HI-YIELD FACTS IN OBSTETRICS [from USMLE CLERKSHIP-OB & handy notes] o Parts [from uterus to lateral wall]: interstitial

from uterus to lateral wall]: interstitial part, isthmus, ampulla, fimbrial end /
infundibulum]
GENERALITIES
Keyterms Chapter 3: Physiology of Normal Mensrual cycle
Ovulation /postconception It is 2 wks < gestational age Menstruation
Gravida Woman who is, or has been pregnant irrespective of the outcome  Average thelarche = 10 y/o [↑ estradiol], pubarche = 11 y/ o [↑ adrenal hormones],
Parity Number of pregnancies reaching viability menarche = 12 y/o [↑ estradiol]
Puerperium 6-8 wks period after delivery  Causes of precocious puberty and manifestations:
Perinatal period Commences at 22 completed wks of gestation & ends 7 Idiopathic – MC cause Thelarche/pubarche/menarche
completed days after birth Tumors of hypothalamic-pituitary stalk Thelarche/pubarche/menarche
Neonatal period From birth to 28 days after birth Inflammation of the hypothalamus Thelarche/pubarche/menarche
Embryonic period 3rd wk to 7th wk after fertilization, when major structures are formed 21-hydroxylase deficiency Pubarche
Previable period Lasts from 11-20 AOG Excess estrogen Thelarche and menarche
Viable period Lasts from 21-40 AOG
Preterm Less than 37 completed wks  Average menses = 3-6 days
Term From 37-42 completed wks  Blood loss in menstruation averages 30-50 ml, should not form clots. > 80 ml is abnormal
Post-term 42 completed wks or more amount of blood loss.
Low birth weight Less than 2500 gms  Phases of menstrual cycle:
Very low birth weight Less than 1500 gms o Menstruation: days 1-4 [1st part of follicular phase]
Extremely low birthweight Less than 1000 gms o Follicular phase [proliferative phase]: days 1-14
Puerperium Time after delivery of placenta up to return of reproductive organs o Ovulation; day 14
to their normal non-pregnant state [usually occur at 6-8 wks] o Luteal phase: days 14-28
 Main events of menstruation: absence of progesterone causes endometrial sloughing.
PHYSIOLOGIC OBSTETRICS  2 main events in follicular phase:
Chapter 2: Anatomy of Female Reproductive Tract o FSH causes follicle maturation and estrogen secretion.
 Functional components: o Estrogen causes endometrial proliferation.
Placental arm Paracrine arm  Main event of ovulation:
Nutritive, endocrine, Pregnancy maintenance, immunologic acceptance, o LH surge causes oocyte to be released.
immunologic AFV & hemostasis, physical protection of fetus  Main events of luteal phase: corpus luteum secretes progesterone w/c causes endometrial
maturation [↓FSH, ↓LH].
 Communication system:
Chapter 4: Endometrium and Decidua
Placental arm Paracrine arm
 Endometrial cycle and histology:
Maternal blood to placental intervillous space, Chroion leave, maternal deciduas
Early proliferative Glands are tubular and short, nuclei are basally located w/
fetal blood confined to capillaries parietalis, amnion
phase abundant mitotic figures
Late proliferative Glands become tortuous w/ cells lining the gland undergoing
 Embryology
phase pseudostratification
Paramesonephric or mullerian ducts Forms uterine tubes [cranial], uterus
Early secretory Glycogen-rich subnuclear vacuoles appear at base of cells
[caudal], and upper part of vagina
Mid-late secretory Endometrium rich in glycogen, decidualization of stromal cells
Urogenital sinus Forms lower part of vagina & vestibule
Premenstrual Intense coiling of spiral arteries w/ PMN infiltration of stroma
Mesonephric system or wolffian duct Forms the epoophoron & paroophorron
Germinal epithelium Forms the ovary
 Sex-steroid hormone induced proliferation:
Pre-ovulatory or follicular phase Estradiol 17-β is secreted by follicles
 6 openings of vestibule:
Post-ovulatory or follicular phase Progesterone secreted by corpus luteum, at 7-8
o Urethra, vagina, bartholin’s ducts [2], paraurethral/ skenes ducts [2]
days after ovulation progest + estrogen declines
 Vagina:
Proliferative phase Estrogen is the predominant hormone, ↑ PTH-
o pH = 4-5
rp, vasodilatation occurs
o blood supply:
Late ssecretory phase + menses Progesterone withdrawal + TGF-β, increase
Upper 1/3 Cervicovaginal branch of uterine A.
endothelin-1, vasoconstriction occurs
Middle 1/3 Inferior vesical A.
Lower 1/3 Middle rectal and internal puddendal A.
 3 portions of deciduas
Decidua basalis Directly beneath site of blastocyst implantation
o lymphatics:
Decidua capsularis Overlies the enlarging blastocyst & is most prominent
Upper 1/3 Iliac nodes
during 2nd month of pregnancy
Middle 1/3 Internal iliac nodes
Decidua parietalis Joins decidua capsularis at 14-16 wks of pregnancy
Lower 1/3 & vulva Inguinal nodes
 Blood supply of endometrium:
 Perineum:
Basal 1/3 Straight arteries
o Blood supply: internal pudendal and its branches [inferior rectal + posterior labial A.]
o Innervation: pudendal nerve Superficial 1/3 Coiled or spiral arteries
o Muscles:
Pelvic diaphragm Levator ani and coccygeus muscles Important facts
Urogenital diaphragm Deep transverse perineal, constrictor urethrae, internal  At 6 days post-fertilization, blastocyst establishes cell to cell contact w/ endometrium.
and external fascial coverings  Restoration of epithelial surface of endometrium is complete by 5 days of endometrial
Perineal body: on w/c converge the bulbocavernosus M., superficial transverse perineal M., cycle.
and external anal sphincter  Subnuclear vacuolization is the 1st histologic indication of progesterone effect.
 Uterus:  Decidua is the source of prolactin in amniotic fluid.
o Wall: endometrium, myometrium and serosa  Nitabuch’s layer is where invading trophoblast meet the decidua, a zone of fibrinoid
o Lymphatics: hypogastric nodes [cervix], internal iliac, nodes to ovarian region and degeneration.
periaortic nodes [body]
o Ligaments: Chapter 5: Placenta and Fetal membranes
Uterosacral lig. O superior part of cervix encircling the rectum, insert over S2-3  Structures:
Cardinal lig. Aka: transverse cerviacal lig. Or Mackenrodt lig. Amnion Tough and tenacious bu pliable membrane, innermost vascular fetal
United firmly to the supravaginal wall of cervix membrane, contiguous w/ amniotic fluid. Amnion layer continuos w/
Round lig. Continuous w/ broad lig. to inguinal canal terminatinng at upper chorion leave is the acellular zona spongiosa. The amnion develops
part of labium majus, holds the ovary in place about 7th-8th day of blastocysts development. It has no muscles, nerves,
lymphatics, and is avascular. It also provides all the tensile strength of
fetal membranes.
 Oviducts:

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Umbilical cord 30-100 cm [ave. 55] length, w/ 2 arteries and 1 vein, 0.8-2.0 cm in 10th wk Spontaneous movement noted
diameter, average of 55 cm. Exracellular matrix of umbilical cord is 3rd lunar month Histological evidence of taste buds
composed of specialized tissue [Wharton’s jelly]. 4th lunar month Complete finger closure
Amniotic fluid Average vol: 1,000 cc at term, 400 cc at midpregnancy, 50 cc at 12 wks 24 or more wks Ability o suck
24-26 wks Fetus hears sounds in uterus
Important facts 28 wks Eye sensitive to light, responsive to vibrations in taste
 Zona pellucida disappears prior to implantation & blastocyst adheres to endometrial
surface [apposition]. Respiratory system
 Leafy chorion/chorion frondosum [fetal part] while chorion leave/bald chorion contains the  Glycerophospholipid composition of mature surfactant:
ghost villi. i. Phosphatidylcholine = 78%
 As emdryo grows further, the decidua capsularis & parietalis form the decidua Vera. ii. Phosphatidylglycerol = 9%
 The impetus for implantation invasion is provided by trophoblasts.  Hormone regulation of surfactant:
 Human placenta is of hemochorioendothelial type. Cortisol Natural stimulus for augmented surfactant synthesis
 Mainstem villi & its ramififications constitute a placental cotyledon. Prolactin Accelerate rate of synthesis of phosphatidylcholine by lungs
 Chorionic villi can be seen in human placenta by 12th day post-fertilization. Estrogen Promote prolactin release
 MC vascular anomaly in humans is absence of 1 umbilical Artery. Thyroxine Accelerate fetal lung maturation
EGF Promote surfactant secretion and increase SP-A [major
Chapter 6: Placental hormones apoprotein surfactant]
Important facts
 ANP is produced in atrial myocytes & is synthesized in placenta. It causes natriuresis, Urinary system
diuresis and vasorelaxation of uterus during pregnancy.  Fetal kidneys star producing urine by 12 wks
 Inhibin acts to inhibit FSH release by the pituitary.  Metanephros is the definitive urinary system.
 Highest carbohydrate content of any human hormone is in HCG [pregnancy hormone]. A  Lecithin is principal surface active component of surfactant.
glycoprotein produced by syncitiotrophoblasts. It is secreted maximally at 8-10 wks AOG.  Phospholipid is the primary surface tension-lowering component of surfactant.
It also acts to rescue or maintain corpus luteum to promote continued estrogen  Surface apoproteins serves to facilitate serve to facilitate forming & reforming of surface
stimulation. film in alveoli during respiration.
 T ½ of HCG is 24 hrs while LH is 2 hrs.  Cortisol is the natural stimlus for augmented surfactant synthesis.
 GH releasing hormaone is also known as somatocrinin.  Urine production = 10 ml/hr at 30 wks, 27 ml/hr at term
 DHEAS is the principal circulating precursor of placental estrone & estradiol.  Amniotic fluid volume:
 Adrenal cortex is the largest organ in fetus, a principal source of estrogen precursors. - Term fetus is able to swallow as much as 450 ml/24 hrs of amniotic fluid
 The primary placental estrogen that enters maternal compartment is estradiol. - At 16-18 wks, fetal urine becomes an important source of amniotic fluid
 Pregnanediol is the principal urinary metabolite of progesterone. 12 wks 50 ml
 Maternal plasma LDL cholesterol is the principal precursor of progesterone biosynthesis in Midpregnancy 400 ml
placenta. 36-38 wks 1000 ml
 5 alpha-reduction of progesterone is the major pathway of progesterone metabolism.
 Major role of relaxin is remodeling of CT of reproductive tract allowing pregnancy Respiration
accommodation & successful parturition.  Respiratory movements are seen at 4 mos.
Endocrine system
Chapter 7: Morphological and Functional development of fetus  Neurohypophysis secretes oxytocin & AVP by 10-12 wks.
 Most frequently used diameters of fetal head: Gonads
Occipitofrontal 11.5 cm From root of nose to occipital bone  Fetal testis secretes testosterone and pregnenolone by 10 wks.
Biparietal 9.5 cm Greatest transverse diameter of the head  Genetic sex is established at time of fertilization
Bitemporal 8.0 cm Greatest distance btw 2 temporal sutures  Sexual development of male and female embryo is identical up to 8 wks.
Occipitomental 12.5 cm Greatest diameter of fetal head  Maleness: testosterone and MIF, its absence in Femaleness
Suboccipitobregmatic 9.5 cm From large fontanelle to occipital bone
Chapter 8: Maternal adaptations to pregnancy
 Plane of occipitofrontal diameter: 34.5 cm [greatest head circumference] Cardiovascular system
 Plane of suboccipitobregmatic: 32 cm [smallest head circumference]  Heart is displaced upwards and outwards due to gravid uterus
 Maximal increase in heart rate during 7-8th mos. w/ average of 10 bpm
Cardiovascular system  CO peaks during 25th-32nd wks [highest at 28th wks] = 30-40%
 Remnants of the following will become:  4 periods of increased CO:
Umbilical vein Ligamentum teres 1. on 28 wks AOG [highest peak]
Umbilical artery Medial umbilical ligament 2. during labor
Urachus Median umbilical ligament 3. immediately postpartum
Tongue remnant [thyroid] Foramen cecum 4. 1st wk of puerperium
Vitelline duct Meckel’s diverticulum  ↑ Plasma volume [50-60%] w/c peaks by 7 mos. → dilutional anemia
Ductus venosus Ligamentum venosum  ↑ Pulse pressure maximum on the 7-8th mos.
Ductus arteriosus [closes at 10-96 hrs] Ligamentum arteriosus  ↓ DBP [note that presence of diastolic murmur in pregnancy is never normal]
Foramen ovale [closes after several mins] Anatomical fusion at 1 yr.  Elevated venous pressure in lower extremities
Fetal coagulation factors Respiratory system
 ↓ factors 2,6,9,10,11,12,13, fibrinogen & plasminogen, ↑ thrombin, normal platelet count  Upward displacement of diaphragm by 4 cm
 ↑ in RR, TV, respiratory minute volume, and airway conductance
Immunocompetence of fetus  ↓ FRC, RV, TPR, and broncho-motor tone [progesterone effect]
 13 wks: fetus is immunologically competent  Lung compliance is unaffected
IgG Transported btw mother to fetus at 16 wks Gastrointestinal system
IgM Produced by fetus in response o infections, adult levels at 9 mos.  Px may have GERD/heartburn [progesterone effect]
B lymphocytes Appear in liver at 9 wks, in blood and spleen at 12 wks  Decreased responsiveness to CCK
T lymphocytes Produced by thymus at 14 wks  Liver of pregnancy – swelling of kuppfer cells
Urinary system
Gastrointestinal tract  Kidneys hypertrophy due to ↑ renal blood flow
 Glucagon identified by 8 wks, insulin detectable by 12 wks  Physiologic hydroureter evident at 1st trimester
 Fetal pancreas noted at 9-10 wks  Estrogen stimulates hypertrophy and elongation of muscles while progesterone promotes
 Swallowing begins at 10-12 wks generalized atony
 Peristalsis a 11 wks AOG  Prone to UTI due to progesterone and pressure changes
Endocrine system
Nervous system and sensory organs  ↑ corpus luteum activity up to 12 wks
8th wk Flexion of fetal neck and trunk  Mild hyperthyroid state due to gland hyperplasia

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  Pituitary gland hypertrophy and hyperplasia  Changes in cervical mucus: beading [progesterone], ferning [estrogen]
 Diabetogenic due to placental degradation of insulin and insulin effects of placental  Perception of fetal movement [quickening]: 16-18 wks [multi], 18-20 wks [primi]
lactogen, estrogen, and progeterone  Different signs of pregnancy:
 Increase oxytocin production near term Presumptive Chadwick sign [6 wks] Discoloration of vaginal mucosa
Placenta Probable Hegars [6-8 wks] Soft compressible isthmus
 HCG is detected in maternal plasma or urine by 8-9 days after ovulation, reaches nadir at Probable Goodell’s [4-8 wks] Cyanosis and softening of cervix
100-130 days, peaks at 60-70 days
 hPl detected as early as 2nd-3rd wk after fertilization, rises steadily at 34-36th wks of  HCG:
pregnancy o Detected in maternal plasma or urine by 8-9 days after ovulation
 progesterone synthesis is accomplished by syncitiotrophoblasts after 6-8 wks of o Peak levels at 60-70 days, Nadir reached at 100-130 days
pregnancy o Urine HCG – preferred method to recognize normal pregnancy [25 mU/ml by 1 wk
Hematologic system after LMP]
 ↑ retic count and RC volume due to erythroid hyperplasia  Radiographic evidence of fetal death:
 ↓ Hct due o increase plasma volume o Spalding sign: overlapping of fetal skull bones due to brain liquefaction
 Total iron requirement = 1 gm or 6-7 mg/day [RDA] o Robert’s sign: gas bubble in fetus
300 mg Fetus and placenta o Exaggeration of fetal spine curvature
200 mg Excreted  Cranial signs of spina bifida on UTZ:
500 mg Erythrocyte production o Small BPD
o Ventriculomegaly
Fetal blood hematopoiesis o Frontal bone scalloping [lemon sign]
Mesoblastic In yolk sac during embryonic period o Abnormal curvature of cerebellum [banana sign]
Hepatic Liver up to near term o Effacement/obliteration of cisterna magna
Myeloid BM starts at 4 mos. fetal age, major site in adults  Scan dating is useful up to 20 wks AOG when menstrual data is unreliable or conflicts with
clinical findings.
Skeletal system  Ideal weight gain:
 Progressive lordosis o 1ST trimester: 1.5-3 lbs
 Increased mobility of pelvis joints o 2nd and 3rd trimester: 0.8 lbs/wk
Immunologic system  Pregnancy is an anabolic state.
 Immuosupressive mechanism by progesterone, estrogen and HCG  The optimal time to screen for glucose intolerance/DM in the pregnant female is at 26-28
 Production of suppressor T cells and AFP by fetus AOG.
Maternal metabolism  By midpregnancy, fat is the primary source of maternal energy.
 Weight gain: at least 25 lbs weight gain  Normal pregnancy is a hyperlipemic as well as glucosuric state.
1st trimester 2 lbs  Diastolic murmurs in pregnancy are never normal.
2nd trimester 11 lbs  Chadwick’s sign: bluish discoloration of vagina and cervix due to congestion of pelvic
vasculature.
3rd trimester 11 lbs
 Constipation may occur secondary to progesterone, w/c relaxes the intestinal smooth
muscle and slows peristalsis.
 Carbohydrate metabolism – pregnancy is diabetogenic due to:
o hPl has anti-insulin effect  Asymptomatic bacteriuria occurs in 5-8% of pregnant women.
o estrogen, progesterone and cortisol induce insulin resistance  OCPs and HRT [combinations of estrogen and progesterone] are the MC cause of
o placenta secretes insulinase w/c cause insulin degeneration melasma or “mask of pregnancy”.
 Protein metabolism  TSH, PTH and calcitonin do not cross the placenta.
o + nitrogen balance at 29th wks  HCG is detectable in maternal serum after implantation has taken place at 8-11 days after
 Fat metabolism – lipemia occurs conception.
 Trophoblasts [rophoecoderm] are the precursor cells for the placenta and membranes.
Acid-base balance  Placenta is the primary producer of steroid hormones after 7 weeks AOG.
 Pregnant women normally hyperventilate to reduce arterial PCO2  HCG maintains the corpus luteum and stimulates adrenal and placental steroidogenesis.
 Partial renal compensation: increase HCO3 secretion  MSAFP peaks btw 10-13 wks AOG then declines thereafter.
 After 1st trimester, placenta is the major source of circulating estradiol.
Chapter 9: Diagnosis of pregnancy  Progesterone concentrations of < 5 ng/ml are diagnostic of fetal death in 1st trimester.
Presumptive Nausea with or w/o vomiting [due to increased HCG levels]  Progesterone concentrations are significantly elevated in: women w/ hydatidiform mole
Sx Urinary disturbances complications of Rh isoimmunization.
Fatigue [due to increased metabolism]
Perception of fetal movement [quickening] = 18-20th wks AOG ANTEPARTUM
[primigravida] and 16-18th wks [multigraviida].  Frequency of visits: < 28 wks – every month, 28-36 wks – every 2-3 wks, 36 wks to
Presumptive Amenorrhea, breast changes [dark areola, erected nipple, delivery – once per week until delivery
signs engorged breast], skin pigmentation [choalasma/mask of  Triple screen: serum AFP, estriol, beta-HCG at 16-18 wks
pregnancy, striae gravidarum, spider telangiectasia (estrogen  Important hallmarks in prenatal visits:
effect), linea nigra], changes in vaginal mucosa, thermal signs [↑ o Pap smear: 1st visit
temp by 0.3-0.5 for > 3 wks due to progesterone effect] o Rh screen – 1st visit
Probable Abdominal enlargement, changes in skin, shape, and consistency o Gonorrhea and Chlamydia – 1st visit
signs of uterus, anatomical cervical changes, Braxton-hicks o 1st sonogram – week 16-18
contractions, ballotment, physical outlining of fetus, (+) preg test o Amniocentesis – week 16-18
Positive Identification of FHT separate from mother, perception of active o Triple screen – week 16-18
evidence fetal movement by physician, UTZ or radiologic evidence o Diabetes screen – week 16-18
o Group B strep culture – week 36.
 NAV occurs in 50% 0f pregnancies, most notably at 6 wks AOG and disappears 6-12 wks  An inaccurate gestational age is the most common reason for an abnormal screen.
later.  After Rh sensitization, a Kleihauer-Bettke test is done to determine the amount of fetal
 Braxton-Hicks contraction: painless, irregular contractions at 28th wks. RBCs in the maternal circulation.
 Quickening – awareness of 1st movement of the baby  RhoGAM administered to Rh-mothers exposed to fetal blood.
 Ballottement noted at 20th wks.  Anti-D titers of > 1:16 require amniocentesis and analysis of amniotic fluid bilirubin].
 Anatomical changes in cervix:  Intrauterine pregnancy seen via vaginal UTZ when beta-HCG > 1,500
o Beaded pattern of cervical mucus due to progesterone  Intrauterine pregnancy seen via abdominal UTZ when beta-HCG > 6,000.
o Ferning pattern due to estrogen seen on 1st half of the cycle  Anti-D titers of > 1:16 require amniocentesis and analysis of amniotic fluid [bilirubin].
 Fetal heart tones:  Oligohydramnios [AFI < 5], may suggest possible fetal compromise due to umbilical cord
o Normal FHT = 110-150 bpm compression.
o UTZ by 8th wks  Polyhydramnios [AFI>20] may signify poor control in a diabeti pregnancy or a diabetic
o Stethoscope by 17-19th wk pregnancy or a fetal anomaly.
o Doppler as early as 10-12th wks  The average woman must consume an additional 300 kcal/day beyond baseline needs.

