A 23-year-old woman is brought to the emergency department by her friend because of a 1-hour episode of confusion. Earlier that night, they were at a dance club, and the patient was very energetic and euphoric. Thirty minutes after arriving, she became agitated and nauseous. She no longer seemed to know where she was or how she got there, and she began talking to herself. She has no major medical illness. She is an undergraduate student at a local college. She does not smoke but drinks 10–14 mixed drinks each week. Her temperature is 38.3°C (100.9°F), pulse is 115/min and regular, respirations are 16/min, and blood pressure is 138/84 mm Hg. She oriented to self but not to time or place. Throughout the examination, she grinds her teeth. Her pupils are 7 mm in diameter and minimally reactive. Her skin is diffusely flushed and diaphoretic. Cardiopulmonary examination shows no abnormalities. Serum studies show:
Na+ 129 mEq/L
K+ 3.7 mEq/L
HCO3- 22 mEq/L
Creatinine 1.2 mg/dL
Glucose 81 mg/dL
Which of the following substances is the most likely cause of this patient's presentation?
Q352
A 30-year-old woman presents complaining of shortness of breath, chest pain, and fatigue. The patient complains of dyspnea upon exertion, generalized fatigue, lethargy, and chest pain associated with strenuous activities. Her history is notable for an atrial septal defect at birth. Her temperature is 99.5°F (37.5°C), blood pressure is 147/98 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 98% on room air. On exam, she has a wide, fixed splitting of S2. Which of the following medications most directly treats the underlying pathophysiology causing this patient's presentation?
Q353
Please refer to the summary above to answer this question
Which of the following is the most appropriate pharmacotherapy?
Patient Information
Age: 30 years
Gender: F, self-identified
Ethnicity: unspecified
Site of Care: office
History
Reason for Visit/Chief Concern: "I'm so anxious about work."
History of Present Illness:
7-month history of sensation that her heart is racing whenever she gives oral presentations at work
she has also had moderate axillary sweating during these presentations and feels more anxious and embarrassed when this happens
feels otherwise fine when she is interacting with her colleagues more casually around the workplace
Past Medical History:
alcohol use disorder, now abstinent for the past 2 years
acute appendicitis, treated with appendectomy 5 years ago
verrucae planae
Medications:
disulfiram, folic acid, topical salicylic acid
Allergies:
no known drug allergies
Psychosocial History:
does not smoke, drink alcohol, or use illicit drugs
Physical Examination
Temp Pulse Resp BP O2 Sat Ht Wt BMI
36.7°C
(98°F)
82/min 18/min 115/72 mm Hg –
171 cm
(5 ft 7 in)
58 kg
(128 lb)
20 kg/m2
Appearance: no acute distress
Pulmonary: clear to auscultation
Cardiac: regular rate and rhythm; normal S1 and S2; no murmurs
Abdominal: has well-healed laparotomy port scars; no tenderness, guarding, masses, bruits, or hepatosplenomegaly
Extremities: no tenderness to palpation, stiffness, or swelling of the joints; no edema
Skin: warm and dry; there are several skin-colored, flat-topped papules on the dorsal bilateral hands
Neurologic: alert and oriented; cranial nerves grossly intact; no focal neurologic deficits
Psychiatric: describes her mood as "okay"; speech has a rapid rate but normal rhythm; thought process is organized
Q354
A 70-year-old man is brought to the emergency department unconscious after a fall. He appears pale and is pulseless. A 12-lead EKG reveals wide, monomorphic sawtooth-like QRS complexes. He undergoes synchronized cardioversion three times at increasing voltage with no effect. Epinephrine is administered with minimal effect. Which drug will minimize his risk of developing multifocal ventricular tachycardia?
Q355
A 27-year-old P1G1 who has had minimal prenatal care delivers a newborn female infant. Exam reveals a dusky child who appears to be in distress. Her neck veins are distended and you note an enlarged v wave. She has a holosystolic murmur. Following echocardiogram, immediate surgery is recommended.
For which of the following conditions was the mother likely receiving treatment during pregnancy?
Q356
A 50-year-old woman presents to the ED 6 hours after ingesting three bottles of baby aspirin. She complains of nausea, vomiting, dizziness, and tinnitus. Her blood pressure is 135/80 mmHg, pulse is 110/min, respirations are 32/min, temperature is 100.1 deg F (37.8 deg C), and oxygen saturation is 99% on room air. Arterial blood gas at room air shows, PCO2 11 mmHg, and PO2 129 mmHg. Blood salicylate level is 55 mg/dL. Management should involve which of the following acid-base principles?
