1. OB-GYN History
2. Antenatal Care
3. Diagnosis of Pregnancy
4. Changes in Normal Pregnancy
5. Placental Development and Physiology
6. Fetal Physiology
7. Intrauterine Fetal Evaluation
8. Pelvimetry
9. Clinical Course of Labor
10. Intrapartum Fetal Monitoring
11. Anesthesia and Analgesia
12. Evaluation of the Newborn
13. Peurperium
14. Contraception
15. Maternal, Fetal and Infant Mortality
16. Abortion
17. Ectopic Pregnancy
18. Late Pregnancy Bleeding
19. Breech Presentation
20. Cephalo-Pelvic Disproportion
21. Multiple Pregnancies
22. Maternal Hypertension
23. Cardiac Disease in Pregnancy
24. Anemias
25. Urinary Tract Infections
26. Premature Rupture of Membranes
27. Thrombophlebitis in Pregnancy
28. Rubella Infection
29. Erythroblastis Fetalis
30. Post Partum Hemmorhage
31. Peurperal Infection
32. Cytogenetics
33. Clinical Genetics
34. Puberty
35. Premenstrual Syndrome
36. Dysmenorrhea
37. Menopause
38. Amenorrhea
39. Hirsutism and Virilization
40. Infertility
41. Congenital Anomalies
42. Vulvar Dermatoses
43. Benign Cervical Lesions
44. Vaginal Infections
45. Cervical Infections
46. Pelvic Inflammatory Disease
47. Endometriosis
48. Adenomyosis
49. Endometrial Hyperplasia
50. Uterine Myomas
51. Pelvic Relaxation
52. Urinary Incontinence
53. Genital Fistulae
54. Vulvar Carcinoma
55. Cervical Cancer
56. Neoplasms of the Corpus Uteri
57. Ovarian Carcinoma
58. Benign Ovarian Neoplasms
59. Functional Ovarian Neoplasms
60. Gestational Trophoblastic Disease
61. Radiation Therapy


I. Age, gravidity, parity
A. Age: age-related risks, young-prematurity, older-syndromes
B. Gravidity: total # of pregnancies
C. Parity: number of Full-term deliveries, Preterm, Abortions/miscarriages, Living children (Florida Power And Light)

II. Chief Complaint: reasons for the pt visit expressed in their own words (COLDEARR or LMNOPQRST); Don't cut to chase on entering room

III. Present illness

A. Pain
1. Dysmenorrhea: painful menstruation (primary or secondary)
2. Dyspareunia: painful intercourse
3. Pelvic pressure
4. Acute pelvic pain: direct or rebound
5. Chronic pelvic pain
6. Vulvar pain or pruritus
B. Bleeding
1. Menorrhagia: excessive bleeding
2. Metrorrhagia: light or heavy bleeding at irregular intervals (like any metro train)
3. Menometrorrhagia: heavy and irregular timing
4. Polymenorrhea: <21 day intervals
5. Oligomenorrhea: few periods
6. Hypomenorrhea: little menstrual bleeding
7. Contact or postcoital bleeding: Cervical CA
C. Abnormal discharge
1. Leukorrhea
2. Nipple discharge
D. Bowel symptoms
1. Diarrhea
2. Constipation
3. Tenesmus
4. Proctorrhagia
E. Urinary symptoms
1. Dysuria
2. Frequency
3. Incontinence
4. Sensations of incomplete voiding
F. Menstruation
1. Menarche
2. Interval
3. Flow (duration and amount)
4. Date of last menstrual period (LMP)
5. Date of preceding LMP
6. Premenstrual tension
7. Breast tenderness
8. Irritability
9. Anxiety
10. Dysmenorrhea
G. Past obstetrical history
1. Gravidity--total # of pregnancies
2. Parity--# of deliveries (FPAL)
3. Abortions
4. Length of gestation
5. Complication during prenatal periods
6. Method of deliveries, complications, outcomes
7. Indications for operative deliveries
8. Characteristics anbd conditions of offsprings
9. Puerperal complications
H. Gynecologic history
1. Prior diagnosis of gynecologic dz
3. Gynecologic surgery
4. Pelvic pain
5. Vulvar or vaginal lesions
6. Bleeding problems
7. Pap smear history
8. Infertility
I. Contraceptive history
1. Actual feelings about contraception
2. Current method
3. Length of use and any problems?
4. If contraceptive method is used, is it well accepted?
5. Well comprehended?
6. Is change desired?
7. Complaints related to the method
8. Prior methods and complications
J. Sexual history
1. Age at first intercourse
2. Number of partners
3. Know exposure to STDs
4. Feelings about sexual function
5. Current problems
6. Libido
7. Orgasmic function
8. Dyspareunia
9. Vaginismus
10. History of sexual abuse
K. Past medical history
1. Medications
2. Allergies
3. Other medical diagnosis
L. Past surgical history
M. Family history
1. CA: colon, breast, ovarian, uterus
N. Social history
1. Habits: social, sexual
P. PE: include thyroid and lymphatics (axillary, groin, supraclavicular)


I. Important factors in the patient's past Medical/Surgical/Obstetrical Hx in assessing current pregnancy

A.Medical: DM, HTN/CV dz, thyroid dz, infectious dz
B.Surgical: prior abdominal surgeries in case of a CS (possible adhesions)
C.OB: date & location of delivery, gestational ages, type of delivery or termination, duration of labor, anesthesia, maternal complications, newborn wt. and gender, fetal or neonatal complications
II. Important factors in the Family and Socio-economic Hx
A.FHx DM, HTN/PIH/CV dz, thyroid dz, congenital malformations, genetic disorders
B.SE: insurance, prenatal care, alcohol or tobacco, drug use, father in home, exposure to pets (cats=toxoplasmosis), maternal education about PNV, etc
III. Complete Physical
A. HEENT (check for thyroid status), CV, lungs, abdomen (gravid? tender?), extremities/skin, neuro (DTRs, CNs), pelvic (uterine size, adnezal masses, tenderness, pap smear)
IV. Evaluate uterine size and determine heart beats
A. From the pubic symphisis to height of fundus. At 16 weeks--halfway between symphisis pubis and umibilcus, 20 weeks--umbilicus. After 22 weeks, fundal height = gestational age; If 2-3 cm off, gut US (IUGR, twins, wrong EDC). Doppler FHTs at 10-12 weeks; US heart activity @ 8 weeks
V. Basic lab data obtained on all pregnant patients, value of each test, normal values for pregnancy
A. Blood type including Rh & Ab screen
B. Rubella immune
C. CBC--hct, WBC, plt
D UA--protein, sugar
E. Glucola at 24-28 weeks (NL<130-140: 1 hour), do 3-hr of abnormal
F. Pap smear
G. RPR, GC, HBsAg, GBS, TB skin test
H. AFP (15-20 Wks): high (open defect of neural tube: anencephaly, open spinal bifida) indication for US; low (Down, etc.)
I. US (10-20 wks): EGA, gender
VI. High-risk Factors
A. Maternal age: >35 = inc. trisomies and SAB; if mom < 30 YO then <2% SAB
B. Race: various dz with race (viz AA with inc. IUGR)
C. SES: inadequate prenatal care from inadequate insurance
D. Marital status: dec. support system
E. parity: inc. risk for postpartum hemorrhage, placental previas, etc.
F. Medical/obstetrical Hx: See "OB-Gyn history"
G. Medical/obstetrical disorders
1. Systemic
2. Specific infections
3. Diabetes
4. Heart disease
5. Chronic HTN
6. Thyroid dysfunction
7. Anemia
8. Isoimmunization
9. Other significant maternal disease
10. Nutrition: vitamins & minerals, folate, iron
11. Emotional disturbance: poor coping skills etc.
VII. Discuss with the Pt
A. Diet
1. Weight gain: ideal is 26-28 lbs (0.5 lbs/week 0-28 wks, 1 lb/wk 28+); excess gain isn't harmful but may be associated with GDM; sudden 3rd trimester gain may be a warning sign of impending pre-eclampsia; inadequate gain (<10 lbs at 28 weeks) associated w/ risk of PTL or IUGR.
2. Vitamins: PNV with iron for Mom, folate for baby
3. Food groups: well-rounded diet
4. Minerals
B. Hygiene
1. Baths: baths & showers OK but be careful to not slip as center of gravity changes
2. Clothing: whatever feels comfortable & appeals to pt
3. Sexuality: intercourse OK except in pts at risk for SAB & PTL or placenta previa; avoid breast stimulation in high risk pts which may induce uterine activity; PGs in seminal fluid may induce labor following coitus near term
4. Douches: bad, may inroduce bacteria into uterine cavity & cause chorioamnionitis with PTL
5. Smoking: bad; inc. risk for abruptions, IUGR, etc.
C. Exercise: same level as before pregnancy; beneficial since maintains feeling of well-being, muscle strength, flexibility, improve posture/muscle tone and dec. some of the common discomforts of pregnancy. Avoid fatigue with heavy housework, employment, lots of stress: PTL
D. Common complaints:
1. Heartburn (especially late in pregnancy)
2. Constipation
3. Sialorrhea
E. Labor: likely to be longer in nulliparous pt; actual labor is CTXs + cervical progression; see much "false labor" or Braxton-Hicks CTXs
F. Danger signs in pregnancy: lots of premature CTXs, VB, premature vaginal LOF (water, clear), anything that makes the mom feel uncomfortable
G. Use of drugs: avoid drugs of any kind if possible & clear with physician before using
H. Plans for future childbearing: considering sterilization
I. Breast feeding: many advantages, ideal for newborn, inexpensive, usually in good supply, nursing accelerates involution of uterus d/t oxytocin stimulation of UC; maternal Ab in BM provide protection in infant against certain infectious dz until infant immune system kicks in @ 3-4 months
J. Outline frequency, number, and clinical factors to be assessed in prenatal visits
1. Every 4 weeks up to 28-30 weeks then every 2 weeks to 36 weeks, then every week until birth. Weight, BP, UA, fundal height, FHT, FM should be recorded at every visit; prenatal labs should be done per above. Leopold maneuver can be tried for malpresentation in a hospital with provisions for immediate CS
K. Prenatal Visits
1. Initial labs: CBC, blood group with Rh type, serologic test for syphilis, rubella, hepatitis B, urine for glucose/protein/ketones/culture
2. 12 weeks: fetal heart tones with doppler
3. 14-16 weeks: assess growth, genetic tests as indicated (amnio, MSAFP), review prenatal
4. 20 weeks: fetoscope, reasses EGA, US
5. 24 weeks: begin maternal education
6. 28 weeks: Rh immune globulin as indicated, GDM screen, risk assessment
7. 30-40 weeks: observe for complications, repeat Hb, fetal surveillance as indicated
8. 41 weeks: plan for postdate pregnancy


I. Four positive signs of pregnancy

A. Demonstration of fetal heart (10-12 weeks by doppler, 16-20 by stethoscope)
B. Examiner appreciation of fetal movement: (examine @ 20-24 wks)
C. Visualization of the fetus: US pick up intrauterine gestational sac @ 5wks, fetal image @ 6-7wks, beating heart @ 8wks, fetal skeleton @ 16wks
II. Use of Ultrasonography in Early Diagnosis
A. Confirm pregnancy dating
B. Measurements of the gestational sac & crown-rump length (CRL)in cm plus 6.5 approximates the estimate GA
III. hCG and LH antigenicity, alpha and beta subunits, ELISA test
A. hCG and LH have same alpha subunits, but different bets subunits-- this is what is detected in pregnancy tests. hCG is produced by syncytiotrophoblast, supports corpus luteum progesterone production, and increases exponentially during the first trimester (inc. 66% every 2 days). The ELISA test uses AB to the beta subunit of hCG
IV. Presumptive Signs of Pregnancy
A. Cessation of menses: reliable in reproductive age women if regular menses prior
B. Breast changes: shortly after LMP, heavy sensation, tingling and soreness
C. Congestions of the vagina: blue-violet hue
D. Skin changes: inc. pigmentation, adbominal striae common
E. Nausea: 1/2 in early pregnancy, between 2 and 12 wks, usually more severe in morning
F. Bladder irritability: common early in pregnancy, resolved by 2nd trimester
G. Fatigue: can be a severe symptom of early pregnancy, usually resolves by 20th week, unclear etiology
H. Perception of fetal movement: described as "fluttering", 16 to 18 weeks if multiparous, several weeks later if primagravida
V. Probable signs: enlargement of the abdomen, uterine changes (size, shape, consistency), cervical changes (effacement), palpation of the fetus, Braxton-Hicks contractions, Endocrine tests


I. Uterine Changes

A. Macroscopic
1. Enlargement
2. Pelvic and ligament pain, weight gain
3. Uterine anomalies, leiomyoma enlargement
B. Uterine blood flow
1. Enlarging uterus compresses iliac veins and IVC; venous return, and thus CO dec. but a compensatory inc. in TRP minimizes dec. in BP. The IVC and pelvic vein compression may exacerbate varicose veins and hemorrhoids. Later in pregnancy, aortic compression may occur which may cause fetal distress when pt in supine position. Blood flow increases to uterus, kidney, and skin (inc. waste & heat loss)
II. Ovarian changes
A. Anatomy and physiology of the corpus luteum of pregnancy
1. CL made up of granulosa cells of the ruptured follicle & theca cells of ovarian stroma which produce progesterone & some estradiol. Life span of 14 days unless rescued by hCG. hCG keeps the luteum viable & producing progesterone to keep the uterus favorable for the developing fetus
III. Vaginal and perineal changes
A. Connective tissue of the perineum: vulva can get engorged, endocervix protrudes into vagina & produces the mucus plug
B. Vaginal secretion (change in pH): discharge increases and is thicker so that many will complain of dryness & dyspareunia
IV. Abdominal wall and skin changes
A. Striae gravidarum: stretch marks from pregnancy weight
B. Diastasis recti: herniation through rectus abdomins muscles
C. Linea nigra - chloasma: MSH and estrogen effect (relationship w/ OCP): LN is pigmentation of midline of the lower abdomen; Cloasma is pigmentation over bridge of nose & under eyes (aka "mask of pregnancy"); fairly uncommon SE of OCP. Melanoma growth may be inc. during pregnancy because of inc. MSH and because some melanomas contain estrogen receptors. If the pt has a melanoa, a therapeutic abortion is recommended if estrogen receptor + as maternal melanomas have been observed to spread to fetus and placenta
D. Vascular spiders, Palmar erythema: also shows up in drunk d/t inc. estrogen
V. Breast changes
A. Macroscopic:
1. Size and nodularity inc., nipple hypertrophy & pigmentation; areolar hypertrophy and pigmentation; colostrum comes in the 2nd day after delivery; contains fat, protein & IgA; after 3-6 days, replaced by mature milk
VI. Metabolism changes
A. Weight gain (responsible factors): fetus, placenta, amniotic fluid, uterus, breasts, blood, interstitial fluid & maternal fat stores
B. Water metabolism (normal distribution of water in the pregnant pt.) in relation to dependent edema: ECF increases and mom is in a state of physiological extracellular hypervolemia. IV volume inc. 50% but dec. albumin means dec. colloid pressure, which contributes to edema. Interstitial volume increases the most in 3rd trimester. Compression of IVC & pelvic veins increases leg edema.
C. Protein metabolism: active transport of aa across placenta means inc. in fetus and dec. in mom
D. Carbohydrate metabolism: facilitated diffusion of glucose means inc. in fetus and dec. in mom (glucose & aa's are baby's food)
E. maternal "accelerated starvation" state
1. Fasting blood sugar levels and response to oral glucose load: should be lower sugar levels than non-gravid but dec. tolerance to oral glucose load in later pregnancy due to diabetogenic hormones secreted by baby
2. Lipolysis, maternal levels of free fatty acids: in first 1/2 of pregnancy, dec. lipolysis; but inc. hPL in later pregnancy increases lipolysis and therefore increases ketone bodies: risk for ketoacidosis
3. Insulin "blocking" effect: hPL antagonized peripheral effects of insulin; secreted by placenta into maternal blood in amounts that parallel placental growth. Progesterone & increased cortisol levels also have an anti-insulin effect
a. Role of HPL: antagonizes insulin
b. Placental steroids (estrogen, progesterone): insulin antagonist
c. Corticosteroid and thyroxin: antagonist
4. Insulin response to carbohydrate intake in pregnancy: In first 1/2 of pregnancy, the anabolic actions of insulin are potentiated in response to glucose but insulin resistance everges in the 2nd 1/2 even though fasting glucose is still lower than in non-pregnant women d/t anti-insulin factors listed above
F. Fat metabolism
1. Hyperlipemia: degree of total and specific lipids: FFAs act as substrates for maternal vs. fetal (glucose & aa) energy use, as they cross placenta passively. The largest lipid fraction change in pregnancy is the rise in fasting triglyceride concentration
2. Starvation effect in pregnancy
VII. Hematologic changes
A. Increase in total blood volume: increase about 50% (dec. albumin by about 30%)
B. Degree of increase in each trimester: magnitude rise correlates with size of fetus & plateaus at 32-34 wks
C. Plasma and red cell mass ratio of increment: RBC mass increases by 30% with Fe supplement & 18% without (about 1/2: hence the dilutional anemia of pregnancy. Optimum hct is 35; hct <27-29 or >39-41 are associated with less favorable outcomes D. Mechanism of increment of red cell mass (erythropoietin)
E. Normal average Hb level in pregnancy
F. Total body iron content in the female
G. Iron storage as related to total content
H. Average iron content of fetus at birth: 300 mg
I. Total iron need: total antepartum need = 800 mg, 300 for fetus and placenta, 500 for hgb mass in mom
J. Excretion average of iron
K. Daily iron requirement
L. Iron content and absorption in commonly used ferrous compounds
M. Maternal blood loss in vaginal and cesarean section deliveries: 500cc for NSVD and 1000cc for CS
N. Coagulation factors
1. Fibrinogen (sedimentation rate): increase by about 50%, clotting factors VII-X all increase in pregnancy
2. Other clotting factors and changes: placenta produces a plasminogen activator inhibitor, Platelets dec. slightly
3. Fibrinolytic activity: placental inhibitor decreases fibrinolytic activity in the body plus the risk of venous stasis and endothelial damage makes pregnancy a hypercoagulable state. Inc. ESR, PT/PTT dec. slightly but no change in clotting time
VIII. Cardiovascular system
A. Heart rate
B. Cardiac silhouette
C. Cardiac volume
D. Heart sounds (heart murmurs)
E. Cardiac output
F. Arterial blood pressure
1. Changes according to trimester
2. Changes according to maternal posture
3. Upper and lower extremities venous pressures
IX. Respiratory tract
A. Anatomic (chest) changes
B. Respiratory rate and tidal volume
C. Minute ventilation
D. Vital capacity
E. Residual volume
F. Lung compliance
X. Urinary system
A. glomerular filtration rate (degree and possible HPL effect)
B. Renal plasma flow
C. Importance of maternal position in renal function at term; i.e., sodium exretion
D. Renal function tests in pregnancy
E. Glycosuria of pregnancy
F. Ureters
XI. Gastrointestinal tract
A. Displacements: Appendix
B. Pyrosis (esophagitis-gastritis)
C. Motility
D. Gastric emptying in labor
E. Gums: Epulis of pregnancy
F. Hemorrhoids and constipation
XII. Liver and gallbladder
A. Liver laboratory studies in pregnancy
B. Alkaline phosphatase activity
C. Serum albumin
D. ALB/globulin ratio
E. Gallbladder function and propensity to stone formation
XIII.Endocrine glands
A. Pituitary: Enlargement, role in pregnancy, labor, and delivery
1. Growth hormone
2. Prolactin: Serum levels in pregnancy; serum levels during
a. Puerperium
b. Lactation
c. Non-lactating mothers
3. Progesterone effect on lactation
B. Thyroid
1. Enlargement
2. Thyroid hormone concentration in pregnancy
a. Thyroid-binding globulin (estrogen effect)
b. Serum thyroxin (T4)
c. Triiodothryonine resin uptake (T3U)
d. Free thyroxin index (FTI)