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  Vaccines safe in pregnancy: hep B, oral polio, tetanus, yellow fever, dipheria Iron 30 mg/day
 Vaccines unsafe in pregnancy: measles, mumps and rubella 60-100 mg for large built, twin fetuses, late pregnancy
 Give immune globulin in pregnancy for exposure to: heap A and B, tetanus, chickenpox 200 mg for overly anemic women
and rabies. 15 mg/day for nonpregaant and lactating women
Calcium + 1200 mg/day for nonpregnant, pregnant and lactating
Chaper 10: Prenatal care phosphorus women
 Estimation of pregnancy duration Zinc 15 mg/day for pregnant women, 12-19 mg/day for
o LMP = count number of days since 1st day of last normal menses nonpregnant, pregnant and lactating women
o 280 days or 40 wks or 9 ½ calendar months Iodine 175 ug/day for pregnant women
 EDC = [1st day of LMP] + 7 days – 3 mos. + 1 year [ex. LMP= 7/10/93, EDC = 4/17/94] 150-200 ug/day for nonpregnant and lactating women
 Height of fundus [in cm] = wks AOG [18-32 wks] Magnesium Pregnancy = 320 mg/day
 Fetal weight in gms = 155 x [fundic ht in cm – n] Nonpregnant = 280 mg/day
o n = 12 if sation below ischial spines [engaged], 11 if above the ischial spines Lactation = 355 mg/day
[unengaged]
o k = 155, constant Chapter 11: Identification of high-risk pregnancy
 Fundal height during pregnancy Maternal age < 18 y.o or nullipara > 30 y.o
Weeks Fundal height Maternal height 60 inches or < 153 cm
12 Above pubic symphysis Maternal weight > 20% of standard weight for height
16 Midpoint btw pubic symphysis and umbilicus Obstetric hx If [+] medical illness
20 At umbilicus
28 6 cm above umbilicus Chapter 15: Immunizations during pregnancy
36 2 cm below xiphoid process  Contraindicated vaccines: measles, mumps and varizella-zoster
40 4 cm below xiphoid process  Vaccines given similar o non-pregnant women: rabies, pneumococcal, meningococcal,
tetanus, hepa A and B
 Leopolds maneuver:  Requested only after 1st trimester: influenza
LM1 Fundal grip What fetal pole occupies the fundus?  Given only as post-exposure prophylaxis: hepa A and B, rabies, tetanus, VZV, measles
LM2 Umbilical grip Which side is the back?
LM3 Pawlick’s grip What fetal part lies above pelvic inlet? Chapter 16: The Pelvis [Passages]
LM4 Pelvic grip Which side is the cephalic prominence?  Pelvic inlet:
o Diameters of inlet:
Findings: 1. Anteroposterior diameters
LM1 Irregular nodular [breech] Round [cephalic] Diagonal conjugate 12 cm Only APD measured clinically
LM2 Linear, convex, bony ridge [back] Numerous nodulations [small parts] True or anatomic conjugate 11 cm DC – 1.2 cm
LM3 Round, ballotable [unengaged] Fixed, knoblike part [engaged] Obstetric conjugate 10 cm DC -1.5-2 cm
LM4 Cephalic prominence on same Cephalic prominence on same side 2. Transverse diameter of inlet 13 cm
side as fetal parts [flexion] as fetal back [extension] 3. Posterior sagittal of inlet 4 cm R and L oblique diameters

 Visit intervals: q 4wks until 28 wks, then q 2-3 wks until 36 wks then weekly thereafter  Plane of greatest diameter: 12.5 cm – anteroposterior diameter
 Lab examinations:  Plane of midpelvis:
Time [wks] Assessment o Landmarks of areas of assessment of midpelvis:
1. prominence of ischial spines
Initially [ASAP] CBC, U/A, blood group & Rh type, PAP smear, Hepa B screen]
2. convergent pelvic sidewalls
8-18 wks UTZ, amniocentesis, chorionic villous sampling
3. shallow concavity of sacrum
15-20 wks MSAFP screening
4. bi-ischial diameter of outlet: < 8 cm
26-28 wks Screen for GDM if indicated, repeat CBC [esp. Hb and Hct] o Diameters of midpelvis:
28 wks Test D-negative women for antibodies Anteroposterior diameter ?
32-36 wks UTZ, repeat CBC, test for STD Transverse diameter [bispinous] 10.5 cm
3rd trimester Hepa B screening Posterior sagittal of midpelvis 4.5 ccm
Note:
 Pelvic outlet:
Give hepa B Ig & vaccine to infans of HBsAg [+] mothers
Anteroposterior diameter of outlet 9.5-11.5 cm
50 g OGCT, if > 130 mg/dl in 1 hr then proceed to 3 hr 100 g OGCT
Triple screen for Down’s syndrome: ↓AFP, ↑ HCG, ↓ unconjugaed estriol Transverse diameter [intertuberous] 11 cm
Posterior sagittal of outlet 7 cm
Chapter 14: Ultrasound in pregnancy
Abdominal UTZ [full bladder] Full bladder acts as acoustic window, pushing uterus out of  Indications for clinical pelvimetry:
pelvis & displacing bowel superiorly o Previous injuries or disease affecting the pelvis
Vaginal UTZ [empty bladder] Small amount of urine pushes the uterus posteriorly out of view o Breech for vaginal delivery, VBAC
 Soft parts of the pelvis: pelvic floor and pelvic diaphragm
 Indications for 1st trimester UTZ
o Establishes uterine pregnancy upon seeing gestational sac [earliest at 5-6 wks]  Forceps delivery is usually indicated in pxs w/ antrophoid pelvis.
o Detection of fetal life and number of fetuses [FHT by 7 wks AOG] Different pelvic types: [refer to OB-GYNE handy notes p. 11]
o Evaluates for retrochorionic hemorrhage, incomplete/complete abortion [if > 600 cc]
o Early dating of pregnancy using: Chapter 18: Parturition
Gestational sac diameter At 5-6 wks  4 phases of parturition:
CRL At 12-14 wks [most accurate] Phase 0 Prelude to Time of contractility and uterine unresposiveness, occurs before
parturition or implantation until 35-38 wks, mediaed by progesterone, cervix
BPD, femoral length Onwards
quiescence remains rigid & unyielding
o Evaluation of uterus and adnexa Phase 1 Preparation to Uterus & cervix undergo anatomic and functional changes, ↑
labor oxytocin in myometrial cells, dependent on uterotonins or
 Indications for 2nd and 3rd trimester UTZ
uterotropin, cervix ripens & dilates
o Fetal viability, number and presentation
Phase 2 Active labor Active uterine contractions occur, 3 stages of labor occur
o Amount of AFV & placental localization [3 cm VFP in 3rd trimester is normal]
o Fetal age and growth by fetal biometry [CRL, BPD, FL] Phase 3 Recovery period Uterine contraction & involution to prevent hemorrhage, initiation
o Evaluation of fetal amniotic structures [reversal of fetal diastolic blood flow in umbilical of lactation and milk ejection for breastfeeding, uterotonins present
artery indicates a severely compromised fetus]
 Uterotropin vs. uterotonins
Chapter 13: Nutrition during pregnancy Uterotropin [ex. gap junctions Acts in myometrium & cervix to produce functional elements to
Calories Daily increase of 300 kcal/day & oxytocin receptors] prepare uterus for effective contraction & cervical softening
Protein Increase to 5-6 gm/day Uterotonins [ex. oxytocin, Causes smooth muscle contraction

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prostaglandin, endothelin]
INTRAPARTUM
 Early signs of labor:
Lightening or ↓ fundic height due to formation of LUS allowing fetal head to Chapter 21: Intrapartum assessment
“baby drop” descend & ↓ AFV  3 types of FHR pattern:
Bloody show Blood-tinged mucus from vagina, considered a late sign Type Characteristics Cause
False labor Irregular interval of contractions, shorter duration, and discomfort Early deceleration Occurs w/ onset of contraction Head compression
confined to lower abdomen or groin Late deceleration Occurs after onset of contraction Uteroplacental insufficiency
Variable MC type, occurs before, during or Cord compression & cessation
 Ferguson’s reflex: mechanical stretching of cervix that enhances uterine contractions deceleration after & even w/o contraction of umbilical blood flow
 Pathologic retraction ring [Bandl ring]: extreme thinning of LUS as in obstructed labor
 Patterns of cervical dilatation [active phase]: maximum diameter is 10 cm  Abnormalities of the 2nd stage of labor may be either protraction or arrest of descent [fetal
Latent phase More variable, affected by sedation head descends < 1 cm/hr in nulliparous and < 2 cm/hr in multiparous]
Active phase Starts at 4cm dilatation  If 30 mins have passed w/o placental extrusion, manual removal of the placenta may be
Acceleration phase Predictive of outcome of labor required.
Phase of maximum slope A good measure of the overall efficiency of  Normal blood flow to nonpregnant uterus – 100 cc/min
the uterus  Normal blood loss for normal vaginal delivery – 300 to 500 ml
Deceleration phase Reflective of fetopelvic relationship  Normal blood loss for normal CS – 800-1000 ml
 False [+] nitrazine test may be cause by vaginal infections w/ trichomonas vaginalis, blood
 Progressive dilatation w/ no change in station in woman of low parity may signify and semen.
fetopelvic disproportion.  A score of > 8 in bishop’s score indicates that the probability of vaginal delivery after labor
 Pattern of descent: hyperbolic curve induction is similar to that after spontaneous labor.
 3 functional divisions of labor:  Vaginal prostaglandins are inserted for ripening of cervix.
Preparatory Affected by sedation & analgesia  Anterior fontanelle: bigger, diamond-shape
Dilatational Rapid rate, unaffected by sedation or analgesia  Posterior fontanelle: smaller, triangle-shape
Pelvic Commences ww/ deceleration phase of cervical dilatation, cardinal  Vaginal delivery is possible only if fetus is mentum anterior.
movements of labor take place  Engagement is measured by palpation of the presenting part of the occiput.
 Ferguson’s reflex: mechanical sretching or stripping of the cervix
 WHO principles of partograph [study Friedman’s curve on OB-GYN handy notes p. 20]  The anterior shoulder is the one closest to the superior portions of the vagina, while the
1. active phase of labor begins at 4 cm cervical dilatation posterior shoulder is losest to the perineum and anus.
2. latent phase of labor should not last longer than 8 hrs  Modified ritgen’s maneuver: allows for delivery of fetal head w/ smallest diameter passing
3. rate of cervical dilatation during active phase of labor & should not be slower than 1 thru the introitus and over the perineum.
cm/hr  Maneuver’s for placental separation:
4. 4 hr lag btw slowing of labor and the need for intervention is unlikely to compromise he o Brandt-andrews maneuver:
fetus o Crede’s maneuver: manual extraction of placenta [after > 30 mins of not being
5. 4 hourly vaginal examinations is recommended expelled]
 MC indication for primary CS: dystocia
 Cardinal movements of labor;  Montevideo units are calculated by increases in uterine pressure above baseline [8-12
Engagement Head enters the brim in transverse biparietal diameter mmHg] multiplied by contraction frequency per 10 minutes.
Asynclitism – slight deflection either anteriorly towards symphysis or  Uterine pressure increases and stages of labor:
posteriorly towards promontory 1st stage 25-50% mmHg ↑ by 3-5 contractions/10 mins
Fismanns obliquity [sagittal suture lies anteriorly], Naegeles’ obliquity 2nd stage 80-100 mmHg ↑ by 5-6 contractions/10 mins
[sagittal suture lies posteriorly]
Descent 1st requisite for normal spontaneous delivery, facilitated by amniotic fluid  Vaginal exams: VE q 4 hrs in latent phase and q 2 hrs in active phase
pressure, fundal pressure, and abdominal muscle contraction  FHT monitoring: q 30 mins [1st stage], and q 15 [2nd stage]
Flexion As head meets resistance of birth canal  Electronic fetal monitoring: q 15 mins [1st stage], and q 5 mins [2nd stage]
Internal rotation Occiput gradually moves anteriorly towards symphysis  Non-stress test: normally there is acceleration in FHR of > 15 bpm above baseline for
Extension Delivery of fetal head occurs at least 15 secs.
External rotation Head undergoes restitution [rotation of head back o its original position] o If at least 2 such acceleration occurs in a 20 mins interval, the fetus is deemed
Expulsion healthy and the test is reactive.
o A non-reactive test may imply that fetus is acidotic, asleep, or drugs administered
 Mechanism of placental extrusion: to mother.
Schultze mechanism Duncan mechanism  Contraction stress test / Oxytocin Challenge test: measure of the uteroplacental
Central type of placental separation Peripheral type of separation function
Fetal surface of placenta Dirty maternal surface o Evaluates reaction of heart rate to contractions induced by nipple stimulation or
oxytocin administration.
 Uterine phases of parturition: o Done when frequency is 3 contractions/10 mins
Phase 1 Prelude to parturition, phase of myometrial smooth muscle o Interpretation:
unresponsiveness and cervical rigidity Positive Consistent & persistent late decelerations of FHT in absence
Phase 2 Morphological and functional changes in myometrium and cervix occur in of uterine hypertonus or supine hypertension
preparation of labor Negative At least 3 contrations in 10 mins, each lasting 40 secs, without
Uterine changes: late deceleration
1. ↑ myometrial oxytocin receptors Suspicious Inconstant late deceleration
2. ↑ gap junctions btw myometrial cells Hyperstimulation Uterine contractions occur more frequent than 2 mins or lasting
3. uterine irritability longer than 90 secs or presence of uterine hypertonus
4. ↑ responsiveness to uterotonics Unsatisfactory Frequency of contractions is < 3 per minutes or tracing is poor
5. formation of LUS
Cervical changes  5 parameters in BPP [read p. 15 of OB-GYN handy notes]: fetal breathing movements
1. collagen breakdown and rearrangement [chest wall], fetal activity [trunk/limb], amniotic fluid index, fetal tone [flexion/extension of
2. ↑ hyaluronic acid and ↓ dermatan sulfate lower extremities], reactivity NST]
Phase 2 Period of uterine contractions w/c causes:  The physiologic basis for using BPP lies in the fact that coordinated fetal activities require
1. cervical dilatation and effacement an intact, non-hypoxic CNS.
2. fetal descent  Reactivity and the normal FHR: normal FHR = 110-160 bpm, baseline refers to a heart
3. delivery of conceptus rate lasting > 10 mins.
Phase 3 Events of puerperium  A fetus < 28 wks GA is neurologically immature and thus is not expected to have a
1. maternal recovery from childbirth “reactive” FHR.
2. maternal contribution to infant survival  Early decelerations: are normal and due to head compressionduring contractions.
3. restoration of fertility

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  Late decelerations: are abnormal and due to uteroplacental insufficiency during Stages Features Nullipara Multipara
contractions. Stage 1 Cervical effacement & dilatation to full dilatation 8 hrs 5 hrs
 The lateral recumbent position [either side] is best for maximizing cardiac output and a. Uterine contractions q 2-3 mins x 40-60 secs
uterine blood flow [in supine position, the vena cava and aortic vessels may be b. FHT q 15 mins
compressed by the gravid uterus] c. I.E q 2 hrs [dilatation should be 1-2 cm/hr]
 Variable decelerations are abnormal and can be mild or severe and are due to d. artificial amniotomy can be done at 4 cm
compression and sometimes head compression. Stage 2 From full dilatation to fetal expulsion 50 mins 20 mins
 Classification of variable decelerations: Contractions are q 1-2 mins x 90 secs
Mild variability < 30 secs and depth > 70-80 bpm Dorsal lithotomy position [to ↑ pelvic diameter]
Moderate variability 30-60 secs and depth < 70-80 bpm Crowning occurs, fetal head delivery by Ritgen’s
Severe variability > 60 secs and depth < 70 bpm maneuver, suctioning and cord care
Stage 3 From delivery to placental expulsion
 Amnioinfusion: infuse normal saline into the uterus thru the intrauterine pressure catheter Schultze – at central placental part, Duncan –
to alleviate cord compression. occurs at the periphery & descends sideways
 Fetal tachycardia: mild = 161-180 bpm, severe > 181 w/c may indicate intrauterine Stage 4 Occurs 1 hr after placental delivery, critical to
infection, severe fetal hypoxia, CHD, or maternal fever. identify postpartum hemorrhage sec. to atony,
 Beat-to-beat variability: single most important characteristic of the baseline FHR. mg by massage, ice packs, and oxytoxics
 At < 28 wks GA, the fetus is neurologically immature, thus decreased variability is
expected.  Signs of placental separation:
 Long-term variability = 3-6 cycles/min. 1. calkin’s sign – uterus becomes globular and firmer
 If an FHR of 160 bpm lasts for > mins, then tachycardia is present. 2. sudden gush of blood
3. uterus rises in abdomen as deched placena drops to lower segment & vagina
 Beat-to-beat variability can be reliably determined only w/ internal FHR monitoring.
4. lengthening of umbilical cord & protrudes out of the introitus
 Prolonged decelerations: isolated decelerations that last 2-10 mins.
 Indications for CS hysterectomy:
 Short-term variability is thought to be the most important predictor of fetal outcome.
1. arrest hemorrhage from uterine atony
 If deceleration has occurred w/o recovery after 2 mins, an emergency C-section is 2. lower segment bleeding
required. 3. laceration of major uterine vessel
 Scalp deceleration is done between decelerations to elicit a reactive acceleration and rule 4. large myoma
out metabolic acidosis. 5. cervical dysplasia /CIS
 Fetal lung maturity must be confirmed before elective induction at < 39 wks AOG, unless
lung maturity can be inferred from other maturity criteria.  Types of lacerations of vagina & perineum:
 Candidates for VBAC: 1 or2 prior LTCS, clinically adequate pelvis, no other uterine scars 1st degree Fourchette, perineal skin, vaginal mucosa [not underlying fascia & muscle]
or previous rupture. 2nd degree Involve fascia & muscle of perineal body but not the anal sphincter
 Contraindications for VBAC: prior classical or T-shaped incision or other transfundal 3 degree
rd From vaginal mucosa, perineal skin, fascia, up to anal sphincter [not rectum]
uterine surgery, contracted pelvis, medical/obstetric complication that precludes vaginal
4 degree
th Extension up to rectal mucosa [repaire first before the vaginal mucoosa]
delivery.
 Prerequisites for forceps delivery: a fully dilated cervix, ROM, engaged fetal head, > +2
 Types of incisions;
station, no cephalopelvic disproportion, empty bladder, and vertex presentation.
Kronig’s incision Vertical incision at LUS
 If delivery occurs w/in 1 hour of analgesia, neonatal depression may occur.
Kerr incision Transverse incision at LUS
 Prophylactic measures against aspiration include fasting for at least 6 hrs prior to
anesthesia and antacid administration before induction. Transverse/Pfannenstiel Curvilinear incision
Maylard incision Transverse incision w/ the rectus divided