Q357
A 72-year-old man of Asian descent seeks evaluation at your medical office and is frustrated about the frequency he wakes up at night to urinate. He comments that he has stopped drinking liquids at night, but the symptoms have progressively worsened. The physical examination is unremarkable, except for an enlarged, symmetric prostate free of nodules. Which of the following should you prescribe based on the main factor that contributes to the underlying pathogenesis?
Q358
An endocrinologist is working with a pharmaceutical research company on a new drug for diabetes mellitus type 2 (DM2). In their experimental studies, they isolated a component from Gila monster saliva, which was found to have > 50% homology with glucagon-like peptide-1 (GLP1). During the animal studies, the experimental drug was found to have no GLP1 agonist effect. Instead, it irreversibly binds DPP-IV with a higher affinity than GLP1. Which of the following drugs has a similar mechanism of action to this new experimental drug?
Q359
A 34-year-old woman presents with acute onset loss of vision and visual disturbances. She says that, several hours ago, her vision began to get dim, and she sees halos around light sources. This was immediately followed by a severe frontal headache. Past medical history is significant for epilepsy. The patient says her anticonvulsant medication was changed recently but she doesn’t remember the name. Slit-lamp examination reveals mild chemosis, injection, and ciliary flush with diffuse stromal haze, along with very shallow peripheral anterior chambers with areas of iridocorneal touch in both eyes. Gonioscopy showed closed angles bilaterally. Which of the following antiepileptic drugs is most likely responsible for this patient’s condition?
Q360
An 85-year-old man presents with the reappearance of his Parkinson’s disease (PD) symptoms over the last few months. He says he has been treated with various drugs over the last 20 years, but that currently his symptoms worsen as he nears the time for his next dose of medication. His movements have been slower lately and it’s difficult to initiate voluntary movements. His past medical history is significant for hypertension. He was diagnosed 10 years ago and was well-managed on medication. His current medications are levodopa/carbidopa, rasagiline, aspirin, and captopril. The vital signs include: pulse 70/min, respiratory rate 15/min, blood pressure 130/76 mm Hg, and temperature 36.7°C (98.1°F). Physical examination reveals the expected ‘pill-rolling’ resting tremor, which is alleviated by movement. Increased tone of arm muscles and resistance to passive movement at the joints is noted. When asked to walk across the room, he has difficulty taking the 1st step and has a stooped posture and takes short, shuffling, rapid steps. Laboratory studies show:
Serum glucose (fasting) 97 mg/dL
Sodium 141 mEq/L
Potassium 4.0 mEq/L
Chloride 100 mEq/L
Cholesterol (total) 190 mg/dL
HDL-cholesterol 42 mg/dL
LDL-cholesterol 70 mg/dL
Triglycerides 184 mg/dL
The patient is started on a drug that increases the efficacy of his current anti-PD medication. Which of the following is most likely the drug that was added to this patient’s current regimen?
Autonomic/CV Drugs US Medical PG Practice Questions and MCQs
Question 351: A 23-year-old woman is brought to the emergency department by her friend because of a 1-hour episode of confusion. Earlier that night, they were at a dance club, and the patient was very energetic and euphoric. Thirty minutes after arriving, she became agitated and nauseous. She no longer seemed to know where she was or how she got there, and she began talking to herself. She has no major medical illness. She is an undergraduate student at a local college. She does not smoke but drinks 10–14 mixed drinks each week. Her temperature is 38.3°C (100.9°F), pulse is 115/min and regular, respirations are 16/min, and blood pressure is 138/84 mm Hg. She oriented to self but not to time or place. Throughout the examination, she grinds her teeth. Her pupils are 7 mm in diameter and minimally reactive. Her skin is diffusely flushed and diaphoretic. Cardiopulmonary examination shows no abnormalities. Serum studies show:
Na+ 129 mEq/L
K+ 3.7 mEq/L
HCO3- 22 mEq/L
Creatinine 1.2 mg/dL
Glucose 81 mg/dL
Which of the following substances is the most likely cause of this patient's presentation?
