Hyperthyroidism Flashcards
Hyperthyroidism treatment
REDUCE THYROID HORMONE SYNTHESIS (THYROXINE) TO TARGET HYPERTHYROIDISM
-Thionamides (propylthiouracil and carbimazole)
-Potassium iodide
-Radioiodine
HELPS WITH SYMPTOMS
-Beta blockers (propranolol)
Clinical use of Thionamides
- 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
Thyroid hormone synthesis
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Thionamides side effects
- Agranulocytosis (usually neutrophil reduction)->rare and reversible on drug withdrawal
- rashes (relatively common side effect)
Thionamides pharmacokinetics
- 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
Potassium iodide clinical effect
- Hyperthyroid symptoms reduced within 1-2 days
- Vascularity and size of thyroid gland reduced within 10-14 days
Potassium iodide pharmacokinetics
- Oral administration (Lugol’s solution=potassium iodide with iodine in water)
- Maximum effects after 10 days continuous administration
Potassium iodide side effects
Allergic reactions (eg: rashes, fever, angio-oedema)
Problems using radioiodine
- avoid close contact with small children for several weeks after receiving radioiodine treatment
- contraindicated in pregnancy and breastfeeding
Radioiodine pharmacokinetics
- 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
Thionamide actions
- 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)
Thionamide follow up
- typically aim to stop anti-thyroid drug treatment after 18 months
- review patient periodically (including thyroid function tests for remission/relapse)
Beta blockers in thyrotoxicosis
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Potassium iodide mechanism of action
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Radioiodine at high doses
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Radioiodine at low doses
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Pretibial myxoedema
- 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)
Exophthalmos
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Plummer’s disease
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Thyroxine effects on the sympathetic nervous system
- 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
Thyroid storm
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
Hyperthyroidism presentation
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Viral (De Quervain’s) thyroiditis presentation
- painful dysphagia
- hyperthyroidism symptoms initially followed by hypothyroidism symptoms
- pyrexia (fever)
- raised ESR (erythrocyte sedimentation rate)
Natural history of viral thyroiditis
- 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
Causes of hyperthyroidism
- Graves’ disease
- Toxic nodular goitre (Plummer’s disease)
Graves’ disease
- 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
Graves’ disease presentation
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Potassium iodide clinical uses
- preparation of hyperthyroid patients for surgery
- severe thyrotoxic crisis
