Peripartum mood disturbances pathophysiology: Difference between revisions

Jump to navigation Jump to search
No edit summary
Line 7: Line 7:


==Pathophysiology==
==Pathophysiology==
===Physiology===
Pathophysiology Of Peripartum mood disturbances- Pathophysiology of Peripartum mood disturbances includes the role of various genes and hormones as described below
The normal physiology of [name of process] can be understood as follows:


===Pathogenesis===
* [[Genetics]] of [[postpartum]] [[depression]]: <ref name="pmid30552910">{{cite journal |vauthors=Payne JL, Maguire J |title=Pathophysiological mechanisms implicated in postpartum [[depression]] |journal=Front Neuroendocrinol |volume=52 |issue= |pages=165–180 |date=January 2019 |pmid=30552910 |pmc=6370514 |doi=10.1016/j.yfrne.2018.12.001 |url=}}</ref><br> [[Estrogen receptor]] alpha gene,  
 
** [[polymorphisms]] in the [[serotonin transporter]] gene,  
*[[Genetics]] of [[postpartum]] [[depression]]: <ref name="pmid30552910">{{cite journal |vauthors=Payne JL, Maguire J |title=Pathophysiological mechanisms implicated in postpartum [[depression]] |journal=Front Neuroendocrinol |volume=52 |issue= |pages=165–180 |date=January 2019 |pmid=30552910 |pmc=6370514 |doi=10.1016/j.yfrne.2018.12.001 |url=}}</ref><br>[[Estrogen receptor]] alpha gene, [[polymorphisms]] in the [[serotonin transporter]] gene, 5-HTT, and the [[gene]] encoding for MAOA and the [[gene]] encoding for [[Catechol-O-methyltransferase]] (COMT), Genetic variants for the [[TPH2 gene]], a SNP in OXT was predictive of both variation in [[breastfeeding]] duration and [[postpartum depression]] scores, an interaction between a SNP in the [[OXTR gene]] and [[methylation]] state was detected in association with [[postpartum]] [[depression]]. In a [[genome]]-wide linkage and association study, the [[Hemicentin 1 gene]] [[Hemicentin 1|(HMNC1]]) had the strongest association with [[postpartum]] [[depression]].
** 5-HTT, and the  
** [[gene]] encoding for MAOA and the  
** [[gene]] encoding for [[Catechol-O-methyltransferase]] (COMT),  
** Genetic variants for the [[TPH2 gene]], a SNP in OXT was predictive of both variation in [[breastfeeding]] duration and [[postpartum depression]] scores, an interaction between a SNP in the [[OXTR gene]] and [[methylation]] state was detected in association with [[postpartum]] [[depression]]. In a [[genome]]-wide linkage and association study, the  
** [[Hemicentin 1 gene]] [[Hemicentin 1|(HMNC1]]) had the strongest association with [[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]].
*[[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]].
Line 19: Line 22:


*[[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]].




Line 46: Line 48:
|}
|}


*[[Neuroinflammatory]] mechanisms in [[postpartum depression]]: <br>There is a negative relationship between [[T-cell]] number and [[postpartum depression]] symptoms, whereas [[IL-6]] and [[IL-1β]] have a significant positive relationship with it.
* [[Neuroinflammatory]] mechanisms in [[postpartum depression]]: <br>There is a negative relationship between [[T-cell]] number and [[postpartum depression]] symptoms, whereas [[IL-6]] and [[IL-1β]] have a significant positive relationship with it.
 
<br />
 
* It is thought that in [[postpartum]] [[psychosis]], immunoneuroendocrine set point is dysregulated with overactivation of the [[immune system]]'s [[macrophage]] and [[monocyte]] arm. <ref name="pmid28713685">{{cite journal |vauthors=Davies W |title=Understanding the pathophysiology of [[postpartum]] [[psychosis]]: Challenges and new approaches |journal=World J Psychiatry |volume=7 |issue=2 |pages=77–88 |date=June 2017 |pmid=28713685 |pmc=5491479 |doi=10.5498/wjp.v7.i2.77 |url=}}</ref>
 


It is thought that in [[postpartum]] [[psychosis]], immunoneuroendocrine set point is dysregulated with overactivation of the [[immune system]]'s [[macrophage]] and [[monocyte]] arm. <ref name="pmid28713685">{{cite journal |vauthors=Davies W |title=Understanding the pathophysiology of [[postpartum]] [[psychosis]]: Challenges and new approaches |journal=World J Psychiatry |volume=7 |issue=2 |pages=77–88 |date=June 2017 |pmid=28713685 |pmc=5491479 |doi=10.5498/wjp.v7.i2.77 |url=}}</ref>


<br />
==Genetics==
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.
[Disease name] is transmitted in [mode of genetic transmission] pattern.

Revision as of 20:58, 2 August 2021

Peripartum mood disturbances Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Peripartum mood disturbances from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Interventions

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Peripartum mood disturbances pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Peripartum mood disturbances pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Peripartum mood disturbances pathophysiology

CDC on Peripartum mood disturbances pathophysiology

Peripartum mood disturbances pathophysiology in the news

Blogs on Peripartum mood disturbances pathophysiology

Directions to Hospitals Treating Psoriasis

Risk calculators and risk factors for Peripartum mood disturbances pathophysiology

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

Pathophysiology Of Peripartum mood disturbances- Pathophysiology of Peripartum mood disturbances includes the role of various genes and hormones as described below

Pathophysiology


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.




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)