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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 II. Methods available for establishing
the diagnosis of PROM A. Temperature, maternal
tachycardia, uterine tenderness; avoid digital
exam. Sterile speculum exam for pooled amniotic fluid
for ferning (salt content inc.), nitrazine (turns blue
at pH>6.5; amniotic fluid 7.1-7.3 with normal vagina
4.5-6.0; false +: blood, semen, vaginal infection);
visually examine cervix dilatation, effacement; fetal
heart tones III. Incidence of PROM and its
relation to SES A. PROM occurs in 8-10% of
term pregnancies, 30% of preterm deliveries (more than
any other cause). IV. Definition of "latent" period A. Delay between PROM and
labor is called the latency period V. Prematurity rate as compared with
the general population A. Accounts for more premature
births than any other cause (20% of PROM = <37wks) VI. Incidence of chorioamnionitis in
cases of PROM A. .5-1% of all pregnancies;
3-5% in cases of prolonged PROM at term; 15-25% in cases
of PPROM; neonatal sepsis more likely in preterm fetus VII. Maternal risk associated with
PROM A. PTL with an unfavorable
cervix, maternal sepsis VIII. Management of a case of PROM at
term and a case at 32 weeks gestation or less A. Term: Immediate induction
suggested
THROMBOPHLEBITIS IN PREGNANCY I. Differential diagnosis of deep and
superficial thrombophlebitis A. Edema, calf-cramping and
tendernes, Homan's sign II. Treatment of superficial and deep thrombophlebitis A. Deep: anticoagulation,
bedrest with leg elevation (20cm), moist heat, elastic
hose once subside III. Anticoagulation management A. Heparin is anticoagulant of
choice (does not cross placenta). OCPs contraindicated. IV. Techniques for making the
diagnosis of deep venous thrombosis and pulmonary embolism A. DVT: Homan's sign, IPG or
Doppler US. Venogram if diagnosis is in doubt. CT with
contrast if iliac, ovarian, or other pelvic venous
thrombosis
RUBELLA INFECTION IN PREGNANCY I. Clinical diagnosis of rubella
infection A. 14-21 d post-exposure.
Prodrome = malaise, fever, HA, conjunctivitis,
lymphadenopathy. Rash = 16-18 d post-exposure,
face/thorax--progressing distally, disappears after 3-4
d. Arthralgias = transient, occurs in 1/3 of women.
Other - encephalitis, neuritis, thrombocytopenic
purpura, heart block II. Serodiagnosis and evaluation of
recent exposure A. Rubella-specific IgM (+ one
week after appearance of rash, present for 4 weeks,
absence does not exclude infection) III. Immunization, vaccine, and
precautions A. All women of child-bearing
years should be checked for immunity. Vaccination
recommended in nonpregnant susceptible patient, avoid
pregnancy for 3 months after vaccine (live vaccine) IV. Effect on the fetus A. Congenital rubella
syndrome: Cataracts, congenital glaucoma, CHD, loss of
hearing, pigmentary retinopathy, purpura, splenomegaly,
jaundice, microcephaly, MR, meningoencephalitis, and
radiolucent bone dz
ERYTHROBLASTOSIS FETALIS I.Mode of inheritance of the Rh factor A. Autosomal Recessive II. Identification of the Rh sensitized patient A. Indirect Coombs test
(serial Rh antibody titers, follow unsensitized mother
throughout pregnancy) III. Pathogenesis and modes of sensitization A. Blood transfusion IV. Rho immune globulin, its use, indications, and dose-volume A. RhIgG: antigen blocking,
clearance and antigen deviation, central inhibition.
Destroys fetal cells that crossed the placenta before
they can stimulate the maternal immune system endogenous
antibodies V.Basic steps in the performance of
indirect (in the mother) and direct (in the fetus) Coomb's test A. Indirect: detects
circulating Ab to RBC D-antigen. The pts seru is
incubated with RBCs of the same blood group, the
antiglobulin test is then done on these RBCs.
Agglutination confirms the presence of circulating Ab to
RBC Ags. VI. Indications and timing of
amniocentesis A. If the titers are > 1:32.
Determination of bilirubin concentration (D450) in
amniotic fluid should be done at 2-wk intervals
beginning at 28 weeks. VII. Use of spectrophotometric
analysis of amniotic fluid and normograms for fetal prognosis;
indications for intrauterine transfusion A. Check OD 450, plot on Liley
curve. Zone I: Rh-negative or only mildly affected; Zone
II: moderately affected; Zone III: high risk for IUFD.
If severe, US @ 14-16 weeks, serial scans q 1-2 weeks.
Hydropic changes indicate Hct<15% (severe sub-q edema &
efusion into serous cavities, i.e. ascites in abdomen).
If severe anemia is suspected, perform PUBS and possibly
transfuse in utero (inject into cord or abdominal
cavity, infuse each 10d to 2-wk until 32-33 wk gestation
then deliver) VIII. Fetal pathophysiology and
feto-placental pathology A. In the Rh sensitized woman,
Ab to the fetal Rh-positive cells crosses the placenta
and destroys the fetal RBCs. Anemia may result that is
severe enough to cause intra-uteral death. Otherwise,
the increase in bilirubin occurs. In utero, the
bilirubin is cleared by the mother. After birth, the
bilirubin builds up causing kernicterus IX. Neurologic consequences of
kernicterus A. High levels of bilirubin is
deposited in the basal ganglia of the brain. It causes a
clinical syndrome of poor feeding, flaccidity,
opisthotonus, seizures, apnea and neonatal death.
