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?

  1. Destroys thyroid follicular cells by beta emission
  2. Blocks the sodium-iodide symporter, preventing iodide uptake
  3. Replaces endogenous thyroxine
  4. Inhibits thyroid peroxidase, blocking thyroid hormone synthesis
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.

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Question 2

What is the mechanism of action of lisinopril?

  1. Blocks the angiotensin II type 1 receptor
  2. Inhibits the sodium-chloride cotransporter in the distal tubule
  3. Inhibits angiotensin-converting enzyme
  4. Blocks beta-1 adrenergic receptors
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.

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Question 3

What is the mechanism of action of naloxone?

  1. Partial agonist at the mu opioid receptor
  2. Competitive antagonist at the benzodiazepine receptor
  3. Inhibits reuptake of noradrenaline and serotonin
  4. Competitive antagonist at the mu opioid receptor
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.

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Question 4

What is the mechanism of action of albuterol?

  1. Muscarinic receptor antagonist
  2. Phosphodiesterase inhibitor
  3. Beta-2 adrenergic receptor agonist
  4. Leukotriene receptor antagonist
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.

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