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Define 3 stages of labor

Labor - cervical changes and regular uterine contractions (firm, every 2-3 min, last up to 60 sec, nl intensity > 40 mm Hg and nl sum total of >200 montevideo units in 10 min interval)

1st stage - onset until full cervical dilation
A. latent - cervix effaces (thins) until dilation of 6 cm
- can be up to 20 hours in nulli, 14 hrs in multip
* if prolonged - NOT an indication for C-section, give pitocin

B. active - more rapid dilation until 10 cm; 1.2 cm/hr in nulli, 1.5 cm/hr in multip
* arrest of active phase if ROM with no progress for 4 hours (w ctx) or 6 hrs (w/out ctx) --> amniotomy, then C-section

2nd stage - 10 cm to delivery of baby
- 3 hours - nulli w epidural
- 2 hours - nulli w/out epi
- 2 hours - multip w epidural
- 1 hour - multip w/out epi
*MCC of arrested second stage is fetal malposition (optimal is occiput anterior); manage with operative vaginal delivery (forceps / vacuum)

3rd stage - delivery until placenta is delivered
- less than 30 min (if longer, try manual extraction)
- bloody show, uterus becomes firm and globular and rises in abdomen, and umbilical cord lengthens


Fetal heart rate monitoring - categories

Fetal heart rate monitoring

Category I - reassuring --> normal baseline and variability, no late or variable decelerations, reactive (2 accelerations of 15+ bpm that last for 15 seconds over a 20 min period)

Category II - represents majority; concerning but not ominous eg tachycardia w/out decelerations
- if minimal variability (non-reactive) - scalp stimulation should induce an acceleration (indicates normal umbilical cord pH >7.2)
- if nonreassuring - fetal scalp electrode to directly measure FHR

Category III - ominous - indicates hypoxia or acidosis e.g. absent baseline variability + recurrent late or variable decelerations, or sinusoidal HR pattern (indicates fetal anemia), or prolonged bradycardia
*indication for C-section if intrauterine resuscitation maneuvers do not work


When to do C-section
Cardinal movements of labor

NO trial of labor with:
- active herpes
- prior classical C-section with vertical incision
- prior abdominal myomectomy with uterine cavity entry
- placenta previa
- vasa previa
- HIV with viral load >1000
- transverse lie / breech presentation

Cardinal movements of labor - engagement, descent, flexion, internal rotation, extension, external rotation


Fetal orientation
1. Lie
2. Presentation
3. Posture / attitude
4. Position

Fetal orientation - can do Leopold maneuvers or U/S to determine

1. Lie - transverse, longitudinal, or oblique

2. Presentation
A. Long - cephalic (compound, face, brow, vertex, ideal) or breech (complete, frank, footlong)
B. Transverse - shoulder presents --> C-section
C. Incomplete - leg coming out

3. Posture / attitude - fetus folds so back is convex, arms crossed, necks flexed

4. Position - relationship of fetus to R or L side
- Vertex - occiput anterior e.g. ROA, OA, LOA ideal, malposition is OT or OP
- Face - chin --> must be mentum anterior for NSVD
- Breech - sacrum

*mentum posterior of cephalic face presentation --> will NOT deliver vaginally


Bishop score - components

Bishop score - >8 --> cervix favorable for spontaneous and induced labor

1. Dilation - how open the internal os of the cervix is
- 10 cm is fully dilated

2. Effacement - length of the cervix from internal to external os (normal is ~4 cm)
- 2 cm is 50% effaced
- as thin as lower uterine segment is 100% effacted

3. Station - relation of fetal head to ischial spines of pelvis
- level of pelvic outlet is +3 station

4. Consistency of cervix - firm, medium soft

5. Position of cervix - posterior, middle, anterior

*labor - cervix goes to soft and anterior


Differential and workup for anemia in pregnancy
1. Microcytic
2. Macrocytic
3. Normocytic

Anemia in pregnancy - Hb < 11 in 1st and 3rd trimesters, 10.5 g/dL in 2nd trimester (<12 in nonpregnant women)

1. Microcytic
A. iron deficiency - therapeutic trial of iron, recheck Hb in 3 weeks
- then evaluation iron stores, Hb electrophoresis

B. Hemoglobinopathies - do Hb electrophoresis
- B thalassemia minor - elevated HbA2 and HbF--> prophylactic folate
- A thalassemia - trait is normal eletrophoresis, ferritin; can have HbH or HbBart's
- sickle cell trait (50% HbS) vs disease (almost 99% HbS)

2. Macrocytic - vitamin B12 and folate deficiency --> MCC is folate

3. Normocytic
A. G6PD deficiency - triggered by nitrofurantoin, sulfa drugs --> jaundice, fatigue, bilirubinuria

B. HELLP - hemolysis, elevated liver enzymes, low platelets

C. Consider bone marrow process (leukemia) if other cell lines eg WBC, platelets also decreased
- do bone marrow bx

D. Anemia of pregnancy - increased demands for iron due to fetus need and expanded maternal blood volume (increase in plasma >> increase in RBC)


Uterine inversion
1. Risk factors
2. Etiology
3. What to do if it happens

Uterine inversion - need to deliver placenta within 30 min in 3rd stage of labor

1. Risk factors - placenta implanted in fundus, placenta accreta

2. Etiology - massive hemorrhage bc uterine atony --> myometrial fibers do not exert tourniquet on spiral arteries --> placental bed pours out blood

3. What to do if it happens - fluid resuscitation
- reduce the uterus
- if initial attempt is unsuccessful, use relaxation agents (halothane, terbutaline, mag sulfate) then try again to reduce the uterus
- then give uterotonic agents (e.g. oxytocin) to prevent it from coming out again
- if unsuccessful, laparotomy


Shoulder dystocia
1. Risk factors
2. Management
3. Complications

Shoulder dystocia - impaction of anterior shoulder behind symphysis pubis
*cannot be predicted or prevented in majority of cases

1. Risk factors - prior shoulder dystocia, fetal macrosomia, maternal gestational diabetes, maternal obesity, prolonged 2nd stage labor
- "turtle sign" - head retracts towards perineum

2. Mgmt - need to deliver < 5 min to avoid compression of umbilical cord
A. Maneuvers
- McRoberts (flex maternal thighs to straighten the sacrum and rotate symphysis pubis)
- apply suprapubic pressure (move fetal shoulder from AP to oblique plane)
B. Episiotomy
C. Fracturing fetal clavicle
D. Put infants head back in pelvis and C-section

3. Neonatal complications - 90% cases have none
- fractured clavicle or humerus (decreased Moro, intact biceps/grasp reflexes); hypoxia
- Erb palsy (C5-C6) --> Affects deltoid, infraspinatus --> arm internally rotated, pronated "waiter's tip sign"; most spontaneously recover
- Klumke Palsy (C8-T1) --> "claw hand" with absent grasp (intact Moro/biceps reflexes), Horner's syndrome
- maternal complication - PPH, vaginal lacerations


Umbilical cord prolapse
1. Risk factors
2. Management
3. Neonatal complications

*DDx for fetal bradycardia

Umbilical cord prolapse - cord protrudes through cervical os

1. Risk factors - unengaged fetal head (-3, -2, -1 station), footlong breech, transverse fetal lie
*engagement - largest diameter of fetal head has negotiated pelvic inlet (0 station)
*do not do AROM with unengaged presentation

2. Management -
- digital exam for cord through cervical os (pulsating)
- elevate the presenting part (trendelenberg)
- immediate C-section

3. Neonatal complications - sustained fetal bradycardia post AROM (<110 bpm for >10 min) --> take maternal pulse first to differentiate fetal pulse from mom's
- improve maternal 02 (100% face mask)
- place patient on side to move uterus from great vessels --> improve blood return
- IVF bolus
- stop oxytocin

*DDx for fetal brady --> cord prolapse, uterine rupture, uterine hyperstimulation 2/2 misoprostol


Uterine atony

1. Risk factors
2. Management
3. DDx

Uterine atony - myometrium does not contract to cut off uterine spiral arteries supplying placental bed "boggy uterus" --> MCC of early PPH (>500 cc blood loss in NSVD and >1000 cc in C-section)
*can exsanguinate in 10-15 min!

1. Risk factors
- magnesium sulfate (for preeclampsia)
- rapid OR prolonged labor/delivery
- prolonged oxytocin stimulation (hyponatermia, hypotension, tachysystole)
- chorioamnionitis
- high parity
- uterine overdistension (macrosomia, multis, hydramnios)

2. Management
- ABCs
- palpate uterine fundus --> if boggy --> oxytocin and bimanual massage
- uterotonic agents --> rectal misoprostol / Cytotec, ergot alkaloid eg Methergine (c/i in HTN), prostaglandin F2ef eg carboprost / Hemabate (c/i in asthma)
- if bleeding continues --> large bore IVs, foleys, blood; Bakri balloon, OR for embolization/ligation of uterine arteries or compression stitches (B-lynch) or hysterectomy

3. DDx - if there is PPH but uterus is firm --> Suspect laceration to genital tract


Postpartum hemorrhage - causes
1. Early
2. Late


1. Early PPH - <24 hours
- MCC is uterine atony
- genital tract laceration
- uterine inversion
- placenta accreta, increta, percreta (can do MRI to dx)
- retained placenta
- coagulopathy

2. Late - >24 hours
- subinvolution of placental state (~2 weeks PP) --> eschar falls off and leads to bleeding; give uterotonic agent
- uterine atony 2/2 retained products conception --> uterine cramping bleeding --> D and C
- infection eg endometritis - uterine fundal tenderness, fever, foul smelling lochia


Serum screening in pregnancy - first and second trimester

1. DDx elevated msAFP
2. DDx decreased msAFP
3. Serum levels associated with:
A. Trisomy 21
B. Trisomy 18
C. Trisomy 13
4. Mgmt

Serum screening: >2 MOM are considered elevated
- first trimester in weeks 11 - 14: PAPPA, bhCG, nuchal translucency
- second trimester screening in weeks 15-20:
---- triple screen - msAFP, estriol, bHCG
---- quad screen - msAFP, estriol, bHCG, inhibin A

1. DDx elevated msAFP - underestimating gestational age (MCC), multis, defects of skin, abd wall, or neural tube; olighydramnios, cystic hygroma, decreased maternal weight, fetal demise

