A patient has been taking digoxin for several years for chronic heart failure is about to receive atropine for another condition. A common effect of digoxin (at therapeutic blood levels) that can be almost entirely blocked by atropine is

Correct Answer: C

Rationale: In this scenario, the correct answer is C) Increased PR interval on the ECG. Digoxin, a medication used for chronic heart failure, can lead to an increased PR interval on the ECG as one of its effects. Digoxin slows down conduction through the atrioventricular (AV) node, prolonging the PR interval. Atropine, on the other hand, is a medication that blocks the effects of the parasympathetic nervous system, including the vagus nerve, which slows down heart rate. By blocking the parasympathetic effects, atropine can counteract the bradycardic effects of digoxin, hence reducing the prolonged PR interval caused by digoxin. Option A) Decreased appetite is not directly related to the pharmacological actions of digoxin or atropine. Option B) Increased atrial contractility is a common effect of digoxin, but atropine does not block this effect. Option D) Headaches are not a typical effect of digoxin or atropine in this context. Educationally, understanding the interactions between medications targeting the autonomic nervous system, such as digoxin and atropine, is crucial for healthcare professionals to ensure safe and effective patient care. This scenario highlights the importance of considering potential drug interactions and their effects on cardiac conduction when managing patients with multiple comorbidities requiring different medications.

Correct Answer: C

Rationale: The correct answer is C) Trimethaphan. Trimethaphan is an antagonist of ganglion type nicotinic receptors. Ganglionic blockers like Trimethaphan act on nicotinic receptors in autonomic ganglia, blocking transmission in both sympathetic and parasympathetic ganglia. This results in decreased sympathetic and parasympathetic tone, leading to effects such as reduced heart rate and blood pressure. Option A, Tubocurarine, is a neuromuscular blocking agent that acts at the neuromuscular junction, not at ganglionic nicotinic receptors. Option B, α-bungarotoxin, is a neurotoxin found in snake venom that binds irreversibly to nicotinic acetylcholine receptors at neuromuscular junctions, not ganglionic receptors. Educational context: Understanding the mechanisms of action of drugs that target the peripheral nervous system is crucial in pharmacology. Knowing the specific receptors targeted by each drug helps in predicting their effects and potential side effects. It is important for healthcare professionals to be able to differentiate between drugs affecting different types of nicotinic receptors for safe and effective patient care.

Correct Answer: A

Rationale: In this scenario, the correct answer is A) Acetazolamide. Acetazolamide is a carbonic anhydrase inhibitor that can lead to hyperammonemia in patients with severe liver disease like cirrhosis. Hyperammonemia can result in encephalopathy, leading to symptoms such as confusion, coma, and even death. Option B) Amiloride is a potassium-sparing diuretic and is not typically associated with causing coma in cirrhotic patients. Option C) Furosemide and Option D) Hydrochlorothiazide are loop and thiazide diuretics, respectively, which do not directly affect ammonia metabolism and are less likely to cause coma in this patient population. Educationally, this question highlights the importance of understanding the pharmacological effects of medications in patients with liver disease. It emphasizes the need for healthcare providers to consider the potential adverse effects of drugs in individuals with compromised liver function to prevent serious complications like hepatic encephalopathy.

Correct Answer: A

Rationale: In the therapy of hypercalcemia, the least likely useful option is A) Thiazide diuretics. Thiazide diuretics can actually exacerbate hypercalcemia by decreasing calcium excretion in the urine, leading to elevated levels of calcium in the blood. This is why thiazide diuretics are contraindicated in patients with hypercalcemia. Option B) Glucocorticoids are sometimes used in the treatment of hypercalcemia because they can help decrease inflammation and reduce calcium absorption in the gut. Option C) Plicamycin is an antibiotic that can be used in the treatment of hypercalcemia by inhibiting bone resorption and reducing calcium levels in the blood. Option D) Parenteral infusion of phosphate can be effective in treating hypercalcemia by promoting the formation of calcium phosphate complexes, which lowers the levels of free calcium in the blood. In an educational context, understanding the mechanisms of action of different drugs in the treatment of hypercalcemia is crucial for healthcare professionals to make informed decisions in clinical practice. It is important to be aware of which medications can exacerbate hypercalcemia and which ones are effective in lowering calcium levels to provide optimal patient care.

Correct Answer: D

Rationale: The correct answer is D) None of the above. In this scenario, the physician is recommending a drug that blocks 5α reductase in the prostate to address the urinary hesitancy associated with benign prostatic hyperplasia. This drug is likely referring to finasteride or dutasteride, which are 5α reductase inhibitors commonly used in the treatment of BPH. Option A) Atropine is a muscarinic antagonist used for conditions like bradycardia or to reduce salivary and bronchial secretions, not for BPH. Option B) Clonidine is an alpha-2 adrenergic agonist primarily used for hypertension or ADHD, not for BPH. Option C) Hydralazine is a direct-acting vasodilator used for hypertension, not for BPH. Understanding the mechanism of action of drugs used in the treatment of BPH is crucial for healthcare professionals to make appropriate prescribing decisions. This question assesses the knowledge of students on the pharmacological management of BPH and the specific drug classes used to address urinary symptoms in this condition. It highlights the importance of tailoring treatment to the underlying pathophysiology of the patient's condition for optimal outcomes.