TOPNOTCH OBSTETRICS AND GYNECOLOGY MAIN HANDOUT BY DR. FAJUTAGANA AND DR.

BANZUELA-CRUZ
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Gynecologic Infections 71
Benign Gynecologic Lesions 76
IMPORTANT LEGAL INFORMATION Neoplastic Disease of the Upper and Lower Genital Tract 82
Family Planning 89
The handouts, videos and other review materials, provided by Topnotch Medical Board
Preparation Incorporated are duly protected by RA 8293 otherwise known as the
Intellectual Property Code of the Philippines, and shall only be for the sole use of the person: PREGNANCY
a) whose name appear on the handout or review material, b) person subscribed to Topnotch
Medical Board Preparation Incorporated Program or c) is the recipient of this electronic
communication. No part of the handout, video or other review material may be reproduced, GUIDE QUESTION:
shared, sold and distributed through any printed form, audio or video recording, electronic
medium or machine-readable form, in whole or in part without the written consent of Pregnancy and Pregnancy Test
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whether intended or otherwise shall be subject to legal action and prosecution to the full
extent guaranteed by law.
• Pregnancy – product of conception implanted typically in
DISCLOSURE uterus or atypically in other locations
The handouts/review materials must be treated with utmost confidentiality. It shall be the DEFINITIONS
responsibility of the person, whose name appears therein, that the handouts/review
materials are not photocopied or in any way reproduced, shared or lent to any person or • Embryo – from time of fertilization until 8 weeks pregnancy (10
disposed in any manner. Any handout/review material found in the possession of another weeks’ gestational age [GA])
person whose name does not appear therein shall be prima facie evidence of violation of RA
8293. Topnotch review materials are updated every six (6) months based on the current • Fetus – after 8 weeks until time of birth
trends and feedback. Please buy all recommended review books and other materials listed • 1st trimester –from 12 weeks up to 14 weeks’ GA
below.
THIS HANDOUT IS NOT FOR SALE! • 2nd trimester –from 12–14 until 24–28 weeks’ GA
• 3rd trimester –from 24–28 weeks until delivery
INSTRUCTIONS • Infant – between delivery and 1 year of age
To scan QR codes on iPhone and iPad o previable – delivered prior to 23–24 weeks
1. Launch the Camera app on your IOS device o preterm – between 24–37 weeks
2. Point it at the QR code you want to scan
3. Look for the notification banner at the top
o term – between 37–42 weeks
of the screen and tap o postterm – beyond 42 weeks
To scan QR codes on Android • Nulligravida – a woman who currently is not pregnant and has
1. Install QR code reader from Play Store
2. Launch QR code app on your device
never been pregnant
3. Point it at the QR code you want to scan • Gravida – a woman who is currently pregnant or has been in the
4. Tap browse website past, irrespective of pregnancy outcome
This handout is only valid for the March 2023 batch. • Nullipara – a woman who has never completed a pregnancy
This will be rendered obsolete for the next batch beyond 20 weeks’ gestation; may not have been or pregnant or
since we update our handouts regularly. may have had an abortion or an ectopic pregnancy
• Primipara – a woman who has been delivered only once of a fetus or
OBSTETRICS AND GYNECOLOGY fetuses born alive or dead with an estimated AOG of at least 20 weeks
• Multipara – a woman who has completed 2 or more pregnancies
– MAIN HANDOUT to 20 weeks’ gestation or more
• Grand multipara – a woman who has had at least 5 births (live
Obstetrics Gynecology or stillborn) that are at least 20 weeks age of gestation
By Shayne C. By Nina Katrina C. • GP-TPAL designation
Fajutagana, MD, DPOGS Banzuela-Cruz, MD, FPOGS o Gravidity, Parity, Term, Preterm, Abortus, Living children
Contributors: Contributors: § Gravidity – number of times a woman has been pregnant
Manuel S. Vidal, Jr, RCh, MD, Shayne C. Fajutagana, MD, DPOGS § Parity – number of pregnancies that led to birth
Jian Kenzo O. Leal, MD, Jian Kenzo O. Leal, MD > 20 wks AOG or infant > 500 g
Anna Rominia d.P. Cruz, MD Anna Rominia d.P. Cruz, MD
§ Preterm – born between 24–37 weeks
TOPIC PAGE § Abortus – pregnancy losses before 20 weeks
Obstetrics Review § Multifetal pregnancy – counts as 1 for TPA, but number
Pregnancy 1 of children alive counts separately for L
Maternal Adaptations in Pregnancy 2 § Grand multipara – a woman whose parity is ≥ 5
Preconceptional and Prenatal Care 3
Early Pregnancy Complications 5 DATING THE PREGNANCY
Ectopic Pregnancy 5 • Developmental age (DA) – number of weeks and days since
Abortion 6 fertilization (conceptional/embryonic age)
Recurrent Pregnancy Loss 7 • Gestational age (GA) – age in weeks and days from last
Gestational Trophoblastic Diseases 7 menstrual period (LMP); + 2 weeks from DA
Labor 9
• Estimated date of confinement (EDC) / estimated date of
Induction and Augmentation of Labor 14
Dysfunctional Labor 14
delivery (EDD) – computed via Naegele’s rule
Delivery 16 o EDC/EDD = LMP – 3 months, + 7 days
Obstetric Hemorrhage 18 o 280 days after LMP; 266 days after LMP if via assisted
Hypertensive Diseases in Pregnancy 22 reproductive technology
Diabetes Mellitus in Pregnancy 23 • Ultrasound - rarely off by 7–8% from GA; Should not differ
Medical Complications in Pregnancy 24 from LMP dating by
Puerperium 34 o >1 week in the first trimester
Gynecology Review o >2 weeks in the second trimester
Developmental Biology of Sex 35 o >3 weeks in the third trimester
Errors in Sexual Determination and Differentiation 37 • Auscultation of fetal heart tones by 20 weeks via stethoscope,
Reproductive Anatomy 38 or 10 weeks via Doppler ultrasound
Reproductive Endocrinology 42 • Quickening usually between 16-20 weeks
Abnormalities of the Menstrual Cycle 48
Amenorrhea 52 DIAGNOSIS
Precocious Puberty 55 Ultrasound
Pediatric Gynecology 56 • Gestational sac seen at 5 weeks on transvaginal ultrasound or at
Hyperandrogenism 56 a beta-hCG of 1,500-2,000 mIU/mL
Infertility 59 • FH motion seen at 6 weeks or at beta-hCG of 5,000-6,000
Menopause 62
mIU/mL
Osteoporosis 64
Urinary Incontinence 65
Pelvic Organ Prolapse 65
Endometriosis 66

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 TOPNOTCH OBSTETRICS AND GYNECOLOGY MAIN HANDOUT BY DR. FAJUTAGANA AND DR. BANZUELA-CRUZ
For inquiries visit www.topnotchboardprep.com.ph or https://www.facebook.com/topnotchmedicalboardprep/
This handout is only valid for the March 2023 PLE batch. This will be rendered obsolete for the next batch since we update our handouts regularly.
Beta-hCG (urine or serum) o reaches nadir at week 24 (24 – 26 weeks in Williams)
• hormone produced by the placenta o between 24 weeks and term, blood pressure returns to pre-
• will rise to a peak of 100,000 mIU/mL by 10 weeks of gestation, pregnancy levels
decrease throughout the second trimester, and then level off at • (Williams) larger cardiac silhouette d/t 1) left and upward
approximately 20,000 to 30,000 mIU/mL in the third trimester. displacement, 2) benign pericardial effusion
• Will turn POSITIVE on urine pregnancy test around the time of
RESPIRATORY SYSTEM
missed menses
• Total lung capacity (TLC) decreases 5% because of elevation
of diaphragm (~4 cm)
Signs Symptoms
• Tidal volume (TV) increases 30–40% à inspiratory capacity
• Bluish discoloration of vagina and cervix • Amenorrhea
(IC) increases
(Chadwick sign) • Nausea and o increased TV lowers blood PCO2 slightly and paradoxically
• Softening and cyanosis of the cervix at or vomiting
causes physiological dyspnea
after 4 wk (Goodell sign) • Breast pain • expiratory reserve volume (ERV) decreases ~20%
• Softening of the uterus after 6 wk (Ladin • Quickening— (15-20% in Williams)
sign) fetal à functional residual capacity (FRC) decreases
• Softening of the uterine isthmus after 6 movement (↓20-30% in Williams)
weeks (Hegar sign) • constant respiratory rate with increased TV à minute
• Breast swelling and tenderness ventilation increases 30–40% à increases alveolar (PAO2) and
• Development of the linea nigra from arterial (PaO2) oxygen levels, decreases PACO2 and PaCO2 levels
umbilicus to pubis
• Telangiectasias
• Palmar erythema

MATERNAL ADAPTATIONS IN PREGNANCY

GUIDE QUESTION:
Maternal Physiology
https://qrs.ly/rtegwwy
Pulmonary changes in pregnancy. From Williams’ Obstetrics, 25th edition.
REPRODUCTIVE SYSTEM Green = increased volumes; Red = decreased volumes
Uterus Increased Decreased Unchanged
• Myometrial hypertrophy > hyperplasia • Inspiratory • Functional • Respiratory rate
• Uterine blood flow increases to 500–750 mL/min capacity (IC) residual capacity • Total lung
o d/t systemic vascular resistance decrease via progesterone, • Tidal volume (FRC) = ERV + RV capacity (FRC +
relaxin, and increased refractoriness to AT II, norepinephrine (VT) o Expiratory IC)*
• Contractions may occur weeks prior to delivery • Resting reserve • Lung
Braxton Hicks True Labor minute volume (ERV) compliance
ventilation o Residual • Maximum
Painless Painful
• Peak volume (RV) breathing
Irregular rhythm, infrequent Rhythmic, frequent
expiratory • Total lung capacity
Cervix does not progress Cervix thins, dilates flow rates • Forced or timed
capacity*
• Airway • Pulmonary vital capacity
Ovaries conductance resistance
• Corpus luteum of pregnancy – max function between 6–7 wks
*unchanged or decreases by < 5% at term
o initially produces progesterone à placenta assumes
production of progesterone à corpus luteum degrades into GASTROINTESTINAL SYSTEM
corpus albicans • Morning sickness – nausea and vomiting in 70% of
• Cervix pregnancies, d/t
o elevations in estrogen, progesterone, and hCG.
• Arias-Stella reaction – loss o may also be due to hypoglycemia à treated with frequent
of polarity, pleiomorphism, snacking
intraluminal budding o typically resolve by 14–16 weeks
o Hyperemesis gravidarum – pathologic morning sickness
associated with weight loss (≥5% of pre-pregnancy weight),
ketosis, and loss of electrolytes
• Eversion -
• gastric emptying time increases (unchanged in Williams) and
marked proliferation of
lower esophageal tone decreases à reflux
cervical glands
o anesthesia may further increase GET (risk factor for
regurgitation and aspiration of gastric contents)
• decreased esophageal tone may cause ptyalism, or spitting
• Ferning –arborization of • large bowel motility decreases à increased water absorption
amniotic fluid due to high and constipation
amounts of salt and estrogen • pelvic vessels congest d/t gravid uterus à increases abdominal
pressure, and with constipation à hemorrhoids
• Goodell’s sign – cervical softening
RENAL SYSTEM
CARDIOVASCULAR SYSTEM • kidneys increase in size, and ureters dilate (R > L) during
• cardiac output increases by 30–50% pregnancy à hydronephrosis of pregnancy: risk factor for
o maximum output at 20–24 weeks and maintained until delivery pyelonephritis
o initially from increased stroke volume à maintained by • relaxin mediates vasodilation à glomerular filtration rate
increased heart rate à stroke volume returns to near pre- (GFR) increases by 50% early in pregnancy (25-50% starting 2nd
pregnancy levels by end of third trimester trimester in Williams) and maintained until delivery à blood urea
• Systemic vascular resistance decreases à fall in arterial nitrogen and creatinine decrease by ~25%
blood pressure • RAAS activation à aldosterone increases à sodium resorption
o due to elevated progesterone, leading to smooth muscle increases
relaxation (and refractoriness to angiotensin II – Williams) o Normonatremia is maintained d/t GFR increase
• systolic pressure decreases 5–10 mm Hg and diastolic pressure o AVP threshold decreases à serum osmolality decreases by
decreases 10–15 mm Hg 10 mOsm/kg
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 TOPNOTCH OBSTETRICS AND GYNECOLOGY MAIN HANDOUT BY DR. FAJUTAGANA AND DR. BANZUELA-CRUZ
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This handout is only valid for the March 2023 PLE batch. This will be rendered obsolete for the next batch since we update our handouts regularly.
HEMATOLOGICAL SYSTEM Total Weight Weight Gain in 2nd and
• plasma volume increases 50% (40-45% in Williams), while RBC Category (BMI) Gain Range 3rd trimester
volume increases 20-30% à physiological anemia of (lb) Mean in lb/wk (range)
pregnancy à hematocrit and hemoglobin decreases Underweight 28-40 1 (1-1.3)
o hypervolemia probably for increased metabolic demand, (<18.5)
protection from impaired venous return, and protection Normal weight 25-35 1 (0.8-1)
against blood loss in delivery (18.5-24.9)
• WBC count increases to ~10.5 million/mL (6-16 million) à Overweight 15-25 0.6 (0.5-0.7)
further increases to >20 million/mL in stressful conditions (25.0-29.9)
• Platelets slightly decrease d/t increased plasma volume and Obese (>=30) 11-20 0.5 (0.4-0.6)
increased peripheral destruction Williams Obstetrics Table 10-4: Recommendations for Total and Rate of Weight Gain in Pregnancy

• Pregnancy is considered hypercoagulable state with • Nutritional requirements

increase in thromboembolic events o Protein: increases from 60 to 70 or 75 g/day
o Levels of fibrinogen and factors VII–X increase o Calcium: 1.5 g/day
o However, clotting and bleeding times do not change o The recommended daily diet allowance (RDA) for Calcium is
o Increased rate of thromboembolic events (may also be due 1200mg/day in Blueprints and 1000mg/day in Williams
to other elements of Virchow’s triad: increased venous stasis o 1500mg/day in patients taking heparin,
& endothelial damage) o Iron: +18mg daily
o Folate (helps prevent NTDs): increases from 0.4 to 0.8
ENDOCRINE SYSTEM mg/day
• Pregnancy is a hyperestrogenic state, mainly d/t o 400 mcg/day supplementation for all until first trimester
o Placenta production, from plasma-borne precursors o 4mg/day for patients with a history of child with NTDs,
produced by maternal adrenal glands Since mahilig sila magtanong ng difference in dosages minsan, to add: 4mg/day
o Ovaries contributing to lesser degree, from estrogen supplementation with folic acid is also advised for patients with Type 2 Diabetes
precursors produced in ovarian theca cells Mellitus (Blueprints and Williams 25th ed) and in patients with seizure disorders
o Fetal well-being was correlated with maternal serum estrogen (Williams 26th ed). Increased folic acid supplementation of around 2-4mg/day is
levels (e.g. low estrogen levels in fetal death and anencephaly) also recommended for patients with ulcerative colitis to counteract the
• In addition to estrogen, placenta produces antifolate actions of sulfasalazine.
Dr. Anna Rominia Cruz
o hCG
§ α subunit of hCG is identical to α subunits of luteinizing
hormone (LH), follicle-stimulating hormone (FSH), and PRECONCEPTIONAL AND PRENATAL CARE
thyroid-stimulating hormone (TSH), whereas tβ subunits differ PRECONCEPTIONAL COUNSELING
§ hCG levels double every ~48 hours during early • Folic acid: Begin 0.4 mg/day one month prior to conception for
pregnancy à peaks at ~10–12 weeks à declines to all patients; then increase to 4mg/day for patients high risk for
steady state after week 15 NTDs
o relaxin • A pre-conceptional hemoglobin A1c level goal below 7% is
§ remodels reproductive tract to accommodate labor recommend for patients with diabetes mellitus
o Human placental lactogen (hPL) • For a woman recently vaccinated with live vaccines (i.e.
§ ensures constant nutrient supply to fetus. hPL, is also varicella-zoster, measles, mumps, rubella, polio, chickenpox, and
known as human chorionic somatomammotropin (hCS) yellow fever), it is recommended to get pregnant at least a month
§ cause lipolysis with increase in circulating free fatty acids after administration
§ acts as insulin antagonist (diabetogenic effect) à insulin
and protein synthesis
• Prolactin levels increased during pregnancy à decreased
PRENATAL CARE
after delivery à increased in response to suckling Initial Visit and First REMARKS
• Pregnancy is considered a euthyroid state, despite subtle Trimester
changes in thyroid hormone production CBC Primarily for hematocrit
o Estrogen stimulates thyroid binding globulin à elevation in Pap smear Screening for cervical CA
total T3 and T4, but free T3 and T4 remain constant (Free T4 Blood type and Rh (-) mothers: should be given
slightly increases in1st trimester, then decreases – Williams) antibody screen RhoGAM at 28 wks
o hCG weakly stimulates thyroid à slight increase in T3 and RPR/VDRL Screening for syphilis
T4 and slight decrease in TSH early in pregnancy Rubella antibody If nonreactive, give vaccine
MUSCULOSKELETAL AND DERMATOLOGICAL SYSTEM screen postpartum
• Change in center of gravity during pregnancy à posture shift Hepatitis B antibody
and lower back strain, which worsens during third trimester screen
• Pregnancy is associated with carpal tunnel syndrome; results Urinalysis and urine
Screen for asymptomatic bacteriuria
from compression of the median nerve; incidence varies, and culture
symptoms are usually self-limited In patients with no history of
VZV titer
• Spider angiomata and palmar erythema occur due to chickenpox
increased estrogen in skin During the 1st or 2nd trimester to
PPD
• hyperpigmentation of nipples, umbilicus, abdominal midline screen for PTB in high risk patients
(the linea nigra), perineum, and face (melasma or chloasma) HIV screening Offered routinely
occur due to increased melanocyte-stimulating hormones and Gonorrhea culture Repeated in the 3rd trimester in
steroid hormones Chlamydia culture high-risk populations
• Breast enlargement typically occurs, pathological enlargement Early screening for Nuchal translucency + serum markers
is termed gigantomastia aneuploidy (hCG, PAPP-A) at 11-14wks
• Colostrum may be produced as early as few months into Second Trimester
pregnancy (but only expressed 2nd day postpartum – Williams) MSAFP/triple or quad MSAFP, beta-hCG, estriol +/- inhibin
screen A at 15-20 weeks
METABOLISM AND NUTRITION 18-20 wks: screening utz for fetal
Caloric equivalent of eating for ~1.15 persons malformation
• An additional 80,000 kcal is needed during pregnancy specially
in the last 20 weeks of gestation Obstetric ultrasound In NTDs:
• Average woman requires 2,000 to 2,500 kcal/day; caloric Banana sign – cerebellum is pulled
requirement increased by 300 kcal/day during pregnancy caudally and flattened
and by 500 kcal/day when breastfeeding Lemon sign –concave frontal bones
o 100-300kcal/d caloric increase is recommended (Williams 26th) For women interested in prenatal
Amniocentesis
o Most gain 20–30 lbs during pregnancy (mean: 28.6 lbs in Williams) diagnosis

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Third Trimester o UTZ for NT + serum PAPP-A and free beta-hCG, or
Hematocrit Hct becomes close to its nadir o Blood test to assess relative quantity of fetal cfDNA for
GDM screening; 75g OGTT based on chromosomes 13, 18, and 21à cfDNA is detected as early as 5
local CPG weeks; offers ↑ detection rate and ↓ false (+) rate
• Second trimester
BLUEPRINTS: o Screening for MSAFP between 15-18 weeks: ↑MSAFP = ↑risk
50g GLT: check after 1hr for NTD, ↓ in some aneuploidies like Down Syndrome
à if ≥ 140 mg/dL*, proceed to do o Between 18-20 weeks: most patients are offered a screening
Glucose loading test glucose tolerance test (GTT) UTZ to screen for common fetal abnormalities (Congenital
*other institutions use a lower threshold of 130 or Anomaly Scan)
135 mg/dL
§ Spina bifida: “lemon” sign (concave frontal bones),
2 or more to diagnose as GDM on
“banana” sign (a cerebellum that is pulled caudally and
100g OGTT:
flattened)
FBS 95 mg/dL; 1hr 180; 2hr 155;
o Also noted are AFV, placental location, and gestational age
3hr 140
RPR/VDRL ---
• Third trimester
at 36 wks (Williams: 35-37 wks); if o RhoGAM is given at 28 weeks to Rh negative patients
GBS culture (+) à IV penicillin once in labor to o Beyond 32-34 weeks, Leopold maneuvers are performed to
prevent neonatal GBS infection determine presentation
BPP – score of 8 to 10 is reassuring o In breech presentation: external cephalic version (ECV) is
Doppler – abnormal findings: offered at 37-38 weeks
decrease, absence, or reversal of
Ultrasound + other diastolic flow in the umbilical artery
tests for fetal well- NST PRENATAL CARE
being https://qrs.ly/zsegwx6
At 35-36 wks: confirm fetal
presentation; if breech, offer ECV at
37 to 38 weeks ROUTINE PROBLEMS OF PREGNANCY
Blueprints 7th edition, Table 1-3: Routine Tests in Prenatal Care
• Back pain – usually in the 3rd trimester when the patient’s
center of gravity has shifted
High-Risk Group Specific Test o Management: mild exercise (like stretching), gentle massage,
Sickle cell prep for heating pads, Tylenol for mild pain, narcotics or muscle
African Americans; Hgb relaxants for severe pain, physical therapy
African American, Southeast Asian
electrophoresis for • Constipation - ↓ bowel motility due to ↑ progesterone à ↑
both water absorption from the GI tract
Family history of genetic disorder o Management: increase oral fluid intake, stool
(e.g., Prenatal genetics referral Prenatal genetics softener/bulking agents, laxatives (avoided during 3rd
hemophilia, sickle cell disease, referral trimester due to risk of preterm labor)
fragile X syndrome), maternal age • Contractions – patients are advised regarding Braxton Hicks
35 or older at time of EDC contractions; dehydration may increase contractions
Prior gestational diabetes, family • Dehydration – due to expanded intravascular space and ↑ third
history Early GLT of diabetes, Early GLT spacing à intravascular volume status is difficult to maintain
Hispanic, Native American, o May cause contractions secondary to cross-reaction of
Southeast Asian, obese vasopressin with oxytocin receptors
Pregestational diabetes, unsure • Edema – compression of IVC and pelvic veins by the uterus à
Dating sonogram at
dates, Dating sonogram at first visit increased hydrostatic pressure in the lower extremities
first visit
recurrent miscarriage o Management: elevation of lower extremities above the heart,
HPN, renal disease, preGDM, prior BUN, Crea, uric acid, sleeping in a lateral decubitus position
preeclampsia, renal transplant, SLE 24h urine collection o Edema of face and hands may indicate preeclampsia
PreGDM, prior cardiac disease, HPN ECG • GERD – relaxation of the LES, increased transit time in the
HbA1c, ophthalmology stomach
PreGDM
for eye exam o Management: may be started on antacids; multiple small
Graves disease TSI meals per day; avoid lying down within 1 hr of eating; H2
All thyroid disease TSH +/- FT4 blockers or PPI may be given
PPD+ CXR after 16 wks AOG • Hemorrhoids - ↑ venous stasis & IVC compression;
Anti Rho, anti-La o Management: topical anesthetic and steroids, prevention of
antibodies (can cause constipation with ↑ fluids, ↑ dietary fiber, use of stool
SLE
fetal complete heart softeners
block • Pica – cravings for inedible items such as dirt/clay; patient is
Blueprints 7th edition, Table 1-4: Initial Screens fin Specific High-Risk Groups
advised to maintain adequate nutrition
ROUTINE PRENATAL VISITS
• Round ligament pain – usually late in 2nd trimester or early in
• The following must be performed and assessed on each follow- 3rd trimester; pain in the adnexa, lower abdomen, or groin; due
up prenatal care visit to rapid expansion of the uterus & stretching of ligamentous
o Blood pressure: ↓ during 1st & 2nd trimesters, slowly returns attachments; usually self-limited
to baseline during the 3rd trimester; ↑BP may be a sign of o Management: warm compress or acetaminophen
preeclampsia
• Urinary frequency – due to ↑ compression of the bladder by
o Weight: large weight gain towards the end of pregnancy can the growing uterus; ↑ intravascular volume & GFR leading to ↑
be a sign of fluid retention and preeclampsia
urine production
o Urine dipstick: presence of protein may be indicative of
• Varicose veins – may be due to relaxation of the venous smooth
preeclampsia, glucose of DM, and leukocyte esterase of UTI
muscle and ↑ intravascular pressure
§ Pregnant women are at an ↑risk for complicated UTI (e.g.
o Management: elevation of the lower extremities, use of
pyelonephritis) due to ↑urinary stasis from mechanical
pressure stockings, referred for surgical therapy if persistent
compression of ureters and progesterone-mediated
beyond 6 months postpartum
smooth muscle relaxation
o Measurement of the uterus: between 20 and 34 weeks,
fundic height in cm correlates closely with AOG in weeks GUIDE QUESTION:
o Auscultation of FHT: after 10-14 weeks, Doppler UTZ is used Prenatal Screening
• First trimester: early screening for aneuploidy is offered https://qrs.ly/9negwxd
between 11-13 weeks either with:
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QUAD SCREENING TABLE
TRISOMY 21 TRISOMY 18 TRISOMY 13 GUIDE QUESTION:
Depends on Antenatal Fetal Testing
MSAFP Decreased Decreased
defect https://qrs.ly/aeegwy7
Depends on
Beta-hCG Increased Decreased
defect
Depends on RECOMMENDED
Estriol Decreased Decreased BPP SCORE INTERPRETATION
defect MANAGEMENT
Depends on No intervention
Inhibin Increased Decreased Normal, non-
defect 10 Repeat test weekly or
Edward asphyxiated fetus
twice weekly
Syndrome Patau 8/10
Other Down (eighteen) Syndrome (Normal AFV) No intervention
remarks Syndrome -choroid plexus (CP) -up to 1 yr of Normal, non-
8/8 Repeat testing per
cysts life asphyxiated fetus
(NST not protocol
-up to 2 yrs of life done)
8/10
Chronic fetal
ANTEPARTUM FETAL ASSESSMENT (Decreased
asphyxia suspected
DELIVER
AFV)
• Oxytocin challenge test or contraction stress test (CST): achieve
DELIVER if:
at least 3 contractions in 10 min; test of uteroplacental function
• AFV abnormal
• Satisfactory test: 3 or more contractions lasting 40 seconds or
• Normal AFV >36 weeks
more in a 10-minute period with favorable cervix
Possible fetal
• Positive CST (abnormal): late fetal heart deceleration (due to 6
asphyxia • Repeat test ≤6
uteroplacental insufficiency) following ≥50% of contractions o If Repeat test > 6:
even if the contraction frequency is < 3 in 10 minutes observe and repeat
• Negative CST (normal): no late or significant variable per protocol
decelerations • Repeat testing on the
• Equivocal-suspicious: intermittent late decelerations or Probable fetal
4 same day
significant variable decelerations asphyxia
• If BPP score ≤6: DELIVER
• Equivocal-hyperstimulatory: FHR decelerations that occur in Almost certain fetal
the presence of contractions more frequent than every 2 0-2 DELIVER
asphyxia
minutes or lasting > 90 seconds
• Unsatisfactory: fewer than 3 contractions in 10 minutes or an NEURAL CONTROL OF BPS ACTIVITY
uninterpretable trace BPS HYPOXIA
• Methods: CNS CENTER AOG
PARAMETER CASCADE
o Oxytocin infusion • Cortex- • 7.5 – 8.5 • Last
o Nipple stimulation Fetal Tone
Subcortical Area wks affected
• Nonstress test (NST): test of fetal condition; most antenatal Fetal
• Cortex-Nuclei • 9 weeks • 3rd
testing units use the NST, beginning at 32 to 34 weeks of Movement
gestation in high-risk pregnancies and at 40 to 41 weeks for Fetal • Ventral surface • 20-21
• 2nd
undelivered patients Breathing of 4th ventricle wks
• Fetal heart rate acceleration in response to fetal movement as • Medulla &
Fetal Heart • 24-26
sign of fetal health Posterior • 1st affected
Reactivity weeks
o ≥32 weeks: acceleration ≥15 bpm from baseline, lasts for Hypothalamus
≥15 secs, but <2 mins from onset to return
o <32 weeks: acceleration ≥10 bpm from baseline, lasts for FETAL BLOOD SAMPLING
≥ 10 secs, but <2 mins from onset to return • Percutaneous umbilical blood sampling – needle is placed
• Considered REACTIVE (reassuring) if there are ≥ 2 transabdominally into the uterus and phlebotomizing the
accelerations in 20 mins; otherwise: NONREACTIVE NST umbilical cord
• Biophysical profile (BPP) o used to asses for fetal anemia (e.g. in Rh isoimmunization), for
• Components (BATMaN): fetal transfusion, karyotyping, and for assessment of fetal
1. Fetal Breathing platelet count
2. Amnionic fluid volume
3. Fetal Tone FETAL LUNG MATURITY
4. Fetal Movement • Lecithin to sphingomyelin ratio (L/s): type II pneumocytes
5. Nonstress test (NST) – may be omitted if all 4 secrete a surfactant that uses phospholipids
sonographic components are normal o Lecithin increases as the lungs mature
COMPONENT SCORE 2 SCORE 0 o Sphingomyelin decreases beyond 32 weeks
≥ 2 accelerations of ≥ 15 0 or 1 o L/S ratio > 2 is associated with only rare cases of RDS
Nonstress
beats/min for ≥ 15 sec acceleration • Levels of phosphatidylglycerol
testa
within 20-40 min within 20-40 min • Saturated phosphatidyl choline
≥ 1 episode of rhythmic < 30 sec of • Presence of lamellar body count
Fetal
breathing lasting ≥ 30 sec breathing within • Surfactant to albumin ration
breathing
within 30 min 30 min
Fetal ≥ 3 discrete body or limb < 3 discrete
movement movements within 40 min movements EARLY PREGNANCY COMPLICATIONS
≥ 1 episode of extremity 0 ECTOPIC PREGNANCY
Fetal tone extension and subsequent extension/flexion • When fertilized egg implants outside uterine cavity
return to flexion events
• fallopian tube in 95%–99% of ectopic pregnancy
A pocket of amniotic fluid
o Implantation in ampulla is 70%, followed by isthmus
that measures at least 2
Largest single (12%) and fimbriae (11%)
Amniotic fluid cm in two planes
vertical pocket • May occur on ovary, cervix, outside of fallopian tube, abdominal
volumeb perpendicular to each
≤ 2 cm wall, or bowel
other
(2 x 2 cm pocket) • > 1:100 of pregnancies are ectopic
aMay be omitted if all four sonographic components are normal. o secondary to increase in assisted fertility, sexually
bFurther evaluation warranted, regardless of biophysical composite score, if transmitted infections, and pelvic inflammatory disease
largest vertical amniotic fluid pocket ≤ 2 cm. • Cardinal signs: vaginal bleeding and/or abdominal pain
with missed menses
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Risk Factors for Ectopic Pregnancy Methotrexate Contraindications
• History of STIs or PID Sensitivity to MTX Intrauterine pregnancy Peptic ulcer disease
• Prior ectopic pregnancy* (STRONGEST RISK FACTOR) Evidence of tubal Active pulmonary
Hepatic, renal, or
• Previous tubal surgery (highest risk – Williams) rupture disease
hematological
• Prior pelvic or abdominal surgery resulting in adhesions Evidence of
Breast feeding dysfunction
immunodeficiency
• Endometriosis
• Current use of exogenous hormones including progesterone
or estrogen ECTOPIC PREGNANCY
• IVF and other assisted reproduction https://qrs.ly/gfegwyc
• DES-exposed patients with congenital abnormalities
• Use of an IUD for birth control
• Smoking ABORTION
*risk of a subsequent ectopic pregnancy is 10% after one prior • 15–25% pregnancies undergo spontaneous abortion (SAB)
ectopic pregnancy and increases to 25% after more than one prior • Abortus – fetus lost before 20 weeks’ gestation or < 500 g
ectopic pregnancy • Complete abortion – expulsion of POC before 20 weeks
• Incomplete abortion – partial expulsion before 20 weeks
DIAGNOSIS OF ECTOPIC PREGNANCY
• Inevitable abortion – no expulsion of POC, but vaginal bleeding
• history: unilateral pelvic or lower abdominal pain and vaginal and dilation of cervix will unlikely result in pregnancy
bleeding • Threatened abortion – any vaginal bleeding before 20 weeks,
• physical examination: tender adnexal mass, small uterus for without dilation of cervix or expulsion of any POC
gestational age, bleeding from cervix • Missed abortion – death of embryo or fetus before 20 weeks
• ruptured ectopic pregnancies: hypotensive, tachycardic, with complete retention of POC
unresponsive • Septic abortion – any abortion complicated with infection
o show signs of peritoneal irritation secondary to
hemoperitoneum
FIRST TRIMESTER ABORTIONS
• laboratory findings: low β-hCG level for gestational age
o In normal intrauterine pregnancy (IUP), should double (or at • 60–80% SABs in first trimester are associated with abnormal
least 2/3 increase) every ~48 hours chromosomes, 95% are due to maternal gametogenesis errors
o In ectopic pregnancy, poorly implanted placenta receive low • 95% usually due to autosomal trisomy (50-60% in Williams)
blood supply à β- hCG levels do not double every 48 hours
o Hematocrit: decreased ruptured ectopic pregnancies MANAGEMENT OF FIRST-TRIMESTER ABORTIONS
• Imaging findings • Stabilize if hypotensive
o gestational sac with yolk sac on UTZ indicates IUP • Incomplete abortion, inevitable abortions, missed abortions –
o in IUP, β-hCG levels should be 1,500–2,000 mIU/mL. allow to finish course, or may be completed via surgical or
o Fetal heartbeat: β-hCG level > 5,000 mIU/mL medical means
o hemorrhaging, ruptured ectopic pregnancy may reveal o Surgical: dilatation and curettage (D&C)
intraabdominal fluid throughout pelvis and abdomen o Medical: prostaglandins ± mifepristone
• Threatened abortion – followed up for possibility of bleeding
MANAGEMENT OF ECTOPIC PREGNANCY o Bed rest and analgesia with acetaminophen
• Surgical procedure o Rh-negative – RhoGAM to prevent isoimmunization
o Exploratory laparotomy – if patient is unstable o Contraceptives if desired
o Exploratory laparoscopy – procedure of choice
o Salpingostomy – resection of ectopic pregnancy, leaving SECOND-TRIMESTER ABORTIONS
fallopian tubes as is • Between 12 to 20 weeks
o Salpingectomy – resection of ectopic pregnancy with • Abnormal chromosomes do NOT often cause late abortions
removal of fallopian tubes • Infection, maternal uterine or cervical anatomic defects,
o Cornual resection – for interstitial pregnancies maternal systemic disease, exposure to fetotoxic agents, and
• Medical management trauma are associated with late abortions
o Methotrexate
§ Factors for success: small ectopic (< 5 cm, serum β-hCG MANAGEMENT OF SECOND-TRIMESTER ABORTIONS
level < 5,000, and w/o fetal heartbeat), reliable ffup
• At 16–24 weeks, dilatation and evacuation may be done or labor
(<3.5 cm – Williams)
induced with oxytocin or prostaglandins
§ single dose regimen (50 mg/m2) IM methotrexate vs
• Aggressive dilatation must be done prior to D&E
multidose regimen (88% vs 93% effectiveness)
• Rule out preterm labor and cervical insufficiency
§ β-hCG levels rise after methotrexate therapy, then fall
10–15% after 4–7 days o Preterm labor – tocolysis
o Cervical insufficiency – cerclage
SINGLE DOSE MULTIDOSE
Up to four doses of GUIDE QUESTION:
One dose; repeat if
Dosing both drugs until serum Second-trimester abortion
necessary
B-hCG declines by 15%
and Cervical insufficiency
Medication https://qrs.ly/niegwyl
Dosage
Methotrexate 50 mg/m2 BSA (D1) 1 mg/kg, D1, 3, 5, 7
CERVICAL INSUFFICIENCY
Leucovorin NA 0.1 mg/kg, D2, 4, 6, 8
Serum B-hCG Days 1 (baseline), 4 Days 1, 3, 5, and 7 • Painless cervical dilation and effacement, often in second
level and 7 trimester à increased exposure of fetal membranes to vaginal
• If serum B-hCG flora and risk of trauma as cervix dilates.
• If serum B-hCG • Possible short-term cramping or contracting à cervical dilation
declines < 15%, give
level does not or vaginal pressure à chorionic and amniotic sacs bulge
additional dose;
Indication for decline by 15%
repeat serum B-hCg through cervix
additional from day 4 to day 7
dose
in 48 hrs and • Cervical insufficiency cause ~15% second-trimester losses
• < 15% decline
compare with
during weekly DIAGNOSIS OF CERVICAL INSUFFICIENCY
previous value;
surveillance
maximum four doses • Dilated cervix on routine examination, ultrasound, or during
Posttherapy bleeding, vaginal discharge, or membrane rupture
Weekly until serum B-hCG undetectable
surveillance • mild cramping or pressure in lower abdomen or vagina
• More cervical dilation than expected with level of contractions
• differentiation between cervical insufficiency and PTL
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o Cervical insufficiency – mild cramping and advancing • hCG: tumor marker for diagnosing the disease and as a tool for
cervical dilation and/or amniotic sac bulging through cervix, measuring the effects of treatment
due to dilated cervix and exposed membranes • most curable gynecologic malignancy d/t sensitivity to
o PTL – contractions/cramping leading to cervical change chemotherapy

MANAGEMENT OF CERVICAL INSUFFICIENCY EPIDEMIOLOGY

• Previable fetus – expectant management or elective termination • decreased rate of GTD in African American women
• Viable fetus – tocolysis and corticosteroids • Low and intermediate rates: North America and Europe
Cerclage – suture at cervical–vaginal junction (McDonald) • Moderate to high rates: Latin America and Asia
(at the internal os level – Williams) or at internal os (Shirodkar) • Highest: among South East Asian women and women in Japan (
(transverse incision of the anterior cervical mucosa at level of 1 in 500 pregnancies)
internal os – Williams) (if without preterm birth but with short
cervix, offer progesterone – Williams) RISK FACTORS
o offer elective cerclage in subsequent pregnancies only if with • most common risk factors: extremes in age and prior history of GTD
history of recurrent midtrimester losses or prior preterm
• <20 years of age: slight increase, >35 years of age: significant
birth with short cervix – Williams)
increase, as well as of malignant disease
o elective cerclage is similar to emergent cerclage (with (adolescents and 36-40 y/o: 2x risk. >40 y/o: 10x risk – Williams)
McDonald or Shirodkar method), usually at 12–14 weeks’ • Nulliparity > multiparity
gestation, maintained until 36-38 weeks (37 weeks – • history of GTD
Williams) o no previous hx: 0.1%
o if cervical cerclage fails à abdominal cerclage is offered at o 1 previous molar pregnancy: 1-2% (0.9% - Williams)
12–14 weeks à mode of delivery is by CS o 2 previous molar pregnancies: 16-28% (20% - Williams)
o If with previous preterm birth, • Diet: low in β-carotene, folic acid, and animal fat
IM 17-hydroxyprogesterone offered until 36 weeks AOG • other possible associated factors: smoking, infertility,
(if without preterm birth but with short cervix, offer spontaneous abortion, blood group A, and a history of OCP use
progesterone – Williams)
COMPLETE MOLAR PREGNANCY
RECURRENT PREGNANCY LOSSES (RPL)
PATHOGENESIS
• recurrent or habitual aborter – three or more consecutive SABs
• result from the fertilization of an enucleate ovum/empty egg,
• < 1% of population diagnosed with recurrent pregnancy loss
one whose nucleus is missing or nonfunctional, by one normal
• Risk of SAB:
sperm that then replicates itself
o after one prior SAB, 20–25%
• all chromosomes are paternally derived
o after two consecutive SABs, 25–30%
• most common karyotype: diploid 46,XX
o after three consecutive SABs, 30–35%
• placental abnormality: noninvasive trophoblastic proliferation
ETIOLOGIES OF RPL à grape-like vesicles
• Similar to spontaneous abortions
• 15% RPL due to antiphospholipid antibody (APA) syndrome Complete mole Incomplete mole
Features
• Possible luteal phase defect and insufficient progesterone (90%) (10%)
Genetics
DIAGNOSIS OF RPL Most common 69,XXY/XXX
46,XX
• obtain parents’ karyotype and POC karyotypes from each SAB karyotype (or XYY – rare)
Chromosomal All paternally
• examine maternal anatomy Extra paternal set
origin derived
• Screening for metabolic/hematologic disorders + APAS panel
Pathology
o lupus anticoagulant
o factor V Leiden deficiency Coexistent fetus Absent Present
o prothrombin G20210A mutation
Fetal RBCs Absent Present
o ANA
o anticardiolipin antibody Chorionic villi Hydropic Few hydropic
o Russell viper venom
o antithrombin III, protein S, and protein C Minimal/
Trophoblasts Severe hyperplasia
• obtain serum progesterone in luteal phase of menstrual cycle no hyperplasia
• cultures from cervix, vagina, endometrium to r/o infection Clinical presentation
Associated
None Present
MANAGEMENT OF RPL embryo
Abnormal vaginal
• patients with chromosomal abnormalities: IVF or Symptoms/signs
bleeding
Missed abortion
preimplantation diagnosis Classic symptomsa Common Rare
• anatomic abnormalities may not be correctable (for Asherman 50% larger for
syndrome à hysteroscopic adhesiolysis; for uterine Uterine size Size = dates
dates
leiomyomas à excision; for congenital genital tract anomalies, 15-25%
disease-specific treatment – Williams) Theca lutein cysts (25-30% - Rare
• cerclage: for cervical insufficiency Williams)
• progesterone: for luteal phase defects hCG levels High Slightly elevated
• low-dose aspirin: for APA syndrome Malignant potential
• SQ heparin (low molecular weight or unfractionated): for Nonmetastatic
15-25% 2-4%
thrombophilia malignant GTD
• appropriate therapy: for maternal systemic diseases Metastatic
4% -
malignant GTD
Follow-up
GESTATIONAL TROPHOBLASTIC DISEASE 14 weeks 8 weeks
Weeks to normal
(GTD) hCG
(9 weeks – (7 weeks –
• abnormal proliferation of trophoblastic (placental) tissue Williams) Williams)
aHyperemesis gravidarum, early preeclampsia, hyperthyroidism,
• four major classifications
o molar pregnancies (80%) anemia, excessive uterine size
Comparison of complete mole vs partial mole. From Blueprints Obstetrics and Gynecology, 7th edition
o persistent GTD and invasive moles (10% to 15%)
o gestational choriocarcinoma (2% to 5%)
o very rare placental site trophoblastic tumors (PSTTs)
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CLINICAL PRESENTATION TREATMENT OF PARTIAL MOLAR PREGNANCY
History • suction D&C
• irregular, heavy vaginal bleeding in the setting of a positive
PROGNOSIS
pregnancy test (97%): most common presenting symptom
o caused by separation of the tumor from the underlying • <5% will develop persistent malignant disease
decidua, resulting in disruption of the maternal vessels. • Similar surveillance strategy with complete moles
• All other symptoms mainly d/t hCG production • average time to normalization of levels: 8 weeks (partial mole) (7
Symptom Percentage weeks – Williams) vs 14 weeks (complete mole) (9 weeks – Williams),
Vaginal bleeding 90-97 2-4 weeks following a normal pregnancy, miscarriage, or termination
Passage of molar vesicles 80 • contraception is warranted to avoid pregnancy interference
Anemia 50
Uterine size larger than dates 30-50 MOLAR PREGNANCY
Bilateral theca lutein cysts 15-25 https://qrs.ly/iaegwyv
Hyperemesis gravidarum 10-25
Preeclampsia 10-15
Hyperthyroidism 10 GESTATIONAL TROPHOBLASTIC NEOPLASIA (GTN)
Trophoblastic pulmonary emboli 2 • 20% of patients with GTD
Common symptoms of molar pregnancy, in descending frequency. From Blueprints Obstetrics and Gynecology, 7th edition.
Physical examination o persistent postmolar pregnancies or invasive molar
• absence of fetal heart sounds pregnancies (75%)
• expulsion of grape-like molar clusters from the vaginal canal o gestational choriocarcinomas (25%)
• palpable large bilateral theca lutein cysts (less frequent) o placental site trophoblastic tumors (rare)
• initially presumed to be a threatened abortion. • diagnosis: plateauing/rising hCG levels after molar evacuation.
• most common presentation: abnormal uterine bleeding >6
Labs and imaging weeks following pregnancy
• hCG levels > >100,000 mIU/mL • staging system: Revised FIGO Staging System
• UTZ: snowstorm pattern d/t chorionic villi swelling • extreme sensitivity to chemotherapy
• theca lutein cysts >6 cm o low-risk disease: single- agent chemotherapy
• definitive diagnosis: histopathological exam of the uterine tissue o high-risk disease: combination chemotherapy.
o surgical intervention: for high-risk patients or for PSTT
TREATMENT OF COMPLETE MOLAR PREGNANCY FIGO staging of malignant GTD
• suction D&C: definitive treatment Stage I Confined to the uterus
o hysterectomy if non-desirous of future pregnancies Stage II Metastases to the pelvis
• uterotonics to minimize blood loos Stage III Metastases to the lung (with or without pelvic
• RhoGAM for Rh-negative women metastases)
• adjunctive anti-hypertensives and beta blockers Stage IV Distant metastases (with or without lung
PROGNOSIS metastases)
• prognosis is excellent: persistent postmolar GTD: 6-32% in Revised FIGO scoring system for GTDa
complete moles, <5% in partial moles Risk factors 0 1 2 4
• serial hCG surveillance Age (yrs) ≤39 ≥40
o 48 hours after evacuation then Antecedent Abort
Mole Term
o every 1 to 2 weeks until negative for 3 consecutive weeks pregnancy us
o then followed monthly for an additional 6 months Pregnancy event to
<4 4-6 7-12 >12
o plateau/rise in hCG is indicative of malignant postmolar GTD tx interval (mos.)
o phantom hCG: (+) hCG but negative urine PT – no tx needed 1,000
10,000-
• contraception: to avoid pregnancy interfering with surveillance Pretx hCG levels <1,00 - >100,00
100,00
• Risk factors for persistent trophoblastic disease (mIU/mL) 0 10,00 0
0
o β-hCG levels >100,000 mIU/mL 0
o ovaries >6 cm (theca lutein cysts > 6 cm – Williams) No. of metastases 0 1-4 5-8 >8
o large uterine sizes (14 to 16 weeks) Splee
Lung,
o may give chemoprophylaxis: methotrexate + folinic n, Brain,
Sites of metastases vagin GI tract
acid/dactinomycin) kidne liver
a
y
Largest tumor size,
PARTIAL MOLAR PREGNANCY including uterine 3-4 5
PATHOGENESIS tumor (cm)
• normal ovum is fertilized by two sperm simultaneously Prior number of Single Multi-
• triploid karyotype with 69 chromosomes, two sets are failed chemotx drugs agent agent
paternally derived a The total score is obtained by adding the individual scores for
• most common karyotype is 69,XXY (80%) each prognostic factor. 0-6 = low risk, ≥7 = high risk
• placenta: focal hydropic villi and trophoblastic hyperplasia Revised FIGO Staging of GTD. From Blueprints Obstetrics and Gynecology, 7th edition

primarily of the cytotrophoblast

PERSISTENT POSTMOLAR GTD AND INVASIVE MOLES
• notable d/t presence of embryo
• 1 in 15,000 pregnancies
• often misdiagnosed as spontaneous or missed abortions
• hydropic chorionic villi and trophoblast proliferation into
• much lower malignant potential than complete moles
the myometrium
CLINICAL PRESENTATION • rarely metastasize and are capable of spontaneous regression
• delayed menses and (+) urine PT • Risk factors
• vaginal bleeding from miscarriage or incomplete abortion in late o hCG > 100,000 mIU/mL
first trimester or early second trimester (90%) o Uterine size >14–16 wk
• physical examination typically normal d/t slightly elevated hCG, o Theca lutein cysts >6cm
(+) fetal heart sounds, uterine size small for gestational age o Coexistent fetus
• UTZ: fetus with cardiac activity, congenital malformations, DIAGNOSIS
and/or IUGR
• Plateau/rise in hCG levels, excessive uterine size, large theca
• “Swiss-cheese” appearance
lutein cysts
• definitive diagnosis: histopathological exam of the uterine tissue
• UTZ: invasion of an intrauterine mass into the myometrium
• Doppler: high vascular flow

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MANAGEMENT MANAGEMENT
• Avoid repeat D&C • Similar treatment for low-risk and high-risk patients
• Single-agent chemotherapy (MTX or dactinomycin) • cure rate: 95% to 100% if low-risk, 50-70% if high-risk
• If with metastases: single agent for low risk, multiagent for high risk • Similar follow-up and surveillance
• Similar follow up and surveillance with GTD
PLACENTAL SITE TROPHOBLASTIC TUMORS (PSTT)
GESTATIONAL CHORIOCARCINOMA
• extremely rare tumors from invasion of the myometrium
• 1 in 20,000 to 40,000; common in Asian or African descent
and vasculature from intermediate cytotrophoblasts of the
• malignant necrotizing tumor: invasion of uterine wall and
placental implantation site
vasculature à necrosis and potentially severe hemorrhage
• absence of villi, intermediate trophoblasts, and (+) hPL (vs
• “the great imitator”
syncytiotrophoblasts, cytotrophoblasts, (+) hCG from other
• pure epithelial tumor: sheets of anaplastic cytotrophoblasts and
types of malignant GTD)
syncytiotrophoblasts in the absence of chorionic villi
• rarely metastasize
• hematogenous spread
DIAGNOSIS
• rate of development:
• most common symptom of PSTT: persistent irregular vaginal
o 50% after a complete molar pregnancy
bleeding
o 25% after a normal-term pregnancy
o 25% after miscarriage, abortion, or ectopic pregnancy • Labs: (+) hPL
• UTZ: uterine mass, less hemorrhage than seen in gestational
DIAGNOSIS choriocarcinomas
• late postpartum bleeding, or abnormal uterine bleeding years
TREATMENT
after an antecedent pregnancy
• symptoms of metastatic disease • generally not sensitive to chemotherapy
• Labs: elevated hCG levels • hysterectomy is the treatment of choice for PSTT
• Imaging: look for metastases (lung CXR, brain/chest/abdominal • multiagent chemotherapy to prevent recurrence
CT/MRI)
LABOR
OBSTETRIC EXAMINATION
• Leopold maneuvers o 3rd – Pawlick grip
o 1st – Fundal grip § Engaged?
§ What occupies fundus? § Engaged – not movable
§ Breech (rump) – large nodular mass § Not engaged – movable
§ Cephalic (head) – hard round ballotable o 4th – Pelvic grip
o 2nd – umbilical grip § What is the prominence?
§ Where is the back? § Brow – resistance to descent of fingers
§ Back – hard and resistant § Flexed – opposite from back
§ Fetal extremities – small and irregular mobile parts § Extended – occiput same side with back

Leopold’s maneuvers. A) Fundal grip. B) Umbilical grip. C) Pawlick grip. D) Pelvic grip. From Blueprints Obstetrics and Gynecology 7th edition
PELVIMETRY

Characteristics of different pelvises. From Blueprints Obstetrics and Gynecology, 6th edition.

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Performing the pelvimetry. From TeachMeAnatomy and Williams’ Obstetrics.

• Diagonals of the pelvic exam

o True conjugate: anteroposterior diameter from uppermost GUIDE QUESTION:
margin of symphysis pubis to sacral promontory Diagnosis of
o Obstetrical conjugate: shortest distance between sacral Ruptured Membranes
promontory and symphysis pubis (typically ≥10 cm, but https://qrs.ly/1zegwzf
cannot be measured directly)
o The obstetrical conjugate is estimated indirectly by RUPTURE OF MEMBRANES
subtracting 1.5–2 cm from diagonal conjugate, feeling for • Premature ROM: before onset of labor
sacral promontory using tips of fingers, and noting position • Prolonged ROM: more than 18 hours
of lower border of pubic symphysis • Preterm premature ROM (PPROM): less than 37 weeks
• Diagnosis
CERVICAL EXAMINATION
o Pool test: positive if with pooling of fluid in the vagina
o Nitrazine test: vagina is acidic (red/orange), amniotic fluid
GUIDE QUESTION: (blue)
Bishop Score o Fern test: estrogens in the AF causes crystallization of salts
https://qrs.ly/r8egwyz à fern pattern
o Oligohydramnios: if there are no other possible causes,
• Bishop score suspect ROM
o Bishop score >8 – cervix favorable for spontaneous and o Amnio dye test or tampon test: indigo carmine is injected
induced labor transabdominally; positive if w/ leakage into tampon
Score 0 1 2 3 o Amnisure rapid test: identify placental α-microglobulin-1
Dilation (cm) Closed 1–2 3–4 ≥5 via immunoassay
Effacement (%) 0–30 40–50 60–70 ≥80
Station –3 –2 –1, 0 ≥+1 INTRAPARTUM ASSESSMENT
Consistency Firm Medium Soft MONITORING FETAL WELL-BEING DURING LABOR
Position Posterior Mid Anterior • Cardiotocograph – has two transducers on fundus (pressure)
The Bishop score. . From Blueprints Obstetrics and Gynecology 7th edition.
o Cervical dilation – assessed using one or two fingers to and fetal heart tone site
determine how open cervix is at level of internal os • Uterine contraction measurements
o Effacement – subjective determination of how much length o Montevideo unit – average of variation of intrauterine
is left of cervix and how effaced pressure from baseline multiplied by number of contractions
o Station – relation of fetal head to ischial spines in a 10-minute period
o Consistency – firm, soft, or somewhere in between o Alexandria unit – Montevideo units multiplied by length of
o Position – from posterior to mid to anterior each contraction
• Fetal heart tracing
FETAL PRESENTATION
• normal range – 110–160 beats per minute
• Vertex – fetal occiput as reference
Baseline • reactive – at least two accelerations of ≥15
• Breech – fetal sacrum as reference
heart rate beats per minute over baseline that last for
o Frank breech:
≥15 seconds within 20 minutes
§ flexed hips
§ extended knees • beat-to-beat variation from baseline
§ feet near fetal head • absent (< 3 beats per minute of variation)
o Complete breech: o worrisome; needs to be repeated
§ flexed hips • minimal (3–5 beats per minute of
§ one or both knees flexed variation)
Variability
§ at least one foot near the breech o may be d/t sleep state or inactivity
o Incomplete or footling breech: • moderate (5–25 beats per minute of
§ one or both hips not flexed variation)
§ foot or knee lies below breech in birth • marked (> 25 beats per minute of
• Face presentation – mentum is reference point variation)
• Shoulder presentation – acromion is reference point • Early decelerations begin and end
approximately at same time as
FETAL POSITION contractions
• based on relationship of fetal occiput to maternal pelvis o result of increased vagal tone
• determined by palpation of sutures and fontanelles secondary to head compression during
o Abnormal fetal position can lead to prolonged labor and contraction
higher rate of cesarean delivery. OT or OP position may be Decelerations • Variable decelerations can occur at any
suspected during prolonged labor. time and tend to drop more than early or
• Asynclitism: Malposition of the fetal head within the pelvis late decelerations
• Sagittal suture approaches sacral promontory à more of o result of umbilical cord compression.
anterior parietal bone presents itself to examining fingers à When cord is trapped under fetal
anterior asynclitism shoulder or around neck à repetitive
• sagittal suture lies close to symphysis à more of posterior variables with contractions
parietal bone will present à posterior asynclitism

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• Late decelerations begin at peak of NORMAL LABOR
contraction and return to baseline after
• Labor – contractions that cause cervical change in either
contraction
effacement or dilation. Prodromal labor or “false labor” is
o result of uteroplacental insufficiency
common in differential diagnosis of labor.
(most worrisome type)
• Difference between false contractions vs true contractions:
o may degrade into bradycardias during
Braxton Hicks True Labor
labor, particularly with stronger
contractions Painless Painful
Irregular rhythm, infrequent Rhythmic, frequent
• transient increases in FHR of ≥ 15 bpm
Accelerations Cervix does not progress Cervix thins, dilates
above baseline and lasting 15 seconds

FETAL HEART TRACING GUIDE QUESTION:

https://qrs.ly/q7egwzu Stages of Labor
https://qrs.ly/s9egx00

PROGRESSION OF LABOR
Functional Divisions of Labor
• Cervix dilates little but connective tissue
Preparatory
components change
Division
• Sedation and conduction analgesia can arrest
Dilatational • Dilation proceeds at its most rapid rate
Division • Unaffected by sedation
Pelvic • From deceleration phase of cervical dilation
Division • Cardinal fetal movements take place
Phases of Cervical Dilation
• Corresponds to the preparatory division
• Ends once dilation of 6 cm is achieved
Latent
Phase • Prolonged latent phase
o Nullipara: > 20 hours
o Multipara: >14 hours
• Corresponds to the dilatational division
• Subdivided into:
o Acceleration phase
o Phase of maximum slope
o Deceleration phase
Active
• Cervical dilation of 3-6 cm or more in the
Phase
presence of uterine contractions
• Rate of cervical dilation
o Nullipara: 1.2 cm/hr
o Multipara: 1.5 cm/hr
• Descent commences at 7-8 cm for nulliparas
Stages of labor
• Stage of cervical effacement and dilation
• Begins when spaced uterine contractions of
1st stage sufficient frequency, intensity, and duration are
attained to bring about effacement to full
cervical dilation
• Stage of fetal expulsion
2nd stage • Complete cervical dilatation to fetal
delivery
• Stage of placental separation and expulsion
3rd stage
• After delivery of fetus to placental delivery

Sample CTG readings demonstrating various patterns of decelerations. A) Early deceleration. B) Late decelerations. C)
Variable decelerations. From Blueprints Obstetrics and Gynecology, 7th edition. STAGES OF LABOR
INTERPRETATIONS OF THE CTG STAGE 1
Normal fetal heart rate tracing • From onset of labor until dilation and effacement of cervix
Category • normal baseline • lasts ~10–12 hours in; divided into latent and active phases
I • moderate variability o latent phase ranges from onset of labor until 6 cm of dilation,
• no variable/late decelerations with slow cervical change
Indeterminate fetal heart tracing § Friedman: active phase began at 3-4 cm cervical dilation
• variable and late decelerations § New threshold: 6 cm of dilation
Category • bradycardia and tachycardia o active phase follows latent phase until complete dilation, and
II • minimal variability is defined by period of time when slope of cervical change
• marked variability against time is at maximum
• absent variability without decelerations § ≥1.0 cm/hour of dilation expected in nulliparous woman
Abnormal fetal heart rate tracing and ≥1.2 cm/hour in multiparous woman
• absent fetal heart variability § Active phase arrest – no change in dilatation or station
Category for 2 hrs even if adequate Montevideo units
• recurrent late/variable decelerations or
III
bradycardia
• sinusoidal pattern à fetal anemia

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1. ENGAGEMENT
• Biparietal diameter (BPD)—the greatest transverse diameter
in an occiput presentation—passes through the pelvic inlet
o Fetal head may engage during the last few weeks of
pregnancy or not until after labor commencement
• Fetal head usually enters the pelvic inlet either transversely or
obliquely.

