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  • 1. Hyperthyroidism partum thyroiditis. <3% will be negative for all 3 autoimmune Abs Anti-microsomal Ab – may be + in Hashimoto’s thyroiditis TSI Thyroid stimulating Immunoglobulin – used when Graves’ dz is suspectedClinical features by all other Abs are negativeGoitre Diffuse ± bruit Nodular Thyroid scan Differentiate btwn types of ↑T4 131GI LOW Diarrhoea Anorexia (I or Graves’ dz: Diffuse uptake N/↑ appetite Steatorrhoea Vomiting Technetium MNG: maximal uptake by active nodulesCardiorespiratory Palpitation Dyspnoea ↑ pulse pressure 99) Toxic adenoma: uptake by adenoma, ↓ uptake by the remaining tissues Sinus tachycardia Angina Exacerbation of Thyroid U/S Differentiate btwn cystic and solid thyroid nodules AF CMP asthma FNAC Differentiate nodule into benign, suspicious or malignant (5%) Cardiac failure Follicular neoplasm – may be either follicular adenoma or CA. Ankle oedema in Indistinguishable on FNAC absence of CFNeuromuscular Nervous / irritable Tremor Proximal Emotional lability Hyperreflexia myopathy Psychosis Clonus Muscle weakness Interpreting TFT T4 T3 TSHDermatological ↑ sweating Onycholysis Spider naevi Pruritus Clubbing Pigmentation Conventional hyperthyroidism ↑ ↑ ↓↓ Alopecia Pretibial Vitiligo T3 – hyperthyroidism N ↑ ↓↓ Palmar erythema myxoedema Subclinical hyperthyroidism N N ↓ / ↓↓Reproductive Amenorrhoea / Infertility / Loss of libido / Primary hypothyroidism ↓ - ↑ oligomenorrhoea spontaneous impotence Subclinical hypothyroidism N - ↑ abortions Secondary hypothyroidism (eg ↓ - ↓↓Ocular Excessive Lid lag / retraction Ophthalmoplegia / hypothalamic or pituitary dz) lacrimation Chemosis diplopia Grittiness Corneal ulceration Papilloedema Exophthalmos Loss of visual acuity Graves’ DiseaseOthers Heat intolerance Fatigue / apathy Lymphadenopathy Thirst Gynaecomastia Osteoporosis Epidemiology • features unique to Graves’ dz are highlighted in blue Usually 30-50 YO • Important complications Genetic factors: a/w HLA-B8, DR3 & DR2 • Stigmata of hyperthyroidism: goitre, tremors, lid lag/retraction, myopathy Trigger: ?viruses / bacteria (E. coli & Yersinia enterocolitica – may possess cell-membrane TSH receptor, causing cross-reactivity of Abs vs host TSH receptor)Causes a/w IDDM & pernicious anaemia cause of >90% of hyperthyroidism in Singapore• Graves’ disease • Iodide induced (eg amiodarone,• MNG contrast dye)• Toxic adenoma • Factitious hyperT4 Features• Thyroiditis (subacute / de Quervain’s, or • TSH induced (eg chorioCA, Diffuse thyroid enlargement + thrill / bruit. May be nodular post partum) hydatidiform mole) Ophthalmopathy • Follicular CA ∼ Lid retraction ∼ Proptosis ∼ Excessive lacrimation ∼ Loss of visual acuity ± visual field defectInvestigations ∼ Conjunctivitis due to corneal oedema or optic n. ∼ Corneal ulceration (due to increased compressionTFT Free T3 & T4, TSH exposure) ∼ DiplopiaTRAb Stimulating TSH-receptor Ab in Graves’ disease (>90%). May also be Pretibial myxoedema (rare): raised pink / purplish plaques on anterior shin to dorsum of foot. blocking causing hypothyroidism a/w pruritis, peau d’orange and coarse hairOther Abs Anti-Thyroid Peroxidase Ab (TPO) & anti-Thyroglobulin Ab (TgAb) – high levels are suggestive of GDz, Hashimoto’s, silent thyroiditis or post-
