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Goiter

Goiter. * Definition: Non-inflammatory, non-neoplastic enlargement of the thyroid gland. * Classification: Simple (non-toxic) goiter. Toxic goiter. SIMPLE (NON-TOXIC) GOITER. Enlargement of the thyroid without toxic manifestations. * Causes: 1. Iodine deficiency.

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Goiter

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  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 folliclessmall 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.

  32. * 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 Hurthlecell metaplasia. • Finally, fibrosis.

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

  34. Subacute granulomatous thyroiditis • Occurs between 30-50 years. • More common in females than males (5:1). • Cause painful thyroid enlargement. • Associated with transient hyperthyroidism. * Pathogenesis: • Associated with viral infection.

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

  36. * 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.

  37. Reidel’s thyroiditis • 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.

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