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OB/GYN: Shelf Review Notes

Table of Contents

Obstetrics.......................................................................................................................................................................................................2
Normal pregnancy / Prenatal care............................................................................................................................................................2
Early Pregnancy Complications..................................................................................................................................................................4
Prenatal Screening...........................................................................................................................................................................................5
Normal L&D........................................................................................................................................................................................................7
Antepartum Hemorrhage..............................................................................................................................................................................9
L&D Complications........................................................................................................................................................................................10
Fetal complications of pregnancy...........................................................................................................................................................11
Hypertension & Pregnancy........................................................................................................................................................................13
Diabetes in pregnancy.................................................................................................................................................................................14
Infectious Diseases in Pregnancy............................................................................................................................................................15
Infections that can affect the fetus (TORCH, etc)........................................................................................................................16
Other Medical Complications of Pregnancy........................................................................................................................................17
Postpartum care / complications............................................................................................................................................................19

Gynecology................................................................................................................................................................................................21
Benign Lower Genital Tract Disorders..................................................................................................................................................21
Benign Upper Genital Tract Disorders..................................................................................................................................................23
Endometriosis / Adenomyosis.................................................................................................................................................................24
Lower reproductive tract infections......................................................................................................................................................25
Upper reproductive tract infections.......................................................................................................................................................27
Pelvic organ prolapse...................................................................................................................................................................................28
Urinary Incontinence...................................................................................................................................................................................29
Puberty...............................................................................................................................................................................................................30
Menopause.......................................................................................................................................................................................................30
Amenorrhea.....................................................................................................................................................................................................31
Menstrual cycle abnormalities.................................................................................................................................................................32
Hirsutism & Virilization..............................................................................................................................................................................33
Contraception / Sterilization....................................................................................................................................................................34
Elective Termination of Pregnancy........................................................................................................................................................35
Infertility and Assisted Reproductive Technologies........................................................................................................................36
Vulvar / Vaginal Neoplasia........................................................................................................................................................................38
Cervical Neoplasia / Cancer.......................................................................................................................................................................39
Endometrial Cancer......................................................................................................................................................................................40
Ovarian Tumors..............................................................................................................................................................................................41
Gestational Trophoblastic Disease..........................................................................................................................................................43
Breast Disease & Breast Cancer...............................................................................................................................................................45
Benign breast disease............................................................................................................................................................................45
Malignant breast disease:.....................................................................................................................................................................46
Other random stuff........................................................................................................................................................................................47

Obstetrics
Normal pregnancy / Prenatal care

Urine preg test: positive around time of missed cycle.


Gestational sac on transvag U/S @ b-hCG of 1500-2000 (5wks)
Fetal heart @ b-hCG of 5-6000 (6wks)
TPAL: remember abortus = < 20 wk losses (TAB/SAB/ectopic)

Dates & stuff


0-8wks = embryo, 8wks-birth = fetus.
0 to 12-14 wks = 1st tri, 12-14 to 24-28 = 2nd tri, > 24-28 wks = 3rd tri.
Viability @ 24 wks or greater, Term @ 37 to 42 wks, Postterm @ > 42 wks
Date with U/S; take LMP if within 1 wk in 1st tri, 2 wks in 2nd, 3 wks in 3rd. Early = more accurate
Do fundal ht > 20 wks, Doppler for fetal heart beat after 10-14 wks
Should feel quickening ~ 16-20 wks
Physiology of pregnancy:
CV:
CO increases 30-50%, most in 1st trimester, SV first, then HR.
SVR decreases (BP falls) 2/2 progesterone, nadir @ wk 24 (then volume increases catch up)
Pulm: Tidal volume increases (bigger breaths, horizontal expansion), TLC decreases (diaphragm
elevated), respiratory rate stays the same, but minute ventilation increases (2/2 tidal volume increase),
so PaO2 increases, PaCO2 decreases (30 mm @ 20 wks), helping baby get oxygen
GI:
N/V in first trimester, should resolve by 14-16 wks, otherwise consider hyperemesis gravidarum
(lose > 5% wt, go into ketosis), encourage frequent snacking.
Prolonged gastric emptying / GES tone lowered 2/2 progseterone = reflux
Decreased motility in large bowel = more water absorbed = constipation
Renal:
kidneys bigger, ureters dilate pyelonephritis
GFR increases (50%) early, 2/2 increased plasma volume, so BUN and Cr drop
Heme:
Plasma volume increases 50% , RBC mass increases 20-30%, dilutional anemia
WBC increases to ~10.5, plts only drop a little (should be > 100)
Hypercoagulable state (more factors VII-X, fibrinogen) although INR/PTT stay the same
Decreased oncotic pressure! Tocolysis with terbutaline can cause pulmonary edema (already
prediposed from decreased oncotic pressure)
Endocrine: lots of estrogen from adrenal precursors converted in placenta.
hCG, LH, FSH, TSH all have same alpha subunit. hCG maintaisn corpus luteum in early pregnancy.
hPL ensures nutrient supply, diabetogenic
PRL increased during pregnancy
TBG increased by estrogen, so total T3/T4 increase but fT4 stays the same

Glucosuria is common in pregnancy!

Nutritional stuff
Folate stuff:
4mg/day folate if previous hx NTD, on carbamazepine or valproate, or pregestational DM
Otherwise 0.4-0.8 mg/day for all other women of reproductive potential
Weight gain in pregnancy: dont ever want to lose weight, just gain less if overwt.
Underweight (BMI < 18.5)

28-40 lbs.
Normal wt (BMI 18.5-24.9)
25-35 lbs.
Overweight (BMI 25-30)

15-20 lbs
Obese (BMI > 30)

11-20 lbs
Add 300kcal/day in pregnancy, 500kcal/day in breastfeeding.
Antenatal screening:
First trimester (NT/ nasal bone on U/S and PAPP-A/free b-hCG bloodwork) @ 11-13 wks
Can do CVS around 9-12 wks if concerns, > 1:200 risk miscarriage
Quad screen (MSAFP, b-hCG, estriol, inhibin A) @ 18-20 wks
Can do amnio after ~ 15wks if concerns, 1:200ish risk miscarriage
Anatomy screening U/S @ 18-20 wks also.
Glucose loading test @ 27-29 wks (earlier if multiples / hx).
GLT: 50g challenge, check in 1 hr, if 140 or more, go to OGTT
OGTT: 100g challenge, measure fasting and at 1,2,3h. Should be less than 95/180/155/140.
6wk PP: 75g challenge, measure in 2 hrs.
BPP: 0 or 2 scoring for AFI, fetal tone, fetal activity, breathing movements, NST
U/S with cord doppler if worried for placental insufficiency (decrease / reversal of flow)
NST: in 20 min, need 2 accels that are 15 bpm above baseline x 15 seconds
U/S if worrisome.
Contraction stress test: get 3 ctx in 10m, analyse FHR
Fetal lung maturity:
L/S ratio > 2 = RDS is rare
also use phosphatidylglycerol, saturated phosphatydal choline, surfactant / albumin ratio, lamellar body ct
Routine pregnancy problems
Lower back pain stretching, gentle excercise, Tylenol, massage, heating pads
Constipation drink water, colace. Avoid laxatives in 3rd tri (increased PTL?)
Contractions if braxton-hicks, drink lots of water (vasopression oxytocin receptors), reassure.
If q10m or less, think PTL & bring in to check cervix. If no change, reassuring.
Edema (compressed IVC) elevate legs, sleep on side if helps, worry for PEC if hands/face
GERD many small meals, start antacids, dont lay down right after eating. H2 blockers / PPI if persists.
Hemorrhoids: 2/2 IVC compression topical anesthetics, steroids, prevent constipation
Pica tell pt to stop, get good nutrition instead. If toxic substance, call poison control or toxicology
consult
Round ligament pain: late in 2nd tri / early in 3rd, adnexa / lower abdomen / shoots to labia. Warm
compresses or acetaminophen.

Urinary frequency: check urine, keep up PO hydration


Varicose veins (LE or vulva) elevate, use compression stockings.

Early Pregnancy Complications


Ectopic:
Unilateral pelvic / lower abd pain, vaginal bleeding, SGA uterus. If ruptured, can see peritoneal signs
Get transvag U/S & bHCG: IUP can be seen on transvag u/s with bHCG of 2000 or so
if less and no IUP seen and patient stable, repeat bHCG in 48 hrs (should double, but wont if
ectopic 2/2 poorly implanted placenta)
If not stable / peritoneal signs of rupture, stabilize (ABC / fluids / blood products / pressors if
needed), then do laparoscopy if stabilized, laparotomy if crashing.
Methotrexate criteria:
hemodynamic stability, nonruptured ectopic pregnancy,
size of ectopic mass <4 cm without a fetal heart rate or <3.5 cm in the presence of a fetal heart rate,
normal liver enzymes and renal function, normal white cell count, and
the ability of the patient to follow up rapidly (reliable transportation, etc.,) if her condition changes
F/u with bHCG (should be 10-15% drop after 4-7d after treatment), if not, 2nd dose MTX
SAB: before 20 wks (later = stillbirth)
Complete if all POC out before 20wks, Incomplete if some but not all POC out by 20 wks, Inevitable if no
POC but VB/ cervical dilation, Threatened if any VB before 20 wks w/o POC expulsion or cervical diation,
Missed if embryo/fetus dies < 20 wks with retention of all POC.
1st trimester: think chromosomes.
Stabilize pt if hypotensive, then check cervix / get bHCG quant, CBC, type & screen, U/S, r/o ectopic
If complete, can follow (if no signs of infection), send tissue to path
If incomplete, inevitable, or missed can finish on own, or do D&C, or give misoprostol
(prostaglandin) to induce cervical dilation / ctx.
If threatened, follow up as o/p, pelvic rest.
If Rh negative, get RhoGAM
2nd trimester: think infection, maternal dz, trauma, cervical defects like insufficiency (late 2nd tri)
If incomplete / missed, can finish on own, induce with high dose oxytocin / prostaglandins, or
go to D&E (need to use laminaria first)
Need to r/o PTL (painful ctx cervical change) / incompetent cervix (painless cervical change)

incompetent cervix: 2/2 surgery, trauma, ?DES, or idiopathic. Can do cerclage, both if hx
in previous pregnancy or in emergency. If elective, place at 14 wks (2/2 chance of 1st
trimester sab). Consider betamethasone / tocolysis if close to 24 wks.
Habitual aborters (3+ consecutive SABs)
W/U:

HSG for maternal anatomy,

karyotypes for translocations (parents / POC),

screen for hypothyroidism / DM / hypercoagulability (Factor V Leiden / prothrombin


G20210A, antiphospholipid ab, Protein C/S),

r/o infection (cx cervix, vagina, endometrium)


Antiphospholipid antibodies

Consider if hx DVT, prolonged DRVVT, anticardiolipin abs, recurrent first trimester losses.

Rx heparin & aspirin


Luteal phase defect (?) controversial, ?not enough progesterone

get luteal phase serum progesterone and/or endometrial bx in luteal phase to look for
proliferative endometrium).
Factor V Leiden: consider if late fetal demise (late 3rd trimester), with head > abdominal, fetal,
humerus lengths, pt with hx of DVT in the past
Tx: may need IVF (translocations, etc), surgery for anomalies, heparin / aspirin, maternal tx
Septic abortion - miscarriage with fever, uterine tenderness, etc.
Need uterine evacuation and broad spectrum abx

Prenatal Screening
Remember PPV = % pts with positive screen that are affected; NPV = % pts with negative screen not affected, +LR
and -LR tell you how to adjust pretest odds to get posttest odds
Remember, for an autosomal recessive disease, the sibling of an affect pt has a chance of being a carrier.
Example: Dads brother has sickle cell disease. Neither parent has been checked. Dad has chance of
being a carrier; Mom has 1/12 (population risk), so risk for affected child is (1/2) x (1/12) x (1/2) x (2/3)
Also remember Hardy-Weinberg: p2 + 2pq + q2 = 1 @ equilibrium where p, q = allele frequencies, p2 / q2 =
homozygotes, 2pq = heterozygotes
Cystic fibrosis: Aut-rec, CFTR gene, chloride channel, commonly deltaF508 / G542x but 1000+ mutations known
sx: lung / cor pulmonale / pancreatic insufficiency / infertility
1/29 Caucasians are carriers; screen parents, then with CVS / amnio if both parents carriers (1/4 risk)
Sickle-Cell: Aut rec, vaso-occlusive crises, hemolytic anemia
Screen mom with hemoglobin electophoresis, then dad if patient carries HBs
Carrier frequency: 1/12 in African Americans
Tay-Sachs: aut rec, hexosamindase A deficiency GM2 gangliosides build up.
Carrier freq: 1/27 in Ashkenazi Jews, also eastern Europeans
3-10mo after birth: hyperacusis, loss of alertness, myoclonic / akenitic seizures, cherry red spot in macula.
Gray matter lysosomal storage disease.
Thalassemias: hemolytic anemia, RBC destroyed in bone marrow / liver / spleen
Beta-thal: AR, in Mediterranean descent (also Asia / Africa). Too few beta chains usually presents
postnatally (when beta normally replaces gamma). Screen with CBC (mild hemolytic anemia with low
MCV), then get Hb electrophoresis (shows more alpha than beta Hgb A2).
Alpha-thal: AR, too few alpha chains. 4 alpha genes, 2/4 mutations can be cis (Asians) or trans (Africans).
If both parents have cis mutations = 25% infants will get severe form; trans = usually will become carrier.
4 genes: fetal hydrops, incompatible with life, splenomegaly, etc. Hb electrophoresis shows no
HbF, no HbA, lots of Hb Barts (4 gammas)
3 genes: HbH disease beta chains build up, oxidative damage destruction, Hb electrophoresis
shows Hb barts & HbH (beta tetramers), barts goes away as gamma chains replaced.
2 genes: trait. Mild phenotype, microcytic anemia.
Screen with CBC, then Hb electrophoresis.

Chromosomal abnormalities
Quad screen: first thing to do = verify the dates & r/o multiple gestation!!
MSAFP

Estriol

B-hCG

Inhibin-A

Trisomy 21

Low

Low

High

High

Trisomy 18

Low

Low

Low

normal

Trisomy 13

depends on defects

depends on defects

depends on defects

depends on defects

NTD

High

Down syndrome: flattened nasal bridge, small size, cup-shaped ear, sandal-gap toes, hypotonia, simian
crease, epicanthic fold, oblique palpebral fissures, protruding tongue, short, broad hands.
Higher rates of stillbirth, miscarriage. IQ 40-90. A/w duodenal atresia, cardiac defects, short
limbs, nasal bone hypoplasia.
echogenic intracardiac focus only has LR of 2.0, so at most doubles pretest odds.
Trisomy 18 = Edward: Clenched fists, overlapping digits, rocker bottom feet, VSD / tetFal, omphalocele,
CDH, NTD, choroid plexus cysts. Fetal / neonatal death.
Trisomy 13 = Patau. holoProsencephaly, cleft lip and Palate, cystic hydroma, single nostril, omphalocele,
hypoPlastic left heart, clubfoot / hand, Polydactyly, overlapping fingers.
Turner syndrome = XO: wide-spaced nipples, shield-like chest, lymphedema, primary amenorrhea,
coarctation of aorta, short 4th metacarpal, receding hairline
Klinefelter syndrome = 47,XXY. small, firm testes, hyalinized seminiferous tubules, infertility,
gynecomastia, MR, elevated gonadotropin levels.