The first stage of labor. From Blueprints Obstetrics and Gynecology, 7th edition.

Figure 22-11 (2). Cunningham, et al. Williams Obstetrics. 25th ed. 2018
THE 3 P’S OF THE ACTIVE PHASE
• Asynclitism
• “powers” are determined by strength and frequency of uterine
o Lateral deflection of the sagittal suture either posteriorly
contractions. Strength of uterine contractions is measured with
toward the promontory or anteriorly toward the symphysis.
IUPC
o Anterior asynclitism: Sagittal suture approaches the sacral
o Considered adequate if > 200 Montevideo units
promontory, more of the anterior parietal bone presents
• If “passenger” is too large for “pelvis” à cephalopelvic
itself to the examining fingers.
disproportion (CPD)
o Posterior asynclitism: Sagittal suture lies close to the
o Development of fetal caput
symphysis, more of the posterior parietal bone will present.
o Molding of fetal skull with palpable overlapping suture
MONITORING OF FETAL-WELL BEING
• Resuscitative maneuvers
o face mask O2
o turn onto left side to decrease inferior vena cava (IVC)
compression and increase uterine perfusion
o discontinue oxytocin
o for hypertonus (a single contraction lasting 2 minutes or
longer) or tachysystole (greater than five contractions in a
10-minute period), may give terbutaline
• If still nonreassuring CTG pattern, operative vaginal/caesarean Figure 22-12. Cunningham, et al. Williams Obstetrics. 25th ed. 2018

delivery may be done PELVIC PLANES

STAGE 2 FALSE
• from time of full dilation until delivery of infant PELVIS
Linea terminalis
• prolonged in nulliparous patient if duration is >2 hours, or >3
hours with an epidural
• prolonged in multiparous women if duration is >1 hour without
an epidural, or >2 hours with an epidural Ischial spines TRUE
• Median duration is 50 minutes in nulliparas and 20 minutes in PELVIS
multiparas
• Repetitive early and variable decelerations are common
CARDINAL MOVEMENTS Ischial
tuberosity

PELVIC INLET
• Landmarks:
o Posterior
§ Promontory
§ Sacral alae
o Lateral
§ Linea
terminalis
o Anterior
§ Pubic rami
§ Symphysis
pubis
• Diameters:
o True/anatomic conjugate
§ 11 cm
§ Promontory to upper margin of symphysis
o Obstetric conjugate
§ >10 cm
§ Promontory to posterior symphysis
§ Subtract 1.5 to 2 cm from diagonal conjugate
o Diagonal conjugate
§ >11.5 cm
§ Promontory to lower margin of symphysis
§ Measured manually

The cardinal movements of labor. From Blueprints Obstetrics and Gynecology, 7th edition.

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5. EXTENSION
• Extension brought about by two forces:
Adequate diagonal o First force, exerted by the uterus, acts more posteriorly,
conjugate: >11.5 cm o Second force, by the resistant pelvic floor and the
symphysis, acts more anteriorly.
Adequate obstetrical o Base of the occiput is in direct contact with the inferior
conjugate: >10 cm margin of the symphysis pubis

Figure 22-11 (4 & 5)). Cunningham, et al. Williams Obstetrics. 25th ed. 2018

6. EXTERNAL ROTATION
• Corresponds to rotation of the fetal body and serves to bring
2. DESCENT its biacromial diameter into relation with the
• First requisite for birth of the newborn. anteroposterior diameter of the pelvic outlet.
• Nulliparas, engagement may take place before the onset of
labor, and further descent may not follow until the onset of the
second stage
• Multiparas, descent usually begins with engagement
• Descent begins at 7 to 8 cm in nulliparas
• Descent is brought about by one or more of four forces:
o pressure of the amniotic fluid,
o direct pressure of the fundus upon the breech with
contractions
o bearing-down efforts of maternal abdominal muscles, and Figure 22-11 (6). Cunningham, et al. Williams Obstetrics. 25th ed. 2018

o extension and straightening of the fetal body. 7. EXPULSION

• Anterior shoulder appears under the symphysis pubis, and
the perineum soon becomes distended by the posterior
Descent shoulder. After delivery of the shoulders, the rest of the body
HYPERBOLIC quickly passes.
Phase of
maximum
slope

Dilata'on Decelera'on
SIGMOID Accelera'on phase
phase

1st stage 2nd stage

of labor of labor
Figure 22-11 (7 & 8). Cunningham, et al. Williams Obstetrics. 25th ed. 2018
PREPARATORY DILATATIONAL PELVIC
DIVISION DIVISION DIVISION

2 4 6 8 10 12 14 16 GUIDE QUESTION:
3. FLEXION Cardinal Movements
• Occurs as the descending head meets resistance, whether from of Labor
the cervix, pelvic walls, or pelvic floor. https://qrs.ly/6qegx07
• Chin is brought into more intimate contact with the fetal
thorax, and the appreciably shorter sub-occipitobregmatic
DELIVERY PROPER
diameter is substituted for the longer occipitofrontal diameter
Normal spontaneous delivery (NSD)
• Upon crowning, perform modified Ritgen maneuver
o forward pressure on fetal chin through perineum + other
hand to hold sub-occipital region of fetal head against
maternal symphysis
• Delivery of head and anterior shoulder
o Grasp sides of head and perform gentle downward traction
Modified Figure 22-13. Cunningham, et al. Williams Obstetrics. 25th ed. 2018 until anterior shoulder appears under pubic arch
4. INTERNAL ROTATION • Delivery of posterior shoulder and fetal body
• the occiput gradually moves toward the symphysis pubis o Gentle upward traction to deliver posterior shoulder
anteriorly from its original position o Rest of body will follow
• Internal rotation is essential for completion of labor.
STAGE 3
• begins after infant delivery until delivery of placenta
• Placental separation usually occurs within 5–10 minutes of
delivery, up to 30 minutes
• Three signs of placental separation
o cord lengthening
o gush of blood
o uterine fundal rebound
o All signs must be observed prior to delivery of placenta
Figure 22-11 (3). Cunningham, et al. Williams Obstetrics. 25th ed. 2018

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Episiotomy AUGMENTATION OF LABOR
Median Mediolateral • intervening to increase pre-existing contractions
Most common Less frequently used • Oxytocin and amniotomy – used for augmentation of labor
Vertical midline incision from Oblique incision from either • Aggressive augmentation (active management of labor) –
posterior fourchette to 5 o’clock or 7 o’clock position leads to shorter labor times
perineal body and cut laterally
Less painful More painful
Less wound infections More wound infections
DYSFUNCTIONAL LABOR
(no mention in Williams) (no mention in Williams) DISORDERS IN THE FIRST STAGE OF LABOR
Usually results to third- and LATENT PHASE ABNORMALITIES
Rarely needs extensions
fourth-degree extensions • Prolonged latent phase
o >20 hours: nullipara
PERINEAL LACERATIONS o >14 hours: multipara
First-degree (I) Mucosa or skin o Management
Extend into perineal body, spares anal § sedation if no contraindication to delaying
Second-degree (II)
sphincter § amniotomy discouraged
Third-degree (III) Extend through anal canal § CS not routinely done
IIIa <50% of external anal sphincter
ACTIVE PHASE – DILATATIONAL DIVISION
IIIb >50% of external anal sphincter
• protracted active phase dilatation
IIIc both external and internal sphincters
o < 1.2 cm/hr for nullipara
Fourth-degree (IV) Rectal mucosa is entered
o < 1.5 cm/hr for multipara
*“Buttonhole” fourth-degree laceration: a laceration through
o d/t CPD, uterine dysfunction
the rectal mucosa into the vagina, but with the sphincter still
• secondary arrest of dilatation
intact.
o > 2 hrs for nullipara, multipara
o d/t malposition, excessive analgesia, CPD
OB ANALGESIA & ANESTHESIA
• Natural childbirth: Lamaze method (relaxation & breathing ACTIVE PHASE – PELVIC DIVISION
techniques) • protracted descent
• Systemic pharmacologic intervention: e.g. fentanyl, nubain, o < 1 cm/hr for nullipara
morphine sulfate; should not be used close to time of expected o < 2 cm/hr for multipara
delivery because they can cross the placenta à depressed • prolonged deceleration phase
infant; may induce maternal respiratory depression and o > 3 hr for nullipara, >1 hr multipara
increased risk of aspiration • arrest of descent
• Pudendal block: pudendal nerve runs posterior to the ischial o > 1 hr for nullipara, multipara
spine at its juncture with the sacrospinous ligament; gives • failure of descent
perineal anesthesia esp for assisted vaginal deliveries o no descent in deceleration phase or second stage of labor
• Local anesthesia: for repair of vaginal, perineal, and
periurethral lacerations MALPRESENTATIONS
• Epidural and spinal anesthesia BREECH PRESENTATION
o epidural for analgesia throughout the active phase and • occurs in 3–4% of all singleton deliveries
delivery; catheter place at L3 to L4; • Factors associated with breech presentation: previous breech
o spinal anesthesia is given a one-time dose of anesthesia into delivery, uterine anomalies, oligohydramnios, multiple
the spinal canal; more rapid onset; more commonly used for gestation, PPROM, hydrocephalus, anencephaly
CS than for vaginal delivery • Complications: cord prolapse, head entrapment, fetal
o Adverse effects: maternal hypotension from decreased neurologic injury (from vaginal breech delivery)
systemic vascular resistance à decreased placental • Planned vaginal breech criteria:
perfusion à fetal bradycardia; maternal respiratory o Favorable pelvis
depression (for high blockade or up to diaphragmatic
o EFW between 2,000 to 3,800 grams
innervation); spinal headache
o Frank or complete breech
• General anesthesia: for emergency CS (e.g. fetal bradycardia, o Skilled OB
hemorrhage from abruptio placenta or placenta previa, cord o Facilities for possible CS available
prolapse); increased risk of aspiration and hypoxia to mother o Woman is informed of risks
and fetus during induction

INDUCTION AND AUGMENTATION OF LABOR

INDUCTION OF LABOR
• attempt to begin labor in nonlaboring patient
• prior to induction of labor, cervix is ripened via
o Prostaglandin E2 gel – risk of uterine hyperstimulation and
tetanic contractions
o Mechanical dilation
§ Foley – inserted into cervix adjacent to amniotic sac,
inflated, and placed on gentle traction à dilates cervix 2–
3 cm within 4–6 hours, but may stay in up to 12 hours.
CARDINAL MOVEMENTS: BREECH
§ Laminaria – small rods of seaweed placed in cervix 1–2
days prior to procedure à rods absorb water which • Engagement & descent:
dilate cervix o Bitrochanteric diameter in oblique diameter
o Prostaglandin E1 (misoprostol) – effective, but banned in o Anterior hip descends more rapidly
country • Internal rotation:
• Agents for induction of labor o 45-degree rotation of hip
o Oxytocin – synthetic analog is used. Oxytocin is normally o Anterior hip toward pubic arch
released from posterior pituitary that causes uterine o Bitrochanteric diameter in AP diameter of outlet
contractions • Lateral flexion: posterior hip over the perineum
o Amniotomy – amnio hook punctures amniotic sac and • External rotation: fetal back turns anteriorly
releases some amniotic fluid à ensure that prolapse of • Internal rotation: Bisacromial diameter in AP plane
umbilical cord has not occurred • Expulsion: posterior neck under symphysis; head born in
flexion
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BREECH DECOMPOSITION
• Goal: Bring fetal feet
within reach
• Two fingers will
push knee away
from midline
• Spontaneous flexion
of extremity follows
• Foot may be grasped
and brought down
Adapted from Cunningham, et al. Williams Obstetrics. 24th ed. 2014

COMPLETE BREECH EXTRACTION

• Both feet grasped
through the vagina
• Ankles held with
second finger
between them
• Feet brought
through the introitus SYMPHYSIOTOMY
with gentle traction • Delivery of
Adapted from Cunningham, et al. Williams Obstetrics. 25th ed. 2018
entrapped
aftercoming head
PARTIAL BREECH EXTRACTION • Divides
• Breech spontaneously symphyseal
delivered to the cartilage to
umbilicus. widen symphysis
• Posterior hip will deliver pubis up to 2.5
from 6 o’clock position cm
• Anterior hip delivers next
• External rotation to
sacrum anterior DÜHRSSEN INCISION
• Fetal bony pelvis grasped • Incision on the cervix at 2 o’clock,
with both hands, using and at 10 o’clock position
cloth towel (additional at 6 o’clock).
o Fingers rest of • Incisions are placed to minimize
anterior superior iliac bleeding from the laterally located
Adapted from Cunningham, et al. Williams Obstetrics.
crest 24th ed. 2014 cervical branches of the uterine
o Thumbs on sacrum artery.

BREECH DELIVERY STEPS • Management

Consent Secure consent o external cephalic version (37-38 weeks AOG) (37 weeks -
Anesthesia Request for anesthesia Williams)
Episiotomy Do episiotomy § manipulation of breech infant into vertex presentation
Partial breech extraction § if successful, 5% to 10% risk of fetus reverting to breech
Spontaneous
Wait! Don’t pull! presentation
delivery
Hold baby until umbilicus is delivered § If unsuccessful, second attempt under spinal anesthesia
Pinard: lateral rotation of thighs, flex at 39 weeks
Legs
knees § If successful: induce labor or continue pregnancy
Delivery when wing of scapula is seen § If second attempt fails, cesarean delivery
Arms Rotate arm to anterior o Trial of breech vaginal delivery
Loveset maneuver § favorable pelvis
Fetal body rests on arm § flexed head
Nape § estimated fetal weight between 2,000–3,800 g
Apply suprapubic pressure
After-coming head Mauriceau-Smellie-Veit maneuver § frank or complete breech
Fetal fractures/injuries;
Inspect FACE PRESENTATION
perineal lacerations
Document Document • Mentum anterior will allow for vaginal delivery
• If mentum posterior or transverse, fetus must rotate to mentum
• Delivery of the AFTERCOMING head: anterior to deliver vaginally; otherwise, cesarean delivery is
o assistant should apply suprapubic pressure to favor flexion necessary
and engagement of fetal head • Often, anencephalic fetuses have face presentation
o Mauriceau-Smellie-Veit maneuver, or
o Use of Piper forceps BROW
• Spontaneous or assisted breech delivery is acceptable. Fetal • A larger diameter must pass through the pelvis
manipulation applied after spontaneous delivery to the level of • Unless the fetus is extremely small (e.g. preterm) or the pelvis is
umbilicus. particularly large, the brow presentation must convert to vertex
• Nuchal arms may be reduced by Loveset maneuver. or face to deliver vaginally

COMPOUND PRESENTATION
• < 1 in 1,000 pregnancies
• common complication is umbilical cord prolapse
• If upper extremity is presenting + vertex → presenting part may
be gently reduced
• If lower extremity is presenting + vertex → CS delivery
• If lower extremity + breech (footling) → CS delivery
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SHOULDER PRESENTATION DELIVERY
• delivered via cesarean section, due to:
OPERATIVE VAGINAL DELIVERY
o increased risk of cord prolapse
o increased risk for uterine rupture • utilized when hastened delivery is indicated (maternal
o difficulty of vaginal delivery exhaustion,* prolonged second stage,* declining fetal status)
*most common maternal indications – Williams
o For dorsoanterior presentation → vertical hysterotomy
• Vaginal delivery may be done if fetal is small (< 800 g) and the COMPLICATIONS
pelvis is large • Scalp laceration and cephalohematoma – most common
• Subgaleal hemorrhage – a rare complication but can be a
MALPOSITION neonatal emergency
• Left OA (LOA) and right OA (ROA) are normal and commonly Forceps delivery Vacuum delivery
complete internal rotation to OA by late first stage or second Higher rate of
stage Higher rate of facial nerve
cephalohematomas, scalp
• If occiput transverse (OT) or occiput posterior (OP), it is called palsy
lacerations, shoulder dystocia
malposition Higher rate of third- and May lead to rare subgaleal
o persistent OT leading to arrest of labor is more common in fourth-degree lacerations hemorrhages
women with platypelloid pelvis
o OP positions may rotate to OA and slow progress in labor FORCEPS DELIVERY
• Blades conforming to curves of maternal pelvis are placed
SHOULDER DYSTOCIA around fetal head à user guides fetal head to proper descent
• difficulty in delivering shoulders, due to impaction of anterior Type of
Criteria
shoulder behind pubic symphysis Procedure
• Fetal complications: humeral/clavicular fractures, brachial • Scalp is visible at introitus without
plexus nerve injuries (Erb palsy), phrenic nerve palsy, hypoxic separating the labia
brain injury, death • Fetal skull has reached pelvic floor
Outlet
• Turtle sign: incomplete delivery of the head or chin tucking up forceps
• Sagittal suture is in AP diameter or
against the maternal perineum ROA/LOA or ROP/LOP
• Head-to-body delivery time >60 seconds (Spong, 1995) • Fetal head is at or on perineum
• Maneuvers for delivering • Rotation does not exceed 45 degrees
o McRoberts maneuver – hyperflexion of maternal hips • Leading point of fetal skull is ≥ +2 but not on
towards maternal abdomen à flattens lumbar spine and the pelvic floor
ventrally rotates maternal pelvis and symphysis à decrease Low forceps • Rotation < 45 degrees (left or right OA to OA,
pelvic inclination, increase AP diameter (does not increase pelvic or left or right OP to OP)
dimensions but frees up anterior shoulder – Williams)
• Rotation > 45 degrees
o Suprapubic pressure—pressure above maternal pubic Midforceps Station above +2 but head engaged
symphysis to dislodge anterior shoulder from behind pubic High forceps Not included in classification
symphysis
• Prerequisites (FORCEPS):
o Rubin maneuver – pressure on either accessible shoulder
o Fully dilated cervix
toward anterior chest wall of fetus to decrease bisacromial
o Occiput/vertex presentation
diameter and free impacted shoulder
o Ruptured membranes
o Wood corkscrew maneuver – pressure behind posterior
o CPD not suspected
shoulder to rotate infant and free anterior shoulder
o Engaged head, experienced operator, emptied bladder
o Delivery of posterior arm/shoulder – sweeping posterior
o Position known, painless (adequate anesthesia)
arm across chest à rotates bisacromial diameter to an
o Size (fetal weight) estimated
oblique diameter of pelvis à frees anterior shoulder
• Other prerequisites: no fetal coagulopathy/demineralization
o Wider episiotomy
disorder, willingness to abandon operative vaginal delivery,
o Cleidotomy – intentional fracture of fetal clavicle
informed consent
o Symphysiotomy – intentional cutting of pubic symphysis
o Gaskin maneuver – placement of patient on hands and FORCEPS PROCEDURE
knees Ask for
o Zavanelli maneuver – placing infant’s head back into pelvis Assistance
Authorization (consent), Anesthesia, Assistance
and performing cesarean delivery Bladder Empty bladder
Cervix Fully dilated; membranes ruptured
SHOULDER DYSTOCIA Station, position, adequate pelvis, if with risks
Determine
https://qrs.ly/f1egx0k for shoulder dystocia
Equipment Quality, functionality
Phantom application; correct pair
Left blade, left hand, maternal left side
MATERNAL HYPOTENSION Pencil grip, vertical insertion, right thumb
Forceps directing
• During pregnancy, BP is as low as 90/50 mm Hg
Lock & support
• BP < 80/40 mm Hg range can lead to poor maternal and uterine Posterior fontanelle 1 cm above plane of shank
perfusion. Common etiologies are: Sagittal suture perpendicular to plane of shank
o vasovagal events Gentle
o regional anesthesia Traction with contraction or pushing
traction
o overtreatment with antihypertensive drugs Handle Traction along axis of canal; do not elevate too
o hemorrhage elevation early
o anaphylaxis Incision Episiotomy
o amniotic fluid embolism (AFE)
Remove forceps when jaw is reachable
• treatment may vary depending on etiology, but aggressive IV
Jaw Inspect for lacerations
hydration and adrenergic medications are a must (prompt
administration of crystalloids and BLOOD – Williams)
Document
• consider benadryl and epinephrine for possible anaphylactic COMPLICATIONS
reaction to adrenergic medications
• Bruising on the face and head
• if AFE occurs, mortality rate is high; definitive diagnosis of AFE:
• Lacerations to the fetal head, cervix, vagina, and perineum
fetal cells in pulmonary vasculature at autopsy
• Facial nerve palsy
• Skull and/or intracranial damage
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HYSTEROTOMY
GUIDE QUESTION: • Low transverse cesarean incision (Kerr) – preferred and
Classification of Forceps Delivery most common uterine incision; associated with less bleeding
https://qrs.ly/xiegx0q and risk of rupture; may be extended to a J incision, U incision, or
T incision
• Low-vertical incision (Krönig) – confined to the lower uterine
VACUUM-ASSISTED DELIVERY segment (LUS)
• vacuum extractor consists of vacuum cup placed on fetal scalp, • Classical cesarean incision – prone to rupture
and suction device connected to cup to create vacuum o Indications
o Suction is created within a cup placed on the fetal scalp such § Densely adhered bladder
that traction on the cup aids fetal expulsion § Leiomyoma occupies the LUS
o Causes less maternal trauma § Cervical cancer
o Proper cup placement over the flexion point: § Massive maternal obesity precluding safe access to the LUS
approximately 3 cm in front of the posterior fontanel and § Placenta previa with anterior implantation
approximately 6 cm from the anterior fontanel § Back-down transverse lie presentation

CESAREAN DELIVERY
INDICATIONS
• Maternal
o Prior cesarean delivery
o Abnormal placentation (e.g. placenta accrete)
o Prior classical hysterotomy
o Unknown uterine scar type Image from www.cambridge.org
o Uterine incision dehiscence
o Select prior surgeries (full-thickness myomectomy,
PRIOR CESAREAN DELIVERY
trachelectomy, pelvic reconstructive surgery)
o Genital tract obstructive mass (e.g. tumor previa) VAGINAL BIRTH AFTER CESAREAN (VBAC)
o Invasive cervical cancer May be considered in patients with:
o HIV or HSV infection • One prior low-transverse hysterotomy
o Perimortem delivery • Nonrecurring indication for prior CS (e.g. malpresentation,
• Maternal-Fetal placenta previa)
o CPD • Inter-delivery interval >18 months
o Failed OVD • Informed consent
o Placenta previa or placental abruption PRIOR INCISION ESTIMATED RUPTURE RATE (%)
• Fetal Classical 2-9
o Nonreassuring fetal status T-shaped 4-9
o Malpresentation Low-vertical 1-7
o Macrosomia One low-transverse 0.2-0.9
o Congenital anomaly Multiple low transverse 0.9-1.8
o Abnormal umbilical cord Doppler study Prior preterm CS “increased”
o Thrombocytopenia Prior uterine rupture
o Prior neonatal birth trauma • LUS 2-6
• Upper uterus 9-32
• Factors for rapid increase of Caesarean delivery rates
This table is lifted from Williams, although Blueprints states that the rates of
o biologic reasons uterine rupture from those with a prior low-transverse CS delivery is 0.5-0.1%
o higher rates of multiple gestations and classical CS delivery is 6-12%(Page 16). Nonetheless, the main take-
o older population away is to emphasize why we offer VBAC in patients with 1 low transverse CS and
o higher rates of overweight and obesity not in those with other types of incision.
o patient preferences toward elective cesarean, also known as Dr. Fajutagana and Dr. Vidal

cesarean delivery on maternal request (CDMR) UTERINE SCAR RUPTURE

o clinician preferences • Most common sign: nonreassuring FHR pattern with variable
• most common indication for primary cesarean delivery – decelerations that may evolve into late decelerations and
failure to progress in labor (remember the 3 P’s!) bradycardia
(dystocia, fetal jeopardy, or abnormal fetal presentation: most common • Other signs and symptoms: abdominal pain, signs of maternal
indications – Williams) hypovolemia, loss of station by pelvic examination, fetal distress
TECHNIQUES • Management: hysterectomy or suture repair with uterine
preservation
LAPAROTOMY
Vaginal birth after Caesarean delivery (VBAC)/ Trial of labor
after Caesarean delivery (TOLAC)
Increased Success of Increased Risk of Uterine
TOLAC Rupture
• More than one prior cesarean
delivery
• Prior vaginal birth
• Prior classical cesarean
• Prior VBAC
• Induction of labor
• Nonrecurring indication
• Use of prostaglandins
for prior C/S (herpes,
Image uploaded by Ylva Vladic Stjernholm
• Use of high amounts of
• Suprapubic transverse incision previa, breech)
oxytocin
o Follow Langer lines; more commonly associated with • Presentation in labor at:
• Time from last cesarean
bleeding, hematoma and nerve damage o > 3 cm dilated
< 18 mos
§ Pfannenstiel – skin incised in a transverse, slightly curvilinear o > 75% effaced
• Uterine infection at time of
manner 3cm above the border of the symphysis pubis
last cesarean
§ Maylard – main difference with Pfannenstiel is that rectus
Decreased Success of Decreased Risk of Uterine
abdominis muscle bellies are transected in this technique
TOLAC Rupture
§ Joel-Cohen – greater use of blunt dissection; a straight 10-
cm transverse skin incision is made 3 cm below the ASIS • Prior C/S for cephalopelvic
§ Misgav Ladach – differs from Joel-Cohen in that the disproportion • Prior vaginal birth
peritoneum is entered bluntly • Induction of labor
Factors affecting outcomes of VBAC/TOLAC. From Blueprints Obstetrics and Gynecology, 7th edition.
• Midline vertical
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MANAGEMENT OF PRETERM LABOR
GUIDE QUESTION:
TOCOLYSIS
Prior Caesarian
• prevent contractions and progression of labor
Section
• goal: delay delivery by at least 48 hours
https://qrs.ly/2regx17
• steroids: enhance fetal lung maturity and reduce risk of preterm
delivery complications
COMPLICATIONS OF LABOR AND DELIVERY • Indications for emergent delivery in preterm labor
o Chorioamnionitis
PRETERM LABOR (PTL)
o non-reassuring fetal testing
• labor before week 37 o significant placental abruption
• Diagnosis: cervical change upon examination
• Differs from cervical insufficiency (silent, painless dilation, and TOCOLYTICS
effacement of cervix) • goal: decrease or halt cervical change due to contractions
o Both can cause preterm delivery (leading cause of fetal • for preterm contractions without cervical change: hydration can
morbidity and mortality in US) decrease number and strength of contractions
• Increased rates due to iatrogenic deliveries, and declined due to • Dehydration increases levels of vasopressin or antidiuretic
policy interventions that avoid unindicated iatrogenic delivery hormone (ADH) à bind to oxytocin receptors à contractions
• Preterm – infants born before 37 weeks’ gestation • Hydration decreases ADH levels à decrease contractions
o extremely preterm (< 28 weeks)
o very preterm (28 to < 32 weeks) Calcium channel blockers (Nifedipine*)
o moderate to late preterm (32 to < 37 weeks) • Calcium channel blockers decrease calcium influx into smooth
• Infant classification by birth weight muscle cells à diminished uterine contractions
o low birth weight (LBW) < 2,500 g (1500 – 2500 g – Williams) • Nifedipine (peripheral vasodilator) side effects: headaches,
o very LBW < 1,500 g (1000 – 1500 g – Williams) flushing, dizziness
o extremely LBW, < 1,000 g (500 – 1000 g – Williams) • Contraindications:
o preload-dependent cardiac lesions and hypotension
CAUSES o use with caution in left ventricular dysfunction
• Uterine distension o use with caution if given with magnesium sulfate (synergistic
o E.g. multifetal pregnancy, hydramnios effect results in respiratory depression)
o Early uterine distension acts to initiate expression of Prostaglandin inhibitors (Indomethacin*)
contraction-associated proteins (CAPs) in the myometrium • prostaglandins increase intracellular calcium level and
• Maternal-fetal stress myometrial gap junction function à increase myometrial
o E.g. Nutrient restriction, obesity, diabetes, psychological stress contractions
o Premature activation of the placental-adrenal endocrine • anti-prostaglandin agents inhibit contractions and may halt labor
axis → increases placental-derived corticotropin-releasing
• Indomethacin—non-steroidal anti-inflammatory drug (NSAID)
hormone (CRH) → early loss of uterine quiescence
that blocks cyclooxygenase, decreases level of prostaglandins
• Premature cervical changes
• Side effects:
o In the epithelial or stromal extracellular matrix
o associated with premature constriction of ductus arteriosus,
o Reduced mechanical competence of the cervix
pulmonary hypertension, and oligohydramnios
• Infection o increased risk of necrotizing enterocolitis and
(1) Transplacental transfer of maternal systemic infection intraventricular hemorrhage in premature fetuses exposed
(2) Retrograde flow of into the peritoneal cavity via the fallopian tubes to indomethacin ≤ 48 hours of delivery
(3) Ascending infection with bacteria from the vagina and
• Contraindications
cervix – the most common entry route
o Platelet/hepatic/renal dysfunction
• Risk factors o gastrointestinal ulcerative disease
o preterm rupture of membranes (ROM); o asthma
o chorioamnionitis;
o multiple gestations; Magnesium sulfate
o uterine anomalies, such as a bicornuate uterus; • decreases uterine tone and contractions by acting as calcium
o previous preterm delivery; antagonist and membrane stabilizer
o maternal prepregnancy weight less than 50 kg; • Side effects:
o placental abruption; o flushing, headaches, fatigue, and diplopia
o maternal disease, including preeclampsia, infections, intra- o > 10 mg/dL: respiratory depression, hypoxia, cardiac arrest
abdominal disease or surgery; o 6–10 mg/dL: deep tendon reflexes (DTRs) are depressed
o substance abuse; and o serial DTR exams: quick assessment for magnesium toxicity
o low socioeconomic status. o pulmonary edema, may be secondary to concomitant IV fluid
• Short-term risks of preterm delivery given to PTL patients
o respiratory distress syndrome (RDS) o bone thinning and fractures if administered >5-7 days – Williams
o intraventricular hemorrhage • Administration: loaded as 6 g bolus over 20 minutes, then 2
o neonatal sepsis g/hour continuous infusion. Use slower infusion in renal
o necrotizing enterocolitis insufficiency.
• Long-term risks of preterm delivery
o bronchopulmonary dysplasia and asthma β-Mimetics (terbutaline*, ritodrine, isoxsuprine)
o neurologic disorders (e.g. cerebral palsy, behavioral • Myosin light-chain kinase (MLK) regulates contraction, which is
problems, learning disabilities) activated by calcium ions–calmodulin interaction
o retinopathy of prematurity (considered short-term • increased cAMP level à calcium sequestered in sarcoplasmic
complication – Williams) reticulum à decreased free calcium ions and uterine
o hearing loss contractions
• Prognosis: > 50% mortality rate for birth at 23 weeks’ gestation, • increased β-agonists à convert ATP to cAMP à activate β2
while mortality rate slightly higher than full-term neonates for receptors on myometrial cells
birth after week 34 • ritodrine and terbutaline: β-mimetics used for PTL
• Previous preterm delivery** – greatest risk factor • Side effects:
Second birth o tachycardia, headaches, and anxiety
Birth outcome o possible pulmonary edema and maternal death (rare)
≤34 weeks AOG
First birth ≥35 weeks 5% o FDA black box warning for pulmonary edema: use of
First birth ≤34 weeks 16% terbutaline IV for >24–48 hours, and ritodrine (pulled out)
First, second birth ≤34 weeks 41% o Subcutaneous terbutaline: stops contractions in uterine
Probability of recurrence of a next preterm labor based on prior outcomes. From Williams’ Obstetrics, 24th edition. hypertonicity leading to abnormal fetal heart tracing

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• Oxytocin antagonists (atosiban*) • < 34 weeks: expectant management; give antibiotics to
• selective oxytocin–vasopressin receptor antagonists, prolonger latency period before onset of labor
theoretically effective tocolytic with minimal side effects o ampicillin with erythromycin (48 hours IV followed by 5
• small clinical studies with no improvement in outcomes days of oral erythromycin and amoxicillin) or azithromycin
(oral) once and 48 hours of IV ampicillin and 5 days of oral
amoxicillin
PRETERM LABOR • patients may elect for spontaneous labor, despite increased risk
https://qrs.ly/apegx1a of infection
o Acceptable if no evidence of infection during presentation
and reassuring fetal status, and patient is counseled
regarding risks of prolonged PROM
PRETERM, PREMATURE RUPTURE OF
MEMBRANES (PPROM) FETAL COMPLICATIONS OF PREGNANCY
FETAL GROWTH DISORDERS
GUIDE QUESTION:
PPROM
https://qrs.ly/dwegx1f GUIDE QUESTION:
IUGR
https://qrs.ly/xbegx23
• preterm rupture of membranes – ROM before week 37
• premature rupture of membranes (PROM) – ROM before
• Phases of fetal growth
onset of labor (8%)
o initial phase of hyperplasia – first 16 weeks; characterized
• preterm premature rupture of membranes (PPROM) – both
by rapid increase in cell number
preterm and premature rupture of membranes occur
o second phase – up to 32 weeks; includes cellular
• prolonged rupture of membranes: ROM lasting >18 hours hyperplasia and hypertrophy
before delivery o after 32 weeks – fetal mass accrues by cellular hypertrophy;
wherein most fetal fat and glycogen are accumulated
PRETERM RUPTURE OF MEMBRANES
• Spontaneous rupture of fetal membranes before week 37:
common cause of PTL, preterm delivery, and chorioamnionitis SMALL FOR GESTATIONAL AGE (SGA) FETUS
• Without intervention, ~50% ROM lead to labor within 24 ETIOLOGIES OF SGA FETUS
hours, and ≤ 75% within 48 hours DECREASED GROWTH POTENTIAL
• gestational age at ROM rates are inversely correlated; ROM at < • usually start small and stay small
26 weeks are more likely to gain additional week compared with • congenital abnormalities cause ~10–15% of SGA infants
> 30 weeks • Many intrauterine infections—particularly cytomegalovirus
• prolonged PPROM: associated with increased risk of (CMV) and rubella—10–15% SGA of infants
chorioamnionitis, abruption, and cord prolapse • Exposure to teratogens (most commonly alcohol and
cigarettes), most chemotherapeutic agents, and other drugs
DIAGNOSIS OF PROM • parental stature or genetic potential – 10% of SGA infants
• Evaluate increased vaginal discharge
• pooling on speculum examination INTRAUTERINE GROWTH RESTRICTION (IUGR)
• positive nitrazine and fern tests • progressively fall off growth curve
• If tests are equivocal: perform ultrasound to examine amniotic • symmetric growth restriction
fluid level o early insult could result in decrease in cell number prior to
• Amnisure test 20 weeks (hyperplastic growth)
• If still unconfirmed, perform amniocentesis dye test and observe o proportionately small
if dye leaks into vagina (tampon test) o occurs early (↓ cell size AND number) with proportionate
• If suspected chorioamnionitis: check maternal temperature, decrease in length, weight, and head circumference (all
WBC count, uterine tenderness, and fetal heart tracing for signs parameters at < 10th percentile)
of infection o likely due to intrinsic growth problems (aneuploidy,
syndromes, congenital infections)
MANAGEMENT OF PRETERM ROM o more likely represented normal, genetically determined
• prematurity risk ≈ infection risk between 32–36 weeks small stature
o up to this point, risk of prematurity drives management • asymmetric growth restriction
o after this point, risk of infection motivates delivery o later pregnancy insults lead to decreased nutrition and
o most common practice: delivery at 34 weeks’ gestation oxygen after 20 weeks (hypertrophic growth)
• For PPROM <34 weeks: antibiotics lead to longer latency period o abdominal circumference > head circumference
before onset of labor o 2/3 of IUGRs
o ampicillin with erythromycin (48 hours IV followed by 5 o might follow a later pregnancy insult (↓ cell size, NOT
days of oral erythromycin and amoxicillin) or azithromycin number);
(oral) once and 48 hours of IV ampicillin and 5 days of oral o disproportionately lagging abdominal growth compared
amoxicillin is recommended with head growth;
• Tocolysis: little to no benefit for PPROM, and may be harmful in o HC remains appropriate for aging (due to “brain sparing” or
chorioamnionitis preferential shunting of oxygen and nutrients to the brain)
o tocolysis: used for 48 hours at earlier GA to gain time to while fetal abdominal circumference is reduced (reflects
administer course of corticosteroids liver size);
• Use corticosteroids up to 36 weeks for fetal benefits, despite o caused by extrinsic growth problems (e.g. placental
immunosuppression concern insufficiency in the 3rd trimester)
SYMMETRICAL ASYMMETRICAL
PREMATURE RUPTURE OF THE MEMBRANES (PROM) • Proportionately small • Disproportionately lagging
• Early insult: abdominal growth
• PROM at term complicates 8% of pregnancies
o ↓ cell number & size* • Late insult:
• Most significant risk: development of chorioamnionitis (risk o Proportionate reduction o ↓ cell size*
increases with length of ROM) of BOTH head & body size o ↓AC
• Normal, genetically • Brain sparing: protected from
MANAGEMENT OF PREMATURE ROM determined small stature full effects of growth restriction
• Antibiotics are recommended for prolonged ROM and unknown • Significant disordered growth
group B streptococcus (GBS) patient status *Fetal growth can be divided into 2 phases: 1) prior to 20 weeks: primarily
• if ROM occurs > 34 weeks: labor is induced/augmented hyperplastic or ↑cell number, 2) after 20 weeks: primarily hypertrophic or ↑cell size
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DIAGNOSIS OF SGA FETUS OLIGOHYDRAMNIOS
• Oligohydramnios and SGA: fundal heights less than expected • + absence of ROM à 40-fold increase in perinatal mortality
o If fundal height < 3 cm than expected, estimate fetal growth • during labor, associated with nonreactive NSTs, fetal heart rate
via ultrasound (FHR) decelerations, meconium, and cesarean delivery due to
o fundal height to screen SGA or LGA: sensitivity < 50% and non-reassuring fetal testing
positive predictive value < 50%
• verify accuracy of pregnancy’s dating ETIOLOGY OF OLIGOHYDRAMNIOS
o serial ultrasound scans for growth every 2 to 3 weeks • Decreased production of amniotic fluid
• Doppler of umbilical artery: to differentiate IUGR fetuses o congenital abnormalities of genitourinary tract
o Diastolic flow should never be absent/reversed o uteroplacental insufficiency
o Manage to term SGA fetus with normal Doppler values, • Increased withdrawal of amniotic fluid
whereas deliver early those with abnormal Doppler values o Rupture of membranes* – most common

MANAGEMENT OF SGA FETUS DIAGNOSIS OF OLIGOHYDRAMNIOS

• Address malnutrition, smoking or alcohol use • AFI is <5; some use deepest vertical pocket of fluid <2 cm
• Low-dose aspirin: history of placental insufficiency, • R/o if
preeclampsia, collagen vascular disorders, or vascular disease o measuring size less than dates
• Heparin + corticosteroids: prior placental thrombosis, o with a history of ruptured membranes
thrombophilias, or antiphospholipid antibody syndrome o with suspicion of IUGR
(aspirin, heparin is ineffective according to ACOG – Williams) o postterm pregnancy
(corticosteroids before 34 weeks AOG – Williams) MANAGEMENT OF OLIGOHYDRAMNIOS
• For nonreassuring fetal status, delivery • If pregnancy at term or postdate, induce labor
• If undelivered, fetal surveillance every 2 to 3 weeks • If fetus with congenital abnormalities, refer patient to maternal–
(every 3-4 weeks – Williams) fetal medicine care for genetic counseling and prenatal
diagnosis
LARGE FOR GESTATIONAL AGE (LGA) FETUS • If severely preterm patients with no other etiology, managed
• LGA – EFW greater than the 90th percentile expectantly with frequent antenatal fetal testing
• Macrosomia – birth weight > 4,500 g • If ROM at term, induce labor if not already in labor
• Mothers with LGA or macrosomic fetuses: increased risk for CS o If meconium or frequent variable decelerations in FHR,
delivery, perineal trauma, and postpartum hemorrhage perform amnioinfusion to increase the AFI
o amnioinfusion dilutes meconium in amniotic fluid à
ETIOLOGY OF LGA FETUS decreased risk of meconium aspiration syndrome
• for fetal macrosomia: classic risk factor is preexisting or o
gestational diabetes mellitus POLYHDRAMNIOS
• Maternal obesity (BMI > 30 or weight > 90 kg) is a “Hydramnios” is used in Williams.
significant risk factor • AFI greater than 20 or 25 (≥24 or 25 – Williams)
• History of LGA infant delivery: increased risk in future • present in 2% to 3% of pregnancies
pregnancies • associated with maternal diabetes and malformations such as
• Increased risk in postterm pregnancies neural tube defects, obstruction of fetal alimentary canal, and
• Multiparity and advanced maternal age are also risk factors fetal hydrops
DIAGNOSIS OF LGA FETUS • majority of cases have no associated diagnosis or cause
• large fetus: size > dates on measurement of fundal height,
ETIOLOGY OF POLYHYDRAMNIOS
Leopold examination may be used by late 3rd trimester
o ultrasound for EFW: fundal height > date by more than 3 cm • more common in pregnancies complicated by
• Verify pregnancy dating o hydrops secondary to high-output cardiac failure
• EFW by ultrasound in late 3rd trimester – patient with diabetes o diabetes – increased circulating glucose can act as osmotic
or previous LGA infant diuretic in fetus
o monozygotic multiple gestations à twin-to-twin transfusion
MANAGEMENT OF LGA FETUS syndrome with polyhydramnios around one fetus and
• LGA prevention: counseling about goals for gestational weight oligohydramnios around the other
gain, including diet and exercise in pregnancy • associated with increase in congenital anomalies
• type 1 and 2 pregestational diabetes or gestational diabetes: risk o obstruction of gastrointestinal tract (e.g., tracheoesophageal
factors for LGA fetuses; benefit from control of blood glucose fistula, duodenal atresia) à fetus unable to swallow amniotic
level during pregnancy fluid à polyhydramnios
• Maternal obesity: independent risk factor for LGA infants;
encouraged to lose weight before conception DIAGNOSIS OF POLYHYDRAMNIOS
• size greater than dates
GUIDE QUESTION: • routine screening of diabetic or multiple-gestation pregnancies,
Disorders of Amniotic Fluid or during an ultrasound performed for other reasons
https://qrs.ly/a4egx24 • Polyhydramnios classification
mild (AFI 25 – 29.9 cm or DVP 8 – 9.9 cm – Williams)
moderate (AFI 30 – 34.9 cm or DVP 10 – 11.9 cm – Williams)
severe (AFI ≥35 cm or DVP ≥12 cm – Williams)
DISORDERS OF THE AMNIOTIC FLUID
• reaches ~800 mL (max volume) at ~28 weeks MANAGEMENT OF POLYHYDRAMNIOS
• fluid balance maintained by: • evaluate for malpresentation (increased risk) during labor
o production of fetal kidneys and lungs • perform ROM in controlled setting only if head is truly engaged
o resorption by fetal swallowing, and interface between in pelvis (increased risk of cord prolapse)
membranes and placenta; disturbance in any of these à • (may do amnioreduction – Williams)
possible pathologic change in amniotic fluid volume
• Ultrasound is used to measure amniotic fluid index (AFI),
calculated by dividing maternal abdomen into quadrants,
measuring largest vertical pocket of fluid in each quadrant in
centimeters, and summing them
o AFI < 5: oligohydramnios
o AFI > 24-25: polyhydramnios

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OLIGOHYDRAMNIOS POLYHYDRAMNIOS
Single deepest pocket (SDP) of SDP of ≥ 8 cm, or
< 2cm, or AFI ≥ 25 cm
Amniotic fluid index (AFI) AFI (cm) SDP (cm)
Definition < 5 cm Mild 25-30 8-12
Moderate 30-35 12-16
Anhydramnios – no measurable pocket of AF Severe >35 >16
• Fetal death • Maternal
• IUGR • Overdistension of the uterus → mother may suffer from dyspnea,
• CS for Non-reassuring FHR pattern orthopnea, pronounced edema
• Preterm delivery • Placental abruption
• Anatomical & functional abnormalities (e.g. • Dysfunctional labor
Complication
skeletal deformations, contractures, and • Postpartum hemorrhage
pulmonary hypoplasia) • Fetal
• Meconium aspiration • Preterm labor
• SGA baby
• Perinatal mortality
• 6 Major Causes (POGS, 2015) • May be due to decreased fetal swallowing/diminished absorption or
1. Underlying fetal abnormality that precludes increased fetal excretion
normal urination (e.g., Potter syndrome, • Idiopathic
polycystic kidney disease, obstruction of the • Congenital anomalies & genetic disorders
genitourinary system) o CNS abnormalities (e.g. spina bifida, anencephaly – from defective
2. PPROM – rupture of membranes is the most swallowing, transudation of CSF & fetal polyuria from lack of ADH)
common cause of oligohydramnios o GIT – esophageal/duodenal atresia
Patho- 3. Isolated / idiopathic form o Cerebral & neuro-muscular disorders
physiology/ 4. Uteroplacental insufficiency - e.g., from o Chromosomal abnormalities
Etiology preeclampsia • DM – fetal polyuria from hyperglycemia and increased osmotic diuresis
5. A complication of multiple pregnancies – i.e., • Multifetal gestation – i.e. twin-to-twin transfusion, twin-reversed
twin-to-twin transfusion arterial perfusion
6. Iatrogenic – e.g., postchorionic villous • Fetal anemia – increased UO from increased cardiac output
sampling, exposure to angiotensin-receptor • Placental tumor – e.g. chorangioma; due to increased transudation from
blockers, ACE inhibitors & NSAIDs enlarged vessels
• Others – fetal hydrops, Bartter syndrome, congenital viral infections (TORCH)
• Methods for increasing AFI: • May do amnioreduction if symptomatic
1. Amnioinfusion: used intrapartum to resolve
Management
variable FHR decelerations
2. Maternal hydration

RH INCOMPATIBILITY SENSITIZED Rh-NEGATIVE PATIENT

• antibody titers ≥ 1:16: associated with fetal hydrops
AND ALLOIMMUNIZATION o Follow-up titers approximately every 4 weeks
o < 1:16, the pregnancy can be managed expectantly
GUIDE QUESTION:
o > 1:16 or greater, begin serial amniocentesis at 16–20 weeks
Rh Incompatibility
§ Rh negative, pregnancy can be followed expectantly
and Alloimmunization
https://qrs.ly/wregx29 § Rh positive, screen fetal anemia using fetal middle
cerebral artery (MCA) Doppler measurements
• sensitization to Rh antigen • Spectrophotometry – light absorption (ΔOD450) by bilirubin
o woman is Rh (-) and fetus is Rh (+)in prior or current will rise in amniotic fluid with increasing fetal hemolysis; plot
pregnancy measurements on Liley curve
o prior blood transfusion • fetal intraperitoneal transfusion, percutaneous umbilical
• In Rh (+) fetus, IgG antibodies cross placenta and cause blood sampling (PUBS) and intrauterine transfusion (IUT):
hemolysis of fetal RBCs treatment for fetal anemia (only if fetal hematocrit is <30% - Williams)
• ABO incompatibility decreases risk of sensitization, due to anti-
A or anti-B antibodies-mediated destruction of RH (+) fetal cells INTRAUTERINE FETAL DEMISE (IUFD)
• 0.5% to 1% of pregnancies and ~1:1,000 term births
COMPLICATIONS OF RH INCOMPATIBILITY • no explanation, usually attributed to “cord accident”
• sensitized patients with Rh-positive fetuses à antibodies cross • retained IUFD greater than 3–4 weeks à possible
placenta à hemolysis hypofibrinogenemia secondary to release of thromboplastic
o resulting anemia à increased extramedullary production of substances from decomposing fetus à disseminated
fetal red cells (erythroblastosis fetalis or fetal hydrops) intravascular coagulation (DIC)
o anemia can cause syndrome with hyperdynamic state, high-
output heart failure, diffuse edema, ascites, pleural effusion, DIAGNOSIS OF IUFD
and pericardial effusion • Prior to 20 weeks AOG – lack of uterine growth or cessation of
o Bilirubin, a breakdown product of RBCs, can cause jaundice symptoms of pregnancy; confirm with serial decrease in hCG
and neurotoxic effects in neonate (UTZ is better – for early pregnancy loss, sonographic findings
include
MANAGEMENT OF RH INCOMPATIBILITY CRL ≥7 mm and no heartbeat
UNSENSITIZED Rh-NEGATIVE PATIENT MSD ≥25 mm and no embryo
• If Rh (-) patient with negative antibody screen, avoid Initial UTZ = gestational sac, (+) yolk sac, then ≥11 days later (-)
sensitization during pregnancy embryo with heartbeat
• If patient may be exposed to fetal blood, give RhoGAM (anti-D Initial UTZ = gestational sac, (-) yolk sac, then ≥14 days later (-)
immunoglobulin, Rh IgG) at 28 weeks and postpartum if embryo with heartbeat
neonate is Rh (+); • After 20 weeks AOG – lack of uterine growth or absence of fetal
o standard dose of RhoGAM (0.3 mg Rh IgG) (per 30 mL of fetal movement noted by mother; confirm with UTZ
whole blood or 15 mL of fetal RBC to be neutralized – Williams) MANAGEMENT OF IUFD
• Kleihauer–Betke test: if placental abruption or any
• Delivery – best treatment
antepartum bleeding occurs; if amount of fetal RBCs > capacity
• Prior to 20 weeks – D&E or mifepristone + misoprostol
of single RhoGAM dose, give additional dosages
• After 20 weeks – induction of labor
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POSTTERM PREGNANCY o vertex then breech (40%)

§ trial of labor if presenting twin is larger
• Beyond 42 weeks AOG or 294 days after LMP
§ breech extraction of second twin is favorable
• 3% to 10% of all pregnancies will go postterm o breech then vertex
• complications of pregnancy may increase after 40 or 41 weeks § vertex second twin usually with abruptio
of gestation § CS if cervix is no longer full dilated or if fetal vertex is
higher than station 0
ETIOLOGY OF POSTTERM PREGNANCY o both breech
• Inaccurate dating – most common • triplets and above: Caesarean delivery
• More common in overweight, obese women • Non-vertex presenting twins compromise 20% (breech-breech
• anencephaly, fetal adrenal hypoplasia, and absent fetal pituitary and breech-vertex combined). Non-vertex presenting twins are
à decrease in circulating estrogens usually delivered via cesarean section. (Blueprints)

DIAGNOSIS OF POSTTERM PREGNANCY COMPLICATIONS OF MULTIFETAL PREGNANCY

• best diagnosis: certain LMP, 1st/2nd trimester UTZ-compatible • Preterm delivery
o Average AOG at age of delivery for twins: 36-37 weeks
MANAGEMENT OF POSTTERM PREGNANCY o for triplets: 33 and 34 weeks
• NST at 41 weeks; twice done at 42 weeks o for quadruplets: 28 and 29 weeks.
• Induction if nonreassuring fetal status OR electively at 41 weeks • Twin-to-twin transfusion syndrome
o secondary to unequal flow within vascular communications
GUIDE QUESTION: between twins à one twin is donor and the other recipient
Multifetal Gestation o managed with serial amnioreduction or laser coagulation of
https://qrs.ly/wgegx2c vascular connections (if severe; controversial if Quintero
Stage I TTSS) ; termination is an option if severe (before 20
weeks AOG – Williams)

MULTIFETAL GESTATION OBSTETRIC HEMORRHAGE

• rate of twinning is ~1:80 pregnancies, with 30% of those
TRADITIONALLY CLASSIFIED BASED ON TIMING:
monozygotic
• frequency of dizygotic twins is lowest in Asians, intermediate in • Antepartum hemorrhage
Caucasians, and higher in African Americans OBSTETRIC CAUSES
Placental abruption (30%), placenta previa
• rate of naturally occurring triplets is ~1:7,000–8,000 Placental
(20%), vasa previa
pregnancies
Maternal Uterine rupture
Fetal Fetal vessel rupture
PATHOGENESIS OF TWINNING
NON-OBSTETRIC CAUSES
MONOZYGOTIC TWINNING Severe cervicitis, polyps, cervical
• from division of fertilized ovum or cells in embryonic disk Cervical
dysplasia/cancer
• If separation occurs before differentiation of trophoblast, Vaginal/vulvar Lacerations, varices, cancer
two chorions and two amnions (Di-Di) result Hemorrhoids, congenital bleeding disorder,
(Within first 72 hrs – Williams) Other
trauma, hematuria
• if separation occurs after trophoblast differentiation and before • Postpartum hemorrhage
amnion formation (days 3 to 8), one placenta, one chorion, and o Early postpartum hemorrhage: first 24 hours
two amnions (Mo-Di) result (Day 4-8 – Williams) o Late postpartum hemorrhage: after the first 24 hours to 12
• Division after amnion formation leads to single placenta, one weeks after delivery
chorion, and one amnion (Mo-Mo) (days 8 to 13) (Day 8-12 – o Occur in response to an abnormality of one of 4 basic
Williams) and, rarely, conjoined or “Siamese” twins (days 13 processes (“4 T’s”)
to 15). 1. Tone – uterine atony
• cell division beyond day 15 or 16 results in singleton fetus 2. Tissue – retained placental tissue or blood clots
3. Trauma – genital tract lacerations or hematomas
DIZYGOTIC TWINNING 4. Thrombin - coagulopathy
• from fertilization of two ova by two sperm
• Risk factors ANTEPARTUM HEMORRHAGE
o more common in Africans PLACENTA PREVIA
o Clomiphene citrate (fertility enhancer) increases rate of
• ≤6% display sonographic evidence of placenta previa on early
dizygotic twinning up to 8%
ultrasound
o multiple embryos in IVF (improve pregnancy rate) increase
• ~3.5–5 per 1,000 births account for ~20% of antepartum
rates of twinning and higher order multiple gestations (30–
hemorrhage
40%)
• occurs in ~1–5% patients with prior cesarean section
o risk of concurrent placenta accreta is ~3%, 11%, 40%, 61%,
DIAGNOSIS OF MULTIFETAL GESTATION
and 67% for one, two, three, four, and five prior cesarean
• Ultrasound sections, respectively
• PE: rapid uterine growth, excessive maternal weight gain, or
palpation of three or more fetal (cranium and breech) DEFINITION OF TERMS
• Labs: elevated β-hCG, human placental lactogen, and maternal • Placenta previa – abnormal implantation of placenta over
serum α-fetoprotein for gestational age (levels may vary internal cervical os (new term encompassing complete or partial
considerably and overlap with those of singletons – Williams) previa – Williams)
• after delivery of the first fetus with palpation of the aftercoming • Complete previa – placenta completely covers internal os
fetus • Partial previa – placenta covers portion of internal os
• Imaging: • Marginal previa – edge of placenta reaches margin of os
o Mo-Di: T sign – juxtaposed amniotic sacs • Low-lying placenta – implantation in lower uterine segment in
o Di-Di: twin peak sign – fusion of two placentae proximity but not extending to internal os (new term encompassing
o Mo-Mo: no intertwin membrane marginal previa or low-lying placenta – Williams)
• Bleeding results from disruptions in placental attachment and
MANAGEMENT OF MULTIFETAL PREGNANCY thinning of lower uterine segment during third trimester. Blood
• Selective reduction down to twins or singleton delivery irritates uterus à stimulates uterine contractions à stimulates
• four possibilities for twin presentation placental separation and bleeding
o both vertex (40%) à trial of labor
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• cervix dilates and effaces in labor à placental separation and • Mode of delivery
unavoidable bleeding à profuse hemorrhage and shock à o asymptomatic without bleeding: outpatient management
significant maternal and fetal morbidity and mortality until cesarean delivery (elective CS by 34 – 37 weeks
o Two-thirds with placenta previa and associated accreta according to SMFM – Williams)
require hysterectomy at delivery (peripartum o Unstoppable labor, fetal distress, and life-threatening
hysterectomy) hemorrhage: immediate cesarean delivery
o placenta accreta may cause spontaneous uterine rupture in o complete/partial placenta previa: delivery by cesarean
second/third trimester à intraperitoneal hemorrhage o low-lying placenta/marginal previa (<2 cm from internal os),
o average blood loss at delivery in placenta accreta is 3,000– and with placental edge < 1–2 cm: delivery by cesarean,
5,000 mL given risk of antepartum hemorrhage
o morbidity and mortality is associated with preterm delivery
(cause of 60% perinatal deaths) PLACENTA ACCRETA SPECTRUM
RISK FACTORS PATHOLOGY
• Maternal age (>35 y/o) • Abnormally firm adherence to myometrium:
• Multiparity o partial or total absence of the decidua basalis and
• Prior uterine surgery (e.g., CS, myomectomy) o imperfect development of the fibrinoid or Nitabuch layer
• Recurrent abortions • Microscopically, placental villi are anchored to muscle fibers
• Smoking rather than to decidual cells.
• Multiple gestation • Cytotrophoblasts may control decidual invasion through factors
• Erythroblastosis such as angiogenesis and growth expression
• History of placenta previa
• Uterine leiomyomas
• Infertility treatment
• Elevated maternal serum AFP (MSAFP) levels
• Assisted reproductive technology used for conception

