Learn — Gynaecology

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Vaginitis

Vaginitis is inflammation of the vagina presenting as an abnormal discharge with itching, soreness or odour, and in the reproductive years it is nearly always one of three conditions: bacterial vaginosis, vulvovaginal candidiasis or trichomoniasis. It matters because the three feel alike to the woman but differ in pH, microscopy, drug and whether the partner must be treated — and because trichomoniasis is a sexually transmitted infection that raises the risk of acquiring HIV and of preterm birth.

Normal vaginal pH is 3.8–4.5, held acid by lactobacilli. A pH above 4.5 points to bacterial vaginosis or trichomoniasis and away from candidiasis, so the pH paper is the single most useful bedside discriminator.
Bacterial vaginosis is an overgrowth of Gardnerella vaginalis and anaerobes with loss of lactobacilli: thin homogeneous grey-white discharge, fishy odour, pH above 4.5, clue cells on saline wet mount and no inflammation — hence vaginosis rather than vaginitis. Treat with metronidazole 400 mg twice daily for 7 days (or 2 g as a single dose); the male partner is not treated.
Vulvovaginal candidiasis is usually Candida albicans: thick white curdy discharge adherent to the vaginal wall, intense itching and soreness, a normal pH of 4.0–4.5, and budding yeasts with pseudohyphae on a 10% potassium hydroxide mount. Treat with fluconazole 150 mg orally as a single dose or clotrimazole 500 mg as a single pessary; in pregnancy use a topical azole for 7 days and avoid oral fluconazole.
Trichomoniasis is Trichomonas vaginalis, a flagellated protozoon: frothy greenish-yellow offensive discharge, vulval soreness, pH above 5, a strawberry cervix (colpitis macularis) in a minority, and motile trichomonads on saline wet mount. Treat with metronidazole 2 g orally as a single dose, or 400 mg twice daily for 7 days, and treat the partner at the same time.
Amsel's criteria diagnose bacterial vaginosis when any three of four are present: homogeneous thin discharge, pH above 4.5, a positive whiff (amine) test with 10% potassium hydroxide, and clue cells on microscopy. Nugent scoring of a Gram-stained smear is the laboratory standard.
Alcohol is avoided during metronidazole and for 24 hours after the last dose (48 hours after tinidazole) because of the disulfiram-like reaction of flushing, vomiting and tachycardia.
Atrophic vaginitis in the postmenopausal woman is not infective: a thin, dry, sometimes blood-stained discharge with pale friable epithelium and a pH above 5, treated with a lubricant and low-dose topical oestrogen.
In pregnancy both bacterial vaginosis and trichomoniasis are associated with preterm labour and premature rupture of the membranes; symptomatic women are treated, and metronidazole may be used in pregnancy.

Syndromic management of PID and vaginitis

Syndromic management is the NACO approach of treating a patient at the very first visit on the basis of a recognisable group of symptoms and signs — a syndrome — rather than waiting for a laboratory diagnosis, using a pre-packed colour-coded kit that covers all the likely organisms for that syndrome. It matters because most Indian primary-care settings have no microbiology and the patient often does not return, while an untreated cervical or upper genital infection ends in infertility, ectopic pregnancy or onward transmission of HIV.

