1/15
Looks like no tags are added yet.
pelvic inflammatory disease
infection of the female reproductive system
very commonly affects fallopian and ovaries
may or may not be sexually transmitted
etiology of PID
multiple types of bacteria and other microorganisms
prevalence of PID
about 4.1% of sexually active women in the US have been treated for PID in their lifetime
predisposing factors of PID
presence of STI
younger than 24
multiple sex partners
prior episodes of vaginitis and cervicitis
causes of PID
N. gonorrhea
C. trachomatis
pathophysiology of PID
microbes ascend through uterus into fallopian tubes (salpingitis)
early stage of inflammation promotes invasion of bacteria into mucosa
tubal walls become edematous
lumen is filled with purulent exudate
tubes becomes obstructed and prevent drainage into uterus
exudate drips from fimbriae onto ovary and surrounding tissue
peritoneal membrane cannot contain infection
what complications may occur in PID
peritonitis
abscesses form and need surgical drainage to prevent life-threatening infection
septicemia from systemic infection if it spreads too much and causes septic shock and even death
adhesions and strictures may affect tubes and ovaries
could cause infertility, ectopic pregnancy, or colon problems
clinical manifestations of PID
lower abdominal pain increasing in intensity = caused by inflammatory process
continual pain that intensifies with ambulation and worsens over time as scar tissue and adhesions form = irritation of inflamed tissue
pelvic exam showing purulent discharge from cervical os- opening in the center of ectocervix = inflammatory and infectious process
fever and chills = infection from vaginitis and cervicitis ascending into uterus and fallopian tubes and out to peritoneal cavity
causes of genital herpes
HSV-2: herpes simplex virus type 2
HSV-1 oral sex or autoinoculation
transmission of either strain of HSV through direct contact with skin or mucous membranes when an infected individual is symptomatic
HSV-1 and HSV-2 can be transmitted without any symptoms being apparent = asymptomatic shedding
impossible to predict when this will occur
prevalence of genital herpes
affects more than 24 million people in the US
acute stage in male genital herpes
causes tingling and burning sensation in inoculation site before lesions appear
then, lesions usually on penis, scrotum, or urethra
blister-type vesicle loaded with herpes viruses
lesion is surrounded by erythema
vesicle ruptures after sexual days, causing painful ulcerated area with watery exudate
crust forms over the ulcer and heals spontaneously in 3-4 weeks
dormant stage in male genital herpes
HS migrates along dermatome to dorsal sacral root ganglion near infection site
virus dormant until reactivated by stress or other infections
migrates back to mucosa or skin
enters host for replication
new vesicle is formed
pathophysiology in female genital herpes
virus causes herpetic lesions located on cervix, vulva, or urethra
risk factor for cervical cancer
same cycle of lesion outbreaks and dormancy as in males
active vaginal or cervical lesions can cause transmission to a neonate during vaginal delivery
frequently leading to severe central nervous system damage or death in a newborn
delivery via C-section is recommended
clinical manifestations in male genital herpes
due to generalized systemic infection: fever, headache, lymphadenopathy
due to localized infection: vesicular herpetic lesions
clinical manifestations in females
systemic infectious signs in acute stage: fever, headache, lymphadenopathy
reddened area surrounds fluid-filled vesicles
herpetic cells increase the risk for cervical cancer
risk for neonates for females with genital herpes
cross contamination from active lesions in vagina or cervix during vaginal childbirth can cause death or severe central nervous system damage
can also affect skin, eyes, mouth
delivery by C-section recommended