A 23-year-old primigravid woman at 8 weeks' gestation is brought to the emergency department by her husband because of increasing confusion and high-grade fever over the past 16 hours. Three days ago, she was prescribed metoclopramide by her physician for the treatment of nausea and vomiting. She has a history of depression. Current medications include fluoxetine. She is confused and not oriented to time, place, or person. Her temperature is 39.8°C (103.6°F), pulse is 112/min, and blood pressure is 168/96 mm Hg. Examination shows profuse diaphoresis and flushed skin. Muscle rigidity is present. Her deep tendon reflexes are decreased bilaterally. Mental status examination shows psychomotor agitation. Laboratory studies show:
Hemoglobin 12.2 g/dL
Leukocyte count 17,500/mm3
Serum
Creatinine 1.4 mg/dL
Total bilirubin 0.7 mg/dL
Alkaline phosphatase 45 U/L
AST 122 U/L
ALT 138 U/L
Creatine kinase 1070 U/L
Which of the following drugs is most likely to also cause the condition that is responsible for this patient’s current symptoms?
Q22
Which of the following compounds is most responsible for the maintenance of appropriate coronary blood flow?
Q23
A 55-year-old female with a history of poorly controlled hyperlipidemia and obesity presents to her primary care physician for a follow-up visit. She reports that she feels well and has no complaints. She currently takes atorvastatin. Her temperature is 99°F (37.2°C), blood pressure is 135/80 mmHg, pulse is 80/min, and respirations are 16/min. Her BMI is 31 kg/m2. Her total cholesterol is 290 mg/dl, triglycerides are 120 mg/dl, and LDL cholesterol is 215 mg/dl. Her physician considers starting her on a medication that forces the liver to consume cholesterol to make more bile salts. Which of the following adverse effects is this patient at highest risk of developing following initiation of the medication?
Q24
A 27-year-old woman comes to the physician because of poor sleep for the past 8 months. She has been gradually sleeping less because of difficulty initiating sleep at night. She does not have trouble maintaining sleep. On average, she sleeps 4–5 hours each night. She feels tired throughout the day but does not take naps. She was recently diagnosed with social anxiety disorder and attends weekly psychotherapy sessions. Mental status examination shows an anxious mood. The patient asks for a sleeping aid but does not want to feel drowsy in the morning because she has to drive her daughter to kindergarten. Short-term treatment with which of the following drugs is the most appropriate pharmacotherapy for this patient's symptoms?
Q25
A 24-year-old woman is brought into the emergency department by an ambulance after swallowing a bottle of pain medication in a suicide attempt. According to her parents, she recently had a fight with her boyfriend and was acting very depressed. She claims to not remember what she had taken. Further inquiry reveals she is experiencing nausea and feeling quite dizzy. She also repeatedly asks if anyone else can hear a ringing sound. Her pulse is 105/min, respirations are 24/min, and temperature is 38.2°C (100.8°F). Examination reveals mild abdominal tenderness. The patient is visibly agitated and slightly confused. The following lab values are obtained:
Arterial blood gas analysis
pH 7.35
Po2 100 mm Hg
Pco2 20 mm Hg
HCO3- 12 mEq/L
Which of the following pain medications did this patient most likely take?
Q26
A 55-year-old woman comes to the emergency room 30 minutes after the sudden onset of chest pain radiating to the left shoulder. Prior to the onset of her symptoms, she was lying in bed because of a migraine headache. Episodes of similar chest pain usually resolved after a couple of minutes. She has smoked one pack of cigarettes daily for 20 years. Her only medication is sumatriptan. An ECG shows ST-segment elevations in the anterior leads. Serum troponins are negative on two successive blood draws and ECG shows no abnormalities 30 minutes later. Administration of which of the following is most likely to prevent further episodes of chest pain in this patient?
Q27
A healthy 48-year-old presents for a well-patient visit. He has no symptoms and feels well. Past medical history is significant for asthma, chronic sinusitis, and nasal polyps. He occasionally takes diphenhydramine for allergies. Both of his parents and an elder brother are in good health. Today, his blood pressure is 119/81 mm Hg, heart rate is 101/min, respiratory rate is 21/min, and temperature 37°C (98.6°F). Routine screening blood work reveals elevated total cholesterol. The patient asks if he should take low-dose aspirin to reduce his risk of stroke and heart attack. Of the following, which is the best response?
