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Give 100 questions and answers for mbbs obg on the following topics Anatomy of female genital tract Physiology of ovulation and menstruation Gametogenesis and fertilisation Developement of female reproductive system Placenta and fetal membranes Puberty and related problems Menopause and related problems Maternal changes during pregnancy Diagnosis of pregnancy Preconceptional and antenatal care AUB Miscarriage Leiomyoma of uterus Normal and abnormal puerperium Sexually transmitted diseases Antepartum and intrapartum fetal surveillance Molar pregnancy

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100 MBBS OBG Questions and Answers

Compiled from standard OBG teaching (Williams, Shaw, Dutta-style content). I checked the library and PubMed for update flags. The library had nothing OBG-specific for these topics beyond the FIGO PALM-COEIN classification, so the rest is from standard OBG teaching. Please confirm drug doses against your current local protocol before clinical use.

1. Anatomy of the female genital tract (Q1-7)

Q1. What are the dimensions and parts of the normal uterus? It measures 7.5 x 5 x 2.5 cm and weighs 50-80 g. The cavity is about 6 cm long (uterine sound 6-9 cm). The parts are the fundus, body (corpus) and cervix, with the isthmus between body and cervix. The body-to-cervix ratio is 2:1 in adults and 1:2 in infants.
Q2. What are the supports of the uterus?
  • Primary supports: pelvic floor muscles (levator ani), perineal body, and the Mackenrodt (transverse cervical/cardinal) ligaments.
  • Other ligamentous supports: uterosacral and pubocervical ligaments.
  • Secondary (peritoneal) supports: round and broad ligaments.
  • The Mackenrodt ligament is the main support against prolapse.
Q3. What is the blood supply of the uterus, and what is the surgical relevance? The uterine artery (anterior division of the internal iliac) supplies the uterus. It anastomoses with the ovarian artery (from the aorta at L2) in the broad ligament. The ureter passes under the uterine artery about 2 cm lateral to the cervix at the level of the internal os ("water under the bridge"). It is at risk of injury during hysterectomy.
Q4. Describe the course of the round ligament. It is a fibromuscular band, 10-12 cm long, and a remnant of the gubernaculum. It arises from the uterine cornu in front of and below the tube. It passes through the deep inguinal ring and inguinal canal and ends in the labium majus. It keeps the uterus anteverted and anteflexed.
Q5. What is the lymphatic drainage of the female genital organs?
  • Ovary and fundus: para-aortic nodes.
  • Fundus also drains along the round ligament to superficial inguinal nodes.
  • Uterine body: internal and external iliac nodes.
  • Cervix: paracervical, obturator, iliac and sacral nodes.
  • Lower third of the vagina and vulva: superficial inguinal nodes.
Q6. Describe the parts of the fallopian tube. The tube is about 10 cm long. The parts are interstitial (1.25 cm), isthmus (2.5 cm, narrowest), ampulla (5 cm, widest) and infundibulum (with fimbriae, 1.25 cm). The ampulla is the usual site of fertilisation and of ectopic pregnancy. The epithelium is ciliated columnar.
Q7. What are the epithelia of the vulva, vagina, cervix and ovary, and what is the transformation zone? The vagina and ectocervix have non-keratinised stratified squamous epithelium. The endocervix has columnar epithelium. The squamocolumnar junction lies between them, and the transformation zone is the area of squamous metaplasia around it, where most cervical neoplasia arises. The ovary is covered by a single layer of cuboidal germinal epithelium. The vagina has no glands.

