Dyspareunia pathophysiology: Difference between revisions
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{{CMG}} {{AE}} | {{CMG}} {{AE}} | ||
==Overview== | ==Overview== | ||
[[Dyspareunia]] is caused by [[medical causes]], [[psychological]] problems, and pathophysiology can be considered as multifactorial, multisystemic, or complex. | [[Dyspareunia]] is caused by [[medical causes]], [[psychological]] problems, and [[pathophysiology]] can be considered as multifactorial, [[multisystemic]], or [[complex]]. [[Dyspareunia]] vary based on the underlying causes. For example, [[Estrogen|estrogen deficiency]] causes [[atrophic vaginitis]] or [[Ectopic|ectopic uterine tissues]] in [[endometriosis]] causes [[dyspareunia]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 22:26, 21 September 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:
Overview
Dyspareunia is caused by medical causes, psychological problems, and pathophysiology can be considered as multifactorial, multisystemic, or complex. Dyspareunia vary based on the underlying causes. For example, estrogen deficiency causes atrophic vaginitis or ectopic uterine tissues in endometriosis causes dyspareunia.
Pathophysiology
Pathophysiology of sexual pain disorders can be considered as:[1][2]
- Multifactorial
- Multisystemic
- Complex
Multifactorial:
- Biological, psychosexual, relational factors can coexist in a woman complaining of coital pain. Over time, these different factors may act as predisposing, precipitating, or perpetuating sexual pain disorders.
Multisystemic: sexual function involves:
- Nervous system
- Endocrine system
- Vascular system
- Immunological systems
- Vaginal ecosystem: Vaginal receptiveness may be further modulated by; psychosexual, mental, interpersonal factors that may result in poor arousal with vaginal dryness. Fear of penetration, general muscular arousal secondary to anxiety, defensive contraction of the peri-vaginal muscles, leading to lifelong vaginismus.
Complex:Coital pain is greater than the simple peripheral tissue damage that may initially trigger the nociceptive component. When It becomes chronic, the pathophysiology of pain may gradually shift from nociceptive, a friend signal that should induce self-protection and defense, to neuropathic, with progressive involvement of the CNS.[3]