HI-YIELD NOTES IN OB-GYNE

1. 1
HI-YIELD FACTS IN OBSTETRICS [from USMLE CLERKSHIP-OB& handy notes]
Keyterms
Ovulation /postconception It is 2 wks < gestational age
Gravida Woman who is, or has been pregnant irrespective of the outcome
Parity Number of pregnancies reaching viability
Puerperium 6-8 wks period after delivery
Perinatal period Commences at 22 completed wks of gestation & ends 7 completed days after birth
Neonatal period From birth to 28 days after birth
Embryonic period 3rd wk to 7th wk after fertilization, when major structures are formed
Previable period Lasts from 11-20 AOG
Viable period Lasts from 21-40 AOG
Preterm Less than 37 completed wks
Term From 37-42 completed wks
Post-term 42 completed wks or more
Low birth weight Less than 2500 gms
Very low birth weight Less than 1500 gms
Extremely low BW Less than 1000 gms
Puerperium Time after delivery of placenta up to return of reproductive organs to their normal
non-pregnant state [usually occur at 6-8 wks]
PHYSIOLOGIC OBSTETRICS
Chapter 2: Anatomy of Female Reproductive Tract
 Functional components:
Placental arm Paracrine arm
Nutritive, endocrine, immunologic Pregnancy maintenance, immunologic acceptance, AFV & hemostasis, physical
protection of fetus
 Communication system:
Placental arm Paracrine arm
Maternal blood to placental intervillous space, fetal blood
confined to capillaries
Chroion leave, maternal deciduas parietalis,
amnion
 Embryology
Paramesonephric or mullerian ducts Forms uterine tubes [cranial], uterus [caudal], and upper part of vagina
Urogenital sinus Forms lower part of vagina & vestibule
Mesonephric system or wolffian duct Forms the epoophoron & paroophorron
Germinal epithelium Forms the ovary
 6 openings of vestibule:
o Urethra, vagina, bartholin’s ducts [2], paraurethral/ skenes ducts [2]
 Vagina:
o pH = 4-5
o blood supply:
Upper 1/3 Cervicovaginal branch of uterine A.
Middle 1/3 Inferior vesical A.
Lower 1/3 Middle rectal and internal puddendal A.
o lymphatics:
Upper 1/3 Iliac nodes
Middle 1/3 Internal iliac nodes
Lower 1/3 & vulva Inguinal nodes
 Perineum:
o Blood supply: internal pudendal and its branches [inferior rectal + posterior labial A.]
o Innervation: pudendal nerve
o Muscles:
Pelvic diaphragm Levator ani and coccygeus muscles
Urogenital diaphragm Deep transverse perineal, constrictor urethrae, internal and external fascial
coverings
Perineal body: on w/c converge the bulbocavernosus M., superficial transverse perineal M., and external anal
sphincter
 Uterus:
o Wall: endometrium, myometrium and serosa
o Lymphatics: hypogastric nodes [cervix], internal iliac, nodes to ovarian region and periaortic nodes [body]
o Ligaments:
Uterosacral lig. superior part of cervix encircling the rectum, insert over S2-3
Cardinal lig. Aka: transverse cerviacal lig. Or Mackenrodt lig.
United firmly to the supravaginal wall of cervix
Round lig. Continuous w/ broad lig. to inguinal canal terminatinng at upper part of labium majus, holds
the ovary in place
 Oviducts:
o Parts [from uterus to lateral wall]: interstitial part, isthmus, ampulla, fimbrial end / infundibulum]
Chapter 3: Physiology of Normal Mensrual cycle
Menstruation
 Average thelarche = 10 y/o [↑ estradiol], pubarche = 11 y/ o [↑ adrenal hormones], menarche = 12 y/o [↑
estradiol]
 Causes of precocious puberty and manifestations:
Idiopathic – MC cause Thelarche/pubarche/menarche
Tumors of hypothalamic-pituitary stalk Thelarche/pubarche/menarche
Inflammation of the hypothalamus Thelarche/pubarche/menarche
21-hydroxylase deficiency Pubarche
Excess estrogen Thelarche and menarche
 Average menses = 3-6 days
 Blood loss in menstruation averages 30-50 ml, should not form clots. > 80 ml is abnormal amount of blood loss.
 Phases of menstrual cycle:
o Menstruation: days 1-4 [1st part of follicular phase]
o Follicular phase [proliferative phase]: days 1-14
o Ovulation; day 14
o Luteal phase: days 14-28
 Main events of menstruation: absence of progesterone causes endometrial sloughing.
 2 main events in follicular phase:
o FSH causes follicle maturation and estrogen secretion.
o Estrogen causes endometrial proliferation.
 Main event of ovulation:
o LH surge causes oocyte to be released.
 Main events of luteal phase: corpus luteum secretes progesterone w/c causes endometrial maturation [↓FSH,
↓LH].
Chapter 4: Endometrium and Decidua
 Endometrial cycle and histology:
Early proliferative phase Glands are tubular and short, nuclei are basally located w/ abundant mitotic figures
Late proliferative phase Glands become tortuous w/ cells lining the gland undergoing pseudostratification
Early secretory Glycogen-rich subnuclear vacuoles appear at base of cells
Mid-late secretory Endometrium rich in glycogen, decidualization of stromal cells
Premenstrual Intense coiling of spiral arteries w/ PMN infiltration of stroma
 Sex-steroid hormone induced proliferation:
Pre-ovulatory or follicular phase Estradiol 17-β is secreted by follicles
Post-ovulatory or follicular phase Progesterone secreted by corpus luteum, at 7-8 days after ovulation
progest + estrogen declines
Proliferative phase Estrogen is the predominant hormone, ↑ PTH-rp, vasodilatation occurs
Late secretory phase + menses Progesterone withdrawal + TGF-β, increase endothelin-1,
vasoconstriction occurs

2. 2
 3 portions of deciduas
Decidua basalis Directly beneath site of blastocyst implantation
Decidua capsularis Overlies the enlarging blastocyst & is most prominent during 2nd month of pregnancy
Decidua parietalis Joins decidua capsularis at 14-16 wks of pregnancy
 Blood supply of endometrium:
Basal 1/3 Straight arteries
Superficial 1/3 Coiled or spiral arteries
Important facts
 At 6 days post-fertilization, blastocyst establishes cell to cell contact w/ endometrium.
 Restoration of epithelial surface of endometrium is complete by 5 days of endometrial cycle.
 Subnuclear vacuolization is the 1st histologic indication of progesterone effect.
 Decidua is the source of prolactin in amniotic fluid.
 Nitabuch’s layer is where invading trophoblast meet the decidua, a zone of fibrinoid degeneration.
Chapter 5: Placenta and Fetal membranes
 Structures:
Amnion Tough and tenacious bu pliable membrane, innermost vascular fetal membrane, contiguous w/
amniotic fluid. Amnion layer continuos w/ chorion leave is the acellular zona spongiosa. The
amnion develops 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.
Umbilical cord 30-100 cm [ave. 55] length, w/ 2 arteries and 1 vein, 0.8-2.0 cm in diameter, average of 55 cm.
Exracellular matrix of umbilical cord is composed of specialized tissue [Wharton’s jelly].
Amniotic fluid Average vol: 1,000 cc at term, 400 cc at midpregnancy, 50 cc at 12 wks
Important facts
 Zona pellucida disappears prior to implantation & blastocyst adheres to endometrial surface [apposition].
 Leafy chorion/chorion frondosum [fetal part] while chorion leave/bald chorion contains the ghost villi.
 As emdryo grows further, the decidua capsularis & parietalis form the decidua Vera.
 The impetus for implantation invasion is provided by trophoblasts.
 Human placenta is of hemochorioendothelial type.
 Mainstem villi & its ramififications constitute a placental cotyledon.
 Chorionic villi can be seen in human placenta by 12th day post-fertilization.
 MC vascular anomaly in humans is absence of 1 umbilical Artery.
Chapter 6: Placental hormones
Important facts
 ANP is produced in atrial myocytes & is synthesized in placenta. It causes natriuresis, diuresis and vasorelaxation
of uterus during pregnancy.
 Inhibin acts to inhibit FSH release by the pituitary.
 Highest carbohydrate content of any human hormone is in HCG [pregnancy hormone]. A glycoprotein produced
by syncitiotrophoblasts. It is secreted maximally at 8-10 wks AOG. It also acts to rescue or maintain corpus luteum
to promote continued estrogen stimulation.
 T ½ of HCG is 24 hrs while LH is 2 hrs.
 GH releasing hormaone is also known as somatocrinin.
 DHEAS is the principal circulating precursor of placental estrone & estradiol.
 Adrenal cortex is the largest organ in fetus, a principal source of estrogen precursors.
 The primary placental estrogen that enters maternal compartment is estradiol.
 Pregnanediol is the principal urinary metabolite of progesterone.
 Maternal plasma LDL cholesterol is the principal precursor of progesterone biosynthesis in placenta.
 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 accommodation & successful
parturition.
Chapter 7: Morphological and Functional development of fetus
 Most frequently used diameters of fetal head:
Occipitofrontal 11.5 cm From root of nose to occipital bone
Biparietal 9.5 cm Greatest transverse diameter of the head
Bitemporal 8.0 cm Greatest distance btw 2 temporal sutures
Occipitomental 12.5 cm Greatest diameter of fetal head
Suboccipitobregmatic 9.5 cm From large fontanelle to occipital bone
 Plane of occipitofrontal diameter: 34.5 cm [greatest head circumference]
 Plane of suboccipitobregmatic: 32 cm [smallest head circumference]
Cardiovascular system
 Remnants of the following will become:
Umbilical vein Ligamentum teres
Umbilical artery Medial umbilical ligament
Urachus Median umbilical ligament
Tongue remnant [thyroid] Foramen cecum
Vitelline duct Meckel’s diverticulum
Ductus venosus Ligamentum venosum
Ductus arteriosus [closes at 10-96 hrs] Ligamentum arteriosus
Foramen ovale [closes after several mins] Anatomical fusion at 1 yr.
Fetal coagulation factors
 ↓ factors 2,6,9,10,11,12,13, fibrinogen & plasminogen, ↑ thrombin, normal platelet count
Immunocompetence of fetus
 13 wks: fetus is immunologically competent
IgG Transported btw mother to fetus at 16 wks
IgM Produced by fetus in response o infections, adult levels at 9 mos.
B lymphocytes Appear in liver at 9 wks, in blood and spleen at 12 wks
T lymphocytes Produced by thymus at 14 wks
Gastrointestinal tract
 Glucagon identified by 8 wks, insulin detectable by 12 wks
 Fetal pancreas noted at 9-10 wks
 Swallowing begins at 10-12 wks
 Peristalsis a 11 wks AOG
Nervous system and sensory organs
8th wk Flexion of fetal neck and trunk
10th wk Spontaneous movement noted
3rd lunar month Histological evidence of taste buds
4th lunar month Complete finger closure
24 or more wks Ability to suck
24-26 wks Fetus hears sounds in uterus
28 wks Eye sensitive to light, responsive to vibrations in taste
Respiratory system
 Glycerophospholipid composition of mature surfactant:
i. Phosphatidylcholine = 78%
ii. Phosphatidylglycerol = 9%
 Hormone regulation of surfactant:
Cortisol Natural stimulus for augmented surfactant synthesis
Prolactin Accelerate rate of synthesis of phosphatidylcholine by lungs
Estrogen Promote prolactin release
Thyroxine Accelerate fetal lung maturation
EGF Promote surfactant secretion and increase SP-A [major apoprotein surfactant]
Urinary system
 Fetal kidneys star producing urine by 12 wks
 Metanephros is the definitive urinary system.
 Lecithin is principal surface active component of surfactant.
 Phospholipid is the primary surface tension-lowering component of surfactant.
 Surface apoproteins serves to facilitate serve to facilitate forming & reforming of surface film in alveoli during
respiration.