  • 2. Pathogenesis Papilloedema, loss of visual acuity or visual field defect: Urgent Rx with Prednisolone TRAb (TSH-receptor IgG Abs) vs thyroid follicular cell stimulates thyroid hormone production 60mg daily. Surgical orbital decompression if no improvement. Ophthalmopathy & dermopathy: immunologically mediated proliferation of fibroblasts which secrete hydrophilic glycosaminoglycans causing increased interstitial fluid content + chronic inflammatory cell infiltrate (usually lymphocytic). May cause optic nerve compression.Clinical course MNG Usually women around 60 YO1. Prolonged periods of ↑T4 of fluctuating severity a/w AF and cardiac failure due to older age group2. Periods of relapses and remission of ↑T4 Rx:3. Single short-lived episode with prolonged remission ± eventual onset of ↓T4 1. Radioiodine – hypoT4 less common 2. Partial thyroidectomy – for tracheal compression or retrosternal extension of goitreAssoc. Non-specific Biochemical Abnormalities 3. Antithyroid drugs NOT useful as relapse occurs after drug withdrawal. LFT: ↑ bilirubin, ALT, AST, GGT, ALP Mild ↑ Ca Glycosuria Toxic Adenoma Follicular adenoma autonomously secreting excess thyroid hormone – negative feedbackManagement inhibits TSH secretion and causes atrophy of the rest of the thyroid gland.1. Carbimazole Usually females >40YO Inhibit tyrosine iodination + immunosuppression (↓ serum TRAb conc) Hyperthyroidism may be mild, and 50% have isolated elevation of T3 only (T3 thyrotoxicosis) Duration: 6-18 mths then try stopping. Consider other Rx if relapse occurs (70%) Rx: Hemithyroidectomy, radioiodine. Post-Rx hypoT4 uncommon due to compensation of Onset of efx: 3-12 wks. Meanwhile, use propanolol for symptomatic control remaining thyroid gland. Antithyroid drugs not useful as relapse invariably follow drug 2 dosing strategy: either give just enough CBZ to keep PT euthyroid, or give excess CBZ withdrawal. & correct hypothyroidism with L-thyroxine replacement ADR: **Agranulocytosis (reversible, requires WBC monitoring. Stop drug and consult Dr Subacute (de Quervain’s) Thyroiditis immediately in the event of a sore throat / fever!), rash, cholestatic hepatitis, Virus induced (Coxsackie, mumps, adenovirus) thyroid inflammation. thrombocytopenia, vasculitis, lupus-like syndrome Usually females 20-40YO Preferred over propylthiouracil due to lower dose (once daily vs tds dosing) a/w pain radiating to angle of jaw and ears, worse on swallowing, coughing, neck movt.2. Subtotal thyroidectomy Tender enlarged thyroid Change antiT4 drug to potassium iodate PO 2 wks pre-Sx: short term inhibition of thyroid Raised thyroid hormone levels for 4-6 wks followed by asymptomatic hypoT4. Full recovery hormone release and reduce gland size and vascularity within 4-6 mths Outcome 1 yr post-Sx: 5% ↑T4, 15% permanently ↓T4, 80% euthyroid. Late onset ↓T4 or Rx: Aspirin / NSAID for pain, propranolol for ↑T4 symptoms, ± prednisolone. ↑T4 common, therefore require continued follow-up.3. Radioiodine Post-partum Thyroiditis Unmasking of subclinical autoimmune thyroid disease Indications: failed medical/Sx Rx, PT w cardiac dz, PT’s preference 4-12 wks for onset of effects Usually presents with ↑T4 symptoms for the first time within 6 mths post-partum. Recurs in subsequent pregnancies, progressing to permanent hypoT4 in the long term. Interim symptom control with β-blocker or carbimazole Rx: Propranolol. No a/w ↑ freq of malignancy or congenital malformation in offspring st Majority devt hypothyroidism (50% in 1 yr) – need f/u with TFT & thyroxine replacement CI: pregnant, breastfeeding, severe Graves’ Ophthalmopathy (may worsen it)4. β-blocker (eg propranolol) Indications for surg: For short term alleviation of symptoms. • Thyrotoxicosis not controlled by drugs Useful for pre-thyroidectomy, or before onset of effects of radioiodine or carbimazole • Compressive symps5. Ophthalmopathy • CA Eyedrops / glasses + side shields • Cosmesis Lateral tarsorrhaphy – for corneal ulceration Extra-ocular muscle Sx: for persistent diplopia. Alternative: prism glasses.