Survivor may have choreoathetosis, mental retardation,
and hearing loss. X. Association of hemolytic disease of
the newborn (HDN) with ABO-incompatibility (incidence, clinical
characteristics) A. ABO incompatibility between
fetus/mother in 20-25%. Only 10% result in clinically
recognized hemolytic process. Results almost exclusively
in A or B infants with O mothers. Kernicterus and anemia
are rare. Jaundice is seen. Coomb's test is negative or
only weakly positive (inc. = more severe) XI. Significance of the Coomb's test
in cases of ABO-incompatibility and fetal prognosis See #10 XII. Protective effect of ABO
incompatibility on RH sensitization A. Sensitization requires an
Rh negative person to be exposed to an Rh positive
antigen. A and B positive blood groups already have Ab
produced to other blood types. These Ab can cause lysis
of RBCs before sensitization can occur when a RBC with
D-antigen is seen XIII.Other antigens A. Duffy dies, Kell kills,
Lewis lives
POSTPARTUM HEMORRHAGE I. Definition of postpartum hemorrhage A. Average blood loss is 500
mL with SVD; Bleeding greater than 1000 mL represents a
postpartum hemorrhage II. Causes, predisposing factors, and
management of immediate and delayed hemorrhage A. Uterine atony (use bimanual
compression, oxytoxic agents)
PUERPERAL INFECTION I. Definition of "puerperal morbidity" II. Predisposing causes A. PROM, Long labor with
multiple exams, Ecsarean delivery III. Pathophysiology of the puerperal
infection IV. Possible extensions or
complications (i.e., septic thrombophlebitis) V. Most common organisms involved A. Endomyometritis most common cause of infection of early puerperium, polymicrobial VI. Clinical course A. S/s: fever uterine
tenderness VII. Management according to clinical
situations and extension of the infection A. IV Abx: 1, single agent Tx
(extended spectrum cephalosporins or penicillins; 2,
Combination therapy (Gentamicin, clindamycin, add
ampicillin if severely ill); 3, Switch to oral Abx if
24-48 hours afebrile
CYTOGENETICS I.Definition of: A. Chromosomes, autosomes, sex
chromosomes II. Mechanism of: A. Numerical chromosomal
alterations 1. Non-disjunction during
the first meiotic division B. Structural chromosomal
alterations 1. Isochromosomes
CLINICAL GENETICS
Know the incidence, responsible chromosomal or genetic alterations, and clinical manifestation of the following disorders and be able to offer appropriate genetic counseling I. Autosomal chromosomal anomalies A. Complete 21 trisomy II. Sex chromosomal anomalies A. Turner syndrome (XO) III. Autosomal dominant genetic
disorders A. Marfan's syndrome IV. Autosomal recessive genetic
disorders A. Cystic fibrosis V. Sex-linked recessive disorders A. Hemophilia A (Factor VIII) VI. Amniocentesis or Chorionic villus
sampling (CVS) A. Understand the risks of the
procedure 1. Amnio: Fetal loss
usually <1/200, early amnio (10-12w) may give higher
losses B. Be able to evaluate the
risk to the fetus when the mother is over 35 YO or has
previously born children with genetic abnormalities
PUBERTY I. Characteristics of premenarchal body
changes A. Growth spurt 1. Usually precedes menarche.
Associated with early puberty in girls (boys 2 years
later). Governed by GH and gonadal sex steroids B. Breast development: 1. Breast development
typically the first physical manifestation of puberty.
Orderly progression through Tanner stages I-V.
Development varies greatly (nutrition and genetics).
Progression from stage 2 to 5 takes 4 years on average
(maybe not 5 until primagravida). Hormonal stim.
required for endocrine function of the breast--Estrogen
for ductal growty, Progesterone and Prolactin for
lobuloalveolar development C. Pubic hair 1. Influenced by pubertal inc.
in adrenal androgens. Breast development and pubic hair
development do not necessarily begin at the same time.
Pubic hair may appear first but usually follows
thelarche D. Axillary hair 1. Axillary hair development
usually begins at breast development stage 3 or 4 E. Cervical mucus II. Definition of menarche, variable
factors influencing the age of occurrence and knowledge of
corticohypothalamic maturation A. Unique hypothalamo-pituitary
responses during puberty 1.GnRH pulsatile secretion a. Detectable after 20
weeks gestation, dec. in first year, nadir @ 6-8 YO,
initiation of puberty driven by increase in pulse
amplitude with no change in pulse frequency 2.Prolactin detected as early
as 12 weeks gestation a. During puberty, levels
rise to adult levels in girls 3.Growth hormone a. Increase in episodic
release and in volume 4.Adrenal androgen a. Inc. in adrenal
steroids (adrenarche) occurs as early as 7-8 YO III. Characteristics of the menstrual cycle during adolescence IV. Characteristics of psychogenic changes of puberty and adolescence
PREMENSTRUAL SYNDROME Pt with premenstrual irritability,
depression, breast tenderness, and fatigue I. Definition of premenstrual syndrome A. No specific definition
universally accepted 1.Symptom comples consistent
with PMS II. Clinical features A. Symptoms 1.Psychologic: Irritability,
emotional lability, anxiety, depression, hostility B. Timing in the menstrual cycle:
Luteal III. Theories of etiology and
pathophysiology A. Neuroendocrine mechanisms may
play important role (abnormalities of serotonin secretion) IV. Evaluation A. Review 2 months of symptom
charts V. Therapies A. Medical 1. Rx with anxiolytics
(buspirone, alprazolam); antidepressants as indicated
(clomipramine, nortriptylene, fluoxetine); suppression
of ovarian function (OCPs, progestins, GnRH agonists) B. Psychosocial 1. Exercise, dietary
alterations (no salt/caffeine/alcohol), stress reduction
DYSMENORRHEA Young female pt complaining of severe
lower abdominal cramps during menses I. Definition of dysmenorrhea A. Painful cyclic periods, lower
abdominal cramping, occurring just before or during menses II. Difference between primary and
secondary dysmenorrhea 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 1. Assoc. with pelvic
pathology, may by s/s of endometriosis, assoc. with inc.