3. 3
 Cortisol is the natural stimlus for augmented surfactant synthesis.
 Urine production = 10 ml/hr at 30 wks, 27 ml/hr at term
 Amniotic fluid volume:
- Term fetus is able to swallow as much as 450 ml/24 hrs of amniotic fluid
- At 16-18 wks, fetal urine becomes an important source of amniotic fluid
12 wks 50 ml
Midpregnancy 400 ml
36-38 wks 1000 ml
Respiration
 Respiratory movements are seen at 4 mos.
Endocrine system
 Neurohypophysis secretes oxytocin & AVP by 10-12 wks.
Gonads
 Fetal testis secretes testosterone and pregnenolone by 10 wks.
 Genetic sex is established at time of fertilization
 Sexual development of male and female embryo is identical up to 8 wks.
 Maleness: testosterone and MIF, its absence in Femaleness
Chapter 8: Maternal adaptations to pregnancy
Cardiovascular system
 Heart is displaced upwards and outwards due to gravid uterus
 Maximal increase in heart rate during 7-8th mos. w/ average of 10 bpm
 CO peaks during 25th-32nd wks [highest at 28th wks] = 30-40%
 4 periods of increased CO:
1. on 28wks AOG [highest peak]
2. during labor
3. immediately postpartum
4. 1st wk of puerperium
 ↑ Plasma volume [50-60%] w/c peaks by 7 mos. → dilutional anemia
 ↑ Pulse pressure maximum on the 7-8th mos.
 ↓ DBP [note that presence of diastolic murmur in pregnancy is never normal]
 Elevated venous pressure in lower extremities
Respiratory system
 Upward displacement of diaphragm by 4 cm
 ↑ in RR, TV, respiratory minute volume, and airway conductance
 ↓ FRC, RV, TPR, and broncho-motor tone [progesterone effect]
 Lung compliance is unaffected
Gastrointestinal system
 Px may have GERD/heartburn [progesterone effect]
 Decreased responsiveness to CCK
 Liver of pregnancy – swelling of kuppfer cells
Urinary system
 Kidneys hypertrophy due to ↑ renal blood flow
 Physiologic hydroureter evident at 1st trimester
 Estrogen stimulates hypertrophy and elongation of muscles while progesterone promotes generalized atony
 Prone to UTI due to progesterone and pressure changes
Endocrine system
 ↑ corpus luteum activity up to 12 wks
 Mild hyperthyroid state due to gland hyperplasia
 Pituitary gland hypertrophy and hyperplasia
 Diabetogenic due to placental degradation of insulin and insulin effects of placental lactogen, estrogen, and
progeterone
 Increase oxytocin production near term
Placenta
 HCG is detected in maternal plasma or urine by 8-9 days after ovulation, reaches nadir at 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 pregnancy
 progesterone synthesis is accomplished by syncitiotrophoblasts after 6-8 wks of pregnancy
Hematologic system
 ↑ retic count and RC volume due to erythroid hyperplasia
 ↓ Hct due o increase plasma volume
 Total iron requirement = 1 gm or 6-7 mg/day [RDA]
300 mg Fetus and placenta
200 mg Excreted
500 mg Erythrocyte production
Fetal blood hematopoiesis
Mesoblastic In yolk sac during embryonic period
Hepatic Liver up to near term
Myeloid BM starts at 4 mos. fetal age, major site in adults
Skeletal system
 Progressive lordosis
 Increased mobility of pelvis joints
Immunologic system
 Immuosupressive mechanism by progesterone, estrogen and HCG
 Production of suppressor T cells and AFP by fetus
Maternal metabolism
 Weight gain: at least 25 lbs weight gain
1st trimester 2 lbs
2nd trimester 11 lbs
3rd trimester 11 lbs
 Carbohydrate metabolism – pregnancy is diabetogenic due to:
o hPl has anti-insulin effect
o estrogen, progesterone and cortisol induce insulin resistance
o placenta secretes insulinase w/c cause insulin degeneration
 Protein metabolism
o + nitrogen balance at 29th wks
 Fat metabolism – lipemia occurs
Acid-base balance
 Pregnant women normally hyperventilate to reduce arterial PCO2
 Partial renal compensation: increase HCO3 secretion
Chapter 9: Diagnosis of pregnancy
Presumptive Sx Nausea with or w/o vomiting [due to increased HCG levels]
Urinary disturbances
Fatigue [due to increased metabolism]
Perception of fetal movement [quickening] = 18-20th wks AOG [primigravida] and 16-18th wks
[multigraviida].
Presumptive
signs
Amenorrhea, breast changes [dark areola, erected nipple, engorged breast], skin pigmentation
[choalasma/mask of pregnancy, striae gravidarum, spider telangiectasia (estrogen effect), linea
nigra], changes in vaginal mucosa, thermal signs [↑ temp by 0.3-0.5 for > 3 wks due to
progesterone effect]
Probable signs Abdominal enlargement, changes in skin, shape, and consistency of uterus, anatomical cervical
changes, Braxton-hicks contractions, ballotment, physical outlining of fetus, (+) preg test
Positive
evidence
Identification of FHT separate from mother, perception of active fetal movement by physician, UTZ
or radiologic evidence
 NAV occurs in 50% 0f pregnancies, most notably at 6 wks AOG, disappears 6-12 wks later.