 Types of episiotomies:
Chapter 19: Mechanism of labor in Occiput or Vertex presentation
Median type Less painful, easy to repair, heals faster but
 Fetal lie - - relation of long axis of fetus to long axis of mother
may extend to rectum if perineal body is short
Longitudinal lie [99%] Long axis of fetus parallels to long axis of uterus
Mediolateral type Used more often
Transverse lie [< 1%] Lies in transverse to 1 of the oblique diameters of uterus
Oblique lie – a variant, unstable
Chapter 22: Analgesia and anesthesia
 For painless labor
 Presentation – part of fetus lying over the inlet o Meperidine: 50-100 mg [Demerol] – readily crosses placenta
o Cephalic [95% of cases]: o Promethazine: 100 mg [Phenergan]
Type Presenting diameter Features o Butorphanol: 1-2 mg – neonatal depression is lesser
Vertex/occiput Suboccipitobragmatic = 9.5 cm Occiput [posterior fontanelle] =PF o Nalbuphine; 15-20 mg, no neonatal depression
Sinciput/mliary Occipiofrontal = 12.5 cm Bregma [anterior fontanelle] =PF o Fentanyl: 50-100 ug
Brow Occipitomenal = 13.5 cm Converted to face by extension o Naloxone: reverses respiratory depression
Face Submentobregmatic = 9.5 cm CS due to ↑ risk of SC injury  Measures important for effective prophylaxis:
o Fasting from solids at least 8 hrs and preferably longer before anesthesia
o Breech [5% of cases] – complication is cord prolapse or entanglement o Use of agents to reduce gastric acidity during induction and maintenance of general
Frank Thighs are flexed on abdomen, legs are extended over anterior anesthesia
breech surface of the body, thus feet of fetus lies close to the head o Skillful tracheal incubation, accompanied by pressure on cricoid cartilage to occlude
Complete Thighs are flexed on abdomen, legs are flexed on thighs and feet esophagus [Sellick maneuver]
breech presents a level of the buttocks o After intubation and during surgery, passage of NGT to empty stomach of all contents
Incomplete 1 or both thighs are extended so that fee and legs are below the o Awake extubation w/ protective airway reflexes intact
breech level of the buttocks o Use of regional techniques when appropriate
o Shoulder or acromion presentation Regional anesthesia
o Compound presentation: prolapse of fetal hand alongside the presenting vertex or  Uterine innervation – pain during 1st stage of labor generated largely from uterus → pain
breech or foot alongside the head. of uterine contractions thru 11th-12th thoracic nerves
 Lower genital tract innervation – pain transmitted thru pudendal nerve w/c posterior
 Position – relation of point of direction to 1 of the 4 quadrants or to transverse diameter of surface of sacrospinous ligament as it attaches to the ischial spine
maternal pelvis. I. Local infiltration
 Points of direction: occiput in cephalic, mentum/chin in face, sacrum in breech, acromion  Lidocaine - most commonly used local anesthetic
in shoulder [LOT is the most common presentation]. II. Pudendal block [S2-4]
 Fetal Attitude [posture/habitus] – relation of fetal parts to 1 another  Goal: to block the pudendal nerve distal to its formation by anterior division of S2-S4 but
proximal to its terminal branches
Chapter 13; Conduct of normal labor and delivery  Maternal complications are uncommon
 Difference between false and true labor [read p. 21 of OB-GYN handy notes]  MC used anesthetic is lidocaine
 Duration of the stages of labor in nulliparas and multiparas  Complication: hematoma formation, convulsion, infection
 3 stages of labor: III. Paracervical block

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  Provides pain relief during 1st stage of labor  Outlet contraction:
 Complication: fetal bradycardia o Interischial tuberous diameter of < 8 cm
IV. Spinal [subarachnoid] block [T8]
 Low spinal block is popular form of analgesia for forceps or vacuum delivery Active phase disorders
V: Epidural anesthesia [T10-S5]  Before diagnosis is made during 1st stage of labor, both of this criteria should be met:
 Complete analgesia for pain of labor & vaginal delivery necessitates block from T10-S5 o Latent phase has been completed, w/ cervix dilated 4 cm or more
o Uterine contraction pattern of 200 montevideo units or more in 1-10 minute period has
POSTPARTUM been present for 2 hours w/o cervical change
 Within 2 weeks, the uterus has descended into the cavity of the true pelvis. Precipitate labor
 When involution is defective, late puerperal hemorrhage may occur.  Effects:
 Rugae reappear by 3rd week. Maternal effects Fetal effects
 Colostrum can be expressed from the nipple by 2nd postpartum day and is secreted by Uterine rupture, exensive Hypoxia, intracranial trauma, Erb-
breasts for 5 days postpartum. laceration, AFE Duchenne palsy
 Colostrum is then onverted to mature milk by 4 weeks postpartum.
 All vitamins except vitamin K are found in human milk. Nulliparas Cervical dilatation 5m/hr or faster
 Women w/ extensive pituitary necrosis [Sheehan syndrome], cannot lactate due to Multiparas Cervical dilatation 10 cm/hr
absence of prolactin.
 Episiotomy incision is typically well-healed and asymptomatic by week 3 of the Chapter 44: Dystocia due to abnormal presentation, position nd development of fetus
puerperium.  Face presentation – w/ head hyperextended so occiput is in contact w/ fetal back
 Ensure that postpartum woman has voided w/in 4 hrs of delivery.  Brow presentation – the portion of fetal head btw he orbital ridge and anterior fontanelle
 Continue iron until 3 mos. postpartum. presents at the pelvic inlet
 After 6 weeks, coitus may be resumed based on pxs desire and comfort.  Transverse lie/shoulder/acromion presentation – long axis of fetus is perpendicular to that
of mother
Chapter 24: Puerperium  Compound presentation – an extremity prolapses alongside the presenting in the pelvis
 Urinary retention in the 1st 24 hrs is due to: simultaneously
1. edema & congestion of vulva, urethra, bladder trigone  Persistent occiput posterior position – may be due to transverse narrowing of the
2. edema & reflex spasm of urethral sphincter midpelvis
3. bladder atony  Deep transverse arrest of the head – associated w/ platypelloid and android pelvis,
 diuresis is greatest from 2nd to 5th day caused by hypotonic uterine dysfunction
 Types of lochia [discharge from uterus after delivery lasting 4-8 wks]:  Shoulder dystocia management:
Lochia rubra 1st 3-4 d Reddish discharge McRobert’s ‘exagerrated lithotomy”, involves flexing thigh upon her own abdomen
Lochia serosa Next 3-4 days Paler & pinkish discharge Wood-Corkscrew Progressively rotating the posterior shoulder 180 degrees in
Lochia alba From 10 day
th Lighter yellow & creamy color maneuver corkscrew fashion
Rubin maneuver Fetal shoulders rocked from side to side applying force on mother’s
 After pains – due to uterne contraction, more intense during breastfeeding abdomen
 Constipation due to pxs inactivity, decrease intraabdominal pressure after delivery & Hibbard maneuver Pressured is applied to infant’s jaw and neck in the direction of
painful perineum mothers rectum
 Weight loss: normal non-pregnant weight is attained in 6 mos. Zavanelli Cephalic replacement into the pelvis followed by cesarean delivery
Average loss of 5 kgs Immediately after delivery
Additional loss of 3 kgs Due to diuresis and skin loss Fetal developmental anomalies
 Fetal macrosomnia – defined as fetal weight > 4,000 gms, possibly due to DM, multiparity,
 Postpartum check-up in 4-8 wks, PAPsmear at 6 mos. large parents/genetic, or postdatism
 Other events after delivery:  Hydrocephalus – consider cephalocentesis & CS delivery; prognosis: uterine rupture
2 wks Uterus descends into the umbilicus, CO returns to normal  Large abdomen – for transabdominal decompression
3 wks Entire endometrium is restored  Conjoined twins
4 wks Uterus regains non-pregnant size
Dystocia due to abnormalities of Pelvis
6 wks Complete extrusion of placental site
 Bony dystocia: contracted inlet, outlet and midpelvis [see clinical pelvimetry]
2-8 wks Dilaed ureters and pelvis return at prepregnant state
 Soft tissue dystocia: uterine myomas or prolapse, cervical stenosis, transverse septum or
6 mos. May approach prepregnant weight
vagina, cystocele, rectocele
2 wks Coitus may be resumed depending on px desire
6-8 wks Return of menstruation and ovulation Chaptter 43: Dystocia due to Abnormality of Powers
 Dystocia/difficult labor is the MC indication for primary CS
PATHOLOGIC OBSTETRICS
 Classification:
A. disorder of preparatory division Nullipara Multipara
Chapter 45: Dystocia, abnormal labor and feto-pelvic disproportion
Prolonged latent phase > 20 hrs > 14 hrs
 Types of uterine dysfunction:
B. protracted active phase of dilatation < 1.2 cm/hr < 1.5 cm/hr
Hypotonic uterine dysfunction Hypertonic uterine dysfunction
C. disorders of pelvic division
No basal hypertonus and uterine Incoordinated uterine dysfunction
Prolonged deceleration phase > 3 hrs > 1 hr
contraction have a normal gradient Either basal tone is elevated or pressure
Secondary arrest of dilatation > 2 hrs > 2 hrs
Occurs during active phase of labor gradient is distorted
Arrest of descent > 1 hr > 1 hr
Responds to x w/ oxytocin Occurs during latent phase
Failure of descent No descent No descent
Usually responds w/ sedation
D. precipitate labor disorders
Precipitate dilatation > 5 cm/hr > 10 cm/hr
 Estimation of fetal head size [Mueller-Hillis maneuver] Precipitate descent > 5 cm/hr > 10 cm/hr
o W/ internal examining fingers note the fetal presenting part in relation of the ischial
spines [station] while thumb is placed over the symphysis pubis to note the degree of
Chapter 47: Forceps Delivery and Vacuum Extraction
overlapping.
 Obstetric forceps
 Pelvic inlet contraction:
 Types of obstetric forceps
o If diagonal conjugate is < 11.5 cm
o Borderline if AP diameter of inlet is 10 cm Molded Simpson’s forceps
o Severe if AP diameter is < 9 cm Rounded Tucker’s forceps
 Midpelvic contraction: For aftercoming head Piper’s forceps
o If sum of interischial spinous diameter [10.5 cm] and posterosagital diameter of For transverse arrest Barton’s forceps
midpelvis [5 cm] falls to 13.5 cm and below  [Refer to p. 45 of OB-GYN handy notes for ACOG classification of Forceps delivery]
o Interischial diameters is < 10 cm  Prerequisites:
o Prominent ischial spines, convergent sidewalls, narrow sacrosciatic notch on vaginal 1. head must be engaged
exam 2. fully dilated cervix

7
 3. known position of vertex  Classification of hypertensive disorders [refer to p. 37 of OB-GYN handy notes]
4. ruptured membranes  Pathophysiology:
5. no CPD o Trophoblastic hypoperfusion, w/ ibgrowth of trophoblastic cells into tunica media of
6. vertex or mentum anterior spiral arterioles results in denervation & loss of muscular and elastic components
causing thinning of walls, dilation & elongation to a “ corkscrew or saw-toothed
Chapter 46: Breech presentation and delivery configuration
 Methods of vaginal breech delivery o Prostacyclin deficiency + abnormal arterioles result in a state of relative
Spontaneous Infant is expelled entirely spontaneously w/o any traction or vasoconstriction
breech delivery manipulation other than support of the infant  Changes in preeclampsia:
Partial breech Infant is delivered spontaneously as far as the umbilicus, but the o ↓ antithrombin 3 and ↑ fibronectin
extraction remainder of the body is extracted/delivered w/ operator traction o ↓ pasma levels of rennin, angioensin 2, and aldosterone, ↑ ADH
Total breech Entire body of the infant is extracted by the obstetrician o ANP is released upon arterial wall distention
extraction o Glomerular capillary wall distention
o Periporal hemorrhagic necrosis – pahognomonic of preeclampsia
 Mechanism of breech delivery: o Subcapsular hematoma w/ epigastric or RUQ pain
Lovesets Delivery of posterior shoulder ahead of the anterior o Principal cerebral lesions: amaurosis and retinal detachment
Kristeller’s The head may be delivered by suprapubic pressure  Roll-over test: increase of at least 20 mmHg in DBP from a left lateral decubitus position to
supine is a positive test
 Methods of delivery of the head:  MAP test = DBP + 1/3 SBP or 1/3 [SBP + 2DBP]
Piper’s forceps Preferred method, the head well engaged, occiput diretly anterior, blades o MAP 2nd trimester = > 90 mmHg, or MAP 3rd trimester = > 105 mmHg predict future
of head PIH.
Mauriceau- The body of the baby is placed on arm of the operator w/ index and the Management:
smellie-veit middle fingers over malar bones  Control of HPN:
o Hydralazine [apresoline] = 5 mg IV bolus w/ increments of 5 mg q 30 mins if DBP does
Bracht Breech is allowed to deliver spontaneously to navel
not improve up o total of 20 mg dose
Prague Body is swung over the mother’s abdomen
o Beta-blockers and Ca+ channel blockers: nifedipine or nicardipine
Pinnard Hand is introduced inside the uterus to reach for popliteal fossa
o ACE inhibitors are not recommended in pregnancy.
 Control of convusion:
 Entrapment of the aftercoming head: o Magnesium sulfate [DOC] = loading dose of 4 g IV bolus + 10 g IM [5g per buttock];
Durhssen’s incision Cervix should be made 7 cm dilated, 3 incisions made 2,6 and 10 maintenance dose = 1-2 g/hr IV drip or 5 g IM q 6 hrs [monitor toxicity using DTR, RR
o’ clock positions > 12, UO >100 cc/4 hrs]
Abdominal rescue Replacement of fetus higher into the vagina and uterus, followed  Optimum time & mode of delivery
by CS delivery  Prevention: low dose aspirin, high dose Ca+
Chapter 48: Cessarean section Chapter 26: Obstetrical hemorrhage
 Delivery of fetus thru abdominal incision [laparotomy], followed by incision of uterine wall  Placenta previa: bleeding due to separation of placenta implanted in the immediate
[hysterotomy]. vicinity of cervical canal.
 [Refer to p. 46 of OB-GYN handy notes for indications of CS delivery] o Bleeding is proportionate to blood loss, usually painless & occurs at 3rd trimester
 Techniques in CS: o [Refer to page 35 of OB-GYN handy notes for differentiation btw placenta previa
o Types of abdominal incision: and abruption placenta].
Median infraumbilicallongitudinal incision o Dx; double set-up, UTZ, MRI
Transverse suprapubic incision More difficult but is stronger & w/ o Types of placenta previa:
Or Pfannenstiel/Bikini type less dehiscence Total placenta previa Internal os is completely covered by placenta
Partial placenta previa Internal os is partially covered by placenta
o Types of uterine incision: Marginal placenta Edge of placenta is at the margin of internal os
Classical CS Longitudinal incision above LUS, strong tendency to rupture Low-lying placenta Placenta implanted at the LUS such that the placental edge
Low-segment incision Low tendency to rupture actually does not reach the internal os but is in close proximity to it
Low transverse/ kerr Preferred due to only moderate dissection of the bladder
Low longitudinal/kronig More bladder dissection but can be extended  Abruption placenta: bleeding may come from separation of placenta located elsewhere
in the uterine cavity, occurs after 20th wk of pregnancy and before birth of fetus
 Vaginal birth after a CS/VBAC: allow a trial of labor under double set-up for all previous o MC etiology is preeclampsia.
CS of 1 low segment incision after excluding in adequate pelvis & unless new indication o Bleeding is proportionate to placental separation.
arises. o Types of abruption:
External Bleeding passes btw membranes and uterus and escapes thru the cervix
Chapter 35: Hypertensive disorders Concealed If it extravasates into amniotic cavity after breaking the membranes, placenta
 Classification: is completely separated yet membranes retain their attachment to uterine wall
Hypertension A BP of at least 140 mmHg or 90 mmHg diastolic, previously defined by Marginal Placental separation is limited to the margin w/ minimal bleeding but w/o
an increase of 30 mmHg systolic or 15 mmHg diastolic over baseline uterine tenderness and pain
values  Vasa previa: bleeding may be the consequence of velamentous insertion of umbilical
Gestational HPN w/o proteinuria occurring after 20 wks AOG or postpartum, BP cord w/ rupture and hemorrhage from a fetal blood vessel at the time of rupture of the
HPN returns to normal < 12 wks postpartum membranes.
Preeclampsia Presence of HPN + proteinuria [300 mg/24 hr or +2 dipstick] occurring  [Read on Handy notes OB-GYNE for classification of abruption placenta p. 34]
after 20 wks AOG except in cases of extensive trophoblastic proliferation  Complications of abruption placenta:
Superimposed ↑ of at least 15 mmHg diastolic or 30 mmHg systolic over baseline o Couvelaire uterus/uterine apoplexy: in w/c the entire uterus may undergo bluish,
preeclampsia hypertensive BP levels purple or copper discoloration due to blood extravasation into myometrium and uterine
Eclampsia Presence of convulsions in a woman w/ preeclampsia serosa.
Superimposed Convulsions + superimposed preeclampsia o Acute renal failure: due to reduced CO and intrarenal vasospasm due to massive
ecclampsia hemorrhage.
Chronic HPN Presence of 140/90 mmHg or greater prior o pregnancy or is detected o DIC
before the 20th wk of pregnancy and persists long after delivery  Complications of placenta previa:
o Placenta accrete
 Severe preeclampsia – presence of one or more of the ffg: o Postpartum hemorrhage
1. SBP of 160 mmHg or DBP of 110 mmHg o IUGR
2. proteinuria of at least 4 g/d or +2, w/ renal involvement o Congenital abnormalities
3. oliguria of < 400 cc/day  IUFD
4. severe headache or visual disturbance o Absence of fetal movement
5. pulmonary edema or cyanosis; IUGR o Confirmed by:
6. HELLP syndrome – hemolysis, elevated liver enzymes & low platelet count 1. spalding’s sign [7 days after fetal death] – opening of the fontanelles
2. hyperflexion of spine

8
 3. crowding of rib shadow Amnionic cysts Results from fusion of amnionic fold, w/ fluid retention
4. robert’s sign Amnion nodosum Made up of fetal ectodermal debris including vernix caseosa w
o Mgt: delivery hair, squames and sebum
o Compication: DIC Amnionic bands May adhere to fetus and impair growth and development of
 Uterine rupture involved structure
o Complete rupture: uterus may communicate directly w/ the peritoneal cavity
o Incomplete rupture: may be separated from peritoneal cavity by visceral peritoneum  Normal Amniotic fluid volumes:
over the uterus or of broad ligament. o Maximum amniotic fluid is at 28 wks; 800 ml
o After 28 wks, amniotic fluid decreases.
Chapter 37: Preterm Birth o At 40 wks, amniotic fluid is at 500 ml.
 Preterm = < 37 wks AOG but > 20 wks AOG  Abnormal amniotic fluid volumes:
 Average birthweight for Filipinos is 2,275 gms o Normal vertical fluid pocket [VFP]= 2-8 cm
 Survival is feasible at 26-27 wks AOG o Oligohydramnios: < 4-5 AFI [VFP = < 2 cm]
 Dx:  MC cause; rupture of membranes
o Regular uterine contractions 5-8 mins or less apart accompanied by 1 of the ffg.  Clinical correlates: IUGR, dysmaturiy syndromes, renal agenesis, urinary tract
1. progressive change in cervix obstruction, pulmonary hypoplasia
2. cervical dilatation of 2 cm or more o Polyhydramnios: > 20-24 AFI or 2 L [VFP = > 8 cm]
3. cervical effacement of 80% or more  Clinical correlates: GI abnormalities, anencephaly, spina bifida, DM, erytroblastosis
o Passage of cervical mucus; low back pains, pelvic pressure, menstrual-like or fetalis, TEF, esophageal aresia
intestinal cramps  Classification:
 Mgt: repair of incompetent cervix, combat infection, tocolytics Mild 8-11 cm
 Tocolytic agents are of greater benefit if given 32-34 wks AOG, includes: Moderate 12-15 cm
o Beta-adrenergic agonists – reduce myometrial contractility by decreasing intracellular Severe > 16
Ca+ & reducing effect of Ca+ on myometrial activation [ex. isoxuprine/duvadilan]
o Magenesium sulfate  Aniotic fluid index [AFI] – summation of the largest vertical pockets of 4 quadrans
o Prostaglandin inhibitors – indomethacin of uterus.
o Ca+ channel blockers  Placentomegaly > 600 gms
 Types of placental abnormalities:
Chapter 38: Post-term Pregnancy [> 42 wks] Placenta succenturiata w/ accessory lobe outside main disc
 Mgt: Extrachorial placenta Membranes do not insert at disc
1. assessment of true gestational age 1. circummarginate Membranes w/o thickening
2. px counseling regarding induction of labor vs. conservative mgt. 2. circumvallate Membranes arise from a cup
3. antepartum surveillance tests: fetal movement counting, NST/CST, FAST, BPP + AFI
Placenta accreta Villi contiguous w/ myometrium
Placenta increta Villi invade the myometrium
Chapter 39: Fetal Growth Disorders
Placent percreta Villi penetrates serosal surface of myometrium
Intrauterine Growth Retardation
 Types:
 Abnormal shapes:
Symmetric IUGR / Insult early in gestation w/ equal decrease in HC, weight & length
type 1 such as in chromosomal anomalies Succenturiate 1 or more small accessory lobes developed in he membranes at a
placenta distance from the periphery of the main placenta
Asymmetric IUGR Insult of later onset such as maternal disease, presents w/ a
/ type 2 characteristic “head sparing” Ring-shaped Because of atrophy of the tissue of the ring
placenta
Membranaceous Placenta develops into a thin membranous structure
 Dx: UTZ measurement of increase in biparietal diameter
Placenta
1. < 2 mm/wk from 13th-34th wk
2. < 1 mm/wk from 35th wk to term Fenestrated The central portion of discoidal plaenta is missing
Circumvallate Placenta presents a central depression surrounded by a thickened,
Chapter 36: Multifetal Pregnancy grayish white ring
 Classification: Circummarginate Ring coincides w/ placental margin
Dizygotic twins Results from maturation and fertilization of 2 separate ova during
[fraternal twins] a single ovulatory cycle  Abnormal adherence:
Monozygotic twins Results from twins that may arise from a single fertilized ovum Accreta Placental villi attached to myometrium
Increta Placental villi invade the myometrium
 Factors: race, heredity, age > 35, parity > 4, maternal size & nutrition, use of ovulating Percreta Placental villi penetrate the myometrium
drugs [clmiphene, gonadotropins]  A consequence of partial or total absence of the decidua basalis and imperfect
 Types: development of fibrinoid layer [Nitabuch’s layer]
1. double ovum w/ 2 chorions, 2 amnions & 2 placenta  Dx: UTZ = lack of usual subplacental sonolucent space or “hypoehoic retroplacental zone”
2. double ovum w/ 2 chorions, 2 amnions & 1 placenta  Safest treatment is prompt hysterectomy.
3. single ovum w/ 2 chorions, 1 amnion & 1 placenta
4. single ovum w/ 1 chorion, amnion & placenta Abnormalities of Umbilical Cord
 Presentation and incidence:  Mean length of umbilical cord: 55-60 cm, >70 [long cord], < 32 [short cord]
o Cephalic-cephalic: 42% Marginal insertion Cord insertion at placental margin , aka Battledore placenta
o Cephalic-breech: 27% Velamentous insertion Umbilical vessels separate in the membranes at a distance from
o Cephalic-transverse: 18% the placental margin
o Breech-breech; 5% Vasa previa Associated w/ velamentous insertion when some of the fetal
 Fetal complications: vessels in membranes cross the region of the internal os and
1. IUGR occupy a position ahead of the presenting part
2. Intertwining of umbilical cords
3. DIC following deah of a twin  Cord abnormalities impending blood flow:
4. collision [both twins in cephalic presentation] & interlocking [chin to chin lock] Knots False knots – due to kinking of vessels to accommodate the length of the cord
5. anomalous anastomotic vascular connections → “twin-twin transfusion syndrome” – True knots – due to active fetal movements
discordant twins w/ larger twin developing hydramnios + polycythemia while smaller Torsion As a result of fetal movements, the cord becomes twisted, fetal circulation
twin develops oligohydramnios + anemia becomes compromised
 Anesthesia and analgesia: epidural anesthesia – preferred Stricture Associated w/ extreme focal deficiency in Wharton jelly, usually assoc. w/ torsion
 Route of delivery: CS – preferred Hematoma Result from rupture of varix [ umbilical vein], w/ effusion of blood into the cord
Cysts True cysts – from remnants of umbilical vesicle or of allantois
Chapter 29: Abnormalities of the Placenta, Fetal Membranes & Amniotic fluid False cysts – from liquefaction of Wharton jelly
Meconium staining Stained amniotic membranes w/in 1-3 h after meconium passage Edema Associated w/ edema of fetus, common w/ macerated fetus
Chorioamnionitis Associated w/ prolonged membrane rupture w/ long membranes
Criteria: Fever > 38, tachycardia [fetal/maternal], maternal leukocytosis

