OB MustKnows

OBSTETRICS
and
GYNECOLOGY
INTEGRATED

OBSTETRICS & GYNECOLOGY INTEGRATED PAGE 1 OF 90

DIAGNOSIS OF PREGNANCY

PRESUMPTIVE SYMPTOMS OF PREGNANCY
1. Nausea with or without vomiting – due to increase in HCG
2. Disturbance in urination
3. Fatigue – due to increase in metabolism
4. Quickening – perception of fetal movement
th th
a. Primigravid: 18 – 20 week AOG
th th
b. Multigravid: 16 – 18 week AOG
5. Breast tenderness and tingling sensation

PRESUMPTIVE SIGNS OF PREGNANCY
1. Amenorrhea
2. Anatomic breast changes:
- Darker areola, erected nipple, engorged breasts
3. Changes in Vaginal Mucosa
th
- Chadwick’s Sign: violaceous discoloration of the vagina due to increased vascularity starting 6 week
4. Skin Pigmentation
- Chloasma (Mask of Pregnancy) – darkening of the skin over the forehead, nose bridge or cheekbones
- Linea Nigra – darkening of the linea alba, areola, nipples, axilla, neck and groins
- Striae gravidarum or Stretch Marks – irregular scars on the abdomen due to separation of underlying collagen
- Spider Telangiectasia – vascular, stellate marks on abdomen that blanches when compressed; due to high levels of
estrogen
5. Thermal Signs:
- Increased temperature by 0.3 to 0.5 for > 3 weeks due to progesterone

PROBABLE EVIDENCE OF PREGNANCY
1. Enlargement of the abdomen
2. Changes in skin, shape and consistency of the uterus
- Cervical Mucus: beaded pattern due to progesterone vs. Ferning Pattern: characteristic of estrogen seem during the first
half of the cycle
3. Anatomical changes in cervix
4. Braxton-Hick’s contractions that are painless and irregular
th
5. Ballotment: Feeling that something is floating or bouncing back inside the abdomen by 20 week AOG
6. Physical outlining of the fetus
7. Positive Pregnancy Test
- β-hCG levels (>25 IU/L)
o Detected 8 – 9 days after ovulation
o Peaks at 60 – 70 days = Hyperemesis Gravidarum

POSITIVE EVIDENCE OF PREGNANCY
1. Identification of fetal heart tones separately from another
a. Normal FHT: 110 – 160 bpm
th th
b. Transvaginal UTZ by 5 – 6 week
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c. Doppler by 10 week
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d. Stethoscope by 20 week
e. Fundic / Umbilical Soufflé: Fetal Pulse
f. Uterine Soufflé: Maternal Pulse
2. Perception of active fetal movement by the examiner
3. Ultrasound or Radiologic Evidence
a. Male: Turtle Sign
b. Female: Burger Sign

RADIOGRAPHIC EVIDENCE OF FETAL DEATH
§ SPALDING’S SIGN – overlapping of fetal skull bones due to liquefaction of the brain
§ Exaggeration of fetal spine curvature
§ ROBERT’S SIGN – gas bubbles in the fetus


MATERNAL ADAPTATIONS OF PREGNANCY

CARDIOVASCULAR SYSTEM
Ø No actual cardiac enlargement but only slight dilation and displacement upwards and outwards due to gravid uterus
Ø ECG may reveal slight axis deviation, occasional T waves, lowering of T waves
th th
Ø Increase in HR, maximal on 7 -8 month (10bpm)
Ø Increase in CO by 30-50%

Mechanisms of Increased CO:
1. Increase in maternal oxygen consumption
2. Hypervolemia of Pregnancy
th
a. Increase plasma volume by 50-65% (peaks by 7 month) à more increase in erythrocyte production à dilutional
anemia
i. Estrogen and progesterone cause increase in hepatic production of plasma renin à stimulates aldosterone
à Na and Water retention
b. Progesterone causes venous relaxation
3. AV shunt effect of placenta
a. Decreased diastolic pressure and widening of pulse pressure
b. High CO and decreased AV oxygen difference

Four Periods of Increased CO:
th
1. On the 28 week of gestation (highest peak of cardiac load) – due to increased plasma volume and oxygen demand
2. During labor – increased flow to the heart from the uterine sinuses, increased HR due to pain and anxiety labor
3. Immediately post-partum – sudden increase in venous return
st
4. During the 1 week of puerperium – mobilization of fluids from the interstitial space into the vascular compartment

Ø Heart Sounds: exaggerated splitting of S1, systolic and soft diastolic murmur, S3
Ø BP: Systolic minimal change but diastolic decrease due to decreased total systemic peripheral resistance, resulting in
th th
increased pulse pressure maximal during 7 -8 month
Ø Venous Pressure: elevated in lower extremities due to:
o Increased blood flow from uterine vein into IVC
o Pressure of gravid uterus on the pelvic veins resulting in edema of legs and hemorrhoids

RESPIRATORY SYSTEM
Ø Upward displacement of the diaphragm by 4 cm
Ø Due to decreased broncho-motor tone as an effect of progesterone

INCREASED DECREASED
Vital Capacity Functional Residual Capacity
Tidal Volume Residual Volume of Air
Respiratory Rate Total Pulmonary Resistance
Airway Conductance

GASTROINTESTINAL SYSTEM
Ø Progesterone effect
Ø Decreased responsiveness to CCK à duodenal and biliary stasis à pancreatitis à hyperlipidemia à cholesterol stones
Ø Liver of Pregnancy: large, granular cytoplasm with small lymphocytic infiltrations, vacuoles and swelling of Kuppfer Cells

URINARY SYSTEM
Ø Increased kidney size due to hypertrophy & increase RBF causing increased renal vascular volume
Ø Physiologic hydroureter of Pregnancy: marked increase in diameter of ureteral lumen, hypotonicity and hypomotility of its
musculature, more pronounced and frequent on the right side
Ø Prone to UTI due to progesterone and pressure changes


ENDOCRINE SYSTEM
th
Ø Normal ovarian function is suppressed: increased corpus luteum activity up to 12 week after which placenta takes over
secretion of estrogen and progesterone
Ø Mild hyperthyroid state due to:
o Gland hyperplasia à slight increase in BMR
o Increased TBG: from estrogen
o Mild iodine deficiency
Ø Hyperparathyroidism: increased calcium for the fetus
Ø Hyperadrenal State: gland hyperplasia with increased steroid production
Ø Diabetogenic due to placental degradation of insulin and anti-insulin effects of placental lactogen, estrogen, progesterone

WEIGHT GAIN
st
1 Trimester 0 – 2 lbs
nd
rd

SKELETAL SYSTEM
Ø Back pain due to lordosis and increased mobility of sacral joints (relaxin)

HEMATOLOGIC SYSMTEM
Ø Dilutional anemia: increased volume due to increase in plasma > increase in RBC
Ø Increased reticulocyte and leukocyte count
Ø Increased blood coagulation factors, increased fibrinogen levels, increased plasminogen and fibrin degradation products
Ø Increased plasma iron binding capacity (transferrin)

Ø Iron Requirement: RDA – 27mg/day
o Total throughout pregnancy: 1 gram divided as:
§ 300 mg – fetus / placenta
§ 200 mg – excreted
§ 500 mg – RBC production
• Fe salts: Fumarate (33% elemental iron), Sulfate (20%)

Ø Fetal Blood Hematopoiesis
o Mesoblastic Period: in yolk sac during embryonic period
o Hepatic Period: liver takes over up to near term
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o Myeloid Period: marrow starts function at 4 month, major site of blood formation in adults

Ø ANEMIA IN PREGNANCY
st
1 Trimester < 11 g/dL
nd
2 Trimester < 12.5 g/dL
rd
3 Trimester < 11 g/dL


PRENATAL CARE

ESTIMATION OF DURATION OF PREGNANCY
1. Last Menstrual Period (LMP)
2. Height of Fundus (in cm): 20 – 34 weeks
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12 Week Above pubic symphysis
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16 Week Halfway between pubic symphysis and umbilicus
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20 Week Umbilicus
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28 Week 6cm above umbilicus
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36 Week 2 cm below xiphoid process
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40 Week 4 cm below xiphoid process
3. Ultrasound Imaging
• Crown-Rump Length (CRL): 4 days – 12 weeks
• Biparietal Diameter: 12 – 20 weeks
• Femur Length: >20 weeks

EXPECTED DATE OF CONFINEMENT (NAEGELE’S RULE)
st
1 day of LMP + 7 days – 3 months + 1 year

LEOPOLD’S MANEUVER
1. Fundal Grip: What part is occupying the fundus?
• Breech: Irregular, Nodular parts
• Cephalic: Round
2. Umbilical Grip: Which side is the back?
• Back: linear, convex, bony ridge
• Small parts: numerous nodulations
3. Pawlick’s Grip: Engaged in Pelvic Inlet?
• Head NOT engaged: round, ballotable, easily displaced
• Engaged: felt as relatively fixed, knob-like
4. Pelvic Grip: attitude of cephalic prominence
• Flexion: cephalic prominence same side as fetal parts
• Extension: same side as fetal back

LABORATORY EXAMINATIONS
TIME ASSESSMENT
ST
1 VISIT CBC, FBS, Urinalysis, Urine Culture
Blood type + Rh Factor
Pap-smear
Rubella IgG, Hep B (HBsAg), Chlamydia & Gonococcal if HR
Syphilis (VDRL/RPR to screen à FTA – AP to confirm)
HIV offered
15 – 20 weeks Fetal Aneuploidy: 11 – 14 / 15 – 20 weeks
Neural Tube Defects: 15 – 20 weeks
Congenital Anomaly Scan: 18 – 22 weeks
24 – 28 weeks CBC
75g OGTT
29 – 41 weeks Syphilis, Chlamydia
Group B Strep: 35 – 37 weeks
HIV: 36 weeks
Chlamydia (+): test of cure after 3 – 4 weeks of treatment
HBsAg (+): give Hep B Ig and Vaccine


FREQUENCY OF VISITS

Ø UNCOMPLICATED
o Every 4 weeks until 28 weeks
o Weekly until birth
Ø COMPLICATED
o Every week until birth
Ø WHO
st
o At least 4 visits at 1 Trimester, 26, 32, 38 weeks

RECOMMENDED DIETARY ALLOWANCES (RDA)
st
1 Tri: ↑ 100 – 300 kcal/day
nd
CALORIES 2 Tri: ↑ 340 kcal/day
rd
3 Tri: ↑ 452 kcal/day
FOLIC ACID Normal: 400 ug/day
Risk for NTD: 4 mg/day
PROTEIN 71 g/day (?)
CARBOHYDRATES 175 g/day
FIBER 28 g/day
FATS Min 15-25 g/day
CALCIUM 1300 mg/day
IRON Single: 27 mg/day
Twins: 60-100 mg/day
st
WOF: ↑ vomiting in 1 tri
FOLATE 600 ug/day
VIT A (Retinol) 750 ug/day (14 – 18)
770 ug/day (19 – 50)
WOF: Teratogenic at
>10,000 IU/day
VIT B1 (Thiamine) 1.4 mg/day
VIT B2 (Riboflavin) 1.4 mg/day
VIT B6 (Pyridoxine) 2 mg/day
VIT B12 2.6 ug/day
NIACIN 28 mg/day
VIT C 80 mg/day (14 – 18)
85 mg/day (19 – 50)
VIT D 15 ug/day


IDENTIFICATION OF HIGH RISK PREGNANCY

Ø Maternal age: <18 years old, Nullipara >35 years old
Ø Maternal Height: ≤ 60 inches or 153 cm
Ø Obese
Ø Social Factors: single, unwed, working, low economic status, diet, smoking, drugs, alcohol
Ø OB History:
• Multiparity • UTI, DM, Hypertension, Nutrition
• PROM, IUGR • Thyroid disease, PTB
• Premature labor • Uterine / Ovarian Disease
• Macrosomia • Previous CS
• Multiple Pregnancies • Abnormal Presentation
• AF abnormalities • Placental Abnormalities

Malnutrition and Fetal Development Mother’s Age: Infant’s Birth Weight:
• Fetal Growth Retardation • Pregnancy in Adolescents: • High Risk Pregnancy: LBW (a
• Congenital Malformations teenagers are encouraged to BW of ≤2500g. NV = 3000 –
• Spontaneous abortions strive for the highest weight 4000g)
• Stillbirth gains recommended to limit • SGA Infants: Complications
• Premature birth fetal growth retardation during delivery than normal
• Low infant weight • Pregnancy in Older Women: weight babies
• Death increases the risk of genetic • Greater chance of having
abnormalities such as Down physical and mental birth
Syndrome defects contracting diseases
and dying early in life
Maternal Health: 3. Preexisting Hypertension 5. Preeclampsia and Eclampsia
1. Preexisting Diabetes - Increases risk of heart attack - Blood flow that supplies
• Maternal Effects and stroke to the mother oxygen and nutrients
- Infertility rates - Fetus: LBW and abruption diminishes which retards
- Episodes of severe hypoglycemia placenta resulting stillbirth fetal growth
- Episodes of severe hyperglycemia - Ideally, BP must be controlled - In some cases, stillbirth
- Spontaneous abortions before a woman gest pregnant (abruption placenta)
- Pregnancy related hypertension - It rapidly progress to
• Fetal Effects 4. Transient Hypertension of eclampsia
- Large (macrosomic) Pregnancy - Preeclampsia demands
- Physical and mental abnormalities - High BP that develops in the prompt medical attention.
nd
- Respiratory Distress 2 half of pregnancy and Treatment focuses on
resolves after childbirth, controlling BP and
2. Gestational Diabetes usually without affecting the convulsion and CS if
- High infant birth weight outcome of the pregnancy necessary
- Birth defects (heart damage, limb
deformities and NTD)

10 DANGER SIGNS OF PRENGNANCY (4-3-2-1)
1. Headache: ↑BP
2. Blurring of Vision: ↑BP
3. Nausea & Vomiting: ↑BP
4. Facial Edema: ↑BP
5. Abdominal Pain: hepatocellular necrosis in HEELP, abruption placenta, premature labor
6. Dysuria: UTI
7. Decreased fetal movement: FDIU
8. Vaginal Bleeding: placenta previa, PROM
9. Vaginal Discharge: Vaginal infection
10. Fever: infection


DYSTOCIA
THE PASSAGES

INLET – SUPERIOR TRAIT
Ø BORDERS:
• ANT: Symphysis Pubis
• LAT: Linea Terminalis
• POST: Sacral Promontory

Ø AP DIAMETERS:
• True Conjugate: 11 cm (DC – 1.2)
• Obstetric Conjugate: 10 cm (DC – 1.5 – 2)
• Diagonal Conjugate: 11.5 – 12.0 cm (measured clinically)

Ø TRANSVERSE DIAMETER: 13 cm
Ø RIGHT & LEFT OBLIQUE DIAMTER: 13 cm

MIDPELVIS: Plane of Least Pelvic Dimensions
Ø AP Diameter: 11.5 cm
Ø Transverse (Bispinous) Diameter: 10 cm
Ø Posterior Sagittal: 4.5 cm

OUTLET – INFERIOR STRAIT
Ø AP Diameter: 9.5 – 11.5 cm
Ø Transverse (Intertuberous) Diameter: 11 cm
Ø Posterior Sagittal: 7 cm

PLANE OF GREATEST DIAMETER – NO OBSTETRIC SIGNIFICANCE
Ø AP Diameter: 12.5 cm

INDICATIONS FOR CLINICAL PELVIMETRY
1. Previous injuries or diseases likely to affect the pelvis
2. Breech for vaginal delivery
3. Vagina Birth After CS (VBAC)

SOFT PART OF PELVIS
Ø Pelvic Floor: muscular part separating pelvic cavity from perineum
o Levator Ani muscles:
§ Pubococcygeus
§ Iliococcygeus
§ Ischiococcygeus

Ø Pelvic Diaphragm: helps in control of the external anal sphincter through the puborectalis and ischiococcygeus; also stabilizes
joints

ADEQUATE PELVIMETRY
1. Diagonal Conjugate >11.5 cm
2. Bispinous Diameter >9.5 cm
3. Pubic Arch >90 degrees
4. Coccyx: moveable
5. Sacral Inclination: Posterior
6. Sidewalls: Divergent
7. Sacrosciatic Notch: Wide (2 ½ fingers)
8. Curvature: Hollow
9. Best indication of Adequacy: Trial of Labor


FEATURES OF PARENT PELVIC TYPES
(Caldwell – Maloy Classification)

GYNECOID ANTHROPOID ANDROID PLATYPELLOID

Shape Round AP Oval Triangular Transverse Oval
Almost equal and Both increased with Posterior segment Both reduced
AP Segment spacious slight anterior short & anterior flat
INLET narrowing segment narrow
Sacrum Well-curved Long & Narrow Inclined forward & Slightly narrow &
straight small
Sacrosciatic Notch Wide & shallow More wide & shallow Narrow & Deep Slightly narrow &
CAVITY small
Sidewalls Straight or slightly Straight or divergent Convergent Divergent
divergent
Ischial Spines Not prominent Not prominent Prominent Not prominent
Pubic Arch Curved Long & curved Long & straight Short &curved
Sub-pubic angle Wide Slight narrow Narrow Very wide (>90)
OUTLET Diameter Normal Normal or Short Short Wide
Delivery No difficulty More incidence of face Difficult delivery No difficulty
to pubis delivery Perineal injuries


THE PASSENGER

FETAL ATTITUDE (Posture or Habitus)
Ø Relation of fetal parts to one another
Ø Head is flexed, back is convex, thighs flexed over abdomen, legs bent at knees, arches of feet on anterior surface of legs

FETAL LIE
Ø Relation of long axis of fetus to long axis of mother
1. Longitudinal Lie (99%): long axis of fetus parallels the long axis of uterus
• Presentation: Cephalic, Breech
2. Transverse Lie (1%): long axis of fetus perpendicular the long axis of uterus
• Presentation: Shoulder
3. Oblique Lie: unstable, becomes either longitudinal or transverse

FETAL PRESENTATION
1. CEPHALIC (95%)
a. Vertex (Occiput)
• Most common because uterus is pyriform
• Posterior fontanel is the presenting part
• Head is fully flexed
• Shortest AP Diameter: Suboccipitobregmatic – 9.5 cm
b. Sinciput (Military)
• Bregma / Anterior Fontanel is the presenting part
• Head partially flexed, transient
• Occipitofrontal Diameter: 12.5 cm
c. Brow
• Head partially extended, transient
• Longest AP diameter: Occipitomental plane – 13.5 cm
d. Face
• Head fully extended
• Submentobregmatic diameter: 9.5 cm
• Indication for CS delivery

2. BREECH
a. Frank: thighs flexed over abdomen, legs extended over anterior body, feet near head
b. Complete: thighs flexed over abdomen, legs flexed over thighs, feet at buttocks level
c. Incomplete: one or both thighs extended, legs & feet below buttocks level
i. Single footling
ii. Double footling

3. SHOULDER (acromion)
4. COMPOUND: Prolapse of the fetal hand alongside the presenting vertex or breech, or foot alongside the head

FETAL POSITION
Ø Relation if the point of direction to one of the four quadrants or to the AP/Transverse diameters of maternal pelvis
Ø Points of direction: occiput in cephalic, mentum in Face, sacrum in breech, acromion in shoulder
Ø Most common position:
o Left Occiput Transverse (40%)
o Right Occiput Transverse (20%)
o Occiput Posterior (20%)


ASSESSMENT OF FETAL WELL-BEING

CLINICAL ASSESSMENT OF FETAL WELL-BEING
1. Serial measurement of maternal weight
2. Fundic height in determining estimated fetal weight
a. Rough estimate at >32 weeks – fundic height of:
i. 30 cm: 6 – 6 ½ lbs
ii. 31 cm: 6 ½ - 7 lbs
iii. 32 cm: 7 – 7 ½ lbs
b. McDonald’s Rule:
• AOG in Weeks = D (in cm) x 8 / 7
c. Johnson’s Rule
• Fetal weight in grams = (Fundic height in cm – n) x 155
• N = 12 if station below spines; 11 (engaged) if station above spines (unengaged)
• Use N + 1 if >200 lbs
3. Fetal Heart Tone: NV = 110 – 160 bpm
4. Fetal Activity acceleration determination
• Count fetal movements starting 1 hour after meals and before bedtime
• NV: 10 kicks in 2 hours
• Go to OB if <3 movements per hour

BIOPHYSICAL ASSESSMENT METHODS
1. Ultrasonography
a. Real Time Sonography: Biophysical Scoring System (BPS) refer to next table
st
i. Fetal tone: 7.5 – 8.5 weeks (1 to appear, last to disappear)
ii. Fetal movement: 9 weeks
iii. Fetal breathing: 20 – 21 weeks
st
iv. Fetal HR: 28 weeks (1 to disappear in hypoxic states) à BPP done at 28 weeks+

• Doppler Flow Velocimetry: assess the uteroplacental circulation & umbilical artery of the fundus

2. Electric Fetal Monitoring
a. Contraction Stress Test / Oxytocin Challenge
• Measure of uteroplacental function
• Evaluates the reaction of HR to contractions induced by nipple stimulation or oxytocin
• Done when 3 contractions / 10 minutes
• Interpretation:
§ Negative: no late or significant variable decelerations, highly predictive of survival
§ Positive: consistent & persistent late decelerations (>50%) of FHR in the absence of uterine hypertonus
or supine hypertension, even if contraction frequency is fever that 3 in 10
§ Suspicious: intermittent late decelerations or significant variable decelerations
§ Hyperstimulation: FHR decelerations that occur in the presence of contractions more frequent than
every 2 minutes or >90 seconds
b. Non-stress Test
• Reactive: at least 2 FHR accelerations of at least 15bpm lasting 15 secs within 20 mins; highly predictive of
intrauterine survival
• Non-Reactive: if otherwise; may imply fetus is acidotic, asleep or drugs were given


ULTRASOUND IN PREGNANCY
1. Abdominal Ultrasound (full bladder): full bladder acts as an acoustic window pushing uterus out of pelvis and displacing bowel
superiorly
2. Vaginal Ultrasound (empty bladder)
st
3. 1 Trimester Ultrasound
a. Establishes uterine pregnancy upon seeing gestational sac (5-6 weeks) esp. if ectopic pregnancy is suspected
b. Detection f embryonic / fetal life (Fetal Heart Movement at 7 weeks) & number of fetuses
c. Evaluation of complicated early pregnancy such as retrochorionic hemorrhage, incomplete or complete abortion
d. Early dating of pregnancy
e. Evaluation of uterus or adnexa
nd rd
4. 2 & 3 Trimester Ultrasound
a. Fetal Viability (FHR & Tone), number and presentation
b. Amount of Amniotic Fluid and Placental Localization
c. Fetal Age & Growth by Biometry
d. Evaluation of fetal anatomic structures (reversal of fetal diastolic blood flow in the umbilical artery indicates a
severely compromised fetus)

BIOPHYSICAL VARIABLE NORMAL (Score = 2) ABNORMAL (Score = 0)
Fetal Abdominal Breathing At least 1 episode of sustained breathing of at Absent or episodes <30 sec
least 30s duration in 30 mins
Gross Body Movement At least 3 discrete body/limb movements in 30 ≤2 episodes
mins (continuous)
Fetal Tone At least 1 episode of active extension with 1 extension with slow return to flexion,
rapid return to flexion of limbs/trunk movement of limb in full extension, or (-) tone
Reactive NST At least 2 episodes of FHR acceleration of < 2 episodes or acceleration of <15 bpm
>15bpm for 155 secs within 20 mins or <15 sec
Qualitative AFV At least 1 pocket of AF thst measures at least 1 No AF pockets or <1 cm in
cm in 2 perpendicular planes or AFI: 5 – 24 cm 2 perpendicular planes

BPS INTERPRETATION:
• 8 – 10 with normal AFV: Reassurance
• 8 due to abnormal AFV: deliver if >37 weeks
• 6: deliver if >36 weeks
• 4: deliver if >32 weeks
• 0 – 2: deliver


PARTURITION

FOUR PHASES OF PARTURITION

PHASE 1: QUIESCENCE Prelude to Parturition (95)
Contractile tranquility & uterine unresponsiveness
Cervical softening but remains firm & unyielding
PHASE 2: ACTIVATION Preparation for Labor
Uterine Preparedness of Labor:
• ↑ oxytocin receptors in myometrial cells
• ↑ number and size of gap junctions
• ↑ responsiveness of uterotonins
• ↑ frequency of painless contractions
Cervical Ripening
PHASE 3: STIMULATION Process of Labor
Uterine Contraction
Cervical effacement & dilation
Fetal & Placental expulsion (3 stages of labor)
PHASE 4: INVOLUTION Parturient Recovery
Uterine involution to prevent hemorrhage
Cervical Repair: restoration of fertility
Breast Feeding: lactation & milk ejection
Regulators: Uterotonins (Oxytocin, endothelin-1)