2. DDx decreased msAFP - overestimation of gestational age (MCC), trisomies, molar pregnancy, increased maternal weight

3. Serum levels associated with:
A. Trisomy 21 - ↓ PAPPA, ↑ bhCG, ↑ Inhibin A, ↓ AFP, ↓ estriol
B. Trisomy 18 - ↓ PAPPA, ↓ bhCG, ↓ Inhibin A, ↓ AFP, ↓ estriol
C. Trisomy 13 (holoprosencephaly, cleft lip, polydacyly, club foot) - results are variable and not generally reported

4. Mgmt - do U/S to determine correct gestational age, look for multis or NT defects, exclude fetal demise


1. Monozygotic - timing of division and chorion/amnion
2. Dizygotic
3. Maternal complication
4. Neonatal complications

1. Monozygotic - timing of division and amnion (innermost placenta), chorion (outer membrane)
A. first 72 hours ie 3 days (morula) --> dichorionic / diamniotic
B. Days 4-8 (blastocyst) --> monochorionic / diamniotic
C. Days 8-12 (implanted) --> monochorionic / monoamniotic
D. After day 13 --> conjoined twins

2. Dizygotic - fertilization of two eggs by two sperms
- incidence ↑ with maternal age, fertility tx
- dichorionic / diamniotic

3. Maternal complication - preeclampsia, GDM, anemia, DVT, PPH, and C-section more common

4. Neonatal complications - preterm delivery, stillbirth, placenta previa
- twin-twin transfusion syndrome (TTTS - one twin has polyhydramnios, polycythemia and other has IUGR, oligohydramnios --> need laser ablation)


HSV infections
1. Primary infection
2. Nonprimary first episode infection
3. Recurrent infection
4. Mgmt in pregnant women with HSV
5. Neonatal herpes

HSV infections - HSV1 (labialis) and 2 (genitals) --> dx via PCR

1. Primary infection - no HSV Ab
- clinical: asx, local sx (burning, herpetic lesions), systemic sx (malaise, fever, n/v), can have urinary retention 2/2 lumbosacral neuropathy
- lesions last ~ 2 weeks

2. Nonprimary first episode infection - first infection HSV2 in pt who has IgG HSV1
- milder sx and less duration than primary

3. Recurrent infection - no systemic sx, lesions last ~9 days, usually with decreasing recurrence over time
- can also have asymptomatic viral shedding

4. Mgmt in pregnant women with HSV - offer oral acyclovir at 36 wks for pt with first episode or recurrence
- no lesions or prodromal sx --> NSVD
- lesions or burning/itching/tingling --> offer C-section

5. Neonatal herpes - encephalitis, herpetic lesions of eyes/skin/mucosa, or asx
- transmission MC due to asx viral shedding during primary or nonprimary first episode at term (mother has no HSV hx)


Antepartum bleeding
Risk factors, clinical presentation, and mgmt for:
1. Placenta previa
2. Placental abruption
3. Vasa previa

Antepartum bleeding - vaginal bleeding post 20 weeks gestation

1. Placenta previa - placenta < 2 cm from cervical os
A. Risk factors - multis, prior C-section, prior D and C, prior previa
- previa increases risk of placenta accreta
B. Clinical - postcoital spotting, painless vaginal bleeding
C. Mgmt - if preterm, pelvic rest and repeat TVUS at term; if there is still previa at term --> pelvic rest, C-section @ 34-37 weeks

2. Placental abruption - placenta detaches from uterus
A. Risk factors - HTN, prior abruption, short cord, trauma (eg MVA), cocaine use, submucosal leiomyomata, hydramnios, smoking, PPROM
B. Clinical - painful vaginal bleeding, Couvelaire uterus (bleed into myometrium), firm tender uterus
- blood clot adherent to placenta, can lead to coagulopathy (DIC) 2/2 hypofibrinogenemia
C. Mgmt - clinical diagnosis, US to r/o previa
- C-section, unless there is fetal demise --> vaginal delivery

3. Vasa previa - umbilical vessels cross internal os in front of fetal presenting part
A. Risk factors - velamentous cord insertion, placenta with accessory lobes, IVF babies, or multis
B. Clinical - sinusoidal FHR (due to fetal anemia) --> fetus can exsanguinate on ROM (abrupt sustained fetal bradycardia)
C. Mgmt -
- diagnose via color Doppler US (middle cerebral artery peak systolic velocity)
- Apt test for fetal nucleated RBCs (determine fetal vs maternal hemorrhage)
- C-section prior to ROM (~35 weeks gestation)


Ectopic pregnancy
1. Risk factors
2. Clinical
3. Mgmt

Ectopic pregnancy - embryo implants not in uterine lining, MC in fallopian tube ampulla

1. Risk factors - prior ectopic, IVF, IUD, prior tubal sx (adhesions), PID, endometriosis, DES-exposed, smoking

2. Clinical - triad: amenorrhea, unilateral pelvic or lower abdominal pain, irregular vaginal bleeding
- palpable tender adnexal mass
- bHCG does not increase appropriately (2x) after 48 hrs
- if ruptured - hypotensive, tachycardic, peritoneal, fever

3. Mgmt - do US (need bHCG > 2000 to visualize IUP)
A. If unruptured -- methotrexate
B. If ruptured (erodes through tissue --> hemorrhage from exposed vessels) -- pelvic US, stabilize (ABCs), and OR for ex lap to coagulate bleeding and resect ectopic
C. if stable and r/o ectopic -- can follow bHCG (should double every 48 hrs)


Spontaneous abortion
1. Risk factors
2. Clinical
3. Mgmt

Spontaneous abortion i.e. miscarriage - pregnancy that ends prior to 20 weeks gestation
- can be complete, incomplete (partial expulsion), inevitable (no expulsion but bleeding), threatened (normal but bleeding), or missed (no expulsion and not bleeding)

1. Risk factors -
- first trimester - due to abnormal chromosomes (most commonly autosomal trisomies due to failures in maternal gametogenesis)
- second trimester - due to infection, anatomic defects, exposure to teratogens, trauma

2. Clinical - vaginal bleeding, cramping, abdominal pain, decreased symptoms of pregnancy

3. Mgmt - give Rhogam if mom is Rh (-), use Kleihauer - Betke test to see how many fetal nucleated RBCs are to dose the rhogam
- threatened (normal pregnancy with bleeding) - pelvic rest
- incomplete, inevitable, missed - medical (misoprostol) or surgical (D and C or Dand E or inducing labor with pitocin and PGEs)
*need to r/o preterm labor and incompetent cervix in second trimester since they can lead to abortions

for patients w recurrent abortions --> check AP Ab (tx - aspirin + heparin), SLE, thyroid, DM, karyotypes


Incompetent cervix (cervical insufficiency)
1. Risk factors
2. Clinical
3. Mgmt

Cervical incompetence - painless dilation and effacement of the cervix, MC in 2nd trimester
*preterm labor is d,e with ctx

1. Risk factors - surgery e.g. D and C, LEEP, conization; uterine anomalies, DES exposure, hx of cervical lacerations with vaginal delivery

2. Clinical - lower abdominal cramping or contractions
- vaginal bleeding --> amniotic sac bulging through cervix --> exposure to vaginal flora --> fever / infection, vaginal discharge, ROM
* "funneled lower uterine segment" on U/S

3. Mgmt - do TVUS to look at cervix
- normal cervix and no hx PTL --> routine prenatal care
- short cervix (<2.5 cm) and no hx PTL --> vaginal progesterone
- normal cervix and hx PTL --> serial TVUS (q2wks) until 24 wks
- short cervix (<2 cm) and hx PTL --> cerclage at 12-14 weeks, serial TVUS (q2 wks) until 24 wks
* give betamethasone from 24 - 37 weeks


DDx for abdominal pain in pregnancy
A. Timing
B. Clinical
C. Mgmt

DDx for abdominal pain in pregnancy:

1. Appendicitis - any time, in RUQ (NOT RLQ), tx is surgery regardless of gestational age + abx

2. Cholecystitis - after 1st trim, RUQ dx via U/S, tx is surgery

3. Ovarian torsion - ~14 weeks or after delivery, acute onset n/v and colicky pain, see complex adnexal mass w/out Doppler flow on US
- tx - lap detorsion, cystectomy, or oophorectomy if necrosis

4. Ectopic - in 1st trim, u/l pelvic pain and spotting, track bHCG (<2x ↑ in 48 hrs), tx is methotrexate or sx

5. Ruptured corpus luteum (secretes E and P to maximize endometrial implantation) - in 1st trim, sudden onset lower abdominal pain + peritoneal signs
- U/S and laparoscopy show hemoperitoneum (pelvic free fluid)
- tx - hemostasis, cystectomy; need progesterone supplement if excised before 10 weeks gestation
*more common in bleeding d/o (vW, heparin)

6. Placental abruption - in 2nd and 3rd trims, crampy midline uterine tenderness and vaginal bleeding; tx - delivery


DDx for pruritus in pregnancy - clinical, mgmt
1. ICO

DDx for pruritus in pregnancy

1. Intrahepatic cholestasis of pregnancy (ICP) - generalized mild pruritus without lesions, worse at night
A. Clinical - in 3rd trimester, clinical dx of exclusion
- extremities (palms and soles) >> trunk
- normal labs initially but after several days of symptoms --> v high LFTs, ALP, Tbili - need to r/o viral hepatitis
- increased risk fetal demise with higher bile acid levels
B. Mgmt - 1st line is antihistamines, topical emollients, then ursodeoxycholic acid, delivery once fetal maturity achieved

2. Pruritic urticarial papules and plaques of pregnancy (PUPPP)
A. Clinical - pruritus and erythematous papules, begins on abdomen and spreads to thighs
- no lab abnormalities
B. Mgmt - topical steroids and antihistamines
- no adverse fetal/maternal outcomes


DDx for pruritus in pregnancy - clinical, mgmt
3. Pemphigoid gestationis
4. Acute fatty liver of pregnancy

3. Pemphigoid gestationis - pruritus followed by extensive patches of cutaneous erythema and then vesicles / bullae
A. Clinical - in 2nd trimester, autoimmune (IgG)
- limbs >> trunk
B. Mgmt - oral corticosteroids

4. AFLP - microvesicular steatosis
A. Clinical - RUQ pain, persistent nausea / vomiting, anorexia, progressive jaundice
- develops over weeks late in third trimester
- increased LFTs, Bili, clotting times
- decreased glucose, cholesterol, albumin, fibrinogen
- can lead to fulminant liver failure (hepatic encephalopathy)
B. Mgmt - delivery! high fetal mortality


