Benign Gynecological Disorders Tory Davis, PA-C Mercy Hospital.
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Transcript of Benign Gynecological Disorders Tory Davis, PA-C Mercy Hospital.
POP Pelvic Organ Prolapse Defects in pelvic support structures
result in pelvic relaxation abnormalities Classified by anatomical location Severity by Stage 0-IV
Anatomic location Anterior vaginal wall
– Cystocele– Bladder prolapses
Posterior wall– Rectocele
Apical wall defect– Uterine prolapse– Vaginal vault prolapse (post-hyst)– Enterocele
Causes Age Parity
– Vag parity 3xRR– >2 deliveries4.5RR
Obesity Hx pelvic surgery
Diseases/conditions– Chronic cough– Constipation
Heavy lifting Menopause Inherent quality of
connective tissue
Symptoms Vaginal fullness Pressure Heaviness Discomfort Dysparunia Reducible mass in
introitus Low back pain
Incomplete void Stress incontinence Frequency Urinary hesitancy Splinting Coital laxity
POP PE Lithotomy position first, standing prn Vulvar ulcerations Relaxed genital hiatus Thin walled, smooth bulging mass
– Varying severity Observed valsalva Check anterior and posterior walls Rectovaginal
Prevention Antepatrum, intrapartum, postpartum
pelvic floor exercises Avoid other reversible/controllable risk
factors Estrogen therapy p menopause to
maintain pelvic tissue tone
Urinary Incontinence 13 million women 30-40% of US women in lifetime Up to 70% do not seek treatment Involuntary loss of urine
– Can be sign, symptom or diagnosed condition 3x more common in women (shorter urethra
and greater likelihood of connective tissue, muscle and nerve injuries)
Etiology of UI Gender Age
– In elderly, 30% increase prevalence with each 5-year age increase
Hormonal status Birthing trauma
– Damage to pelvic floor neuromusculature POP
Types Stress UI: urinary leakage on effort or
exertion Urge UI: leakage immediately
preceded by sense of urgency “Gotta go!”
Mixed UI: Likely most common
UI History Duration Frequency Severity Social implications
– What do I mean? Use of protective items (pads, diapers,
etc) Mental function
Workup Pelvic exam Q tip test for bladder neck
hypermobility Cough stress test Neuro exam Urodynamic studies
Treatment- Stress UI Reduce caffeine and alcohol Fluid restriction Timed voiding Kegels Biofeedback Electric stimulation Pessaries Surgery
Kegel Exercises Focused repetitive voluntary
contractions of pelvic floor musculature Have pt contract muscles as if to
prevent a fart or to stop urine Hold 3-5 seconds, then relax 50-100 reps daily Cure or significant improvement in up
to 75%
Treatment As for SUI plus Drugs! Anticholinergics
– Oxybutinin (Ditropan)– Tolterodine (Detrol)
Available in IR, long-acting or patch Increase bladder capacity, decrease
bladder contractions, improve urgency symptoms in 70%
Benign vulvar/vaginal disorders
Infectious causes: already covered, right? But still need to be considered
Atrophic vaginitis Lichen sclerosis Bartholin glands Vulvodynia
Atrophic vaginitis Hypoestrogenic vagina High pH Thinned vaginal epithelium SX: dryness, spotting, serosanguinous
discharge, dyspareunia Tx: intravaginal estrogen (cream, ring, pv
tablet) Not in women with hx of breast or endometrial cancer, though, right?
