INI CET Obstetrics & Gynecology Syllabus

What are the components of a Bishop score and what does it predict?

The Bishop score assesses cervical favorability for induction using 5 parameters: cervical dilatation, effacement, consistency, position, and fetal station. A higher score (typically ≥6-8) predicts a favorable cervix and successful induction; a low score suggests the need for cervical ripening agents.

What are the categories of cardiotocography (CTG) and the features assessed?

CTG assesses baseline rate (normal 110-160 bpm), variability (normal 5-25 bpm), accelerations (reassuring), and decelerations (early, variable, late). Late decelerations suggest uteroplacental insufficiency; variable decelerations suggest cord compression. Traces are classified as normal/reassuring, suspicious, or pathological, guiding further fetal assessment (e.g., fetal scalp pH).

How is the partograph used to monitor the progress of labor?

The partograph is a graphical record of labor plotting cervical dilatation against time, with alert and action lines. Crossing the alert line warns of slow progress; crossing the action line prompts intervention. It also records contractions, fetal heart rate, descent, maternal vitals, and liquor, helping detect prolonged/obstructed labor early.

What are the indications for cesarean section and the difference in classification by urgency?

Indications: failure to progress/obstructed labor, fetal distress (non-reassuring CTG), malpresentation (breech/transverse), placenta previa or major hemorrhage, cord prolapse, failed instrumental delivery, and previous classical cesarean. Urgency categories: Category 1 (immediate threat to life of mother/fetus), Category 2 (compromise, not immediately life-threatening), Category 3 (early delivery, no compromise), Category 4 (elective).

What are the active management steps of the third stage of labor?

Active management reduces postpartum hemorrhage: (1) administer a uterotonic (oxytocin 10 IU IM) within 1 minute of delivery, (2) controlled cord traction with counter-pressure on the uterus (Brandt-Andrews), and (3) uterine massage after placental delivery. Examine the placenta for completeness.

What are the physiological changes during the postpartum period (involution and lactation)?

Uterine involution: the uterus contracts from ~1 kg to ~50-70 g by 6 weeks; lochia progresses rubra → serosa → alba. Cardiovascular changes reverse with diuresis of excess fluid. Lactation: falling estrogen/progesterone after placental delivery allows prolactin-driven milk production; suckling triggers oxytocin release for milk ejection (let-down).

Define postpartum hemorrhage (PPH) and list its main causes (the 4 T's).

Primary PPH = blood loss ≥500 mL after vaginal delivery (≥1000 mL after cesarean) within 24 h. Causes — the 4 T's: Tone (uterine atony — most common), Trauma (lacerations/rupture), Tissue (retained placenta), and Thrombin (coagulopathy). Management of atony: uterine massage and uterotonics (oxytocin, ergometrine, carboprost, misoprostol).

What is the difference between endometritis and other causes of puerperal pyrexia?

Puerperal pyrexia is fever ≥38°C in the first 24 h to 6 weeks postpartum. Endometritis (the most common cause) presents with fever, uterine tenderness, and foul lochia, treated with broad-spectrum antibiotics. Other causes include wound/perineal infection, mastitis, urinary tract infection, and deep vein thrombosis — remember 'the 5 W's' (womb, wind, water, walk, wound).

What is the difference between postpartum blues, postpartum depression, and postpartum psychosis?

Postpartum 'blues': transient, mild mood lability in the first ~2 weeks, self-limiting. Postpartum depression: persistent depressive symptoms beyond 2 weeks needing treatment (therapy/antidepressants). Postpartum psychosis: a psychiatric emergency with delusions, hallucinations, and disorganized behavior, usually within 2 weeks, requiring urgent admission.

Compare the mechanisms of action of the main hormonal contraceptive methods.

Combined oral contraceptives (estrogen+progestin): inhibit ovulation by suppressing FSH/LH, thicken cervical mucus, thin endometrium. Progestin-only pills: thicken cervical mucus (variable ovulation suppression). DMPA injection/implant: suppress ovulation. Hormonal IUD (levonorgestrel): thickens mucus, thins endometrium. Copper IUD: copper ions are spermicidal/cytotoxic, preventing fertilization (non-hormonal).

What are the absolute contraindications to combined hormonal contraceptives?

Per WHO Medical Eligibility Criteria category 4: history of venous thromboembolism, known thrombogenic mutations, migraine with aura, smoker ≥35 years (≥15 cigarettes/day), uncontrolled hypertension, current breast cancer, active liver disease, complicated valvular heart disease, <6 weeks postpartum if breastfeeding, and major surgery with immobilization.

What are the options for emergency contraception and their windows of use?

Copper IUD: most effective, insert up to 5 days after unprotected intercourse. Ulipristal acetate 30 mg: a progesterone receptor modulator effective up to 120 h (5 days). Levonorgestrel 1.5 mg: effective up to 72 h (declining efficacy). The copper IUD also provides ongoing contraception.