PARACRINE SYSTEM:
Ø Paracrine Arm: amnion, chorion leave, decidua parietalis
Ø Forebag: amniotic fluid trapped between the leading surface of the presenting part and the inner surface of the lower pole
of amniotic fluid
o PG levels are 10x increased
o Created by cervical dilation and effacement
Ø Hindbag: upper compartment, contribution of fetal swallowing, urination & fetal lungs


SIGNS OF LABOR
1. Lightening / Baby Drop: decreased fundic height due to formation of lower uterine segment allowing fetal head to descend,
also decreased amniotic fluid
2. False Labor / Braxton Hicks Contractions: painless, unpredictable, sporadic, non-rhythmic, with no cervical dilatation
3. Bloody Show: spontaneous release of a small amount of blood-tinged mucus from vagina = extrusion of mucus plug
4. Ferguson Reflex: mechanical stretching of cervix enhances uterine activity
5. Pathologic Retraction Ring / Ring of Bandl: extreme thinning of LUS as in obstructed labor, ring becomes very prominent à
uterine rupture

EFFACEMENT, STATION
BISHOP’S SCORE: predicts whether induction of labor will b e required (call PEDS for parturition)
1. Cervical Dilation
2. Cervical Effacement
3. Cervical Consistency
4. Cervical Position
5. Fetal Station

EFFACEMENT STATION
ü Obliteration/taking up of the cervix ü Level to which fetal presenting part has descended in
ü Shortening of the cervical canal from length of 2 cm à maternal pelvis
circular orifice of paper-thin edges ü Ischial Spine: Station 0
ü Upward pulling of muscular fibers of internal OS while ü From ischial spines up: Station -1 to -3
external OS remains temporarily unchanged ü From ischial spines down: Station +1 to +3
ü Progressive dilation with no change in station in women of
low parity may signify fetopelvic disproportion

CERVICAL DILATATION
Ø Degree of Opening of the External OS
Ø True indicator of Labor
Ø Maximum diameter: 10 cm
Ø Fetus may descend as cervix dilates (due to hydrostatic action of amniotic sac)
Ø Pattern of Cervical Dilation: Sigmoid Curve
1. Latent Phase: at start of regular contraction
2. Active Phase: at 4 cm dilatation
a. Acceleration Phase: predictive of outcome
b. Phase of Maximum Slope: measure of overall efficiency
c. Deceleration Phase
Ø Pattern of Descent: Hyperbolic Curve
• Active descent takes place when the cervical dilatation has already advanced but the maximum slope of descent
occurs during maximum slope of cervical dilation

Ø Three Functional Divisions of Labor:
1. Preparatory Division: little cervical dilation; affected by sedation
2. Dilatational Division: most rapid rate of dilatation; unaffected by sedation or conduction analgesia
3. Pelvic Division: starts at deceleration phase of cervical dilatation; cardinal movements of fetus takes place


FRIEDMAN’S CURVE
Stages of Labor

WHO PRINCIPLES OF PARTOGRAPH:
1. Active Phase of Labor begins at 4 cm
2. Latent Phase of Labor should not last beyond 8 hrs
3. Rate of cervical dilatation during the active phase of labor should not be slower than 1 cm/hr
4. A 4-hr lag between slowing of labor and the need for intervention is unlikely to compromise the fetus
5. Hourly vaginal examination is recommended

Obstetric Care Consensus Committee (2016), there are four new recommendations:
1. Admonishes against cesarean delivery in the latent phase of labor. A prolonged latent phase is not an indication for cesarean
delivery.
2. Does not recommend cesarean delivery if labor is progressive but slow – a protraction disorder
→ "Typically managed with observation, assessment of uterine activity, and stimulation of contractions as needed
3. Cervical dilation threshold is now 6 cm
4. Cesarean delivery for active-phase arrest “should be reserved for women at or beyond 6 cm of dilation with ruptured
membranes who fail to progress despite 4 hours of adequate uterine activity, or at least 6 hours of oxytocin administration
with inadequate contractions and no cervical change.”

CARDINAL MOVEMENTS OF LABOR (OCCIPUT ANTERIOR)
1. ENGAGEMENT
• Biparietal diameter (greatest transverse diameter) passes thru pelvic inlet
• Asynclitism: lateral deflection anteriorly towards symphysis or posteriorly towards promontory
• Naegele’s Obliquity / Anterior Asynclitism: sagittal suture lies more posteriorly, anterior parietal bone becoming
leading presenting part; in multiparas
• Fitsmann’s Obliquity / Posterior Asynclitism: sagittal suture lies more anteriorly; posterior parietal bones present
posteriorly; in primigravids
2. DESCENT
st
• 1 requisite for birth
• Forces:
o Pressure of Amniotic Fluid
o Direct pressure of fundus
o Bearing down of abdominal muscles
o Extension and straightening of fetal body
3. FLEXION
• Due to resistance from cervix, pelvis
• Suboccipitobregmatic diameter passes through pelvic inlet
4. INTERNAL ROTATION
• Occiput gradually moves toward symphysis pubis anteriorly / posteriorly towards hollow of sacrum


5. EXTENSION
• Brings base of occiput in contact with inferior margin of SP, head is born
• Forces:
o Uterus posteriorly
o Resistant pelvic floor and SP (acting as a fulcrum), anteriorly
6. EXTERNAL ROTATION
• Restitution to oblique position: direction of head towards opposite ischial tuberosity
• External rotation to transverse position
• Biacromial diameter is presenting
7. EXPULSION
• Delivery of shoulders and entire body

CHANGES IN THE SHAPE OF THE FETAL HEAD

CAPUT SUCCEDANEUM CEPHALHEMATOMA
• Swelling of Scalp • Below periosteum
• Above periosteum • Does not cross sagittal suture
• Crosses sagittal suture
MOLDING
• Overlapping of Bones
o Shortened suboccipitobregmatic diameter
o Lengthened mentovertical diameter
o By external compressive force


CONDUCT OF NORMAL LABOR AND DELIVERY

DIFFERENTIATION OF LABOR
PARAMETER FALSE LABOR TRUE LABOR
Contractions
• Regularity • Irregular • Regular
• Interval • Long • Increasing
• Intensity • unchanged • Increasing
Pain Radiation Hypogastric Hypogastric to Lumbosacral
Dilatation Long & Closed Open & Effacing
Effacement Does not occur Pregresses
Sedation May stop it Not stopped

FIRST STAGE OF LABOR
Ø Average duration:
o Nulliparas: 8 hours
o Multiparas: 5 hours
Ø Sufficient uterine contractions to bring about demonstrable cervical effacement and dilation up to full cervical dilation
Ø No increase in oxygen levels in plasma but PG levels increase in Amniotic Fluid & Maternal Blood

1.
Uterine Contractions
• Active phase of labor
• Moderate contractions (20 – 60 mmHg) every 10 mins to <1 min for 30 – 90 secs
2. Fetal Heart Tone monitoring
• Cases of fetal compromise, preterm, induced or augmented labor, meconium staining, abnormal fetal HR
• Records FHR by UTZ Doppler & uterine contractions by tacodynamometers at fundus
• Low Risk: every 30 mins
• High Risk: every 15 mins
3. Attendance in Labor
• IE every 2 hours
• Cervical dilation at 1 – 2 cm /hr
• Analgesia, IV fluids, bladder function
4. Active Management of Labor
• Artificial amniotomy can be done to shorten first stage of labor and for early detection of meconium staining
• Oxytocin infusion for uterine atony
o If dilatation did not progress ≥ 1 cm/hr
o Started at 6 mU/min to increase at increments of 6 mL/min every 15 mins but not to exceed a total of 60
mL/mon

SECOND STAGE OF LABOR

Ø Full cervical dilatation to expulsion of fetus
Ø Average duration:
o Nulliparas – 50 mins
o Multiparas – 20 mins
Ø Contractions: lasts for 1 min every 1 ½ mins
Ø Monitor:
o Low Risk: every 15 mins
o High Risk: every 5 mins
Ø Increased Maternal Plasma Oxytocin levels
Ø Dorsal Lithotomy increase pelvic outlet

NEW GUIDELINES (Consensus Committee, 2016) before Second- Stage Labor Arrest is Diagnosed:
• Nulliparas – 3hours
• Multiparas – 2 hours


1. Delivery of the Head
• Crowning: head encircled by vulvar ring
• Episiotomy: prevents perineal laceration
2. Ritgen’s Maneuver
• Controls delivery of head with extension to smallest diameters of head pass over introitus
• When vulvar opening is 5 cm wide, towel draped hand should be used to exert forward pressure on the chin of
fetus through the perineum
• Other hand placed on occiput
• Prevents extension episiotomy and fetal contaminations
3. Nasopharyngeal Toilette
• After delivery of head, face of fetus is wiped and nares and throat quickly suctioned
• To prevent aspiration of anitotic fluid and blood
4. Nuchal Cord Care

THIRD STAGE OF LABOR

Ø Time from delivery of the infant to expulsion of placenta

Ø Mechanisms of Placental Expulsion:

SCHULTZE MECHANISM DUNCAN MECHANISM
ü Starts at central portion ü “Dirty Duncan”
ü Placenta descend by dragging the membranes along ü Starts at periphery
this forming some form of inverted sac ü Placenta descends to the vagina sideways & blood
escapes

Ø Signs of Placental Separation:
1. Calkin’s Sign: uterus becomes globular and firmer
2. Sudden gush of blood into the vagina
3. Uterus rises in abdomen
4. Umbilical cord lengthens as placenta descends

Ø Laceration of the Vagina & Perineum:
st nd rd th
1 Degree 2 Degree 3 Degree 4 Degree
ü Fourchette ü Fascia & muscle of ü From vaginal mucosa, ü Up to rectal mucosa
ü Perineal Skin perineal body perineal skin, fascia up (repaired before vaginal
ü Vaginal Mucosa ü NOT anal sphincter to anal sphincter mucosa)
ü NOT underlying fascia & ü NOT rectal mucosa
muscle

Ø Types of Episiotomy:
MEDIAN MEDIOLATERAL
ü Less painful ü More commonly used
ü Easier to repair ü Less severe lacerations
ü Heals faster
ü May extend to rectum if perineal body is short

Ø Suturing Techniques (in sequence):
1. Initial figure-of-eight suture
2. Vaginal Mucosa: interlocking sutures until lower end of hymenal ring, start 1 cm above angle of mucosal defect
3. Subcutaneous & Fascial Layers: continuous sutures
4. Skin: subcuticular or interrupted sutures


Ø OVERSEWING
• Can control an actively bleeding vaginal lesion
• Apposing normal tissue with the aim to cover the bleeding site and serve as a tamponade for the bleed
• Continuous running locked suture

Ø PACKING AND ARTERIAL EMBOLIZATION
• Other methods to control an actively bleeding lesion

Ø HARMFUL PRACTICE
• Oxytocin at any time
• Sustained bearing down before full dilatation
• Massaging and stretching of perineum
• Fundal pressure
• Lithotomy
• Supine
• Rectal exam
• Xray pelvimetry
• Manual exploration for retained placenta
• Lavage of uterus

FOURTH STAGE OF LABOR / POSTPARTUM HEMORRHAGE
Ø 1 hour after delivery of placenta in which it is critical to identify postpartum hemorrhage
Ø Management: uterine massage, ice packs, oxytocin
Ø Vaginal Bleeding:
• Early: >500 cc within 24 hrs post-op
• Late: >500 cc >24 hrs post-op
Ø CS Bleeding: <1000 cc

CAUSE CLINICAL FINDINGS MANAGEMENT
TONE: Uterine Atony Soft uterus palpable above umbilicus Uterine massage
RF: rapid/protracted labor, infection, Oxytocin 20U IV in 1000mL
MgSO4, overdistended uterus
TEAR: Genital Lacerations Contracted uterus, visualized lesions Suture under anesthesia
RF: uncontrolled vaginal delivery, LGA,
forceps/vacuum
TISSUE: Retained Placenta Missing cotyledon Manual uterine exploration, UTZ guided
curettage
TISSUE: Uterine Inversion Failure to palpate uterus Uterine replacement + IV oxytocin
Dark, beefy-appearing bleeding mass at
introitus
TRANSFUSION: coagulopathies


PUERPERIUM
Ø Time after delivery of placenta up to return of reproductive organs to their normal non-pregnant condition (6 – 8 weeks).
Ø Colostrum: first milk, yellowish alkaline fluid, high protein and mineral content, less sugar, larger fat globules
Ø Uterine Involution (Uterine size decrease by 1 – 2 cm/day)
• At level of umbilicus: after placental delivery
th th
• At symphysis pubis: by 10 – 12 day
Ø Failure of Uterus to contract normally due to:
• Uterine atony
• Clot formation at thrombosed placental site
• Retained placental cotyledons
• Inadequate drainage of tissues
• Infection
Ø Slight fever due to vascular & lymphatic engorgement and not due to milk fever (<24 hours)

POST-PARTUM FEVER (PPD – usual postpartum days)
PPD CAUSE CLINICAL FINDINGS MANAGEMENT
0 WIND: Atelectasis Milk – moderate fever Pulmonary exercises
Mild rales on auscultation Ambulation
RF: Emergency CS w/ gen anesthesia
1 – 2 WATER: UTI High fever malaise, CV tenderness Cephalosporin 1 – 2 g PO Q6
(+) Urine CS
RF: Indwelling foley, Multiple IE
2 – 3 WOMB: Endometritis Moderate fever Clindamycin 900 mg IV Q8
Uterine tenderness Gentamicin 500 mg EOD
(-) Abdominal Findings
4 – 5 WOUND: Infection Spiking fever despite antibiotics Antibiotics for Cellulitis
Wound erythema or fluctuance Incision & Drainge; Saline Packs
Wound drainage Secondary Closure
5 – 6 WALK: Septic Pelvic Thrombophlebitis Wide fever swings despite antibiotics IV Heparin 7 – 10 days
Normal abdomen/pelvis
RF: emergency CS, PROM, prolonged
labor
7 – 21 Mastitis Unilateral localized erythema Antibiotics, Drainage
Edema, tenderness
RF: nipple trauma

nd
Ø Cardiac output returns to normal by 2 week
st
Ø Urinary retention in the 1 24 hours due to:
• Edema & congestion of vulva, urethra & bladder trigone
• Edema & reflex spasm of urethral sphincter
• Bladder atony
nd th
Ø Diuresis greatest from 2 – 5 day
Ø Lochia: discharge from uterus during puerperium; odor is heavy & fleshy but not offensive, lasts 4- 8 weeks
• Lochia Rubra: first 3 – 4 days, bloody
• Lochia Serosa: next 3 – 4 days, paler and pinkish
th
• Lochia Alba: from 10 day onwards, white / yellow white due to leukocytes, decreased fluids
• Foul Lochia: secondary to poor healing, infection, retained tissue
Ø After pains: contractions of the flaccid uterus to expel some of the remaining fragments & blood clots especially in multiparas;
more intense during breastfeeding


Ø Constipation due to inactivity, decreased intraabdominal pressure after delivery and painful perineum
Ø Weight Loss
• Average weight loss of 5kg immediately post-op
• Additional 3kg loss due to diuresis and skin loss
• Normal pre-pregnant weight at 6 months
Ø Post-partum blues
Ø Return of Menses & Ovulation
• Menses: in 6 – 8 weeks
• Ovulation: in 5 – 11 weeks
• Delayed with lactation (of 15 mins 7x/day) due to PRL inhibition of GnRH (2 – 18 months)
Ø Post-partum check-up in 4 – 6 weeks
• 75 OGTT at 6 weeks
• BP at 12 weeks
• Papsmear at 6 months

10 STEPS TO SUCCESSFUL BREASTFEEDING
1. Written breastfeeding policy
2. Train staff
3. Inform benefits and management
4. Initiate within 1 hour of birth
5. Show women how to breastfeed and sustain lactation
6. Pure breastfeeding
7. Rooming-in
8. Breastfeed on demand
9. No artificial pacifiers
10. Support group and referral


INTRAPARTUM ASSESSMENT

NORMAL = CATEGORY 1 TRACING
Ø Baseline rate: 110 – 160 bpm
Ø Baseline variability: 6 – 25 bpm (moderate)
Ø No late / variable decelerations
Ø Early decelerations (present or absent)
Ø Accelerations: 2 in 20 mins
• ≥32 weeks: ≥15 bpm for 15 secs – 2 mins
• <32 weeks: ≥10 bpm for 10 secs – 2 mins

ABNORMAL = CATEGORY 3 TRACING
Ø absent baseline FHR variability and one of the following:
• Recurrent late decelerations
• Recurrent variable decelerations
bradycardia
Ø Or sinusoidal pattern: sine wave patterns in FHR baseline with frequency of 3-5/min for ≥20 mins

MANAGEMENT:
Ø Left lateral decubitus: to decompress IVC
Ø Oxygen: facial mask 10 mL/min/nasal cannula for 2 – 3 mL/min
Ø Plain NSS or Plain LR to improve circulation à HYDRATE

FETAL HEART RATE PATTERNS
Ø DECELERATION: decrease of ≥15 bpm for ≥15 sec to <2 mins
Ø PROLONGED DECELERATION: ≥2 mins
Ø BASELINE CHANGE: ≥10 mins

EARLY DECELERATION LATE DECELERATIONS VARIABLE DECELERATIONS
ü Symmetrical to contraction with ü Occurs after contraction onset with ü Onset varies with successive
nadir occurring during peak of nadir occurring after peak of contractions
contraction contraction ü Due to cord compression & cessation
ü Due to head compression ü Due to uteroplacental insufficiency of umbilical blood flow
ü Normal – NO TX NEEDED ü TX: CS Delivery ü TX: Amnioinfusion, IE


FIRST TRIMESTER HEMORRHAGIC DISEASES
ABORTION
Ø Termination of pregnancy 20 weeks AOG or delivery of <500 g fetus
Ø ETIOLOGY:
1. FETAL: abnormal zygote or embryonic development (most common: Autosomal trisomy)
2. MATERNAL: infections, medical disorder (DM, thyroid disease), RT and CT, early removal of corpus luteum, trauma,
malnutrition, alcohol, insecticides, APAS
3. PATERNAL: Advanced age

TYPES UTERINE BLEEDING CERVICAL UTERINE BOW FINDINGS MANAGEMENT
CONTRACTIONS DILATATION SIZE
THREATENED +/- +/- Closed Compatible Intact (+) FHT Bed rest, Uterine
Relaxant
IMMINENT ++ + Open Compatible Intact (+) FHT Watchful
expectancy,
Oxytocin
INEVITABLE +++ ++ Open Incompatible Ruptured (+) FHT Curettage,
Oxytocin
INCOMPLETE +/- ++ Open Incompatible Ruptured/not Passage of Curettage (Ovum
appreciated Meaty or ring forceps)
Material
COMPLETE - +/- Closed Small Not (-) signs of Observe
appreciated pregnancy
MISSED - SPOT Closed Incompatible +/- (-) FHT Prostaglandin,
D&C
HABITUAL +/- + Closed Compatible +/- (+) FHT fast Correct probable
course cause,
incompetent
cervix: cerclage
SEPTIC -/+ +/- Dilated with Incompatible - Hx of D&C
FOUL mechanical Curettage/
SMELLING interference Hysterectomy
DISCHARGE with Antibiotics
& Uterine pregnancy,
tenderness fever


ECTOPIC PREGNANCY
Ø Implantation of fertilized ovum outside the endometrium
Ø MC: TUBAL à 70% ampullary, 12% isthmic
Ø Heterotropic pregnancy: simultaneous intrauterine & ectopic pregnancy

RISK FACTORS:
1. Abnormal FT anatomy secondary to STDs, adhesions
2. Salpingitis
3. ART, POCPs
4. Surgeries for fertility restoration, sterilization, prior ectopic pregnancy
5. Myomas, adnexal masses
6. Smoking

SYMPTOMS: CLASSIC TRIAD SIGNS
1. Colicky abdominal pain 1. Most Common: Wiggling tenderness
2. Amenorrhea of about 6 weeks followed by 2. Uterus smaller than AOG
3. Minimal vaginal bleeding 3. Fullness of uterine cul-de-sac due to hemoperitoneum

DIAGNOSIS:
1. Empty uterus with serum β-hCG >1500 mIU/mL
2. Low progesterone (>25 ng/mL excludes ectopic pregnancy)
3. TVS:
a. (-) gestational sac
b. (+) trilaminar endometrial pattern
c. (+) adnexal mass

MANAGEMENT:
A. MEDICAL
a. Indications: <6 weeks, <3.5 cm, (-) cardiac activity
2
b. Methotrexate IM 50 mg/m BSA: to reabsorb tissue
c. Given with Leucovorin (Folinic Acid)
B. SURGICAL
a. Laparoscopy: if hemodynamically stable
b. Conservative salpingostomy (creation of opening in FT and not closed with suture) vs. salpingotomy (incision of FT
and closed with suture)
c. Radical: Salpingectomy – removal and resection of FT
C. EXPECTANT: If initial β-hCG <200 mIU/mL

GESTATIONAL TROPHOBLASTIC DISEASE
Ø Tumors with abnormal trophoblast proliferation, produces hCG
Ø CLASSIFICATION:
a. Hydatidiform Mole: (+) villi, stromal edema
i. Complete: most common GTD, benign
ii. Partial: with some fetal tissue
iii. Invasive Mole: malignant
b. Nonmolar Trophoblastic Neoplasms:
i. Choriocarcinoma
ii. Placental site trophoblastic tumor
iii. Epitheloid trophoblastic tumor

Ø CLINICAL FINDINGS OF H. MOLE:
• 1 – 2 months of amenorrhea à spotting / hemorrhage
• Rapid Uterine Growth – enlarged uterus (50% of cases in complete mole)
• Nausea & Vomiting (maybe significant), Hyperemesis Gravidarum
• Uterine bleeding
• No fetal motion
• Thyrotoxicosis (possible but not common) ↑FT4 ↓TSH


• Early onset preeclampsia
• Theca Lutein Cyst (enlarged ovaries)
• UTZ:
§ Snowstorm appearance – Complete
§ Thickened, multicystic palcenta – Partial

FEATURE PARTIAL MOLE COMPLETE MOLE
KARYOTYPE 69 XXX or 69 XXY (usually) 46 XX or 46 XY
PATHOLOGY
EMBRYO FETUS Often Present Absent
AMNION, FETAL RBC Often Present Absent
VILLOUS EDEMA Variable, focal Diffuse
TROPHOBLASTIC PROLIFERATION Variable, focal, slight to moderate Variable, slight to severe
ATYPIA Mild Marked
P57 IMMUNOSTAIN (+) (-)
CLINICAL PRESENTATION
DIAGNOSIS Missed Abortion Molar Gestation
UTERINE SIZE Small for dates 50% large for dates (classic sign)
THECA-LUTEIN CYSTS Rare 25 – 30%
INITIAL HCG LEVELS <100,000 mIU/mL >100,000 mIU/mL
MEDICAL COMPLICATIONS (E.G. THYROID) Rare Frequent (eg. Early onset
preeclampsia <24w)
PERSISTENT TROPHOBLASTIC DISEASE / RATE OF GTN 1 – 5% 15 – 20%
PATHOLOGY
GROSS Bunch of grapes, smooth, transparent surface
MICROSCOPICALLY Not all villi are cystically dilated and All villi are cystic, avascular, there
contains blood vessels with is central cistern in the stroma:
nucleated RBC more marked trophoblastic
proliferation

MANAGEMENT:
1. Pre-op evaluation of preeclampsia, hyperthyroidism, IDA, electrolyte problems, metastasis (CXR for lung metastasis)
2. Termination of molar pregnancy

SUCTION CURETTAGE HYSTERECTOMY HYSTEROTOMY
Fast method, minimal blood loss, For those whose family size is No longer acceptable
more common (#1 in young people) complete, >35 years old

3. IV access for blood loss replacement
4. WOF respiratory insufficiency, pulmonary edema, embolism
5. Aspiration of larger theca lutein cysts
6. Post-op β-hCG monitoring within 48 hours then every 1 – 2 weeks until detectable
7. OCP for 1 year to prevent pregnancy (avoid ↑ in β-hCG)
8. Follow-up Exams:
a. β-hCG levels every 2 weeks for 3 months
b. Every month for 6- 12 months
c. Every 6 months for 1 – 2 years
d. Every year after
e. Pelvic exam every 2 weeks until normal then every 3 months


INDICATIONS FOR IMMEDIATE REFERRAL TO A TROPHOBLASTIC DISEASE SPECIALIST:
1. High β-hCG levels >4 weeks post-evacuation (serum level of 30,000 mIU/mL)
2. Persistently elevated β-hCG titer at 14 weeks post-evacuation
3. A rise in β-hCG of ≥10% (2 consecutive determination)
4. Plateauing β-hCG values (<10% fall or rise) at any time after evacuation (minimum of 3 consecutive weekly determination)
5. Clinical or histologic evidence of metastasis at any site
6. Elevation of a previously normal β-hCG titer after evacuation provided the diagnosis of pregnancy is excluded

CHEMOPROPHYLAXIS FOR H. MOLE:
Ø May be useful for patients at high-risk of post-molar GTD and when post-evacuation surveillance is doubtful. The following
features put a patient at risk for post-molar trophoblastic disease:
• Advanced maternal age: ≥35 years old
• Gravidity: ≥4
• Uterine size larger than AOG by ≥6 weeks
• Serum β-hCG titer ≥100,000 mIU/mL
• Theca lutein cyst/s ≥6 cm
• Any medical condition associated with increased trophoblastic proliferation:
§ Preeclampsia
§ Thyrotoxicosis
§ Pulmonary Insufficiency
§ DIC
• Poor patient compliance
Ø Use of chemoprophylaxis in situations of poor follow-up has been questioned. It requires monitoring due to side effects.
Ø Points against prophylaxis:
• Toxic side effects
• Increase in WHO Score Prognostication
• Resistance
Ø One course of Methotrexate IM is given for prophylaxis.
Ø Actinomycin D may be given if with hypersensitivity or liver toxicity.

