A well-dressed couple presents to the emergency department with sudden onset of headache, a sensation of floating, and weakness of arms and legs after eating a plate of shellfish 2 hours ago. They mention that they had experienced tingling of the lips and mouth within 15 minutes of ingesting the shellfish. They also complain of mild nausea and abdominal discomfort. On physical examination, their vital signs are within normal limits. Their neurological examination reveals decreased strength in all extremities bilaterally and hyporeflexia. After detailed laboratory evaluation, the physician confirms the diagnosis of paralysis due to the presence of a specific toxin in the shellfish they had consumed. Which of the following mechanisms best explains the action of the toxin these patients had consumed?
Q122
A 64-year-old woman comes to the physician because of gradually worsening blurry vision in both eyes for 5 months. She has also had intermittent headaches for the past 2 months. She has type 2 diabetes mellitus, osteoarthritis, second-degree heart block, and presbyopia. Her current medications include metformin, lisinopril, and ibuprofen. Examination shows bilateral equal and reactive pupils. The best-corrected visual acuity in each eye is 20/40. There is narrowing of her visual fields bilaterally. Fundoscopic examination shows bilateral narrowing of the outer rim of the optic nerve head and cupping of the optic disk. Intraocular pressure by applanation tonometry is 27 mm Hg in the right eye and 26 mm Hg in the left eye (N=10–21 mm Hg). Gonioscopy shows no abnormalities. Which of the following is the most appropriate next step in management?
Q123
A 14-year-old boy is admitted to the emergency department with acute onset of confusion, malaise, diffuse abdominal pain, nausea, and a single episode of vomiting. He denies ingestion of any suspicious foods, fevers, respiratory symptoms, or any other symptoms preceding his current condition. However, he notes an increase in his liquid consumption and urinary frequency over the last 6 months. On physical examination, he is responsive but somnolent. His blood pressure is 90/50 mm Hg, heart rate is 101/min, respiratory rate is 21/min, temperature is 36.0°C (96.8°F), and SpO2 is 96% on room air. He has facial pallor and dry skin and mucous membranes. His lungs are clear to auscultation, and heart sounds are normal. His abdomen is soft with no rebound tenderness on palpation. Neurological examination is significant for 1+ deep tendon reflexes in all extremities. A dipstick test shows 3+ for ketones and glucose. The patient’s blood tests show the following findings:
RBCs 4.1 million/mm3
Hb 13.7 mg/dL
Hematocrit 56%
Leukocyte count 7,800/mm3
Platelet count 321,000/mm3
Glucose 565 mg/dL
Potassium 5.8 mEq/L
Sodium 136 mEq/L
ALT 15 U/L
AST 17 U/L
Amylase 88 U/L
Bicarbonate 19 mEq/L
BE −3 mEq/L
pH 7.3
pCO2 37 mm Hg
pO2 66 mm Hg
Which of the medications listed below should be administered to the patient intravenously?
Q124
A 25-year-old woman comes into her family doctor’s clinic confused as to how she failed her work-required urine drug test. The patient has no significant past medical history and takes no medications. She states that she does not smoke and denies ever using any alcohol or recreational drugs. The patient’s social history reveals a recent change in her diet. For the past 2-weeks, she was experimenting with a ketogenic diet and using poppy seed bagels as her only source of carbohydrates. Her vital signs and physical examination are within normal limits. Which of the following physical exam findings might be present had this patient really been abusing the class of drug for which she most likely tested positive?
Q125
A 32-year-old woman comes to the clinic with concerns related to her medication. She recently learned that she is pregnant and wants to know if she needs to change anything. She is taking levothyroxine for hypothyroidism. She does not take any other medication. A urine pregnancy test is positive. What should this patient be advised about her medication during pregnancy?
Q126
A 48-year-old man is brought to the emergency department 20 minutes after being rescued from a house fire. He reports headache, metallic taste, abdominal pain, and nausea. He appears confused and agitated. His pulse is 125/min, respirations are 33/min, and blood pressure is 100/65 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 98%. Physical examination shows a bright red color of the skin. His breath smells of bitter almonds. Hyperbaric oxygen therapy and appropriate pharmacotherapy are initiated. The expected beneficial effect of this drug is most likely due to which of the following mechanisms?
