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Sexually Transmitted Infections & Related Conditions — Key Points

General Principles

• STIs are often asymptomatic but can still be transmitted and cause serious future complications.
• They disproportionately affect younger people, though increasingly identified in older adults where diagnosis is often missed.
• One STI found = screen for all others (coexistence is common).
• Modern testing uses multiplex NAATs (nucleic acid amplification tests) — highly sensitive, can detect multiple infections from a single swab/urine sample, including self-taken samples.
• Point-of-care tests exist for HIV and others but have suboptimal sensitivity/specificity.
• Confidentiality and partner notification are critical — partners require simultaneous testing and treatment.
• Always consider safeguarding: screen for sexual exploitation, coercion, domestic abuse, especially in those under 16.

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Taking a Sexual History

• Reason for attendance and symptoms
• Past/current STI history including HIV status
• Sexual partners in the last 3 months, gender, country of origin, condom use, symptoms
• Any forced sex, violence, abuse, or coercion
• For under 16s: age of partner, whether they attend school, family support, safeguarding assessment
• Capacity assessment is mandatory for under 16s without parental consent

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Caring for Transgender & Non-Binary Individuals

• Use preferred pronouns and name
• Establish current anatomy, hormone use, and type of sexual activity to guide testing
• Offer appropriate contraception, STI screening, HPV vaccination, HIV prevention, and cervical screening based on anatomy

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Infective Causes of Vaginal Discharge

Bacterial Vaginosis (BV)

• Not classified as an STI, but associated with sexual activity
• Caused by depletion of lactobacilli → pH rises >4.5; overgrowth of Gardnerella vaginalis and anaerobes
• Diagnosis (Amsel criteria): homogeneous discharge + high pH + clue cells on microscopy + fishy odour with 10% KOH
• Complications: PID, post-hysterectomy cuff cellulitis, preterm birth, miscarriage
• Treatment: oral or intravaginal metronidazole or clindamycin (treat if symptomatic or pre-surgery); partners do NOT need treatment
• Avoid vaginal douching

Vulvovaginal Candidiasis

• Caused by Candida albicans (most common)
• Not an STI — partners without symptoms do not need treatment
• More frequent/persistent in diabetes, immunocompromise, pregnancy
• Diagnosis: microscopy and culture (swab)
• Treatment: topical intravaginal pessaries or oral imidazoles; topical vulval antifungals for symptomatic relief

Trichomoniasis

• Caused by flagellate protozoan Trichomonas vaginalis — is an STI
• Often causes vaginal discharge ± signs of vulvovaginitis; asymptomatic colonisation in up to 50%
• Associated with preterm birth, low birth weight, maternal postpartum sepsis
• Gold standard diagnosis: NAAT (vulvovaginal swab); also culture or wet mount (lower sensitivity)
• Treatment: systemic metronidazole — simultaneous treatment of current sexual partners required

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Cervicitis

Gonorrhoea (Neisseria gonorrhoeae)

• Endocervical infection asymptomatic in up to 50%
• Symptoms: altered vaginal discharge, lower abdominal pain (~25%)
• Rectal infection via anal sex; pharyngeal infection via oral sex (nearly always asymptomatic)
• Ascending infection → PID; rarely → disseminated gonococcal infection (purpuric non-blanching rash + monoarticular arthritis)
• Neonatal conjunctivitis if mother infected at delivery
• Diagnosis: NAAT (vulvovaginal swab); culture required if tested positive before treatment (surveillance for antimicrobial resistance)
• ⚠️ Widespread antimicrobial resistance — requires surveillance
• Treatment: parenteral third-generation cephalosporin (first-line)

Chlamydia (Chlamydia trachomatis)

• Most common bacterial STI; often asymptomatic but causes subclinical PID and complications
• Symptoms: altered vaginal discharge, intermenstrual/post-coital bleeding, abdominal pain; cervicitis may be present
• Can cause reactive monoarthritis (more common in men); neonatal conjunctivitis
• Diagnosis: NAAT (vulvovaginal swab, self-taken)
• Treatment:
  • Non-pregnant: doxycycline
  • Pregnant: azithromycin + test of cure
  • Partner treatment simultaneously required

Mycoplasma genitalium

• Causes cervicitis, endometritis, PID
• Test with vulvovaginal swabs including macrolide resistance testing where possible
• Treatment: doxycycline → azithromycin → moxifloxacin (escalating regimen based on resistance)

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Pelvic Inflammatory Disease (PID)