Hypertensive diseases of pregnancy - define, clinical, mgmt
1. Gestational HTN
2. Chronic HTN
3. Superimposed preeclampsia

Hypertensive diseases of pregnancy - risk for maternal PPH, GDMA, placental abruption; for fetal IUGR, PTL, oligohydramnios

1. Gestational HTN - HTN w/out proteinuria at >20 weeks for at least 4 hours
- risk for IUGR, placental abruption
- deliver at 37 weeks

2. Chronic HTN - BP of 140/90 before pregnancy or <20 weeks, persisting more than 12 weeks postpartum
- antiHTN
- deliver 38-39 weeks

3. Superimposed preeclampsia - patient with chronic HTN that develops preeclampsia - new onset uncontrollable HTN, new onset proteinuria, or severe features


Hypertensive diseases of pregnancy - define, clinical, mgmt
4. Eclampsia

4. Eclampsia - preeclampsia + seizures
- most commonly occur in 3rd trimester just prior to delivery, labor, or 24 hrs postpartum
- seizures can cause posterior shoulder dislocation, death due to intracerebral hemorrhage
- tx - delivery via c-section
- give mag sulfate and monitor for side effects at >8 (1st sign is hyporeflexia, also pulm edema, somnolence, muscle paralysis) --> give calcium gluconate to counteract
- give IV labetalol to control HTN
*can get hypermagnesemia with renal insufficiency (lower dose with higher Cr - so monitor urine output)

5. HELLP - microangiopathic hemolytic anemia, elevated LFTs, low platelets; affects up to 1/5 women with preeclampsia
- n/v, RUQ pain (due to liver capsule distension)
- LFTs up to 1000s, patelets <100K
- due to abnormal placentation --> systemic inflammation --> activates coagulation / complement cascades
- tx - delivery, mag sulfate, antiHTNs

6. PRES - posterior reversible encephalopathy syndrome
- headache, seizures, visual disturbances
- dx via clinical and MRI (Vasogenic edema 2/2 breakdown of BBB)
- tx - antiHTN, antiepileptics, ICU dispo


Hypertensive diseases of pregnancy

A. Pathophys
B. Definition - severe features
C. Risk factors
D. Mgmt
i. Stable
ii. Severe features
iii. HTN emergency


A. Pathophys - to arterial vasospasm and endothelial damage --> hypoxemia, ↑ SVR, ↓ intravascular volume 2/2 third spacing, ↓ oncotic pressure
- typically presents in late third trimester

B. Definition - HTN >140/90 measured 2x 6 hours apart AND 1 of the following:
- new onset proteinuria (>300 mg over 24 hours or urine protein:cr >0.3) at 20+ weeks gestation

OR severe features:
- thrombocytopenia (plt <100K)
- ↑ LFTs (2x nl) or persistent RUQ pain
- AKI (Cr > 1 .1)
- pulmonary edema (sudden onset DOE, crackles, hypoxia)
- new onset visual or cerebral disturbance (headache, hyperreflexia)

C. Risk factors - nulliparity, young or old, black, prior preeclampsia or family hx, chronic HTN or CKD, antiphospholipid syndrome, DM, multis
*obesity is risk factor for gestational HTN and PEC

D. Mgmt
i. Stable, uncomplicated - expectant mgmt (dont need antiHTN), deliver at 37 weeks
ii. Severe features -
<34 weeks - mag sulfate, corticosteroids (betamethasone) over 24 hrs, assess status
>34 weeks - mag sulfate and deliver
iii. HTN emergency (SP>160 or DP>110 for 15+min) or severe features - give IV labetelol, IV hydralazine (if bradycardic and HTN), or oral nifedipine to lower BP and avoid stroke; improve oxygenation
*alpha methyldopa used to treat chronic HTN (slower onset)


Preterm labor (vs cervical insufficiency)
1. Risk factors
2. Assessing risk
3. Management
4. Tocolytics and side effects

Preterm labor - cervical change (2 cm dilated, 80% effaced) with contractions between 20 and 37 weeks
*vs cervical insufficiency which is painless dilation

1. Risk factors - *hx of prior*, PPROM, multis, hx cervical cone biopsy, cocaine, trauma, pyelo, gonococcal cervicitis, uterine anomalies (bicornuate), placental abruption

2. Assessing risk
- fetal fibronectin (after 20 weeks) - if negative, no delivery in the next week
- TVUS to look at cervical length measurement - <25 mm = increased risk

3. Management - if no c/i --> pts at >34 weeks can be managed expectantly
- steroids (betamethasone) for <34 weeks --> tocolytics, which extend gestation by 48 hrs so you can give 2 doses steroids
- 17OHprogesterone from 16 to 36 weeks in high risk women with prior PTL
- penicillin if GBS (+)
- mag sulfate (Ca2+ competitive antagonist, membrane stabilizer) for fetal neuroprotection for <32 weeks --> hyporeflexia, flushing, HA, diplopia, respiratory depression

4. Tocolytics - decreased Ca2+ --> fewer uterine smooth muscle contractions
A. ritodrine, terbutaline (B2 agonists) - smooth muscle relaxation but can cause anxiety, hyperglycemia, hypokalemia, hypotension tachycardia, pulm edema; c/i in diabetes and terbutaline dangerous if given >48 hrs
B. nifedipine (CCB) - headache, flushing, dizziness; c/i at > 34 weeks bc risk of maternal hypotension
C. indomethacin (NSAID blocks PGE -> decreased Ca) - c/i >34 weeks bc it closes DA and can cause fetal renal failure (--> oligohydramnios --> cord compression --> FHR variable decels)


1. Diagnosis tests for ROM
2. Risk factors
3. Management - based on GA (34 wks)
4. Complication - chorioamnionitis

PPROM - Preterm premature ROM prior to onset of labor at <37 weeks; prolonged if >18 hours

1. Diagnosis - gush of fluid from vagina with constant leakage
- pooling of amniotic fluid on speculum exam
- positive nitrazine test (alkaline changes of vaginal fluid)
- positive fern test (cervical mucus ferns under microscope)
- US shows oligohydramnios (single deepest pocket < 2 cm)
- Amnisure - tests placental alpha macrogolobulin 1
- tampon test - seeing if dye injected in amniotic fluid leaks into vagina

2. Risk factors - primary risk factor is genital tract infection (eg BV)
- also prior PPROM, smoking, conization, multis, hydramnios, placental abruption
- can lead to olighydramnios --> cord compression --> variable decels on FHR

3. Management - depends on gestational age
A. <34 weeks -
- no signs of infection --> abx, steroids, observe
- signs of infections --> abx, steroids, Mag (if <32), and deliver

B. > 34 weeks - delivery esp with fetal lung maturity (phosphatidyl glycerol in vaginal fluid)
- abx - ampicillin, erythromycin to prolong latency period

4. Chorioamnionitis --> maternal fever and 1+: fetal or maternal tachycardia, maternal WBC, uterine fundal tenderness, and/or malodorous vaginal discharge
- baby can be septic (pale, lethargic, high temp)
- tx - IV amp and gent and induce labor regardless of gestational age


Congenital intrauterine infections incl presentation, treatment:
1. Parvovirus
2. CMV
3. Toxo
4. Rubella

Congenital intrauterine infections (part of TORCHeS)

1. Parvovirus - fetal aplastic anemia (sinusoidal FHR), hydrops fetalis (excess fluid in 2+ fetal body cavities; caused by parvovirus), hydramnios
- mgmt - intrauterine transfusion, delivery

2. CMV - DNA virus, 90% of congenital CMV is asymptomatic but it is the MC congenital infection in the USA, MCC of retardation and deafness due to viral infection
- hydrops fetalis in first trimester
- microcephaly, periventricular calcifications, sensorineural hearing loss, chorioretinitis, seizures, blueberry muffin rash
- no treatment - prevent! frequent handwashing

3. Toxoplasma - CNS protozoa
- triad (hydrocephalus, intracranial calcifications, chorioretinitis) + ventriculomegaly, IUGR, deafness
- use PCR to diagnose (not serology)
- prevent with pyrimethamine, sulfadiazine
- transmitted via undercooked meats or oocytes from feces of cats

4. Rubella - triad (sensorineural deafness, cataracts, cardiac defects eg patent DA) + microcephaly, purpura / blueberry muffin rash, IUGR, jaundice
- immunize, live attenuated vaccine (give postpartum)
- increased transmission in 1st trimester


1. Risk factors

2. Etiology
A. Asymmetric
B. Symmetric

3. Presentation at birth

4. Mgmt

IUGR - birthweight <10th percentile for gestational age (small and sick)

1. Risk factors -
A. maternal - smoking/cocaine, HTN, cardiac/renal/pulm dz, anemia
B. uterine/placenta - abruption, previa, infection
C. fetal - Multis, aneuploidy, congenital syndromes, structural abnormalities, infection

2. Etiology
A. asymmetric (abdominal circ and femur length are low, head circ normal) --> later insults eg HTN, maternal malnutrition, Factor V leiden mutation
B. symmetric - all are low --> early insults eg chromosomal abnormalities, congenital infection

3. Presentation - loose peeling skin, wide anterior fontanel, thin umbilical cord
- high morbidity e.g. NRDS, necrotizing enterocolitis, meconium aspiration syndrome (respiratory distress), hypothermia
- IUGR babies at risk for developing DMII, obesity, COPD, CVD, stroke as an adult

3. Mgmt - twice weekly NSTs / AFI or weekly BPPs
- reversed end diastolic doppler flow from umbilical artery --> associated with stillbirth w/in 48 hrs
- steroids if <34 weeks, mag sulfate if <32 weeks
- at birth --> send placenta for histopathology, neonatal urine tox screen


Postpartum Endomyometritis
1. Risk factors
2. Presentation
3. Mgmt

Endomyometritis - infection of decidua, myometrium, and parametrial tissues due to ascension of polymicrobial bacteria from normal vaginal flora (MC is staph aureus and strep)

1. Risk factors - C-section (MC), chorioamnionitis, GBS, numerous vaginal exams, operative vaginal delivery, long labor, low SES, multis, young maternal age, chlamydia, manual extraction of placenta

2. Presentation - fever over 100.4F (MCC of fever in woman post C-section) usually on POD2
- uterine fundal tenderness
- purulent foul-smelling lochia

3. Mgmt - IV gentamicin and clindamycin until pt afebrile >24 hours; add amp if GBS infection, infection persists
- if fever does not improve after 2-3 days --> do CT to r/o abscess, infected hematoma, or septic pelvic thrombophlebitis
- if fever is due to wound infection --> open wound


