Hyperthyroidism

Question 1

Hyperthyroidism treatment

Answer 1

REDUCE THYROID HORMONE SYNTHESIS (THYROXINE) TO TARGET HYPERTHYROIDISM
-Thionamides (propylthiouracil and carbimazole)
-Potassium iodide
-Radioiodine
HELPS WITH SYMPTOMS
-Beta blockers (propranolol)

Question 2

Clinical use of Thionamides

Answer 2

• daily treatment of hyperthyroid conditions (eg: Grave’s disease, toxic thyroid nodule/toxic multinodular goitre otherwise known as Plummer’s disease)
• treatment prior to surgery (pre-operative)
• reduction of symptoms while waiting for radioactive iodine to act

Question 3

Thyroid hormone synthesis

Answer 3

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Question 4

Thionamides side effects

Answer 4

• Agranulocytosis (usually neutrophil reduction)->rare and reversible on drug withdrawal
• rashes (relatively common side effect)

Question 5

Thionamides pharmacokinetics

Answer 5

• Orally active
• Carbimazole=pro-drug which must first be converted to Methimazole
• Crosses placenta and is secreted in breast milk (prefer to use PTU rather than Carbimazole)
• Metabolised in liver and excreted in urine
• Plasma half life->6-15 hours

Question 6

Potassium iodide clinical effect

Answer 6

• Hyperthyroid symptoms reduced within 1-2 days

- Vascularity and size of thyroid gland reduced within 10-14 days

Question 7

Potassium iodide pharmacokinetics

Answer 7

• Oral administration (Lugol’s solution=potassium iodide with iodine in water)
• Maximum effects after 10 days continuous administration

Question 8

Potassium iodide side effects

Answer 8

Allergic reactions (eg: rashes, fever, angio-oedema)

Question 9

Problems using radioiodine

Answer 9

• avoid close contact with small children for several weeks after receiving radioiodine treatment
• contraindicated in pregnancy and breastfeeding

Question 10

Radioiodine pharmacokinetics

Answer 10

• Single oral dose administration (~500MBq for Graves’ disease and ~3000MBq for Thyroid cancer)
• 8 day radioactive half life
• negligible radioactivity after 2 months
• Stop anti-thyroid drugs 7-10 days prior to radioiodine treatment

Question 11

Thionamide actions

Answer 11

• inhibition of thyroid peroxidase and hence inhibition of thyroglobulin iodination and inhibition of iodotyrosine coupling-> reduced T3/T4 synthesis and secretion
• may suppress antibody production in Grave’s disease (immunosuppressive effects)
• reduces T4 to T3 conversion in peripheral tissues (propylthiouracil)

Question 12

Thionamide follow up

Answer 12

• typically aim to stop anti-thyroid drug treatment after 18 months
• review patient periodically (including thyroid function tests for remission/relapse)

Question 13

Beta blockers in thyrotoxicosis

Answer 13

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Question 14

Potassium iodide mechanism of action

Answer 14

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Question 15

Radioiodine at high doses

Answer 15

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Question 16

Radioiodine at low doses

Answer 16

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Question 17

Pretibial myxoedema

Answer 17

• Swelling (non-pitting=solid) of shins in patient with Graves’ disease
• Hypertrophy of the shins
• Pitting shows difference between pretibial myxedema and normal oedema of heart failure
• not to be confused with myxoedema (hypothyroidism)

Question 18

Exophthalmos

Answer 18

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Question 19

Plummer’s disease

Answer 19

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Question 20

Thyroxine effects on the sympathetic nervous system

Answer 20

• sensitises beta adrenoceptors to ambient/normal levels of adrenaline and noadrenaline (more effect at the receptors despite being at normal adrenaline level)
• results in apparent sympathetic activation (tachycardia, palpitations, hand tremor, lid lag etc)
• lid lag results from overactive levator palpebrae superioris muscle

Question 21

Thyroid storm

Answer 21

MEDICAL EMERGENCY

Patient is thyrotoxic + at least two of the following key features that increase mortality:

• Hyperpyrexia > 41 degrees celsius (high fever with body temperature rise above 41)
• Accelerated tachycardia (>140bpm) or any arrhythmia
• Cardiac failure
• Delirium/frank psychosis/confusion
• Hepatocellular dysfunction/jaundice

Patient is immediately admitted to hospital and requires aggressive treatment

Question 22

Hyperthyroidism presentation

Answer 22

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Question 23

Viral (De Quervain’s) thyroiditis presentation

Answer 23

• painful dysphagia
• hyperthyroidism symptoms initially followed by hypothyroidism symptoms
• pyrexia (fever)
• raised ESR (erythrocyte sedimentation rate)

Question 24

Natural history of viral thyroiditis

Answer 24

• virus attacks thyroid gland causing inflammation and hence pain/tenderness->causes release of stored thyroxine to give hyperthyroidism
• thyroid gland then shuts down and stops making thyroxine and makes viruses instead->results in hypothyroidism
• Thyroid uptake scan shows no iodine uptake

Question 25

Causes of hyperthyroidism

Answer 25

• Graves’ disease

- Toxic nodular goitre (Plummer’s disease)

Question 26

Graves’ disease

Answer 26

• autoimmune disease
• anti-TSH receptor antibodies bind to and stimulate the TSH receptor to synthesise thyroxine in the thyroid gland
• TSH receptor stimulation causes all cells of the thyroid gland to grow (all cells have TSH receptors)->results in smooth visible goitre and hyperthyroidism

Question 27

Graves’ disease presentation

Answer 27

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Question 28

Potassium iodide clinical uses

Answer 28

• preparation of hyperthyroid patients for surgery

- severe thyrotoxic crisis