GoiterGoiter

* Definition: Non-inflammatory, non-neoplastic

enlargement of the thyroid gland.

* Classification:

•Simple (non-toxic) goiter.

•Toxic goiter.

SIMPLE (NON-TOXIC) GOITERSIMPLE (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.

* 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.

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.

* Morphological features:

a. Parenchymatous goiter:

* Gross picture:

•Symmetrical enlargement.

•Firm in consistency.

•Cut surface is grayish pink.

* Microscopic picture:

•Hyperplastic acini lined by tall columnar cells

and filled with scanty colloid.

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”.

* Microscopic picture:

•The acini are distended with colloid and lined

by flat cells.

•The stroma is scanty.

c. Nodular goiter:

* Gross picture:

•Asymmetrical enlargement.

•Variable: firm areas and soft cystic areas.

•Cut surface is nodular.

* Microscopic picture:

•Multiple nodules, some formed of hyperplastic

acini and others show acini filled with colloid.

•The nodules are surrounded by fibrous tissue.

* 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.

Goiter

Goiter

Goiter

TOXIC GOITERTOXIC GOITER

• Two types;

1. Primary toxic goiter (exophthalmoic goiter or

grave’s disease).

2. Secondary toxic goiter: toxic nodular goiter

or toxic adenoma.

PRIMARY TOXIC GOITER EXOPHTHALMIC GOITER PRIMARY TOXIC GOITER EXOPHTHALMIC GOITER

(GRAVE’S DISEASE) (GRAVE’S DISEASE)

• 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

* 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.

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

Toxic goiter

Toxic goiter:scalloping of colloid inside thyroid follicles

small sized follicles , lymphocytic infiltration,hypervascularity

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

Exophthalmos associating Graves’ disease

Exophthalmos associating toxic goiter

SECONDARY TOXIC GOITERSECONDARY TOXIC GOITER

* 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.

THYROIDITISTHYROIDITIS

• Inflammation of the thyroid.

* Types:

1. Hashimoto’s thyroiditis.

2. Subacute granulomatous thyroiditis

(DeQuervain thyroiditis).

3. Reidel’s (fibrous) thyroiditis.

HASHIMOTO THYROIDITISHASHIMOTO 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.

* Gross picture:

•Symmetrically enlarged thyroid gland.

•Firm inconsistency.

•Intact, non-adherent capsule.

•Cut surface is pale, homogenous and

sometimes nodular.

* 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.

Hashimoto thyroiditis

Hashimoto thyroiditis; Hurthle cell metaplasia

Hashimoto thyroiditis; Hurthle cell metaplasia

* Complications:

•Hypothyroidism.

•Development of other autoimmune diseases.

•Malignant transformation (lymphoma)

SUBACUTE GRANULOMATOUS THYROIDITISSUBACUTE 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.

* Gross picture:

•Unilateral or bilateral enlargement.

•Intact capsule.

•Slightly adherent.

•Cut surface shows scattered firm yellowish

white areas.

* 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.

Granulomatous thyroiditis

REIDEL’S THYROIDITISREIDEL’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.