2. Physiology of ovulation and menstruation (Q8-14)

Q8. Describe the hypothalamic-pituitary-ovarian axis. The hypothalamus releases GnRH in pulses every 60-90 minutes. This stimulates anterior pituitary FSH and LH. FSH acts on granulosa cells and LH acts on theca cells, and together they drive follicular growth, ovulation and sex steroid production. Estrogen, progesterone and inhibin give feedback to the hypothalamus and pituitary.
Q9. State the two-cell, two-gonadotropin theory. LH stimulates theca cells to make androgens (androstenedione, testosterone). FSH stimulates granulosa cells to express aromatase, which converts these androgens to estradiol.
Q10. How does ovulation occur? Rising estradiol (about 200 pg/mL sustained for roughly 50 hours) gives positive feedback and triggers the LH surge. Ovulation follows 34-36 hours after the onset of the surge (10-12 hours after the peak). The mature follicle is about 18-24 mm. LH triggers prostaglandins and proteolytic enzymes that rupture the follicle wall and release the oocyte.
Q11. Compare the ovarian and endometrial phases of the cycle.
  • Follicular phase of the ovary corresponds to the proliferative phase of the endometrium (estrogen driven). Its length is variable.
  • Luteal phase of the ovary corresponds to the secretory phase (progesterone driven). Its length is fixed at about 14 days.
  • Corpus luteum regression leads to progesterone and estrogen withdrawal and then menstruation.
Q12. What is the mechanism of menstruation, and what are the normal parameters? Withdrawal of estrogen and progesterone causes prostaglandin (PGF2-alpha) release and spiral arteriolar vasoconstriction. Ischaemia and matrix metalloproteinases then break down the functional layer. The basal layer is retained. FIGO normal values: cycle 24-38 days, duration up to 8 days, blood loss 5-80 mL.
Q13. What are the histological features of the secretory endometrium? Subnuclear vacuoles appear first (day 16). Glands become tortuous and saw-toothed with secretions. Stromal oedema occurs around day 22-23, and predecidual change around day 25-26 (perivascular first). These features are used for endometrial dating (Noyes criteria).
Q14. What clinical signs indicate ovulation?
  • Cervical mucus becomes clear, watery and elastic (spinnbarkeit) with a ferning pattern, due to estrogen.
  • After ovulation, progesterone abolishes ferning, and the basal body temperature rises by 0.2-0.5 degrees C.
  • Mid-cycle pain (mittelschmerz) may occur.
  • A mid-luteal serum progesterone above 3 ng/mL confirms ovulation. A TVS follicle scan can also be used.

3. Gametogenesis and fertilisation (Q15-20)

Q15. Describe oogenesis and the numbers of oocytes. Primordial germ cells become oogonia, which multiply by mitosis (peak 6-7 million at 20 weeks). They enter meiosis I and arrest at prophase I (diplotene) as primary oocytes, which number 1-2 million at birth and 300,000-400,000 at puberty. About 400-500 are ovulated. Meiosis I completes just before ovulation, producing a secondary oocyte arrested in metaphase II. Meiosis II completes only after sperm penetration.
Q16. Describe spermatogenesis. Spermatogonia become primary spermatocytes, then secondary spermatocytes, then spermatids, and finally spermatozoa by spermiogenesis. The cycle takes about 64-74 days. FSH acts on Sertoli cells and LH on Leydig cells, which produce testosterone.
Q17. What are capacitation and the acrosome reaction? Capacitation is the removal of glycoprotein coat and seminal plasma factors from the sperm head in the female tract (about 7 hours). The acrosome reaction is the release of hyaluronidase and acrosin on binding to ZP3 of the zona pellucida. It lets the sperm penetrate the zona.
Q18. Where and when does fertilisation occur, and how is polyspermy prevented? It occurs in the ampulla within 24 hours of ovulation. The oocyte is viable for 12-24 hours and sperm survive 48-72 hours. The cortical granule reaction (zona reaction) after the first sperm enters makes the zona impermeable. Fusion of pronuclei restores the diploid number (46).
Q19. Outline events from fertilisation to implantation. The zygote divides to form a morula (16 cells, day 3-4). The blastocyst forms around day 5 and the zona is shed. Implantation starts 6-7 days after fertilisation and is completed by day 10-12. Syncytiotrophoblast invades the decidua and hCG appears in maternal blood about 8-9 days after ovulation.
Q20. How does the timing of division determine the type of monozygotic twinning?
  • Day 0-3: dichorionic diamniotic.
  • Day 4-8: monochorionic diamniotic (most common).
  • Day 8-12: monochorionic monoamniotic.
  • After day 13: conjoined twins.