  • 3. Special Problems in Hyperthyroidism Drugs 1. β-blockers IV esmolol, or IV / PO propranololHyperthyroidism & Pregnancy 2. PTU (propylthiouracil) Blocks iodination and conversion of T4 to T3 ↑T4 usually cause anovulatory cycles and infertility 3. Iodine solution Inhibit thyroid hormone release Carbimazole: crosses placenta causing treats fetus which is exposed to TRAb as well. Use 4. Dexamethasone IV 2mg for glucocorticoid support & to block conversion smallest dose possible to prevent fetal hypothyroidism & goitre of free T4 to T3 Breastfeeding: use PTU which is excreted in breast milk to a lesser extent c.f carbimazole. 5. Treat CVS Cx accordingly Eg digoxin, diuretics Radioiodine: absolute CI – causes fetal hypothyroidism. 6. Carbimazole Long term control of ↑T4 with carbimazole.Atrial Fibrillation Dysrhythmias present in 10% of thyrotoxic patients. Increasing incidence with age. Establish euthyroidism, then consider cardioversion (establish stable sinus rhythm in 50%). Thyrotoxic periodic paralysis β-blocker helps control ventricular rate as well. • Periodic weakness a/w hypo K - Cause of hypoK is due to K shift intracellularly Anticoagulation: aspirin in the elderly, warfarin in younger PTs and those with Cardiomegaly • usu Asian males, onset in early adulthood / atrial thrombus. • episodic limb weakness lasting hrs to days • weakness ppted by exercise, onset usu at night during sleep (after strenuous exercise) • strength normal btwn attacks • ECG: ST depression, flattened T waves, U wavesThyroid StormPresentationFever From underlying sepsis or thyroid storm (uncontrolled ↑T4 / post-subtotal thyroidectomy / post-radioiodine Rx)Agitation / confusionTachycardia / AFAccentuated thyrotoxic S/S LOW, tremors etcMultiorgan dysfunction CNS: altered mental state, confusion, agitation, coma etc GI: abdo pain, diarrhoea, vomiting CVS: AF, heart failure, hyper/hypotensionVolume depletion From fever, diarrhoea and increased metabolismS/S of precipitating event Eg sepsis, recent surgeryManagement Supportive1. High flow O22. Monitor ECG, vital signs q10mins, pulse oximetry Digitally signed by DR WANA HLA SHWE3. IV lines and fluid Dextrose-saline with appropriate electrolytes. Beware of DN: cn=DR WANA HLA SHWE, c=MY, precipitating heart failure. o=UCSI University, School of Medicine, KT- Campus, Terengganu, ou=Internal4. Lab invxs FBC Medicine Group, email=wunna. U/E/Cr hlashwe@gmail.com LFT Reason: This document is for UCSI year 4 students. TFT Date: 2009.02.24 14:01:08 +0800 CXR: heart failure and infection ECG; ischaemia, infarction or dysrrhythmia Urinalysis ± C/S if sepsis suspected5. Correct precipitating factors eg sepsis, MI6. Relieve fever Paracetamol, tepid sponging