menometrorrhagia, assoc. with cervical stenosis, follow
Tx of cervical dysplasia III. Pathophysiology of primary
dysmenorrhea (prostaglandins) A. PGF2 IV. Three most common causes of secondary
dysmenorrhea A. endometriosis,
menometrorrhagia, cervical stenosis V. Management of both primary and
secondary dysmenorrhea A. Primary: NSAIDs
MENOPAUSE I. Definition of menopause (climacteric), its average age of occurrence and normal variations A. Exhaustion of
gonadotropin-responsive follicular units in ovary results in
cessation of menses II. Difference between cessation of
ovulation and menopause A. Many reasons for cessation of
ovulation (dietary, body fat, hyperprolactinemia), only one
reason for menopause III. Possible endogenous sources of
estrogen in the postmenopausal female A. Estradiol-17B produced by
peripheral conversion of T and estrone IV. Clinical characteristics, possible
causes, and managment of the vasomotor symptoms (VMS=hot flushes) A. Experienced by 75-85% of
perimenopausal and postmenopausal women, 37-50% of women s/p
BSO; 80% have s/s > 1year, 25% > 5years V. Clinical characteristics and managment of: A. Insomnia 1. Grouped under psychosocial,
perhaps a result of nocturnal hot flashes B. Senile vaginitis 1. Atrophy @ different rates,
most common vulvar symptom is pruritis, vagina becomes
pale and thin, cervical lesions more common (erosion,
ectropion, ulcer C. Senile urethritis 1. Inc. rate of bacteriuria
7-10% D. Osteoporosis 1. Primary osteoporosis occurs
in women between 55 and 70 YO with the most common fx
being vertebrae and long bones. VI. Carciniogenic hazard of estrogen
therapy A. Endometrial CA from unopposed
estrogen action causing endometrial hyperplasia, Rx with
progesterone therapy; Breast CA possible but recent studies
refute. VII. Role of estrogen replacement in the
maintenance of bone mass A. Significant reduction in bone
loss if initiated within 3 years of loss of ovarian
function; Dec. osteoclast activity; role of estrogen in
established osteoporosis is less clear, may prevent further
complications VIII. Contraindications to estrogen
administration A.Absolute: Undiagnosed VB, breast
CA, endometrial CA, active venous thrombosis, known or
suspected estrogen-dependent/sensitive neoplasia, active
liver dz, pregnancy IX. Alternatives to estrogen
administration A. Weight-bearing exercise, vit D,
Calcium (1,000 mg/day), Alendronate, Calcitonin X. Psychosomatic aspect of climacteric
syndrome A. Insomnia & fatigue in 30-40%, may be a result of nocturan hot flashes; Estrogen may combat depression; No direct evidence to support hormonal deprivation as a cause of diminshed sexual response (decline probably circumstance, not potential)
AMENORRHEA I. Define: A. Amenorrhea 1. Failure of
hypothalamic-pituitary-gonadal axis to induce cyclic
changes in the endometrium that causes menses B. Primary amenorrhea 1. No menarche by 16 YO or
within 4 years of thelarche C. Secondary amenorrhea 1. Cessation of menses for at
least 6 months after previously normal menstruation, or
absence of menses for 3 normal intervals with a history
of oligomenorrhea D. Cryptomenorrhea 1. Less than normal flow at
normal intervals F. Hypomenorrhea 1. Shorter than normal
duration of menstruation II. Psychogenic, functional, and
neoplastic pituitary lesions associated with amenorrhea A. Hyperpituitarism (AM fasting) 1.Benign adenoma of
lactotrophes a.Forbes-Albright syndrome
(amenorrhea & hyperprolactinemia) 2.Drugs B.Hypoprolactinemia 1. Sheehan syndrome, head
trauma, neoplasm, hypopituitarism, provocative testing
(TRH stim. test), replacement therapy III. Given an amenorrheic patient with an
organic brain lesion, the student should understand the underlying
pathophysiology responsible for the amenorrhea and suggest
management if indicated A.Hamartomas IV. Given a pt with polycystic ovary
syndrome (PCOS) A. Characteristic clinical
features 1. Hirsutism and acne are
earliest signs B. Anatomic criteria 1. multiple small follicular
cysts (poor granulosa cell development, thickened
luteinized theca C. Common laboratory findings 1. Inc. DHEAS/T/prolactin,
reversal of estradiol/estrone ratio, LH-FSH ratio is
>3:1 D. Microscopic and macroscopic
characteristics of the ovaries 1. IV.B.1 E. Hypothesized pathophysiology of
the syndrome 1. Elevation of LH,
preferential inhibition of FSH; LH induced excess of T
and A'D; Normal granulosa cell aromatization of A'D and
T to estradiol is reduced without requisite FSH levels F. Indications for therapy 1. Antiestrogen effect on
mucus H. Relationship between PCOS,
endometrial hyperplasia, and/or carcinoma V. Given a pt with "post pill" amenorrhea,
the student should know of possible predisposing clinical
situations, mechanism of action of oral contraceptives and possible
induction of "post pill" prolonged amenorrhea A. 1/5 of users have 2- to 3-month
delay in return of fertility compared with barrier users VI. Given a pt with galactorrhea, the
student should know the possible etiologies, pathophysiology,
