- 📝Exam question: aetiology, premalignant lesion, clinical features, FIGO staging and treatment
DEFINITION
Carcinoma of the cervix is a malignant tumour of the uterine cervix, the great majority being squamous-cell carcinomas arising at the squamo-columnar junction (transformation zone); the rest are adenocarcinomas. It is one of the commonest genital cancers in women in developing countries.
NATURAL HISTORY & FIGO STAGES OF CARCINOMA CERVIX
AETIOLOGY AND RISK FACTORS
The central cause is persistent infection with high-risk human papilloma virus (HPV types 16 and 18). Co-factors are early age at marriage/first coitus, multiple sexual partners, high parity, smoking, poor genital hygiene, immunosuppression (HIV), and long-term oral-contraceptive use.
PREMALIGNANT LESION — CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN)
Invasive cancer is preceded by a long premalignant phase — CIN (dysplasia → carcinoma in situ) — over 10–15 years, which is the basis of screening and prevention.
SPREAD
Direct — into the vagina, body of the uterus and parametrium (towards the pelvic wall, ureters, bladder and rectum); lymphatic — to the pelvic (and later para-aortic) nodes; and late blood-borne spread to liver, lung and bone.
CLINICAL FEATURES
Early disease is often asymptomatic (detected on screening). The classic symptoms are post-coital bleeding, irregular intermenstrual or post-menopausal bleeding, and an offensive blood-stained vaginal discharge. Advanced disease causes pelvic/back pain, leg oedema, urinary or rectal symptoms and uraemia from ureteric obstruction.
FIGO STAGING (CLINICAL)
- Stage I — carcinoma strictly confined to the cervix. IA microinvasive (diagnosed only on microscopy, depth ≤ 5 mm); IB clinically visible lesion confined to the cervix.
- Stage II — extends beyond the uterus but not to the pelvic wall or the lower third of the vagina. IIA without parametrial involvement; IIB with parametrial involvement.
- Stage III — extends to the pelvic wall and/or the lower third of the vagina, and/or causes hydronephrosis/non-functioning kidney (IIIA lower vagina, IIIB pelvic wall/hydronephrosis).
- Stage IV — spread beyond the true pelvis or into the bladder/rectal mucosa (IVA), or distant metastasis (IVB).
INVESTIGATIONS
Pap smear and colposcopy with directed biopsy for diagnosis; examination under anaesthesia for clinical staging; cystoscopy and proctoscopy, intravenous urography, and cross-sectional imaging (MRI/CT, or PET) to assess spread.
TREATMENT
- CIN / Stage IA1 — conisation (to preserve fertility) or simple (extrafascial) hysterectomy.
- Stage IA2–IIA (early invasive) — radical hysterectomy (Wertheim's) with pelvic lymphadenectomy, or radical radiotherapy — both give comparable cure; chemoradiation if high-risk features are present.
- Stage IIB–IVA (advanced) — concurrent chemoradiation (external-beam radiotherapy + brachytherapy + cisplatin).
- Stage IVB / recurrence — palliative chemotherapy and supportive/palliative care.
💡CLINICAL PEARL — Prevention is highly effective: HPV vaccination of adolescent girls (primary prevention) and organised screening by Pap cytology, visual inspection with acetic acid (VIA) or HPV-DNA testing (secondary prevention), with treatment of detected CIN before it becomes invasive. - 📝Exam question: definition, causes, investigation of the infertile couple and management
DEFINITION
Infertility is the failure of a couple to conceive after one year of regular, unprotected sexual intercourse. It is primary when conception has never occurred, and secondary when it follows a previous conception. About 10–15% of couples are affected.
INFERTILITY - EVALUATION PATHWAY
CAUSES
- Female factors — ovulatory/endocrine (PCOS, hyperprolactinaemia, thyroid disorders, premature ovarian failure), tubal (pelvic inflammatory disease, tuberculosis, endometriosis, previous surgery), uterine (fibroid, synechiae, anomalies) and cervical factors.
- Male factors — defective spermatogenesis (oligo-/astheno-/azoospermia), varicocele, obstruction, infection, endocrine and sexual/ejaculatory dysfunction.
- Combined and unexplained infertility (normal basic tests in ~10–15%).
INVESTIGATION OF THE INFERTILE COUPLE
Both partners are investigated together.
General
History (duration, coital frequency, menstrual and medical/surgical history) and examination of both partners.
Male
Semen analysis (after 2–3 days' abstinence) is the single most important male test — volume, sperm count, motility and morphology; repeated and supplemented by hormones/imaging if abnormal.
Female
- Tests of ovulation — mid-luteal (day-21) serum progesterone, basal body temperature, ultrasound folliculometry, and LH-surge detection.
- Tests of tubal patency — hysterosalpingography (HSG), laparoscopy and dye (chromopertubation, the gold standard), or sono-salpingography.
- Uterine cavity — ultrasound and hysteroscopy for fibroids, polyps, synechiae and anomalies.
- Ovarian reserve — anti-Müllerian hormone (AMH) and antral follicle count.
MANAGEMENT
- General — correct lifestyle factors (weight, smoking, alcohol), optimise coital timing, and treat infection.
- Ovulatory disorders — ovulation induction with clomiphene citrate or letrozole, and gonadotrophins in resistant cases; dopamine agonists for hyperprolactinaemia.
- Tubal disease — tubal microsurgery in selected cases, otherwise in-vitro fertilisation (IVF).
- Male factor — treat the cause (varicocele ligation, infection); intra-uterine insemination (IUI) for mild defects and ICSI for severe oligospermia/azoospermia.
- Assisted reproduction — IUI, IVF and ICSI for unexplained or refractory infertility; donor gametes and surrogacy where appropriate.
💡CLINICAL PEARL — Approach: always evaluate both partners in parallel and confirm the three essentials of conception — ovulation, patent tubes and adequate sperm — before embarking on treatment. - 📝Exam question: classification of methods, with their mechanism, advantages and limitations
DEFINITION
Contraception is the voluntary prevention of pregnancy by temporary (reversible) or permanent (irreversible) methods, enabling couples to plan the number and spacing of their children.
METHODS OF CONTRACEPTION
CLASSIFICATION
A. Temporary (spacing) methods
- Barrier — male/female condom and diaphragm (with spermicide); prevent sperm–ovum meeting and also guard against sexually-transmitted infection, but have a higher failure rate.
- Hormonal — combined oral pills (oestrogen + progestin) acting mainly by inhibiting ovulation; progestin-only pills, injectable DMPA, subdermal implants, the vaginal ring and the patch. Highly effective; cautions include thromboembolism (oestrogen) and irregular bleeding (progestin).
- Intra-uterine devices — copper IUCD (Cu-T 380A) (a foreign-body and spermicidal copper effect) and the levonorgestrel-releasing IUS (Mirena); long-acting and reversible.
- Natural / fertility-awareness — calendar (rhythm), basal temperature and cervical-mucus methods, withdrawal and lactational amenorrhoea; no side-effects but less reliable.
- Emergency contraception — after unprotected intercourse (see short note).
B. Permanent (terminal) methods
- Female sterilisation — tubal ligation (laparoscopic/minilap, post-partum), occluding the fallopian tubes.
- Male sterilisation — vasectomy (no-scalpel), interrupting the vas deferens; simpler and safer than female sterilisation but requires confirmation of azoospermia.
MEASURING EFFECTIVENESS
Efficacy is expressed by the Pearl index — the number of accidental pregnancies per 100 woman-years of exposure; the lower the index, the more effective the method. Long-acting reversible methods (IUCD, implant) and sterilisation have the lowest indices, while barrier and natural methods have the highest.
NEWER / NON-HORMONAL OPTIONS
Centchroman (ormeloxifene, "Saheli") is a non-steroidal once-weekly oral contraceptive (a selective oestrogen-receptor modulator) suited to lactating women; the levonorgestrel-IUS additionally reduces menstrual loss.
THE IDEAL CONTRACEPTIVE
Should be safe, effective, acceptable, reversible (for spacing), cheap, easy to use and free of side-effects. No single method is ideal; the choice is individualised to the couple's age, parity, family plans, health and preference.
SELECTION (COUNSELLING POINTS)
- Spacing the family — barrier, hormonal or IUCD.
- Completed family — IUCD or sterilisation.
- Postpartum / lactating — progestin-only methods, IUCD (PPIUCD) or lactational amenorrhoea.
- Avoid oestrogen in smokers > 35 years and those with thromboembolic/cardiovascular risk.
💡CLINICAL PEARL — Key point: effectiveness, reversibility and the woman's medical eligibility (WHO eligibility criteria) guide the choice — barrier methods uniquely add protection against sexually-transmitted infection, and long-acting reversible methods (IUCD, implant) give the best "real-use" efficacy. - 📝Exam question: classification, clinical features, complications, staging and management
DEFINITION
Ovarian tumours are neoplasms arising from the ovary; they may be benign or malignant and arise from any of its tissue components. Ovarian cancer is notorious for presenting late ("the silent killer").
CLASSIFICATION OF OVARIAN TUMOURS (WHO)
CLASSIFICATION (WHO, BY TISSUE OF ORIGIN)
- Surface epithelial tumours (~65%) — serous, mucinous, endometrioid, clear-cell and Brenner tumours (the commonest malignant group).
- Germ-cell tumours — benign cystic teratoma (dermoid cyst), dysgerminoma, yolk-sac tumour, choriocarcinoma (common in young women).
- Sex-cord stromal tumours — granulosa-cell, theca-cell, Sertoli–Leydig (often hormone-producing).
- Metastatic tumours — e.g. Krukenberg tumour from the gastrointestinal tract.
CLINICAL FEATURES
Often silent until large or malignant. Symptoms include abdominal swelling/mass, vague discomfort, pressure effects (urinary, bowel), and — in functioning tumours — hormonal effects (precocious puberty, menstrual disturbance, virilisation). Malignancy is suggested by ascites, rapid growth, fixity, nodularity and weight loss.
