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OB-GYN HISTORY I. Age, gravidity, parity A. Age: age-related risks,
young-prematurity, older-syndromes 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 B. Bleeding C. Abnormal discharge D. Bowel symptoms E. Urinary symptoms F. Menstruation G. Past obstetrical history H. Gynecologic history I. Contraceptive history J. Sexual history K. Past medical history L. Past surgical history N. Social history O. ROS ANTEPARTUM CARE I. Important factors in the patient's past Medical/Surgical/Obstetrical Hx in assessing current pregnancy
II. Important factors in the Family and
Socio-economic Hx III. Complete Physical IV. Evaluate uterine size and determine heart beats
V. Basic lab data obtained on all pregnant patients, value of each test, normal values for pregnancy
VI. High-risk Factors
VII. Discuss with the Pt
DIAGNOSIS OF PREGNANCY I. Four positive signs of pregnancy
II. Use of Ultrasonography in Early Diagnosis
III. hCG and LH antigenicity, alpha and beta subunits, ELISA test
IV. Presumptive Signs of Pregnancy
V. Probable signs: enlargement of the abdomen, uterine changes (size, shape, consistency), cervical changes (effacement), palpation of the fetus, Braxton-Hicks contractions, Endocrine tests ÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜÜ PHYSIOLOGIC CHANGES IN NORMAL PREGNANCY I. Uterine Changes
II. Ovarian changes A. Anatomy and physiology of the corpus luteum of pregnancy
III. Vaginal and perineal changes
IV. Abdominal wall and skin changes
V. Breast changes
VI. Metabolism changes
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 VII. Hematologic changes
VIII. Cardiovascular system
IX. Respiratory tract
X. Urinary system
XI. Gastrointestinal tract
XII. Liver and gallbladder
XIII.Endocrine glands
B. Thyroid PLACENTAL DEVELOPMENT AND PHYSIOLOGY I. Characteristics of placental villi II.Characteristics of placental circulation
III. Histologic concept of placental "barrier" IV. Description of the amnion
V. Description of the umbilical cord
VI. Placental hormonal production
VII. Basic mechanisms of placental transfer
FETAL PHYSIOLOGY I. Development of fetal circulatory system
II. Fetal circulation and post-delivery changes
III. Characteristics of fetal hematopoiesis and fetal blood at term
INTRAUTERINE FETAL EVALUATION 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) 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
PELVIMETRY 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 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)
CLINICAL COURSE OF LABOR 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) 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
INTRAPARTUM FETAL MONITORING 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
ANALGESIA AND ANESTHESIA 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 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 II. List at least two acceptable methods
of anesthesia and describe: A. Pharmacologic effects on mother
and fetus
EVALUATION OF THE NEWBORN 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 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 PUERPERIUM 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 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 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) IV. Counsel the puerperal patient
regarding physical activities, sexual activities, and contraception A. Physical activity: slow and
easy, D/C if painful.
CONTRACEPTION I. Discuss the mode of action of each method and explain it to the patient in lay terms A. Coitus interruptus 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 F. IUD 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) 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 III. List the contraindications of each
method A. In general, each method has
contraindications with allergy to the topical application of
barriers or spermicides 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 IV. List the effectiveness of each method
(one year of actual use) A. Coitus interruptus: 82% (23-40%
FR) V. List the advantages and disadvantages
(III above)of each method A. Coitus interruptus: no devices,
no chemicals, no cost, ethical/religious 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 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 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 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)
MATERNAL, FETAL, AND INFANT MORTALITY 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 A. Low birth weight
(blacks>whites) 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
ABORTION I. Definition of "abortion" and
"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) 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 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)
ECTOPIC PREGNANCY 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% 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 1. Ruptured tubal pregnancy:
hCG F. The use of US, culdocentesis,
and diagnostic 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 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
LATE PREGNANCY BLEEDING 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
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 1. shock 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 B. Incidence and probable mechanism 1. 1/200, more common with
inc. parity, incidence decreasing in US 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 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
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)
VI. Clinical, radiographic, and US
evidence of fetal death A. Fetal demise > 20 wks
before onset of labor
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.
BREECH PRESENTATION 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%) 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) 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
FETO-PELVIC DISPROPORTION 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) II. Maternal causes of feto-pelvic
disproportion A. Inlet contraction
(diameters): Obstetric conjugate (unengaged head in
nulliparous pt) 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) 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 V.Power problems A. Tx with pitocin. Primary
uterine inertia in primagravidas, NOT multi-.
Discoordinate CTX, false labor
MULTIPLE PREGNANCIES
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)
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%). 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
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
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)
IX. Antepartum management A. Prevention of prematurity
is primary goal. Prolong gestation, inc. birth weight
and dec. perinatal M&M and dec. maternal complications
HYPERTENSION DISORDERS IN PREGNANCY 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.
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;
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.
VIII. Know the possible electrolyte
and hematologic changes A. Hematologic: Associated
with vasoconstriction and activation of coagulation
system; reduction of platelet count and
hypofibrogenemia.
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
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
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
DIABETES MELLITUS IN PREGNANCY I. Influence of the use of insulin as it applies specifically to: A. Infertility 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 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. 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 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 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
CARDIAC DISEASE IN PREGNANCY I. Two most common types of cardiac
disease in the reproductive age group A. Congenital disorders (ASD
most common--others include VSD and PDA) 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) III. New York Heart Association's
functional classification of cardiac patients A. Class I: No s/s of
decompensation 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
ANEMIAS 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 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 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 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)
URINARY TRACT INFECTION I. Clinical difference between
cystitis, pyelonephritis, and asymptomatic bacteriuria A. Most common medical
complication of pregnancy (10-15%). II. Factors predisposing to acute
pyelonephritis in pregnancy (hormonal, mechanical) A. Hx of UTI, sickle trait,
DM, chronic renal dz, HTN 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 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
PREMATURE RUPTURE OF MEMBRANES (PROM) 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 |