clinical and laboratory findings, and Tx A. Idiopathic galactorrhea VII. Given a pt with anorexia nervosa A. Clinical characteristics VIII. Concerning amenorrhea due to
metabolic or systemic Dz, the student should know of the following
conditions that may be associated with amenorrhea and understand the
pathophysiology, clincial characteristics, laboratory data, and
management A. Thyroid dysfunction 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
HIRSUTISM AND VIRILIZATION Pt with excessive hair growth over the face and abdomen I. Definition of A. Defeminization II. Different etiologies of hirsutism and
virilization A. Genetic and racial 1.Classic congenital
hyperplasia (CAH) a. 21-hyrdoxylase
deficiency. Most common congential enzyme defect in
hyperandrogenism. Adrenals produce insufficient
glucocorticoids or mineralocorticoids (pathway
blocked) with inc. ACTH and shunting to adrenal
precursor steroids 2.Nonclassic CAH a.Late onset of each class
of CAH, manifests near puberty C. Ovarian--androstenedione and
testosterone 1.Polycystic ovarian syndrome
(PCO) a. Most common cause with
ovarian etiology, abnormal LH response to GnRH, inc.
LH suppress FSH, more T and A'D with less conversion
to estradiol without FSH 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 D. Iatrogenic III. Biosynthesis of steroids and androgen
formation in the adrenals and ovaries A. Adrenals 1.Androstenedione to
Testosterone B.Ovary 1.Testosterone IV. Relative potencies of natural
androgens A. Dihydrotestosterone >
Testosterone > Androstenedione > DHEA, DHEAS V. Mechanisms of androgen action and
metabolism A. Stimulate primary and secondary
male sexual characteristics and secondary female sexual
characteristics VI. Management of women with hirsutism of
various etiologies A. Idiopathic 1. CAH: dexamethasone
suppression test, Antiandrogens (cyproterone acetate,
spironolactone), Flutamide C. Ovarian 1. OCP: suppress LH drive of
ovarian androgens, estrogen component stimulates SHBG,
lowers adrenal androgen secretion; Medroxyprogesterone
(suppresses LH secretion, competes with T for
5a-reductase) D. Iatrogenic VII. Significance of ovarian and adrenal
hormone tests A. Establish etiology for hormone
imbalance
INFERTILITY I.Define primary and secondary infertility A. Failure of a couple of
reproductive age to establish a pregnancy within one year of
intercourse without contraception. Primary--female has never
been pregnant; Secondary--after one or more prior,
successful pregnancies. II. List the causes of infertility A. Male: No sperm; Compromised
spermatogenesis (decreased numbers/motility/fertilizing
ability III. Discuss the workup of the infertile
couple A. Male gamete factor--12% 1.Sperm analysis B. Female gamete factor--Ovulatory
dysfunction (11%) 1. BBT charts, Endometrial
biopsy, Serum progesterone, Hormonal profiles (gold
standard), US monitoring of follicular growth, Cervical
mucus changes C. Female genital tract factor 1.Lower genital tract a. Cervical factors
(1%-postcoital test), Immunologic factors
(anti-sperm Ab), Inflammatory processes, Iatrogenic 2.Upper Genital Tract a. Laparoscopy and
Hysteroscopy + Hysterosalpingogram D. Multifactorial(40%) or
Idiopathic(1%) 1. Complete survey IV. Discuss the technique of basal body
temperature recording, its biochemical basis, and its usefulness in
infertility appraisal A.Clearcut stepwise shift of
temperature V. Define and describe the usefulness of
cervical mucus observations: volume, fluidity, "Spinnbarkeit," and
ferning VI. Discuss the significance of uterine
retroflexion, uterine leiomyomas, postabortal infection, and
gonococcal salpingitis on fertility A.Retroflexion: VII. List norms for ejaculate volume, viscosity, sperm density, morphology, and motility VIII. Discuss methods of determining tubal patency A.Laparoscopy, Hysteroscopy,
Hysterosalpingogram (HSG) IX. Discuss the role of laparoscopy A. Diagnostic: allows direct
examination of peritoneal surfaces, assess mobility and
patency of fallopian tubes X. Discuss the therapy of A. Male factor: Prospective
observation, donor insemination, IUI, GIFT, IVG-ET
CONGENITAL ANOMALIES I. Given a pt with an imperforate hymen 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 1. Primary amennorhea,
recurrent pelvic pain, bulging hymen, hematocolpos C. Describe correct management 1. Correct surgically II.Congenital abnormalities of the uterus
due to abnormal Mullerian fusion, should know: A. Different anatomic variations;
i.e., didelphis, arcuate, etc. 1. Mullerian agenesis: failure
of formation of the primordial ducts B. Clinical significance 1.Psychosocial C. Hysterosalpingographic
characteristics
VULVAR DERMATOSES I.Etiology, clinical characteristics, and
Tx of the following common vulvar dermatoses A. Allergic 1. Most common benign
affliction, avoid irritants, apply local fluorinated
hydrocortisones (0.025% to 0.1%) B. Intertrigo & sehorrheic
dermatitis commonly seen with DM 1. Acute problem may be
treated with corn starch and topical fluorinated
hydrocortisones C. Fungal 1. Very common, candidiasis