FETAL COMPLICATIONS
• Preterm delivery and its complications
• PPROM
• IUGR
• Malpresentation
• Congenital abnormalities
PATHOPHYSIOLOGY
• Most likely due to development of lower uterine segment CLASSIFICATION
• Uterine scarring: implantation in lower uterine segment • Depth of invasion:
• >90% low-lying placentas moves away from cervix and out of o Placenta accreta: villi are attached to the myometrium.
lower uterine segment to better vascularized (trophotropism) o Placenta increta: villi actually invade the myometrium, and
o Placenta percreta: villi that penetrate through the
DIAGNOSIS OF PLACENTA PREVIA
myometrium and to or through the serosa
• painless vaginal bleeding. • Extent of adherence:
• First episode or “sentinel” bleed at >28 weeks o Total accreta: abnormal adherence may involve all lobules.
• Placenta accreta (and increta): usually asymptomatic, may o Partial accreta: involves few to several cotyledons
present with hematuria or rectal bleeding if percreta into o Focal accreta: a single lobule is abnormally attached
bladder or rectum
• PE: RISK FACTORS
o soft, spongy tissue in cervix upon examination • Two (2) most important risk factors:
o varices in lower uterine segment or cervix upon speculum o Previa
examination or palpation o Prior cesarean delivery:
• Imaging: § Stat CS > elective CS
o placenta previa: ultrasonography (sensitivity > 95%) § Classical CS
o placenta accreta: ultrasound (sensitivity 77–87%) • Maternal serum:
MANAGEMENT OF BLEEDING PLACENTA PREVIA o MSAFP levels > 2.5 MoM (8x)
o hCG levels > 2.5 MoM (4x)
• Stabilize patient – continuous CTG, IV with two large-bore
• Advanced maternal age with placenta previa
catheters, hematological evaluation with fibrinogen/D-
dimer/fibrin split products • Prior myomectomy or reconstructive surgery
• Kleihauer-Betke test for Rh (-) women – determines extent of • Asherman’s syndrome
fetomaternal transfusion for possible RhoGAM administration • Submucous leiomyomata
• Prepare for catastrophic hemorrhage • Multiparity (>G6)
o Hospitalization DIAGNOSIS
o limited activity (pelvic rest – Williams)
• In some women with no associated previa, accreta may not be
o Hct monitoring (must be >25%)
identified until the third-stage labor
• Prepare for preterm delivery
• Diagnosed via ultrasound with Doppler studies
o steroids: for vaginal bleeding at 24–36 weeks’ gestation to
o Loss of hypoechoic retroplacental zone, which
promote fetal lung maturity
correspond to the decidua basalis, myometrium, and dilated
o Magnesium sulfate: for neuroprotection at 24–32 weeks if
venous channels
delivery is occurring within 24 hours
o Progressive thinning of the retroplacental hypoechoic zone
o Before 32 weeks AOG
to <2mm on serial exams
§ prolong pregnancy (prematurity: main cause of perinatal
o Placental vascular lacunae or “lakes” which represent
mortality associated with placenta previa)
dilated vessels extending from the placenta through the
§ blood transfusion: for moderate to severe bleeding
myometrium (“Swiss cheese” appearance of the
without maternal or fetal compromise
myometrium)
§ tocolytics: for placenta previa with contractions to
o Thinning or focal disruption of the uterine serosa-bladder
prolong pregnancy up to 34 weeks, if mother and fetus
wall complex (placenta percreta)
are stable (limit only to 48 hrs according to Bose et al., but categorically
Parkland Hospital recommends against this – Williams) o Focal mass-like elevation with the same echogenicity as the
§ avoid indomethacin due to platelet inhibition placenta beyond the uterine serosa (placenta percreta)
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MANAGEMENT ABRUPTIO PLACENTA
• Delivery in a tertiary-care facility with a multi-disciplinary
team (OB, urology, gynecologic oncology, anesthesiology, etc.)
• Give corticosteroids between 24-34 weeks for pregnancies at
increased risk of delivery within 7 days.
• If with significant bleeding → CS hysterectomy regardless of AOG
• If asymptomatic, elective CS hysterectomy at 34 to 35 6/7
weeks after giving corticosteroid (POGS CPG, November 2019); GUIDE QUESTION: ABRUPTIO PLACENTA
at 34 weeks (Blueprints) Abruptio Placenta https://qrs.ly/tvegx2s
https://qrs.ly/nuegx2w
o After fetal delivery, extent of placental invasion is assessed
• Placental abruption (abruptio placentae) – premature
WITHOUT attempts at manual placental removal
separation of implanted placenta from uterine wall, resulting in
• Conservative management in select cases in whom accreta was
hemorrhage
not suspected before CS: placenta is left in situ, repair of hysterotomy
• non-clotted blood coursing from injury site may cause further
is done, hysterectomy NOT done, with possible transfer to a higher-
separation of placenta
level facility or do interval (delayed) hysterectomy
• 50% abruptions occur before labor and after 30 weeks, 15%
EPIDEMIOLOGY: PLACENTA PREVIA & ACCRETA occur during labor, and 30% identified on placental inspection
• Placenta previa occurs in 3.5 – 5 per 1,000 births and nearly 20% after delivery
of all antepartum hemorrhage • concealed hemorrhage – bleeding confined in uterine cavity
• Previa occurs in 1-5% of women with a prior CS (20% of abruptions)
• Placenta previa accrete (placenta with accrete): ~5% of cases • revealed or external hemorrhage – blood dissects toward
• The risk of placenta accrete is increased in women with cervix (80% abruptions)
placenta previa in the setting of prior CS delivery • history of previous abruption – strongest risk factor for
• In the setting or placenta previa, the risk of concurrent accrete is abruption (8- to 12-fold risk increase)
o After 1 CS: 3% o After 4 CS: 61% o Risk of abruption in future pregnancy – 10% after one
o After 2 CS: 11% o After 5 CS: 67% abruption and 25% after two abruptions (5.8 – 22% after
o After 3 CS: 40% one, >50% after two abruptions.- Williams)
DIAGNOSIS OF ABRUPTIO PLACENTA
• History: third-trimester vaginal bleeding (80%) associated with
severe abdominal pain (67%) and/or frequent, strong
contractions. ~30% have few or no symptoms
• abruption pain may mimic normal labor, or be painless (if with
GUIDE QUESTION: PLACENTA PREVIA AND posterior placenta)
Abnormal Placentation ACCRETA • PE:
https://qrs.ly/9oegx2f https://qrs.ly/slegx2o o vaginal bleeding and firm, tender uterus
o non-reassuring fetal heart tracing
SUMMARY: Abnormalities of Placentation o Couvelaire uterus – blood infiltrating myometrium to reach
• Occurs when the membranes double back serosa, especially at cornua, à bluish purple myometrium as
over the edge of the placenta forming a seen on surface of uterus
dense ring around the periphery of the • Imaging: 2–25% abruptions diagnosed by ultrasound
Circumvallate (evidenced by retroplacental clot)
placenta
placenta o negative findings on ultrasound do NOT exclude placental
• Often considered a variant of placental
abruption, it is a major cause of 2nd abruption
trimester hemorrhage • Complications: hypovolemic shock, consumptive coagulopathy
Placenta • Occurs when the placenta develops over the MANAGEMENT OF ABRUPTIO PLACENTA
previa internal cervical os
• Stabilize patient – continuous CTG, IV with two large-bore
• Abnormal adherence of part or all of the
catheters, hematological evaluation with fibrinogen/D-
placenta to the uterine wall
Placenta dimer/fibrin split products
accrete • May be associated with a placenta in normal
• Administer RhoGAM for Rh (-) women
locations, but incidence increases in placenta
• Prepare for possible hemorrhage
previa
o cross-matched blood; O-negative may be given in emergency
Placenta • Abnormal placentation in which the placenta
o 1:1:1 RBC:FFP:Plt for massive transfusion
increta invades the myometrium
• Prepare for preterm delivery
• Abnormal placentation in which the placenta o Betamethasone prior to 36 weeks
invades through the myometrium to the o MgSO4 prior to 32 weeks
Placenta uterine serosa
• CS for life-threatening bleeding or nonreassuring fetal status
percreta • Occasionally, placentas may invade into
• Vaginal delivery if controlled bleeding/reassuring fetal status
adjacent organs such as the bladder or
rectum UTERINE RUPTURE
• Occurs when a velamentous cord insertion
causes the fetal vessels to pass over the
Vasa previa internal os GUIDE QUESTION:
• Also seen with velamentous and Uterine Rupture
succenturiate placentas https://qrs.ly/iwegx34
• Occurs when blood vessels insert between
the amnion and the chorion, away from the • 1 in 15,000–20,000 deliveries with no history of uterine surgery
Velamentous o 0.5–0.1% in prior low-transverse cesarean delivery
placenta
margin of the placenta, leaving the vessels
largely unprotected and vulnerable to o 6–12% in prior classical cesarean delivery
compression or injury
• An extra lobe of the placenta is implanted DIAGNOSIS OF UTERINE RUPTURE
at some distance away from the rest of the • History: FHR decelerations with prior scars on uterus
placenta • “popping” sensation or sudden abdominal pain (“In most, however,
Succenturiate there is remarkably little appreciable pain or tenderness” – Williams)
placenta • Fetal vessels may course between the two
lobes, possibly over the cervix, leaving these • PE: fetus may be palpable in extrauterine space, possible vaginal
blood vessels unprotected and at risk for bleeding, and fetal presenting part is suddenly at higher station
rupture than previously

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MANAGEMENT OF UTERINE RUPTURE UTERINE ATONY
• immediate laparotomy and delivery of fetus • leading cause of PPH
• repair rupture site and obtain hemostasis • Diagnosis: soft, enlarged, and boggy uterus
• If large rupture extensions occur, may require hysterectomy • Management
• patient discouraged into future pregnancies, given high risk of o IV oxytocin, given prophylactically after delivery
recurrent rupture o strong uterine massage to assist the uterus in contracting
• avoid trial of labor in subsequent pregnancy, and deliver via o If atony continues
repeat cesarean section between 36–37 weeks § methylergonovine (contraindicated in hypertensive
patients); if persistent, THEN
FETAL VESSEL RUPTURE § Carboprost or Prostaglandin F2α (contraindicated in
• incidence of vasa previa is approximately 1:2,500 pregnancies asthma patients) (contraindicated as well in suspected
• velamentous cord insertion – blood vessels insert between amnionic fluid embolism – Williams)
amnion and chorion away from placenta, instead of inserting § (Williams) Dinoprostone, a Prostaglandin E2 analog
directly into chorionic plate (contraindicated in hypovolemic patients)
o 1% in singleton gestations, 4% to 12% for twin gestations § Misoprostol, a Prostaglandin E1 analog: off-label
(4% to 7% for dichorionic twins and 10% to 12% for uterotonic
monochorionic twins), and 28% to 50% for triplet gestations o If atony is still persistent after medical management
• vessels may cross internal cervical os (vasa previa) à § dilation and curettage (D&C): r/o possible retained POCs
compression by presenting fetal part or tearing when § uterine packing with an inflatable tamponade
membranes are ruptured (Bakri balloon)
o Trophotropism may result to vasa previa – placental § occlusion of pelvic vessels (uterine artery embolization)
atrophy from previous site leaving underlying vessels § If all are unsuccessful, exploratory laparotomy with
running unsupported through membranes over the cervix ligation of pelvic vessels and possible hysterectomy are
o succenturiate lobe – placental lobe that is discrete from rest required
of placenta, in an incomplete atrophy § Bleeding unresponsive to uterotonic agents
• fetal blood loss (even small amounts of blood) or pressure on 1. Bimanual uterine compression
vessels à exsanguination and death 2. Balloon tamponade
3. Surgical procedures – uterine compression sutures (e.g.,
DIAGNOSIS OF FETAL VESSEL RUPTURE B-Lynch sutures), pelvic vessel ligation, and
• History: vaginal bleeding associated with sinusoidal variation of hysterectomy
FHR indicative of fetal anemia RETAINED PRODUCTS OF CONCEPTION
• PE: fetal vessels are palpated and recognized through dilated • Usually, the retained fetal membranes or placental tissue pass in
cervix the lochia
• Imaging: color Doppler if low-lying placenta, succenturiate lobe, • Management:
or placental cord insertion cannot be identified o Manual exploration of cervix
• Labs: Apt test (nucleated fetal RBCs in maternal blood) o UTZ: must have normal uterine stripe
o dilute blood with water, collect supernatant, and combine it o D&C: both diagnostic and therapeutic measures
with 1% NaOH. If mixture is pink, it indicates fetal blood; if o If still with hemorrhage, placenta accreta should be
yellow-brown, it indicates maternal blood suspected
MANAGEMENT OF FETAL VESSEL RUPTURE
UTERINE INVERSION
• emergent cesarean delivery – treatment of ruptured fetal vessel
o 39 weeks recommended for elective cesarean delivery • 1 in 2,500 deliveries (1 in 2000 – 20,000 – Williams)
• immediate transfusion: if considerable blood loss in neonate • uterine fundus turns partially or completely inside out
• with antepartum diagnosis of vasa previa, patients may opt for • life-threatening obstetrical emergency
elective cesarean delivery • Diagnosis
• If electing for trial of labor with history of vasa previa, artificial o fundus of the uterus is attached to the placenta on placental
rupture of membranes is contraindicated delivery a round mass protruding from the cervix or vagina
accompanies by significant vaginal bleeding
POSTPARTUM HEMORRHAGE (PPH) o intense vasovagal response, requiring stabilization with the
aid of an anesthesiologist before manual replacement
• 1-5% of all deliveries
• Management
• blood loss > 500 mL: vaginal delivery and > 1,000 mL: CS
o Manual replacement – first step (call for help is first step à
• early PPH: within 24 hrs, late PPH: after 24 hrs secure blood and large bore IV à evaluate for general
• complications: anesthesia à manual replacement – Williams)
o Disseminated Intravascular Coagulation (DIC) o Uterine relaxants (nitroglycerin or halogenated agents) may
o Sheehan syndrome (pituitary infarct) be given to aid uterine relaxation and replacement. (then if
replaced, stop tocolysis, then administer
GENITAL TRACT LACERATIONS oxytocin/uterotonics – Williams)
• Large drop in Hct after delivery without no visible bleeding o laparotomy if replacement unsuccessful
siteà r/o vaginal wall hematoma
• Low back pain + large drop in Hct à r/o retroperitoneal AMNIOTIC FLUID EMBOLISM
hematoma • 1-2 cases per 100,000 births
• Management • Risk factors include rapid labor, meconium-stained amniotic
o Lacerations: repair fluid, and uterine and pelvic vein tears
o Hematomas: if stable Hct or stable BP, expectant • Due to intravenous embolization of meconium-laden amniotic
management fluid
o If rapidly expanding or tense vaginal hematoma: open • Diagnosis:
hematoma, ligate vessel, and close o Clinical onset during labor or within 30 mins of placental
o If retroperitoneal hematoma: confirm with UTZ or CT, then delivery
embolization o Abrupt onset of cardiorespiratory arrest or both
hypotension and respiratory compromise
GUIDE QUESTIONS: o Overt disseminated intravascular coagulopathy
Postpartum Hemorrhage o No fever ≥ 38C
and Uterine Atony • Abnormal activation of proinflammatory cascades similar to
https://qrs.ly/qeegx3b systemic inflammatory response syndrome (SIRS) causing
pulmonary vasoconstriction and hypertension.
• May develop to disseminated intravascular coagulopathy (DIC)
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GENERAL MANAGEMENT OF HEMORRHAGE DISSEMINATED INTRAVASCULAR COAGULATION

• Simultaneously try to identify source and begin resuscitation • DIC as a sole cause of maternal death is uncommon (0.2% of
• If postpartum, identify presence of atony, retained placental pregnancy-related deaths)
fragments, or lacerations • Tissue factors are release from subendothelial tissue and
• Establish 1 or 2 large-bore IV infusion systems stimulated monocytes provoke cytokine release from
• Infuse crystalloids rapidly; initial fluid is infused in a volume two endothelium causing diffuse activation of coagulation cascades
or three times the estimated blood loss • Placenta abruptio is the most common cause
• Order blood products Other possible obstetric causes: HELLP, amniotic fluid embolism,
• Prepare OR room and assemble surgical and anesthesiology teams sepsis, second-trimester induced abortion, and prolonged
• Inform pediatric neonatology resuscitation team if imminent retention a dead fetus
delivery is possible • Management: remove inciting source of defibrination
• Surgical management if necessary may include • Vigorous fluid resuscitation; recombinant factor VIIa may help
o Uterine compression sutures in severe cases
o Artery lugation • Not recommended: tranexamic acid, unfractionated heparin, and
o Angiographic embolization epsilon-aminocaproic acid
o Aortic compression
o Pelvic packing GUIDE QUESTIONS:
Preeclampsia
BLOOD TRANSFUSION https://qrs.ly/oqegx3d
• Rapid blood infusion should be done when hematocrit < 25
volume percent HYPERTENSIVE DISEASES OF PREGNANCY
• Platelet concentrate infusion: for platelet count less than Gestational Hypertension
<50,000/uL
• SBP≥140 and/or DBP≥90 mmHg on two
• Fresh frozen plasma in doses of 10-15 mL/kg or cryoprecipitate BP occasions at least 4 h apart after 20 wks’
infusion: for prolonged PT/PTT in a woman with surgical gestation in women with previously normal BP
bleeding
Preeclampsia without severe features
• Compatible whole blood: recommended for severe obstetrical
BP • SBP≥140 and/or DBP≥90 mmHg on two
hemorrhage (Hct increases by 3-4% per unit)
occasions at least 4 h apart after 20 wks’
gestation in women with previously normal BP
• ≥300 mg/24 h or protein/creatinine ratio
• and ≥0.3 or dipstick reading of +1 (used only if
Proteinuria other quantitative methods are unavailable)
Preeclampsia with severe features
• SBP≥140 and/or DBP≥90 mmHg on two
BP
occasions at least 4 h apart after 20 wks’
gestation in women with previously normal BP
• SBP≥160 and/or DBP≥110 mmHg
confirmed within a short interval (minutes)
to facilitate antihypertensive therapy
• ≥300 mg/24 h or
• protein/creatinine ratio ≥0.3 or
• and • persistent dipstick reading of +1 (used only
Proteinuria if other quantitative methods are
unavailable)
Or in the absence of proteinuria and severe range blood
pressures, new onset hypertension with the new onset of
any of the following:
Thrombocytopenia • Platelet count < 100,000 μL−1
• Serum creatinine concentrations
Renal insufficiency >1.1 mg/dL or 2x baseline in the
absence of other renal disease
Impaired liver fxn • >2x ALT, AST measurements
Pulmonary edema
Cerebral or visual
symptoms

CHRONIC HYPERTENSION
• hypertension present before conception, before 20 weeks’
gestation, OR persisting > 6 weeks postpartum
• ⅓ chronic pregnant hypertensives develop superimposed
preeclampsia

MANAGEMENT
• ≤ 140/90 mm Hg can be managed expectantly (treat only when SBP
≥ 160 mmHg or DBP ≥105 mmHg according to ACOG – Williams)
• persistently elevated BPs or already on medications: use
antihypertensives
o most common are labetalol and nifedipine
• obtain baseline labs (complete blood count, complete metabolic
panel [CMP]) and baseline 24-hour urine for creatinine
clearance and protein
• obtain baseline ECG to ensure no current cardiac compromise
• initiate low-dose aspirin after 12 weeks to reduce risk of
superimposed preeclampsia

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GESTATIONAL HYPERTENSION
• deliver at 37 weeks’ gestation HYPERTENSION IN PREGNANCY
• prior to 37 weeks, monitor closely for preeclampsia, with twice https://qrs.ly/mjegx3n
weekly BP checks and weekly laboratory testing and antenatal
fetal testing
HELLP SYNDROME
PREECLAMPSIA • rapidly deteriorating liver function, evidence of hemolysis, and
• abnormal development of placental vasculature and thrombocytopenia
maternal systemic endothelial dysfunction • in frank hepatic failure, screen for acute fatty liver of pregnancy
• Fetal effects d/t abnormal placentation à uteroplacental o 1 in 10,000 pregnancies
insufficiency à IUGR and hypoxia o > 50% AFLP have hypertension and proteinuria
• Maternal effects d/t circulating antiangiogenic factors à o fetuses with long-chain hydroxyacyl-CoA dehydrogenase
increased vascular permeability, coagulation activation, deficiency or medium-chain hydroxyacyl-CoA
vasoconstriction à end-organ damage such as dehydrogenase deficiency
o brain (seizure and stroke) o management: maternal stabilization and delivery of fetus
o kidneys (oliguria and renal failure) regardless of gestational age
o lungs (pulmonary edema) • if diagnosed after 34 0/7 weeks, deliver after maternal
o liver (edema and subcapsular hematoma) stabilization
o small blood vessels (thrombocytopenia and disseminated • if diagnosed prior to 34 weeks, deliver 24 to 48 hours after
intravascular coagulation [DIC]) administration of betamethasone and MgSO4 (through 24 hours
• 10% of patients with preeclampsia with severe features develop postpartum)
HELLP syndrome
o HEmolysis, Elevated Liver enzymes, and Low Platelets ACUTE FATTY LIVER OF PREGNANCY (AFLP)
o stillbirth (10% to 15%), neonatal death (20% to 25%). • Unclear whether AFLP is truly in the spectrum of preeclamptic
o patient with HELLP syndrome likely < 36 weeks’ gestation at syndromes
presentation • More than 50% of patients with AFLP will also have
hypertension and proteinuria
EPIDEMIOLOGY • Has a high mortality rate; difficult to distinguish from HELLP
• 5% to 6% of live births but AFLP exhibit evidence of liver failure
• most common – third trimester near term o Elevated ammonia level
o if hypertension occurs in second trimester (14 to 20 weeks), o Blood glucose < 50 mg/dL
consider h-mole or undiagnosed chronic hypertension o Markedly reduced fibrinogen and antithrombin III levels
• 80% develop HELLP syndrome after preeclampsia diagnosis • Management: maternal stabilization → prompt delivery
(30% without severe features, 50% with severe features) regardless of AOG
FOLLOW-UP FOR PREECLAMPSIA PATIENTS
PREECLAMPSIA WITHOUT SEVERE FEATURES • 25–33% recurrence rate in future pregnancies
• delivery at 37 weeks • In chronic hypertension, risk of recurrence is 70%
• magnesium sulfate (MgSO4) may be started for seizure • Low-dose aspirin – for patient with history of preeclampsia,
prophylaxis multiple gestations, chronic hypertension, diabetes, renal
• prior to 37 weeks, inpatient management with very close disease, or autoimmune disease (given 12-28 weeks AOG – Williams)
monitoring of BP, laboratory values, and fetal testing • Calcium– decrease rates subsequent preeclampsia (beneficial only
• possible outpatient care if without co-morbids for high-risk women – Williams)
• (Williams) anti-hypertensives may be started, but benefit remains
only for severe hypertensive patients; for mild-moderate ECLAMPSIA
hypertension, these drugs “at least theoretically can reduce • grand mal seizures in preeclamptic patient with no other causes
uteroplacental perfusion” • assume seizure as eclampsia until proven otherwise
o Adrenergic receptor blockers (peripheral: labetalol, etc; • due to hyperperfusion, endothelial dysfunction, and brain
central: methyldopa, clonidine) edema à breakdown in autoregulation of cerebral circulation
o Calcium channel blocking agents (dihydropyridine:
nifedipine etc, non-DHP: verapamil) MANIFESTATIONS OF ECLAMPSIA
• tonic–clonic in nature and may not be preceded by an aura
PREECLAMPSIA WITH SEVERE FEATURES • may develop before labor (59%), during labor (20%), or after
delivery (21%).
• delivery at 34 weeks
• Most postpartum seizures occur within first 48 hours after
• administer MgSO4 (4–6 g loading dose followed by 1 to 2 g/hour delivery, sometimes occur as late as several weeks after delivery
through 24 hours postpartum) for seizure prophylaxis
• Fetal bradycardia can occur during and after seizure
• BPs ≥ 160 mm Hg/110 mm Hg, manage with antihypertensive
therapies (IV labetalol, IV hydralazine, or PO nifedipine) to bring MANAGEMENT OF ECLAMPSIA
BPs out of severe range given risk of stroke • seizure management: start with ABCs (airway, breathing,
• If stable maternal and fetal conditions, manage expectantly until circulation), though most resolve spontaneously
34 weeks • hypertension management: administer hydralazine or labetalol
• administer betamethasone for fetal lung maturity through 36 to lower BP < 160/110 mm Hg
weeks • seizure prophylaxis and control:
• if delivery is needed, induce labor in appropriate patients o MgSO4 to decrease hyperreflexia (initiate at diagnosis and
continue 12–24 hours after delivery)
CHRONIC HYPERTENSION WITH o raise seizure threshold
SUPERIMPOSED PREECLAMPSIA Serum Concentration
Clinical Response
MgSO4 (mg/mL)
• ≥ ⅓ develop superimposed preeclampsia 4.8–8.4 Therapeutic seizure prophylaxis
• diagnosis: 8 CNS depression
o increasingly elevated BPs and new/worsening proteinuria 10 Loss of deep tendon reflexes
o 24-hour urine protein > 300 mg/24 hours 15 Respiratory depression/paralysis
o In pre-existing baseline renal disease, uric acid > 6.0–6.5 is 17 Coma
differentiates preeclampsia from exacerbation of 20–25 Cardiac arrest
hypertension Side effects of MgSO4 administration. From Blueprints Obstetrics and Gynecology 7th edition.

o Severe superimposed preeclampsia: with severe • In overdose, administer 10 mL 10% calcium chloride or calcium
preeclampsia signs and symptoms gluconate via IV for cardiac protection
• Initiate delivery only after eclampsia controlled
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• prolonged fetal heart rate (FHR) decelerations commonly occur MANAGEMENT OF GDM
during seizure à establish adequate maternal oxygenation and • Initial management is DIETARY (Class A1)
cardiac output • ADA diet plan of 2,200 calories per day
• If FHR abnormalities do not resolve à emergent cesarean delivery (40% carbs, 20% protein, 40% fat – Williams)
• If stable à may induce labor o meal plan: 30–35 kcal/kg of ideal body weight
§ 30–45 g carbohydrates for breakfast
§ 45–60 g carbohydrates for lunch and dinner
GESTATATIONAL DIABETES MELLITUS (GDM) § 15 g carbohydrates for snacks
• impairment in carbohydrate metabolism during pregnancy • monitor blood glucose four times per day, including fasting and
• increased risk of fetal macrosomia, birth injuries, neonatal three postprandial values
hypoglycemia, hypocalcemia, hyperbilirubinemia, and polycythemia • postprandial walking – 15 minutes about 30–40 minutes after meal
• 4- to 10-fold increased risk of developing type 2 diabetes • if > 25–30% blood glucose values elevated, insulin or oral
mellitus (T2DM) during their lifetime hypoglycemic agent is indicated (Class A2) (or if glucose targets
are not achieved consistently. <95 mg/dL for fasting, <120 mg/dL for 2-hr
ETIOLOGY OF GDM postprandial levels; insulin is started if glucose targets are not maintained <140
• human placental lactogen (hPL)/human chorionic mg/dL 1-hr postprandial or <120 mg/dL 2-hr postprandial – Williams)
somatomammotropin (hCS) o short-acting and intermediate-acting insulin at breakfast and
o anti-insulin agents à increased insulin resistance and short-acting insulin at dinner
generalized carbohydrate intolerance § short-acting insulin: Humalog (lispro) or NovoLog
• beta cell hypertrophy in first half of pregnancy à insulin § intermediate-acting insulin: NPH
production greater than insulin resistance o metformin: second-line agent for those not taking insulin
• carbohydrate metabolism abnormalities: appear during late o glyburide: not a first-line treatment
second trimester or early third trimester (both metformin and glyburide are considered second-line
agents – Williams)
EPIDEMIOLOGY Insulin Type and Time Impact Target Glucose
• 1% to 12% of pregnant women Dose Time Seen Level (mg/dL)
• Risk factors: Evening NPH Fasting 70–90
o African-American Morning Humalog Post-breakfast 100–139
o maternal age Morning NPH Post-lunch 100–139
o obesity Evening Humalog Post-dinner 100–139
o family history of diabetes Insulin dosing and target glucose levels during pregnancy. From Blueprints Obstetrics and Gynecology, 7th edition.

o history of a previous infant weighing more than 4,000 g Instructions for Adjusting Insulin Dosage
o previous stillborn infant. 1. Establish a fasting glucose level between 70 and 90 mg/dL
Fetal Complications of DM 2. Adjust only one dosing level at a time
• Macrosomia 3. Do not change any dosage by more than 20% per day
o Traumatic delivery 4. Wait 24 h between dosage changes to evaluate the response
Adjusting insulin dosing. From Blueprints Obstetrics and Gynecology, 7th edition.
o Shoulder dystocia
o Erb palsy WHITE CLASSIFICATION
• determines likely severity of diabetes and its interaction with
• Delayed organ maturity
pregnancy
o Pulmonary
o Hepatic • originally to predict perinatal survival
o Neurologic Classification Description
o Pituitary-thyroid axis Class A1 Gestational diabetes; diet controlled
• Congenital malformations Class A2 Gestational diabetes; insulin controlled
o Cardiovascular defects Class B Onset: age 20 or older Duration: <10 y
o NTDs Class C Onset: age 10–19 Duration: 10–19 y
o Caudal regression syndrome Class D Onset: before age 10 Duration: >20 y
o Situs inversus Class F Diabetic nephropathy
o Duplex renal ureter Class R Proliferative retinopathy
• IUGR Class RF Retinopathy and nephropathy
• Intrauterine death Class H Ischemic heart disease
Maternal complications Class T Prior renal transplantation
White Classification for diabetic women. From Blueprints Obstetrics and Gynecology, 7th edition.
• OB complications: polyhydramnios, preeclampsia, infection,
FETAL SURVEILLANCE
miscarriage, postpartum hemorrhage, ↑CS rate
• Class A2 – NST/BPP between 32 and 36 weeks and until delivery
• DM emergencies: DKA, hypoglycemia, DM coma
on a weekly or biweekly basis (start between 32-34 weeks, then
• Vascular and end-organ involvement: cardiac, renal, weekly/biweekly – Williams)
ophthalmic, peripheral vascular • UTZ to check fetal weight (EFW) between 34 and 37 weeks
• Neurologic: peripheral neuropathy, GI disturbance • if well-controlled on diet, fetal monitoring not common for A1
GDM patients
DIAGNOSIS OF GESTATIONAL DIABETES MELLITUS
DELIVERY MANAGEMENT
• best time to screen: 24 and 28 weeks of gestation in women with
• intrapartum management of diet-controlled GDM same as non-
low risk GDM
diabetic, if no significant hyperglycemia on admission
• to identify T2DM, screen patients with one or more risk factors
• induce labor at 39 weeks, if on insulin or hypoglycemic agent
for GDM during initial prenatal laboratory tests
o long-acting hypoglycemic agents are discontinued
• 50g glucose loading test (fasting and 1hr after): normal fasting
o blood glucose monitored every hour
< 105 mg/dL, 1hr after 50g glucose load < 140 mg/dL
o dextrose and insulin drips to maintain blood glucose within
• If 1hr glucose > 140 mg/dL à proceed to 75- or 100g- glucose reference limits (<120 mg/dL) (maintained at 100 mg/dL – Williams)
tolerance test
• delivery at 37–39 weeks, if poor glycemic control
• elective cesarean delivery, if EFW ≥ 4,500 g (may consider – Williams)
• forceps and vacuum are generally not used if macrosomia is
suspected (increased risk of shoulder dystocia), except in true
outlet forceps for non-reassuring fetal monitoring

PROGNOSIS
• >50% GDM in subsequent pregnancy (48% recurrence – Williams)
• 25–35% overt diabetes within 5 years (50% overt diabetes within
20 years – Williams)

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• if prior GDM, screen for T2DM at postpartum visit and every • Mild to moderate nausea and vomiting until approximately 16
year thereafter (at 4-12 weeks postpartum, then if normal, at least every 3 weeks’ gestation
years – Williams) • Hyperemesis gravidarum: severe unrelenting nausea and
• for GDM infants, increased incidence of childhood obesity and vomiting that may lead to weight loss (≥5% of pre-pregnancy
T2DM during early adulthood and later in life weight), dehydration, ketosis, alkalosis, electrolyte imbalance,
o 8 weeks and transient hepatic dysfunction
• Cause: elevated hCG, progesterone (decreases gastric motility,
relaxes esophageal sphincter), thyroid hormone
GESTATIONAL DIABETES MELLITUS
https://qrs.ly/n6egx40 • Management:
o Mild: Doxylamine + Vitamin B6 plus diphenhydramine or
dimenhydrinate, ginger supplementation with Vitamin B12
o Moderate: Promethazine, metoclopramide,
SELECTED MEDICAL COMPLICATIONS IN prochlorperazine, ondansetron (oral, rectal, parenteral)
PREGNANCY o Severe: IV hydration with thiamine (to prevent Wernicke
GASTROINTESTINAL DISORDERS encephalopathy), parenteral: metoclopramide,
PEPTIC ULCER DISEASE promethazine, or ondansetron
• Gastroduodenal ulcers may be caused by chronic gastritis from
COMPLICATIONS
H. pylori or from NSAID use, but not common in pregnancy.
• Gastroprotection during pregnancy originates from reduced • Weight loss
gastric acid secretion, decreased motility, and increased mucus • Dehydration
secretion. • Ketosis
• Mainstay of management is eradication of H. pylori and • Alkalosis
prevention of NSAID-induced disease. o Loss of HCl
• First-line therapy is H2-receptor blockers or proton-pump o Low K
inhibitors • Transient hepatic dysfunction
• Sucralfate, aluminum salt of sucralfated sucrose inhibits pepsin,
provides protective coating of ulcer base. GASTROESOPHAGEAL REFLUX DISEASE
• 14-day regimen: amoxicillin 1g BID + Clarithromycin 250-500 • Heartburn – main symptom
mg BID + metronidazole 500 mg BID; Plus PPI Omeprazole. • Management
o Small, frequent meals
APPENDICITIS o Head of the elevation, and avoidance of postprandial
• Right lower quadrant pain is most frequent but migrates recumbency
upwards with appendiceal displacement. o Avoidance of “trigger” foods – coffee, fatty & tomato-based
• Pregnancy complications: miscarriage, uterine contractions foods
o Oral antacids – first-line therapy
• Differentials: cholecystitis, labor, pyelonephritis, renal colic,
o Proton-pump inhibitor (Omeprazole) or H2-receptor
placental abruption, or uterine leiomyoma degeneration.
antagonist (Ranitidine)
• MRI is the preferred modality for evaluation of appendicitis in
pregnancy.
• Surgical exploration or evaluation is preferred. HEPATITIS B IN PREGNANCY
• Antimicrobial therapy with second-generation cephalosporin • Clinical presentation: At least half are asymptomatic; if with
or 3rd generation penicillin prior to surgery. symptoms: anorexia, nausea, vomiting, fever, jaundice, or
abdominal pain
HYPEREMESIS GRAVIDARUM • Serologic markers
HBsAg Marker for infection
✔GUIDE QUESTION
Diagnostic for immunity; either from vaccination
The following are common initial complications in cases of severe Anti-HBs
or from natural infection
hyperemesis gravidarum, EXCEPT?
A. Acidosis Anti-HBc Arises only as a result of natural infection
B. Dehydration Present during times of high viral replication/
HbeAg
C. Hypokalemia infectivity, correlates with detectable HBV DNA
D. Mild transaminitis
INTERPRETATION OF HEPATITIS PROFILE
VERTICAL
TEST RESULTS INTERPRETATION
TRANSMISSIONa
HbsAg Negative
Anti-HBc Negative Susceptible 0%
Anti-HBs Negative
HbsAg Negative
Anti-HBc Positive Immune because of natural infection 0%
Anti-HBs Positive
HbsAg Negative
Anti-HBc Negative Immune because of hepatitis B vaccination 0%
Anti-HBs Positive
First trimester: 10%
HbsAg Positive
Third trimester:
Anti-HBc Positive
Acutely infected 80-90%
Anti-HBc IgM Positive
HBeAg- : 10-20%
Anti-HBs Negative
HBeAg+: 90%
HbsAg Positive
Anti-HBc Positive HBeAg- : 2-10%
Chronically infected
Anti-HBc IgM Negative HBeAg+: 80-90%
Anti-HBs Negative
Four interpretations possible:
1. May be recovering from acute HBV infection
HbsAg Negative
2. May be distantly immune, and test is not sensitive enough to detect very low level of anti-HBs
Anti-HBc Positive 0%
in serum
Anti-HBs Negative
3. May be susceptible with false-positive anti-HBc
4. May be an undetectable level of HBsAg present in the serum and the person is a carrier
aAssuming HIV negative, and no HB vaccine and immunoprophylaxis of neonate
Berghella et al. Maternal-Fetal Evidence Based Guidelines 2nd edition. 2011

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• Management ASYMPTOMATIC BACTERIURIA
o Universal screening with HBsAg; If (+), send for hepatitis • >100,000 colonies on urine culture, w/o symptoms of UTI
profile & HBV DNA
• ASB in early pregnancy are 20- to 30-fold more at risk of
o Start antiviral therapy when HBV DNA IS ≥200,000 IU/mL
pyelonephritis
o Vaccine may be given during pregnancy in susceptible women.
• associated with preterm birth and low–birth-weight
o Tenofovir – first-line treatment in pregnancy
• untreated ASB à 25–40% cystitis or pyelonephritis
o Immunoprophylaxis (hepatitis B Ig and vaccine) for infants
born to infected mothers within 12 hours of birth • in sickle-cell disease, rate of ASB doubles to 10%
o Infants who received immunoprophylaxis may be breastfed.
TREATMENT FOR UTI/ASYMPTOMATIC BACTERIURIA
• amoxicillin, nitrofurantoin, trimethoprim/sulfamethoxazole, or
GUIDE QUESTION: cephalexin à all active against Gram-negative bacteria
Hepatitis B in Pregnancy o E. coli causes > 80% ASB and UTIs, remaining is caused by
https://qrs.ly/wnegx45 gram-negative enterobacteria and gram-positive bacteria
• In first trimester, penicillins and cephalosporins are first-line
• In third trimester, use nitrofurantoin or
RENAL AND URINARY TRACT DISORDERS trimethoprim/sulfamethoxazole with caution (may cause
CHRONIC RENAL DISEASE kernicterus in fetuses/neonates with G6PD deficiency)
• ↑ renal blood flow and creatinine clearance during pregnancy • Treatment duration: 7-day antibiotic course
→ in mild renal disease, patients usually experience • Single-dose therapy is not recommended (but single dose
improvement of renal function throughout much of pregnancy nitrofurantoin is effective – Williams)
• In moderate and severe cases: may experience ↓renal function • For cystitis: 7-to 10-day antibiotic course, adjusted depending
in the latter half pregnancy up to the postpartum period on culture sensitivity
• Increased risk for preeclampsia, preterm delivery, GDM, and • obtain test-of-cure culture 2 weeks after completion of therapy
IUGR o If positive test of cure, initiate different regimen for 14 days
• 24-hour urine for creatinine clearance and protein must be • nightly antibiotic prophylaxis for pregnant with two or more
done at least once per trimester UTIs
• Baseline uric acid may be assessed instead of baseline o either nitrofurantoin or trimethoprim/sulfamethoxazole
proteinuria to help diagnose preeclampsia • phenazopyridine (Pyridium) for dysuria or bladder pain
• Status post-renal transplant patients: average AOG at delivery (anesthetic is concentrated in urine) (can cause orange urine)
is 30 weeks; commonly on immunosuppressants
PYELONEPHRITIS
URINARY TRACT INFECTIONS • ascending infection to kidneys (most common complication of
• infection along urinary tract (includes cystitis and lower UTI)
pyelonephritis) • 1% to 2.5% of pregnancies
• in 20% of pregnancies, and up to 10% antepartum • 10–18% recurrence during same pregnancy
hospitalizations • 20% of acute pyelonephritis à multiorgan system involvement
secondary to endotoxemia à sepsis
PATHOGENESIS OF UTI
• 2–8% ARDS, the most severe complication of severe sepsis
• Women are 14 times more likely to develop UTIs vs men, d/t • risk factors for developing pyelonephritis
o shorter urethra in women o pyelonephritis
o exposure of external 1/3 of urethra to pathogenic bacteria o history of vesicoureteral reflux
from vagina and rectum o ASB
o greater incidence of incomplete emptying during voiding • 60% recurrence for non-treated UTIs; < 10% recurrence with
o movement of bacteria into female bladder during sexual suppressive therapy
intercourse • most common organisms in acute antepartum pyelonephritis:
• During pregnancy, risks of UTI increase d/t o E. coli (70%)
o progesterone decreases bladder tone, causes ureteral and o Klebsiella/Enterobacter spp. (3%)
renal pelvis dilation, and decreases ureteral peristalsis o Proteus spp. (2%)
§ urinary stasis along urinary tract à physiologic o gram-positive bacteria, including GBS (10%)
hydronephrosis of pregnancy
o mechanical compression from enlarged uterus à DIAGNOSIS OF PYELONEPHRITIS
obstruction of ureters à additional stasis • History: fever, chills, flank pain, dysuria, urgency, and frequency
o increased capacity and incomplete emptying of bladder à
• PE: fever and costovertebral angle tenderness are often present
vesicoureteral reflux
• Labs: pyuria, bacteriuria, elevated WBC count, WBC casts
o inhibited TLR4 response against uropathogenic E. coli
• static columns of urine in ureters à bladder infection à
TREATMENT OF PYELONEPHRITIS
ascending migration of bacteria to upper urinary tract
• treated aggressively with hospital admission, intravenous (IV)
DIAGNOSIS OF UTI hydration, and antibiotics
• either cystitis/lower UTI or pyelonephritis/upper UTI o IV hydration for common transient renal dysfunction
o Cystitis: syndrome including o IV antibiotics—often cephalosporins (cefazolin, cefotetan, or
§ urinary urgency, frequency, dysuria ceftriaxone) or ampicillin and gentamicin—until afebrile and
§ suprapubic discomfort (tenderness on palpation) asymptomatic for 24–48 hours
without systemic symptoms (high fever and o avoid ampicillin and first-generation cephalosporins
costovertebral angle tenderness) (cephalexin or cefazolin) for E. coli (high resistance
§ possible gross hematuria incidence) (“<50% of E. coli strains are sensitive to ampicillin
§ urine culture positive for bacterial growth in vitro, but cephalosporins and gentamicin generally have
o Pyelonephritis: signs of systemic symptoms excellent activity – Williams)
• gold standard – culture of >100,000 CFU/mL, done between o transition to oral antibiotic regimen for 10–14 days (7-10 days
– Williams)
12-16 weeks AOG
o urine cultures may take 3 to 4 days to become positive à o if one episode of pyelonephritis or ≥ 2 episodes of ASB
and/or cystitis: antimicrobial prophylaxis during pregnancy
urinalysis used as proxy
o urinalysis parameters for UTI
§ (+) leukocyte esterase, nitrates, or hematuria
– Nitrates are sensitive and specific to gram-negative bacteria
§ urine sediment have elevated WBCs and bacteria
• E.coli is the most common species isolated in pregnant women

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CARDIOVASCULAR DISEASES TUBERCULOSIS IN PREGNANCY

*taken from Williams; no discussion in Blueprints
• patients with primary pulmonary hypertension (PH),
• Diagnosis: tuberculin skin test (TST), interferon-gamma release
Eisenmenger physiology, severe mitral or aortic stenosis, and
assay (IGRA)
Marfan syndrome are at high risk of maternal mortality in
• Management
pregnancy
o Latent infection: isoniazid (H) 300 mg daily x 9 months
EISENMENGER SYNDROME, PULMONARY HTN o Active infection: HRZE + pyridoxine
• >50% mortality rate o If with ART: start tx 2-4 weeks after starting TB tx
• most common right-to-left shunts: patent ductus arteriosus and § Resistance to rifabutin, rifampin: pyrazinamide
ventricular septal defect § Aminoglycosides are contraindicated d/t ototoxicity
• often decompensate in third trimester, but risk is concentrated
~2–4 weeks after delivery COAGULATION DISORDERS
• assisted vaginal delivery preferable to elective cesarean • Virchow triad
delivery (pregnancy contraindicated for Group 1 pulmonary HTN: pulmonary o increased coagulation factors
arterial HTN) (may consider epidural analgesia induction and careful attention to
blood loss prevention – Williams) o endothelial damage
VALVULAR DISEASE o venous stasis
• surgical treatment or repair prior to conception for moderate or • increased estrogen in pregnancy
severe disease
• aortic stenosis and aortic insufficiency: decreased afterload to SUPERFICIAL VEIN THROMBOSIS (SVT)
maintain cardiac output (severe aortic stenosis is life- • unlikely to lead to emboli
threatening, so avoid decreased preload – Williams) (for aortic • palpable, usually visible, venous cord that is tender, with local
insufficiency, if with heart failure symptoms, give diuretics and erythema and edema
bed rest – Williams) • symptomatic tx: warm compresses and analgesics
• mitral stenosis: may backup into pulmonary system à
congestive heart failure (vaginal delivery + elective induction – DEEP VEIN THROMBOSIS (DVT)
Williams) • unilateral lower extremity pain and swelling
• pulmonary stenosis : valvuloplasty during pregnancy (severe o > 90% of pregnant women have it in left leg (78-97% - Williams)
stenosis associated with right heart failure and atrial • Conventional imaging: Doppler UTZ (first-line is compression UTZ)
arrhythmias – Williams) • Gold standard: venography
• Tx:
MARFAN SYNDROME o low-molecular-weight heparin (enoxaparin 1 mg/kg BID)
• increased risk of aortic dissection (aortic root diameter > 4 cm) § preferred option d/t no routine checking of activated
• Tx: sedentary lifestyle placed on beta-blockers to decrease partial thromboplastin time (aPTT) and lower risk of
cardiac output (vaginal delivery + regional analgesia and assisted second stage heparin-induced thrombocytopenia
for root diameter <4 cm; elective CS for ≥4 cm – Williams) o unfractionated heparin (goal of aPTT 1.5-2.5 times normal)
§ tx initially with IV heparin, then transition to
PERIPARTUM CARDIOMYOPATHY subcutaneous heparin
• heart failure secondary to dilated cardiomyopathy § side effects: warfarin embryopathy in the 1st trimester
• echocardiogram: dilated heart, EF 20%-40% (nasal hypoplasia, skeletal abnormalities), diffuse CNS
• >34 weeks AOG: risk of remaining pregnant >> premature abnormalities (e.g., optic atrophy)
delivery of fetus
• <34 weeks AOG: administer betamethasone to promote fetal PULMONARY EMBOLUS (PE)
lung maturity, then deliver accordingly • emboli from DVTs travel to right side of heart à block
• heart failure managed with diuretics, digoxin, and vasodilators pulmonary arterial system à pulmonary hypertension, hypoxia
à right-sided heart failure and death
PULMONARY DISEASES • acute onset of shortness of breath, simultaneous onset of
pleuritic chest pain, hemoptysis or tachycardia, and/or
ASTHMA
concomitant signs of DVT
*taken from Williams; no discussion in Blueprints
• Diagnosis
• 20% of pregnant px with mild/moderate asthma have
o CXR may be normal, but may show abrupt termination of
intrapartum exacerbations
vessel and area of radiolucency in lung region beyond PE
• reversible airway obstruction from bronchial smooth muscle
o Spiral CT scan: most common diagnostic
contraction, vascular congestion, mucus, and mucosal edema
o Pulmonary angiography: gold standard. Positive if there are
• in pregnant patients: smaller FRC and increased pulmonary
intraluminal filling defects, or sharp vessel cutoffs
shunting à susceptible to hypoxia and hypoxemia
o ventilation/perfusion (V/Q) scanning: allows visualization
• Diagnosis: Sequential measurement of FEV1 or peak expiratory of perfusion via radioisotope in pulmonary circulation
flow rate (PEFR): best measure of severity § highly specific
• One-third rule: in pregnancy, one-third improves, one-third § if with defects: ventilation scan is performed.
worsens, one-third unchanged Mismatched defects in ventilation and perfusion scans
• Management are suggestive of PE
o Monitoring for moderate to severe patients: measure and • Tx:
record FEV1 or PEFR 2x/day o mild PE: similar to the treatment of DVT
o Treatment o hypotensive or unstable patient: IV heparin
§ Aim: PO2 >60 mm Hg, 90-95% O2 sats o massive PE: streptokinase for thrombolysis in addition to
§ First-line therapy for acute asthma: short-acting β- supportive measures.
adrenergic agonist o Enoxaparin: sometimes used 36 weeks AOG
§ Severe: corticosteroids ± IV MgSO4 or theophylline o Continue tx for 6 months postpartum
§ If nonresponsive: oral prednisone or prednisolone or IV
methylprednisolone, along with beta agonist
o Maintenance: inhaled corticosteroids
GUIDE QUESTION:
Hyperthyroidism in Pregnancy
STATUS ASTHMATICUS
*taken from Williams; no discussion in Blueprints
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• Severe asthma not responding 30-60 mins after intensive tx
• Tx: 100 mg of hydrocortisone given IV every 8 hours during
labor and for 24 hours after delivery
• Prostaglandin F2α or ergotamine derivatives: contraindicated
d/t significant bronchospasm
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THYROID DISEASES NEUROLOGIC AND PSYCHIATRIC DISORDERS

HYPERTHYROIDISM
• Graves disease: most common cause GUIDE QUESTION:
• Management: Seizure Disorders in Pregnancy
o propylthiouracil (PTU): decrease production of T4 + block https://qrs.ly/r5egx49
peripheral conversion to T3
o methimazole: decrease production of T4 only
o use minimal dose possible, since BOTH can cross placenta à
SEIZURE DISORDERS
fetal goiter SEIZURE FREQUENCY
o check initial thyroid-stimulating immunoglobulins (TSI) • During pregnancy: increased seizure frequency (17–33% of
levels (check between 22-26 weeks AOG – Williams), if elevated: fetal pregnancies) (1:200 – Williams)
goiter risk à fetal survey at 18 to 20 AOG + UTZ in the 3rd o Increased circulating estrogen à increased function of P450
trimester enzyme à increased hepatic metabolism of AEDs
o fetal tachycardia may be d/t fetal hyperthyroidism § progesterone: anti-epileptic effects
o follow up TSH and FT4 levels every 6-8 weeks o Increased intravascular volume à increased volume of
distribution (VD) à 50% rise in creatinine clearance that
HYPOTHYROIDISM affects metabolism of carbamazepine, primidone, and the
• Hashimoto thyroiditis: most common cause benzodiazepines à increased metabolism
• ablation or removal of thyroid after Graves disease or cancer: o Added stress, decreased sleep during pregnancy,
second most common cause hyperventilation and pain during labor à lower seizure
threshold
• Levothyroxine supplementation
o Decreased compliance with AEDs* – most important
o increase dose from 25% to 30% (anticipate 25% increase–
Williams) contributor d/t fetal effects concern
o check TSH levels every trimester à must maintain low levels • Best predictor of pregnancy seizure frequency: amount of
by adjusting levothyroxine dose (surveillance every 4-6 weeks) seizures in year prior to pregnancy
o if with history of thyroid cancer: TSH levels must be below
reference range of TSH to prevent recurrence FETAL ANOMALIES AND ADVERSE OUTCOMES WITH AED USE
• risk for fetal anomalies for epileptic patients > baseline
population (4–6% vs. 2–3%)
AUTOIMMUNE DISEASES o fourfold increase in cleft lip and palate
SYSTEMIC LUPUS ERYTHEMATOSUS o threefold increase in cardiac anomalies
• Valproic acid: neural tube defects, neurodevelopmental effects
GUIDE QUESTION: (Malformation risk increased 4-8x)
SLE in Pregnancy • Phenytoin and Phenobarbital: increased malformation rate two-
https://qrs.ly/3regx47 to threefold above baseline
• Lamotrigine and Levetiracetam: lowest risk of malformations
• 20-fold increase in risk for maternal mortality: if with and neurodevelopmental effects
concomitant HTN or renal disease à greater risk of • Mechanisms of teratogenicity
preeclampsia, IUGR, preterm delivery o folate deficiency
• One-third rule: in pregnancy, one-third improves, one-third o epoxide generation
worsens, one-third unchanged MANAGEMENT OF SEIZURES IN PREGNANCY
EARLY PREGNANCY COMPLICATIONS • Goal: Monotherapy with the least teratogenic medication and
• Placental thrombosis à high rate of pregnancy loss (hallmark is the lowest possible dose
second trimester) • if seizure-free for 2–5 years: attempt without AEDs prior to
• Symmetric IUGR by 18-20 wk AOG conception
• Tx: low-dose aspirin, heparin, corticosteroids • Folate supplementation 4mg/day
• Congenital anomaly scan at 19–20 weeks, particularly face and
LATE PREGNANCY COMPLICATIONS central nervous system (CNS)
• Placental thrombosis à IUGR and IUFD • Obtain total and free serum levels of AED monthly
• Frequent antenatal testing by 32 weeks AOG • Optional vitamin K 20 mg QID starting 37 weeks until delivery –
• Tx: low-dose aspirin, subcutaneous heparin, Lovenox reduces risk of spontaneous hemorrhage secondary to
increased vit K metabolism of AEDs
LUPUS FLARES VS PREECLAMPSIA
• Both mediated by antigen-antibody complexes à vasculitis Management of a Pregnant Patient with Seizures or in
• In lupus flare: reduced C3, C4; with active urine sediments, tx Status Epilepticus
with high dose corticosteroids and cyclophosphamide • Assess and establish airway and stable VS
• In preeclampsia: normal C3, C4; no urine sediments; tx by • Assess FHR or fetal status
delivery • Bolus magnesium sulfate, or give 10 g IM
NEONATAL LUPUS • Bolus with lorazepam 0.1 mg/kg, 5.0–10.0 mg at no more
• Two distinct complications than 2.0 mg/min
o Lupus syndrome • Load phenytoin 20 mg/kg, usually 1–2 g at no more than 50
§ skin lesions, hepatosplenomegaly, and low blood counts mg/min
(with positive anti-SSA or SSB – Williams) • Laboratory tests include CBC, metabolic panel, Antiepileptic
o Congenital heart block Drug (AED) levels, and toxicology screen
§ Anti-Ro (SSA) and anti-La (SSB) – cardiospecific, • If fetal testing is not reassuring, move to emergent delivery
damages AV node (SSA>SSB) Management guidelines for pregnant patients presenting with seizures. From Blueprints Obstetrics and Gynecology, 7th
edition.
• Tx: corticosteroids, plasmapheresis, IVIG (maternal plasmapheresis or LABOR AND DELIVERY
IVIG does not reduce risk of heart block – Williams)
• Check AED levels upon admission
o If low: extra dosing or switched to IV benzodiazepines or
phenytoin
• Drug of choice for seizure: phenytoin (vs magnesium used in
preeclamptic patients)

BREASTFEEDING
• Data regarding safety of anticonvulsants are limited
• No obvious deleterious effects have been reported

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SUBSTANCE ABUSE CERVICAL NEOPLASIA

ALCOHOL • In patients with cervical neoplasia and with suspicious lesions,
Fetal alcohol syndrome targeted biopsy may be done. However, endocervical sampling,
• 2-5 drinks/day during pregnancy (no amount of alcohol is safe in endometrial biopsy and treatment of preinvasive lesions are
pregnancy, but binge drinking is associated with higher risks – Williams) unacceptable.
• growth retardation, CNS effects, and abnormal facies • Women with CIN may deliver vaginally
• 1 in 2,000 live births • If higher cancer risk, may repeat colposcopy and cytology/HPV
• Cardiac defects are also particularly associated testing no more frequency than 12 weeks
• Tx: • Hemorrhage from cancer may complicate delivery and
o Counseling program recurrences in the episiotomy scar have been reported thus
o barbiturates for withdrawal most favor cesarean delivery.
o adequate nutrition during pregnancy
CIGARETTE SMOKING UTERINE LEIOMYOMAS
• increased risk for sudden infant death syndrome (but best- • Associated with preterm labor, placental abruption, fetal
documented adverse outcome is fetal growth restriction – Williams) malpresentation, obstructed labor, cesarean delivery, and
• 20% increased risk if <1 pack/day postpartum hemorrhage
• 35% increased risk if >1 pack/day • Morbidity is greatly affected by number, size, and location of
myoma
MARIJUANA
• Submucous myomas may be operated on near term by ligating
• Most common illicit substance used in pregnancy
the stalk vaginally if it is causing bleeding and to avoid avulsion
• Advise to stop use during delivery
COCAINE AND METAMPHETAMINE • Unless the myoma is clearly obstructing the birth canal, trial of
• Cocaine and methamphetamine: associated with abruptio labor may be done
(cocaine), IUGR, preterm labor d/t vasoconstriction à HTN • Myomectomy during cesarean delivery is not recommended
(may mimic preeclampsia) unless there is recalcitrant intraoperative bleeding or if the
• Tx myoma prohibits hysterotomy
o Methamphetamine: detoxification center
o Cocaine: detoxification center, hydralazine OVARIAN MASSES
• Most commonly seen are corpus luteum cysts, endometriomas,
benign cystadenomas, and mature cystic teratomas
POSTPARTUM DEPRESSION
• Most common cause of ovarian hemorrhage is a ruptured corpus
• Postpartum blues: rapid mood swings and appetite, luteum (CL) cyst.
concentration, sleep changes that generally occur within 2-3 o If asymptomatic, may observe
days after delivery, peaking at the fifth day and resolving o If ongoing bleeding is present, progesterone supplementation
within 2 weeks may be needed if CL is removed before 10 weeks
• Postpartum depression: if with symptoms of persisting • Surgical exploration for resection of ovarian masses, if needed,
sadness and disinterest within 6 months of delivery (10-20% can be done at 14-20 weeks AOG.
of women) • Some ovarian masses the result directly from the stimulating
o Physical or verbal abuse is a risk factor effects of pregnancy hormones on the ovarian stroma:
o Associated with serious adverse obstetrical events o PREGNANCY LUTEOMA – rare, benign ovarian neoplasm from
• Management luteinized stromal cells and raises testosterone levels which
o Postpartum blues typically self-limited could cause virilization to the woman and to a female fetus.
o Postpartum depression: SSRIs for as minimum of 6 months Most women are unaffected. Tumors spontaneously regress
to prevent relapse; if with relapse or poor response, consider postpartum
a psychiatric referral o HYPERREACTIO LUTEINALIS – development of multiple,
o Cognitive behavioral therapy large theca-lutein cysts after the first trimester due to
luteinization of the follicular theca interna layer and
SCHIZOPHRENIA IN PREGNANCY stimulation by high HCG. Resolve after delivery
• May be associated with low birth weight, fetal-growth o OVARIAN HYPERSTIMULATION SYNDROME – Multiple
restriction, and preterm delivery ovarian follicular cysts with increased capillary permeability;
• Schizophrenia medications are continued in pregnancy to often a complication of ovulation-induction therapy
prevent recurrence
• Use of atypical antipsychotics are not recommended VULVA AND VAGINA
• Vulvar intraepithelial neoplasia (VIN) and vaginal intraepithelial
NEOPLASTIC DISEASES IN PREGNANCY neoplasia (VAIN) are more common than invasive disease;
• Most common neoplasms during pregnancy are benign. Uterine treated postpartum
leiomyomas and ovarian cysts are the most frequency • Cancer of vagina and vulva are generally a malignancy of older
• Most common gynecologic cancer during pregnancy: cervical women
cancer followed by ovarian malignancies • Treatment is individualized and if incisions are well healed,
vaginal delivery is not contraindicated
• If found in late pregnancy, treatment may be delayed due to slow
progression of the cancer.