4. Development of the female reproductive system (Q21-26)

Q21. What is the embryological origin of the female genital tract? The paramesonephric (Mullerian) ducts arise from the intermediate mesoderm and coelomic epithelium. They fuse caudally to form the uterus, cervix and upper vagina (classically the upper two thirds). The lower vagina arises from the urogenital sinus. The unfused cranial parts form the fallopian tubes.
Q22. How is sex differentiated in the embryo? The SRY gene on the short arm of the Y chromosome drives testis development at about 7 weeks. Sertoli cells secrete anti-Mullerian hormone, which causes Mullerian regression. Leydig cell testosterone maintains the Wolffian ducts. Without SRY the Mullerian ducts persist, the Wolffian ducts regress, and the ovary develops by about 10 weeks.
Q23. Classify Mullerian anomalies. ASRM classes:
  • I: hypoplasia or agenesis (MRKH).
  • II: unicornuate.
  • III: didelphys.
  • IV: bicornuate.
  • V: septate.
  • VI: arcuate.
  • VII: DES-related.
Septate uterus is the most common and has the worst reproductive outcome (recurrent loss). It is treated by hysteroscopic septal resection.
Q24. What is MRKH syndrome? It is Mullerian agenesis with a 46,XX karyotype, normal ovaries and normal secondary sexual characters, including pubic hair. It presents as primary amenorrhoea with absent uterus and upper vagina. Renal anomalies occur in about 30% and skeletal anomalies in some. Treatment is Frank dilators, or surgical neovagina (Vecchietti, McIndoe).
Q25. What are the Wolffian (mesonephric) remnants in females? They are the epoophoron, paroophoron, appendix vesiculosa and Gartner's duct. Gartner's duct cysts lie in the anterolateral vaginal wall. The hydatid of Morgagni is a Mullerian remnant.
Q26. What is an imperforate hymen, and how does it present? It is a failure of canalisation of the vaginal plate or sinovaginal bulbs. It presents in adolescence with primary amenorrhoea, cyclical lower abdominal pain, urinary retention and a bluish bulging hymen from haematocolpos. Treatment is cruciate incision and drainage. A transverse vaginal septum is the differential diagnosis.

5. Placenta and fetal membranes (Q27-33)

Q27. How is the placenta formed? Trophoblast differentiates into cytotrophoblast and syncytiotrophoblast. Villi progress from primary to secondary to tertiary (with fetal vessels) during days 13-21. The chorion frondosum (fetal part) and decidua basalis (maternal part) form the definitive placenta, which is complete by 12-13 weeks.
Q28. Describe the mature placenta. It is discoid, 15-20 cm in diameter and 2.5-3 cm thick. It weighs about 500 g (roughly one sixth of fetal weight) and has 15-20 cotyledons. The fetal surface is smooth and shiny (amnion) with the cord attached. The maternal surface is rough and divided into cotyledons.
Q29. Describe the placental circulation. Maternal blood enters the intervillous space through spiral arteries at about 500-700 mL/min at term. Fetal blood flows through two umbilical arteries (deoxygenated) to the villi and returns in one umbilical vein (oxygenated). The two circulations do not mix.
Q30. What is the placental barrier, and what are its transport mechanisms? Early, it has four layers: syncytiotrophoblast, cytotrophoblast, villous stroma and fetal capillary endothelium. At term the cytotrophoblast is largely lost, and the barrier is thin (vasculosyncytial membrane).
  • Simple diffusion: O2, CO2, urea.
  • Facilitated diffusion: glucose.
  • Active transport: amino acids, calcium, iron.
  • Pinocytosis: IgG.
Q31. Describe the placental hormones.
  • hCG: made by syncytiotrophoblast and maintains the corpus luteum. It peaks at 8-10 weeks and doubles every 48 hours early on. It shares its alpha subunit with LH, FSH and TSH.
  • hPL: anti-insulin and growth-promoting, so it is diabetogenic.
  • Progesterone: the luteo-placental shift occurs at 7-9 weeks.
  • Estrogen (mainly estriol): produced via the fetoplacental unit, since the placenta lacks 17-alpha-hydroxylase and needs fetal adrenal DHEAS.
Q32. Describe the membranes and the amniotic fluid. The amnion (inner, avascular) and chorion form the sac. Amniotic fluid volume peaks at about 800 mL at 34-36 weeks and is about 600 mL at term.
  • Oligohydramnios: AFI below 5 cm or deepest pocket below 2 cm. Causes: PROM, FGR, renal agenesis, post-term.
  • Polyhydramnios: AFI above 24-25 cm or deepest pocket above 8 cm. Causes: diabetes, oesophageal atresia, anencephaly, twins, isoimmunisation.
Q33. Describe the umbilical cord. It is about 50 cm long and contains two arteries, one vein and Wharton's jelly. A single umbilical artery (about 1%) is associated with fetal anomalies. Velamentous insertion can lead to vasa praevia, with a risk of fetal exsanguination on membrane rupture.