CONTRAINDICATIONS TO CHEMOPROPHYLAXIS:
• Hgb <100 mg/dL, Hct <0.30
9
• WBC count <0.3x10
• ANC ≤1.5
• Platelet count <100
• Any active infection
• Liver/Renal dysfunction
• Known allergy to chemoprophylactic drug

SCHEDULE OF MONITORING FOR H. MOLE:
Ø After molar evacuation, all patients must have serial β-hCG monitoring to detect malignant degeneration (Level III, GPP).
Serum β-hCG level is measured.
• 1 week after molar evacuation, then
• Every 2 weeks until level becomes normal (<5 mIU/mL)
• After 3 consecutive biweekly normal levels, the monitoring is every 6 months
• At 2 monthly intervals for the next 6 months to ensure that β-hCG levels remain undetectable for 1 year following
remission.
Ø After evacuation of molar pregnancy, β-hCG levels usually disappear in 8 – 10 weeks.
Ø After normal delivery or miscarriage β-hCG levels become undetectable within 3 – 6 weeks.
Ø More than half of patients will have complete regression of β-hCG to normal within 2 months of evacuation
Ø Continue monitoring β-hCG until it is undetectable for 1 year
Ø Pregnancy is allowed after 6 months of normal serum β-hCG level.


GESTATIONAL TROPHOBLASTIC TUMOR
Ø INVASIVE MOLE
Ø CHORIOCARCINOMA
Ø PLACENTAL SITE TROPHOBLASTIC TUMOR
Ø EPITHELOID TROPHOBLASTIC TUMOR
o The diagnosis of GTN is usually based on persistent level elevation of serum β-hCG level without confirmation by
pathological study. Management is NOT directed by histologic findings.

ETIOLOGY
• ½ follow H. mole CLINICAL FINDINGS OF GTT
• ¼ follow miscarriage or tubal pregnancy • Irregular bleeding with uterine subinvolution
• ¼ follow term / preterm pregnancy • Aggressive invasion, metastasis

DIAGNOSIS
• Plateau of β-hCG for 4x in 3 weeks (days 1, 7, 14, 21)
• Rise in β-hCG >10% during 3 weekly consecutive measurements in 2 weeks (days 1, 7, 14)
• Serum β-hCG detectable for ≥6 months
• Histological diagnosis of choriocarcinoma

ü Excessive trophoblastic overgrowth with extensive tissue invasion by trophoblastic cells & whole villi
ü Deep penetration into the myometrium (even at times the peritoneum, parametrium or vaginal
vault)
ü Almost always arise from a partial or complete mole
INVASIVE MOLE / ü Locally invasive but lacks the tendency for widespread metastasis
CHORIOCARCINOMA ü TREATMENT:
DESTRUENS o SINGLE AGENT CHEMOTHERAPY à Methotrexate
§ 5-day: 0.4 – 0.5 mg/kg IM or IV OD
2
§ Weekly: 50 mg/m IM or IV
o HYSTERECTOMY if complete family size or > 35 years old
ü Extremely malignant carcinoma of chorionic epithelium
ü 2/3 follow a normal delivery, 1/3 follow molar gestation
ü considered anytime there is persistent bleeding after any pregnancy event
ü most common type if term pregnancy or miscarriage
ü rapidly growing
ü invades myometrium and blood vessels à hemorrhage and necrosis
ü TREATMENT:
o SINGLE AGENT OR COMBINATION THERAPY à MAC drug combination
CHORIOCARCINOMA § Methotrexate: 0.3 – 0.4 mg/kg BW/day IM
§ Actinomycin D: 10 – 12 µg/kg BW/day SIVP
§ Cyclophosphamide: 3 mg/kg BW/day PO, or
§ Chlorambucil: 0.2 mg;kg BW/day PO
o HYSTERECTOMY
o EMA-CO CHEMOTHERAPY
§ Course 1 (EMA): Etoposide, Methotrexate, Actinomycin D
§ Course 2 (CO): Vincristine, Cyclophosphamide
ü GTN arising in placental implantation site producing PRL
PLACENTAL SITE ü Follows term, abortion, ectopic, or molar pregnancy
TROPHOBLASTIC ü Presents mainly as bleeding
TUMOR ü TREATMENT:
(PSTT) o HYSTERECTOMY: best treatment
o Adjuvant multi-drug combination
EPITHELOID ü Develops from neoplastic transformation of chorionic type intermediate trophoblast
TROPHOBLASTIC ü Resembles PSTT but the cells are smaller and there is less nuclear pleomorphism
TUMOR ü TREATMENT:
(ETT) o HYSTERECTOMY
o Resistant to chemotherapy


FIGO ANATOMICAL STAGING FOR GTN
STAGE I Confined to uterus
STAGE II Extends outside uterus but limited to genital structures (adnexae, vagina, broad ligament)
STAGE III Extends to lungs with or without known genital involvement
STAGE IV Other metastatic sites

SUBSTAGING: RISK FACTORS:
• A: No risk factor • β-hCG >100, 000 mIU/mL
• B: One risk factor • duration of termination of antecedent
• C: Two risk factors pregnancy to diagnosis >6 months

WHO PROGNOSTIC SCORING SYSTEM

0 1 2 4
AGE ≤40 >40
ANTECEDENT PREGNANCY H mole Abortion Term
INTERVAL MONTHS FROM <4 4 – 6 7 – 12 >12
INDEX OF PREGNANCY
3 3 4 4 5 5
PRE-TREATMENT HCG <10 10 – 10 10 – 10 >10
LARGEST TUMOR SIZE 3 – 4 cm >5 cm
SITES OF METASTASIS Spleen, Kidney GIT Brain, Liver
NUMBER OF METASTASIS 1 – 4 5 – 8
PREVIOUS FAILED Single Drug ≥2 drugs
CHEMOTHERAPY
Ø ≤6: low risk disease treatable by single chemotherapeutic agent
Ø ≥7: high risk disease requiring combination chemotherapy


THIRD TRIMESTER BLEEDING
PLACENTA PREVIA
Ø Placenta is located over or very near the internal os. Four degrees of this abnormality have been recognized:

TYPES:
1. TOTAL/COMPLETE PLACENTA PREVIA à the internal cervical os is completely covered by the placenta
2. PARTIAL PLACENTA PREVIA à the internal os is partially covered by the placenta
3. MARGINAL PLACENTA PREVIA à the edge of the placenta is at the margin of the internal os
4. LOW-LYING PLACENTA à the placenta is implanted in the LUS such that placenta edge actually does not reach the internal
os but is in close proximity to it

1. Multifetal gestation, large placentation
RISK FACTORS 2. Maternal age >35 yo
3. Prior CS
4. Smoking
rd
1. Painless, profuse, sentinel (w/o contraction) bleeding in 3 trimester due to
migration
DIANOSIS 2. TVS for placental localization
3. IE only if delivery planes (double set-up)
4. MRI

ABRUPTIO PLACENTA
Ø Premature separation of normally implanted placenta
Ø Rupture of spiral arteries à retroplacental hemorrhage

ETIOLOGY CLINICAL FINDINGS
1. Pre-eclampsia 1. Sudden onset abdominal pain
2. Chronic Hypertension 2. Diagnosis of exclusion
3. External trauma à external or internal inversion 3. +/- hypovolemic shock, couvelaire uterus /
4. Short umbilical cord uteroplacental apoplexy, AKI, Sheehan syndrome
5. Sudden uterine decompression

CLINICAL CLASSIFICATION OF ABRUPTIO PLACENTA
MILD MODERATE SEVERE
MOTHER Normal CVP ↑pulse ↓CVP, hypotension Shock
FETUS Normal FHT Signs of fetal distress Fetal distress / death
COMPLICATION None, good UO None, marginal UP Renal failure, coagulation
UTERUS Irritability, Pain, Tenderness Irritability, Pain, Severe Severe pain & tenderness,
Tenderness tetanic contractions
BLEEDING <500 mL 500 – 1000 mL >1000 mL
PLACENTAL SEPARATION < 1/6 1/6 – 2/3 >2/3


ABRUPTIO PLACENTA VS. PLACENTA PREVIA

ABRUPTIO PLACENTA PLACENTA PREVIA
HISTORY • Pre-eclampsia or Hypertension • No association with pre-eclampsia
• Single attack of vaginal bleeding which usually • Repeated “warning hemorrhages” often
continues until delivery occurring over a period of weeks
• Abdominal pain • No abdominal pain
ABDOMINAL EXAM • Local uterine tenderness • Normal uterine tone;
• Hypertonic uterus in a concealed abruption • No tenderness
• Patients usually in labor • Patient rarely in labor
• Presenting part not engaged • Presenting part above brim, malpresentation
• Fetal parts maybe difficult to palpate frequently found
• (-) FHT • Fetal parts usually palpable
• (+) FHT
ANCILLIARY AIDS (UTZ) • Placenta demonstrated in the Upper Uterine • Placenta demonstrated in the Lower Uterine
Segment (UUS) Segment (LUS)
VAGINAL EXAMINATION • No placenta within 5 cm of the cervical os • Placenta implanted in the Lower Uterine
Segment (LUS)
MANAGEMENT • No place in expectant management • < 36 weeks, bleeding stopped: expectant
• Massive Bleed management is indicated
o Intensive blood & fluid resuscitation • If bleeding continues: CS delivery (vertical skin
o Oxygen incision)
o Prompt delivery (CS if alive, vaginal
if dead)


PLACENTAL DISORDERS
ABNORMALITIES OF PLACENTAL FETAL MEMBRANES
Ø PLACENTOMEGALY: placenta >600g
Ø Placenta Succenturiata: accessory love outside main disc
Ø Extrachorial Placenta: mebranes do not insert at disc
o Circummarginate: membranes without thickening
§ When the ring does not have central depression
o Circumvallate: membranes arise from a cup
§ If the fetal surface of the placenta presents a central depression surrounded by a gray-white ring

PLACENTA ACCRETA / INCRETA / PERCRETA
Ø Placenta accrete vera: villi contiguous with myometrium
Ø Placenta increta: villi invade myometrium
Ø Placenta precreta: villi penetrate serosal surface of myometrium
Ø Total accrete: adherence of cotyledons
Ø Partial accrete: adherence of few to several cotyledons
Ø Focal accrete: adherence of a single cotyledon

MEMBRANES – CHORIOAMNIONITIS
Ø Full thickness infection of the membranes

Routes of Infection: Pathology: At least 2 of the ff:
o
• Ascending from lower genital tract • Clouding of membrane • Fever of >38 C
(most common) • Foul odor of amniotic fluid • Tachycardia (fetal & maternal)
• Hematogenous spread from • Maternal Leucocytosis
maternal blood Complications:
• Direct spread from endometrium / • PPROM
fallopian tube • Preterm labor
• Iatrogenic contamination during
invasive procedures Management:
• Antibiotics (massive amounts)
• Delivery (definitive treatment, always)

OTHER ABNORMALITIES:
AMNION NODOSUM AMNIOTIC BANDS
A placental lesion consisting of numerous small, light-tan Disruption of the amnion leading to the formation of bands or
nodules on the amnion considered as a hallmark of prolonged strings that entrap the fetus
oligohydramnios


ABNORMALITIES OF AMNIOTIC FLUID
Ø AMNIOTIC FLUID INDEX (AFI)
o Used to measure amniotic fluid
o Calculated by adding the vertical depths of the largest pocket in each of the 4 equal quadrants

UNHYDRAMNIOS No AFV
OLIGOHYDRAMNIOS <5 cm
NORMAL 5 – 24 cm
POLYHYDRAMNIOS > 24 cm

HYDRAMNIOS / POLYHYDRAMNIOS OLIGOHYDRAMNIOS
ü AF >2000 mL ü Paucity of AF at term <500 mL
ü AFI >24 cm ü AFI <5 cm
ü Causes: ü Causes:
§ Fetal anomalies 1. Fetal Congenital Anomalies
• Esophageal atresia, anencephaly / spina bifida • Growth restriction, Demise / IUGR
• Transudation of fluid through exposed meninges • Postterm, ruptured membranes
to the amniotic cavity 2. Drugs
§ Maternal diabetes • PG synthase inhibitors
• Maternal hyperglycemia à fetal hyperglycemia à • ACEI (destroys fetal kidneys)
osmotic diuresis à Increased fetal urination o Placenta
§ Multifetal gestation • Abruption, Twin-Twin Transfusion
o Maternal
• Uteroplacental insufficiency
• HPN, Preeclampsia, Diabetes
o Idiopathic
ü Diagnosis: üMeasure AFI
• Measure largest pocket of AF on UTZ
§ Mild: 8 – 11 cm
§ Moderate: 12 – 15 cm
§ Severe: 16 cm
ü Symptoms: ü Possible Outcomes:
• From pressure exerted within the over distended • Pulmonary hypoplasia
uterus and upon adjacent organs • Limb hypoplasia
• Severe dyspnea • Compressed face
§ Mother will complain of DOB, because • Fetal Death
diaphragm can’t go down properly • Serious deformities including amputation
• Edema of the lower extremities, vulva and • Musculoskeletal deformities
abdominal wall (blood flow back to the heart is
impaired)
• Oliguria due to ureteral obstruction
ü Management: AMNIOINFUSION
• Minor and moderate degrees of hydramnios rarely • Replace fluid into the uterine cavity either
require treatment transvaginally or transabdominally
• Dyspnea, abdominal pain or if ambulation is • Indication: to treat repetitive variable decelerations
difficult à hospitalization • NOTE: routine prophylactic amnioinfusion for
• Bed rest, diuretics, and water & salt restriction à meconium stained amniotic fluid is NOT warranted
ineffective
§ Never use diuretics in polyhydramnios
• Amniotomy: only in term pregnancies
• Indomethacin


COMPLICATIONS OF PREGNANCY
HYPERTENSION

GESTATIONAL HYPERTENSION • BP ≥140/90 mmHg for the first time during pregnancy on 2 occasions 4 hrs apart, after
20 weeks AOG
• No proteinuria
• BP returns to normal before 12 weeks postpartum à transient hypertension
• Final diagnosis made only postpartum
PROTEINURIA • ≥300 mg / 24 hrs
• Crea ≥0.3
• Dipstick +1 reading
PREECLAMPSIA Minimum Criteria:
• BP ≥140/90 mmHg after 20 weeks AOG
• Proteinuria ≥300 mg / 24 hrs or ≥ 1+ dipstick

With Increased certainty of Preeclampsia:
• BP ≥160/110 mmHg after 20 weeks AOG
• Proteinuria 2.0 g / 24 hrs or ≥2+ dipstick
• Renal Insufficiency: SCr >1.2 mg/dL unless known to be previously elevated
3
• Thrombocytopenia: Platelets <100,000 mm
• Microangiopathic Hemolysis (↑LDH)
• Impaired liver function: ↑ ALT or AST
• Persistent headache or other cerebral or visual disturbances
• Persistent epigastric pain
• Pulmonary edema
ECLAMPSIA Preeclampsia + Convulsions before, during, or after labor
CHRONIC HYPERTENSION • BP ≥140/90 mmHg before pregnancy or diagnosed before 20 weeks AOG
• Proteinuria ≥300 mg / 24 hrs or ≥ 1+ dipstick
st
• HPN 1 diagnosed after 20 weeks AOG and persistent after 12 weeks postpartum
SUPERIMPOSED PREECLAMPSIA • New-onset proteinuria 300 mg/24 hrs in hypertensive women but no proteinuria
on Chronic Hypertension before 20 weeks AOG
3
• A sudden increase in proteinuria or BP or Platelet count <100,000 mm in women
with hypertension and proteinuria before 20 weeks AOG

ABN NONSEVERE SEVERE
Diastolic BP <110mmHg ≥100mmHg RISK FACTORS
Systolic BP <160 mmHg ≥160 mmHg • Nulliparous women
Proteinuria ≤2+ ≥3+ o Preeclampsia often in young and nulliparous
Headache Absent Present • Race & Ethnicity (African-American Ethnicity)
Visual Disturbances Absent Present • Genetic Predisposition
Upper Abdl Pain Absent Present • Environmental Factors
Oliguria Absent Present • Chronic Hypertension
Convulsion (eclampsia) Absent Present • Multifetal Gestation
Serum Creatinine Normal Elevated • Maternal Age over 35 years
Thrombocytopenia Absent Present o Older women at greater risk for chronic
Serum transaminase (↑) Absent Marked hypertension with superimposed
FGR Absent Obvious preeclampsia
Pulmonary Edema Absent Present • Obesity


PATHOPHYSIOLOGY PREDICTORS OF PREGNANCY INDUCED HYPERTENSION
1. Placental implantation with abnormal trophoblastic • Roll Over Test – Supine à ↑ pressure on uterus on great
invasion of uterine vessels vessels; only 33% predictive value
2. Immunological intolerance (maladaptation) between • Uric acid
maternal, paternal (placental), and fetal tissues • Fibronectin
3. Maternal maladaptation to cardiovascular or inflammatory • Coagulation activation
changes of normal pregnancy • Oxidative stress
4. Genetic influences • Cytokines
5. Dietary deficiencies • Placental peptides
• Fetal DNA
• Uterine artery Doppler velocimetry

PREVENTION:
DIETARY MANIPULATION CARDIOVASCULAR DRUGS
• Low Salt Diet • Diuretics
• “Calcium Supplement” – 2g/day • Antihypertensive drugs
• Fish Oil Supplement
ANTIOXIDANT ANTITHROMBOTIC DRUGS
• Ascorbic Acid • “Low Dose Aspirin” starting <16 weeks AOG: 80mg/day
• α-tocopherol – Vit E • Aspirin/dypiridamole
• Aspirin + Heparin
• Aspirin + Ketansirin

HELLP SYNDROME – “an indication for delivery” – but does not indicated Immediate CS
• H Hemolysis (↑LDH)
• EL Elevated Liver Enzymes (ALT or AST)
• LP Low Platelet Count

MANAGEMENT:
• DELIVERY: definitive cure
1. Oral Antihypertensives:
a. Beta blockers: Labetalol – 200-240mg/day BID-TID divided doses PO
b. CCB: Nifedipine – 20-120mg/day PO
c. Methyldopa: 05-3g/day BID-TID divided doses PO
2. IV Antihypertensives:
a. Hydralazine (DOC) IV 5 or 10mg every 20-30mins
nd
b. Clonidine (2 DOC) IM 75-150mcg
3. Therapy for Acute Onset Severe Hypertension
a. Labetalol 10-20mg IV then 20-80mg every 20-30mins or 1-2mg/min IV infusion
b. Hydralazine 5mg IV or IM then 5-10mg every 20-40mins then repeat every 3 hrs; 0.5-10mg/hr IV infusion
c. Nifedipine: 10-20mg PO then repeat in 20mins then 10-20mg PO every 2-6hrs
d. D5W 90mL + Nicardipine 10mg, 0.1mg/mL solution at 1mg/hr + 1mg/hr every hr up to 10mg/hr
4. Seizure control: Magnesium Sulfate (seizure prophylaxis)
a. IV Infusion
• Loading Dose: 4-6g in 100mL over 15-20mins
• Maintenance Dose: 2g/hr in 100mL IV Infusion
• Monitor: DTRs, serum magnesium if serum crea ≥1mg/dL
• Discontinue 24hrs after delivery
b. IM Injection
• LD: 4g 20% solution IV at ≤1g/min
• 10g of 50% solution IM, give ½ (5g) per upper outer quadrant of each buttock
• If persisting after 15 mins, give up to 2g 20% solution IV at ≤1g/min
• MD: 5g 50% solution in alternating buttocks every 4hrs
• Monitor: DTRs, RR ≥12/min, UO ≥100mL in previous 24hrs
• Discontinue 24hrs after delivery


c. MgSO4 Toxicity: Calcium Gluconate 10m: 10% solution IV
d. Plasma Magnesium levels maintained at 4-7mEq/L, 4.8 – 8.4 mg/dL or 2.0-3.5mmol/L
e. Breathing weakens if >10mEq/L
f. Respiratory paralysis / arrest if >12mEq/L
5. Other anti-convulsants
a. Diazepam
• LD: 10mg IV over 2mins
• MD: 40mg in 500mL normal saline IV infusion
b. Phenytoin
• Used after diazepam for prevention
6. Induction of labor or CS if vaginal delivery is not imminent or there is fetal compromise

DIABETES MELLITUS

OVERT DM GESTATIONAL DM
FBS 126mg/dL At least 2 of the ff: 75g OGTT
RBS 200mg/dL FBS (GDM) 92mg/dL (5.1mmol/L)
HbA1c 6.5% 1 hour 180mg/dL (10mmol/L)
75g OGTT, 2-hour 200mg/dL 2 hour 140mg/dL (7.8mmol/L)
153mg/dL – new guidelines

GENERAL INSTRUCTIONS FOR OGTT:
1. At least 3 days of normal unrestricted diet containing a minimum of 150mg carbohydrate per day prior to the test
2. Testing should not be done while the patient is sick or under stress on medications that can increase blood glucose levels
3. No smoking permitted during the test
4. Remain at rest during the test
5. Glucose solution must be consumed within 5 mins

PATHOPHYSIOLOGY:
Ø Impairment of peripheral insulin action as a consequence of action of placental lactogens, estrogen, and progesterone.
Ø Insulin does not cross placenta à fetal hyperglycemia
th th th
Ø DM Screening: first visit 24 -28 week, 32-34 week

MATERNAL EFFECTS FETAL EFFECTS
1. Preeclampsia 1. Abortion
2. Coronary Heart Diseaase 2. Preterm Labor and Delivery
3. Difficult / Operative Delivery 3. Polyhydramnios
4. Bacterial Infection 4. Macrosomia, Shoulder Dystocia
5. Diabetic Nephropathy, Retinopathy, Neuropathy 5. Congenital Malformations
6. Diabetic Ketoacidosis 6. Unexplained Fetal Demise

MANAGEMENT:
1. Goals: FBS ≤95mg/dL, 1hr ≤140mg/dL, 2hr ≤120mg/dL
2. Medical nutrition therapy
3. Weight management
4. Low glycemic index food
5. Lifestyle changes
6. Medical: Regular or Rapid-acting Insulin

Ø Oral hypoglycemic are NOT recommended during pregnancy, it is usually recommended that metformin be discontinued
once pregnancy is diagnosed.
Ø Recommended that women diagnosed with gestational diabetes undergo evaluation with a 75g OGTT at 6-12 weeks after
delivery


