Pelvic inflammatory disease pathophysiology: Difference between revisions
Created page with "{{Pelvic inflammatory disease}} {{CMG}} ==Overview== ==References== {{reflist|2}} {{Diseases of the pelvis, genitals and breasts}} nl:Eileiderontsteking [[pt:Doença in..." |
m Bot: Removing from Primary care |
||
| (21 intermediate revisions by 6 users not shown) | |||
| Line 1: | Line 1: | ||
__NOTOC__ | |||
{{Pelvic inflammatory disease}} | {{Pelvic inflammatory disease}} | ||
{{CMG}} | {{CMG}};{{AE}}{{MehdiP}} | ||
==Overview== | ==Overview== | ||
Pelvic inflammatory disease (PID) is an infection that begins in the [[vulva]] or [[vagina]] and spreads upward to involve most of the structures in the [[Female genital tract|female genital system]]. Inflammation and the resulting scarring may lead to adhesions and [[infertility]]. | |||
==Pathophysiology== | |||
===Pathogenesis=== | |||
{| style="float: right; width: 350px;" | |||
| [[Image:Anatomy-1.jpg|right|300px|]] | |||
|} | |||
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 [[Female genital tract|genital tract]] from the organisms. Disturbance of this barrier provides [[Bacteria|vaginal bacteria]] access to the upper genital organs, infecting the [[endometrium]], then [[Salpingitis|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 [[Chlamydia infection|chlamydial]] infections | |||
*untreated [[Gonorrhea|gonoccoal]] infections | |||
*Sexual intercourse | |||
*Retrograde [[menstruation]] | |||
Infection results in [[fibrinous]] or [[suppurative]] [[inflammatory]] damage along the [[Epithelium|epithelial]] surface of the [[fallopian tubes]] and the peritoneal surface which leads to [[Scar|scarring]], [[adhesions]], and possibly partial or total obstruction of the [[fallopian tubes]]. | |||
===Microscopic findings=== | |||
Pelvic inflammatory disease causes a selective loss of [[ciliated]] [[epithelial cells]], which interferes with intratubal [[ovum]] transport, resulting in [[infertility]] or [[ectopic pregnancy]].<ref name="pmid25992748">{{cite journal |vauthors=Brunham RC, Gottlieb SL, Paavonen J |title=Pelvic inflammatory disease |journal=N. Engl. J. Med. |volume=372 |issue=21 |pages=2039–48 |year=2015 |pmid=25992748 |doi=10.1056/NEJMra1411426 |url=}}</ref> | |||
*[[T-cell|T-cell neutrophils]] and [[plasma cells]] accumulation are the [[immune system]] response to the infective [[pathogen]].<ref name="pmid2704001">{{cite journal |vauthors=Patton DL, Kuo CC |title=Histopathology of Chlamydia trachomatis salpingitis after primary and repeated reinfections in the monkey subcutaneous pocket model |journal=J. Reprod. Fertil. |volume=85 |issue=2 |pages=647–56 |year=1989 |pmid=2704001 |doi= |url=}}</ref><ref name="pmid9169748">{{cite journal |vauthors=Van Voorhis WC, Barrett LK, Sweeney YT, Kuo CC, Patton DL |title=Repeated Chlamydia trachomatis infection of Macaca nemestrina fallopian tubes produces a Th1-like cytokine response associated with fibrosis and scarring |journal=Infect. Immun. |volume=65 |issue=6 |pages=2175–82 |year=1997 |pmid=9169748 |pmc=175300 |doi= |url=}}</ref> | |||
===Video=== | |||
{{#ev:youtube|w3D2KPPaAH4}} | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WH}} | |||
{{WS}} | |||
[[Category:Emergency mdicine]] | |||
[[Category:Disease]] | |||
[[ | [[Category:Up-To-Date]] | ||
[[ | |||
[[Category:Infectious disease]] | [[Category:Infectious disease]] | ||
[[Category:Gynecology]] | [[Category:Gynecology]] | ||
Latest revision as of 23:37, 29 July 2020
|
Pelvic inflammatory disease Microchapters |
|
Differentiating Pelvic Inflammatory Disease from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Pelvic inflammatory disease pathophysiology On the Web |
|
American Roentgen Ray Society Images of Pelvic inflammatory disease pathophysiology |
|
Risk calculators and risk factors for Pelvic inflammatory disease pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Overview
Pelvic inflammatory disease (PID) is an infection that begins in the vulva or vagina and spreads upward to involve most of the structures in the female genital system. Inflammation and the resulting scarring may lead to adhesions and infertility.
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
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.
Microscopic findings
Pelvic inflammatory disease causes a selective loss of ciliated epithelial cells, which interferes with intratubal ovum transport, resulting in infertility or ectopic pregnancy.[3]
- T-cell neutrophils and plasma cells accumulation are the immune system response to the infective pathogen.[4][5]
Video
{{#ev:youtube|w3D2KPPaAH4}}
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.
- ↑ Brunham RC, Gottlieb SL, Paavonen J (2015). "Pelvic inflammatory disease". N. Engl. J. Med. 372 (21): 2039–48. doi:10.1056/NEJMra1411426. PMID 25992748.
- ↑ Patton DL, Kuo CC (1989). "Histopathology of Chlamydia trachomatis salpingitis after primary and repeated reinfections in the monkey subcutaneous pocket model". J. Reprod. Fertil. 85 (2): 647–56. PMID 2704001.
- ↑ Van Voorhis WC, Barrett LK, Sweeney YT, Kuo CC, Patton DL (1997). "Repeated Chlamydia trachomatis infection of Macaca nemestrina fallopian tubes produces a Th1-like cytokine response associated with fibrosis and scarring". Infect. Immun. 65 (6): 2175–82. PMC 175300. PMID 9169748.