The vulva comprises the mons pubis, labia majora, labia minora, clitoris, vestibule, urethral meatus, and Bartholin glands (greater vestibular glands). Bartholin glands are located at 4 and 8 o'clock positions in the posterior vestibule and secrete mucus during sexual arousal; they can become infected causing a Bartholin abscess or cyst. The blood supply to the vulva is from the internal pudendal artery (branch of the internal iliac) and the external pudendal artery (branch of the femoral). Lymphatic drainage from the vulva primarily goes to the superficial inguinal lymph nodes, then to the deep inguinal and pelvic nodes. The vulva is innervated by the pudendal nerve (S2-S4) and the ilioinguinal and genitofemoral nerves. The clitoris is a highly sensitive erectile structure homologous to the penis, with two crura, a body, and a glans covered by the prepuce.

The vagina is a fibromuscular canal 7-10 cm in length extending from the vulva to the cervix, with rugal folds that allow distension during childbirth. It has three layers: mucosa (stratified squamous non-keratinized), muscularis (smooth muscle), and adventitia (connective tissue). The cervix is the lower cylindrical portion of the uterus, divided into the supravaginal portion and the vaginal portion (ectocervix). The ectocervix is covered by stratified squamous epithelium, while the endocervical canal is lined by columnar epithelium; the squamocolumnar junction is the transformation zone where most cervical dysplasia arises. Nabothian cysts are retention cysts of cervical glands and are benign. Cervical mucus changes throughout the menstrual cycle: thin and watery (spinnbarkeit) at ovulation under estrogen effect, and thick and tenacious under progesterone effect. The cervix plays a critical role in maintaining pregnancy through its structural integrity and the mucus plug that provides a barrier against ascending infection.

The uterus is a pear-shaped hollow organ with three layers: perimetrium (outer serosal layer), myometrium (thick smooth muscle layer responsible for contractions during labor and menstruation), and endometrium (inner mucosal layer that undergoes cyclic changes under hormonal influence). The uterus is normally anteverted and anteflexed, positioned over the bladder. Prolapse occurs when the pelvic floor muscles and ligaments weaken, allowing the uterus to descend into the vaginal canal; it is graded I-IV using the POP-Q system. Risk factors for prolapse include vaginal childbirth, advanced age, obesity, chronic constipation, and occupations involving heavy lifting. The uterus is supported by the cardinal (Mackenrodt) ligaments laterally, the uterosacral ligaments posteriorly, and the round ligaments anteriorly. The broad ligament is a peritoneal fold that encloses the uterus, fallopian tubes, and ovaries. The arcuate artery gives rise to radial arteries that penetrate the myometrium and become spiral arteries in the endometrium, which are critical for menstruation and implantation.

The fallopian tubes are divided into four segments from lateral to medial: infundibulum (with fimbriae that capture the oocyte at ovulation), ampulla (the longest segment, site of fertilization), isthmus (narrow segment connecting to the uterus), and interstitial/intramural segment (within the uterine wall). Ectopic pregnancies most commonly implant in the ampulla (~70%), followed by the isthmus (~12%), fimbriae (~11%), and interstitial portion (~2-4%). The ovaries are almond-shaped organs held in position by multiple ligaments: the suspensory ligament (infundibulopelvic ligament) containing the ovarian artery and vein, the utero-ovarian ligament attaching to the uterus, and the mesovarium attaching to the broad ligament. The ovarian artery arises directly from the aorta (L2 level) and anastomoses with the ovarian branch of the uterine artery. The right ovarian vein drains into the IVC, while the left ovarian vein drains into the left renal vein - a difference that explains the higher incidence of left-sided ovarian varices.

The pelvic floor is composed of the levator ani (pubococcygeus, iliococcygeus, puborectalis) and the coccygeus muscles, forming a supportive sling for the pelvic organs. The urogenital diaphragm (perineal membrane) is the anterior compartment. A critical surgical relationship: the ureter passes under the uterine artery approximately 2 cm lateral to the cervix - "water under the bridge" - a landmark essential for preventing ureteric injury during hysterectomy. The menstrual cycle has three phases: follicular (day 1-14, FSH stimulates follicular growth and estradiol production, one dominant follicle emerges), ovulation (day 14, LH surge triggers oocyte release 34-36 hours after onset), and luteal (day 15-28, corpus luteum secretes progesterone, endometrial secretory transformation). Endometrial changes parallel the ovarian cycle: proliferative phase (estrogen-driven glandular proliferation), secretory phase (progesterone-induced glandular coiling and secretion), and menstrual phase (progesterone withdrawal causing spiral artery vasospasm and tissue sloughing). The average menstrual cycle is 28 days (range 21-35), with menstruation lasting 4-6 days and blood loss averaging 30-40 mL (abnormal if >80 mL). Hypothalamic GnRH pulses drive pituitary FSH and LH secretion, modulated by estradiol and progesterone negative and positive feedback. Inhibin B from the dominant follicle selectively suppresses FSH in the late follicular phase.

The breast consists of 15-20 lobules (milk-producing alveoli) drained by lactiferous ducts that open at the nipple. Cooper ligaments (suspensory ligaments) support the breast and attach to the skin and pectoral fascia; invasion by cancer causes peau d'orange (lymphatic obstruction) and dimpling. The axillary tail of Spence extends into the axilla and must be included in breast examination. Lymphatic drainage: ~75% to the axillary nodes (anterior/pectoral, posterior/subscapular, lateral, central, apical), ~20% to the internal mammary nodes, and the remainder to supraclavicular and inframammary nodes. The axillary nodes are the most important sentinel nodes for breast cancer staging. The female breast responds to cyclic hormonal changes: estrogen stimulates ductal growth, progesterone stimulates lobular development. Hymen variants include annular, crescentic, cribriform, septate, imperforate (causing hematocolpos and primary amenorrhea). Uterine malformations (Mullerian anomalies) include septate uterus (most common, associated with recurrent pregnancy loss), bicornuate uterus, didelphys uterus (double uterus and cervix, often with longitudinal vaginal septum), unicornuate uterus (associated with renal agenesis on the contralateral side), and arcuate uterus (most benign, usually incidental).

Human chorionic gonadotropin (hCG) is produced by the syncytiotrophoblast and can be detected in serum as early as 8-10 days after conception, with a doubling time of approximately 48-72 hours in early pregnancy until reaching 1000-2000 mIU/mL, after which the doubling time slows to ~96 hours. Urine pregnancy tests detect hCG at levels as low as 20-50 mIU/mL and are typically positive by the first missed menstrual period. Serum beta-hCG is quantitative and useful for monitoring early pregnancy viability and ectopic pregnancy evaluation. Transvaginal ultrasound can visualize a gestational sac at 5 weeks (hCG ~1500-2000 mIU/mL), a yolk sac at 5.5 weeks, a fetal pole with cardiac activity at 6-6.5 weeks. The discriminatory zone is the hCG level above which a gestational sac should be visible (typically 1500-2000 mIU/mL for transvaginal ultrasound); absence of an intrauterine gestational sac above this level raises concern for ectopic pregnancy or early pregnancy failure.

Accurate pregnancy dating is essential for management throughout gestation. By LMP (Naegele's rule): EDD = LMP + 280 days (40 weeks). First-trimester ultrasound with crown-rump length (CRL) is the most accurate method, with an accuracy of +/-5-7 days when performed between 9 and 13 weeks. If the discrepancy between LMP dating and CRL dating exceeds 7 days in the first trimester, the ultrasound date should be used. In the second trimester (14-27 weeks), dating uses head circumference (HC), biparietal diameter (BPD), femur length (FL), and abdominal circumference (AC); accuracy is +/-10-14 days. In the third trimester (≥28 weeks), accuracy decreases to +/-21-30 days. AC is the best single parameter for estimating fetal weight. The Hadlock formula is most commonly used for estimated fetal weight (EFW) calculation.