4. 4
 Braxton-Hicks contraction: painless, irregular contractions at 28th wks.
 Quickening – awareness of 1st movement of the baby
 Ballottement noted at 20th wks.
 Anatomical changes in cervix:
o Beaded pattern of cervical mucus due to progesterone
o Ferning pattern due to estrogen seen on 1st half of the cycle
 Fetal heart tones:
o Normal FHT = 110-150 bpm
o UTZ by 8th wks
o Stethoscope by 17-19th wk
o Doppler as early as 10-12th wks
 Changes in cervical mucus: beading [progesterone], ferning [estrogen]
 Perception of fetal movement [quickening]: 16-18 wks [multi], 18-20 wks [primi]
 Different signs of pregnancy:
Presumptive Chadwick sign [6 wks] Discoloration of vaginal mucosa
Probable Hegars [6-8 wks] Soft compressible isthmus
Probable Goodell’s [4-8 wks] Cyanosis and softening of cervix
 HCG:
o Detected in maternal plasma or urine by 8-9 days after ovulation
o Peak levels at 60-70 days, Nadir reached at 100-130 days
o Urine HCG – preferred method to recognize normal pregnancy [25 mU/ml by 1 wk after LMP]
 Radiographic evidence of fetal death:
o Spalding sign: overlapping of fetal skull bones due to brain liquefaction
o Robert’s sign: gas bubble in fetus
o Exaggeration of fetal spine curvature
 Cranial signs of spina bifida on UTZ:
o Small BPD
o Ventriculomegaly
o Frontal bone scalloping [lemon sign]
o Abnormal curvature of cerebellum [banana sign]
o Effacement/obliteration of cisterna magna
 Scan dating is useful up to 20 wks AOG when menstrual data is unreliable or conflicts with clinical findings.
 Ideal weight gain:
o 1ST trimester: 1.5-3 lbs
o 2nd and 3rd trimester: 0.8 lbs/wk
 Pregnancy is an anabolic state.
 The optimal time to screen for glucose intolerance/DM in the pregnant female is at 26-28 AOG.
 By midpregnancy, fat is the primary source of maternal energy.
 Normal pregnancy is a hyperlipemic as well as glucosuric state.
 Diastolic murmurs in pregnancy are never normal.
 Chadwick’s sign: bluish discoloration of vagina and cervix due to congestion of pelvic vasculature.
 Constipation may occur secondary to progesterone, w/c relaxes the intestinal smooth muscle and slows
peristalsis.
 Asymptomatic bacteriuria occurs in 5-8% of pregnant women.
 OCPs and HRT [combinations of estrogen and progesterone] are the MC cause of melasma or “mask of
pregnancy”.
 TSH, PTH and calcitonin do not cross the placenta.
 HCG is detectable in maternal serum after implantation has taken place at 8-11 days after conception.
 Trophoblasts [rophoecoderm] are the precursor cells for the placenta and membranes.
 Placenta is the primary producer of steroid hormones after 7 weeks AOG.
 HCG maintains the corpus luteum and stimulates adrenal and placental steroidogenesis.
 MSAFP peaks btw 10-13 wks AOG then declines thereafter.
 After 1st trimester, placenta is the major source of circulating estradiol.
 Progesterone concentrations of < 5 ng/ml are diagnostic of fetal death in 1st trimester.
 Progesterone concentrations are significantly elevated in: women w/ hydatidiform mole complications of Rh
isoimmunization.
ANTEPARTUM
 Frequency of visits: < 28 wks – q month, 28-36 wks – q 2-3 wks, 36 wks to delivery – once per week until delivery
 Triple screen: serum AFP, estriol, beta-HCG at 16-18 wks
 Important hallmarks in prenatal visits:
o Pap smear: 1st visit
o Rh screen – 1st visit
o Gonorrhea and Chlamydia – 1st visit
o 1st sonogram – week 16-18
o Amniocentesis – week 16-18
o Triple screen – week 16-18
o Diabetes screen – week 16-18
o Group B strep culture – week 36.
 An inaccurate gestational age is the most common reason for an abnormal screen.
 After Rh sensitization, a Kleihauer-Bettke test is done to determine the amount of fetal RBCs in the maternal
circulation.
 RhoGAM administered to Rh-mothers exposed to fetal blood.
 Anti-D titers of > 1:16 require amniocentesis and analysis of amniotic fluid bilirubin].
 Intrauterine pregnancy seen via vaginal UTZ when beta-HCG > 1,500
 Intrauterine pregnancy seen via abdominal UTZ when beta-HCG > 6,000.
 Anti-D titers of > 1:16 require amniocentesis and analysis of amniotic fluid [bilirubin].
 Oligohydramnios [AFI < 5], may suggest possible fetal compromise due to umbilical cord compression.
 Polyhydramnios [AFI>20] may signify poor control in a diabeti pregnancy or a diabetic pregnancy or a fetal
anomaly.
 The average woman must consume an additional 300 kcal/day beyond baseline needs.
 Vaccines safe in pregnancy: hep B, oral polio, tetanus, yellow fever, dipheria
 Vaccines unsafe in pregnancy: measles, mumps and rubella
 Give immune globulin in pregnancy for exposure to: heap A and B, tetanus, chickenpox and rabies.
Chaper 10: Prenatal care
 Estimation of pregnancy duration
o LMP = count number of days since 1st day of last normal menses
o 280 days or 40 wks or 9 ½ calendar months
 EDC = [1st day of LMP] + 7 days – 3 mos. + 1 year [ex. LMP= 7/10/93, EDC = 4/17/94]
 Height of fundus [in cm] = wks AOG [18-32 wks]
 Fetal weight in gms = 155 x [fundic ht in cm – n]
o n = 12 if sation below ischial spines [engaged], 11 if above the ischial spines [unengaged]
o k = 155, constant
 Fundal height during pregnancy
Weeks Fundal height
12 Above pubic symphysis
16 Midpoint btw pubic symphysis and umbilicus
20 At umbilicus
28 6 cm above umbilicus
36 2 cm below xiphoid process
40 4 cm below xiphoid process
 Leopolds maneuver:
LM1 Fundal grip What fetal pole occupies the fundus?
LM2 Umbilical grip Which side is the back?
LM3 Pawlick’s grip What fetal part lies above pelvic inlet?
LM4 Pelvic grip Which side is the cephalic prominence?
Findings:
LM1 Irregular nodular [breech] Round [cephalic]
LM2 Linear, convex, bony ridge [back] Numerous nodulations [small parts]
LM3 Round, ballotable [unengaged] Fixed, knoblike part [engaged]
LM4 Cephalic prominence on same side as fetal parts
[flexion]
Cephalic prominence on same side as fetal back
[extension]

5. 5
 Visit intervals: q 4wks until 28 wks, then q 2-3 wks until 36 wks then weekly thereafter
 Lab examinations:
Time [wks] Assessment
Initially [ASAP] CBC, U/A, blood group & Rh type, PAP smear, Hepa B screen]
8-18 wks UTZ, amniocentesis, chorionic villous sampling
15-20 wks MSAFP screening
26-28 wks Screen for GDM if indicated, repeat CBC [esp. Hb and Hct]
28 wks Test D-negative women for antibodies
32-36 wks UTZ, repeat CBC, test for STD
3rd trimester Hepa B screening
Note:
Give hepa B Ig & vaccine to infans of HBsAg [+] mothers
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
Chapter 14: Ultrasound in pregnancy
Abdominal UTZ [full bladder] Full bladder acts as acoustic window, pushing uterus out of pelvis & displacing
bowel superiorly
Vaginal UTZ [empty bladder] Small amount of urine pushes the uterus posteriorly out of view
 Indications for 1st trimester UTZ
o Establishes uterine pregnancy upon seeing gestational sac [earliest at 5-6 wks]
o Detection of fetal life and number of fetuses [FHT by 7 wks AOG]
o Evaluates for retrochorionic hemorrhage, incomplete/complete abortion [if > 600 cc]
o Early dating of pregnancy using:
Gestational sac diameter At 5-6 wks
CRL At 12-14 wks [most accurate]
BPD, femoral length Onwards
o Evaluation of uterus and adnexa
 Indications for 2nd and 3rd trimester UTZ
o Fetal viability, number and presentation
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]
o Evaluation of fetal amniotic structures [reversal of fetal diastolic blood flow in umbilical artery indicates a
severely compromised fetus]
Chapter 13: Nutrition during pregnancy
Calories Daily increase of 300 kcal/day
Protein Increase to 5-6 gm/day
Iron 30 mg/day
60-100 mg for large built, twin fetuses, late pregnancy
200 mg for overly anemic women
15 mg/day for nonpregaant and lactating women
Calcium + phosphorus 1200 mg/day for nonpregnant, pregnant and lactating women
Zinc 15 mg/day for pregnant women, 12-19 mg/day for nonpregnant/ pregnant / lactating women
Iodine 175 ug/day for pregnant women
150-200 ug/day for nonpregnant and lactating women
Magnesium Pregnancy = 320 mg/day
Nonpregnant = 280 mg/day
Lactation = 355 mg/day
Chapter 11: Identification of high-risk pregnancy
Maternal age < 18 y.o or nullipara > 30 y.o
Maternal height 60 inches or < 153 cm
Maternal weight > 20% of standard weight for height
Obstetric hx If [+] medical illness
Chapter 15: Immunizations during pregnancy
 Contraindicated vaccines: measles, mumps and varizella-zoster
 Vaccines given similar o non-pregnant women: rabies, pneumococcal, meningococcal, tetanus, hepa A and B
 Requested only after 1st trimester: influenza
 Given only as post-exposure prophylaxis: hepa A and B, rabies, tetanus, VZV, measles
Chapter 16: The Pelvis [Passages]
 Pelvic inlet:
o Diameters of inlet:
1. Anteroposterior diameters
Diagonal conjugate 12 cm Only APD measured clinically
True or anatomic conjugate 11 cm DC – 1.2 cm
Obstetric conjugate 10 cm DC -1.5-2 cm
2. Transverse diameter of inlet 13 cm
3. Posterior sagittal of inlet 4 cm R and L oblique diameters
 Plane of greatest diameter: 12.5 cm – anteroposterior diameter
 Plane of midpelvis:
o Landmarks of areas of assessment of midpelvis:
1. prominence of ischial spines
2. convergent pelvic sidewalls
3. shallow concavity of sacrum
4. bi-ischial diameter of outlet: < 8 cm
o Diameters of midpelvis:
Anteroposterior diameter ?
Transverse diameter [bispinous] 10.5 cm
Posterior sagittal of midpelvis 4.5 ccm
 Pelvic outlet:
Anteroposterior diameter of outlet 9.5-11.5 cm
Transverse diameter [intertuberous] 11 cm
Posterior sagittal of outlet 7 cm
 Indications for clinical pelvimetry:
o Previous injuries or disease affecting the pelvis
o Breech for vaginal delivery, VBAC
 Soft parts of the pelvis: pelvic floor and pelvic diaphragm
 Forceps delivery is usually indicated in pxs w/ antrophoid pelvis.
Different pelvic types: [refer to OB-GYNE handy notes p. 11]
Chapter 18: Parturition
 4 phases of parturition:
Phase 0 Prelude to
parturition or
quiescence
Time of contractility and uterine unresposiveness, occurs before implantation
until 35-38 wks, mediaed by progesterone, cervix remains rigid & unyielding
Phase 1 Preparation to labor Uterus & cervix undergo anatomic and functional changes, ↑ oxytocin in
myometrial cells, dependent on uterotonins or uterotropin, cervix ripens &
dilates
Phase 2 Active labor Active uterine contractions occur, 3 stages of labor occur
Phase 3 Recovery period Uterine contraction & involution to prevent hemorrhage, initiation of lactation
and milk ejection for breastfeeding, uterotonins present
 Uterotropin vs. uterotonins
Uterotropin [ex. gap junctions &
oxytocin receptors]
Acts in myometrium & cervix to produce functional elements to prepare uterus
for effective contraction & cervical softening
Uterotonins [ex. oxytocin,
prostaglandin, endothelin]
Causes smooth muscle contraction