I. Characteristics of placental villi

II.Characteristics of placental circulation

A. Single vein carries oxygenated blood to fetus, paired arteries branches of hypogastric carrying dexoygenated blood to placenta
III. Histologic concept of placental "barrier"

IV. Description of the amnion

A. Chorion and amnion have different anatomic origins
V. Description of the umbilical cord
A. 30-100 cm long, 2 cm diameter, three vessels
VI. Placental hormonal production
A. Human chorionic gonadotrophin (hCG)
B. Human placental lactogen (HPL)
C. Estrogens (role of the fetal adrenal)
VII. Basic mechanisms of placental transfer
A. Diffusion
B. Selective transfer


I. Development of fetal circulatory system

A. DV shunts umbilical oxygenated blood from liver to IVC, foramen ovale, ductus arteriosus
II. Fetal circulation and post-delivery changes
A. Marked fall in pulmonary vascular resistance with lung expantion and increase in oxygen tension, pressure reises systemically from inc. systemic resistance, pressure rises in left ventricle and atrium (change in pressure between atria closes foramen ovale), ductus arteriosus slowly constricts over 16 hours, circulatory instability continues until DA closes
III. Characteristics of fetal hematopoiesis and fetal blood at term
A. HbF and HbA (O2 affinity)


I. Clinical parameters for the assessment of intrauterine fetal growth

A. First trimester: Last menstrual period, pelvic examination, auscultation of heart tones (doppler 10-12 weeks, fetoscope 17-20 weeks), early US (most accurate)
B. Second and Third trimester: US limited, reassignment of EGA requires good historical info.
II. Use of US in the assessment of fetal growth

III. Amniotic fluid analysis for fetal maturity

A. Lecithin-sphingomyelin ratio (L/S)
1. Increases after 34 weeks, correlates with GA-dependent risk of RDS, 1:5 to 2:0 are transitional
B. Phosphatidyl glycerol (PG)
1. Increases after 35 weeks, lab methods simpler and less expensive, PG levels greater than 3% assoc. with low incidence of RDS (<1%)
C. Fluorescence polarization (fpol)
IV. Fetal heart evaluations
A. Contraction stress test (CST)
1. Labor intensive, sensitive but nonspecific
B. Nonstress test (NT)
1. Simpler, not as predictive as CST
C. Biophysical profile (BPP)
1. Developed to improve sensitivity and specificity, sensitive and convenient testing regime for high-risk conditions
a. Fetal breathing movements (FBM), gross body movement, fetal tone, reactive fetal heart rate (FHR), qualitative amniotic fluid volume (AF)
V. Principle of umbilical artery doppler blood flow


I. Planes and diameters of the pelvis (normal average values, borderline and absolute contracture values)

A. Obstetric conjugate: measure diagonal conjugate, exceeds obstetric conjugate by 1.5-2 cm
B. Mid-pelvis: assess prominence of ischial spine
C. Outlet: ischial tuberosity
D. Others: hollowness of sacrum, width of sacrosciatic notch (sacrospinous ligament), subpubic angle (pubic arch)
II. Characteristics of the pelvic joints

III. Pelvic shapes

A. Anthropoid
1. AP diameter of inlet greater than transverse diameter
B. Gynecoid
1. best suited for child bearing, fortunately most common
C. Android
1. not favorable for delivery
D. Platypelloid
1. least common type (flat)


I. Define "labor"

A. Contractions and cervical dilitation
II. Describe the theories of initiation of labor
A. fall in progesterone, inc. estrogen, fetal cortisol production (animal models only, don't hold true in human studies)
III. Define the first, second, and third stages of labor
A. First: onset of contractions to full dilation (10 cm)
B. Second: complete dilation to delivery of baby
C. Third: delivery of baby to delivery of placenta
IV. Using the standard labor curve (Friedman)
A. Define latent phase of labor
1. Contractions without dilitation (20h nulli, 14h multi)
B. Define active phase of labor
1. Rapid progression of dilitation (12h nulli, 5.2h multi)
V. List the common etiologies and management of
A. Prolonged latent phase
1. 20h if multi, 14h if nulli. Analgesia and anesthesia may prolong, Tx with low dose of oxytocin after 12 hours (1-2mU/m)
B. Primary dysfunctional labor
1. < 1 cm/h for nulli, < 1.5 cm/h for multi. 10-15% of labor. Active management (oxytocin, fetal monitoring)
C. Secondary arrest
1. No change for two hours in active labor (5-10% of labor); associated with CPD; oxytocin should cause progression within 2-3 hours
D. Prolonged second stage of labor
1. 2 hours in nulli, 45 minutes in multi; malposition or mild CPD, oxytocin stimulation in appropriate cases, abdominal delivery if previous labor had been abnormal (fetal monitoring, low dose oxytocin, edematous cervical lip reduces chances for vaginal delivery, rotation from OA to OP)
VI. Describe the normal mechanism of labor in the occiput presentation
A. Engagement, Descent, Flexion, Rotation, Extension


I. Basic technical aspects of external and internal fetal heart rate monitoring techniques

A. Top pen = FHT, bottom pen = uterine CTX; external FHM subject to artifacts and affected by maternal body habitus, internal use during labor
II. Normal ranges of fetal heart rate during labor (definition of bradycardia and tachycardia)
A. Baseline rate is the most prominent for average rate between contractions in absence of decelerations, should persist for greater than 15 minutes, normal range 110-160; Tachycardia is > 160 bpm; less than 120 bpm shoul have normal variability to be considered normal variant
III. Characteristics, physiopathology and clinical significance of
A. Beat-to-beat variability
1. Only measurable with fetal scalp monitor, shows control by higher mental functions
B. Early decelerations
1. Most benign, probably normal vagal response, not associated with hypoxia or acidosis, head compression
C. Late decelerations
1. Most concerning periodic change, return to baseline after contraction, smooth shape, usually repetitive, 70% assoc. with suboptimal outcome, placental insufficiency
D. Variable decelerations
1. Most common (50% of all FHT), cord compression, nonuniform shape / duration / depth, fetal risk depends on severity and persistence of decelerations
IV. Significance of fetal pH changes during the intrapartum period
A. pH < 7.20 = fetal acidosis, delivery indicated
B. 7.20-7.25 = concerning, repeat test required within 20-30 minutes
C. 7.25-7.35 = normal


I. List a method of analgesia and describe its effects on the mother and fetus

A. Systemic
1. Maternal: N/V, sedation, dec. gastric motility, respiratory depression
2. Neonatal: CNS depression, Resp. depression, dec. temp regulation,altered neuroadaptive behavior
B. Regional Anesthetic
1. Local only, some s/s of toxicity, minor neonatal effect. Complications are infection and abscess
C. Lumbar Epidural
1. Local effect, minor neonatal effect. Hypotension is common, thrombocytopenia
2. Decreased control and assistance by mother, inc. C/S rate, inc. dystocia
II. List at least two acceptable methods of anesthesia and describe:
A. Pharmacologic effects on mother and fetus
B. Immediate and remote complications of each method


I. Discuss intrauterine fetal respiration

A. Episodic breathing movement occur with inc. frequency during pregnancy to about 30 resp/10 min, esp. during REM and SWS. In utero, so not needed for oxygenation. Gas exchange occurs across placenta w/ NL umbilical O2 sat of 80-85% at PO2of 30 mm Hg. High fetal pulmonary vascular resistance maintained to shunt blood away from lungs
II. Discuss initiation of air breathing
A. Change in resistance to blood flow: high pulmonary vascular resistance in utero is lost at birth by the expansion of the lungs and inc. O2 tension
B. Fall in pulmonary arterial blood pressure: Systemic BP inc. d/t clamping of umblical artery & by catechol release which serves to further inc. pulmonary blood flow (pulmonary arterioles and ductus arteriosus respond in opp. directions to O2 inc. and dec.)
C. High negative intrathoracic pressures: fetal lungs not expanded in utero, high intrathoracic pressure at birth which facilitates lung expansion and breathing, have to work hard to expand lungs
D. Alveolar surface tension (lung surfactant): deficient surfactant causes inc. surface tension and higher intrathoracic pressures to mainain alveoli open therefore more work
III. Discuss known reasons for delayed effective respiratory efforts in the newborn
A. Maternal medication, birth asphyxia, obstruction of the respiratory tract, cerebral trauma, prematurity, massive meconium aspiration, chorioamniotis with maternal fever, prematurity
IV. Describe the APGAR score system
A. Color, Heart rate, Respiratory effort, Muscle tone, Stimulus response 7-10, no resuscitation needed; 4-6, some resuscitation needed; 0-3, aggressive resuscitation.
V. Describe physical characteristics use in the clinical estimation of gestational age
A. Birth weight & body ratios of head circumference, thorax & legs are most commonly used. Consistency of scalp hair, pliability of ear lobes, pigmentation of breasts, presence of upper breast mound, presence of sole creases, presence of scrotal rugae


Recovery process of a mother recently vaginally delivered a term infant. Time from delivery of placenta to return of uterus to a non-gravid state (~6 wks)

I. Describe the normal progressive changes in lochia and uterine size

A. Uterine changes: at level of umbilicus immediately after delivery, midway between symphysis and umbilicus by 1 week PP, pelvic organ by 2 weeks PP, nonpregnant size by 6 weeks PP
B. Lochia: blood, necrotic membrane remnants and decidua shed from uterine cavity, dec. over several weeks
II. Describe the normal recovery process of the skin, cardiovascular, urinary, endocrine, and metabolic systems
A. Skin: Hyperpigmentation d/t inc. estrogen, progesterone, and MSH resolve rather quickly as do angiomata & erythema. Hair loss during 4-20 wks. PP d/t sudden shift of hair follicles from growth phas (anagen) to resting phase (telogen). Striae are mechanically, not hormonally, caused & do not rapidly resolve
B. CV: reversal of pregnancy changes over 2-3 weeks, CO inc. in immediate puerperium d/t inc. venous return, high-risk period for pts with cardiac defects. The 1/3 inc. in blood volume is gone by PPD#3
C. Urinary: GFR remains incresed d/t inc. CO. Diuresis occurs, upper urinary tract dilation persistsfor months PP
D. Endocrine: sudden loss of maternal & placental hormones (progesterone, estrogen, hPL, insulin) at birth contrasted with inc. oxytocin & prolactin
E. Leukocytosis persists, weight loss (5-6 kg at delivery, 3-5 kg first week PP)
III. Describe the normal physiology of lactation and its suppression
A. Lactogenesis results from withdrawal of estradiol and progesterone in human placental lactogen, tactile stimuli results in release of prolactin and oxytocin, composition of milk changes with time, human milk contains better proteins (lactalbumin and lactoferrin) than cow's milk (casein)
B. Lactation suppression: tight bra or binder with ice packs and analgesics
IV. Counsel the puerperal patient regarding physical activities, sexual activities, and contraception
A. Physical activity: slow and easy, D/C if painful.
B. Baths and showers OK, FeSO4 for hct < 30.
C. Pelvic rest for 4-6 weeks (sex, douche, tampons).
D. Begin contraception (OCP, Depo, etc.) at 2 weeks. Watch for inc.bleeding, tenderness, fever, depression


