Antihypertensives — MCQs

Q: A 25 -year-old male presented to the emergency department with head trauma due to a road traffic accident. In the hospital, the patient developed seizures, and an emergency CT scan revealed widespread cerebral edema. Which of the following is the diuretic of choice for cerebral edema in this patient?

A. Mannitol. ***Mannitol*** - **Mannitol** is an osmotic diuretic that creates an osmotic gradient, drawing water from the brain parenchyma into the intravascular space, thereby reducing **cerebral edema**. - Its rapid onset of action and ability to cross an intact blood-brain barrier sparingly makes it the drug of choice for acute management of elevated intracranial pressure due to **cerebral edema**. *Spironolactone* - **Spironolactone** is a potassium-sparing diuretic that primarily acts on the distal tubules to inhibit aldosterone, leading to sodium and water excretion. - It is unsuitable for acute cerebral edema as its diuretic effect is too slow and it does not create the necessary osmotic gradient. *Furosemide* - **Furosemide** is a loop diuretic that inhibits sodium-potassium-chloride co-transporter in the loop of Henle, leading to significant diuresis. - While it can remove fluid, it does not create the same osmotic gradient as mannitol and is less effective at rapidly reducing **intracranial pressure** directly related to cerebral edema. *Hydrochlorothiazide* - **Hydrochlorothiazide** is a thiazide diuretic that primarily acts on the distal convoluted tubule to inhibit sodium reabsorption. - Its diuretic action is too slow and relatively mild for the acute management of severe conditions like **cerebral edema**. *Acetazolamide* - **Acetazolamide** is a carbonic anhydrase inhibitor that reduces CSF production and has a role in chronic management of idiopathic intracranial hypertension. - However, it is not suitable for acute cerebral edema following trauma as its onset is too slow and its diuretic effect is relatively weak compared to osmotic diuretics.

Q: A person was taking an antihypertensive drug and continued taking it despite developing constipation, dry mouth, and dizziness. He was taking it regularly but forgot to take it during a trip abroad and has now developed a hypertensive emergency. Which antihypertensive was he likely taking?

Clonidine. **Clonidine** - The described symptoms of **constipation, dry mouth, and dizziness** are common side effects of **clonidine**, an alpha-2 adrenergic agonist. - The development of a **hypertensive emergency** upon abrupt cessation of the drug strongly suggests clonidine, as it is known for causing **rebound hypertension** due to a sudden increase in sympathetic outflow. *Amlodipine* - **Amlodipine**, a dihydropyridine calcium channel blocker, primarily causes **peripheral edema, headache, and flushing**, not typically constipation or rebound hypertension upon withdrawal. - While it can cause dizziness, the combination of side effects and withdrawal symptoms does not fit amlodipine. *Lisinopril* - **Lisinopril**, an ACE inhibitor, is known for causing **cough and angioedema**. - It does not typically cause constipation, dry mouth, or rebound hypertension upon discontinuation. *Telmisartan* - **Telmisartan**, an angiotensin receptor blocker (ARB), generally has a **favorable side effect profile** and does not commonly cause constipation or dry mouth. - Withdrawal of ARBs does not typically lead to a **hypertensive emergency** in the way clonidine does. *Metoprolol* - **Metoprolol**, a beta-blocker, can cause **fatigue and bradycardia** but does not typically cause the anticholinergic effects (dry mouth, constipation) seen with clonidine. - While abrupt withdrawal of beta-blockers can lead to rebound tachycardia and hypertension, the severity and acute nature of the hypertensive emergency described is more characteristic of clonidine withdrawal.

Q: A patient presents with hypertension and has a history of renal stones, along with several episodes of renal colic. Which diuretic is the most appropriate to use?

Hydrochlorothiazide. **Hydrochlorothiazide** - **Thiazide diuretics** like hydrochlorothiazide reduce urinary calcium excretion, which is beneficial in patients with a history of **calcium renal stones**. - This effect helps prevent the recurrence of renal stones while also treating hypertension. - Among thiazide and thiazide-like diuretics, hydrochlorothiazide has the **most established evidence** for preventing calcium stone recurrence. *Furosemide* - Furosemide is a **loop diuretic** that increases urinary calcium excretion, which would exacerbate the risk of renal stone formation. - While effective for hypertension, its effect on calcium makes it unsuitable for this patient. *Ethacrynic acid* - Ethacrynic acid is also a **loop diuretic** with similar effects to furosemide, including increasing urinary calcium excretion. - This makes it an inappropriate choice for a patient with a history of renal stones. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that works by antagonizing aldosterone, primarily affecting sodium and potassium excretion. - It does not significantly impact urinary calcium excretion in a way that would prevent calcium renal stones, nor is it a first-line agent for hypertension with co-existing renal stones. *Indapamide* - Indapamide is a **thiazide-like diuretic** with some calcium-retaining properties, but it is less effective than hydrochlorothiazide in reducing calcium excretion. - While it can be used for hypertension, **hydrochlorothiazide is preferred** specifically for preventing calcium stone recurrence due to stronger evidence and greater effect on reducing urinary calcium.

Q: Which of the following cardioselective betablockers has been shown to decrease mortality in patients with congestive heart failure?

Bisoprolol. ***Bisoprolol*** - **Bisoprolol** is a highly cardioselective beta-1 blocker that has been extensively studied and proven to reduce mortality and morbidity in patients with **systolic congestive heart failure**. - It is one of the **"big three" beta-blockers** (along with **carvedilol** and **metoprolol succinate**) recommended for chronic heart failure management by major cardiology guidelines, supported by the **CIBIS-II trial**. *Atenolol* - **Atenolol** is a cardioselective beta-1 blocker commonly used for hypertension and angina. - Despite being cardioselective, it has **not been shown to reduce mortality** in patients with chronic heart failure and is generally **not recommended** for this indication due to lack of supportive clinical trial evidence. *Propranolol* - **Propranolol** is a non-selective beta-blocker that blocks both beta-1 and beta-2 receptors. - While effective for conditions like angina and arrhythmias, it is generally **not recommended** for chronic heart failure due to its non-selectivity and lack of evidence for mortality reduction in this specific patient population. *Labetalol* - **Labetalol** is an alpha- and beta-adrenergic blocker, often used in hypertensive emergencies and for managing hypertension in pregnancy. - It is **not indicated** for mortality reduction in chronic heart failure due to its different pharmacological profile and lack of clinical trial evidence supporting its use for this purpose. *Pindolol* - **Pindolol** is a non-selective beta-blocker with **intrinsic sympathomimetic activity (ISA)**, meaning it partially stimulates beta-receptors while blocking the effects of norepinephrine and epinephrine. - Beta-blockers with ISA are generally **contraindicated** in heart failure because their partial agonist activity can potentially worsen myocardial function, and they have not shown any mortality benefit.

Q: A hypertensive patient wants to conceive. Which of the following medications needs to be stopped before pregnancy?

ACE inhibitors. ***ACE inhibitors*** - **ACE inhibitors** are **teratogenic** and can cause **fetal kidney damage**, **oligohydramnios**, and **fetal death** if used during pregnancy. - They should be discontinued before conception or immediately upon pregnancy confirmation, and an alternative safe antihypertensive should be initiated. *Alpha Methyl dopa* - **Alpha-methyldopa** is considered one of the **first-line agents** for managing **hypertension in pregnancy** due to its established safety profile. - It reduces peripheral resistance without significantly affecting renal or uteroplacental blood flow. *Calcium Channel Blockers* - **Calcium channel blockers (CCBs)** like nifedipine and amlodipine are **generally considered safe** for use during pregnancy, especially dihydropyridines. - They are often used as **second-line treatments** for managing hypertension in pregnant women. *Labetalol* - **Labetalol** is a **beta-blocker** that is widely used and considered **safe** for treating **hypertension in pregnancy**. - It effectively lowers blood pressure without significant adverse effects on the fetus. *Hydralazine* - **Hydralazine** is a direct vasodilator that is **safe** for use in pregnancy and is commonly used for **acute management** of severe hypertension in pregnant women. - It has a long history of safe use during pregnancy without teratogenic effects.

Q: A 38-year-old male presents to his primary care doctor with 8 months of uncontrollable anxiety. He states that he experiences overwhelming anxiety and worry in performing just ordinary tasks of daily living. He is started on venlafaxine for treatment of generalized anxiety disorder. Which of the following is a potential side effect of this medication?

Hypertension. ***Hypertension*** - **Venlafaxine** is a serotonin-norepinephrine reuptake inhibitor (SNRI) that can increase **blood pressure**, particularly at higher doses, due to its effect on norepinephrine reuptake. - Patients initiating venlafaxine should have their **blood pressure monitored** regularly. *Priapism* - **Priapism** (a prolonged erection) is a rare but severe side effect more commonly associated with certain atypical antipsychotics (e.g., trazodone) or alpha-blockers, not typically venlafaxine. - While various antidepressant classes can affect sexual function, priapism is not a characteristic side effect of SNRIs like venlafaxine. *Increased urination* - **Increased urination** is not a common or significant side effect of venlafaxine. - Antidepressants can sometimes cause urinary retention or hesitancy due to anticholinergic effects, but venlafaxine has relatively weak anticholinergic properties. *Weight gain* - While some antidepressants, particularly some tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs), are associated with **weight gain**, venlafaxine is often considered weight-neutral or may even cause **modest weight loss** in some individuals. - Significant weight gain is not a primary side effect to anticipate with venlafaxine. *Seizures* - Although any antidepressant can lower the **seizure threshold** to some extent, venlafaxine's risk is generally low and comparable to other antidepressants, especially at therapeutic doses. - A history of seizures often warrants careful consideration when prescribing antidepressants, but seizures are not a common or dose-limiting side effect for most patients taking venlafaxine.

Q: A 56-year-old woman presents to the physician for a routine health maintenance examination. She has no history of a serious illness and takes no medications. She exercises every day and follows a healthy diet. She does not smoke and consumes alcohol moderately. There is no family history of chronic disease. Her blood pressure is 145/92 mm Hg, which is confirmed on a repeat measurement. Her BMI is 23 kg/m2. The physical examination shows no abnormal findings. The laboratory test results show: Serum Total cholesterol 193 mg/dL Low-density lipoprotein (LDL-C) 124 mg/dL High-density lipoprotein (HDL-C) 40 mg/dL Triglycerides 148 mg/dL Her 10-year risk of CVD is 3.6%. Antihypertensive medication is initiated for her elevated blood pressure. Which of the following is the most appropriate additional pharmacotherapy at this time?

Atorvastatin. ***Atorvastatin*** - This patient meets the criteria for initiating a **moderate-intensity statin** due to her **elevated LDL-C (124 mg/dL)**, despite having a 10-year CVD risk below 7.5%. - The patient has **hypertension (BP 145/92 mmHg)** and elevated LDL-C, which are major risk factors for **atherosclerotic cardiovascular disease (ASCVD)**. Current guidelines recommend statin therapy for primary prevention in individuals with LDL-C ≥ 70 mg/dL and multiple ASCVD risk factors. *No pharmacotherapy at this time* - This is incorrect because the patient has several risk factors (hypertension, elevated LDL-C for her age) that warrant intervention, specifically for **dyslipidemia**. - While her 10-year CVD risk is low, individual risk factors such as **hypertension** and **elevated LDL-C** still need to be addressed to prevent future events. *Evolocumab* - **Evolocumab** is a PCSK9 inhibitor, typically reserved for patients with very high LDL-C who cannot achieve target levels with statins, or in cases of **familial hypercholesterolemia**. - It is not a first-line agent for a patient with moderately elevated LDL-C and no history of cardiovascular events. *Cholestyramine* - **Cholestyramine** is a **bile acid sequestrant** used primarily to lower LDL-C, but it can sometimes *increase triglycerides*. - Statins are generally preferred as a first-line therapy because they provide superior LDL-C reduction and have pleiotropic effects, including anti-inflammatory properties, making them more effective for global cardiovascular risk reduction. *Ezetimibe* - **Ezetimibe** works by inhibiting cholesterol absorption and is often used as add-on therapy for patients who cannot reach their LDL-C goals with statins alone, or for those who are **statin-intolerant**. - It is not recommended as initial monotherapy in this patient given their moderate LDL-C elevation and the clear indication for a statin.

A 25 -year-old male presented to the emergency department with head trauma due to a road traffic accident. In the hospital, the patient developed seizures, and an emergency CT scan revealed widespread cerebral edema. Which of the following is the diuretic of choice for cerebral edema in this patient?

A person was taking an antihypertensive drug and continued taking it despite developing constipation, dry mouth, and dizziness. He was taking it regularly but forgot to take it during a trip abroad and has now developed a hypertensive emergency. Which antihypertensive was he likely taking?

A patient presents with hypertension and has a history of renal stones, along with several episodes of renal colic. Which diuretic is the most appropriate to use?

Which of the following cardioselective betablockers has been shown to decrease mortality in patients with congestive heart failure?

A hypertensive patient wants to conceive. Which of the following medications needs to be stopped before pregnancy?

A patient with hypertension, peripheral edema, and chronic kidney disease (CKD) presents for management. Which of the following medications would be the best choice?

A 38-year-old male presents to his primary care doctor with 8 months of uncontrollable anxiety. He states that he experiences overwhelming anxiety and worry in performing just ordinary tasks of daily living. He is started on venlafaxine for treatment of generalized anxiety disorder. Which of the following is a potential side effect of this medication?

A 61-year-old woman presents to her primary care provider with complaints of fatigue, weight gain of 5.5 kg (12.1 lb) and intermittent nausea over the past 4 months. She denies any changes to her diet. She has had type 2 diabetes mellitus for the past 27 years complicated by diabetic neuropathy. Vital signs include: temperature 37.0°C (98.6°F), blood pressure 167/98 mm Hg and pulse 80/min. Physical examination reveals bilateral pitting lower-extremity edema. Fundoscopic examination reveals bilateral micro-aneurysms and cotton wool patches. Her serum creatinine is 2.6 mg/dL. Which of the following is the best initial therapy for this patient?

A 63-year-old woman presents to her physician with hip pain. She has had pain in both hips for almost 5 years, and it has progressed over time. She notes that it gets worse as the day goes on, making it difficult for her to walk her small dog in the evening. She has a little morning stiffness which subsides quickly after she starts to walk. In the last week, her pain became worse. The past medical history includes hypertension, hyperlipidemia, and mild hypothyroidism. She takes captopril, atorvastatin, and levothyroxine. She has also been taking acetaminophen almost every day with a dose increase up to 4,000 mg, but there is no significant decrease in pain. Both of her parents died in their 80's. The blood pressure is 135/85 mm Hg, heart rate is 74/min, respiratory rate is 12/min, and the temperature is 37.0°C (98.6°F). The BMI is 35 kg/m2. On physical examination, the leg strength is normal bilaterally. The neurological exam of both upper and lower extremities is normal. Her gait is difficult to assess due to pain. A radiograph of her left hip joint is shown in the image below. Which of the following is the most appropriate treatment for the patient’s condition?

Q10

A 56-year-old woman presents to the physician for a routine health maintenance examination. She has no history of a serious illness and takes no medications. She exercises every day and follows a healthy diet. She does not smoke and consumes alcohol moderately. There is no family history of chronic disease. Her blood pressure is 145/92 mm Hg, which is confirmed on a repeat measurement. Her BMI is 23 kg/m2. The physical examination shows no abnormal findings. The laboratory test results show: Serum Total cholesterol 193 mg/dL Low-density lipoprotein (LDL-C) 124 mg/dL High-density lipoprotein (HDL-C) 40 mg/dL Triglycerides 148 mg/dL Her 10-year risk of CVD is 3.6%. Antihypertensive medication is initiated for her elevated blood pressure. Which of the following is the most appropriate additional pharmacotherapy at this time?

Antihypertensives US Medical PG Practice Questions and MCQs

Question 1: A 25 -year-old male presented to the emergency department with head trauma due to a road traffic accident. In the hospital, the patient developed seizures, and an emergency CT scan revealed widespread cerebral edema. Which of the following is the diuretic of choice for cerebral edema in this patient?

A. A. Mannitol (Correct Answer)
B. B. Spironolactone
C. C. Furosemide
D. D. Hydrochlorothiazide
E. E. Acetazolamide

Explanation: ***Mannitol*** - **Mannitol** is an osmotic diuretic that creates an osmotic gradient, drawing water from the brain parenchyma into the intravascular space, thereby reducing **cerebral edema**. - Its rapid onset of action and ability to cross an intact blood-brain barrier sparingly makes it the drug of choice for acute management of elevated intracranial pressure due to **cerebral edema**. *Spironolactone* - **Spironolactone** is a potassium-sparing diuretic that primarily acts on the distal tubules to inhibit aldosterone, leading to sodium and water excretion. - It is unsuitable for acute cerebral edema as its diuretic effect is too slow and it does not create the necessary osmotic gradient. *Furosemide* - **Furosemide** is a loop diuretic that inhibits sodium-potassium-chloride co-transporter in the loop of Henle, leading to significant diuresis. - While it can remove fluid, it does not create the same osmotic gradient as mannitol and is less effective at rapidly reducing **intracranial pressure** directly related to cerebral edema. *Hydrochlorothiazide* - **Hydrochlorothiazide** is a thiazide diuretic that primarily acts on the distal convoluted tubule to inhibit sodium reabsorption. - Its diuretic action is too slow and relatively mild for the acute management of severe conditions like **cerebral edema**. *Acetazolamide* - **Acetazolamide** is a carbonic anhydrase inhibitor that reduces CSF production and has a role in chronic management of idiopathic intracranial hypertension. - However, it is not suitable for acute cerebral edema following trauma as its onset is too slow and its diuretic effect is relatively weak compared to osmotic diuretics.

Question 2: A person was taking an antihypertensive drug and continued taking it despite developing constipation, dry mouth, and dizziness. He was taking it regularly but forgot to take it during a trip abroad and has now developed a hypertensive emergency. Which antihypertensive was he likely taking?

A. Amlodipine
B. Clonidine (Correct Answer)
C. Lisinopril
D. Telmisartan
E. Metoprolol

Explanation: **Clonidine** - The described symptoms of **constipation, dry mouth, and dizziness** are common side effects of **clonidine**, an alpha-2 adrenergic agonist. - The development of a **hypertensive emergency** upon abrupt cessation of the drug strongly suggests clonidine, as it is known for causing **rebound hypertension** due to a sudden increase in sympathetic outflow. *Amlodipine* - **Amlodipine**, a dihydropyridine calcium channel blocker, primarily causes **peripheral edema, headache, and flushing**, not typically constipation or rebound hypertension upon withdrawal. - While it can cause dizziness, the combination of side effects and withdrawal symptoms does not fit amlodipine. *Lisinopril* - **Lisinopril**, an ACE inhibitor, is known for causing **cough and angioedema**. - It does not typically cause constipation, dry mouth, or rebound hypertension upon discontinuation. *Telmisartan* - **Telmisartan**, an angiotensin receptor blocker (ARB), generally has a **favorable side effect profile** and does not commonly cause constipation or dry mouth. - Withdrawal of ARBs does not typically lead to a **hypertensive emergency** in the way clonidine does. *Metoprolol* - **Metoprolol**, a beta-blocker, can cause **fatigue and bradycardia** but does not typically cause the anticholinergic effects (dry mouth, constipation) seen with clonidine. - While abrupt withdrawal of beta-blockers can lead to rebound tachycardia and hypertension, the severity and acute nature of the hypertensive emergency described is more characteristic of clonidine withdrawal.

Question 3: A patient presents with hypertension and has a history of renal stones, along with several episodes of renal colic. Which diuretic is the most appropriate to use?

A. Furosemide
B. Hydrochlorothiazide (Correct Answer)
C. Ethacrynic acid
D. Spironolactone
E. Indapamide

Explanation: **Hydrochlorothiazide** - **Thiazide diuretics** like hydrochlorothiazide reduce urinary calcium excretion, which is beneficial in patients with a history of **calcium renal stones**. - This effect helps prevent the recurrence of renal stones while also treating hypertension. - Among thiazide and thiazide-like diuretics, hydrochlorothiazide has the **most established evidence** for preventing calcium stone recurrence. *Furosemide* - Furosemide is a **loop diuretic** that increases urinary calcium excretion, which would exacerbate the risk of renal stone formation. - While effective for hypertension, its effect on calcium makes it unsuitable for this patient. *Ethacrynic acid* - Ethacrynic acid is also a **loop diuretic** with similar effects to furosemide, including increasing urinary calcium excretion. - This makes it an inappropriate choice for a patient with a history of renal stones. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that works by antagonizing aldosterone, primarily affecting sodium and potassium excretion. - It does not significantly impact urinary calcium excretion in a way that would prevent calcium renal stones, nor is it a first-line agent for hypertension with co-existing renal stones. *Indapamide* - Indapamide is a **thiazide-like diuretic** with some calcium-retaining properties, but it is less effective than hydrochlorothiazide in reducing calcium excretion. - While it can be used for hypertension, **hydrochlorothiazide is preferred** specifically for preventing calcium stone recurrence due to stronger evidence and greater effect on reducing urinary calcium.

Question 4: Which of the following cardioselective betablockers has been shown to decrease mortality in patients with congestive heart failure?

A. Propranolol
B. Bisoprolol (Correct Answer)
C. Labetalol
D. Pindolol
E. Atenolol

Explanation: ***Bisoprolol*** - **Bisoprolol** is a highly cardioselective beta-1 blocker that has been extensively studied and proven to reduce mortality and morbidity in patients with **systolic congestive heart failure**. - It is one of the **"big three" beta-blockers** (along with **carvedilol** and **metoprolol succinate**) recommended for chronic heart failure management by major cardiology guidelines, supported by the **CIBIS-II trial**. *Atenolol* - **Atenolol** is a cardioselective beta-1 blocker commonly used for hypertension and angina. - Despite being cardioselective, it has **not been shown to reduce mortality** in patients with chronic heart failure and is generally **not recommended** for this indication due to lack of supportive clinical trial evidence. *Propranolol* - **Propranolol** is a non-selective beta-blocker that blocks both beta-1 and beta-2 receptors. - While effective for conditions like angina and arrhythmias, it is generally **not recommended** for chronic heart failure due to its non-selectivity and lack of evidence for mortality reduction in this specific patient population. *Labetalol* - **Labetalol** is an alpha- and beta-adrenergic blocker, often used in hypertensive emergencies and for managing hypertension in pregnancy. - It is **not indicated** for mortality reduction in chronic heart failure due to its different pharmacological profile and lack of clinical trial evidence supporting its use for this purpose. *Pindolol* - **Pindolol** is a non-selective beta-blocker with **intrinsic sympathomimetic activity (ISA)**, meaning it partially stimulates beta-receptors while blocking the effects of norepinephrine and epinephrine. - Beta-blockers with ISA are generally **contraindicated** in heart failure because their partial agonist activity can potentially worsen myocardial function, and they have not shown any mortality benefit.

Question 5: A hypertensive patient wants to conceive. Which of the following medications needs to be stopped before pregnancy?

A. ACE inhibitors (Correct Answer)
B. Alpha Methyl dopa
C. Calcium Channel Blockers
D. Labetalol
E. Hydralazine

Explanation: ***ACE inhibitors*** - **ACE inhibitors** are **teratogenic** and can cause **fetal kidney damage**, **oligohydramnios**, and **fetal death** if used during pregnancy. - They should be discontinued before conception or immediately upon pregnancy confirmation, and an alternative safe antihypertensive should be initiated. *Alpha Methyl dopa* - **Alpha-methyldopa** is considered one of the **first-line agents** for managing **hypertension in pregnancy** due to its established safety profile. - It reduces peripheral resistance without significantly affecting renal or uteroplacental blood flow. *Calcium Channel Blockers* - **Calcium channel blockers (CCBs)** like nifedipine and amlodipine are **generally considered safe** for use during pregnancy, especially dihydropyridines. - They are often used as **second-line treatments** for managing hypertension in pregnant women. *Labetalol* - **Labetalol** is a **beta-blocker** that is widely used and considered **safe** for treating **hypertension in pregnancy**. - It effectively lowers blood pressure without significant adverse effects on the fetus. *Hydralazine* - **Hydralazine** is a direct vasodilator that is **safe** for use in pregnancy and is commonly used for **acute management** of severe hypertension in pregnant women. - It has a long history of safe use during pregnancy without teratogenic effects.

Question 6: A patient with hypertension, peripheral edema, and chronic kidney disease (CKD) presents for management. Which of the following medications would be the best choice?

A. Aliskiren
B. Beta blocker
C. Prazosin
D. Chlorthalidone (Correct Answer)
E. Furosemide

Explanation: ***Chlorthalidone*** - **Chlorthalidone** is a **thiazide-type diuretic** that is effective in managing hypertension and associated edema, even in patients with moderate CKD (eGFR >30 mL/min/1.73m²). - Its long duration of action and proven cardiovascular benefits make it a good choice for hypertension control in this clinical context. - **Superior to loop diuretics for blood pressure control** and has better evidence for reducing cardiovascular events. *Aliskiren* - **Aliskiren** is a **direct renin inhibitor** that blocks the renin-angiotensin-aldosterone system (RAAS). - However, in patients with CKD, particularly those with existing hypertension and peripheral edema, it is generally **not preferred due to potential risks** of hyperkalemia, renal impairment, and hypotension, especially when combined with ACE inhibitors or ARBs. *Beta blocker* - While **beta-blockers** can treat hypertension, they are **not the first-line choice** for patients with both hypertension and significant peripheral edema. - They also have potential side effects like bradycardia, fatigue, and bronchospasm, and may mask symptoms of hypoglycemia in diabetic patients. *Prazosin* - **Prazosin** is an **alpha-1 adrenergic blocker** that can reduce blood pressure but is primarily used for **hypertension with benign prostatic hyperplasia (BPH)** due to its dilating effect on the bladder neck. - It's **not typically a first-line agent** for essential hypertension with peripheral edema and carries a risk of **first-dose syncope**. *Furosemide* - **Furosemide** is a **loop diuretic** that is more effective than thiazides for managing edema, especially in severe CKD (eGFR <30). - However, for **blood pressure control** in patients with moderate CKD and edema, **thiazide-type diuretics like chlorthalidone are preferred** due to their superior antihypertensive efficacy and cardiovascular benefits. - Loop diuretics have a shorter duration of action and are less effective for chronic hypertension management.

Question 7: A 38-year-old male presents to his primary care doctor with 8 months of uncontrollable anxiety. He states that he experiences overwhelming anxiety and worry in performing just ordinary tasks of daily living. He is started on venlafaxine for treatment of generalized anxiety disorder. Which of the following is a potential side effect of this medication?

A. Hypertension (Correct Answer)
B. Priapism
C. Increased urination
D. Weight gain
E. Seizures

Explanation: ***Hypertension*** - **Venlafaxine** is a serotonin-norepinephrine reuptake inhibitor (SNRI) that can increase **blood pressure**, particularly at higher doses, due to its effect on norepinephrine reuptake. - Patients initiating venlafaxine should have their **blood pressure monitored** regularly. *Priapism* - **Priapism** (a prolonged erection) is a rare but severe side effect more commonly associated with certain atypical antipsychotics (e.g., trazodone) or alpha-blockers, not typically venlafaxine. - While various antidepressant classes can affect sexual function, priapism is not a characteristic side effect of SNRIs like venlafaxine. *Increased urination* - **Increased urination** is not a common or significant side effect of venlafaxine. - Antidepressants can sometimes cause urinary retention or hesitancy due to anticholinergic effects, but venlafaxine has relatively weak anticholinergic properties. *Weight gain* - While some antidepressants, particularly some tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs), are associated with **weight gain**, venlafaxine is often considered weight-neutral or may even cause **modest weight loss** in some individuals. - Significant weight gain is not a primary side effect to anticipate with venlafaxine. *Seizures* - Although any antidepressant can lower the **seizure threshold** to some extent, venlafaxine's risk is generally low and comparable to other antidepressants, especially at therapeutic doses. - A history of seizures often warrants careful consideration when prescribing antidepressants, but seizures are not a common or dose-limiting side effect for most patients taking venlafaxine.

Question 8: A 61-year-old woman presents to her primary care provider with complaints of fatigue, weight gain of 5.5 kg (12.1 lb) and intermittent nausea over the past 4 months. She denies any changes to her diet. She has had type 2 diabetes mellitus for the past 27 years complicated by diabetic neuropathy. Vital signs include: temperature 37.0°C (98.6°F), blood pressure 167/98 mm Hg and pulse 80/min. Physical examination reveals bilateral pitting lower-extremity edema. Fundoscopic examination reveals bilateral micro-aneurysms and cotton wool patches. Her serum creatinine is 2.6 mg/dL. Which of the following is the best initial therapy for this patient?

A. Perindopril (Correct Answer)
B. Diltiazem
C. Hydrochlorothiazide
D. Labetalol
E. Metoprolol

Explanation: ***Perindopril*** - This patient exhibits signs of **diabetic nephropathy**, including a history of long-standing diabetes, elevated blood pressure, peripheral edema, and a significantly increased serum creatinine. **ACE inhibitors** like perindopril are the preferred initial therapy for hypertension in diabetic patients with renal disease, as they **reduce proteinuria** and **slow the progression of kidney damage**. - The presence of **retinopathy** (micro-aneurysms and cotton wool patches) further supports the diagnosis of microvascular complications of diabetes, for which ACE inhibitors offer protective benefits. *Diltiazem* - While **non-dihydropyridine calcium channel blockers** such as diltiazem can reduce proteinuria and are an option for blood pressure control in diabetic nephropathy, they are generally considered **second-line** after ACE inhibitors or ARBs. - They do not offer the same extensive evidence for preventing the progression of renal disease as ACE inhibitors. *Hydrochlorothiazide* - **Thiazide diuretics** can be used as **antihypertensive agents**, but they are **less effective** in patients with a **creatinine clearance below 30 mL/min**, which is likely the case here with a creatinine of 2.6 mg/dL. - They do not provide the specific renoprotective benefits, such as reducing proteinuria, that ACE inhibitors offer in diabetic nephropathy. *Labetalol* - **Labetalol is a beta-blocker/alpha-blocker** that can effectively lower blood pressure. However, it does not offer the specific renoprotective benefits, such as significant reduction in proteinuria or slowing the progression of kidney disease, that **ACE inhibitors** provide in diabetic nephropathy. - While useful for blood pressure control, it's not the **best initial therapy** in this specific context. *Metoprolol* - **Metoprolol is a beta-1 selective beta-blocker** used for hypertension and other cardiac conditions. Similar to labetalol, while it can lower blood pressure, it **does not offer the specific renoprotective advantages** of ACE inhibitors in diabetic patients with nephropathy. - Beta-blockers are generally not the first-line choice for hypertension in diabetic patients with proteinuria, especially when ACE inhibitors are indicated.

Question 9: A 63-year-old woman presents to her physician with hip pain. She has had pain in both hips for almost 5 years, and it has progressed over time. She notes that it gets worse as the day goes on, making it difficult for her to walk her small dog in the evening. She has a little morning stiffness which subsides quickly after she starts to walk. In the last week, her pain became worse. The past medical history includes hypertension, hyperlipidemia, and mild hypothyroidism. She takes captopril, atorvastatin, and levothyroxine. She has also been taking acetaminophen almost every day with a dose increase up to 4,000 mg, but there is no significant decrease in pain. Both of her parents died in their 80's. The blood pressure is 135/85 mm Hg, heart rate is 74/min, respiratory rate is 12/min, and the temperature is 37.0°C (98.6°F). The BMI is 35 kg/m2. On physical examination, the leg strength is normal bilaterally. The neurological exam of both upper and lower extremities is normal. Her gait is difficult to assess due to pain. A radiograph of her left hip joint is shown in the image below. Which of the following is the most appropriate treatment for the patient’s condition?

A. Addition of intra-articular hyaluronic acid injections
B. Switching acetaminophen to meloxicam (Correct Answer)
C. Switching acetaminophen to oral methylprednisolone
D. Increasing the dose of acetaminophen to 6000 mg per day
E. Addition of glucosamine supplementation

Explanation: ***Switching acetaminophen to meloxicam*** - The patient presents with classic symptoms of **osteoarthritis (OA)**, including progressive hip pain, worsening with activity, and minimal morning stiffness, along with radiographic evidence of severe OA (joint space narrowing, osteophytes, subchondral sclerosis, and cysts) in the left hip. As **acetaminophen (paracetamol)** at 4000 mg/day is no longer effective, a **non-steroidal anti-inflammatory drug (NSAID)** like meloxicam is the next appropriate step for pain management in OA, especially given her relatively healthy status for NSAID use. - **Meloxicam** is a selective COX-2 inhibitor, which may have a slightly lower risk of gastrointestinal side effects compared to non-selective NSAIDs, making it a reasonable choice if tolerated. *Addition of intra-articular hyaluronic acid injections* - **Intra-articular hyaluronic acid injections** (viscosupplementation) are sometimes used in knee osteoarthritis, but their effectiveness in **hip osteoarthritis** is less well-established and generally considered for patients who have failed oral therapies and are not yet candidates for surgery. - Given the severe radiographic findings, this patient is likely beyond the stage where these injections would provide significant long-term relief, and oral NSAIDs should be tried first if acetaminophen failed. *Switching acetaminophen to oral methylprednisolone* - **Oral corticosteroids** like methylprednisolone are generally **not recommended** for the long-term management of osteoarthritis due to significant systemic side effects such as osteoporosis, hyperglycemia, and immunosuppression. - While they can provide temporary pain relief due to their anti-inflammatory properties, their chronic use for OA is discouraged. *Increasing the dose of acetaminophen to 6000 mg per day* - The **maximum recommended daily dose of acetaminophen** for adults is generally 3000-4000 mg (3-4 grams) to avoid **hepatotoxicity**. - Increasing the dose to 6000 mg (6 grams) per day would significantly increase the risk of **severe liver damage** and is therefore contraindicated. *Addition of glucosamine supplementation* - **Glucosamine supplementation** has shown **inconsistent efficacy** in clinical trials for osteoarthritis and is generally not recommended as a primary treatment. - There is little evidence to support its ability to slow disease progression or significantly reduce pain in moderate to severe osteoarthritis, particularly when compared to proven pain management strategies like NSAIDs.

Question 10: A 56-year-old woman presents to the physician for a routine health maintenance examination. She has no history of a serious illness and takes no medications. She exercises every day and follows a healthy diet. She does not smoke and consumes alcohol moderately. There is no family history of chronic disease. Her blood pressure is 145/92 mm Hg, which is confirmed on a repeat measurement. Her BMI is 23 kg/m2. The physical examination shows no abnormal findings. The laboratory test results show: Serum Total cholesterol 193 mg/dL Low-density lipoprotein (LDL-C) 124 mg/dL High-density lipoprotein (HDL-C) 40 mg/dL Triglycerides 148 mg/dL Her 10-year risk of CVD is 3.6%. Antihypertensive medication is initiated for her elevated blood pressure. Which of the following is the most appropriate additional pharmacotherapy at this time?

A. No pharmacotherapy at this time
B. Evolocumab
C. Cholestyramine
D. Ezetimibe
E. Atorvastatin (Correct Answer)

Explanation: ***Atorvastatin*** - This patient meets the criteria for initiating a **moderate-intensity statin** due to her **elevated LDL-C (124 mg/dL)**, despite having a 10-year CVD risk below 7.5%. - The patient has **hypertension (BP 145/92 mmHg)** and elevated LDL-C, which are major risk factors for **atherosclerotic cardiovascular disease (ASCVD)**. Current guidelines recommend statin therapy for primary prevention in individuals with LDL-C ≥ 70 mg/dL and multiple ASCVD risk factors. *No pharmacotherapy at this time* - This is incorrect because the patient has several risk factors (hypertension, elevated LDL-C for her age) that warrant intervention, specifically for **dyslipidemia**. - While her 10-year CVD risk is low, individual risk factors such as **hypertension** and **elevated LDL-C** still need to be addressed to prevent future events. *Evolocumab* - **Evolocumab** is a PCSK9 inhibitor, typically reserved for patients with very high LDL-C who cannot achieve target levels with statins, or in cases of **familial hypercholesterolemia**. - It is not a first-line agent for a patient with moderately elevated LDL-C and no history of cardiovascular events. *Cholestyramine* - **Cholestyramine** is a **bile acid sequestrant** used primarily to lower LDL-C, but it can sometimes *increase triglycerides*. - Statins are generally preferred as a first-line therapy because they provide superior LDL-C reduction and have pleiotropic effects, including anti-inflammatory properties, making them more effective for global cardiovascular risk reduction. *Ezetimibe* - **Ezetimibe** works by inhibiting cholesterol absorption and is often used as add-on therapy for patients who cannot reach their LDL-C goals with statins alone, or for those who are **statin-intolerant**. - It is not recommended as initial monotherapy in this patient given their moderate LDL-C elevation and the clear indication for a statin.

Question 11: A 74-year-old man presents to the clinic for a routine health checkup. He has been hypertensive for the past 20 years, and he has had congestive heart failure for the past 2 years. He is currently on captopril and claims to be compliant with his medication. His most recent echocardiogram report shows that his ejection fraction has been decreasing, so the physician decides to add spironolactone to his drug regimen. Which of the following complications should be most closely monitored for in this patient?

A. Hypernatremia
B. Hyperkalemia (Correct Answer)
C. Azotemia
D. Alkalosis
E. Gynecomastia

Explanation: **Hyperkalemia (Correct)** - **Spironolactone** is a **potassium-sparing diuretic** and aldosterone antagonist, which can lead to increased serum potassium levels - The patient is also on **captopril**, an ACE inhibitor, which also decreases aldosterone and can contribute to hyperkalemia - **This combination significantly increases the risk of hyperkalemia**, making it the most critical complication to monitor closely - Hyperkalemia can lead to life-threatening cardiac arrhythmias, requiring immediate attention *Hypernatremia (Incorrect)* - Spironolactone, by blocking aldosterone, mildly promotes **sodium excretion**, making hypernatremia (high sodium) less likely - While other diuretics can cause hyponatremia due to volume depletion, spironolactone's primary risk isn't dysregulation of sodium leading to hypernatremia *Azotemia (Incorrect)* - Azotemia refers to an increase in **urea and creatinine** in the blood, often indicating kidney dysfunction - While spironolactone can sometimes worsen renal function, it's not the most direct or immediate concern for monitoring compared to potassium levels, especially in a stable patient without acute kidney injury - **ACE inhibitors** like captopril can sometimes induce mild azotemia, but monitoring for hyperkalemia is a more direct and significant concern with the addition of spironolactone *Alkalosis (Incorrect)* - **Spironolactone** can cause **metabolic acidosis** (not alkalosis) due to its effect on potassium and hydrogen excretion, making alkalosis an unlikely complication - Most other diuretics, like loop or thiazide diuretics, are more commonly associated with metabolic alkalosis *Gynecomastia (Incorrect)* - While **gynecomastia** is a known side effect of spironolactone due to its **antiandrogenic effects**, it is a chronic side effect that develops over time - This is not an acute or immediately life-threatening complication requiring close monitoring in the same way hyperkalemia does - The immediate focus of monitoring after starting spironolactone is on electrolyte imbalances, particularly potassium levels

Question 12: A 42-year-old African American woman presents to the physician’s office complaining of sudden onset chest pain. She describes the pain as sharp, non-radiating with improvement when she is sitting up and leaning forward. She denies fever, chills, or a cough, but she has had swollen hands and wrists for the past 3 weeks. Medical history is significant for chronic hypertension. She had an appendectomy at age 12. Medications include hydralazine and folic acid. Vital signs are normal except for a low-grade fever. On examination, the patient is in mild distress, especially in the supine position. The metacarpophalangeal and proximal interphalangeal joints are swollen and tender bilaterally. ECG shows diffuse ST elevations. Her antinuclear antibody is negative. Which of the following additional antibodies are expected to be found in this patient’s serum?

A. Anti-cyclic citrullinated antibodies
B. Anti-histone antibodies (Correct Answer)
C. Anti-topoisomerase I antibodies
D. Anti-mitochondrial antibodies
E. Anti-cardiolipin antibodies

Explanation: ***Anti-histone antibodies*** - The patient's symptoms, including **diffuse ST elevations** (suggesting pericarditis) and joint pain, combined with a history of **hydralazine** use, are highly indicative of **drug-induced lupus**. - **Anti-histone antibodies** are positive in over 95% of cases of drug-induced lupus. *Anti-cyclic citrullinated antibodies* - These antibodies are highly specific for **rheumatoid arthritis**, a condition not supported by the clinical picture (e.g., pericarditis, diffuse ST elevation, specific medication history). - While the patient has arthritis, the **acute pericarditis** and **hydralazine use** point away from rheumatoid arthritis. *Anti-topoisomerase I antibodies* - These antibodies are characteristic of **systemic sclerosis (scleroderma)**, particularly the diffuse cutaneous form. - The patient's presentation with acute pericarditis and reversible joint swelling is not typical for **scleroderma**. *Anti-mitochondrial antibodies* - These antibodies are the serological hallmark of **primary biliary cholangitis**, a chronic autoimmune liver disease. - The patient's symptoms are unrelated to liver disease. *Anti-cardiolipin antibodies* - These antibodies are associated with **antiphospholipid syndrome**, which can cause **thrombosis** and recurrent pregnancy loss but does not typically present with the acute pericarditis and joint pain described in this case, nor is it linked specifically to hydralazine. - While lupus can be associated with antiphospholipid syndrome, the most direct antibody for **drug-induced lupus** is anti-histone.

Question 13: A 65-year-old man presents with hypercholesterolemia. Family history is significant for multiple cardiac deaths and other cardiovascular diseases. The patient reports a 40-pack-year smoking history. BMI is 28 kg/m2. Total cholesterol is 255 mg/dL and low-density lipoprotein (LDL) is more than 175 mg/dL. Lifestyle and dietary modifications are recommended, and the patient is prescribed a hypolipidemic drug. He returns for follow-up 4 weeks later complaining of muscle pains. Laboratory findings are significant for a significant increase in serum transaminases. Which of the following drugs is most likely responsible for this patient's symptoms on follow-up?

A. Atorvastatin (Correct Answer)
B. Glyceryl trinitrate
C. Colestipol
D. Gemfibrozil
E. Nifedipine

Explanation: ***Atorvastatin*** - **Statins** (e.g., atorvastatin) are the **first-line treatment for elevated LDL cholesterol** and commonly cause **myopathy** (muscle pain) and **hepatotoxicity** (elevated transaminases). - The combination of **muscle pains** and significantly increased **serum transaminases** is a classic presentation of statin-induced adverse effects. - Given the patient's LDL >175 mg/dL, a statin would be the most appropriate initial hypolipidemic therapy, making this the most likely culprit. *Glyceryl trinitrate* - This is a **nitrate** used for angina, primarily causing **vasodilation**. - **Not a hypolipidemic agent** and would not be prescribed for hypercholesterolemia. - Common side effects include headache, flushing, and hypotension, but not muscle pain or elevated transaminases. *Colestipol* - **Colestipol** is a **bile acid sequestrant** used as a hypolipidemic agent. - Common side effects are gastrointestinal: **constipation**, bloating, and nausea. - Does **not** typically cause muscle pain or elevated liver enzymes. *Gemfibrozil* - **Gemfibrozil** is a **fibrate** primarily used to lower triglycerides and increase HDL, rather than LDL. - While fibrates can rarely cause myopathy and elevated transaminases (especially when combined with statins), they are **not first-line for isolated LDL elevation**. - Given this patient's primary problem is elevated LDL (>175 mg/dL) with normal triglycerides implied, a statin would be prescribed, not a fibrate. *Nifedipine* - **Nifedipine** is a **calcium channel blocker** used for hypertension and angina. - **Not a hypolipidemic agent** and would not be prescribed for hypercholesterolemia. - Common side effects include peripheral edema, headache, flushing, and dizziness, but not muscle pain or elevated transaminases.

Question 14: A 42-year-old man presents to the emergency room complaining of a painful, swollen tongue that is making it hard to talk and swallow. The patient denies trauma, trouble breathing, and skin rashes. The patient has no known allergies and a minimal past medical history, except for newly diagnosed hypertension for which he was just started on a new medication. The patient is afebrile, the blood pressure is 145/110 mm Hg, the heart rate is 88/min, and the O2 saturation is 97% on room air. What is the mechanism of this reaction?

A. Inhibition of 17-alpha-hydroxylase
B. Histamine release
C. Increased angiotensin II due to decreased receptor response
D. Decreased bradykinin degradation (Correct Answer)
E. Decreased levels of C1 inhibitor protein

Explanation: ***Decreased bradykinin degradation*** - The patient's symptoms of **angioedema** (painful, swollen tongue, difficulty talking and swallowing) rapidly developing after starting a new medication for hypertension strongly suggest an **ACE inhibitor-induced** reaction. - ACE inhibitors block the enzyme that normally degrades **bradykinin**, leading to an accumulation of bradykinin, which causes **vasodilation** and increased vascular permeability, manifesting as angioedema. *Inhibition of 17-alpha-hydroxylase* - This mechanism is associated with drugs like **abiraterone**, used in prostate cancer, affecting **steroid hormone synthesis**. - It would lead to changes in sex hormones and mineralocorticoids, not acute angioedema. *Histamine release* - **Histamine release** is characteristic of type I hypersensitivity reactions (allergies) and typically presents with urticaria, pruritus, and bronchospasm, which are absent here. - Angioedema from histamine release is usually accompanied by other **allergic symptoms**, and the patient denies allergies. *Increased angiotensin II due to decreased receptor response* - This describes the mechanism of **angiotensin receptor blockers (ARBs)**, where the body compensates for receptor blockade by increasing angiotensin II levels. - While ARBs can also cause angioedema, the underlying mechanism for the angioedema is often still related to bradykinin accumulation (though less common than with ACE inhibitors), not increased angiotensin II itself causing the swelling. *Decreased levels of C1 inhibitor protein* - This is the mechanism for **hereditary or acquired angioedema** (HAE/AAE), characterized by recurrent episodes of swelling without urticaria, often triggered by stress or trauma. - While it causes similar symptoms, it is not drug-induced in the typical acute presentation following a new medication, and the patient has no history suggesting a chronic condition.

Question 15: A 44-year-old woman comes to the emergency department after waking up with facial swelling and with difficulties speaking and swallowing. She states that she does not have allergies or recently had insect bites. She has a 4-year history of hypertension and type 2 diabetes mellitus controlled with medication. Her pulse is 110/min, respirations are 20/min, and blood pressure is 140/90 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 97%. On physical exam, she appears uncomfortable, with notable swelling of the lips and tongue. The remainder of the examination shows no abnormalities. Serum C4 levels are within normal limits. Which of the following is the most likely underlying mechanism of this patient's symptoms?

A. Impaired bradykinin metabolism (Correct Answer)
B. IgE-mediated histamine release
C. Anaphylactoid reaction
D. Type 2 hypersensitivity reaction
E. Immune-complex deposition

Explanation: ***Impaired bradykinin metabolism*** - The patient's presentation with **angioedema** (facial swelling, difficulty speaking/swallowing due to lip and tongue swelling) without urticaria or pruritus, and **normal C4 levels**, is consistent with **ACE inhibitor-induced angioedema**. - ACE inhibitors (commonly used for hypertension) block angiotensin-converting enzyme, which normally degrades bradykinin. **Impaired bradykinin breakdown** leads to accumulation, causing increased vascular permeability and angioedema. - Normal C4 levels rule out C1 esterase inhibitor deficiency (hereditary angioedema), making drug-induced angioedema the most likely diagnosis in this patient on antihypertensive therapy. *IgE-mediated histamine release* - This mechanism typically causes **urticaria** (hives), pruritus, and often bronchospasm or hypotension, which are not described in this patient. - **Allergic reactions** involving IgE usually involve a clear allergen exposure, which is absent here ("no allergies or recent insect bites"). *Anaphylactoid reaction* - Anaphylactoid reactions involve mast cell and basophil degranulation, releasing histamine and other mediators **without IgE involvement**. - While it can cause angioedema, it often presents with other systemic symptoms like flushing, itching, and respiratory distress. The absence of a clear trigger and presence of isolated angioedema makes bradykinin-mediated angioedema more likely. *Type 2 hypersensitivity reaction* - Type 2 hypersensitivity involves **antibody-mediated cytotoxicity** and cell lysis, seen in conditions like autoimmune hemolytic anemia or Goodpasture syndrome. - This mechanism does not typically manifest as isolated angioedema with facial and airway swelling. *Immune-complex deposition* - This refers to a **Type 3 hypersensitivity reaction**, where antigen-antibody complexes deposit in tissues, leading to inflammation (e.g., serum sickness, lupus nephritis). - This mechanism does not explain the acute, localized angioedema observed in this patient.