There are seven colour-coded kits, one per syndrome, supplied free through designated STI/RTI (Suraksha) clinics, primary health centres and ICTC-linked facilities, and each is given with a fixed counselling package.
Kit 1, grey — urethral discharge, ano-rectal discharge and cervicitis: azithromycin 1 g as a single dose with cefixime 400 mg as a single dose, covering chlamydia and gonorrhoea together.
Kit 2, green — vaginal discharge: secnidazole 2 g as a single dose with fluconazole 150 mg as a single dose, the first covering bacterial vaginosis and trichomoniasis and the second covering candidiasis.
Kit 3, white — non-herpetic genital ulcer: benzathine penicillin 2.4 million units intramuscularly after a test dose, with azithromycin 1 g. Kit 4, blue — the same syndrome in a penicillin-allergic patient: doxycycline 100 mg twice daily for 15 days with azithromycin 1 g.
Kit 5, red — herpetic genital ulcer: acyclovir 400 mg three times daily for 7 days. Kit 7, black — inguinal bubo: doxycycline 100 mg twice daily for 21 days with azithromycin 1 g.
Kit 6, yellow — lower abdominal pain, that is pelvic inflammatory disease: cefixime 400 mg as a single dose, with metronidazole 400 mg twice daily and doxycycline 100 mg twice daily, both for 14 days.
Every kit is issued with the four C's — Counselling, Condom promotion and provision, Contact (partner) treatment, and Compliance with the full course — plus HIV, syphilis and hepatitis B testing with pre- and post-test counselling, and a review at 7 days.
Doxycycline is contraindicated in pregnancy and lactation, so a pregnant woman with lower abdominal pain or discharge is not simply given Kit 6; she is treated with the pregnancy-safe alternative and referred.
Syndromic management has a known weakness: it treats symptomatic patients only, and it cannot detect the asymptomatic cervical infection that causes much of the tubal damage, which is why partner treatment and follow-up are not optional extras.

Pap smear

The Papanicolaou smear is a cytological screening test in which cells are scraped from the transformation zone of the cervix, fixed and stained so that precancerous change can be found years before an invasive cancer develops. It matters because cervical cancer is one of the commonest cancers in Indian women and is almost entirely preventable: the disease has a decade-long precancerous phase, and screening is what finds it while it can still be treated in an outpatient room.

The sample must come from the transformation zone, the squamocolumnar junction where almost all cervical cancers arise: the Ayre's spatula is rotated through 360° at the ectocervix and an endocervical brush is rotated within the canal.
Preparation: no douching, vaginal medication, spermicide or intercourse for 48 hours before, not during menstruation, and no lubricant on the speculum other than warm water.
Fixation is immediate — a conventional smear is spread thinly on a labelled slide and fixed in 95% ethyl alcohol or with a spray fixative within seconds, because air-drying artefact makes the slide unreadable. Liquid-based cytology rinses the brush head into a preservative vial and allows reflex HPV testing from the same sample.
The Bethesda system reports specimen adequacy first, then the result: negative for intraepithelial lesion or malignancy, ASC-US, ASC-H, LSIL, HSIL, atypical glandular cells, adenocarcinoma in situ, or carcinoma.
India's programme under the National Programme for Prevention and Control of Non-Communicable Diseases screens women aged 30 to 65 once every 5 years, and the primary community-level test is visual inspection with acetic acid performed by a trained ANM at the Ayushman Arogya Mandir (formerly the health and wellness centre), with referral of every VIA-positive woman for colposcopy and treatment.
WHO now recommends HPV DNA testing as the preferred primary screening test from the age of 30, repeated every 5 to 10 years in the general population and from 25 years more frequently in women living with HIV. Where cytology is the test used, the ACOG pathway screens from 21 years with cytology alone every 3 years to 29, then HPV testing or co-testing every 5 years to 65.
The positive pathway: HSIL on cytology or a VIA-positive cervix goes to colposcopy with a directed biopsy. A confirmed high-grade lesion is treated by thermal ablation or cryotherapy when the whole lesion is visible and ectocervical, and by LEEP/LLETZ or cold-knife conisation when it is not, or when glandular disease or invasion is suspected.
WHO's elimination targets for 2030 are 90–70–90: 90% of girls fully vaccinated against HPV by 15 years, 70% of women screened with a high-performance test at 35 and again at 45, and 90% of women with disease treated.
A smear is a screening test, not a diagnosis: a negative smear in a woman with postcoital bleeding or a visible cervical lesion is disregarded and she is biopsied.

HPV and vaccine

Human papillomavirus is a double-stranded DNA virus transmitted by sexual and skin-to-skin genital contact, and persistent infection with a high-risk type is the necessary cause of virtually all cervical cancer. It matters because the vaccine works only before exposure — it prevents infection rather than treating it — so the nurse's window is the girl of 9 to 14, years before she is at any risk.