MULTIFETAL PREGANCY

IDENTICAL / MONOZYGOTIC TWIN FRATERNAL / DIZYGOTIC TWIN
• Twins arise from a single fertilized ovum • Fertilization of two separate ova
• “single-ovum”, monozygotic • “double-ovum”, dizygotic
• have increased incidence of discordant malformations

MONOZYGOTIC DIZYGOTIC
• Relatively constant • Increasing Maternal Age
• Largely independent of race, heredity, age & parity • Increasing Parity
• Assisted reproductive therapy • Nutritional Factors
• Pituitary Gonadotropin
• Infertility Therapy
• Assisted Reproductive Therapy

GENESIS OF MONOZYGOSITY DIFFERENTIALS
th
Dichorionic – Diamnionic: division on the 0-4 day Multiple fetuses Hydatidiform mole
th th
Monochorionic – Diamnionic: division on the 4 -8 day Elevation of the uterus by a distended Uterine Myomas
th th
Monochorionic – Monoamnionic: division on the 8 -12 day bladder A closely attached
Conjoined Twins: division >12 days Inaccurate menstrual history adnexal mass
Hydramnios Fetal macrosomia

DETERMINATION OF ZYGOSITY:
1. Ultrasound: # of placenta (chorionicity) gives clue à zygosity (can
determine zygosity as early as the first trimester)
2. Placental Examination – visual examination of the placenta and
membranes
3. Infant Sex & Zygosity
- Twins at the opposite sex are almost always dizygotic
Infants of different blood types are dizygotic

CONJOINED TWINS
1. Anterior: Thoracopagus – most common
2. Posterior: Pypopagus
3. Cephalic: Craniopagus
4. Caudal: Ischiopagus

COMPLICATIONS:
1. Twin Reversed Arterial Perfusion (TRAP) Sequence: rare (1 in 35,000 births) but serious complication of monochorionic,
monozygotic multiple gestation
• Normally formed donor twin who has features of heart failure as well as a recipient twin who lacks a heart (acardius)
and various other structures
• Caused in the embryo by a large artery-to-artery placental shunt, also accompanied by a vein-to-vein shunt
• The perfusion pressure of the donor twin overpowers the recipient twin, who thus receives reverse blood flow from
its twin sibling
2. Twin-Twin Transfusion Syndrome:
• Blood is transfused from a donor twin to its recipient sibling:
DONOR RECIPIENT
• Anemic / Pale • Polycythemic / Plethoric
• Growth may be restricted • Circulatory overload manifests as fetal hydrops
• Oligohydramnios • Poligyhydramnios
• Fetal consequence:
→ Circulatory overload with heart failure
→ Occlusive thrombosis is also much more likely to develop in this setting
→ Polycythemia may lead to severe hyperbilirubinemia and kernicterus


PRE-TERM LABOR
PRE-TERM 20 – 36 6/7 weeks AOG
PREMATURE Delivery before 37 completed weeks
LOW BIRTHWEIGHT <2,500g
VERY LOW BIRTHWEIGHT <1,500g
EXTREMELY LOW BIRTHWEIGHT <1,000g
AVERAGE BIRTHWEIGHT 2,500 – 3,500g
SURVIVAL FEASIBLE At 26 – 27 weeks AOG

RISK FACTORS:
MATERNAL PSYCHOSOCIAL OB HISTORY
• Race • Smoking • Short Interpregnancy Interval
• Age <16yo • Marijuana • Hx of Preterm Birth
• Height <145cm • Alcohol • Low Pregnancy Weight Gain
• Obese III • Stress • Multifetal Pregnancy
• Low Socioeconomic Status • Anxiety • Infections
• Unwanted Pregnancies • Depression • Douching During Pregnancy

PATHOPHYSIOLOGY COMPLICATIONS
• Activation of HPA Axis • Perinatal Mortality
• Infection & Inflammatory Response • Respiratory Distress Syndrome
• Decidual Hemorrhage • Intraventricular Hemorrhage
• Pathological Uterine Distention

DIAGNOSIS MANAGEMENT
1. Persistent uterine contractions of ≥6/hr with: 1. Restriction of physical and sexual activity
a. Cervical dilation ≥3cm, or 2. Correct infection if present
b. Cervical Effacement ≥80% or both 3. Non-Pharma: cervical cerclage to repair incompetent cervix
2. And membrane rupture of bleeding 4. Tocolytics: to relax uterine contractions, best at 32-34weeks AOG
3. Other tests: a. CCBs: Nifedipine (WOF: headache) 10-20mg q3-6hrs until
a. (+) Terbutaline Test contractions are rare, then 30-60mg q8-12hrs for 48 hrs
b. TVS: wedging & short cervix (<2.5cm) b. β-Blockers: Terbutaline – not given to patients with
c. Fetal Fibronectin Test in High Risk asthma
Population c. Oxytocin Receptor Antagonist: Atosiban
5. Corticosteroids: to enhance lung maturation & reduce
cerebroventricular hemorrhage, necrotizing enterocolitis &
neonatal death; given at 26-34 weeks AOG
a. Dexamethasone: 6mg q12 x 4 doses IM/IV
b. Betamethasone: 12mg q24 x 2 doses IM
6. MgSO4: for <33 weeks AOG; for neuroprotection

POSTTERM PREGNANCY: >42 weeks AOG
MATERNAL COMPLICATIONS FETAL COMPLICATIONS
• Difficult deliveries (fetal wt >4.5kg, arrest of dilation, • Stillbirth
nd
prolonged 2 stage with marked caput & molding) • IUGR or Macrosomia & Shoulder Dystocia
• Operative deliveries • Fetal distress & hypoxia
• Postpartum Hemorrhage • Meconium Aspiration Syndrome
• Failed Induction of Labor

FETAL SIGNS OF POST-TERM PREGNANCY: MANAGEMENT:
• OLD MAN FACIES 1. Assessment of True Gestational Age
o Wrinkled, worried look 2. Patient counseling regarding induction of labor
o Open eyes vs. conservative management
o Long nails 3. Anterpartum surveillance tests 2x/week: fetal
movement counting, NST > CST, fetal acoustic
stimulation test, BPP


URINARY TRACT INFECTION (UTI)
ASYMPTOMATIC BACTERIURIA ACUTE CYSTITIS ACUTE PYELONEPHRITIS
st st st
SCREEN 1 prenatal visit 1 prenatal visit 1 prenatal visit
3
>100,000 cfu/mL with ≥1 Pyuria ≥8 pus cells/mm Pyuria ≥5 pus cells/hpf
organisms in 2 consecutive (uncentrifuged) or ≥5 pus cells/hpf (centrifuged) & bacteriruria
midstream specimen or 1 (centrifuged) ≥10,000 cfu of uropathogen/mL
DIAGNOSIS catheterized specimen in urine CS GS, Urine CS, Blood Culture
>8-10 WBCs/hpf in urinalysis (not Urinary frequency, urgency, Chills, fever, flank pain, N&V, C/S
recommended alone) dysuria, bacteriuria LUTS, CVA tenderness
Absence of symptoms
TREATMENT MC Etiologic Agent: E.coli 7 days antibiotic Admit
Nitrofurantoin 100mg every 8hrs x 14 days antibiotics
7days (avoid >35wks AOG)

INTRAUTERINE GROWTH RESTRICTION

CLINICAL IDENTIFICATION
1. Previous undergrown infant in multipara
2. Slowing in fundal measurement (<1cm/week)
3. Slowing of maternal weight gain or girth increase
4. Presence of maternal disease or addictive habits

DIAGNOSIS: measure increase in biparietal diameter by UTZ
th th
1. <2mm/wk from 13 -34 week
th
2. <1mm/wk from 35 -term

TYPE I TYPE II
• Insult Early in Gestation with Equal Decrease in HC, • Insult of Later Onset
Weight And Length • With Characteristic “Sparing Of Head”
• Chromosomal Anomalies
• Increased Morbidity
• Lower Birthweight
• Late Catch-Up


DYSTOCIA
Ø Difficult labor characterized by abnormally slow progress of labor
Ø FOUR DISTINCT ABNORMALITIES
o Abnormalities of the expulsive forces
o Abnormalities of presentation, position, or development of the fetus
o Abnormalities of the maternal bony pelvis
o Abnormalities of soft tissues of the reproductive tract
Ø Abnormalities of the POWERS – uterine contractility and maternal expulsive effort
Ø Abnormalities involving the PASSENGER – the fetus
Ø Abnormalities of the PASSAGE – the pelvis
Ø DESCRIPTORS:
CEPHALOPELVIC DISPROPORTION (CPD) FETOPELVIC DISPROPORTION (FPD)
• Doubtful pelvimetry • Larger passenger or asynclitism
• Malposition of fetal head • Congenital anomalies
• Ineffective uterine contractions • Repeat CPD

ABNORMALITIES OF POWER
ST
• 1 STAGE OF LABOR: contractions of the uterus à cervical dilation, propulsion and expulsion of uterus
ND
• 2 STAGE OF LABOR: contractions of the uterus or involuntary muscular action of abdominal wall – “PUSHING”
Ø 2 TYPES OF UTERINE DYSFUNCTION:
HYPOTONIC UTERINE DUSFUNCTION HYPERTONIC/INCOORDINATE UTERINE DYSFUNCTION
• More common • Basal tone is elevated
• No basal hypertonus • Pressure gradient is distorted (asynchronism)
• Contractions have a normal gradient pattern • Treatment: SEDATION
(synchronous)
• Slight rise in pressure during a contraction is
insufficient to dilate the cervix
• Treatment: OXYTOCIN
NEW DIAGNOSTIC CRITERIA

st nd
Arrest of 1 Stage or Labor: Arrest of 2 Stage of Labor:
• ≥6cm dilation with membrane rupture • ≥2hrs of pushing multiparous women without epidural
• ≥4hrs of adequate contractions (200MVU) • ≥3hrs of pushing nulliparous women without epidural
• or ≥6hrs if contractions are inadequate after oxytocin • ≥3hrs of pushing multiparous women without epidural
• ≥4hrs of pushing nulliparous women without epidural
ABNORMALITIES OF PASSENGER
1. DIFFERENT PRESENTATIONS
a. Breech: Mauriceau Maneuver; Pinnard for frank breech
b. Face: do CS, do not attempt conversion to vertex
c. Brow
d. Transverse Lie: do vertical incision CS, may attempt external version
e. Compound: if arm does not retract out of the way, push upward & head downward by fundal pressure
f. Persistent occiput anterior: manual rotation then spontaneous delivery, forceps or vacuum with episiotomy, or CS
if head above inlet
g. Occiput Transverse Position: give oxytocin, manual rotation or forceps rotation & delivery
h. Shoulder dystocia: McRoberts Maneuver
2. FETAL DEVELOPMENTAL ABNORMALITIES
a. Macrosomia: fetal weight >4500g secondary to DM, multiparity, large parents/genetic/post-term pregnancy
b. Hydrocephalus: do cephalocentesis then CS
c. Large Abdomen: transabdominal decompression
d. Conjoined twins


ABNORMALITIES OF PASSAGE
1. Bony Dystocia
a. Pelvic Capacity
Contracted Inlet AP Diameter <10cm
(Sacral Promontory) Transverse Diameter <12cm
Diagonal Conjugate <11.5cm
Contracted Midpelvis Interspinous Diameter <10cm (suspect), <8cm (sure)
(Ischial Spine) Prominent Spines
Convergent Pelvic Sidewalls
Narrow Sacrosciatic Notch
Contracted Outlet Intertuberous Diameter <8cm
(Bitrochanteric Diameter)
o
Others Pelvic Arch <90
b. Pelvic Fractures
2. Soft Tissue Dystocia: uterine myoma or prolapse, cervical stenosis, transverse septum of vagina, cystocoele, rectocoele

COMPLICATIONS OF DYSTOCIA
MATERNAL EFFECTS FETAL EFFECTS
• Intrapartum infection • Caput Succedaneum
• Uterine rupture • Fetal head molding
• Pathological Retraction Ring • Associated with:
• Pathological Retraction Ring of Bandl – an § Nulliparity
exaggeration of the normal retraction ring § Oxytocin labor stimulation
• Uterine indentation and signifies impending rupture of § Delivery with a vacuum
the LUS extractor
• Fistula Formation • Skull fractures
• Vesicovaginal, vesicovervical or rectovagianl fistulas • Fetal morbidity and mortality
• Pelvic Floor Injury • Brachial plexus injury
• Postpartum Lower Extremity Nerve Injury • Clavicular Fracture
• Footdrop; Sx resolve within 6mos of delivery in most • Humeral fracture
• Most Common MOI: external compression of the
peroneal nerves (inappropriate leg positioning in
stirrups)

MANAGEMENT
Moderate Suprapubic Pressure Hibbard Maneuver
- Pressure is applied to the fetal jaw and neck
in the direction of the maternal rectum,
with strong fundal pressure applied by an
assistant as the anterior shoulder is treed
McRobert’s Manuever Zavanell Maneuver
- Removes legs from stirrups & sharply flex up onto the abdomen à - Cephalic replacement into the pelvis
assistant is also providing suprapubic pressure simultaneously and then cesarean delivery
Woods Corkscrew Maneuver Cleidotomy
- Hand is placed behind the posterior shoulder of the fetus and - Cutting the clavicle with the scissors
o
progressively rotating the posterior shoulder 180 in a corkscrew or other sharp instruments
fashion so the impacted anterior shoulder could be released - Usually used for a dead fetus
Rubin’s Maneuver Symphysiotomy
- Fetal shoulders are rocked from side to side by applying force to the
maternal abdomen
- Pelvic hand reaches the most easily accessible fetal shoulder, which
is then pushed toward the anterior surface of the chest
Deliberate Fracture of the Clavicle
- Pressing the anterior clavicle against the ramus of the pubis to
free shoulder impaction


ABNORMAL LABOR PATTERNS

LABOR PATERN NULLIPARAS MUTIPARAS PREFERRED TX EXCEPTIONAL TX
Prolongation Disorder >20hr >14hr Bed Rest Oxytocin or CS for urgent
(Prolonged Latent Phase) problems
PROTRACTION DISORDER
1. Protracted Active Phase Dilation <1.2cm/hr <1.5cm/hr Expectant & CS for CPD
2. Protracted Descent 1cm/hr <2cm/hr Support
ARREST DISORDERS
1. Prolonged Deceleration >3hr >1hr Oxytocin Rest if exhausted
2. Secondary Arrest of Dilation >2hr >2hr without CPD
3. Arrest of Descent >1hr >1hr
4. Failure of Descent No descent in >1hr CS delivery with
deceleration CPD
nd
phase or 2
Stage
PRECIPITATE DISORDERS
1. Dilation ≥5cm/hr ≥10cm/hr Do not give Oxytocin
2. Descent ≥5cm/hr ≥10cm/hr May give tocolytic


INSTRUMENTAL VAGINAL DELIVERY
INDICATIONS:
1. Pre-requisites
o Fetal head is engaged
o Cervix fully dilated
o Known position of vertex
o Ruptured membranes
o No CPD
o Vertex or Mentum Anterior
2. Maternal Indications
o CVD, Asthma, HPN
o VBAC
o Maternal Exhaustion / Poor Maternal Effort
nd
o Prolonged 2 Stage of Labor
3. Fetal Indications
o Non-reassuring fetal status
o Cord prolapse
o Abruptio Placenta

FORCEPS DELIVERY
TYPES:
1. Simpson
2. Barton – for transverse arrest
3. Piper – for aftercoming head in breech

TYPES OF FORCEPS INDICATIONS
OUTLET FORCEPS Scalp is visible at introitus without separating labia
Fetal skull has reached pelvic floor
Sagittal suture in AP Diameter or ROA/LOA or ROP/LOP
Fetal Head is at or on perineum
o
Rotation does not exceed 45
LOW FORCEPS Leading point of fetal skull is at ≥2cm & not on the pelvic floor
Rotation is:
o
a) ≤45 (LOA/ROA to OA, or LOP/ROP to OP) or
o
b) >45
MIDFORCEPS Station is between 0 and +2cm
Not currently recommended
HIGH FORCEPS Not included and not recommended
ELECTIVE FORCEPS Outlet Forceps + Anesthesia, for training

VACUUM DELIVERY
1. Successful if:
a. Accurate cup application at flexion point
b. Appropriate traction technique
c. Favorable flexed fetal cranial position
d. Low station at time of application
2. Soft, bell-shaped vacuum recommended for uncomplicated OA position
3. Limit to 2-3 “pop-offs” for 15 – 30 mins
4. Prompt CS if failed


CESAREAN SECTION
Ø Delivery of a fetus through an abdominal incision (laparotomy) followed by uterine incision (hysterotomy)
INDICATIONS FOR CS CONTRAINDICATIONS
1. Repeat CS 1. Compromised maternal status
2. CPD 2. Fetus with Trisomy 12/18 or known congenital anomaly
3. Breech in Primigravid that may lead to death (anencephaly)
4. Uterine Dysfuctions
5. Uncontrollable HTN
6. Hemorrhagic Complications (Previa/Abruptio)
7. Multiple Pregnancies
8. Post-Term Pregnancies
9. Fetal Distress
10. Cord Complications
11. Malpresentation
12. Obstructive Lesions in Lower Genital Tract

TECHNIQUES FOR CS
1. LAPAROTOMY
a. Midline Infraumbilical
b. Vertical
c. Transverse (Pfannenstiel, Mayland, Joel Cohen): stronger, less dehiscence

VERTICAL INCISION TRANSVERSE INCISION
Infraumbilical midline vertical incision MODIFIED PFANNENSTIEL INCISION
Should be of sufficient length to allow delivery Low transverse, slightly curvilinear incision at the level fo the
Should correspond with estimated fetal size pubic hairline and extended beyond the lateral borders of the
rectus muscle
Advantage: Advantage:
Can be rapidly extended Cosmetic
Quickest to make Stronger Incision
Less likely to develop dehiscence or hernia
Disadvantages
Suboptimal exposure
Reentry is more difficult due to scarring
MAYLARD INCISION
Rectus muscle divided with scissors and scalpel
Useful in women with scarring resulting from previous
Pfannenstiel incision

Ø Usually either a midline vertical or suprapubic transverse incision is used
Ø Only in special circumstances would a paramedian or midtransverse incision be employed

2. HYSTEROTOMY
a. Classical: longitudinal cut above LUS, not done due to high rupture risk
b. Low Segment: preferred method
i. Transverse (Monroe-Kerr): less bladder dissection, but little extension; easier to repair
ii. Vertical (Kronig, DeLee): more bladder dissection but can be extended


KERR KRONIG CLASSICAL INCISION
Incision is made in the lower uterine Low segment vertical incision Vertical incision in the body of the uterus
segment transversely May extend upward above the LUS & reaching the uterine fundus
Operation of choice
ADVANTAGES DISADVANTAGES INDICATIONS
Easier to repair More extensive dissection of the If the LUS cannot be exposed or entered
Located at a site least likely to rupture bladder safely because of:
during a subsequent pregnancy May extend downward to the cervix 1. Bladder adherent densely from
Does not promote adherence of bowel or and involve the bladder previous surgery
omentum to the incisional line More likely to rupture 2. Myoma
3. Invasive CA of the cervix

Transverse Lie of Large Fetus
Placenta previa with anterior implantation
Very small fetuses with LUS not thinned out
massive maternal obesity where Upper
Uterus is easily accessible

RISKS OF RUPTURE
TYPES OF CS RISK OF RUPTURE
Classical 2 – 9%
T-shaped 4 – 9%
Low Vertical 1 – 7%
Single Low Transverse 0.2 – 0.9%
Multiple Low Transverse 0.8 – 1.8%
Prior Uterine Rupture (Lower) 2 – 6%
Prior Uterine Rupture (Upper) 9 – 32%

INDICATIONS FOR VBAC (Vaginal Birth After CS)
1. Consent
2. No CPD
3. Active Labor
4. Advanced Cervical Dilation
5. Experienced OB Attendant
6. Double Set-up in case of CS
7. Cephalic
8. Small Fetus
9. Prior Vaginal Delivery
10. Prior CS was Low Transverse, Single Scar


MENSTRUAL CYCLE

PROLIFERATIVE STAGE / FOLLICULAR PHASE SECRETORY STAGE / LUTEAL PHASE
Ø Rising estrogen levels à proliferation of stromal & Ø CL produces estrogen & progesterone
epithelial cells Ø Preparation for implantation
Ø Endometrial thickening of 2-3mm, ↑BVs Ø Marked swelling & formation of tortuous glands & BV,
Ø Selection of dominant “ovulatory” follicle ↑lipid & glycogen deposits
Ø Prolonged in anovulation Ø Endometrium 4-6mm thick
Ø Surge of LH 2 days before ovulation

MENSTRUATION
→ ↓ in progesterone and estrogen causes vasospasm of BV & initiates uterine contraction leading to desquamation

CYTOLOGICAL HORMONAL MATURATION INDEX
st rd
Ø 1 number represents parabasal cells, middle number the intermediate cells, the 3 number in the superficial cells
o 0/10/90 – adequate marked estrogen effects
o 20/75/5 – poor estrogen effect
o 100/0/0 – absence of estrogen like in postmenopause
o 0/100/0 – maximum progesterone effect (pregnancy)


ABNORMAL UTERINE BLEEDING
Ø Significant deviation from normal frequency, regularity, heaviness, duration

CLINICAL DIMENSION TERMS
Frequency (Days) Frequent <24
Normal 24-28
Infrequent >28
Regularity: cycle-cycle variation in 12 mos (Days) Absent
Regular ±2-20days
Irregular >20days
Duration (Days) Prolonged >8
Normal >4.5-8
Shortened <4.5
Volume (mL) Heavy >80
Normal 5-80
Light <5

Ø Heavy menstrual bleeding (previously menorrhagia): excessive menstrual blood loss interfering with quality of life
Ø Intermenstrual bleeding (previously metrorrhagia): occurs between clearly defined cyclic & predictable menses
Ø DUB: no longer used
Ø Acute AUB: bleeding in a non-pregnant fertile woman with sufficient quantity to require immediate intervention
Ø Chronic AUB: AUB for the past 6 months

PATHOPHYSIOLOGY (PALM-COEIN CLASSIFICATION)
NORMAL FACTORS FOR HEMOSTASIS:
1. Higher thromboxane level (PGF2) in relation to prostacyclin (PGE2)
2. Fibrin clot formation
3. Stabilization of hemostatic platelet plug

POLYP Endometrial ADENOMYOSIS
HMB Growth of endometrial glands & stroma in the uterine myometrium at a depth of
IMB at least 2.5mm from basalis layer of endometrium
Postmenstrual Bleeding
CLINICAL:
Painful prolonged HMB
Corpus enlarged to 14 weeks
DX: DX:
UTZ, Hysteroscopic Imaging ± Hysteroscopy UTZ
REASONS FOR BLEEDING:
1. Inc endometrial surface
2. Altered PGE/PGF2 balance
3. Hampered myometrial contractility
4. Abnormal myometrial angiogenesis associated with fragile BVs


LEIOMYOMA / FIBROIDS MALIGNANCY / HYPERPLASIA
TYPES: Refer to gyne malignancy section
1. Solitary or Multiple
2. Submucosal (close to cavity)
3. Intramural (in myometrium)
4. Subserosal (close to outer surface)
5. Parasitic (independent of uterus)
CLASSIFICATION:
1. Primary: presence/absence
2. Secondary: submucosal or others
3. Tertiary: submucous, intraural, subserous
CLINICAL:
Ø Uterus asymmetrically enlarged
Ø No tenderness
REASONS FOR BLEEDING:
1. Increased endometrial surface due to mechanical distortion
2. Ulceration & hemorrhage of endometrium overlying submucous fibroids
3. Interference by myomas with normal uterine hemostasis
4. Mechanical compression of venous drainage by myomas at any site
5. Dilation of venous plexuses draining endometrium

COAGULOPATHY OVULATORY DYSFUNCTION
Von Willebrand Disease CLINICAL:
Chronic Anticoagulant Drug Use Unpredictable bleeding
(Warfarin, Heparin, LMWH) Variable amount of flow
HMB
Non-secretory endometrium
MC after menarche (immature HPO axis: (-) predictable cyclic progesterone production from
CL) or just before menopause (decline of inhibin & rise in FSH à luteal out-of-phase events)
Associated with endocrinopathies: PCOS, hypothyroidism, hyperprolactinemia, mental stress,
obesity, anorexia, weight loss, extreme exercise

