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
I. Important factors in the patient's past Medical/Surgical/Obstetrical Hx in assessing current pregnancy
I. Four positive signs of pregnancy
I. Uterine Changes
I. Characteristics of placental villi
II.Characteristics of placental circulation
IV. Description of the amnion
I. Development of fetal circulatory system
I. Clinical parameters for the assessment of intrauterine fetal growth
III. Amniotic fluid analysis for fetal maturity
I. Planes and diameters of the pelvis (normal average values, borderline and absolute contracture values)
III. Pelvic shapes
I. Define "labor"
I. Basic technical aspects of external and internal fetal heart rate monitoring techniques
I. List a method of analgesia and describe its effects on the mother and fetus
I. Discuss intrauterine fetal respiration
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
I. Discuss the mode of action of each method and explain it to the patient in lay terms
I. Define fetal death and fetal mortality rate
II. Define neonatal death and neonatal mortality rate
III. Define perinatal death and perinatal mortality rate
IV. State most common cause of neonatal death
I. Definition of "abortion" and "viability"
II. Incidence and possible etiologies of "spontaneous abortion"
V. Definition of "induced abortion"
I. Define "ectopic pregnancy"
I. Most common obstetrical and nonobstetrical causes of bleeding late in pregnancy
III. Given supected diagnosis of abruption placentae, the student should know:
I. Incidence of breech presentation
VII. Congenial abnormality rate
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
I. Maternal clinical complications related to multiple gestation
VI. Factors influencing incidence of dizygotic twins: above
VII. Clinical and sonographic data useful in the prepartum diagnosis of multiple gestation
I.Define "gestational hypertension"
I. Influence of the use of insulin as it applies specifically to:
II. Identification of patients at high risk for the complication of diabetes mellitus in pregnancy
III. Significance of glycosuria in pregnancy
IV. Difference between plasma and whole blood glucose levels V. Diabetogenic effects of pregnancy and insulin requirements during and after pregnancy VI. Maternal morbidity associated with diabetes VII. Perinatal death rate and infant morbidity rate, congenital anomalies, dystocia due to macrosomia,
hypoglycemia, hypocalcemia, etc. VIII. White's classification of pregnant diabetes
IX. Management of the prenatal period X. Use of passive and active FHR testing and the role of the L/S ratio in diabetic pregnancies XI. Factors considered in deciding the method and time in delivery 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 II. Physiologic factors complicating the diagnosis of abnormal heart function in pregnancy
III. New York Heart Association's functional classification of cardiac patients IV. General management and preferred methods of delivery of the pregnant cardiac patient
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 II. Normal iron and folate metabolism and requirements in non-pregnant and pregnant women III. Incidence, causes, and clinical characteristics of anemia IV. Laboratory findings characteristic of folate deficiency anemia V. Common iron and folic acid compounds available
I. Clinical difference between cystitis, pyelonephritis, and asymptomatic bacteriuria II. Factors predisposing to acute pyelonephritis in pregnancy (hormonal, mechanical) III. Incidence of asymptomatic bacteriuria IV. Association between asymptomatic bacteriuria and acute pyelonephritis V. Association between acute pyelonephritis and premature labor VI. Appropriate antimicrobial therapy VII. How to develop a plan of follow-up in a patient with urinary tract infection in pregnancy
I. Definition of premature ruputure of membranes (PROM) II. Methods available for establishing the diagnosis of PROM III. Incidence of PROM and its relation to SES IV. Definition of "latent" period V. Prematurity rate as compared with the general population VI. Incidence of chorioamnionitis in cases of PROM VII. Maternal risk associated with PROM VIII. Management of a case of PROM at term and a case at 32 weeks gestation or less
I. Differential diagnosis of deep and superficial thrombophlebitis II. Treatment of superficial and deep thrombophlebitis
III. Anticoagulation management IV. Techniques for making the diagnosis of deep venous thrombosis and pulmonary embolism