Diabetes in pregnancy
1. Pregestational diabetes
A. Fetal risks
B. Maternal risks
C. Mgmt

1. Pregestational diabetes - hyperglycemia existing prior to pregnancy; accounts for 10% diabetes in pregnancy

A. Fetal risks - congenital anomalies (cardiac, skeletal, NTD), growth restriction (IUGR), fetal macrosomia (less likely), miscarriage, prematurity

B. Maternal risks - diabetic retinopathy, worsening nephropathy (if already existing), and HTN --> preeclampsia

C. Mgmt - target <105 fasting glucose
- glycemic control during labor to avoid neonatal hypoglycemia after birth
- C-section if big baby to avoid shoulder dystocia


Diabetes in pregnancy
2. Gestational diabetes
A. Screening
B. Risk factors
C. Fetal risks
D. Maternal risks
E. Mgmt

2. Gestational diabetes - hyperglycemia caused by insulin resistance during pregnancy due to increased levels of human placental lactogen
- GDMA1 - controlled with diet; GDMA2 - controlled with insulin

A. Screening - from 24 to 28 weeks Glucola test
(high risk do ASAP) --> 50g glucose and assess after 1-hour --> abnormal >140
*high risk (prior GDM, FHx, or BMI > 30) - do Glucola ASAP
- then 100g GTT and assessing every hour for 3 hours, 2 abnormals needed

B. Risk factors - age > 25, obesity, prior macrosomic infant

C. Fetal risks:
i. anatomic - macrosomia (>4000 g), congenital abnormalities (NTD, cardiac), shoulder dystocia
ii. endocrine - increased insulin --> decreased surfactant --> NRDS, neonatal hypoglycemia
- polycythemia, hyperbilirubinemia, hypocalcemia
iii. polyhydramnios

D. Maternal risks - preeclampsia, risk of C-section, PTL, UTIs

E. Mgmt - diet, insulin or glyburide; goal is fasting glucose <105
- breast-feeding
- 75g GTT at 6- 8 weeks postpartum; should be <126 fasting


Prenatal labs - when they should occur, abnormal findings, ramifications, and mgmt:
1. CBC
2. Blood type and screen
3. Rh factor
4. HIV
5. Rubella
6. STD screening

1. CBC - first visit, Hb up to 10.5 is normal, if lower --> could lead to preterm delivery; do trial of iron

2. Blood type and Screen (indirect coombs) - first visit, Ab screen may indicate isoimmunization --> hemolysis
- Abs: Lewis (lives), Duffy (dies), Kell (kills)

3. Rh factor - first visit, if negative and indirect Coombs shows no isoimmunization--> Give RhoGAM at 28 weeks (to prevent alloimmunization ie anti-Rh Ab titers); if baby is Rh (+) --> give after delivery
- check Rh status in subsequent pregnancies via indirect Coombs (to see if there are Rh+ Ab that can harm baby)

4. HIV - first visit, if positive --> confirm ELISA with Western blot, then HAART with IV ZDV in labor, neonatal HIV testing at 24 hrs, and no breastfeeding

5. Rubella - first visit, if nonimmune --> give live attenuated vaccine postpartum

6. STD screening - first visit
A. RPR or VRDL - for syphilis; need to confirm positive test with FTA-ABS; treat with penicillin, if allergic - desensitize then give penicillin
B. NAAT is gold standard for GCC, treat pt + partner
- gonorrhea --> conjunctivitis (up to 5 days after), blindness, preterm labor; if (+) --> IM ceftriaxone + azithromycin
- chlamydia --> conjuncitivitis (up to 2 weeks after birth), blindness, pneumonia; if (+) --> give azithromycin PO


Prenatal testing - when they should occur, abnormal findings, ramifications, and mgmt:
1. Nuchal translucency
2. Quad screen
3. Screening U/S
4. GBS culture
5. TdaP vaccine
6. Chorionic villus sampling
7. Amniocentesis

1. Nuchal translucency - 11 to 13 weeks, can indicate trisomy --> karyotype, f/u US
- also PAPPA, bHCG --> first-trimester combined test
- also offer cell free DNA screen after 10 weeks (most sensitive for Down syndrome, confirm via karyotyping - CVS or amnio)

2. Quad screen (MSAFP, hCG, Estriol, and Inhibin-A) - 16 to 20 weeks, can indicate trisomy or NTD --> confirm dates via U/S or amniocentesis

3. Screening U/S - 18 to 20 weeks to look for fetal abnormalities

4. GBS culture - 35 to 37 weeks; if (+) - penicillin during labor

5. TdaP vaccine - 28 to 36 weeks - killed vaccine so safe, results in passive transmission of IgG response

6. Chorionic villus sampling - 10 to 13 weeks; for definitive karyotype

7. Amniocentesis - 15 to 20 weeks; for definitive karyotype


1. Pathophysiology
2. Clinical incl perimenopause
3. Mgmt

Menopause - cessation of menses for 12 months; occurs after age 40, mean age is 51

1. Pathophysiology - follicular atresia due to decreased ovarian reserve --> decreased AMH, then inhibin B, then estradiol
*ovaries stop making estrogen, but still make androgens
- persistently elevated LH, FSH

2. Clinical - sx due to low estrogen levels:
- perimenopause - oligomenorrhea (infrequent)
- vasomotor symptoms (hot flushes)
- vaginal and vulvar atrophy
- bone loss --> osteoporosis fracture (MC compression fracture at thoracic spine)

3. Mgmt
A. Hot flushes, sleep disturbances, other vasomotor sx - if woman has uterus and is <60 yo --> HRT (progestin + estrogen) *do for as little time as possible bc of risk of endometrial, breast cancers, PE, stroke, heart disease, which are all c/i (these people are given SSRIs instead)
- if woman is s/p hysterectomy --> just estrogen replacement
- clonidine or gabapentin
B. Irregular menses - progestin or low dose OCP
C. Bone loss - bisphosphonates or raloxifene (SERM, VTE is c/i); DEXA screening at 65+


Ureteral injury
1. Most common locations
2. Clinical
3. Mgmt

Ureteral injury
1. Most common locations - MC is cardinal ligament (attachent of cervix to pelvic walls), contains uterine arteries and ureter traverses just below ("water under the bridge")
- other locations - pelvic brim, UVJ

2. Clinical -
- ureteral ligation: vague flank/ abdominal pain, n/v, fever post op esp after lap hysterectomies --> risk of hydronephrosis, pyuria, hematuria
- bladder perforation - gross hematuria, pain, suprapubic tenderness
- urine leak can cause sepsis, abscess, pyelo

3. Mgmt - IV pyelogram to diagnose
- abx and cysto to r/o kinked ureter
- stenting, repair


Pelvic organ prolapse - types, clinical, and mgmt

Pelvic organ prolapse (POP) - due to defect of pelvic support; family history increases risks, so does age, obesity, chronic constipation

1. Enterocele - defect of pelvic support of uterus and cervix --> small bowel descends into vagina --> feeling of bulging mass in vagina

2. Cystocele - defect of pelvic support of anterior vagina, hypermobile urethra --> stress urinary incontinence with valsalva (cough, sneeze), difficulty voiding
- Q-tip placed in urethra and angle moves with valsalva --> >30 degrees implies urethral hypermobility
- kegels, pessaries, mesh support or fixation

3. Rectocele - defect of pelvic support of rectum --> constipation, difficulty pooping
- posterior colporrhaphy, culdoplasty (since large cul-de-sac can lead to POP)


Urinary incontinence - for each type, describe mechanism, clinical, diagnosis, and treatment

1. Stress
2. Urge

Urinary incontinence

1. Stress (ie outlet incompetence)
A. Mechanism - bladder neck falls out of normal position --> increased intrabdominal pressure transmits to bladder and exceeds outlet (sphincter) resistance --> leakage
- due to intrinsic sphincter dysfunction ("drain pipe urethra"), loss of pelvic support in multips, urethrocele / cystocele
- can also be due to fibroids
B. Clinical - painless and immediate leakage of urine with valsalva (coughing, sneezing)
C. Diagnosis - loss of bladder angle, hypermobile urethra (>30degree on qtip test)
D. Mgmt - kegels, pessaries, urethropexy (sling or fixation) to return urethra back to position; urethral bulking

2. Urge
A. Mechanism - hyperactive / unstable detrusor muscle --> overactive bladder
B. Clinical - leak with urge to void ASAP, delayed leakage after coughing
C. Diagnosis - cytometric examination
D. Mgmt - antimuscarinics eg oxybutynin


Urinary incontinence - for each type, describe mechanism, clinical, diagnosis, and treatment

3. Overflow
4. Fistula

3. Overflow
A. Mechanism - outlet obstruction or detrusor underactivity --> overdistended hypotonic bladder --> incomplete emptying
B. Clinical - dribbling, inability to void
- diabetes, spinal cord injury, or postpartum (2/2 epidural or perineal swelling)
C. Diagnosis - increased postvoid residual (>100 - 150 mL or >1/3 instilled volume)
D. Mgmt - intermittent self-cath to avoid detrusor muscle damage 2/2 wall ischemia

4. Fistula
A. Mechanism - communication bw bladder or ureter and vagina
B. Clinical - constant leakage after labor or sx
C. Diagnosis - dye into bladder showed vaginal discoloration
D. Mgmt - surgical repair


Salpingitis (ie PID)
1. Diagnosis
2. Etiology
3. Clinical
A. Presentation
B. Complications
4. Mgmt incl meds, when to hospitalize

Salpingitis - infection of fallopian tubes
PID - infection of upper female genital tract - includes endometritis, salpingitis, TOA, and pelvic peritonitis

1. Diagnosis (clinical):
- lower abdominal tenderness (due to peritoneal irritation of pelvis)
- cervical motion tenderness (chandelier sign)
- adnexal tenderness

2. Etiology - ascending infection often during menses
- polymicrobial, due to gonorrhea, chlamydia (MCC) --> dx via NAAT (bc no organisms on microscopy)
- IUD, nulliparity, STIs increase risk for PID

3. Clinical
A. Presentation - dyspareunia, fever, postcoital spotting
- cervicitis (friable cervix with purulent d/c), urethritis
B. Complications
- fallopian tubes can become damaged --> tubal occlusion --> chronic pelvic pain, infertility, ectopic pregnancy
- Fitz-Hugh-Curtis - perihepatitis (RUQ pain)
- gonorrhea (sx worse during/after menses) can also cause septic arthritis, painful pustules, pharyngitis
C. TOA = PID + adnexal mass / fullness, fever, WBC, abdominal pain
- complex multiloculated adnexal mass with internal debris on U/S --> needs IV clinda/gent/amp, rupture is sx emergency (U/S drainage or laparoscopy)