ENDOMETRIAL IATROGENIC NOT YET CLASSIFIED
Predictable & cyclic, typical of ovulatory
Breakthrough bleeding Chronic Endometritis
cycles, w/o other identified causes Irregular Bleeding AVM
HMB: primary local disorder of local
Secondary to meds that impact Myometrial Hypertrophy
endometrial hemostasis regulation endometrium, blood coagulation, control
of ovulation
IMB / Prolonged Bleeding: Deficiencies in
molecular mechanisms of endometrial e.g. OCPs, IUD, steroids, tranquilizers,
repair digitalis, Dilantin, rifampicin, griseofulvin

MANAGEMENT
A. MEDICAL MANAGEMENT OF ACUTE HMB: • Cyclic Progesterone:
a. Hormonal Medroxyprogesterone (Provra)
• High dose estrogen 10mg PO OD on days 15 – 26
• High dose combined OCPs • Danazol 200-400mg PO OD
• Progestin b. Non-hormonal: anti fibrinolytic agents,
b. Non-hormonal – Tranexamin acid 1g 3- NSAIDS
4x/day PO during heavy bleeding for 3 days C. Surgical Management of HMB:
a. Dilatation & Curettage: NOT
B. MEDICAL MANAGEMENT OF CHRONIC HMB: RECOMMENDED
st
a. Hormonal b. Endometrial Ablation: 1 line in non-
• Levonorgestrel releasing desirous of pregnancy & no
intrauterine system once every 5 structural/histological abnormality
st
years c. Hysterectomy: NOT 1 line treatment
• Combined OCPs


AMENORRHEA
Ø Absence of menses during the reproductive years
o PRIMARY (<0.1%): absence of menses in a woman who has never menstruated by the age of 16 ½ years
o SECONDARY (<0.7%): absence of menses for an arbitrary time period, usually longer than 6 – 12 months

CLASSIFICATION OF PRIMARY AMENORRHEA:
• (+) breast means estrogen is produced
• (+) uterus means Y chromosome is not present

DELAYED MENSES
• Onset of menses in women >16.5 years who have NO REPRODUCTIVE ABNORMALITY

Breast (-) Breast (+) Breast (-) Breast (+)
Uterus (+) Uterus (-) Uterus (-) Uterus (+)
o
Hypothalamic Failure 2 to inadequate GnRH release Hypothalamic
(Hypogonadotropic Hypogonadism) Etiology

Insufficient GnRH synthesis (Kallman’s Syndrome)

Insufficient GnRH secretion

Congenital Anatomic defects in the CNS (stenosis of the
aqueduct, absence of sellar floor)

CNS Neoplasm
Pituitary Failure Pituitary Etiology

Isolated Gonadotropin insufficiency
(Thalassemia major, retinitis pigmentosa)

Pituitary neoplasia
(pituitary adenoma, chromophobe adenomas)

Mumps encephalitis

Newborn Kernicterus

Prepubertal Hypothyroidism
Gonadal Failure (Hypergonadotropic Hypogonadism) Androgen resistance Agonadism Ovarian
(testicular feminization)
45X Anomalies (Turner’s Syndrome, Mosaicism) 17,20 desmolase Uterine Etiology
Congenital absence of deficiency
Structurally Abnormal X Chromosome uterus (RKH)
46XY, 17α-
Pure Gonadal Dysgenesis (46XX, 46XY with gonad streaks, hydroxylase
Gonadal agenesis) deficiency


SECONDARY AMENORRHEA:
Ø Absence of menses for an arbitrary time period, usually longer than 6 – 12 months
o Asherman Syndrome: post-traumatic/post-curettage intrauterine adhesions or synechiae with ology-/amenorrhea
& infertility
o Sheehan Syndrome: postpartum pituitary necrosis
o Simmon Syndrome: pituitary hemorrhage not related to pregnancy

PUBERTY: SEQUENCE OF EVENTS
EVENT AGE AVG HORMONE
Breast Development 10.8 ± 1.10 10-11 Estradiol
Appearance Of Pubic & Axillary Hairs 11.0 ± 1.21 10.5-11.5 Androgens
(Pubarche)
Maximal Growth Velocity 11-12 11-12 GH
Menarche 12.0 ±1.20 11.5-13 Estradiol

BREAST GROWTH
B1 Prepubertal: elevation of papilla only
B2 Breast budding
B3 Enlargement of breasts with glandula tissue, without separation of breast contours
B4 Secondary mound formed by areola
B5 Single contour of breast and areola

PUBIC HAIR GROWTH
PH1 Prepubertal: no pubic hair
PH2 Labial hair present
PH3 Labial hair spreads over mons pubis
PH4 Slight lateral spread
PH5 Further lateral spread to form inverse triangle and reach medial thighs

PUBERTY INTERVALS
EVENT AGE
B2 – Peak Height Velocity 1.0 ± 0.77
B2 – Menarche 2.3 ± 1.03
B2 – PH5 3.1 ± 1.04
B2-B5 (average duration of puberty) 4.5 ± 2.04


ENDOMETRIOSIS
Ø The presence & growth of the glands and stroma of the lining of the uterus in an aberrant or heterotrpic location

ETIOLOGY: COMMON SITES:
1. Retrograde menstruation • Majority: dependent portions of the pelvis
2. Lymphatic & Vascular Dissemination • The OVARIES are the most common site
3. Metaplasia • Mostly bilateral
4. Genetic predisposition
5. Immunologic changes
6. Hormonal influences
7. Iatrogenic dissemination
1. Ovaries: endometrioma / chocolate cyst
2. Pelvic peritoneum
3. Uterine ligaments
4. Sigmoid Colon
5. Appendix
6. Pelvic lymph nodes
7. Cervix
8. Vagina
9. Fallopian tubes

CARDINAL HISTOLOGIC FEATURES:
• Ectopic endometrial glands
• Ectopic endometrial stroma
• Hemorrhage into the adjacent tissue

SIGNS & SYMPTOMS:
1. CLASSIC SYMPTOMS:
a. Cyclic Pelvic Pain (secondary dysmenorrhea / dyspareunia)
b. Infertility
c. Abnormal Bleeding
2. CLASSIC SIGN:
a. Classic Pelvic Finding: fixed retroverted uterus, with scarring & tenderness posterior to the uterus
i. Tenderness of the pelvic structures, nodularity of the uterosacral ligaments & cul-de-sac
ii. Time of maximum swelling & tenderness – first 2 days of menses

GOLD STANDARD FOR DIAGNOSIS: Laparoscopy
Other diagnostic tools:
• Ultrasound
• MRI

DIFFERENTIAL DIAGNOSIS
• Chronic PID • Ectopic Pregnancy
• Ovarian Malignancy • Appendicitis
• Degeneration of Myoma • Diverticulitis
• Adenomyosis • Primary Dysmenorrhea
• Functional Bowel Disease • Hemorrhage or Torsion of Ovarian Cyst

MANAGEMENT:
SHORT TERM GOALS LONG TERM GOALS
• Relief of Pain • Prevent progression or recurrence
• Promotion of Fertility


1. MEDICAL MANAGEMENT: HORMONAL THERAPY
• Primary Goal:
o Induction of amenorrhea
o To create a state of pseudopregnancy or pseudomenopause
• Agents used:
o Danazol
o GnRH agonists
o Oral Contraceptives
o NSAIDs
• Other Hormonal Agents
o Progestins
o COX-2 Inhibitors
o PPAR-ligands
o Gestrinone
o Aromatase inhibitors

2. SURGICAL THERAPY
• TYPES:
CONSERVATIVE SURGERY DEFINITIVE SURGERY
Resection or destruction of endometrial Removal of both ovaries, the uterus and all visible
implants, lysis of adhesions & attempts to ectopic foci or endometriosis
restore normal anatomy
Goal: removal of all macroscopic, visible areas Reserved for far advanced disease and for whom
of endometriosis with preservation of ovarian future fertility is not a consideration
function & restoration of pelvic anatomy
TAHBSO and REMOVAL of all visible endometriosis
LAPAROSCOPY is commonly recommended

• Factors to consider between medical or surgical management:
o Age
o Symptomatology
o Reproductive desires
• Surgical Therapy:
o The only option for failed medical therapy
o For moderate to severe endometriosis
o Laparoscopy: employed for both diagnostic & therapeutic reasons
§ Commonly recommended as initial approach
§ Advantages:
• Both diagnostic & therapeutic
• Shorter recovery period
• Reduced subsequent postoperative adhesions

3. COMBINATION OF MEDICAL & SURGICAL THERAPY:
• For advanced stages of endometriosis
• Many favors preoperative medical therapy prior to surgery, especially in extensive disease
• Postoperative Medical Therapy is considered depending on the extensiveness of the disease and the success of
surgery


DISORDERS OF PELVIC SUPPORT

URETHROCOELE & CYSTOCOELE
Ø Descent of urethra (urethrocoele) or bladder neck, bladder (cystocoele) into vaginal canal due to rupture or attenuation of
the pubovesical fascia
Ø SIGNS & SYMPTOMS:
o Sensation of fullness
o Pressure of vaginal bulge
o “Failing Out” Sensation
o Urgency
o Incomplete Emptying
o Urinary symptoms, stress incontinence
o Soft, bulging mass on anterior vaginal wall: may be manual reducible
Ø DIAGNOSIS: Hx & PE; patient in lithotomy position asked to strain
Ø DIFFERENTIAL DIAGNOSIS:
o Inflamed and enlarged Skene’s glands – tender and pus is expressed from the urethra
o Diverticula – more reducible, very prominent sensation of a mass, less common
o Bladder tumors – less common
§ Cystocoele & Urethrocoele – softish, pliable and nontender
Ø MANAGEMENT:
o Non-operative
§ Pessary (Smith – Hodge or inflatable)
§ Large tampons
§ Kegel’s Exercises (Pelvic Floor Exercises)
• Simple technique for toning the muscles in the vaginal and perineal area, strengthening them in
preparation for delivery
§ Estrogen Vaginal Creams
o Operative
§ Objective: Repair of all existing support defects
• Anterior and posterior colporrhaphy
• Abdominal retropubic bladder neck suspension – stress incontinence

RECTOCOELE
Ø Protrusion of the rectum into the posterior vaginal wall due to weakness of rectal supports
Ø Heaviness or feeling of falling out in the vagina with constipation or incomplete emptying of rectal vault
o Pelvic Heaviness
o “Falling Out”
o Constipation
o Incomplete Emptying
o Vaginal splinting to effect bowel movement
Ø DIAGNOSIS: History & Physical Examination
Ø MANAGEMENT:
NONOPERATIVE OPERATIVE
• Pessary, Kegel’s, Estrogen cream • Anterior & Posterior colporrhaphy
• Dietary Fibers, Increased fluids • Correction of concomitant enterocoele
• *Colorectal Screening test for GI symptoms • Perineorraphy


ENTEROCOELE
Ø Herniation of the Pouch of Douglas between the uterosacrals into the rectovaginal septum
Ø Usually contains small intestine
Ø Often arises after a hysterectomy (post-abdominal or vaginal hysterectomy)
Ø PREVENTION: incorporation of uterosacrals and cardinals into the vault repair
Ø DIAGNOSIS:
o PE reveals it as a separate bulge above a rectocoele
o Transillumination reveals small bowel shadows in the sac
Ø MANAGEMENT:
o Transabdominal reduction done at the time of the primary repair (Moschovitz repair)

UTERINE PROLAPSE (Descensus, Procidentia)
Ø Protrusion of the cervix and uterus into the barrel of the vagina but often associated with cystocoele, rectocoele and
enterocoele.
Ø Due to injuries of endopelvic fascia, uterosacrals and cardinals, levator ani leading to pelvic floor relaxation
Ø Due to increased pressured or tension on pelvic musculature such as chronic constipation, tumors, BA/COPD, multiparity, old
age, sacral nerve disorder (DM Neuropathy, S1 – S4 injuries)
Ø CLASSIFICATION:
ST
1 Prolapse into the upper barrel of the vagina
ND
2 Prolapse through vaginal barrel up to introitus
RD
3 Cervix & uterus prolapses out through introitus and vagina is exteriorized
Predisposed to dryness & thickening of vaginal epithelium & stasis ulcers
TH
4 Providential: entire uterus as well as anterior & posterior vaginal wall extend
outside the introitus at all times
o Heaviness, fullness, falling out
o “Tumor” bulging out of introitus
o Similar symptoms to cystocoele and rectocoele
o Inflammation and ulcers, pain and bleeding, infection of prolapsed uterus
Ø MANAGEMENT:
o Non-operative: Mild: not treated unless there are symptoms
§ Pessary
§ Estrogen Creams
§ Kegel’s
o Operative: more severe degrees
§ Vaginal hysterectomy with vaginal vault suspension and A&P colporrhaphy
§ Ulcers & infections are treated first & allowed to heal prior to surgery
o If with adhesions and previous surgery:
§ May need abdominal hysterectomy with AP repair or minilap assisted vaginal hysterectomy
§ Manchester (Donald or Fothergill)
• Cervical hypertrophy
§ Colpoclesis (Le Fort or Goodall-Power)
• Older non sexually active women


UROGYNECOLOGY: INCONTINENCE
INNERVATION OF BLADDER & URETHRA
CONTINENCE MICTURITION
BLADDER Sympathetic (NE) Parasympathetic (Ach)
Relaxation à prevents micturition Contraction à Micturition
SPHINCTER Sympathetic (NE) Parasympathetic (Ach)
Contraction à prevents micturition Relaxation à Micturition

RISK FACTORS:
1. Immobility 5. High impact activities 9. Cognitive status 13. Obesity
2. Medication use 6. Pelvic muscle weakness 10. History of fecal impaction 14. Stroke
3. Smoking 7. Pregnancy 11. History of low fluid intake 15. Hypoestrogen state
4. Delirium 8. Childhood nocturnal enuresis 12. DM 16. Race

DIAGNOSTIC PROCEDURES:
1. Urinalysis & Culture: for chronic infections
2. Test for residual urine: catheterization within 10-15 minutes of voiding; residual urine should be <50cc
3. Office cystometrics: sterile saline given through a urinary catheter; measures volume that causes urge to void (NV: 150 –
200mL) and functional capacity (NV 400-500mL) while maintaining continence
4. Stress (Bonney) Test: instill 250cc sterile saline & ask patient to cough
a. Urine spurts out immediately: stress incontinence
b. Urine spurts out after delay: detrusor instability
5. Urethroscopy: visualization of urethra
6. Cystoscopy & Cystometry: best used for diagnosis of detrusor hyperactivity

TYPES OF INCONTINENCE
1. STRESS INCONTINENCE
• Occurs when increased intraabdominal pressure is not transmitted equally to the bladder and the functional urethra
(coughing, sneezing, laughing, lifting)
• Urine loss due to sphincter incompetence without demonstrable contraction of bladder detrusor muscles
o
• Loss of PUV (posterior urethrovesical) angle (Normal: <120 ); Able to stop stream when voiding; Disappears during
the night
2. DETRUSOR DYSSYNERGIA/IRRITABILITY/INSTABILITY
• Involuntary contraction of the bladder during distention with urine or other fluid
• Chronic; urgency-frequency problem, painless urine loss, inability to stop stream and nocturia
• URGE INCONTINENCE: involuntary loss of urine associated with a sudden and strong urge to void
• DETRUSSOR HYPERREFLEXIA: (+) neurologic disorder (stroke, PD)
• DIAGNOSIS: Electronic Urehtrocystometry
• TREATMENT: Bladder retraining, anticholinergic / β-adrenergic agonists (Propantheline, Oxybuntin, Imipramine,
Ephedrine)
3. TRUE INCONTINENCE
• Loss of urine without abnormal bladder function due to fistulas or other damage to the urinary tract
4. OVERFLOW INCONTINENCE
• Old term used to describe chronic retention of urine;
• It occurs when a bladder is overdistented because of its inability to empty
• Caused by a neurologic disorder that interferes with normal bladder reflexes or by partial obstruction of the urethra
à inability to empty à overdistended bladder à overflow
• CLINICAL MANIFESTATIONS:
o Typically, the patient complains of voiding small amounts and still having the feeling that there is urine in the
bladder
o Bladder is non-painful and may be palpable after the patient has voided
o Retention of urine volume is >300mL
o Patient frequently loses small amounts of urine without any control
o COMMONLY SEEN IN PATIENTS WITH:
§ Multiple sclerosis; Trauma
§ Diabetic Neuropathy; Tumors of CNS


GENITAL TRACT INFECTIONS
INFECTIONS OF THE VULVA

ACUTE BACTERIAL CYSTITIS
• Highest incidence in women during their early 20’s
• Reproductive age women are prone to ascending infections
o Shortness of the female urethra
o Distal 1/3 of the urethra is often colonized by bacteria from the vulvar vestibule
• Independent Risk Factors:
o Sexual intercourse
o Use of vaginal diaphragm or spermicide in a premenopausal woman
o Previous UTI
o Recent exposure to antibiotics
• Symptoms:
o Dysuria
o Urgency
o Frequent voiding
• Signs: Suprapubic Tenderness
• Ascending infection from the introitus and distal urethra – most common cause
• Recommended 3-day regimen for Acute Uncomplicated Cystitis
DRUG DOSAGE
Trimethoprim/Sulfamethoxazole 160/180mg q12h
Trimethroprim 100mg q12h
Quinolones
• Ciprofloxacin 250mg q12h
• Enoxacin 400mg q12h
• Lomefloxacin 400mg q12h
• Norfloxacin 400mg q12h
• Ofloxacin 200mg q12h

• Strategies for Recurrent Cystitis in Women


INFECTIONS OF BARTHOLIN’S GLAND
• Caused by an obstruction of the duct at 5 & 7 o’clock position secondary to non-specific inflammation or trauma
• Following obstruction, there is a continued secretion of glandular fluid resulting in cystic dilation
• Develops rapidly over 2- 4 days

SIGNS & SYMPTOMS / CHARACTERISTICS OF A BARTHOLIN’S DUCT CYST
• Asymptomatic
• Cysts may vary from 1 – 8 cm in diameter
• Usually unilateral, tense & non-painful
• Unilocular but occasionally may be multilocular

DIFFERENTIAL DIAGNOSES
• Mesonephric cysts of vagina – more anterior & cephalad in the vagina
• Epithelial inclusion cysts – more superficial
• Rarely: lipoma, fibroma, hernia, vulvar varicosity hydrocele

SIGNS SYMPTOMS
Acute vulvar pain & tenderness (due to rapid enlargement, Erythema; acute tenderness; edema; cellulitis of the
hemorrhage or secondary infection); Dyspareunia; Pain during surrounding subcutaneous tissue
walking

TREATMENT OF BARTHOLIN’S GLAND INFECTION / ENLARGEMENT:
• Asymptomatic cysts in women <40 y/o – no treatment
• Acute adenitis without abscess formation – broad spectrum antibiotic and frequent hot-sitz bath
• Symptomatic Cyst or Abscess – development of a fistulous tract from the dilated duct to the vestibule by “Marsupialization”
(recurrence rate 5-10%)
• Simple Incision & Drainage – (+) tendency to recur
• Insertion of Word Catheter (a short catheter with an inflatable Foley Balloon) through a stab incision in the abscess
• Antibiotic therapy if with associated cellulitis surrounding the abscess
• Biopsy in women >40 y/o to exclude Adenocarcinoma of the Bartholin’s Gland
• Excision – for persistent deep infection or multiple recurrences of abscess; for women >40 y/o; should be performed when
the infection is quiescent

PEDICULOSIS PUBIS SCABIES
• Infestation by the crab louse or pubic louse Phthirus pubis • Itch mite Sarcoptes scabiei
• Hairy areas of the vulva • Widespread over the body without a predilection for hairy
• Travels slowly areas
• Predominant Clinical Symptom of Infestation: constant • Travels rapidly over the skin (2.5cm in 1 minute)
itching in the pubic area secondary to allergic sensitization • Burrows – pathognomonic sign of scabies infection
• Transmitted by direct sexual contact; non-sexual • May present as papules, vesicles or burrows
transmission also documented • May involve the hands, wrists, breasts, vulva, & buttocks
• Most contagious of all STD’s (>90% of sexual partners • Transmitted by close contact
infected after single exposure) • Predominant Clinical Symptom: severe but intermittent
itching; pruritus is more intense at night
DIAGNOSIS DIAGNOSIS
• (+) eggs & adult lice, and “pepper grain” feces adjacent to • (+) burrows: twisted line on the skin surface, with a small
the hair shaft vesicle at one end
• Definitive: microscopic slide by scratching the skin papule • laboratory Work-up: microscopy using scratch technique;
with a needle and placing the crust under a drop of mineral mites lack lateral claw legs but have 2 triangular hairy buds
oil
TREATMENT: Should kill both the adult parasite & eggs TREATMENT: Should kill both the adult parasite & eggs
• Permethrin 1% cream rinse (Nix crème) applied to • Permethrin cream 5% applied to all areas of the body
affected areas & washed off after 10mins from the neck down and washed off after 8-14 hrs.
• Lindane 1% shampoo (Kwell) applied for 4mins then • Ivermectin 02mg/kg orally, repeated in 2 weeks if
washed off necessary


• Pyrethrins with pipronyl butoxide applied & wash off • Lindane 1% 1 oz of lotion or 30g of cream applied thinly
after 10mins to all areas of the body from the neck & thoroughly
• Reevaluate after 1 week washed after 8hrs
• Reevaluate after 1 week
PREVENTION OF REINFECTION:
• Treatment should be prescribed for sexual contacts within the previous 6 weeks and other close household contacts
• Clothing & bleeding should be decontaminated

Etiologic Agent PHTHIRUS PUBIS SARCOPTES SCABIEI
Site of Infection Hairy body parts Non-hairy areas
Movement Slow Rapid
Lesions “Pepper Grain” feces, tiny rough spots Papules, vesicles, burrows
S/Sx Constant Itching Intermittent itching, more intense at night

MOLLUSCUM CONTAGIOSUM: POX VIRUS
• Chronic localized infection
• Spread by skin to skin contact, autoinoculation or by formites
• Widespread infection is most closely related to underlying cellular immunodeficiency (HIV infection, chemotherapy or
corticosteroid administration)
• Characteristic Appearance of Lesion: flesh-colored small nodules or domed papules usually 1-5mm in diameter with
umbilicated center
• Most common complication is superinfection
• DIAGNOSIS:
o Clinical: appearance of lesion
o Microscopy of the white waxy material from inside the nodule: intracytoplasmic molluscum bodies with Wright or
Giemsa Stain
• TREATMENT:
o Self-limiting infection
o Individual papules: injection of local anesthetic followed by evacuation of caseous material or excision of nodule
with a sharp dermal curette. Base of the papule is chemically treated with ferric subsulfate (Monset solution) or 85%
TCA
o Alternative method is Canthardin – a blistering solution

CODYLOMA ACCUMINATA (Venereal Warts): Human Papilloma Virus (HPV)
• Genital, venereal, or anogenital warts
• Most common viral sexually transmitted disease of the vulva, vagina, rectum & cervix
• 30% of infected women – clinically recognizable microscopic lesion
• 70% - unrecognized subclinical infection
• Sexual transmission; autoinoculation, vertical transmission
• Conditions that predispose women to HPV infection: Immunosuppression, DM, Pregnancy, Local Trauma
• S/SX:
o Asymptomatic
o Pain, itching, tendency to bleed when friable, (+) odor when secondarily infected
• MANAGEMENT:
o Depends on the location, size, and extent of the condyloma and whether the woman is pregnant
o Treatment: Chemical, cautery, laser, immunologic therapy, surgery


Treatment of Warts: Patient – Administered
Podofilox 0.5% Solution or Gel (Condylox) Imiquimod 5% Cream (Aldera)
DOSE BID x 3 days, 4 days off up to 4 cycles Daily & qhs, 3x/week up to 16 weeks, wash 6 – 10 mins after
MOA Antimitotic Immune enhancer
SIDE EFFECTS Mild to moderate pain, local irritation Mild to moderate local inflammation
PREGANCY NO NO

Treatment of Warts: Provider – Administered
Cytotherapy Podophyllin Resin Trichloroacetic Acid (TCA)
DOSE Weekly after 1-2wks (no cryoprobe in vagina) Weekly Weekly, “frosting”
MOA Thermal-induced cytolysis Antimitotic Chemical coagulation of CHONs
SIDE EFFECTS Pain, necrosis + blistering Local irritation Pain, adjacent damage (use soap, soda)
PREGANCY OK NO OK

