Thyroid disorders: pharmacotherapy of hypo and hyperthyroidism MCQs With Answer

Introduction: This focused MCQ set covers the pharmacotherapy of thyroid disorders — hypothyroidism and hyperthyroidism — tailored for M.Pharm students studying Pharmacotherapeutics I (MPP 102T). The questions probe mechanisms of action, pharmacokinetics, clinical use, monitoring, adverse effects, drug interactions and special situations such as pregnancy, thyroid storm, myxedema coma and drug-induced thyroid dysfunction. Designed to deepen understanding beyond basic facts, these items emphasize therapeutic decision-making, rationale for drug selection and safe management. Use these questions for self-assessment, exam preparation and to reinforce evidence-based prescribing principles relevant to thyroid hormone replacement and antithyroid therapies.

Q1. Which best describes the primary pharmacologic action of levothyroxine in replacement therapy?

• Acts as synthetic T4 that is converted peripherally to active T3 which binds nuclear thyroid hormone receptors to regulate gene transcription
• Directly binds mitochondrial receptors to increase cellular ATP production
• Inhibits thyroid peroxidase thereby reducing thyroid hormone synthesis
• Blocks sodium-iodide symporter to reduce iodide uptake into the gland

Correct Answer: Acts as synthetic T4 that is converted peripherally to active T3 which binds nuclear thyroid hormone receptors to regulate gene transcription

Q2. Which concomitant medication most commonly reduces oral levothyroxine absorption and may necessitate spacing doses?

• Calcium carbonate supplements
• Beta blockers (e.g., propranolol)
• Potassium iodide
• Glucocorticoids

Correct Answer: Calcium carbonate supplements

Q3. What is the recommended initial approach for initiating levothyroxine in an elderly patient with ischemic heart disease and newly diagnosed hypothyroidism?

• Start low-dose levothyroxine and titrate slowly while monitoring cardiac status
• Begin full replacement dose immediately to normalize TSH quickly
• Use liothyronine (T3) instead because it has faster onset
• Delay treatment unless TSH >50 mIU/L

Correct Answer: Start low-dose levothyroxine and titrate slowly while monitoring cardiac status

Q4. Which laboratory test is the most sensitive and preferred for monitoring adequacy of levothyroxine replacement after dose changes?

• Serum thyroid-stimulating hormone (TSH) measured 4–6 weeks after dose adjustment
• Total T4 measured weekly
• Reverse T3 measured monthly
• Thyroid peroxidase antibody titer annually

Correct Answer: Serum thyroid-stimulating hormone (TSH) measured 4–6 weeks after dose adjustment

Q5. What is the primary mechanism of action of thionamide antithyroid drugs such as methimazole?

• Inhibit thyroid peroxidase–mediated iodination and coupling of thyroglobulin, decreasing thyroid hormone synthesis
• Block sodium-iodide symporter preventing iodide uptake into follicular cells
• Irreversibly destroy thyroid tissue via beta radiation
• Enhance peripheral deiodination of T4 to inactive metabolites

Correct Answer: Inhibit thyroid peroxidase–mediated iodination and coupling of thyroglobulin, decreasing thyroid hormone synthesis

Q6. Which antithyroid drug is preferred during the first trimester of pregnancy to reduce teratogenic risk associated with other agents?

• Propylthiouracil (PTU)
• Methimazole throughout pregnancy
• Radioactive iodine (I-131)
• Saturated solution of potassium iodide (SSKI)

Correct Answer: Propylthiouracil (PTU)

Q7. Which serious hematologic adverse effect must patients on methimazole or PTU be counseled to report immediately?

• Agranulocytosis presenting with fever and sore throat
• Nephrotic syndrome with peripheral edema
• Hemolytic anemia with jaundice
• Deep venous thrombosis

Correct Answer: Agranulocytosis presenting with fever and sore throat

Q8. Which of the following is an absolute contraindication to radioactive iodine therapy for hyperthyroidism?

• Pregnancy
• Mild ophthalmopathy without visual compromise
• Age over 70 years
• Subclinical hyperthyroidism

Correct Answer: Pregnancy

Q9. For symptomatic control of palpitations and tremor in thyrotoxicosis, which drug class is first-line?