INFECTIOUS DISEASES IN PREGNANCY

GUIDE QUESTION:
Bacterial Vaginosis
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VULVOVAGINITIS IN PREGNANCY
BACTERIAL VAGINOSIS (BV)
CLINICAL PRESENTATION
• Asymptomatic (50%)
Williams 26 edition; Figure 66-1 Distribution of Cancer in Pregnant Women
• Fishy smelling discharge
th

• Vaginal pruritus
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DIAGNOSIS DIAGNOSIS
• Amsel’s Criteria (3 out of 4 • KOH (10%) or saline wet prep:
features): o Visualization of pseudohyphae (mycelia)
o Vaginal pH >4.5 and/or budding yeast (conidia)
o Presence of clue cells on a gram • Normal pH (4.0 – 4.5)
stain or wet mount of vaginal
TREATMENT
discharge
o Homogenous, milky-white • Azole creams: Butoconazole, clotrimazole, miconazole,
discharge terconazole (CDC STD Treatment Guidelines, 2010)
o Release of fishy odor when KOH is • Only topical azole therapies (cream, suppository, tablet),
added to the discharge applied for 7 days, are recommended for pregnancy.
• Fluconazole is contraindicated
MATERNAL AND FETAL EFFECTS
• Abortion BV, TRICHOMONIASIS, AND VVC
• Preterm delivery, PROM https://qrs.ly/zpegx4n
• Chorioamnionitis, intraamniotic infection
• Postpartum endometritis
• Post-cesarean wound infection
CDC STD Guidelines (2010) For Pregnant Women GROUP B STREPTOCOCCUS INFECTIONS
• Metronidazole 500 mg/tab BID for 7 days • GBS
• Metronidazole gel 0.75%, one full applicator (5g) intravaginally, o β-hemolytic gram-positive bacteria S. agalactiae
OD for 5 days o cause UTIs, chorioamnionitis, and endomyometritis during
• Clindamycin cream 2%, one full applicator (5g) intravaginally pregnancy
ODHS for 7days o also cause neonatal sepsis (2 to 3 per 1,000 live births)
• Alternatives: (0.2-0.3 per 1,000 live births – Williams)
o Clindamycin 300 mg PO BID for 7 days • 2–50% GBS sepsis mortality rate, depending on GA at delivery
o Clindamycin ovules 100 mg intravaginally ODHS for 3 days o 2% in term infants and 16% in preterm infants
§ Tinidazole should be avoided during pregnancy o GBS is commensal in gastrointestinal (GI) and genitourinary
§ Routine screening is NOT recommended (GU) tracts
• Routine treatment of sex partners NOT recommended. • asymptomatic colonization in pregnant women: 10–35%
DIAGNOSIS OF GBS INFECTION
TRICHOMONAS • rectovaginal culture for GBS colonization: 35-37 weeks
CLINICAL PRESENTATION o positive GBS cultures treated with IV penicillin G at labor or
• Asymptomatic (70%) rupture of membranes (ROM)
• Green-yellow frothy vaginal discharge o GBS results only good for 5 weeks; if negative at 35 weeks of
• Offensive odor gestation, repeat screening at 40 weeks
• “Strawberry” cervix MANAGEMENT OF GBS INFECTION
• Dyspareunia
• treat unknown GBS status at labor that meet certain risk-based
• Vulvovaginal soreness, itching
criteria
• Dysuria, frequency
o experiencing labor before 37 weeks of gestation
• Low back pain
o ROM greater than 18 hours
o temperature >100.4°F
DIAGNOSIS o (Williams) NAAT positive for GBS
• Saline wet mount – motile • treat if with history of GBS UTI or previous infant with GBS
trichomonads independent of screening
• Vaginal pH >4.5 • prophylaxis not indicated if cesarean delivery before ROM and labor
• Culture (Gold standard) • Drug of choice: penicillin G
• Pap smear (liquid-based) o Ampicillin typically used d/t difficulty of proper dose
• DNA probe o if allergic to penicillin but low risk for anaphylaxis (i.e., rash
• Rapid test (antigen detection) allergy): cefazolin (Ancef) for prophylaxis during labor
• NAAT (urine or vaginal swab) o if significant penicillin allergy (i.e., high risk for anaphylaxis):
clindamycin
MATERNAL AND FETAL EFFECTS o If resistant to clindamycin or of unknown susceptibility:,
• Preterm labor and birth vancomycin
• Premature rupture of membranes
• Postpartum endometritis GUIDE QUESTION:
• Low birth weight infant Intraamniotic Infection
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MANAGEMENT
• POGS Clinical Practice Guidelines CHORIOAMNIONITIS
o Metronidazole 2 grams single dose. (CDC STD Treatment
• infection of membranes and amniotic fluid
Guidelines, 2010)
o Partners should be treated • frequent in preterm and prolonged ROM, can occur w/o ROM
o Withhold Metronidazole until after the first trimester • 0.5% to 10% of pregnancies
o Treat symptomatic pregnant women regardless of • histologic chorioamnionitis in up to 20% of term deliveries and
pregnancy stage. (Vaginitis Module, CDC, July 2013) more than 50% of preterm deliveries
• Breastfeeding must be withheld up to 12-24 hours after the • Triple I – intrauterine inflammation, infection or both; most
last dose common precursor of neonatal sepsis
DIAGNOSIS OF CHORIOAMNIONITIS
VULVOVAGINAL CANDIDIASIS (VVC) • combination of fever ≥39°C or 102.2°F based on oral maternal
CLINICAL MANIFESTATIONS temperature with another clinical sign
• Vulvar pruritus – most common o elevated maternal WBC count (>15,000/mL)
• Discharge is thick, white, curdy attached to vaginal walls o purulent fluid from cervical os
• Erythema, irritation o fetal tachycardia (>160 beats per minute)
• External dysuria & dyspareunia o evidence from amniocentesis consistent with microbial
invasion
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• temperature ≥38°C but <39°C is not diagnosis for Triple I; WHAT HAPPENS TO THE WHAT HAPPENS TO THE
two ≥ 38°C, 30 minutes apart with additional clinical factor is MOTHER? BABY?
diagnosis for Triple I • Fatigue • Clinical findings:
• gold standard – culture of amniotic fluid, obtained via • Fever o Low birthweight
amniocentesis • Headache o Hepatosplenomegaly
• Triple I necessitates delivery: exclude other causes • Muscle pain o Jaundice
• if constellation of signs exists at term without other etiology, • Maculopapular rash o Anemia
presume Triple I diagnosis and start treatment • Posterior cervical o Neurologic disease
lymphadenopathy § Micro- or
TREATMENT OF CHORIOAMNIONITIS
• Mostly subclinical hydrocephaly
• initiate IV antibiotics and delivery of fetus o Learning disabilities
• Initial infection confers
• use broad-spectrum coverage • Toxoplasmosis Triad:
immunity
o second- or third-generation cephalosporin or ampicillin and o Chorioretinitis
gentamicin o Intracranial calcifications
o decreased rates of neonatal sepsis and maternal morbidity if o Hydrocephalus
antibiotics are begun intrapartum § *convulsions
• hasten delivery with induction and augmentation by vaginal HOW DO WE MANAGE?
delivery or cesarean delivery (if non-reassuring fetal tracing) • Prevention:
o If cesarean delivery, use either metronidazole or o NO VACCINE
clindamycin, or use broad-spectrum antibiotic which covers o Cooking meat to safe temperatures
anaerobes o Peeling or thoroughly washing fruits and vegetables
o continue antibiotics after cesarean section for 12 to 24 hours o Cleaning cooking surfaces and utensils
o Wearing gloves when changing cat litter or delegating this
duty
GUIDE QUESTION: o Avoiding feeding cats raw or undercooked meat and keeping
Genital Herpes in Pregnancy cats indoors
https://qrs.ly/pjegx50 • Routine screening NOT recommended
• Spiramycin
o Reduce risk of congenital infection
TOXOPLASMOSIS o Acute infection in early pregnancy
• Pyrimethamine, sulfonamides & folinic acid
GUIDE QUESTION: o Eradicate parasites in placenta & fetus
Toxoplasmosis in Pregnancy After 18 weeks or suspected fetal infection
and Congenital Toxoplasmosis
https://qrs.ly/bgegx53 VIRAL INFECTIONS IN PREGNANCY
HERPES SIMPLEX
• Toxoplasma gondii
• Classic presentation: papular eruption with itching and tingling,
• Raw/undercooked meat infected with tissue cysts
then becomes painful and vesicular
• Cat feces with oocysts (litter, soil or water)
o Multiple vulvar and perineal lesions may coalesce, inguinal
• Tachyzoite, bradyzoite, sporozoite
adenopathy may be severe
• Risk of infection increases with duration of pregnancy
o Transient systemic influenza-like symptoms are common
• Endemic in the Philippines (fever, myalgia, malaise)
Tissue cysts containing
bradyzoites in prey • Peripartum transmission – most common route of vertical
transmission
MATERNAL EFFECTS
Oocysts • Preterm labor
Oocysts ingested
Oocysts by animals RISK OF NEONATAL INFECTION
Fecal
contamina6ng
oocysts • Presence of HSV in genital tract
cat li7er • Type of HSV
Soil, water,
and grass • Invasive obstetrical procedure
contaminated • Stage of maternal infection: genital HSV near the time of delivery
>1-2 days with oocysts
NEONATAL INFECTION
Oocysts on unwashed
fruits and vegetable
• (1) Disseminated (25%) – coagulopathy, liver dysfunction,
Oocysts pulmonary failure and death; high mortality and morbidity
• (2) CNS (30%) – seizures, lethargy, irritability, tremors,
temperature dysregulation, bulging fontanelle
• (3) Localized to skin, eye, or mouth

Tachyzoites transmi7ed DIAGNOSIS

transplacentally to fetus • Cell culture
• PCR assays
HOW DO WE DIAGNOSE? • Tzanck smear – (+) multinucleated giant cells
• Serologic tests
o Anti-toxoplasma IgM and IgG MANAGEMENT
• PCR of amniotic fluid or fetal blood • Routine screening for HSV is NOT recommended
• Fetal ultrasound findings: • Acyclovir appears to be safe for use in pregnancy (>36 weeks
o Intracranial calcifications with recurrence)
o Hydrocephaly • Cesarean delivery is indicated for women with active genital
o Liver calcifications lesions or prodromal symptoms
o Hyperechoic bowel, Ascites • Women with HSV may BREASTFEED, if there are no active HSV
o Placental thickening breast lesions. Strict handwashing is advised
o Growth restriction • Valacyclovir and acyclovir may be used during breast feeding.
• Symptomatic partners should be treated. Asymptomatic
partners should be questioned concerning histories of genital
lesions and offered type-specific serologic testing.
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VARICELLA ZOSTER VIRUS (VZV) • The risk of hydrops is directly related to the GA at which
• transmitted by respiratory droplets or close contact and causes maternal infection occurs.
chicken pox o First 12 weeks of gestation: 5% to 10%
o 13 through 20: 5% or less
• attack rate: 60% to 90% (60-95%) after exposure
o beyond the 20th week of gestation: <1%.
• enters mucus membranes and establishes viremia
• Workup: parvovirus IgM and IgG levels.
o prodromal symptoms: headache, malaise, and fever
o followed by diffuse maculopapular rash à vesicular • If studies indicate an acute parvovirus infection (positive IgM
and positive or negative IgG) beyond 20 weeks of gestation:
• incubation period: 10 to 20 days (10-21 days – Williams), with mean
do serial ultrasounds for 12 and up to 20 weeks after
of 14 days
maternal infection is suspected to have occurred
• period of infectivity: 48 hours before rash appears until vesicles
o use Doppler velocimetry to examine the peak systolic
crust over
velocity of the middle cerebral artery (MCA)
• After primary infection, VZV remains dormant in sensory
o increases in peak systolic velocity are associated with fetal
ganglia à reactivated to cause vesicular erythematous skin rash
anemia à cordocentesis should be performed to determine
(herpes zoster or shingles)
the fetal hematocrit à If with anemia, do intrauterine blood
• prior infection with VZV confers lifelong immunity
transfusion
COMPLICATIONS OF VZV INFECTIONS CYTOMEGALOVIRUS (CMV)
VZV pneumonia
• Serologic tests
• risk factor for maternal mortality (mortality is 3% to 14%) o CMV IgG: (+)
(1-2% - Williams)
o IgG avidity index: Low
Congenital varicella syndrome o CMV IgM: (+)
• d/t reactivation of VZV in utero (similar to herpes zoster)
PATHOLOGY
• when mothers are infected between 8-20 weeks AOG, highest
risk in 13-20 weeks • DNA herpesvirus
• Features: • Most common perinatal infection
o skin scarring • Present in body fluids, including breastmilk
o limb hypoplasia • Day-care centers are common source
o chorioretinitis WHAT WILL HAPPEN TO THE BABY?
o microcephaly • Symptomatic CMV Infection (syndrome) – 5 to 10%
• 30% mortality in first month of life o Growth restriction
Neonatal varicella o Microcephaly, intracranial calcifications
• d/t maternal infection in 3rd trimester (5 days before delivery o Chorioretinitis
and up to 48 hours postpartum) à transplacental crossing à o Mental and motor retardation
insufficient cell-mediated immunity of neonate à o Sensorineural deficits
hematogenous dissemination of virus à neonatal varicella o Hepatosplenomegaly, jaundice
• maternal herpes zoster is not associated with congenital o Hemolytic anemia, thrombocytopenic purpura (“blueberry
anomalies or neonatal varicella muffin” baby)
• Other infants may be asymptomatic at birth, but will develop • Asymptomatic; late-onset (majority)
shingles (recurrent herpes zoster outbreaks) later in childhood o Hearing loss o Psychomotor
o Neurologic deficits retardation
MANAGEMENT OF VZV INFECTIONS
o Chorioretinitis o Learning disabilities
• Varicella Zoster Immunoglobulin (VZIG) and/or treatment
with antiviral agents, such as acyclovir or valacyclovir HOW DO WE MANAGE?
o For neonates with varicella disease within 5 days before • Symptomatic treatment
delivery or 2 days after • Passive immunization with CMV Ig (under study)
o (Williams) VariZIG not indicated with known history of varicella • No vaccine available.
• Varivax • Good hygiene and hand washing
o contraindicated in pregnancy to avoid transmission to fetus • Avoid sexual transmission
o for immunization of seronegative mothers prior to conceiving
• VariZIG/ oral acyclovir (800 mg, 5x/day for 7 days), oral GUIDE QUESTION:
valacyclovir (1,000 mg, 3x/day for 7 days) Rubella in Pregnancy
o Both used for postexposure prophylaxis and Congenital Rubella
o Tx within 72 to 96 hours https://qrs.ly/a5egx57
o VariZIG is more recommended, and may extend for up to 10
days post-exposure RUBELLA INFECTION
o If still with disease despite immunoprophylaxis: tx with oral • mild illness in adults
acyclovir or valacyclovir in same dose o nonpruritic, erythematous maculopapular rash
• IV acyclovir o lymphadenopathy that lasts 3 to 5 days
o pneumonia, encephalitis, or disseminated infection and o postauricular adenopathy
those who are immunosuppressed • crosses placenta by hematogenous dissemination
• vaccinated after delivery if treated with postexposure prophylaxis
COMPLICATIONS OF RUBELLA INFECTION
PARVOVIRUS B19 Congenital rubella syndrome
• a DNA virus that causes erythema infectiosum (fifth • congenital infection rate declines with advancing GA
disease), a common childhood illness o 50–80% of infants exposed to virus within 12 weeks AOG
• transmitted primarily by respiratory droplets and infected o Decreased rate of infection after 18 weeks AOG
blood products (up to 90% within 12 weeks; rare incidence after 20 weeks
• the virus is transmitted transplacentally in about 35% of AOG – Williams)
infected women • if maternal infection occurs during organogenesis, any fetal
• infects rapidly dividing cells and is cytotoxic for erythroid organ may be affected; most common are
progenitor cells. o deafness (60–75%)
• Presentation: low-grade fever, malaise, myalgias, arthralgias, o eye defects, such as cataracts or retinopathy (10–30%)
and a red macular “slapped cheek” facial rash, lace-like rash o CNS defects (10–25%)
also may extend to the torso and upper extremities o cardiac malformations (10–20%)
• First-trimester infections have been associated with § most common: patent ductus arteriosus
miscarriage, midtrimester and later infections are associated § pathognomonic: supravalvular pulmonic stenosis
with fetal hydrops.

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DIAGNOSIS OF RUBELLA INFECTION ZIKA VIRUS
• Mothers: IgM titers for primary infection and reinfection • Transmission
• Fetus: o Aedes aegypti mosquitos (Dengue, Chikungunya)
o infant IgM titers (IgM does not cross placenta) o Condomless sex
o IgG titers elevated over time § Vaginal, anal, fellatio (possible)
o fetal immunoglobulins usually cannot be detected before 22 • Onset of symptoms is usually 2-7 days after the mosquito bite
to 24 weeks • Symptoms: headache, fever, red eye, skin rash, knee pain
o PCR testing for rubella antigen: chorionic villi, fetal blood • 1 in 4 people with Zika infection develops symptoms
(cordocentesis), and amniotic fluid (amniocentesis) • Complication: the baby inside the womb od a pregnant mother
o ultrasound examination – best test for serious fetal injury may develop abnormally in the size of its head due to incomplete
TREATMENT OF RUBELLA INFECTION brain development called microcephaly
• no treatment currently • There is no vaccine or specific drug against this virus. Only pain
• Rubella vaccine and fever can be treated.
o if seronegative HOW DO WE PREVENT?
o pre-conception: avoid giving 1 month before conception
• Avoid infection by preventing mosquito bites
o contraindicated in pregnancy; may give postpartum
o Use insect repellants
• Avoid exposure human immunodeficiency virus (HIV) infection o Use window and door screens
• Vertical transmission o Wear long-sleeved shirts and long pants or permethrin-
o 35% to 40% without intervention treated clothing
o decreased viral load decreases vertical transmission risk, but o Once a week empty and scrub, turn over, cover, or throw out
not absolutely protective items that hold water, such as tires, buckets, planters, toys,
or trash containers
GUIDE QUESTION: • People sick with Zika virus should get plenty of rest, drink
HIV in Pregnancy enough fluids, and treat pain and fever with common medicines
https://qrs.ly/rnegx5b • If symptoms worsen, they should seek medical care and advice
immediately to the nearest health facility
• Women planning to conceive or with exposure
HUMAN IMMUNODEFICIENCY VIRUS (HIV) o Delay conception at least 8 weeks after symptom onset or
SCREENING FOR HIV PATIENTS last possible Zika exposure
• offered to pregnant women at first prenatal or preconception • Men with possible Zika exposure
visit on informed “opt-out” basis o Delay conception at least 6 months from symptom onset or
• offered again in third trimester if there are specified risk factors last possible exposure
for HIV infection HOW DO WE DIAGNOSE
• screening test: enzyme immunoassay, antigen/antibody test • Zika virus testing
• confirmatory: Western blot, immunofluorescence o Persons with Zika exposure + symptoms
• if within window of seroconversion and suspected acute HIV o NOT Recommended:
infection, then use plasma HIV PCR and repeat in 2 weeks § Zika exposure with NO symptoms
• performed in intrapartum and/or neonatal periods if serostatus § Planning for conception
is not determined § Assess risk of Zika sexual transmission
ANTEPARTUM MANAGEMENT
CERVICITIS IN PREGNANCY
• Combined antiretroviral therapy (cART) to maintain
undetectable viral load CHLAMYDIA
o infant pre-exposure prophylaxis: transplacental passage of MATERNAL EFFECTS
antiretrovirals • Preterm labor with PROM • Salpingitis
o antiviral use à increased risk of preterm delivery, small for • Postpartum endometritis • Fitz-Hugh-Curtis syndrome
GA infants, and hypertensive disorders • Pelvic inflammatory disease • Reiter’s syndrome
• Tests every three months starting from first visit
o CD4 measurements FETAL EFFECTS
o viral load measurements • Neonatal pneumonia
o baseline blood counts • Ophthalmia neonatorum
o liver and renal function tests
MANAGEMENT
o drug resistance
• Prenatal screening
• Vaccinations:
o hepatitis A and hepatitis B • Treatment during pregnancy (CDC STD Guidelines, 2015)
o pneumococcal vaccinations o Azithromycin 1g PO as single dose, DRUG OF CHOICE
INTRAPARTUM MANAGEMENT • Alternatives: Amoxicillin 500mg PO TID x 7 days, Erythromycin
base or erythromycin ethylsuccinate
• vaginal delivery: women on cART + viral load < 1,000 copies/mL
• Sexual partners during the 60 days preceding the onset of
near delivery (may do CS at 39 weeks AOG – Williams)
symptoms should be evaluated and treated
• CS delivery: women with a viral load >1,000 copies/mL
o 38 weeks AOG GONORRHEA
o zidovudine (ZDV) is recommended 3 hours prior to delivery
DIAGNOSIS
o decreases transmission by 80%
• during labor: minimize contact between infant’s skin and • Culture (Thayer-Martin) – Gold Standard
mucous membranes, maternal blood, and genital secretions • Gram-stain: intracellular gram-negative diplococci
• after delivery: • NAAT
o babies should be bathed immediately • DNA Probe
o ZDV therapy within 12 hours, until 4-6 weeks MATERNAL COMPLICATIONS
o if no maternal antepartum prophylaxis: two-drug (ZDV plus • Septic abortion
nevirapine) or three-drug regimen (ZDV plus nelfinavir and • Preterm delivery, PROM
lamivudine) • Chorioamnionitis
o breastfeeding is contraindicated in HIV-infected woman • Postpartum infection (endometritis, PID)
§ Postnatal HIV transmission from breast milk at 2 years as
• Accessory gland infection (Bartholin and Skene’s gland)
high as 25%.
• Perihepatitis (Fits-Hugh-Curtis syndrome)
§ Counterbalance advantage of bottle-feeding in reducing
• Meningitis and endocarditis (rare, but fatal in pregnancy)
neonatal deaths from AIDS with increases in deaths from
other illnesses, malnutrition, and dehydration
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PERINATAL COMPLICATIONS MATERNAL AND NEONATAL EFFECTS
• Ophthalmia neonatorum • Preterm labor
• Pharyngeal and respiratory tract infection • Congenital syphilis (40-50%)
• Anal canal infection • Neonatal syphilis
MANAGEMENT CONGENITAL SYPHILIS
• Uncomplicated GC infections in pregnancy • Stillbirth, neonatal death, characteristic pale, large placenta
o Ceftriaxone, 250 mg IM, single dose + single dose of • May be asymptomatic (up to 2/3) at birth and develop
Azithromycin 1 g PO (to treat chlamydia co-infection) (CDC symptoms until 3-8 weeks after
STD Guidelines, 2015)
o NEW UPDATE: CDC released an update last Dec 18, 2020 EARLY CONGENITAL LATE CONGENITAL SYPHILIS
increasing the dosing of Ceftriaxone from 250 mg to 500mg SYPHILIS
single IM dose • Non-immune hydrops • Neurological
o Alternative: Gentamicin 450mg IM single dose + • IUGR abnormalities (mental
• Reticuloendothelial retardation, deafness,
Azithromycin, Cefixime 800 mg/tab single dose +
abnormalities (jaundice, hydrocephalus)
Azithromycin
hepatitis, hepatomegaly, anemia) • Dental abnormalities
o All newborns are given ocular prophylaxis (within 1 hr after birth):
• Mucocutaneous lesions (peg-shaped upper incisors/
§ 1% silver nitrate solution, or Hutchinson teeth, mulberry
(rhinitis/snuffles,
§ 1% tetracycline ointment or solution or molars, perioral fissures)
maculopapular rash)
§ 0.5% erythromycin ointment within one hour after birth • Bone abnormalities • Skeletal abnormalities
OTHER CONSIDERATIONS IN PREGNANCY: (periostitis, osteochondritis) (frontal bossing, short and
• Ocular abnormalities protruding mandible, saddle
• Azithromycin (2 g PO): Cephalosporin is not tolerated or nose, flaring scapula, high-
(chorioretinitis, cataract,
allergic to Penicillin arched palate, saber shins,
glaucoma, uveitis)
• Test of cure should be performed 1 week after treatment • CNS abnormalities bilateral knee effusions)
• Pregnant women should NOT be treated with quinolones or (hydrocephalus, seizures,
tetracyclines. hypopituitarism)
GENITAL ULCERS MANAGEMENT
SYPHILIS • Recommended treatment (CDC STD Guidelines, 2015)
• Treponema pallidum o Primary, Secondary, or Early latent (<1 year): Benzathine
• Minute abrasions in vagina are portal of entry penicillin G 2.4 M units single IM dose
• Transplacental transmission is most common o Late latent (>1 year), Latent Syphilis of Unknown Duration,
• Neonatal infection from contact with genital lesions & or Tertiary syphilis with Normal CSF: Benzathine penicillin
membranes G 7.2 M units single IM dose, administered as 3 doses of 2.4
M units IM each at 1-week intervals
PRIMARY SYPHILIS
o Neurosyphilis: Aqueous crystalline penicillin G 18-24 M
units per day administered as 3-4 M units IV Q4 or via
infusions for 10-14 days
• Painless chancre • No proven alternatives to penicillin therapy during pregnancy.
• Non-suppurative Erythromycin may be curative for the mother only.
lymphadenopathy • If with penicillin allergy, oral desensitization is done.
• Quantitative RPR or VDRL titers should be evaluated at 6 and 12
Figure 65-1. Cunningham et al. Williams Obstetrics 25th edition. 2018 mos post-treatment.
SECONDARY SYPHILIS o Four-fold decline by 6 mos post-treatment should be noted.
• Macular rash • Jarisch-Herxheimer reaction often appears after penicillin
(75 - 100%) treatment of women
• Lymphadenopathy (50 - 86%) o Acute febrile reaction accompanied by chills, headache,
• Condyloma lata myalgia, hypotension, tachycardia, and transient
(10 - 20%) accentuation of cutaneous lesions
• Mucous patches o May cause preterm labor and/or fetal distress
(6 – 30%) • Sex partners must be evaluated and treated
• Patchy alopecia (5%)
• Fever, malaise, headache, Figure 65-3. Condyloma lata. Cunningham et al.
PUERPERIUM
arthralgia Williams Obstetrics 25th edition. 2018 ENDOMETRITIS
• Liver and kidney involvement • Polymicrobial infection of the uterine lining that often
• Splenomegaly invades the underlying muscle wall
TERTIARY (LATE) SYPHILIS: RARE • most common after cesarean section (route of delivery is single
• Early latent (subclinical disease acquired within the most significant risk factor – Williams)
preceding 12 mos) vs Late syphilis (diagnosed beyond 12 o Vaginal delivery: 1-2% incidence
mos) vs Latent syphilis of unknown duration o Ruptured membranes, prolonged labor, and multiple
• Gummas cervical examinations: 5-6%
o granulomatous lesions, which destroy soft tissue, cartilage o Intrapartum chorioamnionitis present: 13%
and bone and may be an immunological response to o Cesarean delivery: can reach 50% in some studies, but
treponemal antigens incidence has decreased in the advent of antibiotics
• Cardiovascular syphilis • Risk factors for endometritis
o pathologic lesions of the aortic vasa vasorum; and o Meconium
o Clinically presents as ascending aortic aneurysm, aortic o Chorioamnionitis
insufficiency, or coronary ostial stenosis. o prolonged rupture of membranes.
DIAGNOSIS • Diagnosis:
o Fever**, elevated WBC count, and uterine tenderness, with a
• Screening: VDRL or RPR (reactive)
higher suspicion after CS delivery
• Confirmatory tests: o commonly occurs 5 to 10 days after delivery but may be
• FTA-ABS (e.g. 1:16) suspected when all other sources of infection have been
• TP-PA ruled out
• MHA-TP, TP-PA o UTZ to r/o retained POCs
• Darkfield microscopy showing spirochetes – method of
choice for primary and secondary syphilis
• Lumbar puncture for CSF for neurosyphilis
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• Management: WOUND DEHISCENCE
o broad-spectrum IV antibiotics, or triple antibiotics • Usual healing times: post-operative day 3 if transverse incision,
(for nonsevere metritis, after vaginal delivery, may give oral post-operative day 6-7 if vertical incisions day 6 or 7
or IM antibiotics usually ampicillin + gentamicin – Williams)
• Skin separation after removal of staples/sutures – separation
§ until patient is afebrile for 48 hours; uterine pain and
• If with fascial separation – dehiscence
tenderness are absent; and normal WBC count
• seroma or hematoma may cause wound separation by
o If retained POCs: D&C is performed
preventing tissue apposition
• Management
REGIMEN COMMENTS
“Gold standard”, 90-97% efficacy, once
o Superficial wound separation: secondary intention healing,
daily gentamicin dosing acceptable packing with gauze, or wound vacuum
Clindamycin + PLUS o Dehiscence: OR closure of fascia
gentamicin Ampicillin added to regimen with sepsis
syndrome or suspected enterococcal PUERPERAL MASTITIS
infection
Clindamycin + Gentamicin substitute for renal • d/t patient’s skin flora or the oral flora of breastfeeding infants
aztreonam insufficiency • bilaterally warm, diffusely tender, and firm breasts,
Piperacillin, piperacillin tazobactam, particularly at the time of engorgement or milk letdown
Extended-spectrum
ampicillin/sulbactam, • Management
penicillins
ticarcillin/clavulanate o Dicloxacillin: drug of choice (erythromycin if penicillin-
Cephalosporins Cefotetan, cefoxitin, cefotaxime sensitive; resistant organisms –
Added to other regimens for suspected vancomycin/clindamycin/TMP-SMX – Williams)
Vancomycin
Staphylococcus aureus infections
o If unresponsive: IV antibiotics until afebrile for 48 hours
Metronidazole +
Metronidazole has excellent anaerobic o If unresponsive to IV antibiotics: r/o breast abscess à I&D
ampicillin +
coverage o encouraged to continue breastfeeding, to prevent intraductal
gentamicin
Imipenem/cilastatin, meropenem, accumulation of infected material
Carbapenems o during acute phase of infection: breast pump
ertapenem reserved for special indications
Antibiotic regimens for endometritis following CS deliveries. From Williams Obstetrics, 25th edition.

WOUND COMPLICATIONS GYNECOLOGY REVIEW

CELULLITIS DEVELOPMENTAL BIOLOGY OF SEX
• local erythema around the surgical site + tenderness ✔GUIDE QUESTIONS
• if two symptoms are not present, draw a line around the Genetic female sex is determined by the following factor.
erythema à expands after 12 to 24 hours à highly likely A. Presence SRY gene
cellulitis B. Absence of SRY gene
• Management: broad-spectrum antibiotics, especially targeting C. High levels of estrogen
skin flora D. Low levels of testosterone
Which of the following processes will determine the
ABSCESS development of the fallopian tubes?
• cellulitis not responding to antibiotics + increasing fever, A. Presence of testosterone
evidence of pus, or a palpable fluid collection B. Absence of testosterone
• Management C. Presence of Müllerian-inhibiting factor
o r/o first abscess with incision or UTZ D. Absence of Müllerian-inhibiting factor
o incision and drainage (I&D), wound cleaning, and packing.
o antibiotics are continued until 48 hours afebrile SEX DETERMINATION AND DIFFERENTIATION
o if perineal abscess after third- or fourth-degree lacerations: Processes for determination:
long delayed closure 1. Chromosomal or genetic sex 3. Phenotypic or genital sex
• Necrotizing fasciitis: feared complication 2. Gonadal sex 4. Psychological sex
o loss of initial pain from cellulitis caused by nerve injury Chromosomal sex is basically either XX for female and XY for males.
without change in the visual appearance Gonadal sex from the word “Gonad” which can either be ovaries and
o requires surgical resection of the necrotic tissue testes. Phenotypic sex is how the reproductive organs are expressed
physically i.e. the reproductive tract. Psychological sex is how a person
has been brought up genetically regardless of chromosomal sex
Dr. Banzuela-Cruz

CHROMOSOMAL (GENETIC) SEX

• Established by genetic inheritance at the moment of fertilization
• Determined at time of
fertilization when ovum and
sperm unite
o genetic male
(heterogametic) = XY
pattern
o genetic female
(homogametic) = XX
pattern
• Mutation of genes on an X
chromosome results in
transmission of X-linked
traits
o Examples: hemophilia,
color blindness
• Presence of the Y chromosome is the single most consistent This means that even if there is a hundred X chromosome, as long as there
determinant of maleness is a Y chromosome, that person is genotypically male.
Dr. Banzuela-Cruz
o contains SRY gene responsible for sex determination
KARYOTYPING
o necessary for testes and masculine genital pattern
development • Most accurate method (gold standard)
• Presence of additional X chromosome does not alter • Indications
fundamental maleness dictated by the Y chromosome o Patients who will undergo gender reassignment surgery
o Example: Klinefelter Syndrome (XXY) o Patients with ambiguous genitalia
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GONADAL SEX
• Development of primary sex organs (gonads) in response to genetic sex
• Development of primitive gonad into either
testes or ovary
o outer cortex composed of coelomic
epithelial cells
o inner medulla composed of stromal
mesenchyme which surrounds cords of
epithelial cells
• At 4th to 6th week of gestation, all embryos have
bipotential gonads
o potential to differentiate along either
male or female lines
• Development of the ovary occurs at about the
eleventh or twelfth week
• Two functional X chromosomes are
necessary for optimal development of the ovary
The SRY gene codes for the production of the testes
determining factor which causes the gonadal
medulla to differentiate into the testes. As for the
development of the ovaries, I cannot emphasize
enough that TWO normal and functional X
chromosomes are needed for optimal development
of the ovaries.
Dr. Banzuela-Cruz

PHENOTYPIC (GENITAL) SEX INTERNAL GENITALIA

• Regulation by gonadal sex of the differentiation of the genital • 7 weeks, fetus contains male and female primordial genital ducts:
apparatus o Wolffian ducts (mesonephric duct)
• Influenced mainly by genetics and hormonal factors § have the potential of differentiating into:
• Differentiation of the internal and external genitalia requires - epididymis
presence of hormones or chemical messengers - vas deferens MALE INTERNAL GENITALIA
• Development of phenotypic sex requires: - seminal vesicles
o differentiation of genital ducts (internal genitalia) o Müllerian ducts (paramesonephric ducts)
o differentiation of external genitalia § serves as the anlagen of the:
o hypothalamic differentiation - uterus
- fallopian tube
The development of the reproductive tract is closely associated with the FEMALE INTERNAL GENITALIA
development of the urinary tract. - cervix
Dr. Banzuela-Cruz - upper vagina

Basically, the presence of absence of the SRY gene

will determine whether the bipotential gonad
will differentiate into testes or ovaries. The
testes will produce testosterone and MIH a.k.a.
Anti-Mullerian hormone (AMH). MIH is
important for the development of the uterus,
fallopian tube and the upper 3rd of the vagina. I
always think of Müllerian agenesis when I think
about these structures. Women with MRKH have
XX chromosomes which are necessary in the
proper development of the ovaries but they lack
uterus, fallopian tubes and upper part of the
vagina. Most of the time, the vaginal opening is
also very narrow and require dilation. But these
patients have a clitoris (since testosterone is
absent) so okay naman din. J
Also, I use this mnemonic: W=wolffian=sounds
like a guy “wolf”, M=Mullerian=Mamae (babae)
Dr. Banzuela-Cruz

HORMONAL INFLUENCE
TESTOSTERONE MÜLLERIAN INHIBITING FACTOR (MIF)
• responsible for differentiation of Wolffian ducts to male internal • other names: Anti-Mullerian Hormone (AMH), Mullerian
genitalia at 9 to 10 weeks Regressing Factor (MRF)
• secreted by fetal Leydig cells • glycoprotein hormone produced by Sertoli cells
• does NOT have to be converted to its active product • induces dissolution of Müllerian ducts, therefore inhibiting
(dihydrotestosterone) to act on the Wolffian ducts differentiation of female internal genitalia
o 5-a reductase activity is required for conversion of
testosterone to dihydrotestosterone
o cells do not develop 5-a reductase activity until they have fully
differentiated

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SRY protein in a male embryo

directs the medulla of the
Tes6s Gonadal cortex becomes ovary
bipoten6al gonad to develop
into tes6s. in the absence of SRY protein
1 1
Mullerian duct
An6-Mullerian hormone from
Wolffian duct
tes6s causes the Mullerian
ducts to disappear. 2
Absence of testosterone causes
Wolffian duct to degenerate.
2 Uterus

Prostate Testosterone from tes6s

converts Wolffian duct into Ovary
Seminal seminal vesicle, vas deferens, Absence of an6-Mullerian
vesicle and epididymis. DHT controls hormone allows the Mullerian Fallopian tube (from
prostate development. duct to become the fallopian Mullerian duct)
Vas deferens
3 tube, uterus, and upper part of
Tes6s the vagina.
3 Uterus
Epididymis
Vagina

PHENOTYPIC (GENITAL) SEX

GENITAL DEVELOPMENT
EMBRYOLOGIC STRUCTURES MALE FEMALE
Labioscrotal swelling Scrotum Labia Majora
Urogenital folds Ventral portion of the penis Labia Minora
Phallus (genital tubercle) Penis Clitoris
Urinary bladder Urinary bladder
Prostate gland Urethral and Paraurethral glands
Urogenital sinus Prostatic Utricle Vagina
Bulbourethral glands Greater vestibular glands
Seminal colliculus Hymen
Hydatid of Morgagni
Uterus and Cervix
Paramesonephric duct Appendix of testes
Fallopian Tubes
Upper 1/3 of the vagina
Appendix of epididymis Appendix of vesiculosis
Ductus of epididymis Duct of epoophoron
Mesonephric duct Ductus deferens
Ejaculatory duct Gartner’s Duct
Seminal Vesicle
Ureter
Metanephric duct Renal Pelvis
Ureteric bud Calyces
Collecting system
Metanephric Glomerulus
Mesenchyme Renal Collecting Tubules
Undifferentiated gonad Testes Ovary
Cortex Seminiferous tubules Ovarian Follicles
Medulla Rete Testis Rete Ovarii
Round ligament of uterus
Gubernaculum Gubernaculum testis
Ovarian ligament
BIPOTENTIAL BIPOTENTIAL
MALE FEMALE MALE FEMALE
STRUCTURE STRUCTURE
Regresses GONAD (cortex) Ovaries Glans Penis, Corpus
GENITAL Clitoris,
cavernosum/
TUBERCLE Vestibular bulb
Testis GONAD (medulla) Regresses spongiosum
Epididymis, Penis (Ventral Shaft) GENITAL FOLDS Labia minora
Vas Deferens, WOLFFIAN DUCT Regresses GENITAL
Scrotum, Prepuce Labia majora
Seminal Vesicle SWELLING
Fallopian tubes, female urethra,
Male urethra,
Uterus, Cervix, UROGENITAL lower vagina,
Regresses MÜLLERIAN DUCT Cowper’s gland,
Vagina (upper SINUS Bartholin’s glands,
prostate gland
1/3) Skene’s glands
MALE FEMALE

Genital tubercle Glans penis, corpus cavernosum, Clitoris, vesBbular bulb

corpus spongiosum

Urogenital sinus Urethra, Cowper’s, Prostate Urethra, Skene’s, Bartholin’s

gland, lower vagina
Urogenital fold Ventral sha> of penis Labia minora
Labioscrotal swelling Prepuce, scrotum Labia majora

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SPECIAL CONSIDERATIONS
• Normal FEMALE, hormones may not be essential for differentiation
• Growth of labia to normal size requires estrogen
• Normal FEMALE fetus exposure to excess testosterone during
differentiation causes virilization
o Early: male pattern can result
o After differentiation: enlargement of clitoris may occur
• For newborn with ambiguity of external genitalia
o postpone signing of birth certificate
o do screening test

ERRORS IN SEXUAL DETERMINATION AND

DIFFERENTIATION
NONDISJUNCTION
• Established defect in gametogenesis
• Chromosomes fail to separate therefore both go to one of the TURNER SYNDROME (XO)
daughter cells during meiosis, the other has none https://diffzi.com/turner-syndrome-vs-klinefelter-syndrome/

NONDISJUNCTION OF CHROMOSOMES DURING MEIOSIS

KLINEFELTER SYNDROME (XXY)

OVUM https://diffzi.com/turner-syndrome-vs-klinefelter-syndrome/
X XX O
XX XXX
XO SUPERFEMALE (TRIPLE X SYNDROME)
X Turner
Normal Triple X
Syndrome
• Only one X chromosome is active
XXY o two Barr bodies are present
XY YO • Usually no distinguishable difference between triple X and
Y Klinefelter
SERUM

Normal Lethal normal females

Syndrome
XXY o some studies show increased risk for menstrual
XXX
XY Klinefelter -- irregularities and learning disorders
Triple X
Syndrome
XXO
O --
Turner Syndrome
-- HERMAPHRODITISM
• Disorder of sexual differentiation
Take note that fertilization happens during Meiosis II, where a haploid (either an
X or a Y) sperm fertilize either a haploid or diploid egg cell. If you look at the • Born with both ovarian and testicular tissues
figure above, when the non-disjunction happens during meiosis I, it will yield 2 • Two types:
triploids and 2 haploids. If nondisjunction happens after meiosis I and affects one o TRUE hermaphrodites
of the daughter chromatids, it will yield 2 normal diploids, 1 triploid and a § functional gonads
haploid. To be able to understand non-disjunction better, please see clip below: o PSEUDOhermaphrodites
Dr. Banzuela-Cruz
§ phenotype and genotype do NOT match
§ non-functional gonads
CHROMOSOME
True hermaphrodites are very rare, and studies are limited to animals.
NONDISJUNCTION What happens here is that the SRY gene is transferred to the one of the X
https://qrs.ly/ahbk4tz chromosomes (for XX karyotype). May episode sa KMJS of a True
hermaphrodite, probably with both male and female phenotype but with
a functioning uterus and ovaries.
TURNER SYNDROME Dr. Banzuela-Cruz

• Complete absence of one sex chromosome (Barr body) TESTICULAR FEMINIZATION

o leads to monosomy X (XO genotype) (ANDROGEN INSENSITIVITY)
• Short stature (< 5 feet)
• Genetic males whose target cells lack receptors for testosterone
• Ovarian dysgenesis (streak ovary)
are feminized
• Shield chest with widely spaced nipples
• Male pseudohermaphrodites
• Webbed neck
o male genotype, female phenotype
• Coarctation of the aorta
KLINEFELTER SYNDROME CONGENITAL ADRENAL HYPERPLASIA
• Meiotic nondisjunction leads to a 47, XXY genotype (ADRENOGENITAL SYNDROME)
• Testicular atrophy • Adrenal androgen overproduction in the fetus
• Eunuchoid body shape • Female pseudohermaphrodites
• Tall, long extremities o female genotype, male phenotype
• Gynecomastia o virilization of an XX fetus
• Female hair distribution o ambiguous genitalia
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Turner syndrome is the only monosomy compatible to life. YO is always The labia minora fuse anteriorly to form the frenulum of the clitoris,
lethal. The ovaries of patients with Turner syndrome however are posteriorly forming the posterior fourchette. The labia majora naman
underdeveloped because as we’ve mentioned, 2 functioning X meets anteriorly to form the prepuce and posteriorly to form posterior
chromosomes are needed for the proper development of the ovaries. commissure.
These patients may need a lifetime intake of estrogens to be able to Dr. Banzuela-Cruz

promote development of the secondary sexual characteristics. Those with PERINEUM

Klinefelter’s seem genetically female at birth, hence although genetically
male, they are often raised as females.
Dr. Banzuela-Cruz

REPRODUCTIVE ANATOMY
VULVA
• Includes all structures visible externally from the pubis to the
perineal body:
o Mons pubis o Labia majora and minora
o Clitoris o Vestibule
o Urinary meatus § Hymen
§ Vaginal opening
§ Urethral opening
§ Glandular structures
Mons pubis
Clinical Significance
Prepuce
Clitoris
Frenulum
Labium majus Urethral meatus
Labium minus Anterior vaginal wall
Hymen tags Vaginal orifice
Fossa Perineal body
navicularis

Fourche>e
Anus
Adapted from Lobo, et al. Comprehensive Gynecology. 7th ed. 2017
Boundary Landmark
LABIA MAJORA AND LABIA MINORA Anterior Pubic Symphysis
LABIA MAJORA LABIA MINORA Anterolateral Ischiopubic Rami And Ischial Tuberosities
Ventral portion of the Posterolateral Sacrotuberous Ligaments
Homology Scrotum penis Posterior Coccyx
Skin of the penis
Lining Outer- KSSE Triangle
NKSSE
epithelium Inner- NKSSE • Urogenital triangle
Lie in close apposition Not visible behind the • Boundaries:
Nulliparous Anterior
Inner surface resembles non-separated labia • Superior- pubic rami
women to Superficial
the mucous membrane majora
• Lateral-ischial tuberosities
Gape widely Project beyond the and deep
Multiparous • Posterior: superficial transverse perineal
Inner surface become labia majora
women skin like muscle
• Anal triangle
(+) Hair follicles No hair follicles • ischiorectal fossa, anal canal, anal
Glands (+) Sweat glands No sweat glands Posterior sphincter complex, and branches of the
(+) Sebaceous glands (+) Sebaceous glands internal pudendal vessels and pudendal
nerve
VESTIBULE
• Functionally mature female structure of the urogenital sinus of Urogenital (Anterior) Triangle: SUPERFICIAL SPACE
the embryo. • bounded deeply by the perineal membrane
• Extends from clitoris to posterior fourchette and superficially by Colles fascia
STRUCTURES IN THE VESTIBULE • ischiocavernosus, bulbocavernosus, and
• Non keratinized Stratified squamous Closed
superficial transverse perineal muscles;
epithelium compartment
Bartholin glands; vestibular bulbs; clitoral
• During first coitus, first that ruptures is usually body and crura; and branches of the
HYMEN
at the 6 o’clock position pudendal vessels and nerve
• Caruncle Myrtiformes: Remnants of hymen in Ischiocavernosus
adult female • clitoral erection
muscle
GLANDULAR • Paraurethral Glands “Skene’s Glands” Bulbocavernosus • Bartholin gland secretion
STRUCTURES • Vulvovaginal Glands “Bartholin’s Glands” muscles • Clitoral erection
• Vaginal introitus Superficial
• may be attenuated or even absent
• Urethral opening transverse
6 OPENINGS: • Contributes to the perineal body
• Paired Skene’s glands opening perineal muscles
• Paired Bartholin ducts opening Urogenital (Anterior) Triangle: DEEP SPACE
GLANDULAR STRUCTURES • Lies deep to the perineal membrane and
PARAURETHRAL extends up into the pelvis
VULVOVAGINAL GLANDS
GLANDS • Contents: compressor urethrae and
“BARTHOLIN’S GLANDS” Continuous
“SKENE’S GLANDS” urethrovaginal sphincter muscles, external
space with the
Another Lesser vestibular Greater vestibular urethral sphincter, parts of urethra and
pelvis
Name glands glands vagina, branches of the internal pudendal
Male artery, and the dorsal nerve and vein of the
Prostate Bulbourethral gland clitoris
Homology
Type of Compound alveolar/ • Wedge-shaped spaces found on either side
Tubulo-alveolar Ischiorectal of the anal canal and comprise the bulk of
Gland compound acinar
Adjacent to the 4 and 8 o’clock of the fossae the posterior triangle
Location • Continuous space
urethra vagina
Pathology Urethral diverticulum Bartholin’s cyst/ abscess
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PUDENDAL NERVE AND VESSELS • Vesicovaginal septum

Roots Anterior rami of the 2nd to 4th sacral nerve o Separates the vagina from the bladder and urethra
between the piriformis and coccygeus muscles and exits • Rectovaginal septum
through the greater sciatic foramen in a location o Separates the lower portion of the vagina from the rectum
Course posteromedial to the ischial spine → obturator internus • Rectouterine pouch of Douglas
muscle → pudendal canal (Alcock Canal) → enter the o Separates the upper of the vagina from the rectum
perineum and divides into three terminal branches • Upper vaginal vaults
o Subdivided into anterior, posterior, and two lateral fornices
Terminal Branches: by the uterine cervix
Dorsal Nerve of the Clitoris Skin of the clitoris o Posterior fornix provides surgical access to the peritoneal
Muscles of the anterior triangle cavity
Perineal Nerve
and labial skin Rectouterine pouch of Douglas One of the main
External anal sphincter, the structures that we
Inferior Rectal mucous membrane of the anal palpate during
canal, and the perianal skin rectovaginal exam is
the Pouch of Douglas. A
Landmark for Pudendal feeling of fullness may
Ischial spine
Nerve Block indicate the presence of
Blood Supply Internal pudendal artery fluid, which can either
be due to ovulation or
INTERNAL GENITALIA pwede rin blood due to
ruptured ectopic
VAGINA pregnancy. We rarely
• Thin-walled, distensible, fibromuscular tube that extends from Rectovaginal Vesicovagina do culdocentesis kasi
the vestibule of the vulva to the uterus septum septum may ultrasound naman
na to help us diagnose
• Rugae in reproductive aged women has an accordion like hemoperitoneum
distensibility Dr. Banzuela-Cruz

BLOOD SUPPLY LYMPHATICS NERVES SUPPORT

UPPER Cervico-Vaginal branch of Sympathetic via Cardinal ligaments, uterosacral
1/3 uterine artery External and internal Hypogastric plexus ligaments, and parametria
MIDDLE iliac nodes Parasympathetic via S2-S4 Paravaginal attachments to the pelvic
Inferior Vesical Arteries
2/3 (low density) walls covering the levator ani
LOWER Middle Rectal and General somatic via the
inguinal nodes Urogenital and pelvic diaphragm
1/3 Internal Pudendal Artery Pudendal Nerve
CERVIX UTERUS
• The lower, narrow portion of the uterus • Thick-walled, hollow, muscular organ located
• May vary in shape from cylindric to conical. centrally in the female pelvis
• Usually 2.5 to 3 cm in length and 7 to 8 mm at its widest point • globular
• It consists of predominantly fibrous tissue in contrast to the Description • Inverted pear
primarily muscular corpus of the uterus. • Isthmus: short area of constriction in the
• The vagina is attached obliquely around the middle of the cervix; lower uterine segment
this attachment divides the cervix into an upper, supravaginal • Fundus: dome-shaped top of the uterus
portion and a lower segment in the vagina called the portio • Nulliparous woman is approximately 8 cm
vaginalis long, 5 cm wide, and 2.5 cm thick and weighs
40 to 50 g.
ENDOCERVIX EXOCERVIX Size • Multiparous woman each measurement is
• Supravaginal portion • Portio vaginalis approximately 1.2 cm larger and normal
• Extends from the isthmus uterine weight is 20 to 30 g heavier.
• Extends from the
(Internal Os) to the • The maximal weight of a normal uterus is 110g
squamocolumnar junction to
ectocervix and contains the STRATUM FUNCTIONALE
the external orifice
endocervical canal • responds to fluctuating Zona
• Single layer of mucous hormonal levels Spongiosa
secreting highly ciliated • Non keratinized stratified • Shed during menstruation
columnar epithelium which is squamous epithelium • Supplied by the Spiral Arteries Zona
thrown into folds forming • Hormone Sensitive Endometrium compacta
• Superficial 2/3
complex glands and crypts STRATUM BASALE
• Extensive amount of nerves • Few nerves only • Source of Stratum Functionale after menstruation
• Blood supply: Cervicovaginal branch of uterine artery located at • Supplied by the Straight arteries
the lateral walls • Basal 1/3
• Inner Longitudinal
CLINICAL CORRELATES: Myometrium • Middle oblique
• The major arterial supply to the cervix is located on the lateral • Outer longitudinal
cervical walls at the 3 and 9 o’clock positions, respectively. Serosa • Visceral peritoneum
Therefore a deep figure-of-eight suture through the vaginal
mucosa and cervical stroma at 3 and 9 o’clock helps to reduce FALLOPIAN TUBES
blood loss during procedures such as cone biopsy • The paired uterine tubes extend outward from the superolateral
• The transformation zone encompasses the transition from portion of the uterus and end by curling around the ovary.
stratified squamous epithelium to columnar epithelium. Most • They are between 10 and 14 cm in length and slightly less than
cervical dysplasia develops within this transformation zone 1 cm in external diameter.
• Each tube is divided into four anatomic sections.