6. Puberty and related problems (Q34-39)

Q34. What is the sequence of pubertal events in girls? Thelarche (first sign, 8-13 years), then pubarche, then peak height velocity, then menarche (mean about 12.5-13 years, about 2-2.5 years after thelarche). Adrenarche occurs earlier, at about 6-8 years.
Q35. Describe Tanner staging. Breast stage 1 is prepubertal. Stage 2 is the breast bud, stage 3 is further enlargement, stage 4 is areolar mound, and stage 5 is adult contour. Pubic hair runs from stage 1 (none) to stage 5 (adult distribution). Menarche usually occurs at breast stage 4.
Q36. Define and classify precocious puberty. It is the appearance of secondary sexual characters before 8 years (or menarche before 10 years).
  • Central (GnRH dependent, true): idiopathic in most girls. Other causes are CNS tumours and hypothalamic hamartoma.
  • Peripheral (GnRH independent): ovarian cyst or granulosa cell tumour, McCune-Albright syndrome, CAH, exogenous estrogen.
Treatment of central precocious puberty is a GnRH agonist (leuprolide).
Q37. Define delayed puberty and list causes. It is no breast development by 13 years, or no menarche by 15 years (or 3 years after thelarche).
  • Hypergonadotropic: Turner syndrome, gonadal dysgenesis.
  • Hypogonadotropic: constitutional delay, Kallmann syndrome, hypothalamic causes (weight loss, athletes, chronic illness).
  • Eugonadal: outflow obstruction, MRKH, androgen insensitivity.
Q38. Describe Turner syndrome. Karyotype is 45,XO (or mosaic). Features:
  • Short stature, webbed neck, shield chest and cubitus valgus.
  • Streak gonads with raised FSH and primary amenorrhoea.
  • Coarctation of the aorta, bicuspid aortic valve and horseshoe kidney.
Treatment is growth hormone, then estrogen and cyclic progestin.
Q39. How do you distinguish complete androgen insensitivity from MRKH? Both present as primary amenorrhoea with a blind vagina and absent uterus.
  • Androgen insensitivity: 46,XY, testes, high or normal-male testosterone, scanty or absent pubic and axillary hair, good breast development. Gonadectomy is done after puberty because of malignancy risk, followed by estrogen.
  • MRKH: 46,XX, ovaries, normal pubic hair, female testosterone.

7. Menopause and related problems (Q40-45)

Q40. Define menopause, perimenopause and premature ovarian insufficiency. Menopause is the permanent cessation of menses for 12 months due to loss of ovarian follicular activity. The mean age is about 47-51 years. Perimenopause is the transition, including the year after the final period. Premature ovarian insufficiency is loss of ovarian function before 40 years, with FSH above 25 IU/L on two occasions 4 weeks apart. Causes include idiopathic, Turner mosaics, fragile X premutation, autoimmune disease and chemotherapy or radiotherapy.
Q41. What are the hormonal changes of menopause? FSH rises first (due to falling inhibin B), reaching above 30-40 IU/L, followed by LH. Estradiol falls. Estrone becomes the main estrogen, from peripheral aromatisation of androstenedione in fat. The ovary still secretes some androgens.
Q42. List the clinical features of menopause.
  • Short term: vasomotor symptoms (hot flushes, night sweats), sleep and mood disturbance.
  • Urogenital syndrome: vaginal dryness, dyspareunia, urinary urgency and recurrent UTI.
  • Long term: osteoporosis and cardiovascular risk.
Q43. What are the indications, contraindications and risks of HRT?
  • Indications: troublesome vasomotor symptoms, genitourinary atrophy, premature ovarian insufficiency, and prevention of osteoporosis when other agents are unsuitable.
  • Women with a uterus need a progestogen to prevent endometrial hyperplasia.
  • Contraindications: breast or endometrial cancer, active VTE, unexplained vaginal bleeding, active liver disease, and previous coronary disease or stroke.
  • Risks (WHI, combined E+P): breast cancer, stroke and VTE. Benefit is greatest if started before 60 years or within 10 years of menopause.
  • Non-hormonal options: SSRIs/SNRIs, gabapentin, NK3 antagonist (fezolinetant), and local vaginal estrogen for urogenital symptoms.
Q44. How is postmenopausal osteoporosis diagnosed and treated? DEXA T-score of -2.5 or lower defines osteoporosis (-1 to -2.5 is osteopenia). Treatment: calcium (about 1200 mg/day total), vitamin D, weight-bearing exercise, and bisphosphonates (alendronate). Alternatives are raloxifene, denosumab and teriparatide.
Q45. How do you evaluate postmenopausal bleeding? Any bleeding more than 12 months after the last period is abnormal, and about 10% have endometrial cancer. Start with TVS: endometrial thickness above 4-5 mm needs endometrial sampling (Pipelle) or hysteroscopy. The commonest cause is atrophic vaginitis or endometritis.