Question 16: A 34-year-old gravida 2, para 1 woman at 37+6 weeks of gestation presents for elective cesarean delivery. She says she has been having increased fatigue over the past few weeks. Past medical history includes gestational hypertension for which she has been taking an antihypertensive drug twice daily since week 24. Her vital signs include: temperature 36.7°C (98.0°F), blood pressure 120/75 mm Hg, pulse 127/min. Physical examination reveals generalized pallor. Her laboratory results reveal normocytic anemia with anisocytosis, hemoglobin of 9 g/dL, a differential with 14% lymphocytes, an ESR of 22 mm/hr, and a reticulocyte production index of 3.1. A direct antiglobulin test is positive. LFTs, creatinine, ferritin level, vitamin B12 level, coagulation studies, and urinalysis are normal. Which of the following is the most likely diagnosis in this patient?

A. Drug-induced immune hemolytic reaction (Correct Answer)
B. Hereditary spherocytosis
C. Preeclampsia
D. Normal pregnancy
E. HELLP syndrome

Explanation: ***Drug-induced immune hemolytic reaction*** - The positive **direct antiglobulin test (DAT)** combined with a history of **antihypertensive drug use** in a pregnant patient with **normocytic anemia** and an **elevated reticulocyte production index** strongly suggests a drug-induced immune hemolytic reaction. - Certain antihypertensive medications, such as **alpha-methyldopa**, are known to cause a positive DAT and hemolytic anemia through drug-induced antibody formation. *Hereditary spherocytosis* - Hereditary spherocytosis causes **hemolytic anemia** but typically presents with a **negative DAT** because it is a membrane defect, not an immune-mediated process. - This is usually a lifelong condition that would likely have been diagnosed earlier, not presenting acutely in late pregnancy. - The positive DAT in this case effectively rules out uncomplicated hereditary spherocytosis. *Preeclampsia* - Preeclampsia involves **hypertension** and **proteinuria**, but **autoimmune hemolytic anemia** with a positive DAT is not a typical feature. - The patient's blood pressure is well-controlled at 120/75 mmHg, and both creatinine and urinalysis are normal, ruling out preeclampsia. *Normal pregnancy* - **Physiological anemia of pregnancy** is typically dilutional and mild, and does not present with a **positive DAT** or a significantly elevated **reticulocyte production index** as seen in this case. - The degree of pallor, tachycardia, and the laboratory findings, particularly the positive DAT, indicate a pathological hemolytic process. *HELLP syndrome* - **HELLP syndrome** (Hemolysis, Elevated Liver enzymes, Low Platelets) is characterized by **thrombocytopenia** and **elevated liver enzymes**, neither of which are present in this patient. - While it involves hemolysis, the normal LFTs and absence of thrombocytopenia rule out HELLP syndrome.

Question 17: Four weeks after starting hydrochlorothiazide, a 49-year-old man with hypertension comes to the physician because of muscle cramps and weakness. His home medications also include amlodipine. His blood pressure today is 176/87 mm Hg. Physical examination shows no abnormalities. The precordial leads of a 12-lead ECG are shown. The addition of which of the following is most likely to have prevented this patient's condition?

A. Hydralazine
B. Clonidine
C. Eplerenone (Correct Answer)
D. Torsemide
E. Nifedipine

Explanation: ***Eplerenone*** - The patient's symptoms of **muscle cramps and weakness** after starting hydrochlorothiazide strongly suggest **hypokalemia**, a common adverse effect of thiazide diuretics. The ECG showing **QT prolongation with prominent U waves** further supports hypokalemia. - **Eplerenone** is a potassium-sparing diuretic and aldosterone antagonist that would counteract the potassium loss caused by hydrochlorothiazide, thus preventing hypokalemia. *Hydralazine* - **Hydralazine** is a direct vasodilator primarily used for hypertension that causes **reflex tachycardia and fluid retention**. - It does not influence potassium levels and would not prevent hypokalemia. *Clonidine* - **Clonidine** is a centrally acting alpha-2 agonist that reduces sympathetic outflow, causing **vasodilation and reduced heart rate**. - It has no known effect on potassium balance and would not prevent diuretic-induced hypokalemia. *Torsemide* - **Torsemide** is a loop diuretic, which is also associated with **potassium wasting**, similar to or even more pronounced than thiazide diuretics. - Adding torsemide would worsen, not prevent, the patient's hypokalemia. *Nifedipine* - **Nifedipine** is a dihydropyridine calcium channel blocker that causes **peripheral vasodilation** and does not impact potassium levels. - It would not prevent hydrochlorothiazide-induced hypokalemia.

Question 18: A 55-year-old man with hypertension, hyperlipidemia, type 2 diabetes mellitus, and asthma comes to the physician because of a 2-month history of intermittent dry, hacking cough. He does not have fever, chest pain, or shortness of breath. He does not smoke cigarettes. Current medications include simvastatin, metformin, albuterol, and ramipril. His temperature is 37°C (98.6°F), pulse is 87/min, and blood pressure is 142/88 mm Hg. Cardiopulmonary examination shows no abnormalities. Which of the following is the most appropriate next step in management?

A. Start dextromethorphan and increase frequency of albuterol
B. Stop ramipril and start candesartan (Correct Answer)
C. Stop simvastatin and start atorvastatin
D. Stop ramipril and start lisinopril
E. Stop albuterol and start salmeterol

Explanation: ***Stop ramipril and start candesartan*** - The patient's **dry, hacking cough** is a common side effect of **ACE inhibitors** like ramipril, occurring in up to 20% of patients [1], [4]. Switching to an **angiotensin receptor blocker (ARB)** like candesartan avoids this side effect as ARBs do not inhibit bradykinin breakdown [1], [4]. - Given the patient's other well-controlled chronic conditions and the absence of other respiratory symptoms (fever, chest pain, shortness of breath), an **ACE inhibitor-induced cough** is the most likely diagnosis [2]. *Start dextromethorphan and increase frequency of albuterol* - **Dextromethorphan** is a cough suppressant, but it does not address the underlying cause of the cough if it is medication-induced, and the cough is likely due to the ramipril. - Increasing the frequency of **albuterol** (a short-acting beta-agonist) is inappropriate as the patient does not have symptoms of asthma exacerbation (e.g., shortness of breath, wheezing), and the cough is dry and persistent, not typical of asthmatic bronchoconstriction [3]. *Stop simvastatin and start atorvastatin* - There is no indication to change the **statin** medication. **Simvastatin** is an effective HMG-CoA reductase inhibitor, and it is not associated with cough. - This change would not address the patient's presenting symptom of a dry, hacking cough. *Stop ramipril and start lisinopril* - Both **ramipril** and **lisinopril** are **ACE inhibitors** and share the same mechanism of action [1]. - Switching from one ACE inhibitor to another would likely result in the continuation of the **cough** side effect, as it is a class effect [4]. *Stop albuterol and start salmeterol* - This patient's dry cough is unlikely to be an asthma symptom given the chronic nature and lack of other respiratory symptoms, suggesting the albuterol is not the issue. - **Salmeterol** is a long-acting beta-agonist (LABA) used for maintenance therapy in asthma; switching to it from albuterol would not address a medication-induced cough and could be inappropriate without further asthma assessment [3].

Question 19: A 60-year-old African-American male with no active medical problems presents to his primary care physician for a general checkup. His blood pressure on the previous visit was 145/90, and his blood pressure at this visit is found to be 150/95. He is prescribed hydrochlorothiazide, a thiazide diuretic, to treat his hypertension. The serum level of which of the following is likely to decrease in response to his treatment?

A. Uric acid
B. Cholesterol
C. Glucose
D. Potassium (Correct Answer)
E. Calcium

Explanation: ***Potassium (Correct Answer)*** - **Thiazide diuretics** inhibit the Na-Cl cotransporter in the **distal convoluted tubule**, leading to increased delivery of sodium to the collecting duct - This increased sodium delivery promotes the **exchange of sodium for potassium** and hydrogen ions, resulting in increased potassium excretion - The result is **hypokalemia** (decreased serum potassium), which is a classic adverse effect requiring monitoring - Potassium supplementation or potassium-sparing diuretics may be needed in some patients *Uric acid (Incorrect)* - Thiazide diuretics **decrease the renal excretion of uric acid** by competing for secretion in the proximal tubule - This leads to **hyperuricemia** (increased serum uric acid), not decreased levels - Can potentially precipitate **gout attacks** in susceptible individuals *Cholesterol (Incorrect)* - Thiazide diuretics cause a **slight increase in total cholesterol** and LDL cholesterol, particularly at higher doses - This effect is generally mild and non-progressive with long-term use - Serum cholesterol increases, not decreases *Glucose (Incorrect)* - Thiazide diuretics can **impair glucose tolerance** and raise blood glucose levels - This effect is particularly notable in patients with pre-existing diabetes or metabolic syndrome - Mechanism involves decreased insulin secretion and increased insulin resistance - Results in **hyperglycemia** (increased serum glucose), not decreased levels *Calcium (Incorrect)* - Thiazide diuretics **decrease calcium excretion** by promoting reabsorption in the distal convoluted tubule - This leads to **increased serum calcium** (hypercalcemia), not decreased levels - This effect can be therapeutically useful in patients with hypercalciuria or kidney stones - Can unmask or worsen hypercalcemia in patients with hyperparathyroidism

Question 20: A 52-year-old man presents to his primary care physician for an annual check-up. He says that he has no significant developments over the last year and that he has been feeling well in general. On presentation, his temperature is 98.6°F (37°C), blood pressure is 140/95 mmHg, pulse is 85/min, and respirations are 12/min. This is the third time that he has had elevated blood pressure so his physician suggests that he start taking a medication for hypertension. The patient is a biologist so he researches this medication after returning home. He finds that the medication can either decrease or increase the level of cyclic adenosine monophosphate depending on whether there is endogenous substrate around. Which of the following medications is most likely being described here?

A. Carvedilol
B. Atenolol
C. Propranolol
D. Esmolol
E. Pindolol (Correct Answer)

Explanation: ***Pindolol*** - **Pindolol** is a **beta-blocker** with **intrinsic sympathomimetic activity (ISA)**, meaning it can act as a partial agonist at beta-adrenergic receptors. - In the absence of endogenous sympathetic stimulation, pindolol can **mildly stimulate** the receptor, increasing cAMP; however, in the presence of high sympathetic tone (endogenous substrate), it acts as an antagonist, **blocking** the effect of norepinephrine and decreasing cAMP. *Carvedilol* - **Carvedilol** is a **non-selective beta-blocker** and an **alpha-1 blocker** used in hypertension and heart failure, but it **lacks intrinsic sympathomimetic activity (ISA)**. - Its effects on cAMP are solely antagonistic, blocking the increase caused by endogenous catecholamines. *Atenolol* - **Atenolol** is a **selective beta-1 blocker** (cardioselective) that **lacks intrinsic sympathomimetic activity (ISA)**. - It works by blocking beta-1 receptors in the heart, leading to decreased heart rate and contractility, thereby reducing blood pressure, and consistently reduces cAMP levels. *Propranolol* - **Propranolol** is a **non-selective beta-blocker** that **lacks intrinsic sympathomimetic activity (ISA)**. - It blocks both beta-1 and beta-2 adrenergic receptors, leading to a decrease in heart rate, contractility, and renin release, consistently leading to a reduction in cAMP. *Esmolol* - **Esmolol** is an **ultrashort-acting, selective beta-1 blocker** that **lacks intrinsic sympathomimetic activity (ISA)**. - Due to its rapid onset and short duration of action, it is primarily used intravenously in acute settings for rate control in arrhythmias or hypertension, consistently reducing cAMP.

Question 21: A 63-year-old African American man presents to the emergency department with edema over his face and difficulty breathing. Past medical history is significant for hypertension and dyslipidemia. He recently began lisinopril and atorvastatin several weeks ago. His father died at 80 years from complications of a stroke and his mother lives in a nursing home. His blood pressure is 135/92 mm Hg, the heart rate is 101/min, the respiratory rate is 21/min, the temperature is 37.0°C (98.6°F). Clinical pathology results suggest a normal C1 esterase inhibitor level. Of the following options, which is the most likely diagnosis?

A. Contact dermatitis
B. Facial lymphedema
C. Drug-induced angioedema (Correct Answer)
D. Scleredema
E. Erysipelas

Explanation: ***Drug-induced angioedema*** - The patient's recent initiation of **lisinopril**, an **ACE inhibitor**, is a strong risk factor for developing **angioedema**, particularly in African American individuals. - The presentation of **facial edema** and **difficulty breathing** without signs of urticaria or pruritus, and normal C1 esterase inhibitor levels, is consistent with ACE inhibitor-induced bradykinin-mediated angioedema. *Contact dermatitis* - This condition typically presents with **pruritus**, **erythema**, and sometimes **vesicles** or **bullae**, which are not described in this patient's symptoms. - It is usually localized to the area of contact with an allergen or irritant and would be unlikely to cause such acute respiratory distress without other prominent skin manifestations. *Facial lymphedema* - **Lymphedema** generally develops **gradually** and is characterized by chronic, non-pitting edema due to impaired lymphatic drainage. - It would not typically present with acute onset **difficulty breathing** as a primary symptom. *Scleredema* - **Scleredema** is a rare connective tissue disorder characterized by diffuse, non-pitting hardening and thickening of the skin, often on the back, neck, and face. - It is a **chronic condition** and does not typically cause acute onset of facial edema and respiratory distress. *Erysipelas* - **Erysipelas** is a superficial skin infection characterized by a well-demarcated, erythematous, warm, and tender plaque, often accompanied by fever and systemic symptoms. - The patient's presentation of painless facial edema and difficulty breathing without clear signs of infection makes erysipelas less likely.

Question 22: A 26-year-old male is brought into the emergency room because he collapsed after working out. The patient is a jockey, and he states that he feels dehydrated and has an upcoming meet for which he needs to lose some weight. On exam, the patient has dry mucosa with cracked lips. His temperature is 98.9 deg F (37.2 deg C), blood pressure is 115/70 mmHg, pulse is 105/min, and respirations are 18/min. The patient's blood pressure upon standing up is 94/65 mmHg. His serum Na+ is 125 mEq/L and K+ is 3.0 mEq/L. His urinalysis reveals Na+ of 35 mEq/L and K+ of 32 mEq/L. The abuse of which of the following is most likely responsible for the patient's presentation?

A. Metoprolol
B. Polyethylene glycol
C. Furosemide (Correct Answer)
D. Spironolactone
E. Amiloride

Explanation: ***Furosemide*** - The patient's **hyponatremia** (Na+ 125 mEq/L), **hypokalemia** (K+ 3.0 mEq/L), and signs of **dehydration** (dry mucosa, cracked lips, orthostatic hypotension, tachycardia) are consistent with the overuse of a **loop diuretic**. - **Furosemide** inhibits the Na-K-2Cl cotransporter in the **thick ascending limb of the loop of Henle**, leading to significant excretion of sodium, potassium, and water. - The **high urinary sodium (35 mEq/L) and potassium (32 mEq/L)** confirm **renal wasting**, which is the hallmark of diuretic abuse (as opposed to GI losses or poor intake, which would show low urinary electrolytes). *Metoprolol* - **Metoprolol** is a beta-blocker that primarily reduces heart rate and blood pressure, but it does not cause significant electrolyte disturbances like **hyponatremia** or **hypokalemia**, or profound dehydration. - While it can lower blood pressure, it would not typically cause the combination of **orthostatic hypotension** and electrolyte abnormalities seen here. *Polyethylene glycol* - **Polyethylene glycol** is an osmotic laxative used for constipation or bowel preparation, which can cause fluid and electrolyte imbalances but typically presents with **diarrhea** and more pronounced gastrointestinal symptoms. - Importantly, GI losses would result in **low urinary electrolytes** (kidney conserving electrolytes), not the high urinary Na+ and K+ seen here. *Spironolactone* - **Spironolactone** is a potassium-sparing diuretic, which would typically cause **hyperkalemia** rather than the **hypokalemia** observed in this patient. - It also does not usually cause severe **hyponatremia** or profound dehydration to the extent seen here. *Amiloride* - **Amiloride** is a potassium-sparing diuretic, similar to spironolactone, and would lead to **potassium retention** (hyperkalemia) rather than severe **hypokalemia**. - It has a mild diuretic effect and would not typically cause the profound **electrolyte imbalances** and dehydration observed.

Question 23: A 57-year-old man with a history of long-standing hypertension is brought to the emergency department because of headache, dyspnea, and blurry vision for 2 hours. He says that he forgot to fill his prescription for his antihypertensive medications last week. His blood pressure is 230/130 mm Hg. Intravenous infusion of sodium nitroprusside is begun and the patient's symptoms slowly resolve. The next day, the patient develops confusion, abdominal pain, and flushing of the skin. Laboratory studies show metabolic acidosis and an elevated serum lactic acid concentration. Treatment is started with a drug that directly binds the toxin responsible for the patient's new symptoms. The patient was most likely given which of the following drugs?

A. Amyl nitrite
B. Dimercaprol
C. Penicillamine
D. Hydroxycobalamin (Correct Answer)
E. Sodium thiosulfate

Explanation: ***Hydroxycobalamin*** - The patient's symptoms of **confusion, abdominal pain, flushing**, **metabolic acidosis**, and **elevated lactic acid** after receiving sodium nitroprusside are highly suggestive of **cyanide toxicity**. - **Hydroxycobalamin** is the antidote that directly binds **cyanide** to form cyanocobalamin, which is then excreted in the urine. *Amyl nitrite* - **Amyl nitrite** is an older treatment for cyanide poisoning that works by inducing **methemoglobinemia**, which then binds cyanide. - While it can be used, it does not directly bind the toxin in the same way the scenario describes for the chosen drug. *Dimercaprol* - **Dimercaprol** is a chelating agent primarily used for **heavy metal poisoning**, such as arsenic, mercury, and lead. - It is not indicated for **cyanide toxicity** and would not be effective in this scenario. *Penicillamine* - **Penicillamine** is a chelating agent used for **copper poisoning** (e.g., in Wilson's disease) and rheumatoid arthritis. - It has no role in the treatment of **cyanide poisoning**. *Sodium thiosulfate* - **Sodium thiosulfate** is another antidote for cyanide poisoning that acts as a **sulfur donor**, facilitating the conversion of cyanide to thiocyanate by the enzyme rhodanese. - While it can be used, the question describes a drug that *directly binds* the toxin, which more accurately characterizes the action of hydroxycobalamin.

Question 24: A 47-year-old female with a history of mild asthma, type II diabetes, hypertension, and hyperlipidemia presents to clinic complaining of swelling in her lips (Image A). She has had no changes to her medications within the past two years. Vital signs are stable. Physical exam is notable for significant erythema around and swelling of the lips. The remainder of her exam is unremarkable. What is the mechanism of action of the drug that has caused her current symptoms?

A. Inhibition of voltage-dependent L-type calcium channels
B. Stimulation of the Beta 2 receptor
C. Inhibition of angiotensin-converting enzyme (Correct Answer)
D. Inhibition of HMG-CoA reductase
E. Inhibition of the Na/K/Cl triple transporter of the thick ascending limb

Explanation: ***Inhibition of angiotensin-converting enzyme*** - The patient's presentation with **lip swelling (angioedema)**, combined with a history of **hypertension**, strongly suggests an adverse effect of an **ACE inhibitor**. - ACE inhibitors prevent the breakdown of **bradykinin**, leading to its accumulation which causes vasodilation and increased vascular permeability, resulting in angioedema. *Inhibition of voltage-dependent L-type calcium channels* - This describes the mechanism of **calcium channel blockers (CCBs)**, which commonly cause peripheral edema (swelling of ankles) and constipation, but not typically angioedema. - While CCBs are used for hypertension, the **lip swelling** points away from this class of medication as the cause. *Stimulation of the Beta 2 receptor* - **Beta-2 agonists** are used to treat asthma, causing bronchodilation, and are not typically associated with angioedema. - Common side effects include tremors, tachycardia, and palpitations, but not significant facial swelling. *Inhibition of HMG-CoA reductase* - This is the mechanism of action for **statins**, used to treat hyperlipidemia. - Statins are generally well-tolerated, but can cause **myalgia** and liver enzyme elevation; angioedema is not a characteristic side effect. *Inhibition of the Na/K/Cl triple transporter of the thick ascending limb* - This mechanism describes **loop diuretics**, such as furosemide, which are used to treat hypertension and edema, but they do not cause angioedema. - Side effects include **hypokalemia**, dehydration, and ototoxicity.

Question 25: A 48-year-old woman with a history of type 2 diabetes mellitus presents to her primary care physician with complaints of headaches, fatigue, dry cough, and frequent episodes of bronchospasm. She was diagnosed with moderate nonproliferative diabetic retinopathy by an ophthalmologist last month. Her blood pressure measured in the clinic is 158/95 mmHg. A 24-hour urine collection is obtained and reveals 9.5 g of protein. On physical examination, the patient has diffuse wheezing, jugular venous distention, and 2+ pitting pretibial edema. Labs are notable for a potassium level of 5.2 mEq/L. Which of the following medications is most likely contributing to this patient’s current presentation?

A. Hydralazine
B. Lisinopril (Correct Answer)
C. Amlodipine
D. Losartan
E. Hydrochlorothiazide

Explanation: ***Lisinopril*** - The patient's **dry cough** and **hyperkalemia** (K+ 5.2 mEq/L) are classic adverse effects of **ACE inhibitors** like lisinopril. - **Dry cough** occurs in 10-20% of patients due to **bradykinin accumulation** (ACE normally degrades bradykinin). - **Hyperkalemia** results from decreased aldosterone production due to reduced angiotensin II levels. - The **massive proteinuria (9.5 g/24hr)** is from the patient's **diabetic nephropathy**, NOT caused by lisinopril. In fact, ACE inhibitors are **first-line renoprotective therapy** that **reduces proteinuria** in diabetic nephropathy. - Note: The bronchospasm/wheezing is atypical for ACE inhibitors (which cause dry cough, not bronchospasm) and might suggest concurrent beta-blocker use, but among the listed options, lisinopril best explains the dry cough and hyperkalemia. *Hydralazine* - Hydralazine is a direct **arteriolar vasodilator** that causes **reflex tachycardia**, headache, and fluid retention. - It can cause drug-induced lupus with chronic use, but does **not cause dry cough or hyperkalemia**. *Amlodipine* - Amlodipine is a **dihydropyridine calcium channel blocker** that commonly causes **peripheral edema** (due to preferential arteriolar dilation causing increased capillary hydrostatic pressure). - It does **not cause dry cough or hyperkalemia**, and the edema is typically ankle edema without JVD or systemic fluid overload. *Losartan* - Losartan is an **angiotensin receptor blocker (ARB)** with similar renoprotective effects to ACE inhibitors. - While ARBs can cause **hyperkalemia**, they do **not cause dry cough** because they don't affect bradykinin metabolism. - ARBs are often used as alternatives in patients who develop ACE inhibitor-induced cough. *Hydrochlorothiazide* - Hydrochlorothiazide is a **thiazide diuretic** that typically causes **hypokalemia** (not hyperkalemia) due to increased urinary potassium loss. - It does not cause dry cough and would actually help reduce fluid overload rather than cause it.

Question 26: A 25-year-old female presents to the emergency room with a heart rate of 32 BPM and a blood pressure of 80/40. She was found by emergency medical services with an empty bottle of propranolol that was taken from her grandmother. Her vital signs do not improve despite IV fluids and oxygen. Which of the following is a first line treatment for overdose?

A. Hemodialysis
B. Adenosine
C. Atropine
D. Vagal maneuvers
E. Glucagon (Correct Answer)

Explanation: ***Glucagon*** - **Glucagon** is the first-line antidote for severe beta-blocker overdose due to its ability to increase **intracellular cAMP** independently of beta-adrenergic receptors, thereby bypassing receptor blockade. - This action leads to increased **heart rate** and **contractility**, improving hemodynamic stability. *Hemodialysis* - **Hemodialysis** is generally ineffective for propanolol overdose as it has a large volume of distribution and is highly protein-bound, making it difficult to clear from the body. - It might be considered for other beta-blockers with different pharmacokinetic profiles but is not first-line for propanolol. *Adenosine* - **Adenosine** is contraindicated in beta-blocker overdose as it can worsen **bradycardia** and **hypotension** by directly inhibiting AV nodal conduction. - Its action as an AV nodal blocker would exacerbate the patient's already compromised cardiac function. *Atropine* - **Atropine** may be used in beta-blocker overdose to counteract the **bradycardia** by blocking muscarinic receptors and increasing heart rate. - However, it often provides only a partial or transient effect in severe beta-blocker toxicity and is not as effective as glucagon in restoring hemodynamic stability. *Vagal maneuvers* - **Vagal maneuvers** increase vagal tone, which would further slow the **heart rate** and worsen bradycardia in the context of beta-blocker overdose. - They are used to terminate supraventricular tachycardias, not to treat bradycardia and hypotension from overdose.

Question 27: A 34-year-old man is being evaluated in an emergency clinic for dizziness and headache after a stressful event at work. He also reports that his face often becomes swollen and he occasionally has difficulty breathing during these spells. Family history is significant for his father who died of a stroke and his mother who often suffers from similar facial swelling. The patient’s blood pressure is 170/80 mm Hg. On physical examination, the patient appears well. Which of the following medications is most likely contraindicated in this patient?

A. The patient has no contraindications.
B. Enalapril (Correct Answer)
C. Sulfadiazine
D. Penicillin
E. Losartan

Explanation: **Enalapril** - The patient's presentation with recurrent facial swelling, occasional difficulty breathing, and a family history of similar symptoms in his mother and stroke in his father is highly suggestive of **hereditary angioedema (HAE)**. - **ACE inhibitors**, such as enalapril, are absolutely contraindicated in patients with HAE because they increase bradykinin levels, which can precipitate or worsen angioedema attacks. *The patient has no contraindications.* - The patient's history of recurrent angioedema episodes and a significant family history strongly suggest an underlying condition, likely HAE, which has clear contraindications for certain medications. - Dismissing contraindications without further investigation into the cause of his angioedema would be unsafe and medically negligent. *Sulfadiazine* - **Sulfonamide antibiotics** are not directly contraindicated in HAE. - While some individuals may have allergies to sulfa drugs, there is no specific link between sulfadiazine and triggering HAE attacks. *Penicillin* - Penicillin is a **beta-lactam antibiotic** and is not known to exacerbate or be contraindicated in hereditary angioedema. - Allergic reactions to penicillin are common, but this is a Type I hypersensitivity, distinct from bradykinin-mediated angioedema. *Losartan* - **Angiotensin Receptor Blockers (ARBs)** like losartan generally do not significantly increase bradykinin levels and are typically considered a safer alternative to ACE inhibitors in patients who might develop ACE inhibitor–induced angioedema. - While rare cases of ARB-induced angioedema have been reported, the risk is considerably lower than with ACE inhibitors, making it a less likely contraindication in this context.

Question 28: A 72-year-old man comes to the emergency department because of blurry vision for the past 3 days. He has also had 4 episodes of right-sided headaches over the past month. He has no significant past medical history. His father died of coronary artery disease at the age of 62 years. His temperature is 37.2°C (99°F), pulse is 94/min, and blood pressure is 232/128 mm Hg. Fundoscopy shows right-sided optic disc blurring and retinal hemorrhages. A medication is given immediately. Five minutes later, his pulse is 75/min and blood pressure is 190/105 mm Hg. Which of the following drugs was most likely administered?

A. Nicardipine
B. Hydralazine
C. Nitroprusside
D. Fenoldopam
E. Labetalol (Correct Answer)

Explanation: ***Labetalol*** - This patient presents with **malignant hypertension** given the severely elevated blood pressure (232/128 mm Hg) and signs of **end-organ damage** (blurry vision, optic disc blurring, retinal hemorrhages suggesting hypertensive retinopathy, and new-onset headaches). - **Labetalol** is a mixed alpha- and beta-blocker commonly used in hypertensive emergencies because of its **rapid onset of action** and ability to effectively lower blood pressure without causing significant reflex tachycardia. The decrease in pulse rate from 94/min to 75/min after administration is consistent with its beta-blocking effects. *Nicardipine* - **Nicardipine** is a dihydropyridine calcium channel blocker that primarily causes **vasodilation**, making it effective in hypertensive emergencies. - While it would lower blood pressure, it typically causes **reflex tachycardia** due to vasodilation, which is not observed in this patient (pulse decreased). *Hydralazine* - **Hydralazine** is a direct arterial vasodilator often used in hypertensive emergencies, but it typically causes a more pronounced **reflex tachycardia** than calcium channel blockers. - Its onset of action can also be less predictable, and its use is generally avoided if there's evidence of **coronary artery disease** due to the risk of increased myocardial oxygen demand. *Nitroprusside* - **Nitroprusside** is a powerful balanced arterial and venous vasodilator, leading to a rapid and significant drop in blood pressure. - It is known for causing **reflex tachycardia** and has a risk of **cyanide toxicity** with prolonged use, making its use in this scenario less ideal given the patient's existing elevated pulse. *Fenoldopam* - **Fenoldopam** is a dopamine-1 receptor agonist that causes vasodilation and improves renal blood flow, useful in hypertensive emergencies. - Like other vasodilators, it can cause **reflex tachycardia** and may lead to increased intraocular pressure, which would be a concern in a patient with acute blurry vision.

Question 29: A 67-year-old woman comes to the physician with a 4-month history of chest pain that occurs on exertion. The pain is dull, and she experiences retrosternal pressure when she walks up the stairs to her apartment on the fifth floor. The pain disappears shortly after stopping for one minute. She has hypertension, for which she takes lisinopril and metoprolol daily. She does not smoke or drink alcohol. She is 158 cm (5 ft 2 in) tall and weighs 82 kg (180 lb); BMI is 33 kg/m2. Her pulse is 72/min and blood pressure is 140/85 mm Hg. Cardiac examination shows no murmurs, rubs, or gallops. Fasting lipid studies show: Total cholesterol 196 mg/dL LDL 110 mg/dL HDL 50 mg/dL A resting ECG shows no abnormalities. A week after uneventful initiation of aspirin, the patient is started on atorvastatin. This patient is most likely to develop which of the following?

A. Cholelithiasis
B. Elevated transaminases (Correct Answer)
C. Myositis
D. Flushing
E. Bloating

Explanation: ***Elevated transaminases*** - **Statins** like atorvastatin can cause **hepatotoxicity**, manifesting as elevated liver transaminases (ALT/AST). - Mild, asymptomatic transaminase elevation occurs in **0.5-2% of patients** and is the most likely adverse effect among the listed options. - Routine monitoring of liver function tests is recommended, though clinically significant liver damage is rare. - Transaminase elevations often resolve even with continued therapy. *Cholelithiasis* - **Cholelithiasis** (gallstones) is not a side effect of statins. - While fibrates can increase gallstone risk, statins do not have this association. - The patient's risk factors (age, obesity) are unrelated to atorvastatin initiation. *Myositis* - **Myositis** refers to inflammatory muscle disease with **elevated creatine kinase (CK)** and is a rare complication of statins (<1%). - While muscle-related **symptoms** (myalgias, muscle aches) are the most common statin side effect (10-15%), true **myositis** with CK elevation is uncommon. - There are no muscle symptoms mentioned in this patient's presentation. - Among the listed options, mild transaminase elevation is more likely than frank myositis. *Flushing* - **Flushing** is a common side effect of **niacin** (nicotinic acid), not statins. - The mechanism involves prostaglandin-mediated vasodilation, which can be mitigated by aspirin pre-treatment. *Bloating* - **Bloating** is not a characteristic or common adverse effect of atorvastatin. - While mild GI upset can occur with many medications, bloating is not a typical or distinguishing side effect of statins.

Question 30: A 67-year-old woman with chronic kidney disease, hypertension, and diabetes mellitus presented with congestive heart failure and underwent uneventful 3-vessel coronary artery bypass surgery. Within 20 hours, she was extubated and all infusions except nitroprusside were stopped. On the 4th postoperative day, she deteriorated, exhibiting restlessness, tachypnea, tachycardia, and hypotension. Inotropes, vasopressors and bicarbonate infusions were started. Continuous hemodialysis was initiated, yet lactate levels continued to rise. Her chart clarified that she had received 319 mg of nitroprusside over 72 hours. What is the most likely cause of her condition?

A. Carbon monoxide poisoning
B. Anemia
C. Sulfmethemoglobinemia
D. Methemoglobinemia
E. Cyanide toxicity (Correct Answer)

Explanation: ***Cyanide toxicity*** - The patient received a significant cumulative dose of **nitroprusside** (319 mg over 72 hours), which metabolizes into **cyanide**. - Symptoms like **restlessness**, **tachycardia**, **hypotension**, and **rising lactate levels** despite aggressive management are classic signs of cyanide toxicity, particularly in a patient with **renal impairment** who struggles to clear cyanide. *Carbon monoxide poisoning* - This is less likely as there is no exposure history to **carbon monoxide**, and the clinical picture strongly points to a **nitroprusside-related** complication. - While it can cause lactic acidosis, the primary mechanism of injury is different and not directly related to the drug administered. *Anemia* - This is unlikely to be the primary cause of acute deterioration, as it would typically develop over time and not suddenly manifest with **refractory hypotension** and **lactic acidosis** in this context. - Anemia might exacerbate the condition but does not explain the acute and severe metabolic derangement. *Sulfmethemoglobinemia* - This is a rare condition that causes functional anemia by impairing oxygen transport but is typically caused by exposure to **sulfur-containing drugs** (e.g., sulfonamides) or **hydrogen sulfide**. - It does not explain the specific metabolic acidosis and clinical deterioration seen with nitroprusside overdose. *Methemoglobinemia* - This condition is caused by the oxidation of hemoglobin to **methemoglobin**, which cannot transport oxygen, often induced by drugs like **nitrates** or **local anesthetics**. - While nitroprusside can cause methemoglobinemia, the profound **lactic acidosis** and the specific clinical evolution are more characteristic of cyanide toxicity due to the inhibition of **cellular respiration**.

Question 31: A 36-year-old male is brought to the emergency department for severe chest pain and vomiting. He reports sudden onset 10/10 pain concentrated along his lower chest/epigastric region that radiates to his back for the past 3 hours. He denies any precipitating event, alcohol use, exertion, biliary colic, or family history of coronary artery disease. Medical history is significant for hypertension for which he recently started taking a “water pill.” Electrocardiogram (ECG) demonstrates normal sinus rhythm, and troponins are negative. Additional laboratory findings are shown below: Serum: Na+: 138 mEq/L K+: 3.9 mEq/L Cl-: 101 mEq/L Ca2+: 8.5 mg/dL Total cholesterol: 210 mg/dL (Normal: < 200 mg/dL) Triglycerides: 1,528 mg/dL (Normal: < 150 mg/dL) CRP: 28 mg/dL (Normal: < 3 mg/dL) Amylase: 582 U/L (Normal: 23-85 U/L) Lipase: 1,415 U/L (Normal: 0-160 U/L) What is the best medication for this patient in the long-term following initial stabilization?

A. Aspirin
B. Atorvastatin
C. Gemfibrozil (Correct Answer)
D. Cholestyramine
E. Niacin

Explanation: ***Gemfibrozil*** - This patient presents with signs and symptoms of **acute pancreatitis** secondary to **severe hypertriglyceridemia**. - **Fibrates** like gemfibrozil are the most effective medications for significantly lowering triglyceride levels and are indicated for treating severe hypertriglyceridemia (usually >500 mg/dL) to prevent recurrent pancreatitis. *Aspirin* - **Aspirin** is an antiplatelet agent primarily used for the prevention of cardiovascular events in patients with atherosclerosis. - It does not significantly impact triglyceride levels and is not indicated for the management or prevention of hypertriglyceridemia-induced pancreatitis. *Atorvastatin* - **Statins** (e.g., atorvastatin) are highly effective in lowering LDL cholesterol and have a moderate effect on lowering triglycerides. - However, for severe hypertriglyceridemia (>500 mg/dL), **fibrates** are significantly more potent in reducing triglyceride levels and preventing pancreatitis. *Cholestyramine* - **Cholestyramine** is a bile acid sequestrant primarily used to lower LDL cholesterol by binding bile acids in the intestine. - It does not effectively lower triglyceride levels and can sometimes even increase them, making it inappropriate for this patient's condition. *Niacin* - **Niacin** (nicotinic acid) can lower both triglycerides and LDL cholesterol while raising HDL cholesterol. - However, it is often associated with significant side effects like **flushing** and can worsen insulin resistance, and **fibrates** are generally preferred for severe hypertriglyceridemia due to a more favorable side effect profile and proven efficacy in preventing pancreatitis.

Question 32: A 49-year-old man is diagnosed with hypertension. He has asthma. The creatinine and potassium levels are both slightly elevated. Which of the following anti-hypertensive drugs would be appropriate in his case?

A. Amlodipine (Correct Answer)
B. Hydrochlorothiazide (HCT)
C. Enalapril
D. Spironolactone
E. Propranolol

Explanation: ***Amlodipine*** - **Amlodipine** is a **calcium channel blocker** that is safe and effective in patients with **asthma** as it does not exacerbate bronchoconstriction. - It is **renal protective** and does not significantly affect **potassium levels**, making it ideal for this patient with elevated creatinine and potassium. - This is the **best choice** given all three clinical considerations. *Hydrochlorothiazide (HCT)* - While generally safe in asthma, **HCT** is a **thiazide diuretic** that can worsen renal function and **increase creatinine levels**, which is problematic given the patient's already elevated creatinine. - Although HCT causes **hypokalemia** (low potassium), it is not the preferred agent for managing hyperkalemia, and worsening renal function is a more significant concern here. - **Amlodipine is safer overall** in this patient. *Enalapril* - **Enalapril** is an **ACE inhibitor** that can cause **hyperkalemia**, further worsening the patient's already elevated potassium levels. - It can also transiently increase **creatinine**, particularly in patients with underlying renal impairment, making it an unfavorable option in this scenario. *Spironolactone* - **Spironolactone** is a **potassium-sparing diuretic** that frequently causes **hyperkalemia**, which would be dangerous given the patient's elevated potassium levels. - It is **contraindicated** in patients with significant hyperkalemia or renal impairment. *Propranolol* - **Propranolol** is a **non-selective beta-blocker** that is **contraindicated** in patients with **asthma** as it can cause **bronchospasm** and severe respiratory compromise. - Beta-blockers should be avoided in asthmatic patients.

Question 33: A 55-year-old man comes to the physician because of episodic retrosternal chest pain and shortness of breath for the past 6 months. His symptoms occur when he takes long walks or climbs stairs but resolve promptly with rest. He has a history of chronic obstructive pulmonary disease, for which he takes ipratropium bromide. His pulse is 81/min and blood pressure is 153/82 mm Hg. Physical examination shows mild expiratory wheezing over both lungs. Additional treatment with a beta blocker is considered. Which of the following agents should be avoided in this patient?

A. Betaxolol
B. Esmolol
C. Bisoprolol
D. Atenolol
E. Labetalol (Correct Answer)

Explanation: ***Labetalol*** - **Labetalol** is a **non-selective beta-blocker** with additional **alpha-1 blocking activity**. - Its **non-selective beta-blocking** effects can exacerbate **bronchoconstriction** in patients with **COPD**, leading to worsening respiratory symptoms. *Betaxolol* - **Betaxolol** is a **beta-1 selective blocker (cardioselective)**, meaning it primarily targets the heart. - While no beta-blocker is entirely safe in **COPD**, cardioselective agents are generally preferred due to their reduced risk of **bronchospasm**. *Esmolol* - **Esmolol** is an **ultra-short-acting**, **beta-1 selective blocker** often used for acute cardiac conditions. - Its **cardioselective nature** and rapid metabolism make it relatively safer in patients with **COPD** compared to non-selective agents. *Bisoprolol* - **Bisoprolol** is a **highly beta-1 selective blocker** commonly used for chronic cardiac conditions. - Its high **cardioselectivity** minimizes its impact on **bronchial beta-2 receptors**, making it a safer option for patients with **COPD**. *Atenolol* - **Atenolol** is a **beta-1 selective blocker** used for conditions like hypertension and angina. - Like other cardioselective beta-blockers, it has a lower risk of causing **bronchoconstriction** in patients with **COPD** compared to non-selective agents.

Question 34: A 53-year-old man with hyperlipidemia comes to the physician for a follow-up examination. His home medications include acetaminophen and atorvastatin. Serum studies show elevated total cholesterol and triglyceride concentrations. A drug that activates the peroxisome proliferator-activated receptor alpha is added to his existing therapy. This patient is at highest risk for developing which of the following drug-related adverse effects?

A. Reddish-brown discoloration of urine (Correct Answer)
B. Bleeding from minor trauma
C. Waxing and waning confusion
D. Acutely swollen and painful joint
E. Pruritus and flushing of the skin

Explanation: ***Reddish-brown discoloration of urine*** - This patient is likely being treated with a **fibrate**, a PPAR-alpha agonist, in addition to **atorvastatin** due to persistently elevated triglycerides. - The combination of a fibrate and a statin increases the risk of **rhabdomyolysis**, which can cause **myoglobinuria**, leading to reddish-brown urine and potential **acute kidney injury**. *Bleeding from minor trauma* - This adverse effect is more characteristic of **anticoagulants** (e.g., warfarin, direct oral anticoagulants) or **antiplatelet agents** (e.g., aspirin, clopidogrel). - Fibrates and statins do not typically cause significant bleeding diathesis. *Waxing and waning confusion* - This can be a symptom of various conditions, including **hepatic encephalopathy**, severe electrolyte imbalances, or delirium; it is not a common adverse effect of fibrates or statins. - While statins can rarely cause cognitive side effects, **confusion** of this nature is not a hallmark. *Acutely swollen and painful joint* - This symptom strongly suggests an acute **arthritic flare**, particularly **gout**, caused by hyperuricemia. - While some medications can induce gout (e.g., diuretics), neither fibrates nor statins are commonly associated with this adverse effect. *Pruritus and flushing of the skin* - These are characteristic side effects of **niacin (nicotinic acid)**, another lipid-lowering agent. - Niacin causes prostaglandin-mediated vasodilation, leading to intense **flushing and itching**, which can be severe enough to cause medication non-adherence.

Question 35: A 51-year-old man presents to the urgent care center with a blood pressure of 201/111 mm Hg. He is complaining of a severe headache and chest pain. Physical examination reveals regular heart sounds and clear bilateral lung sounds. Ischemic changes are noted on his electrocardiogram (ECG). What is the most appropriate treatment for this patient’s high blood pressure?

A. IV labetalol - lower mean arterial pressure no more than 25% over the 1st hour (Correct Answer)
B. Oral clonidine - gradually lower blood pressure over 24–48 hours
C. Oral beta-blocker - lower mean arterial pressure no more than 25% over the 1st hour
D. IV labetalol - lower mean arterial pressure no more than 50% over the 1st hour
E. IV labetalol - redose until blood pressure within normal limits

Explanation: ***IV labetalol - lower mean arterial pressure no more than 25% over the 1st hour*** - This patient presents with **hypertensive emergency**, indicated by severe hypertension (BP 201/111 mmHg) and evidence of **acute target organ damage** (severe headache, chest pain, ischemic ECG changes). - **IV labetalol** is an appropriate first-line agent, and the goal is to **gradually reduce** the mean arterial pressure by no more than **25% within the first hour** to prevent hypoperfusion and ischemic events. *Oral clonidine - gradually lower blood pressure over 24–48 hours* - **Oral clonidine** has a slower onset of action and is not suitable for the **urgent reduction** required in a hypertensive emergency. - This approach is more appropriate for **gradual blood pressure reduction** in less severe hypertension or as an adjunct in chronic management. *Oral beta-blocker - lower mean arterial pressure no more than 25% over the 1st hour* - **Oral medications** are generally not preferred for initial management of **hypertensive emergencies** due to their slower onset and less predictable dose titration compared to intravenous agents. - While beta-blockers can be effective, the **oral route** is inappropriate for the acute, rapid control needed for this condition. *IV labetalol - lower mean arterial pressure no more than 50% over the 1st hour* - A rapid reduction of **50% in MAP** within the first hour is too aggressive and carries a significant risk of **hypoperfusion** to vital organs, potentially leading to **stroke**, **myocardial infarction**, or **renal failure**. - The recommended initial reduction is **no more than 25%** in the first hour to maintain adequate organ perfusion. *IV labetalol - redose until blood pressure within normal limits* - Aggressively lowering blood pressure to **"normal limits"** too quickly can cause cerebral, cardiac, or renal **ischemia** due to loss of autoregulation in previously hypertensive patients. - The goal is to first stabilize the patient by reducing the BP by a controlled amount, not to normalize it immediately.

Question 36: A 27-year-old man comes to the physician with his wife because they have been unable to conceive. They have had regular unprotected sex for the past 18 months without using contraception. His wife has been tested and is fertile. The patient began puberty at the age of 13 years. He has been healthy except for an infection with Chlamydia trachomatis 10 years ago, which was treated with azithromycin. He is a professional cyclist and trains every day for 3–4 hours. His wife reports that her husband has often been stressed since he started to prepare for the national championships a year ago and is very conscious about his diet. His temperature is 36.5°C (97.7°F), pulse is 50/min, and blood pressure is 154/92 mm Hg. Physical examination of the husband shows an athletic stature with uniform inflammatory papular eruptions of the face, back, and chest. Genital examination shows small testes. Which of the following is the most likely underlying cause of this patient's infertility?

A. Heat from friction
B. Psychogenic erectile dysfunction
C. Kallmann syndrome
D. Anorexia nervosa
E. Anabolic steroid use (Correct Answer)

Explanation: ***Anabolic steroid use*** - The patient's **athletic stature**, **inflammatory papular eruptions** (acne), **small testes**, and dedication to intense training are highly suggestive of anabolic steroid use. Anabolic steroids suppress endogenous **gonadotropin-releasing hormone (GnRH)**, leading to secondary hypogonadism, testicular atrophy, and infertility. - The history of **Chlamydia trachomatis** 10 years ago is less likely to be the primary cause of current infertility given the effective treatment, and the associated signs point more strongly to steroid use. *Heat from friction* - While prolonged cycling can increase **scrotal temperature**, potentially affecting **sperm quality**, it is unlikely to cause the severe **testicular atrophy** and broad systemic effects (acne, hypertension) seen in this patient. - **Infertility related to heat** typically presents as reduced sperm count or motility, without the endocrine disruptions associated with anabolic steroids. *Psychogenic erectile dysfunction* - **Erectile dysfunction** is not explicitly mentioned as a complaint; the primary concern is infertility despite regular unprotected sex. While stress can contribute to ED, it does not explain the **small testes** or systemic dermatological findings. - **Psychogenic factors** primarily affect the ability to achieve or maintain an erection, not necessarily **sperm production** or testicular size in the absence of other hormonal issues. *Kallmann syndrome* - **Kallmann syndrome** is a genetic condition characterized by hypogonadotropic hypogonadism and **anosmia** (inability to smell) due to defective migration of GnRH neurons. Patients typically present with **delayed puberty** (primary amenorrhea in females, lack of secondary sexual characteristics in males). - This patient began puberty at age 13, which is within the normal range, and there is no mention of anosmia, making Kallmann syndrome unlikely. *Anorexia nervosa* - Anorexia nervosa can lead to **hypogonadism** (due to low GnRH output from caloric restriction and excessive exercise), which might cause small testes and infertility. However, it is typically associated with **low body weight**, which contradicts the patient's athletic stature and professional cyclist status. - While extreme dieting is mentioned, it's in the context of professional cycling, and the other symptoms like **acne** and **hypertension** are not typical findings in anorexia nervosa.

Question 37: A 67-year-old woman presents to her physician for a regular checkup. She is a community-dwelling, retired teacher without any smoking history. She has arterial hypertension and takes hydrochlorothiazide 12.5 mg and valsartan 80 mg daily. She was recently discharged from the hospital after admission for an ulnar fracture she received after a fall from the second step of a ladder in her garden. A year ago, she had a clavicular fracture from tripping over some large rocks in her yard. She does not report lightheadedness or fainting. Her medical history is also significant for an appendectomy 11 years ago. She is in menopause. She mostly consumes vegetables and dairy products. Her height is 163 cm (5 ft 4 in) and weight is 55 kg (123 lb). Her blood pressure is 130/80 mm Hg without orthostatic changes, heart rate is 73/min and regular, respiratory rate is 14/min, and temperature is 36.6°C (97.9°F). Her lungs are clear to auscultation. Cardiac auscultation reveals S2 accentuation over the aorta. The abdomen is mildly distended on palpation; there are no identifiable masses. The neurological examination is unremarkable. Considering the history and presentation, which of the following medications most likely will be prescribed to this patient after additional investigations?