I. Discuss the mode of action of each method and explain it to the patient in lay terms

A. Coitus interruptus
B. Withdrawl prior to ejaculation C. Natural Family Planning/Fertility Awareness Techniques (BBT, Cervical mucus method, Calendar or "rhythm" method)
D. Relates the time of sexual intercourse with the woman's menstrual cycle and avoiding intercourse during the fertile period (preovulation to 48 hours post ovulation)
E. Lactation/Breastfeeding
1. Hypothalamic hypofunction, pituitary unresponsiveness, ovarian refractoriness secondary to increased prolactin releasing hormone
B. Condoms or Vaginal Pouch
1. Barrier or barrier plus spermicide
C. Spermicides (Jellies, creams, foams, supp., tablets, films)
1. Nonoxynol-9, Octoxynol-9, destroy sperm cell membrane so viable sperm reach ovum
D. Diaphragm
1. Barrier plus spermicide
E. Cervical cap
1. Barrier plus spermicide
1. Endometrial reaction--implantation inhibition, bioactive substances such as copper, sperm immobilization
G. Depot Medroxyprogesterone Acetate (Depo-Provera)
1. Inhibition of ovulation by decreasing the levels of FSH/LH and stopping the surge of LH which stimulates ovulation (each 3 months); thicken cervical mucus; create thin, atrophic endometrium
H. Levonorgestrel Implant (Norplant system)
1. 6 subdermal silastic capsules which release levonorgestrel slowly over 5 years causing a sustained blood level of pregestin and preventin ovulation, thicken cervical mucus, keeps endometrium thin and atrophic
I. Oral Contraceptives
1. Combined formulations: negative feedback action due to exogenous estrogen and progestin from OC which act on hypothalamus to inhibit or modify the releasing factor for FSH (E-to block follicular development) and LH (P-so ovulation cannot occur); inhibit ovulation (E & P); thicken cervical mucus and thin endometrium(P)
2. Progestin-only formulations: alterations in cervical mucus and changes of the endometrium; down-regulate E receptors; don't consistently suppress ovulation
J. Abstinence
1. No sperm and egg contact
K. "Morning after" pill
1. Luteolytic effect, out-of-phase endometrium, disordered tubal transport
L. Tubal ligation
1. Blocking fallopian tube by segment removal, cautery, clips, or Fallopr rings to prevent sperm transport to meet ovum
M. Vasectomy
1. Ligation of vas deferens to prevent sperm from leaving the testicle
N. Abortion
1. D&C, D&E, hysterotomy or hysterectomy; medically with PGE2, hypertonic saline or urea
O. Ineffective: postcoital douching, postcoital urination, altered sexual positions, coitus interruptus/withdrawl, lactation
II. For each contraceptive method, list the minor and major complications, their incidence, and reversibility
A. Coitus interruptus: high failure rates, pre-ejaculatory fluid contains sperm, diminished sexual pleasure
B. Rhythm: high failure rate, loss of sexual spontaneity, variations in temp. and vaginal mucus, irregular menses, breastfeeding
C. Breastfeeding: unreliable, feeding must be done on demand, usually requires another form of cotraception, combinatin OCs may decreasre milk supply, lowers estrogen production--vaginal dryness
D. Condoms: decreased sensitivity, interruption of foreplay, allergy to latex
E. Spermicides: inconvenient or messy, importance of timing, allergy to spermicide
F. Diaphragm: requires office visit and prescription, inability of pt to insert/remove, allergy to latex or spermicide, increased risk for cystitis/urethritis/TSS, unsatisfactory for uterine prolapse/retroversion
G. Cervical Cap: office visit and prescription, inability of pt to insert/remove, allergy to latex or spermicide
H. IUD: office visit for insertion, cost, increased risk of PID/ectopic pregnancy, infertility, cramping/bleeding/anemia, expulsion
I. Depo-Provera: spotting/irregular bleeding, amenorrhea, weight gain, bloating, other possible SE
J. Norplant: spotting/irregular bleeding amenorrhea, cost for implantation, minor surgery for removal
K. OCP: fluid retention, acne, leukorrhea, hypomenorrhea, HA, HTN, growth of leiomyomata, thromboembolic complication, altered lipid profile
L. Morning-after pill: nausea, must take within 72 hours
M. Abstinence: lack of intimacy
N. Tubal ligation: Poorly reversible, requires anesthesia, surgical risks of bleeding/infection/injury, no STD protection
O. Vasectomy: Poorly reversible, surgical risks of bleeding/infection, no STD protection, majority develop sperm antibodies, recent concern of effect on prostate
P. Abortion: Surgical risks of infection, injury, bleeding, complications for future fertility, requires trained personnel
III. List the contraindications of each method
A. In general, each method has contraindications with allergy to the topical application of barriers or spermicides
B. OCPs have some absolute and relative contraindications
1. Absolute: Hx of thromboembolic dz, CVA, CAD and MIs or hepatic adenoma; age > 35 if smoker; pregnancy; strong family Hx of malignancy of breast, reproductive system, or any estrogen-dependent tumor; markedly impaired liver function or Hx of jaundice or pruritis of pregnancy
2. Relative: undiagnosed genital tract bleeding; noncompliance or unreliability of pt; smokers < 35 YO; Hx of migraine HA, HTN, of GB dz; DM or FH of DM; sickle cell dz or sickle Cell dz; elective major surgery planned withing next 4 weeks requiring immobilization
3. Medical: hepatic enzyme inducers (barbiturates, carbamazepine, primidone, phenytoin, ethosuximide, and rifampin) and antibiotic therapy both may cause decreased effectiveness of OCs
4. Acronym for physician visit: ACHES
IV. List the effectiveness of each method (one year of actual use)
A. Coitus interruptus: 82% (23-40% FR)
B. Rhythm: 80-90% if dedicated (20-30% FR)
C. Lactation: 2.9-5.9% FR during amenorrheic period, 7.7-17.2% after
D. Condom: 85-95%, 98% with spermicide (10-15% FR)
E. Spermicides: 75-97%, increased with barriers (15% FR)
F. Diaphragm: 80-90%, 98% with spermicide (10-15% FR)
G. Cervical cap: 80-90%, 98% with spermicide
H. IUD: 94-99% (4-6% FR)
I. Depo-Provera: >99%
J. Norplant: >99%
K. OCP: 99% (4-6% FR)
L. Morning-after: 98%
M. Tubal ligation: 99%
N. Vasectomy: 99%
O. Abstinency: 100%
P. Abortion: 99%
V. List the advantages and disadvantages (III above)of each method
A. Coitus interruptus: no devices, no chemicals, no cost, ethical/religious
B. Rhythm: any woman with regular menses, no meds, little equipment, no adverse SE, ethical/religious
C. Lactation: adequate nutrition for newborn, immunity for newborn, child spacing
D. Condoms: inexpensive, no prescription, STD protection
E. Spermicides: no prescription, relatively inexpensive, good back-up method, STD protection
F. Diaphragm: easy to use, some STD protection, reusable, non-hormonal method, low $
G. Cervical cap: reusable for 1 year, non-hormonal, smaller than diaphragm & no increased risk for UTI, some STD protection, can be used with spermicide
H. IUD: very effective, compliance not required, long lasting, non-hormonal
I. Depo-Provera: very effective, compliance, long duration of action, no estrogen component
J. Norplant: very effective, compliance, long duration of action
K. OCP: decreased risk for PID, ectopic pregnancy, breast mass, ovarian and endometrial CA, TSS, dysmenorrhea, PMS, irregular menses, etc.
L. Abstinence: no chance for STD or pregnancy
M. Tubal ligation: permanent, highly effective, non-hormonal, no interruption of sexual activity
N. Vasectomy: Permanent, highly effective, no interruption of sexual activity, office surgery with local anesthesia
O. Morning-after pill: useful if other methods fail, after rape
P. Abortion: implanted pregnancies up to 24 weeks
VI. Recommend the best appropriate method for a specific patient's needs
A. Consider the advantages and disadvantages as they relate to the patient under consideration and choose the method whose profile most effectively meets the patient's needs.
VII. Counsel the patient and her mate concerning the use, reliability, and complications of that particular method
A. Consider advantages, disadvantages, and reliability in advising the couple on the most acceptable from of BC
VIII. Define:
A. Pregnancy rate: # of pregnancies per 1000 women aged 15-44
B. Birth rate: # births per 1000 people
C. Fertility rate: # live births per 1000 women aged 15-44
D. Marriage rate: # marriages per 1000 people
E. Failure of a contraceptive: # pregnancies per 100 women in one year for a certain contraceptive method
IX. Differentiate:
A. Theoretical effectiveness and use-effectiveness
1. Theoretical effectiveness is when always used correctly while use effectiveness is the rate in actual use for a specific method.
B. Contraception and sterilization
1. Contraception is preventing pregnancy in general while sterilization is anatomically preventing an individual from moving gametes to a location where they can meet
X. Discuss:
A. Coitus interruptus or withwrawl: withdrawl of penis prior to ejaculation
B. Postciotal douche: ineffective
C. Prolonged lactation
D. Extravaginal intercourse: form of abstinence
E. Rhythm: maternal practitioner called "Mom"
F. Spermicidal jelly, cream, foam, tablets: spermicide
G. Diaphragm: dome-shaped rubber disc in various sizes
H. Condom: sheath of latex or animal tissue that covers the penis to collect the semen
I. Intrauterine device: plastic device placed in uterine cavity, Paraguard and Progestasert only ones available in US, abortifactant
J. Hormonal contraception
1. Combination "pill": combined estrogen and pregestin formulations in which pills with identical amounts, or varied amounts (biphasic/triphasic) of active ingredients are taken for 21 days followed by 7 days of placebo/no pills
2. "Mini dose" low progestin "pill": pill contains the same dose of progestin on a continuous basis throughout the cycle
3. Morning-after "pill": high dose combination oral contraceptive using 100ug ethinyl estradiol repeated in 12 hours or ethinyl estradiol alone
XI. Sterilization
A. Describe the method and be able to outline it in layman's terms
1. See "method of action"
B. Determine its risks and failure rates
1. Laparascopic (1-2/1000 FR)
2. "fallope" ring application: loop of tube drawn into applicator tube & ring placed on both limbs of loop. Higher FR than fulguration & if done immediately PP (1/100
3. fulguration: Electrocautery of tube
4. Non-puerperal tubal resection: better
5. Postpartum tubal resection: FR slightly higher (2x higher): risks from each are shoulder pain from pneumoperitoneum, ectopic pregnancy, dysfunctional uterine bleeding, depression, regret
6. Vasectomy: (.4% FR) OP procedure, hematoma (5%), sperm granulomas (18%)


I. Define fetal death and fetal mortality rate
Death before complete expulsion or extraction of a product of human conception from the mother excluding pregnancy termination. Fetal mortality rate is the number of stillborn infants/1000 infants born

II. Define neonatal death and neonatal mortality rate
Early: first 7 days of life, Late: after 7 days but before 29. Neonatal mortality rate is the # of neonatal deaths/1000 total births

III. Define perinatal death and perinatal mortality rate
Combination of fetal deaths and neonatal deaths

IV. State most common cause of neonatal death

A. Low birth weight (blacks>whites)
B. Congenital malformations (3% of births)
C. Injury / birth trauma: hypoxic brain injury, birth asphyxia
V. Define maternal death and list three most common causes in the United States
A. Death of a woman from any cause related to or aggravated by pregnancy or its management up to 40 days after the termination of pregnancy
1. emboli
2. PIH
3. PP hemorrhage


I. Definition of "abortion" and "viability"
Abortion and miscarriage both refer to first trimester pregnancy losses (<500g or 20 wks EGA = limits of viability)

II. Incidence and possible etiologies of "spontaneous abortion"

A. Miscarriage is the most common complication of pregnancy, 15% incidence among clinically recognized pregnancies, prevalence inc. with maternal age (12% < 20 YO, 50% >45 YO)
B. Embryonic factors: abnormal germ cells, defective implantation of normal trophoblast, injury to developing embry
C. Chromosomal abnormalities: 60% of first trimester losses, dec. to 7% @ 24 weeks (autosomal trisomies 16/21/22 > monsomy X > triploidy > tetraploidy > translocations > mosaics) and parental factors (balanced translocations)
D. Endocrine:luteal phase defect (no pregesterone secretion by corpus luteum or deficiency of progesterone receptors in endometrium. Hypothyroidism
E. Anatomical abnormalities of uterus: cervical incompetence, uterine structural/formation defects
F. Infectous dz: rubella, herpes, CMV, toxo
G. Systemic dz; nutritional deficiency, DM, SLE (40% SAB rate)
III. Difference between:
A. Threatened abortion: Cervix closed and uneffaced, first trimester bleeding in 25% of pregnancies. No convincing evidence that treatments influence outcome, be sympathetic. Bedrest, progesterone, no sex, evacuation of uterus if bleeding excessive/persistent, cerclage
B. Inevitable abortion: bleeding or SROM with pain and cervical dilation, it's inevitable; deliver or D&C
C. Incomplete abortion: partial passage of products of conception (POC), evacuate uterus to prevent further hemorrhage or infection, follow with methergine/pitocin, always check pathology (mole)
D. Missed abortion: expulsion does not occur for prolonged period after fetal death (>6wks). Suction curretage in first trimester, D&E in second trimester (laminaria pre-op) or prostaglandin E2.
IV. Appropriate plan of management for each clinical situation

V. Definition of "induced abortion"

A. Caused by iatrogenic intervention
VI. Definition of "habitual abortion"
A. Recurrent spontaneous abortion (RSA): three or more consecutive first-trimester losses. Check for uterine abnormalities and rare Ab (lupus anticoagulant, anticardiolipin Ab)


I. Define "ectopic pregnancy"

A. Implantation outside the endometrial cavity. Most common cause of maternal death in first half of pregnancy
II. In reference to tubal pregnancies:
A. Different and most common tubal sites of implantation
1. Tubal--97% (86% in distal half), abdominal, uterine, ovarian
B. Clinical signs and symptoms
1. Symptoms: Abdominal pain~95%, Amenorrhea~85%, VB~60%, Dizziness/fainting~30%, pregnancy symptoms~15%
2. Signs: Adnexal tenderness~85%, Abdominal tenderness~90%, Adnexal mass~50%
C. Significance and sensitivities of standard pregnancy tests and beta-subunit assay in the diagnosis of ectopic pregnancies
1. Serum hCG usually lower than normal; serial values also very helpful, rate of rise slower in ectopic pregnancies.
D. Endometrial and uterine changes
E. List clinical and laboratory data helpful in the differential diagnosis between:
1. Ruptured tubal pregnancy: hCG
2. Acute appendicitis: laparoscopy
3. Acute pelvic inflammatory disease: gonorrhea cultures
4. Torsion of an adnexa: laparoscopy
F. The use of US, culdocentesis, and diagnostic laparoscopy
1. U/S: gold standard in combination with serum hCG, detect early ectopics
2. Culdocentesis: Nonclotted blood with hematocrit >15% in post. cul-de-sac, positive predictive value 70-97%
3. Laparoscopy: direct visualtization, can be performed too early
G. Plan of management in a case of unruptured pregnancy and in a case of ruptured ectopic pregnancy
1. Surgical: salpingostomy except with irreparable tubal rupture, laparoscopic Tx,br> 2. Medical: Methotrexate (folate antagonist, inhibits dihydrofolate reductase so tissues with rapid cell growth most affected), must be unruptured and hCT < 15,000 IU/L


I. Most common obstetrical and nonobstetrical causes of bleeding late in pregnancy

A. Obstetrical: Placenta previa, placental abruption, uterine rupture, velamentous cord, vasa previa, marginal sinus separation, molar gestation
B. Non-obstetrical: cervical / vaginal lesion, Cervicitis, cervical CA, congenital malformation, undetermined

II. Overall incidence of late pregnancy bleeding 3-4%

III. Given supected diagnosis of abruption placentae, the student should know:

A. Definition and incidence of abruptio placentae: Premature separation of the normally implanted placenta > 20 wks, 30% of all late pregnancy bleeding, .8% of all pregnancies
B. Pathophysiology, external and concealed bleeding: Separation is initiated by bleeding into decidua basalis, decidua splits and placenta is sheared off, blood may extravasate into and through myometrium (couvelaire uterus)
C. Associated clinical and obstetrical factors: Maternal HTN, PIH, cocaine-induced, chronic HTN, smoking, short cord, uterine anomalies, advanced maternal age, physical work, poor nutrition, trauma, sudden decompression of overdistended uterus, prior episode (5-15% recur), polyhydramnios, PPROM
D. The clinical characteristics of abruptio placentae: VB--80% (may be concealed bleed), Uterine tenderness or back pain--65%, Fetal distress--60%
E. The maternal complications:
1. shock
2. hemorrhage
3. poor contractile efficiency
4. pituitary necrosis (Sheehan Syndrome)
5. coagulation defect: DIC (marked hypofibrinogenemia)
6. acute renal failure: ATN (d/t low blood volume from bleeding)
F. The fetal complications: immediate and remote but includes fetal hypoxia and death
IV. Given suspected diagnosis of placenta previa, the student should know:
A. Definition and classification of placenta previa: Implantation of the placenta in the lower uterine segment, overlying or reaching the cervix, precedes presenting part at delivery, 20% of all late pregnancy bleeds, 1/200
1. Total: internal os completely covered
2. Partial: os partially covered
3. Marginal: placenta reaches edge of os
4. Low-lying: implanted in lower uterine segment but not to os
B. Incidence and probable mechanism
1. 1/200, more common with inc. parity, incidence decreasing in US
2. Specific cause is unknown.
C. Clinical factors associated with higher incidence of placenta previa
1. Implantation may be affected by abnormality of endometrial vascularity, delayed ovulation, prior endometrial trauma, multiple pregnancy, previous uterine surgery (cesarean, myomectomy)
B. Current methods used to localize the placenta
Ultrasound is diagnostic technique of choice (93-97% accurate) TV is preferred, Definitive Dx by direct palpation only with Double Setup
C. Clinical characteristics of patients with placenta previa
1. Painless VB in third trimester (as early as 20 weeks), blood loss from first bleeding is rarely fatal, mean EGA~32.5 weeks, Use U/S to localize placenta
D. Management of the patient according to gestational age, presence or absence of labor, and degree of vaginal bleeding
1. Light Bleeding/Spotting
H&P (especially time of last intercourse), U/S before vaginal exam to r/o previa, if no previa then cervical exam to evaluate for cervical lesions
2. Moderate to Heavy Bleeding
  • Vitals, fetal monitoring, H&P including trauma, sex, CTXs, bleeding dz, cocaine/tobacco use, assess uterus, fetal presentation & condition (fetal heart monitor)
  • NO VAGINAL or RECTAL EXAM until r/o previa with U/S
  • IV access, T&C 2-4 units PRBCs (give prn per vitals and Hct)
  • Labs: clot tube, CBC, plt, electrolytes, fibrinogen/D-dimer
  • U/S to determine if previa or abruption present (95% sensitivity for previa, poor for abruption)
  • If previa and still bleeding or fetal distress, proceed to C/S
  • If previa & no bleeding, hospitalize with periodic fetal monitoring & U/S or send home if good access to hospital. Pts with previas typically bleed every 2 wks or so with more blood each episode; BMZ Tx & deliver at 36 wks if lungs mature (amniocentesis). If at term, consider amniocentesis for lung maturity then double set-up for delivery
  • If mild abruption & stable fetus, careful observation with continuous fetal monitoring until bleeding and pain resolve
  • If severe abruption & fetus alive, try for double set-uo vaginal delivery with very careful monitoring of FHR; pitocin & AROM
  • If severe abruption and dead fetus, deliver vaginally
  • If no previa or abruption, SSE to look at cervix (lesions, warts) & do CT culture, but these pts usually do not present with heavy bleeding. Cervical exam to make certain pt not in labor before sending home
  • If pt continues to bleed with mom and fetus unstable w/o an established Dx, double set-up exam: have pt ready for C/S then do gentle vaginal exam; if no previa and cervix favorabl, try for vaginal delivery with pitocin
3. Sheehan syndrome: big blood loss causes pituitary to infarct, no hormones (anterior: GH, FSH, LH, prolactin, ACTH, TSH; posterior: oxytocin, ADH), no periods/milk
E. The fetal and maternal prognosis
1. Maternal: <1% mortality from hemorrhage, DIC
2. Fetal: <5% perinatal mortality, prematurity (PPROM), preterm delivery as it is indicated for heavy bleeding, IUGR since lower segment doesn't have the rich blood supply of the fundus

V. Discuss the evaluation and management of other causes of bleeding late in pregnancy
A. Cervicitis: staph, strep, or chlamydia; associated with leukorrhea (WBC in vaginal discharge)
B. Cervical CA: painless VB (esp. post-coital). Most common CA in pregnancy. Endocervical curettage C/I; colposcopy q 6 weeks. Cone bx in 2nd trimester. Complications in 1st trimster=induced ab; 3rd trim=PTL & hemorrhage. Highly invasive CA requires urgent Tx, otherwise manage conservatively during pregnancy
C. Ruptured vasa previa: sudden VB with FHTs which go from tachy to brady to sinusoidal (acidosis); 50-75% perinatal morbidity.