often associated with vaginal infection, tinea cruris,
topical antifungals II. Etiology, clincial presentation, gross
and microscopic characteristics ant Tx of the following inflammatory
lesions of the vulva A. Gonorrheal vulvovaginitis 1. STD, s/s 2-5 days s/p
exposure (urinary frequency, dysuria, vaginal
discharge). Disseminated infection in 2% (fever,
septicemia, dermatitis, arthritis, endocarditis). May
ascend to upper genital tract (menstruation). Dx:
culture N. gonorrhoeae. Rx with ceftriaxone B. Chronic and acute bartholinitis 1. Acute infection often
N.gonorrhoeae or C. trachomatis, with duct obstruction
leading to abscess formation; Tx with drainage for 3-6
weeks with Word catheter C. Chancroid 1. Painful ulcer with ragged
edge, raised border. "Kissing ulcers" across the vulva
can occur. Unilateral, tender adenopathy in 50%.
Incubation period 2-5 days. Etiologic agent: Haemophilsu
ducreyi. Tx with azithromycin D. Chancre 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
BENIGN CERVICAL LESION I. Given a pt with a cervical polyp A. Make proper identification on
the basis of its macroscopic morphology 1. Polyps vary from a few
millimeters to 3cm; pedunculated, soft, smooth, red or
purple; Hyperplastic condition of endocervical
epithelium B. Plan its management 1. Tx by excision after
ligation of base
VAGINAL INFECTIONS I. Know the normal flora of the vagina, its pH, variations of the quality of discharge during the menstrual cycle II. Recognize the s/s of a vaginal infection and make a correct diagnosis by usual clinical and laboratory means of the following: A. Trichomonas vaginalis 1. Profuse yellow, malodorous
discharge, vulvar pruritis, >50% asymptomatic, often
carried in male partners, pH > 4.5, amine odor present
with KOH, wet mount reveals trichomonads; Rx with
metronidazole, 2g single dose, avoid during first 20
weeks of pregnancy B. Candida albicans C. Bacterial vaginosis 1. Overgrowth of aerobic and anaerobic bacteria (Gardnerella vaginalis), vaginal epithelium appears normal, fishy amine odor, sexual transmission unproven; Diagnosis: pH > 4.5, homogenous thin discharge, amine odor with KOH, Clue cells; Rx: Metronidazole 2g D. Herpes simplex 1. 1/3 of women 25-40 YO, 60-85% of sero+ are asymptomatic; primary infection 3-7 days s/p exposure, multiple vesicles coalescing into ulcers, fever, malaise, HA, recurrent shedding, recurring lesions, 75-85% of genital lesions are HSV-2; Diagnosis: viral isolation, serologic testing; Rx: oral acyclovir E. Atrophic vaginitis III. Know: A. Microbiologic characteristics
of the etiologic agents
CERVICAL INFECTIONS I. Differnce between acute and chronic cervicitis (clinical and morphological) A. Acute: Purulent discharge
present, diagnosis made by smears and cultures, superficial
inflammation, Tx with systemic abx II. Most common etiologic agents A. Acute: gonococcus III. Definitions of ectropion and eversion IV. Antimicrobial agents used for specific infections V. Principles of cryotherapy
PELVIC INFLAMMATORY DISEASE Given a pt with suspected acute chlamydial or gonorrheal infection, be able to obtain adequate information from her H&P, and lab data to arrive at an appropriate diagnosis and discuss a plan of management I. Incidence and epidemiology of chlamydial and gonorrheal infections in the United States II. Microbiologic (cultural, morphologic, etc.) characteristics of Neisseria Gonorrhoea and Chlamydia Trachomatis A. Gonorrhoea--gram-negative diplococci that requires Thayer-Martin media III. Incidence of female and male asymptomatic carriers IV. Pathophysiology of ascending gonorrheal and chlamydial infections V. Clinical presentation according to site and degree of infection A. Required: Abdominal tenderness (direct LQ), cervical motion tenderness, Adnexal tenderness; One of the following: leukocyte count > 10,000, temp > 38, gram-negative diplococci on endocervical sample or monocloal antibody for C. trachomatous, pelvic abscess, mucopurulent cervicitis, elevated ESR or C-reactive protein VI. Clinical, pathological and bacteriologic characteristics of pelvic abscesses VII. Medical and/or surgical management as indicated in various clinical situations VIII. Clinical, etiological and physiological characteristics of non-gonococcal pelvic infections (puerperal, postoperative, etc.) IX. Common causes of chronic pelvic discomfort: A. Chronic pelvic inflammatory
disease (pathologic findings) X. Clinical presentations and findings of each of the disorders outlined above XI. Definition of "shock" XII. Basic clinical parameters necessary to make a differential diagnosis between: A. Hypovolemic shock XIII. Pathophysiology of shock according to the type XIV. Most common organisms responsible for septic shock XV. Stepwise management of septic shock
ENDOMETRIOSIS I. Definition of endometriosis A. Presence of both endometrial