I. Clinical diagnosis of rubella infection II. Serodiagnosis and evaluation of recent exposure III. Immunization, vaccine, and precautions IV. Effect on the fetus
I.Mode of inheritance of the Rh factor II. Identification of the Rh sensitized patient
III. Pathogenesis and modes of sensitization
IV. Rho immune globulin, its use, indications, and dose-volume
V.Basic steps in the performance of indirect (in the mother) and direct (in the fetus) Coomb's test VI. Indications and timing of amniocentesis VII. Use of spectrophotometric analysis of amniotic fluid and normograms for fetal prognosis; indications for
intrauterine transfusion VIII. Fetal pathophysiology and feto-placental pathology IX. Neurologic consequences of kernicterus X. Association of hemolytic disease of the newborn (HDN) with ABO-incompatibility (incidence, clinical
characteristics) XI. Significance of the Coomb's test in cases of ABO-incompatibility and fetal prognosis XII. Protective effect of ABO incompatibility on RH sensitization XIII.Other antigens
I. Definition of postpartum hemorrhage II. Causes, predisposing factors, and management of immediate and delayed hemorrhage
I. Definition of "puerperal morbidity" II. Predisposing causes III. Pathophysiology of the puerperal infection IV. Possible extensions or complications (i.e., septic thrombophlebitis) V. Most common organisms involved VI. Clinical course VII. Management according to clinical situations and extension of the infection
I. Characteristics of premenarchal body changes II. Definition of menarche, variable factors influencing the age of occurrence and knowledge of
corticohypothalamic maturation
IV. Characteristics of psychogenic changes of puberty and adolescence
Pt with premenstrual irritability, depression, breast tenderness, and fatigue I. Definition of premenstrual syndrome
II. Clinical features
III. Theories of etiology and pathophysiology IV. Evaluation V. Therapies
Young female pt complaining of severe lower abdominal cramps during menses I. Definition of dysmenorrhea II. Difference between primary and secondary dysmenorrhea III. Pathophysiology of primary dysmenorrhea (prostaglandins) IV. Three most common causes of secondary dysmenorrhea V. Management of both primary and secondary dysmenorrhea
I. Definition of menopause (climacteric), its average age of occurrence and normal variations
II. Difference between cessation of ovulation and menopause III. Possible endogenous sources of estrogen in the postmenopausal female IV. Clinical characteristics, possible causes, and managment of the vasomotor symptoms (VMS=hot flushes) V. Clinical characteristics and managment of:
VI. Carciniogenic hazard of estrogen therapy VII. Role of estrogen replacement in the maintenance of bone mass VIII. Contraindications to estrogen administration IX. Alternatives to estrogen administration X. Psychosomatic aspect of climacteric syndrome I. Define:
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) 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 VI. Given a pt with galactorrhea, the student should know the possible etiologies, pathophysiology, clinical and
laboratory findings, and Tx VII. Given a pt with anorexia nervosa 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
Pt with excessive hair growth over the face and abdomen
I. Definition of II. Different etiologies of hirsutism and virilization III. Biosynthesis of steroids and androgen formation in the adrenals and ovaries IV. Relative potencies of natural androgens V. Mechanisms of androgen action and metabolism VI. Management of women with hirsutism of various etiologies VII. Significance of ovarian and adrenal hormone tests I.Define primary and secondary infertility II. List the causes of infertility III. Discuss the workup of the infertile couple IV. Discuss the technique of basal body temperature recording, its biochemical basis, and its usefulness in
infertility appraisal 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 VII. List norms for ejaculate volume, viscosity, sperm density, morphology, and motility
VIII. Discuss methods of determining tubal patency
IX. Discuss the role of laparoscopy
X. Discuss the therapy of
I. Given a pt with an imperforate hymen II.Congenital abnormalities of the uterus due to abnormal Mullerian fusion, should know:
I.Etiology, clinical characteristics, and Tx of the following common vulvar dermatoses II. Etiology, clincial presentation, gross and microscopic characteristics ant Tx of the following inflammatory
lesions of the vulva I. Given a pt with a cervical polyp
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:
I. Differnce between acute and chronic cervicitis (clinical and morphological)
II. Fetal circulation and post-delivery changes
A. DV shunts umbilical oxygenated blood from liver to IVC, foramen ovale, ductus arteriosus
III. Characteristics of fetal hematopoiesis and fetal blood at term
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
A. HbF and HbA (O2 affinity)
II. Use of US in the assessment of 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.
IV. Fetal heart evaluations
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)
V. Principle of umbilical artery doppler blood flow
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)
II. Characteristics of the pelvic joints
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)
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)
II. Describe the theories of initiation of labor
A. Contractions and cervical dilitation
III. Define the first, second, and third stages of labor
A. fall in progesterone, inc. estrogen, fetal cortisol production (animal models only, don't hold true in
human studies)
IV. Using the standard labor curve (Friedman)
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
V. List the common etiologies and management of
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)
VI. Describe the normal mechanism of labor in the occiput presentation
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)
A. Engagement, Descent, Flexion, Rotation, Extension
II. Normal ranges of fetal heart rate during labor (definition of bradycardia and tachycardia)
A. Top pen = FHT, bottom pen = uterine CTX; external FHM subject to artifacts and affected by
maternal body habitus, internal use during labor
III. Characteristics, physiopathology and clinical significance of
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
IV. Significance of fetal pH changes during the intrapartum period
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
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
II. List at least two acceptable methods of anesthesia and describe:
A. Systemic
1. Maternal: N/V, sedation, dec. gastric motility, respiratory depression
B. Regional Anesthetic
2. Neonatal: CNS depression, Resp. depression, dec. temp regulation,altered neuroadaptive
behavior
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
A. Pharmacologic effects on mother and fetus
B. Immediate and remote complications of each method
II. Discuss initiation of air breathing
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
III. Discuss known reasons for delayed effective respiratory efforts in the newborn
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
IV. Describe the APGAR score system
A. Maternal medication, birth asphyxia, obstruction of the respiratory tract, cerebral trauma, prematurity,
massive meconium aspiration, chorioamniotis with maternal fever, prematurity
V. Describe physical characteristics use in the clinical estimation of gestational age
A. Color, Heart rate, Respiratory effort, Muscle tone, Stimulus response
7-10, no resuscitation needed; 4-6, some resuscitation needed; 0-3, aggressive resuscitation.
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
II. Describe the normal recovery process of the skin, cardiovascular, urinary, endocrine, and metabolic systems
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
III. Describe the normal physiology of lactation and its suppression
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)
IV. Counsel the puerperal patient regarding physical activities, sexual activities, and contraception
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
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
II. For each contraceptive method, list the minor and major complications, their incidence, and reversibility
A. Coitus interruptus
B. Withdrawl prior to ejaculation
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
B. Condoms or Vaginal Pouch
1. Hypothalamic hypofunction, pituitary unresponsiveness, ovarian refractoriness secondary
to increased prolactin releasing hormone
C. Spermicides (Jellies, creams, foams, supp., tablets, films)
1. Barrier or barrier plus spermicide
D. Diaphragm
1. Nonoxynol-9, Octoxynol-9, destroy sperm cell membrane so viable sperm reach ovum
E. Cervical cap
1. Barrier plus spermicide
F. IUD
1. Barrier plus spermicide
G. Depot Medroxyprogesterone Acetate (Depo-Provera)
1. Endometrial reaction--implantation inhibition, bioactive substances such as copper, sperm
immobilization
H. Levonorgestrel Implant (Norplant system)
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
I. Oral Contraceptives
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
J. Abstinence
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
K. "Morning after" pill
1. No sperm and egg contact
L. Tubal ligation
1. Luteolytic effect, out-of-phase endometrium, disordered tubal transport
M. Vasectomy
1. Blocking fallopian tube by segment removal, cautery, clips, or Fallopr rings to prevent
sperm transport to meet ovum
N. Abortion
1. Ligation of vas deferens to prevent sperm from leaving the testicle
O. Ineffective: postcoital douching, postcoital urination, altered sexual positions, coitus
interruptus/withdrawl, lactation
1. D&C, D&E, hysterotomy or hysterectomy; medically with PGE2, hypertonic saline or urea
III. List the contraindications of each method
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
IV. List the effectiveness of each method (one year of actual use)
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
V. List the advantages and disadvantages (III above)of each method
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%
VI. Recommend the best appropriate method for a specific patient's needs
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
VII. Counsel the patient and her mate concerning the use, reliability, and complications of that particular method
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.
