Pelvic inflammatory disease pathophysiology: Difference between revisions
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{{Pelvic inflammatory disease}} | {{Pelvic inflammatory disease}} | ||
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==Overview== | |||
==Pathophysiology== | |||
===Pathogenesis=== | |||
Development of PID is the result of ascension of microorganisms from the cervix or vagina to the upper genital tract including, endometrium, fallopian tubes, ovaries and contiguous pelvic structures. <ref name="pmid20664404">{{cite journal |vauthors=Soper DE |title=Pelvic inflammatory disease |journal=Obstet Gynecol |volume=116 |issue=2 Pt 1 |pages=419–28 |year=2010 |pmid=20664404 |doi=10.1097/AOG.0b013e3181e92c54 |url=}}</ref>The endocervical canal functions as a barrier protecting the normally sterile upper genital tract from the organisms. Disturbance of this barrier provides vaginal bacteria access to the upper genital organs, infecting the endometrium, then endosalpinx, ovarian cortex, pelvic peritoneum, and their underlying stroma. The factors determining the rate of infection ascending to the upper genital tract include:<ref name="pmid12220764">{{cite journal |vauthors=Wiesenfeld HC, Hillier SL, Krohn MA, Amortegui AJ, Heine RP, Landers DV, Sweet RL |title=Lower genital tract infection and endometritis: insight into subclinical pelvic inflammatory disease |journal=Obstet Gynecol |volume=100 |issue=3 |pages=456–63 |year=2002 |pmid=12220764 |doi= |url=}}</ref> | |||
*Untreated chlamydial infections | |||
*untreated gonoccoal infections | |||
*Sexual intercourse | |||
*Retrograde menstruation | |||
<gallery> | |||
image:Anatomy-1.jpg|Anatomy of female genital tract | |||
</gallery> | |||
Infection results in fibrinous or suppurative inflammatory damage along the epithelial surface of the fallopian tubes and the peritoneal surface which leads to scarring, adhesions, and possibly partial or total obstruction of the fallopian tubes. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} |
Revision as of 15:58, 17 October 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Overview
Pathophysiology
Pathogenesis
Development of PID is the result of ascension of microorganisms from the cervix or vagina to the upper genital tract including, endometrium, fallopian tubes, ovaries and contiguous pelvic structures. [1]The endocervical canal functions as a barrier protecting the normally sterile upper genital tract from the organisms. Disturbance of this barrier provides vaginal bacteria access to the upper genital organs, infecting the endometrium, then endosalpinx, ovarian cortex, pelvic peritoneum, and their underlying stroma. The factors determining the rate of infection ascending to the upper genital tract include:[2]
- Untreated chlamydial infections
- untreated gonoccoal infections
- Sexual intercourse
- Retrograde menstruation
-
Anatomy of female genital tract
Infection results in fibrinous or suppurative inflammatory damage along the epithelial surface of the fallopian tubes and the peritoneal surface which leads to scarring, adhesions, and possibly partial or total obstruction of the fallopian tubes.
References
- ↑ Soper DE (2010). "Pelvic inflammatory disease". Obstet Gynecol. 116 (2 Pt 1): 419–28. doi:10.1097/AOG.0b013e3181e92c54. PMID 20664404.
- ↑ Wiesenfeld HC, Hillier SL, Krohn MA, Amortegui AJ, Heine RP, Landers DV, Sweet RL (2002). "Lower genital tract infection and endometritis: insight into subclinical pelvic inflammatory disease". Obstet Gynecol. 100 (3): 456–63. PMID 12220764.