Question

what is the pathophysiology in Hadhimito Thyroiditis?

Answer 1

Hashimoto's thyroiditis:

Hashimoto's thyroiditis is an autoimmune disease that destroys thyroid cells by cell and antibody mediated immune response.

It is the most common cause of hypothyroidism in the developed countries.

This disease is also known as chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis.

Women are mostly affected.

Etiology :

Etiology of hashimoto's thyroiditis is very poorly understood.

Most patient develop antibodies to a variety of thyroid antugens, the most common of which is anti-thyroid peroxidase (anti-TPO).

Others including anti thyroglobulins ( anti-TGs), TSH receptor blocking antibodies.

These antibodies attack the thyroid tissue eventually leading to inadequate production of thyroid hormone.

Pathophysiology :

The development of Hashimoto's thyroiditis is thought to be autoimmune in origin with lymphocytic infiltration and fibrosis as typical features.

Various autoantibodies may be present against thyroid peroxidase, thyroglobulin, and TSH receptor. Although small percentage of people many have non of these antibodies.

Antibody dependent cell mediated cytotoxicity is a substantial factor behind the apoptotic fall out of Hashimoto's thyroiditis.

Activation of cytotoxic T lymphocytes (CD8+ T-cells) in response to cell mediated immune response affected by helper T lymphocytes ( CD4+ T cells) is central to thyroid destruction.

Hashimoto's thyroiditis is an type 4 hypersensitivity.

Recruitment of macrophages is another effect of T lymphocytes activation, with Th1 axis lymphocytes producing inflammatory cytokines within thyroid tissue to further macrophages activation and migration into thyroid gland for direct effect.

Gross morphological changes within the thyroid gland are seen in general enlargement which is far more locally nodular or irregular than more diffuse pattern.

Capsule is intact and the gland is differentiated from the surrounding tissue.

Histologically, hypersensitivity is seen as diffuse parenchymal infiltration of lymphocytes, particularly plasma B cells , which can often be seen as secondary lymphoid follicles.

Atrophy of collied bodies is lined by the Hurtle cells, cells with intensly eosinophilic, granular cytoplasm, a metaplasia from the normal cuboidal cells in the thyroid gland.

The current diagnosis is based on clinical symptoms correlating with laboratory results of elevated TSH with normal to low thyroxine levels.

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