women's health vaginal d/o and menopause

bartholin’s duct cyst and abscess

obstruction of main duct of bartholin’s gland results in retention of secretions and cystic dilation

bartholin’s duct cyst causes

nonSTI infection, thickened mucus and congenital narrowing of duct, secondary infection may result in recurrent abscess formation

bartholin’s gland enlargement in postmenopausal pt should result in

biopsy, but malignancy is <1%

who is bartholin gland abscess m/c in

20-30 yo or w/ sudden increase in sexual activity

pain/tenderness, dyspareunia, difficulty walking/adducting thighs, mass in posterior introitus near 4/8 oclock, erythema, edema, inflammation, fluctuant tender mass when ready for I&D

bratholin’s gland cyst

bartholin’s gland cyst tx

I&D w/ marsupialization, insertion of ward catheter, excision of cyst may be required for postmenopausal pts, ± abx if considerable inflammation develops or for surrounding reinfection

intense pruritis, vulvar skin thin, wrinkled, white, w/ areas of lichenification and hyperkeratosis, anterior parts of labia minora agglutinate, erosion, fissures, subepithelial hemorrhages, ulcerations

lichen sclerosus

lichen sclerosus pathogenesis

m/c vulvar dermatologic d/o, benign chronic inflammatory process, possibly linked to fhx, association w/ human leukocyte antigen, vit A deficiency, autoimmune process preventing conversion of testosterone to dihydrotestosterone resulting in thinning of the skin

lichen sclerosus clinical findings

women over 60 yo, erythema and edema of vulvar skin followed by development of white plaques which unite, intense pruritis leading to scratch itch cycle, telangiectasias and subepithelial hemorrhages from scratching, erosions, fissures, ulcerations, thin/wrinkled/white skin w/ cigarette paper appearance

lichen sclerosus dx

definitive dx biopsy showing thin hyperkeratotic layer, thinning of epithelial layer, flattening of papillae, homogenizaiton of stroma, deep lymphocytic infiltration

lichen sclerosus complications

squamous cell ca in 3-5%, all new lesions must be biopsied, possible reductionin incidence of vulvar carcinoma in those who use topical clobetasol

lichen sclerosus tx

clobetasol dipropionate topical steroid and oral antihistamines, those who do not respond to clobetasol can have tacroliimus, retinoids, antimalarial agents, photodynamic therapy, PRP for sx (works meh)

lichen sclerosus prognosis

chronic, recurs w/ cessation of tx, clobetasol leads to sx resolution in most and reversal of skin changes in about half

lichen simplex chronicus was previously

dystrophy, squamous cell hyperplasia, atopic dermatitis, atopic eczema, neurodermatitis

lichen simplex chronicus

benign epithelial thickening and hyperkeratosis resulting from chronic irritation, scratch itch cycle causes epithelial thickening and moist environment causes maceration and raised white lesion

lichen simplex chronicus dx

biopsy r/o intraepithelial neoplasia and invasive tumor

lichen simplex chronicus tx

sitz baths, lubricants, PO antihisstamines, topical steroids

burning, itching, flu like sx, vesicles develop and erode rapidly resulting in painful erosions/ulcers, each erosion has red halo, lesions spread in serpentine fashion

herpes genitalis

herpes genetalis pathogenesis

virus contaminates secretions and mucosa, entering through microinjuries, erosions provide point of entry to other STIs, virus replicates in dermis/epidermis and stays latent in nearby nerve ganglion, incubation 2-7 days during which shedding can occur, in half of pts asx viral shedding identifiable w/i 1 yr of primary outbreak

herpes prevention

prolonged suppressive therapy for those w/ 6+ recurrences/yr, pts c uncomfortable/painful prodromes or outbreaks, pts c lesions outside area that can be protected w/ condom

herpes genitalis dx

gold standard is viral culture, can use vesicle fluid or scraping from erosion/ulcer, 85% have IgM w/i 21 days of exposure

herpes genitalis complications

pain, discomfort, psych implications, neonatal transmission

herpes genitalis tx

lesions are self limiting, sx tx loose fitting undergarments, cool compresses, sitz baths, oral analgesics, tx acyclovir, valacyclovir, famcivlovir, initial episode doses are higher and taken for longer than recurrent episodes

stress urinary incontinence tx

weight loss, reduce caffeine/alcohol, fluid restriction, timed voiding, pelvic floor muscle exercises, electrical stimulation, pessaries to support bladder neck and urethra, pubovaginal/midurethral slings

type of incontinence linked w/ overactive bladder leading to urgency and frequency and nocturia ± incontinence

urge urinary incontinence

key in lock syndrome

uncontrollable urge to void when unlocking the door after returning home

OAB first line tx

behavioral therapy, bladder training, timed voiding, pelvic floor muscle exercises