8. Maternal changes during pregnancy (Q46-52)

Q46. What are the uterine changes? Weight increases from about 70 g to 1100 g, and capacity from 10 mL to about 5 L. This is hypertrophy and hyperplasia, then stretching. Fundal height: at the symphysis at 12 weeks, midway to the umbilicus at 16 weeks, at the umbilicus at 20-22 weeks, and at the xiphisternum at 36 weeks. Braxton Hicks contractions occur from early pregnancy.
Q47. Name the signs of early pregnancy.
  • Goodell's sign: cervical softening.
  • Chadwick's sign: bluish vaginal discolouration (6-8 weeks).
  • Hegar's sign: isthmus softening (6-10 weeks).
  • Osiander's sign: pulsation in the lateral fornices.
  • Palmer's sign: regular uterine contractions on bimanual examination.
Q48. What are the cardiovascular and haematological changes?
  • Blood volume rises 40-50%. Plasma rises more than red cells, causing physiological anaemia (Hb about 10.5-11 g/dL).
  • Cardiac output rises 30-50% (peaks at 28-32 weeks) and rises further in labour.
  • Heart rate rises 10-15 bpm, and BP falls in mid-pregnancy (SVR is lower).
  • Supine hypotension can occur from aortocaval compression.
  • Pregnancy is hypercoagulable: fibrinogen and factors VII, VIII, X rise, and protein S falls.
Q49. What are the respiratory changes? Tidal volume rises 30-40%, minute ventilation about 40%, and the diaphragm rises about 4 cm. ERV, RV and FRC fall, while vital capacity is unchanged. PaCO2 falls to about 30 mmHg (compensated respiratory alkalosis with bicarbonate 18-21).
Q50. What are the renal changes? GFR and renal plasma flow rise about 50% or more. Serum creatinine falls (about 0.5 mg/dL), as does urea. Glycosuria can be physiological. Ureteric dilatation (right more than left) from progesterone and compression increases UTI and pyelonephritis risk.
Q51. What are the metabolic, endocrine and GI changes?
  • Weight gain is about 11-12 kg overall. Iron requirement totals about 1000 mg.
  • Insulin resistance from hPL (diabetogenic state).
  • Thyroid: TBG and total T4 rise, free T4 is normal, and TSH may fall in the first trimester due to hCG.
  • Progesterone relaxes smooth muscle, causing heartburn, constipation and delayed gastric emptying.
Q52. What are the skin and breast changes? Skin: linea nigra, chloasma (melasma), striae gravidarum, spider naevi and palmar erythema. Breast: enlargement, Montgomery tubercles, secondary areola, and colostrum from about 16 weeks.

