thyroiditis

HASHIMOTO THYROIDITIS
Hashimoto thyroiditis (or chronic lymphocytic thyroiditis) is the most common cause of hypothyroidism It is characterized by gradual thyroid failure because of autoimmune destruction of the thyroid gland.

Pathogenesis.
The Hashimoto thyroiditis is an autoimmune disease in which the immune system reacts against a variety overriding feature of Hashimoto thyroiditis is progressive depletion of thyroid epithelial cells (thyrocyteswhich are gradually replaced by mononuclear cell infiltration and fibrosis. Multiple immunologic mechanisms may contribute to the death of thyrocytes The thyroid is often diffusely enlarged
although more localized enlargement may be seen in some cases. Microscopic examination reveals extensive infiltration of the parenchyma by a mononuclear inflammatory infiltrate containing small lymphocytes, plasma cells, The thyroid follicles are atrophic and  well-developed germinal centers 
Clinical Course
Hashimoto thyroiditis comes to clinical attention as painless enlargement of the thyroid, usually associated with some degree of hypothyroidism, in a middle-aged womanPatients with Hashimoto thyroiditis are at increased risk for developing other concomitant autoimmune diseases, both endocrine (type 1 diabetes, autoimmune adrenalitis), and nonendocrine (systemic lupus erythematosus, myasthenia gravis, and Sj?gren syndrome; see ), and also at increased risk for the development of B-cell non-Hodgkin lymphomas
SUBACUTE (GRANULOMATOUS) THYROIDITIS
Subacute thyroiditis, which is also referred to as granulomatous thyroiditis or De Quervain thyroiditis, occurs much less frequently than does Hashimoto disease. The disorder is most common between the ages of 30 and 50 and, like other forms of thyroiditis, affects women considerably more often than men (3:1 to 5:1).

Pathogenesis.
Subacute thyroiditis is believed to be caused by a viral infection or a postviral inflammatory process  The majority of patients have a history of an upper respiratory infection just before the onset of thyroiditis. clusters of cases have been reported in association with coxsackievirus, mumps, measles, adenovirus, and other viral illnessesThis antigen stimulates cytotoxic T lymphocytes, which then damage thyroid follicular cells.
Morphology
MorphologyHistologically, the changes are patchy and depend on the stage of the disease. Early in the active inflammatory phase, scattered follicles may be entirely disrupted and replaced by neutrophils forming microabscesses. Later, the more characteristic features appear in the form of aggregations of lymphocytes, histiocytes, and plasma cells about collapsed and damaged thyroid follicles. 
The presentation of subacute thyroiditis may be sudden or gradual. It is characterized by pain in the neck, which may radiate to the upper neck, jaw, throat, or ears, particularly when swallowing. Fever, fatigue, malaise, anorexia, and myalgia accompany a variable enlargement of the thyroid The resultant thyroid inflammation and hyperthyroidism are transient, usually diminishing in 2 to 6 weeks, even if the patient is not treatedIt may be followed by a period of transient, usually asymptomatic hypothyroidism lasting from 2 to 8 weeks, but recovery is virtually always complete
SUBACUTE LYMPHOCYTIC (PAINLESS) THYROIDITIS
Subacute lymphocytic thyroiditis, which is also referred to as painless thyroiditis or silent thyroiditis, is an uncommon cause of hyperthyroidism It usually comes to clinical attention because of mild hyperthyroidism, goitrous enlargement of the gland, or both, it is most often seen in middle-aged adults and is more common in women, especially during the postpartum period (postpartum thyroiditis),
Morphology
The most specific histologic features consist of lymphocytic infiltration with hyperplastic germinal centers within the thyroid parenchyma and patch disruption and collapse of thyroid follicles. Unlike in Hashimoto thyroiditis, fibrosis and Hürthle cell metaplasia are not commonly seen The principal clinical manifestation of painless thyroiditis is hyperthyroidism. Symptoms usually develop over 1 to 2 weeks and last from 2 to 8 weeks before subsiding
Graves Disease
Hyperthyroidism owing to hyperfunctional, diffuse enlargement of the thyroid
Infiltrative ophthalmopathy with resultant exophthalmos
? Localized, infiltrative dermopathy, sometimes called pretibial myxedema, which is present in a minority of patients
Pathogenesis
raves disease is an autoimmune disorder in which a variety of antibodies may be present in the serum, including antibodies to the TSH receptor, thyroid peroxisomes, and thyroglobulin. Of these, autoantibodies to the TSH receptor are central to disease pathogenesis
Thyroid-stimulating immunoglobulin (TSI  Thyroid growth-stimulatingimmunoglobulins (TGI): Also directed against the TSH receptor, thyroid growth-stimulating immunoglobulins have been implicated in the proliferation of thyroid follicular epithelium.
TSH-binding inhibitor immunoglobulins (TBII): These anti-TSH receptor antibodies prevent TSH from binding normally to its receptor on thyroid epithelial cells.
The thyroid gland is usually symmetrically enlarged because of diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells
Histologically, the dominant feature is too many cells. The follicular epithelial cells in untreated cases are tall and more crowded than usual. This crowding often results in the formation of small papillae, which project into the follicular lumen and encroach on the colloid The colloid within the follicular lumen is pale, with scalloped margins. Lymphoid infiltrates, consisting predominantly of T cells, with fewer B cells and mature plasma cells, are present throughout the interstitium; germinal centers are common.