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Title: Goiter By Dr. Abdelaty Shawky assistant professor of pathology


1
GoiterBy Dr. Abdelaty Shawkyassistant
professor of pathology
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
    graves disease).
  • 2. Secondary toxic goiter toxic nodular goiter
    or toxic adenoma.

17
Primary toxic goiter exophthalmic goiter
(graves 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 goiterscalloping 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 graves disease. The remaining thyroid
    tissue is inactive. Thyroid hormone secretion is
    autonomous.

28
Thyroiditis
29
  • Inflammation of the thyroid.
  • Types
  • 1. Hashimotos thyroiditis.
  • 2. Subacute granulomatous thyroiditis (DeQuervain
    thyroiditis).
  • 3. Reidels (fibrous) thyroiditis.

30
hashimoto thyroiditis
  • Occurs in middle old age.
  • Common in females more than males (201).
  • 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
Hashimoto thyroiditis
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 30-50 years.
  • More common in females than males (51).
  • 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
Reidels 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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