9. Diagnosis of pregnancy, preconceptional and antenatal care (Q53-60)

Q53. Classify the signs of pregnancy.
  • Presumptive: amenorrhoea, nausea, breast changes, quickening (16-20 weeks).
  • Probable: uterine enlargement, Hegar's sign, ballottement, Braxton Hicks, positive urine hCG.
  • Positive: fetal heart sounds, fetal movements felt by the examiner, and ultrasound visualisation of the fetus. Cardiac activity is seen by about 6 weeks.
Q54. How reliable are pregnancy tests? Urine tests detect hCG at roughly 20-25 mIU/mL, about the time of the missed period. Serum beta-hCG is positive about 8-11 days after conception. False negatives: very early testing and the hook effect. False positives: molar pregnancy, choriocarcinoma, heterophile antibodies.
Q55. How do you calculate the EDD? Naegele's rule: add 7 days to the LMP and 9 months (or subtract 3 months and add 7 days). It assumes a 28-day cycle and 280 days of gestation. First-trimester crown-rump length is the most accurate dating method (about +/- 5-7 days).
Q56. What is preconceptional care?
  • Folic acid 400 mcg daily from 3 months before conception through 12 weeks. A higher dose (4-5 mg) is used with a previous NTD or antiepileptic use.
  • Rubella vaccination if non-immune (avoid conception for 1 month).
  • Optimise diabetes, thyroid disease and hypertension, and stop teratogenic drugs.
  • Counsel on weight, smoking and alcohol, and screen for thalassaemia.
Q57. What is the antenatal visit schedule? WHO recommends 8 contacts (12, 20, 26, 30, 34, 36, 38 and 40 weeks). India recommends a minimum of 4 visits (with PMSMA on the 9th of every month). The traditional schedule is monthly to 28 weeks, fortnightly to 36 weeks, then weekly. The first visit should be before 12 weeks.
Q58. What supplements and immunisations are given in pregnancy?
  • Iron-folic acid (100 mg elemental iron + 500 mcg folate) from the second trimester for 180 days.
  • Calcium 1 g/day from 14 weeks.
  • Td vaccine (two doses 4 weeks apart, or a booster if previously immunised).
  • Albendazole 400 mg once in the second trimester.
  • Influenza and Tdap (27-36 weeks) where available.
  • Low-dose aspirin from 12-16 weeks in women at high risk of pre-eclampsia.
Q59. What does the antenatal abdominal examination include?
  • Fundal height: McDonald's rule, cm approximates weeks +/- 2 from 24-36 weeks.
  • Leopold's manoeuvres: fundal, lateral and two pelvic grips.
  • Engagement is assessed in fifths palpable.
  • FHR: Doppler from 10-12 weeks, Pinard from about 20 weeks.
Q60. What antenatal screening is done?
  • Combined first-trimester screen (11-13+6 weeks): NT, PAPP-A and free beta-hCG. NT above 3 mm raises suspicion.
  • Quadruple test at 15-20 weeks (AFP, hCG, uE3, inhibin A). NIPT is available.
  • Anomaly scan at 18-20 weeks.
  • Danger signs needing immediate care: bleeding, leaking, headache and blurred vision, reduced fetal movements, fever and severe abdominal pain.

10. Abnormal uterine bleeding (Q61-67)

Q61. Define AUB and the normal menstrual parameters. AUB is bleeding from the uterine corpus that is abnormal in regularity, volume, frequency or duration. FIGO normal values: frequency 24-38 days, duration up to 8 days, volume 5-80 mL. Heavy menstrual bleeding (HMB) is excess volume that interferes with quality of life. Older terms (menorrhagia, metrorrhagia, DUB) are no longer recommended.
Q62. Explain the PALM-COEIN classification. Structural causes (PALM): Polyp, Adenomyosis, Leiomyoma, Malignancy and hyperplasia. Non-structural causes (COEIN): Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not yet classified. FIGO introduced this in 2011 (Sabiston describes the same).
Q63. How do you evaluate a woman with AUB?
  • Always exclude pregnancy first.
  • History and examination (BMI, hirsutism, thyroid, speculum and pelvic).
  • CBC, TSH, prolactin, and a coagulation screen (e.g., von Willebrand disease in adolescents).
  • Pelvic ultrasound, then hysteroscopy for intracavitary lesions.
  • Endometrial sampling if age 45 or older, or younger with risk factors (obesity, PCOS, persistent AUB, failed medical therapy).
Q64. What is the pathophysiology of anovulatory AUB (AUB-O)? No ovulation means no corpus luteum and unopposed estrogen. The endometrium proliferates and becomes hyperplastic, then breaks down irregularly. It is common in adolescents and in the perimenopause, and in PCOS and thyroid disease.
Q65. How do you manage acute heavy bleeding? Resuscitate first. Then use tranexamic acid, high-dose estrogen or oral combined pill taper, or high-dose progestin (norethisterone 5 mg TDS or medroxyprogesterone). Foley balloon tamponade can be used. D&C or hysteroscopy is for failure of medical therapy.
Q66. What are the options for long-term management of HMB?
  • First line: LNG-IUS (52 mg), which is the most effective medical option.
  • Others: tranexamic acid, NSAIDs (mefenamic acid), combined OCP, cyclical progestins, GnRH analogues (short term).
  • Surgical: endometrial ablation, myomectomy or polypectomy for structural causes, hysterectomy as definitive treatment.
Q67. Describe endometrial hyperplasia and adenomyosis.
  • Hyperplasia without atypia: low risk of cancer. Treat with LNG-IUS or oral progestins. Atypical hyperplasia/EIN: high cancer risk (complex atypical about 29%), so hysterectomy is advised.
  • Adenomyosis: endometrial glands within the myometrium, presenting with HMB, dysmenorrhoea and a globular tender uterus. MRI shows a junctional zone above 12 mm. Definitive diagnosis is histological.

