You are on page 1of 24

1) Menopause:

Climacteric: a phase in women transitioning from a reproductive state to a non-reproductive


state; includes perimenopause, as well as time before and after
Perimenopause: about 4 years before menopause when cycles become irregular and there are
increased climacteric symptoms
Menopause: cessation of menses for 1 year (avg. age is 50-52 y/o)
-S/S: estrogen deficiency changes
-menstrual cycle alterations
-vasomotor instability (hot flashes)
-mood changes
-skin/nail/hair changes
-cardiovascular events, hyperlipidemia
-incontinence
-Atrophic Vaginitis= thin yellow discharge, pH>5.5, pruritus
-irregular menstrual cycles but no premenstrual sx
-Diagnosis: mostly clinical, increased serum FSH (>35) and LH, decreased estrogen
-Treatment:
-Vasomotor insufficiency/hot flashes: estrogen, progesterone, clonidine, SSRIs,
Gabapentin
-Vaginal atrophy: estrogen (transdermal-Premarin, intravaginal)
-Osteoporosis prevention: Calcium +Vitamin D, weight bearing exercises,
bisphosphonates, calcitonin, estrogen, SERM (Raloxifene, Tamoxifen)
- HRT:
-Estrogen only= most effective tx for menopausal sx, no increased risk of
Breast CA; risks of thromboembolism, endometrial CA(unopposed
estrogen) often used in pts with no uterus
-Estrogen/Progesterone: relief of sx, decreased heart and stroke risk,
decreased osteoporosis and dementia, No increased risk of endometrial
CA, often used if pt still has a uterus; increased risk of Breast CA,
venous thromboembolism
Medical Complications of Menopause:
-Osteoporosis, increased: fractures, cardiovascular risk and lipids
2) Breast Mass:
Benign:
1) Fibrocystic Breast Disorder: fluid-filled breast cyst due to exaggerated response to hormones;
MC breast d/o (esp 30-50y)
-Clinical Manifestations:
-Multiple, mobile, well demarcated areas in breast tissue
-cord-like
-often tender , bilateral, often no axillary involvement nor nipple
discharge
-breast cysts may increase or decrease in size with menstrual
hormonal changes
-Diagnosis: Ultrasound. Bx shows straw-colored fluid (no blood)
-Treatment: Most resolve spontaneously, possible fine needle aspiration removal of fluid
if symptomatic
2) Fibroadenoma of the Breast: 2nd MC benign breast disorder, MC in late teens to early 20s;
composed of glandular and fibrous tissue (collagen arranged in a swirl
-Clinical Manifestations:

-Smooth, well-circumscribed, mobile, rubbery lump


-no axillary involvement nor nipple discharge
-gradually grows over time; may enlarge in pregnancy
-Does not usually wax and wane w/menstruation
-Management:
-Most small tumors resorb w/ time; possible excision (not usually done)
Malignant:
-MC nonskin malignancy in women; 2nd MC cause of cancer death; 1 in 8 lifetime incidence
-Risk Factors:
-Genetic: BRCA 1 and BRCA 2; 1st degree relative w/ breast CA
-age >65 y/o
- Hormonal: increased # of menstrual cycles (nulliparity, late age of 1 st full
term pregnancy >35 y/o, early onset of menarche (<12y/o), late menopause, never having
breastfed.
-Increased estrogen exposure: postmenopausal HRTs and OCPs
-Obesity, ETOH
-75% have no risk factors
-Types: primarily of the milk ducts (ductal) or the lobules which produce the milk
1) Ductal Carcinoma
-Infiltrative ductal carcinoma MC (75%). Associated with lymphatic
METs especially axillary
- Ductal Carcinoma in situ (DCIS). Does not penetrate the basement
membrane
2) Lobular Carcinoma
-infiltrative lobular carcinoma
-Lobular carcinoma in situ (may not progress but associated w/ risk
of invasive BRCA in either breast)
3) Medullary, mucinoid, tubular, papillary, metastatic, mammary Pagets disease
-Clinical Manifestations:
-Early:
1) single, painless, hard, fixed (non-mobile) lump, may be mobile early
on; 80% present w/mass, 90% found by patient, Pain seen in <10%,
may have axillary lymphadenopathy; MC in Upper Outer quadrant
(65%), then Areola (18%)
2) Unilateral nipple discharge: may be bloody, purulent or green
-Later:
-skin or nipple retractions, axillary adenopathy, breast enlargement, erythema,
peau dorange (due to lymphatic obstruction, associated w/ poor prognosis),
edema, pain, fixation of mass to chest wall
-Very late: ulceration, supraclavicular adenopathy, arm edema, mets to: Bone,
Liver, Lung, Brain
-Diagnosis:
-Ultrasound: Recommended initial modality to evaluate breast mass in women <40y/o
(due to high density of breast tissue)
-Mammogram: microcalcifications & speculated masses suspicious for malignancy; not
sensitive in pts w/dense breast tissue (esp pts <40y/o)
-Management:
-Lumpectomy: followed by radiation therapy; allows for breast conservation
-Mastectomy: entire breast removed; indication: diffuse, large tumor, prior to
radiation to breast

- Removal of regional (axillary) lymph nodes: to determine if METs present


- Radiation therapy/ Chemotherapy:
-Radiation: done after lumpectomy and may be done post mastectomy to destroy
residual microscopic tumor cells
-Chemotherapy: done in stage II-IV and inoperable disease, especially estrogen
receptive negative disease (doxorubicin, cyclophosphamide, fluorouracil,
docetaxol)
-Neoadjuvant Endocrine Therapy: tumors may be Estrogen Receptor positive (75%),
Progesterone receptor (65%) positive as well as HER2 positive (25%); HER2 assoc w/
more aggressive tumors
-Anti-estrogen= Tamoxifen (binds and blocks estrogen receptors)
-Aromatase inhibitors: reduces the production of estrogen useful in
postmenopausal ER pos pts with breast CA ex) Letrozole, Anastrozole,
Exemestane
- Monoclonal Ab treatment: useful in patients with HER2 positivity (Human
Epidermal Growth Factor Receptor) ex) Trastuzumab (Herceptin), Lapatinib;
S/E cardiotoxicity
3) Mastitis: Inflammation of the breast
-Can be:
Infection: seen mostly in lactating women secondary to nipple trauma (especially
primagravida); bacteria come from infants mouth/throat
o Etiologies: Most commonly S. Aureus, Strep, possibly Candida
Congestive: bilateral breast enlargement 2-3 days post partum
-Clinical Manifestations:
Infection: unilateral breast pain (esp one quadrant) w/ tenderness, warmth, swelling,
nipple discharge
Congestive: bilateral breast pain and swelling. May have low grade fever and axillary
lymphadenopathy
Breast abscess: induration w/ fluctuance (due to pus). RARE.
-Management:
Infectious: supportive measures (warm compresses, breast pump) + Anti-Staph Abx
(Dicloxacillin, Nafcillin, Cephalosporin, or if fungal- Fluconazole)
o Continue to nurse or use breast pump
Congestive:
o If woman does not want to breast feed: ice packs, tight fitting bra, analgesics,
avoid breast stimulation
o If breast feeding desired: manually empty breast completely until baby is done
breast feeding; local heat, analgesics, continue nursing
Breast abscess: I&D, stop breast feeding from the affected breast
4) Dysfunctional (Abnormal) Uterine Bleeding
-Definition: abnormal frequency/intensity of menses due to nonorganic causes
Organic or structural causes would be PALM: Polyp Adenomyosis Leiomyoma
Malignancy/hyperplasia
Nonorganic or nonstructural causes would be COEIN: Coagulopathy Ovulatory dysfxn
Endometrial Iatrogenic Not yet classified
Normal cycle: 24-38 days w/ menstruation lasting 4.5-8 days (average loss 30ml-80ml)
Amenorrhea: absence of menstrual period