Define abnormal uterine bleeding using the FIGO PALM-COEIN classification.

PALM (structural causes): Polyp, Adenomyosis, Leiomyoma (fibroid), Malignancy/hyperplasia. COEIN (non-structural causes): Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not otherwise classified. It standardizes the etiologic classification of abnormal uterine bleeding in non-pregnant reproductive-age women.

Differentiate primary from secondary dysmenorrhea and primary from secondary amenorrhea.

Primary dysmenorrhea: painful periods without pelvic pathology, due to prostaglandin-mediated uterine contractions. Secondary dysmenorrhea: due to pathology (endometriosis, adenomyosis, fibroids, PID). Primary amenorrhea: no menarche by age 15 (or 13 with no secondary sexual characteristics). Secondary amenorrhea: cessation of periods for ≥3-6 months in a previously menstruating woman.

What is endometriosis, its classic clinical triad, and gold-standard diagnosis?

Endometriosis = endometrial-like tissue outside the uterine cavity (commonly ovaries forming 'chocolate cysts', pelvic peritoneum, uterosacral ligaments). Classic triad: dysmenorrhea, deep dyspareunia, and chronic pelvic pain; also subfertility. Gold-standard diagnosis is laparoscopy with visualization/biopsy; management includes NSAIDs, hormonal suppression, and surgical excision.

Compare uterine fibroids (leiomyomas) by location and their typical symptoms.

Submucosal fibroids (project into cavity): heavy menstrual bleeding and subfertility. Intramural fibroids (within myometrium): bulk symptoms and bleeding. Subserosal fibroids (project outward): pressure effects (urinary frequency, bowel symptoms), may be pedunculated and torse. Fibroids are estrogen-dependent, often regress after menopause.

What are the major histological types of ovarian cancer and the most common overall?

Epithelial tumors are most common (~90%), the leading subtype being high-grade serous carcinoma; others include mucinous, endometrioid, and clear cell. Germ cell tumors (e.g., dysgerminoma, teratoma) occur in younger women; sex cord-stromal tumors (granulosa cell — estrogen; Sertoli-Leydig — androgen) are rarer. Tumor markers: CA-125 (epithelial), AFP/hCG/LDH (germ cell).

What are the gonadotropins and feedback loops of the hypothalamic-pituitary-ovarian (HPO) axis?

Hypothalamic GnRH (pulsatile) stimulates the anterior pituitary to release FSH and LH. FSH drives follicular growth and granulosa cell estrogen production; LH drives theca cell androgen production and triggers ovulation/luteinization. Estrogen exerts negative feedback (low levels) but positive feedback at the mid-cycle peak (LH surge); progesterone and inhibin provide additional negative feedback.

How is the cause of amenorrhea localized using FSH, LH, and prolactin levels?

High FSH/LH: ovarian (hypergonadotropic hypogonadism) — e.g., premature ovarian insufficiency, Turner syndrome. Low/normal FSH/LH: hypothalamic-pituitary (hypogonadotropic hypogonadism) — e.g., stress, weight loss, Kallmann syndrome. High prolactin: prolactinoma/medications suppressing GnRH. Normal levels with absent withdrawal bleed after progestin: consider outflow tract obstruction (e.g., Asherman syndrome).

What is the recommended timing of basic infertility investigations for the couple?

Define infertility as failure to conceive after 12 months of unprotected intercourse (6 months if age ≥35). Male: semen analysis (volume, count, motility, morphology). Female: confirm ovulation (mid-luteal day-21 progesterone), assess tubal patency (hysterosalpingography or laparoscopy with dye), and ovarian reserve (AMH, antral follicle count, day-3 FSH). Also assess uterine cavity (ultrasound/hysteroscopy).

Define and outline the management of polycystic ovary syndrome (PCOS).

PCOS uses the Rotterdam criteria — 2 of 3: oligo/anovulation, clinical or biochemical hyperandrogenism, and polycystic ovaries on ultrasound (≥12 follicles or volume >10 mL), after excluding mimics. Management: weight loss/lifestyle, combined OCP for cycle/androgen control, metformin for insulin resistance, and letrozole (first-line) or clomiphene for ovulation induction in those seeking pregnancy.

Describe the steps and key drugs of assisted reproductive technology (IVF).

IVF steps: (1) controlled ovarian stimulation with FSH/hMG plus a GnRH agonist or antagonist to prevent premature LH surge; (2) trigger final maturation with hCG/GnRH agonist; (3) transvaginal oocyte retrieval ~36 h later; (4) fertilization in vitro (or ICSI for male-factor infertility); (5) embryo culture and transfer; (6) luteal progesterone support. A major complication is ovarian hyperstimulation syndrome (OHSS).