A. Ecstasy (Correct Answer)
B. Cocaine
C. Acetaminophen
D. Diphenhydramine
E. Codeine
Explanation: **Ecstasy**
- The patient's **euphoria, confusion, agitation, teeth grinding (bruxism), mydriasis (7 mm pupils), hyperthermia, tachycardia, hypertension, and hyponatremia** are all characteristic of **MDMA (Ecstasy)** intoxication. These symptoms are consistent with its stimulant and serotonergic effects.
- **Hyponatremia** can occur due to increased antidiuretic hormone (ADH) secretion induced by MDMA, combined with excessive fluid intake (often water) by users trying to combat hyperthermia and dehydration.
*Cocaine*
- While cocaine intoxication can cause **euphoria, agitation, tachycardia, hypertension, and mydriasis**, it typically does not cause the prominent **hyponatremia** seen in this patient.
- **Bruxism** and the specific progression to **confusion and talking to herself** are more suggestive of MDMA's serotonergic effects rather than pure dopaminergic stimulation from cocaine.
*Acetaminophen*
- **Acetaminophen overdose** primarily causes **hepatic toxicity**, which would manifest as elevated liver enzymes, nausea, vomiting, and later jaundice.
- It does not induce the **acute neurological symptoms** (euphoria, agitation, confusion, teeth grinding) or the distinctive **vital sign derangements** (hyperthermia, tachycardia, hypertension) observed in this patient.
*Diphenhydramine*
- **Diphenhydramine overdose** (an antihistamine with anticholinergic properties) would typically present with **anticholinergic toxidrome** symptoms, including dry mouth, blurred vision, urinary retention, dilated pupils, fever, and altered mental status (delirium, hallucinations).
- While it can cause confusion and dilated pupils, the prominent **diaphoresis**, **tachycardia**, and **hyponatremia** are less characteristic of isolated diphenhydramine toxicity.
*Codeine*
- **Codeine** is an opioid, and overdose would cause symptoms of **opioid toxidrome**, such as **respiratory depression, miosis (pinpoint pupils)**, central nervous system depression (sedation, coma), and hypotension.
- The patient's symptoms of alertness, agitation, dilated pupils, hypertension, and tachycardia are directly opposite to what would be expected from codeine intoxication.
Question 352: A 30-year-old woman presents complaining of shortness of breath, chest pain, and fatigue. The patient complains of dyspnea upon exertion, generalized fatigue, lethargy, and chest pain associated with strenuous activities. Her history is notable for an atrial septal defect at birth. Her temperature is 99.5°F (37.5°C), blood pressure is 147/98 mmHg, pulse is 90/min, respirations are 17/min, and oxygen saturation is 98% on room air. On exam, she has a wide, fixed splitting of S2. Which of the following medications most directly treats the underlying pathophysiology causing this patient's presentation?
A. Epoprostenol
B. Metoprolol
C. Lisinopril
D. Nifedipine
E. Bosentan (Correct Answer)
Explanation: ***Bosentan***
- Bosentan is an **endothelin receptor antagonist** that **vasodilates** the pulmonary vasculature, reducing **pulmonary hypertension**. This directly addresses the increased pulmonary artery pressures and subsequent right heart strain caused by long-standing left-to-right shunting from the **atrial septal defect (ASD)**.
- The patient's symptoms (dyspnea, chest pain, fatigue) and signs (elevated pulmonary artery pressure evidenced by a wide, fixed splitting of S2 and systemic hypertension) are consistent with **pulmonary arterial hypertension (PAH)**, likely due to an uncorrected or late-presentation ASD leading to Eisenmenger syndrome.
*Epoprostenol*
- Epoprostenol is a **prostacyclin analog** that causes **vasodilation** and inhibits platelet aggregation, used in severe pulmonary hypertension. While it treats PAH, it is typically reserved for more advanced or rapidly progressive cases, often administered intravenously.
- While it improves symptoms and survival in PAH, **endothelin receptor antagonists** like bosentan are often preferred as first-line oral therapy due to their specific mechanism targeting endothelin's role in PAH pathophysiology and easier administration.
*Metoprolol*
- Metoprolol is a **beta-blocker** used to treat hypertension, angina, and arrhythmias by reducing heart rate and contractility. It would not directly treat PAH.
- In patients with right heart failure secondary to PAH, beta-blockers can sometimes be detrimental by reducing cardiac output, though their use in specific PAH subsets is being investigated.
*Lisinopril*
- Lisinopril is an **ACE inhibitor** that reduces blood pressure by blocking the renin-angiotensin-aldosterone system. It is primarily used for systemic hypertension and heart failure but does not specifically target pulmonary vascular remodeling or vasodilation.