Cryptomenorrhea: light flow or spotting


Menorrhagia: heavy or prolonged bleeding@ normal menstrual intervals
Metrorrhagia: bleeding between menstrual cycles
Menometrorrhagia: irregular intervals w/ varying degrees of bleeding
Oligomenorrhea: infrequent (prolonged cycle length >35 days but <6months)
Polymenorrhagia: frequent cycle interval (<21 days)
-Etiologies:
Chronic Anovulation (90%): seen esp w/ extremes of age (teenagers soon after
menarche or perimenopausal women
o Unopposed estrogen: w/out ovulation, there is no progesterone (unopposed
estrogen)=> increased endometrial overgrowth w/ irregular, unpredictable
shedding (bleeding) as endometrium outgrows its own blood supply=
metrorrhagia, menometrorrhagia, amenorrhea
Ovulatory (10%): regular cyclical shedding, +ovulation w/ prolonged progesterone
secretion (due to low estrogen levels) => increased blood loss from endometrial vessel
dilation and prostaglandins = metrorrhagia
-Diagnosis/Workup
Diagnosis of exclusion: must exclude organic causes (r/o reproductive, systemic,
iatrogenic causes). If w/u shows no evidence of organic cause and negative pelvic
exam= DUB
Workup includes:
o Pregnancy test
o Pelvic exam w/ PAP
o Imaging: TVUS for fibroids, polyps or adenomyosis
o **May need Endometrial biopsy
If endometrial stripe >4mm on TVUS or in women >35y/o to r/o
endometrial hyperplasia or carcinoma
o Malignancy workup if postmenopausal
o Coagulopathy workup: PT/aPTT, CBC
o Assess ovulatory status: biphasic body temp, progesterone levels, urine LH,
estrogen levels
o Consider testosterone and DHEAS levels in women with signs of virilization
-Management:
Goals= control acute bleeding, prevent future bleeding, minimize endometrial cancer risk
Acute severe bleeding: high dose estrogens (ex. IV), high dose OCPs w/ reduction in
dose as bleeding improves. Dilation and Curettage if IV estrogen fails. Can also use
DepoProvera shot as this is Progesterone and will stop acute bleeding.
Anovulatory: (90%):
o OCPs: regulates cycle in anovulatory pts, thins endometrial lining, and reduces
menstrual flow. Decreases endometrial CA risk by reducing unopposed estrogen
o Progesterone: ex. Medroxyprogesterone acetate: 10d q month if estrogen is
contraindicated
o GnRH agonists: Leuprolide causes temporary amenorrhea
o Adolescent mild DUB can be treated w/ iron supplements and observation
o Adolescent mod-severe DUB can be treated with OCPs or progestin only
regimen
o Pts w/contraindications to estrogen can try symptomatic treatment- NSAIDs,
progestin-only regimen or Mirena IUD

Ovulatory (10%):
o OCPs: regulates cycle, thins endometrial lining
o Progesterone: orally or IUD (Mirena reduces bleeding in 79-94%)
o GnRH agonists: Leuprolide w/ add back progesterone reduces GnRH s/e
Surgery: done if not responsive to medical treatment
o Hysterectomy: definitive management
o Endometrial ablation: destruction of endometrium in pts who dont want a
hysterectomy

5) Amenorrhea:
- absence of menses
Primary Amenorrhea: failure of onset of menarche by age 13y/o (in the absence of
secondary sex characteristics) or age 15y/o (with secondary sex characteristics)
-Differential Diagnosis:
o Uterus present, Breasts present:
Outflow obstruction: transverse vaginal septum, imperforate hymen
o Uterus present, Breasts absent:
Elevated FSH, LH= Ovarian Causes
Premature Ovarian Failure (46XX)
o Follicular failure or follicular resistance to LH or FSH
Gonadal dysgenesis (ex Turners syndrome 45X)
o Turners Syndrome: female w/ absent/nonfunctional sex
chromosome. Rudimentary fibrosed ovaries=> primary
amenorrhea, menopause before menarche, delayed
secondary sex characteristics=> short stature, webbed
neck, edema, low hairline, low set ears, widely spaced
nipples
Normal/Low FSH, LH= Hypothalamus-Pituitary Failure
Puberty delay (ex athletes, illness, anorexia)
o Uterus Absent, Breasts present:
Mullerian agenesis (46XX)
Caused by embryologic growth failure of the mullerian duct,
with resultant agenesis or underdevelopment of the vagina,
uterus or both. Ovaries are normal in structure and function as
they have a separate embryologic source.
S/S+PE: normal height, secondary sexual characteristics, body
hair and external genitalia, absence of vagina and/or uterus
Diagnostic evaluation: transabdominal, translabial or transrectal
ultrasonography; three-dimensional ultrasonography or MRI
Management: psychosocial counseling, those with absent
vagina= nonsurgical (vaginal dilators) or surgical creation of a
neovagina
Androgen insensitivity (46XY)
A person who is genetically male (XY) is resistant to androgens
and as a result, the person has some or all of the physical traits of
a woman
S/S+PE: vagina but absence of uterus, little armpit and pubic
hair, breast develop, inguinal hernia w/ testes,