Genital HPV Types
HPV TYPE MORPHOLOGY POTENTIAL FOR CANCER
6, 11 Genital Warts, LSIL, RRP Low (negligible)
40, 42, 53, 57, 66, 84 LSIL Low (negligible)
16, 18, 31, 33, 35, 39 LSIL
45, 51, 52, 56, 58, 59 HSIL High
68, 73, 82 Cancer
61, 62, 67, 69, 70 ? Uncertain

GENITAL ULCERS
SYPHILLIS HERPES CHANCROID LGV DONOVANOSIS
Incubation Period 2-4 wks (1-12 wks) 2-7days 1-14days 3days-6weeks 1-4wks (up to
6mos)
Primary Lesion Papule Vesicle Papule or pustule Papule, pustule or Papule
vesicle
# of Lesions Usually 1 Multiple, may Usually multiple, Usually 1 Variable
coalesce may coalesce
Diameter (mm) 5-15 1-2 2-20 2-10 Variable
Edges Sharply Erythematous Undermined, Elevated, round or Elevated, irregular
demarcated; ragged, irregular oval irregular
elevated, round or
oval
Depth Superficial or deep Superficial Excavated Superficial or deep Elevated
Base Smooth, Serous, Purulent Variable Red & rough
nonpurulent erythematous (beefy)
Induration Firm None Soft Occasionally firm Firm
Pain Unusual Common Usually very tender Variable Uncommon
Lymphadenopathy Firm, nontender, Firm, tender, often Tender, may Tender, may Pseudodenopathy
bilateral bilateral suppurate, usually suppurate,
unilateral loculated, usually
unilateral


PELVIC INFLAMMATORY DISEASE
• >99% of cases result from ascending infection from the bacterial flora of the vagina and cervix.
• Infection occurs along the mucosal surface à bacterial colonization & infection of the endometrium & fallopian tubes à may
extend to the surface of the ovaries & nearby peritoneum (rarely into the adjacent soft tissues, such as the broad ligament &
pelvic blood vessels.
• TWO CLASSIC SEXUALLY TRANSMITTED ORGANISM: N. gonorrheae & C. trachomatis are involved.
o Coexist in the same individual 25-50% of the time
o Endogenous aerobic & anaerobic bacteria also seen
• MAY INCLUDE INFECTION OF ANY OR ALL OF THE FF:
o Endometrium: endometritis
o Oviducts: salpingitis
o Ovaries: oophoritis
o Uterine wall: myometritis
o Uterine serosa & broad ligament: parametritis
o Pelvic peritoneum
• RISK FACTORS:
o Teenagers
o Multiple sexual partners
o Without contraception
• DIAGNOSIS:
o MINIMUM CRITERIA FOR EMPIRIC TREATMENT:
§ Lower abdominal tenderness
§ Adnexal tenderness
§ Cervical motion tenderness
o ROUTINE CRITERIA:
o
§ Oral temp >38 C
§ Abnormal cervical mucopurulent discharge or cervical friability
§ Abundant WBC on saline microscopy of vaginal fluid
§ Elevated ESR; Elevated CRP
§ Lab documentation of cervical infection of N. gonorrheae & C. trachomatis
o DEFINITIVE CRITERIA:
§ Histopathologic evidence of endometritis on endometrial biopsy
§ Transvaginal sonography or MRI techniques showing thickened fluid-filled tubes with or without free pelvic or
tuboovarian complex
§ Laparoscopic abnormalities consistent with PID
§ Although initial treatment can be made before bacteriologic diagnosis of N. gonorrheae & C. trachomatis
infection, such diagnosis emphasizes the need to treat sexual partners
o MANAGEMENT:
§ Outpatient Regimen:
• Ceftriaxone 250mg IM single dose PLUS Doxycycline 100mg BID for 14 days WITH or WITHOUT
Metronidazole 500mg BID for 14 days
• Cefoxitin 2g IM + Probenecid 1g PO single dose PLUS Doxycycline 100mg BID for 14 days WITH or
WITHOUT Metronidazole 500mg BID for 14 days
§ Inpatient Regimen:
• Cefotetan 2g IV every 12 hours PLUS Doxycycline 100mg PO or IV every 12 hours
• Cefoxitin 2g IV every 6 hours PLUS Doxycycline 100mg PO or IV every 12 hours
• Clindamycin 900mg IV every 8 hours PLUS Gentamicin loading dose IV or IM (2mg/kg of body weight)
followed by a maintenance dose (1.5mg/kd) every 8 hours. Single daily dosing may be substituted
• REASSESS:
o After 3 days of treatment:
§ Improving: continue regimen
§ Not improving: consider…
• Wrong diagnosis
• Resistant organism (e.g. enterococcus)
• Mixed abscess, or rupture
• Septic thrombophlebitis


• With 24 hours of Therapeutic Response
o Shift to Oral Doxycycline 100mg BID x 14 days
o Alternative: Clindamycin 450mg QID x 14 days
§ ALTERNATIVE REGIMENT:
• Ampicillin – Sulbactam 3g IV every 6 hours PLUS Doxycycline 100mg PO or IV every 12 hours
• Azithromycin 500mg IV x 1-2 doses followed by 250mg PO for 5-6 days as monotherapy PLUS
Metronidazole 500mg q8 for 12 days
§ ADMIT IF:
• Surgical emergency cannot be ruled out
• Tubo-ovarian abscess
• Pregnancy
• Severe illness, N&V, High Fever
• Unable to follow outpatient regimen
• No response to oral therapy

CERVICITIS
• Endocervicitis: N. gonorrheae & C. trachomatis
• Ectocervicitis: viral (HSV); T. vaginalis
• Mucopurulent Cervicitis

CRITERIA:
1. Gross visualization of yellow mucopurulent material on a white cotton swab
2. Presence of ≥10 PMN leukocytes per microscopic field (magnification x 1000) on Gram-stained smears obtained from the
endocervix

ALTERNATIVE CLINICAL CRITERIA:
1. Erythema and edema in an area of cervical ectopy or associated with bleeding secondary to endocervical ulceration
2. Friability when the endocervical smear is obtained
3. Increased vaginal discharge & intermenstrual vaginal bleeding

SIGNS & SYMPTOMS:
1. Hypertrophic & edematous cervix
2. Vaginal Discharge
3. Deep Dyspareunia
4. Post-coital bleeding

DIAGNOSTIC TOOLS:
1. NAAT (Nucleic Acid Amplification Test) – most sensitive & specific
2. Cultures – less sensitive

GONORRHEA CHLAMYDIA TRACHOMATIS
• Recommended Regimen: • Recommended Regimen:
• Cefixime 500mg single dose PO or • Azithromycin 1g SD or
• Ceftriaxone 125mg IM or • Doxycyline 100mg BID x 7 days
• Ciprofloxacin 500mg SD PO or • Alternative Regimen:
• Ofloxacin 400mg SD PO or • Erythromycin base 500mg QID for 7 days
• Levofloxacin 250mg SD PO • Erythromycin ethylsuccinate 800mg QID for 7 days
• PLUS Chlamydial therapy if infection not ruled out • Ofloxacin 300mg twice daily for 7 days
• Alternative Regimen: • Levofloxacin 500mg for 7 days
• Spectinomycin 2g IM SD or
• Ceftizoxime 500mg IM; Cefoxitin 2g IM, administered
with Probenecid 1g PO; or Cefotaxime 500mg IM or
• Other quinolones such as Gatifloxacin 400mg SD,
Lomefloxacin 400mg SD, Norfloxacin 800mg
• PLUS Chlamydial therapy if infection not ruled out


VAGINITIS
• Normal vaginal discharge: white, floccular, odorless with pH 3.8 – 4.2

TYPICAL FEATURES OF VAGINITIS
CANDIDIASIS/ TRICHOMONIASIS BACTERIAL GARDNERELLA
MONILLASIS VAGINOSIS VAGINALLIS
Signs & Symptoms Increased discharge, Increased discharge Increased discharge Minimal pruritus or
Pruritus, Dysuria, Increased odor (white, thin) vulvar involvement
Burning, Redness Pruritus, Dyuria Increased odor
Excoriation
Examination Findings Thick, curdy discharge, Yellow, frothy discharge Thin, whitish gray Homogenous, gray,
vaginal erythema Strawberry cervix homogenous discharge, rotten fish smell after
Foul smelling sometimes frothy adding 10% KOH (Whiff
test)
pH <4.5 >4.5 >4.5 >4.5
Diagnosis / Wet Mount KOH Smear: yeast cells Wet smear: Clue cells (>20%) shift in Wet smear: Clue cells
& pseudohyphae Motile trichomonads flora >20%
Increased white cells Amine odor after
Hyphae or Spores adding KOH to wet
mount
Comment Can be mixed infection More symptoms at high Greatly decreased
with bacterial vaginosis, vaginal pH lactobacilli (Increased
T. vaginalis, or both, discharge)
and have higher pH Greatly Increased cocci,
bacilli small curved cells
(Increased ordor)
Treatment Miconazole 100mg Vag Metronidazole Metronidazole 500mg Metronidazole
OD x 7 days Tinidazole BID x 7 days Clindamycin
Nystatin 100,000U Vag Metronidazole gel
OD x 14 days 0.75%, 5g intravaginally
OD x 5 days
Clindamycin cream %5,
5g intravaginally qhs x 7
days


BENIGN GYNECOLOGICAL LESIONS
BENIGN VULVAR LESIONS

URETHRAL CARUNCLE BARTHOLIN’S DUCT CYST FIBROMA
Most common large cyst of vulva Most common benign solid tumor of vulva
• Small, fleshy outgrowth • Bartholin’s Glands: rounded, pea- Commonly found in the labia majora
• Distal edge of the urethra sized glands deep in the fine
• Most frequently in perineum
postmenopausal women • At entrance of vagina at 5 & 7 o’clock
• ↓Estrogen à ↓Collagen à • BG duct is 2 cm long, open in a groove
drier, easier to irritate & break between hymen & labia minora in
epithelium posterior lateral wall of vagina
o o
2 to Chronic Irritation or Infection • C/B obstruction of duct 2 to From subcutaneous nodules or deeper CT
• Irritation – usually sexual nonspecific inflammation or trauma
activity • Sexual activity
• If infected, usually associated
with STI
• Classified according to histo • Normally gland not palpable • Slow growing but may attain gigantic
appearance: • If infected, palpable and very painful proportion (involves a muscle: potential
• Papillomatous for size)
• Granulomatous • Low-grade potential for becoming
• Angiomatous malignant
Majority are asymptomatic • Mostly are asymptomatic – unless
they feel mass
Diagnosis by BIOPSY
Initial Therapy: • No tx in women <40 unless infected Tx is operative removal / excision
• Oral or topical estrogen or symptomatic
• Avoidance of irritation • Tx of Choice: “Marsupialization”
• In women >40, marsupialization &
biopsy: to exclude adenocarcinoma
of Bartholin’s gland

CYSTS HEMANGIOMA
• Most common: sebaceous & epidermal inclusion cyst • Malformation of BVs in childhood
• Others: Bartholin’s cyst, apocrine cyst, Skene’s gland cyst • Types:
• Cause: occlusion of ducts/hair follicle 1. Cavernous / Strawberry
• Tx: I&D, excision of EIC 2. Cherry / Senile
3. Angiokeratoma
4. Pyogenic Granuloma

VULVAR PAIN SYNDROMS:
• Vulvodynia: vulvar pain – common
o Accompanied by intolerance to pressure – neurogenic in origin
o Raw, burning: only on stimulus
• Vulvar Pain Syndrome TRIAD
o Severe pain to touch, localized to vaginal vestibule & dyspareunia
o Pain & tenderness localized only to vestibule
o Mild to moderate erythema
• Further subdivided into:
o Vestibulodynia: younger women, most commonly Caucasian
o Dysthenic vulvodynia – peri & post menopausal who have rarely had previous pain
o Allodynia – hyperesthesia, pain related to nonpainful stimuli
• TREATMENT:
o TCAs for social aspect
o 5% Lidocaine Ointment
o Surgucal removal (vestibulectomy) in refractory cases


DERMATOLOGIC CASES OF THE VULVA
PRURITUS CONTACT DERMATITIS PSORIASIS SEBORRHEIC DERMATITIS
• Single most common • Frequent vulvar skin • Common generalized skin • Common chronic skin
gynecological problem (intertriginous areas) disease of unknown origin diseases of unknown
• Can be due to urine/feces • 20% with vulva affected origin
• Rare in mons or vulva
o
• May lead to 2 vulvar pain • Irritation – stinging, • Teenagers – 3% adult • Pale to yellow-red
• Unrelenting with 2 “itch- burning, gone 12h women erythematous, and
scratch” cycles – itching • Allergic – 36-48h to days • Chronic & relapsing edematous covered by
à scratching à after removal; latex, • Usually intertriginous fine, non-adherent scale,
excoriation à healing à semen, therapeutic areas with red to red- usually oily
itching, etc. agents yellow papules à • Mild to severe pruritus
• Common Sx – superficial enlarge, well
vulvar tenderness, circumscribed
burning, pruritus
• Nonspecific diagnosis • Look for delineation for a • Classic silver scales &
with wide range of ddx clue bleeding on gentle
scraping
• Does NOT involve vagina
(like candida) & more well
defined
• Treat primary cause • Withdraw offending • 1% hydrocortisone cream • Hydrocortisone
• Interrupt before substance • fluorinated corticosteroid • Topical ketoconazole
lichenification (white, • Burrow’s solution if chronic fissures
thickened and leathery) • Dry à lubricate, damp à
cornstarch or baby
powder
• Hydrocortisone,
fluorinated
corticosteroids

LICHEN PANUS BEHCET SYNDROME HIDRADENITIS SUPPURATIVA
• Uncommon vulvovaginal dermatosis • AID – Mediterranean & Middle • Rare before puberty, most after
in women >30y/o Eastern menopause
• Uniqe, chronic eruption of shiny, • Recurrent, painful ulcers & papules • Chronic, unrelenting refractory
violaceous papules à hyperrophic • Vulva & oral mucosa infection of skin and subcutaneous
plaque with apocrine glands
• Axilla & anogenital
• Deep scars & pits
• Painful, foul smelling
• Hx of intense emotional stress • Exclusion of ulcerative diseases • Biopsy
• Punch biopsy (herpetic lesions)
• Topical steroid (e.g. clobetasol) • Topical anesthetics • Topical & oral clindamycin
• Oral steroids if severe • Antineoplastic treatment if severe • Antibiotics
(methotrexate, steroids) • Others: antiandrogens, isotretinoin,
cyclosporine, wide excision


BENIGN VAGINAL LESIONS

URETHRAL DIVERTICULUM EPIDERMAL INCLUSION CYST
• A permanent, epithelialized, sac-like projection arising from • Most common vaginal cysts
the posterior urethra • Usually found posterior & lateral walls of lower third of
• SX: vagina (all embryologic urogenital sinus origin) –
• Urinary urgency remember, anterior third come from Mullerian ducts
• Urinary frequency • Cause: birth trauma or gynecologic surgery
• Dysuria • Usually asymptomatic
• DX: • Usually found on pap smear
• Cystourethrogaphy – inject dye, better of the two to • Treatment:
demo the outpouching • Excision: only if they cause dyspareunia or pain
• Cystourethroscopy – insert a small scope in urethra
• DDX:
• UTI
• Gartner’s duct cyst
• Ectopic ureter that empties into urethra
• Skene’s glands cysts
• TX:
• Excision
• Marsupialization

BENIGN LESIONS OF THE CERVIX

POLYP (Endocervical & Cervical) STENOSIS NABOTHIAN CYST
• Most common benign neoplastic • Often occurs in the internal os • Most common cervical cyst
growth • Maybe congenital or acquired • Cause:
Origin: (infection, atrophy, surgery, RT, • Retention mucus cysts of
o
• 2 to inflammation (usually STI) or obstruction) endocervical columnar
• abnormal focal responsiveness to • Sx differ depending on menopausal cells mostly found at the
hormonal stimulation status: transformation zone
Classic Symptoms: • Premenopausal: dysmenorrhea, (where CIN usually starts)
• Intermenstrual bleeding oligomenorrhea, amenorrhea, AUB, • MC in menstruating
• Following contact (insertion, coitus) infertility women
Histologic Subtypes: • Postmenopausal: asymptomatic to
• Adenomatous (80%) – cystic hematoretra, hydrometra, • Gross Appearance: translucent
• Fibrous – vascular pyometra or opaque whitish or yellow
• Inflammatory – fibromyomatous • Diagnosis established by inability to • Vary from micro to
PE: introduce a cervical dilator into the macroscopic size
• Ectocervix: pedunculated, smooth, uterine cavity
reddish-purple to cherry red, fragile • Symptoms:
• Endocerxiv: grayish white with short, Management: • Asymptomatic
broad base • Cervical dilation under Ultrasound
DDX: All fleshy outgrowths of the cervix Guidance • Diagnosis
• Endometrial polyps • If you do D&C must careful to not • Colposcopy with
• Prolapsed myoma cause further scarring & also avoid microscope
• Squamous papilloma injury to the bladder and rectum • No treatment is necessary
• Sarcoma since a cervix under these
• Cervical carcinoma conditions will not be as responsive
• Microglandular hyperplasia to dilations & is scarred
• Retained product of conception • Even more so if there is an
Management: anatomical abnormality such as
• Polypectomy/excision (pedunculated) anteverted or retroverted uterus
• Electrocautery (sessile) • Laminaria tent or T-tube as stent for a
few days


BENIGN LESIONS OF THE UTERUS

ENDOMETRIAL POLYP HEMATOMETRA
o
• Localized overgrowths of endometrial glands and stroma • Uterus is distended with blood 2 to gynatresia (failure of
projecting beyond endometrial surface part of vaginal canal to develop)
• Cause: unknown Common Congenital Causes: Common Acquired Causes:
• Peak age: 40-49 years old • Imperforate hymen • Senile atrophy of
• Mostly: asymptomatic, detected by UTZ • Transverse vaginal endocervical canal &
• Common manifestation: is abnormal uterine bleeding / septum endometrium
intermenstrual bleeding • Congenital absence of • Scarring of the isthmus
• 3 Histological Components: the cervix, vagina, etc. by synechiae
• Endometrial Glands • Cervical stenosis
• Endometrial Stroma • Malignant disease of
• Central Vascular Channels endocervical gland
• Diagnosis: • Usually suspected by hx of amenorrhea & cyclic abdominal
• UTZ, sonohysterogram, biopsy >35y/o pain
• DDX: • Pelvic Exam: mildly tender, globular uterus
• Submucous leiomyoma
• Adenomyoma • Diagnosis – confirmed by:
• Retained products of conception • Ultrasonography – probe the cervix with dilator & with
• Endometrial hyperplasia release of dark brownish black blood
• Endometrial carcinoma • Management:
• Uterine sarcoma • Depends on the operative relief of lower genital
• Management obstruction
• Optimal management is removal by Hysteroscopy with
D & C

LEIOMYOMA / FIBROIDS ADENOMYOSIS
• Benign tumors of muscle origin • “Endometriosis interna”
• The most frequent pelvic tumor & the most common • Histologically: presence of endometrial glands & stroma
tumor in women within the myometrium more than one low power field
th
• Highest prevalence – 5 decade (2.5mm) from the basalis layer endometrium
• Malignant transformation is to 0.3% to 0.7% (into sarcoma) • Pathogenesis: unknown

3 MOST COMMON TYPES: THEORIES
• Intramural: most common • Disruption of the barrier between the endometrium &
• Subserous: if located near BV – hard to remove (bleeding) myometrium
knobby or pedunculated • Trauma to the endometrial-myometrial interface
• Submucous – most likely to cause bleeding, distortiob of
uterine cavity (infertility, abortion) PATHOLOGIC PRESENTATION
• Other types: Intraligamentary & Parasitic Myomas – both • Diffuse involvement of both anterior & posterior
extremely problematic myometrium
• Focal area of involvement or adenomyoma
CURRENT THEORY • Might have a pseudocapsule
• Neoplastic transformation from normal myometrium to
leiomyomata d/t a somatic mutation in the single CLINICAL PRESENTATION
progenitor cell affecting cytokines that affect cell growth • Over 50% are asymptomatic
• Growth may be influenced by estrogen & progesterone • Symptomatic cases – between ages of 35 – 50%
levels
CLASSIC SYMPTOMS
CLINICAL CHARACTERISTICS • Secondary dysmenorrhea
• Rare before menarche, diminish in size after menopause • Menorrhagia
• Enlarges during pregnancy and during OCP use


GROSS APPEARANCE DIAGNOSIS
• Lighter in color than the normal myometrium • Pelvic Examination Findings
• Cut surface: glistening, pearl-white with smooth muscle • Uterus is diffusely enlarged, globular, usually 2-3x
arranged in trabeculated or whorl configuration normal size
• Diagnosis confirmed following histologic examination of
HISTOLOGIC APPEARANCE hysterectomy specimen
• Proliferation of mature smooth muscle cells
• Nonstriated muscle fibers are arranged in interlacing DIAGNOSTIC TOOLS
bundles with variable amount of fibrous connective tissue • Ultrasonography – sensitivity: 53-89%; specificity: 50-89%
in-between • MRI – sensitivity: 88-93%; specificity: 66-91%
• Spin Snout – sensitivity: ruling out; specificity: ruling in
TYPES OF DEGENERATION
Degeneration – when the tumor outgrows its blood supply MANAGEMENT
• Hyaline – mildest; homogenous whorled pattern • No symptoms = no management
• Myxomatous • Goal = stop abnormal bleeding = either a pseudo-pregnant
• Calcific or pseudo-menopausal state
• Cystic
• Fatty NO satisfactory medical management
• Necrosis • GnRH agonist
• Red or Carneous – most acute form, severe pain, localized • Progesterones
peritoneal irritation, tx with NSAIDs 3d (<32 wks AOG); • Progesterone – containing IUD
occurs in 5-10% of gravid women with myomas • Cyclic hormones
• Prostaglandin synthetase (inhibitor?)
CLINICAL MANIFESTATIONS • Relief only provided as long as you can take medicine
• Most common sx:
• Pressure from an enlarging mass HYSTERECTOMY is the definitive treatment
• Pain including dysmenorrhea • H/e, even this cannot completely prevent recurrence
• Abnormal uterine bleeding
• Rapid growth after menopause, consider leiomyosarcoma Factors to consider
• Age
DIAGNOSIS • Parity
• Physical Examination – Internal Examination • Reproductive plans
• Palpation of an enlarged, firm, irregular uterus • Uterine size
• Ultrasonography • Presence of associated pelvic pathology
• Hysteroscopy
• CT Scan or MRI

DIFFERENTIAL DIAGNOSIS
• Pregnancy
• Adenomyosis
• Ovarian neoplasm


MANAGEMENT OF LEIOMYOMA
Observation Small & Asymptomatic
Medical 3-6 months use of:
• GnRH agonists
• Danazol
• Medroxyprogesterone acetate
• RU 486
Operative:
• Myomectomy Classic indications of myomectomy:
• Persistent abnormal bleeding
• Pain or pressure
• Enlargement of an asymptomatic myoma to >8cm in a
woman who has not completed childbearing
Contraindications to myomectomy:
• Pregnancy
• Advanced adnexal disease
• Malignancy
• When enucleation of the myoma results in severe
reduction of endometrial surface that the uterus would
not be functional
• Hysterectomy: definitve treatment Indications for Hysterectomy:
• All indications for myomectomy plus:
• Asymptomatic myomas when the uterus that has
reached the size of 14-16 weeks gestation
• Rapid growth of myoma after menopause
Uterine Artery Embolization Invasive radiology causing ischemia & necrosis of myoma
Contraindication: planning to get pregnant


BENIGN LESIONS OF THE OVARY

Functional Cysts “Non-neoplastic cysts”: most common ovarian mass
TYPES:
1. Follicular Cysts: most common ovarian cyst
2. Corpus Luteum Cysts
3. Theca Lutein Cysts
FOLLICULAR CYSTS
- Most frequent cystic structures in normal ovaries of young menstruating women
- Minimum diameter to be considered a cyst = 2.5 – 3.0 cm
- Dependent on gonadotrophins for growth
- Sx varied and nonspecific to the ovary: most commonly pain
- Management options: observation –
o Majority disappear spontaneously in 4-8 weeks: Reabsorption of the cyst fluid or silent rupture
- Medical management: OCP – ↓FSH production since this is the source of stimulation of the follicles
- Surgery
o For persistent ovarian masses – Cystectomy is commonly done
o Best if by laparoscopy – will allow to possibly see the source or cause & can excise
CORPUS LUTEUM CYSTS
- Corpora lutea that is at least 3 cm in diameter: develop from graafian follicles
- Vary from asymptomatic masses to causing catastrophic & massive intraperitoneal bleeding