COMPLICATIONS
Torsion (axial rotation) causing acute pain, rupture, intracystic/intraperitoneal haemorrhage, infection, pseudomyxoma peritonei (mucinous), and malignant change.
INVESTIGATIONS
Ultrasound (with the morphology/risk index) and Doppler; tumour markers — CA-125 (epithelial), AFP and β-hCG (germ-cell), LDH (dysgerminoma) and inhibin (granulosa); and CT/MRI for staging.
FIGO STAGING OF OVARIAN CANCER
- Stage I — confined to the ovaries (IA one ovary, capsule intact; IB both ovaries; IC capsule breached/surface tumour/malignant washings).
- Stage II — one or both ovaries with pelvic extension.
- Stage III — spread to the peritoneum outside the pelvis and/or retroperitoneal (para-aortic) nodes.
- Stage IV — distant metastasis (liver parenchyma, pleural effusion, etc.).
MANAGEMENT
- Benign tumours — cystectomy (preserving the ovary in young women) or oophorectomy.
- Malignant tumours — staging laparotomy with cytoreductive (debulking) surgery — total hysterectomy, bilateral salpingo-oophorectomy, omentectomy and node sampling — followed by platinum-based chemotherapy (carboplatin + paclitaxel).
- Fertility-sparing surgery for early germ-cell tumours in young women.
💡CLINICAL PEARL — Krukenberg tumour is a metastatic, usually bilateral, solid ovarian tumour from a gastrointestinal primary (commonly stomach), composed of mucin-secreting signet-ring cells; it may secrete hormones and present with abnormal/post-menopausal bleeding. - 📝Exam question: classification, degenerations, clinical features and management
DEFINITION
A fibroid (leiomyoma/myoma) is a benign tumour arising from the smooth muscle of the uterus. It is the commonest benign tumour of the uterus and of the female pelvis, and is oestrogen-dependent (grows in the reproductive years, regresses after menopause).
CLASSIFICATION OF UTERINE FIBROIDS BY SITE
CLASSIFICATION (BY LOCATION)
- Intramural (interstitial) — within the myometrium (commonest).
- Submucous — projecting into the cavity (may become a fibroid polyp); causes the most bleeding.
- Subserous — projecting outward beneath the serosa (may be pedunculated or "wandering").
- Cervical and broad-ligament (intraligamentary) fibroids.
PATHOLOGY
A firm, well-circumscribed, whorled tumour with a false capsule (pseudocapsule) of compressed myometrium that allows easy enucleation; histology shows interlacing bundles of smooth muscle and fibrous tissue.
DEGENERATIONS
- Hyaline (≈ 65%, commonest) — homogeneous, soft, with loss of the whorled pattern.
- Cystic — liquefaction of hyaline areas (may mimic an ovarian cyst).
- Fatty — at/after menopause.
- Calcific (≈ 10%) — in subserous/post-menopausal fibroids ("womb-stone").
- Red (carneous) degeneration — aseptic necrobiosis, typically in the second half of pregnancy/ puerperium, giving a "raw-beef" appearance with a fishy odour (see short note).
- Atrophy after menopause, and rare sarcomatous change (≈ 0.1%).
CLINICAL FEATURES
Often asymptomatic. When symptomatic — menorrhagia/heavy menstrual bleeding (especially submucous), a lower-abdominal mass, pressure effects (urinary frequency, retention, constipation), dysmenorrhoea/pelvic pain, and subfertility or recurrent miscarriage.
COMPLICATIONS
Degenerations, torsion of a pedunculated fibroid, infection, capsular haemorrhage, rare malignant change, and pregnancy-related problems (miscarriage, malpresentation, obstructed labour, PPH).
INVESTIGATIONS
Ultrasound (transvaginal/abdominal) is the main investigation — it confirms the number, size and location of fibroids and distinguishes them from an ovarian mass; saline sonohysterography or hysteroscopy defines submucous fibroids, and MRI helps when the anatomy is complex or before uterine-artery embolisation. Haemoglobin is checked for anaemia from menorrhagia.
FIBROID IN PREGNANCY
Fibroids may enlarge and undergo red degeneration; they predispose to miscarriage, malpresentation, obstructed labour and postpartum haemorrhage. They are managed conservatively in pregnancy (myomectomy is avoided owing to the risk of severe haemorrhage).
MANAGEMENT
- Expectant — small, asymptomatic fibroids with periodic review.
- Medical — for symptom control/pre-operative shrinkage: tranexamic acid and NSAIDs for bleeding, progestins/LNG-IUS, and GnRH analogues or ulipristal to shrink the tumour temporarily.
- Surgical — myomectomy (to preserve fertility) or hysterectomy (completed family); uterine artery embolisation and hysteroscopic resection of submucous fibroids are alternatives.
- 📝Exam question: types and degrees, aetiology, clinical features and management
DEFINITION
Genital (pelvic organ) prolapse is the descent of the pelvic organs — the uterus and/or the vaginal walls with the bladder, rectum or bowel — from their normal anatomical position, due to weakness of the pelvic supports.
TYPES & GRADING OF GENITAL PROLAPSE
TYPES
- Anterior vaginal wall — cystocele (bladder) and urethrocele.
- Posterior vaginal wall — rectocele (rectum) and enterocele (pouch of Douglas/bowel).
- Uterine prolapse — descent of the uterus and cervix.
- Vault prolapse — descent of the vaginal vault after hysterectomy.
DEGREES OF UTERINE PROLAPSE
- First degree — the cervix descends but the external os remains within the introitus.
- Second degree — the cervix protrudes outside the introitus while the uterine body stays inside.
- Third degree (procidentia) — the entire uterus lies outside the introitus, with eversion of the vagina.
The POP-Q system (Pelvic Organ Prolapse Quantification) is the standardised, objective method of grading.
AETIOLOGY
Childbirth trauma (the chief cause — overstretching/tearing of supports in prolonged or instrumental labour, multiparity), oestrogen withdrawal after menopause, chronically raised intra-abdominal pressure (chronic cough, constipation, heavy work, pelvic tumour), and congenital weakness (nulliparous prolapse).
CLINICAL FEATURES
A sense of "something coming down" per vaginum, dragging backache relieved by lying down, a visible mass, and urinary (frequency, incomplete emptying, stress incontinence) or bowel symptoms; long-standing procidentia may develop a decubitus ulcer.
MANAGEMENT
- Prevention — good intrapartum care, avoidance of bearing-down before full dilatation, adequate puerperal rest and pelvic-floor exercises, and treatment of chronic cough/constipation.
- Conservative — pelvic-floor (Kegel) exercises for mild cases, local oestrogen, and a ring/shelf pessary for those unfit for or declining surgery (or in pregnancy).
- Surgical — the definitive treatment: vaginal hysterectomy with pelvic-floor repair (anterior and posterior colporrhaphy) for prolapse with a completed family; the Manchester (Fothergill) operation to conserve the uterus; sacrohysteropexy/sacrocolpopexy for uterine/vault prolapse in younger women; and colpocleisis in the frail elderly.
💡CLINICAL PEARL — Key point: exclude and treat the raised intra-abdominal pressure (cough, constipation) and oestrogen deficiency before and after surgery, or the repair is likely to fail. - 📝Exam question: types, risk factors, clinical features, FIGO staging and management
DEFINITION
Carcinoma of the endometrium is a malignant tumour of the endometrial lining of the uterus, the majority being adenocarcinomas. It is predominantly a cancer of post-menopausal women and is the commonest pelvic genital malignancy in many developed countries.
TYPES OF ENDOMETRIAL CARCINOMA
TYPES
- Type I (≈ 80%, endometrioid) — oestrogen-dependent, arises from endometrial hyperplasia, occurs in younger/peri-menopausal obese women, is well-differentiated and carries a good prognosis.
- Type II (serous, clear-cell) — non-oestrogen-dependent, occurs in older women on an atrophic endometrium, is poorly-differentiated and aggressive.
RISK FACTORS
Conditions of unopposed oestrogen — obesity, nulliparity, late menopause, anovulation/PCOS, oestrogen-only HRT, oestrogen-secreting tumours (granulosa cell) and tamoxifen — together with diabetes, hypertension and Lynch syndrome (HNPCC). The precursor is atypical endometrial hyperplasia.
CLINICAL FEATURES
Post-menopausal bleeding is the cardinal symptom (and any post-menopausal bleeding is endometrial cancer until proven otherwise); peri-menopausal women present with irregular/intermenstrual bleeding, and there may be a blood-stained or watery discharge. Pain and a mass occur late.
INVESTIGATIONS
- Transvaginal ultrasound — an endometrial thickness > 4 mm in a post-menopausal woman with bleeding warrants sampling.
- Endometrial biopsy/aspiration (e.g. Pipelle) or hysteroscopy with dilatation and curettage — the definitive diagnosis.
- MRI/CT for myometrial invasion and spread, and chest imaging.
FIGO STAGING (SURGICAL)
- Stage I — confined to the corpus uteri (IA < ½ myometrial invasion, IB ≥ ½).
- Stage II — invades the cervical stroma but not beyond the uterus.
- Stage III — local/regional spread to serosa/adnexa, vagina/parametrium, or pelvic/para-aortic nodes.
- Stage IV — invasion of bladder/bowel mucosa (IVA) or distant metastasis (IVB).
MANAGEMENT
- Surgery (mainstay) — total hysterectomy with bilateral salpingo-oophorectomy, peritoneal washings and pelvic ± para-aortic lymphadenectomy (surgical staging).
- Adjuvant radiotherapy (vault brachytherapy/pelvic) for intermediate/high-risk disease, and chemotherapy for advanced or high-grade (serous) tumours.
- Progestins — for fertility preservation in selected young women with early well-differentiated tumours, and for advanced/recurrent hormone-responsive disease.
💡CLINICAL PEARL — Prognosis depends mainly on the depth of myometrial invasion and the tumour grade; because bleeding appears early, most cases are diagnosed at Stage I, giving an overall good outcome. - 📝Exam question: sites, risk factors, clinical features, diagnosis and management
DEFINITION
An ectopic pregnancy is the implantation of the fertilised ovum outside the normal uterine (endometrial) cavity. It is a leading cause of maternal death in early pregnancy and a true gynaecological emergency when it ruptures.