Lichen sclerosis Benign chronic inflammatory process Most common vulvar derm d/o Acute phase- red/purple lesions on
non-hair-bearing areas of vulva, perineum, perianal area in hourglass pattern– Erythema and edema– Intense pruritis
Lichen sclerosis Chronic- skin is thin, white, shiny Loss of genital landmarks
– Labia minora fusion– Introital stenosis
Pain/dyspareunia from loss of elasticity Increased risk of squamous cell
carcinoma
Lichen sclerosis Tx Steroids Topical high potency for 3 months,
taper to less potent for maintenance
Bartholin’s gland cyst Obstruction of the duct of the Bartholin’s
gland retention of secretionscystic dilation
Infection can occur– Sx: pain, tenderness, erythema, dyspareunia
with fluctuant mass Drain with Word catheter or marsupialization Excision if recurrent
Vulvodynia Vulvar pain in absence of relevant physical
findings Sx: burning, raw, irritation, hyperalgesia,
allodynia Prevalence 1.5% 2 types:
– Localized provoked 20-30 yrs Vestibular erythema, tenderness, introital pain
– Generalized unprovoked 40 yrs Larger area of pain (?neuropathic, pudendal nerve
injury, referred pain?)
Benign Cervical Disorders Stenosis Nabothian cysts Polyps Already covered: HPV and other STIs,
cervical dysplasia
Cervical stenosis Narrowing of the endocervical canal,
usually at level of internal os Partial to full occlusion of the os Obstruction of menstrual flow (can
lead to amenorrhea) Infertility Pelvic pain
Cervical stenosis etiology Congenital Inflammatory Neoplastic Surgical
– Think of this when treating cervical dysplasia: LEEP causes less stenosis than cold-knife cone biopsy
Nabothian cysts Don’t freak out. Benign Yellowish translucent raised pearl-like
lesions on ectocervix 1 mm to 3 cm Few or multiple
Cervical Polyps Small, pedunculated neoplasms Originate from endocervix Common
– Esp multigravidas over age 20 Mostly benign, but remove and send to
pathology due to malignant change potential
Cervical polyps Asymptomatic or c/o intermenstrual or
postcoital bleeding Sometimes assoc with infertility
– Why? PE: red fragile growth protruding from os
– 2 mm to 3 cm– Not palpable
Remove by grab-n-twist– Larger ones to OR
Adnexal masses Common, usually benign Management dictated by presentation Malignancy must be excluded
– US usually 1st imaging for adnexa– Septations, solid parts and Doppler flow
within lesion are suspicious If likely benign and <6 cm, observe
– Why 6 cm?
Benign ovarian growths Follicular cyst- most common. From
growth of follicle, often doesn’t release the egg– Usually not sx, usually resolve
Corpus luteum cyst Hemorrhagic cyst Dermoid cyst- the cyst with teeth
Cyst management If fluid-filled, monitor with periodic U/S If not, remove it
– Laparoscopic approach most common Also remove if >6 cm to reduce risk of
torsion Prevention with OCPs Tx pain with NSAIDs
PCOS Polycystic Ovarian Syndrome Common (5-10%) female endocrinopathy Oligo or amenorrhea and anovulation Hyperandrogenism
– What’s that look like? Ultrasonographic evidence of polycystic
ovaries Frequently, infertility Insulin resistance
PCOS Does this topic really belong here? Please read the Richardson article “Current
Perspectives in Polycystic Ovary Syndrome” posted on myUNE
Write 1-2 paragraphs on what “system” PCOS belongs in (Endo vs Women's Health)– Defend with supporting evidence from the article
(etiology, clinical features, lab features, treatment, prognosis, etc)
Due Thursday April 15 to me at my next lecture.
Premature Ovarian Failure
Ovaries don’t produce enough estrogen in women < 40– Despite high levels of circulating
gonadotropins Suspect in female <40 with s/s of
estrogen deficiency
S/sx of estrogen deficiency
Atrophic vaginitis Osteopenia/osteoporosis Decreased libido Infertility Menstrual changes
POF Dx High FSH, low estradiol Find cause
– Enzyme defects– Genetic defects – Autoimmune causes (thyroiditis,
Addison’s, hypoparathyroid, myasthenia gravis)
– Environmental factors (chemo, smoking, viruses, surgery)
POF Tx Desiring pregnancy: IVF plus
exogenous hormones to support endometrium
Not desiring pregnancy: HRT until age 50s
Either: psychosocial support