Postpartum thyroiditis pathophysiology: Difference between revisions
Sunny Kumar (talk | contribs) |
Sunny Kumar (talk | contribs) |
||
| Line 4: | Line 4: | ||
{{CMG}}; {{AE}} | {{CMG}}; {{AE}} | ||
==Overview== | ==Overview== | ||
The exact pathogenesis of | 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 inflammatory response to thyroid gland and destroy it, then lead to sudden release of stored thyroid hormone in blood and appearance of clinical and laboratory hyperthyroid picture transiently followed by recovery to euthyroid state or hypothroid state depending on level of destruction of thyroid gland, persistence of inflammatory state, and recovery strength of gland. studies have also shown that pregnancy is stage of reduced immunity to protect fetus from unwanted exposure of immunity which at the end of pregnancy escalate sudden immunity, leading to beginning of slowly evolving autoimmune response to thyroid auto-antigens, in a rapid Se sequences leading to appearance of thyroiditis. Studies are going on in search of exact autoantibody and autoantigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum thyroiditis. TPO autoantibody is significantly linked to occurrence of postpartum thyroiditis. | ||
==Pathophysiology== | ==Pathophysiology== | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
=== Physiology: === | === Physiology: === | ||
*Thyroid is endocrine gland which | *Thyroid is endocrine gland which synthase and secretes thyroid hormones in bloodstream directly. It is regulated by hypothalamus and pituitary gland. Thyroid hormones are of two biochemical structures. , triiodothyronine (T<sub>3</sub>), which is true and potent form and its prohormone, thyroxine (T<sub>4</sub>) majorly is secretory form later converted to T3 in peripheral tissues by deiodinase enzyme. Thyroid hormones has negative feedback on thyroid receptors located on hypothalamus and pituitary gland. Thyroid hormones majorly effects every part of body and maintains metabolic rate by acting on thyroid receptors which are nuclear receptors mediating gene expression. | ||
* | * | ||
Revision as of 20:28, 23 September 2017
|
Postpartum thyroiditis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Postpartum thyroiditis pathophysiology On the Web |
|
American Roentgen Ray Society Images of Postpartum thyroiditis pathophysiology |
|
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. 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 inflammatory response to thyroid gland and destroy it, then lead to sudden release of stored thyroid hormone in blood and appearance of clinical and laboratory hyperthyroid picture transiently followed by recovery to euthyroid state or hypothroid state depending on level of destruction of thyroid gland, persistence of inflammatory state, and recovery strength of gland. studies have also shown that pregnancy is stage of reduced immunity to protect fetus from unwanted exposure of immunity which at the end of pregnancy escalate sudden immunity, leading to beginning of slowly evolving autoimmune response to thyroid auto-antigens, in a rapid Se sequences leading to appearance of thyroiditis. Studies are going on in search of exact autoantibody and autoantigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum thyroiditis. TPO autoantibody is significantly linked to occurrence of postpartum thyroiditis.
Pathophysiology
Pathogenesis
Physiology:
- Thyroid is endocrine gland which synthase and secretes thyroid hormones in bloodstream directly. It is regulated by hypothalamus and pituitary gland. Thyroid hormones are of two biochemical structures. , triiodothyronine (T3), which is true and potent form and its prohormone, thyroxine (T4) majorly is secretory form later converted to T3 in peripheral tissues by deiodinase enzyme. Thyroid hormones has negative feedback on thyroid receptors located on hypothalamus and pituitary gland. Thyroid hormones majorly effects every part of body and maintains metabolic rate by acting on thyroid receptors which are nuclear receptors mediating gene expression.
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].