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OB/GYN Theory Exam - Complete Study Notes

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TOPIC 1: DIAGNOSIS OF PREGNANCY

A. Presumptive Signs (Symptoms felt by the patient - least reliable)

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B. Probable Signs (Detectable by an examiner - more reliable but still not definitive)

Uterine Signs

• Amenorrhea: >6 weeks, soft uterus on bimanual
• Hegar's sign: At 6-8 weeks - the isthmus of uterus becomes extremely soft (compressible between two fingers); the cervix and fundus feel almost separate
• Goodell's sign: Softening of the cervix (like soft rubber vs. firm nose cartilage in non-pregnant)
• Palmer's sign: Regular uterine contractions on bimanual palpation in early pregnancy
• Piskacek's sign: Asymmetric uterine enlargement at the site of placental implantation

Vaginal/Cervical Signs

• Chadwick's sign (Jacquemier's sign): Blue-violet discoloration of vagina and cervix, starting at 6-8 weeks due to increased vascularity
• Osiander's sign: Increased pulsation felt through lateral vaginal fornix

Abdominal Signs

• Uterine enlargement: By 12 weeks uterus becomes palpable above symphysis pubis
• Braxton-Hicks contractions: Painless irregular contractions after 16 weeks
• Ballottement: At 16-18 weeks - dipping the fetus in amniotic fluid and feeling it bounce back

Hormonal (hCG Tests - very reliable but categorized as "probable" because tumors can also secrete hCG)

• Urine pregnancy test: Detects hCG; can be positive around the day of missed period (sensitivity ~25 IU/L)
• Serum beta-hCG: Detectable 8-11 days post-conception (>5 IU/L = positive)
  • Rises geometrically in first 8 weeks
  • Peaks at 8-10 weeks at ~100,000 IU/L
  • Then falls by 90% by end of second trimester
  • Doubles every 48 hours in a normal intrauterine pregnancy (useful to distinguish from ectopic)
  • False positives: heterophile antibodies, human anti-mouse antibodies, trophoblastic tumors

Memory trick: hCG = "human Chorionic Gonadotropin" - it's made by the syncytiotrophoblast to rescue the corpus luteum, maintaining progesterone until the placenta takes over at ~10 weeks.

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C. Positive/Definitive Signs (Absolute proof of pregnancy)

Ultrasound Dating (very important clinically)

• 5-6 weeks: Gestational sac visible (transvaginal)
• 6-7 weeks: Fetal pole + cardiac activity visible
• CRL (Crown-Rump Length): Used from 7-12 weeks - most accurate for gestational age estimation (±5 days)
• BPD (Biparietal Diameter): Used from 13-20 weeks
• After 20 weeks: Accuracy decreases (±2-3 weeks), so early ultrasound is preferred for dating

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TOPIC 2: VOMITING IN PREGNANCY

A. Normal Nausea & Vomiting of Pregnancy (NVP)

• Affects up to 90% of all pregnancies
• Typically begins around 6 weeks, peaks at 8-10 weeks, resolves by 14-16 weeks in most
• Despite being called "morning sickness," it can occur at any time of day
• Cause: rising hCG and estrogen (particularly estradiol) stimulate the chemoreceptor trigger zone
• Also associated with: Helicobacter pylori infection (some evidence), psychological factors, multiple gestation (higher hCG)

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B. Hyperemesis Gravidarum (HG) - The Severe End

Definition

• Weight loss > 5% of pre-pregnancy body weight (some say >10%)
• Volume depletion (dehydration)
• Lab abnormalities: hypokalemia, ketonuria/ketonemia, elevated creatinine

Pathophysiology

• High hCG hyperstimulates thyrotropin receptors (hCG has structural similarity to TSH) - can cause transient hyperthyroidism
• Estrogen slows GI motility (progesterone also contributes)
• Molar pregnancies have extremely high hCG - classic cause of severe HG

Clinical Features

• Severe, persistent vomiting (>3 episodes/day)
• Signs of dehydration: dry mouth, decreased skin turgor, tachycardia, hypotension
• Weight loss
• Ketonuria (early starvation sign - important!)
• Absence of abdominal pain - if pain is present, think of another diagnosis

Differential Diagnosis (must know for exams!)

