Step 2 OB/GYN

What is Nagele’s rule?
due date = LMP + 9 months + seven days
What is developmental age?
number of weeks and days since fertilization. typically used only in research, as the exact date of fertilization is not commonly known
What is gestational age?
number of wks and days measured from the first day of the LMP.
How else can gestational age be determined?

Fundal height: at 20wks, uterus is at the umbilicus and grows approx 1 cm/wk

Quickening, or appreciation of fetal movt: typically occurs at 17-18 wks

Fetal heart tones: can be heard at 10-12 wks by Doppler

Ultrasound: measures fetal crown-rump length (CRL) at 5-12wks and measured biparietal diameter (BPD), femur length (FL), and abd circumference (AC) from 13 wks. U/S measurement of GA is most reliable during the first trimester

How does renal flow change in pregnancy?
increases 25-50%
How does glomerular filtration rate change in pregnancy?
increases early, then plateaus
We will write a custom essay sample on
Any topic specifically for you
For only $13.90/page
Order Now
How does uterine weight change in pregnancy?
increases from about 60-70g to about 900-1200g
How does body weight change in pregnancy?
average 11kg (25lb) increase
What is the standard for diagnosing pregnancy?
B-hCG
– produced by placenta; peaks at 100,000 mIU/mL by 10wks of gestation
– decreases throughout the second trimester; levels off in the third trimester
– hCG levels double approx every 48hrs during early pregnancy. This is often used to diagnose ectopic pregnancy when doubling is abnormal
What is a quantitative B-hCG used for?
– to diagnose and follow ectopic pregnancy
– to monitor trophoblastic disease
– to screen for fetal aneuploidy
What is a quad screen?
1) Maternal serum alpha-fetoprotein
– produced by the fetus, crosses the placenta in small amounts and enters the maternal circulation
– Elevated: assoc w/ open neural tube defects (anencephaly, spina bifida), abd wall defects (gastroschisis, omphalocele), multiple gestation, incorrect gestational dating, fetal death, and placental abnormalities (e.g. placental abruption)
– Decreased: assoc w/ trisomy 21 and 18, fetal demise, and inaccurate gestational dating.
2) inhibin A
3) estriol
4) B-hCG
What quad screen results suggest Trisomy 18?
ALL four decreased
What quad screen results suggest Trisomy 21
decreased AFP and estriol
Increased B-hCG and inhibin A
How does heart rate change in pregnancy?
gradually increases 20%
How does blood pressure change in pregnancy?
gradually decreases 10% by 34 wks, then increases to prepregnancy values
How does stroke volume change in pregnancy?
increases to maximum at 19wks, then plateaus
How does cardiac output change in pregnancy?
rises rapidly by 20%, then gradually increases an additional 10% by 28wks
How does peripheral venous distention change in pregnancy?
progressive increase to term
How does peripheral vascular resistance change in pregnancy?
progressive decrease to term
How does respiratory rate change in pregnancy?
unchanged
How does tidal volume change in pregnancy?
increases by 30-40%
How does expiratory reserve change in pregnancy?
gradual decrease
How does vital capacity change in pregnancy?
unchanged
How does respiratory minute volume change in pregnancy?
increases by 40%
How does blood volume change in pregnancy?
increases by 50% in second trimester
How does hematocrit change in pregnancy?
decreases slightly
How does fibrinogen change in pregnancy?
increases
How do electrolytes change in pregnancy?
unchanged
How does sphincter tone change in pregnancy?
decreases
How does gastric emptying time change in pregnancy?
increases
What is the recommended amount of weight women should gain in pregnancy?
an additional 100-300 kcal/day; 500 kcal/day during breastfeeding
Excessive gain: >1.5kg/mo
Inadequate gain: <1 kg/mo
What are the nutritional guidelines for pregnancy?
folic acid supplements (decrease neural tube defects for all reproductive-age women): 0.4 mg/day
Iron: 30mg/day of elemental iron
Calcium: 1300 mg/day for women <19yo; 1000mg/day >19yo
Vitamin D: 10ug or 400IU/day
Vitamin B12: 2ug/day
What is PAPP-A?
pregnancy-assoc plasma protein A
recommended at wks 9-14 to detect Down Syndrome and Trisomy 18 risk
combined with ultrasound-determined nuchal transparency (fluid in the fetal neck) + B-hCG
What is CVS?
chorionic villus sampling
recommended at wks 10-12
involves transcervical or transabd aspiration of placental (chorionic villi) tissue
What are the advantages and disadvantages of CVS?
Ads
– diagnostic accuracy comparable to that of amnio, available at 10-12wksDisads
– carries risk of fetal loss (1-2%); cannot detect open neural tube defects

What are complications of CVS?
limb defects have been assoc w/ CVS performed </= 9wks
How often should prenatal visits occur?
Wks 0-28: every four wks
Wks 29-35: every 2 wks
Wks 36-birth: every wk
What kind of testing should be completed at the initial prenatal visit?
Heme: CBC, Rh factor, type and screen
ID: UA and culture, rubella ab titer, HBsAg, RPR/VDRL, cervical gonorrhea and chlamydia, PPD, HIV, Pap smear (to check for dysplasia)
If indicated: HbA1c, sickle cell screening
Discuss genetic screening: Tay-Sachs, CF
What kind of prenatal testing should be completed at 9-14wks?
offer Triple Screen
– PAPP-A
– nuchal transparency
– free B-hCG +/- CVS
What kind of prenatal testing should be completed at 15-20wks?
Offer Quad Screen
– AFP
– estriol
– B-hCG
– inhibin A
+/- amniocentesis
What kind of prenatal testing should be completed at 18-20wks?
ultrasound for full anatomic screen
What kind of prenatal testing should be completed at 24-28 wks?
1hr glu challenge test for gestational diabetes screen
What kind of prenatal testing should be completed at 28-30 wks?
RhoGAM for Rh (-) women (after ab screen)
What kind of prenatal testing should be completed at 32-36wks?
GBS; repeat CBC
What kind of prenatal testing should be compeleted at 34-40wks?
cervical chlamydia and gonorrhea cultures, HIV, RPR in high-risk pts
What is an amniocentesis?
recommended 15-20wks
consists of transabdominal aspiration of amniotic fluid using an ultrasound guided needle and eval of fetal cells for genetic studies
What are the advantages and disadvantages of an amniocentesis?
Ads
– detects ~80% of open neural tube defects, ~85% of cases of Down syndrome, and ~60% of cases of trisomy 18Disads
– risks: premature rupture of membranes, chorioamnionitis, and fetal-maternal hemorrhage, which can result in fetal loss (0.5%)

When is an amniocentesis indicated?
– women who will be >35yo at time of delivery
– conjunction w/ an abnormal quad screen
– Rh-sensitized pregnancy to obtain fetal blood type or to detect fetal hemolysis
– to evaluate fetal lung maturity via a lecithin-to-sphingomyelin ratio >/=2.5 or to detect the presence of phosphatidylglycerol (done during the third trimester)
What does FDA Risk Category A suggest of drugs used during pregnancy?

adequate and well-controlled studies in women fail to demonstrate a risk to the fetus in the 1st trimester (and there is no risk in later trimesters). Possibility of fetal harm seems remote.

Ex) Vita B6, Vita E, folic acid (w/in recommended daily allowances)

What does FDA Risk Category B suggest of drugs used during pregnancy?

either animal reproduction studies have not demonstrated risk to the fetus but no adequate and well-controlled studies in pregnant women have been reported, or animal reproduction studies have shown an adverse effect that was not confirmed in controlled studies in women in the 1st trimester (and there is no evidence of risk in later trimesters).

Ex) ampicillin, acetaminophen, buproprion

What does FDA Risk Category C suggest of drugs used during pregnancy?

either studies in animals have revealed adverse effects on the fetus but no controlled studies in women have been reported, or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the fetus

Ex) diphenhydramine, rifampin, AZT

What does FDA Risk category D suggest of drugs used during pregnancy?

positive evidence of human fetal risk exists, but the benefits from use in pregnancy women may be acceptable despite risk

Ex) alcohol, phenytoin, tetracycline

What does FDA Risk Category X suggest of drugs used during pregnancy/

studies in animals or humans have demonstrated fetal abnormalities, or evidence exists of fetal risk based on human experience, or both, and the risk in pregnant women clearly outweighs any possible benefit

Ex) isotretinoin, thalidomide, warfarin

What kinds of fetal defects are assoc w/ ACEIs?
fetal renal tubular dysplasia and neonatal renal failure, oligohydramnios, IUGR, lack of cranial ossification
What kinds of fetal defects are assoc w/ alcohol?
FAS
– growth restriction before and after birth
– MR
– midfacial hypoplasia
– renal and cardiac defects
Consumption of >6 drinks per day is assoc w/ a 40% risk of FAS
What kinds of fetal defects are assoc w/ androgens?
virilzation of females; advanced genital development in males
What kinds of fetal defects are assoc w/ carbamazepine?
neural tube defects, fingernail hypoplasia, microcephaly, developmental delay, IUGR
what kinds of fetal defects are assoc w/ cocaine?
bowel atresias, congenital malformations of the heart, limbs, face, and GU tract; microcephaly; IUGR, cerebral infarctions
What kinds of fetal defects are assoc w/ DES?
clear cell adenocarcinoma of the vagina or cervix, vaginal adenosis, abnormalities of the cervix and uterus or testes, possible infertility
What kinds of fetal defects are assoc w/ lead?
increased spontaneous abortion (SAB) rate; still births
What kinds of defects are assoc w/ lithium?
congenital heart disease (Ebstein’s anomaly)
What kinds of defects are assoc w/ methotrexate?
increased SAB rate
What kinds of defects are assoc w/ organic mecury?
cerebral atrophy, microcephaly, MR, spasticity, seizures, blindness
What kinds of fetal defects are assoc w/ phenytoin?
IUGR, MR, microcephaly, dysmorphic craniofacial features, cardiac defects, fingernail hypoplasia
What kinds of fetal defects are assoc w/ radiation?
microcephaly, MR, medical dx radiation delivery <0.05 Gy to the fetus has no teratogenic risk
What kinds of fetal defects are assoc w/ streptomycin and kanamycin?
hearing loss; CN VIII damage
what kinds of fetal defects are assoc w/ tetracycline?
premanent yellow-brown discoloration of deciduous teeth; hypoplasia of tooth enamel
What kinds of fetal defects are assoc w/ thalidomide?
bilateral limb deficiencies, anotia, microtia, cardiac and GI anomalies
What kinds of fetal defects are assoc w/ Trimethadione and paramethadione?
cleft lip or clef palate, cardiac defects, microcephaly, MR
What kinds of fetal defects are assoc w/ valproic acid?
neural tube defects (spinal bifida); minor cranial defects
What kinds of fetal defects are assoc w/ vitamin A and derivatives?
increased SAB rate, thymic agenesis, cardiovascular defects, craniofacial dysmorphism, microphthalamia, cleft lip, or clef phrase, MR
What kinds of fetal defects are assoc w/ warfarin?
nasal hypoplasia and stippled bone epiphyses, developmental delay, IUGR ophthalmologic abnormalities
What are common sequelae of maternal-fetal infxns?
premature delivery, CNS abnormalities, anemia, jaundice, hepatosplenomegaly, growth retardation
What are the TORCH infxns?
most common pathogens causing maternal-fetal infxns
– Toxoplasmosis
– Other (parvovirus, varicella, Listeria, TB, malaria, fungi)
– Rubella
– CMV
– Herpes
– HIV
– Syphilis
What kinds of animals should pregnant women avoid?
cats
they shouldn’t change a cat’s litterbox
Which is more common, toxo during the first or third trimester?
1st trimester: less common, more severe
3rd trimester: more common, less severe
How does toxoplasmosis affect pregnant women?
transplacental transmission w/ primary infxn occuring via consumption of raw meat or contact w/ cat feces.
Specific findings: hydrocephalus, intracranial calcifications, chorioretinitis, ring-enhancing lesions on head CT
How does rubella affect pregnant women?
transplacental transmission in the 1st trimester.
Specific findings: purpuric “blueberry muffin” rash, cataracts, MR, hearing loss, patent ductus arteriosus (PDA)
How does CMV affect pregnant women?
most common congenital infxn
primarily transmitted transplacentally
specific findings: petechial rash (similar to “blueberry muffin” rash) and periventricular calcifications
How does herpes affect pregnant women?
intrapartum transmission if the mother has active lesions
Causes skin, eye, and mouth infxns or life-threatening CNS/systemic infxn
How does HIV affect pregnant women?
Transmission can occur in utero, at the time of delivery, or via breast milk
Occurs in 13-39% of births to infected mothers
Combination of AZT tx (prenatally, intrapartum, and neonatally for the first six wks of life) and C-section can lower transmission to 2%.
Newborns w/ congenitally acquired HIV are often ASx, failure to thrive, bacterial infxns w/ common organisms, and an increased incidence of upper and lower respiratory diseases may appear early or may be delayed for months to years. HIV + mothers should not breastfeed
How does syphilis affect pregnant women?
Primarily intrapartum transmission
Specific findings: maculopapular skin rash, lymphadenopathy, hepatomegaly, “snuffles” mucopurulent rhinitis, osteitis
Childhood findings: saber shins, saddle nose, CNS involvement and Hutchinson’s traid: peg-shaped upper central incisors, deafness, and interstitial keratitis (photophobia, lacrimation)
What is the definition of SAB?

loss of products of conception prior to the 20th wk of pregnancy.

Approx 60% of chemically evident pregnancies and 15-20% of clinically dx pregnancies terminate in a SAB. More than 80% occur in first trimester

What are the risk factors for an SAB?

