Gynaecology: Summative Revision Notes

Frequency 24–38 days · duration ≤8 days · no intermenstrual/postcoital bleeding · no flooding or large clots. A cycle meeting all four needs no further workup — the "28-day" figure is a population average, not a diagnostic cutoff. Pad count is a subjective proxy for blood loss, not itself a trigger for objective quantification.

Mittelschmerz (brief, one-sided, mid-cycle, from follicular rupture) — benign, no imaging required. Physiologic leucorrhoea (cyclical, odourless, oestrogen-driven, increases around ovulation and premenstrually) — not infection. Neither is a function of age — the specific features drive the decision to investigate, not how young the patient is.

Menstrual, obstetric, contraceptive, and relevant sexual history are taken as a matter of course — not restricted to the stated complaint. Pelvic examination is performed when clinically indicated, not reflexively at every first visit; a chaperone is offered routinely, not only when the patient specifically asks.

Must cover purpose and diagnostic limits, specific risks (bleeding, infection, rare perforation), voluntary nature, the alternative of hysteroscopy if inconclusive, and how results will be communicated. A strong clinical indication never abbreviates this process. A hyperplasia result does not pre-commit the patient to hysterectomy — management options remain hers to choose.

Raises probability of dysplasia but is not itself a diagnosis — triage to colposcopy with directed biopsy, since histology, not the screening combination, confirms or excludes CIN.

FIGO normal cycle: 24–38 days, ≤8 days duration Pad count ≠ objective workup trigger Chaperone offered routinely, not on request ASCUS + HPV+ → colposcopy, not repeat Pap

Types 0–2 (submucosal) bleed disproportionately via cavity distortion; 3–4 (intramural) and 5–7 (subserosal) more often cause bulk/pressure symptoms or are asymptomatic for bleeding. Location, not size alone, drives both classification and management choice — though subserosal fibroids aren't absolutely incapable of any bleeding contribution either.

Immature HPO axis → no corpus luteum → unopposed oestrogen — usually self-limited, but persistent unopposed exposure carries a real endometrial hyperplasia risk, so cycle regulation (not just reassurance) is reasonable if the pattern persists or bleeding is heavy.

Heavy bleeding present since menarche, plus bruising/epistaxis → screen for von Willebrand disease alongside the gynaecological evaluation, not after exhausting it.

Medical first — tranexamic acid/NSAIDs, or hormonal (COCP, LNG-IUS) — before ablation or hysterectomy. "Objectively confirmed" blood loss confirms the diagnosis, not the treatment tier; a normal workup still warrants symptomatic/hormonal management if bothersome.

PALM = structural, COEIN = non-structural Submucosal fibroids bleed most Bleeding since menarche + bruising → screen for vWD Medical therapy before ablation/hysterectomy

Any two of three — oligo/anovulation, clinical or biochemical hyperandrogenism, polycystic ovarian morphology on USG — after excluding other causes (thyroid, prolactin, non-classic CAH). LH:FSH ratio and insulin resistance testing are not required criteria, despite being commonly mistaken for diagnostic components.

Relatively elevated LH drives theca cell androgen synthesis; insulin resistance amplifies this and lowers hepatic SHBG production — more free, biologically active androgen circulates as a result. (Direction matters: insulin resistance lowers SHBG, it does not raise it.)

Rapid-onset, severe virilisation (voice change, clitoromegaly) over months, rather than gradual hirsutism since adolescence, should prompt evaluation for an androgen-secreting tumour or non-classic CAH — tempo of onset is the key discriminator.

Chronic anovulation → unopposed oestrogen → endometrial hyperplasia risk, independent of fertility intentions — ensure regular withdrawal bleeding (cyclical progestin, COCP, or LNG-IUS) regardless of whether pregnancy is desired.

Fertility desired → lifestyle + letrozole (ovulation induction). Fertility not desired → COCP for cycle regulation/endometrial protection. Metformin is an adjunct for metabolic features, not first-line therapy ahead of the goal-specific option.

Rotterdam: any 2 of 3, no required LH:FSH ratio Insulin resistance lowers SHBG, raises free androgen Rapid virilisation ≠ PCOS Letrozole if fertility desired; COCP if not

An endometrioma on ultrasound is highly suggestive but laparoscopy with histological confirmation remains the definitive standard, particularly for peritoneal/superficial implants that imaging cannot see. CA-125 is non-specific and not a required diagnostic marker.

ASRM stage correlates poorly with pain severity — deep infiltrating lesions and local inflammatory/nerve involvement matter more than total visible disease burden. Minimal disease can be severely painful; extensive disease can be relatively painless. This is recognised disease biology, not a diagnostic error.

Without adhesions or distorted anatomy, infertility is driven by an altered peritoneal/inflammatory environment (cytokines, prostaglandins impairing oocyte quality, fertilisation, implantation) — not mechanical blockage, which becomes dominant only in moderate-to-severe disease.