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Chapter 30: Gestational Trophoblastic Disease 1. + cervical glands opposite the placental attachment
 Refers to proliferative abnormalities of trophoblast w/c retains its ability to secrete HCG. 2. whole part of the placenta must be situated below the entrance of uterine vessels
 Classification of GTD [refer to p. 29 of OB-GYN handy notes] or below the entrance of uterine vessels
 Complete vs. partial H. mole [refer to p. 30 of OB-GYN handy notes] 3. attachment of placenta to cervix must be intimate
 FIGO staging for trophoblastic disease [refer to p. 30-31 of OB-GYN handy notes] 4. fetal elements must not be present in corpus uteri
 Most malignant type of GTT is choriocarcinoma  Ovarian pregnancy
 Classic S/sx for complete H. mole: toxemia before 24 wks AOG, uterus large for dates, o Spiegelberg criteria:
absent FHT and fetal parts 1. tube including fimbria ovarica is intact
 Histological structure of complete H. mole: 2. gestational sac is in normal anatomic location of ovary
o Hydrophic degeneration and swelling of the villous stroma 3. the sac is connected to uterus by ovarian ligament
o Absence of blood vessels in the swollen vili 4. definitive ovarian tissue is histologically demonstrated in sac wall
o Proliferation of trophoblastic epithelium to a varying degree  Abdominal pregnancy
o Absence of fetus and amnion o Sonographic criteria:
 Classic UTZ finding; ‘snow-storm pattern” 1. visualization of fetus separate from uterus
 Mgt: 2. failure to visualize the uterine wall between the fetus and urinary bladder
o Replacement of blood loss 3. close approximation of fetal parts to the maternal abdominal wall
o Combat infection if present 4. eccentric position or abnormal fetal attitude and visualization of extrauterine
o Termination of pregnancy either by suction curettage or hysterectomy placental tissue
o Prophylactic chemotherapy [Contraindicated if: hb , 10 gml, WBC < 3 x 10 9/l, platelets o Studdiford criteria:
< 100, 000 m3, and if w/ [+] liver or renal fxn test impairment 1. Tubes appear to normal w/ no evidence of recent or past injury
o Follow-up for signs of persistent disease: 2. There is no uteroplacental fistula or evidence of uterine rupture
3. The pregnancy is exclusively attached to peritoneal surfaces and is early enough
HCG Weekly until normal x 2 values, then q 2 wks x 3 mos, then q
to eliminate the possibility of secondary implantation following tubal nidation
determination monthly x 6-12 mos, then q 6 mos x 1-2 yrs, hen annually
CXR Initially then repeat if abnormal or if HCG plateus or rises
Chapter 41: Congenital Anomalies & Abnormalities of Reproductive tract [read APMC]
Contraception For 1 yr because pregnany will increase HCG levels
 Imperforate hymen
Pelvic exam Q 2 wks until normal then q 3 mos o Primary amenorrhea [cryptomenorrhea] w/ cyclic, crampy pain at puberty
Chapter 31: Gestational Trophoblastic Tumors o Sx: hematocopos → hematometra → hematosalpinx → endometriosis/endometritis
 Hammonds classification of GTT [refer to p. 33 of OB-GYN handy notes] o Bulging membrane at introitus is tx w/ hymenotomy.
 Chemotherapeutic drugs used [refer to p. 33 of OB-GYN handy notes]  Transverse vaginal septum
Type Features Treatment o Associated w/ intrauterine DES exposure
Invasive Invasion of H. mole deep into uterine wall Single-agent chemotherapy o Site: upper 3rd and lower 2/3 of vagina
mole S/Sx: irregular bleeding w/in 6 mos. of [methotrexate] or o Same Sx w/ imperforate hymen, tx by excision
molar evacuation hysterectomy  Mullerain fusion anomalies
Chorio- Syncitiotrophoblast + cytotrophoblast, hx: Chemotherapy – single/multi Complete duplication Asymptomatic
carcinoma exuberant rophoblastic growth w/o villi Hysterectomy Non-communicating uterine horn Cyclic pelvic pains, pelvic mass & ectopic pregnancy
Septate/bicornuate uterus Reproductive wastage, uterine dysfunction, abnormal
Chapter 27: Abortion fetal presentation
 Refers to termination of pregnancy before 20 wks AOG, or delivery of fetus < 500 gms
 Comparative analysis of different types of abortion [refer to p. 27 of OB-GYN handy Chapter 15: Teratology, Drugs, and Medications
notes] Category A Controlled studies in humans have been demonstrated no fetal risk
 Etiologic agents for septic abortion: Category B Animal studies indicate no fetal risk, but there are no human studies or adverse
Anaerobic B. fragilis, strep, clostridium weichii, tetanus effects have been demonstrated in animals, but not in well-controlled
Aerobic e. coli, klebsiella, staph, pseudomonas Human studies
Category C No adequate studies, either animal or human, or there are adverse effects in
 60% of spontaneous abortions in the 1st trimester are a result of chromosomal animal studies but no available human data
abnormalities. Category D Evidence of fetal risk, benefits outweigh the risks
 94% of abortions occur in 1st trimester. Category X Proven fetal risks clearly outweigh any benefits
 Women w/ hx of recurrent abortion have 23% chance of abortion in subsequent
pregnancies that are detectable by UTZ. MEDICAL CONDITIONS AND PREGNANCY
 MC cause ofhabitual or recurrent abortion is Antiphospholipid antibody syndrome/APAS  MC medical complication in pregnancy: diabetes
 Presence of blighted ovum is seen in Inevitable abortion.  Gestational DM probably results from placental lactogen secreted during pregnancy; w/c
has large glucagons-like effects.
Chapter 28: Ectopic pregnancy  Insulin does no cross the placenta → feal hyperglycemia
 Refers to implantation of fertilized ovum outside endometrium.  [Refer to p. 39 of OB-GYN handy notes for Criteria in Dx of GDM]
 Ectopic pregnancy is the leading cause of pregnancy-related death during 1st trimester.  The CNS anomaly most specific to DM is caudal regression.
 Heterotopic pregnancy – simultaneous intrauterine & ectopic pregnancies.  Grave’s disease is the MC cause of thyrotoxicosis in pregnancy. Tx is PTU [drug of
 MC cause is salpingitis or PID. choice] and methimazole.
 Classic triad of Sx: colicky abdominal pain [MC], amenorrhea for 6 wks followed minimal  Sheehan’s syndrome: pituitary ischemia and necrosis associated w/ obstetrical blood loss
vaginal bleeding leading to hypopituitarism. Pxs do not lactate due low levels of prolactin.
 Classic signs: wiggling tenderness [MC], uterus smaller than AOG, fullness of cul-de sac  MC serious medical complication of pregnancy and occurs in 1-2% of pregnant women:
[due to hemoperitoneum] acute pyelonephritis
 Dx:  MC surgical condition in pregnancy: appendicitis
HCG & progesterone Low levels  The 2 MC causes of anemia during pregnancy and puerperium are IDA and acute blood
UTZ criteria [+] adnexal mass, no gestational sac when loss.
HCG levels > 2,500 mIU/ml at 5-6 wks
URINARY TRACT IFECTIONS AND PREGNANCY
 The presence of intrauterine gestational sac rules out ectopic except in heterotopic  Asymptomatic bacteriuria
pregnancy. o Dx:
 Mgt: 1. absence of Sx
Unruptured Medical – methotrexate [for rapid absorption of placental tissue], RU- 2. > 100,000 cfu/ml w/ 1 or more organisms in 2 consecutive midstream specimens or
486 [competes for progesterone binding sites], 1 cathetherized specimen
Surgical – partial salpingectomy, salpingostomy, salpingotomy 3. screening should be done at 1st prenatal visit esp. for diabetics & those w/ previous
Ruptured Radical hysterectomy, total salpingectomy with or w/o oophorectomy, hx of UTI
Conservative – segmental resection 4. test of choice: urine culture [clean catch midstream]
5. U/A alone is not recommended
 Cervical pregnancy o Tx:antibiotics x 7 days w/ follow-up culture after 1 wk
o Rubin’s criteria:  Acute cystitis in pregnancy
o S/Sx: urinary frequency, dysuria & bacteriuria

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 o Dx: pyuria > 8 pus cells/mm3 [uncentrifuged], or > 5 pus cells/hpf [centrifuged] or [+] Parous External os has fishmouth appearance
leukocyte esterase & nitrate test
o Tx: 7 days antibiotics o In normal nonpregnant state, uterus is approximately 6 cm x 4 cm & weighs about 70
 Acute pyelonephritis in pregnancy gms [ovary is 3cm x 2 cm]
o Dx: pyuria [> 5 wbc/hpf centrifuged urine] & bacteriuria [> 10,000 cfu of uropathogen], o Lymphatics: aortic, lumbar and pelvic nodes
gm stain, urine C & S, blood cultures o Nerve supply: hypogastric and ovarian plexus [sympathetic], pelvic N. + S2-4
o Tx: admit, immediate antibiotic therapy for a duration of 14 days [parasympathetic].
o Blood supply:
Note: Antibiotics in pregnancy Uterine A. Large branch of hypogastric A.
Safe antibiotics Use w/ caution Contraindicated Ovarian A. Directly from aorta
Amoxicillin, nitrofurantoin, Aminoglycosides Tetracycline, fluorioquinolones,
cephaalosporins, coamoxiclav, TMP/SMX at 1st TM/SMX at 3rd trimester  Fallopian tube/oviducts
ampicillin-sulbactam, aztreonam & 2nd trimester o Blood supply:
Uterine A. From hypogastric A.
COMPLICATIONS OF PREGNANCY Ovarian A. From aorta
 Magnesium toxicity [7-10 mEq/L] is associated w/ loss of patellar reflexes. Tx w/ calcium
gluconate 10% solution 1 g IV. o Lymphatics; internal iliac and aortic nodes
 Magnesium levels and toxicity: o Innervation: uterine & ovarian plexus, sensory nerves from T11-12, L1
4-7 mg Uterine contractions decreased  Ovaries:
6-12 mg ECG changes, hyporeflexia o Blood supply: ovarian A. [from aorta]
10 mg Loss of deep tendon reflex o Venous drainage:
15 mg Respiratory paralysis, cardiac depression L ovarian V. Drains to L renal V.
R ovarian V. Drains to IVC
 Hydration often stops contractions during preterm labor.
 L:S ratio is normally > 2.0 o Lymphatics: aortic and iliac nodes
 PROM is the MC dx associated w/ preterm delivery. o nerve supply: ovarian, hypogastric and aortic plexuses
 Oxytocin should never be given as undiluted bolus [due to serious hypotension]  Internal pudendal A. – terminal branch of internal iliac A.
 Antibiotics for endometritis: clindamycin + gentamicin  Cardinal ligaments/Mackenrodt’s ligament – provides the major support of uterus & cervix.
 Uterosacral ligament – last to cut in hysterectomy.

HI-YIELD FACTS IN GYNECOLOGY [from GYNE-MISCHELLE & handy notes] Male and Female derivatives of embryonic urogenital structures
Structure Male Female
REPRODUCTIVE ANATOMY Labioscrotal swelling Scrotum Labia majora
Key terms: Urogenital folds Penile urethra Labia minora/nymphae
 Canal of Nuck – tubular process of peritoneum accompanying round ligament into inguinal Genital tubercle Penis Clitoris
canal, generally obliterated in adults. Phallus Penis bulb Vesibular bulbs
 Carunculae myrtiformes – small nodules of fibrous tissue at vaginal orifice w/c are Urogenital sinus Prostate gland Urehral / Skene’s glands
remnants of hymen. Prostatic utricle Vagina
 Cornu – where oviducts enter uterine cavity. Bulbourethral glands Vestibular glands
 Cul-de-sac of Douglas – separates uterus from large intestine Cooper’s glans Bartholin’s glands
 Fimbria ovarica – finger-like projections of distal end of oviducts, attaches oviducts to Mesonephric duct Epididymis Epiophoron
ovary. Ductus deferens Gartner’s duct
 Frankenhauser’s plexus – concentration of both myelinated and non-myelinated nerve Gonad Testis Ovary
fibers in uterosacral lligament supplying primarily the uterus and cervix. Gubernaculums Gubernaculums testis Round lig. of uterus
 Space of Retzius – area btw bladder and symphysis pubis bounded laterally by obliterated
hypogastric A. CONGENITAL ABNORMALITIES OF FEMALE REPRODUCTIVE TRACT
Key terms:
Important Facts  Androgen resistance syndrome – 46 X,Y individual w testis, absent uterus, normal female
 Escutcheon in mons pubis [triangular in female, diamond in male]. phenotype and scanty body hair.
 Labia minora & breast are the only areas of the body rich in sebaceous glands w/o hair  Arcuate uterus – minimum septate uterus
follicles.  Bicornuate uterus – partial lack of fusion of 2 uterine corpura w/ single cervix present.
 Lowest part of embryonic urogenital sinus – vestibule.  Didelphic uterus – compete duplication of uterus and cervix w/o fusion of 2 cavities.
 MC large cystic structure of vulva – Bartholin’s duct cyst.  Rokitansky-Kuster-Hauser syndrome – 46 X,X female w/ mullerian failure showing
 Vagina: absence of all or most of the vagina, cervix, uterus, and FT.
o Normal pH: 3.8 – 7.2  Unicolic/unicornuate uterus – represents a complete arrest of 1 mullerian duct.
o Lower 3rd: close w/ endopelvic fascia & ligament  MC cause of labial fusion is congenital adrenal hyperplasia.
o Middle 3rd: supported by levator ani M.& cardinal ligament [lower part]
o Upper 3rd: supported by cardinal ligament [upper] & parametria HISTORY, P.E, AND PREVENTIVE HEALH CARE
o Blood supply: Keyterms:
Vaginal A. Either directly from uterine A. or as a branch of internal iliac A.  Ectropion – presence of endocervical [glandular] epithelium on potrio vaginalis of cervix;
Pudendal V. Principal venous drainage may result from scarring of external os or congenital.
 Total procidencia – prolapse of uterus and cervix thru introitus
o Nerve supply: vaginal plexus, pudendal nerve; pain fibers [S1-4]  Stages of uterine prolapse;
o Lymphatics: Stage 1 Minimum descent of cervix into vaginal canal
Upper 3rd External iliac nodes Stage 2 Descent of cervix to introitus
Middle 3rd Common & internal iliac nodes Stage 3 Prolapse of cervix or uterus thru introitus
Lower 3rd Common iliac, superficial inguinal & perirectal nodes
 Trichomonas: use 1% NaCl while KOH is used in candidiasis
 Surgical procedures for vagina: colpectomy, colposcopy & colphorrhapy
 Cervix: RAPE, INCEST AND DOMESTIC VIOLENCE
o Blood supply: descending branch of uterine A., cervical A. & azygos A. Key terms
o Lymphatics: obturator, common iliac, internal/external iliac nodes  MC acquired infection in STD is chamydia. [Tx: ceftriaxone and doxycycline]
o Nerve supply: S2-4  Survival time of sperm:
 Majority of arterial supply to cervix is at 3 or 9 o’ clock position. Source Motile sperm Sperm Aid phosphatase
 Removal of narrow lower par of uterus is called trachelectomy. Vagina Up to 8 hrs Up to 7-9 days Variable
 Uterus: Pharynx 6 hrs Unknown 100 IU
Nulliparous External os is round Rectum Undetermined 20-24 hrs 100 IU