Q28
An 82-year-old man comes to the physician complaining of frequent urination, especially at night, and difficulty initiating urination. However, he points out that his symptoms have improved slightly since he started terazosin 2 months ago. He has a history of stable angina. Other medications include nitroglycerin, metoprolol, and aspirin. His blood pressure is 125/70 mm Hg and pulse is 72/min. On examination, the urinary bladder is not palpable. He has a normal anal sphincter tone and a bulbocavernosus muscle reflex. Digital rectal exam shows a prostate size equivalent to three finger pads without fluctuance or tenderness. The 24-hour urinary volume is 2.5 liters. Laboratory studies show:
Urine
Protein negative
RBC none
WBC 1–2/hpf
Hemoglobin negative
Bacteria none
Ultrasonography shows an estimated prostate size of 50 grams, a post-void residual volume of 120 mL, and urinary bladder wall trabeculation without any hydronephrosis. In addition to controlled fluid intake, which of the following is the most appropriate additional pharmacotherapy at this time?
Q29
A 68-year-old man seeks evaluation at an office with a complaint of breathlessness of several months duration. He is able to do his daily tasks, but says that he is not as efficient as before. His breathlessness has been progressive with the recent onset of a dry cough. The past medical history is significant for a cardiac arrhythmia that is being treated with an anti-arrhythmic. He has never smoked cigarettes and is a social drinker. His pulse is 87/min and regular and the blood pressure is 135/88 mm Hg. Bilateral basal inspiratory crackles are present on auscultation of the chest from the back. A chest X-ray image shows peripheral reticular opacities with a coarse reticular pattern. A high-resolution CT scan of the chest reveals patchy bibasilar reticular opacities. Which of the following medications is most likely responsible for this patient’s condition?
Q30
A 36-year-old woman is brought to the emergency department because of lightheadedness, weakness, and abdominal pain for 6 hours. Over the past 3 days, she has also had severe nausea, vomiting, and watery diarrhea. She was diagnosed with pulmonary sarcoidosis 2 years ago. Current medications include prednisone. Her temperature is 38.9°C (102.0°F), pulse is 112/min, and blood pressure is 85/50 mm Hg. Physical examination shows a round face with prominent preauricular fat pads. Her fingerstick blood glucose concentration is 48 mg/dL. Further evaluation is most likely to show which of the following laboratory changes?
Autonomic/CV Drugs US Medical PG Practice Questions and MCQs
Question 21: A 23-year-old primigravid woman at 8 weeks' gestation is brought to the emergency department by her husband because of increasing confusion and high-grade fever over the past 16 hours. Three days ago, she was prescribed metoclopramide by her physician for the treatment of nausea and vomiting. She has a history of depression. Current medications include fluoxetine. She is confused and not oriented to time, place, or person. Her temperature is 39.8°C (103.6°F), pulse is 112/min, and blood pressure is 168/96 mm Hg. Examination shows profuse diaphoresis and flushed skin. Muscle rigidity is present. Her deep tendon reflexes are decreased bilaterally. Mental status examination shows psychomotor agitation. Laboratory studies show:
Hemoglobin 12.2 g/dL
Leukocyte count 17,500/mm3
Serum
Creatinine 1.4 mg/dL
Total bilirubin 0.7 mg/dL
Alkaline phosphatase 45 U/L
AST 122 U/L
ALT 138 U/L
Creatine kinase 1070 U/L
Which of the following drugs is most likely to also cause the condition that is responsible for this patient’s current symptoms?
A. Haloperidol (Correct Answer)
B. Amitriptyline
C. Atropine
D. Dextroamphetamine
E. Succinylcholine
Explanation: ***Haloperidol***
- The patient has **neuroleptic malignant syndrome (NMS)**, caused by metoclopramide (a dopamine D2 receptor antagonist). Key diagnostic features include **muscle rigidity, hyperthermia, autonomic instability, altered mental status, elevated creatine kinase (1070 U/L), and decreased deep tendon reflexes**.
- **Haloperidol** is a first-generation antipsychotic and potent **dopamine D2 receptor antagonist** that is a classic cause of NMS. It would cause the **exact same condition** as metoclopramide.
