Pharmacology · patient case with 4 questions
Reviewing a long medication list
Patient: Female, 55 years old
Chief Complaint: Presents for a comprehensive examination.
Background: Graves disease, hypertension, asthma. She carries a naloxone kit because a family member has opioid use disorder.
Medications: Propylthiouracil · lisinopril · albuterol inhaler · naloxone (rescue kit)
Vital Signs: BP 132/84 mmHg · HR 84 bpm · RR 16
Question 1
What is the mechanism of action of propylthiouracil?
Show answer and explanation
Correct answer: D. Inhibits thyroid peroxidase, blocking thyroid hormone synthesis
- A. Beta-emitting destruction of follicular cells is radioactive iodine (I-131), a different treatment modality.
- B. The sodium-iodide symporter is inhibited by perchlorate and thiocyanate, not by thionamides.
- C. Replacing thyroxine is levothyroxine — the treatment for hypothyroidism, the opposite problem.
- D. CORRECT. Propylthiouracil inhibits THYROID PEROXIDASE, the enzyme that oxidises iodide and couples iodotyrosines. Without it, T3 and T4 cannot be made. Propylthiouracil has a second, distinctive action — it also blocks peripheral 5'-deiodinase conversion of T4 to the more active T3, which is why it is favoured in thyroid storm. Methimazole shares the peroxidase block but not the peripheral effect.
Question 2
What is the mechanism of action of lisinopril?
Show answer and explanation
Correct answer: C. Inhibits angiotensin-converting enzyme
- A. Angiotensin II receptor blockade is the ARBs — losartan, valsartan. They are the substitution when an ACE inhibitor cough is intolerable, because they do not raise bradykinin.
- B. The distal tubule sodium-chloride cotransporter is inhibited by THIAZIDE diuretics such as hydrochlorothiazide.
- C. CORRECT. Lisinopril is an ACE INHIBITOR. Blocking ACE prevents conversion of angiotensin I to angiotensin II, lowering vasoconstriction and aldosterone-driven sodium retention. The same enzyme degrades bradykinin, so bradykinin accumulates — which explains both the dry cough seen in up to a fifth of patients and the rare but dangerous angioedema. Lisinopril is also unusual among ACE inhibitors in not being a prodrug.
- D. Beta-1 blockade is metoprolol and atenolol — a different antihypertensive class entirely.
Note: Worth circulating to the group: at least three files in this series key lisinopril as a diuretic. It is an ACE inhibitor.
Question 3
What is the mechanism of action of naloxone?
Show answer and explanation
Correct answer: D. Competitive antagonist at the mu opioid receptor
- A. Buprenorphine is the mu partial agonist; nalbuphine and butorphanol are agonist-antagonists. Naloxone has no agonist activity at all.
- B. Benzodiazepine receptor antagonism is FLUMAZENIL — the reversal agent for midazolam and diazepam. Confusing the two reversal agents is a classic exam trap.
- C. Monoamine reuptake inhibition describes the SNRI antidepressants, unrelated to opioid reversal.
- D. CORRECT. Naloxone is a pure COMPETITIVE ANTAGONIST with high affinity for the mu opioid receptor. It displaces the agonist and reverses respiratory depression within minutes. The critical clinical caveat: naloxone's duration of action (roughly 30 to 90 minutes) is SHORTER than that of many opioids, so re-narcotisation can follow and the patient must be observed or transported.
Question 4
What is the mechanism of action of albuterol?
Show answer and explanation
Correct answer: C. Beta-2 adrenergic receptor agonist
- A. Muscarinic antagonism is ipratropium and tiotropium, used more in COPD than in acute asthma.
- B. Phosphodiesterase inhibition describes theophylline, an older bronchodilator now rarely used because of its narrow therapeutic index.
- C. CORRECT. Albuterol (salbutamol) is a short-acting selective BETA-2 AGONIST. Beta-2 stimulation raises cyclic AMP in bronchial smooth muscle and relaxes it, giving relief within minutes — this is the rescue inhaler. Its selectivity is relative rather than absolute, so at high doses it spills over to beta-1 and produces tachycardia and tremor.
- D. Leukotriene receptor antagonism is montelukast — a controller, not a rescue medication.