Congenital anomalies:
Organogenesis: wks 3-8 after conception (wks 5-10 EGA). Insult before = probably will lose pregnancy.
Radiation during weeks 8-15 has greatest risk of fetal microcephaly / severe MR
Neural tube defects: defective closure by 4 wks after conception (6 wks EGA). Need folic acid before!
Spina bifida, anencephaly, etc. Elevated AFP
Spina bifida: see lemon sign (concave frontal bones), banana sign (curved cerebellum) on U/S.
Cardiac defects: follow with fetal echo, get peds cards on board. Week 3 (wk 5 EGA) is key time.
VSD: failure of ventricular walls to form
TetFal: overriding aorta, pulmonary stenosis, RV hypertrophy, VSD
Transposition of the great arteries (PA/ Ao into wrong vent)
Coarctation of the aorta: generally preductal if congenital
PDA Eisenmenger syndrome
Hypoplastic left heart: worst outcome with surgery.
Potter sequence: renal failure anhydramnios pulmonary hypoplasia / contractures.
From bilateral renal agenesis, but also if posterior urethral valves / extrophy with obstruction / etc.
Embryology:

Pronephros degenerates.

Mesonephros (Wolffian duct) gives off [ureteric bud urinary collecting system
(tubules, calyces, renal pelvis, ureter)], then degenerates in females, turns into vas /
epidydimis / ejaculatory duct / seminal vesicles if T around in guys.

Metanephros kidney

Paramesonephric duct (Mullerian) Fallopian tubes, uterus, cervix, upper 1/3 of vagina
Fetal anemia: If Rh isoimmunization, hydrops, other concerns for anemia, get PUBS (can get Hct /
transfuse too if needed!)

Normal L&D
Report to the hospital for suspected labor if any of these:
contractions every five minutes for one hour
rupture of membranes
fetal movement less than 10 per two hours
vaginal bleeding.
Breech presentation a/w prematurity, multiples, genetic disorders, polyhydramnios, hydrocephaly, anencephaly,
uterine abnormalities, uterine fibroids. ?oligohydramnios (Williams says it is, uWise says it isnt)
Normal ROM: < 1h prior to onset of labor (>1h = PROM, >18h = prolonged PROM, if < 37wks = PPROM)
Pool, nitrazine (amniotic fluid = alkaline), ferning tests to r/o ROM. Cervical mucus = false + fern
Oligohydramnios in absence of other findings may suggest ROM too.
If really need dx, can inject indigo carmine into amniotic sac look for blue staining of tampon
Bishop score: measure cervical dilation, effacement, station (0-3) and consistency, position (0-2).
Bishop > 8 = favorable for spontaneous labor / induced labor.
0

Position

Posterior

Intermediate

Anterior

Consistency

Firm

Intermediate

Soft

Effacement

0-30%

31-50%

51-80%

>80%

Dilation

0 cm

12 cm

34 cm

>5 cm

Fetal station

-3

-2

-1, 0

+1, +2

Induction / augmentation of labor


Induce with prostagladins, oxytocin, mechanical dilation (Foley bulb), AROM
Indications: postterm, PEC, PROM, nonreassuring fetal testing, IUGR, not pt desire (would be an elective
induction). Dont induce if many prior C/S or nonreassuring settings
Follow with Bishop score favorable. If not progressing, try prostagladin E2 or PGE1M (misoprostol)
to ripen the cervix, or mechanical dilation.
Specific drugs / methods
Prostagladins: cant use if maternal asthma or glaucoma
Pitocin: give it IV.
Amniotomy
Mechanical dilation (30 or 60 cc Foley, dilate over 4-6h)

Augment with oxytocin or amniotomy


Monitor with external monitoring or IUPC, which lets you figure out adequacy of ctx
Uterine perforation in IUPC placement: big gush of amniotic fluid and blood = suspect uterine
perf. Withdraw IUPC, monitor fetus, replace IUPC if the tracing is reassuring.
Montevideo unit: 10m, multiply avg variation of intrauterine pressure from baseline x # ctx
> 200 MVU is generally considered adequate ctx.
Fetal monitoring: external or FSE (but not if fetal thrombocytopenia bleed or HIV/HCV transmission)
Baseline 110-160 with moderate variability, +accels = good!
Decels
Early = increased vagal tone (head compression in ctx)
Variable = umbilical cord compression. Repetitive if cord trapped under shoulder, around neck
Late = uteroplacental insufficiency, worrisome!! Can degrade into bradycardia with stronger ctx
Bradycardia (<110 x 2min = prolonged decel; x 10min = bradycardia):
Face mask, roll onto (L) side, d/c pit, consider terbutaline, check cervix
If cord prolapsed, push it back up to OR
C/S if not getting better.
Cardinal movements: engagement, flexion, descent, internal rotation, extension, external rotation (restitution),
anterior shoulder, posterior shoulder. OA is good
Stages of labor:
Stage 1: onset of labor complete cervical dilation (10-12h if nullip, 6-8 if multip, but big ranges)
Latent phase: onset 3-4 cm, slow change
Active phase: 3-4cm full dilation, fast.

Should have at least 1 cm / hr if nullip, 1.2cm / hr if multip (but usually 2-3 cm/hr)
If below these guidelines, calculate MVU

Active phase arrest if no change in dilation or station x 2h with >200 MVU ctx
Stage 2: complete dilation baby time
Can last 1h if multip, 2h if nullip, and you get a bonus hour if you get an epidural
Lac repair: first degree = superficial, 2nd degree = into perineum, 3rd degree = into sphincter, 4th
degree = into rectum.
Stage 3: baby time placenta time
Retained placenta if > 30m; need to extract manually or curretage if fails (may be 2/2 accreta!)
Stage 4 is technically the name of the immediate postpartum period (not the recovery period)
SVD procedures
Operative vaginal delivery: need complete cervical dilation, head engagement vtx presentation, clinical
assessment of fetal size / maternal pelvis, known position of fetal head, adequate maternal pain control,
and ROM - then can use vacuum / forceps if 2nd stage lasting too long.
If baby needs to come out (e.g. FHR dropping), do operative delivery if crowning / really far down.
Pudendal block if no epidural in place
Episiotomy: midline has easier repair, less pain, less blood loss but more 3rd/4th degree tears than
mediolateral (and for spontaneous delivery without episiotomy!)
No role for routine episiotomy / prophylactic these days.
May use to enlarge vaginal outlet if instruments needed, or if descent arrests

C/Section:
Indications: breech, transverse, shoulder presentations; placenta previa / abruption, fetal intolerance of
labor, nonreassuring fetal status, cord prolapse, prolonged 2nd stage, failed operative vaginal delivery,
active herpes lesions, HIV with VL > 1000, etc. Also multiple prior C/S.
TOLAC: need to have < 1-2 previous C/S, low transverse or low vertical incision without extension into
cervix or upper uterine segment. rupture (pop, decrease in IUPC pressure, FHR decels / brady, abd pain)
to OR immediately!

Antepartum Hemorrhage
DDx: Placenta previa, accreta/increta/percreta, placental abruption, vasa previa / fetal cord rupture
Previa: classically painless vaginal sentinel bleed after 28 wks (3rd trim), but nowadays mostly dx on u/s
Placenta often will move up (repeat u/s in 3rd trimester as lower uterine segment develops)
More common in multiple gestations, hx previa, uterine scars
Vaginal exam contraindicated!
In pregnant pt with 3rd trimester vaginal bleeding, r/o with u/s before digitalizing.
Tx: varies generally pelvic rest, esp after sentinel bleed; hospitalize if Hct drops 3pts, etc.
immediate C/S if unstoppable labor, fetal distress, life-threatening hemorrhage. Stabilize, ABCs,
type & cross, 2x large bore IVs, then kleihauer-Betke RhoGAM
If make it to 36 wks, often will amnio for fetal lung maturity C/S between 36-37 wks
Accreta: usually asymptomatic. Consider if previous C/s and low lying anterior placenta, for instance. Big
problem!
Accreta = abnormal attachment into endometrium; increta = into myometrium, percreta = through to
serosa
Abruption: can be concealed or revealed / external;
classic hx painful 3rd trim vaginal bleeding a/w strong abdominal pain and/or frequent, strong ctx. 30%
are asx, however. Often have firm, tender uterus on exam. If abrupting during C/S, see Couvalaire
uterus (if bleeding dissecting into myometrium, uterus is blue/mottled)
U/S not great for dx: only 2% have retroplacental clot, but usually use U/S to R/O previa
Tx: stabilize, type & cross, 2 large bore IVs, etc.
Uterine rupture: rare. Sudden intense abd pain, vaginal bleeding, nonreassuring fetal testing, FHT disappear,
placental part regresses, IUPC low pressure. Immediate laparotomy & delivery of fetus, then repair!
Fetal cord rupture
Velamentous cord insertion: insert between amnion / chorion away from placenta; vulnerable to
rupture. Vasa previa if cross over the internal os (can tear during delivery or ROM)
Succinuriate placenta (extra lobe with vessels going between the lobes) - also can have vasa previa /
rupture from unprotected cords
Often p/w rupture vaginal bleeding, sinusoidal FHR (anemic).

Can dx a fetal source of blood with Apt test (dilute blood, add 1% NaOH, pink = fetal, yellow/brown =
maternal) or microscopy nucleated fetal RBCs.
Tx: emergent C/S (fetus doesnt have much blood to lose!)

L&D Complications
Preterm labor: labor before 37 wks; preterm ctx / pain (vs cervical insufficiency).
High risk of small baby (IUGR, SGA = small for gestational age, whereas LBW = < 2500 g)
A/w PROM, chorio, multiple gestations, uterine anomalies, previous preterm delivery, small mom,
abruption, PEC / maternal infection, surgery, low SES
Preterm labor and a fever- need to do amniocentesis to rule out chorio before giving steroids for lung
maturity
Preterm contractions: dont do tocolysis unless theres cervical change (no labor unless the cervix is
changing). Instead, observe.
Tocolysis: Trying to buy yourself 48h for betamethasone if < 34 wks for lung maturity.
Class

Examples

Side effects / Contraindications

Notes

Beta-mimetics

Ritodrine*
Terbutaline

Tachycardia, H/A, anxiety


Pulmonary edema
Contraindicated in diabetes

increases ATP cAMP


Ritodrine = continuous IV
Terb = load, then q3-4h

Flushing, H/A, fatigue, diplopia


Lose DTRs (<10), respiratory depression,
hypoxia cardiac arrest (>15)
Contraindicated in myasthenia gravis

No evidence that it
actually delays anything
Ca+ antagonist

Mag sulfate

Ca-channel
blockers
Prostaglandin
inhibitors

Nifedipine

H/A, flushing, dizziness

Indomethacin

Dont use close to term (PDA closure)


Also pulm HTN, oligo 2/2 renal failure,
increased risk necrotizing enterocolitis &
intraventricular hemorrhage

NSAIDs - block COX

* ritodrine (beta-mimetic) is only FDA approved tocolytic


Betamethasone: in addition to RDS prevention, also associated with decreased intracerebral hemorrhage and
necrotizing enterocolitis in the newborn. It has not been associated with increased infection or enhanced growth.
PROM, PPROM, etc: >1h prior to labor = PROM, >18h = prolonged PROM, if < 37wks = PPROM
PROM: biggest risk is for chorio; increased > 18h; give abx ppx if expecting prolonged ROM
Often induce if > 34-36 wks
PPROM: PROM < 37 wks EGA. gush of fluid; dx with pool / fern / nitrazine tampon test if unsure
Risk of chorio starts to outweigh risk of lung immaturity between 32-36 wks; management varies
Management:

Antibiotics can prolong latency up to 5-7 days, so give ampicillin +/- erythromycin
Tocolysis - consider if < 34 wks (controversial in pprom esp without ptl)
Corticosteroids - consider if prior to 32 weeks usually
If at 36 weeks or so, just induce

Malpresentation:
CPD and even macrosomia can try TOL but if failure to progress C/S!
Breech: frank = feet up by head, complete = feet indian style, footling = one foot extended.
Dx by U/S, Leopolds, etc.
Can try ECV after 36-37 wks (spontaneous version would happen before); if fails, may retry @
39wks under epidural anesthesia
Trial of breech vaginal delivery - not so much in the USA. Definitely cant try if nullip, incomplete
breech, EFW > 3,800
C/S is prettty much what happens.
VTX malpresentation
Face: if mentum anterior, may be able to do vaginal delivery; o/w must rotate, careful with
augmentation (pressure edema)
Brow: unless preterm & really small head, must convert to vtx or face to deliver
Shoulder: unless conversion, go for C/S (high risk cord prolapse, rupture, difficult delivery)
Compound:(extremity along with vtx or breech): cord prolapse risk! Can try to reduce, but careful
Persistent LOT / ROT or OP - may need operative vaginal delivery or manual rotation
Shoulder dystocia:
risk increases with fetal macrosomia, cDM/gDM, previous shoulder, obesity, postterm, prolonged 2nd stage
complications: Erb palsy / brachial plexus injury, humerus / clavicle fx, phrenic nerve palsy, hypoxic brain
injury, death.
Dx: turtle sign after prolonged crowning of head
Management: McRoberts / suprapubic pressure, call peds, Rubin (push shoulder across fetal chest),
Woods corckscrew (sweep behind post shoulder rotate, dislodge ant shoulder), deliver posterior arm
/ shoulder.
If that fails, then crazy stuff considered: break fetal clavicle, symphysiotomy, or Zavanelli (shove babys
head back inside & head for the OR!)
Maternal hypotension ddx: vasovagal, regional anesthesia, overtx with antiHTN drugs, hemorrhage, anaphylaxis,
amniotic fluid embolism (high mortality, find fetal cells in pulmonary vasculature at autopsy)
Seizures on L&D: ABCs, assess FHR, then Mag Sulfate bolus lorazepam phenytoin phenobarb

Fetal complications of pregnancy


Growth disorders: if fundal ht differs by 3cm or more, get an U/S
SGA < 10th %ile. Symmetric = think early insult; asymmetric = think later, skull > rest of body
Decreased growth potential (trisomies, Turner, OI, achondroplasia, NTDs, anencephaly, or
intrauterine infections like CMV / rubella, or teratogens like chemo)

IUGR: generally asymmetric (not enough nutrients getting across), a/w smoking
antiphospholipid Ab, SLE, malnutrition, severe chronic renal dz, HTN, anemia in mom, or
placental insufficiency (previa / marginal insertion / thrombosis +/- infarction), or multiples

Check cord doppler to see how placentas doing.


Twin-twin transfusion should be suspected if one big, one small twin.
Generally watch with fetal testing (NST/OCT, BPP, and/or umbilical doppler)
LGA > 90th %ile
Macrosomia = birth wt > 4,500g officially, but some use other definitions - e.g. to offer C/S if
3500g in diabetic mom, or 4000g otherwise

Big risk shoulder dystocia, brachial plexus injuries, low Apgars, hypoglycemia,
polycythemia, hypoCa, jaundice; also childhood leukemia, Wilms tumor, osteosarcoma

A/w maternal obesity, gDM or cDM, postterm, multiparity, AMA

Amniotic fluid disorders:


Max volume 800mL @ 28wks, then falls to 400mL by 40wks.
AFI normal range: 5 to 20-25 (varies by EGA)
Oligohydramnios: AFI < 5.
See nonreactive NST, FHR decels, meconium. can lead to cord compression!
Etiology: not making (GU disorders: renal agenesis, polycystic kidney, obstruction; also chronic
uteroplacental insufficiency) or losing too much (ROM) amniotic fluid.
Management: check BPP, cord doppler, U/S for anomalies. Induce if ROM at term. Can do
amnioinfusion to decrease # of variable decels / dilute meconium
Polyhydramnios: AFI > 20-25. Not as worrisome.
Etiology: not swallowing (GI tract abnormality, duodenal atresia), or making too much (infants of
diabetic mothers osmotic diuretic; or high-output cardiac failure / TTTS)
Risk of cord prolapse: only AROM if sure that head is engaged; check for cord after SROM
Rh incompatibility: all this applies to Rh negative moms only
RhoGAM (anti-D IgG) at 28 wks, postpartum if neonate is Rh positive, and any time theres bleeding!
0.3mg = 1 dose = eradicates 15 mL fetal RBCs. Good enough for normal delivery
Can do Kleihauer-Betke to quantify if abruption, antepartum bleeding
If already sensitized, follow with middle cerebral artery dopplers (faster = more anemic);
(spectrophotometer is another way, older); can do PUBS / in utero transfusion if really anemic
Hydrops = erythroblastosis fetalis. Heart failure, diffuse edema, fluid in 2+ compartments (ascites /
pleural / pericardial effusions), all 2/2 anemia. Jaundice / neurotoxic effects of bilirubin too, but only
after delivery (placenta clears it during pregnancy)
Other causes of hydrops: manage all with antibody titers, amnio, MCA doppler, PUBS / transfusion
Kelly kills, Duffy dies = cause hydrops.
Lewis lives = cause mild hemolytic anemia. ABO causes mild hemolysis too.
Fetal demise: if no explanation, usually attributed to a cord accident
Dx: lack of uterine growth, falling hCG, U/S (<20wks) or lack of fetal movement (> 20 wks)
If > 3-4 wks, can lead to hypofibrinogenemia 2/2 release of thromboplastic substance from decomposing
fetus, and even to DIC! so get a fibrinogen level!