- NMS results from **dopamine D2 receptor blockade** in the basal ganglia and hypothalamus, leading to the characteristic syndrome of rigidity, hyperthermia, and autonomic dysfunction.
*Amitriptyline*
- Amitriptyline is a **tricyclic antidepressant (TCA)** that inhibits reuptake of serotonin and norepinephrine. When combined with SSRIs like fluoxetine, it could potentially contribute to **serotonin syndrome**, not NMS.
- **Serotonin syndrome** presents differently with **hyperreflexia, clonus, mydriasis**, and more prominent GI symptoms—features NOT seen in this patient who has **decreased reflexes** (characteristic of NMS, not serotonin syndrome).
- TCA toxicity typically presents with **anticholinergic effects** (dry mouth, urinary retention, blurred vision) and **cardiac conduction abnormalities** (QRS widening, QT prolongation).
*Atropine*
- Atropine is an **antimuscarinic anticholinergic agent** that does not cause NMS or interact significantly with dopaminergic pathways.
- Atropine toxicity presents as **anticholinergic syndrome**: dry skin (anhidrosis), hyperthermia, delirium, mydriasis, and urinary retention—remembered as "hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter."
- This patient has **profuse diaphoresis** (sweating), which rules out anticholinergic toxicity and is consistent with NMS.
*Dextroamphetamine*
- Dextroamphetamine is a **sympathomimetic stimulant** that increases release of dopamine, norepinephrine, and serotonin, causing a **hyperadrenergic state**.
- While it can cause hyperthermia, tachycardia, and hypertension, it does not typically cause the **severe muscle rigidity** and **marked CK elevation** seen in NMS.
- High doses of amphetamines with SSRIs could theoretically contribute to serotonin syndrome, but this would present with hyperreflexia and clonus, not the decreased reflexes seen here.
*Succinylcholine*
- Succinylcholine is a **depolarizing neuromuscular blocker** used for rapid sequence intubation. It does not affect dopaminergic or serotonergic pathways and does not cause NMS.
- Its major complication is **malignant hyperthermia (MH)** in genetically susceptible individuals (RYR1 or CACNA1S mutations), triggered by volatile anesthetics or succinylcholine itself.
- MH presents with hyperthermia, rigidity, tachycardia, and elevated CK, but occurs in the **perioperative setting** with specific genetic predisposition, not from drug interactions with antidepressants.
Question 22: Which of the following compounds is most responsible for the maintenance of appropriate coronary blood flow?
A. VEGF
B. Epinephrine
C. Nitric oxide (Correct Answer)
D. Histamine
E. Norepinephrine
Explanation: ***Nitric oxide***
- **Nitric oxide (NO)** is a potent **vasodilator** produced by endothelial cells, crucial for relaxing vascular smooth muscle and increasing blood flow.
- In the coronary circulation, NO helps to match oxygen supply with myocardial demand by regulating **coronary artery tone**.
*VEGF*
- **Vascular Endothelial Growth Factor (VEGF)** is primarily involved in **angiogenesis** (formation of new blood vessels) and blood vessel permeability, not immediate regulation of blood flow.
- While important for long-term vascular health and collateral circulation, it does not directly mediate acute changes in **coronary blood flow**.
*Epinephrine*
- **Epinephrine** (adrenaline) primarily causes **vasoconstriction** in many vascular beds via alpha-1 adrenergic receptors, although it can cause vasodilation in skeletal muscle via beta-2 receptors.
- Its overall effect on coronary arteries is complex and can include **increased heart rate and contractility**, which increases myocardial oxygen demand, rather than directly maintaining appropriate coronary blood flow through vasodilation.
*Histamine*
- **Histamine** is a mediator of allergic reactions and inflammation, causing **vasodilation** and increased vascular permeability.
- While it can cause vasodilation, its primary physiological role is not the routine maintenance of **coronary blood flow** under normal conditions.
*Norepinephrine*
- **Norepinephrine** primarily stimulates **alpha-1 adrenergic receptors**, leading to **vasoconstriction** in most vascular beds, including systemic arteries.
- This effect generally reduces blood flow to organs, making it unsuitable for maintaining appropriate and adaptive **coronary blood flow**.