- While it might help with systemic hypertension, it offers no direct benefit for the primary pathophysiology of pulmonary arterial hypertension.
*Nifedipine*
- Nifedipine is a **calcium channel blocker** that causes systemic and, to some extent, pulmonary vasodilation, used for hypertension and angina. However, its use in PAH is typically reserved for a small subset of patients who are **vasoreactive** during acute vasodilator testing.
- For the majority of PAH patients, and especially those with structural heart defects leading to PAH, other vasodilators like endothelin receptor antagonists or prostacyclins are more effective and safer.
Question 353: Please refer to the summary above to answer this question
Which of the following is the most appropriate pharmacotherapy?
Patient Information
Age: 30 years
Gender: F, self-identified
Ethnicity: unspecified
Site of Care: office
History
Reason for Visit/Chief Concern: "I'm so anxious about work."
History of Present Illness:
7-month history of sensation that her heart is racing whenever she gives oral presentations at work
she has also had moderate axillary sweating during these presentations and feels more anxious and embarrassed when this happens
feels otherwise fine when she is interacting with her colleagues more casually around the workplace
Past Medical History:
alcohol use disorder, now abstinent for the past 2 years
acute appendicitis, treated with appendectomy 5 years ago
verrucae planae
Medications:
disulfiram, folic acid, topical salicylic acid
Allergies:
no known drug allergies
Psychosocial History:
does not smoke, drink alcohol, or use illicit drugs
Physical Examination
Temp Pulse Resp BP O2 Sat Ht Wt BMI
36.7°C
(98°F)
82/min 18/min 115/72 mm Hg –
171 cm
(5 ft 7 in)
58 kg
(128 lb)
20 kg/m2
Appearance: no acute distress
Pulmonary: clear to auscultation
Cardiac: regular rate and rhythm; normal S1 and S2; no murmurs
Abdominal: has well-healed laparotomy port scars; no tenderness, guarding, masses, bruits, or hepatosplenomegaly
Extremities: no tenderness to palpation, stiffness, or swelling of the joints; no edema
Skin: warm and dry; there are several skin-colored, flat-topped papules on the dorsal bilateral hands
Neurologic: alert and oriented; cranial nerves grossly intact; no focal neurologic deficits
Psychiatric: describes her mood as "okay"; speech has a rapid rate but normal rhythm; thought process is organized
A. Clonazepam
B. Olanzapine
C. Sertraline
D. Venlafaxine
E. Propranolol (Correct Answer)
Explanation: ***Propranolol***
- This patient presents with symptoms consistent with **performance anxiety** (situational anxiety triggered by public speaking) characterized by a racing heart and sweating. **Propranolol**, a non-selective beta-blocker, is effective in reducing the peripheral physical symptoms of anxiety by blocking adrenergic receptors.
- It works by blunting the **physical manifestations of sympathetic nervous system** activation (e.g., palpitations, tremors, sweating), which can be particularly distressing during performance situations.
*Clonazepam*
- **Clonazepam** is a long-acting benzodiazepine that can be used for anxiety but carries a significant risk of **dependence, tolerance, and withdrawal symptoms**, especially given the patient's history of alcohol use disorder.
- While effective for acute anxiety, its use in performance anxiety should be cautious due to side effects like **sedation** and potential for abuse, making it less appropriate as a first-line treatment in this specific context.
*Olanzapine*
- **Olanzapine** is an atypical antipsychotic primarily used for **schizophrenia** and **bipolar disorder**, or as an augmentation strategy for severe, refractory mood or anxiety disorders.
- Its side effect profile, which includes **metabolic issues** and sedation, makes it an inappropriate choice for treating isolated performance anxiety.
*Sertraline*
- **Sertraline** is an **SSRI** (selective serotonin reuptake inhibitor) often used for generalized anxiety disorder, panic disorder, or social anxiety disorder when symptoms are pervasive and persistent.
- However, for **situational performance anxiety**, which is intermittent and triggered by specific events, SSRIs typically require several weeks to achieve therapeutic effects and are not ideal for immediate symptom relief.
*Venlafaxine*
- **Venlafaxine** is an **SNRI** (serotonin-norepinephrine reuptake inhibitor) indicated for various anxiety disorders, including generalized anxiety disorder and social anxiety disorder.
- Similar to SSRIs, SNRIs take time to become effective and are generally reserved for more **chronic and widespread anxiety**, rather than acute, situational symptoms that can be effectively managed by a beta-blocker.
