1. Goiter

2. * Definition: Non-inflammatory, non-neoplastic enlargement of the thyroid gland.
* Classification:
Simple (non-toxic) goiter.
Toxic goiter.

3. SIMPLE (NON-TOXIC) GOITER
Enlargement of the thyroid without toxic manifestations.
* Causes:
1. Iodine deficiency.
a. Absolute deficiency: in areas far from the sea.
b. Relative deficiency: due to increased demand for iodine at pregnancy, puberty and lactation.
2. Dyshormonogenesis: hereditary deficiency of enzymes necessary for thyroxine formation.
3. Goitrogens: Well-known goitrogens as cabbage, cauliflower which contain thiocyanate which inhibits iodide transport within the thyroid.

4. * Pathogenesis: a. Parenchymatous goiter:
Iodine deficiency → decreased thyroid hormone synthesis → increases TSH secretion → thyroid glands hyperplasia.
The acini are increased in number and lined by tall columnar cells and contain little colloid.
If iodine deficiency is corrected after a short time, the acini return to the normal state.

5. b. Colloid goiter:
When iodine deficiency is corrected after a longer time → the acini are distended with colloid and lined by flat cells.
c. Nodular goiter:
Repeated cycles of iodine deficiency & correction →nodular goiter in which the gland shows multiple nodules of parenchymatous goiter, colloid goiter and areas of fibrosis.

6. * Morphological features:
a. Parenchymatous goiter:
* Gross picture:
Symmetrical enlargement.
Firm in consistency.
Cut surface is grayish pink.

7. * Microscopic picture:
Hyperplastic acini lined by tall columnar cells and filled with scanty colloid.

8. b. Colloid goiter:
* Gross features:
Symmetrical enlargement.
Soft in consistency.
Cut surface is grayish brown in color and may shows cystic spaces filled with glistening colloid “honey comb appearance”.

9. * Microscopic picture:
The acini are distended with colloid and lined by flat cells.
The stroma is scanty.

10. c. Nodular goiter:
* Gross picture:
Asymmetrical enlargement.
Variable: firm areas and soft cystic areas.
Cut surface is nodular.

11. * Microscopic picture:
Multiple nodules, some formed of hyperplastic acini and others show acini filled with colloid.
The nodules are surrounded by fibrous tissue.

12. * Complications of simple goiter:
1. Pressure effects: on esophagus, trachea, and recurrent laryngeal nerve.
2. Secondary hyperthyroidism due to Hyperfunctioning nodules (toxic nodular goiter). No exophthalmos.
3. Malignancy in 2% of cases: follicular carcinoma.

13. Goiter

14. Goiter

15. Goiter

16. Toxic goiter Two types;
1. Primary toxic goiter (exophthalmoic goiter or grave’s disease).
2. Secondary toxic goiter: toxic nodular goiter or toxic adenoma.

17. Primary toxic goiter exophthalmic goiter (grave’s disease)

18. Organ specific autoimmune disease due to auto-antibodies (LATS; long acting thyroid stimulating) stimulating TSH receptors leads to diffuse hyperplasia and hyperfunctioning acini with excess thyroid hormone secretion

19. * Pathological features:
1. Thyroid:
N/E: symmetrically enlarged, firm, with dark red “vascular” cut surface.
M/P: hyperplastic acini lined by columnar cells and filled with faintly stained colloid with peripheral scalloping. The stroma is highly vascular and shows lymphocytic infiltration.

20. Graves’ disease :Diffusely enlarged gland , Can weigh up to 200 g ,Richly vascular

21. Toxic goiter

22. Toxic goiter: scalloping of colloid inside thyroid follicles small sized follicles , lymphocytic infiltration,hypervascularity

23. 2. Exophthalmos: forward protrusion of the eye globe due to edema and degeneration of the retro-orbital muscles “special auto-antibodies react with them”.
3. Diffuse lymphoid hyperplasia: in thymus, tonsil, spleen, guts.
4. Left ventricular hypertrophy “thyrotoxic cardiomyopathy”.
5. Pre-tibial myxedema.
6. Increased basal metabolic rate

24. Exophthalmos associating Graves’ disease

25. Exophthalmos associating toxic goiter

26. Secondary toxic goiter

27. * Causes: A. Toxic nodular goiter: Complicating simple nodular goiter.
Diffuse, nodular enlargement of the thyroid. Some nodules show hyperfunctioning acini. Other acini are inactive.
B. Toxic adenoma:
Complicating thyroid adenoma.
The Hyperfunctioning neoplastic acini are like those of grave’s disease. The remaining thyroid tissue is inactive. Thyroid hormone secretion is autonomous.

28. Thyroiditis

29. Inflammation of the thyroid. * Types:
1. Hashimoto’s thyroiditis.
2. Subacute granulomatous thyroiditis (DeQuervain thyroiditis).
3. Reidel’s (fibrous) thyroiditis.

30. hashimoto thyroiditis
Occurs in middle & old age.
Common in females more than males (20:1).
Cause painless thyroid enlargement.
Associated with hypothyroidism.
* Pathogenesis:
Autoimmune disease in which the immune system reacts against a variety of thyroid antigens.

31. * Gross picture: Symmetrically enlarged thyroid gland.
Firm inconsistency.
Intact, non-adherent capsule.
Cut surface is pale, homogenous and sometimes nodular.

33. * Microscopic picture:
Dense inflammatory infiltrate formed of lymphocytes, plasma cells and macrophages, with sometimes lymphoid follicle formation.
Some acini are atrophied and others show regenerative changes (lined by large cubical cells with deeply esinophilic granular cytoplasm termed (Hurthle cells). This is termed Hurthle cell metaplasia.
Finally, fibrosis.

34. Hashimoto thyroiditis

35. Hashimoto thyroiditis; Hurthle cell metaplasia

36. Hashimoto thyroiditis; Hurthle cell metaplasia

37. * Complications: Hypothyroidism.
Development of other autoimmune diseases.
Malignant transformation (lymphoma)

38. Subacute granulomatous thyroiditis
Occurs between years.
More common in females than males (5:1).
Cause painful thyroid enlargement.
Associated with transient hyperthyroidism.
* Pathogenesis:
Associated with viral infection.

39. * Gross picture: Unilateral or bilateral enlargement. Intact capsule.
Slightly adherent.
Cut surface shows scattered firm yellowish white areas.

40. * Microscopic picture:
Neutrophilic infiltration with variable destruction of the thyroid follicles.
Pools of colloid surrounded by multinucleate giant cells, aggregations of lymphocytes, histiocytes and plasma cells.
Finally, fibrosis, chronic inflammatory cells replace the damaged foci.

41. Granulomatous thyroiditis

42. Reidel’s thyroiditis * Gross picture: * Microscopic picture:
Rare, of unknown cause. Affect both sexes equally.
* Gross picture:
The gland is hard in consistency and adherent to the surrounding structures (simulating malignancy).
* Microscopic picture:
Dense fibrous tissue replacing the thyroid tissue and penetrating the capsule to the surrounding neck structures.