AKT · System
52 conditions across 7 areas.0/52 rated · 0%
Benign oestrogen-dependent smooth-muscle tumours of the uterus — the commonest pelvic tumour in women, more common in Black women. Cause heavy menstrual bleeding, bulk symptoms and subfertility; regress after menopause.
Presence of endometrial tissue within the uterine muscle (myometrium), causing heavy painful periods and a diffusely enlarged tender "boggy" uterus — classically in older, multiparous women near the end of their reproductive years. The key fibroids/endometriosis mimic.
Endometrial-like tissue outside the uterine cavity, responding to cyclical hormones — causing chronic pelvic pain, dysmenorrhoea, deep dyspareunia and subfertility. Laparoscopy is the gold-standard diagnostic.
The commonest endocrine disorder in women of reproductive age. Rotterdam criteria (2 of 3): oligo/anovulation, clinical/biochemical hyperandrogenism, and polycystic ovaries on USS. Associated with insulin resistance and long-term metabolic/endometrial risk.
Fluid-filled ovarian structures — usually benign functional cysts in premenopausal women (follicular/corpus luteal). Risk-of-malignancy (RMI) stratification and the menopausal status guide management; complications include rupture, haemorrhage and torsion.
Twisting of the ovary (± fallopian tube) on its vascular pedicle, compromising blood supply — a gynaecological emergency. Usually involves an enlarged ovary (cyst/mass), causing sudden severe unilateral pain; the ovary is salvaged only by prompt detorsion.
A benign extension of endocervical columnar epithelium onto the ectocervix, exposed to the vaginal environment — common in young women, on the COCP and in pregnancy (high oestrogen). Causes post-coital bleeding and discharge.
Permanent cessation of menstruation from loss of ovarian follicular activity — diagnosed clinically (≥12 months amenorrhoea, average age 51). Perimenopause is the symptomatic transition. Premature ovarian insufficiency = before age 40.
The cluster of vaginal and urinary symptoms from oestrogen deficiency after menopause (formerly "atrophic vaginitis") — dryness, dyspareunia, irritation and recurrent urinary symptoms, responsive to vaginal oestrogen.
A chronic inflammatory skin condition, commonest on the anogenital skin of postmenopausal women, causing intense itch and white atrophic plaques in a figure-of-eight distribution. Carries a small risk of vulval squamous cell carcinoma.
Descent of the pelvic organs (bladder=cystocele, rectum=rectocele, uterus, vault) through weakened pelvic floor support. Driven by childbirth, age, oestrogen deficiency and raised intra-abdominal pressure.
Covered in depth on the Sexual Health page. Listed here as a content-map gynaecology item: thin grey fishy non-itchy discharge with raised pH and clue cells; treated with metronidazole.
Covered in depth on the Sexual Health page. Listed here as a content-map gynaecology item: upper genital tract infection treated empirically with ceftriaxone + doxycycline + metronidazole; always exclude ectopic pregnancy.
Cervical malignancy driven by persistent high-risk HPV (16/18), commonly squamous cell. Largely preventable through HPV vaccination and screening; presents with post-coital, intermenstrual or postmenopausal bleeding.
The NHS cervical screening programme uses HPV-PRIMARY testing: samples are tested for high-risk HPV first, with cytology only as a triage if HPV-positive. Ages 25–64 (3-yearly 25–49, 5-yearly 50–64).
The commonest gynaecological cancer in the UK — usually an oestrogen-driven endometrioid adenocarcinoma presenting with POSTMENOPAUSAL BLEEDING. Risk factors are unopposed-oestrogen states; it usually presents early.
The gynaecological cancer with the highest mortality — usually epithelial (high-grade serous), presenting LATE with vague abdominal symptoms. CA125 and USS (Risk of Malignancy Index) guide referral; BRCA mutations raise risk.
An uncommon malignancy, mostly squamous cell, of older women — arising from HPV-related VIN or from chronic lichen sclerosus. Presents with a persistent vulval lump, ulcer or itch.