6. 6
 Early signs of labor:
Lightening or “baby drop” ↓ fundic height due to formation of LUS allowing fetal head to descend & ↓ AFV
Bloody show Blood-tinged mucus from vagina, considered a late sign
False labor Irregular interval of contractions, shorter duration, and discomfort confined to lower
abdomen or groin
 Ferguson’s reflex: mechanical stretching of cervix that enhances uterine contractions
 Pathologic retraction ring [Bandl ring]: extreme thinning of LUS as in obstructed labor
 Patterns of cervical dilatation [active phase]: maximum diameter is 10 cm
Latent phase More variable, affected by sedation
Active phase
Acceleration phase
Starts at 4cm dilatation
Predictive of outcome of labor
Phase of maximum slope A good measure of the overall efficiency of the uterus
Deceleration phase Reflective of fetopelvic relationship
 Progressive dilatation w/ no change in station in woman of low parity may signify fetopelvic disproportion.
 Pattern of descent: hyperbolic curve
 3 functional divisions of labor:
Preparatory Affected by sedation & analgesia
Dilatational Rapid rate, unaffected by sedation or analgesia
Pelvic Commences ww/ deceleration phase of cervical dilatation,
cardinal movements of labor take place
 WHO principles of partograph [study Friedman’s curve on OB-GYN handy notes p. 20]
1. active phase of labor begins at 4 cm cervical dilatation
2. latent phase of labor should not last longer than 8 hrs
3. rate of cervical dilatation during active phase of labor & should not be slower than 1 cm/hr
4. 4 hr lag btw slowing of labor and the need for intervention is unlikely to compromise he fetus
5. 4 hourly vaginal examinations is recommended
 Cardinal movements of labor;
Engagement Head enters the brim in transverse biparietal diameter
Asynclitism – slight deflection either anteriorly towards symphysis or posteriorly towards
promontory
Fismanns obliquity [sagittal suture lies anteriorly], Naegeles’ obliquity [sagittal suture lies
posteriorly]
Descent 1st requisite for normal spontaneous delivery, facilitated by amniotic fluid pressure, fundal
pressure, and abdominal muscle contraction
Flexion As head meets resistance of birth canal
Internal rotation Occiput gradually moves anteriorly towards symphysis
Extension Delivery of fetal head occurs
External rotation Head undergoes restitution [rotation of head back o its original position]
Expulsion
 Mechanism of placental extrusion:
Schultze mechanism Duncan mechanism
Central type of placental separation Peripheral type of separation
Fetal surface of placenta Dirty maternal surface
 Uterine phases of parturition:
Phase 1 Prelude to parturition, phase of myometrial smooth muscle unresponsiveness and cervical rigidity
Phase 2 Morphological and functional changes in myometrium and cervix occur in preparation of labor
Uterine changes:
1. ↑ myometrial oxytocin receptors
2. ↑ gap junctions btw myometrial cells
3. uterine irritability
4. ↑ responsiveness to uterotonics
5. formation of LUS
Cervical changes
1. collagen breakdown and rearrangement
2. ↑ hyaluronic acid and ↓ dermatan sulfate
Phase 2 Period of uterine contractions w/c causes:
1. cervical dilatation and effacement
2. fetal descent
3. delivery of conceptus
Phase 3 Events of puerperium
1. maternal recovery from childbirth
2. maternal contribution to infant survival
3. restoration of fertility
Chapter 21: Intrapartum assessment
 3 types of FHR pattern:
Type Characteristics Cause
Early deceleration Occurs w/ onset of contraction Head compression
Late deceleration Occurs after onset of contraction Uteroplacental insufficiency
Variable deceleration MC type, occurs before, during or after &
even w/o contraction
Cord compression & cessation of
umbilical blood flow
 Abnormalities of the 2nd stage of labor may be either protraction or arrest of descent [fetal head descends < 1
cm/hr in nulliparous and < 2 cm/hr in multiparous]
 If 30 mins have passed w/o placental extrusion, manual removal of the placenta may be required.
 Normal blood flow to nonpregnant uterus – 100 cc/min
 Normal blood loss for normal vaginal delivery – 300 to 500 ml
 Normal blood loss for normal CS – 800-1000 ml
 False [+] nitrazine test may be cause by vaginal infections w/ trichomonas vaginalis, blood and semen.
 A score of > 8 in bishop’s score indicates that the probability of vaginal delivery after labor induction is similar to
that after spontaneous labor.
 Vaginal prostaglandins are inserted for ripening of cervix.
 Anterior fontanelle: bigger, diamond-shape
 Posterior fontanelle: smaller, triangle-shape
 Vaginal delivery is possible only if fetus is mentum anterior.
 Engagement is measured by palpation of the presenting part of the occiput.
 Ferguson’s reflex: mechanical sretching or stripping of the cervix
 The anterior shoulder is the one closest to the superior portions of the vagina, while the posterior shoulder is
losest to the perineum and anus.
 Modified ritgen’s maneuver: allows for delivery of fetal head w/ smallest diameter passing thru the introitus and
over the perineum.
 Maneuver’s for placental separation:
o Brandt-andrews maneuver:
o Crede’s maneuver: manual extraction of placenta [after > 30 mins of not being expelled]
 MC indication for primary CS: dystocia
 Montevideo units are calculated by increases in uterine pressure above baseline [8-12 mmHg] multiplied by
contraction frequency per 10 minutes.
 Uterine pressure increases and stages of labor:
1st stage 25-50% mmHg ↑ by 3-5 contractions/10 mins
2nd stage 80-100 mmHg ↑ by 5-6 contractions/10 mins
 Vaginal exams: VE q 4 hrs in latent phase and q 2 hrs in active phase
 FHT monitoring: q 30 mins [1st stage], and q 15 [2nd stage]
 Electronic fetal monitoring: q 15 mins [1st stage], and q 5 mins [2nd stage]
 Non-stress test: normally there is acceleration in FHR of > 15 bpm above baseline for at least 15 secs.
o If at least 2 such acceleration occurs in a 20 mins interval, the fetus is deemed healthy and the test is
reactive.
o A non-reactive test may imply that fetus is acidotic, asleep, or drugs administered to mother.

7. 7
 Contraction stress test / Oxytocin Challenge test: measure of the uteroplacental function
o Evaluates reaction of heart rate to contractions induced by nipple stimulation or oxytocin administration.
o Done when frequency is 3 contractions/10 mins
o Interpretation:
Positive Consistent & persistent late decelerations of FHT in absence of uterine hypertonus or supine HPN
Negative At least 3 contrations in 10 mins, each lasting 40 secs, without late deceleration
Suspicious Inconstant late deceleration
Hyperstimulation Uterine contractions occur more frequent than 2 mins or lasting longer than 90 secs or presence
of uterine hypertonus
Unsatisfactory Frequency of contractions is < 3 per minutes or tracing is poor
 5 parameters in BPP [read p. 15 of OB-GYN handy notes]: fetal breathing movements [chest wall], fetal activity
[trunk/limb], amniotic fluid index, fetal tone [flexion/extension of lower extremities], reactivity NST]
 The physiologic basis for using BPP lies in the fact that coordinated fetal activities require an intact, non-hypoxic
CNS.
 Reactivity and the normal FHR: normal FHR = 110-160 bpm, baseline refers to a heart rate lasting > 10 mins.
 A fetus < 28 wks GA is neurologically immature and thus is not expected to have a “reactive” FHR.
 Early decelerations: are normal and due to head compressionduring contractions.
 Late decelerations: are abnormal and due to uteroplacental insufficiency during contractions.
 The lateral recumbent position [either side] is best for maximizing cardiac output and uterine blood flow [in
supine position, the vena cava and aortic vessels may be compressed by the gravid uterus]
 Variable decelerations are abnormal and can be mild or severe and are due to compression and sometimes head
compression.
 Classification of variable decelerations:
Mild variability < 30 secs and depth > 70-80 bpm
Moderate variability 30-60 secs and depth < 70-80 bpm
Severe variability > 60 secs and depth < 70 bpm
 Amnioinfusion: infuse normal saline into the uterus thru the intrauterine pressure catheter to alleviate cord
compression.
 Fetal tachycardia: mild = 161-180 bpm, severe > 181 w/c may indicate intrauterine infection, severe fetal hypoxia,
CHD, or maternal fever.
 Beat-to-beat variability: single most important characteristic of the baseline FHR.
 At < 28 wks GA, the fetus is neurologically immature, thus decreased variability is expected.
 Long-term variability = 3-6 cycles/min.
 If an FHR of 160 bpm lasts for > mins, then tachycardia is present.
 Beat-to-beat variability can be reliably determined only w/ internal FHR monitoring.
 Prolonged decelerations: isolated decelerations that last 2-10 mins.
 Short-term variability is thought to be the most important predictor of fetal outcome.
 If deceleration has occurred w/o recovery after 2 mins, an emergency C-section is required.
 Scalp deceleration is done between decelerations to elicit a reactive acceleration and rule out metabolic acidosis.
 Fetal lung maturity must be confirmed before elective induction at < 39 wks AOG, unless lung maturity can be
inferred from other maturity criteria.
 Candidates for VBAC: 1 or2 prior LTCS, clinically adequate pelvis, no other uterine scars or previous rupture.
 Contraindications for VBAC: prior classical or T-shaped incision or other transfundal uterine surgery, contracted
pelvis, medical/obstetric complication that precludes vaginal delivery.
 Prerequisites for forceps delivery: a fully dilated cervix, ROM, engaged fetal head, > +2 station, no cephalopelvic
disproportion, empty bladder, and vertex presentation.
 If delivery occurs w/in 1 hour of analgesia, neonatal depression may occur.
 Prophylactic measures against aspiration include fasting for at least 6 hrs prior to anesthesia and antacid
administration before induction.
Chapter 19: Mechanism of labor in Occiput or Vertex presentation
 Fetal lie - - relation of long axis of fetus to long axis of mother
Longitudinal lie [99%] Long axis of fetus parallels to long axis of uterus
Transverse lie [< 1%] Lies in transverse to 1 of the oblique diameters of uterus
Oblique lie – a variant, unstable
 Presentation – part of fetus lying over the inlet
o Cephalic [95% of cases]:
Type Presenting diameter Features
Vertex/occiput Suboccipitobragmatic = 9.5 cm Occiput [posterior fontanelle] =PF
Sinciput/mliary Occipiofrontal = 12.5 cm Bregma [anterior fontanelle] =PF
Brow Occipitomenal = 13.5 cm Converted to face by extension
Face Submentobregmatic = 9.5 cm CS due to ↑ risk of SC injury
o Breech [5% of cases] – complication is cord prolapse or entanglement
Frank breech Thighs are flexed on abdomen, legs are extended over anterior surface of the body, thus feet of
fetus lies close to the head
Complete breech Thighs are flexed on abdomen, legs are flexed on thighs and feet presents a level of the buttocks
Incomplete breech 1 or both thighs are extended so that fee and legs are below the level of the buttocks
o Shoulder or acromion presentation
o Compound presentation: prolapse of fetal hand alongside the presenting vertex or breech or foot alongside
the head.
 Position – relation of point of direction to 1 of the 4 quadrants or to transverse diameter of maternal pelvis.
 Points of direction: occiput in cephalic, mentum/chin in face, sacrum in breech, acromion in shoulder [LOT is the
most common presentation].
 Fetal Attitude [posture/habitus] – relation of fetal parts to 1 another
Chapter 13; Conduct of normal labor and delivery
 Difference between false and true labor [read p. 21 of OB-GYN handy notes]
 Duration of the stages of labor in nulliparas and multiparas
 3 stages of labor:
Stages Features Nullipara Multipara
Stage
1
Cervical effacement & dilatation to full dilatation
a. Uterine contractions q 2-3 mins x 40-60 secs
b. FHT q 15 mins
c. I.E q 2 hrs [dilatation should be 1-2 cm/hr]
d. artificial amniotomy can be done at 4 cm
8 hrs 5 hrs
Stage
2
From full dilatation to fetal expulsion
Contractions are q 1-2 mins x 90 secs
Dorsal lithotomy position [to ↑ pelvic diameter]
Crowning occurs, fetal head delivery by Ritgen’s maneuver, suctioning & cord care
50 mins 20 mins
Stage
3
From delivery to placental expulsion
Schultze – at central placental part, Duncan – occurs at the periphery & descends
sideways
Stage
4
Occurs 1 hr after placental delivery, critical to identify postpartum hemorrhage
sec. to atony, mg by massage, ice packs, and oxytoxics
 Signs of placental separation:
1. calkin’s sign – uterus becomes globular and firmer
2. sudden gush of blood
3. uterus rises in abdomen as deched placena drops to lower segment & vagina
4. lengthening of umbilical cord & protrudes out of the introitus
 Indications for CS hysterectomy:
1. arrest hemorrhage from uterine atony
2. lower segment bleeding
3. laceration of major uterine vessel
4. large myoma
5. cervical dysplasia /CIS
 Types of lacerations of vagina & perineum:
1st degree Fourchette, perineal skin, vaginal mucosa [not underlying fascia & muscle]
2nd degree Involve fascia & muscle of perineal body but not the anal sphincter
3rd degree From vaginal mucosa, perineal skin, fascia, up to anal sphincter [not rectum]
4th degree Extension up to rectal mucosa [repaire first before the vaginal mucoosa]