Chromosomal abnormalities

Maternal factors
– maternal trauma, increased maternal age, infxn, dietary deficiencies
– inheritied thrombophilias: Factor V Leiden, prothrombin, antithrombin, proteins C and S, methylene tetrahydrofolate reductase (hyperhomocysteinemia)
– immunologic issues: antiphospholipids abs, alloimmune factors
– anatomic issues: uterine abnormalities, incompetent cervix, cervical conization, loop electrosurgical excision procedure, cervical injury, DES exposure, anatomical abnormalities of the cervix
– endocrine issues: DM, hypothyroidism, progesterone deficiency

Environmental factors: Tabacco, alcohol, caffeine, toxins, drugs, radiation

Fetal factors: anatomic malformation

How is SAB dx?

decreasing level of hCG

U/S: identify the gestational sac 5-6 wks from LMP, a fetal pole at six wks, fetal cardiac activity 6-7wks; accurate dating, a small, irregular intrauterine sac w/o fetal pole on transvaginal U/S is diagnostic of abnormal pregnancy

Maternal Rh type should be determined and RhoGAM given if the type is Rh neg

What is included in a normal obstetric exam?
1) Leopold’s maneuvers: determine fetal lie (longitudinal or transverse) and if possible, fetal presentation (breech or cephalic)
2) Cervical examination: evaluate dilation, effacement, station, cervical position, cervical consistency. Use Bishop score. Confirm or determine fetal presentation. Determine fetal position through palpation of the fetal sutures and fontanelles. Conduct a sterile speculum exam if rupture of membranes is suspected
What is the Bishop score?
used to evaluate the favorability of delivery and the probability of succeeding w/ an induction. Scoring:
0-4: indicates 45-50% chance of failure. Give prostaglandins for induction
5-9: points to a 10% chance of failure. Give pitocin for induction
10-13: assoc w/ very high probability of success. There is no need for intervention for induction
What are the different types of SAB?
– Complete
– Incomplete
– Threatened
– Inevitable
– Missed
– Septic
– Intrauterine fetal demise
– Recurrent
What is a complete SAB?
POC is expelled. Pain ceases, but spotting may persist.
CLOSED OS
U/S shows empty uterus
POC should be sent to pathology to confirm fetal tissueNo further intervention needed

What is an incomplete SAB?
some POC expelled, bleeding/mild cramping. Visible tissue on exam.
OPEN OS
U/S shows retained fetal tissueIntervention: manual uterine aspiration (MUA) or D&C

What is a threatened SAB?
No POC expelled. Uterine bleeding +/- abd pain
CLOSED OS
intact membranes, fetal cardiac motion on U/SIntervention: pelvic rest for 24-48hrs and follow-up U/S to assess the viability of conceptus

What is an inevitable SAB?
No POC expelled. Uterine bleeding and cramps
OPEN OS +/- ROMIntervention: MUA, D&C, misoprostol, or expectant mgmt

What is a missed SAB?
No POC expelled, No fetal cardiac motion, No uterine bleeding. Brownish vaginal discharge
CLOSED OS
No fetal cardiac activity, retianed fetal tissue on U/SIntervention: MUA, D&C, or misoprostol

What is a septic SAB?
endometritis leading to septicemia. Maternal mortality is 10-15%
Hypotension, hypothermia, increased WBC countIntervention: MUA, D&C, IV abx

What is an intrauterine fetal demise?
absence of fetal cardiac activity
Uterus is small for GA; no fetal heart tones or movt on U/SIntervention: induce labor; evacuate the uterus (D&E) to prevent DIC at GA >16wks

What is recurrent SAB?
Early pregnancy: often due to chromosomal abnormalities
Late pregnancy: due to hypercoagulable states (SLE, factor V Leiden, protein S deficiency)
Incompetent cervix: should be suspected w/ hx of painless dilation of cervix and delivery of a normal fetus btw 8 and 32 wksKaryotype both parents. Hypercoagulability work-up in mom. Evaluate for uterine abnormalities

Intervention: surgical cerclage procedures to suture the cervix closed until labor or ROM occurs w/ subsequent removal prior to delivery. Restrict activities

what is the medical procedures for a first trimester therapeutic abortion?
1) oral mifepristone (low dose) + oral/vaginal misoprostol UP TO 49 days GA
2) IM/oral methotrexate + oral/vaginal misoprostol UP TO 49 days GA
3) vaginal or sublingual or buccal misoprostol (high dose), repeated up to three times UP TO 56 days GA
What is the surgical procedure for a first trimester therapeutic abortion?
1) manual aspiration
2) D&C w/ vacuum aspirationBOTH UP TO 13 wks GA

What is the obstetric mgmt for a second trimester therapeutic abortion?
induction of labor (typically w/ prostaglandins, amniotomy, and oxytocin)
UP TO 13-24 wks GA (depending on state laws)
What is the surgical option for a second trimester therapeutic abortion?

D&E

UP TO 13-24 wks GA (depending on state laws)

What are the recommendations for FHR monitoring in pts w/o complications?
Review FHR tracings every 30 min in the first stage of labor and every 15 min in the second stage of labor
What are the recommendations for FHR monitoring in pts w/ complications
Review FHR tracings every 15 min in the first stage of labor and every 5 min in the second stage of labor
What are the components of reading FHR?
Rate (normal = 110-160)
– <110 = bradycardia —caused by congenital heart malformations or severe hypoxia (secondary to uterine hyperstimulation, cord prolapse, or rapid fetal descent) – >160 = tachycardia
—can be caused by hypoxia, maternal fever, fetal anemiaVariability (normal beat to beat variability = 6-25 bpm)
– undetectable variability indicates severe fetal distress
– minimal variability (<6) indicates fetal distress or effects of opioids or mag – marked variability (>25) indicates fetal distress; or may occur before a decrease in variability
– sinusoidal variability: points to serious fetal anemia; may also occur during maternal meperidine use
– accelerations: onset of increase in FHR to a peak in <30sec. Reassuring b/c they indicate fetal ability to appropriately respond to the environment
– decelerations: several types (early, late, variable)

What are the stages of labor?
First stage
– latent
– active
Second
Third
What occurs during the first stage of labor?
Latent: onset of labor to 3-4cm dilation
– primiparous: 6-11hrs
– multiparous: 4-8hrs
– prolonged if excessive sedation and hypertonic uterine contractionsActive: 4cm to complete cervical dilation (10cm)
– primiparous: 4-6hrs (1.2cm/hr)
– multiparous: 2-3hrs (1.5cm/hr)
– prolongation seen w/ cephalopelvic disproportion

what occurs during the second stage of labor?
complete cervical dilation to delivery of infant
– primparous: 0.5-3.0hrs
– multiparous: 5-30min
When baby goes through all cardinal mvts of delivery
What occurs during the third stage of labor?
delivery of infant to delivery of placenta
– primparous and multiparous: 0-0.5 hr
uterus contracts and placenta separates to establish hemostasis
What is an early fetal deceleration?
visually apparent, gradual (onset to nadir in >30sec) decrease in FHR w/ a return to baseline that mirrors the uterine contraction
Etiology: head compression from uterine contraction (normal)
What is a late fetal deceleration?
WORRISOME
visually apparent, gradual (onset to nadir in >30 sec) decrease in FHR w/ return to baseline whose onset, nadir, and recovery occur after the beginning, peak, and end of uterine contraction, respectively
Etiology: uteroplacental insufficiency and fetal hypoxemia
What is a variable fetal deceleration?
an abrupt (onset to nadir in <30sec), visually apparent decrease in FHR below baseline lasting >/= 15 sec but <2 min
Etiology: umbilical cord compression
What are the indications for antepartum fetal surveillance?
used in pregnancies w/ increased risk for fetal demise.
Begin 32-34wks for at risk pts
26-28 if there are multiple worrisome risks
What are the components of antepartum fetal surveillance?
Fetal movt assessment:
– # movts in an hr; assessed by mom
– average is 10 movts q20min
– if decreased movt…Nonstress Test (NST)
– mom is resting in lateral tilt position (prevent supine hypotension)
– FHR monitored externally by Doppler along w/ a tocodynamometer to detect uterine contractions
– Acoustic stimulation can be used
– Results:
—“reactive” (normal response): two accelerations of >/=15 bpm above baseline lasting for at least 15 sec over a 20min period
—“nonreactive”: fewer than two accelerations over a 20 min period. Perform further tests (e.g. biophysical profile). Lack of FHR accelerations may occur w/ any of the following:
—–GA<32 wks —–fetal sleping —–fetal CNS anomalies —–maternal sedative or narcotic administration Contraction Stress Test (CST) – mom in lateral recumbent position – FHR monitored during spontaneous or induced (via nipple stimulation or oxytocin) contractions – reactivity is determined from fetal heart monitoring, as w/ NST – procedure CI in women w/ preterm membrane rupture or known placenta previa; women w/ history of uterine surgery; women who are at high risk for preterm labor – Results: —“Positive” CST: late decelerations following 50% or more of contractions in a 10min window; raises concerns about fetal compromise. DELIVERY NEEDED —“Negative” CST: no late or significant variable decelerations w/in 10 min and at least 3 contractions. Highly predictive of fetal well-being in conjunction w/ a normal NST —“Equivocal” CST: defined by intermittent late decelerations or significant variable decelerations Biophysical profile (BPP) – real-time U/S to assign a score of 2 (normal) or 0 (abnormal) to five parameters –fetal tone –breathing –movement –amniotic fluid volume –NST – Scoring: —8-10: reassuring for fetal well-being —6: considered equivocal. Term pregnancies delivered w/ this profile —0-4: Extremely worrisome for fetal asphyxia; strong consideration should be given to immediate delivery if no other explanation is found Modified BPP (mBPP) – combines NST w/ amniotic fluid index (AFI). Normal if reactive NST and AFI>5cm

Umbilical artery Doppler Velocimetry
– IUGR: reduction and even reversal of umbilical artery diastolic flow. Test is of benefit only when IUGR is suspected

Oligohydramnios (AFI <5 cm) ALWAYS warrants further work-up

Where is the pain in uterine contractions and cervical dilation?
visceral pain at T10-L1
Where is the pain when the fetal head descends and pressure is placed on vagina and perineum?
somatic pain at S2-S4
What are absolute CI to regional anesthesia during delivery?
refractory maternal hypotension
maternal coagulopathy
maternal use of once-daily dose of LMW Heparin w/in 12hrs
untreated maternal bacteremia
skin infxn over the site of needle placement
Increased ICP caused by mass lesion
What is hyperemesis gravidarum?

persistent vomiting not related to other causes, acute starvation (usually large ketonuria), and weight loss

Evaluate Severity:
– ketonemia, ketonuria, hyponatremia, and hypokalemic, hypochloremic metabolic alkalosis
– measure LFTs, serum bilirubin, serum amylase/lipase

More common in first pregnancy, multiple gestations, and molar pregnancies.
– check B-hCG and U/S to r/o molar pregnancy

If “morning sickness” persists after the first trimester, think hyperemesis gravidarum

Increased B-hCG and estradiol implicated

R/O acid reflux, gastroenteritis, hyperthyroidism, neuro conditions

What are the different types of pain relief offered to delivery moms?
Nonpharmacologic
Opiods
Local block (lidocaine)
Epidural
Spinal
Combined spinal epidural
General
What is included in nonpharmacologic pain relief and what are the advantages of this method?
social support, massages, breathing, aromatherapy, ambulation, and repositioning
– no known neg side effects
– works by increasing coping w/ pain rather than eliminating painBUT offers limited pain relief

What are the advantages/disadvantages of using opiods for obstetric analgesia/anesthesia?

ADS: provide an adequate level of pain relief for some women w/o risks assoc w/ regional anesthesia

DISADS: sedative effect of opiods decreases FHR variability and increases the possible need for neonatal naloxone admin and five-min APGAR scores <7

What are the advantages/disadvantages of using local blocks for obstetric analgesia/anesthesia?

ADS: excellent anesthesia before episiotomy and during repair of lacerations; can be used to perform a pudendal block

DISADS: rarely, may cause seizures, hypotension, and cardiac arrhythmias

What are the advantages/disadvantages of using epidural for obstetric analgesia/anesthesia?

ADS: MOST effective form of pain relief; can also be used for C-section or postpartum tubal ligation

DISADS: can result in pruritis, fever, hypotension, and transient FHR deceleration

What are the advantages/disadvantages of using spinal for obstetric analgesia/anesthesia?

ADS: rapid onset analgesia that provides excellent pain relief for procedures of limited duration (30-250min)

DISADS: Limited duration. Puts pts at risk for hypotension, postdural puncture headache, and transient neuro sx

What are the advantages/disadvantages of using combined spinal epidural for obstetric analgesia/anesthesia?

ADS: offers rapid onset of spinal analgesia combined w/ ability to prolong duration of analgesia w/ continuous epidural infusion

DISADS: carries risk of both procedures; may increase risk of bradycardia and emergent cesarean delivery over epidural analgesia alone

What are the advantages/disadvantages of using general anesthesia for obstetric analgesia/anesthesia?