Induces a hypoestrogenic state — long-term use risks accelerated bone mineral density loss. "Add-back" therapy (low-dose oestrogen-progestin) mitigates this and allows longer treatment durations beyond the otherwise limited window.

Laparoscopy + histology = definitive diagnosis Stage ≠ pain severity Minimal disease infertility = inflammatory, not mechanical GnRH agonist + add-back protects bone

pH overlaps between trichomoniasis and BV — the actual discriminator is wet mount morphology, not pH.

CDC minimum criteria: cervical motion, uterine, or adnexal tenderness in a sexually active woman with pelvic pain. Treat now — do not wait for culture or imaging given the reproductive stakes of delay. Many cases are afebrile; fever is not required.

Perihepatitis from transperitoneal/lymphatic spread of pelvic pathogens — "violin-string" capsular adhesions, not parenchymal disease, hence normal gallbladder/LFTs. A specifically recognised PID complication, not coincidental cholecystitis.

Drainage decision is driven by clinical response (failure after 48–72h, rupture, instability/sepsis) — not abscess size alone. Don't stop antibiotics just because fever resolves; full course (often ~14 days) prevents relapse.

Even adequately treated PID leaves cumulative tubal scarring — risk of tubal factor infertility and ectopic pregnancy increases with each episode and does not plateau after the first.

Trich vs BV: wet mount discriminates, not pH PID: treat on clinical criteria, don't wait Fitz-Hugh-Curtis: capsular, not parenchymal TOA decision = response, not size

Clinical diagnosis — 12 consecutive months of amenorrhea at the expected age. FSH testing is reserved for atypical scenarios (suspected POI, post-hysterectomy uncertainty, contraception masking cycles) — not for confirming a typical presentation. FSH fluctuates, it does not rise smoothly, through perimenopause.

A narrowed hypothalamic thermoneutral zone from oestrogen withdrawal — the thermoregulatory centre overreacts to trivial temperature changes; core temperature itself is not genuinely elevated.

Starting HRT within ~10 years of menopause or before age 60 carries a more favourable cardiovascular risk profile than starting later. Intact uterus → combined oestrogen-progestin (oestrogen-only is for post-hysterectomy women only).

Personal history of oestrogen receptor-positive breast cancer is an absolute/near-absolute contraindication to systemic HRT regardless of years disease-free; adding a progestin protects the endometrium but does not neutralise this specific risk.

Local vaginal oestrogen is first-line for isolated GSM — minimal systemic absorption, a different risk category from oral/transdermal therapy, generally usable even with some systemic HRT contraindications.

Menopause = clinical diagnosis, 12 months amenorrhea HRT window: <10 yrs post-menopause / <60 yrs ER+ breast cancer hx = HRT contraindication Local oestrogen for GSM ≠ systemic risk

HPV 16/18 — high-risk, oncogenic, drive the large majority of cervical cancers. HPV 6/11 — low-risk, cause genital warts, not malignancy. Vaccines target the oncogenic types specifically.

Unopposed oestrogen connects obesity (peripheral aromatization in adipose tissue), nulliparity (fewer progesterone-dominant pregnancy periods), and PCOS (chronic anovulation — lack, not excess, of progesterone).

No validated population screening strategy (CA-125 + USG) reduces mortality in average-risk women — CA-125 is non-specific (fibroids, endometriosis) and insensitive in early disease. Screening is reserved for high genetic risk (e.g. BRCA).

Any amount or duration, including a single resolved episode, warrants endometrial workup before attributing to atrophy — endometrial cancer is the most common gynaecological malignancy presenting this way.

HPV 16/18 = cancer; 6/11 = warts Endometrial cancer risk = unopposed oestrogen No effective ovarian cancer screening test exists Postmenopausal bleeding always gets worked up

Mittelschmerz: brief, one-sided, mid-cycle — benign, no workup Fitz-Hugh-Curtis: violin-string capsular adhesions, not parenchymal liver disease Strawberry cervix: trichomoniasis, not bacterial vaginosis Window of opportunity: HRT timing hypothesis for cardiovascular risk Add-back therapy: protects bone during GnRH agonist use

FIGO normal cycle: 24–38 days, ≤8 days duration Rotterdam: any 2 of 3 criteria Menopause: 12 consecutive months amenorrhea TOA: 48–72 hr antibiotic trial before drainage decision HRT window: within ~10 yrs of menopause / before 60 HPV 16/18: oncogenic; 6/11: low-risk/warts ASCUS + HPV+ → colposcopy threshold Endometrial sampling: indicated for ANY postmenopausal bleeding

PID: treat empirically first, never wait for culture/imaging AUB: medical therapy before ablation/hysterectomy PCOS: confirm fertility goal before choosing first-line therapy Postmenopausal bleeding: workup before attributing to atrophy Endometriosis: laparoscopy + histology before calling it definitive Adolescent menorrhagia since menarche: screen for vWD alongside, not after, gynae workup