ECTOPIC PREGNANCY - MANAGEMENT OPTIONS
SITES
Tubal pregnancy (≈ 95%) is commonest — most often in the ampulla, then the isthmus, fimbria and (dangerously) the interstitial/cornual part. Rarer sites are ovarian, cervical, caesarean-scar and abdominal pregnancies.
RISK FACTORS
Anything damaging the tube or delaying ovum transport — pelvic inflammatory disease/salpingitis, previous tubal surgery or previous ectopic, endometriosis, IUCD in situ, assisted reproduction, tubal-ligation failure and smoking.
FATE OF A TUBAL PREGNANCY
The thin-walled tube cannot sustain the pregnancy, which usually ends in one of three ways: tubal abortion (extrusion of the conceptus into the peritoneal cavity, commonest in ampullary pregnancy), tubal rupture (into the peritoneal cavity with severe intraperitoneal haemorrhage, commonest in the narrow isthmus) or, rarely, spontaneous tubal mole/absorption.
CLINICAL FEATURES
The classic triad is amenorrhoea, lower-abdominal pain and abnormal vaginal bleeding (slight, dark). Rupture produces an acute abdomen — severe pain, signs of haemorrhagic shock, shoulder-tip pain (diaphragmatic irritation), abdominal distension, and on examination marked tenderness, cervical excitation/motion tenderness and a tender adnexal fullness.
INVESTIGATIONS
- Urine and serum β-hCG — a sub-optimal rise (failure to double in 48 h) suggests an abnormal pregnancy.
- Transvaginal ultrasound — an empty uterus with an adnexal mass (± gestational sac/cardiac activity) and free fluid in the pouch of Douglas; correlated with the hCG "discriminatory zone".
- Laparoscopy — the gold standard for diagnosis (and treatment); culdocentesis showing non-clotting blood in resource-limited settings.
DIFFERENTIAL DIAGNOSIS
Threatened or incomplete miscarriage, a ruptured or haemorrhagic ovarian cyst, acute pelvic inflammatory disease/salpingitis, torsion of an ovarian mass, and acute appendicitis.
MANAGEMENT
- Expectant — for a small, stable, asymptomatic ectopic with low and falling β-hCG.
- Medical — methotrexate (single-dose, with hCG follow-up) in the stable patient meeting criteria: hCG < 5000 IU/L, mass < 3.5 cm, no fetal cardiac activity and no rupture.
- Surgical — laparoscopic salpingectomy (or salpingostomy if the other tube is damaged) for the stable patient; laparotomy for the ruptured/haemodynamically unstable patient after resuscitation.
- Give anti-D to Rh-negative women.
💡CLINICAL PEARL — Golden rule: consider ectopic pregnancy in any woman of reproductive age with pain and/or bleeding and a positive pregnancy test; a ruptured ectopic with shock needs immediate resuscitation and surgery, not prolonged investigation. - 📝Exam question: definition, causes, evaluation and management
DEFINITION
Abnormal uterine bleeding (AUB) is any uterine bleeding that is abnormal in frequency, regularity, duration or volume in a non-pregnant woman of reproductive age. Dysfunctional uterine bleeding (DUB) is AUB in the absence of any organic (structural), systemic or pregnancy-related cause — a diagnosis of exclusion resulting from a disturbance of the hypothalamo-pituitary-ovarian axis.
AUB - PALM-COEIN CLASSIFICATION
CLASSIFICATION OF AUB — PALM-COEIN (FIGO)
- Structural (PALM) — Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia.
- Non-structural (COEIN) — Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not otherwise classified.
DUB corresponds mainly to the ovulatory and endometrial categories.
TYPES OF DUB
- Anovulatory (≈ 90%) — at the extremes of reproductive life (adolescence and peri-menopause); unopposed oestrogen causes irregular, heavy and prolonged bleeding.
- Ovulatory — regular but heavy menstrual loss, often due to a luteal-phase or endometrial defect.
PATHOPHYSIOLOGY OF ANOVULATORY DUB
In the absence of ovulation no corpus luteum forms, so there is no progesterone to oppose oestrogen. The endometrium proliferates under continuous unopposed oestrogen until it outgrows its blood supply and breaks down irregularly and incompletely — producing the characteristic irregular, heavy and prolonged bleeding.
EVALUATION
A careful menstrual and drug history, examination, and a pregnancy test; pelvic examination and investigations to exclude structural and systemic causes before labelling bleeding as DUB.
INVESTIGATIONS
- Haemoglobin (anaemia), thyroid function and a coagulation screen (especially in adolescents).
- Transvaginal ultrasound for fibroids, polyps and endometrial thickness.
- Endometrial biopsy/hysteroscopy in women > 40 years or with risk factors, to exclude hyperplasia/malignancy.
MANAGEMENT
- Medical (first line) — tranexamic acid and NSAIDs (mefenamic acid) for ovulatory heavy bleeding; combined oral pills or cyclical/continuous progestins; the levonorgestrel-IUS (Mirena) is highly effective; GnRH analogues for short-term control.
- Surgical — endometrial ablation for those who have completed their family and failed medical treatment, and hysterectomy as definitive treatment.
AGE-RELATED APPROACH
In adolescents, anovulatory DUB usually settles with reassurance and hormonal regulation (and a coagulation screen). In the reproductive years, exclude structural causes and use medical therapy/LNG-IUS. In the peri-menopausal woman, the endometrium must be sampled to exclude hyperplasia/malignancy before treatment.
💡CLINICAL PEARL — Key point: always exclude pregnancy and malignancy first; DUB is a diagnosis of exclusion, and in any woman over 40 with abnormal bleeding the endometrium must be sampled before starting hormonal therapy. - 📝Exam question: definition, sites, clinical features, diagnosis and management
DEFINITION
Endometriosis is the presence of functioning endometrial tissue (glands and stroma) outside the uterine cavity. Being hormonally responsive, it bleeds cyclically at the ectopic sites, producing inflammation, adhesions and pain.
ENDOMETRIOSIS - SITES & THEORY
SITES
Most often within the pelvis — the ovary (forming a "chocolate cyst"/endometrioma), the pouch of Douglas, the uterosacral ligaments, the pelvic peritoneum, the recto-vaginal septum and the bladder; rarely at distant sites (umbilicus, scars, lung).
THEORIES OF ORIGIN
Sampson's retrograde menstruation theory (the most accepted), coelomic metaplasia, and lymphatic/ vascular dissemination, with a contribution from genetic and immunological factors.
PATHOLOGY
The ectopic deposits bleed cyclically, producing small "powder-burn"/blue-black lesions on the peritoneum and chocolate cysts (endometriomas) in the ovary (altered, tarry, retained blood), with surrounding fibrosis and dense adhesions. Microscopy shows endometrial glands and stroma with haemosiderin-laden macrophages.
CLINICAL FEATURES
The classic triad is secondary dysmenorrhoea, deep dyspareunia and infertility, with chronic cyclical pelvic pain; there may be cyclical bowel/bladder symptoms. The severity of symptoms correlates poorly with the extent of disease.
EXAMINATION
A fixed retroverted uterus, tender nodularity of the uterosacral ligaments and pouch of Douglas, and a tender adnexal (ovarian) mass.
INVESTIGATIONS
- Ultrasound for an endometrioma; MRI for deep/extensive disease.
- Serum CA-125 may be mildly raised (non-specific).
- Laparoscopy is the gold standard for diagnosis (powder-burn deposits, endometriomas, adhesions) and allows staging (revised ASRM) and biopsy.
COMPLICATIONS
Infertility (the major concern — from adhesions and distorted tubo-ovarian anatomy), chronic pelvic pain, rupture or torsion of an endometrioma, dense pelvic adhesions with bowel/ureteric involvement, and rare malignant change in an endometrioma.
MANAGEMENT
- Medical (to suppress cyclical activity) — NSAIDs for pain; combined oral pills, progestins, the levonorgestrel-IUS, GnRH analogues (with add-back) and danazol.
- Surgical — laparoscopic ablation/excision of deposits, cystectomy of endometriomas and adhesiolysis; definitive surgery (hysterectomy with bilateral salpingo-oophorectomy) for severe disease in women who have completed their family.
- Infertility — surgery improves fertility in mild disease; assisted reproduction (IVF) for those who do not conceive.
- 📝Exam question: diagnostic criteria, features, complications and management
DEFINITION
Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder of reproductive-age women characterised by hyperandrogenism, ovulatory dysfunction and polycystic ovaries. It is the commonest cause of anovulatory infertility.
PCOS - ROTTERDAM CRITERIA (2 OF 3)
DIAGNOSTIC CRITERIA (ROTTERDAM — ESHRE/ASRM)
Diagnosis requires any two of the following three (after excluding other causes):
- Oligo- or anovulation (oligomenorrhoea/amenorrhoea).
- Clinical and/or biochemical hyperandrogenism (hirsutism, acne; raised serum testosterone).
- Polycystic ovaries on ultrasound (≥ 12 small follicles per ovary and/or ovarian volume > 10 mL).
PATHOPHYSIOLOGY
Central features are insulin resistance with compensatory hyperinsulinaemia, an increased LH:FSH ratio, and ovarian/adrenal hyperandrogenism, which together disturb folliculogenesis and ovulation.
CLINICAL FEATURES
Menstrual irregularity (oligo-/amenorrhoea), hirsutism, acne and male-pattern hair loss, obesity (central), infertility, and acanthosis nigricans (a marker of insulin resistance).
INVESTIGATIONS
Serum testosterone, LH and FSH, prolactin and TSH (to exclude mimics); fasting glucose/insulin and an oral glucose-tolerance test, and a lipid profile; transvaginal ultrasound of the ovaries.
DIFFERENTIAL DIAGNOSIS
Other causes of hyperandrogenism/anovulation must be excluded — thyroid dysfunction, hyperprolactinaemia, congenital adrenal hyperplasia (late-onset), Cushing's syndrome and an androgen-secreting tumour (suggested by rapidly progressive virilisation).
