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===Pathogenesis===
===Pathogenesis===
*The exact pathogenesis of postpartum thyroiditis is not fully understood. i
*The exact pathogenesis of postpartum thyroiditis is not fully understood. However, studies have shown that it is an autoimmune disorder in which thyroid tissue antigens are recognized as non-self antigens and our immune cells mediate inflammtory responce to thyrotid gland and destory it. StudIt then lead to sudden release of stored thyroid hormone in blood and appearence of hyperthroid picutre clinically and labortically transiently followed by recovery to euthyroid state or hypothroid state depending on level of distruction of thyroid gland, persistance of inflammtory state, and recovery strenght of gland. itudies have also shown that pregnency is stage of reduced immunity to protect fetus from unwanted exposre of immunty which at the end of pregnecy escalte sudden immunity, leading to begning of slowly evolving autoimmune responce to thyroid auto-antigens, in a rapid Se sequences leading to appearnece thyroidtis. studiesrareoing on in search of exact autoantibody and autoantigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum throiditis. TPO autoantibody is signifcantly linked to occurence of postpartum throidiitis.  
OR
 
*It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [[[hypothesis]] 1], [hypothesis 2], or [hypothesis 3].
=== Physiology: ===
*[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
*Thyroid is endocrine gland which synthise and secrates thyroid hormone in bloodstream directly. It is regulated by hypothelmus and piutary gland.  
*Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
*
*[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
*The progression to [disease name] usually involves the [molecular pathway].
*
*The pathophysiology of [disease/malignancy] depends on the[histological subtype.


==Genetics==
==Genetics==

Revision as of 19:50, 23 September 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Overview

The exact pathogenesis of [ Postpartum thyroiditis] is not fully understood.

OR

It is thought that [ Postpartum thyroiditis] is mediated by either [Autoimmunity], [enviromental factors], or [smoking].

Pathophysiology

Pathogenesis

  • The exact pathogenesis of postpartum thyroiditis is not fully understood. However, studies have shown that it is an autoimmune disorder in which thyroid tissue antigens are recognized as non-self antigens and our immune cells mediate inflammtory responce to thyrotid gland and destory it. StudIt then lead to sudden release of stored thyroid hormone in blood and appearence of hyperthroid picutre clinically and labortically transiently followed by recovery to euthyroid state or hypothroid state depending on level of distruction of thyroid gland, persistance of inflammtory state, and recovery strenght of gland. itudies have also shown that pregnency is stage of reduced immunity to protect fetus from unwanted exposre of immunty which at the end of pregnecy escalte sudden immunity, leading to begning of slowly evolving autoimmune responce to thyroid auto-antigens, in a rapid Se sequences leading to appearnece thyroidtis. studiesrareoing on in search of exact autoantibody and autoantigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum throiditis. TPO autoantibody is signifcantly linked to occurence of postpartum throidiitis.

Physiology:

  • Thyroid is endocrine gland which synthise and secrates thyroid hormone in bloodstream directly. It is regulated by hypothelmus and piutary gland.

Genetics

  • [Disease name] is transmitted in [mode of genetic transmission] pattern.
  • Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
  • The development of [disease name] is the result of multiple genetic mutations.

Associated Conditions

Gross Pathology

  • On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

Microscopic Pathology

  • On microscopic histopathological analysis it hs rer sermblance to Hishimoto thyriodtis but less degree of fibrosis and atrophy , [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

References

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