Diagnostic Evaluation: blood work to check levels of


testosterone, LH, FSH; genetic testing, pelvic ultrasound
Management: removal of testicles that are in the wrong place
after puberty (prevention of cancer), estrogen replacement after
puberty, gender assignment can be a very complex issue
Uterus Absent, Breasts Absent:
RARE. Usually caused by a defect in testosterone synthesis. Presents like
a phenotypic immature girl w/ primary amenorrhea (will often have
intrabdominal testes)

Secondary Amenorrhea: absence of menses for 3 months in a pt w/ previously normal


menstruation (or 9 months in pt who was previously oligomenorrheic)
-Etiologies:
o Pregnancy: MOST COMMON cause, 1st step in amenorrhea w/u is to r/o
pregnancy
o Hypothalamus dysfxn: (35%) disruption of normal pulsatile hypothalamic
secretion of GnRH=> decreased FSH and/or decreased LH secretion by pituitary
Etiologies: hypothalamus d/o, anorexia (or wgt loss 10% below IBW),
exercise, stress, nutritional deficiencies, systemic dx (Celiacs)
Diagnosis: Normal/low FSH & LH, low estradiol, normal prolactin
Management: stimulate Gonadotropin secretion: Clomiphene,
Menotropin (Pergonal)
o Pituitary dysfxn: Prolactin Secreting Pituitary Adenoma (19%)
Diagnosis: decreased FSH, LH; increased prolactin (galactorrhea); MRI
of pituitary sella. Prolactin inhibits GnRH.
Management: transsphenoidal surgery (tumor removal)
o Ovarian disorders: (40%)
Clinical: symptoms of estrogen deficiency (similar to menopause)
Diagnosis:
increased FSH and LH; decreased estradiol= ovarian
abnormalities
Normal/ decreased FSH, LH= pituitary or hypothalamus
Progesterone challenge test: 10mg medroxyprogesterone for 10
days
o If withdrawal bleeding= Ovarian (pt is anovulatory or
oligoovulatory) & there is enough estrogen present
(which built up endometrial lining)
o No withdrawal bleeding=
Hypoestrogenic (Hypothalamus-Pituitary
failure) OR
Uterine: Ashermans or uterine outflow tract
(imperforate hymen)
Types:
1) Polycystic Ovarian Syndrome
Triad: amenorrhea, obesity, hirsutism.
PCOS is due to insulin resistance
Pathophys:

Exact cause unknown but associated w/ abnormal fxn of


hypothalamus-pituitary-ovarian axis=> increased insulin and
LH-driven increase in ovarian androgen production
Clinical manifestations:
Menstrual irregularity: secondary amenorrhea, oligomenorrhea,
DUB
Increased androgen: hirsutism- coarse hair growth midline
structures (face, neck, abdomen), acne, possible male pattern
baldness
Insulin resistance: DMII, obesity, acanthosis nigricans, HTN
Physical Examination
Bilateral enlarged smooth mobile ovaries on bimanual exam
Enlargement is due to immature follicles (not cysts) w/ arrested
development due to abnormal ovarian fxn (due to increased
androgens)
Diagnosis:
Exclude other disorders: thyroid (TSH), Pituitary adenoma
(prolactin levels), ovarian tumors, Cushings (dexamethasone
suppression test)
Labs: increased testosterone, increased DHEA-S (intermediate of
testosterone), LH:FSH ratio 3:1 (normal 1.5:1)
GnRH agonist stimulation test: rise in serum hydroxyprogesteron
Lipid panel (to check for insulin resistance), glucose tolerance
test (for DM)
Pelvic US: bilateral enlarged ovaries w/ peripheral cysts or
string of pearls (not necessary for dx)
Management:
Combination OCPs: mainstay of tx.
-Normalizes bleeding, induces regular menses, treats hirsutism
(suppresses androgen); decreases LH levels, decreases
endometrial hyperplasia. Estrogen stimulates hepatic production
of sex-hormone binding globulin reducing androgen levels.
Progesterone decreases action of testosterone at target organ by
receptor antagonism. Avoid androgenic progesterone (avoid
norgestrel or levonorgestrel)
Anti-androgenic agents for hirsutism: Spironolactone
(structurally similar to testosterone- blocks testosterone
receptors); is teratogenic so must be used w/OCPs
o Leuprolide, Finasteride are other anti-androgenics
Infertility: Clomiphene (selective estrogen receptor modulator)
o Metformin in pts w/ abnormal LH:FSH ratios may
improve menstrual frequency by reducing insulin
Lifestyle changes: diet, exercise, weight loss
Surgical: wedge resection to restore ovulation in pts who desire
to have children in whom clomiphene is ineffective
Complications: increased risk for infertility, increased endometrial
hyperplasia & endometrial carcinoma (from chronic anovulation-

unopposed estrogen); insulin resistance: increased risk of atherosclerosis,


HTN
2) Premature Ovarian Failure
3) Turners syndrome
Uterine disorder: scarring of the uterine cavity
Ashermans Syndrome: Formation of scar tissue in the uterine cavity
Causes: numerous D&Cs, uterine surgery, severe pelvic
infection unrelated to surgery, infection w/ TB or schistosomiasis
S+S: amenorrhea, repeated miscarriages and infertility
Dx:
o Pelvic US: absence of normal uterine stripe.
o Hysteroscopy: to diagnose and treat
Management:
o Surgery to cut and remove the adhesions
o Estrogen treatment: to stimulate endometrial
regeneration of denuded area

6) Premenstrual Syndrome:
Cluster of physical, behavioral, mood changes w/ cyclical occurrence during luteal phase
of menstrual cycle (7-14 days before onset of menses, relieved w/in 2-3 days of menses
onset) & at least 7 days symptom free during the follicular phase
4 phases: Menstrual (Day 1 of cycle), Follicular (1-12 days; estrogen predominates),
Ovulatory (12-14 days; LH surge causes ovulation), Luteal (Ovulation to onset of
menses; progesterone predominates)
PreMenstrual Dysphoric Disorder (PMDD): severe PMS w/ fxnl impairment
Clinical Manifestations:
o Physical: bloating, breast swelling/pain, HA, changes in bowel habits, fatigue,
muscle/joint pain
o Emotional: depression, hostility, irritability, libido changes, aggressiveness
o Behavioral: food cravings, poor concentration, noise sensitivity, loss of motor
senses
Diagnosis: sx seen in luteal phase (7-14 days before menses) w/ sx free follicular phase
(approx. 1 week)
Management:
o Nonpharmacologic: aerobic exercise, consumption of complex carbs and
frequent meals, relaxation training, light therapy, cognitive behavioral therapy,
low salt diet
o Pharmacologic:
SSRIs: for emotional sx (Fluoxetine, Sertraline, Paroxetine, Citalopram)
OCPs: induces anovulation. Drosperinone- containing OCP for PMDD
GnRH: done w. estrogen add back therapy if no response to SSRIs or
OCPs
Refractory breast pain: Danazol, Bromocriptine
Bloating; Spironolactone, calcium carbonate, low salt diet
7) Sexually Transmitted Diseases (characterized by urethritis and cervicitis)
a) Genital Herpes Simplex Virus: 90% caused by HSV II, 10% caused by HSV I (when
HSV I usually spread through oral sex)