ADS: used in emergent c-section and indicated in some cases of FHR abnormality; can be useful in cases where regional anesthesia is absolutely CI or fails

DISADS: requires airway control; carries significant risk of maternal aspiration and neonatal depression (inhaled anesthetic agents readily cross placenta); assoc w/ higher maternal morbidity rates than epidural anesthesia

How is hyperemesis gravidum tx?
1) Admin Vitamin B6
2) doxylamine (antihistamine) PO
3) Promethazine or deminhydrinate PO/PR
4) If severe: metoclopramide, ondansetron, prochlorperazine, or promethazine IM/PO
5) If dehydrated: IV fluids, IV nutritional supplementation, dimenhydrinate IV
What is the difference btw gestational diabetes and pregestational diabetes?
gestational = onset occurs during pregnancy
What classification system is used to risk stratify women with diabetes assoc w/ pregnancy?
White Classification
A1: gestational; insulin not required
A2: gestational; insulin required
B: age of onset 20yrs or older or duration <10yrs
C: age of onset 10-19yrs or duration 10-19yrs
D: age of onset<10yrs or duration >20yrs
F: nephropathy
H: cardiomyopathy
R: proliferating retinopathy
RF: proliferating retinopathy
T: renal transplant
How does gestational diabetes present?
typically ASx
Edema, polyhydramnios, or a large-for-GA infant (>90th percentile) may be warning signsoccurs in 3-5% of all pregnancies, usually in late pregnancy

How is gestational diabetes dx?
1) One hr 50g glu challenge test; venous plasma glucose is measured one hr later (at 24-48wks). Values >/=140mg/dL are considered abnormal
2) Confirm w/ an oral three hr 100g glu tolerance test showing any two of the following: fasting >95mg/dL; one hr>180mg/dL; two hr>155mg/dL, three hrs >140mg/dL
How is gestational diabetes tx?
Mom:
1) start on ADA diet, regular exercise, strict glu monitoring (4x/day). Tight maternal glu control (fasting glu <100; one to two hr postprandial glu <150) improves outcomes
2) add insulin if dietary control is insufficient
Give intrapartum insulin and dextrose to maintain tight control during deliveryFetus:
– Obtain periodic U/S and NSTs to assess fetal growth and well being (30-32wks)
– may be necessary to induce labor at 39-40wks

What are complications of gestational diabetes?
more than 50% pts go on to develop glucose intolerance and/or type 2DM later in life
What are risks of pregestational diabetes?
poorly controlled DM is assoc w/ increased risk of congenital malformations, fetal loss, and maternal/fetal morbidity during labor and delivery
How is pregestational diabetes tx?
Mother:
– renal, ophthalmologic, and cardiac evaluation to assess for end-organ damage.
– strict glu control (w/ diet, exercise, insulin tx, and frequent self-monitoring for type 1 and type 2 DM) to minimize fetal defects
–Fasting AM<90mg/dL
–two-hr postprandial<120mg/dL Fetus: – 18-20wks: u/s to determine fetal age and growth: evaluate for cardiac anomalies and polyhydramnios; quad screen to screen for developmental anomalies – 32-4wks: close fetal surveillance (NST, CST, BPP). Admit if maternal DM has been poorly controlled for fetal parameters are a concern. Serial U/S for fetal growth Delivery and postpartum – maintain normoglycemia (80-100mg/dL) during labor w/ an IV insulin drip and hourly glu measurements – consider early delivery in the setting of poor maternal glu control, preeclampsia, macrosomia, evidence of fetal lung maturity – c-section should be considered for EFW> 4500g
– encourage breastfeeding w/ appropriate increase in caloric intake
– continue glu monitoring postpartum. Insulin needs rapidly decrease after delivery
What lab tests in mom suggest pregestational diabetes?
HgbA1c>8%
UA before 20wks reveals glycosuria
Hyperglycemia in 1st trimester
What is the difference btw gestational and chronic HTN?
Gestational HTN:
– aka PIH
– idiopathic HTN w/o significant proteinuria (<300mg/L) that develops at >20wks’ gestation. 25% will develop preeclampsiaChronic HTN:
– present before conception and at <20wks gestation, may persist >12wks postpartum
– 1/3 may develop superimposed preeclampsia

How are gestational and chronic HTN tx?
Monitor BP closely and tx w/ appropriate anti-HTN (methyldopa, labetalol, nifedipine). DO NOT give ACEIs or diuretics
What are complications that can occur if pregnant pts receive ACEIs or diuretics?
ACEIs: uterine ischemia
Diuretics: low plasma volume to point of uterine ischemia
What are complications of gestational and chronic HTN?
similar to preeclampsia
What is preeclampsia?
new onset HTN (SBP>140 or DBP> 90) and proteinuria (>300mg in 24hrs) occuring at >20wks gestation
What is eclampsia?
new onset grand mal seizures in women w/ preeclampsia
What is HELLP syndrome?
Hemolytic anemia
Elevated liver enzymes
Low plateletVariant of preeclampsia w/ poor prognosis
Clinical manifestations explained by vasospasm leading to hemorrhage and organ necrosis

What are maternal complications of pregestational DM?
DKA (type 1) HHNK (type 2)
preeclampsia/eclampsia
cephalopelvic disproportion (from macrosomia) and need for C-section
preterm labor
infxn
polyhydramnios
postpartum hemorrhage
maternal mortality
What are fetal complications of pregestational DM?
macrosomia or IUGR
cardiac and renal defects
neural tube defects (sacral agenesis)
hypocalcemia
polycythemia
hyperbilirubinemia
IUGR
hypoglycemia from hyperinsulinemia
respiratory distress syndrome
birth injury (shoulder dystocia)
perinatal mortality
What are risk factors for preeclampsia/eclampsia?
nulliparity, African-American ethnicity, extremes of age (<20 or >35), multiple gestation, molar pregnancy, renal disease (due to SLE or type I DM), FHx of preeclampsia, chronic HTN
What are the s/sx of mild preeclampsia?
usually ASx
BP>/= 140/90 on 2 occasions >6hrs apart
Proteinuria (>300mg/24hrs or 1-2 + urine dipsticks)
Edema
What are the s/sx of severe preeclampsia?
BP>160/110 on two occasions >6hrs apart
Renal: proteinuria (>5g/24hrs or 3-4+urine dipsticks) or oliguria (<500 mL/24hrs).
Cerebral changes: headache, somnolence
Visual changes: blurred vision, scotoma
Hyperactive reflexes/clonus
RUQ pain
Hemolysis, elevated liver enzymes, thrombocytopenia (HELLP)
What are the s/sx of eclampsia?
signs preceding eclamptic attack
– HA, visual changes, RUQ/epigastric pain
Seizures are severe if not controlled w/ anticonvulsant tx
What is the classic triad for preeclampsia?
HTN
proteinuria
edema
What is the ONLY cure for preeclampsia/eclampsia?
delivery of fetus
How is preeclampsia tx?
if pts is close to term or preeclampsia worsens, induce delivery w/ IV oxytocin, prostaglandin, amniotomy
if far from term, tx w/ modified bed rest and expectant mgmt
How is severe preeclampsia tx?
1) Control BP w/ labetalol and/or hydralazine (goal <160/110, DBP btw 90-110 to maintain fetal blood flow).
2) Prevent seizures w/ continuous MgSO4 drip
– watch for signs of mg toxicity (Loss of DTRs, respiratory paralysis, coma). Continue seizure prophy for 24hrs postpartum. Tx mg toxicity w/ IV calcium gluconate
3) Delivery by induction of C-section when mother is stable
How is eclampsia tx?
1) ABCs w/ O2
2) seizure control/prophy w/ mg. If seizures recur, give IV diazepam. Monitor mg blood levels and mag toxicity; monitor fetus status. Control BP (labetalol and/or hydralazine). Limit fluids; Foley for strict I/Os.
3) Initiate delivery if pt is stable and convulsions are controlled. Postpartum mgmt is the same as that for preeclampsia. Seizures may occur antepartum, intrapartum, or postpartum. Most w/in 48hrs after delivery
What are complications of preeclampsia?
prematurity
fetal distress
stillbirth
placental abruption
seizure
DIC
cerebral hemorrhage
serous retinal detachment
fetal/maternal death
What are complications of eclampsia?
cerebral hemorrhage
aspiration pneumonia
hypoxic encephalopathy
thromboembolic events
fetal/maternal death
What are possible causes of third trimester bleeding?
Vagina: bloody show, trauma
Cervix: cervical cancer, cervical/vaginal lesion
Placenta: placental abruption, placenta previa
Fetus: fetal bleeding
What is antepartum bleeding?
bleeding that occurs after 20wks gestation
(bleeding before 20wks = threatened abortion)
most common causes: placental abruption, placenta previa
other causes: abnormal placentation (placenta accreta), ruptured uterus, genital tract lesions, and trauma
What is placental abruption?
premature (before delivery) separation of normally implanted placenta
What are risk factors for placental abruption?
HTN
abd/pelvic trauma
tobacco or cocaine use
previous abruption
rapid decompression of an overdistended uterus
excessive stimulation
What are sx of placental abruption?
PAINFUL
Dark vaginal bleeding that does not spontaneously cease
Abd pain, uterine hypertonicity
Fetal distress
How is placental abruption dx?
Clinical dx
Transabdominal/transvaginal U/S sensitivity : 50%
Look for retroplacental clot; most useful for ruling out previa
How is placental abruption tx?
Stabilize pt w/ mild abruption and a premature fetus–>manage expectantly
–hospitalize
–start IV and fetal monitoring
–type and cross blood
–bed restModerate to severe abruption–>IMMEDIATE delivery
— vaginal delivery w/ amniotomy if mother and fetus are stable and delivery is expected soon
–C-section for maternal or fetal distress

What are complications of placental abruption?
Hemorrhagic shock
Coagulopathy: DIC in 10%
Recurrence risk is 5-16% and rises to 25% after 2 previous abruptions
Fetal hypoxia
What is placenta previa?
Abnormal placental implantation
– total: covers cervical os
– marginal: placenta extends to margin of the os
– low-lying: placenta is in close proximity to os
What are risk factors for placenta previa?
prior C-sections, grand multiparity, advanced maternal age, multiple gestation, prior placenta previa
How does placenta previa present?
PAINLESS
bright red blood that often ceases in 1-2 hrs w/ or w/o uterine contractions
Usually no fetal distress
How is placenta previa dx?
transabdominal/transvaginal U/S sensitivity is >95%
Look for an abnormally positioned placenta
How is placenta previa tx?
NO VAGINAL EXAMS!
stabilize pts w/ a premature fetus–>mgmt expectantly
Give tocolytics
Serial U/S to assess fetal growth; resolution of partial previa
Give betamethasone to help w/ fetal lung maturity
Delivery by C-section
–Indications for delivery
—labor
—life-threatening bleeding
—fetal distress
—documented fetal lung maturity
—36wks GA
What are complications of placenta previa?
increased risk of placenta accreta
vasa previa (fetal vessels crossing the internal os
preterm delivery, PROM, IUGR, congenital anomalies
recurrence risk is 4-8%
What is an ectopic pregnancy?
tubal, but can be abd, ovarian, or cervical pregnancy
How does ectopic pregnancy typically present?
abd pain and vaginal spotting/bleeding although some pts are ASx
Assoc w/ etiologies that cause scarring to the fallopian tubes (Hx of PID, pelvic surgery, DES use, or endometriosis)
What is the DDx for ectopic pregnancy?
surgical abd
abortion
ovarian torsion
PID
rupture ovarian cyst
How is ectopic pregnancy dx?
RUPTURED ECOPTIC PREGNANCY UNTIL PROVEN OTHERWISE
1) + pregnancy test and transvaginal u/s showing an empty uterus
2) confirm w/ serial hCG w/o appropriate hCG doubling
How is ectopic pregnancy tx?
Medical tx: methotrexate for small, unruptured tubal pregnancies
Surgical tx: salpingectomy or salpingostomy w/ evacuation (laparoscopy vs. laparotomy)
What are complications of ecoptic pregnancy?
tubal rupture and hemoperitoneum (obstetric emergency)
What is IUGR?
EFW less than 10th percentile for GA
How does IUGR present?
affected infants are commonly born to women w/ systemic diseases that lead to uteroplacental insufficiency (intrauterine infxn, HTN, anemia)
other risk factors: maternal substance, placenta previa, multiple gestations
How is IUGR dx?
1) Confirm serial fundal height measurements w/ U/S
2) U/S the fetus for EFW (although as pregnancy advances, ultrasound fetal weight estimates become increasingly unreliable)
How is IUGR tx?
1) explore underlying etiology and correct if possible
2) if near due date, admin steroids (betamethasone) to accelerate fetal lung maturity
3) perform fetal monitoring w/ NST, CST, BPP, and umbilical artery Doppler velocimetry. A nonreassuring status near term may prompt delivery
What are complications of IUGR?
increase perinatal morbidity and mortality
What is fetal macrosomia?
birth weight> 90th percentile. Common sequela of gestational diabetes
How is fetal macrosomia dx?
dx by weighing newborn at birth (prenatal dx is imprecise)
How is fetal macrosomia tx?
planned C-section delivery may be considered if EFW>5000g in women w/o diabetes and EFW >4500g in women w/ diabetes
What are complications of fetal macrosomia?
increased risk of shoulder dystocia (leading to brachial plexus injury and Erb-Duchenne palsy) as birth weight increases
What is polyhydramnios?
AFI>20 on U/S
– may be present in normal pregnancies, but fetal chromosome developmental abnormalities must be considered
What are causes of polyhydramnios?
maternal DM
multiple gestation
isoimmunization
pulmonary abnormalities (cystic lung malformations)
fetal anomalies (duodenal atresia, tracheoesophageal fistula, anencephaly)
twin-twin transfusion syndrome
How does polyhydramnios present?
usually ASx
How is polyhydramnios dx?
fundal height greater than expected
evaluation includes U/S for fetal anomalies, glu testing for DM and Rh screen
What are complications of polyhydramnios?
preterm labor, fetal malpresentation, cord prolapse
What is oligohydramnios?
AFI<5cm on U/S
Usually ASx, but IUGR or fetal distress may be present
What are causes of oligohydramnios?
fetal urinary tract abnormalities (renal agenesis, GU obstruction), chronic uteroplacental insufficiency, and ROM
How is oligohydramnios dx?
sum of deepest amniotic fluid pocket in all 4 abdominal quadrants on U/S
How is oligohydramnios tx?
r/o inaccurate gestational dates
tx underlying cause, if possible
What are complications of oligohydramnios?
assoc w/ 40x increase in perinatal mortality
musculoskeletal abnormalities (clubfoot, facial distortion), pulmonary hypoplasia, umbilical cord compression, and IUGR
What is Rh isoimmunization?
fetal RBCs leak into maternal circulation, maternal anti-Rh IgG abs form an cross the placenta, leads to hemolysis of fetal Rh RBCs (erythroblastosis fetalis)
What blood type of women are at risk for RH isoimmunization?
Rh neg women who have had previous SAB or TAB as well as among those who have undergone a previous delivery w/ no RhoGAM given
How is Rh isoimmuniztion dx?
sensitized Rh neg mothers w/ titers >1:16 should be closely monitored w/ serial u/s and amniocentesis for evidence of fetal hemolysis
How is Rh isoimmunization tx?
Severe cases: initiate preterm delivery when fetal lungs mature
Prior to delivery: intrauterine blood transfusions may be given to correct a low fetal hematocrit
How is Rh isoimmunization prevented?
If Rh neg at 28wks and father is Rh+ or unknown, give RhoGAM
If baby is Rh+, give RhoGAM postpartum
Give RhoGAM to Rh neg mothers who undergo abortion or who have had placental abruption. T&S critical; follow B-hCG closely and prevent pregnancy for one year
What are complications of Rh isoimmunization?
hydrops fetalis occurs when fetal hemoglobin drops to <7 g/dl
other complications: fetal hypoxia, acidosis, kernicterus, prematurity, death
What is gestational trophoblastic disease (GTD)?
range of proliferative trophoblastic abnormalities that can be benign or malignant
– complete moles
– incomplete (partial) moles
What are complete moles?
usually result from sperm fertilization of an empty ovum, 46XX (paternally derived)
What are incomplete moles?
occur when a normal ovum is fertilized by two sperm (or haploid sperm that duplicates its chromosomes); usually 69XXY and contain fetal tissue
How do moles present?
present w/ first trimester uterine bleeding (most common), hyperemesis gravidarum, preeclampsia/eclampsia at <24wks, uterine size greater than dates
What are risk factors for gestational trophoblastic disease?
extremes of age (<20 or >40yrs) and a diet deficient in folate or beta-carotene
How is gestational trophoblastic disease dx?

