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.
* 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.
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.