4. Mgmt - pelvic US to r/o TOA
- speculum exam - hyperemic friable cervix, mucopurulent exudative discharge (do wet mount to r/o vaginitis)
- GCC test; laparoscopy is gold standard for diagnosis
- treatment - azithromycin or doxy 100 BID for 14 days + ceftriaxone 250 IM (for patient and partner)
- hospitalize if pregnant, unresponsive to tx after 48 hrs, peritoneal signs, TOA


Chronic pelvic pain
1. Define
2. DDx and clinical clues
3. Evaluation
4. Treatment

Chronic pelvic pain
1. Define - persistent pain in lower abdomen / pelvis for >6 months, causing significant effects on daily function, QOL

2. DDx and clinical clues - 30% idiopathic, 30% endometriosis, 20% pelvic adhesions or PID and remaining 20% variety causes

A. GI - bloating, diarrhea/constipation --> IBS, IBD, diverticulitis, hernia
B. Psych - depression, PTSD, anxiety
C. Neuro - burning, radiating --> nerve entrapment, fibromyalgia (trigger points)
- excessive vaginal bleeding (fibroids, adenomyosis)
- dyspareunia, dyschezia (endometriosis)
- hx PID, gyn sx (adhesions)
- cyclic pain s/p BSO (residual ovarian syndrome)

3. Evaluation - r/o pregnancy
- GCC, UA/Ucx, CBC
- pelvic US

4. Treatment - NSAIDs and/or OCPs for 3 month trial, then diagnostic laparoscopy


Vaginal infections - clinical, diagnosis, and treatment

1. Bacterial vaginosis
2. Trichomonas vaginitis
3. Candida vulvovaginitis

Vaginal infections - clinical, diagnosis, and treatment

1. Bacterial vaginosis - overgrowth of anaerobic bacteria which replaces normal lactobacilli, due to Gardnerella
A. Clinical - fishy odor with KOH, gray-white discharge
B. Diagnosis - positive whiff test, pH > 4.5, Clue cells on wet mount (epithelial cells coated with bacteria)
C. Tx - oral or vaginal metronidazole - 500 mg BID for 7 days

2. Trichomonas vaginitis - protozoan that can also inhabit the urethra or Skene's glands
A. Clinical - frothy, green discharge, strawberry red cervix
B. Diagnosis - pH > 4.5, mobile trichomonads on wet mount
C. Tx - oral metronidazole, treat partner too

3. Candida vulvovaginitis - increased risk in DM2, OCP use, Abx use, pregnancy (increased estrogen state)
A. Clinical - cottage cheese discharge, vulvar/vaginal itching and burning --> erythema, swelling, excoriations
B. Diagnosis - pH =< 4.5, pseudohyphae, hyphae, and budding yeast on KOH prep
C. Tx - oral fluconazole, intravaginal imidazole or nystatin


1. Diagnosis

2. Clinical
A. Primary
B. Secondary
C. Latent
D. Tertiary
E. Congenital

3. Treatment

Syphilis - caused by bacteria Treponema pallidum

1. Diagnosis -
- nontreponemal tests - VDRL, RPR; nonspecific, titers fall with tx, *sometimes not positive with primary syphilis*
- specific serologic tests - FTA-ABS; remain positive for life after infection
- darkfield microscopy biopsy
- also assess for HSV via PCR or viral culture or serology --> painFUL ulcers

2. Clinical
A. Primary - shallow, painless, nonexudative genital chancre with indurated edges
B. Secondary - systemic lymphadenopathy, maculopapular "copper penny" rash on palms and soles, condyloma lata (painless flat papules) on genitals
C. Latent - can be early (<1 year) or late (>1 year)
D. Tertiary - tabes dorsalis, aortic aneurysms / aortitis, Argyll Robertson pupil, ataxia and + Romberg
E. Congenital - saddle nose, mulberry molars, saber shins, VIII deafness

3. Treatment
A. Early disease (1, 2, early latent) - one dose IM benzathine penicillin
B. Late disease (late latent, 3) - 3 doses IM benzathine penicillin; neurosyphilis requires IV penicillin

*Vs condyloma acuminata caused by HPV 6 and 11 -- treat with imiquimod, trichloroacetic acid


4. Compare to other causes of ulcers - clinical presentation, tx
B. Chancroid
C. Lymphogranuloma venereum
D. Granuloma inguinale

4. Other ulcers

A. HSV - genital is HSV2
- primary episode is systemic (fever, malalise) and local, vs just local (syphilis)
- vulvar burning and paresthesias, then small, superficial groups of painful ulcers on a red base
- tx - oral acyclovir

B. Chancroid - due to H. ducreyi
- painful ulcer of vulva with ragged edges on necrotic base + tender lymphadenopathy
- school of fish on Gram stain
- tx - oral azithromycin or IM ceftriaxone

C. LV - C. trachomatis L1-L3
- primary - painless papule or shallow ulceration
- secondary - unilateraly painful inguinal LAD --> buboes (enlarged tender nodes) and groove sign (separation of lymph nodes by inguinal ligament)
- tx - doxy or erythromycin

D. Granuloma inguinale - K. ulomatis
- Donovan intracellular inclusion bodies in macrophages
- large painless beefy red ulcers w/out LAD
- tx - doxy or TMP-SMX


Urinary tract infection
For each type - etiology, clinical, and tx
1. Cystitis
2. Urethritis

1. Cystitis - bacterial infection of bladder with >100K CFUs in midstream (non-contaminated) specimen
A. Etiology - infection due to bacteria from GI tract / rectum (NOT STI)
- MCC is E. coli
- also Klebsiella, Pseudomonas, Enterobacter, Proteus, GBS, Staph saprophyticus
B. Clinical - urgency, frequency, dysuria with no fever or flank pain
- hematuria, hesitancy --> hemorrhagic cystitis or kidney stones
C. Tx - do UA/Ucx and sensitivity; 3 days of TMP-SMX unless resistance (cipro BID for 3 days)
*recurrent UTIs can be treated prophylactically with Bactrim

2. Urethritis
A. Etiology - STI --> Chlamydia trachomatis; also Neisseria, Trichomonas
B. Clinical - urethral discharge, dysuria
C. Tx - urethral swabbing for cultures, NAAT;
- doxy (for chlamydia) or azithro in pregnant pts
- IM ceftriaxone (for neisseria)


Urinary tract infection
For each type - etiology, clinical, and tx
3. Urethral syndrome
4. Pyelonephritis

3. Urethral syndrome - recurrent episodes of urgency, dysuria caused by urethral inflammation
A. Etiology - unknown, urine cxs negative
B. Clinical - urgency, frequency, dysuria

4. Pyelonephritis
A. Etiology - starts off as lower UTI
B. Clinical - fever/chills, n/v, CVA tenderness
C. Tx -
i. nonpregnant - oral TMP-SMX or fluoroquinolone for 14 days
ii. pregnant, immunocompromised - hospitalize and give IV amp/gentamicin, ceftriaxone, or zosyn; then suppressive therapy with macrobid for remainder of therapy

*treat pregnant pts with asymptomatic bacteriuria --> 25% chance of developing pyelo (MCC sepsis in pregnancy)


Uterine leiomyomata (ie fibroids)
1. Subtypes
2. Clinical - compare to endometrial polyps
3. Mgmt

Uterine leiomyomata (ie fibroids) - benign smooth muscle tumor surrounded by pseudocapsule

1. Subtypes
- submucosal - on endometrium, protrudes into uterine cavity; associated with recurrent abortion
- intramural - MC, in uterine muscle
- subserosal - on serosa outside of uterus
- can be pedunculated or prolapsed

2. Clinical - most common symptom is menorrhagia (heavy bleeding) --> anemia
- PE - firm, irregular, midline, nontender mass that moves with the cervix
- pelvic pain due to carneous degeneration (2/2 rapid growth) or vascular compromise of a pedunculated one
- contractions due to prolapsed fibroid
- rapid growth (esp after menopause) and hx of pelvic radiation -- could be leiomyosarcoma instead
*endometrial polyps - also in uterus, but lead to metrorrhagia (intermenstrual spotting) w/out uterine enlargement
* differentiate from adenomyosis w pelvic MRI

3. Mgmt - asymptomatic --> no tx; dx via pelvic US
A. Medical
- NSAIDs, progestin therapy (Mirena, OCPs, Depo provera)
- GnRH agonist (Leuprolide) therapy --> shrinks size, used preop bc it is reversible; postmenopausal sx
- f/u 6 mos to monitor size/growth
B. Surgical for symptomatic fibroids
i. myomectomy (if future pregnancy desired AND fibroids caused complications in past pregnancies) - risk of uterine rupture during labor
ii. hysterectomy (MCC of hysterectomy in the US)
iii. uterine artery ligation


For each form - mechanisms, benefits, risks/ contraindications:
1. Barrier
2. Combined hormonal
-- what does estrogen do vs progesterone

1. Barrier - condoms, diaphragms
A. Mechanism - mechanical obstruction
B. Benefits - also provides protection against STIs
C. Risks - need to use each time, lack of spontaneity, allergies to material

2. Combined hormonal (Estrogen and progestin) - OCPs, patch, vaginal ring
A. Mechanism
i. estrogen - inhibits FSH and LH to inhibit ovulation; supports lining to prevent breakthrough bleeding
ii. progesterone - inhibits LH to inhibit ovulation; thickens cervical mucus to inhibit sperm; thins endometrium
B. Benefits - good for pts with dysmenorrhea, IDA, endometriosis, ovarian cysts, acne; decreased risk endometrial/ovarian cancer and benign breast disease
C. Risks - VTE, strokes in pts with migraines with aura, and MI in women over 35 who are heavy smokers; increased risk breast cancer, gallstones
- OCPs can cause or worsen HTN
D. C/i - prior thromboembolic event or CVA, smoking over age of 35, liver tumors, uncontrolled HTN, breast/ endometrial ca, migraines with aura, diabetic retinopathy/nephropathy/PVD


For each form - mechanisms, benefits, risks/ contraindications:
3. Injectable
4. Implant