Standard prenatal visits follow a prescribed schedule: every 4 weeks until 28 weeks, then every 2 weeks from 28 to 36 weeks, then weekly from 36 weeks to delivery. The first prenatal visit includes comprehensive history, physical exam (including pelvic exam if indicated), dating ultrasound, baseline labs (CBC, blood type and Rh, antibody screen, rubella IgG, syphilis RPR, HIV, hepatitis B surface antigen, urinalysis and culture, Pap smear if due, and GC/CT screening). Subsequent visits include serial fundal height measurement (McDonald's rule: cm from pubic symphysis to fundus = weeks' gestation after 20 weeks), fetal heart rate auscultation, blood pressure measurement, urine dipstick for protein and glucose, Leopold maneuvers for presentation, and symptom review. GBS screening (rectovaginal swab) is performed at 35-37 weeks. Cervical length screening by transvaginal ultrasound is recommended at 18-22 weeks for women with prior spontaneous preterm birth.

First-trimester combined screening (11-14 weeks) includes nuchal translucency (NT) ultrasound, serum PAPP-A, and free beta-hCG. Increased NT (≥3.5 mm) is associated with trisomy 21, 18, 13, Turner syndrome, and cardiac anomalies. Cell-free fetal DNA (NIPT/cfDNA) screens for trisomies 21, 18, 13 and sex chromosome aneuploidies with >99% sensitivity for trisomy 21; it is the most sensitive non-invasive screen but remains a screening test - positive results require diagnostic testing (CVS or amniocentesis). Second-trimester quad screen (15-20 weeks) measures AFP, hCG, uE3, and inhibin A; abnormal patterns suggest trisomy 21 (decreased AFP, decreased uE3, increased hCG, increased inhibin A), trisomy 18 (decreased all), or neural tube defect (increased AFP). The anatomic survey (18-22 weeks) evaluates fetal anatomy including brain, spine, heart, chest, abdomen, kidneys, extremities, and placenta. Elevated MSAFP (≥2.5 MoM) requires targeted ultrasound and consideration of amniocentesis.

Universal screening for GDM is performed at 24-28 weeks. The two-step approach: a 50g oral glucose challenge test (non-fasting) with plasma glucose at 1 hour. A value ≥130-140 mg/dL is positive and requires the diagnostic 3-hour 100g OGTT. Carpenter-Coustan criteria: two or more values met or exceeded (fasting ≥95, 1h ≥180, 2h ≥155, 3h ≥140 mg/dL). Cardiovascular changes: cardiac output increases ~40%, heart rate increases 10-15 bpm, SVR decreases. Plasma volume increases ~50% while RBC mass increases only ~25%, producing physiologic anemia (Hb nadir ~10-11 g/dL at 28-32 weeks). Respiratory: tidal volume increases ~40%, PaCO2 decreases to ~28-32 mmHg (compensated respiratory alkalosis). Renal: GFR increases ~50% (serum creatinine decreases to 0.5-0.7 mg/dL), glycosuria is common. Hematologic: WBC count increases, pregnancy is a prothrombotic state. Tdap is recommended at 27-36 weeks every pregnancy. Rho(D) immune globulin (Rhogam) 300 mcg IM is administered at 28 weeks gestation and within 72 hours after any bleeding episode, invasive procedure, or delivery of an Rh-positive infant.

Gestational hypertension is new-onset BP ≥140/90 after 20 weeks without proteinuria or end-organ dysfunction. Preeclampsia is gestational hypertension with proteinuria (≥300 mg/24h or protein/creatinine ratio ≥0.3) or new-onset end-organ dysfunction: thrombocytopenia (<100,000), renal insufficiency (Cr >1.1 or doubling), elevated liver transaminases (2x normal), pulmonary edema, or cerebral/visual symptoms. Severe features: BP ≥160/110, severe headache, visual scotomata, RUQ/epigastric pain, progressive thrombocytopenia. Eclampsia is generalized seizures not attributable to other causes. Delivery is the definitive treatment. Antihypertensives for BP ≥160/110: labetalol 20-40 mg IV, hydralazine 5-10 mg IV, or nifedipine 10-20 mg PO. Magnesium sulfate for seizure prophylaxis: 4-6 g IV loading then 1-2 g/h for 24 hours postpartum.

HELLP syndrome is a variant of severe preeclampsia with Hemolysis (schistocytes, LDH >600, low haptoglobin), Elevated Liver enzymes (AST/ALT ≥70), and Low Platelets (<100,000/uL). Occurs in ~10-20% of severe preeclampsia. Importantly, 15-20% of patients with HELLP do not have hypertension or proteinuria at presentation. Management: delivery regardless of gestational age after maternal stabilization and betamethasone 12 mg IM q24h x2. Platelet transfusion if <20,000-50,000 (before cesarean). Complications include DIC (20-40%), abruptio placentae, acute renal failure, pulmonary edema, subcapsular liver hematoma, and liver rupture. Recovery typically begins 24-48 hours after delivery.

GDM affects ~6-9% of pregnancies, caused by placental hormone-induced insulin resistance. Management: medical nutrition therapy, self-monitoring of blood glucose (fasting ≤95, 1h ≤140, 2h ≤120 mg/dL), and pharmacotherapy if targets not achieved. Insulin is first-line. Metformin is second-line (crosses placenta). Glyburide has higher failure rates and increased macrosomia risk. Fetal surveillance includes twice-weekly NST/AFI. Delivery timing: 39-40 weeks if well-controlled on diet; 39 weeks if on medication; earlier if poorly controlled. Neonatal complications: macrosomia, shoulder dystocia, neonatal hypoglycemia, polycythemia, hyperbilirubinemia, and RDS.

Twins classified by zygosity (dizygotic ~70%, monozygotic ~30%) and chorionicity. Dizygotic are always dichorionic-diamniotic (DCDA). Monozygotic splitting: 0-3 days DCDA (~30%), 4-8 days MCDA (~70%), 8-12 days MCMA (~1%), >12 days conjoined. First-trimester US: lambda sign = dichorionic, T-sign = monochorionic. Complications: preterm labor, preeclampsia (2-3x risk), TTTS in MCDA twins (Quintero staging I-V), IUGR, malpresentation. TTTS management: amnioreduction, laser photocoagulation (Solomon technique). Delivery timing: DCDA 38-39w, MCDA 36-37w, MCMA 32-34w.

Preterm labor: regular contractions with cervical change between 20-36+6 weeks. Management: betamethasone 12 mg IM q24h x2 (24-34w), MgSO4 neuroprotection (<32w), tocolysis (nifedipine, indomethacin, terbutaline) to allow steroid course. PPROM: <34w expectant management with ampicillin + erythromycin for 7 days; ≥34w delivery. IUGR (FGR) is EFW <10th percentile. Umbilical artery Doppler: AREDF indicates severe compromise. MCA Doppler: brain-sparing effect. Management: serial growth scans, BPP/NST, delivery based on Doppler status (normal UA: 37-38w; AREDF: 32-34w with steroids). Polyhydramnios (AFI ≥25): causes include idiopathic, maternal DM, TTTS, fetal GI obstruction. Oligohydramnios (AFI ≤5): causes include ROM, placental insufficiency, renal anomalies, post-term.

First stage: latent (0-6 cm) and active (≥6 cm). Friedman curve: active phase ~1 cm/hr in nulliparas, ~1.2 cm/hr in multiparas. Contemporary data (Zhang) suggests slower active phase is acceptable. Second stage: full dilation to delivery. Nulliparas may push up to 4 hours (3 with epidural), multiparas up to 3 hours (2 with epidural). Cardinal movements: engagement, descent, flexion, internal rotation, extension, external rotation, expulsion. Third stage: placental delivery (Schultze vs Duncan). Active management (oxytocin + controlled cord traction + uterine massage) reduces PPH risk by ~60%. Fourth stage: first 1-2 hours postpartum, monitoring for PPH.

Indications: post-term (≥41-42w), PPROM, preeclampsia, IUGR, GDM, oligohydramnios, macrosomia, fetal demise, chorioamnionitis. Bishop score assesses cervical favorability (≥6-8 predicts success). Ripening methods: prostaglandins (PGE1 misoprostol 25 mcg PV q4-6h, PGE2 dinoprostone), mechanical (Foley bulb 30-60 mL), osmotic dilators. Oxytocin: start 1-2 mU/min, increase by 1-2 q15-30min for 200-250 Montevideo units. Contraindications: placenta previa, vasa previa, transverse lie, prior classical cesarean, active HSV, cord presentation. Failed induction: failure to enter active phase after 24h of oxytocin with ruptured membranes.