glands and stroma outside the uterine cavity II. Common sites of involvement A. Ovary, fallopian tube, cul-de-sacs, broad lig., sigmoid colon III. Histogenesis (theories) A.Coelomic metaplasia: 1. metaplastic transformation of pelvic peritoneum, doubtful (no men, no age inc., pelvis not abdomen) B.Ectopic transplantation of endometrium 1. "Retrograde menstruation", most likely theory C.Induction hypothesis 1. Substances released from shed endometrium induce formation of endometriosis IV. Macroscopic and microscopic characteristics A. Macroscopic: bluish-gray powder
burns, nonpigmented clear vesicles, whit plaques, reddish
petechiae or flame-like areas, scarring, adhesions,
peritoneal pockets, endometriomas (chocolate cysts) V. Relationship to endometroid carcinoma VI. Clinical characteristics A. Most common symptom is pain 1. Secondary dysmennorhea,
worsening primary dysmenorrhea, dyspareunia, noncyclic
diffuse pelvic pain; dyschezia, dysuria, pelvic pain,
backache VII. How to make the diagnosis A. Gold standard is laparoscopy VIII. Surgical or medical management A. Medical--no effect on fertility 1. Danazol--testosterone
derivative, attenuated LH surge, steroidogenic enzyme
pathway inhibitor, hyperandrogenism side effects B. Surgical--Most common approach 1. Vaporize, coagulate,
cauterize, excise lesions; 28% recurrence of pain @
18months, 40% @ 9years; Inc. pregnancy rates if severe;
Gold standared is TAH/BSO
ADENOMYOSIS Given a pt with a suspected diagnosis of adenomyosis of the uterus I. Macroscopic and microscopic characteristics A. Presence of endometrial glands
within myometrium; Endometrial gland foci separated from the
basal layer of lining endometrium by greater than one low
power microscopic field II. Clinical characteristics A. Progressively heavy menstrual flow, inc. dysmenorrhea, enlarging tender uterus III. Management A. Hysterectomy is TOC
ENDOMETRIAL HYPERPLASIA Given a 42 YO pt complaining of irregular vaginal bleeding: I. Describe the pathophysiology (including endocrine characteristics) of "dysfunctional uterine bleeding" II. Describe the microscopic appearance of the endometrium with A. Simple hyperplasia: increased
number of glands III. Discuss the relation of these to adenocarcinoma of the endometrium IV. Discuss the relationship of postmenopausal hyperplasia to adenocarcinoma V. Describe the management of each clinical case according to the histologic pattern and age group
UTERINE MYOMAS I. Incidence of uteine myomas A. Most common pelvic tumor; 1/5-1/4 of women > 35 YO have myomata; Most produce no symptoms; more common in AA than Caucasians; cause of 60% of laparotomies II. Different locations within the uteine wall A. Submucous, Intramural, Subserosal; corpus is most common site III. Macroscopic and microscopic appearance A. Gross appearance is smooth and
glistening white with a whorled and fasciculated pattern IV. Different degenerative changes that can occur in a myoma A. Necrosis can occur and may present with acute pain V. Microscopic criteria for the diagnosis of sarcomatous degeneration VI. Primiary and Secondary signs and symptoms due to uterine myomas A. Most produce no symptoms VII. Role of myomas in cases of infertility and possible behavior of myomas in pregnancy A. Pregnancy 1. Usually inc. in size during pregnancy; Inc. frequency of SAB; Degeneration during 2nd or 3rd trimester may produce symptoms similar to acute abdomen; may result in dystocia during labor VIII. Effect of estrogen upon these tumors A. Leiomyomas are clearly estrogen responsive IX. Indications for: A. Active intervention may be
chosen for usually large tumors, symtomatic tumors or when
the diagnosis is unclear
PELVIC RELAXATION I. Anatomy of the pelvic diaphragm A. Viscerofascial layer 1. Uterus and vagina attach to pelvic walls by fibrous tissue (endopelvic fascia) a. Parametria (cardinal &
uterosacral ligaments) 2. Suburethral endopelvic fascia attaches to the arcus tendineous from pelvis and to the medial border of the levator ani--crucial for urinary continence B.Levator ani muscles 1. Lie below the uterus, vagina, bladder, and rectum. Medial portion is puborectalis (pubococcygeus), Horizontal orientation. Closes urethra, vagina, and rectum by compressing them against the pubic bone II.Factors involved in Pelvic Organ Prolapse A. Inborn strength of connective
tissue 1. damage at childbirth C.Loss of levator function 1. Neuromuscular drainage
during childbirth D.Increased loads on the supportive system 1. Prolonged lifting E. Disturbance of the balance of the structural parts 1. Alteration of vaginal axis
by urethral suspension III. Definition and symptoms of A. Cystocele: IV. Know the indications for nonsurgical and surgical treatment A. Candidates for surgery 1. Prolapse above the hymenal ring a. repair only for
symptoms attributive to prolapse 2. Prolapse below the hymenal ring a. symptomatic
URINARY INCONTINENCE I. Definition of urinary incontinence II. Different types of urinary incontinence in females A. Stress urinary incontinence
(SUI)
GENITAL FISTULAE I.Different types and possible etiologies A. Constant urinary drainage, often after surgical or OB delivery II. Diagnostic techniques used in detection of such fistulae A. Diagnosed by placement of