Figure 3-19a. Lobo, et al. Comprehensive Gynecology. 7th ed. 2017

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SEGMENTS OF THE FALLOPIAN TUBE LIGAMENTS OF THE OVARY
• 2% of ectopic LIGAMENT DESCRIPTION
• 1 to 2 cm in length pregnancy • Formed by the posterior portion of the broad
Intramural
and is surrounded • Ectopic pregnancy at ligament
Interstitial
by myometrium this area result in severe • Attaches to the anterior border of the ovary
maternal morbidity Mesovarium • contains the arterial anastomotic branches of
• The narrow portion • Most highly developed the ovarian and uterine arteries, a plexus of
of the tube that musculature veins, and the lateral end of the ovarian
adjoins the uterus, • Narrowest portion ligament
passes gradually • Preferred portion for • narrow, short, fibrous band that extends from
into the wider, applying clips for Ovarian Ligament the lower pole of the ovary to the uterus
Isthmus
lateral portion. female sterilization
• Preferred portion for • forms the superior and lateral aspect of the
Infundibulopelvic
tubal ligation broad ligament
Ligament
• 12% of ectopic • Contains the ovarian artery, ovarian veins,
(suspensory
pregnancy and accompanying nerves
ligament of the
• 4 to 6 cm in length • Site of fertilization • It attaches the upper pole of the ovary to the
ovary)
and approximately 6 • 80% of ectopic lateral pelvic wall.
mm in inside pregnancy BLOOD SUPPLY OF THE OVARIES
Ampulla diameter. It is wider Ovarian Arteries • Arise directly from the aorta
and more tortuous • Accompany the arteries
in its course than
• Left ovarian vein drains into the left
other segments Ovarian Veins renal vein
• Fimbriated • 5% of ectopic • Right ovarian vein drains into the
extremity pregnancy inferior vena cava
• Tunnel shaped Lymphatic drainage • Aortic nodes
Infundibulum
opening of the distal
Uterine Uterine
end of the fallopian Ovarian
fundus body
Uterine ligament
tube tube
Mesosalpinx
Epoophoron
SEGMENTS OF THE Mesovarium
FALLOPIAN TUBE
https://qrs.ly/mnegx6g
Vesicular
appendix

OVARIES Vagina
• Lies on the posterior aspect of the broad ligament, in the ovarian fossa Abdominal
Ovary External os
os?um
o Immediately adjacent to the ovarian fossa are the external Suspensory ligament
iliac vessels, the ureter, and the obturator vessels and of ovary Ovarian Mesometrium Intravaginal
nerves. fimbra cervix of uterus

• Are attached to the broad ligament by the mesovarium. POSTERIOR ASPECT OF THE BROAD LIGAMENT – SPREAD OUT TO
• They are not covered by peritoneum. DEMONSTRATE THE OVARY
Adapted from Lobo, et al. Comprehensive Gynecology. 7th ed. 2017

DIAPHRAGM AND LIGAMENTS

DESCRIPTION
• Wide but thin muscular layer of tissue that forms the inferior border of the abdominopelvic cavity
• Composed of a broad, funnel-shaped sling of fascia and muscle, it extends from the symphysis pubis to the coccyx and from
one lateral sidewall to the other
PELVIC DIAPHRAGM • Major muscles: coccygeus and levator ani (pubococcygeus, puborectalis, and iliococcygeus)
(endopelvic fascia) • The paired levator ani muscles act as a single muscle and functionally are important in the control of urination, in
parturition, and in maintaining fecal continence
• important in supporting both abdominal and pelvic viscera and facilitates equal distribution of intraabdominal
pressure during activities such as coughing
UROGENITAL • Strong, muscular membrane that occupies the area between the symphysis pubis and ischial tuberosities
DIAPHRAGM • Support the urethra and maintain the ureterovesical junction
(triangular ligament)
• Two wing-like structure that extend from the lateral margins of the uterus to the pelvic walls
• Divide the pelvic cavity into anterior and posterior compartments
• Fallopian tubes
Reproductive structures
• ovaries
Broad ligament
• Ovarian arteries
Vessels:
• Uterine arteries
• Ovarian ligament
Ligaments:
• Round ligament of uterus
• Originated form the densest portion of the broad ligament
Cardinal ligament
• Medially united to the supravaginal wall of the cervix
(Transverse Cervical;
• Provide the major support of the uterus and cervix
Mackenrodt ligament)
• Maintain the anatomic position of the cervix and upper part of the vagina
• From posterolateral to the supravaginal portion of the cervix encircling the rectum then inserts into the fascia over S2, S3
Uterosacral ligament
• serve a role in the anatomic support of the cervix
• Extend from the lateral portion of the uterus, arising below and anterior to origin of the oviducts, that is continuous with the broad
Round Ligament
ligament, outward and downward to the inguinal canal terminating at upper portion of labia majora
Uterine tube Ovarian artery
and vein Ovarian
ligament
The broad ligament contains
various important structure. During
extensive pelvic surgery such as
TAHBSO, the broad ligament is
opened to be able to visualize these
Ovary structures.
Dr. Banzuela-Cruz
Round
ligament

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PELVIS
Pelvic Organs: BLOOD SUPPLY
MAJOR BLOOD SUPPLY TO THE FEMALE REPRODUCTIVE
SYSTEM FALSE PELVIS
Pudenda • Internal Pudendal artery
Vagina • Vaginal Artery of the Uterine Artery
Cervix • Cervicovaginal branch of Uterine artery
Uterus TRUE PELVIS
• Uterine Artery
Fallopian tubes
• Ovarian Artery
Ovaries
PARTICIPANTS IN THE COLLATERAL CIRCULATION OF THE
FEMALE PELVIS
ANT: lower abdomen
• Ovarian artery
False POST: lumbar vertebra
Branches from the • Inferior mesenteric
LATERAL: iliac fossa
Aorta • Lumbar and vertebral
LINEA TERMINALIS
• Middle sacral arteries
SUPERIOR BOUNDARY: Pelvic inlet
Branches from the • Deep iliac circumflex
INFERIOR BOUNDARY: Pelvic outlet
External Iliac Artery • Inferior epigastric artery
True ANTERIOR: Pubic Bones, Ascending Rami Of Ischial Bones,
Branches from the • Medial femoral circumflex artery
Obturator Foramina
Femoral Artery • Lateral femoral circumflex artery LATERAL: Ischial Bones and Sacrosciatic Notch
COMMON INJURIES PELVIC JOINTS
Genitofemoral • Anesthesia in
• Anterior: symphysis pubis/arcuate ligament of the pubis
nerve perineum
• Posterior: sacroiliac
• Interfere with
Radical hysterectomy • Hormonal changes during pregnancy cause laxity of these joints
adduction of the
Iliac and obturator • By 3-5 months POST PARTUM, laxity has regressed
Obturator thigh and hip
node dissection • Symphysis Pubis increase in width also Increase mobility and
nerves • Sensory function
on the medial displacement of the sacroiliac joint
aspect of the thigh WHY THE DORSAL LITHOTOMY POSITION?
Improper placement • Footdrop • Upward gliding of sacroiliac joint is GREATEST in the DORSAL
of legs in the stirrups • Sensory and motor LITHOTOMY POSITION
Peroneal nerve
or prolonged dorsal loss over. The • Outlet increase by 1.5 -2.0 cm
lithotomy position lateral lower leg True conjugate
Damaged due to Obstetric conjugate
Diagonal conjugate symphysis
pressure from lateral • Prohibits flexion of
blade of a self- the hip, patient is
Femoral nerve
retaining retractor not able to lift leg
during an abdominal off the bed
hysterectomy
• In 15-20% of
Anteroposterior
Node dissection of External iliac population, EIA is a diameter
the obturator fossa artery major blood of midpelvis
supply to the pelvis
Inguinal node
Femoral nerve ---
dissection
Straddle or after • Injury producing a
Pudendal
giving anesthetic for very large
artery
second stage labor hematoma
They can ask these in the Anatomy part of the exam. They can also phrase
in a way of a case of prolonged third stage of labor, or complicated
vaginal hysterectomy (both of which place patient in prolonged lithotomy
position) hence, the peroneal nerve may be damaged causing foot drop.
Dr. Banzuela-Cruz

AP
False
pelvis
Posterior
sagiEal
True
pelvis Anterior Linea terminalis
sagiEal

PELVIC TENDENCY AND TYPE

• Determined by the greatest transverse diameter of the inlet and its division into the anterior and the posterior segments
• Anterior – dictates the tendency of the pelvis
• Posterior – dictates the type or character of the pelvis
GYNECOID ANDROID ANTHROPOID PLATYPELLOID
FREQUENCY 50% 20% 25% 5% rarest
INLET SHAPE Round Heart Shaped Vertically oriented oval Horizontally oriented oval
SIDEWALLS Straight Convergent Convergent Divergent, then convergent
ISCHIAL SPINES Non prominent Prominent Prominent Non prominent
Inclined neither anteriorly nor Forward and straight with Straight = pelvis deeper than Well curved and rotated
SACRUM
posteriorly little curvature other 3 types backward
• Increased incidence of Deep • Increased incidence of Face
• Good prognosis for vaginal Transverse Arrest Delivery • Poor prognosis for
SIGNIFICANCE
delivery • Limited posterior space for • Good prognosis for vaginal vaginal delivery
fetal head, poor prognosis delivery

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REPRODUCTIVE ENDOCRINOLOGY
OVERVIEW OF MENSTRUAL CYCLE
36.7
• Spontaneous, cyclical ovulation occurs at 25- to 35-day intervals
36.4
• Cyclical ovulation continues for almost 40 years between menarche
and menopause
• Approximately 400 opportunities for pregnancy, which may occur
with intercourse on any of 1,200 days (includes day of ovulation and
its two preceding days).
• Menstrual cycle days 20 to 24 is the narrow window of endometrial
receptivity to blastocyst implantation.
• Divided in 14-day phases:
Inhibin
Days 0-14 Days 15-28
Phase Phase
Changes in the
Ovarian Cycle Follicular Luteal
ovary
Endometrial Changes in
Proliferative Secretory
Cycle endometrium
Destruction Repair and Secretion by
of functional regeneration uterine glands
zone of functional
Previous references state that the normal menstrual cycle is 28+/-7 days (21-35
zone days)
Dr. Banzuela-Cruz

MENSTRUAL CYCLE
Proliferative Secretory https://qrs.ly/t1egx6j

HPO AXIS • Functional hypothalamic amenorrhea

Please try to understand the HPO axis completely. Most of the questions • Hypogonadotropic hypogonadism (Kallmann syndrome)
in Gynecology has something to do with these. If you are able to • Precocious puberty
comprehend this fully, you can actually derive most of the answers from • Hormone-dependent tumors
here. • Suppression of ovarian
Dr. Banzuela-Cruz
function in PCOS and IVF
• PMS
• DUB
• Contraception GNRH AGONIST
• Suppression of AND ANTAGONIST
spermatogenesis https://qrs.ly/ucegx6s
• Ovulation inhibition
GONADOTROPINS: FSH AND LH
• Structural similarity- Identical α subunits, Different β subunits
• Follicular Stimulating Hormone (FSH) – Acts on the
granulosa cells of the ovarian follicles to stimulate follicular
growth
• Luteinizing Hormone (LH) – Acts on the theca cells and on
Know the difference between positive and negative feedback. Negative the luteal cells to stimulate ovarian steroid hormone
feedback: pag maraming product, the signal to the hypothalamus tells it production
to stop producing the substrate. This is true for most physiologic
functions. Positive feedback happens, however, during Follicular Phase OVARIAN STEROIDS
where an increase in estrogen consequently increases and causes a spike HORMONE ACTIONS
in the Luteinizing hormone (LH surge) signaling ovulation • It represents a group of hormones including
Dr. Banzuela-Cruz
estrone, estradiol, and estriol.
GONADOTROPIN-RELEASING HORMONE • Secretion is regulated by follicle-stimulating
• Regulates secretion of FSH and LH hormone (FSH)
Estrogen
• Secreted in pulsatile manner to be effective • For development of secondary sex
• Released from neurons within the anterior hypothalamus characteristics in females at puberty
(arcuate nucleus of the median basal hypothalamus • Thickens endometrium during the
proliferative phase
• Secretion is regulated by Luteinizing Hormone (LH)
GNRH AGONIST AND ANTAGONIST
• Maintains endometrium during secretory phase
DRUG Progesterone
DRUG NAME MECHANISM OF ACTION • Prepares endometrium for implantation
CLASS
(during pregnancy)
• Buserelin,
Gonadorelin, • Agonist to the GnRH receptor Know the actions of estrogen and progesterone by heart. Most of the
Goserelin, • Interacts with the GnRH receptor questions evolve around these two hormones. Remember: Estrogen-
GnRH
Hostrelin, to elicit its biologic response pampakapal ng matres (endometrium), Progesterone - pampanipis
Agonist
Leuprorelin, • ”flare” response followed by or pangmaintain ng matres. Also remember E1: estrone (menopause),
Naferlin, hypogonadal effect E2: estradiol (most potent, reproductive age), E3: estriol (pregnancy).
Triptorelin Therefore, estrogen is almost always present however the potency of the
• Abarelix, • Competitively and reversibly estrogen varies.
Dr. Banzuela-Cruz
Cetrorelix, bind to GnRH receptors in the
GnRH Degarelix, pituitary gland, blocking the release OVARIAN CYCLE
Antagonist Ganirelix, of luteinizing hormone (LH) and
Elagolix and follicle-stimulating hormone (FSH) This video will explain the hormonal influences involved in the ovarian cycle.
Relugolix from the anterior pituitary
CLINICAL APPLICATIONS OF GNRH ANALOGUES OVARIAN CYCLE
• Activation of pituitary-gonadal function https://qrs.ly/k6bgo90
• Delayed puberty
• Cryptorchidism Dr. Banzuela-Cruz

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FOLLICULAR PHASE 36.7

Follicle Profile
EVENT NUMBERS 36.4
At Birth • 2 Million oocytes
Luteinizing
Puberty • 400,000 follicles
hormone (LH)
Depletion rate • 1,000 Follicle stimulating
(puberty to 35y/o) follicles/month hormone (FSH)
Total follicles released during
• 400 follicles
reproductive age
Atresia (apoptosis) of follicles • 99.9%
Progesterone

Inhibin

Destruction Repair and Secretion by

FOLLICULAR DEVELOPMENT
of functional regeneration uterine glands
zone of functional
zone

OOCYTE CYCLE
• Primary Oocyte
o formed by 5th fetal month
o Started their first meiotic division
o Arrested in Prophase from 5th fetal month until the onset
of puberty
o Will complete the first meiotic division at the onset of
puberty
• Secondary Oocyte
o Formed after completion of Meiotic I
o Release of the first Polar Body During ovulation
o Arrested in Metaphase II until fertilization
o Completion of 2ND Meiotic Division only occurs if there is
fertilization

FOLLICULAR PHASE: FOLLICLE DEVELOPMENT

Withdrawal of estrogen and progesterone during the luteal phase

of the prior cycle

Gradual increase in FSH

FSH stimulates the growth of approximately 5 to 15 primordial

ovarian follicles Follicle Characteristics
• Single layer of granulosa cell surrounding
Primordial
One becomes the dominant follicle and develops and matures the ovum
until ovulation • At puberty, when FSH and LH from the
anterior pituitary gland begin to be secreted
Dominant follicle, destined to ovulate, produces estrogen in significant quantities, the ovaries and the
Primary follicles within them begin to grow
Enhances follicular maturation and increases the production of • Moderate enlargement of the ovum
FSH and LH receptors • Additional layer of granulosa cell in some of
the follicles
• During the first few days of the menstrual
cycle: increase in the concentrations of FSH
and LH
• Elevated FSH causes
o Accelerated growth of 6 to 12 primary
follicles each month
Antral and o Rapid proliferation of granulosa cells
Vesicular
o Formation of THECA CELLS (Spindle
Follicle
cells derived from the ovary interstitium
collect in several layers outside the
granulosa cells)
• Antrum: Forms due to accumulation of
follicular fluid (with high concentration of
estrogen) secreted by the Granulosa cell
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FOLLICULAR PHASE: HORMONE PRODUCTION
OVARIAN STEROID PRODUCTION
• Estrogens synthesis is based on a theory known as the two-cell
theory or the two-cell, two-gonadotropin theory.
• LH stimulates production of androgens (androstenedione) from
cholesterol and pregnenolone in the theca cells.
• The androgens are then transported into the granulosa cells
where FSH stimulates the conversion of androgens to estrogens
(estrone)
• As rising estrogen levels have negative feedback on pituitary
FSH secretion, the dominant follicle is protected from the
decrease in FSH by its increased number of FSH receptors

OVULATION
KEY EVENTS (usually takes 3 to 4 days)
1. Preovulatory follicles increase estrogen secretion 34 to 36 hours before release of ovum with LH surge.
2. LH peaks 10 to 12 hours before ovulation.
3. LH surge triggers the resumption of meiosis in the oocyte and induces production of progesterone and prostaglandins within the follicle
4. The progesterone and prostaglandins, in turn, are responsible for the rupture of the follicular wall with release of the mature ovum or ovulation
5. The ovum usually passes into the adjoining fallopian tube and is swept down to the uterus by the cilia lining the tube
6. Fertilization of the ovum must occur within 24 hours of ovulation or it degenerates
FSHRF LHRF

FSH LH

Estrogens Progesterone
and estrogens

Proliferative Secretory

LUTEAL PHASE
• Constant at 12 to 14 days.
• Luteinization occurs after ovulation when the CL develops.
• CL is a transient endocrine organ that will rapidly regress 9 to
11 days after ovulation

Estrogen LUTEOLYSIS
Luteolysis may be due to the following:
1. ↓levels of circulating LH in the late luteal phase and
2. ↓LH sensitivity of luteal cells
3. Apoptosis
Effects of luteolysis:
1. Drop in circulating estradiol and progesterone levels.
2. Allows follicular development and ovulation during the next
ovarian cycle
3. Signals the endometrium to initiate molecular events that
lead to menstruation.
Remember ovarian cycle: FOLLICULAR, OVULATORY and LUTEAL
Secretory
PHASE. Follicular phase ang star is estrogen, pag luteal phase
Progesterone. This coincides with proliferative and secretory phase of the
Key Events: endometrium.
The granulosa and theca interna cells lining the wall of the follicle Progesterone = progestation hence the corpus luteum produces the
form the corpus luteum under stimulation by LH. progesterone during the early part of the pregnancy. If there is no
pregnancy, the CL will regress.
The corpus luteum synthesizes estrogen and progesterone Dr. Banzuela-Cruz

endometrium to become more glandular and secretory in

preparation for implantation of a fertilized ovum

If fertilization occurs, the developing trophoblast synthesizes

human chorionic gonadotropin the corpus luteum, so that it can
continue production of estrogen and progesterone to support the
endometrium.

This continues until the placenta develops its own synthetic

function at 8 to 10 weeks of gestation.

If fertilization does not occur, the corpus luteum degenerates,

progesterone levels fall, the endometrium is not maintained, and
menstruation occurs.

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ENDOMETRIAL CYCLE
Glands Mitosis
Proliferative
Straight to slightly coiled lined pseudostratified columnar epithelium Mitosis
Endometrium
EARLY SECRETORY PHASE: Scattered mitoses in the
Secretory coiled glands with a slightly widened diameter lined by simple columnar epithelium glands
Endometrium LATE SECRETORY PHASE:
No mitosis
serrated, dilated glands with intraluminal secretion lined by short columnar cells.
Day of
Before 14 15-16 17 18 19-22 23 24-25 26-27 28+
cycle
Post-
ovulatory --- 1-2 3 4 5-8 9 10-11 12-13 14+
day
Cycle Proliferativ Late
'Interval' Early secretory Mid-secretory Menstrual
phases e secretory
Focal
Mitoses
Maximum Subnuclea decidua
Key and Stromal Patchy Extensive Stromal
Mitoses subnuclea r vacuoles around
features subnuclear edema decidua decidua crumbling
r vacuoles present spiral
vacuoles
arteries
Focal
decidua Decidua Extensive
Loose
Loose around throughout decidua. Stromal
Stroma

Same as stroma, Loose Stromal

stroma. spiral stroma. Prominent crumbling.
proliferative scanty stroma edema
Mitoses arteries. Some granulated Hemorrhage
Microscopic mitoses
Edema edema lymphocytes
features of
prominent
functional
Disrupted
zone Straight to Some Dilated
glands.
tightly subnuclear Extensive glands. Dilated glands Luminal Prominent
Glands

"sawtooth" Secretory
coiled vacuoles, subnuclear Some with irregular outline. "sawtooth"
glands exhaustion.
tubules. otherwise as vacuoles subnuclear secretion glands
Regenerating
Mitoses proliferative vacuoles
epithelium

Appearance

Figure 3-16. Lobo, et al. Comprehensive Gynecology. 7th ed. 2017

ENDOMETRIUM: PROLIFERATIVE EARLY SECRETORY PHASE:
• Straight to slightly coiled, tubular glands are lined by • coiled glands with a slightly widened diameter
pseudostratified columnar epithelium with scattered mitoses • lined by simple columnar epithelium that contains clear
• Cyclical replication of: subnuclear vacuoles.
o Epithelial (glandular) cells, • Luminal secretions are seen.
o Stromal (mesenchymal) cells and LATE SECRETORY PHASE:
o Blood vessels • serrated, dilated glands with intraluminal secretion are lined by
• Functionalis layer is shed and regenerated from the deepest short columnar cells.
basalis layer almost 400 times during the reproductive lifetime SECRETORY PHASE Uterine lumen
of most women.
• Day 5 of menses – the epithelial surface of the endometrium
has been restored, and revascularization is in progress.
• Subnuclear Vacuolization
o The first indication of progesterone effects Func%onalis
o Reflects the small but significant increase in progesterone at layer

the time of the LH surge shortly before ovulation

ENDOMETRIUM: SECRETORY ENDOMETRIAL CYCLE
Basalis
• Rapid secretory differentiation layer
https://qrs.ly/ivegx7f
• Well-developed subnuclear vacuoles in all endometrial gland cells
Myometrium
• NO mitoses in the glands
• Rising levels of Progesterone

MENSTRUATION
KEY EVENTS:
• Severe coiling of spiral arteries:
o ↑resistance to blood flow
o ↑hypoxia on the endometrium
• Withdrawal of progesterone causes the endometrium to slough initiating the
menstrual phase
• FSH levels begin to slowly rise in the absence of negative feedback, and
follicular phase starts again
• A menstrual cycle less than 24 days or longer than 35 days or menses that lasts
more than 7 days merits further evaluation
ABNORMALITIES OF THE MENSTRUAL CYCLE
DYSMENORRHEA
• Pain and cramping during menstruation that interferes with normal activities and requires OTC or prescription medication
• Fifty percent of menstruating women suffers from dysmenorrhea
• Ten percent of these are incapacitated for 1 to 3 days each month
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Primary Dysmenorrhea Secondary Dysmenorrhea
• idiopathic menstrual pain without identifiable pathology, often • Painful menses due to underlying pathology
Definition occurring with the initiation of ovulatory menstrual cycles (endometriosis, fibroids, adenomyosis, pelvic
• usually occurs before 20 years old inflammatory disease (PID), cervical stenosis).
• Thought to result from increased levels of endometrial • Cervical stenosis- blood flow obstruction during menses
Etiology prostaglandin production derived from the arachidonic acid • Pelvic adhesions- may be due to infections such as PID
pathway. or tubal disease
• History and the absence of organic causes
Diagnosis • Pain of dysmenorrhea occurs with ovulatory cycles on the first or • Structural Abnormalities: Pelvic ultrasound
second day of menstruation
• Nausea, vomiting, and headache
Associated
• PE: no obvious abnormalities except a generalized tenderness • Dependent on the etiology
Symptoms
throughout the pelvis
• First-line: NSAIDS
• Cervical stenosis - dilatation of the cervix
• Second Line: Oral contraceptive pills (OCP)
Treatment • Pelvic Adhesions - antiprostaglandins, diagnosed and
• Others: progestin-only contraceptives such as Depo-Provera,
treated via laparoscopy
Nexplanon, and levonorgestrel-containing Intrauterine devices (IUDs)

PREMENSTRUAL SYNDROME AND PREMENSTRUAL DYSPHORIC DISORDER

• Characterized by a constellation of physical Blueprints FIGO 2018
and/or behavioral changes that occur in the Normal or “regular” (shortest to
Definition second half of the menstrual cycle. longest cycle variation: <7 to 9 days)
Regularity
• Premenstrual dysphoric disorder is the more Irregular (shortest to longest cycle
severe form of PMS variation: >8 to 10 days)
• headache, weight gain, bloating, breast Patient determined
tenderness, mood fluctuation, restlessness, Flow 35 (55 to Light
Symptoms irritability, anxiety, depression, fatigue, and a volume 60)ml Normal
feeling of being out of control Heavy

• symptoms must occur in the 2 weeks prior to • Usually 30-50 ml

menstruation and resolve following onset of Menstrual blood loss • Average menstrual blood loss:
menses 35 mL
Criteria for
• There must be at least a 7-day symptom-free Average iron loss per cycle • 13 mg
Diagnosis
interval in the first half of the menstrual cycle
• Symptoms must occur in at least two PATTERNS OF ABNORMAL UTERINE BLEEDING
consecutive cycles for the diagnosis to be made. (from Blueprints in OB-GYN, 7th ed)
• unknown but is likely multifactorial and Timing Flow
Bleeding Pattern Description
includes both physiologic and psychological of Cycle Amount
Pathogenesis Regular bleeding,
causes; Women with PMS and PMDD may have
an abnormal response to normal hormonal changes. average every 28
• SSRIs- first line of treatment Normal menstrual days (20-35 days)
Regular Normal
cycle lasting 3-5 days,
• SNRIs
bleeding on average
• Exercise and relaxation techniques 30-50 ml/cycle
• Vitamin supplementation Heavy
o Calcium (600 mg BID) Heavy menstrual (>80 mL/cycle) or
o Vitamin D (800 IU/day) bleeding prolonged (>7 d)
o Vitamin B6 (≤100 mg/day) Regular Heavy
Treatment (formerly menstrual flow
o Magnesium (200 to 360 mg/day) menorrhagia) occurring at regular
o Chasteberry extract (one tablet per day) intervals
• Exercise and relaxation techniques Light menstrual
Regularly timed
• Complex carbohydrate-rich beverage- Improve bleeding
menses but light Regular Light
both the psychological and appetite cravings by (formerly
flow
modulating tryptophan and serotonin Hypomenorrhea)
synthesis Any bleeding
Intermenstrual
between normal
bleeding Normal–
menses, usually Irregular
ABNORMAL UTERINE BLEEDING (formerly
lighter than normal
light
Metrorrhagia)
• Can present in many ways, from infrequent episodes, to menstrual bleeding
excessive flow, or prolonged duration of menses and Heavy irregular Excessive or Irregular Heavy
intermenstrual bleeding bleeding prolonged bleeding
• Oligomenorrhea if the intervals between bleeding episodes vary (formerly at irregular intervals
Menometrorrhagia)
from 35 days to 6 months
Infrequent
• Amenorrhea is defined by no menses for at least 6 consecutive menstrual cycles
Irregular cycles
Irregular Varies
months >35d apart
(Oligomenorrhea)
• Dysfunctional Uterine Bleeding (DUB): obsolete term to describe Frequent regular
Polymenorrhea Regular Normal
idiopathic heavy and/or irregular bleeding that could not be cycles but <21d apart
attributed to another cause following a complete evaluation No menses for
Amenorrhea,
6 or more N/A N/A
AUB is the term used for reproductive age patients with such pathologies. secondary
consecutive months
For Post-menopausal women, we use the term “postmenopausal
bleeding” because PMB requires ruling out of the presence of malignancy No menses by
first either through endometrial biopsy or endometrial curettage age 14 y in the absence
Dr. Banzuela-Cruz of secondary sexual
Amenorrhea, characteristics or No
N/A N/A
CLINICAL GUIDELINES FOR NORMAL MENSTRUATION primary menses by age 16 y in
the presence of
Blueprints FIGO 2018
secondary sexual
Absent(no bleeding)= amenorrhea characteristics
Cycle
Infrequent (>38 days) As you can see from the table primary amenorrhea is defined as having no
Length/ 28 ± 7 days
Normal(>24 to <38 days) menses by 14 years old. This has been lifted from Blueprints OB-GYN. In the
Frequency
Frequent (<24 days) chapter on Amenorrhea (also in Blueprints), primary amenorrhea is absence
4 (up to 7) Normal (<8days) of menses by 15 years old (consistent with Comprehensive Gynecology)
Duration
days Prolonged (>8days) Dr. Banzuela-Cruz

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• Signs/symptoms
o Abnormal bleeding due to
adenomyosis is thought to be a
result of altered uterine
contractility, enlarged
ABNORMAL UTERINE ABNORMAL UTERINE endometrial surface, and
BLEEDING 1 BLEEDING 2 increased endometrial vascularity
https://qrs.ly/sxegx7l https://qrs.ly/zoegx7p o Usually asymptomatic
o Heavy menstrual bleeding
AUB FIGO CLASSIFICATION 2018 (40-60%)
o Profound dysmenorrhea ADENOMYOSIS
(15-30%) https://qrs.ly/rjegx7w
o Heavy menstrual bleeding and
dysmenorrhea are correlated
by the degree of myometrial
invasion
o Other less common: dyspareunia, dyschezia, chronic pelvic
pain, infertility
o On pelvic examination, the uterus is diffusely enlarged,
globular, usually 2-3x the normal size; usually does not
larger than 14 weeks unless with a concomitant pathology
such as a myoma
• Diagnosis:
o Histologic diagnosis: Presence of endometrial glands and
stroma more than one low-powered field (2.5 mm) from the
basalis layer.
o TVS and MRI are sensitive tests
From FIGO 2018 Revisions on abnormal uterine bleeding symptoms and classification of causes of abnormal uterine
§ MRI > Vaginal ultrasound - will differentiate
bleeding in the reproductive years (Munro, et.al, 2018) adenomyosis from uterine myomas preoperatively.
We write diagnosis of AUB based on the PALM-COIEN classification by § Anechoic avascular cysts scattered throughout the
writing the subscript 1 or 0 after the letter. 1 if it’s the cause of the AUB myometrium is pathognomonic for adenomyosis
and 0 if not. Example: if a patient’s AUB is due to an Endometrial Polyp,
we write the diagnosis as: AUB P1-A0-L0-M0-C0-O0-E0-I0-N0.
If it’s a leiomyoma, we write either SM or O followed by the number
(degree). Example: the diagnosis of an intramural myoma is written as
AUB P0-A0-LO4 -M0-C0-O0-E0-I0-N0.
Dr. Banzuela-Cruz

ENDOMETRIAL POLYP (AUB-P)

• Localized overgrowths of endometrial
tissue, containing glands, stroma, and • Management:
Pathology
blood vessels, covered with epithelium o NO satisfactory medical management
• Possible cause: estrogen stimulation § GnRH agonist
• Endometrial glands § Cyclic hormones
3 components: • Endometrial stroma § Prostaglandin synthetase
• Central vascular channels o Hysterectomy is the definitive treatment
Diagnosis • Transvaginal Ultrasound; Hysteroscopy o Levonorgestrel-containing IUD (Mirena) has been found to
substantially decrease bleeding and pain
Management • Operative Hysteroscopy
• 2 most common differentials:
o Uterine myomas
o Dysfunctional uterine bleeding

LEIOMYOMA (AUB-L)
Somatic mutation in a single progenitor cell which
affects cytokines that affect cell growth which may
be affected by estrogen & progesterone
Pathology
Mechanisms by which fibroids cause abnormal
ENDOMETRIAL POLYP
bleeding are varied and depend on size, location,
https://qrs.ly/emegx7s
and number.
Figure 26.4. Lobo, et al. Comprehensive Gynecology. 7th ed. 2017
LEIOMYOMA SUBCLASSIFICATION SYSTEM
ADENOMYOSIS (AUB-A): ENDOMETRIOSIS INTERNA 0 Pedunculated intracavitary
SM –
• Pathology 1 <50% intramural
Submucosal
o presence of endometrial glands and stroma in the uterine 2 ³50% intramural
myometrium. xxxxxxxxxxx 3 Contacts endometrium; 100% intramural
o The presence of ectopic endometrial tissue leads to 4 Intramural
hypertrophy of the surrounding myometrium. 5 Subserosal ³50% intramural
o Glands do not undergo traditional proliferative & secretory O - Others 6 Subserosal <50% intramural
changes 7 Subserosal pedunculated
o Disruption of the barrier between endometrium & myometrium 8 Other (specifically e.g., cervical, parasitic)
• 2 pathological presentations: Two numbers are listed separated by a hyphen. By
o SYMMETRICAL (DIFFUSE): Diffuse involvement of the Hybrid convention, the first refers to the relationship with
leiomyomas the endometrium while the second refers to the
anterior and posterior walls of the uterus resulting in a relationship to the serosa. One example is below.
(affect both
uniformly enlarged uterus (most common); posterior wall Submucosal and subserosal, each with less
endometrium
most involved, not encapsulated and serosa) 2-5 than half the diameter in the endometrial
o ASYMMETRICAL (FOCAL/ADENOMYOMA): Focal areas of and peritoneal cavities, respectively.
pseudo encapsulated areas of adenomyosis resulting in Intracavitary fibroids (type 0) and submucosal fibroids, where more than
asymmetric uterus 50% are intracavitary (type 1) or less than 50% are intracavitary (type 2),
as well as intramural fibroids, which are large, may increase the overall
surface area of the endometrial cavity or alter uterine contractility.
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Primary Excessive uterine production of
AUB-E Endometrial prostacyclin, interfere with uterine
Disorder contractility
AUB-I Iatrogenic Due to medications
Not Otherwise
AUB-N Due to foreign body or trauma
Classified
LEIOMYOMA
https://qrs.ly/joegx7y DIAGNOSTIC APPROACH IN AUB
We write diagnosis of AUB based on the PALM-COIEN classification by
HISTORY
writing the subscript 1 or 0 after the letter. 1 if it’s the cause of the AUB
ONSET OF MENORRHAGIA PROBABLE DIAGNOSIS
and 0 if not. Example: if a patient’s AUB is due to an Endometrial Polyp,
we write the diagnosis as: AUB P1-A0-L0-M0-C0-O0-E0-I0-N0. Immediately after menarche or late Physiologic (anovulation;
If it’s a leiomyoma, we write either SM or O followed by the number 40s & 50s perimenopausal transition)
(degree). Example: the diagnosis of an intramural myoma is written as Since onset of medication; soon after
Medication-induced
AUB P0-A0-LO4 -M0-C0-O0-E0-I0-N0. medication
Dr. Banzuela-Cruz Weight gain or symptoms of
Anovulation
OTHER CAUSES hyperandogenism
Gradual ↑ over months or sudden & Myoma; hyperplasia;
• Includes vulvar, vaginal, cervical, endometrial,
noncyclic carcinoma
Malignancy uterine, and adnexal (ovarian or fallopian tube) CA
Increasing disability from systemic
or • Most common presenting symptom of Chronic disease
disease
Hyperplasia endometrial cancer
(AUB-M) • Risk Factor: Increased circulating levels of LABORATORY TESTS
estrogen • Pregnancy test or sensitive HCG assay
• Present menorrhagia occurred at the time of • CBC (hemoglobin & platelet count)
the first menstrual period • Thyroid function tests (TSH, FT3, FT4)
Coagulopathy • AUB seen in: von Willebrand disease, Prothrombin
• Coagulation profile (adolescent & older women)
(AUB-C) deficiency, Hemophilias A and B, May-Thurner
syndrome, severe sepsis, hypersplenism, leukemia, • Pap smear; screening for STI
and idiopathic thrombocytopenic purpura • Serum ferritin (indirect assessment of iron stores)
• Secondary to alterations in neuroendocrine DIAGNOSTIC TOOLS
function
• Ultrasound
o PCOS, Hypothyroidism, Prolactinemia,
Obesity, Mental stress, Extreme exercise o First-line
Ovulatory diagnostic tool
• The pattern of anovulatory bleeding may be
Dysfunction • Saline infusion
oligomenorrhea, intermenstrual bleeding, or
(AUB-O) Imaging sonography (SIS)
heavy menstrual bleeding
• There is continuous estradiol production o Accurate
WITHOUT corpus luteum formation and evaluation tool
progesterone production. for intracavitary
Primary • Excessive uterine production of prostacyclin, a lesions
Endometrial vasodilatory prostaglandin that opposes
Disorder platelet adhesion and may also interfere with • Both diagnostic &
(AUB-E) uterine contractility therapeutic
Hysteroscopy
• Due to medications such as: • More accurate than
o SERMs D&C
Iatrogenic o GnRH analogues
(AUB-I) o Risperidone and other antipsychotics – can
cause hyperprolactinemia • Endometrial biopsy recommended for:
o Anticoagulation therapy** o Postmenopausal woman with bleeding or premenopausal
• Abnormal bleeding not classified in the woman with heavy/irregular vaginal bleeding.
Not o Postmenopausal women with endometrial cells on pap
previous categories is considered AUB-N.
Otherwise smear or
• Examples of such conditions may include
Classified o Premenopausal women with atypical glandular cells on pap
foreign bodies or trauma
(AUB-N) smear
• Treatment is tailored to the specific cause
In the latest 2018 FIGO Guidelines on Abnormal Uterine Bleeding, drugs that o Breast cancer patients on Tamoxifen who complain of
impair coagulation and drugs that interfere with ovulation now fall under abnormal vaginal bleeding
AUB-Iatrogenic (AUB-I) instead of AUB-C and AUB-O respectively. This is also o Women who are still “menstruating” after 52 years of age.
the case in Blueprints 7th edition. Comprehensive Gynecology 8th edition still
Endometrial biopsy is an outpatient procedure and is a diagnostic tool
follows the FIGO 2011 classification though wherein anticoagulative therapy
with sensitivity and specificity similar to endometrial curettage.
is under AUB-C
Dr. Anna Cruz
Endometrial curettage, however, is both diagnostic and therapeutic and
must be done in actively bleeding patients.
Dr. Banzuela-Cruz

ENDOMETRIAL CANCER MEDICAL MANAGEMENT FOR AUB

https://qrs.ly/31egx83 • Treatment depends on the specific underlying etiology
• In general, structural etiologies for AUB (PALM from the
PALM-COEIN system) generally require surgical correction
MECHANISMS OF BLEEDING
• Therapy for nonstructural causes of AUB (COEIN from the
MECHANISM OF BLEEDING
PALM-COEIN System) should be directed at treatment of the
Stromal congestion within the polyp
underlying cause when a cause is identifiable
AUB-P Polyp leading to venous stasis and apical
necrosis • Most used agents
AUB-A Adenomyosis Altered uterine contractility o Estrogens, Progestogen
Varied and depend on size, location, o Non-steroidal anti-inflammatory drugs (NSAIDs)
and number o Anti-fibrinolytic agents (AFA)
AUB-L Leiomyoma Submucosal fibroids: increase the o Androgenic Steroids (Danazol)
overall surface area of the endometrial o GnRH agonists +/- add back
cavity or alter uterine contractility.
Malignancy or
ESTROGENS
AUB-M Thickens endometrial lining • Rapid growth of endometrium over the denuded & raw
Hyperplasia
AUB-C Coagulopathy Due to coagulative disorders epithelial surfaces.
Ovulatory
Continuous estradiol production • Promotes platelet adhesiveness (large doses of CEE or oral
AUB-O without corpus luteum formation and conjugated equine estrogen)
Dysfunction
progesterone production
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PROGESTOGENS Bleeding Disorder
Bleeding
Typical Treatment
• ↓ synthesis of estrogen receptors Amount
Neoplasms
• Stops endometrial growth
• Hormonal management,
• Support & organize the endometrium in order to have an tranexamic acid, uterine
organized slough to the basalis layer artery embolization,
• Stimulate arachidonic acid formation in endometrium, Uterine fibroids Heavy
myomectomy,
increasing PGF2a/PGE ratio • endometrial ablation,
hysterectomy
NSAIDS
• Hormonal management,
• Prostaglandin synthetase inhibitors that inhibit conversion of Adenomyosis Heavy Mirena IUD, endometrial
arachidonic acid to prostaglandin. ablation hysterectomy
• Cyclooxygenase inhibitors thus block the formation of both Cervical polyps Light • Polypectomy
thromboxane and prostacyclin pathway Benign endometrial • Progestin therapy (if no
• May be used alone or along with hormonal therapy hyperplasia and atypia or desires fertility),
endometrial Varies hysteroscopy with D&C
ANTI-FIBRINOLYTIC AGENTS intraepithelial followed by hysterectomy if
• Potent inhibitors of fibrinolysis neoplasia (EIN) EIN is present
• E-aminocaproic acid (EACA); tranexamic acid (AMCA); para- • Hysterectomy, bilateral
aminomethylbenzoic acid (PAMBA) Endometrial cancer Heavy salpingo-oophorectomy
• Side effects: dizziness, diarrhea, headaches, abdominal pain & • (BSO), ±radiation
allergic manifestation Pregnancy problems
• Tranexamic acid is contraindicated in women using • Expectant management vs.
Pregnancy Varies
delivery
combination hormonal contraception and in women with active
• Expectant management,
thromboembolic disease or history of thromboembolism medical induction, manual
Miscarriage Heavy
ANDROGENIC STEROIDS vacuum evacuation,
• Danazol inhibits gonadotropins. • D&C
• Methotrexate vs. surgical
• Danazol 200 mg and 400 mg daily given over 12 weeks was able
management (usually
to reduce MBL from 25 to 200 ml Ectopic pregnancy Varies
salpingotomy vs.
• Increase interval between bleeding episodes salpingectomy)
• Side effects: weight gain and acne Hormonal problems
GNRH AGONISTS Hypothyroidism Varies • Thyroid hormone replacement
• Leuprolide acetate suppresses gonadotrope secretion of Hyperprolactinemia None • Dopamine agonists
luteinizing hormone and follicle-stimulating hormone that • Combined estrogen /
subsequently suppresses gonadal sex steroid production. progestin pills, patch, or
Anovulation Varies
ring; or cyclic progestin;
TREATMENT OF ACUTE HEMORRHAGE levonorgestrel IUD
Blueprints in Obstetrics and Gynecology, 7th edition
• Therapy to stop the bleeding should be initiated immediately.
Intravenous estrogen (25 mg conjugated estrogen every 4 hours AMENORRHEA
up to 24 hours) Contraindications: DVT, PE PRIMARY AMENORRHEA
• For patients with excessive blood loss who are • The absence of menses in a woman who has never menstruated
hemodynamically stable, high dose oral estrogens can control by the age of 15 years in the presence of normal growth and
the bleeding within 24 to 48 hours secondary sexual characteristics
o 2.5 mg every 4 hours for 14 to 21 days, followed by • Girls who have not menstruated within 5 years of breast
medroxyprogesterone acetate 10 mg/day for 7 to 10 days. development, if occurring by age 10.
• OCP taper can be used for endometrial stabilization. • Breast development (thelarche) should occur by age 13 or
o monophasic pill containing 35 mcg ethinylestradiol given otherwise requires evaluation as well.
three times a day for 3 days, then two times a day for 2 days, • Prevalence in the US: 1% to 2%
and then daily for the remainder of the pack.
• Causes: congenital and chromosomal abnormalities, hormonal
SAMPLE DRUG DOSAGES aberrations, hypothalamic–pituitary disorders
LNG-IUS Once every 5 years • Categories: Outflow Tract Obstruction, end-organ disorders and
Tranexamic acid 1 g TID-QID during heavy bleeding for 3 days central regulatory disorders
200 mg PO TID during heavy bleeding for 3 days
Ibuprofen ETIOLOGIES OF PRIMARY AMENORRHEA
800 mg TID for 5 days
500 mg Loading dose, then 275 mg BID Imperforate hymen
Mefenamic acid
during heavy bleeding for 3 days Transverse vaginal septum
Medroxyprogesterone 10 mg PO OD-TID on cycle days 5-26 Vaginal agenesis
Outflow tract
(MPA) 10 mg PO for 10 consecutive days per month Vaginal atresia
abnormalities
Norethisterone acetate 5 mg PO TID on cycle days 5-26 Testicular feminization
Danazol 200-400 mg PO daily Uterine agenesis with vaginal dysgenesis
Goals of treatment for AUB are to stop acute heavy bleeding and reduce MRKH syndrome
amount of menstrual blood loss. Ovarian agenesis
Dr. Banzuela-Cruz
Gonadal agenesis 46,XX
SURGICAL OPTION FOR AUB Swyer syndrome/gonadal agenesis 46,XY
DILATATION & CURETTAGE (D&C) Ovarian insufficiency
End-organ
Enzymatic defects leading to decreased steroid
• Diagnostic & therapeutic for immediate management of severe bleeding disorders biosynthesis
• Treatment of choice in women with hypovolemia due to DUB Savage syndrome—ovary fails to respond to FSH
• Acute HMB unresponsive to initial medical management. and LH
ENDOMETRIAL ABLATION Turner syndrome
• May be offered as initial treatment for HMB Hypothalamic
Local tumor compression
• Women with medical contraindication against hysterectomy
Trauma
• Women with normal uterus and those with small myoma (<3cm) Tuberculosis
HYSTERECTOMY Central Sarcoidosis
• Performed after investigation to establish cause of HMB Disorders Irradiation
Kallmann syndrome—congenital absence of
• Failed pharmacological treatment
GnRH
• If HMB is causing anemia and/or serious impact to quality of life Pituitary damage from surgery or radiation
Endometrial Ablation and hysterectomy should not be performed in Hemosiderosis deposition of iron in pituitary
Nulligravid patients. So always check age, gravidity and parity.
Dr. Banzuela-Cruz

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Previously primary amenorrhea was defined as absence of menses at 16.5 END-ORGAN DISORDERS
years old. Therefore, in your exam if the choices lack 15 y/o, then the
answer is 16.5 y/o. Also, the presence of breasts means that there is
presence of estrogen, whether from the ovaries or in some cases from
other sources such as in Klinefelter syndrome
Also in Blueprints (table of AUB) , amenorrhea has been defined as
absence of menses by age 14 y in the absence of secondary sexual
characteristics or no menses by age 16 y in the presence of secondary
sexual characteristics. So, note both of these definitions in the exam and
discern whether you are being asked an AUB or an Amenorrhea question.
Dr. Banzuela-Cruz

OUTFLOW TRACT ANOMALIES OVARIAN INSUFFICIENCY

IMPERFORATE HYMEN • Primary Ovarian Insufficiency results in low levels of
• During fetal development, the hymen may fail to canalize, estradiol but elevated levels of gonadotropins:
remaining a sold membrane across the vaginal introitus hypergonadotropic hypogonadism
• Does not allow egress of menstrual blood • Savage syndrome: failure of the ovaries to respond to FSH and
• After a time, patients present with pelvic or abdominal pain LH secondary to receptor defect
from the accumulation and subsequent dilation of the vaginal • Turner Syndrome (45,XO) ovaries undergo rapid atresia that
vault and uterus by menses by puberty, there are usually no primordial oocytes
• Physical Examination: hematocolpos- bulging membrane just • 17-hydroxylase deficiency: results in amenorrhea and absent
outside the introitus with purple-red discoloration behind it of breast development due to lack of estradiol
• Treatment: surgical with a cruciate incision made and the
hymen is sewn open to allow passage of menstrual flow GONADAL AGENESIS WITH 46XY CHROMOSOMES
• Defect in 17-α-hydroxylase or 17,20 desmolase
TRANSVERSE VAGINAL SEPTUM
• No testosterone produced
• May result from failure of the Mü llerian-derived upper vagina to
• MIF is still produced
fuse with the urogenital sinus-derived lower vagina
• Phenotypically female, usually without breast development
• Symptom: young woman who presents with primary
• Testicular feminization syndrome: absence of or defect in
amenorrhea with cyclic pelvic pain
testosterone receptor
• Diagnosis: careful examination of the female genital tract,
• Swyer syndrome: phenotypical picture to that of ovarian
examining for a bulging septum consistent with hematocolpos;
agenesis; no testicular development, MIF not released, (+)
can be differentiated from imperforate hymen by the presence
female internal and external genitalia, but without estrogen so
of a hymenal ring below the septum
breasts will not develop
• Treatment: Surgery correction with resection of the septum
VAGINAL AGENESIS CAUSES OF PRIMARY GONADAL FAILURE
• Patients with Mayer–Rokitansky–Kuster–Hauser syndrome (HYPERGONADOTROPIC HYPOGONADISM)
have Mü llerian agenesis or dysgenesis and may present with • Idiopathic premature ovarian failure
complete vaginal agenesis and the absence of a uterus or • Steroidogenic enzyme defects (primary amenorrhea)
partial vaginal agenesis with a rudimentary uterus and distal • Cholesterol side-chain cleavage
vagina • 3β-ol-Dehydrogenase
• Diagnosis: 46xx with no patent vagina, (+) ovaries in ultrasound • 17-Hydroxylase
• Partial vaginal agenesis or vaginal atresia: rectal exam may • 17-Desmolase
reveal a pelvic mass consistent with a uterus or uterus can be • 17-Ketoreductase
visualized with UTZ, CT or MRI • Testicular regression syndrome
• True hermaphroditism
• Treatment: creation of a neovagina
• Gonadal dysgenesis
TESTICULAR FEMINIZATION • Pure gonadal dysgenesis (Swyer syndrome) (46,XX and 46,XY)
• Also known as Androgen Insensitivity Syndrome • Turner syndrome (45,XO)
• Occurs in 1 in 50,000 women • Turner variants
• Due to dysfunction or the absence of testosterone receptor • Ovarian resistance syndrome (Savage syndrome)
• Phenotypically female with 46XY chromosomes • Autoimmune oophoritis
• Patients have testes, MIF is secreted therefore Mullerian- • Postinfection (e.g., mumps)
derived structures are absent • Postoophorectomy (also wedge resections)
• diminished testosterone sensitivity commonly leads to an • Postirradiation
absence of pubic and axillary hair • Postchemotherapy
• Estrogen is produced: presence of breasts SECONDARY SEXUAL CHARACTERISTICS
• Absent uterus leads to amenorrhea
• Vagina ends as a blind pouch
• Testicular cancer may occur ⨯
(+) Breasts (-) Breasts

Measure
FSH, LH

FSH < 5 IU/L FSH > 20 IU/L

LH < 5 IU/L LH > 40 IU/L

Hypogonadotrophic Hypergonadotrophic
hypogonadism hypogonadism

CNS imaging Karyotyping

CNS tumor 46 XX 45 XO
Ovarian Turner
failure syndrome

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CENTRAL DISORDERS
Hypothalamic Disorders DIAGNOSIS OF PRIMARY AMENORRHEA
BASED ON PHENOTYPIC FEATURES
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SECONDARY AMENORRHEA
• Absence of menses for three months in women with previously
regular cycles or six months in women with a history of irregular
cycles
• Hypothalamus unable to produce GnRH therefore pituitary will • Most common cause: pregnancy
not release FSH and LH • Other causes: anatomic abnormalities, ovarian dysfunction,
• Anovulation and amenorrhea result from this prolactinoma and hyperprolactinemia, and CNS or
hypogonadotropic hypogonadism hypothalamic disorders
• Kallman syndrome: congenital absence of GnRH and is
commonly associated with anosmia OVARIAN
ANATOMIC
DYSFUNCTION
• Disruption of GnRH transport: tumor mass effect, trauma,
• Asherman syndrome • Primary Ovarian
sarcoidosis, tuberculosis, irradiation, or Hand–Schuller–
• Cervical Stenosis Insufficiency
Christian disease
PROLACTINOMA AND
• Defects in GnRH pulsatility: anorexia nervosa, extreme CNS-HYPOTHALAMIC
HYPERPROLACTINEMIA
stress, athletics, hyperprolactinemia, hypothyroidism, rapid or
• Pituitary tumors secreting prolactin • Hypogonadotropic
severe weight loss, and constitutionally delayed pubert
(microadenoma: less than 10mm, Hypogonadism
Pituitary Disorders macroadenoma more than 10mm) • Hypothalamic
• Hypothyroidism Dysfunction
• Idiopathic hyperprolactinemia • Pituitary Disorders
• Drug-induced hyperprolactinemia
• Interruption of normal hypothalamic
pituitary relationship
• Peripheral neural stimulation
• Nipple stimulation
• Spinal cord lesion
• CNS disease
• Rare
• Usually secondary to hypothalamic disorder
• Causes: ANATOMIC
o tumors, infiltration of the pituitary gland, or infarcts of the pituitary • Intrauterine adhesions or synechiae (Asherman
o Surgery or irradiation of pituitary tumors may lead to syndrome):
decreases in or absence of LH and FSH o Obliteration of endometrial cavity
o Hemosiderosis can result in iron deposition in the pituitary, o Endometrial curettage from pregnancy is the most
leading to destruction of the gonadotrophs that produce FSH frequent antecedent factor of IUA.
and LH o Diagnosis
§ Hysterosalpingogram
DIAGNOSIS OF PRIMARY AMENORRHEA BASED ON § Hysteroscopy
PHENOTYPIC FEATURES • Cervical Stenosis
UTERUS ABSENT UTERUS PRESENT o Can manifest as secondary amenorrhea and dysmenorrhea
• Gonadal • Gonadal failure/agenesis o Caused by scarring of the cervical os secondary to surgical
BREASTS or obstetric trauma
agenesis in in 46,XX
ABSENT
46,XY
• Enzyme • Disruption of HYPERPROLACTINEMIA-ASSOCIATED AMENORRHEA
deficiencies in hypothalamic–pituitary • Excess prolactin leads to galactorrhea and amenorrhea
testosterone axis • Amenorrhea results from abnormal FSH and LH secretion due
synthesis • Hypothalamic, pituitary, to alterations in dopamine levels typically seen in
BREASTS
PRESENT
• Testicular or ovarian pathogenesis hyperprolactinemia
feminization similar to that of • PRL release is inhibited by dopamine
• Mü llerian secondary amenorrhea • PRL is stimulated by serotonin and thyrotropin releasing
agenesis or • Congenital abnormalities hormone (TRH)
MRKH of the genital tract SOURCE FEATURES
DIAGNOSTIC FLOWCHART FOR PATIENTS WITH PRIMARY Primary • Elevated TSH and TRH can
AMENORRHEA Hypothyroidism cause hyperprolactinemia
• Dopamine antagonists
o Phenothiazines
o Thioxanthenes
o Butyrophenone
o Diphenylbutylpiperidine
Drug induced
o Dibenzoxazepine
hyperprolactinemia (by
o Dihydroindolone
H-P effect)
o Procainamide derivatives
• Catecholamine-depleting
agents
• False transmitters (α-
methyldopa)

CNS-HYPOTHALAMIC
• Hypogonadotropic-hypogonadism
• Disruption in secretion and transport of GnRH
• Absence of GnRH pulsatility
• Acquired pituitary lesion
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SOURCE FEATURES
• Kallmann syndrome
PEDIATRIC GYNECOLOGY
• Tumors of hypothalamus (craniopharyngioma) GYNECOLOGIC EXAMINATION
• Constitutional delay of puberty • Frog-leg: MOST COMMON. Child has direct view of examiner
Hypothalamic • Severe hypothalamic dysfunction and herself
Dysfunction • Anorexia nervosa • Modified frog-leg: For anxious children. Child between parent’s
• Severe weight loss legs and holds child’s legs in lithotomy position
• Severe stress
• Knee-chest: Older children. Allows visualization of lower and
• Exercise
upper vagina.
• Sheehan syndrome
Pituitary • Panhypopituitarism
o Child with discharge or foreign body.
Disorder • Isolated gonadotropin deficiency o Lateral and downward traction improves visualization
• Hemosiderosis (primarily from thalassemia major) For pediatric patients who can already follow instructions, dorsal
lithotomy position is still the best position to assess gyne problems.
OVARIAN (HYPERGONADOTROPIC HYPOGONADISM) Dr. Banzuela-Cruz

SOURCE FEATURES EXTERNAL GENITALIA

Cystic • Damage to follicles from infection, interference NEWBORN PREPUBERTAL
degeneration with blood supply, depletion from cystectomies • Hymen is thin • Often crescent-shaped; Others
• Previously called premature ovarian failure and annular, cribriform, septate

Hymen
• Idiopathic nonelastic • May protrude upon straining until
• development of hypergonadotropic hypogonadism • Estrogenized 10 y/o
(menopause) before age 40 → thick elastic • CLITORIS: 1-2 cm (prominent)
Premature
• Menopause occurring before 35yo should be redundancy
ovarian
evaluated with a chromosomal analysis
insufficiency • Vaginal epithelium: uncornified,
• Idiopathic POI or with a known cause of early
redder and thinner
ovarian failure are generally treated with estrogen
to decrease the risk of cardiovascular disease and • Puffy labia • 4-6 cm long
osteoporosis majora • Labia majora loses fullness
• Thickened • Labia minora and hymen become
APPROACH TO DIAGNOSIS Vagina labia minora thinner and flatter
1. BHCG- rule out pregnancy • Redundant • Labia minora do not fully cover the
2. History- hypothyroidism, hyperprolactinemia, hymenal folds vaginal vestibule
hyperandrogenism • Mucosa is • Perineum and perivaginal tissues rigid
3. TSH and Prolactin pink & moist and inelastic
• Vaginal pH is • Vaginal pH is neutral or slightly
DIAGNOSTIC FLOWCHART FOR PATIENTS WITH SECONDARY acidic alkaline
AMENORRHEA WITH NORMAL PROLACTIN LEVELS • Mucoid discharge
• Introitus more anterior

PUBERTY
• describes the series of events in which a child matures into a
young adult
• encompasses a series of neuroendocrine and physiologic
changes, which result in the ability to ovulate and menstruate.
• These changes include:
o the development of secondary sex characteristics
o the growth spurt
o achievement of fertility

PUBERTAL CHANGES
• Adrenarche- regeneration of the zona reticularis in the adrenal
cortex and production of androgens and ultimately stimulates
TREATMENT the appearance of pubic hair
• Gonadarche- activation of the hypothalamic–pituitary–gonadal
Hypothyroidism Thyroid hormone replacement
Pituitary Surgical resection
axis, which involves pulsatile gonadotropin-releasing hormone
macroadenomas Bromocriptine (GnRH) secretion stimulating the anterior pituitary to produce
Estrogen and progesterone replacement luteinizing hormone (LH) and follicle-stimulating hormone
Hypoestrogenic (FSH). These, in turn, trigger the ovary to produce estrogens
(OCPs)
Hyperprolactinemia Ovulation induction with Bromocriptine • Pubertal Sequence:
Negative Ovulation induction with Clomiphene citrate o Accelerated growth
Progesterone For unresponsive: human menopausal o Breast development (Thelarche)
Challenge Test gonadotropin or recombinant GnRH o Development of pubic and axillary hair (pubarche)
The main pathophysiology of polycystic ovarian syndrome is actually o Menstruation (menarche)
“insulin resistance”. The target tissues do not let insulin bind to its
receptors leading to hyperglycemia and increase in androgens.
Dr. Banzuela-Cruz
CHANGES AGE DESCRIPTION
• Adrenal gland begins regeneration of the zona reticularis responsible for the secretion of sex steroid hormones
Between 6 and • The adrenal gland produces increased quantities of the androgens dehydroepiandrosterone sulfate (DHEAS),
Adrenarche
8 years DHEA, and androstenedione. Production increases from age 6 to 8 up until 13-15 years
• The primary stimulus of adrenarche is unknown
• Increased pulsatile GnRH secretion from the hypothalamus
• This leads to subsequent pulsatile secretion of LH and FSH from the anterior pituitary.
• Initially, these increases occur mostly during sleep and fail to lead to any phenotypic changes.
Begins around
Gonadarche • As a girl enters early puberty, the LH and FSH pulsatility lasts throughout the day, eventually leading to
age 8 years
stimulation of the ovary and subsequent estrogen release.
• This, in turn, triggers the characteristic breast bud development
• The positive feedback of estradiol also results in the initiation of the LH surge and the ability to ovulate.
Accelerated Around age 9 to • Mean peak growth velocity of about 9cm/year around age 12 years
growth 10 years • Increased pituitary growth hormone secretion in response to sex steroids

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CHANGES AGE DESCRIPTION
• Usually the first phenotypic sign of puberty and occurs in response to the increase in levels of circulating
estrogen.
Thelarche 10 years
• Concomitantly, there is estrogenation of the vaginal mucosa and growth of the vagina and uterus.
• Further development of the breast will continue throughout puberty and adolescence
• Onset of growth of pubic hair years
Pubarche 11 years • Often accompanied by growth of axillary hair. Secondary to the increase in circulating androgens.