NICHD three-tier system: Category I (normal): baseline 110-160 bpm, moderate variability 6-25 bpm, no late/variable decels. Category II (indeterminate). Category III (abnormal): absent variability + recurrent late decels/variable decels/bradycardia/sinusoidal. Early decelerations: head compression, benign. Late decelerations: uteroplacental insufficiency. Variable decelerations: cord compression. Management of Category II/III: position change, IV fluids, oxygen, reduce/stop oxytocin, terbutaline for tachysystole, fetal scalp stimulation. If Category III persists: expedite delivery.

Non-pharmacologic: hydrotherapy, positioning, doula support, nitrous oxide (50% N2O/O2). Pharmacologic: epidural (local anesthetic + opioid) provides excellent relief; CSE offers faster onset. Parenteral opioids: meperidine, fentanyl, nalbuphine - all cross placenta. Meperidine avoid within 2-4h of delivery (neonatal respiratory depression). Complications of epidural: hypotension (IV fluids + ephedrine/phenylephrine), post-dural puncture headache (blood patch), prolonged second stage. Epidural does not increase cesarean rate.

Common indications: prior cesarean, arrest disorders, malpresentation, non-reassuring fetal status, placenta previa, failed induction. Pfannenstiel incision most common. Low transverse uterine incision preferred for VBAC. Complications: infection, hemorrhage, thromboembolism, bladder/bowel/ureter injury. VBAC success rate ~60-80%. Contraindications to TOLAC: prior classical incision, uterine rupture history, >2 prior cesareans. Uterine rupture risk ~0.5-1% for TOLAC with one prior low transverse incision; presents with fetal bradycardia (most common sign). Management: immediate laparotomy, delivery, repair or hysterectomy.

Impaction of anterior shoulder against pubic symphysis. Incidence 0.6-1.4%. Turtle sign: head retracts against perineum. HELPERR: H-Help, E-Evaluate for episiotomy, L-Legs (McRoberts), P-suprapubic Pressure (NOT fundal), E-Enter internal maneuvers (Rubin, Woods corkscrew, delivery posterior arm), R-Roll (Gaskin all-fours). Last resort: Zavanelli maneuver (cephalic replacement + emergency cesarean), intentional clavicular fracture, symphysiotomy. Never apply fundal pressure.

PPH is the leading cause of maternal mortality globally, defined as cumulative blood loss ≥1000 mL or signs of hypovolemia. The 4 Ts: Tone (uterine atony, ~70%, most common), Trauma (lacerations, uterine rupture, episiotomy), Tissue (retained placenta, invasive placentation), Thrombin (coagulopathy, DIC). Stepwise management: Step 1: call for help, ABCs, large-bore IV, fluid resuscitation, type and cross, massive transfusion protocol (1:1:1 RBC:FFP:platelets). Step 2: uterine massage, bimanual compression, oxytocin (10-40 IU in 1L NS). Step 3: second-line uterotonics: methylergonovine (Methergine) 0.2 mg IM, carboprost (Hemabate) 250 mcg IM q15min, misoprostol 600-1000 mcg PR/SL. Step 4: intrauterine balloon (Bakri, 300-500 mL). Step 5: surgical interventions (B-Lynch suture, uterine artery ligation, UAE). Step 6: hysterectomy. Tranexamic acid 1g IV within 3h reduces death (WOMAN trial).

HELPERR: H-Help (mobilize anesthesia, neonatology, nursing). E-Evaluate for episiotomy (generous mediolateral). L-Legs (McRoberts: hyperflex maternal thighs onto abdomen). P-suprapubic Pressure (NOT fundal pressure). E-Enter internal maneuvers: Rubin I/II (rotate anterior shoulder), Woods corkscrew (rotate posterior shoulder 180 degrees), delivery of posterior arm (sweep arm across chest). R-Roll (Gaskin all-fours). If all fail: Zavanelli maneuver (cephalic replacement + emergency cesarean), intentional clavicular fracture, symphysiotomy. Document all maneuvers and times.

Eclampsia seizure: maintain airway, O2, prevent aspiration, lateral positioning. MgSO4 4-6g IV load + 1-2g/h for 24h. If recurrent seizures: additional MgSO4 bolus 2g or lorazepam 2-4mg IV. Monitor toxicity: DTRs, RR, urine output; calcium gluconate 1g IV as reversal. Antihypertensives for BP ≥160/110: labetalol 20mg IV, hydralazine 5-10mg IV, or nifedipine 10-20mg PO. Goal BP 140-155/90-105. Delivery is definitive. Complications: abruption, DIC, pulmonary edema, renal failure, hepatic rupture, intracerebral hemorrhage, PRES.

Risk factors: malpresentation, preterm, polyhydramnios, PROM, low station, multiple gestation, obstetric manipulation. Diagnosis: palpable cord in vagina + sudden fetal bradycardia. Emergency management: call for help, knee-chest/Trendelenburg position, manually elevate presenting part off cord, tocolysis (terbutaline 250 mcg SQ), fill bladder with 500-1000 mL NS. Definitive: if fully dilated and imminent delivery, operative vaginal; otherwise emergency cesarean. Prognosis depends on time from prolapse to delivery and degree of cord compression.

AFE: rare (1-8/100,000), catastrophic, 20-60% maternal mortality. Fetal material enters maternal circulation triggering anaphylactic and procoagulant response. Triad: sudden cardiovascular collapse, DIC, respiratory distress during labor/postpartum. Management: supportive, CPR with left uterine displacement, early intubation, aggressive fluid/vasopressors, massive transfusion, ECMO for refractory arrest. Perimortem cesarean within 4-5 minutes if no ROSC. Placental abruption: premature separation, presents with vaginal bleeding (may be concealed), abdominal pain, uterine hypertonicity, fetal distress. Management based on maternal/fetal status and gestational age. Uterine inversion: Johnson maneuver to push fundus through cervix, tocolytics for cervical relaxation, O'Sullivan hydrostatic technique if needed.

The postpartum period spans delivery through 6-12 weeks. Lochia evolves: rubra (bright red, 1-4 days), serosa (pinkish-brown, 5-9 days), alba (yellowish-white, day 10 to 2-6 weeks). Uterine involution: fundus descends ~1 cm/day, non-palpable by 2 weeks. Afterpains more pronounced in multiparas and during breastfeeding (oxytocin). Vital signs: mild temperature elevation to 38C in first 24h is physiologic. Postpartum blues ("baby blues") affects 40-80%: transient mood lability, tearfulness, irritability beginning 2-3 days postpartum, resolving by day 10-14. The postpartum visit at 6 weeks includes BP, wound healing, depression screening (EPDS), contraceptive counseling.

Prolactin is the primary hormone for milk production; oxytocin is responsible for milk let-down reflex. Exclusive breastfeeding recommended for first 6 months, continued through at least 1 year with complementary foods. Contraindications: maternal HIV (resource-rich settings), active TB, HTLV-1/2, active breast HSV lesions, certain medications (chemotherapy, radioactive compounds), infant galactosemia. Mastitis occurs in 5-10%, typically from milk stasis + S. aureus. Treatment: continue breastfeeding/pumping, antibiotics (dicloxacillin 500 mg QID or cephalexin 500 mg QID for 10-14 days). Breast abscess requires US-guided aspiration or I&D.

PPD affects 10-15% of women, onset within first year. Risk factors: prior depression, depression in pregnancy, poor social support, preterm birth, NICU admission. Screening with EPDS at 6 weeks (score ≥10-13 suggests evaluation). Treatment: CBT/IPT for mild-moderate; SSRIs (sertraline, fluoxetine) first-line pharmacotherapy, safe in breastfeeding. Postpartum psychosis: severe emergency affecting 0.1-0.2%, typically within 2 weeks of delivery. Hallucinations, delusions (often about infant), bizarre behavior, high infanticide risk. Emergency psychiatric hospitalization. Treatment: mood stabilizers (lithium), antipsychotics, ECT for severe. Women with bipolar disorder at highest risk.