• Ascending infection from endocervix to upper reproductive tract
• Caused by chlamydia, M. genitalium, gonorrhoea, or normal vaginal flora
• Diagnosis is clinical: bilateral lower abdominal pain, dyspareunia, altered vaginal discharge, intermenstrual/post-coital bleeding + cervical motion tenderness + cervicitis
• Always exclude pregnancy; test for all STIs
• Start empirical treatment immediately — delay increases risk of complications
• Complications: subfertility, ectopic pregnancy, chronic pelvic pain, Fitz-Hugh–Curtis syndrome (perihepatitis with "violin string" perihepatic adhesions → right upper quadrant pain)
• IUD: consider removal if not responding to treatment (weigh against pregnancy risk if recent unprotected sex)
• Treatment: 2-week course — macrolide or tetracycline + metronidazole + initial parenteral third-generation cephalosporin
• Partners require simultaneous screening and empirical treatment

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Viral STIs

Genital Herpes (HSV)

• Caused by HSV-1 (also orolabial) and HSV-2 — both cause genital herpes
• Latency in sensory ganglia → reactivation with or without symptoms; asymptomatic shedding is a key transmission route
• Recurrence higher with HSV-2; decreases in frequency over time
• Symptoms: genital pain, dysuria, vesicular ulcers
• Pregnancy risks:
  • Primary infection in third trimester → neonatal infection rate up to 41%
  • Recurrent infection at delivery → neonatal herpes risk <3% (maternal IgG crosses placenta)
  • Primary herpes in third trimester → elective pre-labour caesarean section
  • Proven recurrent lesions → vaginal birth may be anticipated
• Treatment: aciclovir (safe and effective; episodic or suppressive regimens)

Genital Warts & HPV

• Warts: benign epithelial tumours caused by HPV types 6 and 11 (~90% of genital warts)
• Oncogenic types 16 and 18 cause ~70% of cervical cancer + other HPV-related cancers (oropharyngeal, penile, anal, vaginal, vulval)
• Most genital HPV infections are subclinical
• HPV vaccination available — highly effective for prevention
• Diagnosis of warts: clinical examination
• Treatment options (optional for benign warts):
  • Ablative: liquid nitrogen, surgical techniques
  • Topical patient-applied: podophyllotoxin or imiquimod
  • In pregnancy: ablative therapies only
• Rarely, large warts obstruct birth canal → caesarean section needed
• Very rarely: neonatal respiratory papillomatosis (caesarean benefit unproven)

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Syphilis (Treponema pallidum)

• Transmitted by direct contact with infective lesions or transplacental passage
• Multisystem disease — frequently misdiagnosed as it mimics many conditions
• Untreated: relapse/remit with late complications appearing years later

Stages of Acquired Syphilis:

• Infectivity declines with time; penicillin-based regimens are curative (reinfection possible)
• Resurgence in gay/bisexual MSM and in pregnant women in recent decades

Congenital Syphilis:

• Screen all pregnant women — riskiest period is infection just before or during pregnancy
• "Negative now" message — women screened early should re-screen if at risk later
• Early congenital features (within 2 years): rash, haemorrhagic rhinitis ("bloody snuffles"), lymphadenopathy/hepatosplenomegaly, skeletal abnormalities, condylomata lata, pseudoparalysis, non-immune hydrops, glomerulonephritis, haemolysis
• Late congenital "stigmata": Hutchinson's incisors, mulberry molars, interstitial keratitis, Clutton joints, saddle nose, sensorineural deafness, frontal bossing, intellectual disability

Diagnosis:

• Serology: treponemal test (EIA) → confirm with second treponemal test + non-treponemal titre
• Can be negative in very early disease → repeat 4–6 weeks later if suspected
• Serological tests usually positive for life even after curative treatment

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HIV

Natural History & Epidemiology

• Acute viral illness → chronic depletion of CD4+ T-lymphocytes → AIDS-defining illnesses
• AIDS-defining illnesses include: invasive cervical cancer, PCP, CMV disease, Mycobacterium tuberculosis, recurrent bacterial infections, CNS lymphoma, Kaposi's sarcoma, and many others
• Cervical pre-cancer is an HIV indicator condition (prevalence of undiagnosed HIV >0.1%)
• Disproportionately affects: sub-Saharan Africans, gay/bisexual MSM, intravenous drug users
• HAART has transformed outcomes — new diagnoses falling globally (>30% worldwide)

Testing

• Recommended for all with AIDS-defining/HIV indicator conditions
• Routine screening in high-prevalence populations (UK: areas >0.2% prevalence, ages 15–59)
• All pregnant women must be screened

Gynaecological Complications

• HIV+ women have higher risk of persistent oncogenic HPV, higher CIN/HSIL incidence → annual cervical screening recommended
• Higher risk of all anogenital HPV-related malignancies, at younger ages