11. Miscarriage (Q68-74)

Q68. Define miscarriage and give the commonest causes. It is loss of pregnancy before viability: below 20 weeks or fetal weight below 500 g (WHO/India). It occurs in 15-20% of clinical pregnancies. Chromosomal abnormalities account for 50-60% (autosomal trisomies, then monosomy X). Others: uterine anomalies, cervical insufficiency, antiphospholipid syndrome, diabetes, thyroid disease, infections.
Q69. Classify miscarriage clinically.
  • Threatened: bleeding, closed os, viable fetus.
  • Inevitable: open os, products not yet expelled.
  • Incomplete: partial expulsion of products.
  • Complete: all products expelled, os closed.
  • Missed: dead fetus retained, closed os, regression of symptoms.
  • Septic: infected products with fever.
Q70. How do you manage a threatened miscarriage? Reassure, confirm viability by ultrasound, and give anti-D to Rh-negative women. Bed rest has no proven benefit. In the PRISM trial, vaginal progesterone 400 mg BD helped women with early bleeding and a history of 3 or more miscarriages (live birth 72% vs 57%). It did not help overall.
Q71. How do you manage missed and incomplete miscarriage? Options are expectant, medical or surgical management.
  • Medical: misoprostol (for incomplete, 600 mcg oral or 400 mcg sublingual; for missed, 800 mcg vaginal, with or without mifepristone 200 mg).
  • Surgical: suction evacuation or MVA (up to 12 weeks).
  • Complete miscarriage needs no evacuation.
  • Give anti-D to Rh-negative women.
Q72. What is recurrent pregnancy loss, and how is it investigated? Two or more (ESHRE/ASRM) or three or more (RCOG) consecutive losses. Investigate:
  • Antiphospholipid antibodies (lupus anticoagulant, anticardiolipin, anti-beta2 glycoprotein I; repeat at 12 weeks).
  • Parental karyotype (balanced translocation in 3-5%).
  • Uterine imaging (3D USG, hysteroscopy), TSH and glucose.
Q73. How is APS in pregnancy treated? Low-dose aspirin plus prophylactic LMWH. APS is the commonest treatable cause. Unexplained recurrent loss is managed with supportive care.
Q74. Describe cervical insufficiency and cerclage. It causes painless mid-trimester dilatation and loss. TVS cervical length below 25 mm before 24 weeks supports the diagnosis.
  • Cerclage types: McDonald (purse-string at the cervicovaginal junction) and Shirodkar (submucosal). Insert at 12-14 weeks and remove at 36-37 weeks.
  • Vaginal progesterone is an alternative for a short cervix.
  • Septic abortion is treated with broad-spectrum antibiotics, then evacuation. The MTP Act (2021 amendment) allows termination up to 20 weeks with one provider's opinion, and 20-24 weeks with two providers for special categories.

12. Leiomyoma of uterus (Q75-80)

Q75. What are the types and pathology of fibroids? Fibroids are benign, monoclonal smooth muscle tumours that depend on estrogen and progesterone. They are the commonest benign uterine tumour. Types are intramural (commonest), subserosal and submucosal (most likely to cause bleeding). Gross: firm, whorled, with a pseudocapsule. Microscopy: interlacing smooth muscle bundles with few mitoses. Genetics: MED12 mutations, t(12;14).
Q76. What are the clinical features? Many are asymptomatic. Symptoms are HMB (especially submucosal), pressure effects (frequency, constipation), pain, infertility and recurrent miscarriage. Examination finds a firm, irregular, nodular uterus that moves with the cervix.
Q77. What are the degenerations of a fibroid?
  • Hyaline (commonest).
  • Cystic, calcific (post-menopausal "womb stone"), fatty.
  • Red (carneous) degeneration: acute pain and low fever, typically in pregnancy. Treated conservatively with analgesia.
  • Sarcomatous change (below 0.5%): rapid growth, especially after menopause.
  • Infection/necrosis, usually of a submucous polyp.
Q78. How is a fibroid diagnosed? Ultrasound is first line. MRI is used for mapping and to differentiate from adenomyosis. Hysteroscopy is used for submucous fibroids. Differential diagnoses are adenomyosis, pregnancy, ovarian tumour and uterine sarcoma.
Q79. How are fibroids managed?
  • Asymptomatic: observe.
  • Medical: tranexamic acid, NSAIDs, LNG-IUS (if cavity not distorted), GnRH analogues (3-6 months, shrink fibroids but regrowth follows), SPRMs, mifepristone.
  • Surgical: myomectomy (fertility desired), hysterectomy (definitive), hysteroscopic resection (submucous), uterine artery embolisation, MRgFUS.
Q80. What is the effect of fibroids in pregnancy? Red degeneration, malpresentation, preterm labour, obstructed labour (cervical or lower segment fibroid), abruption, PPH and retained placenta. Myomectomy at caesarean is generally avoided. After myomectomy, recurrence occurs in 15-30%, and there is a rupture risk in later pregnancy.