Question 23: A 55-year-old female with a history of poorly controlled hyperlipidemia and obesity presents to her primary care physician for a follow-up visit. She reports that she feels well and has no complaints. She currently takes atorvastatin. Her temperature is 99°F (37.2°C), blood pressure is 135/80 mmHg, pulse is 80/min, and respirations are 16/min. Her BMI is 31 kg/m2. Her total cholesterol is 290 mg/dl, triglycerides are 120 mg/dl, and LDL cholesterol is 215 mg/dl. Her physician considers starting her on a medication that forces the liver to consume cholesterol to make more bile salts. Which of the following adverse effects is this patient at highest risk of developing following initiation of the medication?
A. Pruritus
B. Acanthosis nigricans
C. Facial flushing
D. Gallstones (Correct Answer)
E. Fat malabsorption
Explanation: ***Gallstones***
- The physician plans to start a bile acid sequestrant (e.g., cholestyramine, colestipol, colesevelam), which forces the liver to consume cholesterol to make more bile salts, thus reducing LDL.
- An increase in bile acid synthesis and secretion can alter the **cholesterol-to-bile acid ratio** in bile, leading to increased cholesterol saturation and the formation of **cholesterol gallstones**.
*Pruritis*
- While pruritus can be associated with cholestasis (impaired bile flow), it is not a direct or highly common adverse effect of **bile acid sequestrants** themselves.
- Pruritus in hyperlipidemia often relates to severe hypertriglyceridemia not addressed by this class of drug, or in primary biliary cholangitis.
*Acanthosis nigricans*
- **Acanthosis nigricans** is a skin condition characterized by hyperpigmented, velvety plaques, often indicative of **insulin resistance** or malignancy.
- While the patient has obesity, a risk factor for insulin resistance, this condition is not directly caused by or exacerbated by bile acid sequestrants.
*Facial flushing*
- **Facial flushing** is a common adverse effect primarily associated with **niacin (nicotinic acid)**, another lipid-lowering agent.
- Niacin causes vasodilation, but this mechanism is not shared by bile acid sequestrants.
*Fat malabsorption*
- **Bile acid sequestrants** can interfere with the absorption of fat-soluble vitamins (A, D, E, K) due to their binding of bile acids.
- While some gastrointestinal upset can occur, significant **fat malabsorption** leading to steatorrhea is less common with typical doses and is primarily associated with conditions severely impairing bile flow or pancreatic function.
Question 24: A 27-year-old woman comes to the physician because of poor sleep for the past 8 months. She has been gradually sleeping less because of difficulty initiating sleep at night. She does not have trouble maintaining sleep. On average, she sleeps 4–5 hours each night. She feels tired throughout the day but does not take naps. She was recently diagnosed with social anxiety disorder and attends weekly psychotherapy sessions. Mental status examination shows an anxious mood. The patient asks for a sleeping aid but does not want to feel drowsy in the morning because she has to drive her daughter to kindergarten. Short-term treatment with which of the following drugs is the most appropriate pharmacotherapy for this patient's symptoms?
A. Triazolam
B. Phenobarbital
C. Doxepin
D. Suvorexant (Correct Answer)
E. Flurazepam
Explanation: ***Suvorexant***
- This patient presents with **insomnia**, specifically **difficulty initiating sleep**, and requires an agent with a quick onset for short-term use, minimal morning sedation, and suitability for co-morbid **anxiety**. Suvorexant, an **orexin receptor antagonist**, works by blocking wakefulness-promoting signals, providing a good sleep aid without residual daytime drowsiness reported in other classes.
- Its mechanism of action specifically targets wakefulness rather than generally depressing the CNS, making it appropriate for patients who need to function normally the next day, like driving.
*Triazolam*
- **Triazolam** is a short-acting **benzodiazepine** that acts quickly but carries a higher risk of **rebound insomnia** and potential for dependence with prolonged use.
- While it helps with sleep initiation, its anxiolytic properties might be appealing, but the patient's concern about morning sedation makes it less ideal, as benzodiazepines can have residual effects.
*Phenobarbital*
- **Phenobarbital** is a **barbiturate** and a potent CNS depressant primarily used as an anticonvulsant; its use as a sleep aid is highly discouraged due to its **sedative effects**, risk of dependence, and narrow therapeutic index.
- It would cause significant morning drowsiness and is generally not indicated for routine insomnia due to its severe side effect profile.