• Beta-adrenergic blockers such as propranolol
• Calcium channel blockers such as nifedipine
• ACE inhibitors such as enalapril
• Anticholinergics such as atropine

Correct Answer: Beta-adrenergic blockers such as propranolol

Q10. In the acute management of thyroid storm, which immediate intervention is typically instituted to control severe adrenergic manifestations?

• Administer high-dose IV propranolol to control heart rate and reduce peripheral T4→T3 conversion
• Give oral methimazole only and observe
• Provide radioactive iodine to ablate the gland immediately
• Start levothyroxine to stabilize thyroid hormone levels

Correct Answer: Administer high-dose IV propranolol to control heart rate and reduce peripheral T4→T3 conversion

Q11. What is the primary acute effect of administering saturated solution potassium iodide (SSKI) before thyroidectomy or in thyrotoxic crisis?

• Rapidly inhibits thyroid hormone release and decreases vascularity of the gland via the Wolff–Chaikoff effect
• Permanently blocks thyroid peroxidase activity for months
• Stimulates thyroid hormone synthesis for short-term use
• Prevents peripheral conversion of T4 to T3 long-term

Correct Answer: Rapidly inhibits thyroid hormone release and decreases vascularity of the gland via the Wolff–Chaikoff effect

Q12. Why does amiodarone frequently cause thyroid dysfunction?

• It contains large amounts of iodine which can lead to either iodine-induced hypothyroidism or destructive thyrotoxicosis
• It is a potent inhibitor of thyroid peroxidase similar to methimazole
• It stimulates TSH secretion directly from the pituitary
• It competitively antagonizes thyroid hormone receptors in peripheral tissues

Correct Answer: It contains large amounts of iodine which can lead to either iodine-induced hypothyroidism or destructive thyrotoxicosis

Q13. What is the primary effect of lithium on thyroid physiology that can lead to hypothyroidism?

• Inhibition of thyroid hormone release from follicular cells
• Competitive blockade of TSH receptors
• Stimulation of thyroid peroxidase causing hyperfunction
• Enhancement of peripheral deiodination of T4 to T3

Correct Answer: Inhibition of thyroid hormone release from follicular cells

Q14. Which congenital abnormality has been linked to maternal methimazole exposure during early pregnancy?

• Aplasia cutis and other specific embryopathies (scalp and facial defects)
• Neural tube defects exclusively
• Cardiac septal defects only
• Renal agenesis

Correct Answer: Aplasia cutis and other specific embryopathies (scalp and facial defects)

Q15. In myxedema coma, which combination is part of the initial recommended pharmacologic therapy?

• IV levothyroxine plus IV hydrocortisone
• Oral methimazole and propranolol
• Radioactive iodine and potassium iodide
• Oral liothyronine (T3) alone

Correct Answer: IV levothyroxine plus IV hydrocortisone

Q16. Which laboratory pattern is typical of primary hypothyroidism?

• Elevated TSH with low free T4
• Low TSH with high free T4
• Low TSH with low free T4
• Normal TSH with elevated reverse T3 only

Correct Answer: Elevated TSH with low free T4

Q17. Which antithyroid drug is most strongly associated with severe hepatotoxicity and requires monitoring of liver function?

• Propylthiouracil (PTU)
• Methimazole
• Potassium perchlorate
• Propranolol

Correct Answer: Propylthiouracil (PTU)

Q18. Which commonly prescribed therapy increases thyroid-binding globulin and may increase levothyroxine requirements?

• Estrogen therapy (e.g., oral contraceptives or hormone replacement therapy)
• Rifampin therapy
• Metformin therapy
• Amiodarone therapy

Correct Answer: Estrogen therapy (e.g., oral contraceptives or hormone replacement therapy)

Q19. What is the approximate plasma elimination half-life of levothyroxine in a euthyroid adult?

• Approximately 7 days
• Approximately 6 hours
• Approximately 12 hours
• Approximately 30 days

Correct Answer: Approximately 7 days

Q20. How does radioactive iodine (I-131) treat hyperthyroidism at the cellular level?

• Thyroid follicular cells take up iodine via the sodium-iodide symporter and beta emissions cause localized radiation-induced cell death
• It blocks peripheral deiodinases permanently, lowering T3 production
• It competitively inhibits TSH receptor signaling without destroying tissue
• It directly inactivates circulating thyroid hormones in plasma

Correct Answer: Thyroid follicular cells take up iodine via the sodium-iodide symporter and beta emissions cause localized radiation-induced cell death

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