A 50-year-old man with hypertension is started on an ACE inhibitor. Which of the following is the most likely mechanism of action for this class of drugs?

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Question 1 of 5

A 50-year-old man with hypertension is started on an ACE inhibitor. Which of the following is the most likely mechanism of action for this class of drugs?

Correct Answer: B

Rationale: The correct answer is B because ACE inhibitors work by inhibiting the conversion of angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor and also stimulates the release of aldosterone, leading to increased blood pressure. By blocking this conversion, ACE inhibitors help dilate blood vessels and reduce blood pressure. A: Blocking calcium channels is the mechanism of action of calcium channel blockers, not ACE inhibitors. C: Inhibiting aldosterone is the mechanism of action of aldosterone receptor antagonists, not ACE inhibitors. D: Increasing bradykinin levels is a side effect of ACE inhibitors, but not their primary mechanism of action.

Question 2 of 5

This graph shows the concentration-dependent effects of norepinephrine on arterial blood pressure, both alone, and in the presence of a fixed concentration of Drug X. Which type of antagonist is Drug X?

Correct Answer: B

Rationale: The correct answer is B: Non-competitive antagonist. This is because a non-competitive antagonist binds irreversibly to a different site on the receptor compared to the agonist (norepinephrine in this case) and prevents its activation, leading to a decrease in response. In the graph, the presence of Drug X shifts the concentration-response curve of norepinephrine downward without affecting the maximum response, indicating non-competitive antagonism. A: Silent antagonists do not affect the agonist's binding or activity on the receptor. C: Competitive antagonists compete with the agonist for the same binding site on the receptor, affecting potency but not the maximum response. D: Chemical antagonist is a broad term for any antagonist that binds to the agonist or receptor to prevent activation but does not specifically describe the mechanism like non-competitive antagonism does.

Question 3 of 5

A46-year-old woman recently diagnosed with classic migraine had a headache attack at least once a week. Ergotamine was prescribed to prevent the impending attacks. Which of the following actions most likely contributed to the therapeutic effect of the drug in the patient's disorder?

Correct Answer: A

Rationale: The correct answer is A: Constriction of cerebral vessels. Ergotamine is known to constrict cerebral blood vessels, which helps in preventing migraine attacks by reducing the dilation of these vessels that occurs during a migraine. This constriction helps to decrease the pulsatile headache pain associated with migraines. B: Extravasation of plasma into perivascular space is incorrect because it does not contribute to the therapeutic effect of ergotamine in treating migraines. C: Prostaglandin release from vascular endothelium is incorrect because ergotamine works by vasoconstriction rather than affecting prostaglandin release. D: Platelet aggregation in the cerebral vascular bed is incorrect because ergotamine does not target platelet aggregation as a mechanism of action in treating migraines.

Question 4 of 5

A40-year-old woman suffering from chronic classic migraine headaches took three sublingual tablets of ergotamine to abort an impending migraine attack. Which of the following adverse effects were most likely to occur in this patient?

Correct Answer: D

Rationale: The correct answer is D: Nausea and vomiting. Ergotamine is known to commonly cause gastrointestinal side effects such as nausea and vomiting. This is due to its vasoconstrictive effects on blood vessels in the gastrointestinal tract. Visual hallucinations (choice A) are more commonly associated with LSD use, not ergotamine. Postural hypotension (choice B) is more likely to occur with alpha-adrenergic blockers, not ergotamine. Facial flushing (choice C) is more commonly seen with niacin therapy, not ergotamine. Therefore, in this case, the most likely adverse effect for the patient taking ergotamine would be nausea and vomiting due to its vasoconstrictive effects on the gastrointestinal tract.

Question 5 of 5

A66-year-old man suffering from benign prostatic hyperplasia was admitted to the hospital because of severe suprapubic pain and an inability to pass urine for the past 24 hours. On questioning, he said he had been taking diphenhydramine for a few days to relieve itching. Which of the following actions most likely mediated the adverse effect of the drug in this patient?

Correct Answer: A

Rationale: The correct answer is A: Relaxation of the detrusor muscle. Diphenhydramine, an anticholinergic drug, causes relaxation of the detrusor muscle, leading to urinary retention. In benign prostatic hyperplasia, the enlarged prostate already causes obstruction, exacerbating the urinary retention. Therefore, the relaxation of the detrusor muscle due to diphenhydramine worsens the situation by further impairing bladder emptying. Explanation for other choices: B: Constriction of the bladder external sphincter - This would lead to urinary retention, not relieve it. C: Constriction of the prostate capsule - Constriction of the prostate capsule would not relieve urinary retention in benign prostatic hyperplasia. D: Relaxation of the bladder internal sphincter - Relaxation of the bladder internal sphincter would promote bladder emptying, which is opposite to the clinical presentation of urinary retention in this case.

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