1. Endocrine Tutorial

2. Hyperthyroidism Clinical features

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

4. 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

5. 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)

6. Hypothyroidism Clinical features

7. 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

8. 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

9. 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)

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

11. Graves disease Epidemiology –Women, 20-40 yrs, (M:F = 1:7)

12. Graves disease Epidemiology –Women, 20-40 yrs, (M:F = 1:7) Pathogenesis

13. Graves disease Epidemiology –Women, 20-40 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

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

15. Graves disease Microscopic findings Graves diseaseNormal thyroid

16. Graves disease Microscopic findings

17. Hashimoto Thyroiditis Epidemiology

18. Hashimoto Thyroiditis Epidemiology –Women, 45-65 yrs, (M:F = 1:10 to 20)

19. Hashimoto Thyroiditis Epidemiology –Women, 45-65 yrs, (M:F = 1:10 to 20) Pathogenesis

20. Hashimoto Thyroiditis Epidemiology –Women, 45-65 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

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

22. Hashimoto Thyroiditis Microscopic findings

23. Hashimoto Thyroiditis Microscopic findings

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

25. Goitre What is it?

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

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

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

29. 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

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

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

32. 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

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

34. Follicular adenoma Morphology:

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

36. Papillary carcinoma Morphology:

37. Papillary carcinoma Morphology:

38. Causes of hyperparathyroidism Parathyroid hyperplasiaParathyroid adenoma

39. 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

40. Causes of hyperadrenalism hyperplasiacarcinoma adenoma

41. Causes of hypoadrenalism haemorrhage metastases infection (TB)

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

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