• Cholecystitis / cholelithiasis (gallbladder problems - more common in pregnancy due to estrogen)
• Pancreatitis
• Appendicitis
• Gastroenteritis
• Pyelonephritis
• Peptic ulcer
• Ectopic pregnancy (can present with vomiting + abdominal pain)
• Hepatitis
• HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets)
• Fatty liver of pregnancy (acute fatty liver)
• Gestational trophoblastic disease (molar pregnancy - very high hCG)

Investigations

• Urine: ketones, specific gravity (dehydration)
• Blood: CBC, serum electrolytes (K+, Na+), BUN, creatinine, uric acid
• LFTs (liver function)
• TFTs (thyroid - transient hyperthyroidism in HG)
• Ultrasound: to rule out molar pregnancy, multiple gestation

Treatment

• Small, frequent meals; avoid triggers
• Ginger (evidence-based)
• Vitamin B6 (pyridoxine) 25 mg TDS

• Doxylamine + Pyridoxine (Diclegis/Diclectin) - first-line; previously withdrawn due to teratogenicity fears but proven safe and reintroduced
• Antihistamines: promethazine (12.5-25 mg every 4h PO/PR/IV)
• Ondansetron (Zofran): 4-8 mg PO TDS or 8 mg IV; no dystonic reactions; headache is main side effect

• IV fluids: 5% glucose in lactated Ringer's or normal saline (to correct dehydration + reverse ketosis)
• NBM (nil by mouth) initially, then gradual reintroduction of oral fluids once vomiting controlled
• Thiamine (Vitamin B1) supplementation to prevent Wernicke's encephalopathy (a serious complication of prolonged HG)

• Intractable vomiting (not responding to outpatient treatment)
• Persistent ketonuria or electrolyte imbalance after fluid replacement
• Weight loss >10% of pre-pregnancy body weight
• Uncertain diagnosis

Complications of Untreated HG

• Wernicke's encephalopathy (Vitamin B1 deficiency - confusion, nystagmus, ataxia)
• Electrolyte imbalances - hypokalemia can cause cardiac arrhythmias
• Mallory-Weiss tears (mucosal tears at gastroesophageal junction from forceful vomiting)
• Fetal growth restriction (severe cases)

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TOPIC 3: HEMORRHAGE IN PREGNANCY

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A. Antepartum Hemorrhage (APH)

Distribution of APH causes:

• Placenta previa: 7% of APH cases
• Placental abruption: 13%
• Undetermined / local lesions: 80%

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B. Placenta Previa

Definition

• Normal: Placental edge ≥2 cm from internal os
• Low-lying placenta: Placental edge <2 cm from internal os but NOT covering it
• Placenta previa: Placental edge COVERS the internal os

Old classification (still seen in exams): Type I (lateral), Type II (marginal), Type III (partial), Type IV (central/complete)

Incidence & Risk Factors

• Affects ~1 in 200 pregnancies at term (0.5%)
• Risk factors (memory: SCAM-P):
  • Scarring/prior uterine surgery (cesarean section, curettage) - most important
  • Cesarean section history (1 prior CS = 5% risk; >1 prior CS = higher risk)
  • Advanced maternal age (>35 years = 2%; >40 = 5%)
  • Multiparity, prior uterine interventions
  • Placenta previa in prior pregnancy, smoking

Pathogenesis

• Prior endometrial damage leads to poor upper uterine segment endometrium, so the blastocyst implants lower in the uterus
• "Placental migration": The lower segment grows away from the cervix as pregnancy advances, so a low-lying placenta in first trimester often resolves by term (up to 90% of 2nd trimester previews resolve!)

Clinical Features

• Painless, bright red, unprovoked vaginal bleeding (hallmark)
• Bleeding usually stops spontaneously but recurs
• Can occur after intercourse or digital exam
• Uterus is SOFT and non-tender
• Fetal parts may be high/mobile (fetal head not engaged)
• Abnormal lie common (transverse/oblique) due to low-lying placenta

NEVER do a digital vaginal examination in suspected placenta previa - can provoke catastrophic hemorrhage. Only use speculum.