VI. Clinical, radiographic, and US evidence of fetal death
A. Fetal demise > 20 wks before onset of labor
B. Clinical: No FM, small for dates uterus, No FHTs
C. U/S Evidence: No Fetal movement or cardiac activity
D. Radiographic evidence: Robert sign (gas in fetal abdomen), Spalding sign (overlapping of fetal cranium wiht exaggerated curvature of spine)
E. Positive endocrine tests are not reassuring

VII. Complication associated with late pregnancy fetal death
A. Slight possibility of infection, DIC (10%) if fetus retained > 5-6 weeks

VIII. Uterine evacuation techniques in case of fetal death in utero
A. Most will labor within 2-3 weeks of fetal demise, so could possibly manage expectantly; can induce labor with progestin or pitocin if >28 wks if cervix favorable.
B. D&C or D&E, dilate with laminaria the day and night before


I. Incidence of breech presentation

Most common obstetric malpresentation (4% of deliveries)
II. Characteristics of complete and incomplete breech presentation
A. Complete: fetal hips and knees flexed, least common (5%)
B. Incomplete: One or both hips incompletely flexed (single or double footling), poor dilating wedge (25-35%)
C. Frank: hips flexed, legs extended, buttocks most dependent part (65%)
III. Maternal and fetal conditions associated with a higher incidence of breech presentation
A. Maternal: Uterine anomalies (septate, bicornuate, unicornuate), High parity with lax abdominal and uterine musculature, Pelvic obstruction (placenta previa, myomata, other pelvic tumors)
B. Fetal anomalies: head anomalies (anencephaly, hydrocephalus), Chromosomal anomalies (autosomal trisomies), multiple gestation, placenta previa, 50% idiopathic
IV. Mechanism of labor in breech presentation
A. Should have same progression of labor (Friedman curve). Failure to descend to below spine at onset of second stage is indication for C-section. Oxytocin contraindicated in arrest disorders. Second state 30 minutes in multi-, one hour in nullipara. Epidural is indicated, useful in preventing maternal loss of control.
V. Perinatal mortality rates
A. Much higher in breech presentation (4x in term, 2-3x in preterm), much unpreventable. Head trauma, Musculoskeletal trauma, cord prolapse with asphyxiation
VI. Prematurity rates

VII. Congenial abnormality rate

A. Many congenital malformations have a much higher incidence among breech presentations: CNS (hydrocephalus, anencephaly) 1.7%, Trisomy 21 .5%, CV .6%; GI .5%, overall 9%, among term infants who die 50%
VIII. Traumatic morbidity rate in relation to fetal weight
Incidence of breech presentation increases inpressively with decreased fetal weight
IX. Incidence of cord prolapse and its relationship to all breech presentations
.4% with frank, 5-6% with complete, 10% with incomplete
X. Management of the breech delivery
A. External version (Leopold's) can be attempted but not <37 wks. Can pre-treat with tocolytic to relax uterus, can use U/S to guide
B. Deliver to umbilicus, remove 4 cm loop of cord, legs delivered by flexing knees, towel around fetal pelvis and gentle downward traction, fetus delivered to scapulae, fetal body rotated to shoulders in AP position, anteior arm flexed and swept out, fetus rotated 180 degrees to keep breech toward symphysis, delivery of head with Piper forceps, generous episiotomy


Arrest of active phase of cervical dilation or arrest of descent; does not present in latent phase. Think of three P's (power, passenger, pelvis--in that order)

I. Fetal causes of feto-pelvic disproportion

A. malpresentations (breech, face, brow)
B. malpositions (persistent OT--transverse lie; OP)
C. congenital abnormalities: hydrocephalus, fetal ascites, organomegaly, hydrops, NTD
D. Macrosomia: DM, post-dates, genetics, multiparity, >4kg often cause of shoulder dystocia
II. Maternal causes of feto-pelvic disproportion
A. Inlet contraction (diameters): Obstetric conjugate (unengaged head in nulliparous pt)
B. Mid-pelvic contraction (diameters): diameter of mid-pelvis (ischial spines), arrest at 2 or 3+ station
C. Outlet contraction (diameters): diameter of ischial tuberosity (rare alone)
D. Soft tissue obstruction: inflammed and swollen tissue, fibroids, vaginal mass, ovarian cyst, pelvic kidney, sacro-coccygeal teratoma, cervical stenosis, impacted feces, enlarged bladder
III. How presumptive diagnosis of feto-pelvic disproportion is made in labor
A. Secondary arrest of dilation (no change for two hours in active labor), <1.2 cm/h in nulliparous or <1.5 cm/h in multiparous in active phase with adequate CTX (40-60mm Hg q2-4' for 40-90s q CTX)
B. Protracted descent (< 1cm/h in T, < 2cm/h in multi)
If above met then C/S; 50% recurrence rate with C/S; always C/S with repeat classical
IV. Shoulder dystocia
A. McRobert's maneuver to open pelvic outlet, suprapubic pressure, corkscrew maneuver (twist baby), deliver posterior shoulder, break clavicles, Zavanelli, C/S
With these maneuvers, a liberal episiotomy should be cut (fourth degree if necessary)
V.Power problems
A. Tx with pitocin. Primary uterine inertia in primagravidas, NOT multi-. Discoordinate CTX, false labor
B. Inadequate abdominal muscle CTX: diastasis recti, ventral hernias, obesity, previous surgery
C. Inadequate uterine muscle: malformation of uterus (bicornuate), multiple fibroids, tumors, drugs that inhibit uterine CTX (morphine, fentanyl, pudendals, epidurals)


Main idea: multiple gestation increases complications of pregnancy (inc. perinatal M&M, inc. maternal M&M)

I. Maternal clinical complications related to multiple gestation

A. Greater inc. in blood volume / pulse / cardiac output / weight gain (40-44#). Inc. rate of PTL (7-10%), HTN, abruption, anemia, hydramnios, UTI, postpartum hemmorhage, C-Section, Pre-eclampsia

II. Fetal complications related to multiple gestation
A. Prematurity (avg. age ~ 37 weeks, lungs mature ~31-32 weeks)
B. Discordance (>20-25% difference in weight), 10% of twins
C. Vanishing twin (50% of all twin pregnancies in first trimester end up as singleton birth
D. Monoamniotic Twin Pregnancy (d 8-13), cord entangelement and fetal death
E. Dead fetus syndrome (2-7% with fetal death of one > 20 weeks), If monochorionic: high risk for surviving twin (25% die, 50% of survivors have brain damage
F. Hydramnios, malpresentation, placenta previa, abruption, PROM, umbilical cord prolapse, congenital anomalies

III. Etiology of multiple gestation
A. Dizygotic twins (fraternal)
1. heredity important on mother's side, race-specific rates (Africans > Caucasian > Asian) Inc. in women > 35 YO, maternal hx of twins, inc. parity and in obese, fertility drugs (Clomid~10%, Pergonal~30-50%).
2. 1/90 births are twins, 1/3 of which are monozygotes
B. Monozygotic twins (identical)
1. Chance occurrence, inc. slightly with delayed implantation

IV. Anatomic arrangement of the fetal membranes according to the time of division of the embryonic cell; i.e., diamniotic-dichorionic, diamniotic-monochorionic, monoamniotic-monochorionic
A. Dizygotic: two individual placental units
B. < 3 days: diamniotic, dichorionic
C. 3-8 days: diamniotic, monochoionic
D. 8-13 days: monoamnionic
E. > 13 days: conjoined

V. Incidence of monozygotic twins: 3-4/1000

VI. Factors influencing incidence of dizygotic twins: above

VII. Clinical and sonographic data useful in the prepartum diagnosis of multiple gestation

A. Clinical exam misses 1/3 of all twins: uterine size > dates, two fetuses palpated, two heart rates auscultated, Inc. MSAFP / hCG / hPL / estriol, U/S
B. Hx: maternal family hx of dizygotic twinning, use of fertility drugs, maternal sensation of feeling larger than with previous pregnancies,or sensation of excessive fetal movements
C. PE: excessive weight gain, abdominal palpation of an excessive number of fetal parts, auscultation of two separate fetal heart rates that differ by > 10 bpm, rapid uterine growth, size/dates discrepancy--fundal height is usually 4 cm larger that expected.
D. Sonography: >6 wks, separate gestation sacs, > 10 weeks multiple fetal parts may be visualized

VIII. Perinatal mortality with multiple gestation
A. Perinatal M&M >> singletons, mortality rate 5x singletons, MC twins 3x rate of DC twins (twin-twin transfusion)
B. Monoxygotics have 2.5x risk of Di- d/t inc. pre-eclampsia
Respiratory Distress Syndrome~1/2 of perinatal mortality in twins, 2nd twin 2x risk of first d/t birth asphyxia and uteroplacental insufficiency
C. Birth trauma to 2nd twin 4x first
D. Congenital anomalies and stillbirths 1/3 of perinatal mortality, stillbirths 2x singletons. Cerebral hemorrhage 1/10 of perinatal mortality rate

IX. Antepartum management
A. Prevention of prematurity is primary goal. Prolong gestation, inc. birth weight and dec. perinatal M&M and dec. maternal complications
B. Bed rest has been advocated after 24 weeks: maximize uteroplacental flow
C. Pregnancies are usually not permitted to go beyond 38 weeks (inc. perinatal mortality rate >40 wks).
D. Should take rest periods tid; target weight gain 35-45 lbs


I.Define "gestational hypertension"

A. Blood pressure of at least 140/90 mm Hg or a rise of 30 mm systolic or 15 mm diastolic. Blood pressure usually falls during 2nd half of pregnancy.
B. HTN during 2nd half of pregnancy without proteinuria or edema=transient/labile HTN
C. HTN that arises only during pregnancy: PIH, Toxemia, Preeclampsia, EPH Gestosis
D. HTN with Preeclampsia/Eclampsia, Chronic HTN may become worse, Chronic HTN & superimposed Preeclampsia, Transient HTN

II. Define proteinuria in pregnancy
A. Non-pregnant values @ 100-150 mg/24 hours; pregnant state ~ 300 mg/24hr; proteinuria is urine protein concentration > 1 gm/L or >300 mg protein/24hr collection

III. Define gestational edema
A. With severe PIH we may see pulmonary edema and cerebral edema. Edema usually considered pathologic only if generalized and includes hands, face, and legs

IV. Define preeclampsia and know the criteria for "severe preeclampsia"
A. Characterized by HTN (BP >140/90 or SBP>30mm Hg or DBP >15mm Hg), Edema (1+ pitting after 12 hours bedrest or 5# weight gain in 1 week), and Proteinuria; only in humans; usually > 20weeks (unless molar gestation); unknown etiology;
B. Severe: systolic BP>160, diastolic>110 (2 occasions at least 6 hours apar), Proteinuria >5 gm/24 hrs, 3+ to 4+ Semiquantitative proteinuria; epigastric or RUQ pain, elevate LFTs, thrombocytopenia (<100,000), eclampsia, oliguria (<500 ml/24h), cerebral (HA) or visual disturbances, pulmonary edema or cyanosis.
C. Risk factors: primagravida, maternal age, chronic HTN, renal Dz, Family Hx, prior Hx, multiple gestation, DM, molar pregnancy, hydrops fetalis

V. Define eclampsia
A. Occurrence of convulsions, not caused by any coincident neurologic Dz, in a woman whose condition fulfills the criteria for preeclampsia

VI. Define chronic hypertension in pregnancy with and without superimposed preeclampsia
A. Chronic--HTN before 20 weeks gestation or beyond 6 weeks postpartum

VII. Discuss the characteristics and consequences of vasospasm and the abnormal sensitivity of toxemic patients to angiotensin
A. Underlying abnormality is a general alteration in increased vascular sensitivity to pressor hormones and ecosanoids. May be the result of prostacyclin, thromboxane (Inc.) imbalance. Inc. pressor response to angiotensin.
B. Inc. vasoconstriction, Inc. platelet aggregation, Dec. uteroplacental blood flow

VIII. Know the possible electrolyte and hematologic changes
A. Hematologic: Associated with vasoconstriction and activation of coagulation system; reduction of platelet count and hypofibrogenemia.
B. Electrolyte:

IX. Know the incidence, clinical course, prognosis (maternal and fetal) and prophylaxis of preeclampsia
A. Incidence ~ 7% of all pregnancies (20% of nulliparous, 40% with chronic renal dz), 2nd leading cause of maternal death
B. Clincal course:
C. Prophylaxis: Aspirin binds with cylooxygenase enzymes to inhibit thromboxane synthesis. Low dose therapy reduces the risk of preeclampsia. Limit use to high risk population
D. Prognosis: typically resolvs following delivery. D/C usually safe with BP < 160/100. Recurrence rate: mild dz in T (rare), severe pre-E (30-50%), superimposed pre-E (70%)

X. Know the general management, including fetal assessment as it applies to different degrees of severity of preeclampsia
A. Management: 1, prevent convulsions; 2, control BP; 3, delivery
B. Antihypertensive therapy, analgesia-Anesthesia, Hemodynamic monitoring, delivery of the fetus

XI. Know the pharmacologic agents used in the management, their action, toxicity, dosage, and routes of administration
A. Anticonvulsives
1. Magnesium sulfate is the DOC. 4gm IV loading dose, 2-3 gm/hour (keep serum levels 4-8 mg/dL). Loss of patellar reflexes (8-10), respiratory depression (10-15), defective cardiac conduction (>15). Tx with calcium gluconate (1gm IV over 3 min.)
B. Antihypertensive
1. Methyldopa most common. 250-500 mg q6. Recognized safety
2. Hydralazine (Apresoline) @ 5mg IV q 20 minutes to Max dose 40mg. Common adjuvant with methyldopa and labetalol
3. Beta blockers: Labetalol (Normodyne, Trandate), combined alpha/beta-antagonist, 10 mg IV then 20,40,50 up to Max of 300mg. Maternal hepatotoxicity
4. CACB: Nifedipine (Procardia, Adalat) to relax arterial SM, 10mg PO repeat in 30min, then 10-20mg PO q 3-6hr prn
5. Nitroglycerin, relax venous>arterial SM, 10ug/min IV double q 5min; risk for methemoglobinemia
6. ACEI: captopril, assoc. with oligohydramnios and neonatal renal failure.


I. Influence of the use of insulin as it applies specifically to:

A. Infertility
B. Fetal wastage
C. Maternal mortality

II. Identification of patients at high risk for the complication of diabetes mellitus in pregnancy

A. Past diabetes in pregnancy; glycosuria or polyuria, obesity, history of macrosomia (>4,000 gm, 8.8 lbs), habitual abortions, unexplained stillbirths, preeclampsia, polyhydramnios, recurrent UTI; FHx of diabetes, > 30 YO, fetal malformation, HTN

III. Significance of glycosuria in pregnancy

A. Indicates poor control of GDM

IV. Difference between plasma and whole blood glucose levels

V. Diabetogenic effects of pregnancy and insulin requirements during and after pregnancy

A. Hypoglycemia in first half; Hyperglycemia in second half

VI. Maternal morbidity associated with diabetes

A. Preeclampsia
B. Infections
1. Pregnancy predisposes to urinary tract colonization; diabetics at higher risk
C. Hydramnios
1. 10-20% of diabetic pregnancies, especially poorly controlled

VII. Perinatal death rate and infant morbidity rate, congenital anomalies, dystocia due to macrosomia, hypoglycemia, hypocalcemia, etc.

A. Spontaneous abortion not increased except in pts with poor control. Sudden death may be related to GDM. 50% mortality with maternal diabetic ketoacidosis.
B. Congenital anomalies have a 3x overall increase, elevated HgA1c predicts anomalies; unique anomaly: sacral agenesis
C. Hypoglycemia is common
D. Dystocia rate increases due to macrosomia
E. Hypocalcemia presents frequently
F. 5-6x inc. of IRDS, inverse relationship between maternal glucose levels and fetal L/S ratios

VIII. White's classification of pregnant diabetes

A.Class A-1
1. Abnormal 3 hour GTT. Fasting glucose <105 mg/dl. 2 hour postprandial glucose <120 mg/dl. Euglycemia. Non-insulin dependent GDM, diet controlled
B.Class A-2
1. Abnormal 3 hour GTT. Fasting glucose > 105 mg/dl and/or 2 hour postprandial glucose > 120 mg/dl. Gestational diabetes, requiring insulin
C.Class B
1. Overt diabetes with adult onset after 20 years old, and short duration (<10 years)
D.Class C
1. Overt diabetes with relatively young onset (age 10-19) with relatively long duration (10-19 years)
E.Class D
1. Very young onset (age <10 years) or very long duration (>20 years) or evidence of benign retinopathy
F.Class F: Nephropathy
G.Class R: Proliferative retinopathy
H.Class RF: Both renal dz and proliferative retinopathy
I.Class G: Multiple reproductie failures (habitual abortions/stillbirths)
J.Class H: Arteriosclerotic heart dz
K.Class T: Pregnancy after renal transplantation

IX. Management of the prenatal period

A. Diet, Insulin, Monitor glucose levels, 24-hour urine glucose (26 weeks), Hemoglobin A1c, Amniotic fluid glucose, Fetal monitoring
B. Antepartum diet: Check glucose at 0700 (fasting), 2 hours after breakfast , 1600, 2100

X. Use of passive and active FHR testing and the role of the L/S ratio in diabetic pregnancies

A. Perform amniocentesis by 37-38 weeks to assess maturity and induce delivery unless contraindications

XI. Factors considered in deciding the method and time in delivery

A. Size (<4500 EFW), Lung maturity (PG, L/S), CST > NST > BPP

XII. Appropriate use of fluid, electrolytes, glucose, and insulin during delivery and early puerperium


I. Two most common types of cardiac disease in the reproductive age group

A. Congenital disorders (ASD most common--others include VSD and PDA)
B. Eisenmenger's (pulmonary HTN) 25-50% maternal mortality
C. Rheumatic heart dz (90% of RHD seen in pregnancy)
1. On the decline, stenotic murmurs are amplified in pregnancy (CO inc. and obstruction worsens). 2. Big risk is A-fib with subsequent CHF

II. Physiologic factors complicating the diagnosis of abnormal heart function in pregnancy

A. Cardiac output inc. by 40% with peak at 18-24 wks (highest risk for problems)
B. Blood pressure changes. Increase during 1st trimester, dec. during 2nd trimester, then inc. again during third
C. During pregnancy, blood flow to the placenta increases throughout pregnancy, but the size of the fetus increases even more (and it requirement for oxygen). Therefore the oxygen extraction increases and the maternal placental saturation falls

III. New York Heart Association's functional classification of cardiac patients

A. Class I: No s/s of decompensation
B. Class II: No s/s of decompensation at rest, minor limitation of activity. Type I and II pts with mitral stenosis sometimes advance to a higher risk classification.
C. Class III: No s/s of decompensation at rest, marked limitation of activity
1. Need degitalis as well as bed rest beginning @ 20 weeks
D. Class IV: Symptoms of decompensation at rest, increse with activity; Class III & IV represent almost all deaths that occur from heart failure in pregnancy
1. Could be considered candidates for early therapeutic abortions

IV. General management and preferred methods of delivery of the pregnant cardiac patient

A. Management: ASD and RDH patients require bacterial endocarditis prophylaxis and 48 hours PP. Congenital heart disease is generally well tolerated during pregnancy. RHD is managed with limited physical activity, fatigue, and anxiety; prevention or prompt treatment of anema, and prompt treatment of infection
B. Delivery: Labor and delivery are threatening to a cardiac patient, since the work required increases the amount of venous return may alter hemodynamics, the pt should not strain during the second stage of labor as the patient can become anoxic within seconds. Local or general anesthesia shoud be used and a forceps delivery if at all possible because it poses less threat that a C-section. NO PITOCIN PP. Class III and IV should get Swan Gantz catheter to monitor CV status


Pt @ 26 weeks gestation with Hb concentration of 9.0 gm/100 ml

Normal anemia in pregnancy is called "physiologic" because it is a dilutional anemia, due to the fact that blood volume increases 40-50% but red cell mass only increases 25%.