*Doxepin*
- **Doxepin** is a **tricyclic antidepressant** with strong **antihistaminic** properties at low doses, which can be useful for sleep maintenance, but it has a long half-life and can lead to significant **daytime sedation** and anticholinergic side effects.
- Its long half-life makes it unsuitable for a patient who needs to avoid morning drowsiness for driving.
*Flurazepam*
- **Flurazepam** is a long-acting **benzodiazepine** with a prolonged half-life, meaning it would likely cause significant **next-day sedation** and impairment, making it unsuitable for someone who needs to drive in the morning.
- Its long duration of action would counteract the patient's need for a drug without residual daytime effects.
Question 25: A 24-year-old woman is brought into the emergency department by an ambulance after swallowing a bottle of pain medication in a suicide attempt. According to her parents, she recently had a fight with her boyfriend and was acting very depressed. She claims to not remember what she had taken. Further inquiry reveals she is experiencing nausea and feeling quite dizzy. She also repeatedly asks if anyone else can hear a ringing sound. Her pulse is 105/min, respirations are 24/min, and temperature is 38.2°C (100.8°F). Examination reveals mild abdominal tenderness. The patient is visibly agitated and slightly confused. The following lab values are obtained:
Arterial blood gas analysis
pH 7.35
Po2 100 mm Hg
Pco2 20 mm Hg
HCO3- 12 mEq/L
Which of the following pain medications did this patient most likely take?
A. Codeine
B. Indomethacin
C. Gabapentin
D. Aspirin (Correct Answer)
E. Acetaminophen
Explanation: ***Aspirin***
- The patient's symptoms of **tinnitus (ringing sound)**, **nausea**, **dizziness**, **tachycardia**, **tachypnea**, **fever**, and **metabolic acidosis with respiratory alkalosis (pH 7.35, PCO2 20, HCO3 12)** are classic for **salicylate toxicity**.
- Aspirin overdose leads to direct stimulation of the respiratory center, causing **hyperventilation** and **respiratory alkalosis**, while also uncoupling oxidative phosphorylation, leading to **lactic acidosis** and **metabolic acidosis**.
*Codeine*
- Codeine is an **opioid** and overdose typically causes **respiratory depression**, **miosis (pinpoint pupils)**, and potentially **narcosis (stupor)**, which are not seen here.
- The patient exhibits tachypnea and agitation, which contradict opioid toxicity.
*Indomethacin*
- Indomethacin is an **NSAID**; overdose can cause **gastrointestinal upset**, **CNS effects** like headache or confusion, and potentially **renal impairment**.
- It does not typically cause the classic tinnitus or the specific mixed acid-base derangement seen in this patient.
*Gabapentin*
- Gabapentin overdose usually results in **drowsiness**, **ataxia**, **dizziness**, and occasionally **slurred speech**.
- It does not cause tinnitus, fever, or the characteristic acid-base imbalance observed in this clinical scenario.
*Acetaminophen*
- Acetaminophen overdose often presents with **nausea**, **vomiting**, and later **hepatotoxicity** (elevated liver enzymes).
- It does not cause tinnitus, fever, or the specific mixed acid-base disorder characteristic of salicylate poisoning.
Question 26: A 55-year-old woman comes to the emergency room 30 minutes after the sudden onset of chest pain radiating to the left shoulder. Prior to the onset of her symptoms, she was lying in bed because of a migraine headache. Episodes of similar chest pain usually resolved after a couple of minutes. She has smoked one pack of cigarettes daily for 20 years. Her only medication is sumatriptan. An ECG shows ST-segment elevations in the anterior leads. Serum troponins are negative on two successive blood draws and ECG shows no abnormalities 30 minutes later. Administration of which of the following is most likely to prevent further episodes of chest pain in this patient?
A. Aspirin
B. Clopidogrel
C. Propranolol
D. Diltiazem (Correct Answer)
E. Ramipril
Explanation: ***Diltiazem***
- This patient presents with symptoms highly suggestive of **Prinzmetal angina** (vasospastic angina), characterized by sudden-onset chest pain, often at rest or with migraine, transient ST-segment elevations, and negative troponins.
- **Calcium channel blockers** like diltiazem are the cornerstone of treatment for Prinzmetal angina as they effectively prevent coronary artery spasm.
*Aspirin*
- **Aspirin** is an antiplatelet agent used to prevent arterial thrombosis in patients with atherosclerotic disease.
