DO Osteopathic Pharmacology 2 — Questions and Answers
Question 1: A patient on carbamazepine for epilepsy presents with hyponatremia. What is the most likely mechanism?
- Renal wasting of sodium via mineralocorticoid antagonism
- Stimulation of ADH secretion and enhanced ADH activity causing SIADH (Correct answer)
- Inhibition of aldosterone synthesis
- Osmotic diuresis leading to free water retention
Correct answer: Stimulation of ADH secretion and enhanced ADH activity causing SIADH
Carbamazepine stimulates ADH release and potentiates its action on V2 receptors in renal collecting ducts, causing SIADH and hyponatremia.
Question 2: What is the primary mechanism of action of metformin in treating type 2 diabetes mellitus?
- Stimulates insulin secretion from pancreatic beta cells
- Activates AMPK to reduce hepatic gluconeogenesis (Correct answer)
- Inhibits intestinal alpha-glucosidase
- Blocks renal SGLT-2 transporter to enhance glucose excretion
Correct answer: Activates AMPK to reduce hepatic gluconeogenesis
Metformin activates AMP-activated protein kinase (AMPK), which suppresses hepatic glucose production without directly stimulating insulin secretion.
Question 3: A patient on phenelzine (MAOI) eats aged cheddar cheese and develops a severe hypertensive crisis. What is the mechanism?
- Tyramine displaces stored catecholamines from presynaptic vesicles (Correct answer)
- Tyramine directly stimulates alpha-1 adrenergic receptors
- Tyramine inhibits catecholamine reuptake transporters
- Tyramine increases renal renin secretion
Correct answer: Tyramine displaces stored catecholamines from presynaptic vesicles
Without GI MAO to metabolize it, tyramine is absorbed systemically and enters presynaptic terminals where it displaces stored norepinephrine, causing massive NE release.
Question 4: A patient presents with acetaminophen overdose 4 hours after ingestion. What is the correct antidote and its mechanism?
- Flumazenil — benzodiazepine receptor antagonist
- N-acetylcysteine — replenishes glutathione stores (Correct answer)
- Fomepizole — inhibits alcohol dehydrogenase
- Pralidoxime — regenerates acetylcholinesterase
Correct answer: N-acetylcysteine — replenishes glutathione stores
N-acetylcysteine provides cysteine as a glutathione precursor, allowing hepatocytes to detoxify NAPQI before it causes irreversible oxidative damage.
Question 5: A patient with chronic gout is started on allopurinol. What is the mechanism by which allopurinol reduces serum uric acid?
- Inhibits prostaglandin synthesis reducing inflammation
- Increases renal uric acid excretion via OAT transporters
- Inhibits xanthine oxidase reducing uric acid production (Correct answer)
- Blocks URAT1 transporter preventing uric acid reabsorption
Correct answer: Inhibits xanthine oxidase reducing uric acid production
Allopurinol is a xanthine oxidase inhibitor that reduces conversion of hypoxanthine to xanthine and xanthine to uric acid, lowering uric acid production.
Question 6: Which antibiotic class inhibits the 30S ribosomal subunit, is contraindicated in children under 8, and frequently causes photosensitivity?
- Macrolides
- Tetracyclines (Correct answer)
- Fluoroquinolones
- Aminoglycosides
Correct answer: Tetracyclines
Tetracyclines chelate calcium in developing teeth and bone and cause phototoxic skin reactions; they are contraindicated in children under 8 and pregnant women.
Question 7: What is the mechanism underlying aspirin's antiplatelet effect that distinguishes it from other NSAIDs?
- Reversible inhibition of cyclooxygenase-1 in platelets
- Irreversible acetylation of COX-1 permanently blocking thromboxane A2 synthesis (Correct answer)
- Competitive blockade of ADP receptors on platelet membranes
- Inhibition of thromboxane A2 receptors on platelets
Correct answer: Irreversible acetylation of COX-1 permanently blocking thromboxane A2 synthesis
Aspirin irreversibly acetylates the serine residue of COX-1; since anucleate platelets cannot synthesize new enzyme, the antiplatelet effect persists for the platelet's 7-10 day lifespan.
A patient on carbamazepine for epilepsy presents with hyponatremia.
What is the most likely mechanism?