Diagnosis

• Transvaginal Ultrasound (TVUS): Gold standard; more accurate than transabdominal USG
• Follow-up: If previa diagnosed before 32 weeks, repeat USG at 32 weeks; if still present, repeat at 36 weeks

Management

• Admit to labor and delivery
• Hemodynamic assessment + IV access (large bore x2)
• CBC, crossmatch 2-4 units blood, coagulation screen
• Electronic fetal monitoring
• Rh immune globulin for Rh-negative women
• Do NOT perform digital vaginal exam

• Bleeding + ≥36 weeks: Deliver (usually cesarean section)
• Bleeding + <36 weeks + stable: Expectant management (bedrest, monitoring)
• Massive bleeding at any gestation: Emergency CS

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C. Placental Abruption (Abruptio Placentae)

Definition

Types

• Revealed (80%): Blood tracks down between membranes and cervix, exits through vagina - external bleeding visible
• Concealed (20%): Blood collects behind the placenta, no external bleeding - more dangerous
• Mixed: Both

Risk Factors (memory: PAST-HHT)

• Preeclampsia/hypertension (most common association)
• Abdominal trauma
• Smoking, cocaine use
• Thrombophilias
• History of prior abruption (10x increased risk)
• High parity/maternal age
• Twin pregnancy / polyhydramnios (sudden decompression)

Clinical Features

• Painful (severe, constant, board-like uterine pain)
• Dark, mixed blood (if revealed)
• Uterus is hard, tender, "woody" in feel (tetanic contraction)
• Signs of fetal distress (bradycardia, late decelerations)
• Maternal shock out of proportion to visible blood loss (concealed bleeding)
• Can progress to DIC (Disseminated Intravascular Coagulation)

Investigations

• Ultrasound (less sensitive than for previa; up to 50% of abruptions are missed on USG)
• CBC, coagulation profile (PT, aPTT, fibrinogen - DIC screen)
• Kleihauer-Betke test: detects fetal blood cells in maternal circulation

Management

• Mild, preterm, stable: Expectant (hospitalize, monitor closely)
• Severe/fetal distress: Immediate delivery (vaginal if feasible, CS if not)
• Manage DIC aggressively with FFP, platelets, cryoprecipitate

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D. Postpartum Hemorrhage (PPH)

1. Tone (70%) - Uterine atony (uterus fails to contract) - most common cause
2. Tissue (10%) - Retained placenta or placental fragments
3. Trauma (20%) - Genital tract lacerations, uterine rupture, uterine inversion
4. Thrombin (<1%) - Coagulopathy (DIC, inherited disorders)

1. Bimanual compression + uterine massage
2. Oxytocin (IV) - first-line uterotonic
3. Ergometrine / Syntometrine
4. Carboprost (PGF2α) - contraindicated in asthma
5. Misoprostol (sublingual/rectal)
6. Surgical: B-Lynch suture, uterine artery ligation, hysterectomy (last resort)
7. Balloon tamponade (Bakri balloon)
8. Interventional radiology: uterine artery embolization

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TOPIC 4: DEVELOPMENT - PLACENTA, EMBRYO, AMNIOTIC FLUID, UMBILICAL CORD & THEIR ABNORMALITIES

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A. Development of the Placenta

Overview - Week by Week

• Inner cell mass (ICM/embryoblast): Will form the embryo
• Trophoblast (outer layer): Will form the placenta

• Blastocyst implants in the uterine endometrium (now called "decidua" in pregnancy)
• Trophoblast differentiates into:
  • Cytotrophoblast (CTB): Mononuclear, proliferative (the "stem cell" layer)
  • Syncytiotrophoblast (STB): Multinuclear, invasive - invades the decidua and secretes hCG from day 8-10

Chorionic Villi Development - Key stages

1. Primary villi: CTB grows outward, surrounded by STB - solid cellular columns (Week 2)
2. Secondary villi: Extraembryonic mesoderm (ExM) invades the primary villi columns (Week 3)
3. Tertiary villi: Blood vessels form inside villi (angiogenesis begins at 18-20 days); fetal circulation is established by Day 21 - the villi are now fully vascularized (Week 3-4)