- It does not directly prevent coronary artery spasms, which are the underlying cause of Prinzmetal angina.
*Clopidogrel*
- **Clopidogrel** is an antiplatelet agent similar to aspirin, primarily used to prevent arterial thrombosis.
- It would not prevent coronary spasms and is therefore not the most appropriate treatment for Prinzmetal angina.
*Propranolol*
- **Beta-blockers** like propranolol can sometimes worsen vasospastic angina by inhibiting beta-2 mediated vasodilation, leaving alpha-1 vasoconstriction unopposed.
- Their use is generally contraindicated or approached with caution in patients with Prinzmetal angina.
*Ramipril*
- **Ramipril** is an ACE inhibitor, primarily used for hypertension, heart failure, and renal protection.
- It does not directly address coronary artery spasms and would not be effective in preventing episodes of Prinzmetal angina.
Question 27: A healthy 48-year-old presents for a well-patient visit. He has no symptoms and feels well. Past medical history is significant for asthma, chronic sinusitis, and nasal polyps. He occasionally takes diphenhydramine for allergies. Both of his parents and an elder brother are in good health. Today, his blood pressure is 119/81 mm Hg, heart rate is 101/min, respiratory rate is 21/min, and temperature 37°C (98.6°F). Routine screening blood work reveals elevated total cholesterol. The patient asks if he should take low-dose aspirin to reduce his risk of stroke and heart attack. Of the following, which is the best response?
A. Have you had a reaction to aspirin in the past? (Correct Answer)
B. No, because aspirin does not help reduce the risk of stroke and heart attack.
C. Yes, aspirin therapy is recommended.
D. Yes, but only every other day.
E. No, because all chronic sinusitis carries aspirin-complications.
Explanation: ***Have you had a reaction to aspirin in the past?***
- This is the most crucial initial question as the patient's history of **asthma, chronic sinusitis, and nasal polyps** strongly suggests a risk of **aspirin-exacerbated respiratory disease (AERD)**.
- Asking about past reactions helps identify potential contraindications and avoid a severe, potentially life-threatening reaction if aspirin were prescribed.
*No, because aspirin does not help reduce the risk of stroke and heart attack.*
- This statement is incorrect as **low-dose aspirin** is known to **reduce the risk of cardiovascular events**, including stroke and heart attack, in appropriate patients through its antiplatelet effects.
- The decision to prescribe aspirin depends on a careful assessment of individual risk factors and comorbidities, not a blanket dismissal of its efficacy.
*Yes, aspirin therapy is recommended.*
- Recommending aspirin therapy outright without assessing for contraindications is dangerous given the patient's history of **asthma, chronic sinusitis, and nasal polyps**, which is a classic triad for **aspirin-exacerbated respiratory disease (AERD)**.
- Aspirin could precipitate a severe **bronchospasm** or **anaphylactoid reaction** in such individuals.
*Yes, but only every other day.*
- While aspirin dosing regimens vary, the frequency (every other day) is secondary to determining if the patient can safely take aspirin at all, especially with his medical history.
- The fundamental concern is the potential for **aspirin-exacerbated respiratory disease (AERD)**, which would make aspirin contraindicated regardless of the dosing frequency.
*No, because all chronic sinusitis carries aspirin-complications.*
- This statement is an **overgeneralization** as not all cases of chronic sinusitis are associated with aspirin sensitivity or **aspirin-exacerbated respiratory disease (AERD)**.
- While there is an association, especially in patients with the triad of asthma, sinusitis, and nasal polyps, it's not a universal complication for all individuals with chronic sinusitis.
Question 28: An 82-year-old man comes to the physician complaining of frequent urination, especially at night, and difficulty initiating urination. However, he points out that his symptoms have improved slightly since he started terazosin 2 months ago. He has a history of stable angina. Other medications include nitroglycerin, metoprolol, and aspirin. His blood pressure is 125/70 mm Hg and pulse is 72/min. On examination, the urinary bladder is not palpable. He has a normal anal sphincter tone and a bulbocavernosus muscle reflex. Digital rectal exam shows a prostate size equivalent to three finger pads without fluctuance or tenderness. The 24-hour urinary volume is 2.5 liters. Laboratory studies show:
Urine
Protein negative
RBC none
WBC 1–2/hpf
Hemoglobin negative
Bacteria none
Ultrasonography shows an estimated prostate size of 50 grams, a post-void residual volume of 120 mL, and urinary bladder wall trabeculation without any hydronephrosis. In addition to controlled fluid intake, which of the following is the most appropriate additional pharmacotherapy at this time?