-Risk Factors: vaginal, anal or oral sex; even spread when not an active outbreak
-S&S: painful vesicular lesions in bunches of at least 3, they break open and then heal
and go away w/in three weeks; flu-like symptoms such as fever, body aches, or
swollen glands; highly infectious when lesions are present; stress
can precipitate an outbreak
-Diagnosis: usually clinical, can take a culture of the sore if unsure
-Treatment:
First clinical episode: Acyclovir 400mg PO TID for 7-10 days
OR: Famciclovir 250mg PO TID for 7-10 days; Valacyclovir 1g PO BID for 7-10
days
Episodic Therapy for Recurrent episodes: Acyclovir 400mg PO TID for 5 days
o OR Famciclovir 1000mg PO BID for 1 day; Valacyclovir 1g PO QD for
5 days
Suppressive Therapy for Recurrent episodes: Acyclovir 400mg PO BID
o OR: Famciclovir 250mg PO BID; Valacyclovir 1g PO QD
-Complications: painful genital sores, spread to other parts of your body, pregnancy
complications such as miscarriage, early delivery, neonatal herpes which can be fatal
B) Chlamydia Trachomatis
-Risk Factors: vaginal, anal or oral sex
- S&S: may be asymptomatic, mucopurulent cervicitis, increased frequency, dysuria, abdominal
pain, PID, post coital bleeding
If Lymphogranuloma Venereum (LGV): Painless genital ulcer
-Diagnosis: Urethral, Cervical, Vaginal and Urine samples=> Ligase Chain Reaction (LCR)
Cervical and urethral samples= 97% sensitivity; Urine sample= 80% sensitivity
-Treatment:
Azithromycin 1g PO X 1 dose OR Doxycycline 100mg PO BID x 10 days
Treat for Gonorrhea!! Ceftriaxone 250mg IMx1 (co-infection likely)
Treat Partner!
-Complications: PID, infertility, ectopic pregnancy, premature labor
C) Neisseria Gonorrhoeae
-Risk Factors: vaginal, anal or oral sex; presence of columnar cells on a young womans cervix
increases susceptibility
-S&S: may be asymptomatic, vaginal discharge, cervicitis, increased frequency, dysuria
-Diagnosis: Culture of cervix or urethra; gran stain of cervix and vagina could offer immediate
diagnosis
-Treatment:
Ceftriaxone 250mg IM x 1 or Cefixime
Treat for Chlamydia!! (Azithromycin 1 g PO x 1)
Treat partner!
-Complications: PID, infertility, ectopic pregnancy, chronic abdominal pain, reactive arthritis
D) Mycoplasma genitalium
-Risk Factors: vaginal, anal and oral sex
-S&S: may be asymptomatic, pelvic pain, dyspareunia, abnormal discharge, cervicitis (red,
inflamed cervix)
-Diagnosis: cervical culture (Nucleic Acid Amplification Testing NAAT)

-Treatment: Azithromycin 1g PO x 1; if failure then Azithromycin 500mg PO x 1 followed by


250mg QD for 4 days; if failure still, then: Moxifloxacin 400mg QD x 7, 10 or 14 days
-Complications: Urethritis, cervicitis, PID, infertility
E) Trichomoniasis: pear shaped flagellated protozoa
-Risk Factors: vaginal, anal and oral sex
-S&S: vulvular pruritus, erythema, dysuria, dyspareunia, copious malodorous frothy
yellow/green discharge, strawberry cervix- cervical petechiae; Urinary PH >5
-Diagnosis: Mobile protozoa on wet mount, or PCR testing of cervical culture
-Treatment: Metronidazole 2g PO x 1 dose
OR Metronidazole 500mg PO BID x 7 days
SAFE IN PREGNANCY!
Or Tinidazole
MUST treat partner
-Complications: perinatal contraction, increased HIV transmission
8) Vaginitis
a) Bacterial Vaginosis= MC cause of vaginitis
Pathophysiology: decreased lactobacilli acidophilus (normally maintains vaginal pH)=>
overgrowth of normal flora such as Gardnerella vaginalis, anaerobes
S&S: thin, homogenous watery grey-white discharge; fishy odor, possible pruritus,
>50% asymptomatic; urinary pH >5
Diagnosis: Clue cells on microscopic examination (epithelial cells w/ borders obscured
by small bacteria); Positive Whiff test (a fishy odor of vaginal discharge before or after
addition of 10% KOH); vaginal culture
Treatment: Metronidazole 500mg PO BID x 7 days (safe in pregnancy) OR
Clindamycin
Prevention: avoid douching (promotes loss of lactobacilli) and no need to treat partner
Complications: in pregnancy= PROM, preterm labor, choriamnionitis
b) Candida
Pathophysiology: Candida albicans overgrowth (part of normal flora due to change in
normal vaginal environment such as abx use); increased in DM pts, steroid use and
pregnancy
S&S: vaginal and vulvar erythema, swelling, burning, pruritus, burning when urine
touches skin, dysuria, dyspareunia, thick curd-like/ cottage cheese discharge; urinary
pH is normal
Diagnosis: hyphae, yeast on KOH prep or vaginal culture
Treatment: Fluconazole 150 mg PO x 1 dose; or intravaginal antifungal creams:
clotrimazole, Nystatin, Butoconazole, Miconazole (Monistat)
Prevention: Keep vagina dry, 100% cotton underwear, avoid tight fitting clothes, avoid
use of feminine deodorants and bubble baths
9) Pelvic Inflammatory Disease
-ascending infection of the upper reproductive tract (may lead to sepsis, ectopic pregnancy or
infertility
Risk factors: multiple sex partners, unprotected sexual intercourse, prior PID, young,
nulliparous

