Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
THYROID DISORDERS 2 HYPERTHYROIDISM free T3 & T4 thyrotoxicosis Clin effects due to hypermetabolic state & nervous activity. CAUSES Common : Diffuse toxic hyperplasia (Graves) Toxic MNG Toxic adenoma Uncommon : Acute / subacute thyroiditis Hyperfunctioning thyroid Ca ChorioCa / hydatidiform mole TSH secreting pit adenoma* Neonatal thyrotoxicosis (maternal Graves) Struma ovarii Iodide induced hyperthyroidism Iatrogenic *Only one with TSH. All the others have TSH symp DIAGNOSIS Clin & lab TSH (except if TSH secreting pit adenoma) fT4 TRH stim test – injection of TRH, then check level of TSH. If TSH goes up not secondary hyperthyroidism Iodine uptake scans: Diffusely increased Graves Solitary nodule GRAVES’S DISEASE COMMONEST CAUSE OF ENDOGENOUS HYPERTHYROIDISM 3 characteristic findings : Hyperthyroidism Ophthalmopathy (exophthalmos) Dermopathy (pretibial myxoedema) Anti TSH R Abs Thyroid stim Ig (TSI) Thyroid growth stim Ig (TGI) TSH binding inhibitor Igs (TBII) Genetic susceptibility : HLA B8, DR 3 AI D/O – anti TSH R Abs, anti thyroid peroxisome Abs, anti TG Abs TSI (LATS) Bind to TSH R, mimic axn of TSH – fairly specific for Graves TGI – bind to TSH R prolif of follic epith TBII – prevent TSH binding, themselves bind & mimic axn of TSH T cell mediated AI – infiltr ophthalmopathy Incr vol of retro-orbital connective tissue & extra ocular muscle due to: T cell infilt Infl oedema of extra ocular muscle Accum of ECM components Incr amt of fatty tissue Orbital preadipocyte fibroblasts express TSH R’s & become targets of AI attack. T cells perpetuates the AI response Thyroid storm – sudden onset of severe hyperthyroidism MEDICAL EMERGENCY – markedly raised catecholamine levels – death due to arrhythmias Apathetic hyperthyroidism – thyrotoxicosis in elderly; typical features of hyperthyroidism are blunted because of old age & co morbidities THYROIDITIS Inflammation of thyroid Hashimoto Granulomatous (De Quervain) Riedel (Chr sclerosing) Subacute lymphocytic (painless) Painful – infectious, granulomatous HASHIMOTO THYROIDITIS Commonest cause of hypothyroidism in areas of sufficient iodine levels AI, 45 – 65 yrs, F , maybe in chn Genetic component – chrom abN assoc with thyroid autoimmunity eg. Turner synd, Downs synd Pathogenesis : Progressive depletion of thyroid epith cells & replacement by infl infilt & fibrous tissue Sensitisation of auto-reactive CD4+ T helper cells to thyroid Ags is initial event Helper T cell Diff enlargement, pale yellow tan, firm, nodular thyroid Clin – painless goitre, hypothyroid, sometimes 1st get a transient thyrotoxicosis due to disruption of thyroid follicles with secondary release of hormones – HASHITOXICOSIS SUBACUTE (GRANULOMATOUS) THYROIDITIS / DE QUERVAIN 30 – 50 yrs, F Pathogenesis : viral viral Ag itself or thyroid Ag secondary to virus induced host tissue damage, mediated by cytotoxic T cells Clin – pain, fever, fatigue, malaise, transient hyperthroidism (release of preformed hormone) Micros – disrupted follicles, microabscesses, later lympho’s, macro’s, plasma cells surrounding damaged follicles, multinuc GC surrounding colloid, fibrosis may develop SUBACUTE LYMPHOCYTIC (PAINLESS) THYROIDITIS Uncommon Mid aged F, post partum, ?AI Mild enlargement Micros – lymphocytic infilt with hyperplastic germinal centres, disruption of follicles (differs from Hashimoto in that no Hurthle cell change, no fibrosis) RIEDEL THYROIDITIS Rare, unknown aetiology, ?AI Extensive fibrosis hard woody mass (mimic Ca) May be assoc with fibrosis elsewhere in body PALPATION THYROIDITIS Vigorous clin palpation disruption of follicles, MNGC, infl cells No abnormality of TFT’s THANKS