COMPLICATIONS
Anovulatory infertility, type-2 diabetes and metabolic syndrome, dyslipidaemia, obstructive sleep apnoea, and — from chronic unopposed oestrogen — endometrial hyperplasia and carcinoma.
MANAGEMENT
- Lifestyle and weight reduction — the first-line measure; even modest weight loss restores ovulation and improves the metabolic profile.
- Menstrual regulation / endometrial protection — combined oral pills or cyclical progestins.
- Hirsutism — combined pills with anti-androgens (cyproterone, spironolactone), and cosmetic measures.
- Infertility — ovulation induction with letrozole (first line) or clomiphene, adding metformin, then gonadotrophins or laparoscopic ovarian drilling; IVF if these fail.
- Metabolic — metformin for insulin resistance and management of the cardiometabolic risk.
💡CLINICAL PEARL — Long-term surveillance: because of the lifelong cardiometabolic and endometrial risk, women with PCOS need periodic screening for diabetes, dyslipidaemia and hypertension, and endometrial protection (regular withdrawal bleeds) to prevent hyperplasia from chronic unopposed oestrogen. - 📝Exam question: causes, clinical features, diagnosis, management and complications
DEFINITION
Pelvic inflammatory disease (PID) is an acute infection and inflammation of the upper female genital tract — the endometrium (endometritis), fallopian tubes (salpingitis), ovaries (oophoritis) and pelvic peritoneum — usually resulting from ascending infection from the lower genital tract.
PID - ASCENDING INFECTION
CAUSATIVE ORGANISMS
Mostly sexually transmitted — Chlamydia trachomatis and Neisseria gonorrhoeae — usually becoming polymicrobial with anaerobes, Gram-negative bacteria and genital mycoplasmas; tuberculosis causes chronic PID.
ROUTES OF SPREAD
Infection usually ascends from the cervix and vagina along the mucosa to the endometrium, tubes and ovaries, and onto the pelvic peritoneum; less often it spreads by the lymphatics (after delivery/abortion or with an IUCD) or by the blood-stream (tuberculosis).
RISK FACTORS
Multiple sexual partners and young age, a previous episode of PID, recent IUCD insertion or intra-uterine instrumentation (D&C, MTP, HSG), and the post-partum/post-abortal state.
ACUTE AND CHRONIC PID
Acute PID presents with the florid features below; inadequately-treated infection leads to chronic PID — persistent pelvic pain, dyspareunia, menstrual disturbance, a hydrosalpinx/chronic tubo-ovarian mass and dense pelvic adhesions causing infertility.
CLINICAL FEATURES
Lower abdominal/pelvic pain, fever, abnormal vaginal discharge, deep dyspareunia and abnormal bleeding; signs include lower-abdominal tenderness, cervical motion (excitation) tenderness and adnexal tenderness. Fitz-Hugh-Curtis syndrome (perihepatitis) causes right-upper-quadrant pain.
INVESTIGATIONS
- Endocervical/vaginal swabs and NAAT for chlamydia and gonorrhoea; a pregnancy test (to exclude ectopic).
- White-cell count, CRP/ESR; ultrasound/TVS to detect a tubo-ovarian abscess or pyosalpinx.
- Laparoscopy — the gold standard in doubtful or severe cases.
MANAGEMENT
- Broad-spectrum antibiotics covering chlamydia, gonococcus and anaerobes (e.g. ceftriaxone + doxycycline + metronidazole), started empirically.
- Outpatient treatment for mild cases; admit for severe illness, pregnancy, a tubo-ovarian abscess, failure of oral therapy, or an uncertain diagnosis (then intravenous antibiotics).
- Treat the partner and advise abstinence; consider removing an IUCD if there is no response; drain a tubo-ovarian abscess if it does not resolve.
💡CLINICAL PEARL — Complications: chronic pelvic pain, infertility (tubal damage), ectopic pregnancy, tubo-ovarian abscess, recurrent infection and Fitz-Hugh-Curtis perihepatitis — hence the importance of early, adequate treatment and partner management. - 📝Exam question: sites, pathology, clinical features, diagnosis and management
DEFINITION
Genital tuberculosis is tuberculous infection of the female genital tract, caused by *Mycobacterium tuberculosis*. It is almost always secondary to a focus elsewhere (lungs, lymph nodes, gut, urinary tract or bones), reaching the genital tract by haematogenous (mainly), lymphatic or direct spread. It is an important and rising cause of infertility in developing countries.
GENITAL TB - SPREAD & SITES
SITES OF INVOLVEMENT
- Fallopian tubes (≈ 90–100%) — the primary and almost constant site.
- Endometrium (≈ 50%) — by downward spread from the tubes.
- Ovaries (≈ 20–30%), cervix (≈ 5%), and rarely the vagina and vulva.
PATHOLOGY
Tuberculous tubercles with caseation develop in the tubes, which become thickened and may form a "tobacco-pouch" appearance with everted fimbriae, beading, and tubo-ovarian masses or a "frozen pelvis" from adhesions. Endometrial involvement causes destruction and intra-uterine synechiae (Asherman-like), and tubal scarring leads to infertility and a high risk of ectopic pregnancy.
CLINICAL FEATURES
Infertility is the commonest presentation (often the only complaint). Others include menstrual disturbances (oligomenorrhoea, amenorrhoea or abnormal bleeding), chronic pelvic pain, vaginal discharge, and constitutional symptoms (low-grade fever, weight loss, evening rise of temperature); many women are asymptomatic and detected during an infertility work-up.
DIAGNOSIS
- Endometrial biopsy/curettage in the pre-menstrual phase — for histology (tubercles), acid-fast bacilli, culture and PCR (the most useful test); menstrual-blood culture/PCR is an alternative.
- Hysterosalpingography — a rigid, beaded ("pipe-stem") tube, cornual block, calcification, and a distorted/contracted cavity with synechiae.
- Laparoscopy/hysteroscopy — tubercles, tubo-ovarian masses and adhesions, with biopsy.
- Supportive — Mantoux test, chest radiograph, ESR, and a search for an extragenital focus.
MANAGEMENT
- Anti-tubercular therapy (ATT) is the mainstay — the standard four-drug regimen (isoniazid, rifampicin, pyrazinamide, ethambutol) for an intensive phase, followed by a continuation phase, for a total of about 6 months.
- Surgery is reserved for a residual or persistent tubo-ovarian mass, or non-response to ATT.
- Infertility — tubal damage is usually irreversible, so in-vitro fertilisation is the realistic option (tubal surgery has poor results); a severely damaged endometrium carries a poor prognosis.
💡CLINICAL PEARL — Key point: suspect genital tuberculosis in any young woman with infertility and menstrual disturbance, especially with a past history or contact; a pre-menstrual endometrial sample for AFB, culture and PCR is the single most valuable confirmatory test. - 📝Exam question: antecedents, features, staging and management
DEFINITION
Gestational trophoblastic neoplasia (GTN) is the malignant form of gestational trophoblastic disease, comprising invasive mole, choriocarcinoma and placental-site trophoblastic tumour. Choriocarcinoma is a highly malignant tumour of the trophoblast that invades and metastasises early via the blood-stream.
GESTATIONAL TROPHOBLASTIC DISEASE SPECTRUM
ANTECEDENT PREGNANCY
GTN follows a hydatidiform mole in ~50% of cases, an abortion/ectopic in ~25%, and a normal term pregnancy in ~25%. Post-molar GTN is diagnosed when the β-hCG plateaus or rises over consecutive weeks after evacuation.
PATHOLOGY
Choriocarcinoma is a soft, purple, haemorrhagic and necrotic tumour composed of sheets of malignant cyto- and syncytio-trophoblast with no chorionic villi; it invades the myometrium and blood vessels early, which explains its rapid haematogenous spread. An invasive mole, by contrast, retains hydropic villi that penetrate the myometrium. Bilateral theca-lutein cysts may persist owing to the high β-hCG.
CLINICAL FEATURES
Persistent or irregular vaginal bleeding after a molar pregnancy, abortion or delivery, with subinvolution of the uterus and a rising/plateauing β-hCG. Because spread is haematogenous, women may present with features of metastases — lung (commonest — haemoptysis, dyspnoea), vagina (a bluish nodule that bleeds), brain (neurological deficit) and liver.
INVESTIGATIONS
- Serial β-hCG — the tumour marker for diagnosis, monitoring and follow-up.
- Ultrasound of the uterus/pelvis (Doppler shows vascular invasion).
- Metastatic work-up — chest radiograph/CT, CT/MRI brain, and liver imaging.
STAGING AND RISK SCORING
Staged by the FIGO anatomical stages I–IV and risk-stratified by the WHO/FIGO prognostic scoring system (age, antecedent pregnancy, interval, hCG level, tumour size, site and number of metastases, and prior chemotherapy): a score of ≤ 6 is low-risk and ≥ 7 is high-risk, which determines therapy.
MANAGEMENT
- GTN is highly chemosensitive and chemotherapy is the mainstay.
- Low-risk disease — single-agent chemotherapy (methotrexate with folinic-acid rescue, or actinomycin-D).
- High-risk disease — multi-agent chemotherapy (EMA-CO regimen), with surgery/radiotherapy for selected sites (e.g. brain metastases).
- Follow-up with serial β-hCG until normal for a defined period, and reliable contraception during treatment and follow-up.
💡CLINICAL PEARL — Prognosis is excellent — cure approaches 100% in low-risk and ~80–90% in high-risk disease — making GTN one of the few widely-curable solid malignancies, provided β-hCG follow-up after any molar or abnormal pregnancy is maintained. - 📝Exam question: types of incontinence, causes, evaluation and management
DEFINITION
Urinary incontinence is the involuntary loss of urine that is objectively demonstrable and a social or hygienic problem. Stress urinary incontinence (SUI) is the involuntary leakage of urine on effort or exertion (coughing, sneezing, lifting) due to a rise in intra-abdominal pressure exceeding the urethral closure pressure (urethral sphincter incompetence).
