Pelvic inflammatory disease pathophysiology

Pelvic inflammatory disease Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Pelvic Inflammatory Disease from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Pelvic inflammatory disease pathophysiology On the Web

Most recent articles

cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Pelvic inflammatory disease pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Pelvic inflammatory disease pathophysiology

CDC on Pelvic inflammatory disease pathophysiology

Pelvic inflammatory disease pathophysiology in the news

Blogs on Pelvic inflammatory disease pathophysiology

to Hospitals Treating Pelvic inflammatory disease

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

[edit | edit source]

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

[edit | edit source]

### Pathogenesis

[edit | edit source]

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

[edit | edit source]

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

[edit | edit source]

{{#ev:youtube|w3D2KPPaAH4}}

## References

[edit | edit source]

1. ↑ Soper DE (2010). "Pelvic inflammatory disease". Obstet Gynecol. 116 (2 Pt 1): 419–28. doi:10.1097/AOG.0b013e3181e92c54. PMID 20664404.
2. ↑ 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.
3. ↑ Brunham RC, Gottlieb SL, Paavonen J (2015). "Pelvic inflammatory disease". N. Engl. J. Med. 372 (21): 2039–48. doi:10.1056/NEJMra1411426. PMID 25992748.
4. ↑ 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.
5. ↑ 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.

Template:WH Template:WS