HPV 16 and 18 cause about 70% of cervical cancers, and adding types 31, 33, 45, 52 and 58 accounts for about 90%. The low-risk types 6 and 11 cause about 90% of anogenital warts and are not oncogenic.
Most HPV infection is transient and clears within 1 to 2 years; it is persistence of a high-risk type, with the viral E6 and E7 proteins inactivating p53 and the retinoblastoma protein, that produces cervical intraepithelial neoplasia and then invasive cancer over 10 to 20 years.
The vaccines are bivalent (16, 18), quadrivalent (6, 11, 16, 18) and nonavalent (6, 11, 16, 18, 31, 33, 45, 52, 58). All are non-infectious virus-like particle vaccines containing no viral DNA, and all are given intramuscularly into the deltoid.
Schedule: two doses 6 months apart for the primary target group of girls aged 9 to 14 years, and three doses at 0, 1 to 2 and 6 months for those starting at 15 years or older and for immunocompromised people, including those living with HIV.
WHO 2022 endorses a single-dose schedule as an option for girls aged 9–14. India launched nationwide HPV vaccination on 28 February 2026: one dose of Gardasil-4 (quadrivalent), free for girls aged 14 at government facilities — a 90-day campaign, then on routine immunisation days.
CERVAVAC (Serum Institute of India, quadrivalent) was approved by the DCGI in 2022 and is India's first indigenous HPV vaccine.
The vaccine is prophylactic and not therapeutic: it does not clear an existing infection or treat an existing lesion, and a vaccinated woman still needs cervical screening on exactly the same schedule as anyone else.
It is best given before sexual debut, but it is not contraindicated in a sexually active woman. It is deferred in pregnancy — a dose given inadvertently is not a reason to terminate — and it is safe during breastfeeding.
Adverse effects are local and mild: pain, redness and swelling at the site, low-grade fever and headache. Syncope is common enough in adolescents that the recipient is kept seated or lying and observed for 15 minutes after the injection.
Boys benefit too, since HPV causes anal, penile and oropharyngeal cancer as well as genital warts, and gender-neutral vaccination adds herd protection for girls.

Ovarian tumours and tumour markers

Ovarian tumours are neoplasms classified by the cell they arise from — surface epithelial, germ cell and sex-cord stromal — with metastatic deposits such as the Krukenberg tumour as a fourth group. They matter because the ovary is a silent organ: about 70% of epithelial cancers present at stage III or IV with nothing more than vague abdominal symptoms, and it is the tumour marker together with the ultrasound that turns bloating into a diagnosis.

Surface epithelial tumours are the commonest group overall and cause about 90% of ovarian malignancy; the serous type is the commonest, and high-grade serous carcinoma is the classic CA-125-secreting cancer. Mucinous tumours are the ones that grow enormous and cause pseudomyxoma peritonei when they rupture.
Germ cell tumours are the tumours of the young, under 20 years, and the markers name them: dysgerminoma with LDH (the commonest malignant germ cell tumour, and radiosensitive), yolk sac or endodermal sinus tumour with alpha-fetoprotein and Schiller–Duval bodies, choriocarcinoma with beta-hCG, and embryonal carcinoma with both. The mature cystic teratoma or dermoid is the commonest benign ovarian tumour of the reproductive years and the one that undergoes torsion.
Sex-cord stromal tumours secrete hormones: the granulosa cell tumour produces oestrogen and inhibin and presents as precocious puberty in a child or postmenopausal bleeding in an older woman, with Call–Exner bodies on histology; the Sertoli–Leydig cell tumour produces androgens and causes virilisation; thecoma and fibroma are benign.
CA-125 is raised in over 80% of epithelial ovarian cancers but is not a screening test: it also rises in endometriosis, fibroids, pelvic infection, tuberculosis, cirrhosis, heart failure, menstruation and pregnancy. It is most useful in a postmenopausal woman and for monitoring response and recurrence; HE4 with the ROMA index improves specificity.
Krukenberg tumour is a bilateral metastasis to the ovaries, classically from a signet-ring gastric carcinoma, so any bilateral solid ovarian mass demands a search for a primary in the stomach, colon or breast.
Meigs' syndrome is a benign ovarian fibroma with ascites and a right-sided pleural effusion, and both resolve completely once the tumour is removed.
Features that make a mass suspicious on ultrasound: solid or mixed echogenicity, size above 10 cm, bilaterality, thick septa, papillary projections, ascites and abundant central vascularity on Doppler. The risk of malignancy index combines the ultrasound score, the menopausal status and the CA-125.
FIGO staging is surgical: stage I is confined to the ovaries, stage II has pelvic extension, stage III has peritoneal spread beyond the pelvis or retroperitoneal nodes, and stage IV is distant metastasis including a malignant pleural effusion or liver and splenic parenchymal deposits.
Treatment of epithelial cancer is complete cytoreductive surgery with full staging plus platinum-based chemotherapy (carboplatin with paclitaxel); a malignant germ cell tumour in a young woman is usually treated by fertility-sparing unilateral salpingo-oophorectomy with BEP chemotherapy — bleomycin, etoposide and cisplatin.
BRCA1 and BRCA2 mutations carry a high lifetime risk of ovarian cancer and risk-reducing salpingo-oophorectomy is offered once childbearing is complete; long use of the combined oral contraceptive pill substantially lowers the risk in the general population.