STRESS URINARY INCONTINENCE - MECHANISM
TYPES OF URINARY INCONTINENCE
- Stress incontinence — leakage on raised intra-abdominal pressure.
- Urge incontinence — leakage preceded by urgency, from an overactive (detrusor) bladder.
- Mixed — features of both stress and urge.
- Overflow — dribbling from a chronically over-distended bladder (retention).
- Continuous (true) — from a fistula (vesicovaginal/ureterovaginal).
CAUSES / RISK FACTORS OF SUI
Childbirth and pelvic-floor injury (the chief cause — denervation and weakening of the supports), multiparity, menopausal oestrogen deficiency, obesity, chronically raised intra-abdominal pressure (chronic cough, constipation), genital prolapse and previous pelvic surgery.
PATHOPHYSIOLOGY
Continence depends on the urethral closure pressure exceeding the bladder pressure. SUI results from urethral hypermobility (loss of the supports of the bladder neck, so that a rise in intra-abdominal pressure is transmitted unequally to the bladder but not the urethra) and/or intrinsic sphincter deficiency (a weak urethral sphincter), allowing leakage when abdominal pressure rises.
EVALUATION
- History — circumstances, frequency, severity and impact; a bladder diary.
- Examination — demonstrate leakage on the cough stress test, assess prolapse and pelvic-floor tone; a Q-tip test for urethral hypermobility.
- Investigations — urinalysis/culture (exclude infection), a pad test, post-void residual urine, and urodynamic studies (to confirm SUI and exclude detrusor overactivity before surgery); cystoscopy if indicated.
MANAGEMENT
- Conservative (first line) — pelvic-floor muscle (Kegel) exercises, weight reduction, treatment of cough/constipation, bladder training, vaginal oestrogen in post-menopausal women, and a continence pessary; duloxetine in selected cases.
- Surgical — for failure of conservative treatment: the mid-urethral sling (tension-free vaginal tape, TVT / transobturator tape, TOT) is the standard, and Burch colposuspension is an abdominal alternative; periurethral bulking agents for the frail.
💡CLINICAL PEARL — Key point: distinguish stress from urge incontinence before treating — urodynamics confirms the type, since surgery helps stress incontinence but worsens an overactive bladder, which is treated medically (anticholinergics/β3-agonists). - 📝Exam question: risk factors, clinical features, spread, staging and management
DEFINITION
Carcinoma of the vulva is a malignant tumour of the vulva, the great majority being squamous-cell carcinomas. It is predominantly a disease of elderly post-menopausal women and most often arises on the labium majus.
CARCINOMA VULVA - SPREAD
RISK FACTORS
Vulval intraepithelial neoplasia (VIN) and HPV infection (in younger women), lichen sclerosus and chronic vulval dystrophy (in older women), smoking, immunosuppression, chronic irritation, and a history of cervical neoplasia.
PREMALIGNANT LESION
Vulval intraepithelial neoplasia (VIN) — atypical cells confined to the epithelium — is the precursor, analogous to CIN of the cervix.
CLINICAL FEATURES
Long-standing vulval pruritus, a lump, ulcer or warty growth, bleeding, discharge, pain and occasionally a groin swelling (nodal disease). The lesion is often neglected, so women present late.
SPREAD
Direct — to the adjacent vagina, urethra and anus; lymphatic (the main route) — to the inguinal, then femoral, and finally pelvic nodes; blood-borne spread is late.
INVESTIGATIONS
Diagnosis is confirmed by a wedge biopsy of the lesion (with vulvoscopy of the remaining vulva). Spread is assessed by palpation of the groin nodes, cystoscopy/proctoscopy for local extension, and cross-sectional imaging (CT/MRI/PET) of the groin and pelvis; a cervical smear is taken in view of the HPV field association.
FIGO STAGING
- Stage I — tumour confined to the vulva/perineum (IA ≤ 2 cm with stromal invasion ≤ 1 mm).
- Stage II — extension to adjacent structures (lower urethra, vagina, anus) with negative nodes.
- Stage III — spread to the inguino-femoral lymph nodes.
- Stage IV — invasion of upper urethra/bladder/rectum/bone or distant metastasis.
MANAGEMENT
- Early disease — wide local excision with assessment of the groin nodes (sentinel-node biopsy or inguino-femoral lymphadenectomy).
- Operable invasive disease — radical vulvectomy with bilateral inguino-femoral lymphadenectomy.
- Advanced/inoperable disease — radiotherapy or chemoradiation, with surgery where feasible.
- Treat VIN to prevent progression, and counsel on smoking cessation and follow-up.
💡CLINICAL PEARL — Key point: the prognosis depends chiefly on inguinal lymph-node status; any persistent vulval lump, ulcer or non-healing pruritic lesion in an elderly woman must be biopsied rather than treated blindly as infection. - 📝Exam question: primary and secondary, causes, clinical features and management
DEFINITION
Dysmenorrhoea is painful menstruation severe enough to interfere with normal daily activity and to require treatment. It is classified as primary (spasmodic) — without demonstrable pelvic pathology — and secondary (congestive) — due to identifiable pelvic disease.
TYPES OF DYSMENORRHOEA
PRIMARY DYSMENORRHOEA
Occurs in young women, usually beginning 6–12 months after menarche once cycles become ovulatory. The pain is cramping/spasmodic, lower-abdominal, radiating to the back and thighs, starting just before or with the flow and lasting 1–2 days. The cause is excess endometrial prostaglandins (PGF₂α) producing uterine hypercontractility and ischaemia; there is no pelvic pathology.
SECONDARY DYSMENORRHOEA
Appears years after menarche in older women, the pain often congestive, dull, beginning days before the period and relieved by the flow. It is due to underlying pelvic pathology — endometriosis, adenomyosis, fibroids, pelvic inflammatory disease, an IUCD, cervical stenosis or a uterine/ovarian lesion — and is usually accompanied by other symptoms (menorrhagia, dyspareunia, infertility).
Feature Primary Secondary Age / onset Young; 6–12 months after menarche Older; years after menarche Pelvic pathology None Present (endometriosis, fibroid, PID, etc.) Nature of pain Cramping/spasmodic, with the flow Congestive/dull, begins days before flow Associated symptoms Few Menorrhagia, dyspareunia, infertility CLINICAL EVALUATION
History distinguishes the two (age of onset, nature and timing of pain, associated symptoms). In suspected secondary dysmenorrhoea, pelvic examination, ultrasound and, where indicated, laparoscopy are done to find the cause.
MANAGEMENT
Primary dysmenorrhoea
- NSAIDs (the first line) — mefenamic acid/ibuprofen, which inhibit prostaglandin synthesis.
- Combined oral contraceptive pills — suppress ovulation and reduce menstrual prostaglandins (good when contraception is also desired).
- General measures — reassurance, local heat, exercise, and the levonorgestrel-IUS in resistant cases.
Secondary dysmenorrhoea
- Treat the underlying cause (e.g. endometriosis, fibroid, PID, removal of an IUCD), medically or surgically as appropriate.
💡CLINICAL PEARL — Key point: the age of onset and the timing/nature of the pain separate primary from secondary dysmenorrhoea; new or worsening dysmenorrhoea in an older woman should prompt a search for pelvic pathology rather than symptomatic treatment alone. - 📝Exam question: definition, clinical types and their management
DEFINITION
Abortion (miscarriage) is the termination of pregnancy before the period of viability — conventionally before 20 weeks (or a fetal weight under 500 g). When it occurs naturally it is a spontaneous abortion (miscarriage).
CLINICAL TYPES OF ABORTION (MISCARRIAGE)
CAUSES
- Genetic — chromosomal abnormalities of the conceptus (the commonest cause of early miscarriage).
- Maternal — endocrine (luteal-phase defect, uncontrolled diabetes, thyroid disease), uterine (septate uterus, fibroid, cervical incompetence — recurrent mid-trimester loss), infections, and antiphospholipid syndrome.
- Others — severe maternal illness, trauma and environmental factors; many remain unexplained.
CLINICAL TYPES
- Threatened — slight bleeding with a closed cervix; the pregnancy may still continue.
- Inevitable — increasing bleeding and pain with a dilated cervix; the pregnancy cannot be saved.
- Incomplete — part of the products is expelled, the rest retained (continued bleeding, open os).
- Complete — all products expelled; bleeding and pain settle and the uterus is well-contracted.
- Missed — the fetus is dead but retained in utero (no growth, brownish discharge, closed os).
- Septic — abortion complicated by infection of the uterus and its contents.
DIFFERENTIATING THE TYPES
Type Bleeding/pain Cervical os Uterine size Threatened Slight / mild Closed = dates Inevitable Heavy / severe Open = dates Incomplete Variable, continued Open < dates Complete Settles Closed < dates, contracted Missed Brownish, scanty Closed < dates MANAGEMENT
- Threatened — rest, reassurance and observation; confirm viability by ultrasound and serial β-hCG; give anti-D to Rh-negative women.
- Inevitable / incomplete — resuscitate if bleeding is heavy, then evacuate the uterus by suction/manual vacuum aspiration or medically (misoprostol); send products for histology.
- Complete — confirm an empty uterus on ultrasound; usually no intervention.
- Missed — evacuate medically (mifepristone + misoprostol) or surgically; check coagulation if retained long.
- Septic — broad-spectrum intravenous antibiotics and resuscitation, followed by evacuation of the infected products.
💡CLINICAL PEARL — Complications — haemorrhage and shock, sepsis (septic abortion), uterine perforation during evacuation, and (with retained products) coagulopathy — make timely, safe evacuation and asepsis essential. DEFINITION
The Papanicolaou (Pap) smear is an exfoliative cytology test used to screen for premalignant and malignant lesions of the cervix by examining cells shed from the transformation zone.
TECHNIQUE
With the cervix exposed by a speculum, cells are scraped from the squamo-columnar junction using an Ayre's spatula and endocervical brush (or collected in liquid medium), smeared/fixed and stained by the Papanicolaou method.
REPORTING (BETHESDA SYSTEM)
- NILM — negative for intraepithelial lesion/malignancy.