11
 Cervix Up to 5 days Up to 17 days Variable  Classic Sx of intraductal papilloma is spontaneous bloody discharge from 1 nipple.
 Intraductal papilloma and fibrocystic changes are the 2 MC etiology of spontaneous non-
DIAGNOSTIC PROCEDURES milky discharge.
Keyterms  Usual etiology of fat necrosis is trauma.
 Hysterosalpingography – xray whereby uterine cavity and lumina of FT are visualized by  Most accurate conventional method of determining nonpalpable breast CA is
injecting contrast material thru cervical canal. mammography, often mediolateral oblique position.
 Hysteroscopy – direct visualization of endometrial cavity using an endoscope.  Indirect signs of breast CA:
 Laparoscopy – examination and inspection of uterine cavity and pelvic organs by 1. single dilated duct w/ intraductal CA
endoscope. 2. asymptomatic architectural distortion in dense breast
 Sonohysterography – imaging of uterine cavity by instilling saline. 3. developing density
 isolated clusters of tiny calcification are the MC and important diagnostic sign of early CA.
Important facts  Diagnostic test for breast CA is MRI.
 Sonography is the method of choice for locating a missing IUD.  The |presence and number of axilla node metastasis is the single best predictor of
 Endovaginal UTZ is the mainstay in evaluation of pregnant woman w/ 1 st trimester vaginal survival.
bleeding.  Most frequently prescribed hormonal agent for breast CA is tamoxifen/raloxifen.
 CT scan is very accurate in dx cystic teratoma, and is an excellent techique to confirm dx
of ovarian vein thrombosis. DIFFERENTIAL DIAGNOSIS OF MAJOR GYNECOLOGIC PROBLEMS
 Endometrial sampling is the standard diagnostic test to confirm endometritis. Keyterms
 CT is the most accurate in dx of appendicitis.  Hematocolpos – distenion of an obstructed vagina [caused by imperforate hymen or
 Most frequent problem in performing endometrial sampling is cervical stenosis or spasm. transverse vaginal septum] w/ blood products.
 Major complication following endometrial biopsy is uterine perforation.  Hematometria – uterus distended w/ blood secondary to partial or complete obstruction of
 Laparoscopy is adopted as method of choice for female sterilization. any part of lower genital tract.
 Cervical punch biopsy is diagnostic for pxs w/ abnormal papsmear.
Important facts
PEDIATRIC GYNECOLOGY  Implantation bleeding occurs at time of 1st missed menstrual period and last a very short
Keyterms time, may be present 1-2 days w/ flow to menstrual period, it can be seen as brownish-
 Adhesive vulvitis – a self-limiting consequence of chronic vulvitis in w/c denuded tinged cervical mucus.
epithelium of labia minora agglutinates and fuses the 2 labia together.  Common cause of DUB in puberty is anovuation.
 McCune-Albright Syndrome/Polycystic Fibrous dyplasia – triad: café-au lait spots, fibrous  MC benign condition causing postmenopausal bleeding.
dysplasia, and cysts of skull and lung bones.  MC example of recurrent pelvic pain among women.
 Incomplete or pseudoprecosious puberty – premature female sexual maturation and  Pelvic congestion syndrome is characterized by pain and heaviness in pelvis that occurs
uterine bleeding w/o associated ovulation. after arising and becomes worst as day progresses, uterus appears dusky-blue & mottled,
 Precocious puberty – the appearance of secondary sexual maturation at an age > 2.5 often w/ varicosities of veins of broad ligament.
standard deviations below the mean for the population to w/c the child belongs.  MC benign neoplasms of adnexa are serous cystadenoma and benign cystic teratoma
[dermoid cyst].
Important facts  MC benign ovarian neoplasm among different age groups:
 Vulvovaginitis – MC gynecological disease of children and premenarcheal females. Age 19 Benign cystic teratoma
 [+] identification of T. vaginalis, N. gonorrhea, and Chlamydia often indicates sexual Age 20-44 Serous cystadenoma
abuse. Ages 20 to beyond 75 cystadenocarcinoma
 Why is a child susceptible to vulvar infections:
1. they lack labial fat pads and pubic hair  Abdominal masses in young childhood are more likely to be Wilm’s tumor or
2. her vulvar and vaginal epithelium lack protective effects of estrogen thus are sensitive neuroblastomas.
to irritation or infection  Solid or mixed solid and cystic adnexal masses in children include dysgerminoma and
3. labia minora are thin and vulvar skin is red teratoma.
4. vaginal epithelium is of neutral pH providing an excellent medium for bacterial growth.  Majority of adnexal masses in adolescents are functional cysts of ovary [benign cystic
5. her vagina lacks glycogen, lactobacilli, and antibodies to help resists infection. teratoma]. It is also the MC neoplastic masses in reproductive years.
 The major factor in childhood vulvovaginitis is poor perineal hygiene.  Benign fibromas of the ovary may be associated w/ ascites and pleural effusion called
 Classic Sx of E. vermicularis infection is nocturnal vulvar and perineal itching. Meig’s syndrome.
 The classic perineal “figure of 8 or hourglass rash” indicates lichen sclerosus.  Struma ovarii refers to a teratoma w/ thyroid elements present.
 MC cause of bleeding in childhood is foreign bodies, w/c is MC among 3-9 y.o and are  Tumor makers:
due to small wads of toilet tissue. Classic Sx: foul, bloody vaginal discharge. CA-125 Epithelial tumors
 Usual cause of accidental genital trauma is fall [mostly straddle injury]. Serum HCG and AFP Germ-cell tumors
 Calcification in an ovarian mass indcates a dx of ovarian teratoma.
 MC malignancy in preadolescent females is germ cell tumor. BENIGN GYNECOLOGIC LESIONS
 MC malignant neoplasm is dysgerminoma. Keyterms
 MC tumor in children is benign teratoma.  Degeneration of myoma – myoma outgrowths its blood supply and begin to necrose
 MC DDX of abdominopelvic mass in children that is not an ovarian mass is a benign cyst centrally.
of mesentery or omentum.  Endometrial poyp – localized outgrowth of endometrial gland and stroma projecting
 MC cause of pseudoprecocious puberty is an estrogen-secretig ovarian tumor, of w/c the beyond surface of endometrium including is vascular stalk.
MC type is granulose cell tumors.  Gartner’s duct cyst - cyst primarily of mesonephric origin found laterally in vagina.
 DOC for GnRH-dependent precocious puberty is GnRH agonists.  Hidradenoma – rare, small benign vulvar tumor of apocrine sweat glands.
 Spontaneous discharge from nipple is a Sx of intraductal papilloma.  Hydatid cyst of Morgagni – pedunculated, paratubal cysts found near fimbria of oviduct.
 MC of all benign breast conditions is fibrocystic changes. Its classic Sx is cyclic bilateral  Hyperreactio luteinalis – multiple theca lutein cysts causing bilateral ovarian enlargement
breast pain; signs include ↑ engorgement and density of breast, excessive nodularity, during pregnancy.
rapid change and fluctuation in size of cystic tenderness and spontaneous nipple  Leiomyomatosis peritonealis disseminate – benign disease w/ multiple small nodules over
discharge. pelvic surface and abdominal peritoneum mimicking disseminated CA or sarcoma.
 3 clinical stage of fibrocystic changes:  Luteoma of pregnancy – rare, specific, benign hyperplastic reaction of ovarian theca lutein
1st stage / Mazoplasia Breast pain in upper outer quadrant, intense stromal proliferation cells during pregnancy.
2nd stage / Adenosis Seen in early 20s, w/ marked proliferation and hyperplasia of duct,  Nabothian cysts – cervical retention cysts lined by endocervical –type columnar cells.
ductules, and alveolar cells  Syringoma – benign tumor of eccrine sweat glands.
3rd stage / cystic Seen in their 40s, w/ no severe breast pain but there is sudden
phase pain and tenderness w/ a lump, straw-colored fluid Important facts
DOC for fibrocystic changes: Danazol  Urethral curuncle, small fleshy outgrowth at distal end of urethra common in
 MC breast tumor in adolescents is fibroadenomas. It does not produce breast pain and postmenopausal women usually located at ectropion of posterior urethral wall. Common
tenderness. S/Sx includes dysuria, frequency, urgency and pain or tenderness. It is not a precursor for
 MC breast sarcoma is Cystosarcoma phylloides. urethral CA.
 MC breast malignancy is infiltrating ductal CA.

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  Urethral prolapse is MC in children. It appears as annular rosette of friable edematous
prolapsed mucosa. Tx; hot sitz bath and antibiotics, topical estrogen and excision of
redundant mucosa.
 MC large vulvar cyst is Bartholin’s duct cyst [often located at posterolateral aspect]
 MC small vulvar cyst is Epidermal inclusion cyst [often located at anterior half of labia
majora]. It is not related to trauma unlike inclusion cyst of vagina.
 Urethral CA:
o MC in elderly women, usually squamous cell origin, found in distal urethra. S/Sx:
bleeding, frequency, dysuria, urethral mass and tenderness, induration of urethra.
 Most vulvar epidermal cysts do not have sebaceous cells.
 MC benign neoplasm in females is nevus/mole of vulva or vulvar nevi.
 A flat junctional nevus and dysplastic nevus have greatest potential for malignant
transformation.
 MC benign solid tumors of vulva are fibroma [often located at labia majora].
 2nd MC benign vulvar mesenchymal tumors are lipoma [often at labia majora].
 Hidradenoma are treated by excisional biopsy.
 Fox-Fordyce disease are multiple retention cyst of apocrine gland w/ skin inflammation.
 Von Recklinghausen’s Disease are generalized neurofibromatous nodules from neural
sheath associated w/ café-au-lait spots.
 Vulvar hematomas are treated conservatively and by surgery [> 10 cm, expanding].
 Burning vulvar syndrome – persistent vulvodynia w/o any cause.
 Psoriasis is dx by [+] silver scales and bleeding or scraping of plaques.
 Seborrheic dermatitis is characterized by presence of oily scales.
 Lichen planus is characterized by presence of shiny, violaceous papules.
 Urethral diverticulum are MC seen from posterior urethra, middle 3rd], characterized by
dysuria, dyspareunia and dribbling of urine. Classic sign is presence of purulent material
on expression of sub-urethral area.
 MC cystic structure in vagina is inclusion cyst usually found in posterior and lateral walls of
1/3 of the vagina.
 Types of dysontogenic cyst of vagina:
Mesonephros Gartner’s duct cyst
Mullerian cyst Perimesonephrium
Urogenital sinus Vestibular cyst
 Most frequent etiology of trauma to lower genital tract of adult females is coitus, usually a
transverse tear of posterior fornix. Tx: suturing.
 MC benign tumor of cervix is endocervical/cervical polyps.
 Cervical myomas commonly arise from isthmus of uterus.
 Cervical lacerations arise from 3 and 9 o’ clock position. Tx: suturing
 Cervical stenosis often occurs in internal os.
 Endometrial polyp often arises in fundus of uterus.3 components include endometrial
gland and stroma, and central vascular channels.
 Most frequent pelvic tumors are leiomyoma [often found in corps of uterus].
 Submucosal myoma are most troublesome clinically.
 MC form of leiomyomas and is the mildest – hyaline degeneration.
 Most acute form of leiomyomas, often painful – red or carneous degeneration.
 “Spaghetti tumor” is characteristic of intravenous leiomyomatosis.
 MC ovarian cysts are follicular cysts [often located at ovarian cortex].
 Halban’s triad of corpus luteum cyst: delayed menses w/ menorrhagia, unilateral pelvic
pain, & small, tender adnexal mass.
 MC ovarian neoplasms are benign cystic teratom/dermoid cyst/mature teratoma [often
found among prepubertal female and teenagers]. Tx: cystectomy
 MC complication of dermoid cysts is torsion.
 Triad of endometrioma: pelvic pain, dyspareunia and infertility.
 MC benign solid neoplasm of ovary is fibroma.
 Triad of Meig’s syndrome: ovarian fibroma, ascites, hydrothorax.
 “coffee-bean” appearing nucleus is found in Brenner’s tumor/Transitional cell tumors.
 Leiomyomas of oviduct are usually seen in interstitial portion of tubes.
 MC benign tumor of oviduct is Angiomyoma / Adenomatoid tumor.
ENDOMETRIOSIS AND ADENOMYOSIS
Keyterms
 Adenomyosis – growth of endometrial glands and stroma into uterine musculature to a
depth of at least 2.5 mm from basalis layer of endometrium.
 Chocolate cysts – a cystic area of endometriosis in ovary.
 Dyschezia – difficult/painful evacuation of feces from rectum.
 Endometriosis – presence and growth of glands and stroma identical to lining of uterus in
aberrant location.
 Retrograde menstruation – menstrual flow, endometrial cells, and debris, blood flow via
FT into peritoneal cavity. MC etiology.
Doesn’t respond to hormonal stimulation Responds to estrogen
Non-cyclical Cyclical
 Common sites of endometriosis: ovary [MC], cul-de-sac, fallopian tubes, uterosacral
ligaments, bowel. Less common sites: cervix, vagina, bladder. Rare sites: nasopharynx,
lungs
 A 37 y/o female complains of hemoptysis w/ each period: endometriosis of nasopharynx
or lung
 Maximum time on estrogen suppression should be 6 mos. due to adverse effects
 3 cardinal histologic features in endometriosis: ectopic endometrial glands and stroma,
hemosiderin-laden macrophages.
 Classic pelvic finding is fixed, retroverted uterus w/ scarring and tenderness posterior to
uterus. Nodularity of uterosacral ligaments & cul-de-sac of Douglas
 Tx for endometriosis:
o Medical – if < 1-2 cm, primary goal: induction of amenorrhea, drugs used include:
danazol 800 mg/d x 6-9 mos.; GnRH agonists; OCPs; and medroxyprogeserone [for
pxs who has completed childbirth].
o Conservative surgery: laparoscopy or TAHBSO [definitive surgery]
 GIT endometriosis [sigmoid olon and anterior wall of rectum] is the MC site of extrapelvic
endometriosis.
 Most serious consequence of urinary tract endometriosis [often at trigone] is ureteral
obstruction.
 Adenomyosis / endometriosis interna is often found at posterior wall of uterus. Standard
criterion: endometrial gland and stroma > 1 LPF [2.5mm] from basalis layer of
endometrium.
 Classic Sx of adenomyosis: primary & secondary dysmenorrheal and dyspareunia.
 Mgt of adenomyosis:
o Medical: GnRH agonists, cyclic hormone prostaglandin synthetase inhibitors
o Surgery: definitive tx is hysterectomy.
ANATOMIC DEFECTS OF ABDOMINAL WALL AND PELVIC FLOOR
Keyterms
 Cystocele – protrusion of bladder into vagina, significant relaxation of fascial supports of
bladder. Common in women w/ android or anthropoid pelvis.
 Descensus of cervix & uterus [prolapse, procidencia] – protrusion of cervix and uterus into
barrel of vagina.
o 1st degree: prolapse into upper vagina
o 2nd degree: prolapse near uterus
o 3rd [complete]: total prolpase thru introitus
o 4th degree: body of uterus is out of introitus
o Tx:
Nonoperative Pessaries, estrogen
Operative Vaginal hysterectomy w anterior & posterior repair +
perineorrhaphy to reinforce introitus
 Dovetail sign – loss of anterior perianal folds indicates a defect in external anal sphincter
or chronic degree laceration.
 Enterocele – herniation of pouch of Douglas [cul-de-sac] btw uterosacral ligament into
rectovaginal septum, usually contains small bowel.
 Pessary – a prosthesis inserted into vagina to support pelvic structure.
 Urethrocele – protrusion of urethra into vagina, significant loss of fascial supports of
urethra. Common in women w/ gynecoid pelvis.
 MC traumatic cause of rectovaginal fistula is obstetric [due to prolonged 2 nd stage of
labor]. It usually occur in lower 3rd of vagina.
UROGYNECOLOGY
Keyterms
 Genuine stress incontinence – loss of urine when intravesical pressure exceeds maximum
urethral pressure in absence of detrusor acivity.
 Interstitial cystitis – complex inflammatory condition of bladder usually associated w/
altered epithelial permeability, mast cell activation and upregulation of secondary afferent
nerve.
 Overflow incontinence – loss of urine when intravesical pressure exceeds the maximum
urethral pressure secondary to elevtion of intravesical pressure associated w/ bladder
distention but in absence of detrusor activity.
 Reflex incontinence – loss of urine caused by abnormal reflex activity in spinal cord in
absence of sensation that is usually associated w/ desire to micturate.
 True incontinence – loss of urine w/o abnormal bladder function due to fistulas or other
damage to urinary tract
 Urge incontinence – loss of urine associated w/ strong desire to void directly into motor
urge incontinence [uninhibited detrusor contractions] and sensory urge incontinence.

Important facts Important facts

 Classic Sx of endometriosis is cyclic pelvic pain. Its most popular theory is retrograde  Innervation of bladder & urethra:
menstruation. Other Sx: infertility and abnormal bleeding Continence Micturition
 Differences: Bladder Symph [NEp] = relaxation w/c Parasymph [Ach] = contraction
Adenomyosis Endometriosis prevents micturition causing micturition
Usually in older women Young women Sphincter Contraction = prevents micturition Relaxation

13
 o Giemsa/wright stain: [+] Donovan bodies – clusters of dark-staining baceria w/ bipolar
 Resting bladder pressure is btw 20 & 30 cm H2O. safety pin appearance [pathognomonic]
 Highest pressure zone in urethra is about midpoint in functional urethra, roughly 0.5 cm o Mgt: TMP-SMZ, Doxycycline, Erythromycin, Ciprofloxacin
proximal to urogenital diaphragm.  Lymphogranuloma venereum
 For continence to be present, UCP > bladder pressure o Etiology: C. trachomatis
 Cystoscopy and cystometry are best used for Dx of detrusor hyperactivity o S/Sx: tender, enlarged, matted nodes [bubos]
 MC cause of lower urinary tract infection is E. coli. o Classic clinical sign of 2nd stage:: double-genitocrural fold or groove sign
 Common etiologic agents in urethritis include Neisseria and Chlamydia. o Classic sign of 3rd stage: multiple draining sinuses or fistula [rupture bubos]
 MC form of UTI is cystitis. o Dx: CFAb titer – mos frequently used serum mehod
 Common etiologic agents in urethral diverticulum include gonococcus and E. coli. o Mgt: doxycycline, RCN, eryhromycin
 Most urethral diverticula emanate from ventral wall of urethra.  Chancroid
o Soft chancre – painful and tender
 MC urinary incontinence is genuine stress incontinence.
o Hard chancre – asymptomatic
 2nd MC cause of urinary incontinence is urge incontinence.
o Etiology: haemophilus ducreyi
 MC groin hernias in males is inguinal hernia, in females is femoral hernia. o Dx: culture of purulent material - “school of fish”
 Anterior colporrhaphy is indicated for urethrocele and cystocele. o Mgt: erythromycin, ciprofloxacin, azithromycin
 Posterior colporrhaphy is indicated for rectocele.  Syphilis
 Classic Sx in rectocele is “heavy or falling out feeling in vagina w/ constipation or o Etiology: treponema pallidum
imcomplete emptying of rectal vault. o Stages:
 Enterocele is the only type of hernia that can occur after abdominal or vaginal Primary syphilis Hard chancre, painless ulcer
hysterectomy. It is usually due to weakened pouch of Douglas. Important supports in its Secondary syphilis Red macules & papules over palms & soles of feet
prevention are the uterosacral and cardinal ligaments. Latent stage No evidence of diseas
 Mixed incontinence is motor urge incontinence as a result of detrusor overactivity and Tertiary syphilis Gumma [like cold abscesses
stress incontinence.
o Dx: FTA-ABS & MHA-TP
INFECTIONS OF LOWER GENITAL TRACT
o Mgt: PCN G – DOC for syphilis, can cause Jarisch-Herxheimer reaction
Keyterms
 Vaginitis
 Clue cells – epithelial cells w/ clusters of bacterial adherent to external surface, have
o pH > 5.0
granular/stippled appearance and are associated w/ bacterial vaginosis
o 4 diagnostic criteria:
 Donovan bodies – pathognomonic clusters of dark-staining bacteria found in cytoplasm of 1. homogenous-grayish white discharge
large mononuclear cells in pxs w/ granuloma inguinale. 2. vaginal ph > 4.5
 Groove sign – depression btw groups of inflammed nodes producing a double genitocrural 3. [+] whiff test
fold in pxs w/ lymphogranuloma venereum. 4. clue cells > 20% of epithelial cells
 Gumma – infectious granuloma characteristic of late or tertiary syphilis o 3 MC vaginal infections:
 Koilocytosis – histologic appearance of cells w/ perinuclear halo consistent w/ HPV Bacterial vaginosis Candidiasis / Moniliasis Trichomoniasis
infection Gardnerella vaginalis C. albicans / glabrata Trichomonas vaginalis
 Whiff test – smell of vaginal discharge after addition of 10% KOH w/c is [+] for either Musty/fishy odor, pruritus Pruritus, edema, Copious, frothy w/ bubbles,
bacterial vaginosis or trichomonas infections. is rare erythema, odorless malodorous discharge
Gary or white thin sticky White “cottage cheese” Green-yellow “bubbly”
Important facts
[+} clue cells Yeast + pseuudohyphae Flagellated protozoa
 Specific sign of acute bacterial cystitis is suprapubic tenderness.
[+] whiff test ‘fishy amine’ [-] whiff test May be [-/+], hanging drop tech.
 Vulvovaginitis [external dysuria], cystitis [internal dysuria]
Metro or clindamycin Synthetic Imidazoles Metronidazole
 MC pathogens causing acute urethritis: C. trachomatis & N. gonorrheae
pH > 4.5 pH < 4.5 pH < 4.5
 MC etiology is ascendinng infection from introitus and distal urethra.
 Most frequently involved pathogens in uncomplicated lower UTI are E. coli, Staph
 Most prevalent cause of vaginitis is bacterial vaginosis/Non-specific vaginitis.
saprophyticus.
 MC nonviral, non-chlamydial STD of females is Trichomoniasis.
 Gold standard: > 10 5 uropathogens/ml
 Classic sign of trichomoniasis: “colpitis macularis” – strawberry-like appearance of upper
 Mgt of acute bacterial cystitis:
vagina and cervix, [+] patchy erythema
o Acute uncomplicated type: TMP-SMZ x 3 days
 Toxic shock syndrome:
o Complicated type: quinolones BID [DOC]
o S. pyogenes – common in postpartum
o Chronic/pregnant/DM – TMP- SMZ x 7-14 days
o S. aureus – common in children
o Recurrent cystitis – TMP-SMZ, nitrofurantoin
o Mgt: PCN, clindamycin, gentamycin, vancomycin, aminoglycosides
 Bartholin’s duct cyst is located in labia majora while bartholin’s glands are found in base of
 Most specific test for AIDS is PCR.
labia minora.
 Tx of bartholin’s duct cyst is marsupialization [if symptomatic]  Cervicitis – etiology:
Endocervicitis N. gonorrhea and C trachomatis
 Most contagious of all sexually transmitted disease is pediculosis pubis, w/c is caused by
phthirus pubis [crab louse]. Ectocervicitis T. vaginalis
 Scabies is aka “great dermatologic imitator”, caused by Sarcoptes scabiei [itch mite], Sx:
intense pruritus at night, Tx: permethrin 5%  Mucopurulent cervicitis [urethritis in males]
 Characteristic lesion in molluscum contagiosum [by pox virus] is [+] umbilicated papules, o Etiology: Chlamydia trachomatis, gonorrhea
or water wart, Dx: intracytoplasmic molluscum bodies. o Dx: modified-thayer martin [gonorrhea], McCoy cell monolayers [C. trachomatis]
o Tx: azithromycin, doxycycline, erythromycin, ofloxacin
 MC viral sexually transmitted disease is condyloma acuminatum [by HPV].
o HPV 16, and 18 – high risk, associated w/ aneuploid, premalignant & malignant
INFECTIONS OF LOWER GENITAL TRACT
lesions.
o HPV 6, 11 – associated w/ benign, euploid lesions Keyterms
o MC subtype of condyloma acuminatus is cauliflower-shaped.  Fitz-Hugh-Curtis syndrome – syndrome of perihepatic inflammation, origin from
o Progress of the infection is by autoinoculation. transperitoneal or vascular dissemination of either N. gonorrhea or C. trachomatis.
o Classic finding is [+] cells w/ perinuclear bodies  PID – infection of upper genital tract, often use as acute salpingitis
 [Refer to p. 56 of OB-GYN handy notes for clinical features of genital ulcers]  Tubo-ovarian complex – collection of pus w/in an anatomic space created by adherence of
 Genital ulcers/genital herpes organs involving the oviducts, ovaries
o HSV 2 – cause ulceration below waist
o HSV 1 – infects epithelium above waist Important facts
o Latent phase: viruses reside at dorsal root ganglia of S2-4  Endometritis
o Cell culture – gold standard o Etiology: C. trachomatis, N. gonorrhea, S, agalactiae
o Western blot assay – most specific serologic test o Tx: tetracycline - DOC
o Mgt: Acyclovir, famcyclovir, valacyclovir  PID
 Granuloma inguinale [donovanosis] o 3 major sequelae: ectopic pregnancy, chronic pain, infertility
o Etiology: calymmatobacterium granulomatis o MC cause: salpingitis [oviducts], caused by C. trachomatis
o Characteristic lesion of ulcer: beefy-red painless ulcer w/ fresh granulation tissue o Highest risk: menstruating teenager w/ multiple sex partners w/o contraception