Fetal demise & multiples: if one baby dies in utero, check fibrinogen level qweek / biweekly, esp if
unusual bleeding (fibrinogen may decrease coagulopathy!)
Spalding sign - overlapping of fetal skull bones suggesting fetal demise
Tx: D&E if early, or induction of labor (prostaglandins / high dose oxytocin) if late.
Test for TORCH, fetal karyotype, screen for collagen vascular dz / coagulopathies, get fetal autopsy

Postterm pregnancy: > 42 wks. Get a nst at 40 and 41 weeks - don't just send home!
Higher risk to mom & baby (macrosomia, oligo, meconium aspiration, intrauterine demise, dysmaturity
syndrome - look like old man!)
#1 cause is inaccurate dating.
Manage with more frequent visits, fetal testing (NST in wk 40, BPP & NST in 2 visits in wk 41).
Induce if nonreassuring testing or electively if Bishop > 6 wks 40-41; or no matter what > 42
Multiples: higher risk preterm delivery, congenital abnormalities, SGA, malpresentation.
Twins: usually wks 36-37, triplets: usually wks 33-34. Push up testing too!
Twin delivery: Can do TOL if vtx/vtx or vtx/breech if twins concordant / presenting twin is
larger & vtx (grab smaller second twin & pull out breech!)
Triplet delivery: only if vtx/vtx/vtx (rare), usually C/S. Also C/S for more than 3.
Dizygotic twins: 2 ova, 2 sperm. increased FSH can be hereditary, so dizygotic twins can be too
Monozygotic twins: division of fertilized egg.
DiDi if divides on days 1-3, MoDi if 4-8, MoMo if 8-13, conjoined if 13-15
All dizygotic twins are DiDi (dichorionic / diamniotic), monozy twins can be whatever
DiDi: best outcomes. See twin peak sign later in pregnancy
MoDi twins: see two amniotic sacs, one chorion early on U/S. Risk TTTS
MoMo: risk conjoinment, fetal death 2/2 cord entanglement, etc.
Can consider selective reduction if triplets or above
Twin-twin transfusion syndrome (TTTS, aka poly-oli sequence)
One small, oligohydramnios, growth restriction, anemia twin (donor), large, plethoric,
hypervolemic, cardiac failure, polyhydramnios polycythemic / hydropic twin (recipient)
Dx with ultrasound, historically managed with serial amnioreduction, but now laser coagulation
of artery by fetal surgeons improves outcomes.

Hypertension & Pregnancy


Chronic HTN: before conception, < 20 wks EGA, or > 6 wks postpartum. Big risk for PEC.
Treat with antiHTN (usually labetalol / nifedipine) meds.
Get baseline ECG / 24h for Cr / protein to help with PEC dx later.
Superimposed PEC: often dxd with >30/15 increase (either or) in BP + 24h urine elevation. Uric acid >
6.0-6.5 also used, more controversial
Gestational HTN: blood pressure > 140/90 x 2 occasions 4-6h apart, seated.
Severe HTN (> 160 systolic or > 105 diastolic) while in hospital: treat
goal DBP 90-100 (prevent stroke / abruption w/o compromising uterine perfusion)
Hydralazine or labetalol are first choices

Mild Preeclampsia
Risk factors: cHTN, renal dz, also nullip, young or old mom, hx PEC with same dad, living with dad < 1yr
BP 140/90 x 2 and proteinuria > 300 mg / 24h (roughly 2+) and nondependent edema (face/hands)
Can get urine protein/Cr ratio, although not official, for spot check
Contraindications to expectant management remote from term (<32 wks): thrombocytopenia (plt <
100,000), inability to control BP with max doses of 2 antiHTN meds, non-reassuring fetal survellance,
LFTs > 2x ULN, eclampsia, persistent CNS sx, oliguria - need to deliver now!
Tx: Mag sulfate during L&D stay, and 12-24h after. Mag levels (mEq/L):
4-7: therapeutic
7-10: lose DTRs
> 12: respiratory depression
>15: cardiac arrest
If overdose, give calcium (CaCl / Ca gluconate) for cardiac protection
Severe PEC:
> 160 systolic or 110 diastolic x 2 occasions 6h apart; proteinuria > 5g/24h
Can have mild PEC by BP / proteinuria but becomes severe if altered consciousness, H/A or visual
changes, epigastric / RUQ pain, impaired liver fxn (2x nL), oliguria (<400mL/24h), pulmonary
edema, thrombocytopenia (<100)
Tx: need to deliver immediately if > 32 wks or mother crashing. If you can wait, try BMZ & check lung
maturity. Delivery is the cure
Eclampsia: see seizures in L&D above.
ABCs, stabilize mom; Mag sulfate lorazepam phenytoin phenobarb; Lower HTN with hydralazine
Deliver only when mom has stopped seizing (best for fetus too)
HELLP syndrome:
Dx: rapidly deteriorating liver fxn (AST/ALT increases), thrombocytopenia < 100, hemolysis
(schistocytes on peripheral smear, elevated LDH, elevated total bili)
Sx:RUQ pain (liver capsule distention), nausea, vomiting can lead to hepatic rupture!
Acute fatty liver of pregnancy (AFLP): vs HELLP, see elevated ammonia, hypoglycemia (glc < 50), reduced
clotting factors (fibrinogen & antithrombin III) in AFLP (fulminant liver failure!)

Diabetes in pregnancy
GDM: related to hPL, diabetogenic hormone
Not a/w congenital anomalies like pregestational DM (shows up in late 2nd / early 3rd trimester)
But do have incr risk neonatal hypoglycemia, hypoCa, hyperbili, polycythemia; risk of maternal T2DM later
Screen between 24-28 wks as described above. 50g 1h GLT 100g 3h OGTT.
White Classification: GDM A1 = diet controlled, A2 = needs meds / insulin.
B-->D-->C for duration. F=neFropathy, R=Retinopathy, H=Heart dz, T=prior renal Transplant
A2 (not A1) pts: NST or mod BPP starting between 32-36 wks; U/S for EFW between 34-37 wks.
Treat with CHO restricted diet, exercise to enhance postprandial blood sugar control (biggest time in
gDM)

Tx if > 90 FBG, > 140 1h postprandial, > 120 2h postprandial.


Insulin (NPH x 2 doses + short-acting humalog/novolog) is conventional optino
Can also use gyburide / metformin (experimental)
Scheduled delivery @ 39 wks if A2 commonly done; put on dextrose / insulin if needed.
If very poor control, may offer delivery between weeks 37-39.
Offer C/S to pts with EFW > 4,000g (incr risk shoulder dystocia)

Pregestational DM
Risk factor for mom: PEC/eclampsia, SAB, infection, polyhydramnios, PP hemorrhage, C/S
Infants of diabetic mothers
Including gestational DM - higher risk for hypoglycemia, respiratory distress, polycythemia,
hyperbili, hypoCa
Pregestational specifically: if really high HbA1c, think congenital defects (cardiac most common;
also renal / NTD / pretty much all systems. Caudal regression syndrome / sacral agenesis
classic 2/2 disproportionally high risk in poorly controlled diabetics, but not as common as others).
Get HbA1c at outset to see status; then follow closely; good control prior to pregnancy key
Also should get 4mg folate daily (higher risk of NTD).
Diet/exercise meds / insulin as needed!
If poor control (T2 or T1): Should get ECG (esp if HTN), HbA1c, optho consult, etc.
If insulin dependent, offer fetal lung maturity @ 37 wks or IOL @ 38-39wks without testing
Type 1 DM : Prepregnancy control key. Pumps are good. Dont mess with insulin regimen until needed.
Type 2 DM: made worse by pregnancy, may go from diet/exercise or oral meds insulin needs (manage as above)
Fetal testing @ 32 wks, earlier if poor control. Weekly NST / modified BPP for AFI.
Get growth U/S @ 32-36 wks

Infectious Diseases in Pregnancy


UTIs:
#1 for cystitis / asymptomatic bacuria is e. coli. Get U/A, Cx & sensitivity; tx with amox, Macrobid, TMPSMX, or cephalexin x 7d and f/u Cx results. Can also give pyridium for dysuria / bladder pain (local
anesthetic; can turn urine bright orange). Get TOC.
Bigger risk of pyelonephritis (fever, CVA tenderness).
Should be hospitalized, get IV fluids, IV abx (cephalosporin or amp+gent) until afebrile & asx x 48h
Total tx: 10-14d of combined abx.
Prophylactic abx if 2 x [cystitis or asx bacituria] or 1 x pyelonephritis
Bacterial vaginosis:
malodorous discharge / irritation, can be asx. Gardnerella, bacteroides, micoplasma (multiple organisms)
Dx with 3 of: thin, white, homogeneous discharge, whiff test with KOH, pH > 4.5, > 20% clue cells.
increases risk for PPROM, so treat with metronidazole (clinda another option) & get TOC in 1 mo
GBS: causes UTIs, chorio, endomyometritis.
Screen at 35-37 wks with rectovag cx.
If positive, get IV PCN G in labor. If unsure, also get PCN G. Amp / cefazolin / clinda are alternatives.

Chorioamnionitis
Sx: maternal fever, elevated WBC in mom, fundal tenderness, fetal tachycardia.
Can be fooled: elevated T from prostaglandins, tachycardia from terbutaline, WBC elevated in
pregnancy & with labor, or with corticosteroids!
Fundal tenderness + PPROM = chorio until proven otherwise
Do amnio, give IV antibiotics, then speed up delivery time!
On amnio, see high IL6 and low glucose. WBC not a good marker.
Induce / augment if mom & fetus stable, C/S if not

Infections that can affect the fetus (TORCH, etc)


HSV:

if lesions present, C/S to prevent maternal transmission (transmitted in birth canal).


Higher transmission rate if primary infection (IgM, no IgG)
If outbreak in pregnancy, give acyclovir PPx from 36 wks until delivery
in neonate, causes lesions, sepsis, PNA, herpes encephalitis devastation. Give IV acyclovir if infected

VZV: 90% adults immune. Cant vaccinate in pregnancy (live vaccine), but can do before / after
Transplacental spread, a/w congenital malformations (congenital varicella syndrome) if early infection,
or postnatal infection (anywhere from benign disseminated & death) if late in preg
Give VZIG to mom within 96h if no hx chickenpox and exposed during pregnancy (lessens her outbreak,
but doesnt decrease risk transmission to fetus)
Give VZIG to infant if mom has outbreak within 5d before - 2d after delivery
Note: maternal zoster not a/w congenital anomalies
Parvovirus B19: causes erythema infectiosum (fifth dz) - mild infection, red macular slapped cheek rash
Outbreaks in elementary schools, etc. Mild in kids / adults usually
In pregnancy: 1st tri a/w miscarriage, 2nd tri a/w fetal hydrops (attacks fetal erythrocytes hemolytic
anemia, hydrops, death)
If suspected exposure, check parvovirus IgM/IgG. If IgM +, think acute infection. If after 20 wks and acute
infection put baby on anemia protocol (serial U/S, MCA dopplers, PUBS / transfuse if hydrops)
CMV: subclinical / mild viral illness in mom, rarely hepatitis / mono-type picture (rarely diagnosed)
In baby: 10% exposed develop CMV inclusion disease (hepatosplenomeg, thrombocytopenia,
jaundice, cerebral calcs, chorioretinitis, interstital pneumonitis, also MR, high mortality,
sensorineural hearing loss). No tx or PPx available.
Rubella: mom gets mild illness, maculopapular rash, arthralgias, diffuse LAD x 2-4 d
Congenital rubella syndrome in baby, esp high transmission in 1st trimester
Deafness, cardiac anomalies, cataracts, MR. blueberry muffin baby.
Dx with IgM titers. No tx available if acquired.
Mom cant get MMR in pregnancy (live vaccine)
HIV: get viral load suppressed with HAART, AZT=ZDV intrapartum and afterwards to baby to decrease trans.
Do a C/S if VL > 1,000; otherwise can have vaginal or C/S.
Should bottle feed

Gonorrhea:
Screen in pregnant women @ prenatal visit, again in 3rd trim if at risk, with NAAT or cx
Treat: IM ceftriaxone, oral cefixime. Also tx with azithromycin / amoxicillin for chlamydia too
Causes PID only in early pregnancy. A/w preterm delivery, PPROM, other infections.
Neonate: mucosal surfaces affected (eyes, oropharynx, external ear, anoretal mucosa). Can also be
disseminated (arthritis, meningitis)
Chlamydia: transmitted in labor. PNA is the big complication. Often asx, so screen as for GC.
Remember, no tetracycline / doxy in pregnancy, so give azithromycin, amox, or erythromycin
HBV: from sex, blood exposure. Transplacental transmission; can lead to fulminant liver failure, etc.
Screen everybody for HBsAg. If positive, give HBIg / HBV vax for baby after delivery.
Syphillis: T. pallidum, transmitted transplacentally; usually primary or secondary syph (need spirochetes)
Vertical trans: intrauterine fetal demise, late abortion, or congenital syndrome (maculopapular rash,
snuffles, hepatosplenomeg, hemolysis, jaundice, LAD). Dx with IgM antitreponemal ab (remember,
IgM dont cross placenta, so if baby has em theyre infected)
PCN is the only treatment - desensitize and treat with PCN if allergic!!
Later manifestations: CN VIII deafness, saber shins, mulberry molar, saddle nose, Hutchinsons teeth.
Toxoplasma gondii: protazoa, generally subclinical unless immunocompromised , may have vague viral illness
Vertical trans is transplacenta, highest if third trimester acquisition. Stay away from cat feces
Neonate: fevers, seizures, chorioretinitis, hepatosplenomegaly, jaundice, hydro / microcephaly.
Dx with IgM in neonate, or DNA PCR via amnio to guide decision to terminate.
Can treat mom with spiramycin (no teratogenic effects known), but doesnt cross placenta no effect on
baby. So use pyrimethamine / sulfadiazine along with folate to prevent bone marrow suppression if
fetal infection has been documented.