Q127
A 71-year-old man is brought to the emergency department by his wife because of increasing confusion, weakness, and vomiting for 1 day. He has had 5 episodes of vomiting and blurry vision; he told his wife that "everything appears in different colors." He has been unable to recall his wife's name or their address. His wife reports that his drug regimen was adjusted because of worsening tibial edema 1 week ago. He has congestive heart failure, atrial fibrillation, hypothyroidism, and osteoarthritis. Current medications include rivaroxaban, metoprolol, digoxin, levothyroxine, spironolactone, and furosemide. His temperature is 36.7°C (98°F), pulse is 56/min, and blood pressure is 98/68 mm Hg. He is confused and oriented only to person. Neurologic examination shows no focal findings. The abdomen is soft, and there is tenderness to palpation of both lower quadrants without guarding or rebound. There is 1+ pitting edema of both ankles. This patient is most likely to have which of the following ECG findings?
Q128
An 81-year-old man is admitted to the hospital due to acute decompensated heart failure. He has type 2 diabetes mellitus, hypertension, coronary artery disease, and congestive heart failure. Current medications include lisinopril, metformin, and low-dose aspirin. He has smoked one pack of cigarettes daily for 45 years. His temperature is 37.6°C (99.7°F), pulse is 105/min and regular, respirations are 21/min, and blood pressure is 103/64 mm Hg. Laboratory studies show:
Hemoglobin 13.7 g/dL
Leukocyte count 8200/mm3
Serum
Na+ 128 mEq/L
Cl- 98 mEq/L
K+ 4.9 mEq/L
Urea nitrogen 58 mg/dL
Glucose 200 mg/dL
Creatinine 2.2 mg/dL
Which of the following changes in the medication regimen is most appropriate in this patient at this time?
Q129
A 48-year-old woman comes to the physician because of recurrent right upper abdominal pain for 3 weeks. The pain usually occurs after meals and tends to radiate to the right shoulder. She reports that she otherwise feels well. She has more energy since she started an intermittent fasting diet and has rapidly lost 9.0 kg (20 lbs). She is 160 cm (5 ft 3 in) tall and weighs 100 kg (220 lb); BMI is 39.1 kg/m2. Physical examination shows a nontender abdomen. Abdominal ultrasonography shows several small stones in the gallbladder without calcification. When discussing treatment options, she states that she does not wish to undergo surgery and asks about other possibilities. Which of the following is the most appropriate pharmacotherapy to address the underlying cause of this patient's condition?
Q130
A 62-year-old Caucasian male receiving treatment for stable angina experiences intermittent throbbing headaches. What is the most likely cause?
Autonomic/CV Drugs US Medical PG Practice Questions and MCQs
Question 121: A well-dressed couple presents to the emergency department with sudden onset of headache, a sensation of floating, and weakness of arms and legs after eating a plate of shellfish 2 hours ago. They mention that they had experienced tingling of the lips and mouth within 15 minutes of ingesting the shellfish. They also complain of mild nausea and abdominal discomfort. On physical examination, their vital signs are within normal limits. Their neurological examination reveals decreased strength in all extremities bilaterally and hyporeflexia. After detailed laboratory evaluation, the physician confirms the diagnosis of paralysis due to the presence of a specific toxin in the shellfish they had consumed. Which of the following mechanisms best explains the action of the toxin these patients had consumed?
A. Inactivation of syntaxin
B. Increased opening of presynaptic calcium channels
C. Blockade of voltage-gated fast sodium channels (Correct Answer)
D. Inactivation of synaptobrevin
E. Inhibition of acetylcholinesterase
Explanation: ***Blockade of voltage-gated fast sodium channels***
- The symptoms described, particularly **tingling of the lips and mouth**, **sensation of floating**, **weakness**, and **paralysis** after consuming shellfish, are classic for **paralytic shellfish poisoning (PSP)** caused by **saxitoxin**.
- Saxitoxin acts by **blocking voltage-gated fast sodium channels** in excitable membranes (neurons and muscles), preventing depolarization and impulse propagation.