no fetal heartbeat is detected. Pelvic exam may reveal enlarged ovaries (bilateral theca-lutein cysts) or expulsion of grapelike molar clusters into the vagina

Labs: show markedly increased serum B-hCG (usually>100,000 mIU/mL) and pelvic ultrasound reveals a “snowstorm” appearance w/ no gestational sac or fetus present

CXR: show lung metastases; D&C reveals “cluster of grapes” tissue

How is gestational trophoblastic disease tx?
Evacuate the uterus and follow w/ weekly B-hCG.
Treat malignant disease w/ chemotx (methotrexate or dactinomycin) and residual uterine disease w/ hysterectomy; chemotx and irradiation are highly effective for metastases
What are complications of gestational trophoblastic disease?
molar pregnancy may progress to malignant GTD, including invasive moles (10-15%) and choriocarcinoma (2-5%) w/ pulmonary or CNS metastases. Trophoblastic pulmonary emboli may also be seen.
How do multiple gestations present?
characterized by rapid uterine growth, excessive maternal weight gain, and palpation of three or more large fetal parts on Leopold’s maneuvers
How are multiple gestations dx?
ultrasound; hCG, HPL, and MSAFP are elevated for GA
How are multiple gestations tx?
multifetal reduction and selective fetal termination is an option for higher-order multiple pregnancies; antepartum fetal surveillance for IUGR. Mgmt by a high-risk specialist is recommended
What are some complications of multiple gestations?

Maternal: Pts are 6x more likely to be hospitalized w/ complications–e.g. preeclampsia, preterm labor, PPROM, placental abruption, pyelonephritis, postpartum hemorrhage

Fetal: twin-to-twin transfusion syndrome, IUGR, and preterm labor

What are the risk factors for shoulder dystocia?
obesity, diabetes, hx of macrosomic infant, and hx of prior shoulder dystocia
How is shoulder dystocia dx?
dx by prolonged second stage of labor, recoil of the perineum (“turtle sign”), and lack of spontaneous restitution
How is shoulder dystocia tx?

In the event of dystocia, be the mother’s HELPER:

Help reposition
Episiotomy
Leg elevated (McRoberts’ maneuver
Pressure (suprapubic)
Enter the vagina and attempt rotation (Wood’s screw)
Reach for the fetal arm

What conditions is failure to progress assoc w/?
chorioamnionitis
occiput posterior position
nulliparity
elevated birth weight
How is failure to progress dx?

First stage protraction or arrest: labor that fails to produce adequate rates of progressive cervical change

Prolonged second-stage arrest:
– nulliparous: inadequate cervical dilation after >3 hrs w/ regional anesthesia, >2hrs w/o
– multiparous: inadequate cervical dilation after >2 hrs w/ regional anesthesia; >1 hrs w/o

How is failure to progress tx in the first stage?
First stage: failure to have progressive cervical change
– Latent
—Prima: >20hrs
—Multi: >14hrs
—Tx: therapeutic rest via parenteral analgesia; oxytocin; amniotomy; cervical ripening- Active
—Prima: >2hrs
—Multi: >2hrs after reaching 3-4cm
—Tx: amniotomy; oxytocin; C-section if the previous interventions are ineffective

How is failure to progress tx in the second stage?
Arrest of fetal descent:
– Prima>2hrs; >3hrs w/ epidural
—Tx: close observation w/ decrease in epidural rate and continued oxytocin
– Multi: >1hr; >2hrs w/ epidural
—Tx: assisted vaginal delivery (forceps or vacuum). C-section
What are complications of failure to progress?
Chorioamnionitis leads to fetal infxn, pneumonia, and bacteremia
Some 10% of those affected have permanent injury, 11% have a risk of postpartum hemorrhage, and 3.8% are at risk of fourth-degree laceration.
What is spontaneous rupture of membranes?
occurs >1 hr before onset of labor. May be precipitated by vaginal or cervical infxns, abnormal membrane physiology, or cervical incompetence
What is PPROM?
preterm premature rupture of membrane
rupture of membranes occurring at <37 wks’ gestation
What is PROM?
Premature rupture of membrane
defined as rupture >18hrs prior to delivery.
What are the risk factors to PROM?
low SES, young maternal age, smoking, STDs
How does rupture of membranes present?
pts often report a “gush” of clear or blood-tinged amniotic fluid
Uterine contractions may be present
How is rupture of membranes dx?
First Step
– sterile speculum exam reveals pooling of amniotic fluid in the vaginal vault
– nitrazine paper test + (paper turns blue, indicating alkaline pH of amniotic fluid)
– fern test + (ferning pattern is seen under a microscopic after amniotic fluid dries on a glass slide)Second Step
– ultrasound to assess amniotic fluid volume

If unsure: U/S- guided transabdominal instillationo f indigo carmine dye to check for leakage (unequivocal test)

Minimize infxn risk: DO NOT perform digital vaginal exams on women who are not in labor or for whom labor is not planned immediately

Check fetal heart tracing, maternal temperature, WBC count, and uterine tenderness for evidence of chorioamnionitis

How is PROM tx?
Depends on GA and fetal lung maturity
– Term: first check GBS status and fetal presentation; then labor may be induced or the pt can be observed for 24-72
>34-36wks gestation: labor induction may be considered
<32wks gestation: expectant mgmt w/ best rest and pelvic restAbx: given to prevent infxn and to prolong the latency period in the absence of infxn
– if signs of infxn or fetal distress develop, give abx (ampicillin and gentamicin) and induce labor

Antenatal corticosteroids: (betamethasone or dexamethasone x 48hrs)
– can be given to promote fetal lung maturity in the absence of intra-amniotic infxn prior to 32 wks GA

What are complications of PROM?
preterm labor and delivery, chorioamnionitis, placental abruption, cord prolapse
What is preterm labor?
defined as onset of labor between 20-37wks’ gestation
occurs in >10% of all U.S. pregnancies and is the primary cause of neonatal morbidity and mortalityregular uterine contractions + concurrent cervical change at <37wks’ gestation.

