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: don’t 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, don’t 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 won’t 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 ⅔ chance of being a carrier.
● Example: Dad’s brother has sickle cell disease. Neither parent has been checked. Dad has ⅔ 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 Bart’s (4 gammas)
○ 3 genes: HbH disease → beta chains build up, oxidative damage → destruction, Hb electrophoresis
shows Hb barts & HbH (beta tetramers), bart’s 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 isn’t)

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 1 2 3
Position Posterior Intermediate Anterior -
Consistency Firm Intermediate Soft -
Effacement 0-30% 31-50% 51-80% >80%
Dilation 0 cm 1–2 cm 3–4 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). Don’t 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: can’t 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 doesn’t 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: don’t do tocolysis unless there’s 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

Tachycardia, H/A, anxiety increases ATP → cAMP

Ritodrine*
Beta-mimetics Pulmonary edema Ritodrine = continuous IV
Terbutaline
Contraindicated in diabetes Terb = load, then q3-4h

Flushing, H/A, fatigue, diplopia

No evidence that it
Lose DTRs (<10), respiratory depression,
Mag sulfate actually delays anything
hypoxia → cardiac arrest (>15)
Ca+ antagonist
Contraindicated in myasthenia gravis

Ca-channel
Nifedipine H/A, flushing, dizziness
blockers

Don’t use close to term (PDA closure)

Prostaglandin Also pulm HTN, oligo 2/2 renal failure,
Indomethacin NSAIDs - block COX
inhibitors increased risk necrotizing enterocolitis &
intraventricular hemorrhage
* 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, Leopold’s, 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 can’t 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),
Wood’s 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 baby’s
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 placenta’s 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 there’s 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 dx’d 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. Don’t 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, TMP-
SMX, 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. Can’t 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 doesn’t 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 can’t 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 don’t cross placenta, so if baby has ‘em they’re infected)
● PCN is the only treatment - desensitize and treat with PCN if allergic!!
● Later manifestations: CN VIII deafness, saber shins, mulberry molar, saddle nose, Hutchinson’s 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 doesn’t 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 (won’t 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

● Grave’s disease: tx with PTU or MMI (depends on practitioner, PTU is classic but more using MMI now)
● Hashimoto’s: 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 doesn’t 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 won’t 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
A limp limbs flexed active movement
(Muscle tone)
Pulse
P absent < 100 /min > 100 /min
(heart rate)
Grimace cough or sneeze (nose)
G (response to smell or foot absent grimace cry and withdrawal of foot (foot
slap) slap)
Appearance body pink
A blue pink all over
(color) extremities blue
Respiration irregular
R absent good strong cry
(breathing) weak crying

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 won’t 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 (don’t 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 salt-
wasting, 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, can’t 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

Symmetric white, thinned skin on

labia / perineum / perianal. Labia
minora shrink, stick together. Does
Lichen sclerosis
not involve vagina. Caucasian
premenarchal girls and
postmenopausal women.
Usually asx; occ.
pruritis/dyspareuni High potency topical steriods
a. From (clobetasol) 1-2x/d x 6-12 wks
itch/scratch cycle.

Localized thickening of vulvar skin

Squamous cell 2/2 edema Chronic pruritis, Medium potency topical steroids x
hyperplasia Raised white lesion on labia thickened skin 4-6 wks
majora / clitoris
 Shiny, flat, purple papules on inner Pruritis with mild
Vaginal hydrocortisone
labia majora, vagina, vestibule with inflammation to
suppositories; may need surgery /
lacy reticulated pattern; can erode, severe erosion,
dilators for adhesions.
Lichen planus can have vaginal adhesions → remissions /
stenosis. Also on hair-bearing flares, burning,
If postmenopausal, estrogen for
skin/scalp (can → alopecia), oral contact bleeding,
atrophy.
mucous membranes dysparunia.

Thickened white epithelium,

Medium potency topical steroids,
Lichen simplex unilateral usually, well Pruritis, often
antihistamines for itching
chronicus circumscribed, excoriation, worse @ night
Get vulvar bx to r/o badness
lichenified

Red, moist lesions, sometimes scaly,

Vulvar psoriasis a/w scalp / axilla / groin / trunk Asx or occ. pruritis UV light or topical steroids
lesions

Palpable red glandular spots, Asymptomatic

get Bx to r/o adenocarcinoma.
Vaginal adenosis patches on upper ⅓ vagina on A/w DES exposure
Follow (serial exams)
anterior wall in utero.