- ASC-US / ASC-H — atypical squamous cells.
- LSIL and HSIL — low- and high-grade squamous intraepithelial lesions.
- Squamous-cell carcinoma / glandular abnormalities (AGC).
WHEN AND HOW OFTEN
Screening starts at age 21 (or 3 years after first intercourse) and is repeated every 3 years (or with co-testing for HPV every 5 years). An abnormal smear is evaluated by colposcopy and biopsy.
PREREQUISITES AND LIMITATIONS
The smear is best taken in the mid-cycle, avoiding menstruation; the woman should not have douched or used vaginal medication/intercourse for 24–48 hours, and active infection is treated first. It is a screening, not a diagnostic, test and has a false-negative rate (inadequate sampling, an endocervical lesion), so a positive result always needs colposcopy and biopsy for confirmation.
ADVANTAGES
It is simple, inexpensive, painless and performed in the out-patient clinic without anaesthesia, and detects disease in the long premalignant phase — making it ideal for mass screening.
LIQUID-BASED CYTOLOGY & HPV TESTING
Liquid-based cytology (LBC) gives fewer unsatisfactory smears and allows reflex HPV testing from the same vial. Visual inspection with acetic acid (VIA) and HPV-DNA testing are the other screening tools, the latter being highly sensitive and increasingly used as a primary or co-test.
💡CLINICAL PEARL — Value: being simple, cheap and painless, the Pap smear detects cervical disease in the long premalignant phase, allowing cure before invasion — the basis of the fall in cervical-cancer mortality.DEFINITION
Cervical intraepithelial neoplasia (CIN) is a premalignant lesion of the cervix in which atypical (dysplastic) squamous cells are confined to the epithelium above the basement membrane (no invasion). It is the precursor of invasive squamous-cell carcinoma.
GRADING
- CIN I — mild dysplasia; atypical cells in the lower one-third of the epithelium.
- CIN II — moderate dysplasia; lower two-thirds.
- CIN III — severe dysplasia/carcinoma in situ; full thickness involved.
(The Bethesda cytology system groups these as LSIL = CIN I and HSIL = CIN II–III.)
DIAGNOSIS
An abnormal Pap smear leads to colposcopy (acetowhite areas, abnormal vessels) and a directed/punch biopsy for histological confirmation.
MANAGEMENT
- CIN I — often regresses; may be observed with follow-up cytology/colposcopy.
- CIN II–III — treated by excision (LEEP/LLETZ or cold-knife conisation) or ablation (cryotherapy); conisation also provides histology.
NATURAL HISTORY
CIN is caused by persistent high-risk HPV (16, 18) infection. Low-grade lesions (CIN I) frequently regress spontaneously, whereas high-grade lesions (CIN II–III) are more likely to persist and progress to invasive cancer over 10–15 years if untreated — the long latent phase that makes screening effective.
COLPOSCOPY FINDINGS
After acetic acid, CIN shows acetowhite epithelium with punctation, mosaicism and atypical vessels, and is iodine-negative on Schiller's test; the most abnormal area is biopsied.
PREVENTION AND FOLLOW-UP
HPV vaccination and regular screening prevent and detect CIN early. After treatment, women remain under cytology/HPV "test-of-cure" follow-up because the lesion can recur or persist.
💡CLINICAL PEARL — Key point: CIN is asymptomatic and detected only by screening; treating it interrupts progression to invasive cancer, which is why organised screening saves lives.DEFINITION
Tests of ovulation are investigations used in the work-up of infertility to confirm whether and when ovulation is occurring, since ovulation is one of the three essentials of conception.
INDIRECT / CLINICAL TESTS
- Menstrual history — regular cycles with molimina suggest ovulation.
- Basal body temperature (BBT) — a biphasic curve with a mid-cycle rise of ~0.5°C (progesterone thermogenic effect) indicates ovulation has occurred.
- Cervical mucus — loss of ferning/spinnbarkeit after ovulation.
HORMONAL / DIRECT TESTS
- Mid-luteal (day-21) serum progesterone > 10 ng/mL — the best single confirmation of ovulation.
- Urinary LH-surge kits — detect the pre-ovulatory LH surge (ovulation ~24–36 h later).
- Serial transvaginal ultrasound (folliculometry) — follows follicular growth and collapse with appearance of the corpus luteum and free fluid.
- Endometrial biopsy in the luteal phase — secretory endometrium indicates ovulation (now rarely used).
MARKERS OF ANOVULATION
Conversely, a monophasic basal-temperature chart, a low mid-luteal progesterone, and a proliferative (non-secretory) endometrium indicate that ovulation has not occurred — directing attention to ovulation induction in the infertility work-up.
OTHER SUPPORTIVE EVIDENCE
Mid-cycle pain (mittelschmerz), the mid-cycle change to clear elastic mucus, and a premenstrual secretory endometrium on biopsy all support ovulation; the only absolute proof of ovulation, however, is an achieved pregnancy.
💡CLINICAL PEARL — Best practice: a mid-luteal serum progesterone combined with ultrasound folliculometry is the most reliable, objective confirmation of ovulation in clinical practice.DEFINITION
Emergency (post-coital) contraception is the use of a contraceptive method after an act of unprotected or inadequately-protected intercourse to prevent an unintended pregnancy.
METHODS
- Levonorgestrel 1.5 mg orally, as a single dose within 72 hours (the commonest method); earlier is more effective.
- Ulipristal acetate 30 mg orally within 120 hours (a progesterone-receptor modulator, more effective than levonorgestrel).
- Yuzpe regimen — combined oral pills (ethinyl-oestradiol + levonorgestrel) in two doses within 72 hours.
- Copper IUCD inserted within 5 days — the most effective method and gives ongoing contraception.
MECHANISM
Mainly inhibition/delay of ovulation (hormonal methods); the copper IUCD also prevents fertilisation and implantation. It is not an abortifacient and does not disturb an established pregnancy.
INDICATIONS
Unprotected intercourse, a missed or delayed contraceptive (forgotten pills, late injection), a burst or slipped condom, a displaced diaphragm/IUCD, and after sexual assault.
SIDE-EFFECTS
Nausea and vomiting (repeat the dose if vomiting occurs within 2–3 hours), menstrual irregularity, breast tenderness and headache; it does not protect against subsequent acts in the same cycle.
EFFICACY
The copper IUCD is the most effective (failure < 1%); the oral methods reduce expected pregnancies by about 75–85% and work better the earlier they are taken.
COUNSELLING AND FOLLOW-UP
It gives no protection against later acts in the same cycle, so a regular method should be started; the woman is told to return if the next period is over a week late to exclude pregnancy.
💡CLINICAL PEARL — Key point: emergency contraception is for occasional use, not a regular method — its efficacy falls with delay, so it should be taken as early as possible; follow up to confirm the next menses or exclude pregnancy.DEFINITION
Red (carneous) degeneration is an aseptic necrobiosis of a large fibroid, occurring characteristically in the second half of pregnancy and the puerperium. The cause is thought to be vascular (interference with the blood supply of a rapidly-growing fibroid).
PATHOLOGY
The cut surface has a "raw-beef" (red) appearance with a fishy odour (from fatty acids), the colour being due to haemolysed red cells and haemoglobin; microscopy shows necrosis with thrombosed vessels. Partial recovery is possible — hence the term necrobiosis.
CLINICAL FEATURES
In a pregnant woman — acute localised abdominal pain with tenderness over the fibroid, mild fever, vomiting and a moderate leucocytosis; it is an important cause of acute abdomen in pregnancy.
MANAGEMENT
- Conservative — it is self-limiting; treat with rest, analgesics and reassurance.
- Surgery is avoided in pregnancy unless complications (e.g. torsion) supervene.
DIFFERENTIAL DIAGNOSIS
Other causes of acute abdomen in pregnancy must be considered — torsion of a pedunculated fibroid or ovarian cyst, acute appendicitis, abruptio placentae, ureteric colic and accidental haemorrhage; the localised tenderness over a known fibroid and the absence of peritonism point to red degeneration.
INCIDENCE
It complicates about 5–10% of fibroids in pregnancy, typically in the second or early third trimester when a fibroid outgrows its blood supply.
INVESTIGATIONS
Mainly clinical; ultrasound may show a fibroid with mixed echogenicity/cystic change, with a mild leucocytosis and low-grade fever. Other causes of an acute abdomen in pregnancy must be excluded.
COURSE AND PROGNOSIS
It is self-limiting — the pain settles over 3–7 days with conservative care and the prognosis is good; myomectomy is avoided in pregnancy owing to the risk of severe haemorrhage.
💡CLINICAL PEARL — Key point: red degeneration is managed expectantly — recognising it avoids unnecessary surgery in a pregnant woman, as the pain settles over a few days with conservative care.DEFINITION
A Krukenberg tumour is a metastatic (secondary) tumour of the ovary, characteristically bilateral, arising from a gastrointestinal primary — most often the stomach (also colon, breast), and composed of mucin-secreting "signet-ring" cells in a cellular stroma.
PATHOLOGY
The ovaries are usually bilateral, solid and enlarged, retaining the ovarian shape with a smooth surface. Microscopy shows the diagnostic signet-ring cells (mucin pushing the nucleus to one side) scattered in the stroma. Spread to the ovary is transcoelomic, lymphatic and haematogenous.
CLINICAL FEATURES
Features of the primary gastrointestinal cancer, an abdominal/pelvic mass and ascites; the tumour may be hormonally active (oestrogen/androgen), producing menstrual disturbance or post-menopausal bleeding or virilisation.
SPREAD TO THE OVARY
Tumour reaches the ovaries by transcoelomic seeding, lymphatic and haematogenous routes; the bilateral, solid enlargement with preservation of the ovarian outline is characteristic. Peritoneal deposits and ascites are usually present, indicating advanced disease.
GROSS AND MICROSCOPIC APPEARANCE
The ovaries are bilaterally enlarged, solid and smooth, retaining the ovarian shape. Microscopy shows the diagnostic "signet-ring" cells (mucin displacing the nucleus) scattered in a cellular (sarcoma-like) stroma.