What are risk factors to preterm labor?
multiple gestation, infxn, PROM, uterine anomalies, previous preterm labor or delivery, polyhydramnios, placental abruption, poor maternal nutrition, and low SES. Most pts have no identifiable risk factors
How does preterm labor present?
pts may have menstrual-like cramps, onset of low back pain, pelvic pressure, and new vaginal discharge or bleeding
How is preterm labor dx?
– requires regular uterine contractions (>/= 3 contractions of 30sec each over a 30min period) and concurrent cervical change at <37 wks’ gestation
– Assess CI to tocolytics (infxn, nonreassuring fetal testing, placental abruption)
– perform sterile speculum exam to r/o PROM
– Obtain an U/S to r/o fetal or uterine anomalies, verify GA, and assess fetal presentation and amniotic fluid volume
– Obtain cultures for chlamydia, gonorrhea, and GBS. Obtain a UA and urine culture
How is preterm labor tx?
– hydration and best rest
– unless CI, begin tocolytic tx (B-mimetics, MgSO4, CCBs, PGIs) and give steroids to accelerate fetal lung maturation. Give penicillin or ampicillin for GBS prophylaxis if preterm delivery is likely
What are complications of preterm labor?
RDS, intraventricular hemorrhage, PDA, necrotizing enterocolitis, retinopathy of prematurity, bronchopulmonary dysplasia, death
What is fetal malpresentation?
defined as any presentation other than vertex (i.e. head closet to birth canal, chin to chest, occiput anterior).
What are the risk factors for fetal malpresentation?
prematurity, prior breech delivery, uterine anomalies, poly- or oligohydramnios, multiple gestations, PPROM, hydrocephalus, anencephaly, and placenta previa
What is the most common form of fetal malpresentation?
breech presentation= presentation of fetal lower extremities or buttocks into the maternal pelvis
– Frank breech (50-75%): thighs are flexed and the knees are extended
– Footling breech (20%): one or both legs are extended below the buttocks
– Complete breech (5-10%): thighs and knees are flexed
How is fetal malpresentation tx?
Follow: up to 75% spontaneously change to vertex by wk 38
External version: apply directed pressure to the maternal abdomen to turn the infant to vertex. Success rate is roughly 50%.
Trial of breech vaginal delivery: attempt only if delivery is imminent; otherwise contraindicated.
Elective C-section: recommended given the lower risk of fetal morbidity
What are the risk factors of version?
placental abruption and cord compression so be prepared for an emergency C-section if needed.
What are complications of trial of breech vaginal delivery?
cord prolapse and/or head entrapment
What are the maternal factors for C-section?
– prior classical C-section (vertical incision predisposes to uterine rupture w/ vaginal delivery)
– active genital herpes infxn
– cervical carcinoma
– maternal trauma/demise
– HIV infxn
– prior transverse C-section (relative indication)
What prophy should be given to women who undergo a C-section?
sodium citrate should be used to decrease gastric acidity and prevent acid aspiration syndrome
What are the fetal and maternal factors for C-section?
– cephalopelvic disproportion (most common cause of primary C-section)
– placenta previa/placental abruption
– failed operative vaginal delivery
– post-term pregnancy (relative indication)
What are the fetal factors for C-section?
– fetal malposition (e.g. posterior chin, transverse lie, shoulder presentation)
– fetal distress
– cord compression/prolapse
– erythroblastosis fetalis (Rh incompatibility)
What is an episiotomy?
surgical extension of the vaginal opening into the perineum
– Types; Media and mediolateral
What are the complications of episiotomy?
extension to the anal sphincter (third degree) or rectum (fourth degree), which is more common w/ midline episiotomy, as well as bleeding, infxn, dyspareunia, and in rare cases, rectovaginal fistula formation or maternal death
Are episiotomies recommended?
NOT recommended
What is postpartum hemorrhage?
defined as a loss of >500mL of blood for vaginal delivery OR >1000 mL for C-section occurring before, during, or after delivery of the placenta
What are complicates of postpartum hemorrhage?
acute blood loss (potentially fatal), anemia due to chronic blood loss (predisposes to puerperal infxn), and Sheehan’s syndrome (pituitary ischemia and necrosis; the primary cause of anterior pituitary insufficiency in adult females, most commonly presenting as failure to lactate)
What are the risk factors for uterine atony?
– uterine overdistention (multiple gestation, macrosomia, polyhydramnios)
– Exhausted myometrium (rapid or prolonged labor, oxytocin stimulation)
– Uterine infxn
– Conditions interfering w/ contractions (anesthesia, myomas, MgSO4)
What are the risk factors for genital tract trauma?
– precipitous labor
– operative vaginal delivery (forceps, vacuum extraction)
– large infant
– inadequate episiotomy repair
What are the risk factors for retained placental tissue?
placenta accreta/increta/percreta
Placenta previa
uterine leiomyomas
preterm delivery
previous C-section/curettage
How is uterine atony dx?
palpation of soft, enlarged, “boggy” uterus
Most common cause of postpartum hemorrhage (90%)
How is genital tract trauma dx?
manual and visual inspection of the lower genital tract for any laceration >2 cm long
How is retained placental tissue dx?
manual and visual inspection of the placenta and uterine cavity for missing cotyledons.
U/S may also be used to inspect the uterus
How is uterine atony tx?
bimanual uterine massage (usually successful)
Oxytocin infusion
Methergine (methylergonovine) if not hypertensive
Prostaglandin
How is genital tract trauma tx?
surgical repair of the physical defect
How is retained placental tissue tx?
manual removal of remaining placental tissue
curettage w/ suctioning (take care not to perforate the uterine fundus)
What is the ultimate lifesaving tx for all uterine causes of postpartum hemorrhage?
for all uterine causes, when bleeding persists after conventional tx, uterine/internal iliac artery ligation or hysterectomy can be lifesaving
What are the characteristics of postpartum endometritis?
– fever >38 degrees C w/in 36hrs
– uterine tenderness
– malodorous lochia
What are the 7Ws of postpartum fever (10 days postdelivery)?
Womb (endomyometritis)
Wind (atelectasis, pneumonia)
Water (UTI)
Walk (DVT, pulmonary embolism)
Wound (incision, episiotomy)
Weaning (breast engorgement, abscess, mastitis)
Wonder drugs (drug fever)
What are temperature requirements for postpartum infxns?
>/= 38 degrees C for at least two of the first ten postpartum day (not including the first 24hrs)
What are the risk factors for postpartum endometritis?
emergent C-section
PROM
prolonged labor
multiple intrapartum vaginal exams
intrauterine manipulations
delivery
low SES
young age
prolonged ruptured membranes
bacterial colonization
corticosteroid use
How is endometritis tx?
Hospitalize
broad-spectrum empiric IV Abx (clinda and gent) until pts have been afebril for 48hrs (24hrs for chorioamnionitis)
add ampicillin for complicated cases
If persistent postpartum fever is not responsive to broad spectrum abx, what condition must be considered?
septic pelvic thrombophlebitis
– pelvic infxn leads to infxn of the vein wall and intimal damage, leading in turn to thrombogenesis
– clot is invaded by microorganisms
– suppuration follows, w/ liquefaction, fragmentation and finally, septic embolization
How does septic pelvic thrombophlebitis present?
abd and back pain and a picket-fence fever curve (“hectic” fevers) w/ wide swings from normal to as high as 41 degrees C
How is septic pelvic thrombophlebitis dx?
blood cultures and CT looking for a pelvic abscess
How is septic pelvic thrombophlebitis tx?
broad spectrum Abx
anticoagulation w/ heparin x 7-10 days
What is Sheehan’s syndrome?
pituitary ischemia and necrosis that leads to anterior pituitary insufficiency secondary to massive obstetric hemorrhage and shock
How does Sheehan’s syndrome present?
primary cause of anterior pituitary insufficiency in adult females. Most common presenting syndrome is failure to lactate (due to decrease prolactin levels)
other sx: include weakness, lethargy, cold insensitivity, genital atrophy, menstrual disorders
How is Sheehan’s syndrome dx?
established w/ provocative hormonal testing and MRI of the pituitary and hypothalamus to rule out tumor or other pathology
How is Sheehan’s syndrome tx?
replacement of all deficient hormones. However, some pts may recover TSH and even gonadotropin fxn after cortisol replacement alone
What causes breast hypertrophy in pregnancy?
increased estrogen and progesterone
inhibition of prolactin release
What stimulates milk production after delivery?
after delivery of the placenta, hormone levels decrease markedly and prolactin is released, stimulating milk production
What can also stimulate milk production?
periodic infant suckling leads to further release of prolactin and oxytocin, which stimulate myoepithelial cell contraction and milk ejection (“let-down reflex”)
What is colostrum?
“early breast milk” contains protein, fat, secretory IgA, and minerals. W/in one wk postpartum, mature milk w/ protein, fat, lactose, and water is produced
What are the benefits of IgA in colostrum?
provide passive immunity for the infant and protect against enteric bacteria
What conditions is breastfeeding contraindicated?
HIV infxn, active hepatitis (HBV and HCV), and use of certain medications (tetracycline, chloramphenicol, warfarin)
What are some benefits of breastfeeding?
decreased incidence of infant allergies, early upper respiratory tract infxns, and GI infxns; facilitation of mother-child bonding; and maternal weight loss
What is mastitis?
cellulitis of the periglandular tissue caused by nipple trauma from breastfeeding coupled w/ the introduction of bacteria, usually S. aureus from the infant’s pharynx into the nipple ducts. Affects 2-3% nursing women
How does mastitis present?
sx begin 2-4wks postpartum
breast sx are usually unilateral and include breast tenderness, a palpable mass, erythema, edema, warmth, and possible purulent nipple drainage. Significant fever, chills, and malaise may also be seen.
How is mastitis dx?
differentiate from simple breast swelling
Infxn suggested by focal sx, + breast milk culture, an increase in WBC count and fever
How is mastitis tx?
1) continued breastfeeding to prevent accumulation of infected material (or use of breast pump in pts who are no longer breastfeeding)
2) PO abx (dicloxacillin, cephalexin, amoxicillin/clavulanate, azithromycin, clindamycin)
3) if abscess present, treat w/ I&D
Does menarche precede thelarche in women?
no
Thelarche PRECEDS menarche (8-11yrs)
Menarche (10-16yrs)
What occurs during the follicular phase of menstruation?
development of straight glands and thin secretions of the uterine lining (proliferative phase)
increased FSH–>growth of follicles–>increased estrogen production
What is the hormonal profile of ovulation?
LH and FSH spike
What occurs during ovulation?
rupture of the ovarian follicle and release of mature
ruptured follicular cells involute and creates the corpus luteum
What occurs during luteal phase of menstruation?
length of time that the corpus luteum can survive without further LH stimulation
the corpus luteum produces estrogen and progesterone, allowing the endometrial lining to develop thick endometrial glands w/ thick secretions (secretory phase)
In absence of implantation, the corpus luteum cannot be sustained, and the endometrial lining sloughs off
What is the definition of menopause?
cessation of menses for a minimum of 12 months as a result of cessation of follicular development
At what age is premature menopause?
ovarian failure and menstrual cessation before age 40
What are the sx of menopause?
HAVOC
Hot flashes (vasomotor instability)
Atrophy of Vagina
Osteoporosis
Coronary artery diseaseOther sx: insomnia, anxiety/irritability, vaginal bleeding, poor concentration, mood changes, dyspareunia, and loss of libido

How is menopause dx?
Labs: increased FSH and increased LH
DEXA scan to follow bone density for osteoporosis
Lipid profile: increased total cholesterol, decreased HDL
How is menopause tx?
Vasomotor sx:
– HRT (combination of estrogen and progestin)
—WHI STUDI: HRT shown to increase cardiovascular morbidity and mortality and may increase the incidence of breast and endometrial cancers. Rx HRT carefully
—Post-hysterectomy pts do not need progestin. Unopposed estrogen in pts w/ a uterus predisposes to endometrial cancer
– Non-HRT: Venlafaxine and less commonly, clonidine can be given to decrease the frequency of hot flashesVaginal atrophy
– long term: estradiol vaginal ring
– short term: estrogen vaginal cream will relieve sx

Osteoporosis:
– tx w/ daily calcium supplementation and exercise; possibly bisphosphonates

What are the CI of HRT?
vaginal bleeding
suspected or known breast cancer
endometrial cancer
hx of thromboembolism
chronic liver disease
hypertriglyceridemia
What are absolute CI to estrogen-containing hormonal methods (OCPs, NuvaRing, “the patch”?
pregnancy
hx of CAD or DVT
Breast cancer
undx abnormal vaginal bleeding
estrogen-dependent cancer
benign or malignant liver neoplasm
current tobacco use and age >35yo
What are absolute CI to Mirena and Copper IUDs?
known or suspected pregnancy
unexplained vaginal bleeding until dx
current purulent cervicitis
PID that is active (w/in three mo) or recurrent
confirmed sx actinomycosis on culture (but not ASx colonization)
a bicornuate or septate uterus
cervical or uterine cancer
Pap smear w/ squamous intraepithelial lesions or two atypical Pap smears
hx of heart valve replacement or artificial joints
What are CI to Copper IUDs alone?
copper intolerance (allergy to copper, Wilson’s disease)
severe dysmenorrhea and/or menorrhagia
What are the CI to Mirena alone?
Levonorgestrel allergy
breast cancer
acute liver disease or liver tumor
hx of + BRCA
What is unique about combined hormonal contraception methods?
protect against endometrial, ovarian, and breast cancer
How should sexual assault pts be approached?
– Take full hx, including contraceptive use, last time of coitus, condom use prior to assault, drug and alcohol use, hx of STDs, hx of mental illness or deficiency, description of the assailant, location, and time of the assault, circumstances of assault (penile penetration, use of condoms, extragenital acts, use or displays of weapons), and pt’s actions since assault (douching, bathing, brushing teeth, urination/defecation, changing clothes)
– Conduct complete physical exam: making note of any signs of trauma, along w/ a detailed pelvic exam, including a survey of the external genitals, vagina, cervix, and anus.
How is sexual assault dx?
– saline prep for sperm
– gonorrhea and chlamydia smear/culture (including rectal if appropriate)
– serologic testing for HIV, syphilis, HSV, HBV, CMV
– serum pregnancy test
– blood alcohol level; urine tx screen
How is sexual assault tx?
– STD tx (ceftriaxone plus doxycycline)
– HIV risk assessment and possible postexposure prophylaxis
– EC for pregnancy prevent
– refer for psychological counseling
– Arrange for follow-up w/ the same physician or w/ another provider if more appropriate
– Follow-up should include repeat screening for STDs, repeat screening for pregnancy, and a discussion of coping methods w/ appropriate referrals for psychiatric care if needed
Which contraceptive methods have proven to be the most effective (>99%)?
– implanon
– Mirena IUD
– Copper IUD
– Surgical sterilization
What contraceptive methods have proven to be very effective (90-99%)?
– Depo-Provera
– Ortho-Evra (the patch)
– NuvaRing (“the ring”)
– OCPs (combined estrogen and progestin)
– Progestin-only “minipills”
Which contraceptive methods have proven to be moderately effective (75-90%)?
– male condoms
– diaphragm w/ spermicide
– female condom
– fertility awareness methods
Which contraceptive methods have proven to be the least effective (68-74%)?
– withdrawal
– spermicide
What are the etiologies of pediatric vaginal discharge?
– infectious vulvovaginitis
– foreign objects
– candidal infection
– sarcoma botryoides (rhabdomyosarcoma)
What organism often causes pediatric infectious vulvovaginitis?
group A strep
STDs (think possible child abuse)
What must you be concerned about if a pediatric patient presents with a candidal pediatric vaginal discharge?
worry about diabetes!
How does sarcoma botryoides present in the vagina?
“bunches of grapes”
What is the definition of precocious puberty?
Onset of sexual characteristics before age of 8
What are the different types of precocious puberty?
1) Central precocious puberty: results from early activation of hypothalamic GnRH production. Most commonly idiopathic (also known as constitutional or true); may be related to obesity. Can also be caused by CNS tumors
2) Peripheral precocious puberty: aka pseudo-precocious puberty. Results from nonhypothalamic GnRH production
How does precocious puberty usually present?
– Signs of estrogen excess: breast development, possibly vaginal bleeding–>ovarian cysts or tumors
– Signs of androgen excess: pubic and/or axillary hair, enlarged clitoris, acne, and/or increased body odor) suggest adrenal tumors or congenital adrenal hyperplasia (CAH)
How is precocious puberty dx?
1) radiograph of wrist and hand to determine bone age
–if bone age is w/in one yr of chronological age, puberty has not started or has just recently begun
–if bone age is >chronological age by >2yrs, puberty has been present for at least one year or is progressing rapidly
2) Conduct a GnRH agonist (leuprolide) stimulation test
— Central precocious puberty: if LH response is + obtain a cranial MRI to look for CNS tumors
—–in girls 6-8yrs of age w/ signs of precocious puberty, the incidence of CNS tumor is 2% in the absence of other CNS signs
—–If CNS tumors ruled out, constitutional precocious puberty is likely etiology
–Peripheral precocious puberty: if LH response is neg, order the following:
—–U/S of ovaries and/or adrenals to look for ovarian or adrenal cyst/tumors
—–Estradiol: levels will be increased in ovarian cysts or tumors
—–Androgen (DHEA, DHEAS): esp critical in setting of advanced bone age or signs of adrenarche
—–17-OH progesterone: to screen for advanced bone age or adrenarche
What are causes of central precocious puberty (GnRH-dependent)?
constitutional (idiopathic)
Hypothalamic lesions (hamartomas, tumors, congenital malformations)
Dysgerminomas
Hydrocephalus
CNS infxns
CNS trauma/irradiation
Pineal tumors (rare)
NF w/ CNS involvement
Tuberous sclerosis
What are the causes of peripheral precocious puberty (GnRH-indepedent)?
CAH
Adrenal tumors
McCune-Albright Syndrome (polyostotic fibrous dysplasia)
Gonadal tumors
Exogenous estrogen, oral (OCPs) or topical
Ovarian cysts (females)
How is central precocious puberty tx?
1st line: leuprolide
w/ tx, physical changes regress or cease to progress
How is peripheral precocious puberty tx?