8. 8
 Types of incisions;
Kronig’s incision Vertical incision at LUS
Kerr incision Transverse incision at LUS
Transverse/Pfannenstiel Curvilinear incision
Maylard incision Transverse incision w/ the rectus divided
 Types of episiotomies:
Median type Less painful, easy to repair, heals faster but may extend to rectum if perineal body is short
Mediolateral Used more often
Chapter 22: Analgesia and anesthesia
 For painless labor
o Meperidine: 50-100 mg [Demerol] – readily crosses placenta
o Promethazine: 100 mg [Phenergan]
o Butorphanol: 1-2 mg – neonatal depression is lesser
o Nalbuphine; 15-20 mg, no neonatal depression
o Fentanyl: 50-100 ug
o Naloxone: reverses respiratory depression
 Measures important for effective prophylaxis:
o Fasting from solids at least 8 hrs and preferably longer before anesthesia
o Use of agents to reduce gastric acidity during induction and maintenance of general anesthesia
o Skillful tracheal incubation, accompanied by pressure on cricoid cartilage to occlude esophagus [Sellick
maneuver]
o After intubation and during surgery, passage of NGT to empty stomach of all contents
o Awake extubation w/ protective airway reflexes intact
o Use of regional techniques when appropriate
Regional anesthesia
 Uterine innervation – pain during 1st stage of labor generated largely from uterus → pain of uterine contractions
thru 11th-12th thoracic nerves
 Lower genital tract innervation – pain transmitted thru pudendal nerve w/c posterior surface of sacrospinous
ligament as it attaches to the ischial spine
I. Local infiltration
 Lidocaine - most commonly used local anesthetic
II. Pudendal block [S2-4]
 Goal: to block the pudendal nerve distal to its formation by anterior division of S2-S4 but proximal to its terminal
branches
 Maternal complications are uncommon
 MC used anesthetic is lidocaine
 Complication: hematoma formation, convulsion, infection
III. Paracervical block
 Provides pain relief during 1st stage of labor
 Complication: fetal bradycardia
IV. Spinal [subarachnoid] block [T8]
 Low spinal block is popular form of analgesia for forceps or vacuum delivery
V: Epidural anesthesia [T10-S5]
 Complete analgesia for pain of labor & vaginal delivery necessitates block from T10-S5
POSTPARTUM
 Within 2 weeks, the uterus has descended into the cavity of the true pelvis.
 When involution is defective, late puerperal hemorrhage may occur.
 Rugae reappear by 3rd week.
 Colostrum can be expressed from the nipple by 2nd postpartum day, secreted by breasts for 5 days postpartum.
 Colostrum is then converted to mature milk by 4 weeks postpartum.
 All vitamins except vitamin K are found in human milk.
 Women w/ extensive pituitary necrosis [Sheehan syndrome], cannot lactate due to absence of prolactin.
 Episiotomy incision is typically well-healed and asymptomatic by week 3 of the puerperium.
 Ensure that postpartum woman has voided w/in 4 hrs of delivery.
 Continue iron until 3 mos. postpartum.
 After 6 weeks, coitus may be resumed based on pxs desire and comfort.
Chapter 24: Puerperium
 Urinary retention in the 1st 24 hrs is due to:
1. edema & congestion of vulva, urethra, bladder trigone
2. edema & reflex spasm of urethral sphincter
3. bladder atony
 diuresis is greatest from 2nd to 5th day
 Types of lochia [discharge from uterus after delivery lasting 4-8 wks]:
Lochia rubra 1st 3-4 d Reddish discharge
Lochia serosa Next 3-4 days Paler & pinkish discharge
Lochia alba From 10th day Lighter yellow & creamy color
 After pains – due to uterne contraction, more intense during breastfeeding
 Constipation due to pxs inactivity, decrease intraabdominal pressure after delivery & painful perineum
 Weight loss: normal non-pregnant weight is attained in 6 mos.
Average loss of 5 kgs Immediately after delivery
Additional loss of 3 kgs Due to diuresis and skin loss
 Postpartum check-up in 4-8 wks, PAPsmear at 6 mos.
 Other events after delivery:
2 wks Uterus descends into the umbilicus, CO returns to normal
3 wks Entire endometrium is restored
4 wks Uterus regains non-pregnant size
6 wks Complete extrusion of placental site
2-8 wks Dilaed ureters and pelvis return at prepregnant state
6 mos. May approach prepregnant weight
2 wks Coitus may be resumed depending on px desire
6-8 wks Return of menstruation and ovulation
PATHOLOGIC OBSTETRICS
Chapter 45: Dystocia, abnormal labor and feto-pelvic disproportion
 Types of uterine dysfunction:
Hypotonic uterine dysfunction Hypertonic uterine dysfunction
No basal hypertonus and uterine contraction have a
normal gradient
Occurs during active phase of labor
Responds to x w/ oxytocin
Incoordinated uterine dysfunction
Either basal tone is elevated or pressure gradient is
distorted
Occurs during latent phase
Usually responds w/ sedation
 Estimation of fetal head size [Mueller-Hillis maneuver]
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 overlapping.
 Pelvic inlet contraction:
o If diagonal conjugate is < 11.5 cm
o Borderline if AP diameter of inlet is 10 cm
o Severe if AP diameter is < 9 cm
 Midpelvic contraction:
o If sum of interischial spinous diameter [10.5 cm] and posterosagital diameter of midpelvis [5 cm] falls to 13.5
cm and below
o Interischial diameters is < 10 cm
o Prominent ischial spines, convergent sidewalls, narrow sacrosciatic notch on vaginal exam
 Outlet contraction:
o Interischial tuberous diameter of < 8 cm

