vulvovaginitis Flashcards
explain vulgvovaginitis
large variety of conditions that result in inflammation of the vulva and vagina. The causes may be infectious (bacterial vaginosis in most cases) or noninfectious
normal vaginal flora (mainly lactobacilli) keeps pH levels of the vaginal fluids low (4.5)thus preventing the overgrowth of pathogenic and opportunistic organisms.
Disruption of flora (e.g., due to sexual intercourse) predisposes to infection and inflammation.
Atrophic vaginitis is the most common non-infectious cause of vulvovaginitis and frequently affects elderly women after menopauseas a result of decreased estrogen levels. The diagnosis is clinical and treatment includes application of topical estrogen creme.
- labia majora = scrotum
- labia minora = floor of the penile urethra
- clitoris = penis
- Bartholin glands = Cowper glands
vulva anatomy
- entire vulva is covered by a keratinized squamous epithelium
- Hairy regions contain associated hair follicles, sebaceous glands, and apocrine and eccrine sweat glands
- non hairy regions reagions: (labia minora and prepuce), contain sebaceous glands only
- labia majora: skin enclosing fat and smooth muscle.
- labia minora: erectile tissue, made of skin and vascular and connective tissue w/o fat
- clitoris is a highly vascular and innervated, erectile organ betw labia minora
- Bartholin glands: major vestibular glands posterolateral to vaginal introitus
- Ducts of the Skene glands and minor vestibular glands are paraurethral
structures
vulva innervation
clit= DIP
labia: ant&post
Symptoms of vulvovaginal disorders are frequently caused by
irritation of the sensory nerves of the vulva
-
pudendal nerve= inferior hemorrhoidal nerve, the
perineal nerve, and the dorsal nerve of the clitoris - ilioinguinal nerve gives rise to the anterior labial nerves
-
posterior femoral cutaneous nerve gives rise to the posterior
labial nerves
vulva vasculature
- internal iliac artery=>internal pudendal artery,
- femoral artery=>superficial and deep external pudendal
vulva lymphatics
- femoral and inguinal lymph nodes receive the lymphatic drainage
from the vulva - superficial inguinal lymph nodes are the initial site of drainage
- inflammatory conditions of the vulva and distal vaginal
wall are accompanied by an increase in lymphatic drainage, resulting in
tender lymphadenopathy at this site
vagina anatomy
three layers: the mucosa, muscularis, and adventitia
- mucosa: Estrogen stimulates the proliferation and maturation of vaginal epithelial cells, whereas progesterone is inhibitory. lacks glands so lubricated by endocervical secretions
- muscularis: outer longitudinal and inner circular layer
- adventitia: strong sheet of connective tissue. forms the pubocervical fascisa which is fused to the fascia of the pelvic and urogenital diaphragms
nerves vessels, lymphatics of vagina
nerves: lumbar plexus and the pudendal nerve
* pudendal: not as rich distribution of fine sensory nerves as the vulva
arterisal vag supply:
- internal iliac=>vaginal artery <=uterine artery
- cervical branch of the uterine artery=>azygous artery of the vagina
- branches of the pudendal artery
veinous drainage of vagina:
plexus surrounding the vagina, and major vessels follow the arterial course
VAGINAL PHYSIOLOGY
vagina is usually resistant to infection for two reasons:
- marked acidity >(3.8 to 4.2)
- thick protective epithelium
how is acidity maintained
Lactobacilli
- produce of lactic acid and hydrogen peroxide
- toxic to anaerobic bacteria in the vagina
Insults that affect the acidic pH and lead to a more alkaline environment result in a decrease in lactobacilli, with an overgrowth of pathogenic organisms
host factors against vaginal infection (estrogen)
physical barrier (estrogen)
- Estrogen stimulates proliferation and maturation of the vaginal epithelium
- provides a physical barrier to infection
- decreased estrogen levels increase susceptibility to vaginal infections
Lactobacillus (estrogen)
- Mature vaginal epithelium provides glycogen, necessary for lactobacillus metabolism
immune system
- Cellular and humoral immunity plays a role in the normal vaginal defense mechanisms
- immunodef increases susceptibility
facters changing vag env
- Stress, poor diet, and fatigue affect microbiology, pH, immune system
- Foreign bodies alter the pH
- Changes in immune function d/2 HIV infection are associated with recurrent vaginal candidiasis
intercourse
- affects the microenvironment of the vagina because semen has an alkaline pH
- introduces new organisms into the vagina
- STDs affect the microbiology of the vagina, changing the resistance to infection
RF of vulvovaginitis
- Sexual activity
- Recent systemic infection
- antibiotics
- History of diabetes mellitus
- Previous vulvovaginal infections
- Vaginal hygienic practices (e.g., douching)
- Contraceptive methods
general sx of vulvovaginitis
vulvar: bitching
vagina: vcoc
Vulvar symptoms
- Burning: dx= vulvovestibulitis,and vulvodynia
- Itching= allergic rxns
Vaginal discharge description
- Viscosity: Follicular/prolif-phase >mucus is normally watery and abundant; Luteal/secretory-phase > mucus can be thick and viscous
- Consistency: (thick/watery) usually thin
- Color:
Normal discharge = usually white to beige
infection/ foreign body= Green, yellow, or brown discharge
- Odor: may be present w/o pathology. severe, offensive odor occur most often with retained foreign bodies, such as tampons
candida vaginitis
- etio: Candida albicans: inhabitant of the bowel and perianal region.
- Pathogenesis: overgrowth of C. albicans d/2 specific RF:
- Pregnancy
- Immunodeficiency, systemic (diabetes, HIV, immunosuppression)and local (topical corticosteroids)
- After systemic antibiotic treatment)
- Tight clothing, panty hose, and bathing suits (yeast thrives in a dark, warm, moist environment)
Clinical features
- burning sensation, strong pruritus,
- sticky White, crumbly vaginal discharge that may appear like cottage cheese and is typically odorless
- Erythematous vulva and vagina
- dysuria, dyspareunia
Diagnostics:
- Pseudohyphae on wet mount with potassium hydroxide (KOH)
- Vaginal pH within normal range (4–4.5)
- culture not needed
Treatment
Topical azole :creams/ suppository (miconazole, clotrimazole)
oral fluconazole and ketoconazole.