Tx the cause

Ovarian cysts: no intervention is necessary, all cysts will usually regress spontaneously
CAH: Tx w/ glucocorticoids. Surgery is NOT required for the tx of ambiguous genitalia
Adrenal or ovarian tumors: require surgical resection
McCune-Albright syndrome: antiestrogens (tamoxifen) or estrogen synthesis blockers (ketoconazole or testolactone) may be effective

What is the definition of primary amenorrhea/delayed puberty?
absence of menses by age 16 w/ secondary sexual development present, or the absence of secondary sexual characteristics by age 14
What are the causes of delayed puberty (absence of secondary sexual characteristics)?
– Constitutional growth delay: the most common cause
– 1mary ovarian insufficiency: most commonly Turner’s syndrome. Look for a hx of radiation and chemotx
– Central hypogonadism: may be caused by variety of factors, including:
—undernourishment, stress, prolactinemia, or exercise
—CNS tumor or cranial irradiation
—Kallmann’s syndrome (isolated gonadotropin deficiency) assoc w/ anosmia.
What are the causes of primary amenorrhea (secondary sexual characteristics present)?
– Mullerian agenesis: absence of 2/3 of the vagina; uterine abnormalities
– Imperforate hymen: presents w/ hematocolpos (blood in vagina) that cannot escape, along w/ a bulging hymen. Requires surgical opening
– Complete androgen insensitivity: pts present w/ breast development (aromatization of testosterone to estrogen) but are amenorrheic and lack pubic hair
How is primary amenorrhea dx?
1) get a pregnancy test
2) obtain a radiograph to determine if bone age is consistent w/ pubertal onset (>12yrs in girls)
–Constitutional growth delay: (bone age <12yrs) short stature but normal growth velocity –If bone age is >12 and no signs of puberty, obtain LH/FSH and consider where the problem is on the HPA axis
3) U/S may be needed to evaluate the ovaries
4) Obtain a karyotype if suspect Turner’s syndrome
5) If have normal breast development and uterus: measure prolactin and obtain a cranial MRI
What hormonal profile indicates constitutional growth delay?
decrease GnRH
decrease LH/FSH
decrease estrogen/progesterone at prepuberty levels
(puberty has not started yet)
What hormonal profile indicates hypothalamic or pituitary problem?
decreased GnRH
decreased LH/FSH
decrease estrogen/progesterone
(hypogonadotropic hypogonadism)
What hormonal profile indicates that the ovaries have failed to produce estrogen?
increased GnRH
increased LH/FSH
decreased estrogen/progesterone
(hypergonadotropin hypogonadism)
What hormonal profile indicates PCOS or a problem w/ estrogen receptors?
increased GnRH
increased LH/FSH
high estrogen or testosterone
In work up for primary amenorrhea, if have normal pubertal hormone levels, what does this indicate?
anatomic problem (menstrual blood can’t get out)
What are causes of hypogonadotropic hypogonadism?
– Kallmann’s syndrome (GnRH deficiency)
– Tumors, infection, trauma, chronic disease
– Anorexia, excess exercise, weight loss, stress
– Hypothyroidism
– Hyperprolactinoma
What are the causes of hypogonadotropic hypogonadism?
– anorexia, excess exercise, weight loss, stress
– Sheehan’s syndrome
– neoplasms
– panhypopituitarism
– hyperprolactinemia
– hypothyroidism
What are causes of Hypergonadotropic hypogonadism?
– Turner’s syndrome
– premature ovarian failure (chemotx, radiation, idiopathic)
– pure gonadal dysgenesis
– Savage’s syndrome (gonadropin- resistant ovary syndrome)
What causes anovulatory problem?
– androgen insensitivity (increase testosterone, increase estrogen)
– PCOS (increase estrogen, androgen)
– Enzyme deficiency (17alpha- hydroxylase or aromatase)
What are secondary anatomic causes of amenorrhea?
Normal hormone levels!
– Asherman’s syndrome due to endometritis, scarring after delivery, or D&C
– Cervical stenosis
How is primary amenorrhea tx?
– Constitutional growth delay: No tx
– Hypogonadism: Begin HRT w/ estrogen alone at the lowest dose. 12-18mo later, begin cyclic estrogen/progesterone therapy (if the uterus is present)
– Anatomic: requires surgical intervention
What is the first step in the work-up of primary and secondary amenorrhea?
PREGNANCY TEST!
How is secondary amenorrhea dx?
absence of menses for 6 consecutive months in women who have passed menarche
How is secondary amenorrhea dx?
1) Get pregnancy test
2) If neg B-hCG: measure TSH and prolactin
– increased TSH= hypothyroidism
– increased prolactin = (inhibits release of LH and FSH) points to a thyroid pathology. Order an MRI of the pituitary to rule out tumor
– very increased prolactin = suggests a prolactin-secreting pituitary adenoma
3) If normal B-hCG: initiate progestin challenge (10 days of progestin)
– positive progestin challenge (withdrawal bleed): indicates anovulation that is likely due to noncyclic gonadotropin secretion–>PCOS or idiopathic anovulation. Check LH levels and if LH is moderately high, etiology is likely PCOS. Marked elevation of LH can indicate premature menopause
– neg progestin challenge (no bleed): indicates uterine abnormality or estrogen deficiency. Check FSH levels
–increased FSH: indicates hypergonadotropic hypogonadism/ovarian failure
–decreased FSH: obtain a cyclic estrogen/progesterone test. A positive withdrawal bleed points to hypogonadotropic hypogonadism; a neg withdrawal bleed suggests an endometrial or anatomic problem
4) Look for signs of hyperglycemia (polydipsia, polyuria), or hypotension: conduct a 1mg overnight dexamethasone suppression test to distinguish CAH, Cushing’s syndrome, and Addison’s syndrome
5) Look for clinical virilization: measure testosterone, DHEAS, and 17-hydroxyprogesterone
–mild pattern: PCOS, CAH, or Cushing’s syndrome
–moderate to severe pattern: look for an ovarian or adrenal tumor
How is secondary amenorrhea treated?
Hypothalamic: reverse the underlying cause and induce ovulation w/ gonadotropins
Tumors: excision; medical tx for prolactinomas (e.g. bromocriptine, cabergoline)
Premature ovarian failure (age <40yrs): if the uterus is present, tx w/ estrogen plus progestin replacement tx
What is primary dysmenorrhea?
menstrual pain associated w/ ovulatory cycles in the absence of pathologic findings. Caused by uterine vasoconstriction, anoxia, and sustained contractions mediated by an excess of prostaglandin (PGF2alpha)
How does primary dysmenorrhea present?
– low, midline, spasmodic pelvic pain that often radiates to the back or inner thighs
– cramps occur in the first 1-3 days of menstruation and may be associated w/ nausea, diarrhea, headache, and flushing
– no pathologic findings on pelvic exam
How is primary dysmenorrhea tx?
– NSAIDs
– topical heat therapy
– combined OCPs
– Mirena IUD
What is secondary amenorrhea?
menstrual pain for which there is an organic cause:
– endometriosis
– adenomyosis
– tumors
– fibroids
– adhesions
– polyps
– PID
How does secondary amenorrhea present?
Similar to primary dysmenorrhea, but look for pathology.
– palpable uterine mass
– cervical motion tenderness
– adnexal tenderness
– vaginal or cervical discharge
– visible vaginal pathology (mucosal tears, masses, prolapse)
How is secondary amenorrhea dx?
1) Obtain B-hCG to exclude ectopic pregnancy
2) Order:
– CBCPD to r/o infxn or neoplasm
– UA to r/o UTI
– gonococcal/chlamydial swabs to rule out STDs/PID
– Stool guaic to r/o GI pathology
3) Look for pelvic pathology that causes pain
What is the difference between endometriosis and adenomyosis?
endometriosis is functional endometrial glands and stroma OUTSIDE the uterus. Adenomyosis is endometrial tissue IN the myometrium of the uterus.
How does endometriosis present?
presents w/ cyclical pelvic and/or rectal pain and dyspareunia (painful intercourse)
How does adenomyosis present?
presents w/ classic triad of noncyclical pain, menorrhagia, and an enlarged uterus
How is endometriosis diagnosed?
Requires direct visualization by laparoscopy or laparotomy
Classic lesions: blue-black (“raspberry”) or dark brown (“powder-burned”) appearance
Ovaries may have endometriomas (characteristic “chocolate cysts”)
How is adenomyosis diagnosed?
U/S useful but cannot distinguish btw leiomyoma and adenomyosis
MRI can aid in diagnosis but is costly
How is endometriosis tx?

Pharmacologic: inhibit ovulation. First line: combo OCPs; GnRH analogs (leuprolide) and danazol.

Conservative surgical tx: excision, cauterization, or ablation of the lesions and lysis of adhesions. 20% pts can become pregnant after tx

Definitive surgical tx: TAH/BSO +/- lysis of adhesions

How is adenomyosis tx?

Pharmacologic: largely symptomatic relief. First line: NSAIDs + OCPs or progestins

Conservative surgical tx: endometrial ablation or resection using hysteroscopy. Complete eradication of deep adenomyosis is difficult and results in high tx failure

Definitive tx: Hysterectomy is the only definitive tx

What are the complications of endometriosis?
infertility (most common cause among menstruating women >30 yrs of age)
What are the complications of adenomyosis?
rarely, can progress to endometrial carcinoma
What is the definition of abnormal uterine bleeding?
vaginal bleeding that occurs six or more months following the cessation of menstrual function is cancer related until proven otherwise.
What is menorrhagia?
increased amount of flow (>80mL of blood loss per cycle) or prolonged bleeding (flow lasting >8 days); may lead to anemia
What is oligomenorrhea?
an increase length of time btw menses (35-90 days between cycles)
What is polymenorrhea?
frequent menstruation (<21 day cycle); anovular.
What is metrorrhagia?
bleeding btw periods
What is menometrorrhagia?
excessive and irregular bleeding
How is abnormal uterine bleeding diagnosed?
1) obtain B-hCG to r/o ectopic pregnancy
2) order a CBC to r/o anemia
3) Check the following:
– pap smear to r/o cervical cancer
– TFTs to r/o hyper/hypothyroidism and hyperprolactinemia
– obtain plt count, bleeding time, PT/PTT to r/o von Willebrand’s disease and factor XI deficiency
– order u/s to evaluate the ovaries, uterus, and endometrium. Look for uterine masses, polycystic ovaries, and thickness of the endometrium
– If endometrium is >4mm in a postmenopausal woman, obtain an endometrial biopsy. An endometrial biopsy should also be obtained if the pt is >35 yo, obese (BMI>35yo) and diabetic
How is heavy uterine bleeding tx?
1) for hemorrhage, high-dose estrogen IV stabilizes the endometrial lining and stops bleeding w/in one hour
2) If bleeding is not controlled w/in 12-24hrs, a D&C is indicated
How is ovulatory bleeding tx?
Goal: decrease blood loss
1) NSAIDs to decrease blood loss
2) If pt is hemodynamically stable, tx w/ OCPs or Mirena IUD to thicken the endometrium and control the bleeding. If not effective w/in 24hrs, look for alternative dx
How is anovulatory bleeding tx?
Goal: convert proliferative endometrium to secretory endometrium
– give progestins x 10 days to stimulate withdrawal bleeding
– for young pts w/ anovulatory bleeding who may also have a bleeding disorder, give desmopressin followed by a rapid increased in von Willebrand’s factor and factor VIII (lasts roughly six hrs)
What are the tx options for abnormal uterine bleeding if medical mgmt fails?
– D&C: an appropriate diagnostic/therapeutic option
– Hysterectomy: can help identify endometrial polyps as well as aid in the performance of directed uterine biopsies
– Hysterectomy or endometrial ablation: appropriate in women who fail or do not want hormonal tx, have symptomatic anemia, and/or experience a disruption in their quality of life from persistent, unscheduled bleeding.
What are the complications of abnormal uterine bleeding?
– anemia
– endometrial hyperplasia
– +/- carcinoma
What is congenital adrenal hyperplasia?
21-hydroxylase deficiency that can present in its most severe, classic form as a newborn female infant w/ ambiguous genitalia and life-threatening salt wasting. Milder forms present later in life. 11Beta-hydroxylase deficiency is a less common cause of adrenal hyperplasia.
How does CAH present?
excessive hirsutism, acne, amenorrhea and/or abnormal uterine bleeding, infertility, and rarely a palpable pelvic mass.
What is the difference btw hirsutism vs. virilization vs. defeminization?
hirsutism: male hair pattern
virilization: frontal balding, muscularity, clitoromegaly, and deepening of the voice
Defeminization: decrease brest size; loss of feminine adipose tissue
How is CAH dx?
– increased androgens (testosterone > 2ng; DHEAS > 7 ug/mL): r/o adrenal or ovarian neoplasm
– increased serum testosterone: suspect ovarian tumor
– increased DHEAS: suspect an adrenal source (adrenal tumor, Cushing’s syndrome, CAH)
– increased 17-OH progesterone levels (either basally or in response to ACTH stimulation)
What is the differential to hyperandrogenism?
PCOS
21-hydroxylase deficiency (late onset, nonclassic) CAH
21-hydroxylase deficiency- (congenital, classic) CAH
Hypothyroidism
Hyperprolactinemia
Androgen-secreting neoplasm
Cushing’s syndrome
How is CAH tx?
glucocorticoids (prednisone)
To remove hair growth will need: laser ablation, electrolysis, or conventional hair removal techniques must be used to remove unwanted hair
How does the most severe form of PCOS present?
hyperandrogenism
insulin
resistance
acanthosis nigricans
What is PCOS?
most common endocrine disorder in reproductive women
AKA Stein-Leventhal syndrome
What are the diagnostic criteria for PCOS?
1. polycystic ovaries
2. oligo-anovulation
3. clinical or biochemical evidence of hyperandrogenism
How does PCOS present?
High BP
BMI > 30
Stigmata of hyperandrogenism or insulin resistance (menstrual cycle disturbances, hirsutism, obesity, acne, androgenic alopecia, acanthosis nigricans)
What conditions are patients w/ PCOS as risk for?
Type 2 DM
Insulin resistance
Infertility
Metabolic syndrome–insulin resistance, obesity, atherogenic dyslipidemia, HTN
How is PCOS dx?
Labs: (biochemical hyperandrogenemia)
– increased testosterone (total +/- free)
– DHEAS
– DHEA
What other conditions need to be excluded when dx PCOS?
Other causes of hyperandrogenism:
– TSH, prolactin
– 17-OH progesterone to r/o nonclassical CAH
– Consider screening in the setting of clinical sx of Cushing’s syndrome (moon facies, buffalo hump, abd striae) or acromegaly (increased head size)Other causes of metabolic abnormalities:
– 2hr oral glu tolerance test
– fasting lipid and lipoprotein levels (total cholesterol, HDL, LDL, triglycerides)