A. Estrogen plus progestin
B. Denosumab
C. Cholecalciferol (Correct Answer)
D. Atorvastatin
E. Tocopherol

Explanation: ***Cholecalciferol*** - The patient presents with multiple risk factors for **osteoporosis** and potential **vitamin D deficiency**, including postmenopausal status, multiple fragility fractures (ulnar and clavicular), and a diet rich in vegetables but potentially low in vitamin D-fortified products or sun exposure. - **Cholecalciferol (Vitamin D3)** is essential for calcium absorption and bone health, and its supplementation is crucial for preventing and managing osteoporosis, particularly when low levels are suspected. *Estrogen plus progestin* - **Hormone replacement therapy (HRT)** with estrogen plus progestin can prevent osteoporosis, but it is typically not a first-line treatment due to increased risks of breast cancer, cardiovascular events, and stroke, especially in a 67-year-old woman. - Given her age and that she is well past menopause, the risks often outweigh the benefits for bone health alone, and safer alternatives are available for osteoporosis treatment. *Denosumab* - **Denosumab** is a potent antiresorptive agent used for osteoporosis, particularly in patients with a high fracture risk or those who cannot tolerate oral bisphosphonates. - While she has risk factors for osteoporosis, denosumab is usually initiated after a definitive diagnosis of osteoporosis (e.g., via **DEXA scan**) and often after lifestyle modifications and basic supplementation like vitamin D. It's a treatment, not a "most likely prescribed after additional investigation" first step. *Atorvastatin* - **Atorvastatin** is a statin used to lower cholesterol and prevent cardiovascular disease. - While the patient has hypertension, there's no indication in the provided information (e.g., lipid profile, history of cardiovascular events) that she requires atorvastatin at this time. *Tocopherol* - **Tocopherol (Vitamin E)** is an antioxidant that plays a role in various bodily functions but is not directly involved in bone metabolism or the prevention/treatment of osteoporosis. - There is no clinical indication in the patient's history suggesting a need for vitamin E supplementation for her current presentation.

Question 38: A 64-year-old African American female comes to the physician's office for a routine check-up. The patient's past medical history is significant for hypertension, diabetes, and osteoarthritis in her right knee. Her medications include metformin, glimepiride, lisinopril, metoprolol, hydrochlorothiazide, and ibuprofen as needed. Her only complaint is an unremitting cough that started about 3 weeks ago and she has noticed some swelling around her mouth. The drug most likely responsible for her recent symptoms causes its primary renal hemodynamic effect on which part of the kidney?

A. Collecting duct
B. Distal convoluted tubule
C. Juxtaglomerular cells
D. Efferent arteriole (Correct Answer)
E. Afferent arteriole

Explanation: ***Efferent arteriole*** - The patient's symptoms of an **unremitting cough** and **angioedema** (swelling around her mouth) are classic side effects of **ACE inhibitors**, such as **lisinopril**. - ACE inhibitors primarily exert their renal hemodynamic effects by **dilating the efferent arteriole**, leading to a decrease in intraglomerular pressure and glomerular filtration rate. *Collecting duct* - The collecting duct is the primary site of action for **vasopressin (ADH)** and **aldosterone**, regulating water and sodium reabsorption, respectively. - While other medications like **thiazides** (used by the patient) affect distal tubules and collecting ducts indirectly, their direct impact on the collecting duct is not the cause of angioedema or cough. *Distal convoluted tubule* - The distal convoluted tubule is the main site of action for **thiazide diuretics** (e.g., hydrochlorothiazide), which inhibit the Na-Cl cotransporter. - This tubule segment is not directly involved in the mechanism leading to angioedema or cough caused by ACE inhibitors. *Juxtaglomerular cells* - Juxtaglomerular cells are responsible for producing **renin**, which is the initial step in the **renin-angiotensin-aldosterone system (RAAS)**. - While ACE inhibitors block the conversion of angiotensin I to angiotensin II, they do not directly act on the juxtaglomerular cells themselves to cause their side effects. *Afferent arteriole* - The afferent arteriole is primarily regulated by **sympathetic tone** and local factors, and is the main site of action for medications like **NSAIDs** (e.g., ibuprofen, which the patient takes as needed). - While NSAIDs cause **afferent arteriole constriction** and can impair renal function, they do not cause angioedema or a chronic cough.

Question 39: A 68-year-old man presents for his first hemodialysis treatment. He was diagnosed with progressive chronic kidney disease 6 years ago that has now resulted in end-stage renal disease (ESRD). He currently is on a waiting list for a kidney transplant. His past medical history is significant for hypertension and peptic ulcer disease, managed with amlodipine and esomeprazole, respectively. He has diligently followed a severely restricted diet. The patient is afebrile and his vital signs are normal. His latest serum creatinine gives him an estimated glomerular filtration rate (eGFR) of 12 mL/min/1.73 m2. Which of the following should be increased as part of the management of this patient?

A. Protein intake (Correct Answer)
B. Potassium intake
C. Sodium intake
D. Calcium intake
E. Fiber intake

Explanation: ***Protein intake*** - Once a patient with ESRD initiates **hemodialysis**, their protein requirements significantly increase due to protein losses during dialysis and increased catabolism. - While patients with CKD not on dialysis have restricted protein intake, those on dialysis need about **1.2 g/kg/day** of protein to maintain a positive nitrogen balance. *Potassium intake* - Patients with ESRD commonly experience **hyperkalemia** due to impaired renal excretion. - **Potassium intake** is typically restricted in dialysis patients to prevent life-threatening cardiac arrhythmias. *Sodium intake* - **Sodium restriction** is crucial for dialysis patients to manage fluid overload, hypertension, and prevent congestive heart failure. - Increased sodium intake would exacerbate these conditions, leading to adverse outcomes. *Calcium intake* - Patients with ESRD often have complex mineral and bone disorders, including **hyperphosphatemia** and hypocalcemia. - While calcium supplementation may be necessary for some, increasing dietary calcium generally is not the primary intervention and must be carefully balanced with phosphate binders to prevent vascular calcification. *Fiber intake* - While fiber is important for bowel health, there is no specific condition in this patient's profile that warrants a targeted increase in fiber intake in the context of starting hemodialysis. - The most critical dietary adjustments for dialysis patients revolve around protein, fluid, and electrolytes.

Question 40: A 54-year-old man comes to the physician for a follow-up examination after presenting with elevated blood pressures on both arms at a routine visit 1 month ago. He feels well and takes no medications. He is 178 cm (5 ft 10 in) tall and weighs 99 kg (218 lb); BMI is 31 kg/m2. His pulse is 76/min, and blood pressure is 148/85 mm Hg on the right arm and 152/87 mm Hg on the left arm. Physical examination and laboratory studies show no abnormalities. The physician recommends lifestyle modifications in combination with treatment with hydrochlorothiazide. From which of the following embryological tissues does the site of action of this drug arise?

A. Pronephros
B. Mesonephros
C. Ureteric bud
D. Mesonephric duct
E. Metanephric blastema (Correct Answer)

Explanation: ***Metanephric blastema*** - Hydrochlorothiazide, a **thiazide diuretic**, acts primarily on the **distal convoluted tubule (DCT)** of the nephron. - The DCT, along with the glomerulus, Bowman's capsule, proximal convoluted tubule, and loop of Henle, develops from the **metanephric blastema**. *Pronephros* - The **pronephros** is the earliest and most rudimentary kidney structure in human embryonic development, appearing around week 3. - It is **non-functional** and quickly degenerates, not contributing to the definitive adult kidney structures. *Mesonephros* - The **mesonephros** develops after the pronephros and functions as an interim kidney during the first trimester. - While it contributes to parts of the male genital system (e.g., **epididymis**, **vas deferens**), it does not form components of the adult kidney or the distal convoluted tubule. *Ureteric bud* - The **ureteric bud** (an outgrowth of the mesonephric duct) gives rise to the **collecting ducts, renal calyces, renal pelvis**, and **ureters**. - It forms the **collecting system** of the kidney, but not the nephron's filter and reabsorption components like the distal convoluted tubule. *Mesonephric duct* - The **mesonephric duct (Wolffian duct)** is primarily involved in the development of the **male internal genitalia** (e.g., epididymis, vas deferens, seminal vesicles). - In females, it largely **regresses**, and it does not contribute to the formation of the nephron or its tubules.

Question 41: A 33-year-old male presents to his primary care physician with complaints of headaches and muscle weakness. His physical exam is entirely within normal limits except for a blood pressure of 150/95. Subsequent routine blood lab work showed a sodium level of 146 and potassium level of 3.0. What is the best pharmacological therapy for this patient?

A. Fludrocortisone
B. Spironolactone (Correct Answer)
C. Lisinopril
D. Hydrochlorothiazide
E. Propranolol

Explanation: ***Spironolactone*** - This patient's symptoms (hypertension, **hypokalemia**, and **hypernatremia**) are classic for **primary hyperaldosteronism**. **Spironolactone** is an **aldosterone antagonist** that blocks the effects of aldosterone, effectively treating both the hypertension and electrolyte abnormalities. - Aldosterone antagonists directly target the underlying pathology by countering the excessive mineralocorticoid activity, making it the most appropriate pharmacological therapy for primary hyperaldosteronism. *Fludrocortisone* - **Fludrocortisone** is a **mineralocorticoid** used to *replace* aldosterone in conditions like Addison's disease where aldosterone production is deficient. - Administering fludrocortisone in a patient with excessive aldosterone (primary hyperaldosteronism) would worsen their condition by exacerbating hypertension, hypokalemia, and hypernatremia. *Lisinopril* - **Lisinopril** is an **ACE inhibitor** that works by blocking the conversion of angiotensin I to angiotensin II, leading to vasodilation and decreased aldosterone secretion. - While ACE inhibitors can lower blood pressure, they are not the primary treatment for **primary hyperaldosteronism** because the condition involves autonomous aldosterone production **independent of the renin-angiotensin-aldosterone system (RAAS)**. *Hydrochlorothiazide* - **Hydrochlorothiazide** is a **thiazide diuretic** that works by increasing the excretion of sodium and water, thereby lowering blood pressure. - However, thiazide diuretics also increase potassium excretion, which would further worsen the patient's existing **hypokalemia**, making it an inappropriate choice. *Propranolol* - **Propranolol** is a **non-selective beta-blocker** that lowers blood pressure by reducing heart rate and cardiac output. - While useful for hypertension, beta-blockers do not address the underlying electrolyte disturbances characteristic of **primary hyperaldosteronism** and are not a first-line treatment for this specific condition.

Question 42: A 65-year-old woman presents with a complaint of a chronic, dry cough of insidious onset since working with her new primary care physician. She has a longstanding history of diabetes mellitus type 2, hypertension, and hyperlipidemia. She has a 10 pack-year smoking history, but does not currently smoke. What is the best next step?

A. Spirometry
B. Trial of decongestant and first-generation histamine H1 receptor antagonist
C. Monitor esophageal pH
D. Order chest radiograph
E. Review medication list (Correct Answer)

Explanation: ***Review medication list*** - A chronic, dry cough of insidious onset in a patient with **hypertension** who recently started seeing a new physician strongly suggests an **ACE inhibitor-induced cough** as the most likely etiology. - **ACE inhibitors** (e.g., lisinopril, enalapril) cause chronic dry cough in **5-20% of patients** due to accumulation of **bradykinin** and **substance P** in the respiratory tract. - Reviewing the medication list is the **most appropriate first step** to identify the offending agent before pursuing more invasive or costly workup. - If an ACE inhibitor is identified, switching to an **angiotensin receptor blocker (ARB)** typically resolves the cough within 1-4 weeks. *Spirometry* - While spirometry evaluates lung function for conditions like **COPD** or **asthma**, it is less likely to identify the cause of a *new-onset dry cough* in this context without other respiratory symptoms (wheezing, dyspnea). - The patient's 10 pack-year smoking history is relatively modest, and she is a former smoker. - This step would be considered after ruling out more common causes like medication side effects. *Trial of decongestant and first-generation histamine H1 receptor antagonist* - This treatment targets **post-nasal drip**, which typically presents with a *wet cough* rather than a dry cough. - There is no mention of rhinorrhea, nasal congestion, or throat clearing to suggest post-nasal drip. - Using these medications empirically can cause unnecessary **anticholinergic side effects** (confusion, urinary retention, dry mouth) in an elderly patient. *Monitor esophageal pH* - **Gastroesophageal reflux disease (GERD)** can cause chronic cough, but this is a *diagnosis of exclusion* after ruling out more common causes. - GERD-related cough is often accompanied by heartburn, regurgitation, or worse symptoms when lying down. - Esophageal pH monitoring is **invasive and expensive** and should not be a first-line approach. *Order chest radiograph* - A chest X-ray can identify lung pathologies such as **pneumonia**, **masses**, **interstitial lung disease**, or **heart failure**. - However, a dry cough alone without other concerning features (fever, weight loss, dyspnea, hemoptysis, night sweats) does not immediately warrant imaging as the primary first step. - Given the temporal relationship with a new physician and the patient's hypertension, **drug-induced cough** is a more likely and easily investigated initial consideration.

Question 43: A 22-year-old woman comes to the physician for a follow-up examination. She had a spontaneous abortion 3 months ago. Her last menstrual period was 3 weeks ago. She reports feeling sad occasionally but has continued working and attending social events. She does not have any suicidal ideation or tendencies. She does not smoke. Vital signs are within normal limits. Physical examination including pelvic examination show no abnormalities. A urine pregnancy test is negative. She wants to avoid becoming pregnant for the foreseeable future and is started on combined oral contraceptive pills. Which of the following is the patient at risk of developing?

A. Endometriosis
B. Functional ovarian cysts
C. Acne
D. Hypertension (Correct Answer)
E. Premenstrual syndrome

Explanation: **Hypertension** - **Combined oral contraceptives (COCs)** can cause a small but significant increase in blood pressure, leading to **hypertension** in some women. - This risk is dose-dependent and is generally higher with older formulations containing higher estrogen doses. *Endometriosis* - **Combined oral contraceptives** are often used as a treatment for **endometriosis** to suppress ovarian activity and reduce endometrial lesions. - Therefore, COCs typically reduce the risk or symptoms of endometriosis rather than causing it. *Functional ovarian cysts* - **Combined oral contraceptives** work by suppressing ovulation, which is the process that leads to the formation of **functional ovarian cysts**. - As such, COCs actually decrease the incidence of functional ovarian cysts. *Acne* - The estrogen component in **combined oral contraceptives** has an anti-androgenic effect, which can reduce sebum production and improve **acne**. - Many COCs are specifically approved for the treatment of acne, making it an unlikely risk. *Premenstrual syndrome* - **Combined oral contraceptives** can help stabilize hormonal fluctuations throughout the menstrual cycle, often leading to an improvement in symptoms of **premenstrual syndrome (PMS)**. - They are commonly prescribed to manage moderate to severe PMS symptoms.

Question 44: A 45-year-old woman comes to the emergency department because of severe pain in both of her wrist joints and her fingers for the past 24 hours. She has a 6-month history of similar episodes, which are often associated with stiffness for about 90 minutes when she wakes up in the morning. She has hyperlipidemia and hypertension. Two years ago she was diagnosed with peptic ulcer disease, for which she underwent treatment. Current medications include fenofibrate and amlodipine. Vital signs are within normal limits. She is 175 cm (5 ft 9 in) tall and weighs 102 kg (225 lb); BMI is 33 kg/m2. Examination shows swelling and tenderness of the wrists and metacarpophalangeal joints bilaterally. Range of motion is decreased due to pain. There are subcutaneous, nontender, firm, mobile nodules on the extensor surface of the forearm, with the overlying skin appearing normal. Which of the following is the most appropriate treatment for this patient's current symptoms?

A. Prednisolone (Correct Answer)
B. Vitamin D and calcium supplements
C. Methotrexate
D. Sulfasalazine
E. Indomethacin

Explanation: ***Prednisolone*** - This patient presents with an acute flare of what appears to be **rheumatoid arthritis**, characterized by symmetrical polyarticular joint pain, morning stiffness, and subcutaneous nodules. **Glucocorticoids** like prednisolone are highly effective for rapid symptom control in such acute flares. - While other disease-modifying antirheumatic drugs (DMARDs) are used for long-term management, **prednisolone** provides quick anti-inflammatory and immunosuppressive effects to alleviate severe acute symptoms. *Vitamin D and calcium supplements* - These supplements are primarily for **bone health** and are not indicated for the acute management of inflammatory joint pain. - While important for overall health, especially in postmenopausal women or those on chronic steroid therapy, they will not address the patient's acute arthritis symptoms. *Methotrexate* - **Methotrexate** is a cornerstone **disease-modifying antirheumatic drug (DMARD)** for rheumatoid arthritis, used for long-term control to prevent joint damage. - However, it has a slow onset of action (weeks to months) and is not suitable for immediate relief of severe acute symptoms. *Sulfasalazine* - **Sulfasalazine** is another **DMARD** used in rheumatoid arthritis, particularly for patients who cannot tolerate methotrexate. - Similar to methotrexate, it has a delayed onset of action and is not appropriate for resolving an acute and severe flare. *Indomethacin* - **Indomethacin** is a **nonsteroidal anti-inflammatory drug (NSAID)** that can reduce pain and inflammation. However, this patient has a history of **peptic ulcer disease**, which is a contraindication for NSAID use due to the risk of gastrointestinal bleeding. - While effective for acute pain, the patient's medical history makes NSAIDs a risky choice and a systemic corticosteroid is a more appropriate and effective intervention for a severe flare.

Question 45: A previously healthy 45-year-old man comes to the physician for a routine health maintenance examination. He has been having recurrent headaches, especially early in the morning, and sometimes feels dizzy. There is no family history of serious illness. The patient runs 5 miles 3 days a week. He does not smoke or drink alcohol. He is 177 cm (5 ft 10 in) tall and weighs 72 kg (159 lb); BMI is 23 kg/m2. His temperature is 37°C (98.6°F), pulse is 70/min, and blood pressure is 152/90 mm Hg. Physical examination shows no abnormalities. Laboratory studies are within normal limits. Two weeks later, the patient's blood pressure is 150/90 mm Hg in both arms. He is started on an antihypertensive medication. One month later, physical examination shows 2+ pretibial edema bilaterally. This patient was most likely treated with which of the following medications?

A. Prazosin
B. Losartan
C. Propranolol
D. Amlodipine (Correct Answer)
E. Spironolactone

Explanation: ***Amlodipine*** - **Amlodipine** is a **dihydropyridine calcium channel blocker** known to cause **peripheral edema** (like pretibial edema) as a common side effect due to precapillary vasodilation. - The patient's blood pressure was elevated, and after starting an antihypertensive medication, he developed new-onset **2+ pretibial edema**, strongly suggesting this class of medication. *Prazosin* - **Prazosin** is an **alpha-1 adrenergic antagonist** that can cause orthostatic hypotension or reflex tachycardia but is less commonly associated with significant peripheral edema. - While it lowers blood pressure, its side effect profile does not typically include prominent pretibial edema. *Losartan* - **Losartan** is an **angiotensin receptor blocker (ARB)** that works by blocking the effects of angiotensin II. It is generally well-tolerated and less likely to cause peripheral edema compared to calcium channel blockers. - ARBs like losartan do not cause the same degree of precapillary vasodilation that leads to ankle edema. *Propranolol* - **Propranolol** is a **non-selective beta-blocker**. Common side effects include bradycardia, fatigue, and bronchospasm, but not typically peripheral edema. - Beta-blockers primarily reduce heart rate and contractility, and do not cause vasodilation leading to pretibial edema. *Spironolactone* - **Spironolactone** is a **potassium-sparing diuretic** used for hypertension, but also in conditions like heart failure and cirrhosis to reduce fluid retention. It is more likely to cause diuresis and reduce edema, not cause it. - Side effects include hyperkalemia and gynecomastia, but not peripheral edema, as its primary action is to eliminate excess fluid.

Question 46: A 54-year-old African American man presents to the clinic for his first annual well-check. He was unemployed for years but recently received health insurance from a new job. He reports feeling healthy and has no complaints. His blood pressure is 157/90 mmHg, pulse is 86/min, and respirations are 12/min. Routine urinalysis demonstrated a mild increase in albumin and creatinine. What medication is indicated at this time?

A. Hydrochlorothiazide
B. Metoprolol
C. Furosemide
D. Lisinopril (Correct Answer)
E. Amlodipine

Explanation: ***Lisinopril*** - This patient presents with **hypertension (157/90 mmHg)** and **mild albuminuria with elevated creatinine**, indicating early chronic kidney disease (CKD). An **ACE inhibitor (e.g., lisinopril)** is the first-line treatment for hypertension in **any patient with CKD or proteinuria**, regardless of race or ethnicity. - ACE inhibitors are **renoprotective** by reducing intraglomerular pressure and slowing progression of kidney disease. The presence of albuminuria represents a **compelling indication** that overrides other considerations for initial antihypertensive selection. - Note: While ACE inhibitors are typically **less effective** as monotherapy in African Americans without compelling indications, the presence of CKD/proteinuria makes them the preferred agent. *Hydrochlorothiazide* - While a **thiazide diuretic** like hydrochlorothiazide would be an appropriate first-line agent for this African American patient with uncomplicated hypertension, it is **less effective** than an ACE inhibitor in patients with **proteinuria or kidney disease**. - It does not offer the same degree of **renoprotection** as an ACE inhibitor in this clinical scenario with documented albuminuria. *Metoprolol* - **Beta-blockers** like metoprolol are effective antihypertensives but are generally **not considered first-line** for uncomplicated hypertension unless there are compelling indications like heart failure, angina, or history of myocardial infarction. - They also do not provide the specific **renoprotective benefits** seen with ACE inhibitors in patients with albuminuria. *Furosemide* - **Loop diuretics** such as furosemide are potent diuretics primarily used for managing **symptoms of fluid overload** (e.g., heart failure, severe edema) and are not typically the first choice for chronic hypertension without such indications. - For patients with **mild kidney impairment and hypertension without volume overload**, an ACE inhibitor is preferred for its renoprotective effects. *Amlodipine* - **Calcium channel blockers** like amlodipine are effective antihypertensives and would typically be an excellent first-line choice for an African American patient with hypertension. - However, for this patient with **documented albuminuria**, an ACE inhibitor is preferred due to its **specific renoprotective effects** and proven benefit in slowing CKD progression, which amlodipine does not provide.

Question 47: A 27-year-old woman with no past medical history presents to her primary care provider because she has begun to experience color changes in her fingers on both hands in cold temperatures. She reports having had this problem for a few years, but with the weather getting colder this winter she has grown more concerned. She says that when exposed to cold her fingers turn white, blue, and eventually red. When the problem subsides she experiences pain in the affected fingers. She says that wearing gloves helps somewhat, but she continues to experience the problem. Inspection of the digits is negative for ulcerations. Which of the following is the next best step in treatment?

A. Amlodipine (Correct Answer)
B. Thoracic sympathectomy
C. Phenylephrine
D. Propranolol
E. Sildenafil

Explanation: ***Amlodipine*** - This patient exhibits classic symptoms of **Raynaud's phenomenon**, characterized by color changes (white, blue, red) in the digits upon cold exposure, followed by pain. - **Calcium channel blockers** like **amlodipine** are the first-line pharmacologic treatment for Raynaud's, working by dilating peripheral arteries to improve blood flow. *Thoracic sympathectomy* - **Sympathectomy** is a surgical intervention reserved for **severe cases** of Raynaud's phenomenon that are refractory to medical therapy, especially when there is evidence of impending **ischemic damage** (e.g., ulcerations). - This patient currently has a mild presentation without ulcerations, making surgery an overly aggressive initial treatment. *Phenylephrine* - **Phenylephrine** is an **alpha-1 adrenergic agonist** that causes **vasoconstriction**, primarily used as a decongestant or to raise blood pressure in hypotensive states. - Administering a vasoconstrictor would **worsen** Raynaud's symptoms by further reducing blood flow to the digits. *Propranolol* - **Propranolol** is a **beta-blocker** that can potentially **worsen Raynaud's phenomenon** by causing unopposed alpha-adrenergic vasoconstriction, especially with non-selective agents. - Beta-blockers are generally contraindicated in patients with Raynaud's, or should be used with extreme caution if absolutely necessary for another condition. *Sildenafil* - While **sildenafil** (a **phosphodiesterase-5 inhibitor**) can cause vasodilation and has been used off-label for severe Raynaud's, it is typically considered a **second-line or adjunctive treatment** for refractory cases. - **Calcium channel blockers** are the preferred initial pharmacologic therapy due to their proven efficacy and broader availability.

Question 48: A 25-year-old woman presents to the psychiatric emergency department in restraints. She was found trying to break into a deli at midnight. The patient claims that she has an idea that will revolutionize the shipping industry. The patient is not violent but seems highly agitated and is speaking very rapidly about her ideas. She is easily distractible and tells you about many of her other ideas. She has a past medical history of depression and hypertension refractory to treatment. Her current medications include captopril, ibuprofen, and melatonin. A neurological exam is deferred due to the patient's current status. Her pulmonary and cardiovascular exams are within normal limits and mild bilateral bruits are heard over her abdomen. The patient is given haloperidol and diphenhydramine and spends the night in the psychiatric inpatient unit. The patient is started on long-term therapy and is discharged 3 days later. At a follow up visit at her primary care physician, the patient is noted to have a blood pressure of 150/100 mmHg. She is started on chlorthalidone and instructed to return in 3 days. When the patient returns her blood pressure is 135/90 mmHg. She exhibits a fine tremor, and complains of increased urinary frequency. Her pulse is 47/minute, and she is afebrile. Which of the following is the best next step in management?

A. Ultrasound of the renal arteries (Correct Answer)
B. Maintain current medication regimen
C. Increase captopril dose
D. Change diuretics
E. Increase chlorthalidone dose

Explanation: ***Ultrasound of the renal arteries*** - The presence of **bilateral abdominal bruits** and **refractory hypertension** in a young woman despite multiple medications (captopril, chlorthalidone) strongly suggests **renovascular hypertension**, likely due to **fibromuscular dysplasia**. - **Renal artery stenosis** is an important cause of secondary hypertension that requires investigation. Ultrasound of the renal arteries is the appropriate first-line non-invasive investigation to assess for renal artery stenosis. - While the new symptoms (tremor, bradycardia, polyuria) are concerning for **lithium side effects** or toxicity (likely the "long-term therapy" started for bipolar disorder), potentially exacerbated by the thiazide diuretic chlorthalidone, the underlying **secondary hypertension must still be evaluated** to optimize long-term management. - Among the available options, investigating the cause of refractory hypertension is the priority. *Maintain current medication regimen* - The patient's blood pressure remains suboptimally controlled at 135/90 mmHg. - Furthermore, the new symptoms (tremor, bradycardia, increased urinary frequency) suggest possible medication side effects that require investigation, not simply maintenance of the current regimen. *Increase captopril dose* - Increasing the dose of an **ACE inhibitor** (captopril) in a patient with suspected **bilateral renal artery stenosis** can lead to acute kidney injury due to critical reduction in glomerular filtration pressure. - This would not address the underlying cause of secondary hypertension or the new symptoms. *Change diuretics* - While simply changing diuretics does not address the strong clinical suspicion for **renovascular hypertension** indicated by bilateral abdominal bruits in a young patient with refractory hypertension. - The underlying secondary cause must be investigated first before making empiric medication changes. *Increase chlorthalidone dose* - Increasing the thiazide dose might marginally lower blood pressure but does not address the potential underlying **renovascular hypertension**. - Additionally, thiazide diuretics can **increase lithium levels** by reducing renal clearance, and increasing the dose could worsen potential lithium toxicity (explaining the tremor, bradycardia, and polyuria).

Question 49: An 11-year-old boy is brought to the physician by his mother because of teacher complaints regarding his poor performance at school for the past 8 months. He has difficulty sustaining attention when assigned school-related tasks, does not follow the teachers' instructions, and makes careless mistakes in his homework. He often blurts out answers in class and has difficulty adhering to the rules during soccer practice. His mother reports that he is easily distracted when she speaks with him and that he often forgets his books at school. Physical examination shows no abnormalities. The patient is started on the appropriate first-line therapy. This boy is at increased risk for which of the following conditions?

A. Elevated blood pressure (Correct Answer)
B. Serotonin syndrome
C. Increased BMI
D. Prolonged QT interval
E. Decreased perspiration

Explanation: ***Elevated blood pressure*** - This boy's symptoms are highly suggestive of **ADHD** (Attention-Deficit/Hyperactivity Disorder), which is commonly treated with **stimulant medications** like methylphenidate or amphetamines. - Stimulants can cause **cardiovascular side effects**, including **elevated blood pressure** and heart rate, warranting regular monitoring. *Serotonin syndrome* - **Serotonin syndrome** is a risk associated with medications that increase serotonin levels, such as **SSRIs** or MAO inhibitors, which are not typically first-line for ADHD. - Characterized by altered mental status, autonomic dysfunction, and neuromuscular abnormalities, symptoms not directly caused by stimulant therapy. *Increased BMI* - Medications for ADHD, particularly stimulants, are more commonly associated with **decreased appetite** and **weight loss**, not an increased BMI. - **Appetite suppression** leading to difficulty gaining weight is a known side effect in children taking these medications. *Prolonged QT interval* - While some psychiatric medications can prolong the QT interval (e.g., certain antipsychotics or TCAs), **stimulants** used for ADHD are generally not a primary cause of this. - **ECG monitoring** may be considered for patients with pre-existing cardiac conditions, but it's not a common direct side effect for healthy individuals on stimulants. *Decreased perspiration* - Stimulant medications for ADHD can sometimes lead to **increased sweating** (hyperhidrosis) as a side effect, rather than decreased perspiration. - **Autonomic nervous system changes** due to stimulants can include enhanced sympathetic activity, which can manifest as increased sweating.

Question 50: A patient with a history of hypertension and bipolar disorder is seen in your clinic for new-onset tremor, increased urination, and mild dehydration symptoms. Her bipolar disorder has been well-controlled with her current medication regimen. She recently started a new medication for better management of her hypertension. Which of the following medications did she most likely start?

A. Amlodipine
B. Lisinopril
C. Hydrochlorothiazide (Correct Answer)
D. Furosemide
E. Metoprolol

Explanation: ***Hydrochlorothiazide*** - **Thiazide diuretics** are first-line antihypertensive agents that promote **sodium and water excretion**. - Volume depletion from thiazides **decreases renal lithium clearance**, increasing serum lithium levels and causing **lithium toxicity**. - Classic lithium toxicity presents with **tremor, polyuria (nephrogenic diabetes insipidus), polydipsia**, and dehydration. - This represents a critical **drug-drug interaction** between thiazides and lithium. *Incorrect: Amlodipine* - **Calcium channel blocker** (dihydropyridine class) commonly used for hypertension. - Does **not affect lithium levels** or renal clearance. - Side effects include peripheral edema and reflex tachycardia, not the symptoms described. *Incorrect: Lisinopril* - **ACE inhibitor** used as first-line therapy for hypertension. - Does **not significantly affect lithium clearance** (though ACE inhibitors can have minor effects, they don't typically cause clinically significant lithium toxicity). - Common side effects include dry cough and hyperkalemia, not tremor or polyuria. *Incorrect: Furosemide* - **Loop diuretic** that can cause dehydration and polyuria. - Could potentially increase lithium levels through volume depletion, but **thiazides are more commonly implicated** in lithium toxicity. - Furosemide is typically reserved for **resistant hypertension or heart failure**, not as initial therapy. *Incorrect: Metoprolol* - **Beta-blocker** used for hypertension management. - Does **not affect lithium levels** or cause the described symptoms. - Side effects include bradycardia, fatigue, and bronchospasm in susceptible patients.

Question 51: Three weeks after starting a new medication for hyperlipidemia, a 54-year-old man comes to the physician because of pain and swelling in his left great toe. Examination shows swelling and erythema over the metatarsophalangeal joint of the toe. Analysis of fluid from the affected joint shows needle-shaped, negatively-birefringent crystals. Which of the following best describes the mechanism of action of the drug he is taking?

A. Promotion of hepatic LDL secretion
B. Inhibition of hepatic HMG-CoA reductase
C. Inhibition of intestinal cholesterol absorption
D. Inhibition of intestinal bile acid absorption
E. Inhibition of hepatic VLDL synthesis (Correct Answer)

Explanation: ***Inhibition of hepatic VLDL synthesis*** - The patient's symptoms (pain, swelling in the great toe, negatively-birefringent crystals) are classic for **gout**. - **Fibrates** (e.g., gemfibrozil, fenofibrate) are a class of hyperlipidemia medications known to cause hyperuricemia and precipitate gout by inhibiting hepatic VLDL synthesis and increasing catabolism of triglyceride-rich lipoproteins. *Promotion of hepatic LDL secretion* - Medications that promote hepatic LDL secretion are not a primary class of lipid-lowering drugs and are not directly associated with precipitating gout. - The primary goal in hyperlipidemia management is usually to reduce LDL levels, not increase secretion. *Inhibition of hepatic HMG-CoA reductase* - This describes the mechanism of action of **statins**, which are generally not associated with triggering gout and can even have some anti-inflammatory effects. - Statins primarily lower LDL cholesterol by reducing mevalonate synthesis, a precursor to cholesterol. *Inhibition of intestinal cholesterol absorption* - This is the mechanism of action of **ezetimibe**, which specifically blocks the **Niemann-Pick C1-like 1 (NPC1L1)** transporter in the small intestine. - Ezetimibe is not commonly associated with new-onset gout. *Inhibition of intestinal bile acid absorption* - This describes the mechanism of **bile acid sequestrants** (e.g., cholestyramine, colestipol, colesevelam), which bind bile acids in the intestine, preventing their reabsorption. - While they can have various side effects, they are not typically linked to causing gout.

Question 52: A 45-year-old woman presents to a physician with repeated episodes of vertigo for the last 6 months. The episodes usually last for 20–30 minutes, but 2 episodes persisted for more than an hour. The episodes are often associated with severe nausea and vomiting. She has experienced falls after losing her balance during these episodes on 3 occasions, but she has never lost consciousness. However, she reports that after an acute episode is over, she feels unsteady, tired, and nauseated for several hours. For the previous month, she has noted that the acute attacks of vertigo are preceded by a sense of fullness in the ear, hearing an ocean-like roaring sound, and hearing loss on the left side. In between episodes, she is completely normal. There is no history of a known medical disorder, substance use or regular use of medications. The vital signs are within normal limits. The neurologic examination shows normal tone and power in all muscle groups, normal deep tendon reflexes, absence of signs of cerebellar dysfunction, and normal gait. The Dix-Hallpike positional test is negative. The otoscopic exam of both ears does not reveal any significant abnormality. The physician orders an audiogram, which suggests mild low-frequency sensorineural hearing loss on the left side. In addition to lifestyle changes and symptomatic treatment of acute episodes, which of the following is the most appropriate initial treatment to prevent recurrent episodes?

A. Intramuscular dexamethasone
B. Oral diazepam
C. Oral ephedrine
D. Oral prednisone
E. Oral hydrochlorothiazide (Correct Answer)

Explanation: ***Oral hydrochlorothiazide*** - The patient's symptoms (recurrent vertigo, aural fullness, roaring tinnitus, and low-frequency sensorineural hearing loss on one side) are highly characteristic of **Ménière's disease**. - **Diuretics** like hydrochlorothiazide are a cornerstone of prophylactic treatment for Ménière's disease, as they reduce endolymphatic pressure. *Intramuscular dexamethasone* - While corticosteroids (like dexamethasone) can be used to treat **acute, severe attacks** of Ménière's disease, they are not the first-line treatment for **long-term prevention** of recurrent episodes. - Intramuscular administration is typically reserved for severe acute flares or when oral intake is compromised, but not for chronic prophylaxis. *Oral diazepam* - **Diazepam** is a benzodiazepine used to reduce the symptoms of **acute vertigo** and associated nausea and anxiety due to its sedative and anxiolytic properties. - It is a **symptomatic treatment** during an acute attack and does not prevent recurrent episodes of Ménière's disease. *Oral ephedrine* - Ephedrine is a **sympathomimetic** drug, primarily used as a decongestant and bronchodilator. - It has no established role in the treatment or prevention of Ménière's disease or other forms of vertigo. *Oral prednisone* - **Prednisone** is an oral corticosteroid that can be used to manage acute flares of Ménière's disease, similar to dexamethasone, by reducing inflammation and endolymphatic pressure. - However, for **long-term prevention**, diuretics are generally preferred due to a more favorable side effect profile and sustained efficacy compared to chronic steroid use.

Question 53: A 38-year-old man is brought to the emergency department 35 minutes after an episode of loss of consciousness. He was having dinner with a client when his left arm suddenly became weak and numb. A few minutes later he became tense and his arms and legs began jerking violently, following which he lost consciousness. He has no recollection of this event. He works as a business consultant. He has a history of asthma and major depressive disorder. Current medication include an albuterol inhaler and doxepin. He increased the dose of doxepin one week ago because he felt the medication was not helping. He drinks two to three beers on the weekend. He admits to using cocaine 4–5 times per week. On arrival, he is alert and oriented to person, place, and time. His speech is slurred. His temperature is 37°C (98.6F), pulse is 96/min, and blood pressure is 155/90 mm Hg. The pupils are equal and reactive to light. Neurologic exam shows left facial droop. There is 3/5 strength in the left arm. Which of the following is the most likely underlying mechanism of this patient's symptoms?

A. Lowered seizure threshold (Correct Answer)
B. Tear in the carotid artery
C. Vasospasm of cerebral vessels
D. Ruptured berry aneurysm
E. Antagonism on M3 receptor

Explanation: ***Lowered seizure threshold*** - The patient's history of **cocaine use** and recent **increase in doxepin** dosage are significant risk factors, as both can lower the seizure threshold. Cocaine is a known CNS stimulant, and tricyclic antidepressants like doxepin can induce seizures, especially at higher doses or in overdose. - The description of focal weakness followed by generalized tonic-clonic activity, and post-ictal slurred speech and neurological deficits (left facial droop, left arm weakness), is consistent with a **focal seizure with secondary generalization**, followed by a Todd's paralysis. *Tear in the carotid artery* - A carotid artery dissection can lead to **ischemic stroke** symptoms, but the sudden onset of focal weakness followed by generalized tonic-clonic seizures is not the typical presentation. - While it could cause a stroke, the preceding seizure activity points away from dissection as the primary underlying mechanism of the *initial* event described. *Vasospasm of cerebral vessels* - Cerebral vasospasm primarily occurs in conditions like **subarachnoid hemorrhage** (SAH) and can cause delayed cerebral ischemia. - While cocaine use can induce vasospasm, the clinical picture of a focal seizure progressing to generalized tonic-clonic activity is not the direct consequence of vasospasm itself, although vasospasm could theoretically lead to ischemia which then triggers a seizure. *Ruptured berry aneurysm* - A ruptured berry aneurysm typically presents as a **sudden, severe "thunderclap" headache** due to subarachnoid hemorrhage, often followed by rapid deterioration of consciousness. - While seizures can occur with SAH, the progression described (focal weakness to tonic-clonic seizure, and post-ictal state with focal neurological signs) is more indicative of a primary seizure event rather than a ruptured aneurysm. *Antagonism on M3 receptor* - Doxepin, a tricyclic antidepressant, primarily exerts its effects through **norepinephrine and serotonin reuptake inhibition**, and also has significant **anticholinergic (M3 receptor antagonism)** and antihistaminergic properties. - While anticholinergic effects can cause confusion or delirium, they do not directly explain the sudden onset of focal weakness followed by generalized tonic-clonic seizures.

Question 54: A 53-year-old woman presents to a physician for a regular check-up. She has no complaints, but notes that she has been anxious and easily irritable for no particular reason over the past year. Six months ago, she was diagnosed with grade I arterial hypertension and prescribed lifestyle modification and weight loss to control her blood pressure. She currently takes aspirin (81 mg) and rosuvastatin (10 mg) daily. The vital signs are as follows: blood pressure 145/80 mm Hg, heart rate 81/min, respiratory rate 14/min, and temperature 36.6℃ (97.9℉). She weighs 91 kg (213.8 lb), the height is 167 cm (5.5 ft), and the BMI is 32.6 kg/m2. The physical examination is unremarkable. Blood testing was performed, and the results are shown below. Plasma glucose 109.9 mg/dL (6.1 mmol/L) Plasma triglycerides 185.8 mg/dL (2.1 mmol/L) Na+ 141 mEq/L K+ 4.2 mEq/L The patient was prescribed atenolol. If the medication alone affects the patient’s measurements, which laboratory finding would you expect to note several weeks after the treatment is initiated?

A. Plasma glucose 54 mg/dL (3.0 mmol/L)
B. Plasma triglycerides 150.4 mg/dL (1.7 mmol/L) (Correct Answer)
C. Na+ 137 mEq/L
D. Na+ 148 mEq/L
E. K+ 2.6 mEq/L

Explanation: ***Plasma triglycerides 150.4 mg/dL (1.7 mmol/L)*** - Beta-blockers, including atenolol, can cause **modest increases in triglycerides** (typically 10-20%) and **decreases in HDL cholesterol**. - However, a **decrease in triglycerides** from 185.8 to 150.4 mg/dL would be **unexpected and beneficial** if it occurred, but is **not a typical effect** of beta-blockers. - Among the options provided, this represents the **least implausible change**, though it goes in the opposite direction of the expected effect. - Note: The patient is already on rosuvastatin, which affects lipids, but the question specifies "medication alone" referring to atenolol. *Plasma glucose 54 mg/dL (3.0 mmol/L)* - While beta-blockers can **mask hypoglycemia symptoms** and slightly impair glucose tolerance, atenolol as a β1-selective agent has **minimal effect on glucose metabolism** in non-diabetic patients. - Severe hypoglycemia (54 mg/dL) would **not be expected** in a non-diabetic patient taking atenolol alone. *Na+ 137 mEq/L* - Beta-blockers are **not associated with hyponatremia** or significant changes in serum sodium. - A decrease from 141 to 137 mEq/L is within normal variation and **not a recognized pharmacological effect** of atenolol. *Na+ 148 mEq/L* - Beta-blockers do **not cause hypernatremia**. - An increase to 148 mEq/L would suggest **dehydration or other causes**, not atenolol therapy. *K+ 2.6 mEq/L* - Beta-blockers can cause **mild hyperkalemia** (increased potassium), not hypokalemia, by inhibiting β2-receptor-mediated cellular potassium uptake and reducing renin-aldosterone activity. - **Hypokalemia (2.6 mEq/L) is the opposite** of what would be expected and would suggest other causes such as diuretic use or GI losses.

Question 55: A 58-year-old male with a history of congestive heart failure and hypertension comes to you with the chief complaint of new-onset cough as well as increased serum potassium in the setting of a new medication. Which of the following medications is most likely responsible for these findings?

A. Lisinopril (Correct Answer)
B. Metoprolol
C. Furosemide
D. Amiodarone
E. Digoxin

Explanation: ***Lisinopril*** - **Lisinopril** is an ACE inhibitor, which can cause a **persistent dry cough** due to the accumulation of bradykinin. - ACE inhibitors can also cause **hyperkalemia** by inhibiting aldosterone secretion, which normally promotes potassium excretion. *Metoprolol* - **Metoprolol** is a beta-blocker that primarily decreases heart rate and blood pressure; it is not typically associated with cough or hyperkalemia. - While it can be used in CHF, its common side effects include bradycardia and fatigue, not the described symptoms. *Furosemide* - **Furosemide** is a loop diuretic that promotes potassium excretion, leading to **hypokalemia**, not hyperkalemia. - It does not typically cause cough; instead, it can help reduce fluid accumulation in the lungs associated with CHF. *Amiodarone* - **Amiodarone** is an antiarrhythmic drug known for several significant side effects, including **pulmonary fibrosis** (which can cause cough) and thyroid dysfunction. - However, it does not typically cause hyperkalemia; instead, it can cause changes in electrolyte levels, but not the specific combination seen here. *Digoxin* - **Digoxin** is a cardiac glycoside used to increase cardiac contractility and slow heart rate in heart failure and arrhythmias. - It does not typically cause cough or hyperkalemia; its toxicity is often associated with nausea, visual disturbances, and arrhythmias.

Question 56: A new drug has been shown to block epithelial sodium channels in the cortical collecting duct. Which of the following is most likely to be decreased upon drug administration?

A. Urea reabsorption in the collecting tubules
B. Hydrogen ion secretion in the collecting tubules
C. Potassium secretion in the collecting tubules (Correct Answer)
D. Sodium secretion in the collecting tubules
E. Sodium chloride reabsorption in the distal tubule

Explanation: ***Potassium secretion in the collecting tubules*** - Blocking **epithelial sodium channels (ENaC)** in the cortical collecting duct reduces sodium reabsorption, which in turn diminishes the electrochemical gradient driving **potassium secretion** into the lumen. - This is because sodium reabsorption creates a more negative luminal charge, attracting potassium ions to move from the cell into the tubule. - This is the mechanism of **potassium-sparing diuretics** like amiloride and triamterene. *Urea reabsorption in the collecting tubules* - Urea **reabsorption** primarily occurs in the **medullary collecting duct** via urea transporters (UT-A1, UT-A3) and is influenced by the inner medullary osmolarity and ADH. - Blocking ENaC would primarily affect sodium flux and potassium secretion, with minimal direct impact on urea reabsorption in the collecting duct. *Hydrogen ion secretion in the collecting tubules* - **Hydrogen ion (H+) secretion** occurs in the collecting tubules via intercalated cells (α-intercalated cells), which is important for acid-base balance. - While blocking ENaC can indirectly reduce H+ secretion (by decreasing the lumen-negative potential), the primary and most significant effect is on **potassium secretion**, making this a less likely answer. *Sodium secretion in the collecting tubules* - The primary function of ENaC is to **reabsorb sodium** from the tubular lumen back into the blood, not to secrete it. - Sodium is not normally secreted in the collecting tubules; blocking ENaC would decrease sodium **reabsorption**, not affect sodium secretion. *Sodium chloride reabsorption in the distal tubule* - **Sodium chloride reabsorption** in the distal convoluted tubule is mainly mediated by the **thiazide-sensitive Na-Cl co-transporter (NCC)**. - ENaC are predominantly located in the cortical collecting duct (downstream from the DCT), so blocking them would not directly impact NaCl reabsorption in the distal tubule.

Question 57: A 1-week-old male newborn is brought to the physician for the evaluation of persistent irritability and crying. He was born at 36 weeks' gestation. Pregnancy was complicated by polyhydramnios. His mother reports that she nurses him frequently and changes his diapers 18–20 times per day. He is at the 5th percentile for length and 10th percentile for weight. Physical examination shows a triangular face with a prominent forehead and large, protruding ears. Serum studies show: Na+ 129 mEq/L K+ 2.8 mEq/L Cl- 90 mEq/L Ca2+ 8.0 mg/dL HCO3- 32 mEq/L Arterial blood gas analysis shows a pH of 7.51. The effects of this patient's condition are most similar to the long-term administration of which of the following drugs?

A. Triamterene
B. Acetazolamide
C. Tolvaptan
D. Mannitol
E. Bumetanide (Correct Answer)

Explanation: ***Bumetanide*** - The patient's presentation of polyhydramnios, **hypokalemia**, **hypochloremia**, **metabolic alkalosis**, and **failure to thrive** is highly suggestive of **Bartter syndrome**. - **Bartter syndrome** is a genetic disorder affecting the **Na-K-2Cl cotransporter (NKCC2)** in the **thick ascending limb of the loop of Henle**, mimicking the effects of chronic loop diuretic use like bumetanide. *Triamterene* - **Triamterene** is a **potassium-sparing diuretic** that acts on the **collecting duct** by blocking epithelial sodium channels, leading to sodium excretion and **potassium retention**. - Its long-term use would cause **hyperkalemia** and potentially **metabolic acidosis**, which contradicts the patient's presentation of hypokalemia and metabolic alkalosis. *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** that primarily acts on the **proximal tubule**, leading to increased excretion of bicarbonate, sodium, and potassium. - Long-term use typically results in a **hyperchloremic metabolic acidosis**, which is opposite to the metabolic alkalosis observed in the patient. *Tolvaptan* - **Tolvaptan** is a **vasopressin (V2) receptor antagonist** used to treat **hyponatremia** by increasing free water excretion. - Its primary effect is on water balance and sodium concentration, and it does not typically cause the significant electrolyte disturbances (hypokalemia, hypochloremia, metabolic alkalosis) seen in this patient. *Mannitol* - **Mannitol** is an **osmotic diuretic** that works by increasing the osmolarity of the glomerular filtrate, leading to decreased water reabsorption throughout the nephron. - While it can cause electrolyte imbalances, it primarily leads to **volume depletion** and can affect sodium levels, but it doesn't specifically mimic the profile of hypokalemia and metabolic alkalosis seen in Bartter syndrome.

Question 58: A 55-year-old man presents to the emergency department complaining of mild vision changes, dizziness, and severe pain in the chest for the past hour. He has also been experiencing nausea since this morning and has already vomited twice. Past medical history includes poorly controlled type 2 diabetes and end-stage renal disease requiring dialysis. His blood pressure is 210/100 mm Hg, pulse is 110/min, and respirations are 18/min. Ophthalmic examination of his eyes show papilledema and flame-shaped hemorrhages and he is diagnosed with hypertensive emergency. Treatment involves rapidly lowering his blood pressure, and he is started on intravenous sodium nitroprusside while emergent dialysis is arranged. Which of the following cardiac pressure-volume loops closely represents the action of the drug he has been administered, where blue represents before administration and purple represent after administration?