*Inactivation of syntaxin*
- **Syntaxin** is a **SNARE protein** involved in the fusion of synaptic vesicles with the presynaptic membrane, essential for neurotransmitter release.
- Toxins like **botulinum neurotoxins** (specifically serotypes C1, A, E) can cleave syntaxin, leading to **flaccid paralysis** by preventing acetylcholine release. However, the onset and nature of symptoms (e.g., tingling, sensation of floating) differ from botulism.
*Increased opening of presynaptic calcium channels*
- Increased opening of **presynaptic calcium channels** would lead to **exaggerated neurotransmitter release**, resulting in symptoms like **spasms** or **tetany**, not flaccid paralysis or weakness.
- Examples include **black widow spider venom** (alpha-latrotoxin), which causes a massive influx of presynaptic calcium and widespread acetylcholine release.
*Inactivation of synaptobrevin*
- **Synaptobrevin** (also known as VAMP) is another **SNARE protein** located on synaptic vesicles, crucial for neurotransmitter release.
- **Tetanus toxin** and **other botulinum neurotoxins** (serotypes B, D, F, G) specifically cleave synaptobrevin, preventing vesicle fusion and neurotransmitter release, leading to **spastic paralysis** (tetanus) or **flaccid paralysis** (botulism).
*Inhibition of acetylcholinesterase*
- **Acetylcholinesterase inhibitors** prevent the breakdown of **acetylcholine** in the synaptic cleft, leading to an **accumulation of acetylcholine** and continuous stimulation of cholinergic receptors.
- This would result in symptoms like **salivation, lacrimation, urination, defecation, gastrointestinal upset, emesis (SLUDGE)**, muscle fasciculations, and eventually paralysis due to prolonged depolarization block, which is not consistent with the primary symptoms experienced by the patients.
Question 122: A 64-year-old woman comes to the physician because of gradually worsening blurry vision in both eyes for 5 months. She has also had intermittent headaches for the past 2 months. She has type 2 diabetes mellitus, osteoarthritis, second-degree heart block, and presbyopia. Her current medications include metformin, lisinopril, and ibuprofen. Examination shows bilateral equal and reactive pupils. The best-corrected visual acuity in each eye is 20/40. There is narrowing of her visual fields bilaterally. Fundoscopic examination shows bilateral narrowing of the outer rim of the optic nerve head and cupping of the optic disk. Intraocular pressure by applanation tonometry is 27 mm Hg in the right eye and 26 mm Hg in the left eye (N=10–21 mm Hg). Gonioscopy shows no abnormalities. Which of the following is the most appropriate next step in management?
A. Surgical trabeculectomy
B. Topical pilocarpine therapy
C. Topical latanoprost therapy (Correct Answer)
D. Laser iridotomy
E. Topical timolol
Explanation: ### ***Topical latanoprost therapy***
- This patient's presentation, including elevated **intraocular pressure**, **bilateral visual field narrowing**, and **optic disc cupping**, is highly suggestive of **primary open-angle glaucoma (POAG)**.
- **Topical prostaglandin analogs** like latanoprost are the **first-line treatment** for POAG due to their efficacy in reducing intraocular pressure by increasing **uveoscleral outflow**.
- Latanoprost is particularly appropriate for this patient given her **second-degree heart block**, as it avoids the cardiac effects associated with beta-blockers.
### *Surgical trabeculectomy*
- **Trabeculectomy** is a surgical procedure typically reserved for cases where medical therapy fails to adequately control intraocular pressure or when there is progressive visual field loss despite maximal medical treatment.
- It is generally not the initial management step for newly diagnosed **primary open-angle glaucoma (POAG)**.
### *Topical pilocarpine therapy*
- **Pilocarpine** is a **miotic agent** that increases **trabecular outflow** but is generally considered a second or third-line agent for glaucoma due to its significant side effects, such as **ciliary spasm**, **brow ache**, and **miosis**, which can impair vision, especially in older patients.
- It is not the preferred initial therapy over prostaglandin analogs or beta-blockers.
### *Laser iridotomy*
- **Laser iridotomy** is the definitive treatment for **angle-closure glaucoma** where the iris blocks the trabecular meshwork.