INVESTIGATIONS AND MANAGEMENT
Ultrasound shows bilateral solid masses; tumour markers and gastrointestinal endoscopy are done to find the primary. Treatment is directed at the primary tumour with cytoreduction where feasible; the response to chemotherapy is poor.
💡CLINICAL PEARL — Key point: bilateral solid ovarian tumours should always prompt a search for a gastrointestinal (especially gastric) primary; the prognosis is poor as the disease is usually advanced at diagnosis, and treatment is directed at the primary tumour with cytoreduction where feasible.DEFINITION
A hydatidiform mole is a form of benign gestational trophoblastic disease characterised by abnormal proliferation of the trophoblast with hydropic (vesicular) swelling of the chorionic villi, so that the products resemble a "bunch of grapes".
TYPES
Complete mole Partial mole Karyotype 46,XX (entirely paternal) Triploid (69,XXX/XXY) Fetus Absent Present (abnormal) Villous swelling Diffuse Focal β-hCG / malignant potential Very high; higher Lower; low CLINICAL FEATURES
Amenorrhoea followed by vaginal bleeding, a uterus large for dates, severe hyperemesis, early pre-eclampsia, expulsion of grape-like vesicles, and bilateral theca-lutein cysts.
INVESTIGATIONS AND MANAGEMENT
- Ultrasound — a "snow-storm" appearance with no fetus; a very high serum β-hCG.
- Suction evacuation of the uterus, with anti-D for Rh-negative women.
- Serial β-hCG follow-up with contraception to detect persistent/malignant GTN (which follows 15–20% of complete moles).
COMPLICATIONS
Haemorrhage and anaemia, hyperemesis and early pre-eclampsia, hyperthyroidism (hCG cross- reactivity), trophoblastic pulmonary embolisation at evacuation, and progression to persistent/malignant GTN.
💡CLINICAL PEARL — Key point: after evacuation, serial β-hCG monitoring with reliable contraception is essential to detect post-molar GTN early — a rising or plateauing hCG signals malignant change needing chemotherapy.DEFINITION
A vesicovaginal fistula (VVF) is an abnormal communication between the urinary bladder and the vagina, resulting in continuous, involuntary escape of urine through the vagina.
CAUSES
- Obstetric (commonest in developing countries) — pressure necrosis from prolonged/obstructed labour, and instrumental/operative delivery injury.
- Gynaecological/surgical — injury during hysterectomy or pelvic surgery.
- Radiation for pelvic malignancy, and advanced cervical/vaginal carcinoma.
CLASSIFICATION
VVF is classified by site (juxta-urethral, mid-vaginal, juxta-cervical/vault), by size, and by complexity (simple vs complex — large, scarred, radiation-induced, or involving the ureter/urethra), which together determine the route and difficulty of repair.
CLINICAL FEATURES AND DIAGNOSIS
Continuous dribbling of urine per vaginum with a constantly wet, excoriated vulva. Diagnosis is by speculum examination, the dye (methylene-blue/three-swab) test to locate and distinguish it from a ureterovaginal fistula, and cystoscopy with imaging (IVU) to assess the ureters.
MANAGEMENT
- Small, fresh fistulae — continuous bladder catheter drainage may allow spontaneous healing.
- Surgical repair — usually after about 3 months (once inflammation settles), by the vaginal or abdominal route, with interposition of healthy tissue.
INVESTIGATIONS (DETAIL)
The three-swab (dye) test — methylene blue is instilled into the bladder and three swabs are placed in the vagina; staining of the upper swab suggests a ureterovaginal and of the lower/middle swab a vesicovaginal fistula. Cystoscopy, examination under anaesthesia and intravenous urography define the site, size and ureteric relations.
PRINCIPLES OF REPAIR
Repair is by the vaginal or abdominal route with wide mobilisation and tension-free, layered closure and, where needed, interposition of healthy tissue (e.g. Martius graft); a catheter is left for continuous drainage afterwards.
💡CLINICAL PEARL — Prevention — good intrapartum care with use of the partograph to avoid obstructed labour — is the key, since obstetric VVF is largely preventable.DEFINITION
Adenomyosis is the presence of endometrial glands and stroma within the myometrium (at least one high-power field below the endo-myometrial junction), with surrounding myometrial hypertrophy. It is sometimes called "internal endometriosis".
PATHOLOGY
The uterus is uniformly and symmetrically enlarged (rarely beyond 12 weeks' size) with a thickened, trabeculated myometrium; the cut surface shows whorled muscle with small haemorrhagic cystic spaces. It may be diffuse or, less often, localised (an adenomyoma), and frequently coexists with fibroids and endometriosis.
CLINICAL FEATURES
— progressively severe
secondary dysmenorrhoea
and
menorrhagia
, with a
uniformly enlarged, bulky, tender uterus
("globular" uterus).
DIAGNOSIS
Transvaginal ultrasound (a heterogeneous, asymmetrically thickened myometrium with cysts) and MRI (a thickened junctional zone) suggest it; the definitive diagnosis is histological after hysterectomy.
MANAGEMENT
- Medical — symptomatic relief with NSAIDs and tranexamic acid; the levonorgestrel-IUS, progestins or GnRH analogues reduce bleeding and pain.
- Definitive — hysterectomy in women who have completed their family and failed medical treatment.
ASSOCIATIONS AND INVESTIGATIONS
It is associated with multiparity and previous uterine surgery/curettage and commonly coexists with fibroids and endometriosis. On transvaginal ultrasound the myometrium is heterogeneous with cystic spaces, and MRI shows a thickened junctional zone (> 12 mm) — both suggestive but not diagnostic.
💡CLINICAL PEARL — Key point: suspect adenomyosis in a parous, peri-menopausal woman with the triad of menorrhagia, dysmenorrhoea and a symmetrically enlarged tender uterus; it commonly coexists with fibroids.DEFINITION
Amenorrhoea is the absence of menstruation. Primary amenorrhoea — failure to menstruate by 15 years with normal secondary sexual characteristics (or by 13 years in their absence). Secondary amenorrhoea — cessation of menstruation for 6 months (or three cycles) in a woman who previously menstruated.
PHYSIOLOGICAL CAUSES
Before puberty, during pregnancy and lactation, and after the menopause.
PATHOLOGICAL CAUSES (BY LEVEL)
- Outflow tract/uterus — imperforate hymen, transverse vaginal septum, Müllerian agenesis (Rokitansky), and Asherman's syndrome (intra-uterine adhesions).
- Ovary — gonadal dysgenesis (Turner's syndrome), premature ovarian failure and PCOS.
- Pituitary — prolactinoma/hyperprolactinaemia and Sheehan's syndrome.
- Hypothalamus — stress, excessive exercise, weight loss/anorexia, and chronic illness.
INVESTIGATIONS
A pregnancy test first, then serum FSH/LH, prolactin and TSH, a progesterone challenge, and ultrasound/karyotype as indicated to localise the cause.
MANAGEMENT (PRINCIPLE)
Treatment is directed at the cause — relieving an outflow obstruction (e.g. cruciate incision of an imperforate hymen), dopamine agonists for hyperprolactinaemia, ovulation induction or cyclical oestrogen-progestogen for ovarian/hypothalamic causes, and hormone replacement in premature ovarian failure or gonadal dysgenesis.
💡CLINICAL PEARL — Key point: pregnancy is the commonest cause of secondary amenorrhoea and must be excluded before any further work-up.DEFINITION
Menopause is the permanent cessation of menstruation due to loss of ovarian follicular activity, diagnosed retrospectively after 12 months of amenorrhoea. It occurs at an average age of about 50 years.
FEATURES (OF OESTROGEN DEFICIENCY)
- Vasomotor — hot flushes and night sweats.
- Urogenital atrophy — vaginal dryness, dyspareunia and urinary symptoms.
- Long-term — osteoporosis (fracture risk) and an increased cardiovascular risk; mood and sleep disturbance.
HORMONE REPLACEMENT THERAPY (HRT)
- Composition — oestrogen for symptom relief, combined with a progestogen in women with a uterus (to protect the endometrium from unopposed-oestrogen hyperplasia/cancer); oestrogen alone after hysterectomy.
- Indications — troublesome vasomotor/urogenital symptoms and premature menopause; benefits include symptom relief and bone protection.
- Risks — venous thromboembolism, a small increase in breast cancer (combined HRT) and endometrial cancer (unopposed oestrogen).
- Contraindications — oestrogen-dependent cancer, undiagnosed bleeding, active thromboembolism and severe liver disease.
DIAGNOSIS AND NON-HORMONAL MEASURES
The diagnosis is clinical (12 months' amenorrhoea at the appropriate age), with a raised FSH where confirmation is needed. Non-hormonal options for those who cannot take HRT include lifestyle measures, SSRIs/SNRIs or clonidine for flushes, vaginal moisturisers/local oestrogen for atrophy, and calcium/vitamin-D with bisphosphonates for bone protection.
💡CLINICAL PEARL — Principle: use the lowest effective dose for the shortest necessary time, and always add a progestogen in a woman with an intact uterus.DEFINITION
Vaginal candidiasis (moniliasis) is a fungal infection of the vagina and vulva, most commonly caused by Candida albicans, producing a characteristic itchy, curdy discharge.
PREDISPOSING FACTORS
Pregnancy, diabetes mellitus, broad-spectrum antibiotics, immunosuppression (HIV), corticosteroids and oral-contraceptive use — conditions that alter the vaginal flora or glycogen content.
CLINICAL FEATURES
Intense vulval pruritus with a thick, white, curdy ("cottage-cheese") discharge, vulval erythema, soreness and superficial dyspareunia; the vaginal pH usually remains normal (< 4.5).
DIAGNOSIS AND TREATMENT
- Diagnosis — a wet-mount / KOH preparation showing budding yeasts and pseudohyphae, or culture.
- Treatment — topical imidazoles (clotrimazole pessary/cream) or oral fluconazole; correct the predisposing factors and treat recurrent/severe disease for longer.
