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*[[Epigenetic]] mechanisms of [[postpartum depression]]<br>In women with [[postpartum depression]], there was a substantial interaction between [[OXTR]] [[DNA methylation]], [[estradiol]], and the ratio of [[allopregnanolone]] to [[progesterone]]. Alterations in [[DNA methylation]] of the [[OXTR gene]] are adversely linked with [[blood]] [[estradiol]] levels in women with [[postpartum depression]]. As a result, [[epigenetic]] alterations can affect [[metabolic]] processes linked to [[postpartum depression]].
*[[Epigenetic]] mechanisms of [[postpartum depression]]<br>In women with [[postpartum depression]], there was a substantial interaction between [[OXTR]] [[DNA methylation]], [[estradiol]], and the ratio of [[allopregnanolone]] to [[progesterone]]. Alterations in [[DNA methylation]] of the [[OXTR gene]] are adversely linked with [[blood]] [[estradiol]] levels in women with [[postpartum depression]]. As a result, [[epigenetic]] alterations can affect [[metabolic]] processes linked to [[postpartum depression]].
[[File:A-hypothetical-mechanism-by-which-depression-during-pregnancy-and-postpartum-may.png|alt=Pathophysiology|right|327x327px|Post partum depression]]


*[[Neuroendocrine]] mechanisms of [[postpartum depression]]: <br>In [[postpartum depression]], there is an interaction between the [[Hypothalamus]]-[[pituitary]]-[[gonadal]] (HPG) and [[Hypothalamus]]-[[Pituitary]]-[[Adrenal]]([[HPA]]) axis. [[HPA axis]] function has been found to be influenced by [[reproductive]] [[hormones]] and vice versa. As a result, any change in [[reproductive hormones]] may cause [[stress hormone]] levels to fluctuate, resulting in [[postpartum depression]].  Alterations of the [[HPA axis]]' function may also affect [[reproductive]] [[hormone]] levels, contributing to [[postpartum depression]].
*[[Neuroendocrine]] mechanisms of [[postpartum depression]]: <br>In [[postpartum depression]], there is an interaction between the [[Hypothalamus]]-[[pituitary]]-[[gonadal]] (HPG) and [[Hypothalamus]]-[[Pituitary]]-[[Adrenal]]([[HPA]]) axis. [[HPA axis]] function has been found to be influenced by [[reproductive]] [[hormones]] and vice versa. As a result, any change in [[reproductive hormones]] may cause [[stress hormone]] levels to fluctuate, resulting in [[postpartum depression]].  Alterations of the [[HPA axis]]' function may also affect [[reproductive]] [[hormone]] levels, contributing to [[postpartum depression]].





Revision as of 20:47, 2 August 2021

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunita Kumawat, M.B.B.S[2]

Overview

Many pathological mechanisms are involved in postpartum depression which interact with one another.

Pathophysiology

Physiology

The normal physiology of [name of process] can be understood as follows:

Pathogenesis

Pathophysiology
Post partum depression


GABA Glutamate Serotonin Dopamine
GABA which is an inhibitory neurotransmitter in the brain Glutamate is the excitatory neurotransmitter in the brain Serotonin to 5HT1A receptors is decreased in the following brain regions Mutations in DR1
Level is inversely related with the depression symptoms in the postpartum period postpartum depression its level are increased in the medial prefrontal cortex mesiotemporal and anterior cingulate cortices. Relates to the attention and affection of mother for the baby
In postpartum depression decreased in the dorsolateral prefrontal cortex.

It is thought that in postpartum psychosis, immunoneuroendocrine set point is dysregulated with overactivation of the immune system's macrophage and monocyte arm. [2]

Genetics

[Disease name] is transmitted in [mode of genetic transmission] pattern.

OR

Genes involved in the pathogenesis of [disease name] include:

  • [Gene1]
  • [Gene2]
  • [Gene3]

OR

The development of [disease name] is the result of multiple genetic mutations such as:

  • [Mutation 1]
  • [Mutation 2]
  • [Mutation 3]

Associated Conditions

Conditions associated with [disease name] include:

  • [Condition 1]
  • [Condition 2]
  • [Condition 3]

Gross Pathology

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

Microscopic Pathology

On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

References

  1. Payne JL, Maguire J (January 2019). "Pathophysiological mechanisms implicated in postpartum [[depression]]". Front Neuroendocrinol. 52: 165–180. doi:10.1016/j.yfrne.2018.12.001. PMC 6370514. PMID 30552910. URL–wikilink conflict (help)
  2. Davies W (June 2017). "Understanding the pathophysiology of [[postpartum]] [[psychosis]]: Challenges and new approaches". World J Psychiatry. 7 (2): 77–88. doi:10.5498/wjp.v7.i2.77. PMC 5491479. PMID 28713685. URL–wikilink conflict (help)