- The patient's **gonioscopy showed no abnormalities**, indicating an **open-angle**, ruling out angle-closure glaucoma.
### *Topical timolol*
- **Topical timolol**, a **beta-blocker**, lowers intraocular pressure by **decreasing aqueous humor production**. While it is an effective first-line agent for POAG, it should be used with caution in patients with **second-degree heart block** due to potential cardiac effects from systemic absorption.
- Latanoprost is preferred in this patient given her cardiac comorbidity, as it offers once-daily dosing and avoids beta-blocker-related cardiac risks.
Question 123: A 14-year-old boy is admitted to the emergency department with acute onset of confusion, malaise, diffuse abdominal pain, nausea, and a single episode of vomiting. He denies ingestion of any suspicious foods, fevers, respiratory symptoms, or any other symptoms preceding his current condition. However, he notes an increase in his liquid consumption and urinary frequency over the last 6 months. On physical examination, he is responsive but somnolent. His blood pressure is 90/50 mm Hg, heart rate is 101/min, respiratory rate is 21/min, temperature is 36.0°C (96.8°F), and SpO2 is 96% on room air. He has facial pallor and dry skin and mucous membranes. His lungs are clear to auscultation, and heart sounds are normal. His abdomen is soft with no rebound tenderness on palpation. Neurological examination is significant for 1+ deep tendon reflexes in all extremities. A dipstick test shows 3+ for ketones and glucose. The patient’s blood tests show the following findings:
RBCs 4.1 million/mm3
Hb 13.7 mg/dL
Hematocrit 56%
Leukocyte count 7,800/mm3
Platelet count 321,000/mm3
Glucose 565 mg/dL
Potassium 5.8 mEq/L
Sodium 136 mEq/L
ALT 15 U/L
AST 17 U/L
Amylase 88 U/L
Bicarbonate 19 mEq/L
BE −3 mEq/L
pH 7.3
pCO2 37 mm Hg
pO2 66 mm Hg
Which of the medications listed below should be administered to the patient intravenously?
A. Insulin detemir
B. Regular insulin (Correct Answer)
C. Cefazolin
D. Potassium chloride
E. Isophane insulin
Explanation: **Regular insulin**
- The patient presents with **diabetic ketoacidosis (DKA)**, characterized by **hyperglycemia** (glucose 565 mg/dL), **ketonuria** (ketones 3+), and **metabolic acidosis** (pH 7.3, bicarbonate 19 mEq/L, BE -3 mEq/L). **Intravenous regular insulin** is the cornerstone of DKA treatment to lower blood glucose and resolve ketosis.
- Regular insulin is the only type of insulin that can be administered intravenously and has a **rapid onset** and **short duration of action**, allowing for precise titration and quick correction of severe hyperglycemia and acidosis.
*Insulin detemir*
- **Insulin detemir** is a **long-acting insulin analog** primarily used for basal insulin replacement, not for acute management of severe hyperglycemia or DKA.
- It has a **slow onset of action** (1-2 hours) and a prolonged duration (up to 24 hours), making it unsuitable for the urgent and rapid correction required in DKA.
*Cefazolin*
- **Cefazolin** is a **first-generation cephalosporin antibiotic** used to treat bacterial infections.
- This patient's symptoms are consistent with DKA, not a bacterial infection, and there is no indication for antibiotic therapy.
*Potassium chloride*
- Despite the patient's **hyperkalemia** (potassium 5.8 mEq/L) at presentation, DKA treatment with insulin will shift potassium intracellularly, leading to **hypokalemia**.
- **Potassium chloride** is typically added to IV fluids **after insulin therapy has begun and potassium levels start to drop**, to prevent severe hypokalemia, not as an initial treatment when levels are already high.
*Isophane insulin*
- **Isophane insulin (NPH)** is an **intermediate-acting insulin** that is administered subcutaneously.
- It has a **delayed onset of action** (2-4 hours) and cannot be given intravenously, making it inappropriate for the acute management of DKA.
