vulvovaginitis Flashcards

1
Q

explain vulgvovaginitis

A

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.

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2
Q
  1. labia majora = scrotum
  2. labia minora = floor of the penile urethra
  3. clitoris = penis
  4. Bartholin glands = Cowper glands
A
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3
Q

vulva anatomy

A
  • 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
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4
Q

vulva innervation

clit= DIP

labia: ant&post

A

Symptoms of vulvovaginal disorders are frequently caused by
irritation of the sensory nerves of the vulva

  1. pudendal nerve= inferior hemorrhoidal nerve, the
    perineal nerve, and the dorsal nerve of the clitoris
  2. ilioinguinal nerve gives rise to the anterior labial nerves
  3. posterior femoral cutaneous nerve gives rise to the posterior
    labial nerves
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5
Q

vulva vasculature

A
  1. internal iliac artery=>internal pudendal artery,
  2. femoral artery=>superficial and deep external pudendal
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6
Q

vulva lymphatics

A
  • 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
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7
Q

vagina anatomy

A

three layers: the mucosa, muscularis, and adventitia

  1. mucosa: Estrogen stimulates the proliferation and maturation of vaginal epithelial cells, whereas progesterone is inhibitory. lacks glands so lubricated by endocervical secretions
  2. muscularis: outer longitudinal and inner circular layer
  3. adventitia: strong sheet of connective tissue. forms the pubocervical fascisa which is fused to the fascia of the pelvic and urogenital diaphragms
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8
Q

nerves vessels, lymphatics of vagina

A

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

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9
Q

VAGINAL PHYSIOLOGY

A

vagina is usually resistant to infection for two reasons:

  1. marked acidity >(3.8 to 4.2)
  2. thick protective epithelium
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10
Q

how is acidity maintained

A

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

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11
Q

host factors against vaginal infection (estrogen)

A

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
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12
Q

facters changing vag env

A
  • 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

  1. affects the microenvironment of the vagina because semen has an alkaline pH
  2. introduces new organisms into the vagina
  3. STDs affect the microbiology of the vagina, changing the resistance to infection
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13
Q

RF of vulvovaginitis

A
  1. Sexual activity
  2. Recent systemic infection
  3. antibiotics
  4. History of diabetes mellitus
  5. Previous vulvovaginal infections
  6. Vaginal hygienic practices (e.g., douching)
  7. Contraceptive methods
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14
Q

general sx of vulvovaginitis

vulvar: bitching

vagina: vcoc

A

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
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15
Q

candida vaginitis

A
  • etio: Candida albicans: inhabitant of the bowel and perianal region.
  • Pathogenesis: overgrowth of C. albicans d/2 specific RF:
  1. Pregnancy
  2. Immunodeficiency, systemic (diabetes, HIV, immunosuppression)and local (topical corticosteroids)
  3. After systemic antibiotic treatment)
  4. 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.

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16
Q

CHRONIC RECURRENT CANDIDAL INFECTIONS

A

Failure to complete a full course of therapy

women with HIV infection

Chronic antibiotic therapy

Infection with a resistant organism such as C. tropicalis or T glabrata

rx Sexual transmission from the male partner

Allergic reaction to partner’s semen or a vaginal spermicide

Diabetes – patients should have a fasting serum glucose level if they
have recurrent infections

17
Q

Bacterial vaginosis

most common vaginal infection in women

ABCDEFG: Amsel criteria, bacterial vaginosis, clue cells, discharge (gray or milky), electrons (pH of vaginal secretions = alkali), fishy odor of discharge, gestation (increased risk for abortion)

A
  • Pathogen: Gardnerella vaginalis (a gram-variable rod) but polymicrobial
  • Pathogenesis:
  1. Lower concentrations of Lactobacillus causesovergrowth of Gardnerella vaginalis
  2. Sexual intercourse is the primary risk factor, but it is not considered an STD
  3. intrauterine devices (IUDs), douching, and pregnancy

Clinical features

  • Commonly asymptomatic(50%): Pruritus and pain are uncommon
  • Increased vaginal discharge, usually gray or milky with fishy odor