HIV in Pregnancy — Management

1. Confirm HIV status in all pregnant women
2. Effective HAART → achieve undetectable viral load (VL)
3. Most vertical transmission occurs during birth or breastfeeding; intrauterine infection unusual (increased risk with amniocentesis)
4. Pre-labour caesarean section if VL is detectable
5. Avoid: prolonged rupture of membranes, fetal scalp electrodes, procedures that breach infant's skin
6. Breastfeeding: formula feeding preferred if safe; if breastfeeding chosen (with good VL control):
   • Exclusive breast milk, rapid weaning, no mixed feeding
   • Do not feed from breast with mastitis or cracked nipples
   • Monthly VL monitoring for mother and infant
7. With optimal management, vertical transmission rates are extremely low

Contraception

• Many antiretrovirals interact with hormonal contraceptives (reduced efficacy) — check the University of Liverpool HIV Drug Interactions tool
• Non-hormonal contraception (condoms, IUDs) appropriate in most cases

Preconception

• For sero-discordant couples: undetectable VL eliminates sexual transmission
• Screen and treat coexistent STIs
• Fertility treatment is appropriate within regulatory frameworks

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Recommended Guidelines & Resources

• BASHH guidelines (British Association for Sexual Health and HIV)
• BHIVA guidelines (British HIV Association)
• CDC STI treatment guidelines
• University of Liverpool HIV Drug Interactions

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Malignant Disease of the Uterus — Key Points

Overview

• Uterine cancer = tumours arising from the uterine corpus (body)
• Most common: endometrial tumours (from the endometrium)
• Rare: sarcomas (from the myometrium), ~5% of all uterine cancers

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Endometrial Cancer

Incidence

• Most common gynaecological malignancy in high-income countries
• 417,000 new diagnoses globally in 2020; lifetime risk in the UK ~1 in 36
• Mean age of diagnosis: 62 years
• ~15% occur before menopause
• Incidence rising due to: ageing population, less hysterectomy for benign disease, obesity epidemic

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Classification

Historical: Type 1 vs Type 2

Molecular Classification (Cancer Genome Atlas — 4 groups):

1. p53-abnormal — poorest prognosis; benefits most from adjuvant chemotherapy; includes serous, clear cell, carcinosarcoma (and some endometrioid)
2. POLE-mutant — exceedingly good outcomes; very low recurrence; <1% disease-specific mortality
3. MMR-deficient — intermediate stage-dependent prognosis; ~10% associated with Lynch syndrome
4. No specific molecular profile (NSMP) — mostly hormone receptor-positive endometrioid; intermediate to excellent prognosis

Molecular classification is more accurate than histological subtype alone and increasingly guides treatment and prognosis.

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Aetiology & Risk Factors

• Obesity → anovulatory cycles + aromatization of androgens → androgens in adipose tissue → continuous postmenopausal oestrogen
• Insulin & IGF-1 stimulate endometrial proliferation → explains higher risk in type 2 diabetes
• Tamoxifen: antioestrogenic in breast, but stimulatory in endometrium
• Lynch syndrome (autosomal dominant): pathogenic variants in mismatch repair (MMR) genes — MLH1, MSH2, MSH6, PMS2 → lifetime endometrial cancer risk 40–60%; accounts for ~3% of all endometrial cancers; also associated with colorectal, ovarian, and urothelial tumours

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Prevention

• Healthy weight + exercise, hormonal contraceptives, IUDs all reduce risk
• Lynch syndrome patients: offered prophylactic hysterectomy after childbearing completion
• Aspirin is protective against cancer in Lynch syndrome

Screening

• No evidence to support population or high-risk group screening currently

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Clinical Features

• Postmenopausal bleeding (PMB) — the classic "red flag" presentation; 5–10% of PMB = gynaecological malignancy
• Premenopausal: heavy, irregular, or intermenstrual bleeding
• Advanced disease: pelvic pain, urinary/bowel dysfunction, respiratory symptoms
• Incidental finding: abnormal glandular cytology on cervical screening
• Signs: bleeding from cervical os on speculum; bulky uterus on bimanual exam (often normal)

• Always investigate PMB — never dismiss
• Inspect external genitalia + speculum exam to exclude vulval, vaginal, cervical cancer
• Physical exam may be completely normal in endometrial cancer
• Benign causes: unscheduled HRT bleeding, vaginal atrophy

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Diagnosis & Investigation of PMB

1. TVUSS (transvaginal ultrasound scan)
   • Measures endometrial thickness
   • Endometrium <4 mm → cancer very unlikely; no further investigation needed
   • Endometrium ≥4 mm → proceed to hysteroscopy and/or biopsy
2. Hysteroscopy
   • Done outpatient where possible (GA needed for cervical stenosis, poor tolerance, or patient request)
   • Thin scope visualizes endometrium → directed biopsy of abnormal areas
3. Endometrial biopsy
   • Histology reports: tumour type (endometrioid vs other) and grade
   • Atypical hyperplasia = premalignant; risk of progression to cancer: 25–50%
   • Immunohistochemistry (p53 + MMR) and next-generation sequencing (POLE) → enables molecular classification
   • MMR-deficient → prompt genetic counselling for Lynch syndrome

