Endocrine Tutorial

Hyperthyroidism Clinical features

Hyperthyroidism Clinical features –CVS: tachycardia, palpitations, atrial fib –CNS: tremor, anxiety, lability, insomnia –Heat intolerance; warm, moist, flushed skin –Weight loss with increased appetite

Hyperthyroidism Clinical features –CVS: tachycardia, palpitations, atrial fib –CNS: tremor, anxiety, lability, insomnia –Heat intolerance; warm, moist, flushed skin –Weight loss with increased appetite Causes

Hyperthyroidism Clinical features –CVS: tachycardia, palpitations, atrial fib –CNS: tremor, anxiety, lability, insomnia –Heat intolerance; warm, moist, flushed skin –Weight loss with increased appetite Causes –Graves disease –Exogenous thyroid hormone –Functioning multinodular goitre/thyroid adenoma –Thyroiditis –Secondary (hypothal/pituitary dysfunction)

Hypothyroidism Clinical features

Hypothyroidism Clinical features –CVS: bradycardia, cardiomegaly, pericardial effusion –CNS: slowed mental activity, apathy, fatigue, cretinism –Cold intolerance; cool skin; myxedema; hair loss –Weight gain with decreased appetite –Coarsening of features

Hypothyroidism Clinical features –CVS: bradycardia, cardiomegaly, pericardial effusion –CNS: slowed mental activity, apathy, fatigue, cretinism –Cold intolerance; cool skin; myxedema; hair loss –Weight gain with decreased appetite –Coarsening of features Causes

Hypothyroidism Clinical features –CVS: bradycardia, cardiomegaly, pericardial effusion –CNS: slowed mental activity, apathy, fatigue, cretinism –Cold intolerance; cool skin; myxedema; hair loss –Weight gain with decreased appetite –Coarsening of features Causes –Hashimoto thyroiditis –Surgery / Radiation / Drug-induced –Infiltration by tumour –Secondary (hypothal/pituitary dysfunction)

Graves disease Epidemiology –What type of people get Graves disease?

Graves disease Epidemiology –Women, yrs, (M:F = 1:7)

Graves disease Epidemiology –Women, yrs, (M:F = 1:7) Pathogenesis

Graves disease Epidemiology –Women, yrs, (M:F = 1:7) Pathogenesis –Autoimmune disorder –Activation of thyroid by thyroid autoantibodies Anti-TSH R, anti-thyroglobulin, anti-T3/T4 –Associated with certain HLA types –Associated with other AI disorders Hashimoto thyroiditis, pernicious anaemia, rheumatoid arthritis

Graves disease Gross findings –Mild symmetrical thyroid enlargement –Eyes: exophthalmos, lid retraction, lid lag –Skin: pretibial myxedema

Graves disease Microscopic findings Graves diseaseNormal thyroid

Graves disease Microscopic findings

Hashimoto Thyroiditis Epidemiology

Hashimoto Thyroiditis Epidemiology –Women, yrs, (M:F = 1:10 to 20)

Hashimoto Thyroiditis Epidemiology –Women, yrs, (M:F = 1:10 to 20) Pathogenesis

Hashimoto Thyroiditis Epidemiology –Women, yrs, (M:F = 1:10 to 20) Pathogenesis –Autoimmune disorder –Destruction of thyroid by thyroid autoantibodies Anti-TSH R, anti-thyroglobulin –Associated with certain HLA types –Associated with other AI disorders SLE, pernicious anaemia, rh. Arthritis, Sjogrens, IDDM, Graves –May cause transient hyperthyroidism in early stages –Gradual destruction and fibrosis  hypothyroidism

Hashimoto Thyroiditis Gross findings –Enlarged pale thyroid initially –Atrophic thyroid eventually

Hashimoto Thyroiditis Microscopic findings

Hashimoto Thyroiditis Microscopic findings

Thyroiditis Painful –Infectious Adjacent sinusitis, mycobacteria, fungi –Subacute (granulomatous) Post viral Painless –Hashimoto’s –Fibrous Fibrosis, atrophy, hypothyroidism

Goitre What is it?

Goitre What is it? –Enlarged thyroid –Due to impaired thyroid hormone synthesis

Goitre What is it? –Enlarged thyroid –Due to impaired thyroid hormone synthesis Causes

Goitre What is it? –Enlarged thyroid –Due to impaired thyroid hormone synthesis Causes –Iodine deficiency –Goitrogens –Inherited disorders

Goitre Pathogenesis –Hyperplasia of follicular epithelium –Increased thyroid hormone release (decreased colloid) –Involution of follicles when enough thyroid hormone released –Accumulation of colloid Two forms: –Diffuse –Multinodular

Goitre Gross findings –Diffuse: Diffuse enlargement without nodules –Multinodular:

Goitre Microscopic findings –Diffuse (initial hyperplastic stage): Hyperplastic and hypertrophied follicles Decreased colloid –Diffuse (involution stage) Dilated follicles, atrophic epithelium Abundant colloid

Goitre Microscopic findings –Multinodular goitre: –Recurrent episodes of stimulation and involution Hyperplastic and hypertrophied follicles with decreased colloid Dilated follicles with atrophic epithelium and abundant colloid Haemorrhage, fibrosis, calcification, cyst formation

Thyroid neoplasms Risk factors –M:F = 1:4 –Radiation therapy –Hashimoto’s –Multinodular goitre Types –Follicular adenoma –Carcinoma Papillary Follicular Anaplastic Medullary

Follicular adenoma Morphology:

Follicular carcinoma Morphology: –Same as follicular adenoma! BUT –Vascular / capsular invasion –Haematogenous mets

Papillary carcinoma Morphology:

Papillary carcinoma Morphology:

Causes of hyperparathyroidism Parathyroid hyperplasiaParathyroid adenoma

Hyperadrenalism Presentation –Cushing’s syndrome –Conn’s syndrome Causes –Primary Hyperplasia, adenoma, carcinoma –Secondary Hypothalamic/pituitary disorders Ectopic ACTH secretion Activation of renin-angiotensin system

Causes of hyperadrenalism hyperplasiacarcinoma adenoma

Causes of hypoadrenalism haemorrhage metastases infection (TB)

Pancreatic islet cell tumour + Pituitary adenoma + Parathyroid hyperplasia = MEN I

Medullary carcinoma of thyroid + Phaeochromocytoma + Parathyroid hyperplasia = MEN II