Semen analysis

Semen analysis is the first and most informative investigation in an infertile couple: it measures the volume, concentration, total number, motility, morphology and vitality of the ejaculate against agreed reference limits. It matters because a male factor is present in about 40 to 50% of infertile couples, the test is cheap and non-invasive, and doing it first spares the woman a series of invasive investigations that may prove unnecessary.

WHO sixth edition (2021) lower reference limits, which are fifth-centile values from fertile men: semen volume 1.4 mL, sperm concentration 16 million per mL, total sperm number 39 million per ejaculate, total motility 42%, progressive motility 30%, normal morphology 4%, vitality 54% and pH 7.2 or above.
Collection: 2 to 7 days of sexual abstinence, produced by masturbation into a clean wide-mouthed sterile container — never into an ordinary condom, which is spermicidal, and never by coitus interruptus — with the whole ejaculate collected, kept at body temperature and delivered to the laboratory within 1 hour, the time of production written on the container.
These are reference limits, not a pass mark: a man below them can father a child and a man above them may not. The test is repeated after 2 to 3 weeks before any conclusion, and after about 3 months when a treatment effect is being judged, because a cycle of spermatogenesis takes roughly 74 days.
The vocabulary: oligozoospermia is a low concentration, asthenozoospermia low motility, teratozoospermia few normal forms, oligoasthenoteratozoospermia all three together, azoospermia no sperm in the centrifuged deposit of two separate samples, aspermia no ejaculate at all, and necrozoospermia all sperm dead.
Azoospermia splits into obstructive — normal testicular volume with a normal FSH, from vasal agenesis, post-infective obstruction or vasectomy, with sperm retrievable for ICSI — and non-obstructive, with small testes and a high FSH, from Klinefelter syndrome, Y-chromosome microdeletion, cryptorchidism, mumps orchitis or chemotherapy.
Reversible contributors worth correcting: varicocele, scrotal heat from tight clothing, hot baths, long driving or a laptop on the lap, smoking, alcohol, anabolic steroids and testosterone supplements, obesity, poorly controlled diabetes, and drugs such as sulfasalazine, ketoconazole, cimetidine and spironolactone.
Give the result to both partners together and in private, with the point made plainly that one abnormal report is not a diagnosis of infertility and that intrauterine insemination, ICSI and donor options exist.

The menstrual cycle — hormones, ovarian and endometrial phases

The menstrual cycle is the monthly sequence in which the hypothalamus, pituitary, ovary and endometrium prepare for a pregnancy and, when none occurs, shed the preparation as menstrual bleeding; it is counted from the first day of bleeding and lasts 21 to 35 days, with a median of 28. The ovary runs a follicular phase, ovulation and a luteal phase, the endometrium the matching menstrual, proliferative and secretory phases, and four hormones — FSH, LH, oestradiol and progesterone — set the timing, with the luteal phase fixed at about 14 days so that every variation in cycle length lies before ovulation.