Recognition is critical; visual estimation underestimates by 30-50%. Use quantitative measurement. Stepwise: (1) Bimanual massage, explore for retained products or uterine rupture. (2) Oxytocin 10 IU slow IV or 10-40 IU in 1L NS infusion. (3) Second-line uterotonics: methylergonovine 0.2 mg IM (avoid if HTN), carboprost 250 mcg IM (avoid if asthma), misoprostol 600-1000 mcg SL/PR. (4) Intrauterine balloon (Bakri, 300-500 mL, ~85% success). (5) Compression sutures (B-Lynch, Hayman). (6) Uterine artery ligation or UAE. (7) Hysterectomy as life-saving last resort. Tranexamic acid 1g IV within 3 hours reduces PPH death.

Lactational amenorrhea (LAM): >98% effective in first 6 months if exclusive breastfeeding, amenorrheic, <6 months. Progestin-only methods safe immediately: POP, DMPA, implant. IUDs can be inserted immediately after delivery (higher expulsion ~10-15%) or delayed to 4-6 weeks. Copper IUD and LNG-IUD both options. Combined hormonal contraceptives (estrogen-containing) may decrease milk supply; avoid first 3-4 weeks (no VTE risk) or 6 weeks (with VTE risk). Sterilization: postpartum tubal ligation (minilaparotomy) within 48h, or interval laparoscopy at 6-8 weeks. Vasectomy for male partner.

Perineal lacerations: first-degree (skin), second-degree (muscles), third-degree (anal sphincter), fourth-degree (rectal mucosa). Episiotomy: mediolateral preferred. Post-repair care: ice packs, sitz baths, NSAIDs, stool softeners. Cesarean wound care: keep incision dry, remove dressing at 24h, shower allowed after 48h. Monitor for seroma, hematoma, infection (erythema, purulent drainage, fever). Wound infection rate 3-15%, treat with opening, wound culture, antibiotics (cover MRSA + gram negatives + anaerobes). Prophylactic cefazolin 2-3g IV before incision reduces infection by ~60%.

Primary amenorrhea: no menarche by age 15 with secondary sexual characteristics, or by 13 without. Causes with uterus present: hypothalamic (functional hypothalamic amenorrhea from stress, low weight, exercise), pituitary (prolactinoma, Sheehan), ovarian (gonadal dysgenesis/Turner, POI), thyroid, outflow tract obstruction (imperforate hymen), PCOS. Without uterus: Mullerian agenesis (MRKH, 46,XX, normal secondary sex characteristics) and androgen insensitivity syndrome (AIS, 46,XY, absent uterus, blind vaginal pouch). Secondary amenorrhea: no menses for 3 cycles or 6 months. Most common cause: pregnancy (check hCG first). Other causes: hypothalamic (~35%), PCOS, POI, hyperprolactinemia, thyroid disorders, Asherman syndrome (intrauterine adhesions from D&C). Workup: hCG, FSH, LH, TSH, prolactin. FSH >40 suggests ovarian failure. Progestin challenge: withdrawal bleed indicates adequate estrogen and patent outflow tract.

AUB is deviation from normal menstrual parameters. PALM (structural): Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia. COEIN (non-structural): Coagulopathy (VWD most common), Ovulatory dysfunction (PCOS, perimenopausal, thyroid/prolactin), Endometrial, Iatrogenic (anticoagulants, hormonal contraceptives), NOS. Evaluation: CBC, ferritin, TSH, prolactin, hCG, coagulation screen. TVUS first-line imaging. SIS for focal pathology. Endometrial biopsy indicated in women ≥45, and younger with risk factors (obesity, PCOS, tamoxifen, Lynch, persistent anovulatory bleeding). Management depends on cause: hormonal therapy (OCPs, progestins, LNG-IUD), tranexamic acid (reduces bleeding ~40%), NSAIDs, endometrial ablation (completed childbearing), hysterectomy (definitive).

PCOS affects 6-12%, most common cause of anovulatory infertility. Diagnosis: 2 of 3 Rotterdam criteria: (1) oligo/anovulation, (2) clinical/biochemical hyperandrogenism, (3) PCO morphology on US (≥20 follicles/ovary and/or volume ≥10 mL). Exclude: thyroid disease, hyperprolactinemia, NCAH (17-OHP), Cushing. Associated: insulin resistance (50-70%), obesity, impaired glucose tolerance, T2DM (3-7x risk), dyslipidemia, NAFLD. Management: lifestyle (5-10% weight loss restores ovulation in 30-50%), COCs (cycle regulation, hirsutism, endometrial protection), metformin (insulin sensitivity), spironolactone (hirsutism). Fertility: letrozole (first-line, higher live birth than clomiphene), metformin adjunct, gonadotropins. Long-term: endometrial cancer prevention, CVD risk, T2DM screening every 1-3 years.

Primary dysmenorrhea: painful menses without pelvic pathology, begins 6-12 months after menarche. Prostaglandin-mediated myometrial contractions. Symptoms: cramping lower abdominal pain radiating to back/thighs, N/V, diarrhea. Treatment: NSAIDs (ibuprofen, naproxen, mefenamic acid) started at onset, continued 1-2 days. OCPs as second-line. Secondary dysmenorrhea: from underlying pathology (endometriosis, adenomyosis, fibroids, PID). Onset years after menarche (>25). Suspicious: progressive worsening, pre/post-menstrual pain, dyspareunia, AUB, infertility. Diagnosis: history, TVUS, laparoscopy if endometriosis suspected.

PMS affects 20-30%: physical and affective symptoms in luteal phase, resolve within 4 days of menses. PMDD (3-8%): severe affective symptoms (depressed mood, anxiety, affective lability, anger/irritability) with functional impairment. Diagnosis requires prospective daily symptom charting for 2 cycles. First-line for PMDD: SSRIs/SNRIs (sertraline, fluoxetine, paroxetine) continuously or luteal phase only. SSRIs work faster in PMDD (within days). COCs with drospirenone (24/4 regimen) also effective. GnRH agonists with add-back for severe refractory. Lifestyle: exercise, diet, CBT, calcium 1200 mg/day, vitamin B6, magnesium.

Menorrhagia is >80 mL blood loss per cycle: changing pads/tampons every 1-2h, large clots, flooding. PBAC score ≥100 suggests HMB. Workup: CBC, ferritin, TSH, coagulation panel, TVUS, SIS, endometrial biopsy if indicated. Medical management: LNG-IUD (Mirena, first-line, reduces blood loss 70-90%), tranexamic acid 1.3g PO TID during menses, NSAIDs, COCs, oral progestins. Surgical: endometrial ablation (completed childbearing, benign pathology), myomectomy (fibroids), hysterectomy (definitive). LNG-IUD candidacy: excellent for HMB and contraception. Safe in nulliparous women and adolescents. Ideal for endometrial protection in PCOS, obesity, tamoxifen users.

COCs contain ethinyl estradiol (10-35 mcg) + progestin. Mechanisms: ovulation inhibition, thickened cervical mucus, endometrial atrophy. Non-contraceptive benefits: regulate cycles, reduce dysmenorrhea, improve acne, reduce ovarian cancer risk (~50%), endometrial cancer risk (~50%), colorectal cancer, and PID. Risks: VTE (increased 3-4x, highest in first year, absolute risk ~3-10 per 10,000 woman-years), arterial thrombosis (MI, stroke - especially smokers >35 and migraine with aura), breast cancer (slight increase, RR ~1.2), cervical cancer, hepatic adenoma. WHO Category 4 contraindications: age ≥35 + smoking ≥15/day, uncontrolled HTN (≥160/100), migraine with aura, current/past VTE, known thrombophilia, ischemic heart disease/stroke, complicated valvular disease, active liver disease, breast cancer.