Causative Bacteria: N. gonorrhea, Chlamydia, anaerobes, H. flu


Clinical Manifestations:
o Pelvic/lower abdominal pain, dysuria, dyspareunia, vaginal discharge, N/V
o Chandelier sign: cervix/uterine/adnexal tenderness to palpation & rotation so
severe they seem to raise off the bed as if reaching for the chandelier
Physical Exam:
o All 3 of: abdominal tenderness, adnexal tenderness, cervical motion tenderness
o Plus 1 or more of: temp >38C, WBC> 10,000, pus on culdocentesis or
laparoscopy, pelvic abnormality on bimanual exam or ultrasound, increased ESR
or CRP
Diagnosis:
o Pelvic US
o If uncertain or no improvement w/ Abx tx: Laparoscopy
Treatment:
o Outpatient: Doxycycline 100mg BID x 14 days + Ceftriaxone 250mg PO x 1
dose (treats Gonorrhea & Chlamydia)
o Inpatient: Doxycycline + 2nd generation cephalosporin
Reasons to hospitalize: pregnancy, pt does not respond to oral abx
therapy for 3 days, pt is unable to tolerate outpatient regimen, pt has
severe illness (n/v, high fever), pt has tubo-ovarian abscess
Complications:
o Fitz-Hugh Curtis Syndrome: hepatic fibrosis/ scarring or peritoneal involvement.
RUQ pain
o Chronic pelvic pain
o Menometrorrhagia
o Dyspareunia
o Infertility
o Endometriosis

10) Endometriosis: presence of normal endometrial tissue (stroma and gland) outside the uterine
cavity; ectopic endometrial tissue responds to cyclical hormonal changes; 15% of US population
MC sites of ectopic endometrial tissue: ovaries (MC), posterior cul de sac, broad &
uterosacral ligaments, rectosigmoid colon, bladder & distal ureter
Risk factors: nulliparity, family hx, early menarche, onset <35y/o
S&S:
o Classic triad: cyclic premenstrual pelvic pain, dysmenorrhea, dyspareunia
o Dyschezia (painful defecation)
o Pre/post menstrual spotting
o Infertility (MC cause of infertility)
o PE: usually normal; possible fixed tender adnexal masses
Diagnosis:
o Laparoscopy w/ biopsy= definitive diagnosis (used to visualize structures for
presence of tissue)
o Endometrioma: endometriosis involving the ovaries large enough to be
considered a tumor, usually filled w/ old blood appearing chocolate colored
chocolate cyst

Treatment:
o Medical: ovulation suppression
Premenstrual pain: Combined OCPs + NSAIDS
Progesterone tx: suppresses GnRH, causes endometrial tissue atrophy,
suppresses ovulation
Leuprolide: GnRH analog causes pituitary FSH/LH suppression
Danazol: testosterone (induces pseudomenopause by suppressing FSH &
LH & mid cycle surge)
o Surgical:
Conservative laparoscopy w/ ablation: used if fertility desired (preserves
uterus and ovaries)
TAH-BSO (Total Abdominal Hysterectomy w/ Salpingoophorectomy): if
no desire to conceive

11) Urinary Tract Infection:


-Risk factors:
Young women: sexual intercourse, use of spermicidal (esp w/ diaphragm)
Pregnant: progesterone & estrogen=> ureter dilation, inhibit bladder peristalsis
Postmenopausal: decreased bladder tone, estrogen deficiency altering vaginal flora
-Etiologies:
E. coli (80%) MC organism in complicated/uncomplicated cases
Gram neg uropathogens: proteus, enterobacter, klebsiella, pseudomonas (usually
ascending infection)
Staph Saprophyticus: esp among sexually active women
-Clinical Manifestations:
a) Acute uncomplicated cystitis (bladder infection)
Dysuria (burning), increased frequency, urgency, hematuria, suprapubic discomfort
b) Pyelonephritis (kidney infection)
Fever & tachycardia, back/flank pain, CVA tenderness, N/V
-Diagnosis:
Urinalysis:
o Pyuria (>5 WBC/hpf (esp >10)), + leukocyte esterase;
o WBC casts= pyelonephritis
o + nitrites (90% bacteria causing UTIs)
o Hematuria
o Cloudy urine
o Increased pH w/ Proteus
Dipstick:
o Leukocyte esterase, nitrites, hematuria
Urine Culture: CFU/ml of organism > 100,000 is definitive diagnosis
-DDX: vaginitis
-Treatment:
-Acute Uncomplicated Cystitis

Nitrofurantoin monohydrate/macrocrystals (100 mg orally twice daily for 5 days);


Nitrofurantoin should be avoided if there is suspicion for early pyelonephritis, and is
contraindicated when creatinine clearance is <60 mL/minute.
Trimethoprim-sulfamethoxazole (TMP-SMX; one double strength tablet [160/800 mg]
twice daily for 3 days);
Fosfomycin (3 grams single dose) Fosfomycin should be avoided if there is suspicion for
early pyelonephritis.
Pivmecillinam (400 mg orally twice daily for 3 to 7 days); Pivmecillinam is an extended
gram-negative spectrum penicillin used only for treatment of UTI. It is not available in the
United States but is an agent of choice in many Nordic countries due to low resistance rates
and low propagation of resistance. Pivmecillinam should be avoided if there is suspicion for
early pyelonephritis.

Treatment in pregnancy: 7-14 days of amoxicillin, augmentin, cephalexin, macrobid,


fosfomycin, cefpoxidime; sulfisoxazole (safe except in last days of pregnancy=>
kernicterus)

-Pyelonephritis:

500 mg of oral ciprofloxacin (Cipro) twice per day for seven days; 1,000 mg of
extended-release ciprofloxacin once per day for seven days; or 750 mg of
levofloxacin (Levaquin) once per day for five days. These options are
appropriate in areas where the prevalence of resistance to fluoroquinolones does
not exceed 10 percent.

Oral trimethoprim/sulfamethoxazole (Bactrim, Septra) at a dosage of 160


mg/800 mg twice per day for 14 days is an appropriate treatment choice for
women with acute pyelonephritis if the uropathogen is known to be susceptible.

Initial treatment of women with acute pyelonephritis who require hospitalization


should include an intravenous antimicrobial regimen, such as a fluoroquinolone,
an aminoglycoside (with or without ampicillin), an extended-spectrum
cephalosporin or penicillin (with or without an aminoglycoside), or a
carbapenem.

