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?
Q22
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?
Q23
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?
Q24
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?
Q25
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?
Q26
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?
Q27
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?
Q28
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?
Q29
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?
Q30
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?
Antihypertensives US Medical PG Practice Questions and MCQs
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**.