Structure of the Mature Placenta

• Disc-shaped, approximately 500g at term, 20 cm diameter, 2.5 cm thick
• Has 2 surfaces:
  • Fetal surface: Smooth, covered by amnion; umbilical cord attaches here; chorion/chorionic plate lies beneath
  • Maternal surface: Raw, lobulated into 15-20 cotyledons; attached to the decidua basalis

Placenta at Term

• Consists of villous tree with massively increased surface area for exchange
• Placental exchange occurs across the vasculosyncytial membrane (STB + CTB + basement membrane + fetal endothelium)
• Exchange by: simple diffusion (O2, CO2), facilitated diffusion (glucose), active transport (amino acids, iron), and pinocytosis (immunoglobulins)

Functions of the Placenta

1. Respiratory - O2/CO2 exchange (fetal Hb has higher O2 affinity than maternal Hb - Bohr effect helps)
2. Nutritional - Glucose, amino acids, fatty acids to fetus
3. Excretory - Fetal metabolic waste (urea, bilirubin) passed to mother
4. Endocrine - Secretes hCG, hPL (human placental lactogen), progesterone, estrogen
5. Immunological - IgG transfer (passive immunity to fetus); also acts as immunological barrier

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B. Embryonic Development

Key Timeline (fertilization age)

The Three Germ Layers and What They Form:

Gastrulation - Key Concept

• Primitive streak appears in the epiblast on Day 14-16 at the posterior end of the embryo disk
• Epiblast cells migrate through the streak, changing from epithelial to mesenchymal cells (EMT)
• This ingression process creates the three germ layers
• The primitive node (at the anterior end of the streak) is the organizer - expresses Shh, FGF, Nodal
• Importantly: left-right asymmetry is established here (cilia at the node create leftward fluid flow)

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C. Amniotic Fluid

Origins and Dynamics

• Amniotic fluid is derived from:
  • Transudation through fetal skin (before keratinization)
  • Secretion from amniotic epithelium
  • Filtration from maternal blood

• Fetal urine becomes the main source of amniotic fluid
• Resorbed mainly by fetal swallowing (~500 mL/day at term)
• Minor resorption via: intramembranous pathway (across fetal membranes directly into fetal vessels)

Normal Volumes:

Functions of Amniotic Fluid:

1. Cushions the fetus from trauma
2. Space for fetal movement - allows normal limb and lung development
3. Lung development - fetal breathing movements with AF essential for lung growth
4. Bacteriostatic - helps maintain sterile intrauterine environment
5. Temperature regulation
6. Fetal diagnosis - amniocentesis for chromosomal/genetic studies

Abnormalities of Amniotic Fluid:

• Causes: (think "fetus can't swallow" or "fetus makes too much urine")
  • Fetal structural anomalies:
    • Esophageal atresia / duodenal atresia (can't swallow AF) - most common fetal cause
    • Anencephaly (failure of swallowing reflex)
    • Tracheo-esophageal fistula
  • Maternal diabetes (fetal hyperglycemia causes osmotic diuresis = more fetal urine)
  • Multiple pregnancy, hydrops fetalis
  • Idiopathic (50%)
• Complications: preterm labour, malpresentation, cord prolapse, PPH (overdistended uterus), maternal respiratory difficulty

• Causes: (think "fetus can't make urine" or "fluid leaks")
  • Renal agenesis (bilateral) = Potter sequence/syndrome (most important cause)
  • Posterior urethral valves (boys) - urinary obstruction
  • PPROM (preterm premature rupture of membranes) - fluid leaks
  • Placental insufficiency / IUGR (fetal hypoxia → kidney vasoconstriction → less urine)
  • Post-term pregnancy (placental aging, reduced perfusion)
• Complications: Potter sequence (pulmonary hypoplasia, limb contractures, flat facies), umbilical cord compression, fetal distress

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D. Umbilical Cord

Normal Development

• The umbilical cord develops from the body stalk (connecting stalk) + yolk stalk + allantois
• The body stalk is formed from extraembryonic mesoderm cells streaming from the caudal end of the embryo to line the trophoblastic cavity
• The allantois (a diverticulum from the hindgut) grows into the body stalk and carries the blood vessels
• The amnion wraps around the entire cord and strongly adheres to it
• By term: cord is ~50-60 cm long and ~1-2 cm thick