Other Medical Complications of Pregnancy


Hyperemesis gravidarum: persisting past wk 16; very common in setting of molar pregnancy (document IUP!)
Maintain FEN/GI status! Can get hypoCl hypoK met acidosis (use NS + D5W). Can use antiemetics safely,
also B12 supplementation. Small frequent meals.
Seizure disorders: Increase in pregnancy. Watch doses (increased GFR faster clearance).
Phenobarb / primidone / phenytoin = folate antagonists NTD risk. Valproic acid NTDs too
Take lots of folate prior to pregnancy, follow AFP, may or may not decide to switch (to single AED, lowest
possible dose) - but seizures are bad for baby too
Maternal cardiac disease: remember, 50% CO increase.
Highest risk with primary pulmonary HTN, Eisenmenger physiology, severe MS / AS, or Marfan
ACEi, coumadin contraindicated in pregnancy, diuretics risky too.
May do assisted vaginal delivery to avoid valsalva - better than C/S results.
Remember big fluid shifts PP (autotransfusion) big demand on heart.
Hx MI: get baseline ECG

Eisenmenger syndrome / pulmHTN


Really bad, up to 50% mortality, especially postpartum 2-4 wks (follow closely!
Eisenmenger: from R L shunts (PDA, VSD).
Valvular disease:
SBE ppx during labor if valuvular disorder.
Consider fixing MS/AS 1 yr prior to pregnancy. If really bad, may even do it while pregnant!
AS sx may get better early in pregnancy (as SVR decreases, less afterload)
MS pts may not be able to meet increased CO CHF sx!
Mitral valve prolapse: small % of women with sx (anxiety, palpitations, atypical chest pain, and
syncope). If pt has sx, beta-blockers are given to decrease sympathetic tone, relieve chest pain and
palpitations, and reduce the risk of life-threatening arrhythmias.
Marfan syndrome: watch out for aortic dxn / rupture.
Should be on beta blockers & not exert self during pregnancy
Peripartum cardiomyopathy: dilated cardiomyopathy before / during / after delivery
EF drops to 20-40%. Manage with diuretics, digoxin, vasodilators like HF pt.
Management: if > 34wks, deliver. If earlier, BMZ check lung maturity

Maternal renal disease: pregnancy can make it worse; higher risk PEC.
Screen qtrimester with 24h urine for Cr/prot; antenatal testing from 32-34 wks onward.
If s/p transplant, may need to increase meds to avoid rejection (higher Vd)
Maternal coagulopathies
Pregnancy extra coagulable. mechanism not precisely known.
Higher risk pelvic vain thrombus 2/2 IVC compression).
Superficial vein thrombosis: painful, visible venous cord. Rx warm compress / analgesic (wont cause
PE) and watch for si / sx of DVT/PE
DVT: treat with IV heparin subQ heparin for rest of pregnancy.
No coumadin nasal hypoplasia, skeletal problems
PE: get EKG, spiral CT. Rx IV heparin subQ heparin / LMW heparin
Will switch to unfractionated heparin @ 36 wks - shorter half life, so can d/c if presents to L&D
Can switch to Coumadin x 6mo postpartum
If unstable / massive, consider tPA / thrombectomy
Maternal thyroid disease
Graves disease: tx with PTU or MMI (depends on practitioner, PTU is classic but more using MMI now)
Hashimotos: levothyroxine.
SLE:

Early pregnancy: high risk loss in 1st/2nd trimester 2/2 placental thrombosis, esp if antiphospholipid Ab
Later pregnancy: also can lose 2/2 thrombosis. Antenatal testing @ 32wks onwards. Higher risk PEC
Lupus flares: can look like PEC, but have low complement.
If flaring, try high dose steroids cyclophosphamide if that doesnt work. If PEC, deliver.
Neonatal problems: can get irreversible congenital heart block 2/2 anti-Ro (and anti-La, but more Ro)
antibodies which cross-react with fetal cardiac conduction system.
Screen for anti-Ro at first visit; interventions vary.
Substance abuse:

Alcohol: FAS possible with > 2-5 drinks / day. Growth retardation, CNS effects, abnormal facies, cardiac
defects, etc. If in withdrawal, try barbituates instead of benzos (less teratogenic)
Caffeine: > 1 cup coffee (150 mg) may increase miscarriages
Cigarettes: a/w SAB, preterm birth, placental abruption, LBW risk, also higher risk SIDS. Stop!
Cocaine: a/w placental abruption, IUGR, preterm birth.
Opiates: heroin, methadone most common. No teratogenicity. Risk is with withdrawal put on NAS
protocol with tincture of opium, etc for baby.

Other stuff:
Asthma in pregnancy: chronic tx: short-acting beta agonists, then inhaled corticosteroids or cromolyn,
then theophylline. acute tx: subq terbutaline, systemic corticosteroids.
Pruritis gravidarum: mild variant of intrahepatic cholestasis of pregnancy; retain bile salt dermis
deposits pruritis; use antihistamines / topical emollients initially, then can try cholestyramine
ursodeoxycholic acid if really bad.
If appendicitis suspected, get a graded compression ultrasound (best for eval - CT has lots of radiation)
Depression: Paxil is class D (increased risk fetal cardiac malformations & persistent pulmonary HTN)

Postpartum care / complications


Newborn - immediate postpartum assessment
Magnesium used for mom watch for decreased respiratory effort (may require bagging)
Septic infants (e.g. chorio, GBS unknown, etc) often pale, lethargic, high temperature. A foul smell at
delivery can be a warning sign.
No respiratory effort bag, prepare to intubate
suction a good idea, but wont cause respiratory effort
stimulation might not be enough if baby really down.
Naloxone contraindicated if possible hx of opiate abuse by mother (baby would go into
withdrawal, which could be life threatening)
Sign

0 points

1 point

2 points

Activity
(Muscle tone)

limp

limbs flexed

active movement

Pulse
(heart rate)

absent

< 100 /min

> 100 /min

Grimace
(response to smell or foot
slap)

absent

grimace

cough or sneeze (nose)


cry and withdrawal of foot (foot
slap)

Appearance
(color)

blue

body pink
extremities blue

pink all over

Respiration
(breathing)

absent

irregular
weak crying

good strong cry

Postpartum hemorrhage: defined as 500cc if vaginal delivery, 1000cc if c/s


First step: fluids, type & cross for blood, send coags (consumptive coagulopathy)
If hypotensive, worry about Sheehan syndrome

If bleeding wont stop in OR, can try B-lynch sutures to compress, then may start having to tie off bigger
vessels
DDx:
vaginal lacs / hematomas, cervical lacs (fix),
uterine atony (everybody gets Pit ppx postpartum, uterotonics below),
retained POC (examine / may need D&C),
accreta,
rupture (rare),
inversion (too uch cord traction; need to replace manually; if not GETA laparotomy).
Uterotonics - route of administration
Oxytocin is administered as a rapid infusion of a dilute solution (20-80 units in a liter) and not as
an IV bolus.
Prostaglandin F2 should be administered intramuscularly. It could also be injected directly into
the uterine muscle.
Neither prostaglandin F2 nor methylergonovine should ever be administered IV, as they can
lead to severe bronchoconstriction and stroke, respectively.
Uterotonics: contraindications
Methylergotavine (methergine) - hypertension & preeclampsia (constricts smooth muscle and
exacerbates HTN)
Hemeabate (prostaglandin f2) - asthma (bronchoconstrictor)

Endomyometritis
Polymicrobial infection, more common after C/S, higher risk if chorio / meconium / prolonged ROM
Si/Sx: fever, high WBC, uterine tenderness, esp 5-10d after delivery but can be several weeks
Workup: r/o retained POC with U/S. If retained POC, do blunt curettage (PP uterus can rupture!)
Rx: broad spectrum IV abx until afebrile x 48h, no uterine pain / tenderness, normal WBC
Breastfeeding
To suppress lactation: breast binders, ice packs, analgesics, avoid nipple stimulation (not bromocriptine
or other meds which can cause rebound engorgement and thromboembolic events!)
Breastfeeding candidiasis: onset of pain in breast when feeding, sore / sensitive nipples. Exam: pink
shiny nipples with peripheral peeling.
Signs that a baby is getting sufficient milk: 3-4 stools in 24 hours, 6 wet diapers in 24 hours, weight gain
and sounds of swallowing.
Breast engorgement? Try feeding more often, taking showers, NSAIDs before feeding. Can actually lead to
fever (low grade, with breast engorged and/or hx of trouble breastfeeding)
Prolactin causes milk production, oxytocin causes milk letdown
Progesterone-only contraceptives are best in puerperium (dont interfere with milk let-down) - like Depo
Other Postpartum Stuff
Postpartum depression if longer than 2 weeks, ambivalence towards newborn, etc. (vs blues)
Can use SSRIs, safe for breastfeeding.
Postpartum fever ddx
Endometritis - uterine tenderness, hx of d&c or c/s, fever and tachycardia. See above.
Mastitis: fever, elevated WBC, focal tenderness & erythema, one breast warmer.

Use dicloxacillin as first line abx, keep breastfeeding!.

Admit if no response to abx in 48h; suspect breast abscess & get imaging.
Breast engorgement
Septic thrombophlebitis - absence of other findings, no uterine tenderness but just a fever
without other signs. May be able to dx on lower extremity / pelvic ct - involves pelvic veins. Rx
abx and anticoagulants.

Gynecology
Benign Lower Genital Tract Disorders
Congenital anomalies
Labial fusion: 2/2 exogenous androgens or CAH (21-hydroxylase deficiency) - check 17-OH progest
If CAH, treat with cortisol (suppresses ACTH inhibits adrenal activity less androgens). If saltwasting, give mineralocorticoids back too (fludrocortisone). Surgery to reconstruct
Imperforate hymen: buildup of secretions (hydrocolpos / mucocolpos) in vagina, primary amenorrhea
+ cyclic pelvic pain at puberty. Surgery.
Transverse vaginal septum: 2/2 incomplete canualization between mullerian upper vagina & urogenital
sinus-derived lower vagina. Can present like imperforate hymen, but exam shows short vagina with blind
pouch U/S & MRI show upper vagina & uterus. Surgery.
Vaginal atresia: lower vagina (from urogenital sinus) fails to develop. Primary amenorrhea, cyclic pelvic
pain too - but no introitus (vaginal dimple) instead; confirm dx with U/S or MRI, then surgery (e.g.
vaginal pull-throguh)
Vaginal agenesis = mullerian agenesis = mayer-rokitanksy-kuster-hauser syndrome.
Congenital absence of vagina as well as hypoplasia or absence of cervix, uterus, fallopian tubes.
Normal external genitalia & secondary sex characteristics (normal ovaries), 46,XX.
Primary amenorrhea in adolescence. Dx on U/S or MRI.
Can create neovagina with surgery (McIndoe - buttock skin graft reconstructed) or serial dilators
(Frank/Ingram). Clearly, cant carry pregnancy w/o uterus (but can use surrogate with her eggs)
Epithelial disoders of vulva / vagina
bx all vulvar lesions! If vaginal, bx via colpo
For tx, avoid tight-fitting clothes, bubble baths, douching, etc.
Physical findings

Symptoms

Treatment

Lichen sclerosis

Symmetric white, thinned skin on


labia / perineum / perianal. Labia
minora shrink, stick together. Does
not involve vagina. Caucasian
premenarchal girls and
postmenopausal women.

Usually asx; occ.


pruritis/dyspareuni
a. From
itch/scratch cycle.

High potency topical steriods


(clobetasol) 1-2x/d x 6-12 wks

Squamous cell
hyperplasia

Localized thickening of vulvar skin


2/2 edema
Raised white lesion on labia
majora / clitoris

Chronic pruritis,
thickened skin

Medium potency topical steroids x


4-6 wks

Shiny, flat, purple papules on inner


labia majora, vagina, vestibule with
lacy reticulated pattern; can erode,
can have vaginal adhesions
stenosis. Also on hair-bearing
skin/scalp (can alopecia), oral
mucous membranes

Pruritis with mild


inflammation to
severe erosion,
remissions /
flares, burning,
contact bleeding,
dysparunia.

Lichen simplex
chronicus

Thickened white epithelium,


unilateral usually, well
circumscribed, excoriation,
lichenified

Pruritis, often
worse @ night

Medium potency topical steroids,


antihistamines for itching
Get vulvar bx to r/o badness

Vulvar psoriasis

Red, moist lesions, sometimes scaly,


a/w scalp / axilla / groin / trunk
lesions

Asx or occ. pruritis

UV light or topical steroids

Vaginal adenosis

Palpable red glandular spots,


patches on upper vagina on
anterior wall

Asymptomatic
A/w DES exposure
in utero.

get Bx to r/o adenocarcinoma.


Follow (serial exams)

Lichen planus

Vaginal hydrocortisone
suppositories; may need surgery /
dilators for adhesions.
If postmenopausal, estrogen for
atrophy.

Vulvar vestibulitis - constellation of sx including severe pain on vestibular touch or attempted vaginal
entry, tenderness to pressure and erythema of various degrees, often sudden onset, sharp / rawness in
nature. Vulva / vestibule only. can be worsened when biking, tight shorts, tampon insertion, etc.
Tx - tricyclic antidepressants to block sympathetic afferent pain loops, pelvic floor
rehabilitation, biofeedback, and topical anesthetics. Surgery with vestibulectomy is
recommended for patients who do not respond to standard therapies and are unable to tolerate
intercourse.
Cysts, etc:
Epidermal inclusion cysts on vulva: Usually go away, I&D if superinfected
Sebacous cysts: same as above, just accumulating sebum
Apocrine sweat gland cysts - can be occluded, abscesses hidradenitis supperativa if multiple abscesses
form. Excise or I&D; give abx if cellulitis
Skenes gland cyst (near urethral meatus) Bartholins duct cyst - B=below introitus.
If small (1-2 cm), watch and/or sitz bath
If bigger / symptomatic, can I&D & place Word catheter x 4-6 wks
If woman over 40, biopsy to r/o rare bartholins gland carcinoma
If recurrent, can marsupialize (suture cyst wall to vaginal mucosa to prevent reforming)
If abscess (infected looking), only treat if N. gonorrhea isolated, otherwise I&D sufficient.

If refractory or cellulitis too, can use anti-staph agents.


Gartners duct cysts: remnants of mesonephric ducts (Wolffian), which normally regress in females
Found on anterolateral aspect of upper vagina, usually asx but can p/w dyspareunia / pain with
tampon use. Can remove surgically if needed; can bleed (may need to use vasopressin)

Benign solid tumors:


Lipomas: only remove if symptomatic
Hemangiomas: red, will regress, found in infants, can bleed 2/2 trauma.
Benign cervical lesions:

Congenital: can see double cervix = bicollis if 2 uteri or other anomalies 2/2 in utero DES exposure
(higher risk of clear cell adenocarcinoma of cervix / vagina).
Cysts on cervix
retention = nabothian from blockage of endocervical gland, usually asx, no tx needed
mesonephric (from wolffian ducts), or endometrial implants too
Cervical polyps: pedunculated or broad based. Usually asx but can be a/w spotting.
Not premalignant, but remove - can mask irregular bleeding from other source!
Cervical fibroids: can cause intermenstrual bleeding, dyspareunia, bladder / rectal pressure, L&D
problems. Remove as possible.

Benign Upper Genital Tract Disorders


Congenital anomalies:
Upper structures formed from fusion of paramesonephric = mullerian ducts. Lower vagina from UG
sinus
Septate uterus, etc - often a/w inguinal hernias & urinary tract anomalies (get imaging to eval!)
Bicornate or septate uteri a/w 2nd trim pregnancy loss, malpresentation, PTL, etc.
generally will require no treatment unless symptomatic
Uterine leiomyomas = fibroids
Estrogen responsive monoclonal smooth muscle proliferation surrounded by pseudocapsule
Common in women of childbearing age can enlarge in pregnancy regress in menopause
More common in AA pts for unknown reasons
Higher risk with multip, nonsmoking, hypertensive, perimenopausal women
OCPs protective.
Only require treatment if bleeding / sx / problems with fertility
Submucosal bleed, take out under hysteroscopy. Intramural = most common, subserosal too - remove
these via myomectomy.
Dx with pelvic ultrasound. MRI fi need to distinguish from adenomyosis.
Treatment
Medical therapy: Provera, Lupron (decrease estrogen) - remember GnRH agonists can cause more
bleeding initially. Lupron usually used to shrink size / stop bleeding before surgery (fibroids will
go back to previous size very quickly)
IR: can do uterine artery embolization
Surgical: myomectomy if fertility desired, but more morbid / recur. Hysterectomy definitive.
Endometrial polyps: benign overgrowths,
common in women 40-50 y/o, p/w bleeding between periods (metrorrhagia, also meno / menometro)
Dx with U/S & sonohystogram. If > 35, need endometrial biopsy if bleeding.
Benign, but can mask bleeding from other sources.
Endometrial hyperplasia: common cause of abnormal uterine bleeding
2/2 unopposed estrogen exposure (anovulatory cycles, etc) can progress to carcinoma
Obesity, nullips, late menopause, early menarche, exogenous estrogen w/o progesterone, PCOS,
chronic anovulation, estrogen producing tumors (granulosa-theca cell), tamoxifen. Also HTN / DM
P/w oligomenorrhea / amenorrhea, then excessive / irregular bleeding.

