FMGE Obstetrics & Gynecology Flashcards

24 sample cards from the Obstetrics & Gynecology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Describe the key physiological changes of the postpartum period (puerperium).

   Puerperium lasts ~6 weeks. Uterus involutes (returns to pelvis by 2 weeks, normal size by 6 weeks); lochia progresses rubra→serosa→alba; lactation established (prolactin + oxytocin let-down); diuresis clears excess fluid; menstruation returns ~6–8 weeks if not breastfeeding.

2. Define primary postpartum hemorrhage and recall the 'four Ts' of its causes.

   Primary PPH = blood loss ≥500 mL (vaginal) or ≥1000 mL (cesarean) within 24 h of delivery. Causes — Tone (uterine atony, commonest ~70%), Trauma (lacerations/rupture), Tissue (retained placenta), Thrombin (coagulopathy).

3. What is the stepwise uterotonic management of atonic PPH?

   Uterine massage + oxytocin (first-line), then ergometrine (avoid in hypertension), carboprost/PGF2α (avoid in asthma), and misoprostol. If medical measures fail: balloon tamponade, B-Lynch suture, uterine artery/internal iliac ligation, and finally hysterectomy.

4. Compare the typical-use failure rates and mechanisms of combined oral contraceptive pills versus copper IUD versus etonogestrel implant.

   COCP: inhibits ovulation (estrogen+progestin); typical failure ~7%. Copper IUD: spermicidal/inflammatory, prevents fertilization; failure <1%, lasts 10 yrs. Etonogestrel implant: inhibits ovulation + thickens cervical mucus; failure <0.1% (most effective reversible method), lasts 3 yrs.

5. What are the WHO Medical Eligibility Category 4 (absolute) contraindications to combined hormonal contraceptives?

   Examples: <6 weeks postpartum and breastfeeding, smoking ≥15/day at age ≥35, history of VTE/DVT/PE, known thrombogenic mutations, history of stroke or ischemic heart disease, migraine with aura, current breast cancer, severe hypertension, and active liver disease.

6. Define the PALM-COEIN classification of abnormal uterine bleeding.

   Structural causes (PALM): Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia. Non-structural (COEIN): Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not otherwise classified.

7. Define primary versus secondary amenorrhea.

   Primary amenorrhea: no menses by age 15 with normal secondary sexual characteristics, or by 13 with none. Secondary amenorrhea: absence of menses for ≥3 cycles or ≥6 months in a previously menstruating woman (commonest cause: pregnancy).

8. Differentiate fibroids (leiomyoma), adenomyosis, and endometriosis.

   Fibroid: benign smooth-muscle tumor of myometrium (estrogen-dependent), causes menorrhagia/bulk symptoms. Adenomyosis: endometrial glands within the myometrium → enlarged tender 'globular' uterus, dysmenorrhea. Endometriosis: endometrial tissue outside the uterus (ovary/peritoneum) → dysmenorrhea, dyspareunia, infertility; chocolate cysts on ovary.

9. How do the common gynecological cancers classically present and what is the principal risk reduction strategy for each?

   Cervical: postcoital bleeding (HPV-linked; prevent with HPV vaccine + Pap screening). Endometrial: postmenopausal bleeding (unopposed estrogen). Ovarian: vague abdominal symptoms, late presentation (CA-125). Vulvar: pruritus/lump. Choriocarcinoma: bleeding with very high β-hCG.

10. Outline the hypothalamic-pituitary-ovarian axis and the 'two-cell, two-gonadotropin' theory of estrogen synthesis.

    Hypothalamus releases GnRH (pulsatile) → pituitary releases FSH and LH → ovary produces estrogen/progesterone with negative/positive feedback. Two-cell theory: LH stimulates theca cells to make androgens from cholesterol; FSH stimulates granulosa cells (aromatase) to convert androgens to estrogen.

11. What is the recommended order of basic infertility evaluation in a couple?

    Semen analysis (male factor), assessment of ovulation (mid-luteal day-21 progesterone, cycle history), and tubal patency (hysterosalpingography or laparoscopy with dye/chromopertubation). Also assess ovarian reserve (AMH, antral follicle count) and rule out anatomical/uterine factors.

12. Define the WHO lower reference limits for a normal semen analysis (key parameters).

    Volume ≥1.5 mL, sperm concentration ≥15 million/mL, total count ≥39 million/ejaculate, total motility ≥40% (progressive ≥32%), and normal morphology ≥4% (strict criteria).

13. Differentiate IVF from ICSI and name the most serious complication of ovarian stimulation in ART.

    IVF (in-vitro fertilization): eggs and sperm combined in a dish, fertilization occurs spontaneously. ICSI: a single sperm is injected directly into the oocyte (used for severe male-factor infertility). Most serious complication: ovarian hyperstimulation syndrome (OHSS) — capillary leak, ascites, hemoconcentration, thromboembolism risk.