Normal values: cycle length 21 to 35 days; bleeding 2 to 7 days (average 4 to 5); blood loss 20 to 80 mL with an average of about 35 mL, over 80 mL being heavy menstrual bleeding; menstrual blood does not clot because the endometrium releases plasmin, so clots mean the loss is heavy. Menarche is at about 12 to 14 years and menopause at about 45 to 50.
Days 1 to about 13, the follicular phase: FSH, released as the previous corpus luteum’s progesterone, oestrogen and inhibin fall, recruits a cohort of antral follicles; by day 5 to 7 one dominant follicle is selected and its granulosa cells make rising oestradiol (theca cells make androgen under LH, granulosa cells convert it under FSH), which suppresses FSH so the rest undergo atresia.
Days 5 to 14 in the endometrium, the proliferative phase: oestradiol regrows the functional layer from the basal layer — straight tubular glands, thin stroma, lengthening spiral arteries — from about 2 mm after menses to 8 to 12 mm at ovulation, and it thins the cervical mucus into the clear, stretchy (spinnbarkeit 8 to 10 cm), ferning mucus that admits sperm.
The LH surge: once oestradiol has stayed above about 200 pg/mL for two days its feedback on the pituitary turns positive, LH (with a smaller FSH peak) surges on day 12 to 13, and ovulation follows 24 to 36 hours after the surge begins (most often 34 to 36) and 10 to 12 hours after its peak — a urinary LH kit turns positive about a day before the egg is released.
Ovulation, about day 14 in a 28-day cycle: the Graafian follicle, 18 to 25 mm on ultrasound, ruptures and the secondary oocyte is picked up by the fimbria; it survives 12 to 24 hours and sperm survive 3 to 5 days, so the fertile window is the five days before ovulation and the day itself. Mid-cycle pain (mittelschmerz) and a small ovulation spot are common and normal.
Days 15 to 28, the luteal phase: the ruptured follicle becomes the corpus luteum under LH and secretes progesterone (peak about day 21, seven days after ovulation — a serum progesterone above 3 ng/mL then confirms ovulation) and a second, smaller rise of oestradiol; without hCG it regresses by day 26 to a corpus albicans, and the luteal phase keeps its 14 days (12 to 16) whatever the cycle length.
The secretory endometrium under progesterone: tortuous saw-toothed glands full of glycogen, a swollen oedematous stroma, coiled spiral arteries and a decidua-like reaction — ready for the implantation window of days 20 to 24, six to ten days after ovulation; the cervical mucus turns thick, scanty and cellular and ferning disappears.
Progesterone is thermogenic: the basal body temperature rises 0.3 to 0.5 °C after ovulation and stays up until the next period, so a biphasic chart proves ovulation only in retrospect, and the temperature method of contraception counts its safe days from the third day after the rise.
Menstruation, days 1 to 4 or 5: the corpus luteum’s collapse withdraws progesterone and oestrogen, the spiral arteries go into spasm, the functional layer (stratum compactum and spongiosum) becomes ischaemic and is shed while the basal layer survives to regenerate — prostaglandin F2-alpha from the shed tissue drives the cramps of primary dysmenorrhoea, which is why NSAIDs relieve it.
If fertilisation occurs, hCG from the syncytiotrophoblast rescues the corpus luteum from about day 8 to 9 after ovulation and keeps it making progesterone until the placenta takes over at 7 to 10 weeks (the luteo-placental shift) — so a missed period is the first sign of pregnancy and a urine hCG test is usually positive around the day the period was due.
Calendar (rhythm) method: the first fertile day is the shortest cycle minus 18 and the last is the longest cycle minus 11 — the arithmetic of a fixed 14-day luteal phase, 3 to 5 days of sperm survival and a day of ovum survival.

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