Uterine bleeding in postmenopausal women: endometrial hyperplasia / cancer until proven


otherwise!
Classification: if atypia, often have coexistent endometrial cancer!
Simple hyperplasia - just proliferation of both stromal / glandular elements
Complex hyperplasia - just glands proliferating, no cytologic atypia
Atypical simple hyperplasia - cellular atypia, mitotic figures too
Atypical complex hyperplasia - most severe form, atypia + proliferating glands, 29% risk
progression to carcinoma
Dx: need tissue dx: endometrial bx is first line; can do D&C if needed afterwards / bx not possible.
Management:
If just hyperplasia (simple / complex / SAH / CAH), can treat with progestin therapy (Provera to
induce withdrawal bleed, or Mirena, etc) x 3 mo, then repeat endometrial bx to see regression
If CAH, often treat with hysterectomy (high risk coexistent endometrial cancer or developing it
later). Can follow closely if fertility preservation important, however.

Ovarian cysts
Functional - normal functioning cysts
Follicular = most common. From failure of follicle to rupture. 3-8cm. Asx, unilateral but can be
tender. Higher risk of torsion if greater than 4-5 cm. Resolve in 60-90d
Corpus luteum cyst: when corpus luteum fails to regress after 14d, or enlarges, or becomes
hemorrhagic. Can delay menses / cause unilateral lower quadrant pain. Can rupture
hemoperitoneum. Feel more firm on exam.
Theca lutein cysts - large, bilateral cysts, clear, straw-colored fluid. From stimulation by abnormally
high B-hCG (molar pregnancy, choriocarcinoma, ovarian induction therapy)
Warning signs:
Ovarian torsion: classically waxing / waning pain & nausea. Concern if > 4cm
If premenarchal or postmenopausal, think neoplasm & do ex-lap
If persist > 60 days, are solid or complex on U/S, or larger than 8 cm in reproductive woman,
think neoplasm diagnostic laparoscopy or laparotomy.
Follow up with pelvic ultrasounds serially to check for cyst resolution;
CA-125 if concerned for cancer
Start patients on oral contraceptives during observation period (to prevent future cysts)
Cystectomy / evaluation via laparoscopy / laparotomy if no resolution in 60-90d

Endometriosis / Adenomyosis
Endometriosis: Endometrial glands / stroma outside of endometrial cavity
endometrioma = cystic collection in ovary (chocolate cyst)
Severity of sx doesnt correlate with amount of endometriosis
Dx: really need surgical confirmation by direct visualization
Sx: cyclic pelvic pain starting 1-2 wks before menses, peaking 1-2d prior to menses, then subsiding
Also dysmenorhea, dyspareunia, abnl bleeding, infertility
Tx:
expectant management if minimal sx or trying to conceive
medical: suppress / atrophy endometrial tissue

OCPs / progestins to create pseudopregnancy (suppress menstruation)


Danzol (androgen derivative; can cause acne/hirsutism/virilization) or Lupron (GnRH
agonist; causes menopausal sx) to create pseudomenopause (suppress FSH / LH; ovaries
dont create estrogen less sx).
Can use add back therapy with small amt estrogen along with Lupron to minimize
sx of menopause, lessen bone loss.
surgical: laparoscopy + fulgaration for implants, laparoscopic cystectomy for endometriomas

Definitive = TAH/BSO, lysis of adhesions, fulgaration

Adenomyosis: endometrial tissue (stroma) in to uterine myometrium.


High levels of estrogen endometrial basalis layer undergoes hyperplasia invades
Usually in fundus, posterior uterine wall
Adenomyoma - can be an isolated region, but vs fibroid has no pseudocapsule.
Sx: often asx; can have secondary dysmenorrhea, menorrhagia
Signs: diffusely enlarged globular, boggy uterus. Can be slightly tender.
Dx: pelvic U/S often first, then MRI if adenomyosis on ddx (more accurate).
Only definitive dx after hysterectomy!
Need to distinguish - dont want to go in for myomectomy for fibroids and find adenomyosis (would
have to do a TAH!)
Treatment:
Since stromal, not glands, not responsive to OCPs / hormones.
Can try to treat with NSAIDs / OCPs / progestins anyway
Hysterectomy is only definitive treatment!

Lower reproductive tract infections


UTIs: Need to r/o pyelo (no fever, no CVA tenderness). Treat for E. coli, etc. with oral abx.
DDx: Interstitial cystitis: chronic inflammation of bladder recurrent irritative urinary sx (urgency,
frequency) for long time w/o infection, also pelvic pain (dyspareunia, etc).
Vulvitis: usually candidasis. If chronic, always rule out malignancy. Could also be 2/2 irritants, etc.
Ulcers:
Syphillis (T. pallidum).
Primary = chancre on exposed mucosa, painless / red / round / firm / well circumscribed.
Develops 3wks after exposure; some LAD too.
Secondary = disseminated. maculopapular rash including palms / soles 1-3mo after exposure
Latent: early if < 1yr, late if > 1 yr
Tertiary = uncommon, years later. granulomas / gummas of skin, cardiovascular syphilis
(aortitis), neurosyphilis (tabes dorsalis, general paresis).
Dx:

dark field microscopy from chancre / granuloma is gold standard

RPR/STS FTA-ABS for serology / screening.


Tx: PCN G 2.4M units x 1; if late latent, do it weekly x 3 wks.

Alternatives: tetracycline PO 4x/day x 2wks, doxy 100mg PO BID x 2wks, or ceftriaxone


1gm IM/IV daily x 8-10d, but desensitize & give PCN, especially in pregnancy!

If neurosyphilis, need IV PCN G q4h x 10-13d.

Follow RPR / VRDL titers - should see decrease @ 6mo, nonreactive @ 12-24mo
Jarisch-herxheimer rxn: from death of spirochetes; after starting PCN, fever, chills, H/A, myalgia,
malaise, pharyngitis, rash w/in 24h. Shouldnt prevent / delay therapy

HSV:

grouped vesicles / ulcers with burning, pruritis.


Dx: DNA PCR, or Tzanck smear classically.
Rx:

Primary infection: acyclovir, famciclovir, valacyclovir

If severe or immunocompromised, IV acyclovir

If recurrent, oral acyclovir x 5d

Chronic infection: valacyclovir can lessen transmission, reduce outbreaks

If pregnant, C/S
Chancroid (H. ducreyi).
Painful, well-demarcated, non-indurated ulcer with painful supperative inguinal LAD
Very rare in USA.
Dx with culture (chocolate agar), hard to do.
Tx with ceftriaxone IM x1, azithro PO x 1, or longer cipro / erythro regimens. treat partners too
LGV (C. trach L1-3)
First stage: painless, transient local lesion (papule / ulcer) Secondary stage: inguinal
syndrome (painful enlargment / inflammation of inguinal nodes, fever / H/A / malaise, anorexia)
Tertiary stage: anogenital syndrome (proctocolitis, rectal stricture, rectovaginal stricture,
elephantiasis.
Dx: clinical suspicion, can also use cx / immunofluorescence / NAAT
Rx: doxycycline 100 mg PO BID or erithroymycin x 21 days.

Non-ulcerated lesions
Condyloma acuminata (genital warts) - caused by HPV
Raised papillomatous wart can grow to large pedunculated lesions. Bx if uncertain
Prevent with gardasil.

Treat with local excision, cryo, topical TCA or 5FU

Can also use imiquimod or podofilox self-treatment if motivated


Molluscum contagiosum (pox virus)
Small umbilicated water warts, anywhere except hands / feet. Clinical dx.
Rx: local excision or TCA / cryotherapy
Vaginal infections
Bacterial vaginosis: shift from lactobacillis other microorganisms, incl Gardnerella
Dx: 3 of [whiff test, thin white homogenous discharge, > 20% clue cells, nitrazine pH > 4.5]
Tx: metranidazole 500mg PO BID x 7d or clinda. PO > topical for efficacy. No EtOH with metro
Candidaisis
A/w diabetes, recent abx, immunocompromise, intercourse, etc.
Sx: Pruritis, burning, dysuria, dyspareunia, discharge
On exam: satellite lesions, cottage cheese-like discharge
Dx: KOH prep showing branching hyphae & spores
Tx: azoles

Topical / suppository = miconazole, terconazole; Nystatin too


PO: fluconazole = Diflucan 150 mg PO x 1
If recurrent, consider non-albicans species (can be resistant to azoles); try longer duration
and may need weekly PO fluconazole x 6mo
Trichomonas vaginalis: STD, unicellular anaerobic flagellated protozoa
Sx: profuse discharge (yellow / gray / green / frothy) with unpleasant odor, pruritis, worse just
after menses 2/2 vaginal pH increase
Exam: pH in 6-7 range, vulvar erythema / edema / pruritis, strawberry cervix (but only 10%)
Dx: wet prep trichomonads; NAAT is more sensitive, cx rarely done but most sensitive / specific
Tx: metronidazole 2g PO x1 and treat partner as wel

Vs BV tx, which is for 7d and no partner treatment needed

Mucopurulent cervicitis: cervical motion tenderness without other PID sx


N. gonorrhea
Gonorrheal cervicitis: classically sx peak during & after menses. Can infect anal canal, urethra,
oropharynx, bartholin glands too. In neonates, can cause conjunctivitis. Disseminated = fevers,
erythematous macular skin rash, arthritis, etc.
Dx: Gram negative dipplococcus; can gram stain or isolate with Thayer-Martin media, although
NAAT on urine / cervical specimens is now #1
Tx: ceftriaxone 125 mg IM x 1 or cefixime 400mg PO x 1;

also treat with azithro PO x1 for CT unless ruled out by NAAT


Chlamydia trachomatis
Ocular, respiratory, reproductive tract infections. Urethritis, etc. too.
Dx: NAAT (intracellular, so gram stain / cx not good)
Tx: azithromycin 1g PO x1 or BID doxy x 7d (but not in pregnancy)

Upper reproductive tract infections


Endometritis / endomyometritis (depending on depth of invasion)
Usually 2/2 instrumentation (C/S, D&E, D&C, IUD placement, but also vaginal delivery)
Probably also concomittant with most PID
Uterine tenderness, fever, elevated WBC with recent hx of instrumentation, no adnexal pain
Polymicrobial - treat with clinda + gentamicin IV if severe; if chlamydia suspected, add doxy
Treat until afebrile / stable x 24-48h; no need to continue PO afterwards
PID

Higher risk infertility, ectopics afterwards.


Sx: abdominal / adnexal pain; can be unilat / bilat, may be absent, also vaginal discharge / bleeding / UTI
sx. Fever is actually less common (20%).
Fitz - Hugh - Curtis syndrome = perihepatitis; RUQ pain and LFT elevations too
Dx: Pelvic pain + one or more of [cervical motion, uterine, or adnexal tenderness]
Fever, elevated WBC, mucopurulent cervical discharge, elevated ESR/CRP are supportive
Get cervical cultures for etiology, but usually polymicrobial (cx results dont affect tx)

GC/CT are most common, but also anaerobes, E. coli, H. flu, gardnerella, strep
Definitive dx with laparoscopy / pelvic imaging with PID findigns / endometrial bx

Tx: hospitalize (esp if teenagers, nullips, noncompliant), get fluid status under control
IV abx: broad spectrum cephalosporin (e.g. cefoxitin) and doxycycline (for atypicals)
After 24h afebrile, can d/c IV abx but continue doxy. If allergic, can use clinda + gent
For o/p tx, ceftriaxone IM x1 + PO doxy +/- metronidazole x 14d

Tubo-ovarian abscess: most commonly with PID.


Sx: PID + fever, leukocytosis with left shift, elevated ESR
Dx with PID & adnexal / cul-de-sac mass
Tx: can often avoid surgical treatment (unless peritoneal / ruptured)
Give amp + gent IV along with [clinda or metro] for anaerobes
Treat until afebrile 24-48h, pelvic exam OK. Can convert to PO for total 10-14d course
May need to drain if no response to abx in 48h; may rarely need unilateral salpingoopherectomy
Toxic shock syndrome: now uncommon, was often 2/2 long term tampon use; 2/2 S. aureus producing TSST-1
high fever, hypotension, diffuse erythematous macular rash, desquamation of palms / soles 1-2wks
later, GI disturbances, renal failure, plts < 100k, alteration in consciousness, etc.
Blood cx often negative (toxin absorbed via vaginal mucosa)
Tx: always hospitalize; fix hypotension / fluid status first.
Abx decrease risk of recurrence only (clinda + vanc) but since its toxin-mediated, doesnt shorten
current infections course.
HIV: ELISA for screening Western for confirmation; then get VL / CD4. Get em on HAART.
Increased risk cervical cancer - so do Pap smears initially and at 6mo, then yearly if negative.

Pelvic organ prolapse

1st degree = structure in upper of vagina; 2nd degree = to level of introitus, 3rd degree= outside of
vagina, 4th degree = whole structure outside of vagina. POP-q can quantify more precisely.
Bigger problem in post-menopausal women 2/2 decreased estrogen, more vaginal deliveries.
Also increased risk with chronic increased abdominal pressure (chronic cough, constipation,
repeated heavy lifting, large pelvic tumors).
Do a split-speculum exam. May also need urine cx, cystoscopy, urethroscopy, urinary studies,
anoscopy, sigmoidoscopy, defecography depending on presentation.

Part of vaginal wall

Whats prolapsing?

Notes / Specific Surgical Treatment

Anterior

Cystocele, urethrocele

Cystocele: anterior colporrhapathy (remove excess anterior vaginal


mucosa, plicate endopelvic fascia to resuspend bladder)

Posterior

Rectocele, enterocele

Rectocele: posterior colporrhopathy (similar to above, but rectal


fascia plicated posterior, excess posterior vaginal wall removed)
Enterocele: vaginal enterocele repair (repair & plicate rectovaginal
fascia / posterior vaginal wall)

Top

Uterus

Vaginal hysterectomy + McCall culdoplasty (plicate uterosacral


ligaments to reduce risk of future vault prolapse

Anywhere

Vaginal vault prolapse

Sacrospinous ligament suspension: suture endopelvic fascia of

vaginal apex to sacrospinous ligament (vaginal approach)


Abdominal sacral colpopexy: use mesh, attach vaginal apex to sacrum
(abdominal approach)

(collapsing after
hysterectomy)

Treatment: Kegels, pessaries, estrogen replacement if postmenopausal, or surgery as above.

Urinary Incontinence
Nerves: CNS inhibits; parasympathetic pelvic nerve from S2-S4 helps urinate, as does somatic pudendal nerve.