methylene blue into bladder
VULVAR CARCINOMA Given a 65 YO F with a 3 cm pruritic lesion on the vulva I. Procedures required to properly diagnose vulvar disease, including the use of toluidine blue and a simple technique of vulvar biopsy A. Biopsy II. Incidence, natural history, macroscopic, microscopic, and symptoms of squamous cancer of the vulva A. CIS: 3-4% of all primary
malignancies of the genital canal; delay in diagnosis can be
extreme; 3rd and 4th decade of life; appearance varies
greatly (bowenoid = scaly, red, blackened; others--almost
entirely white or red); biopsy crucial III. Lymphatic drainage of the vulva A. Inguinal, femoral and external iliac nodes IV. Basis of management for carcinoma in situ (CIS) and invasive carcinoma of the vulva A. Surgical excision after determination of nodal involvement; localized lesion--wide local excision; multifoci lesions--skinning vulvectomy
CERVICAL CANCER I. Death rate due to cervical cancer in different populations A. 7th most common cancer of women in US; worldwide it is still the leading site of CA in women (500,000 cases annually) II. Risk factors and epidemiologic associations of populations at risk for premalignant and malignant disease of the cervix A. Practically never encountered
in virgins (promoting factor or carcinogen likely sexually
transmitted-HPV 16 & 18) III. Microscopic characteristics of cervical carcinoma and common sites of origin A. Cervical intraepithelial neoplasia (CIN), grades 1,2, and 3 1. Squamous cell carcinoma
represents 85% to 95% of cervical CAs; three grades B. Microinvasive carcinoma 1. depth < 3mm from BM; no vascular or lymphatic space involvement; incidence of lymph node involvement < 1%; may Tx with simple TAH or cone biopsy C. Invasive carcinoma 1. 10-15% of cervical CAs; approximately the same prognosis and clinical behavior as squamous cell CA; same staging and Tx IV. Clinical presentation and symptoms related to carcinoma of the cervix A. Hx: Abnormal VB or discharge,
excessive heavy or prolonged menses, postcoital bleeding;
pelvic pressure or pain V. Diagnostic techniques for cervical carcinoma A. Exfoliation cytology, individual diagnosis and population 1. Mass screening, economical, includes endocervical canal, detects adenocarcinoma, false negative 10-35% B. Schiller's test (pitfalls and
use) 1. Technique a. Localizes lesion, evaluates extent of lesion, differentiates inflammatory atypia from neoplasiakdiff. invasive from non-invasive cervical lesions 2. Colposcopic findings with normal epithelium a. smooth, pink, indefinitely outlined vessels, no change after application of aceitc acic 3. Colposcopic findings with abnormal epithelium a. Variations from above D. Biopsy of the cervix 1. Random biopsies E. Conization of the cervix, indications and contraindications VI. Clinical stages of carcinoma of the cervix (FIGO)--see charts VII. Three principal methods of treating invasive carcinoma of the cervix and their indications
VIII. Five-year survival rates for each stage of the disease A. 0--100%; IB--85%; IIA--70-75%; IIB--60-65%; IIIB--25-40%; IV--5-10%
ADENOCARCINOMA OF THE CORPUS UTERI I. Relative frequency of endometrial carcinoma and geographical, racial, and ethnic factors that influence it A. Most common female pelvic
malignancy in the US; 33,000 cases annually; Increasing
incidence II. Incidence by age group of endometrial carcinoma A. Dz of postmenopausal women~61 YO III. Macroscopic characteristics of endometrial carcinoma IV. Microscopic characteristics of endometrial carcinoma V. Relationship between hyperplasia and endometrial carcinoma A. Suggested screening with transvaginal US; < 5 to 6 mm usually atrophic VI. Relationship of estrogen to endometrial carcinoma A. OCPs are protective (prevent ~
2,000 cases per year) VII. Clinical stages of endometrial carcinoma (FIGO): see charts VIII. Clincal characteristics of the patient at risk (estrogen metabolism) A. Abnormal bleeding is most important symptom, seen in a postmenopausal female, menstrual abnormalities, inc. flow, lower abd. pain or pressure, symptoms of anema IX. Likelihood of endometrial cancer in postmenopausal women with uterine bleeding X. Use of vaginal cytology, endometrial biopsies, endometrial washings, and fractional dilatation and curettage in the diagnosis of endometrial carcinoma A. Diagnosis made by sampling endometrium (curette biopsy 90% accurate; vacuum curettage ~ 100% accurate; pap smear is not helpful XI. Basis of surgical therapy in the treatment of endometrial carcinoma A. Surgical staging via exploratory laparotomy & peritoneal cytology; TAH/BSO, responds poorly to other Tx XII. Treatment of women with advanced or recurrent tumor A. Radiotherapy, Progestins (1/3 of pts respond, better if highly differentiated and have receptors), Chemotherapy (disappointing results-cisplatin + cytoxan + doxorubicin)
OVARIAN CANCER I. Approximate incidence of ovarian cancer and the risk by age groups A. Most frequent cause of death
