Here are the answers to all 17 pharmacology MCQs from the PDF, with brief rationale:
1. Pheochromocytoma - preoperative management
b. Start Phenoxybenzamine first, followed by Propranolol if needed
Alpha-blockade (phenoxybenzamine) must precede beta-blockade to prevent unopposed alpha-mediated vasoconstriction and hypertensive crisis if a beta-blocker is given first.
2. Hypotension with marked bradycardia
a. Dopamine
Dopamine has alpha, beta-1, and dopaminergic activity - it raises both heart rate/contractility (beta-1) and blood pressure (alpha), unlike noradrenaline/phenylephrine which are pure alpha-agonists and can cause reflex bradycardia.
3. Chronic gout, long-term use after acute attack resolves
a. Allopurinol
Xanthine oxidase inhibitor for long-term urate-lowering prophylaxis; never started during an acute flare.
4. Resting tremor 3 weeks after starting psychiatric medication
a. Typical antipsychotics
D2 receptor blockade in the nigrostriatal pathway produces drug-induced parkinsonism (tremor, rigidity, bradykinesia).
5. Pulmonary arterial hypertension
c. Bosentan
Endothelin receptor antagonist that reduces pulmonary vascular resistance/pressure.
6. SLE - long-term disease control
a. Hydroxychloroquine
Antimalarial that is the backbone drug for maintenance therapy in SLE, reducing flares and organ damage over time.
7. Hypertensive emergency (230/110, headache, blurred vision, end-organ damage)
c. Sodium nitroprusside
Rapid-acting IV vasodilator, titratable, drug of choice for hypertensive emergencies.
8. Bipolar disorder - maintenance therapy
a. Lithium
First-line mood stabilizer for long-term prophylaxis of manic and depressive episodes.
9. Triptans - mechanism
b. 5-HT₁B/5-HT₁D receptor (agonist)
Causes cranial vasoconstriction and inhibits release of vasoactive neuropeptides, aborting acute migraine attacks.
10. Multibacillary leprosy - WHO MDT regimen (adult)
b. Rifampicin 600 mg once monthly (supervised) + Clofazimine 300 mg once monthly (supervised) + 50 mg daily + Dapsone 100 mg daily, for 12 months
11. Lineweaver-Burk plot - uncompetitive inhibition
I viewed the graph image on that page. The four quadrants show:
- Top-left: lines intersect on the y-axis (same Vmax, different Km) → competitive inhibition
- Top-right: two parallel lines (same slope, inhibitor line shifted up/left, no intersection point) → this is the classic signature of uncompetitive inhibition, where both Km and Vmax decrease proportionally
- Bottom-left: lines with negative slope converging on the x-axis (same Km, different Vmax) → pure noncompetitive inhibition
- Bottom-right: lines intersecting to the left of the y-axis, above the x-axis → mixed inhibition
Answer: the top-right graph (parallel lines) represents uncompetitive inhibition.
12. Aspirin (salicylate) overdose - enhancing elimination
b. IV sodium bicarbonate to achieve urinary alkalinization
Alkalinizing the urine ion-traps salicylate (a weak acid) in its ionized form, markedly increasing renal excretion. (Charcoal/lavage only help early gastric decontamination, not elimination once absorbed; N-acetylcysteine is for paracetamol, not aspirin.)
13. LOX pathway - selective cysteinyl leukotriene (CysLT1) receptor blocker
b. Montelukast
(Zileuton inhibits 5-lipoxygenase itself rather than blocking the receptor.)
14. Chlorthalidone-induced hyperglycemia mechanism
a. Chlorthalidone causes hypokalemia, which reduces insulin secretion from pancreatic beta-cells
This hypokalemia-mediated impairment of insulin release is the accepted mechanism for thiazide/thiazide-like diuretic hyperglycemia.
15. Trauma with hemoperitoneum, hypotensive/tachycardic - induction agent
d. Ketamine
Preserves sympathetic tone and blood pressure (unlike propofol/thiopentone, which cause vasodilation and myocardial depression that would worsen hypovolemic shock).
16. Multiple myeloma - proteasome inhibitor
a. Bortezomib
17. Tumor lysis syndrome - rapid lowering of serum uric acid
b. Pegloticase
Among the listed options, pegloticase is a PEGylated recombinant uricase that enzymatically degrades existing uric acid to allantoin, acting rapidly - the same mechanism class as rasburicase (the true first-line drug for TLS, though not listed here). Allopurinol/febuxostat only block new urate production (xanthine oxidase inhibitors) and act too slowly for an emergency; probenecid increases renal urate excretion and is actually contraindicated in TLS (risk of intratubular urate precipitation).
18. Bipolar patient, 6 months of treatment: tremor, polyuria/polydipsia, weight gain, hypothyroidism
c. Lithium
Classic chronic lithium toxicity/side-effect profile: fine tremor, nephrogenic diabetes insipidus (polyuria/polydipsia), weight gain, and hypothyroidism (inhibits thyroid hormone release).
A couple of notes on the file: pages 15 and 18 each had a blank option "e." with no text, and page 1 was blank (likely a title page) - these didn't affect the answers above. If you want, I can also format this into an answer key/PDF for printing.