13. Normal and abnormal puerperium (Q81-86)

Q81. Define the puerperium and describe involution. It runs from delivery of the placenta to 6 weeks (42 days). The uterus weighs about 1000 g after delivery and about 60 g by 6 weeks, with the fundus descending about 1 cm/day. Lochia: rubra (1-4 days), serosa (5-9 days) and alba (10-15 days). Foul lochia suggests infection. Subinvolution is caused by retained products, infection, fibroids or a full bladder.
Q82. Describe the physiology of lactation. Prolactin drives milk synthesis. Oxytocin drives let-down (milk ejection reflex). Progesterone withdrawal after delivery triggers lactogenesis (milk comes in at 2-3 days). WHO recommends breastfeeding within 1 hour and exclusive breastfeeding for 6 months. The lactational amenorrhoea method is over 98% effective if exclusive, amenorrhoeic and within 6 months.
Q83. What is puerperal pyrexia, and how is it managed? Temperature of 38 degrees C or higher on two occasions 24 hours apart in the first 10 days (excluding the first 24 hours). Causes: genital tract infection (endometritis is commonest), UTI, mastitis, wound infection, DVT. Organisms: group A streptococcus, E. coli, Bacteroides, anaerobic streptococci, Staph aureus. Treat with cultures and broad-spectrum antibiotics (clindamycin + gentamicin for endometritis), and remove retained products.
Q84. Define PPH and outline its management. PPH is blood loss above 500 mL after vaginal delivery (above 1000 mL after caesarean), or any loss causing haemodynamic instability. Primary is within 24 hours, secondary is from 24 hours to 12 weeks. Causes (4 Ts): Tone (commonest), Trauma, Tissue, Thrombin. Prevent with AMTSL (oxytocin 10 IU IM, controlled cord traction, uterine massage).
  • Treat with oxytocin, ergometrine (avoid in hypertension), carboprost (avoid in asthma), misoprostol and tranexamic acid 1 g IV.
  • Then bimanual compression, balloon tamponade, B-Lynch suture, uterine or internal iliac artery ligation, and hysterectomy.
Q85. What are the postpartum psychiatric disorders?
  • Baby blues: days 3-5, 50-80%, self-limiting.
  • Postpartum depression: 10-15%. Screen with EPDS.
  • Puerperal psychosis: 0.1-0.2%, onset within 2 weeks, a psychiatric emergency (risk with bipolar disorder).
Q86. How are mastitis and breast abscess managed? Staph aureus is the usual organism. Mastitis is treated with continued breastfeeding or expression, analgesia and cloxacillin or flucloxacillin. An abscess needs ultrasound-guided aspiration or incision and drainage.

14. STDs, and antepartum and intrapartum fetal surveillance (Q87-94)

Q87. Describe syphilis and its treatment. Caused by Treponema pallidum.
  • Primary: painless indurated chancre. Secondary: rash and condylomata lata. Tertiary: gumma.
  • Diagnosis: darkfield microscopy; VDRL/RPR (screening) and TPHA/FTA-ABS (confirmatory).
  • Treatment: benzathine penicillin 2.4 MU IM single dose for early disease, weekly x3 for late latent disease. Penicillin is the only option in pregnancy.
  • Congenital syphilis: snuffles, saddle nose, Hutchinson teeth, interstitial keratitis, deafness.
Q88. How do the common causes of vaginal discharge differ?
  • Bacterial vaginosis: thin grey discharge, pH above 4.5, positive whiff test, clue cells (Amsel criteria). Treat with metronidazole 400-500 mg BD for 7 days.
  • Trichomonas: frothy yellow-green discharge, strawberry
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