What is ovarian hyperstimulation syndrome (OHSS)?

OHSS is an iatrogenic complication of ovarian stimulation, mediated by VEGF-driven increased capillary permeability after hCG. Features: enlarged ovaries, ascites, hemoconcentration, third-spacing of fluid, and risk of thromboembolism, renal failure, and pleural effusion in severe cases. Risk factors include PCOS, high estradiol, and high follicle counts; GnRH-antagonist protocols reduce risk.

Compare clomiphene citrate and letrozole for ovulation induction.

Clomiphene is a selective estrogen receptor modulator that blocks hypothalamic estrogen receptors, increasing GnRH/FSH; side effects include anti-estrogenic endometrial/cervical mucus effects and multiple pregnancy. Letrozole is an aromatase inhibitor that lowers estrogen, raising FSH; it is now first-line in PCOS (higher live-birth rates, less anti-estrogenic effect on endometrium).

Differentiate stress, urge, and mixed urinary incontinence.

Stress incontinence: leakage on increased intra-abdominal pressure (cough, sneeze) due to urethral sphincter/support weakness; treated with pelvic floor exercises and mid-urethral sling. Urge incontinence (overactive bladder): sudden urgency with leakage from detrusor overactivity; treated with bladder training and antimuscarinics/beta-3 agonists. Mixed incontinence: features of both.

How is pelvic organ prolapse classified by compartment, and what defines uterine procidentia?

By compartment: anterior (cystocele — bladder), posterior (rectocele — rectum, enterocele — small bowel), and apical (uterine/vault prolapse). Severity is graded by the POP-Q system. Procidentia is complete uterine prolapse with the entire uterus protruding outside the vaginal introitus (stage IV). Management ranges from pelvic floor therapy and pessaries to surgical repair.

Differentiate the common sexually transmitted infections by causative organism and key feature.

Chlamydia trachomatis (often asymptomatic, leading cause of PID/infertility). Neisseria gonorrhoeae (purulent discharge, PID). Trichomonas vaginalis (frothy yellow-green discharge, 'strawberry cervix'). Treponema pallidum (syphilis — painless chancre). Herpes simplex (painful vesicles/ulcers). HPV (genital warts; oncogenic types 16/18 cause cervical cancer). Bacterial vaginosis (Gardnerella — not strictly an STI; clue cells, fishy odor).

What are the hormonal changes and clinical features of menopause, and what defines premature ovarian insufficiency?

Menopause = 12 consecutive months of amenorrhea (mean age ~51); due to ovarian follicular depletion, estrogen falls and FSH/LH rise markedly. Features: vasomotor symptoms (hot flushes, night sweats), vaginal atrophy/dryness, mood changes, and long-term osteoporosis and cardiovascular risk. Premature ovarian insufficiency is menopause before age 40 with elevated FSH.

What are the indications, benefits, and risks of menopausal hormone therapy (HRT)?

HRT relieves vasomotor symptoms and urogenital atrophy and protects against osteoporosis. Women with a uterus need estrogen PLUS progestogen (to prevent endometrial hyperplasia/cancer); estrogen-only is for those after hysterectomy. Risks: increased venous thromboembolism and stroke (oral), and a small increased breast cancer risk with combined long-term use; benefits/risks depend on age and time since menopause.

Outline cervical cancer screening, the main risk factor, and the most common histological type.

Cervical cancer is caused mainly by persistent high-risk HPV infection (types 16 and 18 most common). Screening: HPV DNA testing and/or cervical cytology (Pap smear), with HPV vaccination for primary prevention. The most common histological type is squamous cell carcinoma (from the transformation zone), followed by adenocarcinoma. It spreads by direct local extension and lymphatics.

Differentiate type I and type II endometrial cancer and state the cardinal symptom.

The cardinal symptom is postmenopausal bleeding (investigate with transvaginal ultrasound for endometrial thickness and endometrial biopsy). Type I (endometrioid, most common): estrogen-dependent, arises from hyperplasia, associated with obesity/unopposed estrogen/PCOS/tamoxifen, better prognosis. Type II (serous/clear cell): non-estrogen-dependent, occurs in older women, p53 mutations, more aggressive with poorer prognosis.

What is gestational trophoblastic disease, and how do complete and partial hydatidiform moles differ?

GTD is abnormal trophoblast proliferation. Complete mole: 46,XX (entirely paternal, empty ovum fertilized), no fetal tissue, diffuse 'snowstorm' vesicles, very high hCG, higher malignant potential. Partial mole: triploid (69 chromosomes, two sperm), some fetal/embryonic tissue present, lower hCG. Treatment is suction evacuation with serial hCG follow-up to detect persistent trophoblastic disease/choriocarcinoma.