Question 354: A 70-year-old man is brought to the emergency department unconscious after a fall. He appears pale and is pulseless. A 12-lead EKG reveals wide, monomorphic sawtooth-like QRS complexes. He undergoes synchronized cardioversion three times at increasing voltage with no effect. Epinephrine is administered with minimal effect. Which drug will minimize his risk of developing multifocal ventricular tachycardia?
A. Amiodarone (Correct Answer)
B. Ibutilide
C. Sotalol
D. Dofetilide
E. Procainamide
Explanation: ***Amiodarone***
- **Amiodarone** is a Class III antiarrhythmic, but it has properties of all four Vaughn-Williams classes, making it effective for a wide range of arrhythmias. It is often a first-line agent for both **ventricular tachycardia** and **ventricular fibrillation**.
- Its broad spectrum of action helps to stabilize the myocardial electrical activity and reduce the likelihood of developing additional, polymorphic ventricular arrhythmias like **multifocal ventricular tachycardia**.
*Ibutilide*
- **Ibutilide** is a Class III antiarrhythmic primarily used for the rapid conversion of **atrial fibrillation** and **atrial flutter** to sinus rhythm by selectively prolonging the action potential duration.
- While it prolongs repolarization, it is associated with a risk of **Torsades de Pointes**, a polymorphic ventricular tachycardia, and would not minimize the risk of multifocal ventricular tachycardia, but rather could induce it.
*Sotalol*
- **Sotalol** is a beta-blocker with Class III antiarrhythmic properties, used for both atrial and ventricular arrhythmias.
- Like ibutilide, it also carries a risk of inducing **Torsades de Pointes** due to its action potential prolonging effects, making it unsuitable for minimizing the risk of multifocal ventricular tachycardia in this context.
*Dofetilide*
- **Dofetilide** is a pure Class III antiarrhythmic agent specifically used for the maintenance of sinus rhythm in patients with **atrial fibrillation** or **atrial flutter**.
- It works by blocking the delayed rectifier potassium current, but similar to ibutilide and sotalol, it has a significant risk of **QT prolongation** and **Torsades de Pointes**, thus increasing the risk of polymorphic ventricular tachycardia.
*Procainamide*
- **Procainamide** is a Class IA antiarrhythmic drug that slows conduction and prolongs refractoriness in the atria, ventricles, and accessory pathways. It is used for both supraventricular and ventricular arrhythmias.
- While it can be effective for some ventricular arrhythmias, it is also associated with a risk of **prolonging the QT interval** and inducing **Torsades de Pointes**, especially in patients with structural heart disease or electrolyte imbalances, making it less ideal for minimizing the risk of multifocal ventricular tachycardia compared to amiodarone.
Question 355: A 27-year-old P1G1 who has had minimal prenatal care delivers a newborn female infant. Exam reveals a dusky child who appears to be in distress. Her neck veins are distended and you note an enlarged v wave. She has a holosystolic murmur. Following echocardiogram, immediate surgery is recommended.
For which of the following conditions was the mother likely receiving treatment during pregnancy?
A. Bipolar disorder (Correct Answer)
B. Hypothyroidism
C. Depression
D. Hypertension
E. Diabetes
Explanation: ***Bipolar disorder***
- The newborn's symptoms, including a **holosystolic murmur**, **distended neck veins** with an **enlarged v wave**, and cyanosis, are highly suggestive of **Ebstein's anomaly**.
- **Ebstein's anomaly** is a congenital heart defect strongly associated with maternal **lithium use** during pregnancy, a common treatment for bipolar disorder.
*Hypothyroidism*
- Maternal hypothyroidism is associated with an increased risk of miscarriage, stillbirth, and neurodevelopmental problems in the child, but not specifically with Ebstein's anomaly.
- Treatment for hypothyroidism primarily involves thyroid hormone replacement, which is not linked to this specific cardiac defect.
*Depression*
- While various antidepressant medications can be taken during pregnancy, none are specifically linked to Ebstein's anomaly.
- Maternal depression itself can impact fetal development due to stress, but not typically through this specific congenital heart defect.
*Hypertension*
- Maternal hypertension is associated with conditions like **pre-eclampsia**, fetal growth restriction, and preterm birth, but not specifically with Ebstein's anomaly.
- Antihypertensive medications generally do not cause this specific congenital heart defect.