3. Injectable - depot medroxyprogesterone acetate (Depo provera) --> progestin only; every 3 months
A. Mechanism - inhibits ovulation (inhibits LH surge), thickens cervical mucus to inhibit sperm, thins endometrium
B. Benefits - pts with IDA, breastfeeding, sickle cell, epilepsy, cysts, endometriosis, dysmenorrhea
C. Risks / contraindications - causes osteopenia (reversible), weight gain, depression
- takes while for ovulation to be restored (10 months)

4. Implant - etonorgestrel implant in arm (Nexplanon) --> progestin only
A. Mechanism - inhibits ovulation, thickens cervical mucus to inhibit sperm, thins endometrium
B. Benefits - lasts 3 years, for pts breastfeeding, with IDA, cysts, endometriosis, dysmenorrhea
C. Risks - irregular vaginal bleeding
D. C/i - liver tumors, breast ca, hx VTEs/PE/MI (similar to OCPs bc its systemic progesterone)


For each form - mechanisms, benefits, risks/ contraindications:
5. IUD - levonorgestrel
6. IUD - copper

5. IUD - levonorgestrel (Mirena)
A. Mechanism - thickens cervical mucus to inhibit sperm, thins endometrium to prevent implantation; does NOT inhibit ovulation
B. Benefits - long-term, reversible; decreased bleeding, breastfeeding
C. Risks / contraindications - current STI, PID, malignant gestational trophoblastic disease, breast / cervical / endometrial ca (but NOT ovarian cancer), uterine fibroids or abnormalities distorting uterine cavity

6. IUD - copper
A. Mechanism - inhibits sperm viability and migration, damages ovum; does NOT inhibit ovulation
B. Benefits - long-term, reversible; most effective emergency contraceptive (up to 5 days post)
C. Risks / contraindications - Wilson disease, current STI or PID, cervical / endometrial ca, uterine fibroids or abnormalities distorting uterine cavity
- increased risk heavy periods, cramping


Breast masses
Treatment algorithm based on age (> 30)

Clinical, diagnosis, treatment
1. Fibrocystic changes

Palpable breast mass: triple test is clinical exam, imaging, and biopsy
A. 30 or older - mammo +/- US --> core biopsy if suspicious for malignancy
--> simply cyst - FNA; excise and send for cytology if bloody, mass persists, or fluid reaccumulates
--> palpable solid mass - core needle biopsy
--> nonpalpable solid mass - wire-guided excisional bx

B. younger than 30 - US +/- mammo
--> simple cyst - same as for >30 yo pts
--> complex cyst / palpable solid mass --> FNA; if not enough tissue obtained, or mass is large/suspicious, then excisional biopsy

1. Fibrocystic changes - most common benign breast condition
- exaggerated response to ovarian hormones --> mass size increases before menses
A. Clinical - multiple, irregular lumps --> diffuse breast nodularity bilaterally
- cyclic, painful, engorged breasts before menstruation, sometimes green discharge
- more common in premenopausal
B. Diagnosis - FNA or core needle biopsy
C. Tx - decrease caffeine and chocolate; NSAIDs, OCPs, oral progestin, danazol (weak antiestrogen), vit E and B6


Breast masses - clinical, diagnosis, treatment
2. Fibroadenoma
3. Intraductal papilloma
4. Breast cancer
5. Fat necrosis

2. Fibroadenoma - benign smooth muscle tumor
- MCC breast mass in women <25
A. Clinical - firm, nontender, rubbery, mobile mass on upper outer quadrant
B. Diagnosis - FNA for cytology (BUT only one that does not require tissue diagnosis) to r/o cystosarcoma phyllodes (large low-grade malignancy --> wide local excision)
C. Tx - if small and not growing --> careful observation
- if large --> excisional biopsy

3. Intraductal papilloma
A. Clinical - benign and solitary --> MCC unilateral serosanguineous nipple discharge with absence of mass
B. Diagnosis - core needle biopsy, physical exam
C. Tx - ductogram, excision of involved ducts

4. Breast cancer - invasive ductal carcinoma (MC), invasive lobular, Paget (adenocarcinoma), inflammatory (aggressive)
A. Clinical - irregular, fixed mass with LAD
- Paget is eczematous painful changes, inflammatory is peau d'orange, painful edematous red breasts
- risk factors - AGE, HRT, nulliparity, alcohol consumption, early menarche / late menopause, FHx, white
B. Diagnosis - mammo, biopsy, stage via TNM system
C. Tx - BCT (lumpectomy with radiation) and SNLB
- ER (+) - tamoxifen (SERM --> hot flushes, VTE, endometrial hyperplasia)

5. Fat necrosis - similar to breast cancer (dimpling, mixed mass) but US shows hyperechoic mass and biopsy shows fat globules and foamy histiocytes
- excisional bx to r/o cancer


1. Causes
2. Clinical
3. Mgmt

Hyperprolactinemia - PRL > 20 ng /mL

1. Causes
- drugs eg OCPs, antHTN, TCAs, antipsychotics
- hypothyroidism (TRH elevates TSH and PRL)
- pituitary adenoma
- empty sella syndrome
- acromegaly
- renal disease / failure
- chest surgery or trauma (implants, T2 dermatome herpes)

2. Clinical
- galactorrhea - white watery b/l breast discharge
- oligomenorrhea or amenorrhea (high PRL --> increased dopa --> interrupts pulsatile GnRH --> inhibits FSH, LH --> decreased estradiol)

3. Mgmt - obtain PRL levels after fasting and no breast stimulation for 24 hrs, get TSH and MRIbrain
- anterior pituitary adenoma -- bromocriptine, cabergoline (dopamine agonist) if symptomatic (bitemporal hemianopsia, headache) or transphenoidal resection
- hypothyroidism - levothyroxine
- hyperPRL but nl E2 --> periodic progestin withdrawal


1. Diagnosis
2. Clinical
3. Mgmt

1. Diagnosis - 2 out of 3:
- oligmenorrhea / amenorrhea (2/2 anovulation)
- hyperandrogenism --> increased testosterone (secreted by ovary) and DHEA-S (secreted by adrenals), not otherwise explained by hyperPRL,Cushing, thyroid, CAH, etc.
- evidence of multiple ovarian cysts "string of pearls" on TVUS
also high GnRH, increased LH:FSH ratio also seen often (not always) --> no LH surge --> anovulation

2. Clinical - onset in menarche of androgen excess (acne, hirsutism, temporal balding), chronic menstrual irregularities
- obesity -- insulin resistance --> low SHBG --> high testosterone
- at risk for DM, endometrial / ovarian cancers, hyperlipidemia, cardiovascular disease

3. Mgmt - weight loss via diet and exercise
- will bleed in response to progestin challenge
- OCPs to regulate menstrual cycles
- to induce ovulation --> clomiphene citrate (BMI < 30) or letrozole aromatase inhibitor (BMI > 30)


Hirsutism - clinical presentation, diagnosis, and treatment of:
1. Cushing syndrome
2. Adrenal tumor

Hirsutism - MCC is PCOS

1. Cushing syndrome - increased cortisol
A. Clinical - buffalo hump, violaceous striae, HTN, central obesity, osteoporosis, amenorrhea
B. Diagnosis
- high ACTH - dexamethasone suppression test --> Cushing disease (ACTH pituitary adenoma) vs ectopic ACTH secretion
- low ACTH - adrenal tumor vs exogenous corticosteroids
C. Tx - surgical

2. Adrenal tumor
A. Clinical - rapid onset virilism (clitoromegaly, male balding, acne, voice deepening); abdominal mass
B. Diagnosis - increased DHEA-S (produced by adrenals)
C. Tx - surgical


Hirsutism - clinical presentation, diagnosis, and treatment of:
3. CAH
4. Sertoli-Leydig tumor
5. Aromatase deficiency
vs 5AR deficiency

3. Congenital adrenal hyperplasia (CAH)
- MCC is 21OH deficiency --> Decreased cortisol, aldosterone but increased sex hormones
A. Clinical -
- at birth - hypotension, ambiguous genitalia and salt wasting
- at puberty - precocious puberty in men and virilization in women
B. Diagnosis - elevated morning fasting 17hydroxyprogesterone, increased renin / low BP, high K+
C. Tx - replace cortisol, aldosterone; antiandrogens (spironolactone, OCPs)

4. Sertoli-Leydig tumor - androgen-secreting ovarian tumor
A. Clinical - rapid onset hirsutism, virilization, adnexal mass
B. Diagnosis - elevated testosterone level
C. Tx - surgical
*estrogen counterpart is granulosa cell tumor --> precious puberty in girls

5. Aromatase deficiency - cannot convert androgens to estrogens
A. Clinical - masculinization of XX infants --> normal internal genitalia but ambiguous external genitalia, external virilization (clitoromegaly)
- osteoporosis, delayed puberty
- maternal virilization during pregnancy
B. Diagnosis - high levels of FSH, LH, testosterone, androstenedione but undetectable estrogen levels
C. 5alphareductase deficiency (AR) - cannot convert testosterone to DHT --> feminization of XY infants until virilization at puberty; increased testosterone, LH, estrogen


1. Normal puberty stages
Definition, causes, and mgmt of:
2. Precocious puberty

1. Normal puberty stages
- thelarche (breast bud by 13 yrs) --> adrenarche (axillary and pubic hair) --> growth spurt --> menarche (by 16 yrs)

2. Precocious puberty - developing secondary sexual characteristics in girls <8 and boys <9
- MCC is idiopathic (central cause), dx of exclusion
A. Central cause - early maturation of HPG axis
- e.g. brain tumors, hydrocephalus, idiopathic - normal FSH, LH
- treat with GnRH agonists eg leuprolide

B. Peripheral cause - excess secretion of sex hormones
- e.g. granulosa cell tumor, CAH, McCune-Albright (menses before thelarche/adrenarche), adrenal tumor - low FSH, LH
- does not respond to GnRH agonists, need to block production based on cause
---> CAH - glucocorticoids
---> ovarian cysts - regress spontaneously
---> ovarian, testicular, adrenal tumors - surgery

*hypothyroidism causes delayed bone age, all other causes cause precocious puberty with accelerated bone age


Definition, causes, and mgmt of:
3. Delayed puberty

3. Delayed puberty - lack of secondary sexual characteristics by 14 years

A. Hypergonadotropic hypogonadism - high FSH, low estrogen
i. Causes
- MCC is gonadal dysgenesis e.g. Turner syndrome (streak ovaries do not produce estrogen) - short, webbed neck, shield chest; Klinefelter (XXY)
- CAH eg 17hydroxylase deficiency
- gonadotropin resistance - Leydig cell hypoplasia, FSH insensitivity
- also acquired causes eg orchitis, premature ovarian failure, chemo/radiation
ii. Mgmt - unopposed estrogen until breasts are formed, then progestins (via OCPs)