POP/minipill: norethindrone 0.35 mg or drospirenone 4 mg; mechanism: thickens cervical mucus, may impair ovulation. Must take at same time daily (<3h window for norethindrone). Safe in breastfeeding. DMPA (Depo-Provera): 150 mg IM q12-13wk; ovulation inhibition; typical failure <0.2%. Side effects: irregular bleeding, weight gain (2-5 kg/yr), bone density concern (duration-limited to 2 years in FDA labeling; WHO no restriction). Return to fertility delayed 9-12 months. Implant (Nexplanon): single rod, 3-5 years, failure rate <0.05%. Side effects: irregular bleeding (60-80%), amenorrhea ~20%, mood changes. Immediate return to fertility upon removal.

LARC methods (IUDs and implant) are most effective reversible contraceptives (failure <1%). LNG-IUDs: Mirena (52 mg LNG, 7-8 years, FDA-approved for HMB), Kyleena (19.5 mg, 5 years), Skyla (13.5 mg, 3 years). Mechanisms: endometrial atrophy, thickened cervical mucus, impaired sperm motility. Mirena reduces menstrual blood loss by 70-90% at 3-6 months. Copper IUD (Paragard T380A): non-hormonal, 10-12 years, also emergency contraception (up to 5 days). Side effects: heavier/longer menses, dysmenorrhea. Complications: perforation (~1-2/1000), expulsion (2-10%, highest immediate postpartum), PID (first 21 days after insertion in at-risk). Safe in nulliparous, adolescents, postpartum (including immediate post-placental insertion).

Three methods: levonorgestrel (Plan B), ulipristal acetate (Ella), copper IUD. LNG-EC (Plan B): 1.5 mg single dose, effective within 72h (some efficacy to 120h), OTC. Mechanism: inhibits or delays ovulation. Efficacy reduced if BMI >25; may be ineffective if BMI >30. Ulipristal (Ella): 30 mg single dose, effective within 120h, prescription needed. Progesterone receptor modulator, can delay ovulation after LH surge. Superior to LNG-EC at all time points; maintains efficacy across BMI (though reduced if BMI >35). Copper IUD: >99% effective, up to 5 days after UPSI, provides ongoing contraception. LNG-IUD may also be used as EC. EC does not interrupt established pregnancy.

Male condoms: typical failure ~13% (perfect ~2%). Advantages: STI protection (HIV, GC, CT, HSV, HPV, trichomonas), no hormones, low cost. Female condom: failure ~21%. Diaphragm/cervical cap: used with spermicide, failure ~12-17%. Spermicide alone (nonoxynol-9): failure ~21-28%; frequent use may increase HIV transmission. Sterilization: tubal ligation (failure ~0.5%/5yr). Methods: postpartum minilaparotomy (Pomeroy), interval laparoscopy (rings/clips, bipolar cautery, salpingectomy). Salpingectomy reduces ovarian cancer risk (~30-50% for high-grade serous) and is increasingly recommended. Vasectomy: outpatient, no-scalpel technique, failure ~0.15%. Confirm azoospermia at 2-3 months or 20 ejaculations before relying on it. Reversal possible but not guaranteed. Counsel about LARC as equally effective, reversible alternative.

WHO MEC provides evidence-based guidance (categories 1-4). Quick Start: start hormonal contraception immediately at the visit if pregnancy reasonably excluded. COCs/POPs: start immediately, backup 7 days. DMPA: immediate, no backup if within first 7 days. IUDs/implant: any time if pregnancy excluded. "LARC first" approach: offer IUDs or implant as first-line for most women including adolescents (highest efficacy, safety, satisfaction). Discontinuation: fertility returns immediately (except DMPA: delayed up to 9-12 months). Counseling about common myths: IUDs safe in nulliparous and adolescents; do not cause infertility; do not migrate.

Candida: C. albicans (~80-90%), thick white discharge, itching, KOH + pseudohyphae, pH ≤4.5. Treatment: azoles topical or fluconazole 150 mg PO x1. Recurrent: fluconazole 150 mg q72h x2-3 then weekly x6 months. BV: thin gray discharge, fishy odor, clue cells, pH >4.5, positive Whiff test. Treatment: metronidazole 500 mg PO BID x7d or metronidazole gel or clindamycin cream. Recurs ~30-50% in 3 months. Trichomonas: frothy yellow-green discharge, strawberry cervix, motile trichomonads on wet mount. Treatment: metronidazole 2g PO x1 or 500 mg BID x7d. Treat partner. Avoid alcohol.

Chlamydia: most common reported STI (~1.8M/yr US). Often asymptomatic (70-80%). Symptoms: mucopurulent cervicitis, dysuria, postcoital bleeding. Diagnosis: NAAT (urine, vaginal, cervical swab). Treatment: doxycycline 100 mg PO BID x7d (preferred) or azithromycin 1g x1. Screen all sexually active women <25 annually. Complications: PID, Fitz-Hugh-Curtis, infertility, ectopic pregnancy. Gonorrhea: gram-negative intracellular diplococci. Often co-infects. Treatment: ceftriaxone 500 mg IM x1 (1g if ≥150 kg) plus treatment for chlamydia. DGI: ceftriaxone 1g IV q24h + azithromycin 1g. Emerging resistance: avoid cefixime and azithromycin monotherapy.

Polymicrobial infection of upper genital tract. Minimum diagnostic criteria: cervical motion tenderness, uterine tenderness, or adnexal tenderness. Additional criteria: fever ≥38.3C, mucopurulent discharge, elevated ESR/CRP, GC/CT positive. Outpatient treatment: ceftriaxone 500 mg IM x1 + doxycycline 100 mg PO BID x14d + metronidazole 500 mg PO BID x14d. Inpatient indications: severe illness, N/V, pregnancy, failed outpatient, TOA, immunocompromised. Inpatient regimen: cefoxitin 2g IV q6h + doxycycline 100 mg IV/PO BID, then PO to complete 14d. Complications: TOA, infertility (risk ~10% after first episode, ~50% after third), ectopic pregnancy (6-10x risk), chronic pelvic pain (~20%). Fitz-Hugh-Curtis: perihepatitis with "violin-string" adhesions.

Low-risk HPV (6, 11) cause genital warts; high-risk (16, 18, 31, 33, 45, 52, 58) cause cervical, vulvar, vaginal, anal, oropharyngeal cancers. 90% of infections clear within 2 years. Persistent high-risk HPV is necessary for cervical carcinogenesis. Genital warts: patient-applied (podofilox, imiquimod, sinecatechins) or provider-administered (cryotherapy, TCA, excision). Cervical screening (USPSTF): start at 25. Ages 25-65: primary HPV q5y (preferred) or co-testing q5y or Pap q3y. ASCCP guidelines: HPV 16/18+ with any cytology, HPV+ ASC-US, HPV+ LSIL all require colposcopy. CIN2/3: LEEP or cold knife cone. HPV vaccine (Gardasil 9): 9-valent, recommended 11-12 (2 doses if <15, 3 if ≥15 or immunocompromised), catch-up to 26, shared decision 27-45.

Universal opt-out HIV screening at first prenatal visit, repeat in third trimester for high-risk. All HIV+ pregnant women should be on ART regardless of CD4 (goal VL <50 at delivery). Preferred regimens: TDF/FTC or ABC/3TC + DTG or RAL. Scheduled cesarean at 38w if VL >1000 at 36w. Avoid internal fetal monitoring, artificial ROM, episiotomy if viremic. Breastfeeding contraindicated in resource-rich settings. Infant: AZT prophylaxis for 4-6 weeks. Infant HIV testing by PCR at birth, 2-4w, 6-8w, 4-6m, 12-18m.

Genital HSV: primary infection near term has highest neonatal transmission risk (~30-50% vs <1-3% for recurrent). Acyclovir 400 mg PO TID or valacyclovir 500 mg PO BID starting at 36w reduces recurrence and need for cesarean. Cesarean if active genital lesions or prodromal symptoms at delivery. Neonatal HSV: high-dose IV acyclovir. Syphilis: screen all pregnant women at first visit (RPR/VDRL). Treatment: benzathine penicillin G 2.4 million units IM x1 (early) or weekly x3 (late/latent). Penicillin desensitization if allergic. Congenital syphilis: stillbirth, hydrops, neonatal death; treatment: IV aqueous penicillin G 50,000 U/kg q12h x7d then q8h x3d (total 10d).