● 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
● Skene’s gland cyst (near urethral meatus) -
● Bartholin’s 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 bartholin’s 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.
● Gartner’s 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 ⅓ 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 doesn’t 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
don’t 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 - don’t 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. Shouldn’t 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 don’t 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 it’s toxin-mediated, doesn’t shorten
current infection’s 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 ⅔ 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 What’s prolapsing? Notes / Specific Surgical Treatment

Cystocele: anterior colporrhapathy (remove excess anterior vaginal

Anterior Cystocele, urethrocele
mucosa, plicate endopelvic fascia to resuspend bladder)

Rectocele: posterior colporrhopathy (similar to above, but rectal

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

Vaginal hysterectomy + McCall culdoplasty (plicate uterosacral

Top Uterus
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)
(collapsing after
Abdominal sacral colpopexy: use mesh, attach vaginal apex to sacrum
hysterectomy)
(abdominal approach)

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:
Sx on exertion or
Pelvic relaxation & ● Use sling if hypermobile & intrinsic sphincteric
straining (cough / deficiency combined
urethral
laugh / exercise)
Stress hypermobility, can also ● Use retropubic urethropexy if stress incontinence
be due to intrinsic for hypermobility alone (sling can be obstructive as
Cotton swab test for
sphincter deficiency well - higher rate of retention, voiding dysfunction).
hypermobile urethra
● Use urethral bulking if stress incontinence for
intrinsic sphincteric deficincy alone

Alz dz, stroke, Parkinson’s, MS, diabetes → no central

Involuntary urine inhibition of detrusor contraction
Detrusor overactivity
loss with sudden
Urge urgency whether or Start tx with bladder training, Kegels, behavior
Most is idiopathic; also
not bladder is full; Med tx: anticholinergics (oxybutynin), smooth muscle
with CNS injury
frequency & nocturia relaxants (detrol / tolterodine).
No role for surgery in urge incontinence

Mixed symptoms of Both stress & detrusor imipramine (TCA) especially good if mixed incontinence
Mixed
above activitity (both anticholinergic & alpha-adrenergic)

Meds:
● Reduce urethral closing pressure (prazosin,
Poor / absent bladder
Frequent / constant terazosin, phenoxybenzamine)
contractions (or more
Overflow dribbling, also stress / ● Striated muscle relaxants (diazepam, dantrolene)
rarely obstruction) →
urge incontinence. ● Cholinergic agents (bethanecol) to increase
retention → overflow
contractility
Intermittent self-cathing used too.

Dx with indigo
carmine instilled into Urinary fistula after
Fix fistula (surgery)
Bypass bladder, then tampon. pelvic surgery or
Use abx for UTI / estrogen if postmenopausal / etc
Can use IVP / radiation, esp TAH
cystogram / etc too
 Nursing home,
Functional geriatrics, poor Can’t get to bathroom Fix social situation, psych consult, SW, etc.
mobility

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 1-
3d 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 (Crohn’s, appendicitis, myomectomy, other surgeries) - can’t 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 Asherman’s / 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 / you’re 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 can’t 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 17-
hydroxyprogesterone to build up (gets shunted down androgen pathway). Also don’t 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: Asherman’s, 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, Cushing’s, CAH, etc - get appropriate labs
● Others: Luteal phase defect (controversial), Turner’s 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 doesn’t 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 Clomid

(PCOS, mild hypothalamic amenorrhea) 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 Huntington’s, 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 can’t 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, don’t do lymphadenectomy (if metastasized, high mortality).

Vaginal Cancer
● VAIN is premalignant form; classified I-II-IIII (III = > ⅔ 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 ⅓ 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 ⅓ vagina → surgical resection
■ Large (>2cm) or in lower ⅔ 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! Don’t 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 (can’t 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 can’t be used for staging; also, staging doesn’t change based on operative findings
○ Stage I: confined to cervix
○ Stage II: beyond cervix but not to lower ⅓ vagina or pelvic sidewalls
○ Stage III: to pelvic sidewalls or lower ⅓ 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, teratoma, dysgerminoma, endodermal Granulosa-theca cell tumors,

mucinous, endometriod, clear cell, sinus tumor, choriocarcinoma, Sertoli-Leydig cell tumors,
Brenner, undifferentiated embryonal carcinoma 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 Marker

No differentiation Most common malignant germ cell tumor

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

Embryonal Starting to differentiate

carcinoma towards one of below

Endodermal sinus Differentiation:

AFP
tumor Extraembryonic (yolk sac)

Differentiation:
Choriocarcinoma hCG
Trophoblastic (placental)

Benign cystic mature teratoma = dermoid cyst = most

common germ cell tumor! Cystic, has skin / hair / teeth /
Differentiation: etc
Teratoma
Embryonic (fetal) ● 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, don’t 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 ½, nullips, infertility
● Usually asymptomatic
○ (classic = “Latzko’s 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 Yes coexistent fetus / RBC

Hydropic (swollen, ‘grape like’) villi No hydropic villi

Presentation No embryo Yes embryo

Presents with abnormal vaginal bleeding Presents like missed Ab
Classic sx* common Classic sx rare
Uterus S>>D Uterus S=D
Theca lutein cysts in 25% Rare theca lutein cysts

hCG really high (>100,000), hCG slightly elevated,

takes 14 wks to normalize takes 8 wks to normalize

Malignant? 15-25% nonmetastatic malignancy 2-4% nonmetastatic

4% metastatic malignancy not metastatic
*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 can’t 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 member’s 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 ½, 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 (can’t see on
mammograms and can’t 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 d’orange
● 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.