What other tests can be used to dx PCOS?
– U/S: look for >8 small, subcapsular follicles forming a “pearl necklace” sign
– Gonadotropins: Increased LH/FSH ratio (>2:1)
– Fasting insulin levels
– 24hr urine for free cortisol: adult-onset CAH or Cushing’s syndrome
How is PCOS tx for women who are not attempting to conceive?
Tx w/ a combo of OCPs, progestin, and metformin (or other insulin-sensitizing agents)
How is PCOS tx for women who are trying to conceive?
Clomiphene +/- metformin is first-line tx for ovulatory stimulation
How is Hirsutism tx?
combo OCPs are first line; antiandrogens (spironolactone, finasteride) and metformin may also be used
What kind of tx can be given to PCOS pts to reduce cardiovascular risk factors and lipid levels?
advice on: diet, weight loss, and exercise plus potentially lipid-controlling medication
What are the complications of PCOS?
increase risk of early onset type 2 DM
increase risk of miscarriages
increase risk of long-term risk of breast and endometrial cancer due to unopposed estrogen secretion
How is infertility defined?
defined as inability to conceive after 12 months of normal, regular, unprotected sexual activity
What is the difference between primary and secondary infertility?
Primary: no prior pregnancies
Secondary: at least one prior pregnancy
What are the male causes of infertility?
– testicular injury or infection
– meds (corticosteroids, cimetidine, spironolactone)
– thyroid or liver disease
– signs of hypogonadism
– varicocele
What is the work-up for male causes of infertility?
TSH
prolactin
karyotype (r/o Klinefelter’s syndrome)
Semen analysis
What is the tx of male causes of infertility?
tx of hormonal deficiency
intrauterine insemination
donor insemination
in vitro fertilization
intracytoplasmic sperm injection
What are ovulatory factors that affect infertility?
age (incidence increases w/ age)
sx of hyper-hypothyroidism
galatorrhea
menstrual cycle abnormalities
How are ovulatory factors that affect infertility dx?
basal body temp
ovulation predictor
midluteal progesterone
early follicular FSH +/- estradiol level (ovarian reserve)
TSH, prolactin, androgens
ovarian sonography (antral follicle count)
endometrial biopsy (luteal phase defect)
How are ovulatory factors that affect infertility tx?
Tx depends on the etiology (e.g. levothyroxine, dopamine)
Induction of ovulation w/ clomiphene, gonadotropins, and pulsatile GnRH
IUI
IVF
What are the tubal/pelvic factors that affect infertility?
Hx of PID
appendicitis
endometriosis
pelvic adhesions
tubal surgery
How are tubal/pelvic factors that affect infertility dx?
hysterosalpingogram
endometrial biopsy
How are tubal/pelvic factors that affect infertility tx?
laparoscopic resection or ablation of endometriomas or fibroids
IVF
What are cervical factors that affect infertility
abnormal Pap smears
postcoital bleeding
cryotherapy
conization
DES exposure in utero
How are cervical factors that affect infertility dx?
Pap smear
Physical exam
Antisperm antibodies
How are cervical factors that affect infertility tx?
IUI w/ washed sperm
IVF
How do cyst and abscess of Bartholin’s duct present?
obstruction of the gland leads to pain, swelling, and abscess formation.
– presents w/ periodic painful swelling on either side of the introitus and dyspareunia
– a fluctuant swelling 1-4cm in diameter is seen in the inferior portion of either labium minus
– tenderness is evidence of active infection
How are cysts/abscess of Bartholin’s duct tx?

ASx cysts do not require therapy–>frequent warm soaks may be helpful

If abscess develops–>aspiration or I&D. Culture for Chlamydia and other pathogens

Abx unnecessary unless cellulitis is present

What is vaginitis?
spectrum of conditions that cause vulvovaginal sx such as itching, burning, irritation, and abnormal discharge.
What are the most common causes of vaginitis?
– bacterial vaginosis
– vulvovaginal candidiasis
– trichomoniasis
What are the keys to dx bacterial vaginosis?
odor, increased discharge
mild vulvar irritation
homogenous, grayish-white, fishy/stale odor
“clue cells”
+ Whiff test (fishy smell)
What are the keys to dx trichomonas?
increase discharge, odor, pruritus, dysuria
“strawberry petechiae” in the upper vagina/cervix
profuse, malodorous, yellow-green, frothy
motile trichomonads (flagellated organisms that are slightly larger than WBCs)
What are the keys to dx candidal vaginal infxn?
pruritis, dysuria, increased discharge
erythematous, excoriated vulva/vagina
thick, white, curdy texture w/o odor
Hyphae
How is bacterial vaginosis tx?
Po or vaginal metronidazole or clindamycin
How is Trichomonas tx?
single-dose PO metronidazole or tinidazole.
TREAT PARTNERS; test for other STDs
How is vaginal yeast tx?
topical azole or PO fluconazole
What are complications of bacterial vaginosis?
chorioamnionitis/endometritis
infxn
preterm delivery
miscarriage
PID
What are complications of trichomonas?
chorioamnionitis/endometritis
infxn
perterm delivery
miscarriage
PID
What are complications of vaginal yeast infxn?
oral azoles should be avoided in pregnancy
What are some normal secretions of the vagina?
midcycle estrogen surge: clear, elastic, mucoid secretions
luteal phase/pregnancy: thick and white secretions; adhere to the vaginal wall
What are the risk factors for bacterial vaginosis?
pregnancy
>1 sexual partner
female sexual partner
frequent douching
What are the risk factors for trichomonas?
an STD
unprotected sex w/ multiple partners
What are the risk factors for yeast infxn of the vagina?
DM
broad spectrum abx use
pregnancy
corticosteroids
HIV
OCP use
IUD use
young age at first intercourse
increase frequency of intercourse
What is cervicitis?
inflammation of uterine cervix
What are causes of cervicitis?
Chlamydia, gonococcus, Trichomonas, HSV, HPV, trauma, radiation, exposure, malignancy
How does cervicitis present?
yellow-green mucopurulent discharge; + cervical motion tenderness; absence of other signs of PID
What is PID?
polymicrobial infxn of upper genital tract that is associated w/ Neisseria gonorrhea, Chlamydia, and endogenous aerobes/anaerobes
What are risk factors for PID?
douching, smoking, multiple sex partners, and prior STDs and/or PID
What are acute causes of pelvic pain?
Appendicitis
Ruptured ovarian cyst
Ovarian torsion/abscess
PID
Ectopic pregnancy
How does PID present?
lower abd pain, fever, chills, menstrual disturbances, and a purulent cervical discharge
Cervical motion tenderness (chandelier sign) and adnexal tenderness
How is PID dx?
Acute lower abd pain or pelvic pain
– uterine tenderness
– adnexal tenderness
– cervical motion tenderness
WBC count >10,000
Order B-hCG and u/s to r/o pregnancy and to evaluate for the possibility of tubo-ovarian abscess
U/S: noninvasive means of dx PID Look for:
– thickening or dilation of the fallopian tubes
– fluid in the cul-de-sac
– multicystic ovary
– tubo-ovarian abscess
How is PID tx?
Abx tx ASAP while awaiting culture results. All Sex partners should be examined and tx appropriately
Outpt regimens:
1) Ofloxacin or levofloxacin x 14 days +/- flagyl x 14 days
2) Ceftriaxone IM x 1 dose or cefoxitin plus probenecid + doxycycline x 14 days +/- flagyl x 14 daysInpt regimens:
– Cefoxitin or cefotetan plus doxycycline x 14 days
– clindamycin plus gentamicin x 14 days

What are surgical options to tx PID?
– drainage of a tubo-ovarian/pelvic abscess is appropriate if teh mass persists after antibiotic tx; the abscess is >4-6cm; or the mass is in the cul-de-sac in the midline and drainable through the vagina
– If abscess is dissecting the rectovaginal septum and is fixed to the vaginal membrane, colpotomy drainage is appropriate
– If pt’s condition deteriorates, perform exploratory laparotomy
– Surgery may range from TAH/BSO w/ lysis of adhesions in severe cases to conservative surgery for women who desire to maintain fertility
What are complications of PID?
– 25% of women w/ acute disease develop repeated episodes of infxn, chronic pelvic pain, dyspareunia, ectopic pregnancy, infertility
– RUQ pain (Fitz-Hugh- Curtis syndrome) may indicate an associated perihepatitis (abnormal liver fxn, shoulder pain)
– risk of infertility increases w/ repeated episodes of salpingitis
What is toxic shock syndrome?
caused by preformed S. aureus toxin (TSST-1)
occurs w/in 5 days of the onset of a menstrual period in women who have used tampons
How does TSS present?
abrupt onset of fever, vomiting, and watery diarrhea, w/ fever 38.9 or higher
diffuse macular erythematous rash
nonpurulent conjunctivitis is common
desquamation, especially of the palms and soles, generally occurs during recovery w/in 1-2 wks of illness
How is TSS dx?
blood cultures are neg b/c sx result from preformed txin and are not due to invasive properties of the organism
How is TSS tx?
– rapid rehydration
– antistaphlococcal drugs (nafcillin, oxacillin); vanco if have a penicillin allergy
– corticosteroids can reduce the severity of illness and decreased fever
– manage renal or cardiac failure
What are the complications of TSS?
the mortality rate is 3-6%
– ARDS, intractable, hypotension, hemorrhage secondary to DIC
What are fibroids?
most common benign neoplasm of the female genital tract
Tumor is discrete, round, firm, and often multiple and is composed of smooth muscle and connective tissue. Tumors are estrogen and progesterone sensitive, so they often increase in size during pregnancy and decrease after menopause
What are malignant transformations of fibroids?
leiomyosarcoma
How do fibroids present?
Most are ASx
Sx:
– bleeding: longer, heavier periods; anemia
– pressure: pelvic pressure and bloating; constipation and rectal pressure; urinary frequency or retention
– pain: secondary dysmenorrhea, dyspareunia
– pelvic sx: firm, nontender, irregular enlarged (“lumpy-bumpy”) or cobblestone uterus may be seen
How are fibroids dx?
CBC: look for anemia
U/S: look for uterine myomas; exclude ovarian masses
MRI: delineate intramural and submucous myomas
What are the pharmacologic tx of fibroids?
NSAIDs
combined hormonal contraception
Medroxyprogesterone acetate or danazol to slow or stop bleeding.
GnRH analogs (leuprolide or nafarelin) to decrease the size of myomas, suppress further growth, and decrease surrounding vascularity (for prior to surgery also)
What are the surgical tx of fibroids?
emergent surgery is indicated for torsion of the a pedunculated myoma
– women of childbearing years: myomectomy or hysteroscopy w/ leiomyoma resection
– women who have completed childbearing: total or subtotal abd or vaginal hysterectomy
– uterine artery embolization (~25% will need further invasive tx)
What are the complications of fibroids?
infertility may be due to myoma that distorts the uterine cavity and plays a role similar to that of an IUD
What must be ruled out in a uterine mass that continues to grow after menopause?
malignancy
What are the two types of endometrial cancer?

Type I: endometroid adenocarcinomas derive from atypical endometrial hyperplasia (most common female reproductive cancer in the US)

Type II: serous or clear cell histology

How does endometrial cancer present?

Type I: vaginal bleeding (early finding), pain, (late finding); metabolic syndrome

Type II: no vaginal bleeding

How is endometrial cancer dx?
endometrial/endocervical bx
vaginal U/S shows a thickened endometrium leading to hypertrophy and neoplastic change
How is endometrial cancer tx?

Type I: high-dose progestins for women of childbearing age/ TAH/BSO +/- radiation for postmenopausal women

Type II: TAH/BSO w/ adjuvant chemotx for advanced stage cancer

What strains of HPV are implicated in cervical cancer?
HPV 16: squamous cell carcinoma
HPV 18: adenocarcinoma
What are the risk factors for cervical cancer?
immunosuppression
infection w/ HIV
Hx of STDs
tobacco use
high parity
OCPs
What strains does the Gardisil vaccine protect against?
Type 6, 11, 16, 18
Are hormonal contraceptives protective against endometrial cancer?
YES
How does cervical cancer present?
metrorrhagia, postcoital spotting, and cervical ulceration are the most common signs
bloody or purulent, malodorous, nonpruritic discharge may appear after invasion
What are the screening guidelines for cervical cancer?
– Starting at 21 or no more than 3 yrs after becoming sexually active
– women >/= 30 yo who have had three consecutive normal tests may increase their screening interval to once every three years
– for women >/= 30yo, HPV DNA testing for high-risk strands may be used for screening as well.
– screening should be d/c for women >/= 70yo who have had three or more normal Pap smears.
– Women w/ DES exposure and/or immunocompromised status (including HIV positivity) should continue as long as they do not have a life-limiting condition
What are the follow-up steps for Pap result of atypical glandular cells?
< 35yo w/ no endometrial cancer risk factors: – proceed to colposcopy, endocervical curettage (ECC), and HPV DNA testing >/= 35yo +endometrial cancer factors, or abnormal bleeding
– all above and add endometrial biopsy
What are the follow-up steps for Pap result of Atypical squamous cells of undetermined significance?
</= 21yo – repeat Pap at 12 months. If Pap smear is neg or reveals ASC-US or LSIL, repeat at 12mo >21yo
– immediate colposcopy, HPV DNA testing and repeat Pap smear at 6 mo
What are the follow-up steps for Pap result of low grade squamous intraepithelial lesions?
</= 21yo – repeat Pap smear at 12 mo. If pap smear is neg or reveals ASC-US or LSIL, repeat at 12 mo >21yo
– immediate colposcopy
What are the follow-up steps for Pap smear result of high grade squamous intraepitheial lesions or atypical squamous cells suspicious of high-grade dysplasia?
immediate colposcopy is indicated for ALL age groups
How is CIN I tx?
CLOSE OBSERVATION
>21yo: Pap smear at 6-12mo and/or HPV DNA testing at 12 mo is indicated
<21yo: HPV testing NOT recommended
After two neg Paps or a neg DNA test, pts can be managed w/ routine annual follow-upIf persistent CIN I can be treated w/ ablative (cryotherapy or laser ablation) or excisional therapy (loop electrosurgical excision procedure (LEEP); laser and cold-knife conization)

How is CIN II and III tx?

ablative (cryotherapy or laser ablation) or excisional therapy (LEEP; laser and cold-knife conization)

Hysterectomy is a tx option for recurrent CIN II or III

How is CIN I, II or III w/ neg margins followed-up?
Pap smear at 12mo and/or HPV testing
How is CIN II or III w/ + margins followed- up?

