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.
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 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
(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 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.
THYROIDITIS
• Inflammation of the thyroid.

* Types:
1. Hashimoto’s thyroiditis.

2. Subacute granulomatous thyroiditis

(DeQuervain thyroiditis).

3. Reidel’s (fibrous) thyroiditis.

 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.
* 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 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 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.