Postpartum thyroiditis pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*The exact pathogenesis of postpartum thyroiditis is not fully understood. | *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. | |||
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==Genetics== | ==Genetics== | ||
Revision as of 19:50, 23 September 2017
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Postpartum thyroiditis Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Postpartum thyroiditis pathophysiology On the Web |
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American Roentgen Ray Society Images of Postpartum thyroiditis pathophysiology |
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Risk calculators and risk factors for Postpartum thyroiditis pathophysiology |
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].