A. Finasteride (Correct Answer)
B. Oxybutynin
C. Tadalafil
D. Tamsulosin
E. No additional pharmacotherapy at this time
Explanation: ***Finasteride***
- This patient exhibits symptoms of **benign prostatic hyperplasia (BPH)** with a prostate size of 50 grams and a post-void residual volume of 120 mL, indicating an enlarged prostate contributing to his lower urinary tract symptoms (LUTS)
- **Finasteride**, a **5-alpha reductase inhibitor**, reduces prostate size by inhibiting the conversion of testosterone to dihydrotestosterone, making it an appropriate addition to his current alpha-blocker therapy
- Given his stable angina and current medications including nitroglycerin, finasteride works via a different mechanism than alpha-blockers and directly addresses the underlying prostate enlargement
- Combination therapy with an alpha-blocker and 5-alpha reductase inhibitor is recommended for patients with moderate-to-severe BPH symptoms and prostate enlargement >40 grams
*Oxybutynin*
- **Oxybutynin** is an **anticholinergic medication** used to treat **overactive bladder** symptoms like urgency and frequency
- While the patient has frequency, his primary issue is bladder outflow obstruction from BPH, and anticholinergics can worsen urinary retention in patients with obstructive symptoms
- Contraindicated in men with significant post-void residual volumes
*Tadalafil*
- **Tadalafil** is a **phosphodiesterase-5 (PDE5) inhibitor** FDA-approved for BPH treatment at lower doses
- It acts by relaxing smooth muscle in the prostate and bladder neck, improving urinary flow
- However, it does not reduce prostate size, which is significant in this patient (50 grams), and would not address the underlying progressive enlargement
- Could be considered as an alternative but finasteride is more appropriate for size reduction in moderate-to-severe BPH
*Tamsulosin*
- **Tamsulosin** is a selective **alpha-1A blocker** that relaxes smooth muscle in the prostate and bladder neck
- The patient is already on terazosin, another alpha-blocker, so adding tamsulosin would be redundant and not provide additional benefit through a different mechanism
- Switching from terazosin to tamsulosin (more selective) could be considered but doesn't address the question of "additional pharmacotherapy"
- Adding another alpha-blocker increases risk of orthostatic hypotension without targeting prostate size reduction
*No additional pharmacotherapy at this time*
- The patient's objective findings including a post-void residual volume of 120 mL (normal <50 mL) and 50-gram prostate indicate significant BPH requiring additional treatment
- Although he has improved slightly on terazosin, the persistently elevated post-void residual suggests inadequate treatment response
- Additional treatment targeting prostate size reduction is warranted to prevent complications like acute urinary retention, bladder decompensation, or renal compromise from chronic obstruction
Question 29: A 68-year-old man seeks evaluation at an office with a complaint of breathlessness of several months duration. He is able to do his daily tasks, but says that he is not as efficient as before. His breathlessness has been progressive with the recent onset of a dry cough. The past medical history is significant for a cardiac arrhythmia that is being treated with an anti-arrhythmic. He has never smoked cigarettes and is a social drinker. His pulse is 87/min and regular and the blood pressure is 135/88 mm Hg. Bilateral basal inspiratory crackles are present on auscultation of the chest from the back. A chest X-ray image shows peripheral reticular opacities with a coarse reticular pattern. A high-resolution CT scan of the chest reveals patchy bibasilar reticular opacities. Which of the following medications is most likely responsible for this patient’s condition?
A. Verapamil
B. Amiodarone (Correct Answer)
C. Digoxin
D. Lidocaine
E. Sotalol
Explanation: ***Amiodarone***
- Amiodarone is a well-known antiarrhythmic drug that can cause **pulmonary toxicity**, leading to conditions like **pulmonary fibrosis**, which manifests as progressive breathlessness, dry cough, and basal crackles.
- The imaging findings of **peripheral reticular opacities** and **bibasilar reticular opacities** on HRCT are classic for drug-induced interstitial lung disease, highly suggestive of amiodarone toxicity in this context.