14
 o Cervicitis is not included in PID Consistency Cystic Solid
o Mode of infection: ascending infection from bacterial flora of vagina Surface Smooth Irregular
o Triad: fever, elevated ESR, adnexal tenderness and mass Mobility Mobile Fixed
o MC complain is lower abdominal pain [hallmark] Weight loss, ascites, color flow Absent Present
o Laparoscopy is the gold standard for Dx of PID  Cervical dysplasia almost always forms at transformation zone.
o [Refer to p. 58 of OB-GYN handy notes for CDC guidelines in DX of Acute PID]  Papsmear only gives cytology while colposcopy and biopsy are needed for histology; w/c
o Mgt: ofloxacin, metronidazole, clindamycin, ceftriaxone, cefoxitin, doxycycline is needed for diagnosis, staging and treatment.
 Actinomyces infection  A papsmear [+] for CIN shows chromatin clumping, and decreased cytoplasm resulting in
o Etiology: actinomyces israelli
higher nucleus/cytoplasm ratio.
o Dx: [+] tubo-ovarian abscess – sulfur granules in gm [+] filaments
 90% of women w. abnormal cytologic findings can be adequately evaluated w/
 Pelvic tuberculosis colposcopy.
o Etiology: M. tb, M. bovis
 Indications for cone bopsy/LEEP:
o Primary and predominant site of pelvic Tb are the oviducts.
o Inadequate view of transformation zone on colposcopy
o Other sites: endometrium, ovaries
o [=] ECC
o Gross appearance: “tobacco-appearance” in FT
o + grade 2 discrepancy between colposcopic biopsy and papsmear
o Classic histologic features: giant cells, granulomas, caseous necrosis
o Tx of HGSIL and adenocarcinoma n situ
o Mgt: INH, pyrazinamide, rifampicin, streptomycin
 Indications for cryotherapy:
o Tx of LGSIL or HGSIL only if it is a lesion completely visualized on colposcopic exam
PRINCIPLES OF RADIATION TX & CHEMOTHERAPY IN GYNECOLOGIC CANCER
Keyterms  Indications for laser therapy:
o Excision or ablasion of CIN
 Brachytherapy – a radiotherapy in w/c source is applied to tumor thru needles implanted
o Ablation during laparoscopic surgery [ex. Endometriosis]
into tumor [interstitial], or placed in vagina or cervical canal [internal].
 Fractionation - direct radiotherapy tx into numerous small doses to reduce damage o
MALIGNANT DISEASE OF THE CERVIX
normal tissue
Keyterms
 Teletherapy – a form of radiotherapy w/ placement of radioactive source of a distance
 Barrel-shaped cervix – contains large CA generally of endocervical origin that has
from px [external treatment]
replaced much of the cervix causing its diameter to widen [>4cm].
 Modified radical hysterectomy – removes uterus and cervix and some paracervical tissue
Important facts
but does no dissect ureters distal to uterine arteries.
 Radiation primarily acts on cells in M phase, making rapidly proliferating cells the most
 Persistent tumor – identification of invasive disease at site of primary tx at < 6 mos. after
radiosensitive.
therapy.
 Most chemotherapeutic drugs are severely myelosuppressive except bleomycin and
 Radical hysterectomy – removes uterus, upper 3rd of vagina, cervix and paracervical-
vincristine.
parametrial tissue. Pelvic ureters are dissected to the uterovesical junction. It is usually
 Adverse effects of some chemotherapeutic drugs:
combined w/ pelvic LN dissection.
Vincristine & cisplatin Severe peripheral neurotoxicity
 Recurrent tumor – identification of invasive disease 6 mos. or more after therapy.
Bleomycin Severe pulmonary toxicity
Doxurubicin Severe cardiomyopathy Important facts
Cisplatin Nephrotoxic and myelosuppressive  Most squamous cell CA of cervix is large cell, nonkeratinizing type.
Taxol Severe neuropenia and neurotoxicity  Carcinoma of the cervix
o HPV 18 – common in adenocarcinoma
INTRA-EPITHELIAL NEOPLASIA OF CERVIX o HPV 16 – common in SCCA [more common]
Keyterms  [Refer to p. 66 of OB-GYN handy notes for classification of Cervical CA]
 CA in situ – gives rise to or is usually present in vicinity of invasive CA, full thickness of  [Refer to p. 67 of OB-GYN handy notes for clinical stages of Cervix uteri]
epithelium is replaced by neoplastic cells  Tumor marker for adenocarcinoma is CA-125.
 CIN – premaalignant change in cervical epithelium that can progress to cervical CA  Definitive dx of microinvasive CA is established by cervical conization.
 Conization – excisional technique to remove a cone-shaped central core of cervix for Dx  Microinvasive cervical CA effectively tx by total hysterectomy.
and Tx of intraepithelial neoplasia
 Most cervical CA are treated by irradiation [teleherapy and brachytherapy].
 Cryotherapy – freezing of cervix to abate abnormal epithelium
 Cervical CA is the 3rd MC malignancy of lower genital tract.
 Dysplasia
 Cervical CA is the 3rd MC gynecologic malignancy [breast CA -1st, ovarian CA – 2nd]
Mild Involves 1/3 of epithelium [CIN 1]
 Symptoms of cervical CA become evident when cervical lesions are of moderate size,
Moderate Involves 2/3 of epithelium [CIN 2] looks like “cauliflower”.
Severe Involves full thickness of epithelium [CIN 3]  Cancers that metastasize to cervix: RIBE [rectal, intra-abdominal, bladder, endometrial]
 Uremia and pyelonephritis are common causes of death in cervical CA.
 Endocervical curettage – obtain cervical tissue for histologic section
 Koilocytosis – associated w/ HPV infection, including perinuclear cavitation and nuclear MALIGNANT DISEASES OF FALLOPIAN TUBE
atypicality Keyterms
 Leukoplakia – described an area that appears white to naked eye even before application  Hydrops tubae profluens – sx complex of abnormal vaginal discharge preceded by pain
of 3% acetic acid. and a mass that may disappear after the discharge is noted.
 Mosaic pattern – rosette appearance of capillary vessels in transformation zone  Tubal CA staging:
 Punctation – stippled appearance of capillary vessels in transformation zone Stage 1 Confined to tubes
Stage 2 Spread to ovaries or pelvic tissue
Important facts Stage 3 Intraperitoneal spread or involvement of retroperitoneal nodes
 Risk of progression for CIN I to a higher grade is 16%. Stage 4 Metastasis to liver parenchyma, outside peritoneum, or malignant cells in
 Precise of cause of CIN is unknown but associated w/ sexual activity and HPV infection pleural fluid
 Cigarette smoking increases risk for IN, while vitamin A and E decreases risk for CIN.
 PAP smear is done by taking samples from endo/ectocervix, and lateral vaginal wall. Important facts
 [Refer to p. 65 for Modified Bethesda Classification of PAP smear in OB-GYN handy  80-90% of FT malignancy are metastatic from other sites usually from ovaries , uterus, or
notes] GIT.
 Abnormal colposcopic findings:  Pathognomonic for tubal pregnancy: abnormal vaginal discharge/bleeding, lower
1. Punctation or red stippling abdominal pain, and adnexal tenderness in postmenopausal women. [triad]
2. aceowhite epithelium  Peritoneum is the most frequent site of metastatic spread in tubal CA.
3. leukoplakia  Chemotherapy w/ cisplatin prolongs survival in tubal CA.
4. mosaic pattern of sharp-bordered lesions w/ vessels
 HIV infected pxs have highest risk when CD4 counts < 200. GESTATIONAL TROPHOBLASTIC DISEASE
 HPV infections spontaneously regress w/in 2 years. Keyterms
 Goal of tx in CIN: eradication of all abnormal tissue.  Choriocarcinoma – highly malignant trophoblastic neoplasia, both cytotrophic and
 Benign vs. Malignant lesions syncytiotrophic growth in malignant fusion.
Characteristic Benign Malignant  Complete mole – molar pregnancy w/ swelling of all placental villi, absent fetal tissue
Occurrence Unilateral Bilateral

15
  High-risk GTD – px w/ pretreatment serum HCG > 40, 000 mIU/ml or > 4 mos. duration of
disease or previous chemotherapy failure, brain or liver metastasis NEOPLASTIC DISEASE OF OVARIES
 Hydatidiform mole – placental abnormality involving swollen placental villi and Keyterms
trophoblastic hyperplasia w/ loss of fetal blood vessels, may spread to extrauterine sites.  AFP – secretory product of endodermal sinus tumors in serum and serves as specific
 Low-risk GTD – pxs w/ metastatic disease outside uterus excluding brain, liver, serum tumor marker.
HCG < 40, 000 mIU/ml, duration < 4 mos. w/ no prior chemotherapy.  Brenner tumors – resembling urothelium and so called “Walthard nest of ovary”, mixed w/
 Partial mole – molar pregnancy w/ some normal and swollen villi, fetal cord, and amniotic ovarian stroma.
membrane elements.  Clear cell tumor/mesonephroma – an ovarian neoplasm consists of clear cells w/ glycogen
 Placental site trophoblastic tumor – rare GTT arising from uterus and secretes HPL and or “hobnail cells” resemble clear cell tumors from endocervix, endometrium and vagina.
HCG, often resistant to chemotherapy.  Dermoid – benign, cystic germ cell tumor [cystic teratoma] w/ elements of all 3 germ
 Stages of GTT: layers, MC ovarian neoplasm in < 30 y.o
Stage 1 Confined to corpus uteri  Dysgerminoma – MC ovarian malignant germ cell tumors, w/ primitive germ cells.
Stage 2 Metastasis to pelvis and vagina  Endodermal sinus tumor – malignant germ cell tumor, recapitulates extraembryonic tissue
Stage 3 Metastasis to lungs and resembles yolk sac of rodent placenta.
Stage 4 Distant metastasis [liver, brain, etc.]  Endometriod tumor – ovarian epithelial tumor whose cells resemble uterine endometrial
adenocarcinoma.
 Theca-lutein cells – ovarian enlargements occurring w/ H mole and consists of theca lutein  Epithelial stromal tumors – MC type of ovarian neoplasms, from surface [coelomic
cells, regresses after tx of mole. epithelium and ovarian stroma].
 DNA of complete mole is always paternal while DNA of partial mole is both maternal and  Fibroma – MC benign ovarian solid tumors, compost of stromal cells and fibroblasts, and
paternal. are associated w/ ascites and hydrothorax in Meig’s syndrome.
 All early [< 20 weeks] preeclampsia is molar pregnancy  Germ cell tumors – 2nd MC type of ovarian tumors, containing cells that recapitulate
 GTN secrete HCG, lactogen and thyrotropin. embryonic tissue [ecto, meso, endoderm]
 “Sheets of trophoblast” w/ extensive hemorrhage and necrosis is diagnostic of  Gonadoblastoma – arises from abnormal dysgenetic gonads and consists of sex cords
choriocarcinoma. [it also has no villi] stromal elements and germ cells.
 Granulosa-theca cell tumor – sex cord stromal tumors that secretes estrogens and
Important facts consists of granulosa cells [sex cord] and ovarian stromal cells [theca cells, fibroblasts],
 Trophoblastic tissues normally regresses w/in 2-3 wks after delivery demonstrates “Call-Exner bodies” [eosinophilic bodies in granulose cells].
 Finding of trophoblastic cells in uterus > 3 wks after delivery signifies a [+]  Krukenberg tumor – metastasis to ovary, bilateral, w/ signet ring cells from GIT, most
choriocarcinoma frequently from stomach and large intestine.
 TOC for placental site trophoblastic tumor/trophoblastic pseudotumor is hysterectomy.  Pseudomyxoma peritonei – intraperitoneal spread of mucin-secreting cells from ovarian
 H mole mucinous cystadenoma or cystadenocarcinoma or from appendix leading to recurrent
o A prior H mole is a major risk factor for development of gestational choriocarcinoma. abdominal masses and bowel obstruction.
o MC presenting Sx is abnormal bleeding.  Small cell CA – highly virulent, often accompanied by hypercalcemia.
o Dxtic aid: snowstorm pattern on UTZ  Stages of ovarian CA:
o Most effective method of emptying uterus in molar pregnancy is by suction curettage. Stage 1 Confined to 1 or both ovaries
 Gestational trophoblastic neoplasia Stage 2 Extension to pelvic structures
o Most frequent site of metastatic GTT are the lungs, less frequent are liver, brain, ovary Stage 3 Extension to outside pelvis or retroperitoneal/inguinal nodes
and vagina. Stage 4 Extends outside peritoneal cavity or liver parenchyma
o Non-metastatic GTT: methotrexate, actinomycin D, citravorum
o High-risk GTT: methrotrexate, actinomycin D, chlorambucil or cyclophosphamide  Struma ovarii – specialized ovarian stroma consists of thyroid tissue component.
o Pxs treated for GTT should not become pregnant for 6-12 mos. after tx to allow
accurate assessment of B-HCG levels. Important facts
 Risk of developing a molar pregnancy after a primary molar pregnancy is 20-40x greater  Ovarian Ca is the 2nd MC malignancy of the lower part of female genital tract. [endometrial
than initial risk. > ovarian > cervix]. It has the highest mortality because of its late detection.
 Pxs w/ ovarian CA are at increased risk for breast and endometrial CA.
NEOPLASTIC DISEASE OF THE VULVA  Most frequent ovarian neoplasms are epithelial stromal tumors.
Keyterms  [Refer to p. 70 of OB-GYN handy notes for classification of ovarian neoplasms]
 Keye’s punch – used to biopsy the vulva  [Refer to p. 72 of OB-GYN handy notes for Sassone’s criteria in Dx of Ovarian
 Lichen sclerosus – vulvar abnormality usually characterized by thinning of epithelium w/ Malignancy + FIGO classification]
loss of subcutaneous adnexal structure, hyalinization of superficial dermis and  Serous tumors are the most frequent ovarian epithelial tumors. It also has the worst
lymphocytic infiltrates below zone of dermal homogenization. prognosis.
 Microinvasive vulvar CA – superficially invasive CA of vulva not associated w/ LN  MC malignancy among teens and early 20s are germ cell tumors.
metastasis. Lesion < 2 cm in diameter, invasion of 1 mm into stroma.  Tumor markers:
 Paget’s disease of vulva – itchy, usually erythematous lesion containing large cells same P53 tumor suppressor gene, CA-125 Ovarian epithelial CA
to paget’s disease of breast. c-myc oncogene Serous CA
 Stages of vulvar CA: k-ras oncogene Borderline ovarian CA
Stage 1 < 2cm, confined to vulva and perineum Serum LDH Dysgerminoma
Stage 2 > 2cm, confined to vulva and perineum AFP Endodermal sinus tumors
Stage 3 Extends to anus or lower urethra, unilateral LN metastasis hCG Choriocarcinoma
Stage 4 Spreads to bladder, rectum, pelvic bone, or upper urethra or
nonvulvar site, bilateral LN metastasis
 Benign conditions w/ elevated CA-125:
1. endometriosis 4. pregnancy
Important facts 2. hemorrhagic ovarian cysts 5. leiomyoma
 Vulvar CA 3. liver disease 6. PID
o Mostly are squamous cell CA [usually in postmenopausal women]  MC germ cell tumors are benign cystic teratoma / dermoids
o Major Sx: pruritus  MC malignant germ cell umor is dysgerminoma.
o MC vulvar atypia is lichen sclerosus.
 Immature teratoma – multiple agent chemotherapy
o HPV types 6 and 11 are most frequently associated w/ benign vulvar warts.
o VAC regimen: vincristine, actinomycin D and cycophosphamide
o Most lesions are located at posterior perineal area.
o VBP regimen: vinblastine, bleomycin, cisplatin
 Melanoma is the MC non-squamous cell malignancy of vulva.
 Embryonal CA is dx by both HCG and AFO [+]
o Pigmented lesions of vulva are usually junctional nevi.
 Polyembryomas is dx by both HCG and HPL [+]
o Mostly occur at labia minora or clitoris.
o 2 MC varieties: superficial spreading melanoma and nodular melanoma.  Most frequently found elements in mixed germ cell tumors are dysgerminomas and
teratomas.
 Intraepithelial vulvar neoplasia spontaneously regress, VIN 3 has 3-4 % risk of
progression to invasive CA.  Metastatic ovarian cell tumors frequently originate from endometrium and fallopian tube.
 A basal cell CA of vulva is treated by wide local excision.  Most ovarian neoplasms are dx at stage 3 or 4.
 MC site of vulvar dysplasia: labia majora  Majority of ovarian epithelial tumor cell types recapitulate mullerian-type epithelium
[serous-endosalpinx, mucinous-endocervix, endometrioid-endometrium].
 AdenoCA of vagina is associated w/ DES, and often presents in the young.