Question 124: A 25-year-old woman comes into her family doctor’s clinic confused as to how she failed her work-required urine drug test. The patient has no significant past medical history and takes no medications. She states that she does not smoke and denies ever using any alcohol or recreational drugs. The patient’s social history reveals a recent change in her diet. For the past 2-weeks, she was experimenting with a ketogenic diet and using poppy seed bagels as her only source of carbohydrates. Her vital signs and physical examination are within normal limits. Which of the following physical exam findings might be present had this patient really been abusing the class of drug for which she most likely tested positive?
A. Tachypnea
B. Myalgia
C. Anhidrosis
D. Conjunctival injection
E. Miosis (Correct Answer)
Explanation: ***Miosis***
- Poppy seeds can cause a false positive for **opiates** (morphine/codeine) on urine drug screens. Acute opiate intoxication typically causes **miosis** (pinpoint pupils) due to parasympathetic stimulation.
- Other signs of acute opiate intoxication include **respiratory depression** and **CNS depression**.
*Tachypnea*
- **Tachypnea** (increased respiratory rate) is not a typical sign of acute opiate intoxication; rather, **bradypnea** or **respiratory depression** is characteristic.
- Tachypnea is more commonly seen with stimulant abuse, anxiety, or metabolic acidosis.
*Myalgia*
- **Myalgia** (muscle pain) is a common symptom of **opiate withdrawal**, not acute intoxication.
- During acute opiate use, patients more commonly experience analgesia.
*Anhidrosis*
- The class of drugs involved here is **opiates**, which typically cause **diaphoresis** (sweating), not anhidrosis (absence of sweating).
- Anhidrosis can be a symptom of certain neurological conditions or anticholinergic toxicity.
*Conjunctival injection*
- **Conjunctival injection** (red eyes) is more commonly associated with **cannabis use**.
- Opiate intoxication typically causes **miosis** and sometimes mild conjunctival changes but not prominent injection.
Question 125: A 32-year-old woman comes to the clinic with concerns related to her medication. She recently learned that she is pregnant and wants to know if she needs to change anything. She is taking levothyroxine for hypothyroidism. She does not take any other medication. A urine pregnancy test is positive. What should this patient be advised about her medication during pregnancy?
A. She can continue taking her medication at the usual dose
B. She should be switched to an alternative medication
C. Her medication dose should be increased by 30% (Correct Answer)
D. She should stop taking her medication immediately
E. The decision should be based on an evaluation of fetal risks and maternal benefits
Explanation: ***Her medication dose should be increased by 30%***
- During pregnancy, **levothyroxine** requirements typically increase by **25-50%** due to increased maternal metabolism, estrogen-induced increases in thyroid-binding globulin, and fetal thyroid hormone needs.
- An increase of approximately **30%** is a common initial adjustment, with further titration based on TSH levels.
*She can continue taking her medication at the usual dose*
- Continuing the usual dose of **levothyroxine** without adjustment is likely to result in **suboptimal thyroid hormone levels**, as pregnancy significantly increases the demand for thyroid hormones.
- **Maternal hypothyroidism** during pregnancy is associated with adverse outcomes for both the mother and the fetus, including pre-eclampsia, preterm birth, and impaired neurodevelopment in the child.
*She should be switched to an alternative medication*
- **Levothyroxine** is the **treatment of choice** for hypothyroidism during pregnancy and is considered safe for both mother and fetus.
- There is typically no medical reason to switch to an alternative medication for treating hypothyroidism during pregnancy.
*She should stop taking her medication immediately*
- Discontinuing **levothyroxine** immediately would lead to uncontrolled **maternal hypothyroidism**, which poses a significant risk to the developing fetus, impacting neurodevelopment and increasing the risk of obstetric complications.
- **Thyroid hormone** is crucial for proper fetal growth and development, especially in the first trimester before the fetal thyroid gland is fully functional.
*The decision should be based on an evaluation of fetal risks and maternal benefits*
- While evaluating fetal risks and maternal benefits is generally prudent for medication decisions in pregnancy, for **levothyroxine**, the **benefits overwhelmingly outweigh any risks**, and maintaining optimal thyroid function is critical.
- The primary decision regarding **levothyroxine** in pregnancy is not whether to continue but rather how to **adjust the dose** to meet increased physiological demands.
