Hyperthyroidism & thyroid cancer flashcards
28 high-yield MRCP Part 1 cards from the Intellect Medicos Endocrinology & Diabetes course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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What is the most common cause of thyrotoxicosis?
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Graves' disease.
Why? It is caused by TSH-receptor-stimulating autoantibodies.
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Which antibody test confirms Graves' disease?
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TSH receptor antibodies (TRAb).
Why? Radioisotope uptake is diffuse and increased in Graves, focal in a toxic nodule and low in thyroiditis.
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Which drug is used first to control the adrenergic symptoms of thyrotoxicosis?
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Propranolol.
Why? It controls palpitations, tremor and anxiety while antithyroid drugs take weeks to act.
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What is the first-line antithyroid drug for Graves' disease outside pregnancy?
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Carbimazole, titrated to euthyroidism and usually continued for 12–18 months.
Why? Block-and-replace (high-dose carbimazole plus levothyroxine) is an alternative but not used in pregnancy.
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What is carbimazole's active metabolite?
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Methimazole (thiamazole).
Why? It inhibits thyroid peroxidase, blocking synthesis of new thyroid hormone.
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What is the most serious adverse effect of carbimazole, and what must patients be told?
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Agranulocytosis — report sore throat, fever or mouth ulcers urgently for a full blood count.
Why? Check a full blood count before starting. If agranulocytosis is confirmed, stop and do not restart any antithyroid drug. Routine FBC monitoring is not recommended.
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Which serious adverse effect of carbimazole was highlighted by the MHRA in 2019, requiring permanent withdrawal?
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Acute pancreatitis.
Why? Re-challenge can cause recurrence, so carbimazole must not be restarted.
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What is the major serious adverse effect of propylthiouracil (PTU)?
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Hepatotoxicity (can cause liver failure).
Why? This is why PTU is mainly reserved for the first trimester of pregnancy and thyroid storm.
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Besides blocking thyroid hormone synthesis, what extra action does propylthiouracil have?
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It blocks peripheral conversion of T4 to T3.
Why? This makes it useful in thyroid storm.
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Which antithyroid drug is preferred in the FIRST trimester of pregnancy?
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Propylthiouracil.
Why? Carbimazole is linked to congenital abnormalities during organogenesis. Switch to carbimazole in the second and third trimesters because PTU is hepatotoxic.
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When treating hyperthyroidism in pregnancy, what free T4 level is targeted?
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The upper limit of the normal reference range, using the lowest effective dose.
Why? Antithyroid drugs cross the placenta; overtreatment causes fetal hypothyroidism and goitre.
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What is the main absolute contraindication to radioiodine, and how long should conception be avoided afterwards?
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Pregnancy (and breastfeeding); avoid conception for 4–6 months after treatment.
Why? Radioiodine crosses the placenta and destroys the fetal thyroid.
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Which pre-existing condition may be worsened by radioiodine therapy?
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Active thyroid eye disease (Graves' orbitopathy).
Why? It is a relative contraindication; steroid cover can be used.
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What is the biggest modifiable risk factor for Graves' orbitopathy?
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Smoking.
Why? Stopping smoking, restoring euthyroidism and avoiding hypothyroidism all help eye disease.
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What is the treatment for ACTIVE, SEVERE Graves' orbitopathy?
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High-dose glucocorticoids (usually IV methylprednisolone).
Why? Steroids are reserved for active severe disease; sight-threatening optic nerve compression may need urgent decompression.
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What is the treatment of choice for toxic multinodular goitre?
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Radioiodine.
Why? Antithyroid drugs control it short-term but relapse is common because nodules are autonomous. Surgery is used for large or compressive goitres.
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A thyrotoxic woman has a painful tender goitre after a flu-like illness, raised ESR and globally low radioiodine uptake. What is the diagnosis?
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Subacute (de Quervain's) thyroiditis.
Why? Viral inflammation releases stored hormone (hence low uptake), followed by a hypothyroid phase and recovery.
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What is the treatment of thyroid pain in de Quervain's thyroiditis?
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NSAIDs or aspirin; prednisolone in more severe cases.
Why? It is usually self-limiting. Antithyroid drugs are not useful because no new hormone is being made.
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How is the hyperthyroid phase of postpartum thyroiditis treated?
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Beta-blocker (e.g. propranolol) for symptoms; antithyroid drugs are not indicated.
Why? It is a destructive thyroiditis (anti-TPO positive). The later hypothyroid phase may need levothyroxine.
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How is type 2 amiodarone-induced thyrotoxicosis treated?
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Glucocorticoids (e.g. prednisolone).
Why? Type 2 is a destructive thyroiditis in a normal gland: IL-6 is raised and radioiodine uptake is low.
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How is type 1 amiodarone-induced thyrotoxicosis treated?
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Antithyroid drugs (e.g. carbimazole).
Why? Type 1 is iodine-induced excess hormone synthesis in an abnormal gland (e.g. nodular goitre); uptake is normal or high.
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Which scoring system is used to diagnose thyroid storm?
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The Burch–Wartofsky point scale (score >45 suggests thyroid storm).
Why? Diagnosis is clinical — fever, tachycardia, agitation/delirium, GI upset — so do not wait for TFTs.
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In thyroid storm, why is Lugol's iodine given only AFTER the thionamide (e.g. PTU)?
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So that the iodine cannot be used as substrate to make more thyroid hormone.
Why? Iodine then blocks hormone release (Wolff–Chaikoff effect). Propranolol, steroids and supportive care are given alongside.
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What is the most common type of thyroid cancer?
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Papillary carcinoma (about 70%).
Why? It often affects young women, spreads to lymph nodes and has an excellent prognosis.
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Which thyroid cancer arises from parafollicular C cells, and what tumour marker does it secrete?
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Medullary thyroid carcinoma; calcitonin.
Why? About 20–25% are familial (RET mutation), for example as part of MEN 2.
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Why can fine-needle aspiration not distinguish follicular carcinoma from follicular adenoma?
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Malignancy is defined by capsular or vascular invasion, which needs full histology of the excised nodule.
Why? Follicular carcinoma spreads mainly by the blood (haematogenous), unlike papillary.
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After total thyroidectomy for differentiated thyroid cancer, which blood test is the tumour marker for recurrence?
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Serum thyroglobulin.
Why? With no thyroid tissue left, detectable thyroglobulin suggests residual or recurrent disease. Recombinant TSH (thyrotropin alfa) can stimulate it without stopping levothyroxine.
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After total thyroidectomy and radioiodine for differentiated thyroid cancer, why is levothyroxine initially given at TSH-suppressive doses?
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TSH stimulates growth of thyroid cancer cells, so suppressing it (to below 0.1 mU/L) reduces recurrence.
Why? NICE reassesses at 9–12 months: with an excellent response the TSH target is relaxed to 0.3–2.0 mU/L for life; it stays suppressed if there is persistent or recurrent disease.
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