Download THYROID DISORDERS 2

THYROID DISORDERS 2
HYPERTHYROIDISM
 free T3 & T4  thyrotoxicosis
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 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
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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
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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
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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
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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
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