A. Diagram B (Correct Answer)
B. Diagram E
C. Diagram A
D. Diagram C
E. Diagram D

Explanation: ***Diagram B*** - Sodium nitroprusside is a **balanced vasodilator**, meaning it reduces both **preload** (venous return) and **afterload** (arterial resistance). - This typically results in a decrease in both **end-diastolic volume** (due to reduced preload) and **systolic pressure**/end-systolic volume (due to reduced afterload), as shown by the shift in Diagram B. *Diagram E* - This loop represents an increase in **contractility** and a decrease in **afterload**, which is not the primary action of nitroprusside. - While nitroprusside causes vasodilation, it doesn't directly increase contractility; it primarily works by reducing the heart's workload. *Diagram A* - This diagram shows a significant increase in **preload** (increased end-diastolic volume) with a minimal change in afterload, which is inconsistent with sodium nitroprusside's action as a vasodilator. - Nitroprusside would decrease preload rather than increase it. *Diagram C* - This loop depicts a significant increase in **afterload** (higher systolic pressure) and **preload** (increased end-diastolic volume), which is contrary to the effects of a vasodilator like sodium nitroprusside. - Nitroprusside aims to lower blood pressure and reduce cardiac workload. *Diagram D* - This diagram illustrates a substantial increase in **contractility** with a relatively unchanged afterload, which is not the expected effect of sodium nitroprusside. - Nitroprusside primarily acts on vascular smooth muscle to cause relaxation, not on myocardial contractility.

Question 59: A 54-year-old woman comes to the physician for a follow-up examination after presenting with elevated blood pressure readings during her last two visits. After her last visit 2 months ago, she tried controlling her hypertension with weight loss before starting medical therapy, but she has since been unable to lose any weight. Her pulse is 76/min, and blood pressure is 154/90 mm Hg on the right arm and 155/93 mm Hg on the left arm. She agrees to start treatment with a thiazide diuretic. In response to this treatment, which of the following is most likely to decrease?

A. Serum uric acid levels
B. Urinary calcium excretion (Correct Answer)
C. Serum glucose levels
D. Urinary potassium excretion
E. Urinary sodium excretion

Explanation: ***Urinary calcium excretion*** - Thiazide diuretics work by inhibiting the **Na-Cl cotransporter** in the **distal convoluted tubule**, which leads to decreased sodium reabsorption and subsequently increased calcium reabsorption. - This property makes thiazides useful in treating conditions like **hypercalciuria** and preventing **calcium-containing kidney stones**. *Serum uric acid levels* - Thiazide diuretics are known to **increase serum uric acid levels** by inhibiting its secretion in the proximal tubule. - This can precipitate or worsen **gout attacks**, a known side effect of these medications. *Serum glucose levels* - Thiazide diuretics can cause **increased serum glucose levels** by impairing insulin secretion and promoting insulin resistance. - This effect is more pronounced at higher doses and in patients with pre-existing metabolic risk factors. *Urinary potassium excretion* - Thiazide diuretics **increase urinary potassium excretion**, often leading to **hypokalemia**. - This occurs because decreased sodium reabsorption in the distal convoluted tubule leads to increased sodium delivery to the collecting duct, stimulating an exchange for potassium. *Urinary sodium excretion* - The primary mechanism of action of thiazide diuretics is to inhibit sodium reabsorption in the distal convoluted tubule, which directly leads to an **increase in urinary sodium excretion**. - This increased sodium excretion is what drives their diuretic and antihypertensive effects.

Question 60: A 21-year-old male presents to the emergency department with generalized weakness and fatigue. His past medical history is significant for hypertension refractory to several medications but is otherwise unremarkable. He is afebrile, his pulse is 82/min, respirations are 18/min, and blood pressure is 153/94 mmHg. Labs are as follows: Sodium: 142 mEq/L Potassium: 2.7 mEq/L Bicarbonate: 36 mEq/L Serum pH: 7.5 pCO2: 50 mmHg Aldosterone: Decreased Based on clinical suspicion, a genetic screen is performed, confirming an underlying syndrome due to an autosomal dominant gain of function mutation. Which of the following medications can be given to treat the most likely cause of this patient's symptoms?

A. Thiazide diuretics
B. Amiloride (Correct Answer)
C. Mannitol
D. Acetazolamide
E. Loop diuretics

Explanation: ***Amiloride*** - The patient's presentation with **hypertension**, **hypokalemia**, **metabolic alkalosis**, and **decreased aldosterone** despite these findings is characteristic of **Liddle's Syndrome**. - **Amiloride** is a potassium-sparing diuretic that directly blocks the **epithelial sodium channel (ENaC)** in the collecting duct, which is overactive in Liddle's Syndrome due to a gain-of-function mutation. *Thiazide diuretics* - While commonly used for hypertension, **thiazide diuretics** work by inhibiting the Na+/Cl- cotransporter in the distal convoluted tubule and would likely worsen the **hypokalemia** in Liddle's Syndrome. - They do not address the primary pathophysiology of **ENaC overactivity** in the collecting duct. *Mannitol* - **Mannitol** is an osmotic diuretic primarily used to reduce intracranial pressure or treat cerebral edema. - It acts in the renal tubule to inhibit water reabsorption and is not indicated for the management of **hypertension** or **electrolyte disturbances** seen in Liddle's Syndrome. *Acetazolamide* - **Acetazolamide** is a carbonic anhydrase inhibitor that acts primarily in the proximal tubule to block bicarbonate reabsorption. - It is used for conditions like glaucoma, altitude sickness, and metabolic alkalosis, but it is not effective for the **sodium retention** and **potassium wasting** characteristic of Liddle's Syndrome. *Loop diuretics* - **Loop diuretics** like furosemide work by inhibiting the Na+/K+/2Cl- cotransporter in the thick ascending limb of the loop of Henle. - Similar to thiazides, they would exacerbate the **hypokalemia** in a patient with Liddle's Syndrome and do not target the underlying cause of **ENaC overactivity**.

Question 61: A 67-year-old gentleman with a history of poorly controlled diabetes presents to his primary care physician for a routine examination. He is found to be hypertensive on physical exam and is started on a medication that is considered first-line therapy for his condition. What should the physician warn the patient about before the patient takes his first dose of the medication?

A. Hypothermic episodes
B. Hyperthermic episodes
C. Hypertensive episodes
D. Hypotensive episodes (Correct Answer)
E. Anuric episodes

Explanation: ***Hypotensive episodes*** - **First-line antihypertensive medications** (e.g., ACE inhibitors, ARBs, thiazide diuretics) commonly cause a drop in blood pressure, especially with the **first dose** or in patients who are volume-depleted. - Patients with **diabetes** are often predisposed to orthostatic hypotension due to autonomic neuropathy, making them more susceptible to symptomatic hypotension. *Hypothermic episodes* - **Hypothermia** (abnormally low body temperature) is not a common side effect of first-line antihypertensive medications. - While certain medications can affect thermoregulation, it is not a primary concern for typical antihypertensives. *Hyperthermic episodes* - **Hyperthermia** (abnormally high body temperature) is not a common side effect of first-line antihypertensive medications. - Some drugs can rarely cause drug-induced fever, but it's not a standard warning for initial dosing of antihypertensives. *Hypertensive episodes* - The purpose of antihypertensive medication is to **lower blood pressure**, not raise it; therefore, the medication would not cause hypertensive episodes. - A paradoxical increase in blood pressure is extremely rare and not a typical warning for first-line therapy. *Anuric episodes* - **Anuria** (absence of urine production) is a severe kidney dysfunction and is not a common initial side effect of first-line antihypertensive medications, although some, like ACE inhibitors, can acutely reduce glomerular filtration in specific high-risk patients. - While **acute kidney injury** requiring monitoring can occur, especially with ACE inhibitors/ARBs, complete anuria as a warning for initial dosing is not typical.

Question 62: A 39-year-old man is admitted to the hospital with profuse diarrhea. His wife says that it started yesterday and since then the patient has passed over 15 liters of watery stools which have become progressively clear and odorless. Over the past 2 days, the patient has only eaten homemade food. His wife and daughter do not have any symptoms. His wife says that he returned from a trip to rural India 2 days before the symptoms began. He has a history of gastroesophageal reflux disease. His vitals are as follows: blood pressure 95/70 mm Hg, heart rate 100/min, respiratory rate 21/min, and temperature 35.8°C (96.4°F). The patient appears fatigued and pale. His skin elasticity and turgor are decreased. Cardiac auscultation reveals a holosystolic murmur that changes characteristics with changes in the patient’s position. The chronic intake of which of the following drugs could predispose the patient to this condition?

A. Ibuprofen
B. Aspirin
C. Pantoprazole (Correct Answer)
D. Levocetirizine
E. Propranolol

Explanation: ***Pantoprazole*** - The patient presents with classic symptoms of **cholera**, including rapid onset of **voluminous, watery, odorless stools** after returning from an endemic area (rural India). - **Proton pump inhibitors (PPIs)** like pantoprazole reduce stomach acidity, which can lower the infectious dose of *Vibrio cholerae* required to cause disease, thereby increasing susceptibility. *Ibuprofen* - **NSAIDs** like ibuprofen primarily inhibit prostaglandin synthesis, which can cause gastrointestinal side effects such as gastritis, ulcers, and bleeding. - They do not directly predispose to cholera infection by altering gastric pH or affecting bacterial colonization. *Aspirin* - **Aspirin**, an NSAID and antiplatelet agent, can cause gastrointestinal irritation and bleeding, especially at high doses. - It does not significantly alter gastric pH in a way that would predispose to cholera beyond general stomach upset, nor does it affect immune response to enteric pathogens. *Levocetirizine* - **Levocetirizine** is an antihistamine used for allergic conditions. - It has no known effect on gastric acidity or susceptibility to gastrointestinal infections like cholera. *Propranolol* - **Propranolol** is a beta-blocker used for conditions like hypertension, angina, and anxiety. - It does not affect gastric pH or the immune response to enteric pathogens, and therefore, does not predispose to cholera.

Question 63: A 62-year-old woman with no significant past medical history presents with progressive dyspnea on exertion over the past 6 months. Echocardiogram reveals elevated pulmonary artery pressure (PAP) of 55 mmHg with normal left ventricular ejection fraction and no evidence of left-sided valvular disease. Right heart catheterization confirms mean PAP of 50 mmHg with pulmonary capillary wedge pressure of 10 mmHg. Intraoperative administration of intravenous adenosine causes the PAP to decrease to 35 mmHg. What pharmacological therapy is most likely to provide long-term benefit for this patient?

A. Amlodipine (Correct Answer)
B. Bosentan
C. Epoprostenol
D. Sildenafil
E. Adenosine

Explanation: ***Amlodipine*** - The patient has **idiopathic pulmonary arterial hypertension (PAH, Group 1 PH)** confirmed by elevated mean PAP >20 mmHg with normal pulmonary capillary wedge pressure (≤15 mmHg), excluding left heart disease. - The **positive acute vasodilator response** (PAP drop >10 mmHg to <40 mmHg) during right heart catheterization indicates **vasoreactivity**, which predicts favorable response to **calcium channel blockers (CCBs)**. - **Amlodipine** or other CCBs (nifedipine, diltiazem) are the **first-line long-term therapy** for vasoreactive idiopathic PAH, with some patients achieving near-normalization of PAP. - Only about **10% of idiopathic PAH patients** are vasoreactive, making this finding clinically significant. *Bosentan* - **Bosentan** is an **endothelin receptor antagonist** used for **PAH (Group 1)**. - While effective for PAH, it is typically reserved for patients who are **non-vasoreactive** or who fail CCB therapy. - Given this patient's positive vasodilator response, a **CCB trial is preferred first** due to better long-term outcomes in vasoreactive patients. *Epoprostenol* - **Epoprostenol** is a **prostacyclin analog** used for severe **PAH**, particularly WHO functional class III-IV. - It requires **continuous intravenous infusion** and is reserved for more advanced or refractory PAH. - Not appropriate as **first-line therapy** in a vasoreactive patient who can be treated with oral CCBs. *Sildenafil* - **Sildenafil** is a **phosphodiesterase-5 inhibitor** effective for **PAH**. - Like bosentan, it is used for patients who are **non-vasoreactive** or have failed CCB therapy. - In a vasoreactive patient, **CCBs are preferred** due to superior long-term outcomes in this subset. *Adenosine* - **Adenosine** is an **ultrashort-acting vasodilator** used as a **diagnostic agent** during right heart catheterization to assess vasoreactivity. - It has a half-life of seconds and is **not suitable for long-term therapy**. - Alternative agents for vasoreactivity testing include inhaled nitric oxide and intravenous epoprostenol.

Question 64: A 50-year-old man comes to the physician for his annual health maintenance examination. The patient feels well. He has a history of hypertension, for which he currently takes lisinopril. He has smoked a pack of cigarettes daily for 20 years. He drinks 5–6 beers on weekends. He is 181 cm tall (5 ft 11 in), weighs 80 kg (176.4 lbs); BMI is 24.6 kg/m2. His pulse is 75/min, blood pressure is 140/85 mm Hg, and respirations are 18/min. Physical examination is unremarkable. Laboratory studies show: Total cholesterol 263 mg/dL High-density lipoprotein cholesterol 36 mg/dL Triglycerides 180 mg/dL In addition to dietary and lifestyle modification, administration of which of the following agents is the most appropriate next step in management?

A. Peroxisome proliferator-activated receptor alpha activator
B. Proprotein convertase subtilisin kexin 9 inhibitor
C. Bile acid resins
D. HMG-CoA reductase inhibitor (Correct Answer)
E. Cholesterol absorption inhibitor

Explanation: ***HMG-CoA reductase inhibitor*** - This patient has multiple **cardiovascular risk factors** (hypertension, smoking, low HDL, elevated LDL-c calculated from total cholesterol and triglycerides) and elevated LDL-c. An **HMG-CoA reductase inhibitor (statin)** is the first-line pharmacotherapy in such cases to reduce the risk of atherosclerotic cardiovascular disease events. - Statins effectively lower **LDL-c**, which is the primary target for cholesterol reduction in patients at high risk for cardiovascular disease. *Peroxisome proliferator-activated receptor alpha activator* - **Fibrates** (PPAR-α activators) are primarily used to lower **triglycerides** and increase HDL, and are not the first-line choice for lowering elevated LDL-c in high-risk patients. - They are typically reserved for severe hypertriglyceridemia not controlled by statins, or in patients intolerant to statins whose primary lipid issue is hypertriglyceridemia. *Proprotein convertase subtilisin kexin 9 inhibitor* - **PCSK9 inhibitors** are potent LDL-c lowering agents, but they are typically used as **adjunctive therapy** in patients with high cardiovascular risk who have not achieved adequate LDL-c reduction with maximum tolerated statin therapy, or in patients with familial hypercholesterolemia. - Given that this patient has not yet started statin therapy, a PCSK9 inhibitor is not the initial treatment strategy. *Bile acid resins* - **Bile acid resins** (e.g., cholestyramine) lower LDL-c by binding to bile acids in the intestine, but they are **less effective** than statins and can sometimes increase triglycerides. - They are generally not the first-line choice for primary LDL-c reduction due to their side effect profile (e.g., GI upset) and lower efficacy compared to statins. *Cholesterol absorption inhibitor* - **Ezetimibe** (a cholesterol absorption inhibitor) reduces cholesterol absorption in the small intestine, leading to lower LDL-c. - It is often used as an **add-on therapy** to statins or as monotherapy in statin-intolerant patients, but not as the initial drug of choice when a statin is indicated and tolerated.

Question 65: A 51-year-old woman presents to the emergency department with a 2-day history of bilateral lower extremity swelling. She says that her legs do not hurt, but she noticed she was gaining weight and her legs were becoming larger. Her past medical history is significant for morbid obesity, hypertension, and hypercholesterolemia. She says the swelling started after she was recently started on a new medication to help her blood pressure, but she does not remember the name of the medication. Which of the following is most likely the mechanism of action for the drug that was prescribed to this patient?

A. Potassium-sparing diuretic
B. Inhibition of calcium channels (Correct Answer)
C. Inhibition of enzyme in the lung
D. Potassium-wasting diuretic
E. Inhibition of hormone receptor

Explanation: ***Inhibition of calcium channels*** - The patient's presentation of **bilateral lower extremity swelling** (peripheral edema) after starting a new blood pressure medication is a classic side effect of **calcium channel blockers (CCBs)**, particularly dihydropyridine CCBs like amlodipine. - CCBs cause **vasodilation of arterioles**, leading to increased hydrostatic pressure in the capillaries and subsequent fluid extravasation into the interstitial space. *Potassium-sparing diuretic* - **Potassium-sparing diuretics** primarily work in the collecting duct to increase sodium excretion and retain potassium, without causing or significantly worsening peripheral edema. - They are used to treat hypertension and heart failure, but their mechanism does not directly cause dependent edema in the way described. *Inhibition of enzyme in the lung* - This description most closely refers to the **angiotensin-converting enzyme (ACE)**, which is inhibited by ACE inhibitors used for hypertension. - **ACE inhibitors** typically do not cause peripheral edema; their common side effects include cough and angioedema (though less common). *Potassium-wasting diuretic* - **Potassium-wasting diuretics** (e.g., loop or thiazide diuretics) increase urine output and are used to *reduce* fluid retention and swelling, not cause it. - While they can lower blood pressure, they would alleviate, rather than induce, bilateral lower extremity swelling. *Inhibition of hormone receptor* - This mechanism could refer to several classes of antihypertensives, such as **beta-blockers** (inhibiting adrenergic receptors) or **angiotensin receptor blockers (ARBs)** (inhibiting angiotensin II receptors). - Neither beta-blockers nor ARBs are typically associated with prominent bilateral lower extremity swelling as a common side effect.

Question 66: A 70-year-old man presents to his primary care physician for a general checkup. He states that he has been doing well and taking his medications as prescribed. He recently started a new diet and supplement to improve his health and has started exercising. The patient has a past medical history of diabetes, a myocardial infarction, and hypertension. He denies any shortness of breath at rest or with exertion. An ECG is performed and is within normal limits. Laboratory values are ordered as seen below. Serum: Na+: 139 mEq/L Cl-: 100 mEq/L K+: 6.7 mEq/L HCO3-: 25 mEq/L Glucose: 133 mg/dL Ca2+: 10.2 mg/dL Which of the following is the most likely cause of this patient's presentation?

A. Medication (Correct Answer)
B. Acute renal failure
C. Hemolysis
D. Dietary changes
E. Rhabdomyolysis

Explanation: ***Medication*** - The patient's **hyperkalemia** (K+ 6.7 mEq/L) despite feeling well, suggests a common side effect of medications, particularly those used for his pre-existing conditions like **hypertension** (**ACE inhibitors**, **ARBs**, **spironolactone**) and **diabetes**. - Medications are a frequent cause of asymptomatic electrolyte abnormalities, and given his complex medical history and the absence of acute symptoms, this is the most likely culprit. *Acute renal failure* - While acute renal failure can cause **hyperkalemia**, it typically presents with other symptoms such as **oliguria**, **fluid retention**, or other signs of organ dysfunction, which are not described. - The patient is reported to be "doing well" without **shortness of breath** or other acute complaints, making acute renal failure less likely as the primary cause of isolated hyperkalemia. *Hemolysis* - **Hemolysis** can release intracellular potassium, leading to **pseudohyperkalemia**, but it would typically be suspected in cases of **blood draw errors** or conditions causing red blood cell breakdown, none of which are indicated. - The patient's presentation does not include any signs or symptoms suggestive of red cell destruction. *Dietary changes* - While an extremely **high-potassium diet** or certain **supplements** could contribute to hyperkalemia, it is less common for dietary changes alone to cause such a significant elevation in a patient with normal organ function. - Given his medical history, medication-induced hyperkalemia is a more direct and common explanation. *Rhabdomyolysis* - **Rhabdomyolysis** involves the breakdown of muscle tissue, releasing potassium and other intracellular contents, but it is usually associated with significant **muscle pain**, **weakness**, and elevated **creatine kinase**. - The patient denies these symptoms and has no other indicators pointing towards severe muscle injury.

Question 67: A 69-year-old man with hypertension and congestive heart failure is brought to the emergency department because of a 9-day history of worsening shortness of breath and swelling of his legs. His respirations are 25/min, and blood pressure is 160/98 mm Hg. Pulse oximetry on 5 L O2 via nasal cannula shows an oxygen saturation of 92%. Examination shows 2+ pretibial edema bilaterally. Crackles are heard at both lung bases. ACE inhibitors are being considered for this patient's treatment. The enzyme that these medications inhibit, which is responsible for bradykinin breakdown, is primarily produced in which of the following?

A. Pulmonary endothelium (Correct Answer)
B. Atria
C. Juxtaglomerular cells
D. Zona glomerulosa
E. Liver

Explanation: ***Pulmonary endothelium*** - The **pulmonary endothelium** is rich in **angiotensin-converting enzyme (ACE)**, which is responsible for the breakdown of **bradykinin**. - Medications like **ACE inhibitors** block this enzyme, leading to increased bradykinin levels, which can cause side effects like **cough** and **angioedema**. *Atria* - The **atria** produce **atrial natriuretic peptide (ANP)** in response to stretch, which plays a role in fluid and electrolyte balance but not directly in bradykinin breakdown. - ANP promotes **vasodilation** and **natriuresis**, contributing to blood pressure regulation. *Juxtaglomerular cells* - **Juxtaglomerular cells** in the kidney produce **renin**, an enzyme that initiates the **renin-angiotensin-aldosterone system** by converting angiotensinogen to angiotensin I. - Renin production is stimulated by reduced renal perfusion pressure, sympathetic activity, and decreased sodium delivery to the macula densa. *Zona glomerulosa* - The **zona glomerulosa** of the adrenal cortex produces **aldosterone**, a mineralocorticoid that regulates sodium and potassium balance. - Aldosterone's primary role is in salt and water retention, and it does not directly participate in bradykinin metabolism. *Liver* - The **liver** is involved in the synthesis of many plasma proteins, clotting factors, and detoxification processes, but it is not the primary site for bradykinin breakdown. - While the liver metabolizes many substances, **ACE activity** for bradykinin degradation is concentrated in the pulmonary endothelium.

Question 68: A 70-year-old man with a history of poorly controlled congestive heart failure comes to the physician for a follow-up examination. At his previous visit 4 months ago, a new drug was added to his treatment regimen. He reports that his dyspnea and peripheral edema have improved. His pulse is 70/min and blood pressure is 110/80 mm Hg. Physical examination shows bilateral, mildly tender enlargement of breast tissue. This patient's physical examination finding is most likely caused by a drug that acts at which of the following sites in the kidney?

A. Cortical collecting duct (Correct Answer)
B. Thick ascending limb
C. Early distal convoluted tubule
D. Efferent arteriole
E. Juxtaglomerular apparatus

Explanation: ***Cortical collecting duct*** - The patient's symptoms of improved dyspnea and peripheral edema, along with **gynecomastia**, strongly suggest the use of **spironolactone**. - Spironolactone is an **aldosterone antagonist** that acts on the mineralocorticoid receptors in the **cortical collecting duct**, leading to increased sodium and water excretion and potassium retention, while also causing gynecomastia as a common side effect. *Thick ascending limb* - Medications acting here are **loop diuretics** (e.g., furosemide), which are potent diuretics but do not typically cause gynecomastia. - While loop diuretics improve heart failure symptoms, they do not explain the **tender breast enlargement**. *Early distal convoluted tubule* - **Thiazide diuretics** (e.g., hydrochlorothiazide) act at this site, inhibiting sodium and chloride reabsorption. - Thiazides improve heart failure symptoms but are not associated with **gynecomastia**. *Efferent arteriole* - Medications that act on the efferent arteriole (e.g., **ACE inhibitors** and **ARBs**) can improve heart failure, but they do not typically cause gynecomastia. - These drugs primarily reduce afterload and preload, and prevent cardiac remodeling. *Juxtaglomerular apparatus* - The juxtaglomerular apparatus is involved in **renin secretion**, which is regulated by beta-blockers or direct renin inhibitors. - While these drugs are used in heart failure, they do not cause **gynecomastia**.

Question 69: A 42-year-old man presents to his primary care physician for preventative care. He does not have any current complaint. His father died of diabetic nephropathy. Vital signs include a temperature of 36.7°C (98.06°F), blood pressure of 150/95 mm Hg, and pulse of 90/min. His fasting blood glucose is 159 mg/dL (on 2 occasions) and HbA1c is 8.1%. The patient is started on metformin and lifestyle modifications. 3 months later, he comes for a follow-up visit. His serum blood glucose is 370 mg/dL and HbA1C is 11%. The patient currently complains of weight loss and excessive urination. Which of the following is the optimal therapy for this patient?

A. A thiazolidinedione added to metformin
B. Basal-bolus insulin (Correct Answer)
C. Basal insulin added to metformin
D. A sulfonylurea added to metformin
E. A sodium-glucose cotransporter 2 inhibitor added to metformin

Explanation: ***Basal-bolus insulin*** - This patient presents with an HbA1C of 11% and symptoms of **polyuria** and **weight loss**, indicating significant hyperglycemia. Due to the high HbA1c and symptomatic presentation despite initial metformin and lifestyle modifications, **aggressive glucose lowering** is required to prevent acute complications and long-term organ damage. - Basal-bolus insulin therapy provides both continuous basal insulin to control fasting glucose and prandial boluses to manage post-meal glucose spikes, offering the most comprehensive and effective glucose control in severe hyperglycemia. *A thiazolidinedione added to metformin* - Thiazolidinediones (TZDs) like pioglitazone improve insulin sensitivity and are used as a second-line agent, but they have a **slow onset of action** and are generally insufficient for patients with such severe hyperglycemia (HbA1c 11%). - TZDs can take several weeks to reach maximal effect and are not potent enough for immediate and significant glucose reduction in symptomatic patients with markedly elevated HbA1c. *Basal insulin added to metformin* - While adding basal insulin to metformin is a common step for patients whose HbA1c is a few points above target, an HbA1c of 11% with symptoms of weight loss and polyuria indicates **more severe insulin deficiency** or resistance requiring more comprehensive insulin replacement. - Basal insulin alone would not adequately address post-prandial hyperglycemia, which is likely contributing significantly to the overall high HbA1c. *A sulfonylurea added to metformin* - Sulfonylureas stimulate insulin release from pancreatic beta cells, but their efficacy is limited, and they carry a risk of **hypoglycemia** and weight gain. - Given the patient's very high HbA1c of 11%, sulfonylureas would likely be insufficient to achieve target glycemic control and might lead to significant side effects without achieving adequate glucose lowering. *A sodium-glucose cotransporter 2 inhibitor added to metformin* - SGLT2 inhibitors promote glucose excretion in the urine and offer cardiovascular and renal benefits, but they are generally less potent in reducing HbA1c compared to insulin, especially in patients with severe hyperglycemia. - While beneficial for some, they would not provide the rapid and substantial glucose reduction needed for a patient with an HbA1c of 11% and acute symptoms.

Question 70: A 63-year-old woman presents with dyspnea on exertion. She reports that she used to work in her garden without any symptoms, but recently she started to note dyspnea and fatigue after working for 20–30 minutes. She has type 2 diabetes mellitus diagnosed 2 years ago but she does not take any medications preferring natural remedies. She also has arterial hypertension and takes torsemide 20 mg daily. The weight is 88 kg and the height is 164 cm. The vital signs include: blood pressure is 140/85 mm Hg, heart rate is 90/min, respiratory rate is 14/min, and the temperature is 36.6℃ (97.9℉). Physical examination is remarkable for increased adiposity, pitting pedal edema, and present S3. Echocardiography shows a left ventricular ejection fraction of 51%. The combination of which of the following medications would be a proper addition to the patient’s therapy?

A. Metoprolol and indapamide
B. Enalapril and bisoprolol (Correct Answer)
C. Spironolactone and fosinopril
D. Indapamide and amlodipine
E. Valsartan and spironolactone

Explanation: ***Enalapril and bisoprolol*** - This patient presents with **heart failure with preserved ejection fraction (HFpEF)**, characterized by symptoms of heart failure (dyspnea, fatigue, edema, S3 sound) with an LVEF >50%. She also has **uncontrolled hypertension** (BP 140/85) and a **heart rate of 90/min**. - **Important:** Unlike HFrEF, **ACE inhibitors and beta-blockers have NOT demonstrated mortality benefit in HFpEF** (CHARM-Preserved, PEP-CHF trials). However, they remain important for **blood pressure control** and **symptom management** in patients with HFpEF and comorbid hypertension. - **Enalapril** (ACE inhibitor) helps control blood pressure through reduction of preload and afterload. **Bisoprolol** (beta-blocker) provides **heart rate control** (patient's HR is 90/min) and further blood pressure reduction. Both medications address her inadequately controlled hypertension while managing symptoms. - **Note:** Current guidelines emphasize SGLT2 inhibitors as first-line therapy for HFpEF (not offered here), along with diuretics for volume management (patient is already on torsemide) and aggressive treatment of comorbidities like hypertension and diabetes. *Metoprolol and indapamide* - Metoprolol is a beta-blocker that could help with rate and blood pressure control. However, **indapamide is a thiazide-like diuretic** that is redundant since the patient is already on **torsemide** (a loop diuretic) for volume management. - This combination lacks an **ACE inhibitor or ARB** for optimal blood pressure control and neurohormonal modulation, which is important even in HFpEF for managing hypertension and its consequences. *Spironolactone and fosinopril* - **Spironolactone** (mineralocorticoid receptor antagonist) showed modest benefit in reducing HF hospitalizations in the TOPCAT trial for HFpEF. **Fosinopril** is an ACE inhibitor appropriate for blood pressure control. - However, the patient has a **heart rate of 90/min**, indicating need for **rate control** which neither spironolactone nor fosinopril provides. A **beta-blocker would be more appropriate** to address both rate control and blood pressure. - Additionally, while spironolactone has some evidence in HFpEF, the combination with an ACE inhibitor **without rate control** is suboptimal for this patient's presentation. *Indapamide and amlodipine* - **Indapamide** (thiazide-like diuretic) is **redundant** since the patient is already on torsemide. **Amlodipine** (calcium channel blocker) is effective for hypertension but can cause **peripheral edema**, which this patient already has (pitting pedal edema). - **Calcium channel blockers are not recommended in heart failure** due to lack of mortality benefit and potential to worsen fluid retention. This combination does not address the underlying HFpEF pathophysiology or provide optimal symptom management. *Valsartan and spironolactone* - **Valsartan** (ARB) is appropriate for blood pressure control and is an alternative to ACE inhibitors. **Spironolactone** has modest evidence for reducing hospitalizations in HFpEF (TOPCAT trial). - However, similar to the fosinopril/spironolactone combination, this lacks a **beta-blocker for heart rate control** (patient's HR is 90/min). Rate control is important for optimizing diastolic filling time in HFpEF and controlling blood pressure. - While this combination has theoretical benefits, **enalapril and bisoprolol** better addresses both blood pressure control and rate control simultaneously.

Question 71: A 58-year-old man is rushed to the ER in the middle of the night with severe chest pain. He arrives in the ER short of breath, sweating, and looking terrified. His blood pressure is noted to be 250/140, and he is immediately administered nitroprusside. His blood pressure is controlled, but he soon develops confusion and lactic acidosis. Which of the following best explains these findings?

A. Cyanide toxicity (Correct Answer)
B. Hypoventilation
C. Cough
D. Decreased intracranial pressure
E. Hyperkalemia

Explanation: ***Cyanide toxicity*** - **Nitroprusside** metabolizes into nitric oxide and five **cyanide ions**, which can overwhelm the body's detoxification capacity, especially in patients with prolonged infusion or impaired renal function. - Symptoms such as **confusion** and **lactic acidosis** are classic signs of **cyanide toxicity**, resulting from inhibition of cellular respiration and oxygen utilization. *Hypoventilation* - While some medications can cause hypoventilation, **nitroprusside** primarily affects vascular smooth muscle and does not directly depress respiratory drive. - The patient's **shortness of breath** initially was more likely due to a hypertensive emergency or underlying cardiac event, not hypoventilation due to nitroprusside. *Cough* - **Cough** is not a common side effect of **nitroprusside**; rather, it is often associated with ACE inhibitors or certain respiratory conditions. - The acute presentation of this patient suggests a different etiology for any respiratory distress he might be experiencing. *Decreased intracranial pressure* - **Nitroprusside** is a potent vasodilator and can actually cause a **dose-dependent increase in intracranial pressure**, not a decrease, due to increased cerebral blood flow. - This effect is particularly concerning in patients with pre-existing elevated ICP. *Hyperkalemia* - **Hyperkalemia** is not typically associated with **nitroprusside** administration. - Medications like ACE inhibitors, ARBs, or potassium-sparing diuretics are more commonly linked to hyperkalemia.

Question 72: An 81-year-old man with a history of congestive heart failure presents to his cardiologist because he has been feeling increasingly short of breath while lying down. Specifically, he says that he is now no longer able to sleep flat on the bed and instead has to be propped up on multiple pillows. In addition, he has been experiencing increased swelling in his legs. Finally, he reports that he has been experiencing muscle cramping and weakness. He reports that he has been taking a diuretic as prescribed and adhering to a low-salt diet. Physical exam reveals crackles on lung auscultation bilaterally and 2+ pitting edema in his legs bilaterally. Left ventricular ejection fraction (LVEF) is measured by echocardiogram and found to be 36%. This is decreased from his last measurement of 41%. He is put on a second diuretic that has an additional effect that corrects an electrolyte imbalance in this patient. Which of the following medications is consistent with this description?

A. Acetazolamide
B. Furosemide
C. Spironolactone (Correct Answer)
D. Hydrochlorothiazide
E. Amiloride

Explanation: ***Spironolactone*** - The patient exhibits symptoms of worsening **heart failure** (orthopnea, bilateral crackles, leg edema, decreased LVEF) despite being on a diuretic, suggesting he is likely developing diuretic-induced **hypokalemia** due to chronic diuresis. The **muscle cramping and weakness** are consistent with **hypokalemia**. - **Spironolactone** is an **aldosterone antagonist** that acts as a potassium-sparing diuretic, thus correcting the electrolyte imbalance (hypokalemia) and also improving heart failure outcomes with proven mortality benefit (RALES trial). *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** primarily used for glaucoma, urinary alkalinization, and altitude sickness; it is a weak diuretic. - While it causes bicarbonate excretion, it is not typically used for chronic heart failure or to specifically correct hypokalemia. *Furosemide* - **Furosemide** is a **loop diuretic** that is already likely the initial diuretic the patient is on, given his history of heart failure. - It works by inhibiting the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle and is known to cause **hypokalemia**, not correct it. *Hydrochlorothiazide* - **Hydrochlorothiazide** is a **thiazide diuretic** that inhibits Na-Cl cotransport in the distal convoluted tubule. - Similar to loop diuretics, it also causes significant potassium loss and would worsen, rather than correct, hypokalemia. *Amiloride* - **Amiloride** is an **epithelial sodium channel (ENaC) inhibitor** in the collecting duct, making it a potassium-sparing diuretic. - While it helps correct hypokalemia, it lacks the aldosterone antagonism of spironolactone and has no proven mortality benefit in heart failure, making it a less appropriate choice for this patient.

Question 73: A 67-year-old man with a history of diabetes mellitus type II and a previous myocardial infarction presents to your office for a routine examination. His blood pressure is found to be 180/100 mmHg. Which drug is the first-line choice of treatment for this patient's hypertension?

A. Hydrochlorothiazide
B. Prazosin
C. Lisinopril (Correct Answer)
D. Isoproterenol
E. Amlodipine

Explanation: ***Lisinopril*** - **ACE inhibitors** (like lisinopril) are first-line for patients with hypertension and **diabetes mellitus** due to their **renal protective effects** and ability to slow the progression of diabetic nephropathy. - They are also beneficial post-myocardial infarction as they **reduce ventricular remodeling** and improve long-term outcomes. *Hydrochlorothiazide* - While **thiazide diuretics** can be used for hypertension, they may **worsen glucose control** in diabetic patients and are not preferred as first-line in the presence of diabetes and a history of MI. - They primarily act by reducing blood volume and peripheral resistance but lack the specific **cardio-renal protective benefits** of ACE inhibitors. *Prazosin* - **Alpha-1 blockers** like prazosin are generally not recommended as first-line monotherapy for hypertension due to potential side effects such as **orthostatic hypotension** and a higher risk of cardiovascular events compared to other classes. - Their use is typically reserved for patients with concomitant **benign prostatic hyperplasia (BPH)** or as add-on therapy. *Isoproterenol* - **Isoproterenol** is a non-selective beta-agonist primarily used for **bradycardia** or **heart block**, not for the treatment of hypertension. - It would actually **increase heart rate and contractility**, exacerbating hypertension rather than treating it. *Amlodipine* - **Calcium channel blockers** like amlodipine are effective antihypertensives and can be used in patients with diabetes, but **ACE inhibitors** are generally preferred as first-line in patients with both diabetes and a history of MI due to their direct **renoprotective** and **cardioprotective** benefits. - While effective for blood pressure control, amlodipine does not offer the same degree of **renal benefit** in diabetic nephropathy or post-MI remodeling as ACE inhibitors.

Question 74: A 51-year-old woman comes to the physician because of a 6-month history of fatigue and increased thirst. She has no history of serious medical illness and takes no medications. She is 163 cm (5 ft 4 in) tall and weighs 72 kg (160 lb); BMI is 28 kg/m2. Her fasting serum glucose concentration is 249 mg/dL. Treatment with an oral hypoglycemic agent is begun. Which of the following best describes the mechanism of action of the drug that was most likely prescribed for this patient?

A. Decreased carbohydrate hydrolysis
B. Increased insulin release
C. Decreased hepatic gluconeogenesis (Correct Answer)
D. Decreased glucagon release
E. Increased renal glucose elimination

Explanation: ***Decreased hepatic gluconeogenesis*** - The patient presents with symptoms of **diabetes mellitus** (fatigue, increased thirst, and a fasting glucose of 249 mg/dL). Given her BMI of 28 kg/m2, **Type 2 Diabetes** is highly likely, and the initial treatment for such patients, especially those not excessively obese, is often **metformin**. - **Metformin** works primarily by inhibiting **hepatic gluconeogenesis** and, to a lesser extent, by increasing insulin sensitivity in peripheral tissues. *Increased insulin release* - This mechanism is characteristic of **sulfonylureas** (e.g., glipizide, glyburide) and **meglitinides** (e.g., repaglinide), which stimulate insulin secretion from pancreatic beta cells. - While these can be used in Type 2 Diabetes, they are typically not the first-line oral hypoglycemic agent due to the risk of **hypoglycemia** and weight gain, making metformin a more likely initial choice. *Decreased carbohydrate hydrolysis* - This mechanism is associated with **alpha-glucosidase inhibitors** (e.g., acarbose, miglitol), which delay the breakdown and absorption of carbohydrates in the gut. - These drugs are less commonly prescribed as initial monotherapy for Type 2 Diabetes due to side effects like **flatulence** and diarrhea, and their moderate efficacy. *Decreased glucagon release* - Although reducing glucagon release is beneficial in diabetes, this is the primary mechanism of action for drugs like **GLP-1 receptor agonists** (e.g., exenatide, liraglutide) and **DPP-4 inhibitors** (e.g., sitagliptin, saxagliptin), which also affect insulin secretion and gastric emptying. - These are often considered second-line agents or used in combination therapy, not typically the first oral medication prescribed. *Increased renal glucose elimination* - This is the mechanism of action for **SGLT2 inhibitors** (e.g., dapagliflozin, empagliflozin), which block glucose reabsorption in the renal tubules, leading to increased urinary glucose excretion. - While effective, SGLT2 inhibitors are often not the very first oral medication chosen, especially given metformin's long-standing role as a first-line agent.

Question 75: A 51-year-old woman is brought to the emergency department after not being able to urinate for the past 12 hours. She also complains of a headache that is sharp in nature, 9/10, without radiation, and associated with nausea and vomiting. She neither smokes cigarettes nor drinks alcohol. She complains that her fingers have become numb and very painful on exposure to cold weather during the last few months. She has also noticed her fingers change color from blue to pale to red on cold exposure. Her face looks shiny with thickened, wrinkle-free skin. She has had joint pain and stiffness for the last 20 years. She takes over-the-counter omeprazole for heartburn, which she says improves her symptoms. She has unintentionally lost 9 kg (20 lb) in the last 6 months. She has no previous history of diabetes, hypertension, chest pain, orthopnea, or paroxysmal nocturnal dyspnea. Her mother has rheumatoid arthritis for which she takes methotrexate, and her father takes medications for hypertension and hypercholesterolemia. Her temperature is 37°C (98.6°F), blood pressure is 210/120 mm Hg, pulse is 102/min, respiratory rate is 18/min, and BMI is 22 kg/m2. Laboratory test Complete blood count: Hemoglobin 9.5 g/dL Leukocytes 15,500/mm3 Platelets 90,000/mm3 Serum haptoglobin 20 mg/dL (30–200 mg/dL) Serum creatinine 2.3 mg/dL Blood urea nitrogen 83.5 mg/dL The peripheral blood film of the patient shows the following. Which of the following would be the most appropriate treatment for this patient?

A. Nitroprusside
B. Renal transplantation
C. Ramipril (Correct Answer)
D. Dialysis
E. Labetalol

Explanation: ***Ramipril*** - This patient presents with **scleroderma renal crisis (SRC)**, characterized by new-onset **malignant hypertension**, **acute kidney injury**, and features of **microangiopathic hemolytic anemia**. **ACE inhibitors** like ramipril are the **first-line treatment** for SRC, regardless of the blood pressure, as they can reverse renal ischemia and improve kidney function. - The patient's presentation with **Raynaud phenomenon**, **thickened skin** (sclerodactyly leading to "wrinkle-free" appearance), **esophageal dysmotility** (heartburn managed with omeprazole), and **unintentional weight loss** over many months are all consistent with systemic sclerosis, which predisposed her to SRC. *Nitroprusside* - While nitroprusside is a potent vasodilator used in **hypertensive emergencies**, it is **contraindicated** in scleroderma renal crisis. - Its rapid reduction in blood pressure can exacerbate renal hypoperfusion and worsen kidney function in SRC. *Renal transplantation* - Renal transplantation is a treatment option for **end-stage renal disease**, but it is **not the initial management** for acute kidney injury in the context of scleroderma renal crisis. - The priority is to stabilize the patient's condition and preserve existing renal function with ACE inhibitors. *Dialysis* - Dialysis is indicated for **severe kidney failure** or uremia, which may develop if SRC is not adequately treated or if kidney function rapidly deteriorates. - However, the primary goal in SRC is to prevent progression to dialysis through prompt and aggressive ACE inhibitor therapy, making it not the most appropriate initial treatment. *Labetalol* - Labetalol is a **beta-blocker with alpha-blocking activity** used to treat **hypertensive emergencies**, but it is generally **not the first-line agent for SRC**. - While it can lower blood pressure, ACE inhibitors are specifically preferred in SRC due to their targeted effect on the **renin-angiotensin-aldosterone system (RAAS)** and ability to reverse renal ischemia.

Question 76: A 45-year-old diabetic man presents to your office for routine follow-up. One year ago, the patient’s hemoglobin A1C was 7.2% and the patient was encouraged to modify his diet and increase exercise. Six months ago, the patient’s HA1C was 7.3%, and you initiated metformin. Today, the patient has no complaints. For which of the following co-morbidities would it be acceptable to continue metformin?

A. Prior hospitalization for alcoholic hepatitis
B. Hepatitis C infection
C. Mild chronic obstructive pulmonary disease (Correct Answer)
D. Headache and family history of brain aneurysms requiring CT angiography
E. Recent diagnosis of NYHA Class II congestive heart failure

Explanation: ***Mild chronic obstructive pulmonary disease*** - **Metformin is safe** in patients with **stable, mild COPD** as respiratory disease alone is **not a contraindication** to metformin use. - COPD does not increase the risk of **lactic acidosis**, the primary safety concern with metformin, as long as tissue perfusion and renal function are adequate. - The benefits of metformin for glycemic control are maintained without additional respiratory risks. *Prior hospitalization for alcoholic hepatitis* - **Metformin is contraindicated** in **severe or decompensated liver disease** due to increased risk of **lactic acidosis**. - A history of **alcoholic hepatitis requiring hospitalization** suggests significant hepatic impairment that could compromise lactate clearance. - The liver plays a key role in lactate metabolism, and impaired function substantially increases lactic acidosis risk. *Hepatitis C infection* - While **chronic compensated liver disease** (including Hepatitis C) is no longer considered an absolute contraindication per updated FDA guidance (2016-2017), the presence of Hepatitis C raises concerns about **potential liver dysfunction**. - Without confirmation of **normal liver function and preserved renal function**, metformin use requires caution. - Metformin should be avoided if there is evidence of **hepatic decompensation** or significantly elevated transaminases. *Headache and family history of brain aneurysms requiring CT angiography* - The concern is the **IV contrast dye** used during **CT angiography**, which can cause **acute kidney injury** in susceptible patients. - Traditional guidance recommends **holding metformin** before contrast procedures and for 48 hours after to prevent contrast-induced nephropathy and subsequent **lactic acidosis**. - Though recent evidence suggests this risk is lower with modern iso-osmolar contrast and preserved renal function, temporary discontinuation remains standard practice for patient safety. *Recent diagnosis of NYHA Class II congestive heart failure* - Historically, **CHF was considered a contraindication** to metformin due to concerns about lactic acidosis from poor tissue perfusion. - However, current evidence and guidelines (2020s) demonstrate that metformin is **generally safe and may be beneficial** in **stable NYHA Class II-III CHF** with preserved renal function. - The qualifier "**recent diagnosis**" suggests a potentially **unstable period** where cautious monitoring is warranted, making this scenario less clearly acceptable for continuation without further clinical assessment and stability confirmation.

Question 77: A 45-year-old woman presents to your office with a serum glucose of 250 mg/dL and you diagnose diabetes mellitus type II. You intend to prescribe the patient metformin, but you decide to order laboratory tests before proceeding. Which of the following basic metabolic panel values would serve as a contraindication to the use of metformin?

A. HCO3- > 30
B. Na+ > 140
C. K+ > 4.0
D. Glucose > 300
E. Creatinine > 2.0 (Correct Answer)

Explanation: ***Creatinine > 2.0*** - An elevated **serum creatinine** level indicating significant renal impairment is a contraindication to metformin use, as it markedly increases the risk of **lactic acidosis**. - **Metformin** is primarily excreted by the kidneys unchanged, and impaired renal function leads to drug accumulation and potential toxicity. - Traditional contraindication thresholds include serum creatinine >1.5 mg/dL in men or >1.4 mg/dL in women; a value **>2.0 mg/dL** clearly indicates significant renal dysfunction requiring avoidance of metformin. - Current guidelines emphasize using **eGFR** (contraindicated if <30 mL/min/1.73m²), but creatinine remains a key marker of renal function on basic metabolic panels. *HCO3- > 30* - An elevated **bicarbonate level** (HCO3-) above 30 mEq/L typically indicates **metabolic alkalosis**, which is not a direct contraindication for metformin. - While metabolic alkalosis should be investigated, it does not pose the specific risk of lactic acidosis associated with renal dysfunction and metformin use. *Na+ > 140* - A slightly elevated **sodium level** (Na+) above 140 mEq/L (normal: 135-145 mEq/L) is often associated with **dehydration** or other electrolyte imbalances and is not a contraindication for metformin. - While significant electrolyte imbalances should be addressed, mild hypernatremia does not directly increase the risk of metformin-induced lactic acidosis. *K+ > 4.0* - A potassium level of >4.0 mEq/L is within the **normal range** (typically 3.5-5.0 mEq/L) and is not a contraindication for metformin. - Significant hyperkalemia or hypokalemia would require evaluation and management, but a normal or slightly elevated potassium level does not preclude metformin use. *Glucose > 300* - While a blood **glucose level** >300 mg/dL indicates poorly controlled diabetes, this is actually an **indication** for initiating glucose-lowering therapy like metformin, not a contraindication. - Metformin's primary therapeutic purpose is to lower elevated glucose levels, and severe hyperglycemia itself does not increase the risk of metformin's specific adverse effects.

Question 78: A 57-year-old woman comes to the physician because of a 2-week history of swelling of both her feet. It improves a little bit with elevation but is still bothersome to her because her shoes no longer fit. She has type 2 diabetes mellitus treated with metformin and linagliptin. She was diagnosed with hypertension 6 months ago and started treatment with amlodipine. Subsequent blood pressure measurements on separate occasions have been around 130/90 mm Hg. She otherwise feels well. Today, her pulse is 80/min, respirations are 12/min, and blood pressure is 132/88 mm Hg. Cardiovascular examination shows no abnormalities. There is pitting edema of both ankles. Which of the following would have been most likely to reduce the risk of edema in this patient?