Endometriosis affects 6-10% of reproductive-age women, up to 50% with infertility, and ~70% with chronic pelvic pain. Implantation sites: ovaries (endometriomas, "chocolate cysts"), uterosacral ligaments, pouch of Douglas, rectovaginal septum, bladder, bowel. Sampson theory: retrograde menstruation. Symptoms: dysmenorrhea (progressive), dyspareunia (deep), infertility, dyschezia, dysuria, chronic pelvic pain, fatigue. Diagnosis: TVUS (endometrioma: ground-glass cyst with low-level echoes, no papillary projections). MRI for deep infiltrating disease. Laparoscopy with histology is gold standard. Staging: rASRM I-IV. Treatment: NSAIDs, COCs (cyclic or continuous), progestins (norethindrone acetate, DMPA, LNG-IUD), GnRH agonists (leuprolide with add-back), GnRH antagonists (elagolix, relugolix), aromatase inhibitors. Surgical: laparoscopic excision (gold standard), ablation, presacral neurectomy, hysterectomy with BSO (definitive for severe refractory). Fertility: excision improves spontaneous pregnancy rates; IVF often needed.

Affect 70-80% by age 50, higher in African American women. Classification: submucosal (heavy bleeding, infertility), intramural (menorrhagia, bulk symptoms), subserosal (pressure, torsion). Symptoms: menorrhagia, dysmenorrhea, pelvic pressure, urinary frequency, constipation, infertility. Diagnosis: TVUS first-line, SIS for submucosal, MRI for pretreatment mapping. Management: asymptomatic: observation. Medical: NSAIDs, tranexamic acid, COCs, LNG-IUD, GnRH agonists (shrink fibroids ~40-50%). Surgical: myomectomy (abdominal, laparoscopic, hysteroscopic) for fertility preservation. UAE (uterine artery embolization): reduces volume 40-60%. MRgFUS: thermal ablation. Hysterectomy: definitive. Pregnancy: growth in first trimester, red degeneration (conservative management), malpresentation, PPH risk. Myomectomy during cesarean avoided.

Ectopic endometrial tissue within myometrium causing smooth muscle hyperplasia. Affects multiparous women aged 40-50, but increasingly recognized in younger women. Symptoms: menorrhagia (50-60%), severe progressive dysmenorrhea, chronic pelvic pain, symmetric globular enlarged uterus. Diagnosis: TVUS shows heterogeneous myometrium, myometrial cysts, "Swiss cheese" appearance. MRI: junctional zone ≥12 mm diagnostic, 8-12 mm borderline. Management: NSAIDs, LNG-IUD (first-line medical), COCs continuous, oral progestins, GnRH agonists (temporary). Hysterectomy is definitive for severe symptoms after childbearing. Fertility: associated with infertility, preterm birth, SGA, PPROM. GnRH agonist before IVF may improve outcomes.

Functional cysts: follicular (unruptured, <5 cm, resolves in 1-2 cycles), corpus luteum (can be >10 cm, may rupture causing hemoperitoneum), theca lutein (high hCG: molar, multiple gestation, OHSS). Simple cysts on US: thin-walled, anechoic, no septations, no solid components. Benign neoplasms: dermoid (mature cystic teratoma, most common germ cell tumor, bilateral 10-15%, Rokitansky nodule, contains hair, teeth, fat), serous cystadenoma, mucinous cystadenoma. Management based on size, appearance, symptoms, CA-125, risk stratification (RMI, IOTA simple rules, O-RADS). Expectant for simple cysts <5 cm in reproductive-age. Surgical indications: complex features, size >5-10 cm, persistent, symptomatic, elevated CA-125, or premenopausal with O-RADS 3+. Dermoid treatment: ovarian cystectomy.

Anterior compartment: cystocele (bladder prolapse into vagina). Posterior: rectocele (rectum) and enterocele (small bowel). Apical: uterine prolapse or vaginal vault prolapse after hysterectomy. POP-Q staging 0-IV. Risk factors: vaginal childbirth (most significant), age, obesity, chronic constipation, heavy lifting, genetic connective tissue disorders. Symptoms: vaginal bulge/pressure, urinary incontinence (stress or urgency/overflow), incomplete bladder emptying, fecal urgency or incontinence, sexual dysfunction. Management: pelvic floor physical therapy (Kegel exercises), pessary (ring, Gellhorn, cube), topical estrogen. Surgical: anterior/posterior colporrhaphy, sacrospinous ligament fixation, uterosacral ligament suspension, sacrocolpopexy (abdominal or laparoscopic, best for apical prolapse, mesh may be used). Hysterectomy for uterine prolapse. Mesh controversy: transvaginal mesh complications (erosion, pain) led to FDA restrictions.

PCOS: discussed in menstrual disorders section. Asherman syndrome: intrauterine adhesions from prior D&C, endometritis, causing secondary amenorrhea, cyclic pain, infertility, recurrent pregnancy loss. Diagnosis: hysterosalpingography, saline infusion sonography, or hysteroscopy (gold standard). Treatment: hysteroscopic adhesiolysis, post-operative estrogen to regenerate endometrium, balloon stent to prevent re-formation. Recurrence common. Endometrial polyps: focal overgrowth of endometrial glands and stroma, can cause AUB, postmenopausal bleeding, infertility. Diagnosis: SIS or hysteroscopy. Treatment: hysteroscopic polypectomy. Cervical polyps: typically benign, removed if symptomatic or suspicious. Nabothian cysts: cervical inclusion cysts, benign, no treatment needed. Ovarian remnant syndrome: residual ovarian tissue after oophorectomy causing cyclic pain; difficult diagnosis, treat with surgery. Paraovarian cysts: from Wolffian remnants, typically benign, manage conservatively.

Endometrial cancer is the most common gynecologic cancer in the developed world (~65,000 cases/yr US). Type I (endometrioid, 80%): estrogen-driven, associated with obesity, PCOS, unopposed estrogen, tamoxifen; generally good prognosis, often low-grade, early-stage. Type II (serous, clear cell, 10-20%): not estrogen-driven, more aggressive, higher grade, advanced stage at diagnosis, poorer prognosis. Lynch syndrome (hereditary non-polyposis colorectal cancer, HNPCC) accounts for 2-5% of endometrial cancers; associated with MLH1, MSH2, MSH6, PMS2 mutations. Presentation: postmenopausal bleeding (most common, 90%), abnormal uterine bleeding in perimenopausal women. Workup: transvaginal US (endometrial thickness >4-5 mm in postmenopausal, >16 mm in premenopausal warrants biopsy), office endometrial biopsy (Pipelle, sensitivity ~90% for cancer). If insufficient or high suspicion: hysteroscopy with D&C. Diagnosis: FIGO grade 1-3. Staging: surgical (TAH + BSO + pelvic/para-aortic lymphadenectomy). Management: early-stage (I-II): surgery first, adjuvant radiation if high-risk (deep myometrial invasion, high-grade, serous/clear cell, cervical involvement). Advanced (III-IV): surgery + chemotherapy (carboplatin + paclitaxel) + radiation. Hormonal therapy (progestins) for atypical hyperplasia or grade 1 cancer in women who desire fertility preservation. Surveillance: every 3-6 months for 2-3 years then annually. Lynch screening: universal tumor testing (MMR IHC or MSI) for all endometrial cancers.