among all genital tract CA, overall 5-year survival ~ 30% II. Histogenesis, incidence, macroscopic, and microscopic characteristics and biological behavior of: A. Epithelial malignancies 1. >60% of all ovarian
neoplasms and >90% of malignant tumors; Probably derived
from ovarian surface wpithelium within epithelial
inclusion cysts in cortex; Classified by predominant
pattern and differentiation; Degree of cellular
proliferation, atypia, and stromal invation determines
benign low malignant potential or carcinoma B. Metastatic tumors to the ovaries: ? III. Common chlinical presentations and means of diagnosing ovarian carcinoma A. S/S: vague or absent (pelvic or
abd discomfort, urinary frequency, GI alteration, abdominal
fullness, early satiety with larger lesions, abnormal VB in
15%); endocrine (menstrual irregularities, estrogen
production with granulosa cell tumors=postmenopausal bleed &
precocious puberty, testosterone secretion = virilization in
50% of pts with Sertoli-Leydig tumors) IV. Management of: A. Benign: Unilateral, Cystic,
Mobile, Smooth, Smaller than 8 cm (7 cm is a tennis ball) 1. Ovarian cystic structure
>5cm followed for 6-8 weeks without regression D. Palpable ovary in a postmenopausal female 1. In the premenarchal or postmenopausal period any ovarian enlargement should result in surgical intervention E. 5 cm cystic adnexal mass in a young female 1. 95% of ovarian cysts smaller than 5cm in diameter are nonneoplastic; OCP for more rapid regression of functional cysts F. 10 cm cystic adnexal mass in a young female 1. Any mass larger than 10cm should be surgically explored G. Firm adnexal mass in a young female 1. Firm masses are an indication for surgery H. Any adnexal mass in a pt 40 YO or older 1. Determine menopausal V. FIGO clinical stages of ovarian carcinoma: see charts VI. Principle of managing epithelial ovarian carcinoma A. Surgery--TAH/BSO, omentectomy,
debulking VII. Approximate overall five-year survival rate for ovarian malignancies and the five-year survival rate as it pertains to each clinical state A. Overall~30% Stage I: 70%, Stage II: 25%, Stage III: 12%, Stage IV: 5%
BENIGN OVARIAN NEOPLASMS I. Histologic classification
2. Mucinous cystadenoma 3. Pseudomyxoma peritonei a. From spillage of mucinous contents into peritoneal cavity, biologically malignant, histologically benign, can result in progressive malnutrition 4. Cystadenofibroma a. Variant of serous cystadenoma, less common, partially cystic & partially solid, usually benign and unilateral, surface with broad papillae or deep sulci, Tx varies with age and associated findings 5. Brenner tumor a. 1-2% of all ovarian tumors, gross characteristics similar to fibroma, rarely malignant, 5-13% B, >50YO, arise from Walthard cell rests, 10-15cm, solid, can be assoc. with Meigs syndrome (ascites & hydrothorax), Tx: excision or oophorectomy B. Gonadal Stromal Tumors 1. Thecoma a. See "Functiona1 Ovarian Neoplasms--Granulosa-theca cell tumors" 2. Hilus cell tumor a. See "Functional Ovarian Neoplasms--Hilus cell tumors" C.Nonintrinsic Connective Tissue Tumors 1.Ovarian fibroma a. Middle-aged pts (avg~48 YO), connective tissue of ovarian cortical stroma or possibly inactive endstage thecoma, 2-10% B, ~6cm, can be assoc. with Meigs syndrome, Tx: removal D.Germ Cell Tumors 2.Struma ovarii a. unique benign cystic teratoma with thyroid tissue, resembles dermoid externally, 5% produce s/s of thyrotoxicosis 3.Gonadoblastoma a. See "Functional Ovarian Neoplasms--Gonadoblastoma" II. Incidence and frequency of bilaterality in the most common tumors III. Gross and microscopic appearance IV. Clinical characteristics and treatment FUNCTIONAL OVARIAN NEOPLASMS Germ cell and stromal ovarian tumors I. Dysgerminoma II. Granulosa-theca cell tumors III. Gonadoblastoma IV. Adrenal rest ovarian tumors V. Hilus cell tumors VI. Know:
TROPHOBLASTIC DISEASE In a pt with suspected molar pregnancy the student should know: I. Epidemiology of molar pregnancies II. Clinical characteristics usually associated with a molar pregnancy III. Differences in the curves of gonadotropin titers between normal and trophoblastic pregnancies IV. Frequency and histologic and clinical characteristics of the malignant degeneration of molar pregnancies V. Uterine evacuation techniques for cases of trophoblastic disease VI. Program for appropriate follow-up designed to determine whether there is persistent trophoblastic ticcue after evacuation VII. Pharmacologic characteristics and rationale for use of chemotherapeutic agents in the treatment of trophoblastic disease VIII. Indication for treatment of trophoblastic disease IX. Classification of trophoblastic disease RADIATION THERAPY I. Characteristics of radium, cesium, and cobalt II. Concept of the MEV (million electron) III. Concept of wavelength, penetrability IV. Definition of rad or Gray V. Variation of radiation intensity with distance (inverse square law) VI. Rationale of internal versus external radiation application VII. Short and long-term effects of radiotherapy on normal body tissues |
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