I. Definition of anemia in pregnancy and midtrimester, term, and puerperal average variations of Hb content

A. Pregnancy anemia becomes pathologic when hemataocrit <30% or Hb < 10 g/dL
B. Hb content: Normal~13, 1st trimester~12.2, 2nd trimester~10.9, 3rd~11.0, Delivery~12.4, PP~11.5

II. Normal iron and folate metabolism and requirements in non-pregnant and pregnant women

A. Non-pregnant absorb 10% of intake gives 1-1.5 mg/d, Pregnant absorb 20% to give 2.3 mg/d but need A. 3.5 mg/d so regular diet is not sufficient
B. Fe: 1000 mg total requirement, 500 mg to inc. maternal RBC mass, 300 mg transported to fetus & placenta, 200 mg daily loss, Inc. during 2nd half of pregnancy
C. Folate: Non-pregnant (50-100 ug); Pregnant (150-400 ug), usually see in second trimester because folate deficiency takes about 18-20 weeks to develop

III. Incidence, causes, and clinical characteristics of anemia

A. Iron-deficiency anemia: complicates 15-25% of all pregnancies (most common 75%); caused by greatly increased demand; RBC indices, visualization of peripheral smear (microcytic-hypochromic anemia), serum iron / ferritin / iron-binding capacity
B. Folate-deficiency anemia: complicates 1% of pregnancies, more common with multiple gestation; caused by inc. demand; Fasting folate < 3 mg/mL Anemic pt with macrocytic changes of peripheral smear with hypersegmented neutrophils
C. Vitamin B12 deficiency (pernicious anemia): Exceedingly rare; Diphylobothrium latum, dec. intrinsic factor; Megaloblastic anemia (neurologic symptoms), Vit B12 < 50 pg/mL sugges PA Anemia causes fatigue and decreased exercise tolerance

IV. Laboratory findings characteristic of folate deficiency anemia

A. Serum Fe = <30 ug/dL, Unsaturated binding capacity = >400 ug/dL, Transferrin = <16% saturation, Ferritin = < 10 ug/L

V. Common iron and folic acid compounds available

A. Ferrous sulfate 300 mb, BID to TID; ferrous gluconate; Ferrous (fumarate)
B. Folate contained in most PNVs


I. Clinical difference between cystitis, pyelonephritis, and asymptomatic bacteriuria

A. Most common medical complication of pregnancy (10-15%).
B. Cystitis: Pyuria requires > 50 leukocytes per HPF on spun specimen
C. Pyelonephritis: Fever, CVA tenderness, pyuria, bacteriuria, frequently associated with PTL
D. Asymptomatic bacteriuria: 100,000 organisms/mm3 in asymptomatic pt

II. Factors predisposing to acute pyelonephritis in pregnancy (hormonal, mechanical)

A. Hx of UTI, sickle trait, DM, chronic renal dz, HTN
B. Asymptomatic bacteriuria, hormonal dilation, ureteral hypoperistalsis (progesterone), pressure of the pregnant uterus against the ureters causing stasis

III. Incidence of asymptomatic bacteriuria

A. 4-10% of sexually active women, 2x as high in women with sickle cell trait.

IV. Association between asymptomatic bacteriuria and acute pyelonephritis

A. Inc. risk of pyelonephritis 25-30% if untreated

V. Association between acute pyelonephritis and premature labor

A. Acute pyelonephritis causes sepsis and dehydration and is associated with PROM and preterm labor

VI. Appropriate antimicrobial therapy

A. Asymptomatic bacteriuria: Adequate hydration. Ampicillin, Nitrifurantoin, TMP/SMO (avoid in first trimester & near term), Repeat culture one week after therapy and every 4-6 weeks
B. Cystitis: Culture first then SAA
C. Pyelonephritis: Hospitalization--cefoxitin 1-2g q6h + hydration (200 mL/h) then switch to oral antibiotics when afebrile 24 hrs and discharge after 24 hours on oral. Complete a 10 d course and watch. If lack of inprovement, add gentamicin. Still febrile 4-5 days later, consider perinephric abscess.

VII. How to develop a plan of follow-up in a patient with urinary tract infection in pregnancy

A. Asymptomatic bacteriuria: follow-up 6-12 weeks with clean catch specimen Acute pyelonephritis: above. Recurrence rate 10-18% but reduce to 3% with suppression or close f/u. Suppression = 100 mg nitrofurantoin qhs


I. Definition of premature ruputure of membranes (PROM)

A. Rupture of fetal membranes before the onset of labor (10% near term, normal variant). Before 37 weeks is called PPROM
B. Risk factors: polyhydramnios, cerclage, amniocentesis, abruption, infection, twins, cervicitis, GBS, fetal anomalies, incompetent cervix, abruptio placentae, idiopathic

II. Methods available for establishing the diagnosis of PROM

A. Temperature, maternal tachycardia, uterine tenderness; avoid digital exam. Sterile speculum exam for pooled amniotic fluid for ferning (salt content inc.), nitrazine (turns blue at pH>6.5; amniotic fluid 7.1-7.3 with normal vagina 4.5-6.0; false +: blood, semen, vaginal infection); visually examine cervix dilatation, effacement; fetal heart tones

III. Incidence of PROM and its relation to SES

A. PROM occurs in 8-10% of term pregnancies, 30% of preterm deliveries (more than any other cause).
B. Relatively more common with lower SES, #1 cause of pre-term delivery (inc. smoking ?)

IV. Definition of "latent" period

A. Delay between PROM and labor is called the latency period
B. Longer latent period in pts further from term (50% labor within 24 hours, 75-90% within 7 days
C. 90% of term and 50% of preterm are in labor < 24 hours with PROM. 85% preterm and 50% previable (<25 weeks) patients are in labor < 1 week

V. Prematurity rate as compared with the general population

A. Accounts for more premature births than any other cause (20% of PROM = <37wks)

VI. Incidence of chorioamnionitis in cases of PROM

A. .5-1% of all pregnancies; 3-5% in cases of prolonged PROM at term; 15-25% in cases of PPROM; neonatal sepsis more likely in preterm fetus

VII. Maternal risk associated with PROM

A. PTL with an unfavorable cervix, maternal sepsis
B. Infection--Chorioamnionitis (maternal fever, fetal tachycardia)
C. Endometritis--infection spreads from endometrium to myometrium and even parametrium

VIII. Management of a case of PROM at term and a case at 32 weeks gestation or less

A. Term: Immediate induction suggested
B. SSE, prolonged heart rate monitoring, r/o infection, favorable=induction, unfavorable cervix= 12-24h for spontaneous labor
C. 32 wks: Fetal monitor. Consider steroids, Betamethasone 12 mg IM q 24h x 2, but controversial since rupture itself stimulates fetal lung maturation. Do an initial SSE to assess cervix then avoid exams. Monitor temperature. Check for oligohydramnios with U/S (AFI = add up all vertical measurements of fluid pockets, <4cm = oligo OR measure any pocket sin cord and if <1cm has oligo). Watch for signs of chorio: temp >38 without other sites for infection, fetal tachycardia, uterine irritability on NST. If you see these things, give abx, induce and watch for fetal distress. If distress then C/S. If no chorio develops, obtain vag pool/amnio for fetal lung maturity sometime after 36 weeks and if positive then induce. Consider prophylactic abx (may prolong latent period, Tx of GBS clearly reduces neonatal sepsis)


I. Differential diagnosis of deep and superficial thrombophlebitis

A. Edema, calf-cramping and tendernes, Homan's sign
B. Deep: Clinical Dx not reliable, 50% with signs have no DVT, 30% with DVT have no signs. Diagnosis is best made by impedance plethysmography (IPG) or Doppler US; Limited venography may be useful in 3rd trimester
C. Superficial: 1/600 pregnancies, 1/100 in puerperium, painful/red/tender superficial vein

II. Treatment of superficial and deep thrombophlebitis

A. Deep: anticoagulation, bedrest with leg elevation (20cm), moist heat, elastic hose once subside
B. Superficial: Bedrest, limb elevation, moist heat, analgesics, no anticoagulation

III. Anticoagulation management

A. Heparin is anticoagulant of choice (does not cross placenta). OCPs contraindicated.
B. Initial Tx: IV heparin for 10-14 days. Keep activated PTT 1.5-2x pretreatment level; stop with onset of labor, restart 12-24 hours PP

IV. Techniques for making the diagnosis of deep venous thrombosis and pulmonary embolism

A. DVT: Homan's sign, IPG or Doppler US. Venogram if diagnosis is in doubt. CT with contrast if iliac, ovarian, or other pelvic venous thrombosis
B. PE: tachycardia, tachypnea, dyspnea; most important test is Tc99 perfusion scan coupled with Xe133 ventilation scan (V/Q scan)


I. Clinical diagnosis of rubella infection

A. 14-21 d post-exposure. Prodrome = malaise, fever, HA, conjunctivitis, lymphadenopathy. Rash = 16-18 d post-exposure, face/thorax--progressing distally, disappears after 3-4 d. Arthralgias = transient, occurs in 1/3 of women. Other - encephalitis, neuritis, thrombocytopenic purpura, heart block

II. Serodiagnosis and evaluation of recent exposure

A. Rubella-specific IgM (+ one week after appearance of rash, present for 4 weeks, absence does not exclude infection)
B. Four-fold rise in IgG or seroconversion of IgG evidence of infection. ELISA, IFI, Hemagglutination ingibition

III. Immunization, vaccine, and precautions

A. All women of child-bearing years should be checked for immunity. Vaccination recommended in nonpregnant susceptible patient, avoid pregnancy for 3 months after vaccine (live vaccine)

IV. Effect on the fetus

A. Congenital rubella syndrome: Cataracts, congenital glaucoma, CHD, loss of hearing, pigmentary retinopathy, purpura, splenomegaly, jaundice, microcephaly, MR, meningoencephalitis, and radiolucent bone dz
B. Month 1: 50% risk, M2--25%, M3--10%, 2nd trimester--1% risk, no risk after 20 weeks


I.Mode of inheritance of the Rh factor

A. Autosomal Recessive
B. Caused by incompatability between fetal and maternal blood (Rh-negative mother becomes sensitized, Rh-positive fetus at risk for hemolytic anemia)

II. Identification of the Rh sensitized patient

A. Indirect Coombs test (serial Rh antibody titers, follow unsensitized mother throughout pregnancy)

III. Pathogenesis and modes of sensitization

A. Blood transfusion
B. Abortion
E. Ectopic pregnancy
D. Fetal-maternal bleeding

IV. Rho immune globulin, its use, indications, and dose-volume

A. RhIgG: antigen blocking, clearance and antigen deviation, central inhibition. Destroys fetal cells that crossed the placenta before they can stimulate the maternal immune system endogenous antibodies
B. All Rh-negative women with any type of abortal episode should receive 50ug RhIgG; Amniocentesis testing: Rh-negative woman should receive 300ug; Postpartum: 300 ug within 72 hours of delivery.
C. Do not administer to IC+ women, only adds fuel to the fire

V.Basic steps in the performance of indirect (in the mother) and direct (in the fetus) Coomb's test

A. Indirect: detects circulating Ab to RBC D-antigen. The pts seru is incubated with RBCs of the same blood group, the antiglobulin test is then done on these RBCs. Agglutination confirms the presence of circulating Ab to RBC Ags.
B. Direct: binding of IgG autoantibody to the red cell surface. Rabbit anti-sera (one to Ig and the other to complement) is added and when these mix with RBCs that are coated with Ig or complement, agglutination occurs

VI. Indications and timing of amniocentesis

A. If the titers are > 1:32. Determination of bilirubin concentration (D450) in amniotic fluid should be done at 2-wk intervals beginning at 28 weeks.

VII. Use of spectrophotometric analysis of amniotic fluid and normograms for fetal prognosis; indications for intrauterine transfusion

A. Check OD 450, plot on Liley curve. Zone I: Rh-negative or only mildly affected; Zone II: moderately affected; Zone III: high risk for IUFD. If severe, US @ 14-16 weeks, serial scans q 1-2 weeks. Hydropic changes indicate Hct<15% (severe sub-q edema & efusion into serous cavities, i.e. ascites in abdomen). If severe anemia is suspected, perform PUBS and possibly transfuse in utero (inject into cord or abdominal cavity, infuse each 10d to 2-wk until 32-33 wk gestation then deliver)

VIII. Fetal pathophysiology and feto-placental pathology

A. In the Rh sensitized woman, Ab to the fetal Rh-positive cells crosses the placenta and destroys the fetal RBCs. Anemia may result that is severe enough to cause intra-uteral death. Otherwise, the increase in bilirubin occurs. In utero, the bilirubin is cleared by the mother. After birth, the bilirubin builds up causing kernicterus

IX. Neurologic consequences of kernicterus

A. High levels of bilirubin is deposited in the basal ganglia of the brain. It causes a clinical syndrome of poor feeding, flaccidity, opisthotonus, seizures, apnea and neonatal death. Survivor may have choreoathetosis, mental retardation, and hearing loss.

X. Association of hemolytic disease of the newborn (HDN) with ABO-incompatibility (incidence, clinical characteristics)

A. ABO incompatibility between fetus/mother in 20-25%. Only 10% result in clinically recognized hemolytic process. Results almost exclusively in A or B infants with O mothers. Kernicterus and anemia are rare. Jaundice is seen. Coomb's test is negative or only weakly positive (inc. = more severe)

XI. Significance of the Coomb's test in cases of ABO-incompatibility and fetal prognosis

See #10

XII. Protective effect of ABO incompatibility on RH sensitization

A. Sensitization requires an Rh negative person to be exposed to an Rh positive antigen. A and B positive blood groups already have Ab produced to other blood types. These Ab can cause lysis of RBCs before sensitization can occur when a RBC with D-antigen is seen

XIII.Other antigens

A. Duffy dies, Kell kills, Lewis lives


I. Definition of postpartum hemorrhage

A. Average blood loss is 500 mL with SVD; Bleeding greater than 1000 mL represents a postpartum hemorrhage

II. Causes, predisposing factors, and management of immediate and delayed hemorrhage

A. Uterine atony (use bimanual compression, oxytoxic agents)
B. Retained placental fragments
C. Lacerations


I. Definition of "puerperal morbidity"

II. Predisposing causes

A. PROM, Long labor with multiple exams, Ecsarean delivery

III. Pathophysiology of the puerperal infection

IV. Possible extensions or complications (i.e., septic thrombophlebitis)

V. Most common organisms involved

A. Endomyometritis most common cause of infection of early puerperium, polymicrobial

VI. Clinical course

A. S/s: fever uterine tenderness

VII. Management according to clinical situations and extension of the infection

A. IV Abx: 1, single agent Tx (extended spectrum cephalosporins or penicillins; 2, Combination therapy (Gentamicin, clindamycin, add ampicillin if severely ill); 3, Switch to oral Abx if 24-48 hours afebrile
B. Failure to respond: consider abscess, appendicitis, necrotizing fascitis


I.Definition of:

A. Chromosomes, autosomes, sex chromosomes
B. Karyotype: i.e., metacentric, submetacentric, acrocentric
C. Mitosis (phases)
D. Meiosis (phases)
E. Fertilization
F. Nidation

II. Mechanism of:

A. Numerical chromosomal alterations
1. Non-disjunction during the first meiotic division
2. Anaphase lag during second meiotic division
3. Non-disjunction occurring after zygote formation (mosaicism)
B. Structural chromosomal alterations
1. Isochromosomes
2. Deletions
3. Translocations


Know the incidence, responsible chromosomal or genetic alterations, and clinical manifestation of the following disorders and be able to offer appropriate genetic counseling

I. Autosomal chromosomal anomalies

A. Complete 21 trisomy
B. Translocation 15/21

II. Sex chromosomal anomalies

A. Turner syndrome (XO)
B. Klinefelter syndrome (XXY)

III. Autosomal dominant genetic disorders

A. Marfan's syndrome
B. Myotonic dystrophy
C. Osteogenesis imperfects
D. Neurofibromatosis

IV. Autosomal recessive genetic disorders

A. Cystic fibrosis
B. Hemoglobinopathies
C. Muscular dystrophy (recessive types)
D. Congenital adrenal hyperplasia

V. Sex-linked recessive disorders

A. Hemophilia A (Factor VIII)
B. Testicular feminization syndrome

VI. Amniocentesis or Chorionic villus sampling (CVS)

A. Understand the risks of the procedure
1. Amnio: Fetal loss usually <1/200, early amnio (10-12w) may give higher losses
2. CVS: .8% procedure-related loss rate, small incidence of limb reduction defects
B. Be able to evaluate the risk to the fetus when the mother is over 35 YO or has previously born children with genetic abnormalities
C. Be able to list current indications for intrauterine genetic testing