Workup:
Voiding diary (when are you leaking?)
Do U/A and UCx to r/o infection
Can get urodynamics, PVR, etc.
Standing stress test: stand over towel & cough.
Type

Dx

Etiology

Notes / Tx
Start with behavior /biofeedback / training / Kegels /
pessaries / etc, but may need to go to surgery:

Stress

Sx on exertion or
straining (cough /
laugh / exercise)
Cotton swab test for
hypermobile urethra

Urge

Involuntary urine
loss with sudden
urgency whether or
not bladder is full;
frequency & nocturia

Mixed

Mixed symptoms of
above

Pelvic relaxation &


urethral
hypermobility, can also
be due to intrinsic
sphincter deficiency

Detrusor overactivity
Most is idiopathic; also
with CNS injury

Use sling if hypermobile & intrinsic sphincteric


deficiency combined

Use retropubic urethropexy if stress incontinence


for hypermobility alone (sling can be obstructive as
well - higher rate of retention, voiding dysfunction).

Use urethral bulking if stress incontinence for


intrinsic sphincteric deficincy alone

Alz dz, stroke, Parkinsons, MS, diabetes no central


inhibition of detrusor contraction
Start tx with bladder training, Kegels, behavior
Med tx: anticholinergics (oxybutynin), smooth muscle
relaxants (detrol / tolterodine).
No role for surgery in urge incontinence

Both stress & detrusor


activitity

imipramine (TCA) especially good if mixed incontinence


(both anticholinergic & alpha-adrenergic)

Overflow

Frequent / constant
dribbling, also stress /
urge incontinence.

Poor / absent bladder


contractions (or more
rarely obstruction)
retention overflow

Meds:
Reduce urethral closing pressure (prazosin,
terazosin, phenoxybenzamine)
Striated muscle relaxants (diazepam, dantrolene)
Cholinergic agents (bethanecol) to increase
contractility
Intermittent self-cathing used too.

Bypass

Dx with indigo
carmine instilled into
bladder, then tampon.
Can use IVP /
cystogram / etc too

Urinary fistula after


pelvic surgery or
radiation, esp TAH

Fix fistula (surgery)


Use abx for UTI / estrogen if postmenopausal / etc

Functional

Nursing home,
geriatrics, poor
mobility

Cant get to bathroom

Fix social situation, psych consult, SW, etc.

Stress incontinence: Use sling if hypermobile & intrinsic sphincteric deficiency combined
Use retropubic urethropexy if stress incontinence for hypermobility alone (sling can be obstructive as
well - higher rate of retention, voiding dysfunction).
Use urethral bulking if stress incontinence for intrinsic sphincteric deficincy alone

Puberty

Adrenarche (zona reticularis in adrenal starts making androgens), then gonadarche (pulsatile GnRH)
Adrenarche: ages 6-8; Gonadarche around age 8
Thelarche (~10 y/o) pubarche (~11) growth spurt peak velocity (9-10) menarche (12-13, or
usually ~2.5yrs after thelarche). Earlier in AA, later in Caucasians / thin girls / etc.
True precocious puberty (due to pulsatile GnRH secretion) - treat with nonpulsatile GnRH

Menopause
Definition: 12 months of amenorrhea after last menstrual period. Avg age 51, but big range.
Perimenopause before that point - can still have periods! Get OCPs, not HRT
Sx: Hot flashes, mood changes, insomnia, dyspareunia. Sx usually disappear w/in 12 mo
Signs: vaginal / cervical atrophy
Decreased estrogen, FSH elevation / LH too, but just supportive (not diagnostic)
Also increased coronary artery disease risk, accelerated bone resorption osteoporosis
Osteoporosis:
Osteoporotic fx hx - can treat with bisphosphonates right away without waiting for dexa results
Osteoporosis risk: consider getting DEXA (everybody @ 65 y/o, or @ 60 y/o if high risk)
Treatment
Bisphosphonates (if pathologic fx of hip or vertebrae, other fx and T-score -1.0 to -2.5, or T
score < -2.5).
Should be taking 1000-1500 mg Ca daily no matter what; if osteoporotic, 800 IU vitD too.
SERMs help with osteoporosis too.
Hormone replacement therapy
Unopposed estrogen endometrial hyperplasia endometrial cancer,
so if still have a uterus, need progestins too
Combined HRT: short period of time (6-12 mo), smallest dose
Helps prevent osteoporosis
Contraindicated if chronic liver dz, pregnant, breast / ovarian / uterine Ca, hx DVT
In WHI, actually more CV-related complications in combined hormonal group.
Irregular vaginal bleeding is a contraindication too - need to get a biopsy first
Can also try SSRIs for flushing / mood sx, but not great; also vaginal estrogen for atrophy / dryness
Resumption of bleeding is the #1 reason that women stop hormone replacement therapy

Amenorrhea
Primary amenorrhea - no menarche by age 16 or 4 years after thelarche
Outflow tract anomalies: imperforate hymen transverse vaginal septum, vaginal atresia
All treated with surgery
Mullerian agenesis = MRKH syndrome - pt with no menses, blind pouch vagina, but normal body hair
get a renal ultrasound to check for other commonly associated abnormalities.
Androgen insensitivity, pt with primary amenorrhea with absence of body hair
Get a karyotype to confirm 46,XY
Do have testes MIF secreted no mullerian structures; blind pouch vagina
Swyer syndrome: 46,XY with congenital absence of testes
NO MIF mullerian structures present, as opposed to AIS
Ovarian failure: see low estrogen but high gonadotropins
Savage syndrome: no LH/FSH response 2/2 receptor defect
Turner syndrome (45,XO) - rapid atresia of ovaries no estrogen
Kallman syndrome - no menses, no secondary sex characteristics, normal external genitalia.
Central disorder - low GnRH low FSH/LH low estrogen (labs look like anorexia, etc)
Dx with olfactory challenge. Tx with pulsatile GnRH
Pt 16 years old or younger - just reassure if no menses yet!

Secondary amenorrhea
Pregnancy is #1 cause!
Anatomic abnormalities:
Asherman syndrome (intrauterine synechiae in pt s/p myomectomy, C/S, D&C, endometritis)
Cervical stenosis 2/2 surgical, obsetric trauma
Premature ovarian failure - often idiopathic, also 2/2 torsion, surgery, infection, radiation, chemo
Symptoms of menopause before age 40; do chromosomes if < 35 y/o
PCOS = Stein-Leventhal syndrome
chronic anovulation, oligomenorrhea / amenorrhea, hirsutism, obesity, enlarged polycystic ovaries
Increased LH:FSH ratio kills follicle, more androgens hirsutism
Treat with OCPs / cyclic progestins / Depo to suppress endometrial hyperplasia / etc

Treat with Clomid if fertility desired, however.


Screen these pts for for T2DM
Hyperprolactinemia: amenorrhea, galactorrhea
Prolactinoma is #1 cause; rx with cabergoline / bromocriptine (dopamine agonists) if
asymptomatic / microadenoma, or surgery if big & causing problems
Hypothyroidism increased TSH increases PRL secretion as well
Meds: dopamine agonists (Haldol, Reglan, other antipsychotics), TCAs, MAOis
Everybody should get imaging to r/o prolactinoma.
H-P-A axis disruption: stress, anorexia, etc.
Workup of secondary amenorrhea:
beta-HCG first, then TSH / PRL levels, MRI of sella if needed
Progesterone challenge test if PRL normal

if withdrawal bleeding present, outflow tract is patient & estrogen present in good enough
quantities.

Think anovulation (PCOS, ovarian / adrenal tumors , Cushing syndrome, thyroid disorders,
adult-onset CAH).

These patients should all get progesterone to prevent endometrial hyperplasia


if withdrawal bleeding absent, then do combined estrogen / progesterone challenge

If still no bleeding, think outflow tract obstruction

If bleeding present now, think not enough estrogen - get LH/FSH levels
If LH/FSH normal or low, think hypothalamus or pituitary
If LH/FSH high, think premature ovarian failure

Menstrual cycle abnormalities


Dysmenorrhea: menstrual pain / cramping interfering with normal activities
Treatment for primary dysmenorrhea (idiopathic)
NSAIDs (inhibit endometrial prostaglandin production). Take at onset of menses continue 13d as needed. Can also use COX-2 inhibitors, but worry about side effects.
OCPs are second line. Can also try heating pads, exercise, massage, etc. Surgical therapy not helpful
Treatment for secondary dysmenorrhea
Cervical stenosis: dilate (surgical or laminaria)
Pelvic adhesions (Crohns, appendicitis, myomectomy, other surgeries) - cant see on imaging.

Rx NSAIDs, laparoscopy if recalcitrant


PMS/PMDD: happens in second half of menstrual cycle (luteal).
Bloating, wt gain, H/A, breast tenderness, moodiness, etc. Multifactorial.
PMDD = worse sx, interfere with life, etc.
Rx mood diary, try vitamin B6 and stuff like that, then, SSRIs if that treatment fails. OCPs help too (e.g.
Yaz, has low dose estrogen + drospirinone, a spironolactone with antiandrogen activity)
Menorrhagia: excessive flow duration (>7d) or volume (>80 mL/cycle)
Etiologies: fibroids, adenomyosis, polyps, endometrial hyperplasia.
If in young pt, check for bleeding disorders (F5L, vWB dz, ITP, plt dysfxn, malignancy)
Hypomenorrhea: regularly timed, light flow.
Think A: athletes & anorexics (hypothalamic) or Ashermans / anatomical.
Could also be 2/2 Depo / Mirena / OCP
Metrorrhagia: bleeding between periods.
Think cervical lesions (polyp, eversion, carcinoma) or endometrial (polyps or carcinoma)
Menometrorrhagia: heavy bleeeding & between periods. Similar ddx to menorrhagia.
Oligomenorrhea: > 35d between cycles. Similar to amenorrhea etiologies.
PCOS, chronic anovulation, pregnancy on list too, also thyroid disorders
If > 6 mo, then secondary amenorrhea
If prolonged & pt is obese / youre concerned for anovulatory cycles, get endometrial bx even if < 35 y/o

Polymenorrhea: < 21d between cycles. Often caused by anovulation


Dysfunctional uterine bleeding (DUB): diagnosis of exclusion (abnormal bleeding & no other etiology)
Usually 2/2 anovulation no corpus luteum no progesterone no withdrawal; endometrium just
grows until blood supply cant keep up, then breakds down.
W/u for hypothyroidism, hyperPRL, hyperandrogenism, PMOF
ANY WOMAN OVER 35 WITH ABNORMAL UTERINE BLEEDING GETS AN ENDOMETRIAL BX
Also true for obese women < 35 with extended oligomenorrhea
Tx:
If acutely hemorrhaging, give IV estrogen for quick relief (but risk DVT/PE) or oral estrogens if
hemodynamically stable (lower risk, but takes 24-48h)
For chronic DUB, use NSAIDs to decrease blood loss, regulate periods with OCPs or progestin only
if estrogen contraindicated
If refractory, consider surgery (D&C is first step endometrial ablation if done with kids).
Hysterectomy is definitive treatment; can leave ovaries too.
Postmenopausal bleeding: always abnormal! Atrophy is #1 cause, but rule out cancer. HRT can cause too.
Also check for non-GYN causes (hemorrhoids, anal fissures, rectal prolapse, lower GI tumors, urethral
caruncles)
W/U: CBC, TSH, PRL, FSH; Pap smear, DRE, tumor markers if adnexal mass identified, endometrial
biopsy. Image with pelvic U/S, sonohysterogram, MRI to get endometrial stripe thickness.
Hysteroscopy for polyps / fibroids, and D&C also useful.

Hirsutism & Virilization


Hirsuitism: more terminal hair; pubic hair changes to male diamond
Virilization: male features develop (voice deepens, balding, muscle mass increases, clitoromegaly, breast atrophy)
Sources of androgens: can be adrenal (DHEAS elevated) or ovarian; both result in increased free T levels.

Adrenal disorders:
Cushing syndrome: Cushing disease if from ACTH-secreting pituitary adenoma; also can be paraneoplastic
or 2/2 adrenal tumor (which would suppress ACTH). Get overnight dexamethasone suppression test
(should decrease endogenous production if normal negative feedback); or 24h urine for cortisol
Congenital adrenal hyperplasia - usually 21alpha-hydroxylase deficiency, causing 17hydroxyprogesterone to build up (gets shunted down androgen pathway). Also dont make cortisol or
mineralocorticoids (adrenal insufficiency - hypotension, etc, and salt wasting); if female, can present with
ambiguous genitalia at birth or have late onset virilization.
Can also be 11-beta hydroxylase (precursor builds up with mineralocorticoid activity, so
hypertensive) or 3B-HSD deficiency too.
Always check 17-OHP level; can confirm with ACTH stim check 17OHP 1h later (big rise =
CAH). Lower elevations can be c/w late-onset CAH or heterozygotes
Can suppress adrenal production with prednisone 5mg qhs

Ovarian disorders: nonneoplastic


PCOS (see above)
Theca lutein cysts: LH theca cells androgens granulosa cells estrogens normally
These cysts make too many androgens! A/w molar pregnancy. Dx with Bx
Stromal hyperplasia / hyperthecosis: pts age 50-70, uniformly enlarged ovaries, large & fleshy
Areas of high utilization inside hyperplastic stroma
Can generally treat these with OCPs, which suppress LH/FSH and increase SHBG
GnRH agonists + add-back estrogen are another option
Ovarian disorders: neoplastic
Functional tumors - Sertoli-Leydig (arrhenoblastoma) - make androgens, usually in young women
If rapid onset over months, be concerned for Sertoli-Leydig cell tumors (commonly diagnosed in
women between the ages of 20-40, and are most often unilateral). T elevated, LH/FSH suppressed.
Granulosa-theca cell tumors generally make estrogens but may make androgens too
Pregnancy - can have luteomas (benign tumor growing in response to b-HCG virilization of pt, fetus!)
Drugs: steroids, minoxidil, phenytoin, diazoxinde, cyclosporin can all cause virilization
Idiopathic hirsutism: can try finasteride (inhibits 5-alpha reductase) or sprionolactone (antiandrogen)
These in addition to OCPs; Lupron / Depo-provera are also reasonable 2nd line if not on OCPs
Other stuff
Hair loss postpartum - high estrogen levels in pregnancy cause increased synchronicity of hair growth, so
that there can be significant alopecia afterwards (all hair in same phase, falls out at same time) - nothing to
worry about.

Contraception / Sterilization
Stuff that kind of works
Periodic abstinence (ha!) with ovulation kits, calendars; coitus interruptus, lactational amenorrhea
(but will start to ovulate before return of menstration usually in 6-12 mo)
Stuff that works better
Condoms: 15% failure rate, but protect against STDs
Birth control pills: 8% real life failure rate; decrease ovarian / endometrial cancer, etc. Can get nausea,
h/a, breakthrough bleeding, wt gain
Estrogen and progesterone. Have to remember to take every day
Progesterone only: have to take at same time every day, higher failure rate. Decrease PID risk, OK
for use during nursing as well.
Bleeding every month, every 3 months, or continuous dosing (more breakthrough bleeding)
How to start:

Starting on day 1 of cycle: least likely to ovulate during cycle

Sunday start: backup for 7 days, leaves next weekend free.

Anytime start is actually fine: just backup method for 7 days


Side effects of COC: risk of DVT / PE / CVA / MI / HTN (lower with low dose). Also cholelithiasis,
cholecystitis, benign liver adenomas

Depo: Progesterone. Shot in arm every 3 months. Can cause irregular bleeding, especially at beginning,
which bothers some people more than others. Also decreased bone density (reversible). can cause
depression, wt gain, hair loss, h/a. Can lead to amenorrhea. May take 6-18mo for fertility to return.
Implanon: 3 years, progestin implant, most women have lighter periods (some none at all), really effective
but can have irregular / unpredictable light bleeding
IUDs: Longer term, very effective
Mirena: progesterone. 5 years. Lighter or no periods.
Paragard: copper. 10 years. Can cause irregular bleeding.
Less common stuff:
patch (not if overwt > 198 lbs or high thromboembolism risk),
nuvaring (3 wks in, 1 wk out, or 3mo in with changes, 1 wk out, 0.8% failure rate),
diaphragm (fit by clinician; leave in place 6-8h after intercourse, risk toxic shock syndrome),
cervical cap (fitted by clinician, use with spermicide can be hard to use),
spermicides (nonoxyl-9, etc, should use with condoms, can irritate mucosa & increase STI
transmission)

Emergency contraception - Plan B (progestin only) within 72h. Need Rx if < 18, OTC if > 18.
Plan B, the levonorgestrel pills can be taken in one or two doses and cause few side effects. Oral
contraceptives need to be taken 12 hours apart if using those.