Normal Structure of Umbilical Cord (cross-section):

• 2 umbilical arteries (carry deoxygenated blood FROM fetus TO placenta)
• 1 umbilical vein (carries oxygenated blood FROM placenta TO fetus)
• Embedded in Wharton's jelly (gelatinous connective tissue made of mucopolysaccharides - protects the vessels)
• Covered externally by amnion

Memory trick: 2 arteries, 1 vein - "A vein is Valuable, so only one; arteries are Abundant, so two"

Abnormalities of the Umbilical Cord:

• Incidence: ~1% of singleton pregnancies, higher in twins
• Associated with: congenital anomalies in 20-30% (cardiac, renal, chromosomal)
• Screen with detailed anatomy scan and fetal echocardiography

• Short cord (<35 cm): associated with fetal movement restriction, can cause abruption in labour
• Long cord (>100 cm): associated with cord entanglement, true knots, cord prolapse

• Cord descends through cervix ahead of the presenting part after membrane rupture
• Obstetric emergency - cord gets compressed between presenting part and pelvis → fetal hypoxia
• Risk factors: unengaged head, abnormal lie, polyhydramnios, multiparity, long cord, artificial rupture of membranes
• Management: Elevate presenting part manually, emergency CS

• Occur due to fetal movements, associated with long cords and polyhydramnios
• Can tighten during labor → fetal distress/death

• Cord loops around the fetal neck (common - ~25% of deliveries)
• Single loop: usually not clinically significant
• Multiple tight loops: can cause fetal heart rate decelerations in labor

• Cord inserts into the membranes rather than the placental disc
• Vessels travel unprotected through the membranes
• If vessels cross the internal os = Vasa Previa (very dangerous)

• Fetal blood vessels run across the internal cervical os, unprotected by Wharton's jelly or placenta
• If membranes rupture, these vessels tear → fetal exsanguination (massive fetal hemorrhage)
• Hallmark: painless vaginal bleeding at membrane rupture + sudden, severe fetal bradycardia
• APT test (alkali denaturation test) or Kleihauer-Betke: detects fetal Hb in vaginal blood
• Management: Elective CS at 35-36 weeks if diagnosed antenatally (good prognosis if detected)

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E. Placental Abnormalities

• Accreta: Villi attach directly to myometrium (no decidua)
• Increta: Villi invade INTO myometrium
• Percreta: Villi penetrate THROUGH myometrium (can reach bladder/bowel) - most severe
• Risk: Prior cesarean section + placenta previa (scar + low implantation = very high risk)
• Management: Plan for major hemorrhage, often requires hysterectomy

• Extra lobe of placenta separated from the main disc, connected by vessels running through the membranes
• Risk: If this lobe is retained after delivery → PPH; if vessels cross the os → vasa previa

• Fetal surface is smaller than the maternal surface; membranes fold back on themselves at the edge
• Associated with: APH, preterm labour, IUGR

• Chorioangioma: Benign vascular tumor; if large → polyhydramnios, fetal hydrops, preterm labour
• Gestational Trophoblastic Disease (GTD): Hydatidiform mole → can progress to choriocarcinoma

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Quick Revision Summary Table

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• Creasy & Resnik's Maternal-Fetal Medicine: Principles and Practice
• Tietz Textbook of Laboratory Medicine, 7th Edition
• Tintinalli's Emergency Medicine: A Comprehensive Study Guide
• Berek & Novak's GynecologyAll four topics are covered! Here's a quick orientation to what you just got:

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What's Covered - Quick Map

• The placenta previa vs abruption comparison table is almost always in exams
• hCG peaks at 8-10 weeks = ~100,000 IU/L, then falls
• SUA = always screen for other anomalies
• Vasa previa = painless bleed at rupture + sudden fetal bradycardia = emergency CS
• Potter sequence = bilateral renal agenesis → oligohydramnios → pulmonary hypoplasia
• Wernicke's encephalopathy = complication of prolonged HG (give Vitamin B1/thiamine)