Transcript - Northent
BENIGN THYROID DISORDERS Regional SpR Teaching Woo-Young Yang ST5 CLASSIFICATION Simple Non-Toxic Toxic Inflammatory Neoplastic Rare CLASSIFICATION Simple Non-Toxic Iodine Difficiency Multinodular Goitre Solitary Nodule Physiological Toxic Grave’s Disease Plummer’s Disease Inflammatory Hashimoto’s Thyroiditis De Quervain’s Thyroiditis Riedel’s Thyroiditis Neoplastic Follicular Papillary Medullary Anaplastic Lymphoma Metastatic Rare Infective Iatrogenic IODINE DIFFICIENCY Epidemiology Commonest cause of goitre and hypothyroidism world wide Not common in the western world Pathophysiology Insufficient iodination of thyroglobulin Decrease in Thyroid Hormone Increase in TSH Diffuse hyperplasia(+/- multinodular appearance) Pregnancy Increased demand on maternal iodine Worsening features with subsequent pregnancies Treatment Iodine Replacement EUTHYROID MNG Epidemiology Incidence by Palpation – 10% Incidence by Imaging – up to 50% Aetiology Benign Colloid cyst Simple cyst Adenoma Infection Malignant INVESTIGATIONS Serological TFT Serum Calcitonin? FNAC USS ((useful in looking for malignant features such as microcalcification and capsular invasion/increased vascularity)) CT/MRI – for retrosternal component Tc99/I123 Scintigraphy – NOT useful in MNG/SN ((BTA and ATA, incidence of cancer 10% in cold nodules)) TREATMENT Surgery Cosmetic Compressive symptom Suspicion for cancer Radioiodine Indicated if unfit for surgery Regression of the goitre size SOLITARY NODULES Mx is broadly similar to MNG Cystic nodules Many resolve spontaneously Larger cysts tend to recur Treatment Simple aspiration and expectant approach with small cysts(<3ml) Surgery for the larger ones(10% cancer risk) CLASSIFICATION Simple Non-Toxic Iodine Difficiency Multinodular Goitre Solitary Nodule Physiological Grave’s Disease Plummer’s Disease Toxic Inflammatory Hashimoto’s Thyroiditis De Quervain’s Thyroiditis Riedel’s Thyroiditis Neoplastic Follicular Papillary Medullary Anaplastic Lymphoma Rare Infective Iatrogenic HYPERTHYROIDISM – CLINICAL FEATURES Cardiac Tachycardia, AF High output congestive heart failure Irritability Anxiety Heat intolerance Metabolic Weight loss Increased appetite Dermatological Thermoregulatory Neuopsychiatric Hormonal GI Irregular menstruation Misc Fine tremor Thyroid bruit Diarrhoea Hair loss and brittle nails HYPOTHYROIDISM – CLINICAL FEATURES Cardiac Bradycardia Cold intolerance Depression Mental impairment Constipation Hormonal GI Dermatological Dry skin Myxoedema Metabolic Weight gain Decreased appetite Glucose intolerance Neuopsychiatric Thermoregulatory Irregular menstruation Misc Hoarseness GRAVE’S DISEASE Epidemiology Commonest cause of hyperthyroidism(60%) UK incidence 80/100,000 Pathophysiology Autoantibodies against TSH receptor Stimulation of thyroid gland hyperplasia Autonomous production of T3 and T4 Association with other organ-specific autoimmune diseases Pernicious anaemia, DM, Addison Disease, Myesthenia Gravis HLA-DR3, B8 GRAVE’S DISEASE – CLINICAL PRESENTATION Thyroid Manifestations Diffuse symmetrical goitre +/- bruits Hyperthyroidism Extrathyroid Manifestations Acropachy Myxoedema Grave’s ophthalmopathy GRAVE’S OPHTHALMOPATHY Pathophysiology Lymphocytic infiltration and glycosaminoglycan deposition Extraocular muscle swelling Periorbital fat proliferation GRAVE’S OPHTHALMOPATHY Clinical Features Proptosis greater than 22 mm Lid retraction and lid lag Conjunctival oedema and corneal ulceration Oculomotor problem Decreasing visual acuity Rx options High dose steroids Radiotherapy Surgical – alignment/decompression TOXIC MULTINODULAR GOITRE Epidemiology Commonly found in the elderly Pathophysiology Jod-Baselow Phenomenon ((exact mechanism is obscure. Background iodine deficiency, followed by iodine Xs, leading to unmasking hyperthyroidism. Normal follicular architecture becomes disrupted, leading to inefficient iodine trapping)) ‘T3 toxicosis’ – subclinical hyperthyroidism ((importance of T3 measurement)) TOXIC ADENOMA Plummer’s Disease Epidemiology Rare – 2 % of hyperthyroidism Younger than Toxic MNG Pathophysiology Somatic, non-inherited TSH receptor mutation Autonomous TSHR activation and TOXIC GOITRE - INVESTIGATIONS TFT Thyroid Autoantibodies TPO ((actually the most senstive marker of grave’s disease – 45% for TSH R)) Thyroglobulin TSH receptor Scintigraphy Distinction between toxic nodule and Grave’s disease TOXIC GOITRE - TREATMENT Difference between Grave’s disease and Toxic MNG/Adenoma Grave’s disease may go into remission(30%) Toxic MNG/Adenoma does not go into remission Treatment Options Antithyroid Drugs Radioiodine Surgery ANTITHYROID DRUGS Thionamides Carbimazole, Methimazole, Popylthiouracile(PTU) Pharmacophysiology Inhibition of the organification and oxidation of iodine T4/T3 synthesis inhibition ? Immunomodulation effect for Grave’s disease? Side effects Deranged LFT - rarely drug-induced hepatitis Agranulocytosis(1/1,000) OTHER DRUGS Beta-blocker Propranolol Anticoagulants AF management RADIOIODINE 131 First treatment of choice for Grave’s Disease and MNG PO administration Pharmacophysiology Beta radiation – DNA damage and apoptosis (different from I 123, which emits gamma rays) Dose ? Titration 400 – 600 MBq sufficient for both Grave’s and Toxic MNG RADIOIODINE 131 Side effect Hypothyroidism Thyroiditis Safety? Outpatient treatment Avoid contact with children ((sleep alone/no sharing utensils)) Contraindication Pregnancy Breast feeding TOXIC GOITRE - SURGERY Indications Refractory to radioiodine Patient’s rejection of radioiodine Severe ophthalmopathy Pregnancy with uncontrolled disease Cosmetic Pre-op Preparation Antithyroid treatment Potassium Iodide if antithyroid drug not tolerated ((saturates the thyroid with iodine, then the gland turns off the absorption mechanism)) TOXIC GOITRE - SURGERY Grave’s Disease Toxic Adenoma Total thyroidectomy Thyroid Lobectomy Toxic SMG ? Subtotal thyroidectomy HYPERTHYROIDISM IN PREGNANCY Grave’s Disease Thionamides are safe in pregnancy PTU is preferred as less drug is delivered to foetus Intra-partum – Transient Hyperthyroidism of hyperemesis gravidarum ((betaHCG and TSH share the same subunit)) Post-partum Thyroiditis ((distinction by autoAb, clinical signs, iodine uptake(postpartum))) INFLAMMATORY GOITRES HASHIMOTO’S THYROIDITIS Anti-TPO/Thyroglobulin/TSHR autoAb Initial transient hyperthyroidism due to cellular destruction and release of the preformed thyroid hormones Subsequent hypothyroidism Rubbery diffuse thyroid enlargement Treatment Thyroid replacement Surgery if necessary INFAMMATORY GOITRES – DE QUERVAIN’S SUBACUTE THYROIDITIS Granulomatous inflammation of the thyroid gland ? 2y to viral infection Subacute course over weeks/months Tender symmetrical diffusely enlarged goitre Phases hyperthyroid – hypothyroid – euthyroid(recovery) Treatment Thyroid status control NSAIDs INFLAMMATORY GOITRES – RIEDEL’S FIBROSING THYROIDITIS Chronic Inflammation and Fibrosis of Thyroid Gland Very rare – 1.6/100,000 Uncertain Pathophysiology ? Autoimmune ? Part of systemic fibrosis Spread of the fibrosis outside the thyroid gland – can cause RLN dysfunction/tracheal compression/hypoparathyroidism RIEDEL’S FIBROSING THYROIDITIS Clinical features Extent of hypothyroidism depends on extent of fibrosis of the gland Hard wooden goitre WITHOUT cervical lymphadenopathy May have extra-cervical involvements – retroperitoneal fibrosis/mediastinal fibrosis Investigation Neither FNAC nor Imaging can reliably distinguish Riedel’s Fibrosing Thyroiditis from malignancy ? PET-CT? Open surgical biopsy is required by wedge resection RIEDEL’S THYROIDITIS Medical Treatment Steroid Tamoxifen ((not by oe inhibition but by grow factor level decrease therefore fibroblasts Thyroid hormone replacement Surgical Treatment down)) Wedge Resection Further surgical Rx not recommended due to the extensive fibrosis Prognosis self-limiting, good prognosis THANK YOU