9. 9
Active phase disorders
 Before diagnosis is made during 1st stage of labor, both of this criteria should be met:
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 been present for 2
hours w/o cervical change
Precipitate labor
 Effects:
Maternal effects Fetal effects
Uterine rupture, exensive laceration, AFE Hypoxia, intracranial trauma, Erb-Duchenne palsy
Nulliparas Cervical dilatation 5 cm/hr or faster
Multiparas Cervical dilatation 10 cm/hr
Chapter 44: Dystocia due to abnormal presentation, position nd development of fetus
 Face presentation – w/ head hyperextended so occiput is in contact w/ fetal back
 Brow presentation – the portion of fetal head btw he orbital ridge and anterior fontanelle presents at the pelvic
inlet
 Transverse lie/shoulder/acromion presentation – long axis of fetus is perpendicular to that of mother
 Compound presentation –an extremity prolapses alongside the presenting in the pelvis simultaneously
 Persistent occiput posterior position – may be due to transverse narrowing of the midpelvis
 Deep transverse arrest of the head – associated w/ platypelloid and android pelvis, caused by hypotonic uterine
dysfunction
 Shoulder dystocia management:
McRobert’s ‘exagerrated lithotomy”, involves flexing thigh upon her own abdomen
Wood-Corkscrew maneuver Progressively rotating the posterior shoulder 180 degrees in corkscrew fashion
Rubin maneuver Fetal shoulders rocked from side to side applying force on mother’s abdomen
Hibbard maneuver Pressured is applied to infant’s jaw and neck in the direction of mothers rectum
Zavanelli Cephalic replacement into the pelvis followed by cesarean delivery
Fetal developmental anomalies
 Fetal macrosomnia – defined as fetal weight > 4,000 gms, possibly due to DM, multiparity, large parents/genetic,
or postdatism
 Hydrocephalus – consider cephalocentesis & CS delivery; prognosis: uterine rupture
 Large abdomen – for transabdominal decompression
 Conjoined twins
Dystocia due to abnormalities of Pelvis
 Bony dystocia: contracted inlet, outlet and midpelvis [see clinical pelvimetry]
 Soft tissue dystocia: uterine myomas or prolapse, cervical stenosis, transverse septum or vagina, cystocele,
rectocele
Chaptter 43: Dystocia due to Abnormality of Powers
 Dystocia/difficult labor is the MC indication for primary CS
 Classification:
A. disorder of preparatory division
Prolonged latent phase
Nullipara
> 20 hrs
Multipara
> 14 hrs
B. protracted active phase of dilatation < 1.2 cm/hr < 1.5 cm/hr
C. disorders of pelvic division
Prolonged deceleration phase
Secondary arrest of dilatation
Arrest of descent
Failure of descent
> 3 hrs
> 2 hrs
> 1 hr
No descent
> 1 hr
> 2 hrs
> 1 hr
No descent
D. precipitate labor disorders
Precipitate dilatation
Precipitate descent
> 5 cm/hr
> 5 cm/hr
> 10 cm/hr
> 10 cm/hr
Chapter 47: Forceps Delivery and Vacuum Extraction
 Obstetric forceps
 Types of obstetric forceps
Molded Simpson’s forceps
Rounded Tucker’s forceps
For aftercoming head Piper’s forceps
For transverse arrest Barton’s forceps
 Prerequisites:
1. head must be engaged
2. fully dilated cervix
3. known position of vertex
4. ruptured membranes
5. no CPD
6. vertex or mentum anterior
Chapter 46: Breech presentation and delivery
 Methods of vaginal breech delivery
Spontaneous breech
delivery
Infant is expelled entirely spontaneously w/o any traction or manipulation other than
support of the infant
Partial breech
extraction
Infant is delivered spontaneously as far as the umbilicus, but the remainder of the body is
extracted/delivered w/ operator traction
Total breech extraction Entire body of the infant is extracted by the obstetrician
 Mechanism of breech delivery:
Lovesets Delivery of posterior shoulder ahead of the anterior
Kristeller’s The head may be delivered by suprapubic pressure
 Methods of delivery of the head:
Piper’s forceps Preferred method, the head well engaged, occiput diretly anterior, blades of head
Mauriceau-smellie-
veit
The body of the baby is placed on arm of the operator w/ index and the middle fingers over
malar bones
Bracht Breech is allowed to deliver spontaneously to navel
Prague Body is swung over the mother’s abdomen
Pinnard Hand is introduced inside the uterus to reach for popliteal fossa
 Entrapment of the aftercoming head:
Durhssen’s incision Cervix should be made 7 cm dilated, 3 incisions made 2,6 and 10 o’ clock positions
Abdominal rescue Replacement of fetus higher into the vagina and uterus, followed by CS delivery
Chapter 48: Cessarean section
 Delivery of fetus thru abdominal incision [laparotomy], followed by incision of uterine wall [hysterotomy].
 Techniques in CS:
o Types of abdominal incision:
Median infraumbilicallongitudinal incision
Transverse suprapubic incision
Or Pfannenstiel/Bikini type
More difficult but is stronger & w/ less dehiscence
o Types of uterine incision:
Classical CS Longitudinal incision above LUS, strong tendency to rupture
Low-segment incision
Low transverse/ kerr
Low longitudinal/kronig
Low tendency to rupture
Preferred due to only moderate dissection of the bladder
More bladder dissection but can be extended
 Vaginal birth after a CS/VBAC: allow a trial of labor under double set-up for all previous CS of 1 low segment
incision after excluding in adequate pelvis & unless new indication arises.

10. 10
Chapter 35: Hypertensive disorders
 Classification:
Hypertension A BP of at least 140 mmHg or 90 mmHg diastolic, previously defined by an increase of 30
mmHg systolic or 15 mmHg diastolic over baseline values
Gestational HPN HPN w/o proteinuria occurring after 20 wks AOG or postpartum, BP returns to normal <
12 wks postpartum
Preeclampsia Presence of HPN + proteinuria [300 mg/24 hr or +2 dipstick] occurring after 20 wks AOG
except in cases of extensive trophoblastic proliferation
Superimposed
preeclampsia
↑ of at least 15 mmHg diastolic or 30 mmHg systolic over baseline hypertensive BP levels
Eclampsia Presence of convulsions in a woman w/ preeclampsia
Superimposed ecclampsia Convulsions + superimposed preeclampsia
Chronic HPN Presence of 140/90 mmHg or greater prior o pregnancy or is detected before the 20th wk
of pregnancy and persists long after delivery
 Severe preeclampsia – presence of one or more of the ffg:
1. SBP of 160 mmHg or DBP of 110 mmHg
2. proteinuria of at least 4 g/d or +2, w/ renal involvement
3. oliguria of < 400 cc/day
4. severe headache or visual disturbance
5. pulmonary edema or cyanosis; IUGR
6. HELLP syndrome – hemolysis, elevated liver enzymes & low platelet count
 Classification of hypertensive disorders [refer to p. 37 of OB-GYN handy notes]
 Pathophysiology:
o Trophoblastic hypoperfusion, w/ ibgrowth of trophoblastic cells into tunica media of spiral arterioles results in
denervation & loss of muscular and elastic components causing thinning of walls, dilation & elongation to a “
corkscrew or saw-toothed configuration
o Prostacyclin deficiency + abnormal arterioles result in a state of relative vasoconstriction
 Changes in preeclampsia:
o ↓ antithrombin 3 and ↑ fibronectin
o ↓ pasma levels of rennin, angioensin 2, and aldosterone, ↑ ADH
o ANP is released upon arterial wall distention
o Glomerular capillary wall distention
o Periporal hemorrhagic necrosis – pahognomonic of preeclampsia
o Subcapsular hematoma w/ epigastric or RUQ pain
o Principal cerebral lesions: amaurosis and retinal detachment
 Roll-over test: increase of at least 20 mmHg in DBP from a left lateral decubitus position to supine is a positive
test
 MAP test = DBP + 1/3 SBP or 1/3 [SBP + 2DBP]
o MAP 2nd trimester = > 90 mmHg, or MAP 3rd trimester = > 105 mmHg predict future PIH.
Management:
 Control of HPN:
o Hydralazine [apresoline] = 5 mg IV bolus w/ increments of 5 mg q 30 mins if DBP does not improve up o total
of 20 mg dose
o Beta-blockers and Ca+ channel blockers: nifedipine or nicardipine
o ACE inhibitors are not recommended in pregnancy.
 Control of convusion:
o Magnesium sulfate [DOC] = loading dose of 4 g IV bolus + 10 g IM [5g per buttock]; maintenance dose = 1-2
g/hr IV drip or 5 g IM q 6 hrs [monitor toxicity using DTR, RR > 12, UO >100 cc/4 hrs]
 Optimum time & mode of delivery
 Prevention: low dose aspirin, high dose Ca+
Chapter 26: Obstetrical hemorrhage
 Placenta previa: bleeding due to separation of placenta implanted in the immediate vicinity of cervical canal.
o Bleeding is proportionate to blood loss, usually painless & occurs at 3rd trimester
o Dx; double set-up, UTZ, MRI
o Types of placenta previa:
Total placenta previa Internal os is completely covered by placenta
Partial placenta previa Internal os is partially covered by placenta
Marginal placenta Edge of placenta is at the margin of internal os
Low-lying placenta Placenta implanted at the LUS such that the placental edge actually does not reach
the internal os but is in close proximity to it
 Abruptio 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
o MC etiology is preeclampsia.
o Bleeding is proportionate to placental separation.
o Types of abruption:
External Bleeding passes btw membranes and uterus and escapes thru the cervix
Concealed If it extravasates into amniotic cavity after breaking the membranes, placenta is completely separated
yet membranes retain their attachment to uterine wall
Marginal Placental separation is limited to the margin w/ minimal bleeding but w/o uterine tenderness and pain
 Vasa previa: bleeding may be the consequence of velamentous insertion of umbilical cord w/ rupture and
hemorrhage from a fetal blood vessel at the time of rupture of the membranes.
 [Read on Handy notes OB-GYNE for classification of abruption placenta p. 34]
 Complications of abruption placenta:
o Couvelaire uterus/uterine apoplexy: in w/c the entire uterus may undergo bluish, purple or copper
discoloration due to blood extravasation into myometrium and uterine serosa.
o Acute renal failure: due to reduced CO and intrarenal vasospasm due to massive hemorrhage.
o DIC
 Complications of placenta previa:
o Placenta accrete
o Postpartum hemorrhage
o IUGR
o Congenital abnormalities
 IUFD
o Absence of fetal movement
o Confirmed by:
1. spalding’s sign [7 days after fetal death] – opening of the fontanelles
2. hyperflexion of spine
3. crowding of rib shadow
4. robert’s sign
o Mgt: delivery
o Compication: DIC
 Uterine rupture
o Complete rupture: uterus may communicate directly w/ the peritoneal cavity
o Incomplete rupture: may be separated from peritoneal cavity by visceral peritoneum over the uterus or of
broad ligament.
Chapter 37: Preterm Birth
 Preterm = < 37 wks AOG but > 20 wks AOG
 Average birthweight for Filipinos is 2,275 gms
 Survival is feasible at 26-27 wks AOG
 Dx:
o Regular uterine contractions 5-8 mins or less apart accompanied by 1 of the ffg.
1. progressive change in cervix
2. cervical dilatation of 2 cm or more
3. cervical effacement of 80% or more
o Passage of cervical mucus; low back pains, pelvic pressure, menstrual-like or intestinal cramps
 Mgt: repair of incompetent cervix, combat infection, tocolytics
 Tocolytic agents are of greater benefit if given 32-34 wks AOG, includes:
o Beta-adrenergic agonists – reduce myometrial contractility by decreasing intracellular Ca+ & reducing effect of
Ca+ on myometrial activation [ex. isoxuprine/duvadilan]
o Magenesium sulfate
o Prostaglandin inhibitors – indomethacin
o Ca+ channel blockers