TRIAD
1. Delayed menses followed by spotting
2. Unilateral pelvic pain
3. Small tender adnexal mass

DDX
• Ectopic pregnancy – d/t s/sx of adnexal mass, AUB, and abdominal pain
• Adnexal torsion
• Ruptured endometrioma

Management
• Surgical exploration: cystectomy (lap)
• Just like follicular cysts – only if persistent
THECA LUTEIN CYSTS: almost always bilateral, moderate to massive enlargement of the ovaries

Etiology: (associated with molar pregnancies, hypothyroidism)
• Prolonged or excessive stimulation of ovaries by endo or exogenous gonadotrophins (IVF pts) or
• ↑Ovarian sensitivity to gonadotrophins

Complications:
• Torsion or pedicle or intraperitoneal bleeding

Treatment: Observation
• Most will regress gradually
• Cannot excise: heavily engorged with BVs à may cause hemorrhage

FOLLICULAR CORPUS LUTEUM THECA LUTEIN
Persistence of dominant follicle Failure of CL to regress From prolonged stim by hCG
Translucent, thin walled, filled with clear Smooth, red to brown gray-white if Hyperreactio luteinalis (multiple cysts),
water to straw-colored fluid chronic honeycomb appearance, straw-colored
fluid
UTZ: <8cm, simple & unilocular Larger, simple, unilateral & unilocular Multicystic, partially solid, bilateral;


BENIGN NEOPLASMS OF THE OVARY

EPITHELIAL
1. Serous Cystadenoma • Most common epithelial tumor
• Solid variant: adenofibroma, cystadenofibroma
• Closely related
o Both benign firm tumors
o Consist of fibrous & epithelial (*serous) components
o Preponderance of connective tissue (25% of mass)
• Cystadenofibroma – have areas with cysts
• Adenofibromas – usually small fibrous tumors on vary surface
o Bilateral – 20-25%
o Postmenopausal women
o 1-14 cm diameter
• Large tumors à pressure sx or rarely, adnexal torsion
• TX: TABHSO (since it occurs postmenop)
2. Mucinous Cystadenoma • Enormous
• Multilocular with mucoid substance
3. Brenner Tumor • Transitional cell tumor
• Solid mass of epithelial cells surrounding fibrous stroma
• Generally asymptomatic (incidental finding)
o Unilateral: 85-95%
• Origin: likely metaplasia from coelomic epithelium à uroeptihelium
• Gross: smooth, firm, gray-white, solid (resemble fibroma) & slow growing
• Yellow tinge on cut section
• Histology: coffee bean nucleus, pale epithelial cells similar to UB
• Management: simple excision (h/e, depends on age of patient)
GERM CELL
1. Benign Cystic Teratoma Most common slow growing ovarian tumor
Most common tumor in pre-pubertal females
All 3 germ layers (+) with nipple in the cyst: tubercle of Rokitansky
Most common complication torsion of the pedicle

Gross
• Surface: smooth, shiny, opaque white color
• Cut-section: thick sebaceous fluid, with tangled masses of hair & firm areas of cartilage
& teeth

Etiology
st
• Single germ cell after the 1 meiotic division, from totipotential stem cell
• Chromosomal make up: 46XX
• Associated with 3 medical condition:
o Thyrotoxicosis
o Autoimmune Hemolytic Anemia
o Carcinoid Syndrome

Diagnosis
• Palpation: Kustner’s Sign: dermoid floats upward in abdomen, elongating ovarian
pedicle causing them to lie anterior & superior to uterus
• Ultrasonography – 95% predictive value

Management
• Surgical: oophorocystectomy
o Laparotomy
o Laparoscopy


STROMAL
1. Fibroma • Most common benign, solid neoplasm of the ovary
• Arise from the undifferentiated fibrous stroma of the ovary
• Extremely slow growing
• Incidence of associated ascites is directly related to size of the tumor
• Average age of affected women: 48 years
• Symptoms:
o Pressure on adjacent structures
o Abdominal enlargement
• MEIG’S SYNDROME: ovarian fibroma, ascites & hydrothorax
• Grossly:
o Heavy, solid, well-encapsulated & grayish white
o Cut surface: homogenous white or yellowish white solid tissue with trabeculated or
whorled appearance
• Histologically: connective tissue, stromal cells, & varying amount of collagen, spindle-
shaped, mature fibroblast
• Management: surgery (TAH-BSO)
ENDOMETRIOSIS
- The presence & growth of the glands & stroma of the lining of the uterus in an aberrant or heterotopic location
- A benign but progressive disease

THEORIES ON ITS ETIOLOGY
1. Retrograde Menstruation
2. Metaplasia
- Endometriosis arises from metaplasia of the coelomic epithelium or proliferation of the embryonic rests
3. Lymphatic & Vascular Metastasis
- The endometrium is transplanted via lymphatic & vascular system
4. Immunologic Changes
- Altered function of immune-related cells, cell-mediated & humoral components
5. Genetic Predisposition
- Deletion of genes, specifically increased heterogenicity of chromosome 17 & aneuploidy
6. Hormonal Influences
- Exposure to dioxin & endocrine disruptors
7. Iatrogenic Dissemination
- Endometrial glands & stroma are implanted during surgical procedure

GROSS PATHOLOGIC CHANGES
• Visual manifestation is protean & have many appearances

ANATOMIC DISTRIBUTION

Common Sites Rare Sites
• Ovaries • Umbilicus
• Pelvic peritoneum • Episiotmy scar
• Uterine ligaments • Bladder
• Sigmoid colon • Kidney
• Pelvic LN • Lungs
• Cervix • Arms
• Vagina • Legs
• Fallopian tubes • Nasal mucosa
• Spinal colum


Terminologies used to describe Peritoneal Endometriosis: Cardinal Histologic Features
• Powder-burn, puckered black lesions • Ectopic Endometrial Glands
• Vascular glandular papules • Ectopic Endometrial Stroma
• Vesicular lesions • Hemorrhage into the Adjacent Tissue
o Serous, surrounded by marked vascularization
o Red hemorrhage Symptoms
• Red, flame-like hypervascularized area • One in 3 women are asymptomatic
• Petechial peritoneum • Classic Symptoms:
o
• Discolored area: yellow-brown, blue, white o Cyclic pelvic pain (2 dysmenorrhea)
• White scarring o Infertility
• Peritoneal defects
• Cribriform peritoneum Signs
• Subovarian adhesions • Classic pelvic finding: fixed retroverted uterus, with
scarring & tenderness posterior to the uterus
o Tenderness of the pelvic structures, nodularity of the
uteroscaral ligaments & cul-de –sac
st
o Time of maximum swelling & tenderness – 1 2 days of
menses
Gold Standard for Diagnosis: LAPAROSCOPY MANAGEMENT
• Staged according to the updated scoring system of the • Short-term Goals:
American Society of Reproductive Medicine o Relief of pain
o Promotion of fertility
Other diagnostic tools: • Long-term Goals:
• Ultrasound o Prevent progression or recurrence
• MRI
MEDICAL MANAGEMENT
Differential Diagnosis (all cause pain) • Aim: suppression of lesions & associated sx by induction of
• Chronic PID amenorrhea without inducing hypoestrogenism
• Ectopic Pregnancy Agents used Other hormonal agents
• Ovarian Malginancy Danazol Progestins
• Appendicits GnRH Agonists Dienogest
• Degeneration of Myoma OCPs PPAR-ligands
• Diverticulitis NSAIDs Gestrione
• Adenomyosis Aromatase inhibitors
• Primary dysmenorrhea
• Fuctional Bowel Disease Surgical Therapy
• Hemorrhage or Torsion of Ovarian Cyst • For moderate to severe endometriosis
• The only option for failed medical therapy
• Conservative Surgery: resection or destruction of
endometrial implants, lysis of adhesions and attempts to
restore normal anatomy
• Definitive Surgery: TAHBSO and all visible ectopic foci of
endometriosis (regardless, still a 3-10% recurrence rate)

Combination of medical & surgical therapy
• For advanced stages of endometriosis


GYNECOLOGIC MALIGNANCIES
BENIGN VS. MALIGNANT MASSES

CHARACTERISTIC BENIGN MALIGNANT
Mobility Mobile Fixed
Consistency Cystic Solid
Surface Smooth Irregular
Laterality Unilateral Bilateral
Age Group Reproductive age Pre-pubertal
Postmenopausal
OCP users
Weight Loss Absent Present
ULTRASOUND
Size <8cm >8cm
Consistency Cystic Solid or mixed
No solid components Multilocular
Calcifications Multicystic
Nodular, papillary
Irregular walls & septa
Associated Features Calcifications Ascites
Peritoneal mass
Lymphadenopathy
Color flow

CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN)
-Pre-malignant changes in cervical epithelium usually in the transformation zone that can progress to cervical CA

Risk Factors:
1. HPV 6. smoking tobacco by-products in cervical
2. High sexual activity / multiple sexual mucus weakens immune system & harder
partners to fight HPV infection
3. Intercourse at an early age 7. alcohol
4. Low Socioeconomic Status 8. OCPs >5 years
5. Genetic Predisposition 9. DES exposure

PAP-SMEAR:
- Screening starts at 21 years old or 3 years after onset of sexual activity not less than 21 years old
- Atypia: increased N:C ration, hyperchromasia, perinuclear halo, irregularity in nucleus, clumping of chromatin

RESULTS INTERVENTION
Normal limits Routine screening
Inflammation without atypia Treat inflammation
Inflammation with atypia Treat inflammation, repeat pap
Atypical squamous cells of uncertain significance (ASCUS) Colposcopy & biopsy or repeat pap smear after 3 mos; HPV
DNA Testing
Cannot exclude HSIL (ASC-H) Colposcopy
Low grade SIL – koilocytes & CIN 1
High grade SIL – CIN 2 & 3 Colposcopy ± biopsy & endocervical curettage
Squamous Cell CA

FINDINGS:
• KOILOCYTOSIS: perinuclear cavitation & nuclear atypicality
o An initial indicator
o Eosinophilic squamous cells with perinuclear empty cavity
o Cytoplasmic thickening
o Moderate nuclear enlargement


• CIN I: mild dysplasia, abnormal cells up to 1/3 of basal epithelium
o Usually these disappear SPONTANEOUSLY within weeks to months
o Treatment is no longer recommended at any age
ü Except when lesion persists for at least 1 year
ü Or if <21 persists for at least 1 year
ü Or if <21 persists >24 months
ü Follow up to ensure regression
• CIN II: moderate dysplasia, abnormal cells up to 2/3 of basal epithelium
o The process is still reversible at this stage with 40% disappearing spontaneously without treatment
o Women <21 are not treated
o >21 years old: followed and treated IF condition progresses to CIN III
• CIN III / CA-in-situ: severe dysplasia, abnormal cells involving full thickness
o Believed to be the PRECURSOR to Invasive CA
o TREATMENT IS RECOMMENDED – most cases will progress

COLPOSCOPY
Abnormal Findings:
LGSIL HGSIL
Punctuation/Red Stippling Mild Coarse
Acetowhite Epithelium (+) Dense
Leukoplakia (+)
Mosaicism Mild Coarse
Ulcerations (+)

MANAGEMENT:
CIN I Observation
Repeat colposcopy at 6 mos, 1 year
CIN II Ablative Therapy: cryotherapy, CO2 Laser Ablation, LEEP, cold-knife cone
Fertility Undesired Hysterectomy

SUMMARY: MANAGEMENT OF CIN:
PAP RESULT 21 – 24 years old >24 years old
LESSER ABNS Repeat cytology at 12mos Co-Testing at 12mos
ASCH Observation Follow-up Co-Testing at Follow-up
COLPO & Cyto Adequate Inadequate 12 & 24 months Adequate Inadequate
colposcopy colposcopy OR colposcopy colposcopy
Diagnostic
Every 6mos for 2 years CIN 2 CIN 3 Excisional Recurrent CIN 2,3
Procedure
(if colposcopy is OR Endocervical
adequate & Review of Sampling CIN 2,3
HSIL endocervical sampling Adequate TREATMENT cytological, TREATMENT Diagnostic
is (-). Otherwise, a colposcopy histological & Excisional
diagnostic excisional Excision or colposcopic Excision or Procedure
procedure is indicated) CIN 2 Ablasion of findings Ablasion of
Tzone Tzone


CERVICAL CANCER
rd
• 3 most common malignancy in the female reproductive tract
• TYPES:
1. SQUAMOUS CELL CARCINOMA
- Degree of differentiation (G1-G3) but there is NO consensus if grading in cervical cancer is a major prognostic factor
a) Large Cell (Keratinizing or Non-Keratinizing)
o Most are of large cell, non-keratinizing type
o But many are keratinized with squamous pearls seen on histo
b) Small Cell
o Rare
o Affected women are ~10 years younger than those with SCCA
o Cells are small & anaplastic with little cytoplasm
o Aggressive & spread to multiple sites such as bone, liver, skin, brain
c) Verrucous
o Rare & morphologically similar to that of the vulva
o These are warty masses, large & bulbous. They rarely mets but maybe admixed with the more virunlent typical
squamous cell CA which has more likely potential for mets

2. ADENOCARCINOMA
- ↑Risk – do not appear to have usual sexual factors associated with SCCA
- associated with HPV DNA, OCP use, lack of Cervical cytology screening
a) Typical (endocervical)
b) Endometrioid
c) Clear Cell
o Associated with DES exposure in utero but may also develop spontaneously
d) Adenoid Cystic (Basaloid Cylindroma)
o Rare & aggressive & resemble cylindromas of the salivary glands & basal cell CA of the skin
o They are more common in those >60 years old
e) Adenoma Malignum (minimal deviation adenocarcinoma)
o Rare but virulent type of AdenoCA
o Appear innocuous microscopically as they consist of well differentiated mucinous glands
o H/E, they have a tendency to be deeply invasive & to mets early
o Pts with Peutz-Jeghers syndrome have an increased risk for this tumor

3. MIXED CARCINOMA
a. Adenosquamous
o Consists of Squamous CA & AdenoCA elements
o They occur frequently in PREGNANT women
b. Glassy Cell
o Virulent variety & are made of large cells with cytoplasm like a ground glass appearance
o Mets early to the LN & Distant Sites & are FATAL

CLINICAL FINDINGS
Ø Most common: vaginal bleeding (post-coitus, IMB)
Ø Brownish, foul smelling vaginal discharge
Ø PE:
o Exophytic: cauliflower like
o Endophytic: barrel shaped; adenoCA
DIAGNOSIS: Biopsy
STAGING:
• Clinically: mainstay of treatment is NOT surgery
• Tools that can be used: all “-oscopy” except laparoscopy (surgical)
• Proctosigmoidoscopy & cystoscopy to r/o bladder/bowel invasion
• Cannout use MRI, CT Scan, UTZ as part of staging since not all institutions have them
• Mets work-up: RFTs, LFTs, KUB-IVP, barium enema, CXR, skeletal survey (not bone scan) à for management purposes only,
will not change staging)


TREATMENT:
• Early Stage:
o Surgery
§ Advantage
• Preserve Ovaries
• Explore intraoperatively
• Preserve sexual function
o Concurrent chemotherapy & radiotherapy (Chemoradiation) à cisplatin with pelvic EBRT + brachytherapy
• Late Stage: concurrent chemotherapy & radiotherapy (CRT)
• Unable to Receive Chemotherapy: may do RT alone
• Pregnant: delay tx then do CS at 34-36 weeks up to stage IIA2, otherwise do chemoradiation

2009 FIGO STAGING OF CERVICAL CANCER

Stage I The CA is strictly confined to the cervix (extension to the corpus would be disregarded)
IA Invasive CA which can be diagnosed only by miscroscopy, with deepest invasion ≤5mm & largest
extension ≤7mm
IA1 Measured stromal invasion of ≤3.0 mm in depth and extension of ≤7.0mm
IA2 Measured stromal invasion of >3.0 mm in depth and not >5.00mm with an extension of not> 7.0mm
IB Clinically visible lesions limited to the cervix uteri or pre-clinical cancers greater than Stage IA*
IB1 Clinically visible lesion ≤4.0 cm in greatest dimension
IB2 Clinically visible lesion >4.0 cm in greatest dimension
Stage II Cervical carcinoma invades beyond the uterus but NOT to the pelvic wall or to the lower third of the vagina
IIA Without parametrial invasions
IIA1 Clinically visible lesion ≤4.0 cm in greatest dimension
IIA2 Clinically visible lesion >4.0 cm in greatest dimension
IIB With obvious parametrial invasions
Stage III The tumor extends to the pelvic wall and/or involves the lower third of the vagina and/or causes hydronephorisis or
non-functioning kidney**
IIIA Tumor involves lower third of vagina, with NO extension to the pelvic wall
IIIB Extension to the pelvic wall and/or hydronephrosis or non-functioning kidney
Stage IV The carcinoma has extended beyond the true pelvis or has involved (biopsy proven) the mucosa of the bladder or
rectum. A bullous edema, as such, does not permit a case to be allotted to Stage IV
IVA Spread of the growth to adjacent organs
IVB Spread of the growth to distant organs

ENDOMETRIAL HYPERPLASIA
• Exaggerated proliferative response of the endometrium
• Benign (E>>>P)

Classification of Endometrial Hyperplasia (WHO)
SIMPLE COMPLEX ATYPICAL SIMPLE ATYPICAL COMPLEX
HYPERPLASIA HYPERPLASIA HYPERPLASIA HYPERPLASIA
• Endometrium with dilated glands • Glands are crowded with very • Contain glands with cytologic atypia
• Some outpouching & abundant little endometrial stroma • (+) increase in the N:C ration
endometrial stroma • Very complex gland pattern • Irregularity in the size & shape of the nuclei
• Cystic hyperplasia (dilation of the outpouching formations • Greatest malignant potential (29% rate of
endometrial glands) • Variant of adenomatous progression to cancer)
• “swiss-cheese hyperplasia” hyperplasia with moderate to
• weakly premalignant (1% rate of severe degrees of
progression to cancer) architectural atypia but with
no cytologic atypia
• Low premalignant potential
(3% rate of progression to
cancer)


CLINICAL PRESENTATION:
• ABNORMAL UTERINE BLEEDING
• Younger patients: hyperplasia may develop during anovulatory cycles and maybe even detected after a prolonged period of
oligomenorrhea or amenorrhea
• Most common in perimenopausal period

CLINICAL EVALUATION:
• Premenopausal women with irregular vaginal bleeding and post menopausal women with any vaginal bleeding should be
evaluated with endometrial sampling or a D&C.

DIAGNOSTIC ADJUCT:
• Transvaginal Ultrasound: NORMAL ENDOMETRIAL THICKNESS
o Adolescent ?
o Reproductive Age
§ Proliferative Phase = 5 – 8 mm
§ Periovulatory Phase = 6 – 10 mm
§ Secretory Phase = 7 – 14 mm
o Postmenopause <5mm

THICKENED ENDOMETRIUM:
• ≥5mm in postmenopausal women
• ≥15mm in the premenopausal women warrant further investigation with sonography, transvaginal color Doppler and/or
endometrial tissue sampling

SCHEMATIC DIAGRAM OF ENDOMETRIAL HYPERPLASIA MANAGEMENT FOR REPRODUCTIVE PATIENTS


SCHEMATIC DIAGRAM OF ENDOMETRIAL HYPERPLASIA MANAGEMENT FOR POST-REPRODUCTIVE PATIENTS

MANAGEMENT:
PREMENOPAUSAL POSTMENOPAUSAL
Without ATYPIA OCP x 6 cycles If desirous of uterine preservation or if poor
MPA 10-20mg OD x 14 days surgical risk, same as premenopausal
UTZ & sample endometrium after 3 months
-If normal: MPA 5mg x 10 days/mo x 12mos If not, EHBSO
-If persistent: MPA 40-100mg OD x 3mos then
repeat biopsy
With ATYPIA Desirous Pregnancy: EHBSO
-MPA 10-20mg OD x 3 mos
-Megestrol acetate 40-200mg/day
DMPA 150mg IM every 3 mos
LNG-IUS 1-5 years

Not Desirous of Pregnancy:
-EH±BSO


ENDOMETRIAL CARCINOMA
• Most common malignancy of genital tract
• Most common in perimenopausal & postmenopausal
• Most common symptom: AUB

TYPES OF ENDOMETRIAL CANCER:
TYPE I TYPE II
PROTOTYPE ENDOMETROID CA SEROUS PAPILLARY
TYPICAL PATIENT PERI- OR EARLY POSTMENOPAUSE LATE POSTMENOPAUSE
BACKGROUND ENDOMETRIUM Hyperplastic Atrophic
GRADE Low High
ESTROGEN DEPENDENCE Dependent Non-dependent
ESTROGEN RECEPTORS Usually positive Negative
PROGNOSIS Better
Pathophysiology:
• Chronic unopposed estrogen stimulation
• Atypical complex hyperplasia precursor

RISK FACTORS:
INCREASES RISK DECREASES RISK
• Unopposed strogen stimulation • Ovulation
• Unopposed menopausal estrogen (4-8x) replacement • Progestin therapy
therapy • Combination OCP
• Menopause after 52 years (2.4x) • Menopause before 49 years old
• Obesity (2-5x) • Normal weight
• Nulliparity (2-3x) • Multiparity
• Diabetes (2.8x) • Tubal ligation & hysterectomy with ovarian conservation
• Feminizing ovarian syndrome
• Tamoxifen therapy for Breast CA

ROUTE OF SPREAD:
Four major channels of lymphatic drainage from the uterus that serve as sites for extrauterine spread of tumor:
1. A small lymphatic branch along the round ligament that runs to the inguinal femoral nodes
2. Lymphatic branches from the fallopian tubes
3. Ovarian pedicles (infundibulopelvic ligaments), which are large lymphatics that drain into the paraaortic nodes
4. The broad ligament lymphatics that drain directly to the pelvic nodes
• Pelvic and paraaortic node drainage sites (2,3, and 4) are the most important clinically
• The frequency of nodal involvement becomes much greater with higher grade and with greater depth of myometrial invasions

DEGREE OF DIFFERENTIATION:
G1 Well differentiated <6% solid components
G2 Moderately differentiated 6% to 50% solid components
G3 Poorly differentiated >50% solid components

MANAGEMENT:
1. Basic treatment: TAHBSO, node sampling, peritoneal washing
2. Adjuvant: radiation, hormone, tx if progesterone receptor postivie
3. Advanced / Recurrent: high dose progestin or CT


2009 FIGO STAGING OF ENDOMETRIAL CANCER
Stage I G123 Tumor confined to the corpus
IA No or less than half myometrial invasion
IB Invasion half or more of the myometrium
Stage II G123 Tumor invades the cervical stroma but does not extend beyond the uterus
NOTE: Endocervical glandular involvement should be considered as Stage I and no
longer Stage II
Stage III Local and/or regional spread of the tumor
IIIA Tumor invades serosa and/or adnexa*
IIIB Vaginal metastases and/or parametria*
IIC Metastasis to the lymph nodes*
IIIC1 Positive pelvic lymph nodes
IIIC2 Positive paraaortic LN ± pelvic LN
NOTE: Positive cytology has to be reported separately without changing the stage
Stage IV Tumor invades bladder and/or bowel mucosa and/or distant metastasis
IVA Tumor invades bladder and/or bowel mucosa
IVB Distant metastases, including intra-abdominal metastases and/or inguinal LN

UTERINE SARCOMA
• Comprises <5% of uterine malignancies are much less frequent than endometrial carcinomas

2009 FIGO STAGING OF UTERINE SARCOMA: LEIOMYOSARCOMA
Stage I Tumor limited to uterus

IA <5cm
IB >5cm
Stage II Tumor extends to the pelvis
IIA Adnexal involvement
IIB Tumor extends to extrauterine pelvic tissues
Stage III Tumor invades abdominal tissues (not just protruding into the abdomen)
IIIA 1 site
IIIB >1 site
IIC Metastasis to pelvic and/or paraaortic LN
Stage IV
IVA Tumor invades bladder or rectum
IVB Distant metastasis