16
  Malignant germ cell tumors are usually unilateral except dysgerminomas and teratomas.  Abnormal vaginal bleeding is the MC complaint in endometrial hyperplasia.
 Risk of ovarian CA is decreased by OCPs use, BTL, and hysterectomy.  Most important prognostic factor in uterine tumors is the level of estrogen and
 2nd MC gynecologic malignancy and is the 5TH MC cancer in women: ovarian CA progesterone.
 It is also the deadliest of all gynecologic malignancy  Leiomyosarcomas are the MC type of uterine tumors.
 MC type of ovarian CA: serous type of epithelial ovarian CA  TOC for mullerian adenosarcoma is TAHBSO.
 A postmenopausal woman w/ widening girth notices that she can no longer button her  Most pxs who develop endometrial CA are btw 50-65 y.o [peri/posmenopausal years]. It is
pants: ovarian CA the MC malignancy of the genital tract.
 Ovarian CA metastasis to umbilicus is “Sister Mary Joseph’s nodules”  [Refer to p. 69 of OB-GYN handy notes for FIGO classification of Endometrial CA]
 Ovarian and endometrial CA is staged surgically and not clinically unlike cervical CA w/c is  [Refer to p. 68 of OB-GYN handy notes for classication of Endometrial hyperplasia]
staged clinically.  Chronic unopposed estrogen stimulation leads to endometrial hyperplasia and
 MC type of ovarian GCT: dysgerminioma [tumor marker – LDH] adenocarcinoma. Other predisposing factors include obesity, nulliparity, late menopause
 Most aggressive GCT: endodermal sinus tumor [characterized by schiller-duval bodies] and DM.
 Embryonal and choriocarcinoma tumor marker: beta-HCG  Cytologic atypia w/ endometrial hyperplasia is the most important factor in determining
 GCTs are very chemosensitive. premalignant potential.
 Least common gynecologic malignancy: fallopian cell CA [usually adenoCA]  Key determinant to risk of nodal spread is the depth of myometrial invasion w/c is often
 Pathognomonic finding in fallopian tube CA: hydrops tubae perfluens related to tumor grade.
 In any postmenopausal bleeding or discharge that cannot be explained by endometrial  Histologic variants of enometril CA w/ poor prognosis include serous CA and clear cell CA.
biopsy, fallopian cell CA should be considered.  Most frequent sites of distant metastasis of adenoCA of endometrium are the lungs,
retroperitoneal nodes and abdomen.
NEOPLASTIC DISEASE OF VAGINA  CA-125 > 35 U/ml usually suggest extrauterine disease
Keyterms  Recurrences of uterine myomas are most frequent in pelvis, abdomen and lungs.
 Clear cell adenocarcinoma – a vaginal or cervical malignancy occur primarily after 14 y/o,  Metastatic endolymphatic stromal myosis is tx by progestin [200 mg/d].
often associated w/ prenatal exposure to DES.
 Pelvic exenteration – extensive pelvic operation to treat central pelvic recurrence of NEOPLASTIC DISEASE OF THE ENDOMETRIUM
cervical CA after radiation, a total exenteration involving removal of bladder, uterus, cervix Important facts
and rectum. An anterior exenteration spares the rectum while posterior exenteration  MC gynecologic CA: endometrial CA
spares the bladder.  Gold standard for diagnosing endometrial hyperplasia and CA: biopsy
 Pseudosarcoma botryoides – benign tumor occurring in vagina of infants and pregnant  MC subtype of endometrial CA: endometriod [ciliaed adenoarcinoma]
females.  Subtype w/ very poor prognosis: papillary serous CA
 Sarcoma botryoides / embryonal rhabdomyosarcoma – rare, often fatal vaginal  Grade is the most important prognostic indicator in endometriod CA.
malignancy occurring in infants and children.  Side effects of chemotherapeutic dugs: doxyrubicin [cardiotoxicity], cisplatin
 Staging of vaginal tumors: [nephrotoxicity], ifosphamide [hemorrhagic cystiis], etopiside [blood dyscrasia], bleomycin
Stage 0 CIS [pulmonary fibrosis]
Stage 1 CA limited to vaginal wall
Stage 2 CA involving subvaginal tissuebut not extend thru pelvic wall REPRODUCTIVE ENDOCRINOLOGY
Stage 3 CA extending to pelvic wall Keyterms
Stage 4 CA extending beyond true pelvis or involving mucosa of  Activin – same structure to inhibin, stimulates pituitary FSH release and ovarian estradiol
bladder or rectum formation.
 Arcuate nucleus – lies on medial part of hypothalamus above median eminence, major
 VAIN 1 / LGSIL – least severe type, mild dysplasia, located in lower 3rd epithelium source of GnRH secretion.
 VAIN 2 – intermediate severity, moderate dysplasia, a lower 2/3 of epithelium  Beta-endorphin – potent opioid peptide in hypothalamus and pituitary, it inhibits LH
 VAIN 3 – most severe type, severe dysplasia and CIS, full thickness of epithelium secretion.
 FSH – stimulates granulosa cell synthesis in females
Important facts  Inhibin – produced by ovarian granulose cells w/c inhibits FSH secretion.
 VAIN 2 an 3 are combined into high-grade squamous epithelial lesion  LH – stimulates ovarian steroid synthesis in females.
 Radiation tx is the most frequent mode of treatment for SCCA of vagina.  SHBG – serum globulin w/ high affinity to dihydroestosterone, testosterone, estradiol and
 MC sx is vaginal bleeding or discharge. androgens.
 Most cases of VAIN occur in upper 1/3 of vaginal epithelium.
 VAIN can be treated by excision, laser or 5-FU. Important facts
 MC primary vaginal malignancy is squamous cell CA.  Control of reproduction:
 Most CA occurring in vagina is metastatic. Locus Messenger prod. Stimulant prod. Inhibitory prod.
 Vaginal CA constitutes < 2% of gynecologic malignancy. Higher brain NEp, dopa, endorphins Estrogen Estrogen
 Clear cell adenoCA of vagina is associated w/ prenatal DES exposure. areas
Hypothalamus GnRH NEp, progesterone, Endorphins, dopa,
NEOPLASTIC DISEASE OF THE UTERUS estrogen estrogen, androgen,
Keyterms Anterior FSH, LH GnRH, estrogen, Estrogen, androgen,
 Endolymphatic stromal myosis – low grade, < 10 mitoses/10 hpf endometrial stromal pituitary androgen,progesterone inhibin
sarcoma Ovary Estrogen, androgens & FSH, LH GnRH, FSH, LH
 Endometrial CA grading: progesterone
Grade 1 Well-differentiated Adenocanthoma
Grade 2 Intermediate  Cell bodies that produce GnRH are located in anterior hypothalamus and medial
Grade 3 Poorly differentiated Adenosquamous CA basal/tuberal hypothalamus.
 Tanycytes are specialized ependymal cells from lumen of 3rd ventricle into outermost zone
of median eminence.
 Endometrial CA staging:
 PGE2 is luteotrophic while PGF2α is luteolytic.
Stage 1 Confined to uterine corpus
 Normal number of oocytes;
Stage 2 Involves corpus and cervix
At birth 2M
Stage 3 Spreading outside uterus but confined in pelvis
At 7 mos. AOG 6M
Stage 4 Spreading outside pelvis or into mucosa of bladder/rectum
Neonatal period 2M
Menarche 400, 000
 Complex hyperplasia – glands are irregular in shape and often close together, low
If ovulated < 500
malignant potential
 Simple hyperplasia – consisting of proliferating glands, some dilated and w/ abundant
stroma.  Events in follicular stimulation:
Recruitment Days 1-4
Important facts Selection Days 5-7
 Postmenopausal bleeding and abnormal perimenopausal bleeding are the primary Sx of Dominance Days 8-12
endometrial CA. Follicle monitoring Done at days 8, 10, and 12 [UTZ]

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  Pelvic congestion syndrome – valvular engorgement of uterus and vessels of broad
 Summary of ovarian cycle: ligament & lateral pelvic walls, w/c may lead to chronic pelvic pain.
Follicular phase Estradiol Growth & maturation of graafian follicle  PMS – group of Sx, both physical & behavioral, that occur in 2nd half of menstrual cycle &
Luteal phase ↑ progesterone & Growth & maturation of corpus luteum often interfere w/ work & personal relationships, ffd by period entirely free of Sx.
estradiol
Premenstrual ↓ progesterone & Regression of corpus luteum, a “cohort of Important facts
phase estrogen follicles” start o develop  ↑ PGF2α levels were found in secretory endometrium than proliferative.
 TOC for primary dysmenorrhea is prostaglandin synthetase inhibitors [NSAIDS]
 Summary of menstrual cycle:  OCP – DOC for pxs who desire contraception.
Proliferative phase or Estrogen causes proliferation of stromal & epithelial cells,  Factors affecting prevalence & severity of dysmenorrhea:
estrogen phase endometrium thickens [2-3 mm] w/ vessel proliferation, LH surge Hx of vaginal delivery Decreased
occurs 2 days before ovulation OCP use Decreased
Secretory phase or Progesterone is secreted from corpus luteum, marked swelling & Smoking Decreased
progesterone phase formation of tortous glands and vessels, ↑ lipid & glycogen deposits, Duration & amount of menstrual flow Increased
endometrium thickens about 4-6 mm Early menarche Increased
Menstruation ↓ in progesterone & estrogen secretions causing vasospasm of blood Family hx among mothers and sisters Increased
vessels & initiates uterine contracion leading to desquamation
 MC causes of secondary dysmenorrhea: endometriosis>adenomyosis, IUD
 Cytologic hormonal maturation index:  Common historical findings in PMS pxs include a [+] hx of maternal PMS, low levels of
o 1st number [parabasal cells], middle [intermediate], 3rd number [superficial cells] exercise, younger age, and higher parity.
o Ex: 0/10/90 = adequate marked estrogen effect; 200/75/5 = poor estrogen effect;  Bromocriptine is effective in relieving breast tenderness in PMS.
100/0/0 = no estrogen [ex. postmenopausal], 0/100/0 = maximum progesterone effect
[ex. pregnancy] ABNORMAL UTERINE BLEEDING
 Most feminizing Sx are abnormal menstruation or menorrhagia. Keyterms
 Most musculinizing Sx is hirsutism.  Amenorrhea – no menses for at least 6 mos.
 Morphologic changes after ovulation:  DUB – excessive uterine bleeding w/ no demonstrable organic cause [gental/extragenital],
Day 25 Pseudodecidual reaction occurs MC due to abnormality of endocrine origin particularly anovulation.
Day 23 Active glandular secretion and stromal edema  Intermenstrual bleeding – bleeding of variable amounts btw regular menses.
Day 18 Basal vacuolation occurs  Menometrorrhagia – prolonged uterine bleeding occurring at irregular intervals.
 Menorrhagia or hypermenorrhea – prolonged [> 7 days] or excessive [> 80 ml] uerine
 Important events in menstrual cycle: bleeding occurring at regular intervals.
Day 5 Glandular & stromal mitosis  Metrorrhagia – uterine bleeding occurring at irregular but frequent intervals, amount being
Day 16 Basal vacuolation variable.
Day 22 Active glandular secretion & stromal edema  Oligomenorrhea – infrequent uterine bleeding at intervals between 35 days to 6 mos.
Day 26 Pseudodecidualization  Polymenorrhea – uterine bleeding occurring at regular intervals of < 21 days, or 16-23 d.

 In humans, GnRH is secreted in pulsatile manner w/ T1/2 of 2-4 mins. It is more rapid in Important facts
follicular phase [1 pulse/hr], luteal phase [1 pulse/2-3 hrs]  Mean duration of menses is 4 days.
 NEp stimulates GnRH release while serotonin inhibits it.  Methods to quantify blood loss include:
 Principal metabolite of serotonin is 5-HIAA. o Radioisotope labeling of RBCs
 Neuropeptide-Y stimulate pulsatile GnRH release and in pituitary it potentiates o Photometric measurement to quantify hematin collected onto sanitary napkins – MC
gonadotropin response to GnRH. o Alkaline hematin method – most precise
 Somatostatin inhibits releaseof GH, prolatin and TSH.  Mean amount of MBL in normal women is about 35 ml.
 Leuprolide acetate is a GnRH agonists while Nal-Glu is a potent GnRH antagonist.  MC cause of DUB in postmenarcheal and premenopausal yrs is anovulation secondary to
 Main action of LH is to stimulate androgen synthesis by theca cells and progesterone alterations in neuroendocrinologic function.
synthesis by corpus luteum  2 mechanisms of hemostasis during menses:
 Prostanoids produced by endometrium; PGE2, PGF2α, PGI2, and TXA2 o Hemostatic plug formation – most important mechanism in functional endometrium
 Ovary secretes 3 primary steroids: estradiol [follicle], progesterone [corpus luteum] and o Vasoconstriction – most important mechanism in basalis layer
androstenedione [stroma].  Progestins are the TOC for women w/ anovulatory DUB. It produces normal bleeding
 Ovary lacks the ffg enzymes: 21-hydroxylase, 11-β hydroxylase and 18-hydroxylase. episode after estrogen is withdrawn.
 Estrone sulfate is the largest component of the pool of circulating estrogens.  D and C is the TOC for women w/ DUB who suffer hypovolemia/hypotension and for older
 Pregnanediol-3-glucuronide is the major urinary metabolite of progesterone. women who are at risk for endometrial neoplasia.
 Estradiol inhibits FSH while progesterone inhibits LH.  Hysterectomy is indicated for women w/ persistent ovulatory DUB, or w/ leiomyomas and
 Mean average of menarche = 13 y.o, for menopause = 51 y.o uterine prolapse. [alternatives: D and C, ablation]
 Duration of menses = 38 yrs  Postcoital bleeds suggests trauma, infections or cervical cancer.
 Mean duration of menstrual cycle length = 28 + 7 days  Always do an endometrial biopsy when encountering postmenopausal bleeding because
o Short cycles = < 21 days [polymenorrhea] of he strong possibility of endometrial cancer.
o Longer cycles = > 35 days [oligmenorrhea]  Other bleeding tips:
 Mean duration of menstrual flow = 4 + 2 days o Postcoital bleed in pregnant woman: consider placenta previa
o Postcoital bleeding in non-pregnant woman: consider cervical cancer
 Subnuclear vacuolization is the 1st histological indication of the effect of progesterone but
o Postmenopausal bleeding: consider endometrial cancer
is not evidence that ovulation has occurred.
o Premenopausal bleeding: consider PCOD
 T1/2 of LH IS 30 mins while FSH is 3.9 hrs
 Summary of tx for DUB:
 Progestin challenge tests: give progestin for 5 days then stop. This simulates
Observation For mild bleeding
progesterone withdrawal. If ovaries are secreting estrogen, sloughing will occur and
menses results. No menses indicates no ovaries, no estrogen, or blood flow obstruction. OCP For pxs who are sexually active
 Prolactin inhibits GnRH pulsations and therefore inhibits ovulation. Progesterone If not sexually active, premenopausal women
Clomiphene If w/ infertility problems, induction of ovulation
PRIMARY AND SECONDARY DYSMENORRHEA
Keyterms  Average loss of iron in each menses is 13 mg.
 Dysmenorrhea – painful cramping sensation in lower abdomen accompanied by sweating,  Organic cause of abnormality in uterine bleeding vs. DUB
tachycardia, HA, NAV, diarrhea, tremulousness w/c occur just before or during menses. Organic cause DUB
o Primary dysmenorrhea – begin at or shorlty after menarche [ovulatory cycle], not Any age Extremes of age
associated w/ pelvic pathologic conditions. [< 20 yo] Ovulatory Anovulatory [MC cause]
o Secondary dysmenorrhea – arises after menarche [anovulatory cycle] and is Regular, cyclic dysmenorrhea Irregular, non-cyclic, no pain
associated w/ other pelvic conditions. [>20 y.o] Not responsive to treatment Responsive to hormonal tx
 Mitteschmerz – midcycle pelvic pain usually related to ovulation, unknown mechanism. Secretory endomerium Proliferating or hyperplastic

18
 Biphasic BBT Monophasic BBT o Polycystic ovarian disease [PCOD]: ↑ estrogen levels cause ↑ LH levels w/c cause
abnormal follicular growth and androgen secretion.
 Summary for DUB: o Ashermann’s syndrome: uterine scarring and adhesions after D and C.
Menorrhagia Regular Prolonged Excessive  Classification [primary amenorrhea w/ normal female external genitalia]
Metrorrhagia Irregular + prolonged Normal Absent breast, uterus A. gonadal failure – Turners syndrome, gonadal dysgenesis,
Menometrorrhagia Irregular + prolonged Excessive present 17α-hydroxylase deficiency w/ 46 XX
Hypermenorrhea Regular Normal Excessive B. hypothalamic failure – kallmann syndrome
Hypomenorrhea Regular Normal or ↓ Less C. pituitary failure
Oligomenorrhea Irregular Variable [>35d] Scanty Breast present, A. androgen resistance [testicular feminization]
absent uterus B. congenital absence of uterus [uterovaginal agenesis]
Polymenorrhea Regular Regular [<21d] Normal
Absent breast & B. 17, 20 desmolase deficiency
uterus C. Agonadism
PRIMARY AND SECONDARY AMENORRHEA
D. 17α-hydroxylase deficiency w/ 46 XY
Keyterms
Present breast & A. hypothalamic C. ovarian etiology
 Androgen resistance syndrome / testicular feminization – 46 XY, w/ testes and normal
uterus B. pituitary D. uterine etiology
male testosterone levels, normal female phenotype, absent uterus, scanty body hair.
 Ashermann’s syndrome – post-traumatic/post-curettage intrauterine adhesions or
Presumptions:
synenchiae w/ oligomenorrhea/amenorrhea or infertility
 Chromophobe adenoma – non-hormone secreting pituitary tumor w/c can disrupt normal  breast present means that estrogen is produced
pituitary function and thus produce decreased gonadotropin levels.  uterus present means Y chromosome is absent
 Congenital absence of uterus and vagina / uterovaginal agenesis / Rokitansky-Kuster-
Hauser syndrome – 46 XX, w/ normal ovarian function resulting in failure of uterus and HYPERPROLACTINEMIA, GALACTORRHEA, AND PITUITARY ADENOMAS
Keyterms
vagina to form.
 Bromocriptine – dopa-receptor agonists use to treat hyperprolactnemia.
 Cryptomenorrhea – menstruation w/o egress of menses thru introitus.
 Carbegoline – dopa-receptor agonist that directly inhibits secretion of prolactin from
 Delayed menarche – onset of menses in female older than 16.5 y.o who have no
pituitary and is an effective tx for hyperprolactinemia.
reproductive abnormality.
 Empty-sella syndrome – an intrasellar extension of subarachnoid space resulting in
 Gonadal failure – failure of gonads to develop, either be:
compression of pituitary gland and an enlarged sella turcica associated w/ galactorrhea
o Gonadal dysgenesis – if karyotype is abnormal
o Gonadal agenesis – if karyotype is normal and hyperprolactinemia.
 Galactorrhea – non-puerperal secretion from breast of watery or milky fluid that contains
 Gonadotropin-resistant ovarian syndrome / ovarian hypofolliculogenesis – premature
either pus or blood.
ovarian failure in w/c ovary contains normally appearing primordial follicles but no follicular
development  Hyperprolactinemia – levels of circulating prolactin above normal [> 20-25 ng/ml] that can
cause galactorrhea or amenorrhea or both.
 Hypogonadotrophic hypogonadism – failure of ovaries to develop as a result of low
amounts of circulatory gonadotropins. When anosmia is present, it is called Kallman  PIF – neurotransmitter [dopa] that inhibits prolactin synthesis and release.
syndrome [FSH > 30 mIUml].  Prolactinoma – MC pituitary tumor arising from chromophobic cells that secrete prolactin.
 Hypothalamic dysfunction – secondary amenorrhea caused by abnormal pattern of GnRH
pulsatility & circulatory estradiol levels > 40 pg/ml. Important facts
 Hypothalamic failure – secondary amenorrhea due to abnormal pattern of GnRH pulsatility  Main function of Prolactin is to stimulate growth of mammary tissue as well as produce &
& estradiol levels < 40 pg/ml. secrete milk into alveoli.
 Intrauterine adhesions / synechiae/ Ashermann’s syndrome – fibrous tissue  Major physiologic inhibitor of prolactin release is dopamine.
partially/completely obliterates uterine cavity.  Most frequent cause of slightly elevated prolactin levels is stress.
 Pituitary destruction – damage or necrosis of pituitary gland caused by anoxia, thrombosis  Diagnostic test of choice for prolactinoma is MRI.
or hemorrhage. It is known as Sheehan’s syndrome when related to pregnancy and  Main Sx in hyperprolactemia are galactorrhea and amenorrhea.
Simmond’s disease when unrelated to pregnancy.
 Polycystic ovarian syndrome – characterized by excessive androgen production, HYPERANDROGENISM
inappropriate gonadotropin secretion & chronic anovulation, begins perimenarcheally Keyterms
manifesting w/ hyperandrogenism [hirsutism, oligo/amenorrhea]  Acanthosis nigricans – dark, raised hyperpigmentation of skin found on nape and axilla.
 Premature ovarian failure – cessation of menses due to depletion of ovarian follicles or  Crytic hyperandrogenism – elevated levels of circulating androgens w/o clinical
failure of primordial follicles to respond to gonadotropins. manifestation of hirsutism or acne, accompanied by anovuation.
 Sheehan’s syndrome – postpartum pituitary necrosis  Hilus cell tumor – small testosterone-secreting ovarian tumor developing after
 Sigmond’s syndrome – pituitary hemorrhage not related to pregnancy menopause.
 Hyperandrogenic chronic anovulation – consists of endocrine findings in polycystic ovarian
Important facts syndrome w/o morphologic and sonographic findings of polycystic ovaries.
 1st sign of puberty is appearance of breast budding followed by appearance of pubic hair.  Idiopathic hirsutism [constitutional/familial hirsutism] – MC d/o associated w/ androgen
 Earliest sign of puberty is breast budding & menarche. excess, due to increased peripheral androgen metabolism, normal circulating levels of
 Mean interval btw breast budding and menarche is 2-3 yrs. testosterone and DHEAS.
 Arbitrary age of primary amenorrhea is 16 ½ yrs.  PCOS – characterized by excessive ovarian androgen production, abnormal gonadotropin
secretion, chronic anovulation, w/ morphologic changes in ovary consisting of multiple
 Ratio of fat to both total body weight & lean body weight is the most relevant factor tha
small subcapsular follicles, increased stromal tissues & ovarian enargement.
determines time of onset f puberty and menstruation.
 Sertoli or leydig cell tumors – testosterone secreting ovarian tumors usually unilateral.
 The most frequent antecedent factor of intrauterine adhesions is endometrial curettage
associated w/ pregnancy. It is confirmed by hysterography or hysteroscopy.  Spironolactone – aldosterone antagonist acting as anti-androgen by binding to peripheral
 MC cause of secondary amenorrhea in adolescent women is anorexia nervosa, w/c is due androgen receptor w/o inducing androgenic activity. It also inhibits steroidogenesis by
to hypothalamic dysfunction. interfering w/ ovarian enzymatic activity in pilosebaceous unit.
 MC cause of primary amenorrhea is gonadal failure.  Stromal hyperthecosis – characterized by nests of luteinized theca cells w/in stroma of
bilaterally enlarged ovaries, associated w/ virilization.
 2nd MC cause of primary amenorrhea is uterovaginal agenesis.
 Dx of gonadal failure or hyeprgonadotrophic hypogonadism can be established by FSH
Important facts
levels > 30 mIU/ml.
 Major androgen produced by ovaries is testosterone, for adrenal gland is DHEAS.
 MC non-prolactin secreting pituitary tumors are chromophobe adenomas.
 Ovaries secrete about 0.1 mg of testosterone/day from thce-stromal cells
 MC mullerian anomaly is imperforate hymen. Tx: cruciate incision
 MC cause of androgen excess in females is idiopathic hirsutism.
 MC form of hypogonadism in females is Turner’s syndrome.
 “Halo sign” in UTZ is characteristic of PCOS. Its S/Sx include amenorrhea, hirsutism and
 MC cause of delayed puberty is constitutional delay.
obesity.
 Some etiologies of amenorrhea:
 MC cause of sexual ambiguity in newborn is congenital adrenal hyperplasia.
o Kallman’s syndrome: congenital lack of GnRH
 Spironolactone is the TOC for PCOS and idiopathic hirsutism.
o Sheehan’s syndrome: pituitary infarction resulting from hypotension during delivery,
 Summary of tx for hirsutism:
usually resulting from hemorrhage.
o Premature ovarian failure: menopause before age 35 If w/ ↑ testosterone, excess ovarian androgen production OCPs
o Savage’s syndrome: ovarian resistance to FSH/LH If w/ ↑ DHEAS, excess androgen secretion Dexamethasone
o Turner’s syndrome [XO karyotype]: ovarian dysgenesis If neither is increased Spironolactone