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

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

13. 13
MEDICAL CONDITIONS AND PREGNANCY
 MC medical complication in pregnancy: diabetes
 Gestational DM probably results from placental lactogen secreted during pregnancy; w/c has large glucagons-like
effects.
 Insulin does no cross the placenta → feal hyperglycemia
 [Refer to p. 39 of OB-GYN handy notes for Criteria in Dx of GDM]
 The CNS anomaly most specific to DM is caudal regression.
 Grave’s disease is the MC cause of thyrotoxicosis in pregnancy. Tx is PTU [drug of choice] and methimazole.
 Sheehan’s syndrome: pituitary ischemia and necrosis associated w/ obstetrical blood loss leading to
hypopituitarism. Pxs do not lactate due low levels of prolactin.
 MC serious medical complication of pregnancy and occurs in 1-2% of pregnant women: acute pyelonephritis
 MC surgical condition in pregnancy: appendicitis
 The 2 MC causes of anemia during pregnancy and puerperium are IDA and acute blood loss.
URINARY TRACT IFECTIONS AND PREGNANCY
 Asymptomatic bacteriuria
o Dx:
1. absence of Sx
2. > 100,000 cfu/ml w/ 1 or more organisms in 2 consecutive midstream specimens or 1 cathetherized
specimen
3. screening should be done at 1st prenatal visit esp. for diabetics & those w/ previous hx of UTI
4. test of choice: urine culture [clean catch midstream]
5. U/A alone is not recommended
o Tx:antibiotics x 7 days w/ follow-up culture after 1 wk
 Acute cystitis in pregnancy
o S/Sx: urinary frequency, dysuria & bacteriuria
o Dx: pyuria > 8 pus cells/mm3 [uncentrifuged], or > 5 pus cells/hpf [centrifuged] or [+] leukocyte esterase &
nitrate test
o Tx: 7 days antibiotics
 Acute pyelonephritis in pregnancy
o Dx: pyuria [> 5 wbc/hpf centrifuged urine] & bacteriuria [> 10,000 cfu of uropathogen], gm stain, urine C & S,
blood cultures
o Tx: admit, immediate antibiotic therapy for a duration of 14 days
Note: Antibiotics in pregnancy
Safe antibiotics Use w/ caution Contraindicated
Amoxicillin, nitrofurantoin,
cephaalosporins, coamoxiclav, ampicillin-
sulbactam, aztreonam
Aminoglycosides
TMP/SMX at 1st& 2nd
trimester
Tetracycline, fluorioquinolones, TM/SMX
at 3rd trimester
COMPLICATIONS OF PREGNANCY
 Magnesium toxicity [7-10 mEq/L] is associated w/ loss of patellar reflexes. Tx w/ calcium gluconate 10% solution 1
g IV.
 Magnesium levels and toxicity:
4-7 mg Uterine contractions decreased
6-12 mg ECG changes, hyporeflexia
10 mg Loss of deep tendon reflex
15 mg Respiratory paralysis, cardiac depression
 Hydration often stops contractions during preterm labor.
 L:S ratio is normally > 2.0
 PROM is the MC dx associated w/ preterm delivery.
 Oxytocin should never be given as undiluted bolus [due to serious hypotension]
 Antibiotics for endometritis: clindamycin + gentamicin
HI-YIELD FACTS IN GYNECOLOGY [from GYNE-MISCHELLE & handy notes]
REPRODUCTIVE ANATOMY
Key terms:
 Canal of Nuck – tubular process of peritoneum accompanying round ligament into inguinal canal, generally
obliterated in adults.
 Carunculae myrtiformes – small nodules of fibrous tissue at vaginal orifice w/c are remnants of hymen.
 Cornu – where oviducts enter uterine cavity.
 Cul-de-sac of Douglas – separates uterus from large intestine
 Fimbria ovarica – finger-like projections of distal end of oviducts, attaches oviducts to ovary.
 Frankenhauser’s plexus – concentration of both myelinated and non-myelinated nerve fibers in uterosacral
lligament supplying primarily the uterus and cervix.
 Space of Retzius – area btw bladder and symphysis pubis bounded laterally by obliterated hypogastric A.
Important Facts
 Escutcheon in mons pubis [triangular in female, diamond in male].
 Labia minora & breast are the only areas of the body rich in sebaceous glands w/o hair follicles.
 Lowest part of embryonic urogenital sinus – vestibule.
 MC large cystic structure of vulva – Bartholin’s duct cyst.
 Vagina:
o Normal pH: 3.8 – 7.2
o Lower 3rd: close w/ endopelvic fascia & ligament
o Middle 3rd: supported by levator ani M.& cardinal ligament [lower part]
o Upper 3rd: supported by cardinal ligament [upper] & parametria
o Blood supply:
Vaginal A. Either directly from uterine A. or as a branch of internal iliac A.
Pudendal V. Principal venous drainage
o Nerve supply: vaginal plexus, pudendal nerve; pain fibers [S1-4]
o Lymphatics:
Upper 3rd External iliac nodes
Middle 3rd Common & internal iliac nodes
Lower 3rd Common iliac, superficial inguinal & perirectal nodes
 Surgical procedures for vagina: colpectomy, colposcopy & colphorrhapy
 Cervix:
o Blood supply: descending branch of uterine A., cervical A. & azygos A.
o Lymphatics: obturator, common iliac, internal/external iliac nodes
o Nerve supply: S2-4
 Majority of arterial supply to cervix is at 3 or 9 o’ clock position.
 Removal of narrow lower par of uterus is called trachelectomy.
 Uterus:
Nulliparous External os is round
Parous External os has fishmouth appearance
o In normal nonpregnant state, uterus is approximately 6 cm x 4 cm & weighs about 70 gms [ovary is 3cm x 2
cm]
o Lymphatics: aortic, lumbar and pelvic nodes
o Nerve supply: hypogastric and ovarian plexus [sympathetic], pelvic N. + S2-4 [parasympathetic].
o Blood supply:
Uterine A. Large branch of hypogastric A.
Ovarian A. Directly from aorta
 Fallopian tube/oviducts
o Blood supply:
Uterine A. From hypogastric A.
Ovarian A. From aorta
o Lymphatics; internal iliac and aortic nodes
o Innervation: uterine & ovarian plexus, sensory nerves from T11-12, L1