*Diabetes*
- Maternal diabetes can lead to **macrosomia**, **hypoglycemia**, and an increased risk of various congenital anomalies, including **ventricular septal defects** and **transposition of the great arteries**.
- However, it is not specifically linked to Ebstein's anomaly, which is more characteristic of lithium exposure.
Question 356: A 50-year-old woman presents to the ED 6 hours after ingesting three bottles of baby aspirin. She complains of nausea, vomiting, dizziness, and tinnitus. Her blood pressure is 135/80 mmHg, pulse is 110/min, respirations are 32/min, temperature is 100.1 deg F (37.8 deg C), and oxygen saturation is 99% on room air. Arterial blood gas at room air shows, PCO2 11 mmHg, and PO2 129 mmHg. Blood salicylate level is 55 mg/dL. Management should involve which of the following acid-base principles?
A. Serum neutralization, urine alkalization
B. Serum alkalization, urine alkalization (Correct Answer)
C. Serum neutralization, urine acidification
D. Serum acidification, urine acidification
E. Serum acidification, urine alkalization
Explanation: ***Serum alkalization, urine alkalization***
- Managing **aspirin overdose** involves **aggressive serum alkalization** to promote the shift of salicylic acid from the cells into the bloodstream, where it remains ionized and cannot freely diffuse into the CNS. This also reduces its toxicity by increasing the proportion of the ionized form.
- Subsequently, **urine alkalization** with **sodium bicarbonate** is used to trap the ionized salicylate in the renal tubules, preventing reabsorption and enhancing its excretion.
*Serum neutralization, urine alkalization*
- This option is flawed because the goal is not to "neutralize" the serum pH to a neutral 7.0 but rather to raise it above normal towards an alkaline state (typically pH 7.45-7.55) to enhance salicylate elimination.
- While urine alkalization is correct, the idea of serum neutralization is incorrect and could lead to inadequate treatment.
*Serum neutralization, urine acidification*
- This approach is entirely incorrect for **salicylate toxicity** as **acidifying the urine** would promote the reabsorption of salicylic acid from the renal tubules, worsening toxicity.
- Serum neutralization, as mentioned, is not the correct term or goal for managing **aspirin overdose**.
*Serum acidification, urine acidification*
- This strategy would be **dangerous** in the context of **salicylate overdose** as it would significantly increase the proportion of **non-ionized salicylic acid**, allowing it to more readily cross cell membranes, including the blood-brain barrier, thereby increasing systemic and central nervous system toxicity.
- It would also drastically reduce elimination.
*Serum acidification, urine alkalization*
- **Serum acidification** is contraindicated in **salicylate poisoning** as it drives salicylate into the tissues, exacerbating its toxicity, particularly in the central nervous system.
- While urine alkalization is correct for enhancing elimination, combining it with serum acidification would counteract its benefits and worsen patient outcomes.
Question 357: A 72-year-old man of Asian descent seeks evaluation at your medical office and is frustrated about the frequency he wakes up at night to urinate. He comments that he has stopped drinking liquids at night, but the symptoms have progressively worsened. The physical examination is unremarkable, except for an enlarged, symmetric prostate free of nodules. Which of the following should you prescribe based on the main factor that contributes to the underlying pathogenesis?
A. Prazosin
B. Tamsulosin
C. Leuprolide
D. Phenylephrine
E. Finasteride (Correct Answer)
Explanation: ***Finasteride***
- This medication is a **5-alpha reductase inhibitor** that reduces the size of the prostate by decreasing the conversion of testosterone to **dihydrotestosterone (DHT)**, the primary androgen responsible for prostate growth.
- Given the patient's enlarged prostate and symptoms of **nocturia** that have progressively worsened despite behavioral changes, addressing the underlying stromal and epithelial proliferation of **benign prostatic hyperplasia (BPH)** is key.
*Prazosin*
- **Prazosin** is an **alpha-1 adrenergic antagonist** that works by relaxing the smooth muscle in the prostate and bladder neck, which can improve urine flow but does not address the underlying prostatic hypertrophy.
- While it can alleviate symptoms of BPH, it does not treat the **main pathogenic factor** (prostate enlargement due to DHT) that contributes to the worsening condition.
*Tamsulosin*
- **Tamsulosin** is a selective **alpha-1A adrenergic blocker** that primarily relaxes smooth muscle in the prostate and bladder neck, improving urinary flow with fewer cardiovascular side effects compared to non-selective alpha blockers.