Question 126: A 48-year-old man is brought to the emergency department 20 minutes after being rescued from a house fire. He reports headache, metallic taste, abdominal pain, and nausea. He appears confused and agitated. His pulse is 125/min, respirations are 33/min, and blood pressure is 100/65 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 98%. Physical examination shows a bright red color of the skin. His breath smells of bitter almonds. Hyperbaric oxygen therapy and appropriate pharmacotherapy are initiated. The expected beneficial effect of this drug is most likely due to which of the following mechanisms?
A. Synthesis of 2,3-bisphosphoglycerate
B. Formation of methemoglobin (Correct Answer)
C. Inhibition of cytochrome c oxidase
D. Dissociation of carboxyhemoglobin
E. Reduction of ferric iron
Explanation: ***Formation of methemoglobin***
- This patient's symptoms (headache, confusion, bright red skin, bitter almond breath, high pulse oximetry despite severe symptoms) are classic for **cyanide poisoning**.
- Many antidotes for cyanide poisoning, such as **nitrites**, work by forming **methemoglobin**, which has a higher affinity for cyanide than cytochrome c oxidase, thus detaching cyanide from the enzyme and allowing cellular respiration to resume.
*Synthesis of 2,3-bisphosphoglycerate*
- **2,3-bisphosphoglycerate (2,3-BPG)** helps regulate oxygen release from hemoglobin in red blood cells.
- While important for oxygen delivery, increasing 2,3-BPG is not a direct therapeutic mechanism for **cyanide poisoning**.
*Inhibition of cytochrome c oxidase*
- **Cyanide** itself inhibits cytochrome c oxidase, leading to cellular hypoxia despite adequate oxygen supply.
- The therapeutic goal is to reverse this inhibition, not to further inhibit the enzyme.
*Dissociation of carboxyhemoglobin*
- **Carbon monoxide poisoning**, not cyanide poisoning, causes carboxyhemoglobin formation and presents with cherry-red skin, but there is no foul-smelling breath.
- Dissociating carboxyhemoglobin is relevant for carbon monoxide poisoning, not cyanide poisoning.
*Reduction of ferric iron*
- Reducing ferric iron (Fe3+) back to ferrous iron (Fe2+) would reverse **methemoglobinemia**, which is often a side effect of some cyanide antidotes.
- The therapeutic strategy for cyanide poisoning involves *inducing* methemoglobinemia to sequester cyanide.
Question 127: A 71-year-old man is brought to the emergency department by his wife because of increasing confusion, weakness, and vomiting for 1 day. He has had 5 episodes of vomiting and blurry vision; he told his wife that "everything appears in different colors." He has been unable to recall his wife's name or their address. His wife reports that his drug regimen was adjusted because of worsening tibial edema 1 week ago. He has congestive heart failure, atrial fibrillation, hypothyroidism, and osteoarthritis. Current medications include rivaroxaban, metoprolol, digoxin, levothyroxine, spironolactone, and furosemide. His temperature is 36.7°C (98°F), pulse is 56/min, and blood pressure is 98/68 mm Hg. He is confused and oriented only to person. Neurologic examination shows no focal findings. The abdomen is soft, and there is tenderness to palpation of both lower quadrants without guarding or rebound. There is 1+ pitting edema of both ankles. This patient is most likely to have which of the following ECG findings?
A. Low QRS voltage
B. Increased PR interval (Correct Answer)
C. Mobitz type 2 atrioventricular block
D. Prolonged QT interval
E. Peaked T waves
Explanation: ***Increased PR interval***
- The patient's symptoms (confusion, weakness, vomiting, blurry vision with "everything appears in different colors," bradycardia) are classic signs of **digoxin toxicity**. Digoxin primarily affects the **AV node**, leading to slowed conduction and thus an **increased PR interval** on ECG.
- The recent adjustment of his diuretic regimen (spironolactone and furosemide) for worsening edema suggests possible **hypokalemia** or **renal impairment**, which can precipitate digoxin toxicity even at therapeutic levels.
*Low QRS voltage*
- **Low QRS voltage** is typically associated with conditions like **pericardial effusion**, severe hypothyroidism, or diffuse myocardial disease, which are not directly suggested by the patient's acute presentation.