A. Use of compression stockings
B. Addition of enalapril (Correct Answer)
C. Addition of furosemide
D. Addition of chlorpheniramine
E. Use of nifedipine instead

Explanation: ***Addition of enalapril*** - The patient is likely experiencing **amlodipine-induced edema**, a common side effect of dihydropyridine calcium channel blockers due to precapillary vasodilation. - Adding an **ACE inhibitor (e.g., enalapril)** can counteract this effect by causing postcapillary vasodilation, thereby reducing hydrostatic pressure in the capillaries. *Use of compression stockings* - While compression stockings can help with **venous insufficiency or lymphedema**, they do not address the underlying pharmacological cause of amlodipine-induced edema. - They primarily aid in reducing fluid accumulation by **increasing interstitial pressure externally**, but a medication change would be more effective. *Addition of furosemide* - Furosemide is a **loop diuretic** primarily used for fluid overload associated with conditions like heart failure or renal failure, or for severe hypertension. - It would not specifically counteract the mechanism of amlodipine-induced edema and would primarily address the symptom (edema) rather than the underlying cause, potentially leading to **dehydration or electrolyte imbalances**. *Addition of chlorpheniramine* - Chlorpheniramine is an **antihistamine** typically used to treat allergic reactions, such as rhinitis or hives. - It has no role in managing **edema caused by calcium channel blockers**, as the edema is due to hemodynamic changes, not an allergic response. *Use of nifedipine instead* - Nifedipine is also a **dihydropyridine calcium channel blocker** with a similar mechanism of action to amlodipine, causing precapillary vasodilation. - Switching to nifedipine would likely result in the **same side effect of peripheral edema**, as the mechanism of action is largely identical.

Question 79: A 58-year-old male presents to the clinic for a follow-up visit. He takes metformin every day and says that he is compliant with his medication but can not control his diet. Three months prior, his HbA1c was 8.2% when he was started on metformin. He does not have any complaints on this visit. His temperature is 37°C (98.6°F), respirations are 15/min, pulse is 67/min and blood pressure is 122/88 mm Hg. His BMI is 33. Physical examination is within normal limits. Blood is drawn for laboratory tests and the results are given below: Fasting blood glucose 150 mg/dL Glycated hemoglobin (HbA1c) 7.2 % Serum Creatinine 1.1 mg/dL BUN 12 mg/dL The physician wants to initiate another medication for his blood glucose control, specifically one that does not carry a risk of weight gain. Addition of which of the following drugs would be most suitable for this patient?

A. Sitagliptin (Correct Answer)
B. Glimepiride
C. Rosiglitazone
D. Glyburide
E. Pioglitazone

Explanation: ***Sitagliptin*** - This is a **dipeptidyl peptidase-4 (DPP-4) inhibitor** that enhances incretin effects, leading to glucose-dependent insulin secretion and suppressed glucagon. - DPP-4 inhibitors like sitagliptin are **weight-neutral** and pose a low risk of hypoglycemia, making them suitable additions for patients who need further glycemic control without weight gain, especially with their current BMI. *Glimepiride* - This is a **sulfonylurea** that stimulates insulin release from pancreatic beta cells independently of glucose levels. - Sulfonylureas are associated with a **risk of weight gain** and hypoglycemia, which is an undesirable effect for this patient. *Rosiglitazone* - This is a **thiazolidinedione (TZD)** that improves insulin sensitivity in peripheral tissues and the liver. - TZDs, including rosiglitazone, are associated with **weight gain** due to fluid retention and increased adipogenesis, and can also cause congestive heart failure. *Glyburide* - This is also a **sulfonylurea**, similar to glimepiride, that stimulates insulin secretion. - Like other sulfonylureas, glyburide carries a significant risk of **weight gain** and hypoglycemia, making it less ideal for this patient. *Pioglitazone* - This is another **thiazolidinedione (TZD)** that improves insulin sensitivity. - Pioglitazone is known to cause **weight gain** and fluid retention, and it has a black box warning for exacerbating heart failure.

Question 80: A 54-year-old African American male presents to the emergency department with 1 day history of severe headaches. He has a history of poorly controlled hypertension and notes he hasn't been taking his antihypertensive medications. His temperature is 100.1 deg F (37.8 deg C), blood pressure is 190/90 mmHg, pulse is 60/min, and respirations are 15/min. He is started on a high concentration sodium nitroprusside infusion and transferred to the intensive care unit. His blood pressure eventually improves over the next two days and his headache resolves, but he becomes confused and tachycardic. Labs reveal a metabolic acidosis. Which of the following is the best treatment?

A. Sodium nitrite (Correct Answer)
B. Bicarbonate
C. Methylene blue
D. Ethanol
E. Glucagon

Explanation: ***Sodium nitrite*** - This patient is exhibiting symptoms of **cyanide toxicity** (confusion, tachycardia, metabolic acidosis) due to prolonged high-dose **sodium nitroprusside** infusion. - Sodium nitrite works by inducing **methemoglobinemia**, which then binds to cyanide to form **cyanmethemoglobin**, thereby detoxifying the cyanide. - **Note:** In clinical practice, sodium nitrite is typically combined with **sodium thiosulfate** (which converts cyanide to thiocyanate for renal excretion), and **hydroxocobalamin** is now preferred as first-line therapy. However, among the options listed, sodium nitrite is the most appropriate antidote. *Bicarbonate* - While metabolic acidosis is present, **bicarbonate** only addresses the symptom (acidosis) and does not treat the underlying cause of **cyanide poisoning**. - Without addressing the cyanide, the acidosis will persist or worsen. *Methylene blue* - **Methylene blue** is used to treat **methemoglobinemia**, not cyanide toxicity. - In this scenario, inducing methemoglobinemia with sodium nitrite is part of the treatment for cyanide poisoning, not reversing it. *Ethanol* - **Ethanol** is used to treat **methanol** or **ethylene glycol poisoning** by competitively inhibiting alcohol dehydrogenase. - It has no role in the treatment of **cyanide toxicity**. *Glucagon* - **Glucagon** is primarily used to treat **beta-blocker overdose** or severe **hypoglycemia**. - It does not have any therapeutic effect in cases of **cyanide poisoning**.

Question 81: A 58-year-old woman presents to her physician complaining of a headache in the occipital region for 1 week. Past medical history is significant for essential hypertension, managed with lifestyle modifications and 2 antihypertensives for the previous 6 months. Her blood pressure is 150/90 mm Hg. Neurological examination is normal. A third antihypertensive drug is added that acts as a selective α2 adrenergic receptor agonist. On follow-up, she reports that she does not have any symptoms and her blood pressure is 124/82 mm Hg. Which of the following mechanisms best explains the therapeutic effect of this new drug in this patient?

A. Vasodilation of peripheral arteries
B. Vasodilation of peripheral arteries and peripheral veins
C. Decreased peripheral sympathetic outflow (Correct Answer)
D. Negative inotropic effect on the heart
E. Vasodilation of peripheral veins

Explanation: ***Decreased peripheral sympathetic outflow*** - Selective **α2 adrenergic receptor agonists** (e.g., clonidine, guanfacine, methyldopa) act **centrally in the brainstem** (nucleus tractus solitarius and rostral ventrolateral medulla) to reduce **sympathetic nervous system activity**. - This **central action** leads to a **decrease in peripheral sympathetic outflow**, resulting in reduced heart rate, decreased cardiac output, and peripheral vasodilation, all contributing to lower blood pressure. - This is the **primary mechanism** of antihypertensive action for central α2 agonists. *Vasodilation of peripheral arteries* - While central α2 agonists do cause some peripheral vasodilation, this is an **indirect effect** of **reduced sympathetic tone**, not a primary direct action on peripheral arteries. - Their main mechanism of action is **central**, decreasing the overall sympathetic drive to the vasculature. *Vasodilation of peripheral arteries and peripheral veins* - This option describes a broader effect, and while some vasodilation occurs, it doesn't pinpoint the **primary mechanism of action** of central α2 agonists. - Drugs like alpha-1 blockers (prazosin, doxazosin) or direct vasodilators (hydralazine, minoxidil) would have a more pronounced direct effect on both arterial and venous smooth muscle. *Negative inotropic effect on the heart* - While central α2 agonists can **reduce heart rate** (bradycardia) and cardiac output due to decreased sympathetic stimulation, a **negative inotropic effect** (decreased myocardial contractility) is not their primary or most significant mechanism. - **Beta-blockers** are primarily known for their negative inotropic and chronotropic effects on the heart. *Vasodilation of peripheral veins* - Similar to arterial vasodilation, this is an **indirect effect** of **reduced sympathetic tone**, not the primary mechanism of action of central α2 agonists. - Direct venodilators like **nitrates** would primarily target peripheral veins to reduce preload.

Question 82: A 57-year-old woman presents to the emergency room with complaints of severe headache, vomiting, neck stiffness, and chest pain that have developed over the last several hours. Her past medical history is notable for diabetes, hypertension, and dyslipidemia. Her temperature is 99.0°F (37.2°C), blood pressure is 197/124 mm Hg, pulse is 120/min, respirations are 19/min, and oxygen saturation is 98% on room air. Physical examination is significant for papilledema. Urinalysis reveals gross hematuria and proteinuria. Which of the following is the next best step in management for this patient?

A. Hydralazine
B. Esmolol
C. Lisinopril
D. Propranolol
E. Nitroprusside (Correct Answer)

Explanation: ***Nitroprusside*** - This patient presents with **malignant hypertension** (BP 197/124 mm Hg) with **hypertensive encephalopathy** (severe headache, vomiting, papilledema, neck stiffness) and **acute kidney injury** (gross hematuria, proteinuria), constituting a hypertensive emergency requiring immediate IV therapy. - **Nitroprusside** is a potent **arterial and venous vasodilator** with immediate onset (seconds) and short half-life (2 minutes), allowing rapid and titratable blood pressure reduction in hypertensive emergencies. - Among the options provided, nitroprusside offers the most **rapid and precise BP control** necessary for this life-threatening situation with end-organ damage. - Note: While newer agents like nicardipine or clevidipine are often preferred in modern practice due to better side effect profiles, nitroprusside remains effective when these alternatives are unavailable. *Esmolol* - Esmolol is a **short-acting IV beta-blocker** particularly useful in hypertensive emergencies associated with **aortic dissection**, myocardial ischemia, or postoperative hypertension where heart rate control is critical. - While it could help with this patient's tachycardia, it provides less potent vasodilation and BP reduction compared to nitroprusside in hypertensive encephalopathy. - Beta-blockade alone may be insufficient for the degree of BP reduction needed in this emergency. *Hydralazine* - Hydralazine is a direct arterial vasodilator primarily used for **hypertensive emergencies in pregnancy** (pre-eclampsia/eclampsia). - Its **unpredictable BP response**, slower onset (10-20 minutes IV), and tendency to cause **reflex tachycardia** make it less ideal for precise BP control in this critical situation. - The patient already has tachycardia (120/min), which would be worsened by hydralazine. *Lisinopril* - Lisinopril is an oral **ACE inhibitor** used for chronic hypertension management and renal protection. - It is **inappropriate for hypertensive emergencies** because: (1) oral route has delayed, unpredictable absorption; (2) onset of action is hours, not minutes; (3) cannot be rapidly titrated. - Hypertensive emergencies require immediate IV therapy with titratable agents. *Propranolol* - Propranolol is an oral **non-selective beta-blocker** used for chronic hypertension, angina, and certain arrhythmias. - Like lisinopril, it is unsuitable for acute management due to **slow onset** (oral formulation), lack of titratability, and insufficient vasodilatory effect for severe hypertension. - Beta-blockade without vasodilation is inadequate for hypertensive encephalopathy.

Question 83: A 78-year-old Caucasian male actor presents to your office complaining of a dry, non-productive cough. He has a history of hypertension, diabetes, and coronary artery disease and he follows a complicated regimen of medications to treat his multiple co-morbidities. Which of the following medications is most likely to be associated with his chief complaint?

A. Aspirin
B. Lisinopril (Correct Answer)
C. Hydrochlorothiazide
D. Metoprolol
E. Nifedipine

Explanation: ***Lisinopril*** - **Angiotensin-converting enzyme (ACE) inhibitors** like lisinopril are well-known to cause a **persistent dry, non-productive cough** in approximately 5-20% of patients. - This cough is thought to be due to the accumulation of **bradykinin** and **substance P** in the airways. *Aspirin* - While aspirin can cause respiratory symptoms in some individuals, it is typically associated with **aspirin-exacerbated respiratory disease (AERD)**, which involves **bronchospasm** and nasal polyps, not a persistent dry cough as a primary side effect. - Aspirin's common side effects are usually gastrointestinal, such as **gastric irritation** or bleeding. *Hydrochlorothiazide* - Hydrochlorothiazide is a **thiazide diuretic** primarily used for hypertension. - It works by inhibiting sodium reabsorption in the distal convoluted tubule and is not typically associated with **chronic dry cough** as a side effect. *Metoprolol* - Metoprolol is a **beta-blocker** used for hypertension, angina, and arrhythmias. - While beta-blockers can cause **bronchospasm** in susceptible individuals (especially those with asthma), they are not commonly linked to a persistent **dry, non-productive cough** in the general population. *Nifedipine* - Nifedipine is a **calcium channel blocker** (dihydropyridine type) used for hypertension and angina. - Common side effects include **peripheral edema**, headache, and flushing, but it is not known to cause a **dry cough**.

Question 84: A 55-year-old man presents to the emergency department with a headache, blurry vision, and abdominal pain. He states that his symptoms started several hours ago and have been gradually worsening. His temperature is 99.3°F (37.4°C), blood pressure is 222/128 mmHg, pulse is 87/min, respirations are 16/min, and oxygen saturation is 99% on room air. Physical exam is notable for an uncomfortable and distressed man. The patient is started on an esmolol and a nitroprusside drip thus lowering his blood pressure to 200/118 mmHg. The patient states that he feels better, but complains of feeling warm and flushed. An hour later, the patient seems confused and states his headache has resurfaced. Laboratory values are ordered as seen below. Serum: Na+: 138 mEq/L Cl-: 101 mEq/L K+: 4.4 mEq/L HCO3-: 17 mEq/L BUN: 31 mg/dL Glucose: 199 mg/dL Creatinine: 1.4 mg/dL Ca2+: 10.2 mg/dL Which of the following is the best treatment for this patient?

A. Labetalol
B. Insulin
C. Hydroxocobalamin (Correct Answer)
D. IV fluids
E. Amyl nitrite

Explanation: ***Hydroxocobalamin*** - The patient's worsening confusion, headache, and metabolic acidosis (HCO3- of 17 mEq/L) despite some improvement in blood pressure, coupled with the use of **nitroprusside**, strongly suggest **cyanide toxicity**. - **Hydroxocobalamin** is the preferred antidote for cyanide toxicity as it directly binds to **cyanide** to form cyanocobalamin, which is then safely excreted in the urine. *Labetalol* - While **labetalol** is an effective antihypertensive, it does not address the underlying **cyanide toxicity** caused by the nitroprusside drip. - Continuing to optimize blood pressure without addressing the toxicity will not resolve the patient's neurological symptoms and metabolic derangements. *Insulin* - The patient has a slightly elevated **glucose** (199 mg/dL), but this is likely a stress response and not the primary cause of his acute neurological decline and **metabolic acidosis**. - Administering **insulin** without addressing the cyanide toxicity would be inappropriate and could lead to other complications like hypoglycemia. *IV fluids* - **IV fluids** might be supportive in a critically ill patient, but they do not treat **cyanide toxicity** or reverse the metabolic acidosis. - The primary issue is systemic poisoning, not dehydration or volume depletion. *Amyl nitrite* - **Amyl nitrite** is an older antidote for cyanide poisoning that works by inducing **methemoglobinemia** to bind cyanide. - It is less effective and has more side effects than hydroxocobalamin, especially given the patient's existing hemodynamic instability.

Question 85: A 59-year-old female is brought to the emergency department with an acute onset of weakness in her left hand that started 3 hours ago. She has not had numbness or tingling of the hand. Other than recent episodes of blurry vision and headaches, her medical history is unremarkable. She has one daughter who was diagnosed with multiple sclerosis at age 23. Her temperature is 36.7°C (98°F), pulse is 80/min, and blood pressure is 144/84 mm Hg. Examination shows facial erythema. There are mild scratch marks on her arms and torso. Left hand strength is slightly decreased and there is mild dysmetria of the left hand finger-to-nose testing. The remainder of the neurological examination shows no abnormalities. Her laboratory studies shows: Hematocrit 55% Leukocyte count 14,500/mm3 Segmented neutrophils 61% Eosinophils 3% Lymphocytes 29% Monocytes 7% Platelet count 690,000/mm3 Her erythropoietin levels are decreased. CT scan of the head without contrast shows two focal areas of hypo-attenuation in the right parietal lobe. Which of the following is the most appropriate treatment to prevent complications of this patient's underlying condition?

A. Busulfan
B. Repeated phlebotomies (Correct Answer)
C. Glucocorticoid therapy
D. Radiation therapy
E. Imatinib therapy

Explanation: ***Repeated phlebotomies*** * This patient's symptoms (headaches, blurry vision, facial erythema, weakness, elevated hematocrit, and platelet count, and decreased erythropoietin) are highly suggestive of **polycythemia vera**. Repeated phlebotomies are the first-line treatment to reduce the **hematocrit** to less than 45%, thereby reducing the risk of **thrombotic events** (like stroke or transient ischemic attacks, which the patient has experienced). * The goal of phlebotomy is to alleviate symptoms by decreasing **blood viscosity** and preventing further complications such as **thrombosis** and **hemorrhage**, which are common in polycythemia vera. *Busulfan* * **Busulfan** is an **alkylating agent** used in specific hematological malignancies, often in cases resistant to conventional therapies or in older patients with very high risk. It is not the first-line treatment for polycythemia vera given the availability of less toxic options. * While it can suppress marrow production, its use is typically reserved for patients who do not tolerate phlebotomy or **hydroxyurea**, or who have severe symptoms unresponsive to these treatments. *Glucocorticoid therapy* * **Glucocorticoids** are primarily used for their **anti-inflammatory** and **immunosuppressive** effects. They are not effective in treating the underlying **myeloproliferative disorder** of polycythemia vera. * They might be used in certain hematological conditions, such as autoimmune hemolytic anemia or specific lymphomas, but are not indicated for management of **polycythemia vera**. *Radiation therapy* * **Radiation therapy** (e.g., phosphorus-32) has been used historically for polycythemia vera but is now rarely used due to its **leukemogenic potential** and the availability of safer alternatives. * It is not a standard or appropriate first-line treatment given the risks associated with increasing the potential for **secondary malignancies.** *Imatinib therapy* * **Imatinib mesylate** is a **tyrosine kinase inhibitor** specifically targeting the **BCR-ABL fusion protein** in **chronic myeloid leukemia (CML)** and other **KIT-positive** tumors. * Polycythemia vera is driven by the **JAK2 V617F mutation** (or less commonly other **JAK2 mutations**), not BCR-ABL, making imatinib ineffective for this condition.

Question 86: A 44-year-old man comes to the emergency department because of a severe headache and blurry vision for the past 3 hours. He has hypertension treated with hydrochlorothiazide. He has missed taking his medication for the past week as he was traveling. He is only oriented to time and person. His temperature is 37.1°C (98.8°F), pulse is 92/min and regular, and blood pressure is 245/115 mm Hg. Cardiopulmonary examination shows no abnormalities. Fundoscopy shows bilateral retinal hemorrhages and exudates. Neurologic examination shows no focal findings. A complete blood count and serum concentrations of electrolytes, glucose, and creatinine are within the reference range. A CT scan of the brain shows no abnormalities. Which of the following is the most appropriate pharmacotherapy?

A. Sublingual nifedipine
B. Oral captopril
C. Intravenous nitroprusside (Correct Answer)
D. Oral clonidine
E. Intravenous mannitol

Explanation: ***Intravenous nitroprusside*** - The patient presents with **hypertensive emergency**, characterized by **severe hypertension** (245/115 mmHg) with **acute end-organ damage**, including altered mental status and retinal hemorrhages/exudates. - **Intravenous nitroprusside** is a potent, rapidly acting vasodilator making it an excellent choice for immediate and controlled reduction of blood pressure in such critical situations. *Sublingual nifedipine* - **Sublingual nifedipine** can cause a sudden and uncontrolled drop in blood pressure, leading to **ischemia** due to inadequate perfusion of vital organs. - It also has a less predictable and slower onset of action compared to intravenous agents, making it unsuitable for acute hypertensive emergencies. *Oral captopril* - **Oral captopril** has a slower onset of action and is less suitable for the acute management of a **hypertensive emergency** where immediate and precise blood pressure control is crucial. - While an ACE inhibitor, its oral administration does not provide the rapid titratability needed to safely lower dangerously high blood pressures. *Oral clonidine* - **Oral clonidine** also has a relatively slow onset of action and its effects can be variable, making it less ideal for the acute, emergent management of **severe hypertension** with end-organ damage. - It is more appropriate for urgent but non-emergent hypertension or chronic management, not for situations requiring immediate and controlled blood pressure reduction. *Intravenous mannitol* - **Intravenous mannitol** is an osmotic diuretic primarily used to reduce **intracranial pressure** or to promote diuresis. - It does not directly lower blood pressure effectively in a hypertensive emergency and is not a primary antihypertensive agent.

Question 87: A 62-year-old man presents to the emergency department with chest pain. He was at home watching television when he suddenly felt chest pain that traveled to his back. The patient has a past medical history of alcoholism, obesity, hypertension, diabetes, and depression. His temperature is 98.4°F (36.9°C), blood pressure is 177/118 mmHg, pulse is 123/min, respirations are 14/min, and oxygen saturation is 97% on room air. Physical exam reveals a S4 on cardiac exam and chest pain that seems to worsen with palpation. The patient smells of alcohol. The patient is started on 100% oxygen and morphine. Which of the following is the best next step in management?

A. NPO, IV fluids, serum lipase
B. Nitroprusside
C. Labetalol (Correct Answer)
D. Aspirin
E. CT scan

Explanation: ***Labetalol*** - This patient's presentation with **sudden-onset chest pain radiating to the back**, **hypertension**, **tachycardia**, and a history of uncontrolled hypertension strongly suggests **aortic dissection**. - **Labetalol** is an ideal initial step to rapidly reduce both heart rate and blood pressure, which is crucial in preventing further extension of the dissection. *NPO, IV fluids, serum lipase* - While **alcoholism** is a risk factor for **pancreatitis**, the classic presentation of **sudden-onset chest pain radiating to the back** with **severe hypertension** is not typical for pancreatitis. - Although ruling out pancreatitis might be considered later, it's not the immediate priority over stabilizing a suspected dissection. *Nitroprusside* - **Nitroprusside** is a powerful vasodilator that lowers blood pressure but does not adequately control the **heart rate**. - In **aortic dissection**, isolated blood pressure reduction without concomitant heart rate control can increase **shear stress** on the aortic wall, potentially worsening the dissection. *Aspirin* - **Aspirin** is used in the management of **acute coronary syndromes** to prevent platelet aggregation. - In a suspected **aortic dissection**, aspirin is **contraindicated** as it can increase the risk of bleeding if surgical intervention is required. *CT scan* - A **CT scan** of the chest is the diagnostic test of choice for **aortic dissection** and would be performed soon. - However, the **initial management priority** is to stabilize the patient hemodynamically by reducing heart rate and blood pressure *before* proceeding with imaging to prevent further aortic injury.

Question 88: A 28-year-old woman, gravida 1, para 0, at 32 weeks' gestation is admitted to the hospital for the management of elevated blood pressures. On admission, her pulse is 81/min, and blood pressure is 165/89 mm Hg. Treatment with an intravenous drug is initiated. Two days after admission, she has a headache and palpitations. Her pulse is 116/min and regular, and blood pressure is 124/80 mm Hg. Physical examination shows pitting edema of both lower extremities that was not present on admission. This patient most likely was given a drug that predominantly acts by which of the following mechanisms?

A. Inhibition of β1, β2, and α1 receptors
B. Inhibition of angiotensin II production
C. Activation of α2 adrenergic receptors
D. Inhibition of sodium reabsorption
E. Direct dilation of the arterioles (Correct Answer)

Explanation: ***Direct dilation of the arterioles*** - The development of **headache**, **palpitations**, and **tachycardia** (pulse 116), along with a reduction in blood pressure (124/80 mm Hg) and new-onset **pitting edema**, suggests a direct arterial vasodilator like **hydralazine**. - **Hydralazine reduces peripheral vascular resistance** by directly relaxing vascular smooth muscle, primarily in arterioles, leading to reflex tachycardia and fluid retention as compensatory mechanisms. *Inhibition of β1, β2, and α1 receptors* - Labetaolol, which is commonly used in pre-eclampsia and acts by inhibiting β1, β2, and α1 receptors, would typically lead to a **decrease in heart rate and sympathetic compensation**, not palpitations and increased pulse. - While it lowers blood pressure, it would not typically cause **reflex tachycardia and new-onset edema** to this extent unless there is an underlying cardiac issue or overdose. *Inhibition of angiotensin II production* - Inhibitors of angiotensin II production (like ACE inhibitors or ARBs) are **contraindicated in pregnancy** due to their teratogenic effects, especially in the second and third trimesters. - They typically do not cause **reflex tachycardia and palpitations** as primary side effects, but rather dry cough (ACE inhibitors) or hyperkalemia. *Activation of α2 adrenergic receptors* - **Alpha-2 adrenergic agonists** (e.g., methyldopa, clonidine) reduce sympathetic outflow from the central nervous system, leading to a **decrease in heart rate and blood pressure**. - While effective for hypertension in pregnancy, they are more associated with **sedation and dry mouth** rather than palpitations and reflex tachycardia, and they do not typically cause significant peripheral edema. *Inhibition of sodium reabsorption* - Medications that inhibit sodium reabsorption are **diuretics**. While diuretics can help manage edema, they primarily lower blood pressure by reducing blood volume, and are not typically the immediate go-to for acute severe hypertension in pregnancy. - Diuretics would **reduce edema**, not cause new-onset pitting edema, and would not typically cause reflex tachycardia as seen in this patient unless there is profound hypovolemia leading to a compensatory increase in heart rate.

Question 89: A 73-year-old woman is brought to the emergency department because of a 1-day history of skin lesions. Initially, she experienced pain in the affected areas, followed by discoloration of the skin and formation of blisters. Four days ago, the patient was started on a new medication by her physician after failed cardioversion for intermittent atrial fibrillation. She lives alone and does not recall any recent falls or trauma. She has hypertension treated with metoprolol and diabetes mellitus treated with insulin. Her temperature is 37°C (98.6°F), pulse is 108/min and irregularly irregular, and blood pressure is 145/85 mm Hg. Examination of her skin shows well-circumscribed purple maculae, hemorrhagic blisters, and areas of skin ulceration over the breast, lower abdomen, and gluteal region. Which of the following is the strongest predisposing factor for this patient's condition?

A. Deficiency of a natural anticoagulant (Correct Answer)
B. Major neurocognitive disorder
C. Formation of antibodies against a platelet antigen
D. Mutation in clotting factor V
E. Damaged aortic valve

Explanation: ***Deficiency of a natural anticoagulant*** - The sudden onset of **painful skin lesions**, followed by **purpuric maculae**, **hemorrhagic blisters**, and **skin necrosis**, particularly after commencing a new medication for atrial fibrillation suggests **warfarin-induced skin necrosis**. - This condition is classically triggered when **warfarin** is initiated in patients with a pre-existing **deficiency of protein C** or protein S, leading to a transient hypercoagulable state due to rapid depletion of these natural anticoagulants. *Major neurocognitive disorder* - While neurocognitive disorders can affect medication adherence and overall health management, they do not directly predispose to **warfarin-induced skin necrosis**. - There is no information in the vignette to suggest the patient has a significant neurocognitive disorder, and her ability to recall medical history seems intact. *Formation of antibodies against a platelet antigen* - This scenario describes **heparin-induced thrombocytopenia (HIT)**, where antibodies bind to **platelet factor 4 (PF4)** complexed with heparin, leading to platelet activation and thrombosis. - The patient was not on heparin, and the clinical presentation of painful skin lesions with necrosis is more consistent with paradoxical thrombosis from warfarin. *Mutation in clotting factor V* - A mutation in clotting factor V, specifically **Factor V Leiden**, leads to **resistance to activated protein C (APC)**, increasing the risk of venous thromboembolism. - While it is a **thrombophilic state**, it typically causes deep vein thrombosis or pulmonary embolism and does not directly cause warfarin-induced skin necrosis in the absence of warfarin therapy. *Damaged aortic valve* - A damaged aortic valve, such as in **aortic stenosis** or **aortic regurgitation**, can lead to **turbulent blood flow**, which may predispose to thrombosis or hemolysis or be a source of emboli. - However, valve damage itself does not directly cause the specific syndrome of **warfarin-induced skin necrosis** with its characteristic rapid onset and dermatological findings.

Question 90: A 37-year-old man comes to the physician for a follow-up examination. He is being evaluated for high blood pressure readings that were incidentally recorded at a routine health maintenance examination 1 month ago. He has no history of serious illness and takes no medications. His pulse is 88/min and blood pressure is 165/98 mm Hg. Physical examination shows no abnormalities. Serum studies show: Na+ 146 mEq/L K+ 3.0 mEq/L Cl- 98 mEq/L Glucose 77 mg/dL Creatinine 0.8 mg/dL His plasma aldosterone concentration (PAC) to plasma renin activity (PRA) ratio is 36 (N = < 10). A saline infusion test fails to suppress aldosterone secretion. A CT scan of the adrenal glands shows bilateral adrenal abnormalities. An adrenal venous sampling shows elevated PACs from bilateral adrenal veins. Which of the following is the most appropriate next step in management?

A. Propranolol therapy
B. Unilateral adrenalectomy
C. Amiloride therapy
D. Bilateral adrenalectomy
E. Eplerenone therapy (Correct Answer)

Explanation: ***Eplerenone therapy*** - The patient's presentation is consistent with **primary hyperaldosteronism** (resistant hypertension, hypokalemia, elevated PAC/PRA ratio, and non-suppression with saline infusion). The bilateral adrenal abnormalities on CT and elevated PACs from bilateral adrenal veins indicate **bilateral adrenal hyperplasia**. - **Eplerenone** is a selective **aldosterone antagonist** that blocks the effects of aldosterone, making it the most appropriate medical therapy for bilateral adrenal hyperplasia. *Propranolol therapy* - **Propranolol** is a **beta-blocker** primarily used for hypertension, angina, and arrhythmias, but it does not specifically address the underlying pathology of primary hyperaldosteronism, which is excessive aldosterone production. - While it can lower blood pressure, it would not correct the **hypokalemia** or the fundamental hormonal imbalance. *Unilateral adrenalectomy* - **Unilateral adrenalectomy** is the treatment of choice for **unilateral adrenal adenoma** (Conn's syndrome) causing primary hyperaldosteronism. - In this case, the patient has **bilateral adrenal abnormalities** and elevated PACs from **bilateral adrenal veins**, indicating bilateral hyperplasia, which is not amenable to unilateral surgery. *Amiloride therapy* - **Amiloride** is a **potassium-sparing diuretic** that directly inhibits sodium channels in the collecting duct, thereby reducing potassium excretion. - While it can help with **hypokalemia**, it is less effective than aldosterone antagonists like eplerenone in blocking the full spectrum of aldosterone's effects and is not the first-line pharmacologic treatment for bilateral adrenal hyperplasia. *Bilateral adrenalectomy* - **Bilateral adrenalectomy** would cure the hyperaldosteronism but would lead to **adrenal insufficiency**, requiring lifelong glucocorticoid and mineralocorticoid replacement. - This invasive procedure is generally reserved for cases where medical management fails or specific genetic syndromes, and is not the first-line approach for bilateral adrenal hyperplasia given the availability of effective pharmacotherapy.

Question 91: A 64-year-old female presents with acute right wrist pain after she lost her balance while reaching overhead and fell from standing height. Her right wrist radiographs show a fracture of her right distal radius. A follow-up DEXA bone density scan is performed and demonstrates a T-score of -3.5 at the femoral neck and spine. Her medical history is significant for hypertension, for which she is not currently taking any medication. She has not had a previous fracture. Which of the following antihypertensive agents would be preferred in this patient?

A. Furosemide
B. Propranolol
C. Lisinopril
D. Amlodipine
E. Hydrochlorothiazide (Correct Answer)

Explanation: ***Hydrochlorothiazide*** - This patient has osteoporosis, indicated by a **T-score of -3.5** and a **fragility fracture** (distal radius fracture from a fall from standing height). **Thiazide diuretics** like hydrochlorothiazide reduce urinary calcium excretion and can increase bone mineral density, offering a dual benefit for both hypertension and osteoporosis. - The **calcium-sparing effect** of thiazide diuretics makes them a preferred choice in hypertensive patients with osteoporosis. *Furosemide* - Furosemide is a **loop diuretic** that significantly increases **urinary calcium excretion**, which can worsen osteoporosis. - It is typically used for conditions requiring more potent diuresis, such as heart failure or severe edema, rather than essential hypertension with osteoporosis. *Propranolol* - Propranolol is a **non-selective beta-blocker** that can exacerbate underlying **bronchospasm** in patients with asthma or COPD, though none are mentioned here. - Beta-blockers do not have a direct beneficial effect on **bone mineral density** or osteoporosis. *Lisinopril* - Lisinopril is an **ACE inhibitor** that is effective for hypertension and beneficial in patients with chronic kidney disease or heart failure. - While effective for hypertension, it does not offer the **calcium-sparing benefits** that are particularly helpful for this patient's concurrent osteoporosis. *Amlodipine* - Amlodipine is a **calcium channel blocker** that is effective for hypertension and can be beneficial in patients with angina. - It does not offer any direct benefits for **bone health** or osteoporosis.

Question 92: A 46-year-old African American man presents to the physician with dyspnea on exertion for the past 2 months. He also has occasional episodes of coughing at night. He says that he has been healthy most of his life. He is a non-smoker and a non-alcoholic. He does not have hypercholesterolemia or ischemic heart disease. His father died due to congestive heart failure. On physical examination, the pulse rate was 116/min, the blood pressure was 164/96 mm Hg, and the respiratory rate was 20/min. Chest auscultation reveals bilateral fine crepitations at the lung bases. A complete diagnostic work-up suggests a diagnosis of hypertension with heart failure due to left ventricular dysfunction. Which of the following drug combinations is most likely to benefit the patient?

A. Amlodipine-Atenolol
B. Amlodipine-Valsartan
C. Metoprolol-Atorvastatin
D. Isosorbide dinitrate-Hydralazine (Correct Answer)
E. Atenolol-Hydrochlorothiazide

Explanation: ***Isosorbide dinitrate-Hydralazine*** - This combination is specifically **guideline-recommended for self-identified African American patients with heart failure with reduced ejection fraction (HFrEF)** based on the A-HeFT trial, which demonstrated significant mortality benefit in this population. - **Hydralazine reduces afterload** through direct arterial vasodilation, while **isosorbide dinitrate reduces preload** through venodilation, providing synergistic hemodynamic benefits that improve symptoms and survival. - This combination is typically used as **adjunctive therapy** to standard HF medications (ACE inhibitors/ARBs, beta-blockers, diuretics). *Amlodipine-Atenolol* - **Atenolol, a non-selective beta-blocker**, lacks proven mortality benefit in heart failure and is not among the preferred beta-blockers (carvedilol, metoprolol succinate, or bisoprolol) for HFrEF management. - **Amlodipine, a dihydropyridine calcium channel blocker**, is not a first-line agent for heart failure treatment and does not provide mortality benefit in HFrEF, though it can be used for additional blood pressure control if needed. *Amlodipine-Valsartan* - **Valsartan is an ARB (angiotensin receptor blocker)**, which is indeed a cornerstone therapy for heart failure, but this combination does not provide the additional mortality benefit specifically demonstrated for African American patients with HFrEF. - While guideline-directed medical therapy including ARBs is important, the **hydralazine-nitrate combination offers proven incremental benefit** in this specific patient population when added to standard therapy. *Metoprolol-Atorvastatin* - **Metoprolol succinate** is an appropriate beta-blocker for heart failure when titrated properly, but this combination lacks the specific mortality benefit proven for African American patients with HFrEF. - **Atorvastatin is a statin** used for lipid management and cardiovascular risk reduction, but the patient has no documented hypercholesterolemia or ischemic heart disease, making this combination less appropriate. - Statins do not directly address heart failure pathophysiology or provide mortality benefit in HFrEF in the absence of other indications. *Atenolol-Hydrochlorothiazide* - **Atenolol** is not a preferred beta-blocker for heart failure due to its lack of proven mortality benefit compared to carvedilol, metoprolol succinate, or bisoprolol. - **Hydrochlorothiazide, a thiazide diuretic**, helps manage fluid overload and hypertension but does not offer the mortality reduction or comprehensive hemodynamic benefits of the hydralazine-nitrate combination specifically proven in this patient population.

Question 93: A 44-year-old man presents to the emergency department with weakness. He states that he has felt progressively more weak over the past month. He endorses decreased libido, weight gain, and headaches. His temperature is 97.0°F (36.1°C), blood pressure is 177/108 mmHg, pulse is 80/min, respirations are 17/min, and oxygen saturation is 98% on room air. Physical exam is notable for an obese man who appears fatigued. He has abdominal striae, atrophied arms, and limbs with minimal muscle tone. His ECG is notable for a small upward deflection right after the T wave. A fingerstick blood glucose is 225 mg/dL. The patient's underlying condition will be addressed definitively, but in the interim, which of the following is the most appropriate pharmacologic agent for managing his hypertension?

A. Metoprolol (Correct Answer)
B. Torsemide
C. Hydrochlorothiazide
D. Insulin
E. Eplerenone

Explanation: ***Metoprolol*** - This patient presents with signs and symptoms consistent with **Cushing's syndrome**, including truncal obesity, thin extremities, striae, hypertension, hyperglycemia, and weakness (likely from hypokalemia, as evidenced by the U wave on ECG). - The severe hypertension (177/108 mmHg) requires immediate management while the underlying Cushing's syndrome is being addressed definitively. - **Beta-blockers like metoprolol** are appropriate for managing hypertension in Cushing's syndrome as they counteract the increased cardiac output and sympathetic activation caused by cortisol excess without worsening the metabolic complications. - Unlike thiazide or loop diuretics, beta-blockers do not worsen hyperglycemia or hypokalemia, both of which are already present in this patient. *Torsemide* - **Torsemide** is a loop diuretic that can cause **hypokalemia**, which would worsen this patient's existing hypokalemia (U wave on ECG) and muscle weakness. - Loop diuretics are not first-line agents for hypertension in Cushing's syndrome unless there is evidence of fluid overload, which is not present in this case. *Hydrochlorothiazide* - **Hydrochlorothiazide** is a thiazide diuretic that can worsen both **hyperglycemia** and **hypokalemia**. - This patient already has hyperglycemia (225 mg/dL) and evidence of hypokalemia (U wave on ECG), making thiazides a poor choice. - Thiazides would exacerbate the metabolic complications of Cushing's syndrome. *Insulin* - While insulin would address the hyperglycemia, the question specifically asks about managing the **hypertension**, not the hyperglycemia. - Insulin does not lower blood pressure and would not address the immediate cardiovascular risk from severe hypertension. *Eplerenone* - **Eplerenone** is a selective aldosterone antagonist used primarily for primary hyperaldosteronism or heart failure. - While it can lower blood pressure, the primary pathophysiology in Cushing's syndrome is **cortisol excess**, not aldosterone excess. - Additionally, eplerenone can cause hyperkalemia, which, while potentially beneficial in this hypokalemic patient, makes it less predictable and not first-line for hypertension management in this context.

Question 94: A 75 year-old gentleman presents to his general practitioner. He is currently being treated for hypertension and is on a multi-drug regimen. His current blood pressure is 180/100. The physician would like to begin treatment with minoxidil or hydralazine. Which of the following side effects is associated with administration of these drugs?

A. Persistent cough
B. Cyanosis in extremities
C. Fetal renal toxicity
D. Systemic volume loss
E. Reflex tachycardia (Correct Answer)

Explanation: ***Reflex tachycardia*** - Both **minoxidil** and **hydralazine** are direct arterial vasodilators, causing a significant drop in **peripheral vascular resistance**. - This vasodilation triggers a **baroreflex response**, leading to an increase in heart rate and **cardiac contractility** to maintain cardiac output, resulting in reflex tachycardia. *Persistent cough* - **Persistent cough** is a common side effect associated with **ACE inhibitors**, such as lisinopril or enalapril, due to the accumulation of **bradykinin**. - This side effect is not typically seen with **minoxidil** or **hydralazine**, which act directly on vascular smooth muscle to cause vasodilation. *Cyanosis in extremities* - **Cyanosis** (bluish discoloration of the skin and mucous membranes) usually indicates **hypoxemia** or poor peripheral perfusion. - While sometimes associated with severe cardiogenic shock or specific drug toxicities like methemoglobinemia (not related to minoxidil or hydralazine), it is not a direct or typical side effect of these vasodilators. *Fetal renal toxicity* - **Fetal renal toxicity**, including **fetal renal dysfunction** and **oligohydramnios**, is a well-known risk associated with **ACE inhibitors** and **ARBs** during pregnancy. - Neither **minoxidil** nor **hydralazine** are primarily linked to this specific fetal adverse effect, though hydralazine can be used in pregnancy for severe hypertension. *Systemic volume loss* - **Systemic volume loss** is usually caused by conditions like **dehydration**, excessive diuresis, or hemorrhage. - While vasodilators can reduce blood pressure, they do not directly cause **systemic volume depletion**; rather, the reflex response to vasodilation can include fluid retention to counteract the blood pressure drop.

Question 95: A 57-year-old man presents to his physician with the complaint of a painful toe joint on his right foot. He states that the onset of pain came on suddenly, waking him up in the middle of the night. On physical exam, the metatarsophalangeal (MTP) joint of the big toe is swollen and erythematous. The physician obtains information regarding his past medical history and current medications. Which of the following medications would have the potential to exacerbate this patient’s condition?

A. Indomethacin
B. Methotrexate
C. Allopurinol
D. Hydrochlorothiazide (Correct Answer)
E. Colchicine

Explanation: ***Hydrochlorothiazide*** - **Thiazide diuretics** like hydrochlorothiazide can **increase serum uric acid levels** by inhibiting uric acid secretion in the renal tubules, thereby precipitating or exacerbating **gout attacks**. - The patient's presentation of sudden-onset, painful, red, and swollen **metatarsophalangeal (MTP) joint of the big toe** is classic for **gout**, a condition caused by uric acid crystal deposition. - Thiazide diuretics are a well-known risk factor for hyperuricemia and gout exacerbations. *Indomethacin* - **Indomethacin** is a **nonsteroidal anti-inflammatory drug (NSAID)** commonly used as first-line treatment for acute gout attacks. - It would alleviate, not exacerbate, the patient's condition. *Methotrexate* - **Methotrexate** is an **immunosuppressant** used for rheumatoid arthritis and other inflammatory conditions. - At standard rheumatologic doses, methotrexate does **not typically cause hyperuricemia** or exacerbate gout. - It is not associated with increased risk of gout attacks. *Allopurinol* - **Allopurinol** is a **xanthine oxidase inhibitor** used for the long-term management of gout by **reducing uric acid production**. - While it prevents gout long-term, **initiating or adjusting allopurinol during an acute attack** can transiently worsen symptoms due to rapid changes in uric acid levels causing crystal mobilization. - However, it does not increase uric acid levels like thiazide diuretics do. *Colchicine* - **Colchicine** is an **anti-inflammatory agent** specifically used for the treatment and prophylaxis of gout attacks. - It helps reduce inflammation caused by uric acid crystals and would improve the patient's condition.

Question 96: A 62-year-old man comes to the physician for a follow-up examination. For the past year, he has had increasing calf cramping in both legs when walking, especially on an incline. He has hypertension. Since the last visit 6 months ago, he has been exercising on a treadmill four times a week; he has been walking until the pain starts and then continues after a short break. He has a history of hypertension controlled with enalapril. He had smoked 2 packs of cigarettes daily for 35 years but quit 5 months ago. His temperature is 37°C (98.6°F), pulse is 84/min, and blood pressure is 132/78 mm Hg. Cardiopulmonary examination shows no abnormalities. The calves and feet are pale. Femoral pulses can be palpated bilaterally; pedal pulses are absent. His ankle-brachial index is 0.6. Which of the following is the most appropriate next step in management?

A. Vancomycin and piperacillin
B. Operative vascular reconstruction
C. Rest and orthotic braces
D. Clopidogrel and simvastatin (Correct Answer)
E. Percutaneous transluminal angioplasty and stenting

Explanation: ***Clopidogrel and simvastatin*** - This patient presents with classic symptoms of **peripheral artery disease (PAD)**, indicated by **calf cramping with exertion (claudication)**, absent pedal pulses, pale extremities, and an **ankle-brachial index (ABI) of 0.6**. - **Clopidogrel** is an antiplatelet agent used for secondary prevention of cardiovascular events in PAD, and **simvastatin** is a statin to manage dyslipidemia and stabilize atherosclerotic plaques, both crucial components of initial medical management for PAD. *Vancomycin and piperacillin* - This combination of **broad-spectrum antibiotics** is typically used to treat severe bacterial infections, often in hospitalized patients. - There are no signs or symptoms of infection in this patient's presentation. *Operative vascular reconstruction* - **Operative vascular reconstruction** is an invasive procedure generally reserved for patients with **critical limb ischemia**, rapidly worsening claudication, or failed conservative management. - This patient's symptoms, while significant, do not yet indicate a need for immediate surgical intervention, especially given his recent positive lifestyle changes. *Rest and orthotic braces* - While rest is a component of managing claudication, and orthotic braces might be used for specific foot or joint issues, neither addresses the **underlying atherosclerosis** causing the PAD. - **Supervised exercise programs** including walking until the pain starts and resting, then resuming, are beneficial, but rest alone or orthotics are insufficient primary treatments for PAD. *Percutaneous transluminal angioplasty and stenting* - **Percutaneous transluminal angioplasty and stenting (PTAS)** is an interventional procedure used to revascularize arteries in PAD. - Similar to surgical reconstruction, PTAS is typically considered after **failed medical therapy and supervised exercise programs**, or for more severe symptoms like critical limb ischemia, which is not currently present.

Question 97: A 67-year-old man comes to the clinic for establishment of care. He recently retired and moved to Florida with his wife. His past medical history includes hypertension, diabetes, chronic back pain, and hyperlipidemia. According to the patient, he takes lisinopril, metformin, atorvastatin, acetaminophen, and methadone. His previous doctor prescribed methadone for breakthrough pain as he has been having more severe pain episodes due to the recent move. He is currently out of his methadone and asks for a refill on the prescription. A physical examination is unremarkable except for mild lower extremity edema bilaterally and diffuse lower back pain upon palpation. What is the best initial step in the management of this patient?

A. Refer the patient to a pain management clinic
B. Inform the patient that methadone is not the best option and do not prescribe
C. Encourage the patient to switch to duloxetine
D. Assess the patient's pain medication history (Correct Answer)
E. Prescribe a limited dose of methadone for breakthrough back pain

Explanation: ***Assess the patient's pain medication history*** - It is crucial to gather a comprehensive **pain medication history** for a new patient on long-term opioids, especially when they are requesting a refill for a potentially high-risk medication like **methadone**. This includes understanding the duration of use, previous dosages, other medications tried, and the effectiveness of prior treatments. - A comprehensive assessment helps to identify potential risks, such as **opioid tolerance**, dependence, or drug-drug interactions, and allows the physician to make an informed decision regarding the patient's ongoing pain management plan in accordance with **CDC guidelines** on opioid prescribing. *Refer the patient to a pain management clinic* - While referral to a pain management clinic may be appropriate later, the **initial step** should involve a thorough assessment by the primary care physician to understand the patient's immediate needs and history, especially given the new patient encounter. - A direct referral without an initial evaluation could delay critical care decisions related to safe opioid prescribing and **withdrawal prevention**. *Inform the patient that methadone is not the best option and do not prescribe* - Simply refusing to prescribe methadone without a proper assessment and alternative plan can lead to **opioid withdrawal** and non-adherence to care, which can be dangerous for the patient. - While methadone has significant risks, abruptly discontinuing it without a transition plan is generally discouraged, as it can cause severe **rebound pain** and withdrawal symptoms. *Encourage the patient to switch to duloxetine* - Duloxetine is an appropriate medication for **neuropathic pain** and **chronic musculoskeletal pain**, but it's not an immediate solution for breakthrough pain in a patient accustomed to methadone and should only be considered after a full assessment and discussion of risks and benefits. - Switching to duloxetine without a clear understanding of the patient's current pain control, opioid dependence, and potential for withdrawal is premature and could exacerbate the patient's pain and lead to severe **withdrawal symptoms**. *Prescribe a limited dose of methadone for breakthrough back pain* - Prescribing methadone without a complete and thorough assessment of the patient's pain history, current dosage, and potential interactions with other medications is not safe practice, especially for a **new patient**. - Methadone has a **long and variable half-life**, making it prone to accumulation and overdose, and requires careful titration and monitoring, which cannot be done without a full history.