Between 12 and • As gonadal estrogen production

13 years or 2.5 • Increases during puberty, it increases sufficiently to stimulate endometrial proliferation, ultimately
Menarche years after the resulting in the start of menses usually irregular for the first 1 to 2 years after menarche, reflecting
development of anovulatory cycles
breast buds
There are inconsistencies in the sequence of these changes in blueprints. The text mentions that accelerated growth precedes menarche (which is consistent with
Comprehensive gynecology). In the table however, the first sign of puberty is breast development. In comprehensive gynecology, the sequence are as follows:
increase in growth velocity followed by either thelarche or adrenarche then followed by a period of maximal growth velocity then menarche
Dr. Banzuela-Cruz

CLASSIFICATION DESCRIPTION CLASSIFICATION DESCRIPTION

Breast Growth Pubic Hair Growth
Stage 1 Preadolescent: elevation of papilla only PH1 Prepubertal-no pubic hair
Breast budding: elevation of breast and PH2 Labial hair present
Stage 2
papilla; areolar enlargement ‘PH3 Labial hair spreads over mons pubis
Further enlargement of breasts and areola PH4 Slight lateral spread
Stage 3
without separation of breast contours Further lateral spread to form inverse triangle
PH5
Stage 4 Secondary mound formed by areola and reach medial thighs
Mature stage: projection of papilla only as
Stage 5
areola recesses to breast contour

Adapted from Lobo, et al. Comprehensive Gynecology. 7th ed. 2017

SEQUENCE OF PREPUBERTAL CHANGES ABNORMAL PUBERTY

• Precocious Puberty- pubarche or thelarche before 7 years of
age in Caucasian girls and before 6 years of age in African
American girls
• Delayed puberty-Absent or incomplete breast development by
the age of 12 years
DELAYED MENARCHE
• Menarche delayed up to 15 y/o if involved in strenuous
exercise before menarche.
• They sufficient estrogen to produce some breast development
and no need for extensive endocrinologic evaluation.
• Emotional stress can inhibit the GnRH axis. Corticotropin
releasing hormone (CRH) inhibits GnRH
Decrease levels of Leptin is one of the primary reasons why prepubertal
athletes sometimes experience primary amenorrhea. Also, those with
anorexia nervosa.
Dr. Banzuela-Cruz

Average age and age range for the onset of the major physical changes associated with puberty
EVENT AGE HORMONE PRECOCIOUS PUBERTY
Breast development (Thelarche) 10-11 Estradiol • Thelarche before 7 years of age in Caucasian girls and before 6
Appearance of pubic and years of age in African American girls
10.5-11.5 Androgens
axillary hairs (Pubarche) • Complete evaluation of precocious puberty at 8 years of age
Maximal growth velocity 11-12 11-12 GH The first sign of Puberty is breast budding, the latest is menarche. Again,
Menarche 11.5-13 Estradiol you need to review the HPO axis for this.
Dr. Banzuela-Cruz

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PREMATURE THELARCHE
• Isolated unilateral/bilateral breast development: only sign of
secondary sexual maturation.
o No axillary or pubic hair development
• Features:
o First 2 years of life and ages 6 and 8.
o Breast buds enlarge (asymmetric)
o Nipple development is absent.
o Normal linear growth & bone age.
o Benign, self-limiting
• Etiology
o Transient ovarian follicular activity
o Exogenous source (e.g. environment or diet)
PREMATURE PUBARCHE OR ADRENARCHE
PRECOCIOUS PUBERTY TYPES • Pubarche: Early isolated development of pubic hair
• GnRH dependent (complete; true) o Non-progressive, no clitoral hypertrophy
• GnRH independent (incomplete; pseudo) o Some with abnormal EEG without neuro disease
• Premature thelarche o Bone age not advanced
• Premature adrenarche o ↑ androgen (DHEA & DHEA-S) by adrenal glands.
• Adrenarche: Isolated early development of axillary hair
GNRH-DEPENDENT o Many evolve into PCOS
• 80% of cases o Measure testosterone and 17-OH progesterone
• No genital, intellectual or psych abnormality DIAGNOSIS
Idiopathic • Premature maturation of HPO axis (3-4 y/o)
• LH>5 mIU/ml - diagnostic
• History and PE
o Primary: r/o life threatening neoplasms of ovary, adrenal or
• Lesions at hypothalamus near 3rd ventricle, tuber CNS
cinereum, or mamillary bodies o Secondary: delineate speed of maturation
• Major CNS diseases associated: o Acceleration of growth: one of earliest clinical features of
o TB precocious puberty
CNS Lesion o Encephalitis • Laboratory tests
o Trauma o Brain imaging, EEG’s
o Hamartomas o Ultrasound, CT or MRI of abdomen
o Craniopharyngioma o Serum FSH, LH, TSH, PRL, E2, testosterone, DHEA-S, hCG,
o Hydrocephalus androstenedione, 17-OH progesterone, T3 and T4
• Primary thyroid insufficiency (e.g. Hashimoto • GnRH agonist stimulation test
thyroiditis), leads to increase TSH and o Differentiates incomplete from true precocious puberty
1° Hypo-
gonadotropins or Van Wyk-Grumbach syndrome
thyroidism
• Bone age is retarded – unique to hypothyroidism TREATMENT
• Girls ages 6 and 8 years. • Indications for medical tx:
In GnRH dependent precocious puberty, the bone growth is also advanced o Menarche <8 y/o
for age. Although Primary hypothyroidism is GnRH dependent PP, bone o Progressive thelarche & pubarche
age is retarded. o Bone age >2 yrs of chronological age
Precocious puberty is a rare complication of prolonged primary • Goals of therapy:
hypothyroidism. Exact mechanism is unknown but some states that since the o Reduce gonadotropin secretions
levels of thyroid hormones are decreased, there is compensatory production of o Reduce of counteract the peripheral actions of sex steroids
GnRH since Thyrotropin and GnRH share the same alpha subunit.
Dr. Banzuela-Cruz o Decrease the growth rate to normal
GNRH-INDEPENDENT o Slow skeletal maturation to allow maximal adult height.
• Surgical treatment
• Granulosa cell tumor: >8cm; most common
Ovarian o Removal of tumor or lesion producing excess hormones.
• Others: thecoma, luteoma, teratoma, Sertoli-Leydig,
tumor
follicular cyst, choriocarcinoma, dysgerminoma
• Medical treatment:
o GnRH agonist (Leuprolide) – GnRH dependent drug of
• Feminizing (isosexual) or virilizing
(heterosexual) effects choice
• If treated during neonatal period, normal o Aromatase inhibitors (letrozole) or estrogen receptor
Adreno- puberty ensues. antagonist (fulvestrant) – McCune Albright
cortical • If untreated, develops virilizing features.
• If treated late, feminizing features appear. SUMMARY
• Tests: adrenal imaging, 21- or 11B-OHase or 3B- GnRH- GnRH-
ol dehydrogenase DEPENDENT INDEPENDENT
• Activation of HPO • Production of sex
• Mutation in G3 protein activating adenylate cyclase Pathology
axis hormones
• Constant stimulation of FSH, LH, TSH & GH
McCune • Idiopathic • Ovarian (e.g. GCT)
• Vaginal bleeding – first sign • CNS lesion • Adrenal
Albright Etiology
• Triad: café-au-lait spots, polyostotic fibrous • Hypothyroidism • McCune-Albright
dysplasia, cysts of skull and long bones • Iatrogenic (factitious)
Iatrogenic/ • Applied hormonal cream or ingested OCPs or FSH, LH ↑ ↓
factitious hormones. E2 or T ↑ ↑
DHAS ↑ ↑
McCune Albright Syndrome Triad:
GnRH
Pubertal Flat
response

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PHYSICAL FINDINGS AMONG PATIENTS WITH VARIOUS PRECOCIOUS PUBERTY SYNDROMES
GnRH – DEPENDENT AND GnRH- INDEPENDENT SYNDROMES
PREMATURE PREMATURE
FINDINGS McCUNE-ALBRIGHT
THELARCHE ADRENARCHE IDIOPATHIC CNS TUMOR HYPOTHYROID
SYNDROME
Breast
Yes No Yes Yes Yes Yes
enlargement
Pubic hair No Yes Yes Yes Yes Unusual
Vaginal bleeding No No Yes Yes Yes Yes
Virilizing signs No No No No No No
Normal to
Bone age Normal Advanced Advanced Advanced Normal or retarded
minimally advanced
Neurological
No No No Yes Yes No
deficit
Abdominopelvic
No No Occasional No No Occasional
mass
ISOSEXUAL (FEMINIZING) HETEROSEXUAL (VIRILIZING)
FINDINGS OVARIAN OVARIAN ADRENAL ADRENAL
ADRENAL TUMORS FACTITIOUS
TUMORS TUMORS TUMORS HYPERPLASIA
Breast
Yes Yes Yes Yes Yes Yes
enlargement
Pubic hair Yes Yes Yes Yes Yes Yes
Vaginal bleeding Yes Yes Yes Yes Yes Yes
Virilizing signs No Yes No Yes Yes Yes
Bone age Advanced Advanced Advanced Advanced Advanced Advanced
Neurological
No No No No No No
deficit
Abdominopelvic
Usually, No No Occasional No No
mass
Lobo, et al. Comprehensive Gynecology. 7th ed. 2017

HYPERANDROGENISM (ANDROGEN EXCESS) • Adrenal gland is divided into two components:

• Responsible for glucocorticoid,
• Hyperandrogenism can be due primarily to adrenal or ovaria
mineralocorticoid, and androgen synthesis
disorder
• 3 layers:
• In the adrenals, steroid hormones is stimulated by ACTH thus
o Zona glomerulosa: outer layer produces
elevated ACTH levels increase all the steroid hormones,
aldosterone via the enzyme aldosterone
including androgen Adrenal synthase and is regulated primarily by the
• In the ovary, any increase in LH or in the LH:FSH ratio appears cortex renin–angiotensin system
to lead to excess androgen production
o Zona fasciculata and zona reticularis:
• Tumors of both adrenals and ovary can also lead to excess androgens inner layer; produce both cortisol and
• Regardless of the source, elevated androgens lead to hirsutism androgens because of the presence of
and possible virilism. the 17α-hydroxylase enzyme; highly
NORMAL ANDROGEN SYNTHESIS regulated by ACTH
Adrenal • Produces catecholamines
medulla
ANDROGEN EXCESS IN FEMALE
• Hirsutism – increase in terminal hair on face, chest, back, lower
abdomen, and inner thighs in women; characterized by the
development of pubic hair as a male escutcheon (diamond
shaped) as opposed to the triangular female escutcheon
• Virilization – development of male features such as deepening
of voice, frontal balding, increased muscle mass, clitoromegaly,
breast atrophy, and male body habitus
Hirsutism cut-off:
>7 or 8 (Caucasian or African American)
>3 (Asian)
Dr. Banzuela-Cruz

Differential Diagnosis of hirsutism and Virilization

SOURCE DIAGNOSIS
• Exogenous, iatrogenic
Nonspecific
• Abnormal gonadal or sexual development
MARKERS FOR ANDROGEN PRODUCTION
• Androgen excess in pregnancy, luteoma,
SOURCE DIAGNOSIS Pregnancy
hyperreaction luteinalis
Ovary Testosterone Periphery • Idiopathic hirsutism
Adrenal gland DHEAS • Polycystic ovary syndrome
Periphery 3-alpha-diol-G • Functional or idiopathic hyperandrogenism
Adapted from Lobo, et al. Comprehensive Gynecology. 7th ed. 2017 Ovary
• Stromal hyperthecosis
Conversion of testosterone to DHT is the cause of hirsutism in the female, while
• Ovarian tumors
its conversion in the adipose tissue to estradiol causes anovulation in cases of
PCOS (constant elevated levels of estrogen → no LH surge→ no ovulation) • Adrenal tumors
Adrenal
Dr. Banzuela-Cruz • Cushing syndrome
gland
ADRENAL PRODUCTION • Adult-onset congenital adrenal hyperplasia
Lobo, et al. Comprehensive Gynecology. 7th ed. 2017

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MODIFIED FERRIMAN GALLWEY SCORE

FIGURE 40.1. Lobo, et al. Comprehensive Gynecology. 7th ed. 2017

HYPERANDROGENISM SOURCE: ADRENALS • Treatment

SOURCE FEATURES o Anti-androgen that block peripheral testosterone action or
• Adenomas cause glucocorticoid excess; interfere with 5a-RA
Adrenal
virilizing symptoms are rare
tumors
• Carcinomas are rapidly progressive and lead to
(Androgen-
marked elevations in glucocorticoid,
producing)
mineralocorticoid and androgen steroids
• Excess production of cortisol HYPERANDROGENISM SOURCE: OVARIES
• May be caused by pituitary adenoma, ectopic
SOURCE FEATURES
sources of ACTH, tumors of adrenal gland
• Most common cause: Cushing Disease • Characterized by androgen excess,
(pituitary adenoma that hypersecretes ACTH) ovulatory dysfunction, and/or polycystic
• Clinical findings: ovaries
PCOS
o Hirsutism • present with a constellation of symptoms,
o Menstrual irregularity including hirsutism, virilization,
Cushing anovulation, amenorrhea, and obesity
o Central obesity
Syndrome • Hyperplasia: common between ages 50 and
o Dorsal neck fat pads
Stromal 70 and can cause hisutism
o Abdominal striae
hyperplasia • Hyperthecosis: characterized by foci of
o Muscle wasting & weakness and
• Diagnostics: utilization within the hyperplastic stroma
hyperthecosis • Ovaries appear enlarged and fleshy
o Overnight dexamethasone suppression
test: (+) if elevated cortisol • Sertoli-Leydig tumors
o 24-hour urinary free cortisol o Rapid virilization; reproductive years
• Late night salivary cortisol – most accurate Ovarian o Palpable; less common
• Defect in 21-OHase or 11B-OHase (less neoplasm • Hilus cell tumors
common) o Rapid virilization; after menopause
• Accumulation of 17-OH progesterone & o Non-palpable
androstenedione; androstenedione converted
to testosterone
• Severe form (early): sexual ambiguity of newborn
HYPERANDROGENISM MANAGEMENT
Congenital
Adrenal • Mild form (late): hirsutism in 2nd or 3rd decade WORK-UP
Hyperplasia of life • Testosterone (unbound) • 17-OH progesterone
o irregular menses or amenorrhea • Free androgen index • Ultrasound, CT or MRI
o Accelerated growth (6-8 y/o) and short • DHEAS
ultimate height
TREATMENT
o Elevated 17-OHprogesterone
• Treatment: Corticosteroids or OCP • Adrenal nonneoplastic androgen suppression
o Glucocorticoids such as prednisone, 5mg nightly
o Finasteride inhibits 5a reductase enzyme thus diminishing
HYPERANDROGENISM SOURCE: PERIPHERAL peripheral conversion of testosterone to DHT
IDIOPATHIC HIRSUTISM o Antiandrogens (spironolactone): temporizing
• Hirsutism • Ovarian or adrenal tumors: underlying disorders should be treated
• Regular menses with normal androgen levels (DHEAS and • Ovarian nonneoplastic androgen production can be suppressed
Testosterone) with oral contraceptives that will suppress LH and FSH as well
• ↑3a-diol-G due to ↑5a-reductase activity (5a-RA) as increase SHBG
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• Progesterone therapy can be used alone in patients with
contraindications to estrogen
• GnRH agonists can also be used to suppress LH and FSH
• Hirsutism
o Waxing, depilatories, and electrolysis

POLYCYSTIC OVARIAN SYNDROME

• Previously known as the Stein-Leventhal syndrome
• Any 2 of the ff: (Rotterdam Criteria)
1. Menstrual irregularity (anovulation)
2. Hyperandrogenism
• Clinical hyperandrogenism: acne, alopecia, hirsutism
• Biochemical hyperandrogenism: elevated testosterone;
androstenedione and dehydroepiandrosterone sulfate
(DHEAS) may be considered
3. Polycystic ovaries on ultrasound
• Pathophysiology:
o ↑LH secretion with enhanced theca cell responsiveness lead
to excess ovarian androgen
o ↑androgen inhibit negative feedback on hypothalamic
GnRH pulse causing rapid LH pulse. PATHOPHYSIOLOGIC CONCEPT OF POLYCYSTIC OVARY SYNDROME
o ↑androgen due to android obesity, visceral fat deposition, (PCOS)
and dyslipidemia → insulin resistance Figure 41-14. Lobo, et al. Comprehensive Gynecology. 7th ed. 2017
Increased luteinizing hormone (LH) secretion, together with enhanced
o ↓SHBG, due to hyperandrogenemia, obesity &
theca cell responsiveness, drives the production of excess ovarian
hyperinsulinemia. → ↑active testosterone androgen. Increased androgen production may inhibit steroid negative
o ↑androgen → ↑follicle number and size; enhance GC feedback effects on hypothalamic gonadotropin-releasing hormone pulse
responsiveness to FSH generation to account for the rapid LH pulse frequency observed in
women with PCOS. In addition, increased androgen levels are associated
with android obesity, visceral fat deposition, and dyslipidemia, all of
which may contribute to insulin resistance. Independently,
hyperandrogenemia, obesity, and hyperinsulinemia may decrease sex
hormone-binding globulin, thereby increasing bioactive testosterone.
Finally, increased androgen may have direct effects on the ovary to
increase follicle number and follicle size and possibly enhance granulosa
cell responsiveness to follicle-stimulating hormone (FSH). E2, Estradiol.
Compre Gyne

PCOS
https://qrs.ly/owegxb8

MENSTRUAL IRREGULARITIES
• Oligomenorrhea (cycles over 35 days)
• Menstrual frequency of every few months
• Frank amenorrhea (over 6 months missed)

PCOS: ANOVULATION
• Normal as part of the pubertal
< 1 year post menarche
transition
> 1 to < 3 years post
• < 21 or > 45 days
menarche
>3 years post menarche to • < 21 or > 35 days or < 8 cycles
perimenopause per year
• > 90 days for any one cycle
1 year post menarche • Primary amenorrhea by age 15
or > 3 years post thelarche
• By age 15 or > 3 years post
Primary amenorrhea
thelarche
PCOS: ULTRASOUND
• The presence of 12 or more
follicles measuring 2 to 9
millimeters in diameter
• An increased ovarian volume
greater than 10 cm3
• Omitted in the diagnosis: follicle
Lobo, et al. Comprehensive Gynecology. 7th ed. 2017
distribution, bilateral appearance,
stromal echogenicity:

In the newest ESHRE guidelines for Polycystic Ovarian Syndrome (2018),

the cut off value to consider polycystic ovaries on ultrasound varies
depending on the frequency bandwidth of the ultrasound transducer. For
newer ultrasound transducers with a bandwidth of 8MHz, the threshold
for PCO is a follicle count of 20 or more per ovary and/or an ovarian
volume of at least 10 ml, ensuring that no corpora lutea, cysts, or
dominant follicles are present.
Dr. Anna Rominia Cruz

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CONSEQUENCES OF PCOS

CAUSES OF INFERTI LITY

FEMALE FACTORS INFERTILITY
Polycystic ovarian syndrome (PCOS)
Advanced maternal age
OVULATORY
Primary ovarian insufficiency (POI)
(32%)
Hypothalamic amenorrhea
Hyperprolactinemia
PID
TUBAL Tubal ligation
(34%) Pelvic adhesions
Endometriosis (15%)
Congenital malformations
Fibroids
UTERINE
Uterine polyps
Intrauterine synechiae (Asherman syndrome)
Mü llerian duct abnormalities
CERVICAL
PCOS TREATMENT Cervical stenosis
COMPLAINT TREATMENT OPTIONS FECUNDABILITY
Letrozole, clomiphene, with or without • Fecundability: the ability to achieve pregnancy in one menstrual
Infertility metformin, gonadotropins, ovarian cycle
cautery (“drilling”) • Normal monthly fecundability is 20 to 25% for the first 3
Oral contraceptive + antiandrogen
months followed by 15% during the next 9 months
Skin manifestations (spironolactone, finasteride), GnRH
• 60% of couples conceive within 6 months
agonists
Abnormal bleeding Cyclic progestogen, oral contraceptives • 80-90% conceive within 12 months
Weight, metabolic Diet/lifestyle management, metformin
FEMALE FACTOR INFERTILITY
concerns
Adapted from Lobo, et al. Comprehensive Gynecology. 7th ed. 2017 OVULATORY/OVARIAN DISORDERS
Both Clomiphene and Letrozole are first line treatment for PCOS, but
WHO
cornerstone management of PCOS is still lifestyle modification. As I’ve DISEASE TREATMENT
mentioned, insulin resistance is the pathophysiology of PCOS.
GROUP
Dr. Banzuela-Cruz Pulsatile
gonadotropin-
TREATMENT OF SUBFERTILITY Hypogonadotropic hypogonadal releasing
• Clomiphene (mainstay first-line) 1 anovulation hormone (GnRH)
Hypothalamic amenorrhea therapy or
Ovulation • Letrozole (first-line due to its cost-
human
induction effectiveness)
gonadotropins
agents • Metformin Normogonadotropic
• Low-dose gonadotropin (second line) normoestrogenic anovulation
Adjunctive • Dexamethasone PCOS – the most common
2 --
therapy • Dopamine agonists cause of oligo-ovulation and
(rarely used) • Thiazolidinediones anovulation among all
• Ovarian drilling (diathermy)- used in women
Clomiphene and Low dose gonadotropin Hypergonadotropic
failure hypoestrogenic anovulation
Invasive Egg donation,
• In-vitro fertilization – use in women who primary ovarian insufficiency
therapy gestational
3 [POI]
fail to conceive with ovulation induction surrogacy, or
decreased ovarian reserve—
over 6 cycles and with other causes of adoption
the oocyte-related decline in
infertility fertility
4 Hyperprolactinemic anovulation --
INFERTILITY
TUBAL FACTOR
• Failure of a couple to conceive after 12 months of unprotected
sexual intercourse Tubal disease and pelvic adhesions result in infertility by
• Indications for Investigation: preventing the transport of the oocyte and sperm through the
1. >35 y/o with no pregnancy 4. Uterine disease fallopian tube, which is usually caused by pelvic inflammatory
after 6 months 5. Severe endometriosis disease
2. Oligo/amenorrhea 6. Know male factor Condition Treatment
3. Tubal obstruction Microsurgical tuboplasty with
Tubal occlusion caused by
tubal re-anastomosis or
For women older than 35 years old, infertility should be investigated if no prior infection or from
pregnancy has occurred for 6 months provided that there is regular (3x a neosalpingostomy
prior tubal ligation
week) sexual intercourse In-vitro Fertilization
Dr. Banzuela-Cruz Hydrosalpinges Salpingectomy then IVF

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UTERINE AND CERVICAL FACTORS ALGORITHM OF EVALUATION OF TREATMENT

Condition Treatment
Operative hysteroscopy
Uterine synechiae, myomectomy for treatment
Uterine
septae, polyps, or after recurrent pregnancy
Factors
submucosal fibroids loss or when symptomatic
fibroids have been identified
Cervical stenosis: surgical or
Mü llerian duct mechanical dilation of the
Cervical
abnormalities endocervical canal,
Factors
Cervical stenosis Intrauterine insemination; if
refractory IVF

ENDOMETRIOSIS
Can invade local tissues and cause severe
inflammation and adhesions
Can interfere with tubal mobility, cause tubal
obstruction, or result in tubal or ovarian
Pathology
adhesions that contribute to infertility by
holding the fallopian tube away from the ovary, EVALUATION AND LABORATORY TESTS
obstructing the tube, or by trapping the released
oocyte. • Medical history
There is no role for medical management o Any pregnancy complications if previously pregnant
Fertility rates can be improved by surgical ligation o Previous pelvic surgery of any type
Treatment of periadnexal adhesions and excision, o Significant dysmenorrhea
coagulation, vaporization, or fulguration of o Dyspareunia or sexual dysfunction
endometrial implants typically via laparoscopy o Abnormal cervical cytology or procedures to treat cervical
abnormalities
o Use of medication, drugs, and tobacco.
MALE FACTOR INFERTILITY o Any symptoms suggestive of endocrine disorders (weight
COMMON ETIOLOGIES OF MALE FACTOR INFERTILITY changes, skin changes, etc.)
Cryptorchidism (congenital) • Family History
Abnormal semen Mumps orchitis
o Genetically related illnesses
Antisperm antibodies
o Birth defects
Hypogonadotropic hypogonadism
Endocrine disorders o History of age of menopause in female family members.
Thyroid disease
Radiation
• Physical exam
Environmental o Extremes of body mass
Heat
exposures o Skin changes
Chemicals
Klinefelter syndrome o Thyroid size
Genetic Immobile cilia syndrome o Breast secretion
Cystic fibrosis o Abnormal pain on abdominal or pelvic exam
Erectile dysfunction o Assessment of the vagina and cervix
Sexual dysfunction Ejaculation failure
VAGINAL ULTRASOUND
Retrograde ejaculation
Varicocele • Abnormalities of the uterus (e.g., Fibroids)
Structural factors Testicular torsion • Endometrial thickness
Vasectomy • Pelvic masses
No identifiable cause • Ovarian morphology (polycystic appearance or unusually small)
Unexplained
Idiopathic abnormal semen
SEMENALYSIS
Drugs that decrease semen quality and quantity • The male partner should be advised to abstain from ejaculation
MEDICATIONS EXOGENOUS EXPOSURES for 2 to 3 days before collection of the semen sample, because
• Cimetidine • Anabolic steroids frequent ejaculation lowers seminal volume and occasionally
the sperm count in some individuals
• Sulfasalazine • Marijuana
• The entire specimen be collected, because the initial fraction
• Spironolactone • Alcohol abuse
contains the greatest density of sperm.
• Antidepressants • Heroin/cocaine abuse
• The sperm analysis is a subjective test and that there is a fair
• Metoclopramide
degree of variability from test to test in the same man.
• Chemotherapeutic agents
• The semen profile reflects sperm production, which occurred 3 months
• Beta blockers
earlier, which is important to note if there were illness at that time
• Nitrofurans
• Parameters used to evaluate the semen include volume,
Varicocele is the most common reversible cause of male factor viscosity, sperm density, sperm morphology and sperm motility.
infertility
• The characteristics of semen may vary over time and undergo
normal biological variability, if an abnormality is found, it is best
DIAGNOSTIC EVALUATION
to repeat test in two or three occasions
Semen analysis normal parameters
Volume >2.0 mL
pH 7.2-7.8 INFERTILITY
Concentration >20 million/mL – SEMEN ANALYSIS
Morphology >30% normal forms https://qrs.ly/mzegxbd
Motility >50% with forward progression
WBC <1 million/mL EVALUATION AND LABORATORY TESTS:
Endocrine evaluation FEMALE INFERTILITY
To assess for parenchymal SERUM PROGESTERONE
Testosterone, prolactin, LH,
damage to testes and • For women with regular cycles
and FSH
hypogonadism • Should be measured in the midluteal phase (days 21 to 23) to
Karyotype and a Y- provide indirect evidence of ovulation as well as normal luteal
Cases of azoospermia chromosome microdeletion function.
genetic testing • > 10 ng/mL indicative of adequate luteal function
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FOR WOMEN WITH OLIGOMENORRHEA: PROGNOSIS
Treat with agents that induce ovulation regardless of whether they Highest
have occasional ovulatory cycles. Probability
Anovulation is the only abnormality
• direct or indirect measurement of progesterone is of
Conception
UNNECESSARY until after therapy is initiated.
Tubal disease
DIAGNOSTIC TESTS DONE Sperm abnormality
Lower
Infertile couples with no demonstrable cause of
• CBC Probability
infertility have their best prognosis for conception
• Blood type, RH of
without treatment for about 2 years after the initial
• Rubella status Conception
infertility evaluation is completed, and a poor
• Pap smear obtained within 3 years prognosis thereafter
• Comprehensive screening for carrier status including fragile X Afford The
and cystic fibrosis Highest IVF
Pregnancy GAMETE INTRAFALLOPIAN TRANSFER (GIFT)
• Routine infections disease screening (for chlamydia and
Rates
gonorrhea)
• Infectious disease screening (syphilis, HIV, hepatitis, etc.) in Hysterosalpingogram (HSG) – with dye and uses X-ray
high-risk cases and for couples undergoing insemination or IVF Hysterosalpingosonogram (HSSG) – with dye and uses ultrasound
• TSH (Values greater than 2.5 mIU/m: but lower than 4.4 uU/mL Saline Infusion Sonohysterogram (SISH) – uses ultrasound and
is abnormal in a woman presenting with infertility) introduction of saline to the uterus
• Prolactin Dr. Banzuela-Cruz

TREATMENT: ANOVULATION
WOMEN OLDER THAN 35 CLOMIPHENE CITRATE (FIRST LINE):
Serum FSH and estradiol (E2) should be obtained on cycle day 2 or 3 • competes with estrogen-binding sites on hypothalamus;
< 10 mIU/mL: normal increase FSH, increase in E2
10-15mIU/mL: borderline ovarian reserve • given daily for 5 days beginning on days 3 to 5 after the onset or
Serum
> 20 mIU/mL spontaneous menses or withdrawal bleeding induced with
FSH
o bad prognosis; Suggests decreased progesterone
ovarian reserve
• If elevated (>70 pg/mL) on D2 or 3 may METFORMIN
Estradiol • Can be considered an adjunctive treatment for ovulation
independently suggest a decreased prognosis
(E2) • MOA in inducing ovulation is both through reducing insulin
regarding ovarian reserve
resistance as well as directly stimulating the ovary.
• DOSE 1500 mg/day [begun at 500 mg and titrated up over
several weeks due to gastrointestinal effects
• When metformin alone is prescribed for anovulatory, women
who wish to conceive, the ovulation rate is
• approximately 60%
LETROZOLE
• MOA: inhibition of E2 production during the 5 days of
administration, with a negative feedback causing an increase in
the LH:FSH ratio, much like the response to clomiphene.
• Short-acting, hence the problems of thick cervical mucus or a
ANTIMULLERIAN HORMONE (AMH) thin endometrium associated with clomiphene have not been
• Produced by ovarian granulosa cells and decreases with age reported with letrozole
• At 0.05 ng/mL, menopause occurs within 4-5 years • Dose 2.5 mg or 5 mg for 5 days like clomiphene, beginning on
• May suggest decreased ovarian reserve at levels <0.5 ng/mL cycle days 3 to 5.
• Increased levels suggest a large cohort of follicles, such as in GONADOTROPINS
patients with polycystic ovarian syndrome
• for ovulation induction when estrogen levels are low.
ANTRAL FOLLICLE COUNT (AFC) • Low serum E2 levels (usually < 30 pg/mL) or lack of withdrawal
bleeding after progestogen administration signifies a state that
• Measuring the number of antral follicles present on days 2 to 4
will be unresponsive to oral therapies (clomiphene, letrozole)
measuring 2 to 10 mm in diameter
that are dependent on a negative feedback system
• Presence of 4-10 follicles is a good sign of ovarian reserve • in clomiphene/letrozole failures
• It is essential to monitor treatment carefully with frequent
HYSTEROSALPINGOGRAM (HSG)
• measurement of estrogen levels and ovarian ultrasonography
During the week following the end of
• The physiology is to increase the serum FSH above a critical
Schedule menses to avoid irradiating a possible
pregnancy (days 5-10) threshold level
• Starting Dose: 150IU with FSH
History of salpingitis in the recent past or if • Determine E2 levels and do UTZ after 5 days then every other
Contraindication
there is tenderness on pelvic exam.
day until follicle reaches 18mm diameter
• Advise timed intercourse if with normal semen and good
Prophylactic Doxycycline (100 mg twice a day for 3
antibiotics days starting 1 day before the procedure)
cervical mucus
• Ovulation should occur between 36 – 48 hours after the trigger
(+) hydrosalpinx of HCG
Continue doxycycline for 1 week.
on HSG
• Adverse effect: Ovarian Hyperstimulation Syndrome
Tubal reconstructive surgery not necessary
1 oviduct
Do dx laparoscopy to detect peritubal
patent
adhesions OVULATION INDUCTION
Normal endometrial https://qrs.ly/z1egxbi
No need for hysteroscopy
cavity
Large Laparoscopic salpingectomy followed by IVF-
hydrosalpinx Embryo transfer (ET)
Extent of tubal Do dx laparoscopy in the follicular phase of the ETIOLOGY INTERVENTION
disease unclear cycle • IUA: hysteroscopic lysis of adhesions
Uterine • Leiomyoma: myomectomy
factor • TB: “pipe-stem” tube; anti-Koch’s treatment; IVF
• Endometriosis: cauterization, cystectomy, IUI, IVF

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ETIOLOGY INTERVENTION MENOPAUSE
• COS + preovulatory IUI or IVF. • 12 months of amenorrhea after the FMP in the absence of any
• COS should be performed with either clomiphene other pathologic or physiologic causes
Unexplained citrate or HMG.
Infertility
• Characterized by complete, or near complete, ovarian follicular
• Older women (>42 y/o) should proceed directly to
IVF because of reduced efficacy of COS in such depletion and absence of ovarian estrogen secretion
women • The estrogen and FSH levels stabilize 2 years after the FMP.
Symptoms generally begin to dissipate at this time.
TREATMENT: MALE FACTOR INFERTILITY • Range: 45 and 55 years (average: 51 years old)
History • Late menopause (after 55 years old): 5%
• Early menopause (between 40 to 45 yo): 5%
• Decrease in breast size and change in texture
• Increases in abdominal circumference and
upper abdominal weight gain
• Vulvovaginal atrophy (VVA)
Physical • Increase in the BMI
Examination • Skin changes- loss of elasticity
• Hair changes- loss of pubic hair, female
pattern baldness, and excessive growth of
terminal facial hair
• Dry eyes
Endocrinologic
• FSH levels > 40 IU/L
marker

CLIMACTERIC
• Period of time when a woman passes from reproductive stage to
Figure 42.19. Lobo, et al. Comprehensive Gynecology. 7th ed. 2017
non-reproductive stage.
IN VITRO FERTILIZATION • Includes perimenopause, menopause and postmenopausal years
Indications for IVF Bilateral tubal occlusion
as primary therapy Severe male factor GENITAL URINARY SYNDROME OF MENOPAUSE (GSM)
Strategy for a • vulvovaginal atrophy (VVA), such as dryness with itching,
Generation of good-quality embryos
successful IVF discharge, dyspareunia, and urinary system changes, such as
IVF that is carried out in a natural cycle incontinence and dysuria
Only 1 oocyte and 1 embryo can be
expected HORMONE PRODUCTION
In vitro maturation (IVM) of oocytes is
Unstimulated
carried out followed by ICSI
• AFTER Menopause
IVF o FSH increase 10-20x
Usually done in anovulatory women with
PCOS o LH increase 3x
Advantage of easy aspiration and o Androstenedione: principal steroid secreted by ovary
eliminating risk of hyperstimulation o Testosterone production decreases by 25%
Can be used if the infertile woman with o SHBG decreases
GIFT Gamete functioning oviducts. o Estradiol levels markedly decline
Intrafallopian Both oocytes and sperm are placed into o Androgen/estrogen ratio drastically increase
Transfer (GIFT) the oviduct through a catheter at the o DHEA and DHEA-S decrease
time of laparoscopy or minilaparotomy
ZIFT Zygote MENOPAUSAL SYMPTOMS AND LONG-TERM EFFECTS
The oocytes are fertilized in vitro and
Intrafallopian (Mnemonic: FSH > 40 IU/L)
transferred 24 hours later
Transfer (ZIFT) F Flushes, forgetful (Alzheimer disease)
TET Tubal Embryo Embryos are transferred 8 to 72 hours Sweats at night, sad (depression), stoke, skeletal
Transfer (TET) after fertilization. S changes (accelerated bone loss leading to osteoporosis),
skin changes, sexual dysfunction
H Headaches, heart disease
I Insomnia
MENOPAUSE Urinary symptoms (stress and urge incontinence),
MENOPAUSAL TRANSITION (PERIMENOPAUSE) U
urogenital atrophy (loss of pelvic floor muscles)
• Transition from normal ovulatory cycles to menopause because L Libido decreases
of progressive ovarian failure Remember that an FSH level >40 IU/L is the blood test to confirm menopause.
• Hallmark of Perimenopause: Skipped periods, or longer MENOPAUSE & FAT
intervals (40-60 days)
• Symptoms can begin from 2 to 8 years prior to the final
menstrual period
o Vasomotor symptoms, (VMS) including night sweats and
daytime hot flashes, mood swings, including irritability and
depression, insomnia, and sleep disturbances
HORMONE LEVELS ↑ Body fat = ↑ Androstenedione conversion to estrone
= ↑ circulating level of estrogen
• Decreased inhibin, increased FSH
HORMONE LEVELS DURING PERIMENOPAUSE
Decreased due to diminished in the number of
Inhibin B
follicles
FSH Increased
Progesterone Low
Fluctuates but in general are preserved until
Estradiol late perimenopause when both estradiol and
FSH can fluctuate

MENOPAUSE
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SIGNS & SYMPTOMS COGNITIVE FUNCTION

FAT AND WEIGHT • Effects of estrogen on the CNS:
• á in total body weight and total body fat o ↑ synapses & neuronal growth
o Protects against neuronal oxidative cytotoxicity
• áwaist-to-hip ratio
o Reduces concentration of amyloid protein deposits
• Shift of fat distribution from a gynecoid to android type
o Enhances cerebral blood flow, which increases glucose &
• Prevented by ERT
oxygen provision
SKIN
CARDIOVASCULAR DISEASE
• Decline in collagen content and skin thickness
• Protective effects of estrogen:
• Estrogen effects: o Elevation of HDL cholesterol
o Arrest/avoidance of wrinkles o Reduced total cholesterol, as well as LDL
o Reduces collagen turnover & improves quality
• Predictors of cardiovascular events:
HOT FLUSH/FLASH o HTN o DM
• Hallmark of female climacteric o Smoking o High BMI
• ↓ in circulating level of estrogen alters the hypothalamic o Dyslipidemia (low LDL) o Metabolic syndrome
thermoregulation BONE CHANGES
• Sudden sensation of heat in chest area radiating to the head & • Loss of trabecular bone (spine) > loss of cortical bone with
neck, accompanied by: estrogen deficiency.
o Reddening of skin • Vertebral bone fracture most common
o ↑heart rate
• Osteoporosis: bone formation does not keep pace with bone
o Profuse sweats (night sweats)
reduction
o Anxiety, irritability, palpitations and panic
• Diagnosis: Bone mineral density assessment by DEXA
• Differentials:
o Pheochromocytoma, carcinoid, leukemias, pancreatic MANAGEMENT OPTIONS
tumors, thyroid disease, or psychosomatic Symptoms and treatment options
MENOPAUSAL SYMPTOM TREATMENT OPTION
SLEEP DISTURBANCE
BP and lipid control medications,
• Difficulty falling asleep Cardiovascular changes smoking cessation, weight loss,
• Frequent awakenings exercise
• Difficulty falling back to sleep MHT, calcium, Vitamin D,
• Associated with hot flush/flash bisphosphonates, calcitonin, SERMs,
Osteoporosis prevention weight-bearing exercise, and decrease
• Insomnia
smoking and caffeine and alcohol
DEPRESSED MOOD intake
• Associated with sleep problems & hot flush/flash MHT, SSRIs, SNRIs, gabapentin,
VMS (hot flashes, night
• Risk factors: clonidine, behavioral changes (cooling
sweats)
pillow, sweat-wicking pajamas, fan)
o History of depressive disorders
Genitourinary syndrome of Low-dose vaginal estrogen, water-
o Poor physical health
menopause (vaginal based lubricant, vaginal moisturizers
o Life stressors dryness, dyspareunia, Ospemifine 60 mg (selective estrogen
o Surgical menopause incontinence, dysuria) receptor agonist or SERM)
o Long perimenopause Mood disturbances MHT, SSRIs, SNRIs, counseling
VULVOVAGINAL SYMPTOMS HORMONE REPLACEMENT THERAPY
• Declining estrogen results in dryness, itchiness, burning and • Benefits
dyspareunia o Alleviate menopausal symptoms (e.g. hot flushes, sleep
• Pathophysiology: disturbance, urogenital complaints
o ↓ in blood flow lead to paler, less well-nourished epithelium o Reduced muscle & joint pains, mood swings, sexual
& decrease collagen & elastic fibers dysfunction
o ↑ fibrin & connective tissue lead to thinning, loss of rugae, o Reduced urogenital atrophy & UTI
↓vaginal elasticity o ↓ osteoporosis-related fractures
o ↓ in acid mucopolysaccharides and hyaluronic acid lead to
dryness & less acid pH • Contraindications
o ↓ lubrication with sexual stimulus contribute to dyspareunia o Current, past or suspected breast cancer
• Vaginal changes o Known or suspected estrogen-dependent malignant tumor
o Shortens, narrows with loss of fornices & distensibility o Undiagnosed genital bleeding
o End-stage rigid & contracted vagina o Untreated endometrial hyperplasia
o Venous thromboembolism
SEXUAL DYSFUNCTION o Angina or MI
• Painful sex from atrophy & dryness o Untreated HPN
• Changes in libido & arousal o Active liver disease
• Factors: o Hypersensitivity to HRT
o Personal relationships o Stressors o Porphyria cutanea tarda (absolute contraindication)
o Socioeconomic conditions o Absence of sexual
thoughts & fantasies OSTEOPOROSIS
GENITOURINARY TRACT
RISK FACTORS MNEMONIC FOR OSTEOPOROSIS
LOSS OF ESTROGEN CLINICAL SIGNIFICANCE
SHATTERED Family
• ↓ Collagen content of the S Steroid use (>5 mg/d of prednisone)
structures that support the • Uterine descensus or
Hyperthyroidism/hyperparathyroidism/
uterus (ligaments), pelvic prolapse H
hypercalciuria
relaxation
A Alcohol (>3/d) and tobacco (active or passive) use
• ↓ Collagen in the endopelvic
T Thin (BMI < 22, weight < 127 lbs)
fascial tissue in the vaginal • Cystocele, rectocele
T Testosterone low, hypogonadism
wall
E Early menopause
• Urinary urge
• Atrophic changes in the R Renal or liver failure
incontinence, urinary
urinary tract lining and loss of Erosive/inflammatory bone disease (e.g.,
frequency, dysuria, and E
ureteral tone rheumatoid arthritis, myeloma)
nocturia
D Dietary Ca low/malabsorption or diabetes mellitus type I
Family Family history/genetics
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• Bone mineral density (BMD) screening should Continuous The loss of urine at all times, possibly due to
begin at age 65 years for all women. (urinary) a urinary fistula secondary to surgery,
• Postmenopausal women under the age of 65 incontinence radiation, or obstructed labor
years should be screened if they have significant The loss of urine due to a physical or
Screening Functional
risk factors including history of fragility fracture, psychological (e.g., dementia) inability to
(urinary)
weight <127 lbs, parent with a history of hip respond to voiding cues. Often seen in
incontinence
fracture, current smoking, alcoholism, or nursing home patients and geriatric patients
rheumatoid arthritis
• Gold Standard: dual-energy X-ray absorptiometry RISK FACTORS
(DXA) of the lumbar spine and hip Stress Urgency
Mixed
• Diagnostic Interpretation Incontinence incontinence
Diagnosis o Normal: T-scores ≥−1.0 • Age • Age • Age
o Low bone mass (osteopenia):T-scores • Obesity • Diabetes
<−1.0 to >−2.5 • Pregnancy and mellitus
o Osteoporosis: T-scores ≤−2.5 vaginal delivery
• Lifestyle changes • Genetics
• Weight-bearing exercise (such as walking, hiking, • Diabetes Mellitus
and stair climbing) and muscle-strengthening • Hormonal status
exercise • Pelvic Surgery
• Adequate calcium and vitamin D intake • Smoking
• Reduction in active and passive smoking and • Chronic cough
alcohol intake • Medications
• Medications for prevention: bisphosphonates,
zoledronic acid, raloxifene, MHT, slow-release DIAGNOSTIC EVALUATION
sodium fluoride • Goal: Distinguish between stress incontinence and urgency
• Medications for treatment incontinence
o Bisphosphonates (etidronate, alendronate, • Used to document the specific circumstances
risedronate, ibandronate, and zoledronic Voiding diary or of the patient’s voiding habits (e.g., intake,
acid) - inhibition of osteoclast resorption of bladder chart amount voided, leak volume, associated
bone activity, and urgency presence).
o SERM (raloxifene, droloxifene , and Urinalysis with
tamoxifen)- inhibit bone resorption; used • Rule-out infection as a cause of
microscopy and
incontinence
in the prevention of vertebral fractures but urine culture
not for hip fracture prevention • Genuine stress incontinence- fill bladder
o Tibolone 2.5 mg (structurally related to 19- Urinary stress with 300ml saline, with urine leakage with
nor progestins) – mixed estrogenic, test coughing then postvoid residual (PVR) is
Treatment antiestrogenic, androgenic and obtained by catheterization
progestogenic properties); for the • Diagnose a hypermobile urethra associated
Cotton swab test
treatment of osteoporosis and also with stress incontinence.
beneficial for vasomotor symptoms • Reserved for patients contemplating
o Denosumab 60 mg SQ every 6 months - surgery and for those in whom a clear
monoclonal antibody to receptor activator diagnosis cannot be made on preliminary tests
of nuclear factor-κB ligand, which blocks • Three major components:
proliferation and differentiation of o Evaluation of urethral function
osteoclasts, resulting in decreased bone Urodynamics (urethrocystometry and urethral
pressure profilometry)
resorption and increased BMD; secondary
o Bladder filling (cystometry)
agent for women intolerant to other
o Bladder emptying (uroflowmetry and
treatment
voiding cystometry or pressure flow
o Calcitonin 50IU SQ daily or 200 IU studies).
intranasally- antiresorptive treatment.
o Parathyroid hormone- stimulates
osteoblastic activity; increases bone mass
in women with significant osteoporosis but
must not be taken longer than 18 months
o Elemental calcium 1500 mg daily if no
agents are being used to inhibit resorption
o 400 to 800 IU of vitamin D should also be
ingested

URINARY INCONTINENCE
PATHOLOGY
• Failure of the bladder to store and empty urine appropriately
• 3 main types
o Stress incontinence
o Urgency incontinence
o Mixed incontinence
Stress (urinary) Involuntary loss of urine on effort or physical TREATMENT
incontinence exertion, or on sneezing or coughing Stress Incontinence Urgency incontinence
Urgency
Involuntary loss of urine associated with • Low-dose vaginal estrogen • Depend on the etiology of
(urinary)
incontinence
urgency • Incontinence pessaries disease
• Surgery (tension-free • Idiopathic urgency- managed
Involuntary loss of urine associated with
Mixed (urinary) midurethral sling) with a combination of
urgency and also with effort or physical
incontinence lifestyle and behavior
exertion or on sneezing or coughing
The loss of urine due to poor or absent modifications, medication,
Overflow bladder contractions or bladder outlet and sometimes surgery
(urinary) obstruction that leads to urinary retention Lifestyle and behavioral modifications include weight loss, caffeine
incontinence with overdistension of the bladder and restriction, smoking cessation, fluid management, bladder training,
overflow incontinence pelvic floor muscle exercises (Kegel exercises), and physical therapy
(biofeedback, magnetic therapy, and electrical stimulation)
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PELVIC ORGAN PROLAPSE (POP)

• Failure of various anatomic structures to support the pelvic
viscera
• the descent of one or more of the vaginal walls or cervix:
o anterior vaginal wall prolapse (cystocele, urethrocele,
paravaginal defect)
o posterior vaginal wall prolapse (rectocele or enterocele),
uterine/cervical prolapse
o vaginal vault prolapse – in cases of post hysterectomy
RISK FACTORS FOR DEVELOPMENT OF PELVIC ORGAN
PROLAPSE
Vaginal childbirth
Aging
Obesity
Diabetes
Genetic conditions/connective tissue disorders
Neurologic injury
POSSIBLE ASSOCIATIONS WITH PELVIC ORGAN PROLAPSE
Prior pelvic surgery
Hysterectomy
Constipation
Irritable bowel syndrome
Episiotomy MANAGEMENT: SURGICAL
Higher weight of the largest infant delivered vaginally VAGINAL ABDOMINAL
Chronic cough and respiratory diseases ANTERIOR
Exercise Burch
Cystocele/ Anterior colporrhaphy, colposuspension,
Heavy lifting
Cystourethrocele Paravaginal repair Paravaginal repair,
Lower education Sacrocolpopexy
Lobo, et al. Comprehensive Gynecology. 7th ed. 2017
POSTERIOR
• Symptoms: Rectocele Posterior colporrhaphy Sacrocolpopexy
o Lower Urinary Tract: Urinary incontinence, Frequency, MIDLINE
urgency, nocturia, Voiding difficulty: slow stream, Sacrospinous fixation, Sacrohysteropexy,
incomplete emptying, obstruction, Urinary splinting Prespinous fixation Sacrocolpopexy,
Uterine
o Bowel: Constipation, Straining, incomplete evacuation, (iliococcygeal), Uterosacral
prolapse/
Uterosacral fixation/plication,
Bowel splinting, Anal incontinence Vault prolapse/
fixation/plication, Culdoplasty
o Sexual Symptoms: Interference with sexual activity, Enterocele
McCall’s culdoplasty, (Moschowitz/
Dyspareunia, Decreased sexual desire Colpocleisis Halban)
o Other Symptoms: Pelvic pressure, heaviness, pain,
Wag malito, POP is different from uterine inversion. POP in Tagalog is “bua”.
Presence of vaginal bulge/mass, Low back pain, Tampon not
In POP, nawawalan ng support yung uterus. Imagine that the supporting
retained, Quality of life impacts structures and ligaments of the uterus are rubber bands. Pag maraming times
STAGING (POP-Q) na nanganak, these rubber bands lose their elasticity na eventually nawawala
0 No Descent na resulting to the uterus, along with its attachment to the bladder and the
I Leading point >1 cm above hymen rectum, to prolapse. That’s why one of the risk factors for developing POP is
the number of NSDs as well as the birthweight of the babies. No one has died
II Leading point 1 cm above or 1 cm below the hymen
from POP though, so if the question in the boards gave you a patient who is an
III Leading point >1 cm below the hymen but less than TVL (-2) unlikely candidate for surgery, opt for conservative management such as
IV Leading point is more than TVL (-2). Complete eversion. placement of the pessary.
Dr. Banzuela-Cruz

ENDOMETRIOSIS
• Presence and growth of the glands and stroma of the lining of
the uterus in an aberrant or heterotopic location
• The classic symptom of endometriosis is pelvic pain

PELVIC ENDOMETRIOSIS
https://qrs.ly/z3egxby

THEORIES ON THE ETIOLOGY

• Retrograde menstruation (SAMPSON THEORY):
Implantation of endometrial cells shed during menstruation,
growing as homologous grafts under hormonal influence
• Lymphatic and Vascular dissemination (HALBAN THEORY):
POP-Q SCORING The endometrium is transplanted via lymphatic and the
https://qrs.ly/owegxbr vascular system. Best explains endometrial implants found in
remote sites. Hematogenous dissemination of endometrium is
the best theory to explain endometriosis of the forearm and
MANAGEMENT: CONSERVATIVE thigh, as well as multiple lesions in the lung.
• Pelvic floor muscle training (PFMT) • Metaplasia (COELOMIC METAPLASIA THEORY): Following an
o Delivered by physiotherapist for symptomatic women “induction phenomenon”, endometriosis arises from metaplasia
o Symptomatic women who declined surgery. of the coelomic epithelium or proliferation of the embryonic
• Pessary rests which explains endometriosis in prepubertal girls, women
o Fitted in all women regardless of site or severity of prolapse with congenita absence of uterus, and rarely in men.
o Types: • Iatrogenic: Endometrial glands and stroma are implanted
§ Support pessaries during surgical procedure i.e. endometriosis on abdominal
§ Space-occupying pessaries incision site

