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?
Q52
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?
Q53
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?
Q54
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?
Q55
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?
Q56
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?
Q57
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?
Q58
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?
Q59
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?
Q60
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?
Antihypertensives US Medical PG Practice Questions and MCQs
Question 51: 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 52: 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 53: 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 54: 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 55: 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 56: 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 57: 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 58: 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 59: 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 60: 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.