- Like prazosin, it helps with symptom relief but does not target the **hormone-driven growth** of the prostate, which is the underlying cause of the worsening condition.
*Leuprolide*
- **Leuprolide** is a **GnRH agonist** mainly used in advanced prostate cancer or endometriosis; it suppresses gonadotropin release and, consequently, testosterone production.
- It is not indicated for the management of **benign prostatic hyperplasia (BPH)**, which is the more likely diagnosis given the patient's presentation and symmetrical, non-nodular prostate.
*Phenylephrine*
- **Phenylephrine** is an **alpha-1 adrenergic agonist** that causes vasoconstriction and can contract the smooth muscle of the bladder neck, leading to increased outflow resistance.
- This would **worsen rather than improve** the patient's symptoms of urinary obstruction and is contraindicated in BPH.
Question 358: An endocrinologist is working with a pharmaceutical research company on a new drug for diabetes mellitus type 2 (DM2). In their experimental studies, they isolated a component from Gila monster saliva, which was found to have > 50% homology with glucagon-like peptide-1 (GLP1). During the animal studies, the experimental drug was found to have no GLP1 agonist effect. Instead, it irreversibly binds DPP-IV with a higher affinity than GLP1. Which of the following drugs has a similar mechanism of action to this new experimental drug?
A. Metformin
B. Sitagliptin (Correct Answer)
C. Canagliflozin
D. Pramlintide
E. Exenatide
Explanation: ***Sitagliptin***
- This drug is a **dipeptidyl peptidase-4 (DPP-4) inhibitor**, which works by preventing the breakdown of **endogenous GLP-1** and other incretin hormones.
- By inhibiting DPP-4, sitagliptin increases the availability of GLP-1, leading to **glucose-dependent insulin secretion** and reduced glucagon secretion.
- **Note:** While sitagliptin is a **reversible** DPP-4 inhibitor and the experimental drug is described as irreversible, sitagliptin shares the same **target enzyme (DPP-4)** and overall therapeutic mechanism, making it the closest match among the options provided.
*Metformin*
- Metformin is a **biguanide** that primarily reduces **hepatic glucose production** and improves insulin sensitivity in peripheral tissues.
- Its mechanism does not involve direct interaction with DPP-4 or GLP-1 pathways, unlike the experimental drug.
*Canagliflozin*
- Canagliflozin is a **sodium-glucose co-transporter 2 (SGLT2) inhibitor** that blocks glucose reabsorption in the kidneys, leading to **increased urinary glucose excretion**.
- Its action is independent of insulin and does not involve the incretin system or DPP-4 inhibition.
*Pramlintide*
- Pramlintide is an **amylin analog** that works by slowing gastric emptying, suppressing glucagon secretion, and promoting satiety.
- It is administered via injection and acts synergistically with insulin, but does not affect DPP-4 enzyme activity.
*Exenatide*
- Exenatide is a **glucagon-like peptide-1 (GLP-1) receptor agonist** that directly mimics the action of GLP-1, stimulating insulin release and suppressing glucagon.
- Notably, exenatide is also derived from Gila monster saliva (similar to the experimental drug's origin), but it acts as a GLP-1 agonist rather than a DPP-4 inhibitor, which is the opposite mechanism described for the experimental drug.
Question 359: A 34-year-old woman presents with acute onset loss of vision and visual disturbances. She says that, several hours ago, her vision began to get dim, and she sees halos around light sources. This was immediately followed by a severe frontal headache. Past medical history is significant for epilepsy. The patient says her anticonvulsant medication was changed recently but she doesn’t remember the name. Slit-lamp examination reveals mild chemosis, injection, and ciliary flush with diffuse stromal haze, along with very shallow peripheral anterior chambers with areas of iridocorneal touch in both eyes. Gonioscopy showed closed angles bilaterally. Which of the following antiepileptic drugs is most likely responsible for this patient’s condition?
A. Tiagabine
B. Zonisamide
C. Lamotrigine
D. Gabapentin
E. Topiramate (Correct Answer)
Explanation: ***Topiramate***
- **Topiramate** is strongly associated with acute angle-closure glaucoma, often presenting with **myopic shift** and **ciliary body edema**, leading to closure of the anterior chamber angle.
- The patient's symptoms of **acute vision loss**, **halos around lights**, **severe frontal headache**, and findings of **shallow anterior chambers** with **closed angles bilaterally** are classic for topiramate-induced angle closure.