B. Hypogonadotropic hypogonadism - low FSH, low estrogen
i. Causes
- primary eg Kallman syndrome
- secondary:
----- hypothalamic dysfunction due to eating disorders, chronic illness, stress
----- primary hypothyroidism, Cushing, craniopharyngioma
ii. Mgmt - MRI to r/o tumor, then same estrogen / hormone replacement therapy
--- GnRH agonist for Kallman syndrome


1. Primary vs secondary
2. Differentiate the 2 MCC of primary
3. Other causes of primary amenorrhea

1. Amenorrhea
- Primary - no menarche by age 16 with nl breast devlpt
- Secondary - absence of menses > 6 mos in previously menstruating woman

2. Primary amenorrhea - absent uterus, upper vagina --> blind vaginal pouch

A. Mullerian agenesis (Mayer-Rokitansky-Kuster-Hauser syndrome) - congenital absence of devlpt of uterus, cervix and fallopian tubes in 46,XX female
- normal breasts bc of ovaries (gonads develop due to lack of SRY gene)
- normal testosterone, normal pubic hair
- pts usually also have urinary tract / renal abnormality

B. Androgen insensitivity - receptor defect in which 46,XY individuals are phenotypically female with nl breast devlpt
- functional testes that secrete AMH --> Mullerian ducts regress; and also testosterone (but no response since no receptors) --> so Wolffian ducts degenerate, no male sex characteristics (voice deepening, pubic hair)
- urogenital sinus defaults to external female genitalia (instead of penis/scrotum), testosterone peripherally converted to estrogen (--> breasts)
- high testosterone, LH, estrogen
- need gonadectomy (removal of testes) after puberty due to risk of developing malignancy

3. Other causes of primary:
- Turner 45,X - amenorrhea with streak ovaries, delayed breast devlpt, normal uterus and vagina; estrogen and GH therapy to prevent osteoporosis, promote devlpt of sec sex characteristics
- transverse vaginal septum - no canalization of vagina bw Mullerian top 1/3 and urogenital lower 2/3
- imperforate hymen - cyclic pelvic pain


3. Workup of secondary and DDx
4. Mgmt

3. Workup of secondary amenorrhea:
A. pregnancy test (MCC secondary amenorrhea)
B. PRL, TSH levels --> hypothyroid, hyperPRL
C. progestin challenge test --> if bleeding, probably PCOS (increased estrogen) or immature HPO axis
--> if not bleeding -->
D. estradiol, FSH, LH levels --> if normal E2, probably outflow tract problem (cervical stenosis, Asherman syndrome ie intrauterine adhesions that damage decidua basalis layer)
Ei. if low estradiol, high FSH/LH --> premature ovarian failure or Turner syndrome
Eii. if low estradiol, low FSH/LH --> hypothalamic (weight loss, stress), or pituitary (Sheehan, irradiation)

4. Mgmt
- diagnose Asherman via hysterosalpingogram --> irregular filling defects
- gold standard is hysteroscopy, operative hysteroscopy allows transection of adhesions


For each cause - clinical presentation, diagnosis, and mgmt:
1. Ovulatory dysfunction
2. Uterine disorder
3. Male factor
4. Tubal disorder
5. Peritoneal factor

Infertility - 1 year inability to conceive with unprotected sex

1. Ovulatory dysfunction eg PCOS, hypothalamic disturbances, premature ovarian failure
A. Clinical - irregular menses, obesity
B. Dx - basal body temperature chart (biphasic is nl), LH surge urine test kit
C. Mgmt - clomiphene citrate

2. Uterine disorder eg fibroids
A. Clinical - recurrent pregnancy losses
B. Dx - hysterosalpingogram
C. Mgmt - hysteroscopy

3. Male factor
A. Clinical - hernia, varicocele, mumps
B. Dx - semen analysis
C. Mgmt - repair, IVF

4. Tubal disorder
A. Clinical - hx GCC, PID (Salpingitis)
B. Dx - hysterosalpingogram
C. Mgmt - laparoscopy, IVF

5. Peritoneal factor eg endometriosis
A. Clinical - dysmenorrhea, dyspareunia, dyschezia
B. Dx - laparoscopy
C. Mgmt - laparoscopy for excision/ablation


Endometrial cancer
1. Risk factors
2. Type I vs Type II
3. Endometrial biopsy indications
4. Mgmt

Endometrial cancer - MC female genital tract malignancy

1. Risk factors
- estrogen exposure w/out progesterone --> early menarche / late menopause, anovulation, nulliparity, obesity, PCOS
- older age, hx infertility
- HTN, DM2 (independent risk factors)
- Lynch syndrome (colon, endometrial, colon ca)
- complex atypical endometrial hyperplasia

2. Type I - estrogen dependent, in early menopausal patient, lower grade, adenocarcinoma; precursor is hyperplasia; in women with classic risk factors
Type II - aggressive, papillary serous or clear cell; in thin, late menopausal women with regular menses

3. EMB indications (can also do TVUS for endometrial stripe, nl is <11 mm --> thickened in postmenopausal but can be normal in premenopausal)
- >45 -- AUB or postmenopausal bleeding
- <45 -- AUB + estrogen (obesity, anovulation) or Lynch
- > 35 with atypical glandular cells on pap smear

4. Mgmt -
- for low-grade cancer - can do high dose progestin therapy with endometrial sampling so woman can have kids; afterwards --> surgery
- hysteroscopy for surgical staging --> TAHBSO


Cervical cancer
1. Risk factors
2. Clinical presentation
3. Screening
4. Mgmt

Cervical cancer - 2nd MC gyn malignancy

1. Risk factors - smoking, HIV, multiple sexual partners, STDs, low SES, HPV infection (16 and 18)

2. Clinical presentation - abnormal vaginal bleeding eg postcoital spotting
- arises in squamocolumnar junction (transition zone) of cervix --> MC type is squamous cell carcinoma
- can lead to hydronephrosis bc it spreads through cardinal ligaments towards pelvic sidewalls --> MCC death is uremia 2/2 b/l ureteral obstruction

3. Screening --> colposcopy and bx if abnormal
*if pap is ASCUS, do HPV typing first, then colpo if + or repeat cotesting in 3 yrs if -
* if pap is HSIL --> can do immediate LEEP
- paps w/out HPV co-testing every 3 yrs starting at 21
- paps w HPV co-testing every 5 yrs starting at 30
- no more pap tests if no abnormal history + 3 consecutive negatives starting at 65

4. Mgmt - clinical staging
- cervical biopsy when lesion is seen
- early --> sx (radical hysterectomy) or radiation
- late --> chemo (cisplatin) + radiation


Ovarian tumors - types, clinical presentation, and mgmt of:
1. Germ cell tumors
2. Epithelial tumors

Ovarian cancer risk factors: unopposed estrogen exposure (PCOS, obesity, endometriosis), more ovulatory cycles (age, infertility), and genetics (BRCA 1/2, Lynch)
* decreased risk with breastfeeding, OCPs (anovulation)

1. Germ cell tumors
A. Types - benign cystic teratoma (MC), struma ovarii, choriocarcinoma, dysgerminoma (hCG, LDH), endodermal sinus tumor (yolk sac - AFP)
B. Clinical - in young women 20-30 years, can cause torsion
C. Mgmt - use US to diagnose (eg teratoma is a complex cystic structure - hyperechoic nodules and calcifications); treat via cystectomy or u/l oophorectomy

2. Epithelial tumors
A. Types - serous (MC, usually b/l), mucinous (u/l, grows v large and can lead to pseudomxyomaperitonei --> recurrent SBO), endometrioid, brenner (transitional cell), clear cell
B. Clinical - primarily in postmenopausal or BRCA 1/2 mutations
- adnexal mass, SBO, pleural effusion, ascites (SOB, abdominal distension), pelvic pain
C. Mgmt - CA-125 biomarker level (in postmenopausal pt) + pelvic US
- exlap for cancer resection, staging, debulking, possible hysterectomy + BSO
*do NOT do biopsy (could spread cancerous cells)
- postop chemo (taxane, cisplatin)
* Ovarian cancer - 3rd MC gyn malignancy but leading cause of death (MCC is cachexia due to small bowel mets)


Ovarian tumors - types, clinical presentation, and mgmt
3. Sex cord stromal tumors
4. When to observe vs operate

3. Sex cord stromal tumors - functional neoplasms in either ovaries or testicles
A. Types - granulosa cell (MC), Sertoli-Leydig, thecoma, fibroma
B. Clinical - depends on type (precocious puberty, virilization)
C. Mgmt - solid on U/S

4. General mgmt
A. In prepubertal --> operate if >2 cm
B. In reproductive age --> observe if <5 cm (probably physiologic cyst eg follicular, corpus luteal) and operate if >7 cm
C. In menopausal, operate if >5 cm

*functional ovarian cyst - result of normal ovulation; U/S shows unilocular simple cyst


Vulvar disorders
Clinical presentation and mgmt of:
1. Lichen sclerosis
2. Lichen planus
3. Atrophic vaginitis

Vulvar disorders

1. Lichen sclerosis - inflammatory skin condition of vulva only
A. Clinical - epithelial thinning (Cigarette paper quality), white plaques, hyperkeratosis, resorption of clitoris, labial fusion
- seen in postmenopausal women
B. Mgmt - vulvar biopsy (increased risk squamous cell carcinoma), corticosteroids (clobetasol)

2. Lichen planus - inflammatory skin condition
A. Clinical - affects skin, oral cavity, vulva, vagina --> lacy, reticulated rash (purple papules with white striae); chronic burning and itching; can cause vaginal adhesions
B. Mgmt - corticosteroids (clobetasol)

3. Atrophic vaginitis - postmenopausal genitourinary syndrome --> loss of vaginal wall elasticity f
A. Clinical - vaginal bleeding, dyspareunia
- also urinary sx eg UTIs, urgency, frequency, and incontinence
- sparse pubic hair, loss of rugae, fissures; elevated vaginal pH > 5, narrowed introitus
B. mgmt - vaginal estrogen, UA/UCx to dx concurrent infection


Vulvar disorders
4. Lichen simplex chronicus
5. Bartholin gland abscess
6. Vulvar cancer

4. Lichen simplex chronicus
A. Clinical - itch/scratch cycle --> thickened skin with excoriations
B. Mgmt - give diphenydramine so they sleep through night and don't scratch