*Verapamil*
- Verapamil, a calcium channel blocker, is used for arrhythmias but is not typically associated with **pulmonary fibrosis** or significant interstitial lung disease.
- Its common side effects include constipation, bradycardia, and hypotension, not respiratory pathology like that described.
*Digoxin*
- Digoxin is a cardiac glycoside used for heart failure and arrhythmias, but it does not cause **interstitial lung disease** or pulmonary fibrosis.
- Toxicity usually presents with gastrointestinal symptoms, visual disturbances, and cardiac arrhythmias.
*Lidocaine*
- Lidocaine is an antiarrhythmic often used intravenously for acute arrhythmias, but it is not linked to **chronic pulmonary toxicity** or fibrosis.
- Side effects are primarily neurological (dizziness, seizures) and cardiovascular (arrhythmias, hypotension).
*Sotalol*
- Sotalol is a beta-blocker with potassium channel blocking properties used for arrhythmias, but it is not associated with **drug-induced pulmonary fibrosis**.
- Its main side effects include bradycardia, fatigue, and potential for torsades de pointes.
Question 30: A 36-year-old woman is brought to the emergency department because of lightheadedness, weakness, and abdominal pain for 6 hours. Over the past 3 days, she has also had severe nausea, vomiting, and watery diarrhea. She was diagnosed with pulmonary sarcoidosis 2 years ago. Current medications include prednisone. Her temperature is 38.9°C (102.0°F), pulse is 112/min, and blood pressure is 85/50 mm Hg. Physical examination shows a round face with prominent preauricular fat pads. Her fingerstick blood glucose concentration is 48 mg/dL. Further evaluation is most likely to show which of the following laboratory changes?
A. Decreased norepinephrine
B. Decreased aldosterone
C. Decreased corticotropin-releasing hormone
D. Increased cortisol
E. Increased adrenocorticotropic hormone (Correct Answer)
Explanation: ***Increased adrenocorticotropic hormone***
- This patient presents with **adrenal crisis** (hypotension, hypoglycemia, GI symptoms during acute illness). While she has been on chronic prednisone for sarcoidosis, the underlying cause of her adrenal insufficiency is likely **primary adrenal insufficiency** from **sarcoid infiltration of the adrenal glands**, rather than simple steroid-induced suppression.
- In **primary adrenal insufficiency**, the adrenal glands themselves fail to produce cortisol and aldosterone. This leads to **loss of negative feedback** on the hypothalamus and pituitary, resulting in **compensatory elevation of ACTH**.
- The Cushingoid features indicate chronic steroid exposure, but the acute decompensation during illness with severe hypotension and hypoglycemia suggests the **adrenal glands can no longer respond** adequately, even to endogenous or therapeutic steroids. This points to primary adrenal failure (Addison's disease) secondary to sarcoidosis.
- Sarcoidosis can cause **granulomatous infiltration of the adrenal glands**, leading to primary adrenal insufficiency in 1-5% of cases.
*Decreased norepinephrine*
- In states of hypotension and shock, the sympathetic nervous system is activated to **increase norepinephrine** release to maintain blood pressure.
- Decreased norepinephrine would worsen hypotension and is not expected in adrenal crisis.
*Decreased aldosterone*
- While aldosterone is indeed **decreased in primary adrenal insufficiency** and contributes to hypotension and hyperkalemia, this is a direct consequence of adrenal gland failure, not a compensatory pituitary response.
- The question asks for the most likely laboratory finding on "further evaluation," which typically refers to the **diagnostic hormonal changes** - elevated ACTH is the key finding that distinguishes primary from secondary adrenal insufficiency.
*Decreased corticotropin-releasing hormone*
- In primary adrenal insufficiency, **CRH and ACTH are both elevated** due to loss of negative feedback from cortisol.
- Decreased CRH would only occur in tertiary adrenal insufficiency (hypothalamic dysfunction) or in cases of chronic exogenous steroid use causing **secondary** adrenal insufficiency - but the severity of this patient's presentation suggests primary adrenal failure.
*Increased cortisol*
- Cortisol levels are **low or undetectable** in adrenal crisis, which is the underlying pathophysiology causing hypotension, hypoglycemia, and inability to respond to stress.
- Increased cortisol would contradict the diagnosis of adrenal crisis.