14. State the Rotterdam criteria for diagnosing polycystic ovary syndrome (PCOS).

    Two of three required (after excluding mimics): (1) oligo/anovulation, (2) clinical or biochemical hyperandrogenism (hirsutism, raised free testosterone), (3) polycystic ovaries on ultrasound (≥12 follicles 2–9 mm and/or ovarian volume >10 mL).

15. What is the first-line agent for ovulation induction in PCOS and its mechanism, plus the second-line oral option?

    Letrozole (an aromatase inhibitor that lowers estrogen, increasing FSH) is now first-line. Clomiphene citrate (a selective estrogen receptor modulator blocking hypothalamic estrogen feedback → increased FSH/LH) is the classic alternative. Metformin helps insulin resistance; gonadotropins are used if oral agents fail.

16. Classify urinary incontinence into stress, urge, and overflow types with their causes.

    Stress incontinence: leakage with cough/exertion due to urethral sphincter/pelvic floor weakness (raised intra-abdominal pressure). Urge incontinence: detrusor overactivity → sudden urgency. Overflow incontinence: chronic retention/bladder outlet obstruction. Diagnosis aided by urodynamics.

17. What is the first-line treatment for stress incontinence versus urge (overactive bladder) incontinence?

    Stress: pelvic floor muscle (Kegel) exercises first-line; surgery (mid-urethral sling/colposuspension) if refractory. Urge/OAB: bladder training and lifestyle, then antimuscarinics (oxybutynin, solifenacin) or beta-3 agonist (mirabegron).

18. Describe the POP-Q staging concept for pelvic organ prolapse and name the prolapse types by compartment.

    POP-Q measures descent relative to the hymen (Stage 0 no prolapse to Stage IV complete eversion). Types: cystocele (anterior/bladder), rectocele (posterior/rectum), enterocele (small bowel), uterine prolapse, and vaginal vault prolapse (post-hysterectomy). Conservative: pessary/pelvic floor exercises; surgical repair if symptomatic.

19. Match the common sexually transmitted infections to their causative organisms.

    Gonorrhea — Neisseria gonorrhoeae; Chlamydia — Chlamydia trachomatis; Syphilis — Treponema pallidum (painless chancre); Chancroid — Haemophilus ducreyi (painful ulcer); Genital herpes — HSV-2; Trichomoniasis — Trichomonas vaginalis (strawberry cervix); Genital warts/cervical cancer — HPV.

20. Differentiate the three common causes of vaginitis by discharge and diagnostic finding.

    Bacterial vaginosis: thin grey fishy discharge, clue cells, positive whiff test, pH >4.5 (Gardnerella). Candidiasis: thick white 'cottage cheese' discharge, pseudohyphae, normal pH, itching. Trichomoniasis: frothy yellow-green discharge, motile trophozoites, strawberry cervix, pH >4.5.

21. Define menopause and list the typical hormonal changes and vasomotor/genitourinary symptoms.

    Menopause = permanent cessation of menses, diagnosed retrospectively after 12 months of amenorrhea (average age ~51). Hormones: high FSH and LH, low estradiol. Symptoms: hot flushes/night sweats (vasomotor), vaginal atrophy/dryness, dyspareunia, mood changes, and long-term osteoporosis and cardiovascular risk.

22. What organism causes nearly all cervical cancers, and which HPV types and histologic type predominate?

    Human papillomavirus (HPV), especially high-risk types 16 and 18 (cause ~70% of cases). The commonest histologic type is squamous cell carcinoma (arising at the transformation zone); prevention is HPV vaccination plus Pap/HPV screening.

23. Identify the key risk factors and classic presentation of endometrial carcinoma.

    Risk factors are states of unopposed estrogen: obesity, nulliparity, late menopause, early menarche, PCOS, tamoxifen, and Lynch syndrome. Classic presentation: postmenopausal bleeding. Commonest type: endometrioid adenocarcinoma; diagnosis by endometrial biopsy.

24. What tumor marker and inheritance pattern are linked to epithelial ovarian cancer, and what defines gestational trophoblastic disease including a key follow-up rule?

    Epithelial ovarian cancer: marker CA-125; familial cases linked to BRCA1/BRCA2 mutations; presents late ('silent killer'). Gestational trophoblastic disease: abnormal trophoblast proliferation (hydatidiform mole — 'snowstorm' on USG with markedly elevated β-hCG; choriocarcinoma). After molar evacuation, monitor serial β-hCG to detect persistent/malignant disease and avoid pregnancy during follow-up.

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