2. • These disorders include thyroiditis, and antibody-
mediated disturbances in thyroid function that are not
necessarily associated with inflammation (exemplified
by Graves disease).
• Thyroiditis encompasses a diverse group of disorders
characterized by some form of thyroid inflammation.
• The three most common and clinically significant
subtypes:
(1) Hashimoto thyroiditis.
(2) Granulomatous (de Quervain) thyroiditis.
(3) Subacute lymphocytic thyroiditis.
3. 1= Hashimoto Thyroiditis:
• Also known as ‘Chronic Lymphocytic Thyroiditis or
diffuse lymphocytic thyroiditis, struma lymphomatosa
or goitrous autoimmune thyroiditi’.
• Hashimoto thyroiditis is the most common cause of
hypothyroidism in areas of the world where iodine
levels are sufficient.
• Gradual thyroid failure secondary to autoimmune
destruction of the thyroid gland.
• prevalent between 45 and 65 years of age and is
more common in women with a female to male ratio of
10: 1 to 20:1.
• Although it is primarily a disease of older women, it can
occur at any age, including childhood.
4. • Regions where iodine intake is highest have higher
incidence of Hashimoto’s thyroiditis e.g. in Japan
and the United States.
• Pathogenesis:
• Circulating autoantibodies against thyroid antigens.
1. Other autoimmune disease association.
2. Immune destruction of thyroid cells (CD8+ T
cytotoxic cells).
3. Detection of autoantibodies.
4. Inhibitory TSH-receptor antibodies.
5. Genetic (50%first degree relatives and 40% in
monozygotic twins).
• HLA-DR3 and HLA-DR5 subtypes.
5.
6.
7. • Morphology:
• Macroscopically - The thyroid usually is diffusely and
symmetrically enlarged.
• Microscopically –
• Parenchyma infiltration by mononuclear
inflammatory ‘small lymphocytes, plasma cells, and
well-developed germinal cells.
• Hürthle or oxyphil cells or Askanazy cells = atrophic
thyroid follicle lined by epithelial cells which abundant
of eosinophilia, granular cytoplasm, which later all
these leads to metaplasia.
• Finally the Interstitial connective tissue is increased
and may be abundant and causes more fibrosis ‘fibrosis
variant’
9. • Clinical feature:
1. Painless enlargement.
2. Enlargement ‘symmetric and diffuse, or localized
to raise suspicion for neoplasm’.
3. Hypothyroidism develops gradually.
4. Secondary release of thyroid hormones
(hashitoxicosis).
5. Hashimoto thyroiditis may increase risk for the
development of B-cell non-Hodgkin lymphomas.
10.
11.
12. 2= Subacute Granulomatous
(deQuervain) Thyroiditis:
• Also called ‘giant cell thyroiditis’.
• Less common than Hashimoto disease.
• 30 and 50 years of age more in female.
• Causes:
• Viral infection ‘history of an upper-respiratory
infection’.
• The process spontaneously remits.
• Morphology:
• Macroscopically – The gland is firm, with an intact
capsule, and may be unilaterally or bilaterally
enlarged.
13. • Microscopically –
• Extravasation of colloid, and infiltrating
neutrophils.
• Later on time the neutrophili are replaced by
lymphocytes, plasma cells, and macrophages.
• The extravasated colloid provokes an excited
granulomatous reaction with giant cells.
• Healing occurs by resolution of inflammation and
fibrosis.
• Clinical feature:
• Acute onset.
• Neck pain and tender of firm enlarged mass.
• Sign and symptoms of hypethyrodism.
• Transient hyperthyroidism.
14.
15.
16. • Diagnosis:
• Clinical.
• Thyroid testing and TSH.
• Radioactive iodine uptake should be measured to
confirm the diagnosis.
• Increased WBC and ESR.
• Treatment:
1. Nonsteroidal anti-inflammatory drugs (nsaids).
2. High dose corticosteroids.
17. 3= Subacute Lymphocytic
Thyroiditis:
• Also called silent or painless thyroiditis.
• The onset follows pregnancy (postpartum
thyroiditis).
• Autoimmune,circulating antithyroid antibodies.
• Middle-aged women.
• Clinical feature:
• Painless neck mass.
• Hyperthyroidism followed by euthanoid state
within month, then hypothyroidism.
20. Riedel Thyroiditis:
• •Less common form of thyroiditis.
• Etiology: It is unknown, but the presence of
circulating antithyroid antibodies in most
patients suggests an autoimmune etiology.
• Gross: Thyroid is stony hard and fixed which
clinically simulates a thyroid carcinoma.
• Microscopy: Shows extensive fibrosis involving
the thyroid and contiguous neck structures.
21.
22. • Autoimmune process in which serum IgG Abs bind to
the thyroid TSH receptors and produce stimulation of
thyroid hormone production.
• These Abs called thyroid – stimulating antibodies
(TSAb).
• 20 and 40 years of age.
• Pathogenesis:
• Autoantibodies against the TSH receptor that bind to,
and stimulate, thyroid follicular cells independent of
endogenous trophic hormones.
• Thyroid-stimulating immunoglobulin (TSI).
• Thyroid growth-stimulating immunoglobulins.
• TSH-binding inhibitor immunoglobulins.
28. Eugogo classification:
• NOSPECS
• Grade 0 : No signs or symptoms
• Grade1: Only signs no symptoms
• Grade2: Soft tissue involvement
• Grade3: Proptosis
• Grade4: Eextraocular muscle involvement
• Grade5: Corneal involvement
• Grade6: Sight loss with optic nerve involvement
29. • Morphology:
• Macroscopically - Diffuse hypertrophy and
hyperplasia of thyroid follicular epithelial cells.
• The gland is usually smooth and soft, and its
capsule is intact.
• Microscopically –
• Follicular epithelial cells in untreated cases are tall,
columnar, and more crowded than usual.
• The colloid within the follicular lumen is pale, with
scalloped margins.
• Changes in extrathyroidal tissues include
generalized lymphoid hyperplasia.