12) Cervical Cancer (3rd MC gynecologic CA; 1st= endometrial CA. 2nd= ovarian CA)
Risk Factors:
o Early onset of sexual activity, increased # of partners, smoking, CIN (Cervical
Intraepithelial Neoplasm), DES exposure, Immunosuppression, STDs
2 Types:
o Squamous (90%)
o Adenocarcinoma (10%)
Clear cell carcinoma linked w/ DES exposure
Takes on average 2-10 years for carcinoma to penetrate the basement membrane
Clinical Manifestations:
o Post coital bleeding/spotting (1st symptom)
o Metorrhagia
o Pelvic pain
o Watery vaginal discharge
Diagnosis: Colposcopy w/ biopsy
o Screening= PAP smear w/ cytology
Management:
o Stage O: Carcinoma in situ
Local treatment:
Excision (LEEP, Cold knife conization)
Ablation tx (cryotherapy or laser)
TAH-BSO (total abdominal hysterectomy-bilateral salpingooophorectomy)
o Stage Ia1: microinvasion
Surgery: Conization, TAH-BSO, XRT
o Other stage I, IIA
TAH-BSO; XRT+ Chemo tx (Cisplatin)
o Stage IIb-Iva: Locally advanced; II- extends locally beyond cervix, III- lower 1/3
of vagina, IV- Local METS (bladder, rectum)
XRT+ Chemo (Cisplatin w/ 5FU)
o Ivb or recurrent: Distant Mets
Palliative XRT, Chemo (surgery is not likely to be curative)
Prevention: Gardasil vaccine vs HPV 6, 11, 16, 18; 3 doses in 6 mos; age 11-26; CI if
immunosuppressed, pregnant or lactating
Screening Guidelines:
o 21-29 y/o: PAP and HPV every 3 years
o 30-65 y/o: PAP and HPV every 5 years

13) Rectocele/Cystocele:
Rectocele: distal sigmoid colon into posterior distal vagina
Cystocele: posterior bladder herniating into the anterior vagina
Uterine prolapse: uterine herniation into the vagina
Enterocele: pouch of douglas (small bowel) into the upper vagina
Risk Factors:
o Weakness of pelvic support structures (MC after childbirth)
o Increased pelvic floor pressure due to:
Multiple vaginal births
Obesity
Repeated heavy lifting
Grades:
o I: descent into upper 2/3 of vagina
o II: cervix approaches introitus
o III: outside introitus
o IV: entire uterus outside of vagina= complete prolapse

Clinical Manifestations:
o Pelvic Fullness, heaviness falling out sensation
o Lower back pain (esp w/ prolonged standing)
o Vaginal bleeding, purulent discharge
o Urinary frequency, urgency, stress incontinence
PE: bulging mass esp w/ increased intrabdominal pressure (such as Valsalva)
Management:
o Prophylactic: Kegel exercises, weight control
o Nonsurgical: pessaries, estrogen treatment (improves atrophy)
o Surgical: hysterectomy; uterosacral or sacrospinous ligament fixation

14) Chadwicks/ Hegars sign


Chadwicks sign: cervix & vulva bluish color at 8-12 weeks
Hegars sign: uterine isthmus softening after 6-8 weeks gestation
15) Gestational Diabetes
Clinical Definition: glucose intolerance or DM during pregnancy=> hyperglycemia
o Patho: caused by placental release of human placental lactogen (HPL) which
antagonizes insulin (works similar to growth hormone as a counter regulatory
hormone increasing glucose availability for the fetus)
Risk Factors:
o Family or prior h/o GDM, spontaneous abortion, h/o infant > 4,000g at birth,
multiple gestations, obesity, older maternal age
Clinical manifestations:
o Mother may present w/ hyperglycemia, hypoglycemia, recurrent infections
Appropriate Diagnostic Evaluation:
o Screening: 1 hr Glucose Tolerance Test
50g oral glucose challenge test (nonfasting) @ 24-28 weeks
If >140mg/dl after 1 hour=> perform 3hr oral GTT
o 3 hour 100g oral Glucose Tolerance Test (GTT): gold standard
Positive for GDM if: 1h >180, 2h>155, 3h>140
o Glucosuria
Management:
o Insulin: tx of choice (does not cross placenta more natural); goal is fasting
glucose <95.
NPH/Regular insulin 2/3 in AM, 1/3 in PM
.8 IU/kg 1st trimester; 1.0 IU/kg in 2nd trimester; 1.2 IU/kg in 3rd trimester
o Glyburide: only oral hypoglycemic that does not cross the placenta, but higher
risk of eclampsia
o Early delivery @ 38 weeks; C-section if child is macrosomic (big body..
>4,000g)
Clinical significance of gestational diabetes
o Fetal demise
o Placenta abruption
o Shoulder dystocia
o Neonate hypoglycemia
o Excessive fetal growth
o Increased risk of miscarriage
o Congenital malformation
o Preterm labor
16) Placenta Previa Previa=Painless
Definition: abnormal placenta implantation on or close to cervical os
o Partial= partial covering of cervix ahead of fetal presenting part
o Complete= total coverage
o Marginal= w/in 2-3cm of os
Clinical Manifestation:
o 3rd trimester bleeding

o Sudden onset of PAINLESS bleeding (bright red)


o Resolves w/in 1-2 h
o NO ABDOMINAL PAIN
o Uterine soft NONTENDER
Fetal Heart Rate: normal (no fetal distress usually)
Diagnosis: Pelvic US to localize placenta; DO NOT DO PELVIC EXAM
Management:
o Hospitalization: for stabilization, bed rest
o Stabilize fetus:
Tocolytics: Mg sulfate- inhibits contractions
Amniocentesis: to test amniotic fluid for fetal lung maturity (surfactant)
Steroids given between 24-34 weeks to increase lung maturity
o Delivery when stable:
Possibly vaginal if partial/marginal
C-section: if complete
Risk Factors:
o Multiparity, increased age, uterine surgery, cocaine, smoking

Abruptio Placenta: Abruptio=Abdominal Pain


Definition: premature separation of placenta from uterine wall
Clinical presentation:
o 3rd trimester bleeding- continuous often dark red
o SEVERE ABDOMINAL PAIN (painful bleeding)
o Rigid uterus
Fetal Heart Rate: fetal bradycardia (fetal distress bc it interferes w/ fetal oxygenation)
Diagnosis:
o Pelvic US
o DO NOT DO PELVIC EXAM
Management:
o Hospitalization for hemodynamic stabilization
o IMMEDIATE delivery
Can lead to DIC
Risk Factors:
o MATERNAL HTN MC cause
o Smoking, ETOH, cocaine, folate deficiency, high parity, increased age,
chioramnitis
Vasa Previa: fetal vessels traverse the fetal membranes over the cervical os
Clinical presentation:
o PAINLESS vaginal bleed (rupture of membranes); fetal bleeding
Fetal Heart Rate:
o Fetal Bradycardia (fetal distress)