- While the patient has hypothyroidism, acute digoxin toxicity does not primarily cause low QRS voltage.
*Mobitz type 2 atrioventricular block*
- While digoxin toxicity can cause various arrhythmias, **Mobitz type 2 AV block** (characterized by constant PR interval before a dropped beat) usually indicates issues deeper in the His-Purkinje system.
- **First-degree AV block** (increased PR interval) and **Wenckebach (Mobitz type 1) AV block** are more common manifestations of digoxin's direct inhibitory effect on the AV node.
*Prolonged QT interval*
- A **prolonged QT interval** is associated with an increased risk of **Torsades de Pointes** and can be caused by certain antiarrhythmics (e.g., amiodarone, sotalol) or electrolyte imbalances, but it is not a direct or typical ECG finding of digoxin toxicity.
- Digoxin toxicity is more commonly associated with a **shortened QT interval** or "scooping" of the ST segment.
*Peaked T waves*
- **Peaked T waves** are a hallmark of **hyperkalemia**, an electrolyte disturbance that can cause cardiac arrhythmias and muscle weakness.
- While electrolyte imbalances can contribute to digoxin toxicity, peaked T waves themselves are not a direct consequence of digoxin.
Question 128: An 81-year-old man is admitted to the hospital due to acute decompensated heart failure. He has type 2 diabetes mellitus, hypertension, coronary artery disease, and congestive heart failure. Current medications include lisinopril, metformin, and low-dose aspirin. He has smoked one pack of cigarettes daily for 45 years. His temperature is 37.6°C (99.7°F), pulse is 105/min and regular, respirations are 21/min, and blood pressure is 103/64 mm Hg. Laboratory studies show:
Hemoglobin 13.7 g/dL
Leukocyte count 8200/mm3
Serum
Na+ 128 mEq/L
Cl- 98 mEq/L
K+ 4.9 mEq/L
Urea nitrogen 58 mg/dL
Glucose 200 mg/dL
Creatinine 2.2 mg/dL
Which of the following changes in the medication regimen is most appropriate in this patient at this time?
A. Begin vancomycin therapy
B. Discontinue aspirin therapy
C. Begin nitroprusside therapy
D. Discontinue metformin therapy (Correct Answer)
E. Begin hydrochlorothiazide therapy
Explanation: ***Discontinue metformin therapy***
- The patient has **acute decompensated heart failure** with **acute kidney injury** (creatinine 2.2 mg/dL, BUN 58 mg/dL). Metformin is **contraindicated in acute kidney injury** due to the significantly increased risk of **lactic acidosis**.
- With renal failure, metformin excretion is impaired, leading to drug accumulation and dangerous elevations in lactic acid levels. **Immediate discontinuation** is critical to prevent this life-threatening complication.
- Current guidelines recommend avoiding metformin when eGFR <30 mL/min or creatinine >1.5 mg/dL in males.
*Begin vancomycin therapy*
- There is **no indication of bacterial infection** (normal leukocyte count 8200/mm³, only mild temperature elevation to 37.6°C, no localizing signs).
- Initiating broad-spectrum antibiotics like vancomycin without clear evidence of infection contributes to **antibiotic resistance** and potential adverse effects.
*Discontinue aspirin therapy*
- The patient has a history of **coronary artery disease** and **congestive heart failure**, making him high risk for acute coronary events.
- Aspirin provides crucial **antiplatelet therapy** for secondary prevention of cardiovascular events in this patient population and should be continued.
*Begin nitroprusside therapy*
- Nitroprusside is a potent vasodilator used in **hypertensive emergencies** or severe heart failure with elevated blood pressure.
- This patient currently has **hypotension** (BP 103/64 mm Hg), and nitroprusside would further lower blood pressure, potentially causing cardiovascular collapse and end-organ hypoperfusion.
*Begin hydrochlorothiazide therapy*
- While diuretics are used in heart failure, hydrochlorothiazide is a **thiazide diuretic** primarily effective with preserved renal function (eGFR >30 mL/min).