VIII. Define:
A. Consider advantages, disadvantages, and reliability in advising the couple on the most acceptable
from of BC
IX. Differentiate:
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
X. Discuss:
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
XI. Sterilization
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
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%)
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
Early: first 7 days of life, Late: after 7 days but before 29. Neonatal mortality rate is the # of neonatal
deaths/1000 total births
Combination of fetal deaths and neonatal deaths
V. Define maternal death and list three most common causes in the United States
A. Low birth weight (blacks>whites)
B. Congenital malformations (3% of births)
C. Injury / birth trauma: hypoxic brain injury, birth asphyxia
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
Abortion and miscarriage both refer to first trimester pregnancy losses (<500g or 20 wks EGA = limits
of viability)
III. Difference between:
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)
IV. Appropriate plan of management for each clinical situation
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.
VI. Definition of "habitual abortion"
A. Caused by iatrogenic intervention
A. Recurrent spontaneous abortion (RSA): three or more consecutive first-trimester losses. Check for
uterine abnormalities and rare Ab (lupus anticoagulant, anticardiolipin Ab)
II. In reference to tubal pregnancies:
A. Implantation outside the endometrial cavity. Most common cause of maternal death in first half of
pregnancy
IV. Given suspected diagnosis of placenta previa, the student should know:
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%
C. Significance and sensitivities of standard pregnancy tests and beta-subunit assay in the diagnosis of
ectopic pregnancies
2. Signs: Adnexal tenderness~85%, Abdominal tenderness~90%, Adnexal mass~50%
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
F. The use of US, culdocentesis, and diagnostic laparoscopy
2. Acute appendicitis: laparoscopy
3. Acute pelvic inflammatory disease: gonorrhea cultures
4. Torsion of an adnexa: laparoscopy
1. U/S: gold standard in combination with serum hCG, detect early ectopics
G. Plan of management in a case of unruptured pregnancy and in a case of ruptured ectopic
pregnancy
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
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
II. Overall incidence of late pregnancy bleeding 3-4%
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
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
F. The fetal complications: immediate and remote but includes fetal hypoxia and death
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)
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
V. Discuss the evaluation and management of other causes of bleeding late in pregnancy
1. Total: internal os completely covered
B. Incidence and probable mechanism
2. Partial: os partially covered
3. Marginal: placenta reaches edge of os
4. Low-lying: implanted in lower uterine segment but not to os
1. 1/200, more common with inc. parity, incidence decreasing in US
C. Clinical factors associated with higher incidence of placenta previa
2. Specific cause is unknown.
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
E. The fetal and maternal prognosis
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
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
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
VI. Clinical, radiographic, and US evidence of fetal death
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.
VII. Complication associated with late pregnancy 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
VIII. Uterine evacuation techniques in case of fetal death in utero
A. Slight possibility of infection, DIC (10%) if fetus retained > 5-6 weeks
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
II. Characteristics of complete and incomplete breech presentation
Most common obstetric malpresentation (4% of deliveries)
III. Maternal and fetal conditions associated with a higher incidence of 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%)
IV. Mechanism of labor in 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
V. Perinatal mortality rates
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.
VI. Prematurity rates
A. Much higher in breech presentation (4x in term, 2-3x in preterm), much unpreventable. Head trauma,
Musculoskeletal trauma, cord prolapse with asphyxiation
VIII. Traumatic morbidity rate in relation to fetal weight
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%
IX. Incidence of cord prolapse and its relationship to all breech presentations
Incidence of breech presentation increases inpressively with decreased fetal weight
X. Management of the breech delivery
.4% with frank, 5-6% with complete, 10% with incomplete
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
II. Maternal 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
III. How presumptive diagnosis of feto-pelvic disproportion is made in labor
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
IV. Shoulder dystocia
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
V.Power problems
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)
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)
II. Fetal 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
III. Etiology of 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
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 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%).