Diagnosis:
o Pelvic US: vessels crossing os

APT test: blood from vagina, add sodium hydroxide. Fetal blood stays pink,
maternal blood brown/yellow
Management:
o Immediate C-Section
o

17) Pre-eclampsia/ Eclampsia


-Pre-eclampsia: HTN+Proteinuria
Risk Factors: nulliparity, extremes of age, African American
Clinical Presentation:
o Sx of HTN: headache, visual sx
o Fetal growth restriction.
o Edema (caused by proteinuria=> decreased oncotic pressure)
o Possible RUQ pain (starting to affect liver)
Diagnosis:
o Mild: BP >140/90 on 2 separate occasions @ least 6h apart but no > 1 wk apart
Proteinuria: >300mg/24h (or >+1 on dipstick)
o Severe: BP>160/110
Proteinuria: >5g/24h or (3+ on dipstick)
Oliguria: <500ml/24h
Thrombocytopenia, possible DIC
HELLP syndrome (Hemolytic Anemia, Elevated Liver Enzymes, Low
Platelets)
Management:
o Mild: Delivery only cure
Performed @ 34-36 wks; steroids given to mature lungs
Supportive: daily wgts, BP & dipstick weekly, bed rest
o Severe: Delivery only cure (@34-36 wks)
Hospitalization: low salt, Mg sulfate (prevent eclampsia)
BP meds: started if BP >180/110- Hydralazine, Labetalol, Nifedipine
Complications:
o Abruption placenta, renal failure, hepatic hematoma/hepatic rupture,
uteroplacental insufficiency, eclampsia, intracerebral hemorrhage
-Eclampsia: HTN+Proteinuria+Seizures
Greatest risk of occurrence just prior to delivery (75%), during labor and w/in the first 24
hr period postpartum
Clinical presentation:
o Abrupt tonic clonic seizures 1-2 min, then post ictal state
o HA, visual changes, cardiorespiratory arrest
Diagnosis:
o Same as preeclampsia + seizures
o Hyperreflexia
Management:
o ABCDs 1st
o Magnesium sulfate: for seizures; Lorazepam 2nd line- only if refractory to tx
o Delivery of fetus: once pt is stabilized
o BP meds: Hydralazine, Labetalol

18) Potential medical complications late in pregnancy


Pre-term labor:
o Definition: regular uterine contractions w/ progressive cervical changes
(effacement & dilation) before 37 wks gestation; MC cause of perinatal mortality
(70%)
o Clinical manifestation: cramps, uterine contractions, back pain, pelvic pressure,
vaginal discharge
o Diagnosis:
Pelvic exam: assess cervical dilation & effacement:
if >2cm or >80% effacement preterm labor likely
Nitrazene pH paper test
If pH >6.5- likely PROM
Normal vaginal pH 3.8-4.2
Fern test:
Mixture of estrogen & amniotic fluid causes crystallization on
microscope
Presence of fetal fibronectin between 20-34 weeks strongly suggests
preterm labor
Rule out infections: UTI, Group B strep.
If L:S ratio <2:1= fetal lung immaturity (lecithin-sphingomyelin)
o Test of the amniotic fluid
o Management:
Tocolytics: suppress uterine contraction; given for 48 h to delay delivery
so steroids can take full effect on the fetus. Dont delay if intrauterine
infection
Beta2agonists: Terbutaline, Ritodrine
o S/E of terbutaline: pulmonary edema
Magnesium Sulfate: must be admitted if administered
o MOA: calcium antagonist
Nifedipine (CCB)
o Not given concurrently w/ Magnesium
Indomethacin
o Inhibits prostaglandin-mediated uterine contraction
Antenatal corticosteroids: to enhance fetal lung maturity (esp if L:S ratio
<2:1)
Antibiotics: GBS prophylaxis if needed (to prevent neonatal GBS
induced meningitis, septicemia or pneumonia)
Done if PROM or culture positive
Premature rupture of membranes
o Definition: rupture of chorioamniotic membrane before onset of labor
o Risk factors: STDs, smoking, prior pre-term delivery, multiple gestations
o Diagnosis:
Nitrazine test: amniotic fluid pH>7.1
Fern test of amniotic fluid
+ if Fern pattern due to crystallization of estrogen & amniotic
fluid
Sterile speculum exam: look for infection

Management:
Await for spontaneous labor or induction of labor (with oxytocin or
prostaglandin gel)
Monitor for infection (infection is MC complication of PROM)
Placental abruption (done w/ placenta previa)
o

19) Prenatal care


Recommended routine prenatal testing
o Every visit: vital signs, weight/height/BMI, fetal assessment from 10 th week
(FHT), Urine dip for protein and glucose, Fundal height
o Frequency:
Initial office visit at 8-10 weeks of pregnancy
Every 4 weeks for first 28 weeks
Every 2-3 wks until 36 weeks
Every week after 36 weeks
o 8-10 weeks (1st trimester)
Blood type and screen (Rh)
CBC for H&H.MCV
Platelet Count
Hepatitis B surface antigen (HBsAg).
Syphilis screening.
Chlamydia and Gonorrhea screening
Screening for gestational diabetes if at high risk
Pre-pregnancy BMI >30kg/m
Personal hx of GDM
Known impaired glucose metabolism
HIV testing
Cervical Cancer Screening (if the patient is due).
Urine C&S and urine dip for protein and glucose.
o 11-14 weeks (1st trimester)
When FHT should be heard w/ Doppler
If AMA @ 12 wks offer AFP and high resolution US for Downs
o 15-20 weeks (2nd trimester)
Ultrasound at 18-20 weeks
MSAFP (neural tube defect screening)
If increased then neural tube defects
If decreased, then down syndrome
Triple Screen (AFP, hCG, estriol) (16 wks)
65% detection rate for Downs Syndrome
o 24-28 weeks (2nd + 3rd trimester)
1 hr Glucose Tolerance Test
Hematocrit
Tdap administration?.. (27-36 wks)
Repeat type and screen, if Rh (-) administer Rh-immune globulin

36 weeks (3rd trimester)