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• Genetic predisposition: Incidence of endometriosis in • GnRH agonist (Leuprolide)
relatives of women with the disease: 7-fold increase Medical • 3.75mg IM/ month
• Immunologic changes: Those who develop endometriosis oophorectomy • Side effects: hot flushes, vaginal dryness,
have more peritoneal macrophages that are larger. These insomnia and decrease in mineral bone content
hyperactive cells secrete multiple growth factors and cytokines Pseudo- • High dose OCP
that enhance the development of endometriosis. pregnancy state • OCP single daily monophasic for 6-9 months
• Hormonal influences • Oral Contraceptives
DISEASE OF CLINICAL CONTRAST o Combined oral contraceptive pills
CHARACTERISTICS CONTRASTS o Single daily monophasic oral contraceptive
• Widespread • Progestins
Benign Disease Locally invasive • Disseminated foci o For those who cannot tolerate high dosage of estrogen
• Proliferates in pelvic LN o DMPA 150mg IM every 3 months
Minimal Disease • Severe pain o Breakthrough spotting or bleeding
Many large endometriomas • Asymptomatic patient SURGICAL MANAGEMENT
Cyclic hormones cause • Continuous hormone • Failed medical therapy
growth • reverse growth pattern • Far advanced diseases
LOCATION OF IMPLANTS IN THE PELVIS • Future fertility is not a consideration
• In cases of acute rupture of large endometriomas, ureteral
• The majority of endometrial implants are located in the
obstruction, compromise in large bowel’s function
dependent portions of the female pelvis
• Ovarian endometriosis of >2cm
• Adnexal enlargements of more than >8cm
• Sites: • Conservative
o ovaries- most common o Resection or destruction of endometrial implants
o pelvic peritoneum over o Removal of all macroscopic, visible areas of endometriosis
the uterus with preservation of ovarian function and restoration of
o anterior and posterior pelvic anatomy
cul-de-sac o lysis of adhesions
o uterosacral, round, and • Definitive
broad ligaments o TAHBSO and removal of all visible endometriosis
o pelvic lymph nodes o Reserved for far advanced disease and for whom future
fertility is not a consideration
o Laparoscopy:
§ employed for both diagnostic and therapeutic reasons
The weirdest endometriotic implant I’ve seen is located on a woman’s
knee. Every time she menstruated, the implant grew in size and § Commonly recommended as initial approach
disappeared once she reached menopause. § Advantages:
Dr. Banzuela-Cruz - Both diagnostic and therapeutic
SYMPTOMS - Shorter recovery period
• Asymptomatic in 1 in 3 women - Reduced subsequent postoperative adhesions
• Classic Symptoms: cyclic pelvic pain and infertility o Combination of medical and surgical therapy:
• Common symptoms: pelvic heaviness, dyspareunia § For advanced stages of endometriosis
• Abnormal Bleeding (15-20%) – premenstrual spotting or § Postoperative medical therapy is considered depending on
menorrhagia the extensiveness of the disease and the success of surgery
• GI and Urinary Tract Symptoms: Cyclic abdominal pain, Recommended strategy for the management of women with
intermittent constipation, diarrhea, dyschezia, urinary endometriosis and pain symptoms
frequency, dysuria, and hematuria. Bowel obstruction and
hydronephrosis may occur. One rare clinical manifestation of
• Rare: Catamenial hemothorax and ascites
CLINICAL FINDINGS
• Classic pelvic finding: Fixed retroverted uterus, with scarring
and tenderness posterior to the uterus
o Tenderness of the pelvic structures, nodularity of the
uterosacral ligaments and cul-de-sac
• Advanced cases: extensive scarring and narrowing of the
posterior vaginal fornix
• Ovaries may be enlarged and tender and are often fixed to the
broad ligament or lateral pelvic sidewall
• Gold standard for diagnosis: Laparoscopy
PELVIC ENDOMETRIOSIS ENDOMETRIOSIS
Location • Aberrant location or outside the uterus
• Other diagnostic tools:
Etiology • Retrograde menstruation
o Ultrasound - no specific pattern; may help distinguish an
Cyclic • Responds to cyclic changes in ovarian hormone
endometrioma from other adnexal abnormalities.
changes production
o MRI- Provides the best diagnostic tool for endometriosis;
Prevalence • Nulliparous women
not always a practical modality for its diagnosis.
Symptoms • Dysmenorrhea and infertility
MANAGEMENT Signs • fixed, tender uterus with scarring and
• Short Term Goals tenderness posterior to the uterus (no
o Relief of pain enlargement)
o Address Infertility Diagnosis • Laparoscopy
• Long Term Goal Treatment • Medical and Surgical
o Prevent progression or recurrence Technically, we call aberrant endometrial glands and stroma in the
MEDICAL MANAGEMENT myometrium as adenomyosis, while those found in the ovaries are called
endometriomas or chocolate cysts.
• PRIMARY GOAL: INDUCTION OF AMENORRHEA Dr. Banzuela-Cruz
Pseudo- • Anti-estrogen, hyperandrogenic effect (Danazol)
menopause • 400 to 800 mg/day for 6 months
Effect • Side effects: acne, weight gain, hot flushes

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GYNECOLOGIC INFECTIONS SIGNS AND SYMPTOMS

• Non-specific symptoms
INFECTIONS OF THE UPPER GENITAL TRACT
• The most frequent symptom: new-onset lower abdominal and
PID is a spectrum of disease which can present as an acute abdomen so
pelvic pain
it’s very important to know the sexual history of the patient. Tubo-
ovarian complex is a radiologic diagnosis of salpingo-oophoritis and is • 5-10% of women with acute PID develop symptoms of
treated by broad spectrum antibiotics. Again, management for PID even perihepatic inflammation, the Fitz-Hugh–Curtis syndrome
if with TOA is still medical. o Right upper quadrant pain, pleuritic pain, and tenderness in
Dr. Banzuela-Cruz the right upper quadrant when the liver is palpated. The
ENDOMETRITIS pain may radiate to the shoulder or into the back.
• Infection of the endometrium o Liver transaminase levels may be elevated
• Endomyometritis: infection invades the myometrium
• Chronic Endometritis: often asymptomatic but may lead to
other pelvic infections. Suspected if with chronic irregular
bleeding, discharge and pelvic pain, diagnosed with
endometrial biopsy showing plasma cells
RISK FACTORS
• Retained products of conception
• Sexually Transmitted disease
• Intrauterine foreign bodies or growths
• Instrumentation of the uterine cavity
• Cesarean delivery
• Minimally invasive transcervical gynecologic procedures
• IUD placement
TREATMENT
• Clindamycin 900 mg IV every 8 hours OR cefoxitin 2 g IV every
6 hours + Gentamicin loaded with 2 mg/kg IV and then
maintained with 1.5 mg/kg IV every 8 hours PID COMPLICATIONS
• Single daily IV dosing of gentamicin (5 mg/kg every 24 hours) • Infertility • Ectopic pregnancy
may be substituted for 8-hour dosing o 1 episode: 12% • Chronic pelvic pain
• Treatment course continues until clinical improvement and o 2 episodes: 20% • Dyspareunia
afebrile status for 24 to 48 hours o 3 or more: 40% • Pelvic adhesions
• Oral antibiotic therapy is not required following successful DIAGNOSIS
parenteral treatment MINIMUM ADDITIONAL DEFINITIVE
• In nonpuerperal infections where chlamydial infection may be CRITERIA CRITERIA CRITERIA
the suspected cause, doxycycline should be added to the • Empirical • Oral temperature • Histopathologic
regimen for a total of 14 days treatment of PID >38C evidence of
• Chronic Endometritis: 10-14 day course of Doxycycline, should be initiated • Abnormal cervical endometritis on
100mg BID PO in sexually active or vaginal discharge endometrial
young women and (mucopurulent) biopsy
PELVIC INFLAMMATORY DISEASE (PID) others at risk for • Presence of • Transvaginal
• An infection of the upper female genital tract including any STIs if the following abundant WBCs sonography or
combination of endometritis, salpingitis, tubo-ovarian abscess minimum criteria on microscopy of MRI showing
(TOA), and pelvic peritonitis are present and no vaginal secretions thickened fluid-
other causes(s) for • Elevated filled tubes, with
• Traditionally associated with N. gonorrhoeae and C. trachomatis infections
the illness can be erythrocyte or without free
• Cultures from women with PID are likely to be polymicrobial: identified: sedimentation rate pelvic fluid or
Bacteroides species, Gardnerella, Escherichia coli, Haemophilus • Lower abdominal tubo-ovarian
• Elevated C-
influenzae, and Streptococci tenderness or complex
reactive protein
PID SPECTRUM • Adnexal • Laparoscopic
• Laboratory
tenderness or documentation of abnormalities
• Cervical motion cervical infection consistent with
tenderness with N. PID
gonorrhoeae or C.
trachomatis
CRITERIA FOR HOSPITALIZATION
• Surgical emergencies (e.g., Appendicitis) cannot be excluded
• Tubo-ovarian abscess
• Pregnancy
• Severe illness, nausea and vomiting, or high fever
• Unable to follow or tolerate an outpatient oral regimen
RISK FACTORS
• No clinical response to oral antimicrobial therapy
• Gross indicators of frequency of exposure to STI’s and PID:
o Age at first coitus, marital status, number of sexual partners PID TREATMENT (CDC GUIDELINES 2021)
• History of STI’s and PID Parenteral Treatment
• Young age: 15-25 y/o • Recommended Parenteral Regimens
• nonwhite and non-Asian ethnicity Ceftriaxone 1g every 24 hours
• multiple partners Plus
• recent history of douching Doxycycline 100mg orally or IV every 12 hours
• prior history of PID Plus
• Cigarette smoking Metronidazole 500mg orally or IV every 12 hours
OR
Cefotetan 2 g IV every 12 hours PLUS
Doxycycline 100 mg orally or IV every 12 hours
OR
Cefoxitin 2 g IV every 6 hours PLUS
Doxycycline 100 mg orally or IV every 12 hours

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• Alternative Parenteral Regimen
Ampicillin/Sulbactam 3 g IV every 6 hours PLUS
Doxycycline 100 mg orally or IV every 12 hours
OR
Clindamycin 900 mg IV every 8 hours PLUS
Gentamicin loading dose IV or IM (2 mg/kg),
followed by a maintenance dose (1.5 mg/kg) every 8 hours.
Single daily dosing (3–5 mg/kg) can be substituted

• Intramuscular/Oral Treatment • Pelvic CT, laparoscopy

o Recommended Intramuscular/Oral Regimens TREATMENT
Ceftriaxone 500 mg* IM in a single dose PLUS • Medical Management
Doxycycline 100 mg orally twice a day for 14 days o Same as that of the parenteral treatment for PID
WITH o Course can be monitored by symptoms, clinical examination,
Metronidazole 500 mg orally twice a day for 14 days temperature, WBC count, and imaging study
OR o Repeat pelvic examination is performed after the patient has
Cefoxitin 2 g IM in a single dose AND Probenecid, 1 g orally been afebrile for 24-48 hours
administered concurrently in a single dose PLUS o If responsive to medical management, sift to oral antibiotics
Doxycycline 100 mg orally twice a day for 14 days with to complete 10-14 day course with doxycycline plus
Metronidazole 500 mg orally twice a day for 14 days clindamycin or metronidazole.
OR • Surgical Management
Other parenteral third-generation cephalosporin (e.g., o More serious TOA, either unresponsive to antibiotic therapy
ceftizoxime or cefotaxime) or with gross rupture
PLUS Doxycycline 100 mg orally twice a day for 14 days o Ultrasound-guided drainage or laparoscopy
with o Unilateral salpingooophorectomy: curative therapy for
Metronidazole 500 mg orally twice a day for 14 days unilateral TOA
*For persons weighing >150mg, 1g ceftriaxone should be o Total Abdominal hysterectomy and Bilateral
administered salpingooophorectomy: for bilateral TOA
FOLLOW-UP
• Should demonstrate clinical improvement (e.g. defervescence; TOXIC SHOCK SYNDROME
reduction in direct or rebound abdominal tenderness; and • TSS
reduction in uterine, adnexal, and cervical motion tenderness) • Cause by colonization or infection by Staphylococcus aureas that
within 3 days after initiation of therapy. produce an epidermal toxin- toxic shock syndrome toxin-1
• If no clinical improvement has occurred within 72 hours after (TSST-1)
outpatient IM/oral therapy, hospitalization, assessment of the • Incidence correlated with high absorbency tampons and
antimicrobial regimen, and additional diagnostics (including menstruation in approximately 50-70% of cases
consideration of diagnostic laparoscopy for alternative • 2-8% mortality rate
diagnoses) are recommended.
DIAGNOSIS
• All women who have received a diagnosis of chlamydial or
gonococcal PID should be retested 3 months after treatment • High fever (>38.9°C or 102°F)
• If retesting at 3 months is not possible, these women should be • Hypotension
retested whenever they next present for medical care in the 12 • diffuse erythematous macular rash
months following treatment • desquamation of the palms and soles 1 to 2 weeks after the acute
illness, and multisystem involvement of three or more organ
TESTING OF PARTNERS systems.
• Men who have had sexual contact with a woman with PID during the • Gastrointestinal disturbances (abdominal pain, vomiting, and
60 days preceding her onset of symptoms should be evaluated, diarrhea)
tested, and presumptively treated for chlamydia and gonorrhea • Myalgias
PID SEQUELAE • mucous membrane hyperemia
• ectopic pregnancy • increased blood urea nitrogen and creatinine, platelet count less
• Infertility than 100,000, and alteration in consciousness
• Chronic pelvic pain • Blood cultures are often negative, possibly because the exotoxin
• Subsequent PID is absorbed through the vaginal mucosa
TREATMENT
TUBO-OVARIAN ABSCESS (PYOSALPIX) • Hospitalization is always indicated due to high mortality rate
• Sequelae of persistent PID • Hemodynamically unstable: ICY
• Tubo-ovarian complexes (TOC): not walled off like true • Supportive treatment of hypotension with IV fluids and pressors
abscess and thus are more responsive to antimicrobial theral • IV antibiotics: Clindamycin plus vancomycin for empiric treatment
• Progression from PID to TOA: 3-16% • MRSA TSS: clindamycin plus vancomycin or linezolid
• HIV-infected women with PID are at an increased risk for • MSSA TSS: clindamycin plus nafcillin or oxacillin
developing TOA • Treatment duration: 14 days

DIAGNOSIS
• Clinical in the setting of PID with appreciation of an adnexal or
posterior cul-de-sac mass of fullness
• 90% will complain of abdominal and/or pelvic pain
• 60-80% will have fever and leukocytosis
• Cultures swab and blood culture to rule out sepsis
• Culdocentesis: gross pus
• Ultrasound: imaging study of choice
o complex solid/cystic mass.
o elongated, dilated, fluid-filled mass with partial septae and
thick walls. Incomplete septae within the tubes is a sensitive
sign of tubal inflammation or an abscess.
o ‘cogwheel’ sign resulting from thickened endosalpingeal
folds

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LOWER GENITAL TRACT INFECTIONS

NONULCERATIVE VULVAR INFECTIONS
MOLLUSCUM
PEDICULOSIS SCABIES CONDYLOMA ACUMINATUM
CONTAGIOSUM
CAUSE • Phthirus pubis (crab louse) • Sarcoptic scabei • Pox virus • HPV 6, 11
• Most contagious of all • Widespread over hairy • Flesh-colored, dome- • Genital, venereal, or anogenital
STI’s parts of body shaped papules with an warts
• Pubic pruritus • Severe intermittent umbilicated center • Most common viral STD of the
CLINICAL • Confined to hairy areas itching at night • Autoinoculation, contact, vulva, vagina, rectum and cervix
of vulva • “burrow in the skin” fomites
• Eggs, lice & pepper (pathognomonic) • Asymptomatic & mildly
grain feces in hair shafts contagious
• Permethrin • Permethrin • Self-limiting • Chemical, Cautery, Immunologic
• Pyrethrin • Lindane • Excision with treatment of • therapy, surgery
TREATMENT
• Malathion base
• Ivermectin o Monsel solution, TCA
• Direct sexual contact • Close contact • skin to skin contact; • Sexual transmission;
but non-sexual autoinoculation; fomites Autoinoculation
transmission also • Predisposing Factors:
TRANSMISSION documented • Immunosuppression, Diabetes,
• 90% of sexual partners Pregnancy, local trauma
infected after single
• Most contagious of all STD’s
-- • Severe but intermittent • Complications: • Pigmented, indurated, fixed or
itching o Superinfection ulcerated; Cauliflower-like lesions
• Pruritus is more intense that can be asymptomatic or may
SYMPTOMS
at night present with pain, itching, tendency
to bleed when friable, (+) odor
when secondarily infected
• eggs and adult lice, and • Papules, vesicles or burrows • flesh-colored small --
“pepper grain” feces • Burrows: nodules or domed papules
• adjacent to the hair pathognomonic sign of usually 1-5 mm in
shaft scabies infection diameter with umbilicated
• Appears as a twisted line center
GROSS EXAM
on the skin surface, with
a small vesicle at one end
• May involve the hands,
wrists, breasts, vulva,
and buttocks
• Direct microscopy • Microscopy using scratch • Microscopy of the white • Direct inspection; Biopsy When
technique (mites lack waxy material from inside lesions do not respond to standard
lateral claw legs but have the nodule: therapy or when condition
DEFINITIVE
2 triangular hairy buds) intracytoplasmic accelerates during
DIAGNOSIS
molluscum bodies with • Therapy, Immuno-compromised
Wright or Giemsa stain; woman or lesions are pigmented,
Clinical Diagnosis indurated, fixed or ulcerated growths
• Goal: kill both the adult • Goal: Kill both the adult • Individual papules • Patient administered: Podofilox
parasite and eggs parasite and the eggs injection of local anesthetic 0.5% Solution or Gel; Imiquimod
• Permethrin 1% cream • Permethrin cream 5% and evacuation of caseous 5% Cream (contraindicated to
rinse applied to affected applied to all areas of the material pregnant patients)
areas and washed off body from the neck • excision of nodule with a • Provider administered:
after ten minutes down and washed off sharp dermal curette base Cryotherapy; Podophyllin Resin;
• Pyrethrins with after 8-14 hrs of the papule chemically Trichloroacetic Acid (TCA)
piperonyl butoxide • Ivermectin 0.2 mg/kg treated with ferric
TREATMENT
• Alternative: orally, repeated in 2 subsulfate (Monsel
• Malathione 0.5% lotion weeks if necessary solution) or 85% TCA
applied for 8 –12 hrs • Lindane 1% 1 oz of lotion • Cantharidin
and washed off or 30g of cream applied
• Ivermectin 250 ug/kg thinly to all areas of the
repeated in 2 weeks body from the neck down
and thoroughly washed
after 8 hours.

ULCERATED LESIONS
SYPHILIS HERPES CHANCROID LGV
Incubation period • 7-14 days • 2–10 days • 4-7 days • 3 –12 days
Primary lesion • Papule • Vesicle • Papule, pustule • Papule, vesicle
Number of lesions • Single • Multiple • 1-3, occasionally • Single
more
Size (mm) • 5–15 • 1–3 • 2–20 • 2–10
Pain • No • Yes • Yes • No
Diagnostic Test Dark-field microscopy • Viral culture • Gram stain with • Complement fixation
RPR/microhemagglutination assay for “school of fish”
Treponema pallidum (MHA-TP)/FTAABS appearance
Treatment • Penicillin • Acyclovir • Ceftriaxone or • Doxycycline
Azithromycin

SYPHILIS
• Chronic complex systemic disease cause by Treponema pallidum
o T. pallidum – anaerobic, elongated, tightly wound spirochete; can penetrate the skin or mucous membrane
• Patients are contagious during the primary, secondary and probably the 1st year of latent syphilis

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STAGES OF SYPHILIS
Primary • Chancre: solitary, painless ulcer (chancre); heals spontaneously
• Systemic disease
Secondary • Rashes – red macules and papules over the palms of the hands and the soles of the feet
• Vulvar lesions – mucous patches and condyloma latum associated with painless adenopathy
Latent • Follows secondary stage; Positive serology without symptoms or signs of the disease
Tertiary • Potentially destructive effects on the central nervous, cardiovascular, and musculoskeletal systems
• optic atrophy, tabes dorsalis, generalized paresis, aortic aneurysm, gummas (similar to a cold abscess with a necrotic center and the
Late
obliteration of small vessels by endarteritis) of the skin and bones
Transmission • Sexual contact; oral-genital contact
Screening • VDRL (Venereal Disease Research Laboratories) or RPR (Rapid Plasma Reagin)
Definitive • Treponema Immobilization Test; FTA-ABS; MHA-TP
Diagnosis • Darkfield - thin, silvery spiral motile organism
• Primary and Secondary Phase: Benzathine Penicillin G, 2.4 million units IM
• Early Latent Phase: Benzathine Penicillin G, 2.4 million units IM SD
• Late Latent Phase: Benzathine penicillin G 2.4 million units IM at one week intervals x 3 doses
• Tertiary Syphilis with normal CSF exam: Benzathine Penicillin G 7.2 million units total administered as 3 doses of
Treatment 2.4 million units IM at 1-week intervals
• Neurosyphilis: Aqueous crystalline penicillin G, 18-24 million units administered 3-4 million units IV every 4 hours
or continuous infusion for 10-14 days
• Alternative Regimen for Neurosyphilis
o Procaine penicillin G 2.4 million units IM once daily plus Probenecid 500mg orally 4 times a day, both for 10 to 14 days
HERPES
• Asymptomatic shedding
Transmission
• Recurrent, incurable, highly contagious
• Primary infections usually begin with flu-like symptoms, including malaise, myalgias, nausea, diarrhea, and fever.
S/Sx of
• Vulvar burning and pruritus precede the multiple vesicles that appear next and usually remain intact for 24 to 36 hours before
Primary
evolving into painful genital ulcers
Infection
• Ulcers require 10 to 22 days to heal
• Related to the onset of menstrual period or emotional stress
• May be asymptomatic; most are half as severe as primary infection
Recurrence
• Prodrome: sacroneuralgia, vulvar burning, tenderness and pruritus for a few hours to 5 days before vesicle formation
• HSV – resides in a latent phase in the dorsal root ganglia of S2, S3 and S4
• Clinical inspection; Viral culture positive in primary episodes
• PCR: most accurate and sensitive
Definitive
• Western blot assay for antibodies to HSV: most specific method for diagnosing recurrent, unrecognized or subclinical
Diagnosis
herpes
• HSV culture; ELISA and Immunoblot test

TREATMENT FOR HERPES INFECTION

INDICATION VALACYCLOVIR ACYCLOVIR FAMCICLOVIR
First clinical 1000 mg BID for 7-10 days 200 mg 5x a day or 400 mg TID 250 mg TID for 7-10 days
episode for 7-10 days

Recurrent 1000 mg daily for 5 days or 500 mg BID 400 mg TID for 5 days or 800 mg BID 125 mg BID for 5 days 500 mg once
episodes for 3 days for 5 days or 800 mg TID for 2 days then 250 mg BID for 2 days; 100 mg
BID for 1 day
Daily 1000 mg daily (>10 recurrences per year) 400 mg BID or 1000 mg/day 250 mg BID
suppressive or 500 mg daily (<9 recurrences/ year)
therapy

CHANCROID LYMPHOGRANULOMA VENEREUM (LGV)

• Sexually transmitted, acute, ulcerative disease • Chronic infection of lymphatic tissue, mostly
Transmission Transmission
of the vulva affecting the vulva
• Painful and tender ulcer Etiologic
• Chlamydia trachomatis
• Tender suppurative inguinal adenopathy Agent
S/Sx (buboes) • Culture, direct immunofluorescence or
• Genital ulcers of chancroid facilitate the nucleic acid detection of C. trachomatis of pus
transmission of HIV infection Diagnosis or aspirate from an infected node
Etiologic • Haemophilus ducreyi – highly contagious • Complement fixation antibody titer >1:64 is
Agent small gram-negative rod indicative of infection
Diagnosis • ”school of fish” in microscopy • Doxycycline 100 mg twice daily for at least 21
• Azithromycin 1 gm orally days
• Ceftriaxone 250 mg IM in a single dose Treatment • Alternative: Azithromycin 1g orally once a
Treatment week for 3 weeks
• Ciprofloxacin 500 mg twice daily x 3 days
• Erythromycin base 500 mg TID x 7 days • Erythromycin base 500 mg QID for 21 days
Three Phases
• Shallow painless ulcer of the vestibule or labia,
Primary
which resolves
Infection
• Spontaneously
• Bubo: Painful adenopathy in inguinal and
Secondary
perirectal areas
Infection
• Groove sign: enlarged lymph node, tender and matted
• Formation of multiple draining sinuses and fistula
• Extensive destruction of the external genitalia and
Tertiary
anorectal region leading to secondary extensive scarring
Infection
which can lead to elephantiasis, multiple fistulas,
stricture formation of the anal canal and rectum

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VAGINAL INFECTIONS
FINDINGS ON
CONDITION SYMPTOMS AND SIGNS pH WET MOUNT COMMENT
EXAMINATION
Clue cells (>20%)
Increased discharge Thin, whitish gray, Greatly decreased lactobacilli
Bacterial shift in flora
(white, thin) homogeneous discharge, >4.5 Greatly increased cocci
vaginosis Amine odor after adding
Increased odor cocci, sometimes frothy Small, curved rods
KOH to wet mount
Increased discharge
Can be mixed infection with
(white, thick)
Thick, curdy discharge bacterial vaginosis, T.
Candidiasis Dysuria <4.5 Hyphae or spores
Vaginal erythema vaginalis, or both, and have
Pruritus
higher pH
Burning
Increased discharge
Yellow, frothy discharge,
(yellow, frothy) Motile trichomonads More symptoms at higher
Trichomoniasis with or without vaginal or >4.5
Increased odor Increased white cells vaginal pH
cervical erythema
Dysuria, Pruritus
Lobo, et al. Comprehensive Gynecology. 7th ed. 2017

When faced with questions regarding vaginal discharge, read them very carefully to assess whether you are being asked of a physiologic or pathologic discharge.
Any discharge with color or abnormal scent is usually pathologic. Gram stain is the gold standard in diagnosing bacterial vaginosis but in low resource setting,
Nugent’s criteria may be utilized. Sexual history can also give you a clue that you are being asked of mucopurulent cervicitis or Trichomoniasis.
Dr. Banzuela-Cruz

• Normal Physiologic vaginal discharge • Alternative regiment

o Contains cervical and vaginal epithelial cells, normal o Clindamycin 300 mg BID daily for 7 days
bacterial flora, water, electrolytes, other chemicals o Clindamycin ovules 100 g intravaginally at HS for 3 days
o pH 4.0
o Lactobacilli, S. epidermidis, E.coli, Diphtheroids, Streptococci
TRICHOMONIASIS
• Three common infections of the vagina are produced by: Etiologic Trichomonas vaginalis – unicellular
o Fungus (candidiasis) agent intracellular, anaerobic, flagellated protozoon
o Protozoon (trichomonas) Transmission Sexually transmitted; inhabits the vagina and
o Synergistic bacterial infection (bacterial vaginosis) lower urinary tract, Skene’s ducts in the female
• Symptoms associated with vaginal infection: S/Sx Profuse “frothy "discharge with
o Vaginal discharge o Odor unpleasant odor; Erythema and edema of
o Superficial dyspareunia o Vulvar burning the vulva and vagina; “strawberry” cervix
o Dysuria and upper vagina; Vulvar pruritus; Dysuria
Diagnosis NSS smear / wet smear – visualization of the
BACTERIAL VAGINOSIS trichomonas organism
• Reflects a shift in vaginal flora from lactobacilli-dominant to Treatment • Metronidazole, 500mg 2x a day for 7 days
mixed flora (genital microplasmas, G. vaginalis, and anaerobes, • Metronidazole 2g single dose
such as peptostreptococci, and Prevotella, and Mobiluncus sp.) (Recommended regimen for Men)
• No causative agent has been identified • Alternative Regimen
• “Sexually associated” o Tinidazole 2 gm orally in a single dose
• Absence of inflammation in biopsies hence the term vaginosis CANDIDIASIS
rather than vaginitis Etiologic Produced by a ubiquitous, airborne, gram-
RISK FACTORS agent positive fungus (Candida albicans, C. glabrata, C
.tropicalis) commensal saprophytic organisms
• New or multiple sexual partners
on the mucosal surface of the vagina, which
• Women who have sex with women become opportunistic when the vaginal
• Douching at least monthly or within the prior 7 days ecosystem is disturbed.
• Social stressors Classification • Uncomplicated: Sporadic, infrequent, Mild-
DIAGNOSIS: to-moderate, Likely C albicans
• Gold standard for Diagnosis: Gram Stain • Complicated or Recurrent: Severe, Non-
o Gram Stain – presence of “clue cells” and decreased number albicans, DM, Pregnancy,
of lactobacilli (Nugent’s Criteria) Immunosuppression
Gardnerella and Signs • Pruritus, vulvar burning, external dysuria,
Lactobacillus Curved Gram Symptoms dyspareunia
SCORE Bacteroides
morphotypes variable rods
morphotypes • Shallow erosions on the labia and perineum;
0 4+ 0 0 Plaques of white cheesy discharge
1 3+ 1+ 1+ or 2+ Diagnosis • KOH (10-20%) smear: filamentous forms,
2 2+ 2+ 3+ or 4_ mycelia, hyphae, pseudohyphae
3 1+ 3+ - • Culture with Nickerson or Saboraud
4 0 4+ - medium – useful when KOH smear is
negative or when a woman has recently
treated herself with an antifungal
Treatment • Intravaginal regimens: Butoconazole,
clotrimazole, miconazole, nystatin,
tioconazole, terconazole
• Amsel’s Clinical Criteria (3 out of 4 is diagnostic) • Oral regimen Fluconazole 150 mg, single dose
o Homogenous vaginal discharge • Treatment of recurrent candidiasis
o pH ≥ 4.5 o Initial Therapy
o Amine-like odor when mixed with KOH (whiff test) § Four or more episodes of symptomatic
o Wet smear demonstrates clue cells greater in number than VVC within 1 year
20% of the of vaginal epithelial cells § 7–14 days of topical therapy or a 100-
TREATMENT mg, 150-mg, or 200-mg oral dose of
fluconazole every third day for a total of
• Recommended regimen 3 doses [day 1, 4, and 7]
o Metronidazole 500 mg twice daily for 7 days o Suppressive Maintenance Therapy
o Metronidazole gel 0.75%, 5 g intravaginally once daily for 5 d § Oral fluconazole (100-mg, 150-mg, or
o Clindamycin cream 5%, 5 g intravaginally qhs for 7 days 200-mg dose) weekly for 6 months
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From Blueprints:
CERVICITIS • Ceftriaxone 250 mg IM or Cefixime 400 mg
• Inflammatory process associated with trauma, inflammatory PO PLUS Chlamydia therapy if not ruled out
systemic disease, neoplasia, and infection • Alternative regimens
• Ectocervicitis viral (HSV) o Spectinomycin 2 grams IM in a single
o severe vaginitis (e.g., “strawberry cervix”) dose or Ceftizoxime 500 mg IM; or
o associated with T. vaginalis infection) or C. albicans Cefoxitin 2g IM, administered with
• Endocervicitis C. trachomatis or N. gonorrhoeae probenecid 1g orally; or
o Bacterial vaginosis and M. genitalium o Cefotaxime 500 mg IM; Azithromycin 2
grams
MUCOPURULENT CERVICITIS Treatment o PLUS Chlamydia therapy if not ruled out
• Gross visualization of yellow mucopurulent
material on a white cotton swab CDC 2021:
Criteria • Presence of 10 or more PMN leukocytes per • Ceftriaxone 500 mg IM single dose for
hpf on gram-stained smears obtained from persons weighing <150kg (1 gram is weight >
the endocervix 150kg)
• Erythema and edema in an area of cervical • Alternative regimens
ectopy or associated with bleeding secondary o Gentamicin 240mg IM in a single dose plus
Alternative to endocervical ulceration Azithromycin 2g orally in a single dose OR
Criteria • Friability when the endocervical smear is obtained o Cefixime 800mg orally in a single dose
• Increased vaginal discharge and • PLUS Chlamydia therapy if not ruled out
intermenstrual vaginal bleeding Blueprints uses the 2015 CDC recommendation of Ceftriaxone 250mg IM
Pathogens • Chlamydia trachomatis and Neisseria gonorrhea as treatment for mucopurulent cervicitis, but the newer CDC guidelines is
recommending a dose of 500 mg. It depends on what source will they be
• Hypertrophic and edematous cervix
using in the board exam.
Signs • Vaginal discharge Dr. Banzuela-Cruz
Symptoms • Deep dyspareunia
• Postcoital bleeding. CHLAMYDIA TRACHOMATIS
Description • Obligatory intracellular organism
MUCOPURULENT CERVICITIS: NEISSERIA GONORRHEA • Gold Standard: Nucleic Acid Amplification
• Gram-negative diplococci found in the Test (NAAT)
epithelium of the genitourinary tract, rectum, Diagnosis • Culture
Description pharynx or the eye • Microscopy: Direct immunofluorescence test –
• Localized acute infection resulting to Elementary bodies
bacteremia/disseminated infection Blueprints:
• Azithromycin 1 gm single dose
• Gold Standard: Nucleic Acid Amplification
• Doxycycline 100 mg bid x 7days
Test (NAAT)
• Alternative regimen:
• Culture; Gram stain
• Erythromycin base 500 mg qid for 7 days
• Enzyme immunoassay • Erythromycin ethylsuccinate 800 mg qid for 7
Diagnosis • Nucleic Acid Hybridization Test days
• Microscopy: Gram - stained smear of the Treatment • Ofloxacin 300 mg twice daily for 7 days
endocervical swab: • Levofloxacin 500 mg for 7 days
• gram negative intracellular diplococci
CDC 2021:
• Doxycycline 100 mg bid x 7days
• Alternative Regimen:
o Azithromycin 1 gm single dose OR
• Levofloxacin 500 mg for 7 days

BENIGN GYNECOLOGIC LESIONS

VULVA AND VAGINA
CONGENITAL ANOMALIES
• May be associated with concomitant anomalies in the upper reproductive tract and genital urinary tract
• Include:
1. Clitoral Anomalies 4. Transverse Vaginal Septum
2. Labial Fusion 5. Vaginal Atresia
3. Imperforate hymen 6. Vaginal Agenesis

ABNORMALITY CAUSE PRESENTATION DIAGNOSIS TREATMENT

• excess androgens
• Exogenous androgen • Elevated 17α-
exposure (more • Ambiguous genitalia hydroxyprogesterone
Labial Fusion common) • Hyperandrogenism or 17-ketosteroid • Cortisol + surgery
• Enzymatic error: 21- • 75% adrenal crisis with salt wasting with decreased
hydroxylase deficiency serum cortisol
(may lead to CAH)
• Failure of the central • Hydrocolpos / mucocolpos
portion of hymenal • Hematocolpos / hematometra
Imperforate • Usually diagnosed at
membrane to • Primary amenorrhea with cyclic pelvic pain • Surgery
Hymen puberty
degenerate into • Tense, bulging hymen
hymenal ring • álower abdominal girth

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ABNORMALITY CAUSE PRESENTATION DIAGNOSIS TREATMENT
• Hematocolpos/hematometra • Usually diagnosed at
Transverse • Septa usually lie near the junction between puberty
• Failure of the Mullerian
Vaginal the lower 2/3 and upper 1/3 of the vagina • Ultrasound and MRI • Surgery
tubercle to canalize
Septum • Short vagina appearing to end in a blind pouch to locate/characterize
• S/sx similar to imperforate hymen the septum
• Pelvic ultrasound
• Failure of the urogenital
• Absence of introitus and MRI: large • Vaginal Pull-
Vaginal sinus to contribute the
• Presence of vaginal dimple hematocolpos and Through
Atresia lower portion of the
• Primary amenorrhea with cyclic pelvic pain presence of upper Procedure
vagina
reproductive tract
• Serial vaginal
• Absence of vagina and • Phenotypically and genotypically female
Vaginal dilators
absence or hypoplasia • Primary amenorrhea • Pelvic ultrasound
Agenesis • McIndoe procedure
of all parts of the cervix, • Associated urologic and skeletal and MRI
(MRKH) (neovagina
uterus and fallopian tubes abnormalities
creation)

CLITORAL ANOMALIES VULVAR AND VAGINAL DERMATOSES

• Causes: • Broad spectrum of atrophic and hypertrophic conditions
o Androgen stimulation characterized by skin changes due to variety of etiologic agents
o Exogenous androgen exposure (more common) • Require histologic examination
• Presentation: • Includes:
o Enlarged clitoris (Normal size: 1-1.5 cms long, 0.5 cm wide) 1. Lichen Simplex chronicus
o Occurs in infants with congenital adrenal hyperplasia 2. Lichen Planus
DISORDER CAUSE SIGNS AND SYMPTOMS TREATMENT
• High-potency topical steroid
• White, thinned skin on labia, perineum, and
ointment (clobetasol or
unknown, but it perianal region; resorption of the labia minora
halobetasol 0.05%); 1−2×/d
may be into the labia majora, clitoral phimosis, narrowed
for 6–12 wk, then a
Lichen autoimmune introitus
maintenance dosing vs.
Sclerosus related with • Not found in the vagina
episodic flare treatment with
(LS) secondary genetic • Can scar
topical steroid
and hormonal • Often asymptomatic, may be pruritic
• Refractory : SQ triamcinolone
influences • Dysuria, dyspareunia
• Pelvic floor PT for vaginal
• Chronic waxing and waning
dilator therapy.
• Bright red erosions with white borders • High-potency topical steroids
(Wickham’s striae) of the inner labia minora and (same with LS)
Atrophic
Lichen vestibule • If prominent erosions, short
inflammatory
planus • Pruritus with mild inflammation to severe course of PO prednisone 40 to
condition
erosions 60 mg PO
• Can have itching, burning, irritation, dyspareunia
Reactive changes to
Lichen
chronic scratching
Simplex Valvular pruritus Medium- to high potency
and rubbing rather
chronicus • Thickened white epithelium, slight scaling Topical steroids 2–3×/d for 6
than
(LSC) • Usually unilateral and circumscribed or more weeks
hyperkeratotic
(eczema)
changes

May be a feature Red moist lesions; often nonspecific with poor

Vulvar
of psoriasis margins and slight scaling • Medium potency steroids
psoriasis
Etiology unknown Asymptomatic; pruritus

BENIGN CYSTS AND TUMORS • Differential diagnosis:

• Occlusion of pilosebaceous ducts, sebaceous ducts and apocrine (Large epidermal cysts)
sweat glands o fibromas, lipomas,
hidradenomas
• Treatment is only needed if lesions become symptomatic or infected
• Treatment: none
• Includes:
o If infected - local
o Epidermal Inclusion Cyst
heat application,
o Sebaceous Cyst •
o Apocrine seat gland cyst incision and drainage • EPIDERMAL INCLUSION CYSTS
o Skene’s duct cyst o Recurrently infected • Small, usually solitary lesions, lined
cysts or with pain - with squamous epithelium and
o Bartholin’s duct cyst and abscess
excised when acute contain tissue that would normally be
o Gartner’s duct cyst exfoliated.
inflammation has
EPIDERMAL INCLUSION CYSTS subsided
•

• Histology SEBACEOUS CYST

o Epithelial lining keratinized, stratified squamous • Most common tumor found on the vulva (together with EIC)
epithelium with a center of cellular debris that grossly • Cause: Occlusion of sebaceous duct
resembles sebaceous material. • S/sx:
o Most epidermal cysts do not have sebaceous cells or o Often multiple and asymptomatic
sebaceous material o Sebum accumulates within the cyst
• Features: multiple cysts, majority less than 1 cm in diameter. o May become superinfected with local flora
• Presentation: Asymptomatic unless secondarily infected. • Treatment: Incision and drainage

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APOCRINE SWEAT GLAND CYST GARTNER’S DUCT CYST
• Fox- Fordyce Disease: Microcystic disease • Dysontogenic cyst
• Hidradenitis suppurativa: Multiple infected abscesses • Cause:
• Cause: o Remnants of mesonephric ducts of the wolffian system
o Occlusion of apocrine gland ducts in the mons pubis and o Submucosal along anterior or lateral wall of the upper
labia majora vagina
• S/sx: • S/SX:
o Pruritic and foil smelling o Asymptomatic
• Treatment: o May present during adolescence with dyspareunia or
o Wide local excision difficulty in inserting tampons
o Incision and drainage • Treatment:
o Overlying cellulitis: antibiotics o Excision
PARAURETHRAL GLAND CYST o IVP and cystoscopy performed preoperatively
o Vasopressin perioperatively
• Skene’s Duct cyst
• Cause: Chronic inflammation of the gland causing obstruction URETHRAL CARUNCLE
of the duct • Features
• S/sx: May be superinfected o Outgrowth of distal edge of urethra
• Treatment: Incision and drainage o Due to chronic irritation or infection
BARTHOLIN’S DUCT CYST AND ABSCESS o Mostly seen in postmenopausal women
• Bartholin’s Gland • Clinical Presentation
o Located entrance of o Majority are asymptomatic
the vagina at 5 to 7 o often secondarily infected, producing ulceration and
o’clock position bleeding.
o Duct approximately o point tenderness after contact with undergarments or
2 cm long, and open during intercourse.
in a groove between o Ulcerative lesions usually produce spotting on contact more
the hymen and labia commonly than hematuria
minora in the • Diagnosis: biopsy
posterior lateral wall o Histologic appearance: caruncle is composed of transitional
of the vagina and stratified squamous epithelium with a loose connective
• Most common large cyst of the vulva tissue. Often the submucosal layer contains relatively large
dilated veins
BARTHOLIN’S • Classified according to histologic appearance:
CYST ABSCESS
DUCT o Papillomatous, granulomatous, & angiomatous
• Found in the labia majora and duct • Initial therapy:
Location orifices are at the base of the labia o Avoidance of irritation
minora just distal to the hymen o Estrogen (oral or topical)
Size • 1 – 8 cm o Cryosurgery, fulguration, excision
Laterality • Often unilateral but may be bilateral
URETHRAL DIVERTICULUM
• Obstruction (cyst)
Pathophysiology • Cause: Permanent epithelialized sac-like projection
• Polymicrobial infection or STI (abscess)
• Develops rapidly (2-4 • Signs and Symptoms:
days) o 3 D’s of Diverticulum: Dysuria, Dyspareunia, Dribbling of
Signs • Tense Urine
• Erythema, tenderness,
edema • Diagnostics
o Voiding cystourethrography
• Acute vulva pain
o Cystourethroscopy
Symptoms • Nonpainful • Dyspareunia
• Treatment: Treat if persistence of symptoms or recurrent
• Pain during walking
infection via excision
• No treatment: 1 - 2cms and not causing
any symptoms NEVUS
o Sitz bath • commonly referred to as a mole, is a localized nest or cluster of
§ For pain relief melanocytes
§ Decrease healing time • Differentials: hemangiomas, endometriosis, malignant melanoma,
o Word catheter placement vulvar intraepithelial neoplasia, and seborrheic keratosis.
§ Office setting
§ Balloon tip placed inside cyst BENIGN DYSPLASTIC
and inflated and left in place for • Flat, elevated, or
General • Commonly 6 to 20 mm
4-6 wks. pedunculated
Treatment
o Marsupialization: the entire cyst or Border • Sharp • Diffuse margination
abscess is incised and sutured to the
• Speckling of color;
vaginal mucosa
Color • Even additional red, white, or
o Excision biopsy
blue hues
§ Women older than 40yo to rule
out adenocarcinoma Shape • Symmetrical • Asymmetry
§ For recurrent Bartholin's duct • Diagnosis: Clinical
cyst or abscess • Treatment: Proper excisional biopsy should be three-dimensional
o Antibiotics: N. gonorrhea and adequate in width and depth. Approximately 5 to 10 mm of
(10%); S. aureus normal skin surrounding the nevus should be included, and the
biopsy should include the underlying dermis as well
• Malignant melanoma
MANAGEMENT OF o Clinical features of an early malignant melanoma may be
BARTHOLIN ABSCESS remembered by thinking ABCD: asymmetry, border
https://qrs.ly/8jegxc3 irregularity, color variegation, and a diameter usually >6
mm.

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HEMANGIOMA • Signs/symptom
• Rare malformations of blood vessels rather than true o Post-coital bleeding
neoplasms. • Differentials
• They are usually single, 1 tov2 cm in diameter, flat, and soft, and o Endometrial polyp, prolapsed myoma, retained products of
they range in color from brown to red or purple. conception, squamous papilloma, sarcoma, Cervical cancer
• Histologically, the multiple channels of hemangiomas are • Management
predominantly thin-walled capillaries arranged randomly and o Polypectomy
separated by thin connective tissue septa NABOTHIAN CYSTS
• Most hemangiomas are asymptomatic; occasionally they may • Retentions mucus cysts of endocervical columnar cells usually
become ulcerated and bleed. at the transformation zone
• Management: • Gross appearance:
o Resection or excisional biopsy o translucent or opaque whitish or yellow
o Cryosurgery or argon laser o Vary from microscopic to macroscopic size
FIBROMA • Asymptomatic
• No treatment necessary
• Most common benign solid tumor of the vulva
• Gross: smooth surface and a distinct contour.
• On cut surface: Tissue is gray-white. Fat or muscle cells CERVICAL STENOSIS
microscopically may be associated with the interlacing • Often occurs in the internal os
fibroblasts. • Maybe congenital or acquired
• Have a low-grade potential for becoming malignant. • Symptoms differ depending on the menopausal status of the
• Symptoms: woman
o Asymptomatic: Smaller fibromas • Diagnosis:
o Pressure symptoms o Inability to introduce a cervical dilator into the uterine
o Acute pain during degeneration cavity
• Indications for operative removal • Management:
o Symptomatic o Cervical dilatation under ultrasound guidance
o grows larger o Laminaria tent or T-tube as stent for a few days
o Cosmetic reasons
LIPOMA CERVICAL MYOMA
• Second most frequent type of • Smooth, firm, solitary masses mostly arising from the isthmus
benign vulvar mesenchymal • Most are small and asymptomatic
tumor • Expanding myomas produce symptoms secondary to
• slow-growing, circumscribed mechanical pressure on adjacent organs
tumors of fat cells arising • Diagnosis: Inspection and Palpation
from the subcutaneous tissue • Management:
of the vulva o Asymptomatic and small – maybe observed
• Unless extremely large, • o Occurrence and persistence of symptoms are indications for
lipomas do not produce • Skin-colored pedunculated lipoma treatment
symptoms. of labium major. Histologically,
• Diagnostics: CT scan and MRI lipomas are usually more
• Treatment for large tumors: homogeneous than fibromas.
• Figure 15.7. Lobo, et al. Comprehensive Gynecology. 7th
Excision ed. 2017

CERVIX
CERVICAL POLYP
• Pathology
o Most common benign neoplastic growth of cervix
o Most common in multiparous
o Secondary to inflammation or abnormal focal
responsiveness to hormones
o Ulceration of the stalk’s most dependent portion causes
bleeding.
o Endocervical polyps: cherry red
o Cervical polyps: grayish white
o Adenomatous type (80%)
UTERUS
BENIGN LESIONS OF THE UTERUS
ENDOMETRIAL POLYP LEIOMYOMA ADENOMYOSIS
• Localized overgrowths of the
• Benign tumors
endometrial glands and stroma • Derived from aberrant glands of the BASALIS layer of the
Description of muscle cell
projecting beyond the endometrial endometrium
origin
surface
• Classic symptoms: dysmenorrhea and menorrhagia
Signs and
• Asymptomatic • FIBROIDS • Classic pelvic exam: Diffusely enlarged uterus (2-3 x
Symptoms
larger)
• Myomectomy, • NO satisfactory medical management
Management • Hysteroscopic removal
Hysterectomy • Hysterectomy

ENDOMETRIAL POLYP • Abnormal Uterine Bleeding

Clinical
• Localized benign overgrowths of endometrial o Metrorrhagia, menorrhagia or
Manifestations
glands and stroma over a vascular core menometrorrhagia, post-coital bleeding
Pathology • Vary in size from millimeters to several • Presence- Pelvic Ultrasound
Diagnostic
centimeters and may be pedunculated or • Size- Sonohysterogram
Evaluation
sessile and single or multiple • Number of polyps- Hysteroscopy
Treatment • Removal of Polyp

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LEIOMYOMA MEDICAL THERAPIES

• Benign monoclonal tumors, with each tumor Medical Therapies for Uterine Leiomyomas
resulting from propagation of a single muscle (Mnemonic: GO PAN AM)
cell • GnRH agonists (Nafarelin Acetate, Leuprolide Acetate
Pathogenesis G
• The normal myocytes are transformed to Depot, And Goserelin Acetate)
abnormal myocytes, which are then stimulated • Progestins (Medroxyprogesterone Acetate, Mirena IUD,
O
to grow into tumors Norethindrone Acetate)
• submucosal (beneath the endometrium), P • Oral contraceptive pills
Location • intramural (in the muscular wall of the uterus) A • Antifibrinolytics (tranexamic acid)
• subserosal (beneath the uterine serosa) N • Nonsteroidal anti-inflammatory drugs
• Medical: GnRH agonists, progestins, oral A • Androgenic steroids (Danazol and Gestrinone)
contraceptive pills, antifibrinolytics, NSAIDs, M • Mifepristone (Mifeprex, Korlyn, RU-486
Treatment androgenic steroids, mifepristone
• Myomectomy SURGICAL PROCEDURES
• Hysterectomy
• Conservative
SYMPTOMS
o Myomectomy
CLINICAL SYMPTOMS OF UTERINE LEIOMYOMAS § For preservation of Fertility
Mnemonic: FIBROIDS § Hysteroscopic myomectomy: first-line for the
F • Frequency and retention of urine, hydronephrosis management of symptomatic INTRACAVITARY myomas
I • Iron-deficiency anemia § Abdominal myomectomy- for myomas exceeding 5-8 cm,
• Bleeding abnormalities (menorrhagia, metrorrhagia, multiple myomas or when deep intramural myomas are
B
menometrorrhagia, postcoital spotting), bloating present
• Reproductive difficulties (dysfunctional labor, premature § Laparoscopic myolysis: alternative to myomectomy or
R labor/delivery, fetal malpresentation, increased need for CS hysterectomy for selected women who wish to preserve
delivery
their uterus but do not desire future fertility
O • Obstipation, rectal pressure § Selective Uterine artery occlusion
I • Infertility (failed implantation, spontaneous abortion) o Definitive Surgery
D • Dysmenorrhea, dyspareunia § Hysterectomy
S • Symptomless (most common) • Indications for surgical intervention
DIAGNOSIS o Abnormal uterine bleeding, causing
• Uterine size, as assessed by bimanual anemia
Pelvic examination, correlates well with uterine o Severe pelvic pain or secondary
Examination size and weight at pathologic examination, amenorrhea
even in most obese women o Uncertainty if mass is a fibroid or
• Typically used to confirm the diagnosis of myomas another type of tumor
• A complementary transabdominal o Urinary frequency, retention, or
ultrasound evaluation may be of value in hydronephrosis
selected cases such as large volume uteri o Growth after menopause
• Sonohysterography or saline infusion o Recurrent miscarriage or infertility
Transvaginal
sonography (SIS)
Ultrasound o Rapid increase in size
• Color doppler SHG may be useful in
distinguishing polyp from submucosal myomas Remember, myomas feed on estrogen. So medical management mainly
based on the vascularity of the lesions: involves medications which inhibit production of estrogen including
• Polyps: a single feeding vessel synthetic progesterone. Again, pag mataas ang progesterone, it inhibits
• Myoma: several vessels secretion of GnRH, and FSH therefore decreasing the production of
Hystero- • remains mandatory in the evaluation of estrogen.
Dr. Banzuela-Cruz
salpingography infertility
• Diagnostic hysteroscopy and SIS are
Hysteroscopy equivalent diagnostic tools for the detection ADENOMYOSIS
of intrauterine myomas and polyps • ADENOMYOSIS • ADENOMYOMA
• TVS is as efficient as MRI in detecting myoma • The presence of endometrial • A well-circumscribed collection
presence. However, MRI is more accurate tissue in the uterine of endometrial tissue within
for exact myoma mapping and should be myometrium leading to the uterine wall.
preferred when such mapping is important abnormal bleeding and pain. • They may also contain smooth
MRI • Recommended for preop evaluation when • The uterus becomes soft and muscle cells and are not
advanced surgery of myomas is planned especially globular. Treatment: Progestin- encapsulated.
for patients who want to preserve fertility containing • Adenomyomas can also
• MRI is superior to TVS for the diagnosis of • Management: IUD prolapse into the endometrial
adenomyosis • Definitive treatment: cavity similar to a classic
Hysterectomy endometrial polyp.
DEGENERATION OF LEIOMYOMA
TYPE OF DEGENERATION FALLOPIAN TUBES
• 65%
• Mildest form of degeneration characterized by PARATUBAL CYSTS
Hyaline
loss of smooth muscle cells that are replaced by • Vary in size from 0.5 cm to 20 cm in diameter
fibrous connective tissue • Hydatid cysts of Morgagni – pedunculated and near the fimbrial
• Occurs in 5-10% of pregnant women end of the oviduct
Carneous
• Can cause severe pain and peritoneal irritation • Majority are accessory lumina of the fallopian tubes
or red
• Characterized by extensive coagulative necrosis • Often difficult to differentiate from an ovarian mass
• Due to the deposition of calcium phosphates and • May grow rapidly during pregnancy
Calcific carbonates brought about by the continued diminished • Treatment: Simple excision
blood supply and ischemic necrosis of tissue
Cystic or • Characterized by accumulation of edema fluid and
hydropic often associated with collagen deposition
• Result from adipose metaplasia in myomas. It
Fatty contains an admixture of smooth muscle and
mature adipose tissue
• May be a misnomer. It is unknown whether
Malignant myomas degenerate into leiomyosarcomas or
whether they arise spontaneously

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OVARY BENIGN CYSTS/TUMORS

PELVIC EXAM FINDINGS • Functional
FEATURE BENIGN MALIGNANT o Follicular cysts
Mobility • Mobile • Fixed o Corpus luteum cysts
Consistency • Cystic • Solid o Theca-lutein cysts
Tumor surface • Smooth • Irregular • Benign Cysts/Tumors
Laterality • Unilateral • Bilateral o Dermoid cyst (mature teratoma)
• Pre pubertal mass o Endometriomas
• Reproductive • Post-menopausal women o Fibroma
Age group
age • Any mass in reproductive o Brenner tumor (transitional cell tumors)
age women taking OCP o Adenofibroma & cystadenofibroma
RISK FACTORS • General Facts
INCREASED RISK DECREASED RISK o 75% of ovarian mass in women in reproductive age are
• Family history; BRCA-1 gene functional cysts
• Decreased ovulatory age o Functional cysts – most common cause of simple cystic
• Obesity
o Breast feeding
• Endometriosis, PID, high meat & fat
o OCP, aspirin,
adnexal mass in the reproductive age
diet (epithelial type)
NSAIDs o Benign cystic teratoma – most common cause of complex
• Smoking – mucinous epithelial type o Increasing parity adnexal mass
• Increased ovulatory age • Tubal ligation o Pregnancy – most common cause of pelvic mass
o Infertility hysterectomy with
o Nulliparity ovarian conservation
o Late menopause
• Carotenoids, tea
o Late childbearing
FOLLICULAR CYST CORPUS LUTEUM CYST THECA LUTEIN CYST
• Failure of the corpus luteum to regress
• prolonged or excessive stimulation by
• Persistence of dominant follicle during the luteal phase
endo/exogenous gonadotropins (hCG)
Patho • Failure of a follicle to rupture during the • Halban’s triad: spotting with delay in
• Increased sensitivity to gonadotropins
follicular maturation phase menses; unilateral pelvic pain; small,
• Massive ovaries (10 cm)
tender, adnexal mass
• Hypereactio luteinalis (multiple luteinized
• Translucent and thin walled • Smooth, red to brown
follicular cysts)
Gross • Filled with clear, watery to straw colored • gray white if chronic
• Honeycomb appearance
fluid • Potential for bleeding
• (+) straw colored fluid
• Usually less than 8 cm • Larger
• Multicystic (Partially solid/partially cystic)
UTS • Unilateral, Simple and unilocular in • Simple, unilateral and unilocular in
• bilateral
structure structure

MANAGEMENT STROMAL TUMOR

• Diagnosis: • Most common benign solid tumor of the ovary
o Pregnancy test • Extremely slow growing and unilateral
o Vaginal ultrasound • Whorled pattern on cross section
• Observation Fibroma • Meig’s Syndrome:
o Repeat ultrasound after 6-8 weeks for Follicular and Corpus 1. Ovarian Fibroma
Luteum Cysts 2. Ascites
o Theca Lutein will regress after pregnancy 3. Hydrothorax
• Laparoscopy ADNEXAL MASS:
o Adnexal Mass after menopause or before puberty LABORATORY TESTS & SERUM BIOMARKERS
o Solid adnexal mass (regardless of age)
• Pregnancy Test
o Cystic mass >8cm Laboratory tests
• Serial quantitative B-HCG to evaluate
o Cystic mass of 5-8 cm persisting more than 8 weeks in a to be requested
suspected ectopic pregnancy
menstruating woman should be based
• CBC: elevated WBC may indicate PID or
• Explore laparotomy for adnexal torsion on associated
TOA, or pelvic abscess from colonic or
symptoms
appendiceal pathology
BENIGN OVARIAN TUMORS • Does not need to be measured on all
EPITHELIAL TUMOR premenopausal women with simple
Serum cancer
• Most frequent ovarian epithelial tumors ovarian cyst on ultrasound
Serous antigen (CA)-125
Cystadenoma • Not recommended for differentiating
• Resembles the fallopian tubes
between benign and malignant adnexal mass
• Can reach enormous size
• Should be measured in all women under the
Mucinous • Multilocular with mucoid substance within LDH, AFP and
age of 40 with complex ovarian mass because
cystadenoma • Resembles cells of endocervix or intestinal hCG
of the likelihood of germ cell tumors
epithelium
• Transitional cell tumor ADNEXAL MASS: IMAGING
• Solid mass or nests of epithelial cells and a • Primary imaging modality: Grey scale, high frequency, 2D
Brenner surrounding fibrous stroma transvaginal ultrasound with color Doppler imaging
Tumor • Epithelium similar to transitional epithelium • UTS should be used to identify specific diagnosis, differentiate
of the urinary bladder
from a non-gynecologic pathologies, differentiate benign from
• Epithelial cells: “coffee bean”-appearing nucleus
malignant masses, or to evaluate extent of the disease
GERM CELL TUMOR
• Computerized tomography (CT) and MRI- reserved for
• Dermoid cysts/ Mature teratoma secondary evaluation of concerning abdominal processes,
Benign Cystic
• 80% occur in reproductive life complex masses, and suspected malignancy
teratoma
• Most common neoplasm in prepubertal female • CA-125- obtained from patients who are at high risk for ovarian
cancer; refer to Gynecologic Oncology if more than 200

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ULTRASOUND FINDINGS ULTRASOUND FINDINGS (IOTA SIMPLE RULES)
FEATURE BENIGN MALIGNANT Rules of predicting a malignant tumor (M-rules)
Size • <8 cm • >8 cm M1 • Irregular solid tumor
• Solid or Mixed M2 • Presence of ascites
• Cystic • Multilocular M3 • At least four papillary structures
• No solid • Multicystic • Irregular multilocular solid tumor with largest
Consistency M4
compartments • Nodular, Papillary diameter ≥ 100 mm
• No septations • Irregular walls and M5 • Very strong blood flow (color score 4)
septa Rules of predicting a benign tumor (B-rules)
Laterality • Unilateral • Bilateral B1 • Unilocular
• Ascites • Presence of solid components with the largest
Associated B2
• Calcifications • Peritoneal masses diameter < 7 mm
features
• Lymphadenopathy B3 • Presence of acoustic shadows
• Smooth multilocular tumor with largest diameter
B4
<100mm
B5 • No blood flow (color score 1)

AGE TYPE SIZE (CM) MANAGEMENT

Premenarchal Any >2 cm Surgical Evaluation
<5 No follow-up necessary
Simple >5 and <7 Repeat ultrasound in 1 year
>7 Further imaging or surgical evaluation if change
<5 No follow-up necessary
Hemorrhagic
Reproductive >5 Repeat ultrasound in 6–12 wk
Repeat ultrasound in 6–12 wk. Then if not surgically
Endometrioma Any
removed, follow yearly
MRI and/or
Nodule without flow or multiple thin septations Any
surgical evaluation
<1 No follow-up necessary
Simple >1 and ≤7 Repeat ultrasound in 1 y
Post- >7 Further imaging or surgical evaluation
menopausal Early Menopause: repeat ultrasound in 6–12 wk
Hemorrhagic Any
Late menopause: surgical evaluation
Nodule without flow or multiple thin septations Any Surgical evaluation or MRI
RISK FACTORS
To be able to understand functional cyst, you have to understand the
ovarian cycle. Remember, the follicular cyst, after ovulation will turn to • Compromised immune system (genetic, iatrogenic, infectious)
a corpus luteum. When no ovulation happens, the mature follicular cyst • Increased risk for HPV infection
will persist and grow in size resulting to follicular cyst. If no luteolysis o Early coitarche
happens, the CL will persist giving rise to corpus luteum cyst. o Multiple sexual partners (>/= 6)
Dr. Banzuela-Cruz
o History of STI
o OCP use
NEOPLASTIC DISEASE OF THE LOWER o History of vulvovaginal dysplasia
GENITAL TRACT • Smoking (Squamous Cell CA, not Adeno CA)
CERVIX
PRIMARY PREVENTION:
HUMAN PAPILLOMA VIRUS • Human Papillomavirus Vaccination
RISK HPV SEEN IN: o Bivalent (16,18)
Low • 6, 11, 40, • seen in CIN I or condyloma o Quadrivalent (6,11,16,18)
41, 42 acuminata o Nonavalent (6, 11, 16, 18, 31, 33, 45, 52, and 58)
Intermediate • 31, 33, 35, • seen in HSIL (CIN II/III) o Schedule: 3 doses given at 0,1,6
51, 52
High • 16, 18, 45, • seen in invasive CA
58
Majority of cases are associated with infection of one or more types of HPV
which is sexually transmitted.