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  3 markers of androgen production: o MC cause of primary amenorrhea: gonadal dysgenesis
Ovary Testosterone o MC cause of fetal morbidity and mortality: preterm labor
Adrenal gland DHEAS o MC reason for neonatal sepsis: chorioamnionitis [GBS, E. coli]
Peripheral 3α–diol-G o MC congenital adrenal hyperplasia: 21-hydroxyase deficiency
 High LH: FSH ratio in the context of androgen excess indicates that ovary is the source.
 Hair-Van syndrome triad: acanthosis nigricans, hyperandrogenism, insulin resistance.  A baby w ambiguous genitalia, dangerously hypotensive, and w/ elevated 17-
hydroxyproesterone: 21-hydroxylase deficiency
INFERTILITY  11-β hydroxylase deficiency: low cortisol, high mineral corticoids [hypertensive], and high
Keyterms androgens + elevated 11-deoxycortisol.
 Artificial insemination – sperm placed in female reproductive tract other than by sex. It is  21-hydroxylase deficiency: low cortisol and mineral corticoids [hypotensive], high
also known as donor or therapeutic donor insemination. androgens + 17-hydroxyprogesterone is elevated.
 Asthenospermia – loss or reduction of motility of spermatozoa.  24 y/o obese woman w/ facial hair comes in w/ complaints of amenorrhea. LH: FSH ratio
 Azoospermia – absence of sperm in semen. [i.e Klinefelter, varicocele] is elevated: PCOS [tx w/ OCPs]
 Clomiphene citrate – given to induce ovulation in anovulatory females w/ circulating  A baby w/ ambiguous genitalia is born to a mother who complains of increased facial hair
estradiol levels of > 40 pg/ml. growth over the last few months: luteoma of pregnancy
 Gamete intrafallopian transfer [GIFT] – placement of human ova and sperm into distal end
of oviduct. Pelvic pain
 In vitro fertilization [IVF] – fertilization of human ova by sperm in the lab.  Chronic pelvic pain is defines as > 6 mos. of pain.
 Infertility – inability of couples of reproductive age to establish a pregnancy by having  MC cause of chronic pelvic pain: PID
sexual intercourse w/in a certain period of time [usually 1 yr]  Pelvic pain associated w/ ovulation: mittelschmerz
 Oligospermia - < 20 M sperm/ml of semen  Final conclusive step in diagnosing pelvic pain: laparoscopy
 Ovarian hyperstimulation syndrome – ovarian enlargement to a diameter of > 6 cm due to  MC cause of acute pelvic pain ruptured cysts
stimulation of multiple follicles.
 Primary infertility – occurs in woman who has never been pregnant Pelvic masses
 Salpingitis isthmica nodosa – diverticula of endosalpinx in muscularis of isthmic part of  Histories suggestive of diagnosis:
oviduct. Context in w/c pelvic mass is found Likely diagnosis
 Secondary infertility – it occur after 1 or more pregnancy Painless abnormal uterine bleeding Leiomyoma
 Spinbarkeit – property of elasticity or disensibiity of cervical mucus. Amenorrhea Pregnancy, ovarian cysts
 Teratozoosermia – greater than normal incidence of abnormal forms of sperm in semen Dysmenorrhea Endometriosis
analysis. Reproductive age Preganancy, ovarian cysts, leiomyoma,
TOA, ovarian neoplasm
Important facts Postmenopausal Neoplasm
 Measurement of LH by urinary LH immunoassays is the best way to detect optimal time to Hx of PID S/sx of systemic illness [TOA, adhesion]
have intercourse or insemination. Hx of surgery/endometriosis Adhesions
 Clomiphene citrate is the TOC for females w oligomenorrhea as well as amenorrhea who
have sufficient ovarian estradiol production. S/E: ovarian cyst formation  MC causes of undiagnosed pelvic masses: leiomyomas
 Intracytoplasmic sperm injection is now the TOC for all causes of male infertility as well as  Diagnostic tests for various causes of pelvic masses:
for those w/ no known cause of infertility. Ovarian cysts PE + UTZ for confirmation
 If GnRH is used for ovulation induction, it needs to be administered in a pulsatile manner Leiomyomas PE + UTZ, hysteroscopy for confirmation
at intervals of 1-2 hours. Ovarian neoplasm UTZ, CT scan, CA-125, family hx, age suspicion
 [Refer to p. 76-77 of OB-GYN handy notes for causes of Infertility] Endometrial neoplasm ECC and D and C
Tubo-ovarian abscess Hx of PID, tender mass, KUB xray [ileus]
MENOPAUSE
Keyterms  MC functional ovarian cysts: follicular cyst
 Atrophic vaginitis – inflammation of vaginal epithelium due to atrophy secondary to  MC indication for hysterectomy leiomyoma
decreased circulating estrogen.  Extremely rarely do leiomyomas progress to malignancy [leiomyosarcoma]
 Climacteric – physiologic product in female life during w/c there is regression of ovarian  MC type of leiomyomas: subserous type
function. Apparent clinically over 3-5 yrs around menopause.
 Leiomyomas/fibroids are hormonally responsive smooth muscle tumors.
 HRT – administration of estrogen and progestin.
 Changes in uterine fibroids over time: hyaline degeneration, calcification, red
 Hot flush – pathognomonic sign of menopause caused by decreased in circulating degeneration [painful interstitial hemorrhage w/ pregnancy, and cystic degeneration]
estrogen levels.
 Uterine locations of leiomyomas:
 Menopause – complete or permanent cessation of menses indicated by finl menstrual
Submucous Just below endometrium, tend o bleed Menorrhagia
period, often during the climacteric. Interval of 6-12 mos. is needed, usual age: 45-55 y.o
Intramural w/in the uterine wall Menorrhagia
 Premature ovarian failure / premature menopause – cessation of menses due to depletion
Subserous Just below he serosa/peritoneum Torsion
of ovarian follicles before age 35-40.
 Raloxifene – estrogen agonist effect on bone by suppressing bone resorption & an
 Pregnancy w/ fibroids does carry increased risk for preterm labor and feral
estrogen antagonist effect on endometrium and breast tissue.
malpresentation.
 Selective estrogen receptor stimulator [SERM] – agents that bind to estrogen receptor and
have estrogen agonist effect on other tissue.
Sexually transmitted diseases
 Tibolone – synthetic steroid w/ estrogenic, progestogenic and androgenic activity, reduces
 Gold standard for diagnosis of PID: laparoscopy
hot flushes, increases bone density and does not stimulate endometrial proliferation when
given orally.  Chandelier sign: when you touch the cervix, there is so much pain that she jumps to the
chandelier.
Important facts  Common causative agents in PID: N. gonorrhea, C. trachomatis, E. coli, Bacteroides
 Initial fall in inhibin levels is the 1st index of declining ovarian function.  Gold standard for diagnosis of gonorrhea: culture on Thayer-Martin agar
 Most effective tx for hot flushes is estrogen, alternative is progestogen.  There is 50-90% chance of transmission after 1 exposure to gonorrhea.
 Spine and hip are the MC location of osteoporotic fractures.  Fitz-Hugh-Curtis perihepatitis presents as RUQ pain, fever, nausea and vomiting. It can
 Contraindications to estrogen treatment: presence of breast or endometrial CA, active be caused by chlmydia or gonorrhea.
thrombophlebitis and undiagnosed AUB.  Use erythromycin rather than doxyycline for pregnant women or children w/ chlamydia.
 Median age of onset of menopause is 47.5 yrs, and is median length is 4 yrs.  CS delivery is indicated for active herpes infection.
 A very specific test in dx of AIDS western blot
 Whiff test: combining vaginal secretions w 10% KOH: amines released will give fishy odor,
indicating a [+] tests
Important Gynecologic concepts
 Some most common:
o MC cause of hirsutism: PCOD
o MC reason for hospitalization in women of reproductive age: endometriosis
o MC post-operative complication: pulmonary atelectasis

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 MISCELLANEOUS [OBSTETRICS & GYNECOLOGY] Main lesion in syphilis Endarteritis
MC neonatal infection or white plaques in children Thrush [candidal stomatitis]
Most common MC site of metastatic trophoblastic disease Lungs
MC cause of gynecologic malignancy Endometrial CA MC CA of placenta – benign Cavernous hemangioma [vs. chorioangioma]
MC CA in women Leiomyoma MC placental lesion Placental infarcts
MC liver CA associated w/ OCP use Hepatocellular adenoma MC Sx in placenta previa Painless vaginal bleeding
MC CA invading female GUT Endometrial adenoCA In abruption placenta Painful vaginal bleeding
MC type of endometrial adenoCA Endometrial CA MC pregnancy complication in women w/ Abortion
MC form of ductal CA in-situ of breast Comedo DCIS unicornuate uterus
MC CA of breast – primary, malignant Invasive ductal CA MC serious medical complication of pregnancy Pyelonephritis
Least common CA of the breast Papillary CA MC serious liver disease in pregnancy Hepatitis
MC CA of breast – primary, benign Fibroadenoma MC cause of Cushing syndrome in pregnancy Benign adrenal tumor
MC congenital anomaly of breast Supernumerary nipples [vs. accessory nipples] MC benign mesenteric masses Chylous or mesenteric cyst
MC malignant neoplasm of breast w/ calcifications Ductal CA in situ MC cause of SAH during pregnancy Ruptured cerebral aneurysm
MC breast disorder/breast mass Fibrocystic changes Most likely cause of spider angioma in pregnancy Estrogen
MC breast CA presenting w/ architectural distortion Lobular CA Most important characteristic of baseline FHR Beat-to-beat variability
w/o a discrete density Most sensitive method to dx CMV infection CMV IgM titer
MC mammographic presentation of an invasive CA Speculated density MC method of family planning Tubal sterilization
MC cause of bloody nipple discharge in F > 50 y.o Ductal papilloma MC complication of multiple gestation Preterm delivery
MC cause of green, straw-colored nipple discharge Fibrocystic disease MC complication of SLE during pregnancy HPN
MC cause of breast mass after a trauma Fat necrosis MC neurologic abnormality in neonatal period Asphyxial brain injury
MC breast mass in postmenopausal women Breast carcinoma MC neurologic disorder of neonatal period Hypotonia
MC CA of connective tissue/soft issue – benign Lipoma MC congenital anomaly of he nervous system Myelomeningocoele
MC site of origin of metastatic tumor to ovary Stomach [Krukenberg tumor] MC cause of neonatal sepsis Chorioamnionitis
MC site of vaginal epithelial tumor Upper part of posterior wall MC cause of primary amenorrhea Gonadal dysgenesis
MC CA of ovary during pregnancy Dysgerminoma MC cause of fetal morbidity & mortality Preterm labor
MC CA of ovary – benign, primary Serous cystadenoma MC cause of acute & chronic pelvic pain Rupture ovarian cyst & PID
MC CA of ovary – malignant, primary Serous cystadenocarcinoma MC type of fistula formation after prolonged Vesico-vaginal fistula
MC CA of ovary – benign Mature teratoma [epithelial tumors] obstructive labor
MC germ cell tumor of ovary Mature cystic teratoma MC cause of undiagnosed pelvic masses Leiomyomas
MC germ cell tumor of anterior mediastinum Seminoma MC functional ovarian cyst Follicular cyst
Most important criteria for dx btw borderline Stromal invasion MC reason for hospitalization in women of Endometriosis
ovarian tumor & frank CA reproductive age
MC uterine site for implantation Upper posterior wall MC indication for hysterectomy Leiomyomas
MC finding in uterine rupture Fetal distress MC used test to detect APAS antibodies ELISA
MC CA of uterus – primary Leiomyoma Most specific clotting test to identify lupus Platelet neutralization
MC CA of uterus adenoCA MC source of cerebral artery embolism during Heart
MC CA of vulvar & cervix SCCA pregnancy
MC CA of testicles & the most malignant chorioCA MC pregnancy complication of benign ovarian cyst Torsion
MC CA of testicles [overall] Seminoma MC fetal presentation to enter the pelvis LOT
MC CA in uncircumcised men SCCA MC cause of oligohydramnios Renal anomalies
Most radiosensitive testicular tumor Seminoma MC cause of innocent heart murmur in childhood Still’s murmur
MC germinal tumor in males Seminoma MC type of conjoined twin Thoracophagus
MC fusion defect of the urethra in men Hypospadias MC intrapartum presentation of twins Cephalic-cephalic
MC metastatic site of prostate CA Pelvis Most critical period w/ regards to developmental Embryonic period
MC cause of acute urinary retention in men BPH malformations
MC cause of venereal disease in men Non-gonococcal urethritis Most likely the cause of fetal-maternal hemorrhage Chorioangioma
MC cause of UTI in males Prostatic hypertrophy MC inherited bleeding disorder Von willebrand disease
MC CA of breast in males Infiltrating ductal CA Most significant fetal consequence of GDM Macrosomia
MC cause of PID N. gonorrhea > C. trachomatis MC birth defect in women w/ overt DM CHD
MC cause of UTI in young women E. coli, S. saprophyticus Most appropriate method of contraception for DM Sterilization
MC cause of STD [overall] Chlamydia MC maternal complication of hydramnios Abruption placenta
MC cause of STD in adolescents Condyloma acuminatum MC recognizable COD in fetus Abruption placenta
MC cause of venereal disease in women Gonorrhea MC cause of severe DIC in pregnancy Abruption placenta
MC cause of ectopic tubal pregnancy PID MC cause of PP he requiring hysterectomy Placenta accrete
MC cause of vaginitis & vulvar infections / pruritus Candidiasis [C. albicans] MC cause of primary LTCS Dystocia
MC cause of vulvovaginitis Candidiasis & moniliasis MC postpartum complication of precipitous labor Hemorrhage
MC viral cause of vulvo-vaginal infections HPV [condyloma acuminatum] MC breech presentation Frank breech
MC bacterial cause of vulvo-vaginal infections G. vaginalis MC finding in molar pregnancy Increase uterine size
MC cause of hemosalpinx Ectopic pregnancy [MC complaint = pain] MC finding in uterine rupture Fetal distress
MC cause of suppurative salpingitis Gonococcus Most significant factor in postpartum metritis Route of delivery
MC cause of ambiguous genitalia Androgenital syndrome Most ideal anesthetic for replacing inverted uterus Halothane
MC chromosomal anomaly in early spontaneous 45 X Most ideal anesthetic for non-OB surgery at preg. General anesthesia
abortion MC extrauterine disease requiring surgical Appendicitis
MC chromosomal anomaly in 1st trimester abortion Autosomal trisomy treatment during pregnancy
MC chromosomal anomaly in cystic hygroma in 2nd Monosomy X MC cause of episiotomy breakdown Infection
or 3rd trimester MC cause of dystocia Pelvic contraction & uterine dysfunction
MC chromosomal anomaly associated w/ choroids Trisomy 18 MC cause of uterine rupture Separation of previous CS scar
plexus cyst MC cause of fetal tachycardia Maternal fever
MC chromosomal disorder Down’s syndrome or trisomy 21 Most reliable sign of fetal compromise Reduced baseline variability
MC ectopic tubal implantation site Ampulla MC deceleration pattern during labor Variable deceleration
Most definitive treatment for CIN Hysterectomy Most reliably detected part of fetal ECG R wave peak
Most sensitive pregnancy test b-HCG Earliest morphologic evidence of ovulation found in Basal vacuolation
Most specific test of Amniotic fluid to exclude intra- Gram stain endometrium
amniotic infection MC site of endometriosis Ovaries
MC cause of stillbirth Syphilis MC site of breast CA Upper outer quadrant

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RAPID REVIEW
Treatment for breastfeeding mastitis
MC cause of non-obstetric postpartum death
Postmaturity syndrome characteristics
Cardinal movements of labor
A pregnant w/ Hct = 10, is this normal?
Test used to detect NTDs
Test at 10th wk AOG to screen for
chromosomal abnormalities
Antihypertensive in px w/ severe preeclampsia
Abnormal HR pattern in CST
Seizure prophylaxis in severe preeclampsia
Cure for ecclmpsia & preeclampsia
Cause of erythroblastosis fetalis
Cause of hydrops fetalis
Preeclampsia in 1st trimester is
Primary causes of 3rd trimester bleeding
Chromosomal pattern of complete mole
Molar pregnancy containing fetal tissue
Antibiotics w/ teratogenic effects
Shortest AP diameter of pelvis
Meds given to accelerate fetal lung maturity
MC cause of postpartum hemorrhage
Tx of postpartum hemorrhage
Typical antibiotics for GBS prophylaxis
Px fails to lactate after CS w/marked blood
loss
Cause of amenorrhea w/ normal prolactin, no
response to estrogen, progesterone challenge
& hx of D and C
Therapy for PCOS
Medication used to induce ovulation
Dxtic step required in postmenopausal women
w/ vaginal bleeding
Indications for medical treatment of ectopic
pregnancy
Medical options for endometriosis
Uterine bleeding at 8 wks AOG, no products
expelled, cervical os is closed
Uterine bleeding at 18 wks AOG, no products
expelled, membrane ruptured, cervical os
open
Laparoscopic findings in endometriosis
Natural history of melanoma
Px w/ increased vaginal discharge & petechial
patches in upper vagina & cervix
Tx for bacterial vaginosis
Contraception that protects against PID
Unopposed estrogen is contraindicated in
Px w/ recent PID & RUQ pain
Annual screening for women w/ strong family
hx of ovarian CA
Lab values suggestive of menopause
MC cause of female infertility
2 consecutive findings of ASCUS, next step?
Continue BF & give PO antibiotics
Thromboembolic disease
Oligohydramnios & passage of meconium in
utero, “scrawny” neonate w/ dry, peeling skin
Engagement, descent, flexion, internal
rotation, extension, external rotation,
expulsion
No. a Hct < 11 should raise IDA suspect
AFP or amniocentesis
Chorionic villous sampling
Hydralazine & labetalol
Late decelerations [fetal hypoxia]
IV magnesium sulfate
Delivery
Maternal antibodies against infant’s Rh-[+]
RBC result in fetal RBC hemolysis
↓ protein production by fetal liver leading to ↓
oncotic pressure, edema & cardiac failure
H mole
Abruption placenta & placenta previa
46, XX
Partial mole
TCN, fluoroquinolones, aminoglycosides,
sulfonamides
Obstetric conjugate [btw sacral & pubis]
Betamethasone or dexamethasone x 48 hrs
Uterine atony
Uterine massage or oxytocin
IV PCN or ampicillin
Sheehan’s syndrome [postpartum necrosis]
Ashermann’s syndrome
Weight loss & OCPs
Clomiphene citrate
Endometrial biopsy
Stable, unruptured ectopic pregnancy of < 3.5
cm at 6 wks gestation
OCPs, danazol, GnRH agonists
Threatened abortion
Inevitable abortion
“chocolate cysts & powder burns”
Regresses after menopause
Trichomonas vaginitis
Oral or topical metronidazole
OCP & barrier contraception
Endometrial or estrogen receptor [+] CA
Fitz-Hugh-Curtis syndrome
CA-125 & transvaginal UTZ
Elevated serum FSH
Endometriosis
Colposcopy & endocervical curettage
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