Legal ending of pregnancy under the Abortion Act 1967 (two doctors’ agreement; commonly under 24 weeks for risk to physical/mental health). Provided medically (mifepristone + misoprostol) or surgically; anti-D for rhesus-negative women in some circumstances.
Implantation of a pregnancy outside the uterine cavity — most commonly the fallopian tube. A leading cause of first-trimester maternal death; presents with pain and bleeding at 6–8 weeks and can rupture catastrophically.
Loss of a pregnancy before 24 weeks (miscarriage); intrauterine/stillbirth from 24 weeks. Types: threatened, inevitable, incomplete, complete, missed. Managed expectantly, medically or surgically.
Severe, persistent nausea and vomiting of pregnancy causing dehydration, weight loss (>5%) and electrolyte/ketone disturbance — beyond ordinary morning sickness. Associated with high βhCG (multiple/molar pregnancy).
Gestational trophoblastic disease: abnormal proliferation of trophoblast. Complete mole (empty egg + paternal DNA, 46XX, no fetus) or partial mole (triploid, some fetal parts). Presents with bleeding, a large-for-dates uterus and very high βhCG; needs hCG surveillance for malignant transformation (choriocarcinoma).
Spans gestational hypertension (new BP ≥140/90 after 20 weeks, no proteinuria), pre-eclampsia (hypertension + proteinuria/organ involvement after 20 weeks) and eclampsia (seizures). A leading cause of maternal/fetal morbidity.
Either gestational diabetes (glucose intolerance first recognised in pregnancy) or pre-existing type 1/2 diabetes. Raises risks of macrosomia, shoulder dystocia, neonatal hypoglycaemia, pre-eclampsia and congenital anomaly (pre-existing).
Pregnancy and the puerperium are prothrombotic (Virchow’s triad) — VTE is a leading direct cause of maternal death. Risk is highest postpartum. Assessed with a risk score; treated and prevented with LMWH (NOT warfarin/DOACs).
Haemolytic disease of the fetus/newborn from maternal IgG antibodies (classically anti-D) crossing the placenta to destroy fetal red cells. Prevented by routine anti-D prophylaxis in rhesus-negative women; causes fetal anaemia/hydrops and neonatal jaundice.
Maternal obesity (BMI ≥30) raises risks across pregnancy: gestational diabetes, pre-eclampsia, VTE, macrosomia, shoulder dystocia, caesarean, and anaesthetic/wound complications. Managed with extra surveillance and prophylaxis.
Pregnancy with more than one fetus. Chorionicity (determined by USS in the first trimester) drives risk — monochorionic twins share a placenta and risk twin-to-twin transfusion syndrome. Higher rates of all pregnancy complications.
Jaundice or deranged liver function in pregnancy — most commonly intrahepatic cholestasis of pregnancy (obstetric cholestasis): pruritus (esp. palms/soles) WITHOUT a rash and raised bile acids, carrying a risk of stillbirth.
Bleeding from the genital tract from 24 weeks’ gestation until birth. The three discriminators to separate are placenta praevia (painless), placental abruption (painful) and vasa praevia (painless bleeding + fetal distress after membrane rupture). NEVER do a digital vaginal exam until praevia is excluded.
Placenta lying wholly or partly over the lower uterine segment/internal os. Classically causes PAINLESS antepartum bleeding; diagnosed on USS and managed to avoid digital examination and to plan caesarean delivery.
Premature separation of a normally sited placenta before delivery, causing PAINFUL antepartum bleeding and a tense tender uterus, with risk of fetal compromise and maternal DIC. Bleeding may be concealed (shock out of proportion to visible loss).
Unprotected fetal blood vessels (from a velamentous cord insertion or succenturiate lobe) running through the membranes over the cervical os. When the membranes rupture, the vessels tear — causing PAINLESS bleeding of FETAL blood with rapid fetal exsanguination.
A group of intrapartum emergencies the exam tests by their specific manoeuvre/response: shoulder dystocia (McRoberts), cord prolapse, malpresentation and preterm labour. Each has a defining first action.