SECONDARY PREVENTION: CYTOLOGY

ACS (2012)/ASCCP/ASCP Screening PSCPC 2012
POPULATION ACS 2020
Recommendation Screening Recommendation
• No screening (Screening should begin
Age <25 • Cytology alone every 3 years starting at
• No screening approximately 3 years after the onset of vaginal
years old age 21yo
intercourse, but not earlier than 21 years old.)
• Preferred: Starting at age
• Cytology alone every 3 years until age • Due to the disease burden and low sensitivity of
25 y, primary HPV test
25-65 years 29yo cytology in the local setting, either annual
alone every 5 y
old • Preferred: HPV and Cytology “co-testing” screening using conventional cytology or
• Acceptable: Cotesting
every 5 years. biennial screening with liquid based cytology is
every 5 years or cytology
• Acceptable: Cytology alone every 3 years recommended.
alone every 3 years
• Screening is not recommended for women >65 years of age who • Screening with Pap test or HPV testing is not recommended for
have had three consecutive negative Pap tests or two women who have had a hysterectomy with removal of the cervix
consecutive negative HPV tests, provided they have had no and who do not have a history of CIN2+.
history of high-grade dysplasia (CIN2/3) or cancer (CIN2+) in Again, no Pap smear for those younger than 21y/o unless pregnant
the past 20 years. However, women presenting at age because burden of the disease as well as prevalence is low in this
• 65 years of age or older who have not had previous screening population. For pregnant patients, however, obtaining a Pap smear
should be included during the first PNCU regardless of age.
should undergo Pap and HPV testing. Dr. Banzuela-Cruz

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CERVICAL CYTOLOGY REPORTING: THE BETHESDA SYSTEM
CYTOLOGIC ABNORMALITY
• Most common squamous abnormality
• Few cells may show features associated with squamous
ASC-
intraepithelial lesions, but there are few of these cells
US
present or the changes are not consistent with a more
precise diagnosis
• Atypical squamous cells, cannot exclude a higher-grade
ASC-
lesion
H
• Colposcopy
• Often found to be consistent with histology reports of
low-grade dysplasia or cervical intraepithelial neoplasia
LSIL 1 (CIN 1)
• LSIL may resolve spontaneously or progress to more
severe dysplasia MANAGEMENT OF CYTOLOGIC ABNORMALITIES
• Indicates more severe dysplasia or CIN 2/3 I 21-24 y/o >24 y/o
• If unmanaged, approximately 20% of patients with HSIL • Reflex Testing or • HPV testing
HSIL will progress to cervical cancer. ASC-US repeat Cytology • Repeat cytology
• All patients with HSIL should be evaluated with after 12 months after 12 months
colposcopy, • HPV negative*
AG- • Recommended that all women with AGC undergo (may repeat Co-test
US colposcopy with endocervical sampling • Repeat Cytology after 1 year)
LSIL
after 12 months • HPV positive*
• HPV unknown*
• *Colposcopy
ASC-H • COLPOSCOPY
• Colposcopy with
HSIL • Colposcopy
ECC or LEEP
• Colposcopy with ECC and Endometrial
AGC
Sampling
Atypical
Endometrial • Endometrial and Endocervical curettage
Cells

Comparison of 2012 and 2019 consensus recommendations for management of common abnormalities — American Society for
Colposcopy and Cervical Pathology
Current Pap Management By 2012 Management By 2019
Current HPV Result Previous Result
Test Result Guidelines Guidelines
Repeat HPV test with or
Repeat pap plus HPV
Negative ASC-US unknown or HPV negative* without concurrent pap
testing in 3 yrs
test in 3 yrs
Repeat pap plus HPV Repeat HPV test with or
Negative LSIL unknown or HPV negative* testing in 1 yr preferred, without concurrent pap
colposcopy acceptable test in 1 yr
Negative ASC-H noncontributory Colposcopy Colposcopy
Noncontributory agc noncontributory Colposcopy Colposcopy
Repeat HPV test with or
Repeat pap plus HPV
Positive NILM unknown or HPV negative* without concurrent pap
testing in 1 yr
test in 1 yr
Positive NILM HPV positive† Colposcopy Colposcopy
Positive for genotype
HPV 16, HPV 18, or NILM noncontributory Colposcopy Colposcopy
both
Positive for genotype Not applicable, genotyping
HPV 16, HPV 18, or ASC-US or LSIL noncontributory not recommended for ASC- Colposcopy
both US or LSIL in 2012
positive ASC-US or LSIL Unknown or HPV positive Colposcopy Colposcopy
Negative screening results with HPV Repeat HPV test with or
positive ASC-US or LSIL testing or HPV plus pap testing within Colposcopy without concurrent pap
the previous 5 yrs test in 1 yr§
Repeat HPV test with or
Colposcopy confirming the absence of
Positive ASC-US or LSIL Colposcopy without concurrent Pap
high-grade lesion within the past yr
test in 1 yr
Colposcopy or expedited
Positive ASC-H Noncontributory Colposcopy
treatment
Positive untyped,
positive for genotype Colposcopy or expedited Colposcopy or expedited
HSIL Noncontributory
other than HPV 16, or treatment treatment
negative
Positive for genotype HSIL Noncontributory Colposcopy or expedited Expedited treatment
HPV 16 treatment

RISK-BASED FRAMEWORK MANAGEMENT TREATMENT FOR DYSPLASIA

1. Expedited treatment preferred ABLATIVE EXCISIONAL
2. Expedited treatment or colposcopy acceptable • Procedures
3. Colposcopy recommended • Cryotherapy • Loop Electrosurgical Excision
4. Repeat test in 1 year • CO2 ablation Procedure (LEEP)
5. Repeat test in 3 years • Cold-knife conization
6. Return to routine screening at 5-year intervals

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ABLATIVE EXCISIONAL • Schiller’s (Lugol’s) iodine test
Criteria • Lugol’s is a concentrated solution
• No suspicion of glandular • Provides specimen for further of iodine that reacts with the
involvement or invasive pathologic studies glycogen in normal squamous
cancer. • Suspected microinvasion epithelium to make it appear dark
• Satisfactory colposcopy with • Adenocarcinoma in situ or brown
visualization of entire other glandular abnormalities • Original and newly formed mature
cervical squamocolumnar • Unsatisfactory colposcopy squamous metaplastic epithelium
junction in which the transformation is glycogenated, whereas CIN and
• Biopsy confirming presence zone is not fully visualized invasive cancer contain little or no
of CIN; abnormal cytology • Lack of correlation between glycogen
alone is not sufficient cytology and colposcopy/
• Lesion does not involve the biopsies CERVICAL INTRAEPITHELIAL NEOPLASIA
endocervical canal and • Unable to rule out invasive
negative endocervical • Premalignant changes in the cervical epithelium that has the
disease
curettage (if available) potential to progress to cervical cancer
• Lesion extending into the
endocervical canal • Histologic features: cellular immaturity, cellular
• Endocervical curettage disorganization, nuclear abnormalities, and increased mitotic
showing CIN or a glandular activity
abnormality • Severity of CIN is determined by the portion of epithelium
• Recurrence after an showing disordered growth and development
ablative or previous
CLASSIFICATION OF CIN
excisional procedure
• Cellular dysplasia confined to the basal third of
FOLLOW-UP CIN I
the epithelium (mild dysplasia)
• The rate of recurrent or persistent disease following excisional • Cellular dysplasia encompassing the lower two-
or ablative treatment for CIN 2/3 is 5% to 17%, with no CIN II
thirds of the epithelium (moderate dysplasia)
significant differences in outcomes between the different • Cellular dysplasia encompassing more than two-
treatment thirds of the epithelial thickness (severe
• Co-testing with cervical cytology and HPV at 12 and 24 months. CIN III
dysplasia), including full-thickness lesions
o If both co-tests are negative, the woman can return to routine (formerly carcinoma in situ or CIS)
screening
o If any test is abnormal, colposcopy with endocervical sampling TREATMENT FOR DYSPLASIA
is recommended. ABLATIVE EXCISIONAL
Criteria
PRINCIPLES OF COLPOSCOPY
• No suspicion of glandular • Provides specimen for
Normal transformation zone involvement or invasive further pathologic studies
cancer. • Suspected microinvasion
• Satisfactory colposcopy • Adenocarcinoma in situ or
with visualization of entire other glandular
cervical squamo-columnar abnormalities
junction • Unsatisfactory colposcopy
• Biopsy confirming in which the transformation
presence of CIN; abnormal zone is not fully visualized
cytology alone is not • Lack of correlation between
sufficient cytology and colposcopy/
• Lesion does not involve biopsies
the endocervical canal and • Unable to rule out invasive
negative endocervical disease
curettage (if available) • Lesion extending into the
endocervical canal
Application of green filter
• Endocervical curettage
showing CIN or a glandular
abnormality
• Recurrence after an
ablative or previous
excisional procedure
• Procedures
• Cryotherapy • Loop Electrosurgical
Acetowhitening • CO2 ablation Excision Procedure (LEEP)
• Addition of 3-5% Acetic Acid • Cold-knife conization
• Depends on the amount of nuclear protein
FOLLOW-UP
• The rate of recurrent or persistent disease following excisional or
ablative treatment for CIN 2/3 is 5% to 17%, with no significant
differences in outcomes between the different treatment
• Co-testing with cervical cytology and HPV at 12 and 24 months.
o If both co-tests are negative, the woman can return to
routine screening
o If any test is abnormal, colposcopy with endocervical
sampling is recommended.

GYNECOLOGIC
MALIGNANCIES
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CERVICAL CANCER Note: Lymph vascular space invasion (LVSI) is not part of the
staging but should be reported.
RISK FACTORS
• Third most common malignancy of the lower female genital Staging for cervical cancer is clinical meaning once you perform IE,
Bimanual exam, rectal exam, and imaging studies, you have already
tract (most common is endometrial then ovarian)
staged the Ca.
• 2/3 are diagnosed in advanced stage Dr. Banzuela-Cruz
o HPV – necessary cause of cervical cancer TREATMENT
o Parity of 7 or more STAGE TREATMENT
o OCP use >5 years with HPV • Desirous of pregnancy with LVSI
o Current smokers & younger age at smoking o (-) margins: BLND
o Co-infected with Chlamydia or HSV-2 o (+) margins: repeat cone biopsy/trachelectomy
IA1
o HIV + BLND +/- PALS
o Early age at sex <14 y/o • Not desirous of pregnancy
o Sex partners >6 o EH +/- BSO (+BLND if +LVSI)
o Pregnancy <17 years old • Desirous of pregnancy
o No screening o Radical vaginal or abdominal trachelectomy +
o Low socio-economic status IA2 pelvic lymphadenectomy
o Poor access to healthcare services, poor nutrition, etc. • Not desirous of pregnancy
MAJOR CATEGORIES OF CERVICAL CARCINOMA o RH, BLND +/- BSO
• Squamous Cell Carcinomas IB1, •
RH, BLND +/- PALS +/- BSO
IIA1 •
Chemotherapy and pelvic EBRT + brachytherapy
o Large cell (keratinizing or nonkeratinizing)
o Small cell •
Chemotherapy and pelvic EBRT + brachytherapy
o Verrucous •
Chemotherapy and pelvic EBRT followed by RHBSO
IB2,
+/- PALS and selective pelvic lymphadenectomy.
• Adenocarcinomas IIA2
• Primary RHBSO, BLND +/- PALS followed by adjuvant
o Typical (endocervical)
chemoradiation
o Endometrioid
IIB- • Chemotherapy and pelvic EBRT + brachytherapy
o Clear cell
IVA • EBRT + brachytherapy + platinum-based chemotherapy
o Adenoid cystic (basaloid cylindroma)
• Cisplatin-based chemotherapy + individualized RT for
o Adenoma malignum (minimal deviation adenocarcinoma) IVB
control of pelvic disease and other symptoms
• Mixed Carcinomas
PALS – paraaortic lymph node sampling; EBRT – external beam radiotherapy
o Adenosquamous
• Concurrent Chemoradiation: Current standard of care and
o Glassy cell carcinoma
mainstay of treatment
HISTOLOGIC FEATURES • Surgery: Cone Biopsy and Radical trachelectomy (if desirous of
• Squamous cell CA pregnancy) for stage IA1
o Arising from ectocervix Before we proceed, it is important that you know the mainstay treatment
o Most common (85-90%) for the following carcinoma is concurrent chemoradiation. Surgery is
• Adenocarcinoma only for early stages of the carcinoma (until IIA2)
o Arising from endocervical columnar epithelium (10-15%) Dr. Banzuela-Cruz

• Gross examination
o Exophytic or cauliflower-like
o Endophytic or barrel-shaped
PATTERN OF SPREAD
• Spread to adjacent tissues like vagina, uterus RISK FACTORS AND
STAGING AND TREATMENT
• Lymphatic spread SCREENING FOR CERVICAL
OF CERVICAL CANCER
CANCER
CLINICAL PRESENTATION https://qrs.ly/z8egxck
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• Vaginal bleeding
o Most common symptom PREMALIGNANT DISEASES OF THE VULVA
o Post-coital bleeding CLASSIFICATION OF VULVAR ATYPIA
o Intermenstrual bleeding • Squamous cell hyperplasia (formerly hyperplastic dystrophy)
• Brownish, foul-smelling vaginal discharge • Lichen sclerosus
Stage I: Cancer confined to the cervix • Intraepithelial neoplasia
IA Microscopic cancer depth ≤5 mm and extension ≤7 mm o VIN I: Mild dysplasia (lower third involvement)
IA1 Stromal invasion ≤3 mm and extension ≤7 mm o VIN II: Moderate dysplasia (half to two-thirds)
IA2 Stromal invasion >3 mm and ≤5 mm with extension ≤7 mm o VIN III: Severe dysplasia–carcinoma in situ (more than two-
Cancer confined to the cervix clinically visible or thirds of epithelium involved)
IB
exceeds the dimensions for IA • Others
IB1 ≤4 cm in greatest diameter o Paget disease
IB2 >4 cm in greatest diameter o Melanoma in situ (level 1)
Stage II: Cancer extends beyond cervix but not to pelvic LICHEN SCLEROSUS
wall or lower third of vagina
• 5-15% risk of CA in postmenopausal women
IIA Without parametrial invasion
• Cumulative incidence of squamous cell carcinoma of the vulva
IIA1 ≤4 cm in greatest diameter for women with prior lichen sclerosis was 6.7%
IIA2 >4 cm in greatest diameter • S/SX: Pruritus
IIB With parametrial invasion • Pathology:
Stage III: Cancer extends to pelvic wall and/or involves o Thin, bluish, parchment like appearance with labial fusion,
lower third of vagina and/or causes hydronephrosis or scarring, and contracture
non-functioning kidney o Thickening or hyperkeratosis of the surface layers and
Tumor involves lower third of vagina, no extension to inflammation is usually present
IIIA
pelvic wall • Diagnosis: Biopsy
Extension to pelvic wall and/or hydronephrosis or • Treatment:
IIIB
non-functioning kidney o Testosterone cream
Stage IV: Cancer extends beyond true pelvis or has o High potency topical steroids: Clobetasol or halobetasol
involved (biopsy proven) mucosa of bladder or rectum
IVA Cancer spread to adjacent organs
IVB Cancer spread to distant organs

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SQUAMOUS CELL HYPERPLASIA DIAGNOSIS AND ENDOMETRIAL SAMPLING

• Formerly called hyperplasic dystrophy • Endometrial biopsy
• Elongation & widening of rete ridges, which may be confluent • Endometrial curettage
• White firm cartilaginous lesions with hyperkeratotic changes • Hysteroscopy
o Whitish lesions, vulvar tissues appear thickened MANAGEMENT FOR PREMENOPAUSAL WOMEN
o More focal or multifocal HISTOLOGIC
• S/Sx: Chronic pruritus and thickened skin MANAGEMENT
TYPE
• Diagnosis: Biopsy • For simple hyperplasia: OCP x 6 cycles
• Treatment: Medium potency topical steroids • MPA 10-20 mg OD x 14 days
PAGET DISEASE Hyperplasia • Do UTS & sample endometrium after 3 mos:
• Pathology: WITHOUT o Normal: MPA, 5mg x 10days/month for
o Rare intraepithelial disorder in vulva atypia 12 months
o Resembles Paget disease of breast o Persistent: increase dose 40-100mg daily
• Cause: Associated with adenocarcinoma of vulva, vagina & anus for 3 months, then repeat biopsy
• S/SX: • If desirous of pregnancy
1. Continuous MPA 10-20mg OD x 3 months
o Reddish eczematoid appearance
2. Megestrol acetate 40-200mg OD
o Itchiness – common problem
3. DMPA 150mg every 3 months
• Diagnosis: Biopsy 4. LNG-IUS for 1-5 years
• Treatment: Surgery • Do UTS & sample endometrium after 3 mos:
Hyperplasia o Normal: decrease MPA 10mg OD x 14
WITH days for 12 more months
atypia o Persistent: increase MPA to 40-100mg
daily for 3 months, OR shift to Megestrol
acetate 40mg 2-4x a day for 3 months
then repeat biopsy, if persistent: EH +/-
BSO
• No desire for pregnancy
o EH +/- BSO

MANAGEMENT FOR POSTMENOPAUSAL WOMEN

HISTOLOGIC
MANAGEMENT
TYPE
Hyperplasia • If desirous for uterine preservation, of if poor
WITHOUT surgical risk, same as in premenopausal
Vulvar epidermis with Paget disease. Paget cells are large pale cells; occur atypia • If not desirous of uterine preservation, EHBSO
in nests and infiltrate upward through the epithelium. Hyperplasia
• EHBSO
WITH atypia
NEOPLASTIC DISEASES OF THE UTERUS • Other non-surgical treatment options
ENDOMETRIAL HYPERPLASIA 1. Danazol 400mg daily x 3months
2. GnRH analogues +progestin combination
SIMPLE HYPERPLASIA
o Norethisterone acetate 500mg weekly x 3 months
• Irregularity in the shape of glands with cystic alterations o Goserelin, 3.6mg or Leuprorelin 3.75mg depot monthly for 6
• Abundant stroma between glands months OR Goserelin, 10.8mg or Leuprorelin 11.25mg depot
• Glands cystically dilated with occasional outpouchings, focal crowding every 3 months for 6 months
• Lined by pseudostratified tall columnar epithelium
• Glands separated by abundant cellular stroma ENDOMETRIAL CANCER
RISK FACTOR: Unopposed estrogen stimulation of the endometrium
COMPLEX HYPERPLASIA • Unopposed estrogen stimulation
• Highly crowded glands with little stroma • Unopposed menopausal estrogen (4-8x)
• Complex glandular outlines with papillary intraluminal folding replacement therapy
• Pseudostratified tall columnar epithelium lined glands • Menopause after 52 years (2.4x)
• Obesity (2-5x)
ATYPIA Increases the
• Nulliparity (2-3x)
Risk
• Loss of polarity • Diabetes (2.8x)
• Increased N:C ratio • Insulin resistance
• Irregular size and shape • Estrogen secreting ovarian tumors
• Prominent nucleoli • Polycystic ovarian syndrome
• Thick nuclear membrane • Tamoxifen therapy for breast cancer
• Ovulation
• Progestin therapy
Diminishes the
• Combination oral contraceptives
Risk
• Menopause before 49 years
• Multiparity
SYMPTOMS, SIGNS, AND DIAGNOSIS
• Symptoms
o Postmenopausal bleeding, abnormal premenopausal
bleeding, and perimenopausal bleeding are the primary
symptoms of endometrial carcinoma.
• Diagnosis: Biopsy of the endometrium
• Histologic Classification
o Typical endometrioid adenocarcinoma
o Adenocarcinoma with squamous elements
(adenoacanthoma or adenosquamous ca)
Rate of Progression
to Cancer
o Clear cell carcinoma –poor prognosis
o Serous carcinoma –poor prognosis
Simple Hyperplasia without Atypia 1%
o Secretory carcinoma
Complex Hyperplasia without Atypia 3%
o Mucinous carcinoma
Complex Hyperplasia with Atypia 29%
o Squamous carcinoma
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DEGREE OF DIFFERENTIATION SARCOMAS
G1 Well differentiated Less than 6% solid components UTERINE SARCOMAS
Moderately TYPE FEATURES TREATMENT
G2 6% to 50% solid components
differentiated • EH
G3 Poorly differentiated More than 50% solid components *BSO, BLND are
• Leiomyosarcoma
not mandatory
TYPES OF ENDOMETRIAL CANCER (30%)
• Adjuvant:
TYPE 1 TYPE 2
Pure sarcoma Doxorubicin
Prototype Endometrioid Ca Serous Papillary
• Endometrial • EH+BSO
Peri- Or Early
Typical Patient Late Postmenopause stromal sarcoma • PFC, Pelvic/PALS
Postmenopause
Background
(adenosarcoma) • Adjuvant: Pelvic
Hyperplastic Atrophic 10% EBRT
Endometrium
Grade Low High • EH+BSO
Estrogen • PFC, BLND, IO
Dependent Non-dependent • Consist of
Dependence Carcinosarcoma • Peritoneal biopsy
carcinoma and
Estrogen
(MMMT) • Adjuvant: Pelvic
Usually Positive Negative sarcoma elements
Receptors EBRT or Cisplatin
+ Ifosfamide
Prognosis Better Poorer
Müllerian
• EH+BSO
STAGING FIGO 2009 / 2018 adenosarcoma
Stage I • Tumor confined to the corpus • Aggressive
G123 behavior
IA • No or less than half myometrial invasion • Poor prognosis
IB • Invasion half or more of the myometrium • Confused with • EH+BSO
Undifferentiated
lymphoma, • PFC, Pelvic/PALS
Stage II • Tumor invades the cervical stroma but does
leukemia, high-
G123 not extend beyond the uterus grade endometrial
* NOTE: Endocervical glandular involvement should be cancer
considered as Stage 1 and no longer stage II
Stage III • Local and/or regional spread of the tumor
III A • Tumor invades serosa and / or adnexa*
NEOPLASTIC DISEASES OF THE OVARIES
III B • Vaginal and / or parametrial involvement OVARIAN CANCER
III C • Metastasis to the pelvic or para-aortic lymph nodes* WHO Classification
C1 o Positive pelvic lymph nodes • Serous
C2 o Positive para-aortic LN +/- pelvic lymph nodes • Mucinous
• EPITHELIAL
*Positive cytology has to be reported separately • Endometrioid
NOTE: • 65%
without changing the stage • Clear cell (Mesonephroid)
Stage IV • Tumor invades bladder and/or bowel • Brenner
mucosa, and /or distant metastasis • Granulosa cell
IVA • SEX CORD
• Tumor invades bladder and/or bowel mucosa • Thecoma-fibroma
IVB • < 0.01
• Distant metastases, including intra-abdominal • Sertoli-Leydig
metastases and/or inguinal lymph nodes • GERM CELL • Primitive (dysgerminoma, yolk sac)
Since the most common symptom of endometrial Ca is AUB, endometrial biopsy • 6% • Teratoma
will point us whether carcinoma is present. Staging is surgical. Mainstay • GERM CELL-SEX
procedure for endometrial Ca is Extrafascial hysterectomy except for stage II • Gonadoblastoma
CORD < 0.01
because it includes cervical invasion (cervix=radical hysterectomy).
Dr. Banzuela-Cruz
• Tumors of rete ovarii
STAGING & TREATMENT • Small cell ca
• MISC
• Initial management of endometrial cancer includes: • Large cell ca
o Extrafascial hysterectomy (EH) • Wilms tumor
o Bilateral salpingo-oophorectomy (BSO)
o Para-aortic lymphadenectomy (PALS)
• Exceptions to surgical approach: OVARIAN TUMORS
o Poor surgical risk patients. Initially undergo complete https://qrs.ly/voegxco
radiotherapy with or w/o chemotherapy.
o Non-resectable disease
o Well-differentiated lesion and contraindication to TUMOR MARKERS
anesthesia & unsuited for radiotherapy. TUMOR
TYPE AGE HISTOLOGY
ST LOCATION TREATMENT MARKERS
• *EH+BSO, PFC, BLND • Serous
o Vaginal brachytherapy (AG3, • Mucinous
I Confined to corpus
BG1-G2) • CA-125 • Endometroid
Epithelial Older
o Pelvic EBRT (BG3) • CEA • Clear cell
Extension to (Mesonephroid)
• RH+BSO
II cervix, but not • Brenner
• PFC, BLND
beyond uterus • Dysgerminoma
• *EH+BSO, PFC, BLN eval, • Endodermal sinus
Debulking • LDH
Germ • Embryonal
o Chemotherapy + pelvic EBRT Young • hCG
Cell choriocarcinoma
(A) • AFP
Outside uterus, • Teratoma
III o Chemotherapy + pelvic EBRT • Mature teratoma
within pelvis
+ vaginal brachytherapy (B, • Estrogen • Granulosa-theca
C1) Sex cord All
• Testosterone • Sertoli-Leydig
o Chemotherapy + EFRT +
vaginal brachytherapy (C2)
Invades bladder
and/or bowel
IV • EH+BSO Debulking
mucosa, +/-
distant metastasis
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OVARIAN TUMORS COMPLETE SURGICAL STAGING
Serous • Most frequent ovarian epithelial tumors • Staging is surgical and based on the operative findings at the
Cystadenoma • Resembles the fallopian tubes commencement of the procedure
• Can reach enormous size • Staging
• Multilocular with mucoid substance o Laparotomy: Midline longitudinal incision
Mucinous
within o Peritoneal fluid cytology
cystadenoma
EPITHELIAL

• Resembles cells of endocervix or o Systematic exploration of the abdominal cavity

intestinal epithelium o TH with bilateral salpingo-oophorectomy
• Transitional cell tumor o Infracolic omentectomy
• Solid mass or nests of epithelial cells o Lymph node evaluation (Pelvic and Para aortic )
and a surrounding fibrous stroma o Random biopsy of abdominal peritoneum and suspicious
Brenner
• Epithelium similar to transitional areas
Tumor
epithelium of the urinary bladder
o Tumor Debulking
• Epithelial cells have “coffee bean”-
o Appendectomy if mucinous adenocarcinoma
appearing nucleus
Staging for ovarian carcinoma is through surgery.
• Dermoid cysts/ Mature teratoma Dr. Banzuela-Cruz
SURGERY
GERM
CELL

Benign Cystic • 80% occur in reproductive life

teratoma • Most common neoplasm in • Conservative surgery: Unilateral Salpingo-Oophorectomy
prepubertal female • Criteria:
• Most common benign solid tumor of o Stage IA
the ovary o Well-differentiated tumor
• Extremely slow growing and unilateral o Peritoneal fluid cytology is negative for malignant cells
STROMAL

• Whorled pattern on cross section o Omentum and peritoneal biopsies are negative for
Fibroma metastasis
• Meig’s Syndrome:
1. Ovarian Fibroma o Young woman desirous of pregnancy
2. Ascites
3. Hydrothorax

STAGING
ST LOCATION A B C
• 1 or 2 ovaries with rupture/ spill
• C1: surgical spill
I • Confined to ovaries or FT • 1 ovary only • 2 ovaries • C2: ruptured before surgery
• C3: positive malignant cells in
the peritoneal fluid
• 1 or 2 ovaries/FT +
• Extension /
• Pelvic extension (below pelvic • Extension to pelvic
II implants on uterus, --
brim) or primary peritoneal intraperitoneal tissues
FT or ovaries
cancer
• Stage II PLUS • (+) RPLN • Visible peritoneal mets beyond
• Visible peritoneal mets
• Spread to peritoneum outside • Microscopic pelvis >2 cm; w/ or w/o mets to
III beyond pelvis up to 2 cm; w/
the pelvis and/or mets to extrapelvic RPLN; extension of tumor to
or w/o mets to RPLN
retroperitoneal LN peritoneal mets capsule of liver & spleen
• Parenchymal met and mets to
• Distant metastases excluding • Pleural effusion with
IV extra-abdominal organs --
peritoneal surfaces (+) PFC
(including inguinal LN)
IC1 to IC3 is new in the ovarian cancer staging. Inadvertent rupture during surgery is IC1. This staging is also used for Fallopian tube carcinoma and Primary
peritoneal carcinoma. It has been postulated that high grade ovarian serous carcinoma actually comes from the fimbria of the fallopian tubes hence it has been
proposed that bilateral fimbriectomy offers protection from development of this kind of ovarian Ca. Kaya ako, I perform this instead of BTL when the patient
requests permanent sterilization method.
Dr. Banzuela-Cruz

OVARIAN TUMOR: EPITHELIAL-STROMAL DIAGNOSTIC TOOLS

HISTOLOGY • Pelvic Ultrasound: Primary tool for evaluation pelvic mass
• MRI and CT Scan
• Serous Tumors
o Pelvis and abdomen to assess the spread of the disease
o are the most frequent ovarian epithelial tumors
o Resembles fallopian tubes • Barium Enema and IVP
o To distinguish primary or secondary ovarian cancer
• Mucinous Tumors
o Epithelial cells filled with mucin
o Resembles endocervix/GIT
OVARIAN TUMOR: GERM CELL
• Clear Cell CLINICAL FEATURES
o Contains cell with abundant glycogen (HOBNAIL CELLS) • Most common ovarian malignancy in women < 30 years old
o Associated with DES exposure • Grow rapidly, usually unilateral, and are at stage 1a at diagnosis
• Endometrioid: Epithelial cells resembling the endometrium (compared to epithelial tumors)
• Brenner: Resembles the transitional cells of the urinary bladder • Clinical manifestation
o Pelvic pain due to rapid growth, hemorrhage, and necrosis
CLINICAL FINDINGS
o Pressure symptoms on the bladder or rectum
• Signs & Symptoms o 85% will have abdominal pain and pelvic mass
o Early disease is nearly always almost ASYMPTOMATIC • Management
o Vague pelvic pressure o Benign teratoma
o Abdominal fullness and bloating § Ovarian cystectomy or oophorectomy
o 80% of patients have elevated CA-125 o Malignant
o Advanced diseases may present with ascites and metastasis § If fertility is desired – Unilateral Salpingo-oophorectomy
to the umbilicus § No desire for fertility – TAHBSO
• Pelvic Exam findings
o Solid fixed, irregular pelvic mass

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• Pathology FAMILY PLANNING
Tier Effectiveness Types
Highly effective (fewer • IUDs
than 1 pregnancy per • Implants
Tier 1
100 women in 1 year) • Male and female
sterilization
Very effective (7 to 12 • Injectables
pregnancies per 100 • Pills
Tier 2 women in 1 year) • Patches
• Ring
Effective (18 or more • Barrier methods
pregnancies per 100 • Lactational
Tier 3 women in 1 year) amenorrhea
• Fertility awareness
methods
HISTOLOGY & TUMOR MARKER Generally, under tier 1 contraceptive methods, you would have
GERM CELL sterilization and the long acting reversible contraceptives (LARC) while
TUMOR
TUMOR HISTOLOGY coitus-related methods and more user-dependent methods would fall
MARKER
(MALIGNANT) under tiers 2 and 3. But recently, in choosing the most appropriate
• Germ cells stroma infiltrated contraceptive method for your patients, it would be best to use the WHO
with lymphocytes Medical Eligibility Criteria (MEC) to be able to consider her medical
Dysgerminoma LDH
• 10% are bilateral conditions.
Dr. Anna Rominia Cruz
• Analogous to seminoma of the testes
Endodermal
• Schiller Duval bodies – numerous TIER 1: INTRAUTERINE DEVICE (IUD)
sinus tumor or AFP
hyaline droplets
Yolk sac tumor • Copper IUD
• Hemorrhagic o Copper T 380A IUD (Paragard)
Choriocarcinoma • Highly malignant cytotrophoblast hCG o Copper impedes sperm transport and viability in the cervical
and Syncytiotrophoblast mucus
• Consists of immature embryonic o Most effective emergency contraceptive method
Immature
structures admixed with mature AFP
teratoma o Can last up to 10 years
elements
• LNG-IUS (Levonorgestrel intrauterine system) or Mirena
OVARIAN TUMOR: SEX CORD o 20μg of levonorgestrel (LNG) released everyday
o Primary effect of the progestin in the LNG-IUS: to thicken
GRANULOSA THECA CELL SERTOLI LEYDIG
TUMOR (75%) CELL TUMOR cervical mucus, impeding sperm penetration and access to
• Sex Cord: Granulosa • Sex Cord: Sertoli the upper genital tract
COMPONENT
• Stroma: Theca • Stroma: Leydig o Decreases tubal motility and also produces a thin, inactive
• Granulosa cells have endometrium.
grooved “coffee bean” nuclei
• Resemble fetal o The low levels of circulating steroid sometimes inhibit
MICROSCOPIC and are arranged in small ovulation
testes
clusters around a central o May be used for 5 years
cavity (Call-Exner bodies)
• Functionally TIER 1: SUBDERMAL IMPLANTS (Nexplanon)
HORMONES • Functionally estrogenic
testosterogenic • Contains 68 mg of Etonorgestrel (ENG)
• Premenarchal:
• Masculinization • Approved for use up to 3 years
Precocious puberty
• Hirsutism • Extremely effective, and is easy to insert and remove
• Premenopausal:
SYMPTOMS • Temporal • Does not result in a decrease of bone mineral density
Menstrual irregularities
recession • MOA: ovulation inhibition implant and thickening of the
• Postmenopausal:
• Deeper voice cervical mucus
Bleeding
• Young women: Unilateral
MANAGEMENT salpingooophorectomy
TIER 1: PERMANENT STERILIZATION
Postmenopausal: TAH/BSO • Vasectomy
Sex cord stromal tumors are functioning tumors meaning these tumors o Low cost
secrete either estrogen (Granulosa cell) or testosterone (Sertoli Leydig) o Office procedure with only local anesthesia
therefore meron silang estrogen or testosterone as evident through their o Efficacy is easily verified through a semenalysis after the
symptoms. Like a menopausal woman who suddenly menstruates again procedure
may have Granulosa theca cell tumor. o 13 to 20 ejaculations is necessary after the procedure before
Dr. Banzuela-Cruz
sterility
MATCHING TYPE • Bilateral tubal ligation or Fimbriectomy
A. Sertoli –Leydig tumor E. Dysgerminoma o May be done transabdominally, laparoscopically, or
B. Granulosa –theca tumor F. Dermoid
transcervically
C. Choriocarcinoma G. Struma ovarii
D. Yolk sac tumor H. Tubercle of Rokitansky o May be done immediately after a cesarean section or in cases
Most common benign tumor for <30 y/o of post vaginal delivery, an infraumbilical minilaparotomy
Schiller-Duvall bodies incision is done
Call-Exner bodies
TIER 2: INJECTABLE SUSPENSION
Precocious puberty in children
Nipple projections in dermoids • Depo-Provera, or depo-medroxyprogesterone acetate
Presents as virilization (DMPA) injectable
Numerous hyaline droplets • Given in a dose of 150 mg intramuscularly (IM) or 104 mg
Presence of thyroid tissue in the ovary subcutaneously (SC) every 3 months Inhibits ovulation, keeps
Tumor marker is HCG endometrium thin, keeps cervical mucus thin
Tumor marker is AFP • Return of fertility- 6 months to 1 year
Tumor marker is LDH • Clinical side-effects
Analogous to seminoma in males
o Irregular bleeding patterns
Composed of malignant syncytiotrophoblast
and cytotrophoblast
o Weight changes
Presents as vaginal bleeding in adults o Headaches
Most common malignant tumor <30 y/o o Mood changes
Eosinophilic bodies surrounded by granulosa cells o Bone loss
FDBBHADGCDEECBEB

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 TOPNOTCH OBSTETRICS AND GYNECOLOGY MAIN HANDOUT BY DR. FAJUTAGANA AND DR. BANZUELA-CRUZ
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• Non-contraceptive Health Benefits Absolute contraindications Relative contraindications
o reduces the risk of developing iron deficiency anemia and • Thromboembolism • Uterine fibroids
PID. The reduction in risk of endometrial cancer in women • Pulmonary embolism • Lactation
o Reduces the incidence of primary dysmenorrhea, symptoms • Coronary artery disease • Diabetes mellitus
of endometriosis, ovulation pain, and functional ovarian cysts • Cerebrovascular accident • Sickle-cell disease
because it inhibits ovulation. • Smokers older than 35 y • Hepatic disease
o Many believe that DMPA also reduces seizure frequency in • Breast/endometrial CA • Hypertension
women with epilepsy. In some studies, DMPA seems to have • Unexplained vaginal • Systemic lupus
beneficial effects on sickle cell pain crises. bleeding erythematosus
• Clinical Recommendations: DMPA can be started at any time • Abnormal liver function • Age 40 years and older and
during the menstrual cycle as long as the woman and her • Known or suspected high risk for vascular
provider are reasonably certain that she is not pregnant. If pregnancy disease
given later than 7 days into the menstrual cycle, backup • Severe • Migraine headaches
contraception should be used for 7 days. hypercholesterolemia • Seizure disorders
TIER 2: COMBINED ORAL CONTRACEPTIVE PILLS • Severe • Elective surgery
• Mechanism of Action hypertriglyceridemia
Blueprints Obstetrics and Gynecology, Table 24-6
o Combination oral contraceptives suppress gonadotropins
o Contraceptive steroids prevent ovulation mainly by TIER 2: PROGESTIN ONLY PILLS (POP)
interfering with release of gonadotropin-releasing hormone • Low dose progestin and no estrogen i.e. Norethindrone or
(GnRH) from the hypothalamus. Norgestrel
o Contraceptive steroids directly suppress the pituitary gland • Taken every day without a steroid-free interval
• ESTROGEN • Primary MOA: Cervical mucus thickening as the dose of
o Prevents a rise in follicle-stimulating hormone (FSH) and progestin in POPs is less than the ovulation inhibition dose
enhances the effect of the progestin component
• PROGESTERONE TIER 2: CONTRACEPTIVE PATCH
o Inhibits ovulation and, specifically, the luteinizing hormone
• Contains 75 ug ethinyl estradiol and 6 mg norelgestromin
(LH) surge
(Xulane)
• Ovulation Inhibition Dose - The lowest amount of a progestin
• Applied for 3 weeks then followed by a patch-free week to
needed to suppress LH
induce bleeding
• Secondary effects: Changes in the cervical mucus (which
• Applied to upper outer arm, lower abdomen, upper torso, or
prevent sperm transport into the uterus), the fallopian tube
buttocks
(which interfere with gamete transport), and the endometrium
(which reduce the likelihood of implantation)
TIER 2: CONTRACEPTIVE VAGINAL RING
• Proper Use
• Contains 2.7 mg ethinyl estradiol and 11.7 mg etonogestrel
• Monthly COCs
o 21 pills-21 active tablets taken every day then 7 pill-free days • Placed in the vagina for 21 days then removed for 7 days
o 22 pills-22 active tablets taken every day then 6 pill-free days • Steroids pass through the vaginal epithelium then directly into
o 24 pills-24 active tablets taken every day then 4 pill-free days the circulation
o 28 pills- 21 active pills taken every day followed by 7
inactive/non-hormonal pills of different color. No pill-free or TIER 3: BARRIER METHODS
rest days • Diaphragm – thin, dome-shaped membrane of latex rubber or
• Continuous COCs silicone with a flexible spring modeled into the rim
o Active pills are taken for 365 days of each year • Cervical cup – silicone or rubber that fits the cervix
o Extended cycle preparations • Both diaphragm and cervical cup must be used with a
o Active pills are taken for 12 weeks followed by a one-week spermicide and be left in place for at least 8 hours after the last
pill free period for withdrawal bleeding coital act
• How to Take COCs • Male condom – latex condoms provide protection against
o Take one pill regularly, preferably at the same time every day sexually transmitted diseases but must be stored in a cool dry
o Start within the first 5 days of the menstrual period. However place not exceeding 37.7C and is not compatible with oil-based
if the client is certain that she is not pregnant, it can be lubricants
started anytime but a backup method is required for 7 days if • Female condom – soft, loose-fitting polyurethane sheath with
started after the 7th day of menses Start the COCs as two flexible rings; intended for one-time use only
prescribed (Quick Start). This method may improve the
initiation of use but a backup method is required for 7 days if TIER 3: FERTILITY AWARENESS METHODS
started after the 7th day of menses. • Refraining from sexual intercourse during the fertile period
• Missed Pills: Take a missed hormonal pill as soon as possible • Effective with correct and consistent use
then keep taking pills as usual, one each day (She may take 2 • Not advisable for patients with irregular menstruation
pills at the same time or on the same day) • Do not protect against sexually transmitted infections
• Safety • Calendar method (Rhythm): fertile period computed by
o COCs do not disrupt an existing pregnancy, but should be o Start: Shortest recorded cycle minus 18
stopped o End: Longest recorded cycle minus 11
o COCs do not cause birth defects and will not harm the fetus o Example: A woman with a shortest cycle of 25 days and with
even if the woman becomes pregnant while taking the pills or longest recorded cycle of 34 days should refrain from sexual
accidentally starts the pill when she is already pregnant intercourse on days 7 (25-18) to 23 (34-11)
• Drug Interaction: Effectiveness of COCs are reduced with • Standard Days Method (SDM) – Abstain from days 8-19; may
rifampicin, phenytoin, phenobarbital, carbamazepine, only be used among women with cycles of 26-32 days
primidone and ethosuximide • Basal Body Temperature Method (BBT ) – refrain from
• Side effects: Spotting, amenorrhea, nausea, breast tenderness, intercourse from the first days of menses until 3 days after the
headaches and depression temperature rise of 0.2-0.5 degrees
• There is no delay of return to fertility after COCs are discontinued • Billings Ovulation Method or Cervical Mucus Method – refrain
from vaginal intercourse from the presence of clear, wet, and
slippery mucus until the 4th day after her peak day of menses
• Symptothermal method (STM) – Abstain when there are
secretions until both the 4th day after the peak cervical
secretions and the 3rd full day after the rise in basal body
temperature

TOPNOTCH MEDICAL BOARD PREP OB-GYNE MAIN DIGITAL HANDOUT BY DRS. SORIANO, BANZUELA-CRUZ & FAJUTAGANA Page 90 of 91
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 TOPNOTCH OBSTETRICS AND GYNECOLOGY MAIN HANDOUT BY DR. FAJUTAGANA AND DR. BANZUELA-CRUZ
For inquiries visit www.topnotchboardprep.com.ph or https://www.facebook.com/topnotchmedicalboardprep/
This handout is only valid for March 2023 PLE batch. This will be rendered obsolete for the next batch since we update our handouts regularly.
• Two-day method – Once with secretions of any time and • Gold standard of use is Levonorgestrel (Plan B pill) and is
consistency, refrain from intercourse on that day and the day most effective if given within 72 hours
after • Copper IUD is the most effective emergency contraception
• Saliva Ovulation Method – refrain from intercourse on days that • YUZPE REGIMEN:
a Ferning pattern is observed on saliva o COCs may be used in the absence of levonorgestrel-only pills
o Initial dose started as soon as possible and at most within 72
LACTATION AMENORRHEA (LAM) hours of unprotected intercourse then repeated 12 hours
• Three requirements are met: after
o Menstruation has not returned o Dose: 100 mcg ethinyl estradiol plus 0.5 mg levonorgestrel or
o Fully or nearly fully breastfeeding 1.0 mg DL-norgestrel
o Baby is less than six months old The number of pills you take for the Yuzpe method varies depending on
• Definition of full breastfeeding the formulation of the COC pill you will be using. For example, if you use
the Trust pill na available dito sa Philippines, one pill has a formulation
o Breastfeeding on demand
of 30 mcg EE + 125 mcg LNG. So to achieve the required dose of 100 mcg
o 10-12 times a day EE plus 0.5 mg LNG, you’ll have to take 4 pills per intake. Pag nagsearch
o Daytime feeding no more than four (4) hours apart kayo, di laging applicable ang 2 pills initially and 2 pills after 12 hours
o Night time feeding no more than six (6) hours apart ah! It depends on the pill formulation. Stay safe. J
Dr. Anna Rominia Cruz

EMERGENCY CONTRACEPTION
• Best given within the first 72 hours
• May be used up to 120 hours after sexual intercourse END OF OBSTETRICS AND GYNECOLOGY
• Criteria: there is a risk of pregnancy, patient presents within - MAIN HANDOUT
five days from the assault, and patient has a negative pregnancy
test

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Re-reading is inefficient. Here are 8 tips for studying smarter. "One example is if you were learning about how the neuron transmits electricity. One of
(from http://www.vox.com/2014/6/24/5824192/study-smarter-learn- the things we know if that if you have a fatty sheath surround the neuron, called a myelin
better-8-tips-from-memory-researchers) sheath, it helps the neuron transmit electricity more quickly.
"So you could liken this, say, to water running through a hose. The water runs quickly
The way most students study makes no sense.
through it, but if you puncture the hose, it's going to leak, and you won't get the same flow.
That's the conclusion of Washington University in St. Louis psychologists Henry Roediger
And that's essentially what happens when we age — the myelin sheaths break down, and
and Mark McDaniel — who've spent a combined 80 years studying learning and memory,
and recently distilled their findings with novelist Peter Brown in the book Make It Stick: The transmissions become slower."
Science of Successful Learning. 4) Draw out the information in a visual form
The majority of students study by re-reading notes and textbooks — but the "A great strategy is making diagrams, or visual models, or flowcharts. In a beginning
psychologists' research, both in lab experiments and of actual students in classes, shows psychology course, you could diagram the flow of classical conditioning. Sure, you can read
this is a terrible way to learn material. Using active learning strategies — like flashcards, about classical conditioning, but to truly understand it and be able to write down and
diagramming, and quizzing yourself — is much more effective, as is spacing out studying describe the different aspects of it on a test later on — condition, stimulus, and so on — it's
over time and mixing different topics together. a good idea to see if you can put it in a flowchart.
McDaniel spoke with me about the eight key tips he'd share with students and teachers "Anything that creates active learning — generating understanding on your own — is
from his body of research. very effective in retention. It basically means the learner needs to become more involved
and more engaged, and less passive."
1) Don't just re-read your notes and readings
"We know from surveys that a majority of students, when they study, they typically re- 5) Use flashcards
read assignments and notes. Most students say this is their number one go-to strategy. "Flashcards are another good way of doing this. And one key to using them is actually re-
“when students re-read a textbook chapter, they show no improvement in learning” testing yourself on the ones you got right.
"We know, however, from a lot of research, that this kind of repetitive recycling of “keeping a correct card in the deck and encountering it again is more useful”
information is not an especially good way to learn or create more permanent "A lot of students will answer the question on a flashcard, and take it out of the deck if
memories. Our studies of Washington University students, for instance, show that when they get it right. But it turns out this isn't a good idea — repeating the act of memory
they re-read a textbook chapter, they have absolutely no improvement in learning over retrieval is important. Studies show that keeping the correct item in the deck and
those who just read it once. encountering it again is useful. You might want to practice the incorrect items a little more,
"On your first reading of something, you extract a lot of understanding. But when you do but repeated exposure to the ones you get right is important too.
the second reading, you read with a sense of 'I know this, I know this.' So basically, you're "It's not that repetition as a whole is bad. It's that mindless repetition is bad."
not processing it deeply, or picking more out of it. Often, the re-reading is cursory — and it's 6) Don't cram — space out your studying
insidious, because this gives you the illusion that you know the material very well, when in
"A lot of students cram — they wait until the last minute, then in one evening, they repeat
fact there are gaps."
the information again and again. But research shows this isn't good for long term memory.
2) Ask yourself lots of questions It may allow you to do okay on that test the next day, but then on the final, you won't retain
"One good technique to use instead is to read once, then quiz yourself, either using as much information, and then the next year, when you need the information for the next
questions at the back of a textbook chapter, or making up your own questions. Retrieving level course, it won't be there.
that information is what actually produces more robust learning and memory. “practice a little bit one day, then two days later”
“retrieving information is what produces more robust learning and memory” "This often happens in statistics. Students come back for the next year, and it seems like
"And even when you can't retrieve it — when you get the questions wrong — it gives you they've forgotten everything, because they crammed for their tests.
an accurate diagnostic on what you don't know, and this tells you what you should go back "The better idea is to space repetition. Practice a little bit one day, then put your
and study. This helps guide your studying more effectively. flashcards away, then take them out the next day, then two days later. Study after study
"Asking questions also helps you understand more deeply. Say you're learning about shows that spacing is really important."
world history, and how ancient Rome and Greece were trading partners. Stop and ask 7) Teachers should space out and mix up their lessons too
yourself why they became trading partners. Why did they become shipbuilders, and learn
"Our book also has information for teachers. And our educational system tends to
to navigate the seas? It doesn't always have to be why — you can ask how, or what.
promote massed presentation of information as well.
"In asking these questions, you're trying to explain, and in doing this, you create a better
"In a typical college course, you cover one topic one day, then on the second day, another
understanding, which leads to better memory and learning. So instead of just reading and
topic, then on the third day, another topic. This is massed presentation. You never go back
skimming, stop and ask yourself things to make yourself understand the material." and recycle or reconsider the material.
"But the key, for teachers, is to put the material back in front of a student days or weeks
later. There are several ways they can do this. Here at Washington University, there are
some instructors who give weekly quizzes, and used to just put material from that week's
classes on the quiz. Now, they're bringing back more material from two to three weeks ago.
3) Connect new information to something you already know One psychology lecturer explicitly takes time, during each lecture, to bring back material
"Another strategy is, during a second reading, to try relating the principles in the text to from days or weeks beforehand.
something you already know about. Relate new information to prior information for better
“the key, for teachers, is to put the material back in front of a student days or weeks later”
learning.
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 TOPNOTCH OBSTETRICS AND GYNECOLOGY MAIN HANDOUT BY DR. FAJUTAGANA AND DR. BANZUELA-CRUZ
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"This can be done in homework too. It's typical, in statistics courses, to give homework in
which all of the problems are all in the same category. After correlations are taught,
a student's homework, say, is problem after problem on correlation. Then the next week, T
tests are taught, and all the problems are on T tests. But we've found that sprinkling in
questions on stuff that was covered two or three weeks ago is really good for retention.
"And this can be built into the content of lessons themselves. Let's say you're taking an
art history class. When I took it, I learned about Gauguin, then I saw lots of his paintings,
then I moved on to Matisse, and saw lots of paintings by him. Students and instructors both
think that this is a good way of learning the painting styles of these different artists.
"But experimental studies show that's not the case at all. It's better to give students an
example of one artist, then move to another, then another, then recycle back around. That
interspersing, or mixing, produces much better learning that can be transferred to paintings
you haven't seen — letting students accurately identify the creators of paintings, say, on a
test.
"And this works for all sorts of problems. Let's go back to statistics. In upper level classes,
and the real world, you're not going to be told what sort of statistical problem you're
encountering — you're going to have to figure out the method you need to use. And you
can't learn how to do that unless you have experience dealing with a mix of different types
of problems and diagnosing which requires which type of approach."
8) There's no such thing as a "math person"
"There's some really interesting work by Carol Dweck, at Stanford. She's shown that
students tend to have one of two mindsets about learning.
“it turns out that mindsets predict how well students end up doing”
"One is a fixed learning model. It says, 'I have a certain amount of talent for this topic —
say, chemistry or physics — and I'll do well until I hit that limit. Past that, it's too hard for
me, and I'm not going to do well.' The other mindset is a growth mindset. It says that
learning involves using effective strategies, putting aside time to do the work, and engaging
in the process, all of which help you gradually increase your capacity for a topic.
"It turns out that the mindsets predict how well students end up doing. Students with
growth mindsets tend to stick with it, tend to persevere in the face of difficulty, and tend to
be successful in challenging classes. Students with the fixed mindset tend not to.
"So for teachers, the lesson is that if you can talk to students and suggest that a growth
mindset really is the more accurate model — and it is — then students tend to be more open
to trying new strategies, and sticking with the course, and working in ways that are going
to promote learning. Ability, intelligence, and learning have to do with how you approach it
— working smarter, we like to say.

TOPNOTCH MEDICAL BOARD PREP OB-GYNE MAIN DIGITAL HANDOUT BY DRS. SORIANO, BANZUELA-CRUZ & FAJUTAGANA Appendix
For inquiries visit www.topnotchboardprep.com.ph or email us at [email protected]
This handout is only valid for the March 2023 PLE batch. This will be rendered obsolete for the next batch since we update our handouts regularly.