Diagnostics: vaginal discharge sample

  • Amsel’s criteria: 3 of 4 must apply to confirm diagnosis
  • Whiff test; add 1–2 drops of 10% KOH to vaginal fluid → intensification of the fishy odor
  • Vaginal pH > 4.5 (alkali) between 5.0 and 5.5
  • Clue cells: v_aginal epithelial cells covered with bacteria_ identified on wet mount preparation (pic)

Treatment: both topical and systemic agents 90% effective

systemic

  • First-line: oral metronidazole 500 mg twice daily for 7 days or a single, 2-g dose
  • Alternative: clindamycin

topical

  • Intravaginal 2% clindamycin cream is used at bedtime for 7 days
  • Intravaginal metronidazole is applied once a day for 5 days
18
Q

bacterial vaginosis special considerations

A

Treatment during pregnancy is critical; data suggest an association of
adverse maternal and fetal outcomes with bacterial vaginosis

Clindamycin may be used throughout pregnancy

Metronidazole may be used after the first trimester

Patients with recurrences

  • should be screened for STDs
  • Sexual partners should be treated
19
Q

what is amsel criteria

A

3 of the 4criteria are positive, the patient has bacterial vaginosis

  1. homogeneous vaginal discharge,
  2. pH of the vagina being > 4.5,
  3. the presence of clue cells in gram stained vaginal discharge smears
  4. positive whiff test.
20
Q

TRICHOMONAS VAGINALIS

After sex, burn the foul, green tree (trichomonas)!

A
  • Pathogen: Trichomonas vaginalis Anaerobic, motile protozoan with flagella
  • Transmission: STD = trichomonads can be recovered from 70% to 80% of the male partners of the infected

Clinical features= involvies vaginal epithelium, Skene glands, Bartholin glands, and urethra

  • Vulvovaginal pruritus, burning sensation,
  • Frothy, purulent , yellow-green, discharge that’s Foul-smelling
  • dyspareunia,|(painful sex) dysuria,

Diagnosis

edema or erythema of the vulva w/ strawberry cervix (punctations)

Pap smears positive in as many as 65% confirm w/ wet mount d-2 false +ve

Saline wet mount of vaginal smear: protozoa with multiple flagella (pic)

pH of vaginal discharge > 4.5 between 5.0 and 7.0

21
Q

TRICHOMONAS VAGINALIS - TREATMENT

A

oral metronidazole or tinidazole

  • Vaginal rx alone is ineffective (multiple sites of infection) and systemic agents are necessary
  • If both partners are treated simultaneously, cure rates of 90%
  • disulfiram-like reaction occurs topt abstain from alcohol
  • Resistant require IV metronidazole, but resistant trichonomonas is rare and usually assoc w/ uncompliance
  • Metronidazole is contraindicated for use during the first trimester of
    pregnancy
  • Infected patients should be screened for other STDs
22
Q

ATROPHIC VAGINITIS

A
  • Etiology= 1) Low estrogen levels (e.g., after menopause, breast feeding bilateral oophorectomy, radio-/chemotherapy, immunological disorders) 2) Atrophy of epithelium in vagina and vulva 2ndary to reduced estrogen
  • vaginal epithelium becomes thin; vulvar structures may atrophy
  • glycogen also decreases,

Clinical features

  • Decreasing labial fat pad Commonly associated with receding pubic hair
  • Vaginal soreness & dryness causing Dyspareunia
  • Discharge

Diagnostics: clinical diagnosis

  • The vagina is often pale with punctate hemorrhagic spots throughout
    the vaginal wall
  • There absence of superficial epithelial cells and a predominance
    of parabasal cells
  • leukorrhea
  • atrophic, sometimes inflamed vaginal walls
  • pH becomes alkaline
  • infection is not identified on a wet mount preparation

Treatment:

  • estrogen cream (topical) or tablets (systemic)
  • respond to short-term therapy but recur on discontinuation

-estrogen subs increases the risk of endometrial and breast cancer!