14. 14
 Ovaries:
o Blood supply: ovarian A. [from aorta]
o Venous drainage:
L ovarian V. Drains to L renal V.
R ovarian V. Drains to IVC
o Lymphatics: aortic and iliac nodes
o nerve supply: ovarian, hypogastric and aortic plexuses
 Internal pudendal A. – terminal branch of internal iliac A.
 Cardinal ligaments/Mackenrodt’s ligament – provides the major support of uterus & cervix.
 Uterosacral ligament – last to cut in hysterectomy.
Male and Female derivatives of embryonic urogenital structures
Structure Male Female
Labioscrotal swelling Scrotum Labia majora
Urogenital folds Penile urethra Labia minora/nymphae
Genital tubercle
Phallus
Penis
Penis bulb
Clitoris
Vesibular bulbs
Urogenital sinus Prostate gland
Prostatic utricle
Bulbourethral glands
Cooper’s glans
Urehral / Skene’s glands
Vagina
Vestibular glands
Bartholin’s glands
Mesonephric duct Epididymis
Ductus deferens
Epiophoron
Gartner’s duct
Gonad Testis Ovary
Gubernaculums Gubernaculums testis Round lig. of uterus
CONGENITAL ABNORMALITIES OF FEMALE REPRODUCTIVE TRACT
Key terms:
 Androgen resistance syndrome – 46 X,Y individual w testis, absent uterus, normal female phenotype and scanty
body hair.
 Arcuate uterus – minimum septate uterus
 Bicornuate uterus – partial lack of fusion of 2 uterine corpura w/ single cervix present.
 Didelphic uterus – compete duplication of uterus and cervix w/o fusion of 2 cavities.
 Rokitansky-Kuster-Hauser syndrome – 46 X,X female w/ mullerian failure showing absence of all or most of the
vagina, cervix, uterus, and FT.
 Unicolic/unicornuate uterus – represents a complete arrest of 1 mullerian duct.
 MC cause of labial fusion is congenital adrenal hyperplasia.
HISTORY, P.E, AND PREVENTIVE HEALH CARE
Keyterms:
 Ectropion – presence of endocervical [glandular] epithelium on potrio vaginalis of cervix; may result from scarring
of external os or congenital.
 Total procidencia – prolapse of uterus and cervix thru introitus
 Stages of uterine prolapse;
Stage 1 Minimum descent of cervix into vaginal canal
Stage 2 Descent of cervix to introitus
Stage 3 Prolapse of cervix or uterus thru introitus
 Trichomonas: use 1% NaCl while KOH is used in candidiasis
RAPE, INCEST AND DOMESTIC VIOLENCE
Key terms
 MC acquired infection in STD is chamydia. [Tx: ceftriaxone and doxycycline]
 Survival time of sperm:
Source Motile sperm Sperm Aid
phosphatase
Vagina Up to 8 hrs Up to 7-9 days Variable
Pharynx 6 hrs Unknown 100 IU
Rectum Undetermined 20-24 hrs 100 IU
Cervix Up to 5 days Up to 17 days Variable
DIAGNOSTIC PROCEDURES
Keyterms
 Hysterosalpingography – xray whereby uterine cavity and lumina of FT are visualized by injecting contrast
material thru cervical canal.
 Hysteroscopy – direct visualization of endometrial cavity using an endoscope.
 Laparoscopy – examination and inspection of uterine cavity and pelvic organs by endoscope.
 Sonohysterography – imaging of uterine cavity by instilling saline.
Important facts
 Sonography is the method of choice for locating a missing IUD.
 Endovaginal UTZ is the mainstay in evaluation of pregnant woman w/ 1st trimester vaginal bleeding.
 CT scan is very accurate in dx cystic teratoma, and is an excellent techique to confirm dx of ovarian vein
thrombosis.
 Endometrial sampling is the standard diagnostic test to confirm endometritis.
 CT is the most accurate in dx of appendicitis.
 Most frequent problem in performing endometrial sampling is cervical stenosis or spasm.
 Major complication following endometrial biopsy is uterine perforation.
 Laparoscopy is adopted as method of choice for female sterilization.
 Cervical punch biopsy is diagnostic for pxs w/ abnormal papsmear.
PEDIATRIC GYNECOLOGY
Keyterms
 Adhesive vulvitis – a self-limiting consequence of chronic vulvitis in w/c denuded epithelium of labia minora
agglutinates and fuses the 2 labia together.
 McCune-Albright Syndrome/Polycystic Fibrous dyplasia – triad: café-au lait spots, fibrous dysplasia, and cysts of
skull and lung bones.
 Incomplete or pseudoprecosious puberty – premature female sexual maturation and uterine bleeding w/o
associated ovulation.
 Precocious puberty – the appearance of secondary sexual maturation at an age > 2.5 standard deviations below
the mean for the population to w/c the child belongs.
Important facts
 Vulvovaginitis – MC gynecological disease of children and premenarcheal females.
 [+] identification of T. vaginalis, N. gonorrhea, and Chlamydia often indicates sexual abuse.
 Why is a child susceptible to vulvar infections:
1. they lack labial fat pads and pubic hair
2. her vulvar and vaginal epithelium lack protective effects of estrogen thus are sensitive to irritation or infection
3. labia minora are thin and vulvar skin is red
4. vaginal epithelium is of neutral pH providing an excellent medium for bacterial growth.
5. her vagina lacks glycogen, lactobacilli, and antibodies to help resists infection.
 The major factor in childhood vulvovaginitis is poor perineal hygiene.
 Classic Sx of E. vermicularis infection is nocturnal vulvar and perineal itching.
 The classic perineal “figure of 8 or hourglass rash” indicates lichen sclerosus.
 MC cause of bleeding in childhood is foreign bodies, w/c is MC among 3-9 y.o and are due to small wads of toilet
tissue. Classic Sx: foul, bloody vaginal discharge.
 Usual cause of accidental genital trauma is fall [mostly straddle injury].
 Calcification in an ovarian mass indcates a dx of ovarian teratoma.
 MC malignancy in preadolescent females is germ cell tumor.
 MC malignant neoplasm is dysgerminoma.
 MC tumor in children is benign teratoma.
 MC DDX of abdominopelvic mass in children that is not an ovarian mass is a benign cyst of mesentery or
omentum.
 MC cause of pseudoprecocious puberty is an estrogen-secretig ovarian tumor, of w/c the MC type is granulose
cell tumors.
 DOC for GnRH-dependent precocious puberty is GnRH agonists.
 Spontaneous discharge from nipple is a Sx of intraductal papilloma.
 MC of all benign breast conditions is fibrocystic changes. Its classic Sx is cyclic bilateral breast pain; signs include
↑ engorgement and density of breast, excessive nodularity, rapid change and fluctuation in size of cystic
tenderness and spontaneous nipple discharge.

15. 15
 3 clinical stage of fibrocystic changes:
1st stage /
Mazoplasia
Breast pain in upper outer quadrant, intense stromal
proliferation
2nd stage / Adenosis Seen in early 20s, w/ marked proliferation and hyperplasia
of duct, ductules, and alveolar cells
3rd stage / cystic
phase
Seen in their 40s, w/ no severe breast pain but there is
sudden pain and tenderness w/ a lump, straw-colored fluid
DOC for fibrocystic changes: Danazol
 MC breast tumor in adolescents is fibroadenomas. It does not produce breast pain and tenderness.
 MC breast sarcoma is Cystosarcoma phylloides.
 MC breast malignancy is infiltrating ductal CA.
 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-milky discharge.
 Usual etiology of fat necrosis is trauma.
 Most accurate conventional method of determining nonpalpable breast CA is mammography, often mediolateral
oblique position.
 Indirect signs of breast CA:
1. single dilated duct w/ intraductal CA
2. asymptomatic architectural distortion in dense breast
3. developing density
 isolated clusters of tiny calcification are the MC and important diagnostic sign of early CA.
 Diagnostic test for breast CA is MRI.
 The |presence and number of axilla node metastasis is the single best predictor of survival.
 Most frequently prescribed hormonal agent for breast CA is tamoxifen/raloxifen.
DIFFERENTIAL DIAGNOSIS OF MAJOR GYNECOLOGIC PROBLEMS
Keyterms
 Hematocolpos – distenion of an obstructed vagina [caused by imperforate hymen or transverse vaginal septum]
w/ blood products.
 Hematometria – uterus distended w/ blood secondary to partial or complete obstruction of any part of lower
genital tract.
Important facts
 Implantation bleeding occurs at time of 1st missed menstrual period and last a very short time, may be present 1-
2 days w/ flow to menstrual period, it can be seen as brownish-tinged cervical mucus.
 Common cause of DUB in puberty is anovuation.
 MC benign condition causing postmenopausal bleeding.
 MC example of recurrent pelvic pain among women.
 Pelvic congestion syndrome is characterized by pain and heaviness in pelvis that occurs after arising and becomes
worst as day progresses, uterus appears dusky-blue & mottled, often w/ varicosities of veins of broad ligament.
 MC benign neoplasms of adnexa are serous cystadenoma and benign cystic teratoma [dermoid cyst].
 MC benign ovarian neoplasm among different age groups:
Age 19 Benign cystic teratoma
Age 20-44 Serous cystadenoma
Ages 20 to > 75 cystadenocarcinoma
 Abdominal masses in young childhood are more likely to be Wilm’s tumor or neuroblastomas.
 Solid or mixed solid and cystic adnexal masses in children include dysgerminoma and teratoma.
 Majority of adnexal masses in adolescents are functional cysts of ovary [benign cystic teratoma]. It is also the MC
neoplastic masses in reproductive years.
 Benign fibromas of the ovary may be associated w/ ascites and pleural effusion called Meig’s syndrome.
 Struma ovarii refers to a teratoma w/ thyroid elements present.
 Tumor makers:
CA-125 Epithelial tumors
Serum HCG and AFP Germ-cell tumors
BENIGN GYNECOLOGIC LESIONS
Keyterms
 Degeneration of myoma – myoma outgrowths its blood supply and begin to necrose centrally.
 Endometrial poyp – localized outgrowth of endometrial gland and stroma projecting beyond surface of
endometrium including is vascular stalk.
 Gartner’s duct cyst - cyst primarily of mesonephric origin found laterally in vagina.
 Hidradenoma – rare, small benign vulvar tumor of apocrine sweat glands.
 Hydatid cyst of Morgagni – pedunculated, paratubal cysts found near fimbria of oviduct.
 Hyperreactio luteinalis – multiple theca lutein cysts causing bilateral ovarian enlargement during pregnancy.
 Leiomyomatosis peritonealis disseminate – benign disease w/ multiple small nodules over pelvic surface and
abdominal peritoneum mimicking disseminated CA or sarcoma.
 Luteoma of pregnancy – rare, specific, benign hyperplastic reaction of ovarian theca lutein cells during pregnancy.
 Nabothian cysts – cervical retention cysts lined by endocervical –type columnar cells.
 Syringoma – benign tumor of eccrine sweat glands.
Important facts
 Urethral curuncle, small fleshy outgrowth at distal end of urethra common in postmenopausal women usually
located at ectropion of posterior urethral wall. Common S/Sx includes dysuria, frequency, urgency and pain or
tenderness. It is not a precursor for urethral CA.
 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 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].

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 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.
Important facts
 Classic Sx of endometriosis is cyclic pelvic pain. Its most popular theory is retrograde menstruation.Other Sx:
infertility and abnormal bleeding
 Differences:
Adenomyosis Endometriosis
Usually in older women Young women
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
 Dovetailsign – 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 2nd 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
 Innervation of bladder & urethra:
Continence Micturition
Bladder Symph [NEp] = relaxation w/c prevents micturition Parasymph [Ach] = contraction causing micturition
Sphincter Contraction = prevents micturition Relaxation
 Resting bladder pressure is btw 20 & 30 cm H2O.
 Highest pressure zone in urethra is about midpoint in functional urethra, roughly 0.5 cm proximal to urogenital
diaphragm.
 For continence to be present, UCP > bladder pressure
 Cystoscopy and cystometry are best used for Dx of detrusor hyperactivity
 MC cause of lower urinary tract infection is E. coli.
 Common etiologic agents in urethritis include Neisseria and Chlamydia.
 MC form of UTI is cystitis.
 Common etiologic agents in urethral diverticulum include gonococcus and E. coli.
 Most urethral diverticula emanate from ventral wall of urethra.
 MC urinary incontinence is genuine stress incontinence.
 2nd MC cause of urinary incontinence is urge incontinence.
 MC groin hernias in males is inguinal hernia, in females is femoral hernia.
 Anterior colporrhaphy is indicated for urethrocele and cystocele.
 Posterior colporrhaphy is indicated for rectocele.
 Classic Sx in rectocele is “heavy or falling out feeling in vagina w/ constipation or incomplete emptying of rectal
vault.