OAB second line tx

pharmacologic, antimuscarinics or anticholinergics have become mainstay, detrusor muscle is heavily populated w/ cholinergic receptor

OAB third line tx

botox in detrusor muscle, sacral neuromodulation focuses on sensory nerve signals from bladder to reduce bladder activity, posterior tibial nerve stimulation

mixed incontinence

stress and urge incontinence occur simultaneously, pts preemptively urinate to avoid full bladder and consequently condition bladder to low functional capacity creating premature signaling of bladder fullness and frequent urge sx

mixed incontinence tx

tailored to sx that are more impactful on pt’s life

loss of urine w/o awareness or continuous dribbling/wetness sensation

overflow incontinence

overflow incontinence

involuntary loss of urine associated w/ bladder overdistention in the absence of detrusor contraction

who does overflow incontinence occur in

classically men who have outlet obstruction secondary to prostatic enlargement, uncommon in women but typically due to increased outlet resistance from advanced vaginal prolapse causing kink in the urethra

pt c overflow continence may c/o need to

strain or apply suprapubic pressure in order to void

overflow incontinence tx

tx underlying cause, may need to utilize intermittent catheterization, alpha adrenergic blockers (tamsulosin) can facilitate bladder emptying by relaxing bladder neck tone

incontinence prognosis

spontaneous resolution is not normal, sx generally stabilize or progress, fundamentally affects qol, most learn coping skills/adaptive measures but others develop significant psychosocial maladaptive behaviors

cystocele

bladder prolapses into anterior vaginal wall

rectocele

rectum prolapses into posterior vaginal wall

cervicouterine or enterocele

atypical prolapse

anterior vaginal prolapse

anterior vaginal wall defect in which bladder is frequently associated w/ prolapse

locations of anterior wall defects

paravaginal, midline, transverse

apical prolapse

uterine prolapse, vaginal vault prolapse (post hysterectomy), enterocele (apical vaginal wall defect in which bowel is contained w/i prolapsed segment, m/c in post hysterectomy)

POP grading and staging

grade described w/ Baden Walker system w/ scale of 0-4 based on position relative to hymen, stage described using POP-Q system and is preferred method as more objective

POP dx

sensation of vaginal fullness/presure/heaviness/something falling out/sitting on a ball, vaginal discomfort, presence of soft reducible mass bulging into vagina and distending through vaginal introitus, increased bulging and descent of vaginal wall w/ straining or coughing, back/pelvic pain

POP urinary sx

incomplete emptying, stress incontinence, urinary frequency, urinary hesitancy, need to push bladder up to void (splinting)

POP risk factors

increasing age, increasing parity, obesity, hx of pelvic surgery, hysterectomy, chronic cough from lung dz, straining from chronic constipation, occupations requiring heavy lifting, inherent quality of connective tissue

POP clinical findings

prolapse can be noted on pelvic exam, pt may be asked to cough/valsalva to reproduce bulging, must eval urinary function, imaging can be utilized if dx cannot be made clinically

POP tx

extent/choice of tx should reflect degree of impact on pt’s qol, conservative measures such as pessaries can provide adequate sx relief, surgery can be performed if significant hindrance on qol

natural menopause dx

12 mo amenorrhea w/ no obvious pathologic cause, estradiol <20 FSH 21-100

induced menopause

permanent cessation of menstruation after b/l oophorectomy or ablation of ovarian function (chemo/radiation)

perimenopause/menopause transition

menstrual cycle and hormonal changes that occur a few years before and 12 mo after final menstrual period resulting from natural menopause

menopause pathogenesis 

high levels of FSH appear to stimulate residual follicles to secrete bursts of estradiol, occasionally estradiol levels rise 2-3x nl likely reflecting recruitment of more than 1 follicle for ovulatin, first oocytes responsive to gonadotropins disappear from the ovary, then few remaining oocytes that do not respond to gonadotropins

what is associated w/ early menopause

smoking

vaginal rugae flatten and epithelium thins, symptomatic atrophic vaginitis, reduction of mucus secretion, vaginal dryness, dyspareunia, uterine atrophy, regression of breast size, disappearance of cyclic breast pain

menopause

how long do menopausal vasomotor sx last

average 1-6 yrs, up to 15 years

menopause PE

elevated BP from arterial constriction, weight gain, decrease in height from op, breasts increase in fatty deposition and show involution, vaginal dryness, urogenital atrophy, arthralgias, sarcopenia

menopause tx

sx hormonal therapy to tx moderate to severe vasomotor sx, combo HRT estrogen/progestin relatively low risk in women in early menopause, vaginal estrogen creams tx symptomatic dyspareunia caused by atrophic vaginitis

menopause prognosis

transition and postmenopausal stages may last several yrs, w/ tx prognosis of sx is very good