- This patient has **elevated creatinine (2.2 mg/dL)**, indicating acute kidney injury, which would significantly limit the efficacy of hydrochlorothiazide. **Loop diuretics** (furosemide) would be more appropriate if diuresis is needed in the setting of renal impairment.
Question 129: A 48-year-old woman comes to the physician because of recurrent right upper abdominal pain for 3 weeks. The pain usually occurs after meals and tends to radiate to the right shoulder. She reports that she otherwise feels well. She has more energy since she started an intermittent fasting diet and has rapidly lost 9.0 kg (20 lbs). She is 160 cm (5 ft 3 in) tall and weighs 100 kg (220 lb); BMI is 39.1 kg/m2. Physical examination shows a nontender abdomen. Abdominal ultrasonography shows several small stones in the gallbladder without calcification. When discussing treatment options, she states that she does not wish to undergo surgery and asks about other possibilities. Which of the following is the most appropriate pharmacotherapy to address the underlying cause of this patient's condition?
A. Ezetimibe
B. Hydromorphone
C. Ursodeoxycholic acid (Correct Answer)
D. Gemfibrozil
E. Colestipol
Explanation: ***Ursodeoxycholic acid***
- This medication is a **bile acid** that can dissolve **cholesterol gallstones** by reducing cholesterol synthesis and secretion into bile, and by stabilizing the gallbladder membrane.
- It is appropriate for patients with **symptomatic gallstones** who are poor surgical candidates or refuse surgery, especially when the stones are small and non-calcified.
*Ezetimibe*
- This drug works by inhibiting the absorption of **cholesterol** from the small intestine.
- While it lowers cholesterol, it is not a primary treatment for dissolving existing **gallstones**.
*Hydromorphone*
- This is an **opioid analgesic** used for managing severe pain.
- It would only mask the symptoms of gallstones and does not address the underlying pathology or dissolution of the stones.
*Gemfibrozil*
- This fibrate medication primarily lowers **triglycerides** and can also increase HDL cholesterol.
- It works by activating peroxisome proliferator-activated receptor alpha (PPAR-alpha) but is not indicated for dissolving gallstones.
*Colestipol*
- This is a **bile acid sequestrant** that binds bile acids in the intestine, preventing their reabsorption and increasing their excretion.
- While it lowers cholesterol, it can actually **increase the risk of gallstone formation** by altering bile composition rather than dissolving them.
Question 130: A 62-year-old Caucasian male receiving treatment for stable angina experiences intermittent throbbing headaches. What is the most likely cause?
A. Transient ischemic attack
B. Beta adrenergic inactivation
C. Acute hemorrhage
D. Vasodilation of cerebral arteries (Correct Answer)
E. Elevated creatine kinase
Explanation: ***Vasodilation of cerebral arteries***
- Many medications used to treat **stable angina**, such as **nitrates**, achieve their therapeutic effect through **vasodilation**.
- This vasodilation can extend to the **cerebral arteries**, leading to an increase in intracranial arterial pulsatility, which is often perceived as a **throbbing headache**.
*Transient ischemic attack*
- A TIA typically presents with **focal neurological deficits** (e.g., weakness, numbness, speech difficulties) that resolve within 24 hours, not primarily with isolated headaches.
- While headache can occur, it's not the hallmark symptom and usually accompanies other transient neurological symptoms.
*Beta adrenergic inactivation*
- **Beta-blockers**, while used for angina, typically do not cause throbbing headaches; in fact, they are sometimes used to prevent migraines.
- **Inactivation** or withdrawal of beta-blockers might cause rebound symptoms but regular use is not linked to this type of headache.
*Acute hemorrhage*
- An **acute hemorrhage**, especially in the brain, often causes a **sudden, severe "thunderclap" headache** accompanied by neurological deficits, altered mental status, or signs of meningeal irritation, which are not described here as intermittent or mild.
- The description of "intermittent throbbing headaches" does not fit the typical presentation of an acute intracranial hemorrhage.
*Elevated creatine kinase*
- **Elevated creatine kinase (CK)** indicates muscle damage and is not directly related to headaches.
- While some medications (e.g., statins) can cause myopathy and elevated CK, this is not a common cause of headaches, particularly throbbing ones.