Ovarian cancer is the most lethal gynecologic cancer, often called the "silent killer" because symptoms are vague (bloating, early satiety, pelvic/abdominal pain, urinary urgency) and most present at advanced stage (III-IV). Epithelial ovarian cancer accounts for ~90%: high-grade serous (most common, associated with BRCA1/BRCA2, TP53 mutations), low-grade serous, mucinous, endometrioid, clear cell. Germ cell tumors: dysgerminoma (most common germ cell malignancy, radiosensitive, LDH+, similar to testicular seminoma), yolk sac tumor (AFP+), immature teratoma, embryonal carcinoma, choriocarcinoma (hCG+). Sex cord-stromal: granulosa cell tumor (produces estrogen, causes precocious puberty or postmenopausal bleeding, inhibin B+), Sertoli-Leydig cell tumor (produces androgens, causes virilization). Risk factors: nulliparity, early menarche/late menopause, family history (BRCA1: ~40% lifetime ovarian cancer risk, BRCA2: ~15%), Lynch syndrome, endometriosis (clear cell and endometrioid). Protective: OCP use (50% risk reduction), multiparity, breastfeeding, tubal ligation/salpingectomy. Screening: not recommended in average-risk women (USPSTF Grade D). High-risk: transvaginal US + CA-125 q6-12m starting at 30-35 (BRCA1) or 40-45 (BRCA2). Diagnosis: pelvic US (complex mass with septations, solid components, papillary projections, ascites), CA-125, HE4, ROMA index. Definitive: surgical staging via midline laparotomy: TAH + BSO + omentectomy + peritoneal biopsies + lymphadenectomy + optimal cytoreduction (residual disease <1 cm). Treatment: surgical cytoreduction followed by carboplatin + paclitaxel chemotherapy. Targeted therapy: PARP inhibitors (olaparib, niraparib, rucaparib) for BRCA-mutated/HRD-positive; bevacizumab (anti-VEGF). Interval debulking after 3 cycles of chemo if unable to achieve optimal primary cytoreduction. Germ cell: BEP (bleomycin, etoposide, cisplatin) chemotherapy, highly curable. Surveillance: CA-125, exam, CT imaging q3-6 months.

Cervical cancer is HPV-related (high-risk types 16 and 18 responsible for ~70%). It is preventable through vaccination and screening. Staging: clinical (FIGO) based on exam under anesthesia, cystoscopy, proctoscopy, imaging (MRI, PET-CT). Stage I: confined to cervix (IA1: microscopic stromal invasion <3 mm; IA2: 3-5 mm; IB: clinically visible or >5 mm). Stage II: beyond cervix but not to pelvic wall. Stage III: extends to pelvic wall or lower third vagina, or hydronephrosis. Stage IV: involves bladder/rectum or distant mets. Treatment: microinvasive (IA1): conization or simple hysterectomy. IA2-IB1: radical hysterectomy (Type III) with pelvic lymphadenectomy or radiation (external beam + brachytherapy). Locally advanced (IB3-IVA): chemoradiation with cisplatin (weekly x5-6 cycles). Metastatic (IVB): platinum-based chemotherapy (cisplatin + paclitaxel + bevacizumab). Recurrent: pembrolizumab for PD-L1 positive, tisotumab vedotin. Fertility-sparing options: conization (IA1), radical trachelectomy (IA2-IB1, <2 cm). Post-treatment surveillance: Pap + HPV co-test q3-6 months for 2 years, then q6-12m for 3-5 years, then annually.

Vulvar cancer: ~90% squamous cell carcinoma, typically in postmenopausal women (mean age 65-70). Two pathways: HPV-related (younger, multifocal, associated with VIN) and HPV-independent (older, associated with lichen sclerosus, TP53 mutations). Less common: vulvar melanoma (second most common, more aggressive), basal cell, Paget disease (intraepithelial adenocarcinoma, associated with underlying adenocarcinoma in ~20%). Presentation: vulvar mass, itching, bleeding, pain. Diagnosis: biopsy of suspicious lesion. Staging: surgical (FIGO). Treatment: Stage I: wide local excision with 1-2 cm margins + sentinel lymph node biopsy (if >1 mm invasion). Stage II/III: radical local excision + inguinofemoral lymphadenectomy ± radiation. Advanced: chemoradiation. Sentinel node biopsy reduces morbidity of complete lymphadenectomy. Vaginal cancer: rare, ~90% squamous (HPV-related), typically in women aged 60-80. Clear cell adenocarcinoma associated with in-utero DES exposure. Treatment: radiation for most (brachytherapy + external beam), surgery for early proximal lesions. Both vulvar and vaginal cancer require close follow-up due to high recurrence risk.

GTD encompasses molar pregnancy and gestational trophoblastic neoplasia (GTN). Complete mole: 46,XX (androgenetic, all paternal chromosomes), no fetal tissue, diffuse hydropic villi, hCG very high, risk of malignant transformation ~15-20%. Partial mole: 69,XXX or 69,XXY (triploid, two paternal sets + one maternal), fetal tissue may be present, focal hydropic changes, lower hCG, malignant risk <5%. Presentation: vaginal bleeding, excessive uterine size, theca lutein cysts, hyperemesis, preeclampsia <20w. Diagnosis: US (complete mole: "snowstorm" pattern, no fetal parts; partial: hydropic villi + fetal parts), hCG markedly elevated. Management: suction D&C (preferred), Rhogam if Rh-negative, serial hCG monitoring weekly until negative x3, then monthly x6-12. Contraception (avoid pregnancy) during monitoring. GTN: persistent hCG elevation after molar pregnancy (or after non-molar pregnancy). Staging: FIGO I-IV + WHO prognostic scoring (<7 = low risk, ≥7 = high risk). Low-risk GTN: single-agent chemotherapy (methotrexate 0.4 mg/kg/day IV x5d q14d or dactinomycin 10-12 mcg/kg/day IV x5d q14d). High-risk GTN: multi-agent EMACO (etoposide, methotrexate, dactinomycin, cyclophosphamide, vincristine). Excellent cure rates (>95% for low-risk, 80-90% for high-risk). hCG monitoring for 12 months after chemotherapy.

BRCA1/BRCA2 testing: indicated for women with ovarian cancer (any type), breast cancer at ≤45 or triple-negative ≤60, male breast cancer, Ashkenazi Jewish ancestry, or family history suggestive. Management of BRCA carriers: enhanced breast screening (mammogram + breast MRI alternating q6m starting at 25-30), risk-reducing salpingo-oophorectomy (RRSO) at 35-40 (BRCA1) or 40-45 (BRCA2), consideration of risk-reducing mastectomy. RRSO reduces ovarian cancer risk by ~80% and breast cancer risk by ~50%. Salpingectomy alone (with delayed oophorectomy) being studied. Lynch syndrome: universal tumor screening for all endometrial cancers (MMR IHC or MSI). Management: colonoscopy q1-2y starting 20-25, prophylactic hysterectomy + BSO after childbearing, annual endometrial biopsy, urinalysis for urothelial cancer. Fertility preservation: oocyte/embryo cryopreservation, ovarian tissue cryopreservation (experimental). Options for women with gynecologic cancers: conization/trachelectomy (cervical), hormonal therapy for endometrial cancer (grade 1, stage IA), and oocyte preservation before gonadotoxic chemotherapy. Oncofertility counseling should be offered to all reproductive-age patients at diagnosis.

Menopause is the permanent cessation of menses for 12 consecutive months due to ovarian follicle depletion, with declining estradiol and rising FSH/LH. Average age of natural menopause is 51 years (range 45-55). Perimenopause (menopausal transition) lasts ~4-8 years, characterized by irregular cycles, vasomotor symptoms, sleep disturbances, mood changes, and variable FSH levels (periodically elevated, then normal). Premature menopause (<40 years) is called premature ovarian insufficiency (POI). Diagnosis: FSH >25 IU/L on two occasions 4 weeks apart in a woman with amenorrhea >12 months. No single test is diagnostic for perimenopause; diagnosis is clinical based on menstrual pattern and symptoms. The STRAW+10 staging system classifies reproductive aging. AMH is low and declines further but not routinely used. Postmenopausal hormonal changes: low estradiol (<15-20 pg/mL), high FSH (>25-100 IU/L), decreased inhibin B, increased GnRH. Long-term effects of estrogen deficiency: vasomotor symptoms, urogenital atrophy, osteoporosis, increased cardiovascular risk, cognitive changes, skin changes.