I. Characteristics of premenarchal body changes

A. Growth spurt
1. Usually precedes menarche. Associated with early puberty in girls (boys 2 years later). Governed by GH and gonadal sex steroids
B. Breast development:
1. Breast development typically the first physical manifestation of puberty. Orderly progression through Tanner stages I-V. Development varies greatly (nutrition and genetics). Progression from stage 2 to 5 takes 4 years on average (maybe not 5 until primagravida). Hormonal stim. required for endocrine function of the breast--Estrogen for ductal growty, Progesterone and Prolactin for lobuloalveolar development
C. Pubic hair
1. Influenced by pubertal inc. in adrenal androgens. Breast development and pubic hair development do not necessarily begin at the same time. Pubic hair may appear first but usually follows thelarche
D. Axillary hair
1. Axillary hair development usually begins at breast development stage 3 or 4
E. Cervical mucus

II. Definition of menarche, variable factors influencing the age of occurrence and knowledge of corticohypothalamic maturation

A. Unique hypothalamo-pituitary responses during puberty
1.GnRH pulsatile secretion
a. Detectable after 20 weeks gestation, dec. in first year, nadir @ 6-8 YO, initiation of puberty driven by increase in pulse amplitude with no change in pulse frequency
2.Prolactin detected as early as 12 weeks gestation
a. During puberty, levels rise to adult levels in girls
3.Growth hormone
a. Increase in episodic release and in volume
b. necessary for skeletal, muscle growth
4.Adrenal androgen
a. Inc. in adrenal steroids (adrenarche) occurs as early as 7-8 YO
III. Characteristics of the menstrual cycle during adolescence

IV. Characteristics of psychogenic changes of puberty and adolescence


Pt with premenstrual irritability, depression, breast tenderness, and fatigue

I. Definition of premenstrual syndrome

A. No specific definition universally accepted
B.Most require three findings
1.Symptom comples consistent with PMS
2.Symptoms must occur exclusively in luteal phase
3.Symptoms must be severe enough to cause disruption of lifestyle

II. Clinical features

A. Symptoms
1.Psychologic: Irritability, emotional lability, anxiety, depression, hostility
2.Somatic: Mastalgia, bloating, HA, fatigue, insomnia
3.Cognitive: Inability to concentrate, confusion
4.Social Behavior: craving carbohydrates, withdraw, arguing
B. Timing in the menstrual cycle: Luteal
C. Complications

III. Theories of etiology and pathophysiology

A. Neuroendocrine mechanisms may play important role (abnormalities of serotonin secretion)

IV. Evaluation

A. Review 2 months of symptom charts

V. Therapies

A. Medical
1. Rx with anxiolytics (buspirone, alprazolam); antidepressants as indicated (clomipramine, nortriptylene, fluoxetine); suppression of ovarian function (OCPs, progestins, GnRH agonists)
B. Psychosocial
1. Exercise, dietary alterations (no salt/caffeine/alcohol), stress reduction


Young female pt complaining of severe lower abdominal cramps during menses

I. Definition of dysmenorrhea

A. Painful cyclic periods, lower abdominal cramping, occurring just before or during menses

II. Difference between primary and secondary dysmenorrhea

1. Painful periods not accompanied by pelvic pathologic conditions. Onset begins at or shortly after menarche. Cramping or labor-like pain, usually lasts 48-72 hours, with pain starting a few hours prior to or after onset of menstruation.
2. Usually nulliparous young women with normal pelvic exam, etiology is PGF2, Rx with NSAIDs
1. Assoc. with pelvic pathology, may by s/s of endometriosis, assoc. with inc. menometrorrhagia, assoc. with cervical stenosis, follow Tx of cervical dysplasia

III. Pathophysiology of primary dysmenorrhea (prostaglandins)


IV. Three most common causes of secondary dysmenorrhea

A. endometriosis, menometrorrhagia, cervical stenosis

V. Management of both primary and secondary dysmenorrhea

A. Primary: NSAIDs
B. Secondary: laparoscopy, presacral neurectomy, hysterectomy


I. Definition of menopause (climacteric), its average age of occurrence and normal variations

A. Exhaustion of gonadotropin-responsive follicular units in ovary results in cessation of menses
B. Age range 48-55 YO with median age~51: hot flushes (VMS), night sweats, vaginal dryness/atrophy, dyspareunia, leukorrhea, urinary incontinence, skin atrophy, emotional lability, depression, fx, abnormal uterine bleeding
C.Risk factors: fair skin, thin body habitus, FHx, early menopause (<40), smoking, alcohol, chronic illness, corticosteroids, inactivity, inadequate calcium, hyperthyroidism
D.Significant variations in menopausal s/s from one group to another

II. Difference between cessation of ovulation and menopause

A. Many reasons for cessation of ovulation (dietary, body fat, hyperprolactinemia), only one reason for menopause

III. Possible endogenous sources of estrogen in the postmenopausal female

A. Estradiol-17B produced by peripheral conversion of T and estrone
B. In postmenopausal women, the principle estrogen is estrone: 1/3 potency of estradiol, periperhal conversion of T and A'D

IV. Clinical characteristics, possible causes, and managment of the vasomotor symptoms (VMS=hot flushes)

A. Experienced by 75-85% of perimenopausal and postmenopausal women, 37-50% of women s/p BSO; 80% have s/s > 1year, 25% > 5years
B. Not a peripheral cause, no dif. in ratio or absolute levels of LH to FSH or in total estrogens in those with or w/o flashes, don't occur in women with gonadal dysgenesis never exposed to estrogen
C. Temporal relationship with LH pulse
D. Hypothalamic factors probably responsible (four NTs in preoptic and ant. hypothalamic nuclei: GnRH, norepinephrine, dopamine, B-endorphin)
E. Estrogen deficiency primary abnormality: Rx with exogenous estrogen (options are: medroxyprogesterone acetate, bellergal, clonidine)

V. Clinical characteristics and managment of:

A. Insomnia
1. Grouped under psychosocial, perhaps a result of nocturnal hot flashes
B. Senile vaginitis
1. Atrophy @ different rates, most common vulvar symptom is pruritis, vagina becomes pale and thin, cervical lesions more common (erosion, ectropion, ulcer
C. Senile urethritis
1. Inc. rate of bacteriuria 7-10%
D. Osteoporosis
1. Primary osteoporosis occurs in women between 55 and 70 YO with the most common fx being vertebrae and long bones.
2. Secondary osteoporosis is bone loss and fx caused by a specific dz
3. 1/3 of all women will develop some complication of osteoporosis

VI. Carciniogenic hazard of estrogen therapy

A. Endometrial CA from unopposed estrogen action causing endometrial hyperplasia, Rx with progesterone therapy; Breast CA possible but recent studies refute.

VII. Role of estrogen replacement in the maintenance of bone mass

A. Significant reduction in bone loss if initiated within 3 years of loss of ovarian function; Dec. osteoclast activity; role of estrogen in established osteoporosis is less clear, may prevent further complications

VIII. Contraindications to estrogen administration

A.Absolute: Undiagnosed VB, breast CA, endometrial CA, active venous thrombosis, known or suspected estrogen-dependent/sensitive neoplasia, active liver dz, pregnancy
B.Relative: Uterine leiomyoma, endometriosis, Hx of cholelithiasis, Hx of migraine, hypertriglyceridemia, Hx of pregnancy related thrombosis, Hx of oral contraceptive-related thrombosis, liver dz, poorly controlled HTN

IX. Alternatives to estrogen administration

A. Weight-bearing exercise, vit D, Calcium (1,000 mg/day), Alendronate, Calcitonin
B. Supplement estrogen with progestin administration
C. Topical estrogen for vaginal atrophy
D. medroxyprogesterone acetate, bellergal, clonidine

X. Psychosomatic aspect of climacteric syndrome

A. Insomnia & fatigue in 30-40%, may be a result of nocturan hot flashes; Estrogen may combat depression; No direct evidence to support hormonal deprivation as a cause of diminshed sexual response (decline probably circumstance, not potential)


I. Define:

A. Amenorrhea
1. Failure of hypothalamic-pituitary-gonadal axis to induce cyclic changes in the endometrium that causes menses
B. Primary amenorrhea
1. No menarche by 16 YO or within 4 years of thelarche
C. Secondary amenorrhea
1. Cessation of menses for at least 6 months after previously normal menstruation, or absence of menses for 3 normal intervals with a history of oligomenorrhea
D. Cryptomenorrhea
E. Oligomenorrhea
1. Less than normal flow at normal intervals
F. Hypomenorrhea
1. Shorter than normal duration of menstruation
II. Psychogenic, functional, and neoplastic pituitary lesions associated with amenorrhea
A. Hyperpituitarism (AM fasting)
1.Benign adenoma of lactotrophes
a.Forbes-Albright syndrome (amenorrhea & hyperprolactinemia)
1. Sheehan syndrome, head trauma, neoplasm, hypopituitarism, provocative testing (TRH stim. test), replacement therapy

III. Given an amenorrheic patient with an organic brain lesion, the student should understand the underlying pathophysiology responsible for the amenorrhea and suggest management if indicated


IV. Given a pt with polycystic ovary syndrome (PCOS)

A. Characteristic clinical features
1. Hirsutism and acne are earliest signs
B. Anatomic criteria
1. multiple small follicular cysts (poor granulosa cell development, thickened luteinized theca
C. Common laboratory findings
1. Inc. DHEAS/T/prolactin, reversal of estradiol/estrone ratio, LH-FSH ratio is >3:1
D. Microscopic and macroscopic characteristics of the ovaries
1. IV.B.1
E. Hypothesized pathophysiology of the syndrome
1. Elevation of LH, preferential inhibition of FSH; LH induced excess of T and A'D; Normal granulosa cell aromatization of A'D and T to estradiol is reduced without requisite FSH levels
F. Indications for therapy
G. Mechanism of action of clomiphene citrate
1. Antiestrogen effect on mucus
H. Relationship between PCOS, endometrial hyperplasia, and/or carcinoma

V. Given a pt with "post pill" amenorrhea, the student should know of possible predisposing clinical situations, mechanism of action of oral contraceptives and possible induction of "post pill" prolonged amenorrhea

A. 1/5 of users have 2- to 3-month delay in return of fertility compared with barrier users

VI. Given a pt with galactorrhea, the student should know the possible etiologies, pathophysiology, clinical and laboratory findings, and Tx

A. Idiopathic galactorrhea
B. Phenothiazine-induced amenorrhea-galactorrhea
C. Hypothyroidism and amenorrhea-galactorrhea
D. Prolactin-secreting pituitary adenoma

VII. Given a pt with anorexia nervosa

A. Clinical characteristics
B. Laboratory findings
C. Possibl etiology
D. Recommended management

VIII. Concerning amenorrhea due to metabolic or systemic Dz, the student should know of the following conditions that may be associated with amenorrhea and understand the pathophysiology, clincial characteristics, laboratory data, and management

A. Thyroid dysfunction
B. Diabetes mellitus
C. Cushing's disease
D. Adrenal tumors
E. Cushing's syndrome
1. An estimate of cortisol secretion is indicated in women with amennorhea who present with stigmata of Cushing syndrome (truncal obesity, striae). Basal circulating level of 17-hydroxyprogesterone or 24-hour urinary excretion oof pregnanetriol
F. Nutritional deficiencies
G. Chronic nephritis
H. Liver cirrhosis


Pt with excessive hair growth over the face and abdomen

I. Definition of

A. Defeminization
B. Hirsutism: Excessive hair growth in androgen-dependent areas of skin; most common finding assoc. with androgen excess; frequently accompanied by acne vulgaris
C. Virilization: Regression of femle body characteristics and acquisition of male body characteristics; always assoc. with pathologic state of androgen excess

II. Different etiologies of hirsutism and virilization

A. Genetic and racial
B. Adrenal--androstenedione & DHEA/DHEASM
1.Classic congenital hyperplasia (CAH)
a. 21-hyrdoxylase deficiency. Most common congential enzyme defect in hyperandrogenism. Adrenals produce insufficient glucocorticoids or mineralocorticoids (pathway blocked) with inc. ACTH and shunting to adrenal precursor steroids
b. 11 B-hydroxylase deficiency. 11-deoxycorticosterone produced in excess
c. 3B-hydroxysteroid dehydrogenase, 4-5 isomerase deficiency. Dec. production of all three steroid classes. Female without secondary sex characteristics. Hirsutism due to DHEA overproduction
2.Nonclassic CAH
a.Late onset of each class of CAH, manifests near puberty
C. Ovarian--androstenedione and testosterone
1.Polycystic ovarian syndrome (PCO)
a. Most common cause with ovarian etiology, abnormal LH response to GnRH, inc. LH suppress FSH, more T and A'D with less conversion to estradiol without FSH
a. Similar clinical features to PCO
3.Obesity, insulin resistance, acanthosis nigricans
a. Androgen levels inc. by obesity (dec. SHBG, inc. production) often coupled with PCO
a. Rare cause. commonly present with amenorrhea with rapidly progressive virilization
1 Sertoli-Leydig: large amounts of T
2 Hilar cell, mixed gonadal stromal: postmenopausal
3 Others (dysgerminomas, teratomas, Brenner, serous cystadenoma, Krukenberg): inc. A'D
4 Luteoma of pregnancy: rare, regresses
D. Iatrogenic
E. Physiologic (puberty-pregnancy-menopause)

III. Biosynthesis of steroids and androgen formation in the adrenals and ovaries

A. Adrenals
1.Androstenedione to Testosterone
2.DHEA/DHEAS to Androstenedione to Testosterone
3.DHT derived from peripheral conversion of A'D
2.Androstenedione to Testosterone

IV. Relative potencies of natural androgens

A. Dihydrotestosterone > Testosterone > Androstenedione > DHEA, DHEAS

V. Mechanisms of androgen action and metabolism

A. Stimulate primary and secondary male sexual characteristics and secondary female sexual characteristics
B. Initiate pubarche and adrenarche

VI. Management of women with hirsutism of various etiologies

A. Idiopathic
B. Adrenal
1. CAH: dexamethasone suppression test, Antiandrogens (cyproterone acetate, spironolactone), Flutamide
C. Ovarian
1. OCP: suppress LH drive of ovarian androgens, estrogen component stimulates SHBG, lowers adrenal androgen secretion; Medroxyprogesterone (suppresses LH secretion, competes with T for 5a-reductase)
D. Iatrogenic

VII. Significance of ovarian and adrenal hormone tests

A. Establish etiology for hormone imbalance


I.Define primary and secondary infertility

A. Failure of a couple of reproductive age to establish a pregnancy within one year of intercourse without contraception. Primary--female has never been pregnant; Secondary--after one or more prior, successful pregnancies.

II. List the causes of infertility

A. Male: No sperm; Compromised spermatogenesis (decreased numbers/motility/fertilizing ability
B. Female: Systemic illness, Subtle hyperprolactinemia or hypothyroidism, Ovarian failure, hypothalamic amennorrhea, Polycystic Ovarian dz, Progesterone supplementation

III. Discuss the workup of the infertile couple

A. Male gamete factor--12%
1.Sperm analysis
B. Female gamete factor--Ovulatory dysfunction (11%)
1. BBT charts, Endometrial biopsy, Serum progesterone, Hormonal profiles (gold standard), US monitoring of follicular growth, Cervical mucus changes
C. Female genital tract factor
1.Lower genital tract
a. Cervical factors (1%-postcoital test), Immunologic factors (anti-sperm Ab), Inflammatory processes, Iatrogenic
2.Upper Genital Tract
a. Laparoscopy and Hysteroscopy + Hysterosalpingogram
b. Uterine factor (1%), tubal occlusion/adhesions (8%), endometriosis (17%)
D. Multifactorial(40%) or Idiopathic(1%)
1. Complete survey

IV. Discuss the technique of basal body temperature recording, its biochemical basis, and its usefulness in infertility appraisal

A.Clearcut stepwise shift of temperature

V. Define and describe the usefulness of cervical mucus observations: volume, fluidity, "Spinnbarkeit," and ferning

VI. Discuss the significance of uterine retroflexion, uterine leiomyomas, postabortal infection, and gonococcal salpingitis on fertility

B.Leiomyomas: inc. in size during pregnancy, inc. frequency of SAB
C.postabortal infcn:

VII. List norms for ejaculate volume, viscosity, sperm density, morphology, and motility

VIII. Discuss methods of determining tubal patency

A.Laparoscopy, Hysteroscopy, Hysterosalpingogram (HSG)

IX. Discuss the role of laparoscopy

A. Diagnostic: allows direct examination of peritoneal surfaces, assess mobility and patency of fallopian tubes
B. Therapeutic: Lyse adhesions, destroy endometriosis implants

X. Discuss the therapy of

A. Male factor: Prospective observation, donor insemination, IUI, GIFT, IVG-ET
B. Tubal disease: Tuboplasties @ laparotomy, IVF-ETm
C. Endometriosis: Prospective observation, suppression with medication, conservatiave resection at laparotomy, IUI, GIFT, IVF-ET
D. Pelvic adhesions: Laser laparoscopy or lysis of adhesions, IVF-ET
E. Amenorrhea: Directed therapies for endocrine dzs, clomiphene, human menopausal gonadotropin or GnRH


I. Given a pt with an imperforate hymen

A.Describe anatomic variations of the hymen and vagina
1. Hymen: Imperforate hymen, Cribiform hymen
2. Vagina: Congenital absence (Uterus absent: Mayer-Rokitansky-Kuster-Hauser Syndrome/Mullerian agenesis, Androgen insensitivity syndrome; Uterus present: Transverse vaginal septum, Longitudinal vaginal septum
B. Describe common symptoms and physical findings detected after onset of puberty in women with vaginal outflow obstruction
1. Primary amennorhea, recurrent pelvic pain, bulging hymen, hematocolpos
C. Describe correct management
1. Correct surgically

II.Congenital abnormalities of the uterus due to abnormal Mullerian fusion, should know:

A. Different anatomic variations; i.e., didelphis, arcuate, etc.
1. Mullerian agenesis: failure of formation of the primordial ducts
2. Uterus didelphys: failure of fusion of the primordial ducts
3. Medium septum: failure of dissolution of the septum between the fused ducts
B. Clinical significance
C. Hysterosalpingographic characteristics
D. Significance in reproductive function


I.Etiology, clinical characteristics, and Tx of the following common vulvar dermatoses

A. Allergic
1. Most common benign affliction, avoid irritants, apply local fluorinated hydrocortisones (0.025% to 0.1%)
B. Intertrigo & sehorrheic dermatitis commonly seen with DM
1. Acute problem may be treated with corn starch and topical fluorinated hydrocortisones
C. Fungal
1. Very common, candidiasis often associated with vaginal infection, tinea cruris, topical antifungals

II. Etiology, clincial presentation, gross and microscopic characteristics ant Tx of the following inflammatory lesions of the vulva

A. Gonorrheal vulvovaginitis
1. STD, s/s 2-5 days s/p exposure (urinary frequency, dysuria, vaginal discharge). Disseminated infection in 2% (fever, septicemia, dermatitis, arthritis, endocarditis). May ascend to upper genital tract (menstruation). Dx: culture N. gonorrhoeae. Rx with ceftriaxone
B. Chronic and acute bartholinitis
1. Acute infection often N.gonorrhoeae or C. trachomatis, with duct obstruction leading to abscess formation; Tx with drainage for 3-6 weeks with Word catheter
C. Chancroid
1. Painful ulcer with ragged edge, raised border. "Kissing ulcers" across the vulva can occur. Unilateral, tender adenopathy in 50%. Incubation period 2-5 days. Etiologic agent: Haemophilsu ducreyi. Tx with azithromycin
D. Chancre
E. Granuloma inguinale
1. Sexual or GI transmission. Soft, red, painless gramuloma. Nodes enlarged, painless, not suppurative. Calymmatobacterium granulomatis (intracellular, difficult to isolate). Diagnosis: biopsy specimen with Donovan bodies (bipolar staining bodies within mononuclear bodies). Rx with doxycycline
F. Lymphogranuloma venereum
1. Incubation period 2-5 days. Primary, painless, genital or anorectal ulcer. 2-3 weeks later, multiple confluent suppurative nodes. Chlamydia immunoytpes. Diagnosis: microimmunofluorescent antibody test. Rx with doxycycline
G. Herpes simplex infection
1. 1/3 of women 25-40 YO, 60-85% of sero+ are asymptomatic; primary infection 3-7 days s/p exposure, multiple vesicles coalescing into ulcers, fever, malaise, HA, recurrent shedding, recurring lesions, 75-85% of genital lesions are HSV-2; Diagnosis: viral isolation, serologic testing; Rx: oral acyclovir
H. Condyloma acuminatum
1. Warty growth caused by HPV 6 & 11. Lesions grow during pregnancies. Do biopsy prior to therapy. Tx: podophyllin (not in pregnancy), trichloracetic acid (TCA), laser, EC, or cryotherapy, Tx recurrence with 5-FU
I. Condyloma latum
1. Warty growth caused by Treponema pallidum.
J. Lichen sclerosis et atrophicus
1. Nonspecific, patchy, white alteration of the labial skin. Moderate hyperkeratosis, thinning of epithelium, underlying collagenization, inflammatory infiltrate. Rx with local hydrocortisone if prepubertal, topical testosterone if postmenopausal


I. Given a pt with a cervical polyp

A. Make proper identification on the basis of its macroscopic morphology
1. Polyps vary from a few millimeters to 3cm; pedunculated, soft, smooth, red or purple; Hyperplastic condition of endocervical epithelium
B. Plan its management
1. Tx by excision after ligation of base


I. Know the normal flora of the vagina, its pH, variations of the quality of discharge during the menstrual cycle

II. Recognize the s/s of a vaginal infection and make a correct diagnosis by usual clinical and laboratory means of the following:

A. Trichomonas vaginalis
1. Profuse yellow, malodorous discharge, vulvar pruritis, >50% asymptomatic, often carried in male partners, pH > 4.5, amine odor present with KOH, wet mount reveals trichomonads; Rx with metronidazole, 2g single dose, avoid during first 20 weeks of pregnancy B. Candida albicans 1. Vulvar and vaginal pruritis, curd-like vaginal discharge, causes >90% of yeast infections; Etiology: changes in host resistance or local bacterial flora, pregnancy, DM, Abx therapy, immunosuppressive drugs, pH is normal, diagnosis by wet mount (KOH shows hyphae); Rx with local antifungals or oral fluconazole
C. Bacterial vaginosis
1. Overgrowth of aerobic and anaerobic bacteria (Gardnerella vaginalis), vaginal epithelium appears normal, fishy amine odor, sexual transmission unproven; Diagnosis: pH > 4.5, homogenous thin discharge, amine odor with KOH, Clue cells; Rx: Metronidazole 2g
D. Herpes simplex
1. 1/3 of women 25-40 YO, 60-85% of sero+ are asymptomatic; primary infection 3-7 days s/p exposure, multiple vesicles coalescing into ulcers, fever, malaise, HA, recurrent shedding, recurring lesions, 75-85% of genital lesions are HSV-2; Diagnosis: viral isolation, serologic testing; Rx: oral acyclovir
E. Atrophic vaginitis
III. Know:
A. Microbiologic characteristics of the etiologic agents
B. Clinical presentation
C. Predisposing factors, if any
D. Macroscopic appearance
E. Microscopic appearance and technique used to identify them
F. Managment


I. Differnce between acute and chronic cervicitis (clinical and morphological)

A. Acute: Purulent discharge present, diagnosis made by smears and cultures, superficial inflammation, Tx with systemic abx
B.Chronic: 90-95% of parous women, cervical erosion (lose strat. squamous epithelium), reparative attempts result in sealing of the gland necks may = nabothian cysts; s/s = yellowish/white, thick discharge, intermenstrual bleeding, backache, trigone irritation ("honeymoon bladder"; Tx with EC,laser, or cryotherapy
II. Most common etiologic agents
A. Acute: gonococcus

III. Definitions of ectropion and eversion

IV. Antimicrobial agents used for specific infections

V. Principles of cryotherapy


Given a pt with suspected acute chlamydial or gonorrheal infection, be able to obtain adequate information from her H&P, and lab data to arrive at an appropriate diagnosis and discuss a plan of management

I. Incidence and epidemiology of chlamydial and gonorrheal infections in the United States

II. Microbiologic (cultural, morphologic, etc.) characteristics of Neisseria Gonorrhoea and Chlamydia Trachomatis

A. Gonorrhoea--gram-negative diplococci that requires Thayer-Martin media

III. Incidence of female and male asymptomatic carriers

IV. Pathophysiology of ascending gonorrheal and chlamydial infections

V. Clinical presentation according to site and degree of infection

A. Required: Abdominal tenderness (direct LQ), cervical motion tenderness, Adnexal tenderness; One of the following: leukocyte count > 10,000, temp > 38, gram-negative diplococci on endocervical sample or monocloal antibody for C. trachomatous, pelvic abscess, mucopurulent cervicitis, elevated ESR or C-reactive protein

VI. Clinical, pathological and bacteriologic characteristics of pelvic abscesses

VII. Medical and/or surgical management as indicated in various clinical situations

VIII. Clinical, etiological and physiological characteristics of non-gonococcal pelvic infections (puerperal, postoperative, etc.)

IX. Common causes of chronic pelvic discomfort:

A. Chronic pelvic inflammatory disease (pathologic findings)
B. Endometriosis
C. Leiomyoma degeneration
D. Lumbo-sacral degeneration
E. Diverticulosis
F. Myofascial pain

X. Clinical presentations and findings of each of the disorders outlined above

XI. Definition of "shock"

XII. Basic clinical parameters necessary to make a differential diagnosis between:

A. Hypovolemic shock
B. Cardiogenic shock
C. Septic (bacterial) shock

XIII. Pathophysiology of shock according to the type

XIV. Most common organisms responsible for septic shock

XV. Stepwise management of septic shock


I. Definition of endometriosis

A. Presence of both endometrial glands and stroma outside the uterine cavity
B. "A constellation of bastard uteri causing a monthly orchestration of pain" Dr. Johnson.

II. Common sites of involvement

A. Ovary, fallopian tube, cul-de-sacs, broad lig., sigmoid colon

III. Histogenesis (theories)

A.Coelomic metaplasia:
1. metaplastic transformation of pelvic peritoneum, doubtful (no men, no age inc., pelvis not abdomen)
B.Ectopic transplantation of endometrium
1. "Retrograde menstruation", most likely theory
C.Induction hypothesis
1. Substances released from shed endometrium induce formation of endometriosis

IV. Macroscopic and microscopic characteristics

A. Macroscopic: bluish-gray powder burns, nonpigmented clear vesicles, whit plaques, reddish petechiae or flame-like areas, scarring, adhesions, peritoneal pockets, endometriomas (chocolate cysts)
B. Microscopic: glands and stroma, glands frequently cystic, majority of implants do not exhibit cyclicity; giant mitochondria, nuclear channel system

V. Relationship to endometroid carcinoma

VI. Clinical characteristics

A. Most common symptom is pain
1. Secondary dysmennorhea, worsening primary dysmenorrhea, dyspareunia, noncyclic diffuse pelvic pain; dyschezia, dysuria, pelvic pain, backache
2. Others: infertility, GI involvement, UTI, pulmonary dz, nervous system dz, no pathognomonic physical findings, cul-de-sac tenderness, US ligament nodularity and tenderness, palpable enometrial adnexal mass

VII. How to make the diagnosis

A. Gold standard is laparoscopy
B. MRI is highly sensitive (90%) and specific (98%) for endometriomas
C. Can also use CA-125, US, placental protein 14, endometrial antibodies but each has insufficient sensitivity or specificity

VIII. Surgical or medical management

A. Medical--no effect on fertility
1. Danazol--testosterone derivative, attenuated LH surge, steroidogenic enzyme pathway inhibitor, hyperandrogenism side effects
2. Progestins--produce decidualization, usual SEs
3. OCPs--little data
5. GnRH agonist--downregulation of native GnRH, menopausal s/s
B. Surgical--Most common approach
1. Vaporize, coagulate, cauterize, excise lesions; 28% recurrence of pain @ 18months, 40% @ 9years; Inc. pregnancy rates if severe; Gold standared is TAH/BSO
2. Indications: when meds fail, pain mod. to severe, endometrioma > 1cm, definitive Tx after childbearing years


Given a pt with a suspected diagnosis of adenomyosis of the uterus

I. Macroscopic and microscopic characteristics

A. Presence of endometrial glands within myometrium; Endometrial gland foci separated from the basal layer of lining endometrium by greater than one low power microscopic field
B. Usually diagnosed by pathologist as incidental finding (20% of hysteroscopy specimens); correctly diagnosed only 10% of time prior to surgery

II. Clinical characteristics

A. Progressively heavy menstrual flow, inc. dysmenorrhea, enlarging tender uterus

III. Management

A. Hysterectomy is TOC


Given a 42 YO pt complaining of irregular vaginal bleeding:

I. Describe the pathophysiology (including endocrine characteristics) of "dysfunctional uterine bleeding"

II. Describe the microscopic appearance of the endometrium with

A. Simple hyperplasia: increased number of glands
B. Cystic hyperplasia: glands are dilated
C. Adenomatous hyperplasia: irregular glands with crowding
D. Squamous metaplasia:

III. Discuss the relation of these to adenocarcinoma of the endometrium

IV. Discuss the relationship of postmenopausal hyperplasia to adenocarcinoma

V. Describe the management of each clinical case according to the histologic pattern and age group


I. Incidence of uteine myomas

A. Most common pelvic tumor; 1/5-1/4 of women > 35 YO have myomata; Most produce no symptoms; more common in AA than Caucasians; cause of 60% of laparotomies

II. Different locations within the uteine wall

A. Submucous, Intramural, Subserosal; corpus is most common site

III. Macroscopic and microscopic appearance

A. Gross appearance is smooth and glistening white with a whorled and fasciculated pattern
B. Microscopic appearance is interlacing pattern of smooth muscle

IV. Different degenerative changes that can occur in a myoma

A. Necrosis can occur and may present with acute pain

V. Microscopic criteria for the diagnosis of sarcomatous degeneration

VI. Primiary and Secondary signs and symptoms due to uterine myomas

A. Most produce no symptoms
B. Bleeding (often excessive or prolonged menses, exact mechanism
C. Pressure (voiding difficulties, constipation, urethral comression)
D. Pain (degeneration, sensation of pelvic heaviness or bearing down may occur
E. Abdominal distension
F. Infertility (always evaluate for other causes)

VII. Role of myomas in cases of infertility and possible behavior of myomas in pregnancy

A. Pregnancy
1. Usually inc. in size during pregnancy; Inc. frequency of SAB; Degeneration during 2nd or 3rd trimester may produce symptoms similar to acute abdomen; may result in dystocia during labor

VIII. Effect of estrogen upon these tumors

A. Leiomyomas are clearly estrogen responsive

IX. Indications for:

A. Active intervention may be chosen for usually large tumors, symtomatic tumors or when the diagnosis is unclear
B. Myomectomy
C. Hysterectomy
D. Subtotal hysterectomy


I. Anatomy of the pelvic diaphragm

A. Viscerofascial layer
1. Uterus and vagina attach to pelvic walls by fibrous tissue (endopelvic fascia)
a. Parametria (cardinal & uterosacral ligaments)
b. Paracolpia
2. Suburethral endopelvic fascia attaches to the arcus tendineous from pelvis and to the medial border of the levator ani--crucial for urinary continence
B.Levator ani muscles
1. Lie below the uterus, vagina, bladder, and rectum. Medial portion is puborectalis (pubococcygeus), Horizontal orientation. Closes urethra, vagina, and rectum by compressing them against the pubic bone

II.Factors involved in Pelvic Organ Prolapse

A. Inborn strength of connective tissue
B. Loss of connective tissue strength
1. damage at childbirth
2. deterioration with age
3. poor collagen repair
C.Loss of levator function
1. Neuromuscular drainage during childbirth
2. Metabolic dzs that affect muscle fcn
D.Increased loads on the supportive system
1. Prolonged lifting
2. Chronic coughing from chronic pulmonary dz
E. Disturbance of the balance of the structural parts
1. Alteration of vaginal axis by urethral suspension
2. Failure to reattach the cardinal ligaments at hysterectomy

III. Definition and symptoms of

A. Cystocele:
B. Rectocele: anterior rectal wall and overlying vagina protrude below hymenal ring; hallmark is formation of a pocket which allows anterior rectal wall to bulge below introitus; stool can become trapped
C. Urethrocele
D. Enterocele: cul-de-sac becomes distended with intestine and bulges the posterior wall outward; types: pulsion, traction
E. 1st, 2nd, and 3rd degree uterine prolapse

IV. Know the indications for nonsurgical and surgical treatment

A. Candidates for surgery
1. Prolapse above the hymenal ring
a. repair only for symptoms attributive to prolapse
b. consider "pessary test"
2. Prolapse below the hymenal ring
a. symptomatic
b. asymptomatic may be assoc. with recurrent UTI & ureteral dilation


I. Definition of urinary incontinence

II. Different types of urinary incontinence in females

A. Stress urinary incontinence (SUI)
B. Detrusor dysfunction (UI)
C. Neurogenic
D. Psychogenic incontinence
E. Congential malformations
F. Fistulae


I.Different types and possible etiologies

A. Constant urinary drainage, often after surgical or OB delivery

II. Diagnostic techniques used in detection of such fistulae

A. Diagnosed by placement of methylene blue into bladder
B. Types: Vesicovaginal, Ureterovaginal, Urethrovaginal


Given a 65 YO F with a 3 cm pruritic lesion on the vulva

I. Procedures required to properly diagnose vulvar disease, including the use of toluidine blue and a simple technique of vulvar biopsy

A. Biopsy

II. Incidence, natural history, macroscopic, microscopic, and symptoms of squamous cancer of the vulva

A. CIS: 3-4% of all primary malignancies of the genital canal; delay in diagnosis can be extreme; 3rd and 4th decade of life; appearance varies greatly (bowenoid = scaly, red, blackened; others--almost entirely white or red); biopsy crucial
B. Squamous cell most common: 65-70% are mature, pearl-forming tumors; Avg age ~ 65 YO; s/s: pruritus, lump, local irritation

III. Lymphatic drainage of the vulva

A. Inguinal, femoral and external iliac nodes

IV. Basis of management for carcinoma in situ (CIS) and invasive carcinoma of the vulva

A. Surgical excision after determination of nodal involvement; localized lesion--wide local excision; multifoci lesions--skinning vulvectomy


I. Death rate due to cervical cancer in different populations

A. 7th most common cancer of women in US; worldwide it is still the leading site of CA in women (500,000 cases annually)

II. Risk factors and epidemiologic associations of populations at risk for premalignant and malignant disease of the cervix

A. Practically never encountered in virgins (promoting factor or carcinogen likely sexually transmitted-HPV 16 & 18)
B. Risk factors: early onset of sexual activity, multiple sexual partners, smoking, early parity, Hx of STD, immunocompromised

III. Microscopic characteristics of cervical carcinoma and common sites of origin

A. Cervical intraepithelial neoplasia (CIN), grades 1,2, and 3
1. Squamous cell carcinoma represents 85% to 95% of cervical CAs; three grades
2. CIN I--mild; 5% of squamous cell CAs, well-differentiated, keratin, pearl formation, few mitoses
3. CIN II--moderate; 85% of squamous cell CAs, no intracellular bridges and little keratin, pearl formation, inc. number of mitotic figures
4. CIN III--severe, CIS; 10% of squamous cell CAs, rapid growth rate, numerous mitoses, difficult to identify as squamous cell origin
5. Exophytic growth (64%): friable, granular, red & yellow fungating mass, usually ulcerative & bleeds freely
6. Endophytic tumore: may be deceptive on exam; may only present as cervical enlargement;
B. Microinvasive carcinoma
1. depth < 3mm from BM; no vascular or lymphatic space involvement; incidence of lymph node involvement < 1%; may Tx with simple TAH or cone biopsy
C. Invasive carcinoma
D. Adenocarcinoma
1. 10-15% of cervical CAs; approximately the same prognosis and clinical behavior as squamous cell CA; same staging and Tx