Question 98: A 60-year-old man presents to the office for a scheduled follow-up visit. He has had hypertension for the past 30 years and his current anti-hypertensive medications include lisinopril (40 mg/day) and hydrochlorothiazide (50 mg/day). He follows most of the lifestyle modifications recommended by his physician, but is concerned about his occasional occipital headaches in the morning. His blood pressure is 160/98 mm Hg. The physician adds another drug to his regimen that acts centrally as an α2-adrenergic agonist. Which of the following second messengers is involved in the mechanism of action of this new drug?

A. Calcium ions
B. Inositol triphosphate
C. Cyclic guanosine monophosphate
D. Cyclic adenosine monophosphate (Correct Answer)
E. Diacylglycerol

Explanation: ***Cyclic adenosine monophosphate*** - The physician likely added **clonidine or methyldopa**, both of which are **central α2-adrenergic agonists** used to treat hypertension. - Activation of **α2-adrenergic receptors** leads to the **inhibition of adenylyl cyclase** and a decrease in **intracellular cyclic AMP (cAMP) levels**, which is the second messenger. *Calcium ions* - While calcium ions are crucial second messengers in many cellular processes, they are primarily involved in the mechanism of action of **α1-adrenergic receptors** and **voltage-gated calcium channels**, not directly inhibited by α2-agonists. - **α2-adrenergic agonism** primarily acts to *reduce* neuronal excitability, which can indirectly affect calcium flux but does not directly involve calcium as the primary second messenger. *Inositol triphosphate* - **Inositol triphosphate (IP3)** is a second messenger primarily associated with the activation of **Gq protein-coupled receptors**, leading to the release of intracellular calcium. - This pathway is characteristic of **α1-adrenergic receptors**, which cause vasoconstriction, and is antagonistic to the α2-agonist mechanism. *Cyclic guanosine monophosphate* - **Cyclic GMP (cGMP)** is a key second messenger in processes such as **vasodilation mediated by nitric oxide** and the action of ANP/BNP. - **α2-adrenergic agonists** do not directly modulate cGMP levels as their primary mechanism of action. *Diacylglycerol* - **Diacylglycerol (DAG)** is a second messenger, along with IP3, produced from the hydrolysis of **PIP2** by phospholipase C, following activation of **Gq protein-coupled receptors**. - This pathway is associated with **α1-adrenergic receptor activation**, not the inhibitory pathway initiated by central α2-adrenergic agonists.

Question 99: A 56-year-old man comes to the office complaining of a dry cough for 2 months. His medical history includes a recent myocardial infarction (MI), after which he was placed on several medications. He is currently on ramipril, clopidogrel, digoxin, lovastatin, and nitroglycerin. He does not smoke cigarettes and does not drink alcohol. He denies a history of bronchial asthma. Examination of the chest is within normal limits. Which of the following medications may have caused his symptom?

A. Clopidogrel
B. Ramipril (Correct Answer)
C. Digoxin
D. Nitroglycerin
E. Lovastatin

Explanation: ***Ramipril*** - **Ramipril** is an **ACE inhibitor** commonly associated with a **dry cough** due to the accumulation of **bradykinin** in the respiratory tract. - The cough typically develops within **weeks to months** of starting the medication and resolves upon discontinuation. *Clopidogrel* - **Clopidogrel** is an **antiplatelet medication** that inhibits platelet aggregation. - It is known for side effects like increased **bleeding risk**, but **dry cough** is not a characteristic adverse effect. *Digoxin* - **Digoxin** is a cardiac glycoside used to treat **heart failure** and **atrial fibrillation**. - Its common side effects include **gastrointestinal upset**, **visual disturbances**, and **cardiac arrhythmias**, not a chronic cough. *Nitroglycerin* - **Nitroglycerin** is a **vasodilator** used for angina. - The most common side effects are **headache**, **dizziness**, and **hypotension**, but it does not typically cause a persistent dry cough. *Lovastatin* - **Lovastatin** is an **HMG-CoA reductase inhibitor** used to lower cholesterol. - Common side effects include **myalgia**, **gastrointestinal complaints**, and **elevated liver enzymes**, but a dry cough is not a recognized side effect.

Question 100: A 38-year-old man presents to his physician with recurrent episodes of facial swelling and abdominal pain. He reports that these episodes started when he was approximately 16 years of age. His mother also has similar episodes of swelling accompanied by swelling of her extremities. The vital signs include: blood pressure 140/80 mm Hg, heart rate 74/min, respiratory rate 17/min, and temperature 36.6℃ (97.8℉). His physical examination is unremarkable. The laboratory work-up shows the following findings: Test Result Normal range C1 esterase inhibitor 22% > 60% Complement C4 level 9 mg/dL 14–40 mg/dL Complement C2 level 0.8 mg/dL 1.1–3.0 mg/dL Complement component 1q 17 mg/dL 12–22 mg/dL Which of the following anti-hypertensive medications is contraindicated in this patient?

A. Amlodipine
B. Fosinopril (Correct Answer)
C. Atenolol
D. Indapamide
E. Valsartan

Explanation: ***Fosinopril*** - This patient presents with symptoms and lab findings consistent with **hereditary angioedema (HAE)**, characterized by recurrent episodes of **facial swelling** and **abdominal pain**, low C1 esterase inhibitor, and low C4/C2 levels. **ACE inhibitors** like fosinopril are absolutely **contraindicated in HAE** because they can trigger life-threatening angioedema attacks by increasing bradykinin levels. - The family history of similar swelling further supports the diagnosis of HAE, making any medication that exacerbates bradykinin a significant risk. *Amlodipine* - **Dihydropyridine calcium channel blockers** such as amlodipine are generally considered safe in patients with angioedema and do not interfere with the bradykinin pathway. - They are a suitable option for hypertension management in these patients. *Atenolol* - **Beta-blockers** like atenolol are generally safe for managing hypertension in patients with a history of angioedema, as they do not affect the complement or bradykinin systems. - There is no evidence to suggest that atenolol would worsen angioedema symptoms. *Indapamide* - **Thiazide diuretics** such as indapamide are safe and effective antihypertensive agents in patients with angioedema. - They work by increasing sodium and water excretion and do not interact with the pathways involved in angioedema. *Valsartan* - **Angiotensin receptor blockers (ARBs)** like valsartan are generally considered safer than ACE inhibitors in patients with angioedema, although a small risk of angioedema still exists due to their weak effect on bradykinin. - However, the primary family of drugs to avoid in HAE is ACE inhibitors due to their direct and significant impact on bradykinin degradation.

Question 101: A 31-year-old African American woman presents to her primary care provider complaining of stiff, painful fingers. She reports that her symptoms started 2 years ago and have gradually worsened. Her pain is not relieved by ibuprofen or acetaminophen. She is most concerned about having occasional episodes in which her fingers become extremely painful and turn white then pale blue. Her past medical history is notable for hypertension but she has previously refused to take any medication. She works as a postal worker and spends most of her time outside. Physical examination reveals induration of her digits with loss of skin fold wrinkles. She has limited finger range of motion. She would like to know if she can do anything to address her intermittent finger pain as it is affecting her ability to work outside in the cold. Which of the following medications is most appropriate to address this patient’s concerns?

A. Methotrexate
B. Enalapril
C. Diltiazem
D. Nifedipine (Correct Answer)
E. Ambrisentan

Explanation: ***Nifedipine*** - Nifedipine, a **dihydropyridine calcium channel blocker**, is the first-line treatment for **Raynaud's phenomenon**, which is suggested by the patient's episodic finger discoloration (white then pale blue) and pain, especially exacerbated by cold. - This medication works by **vasodilation**, which improves blood flow to the digits and reduces the frequency and severity of vasospastic attacks. *Methotrexate* - Methotrexate is a **disease-modifying antirheumatic drug (DMARD)** primarily used for inflammatory conditions like **rheumatoid arthritis** or **psoriatic arthritis**. - While the patient's symptoms could suggest a connective tissue disease like **scleroderma**, methotrexate would address the underlying inflammatory/autoimmune process, not the acute vasospastic episodes of Raynaud's phenomenon. *Enalapril* - Enalapril is an **ACE inhibitor** used primarily for **hypertension** and heart failure. - While the patient has hypertension, enalapril would not directly address her intermittent finger pain and discoloration attributable to Raynaud's phenomenon. *Diltiazem* - Diltiazem is a **non-dihydropyridine calcium channel blocker** used for hypertension, angina, and arrhythmias. - While calcium channel blockers are used for Raynaud's, **diltiazem is less preferred than dihydropyridines like nifedipine** for this specific indication due to its different mechanism of action and potential side effect profile. *Ambrisentan* - Ambrisentan is an **endothelin receptor antagonist** primarily used for **pulmonary arterial hypertension**. - It is not indicated for the direct management of Raynaud's phenomenon in the absence of pulmonary hypertension.

Question 102: A 57-year-old otherwise healthy male presents to his primary care physician for a check-up. He has no complaints. His blood pressure at the previous visit was 160/95. The patient did not wish to be on any medications and at the time attempted to manage his blood pressure with diet and exercise. On repeat measurement of blood pressure today, the reading is 163/92. His physician decides to prescribe a medication which the patient agrees to take. The patient calls his physician 6 days later complaining of a persistent cough, but otherwise states that his BP was measured as 145/85 at a local pharmacy. Which of the following is a contraindication to this medication?

A. Congestive heart failure
B. Black race
C. Bilateral renal artery stenosis (Correct Answer)
D. Chronic obstructive pulmonary disease
E. Gout

Explanation: ***Bilateral renal artery stenosis*** - The patient's developing **cough** after starting a new antihypertensive suggests he was likely prescribed an **ACE inhibitor**. - **Bilateral renal artery stenosis** is a strong contraindication for ACE inhibitors due to the risk of precipitating **acute kidney injury**, as these medications rely on efferent arteriolar vasodilation to maintain renal perfusion when there's reduced afferent flow. *Congestive heart failure* - **ACE inhibitors** are often a **first-line treatment** for heart failure due to their ability to improve cardiac remodeling and reduce mortality. - They are used to prevent ventricular remodeling and reduce afterload, making this an indication, not a contraindication. *Black race* - While ACE inhibitors may be **less effective as monotherapy** in black patients, they are not contraindicated and can be effectively used in combination with other antihypertensives, such as **thiazide diuretics** or **calcium channel blockers**. - **African Americans** often respond better to calcium channel blockers and diuretics for hypertension but ACE inhibitors are not absolutely contraindicated. *Chronic obstructive pulmonary disease* - **ACE inhibitors** are **not contraindicated** in COPD, as they do not affect bronchial smooth muscle tone. - **Beta-blockers**, not ACE inhibitors, are typically avoided or used with caution in patients with reactive airway diseases like asthma or severe COPD. *Gout* - **ACE inhibitors** do not significantly impact **uric acid levels** and are generally safe for use in patients with gout. - In contrast, **thiazide diuretics** can increase uric acid levels and worsen gout, but this is not the medication indicated by the patient's cough.

Question 103: A 65-year-old man with a history of hypertension visits your office. His blood pressure on physical examination is found to be 150/90. You prescribe him metoprolol. Which of the following do you expect to occur as a result of the drug?

A. Increased serum renin levels as a consequence of ß2 receptor antagonism
B. Decreased PR interval on EKG
C. Increased serum renin levels as a consequence of ß1 receptor antagonism
D. Decreased serum renin levels as a consequence of ß2 antagonism
E. Decreased serum renin levels as a consequence of ß1 receptor antagonism (Correct Answer)

Explanation: ***Decreased serum renin levels as a consequence of ß1 receptor antagonism*** - Metoprolol is a **selective beta-1 blocker**, primarily acting on beta-1 adrenergic receptors in the heart and kidneys. - Antagonism of **renal beta-1 receptors** reduces **renin secretion** from the juxtaglomerular cells, leading to decreased angiotensin II and aldosterone levels, and ultimately lower blood pressure. *Increased serum renin levels as a consequence of ß2 receptor antagonism* - This is incorrect because beta-2 receptor stimulation generally leads to some **renin release**, and their antagonism would not inherently cause an increase in renin. - Moreover, metoprolol primarily antagonizes **beta-1 receptors**, not beta-2 receptors, at typical therapeutic doses. *Decreased PR interval on EKG* - Beta-blockers like metoprolol decrease the **sinoatrial node firing rate** and **atrioventricular (AV) nodal conduction velocity**. - This effect would typically **increase** (prolong) the **PR interval** on an EKG, not decrease it. *Increased serum renin levels as a consequence of ß1 receptor antagonism* - This is incorrect because **beta-1 receptor stimulation** *increases* renin release, so **beta-1 receptor antagonism** would *decrease* renin levels. - The direct effect of beta-1 blockade in the kidneys is to reduce renin secretion. *Decreased serum renin levels as a consequence of ß2 antagonism* - This is incorrect. While some beta-2 receptors are present in the kidneys, their role in renin release is less prominent than **beta-1 receptors**. - The primary mechanism by which metoprolol reduces renin is through its **beta-1 receptor antagonism**.

Question 104: A 56-year-old man with hypertension comes to the physician for a follow-up examination. His blood pressure is 165/92 mm Hg on the left arm and 162/90 mm Hg on the right arm. He reports that he is compliant with his medication and exercise regimen. The physician adds a drug to his antihypertensive medication regimen. This drug increases serum renin, angiotensin I, and angiotensin II levels, and decreases serum aldosterone levels, without affecting bradykinin levels. Which of the following drugs was most likely added to this patient's medication regimen?

A. Lisinopril
B. Aliskiren
C. Triamterene
D. Metoprolol
E. Candesartan (Correct Answer)

Explanation: ***Candesartan*** - **Candesartan** is an **Angiotensin Receptor Blocker (ARB)**. ARBs block the AT1 receptor, preventing angiotensin II from exerting its effects, including vasoconstriction and aldosterone release. - By blocking the AT1 receptor, ARBs lead to a compensatory increase in renin, angiotensin I, and angiotensin II levels due to the interrupted negative feedback loop, while lowering aldosterone; they do not affect bradykinin metabolism. *Lisinopril* - **Lisinopril** is an **ACE inhibitor**, which prevents the conversion of angiotensin I to angiotensin II, leading to decreased angiotensin II and aldosterone levels. - ACE inhibitors also inhibit the breakdown of **bradykinin**, leading to increased bradykinin levels, which is a key differentiating feature not described in the question. *Aliskiren* - **Aliskiren** is a **direct renin inhibitor**; it directly inhibits renin, thus decreasing the production of angiotensin I, angiotensin II, and subsequently aldosterone. - This drug would decrease, not increase, serum renin, angiotensin I, and angiotensin II levels. *Triamterene* - **Triamterene** is a **potassium-sparing diuretic** that blocks sodium channels in the collecting duct, leading to increased sodium excretion and potassium retention. - It does not directly affect the **renin-angiotensin-aldosterone system (RAAS)** in the manner described, nor does it affect bradykinin levels. *Metoprolol* - **Metoprolol** is a **beta-blocker** that primarily reduces heart rate, cardiac output, and renin release from the kidneys. - It would therefore tend to *decrease* renin activity, and consequently lower angiotensin II and aldosterone, which contradicts the described hormonal changes.

Question 105: A 50-year-old woman comes to the physician because of intermittent pain and numbness in her right hand for 6 weeks. She has a pins-and-needles sensation that worsens at night and is relieved when she shakes her hand. She also has episodic left knee pain throughout the day. She has a history of hypertension controlled with lisinopril. She takes over-the-counter medications for constipation. Her BMI is 35 kg/m2. Her mother has a history of rheumatoid arthritis. She looks fatigued. Her pulse is 57/min and blood pressure is 120/75 mm Hg. On physical examination, there is normal range of motion in the wrists and digits. Sensation is decreased to light touch in the thumb and index finger. There is no thenar muscle atrophy. Deep tendon reflexes are 1+ and there is mild edema in the legs. Which of the following treatments is most likely to benefit the patient?

A. Surgical decompression
B. Oral prednisone
C. Methotrexate
D. L-thyroxine (Correct Answer)
E. Ibuprofen

Explanation: ***L-thyroxine*** - The patient's symptoms of **fatigue** and **bradycardia (pulse 57/min)**, along with a high BMI and leg edema, suggest **hypothyroidism** as a contributing factor to her carpal tunnel syndrome. Subclinical hypothyroidism is a common cause of neuropathy and can be easily treated with thyroid hormone replacement. - **L-thyroxine** replacement would address the underlying metabolic derangement, potentially resolving the nerve compression symptoms and improving overall systemic function. *Surgical decompression* - While recommended for severe carpal tunnel syndrome, the absence of **thenar atrophy** and **normal range of motion** suggests her condition is not yet severe enough to warrant immediate surgery, especially without addressing potential underlying causes. - This is typically reserved for cases unresponsive to conservative management or with objective signs of severe nerve damage. *Oral prednisone* - **Corticosteroids** can provide short-term relief for carpal tunnel syndrome by reducing inflammation, but they do not address the underlying cause and are not a long-term solution. - Their use is generally reserved for acute flares or as a temporary measure, not as primary treatment for chronic symptoms with a likely systemic cause. *Methotrexate* - This medication is a **disease-modifying antirheumatic drug (DMARD)** primarily used for autoimmune conditions like **rheumatoid arthritis** or psoriatic arthritis. - The patient's symptoms are more consistent with carpal tunnel syndrome exacerbated by an underlying metabolic issue, rather than an inflammatory arthropathy, making methotrexate inappropriate. *Ibuprofen* - **NSAIDs** like ibuprofen can help manage pain and inflammation but do not address the underlying **nerve compression** or the potential systemic cause (hypothyroidism) of her carpal tunnel syndrome. - It would offer only symptomatic relief without treating the root problem, and chronic use can have side effects.

Question 106: A 45-year-old man comes to the physician for a follow-up examination after being diagnosed with hypertension 6 months ago. He has cut salt out of his diet and started exercising regularly, but home blood pressure measurements continue to be elevated. His blood pressure is 160/85 mm Hg. An antihypertensive medication is prescribed that decreases blood pressure by decreasing the transmembrane calcium current across vascular smooth muscle cells. Side effects include peripheral edema and flushing. Which of the following best describes why this drug does not affect skeletal muscle contraction?

A. Skeletal muscle contraction occurs independently of extracellular calcium influx (Correct Answer)
B. Skeletal muscle preferentially expresses N-type and P-type calcium channels
C. Skeletal muscle calcium channels do not undergo conformational change when bound to this drug
D. Skeletal muscle ryanodine receptor activation occurs independently of membrane depolarization
E. Skeletal muscle lacks voltage-gated L-type calcium channels

Explanation: ***Skeletal muscle contraction occurs independently of extracellular calcium influx*** - Skeletal muscle contraction is primarily initiated by the release of **intracellular calcium** from the **sarcoplasmic reticulum** via **ryanodine receptors (RyRs)**. - While L-type calcium channels (dihydropyridine receptors, DHPRs) are present in skeletal muscle, their main role is to act as **voltage sensors** that mechanically activate RyRs, rather than to provide significant calcium influx for contraction. *Skeletal muscle preferentially expresses N-type and P-type calcium channels* - **N-type** and **P/Q-type calcium channels** are primarily found in **neurons** at presynaptic terminals, where they mediate neurotransmitter release. - While skeletal muscle does have calcium channels, the primary voltage-gated channels involved in excitation-contraction coupling are **L-type calcium channels (DHPRs)**, not N or P-type. *Skeletal muscle calcium channels do not undergo conformational change when bound to this drug* - This statement is incorrect because the drug class in question, **dihydropyridine calcium channel blockers**, specifically acts on L-type calcium channels (DHPRs). - While the drug may bind to skeletal muscle DHPRs, the functional consequence is less significant because **skeletal muscle contraction** is not highly dependent on extracellular calcium influx through these channels. *Skeletal muscle ryanodine receptor activation occurs independently of membrane depolarization* - This statement is incorrect. **Skeletal muscle ryanodine receptors (RyRs)** are directly activated by a **conformational change** in the adjacent **dihydropyridine receptors (DHPRs)** in response to **membrane depolarization**. - This mechanical coupling is triggered by the action potential spreading along the muscle fiber, leading to calcium release. *Skeletal muscle lacks voltage-gated L-type calcium channels* - This statement is incorrect. Skeletal muscle actually contains **voltage-gated L-type calcium channels (DHPRs)** in its T-tubule membranes. - However, in skeletal muscle, these channels primarily function as **voltage sensors** that mechanically trigger the release of calcium from the sarcoplasmic reticulum, rather than allowing significant calcium influx to directly initiate contraction.

Question 107: A 47-year-old farmer presents to his primary care physician for the first time appointment. The patient has never seen a doctor and states that he is in good health. He has worked as a farmer for the past 30 years and has no complaints. His temperature is 98.9°F (37.2°C), blood pressure is 197/118 mmHg, pulse is 90/min, respirations are 14/min, and oxygen saturation is 98% on room air. Physical exam is notable for an obese man in no current distress. Laboratory values are seen below. Serum: Na+: 139 mEq/L Cl-: 101 mEq/L K+: 5.2 mEq/L HCO3-: 25 mEq/L BUN: 34 mg/dL Glucose: 179 mg/dL Creatinine: 2.1 mg/dL Ca2+: 10.2 mg/dL Which of the following is the best management of this patient's blood pressure?

A. Lisinopril
B. Hydrochlorothiazide (Correct Answer)
C. Nicardipine
D. Carvedilol
E. Metoprolol

Explanation: ***Hydrochlorothiazide*** - This patient has **severe hypertension with renal impairment** (Cr 2.1 mg/dL) and **hyperkalemia** (K+ 5.2 mEq/L), making a **thiazide diuretic** the best initial choice. - **Thiazides lower potassium levels**, addressing the hyperkalemia that contraindicates ACE inhibitors in this patient. - **Effective for hypertension** at this level of renal function (creatinine < 2.5 mg/dL) and recommended as **first-line therapy** per ACC/AHA guidelines. - While thiazides can worsen glucose slightly, this is a **minor concern compared to the risk of worsening hyperkalemia** with ACE inhibitors. *Lisinopril* - Although **ACE inhibitors** have **renoprotective effects** and are beneficial in diabetic nephropathy, they are **relatively contraindicated** in this patient due to **existing hyperkalemia** (K+ 5.2 mEq/L). - ACE inhibitors **increase potassium** by reducing aldosterone secretion, risking **dangerous hyperkalemia** (potentially > 6.0 mEq/L). - In patients with **renal impairment and hyperkalemia**, ACE inhibitors can precipitate **acute kidney injury** and life-threatening arrhythmias. - The hyperkalemia must be addressed first before considering ACE inhibitor therapy. *Nicardipine* - **Nicardipine** is a **dihydropyridine calcium channel blocker** used primarily for **hypertensive emergencies** requiring rapid IV blood pressure reduction. - This patient has **severe asymptomatic hypertension** without acute end-organ damage (no acute distress, stable vitals), making this **chronic hypertension** requiring oral management, not an emergency. *Carvedilol* - **Carvedilol** is a **non-selective beta-blocker with alpha-blocking activity** used for hypertension with co-existing **heart failure** or **post-MI**. - No evidence of heart failure or coronary disease in this presentation, making it **not first-line**. - Beta-blockers can **mask hypoglycemic symptoms** in diabetic patients and may worsen **insulin resistance**. *Metoprolol* - **Metoprolol** is a **selective beta-1 blocker** that can be used for hypertension but is **not preferred first-line** in this clinical scenario. - Like other beta-blockers, it can **worsen glucose control** and **mask hypoglycemia** in diabetic patients. - Does not address the **hyperkalemia** or provide the blood pressure efficacy needed in this patient with severe hypertension and metabolic concerns.

Question 108: A 45-year-old man presents with a chief complaint of pain in the great toe. He has a history of gout, which is under control. He was diagnosed with diabetes 5 years ago and is currently taking metformin. He was recently diagnosed with hypertension and was placed on a hypertensive drug. He is a non-smoker and does not abuse alcohol. The family history is significant for ischemic heart disease in his father. His current blood pressure is 136/84 mm Hg and the pulse is 78/min. The physical examination did not reveal any abnormalities. He uses over-the-counter multivitamin supplements. Which of the following drugs could have resulted in these symptoms?

A. Angiotensin-converting enzyme (ACE) inhibitors
B. Angiotensin II receptor blockers (ARBs)
C. Thiazide diuretics (Correct Answer)
D. Calcium channel blockers (CCBs)
E. Beta-blockers

Explanation: ***Thiazide diuretics*** - **Thiazide diuretics** can increase serum uric acid levels by reducing its renal excretion, thereby precipitating a **gout flare**, especially in individuals with a pre-existing history of gout. - This patient's history of gout and recent initiation of a hypertensive drug strongly suggest that a thiazide diuretic is the most likely cause of his current symptoms. *Angiotensin-converting enzyme (ACE) inhibitors* - **ACE inhibitors** are generally favorable for patients with gout as they tend to **lower uric acid levels** or have no significant impact on them. - They are often preferred for hypertension in patients with diabetes due to their **renal protective effects**. *Angiotensin II receptor blockers (ARBs)* - Some **ARBs**, particularly **losartan**, have a **uricosuric effect**, meaning they can lower uric acid levels and are thus beneficial for patients with gout. - ARBs, in general, are not associated with increasing uric acid or triggering gout flares. *Calcium channel blockers (CCBs)* - **CCBs** are considered **neutral or beneficial** in terms of uric acid metabolism and gout. - They do not typically cause hyperuricemia or gout flares. *Beta-blockers* - **Beta-blockers** are generally considered to have a **neutral effect** on uric acid levels. - They are not known to precipitate gout attacks.

Question 109: A patient presents to the clinic with symptoms of dizziness on standing up. He says it started soon after he was diagnosed with hypertension and started taking treatment for it. He has no other medical history. The physician decides to switch to another antihypertensive that does not cause orthostatic hypotension. Which of the following should be the drug of choice for this patient?

A. Clonidine
B. Methyldopa
C. Enalapril
D. Amlodipine (Correct Answer)
E. Propranolol

Explanation: ***Amlodipine*** - Amlodipine is a **dihydropyridine calcium channel blocker** that causes **peripheral vasodilation** but does **NOT typically cause orthostatic hypotension** because it maintains blood pressure across postural changes. - Unlike centrally acting agents, amlodipine does **not impair baroreceptor reflexes** or reduce sympathetic tone, allowing normal cardiovascular compensation when standing. - It is an excellent choice for patients who experienced orthostatic hypotension with other antihypertensives, as it effectively lowers blood pressure without postural effects. - Common side effects include **peripheral edema** and **reflex tachycardia**, but not orthostatic symptoms. *Enalapril* - As an **ACE inhibitor**, enalapril is generally well-tolerated but can cause **first-dose hypotension**, particularly in volume-depleted or elderly patients. - While less likely than centrally acting agents to cause orthostatic hypotension, it is not the best choice when specifically avoiding this adverse effect. - ACE inhibitors work on the **renin-angiotensin-aldosterone system** and are preferred in patients with diabetes or heart failure. *Clonidine* - Clonidine is a **centrally acting alpha-2 agonist** that reduces sympathetic outflow and commonly causes **significant orthostatic hypotension** due to impaired cardiovascular reflexes. - It can also cause **sedation, dry mouth**, and **rebound hypertension** with abrupt withdrawal. - This drug would worsen the patient's orthostatic symptoms. *Methyldopa* - Methyldopa is another **centrally acting alpha-2 agonist** that frequently causes **orthostatic hypotension** by reducing sympathetic tone. - It is primarily used for **pregnancy-induced hypertension** due to its safety profile in pregnancy. - This drug would be inappropriate for a patient experiencing orthostatic symptoms. *Propranolol* - Propranolol is a **non-selective beta-blocker** that can occasionally cause orthostatic symptoms, though this is not a primary adverse effect. - It reduces **cardiac output** and **heart rate**, which may impair compensation for postural changes in some patients. - Beta-blockers can also cause **fatigue, bradycardia**, and mask **hypoglycemia symptoms** in diabetic patients.

Question 110: A 27-year-old G1P0 woman at 25 weeks estimated gestational age presents with a blood pressure of 188/99 mm Hg during a routine prenatal visit. She has no symptoms, except for a mild headache. The patient's heart rate is 78/min. An injectable antihypertensive along with a beta-blocker is administered, and her blood pressure returns to normal within a couple of hours. She is sent home with advice to continue the beta-blocker. The patient returns after a couple of weeks with joint pain in both of her knees and fatigue. A blood test for anti-histone antibodies is positive. Which of the following is the mechanism of action of the intravenous antihypertensive medication most likely used in this patient?

A. Potassium channel activation
B. Calcium channel antagonism
C. Release endogenous nitric oxide
D. Interference with action of inositol trisphosphate (IP3) on intracellular calcium release (Correct Answer)
E. Inhibition of phosphodiesterase enzyme

Explanation: ***Interference with action of inositol trisphosphate (IP3) on intracellular calcium release*** - The clinical presentation of hypertension, especially during pregnancy, followed by **joint pain** and ** positive anti-histone antibodies**, strongly suggests **drug-induced lupus**. - **Hydralazine** is a common cause of **drug-induced lupus** and acts by interfering with **IP3-mediated calcium release**, causing **vasodilatation**. *Potassium channel activation* - Medications like **minoxidil** and **diazoxide** activate potassium channels, leading to **hyperpolarization** and **vasorelaxation**. - While effective antihypertensives, they are not typically associated with **drug-induced lupus**. *Calcium channel antagonism* - **Calcium channel blockers** (e.g., nifedipine, amlodipine) reduce intracellular calcium, leading to **smooth muscle relaxation**. - These medications are generally safe in pregnancy but are not linked to **anti-histone antibody formation** or **drug-induced lupus**. *Release endogenous nitrous oxide* - **Nitrates** (e.g., nitroglycerin) release **nitric oxide**, which activates **guanylyl cyclase** and leads to **vasodilatation**. - While used in hypertensive emergencies, they are not a common cause of **drug-induced lupus**. *Inhibition of phosphodiesterase enzyme* - **Phosphodiesterase inhibitors** (e.g., sildenafil) increase intracellular levels of **cAMP** or **cGMP**, leading to **vasodilatation**. - These drugs are not the primary treatment for acute severe hypertension in pregnancy and do not typically cause **drug-induced lupus**.

Question 111: A 52-year-old woman with type 2 diabetes, treated with metformin, presents for a routine physical examination. Her vital signs are: pulse 85/min, respiratory rate 15/min, blood pressure 162/96 mm Hg, and temperature 37.0°C (98.6°F). A first-line antihypertensive drug is initiated. Which of the following is the most likely effect of this medication on the following parameters? Parameters (in order): 1. 24-hour urine sodium 2. Aldosterone 3. Angiotensin II 4. Peripheral vascular resistance 5. Renin

A. Increased Decreased Decreased Decreased Increased (Correct Answer)
B. Increased Decreased Increased Decreased Increased
C. Increased Increased Increased Increased Increased
D. Decreased Increased Increased Decreased Increased
E. Increased Decreased Decreased Decreased Decreased

Explanation: ***Increased, Decreased, Decreased, Decreased, Increased*** * Given the patient's **type 2 diabetes** and **hypertension**, an **ACE inhibitor** or **ARB** would likely be initiated as a first-line agent due to their renoprotective effects and ability to control blood pressure. * These drugs block the conversion of **angiotensin I to angiotensin II (ACE inhibitors)** or block **angiotensin II receptors (ARBs)**, leading to **decreased angiotensin II** and subsequent **decreased aldosterone**, **decreased peripheral vascular resistance**, and a **reflex increase in renin**. **Sodium excretion** would increase due to decreased aldosterone. *Increased, Decreased, Increased, Decreased, Increased* * This option incorrectly suggests an **increase in Angiotensin II (Ang II)** which would not occur with ACE inhibitors or ARBs, as these drugs work to lower Ang II levels. * A decrease in peripheral vascular resistance is consistent, but the overall profile of hormonal changes is inaccurate for a first-line agent like an ACE inhibitor. *Increased, Increased, Increased, Increased, Increased* * This option suggests an overall increase in most parameters, which would indicate a drug that activates the **renin-angiotensin-aldosterone system (RAAS)** rather than inhibiting it. * An **increase in peripheral vascular resistance** means the drug either constricts blood vessels or has no effect, which contradicts the goal of an antihypertensive. *Decreased, Increased, Increased, Decreased, Increased* * This option states **decreased 24-hour urine sodium**, which is inconsistent with the action of ACE inhibitors or ARBs, as the reduction in aldosterone should lead to increased sodium excretion. * While **decreased peripheral vascular resistance** and **increased renin** are plausible, the rise in aldosterone and Ang II in conjunction with decreased sodium excretion makes this option less likely. *Increased, Decreased, Decreased, Decreased, Decreased* * This option proposes a **decrease in renin**, which would happen with direct renin inhibitors but not with ACE inhibitors or ARBs where a *reflex increase* in renin is expected due to the blockade of the negative feedback loop. * Most other parameters align with ACE inhibitor/ARB action, but the **renin** change is incorrect for this class of drugs.

Question 112: A 55-year-old man with type 2 diabetes mellitus comes to the physician for a routine health maintenance. He feels well. His blood pressure is 155/60 mm Hg. Physical exam shows no abnormalities. Laboratory studies show a glucose concentration of 150 mg/dL and a hemoglobin A1c concentration of 9%. Treatment with lisinopril is initiated. Which of the following findings would be expected two days after initiating lisinopril therapy? | Glomerular filtration rate | Renal plasma flow | Filtration fraction | |----------------------------|-------------------|---------------------|

A. ↓ no change ↓
B. ↓ ↓ no change
C. ↑ no change ↑
D. ↓ ↑ ↓ (Correct Answer)
E. ↓ ↓ ↑

Explanation: ***↓ GFR, ↑ RPF, ↓ FF (Correct Answer)*** - Lisinopril, an **ACE inhibitor**, causes **vasodilation of the efferent arteriole**, leading to a decrease in **glomerular hydrostatic pressure**. This results in a **decreased glomerular filtration rate (GFR)**. - The decrease in efferent arteriolar resistance leads to a slight **increase in renal plasma flow (RPF)**. - The **filtration fraction (FF = GFR/RPF)** therefore **decreases** as GFR falls while RPF increases. - This initial decrease in GFR is expected and typically stabilizes; the long-term renoprotective benefits outweigh this transient effect, especially in diabetic patients. *↓ GFR, no change RPF, ↓ FF* - This option correctly predicts a decrease in GFR and FF but incorrectly states no change in RPF. - ACE inhibitors cause efferent arteriolar dilation, which typically results in a **slight increase in RPF**, not "no change." *↓ GFR, ↓ RPF, no change FF* - This option incorrectly predicts a decrease in RPF. ACE inhibitors cause **efferent vasodilation**, which increases or maintains RPF, not decreases it. - A decrease in both GFR and RPF with no change in FF would imply proportional decreases, which is not the characteristic action of ACE inhibitors. *↑ GFR, no change RPF, ↑ FF* - This option incorrectly predicts an increase in GFR and FF. - Lisinopril, by dilating the efferent arteriole, **reduces glomerular hydrostatic pressure** and thus **reduces GFR**, not increases it. - An increase in filtration fraction contradicts the expected pharmacologic effect. *↓ GFR, ↓ RPF, ↑ FF* - This option incorrectly predicts an increase in filtration fraction. - While it correctly shows decreased GFR, the **decrease in RPF is incorrect** (should increase or remain stable). - An increased FF would only occur if GFR decreased proportionally less than RPF, which is opposite to ACE inhibitor effects.

Question 113: A 69-year-old woman is brought to the clinic for difficulty breathing over the past 2 months. She denies any clear precipitating factor but reports that her breathing has become progressively labored and she feels like she can’t breathe. Her past medical history is significant for heart failure, diabetes mellitus, and hypertension. Her medications include lisinopril, metoprolol, and metformin. She is allergic to sulfa drugs and peanuts. A physical examination demonstrates bilateral rales at the lung bases, pitting edema of the lower extremities, and a laterally displaced point of maximal impulse (PMI). She is subsequently given a medication that will reduce her volume status by competitively binding to aldosterone receptors. What is the most likely drug prescribed to this patient?

A. Spironolactone (Correct Answer)
B. Atorvastatin
C. Furosemide
D. Amiloride
E. Hydrochlorothiazide

Explanation: ***Spironolactone*** - The patient's symptoms (difficulty breathing, bilateral rales, pitting edema, displaced PMI) are consistent with **worsening heart failure**. - **Spironolactone** is an **aldosterone antagonist** that competitively binds to aldosterone receptors, leading to diuresis and beneficial effects in heart failure by reducing fluid retention and cardiac remodeling. *Atorvastatin* - **Atorvastatin** is a **HMG-CoA reductase inhibitor** used to lower cholesterol. - While heart failure patients often have dyslipidemia, atorvastatin does not directly address acute fluid overload or improve volume status in the way described. *Furosemide* - **Furosemide** is a **loop diuretic** that also reduces volume status, but it acts by inhibiting the Na-K-2Cl cotransporter in the loop of Henle, not by competitively binding to aldosterone receptors. - Although it would be used in this patient, it does not match the mechanism of action specified in the question. *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that acts by blocking epithelial sodium channels (ENaC) in the collecting duct. - It does not competitively bind to aldosterone receptors, which is the specific mechanism mentioned in the question. *Hydrochlorothiazide* - **Hydrochlorothiazide** is a **thiazide diuretic** that inhibits the Na-Cl cotransporter in the distal convoluted tubule. - It does not act by competitively binding to aldosterone receptors, and its diuretic effect is generally weaker than loop diuretics, making it less suitable for acute severe fluid overload.

Question 114: A 34-year-old woman comes to the physician for a follow-up appointment because of a blood pressure of 148/98 mm Hg at her last health maintenance examination four weeks ago. She feels well. She has a 20-year history of migraine with aura of moderate to severe intensity. For the past year, the headaches have been occurring 1–2 times per week. Her only medication is sumatriptan. She runs two to three times a week and does yoga once a week. She is sexually active with her husband and uses condoms inconsistently. Her father has type 2 diabetes mellitus and hypertension. Her temperature is 37.2°C (99.0°F), pulse is 76/min, respirations are 12/min, and blood pressure is 143/92 mm Hg. A repeat sitting blood pressure 20 minutes later is 145/94 mm Hg. Physical examination is unremarkable. Which of the following is the most appropriate pharmacotherapy for this patient?

A. Losartan
B. Lisinopril
C. Hydrochlorothiazide
D. Propranolol (Correct Answer)
E. Prazosin

Explanation: ***Propranolol*** - This patient has a history of **migraine with aura** and **hypertension**. Beta-blockers like propranolol are effective in treating both conditions, making it an appropriate choice. - Beta-blockers are a good option for hypertension management in patients with co-existing conditions such as migraine prophylaxis, especially since the patient is already experiencing frequent migraines. *Losartan* - Losartan is an **ARB (angiotensin receptor blocker)**, effective for hypertension. However, it does not offer additional benefits for migraine prophylaxis. - While ARBs are renoprotective and good for diabetes-related hypertension, this patient's hypertension is not solely related to diabetes, and her primary co-morbidity is migraine. *Lisinopril* - Lisinopril is an **ACE inhibitor**, a first-line agent for hypertension, but it does not treat migraine effectively. - ACE inhibitors are also **contraindicated in pregnancy**, and this patient is sexually active with inconsistent condom use, raising potential concerns if she were to become pregnant. *Hydrochlorothiazide* - Hydrochlorothiazide is a **thiazide diuretic** and a first-line antihypertensive agent. It is not indicated for migraine prophylaxis. - While effective for hypertension, it would not address the patient's severe and frequent migraines. *Prazosin* - Prazosin is an **alpha-1 blocker** used for hypertension, particularly beneficial for benign prostatic hyperplasia, which is not relevant here. - It is not a first-line agent for essential hypertension and does not have a role in migraine prophylaxis.

Question 115: A 25-year-old man comes to the physician because he and his wife have been unable to conceive despite regular unprotected sex for the past 15 months without using contraception. His wife has been tested and is fertile. The patient began puberty at the age of 14 years. He was treated for Chlamydia trachomatis 6 years ago. He is a professional cyclist and trains every day for 3–4 hours. He feels stressed because of an upcoming race. His blood pressure is 148/92 mm Hg. Physical examination of the husband shows a tall, athletic stature with uniform inflammatory papular eruptions of the face, back, and chest. Genital examination shows small testes. Which of the following is the most likely underlying cause of this patient's infertility?

A. Scrotal hyperthermia
B. Anabolic steroid use (Correct Answer)
C. Psychogenic erectile dysfunction
D. Kallmann syndrome
E. Klinefelter syndrome

Explanation: ***Anabolic steroid use*** - The patient's **tall, athletic stature**, **hypertension**, and diffuse **inflammatory papular eruptions** (acne) are classic signs of anabolic steroid use. - Anabolic steroids suppress endogenous **gonadotropin-releasing hormone (GnRH)**, leading to secondary hypogonadism, **testicular atrophy** (small testes), and infertility. *Scrotal hyperthermia* - While professional cycling can lead to increased scrotal temperature, this would cause more generalized damage to spermatogenesis, not necessarily lead to **acne**, **hypertension**, or **testicular atrophy** to the degree suggested. - The primary impact is on **sperm motility** and **morphology**, not typically accompanied by the systemic signs of androgen excess. *Psychogenic erectile dysfunction* - This patient is presenting with **infertility**, not primary erectile dysfunction, and his wife is confirmed fertile. - While psychological stress can impact fertility, the multitude of specific physical findings point away from a purely psychogenic cause. *Kallmann syndrome* - Kallmann syndrome is characterized by **anosmia/hyposmia** and **delayed puberty** due to GnRH deficiency. - The patient started puberty at 14, indicating a normal onset, and no mention of olfactory deficits is made. *Klinefelter syndrome* - Klinefelter syndrome (47,XXY) is a genetic disorder associated with **primary hypogonadism**, **tall stature**, and **gynecomastia**. - While it can cause small testes and infertility, the patient's prominent **acne** and **hypertension** are not typical features, and puberty was not delayed.

Question 116: A 58-year-old man presents for a follow-up appointment. He recently was found to have a history of stage 2 chronic kidney disease secondary to benign prostatic hyperplasia leading to urinary tract obstruction. He has no other medical conditions. His father died at age 86 from a stroke, and his mother lives in an assisted living facility. He smokes a pack of cigarettes a day and occasionally drinks alcohol. His vital signs include: blood pressure 130/75 mm Hg, pulse 75/min, respiratory rate 17/min, and temperature 36.5°C (97.7°F). His physical examination is unremarkable. A 24-hour urine specimen reveals the following findings: Specific gravity 1,050 pH 5.6 Nitrites (-) Glucose (-) Proteins 250 mg/24hrs Which of the following should be prescribed to this patient to decrease his cardiovascular risk?

A. Enalapril (Correct Answer)
B. Ezetimibe
C. Amlodipine
D. Carvedilol
E. Aspirin

Explanation: ***Enalapril*** - **Enalapril**, an ACE inhibitor, is indicated for patients with **chronic kidney disease** and **proteinuria** to reduce cardiovascular risk and slow kidney disease progression. - The patient has stage 2 CKD and **250 mg/24hrs of protein in urine**, which, when coupled with hypertension, makes ACE inhibitors the preferred choice to mitigate cardiovascular risk. *Ezetimibe* - **Ezetimibe** is a **cholesterol absorption inhibitor** used to lower LDL-C, but there is no information in the vignette to suggest hyperlipidemia. - It is an inappropriate choice without evidence of dyslipidemia or a strong indication for lipid-lowering therapy. *Amlodipine* - **Amlodipine** is a **calcium channel blocker** used to treat hypertension but does not provide specific renal-protective benefits in patients with proteinuria. - It would be a consideration for blood pressure control if an ACE inhibitor were contraindicated or insufficient. *Carvedilol* - **Carvedilol** is a **beta-blocker** used for hypertension, heart failure, and post-MI, but there is no indication for its use here. - It is not the first-line agent for cardiovascular risk reduction in patients with chronic kidney disease and proteinuria without other specific cardiac indications. *Aspirin* - **Aspirin** is used for primary or secondary prevention of cardiovascular events due to its **antiplatelet effects**. However, in the absence of established cardiovascular disease, its use for primary prevention in CKD patients needs careful consideration of bleeding risk. - While patients with CKD are at higher cardiovascular risk, an ACE inhibitor addresses both the hypertension and proteinuria, which directly contribute to cardiovascular and kidney disease progression in this patient.

Question 117: A 66-year-old man presents to the emergency room with blurred vision, lightheadedness, and chest pain that started 30 minutes ago. The patient is awake and alert. His history is significant for uncontrolled hypertension, coronary artery disease, and he previously underwent percutaneous coronary intervention. He is afebrile. The heart rate is 102/min, the blood pressure is 240/135 mm Hg, and the O2 saturation is 100% on room air. An ECG is performed and shows no acute changes. A rapid intravenous infusion of a drug that increases peripheral venous capacitance is started. This drug has an onset of action that is less than 1 minute with rapid serum clearance than necessitates a continuous infusion. What is the most severe side effect of this medication?

A. Status asthmaticus
B. Increased intraocular pressure
C. Cyanide poisoning (Correct Answer)
D. Intractable headache
E. Lupus-like syndrome

Explanation: ***Cyanide poisoning*** - The drug described is likely **nitroprusside**, a potent vasodilator used in hypertensive emergencies, which is rapidly metabolized to **cyanide**. - **Cyanide accumulation** can occur, especially with prolonged infusions or in patients with renal impairment, leading to severe metabolic acidosis, lactic acidosis, and neurological dysfunction. *Status asthmaticus* - While some medications can exacerbate asthma, nitroprusside is not typically associated with inducing **status asthmaticus**. Its primary action is vasodilation, not bronchoconstriction. - This is an acute respiratory emergency characterized by severe, persistent asthma symptoms unresponsive to initial bronchodilator therapy, which is unrelated to nitroprusside's mechanism of action. *Increased intraocular pressure* - This side effect is more commonly associated with drugs that affect aqueous humor dynamics, such as certain **ophthalmic medications** or systemic steroids, not nitroprusside. - Nitroprusside's vasodilatory effects do not directly cause a significant or dangerous increase in **intraocular pressure**. *Intractable headache* - **Headache** is a common side effect of vasodilators like nitroprusside due to cerebral vasodilation, but it is typically manageable and is generally not the most severe or life-threatening complication. - While uncomfortable, it does not carry the same systemic toxicity risk as cyanide poisoning. *Lupus-like syndrome* - A **lupus-like syndrome** is a known side effect of certain drugs like **hydralazine** and **procainamide**, which can induce systemic lupus erythematosus-like symptoms. - Nitroprusside is not associated with this autoimmune-like reaction.

Question 118: A 56-year-old man presents for an annual checkup. He has no complaints at the moment of presentation. He was diagnosed with diabetes mellitus a year ago and takes metformin 1000 mg per day. The patient also has a history of postinfectious myocarditis that occurred 15 years ago with no apparent residual heart failure. His family history is unremarkable. He has a 15-pack-year history of smoking, but he currently does not smoke. He is a retired weightlifting athlete who at the present works as a coach and continues to work out. His BMI is 29 kg/m2. The blood pressure is 120/85 mm Hg, heart rate is 85/min, respiratory rate is 14/min, and temperature is 36.6℃ (97.9℉). Physical examination is only remarkable for an increased adiposity. The ECG is significant for increased R amplitude in leads I, II, and V3-6 and an incomplete left bundle branch block. Which of the following is most likely included in the treatment regimen of this patient?

A. Fosinopril (Correct Answer)
B. No management is required since the patient is asymptomatic
C. Amlodipine
D. Diltiazem
E. Furosemide

Explanation: ***Fosinopril*** - This patient has risk factors for **cardiovascular disease** including a history of **diabetes mellitus**, a 15-pack-year smoking history, and a history of **postinfectious myocarditis**, which together warrant the use of an **ACE inhibitor** for cardioprotection. - While his blood pressure is currently well-controlled, **ACE inhibitors** like fosinopril are recommended for patients with diabetes and/or a history of cardiac issues for their **renoprotective** and **cardioprotective effects**, irrespective of blood pressure, especially given his ECG findings suggesting some degree of ventricular enlargement. *No management is required since the patient is asymptomatic* - Despite being asymptomatic, the patient has several significant **cardiovascular risk factors** (diabetes, past smoking, history of myocarditis) that necessitate active management to prevent future adverse events. - Ignoring these risk factors would be a missed opportunity for **primary prevention** in a patient who could benefit from a cardioprotective regimen. *Amlodipine* - **Amlodipine** is a calcium channel blocker primarily used to treat hypertension and angina, but it does not offer the same **cardioprotective** and **renoprotective benefits** as ACE inhibitors in patients with diabetes or a history of heart disease. - While it could be considered for blood pressure control, it's not the first-line choice for organ protection in this scenario. *Diltiazem* - **Diltiazem** is a non-dihydropyridine calcium channel blocker used for hypertension, angina, and rate control in arrhythmias. Like amlodipine, it lacks the specific **organ-protective benefits** of ACE inhibitors for patients with diabetes and/or a history of myocarditis. - It would be a less suitable first-line option compared to an ACE inhibitor for reducing cardiovascular risk. *Furosemide* - **Furosemide** is a loop diuretic primarily used to manage fluid overload in conditions like heart failure or edema. The patient shows no signs of **congestive heart failure** or fluid retention. - Administering a diuretic without an indication for volume management would be inappropriate and could lead to **dehydration** or electrolyte imbalances.