Indicated sooner than 72h if possible and no later than 120h

Can insert second dose of ocps per vagina or take an antiemetic 1 hr before administration
to decrease nausea/vomiting (major side effect
Copper IUD can be put in within 5-8 days, actually the most effective form of emergency
contraception
Sterilization
Tubal ligation
Can be done laparoscopically (clips, cautery, banding)or hysteroscopically (Essure, Adiana);
Can do immediately postpartum through small subumbilical incision
Essure - takes 12 weeks, use backup birth control until HSG confirms complete occlusion
Leads to a slightly decreased risk of ovarian cancer (mechanism unknown)
Age < 30 have highest regret for procedure
Vasectomy:
Not immediately effective! Use alternate contraception until repeat semen analysis in 6-8wks
Simpler, safer, more effective than BTL
Can form antisperm antibodies, but no long-term effects.

Elective Termination of Pregnancy

Surgical options
Manual vacuum aspiration - more than 99% effective but needs to be 7-8 wks EGA or less
D&C up to 16 wks
D&E after 16 wks - use laminaria first, then introduce large cannula; may need forceps

can use U/S to guide.


Medical abortion
Mifepristone: progesterone antagonist.

Can use up to 49d from LMP.

Use with PO or PV prostoglandin analog (misoprostol) 36-48h later

Confirm completion in 2 wks with serum b-HCG or U/S


Methotrexate - inhibits DHFR / interferes with DNA synth / prevents placental villi proliferation

Used off label as abortifacent (but approved for ectopics) within 49d of LMP

Also use with misoprostol 6-7d later

Confirm completion in 2 wks with serum b-HCG or U/S


Both decline greatly in efficacy after 7 wks. If fail, need to do suction D&C
Side effects: abd pain, cramps, N/V/D, excessive bleeding
Induction of labor also an option if 2nd trimester (esp if later on)
cervical ripening agents, amniotomy, high-dose oxytocin
use fetacidal agents (intraamniotic saline / digoxin / intracardiac KCl) to prevent live birth

Other stuff:
If tissue needed for karyotype, etc should do medical abortion (mifepristone / misoprostol prior to 49
days, or induction with prostaglandins if 8 0/7 or later).
Make sure to give RhoGAM if Rh negative (at time of termination) - both medical & surgical!
Give abx (doxy, ofloxacin, or ceftriaxone) to prevent postabortion endometritis
Rough guide: termination is legal if < 24 wks (threshold of viability) or later if abnormality incompatible
with life

Infertility and Assisted Reproductive Technologies


Normal fecundity (ability to get pregnant in one cycle):
20-25% in first 3 mo, then 15% in next 9 mo (80-90% within 12 mo)
Start workup after one year
Female factor (45-55%)
Ovulatory disorders: PCOS / advanced maternal age most common
Track menstrual cycle with basal body temp chart, mid-luteal progesterone
Clomiphine citrate challenge test: give clomiphine on days 5-9, then measure FSH on days 3 and
10. If FSH high, suggests that ovarian reserve diminished (not making estrogen, so FSH incr)
Tubal factors: PID adhesions, hx ectopics, endometriosis, previous surg adhesions
May need HSG for tubal patency and/or laparoscopy to look for adhesions / endometriosis
GC/CT cx and Pap smears as well
Uterine / cervical factors: Ashermans, DES exposure, cervical stenosis (after conization, 4+ mechanical
dilations, cauterization - also cause inadequate mucous production)
Progestin challenge test & combined estrogen / progesterone challenge to look for endometrial
suitability
Pelvic U/S to look for fibroids, adenomyosis, cancer, polyps, etc. Hysteroscopy is next step
Endocrine: hypothyroid, hyperPRL, Cushings, CAH, etc - get appropriate labs
Others: Luteal phase defect (controversial), Turners syndrome / translocations, etc.
Treatment options
Clomiphine citrate: SERM, estrogen antagonist at hypothalamus, stimulates GnRH production increased
LH/FSH surges ramps up follicular development

Letrozole: aromatase inhibitor, decreases peripheral estrogen production more GnRH more LH/FSH
more follicles, etc. Decreases peripheral estrogen (good for fertility in breast cancer pts, etc)
Metformin: insulin sensitizer (biguanide), but some studies suggest it doesnt help in PCOS
Human menopausal gonadotropins: purified FSH/LH, next line after Clomid
Follistatins (Follistim) - recombinant FSH, stimulates follicular development
Recombinant hCG - similar to LH, used to trigger ovulation after follicle stimulation
Pulsatile GnRH - can be used to increase FSH/LH release. Often used for HPA axis failure (e.g. low wt)
Can try surgery too - for endometriosis, or tuboplasty with reanastamosis (although many go straight to
IVF), or uterine factors (cut synechiae, remove polyps, etc)

Male factor infertility (35%)


Check semen analysis. Avoid tight underwear, saunas, hot tubs, excess radiation / heat / some meds /
steroids / marijuana /etc.
Normal semen: > 2mL, pH 7.2-7.8, > 20 million / mL sperm with > 30% normal forms, > 50% with forward
progression (motility), < 1 million WBC / mL
Can use ICSI if low sperm density or impaired motility
Unexplained etiology (10%)
Often try IVF ICSI donor sperm
If no cause found, some studies suggest that therapy has no higher success than no treatment at all - 60%
eventually become pregnant over 3-5 years no matter what.
Problem

Try

Absent or infrequent ovulation


(PCOS, mild hypothalamic amenorrhea)

Clomid
Letrozole

Pituitary gland not making LH/FSH, or bfails

Human menopausal gonadotrophin

Really bad hypothalamic amenorrhea

Recombinant GnRH

Poor sperm motility, low sperm count

ICSI

Azoospermia

Donor sperm

Ovarian failure (advanced maternal age or PMOF)

Donor egg

Complications:
Multiple gestations
Ovarian hyperstimulation syndrome (OHSS) - ovarian enlargement, can lead to torsion / rupture, can be
complicated by ascites / pleural effusion / hemoconcentration / hypercoagulability / renal failure / even
death
Preimplantation genetic diagnosis: evaluate embryo for genetic abnormalities before implanting into uterus
e.g. for pt with hx of Huntingtons, sickle cell, etc
Preimplantation genetic screening: screen for conditions, usually chromosomal, screening for aneuploidy
e.g. for advanced maternal age, etc.

Vulvar / Vaginal Neoplasia


Preinvasive Vulvar Disease: either squamous (VIN) or nonsquamous (Paget / melanoma in situ)
VIN: cellular atypia within epithelium. VIN I/II/III based on depth of involvement.
Risks: HPV 16/18 associated (if younger pt, HPV associated, faster / more aggressive; if older
often not HPV-associated and slower moving), also smoking / immunocompromise.
Dx: many asx & picked up on exam, also pruritis / irritation / dysuria. PE: flat or raised, red or
white or pigmented, can be multifocal. Need colpo to look for additional lesions
Management: get bx to look for invasion; if no invasion, wide local excision with split-thickness
skin graft afterwards. Can also do laser vaporization - but bx first, since no tissue left behind.

If younger, can try 5-FU / imiquimod to preserve anatomy, but cant be invasive and need
to follow up closely (lower effectiveness)

If older, may chose vulvar vulvectomy

Close follow up (1/3 will recur) - colpo q6mo x 2y then annually


Paget disease of vulva: rare, intrapithelial neoplasia a/w coexistent adenocarcinoma
Dx: chronic inflammatory changes (hyperemia, well demarcated thickening / excoritation), often
velvety red lesions white plaques after chronic itching 2/2 pruritis. Most common in pts > age
60 with vulvar pruritis / vulvodynia
a/w breast cancer (although not as much as paget disease of breast),
May be confused with lichen sclerosis, although paget disease has more hyperkeratotic
appearance and doesn't respond to steroids.
Tx: wide local excision but high recurrance rate; fatal if spreads to LNs
Melanoma should be on DDx as well; often p/w invasion.
Vulvar cancer
Most commonly squamous cell carcinoma, also melanoma / BCC / soft tissue sarcomas
Most lesions unifocal on labia majora, can have varied appearance. Mostly older women (65 is avg age).
Spreads via lymphatics & direct extension
Risk factors: menopause, smoking, VIN/CIN, HPV, immunocompromise, hx cervical cancer
Tx if bx proven - need radical vulvectomy and bilateral inguinal lymph node dissection.
If microinvasive (bx of small (<2 cm), well-differentiated lesion, with invasion <1.0 mm), then
and only then can you consider wide local excision.
If metastatic, use pelvic radiation as adjunct.
If melanoma, dont do lymphadenectomy (if metastasized, high mortality).
Vaginal Cancer
VAIN is premalignant form; classified I-II-IIII (III = > epithelium thickness)
A/w CIN, cervical cancer, condylomas, HPV, etc. (majority have neoplasia / Ca of vulva/cervix)
Dx: Almost always asymptomatic but can have some spotting or discharge; picked up on Pap

Consider if persistent abnormal Pap but no neoplasia on cervical bx

Bx the lesions!
Tx: local excision.

If invasion ruled out, can try laser vaporization or 5-FU (esp if multiple lesions or
immunocompromised)

Get close follow up with colpo


Vaginal cancer: mostly SCC; adenoCa / sarcoma / melanoma less common.

Consider clear cell adenocarcinoma if hx of in utero DES exposure


Usually posterior wall, upper vagina; spreads via lymphatics or hematogenous
Mostly older women > 60
Dx: postmenopausal bleeding / postcoital spotting / watery or bloody discharge.

Often may be diagnosed on Pap


W/U and staging: CXR, cystoscopy, sigmoidoscopy, IVP for local invasion
Tx:

Small in upper vagina surgical resection

Large (>2cm) or in lower vagina or stage III/IV radiation therapy alone

If adenocarcinoma, treat similarly.

Cervical Neoplasia / Cancer


Pap smears - timing
Start at age 21 regardless of sexual hx (ACOG 2009)
If ascus and under 20 (who knows why they got a pap) repeat in 12 mo.
Women from ages 21 to 30 be screened every two years instead of annually, using either the standard Pap
or liquid-based cytology.
Women age 30 and older who have had three consecutive negative cervical cytology test results may be
screened once every three years with either the Pap or liquid-based cytology.
Women with certain risk factors may need more frequent screening, including those who have HIV, are
immunosuppressed, were exposed to diethylstilbestrol (DES) in utero, and have been treated for cervical
intraepithelial neoplasia (CIN) 2, CIN 3, or cervical cancer.
If total hysterectomy for benign condition, no more PAPs.
If supracervical hysterectomy & still have cervix - regular Paps
Defer Pap smear if bleeding present (messes up results)
Pap results & futher workup
ASC - many have severe dysplasia.
ASC-US - reflex HPV testing. If positive, then colpo. If not then repeat Pap in 1 year
ASC-H or LSIL / HSIL or atypical glandular cells get colpo! Dont bother with HPV.
Colpo results
Worrisome: acetowhite changes, mosaicism, punctations, atypical vessels biopsy these!
Path results:
CIN I = repeat cytology q6mo x 2 or repeat HPV testing in 1 year
CIN II / III: treat with surgical excision (LEEP > cold knife cone)
After colpo, need to do a cone / Leep excision if adenoCa in situ, positive endocervical curretage (LSIL,
HSIL, etc), unsatisfactory colpo (cant visualize entire transition zone, etc), or big discrepancy between
Pap & bx results (e.g. HSIL on Pap, then normal colpo need excision!)
LEEP complications: cervical stenosis, insufficiency, infection, bleeding.
CIN

Disordered growth & development, starting at basal layer.


Most commonly during menarche and after pregnancy (more metaplasia) metaplasia of transition
zone

HPV 16/18/31/45 are high risk types - get em Gardasil


Other risk factors: cig smoking, immunodeficiency (HIV)

Cervical cancer: 80% SCC, most of rest is adenoCa (think clear cell adenoCa with DES exposure in utero)
High risk serotypes, immunosuppression, etc (cervical cancer = HIV-defining illness)
Dx: usually asx (need to screen with Paps!). Can have postcoital bleeding, see mass on spec exam, etc
Cancer can only be diagnosed with tissue bx, not with Pap!
Staging is clinical (only GYN cancer with clinical staging) - look for invasion to adjacent structures /
metastasis (EUA, CXR, cystoscopy, proctoscopy, IVP, barium enema).
MRI / CT cant be used for staging; also, staging doesnt change based on operative findings
Stage I: confined to cervix
Stage II: beyond cervix but not to lower vagina or pelvic sidewalls
Stage III: to pelvic sidewalls or lower of vagina
Stage IV: beyond pelvis, or into bladder/rectum, or distant mets
Treatment:
If preinvasive / microinvasive (stage I-Ia) simple hysterectomy

consider cold knife cone if fertility highly desired


If early (stage Ia-2 to IIa) radiation or radical hysterectomy + bilat LN dxn

Includes parametria, upper vaginal cuff, uterosacral / cardinal ligaments, vascular supply

Decision based on age, ability to tolerate surgery, ?nearby rad facilities

If young, may lean towards surgery (keep ovaries!0


If advanced (IIb-IV), treat with chemoradiation (cisplatin-based + internal & external rad)
If recurrent, can treat with pelvic exenteration & get 50% survival
Palliation: cisplatin chemo and/or palliative radiation

Endometrial Cancer
#1 common / curable GYN cancer in USA
Risk factors: unopposed estrogen (obesity, chronic anovulation, nullip, late menopause, exogenous
unopposed estrogen, early menarche, tamoxifen use), also HTN / DM, HNPCC, breast Ca hx, BRCA 1
Protective: OCPs, combination HRT, high parity, pregnancy, physical activity, smoking (weird.
Subtypes
Younger women: type I, estrogen-dependent, more favorable prognosis.
Older thin white women: type II, non-estrogen dependent, less favorable
Most are endometriod adenocarcinoma, with complex atypical hyperplasia as precursor
Extension is direct to cervix / outward through myometrium lymphatics eventually; heme less common
Grade is most important prognostic factor
Sx: postmenopausal / abnormal vaginal bleeding. can also see pelvic pain / mass / wt loss if advanced
Dx: endometrial biopsy D&C (if suspicious findings on EMB)
Also get TSH, PRL, FSH as part of w/u; may also get CA-125 (if super high, maybe advanced), Pap
Pelvic U/S (postmenopausal should have endometrial stripe < 4-5mm).

Even if normal endometrial stripe & pelvic U/S, need to get tissue (EMB/D&C)
Staging:
Stage I: Ia limited to myometrium, Ib/c into myometrium
Stage II: cervical invasion
Stage III: into serosa / peritoneum / vagina / pelvic or periaortic LN

Stage IV: invades bowel / bladder, or distant mets


Treatment:
Stage I / II: TAH-BSO (get rid of ovaries less estrogen); may also need LN dxn and/or rads
Stage III / IV: TAH-BSO + radiation + pelvic / periaortic LN sampling
Advanced/recurrent: high dose progestins; ?chemo
Good 5 year survival!