5. Bartholin gland abscess
A. Clinical - polymicrobial (incl anaerobic), not due to STIs
- painful masses at 5 or 7oclock
B. Mgmt - Word balloon catheter in gland, marsupialization (fixation of cyst wall to vulva)

6. Vulvar cancer
A. Clinical - most common squamous cell carcinoma, spreads to ipsilateral inguinal lymph nodes
B. Mgmt - radical vulvectomy

Also vulvar psoriasis (salmon plaques with silver scales)


1. Clinical
2. Physical exam findings - compare to adenomyosis
3. Intraop findings
4. Treatment

Endometriosis - endometrial glands and stroma outside the uterus

1. Clinical - hallmark is cyclical pelvic pain beginning 1-2 weeks pre, peaking 1-2 days pre-menses, subsiding at onset of menses
- 3D's = dysmenorrhea, dyspareunia, dyschezia
- or asymptomatic, or progression to chronic pelvic pain
- cause of infertility (2/2 adhesions, inflammation)

3. PE - fixed, immobile uterus, can be tilted laterally due to adhesions
* adenomyosis (MC in older multips)- endometrial tissue in myometrium --> soft, boggy, globular and uniformly enlarged uterus; dysmenorrhea and heavy menstrual bleeding --> tx - Mirena, hysterectomy

3. Intraop findings - adhesions, powder burn lesions, flesh colored / dark nodules, collections of chocolate fluid (endometrioma aka "chocolate cysts" --> homogenous cystic appearance on US)

4. Treatment:
A. asymptomatic - observe, no treatment indicated
B. symptomatic
i. medical
- leuprolide (GnRH agonist, temporary action) or danazol (androgen derivative) --> inhibit LH and FSH surges --> suppress estrogen stimulation of ectopic endometrial glands
*clomiphene if trying to conceive
ii. surgical
- laparoscopy and excision of implants / ablation


Risk factors, presentation, and mgmt of:
1. Intrauterine fetal demise
2. Uterine rupture

1. Intrauterine fetal demise (IUFD) at > 20 weeks and before onset of labor
A. Risk factors - obesity, HTN, DM2, smoking, drug use
B. Clinical - Diagnosis via absence of fetal cardiac activity on US (FHR nonstress test / Doppler can be false negative)
- or nonviable fetuses with FHR (anencephaly, b/l renal agenesis, acardia, holoprosencephaly)
C. Mgmt -
- <24 weeks --> D and E
- >24 weeks --> induce vaginal delivery
- fetal autopsy and placental evaluation
- maternal testing for antiphospholipids and fetomaternal hemorrhage

2. Uterine rupture
A. Risk factors - weakened uterine wall --> prior uterine surgery (C-section, myomectomy), congenital uterine anomalies, fetal macrosomia / multis, trauma
B. Clinical factors - sudden excruciating abdominal pain, vaginal bleeding, abdominally palpable fetal parts
- maternal hypotension and tachycardia (2/2 hemorrhage)
- loss of fetal station (pathognomonic), cessation of contractions
- abnormal FHR --> persistent variable decelerations
C. Mgmt - laparotomy and delivery through rupture site; rupture repair or hysterectomy


Risk factors, presentation, and mgmt of:
3. Amniotic fluid embolism

3. Amniotic fluid embolism - amniotic fluid enters maternal circulation through placental insertion site, cesarean incision site, endocervical veins --> inflammatory response with vasospasm

A. Risk factors - advanced maternal age, gravida >5, C-section, placenta previa, placental abruption, preeclampsia

B. Clinical - cardiogenic shock, DIC (purpuric rash, bleeding from IV lines), hypoxemic respiratory failure, seizures, coma

3. Tx - respiratory and hemodynamic support (intubation, ventilation)
- dx of exclusion after eclampsia, cardiomyopathy, PE


Spontaneous abortions
For each type, describe clinical presentation and treatment:
1. Threatened abortion
2. Inevitable abortion
3. Incomplete abortion

1. Threatened abortion - <20 weeks with vaginal spotting / bleeding but NO cervical dilation or passage of tissue, due to:
A. Viable intrauterine pregnancy (50%)
B. Spontaneous abortion (35%)
C. Ectopic pregnancy (15%)
- if stable, f/u hCG level in 48 hrs
- abnl hCG rise (<66%) --> D and C --> miscarriage (chorionic villi on path) or ectopic (no villi, give IM methotrexate)
- give RhoGAM if Rh (-), or can lead to hydrops later on

2. Inevitable abortion - pregnancy < 20 weeks with uterine cramping, bleeding, and cervical dilation (open os) but NO passage of tissue yet
*differentiate from incompetent cervix (painless cervical dilation)
- tx - expectant mgmt, medical (vaginal misoprostol), or surgical (D and C)

3. Incomplete abortion - pregnancy < 20 weeks with cramping, bleeding, and cervical dilation (open os) AND passage of some tissue but also retained tissue
- tx - expectant mgmt, medical (vaginal misoprostol), or surgical (D and C)


Spontaneous abortions
For each type, describe clinical presentation and treatment:
4. Septic abortion
5. Missed abortion
6. Complete abortion

4. Septic abortion - retained POC from missed or incomplete abortion, or elective abortion
- f/c, heavy bleeding, malodorous vaginal d/c, dilated cervix and boggy tender uterus
- broad-spectrum abx (gent and clinda) then curettage after 4 hours

5. Missed abortion - pregnancy < 20 weeks with fetal demise but no sx (no cramping, bleeding)
- tx - expectant mgmt, medical (vaginal misoprostol), or surgical (D and C)

6. Complete abortion - pregnancy < 20 weeks where all POC have passed, cervix is closed, resolved cramping and bleeding
- tx - follow hCG levels to zero


Spontaneous abortions
For each type, describe clinical presentation and treatment:
7. Molar pregnancy (hydatidiform mole)
8. Choriocarcinoma

7. Molar pregnancy - trophoblastic placental tissue without fetus; increased risk among asians, multiple miscarriages, <20 or >40, prior moles
- Complete mole - XX or XY (enucleated egg + sperm), no fetal parts, increased risk GTD
- Partial mole - XXX, XXY, or XYY (egg + 2 sperm), fetal parts

A. Clinical - vaginal bleeding, absence of FHR, size greater than dates, early preeclampsia at <20 weeks
- hyperemesis, hyperthyroidism
- v high beta hCG (>100,000) --> hyperstimulation of ovaries --> theca lutein cyts (b/l multilocular ovarian cysts that resolve)
- Diagnosis - U/S shows snowstorm pattern
B. Tx - D and C, monitor hCG weekly until undetectable and then 6 months post for choriocarcinoma (so give contraception for 6 mos)

8. Choriocarcinoma - metastatic form of gestational trophoblastic neoplasia (no chorionic villi present)
- diagnose via + bHCG (NO biopsies bv lesions vascular)
A. Clinical - postpartum woman with enlarged uterus, irregular vaginal bleeding
- pulmonary symptoms, and multiple infiltrates on CXR (lungs MC site of mets)
B. Tx - methotrexate or hysterectomy


Fetal heart rate monitoring
1. Normal heart rate
A. Tachy
B. Brady

2. Variability

3. Accelerations

Fetal heart rate monitoring

1. Normal - baseline (avg HR in 10 min window) is 110 - 160 bpm with accelerations and variability
A. Tachy --> due to chorioamnionitis (maternal fever), hyperthyroid
B. Brady - FHR <110 for >10 minutes --> due to preuterine (maternal hypoxia 2/2 epidural, seizure, PE, AFE), uteroplacental (placental previa or abruption), or postplacental (cord prolapse, vasa previa)

2. Variability - bw 6 - 25 bpm
- decreased variability --> baby could be sleeping (do scalp stimulation to induce acceleration) or could be acidotic

3. Accelerations - normal! abrupt increase in FHR >15 bpm for >15 sec


Fetal heart rate monitoring

4. Decelerations - etiologies and interventions
A. Early
B. Late
C. Variable
D. Prolonged

4. Decelerations - abrupt decrease in FHR <15 bpm for 15 sec - 2 min (prolonged decel = 2-10 min)

A. Early - when ctx begins and recovers when ends --> physiological, benign (2/2 vagal tone from fetal head compression)

B. Late - begin at peak of ctx --> due to fetal hypoxia (uteroplacental insufficiency 2/2 chronic HTN, postterm)
- recurrent late --> due to fetal acidemia
- move mom to LLD, give 02 and IVF, d/c pitocin

C. Variable - abrupt in decline and resolution (<30 sec from onset to nadir) --> due to cord compression, cord prolapse, or oligohydramnios
- if persistent (with >50% ctx) --> maternal repositioning to LLD, then amnioinfusion for repetitive variable decels to decrease risk C-section

D. Prolonged decels
- tachysystole (>5 ctx in 10 min) --> stop pitocin, give B2 agonist tocolytic e.g. terbutaline or nitroglycerin
- hypotension 2/2 epidural --> give IVF bolus or ephedrine
- rapid cervical dilation --> positional changes (place in LLD left lateral decubitus to avoid compression of IVC)
- umbilical cord prolapse --> C-section
- placental abruption --> support BP, C-section
- uterine rupture --> C-section


External cephalic version - indications

external cephalic version - manual conversion of fetus from breech to vertex
- do if >37 weeks, no c/I to vaginal delivery (placenta previa, herpes, prior classical C-section) or to ECV (waters broken, abnormal FHR, oligohydramnios, multis)
- if ECV fails --> C-section by 39 weeks

*if presentation is breech at labor (eg waters have broken) --> do C-section

internal podalic version - breech extraction of malpresenting second twin, preferable to C-section


Hyperemesis gravidarum
1. Risk factors
2. Clinical
3. Lab values
4. Treatment esp compared to morning sickness
5. Complication

Hyperemesis gravidarum

1. Risk factors - prior hx, multis, mole

2. Clinical - severe, persistent vomiting with dehydration, hypotension, and >5% loss of prepregnancy weight

3. Lab values - ketonuria, hypochloremic hypokalemic MA, hemoconcentration

4. Treatment - fluids (NS w 5% dextrose), antiemetics, admission to hospital, corticosteroids if tx unresponsive
vs morning sickness - vitamin B6, doxylamine, ginger; resolves by week 16

5. Complication - Wernicke encephalopathy (AMS, nystagmus, gait ataxia) 2/2 thiamine deficiency --> hypoglycemia, elevated LFTs due to vomiting