Question 119: A 48-year-old man comes to the physician because of a 3-month history of fatigue, polyuria, and blurry vision. His BMI is 33 kg/m2 and his blood pressure is 147/95 mm Hg. Laboratory studies show a serum glucose concentration of 192 mg/dL and hemoglobin A1c concentration of 7.2%. Urinalysis shows 1+ glucose, 1+ protein, and no ketones. Which of the following is the most appropriate pharmacotherapy to prevent cardiovascular disease in this patient?

A. Lisinopril therapy (Correct Answer)
B. Gemfibrozil therapy
C. Insulin therapy
D. Aspirin therapy
E. Sleeve gastrectomy

Explanation: ***Lisinopril therapy*** - This patient has **hypertension**, **diabetes mellitus** (elevated blood glucose and HbA1c), and **proteinuria**, all of which significantly increase **cardiovascular risk**. **ACE inhibitors** like lisinopril are first-line therapy for hypertension in patients with diabetes and proteinuria, as they offer both blood pressure control and renal protection, thereby reducing cardiovascular events. - The medication's **renoprotective effect** in diabetic nephropathy, by reducing intraglomerular pressure and proteinuria, directly contributes to cardiovascular disease prevention by preserving kidney function. *Gemfibrozil therapy* - **Gemfibrozil** is a **fibrate** primarily used to treat **severe hypertriglyceridemia** and to a lesser extent, to raise HDL cholesterol. While dyslipidemia is common in diabetics, this patient's lipid profile is not provided, and there's no indication of severe hypertriglyceridemia that would prioritize gemfibrozil over blood pressure control and renal protection. - While addressing dyslipidemia can contribute to cardiovascular risk reduction, it is not the most appropriate initial or primary pharmacotherapy for this patient's constellation of risk factors, especially given the presence of proteinuria indicating kidney involvement. *Insulin therapy* - The patient's diabetes diagnosis (HbA1c of 7.2%) indicates elevated glucose, but it is not severe enough to immediately warrant **insulin therapy** given the patient's **BMI of 33 kg/m2**, suggesting type 2 diabetes that typically begins with oral hypoglycemics. - While glucose control is crucial, insulin does not directly address the **cardiovascular risk from hypertension and proteinuria** as effectively as an ACE inhibitor would. *Aspirin therapy* - **Aspirin** is considered for **primary prevention of cardiovascular disease** in select diabetic patients, typically those with an increased 10-year atherosclerotic cardiovascular disease (ASCVD) risk and low bleeding risk. - However, aspirin's benefit for primary prevention is less clear than that of **renoprotective antihypertensives** in patients with proteinuria, and bleeding risk must be considered. Furthermore, addressing hypertension and proteinuria is a more immediate and impactful intervention for this patient's overall cardiovascular risk profile. *Sleeve gastrectomy* - **Sleeve gastrectomy** is a form of **bariatric surgery** indicated for significant obesity (BMI typically >40 kg/m2 or >35 kg/m2 with comorbidities) to induce substantial weight loss. While weight loss would certainly improve diabetes and hypertension, it is a surgical intervention and not a "pharmacotherapy." - This option does not address the immediate need for pharmacologic management of **hypertension and proteinuria**, which are critical for preventing cardiovascular and renal complications.

Question 120: A 35-year-old man comes to the physician because of several episodes of crushing substernal chest pain on exertion over the past 6 weeks. The pain occurs when he goes for his morning run and disappears if he slows down to a walk. The patient is concerned because two of his uncles died of myocardial infarction in their early 50s. Physical examination shows yellow plaques on both the palms. An ECG shows no abnormalities. Serum lipid studies show: Total cholesterol 650 mg/dL HDL cholesterol 30 mg/dL VLDL cholesterol 185 mg/dL Triglycerides 800 mg/dL Chylomicron remnants elevated Which of the following is the most likely cause of this patient's symptoms?

A. Decreased apolipoprotein C-II
B. Defective apolipoprotein E (Correct Answer)
C. Defective apolipoprotein B-100
D. Hepatic overproduction of VLDL
E. Decreased apolipoprotein B-48

Explanation: ***Defective apolipoprotein E*** - The patient's presentation with **eruptive xanthomas** (yellow plaques on palms), very high **triglycerides (800 mg/dL)**, elevated **VLDL cholesterol (185 mg/dL)**, and elevated **chylomicron remnants** strongly suggests **dysbetalipoproteinemia type III (familial dysbetalipoproteinemia)**. - This condition is caused by a defect in **apolipoprotein E**, which is crucial for the uptake of **chylomicron remnants** and **VLDL remnants (IDL)** by the liver. Its defect leads to their accumulation. *Decreased apolipoprotein C-II* - A deficiency in **apolipoprotein C-II** would lead to impaired activation of **lipoprotein lipase**, resulting in significantly elevated **chylomicrons** and **VLDL**. - While triglycerides would be very high, this condition primarily impacts the initial breakdown of triglycerides from chylomicrons and VLDL, and is most often associated with **recurrent pancreatitis**. *Hepatic overproduction of VLDL* - This mechanism can contribute to high triglycerides and **VLDL**, but it typically does not cause the marked elevation of **chylomicron remnants** seen in this patient. - It is often seen in conditions like **metabolic syndrome** or **familial hypertriglyceridemia**, but without the specific apolipoprotein E defect. *Defective apolipoprotein B-100* - A disease involving **defective apolipoprotein B-100** (e.g., familial defective ApoB-100) or deficient LDL receptors primarily causes **familial hypercholesterolemia**, characterized by very high **LDL cholesterol**. - This patient's lipid profile shows significantly elevated triglycerides, VLDL, and chylomicron remnants, rather than isolated high LDL. *Decreased apolipoprotein B-48* - **Apolipoprotein B-48** is essential for the synthesis and secretion of **chylomicrons** from the intestine. - A decrease in ApoB-48 would lead to **hypobetalipoproteinemia** or **abetalipoproteinemia**, characterized by very low or absent **triglycerides and cholesterol**, which is contrary to this patient's findings.

Question 121: A 50-year-old man with hypertension comes to the physician for a routine follow-up evaluation. His blood pressure is 146/98 mm Hg. The physician wishes to prescribe lisinopril. The patient says that his blood pressure is high when he is “anxious” and requests alprazolam instead of lisinopril. Which of the following is the most appropriate initial response by the physician?

A. “I would recommend fluoxetine because alprazolam can cause dependence.”
B. “Lisinopril is more effective to treat hypertension. If you do not control your high blood pressure, you may develop a stroke.”
C. “What have you heard about the use of alprazolam to treat high blood pressure?” (Correct Answer)
D. “Anxiety can cause temporary spikes in blood pressure, but it does not cause a long-term increase in blood pressure.”
E. “I would recommend consultation with a psychiatrist.”

Explanation: ***"What have you heard about the use of alprazolam to treat high blood pressure?"*** - This response demonstrates **empathy** and an interest in the patient's perspective, which is crucial for building trust and shared decision-making. - It allows the physician to understand the patient's **misconceptions** about alprazolam and hypertension, paving the way for a more effective discussion. *"I would recommend fluoxetine because alprazolam can cause dependence."* - While fluoxetine is a valid treatment for anxiety and alprazolam does carry a risk of dependence, this response **prematurely dismisses** the patient's concerns without exploring them. - It introduces a new medication without first understanding the **patient's existing beliefs** or reasons for requesting alprazolam. *"Lisinopril is more effective to treat hypertension. If you do not control your high blood pressure, you may develop a stroke."* - This statement is medically accurate regarding the treatment of hypertension and its risks but is **dismissive** of the patient's expressed concerns about anxiety. - It uses a **fear-based approach** rather than an empathetic or educational one, which can hinder patient engagement and adherence. *"Anxiety can cause temporary spikes in blood pressure, but it does not cause a long-term increase in blood pressure."* - This statement provides medical information but **does not address the patient's direct request** for alprazolam or explore their underlying reasons. - It also fails to acknowledge the potential link between chronic anxiety and its impact on overall cardiovascular health, or that an underlying anxiety disorder *can* contribute to sustained hypertension in some individuals. *"I would recommend consultation with a psychiatrist."* - While a psychiatric consultation might eventually be appropriate if an anxiety disorder is confirmed, this is a **premature referral** without first understanding the patient's perspective or attempting to address their immediate concerns. - It may make the patient feel dismissed or that their concerns are being unduly pathologized.

Question 122: A 45-year-old man presents to his primary care physician for a wellness checkup. He states that he feels fatigued at times but feels near his baseline. The patient smokes 1 pack of cigarettes per day, drinks alcohol occasionally, and has a past medical history of poorly controlled diabetes. His temperature is 98.6°F (37.0°C), blood pressure is 167/108 mmHg, pulse is 80/min, respirations are 10/min, and oxygen saturation is 98% on room air. Physical exam reveals an overweight man with a ruddy complexion. Bilateral gynecomastia is noted for which the patient inquires about cosmetic surgery as a treatment. Laboratory values are ordered as seen below. Hemoglobin: 14 g/dL Hematocrit: 42% Leukocyte count: 6,500/mm³ with normal differential Platelet count: 185,000/mm³ Serum: Na+: 142 mEq/L Cl-: 102 mEq/L K+: 3.2 mEq/L HCO3-: 31 mEq/L BUN: 27 mg/dL Glucose: 173 mg/dL Creatinine: 1.5 mg/dL Ca2+: 9.8 mg/dL A CT scan demonstrates bilateral abnormal adrenal masses. What is the most appropriate initial treatment?

A. Measure aldosterone and renin levels
B. Amiloride
C. Spironolactone (Correct Answer)
D. Eplerenone
E. Bilateral adrenalectomy

Explanation: ***Spironolactone*** - The patient presents with **hypertension**, **hypokalemia** (K+ 3.2 mEq/L), **metabolic alkalosis** (HCO3- 31 mEq/L), **bilateral adrenal masses**, and **gynecomastia**, which are highly suggestive of **primary hyperaldosteronism** (Conn's syndrome), specifically **bilateral adrenal hyperplasia**. - **Spironolactone** is an **aldosterone antagonist** that blocks mineralocorticoid receptors, thereby treating the hypertension and correcting the hypokalemia and metabolic alkalosis. - It is the **first-line medical treatment** for **bilateral adrenal hyperplasia**, as surgery is typically reserved for unilateral adenomas. - The existing gynecomastia noted in this patient is consistent with hyperaldosteronism and may be exacerbated by spironolactone's anti-androgenic effects, but this does not preclude its use as initial therapy. *Measure aldosterone and renin levels* - While measuring aldosterone and renin levels (aldosterone-to-renin ratio) is crucial for **diagnosing** primary hyperaldosteronism, this question asks for initial **treatment**. - The clinical presentation (hypertension, hypokalemia, metabolic alkalosis, bilateral adrenal masses) already strongly suggests the diagnosis, and treatment would be initiated after diagnostic confirmation. *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that blocks epithelial sodium channels in the collecting duct, reducing sodium reabsorption and potassium excretion. - While it can help manage hypokalemia and hypertension in hyperaldosteronism, it is **less effective** than spironolactone in directly antagonizing aldosterone's effects and is considered a second-line agent. *Eplerenone* - **Eplerenone** is a **selective aldosterone antagonist** with fewer anti-androgenic side effects compared to spironolactone (less gynecomastia, erectile dysfunction). - While equally effective for treating hyperaldosteronism, **spironolactone** remains the first-line choice due to its established efficacy, longer track record, and lower cost. - Eplerenone may be preferred in patients who develop intolerable anti-androgenic side effects from spironolactone. *Bilateral adrenalectomy* - **Bilateral adrenalectomy** would result in permanent adrenal insufficiency requiring lifelong glucocorticoid and mineralocorticoid replacement. - Surgery is typically reserved for **unilateral aldosterone-producing adenomas** (after lateralization studies) where unilateral adrenalectomy can be curative. - For bilateral adrenal hyperplasia, **medical management** with mineralocorticoid receptor antagonists is the preferred approach.

Question 123: A 47-year-old woman comes to the physician for a follow-up examination. She has type 1 diabetes mellitus, end-stage renal disease, and was recently started on erythropoietin for anemia. Her last hemodialysis session was yesterday. Current medications also include insulin, calcitriol, and sevelamer. She appears well. Her pulse is 68/min and regular, respirations are 12/min, and blood pressure is 169/108 mm Hg. Her blood pressure was normal at previous visits. Examination shows normal heart sounds. There are no carotid, femoral, or abdominal bruits. The lungs are clear to auscultation. Laboratory studies show a hemoglobin concentration of 12 g/dL, a serum creatinine concentration of 3.4 mg/dL, and BUN of 20 mg/dL. Which of the following is the most likely cause of this patient's hypertension?

A. Autonomic neuropathy
B. Erythropoietin therapy (Correct Answer)
C. Hypervolemia
D. Hypoglycemia
E. Calcitriol therapy

Explanation: ***Erythropoietin therapy*** - **Erythropoietin (EPO)** can cause or exacerbate hypertension, particularly in patients with chronic kidney disease, by increasing peripheral vascular resistance and vasoconstriction. - The patient was recently started on erythropoietin, and her blood pressure was normal at previous visits, suggesting a direct link. *Autonomic neuropathy* - While common in **diabetic patients**, autonomic neuropathy typically leads to **orthostatic hypotension**, not an acute elevation in systolic and diastolic blood pressure. - It would not explain the sudden onset of hypertension in a patient whose blood pressure was previously normal. *Hypervolemia* - The patient had hemodialysis yesterday, which generally removes excess fluid, making **hypervolemia** less likely as the primary cause of acute hypertension. - Clinical signs of hypervolemia (e.g., pulmonary edema, JVD) are absent, as the lungs are clear and she appears well. *Hypoglycemia* - **Hypoglycemia** can cause sympathetic activation and lead to a temporary increase in blood pressure, but it is usually associated with other symptoms like palpitations, sweating, and tremor. - It would also not explain sustained hypertension, and there is no indication of hypoglycemia in the patient's presentation. *Calcitriol therapy* - **Calcitriol**, a form of vitamin D, is used to manage secondary hyperparathyroidism in ESRD but is not directly associated with causing **acute hypertension**. - Its effects primarily relate to calcium and phosphorus metabolism, not direct blood pressure regulation.

Question 124: A 35-year-old woman presents to the emergency department with swelling of her face and abdominal pain. She states she was outside doing yard work when her symptoms began. The patient has a past medical history of recently diagnosed diabetes and hypertension. Her current medications include lisinopril, metformin, and glipizide. Her temperature is 99.5°F (37.5°C), blood pressure is 149/95 mmHg, pulse is 90/min, respirations are 15/min, and oxygen saturation is 99% on room air. On physical exam, the patient's cardiac and pulmonary exam are within normal limits. Dermatologic exam reveals edema of her hands, lips, and eyelids. There is mild laryngeal edema; however, the patient is speaking clearly and maintaining her airway. Which of the following is appropriate long-term management of this patient?

A. Danazol
B. Discontinue lisinopril (Correct Answer)
C. Prednisone
D. Ecallantide
E. Fresh frozen plasma

Explanation: ***Discontinue lisinopril*** - The patient's presentation with **facial edema**, **abdominal pain**, and mild **laryngeal edema** after starting lisinopril is highly suggestive of **angioedema induced by ACE inhibitors**. Discontinuing the causative agent is the primary long-term management. - **ACE inhibitors** like lisinopril can inhibit the breakdown of **bradykinin**, leading to its accumulation and subsequent vascular leakage and angioedema. This is a common and potentially life-threatening side effect. *Danazol* - **Danazol** is an **attenuated androgen** sometimes used for long-term prophylaxis in **hereditary angioedema** to increase C1 esterase inhibitor levels. However, it is not indicated for ACE inhibitor-induced angioedema, which is not due to a C1-INH deficiency. - Its use is associated with significant **androgenic side effects**, making it unsuitable for this patient's condition. *Prednisone* - **Prednisone**, a corticosteroid, is typically used to manage **allergic reactions** and reduce inflammation. However, **ACE inhibitor-induced angioedema** is a **bradykinin-mediated process**, not histamine-mediated, and thus does not respond to corticosteroids or antihistamines. - Administering prednisone would not address the underlying cause of bradykinin accumulation and would expose the patient to unnecessary side effects. *Ecallantide* - **Ecallantide** is a **kallikrein inhibitor** used for the acute treatment of hereditary angioedema. It works by blocking the enzyme kallikrein, which is involved in bradykinin production. - While effective in acute episodes of hereditary angioedema, it is not a long-term management strategy for ACE inhibitor-induced angioedema, particularly after the acute phase has resolved by removing the offending agent. *Fresh frozen plasma* - **Fresh frozen plasma (FFP)** contains all clotting factors, including C1 esterase inhibitor, and is used in certain severe cases of **hereditary angioedema** as an acute treatment, especially when C1-INH concentrate is unavailable. - FFP is not indicated for long-term management of ACE inhibitor-induced angioedema, as the underlying problem is not a deficiency of C1 esterase inhibitor but rather bradykinin accumulation due to ACE inhibition.

Question 125: A 64-year-old gentleman with hypertension is started on a new diuretic medication by his primary care physician because of poor blood pressure control on his previous regimen. Before starting, he is warned by his physician that the new medication may have side effects including hypokalemia and metabolic alkalosis. Furthermore it may cause alterations in his metabolites such as hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia. What is the mechanism of the class of diuretic most likely being recommended by the physician?

A. Aldosterone receptor inhibitor
B. NKCC inhibitor in loop of Henle
C. NCC inhibitor in distal tubule (Correct Answer)
D. ENaC inhibitor in collecting duct
E. Osmotic diuresis

Explanation: ***NCC inhibitor in distal tubule*** - The side effects described (hypokalemia, metabolic alkalosis, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia) are characteristic of **thiazide diuretics**, which work by inhibiting the **Na-Cl cotransporter (NCC)** in the distal convoluted tubule. - This inhibition leads to increased sodium and water excretion, while also diminishing calcium excretion, contributing to hypercalcemia. *Aldosterone receptor inhibitor* - **Aldosterone antagonists** (e.g., spironolactone, eplerenone) primarily cause **hyperkalemia** and **metabolic acidosis**, which is the opposite of what is described in the clinical scenario. - They also do not typically cause hyperglycemia, hyperlipidemia, or hyperuricemia. *NKCC inhibitor in loop of Henle* - **Loop diuretics** (e.g., furosemide, bumetanide) inhibit the **Na-K-2Cl cotransporter (NKCC)** in the thick ascending limb of the loop of Henle. While they cause hypokalemia and metabolic alkalosis, they generally lead to **hypocalcemia** due to increased calcium excretion, not hypercalcemia. - They are also not typically associated with chronic hyperglycemia or hyperlipidemia to the same extent as thiazides. *ENaC inhibitor in collecting duct* - **ENaC inhibitors**, also known as potassium-sparing diuretics (e.g., amiloride, triamterene), block the epithelial sodium channel in the collecting duct. - Their primary side effect is **hyperkalemia**, which contradicts the described hypokalemia. *Osmotic diuresis* - **Osmotic diuretics** (e.g., mannitol) act by increasing the osmolality of the tubular fluid, leading to reduced water reabsorption. - Their side effect profile is different, often involving fluid and electrolyte imbalances but not typically the specific metabolic alterations mentioned (hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia) in the context of long-term hypertension management.

Question 126: A 68-year-old man presents to the clinic for a regular health checkup. He is hypertensive and was diagnosed with congestive heart failure last year. He has hyperlipidemia but does not take any medication for it. Although he takes his antihypertensive medications regularly, his blood pressure recordings at home tend to range between 150/98 and 160/90 mm Hg. Today, his blood pressure is 147/96 mm Hg. The doctor decides to add indapamide to his medication list and asks the patient to follow up within 2 weeks. The patient is compliant with the medication. He comes back to the physician in just one week complaining of muscle cramping and weakness. Which of the following is the most likely cause of his symptoms?

A. Hypoglycemia
B. Hypokalemia (Correct Answer)
C. Hyperuricemia
D. Hyperlipidemia
E. Hypocalcemia

Explanation: ***Hypokalemia*** - Indapamide is a **thiazide-like diuretic** that can cause **potassium wasting**, leading to hypokalemia. - **Muscle cramping** and **weakness** are classic symptoms of hypokalemia, as potassium is crucial for normal muscle function. *Hypoglycemia* - Hypoglycemia is characterized by symptoms such as **shakiness**, **sweating**, **dizziness**, and **confusion**, which are not reported here. - There is no indication of diabetes or medications that would significantly drop blood glucose in this patient. *Hyperuricemia* - Hyperuricemia can lead to **gout**, presenting with acute, severe joint pain and inflammation, typically in the big toe. - While indapamide can cause hyperuricemia, it generally does not cause muscle cramping and weakness as its primary manifestation. *Hyperlipidemia* - Hyperlipidemia itself is typically **asymptomatic** and only causes symptoms when it leads to complications like atherosclerosis. - This condition does not directly cause acute muscle cramping and weakness. *Hypocalcemia* - Hypocalcemia can cause muscle cramps and spasms (tetany), but it often presents with additional symptoms like **paresthesias**, **Chvostek's sign**, or **Trousseau's sign**. - Indapamide is more likely to cause hypokalemia than hypocalcemia, and direct evidence for a calcium imbalance is not provided.

Question 127: A 58-year-old man presents with a sudden-onset severe headache and vomiting for the past 2 hours. Past medical history is significant for poorly controlled hypertension, managed with multiple medications. His blood pressure is 188/87 mm Hg and pulse is 110/min. A non-contrast CT of the head is unremarkable and cerebrospinal fluid analysis is within normal limits, except for an RBC count of 5.58 x 106/mm3. Labetalol IV is administered. Which of the following medications should also be added to this patient’s management?

A. Nifedipine
B. Ecosprin
C. Nimodipine (Correct Answer)
D. Furosemide
E. Verapamil

Explanation: ***Nimodipine*** - This patient presents with symptoms suggestive of a **subarachnoid hemorrhage (SAH)**, including a sudden severe headache, vomiting, and **xanthochromia** (high RBC count in CSF) despite a normal CT. **Nimodipine** is a calcium channel blocker specifically used in SAH to prevent **cerebral vasospasm**, a common and devastating complication. - Cerebral vasospasm can lead to **delayed cerebral ischemia** and further neurological deficits, and nimodipine has been shown to improve neurological outcomes. *Nifedipine* - **Nifedipine** is a dihydropyridine calcium channel blocker used for hypertension but is not indicated for the prevention of cerebral vasospasm in SAH. - Its use in SAH could potentially lead to systemic hypotension without the specific cerebrovascular benefits of nimodipine, potentially worsening cerebral perfusion. *Ecosprin* - **Ecosprin (aspirin)** is an antiplatelet agent used for thrombosis prevention but is **contraindicated** in acute SAH due to its antiplatelet effect, which could worsen bleeding. - There is no indication for antiplatelet therapy in the immediate management of SAH. *Furosemide* - **Furosemide** is a loop diuretic used to manage fluid overload, hypertension, or cerebral edema. - While hypertension is partially present, furosemide is not directly indicated for the management or prevention of complications of SAH, and its diuretic effect could lead to dehydration, which may exacerbate hypovolemia. *Verapamil* - **Verapamil** is a non-dihydropyridine calcium channel blocker primarily used for arrhythmias and hypertension. - It is not specifically indicated or shown to be effective in preventing cerebral vasospasm after SAH, unlike nimodipine.

Question 128: A 41-year-old African American man presents to his primary care physician a few months after being found to have a blood pressure of 152/95 mmHg. The patient denies any current symptoms, having any past medical history, or prior hospitalizations. He does not take any medications but takes one multivitamin daily. His blood pressures on three separate occasions have been 151/93 mmHg, 150/90 mmHg, and 155/97 mmHg. In today’s visit, his blood pressure is 149/91 mmHg despite exercise and dietary modifications. Physical examination is unremarkable. After extensive work-up he is started on appropriate monotherapy for his hypertension. Which of the following laboratory abnormalities may be found on follow-up testing?

A. Hyperkalemia
B. Hypermagnesemia
C. Hypolipidemia
D. Hypercalcemia (Correct Answer)
E. Hypouricemia

Explanation: **Hypercalcemia** - This African American patient with stage 2 hypertension unresponsive to lifestyle modifications requires pharmacologic therapy. - **First-line options** for African American patients include **thiazide diuretics** or **calcium channel blockers** (per ACC/AHA guidelines). - Given the question asks about hypercalcemia, the appropriate monotherapy is a **thiazide diuretic** (e.g., chlorthalidone, hydrochlorothiazide). - Thiazide diuretics **inhibit calcium excretion** in the distal convoluted tubule, leading to increased calcium reabsorption and potential **hypercalcemia**. - This is a well-known side effect that requires monitoring during thiazide therapy. *Hyperkalemia* - **Thiazide diuretics** cause **hypokalemia** (low potassium), not hyperkalemia, by increasing potassium excretion in the distal tubule. - Hyperkalemia is associated with **potassium-sparing diuretics** (spironolactone, amiloride), **ACE inhibitors**, or **ARBs**. *Hypermagnesemia* - **Thiazide diuretics** increase urinary magnesium excretion, potentially causing **hypomagnesemia**, not hypermagnesemia. - Hypermagnesemia is rare and typically seen with renal failure or excessive magnesium supplementation. *Hypolipidemia* - **Thiazide diuretics** can cause **mild dyslipidemia** (increased LDL cholesterol and triglycerides), not hypolipidemia. - Hypolipidemia (abnormally low lipid levels) is not a recognized side effect of antihypertensive therapy. *Hypouricemia* - **Thiazide diuretics** decrease uric acid secretion in the proximal tubule, leading to **hyperuricemia** and potential gout precipitation. - Hypouricemia would not be expected with thiazide therapy.

Question 129: A 56-year-old Caucasian male presents to the clinic to establish care. He has never seen a physician and denies any known medical problems. Physical examination is notable for central obesity, but the patient has regular heart and lung sounds. He has a blood pressure of 157/95 mm Hg and heart rate of 92/min. He follows up 2 weeks later, and his blood pressure continues to be elevated. At this time, you diagnose him with essential hypertension and decide to initiate antihypertensive therapy. Per the Joint National Committee 8 guidelines for treatment of high blood pressure, of the following combinations of drugs, which can be considered for first-line treatment of high blood pressure in the Caucasian population?

A. ACE inhibitor, ARB, CCB, or thiazide (Correct Answer)
B. ACE inhibitor, angiotensin receptor blocker (ARB), beta-blocker (BB), or thiazide
C. ACE inhibitor, ARB, CCB, or loop diuretic
D. ACE inhibitor, ARB, alpha-blocker, or loop diuretic
E. ACE inhibitor, ARB, alpha-blocker, or direct vasodilator

Explanation: **ACE inhibitor, ARB, CCB, or thiazide** - The **JNC 8 guidelines** recommend **ACE inhibitors**, **ARBs**, **calcium channel blockers (CCBs)**, and **thiazide diuretics** as first-line agents for essential hypertension in the general non-Black population. - These drug classes have demonstrated efficacy in reducing cardiovascular events and are generally well-tolerated. *ACE inhibitor, angiotensin receptor blocker (ARB), beta-blocker (BB), or thiazide* - While **ACE inhibitors**, **ARBs**, and **thiazides** are first-line, **beta-blockers** are generally not considered first-line for uncomplicated hypertension unless there are specific compelling indications (e.g., post-MI, heart failure). - **Beta-blockers** are less effective than other first-line agents in preventing stroke in the elderly and may have more side effects in some populations. *ACE inhibitor, ARB, CCB or loop diuretic* - **ACE inhibitors**, **ARBs**, and **CCBs** are first-line options, but **loop diuretics** are typically reserved for patients with fluid overload or chronic kidney disease, not for initial management of essential hypertension. - **Loop diuretics** have a shorter duration of action and a greater electrolyte-wasting effect compared to thiazide diuretics, making them less suitable for long-term monotherapy. *ACE inhibitor, ARB, alpha-blocker, or loop diuretic* - **Alpha-blockers** and **loop diuretics** are not considered first-line agents for essential hypertension. **Alpha-blockers** are typically used for benign prostatic hyperplasia or as add-on therapy for resistant hypertension. - **Alpha-blockers** can cause significant orthostatic hypotension, particularly with the first dose, and have not shown the same cardiovascular protective benefits as true first-line agents. *ACE inhibitor, ARB, alpha-blocker, or direct vasodilator* - **Alpha-blockers** and **direct vasodilators** (e.g., hydralazine, minoxidil) are not first-line treatments for essential hypertension. - **Direct vasodilators** are potent but often cause reflex tachycardia and fluid retention, requiring co-administration with other agents, and are typically reserved for severe or resistant hypertension.

Question 130: A 53-year old man presents for a well physical examination. He reports his diet is suboptimal, but otherwise reports a healthy lifestyle. He has no past medical history and only takes a multivitamin. He has a blood pressure of 116/74 mm Hg and a pulse of 76/min. On physical examination, he is in no acute distress, has no cardiac murmurs, and his lung sounds are clear to auscultation bilaterally. You order a lipid panel that returns as follows: LDL 203, HDL 37, TG 292. Of the following, which medication should be initiated?

A. Ezetimibe 10 mg daily
B. Colesevelam 3.75 grams daily
C. Atorvastatin 40 mg daily (Correct Answer)
D. Fenofibrate 145 mg daily
E. Simvastatin 10 mg daily

Explanation: ***Atorvastatin 40 mg*** - This patient has a **very high LDL level of 203 mg/dL** and is over 40 years old, placing him in a high-risk group that warrants initiation of a **high-intensity statin** for primary prevention of cardiovascular disease. - **Atorvastatin 40 mg** is a high-intensity statin known to reduce LDL cholesterol by 50% or more, which is appropriate for this patient's elevated risk. *Ezetimibe 10 mg daily* - **Ezetimibe** works by inhibiting cholesterol absorption in the small intestine and is typically used as an add-on therapy for patients who do not achieve their LDL goals with statins alone, or for those who are statin-intolerant. - It is not a first-line monotherapy for a patient with such significantly elevated LDL cholesterol. *Colesevelam 3.75 grams daily* - **Colesevelam** is a bile acid sequestrant that lowers LDL by increasing its fecal excretion; however, it has a more modest LDL-lowering effect compared to statins and can sometimes increase triglycerides. - It is not the most effective or appropriate first-line agent, especially given the patient's existing elevated triglyceride levels. *Fenofibrate 145 mg daily* - **Fenofibrate** is primarily used to lower **triglycerides** and can mildly raise HDL, but it has minimal effect on LDL cholesterol. - While the patient has elevated triglycerides, his primary and most significant lipid abnormality requiring immediate intervention for cardiovascular risk reduction is his severely elevated LDL. *Simvastatin 10 mg daily* - **Simvastatin 10 mg** is a **low-intensity statin** dose (typical range: 10-20 mg), which is not sufficient for a patient with an LDL of 203 mg/dL and high cardiovascular risk. - Guidelines recommend a **high-intensity statin** like atorvastatin 40-80 mg or rosuvastatin 20-40 mg for such elevated LDL levels.

Question 131: A 65-year-old Caucasian man visits the nephrology outpatient clinic for a follow-up appointment. He was previously diagnosed with stage G3a chronic kidney disease (CKD) and albuminuria stage A2. He follows strict dietary recommendations and takes enalapril. He has a history of benign prostatic hyperplasia which has been complicated by urinary tract obstruction. His vitals are stable, and his blood pressure is within the recommended limits. His most recent laboratory studies are as follows: Serum sodium 140 mEq/L Serum potassium 5.8 mEq/L Serum chloride 102 mEq/L Serum phosphate 4.0 mg/dL Hemoglobin 11.5 mg/dL Albumin excretion rate (AER) 280 mg/day Which of the following is the best strategy in the management of this patient?

A. Observation
B. Addition of furosemide
C. Addition of patiromer (Correct Answer)
D. Addition of sevelamer
E. Removal of enalapril

Explanation: ***Addition of patiromer*** - The patient has **hyperkalemia** (serum potassium 5.8 mEq/L) which is exacerbated by his enalapril use and CKD; **patiromer** is a potassium binder that can effectively lower serum potassium without necessitating discontinuation of essential medications like ACE inhibitors. - Patiromer is a good choice for chronic hyperkalemia in patients with **CKD** who require drugs that can increase potassium, such as **ACE inhibitors**, helping to maintain the benefits of these renoprotective agents. *Observation* - The patient's **serum potassium is elevated at 5.8 mEq/L**, which is a potentially dangerous level requiring intervention, not just observation. - Hyperkalemia can lead to **life-threatening cardiac arrhythmias**, necessitating active management rather than a wait-and-see approach. *Addition of furosemide* - While furosemide can promote potassium excretion, its primary role is fluid removal and relief of congestion, and it may not be sufficient to address significant hyperkalemia in a patient on an **ACE inhibitor** with CKD. - Furosemide would not directly counteract the potassium-retaining effect of **enalapril** as effectively as a potassium binder would, especially in the context of controlled blood pressure and no overt fluid overload. *Addition of sevelamer* - **Sevelamer** is a phosphate binder primarily used to manage **hyperphosphatemia** in CKD patients, which this patient does not have (serum phosphate 4.0 mg/dL is within normal limits). - Its mechanism of action does not involve **potassium binding** or excretion, making it ineffective for the patient's hyperkalemia. *Removal of enalapril* - **Enalapril** is crucial for its **renoprotective effects**, including reducing proteinuria (AER 280 mg/day) and controlling blood pressure in CKD patients. - Discontinuing enalapril would remove these benefits and could worsen kidney disease progression and proteinuria, while there are other strategies (like **patiromer**) to manage the side effect of hyperkalemia.

Question 132: A 63-year-old man with high blood pressure, dyslipidemia, and diabetes presents to the clinic for routine follow-up. He has no current complaints and has been compliant with his chronic medications. His blood pressure is 132/87 mm Hg and his pulse is 75/min and regular. On physical examination, you notice that he has xanthelasmas on both of his eyelids. He currently uses a statin to lower his LDL but has not reached the LDL goal you have set for him. You would like to add an additional medication for LDL control. Of the following, which statement regarding fibrates is true?

A. Fibrates inhibit the rate-limiting step in cholesterol synthesis
B. Fibrates can potentiate the risk of myositis when given with statins (Correct Answer)
C. Fibrates can cause significant skin flushing and pruritus
D. Fibrates can increase the risk of cataracts
E. The primary effect of fibrates is to lower LDL

Explanation: ***Fibrates can potentiate the risk of myositis when given with statins*** - **Fibrates** and **statins** can both independently cause muscle toxicity (myopathy, rhabdomyolysis). - When used concomitantly, especially **gemfibrozil** with statins, there is an **increased risk of muscle adverse events** due to pharmacokinetic interactions that raise statin levels. - This combination requires careful monitoring and is often avoided; **fenofibrate** is preferred over gemfibrozil when combination therapy is needed. *Fibrates inhibit the rate-limiting step in cholesterol synthesis* - This statement describes the mechanism of action of **statins**, which inhibit **HMG-CoA reductase**, the rate-limiting enzyme in cholesterol synthesis. - Fibrates, on the other hand, act primarily by activating **PPAR-alpha receptors**, leading to altered lipid metabolism (increased lipoprotein lipase activity, decreased VLDL synthesis). *Fibrates can cause significant skin flushing and pruritus* - **Niacin (nicotinic acid)** is the lipid-modifying agent most commonly associated with significant **skin flushing and pruritus**, mediated by prostaglandin release. - Fibrates do not cause significant flushing; their side effects include GI disturbances, gallstones, and potential muscle toxicity. *Fibrates can increase the risk of cataracts* - This is **not an established adverse effect** of the fibrate class. - While **clofibrate** (an older, largely discontinued fibrate) showed some association with cataracts in older studies, this is not a recognized risk with modern fibrates like **fenofibrate** and **gemfibrozil**. - Current fibrate therapy does not require routine ophthalmologic monitoring for cataracts. *The primary effect of fibrates is to lower LDL* - The primary effect of **fibrates** is to significantly **lower triglycerides** (by 30-50%) and **increase HDL cholesterol** levels (by 10-20%). - While they can cause a modest decrease in LDL cholesterol (10-15%), this is not their primary or most pronounced lipid-modifying effect. - Fibrates are primarily indicated for **hypertriglyceridemia** and mixed dyslipidemia.

Question 133: A 30-year-old man comes to the physician after receiving a high blood pressure reading of 160/90 mm Hg at an annual employee health check-up. During the past few months, the patient has had occasional headaches and mild abdominal pain, both of which were relieved with ibuprofen. He has also had several episodes of heart palpitations. He has no history of serious illness. His mother and father both have hypertension. He has smoked one pack of cigarettes daily for the past 10 years and drinks one glass of wine daily. He occasionally smokes marijuana. He appears pale. His temperature is 36.8°C (98.2°F), pulse is 103/min, and blood pressure is 164/102 mm Hg. Physical examination shows no abnormalities. Laboratory studies show: Hemoglobin 15.3 g/dL Leukocyte count 7,900/mm3 Platelet count 223,000/mm3 Serum Na+ 138 mEq/L K+ 4.6 mEq/L Cl- 103 mEq/L Urea nitrogen 14 mg/dL Glucose 90 mg/dL Creatinine 0.9 mg/dL Plasma metanephrines 1.2 nmol/L (N < 0.5 nmol/L) Urine toxicology screening is positive for tetrahydrocannabinol (THC). Renal doppler shows no abnormalities. A CT scan of the abdomen shows a mass in the left adrenal gland. Which of the following is the most appropriate next step in management of this patient?

A. Resection of adrenal mass
B. Phenoxybenzamine (Correct Answer)
C. Propranolol
D. Metoprolol
E. MIBG therapy

Explanation: ***Phenoxybenzamine*** - The patient's presentation with **hypertension**, **palpitations**, and significantly elevated **plasma metanephrines** (1.2 nmol/L vs. normal < 0.5 nmol/L), along with an **adrenal mass**, strongly suggests a **pheochromocytoma**. - **Alpha-blockade** with phenoxybenzamine is the crucial first step to control blood pressure and prevent a **hypertensive crisis** during subsequent surgical resection. *Resection of adrenal mass* - While surgical resection is the **definitive treatment** for pheochromocytoma, it should **not be performed before adequate alpha-blockade**. - **Unprepared surgery** can lead to a fatal hypertensive crisis due to uncontrolled catecholamine release during manipulation of the tumor. *Propranolol* - Propranolol is a **non-selective beta-blocker** and should **not be initiated before alpha-blockade** in pheochromocytoma. - Blocking beta-adrenergic receptors can lead to **unopposed alpha-adrenergic vasoconstriction**, potentially worsening hypertension and causing a crisis. *Metoprolol* - Metoprolol is a **selective beta-1 blocker** and, like other beta-blockers, should **not be used before alpha-blockade** in pheochromocytoma. - While it may have fewer peripheral vasoconstrictive effects than non-selective beta-blockers, the risk of unopposed alpha-stimulation remains significant. *MIBG therapy* - **Metaiodobenzylguanidine (MIBG) therapy** is a form of **radiotherapy** used for metastatic or inoperable pheochromocytoma/paraganglioma. - It is **not the initial management** for a resectable adrenal mass in a patient with a newly diagnosed pheochromocytoma.

Question 134: A 44-year-old woman presents with increased thirst and frequent urination that started 6 months ago and have progressively worsened. Recently, she also notes occasional edema of the face. She has no significant past medical history or current medications. The patient is afebrile and the rest of the vital signs include: blood pressure is 120/80 mm Hg, heart rate is 61/min, respiratory rate is 14/min, and temperature is 36.6°C (97.8°F). The BMI is 35.2 kg/m2. On physical exam, there is 2+ pitting edema of the lower extremities and 1+ edema in the face. There is generalized increased deposition of adipose tissue present that is worse in the posterior neck, upper back, and shoulders. There is hyperpigmentation of the axilla and inguinal areas. The laboratory tests show the following findings: Blood Erythrocyte count 4.1 million/mm3 Hgb 12.9 mg/dL Leukocyte count 7,200/mm3 Platelet count 167,000/mm3 Fasting blood glucose 141 mg/dL (7.8 mmol/L) Creatinine 1.23 mg/dL (108.7 µmol/L) Urea nitrogen 19 mg/dL (6.78 mmol/L) Urine dipstick Glucose +++ Protein ++ Bacteria Negative The 24-hour urine protein is 0.36 g. Which of the following medications is the best treatment for this patient’s condition?

A. Metoprolol
B. Insulin
C. Enalapril (Correct Answer)
D. Furosemide
E. Mannitol

Explanation: ***Enalapril*** - This patient presents with signs of **Type 2 Diabetes Mellitus (T2DM)** (BMI 35.2, fasting blood glucose 141 mg/dL, hyperpigmentation of axilla/inguinal areas suggesting **acanthosis nigricans**) and **diabetic nephropathy** (proteinuria 0.36g/24h, progressively worsening edema, elevated creatinine). **ACE inhibitors** like enalapril are first-line for managing proteinuria and slowing the progression of diabetic nephropathy, even in patients with normal blood pressure. - Enalapril helps reduce **glomerular pressure** and **proteinuria**, which is crucial for kidney protection in diabetes. *Metoprolol* - Metoprolol is a **beta-blocker** primarily used for hypertension, angina, and heart failure. - While it can be used in patients with diabetes, it does not directly address the **proteinuria** or provide renal protection in the same way an ACE inhibitor does. *Insulin* - While the patient has elevated fasting blood glucose, indicating **diabetes**, insulin is typically reserved for patients who fail oral hypoglycemic agents or have significantly higher glucose levels, or Type 1 Diabetes. - In this case, the primary concern requiring immediate targeted treatment is the **proteinuria and early diabetic nephropathy**, which insulin won't directly treat. *Furosemide* - Furosemide is a **loop diuretic** used to treat **edema** and fluid overload. - Although the patient has edema, furosemide would only treat the symptom and not the underlying cause of the **diabetic nephropathy** or provide specific renal protection. *Mannitol* - Mannitol is an **osmotic diuretic** primarily used to decrease intracranial pressure or intraocular pressure. - It is not indicated for chronic management of **edema** or **diabetic nephropathy**.

Question 135: A 61-year-old obese man with recently diagnosed hypertension returns to his primary care provider for a follow-up appointment and blood pressure check. He reports feeling well with no changes since starting his new blood pressure medication 1 week ago. His past medical history is noncontributory. Besides his blood pressure medication, he takes atorvastatin and a daily multivitamin. The patient reports a 25-pack-year smoking history and is a social drinker on weekends. Today his physical exam is normal. Vital signs and laboratory results are provided in the table. Laboratory test 2 weeks ago Today Blood pressure 159/87 mm Hg Blood pressure 164/90 mm Hg Heart rate 90/min Heart rate 92/min Sodium 140 mE/L Sodium 142 mE/L Potassium 3.1 mE/L Potassium 4.3 mE/L Chloride 105 mE/L Chloride 103 mE/L Carbon dioxide 23 mE/L Carbon dioxide 22 mE/L BUN 15 mg/dL BUN 22 mg/dL Creatinine 0.80 mg/dL Creatinine 1.8 mg/dL Magnetic resonance angiography (MRA) shows a bilateral narrowing of renal arteries. Which of the following is most likely this patient's new medication that caused his acute renal failure?

A. Clonidine
B. Verapamil
C. Hydralazine
D. Captopril (Correct Answer)
E. Hydrochlorothiazide

Explanation: ***Captopril*** - The patient has **bilateral renal artery stenosis** and develops **acute renal failure** after starting a new blood pressure medication. **ACE inhibitors** (like captopril) and **angiotensin receptor blockers (ARBs)** are nephrotoxic in such patients. - In bilateral renal artery stenosis, the kidneys rely on **angiotensin II** to constrict the efferent arterioles, maintaining **glomerular filtration pressure**. ACE inhibitors block angiotensin II production, leading to a significant drop in glomerular filtration and acute kidney injury. *Clonidine* - Clonidine is an **alpha-2 adrenergic agonist** that lowers blood pressure by reducing sympathetic outflow from the central nervous system. - It is **not directly nephrotoxic** and would not typically cause acute renal failure, especially in the context of renal artery stenosis. *Verapamil* - Verapamil is a **non-dihydropyridine calcium channel blocker** that reduces heart rate and blood pressure. - While it can affect renal hemodynamics, it does not typically cause **acute renal failure** or have a contraindication in bilateral renal artery stenosis like ACE inhibitors. *Hydralazine* - Hydralazine is a **direct arterial vasodilator** that lowers blood pressure. - It is **not associated with acute renal failure** in the setting of renal artery stenosis and would not acutely worsen kidney function. *Hydrochlorothiazide* - Hydrochlorothiazide is a **thiazide diuretic** that lowers blood pressure by increasing sodium and water excretion. - While it can cause **prerenal azotemia** due to volume depletion, it does not directly lead to the severe acute renal failure seen with ACE inhibitors in bilateral renal artery stenosis.

Question 136: A 68-year-old man with hypertension comes to the physician because of fatigue and difficulty initiating urination. He wakes up several times a night to urinate. He does not take any medications. His blood pressure is 166/82 mm Hg. Digital rectal examination shows a firm, non-tender, and uniformly enlarged prostate. Which of the following is the most appropriate pharmacotherapy?

A. Finasteride
B. α-Methyldopa
C. Phenoxybenzamine
D. Terazosin (Correct Answer)
E. Tamsulosin

Explanation: ***Terazosin*** - **Terazosin** is an alpha-1 blocker that relaxes the smooth muscles in the prostate and bladder neck, improving urine flow and relieving symptoms of **benign prostatic hyperplasia (BPH)**. - It also has the added benefit of lowering blood pressure, making it suitable for this patient with both **BPH** and **hypertension**. *Finasteride* - **Finasteride** is a 5-alpha reductase inhibitor that reduces prostate volume by inhibiting the conversion of testosterone to **dihydrotestosterone (DHT)**. - While effective for **BPH**, it takes longer to show benefits (6-12 months) and does not address the patient's **hypertension**. *α-Methyldopa* - **α-Methyldopa** is a centrally acting alpha-2 adrenergic agonist used to treat **hypertension**, particularly in pregnancy. - It does not have a direct effect on prostate smooth muscle and would not alleviate the patient's urinary symptoms. *Phenoxybenzamine* - **Phenoxybenzamine** is a non-selective, irreversible alpha-adrenergic blocker primarily used for **pheochromocytoma** to control blood pressure. - Its non-selective nature and side effect profile make it less suitable for chronic management of **BPH** and **hypertension** compared to selective alpha-1 blockers. *Tamsulosin* - **Tamsulosin** is a selective alpha-1A adrenergic blocker that specifically targets the prostate, rapidly improving **BPH** symptoms with less effect on blood pressure. - While it effectively treats **BPH**, unlike terazosin, it does not offer the additional advantage of lowering the patient's elevated blood pressure.

Question 137: A 65-year-old African-American man comes to the physician for a follow-up examination after presenting with elevated blood pressure readings during his last visit. He has no history of major medical illness and takes no medications. He is 180 cm (5 ft 9 in) tall and weighs 68 kg (150 lb); BMI is 22 kg/m2. His pulse is 80/min and blood pressure is 155/90 mm Hg. Laboratory studies show no abnormalities. Which of the following is the most appropriate initial pharmacotherapy for this patient?

A. Chlorthalidone (Correct Answer)
B. Captopril
C. Metoprolol
D. Valsartan
E. Aliskiren

Explanation: ***Chlorthalidone*** - **Thiazide diuretics** (like chlorthalidone) are recommended as **first-line agents** for hypertension in most patients, and particularly for African-American patients, due to their superior efficacy and cardiovascular outcome benefits. - This patient has uncomplicated hypertension, normal BMI, and no comorbidities, making a thiazide diuretic an appropriate initial choice. *Captopril* - **ACE inhibitors** (like captopril) are first-line agents but are generally less effective as monotherapy in African-American patients compared to thiazide diuretics or calcium channel blockers. - While useful in conditions like diabetes or chronic kidney disease, which this patient does not have, its use as an initial standalone therapy in this demographic is not preferred. *Metoprolol* - **Beta-blockers** (like metoprolol) are not recommended as first-line therapy for uncomplicated hypertension unless there are specific compelling indications (e.g., angina, post-myocardial infarction). - Their efficacy in preventing cardiovascular events as monotherapy in uncomplicated hypertension is generally inferior to other first-line agents. *Valsartan* - **ARBs** (like valsartan) are similar to ACE inhibitors in their efficacy and are generally less effective as monotherapy in African-American patients without compelling indications. - They are often chosen for patients who cannot tolerate ACE inhibitors due to cough, but this patient has no such indications. *Aliskiren* - **Direct renin inhibitors** (like aliskiren) are not considered first-line therapy for hypertension and are generally reserved for specific cases or when other first-line agents are not sufficient or contraindicated. - They have not demonstrated superior outcomes compared to other established antihypertensive agents that would warrant their initial use.