Ovarian Tumors
Worry about pelvic mass if >8cm, solid or cystic+solid, nodular, multilocular, + doppler flow, bilateral
3 categories: epithelial, germ cell, or stroma.
Metastatic - usually GI tract (Krukenberg), breast, endometrium
Usually spreads via direct exfoliation; can be lymphatic too, more rarely hematogenous
Epithelial tumors (65-70%)

Germ cell tumors (15-20%)

Sex cord stromal (5-10%)

20+ years (esp older)

0-25+ years

All ages

Serous cystadenocarcinoma,
mucinous, endometriod, clear cell,
Brenner, undifferentiated

teratoma, dysgerminoma, endodermal


sinus tumor, choriocarcinoma,
embryonal carcinoma

Granulosa-theca cell tumors,


Sertoli-Leydig cell tumors,
fibromas

Epithelial: #1 most common


Thought to be 2/2 chronic uninterrupted ovulation malignant transformation
Early menarche, infertility, late menopause, nulliparity, delayed childbearing, increasing age
OCPs are protrective (50% if on OCP x 5yrs), also tubal ligation / hysterectomy
10-15% have familial syndrome (e.g. BRCA 1>2 or HNPCC)
Sx: asx or vague, nonspecific complains (lower abd pain, bloating, distention, early satiety, other GI sx,
urinary frequency / dysuria / pelvic pressure when more advanced, ascites if later)
PE: fixed, solid, irregular pelvic mass +/- ascites. Met to umbilicus = Sister Mary Joseph nodule.
Dx: Pelvic U/S; CT/MRI can be helpful too, then look for mets / other primaries (barium enema, IVP, etc)
Get a CA-125. If wondering about other types of tumors, alpha-fetoprotein, LDH, hCG too.
Staging: surgical (TAHBSO, omentectomy, peritoneal washings, Pap smear of diaphragm, sampling of
pelvic / periarotic lymph nodes).
Many present in stage III/IV (2/2 vauge symptoms) and 5-yr survival low.
Goal is optimal debulking (no tumor > 1cm left behind)
Usually do adjuvant carboplatin + paclitaxel

If optimal debulking achieved, can do intraperitoneal chemo if tolerated.


Most common type: serous cystadenocarcinoma, but types can vary from borderline to high malignancy
CA-125 elevated in 80% epithelial tumors - not for screening, but to track tx / recurrence
Can also get CT scans to follow serially
Germ Cell
Most grow rapidly, limited to one ovary, stage I at time of diagnosis, curable! 95% benign
Sx: capsule distention pain, hemorrhage, necrosis acute pelvic pain; can also torse / rupture

Type

Differentiation

Notes

Dysgerminoma

No differentiation
(totipotent)

Most common malignant germ cell tumor


LDH
Uniquely radiosensitive! but still do chemo (better fertility)

Embryonal
carcinoma

Starting to differentiate
towards one of below

Endodermal sinus Differentiation:


Extraembryonic (yolk sac)
tumor
Choriocarcinoma

Teratoma

AFP

Differentiation:
Trophoblastic (placental)

Differentiation:
Embryonic (fetal)

Marker

hCG
Benign cystic mature teratoma = dermoid cyst = most
common germ cell tumor! Cystic, has skin / hair / teeth /
etc
Do a cystectomy for definitive dx & to r/o
malignancy!
Immature teratoma = malignant version

Treatment:
for benign tumors (mature teratomas) cystectomy or oophorectomy
for malignant tumors, unilateral salpingo-oophorectomy if fertility desired, or TAH/BSO
everything except stage IA dysgerminomas / immature teratomas gets multiagent chemo

Usually BEP = bleomycin, etoposide, cisplatin=Platinol

Can follow response with tumor markers


Dysgerminomas are uniquely radiosensitive - but often still do combo chemo to protect fertility

Sex cord-stromal tumors


Generally low grade, dont recur, usually unilateral
Treatment with unilateral sapingooophorectomy
No role for chemo or radiation in these tumors

Granulosa-Theca cell tumors are #1 (70%), can happen at any age


Functional: can make lots of estrogens endometrial hyperplasia, cancer 2/2 stimulation!
See Call-Exner bodies (pathognomonic) - with grooved coffee-bean nuclei
Sx: can cause precocious puberty, feminization, menstrual irreg, secondary amenorrhea,
postnemopausal bleeding 2/2 high estrogen.
Dx: high estradiol, inhibin A/B.

Sertoli-Leydig cell tumors are more rare; mostly in women < 40


Like the ovary grew a little pair of testicles: making androgens
Sx: see virilizing effects (breast atrophy, hirsutism, deepend voice, etc) + oligo / amenorrhea.

Ovarian fibroma: derived from mature fibroblasts, not functional


Can be a/w ascites: tumor + ascites + right hydrothorax = Meigs syndrome

Fallopian tube cancers: really rare, usually adenocarcinoma,


Behave like ovarian cancer (peritoneal spread, ascites)
More frequently in caucasians, BRCA , nullips, infertility
Usually asymptomatic
(classic = Latzkos triad, profuse watery discharge + pelvic pain + pelvic mass but only in 15%)
hydrops tubae profluens (intermittent hydrosalpinx) = spontaneous or pressure-induced
watery / blood tinged vaginal discharge that makes abdominal mass shrink
W/U: Pelvic U/S, CA-125 can be up, cervical cytology rarely shows malignancy
Usually dx @ surgery (since so rare); stage surgically
Treat like epithelial ovarian carcinoma (TAHBSO,omentectomy, cytoreduction, peritoneal sampling,
LN sampling, etc) and then carboplatin + paclitaxil

Gestational Trophoblastic Disease


From abnormal proliferation of placental = trophoblastic tissue (unique - fetal origin)
make hCG (tumor marker; for dx & following progression)
Remember hCG has common alpha subunit with LH/FSH/TSH

can result in theca lutein cysts, hyperthyroidism, early PEC, hyperemesis


Malignant versions very chemosensitive (really curable; can preserve fertility)
Benign GTD = molar pregnancies = hyatidiform moles
Highest in Asian women esp Japan (1/500!); extreme age, prior GTD; nullips are big risk factors too
Dx: sx as described above, bleeding + early PEC, hyperthyroidism, etc.
PE: Uterus S>D; may see grape like clusters at os, palpate big theca lutein cysts
Pelvic U/S: snowstorm pattern
Definitive dx: pathologic examination

Complete / Classic Mole (90%)

Partial / Incomplete Mole (10%)

Genetics

46,XX (all paternal)

69,XXY (extra paternal set)

Pathology

No coexistent fetus / fetal RBC


Hydropic (swollen, grape like) villi

Yes coexistent fetus / RBC


No hydropic villi

Presentation

No embryo
Presents with abnormal vaginal bleeding
Classic sx* common
Uterus S>>D
Theca lutein cysts in 25%

Yes embryo
Presents like missed Ab
Classic sx rare
Uterus S=D
Rare theca lutein cysts

hCG really high (>100,000),


takes 14 wks to normalize

hCG slightly elevated,


takes 8 wks to normalize

15-25% nonmetastatic malignancy


4% metastatic malignancy

2-4% nonmetastatic
not metastatic

Malignant?

*hyperemiesis gravidarum, early PEC, hyperthyroidism, anemia, really big uterus S>>D

Treatment: IMMEDIATE D&C followed by IV oxytocin


Get baseline hCG first; Rh status to see if RhoGAM needed, CXR optional(?)
May need antiHTN meds if preeclamptic
May need beta blockers (propranolol) if thyroid storm
May do hysterectomy if done childbearing

Prognosis: 95-100% cure rate; 15-25% persistent disease


so follow up closely with serial hCGs until negative x 3 consecutive weeks, then monthly
prevent pregnancy during the followup (otherwise cant monitor hCG) with OCPs!!

Malignant GTD
Types
Persistent / invasive moles (75%)

Arise after evacuation of molar pregnancy: hydropic villi / tropoblasts invade myomet.

Rarely metastasize; can regress spontaneously

Dx: plateauing / rising hCG after tx for molar pregnancy, can have uterine bleeding

Tx: single agent chemo (MTX / actinomycin D) if low risk, multiagent if high risk

Choriocarcinoma (25%)

Pure epithelial tumor; sheets of anaplastic cytotrophoblasts without villi.

Tissue diagnosis is the standard in establishing a diagnosis of most all malignancies, with
the exception of choriocarcinoma. Only a positive beta-HCG in a reproductive-aged
woman who has a history of a recent pregnancy (term, miscarriage, termination, mole)
is necessary to establish the diagnosis

Malignant, necrotizing, arises weeks/years after pregnancy

Often metastatic, can spread hematogenously (lungs / vagina / pelvis / brain / liver / GI)

Present with late postpartum bleeding or irregular bleeding years later


Mets to lungs cough, resp distress, hemoptysis

Get hCG, CBC/coags, pelvic U/S (doppler really vascular), CXR/chest CT for lungs,
abd/pelvic CT or MRI to look for mets as well.

Tx: single agent chemo / multiagent chemo depending on prognosis

PSTT (really rare) = placental site trophoblastic tumors

Arise from placental implantation site; no villi, intermediate trophoblasts proliferating

Persistent irregular vaginal bleeding + big uterus

Chronic low levels of hCG (no syncitiotrophoblasts proliferating)

Treat with hysterectomy multiagent chemo 1 week later to prevent recurrence

Malignant GTD in general:


Metastatic if beyond uterus; bad prognosis if metastatic and bHCG > 40,000, duration > 4mo, mets
to brain or liver, chemo failure, GTD after a term pregnancy

Staging not clinically useful


Really chemosensitive - NO ROLE FOR SURGERY unless high risk or PSTT
Follow bHCG

Breast Disease & Breast Cancer


Nerves around the breast / injuries
intercostobrachial nerve through axilla; sensory to upper medial arm
long thoracic nerve (C5-7) serratus anterior (winged scapula)
thoracodorsal nerve latissimus dorsi
SBE: monthly 5d after menses, CBE: yearly
Mammograms:
Should have yearly mammogram starting at age 40; continue as long as the woman is in good health
No upper age limit!
If strong FHx breast cancer (mother or sister), mammogram screening 5 yrs earlier than youngest
family members diagnosis or 10 years if family member was premenopausal.
Breast pain (mastalgia / mastdynia)
If cyclic, can be 2/2 PMS, normal hormonal fluctuations, fibrocystic change
If no signs of malignancy and really low risk, reassure NSAIDs, support bra, warm compresses
Consider U/S if hx trauma or mammogram if higher risk for cancer
Nipple discharge: mostly normal physiologic
DDx
Worrisome: spontaneous, bloody / SS, unilateral, persistent, from single duct, a/w mass
Bloody: think intraductal papilloma / invasive papillary cancer
Galactorrhea: think pregnancy, pituitary adenomas, hypothyorid, stress, OCPs/antiHTN/antipsychotics
Serous: think normal menses, OCPs, fibrocystic change, early pregnancy
Yellow-tinged: think fibrocystic change, galactocele
Green, sticky: think duct ectasia
Purulent: think breast abscess
Breast masses
Never dismiss a mass just because mammogram is negative
Think malignant if firm, nontender, poorly circumscribed, immobile
W/U: get U/S for women < 30, mammogram for women > 30
If concerning on imaging or exam, get tissue

Cystic aspirate ; excise cyst if bloody fluid or persistent

Solid
fine needle aspiration if < 30 excisional bx if FNA fails, or nondiagnostic
core needle biopsy if > 30

Nonpalpable excisional bx under needle / wire guidance

Benign breast disease

Fibrocystic change:
Painful breast masses that are multiple / bilateral, hormonal response, fluctuates in cycle
Peak incidence in women 30-40 years old

Treat with less caffeine, tea, chocolate (controversial), avoiding trauma, using support bra
Not associated with increased cancer risk
Fibroadenoma
Benign tumor with glandular / stromal components
Usually solitary but can be bilateral; rubbery / nontender, can change during cycle
Peak incidence in women 20-35 years old
Classic fibroadenoma in a woman < 30 may be only solid breast mass not requiring tissue dx

Follow clinically if stable!


If concerned, get FNA for cytology to r/o cancer or phyllodes tumor, or excise if large/bothersome
Cystosarcoma phylloides:
rare variant of fibroadenoma; any age but mostly premenopausal women
large, bulky, mobile mass, smooth, well circumscribed, grows quickly
most benign but may degenerate; need to make pathologic dx after wide local excision with 1cm
margin; if really big simple mastectomy
Intraductal papilloma:
benign solitary lesion from epithelial lining of lactiferous ducts; rarely degenerate into malignancy
#1 cause of bloody nipple discharge in absence of mass

but send S/S discharge for cytology to r/o invasive papillary carcinoma
Tx: excise involved ducts.
Mammary duct ectasia:
Subacute inflammation of ducts dilation inflammation
Usually at or after menopause
Nipple discharge, noncyclic breast pain, nipple retraction, often bilateral
Get mammogram / excisional bx to r/o carcinoma

Malignant breast disease:

Risks: increasing age is big one, also personal hx, first degree family hx, esp higher if family member
premenopausal or male, BRCA , ionizing radiation at young age (Hodgkin lymphoma), atypical ductal or
lobular hyperplasia on bx.
Survival rates similar for pregnant / lactating women with breast cancer.
OCP use - no evidence of risk factor.
Dx: often SBE / CBE / mammmo; masses / skin change / dimpling; bloody discharge should be ruled out
50% of tumors in upper outer quadrant.
Mets: to bone, liver, lung, pleura, brain, LNs

Noninvasive disease:
Lobular carcinoma in situ (LCIS) - neoplastic epithelial cells in breast lobules without invasion of stroma
multicentric & bilateral; often picked up incidentally on bx for another finding (cant see on
mammograms and cant palpate on PE)
premalignant lesion - 25-30% risk of invasive breast cancer w/in 15 yrs in either/both breasts
Tx: Observe only; may consider SERM to decrease risk - otherwise close followup
Ductal carcinoma in situ (DCIS) - malignant epithelial cells in mammary ducts, not stroma
Higher capacity to progress to outright invasive ductal cancer in same site
Mammogram clustered microcalcs +/- palpable mass
Dx: needal localization bx or excisional bx if palpable

Tx: surgical excision of all microcalcifications with wide margins

May need simple mastectomy if extensive only

Invasive disease:
Types
Infiltrating ductal carcinoma (70%) - from ductal epithelium, usually unilateral
Invasive lobular carcionoma (10-20%) - from lobular epithelium, often bilateral
Paget disease of nipple (1-3%) - often with DCIS / invasive carcinoma in subareolar area

Malignant cells invade nipple epidermis eczematous changes w/ scaling, erosion, etc.
Inflammatory breast carcinoma (1-4%) - really aggressive, poorly differentiated

Dermal lymphatic invasion peau dorange


Treatment:
Modified radical mastectomy or [lumpectomy + radiation] but need to be able to get rads

Get sentinel LN biopsy

Breast reconstruction afterwards


Hormone status: ER/PR+ = better prog, HER2/neu = worse prognosis

If ER+, usually use tamoxifen x 5 yrs; letrozole / anstrozole (aromatase inhibitors) even
better if postmenopausal (most estrogen coming from fat!)
Remember tamoxifen predisposes to endometrial cancer!

If HER2/neu+, may try trastuzumab (mAb vs HER2/neu)


Metastatic / recurrent

ER-: combo chemo

ER+:
consider oophorectomy / GnRH antagonists if premenopausal,
consider tamoxifen / aromatase inhibitors if postmenopausal
Systemic adjuvant chemo along with hormonal therapy if indicated often used
Prognosis: stage is #1 predictor, also ER/PR status and lymph node status
F/U:
PE q3-6mo x 3y, then space to q6mo x 2y, then q12mo
Mammogram @ 6mo, then annually
Avoid HRT

Other random stuff


Postop nerve problems
Low transverse incision: can damage the iliohypogastric or ilioinguinal nerves (both pass through
psoas and then go through transversus abdominus to anterior abdominal wall, where they run between
internal and external oblique. At risk if low transverse incision extended beyond lateral border of rectus
mm.
Iliohypogastric provides cutaneous sensation to the groin and the skin overlying the pubis.
Ilioinguinal provides cutaneous sensation to the groin, symphysis, labium and upper inner thigh.