Blood loss ≥500 mL after vaginal birth (≥1000 mL after caesarean), or any loss causing compromise. Primary PPH (<24h) is most often uterine ATONY (the commonest cause); the four causes are the "4 Ts" — Tone, Trauma, Tissue, Thrombin.
Infection of the chorion, amnion and amniotic fluid, usually ascending after prolonged rupture of membranes — a maternal and fetal emergency requiring delivery and antibiotics.
Too much (polyhydramnios) or too little (oligohydramnios) amniotic fluid on USS. The volume points to a cause: polyhydramnios suggests reduced fetal swallowing or excess urine; oligohydramnios suggests reduced fetal urine output or fluid loss.
Involuntary urine leakage. The two core types behave oppositely and have opposite first-line treatments: STRESS (leak on cough/effort — sphincter/pelvic-floor weakness) vs URGENCY/overactive bladder (sudden urgency ± leak — detrusor overactivity); many women have a MIXED picture, treated by the predominant type.
GBS colonises the vagina/rectum of ~20–25% of women and is the leading cause of EARLY-ONSET neonatal sepsis. The UK uses a RISK-BASED intrapartum antibiotic prophylaxis (IAP) strategy — it does NOT offer universal antenatal screening (unlike the USA).
A combined oestrogen/progestogen pill that mainly inhibits ovulation. Highly effective with perfect use but typical-use failure ~9%. Offers non-contraceptive benefits (cycle control, ↓ovarian & endometrial cancer) but the oestrogen drives the key contraindications.
An oestrogen-free pill — the go-to oral method when oestrogen is contraindicated (migraine with aura, breastfeeding, VTE risk, smokers ≥35). Traditional POPs thicken cervical mucus; desogestrel additionally inhibits ovulation. Taken continuously with no break.
A single subdermal progestogen rod lasting 3 years — the MOST EFFECTIVE reversible method (<1% failure, "fit and forget"). Inhibits ovulation. The main drawback is an unpredictable bleeding pattern, the commonest reason for early removal.
A progestogen depot injection (medroxyprogesterone acetate) every 13 weeks that inhibits ovulation. Effective and discreet, but unique among methods for a reversible reduction in bone mineral density and for delaying the return of fertility by up to a year.
A progestogen-releasing intrauterine device (LARC, 5–8 years depending on brand) that thins the endometrium and thickens cervical mucus. Doubles as treatment for heavy menstrual bleeding and as the progestogen component of HRT — periods usually become light or absent.
A non-hormonal intrauterine device (LARC, 5–10 years) — copper is toxic to sperm and ova and inhibits implantation. The only hormone-free LARC, and the MOST EFFECTIVE emergency contraception. The trade-off is heavier, more painful periods.
Prevents pregnancy after unprotected sex (UPSI) or contraceptive failure. Three options with different windows and mechanisms — the copper IUD is by far the most effective and the only one that works after ovulation; the oral methods only delay ovulation.
Obstruction of a Bartholin gland duct causes a cyst; secondary infection causes a painful abscess. A common cause of a unilateral, posterolateral vulval (introital) swelling.
A rare but life-threatening third-trimester liver failure from microvesicular fatty infiltration. It overlaps with the pre-eclampsia/HELLP spectrum but is distinguished by HYPOGLYCAEMIA, coagulopathy and frank liver failure. The treatment is prompt delivery.
Painful menstruation WITHOUT identifiable pelvic pathology, caused by excess endometrial prostaglandins. It begins soon after menarche; the contrast is secondary dysmenorrhoea (endometriosis/adenomyosis/fibroids), which starts later and has other features.
Proliferation of the endometrium from unopposed oestrogen — a precursor to endometrial cancer, especially with atypia. A key cause of abnormal/postmenopausal bleeding and the reason oestrogen-only HRT is contraindicated with an intact uterus.
Failure to conceive after 12 months of regular unprotected intercourse (roughly every 2–3 days). About 84% of couples conceive within a year. Causes divide roughly into male factor (30%), ovulatory (25%), tubal (20%) and unexplained (25%) — which is why BOTH partners are investigated from the outset.