B. Monozygotic twins (identical)
2. 1/90 births are twins, 1/3 of which are monozygotes
1. Chance occurrence, inc. slightly with delayed implantation
V. Incidence of monozygotic twins: 3-4/1000
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
VIII. Perinatal mortality with 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
IX. Antepartum management
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
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
II. Define proteinuria in pregnancy
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
III. Define gestational edema
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
IV. Define preeclampsia and know the criteria for "severe preeclampsia"
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
V. Define eclampsia
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
VI. Define chronic hypertension in pregnancy with and without superimposed preeclampsia
A. Occurrence of convulsions, not caused by any coincident neurologic Dz, in a woman whose
condition fulfills the criteria for preeclampsia
VII. Discuss the characteristics and consequences of vasospasm and the abnormal sensitivity of toxemic patients
to angiotensin
A. Chronic--HTN before 20 weeks gestation or beyond 6 weeks postpartum
VIII. Know the possible electrolyte and hematologic changes
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
IX. Know the incidence, clinical course, prognosis (maternal and fetal) and prophylaxis of preeclampsia
A. Hematologic: Associated with vasoconstriction and activation of coagulation system; reduction of
platelet count and hypofibrogenemia.
B. Electrolyte:
X. Know the general management, including fetal assessment as it applies to different degrees of severity 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%)
XI. Know the pharmacologic agents used in the management, their action, toxicity, dosage, and routes of
administration
A. Management: 1, prevent convulsions; 2, control BP; 3, delivery
B. Antihypertensive therapy, analgesia-Anesthesia, Hemodynamic monitoring, delivery of the fetus
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.
A. Infertility
B. Fetal wastage
C. Maternal mortality
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
A. Indicates poor control of GDM
A. Hypoglycemia in first half; Hyperglycemia in second half
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
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
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
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
A. Perform amniocentesis by 37-38 weeks to assess maturity and induce delivery unless
contraindications
A. Size (<4500 EFW), Lung maturity (PG, L/S), CST > NST > BPP
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
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
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
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
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
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
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
A. Serum Fe = <30 ug/dL, Unsaturated binding capacity = >400 ug/dL, Transferrin = <16% saturation,
Ferritin = < 10 ug/L
A. Ferrous sulfate 300 mb, BID to TID; ferrous gluconate; Ferrous (fumarate)
B. Folate contained in most PNVs
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
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
A. 4-10% of sexually active women, 2x as high in women with sickle cell trait.
A. Inc. risk of pyelonephritis 25-30% if untreated
A. Acute pyelonephritis causes sepsis and dehydration and is associated with PROM and preterm labor
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.
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
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
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
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 ?)
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
A. Accounts for more premature births than any other cause (20% of PROM = <37wks)
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
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
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)
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
A. Deep: anticoagulation, bedrest with leg elevation (20cm), moist heat, elastic hose once subside
B. Superficial: Bedrest, limb elevation, moist heat, analgesics, no anticoagulation
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
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)
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
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
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)
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
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)
A. Indirect Coombs test (serial Rh antibody titers, follow unsensitized mother throughout pregnancy)
A. Blood transfusion
B. Abortion
E. Ectopic pregnancy
D. Fetal-maternal bleeding
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
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
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.
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)
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
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.
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)
See #10
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
A. Duffy dies, Kell kills, Lewis lives
A. Average blood loss is 500 mL with SVD; Bleeding greater than 1000 mL represents a postpartum
hemorrhage
A. Uterine atony (use bimanual compression, oxytoxic agents)
B. Retained placental fragments
C. Lacerations
A. PROM, Long labor with multiple exams, Ecsarean delivery
A. Endomyometritis most common cause of infection of early puerperium, polymicrobial
A. S/s: fever uterine tenderness
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
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
III. Characteristics of the menstrual cycle during adolescence
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
4.Adrenal androgen
b. necessary for skeletal, muscle growth
a. Inc. in adrenal steroids (adrenarche) occurs as early as 7-8 YO
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
A. Symptoms
1.Psychologic: Irritability, emotional lability, anxiety, depression, hostility
B. Timing in the menstrual cycle: Luteal
2.Somatic: Mastalgia, bloating, HA, fatigue, insomnia
3.Cognitive: Inability to concentrate, confusion
4.Social Behavior: craving carbohydrates, withdraw, arguing
C. Complications
A. Neuroendocrine mechanisms may play important role (abnormalities of serotonin secretion)
A. Review 2 months of symptom charts
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
A. Painful cyclic periods, lower abdominal cramping, occurring just before or during menses
A.Primary
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.
