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]

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References[edit | edit source]

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