Vasomotor symptoms (VMS) affect ~80% of women during perimenopause and early postmenopause. Mechanism: estrogen withdrawal destabilizes the hypothalamic thermoregulatory center, narrowing the thermoneutral zone such that small core temperature fluctuations trigger heat dissipation responses (vasodilation, sweating). Hot flashes: sudden sensation of intense heat, often with sweating, palpitations, anxiety, lasting 1-5 minutes, sometimes followed by chills. They are most severe in the first 1-2 years after final menses but can persist 7-10 years or longer. Triggers: stress, caffeine, alcohol, spicy foods, warm ambient temperature. Management: menopause hormone therapy (HT) is the most effective treatment (reduces frequency and severity by ~75-90%). Non-hormonal pharmacologic options for women with contraindications to HT: SSRIs/SNRIs (paroxetine 7.5 mg daily - the only FDA-approved non-hormonal option; venlafaxine 37.5-75 mg, desvenlafaxine, escitalopram), gabapentin 300-900 mg/day, pregabalin, clonidine 0.1-0.2 mg/day. Lifestyle modifications: layered clothing, fans, avoiding triggers, weight loss, smoking cessation. Cognitive behavioral therapy and hypnosis have evidence for efficacy. Oxybutynin (anticholinergic) emerging option but side effects limit use.

GSM encompasses vulvovaginal atrophy (VVA) and lower urinary tract symptoms due to estrogen deficiency. Affects ~50% of postmenopausal women. Symptoms: vaginal dryness, dyspareunia, itching/burning, decreased lubrication, recurrent UTIs, urinary urgency, frequency, and urge incontinence. Examination: pale, thin, smooth vaginal mucosa, loss of rugae, introital narrowing, urethral caruncle. Vaginal pH >5 is suggestive. Treatment: first-line: non-hormonal vaginal moisturizers (Replens, Hyalofemme) used 2-3 times/week and lubricants for intercourse. Second-line (more effective): low-dose vaginal estrogen (estradiol cream 0.5-1g, conjugated equine estrogen cream 0.5g, estradiol tablet 10 mcg, estradiol vaginal ring 2 mg/90 days). Vaginal estrogen is safe (minimal systemic absorption, no need for progestin). Ospemifene: oral SERM (selective estrogen receptor modulator) for moderate-severe dyspareunia; increases endometrial thickness (theoretical risk, monitor). DHEA vaginal insert (prasterone) 6.5 mg daily: improves all GSM domains. Systematic HT also improves GSM but may not resolve symptoms. Recurrent UTIs in postmenopausal women: vaginal estrogen reduces UTI recurrence.

HT is the most effective treatment for moderate-severe vasomotor symptoms and also prevents bone loss and treats GSM. Regimens: systemic estrogen (oral estradiol 0.5-2 mg, conjugated equine estrogen 0.3-0.625 mg, transdermal estradiol 0.025-0.1 mg patch/gel/spray) + progestogen (micronized progesterone 100-200 mg or progestin) in women with a uterus to prevent endometrial hyperplasia/cancer. Estrogen alone for women post-hysterectomy. Continuous combined regimen (daily estrogen + daily progestin/MP) for postmenopausal (no bleeding expected after 6 months). Sequential/cyclic regimen for perimenopausal women (estrogen daily + progestin 12-14 days/month) causing scheduled withdrawal bleeding. Bioidentical hormones: custom-compounded bioidentical HT has no proven benefit over FDA-approved HT and is not recommended due to lack of regulation and safety data. Benefits (WHI and subsequent re-analyses): VMS relief (most effective), prevents bone loss and fractures (hip, vertebral), improves quality of life, reduces colorectal cancer risk. Risks: VTE (oral > transdermal, absolute risk increase ~2-4/10,000 woman-years), stroke (increases with age, oral estrogen), breast cancer (increased risk with estrogen + progestin after ~5 years of use, RR ~1.25; estrogen alone shows no increase or decreased risk in WHI), gallbladder disease (oral). Timing hypothesis: the benefit-risk profile is most favorable when HT is initiated within 10 years of menopause or before age 60 for symptomatic women. Start at the lowest effective dose, use for the shortest duration needed for symptom management (usually 3-5 years, can be longer for severe symptoms with appropriate monitoring). Contraindications: known/suspected pregnancy, undiagnosed genital bleeding, known/suspected breast cancer, estrogen-dependent cancer, active VTE, active arterial thromboembolic disease, untreated hypertension, active liver disease, known thrombophilia (factor V Leiden, prothrombin mutation). Tibolone: synthetic steroid with estrogenic, progestogenic, and androgenic activity; used in Europe for VMS and bone protection. BZA/SERM combinations: conjugated estrogen + bazedoxifene (Duavee) provides endometrial protection without progestin; reduces VMS and prevents bone loss.

Osteoporosis is a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration leading to increased fracture risk. Postmenopausal osteoporosis results from accelerated bone loss due to estrogen deficiency (estrogen normally inhibits osteoclast activity). Screening: DXA (dual-energy x-ray absorptiometry) at age 65 for average-risk women, earlier (age 50-64) with risk factors (fragility fracture, parental hip fracture, low body weight, smoking, glucocorticoid use, RA, secondary causes). T-score interpretation: -1.0 or above = normal; -1.0 to -2.5 = osteopenia; -2.5 or below = osteoporosis; -2.5 or below + fragility fracture = severe/established osteoporosis. FRAX tool: estimates 10-year probability of hip fracture and major osteoporotic fracture. Treatment thresholds: hip or vertebral fracture (any T-score); T-score ≤-2.5 (osteoporosis); osteopenia with FRAX 10-year hip risk ≥3% or major risk ≥20%. Management: calcium 1200 mg/day total (diet + supplement if needed, max 500-600 mg elemental per dose), vitamin D 800-1000 IU/day, weight-bearing exercise (walking, jogging, resistance training 30 min/day), fall prevention (home safety, balance training, vision correction). Pharmacologic: first-line: bisphosphonates (alendronate 70 mg weekly, risedronate 35 mg weekly, ibandronate 150 mg monthly, zoledronic acid 5 mg IV yearly). Atypical femur fracture and osteonecrosis of the jaw (ONJ) with long-term bisphosphonates; consider drug holiday after 3-5 years. Second-line: denosumab (Prolia) 60 mg SQ q6 months (potent antiresorptive, no drug holiday, rebound fractures if delayed). Raloxifene (SERM) 60 mg daily: reduces vertebral fractures, reduces breast cancer risk, no effect on hip/non-vertebral, increases VTE risk. Teriparatide (Forteo) 20 mcg SQ daily: anabolic therapy (PTH analog), reserved for severe osteoporosis or bisphosphonate failure, limited to 2 years. Abaloparatide (Tymlos): similar to teriparatide, SQ daily, 2-year limit. Romosozumab (Evenity): monoclonal antibody neutralizing sclerostin, anabolic + antiresorptive, 1 year of monthly SQ injections, then transition to antiresorptive. Sequential therapy: anabolic (teriparatide/abaloparatide/romosozumab) followed by antiresorptive (bisphosphonate/denosumab) for maximum benefit. Monitoring: DXA every 1-2 years until stable, then every 2-5 years.

Fall prevention is a critical component of osteoporosis management. Interventions: home safety assessment (remove rugs, improve lighting, grab bars), medication review (deprescribe sedatives, antihypertensives if orthostatic), vision assessment, balance/gait training (Tai Chi, PT), vitamin D supplementation, hip protectors for high-risk individuals. Secondary causes of osteoporosis: glucocorticoids, hyperthyroidism, hyperparathyroidism, Cushing syndrome, hypogonadism, eating disorders, malabsorption (celiac, IBD), chronic kidney disease, multiple myeloma, medications (SSRIs, PPIs, aromatase inhibitors, Depo-Provera, GnRH agonists, TZDs, loop diuretics, heparin). Evaluation: CBC, Cr, Ca, P, 25-OH vitamin D, PTH, TSH, LFTs, SPEP (if vertebral fracture or anemia), 24h urine calcium, celiac panel, consider testosterone (men). Bone turnover markers (P1NP, CTX) monitor treatment response but not routinely used. Sequential therapy: for patients at very high risk (T-score <-3, prior fragility fracture, multiple risk factors), start with anabolic therapy (teriparatide, abaloparatide, romosozumab) for 1-2 years, then transition to antiresorptive (bisphosphonate or denosumab). Non-pharmacologic: adequate protein intake (1-1.2 g/kg/day), smoking cessation, limit alcohol (≤1 drink/day). Hip fractures require surgical repair within 24-48h; post-op bisphosphonate or denosumab reduces second fracture risk by ~50%.