B.Secondary
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
A. PGF2
A. endometriosis, menometrorrhagia, cervical stenosis
A. Primary: NSAIDs
B. Secondary: laparoscopy, presacral neurectomy, hysterectomy
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
A. Many reasons for cessation of ovulation (dietary, body fat, hyperprolactinemia), only one reason
for menopause
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
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)
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
A. Endometrial CA from unopposed estrogen action causing endometrial hyperplasia, Rx with
progesterone therapy; Breast CA possible but recent studies refute.
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
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
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
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)
II. Psychogenic, functional, and neoplastic pituitary lesions associated with amenorrhea
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
A. Hyperpituitarism (AM fasting)
1.Benign adenoma of lactotrophes
B.Hypoprolactinemia
a.Forbes-Albright syndrome (amenorrhea & hyperprolactinemia)
2.Drugs
3.Hypothyroidism
1. Sheehan syndrome, head trauma, neoplasm, hypopituitarism, provocative testing (TRH
stim. test), replacement therapy
A.Hamartomas
B.Craniopharyngiomas
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
A. 1/5 of users have 2- to 3-month delay in return of fertility compared with barrier users
A. Idiopathic galactorrhea
B. Phenothiazine-induced amenorrhea-galactorrhea
C. Hypothyroidism and amenorrhea-galactorrhea
D. Prolactin-secreting pituitary adenoma
A. Clinical characteristics
B. Laboratory findings
C. Possibl etiology
D. Recommended 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
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
A. Genetic and racial
B. Adrenal--androstenedione & DHEA/DHEASM
1.Classic congenital hyperplasia (CAH)
C. Ovarian--androstenedione and testosterone
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
2.Nonclassic CAH
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
a.Late onset of each class of CAH, manifests near puberty
1.Polycystic ovarian syndrome (PCO)
D. Iatrogenic
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
2.Hyperthecosis
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
4.Neoplasms
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
E. Physiologic (puberty-pregnancy-menopause)
A. Adrenals
1.Androstenedione to Testosterone
B.Ovary
2.DHEA/DHEAS to Androstenedione to Testosterone
3.DHT derived from peripheral conversion of A'D
1.Testosterone
2.Androstenedione to Testosterone
A. Dihydrotestosterone > Testosterone > Androstenedione > DHEA, DHEAS
A. Stimulate primary and secondary male sexual characteristics and secondary female sexual
characteristics
B. Initiate pubarche and adrenarche
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
A. Establish etiology for hormone imbalance
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.
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
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
D. Multifactorial(40%) or Idiopathic(1%)
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%)
1. Complete survey
A.Clearcut stepwise shift of temperature
A.Retroflexion:
B.Leiomyomas: inc. in size during pregnancy, inc. frequency of SAB
C.postabortal infcn:
D.PID:
A.Laparoscopy, Hysteroscopy, Hysterosalpingogram (HSG)
A. Diagnostic: allows direct examination of peritoneal surfaces, assess mobility and patency of fallopian
tubes
B. Therapeutic: Lyse adhesions, destroy endometriosis implants
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
A.Describe anatomic variations of the hymen and vagina
1. Hymen: Imperforate hymen, Cribiform hymen
B. Describe common symptoms and physical findings detected after onset of puberty in women with
vaginal outflow obstruction
2. Vagina: Congenital absence (Uterus absent: Mayer-Rokitansky-Kuster-Hauser
Syndrome/Mullerian agenesis, Androgen insensitivity syndrome; Uterus present:
Transverse vaginal septum, Longitudinal vaginal septum
1. Primary amennorhea, recurrent pelvic pain, bulging hymen, hematocolpos
C. Describe correct management
1. Correct surgically
A. Different anatomic variations; i.e., didelphis, arcuate, etc.
1. Mullerian agenesis: failure of formation of the primordial ducts
B. Clinical significance
2. Uterus didelphys: failure of fusion of the primordial ducts
3. Medium septum: failure of dissolution of the septum between the fused ducts
1.Psychosocial
C. Hysterosalpingographic characteristics
D. Significance in reproductive function
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
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
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
III. Know:
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
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
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
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. squamou