IV. Clinical presentation and symptoms related to carcinoma of the cervix

A. Hx: Abnormal VB or discharge, excessive heavy or prolonged menses, postcoital bleeding; pelvic pressure or pain
B. PE: Inspection and palpation of cervix, vagina, pelvis, rectum; abdomen, supraclavicular/inguinal nodes; Cervical lesion may appear exophytic, endophytic, ulcerative, friable, granular, necrotic, bloody, or indurated

V. Diagnostic techniques for cervical carcinoma

A. Exfoliation cytology, individual diagnosis and population
1. Mass screening, economical, includes endocervical canal, detects adenocarcinoma, false negative 10-35%
B. Schiller's test (pitfalls and use)
C. Colposcopy
1. Technique
a. Localizes lesion, evaluates extent of lesion, differentiates inflammatory atypia from neoplasiakdiff. invasive from non-invasive cervical lesions
2. Colposcopic findings with normal epithelium
a. smooth, pink, indefinitely outlined vessels, no change after application of aceitc acic
3. Colposcopic findings with abnormal epithelium
a. Variations from above
D. Biopsy of the cervix
1. Random biopsies
2. Colposcopically directed biopsies
E. Conization of the cervix, indications and contraindications

VI. Clinical stages of carcinoma of the cervix (FIGO)--see charts

VII. Three principal methods of treating invasive carcinoma of the cervix and their indications

A. Cryotherapy: reproductive desires, no tissue for biopsy
B. Laser: no tissue sampling
C. Electrosurgical excision: stage 0
D. Radiotherapy: from IA1 on
E. TAH: through IA2
F. Radica hysterectomy: from IB on

VIII. Five-year survival rates for each stage of the disease

A. 0--100%; IB--85%; IIA--70-75%; IIB--60-65%; IIIB--25-40%; IV--5-10%


I. Relative frequency of endometrial carcinoma and geographical, racial, and ethnic factors that influence it

A. Most common female pelvic malignancy in the US; 33,000 cases annually; Increasing incidence
B. Risk factors: obesity, nulliparity, early menarche, late menopause, chronic anovulation, Caucasian, exogenous unopposed estrogen, Hx or breast or ovarian CA, pelvid radiation Tx; DM, HTN are associated med ical problems

II. Incidence by age group of endometrial carcinoma

A. Dz of postmenopausal women~61 YO

III. Macroscopic characteristics of endometrial carcinoma

IV. Microscopic characteristics of endometrial carcinoma

V. Relationship between hyperplasia and endometrial carcinoma

A. Suggested screening with transvaginal US; < 5 to 6 mm usually atrophic

VI. Relationship of estrogen to endometrial carcinoma

A. OCPs are protective (prevent ~ 2,000 cases per year)
B. Unopposed exogenous estrogens inc. risk of CA (survival rates are excellent, progesterone offers protective effect)
C. Tamoxifen may inc. risk of endometrial CA

VII. Clinical stages of endometrial carcinoma (FIGO): see charts

VIII. Clincal characteristics of the patient at risk (estrogen metabolism)

A. Abnormal bleeding is most important symptom, seen in a postmenopausal female, menstrual abnormalities, inc. flow, lower abd. pain or pressure, symptoms of anema

IX. Likelihood of endometrial cancer in postmenopausal women with uterine bleeding

X. Use of vaginal cytology, endometrial biopsies, endometrial washings, and fractional dilatation and curettage in the diagnosis of endometrial carcinoma

A. Diagnosis made by sampling endometrium (curette biopsy 90% accurate; vacuum curettage ~ 100% accurate; pap smear is not helpful

XI. Basis of surgical therapy in the treatment of endometrial carcinoma

A. Surgical staging via exploratory laparotomy & peritoneal cytology; TAH/BSO, responds poorly to other Tx

XII. Treatment of women with advanced or recurrent tumor

A. Radiotherapy, Progestins (1/3 of pts respond, better if highly differentiated and have receptors), Chemotherapy (disappointing results-cisplatin + cytoxan + doxorubicin)


I. Approximate incidence of ovarian cancer and the risk by age groups

A. Most frequent cause of death among all genital tract CA, overall 5-year survival ~ 30%
B. 30 types of tumors in three main categories: Epithelial, Gonadal stroma, Germ cell
C. 18,500-22,000 new cases/year; 11,500-15,000 deaths/year; 5th most frequent CA in women; 4th leading cause of CA death (lung, breast, colon); highest in Scandinavia, lowest in 3rd world & Japan, US~7/100,000; 50-59 YO and inc. with age; Epithelial most common but in children are germ cell
D. Risk factors: Caucasian, 50-70, low parity, dec. fertility, delayed child-bearing, FHx of 1st degreee rel., Peutz-Jeghers syndrome, Turner Syndrome
E. Environmental/diet, genetic, endocrine milleau (dec. with OCP/pregnancy)

II. Histogenesis, incidence, macroscopic, and microscopic characteristics and biological behavior of:

A. Epithelial malignancies
1. >60% of all ovarian neoplasms and >90% of malignant tumors; Probably derived from ovarian surface wpithelium within epithelial inclusion cysts in cortex; Classified by predominant pattern and differentiation; Degree of cellular proliferation, atypia, and stromal invation determines benign low malignant potential or carcinoma
2. Serous, Mucinous, Endometrioid, Clear-Cell, Malignant mixed mesodermal, Undifferentiated
B. Metastatic tumors to the ovaries: ?

III. Common chlinical presentations and means of diagnosing ovarian carcinoma

A. S/S: vague or absent (pelvic or abd discomfort, urinary frequency, GI alteration, abdominal fullness, early satiety with larger lesions, abnormal VB in 15%); endocrine (menstrual irregularities, estrogen production with granulosa cell tumors=postmenopausal bleed & precocious puberty, testosterone secretion = virilization in 50% of pts with Sertoli-Leydig tumors)
B. PE: empty bladder & rectum, check for presence of ascites, uterine displacement
C. Findings (vary): bilaterality, mobility, consistency, abdominal distension (ascites, huge masses), uterine displacement

IV. Management of:

A. Benign: Unilateral, Cystic, Mobile, Smooth, Smaller than 8 cm (7 cm is a tennis ball)
B. Malig: Bilateral, Solid, Fixed, Irregular, Ascites, Rapid growth rate, Cul-de-sac nodules
C. Indications for surgery:
1. Ovarian cystic structure >5cm followed for 6-8 weeks without regression
2. Any solid ovarian lesion
3. Any ovarian lesion with papillary vegetation on the cyst wall
4. Any adnexal mass greater than 10cm in diameter
5. Ascites
6. Palpable adnexal mass in a premenarchal or postmenopausal patient
7. Torsion or rupture suspected
D. Palpable ovary in a postmenopausal female
1. In the premenarchal or postmenopausal period any ovarian enlargement should result in surgical intervention
E. 5 cm cystic adnexal mass in a young female
1. 95% of ovarian cysts smaller than 5cm in diameter are nonneoplastic; OCP for more rapid regression of functional cysts
F. 10 cm cystic adnexal mass in a young female
1. Any mass larger than 10cm should be surgically explored
G. Firm adnexal mass in a young female
1. Firm masses are an indication for surgery
H. Any adnexal mass in a pt 40 YO or older
1. Determine menopausal

V. FIGO clinical stages of ovarian carcinoma: see charts

VI. Principle of managing epithelial ovarian carcinoma

A. Surgery--TAH/BSO, omentectomy, debulking
B. Chemotheraphy--cisplatin after debulking to < 2cm
C. Radiation theryapy--more morbid than chemo.
D. Tumor markers--hCG, CA-125

VII. Approximate overall five-year survival rate for ovarian malignancies and the five-year survival rate as it pertains to each clinical state

A. Overall~30% Stage I: 70%, Stage II: 25%, Stage III: 12%, Stage IV: 5%


I. Histologic classification

A. Epithelial
1. Serous cystadenoma
a. 15-25% of all benign ovarian tumors, 20-50 YO, 5-15cm, B in 12-50%, derived from surface epithelium of ovary, resembles mucosa of the oviduct, may find adjacent psammoma bodies (calcific concretions~x-ray), often asymptomatic, Tx: TAH/BSO or conservative for reproductive years
2. Mucinous cystadenoma
a. 16-30% of all benign neoplasms, B in only 5-7%, rarely malignant, 20-40 YO, differentiation of ovarian surface epithelium to endocervical type of mullerian duct epithelium (tall, columnar cells), often very large (15-30cm), completely cystic & multilocular, Tx: young--unilateral oophorectomy, older--TAH/BSO
3. Pseudomyxoma peritonei
a. From spillage of mucinous contents into peritoneal cavity, biologically malignant, histologically benign, can result in progressive malnutrition
4. Cystadenofibroma
a. Variant of serous cystadenoma, less common, partially cystic & partially solid, usually benign and unilateral, surface with broad papillae or deep sulci, Tx varies with age and associated findings
5. Brenner tumor
a. 1-2% of all ovarian tumors, gross characteristics similar to fibroma, rarely malignant, 5-13% B, >50YO, arise from Walthard cell rests, 10-15cm, solid, can be assoc. with Meigs syndrome (ascites & hydrothorax), Tx: excision or oophorectomy
B. Gonadal Stromal Tumors
1. Thecoma
a. See "Functiona1 Ovarian Neoplasms--Granulosa-theca cell tumors"
2. Hilus cell tumor
a. See "Functional Ovarian Neoplasms--Hilus cell tumors"
C.Nonintrinsic Connective Tissue Tumors
1.Ovarian fibroma
a. Middle-aged pts (avg~48 YO), connective tissue of ovarian cortical stroma or possibly inactive endstage thecoma, 2-10% B, ~6cm, can be assoc. with Meigs syndrome, Tx: removal
D.Germ Cell Tumors
1.Benign cystic teratoma (dermoid)
a. 18-25% of all ovarian neoplasms, 20-40 YO, almost always benign, 12% B, 5-10cm, arises from primordial germ cells (sebaceous material, teeth, sweat glands, nervous tissue, skin), often solid, 30-50% seen on XR d/t teeth), Tx: excision of cyst with ovarian conservation
2.Struma ovarii
a. unique benign cystic teratoma with thyroid tissue, resembles dermoid externally, 5% produce s/s of thyrotoxicosis
a. See "Functional Ovarian Neoplasms--Gonadoblastoma"

II. Incidence and frequency of bilaterality in the most common tumors

III. Gross and microscopic appearance

IV. Clinical characteristics and treatment


Germ cell and stromal ovarian tumors

I. Dysgerminoma

A. Most common malignant germ cell tumor-50%; 2% of all malignant ovarian neoplasms; 75% of pts 10-30 YO; 2% of nonpregnant women have +pregnancy test
B. Solid fleshy tumor~15cm diameter; aggregates of large polygonal cells with lymphocyte infiltration, syncitiotrophoblast may be present, produce hCG
C. 5-year survival rate (63% for adv. case, 96% for stage IA), 75% have stage I dz, occasionally bilateral, highly sensitive to radiation and chemo. (VP-16, bleomycin, cisplatin=VBP)

II. Granulosa-theca cell tumors

A. 1-3% of all ovarian neoplasma, 40% after menopause, 5% before puberty, most pts are symptomatic (<5% asymptomatic, 75% with endocrine manifestations, 10% with endometrial adenocarcinoma.
B. Circumscribed, varied consistency, hemorrhage & necrosis; small round cells (longitudinal groove=coffee bean appearance), theca cells, many patterns, Call-Exner bodies; Juvenil granulosa with mitotic figures, atypia, 15% metastases; cystic assoc. with hirsutism or virilization, rare metastases
C. LMP, 90% are stage IA, 10-year survival 86-96% for stage I; TAH/BSO is std Tx, USO in young women; Tx recurrence with surgery or radiation
D. Thecoma: 12% of feminizing mesenchymomas, 2% of all ovarian tumors, uncommon <35 YO, postmenopausal, from ovarian cortical stroma, unilateral, almost never malignant, 15-20cm, marked luteinization (no hormone activity in 25%), most frequent symptom is postmenopausal bleeding, can be assoc. with Meigs syndrome.

III. Gonadoblastoma

A. Most common neoplasm of abnormal gonads, abnormal sexual development; 80% are phenotypic females (90% have Y chromosome=T-fem, some are virilized); mixture of germ cells and gonadal stroma cells, 50% are overgrown by germinoma
B. Large range of tumor size
C. Any pt with gonadal dysgenesis and Y chromosome runs risk of developing germ cell tumor--prophylactic removal of gonadal tissue after puberty, 25% incidence of malignancy; TAH/BSO

IV. Adrenal rest ovarian tumors

V. Hilus cell tumors

A. Extremely rare~50 cases in lit, s/s are masculinization d/t high levels of testosterone; Tx: unilateral oophorectomy

VI. Know:

A. Histogenesis and incidence
B. Macroscopic and microscopic characteristics
C. Degree of malignancy, clinical behavior, management


In a pt with suspected molar pregnancy the student should know:

I. Epidemiology of molar pregnancies

A. 1/1500 1/2000 in US = 3000/year; 500 to 750 malignant GTNs/year; more common (5-15x) in Far East & SE Asia; Previous molar inc. risk by 4--5x; Inc. risk at both ends of reproductive age; Nutritional factors; Partial moles about 10%; Invasive mole follows about 10-15% of complete moles; Choriocarcinoma complicates about 1/40 moles (1/5000 ectopics, 1/15,000 abortions, 1/150,000 normal pregnancies)

II. Clinical characteristics usually associated with a molar pregnancy

A. U/S is diagnostic method of choice; Pt often presents with VB, uterine enlargement in absence of FHT

III. Differences in the curves of gonadotropin titers between normal and trophoblastic pregnancies

IV. Frequency and histologic and clinical characteristics of the malignant degeneration of molar pregnancies

A. 1/40 to choriocarcinoma; Sequelae: molar proliferation without invation (retained mole), invasive mole, choriocarcinoma, clinically identified metastatic GTN without histologic diagnosis; signs: rising hCG, hCG plateau for 3 or more consecutive weeks, appearance of metastases, histologic evidence of invasive mole or choriocarcinoma

V. Uterine evacuation techniques for cases of trophoblastic disease

A. Perform suction prepared to convert to laparotomy and obtain central hemodynamic monitoring if needed; hysterectomy

VI. Program for appropriate follow-up designed to determine whether there is persistent trophoblastic ticcue after evacuation

A. Initial: B-hCG, PE with pelvic exam, CXR; Surveillance: hCG every week until neg., then every 2-4 weeks to confirum regression, every 1-2 months for 6-12 months, start contraception (OCPs)

VII. Pharmacologic characteristics and rationale for use of chemotherapeutic agents in the treatment of trophoblastic disease

A. Very sensitive to chemotherapy~100%; reduces malignant sequelae in high-risk pts; not routinely recommended if uncomplicated mole & reliable pt; MTX

VIII. Indication for treatment of trophoblastic disease

A. Suction curretage has low complication rate w/ uterine size < 16 weeks; Excessive uterine enlargement my predispose to pulmonary complications (trophoblastic deportation, preeclampsia, fluid overload); Uterine size > 16 weeks mandate further pre-op assessment (EKG, heart ejection fraction, assess valvular fcn); suction or hysterectomy (completeed childbearing, desire sterilization, cuts malignancy from 20% to 5%)

IX. Classification of trophoblastic disease

A. Partial: identifiable fetus, normal/hydropic villi, fetal vessels & RBCs, haploid maternal and two haploid paternal (triploid--dispermic fertilization), <5% require chemo for malignant GTN; rare clinical mole diagnosis or uterus large for dates with <10% with malignant sequlae
B. Complete: hydropic villi, lack fetus & membranes, all secrete hCG (marker), uniformly diploid (paternal 46, XX), 1/3-1/2 with uterine enlargement > than EGA, common clinical diagnosis
C. Invasive mole = chorioadenoma destruens, complete mole which invades myometrium, seen w/in 6 mos of molar evacuation, underdiagnosed d/t high hysterectomy rate
D. Choriocarcinoma: highly anaplastic, no villi, rapidly invades & metastasizes (lung & vagina), 1/2 preceded by hydatidiform mole
E. Placental Site Tumor: locally invasive neoplasm derived from intremediate cells of placenta, rare, rare systemic metastases, more resistant to chemo than other GTNs, hysterectomy
F. Stage I: confined to uterine corpus; Stage II: vaginal or pelvic metastases; Stage III: lung metastases; Stage IV: other mets


I. Characteristics of radium, cesium, and cobalt

A. Selective destruction of tissue forms the basis of therapeutic radiology (neoplastic cells are killed more easily, radiosensitivity and radiocurability are not identical, cervical CA is relatively radioinsensitive but curable)

II. Concept of the MEV (million electron)

III. Concept of wavelength, penetrability

A. energy and penetrating power are dependent on proton wavelength;

IV. Definition of rad or Gray

A. rad = Unit of exposure
B. centigray cGy = unit of absorption (1 Gray = 100 rads = 100 cGy)

V. Variation of radiation intensity with distance (inverse square law)

A. Intensity of radiation decreases with distance

VI. Rationale of internal versus external radiation application

A. External: Supervoltage radiation has a reduced skin effect compared with orthovoltage; Isodose curves represent tisue part receiving equivalent doses
B. Internal: Less local tissue irradiation to achieve therapeutic levels at desired target location

VII. Short and long-term effects of radiotherapy on normal body tissues