Repeat Gonorrhea and Chlamydia
Group B strep culture
o 41 weeks:
Baseline non-stress test (NST) or contraction stress test (CST), US,
biophysical profile (BPP)
Discuss labor induction >41 weeks
Significance of fundal height:
o Definition: distance from the pubic bone to the top of the uterus measured in
centimeters
o Used as a tool for gauging fetal growth and gestational age
o After 16 wks, fundal hgt measurement often matches the number of weeks
youve been pregnant
Ex: 27 wks pregnant= 27cm
o Fundal hgt discrepancies:
High BMI, full bladder, carrying twins or other multiples
Slow fetal growth
Rapid fetal growth
Too little amniotic fluid (oligohydramnios)
Too much amniotic fluid (polyhydramnios)
Uterine fibroids
A baby prematurely descending into the pelvis or settling into a breech or
other unusual position
o Depending on circumstance doctor may recommend US to determine cause
Normal Fetal Heart Rate:
o 120-160bpm
Approaches to morning sickness treatment
o Morning sickness definition:
N/V up until 16 wks due to oversensitivity of pregnancy hormones
o Hyperemesis Gravidarum:
severe, excessive form of morning sickness associated w/ wgt loss,
electrolyte imbalance. Develops during 1st/2nd trimester (persists >16 wks
gestation)
wgt loss 5% of pre-pregnant wgt
acidosis (from starvation), metabolic hypochloremic alkalosis (vomiting)
o Risk factors:
Primagravida, previous hyperemesis in past pregnancy, multiple
gestations, molar pregnancy
o Management:
Fluids, electrolytes, multivitamin, trans-parenteral nutrition if severe.
Early treatment: high protein foods, small/frequent meals, avoiding
spicy/fatty foods
Anti-emetics:
pyridoxine (Vit B6) +/- doxylamine (1st line)
Promethazine, dimenhydrinate
Reglan
o

20) Gestational Trophoblastic Disease


Definition: a group of pregnancy-related tumors including: hydatiform mole (partial or
complete), invasive mole, choriocarcinoma and placental site trophoblastic tumor. These
tumors are rate and they appear when cells in the womb start to proliferate
uncontrollably.
1) Hydatiform mole: neoplasm due to abnormal placental development with trophoblastic
tissue proliferation arising from gestational tissue (not maternal) origin. 80% benign

Types:
o Complete Molar pregnancy: egg with no DNA fertilized by 1 or 2 sperm.
46XX all paternal chromosomes.
Associated with higher risk of malignancy
o Partial Molar pregnancy: an egg is fertilized by 2 sperm (or 1 sperm that
duplicates its chromosomes). There may be development of the fetus but it is
always malformed and never viable
Risk Factors: prior molar pregnancy or extremes of age <20y or
>35 y; Asian
Pathophysiology:
o Abnormal pregnancy in which a nonviable fertilized egg implants in uterus with
a nonviable pregnancy which will fail to come to term => abnormal placental
development
Clinical Manifestations:
o Painless vaginal bleeding may begin @ 6 weeks- 4th/5th months MC. Possible
brownish discharge
o Uterine size/date discrepancies (ex larger than expected)
o Preeclampsia before 20 weeks
o Hyperemesis Gravidarum: due to significant hormonal changes
Diagnosis:
o B-HCG: markedly elevated (>100,000)
o Very low maternal serum a-fetoprotein
o Ultrasound: snowstorm or cluster of grapes appearance & absence of fetal
parts & heart sounds.
Cluster of grapes= enlarged cystic chorionic villi
Complete: no products of conception seen
Partial: gestational sac seen
Management:
o Uterine Suction curettage: as soon as possible to avoid risk of choriocarcinoma
development; pts followed weekly until B-HCG levels fall to an undetectable
level
o If METs: chemotherapy which destroys trophoblastic tissue. Suspect if B-HCG
rises or plateaus after tx, continue hemorrhage after tx, vaginal tumor or pelvic
mass presence
2) Invasive mole
o Same histopathologic characteristics of a hydatidiform mole, but invasion of the
myometrium with necrosis and hemorrhage occurs or pulmonary METs are
present
3) Choriocarcinoma

Have sheets of trophoblasts and hemorrhage. Aneuploid and can be


heterozygous.
o METs to lungs MC, lower genital tract (purple black nodules), pelvic mass
o Preceded by:
o 50% hydatidiform mole
o 25% abortion
o 3% ectopic pregnancy
o 22% full term pregnancy
4) Placental Site Trophoblastic Tumor
o Intermediate trophoblasts are found infiltrating the myometrium w/o causing
tissue destruction
o Contain human placental lactogen (hPL)
o Have persistent low levels of serum HCG (100-1000)
o Treatment is: hysterectomy w/ ovarian conservation
o

21) Ectopic Pregnancy


Definition: implantation of fertilized ovum outside of the uterine cavity
o MC in fallopian tube esp ampulla (98.3%), abdomen (1.4%), ovarian/cervix
(0.15%)
Risk Factors:
o High: PID, previous ectopic, h/o tubal ligation, endometriosis, IUD use, assisted
reproduction
o Middle risk: infertility, h/o genital infections, multiple partners
Clinical Manifestations:
o Triad: unilateral pelvic/abdominal pain, vaginal bleeding, amenorrhea
(pregnancy)
This triad also seen w/ threatened abortion which is MC than ectopic
o If ruptured or rupturing Ectopic:
Severe abdominal pain, dizziness, N/V, syncope, signs of shock (from
hemorrhage).
o Atypical: vague symptoms, menstrual irregularities
Physical Exam:
o Cervical motion tenderness, adnexal mass
o Possible mild uterine enlargement
Diagnosis:
o Serial Quantitative B-HCG: should double q24-48h
In ectopic, fails to double (rises <66% expected, decreases or plateaus)
If initial value <1500, repeat q2-3 days
o Transvaginal Ultrasound: presence (or absence) of pregnancy w/in or outside
uterus
Absence of gestational sac w/ levels B-HCG> 2,000 strongly suggest
ectopic or nonviable IUP
o Culdocentesis: nonclotted blood present
o Laparoscopy: may be used if unstable or ruptured
Management:
o Unruptured/stable:
Methotrexate: destroys trophoblastic tissue (disrupts cell multiplication)

Multiple dose: methotrexate + leucovorin x 4 doses (B-HCG


monitoring day 0 then odd numbered days. Successful if B-HCG
drops 15% between 2 successive draws)
Single dose or double dose: monitor B-HCG on days 0, 4, 7
should drop 15% by day 4-7
Indications: hemodynamically stable pts, early gestation <4cm,
B-HCG < 5,000
Contraindication: ruptured ectoic or h/o TB, B-HCG>5,000,
+fetal heart activity
RhoGAM if mother is Rh negative. Use contraception for at least
2 months

Ruptured:
Laparoscopic salpingostomy (surgical incision into a fallopian tube): 1 st
choice
May need to do reparative procedure to save reproductive organs
OR Salpingectomy (removal of fallopian tube)
Give RhoGAM if mother Rh-

You might also like