Question 138: An 11-year-old boy presents to his pediatrician with muscle cramps and fatigue that have progressively worsened over the past year. His mom says that he has always had occasional symptoms including abdominal pain, muscle weakness, and mild paresthesias; however, since starting middle school these symptoms have started interfering with his daily activities. In addition, the boy complains that he has been needing to use the restroom a lot, which is annoying since he has to ask for permission to leave class every time. Labs are obtained showing hypokalemia, hypochloremia, metabolic alkalosis, hypomagnesemia, and hypocalciuria. The most likely cause of this patient's symptoms involves a protein that binds which of the following drugs?

A. Furosemide
B. Mannitol
C. Spironolactone
D. Amiloride
E. Hydrochlorothiazide (Correct Answer)

Explanation: ***Hydrochlorothiazide*** - This patient's symptoms (muscle cramps, fatigue, polyuria, abdominal pain, muscle weakness) along with lab findings (hypokalemia, hypochloremia, metabolic alkalosis, hypomagnesemia, hypocalciuria) are classic for **Gitelman syndrome**. - Gitelman syndrome is caused by a defect in the **thiazide-sensitive NaCl co-transporter (NCC)** in the distal convoluted tubule, which is the target of **thiazide diuretics** like hydrochlorothiazide. *Furosemide* - Furosemide is a **loop diuretic** that acts on the **Na-K-2Cl co-transporter (NKCC2)** in the thick ascending limb of the loop of Henle. - While loop diuretics can cause similar electrolyte imbalances, Gitelman syndrome presents with **hypocalciuria**, whereas loop diuretics typically cause **hypercalciuria**. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that acts as an **aldosterone antagonist** in the collecting duct. - It would typically lead to hyperkalemia, not the hypokalemia seen in this patient. *Amiloride* - Amiloride is a **potassium-sparing diuretic** that inhibits the **epithelial sodium channel (ENaC)** in the collecting duct. - Like spironolactone, it is associated with **hyperkalemia**, which contradicts the patient's presentation of hypokalemia. *Mannitol* - Mannitol is an **osmotic diuretic** that works in the renal tubule, particularly the proximal tubule and descending limb of the loop of Henle, where it is not reabsorbed. - It primarily increases urinary output to reduce intracranial or intraocular pressure and does not typically cause the specific electrolyte abnormalities seen in Gitelman syndrome.

Question 139: A 66-year-old woman presents to the emergency department with lower extremity pain. She reports that she has had worsening pain in her left calf over the past year while walking. The pain improves with rest, but the patient notes that she now has to stop walking more frequently than in the past to relieve the pain. The patient’s past medical history is otherwise notable for hypertension and coronary artery disease. Her home medications include hydrochlorothiazide and lisinopril. Her family history is significant for diabetes mellitus in her father. On physical exam, her left lower extremity is slightly cool to the touch with palpable distal pulses. The skin of the left lower extremity appears smooth and shiny below the mid-calf. Laboratory testing is performed and reveals the following: Serum: High-density lipoprotein (HDL): 60 mg/dL Low-density lipoprotein (LDL): 96 mg/dL Triglycerides: 140 mg/dL This patient should be started on which of the following medication regimens?

A. Aspirin and cilostazol
B. Aspirin only
C. Aspirin and atorvastatin (Correct Answer)
D. Atorvastatin and cilostazol
E. Atorvastatin only

Explanation: ***Aspirin and atorvastatin*** - The patient presents with classic symptoms and signs of **peripheral artery disease (PAD)**, including **intermittent claudication** (pain with walking, relieved by rest), **cool extremity**, and **trophic skin changes** (smooth, shiny skin). - Both **aspirin** (for antiplatelet activity to reduce thrombotic events) and a **statin** like atorvastatin (for lipid lowering and plaque stabilization) are crucial for managing PAD and reducing cardiovascular risk due to her history of hypertension and coronary artery disease. *Aspirin and cilostazol* - **Aspirin** is appropriate for its antiplatelet effects, but **cilostazol** is primarily used to improve claudication symptoms and does not address the underlying lipid abnormalities or the need for cardiovascular risk reduction as comprehensively as a statin. - While cilostazol can alleviate symptoms, it's not a first-line agent for overall cardiovascular risk reduction in PAD when dyslipidemia is also a concern. *Aspirin only* - **Aspirin** is essential for secondary prevention of cardiovascular events in PAD, but it does not address the patient's **lipid profile** which, while within "normal" limits by some metrics, warrants statin therapy given her high-risk cardiovascular history (hypertension, CAD, PAD). - Optimal management of PAD involves both antiplatelet therapy and intensive lipid lowering. *Atorvastatin and cilostazol* - **Atorvastatin** is appropriate for lipid lowering and cardiovascular risk reduction in PAD. However, omitting **aspirin** means missing a crucial component of antiplatelet therapy for PAD, which significantly reduces the risk of serious thrombotic events. - **Cilostazol** helps with symptoms but does not replace aspirin's role in preventing cardiovascular morbidity and mortality. *Atorvastatin only* - **Atorvastatin** is vital for its pleiotropic effects, including plaque stabilization and lipid lowering, in a patient with PAD and other cardiovascular risk factors. - However, managing PAD optimally requires concurrent **antiplatelet therapy** (e.g., aspirin) to reduce the risk of thrombotic events, which is not included in this regimen.

Question 140: A 53-year-old man seeks evaluation from his physician with concerns about his blood pressure. He was recently told at a local health fair that he has high blood pressure. He has not seen a physician since leaving college because he never felt the need for medical attention. Although he feels fine, he is concerned because his father had hypertension and died due to a heart attack at 61 years of age. He does not smoke cigarettes but drinks alcohol occasionally. The blood pressure is 150/90 mm Hg today. The physical examination is unremarkable. Labs are ordered and he is asked to monitor his blood pressure at home before the follow-up visit. Two weeks later, the blood pressure is 140/90 mm Hg. The blood pressure measurements at home ranged from 130/90 to 155/95 mm Hg. An electrocardiogram (ECG) is normal. Lab tests show the following: Serum glucose (fasting) 88 mg/dL Serum electrolytes: Sodium 142 mEq/L Potassium 3.9 mEq/L Chloride 101 mEq/L Serum creatinine 0.8 mg/dL Blood urea nitrogen 10 mg/dL Cholesterol, total 250 mg/dL HDL-cholesterol 35 mg/dL LDL-cholesterol 186 mg/dL Triglycerides 250 mg/dL Urinalysis: Glucose negative Ketones negative Leucocytes negative Nitrite negative RBC negative Casts negative Regular exercise and a 'heart healthy diet' are advised. He is started on lisinopril for hypertension. Which of the following medications should be added to this patient?

A. Atorvastatin (Correct Answer)
B. Cholestyramine
C. Niacin
D. Orlistat
E. Gemfibrozil

Explanation: ***Atorvastatin*** - The patient has significantly **elevated LDL-cholesterol (186 mg/dL)** and **total cholesterol (250 mg/dL)**, alongside a family history of premature cardiovascular disease and established hypertension, placing him at high risk for atherosclerotic cardiovascular disease (ASCVD). - **Statins (HMG-CoA reductase inhibitors)** are the first-line therapy for managing dyslipidemia in patients with high ASCVD risk, effectively lowering LDL-cholesterol and reducing cardiovascular events. *Cholestyramine* - This is a **bile acid sequestrant** that works by binding bile acids in the intestine, preventing their reabsorption. - While it lowers LDL-cholesterol, **bile acid sequestrants** are generally considered second-line agents for dyslipidemia due to potential gastrointestinal side effects and often less potent LDL reduction compared to statins. *Niacin* - Niacin primarily raises **HDL-cholesterol** and can lower triglycerides, but its role in reducing ASCVD events has been less convincing in recent trials. - It is also associated with significant side effects like **flushing and hepatotoxicity**, making it a less preferred option for initial management of LDL-cholesterol. *Orlistat* - Orlistat is a **pancreatic lipase inhibitor** used for **weight management** by reducing dietary fat absorption. - It is not indicated as a primary medication for managing dyslipidemia or hypertension directly, though weight loss can indirectly improve these conditions. *Gemfibrozil* - Gemfibrozil is a **fibrate** primarily used to **lower elevated triglycerides** and modestly increase HDL-cholesterol. - While the patient has elevated triglycerides (250 mg/dL), his primary lipid abnormality and highest ASCVD risk factor is the significantly elevated LDL-cholesterol, for which statins are more effective and first-line.

Question 141: A 55-year-old man presents to his primary care provider with increased urinary frequency. Over the past 3 months, he has been urinating 2-3 times more often than usual. He has started to feel dehydrated and has increased his water intake to compensate. He works as a bank teller. He has a 25-pack-year smoking history and drinks 8-10 beers per week. His temperature is 98°F (36.8°C), blood pressure is 114/68 mmHg, pulse is 100/min, and respirations are 18/min. Capillary refill is 3 seconds. His mucous membranes appear dry. The patient is instructed to hold all water intake. Urine specific gravity is 1.002 after 12 hours of water deprivation. The patient is given desmopressin but his urine specific gravity remains relatively unchanged. Which of the following is the most appropriate pharmacologic treatment for this patient's condition?

A. Desmopressin
B. Furosemide
C. Metolazone (Correct Answer)
D. Spironolactone
E. Mannitol

Explanation: ***Metolazone*** - The patient's inability to concentrate urine after water deprivation (urine specific gravity 1.002) and lack of response to desmopressin indicate **nephrogenic diabetes insipidus**. - **Thiazide diuretics** like metolazone are effective for nephrogenic diabetes insipidus, as they induce a state of mild volume depletion, increasing proximal tubule reabsorption of sodium and water, thereby reducing the amount of filtrate reaching the collecting ducts. *Desmopressin* - Desmopressin is an antidiuretic hormone (ADH) analog used to treat **central diabetes insipidus**, where the pituitary gland does not produce enough ADH. - The patient's lack of response to desmopressin rules out central diabetes insipidus, indicating an issue with the kidneys' response to ADH. *Furosemide* - Furosemide is a **loop diuretic** that works by inhibiting the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle, leading to significant diuresis. - While it causes increased urine output, it is not the primary treatment for diabetes insipidus and would exacerbate the dehydration in this patient. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that acts as an aldosterone antagonist in the collecting duct. - It is used to treat conditions like hyperaldosteronism, heart failure, and edema, but not diabetes insipidus. *Mannitol* - Mannitol is an **osmotic diuretic** that increases the osmolality of the glomerular filtrate, preventing water reabsorption. - It is primarily used to reduce intracranial or intraocular pressure and would worsen dehydration in a patient with diabetes insipidus.

Question 142: A 62-year-old man comes to the physician for an annual health maintenance examination. He has a history of stable angina, gout, and hypertension. His medications include lisinopril and aspirin. He has smoked a pack of cigarettes daily for 20 years. He drinks 5–6 beers on the weekends. His blood pressure is 150/85 mm Hg. Laboratory studies show a total cholesterol of 276 mg/dL with an elevated low-density lipoprotein (LDL) concentration and low high-density lipoprotein (HDL) concentration. Administration of which of the following agents is the most appropriate next step in management?

A. Peroxisome proliferator-activated receptor alpha activator
B. Cholesterol absorption inhibitor
C. HMG-CoA reductase inhibitor (Correct Answer)
D. Bile acid resin
E. Proprotein convertase subtilisin kexin 9 inhibitor

Explanation: ***HMG-CoA reductase inhibitor*** - This patient has a history of **stable angina**, **hypertension**, and **dyslipidemia** (elevated LDL, low HDL), placing him at high risk for cardiovascular events. **Statins** (HMG-CoA reductase inhibitors) are first-line therapy for reducing LDL cholesterol and cardiovascular risk in such patients. - They work by **inhibiting the rate-limiting step of cholesterol synthesis** in the liver, leading to an upregulation of LDL receptors and increased clearance of LDL from the blood. *Peroxisome proliferator-activated receptor alpha activator* - These agents, like **fibrates**, primarily reduce **triglycerides** and can increase HDL, but they are less effective at lowering LDL compared to statins. - They are typically used for patients with **severe hypertriglyceridemia** or in combination with statins if significant HDL or triglyceride issues persist. *Cholesterol absorption inhibitor* - **Ezetimibe** works by preventing the absorption of cholesterol in the small intestine. - While effective at lowering LDL, it is generally used as an **add-on therapy to statins** or for patients unable to tolerate statins, rather than as a first-line agent in high-risk patients. *Bile acid resin* - **Bile acid sequestrants** (e.g., cholestyramine) work by binding bile acids in the intestine, preventing their reabsorption and increasing their excretion. - This leads to increased hepatic synthesis of bile acids from cholesterol, lowering LDL, but they can cause **gastrointestinal side effects** and are generally less potent and less tolerated than statins. *Proprotein convertase subtilisin kexin 9 inhibitor* - **PCSK9 inhibitors** are highly effective at lowering LDL cholesterol by preventing the degradation of LDL receptors, thereby increasing LDL clearance. - They are typically reserved for patients with **familial hypercholesterolemia** or those with established cardiovascular disease who have not achieved adequate LDL lowering with maximally tolerated statin therapy, often due to their high cost and subcutaneous administration.

Question 143: A 58-year-old chronic smoker known to have chronic bronchitis for the last 20 years presents to his physician for a scheduled follow-up visit. He mentions that over the last month he has been having difficulty breathing, especially after climbing stairs. He also says that he has had similar episodes in the past, which were relieved with the use of inhaled bronchodilators, but recently the breathlessness has ceased to respond to them. He also mentions frequent pain in the right upper quadrant of the abdomen. On physical examination, his temperature is 37°C (98.6°F), the pulse is 96/min, the blood pressure is 124/82 mm Hg, and the respirations are 26/min. Auscultation of the chest reveals wheezing bilaterally and a loud pulmonic component of the second heart sound. Two-dimensional echocardiography shows a dilated right ventricle with increased wall thickness. Right heart catheterization is performed, which indicates a pulmonary artery pressure of 30 mm Hg and a pulmonary capillary wedge pressure of 13 mm Hg. There is a significant drop in pulmonary artery pressure after the administration of inhaled nitric oxide. In addition to continued appropriate management of chronic bronchitis, which of the following medications is most likely to improve symptoms in the patient?

A. Captopril
B. Hydralazine
C. Diltiazem (Correct Answer)
D. Losartan
E. Isosorbide mononitrate

Explanation: ***Diltiazem*** - This patient presents with **pulmonary hypertension** secondary to chronic obstructive pulmonary disease (COPD) along with **vasoreactivity** (indicated by the response to inhaled nitric oxide). - **Calcium channel blockers** like diltiazem are effective in vasoreactive pulmonary hypertension by causing pulmonary vasodilation, reducing pulmonary artery pressure, and improving right ventricular function. *Captopril* - **Angiotensin-converting enzyme (ACE) inhibitors** primarily act as systemic vasodilators and are used in systemic hypertension and heart failure. - They are **not indicated** for the primary treatment of pulmonary hypertension and do not target the underlying pulmonary vascular remodeling or vasoreactivity. *Hydralazine* - **Direct arterial vasodilators** like hydralazine primarily reduce systemic vascular resistance and are used in systemic hypertension. - They are **not typically used** in pulmonary hypertension as their effects on the pulmonary vasculature are less specific and beneficial compared to other agents. *Losartan* - **Angiotensin receptor blockers (ARBs)**, like ACE inhibitors, are primarily used for systemic hypertension and heart failure. - They have **no significant role** in the treatment of pulmonary hypertension, especially in the context of vasoreactivity. *Isosorbide mononitrate* - **Nitrates** are primarily venodilators and are used in coronary artery disease to reduce preload and in some cases of heart failure. - While they can have some pulmonary vasodilatory effect, they are **not the primary treatment** for pulmonary hypertension, particularly in vasoreactive cases, and their benefit is less pronounced compared to calcium channel blockers.

Question 144: A 55-year-old woman presents to the emergency department with chest pain, shortness of breath, and weakness. She has no known past medical history and generally refuses to see a physician for health issues. Review of systems is notable for chronic, severe gastroesophageal reflux disease and chronic diarrhea. Her temperature is 98.3°F (36.8°C), blood pressure is 177/105 mmHg, pulse is 88/min, respirations are 14/min, and oxygen saturation is 97% on room air. Laboratory values are ordered as seen below. Hemoglobin: 10 g/dL Hematocrit: 30% Leukocyte count: 4,500/mm^3 with normal differential Platelet count: 192,400/mm^3 Serum: Na+: 139 mEq/L Cl-: 101 mEq/L K+: 6.3 mEq/L BUN: 65 mg/dL Glucose: 99 mg/dL Creatinine: 3.1 mg/dL Notably, the patient requires nursing to help her with most tasks such as putting on her gown and manipulating a cup of water given poor mobility of her hands. She also has recurrent episodes of severe hand pain, which self resolve. The patient is given calcium, insulin, and dextrose and started on dialysis. Which of the following is the most appropriate medical therapy for this patient?

A. Labetalol
B. Nifedipine
C. Furosemide
D. Hydrochlorothiazide
E. Captopril (Correct Answer)

Explanation: ***Captopril*** * Given the patient's presentation with **scleroderma renal crisis** (hypertension, elevated creatinine, and new-onset anemia), an **ACE inhibitor** like captopril is the **first-line treatment** for blood pressure control and prevention of further renal damage. * **ACE inhibitors** are crucial for managing the severe hypertension and are the only class of antihypertensive agents shown to improve outcomes in scleroderma renal crisis. *Labetalol* * While labetalol can adequately control blood pressure, it is a **beta-blocker**, which is not the preferred first-line treatment for scleroderma renal crisis. * Beta-blockers may also **worsen Raynaud's phenomenon**, which can be associated with scleroderma. *Nifedipine* * Nifedipine, a **calcium channel blocker**, can lower blood pressure but is not the first-line agent for scleroderma renal crisis. * While effective for **Raynaud's phenomenon**, it does not provide the specific renal protection offered by ACE inhibitors in this context. *Furosemide* * Furosemide is a **loop diuretic** primarily used for fluid overload and is not indicated as a primary antihypertensive agent in this scenario, especially given the patient's **acute kidney injury**. * Diuretics may exacerbate **hypovolemia**, which can worsen renal perfusion in patients with renal crisis. *Hydrochlorothiazide* * Hydrochlorothiazide is a **thiazide diuretic** primarily used for uncomplicated hypertension and fluid retention. * It is **ineffective** in patients with a **creatinine clearance below 30 mL/min**, which this patient likely has given a creatinine of 3.1 mg/dL.

Question 145: A 71-year-old African American man diagnosed with high blood pressure presents to the outpatient clinic. In the clinic, his blood pressure is 161/88 mm Hg with a pulse of 88/min. He has had similar blood pressure measurements in the past, and you initiate captopril. He presents back shortly after initiation with extremely swollen lips, tongue, and face. After captopril is discontinued, what is the most appropriate step for the management of his high blood pressure?

A. Initiate a beta-blocker
B. Switch to ramipril
C. Initiate a thiazide diuretic (Correct Answer)
D. Reinitiate captopril
E. Initiate an ARB

Explanation: ***Initiate a thiazide diuretic*** - The patient experienced **angioedema** after taking **captopril**, which is an **ACE inhibitor**. This is a life-threatening adverse effect, and it indicates that all **ACE inhibitors** should be avoided in the future. - Due to the risk of angioedema, a different class of antihypertensive should be used. Given his African American ethnicity, a **thiazide diuretic** or **calcium channel blocker** would be an appropriate initial choice for monotherapy if hypertension is stage 1, or combination therapy if stage 2 hypertension, otherwise, a second agent, such as a **calcium channel blocker**, can be added. *Initiate a beta-blocker* - While beta-blockers are a class of antihypertensive drugs, they are generally not preferred as **first-line monotherapy** for **hypertension**, especially in older African American patients, unless there are specific comorbidities like heart failure or coronary artery disease. - The most appropriate first-line choice after **ACE inhibitor-induced angioedema** would be a thiazide diuretic or calcium channel blocker, as per ACC/AHA guidelines for primary hypertension. *Switch to ramipril* - **Ramipril** is also an **ACE inhibitor**, and the patient experienced **angioedema** with **captopril** (another ACE inhibitor). - Cross-reactivity and recurrence of angioedema are high with other ACE inhibitors, making this choice extremely dangerous and contraindicated. *Reinitiate captopril* - The patient developed **angioedema**, a severe and potentially fatal hypersensitivity reaction, to **captopril**. - Reinitiating the same drug could lead to recurrent, and potentially more severe, angioedema and is therefore absolutely contraindicated. *Initiate an ARB* - **Angiotensin receptor blockers (ARBs)**, while a different class from ACE inhibitors, act on the renin-angiotensin system and carry a **small but significant risk of cross-reactivity** leading to angioedema, especially in patients who have experienced it with an ACE inhibitor. - Given the life-threatening nature of angioedema, it is generally recommended to avoid ARBs if a patient has a history of ACE inhibitor-induced angioedema.

Question 146: A 50-year-old woman presents with a severe headache and vomiting. She says that symptoms onset after attending a wine tasting at the local winery. She says that her headache is mostly at the back of her head and that she has been nauseous and vomited twice. Past medical history is significant for depression diagnosed 20 years ago but now well-controlled with medication. She also has significant vitamin D deficiency. Current medications are phenelzine and a vitamin D supplement. The patient denies any smoking history, alcohol or recreational drug use. On physical examination, the patient is diaphoretic. Her pupils are dilated. Which of the following is most likely to be elevated in this patient?

A. Blood pressure (Correct Answer)
B. Temperature
C. Creatine phosphokinase
D. Aspartate aminotransferase
E. Serum creatinine

Explanation: ***Blood pressure*** - The patient is taking **phenelzine**, a **monoamine oxidase inhibitor (MAOI)**. Consuming **tyramine-rich foods**, such as **wine** and fermented products, while on an MAOI can trigger a **hypertensive crisis**. - Symptoms like severe headache (especially occipital), vomiting, diaphoresis, and dilated pupils are consistent with a **hypertensive crisis** induced by a **tyramine reaction**. *Temperature* - While fever can accompany a hypertensive crisis, it is not the most direct or consistently elevated vital sign in this specific scenario, which primarily describes symptoms related to **vasoconstriction** and **sympathetic overactivity**. - Other conditions like **neuroleptic malignant syndrome** or **serotonin syndrome** are more typically associated with prominent hyperthermia, but the clinical picture here points more strongly to a tyramine reaction. *Creatine phosphokinase* - An elevated **creatine phosphokinase (CPK)** often indicates **muscle damage** or **rhabdomyolysis**. While severe hypertensive crises can sometimes lead to organ damage, CPK elevation is not a primary or immediate expected finding. - This is more commonly elevated in conditions like **malignant hyperthermia**, **rhabdomyolysis**, or **myocardial infarction**, none of which are directly suggested by the initial presentation. *Aspartate aminotransferase* - **Aspartate aminotransferase (AST)** is an enzyme primarily associated with **liver damage**, although it can also be elevated in muscle or cardiac injury. There is no information in the vignette to suggest liver pathology. - While severe organ damage can occur in prolonged or extreme hypertensive crises, **AST elevation** is not an immediate or characteristic feature of an acute **tyramine reaction**. *Serum creatinine* - **Serum creatinine** is a marker of **kidney function**. While kidney injury can occur in severe, prolonged hypertension, it is not an immediate finding expected during the acute onset of a **hypertensive crisis** from a tyramine reaction. - There is no clinical information provided that would directly indicate immediate and significant renal impairment in this acute setting.

Question 147: A 52-year-old man comes to the physician for a routine health maintenance examination. He feels well. His blood pressure is 125/70 mm Hg. His glomerular filtration rate is calculated to be 105 mL/min/1.73 m2 and glucose clearance is calculated to be 103 mL/min. This patient is most likely being treated with which of the following agents?

A. Ifosfamide
B. Acarbose
C. Canagliflozin (Correct Answer)
D. Glipizide
E. Metformin

Explanation: ***Canagliflozin*** - The key finding is that **glucose clearance (103 mL/min) approximately equals GFR (105 mL/min)**, indicating nearly complete failure of glucose reabsorption. - **Canagliflozin** is an **SGLT2 inhibitor** that blocks the sodium-glucose cotransporter 2 in the proximal tubule, preventing glucose reabsorption. - This causes filtered glucose to be excreted in urine, resulting in **glucose clearance approaching GFR** - exactly what is seen in this patient. - SGLT2 inhibitors are increasingly used as first-line agents in Type 2 Diabetes, especially with cardiovascular or renal benefits. *Metformin* - **Metformin** is a biguanide that decreases hepatic gluconeogenesis and increases peripheral insulin sensitivity. - It does **NOT affect renal glucose handling** or glucose clearance, which would remain near zero in patients on metformin. - The elevated glucose clearance in this patient rules out metformin monotherapy. *Ifosfamide* - **Ifosfamide** is an alkylating chemotherapy agent used for cancer treatment, not diabetes management. - It can cause **Fanconi syndrome** (proximal tubule dysfunction) leading to glycosuria, but this would also cause decreased GFR, proteinuria, and electrolyte abnormalities. - This patient's normal GFR and otherwise normal presentation makes ifosfamide-induced toxicity unlikely. *Acarbose* - **Acarbose** is an alpha-glucosidase inhibitor that slows carbohydrate absorption in the intestine. - It works in the **GI tract**, not the kidneys, and does not affect glucose clearance. - It would not explain the elevated renal glucose excretion seen here. *Glipizide* - **Glipizide** is a sulfonylurea that stimulates pancreatic insulin release. - It does **NOT affect renal glucose handling** and would not cause elevated glucose clearance. - The patient's glucose clearance pattern is inconsistent with sulfonylurea therapy.

Question 148: A 57-year-old man comes to the physician because of sudden-onset fever, malaise, and pain and swelling of his wrists and ankles that began a week ago. One month ago, he was started on hydralazine for adjunctive treatment of hypertension. His temperature is 37.8°C (100°F). Examination shows swelling, tenderness, warmth, and erythema of both wrists and ankles; range of motion is limited. Further evaluation is most likely to show an increased level of which of the following autoantibodies?

A. Anti-Jo-1
B. Anti-dsDNA
C. Anti-β2-glycoprotein
D. Anti-histone (Correct Answer)
E. Anti-Smith

Explanation: ***Anti-histone*** - The patient's presentation with **fever, malaise, polyarthritis**, and recent initiation of **hydralazine** strongly suggests **drug-induced lupus erythematosus (DILE)**. - **Anti-histone antibodies** are the most common and characteristic autoantibody found in over 95% of cases of DILE. *Anti-Jo-1* - **Anti-Jo-1 antibodies** are positive in a subset of patients with **polymyositis** and **dermatomyositis**, often associated with interstitial lung disease and "mechanic's hands." - These conditions typically involve **proximal muscle weakness** rather than predominantly joint pain and swelling as seen here. *Anti-dsDNA* - **Anti-dsDNA antibodies** are highly specific for **systemic lupus erythematosus (SLE)**, but are rarely positive in drug-induced lupus erythematosus (DILE). - While DILE shares some features with SLE, the presence of these antibodies would favor a diagnosis of idiopathic SLE. *Anti-β2-glycoprotein* - **Anti-β2-glycoprotein antibodies** are associated with **antiphospholipid syndrome (APS)**, which presents with arterial or venous thrombosis and recurrent pregnancy loss. - The patient's symptoms are primarily inflammatory arthritis, not thrombotic events. *Anti-Smith* - **Anti-Smith antibodies** are highly specific for **systemic lupus erythematosus (SLE)** and are rarely positive in drug-induced lupus erythematosus (DILE). - Although highly specific for SLE, they are present in a minority of SLE patients (20-30%) and are not characteristic of DILE.

Question 149: A simple experiment is performed to measure the breakdown of sucrose into glucose and fructose by a gut enzyme that catalyzes this reaction. A glucose meter is used to follow the breakdown of sucrose into glucose. When no enzyme is added to the sucrose solution, the glucose meter will have a reading of 0 mg/dL; but when the enzyme is added, the glucose meter will start to show readings indicative of glucose being formed. Which of the following diabetic pharmacological agents, when added before the addition of the gut enzyme to the sucrose solution, will maintain a reading of 0 mg/dL?

A. Metformin
B. Acarbose (Correct Answer)
C. Exenatide
D. Glyburide
E. Insulin

Explanation: ***Acarbose*** - **Acarbose** is an **alpha-glucosidase inhibitor** that reduces the digestion and absorption of carbohydrates like sucrose in the small intestine. - By inhibiting the enzyme that breaks down sucrose into glucose and fructose, it would prevent the formation of glucose, thus maintaining a reading of **0 mg/dL** in the experiment. *Metformin* - **Metformin** primarily acts by decreasing **hepatic glucose production** and increasing **insulin sensitivity** in peripheral tissues. - It does not directly inhibit enzymes involved in the breakdown of dietary carbohydrates like sucrose in the gut. *Exenatide* - **Exenatide** is a **glucagon-like peptide-1 (GLP-1) receptor agonist** that enhances glucose-dependent insulin secretion, suppresses glucagon secretion, and slows gastric emptying. - Its mechanism of action does not involve direct inhibition of carbohydrate-digesting enzymes in the gut. *Glyburide* - **Glyburide** is a **sulfonylurea** that stimulates **insulin release** from pancreatic beta cells by binding to and closing ATP-sensitive potassium channels. - It does not interfere with the enzymatic breakdown of sucrose into glucose in the isolated gut enzyme system. *Insulin* - **Insulin** is a hormone that facilitates the uptake of glucose by cells and promotes its storage, thereby lowering blood glucose levels. - It has no direct inhibitory effect on the enzyme that breaks down sucrose into glucose in the gut lumen.

Question 150: A patient presents with periods of severe headaches and flushing however every time they have come to the physician they have not experienced any symptoms. The only abnormal finding is a blood pressure of 175 mmHg/100 mmHg. It is determined that the optimal treatment for this patient is surgical. Prior to surgery which of the following noncompetitive inhibitors should be administered?

A. Phentolamine
B. Isoproterenol
C. Atropine
D. Propranolol
E. Phenoxybenzamine (Correct Answer)

Explanation: ***Phenoxybenzamine*** - This patient likely has a **pheochromocytoma**, which explains the episodic headaches, flushing, and hypertension. **Phenoxybenzamine** is a **non-competitive, irreversible alpha-adrenergic blocker** that is crucial for preoperative preparation to prevent a **hypertensive crisis** during surgery. - Its **irreversible binding** provides sustained alpha blockade, essential to control blood pressure and avoid catecholamine-induced surges during tumor manipulation. *Phentolamine* - **Phentolamine** is a **competitive alpha-adrenergic blocker** used to manage acute hypertensive episodes, but it has a shorter duration of action. - It is not preferred for sustained preoperative alpha blockade due to its **reversible nature** and potential for drug washout during surgery, which could lead to catecholamine surges. *Isoproterenol* - **Isoproterenol** is a **beta-adrenergic agonist** that increases heart rate and contractility, and causes bronchodilation. - It would be contraindicated in a patient with pheochromocytoma as it could worsen hypertension and cardiac symptoms by stimulating beta receptors that are already overly sensitive to endogenous catecholamines. *Atropine* - **Atropine** is a **muscarinic acetylcholine receptor antagonist** that blocks parasympathetic effects, like bradycardia and salivation. - It has no role in managing hypertension or the catecholamine excess seen in pheochromocytoma. *Propranolol* - **Propranolol** is a **non-selective beta-adrenergic blocker** that can be used to control tachycardia and arrhythmias in pheochromocytoma, but only *after* adequate alpha-blockade has been established. - Using **propranolol alone** or before alpha-blockade can lead to **unopposed alpha-adrenergic stimulation**, resulting in a severe, life-threatening hypertensive crisis.

Question 151: A physician is choosing whether to prescribe losartan or lisinopril to treat hypertension in a 56-year-old male. Relative to losartan, one would expect treatment with lisinopril to produce which of the following changes in the circulating levels of these peptides?

A. Aldosterone increase; bradykinin decrease
B. Angiotensin II increase; bradykinin decrease
C. Renin decrease; angiotensin I increase
D. Bradykinin increase; angiotensin II decrease (Correct Answer)
E. Renin decrease; angiotensin II increase

Explanation: ***Bradykinin increase; angiotensin II decrease*** - **Lisinopril** is an **ACE inhibitor**, which directly blocks the conversion of **angiotensin I** to **angiotensin II**, leading to a decrease in circulating **angiotensin II** levels. - ACE is also responsible for the breakdown of **bradykinin**, so inhibiting ACE with lisinopril will lead to an **increase in bradykinin** levels, contributing to vasodilation but also the characteristic cough. *Aldosterone increase; bradykinin decrease* - **Lisinopril** (an ACE inhibitor) decreases **angiotensin II**, which in turn leads to a **decrease in aldosterone** synthesis and release, not an increase. - **Bradykinin** levels would increase due to ACE inhibition, as ACE is involved in its degradation. *Angiotensin II increase; bradykinin decrease* - **Lisinopril** directly inhibits the enzyme responsible for producing **angiotensin II**, thus leading to its **decrease**, not an increase. - **Bradykinin** levels would increase because its degradation pathway (via ACE) is blocked, not decrease. *Renin decrease; angiotensin I increase* - **Lisinopril** reduces the negative feedback on **renin** release, leading to an **increase in renin** levels, not a decrease. - While ACE is inhibited by lisinopril, this leads to an accumulation of its substrate, **angiotensin I**, resulting in an increase of angiotensin I. *Renin decrease; angiotensin II increase* - As an ACE inhibitor, lisinopril would lead to an **increase in renin** due to reduced negative feedback from angiotensin II, not a decrease. - **Angiotensin II** levels would **decrease** because its production from angiotensin I is directly inhibited by lisinopril.

Question 152: A 60-year-old woman sought evaluation at an urgent care clinic after developing breathlessness 30 minutes earlier. She also developed swelling of the tongue and lips. She has heart failure and was recently diagnosed with hypertension. She was started on a medication, the first dose of which she took this afternoon before her symptoms started. Her blood pressure is 167/88 mm Hg, the respiratory rate is 17/min, and the pulse is 78/min. The physical examination reveals a skin rash on the back and abdomen. There is a mild swelling of the lips and tongue. Chest auscultation does not reveal any abnormal breath sounds. Which of the following medications most likely led to her current symptoms?

A. Hydrochlorothiazide (HCTZ)
B. Captopril (Correct Answer)
C. Amlodipine
D. Clonidine
E. Propranolol

Explanation: ***Captopril*** - The symptoms of **angioedema**, including tongue and lip swelling, and breathlessness, are classic adverse effects of **ACE inhibitors** like captopril. - Angioedema can occur even after the **first dose** and is more common in patients treated for hypertension and heart failure. *Hydrochlorothiazide (HCTZ)* - While HCTZ can cause allergic reactions, severe angioedema with acute breathlessness and tongue/lip swelling as the primary presentation is **rare** with this drug. - Common side effects include electrolyte imbalances, **orthostatic hypotension**, and photosensitivity, none of which are described as the main acute issue here. *Amlodipine* - Amlodipine, a **calcium channel blocker**, does not typically cause angioedema or acute breathlessness and lip/tongue swelling. - Its common side effects include **peripheral edema**, headache, and flushing. *Clonidine* - Clonidine is an **alpha-2 adrenergic agonist** used for hypertension. It primarily causes central nervous system depression, such as **sedation** and **dry mouth**. - It does not cause angioedema, tongue/lip swelling, or acute breathlessness. *Propranolol* - Propranolol is a **non-selective beta-blocker** and can cause **bronchospasm** in susceptible individuals, leading to breathlessness. - However, it does not typically cause angioedema with lip and tongue swelling.

Question 153: A 45-year-old man was shown to have a blood pressure of 142/90 mm Hg at a health fair. Despite modifying his lifestyle, his blood pressure remained elevated on 2 separate subsequent occasions. He was prescribed an anti-hypertensive medication. After 3 weeks, the swelling of the lips shown in the accompanying photograph was observed. What is the most likely cause of this finding?

A. Hydrochlorothiazide
B. Lisinopril (Correct Answer)
C. Amlodipine
D. Verapamil
E. Furosemide

Explanation: ***Lisinopril*** - The patient developed **angioedema**, a known side effect of **ACE inhibitors** like lisinopril, which presents as swelling of the lips, face, and sometimes airways. - ACE inhibitors block the degradation of **bradykinin**, leading to its accumulation and subsequent vasodilation and increased vascular permeability. *Hydrochlorothiazide* - This is a **thiazide diuretic** commonly used for hypertension. - While it can cause various side effects (e.g., electrolyte imbalances, photosensitivity), **angioedema** is not a characteristic or common adverse effect. *Amlodipine* - Amlodipine is a **calcium channel blocker**. - Common side effects include peripheral edema (swelling of ankles/feet), headache, and flushing, but not typically **angioedema of the lips**. *Verapamil* - Verapamil is a **non-dihydropyridine calcium channel blocker**. - Side effects include constipation, bradycardia, and AV block; **angioedema is not a known adverse reaction**. *Furosemide* - Furosemide is a **loop diuretic**. - Its main side effects include electrolyte disturbances, dehydration, and ototoxicity; there is **no association with angioedema**.

Question 154: A 62-year-old man comes to the physician for a follow-up examination. One month ago, therapy with lisinopril was initiated for treatment of hypertension. His blood pressure is 136/86 mm Hg. Urinalysis shows a creatinine clearance of 92 mL/min. The patient's serum creatinine concentration is most likely closest to which of the following values?

A. 1.7 mg/dL
B. 1.1 mg/dL (Correct Answer)
C. 2.0 mg/dL
D. 1.4 mg/dL
E. 2.3 mg/dL

Explanation: ***1.1 mg/dL*** - For a 62-year-old man with a **creatinine clearance of 92 mL/min**, the serum creatinine can be estimated using the **Cockcroft-Gault relationship**. - With CrCl of 92 mL/min (near-normal for age), the baseline serum creatinine would be approximately **0.9-1.0 mg/dL** for a typical male patient. - **Lisinopril (ACE inhibitor)** commonly causes a **mild increase in serum creatinine (10-20%)** due to reduced efferent arteriolar tone, which is acceptable if <30% increase and creatinine clearance remains adequate. - Therefore, **1.1 mg/dL** represents the expected value: baseline creatinine consistent with CrCl of 92 mL/min plus the typical mild ACE inhibitor-induced elevation. *1.4 mg/dL* - A serum creatinine of **1.4 mg/dL** would be inconsistent with a creatinine clearance of **92 mL/min** in this patient. - Using the Cockcroft-Gault formula for a 62-year-old male, a creatinine of 1.4 mg/dL would correspond to a **CrCl of approximately 65-70 mL/min**, not 92 mL/min. - This would represent a more significant decrease in GFR than is present in this patient. *1.7 mg/dL* - A serum creatinine of **1.7 mg/dL** is far too high for a creatinine clearance of **92 mL/min**. - This level would correspond to a **CrCl of approximately 50-55 mL/min** in a 62-year-old male, indicating **moderate renal impairment**. - Such an elevation with ACE inhibitors would warrant investigation for **bilateral renal artery stenosis** or other significant renal pathology. *2.0 mg/dL* - A serum creatinine of **2.0 mg/dL** would indicate **significant renal dysfunction** with an estimated CrCl of approximately **40-45 mL/min**, not the 92 mL/min observed. - This degree of elevation is incompatible with the measured creatinine clearance. - Would suggest **acute kidney injury** or **severe bilateral renal artery stenosis** and require immediate ACE inhibitor discontinuation. *2.3 mg/dL* - A serum creatinine of **2.3 mg/dL** indicates **severe renal impairment** with an estimated CrCl well below 40 mL/min. - This is completely incompatible with the measured **creatinine clearance of 92 mL/min**. - Would represent **acute kidney injury** requiring urgent evaluation and medication adjustment.

Question 155: A 45-year-old woman comes to the physician because of a 2-week history of fatigue and excessive thirst. During this period, she has not been able to sleep through the night because of the frequent urge to urinate. She also urinates more than usual during the day. She drinks 4–5 liters of water and 1–2 beers daily. She has autosomal dominant polycystic kidney disease, hypertension treated with lisinopril, and bipolar disorder. Therapy with valproic acid was begun after a manic episode 3 months ago. Vital signs are within normal limits. Irregular flank masses are palpated bilaterally. The remainder of the examination shows no abnormalities. Laboratory studies show: Serum Na+ 152 mEq/L K+ 4.1 mEq/L Cl− 100 mEq/L HCO3− 25 mEq/L Creatinine 1.8 mg/dL Osmolality 312 mOsmol/kg Glucose 98 mg/dL Urine osmolality 190 mOsmol/kg The urine osmolality does not change after 3 hours despite no fluid intake or after administration of desmopressin. Which of the following is the most appropriate next step in management?

A. Further water restriction
B. Begin infusion of 3% saline
C. Desmopressin therapy
D. Hydrochlorothiazide therapy (Correct Answer)
E. Amiloride therapy

Explanation: ***Hydrochlorothiazide therapy*** - The patient's presentation of polyuria, polydipsia, hypernatremia, and inappropriately low urine osmolality, unresponsive to **desmopressin**, indicates **nephrogenic diabetes insipidus (NDI)**. - **Thiazide diuretics**, such as hydrochlorothiazide, induce mild volume depletion, which stimulates proximal tubular water and solute reabsorption, effectively reducing water delivery to the collecting duct and ameliorating symptoms of NDI. - This is the first-line treatment for NDI regardless of underlying etiology. *Further water restriction* - While the patient exhibits polydipsia, further water restriction would exacerbate her **hypernatremia** and dehydration without addressing the underlying inability to concentrate urine. - This would lead to increased thirst and potentially more severe electrolyte imbalances. *Begin infusion of 3% saline* - The patient already has **hypernatremia (Na+ 152 mEq/L)**; infusing **hypertonic saline** would dangerously worsen this condition and increase serum osmolality. - This intervention is used for severe hyponatremia, not hypernatremia. *Desmopressin therapy* - The diagnostic test showed that the urine osmolality did not change after **desmopressin administration**, indicating a lack of renal response to ADH. - This confirms **nephrogenic diabetes insipidus**, making exogenous ADH (desmopressin) ineffective as a treatment. *Amiloride therapy* - **Amiloride**, a potassium-sparing diuretic, is specifically used to treat **lithium-induced NDI** by blocking ENaC channels and reducing lithium uptake in principal cells. - This patient is on **valproic acid** (not lithium) for bipolar disorder, making amiloride inappropriate. - Her NDI is likely multifactorial, related to her ADPKD with chronic kidney disease (creatinine 1.8 mg/dL) and possibly valproic acid, but **thiazide diuretics remain first-line regardless of etiology**.

Question 156: A 60-year-old man comes to the physician because of flank pain, rash, and blood-tinged urine for 1 day. Two months ago, he was started on hydrochlorothiazide for hypertension. He takes acetaminophen for back pain. Examination shows a generalized, diffuse maculopapular rash. Serum studies show a creatinine concentration of 3.0 mg/dL. Renal ultrasonography shows no abnormalities. Which of the following findings is most likely to be observed in this patient?

A. Dermal IgA deposition on skin biopsy
B. Urinary eosinophils (Correct Answer)
C. Mesangial IgA deposits on renal biopsy
D. Crescent-shape extracapillary cell proliferation
E. Urinary crystals on Brightfield microscopy

Explanation: ***Urinary eosinophils*** - The patient's presentation with **flank pain**, **rash**, **blood-tinged urine**, and **acute kidney injury** after starting hydrochlorothiazide is highly suggestive of **acute interstitial nephritis (AIN)**. - **Urinary eosinophils** are a classic, though not always present, finding in **drug-induced AIN**, indicating an allergic inflammatory response in the kidney. *Dermal IgA deposition on skin biopsy* - **Dermal IgA deposition** is characteristic of **IgA vasculitis (Henoch-Schönlein purpura)**, which typically involves palpable purpura, arthralgias, abdominal pain, and nephritis, but does not usually present as a maculopapular rash directly caused by a drug. - While IgA vasculitis can cause a rash and renal involvement, the temporal relationship with a new medication and the diffuse maculopapular nature of the rash point away from this diagnosis. *Mesangial IgA deposits on renal biopsy* - **Mesangial IgA deposits** are the hallmark of **IgA nephropathy**, which typically presents with recurrent episodes of gross hematuria (often synpharyngitic) or persistent microscopic hematuria and proteinuria, not primarily with an acute, drug-induced rash and flank pain. - While IgA nephropathy can cause renal dysfunction and hematuria, the acute onset and systemic allergic features are not characteristic. *Crescent-shape extracapillary cell proliferation* - **Crescent-shape extracapillary cell proliferation** is characteristic of **rapidly progressive glomerulonephritis (RPGN)**, which causes a rapid decline in renal function often associated with severe hematuria and proteinuria. - While the patient has acute kidney injury and hematuria, the rash and flank pain in the context of new medication are more indicative of AIN than primary glomerulonephritis leading to crescents. *Urinary crystals on Brightfield microscopy* - **Urinary crystals** can be seen in conditions like **kidney stones** or **acute uric acid nephropathy**, which might cause flank pain and hematuria. However, the presence of a rash and the temporal association with hydrochlorothiazide do not align with these conditions. - Furthermore, renal ultrasonography showed no abnormalities, making kidney stones less likely to be the primary cause of symptoms.

Question 157: A 52-year-old man presents to the emergency department with chest pain radiating to his left jaw and arm. He states that he had experienced similar symptoms when playing basketball. The medical history is significant for diabetes mellitus, hypertension, and GERD, for which he takes metformin, hydrochlorothiazide, and pantoprazole, respectively. The blood pressure is 150/90 mm Hg, the pulse is 100/min, and the respirations are 15/min. The ECG reveals ST elevation in leads V3-V6. He is hospitalized for an acute MI and started on treatment including lisinopril. The next day he complains of dizziness and blurred vision. Repeat vital signs were as follows: blood pressure 90/60 mm Hg, pulse 72/min, and respirations 12/min. The laboratory results were as follows: Serum chemistry Sodium 143 mEq/L Potassium 4.1 mEq/L Chloride 98 mEq/L Bicarbonate 22 mEq/L Blood urea nitrogen 26 mg/dL Creatinine 2.3 mg/dL Glucose 120 mg/dL Which of the following drugs is responsible for this patient's lab abnormalities?

A. Lisinopril (Correct Answer)
B. Nitroglycerin
C. Pantoprazole
D. Atorvastatin
E. Digoxin

Explanation: ***Lisinopril*** - The patient's **hypotension** (90/60 mmHg), **dizziness**, **blurred vision**, and elevated **creatinine** (2.3 mg/dL) with elevated **BUN** (26 mg/dL) one day after starting lisinopril strongly suggest **acute kidney injury (AKI)** induced by the ACE inhibitor. - **ACE inhibitors** like lisinopril can cause AKI, especially in patients with pre-existing renal impairment or those with conditions that make them susceptible to reduced renal perfusion, such as **atherosclerotic renovascular disease** (which can be associated with uncontrolled hypertension and diabetes). *Nitroglycerin* - **Nitroglycerin** primarily causes **vasodilation**, which can lead to **hypotension** and **headache** or **dizziness**, but it is not directly associated with a rapid increase in **creatinine** or **BUN** to this extent, indicative of AKI. - While it could contribute to hypotension, it wouldn't explain the acute renal dysfunction observed in this patient. *Pantoprazole* - **Pantoprazole**, a **proton pump inhibitor**, is generally well-tolerated but can rarely cause **acute interstitial nephritis**, which might lead to AKI over a longer period. - However, it would not typically cause such a rapid and significant increase in **BUN** and **creatinine** immediately after an MI and starting other medications, and it's less likely to be the primary cause of acute decompensation compared to an ACE inhibitor in this context. *Atorvastatin* - **Atorvastatin** is a **HMG-CoA reductase inhibitor** used for lipid lowering. Its main side effects include **myopathy** and **liver dysfunction**, neither of which are reflected in the presented symptoms or lab findings. - It does not directly cause **hypotension** or acute **renal dysfunction**. *Digoxin* - **Digoxin** is a **cardiac glycoside** used to treat heart failure and arrhythmias. Its toxicity can cause **nausea**, **vomiting**, **arrhythmias**, and **visual disturbances** (e.g., blurred or yellow vision). - While visual disturbances are present, digoxin is not associated with acute **hypotension** or acute **kidney injury** characterized by elevated **BUN** and **creatinine**.

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Antihypertensives — MCQs

Antihypertensives — MCQs

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