RECURRENT AND COMPLICATED DISEASE
Recurrent candidiasis (four or more episodes a year) warrants a search for diabetes or immunosuppression and a longer suppressive course. In pregnancy it is common (high oestrogen and glycogen) and treated with topical azoles; oral fluconazole is generally avoided.
PATHOPHYSIOLOGY
*Candida* is a commensal of the vagina and gut; disease results when altered conditions (raised oestrogen/glycogen, antibiotics suppressing lactobacilli, immunosuppression) allow overgrowth and tissue invasion of the vulvovaginal epithelium.
💡CLINICAL PEARL — Key point: recurrent candidiasis should prompt a search for diabetes or immunosuppression; the male partner is treated only if symptomatic.DEFINITION
The Manchester (Fothergill) operation is a uterus-conserving operation for uterovaginal prolapse, particularly when there is cervical (supravaginal) elongation, in a woman who wishes to retain her uterus.
COMPONENTS (THREE STEPS)
- Amputation of the elongated cervix.
- Plication and shortening of the cardinal (Mackenrodt) ligaments in front of the cervix (the Fothergill stitch), which elevates and supports the uterus.
- Anterior colporrhaphy (for the cystocele) and posterior colpoperineorrhaphy as required.
INDICATIONS
Uterovaginal prolapse with cervical elongation in a younger woman wishing to preserve the uterus/ menstruation or who is unfit for hysterectomy.
ADVANTAGES AND LIMITATIONS
Advantages — the uterus is conserved, it is quicker and less major than hysterectomy, and it corrects the cystocele and cervical elongation. Limitations — it does not remove the (potentially diseased) uterus, is unsuitable when childbearing is complete, and has the complications below.
OUTCOME AND CONTRAINDICATIONS
It corrects the prolapse while conserving the uterus and menstruation. It is not suitable when further childbearing is desired (risk of cervical incompetence) or when the uterus itself is diseased, and the cardinal- ligament plication may make a subsequent pregnancy high-risk.
💡CLINICAL PEARL — Complications: cervical stenosis (haematometra, dysmenorrhoea, infertility), cervical incompetence and mid-trimester loss/preterm labour in a future pregnancy, and recurrence of the prolapse. For these reasons it is less favoured than vaginal hysterectomy when childbearing is complete.DEFINITION
Medical termination of pregnancy (MTP) is the legally permitted, deliberate termination of pregnancy by a registered medical practitioner under the provisions of the MTP Act, 1971 (amended 2021) in India.
LEGAL GESTATIONAL LIMITS (INDIA)
- Up to 20 weeks — on the opinion of one registered medical practitioner.
- 20–24 weeks — on the opinion of two practitioners, for specified categories (e.g. survivors of rape, minors, change in marital status, fetal abnormality, disability).
- Beyond 24 weeks — only for substantial fetal abnormality, on the approval of a Medical Board.
INDICATIONS
Risk to the life or physical/mental health of the woman, substantial fetal abnormality, pregnancy from rape/incest, and contraceptive failure (for any woman and her partner).
METHODS
- Medical — mifepristone followed by misoprostol (up to about 9 weeks).
- Surgical — suction evacuation / manual vacuum aspiration (up to ~12–14 weeks), and dilatation and evacuation later.
COMPLICATIONS
Immediate — haemorrhage, uterine perforation, cervical injury and anaesthetic complications. Delayed — incomplete abortion, pelvic infection/sepsis, and failed termination with a continuing pregnancy. Remote — cervical incompetence, intra-uterine adhesions and (with repeated procedures) menstrual disturbance.
PRE-REQUISITES
The procedure requires the informed written consent of the woman, performance by a registered medical practitioner with the prescribed training, at a government-approved place, with maintenance of the woman's confidentiality.
💡CLINICAL PEARL — Always provide anti-D to Rh-negative women and post-abortion contraception; confidentiality of the woman is protected under the Act.DEFINITION
A Bartholin's cyst is a retention cyst formed by obstruction of the Bartholin's (greater vestibular) gland duct, with accumulation of secretion; a Bartholin's abscess is an infected, suppurating cyst.
CAUSE
Blockage of the duct (by inflammation/inspissated secretion); the abscess is usually caused by E. coli, gonococcus, staphylococci and anaerobes.
CLINICAL FEATURES
Cyst — a painless, tense, cystic swelling in the posterolateral part of the introitus (lower third of the labium majus). Abscess — a painful, hot, red, tender swelling with difficulty in sitting/walking, sometimes with fever.
MANAGEMENT
- Small asymptomatic cyst — observation.
- Symptomatic cyst — marsupialisation (creating a permanent new duct opening) to preserve gland function.
- Abscess — incision and drainage (or marsupialisation) with antibiotics; a Word catheter may be placed to keep the cavity draining.
COMPLICATIONS AND RECURRENCE
An untreated abscess may rupture spontaneously or recur; recurrence after simple incision is common (hence marsupialisation is preferred), and a chronic cyst may cause dyspareunia. Cellulitis of the vulva and, rarely, necrotising infection can complicate an abscess.
ANATOMY AND DIFFERENTIAL DIAGNOSIS
The Bartholin's (greater vestibular) glands lie in the posterolateral wall of the lower vagina and secrete lubricating mucus through a duct opening into the vestibule. The swelling is distinguished from a cyst of the canal of Nuck, an inclusion/sebaceous cyst, and — in the elderly — carcinoma of the gland.
💡CLINICAL PEARL — Note: a Bartholin swelling appearing for the first time in a woman over 40 should be biopsied to exclude the rare carcinoma of the gland.DEFINITION
Trichomoniasis is a sexually transmitted infection of the vagina caused by Trichomonas vaginalis, a flagellated motile protozoan.
CLINICAL FEATURES
A profuse, frothy, greenish-yellow, offensive vaginal discharge with vulval itching and soreness, dysuria and dyspareunia; on examination a "strawberry" cervix (punctate haemorrhages) may be seen, and the vaginal pH is raised (> 4.5).
DIAGNOSIS
Wet-mount microscopy of the discharge shows the motile, flagellated trichomonads; culture and NAAT are more sensitive. A positive amine (whiff) test may coexist.
TREATMENT
- Metronidazole (single 2 g dose or a 7-day course) — oral, since the infection is vaginal and urethral.
- Treat the sexual partner simultaneously (it is an STI) and advise abstinence until both are cured; screen for other sexually transmitted infections.
COMPLICATIONS
Trichomoniasis is associated with preterm labour and low birth weight in pregnancy, an increased risk of acquiring and transmitting HIV and other sexually transmitted infections, and ascending infection/PID; the "strawberry cervix" reflects the intense inflammation.
ORGANISM AND TRANSMISSION
*Trichomonas vaginalis* is an anaerobic flagellated protozoan transmitted almost exclusively sexually; it infects the vagina, urethra and paraurethral glands, with an incubation period of about 4–28 days.
NOTE ON TREATMENT
The patient is advised to avoid alcohol while taking metronidazole (a disulfiram-like reaction); metronidazole is also used (with caution) in pregnancy.
💡CLINICAL PEARL — Key point: because it is sexually transmitted, partner treatment is essential; in pregnancy it is associated with preterm labour and low birth weight.DEFINITION
Tumour markers are substances (usually proteins) produced by tumour cells or by the body in response to a tumour, measurable in blood and used mainly to monitor treatment response and detect recurrence (and to support diagnosis), rather than for screening.
IMPORTANT GYNAECOLOGICAL MARKERS
Marker Associated tumour CA-125 Epithelial ovarian cancer (also raised in endometriosis, PID, fibroids) AFP Yolk-sac (endodermal sinus) tumour of ovary β-hCG Choriocarcinoma/GTN; germ-cell (choriocarcinoma) tumours LDH Dysgerminoma Inhibin / oestradiol Granulosa-cell (sex-cord stromal) tumour CEA Mucinous ovarian tumours SCC antigen Squamous-cell carcinoma of the cervix PRINCIPLE AND LIMITATIONS
An ideal marker is both specific and sensitive; in practice most gynaecological markers lack the specificity needed for screening (CA-125 is raised in many benign conditions) and are used chiefly for supporting a diagnosis, monitoring the response to treatment and detecting recurrence of a known tumour.
💡CLINICAL PEARL — Key point: markers are most useful for monitoring a known tumour — a falling level indicates response and a rising level recurrence; most lack the specificity needed for population screening (CA-125 is also raised in many benign conditions).DEFINITION
Dilatation and curettage (D&C) is a gynaecological procedure in which the cervix is dilated and the endometrium is scraped (curetted) for diagnostic or therapeutic purposes.
INDICATIONS
- Diagnostic — endometrial sampling in abnormal/post-menopausal uterine bleeding (to exclude hyperplasia/ malignancy) and to investigate infertility (now often replaced by Pipelle biopsy and hysteroscopy).
- Therapeutic — evacuation of retained products of conception (incomplete/missed abortion), removal of an endometrial polyp, and evacuation of a molar pregnancy.
TECHNIQUE
Under anaesthesia, with the patient in lithotomy and full aseptic precautions: the uterine size/position is assessed, the cervix dilated with Hegar's dilators, and the cavity curetted with a sharp/blunt curette (or emptied by suction); products are sent for histology.
FRACTIONAL CURETTAGE
In suspected malignancy, a fractional (separate) curettage is done — the endocervix is curetted first and then the uterine cavity, the specimens being labelled separately — to determine whether disease has involved the cervix, which alters the stage and management.
TYPES AND CONTRAINDICATIONS
Types include simple, fractional (separate endocervical then endometrial), and suction curettage. It is contraindicated in pregnancy (unless the aim is evacuation), in acute pelvic infection and with an uncorrected bleeding disorder; an acute infection is treated first.
PREPARATION
It is performed under general/regional anaesthesia in the lithotomy position with full asepsis, after a bimanual examination to assess uterine size and position.
💡CLINICAL PEARL — Complications: uterine perforation, cervical injury, haemorrhage, infection, and intra-uterine adhesions (Asherman's syndrome) from over-vigorous curettage — hence gentle technique and a clear indication are essential.MBBS Adda · mbbsadda.in Page 3