Pap smear at 6mo; consider repeat ECC

If margins unknown, obtain a Pap smear at 6mo and HPV DNA testing at 12mo

How is microinvasive cervical cancer tx?
cone bx and close follow-up or simple hysterectomy
How is Stages IA2, IB1, and IIA cervical cancer tx?
may be treated either w/ radical hysterectomy w/ concomitant radiation and chemotx or w/ radiation plus chemotx alone
What is Stages IB2, IIB, III, and IV cervical cancer tx?
tx w/ radiation tx plus concurrent cisplastin-based chemotx
What type of cancer is vulvar cancer predominantly?

90-95% squamous lesions occurring in women >50yo

melanoma
basal cell carcinoma
adenocarcinoma
sarcoma
Bartholin’s gland tumors
metastatic disease

What are the risk factors for vulvar cancer?
HPV (16,18, 31)
lichen sclerosis
infrequent medical exams
diabetes
obesity
HTN
CV disease
immunosuppression
How does vulvar cancer present?
presents w/ pruritus, pain, ulceration of the mass
Early: lesions may appear white, pigmented, raised, thickened, nodular, ulcerative
Late: presents w/ large, cauliflower-like or hard ulcerated area in the vulva
How is vulvar cancer dx?
1) punch biopsy for any suspicious lesions
VIN I and II: associated w/ mild and moderate dysplasia
VIN III: carcinoma in situ
How is vulvar precancerous lesions tx?
reduce irritative or other predisposing causes. Topical corticosteroids (e.g. betamethasone, clobetasol) and crotamiton are particularly effective for pruritus
How is high-grade VIN tx?
topical chemotx, laser ablation, wide location excision, skinning vulvectomy, and simple vulvectomy
How is invasive vulvar cancer tx?
treated w/
1) radical vulvectomy and regional lymphadenectomy
2) wide local excision of the primary tumor w/ inguinal lymph node dissection +/- preoperative radiation, chemotx, or both
What type of cancer is vaginal cancer in postmenopausal women?
squamous cell carcinoma
What are risk factors for vaginal cancer?
immunosuppression
chronic irritation (long-term pessary use or prolapse of female organs)
low SES
radiation for cervical cancer
hysterectomy for dysplasia
multiple sexual partners
DES exposure
How does vaginal cancer present?
characterized by abnormal vaginal bleeding, an abnormal discharge or postcoital bleeding
presents in the upper third of the vagina in 75% of pts
How is vaginal cancer dx?
cytology, colposcopy and biopsy
How is vaginal cancer tx?
– local excision of involved areas when they are few and small
– extensive involvement of the vaginal mucosa may require partial or complete vaginectomy
– invasive disease requires radiation tx or radical surgery
What are the risk factors of ovarian cancer?
– age
– low parity
– decreased fertility
– delayed childbearing
– + FHx
– BRCA1 mutation and BRCA2 mutation
– Lynch II syndrome or HNPCC
– OCPs taken for 5yrs or more decrease risk by 29%
How do benign and malignant ovarian tumors present?
– Generally ASx
– mild, nonspecific GI sx or pelvic pressure/pain
– early disease: typically not detected on routine pelvic exam
– Some 75% of woman present w/ advanced malignant disease (abd pain, bloating, palpable abd mass, and ascites)
What tumor markers are used to monitor progression and recurrence of ovarian cancer?
CA-125
What must be ruled out if a palpable ovarian or adnexal mass in a premenarchal or postmenopausal pt?
ovarian neoplasm
What does increased CA-125 indicate in premenopausal women?
endometriosis
What does increased CA-125 indicate in postmenopausal women?
increased likelihood that the ovarian tumor is malignant
What are characteristics of a benign pelvic mass?
mobile
cystic
unilateral
smooth
What are characteristics of a malignant pelvic mass?
fixed
solid/firm
bilateral
nodular
What are characteristics of a benign adnexal mass via transvaginal U/S?
<8 cm
cystic
unilocular
unilateral
calcifications
What are characteristics of a malignant adnexal mass via transvaginal U/S?
>8 cm
solid or cystic and solid
multilocular
bilateral
ascites
How are ovarian masses tx in premenarchal women?
Masses > 2cm require exploratory laparotomy
How are ovarian masses tx in premenopausal women?
1) observe for 4-6wks for ASx, mobile, unilatera, simple cystic masses <8-10cm. Most will resolve spontaneously 2) Surgical eval for masses >8-10cm as well as for those that are unchanged on repeat pelvic exam and U/S
How are ovarian masses tx in postmenopausal women?

ASx: unilateral simple cysts <5cm in diameter w/ a normal CA-125 should be closely followed w/ U/S

Palpable masses warrant surgical evaluation by exploratory laparotomy

How is ovarian cancer tx surgically?

surgical staging followed by TAH/BSO w/ omentectomy and pelvic and para-aortic lymphadenectomy

benign neoplasms warrant tumor removal or unilateral oophorectomy

What ovarian tumor marker is used to follow endodermal sinus tumors?
AFP
What ovarian tumor marker is used to follow embryonal carcinoma?
AFP, hCG
What ovarian tumor marker is used to follow choriocarcinoma?
hCG
What ovarian tumor marker is used to follow dysgerminoma?
LDH
What ovarian tumor marker is used to follow granulosa cell tumors?
inhibin
Do postmenopausal ovarian tumor pts receive postoperative chemo?
Yes, routine except for women w/ early-stage or low-grade ovarian cancer
In what types of ovarian tumor pts receive radiation tx?
dysgerminomas
What kind of prevention can be done for ovarian cancer?
Women w/ BRCA1 mutation should be screened annually w/ U/S and CA-125 testing
Prophy oophorectomy is recommended by age 35 or whenever childbearing isOCP use to decrease risk

What are the risk factors for pelvic organ prolapse?
vaginal birth (particularly w/ use of forceps)
genetic predisposition
advancing age
prior pelvic surgery
connective tissue disorders
increased intra-abdominal pressure assoc w/ obesity or straining w/ chronic constipation
How does pelvic organ prolapse present?
sensation of a bulge or protrusion in the vagina
urinary or fecal incontinence, a sense of incomplete bladder emptying, and dyspareunia are also seen
How is pelvic organ prolapse dx?
women perform the Valsalva maneuver while in the lithotomy position
How is pelvic organ prolapse tx?
supportive measures include a high-fiber diet and weight reduction in obese pts and limitation of straining and lifting
pessaries may temporarily reduce prolapse and are helpful in women who do not wish to undergo surgery or who are chronically ill
Most common surgical procedure: vaginal or abdominal hysterectomy w/ vaginal vault suspension
What are the causes of urinary incontinence w/o specific urogenital pathology?
Delirium/confusional state
Infxn
Atrophic urethritis/vaginitis
Pharmaceutical
Psychiatric causes (esp depression)
Excessive urinary output (hyperglycemia, hypercalcemia, CHF)
Restricted mobility
Stool impaction
How is total urinary incontinence presented?
uncontrolled loss at all times and in all positions
exclude fistula
What is the mechanism of total urinary incontinence?
loss of sphincteric efficiency (previous surgery, nerve damage, cancer infiltration). Abnormal connection btw the urinary tract and skin (fistula)
What is the tx for total urinary incontinence?
surgery
How does stress incontinence present?
occurs after increase in intra-abdominal pressure (coughing, sneezing, lifting)
What is the mechanisms of stress incontinence?
urethral sphincteric insufficiency due to laxity of pelvic floor musculature; common in multiparous women or after pelvic surgery
How is stress incontinence tx?
kegel exercises and pessary
vaginal vault suspension surgery
How does urge incontinence present?
strong, unexpected urge to void that is unrelated to position or activity
spasticity, flaccidity, rectal sphincter tone
What is the mechanism of urge incontinence?
detrusor hyperreflexia or sphincter dysfxn due to inflammatory conditions or neurgenic disorders of the bladder.
How is urge incontinence tx?
anticholinergic medications or TCAs; behavioral training (biofeedback)
How does overflow incontinence present?
chronic urinary retention, distended bladder
What is the mechanism of overflow incontinence?
chronically distended bladder w/ increased intravesical pressure that just exceeds the outlet resistance, allowing a small amount of urine to dribble out
How is overflow incontinence tx?
placement of urethral catheter in acute settings
tx underlying diseases. Timed voiding.
How is urinary incontinence dx?
1) Obtain UA and urine culture to exclude UTI
2) voiding diary; possible urodynamic testing
3) serum Cr to exclude renal dysfxn
4) cystogram to demonstrate fistula sites and descensus of the bladder neck
What is the differential dx for breast mass?
fibrocystic disease
fibroadenoma
mastitis/abscess
fat necrosis
breast cancer
What is breast fibrocystic change?
most common of all benign breast conditions
exaggerated stromal tissue response to hormones and growth factors
Findings: cysts (gross and microscopic), papillomatosis, adenosis, fibrosis, and ductal epithelial hyperplasia
How does fibrocystic change present?
– cyclic bilateral mastalgia and swelling, w/ sx most prominent just before menstruation
– rapid fluctuation in the size of the masses in common
– other sx: irregular, bumpy consistency to the breast tissue (“oatmeal w/ raisins”)
How is fibrocystic change dx?
FNA: discrete mass that is suggestive of a cyst is indicated to alleviate pain as well as to confirm the cystic nature of the mass
Excisional bx: if no fluid is obtained or if fluid is bloody on aspiration
How is fibrocystic change tx?
dietary modifications (e.g. caffeine restriction)
danazol may be given for severe pain but is rarely used in the view of its side effects (acne, hirsutism, edema)
consider use of OCPs, which decrease hormonal fluctuations
What is fibroadenoma?
benign, slow-growing breast tumor w/ epithelial and stromal components. Most common breast lesion in women <30yo.
What is cystosarcoma phyllodes?
large fibroadenoma
How does fibroadenoma present?
round/ovoid, rubbery, discrete, relatively mobile, nontender mass 1-3cm in diameter
usually solitary, although up to 20% of pts develop multiple fibroadenomas
Tumors do not change during the menstrual cycle.
Does not occur after menopause unless the pt is on HRT
How is fibroadenoma dx?
breast u/s can differentiate cystic from solid masses.
needle biopsy or FNA
excision w/ pathologic exam if the dx remains uncertain
How is fibroadenoma tx?
excision is curative, but recurrence is common
What are the risk factors for breast cancer?
– female gender, older age
– personal hx of breast cancer
– breast cancer in a first-degree relative
– BRCA1 and BRCA2 mutations (assoc w/ early onset)
– a high-fat and low-fiber diet
– hx of fibrocystic change w/ cellular atypia
– increased exposure to estrogen (nulliparity, early menarche, late menopause, first full-term pregnancy after age 35)
What are the early findings of breast cancer?
single, nontender, firm-to-hard mass w/ ill-defined margins or as mammographic abnormalities w/ no palpable
What are later findings of breast cancer?
skin or nipple retraction, axillary lymphadenopathy, breast enlargement, redness, edema, pain, fixation of the mass to the skin or chest wall
What are late findings of breast cancer?
– ulceration; supraclavicular lymphadenopathy; edema of the arm; metastases to bone, lung, and liver
– prolonged unilateral scaling erosion of the nipple w/ or w/o discharge (Paget’s disease of the nipple)
How does metastatic disease present/
back or bone pain, jaundice, weight loss
firm or hand axillary node >1cm
axillary nodes that are matted or fixed to the skin (stage III); ipsilateral supraclavicular or infraclavicular nodes (Stage IV)
How is breast cancer dx in postmenopausal women?
mammography: look for increased density w/ microcalcifications and irregular borders. Can detect lesions roughly two years before they become clinically palpable
How is breast cancer dx in premenopausal women?
U/S (<30yo), which can distinguish a solid mass from a benign cyst
What are the tumor markers used in breast cancer?
CEA and CA 15-3 and CA27-29
What is the receptor status of tumor (breast cancer)?
ER
PR
HER2/neu
What labs can be followed in breast metastatic disease?
increased ESR
increased alkaline phosphatase (liver and bone metastases)
increased calcium
What imaging can be followed in breast metastatic disease?
CXR
CT of chest, abd, pelvis, and brain
Bone scan
How is breast cancer tx pharmacologically?
All hormone receptor +—>pts receive tamoxifen
ER neg–>receive chemo
Trastuzumab: mAB that binds to HER2/neu receptors on the cancer cell, is highly effective in HER2/neu-expressive cancers
How is breast cancer tx surgically?
– partial mastectomy (lumpectomy): plus axillary dissection followed by radiation tx
– modified radical mastectomy (total mastectomy plus axillary dissection)
What are the CI to breast conserving tx?
large tumor size, subareolar location, multifocal tumors, fixation to the chest wall, or involvement of the nipple or overlying skin
How should Stage IV breast cancer be tx?
radiotherapy and hormonal tx
mastectomy may be required for local sx control