Q- Isoniazid-induced peripheral neuropathy is caused by deficiency of which vitamin?
A- Vitamin B6
B- Vitamin B12
C- Vitamin B1
D- Folate
A- Vitamin B6- Isoniazid increases pyridoxine excretion and inhibits its activation, causing a functional B6 deficiency that leads to peripheral neuropathy. This is prevented by co-administering pyridoxine.
Q- Furosemide-induced ototoxicity results from disrupted ion transport in which structure?
A- Organ of Corti hair cells
B- Vestibular apparatus
C- Stria vascularis of the cochlea
D- Auditory nerve
C- Stria vascularis of the cochlea- Loop diuretics inhibit the Na-K-2Cl cotransporter in the stria vascularis, disrupting the endolymph ionic gradient and causing usually reversible ototoxicity, especially with high-dose or rapid IV administration.
Q- Thiazide diuretics increase digoxin toxicity primarily through which electrolyte disturbance?
A- Hypercalcemia
B- Hyponatremia
C- Hypomagnesemia
D- Hypokalemia
D- Hypokalemia- Potassium competes with digoxin for the same binding site on Na+/K+-ATPase. Thiazide-induced hypokalemia reduces this competition, allowing digoxin to bind more effectively and worsening toxicity.
Q- Leucovorin rescues normal cells from methotrexate toxicity by bypassing inhibition of which enzyme?
A- Thymidylate synthase
B- Dihydrofolate reductase
C- Ribonucleotide reductase
D- DNA polymerase
B- Dihydrofolate reductase- Methotrexate inhibits dihydrofolate reductase, blocking folate activation needed for DNA synthesis. Leucovorin is a reduced folate that bypasses this block, rescuing normal cells from toxicity.
Q- Tamoxifen increases endometrial cancer risk because it acts as a partial estrogen agonist in which tissue?
A- Breast
B- Bone
C- Endometrium
D- Liver
C- Endometrium- As a selective estrogen receptor modulator (SERM), tamoxifen antagonizes estrogen receptors in breast tissue but acts as a partial agonist in the endometrium, raising the risk of endometrial hyperplasia and cancer.
Q- A patient treated with a nonselective beta blocker develops hypoglycemia that is difficult to recognize. What explains the masking of hypoglycemia symptoms?
A- Alpha receptor blockade
B- Beta-1 receptor stimulation
C- Beta-2 receptor blockade
D- Muscarinic receptor blockade
C- Beta-2 receptor blockade- Nonselective beta blockers inhibit β₂-mediated glycogenolysis and mask adrenergic warning symptoms like tachycardia, making hypoglycemia harder to detect.
Q- A patient with hyperlipidemia is treated with cholestyramine. What is the primary mechanism by which this drug lowers cholesterol?
A- Decreases hepatic cholesterol synthesis
B- Inhibits intestinal cholesterol absorption
C- Increases bile acid excretion in stool
D- Stimulates lipoprotein lipase
C- Increases bile acid excretion in stool- Cholestyramine binds bile acids in the intestine, preventing their reabsorption. The liver then uses more cholesterol to synthesize new bile acids, lowering LDL levels.
Q- A patient receiving long-term glucocorticoid therapy develops osteoporosis. What is the main mechanism responsible for this effect?
A- Decreased calcium absorption and increased bone resorption
B- Decreased osteoclast activity
C- Increased vitamin D activation
D- Increased calcium reabsorption in bone
A- Decreased calcium absorption and increased bone resorption- Glucocorticoids decrease intestinal calcium absorption and increase osteoclast activity, leading to bone loss and osteoporosis.