- Topiramate is a **sulfonamide derivative** that causes ciliochoroidal effusion, leading to anterior rotation of the ciliary body and forward displacement of the lens-iris diaphragm.
*Tiagabine*
- **Tiagabine** is associated with central nervous system side effects such as dizziness, somnolence, and confusion.
- It is not typically linked to ophthalmological side effects involving acute angle-closure glaucoma.
*Zonisamide*
- **Zonisamide** is also a **sulfonamide derivative** and can rarely cause acute angle-closure glaucoma through a similar mechanism to topiramate.
- However, **topiramate** is more commonly and strongly associated with this adverse effect.
- Zonisamide is also known for other side effects like kidney stones and metabolic acidosis.
*Lamotrigine*
- **Lamotrigine** is primarily known for skin reactions such as Stevens-Johnson syndrome and toxic epidermal necrolysis.
- Ocular side effects are generally mild and do not include acute angle-closure glaucoma.
*Gabapentin*
- **Gabapentin** common side effects include drowsiness, dizziness, and peripheral edema.
- It is not associated with acute angle-closure glaucoma or the specific constellation of ocular symptoms described.
Question 360: An 85-year-old man presents with the reappearance of his Parkinson’s disease (PD) symptoms over the last few months. He says he has been treated with various drugs over the last 20 years, but that currently his symptoms worsen as he nears the time for his next dose of medication. His movements have been slower lately and it’s difficult to initiate voluntary movements. His past medical history is significant for hypertension. He was diagnosed 10 years ago and was well-managed on medication. His current medications are levodopa/carbidopa, rasagiline, aspirin, and captopril. The vital signs include: pulse 70/min, respiratory rate 15/min, blood pressure 130/76 mm Hg, and temperature 36.7°C (98.1°F). Physical examination reveals the expected ‘pill-rolling’ resting tremor, which is alleviated by movement. Increased tone of arm muscles and resistance to passive movement at the joints is noted. When asked to walk across the room, he has difficulty taking the 1st step and has a stooped posture and takes short, shuffling, rapid steps. Laboratory studies show:
Serum glucose (fasting) 97 mg/dL
Sodium 141 mEq/L
Potassium 4.0 mEq/L
Chloride 100 mEq/L
Cholesterol (total) 190 mg/dL
HDL-cholesterol 42 mg/dL
LDL-cholesterol 70 mg/dL
Triglycerides 184 mg/dL
The patient is started on a drug that increases the efficacy of his current anti-PD medication. Which of the following is most likely the drug that was added to this patient’s current regimen?
A. Entacapone (Correct Answer)
B. Atorvastatin
C. Benztropine
D. Selegiline
E. Bromocriptine
Explanation: ***Entacapone***
- The patient is experiencing motor fluctuations, specifically "wearing-off" phenomena, where symptoms worsen before the next dose of **levodopa/carbidopa** is due. Entacapone, a **COMT inhibitor**, prolongs the half-life of levodopa, increasing its availability to the brain.
- This drug acts by inhibiting the peripheral breakdown of levodopa by **catechol-O-methyltransferase (COMT)**, thereby increasing the amount of levodopa that crosses the blood-brain barrier.
*Atorvastatin*
- Atorvastatin is a **statin medication** used to lower cholesterol levels and is not indicated for the management of Parkinson's disease symptoms.
- While the patient's lipids show high triglycerides and low HDL, the question specifically asks for a drug to improve Parkinson's symptoms.
*Benztropine*
- Benztropine is an **anticholinergic medication** used to treat tremors and rigidity in Parkinson's disease.
- However, it is generally avoided in elderly patients due to its potential to cause cognitive side effects and is not primarily used to address "wearing-off" phenomena.
*Selegiline*
- Selegiline is a **monoamine oxidase-B (MAO-B) inhibitor** that prevents the breakdown of dopamine in the brain, and it is already part of the patient's current regimen (rasagiline is also an MAO-B inhibitor).
- While it helps with PD symptoms, adding another MAO-B inhibitor or increasing its dose would not directly address the "wearing-off" phenomenon as effectively as a COMT inhibitor.
*Bromocriptine*
- Bromocriptine is a **dopamine agonist** that directly stimulates dopamine receptors in the brain.
- While dopamine agonists can be used in Parkinson's disease, they are typically considered for early-stage disease or as an adjunct, and are not the first-line choice for levodopa "wearing-off" in an elderly patient.