Pharmacology · patient case with 5 questions
Bone biology and drug mechanisms
Scenario: One histology item followed by a run of mechanism-of-action questions.
Question 1
Which of the following is associated with bone resorption?
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Correct answer: D. Howship lacunae
- A. The endosteum is the membrane lining the medullary cavity. It contains osteoprogenitor cells and is a site of both formation and resorption, but it is not the resorption feature itself.
- B. Canaliculi are the tiny channels housing osteocyte processes; they permit communication and mechanosensation, not resorption.
- C. Haversian canals carry the neurovascular bundle at the centre of each osteon — a structural feature of compact bone.
- D. Correct. Howship lacunae are the scalloped depressions on a bone surface excavated by actively resorbing osteoclasts, which sit within them behind a ruffled border and sealing zone.
Question 2
What is the mechanism of action of albuterol?
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Correct answer: B. Beta-2 adrenergic agonist
- A. A beta-1 blocker slows the heart and lowers contractility; blocking beta receptors would worsen bronchospasm, not relieve it.
- B. Correct. Albuterol is a short-acting selective beta-2 agonist. Stimulating beta-2 receptors on bronchial smooth muscle raises cyclic AMP and relaxes the airway — the rescue inhaler in asthma.
- C. Muscarinic antagonists such as ipratropium do bronchodilate, but by a different route, and albuterol is not one of them.
- D. Leukotriene antagonists such as montelukast are controller medications taken orally, not rescue bronchodilators.
Question 3
What is the mechanism of action of lisinopril?
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Correct answer: B. Angiotensin-converting enzyme inhibitor
- A. ARBs such as losartan block the receptor instead of the enzyme; they do not raise bradykinin, so cough is uncommon.
- B. Correct. Lisinopril blocks the conversion of angiotensin I to angiotensin II, lowering vasoconstriction and aldosterone release. The rise in bradykinin explains the characteristic dry cough and the risk of angioedema.
- C. Calcium channel blockers such as nifedipine relax vascular smooth muscle and are the group associated with gingival enlargement.
- D. Thiazides such as hydrochlorothiazide act at the distal convoluted tubule and cause hypokalaemia and xerostomia.
Question 4
What is the mechanism of action of the statins?
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Correct answer: D. Inhibit HMG-CoA reductase, reducing hepatic cholesterol synthesis
- A. Fibrates act through PPAR-alpha to raise lipoprotein lipase activity and lower triglycerides.
- B. Bile acid sequestrants such as cholestyramine work that way — a different class.
- C. Ezetimibe blocks intestinal cholesterol absorption at the NPC1L1 transporter.
- D. Correct. Statins competitively inhibit HMG-CoA reductase, the rate-limiting enzyme of hepatic cholesterol synthesis. The liver responds by upregulating LDL receptors, clearing LDL from the blood.
Note: The dental relevance: statins carry a risk of myopathy, and that risk rises with drugs sharing the CYP3A4 pathway — azole antifungals and erythromycin among them.
Question 5
What is the mechanism of action of triamterene?
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Correct answer: B. Blocks sodium channels in the distal tubule, sparing potassium
- A. The Na-K-2Cl cotransporter is the target of loop diuretics such as furosemide, which waste potassium heavily.
- B. Correct. Triamterene blocks epithelial sodium channels in the distal tubule and collecting duct. Because potassium secretion is coupled to sodium reabsorption there, blocking sodium entry retains potassium — hence potassium-sparing.
- C. Acetazolamide inhibits carbonic anhydrase and is used for glaucoma and altitude sickness, not routine blood-pressure control.
- D. Spironolactone is the aldosterone receptor antagonist. It is also potassium-sparing but reaches the same endpoint by a different route.