2009 FIGO STAGING OF UTERINE SARCOMA: LEIOMYOSARCOMA
Stage I Tumor limited to uterus

IA Tumor limited to endometrium/endocervix with no myometrial invasion
IB ≤ half myometrial invasion
IC > half myometrial invasion
Stage II Tumor extends to the pelvis
IIA Adnexal involvement
IIB Tumor extends to extrauterine pelvic tissues
Stage III Tumor invades abdominal tissues (not just protruding into the abdomen)
IIIA 1 site
IIIB >1 site
IIC Metastasis to pelvic and/or paraaortic LN
Stage IV
IVA Tumor invades bladder or rectum
IVB Distant metastasis


OVARIAN, FALLOPIAN TUBES AND PRIMARY PERITONEAL CANCER
Differential Diagnosis of Adnexal Mass:
ORGAN CYSTIC SOLID
Ovary Functional cyst Neoplasm
Neoplastic cyst Benign
Benign Malignant
Malignant
Endometriosis
Fallopian Tube Tuboovarian abscess Tuboovarian abscess
Hydrosalphinx Ectopic pregnancy
Parovarian cyst Neoplasm
Uterus Intrauterine pregnancy in bicornuate Pedunculated or intraligamentous
uterus myoma
Bowel Sigmoid or cecum distended with gas or Diverticulitis
feces Ileitis
Appendicitis
Colonic cancer
Miscellaneous Distended bladder Abdominal wall hematoma or abscess
Pelvic kidney Retroperitoneal neoplasm
Urachal cyst

SYMPTOMS INDICATIONS FOR SURGERY

• Initially are asymptomatic • Ovarian cystic structure >5cm that has been observed 6-8
• Lower abdominal discomfort weeks without regression
• Pelvic pain • Any solid ovarian lesions
• Dyspareunia • Any ovarian lesion with papillary vegetation on the cyst wall
• Abdominal enlargement • Any adnexal mass >10cm
• Frequent urination • Palpable adnexal mass in premenarchal or postmenopausal
• Constipation • Torsion or rupture suspected

FREQUENCY OF OVARIAN NEOPLASM (WHO Classification)
CLASS FREQUENCY (%)
Epithelial Stromal (Common Epithelial) Tumors 65
Germ Cell Tumors 20 – 25
Sex Cord-Stromal Tumors 6
Lipid (lipoid) Cell Tumors <0.01
Gonadoblastoma <0.01
Soft-tissue Tumors (not specific to the ovary)
Unclassified Tumors
Secondary (Metastatic) Tumors
Tumor-like Conditions (not true neoplasm)


1. EPITHELIAL OVARIAN NEOPLASMS
- Arise from inclusion cysts lined with surface (coelomic) epithelium within adjacent ovarian stroma
- (+) pelvic pressure, abdominal fullness and bloating
- Marker: CA-125
a. Serous: most common epithelial tumor, (+) psammoma bodies
i. High Grade – worse prognosis
ii. Composed of ciliated epithelial cells that resemble those of the fallopian tube
b. Mucinous: consist of epithelial cells filled with mucin, resembling cells of the endocervix or intestinal cells
c. Clear Cell Carcinoma: most clear cell neoplasms of the ovaries are carcinomas
i. Hobnail Cells (abundant glycogen)
ii. Most common epithelial ovarian neoplasm to be associated with paraneoplastic hypercalcemia
iii. Relationship with endometriosis is strongest among all types of ovarian carcinoma
d. Endometrioid Adenorcarcinoma: consist of cells resembling those of the endometrium
e. Brenner Tumor: resemble bladder transitional cells
i. Grossly identical to a fibroma of the ovary
ii. Arise from Walthard Cell Rests

2. GERM CELL TUMOR
- Most common ovarian CA in women <30 years old
- Pelvic pain due to rapid growth and hemorrhage
a. Dysgeminoma: most common malignant GCT (-seminoma)
i. Marker: LDH
b. Endodermal Sinus: Schiller Duval bodies – numerous hyaline droplets
i. Marker: AFP
c. Teratoma
i. Marker: AFP
d. Choriocarcinoma: hemorrhagic, highly malignant cytoplasm & syncitiotrophoblast
i. Marker: hCG

3. SEX CORD STROMA
a. Granulosa-Theca: Call-Exner Bodies – coffee bean nuclei in clsuters around central cavity; estrogenic
i. SSx: Precocious puberty, AUB, PMB
b. Sertoli-Leydig: resembles fetal testes; testosterogenic
i. SSx: masculinization, hirsutism

CLASSIFICATION OF OVARIAN NEOPLASMS
Origin SURFACE EPITHELIAL GERM CELL SEXCORD-STROMAL METS
Overall Frequency 65-70% 15-20% 5-10% 5%
% of Ovarian CA 90% 3-5% 2-3% 5%
Markers CA-125, CEA LDH, hCG, AFP Estrogen, Testosterone
Age Group >20 yo 0-25 yo All Ages Varied
Types Serous: mc Teratoma Firbroma
Mucinous Dysgerminoma Grnaulosa-Theca
Endometroid Endodermimal Sinus Tumor Sertoli-Leydig
Clear Cell Choriocarcinoma
Brenner
Cystadenofibroma


2009 FIGO STAGING OF OVARIAN CARCINOMA
STAGE I Growth limited to the ovaries
IA Growth limited to one ovary; no ascites present containing malignant cells; no tumor
on the external surfaces; capsule intact
IB Growth limited to both ovaries; no ascites present containing malignant cells; no
tumor on the external surfaces; capsule intact
IC Tumor stage IA or IB but with tumor on the external surface of one or both ovaries
IC1 Surgical spill
IC2 Capsule ruptured before surgery or tumor on ovarian or FT surface
IC3 Ascites present containing malignant cells or positive peritoneal washings
STAGE II Growth involving one or both ovaries with pelvic extension
IIA Extension and/or metastases to uterus and/or tubes
IIB Extension to other pelvic tissues
IIC Tumor stage IIA or IIB but with tumor on the surface of one or both ovaries; or with
capsule(s) ruptured; or with ascites present containing malignant cells or positive
peritoneal washings
STAGE III Tumor involving one or both ovaries with peritoneal implants outside the pelvis
and/or positive retroperitoneal or inguinal nodes; superficial liver metastasis equals
Stage III; tumor is limited to the true pelvis but with histologically verifies malignant
extension to small bowel or omentum
IIIA Tumor grossly limited to the true pelvis with negative nodes with histologically
confirmed microscopic seeding of abdominal peritoneal surfaces
IIIB Tumor of one or both ovaries histologically confirmed implants of the abdominal
surfaces none exceeding 2cm in diameter nodes are negative
IIIC Abdominal implants 2cm in diameter and/or positive retroperitoneal or inguinal
nodes
STAGE IV Growth involving one or both ovaries with distant metastasis; if pleural effusion is
present, there must be positive cytologic test result to allot a case to Stage IV;
parenchymal liver metastasis equals Stage IV
IVA Pleural effusion with positive cytology
IVB Parenchymal mets with mets to extra-abdomonal organs (including inguinal LN & LN
outside the abdominal cavity)

VULVAR INTRAEPITHELIAL NEOPLASIA AND CANCER

VULVAR ATYPIA: CLASSIFICATION
• Squamous Cell Hyperplasia (formerly Hyperplastic Dystrophy)
• Lichen Sclerosus
• Intraepithelial Neoplasia
o VIN I: Mild Dysplasia
o VIN II: Moderate Dysplasia
o VIN III: Severe Dysplasia
• Others:
o Paget’s Disease
o Melanoma In-Situ (Level 1)

LICHEN SCLEROSUS SQUAMOUS HYPERPLASIA
GROSS Vulvar skin is thin & there maybe scarring & contracture Tissues of vulva appear thickened
Fissuring of the skin, accompanied by excoriation Hyperkeratotic
secondary to itching Focal or multifocal whitish or reddish
Hyperkeratosis is occasionally present
Diffuse whitish change
MICRO Markedly thinned epithelium Elongation & widening of rete ridges
Loss of blunting or rete ridges
TX Testosterone cream; topical steroids Steroids


VULVAR INTRAEPITHELIAL NEOPLASIA (VIN)
- Usually marked by a loss of maturation process usually seen in squamous epithelium as well as an increase in mitotic
activity and in the nuclear-cytoplasmic ratio
- RISK FACTORS:
o HPV 16 and 18
o Obesity
o Chronic Hypertension
- HPV Types 6 and 11 – found most frequently in BENIGN vulvar warts
- HPV Types 16, 18, 31, 33, and 35 – more frequently associated with intraepithelial neoplasia or invasive carcinoma
- Most Common SSX: Itching
- Treatment: Excision, Vaporization

Mild Dysplasia (Atypia) – involve the lower third of the epithelium VIN I – mild atypia
Moderate Dysplasia (Atypia) – ½ to 2/3 of the epithelium is involved VIN II – moderate atypia
Severe Dysplasia (Atypia) - >2/3 of the epithelium is affected VIN III – severe atypia as well as carcinoma in-situ
Carcinoma In-Situ – involves the full thickness of the epithelium

VULVAR CARCINOMA
• SQUAMOUS CELL CARCINOMA: most common; 90% of Primary Vulvar Malignancies
• Most common in women >60 years old
• Gross: raised, flat, ulcerated, plaquelike, or polypoid mass
• SPREAD:
o Tumors in the middle of either labium: drain into the ipsilateral femoral-inguinal nodes
o Perineal nodes: spread to either the left of right side
o Tumors in the clitoral or urethral areas can also spread to either side
o From the inguinal-femoral nodes, the lymphatic spread of the tumor is cephalad to the deep pelvic iliac and
obturator nodes
• Most common ssx: itching
• Treatment: wide radical vulvar excision and bilateral inguino-femoral node dissection

2009 FIGO STAGING OF VULVAR CARCINOMA
STAGE I Tumor confined to vulva
IA Lesions ≤2 cm in size, confined to the vulva or perineum and with stromal invasion
≤1.0mm, no nodal metastasis
IB Lesions >2 cm in size, with stromal invasion >1.0mm confined to the vulva or
perineum, with negative nodes
STAGE II TUMOR OR ANY SIZE WITH EXTENSION TO ADJACENT PERINEAL STRUCTURE
(1/3 lower urethra, 1/3 lower vagina, anus) no negative nodes
STAGE III TUMOR OR ANY SIZE WITH EXTENSION TO ADJACENT PERINEAL STRUCTURE
(1/3 lower urethra, 1/3 lower vagina, anus) with positive inguino-femoral lymph
nodes
IIIA (i) with 1 lymph node metastasis (>5mm) or
(ii) 1-2 lymph node metastasis (<5mm)
IIIB (i) with ≥2 lymph node metastasis (>5mm) or
(ii) with ≥3 lymph node metastasis (<5mm)
IIIC With positive nodes, with extracapsular spread
STAGE IV TUMOR INVADES OTHER REGIONAL (2/3 upper urethra, 2/3 upper vagina) or
DISTANT STRUCTURE
IVA Tumor invades any of the following:
(i) Upper urethral and/or vaginal mucosa, bladder mucosa, rectal mucosa or fixed to
pelvic bone or.
(ii) Fixed or ulcerated inguino-femoral lymph nodes
IVB Any distant metastasis including pelvic lymph ndoes


VAGINAL INTRAEPITHELIAL NEOPLASIA (VAIN)
RISK FACTORS
• HIV infection
• Cigarette smoking
• Previous radiation of the genital tract
• Immunosuppressive therapy
DETECTION & DIAGNOSIS
• Cytologic screening
• Biopsy
• Vaginal calposcopic examination is usually performed to identify the areas requiring biopsy (uses Acetic Acid & Lugol’s
Iodine)
• Repeat pap smear is taken before the colposcopic examination
GROSS
• Most cases no identifiable lesion; occasionally, epithelium appears raised, roughened and white or pink
• Usually located in the upper half of the vagina or along the vaginal cuff suture line
• Multifocal or diffuse
MICROSCOPIC
• Nuclear abnormalities: enlargement with irregular shape, hyperchromasia
• Increased mitotic activity, abnormal mitotic figures, acanthosis, dyskeratosis

LOW GRADE SIL
• VAIN I – Mild Dysplasia
HIGH GRADE SIL
• VAIN II – Moderate Dysplasia
• VAIN III – Severe Dyspalasia to CIS

MANAGEMENT
• The principles of managing vain are to rule out and prevent invasive disease and to preserve vaginal function
• VAIN I, particularly those lesions associated with low-risk strains of HPV, can be observed, provided the patient is compliant
with follow up
• VAIN II & VAIN III are generally treated

TREATMENT OPTIONS
A. Topical 5-fluorouracil (5-FU) cream
B. CO2 Laser Vaporization
C. Wide Local Excision (Upper Vaginectomy): VAIN III
o The choice of treatment depends largely on the number of lesions, their location and the level of concern for
possible invasion

VAGINAL CANCER

TUMOR PREDOMINANT AGE CLINICAL
TYPE (YEARS) CORRELATIONS
Endodermal Sinus Tumor (AdenoCA) <2 Extremely rare, α-fetoprotein secretion, often fatal,
multimodality therapy
Sarcoma Botryoides <8 Aggressive malignancy, multimodality therapy
Clear-Cell AdenoCA >14 Associated with intrauterine exposure to diethylstilbestrol
Melanoma >50 Very rare, poor survival
Squamous Cell CA >50 Most common primary vaginal cancer

SYMPTOMS:
• Most common symptom: abnormal bleeding or discharge
• Pain is usually a symptom of an advanced tumor
• Urinary frequency is reported in the case of anterior wall tumors
• Constipation or tenesmus may be reported when the tumors involve the posterior vaginal wall
• Usually diagnosed by direct biopsy of the tumor mass


2009 FIGO STAGING OF VULVAR CARCINOMA
STAGE I The carcinoma is limited to the vaginal wall
STAGE II The carcinoma has involved the subvaginal tissue but has not extended to the pelvic
wall
STAGE III The carcinoma has extended to the pelvic wall
STAGE IV The carcinoma has extended beyond true pelvis or has involve the mucosa of bladder
or rectum; bullous edema as such does not permit a case to be allotted to stage IV
IVA Tumor invades bladder and/or rectal mucosa and/or direct extension beyond true
pelvis
IVB Spread to distant organs

MANAGEMENT: TREATMENT AND PERFORMANCE STATUS

DEFINITION OF RESPONSE TO TREATMENT
RESPONSE WHO CHANGE IN CROSS PRODUCT (CP) RECIST CAHNGE IN MAXIMAL DIAMETER (MD)
Complete Complete resolution of all evidence of disease lasting at Complete resolution of all evidence of disease
least 1 month
Partial Decrease of 50% in product of diameters (max and min) Decrease of 30% in baseline sum longest diameters of all
of all measurable lesions lasting at least 1 month measurable disease without new lesions
without new lesions
Stable Decrease of <50% or increase of <25% in product of Decrease of 30% in baseline sum longest diameters of all
diameters of all measurable disease measurable disease without new lesions
Progression Increase of 25% in measureable lesions as described Increase of 20% in baseline sum longest diameters of all
above or identification of new lesions measureable disease or identification of new lesions

Measureable disease: solid tumor assessed by CT Scan (>10mm) or by UTZ (>20mm)
Non-measureable disease: lesions measuring by <10mm by CT or <20mm by UTZ
• Cystic lesions, ascites

PERFORMANCE STATUS SCORING
ECOG/COG KARNOFSKY SCORE ACTIVITY LEVEL
0 90-100 Fully active
Unrestricted ADLs
1 70-80 Ambulatory but restricted in strenuous activity
2 50-60 Ambulatory but capable of self care
Unable to work
Out of bed >50% of working hours
3 30-40 Limited to self care
Confined to bed or chair >50% of working hours
Needs special assistance
4 10-20 Completely disabled
No self care
5 0 Dead


MENOPAUSE
- Permanent cessation of menstruation caused by failure of ovarian follicular development and estradiol production in the presence
of elevated gonadotropin levels
- 12 months of amenorrhea after final menstrual period
- Mean age of Filipino menopause: 47 – 48 years old

PERIMENOPAUSAL TRANSITION
• The time between the onset of irregular menses and permanent cessation of menstruation
• The average duration is about 4 years.
• A variable time beginning a few years before and continuing after the event of menopaues, and climacteric.

Climacteric
- The physiologic period in a woman’s life during which there is regression of ovarian function.
- Time after the cessation of reproductive function

Age of Menopause
- The primary determinate of age of menopause is genetic.
- By age 58, 97% of women will have gone through menopause

PATHOPHYSIOLOGY / HORMONAL CHANGES:
• Basic feature is depletion of ovarian follicles
o With degeneration of granulosa and theca cells
o While stromal cells continue to produce the androgens, androstenedione and testosterone

PERIMENOPAUSE MENOPAUSE
Gametogenic Ovarian Failure 1. Marked reductions in ↓E2 and estrone
1. ↓Ovarian inhibin productive accompanied by an ↑Pituitary FSH (↓E1).
release 2. ↑FSH & ↑LH
2. ↑Activin 3. ↓Ovarian inhibin production
3. ↓Ovarian estrogen production (Major reduction ~ 6mos before 4. Serum prolactin levels very slightly
menopause decreased
4. Very slow decline in androgen status 5. Very slow decline in androgen status

EFFECTS OF HYPOESTROGENISM: LONG TERM EFFECTS:
CNS Hot flush Bones Osteopenia
Disturbed sleep Osteoporosis
Depressed mood Fracture
Cognitive decline CVS CVD
Dementia (Alzheimer’s Disease) Cancer Breast
Collagen Bone Colon
Skin
Pelvic Structure
Urinary System
Genital Atrophy Vaginal Dryness
Atrophic Vaginitis
Dyspareunia

TREATMENT:
a) ERT: Biphosphonates (Alendronate-Fosamax), SERMs (Raloxifene, Tamoxifen)
b) Calcium 1500mg/day & Vitamin D 1500mg/day
c) Weight bearing exercises


INFERTILITY
- Inability of couples of reproductive age to establish a pregnancy by having sexual intercourse with a certain period of time,
usually 1 year
o PRIMARY: if the woman has never been pregnant
o SECONDARY: if it occurs after one or more pregnancies

FECUNDABILITY
- Probability of conception occurring in a population of couples in a given period of time, usually 1 month; NV: 20%

FEMALE FACTORS:
ETIOLOGY CAUSES MANAGEMENT
Ovulatory PCOS Ovulation induction
Advanced maternal age
Hyperprolactinemia
Hypothyroidism
Tubal PID Laparoscopic lysis of adhesions
Tubal ligation Tuboplasty with tubal reanastomosis
Pelvic adhesions IVF
Endometriosis
Uterine Congenital malformation Operative hysterectomy
Submucosal fibroids
Uterine polyps
Asherman’s syndrome
Luteal phase defect
Cervical Cervical stenosis Surgical or mechanical dilation
Cervicitis IVF
Unfavorable mucus
Endometriosis Remove surgically

MALE FACTORS:
ETIOLOGY CAUSES MANAGEMENT
Abnormal Semen Cryptorchidism
Mumps orchitis
Anti-sperm antibodies
Endocrine Hypogonadotropic hypogonadism hMG
Thyroid disease
Environment Radiation
Heat
Genetics Klinefelter’s syndrome
Immobile cilia syndrome
Sexual Dysfunction Erectile dysfunction IUI
Ejaculation failure Intra-cytoplasmic sperm
Retrograde ejaculation Artifial insemination of donor sperm if
Structural Defects Varicocoele necessary
Vasectomy
Testicular torsion


DIAGNOSIS:
I. OVULATION DOCUMENTATION
a. History
b. Midluteal progesterone level (>10ng/mL)
c. Basal body temperature (midcycle elevation)
d. Endocrine evaluation
e. Endometrial biopsy: proliferative changes only
rd
f. Ovarian reserve: clomiphene citrate challenge test in >35 years old (if FSH on 3 day ≥12mIU/mL à impending
ovarian failure
g. Pelvic ultrasound: uterine structural defects
II. SPERM ANALYSIS
a. 2-3 specimens within 2-4hrs collection after ≥2-3 days of abstinence
Volume 1.5 – 5.0 mL
Ph >7.2 (alkaline)
Viscosity <3 (scale 0 -4); viscid
Sperm Concentration >20 million/mL (20-150M)
Total Sperm Number >39 million ejaculate
Percent Motility >50% active motile sperm in 4 hours
Forward Progression >2 (scale 0 – 4)
Normal Morphology 60-80% sperm heads are normal
Round Cells <5 million mL
Sperm Agglutination < (Scale 0 -3)
Liquefaction Complete within 10-30 mins

III. HYSTEROSALPINGOGRAM
IV. LAPAROSCOPY
a. When HSG shows potentially correctible cause
b. To confirm tubal potency
c. For tubal reconstructive surgery

IN VITRO FERTILIZATION
• For women who had no functioning oviducts as a result of severe tubal disease
• For women with severe endometriosis
• For couples with male factor or unexplained fertility

GIFT • Gamete Intrafallopian Transfer (GIFT)
• Can be used if the infertile woman has functioning oviducts
• With this technique both oocytes and sperm are placed into the oviduct
through a catheter at the time of laparoscopy or mini laparotomy
ZIFT • Zygote Intrafallopian Transfer (ZIFT)
• Oocytes are fertilzif in vitro & trasnfered 24 hours later
TET • Tubal Embryo Transfer
• Embryos are transferred 8-72 hours after fertilization


POLYCYSTIC OVARIAN SYNDROME
STEIN-LEVENTHAL SYNDROME:
• PCOS
• Amenorrhea
• Hirsutism
• Obesity
• Infertility

PCOS: Diagnostic Criteria
1990 NIH: requires both criteria 2003 ESHRE/ASRM: requires 2 of 3 AEPCOS 2006: Requires #1 + either/both
criteria #2, #3
1. Chronic anovulation (OA) 1. Oligo- and/or anovulation (OA) 1. Clinical and/or biochemical signs of
2. Clinical and/or biochemical signs of 2. Clinical and/or biochemical signs of hyperandrogenism (HA)
hyperandrogenism (HA) hyperandrogenism (HA) 2. Anovulation
3. Polycystic Ovaries (PCO) 3. Polycystic Ovaries (PCO)

DIFFERENTIAL DIAGNOSIS:
• Syndromes of severe insulin resistance (HAIR-AN* Syndrome)
• 21-hydorxylase deficient non-classic adnernal hyperplasia
• Cushing’s Syndrome
• Androgen Secreting Neoplasms
• High-dose exogenous androgens
• Hyperprolatinemia
• Thyroid dysfunction

CLINICAL 1. Hirsutism Primary indicator
2. Acne Potential marker
3. Androgenic Alopecia Poor marker
BIOCHEMICAL 1. Free testosterone Most sensitive methods
2. Free androgen index Most sensitive methods
3. Total T Not sensitive
4. DHEAS May be increased but not routine
5. Androstenedione Little data

PATHOPHYSIOLOGY:
• LH/FSH Ratio >3 due to:
o Tonically elevated LH à androgen production by Theca Cells
o Decreased FSH à increased conversion of androgen to estrogen through aromatase

OTHER CLINICAL FINDINGS:
Chronic Anovulation: increase risk of endometrial CA TREATMENT:
Infertility: due to abnormal folliculogenesis • Cyclic progestins or OCP
Hyperandrogenism: hirsutism, oily skin, acne • Clomiphene Citrate, HMG, FSH
Obesity: estrogen by peripheral conversion

WOF: Metabolic Syndrome
(Criteria 3 out of 5)
Waist Circumference: >88cm
HDL: <50mg/dL
Triglycerides: >150mg/dL
BP: >130/85mmHg
FBS: >110mg/dL


PCOS: Symptom-Based Therapy

HYPERANDROGENISM
• OCPs HYPERINSULINEMIA

• Anti-androgens • Insulin sensitizing agents
• GnRH Agonists • Weight loss
• Electrolysis • Life-long health assessments
• Depilatory Creams
OBESITY UNOPPOSED ESTROGEN

• Diet • Progestins
• Exercise • OCPs
• Behavior Modification • Endometrial Ablation
• Hysterectomy
HYPERANDROGENISM ANOVULATION
• OCPs • Clomiphene citrate
• Progestins • Gonadotropins
• GnRH Analogs • Laparoscopic Surgery
• Endometrial Ablation • Insulin sensitizing agents
• Hysterectomy • Aromatase inhibitors
• In vitro fertilization


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OBSTETRICS

NEW DIAGNOSTIC CRITERIA

Stage I Tumor limited to uterus

2009 FIGO STAGING OF UTERINE SARCOMA: LEIOMYOSARCOMA

Stage I Tumor limited to uterus

SYMPTOMS INDICATIONS FOR SURGERY

OBESITY UNOPPOSED ESTROGEN

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