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Staging (FIGO)

• Low-grade stage IA → surgery at local hospital
• High-grade or stage IB+ → surgery at cancer centre (improves outcomes)

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Management

Surgery (Mainstay)

• Total hysterectomy + bilateral salpingo-oophorectomy (BSO)
• Minimally invasive (laparoscopic or robotic) = preferred — equivalent oncological outcomes + fewer complications, faster recovery
• Lymph node assessment:
  • High-risk features → pelvic and para-aortic node dissection (staging info but does not improve survival; increases morbidity)
  • Sentinel lymph node biopsy — emerging replacement for full dissection; provides same staging with lower perioperative risk

Adjuvant Treatment

• Given for high/intermediate risk of relapse
• Radiotherapy:
  • Vaginal brachytherapy — reduces local recurrence (for local disease)
  • Brachytherapy + external beam pelvic radiotherapy — for stage III
  • Does not improve overall survival
• Chemotherapy: for high-risk tumours; most beneficial for p53-abnormal tumours (highest relapse risk)

Hormone Therapy (Fertility-Sparing / Unfit for Surgery)

• High-dose oral or intrauterine progestin for:
  • Atypical hyperplasia
  • Low-grade stage IA endometrioid tumours
• ⚠️ Relapse rates are high
• Premenopausal patients: refer to specialist for egg retrieval/surrogacy counselling
• Hysterectomy with ovarian conservation is an option for premenopausal low-grade early-stage disease (avoids surgical premature menopause without impairing survival)

Advanced & Recurrent Disease

• Treated with surgery, chemotherapy, radiotherapy, and/or hormone therapy based on extent, location, and molecular profile
• Immune checkpoint inhibitors (e.g. dostarlimab): licensed for advanced/recurrent MMR-deficient endometrial cancers
• New systemic therapies targeted to molecular profile offer improved outcomes

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Prognosis

• Overall 5-year survival: 76%
• Adverse prognostic features: advanced age, grade 3, non-endometrioid histology, p53-abnormal, deep myometrial invasion, lymphovascular space invasion, nodal involvement, distant metastases

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Endometrial Cancer in Young Women

• Young-onset endometrial cancer is a feature of Lynch syndrome
• PCOS and obesity are risk factors for sporadic premenopausal cancer
• Being diagnosed during infertility investigation = "two devastating diagnoses at once"
• Fertility-sparing options only valid for atypical hyperplasia or low-grade stage IA
• Hormone therapy has moderate response but high relapse rates
• Ovarian stimulation for egg retrieval + surrogacy should be discussed with a specialist

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Sarcomas of the Uterus (~5% of uterine cancers)

Pure Sarcomas

Leiomyosarcoma

• Rare tumours of the myometrium
• In 0.75% of cases: malignant transformation of benign fibroids
• Presents: rapidly growing pelvic mass + pain
• Pre-op diagnosis difficult; MRI may show necrosis within fibroid (suggestive of malignant change)
• Uterus: enlarged and soft on palpation
• Treatment: surgery ± adjuvant treatment if mitotic count >10 mitoses per high-powered field
• Metastatic spread: vascular → lung, brain

Endometrial Stromal Sarcoma

• Occurs in perimenopausal patients
• Presents: irregular bleeding + soft, enlarged uterus
• Majority are low grade
• Treatment: surgery (main treatment)

Heterologous Sarcomas

• Sarcomatous tissue not normally found in the uterus (striated muscle, bone, cartilage)
• Most common: rhabdomyosarcoma
  • May present in children as a grape-like mass protruding from cervix with watery discharge
  • Histology: primitive rhabdomyoblasts
  • High recurrence rates with distant metastases

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Key Learning Points Summary

1. Endometrial cancer = most common gynaecological malignancy in the UK
2. Obesity and hyperoestrogenic states are the main aetiological drivers
3. Most present with PMB; 5–10% of PMB cases = gynaecological malignancy; 15% of endometrial cancers occur premenopausally
4. Endometrial biopsy and/or hysteroscopy = gold standard for diagnosis; MRI defines disease extent
5. Total hysterectomy + BSO = treatment of choice for most patients
6. Majority present as stage I disease; overall 5-year survival = 76%
7. Non-endometrioid histology, p53-abnormal, high grade, and advanced stage = worst outcomes

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Malignant Disease of the Ovary — Key Points

Overview

• Second most common gynaecological malignancy
• Primary cause of death from gynaecological cancer in the UK
• ~7,500 new cases and 4,200 deaths per year in the UK
• Overall 5-year survival: 46% — poor due to late presentation
• Excellent prognosis when detected early
• Many ovarian cancers now believed to originate in the fallopian tube, not the ovarian surface epithelium

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Incidence

• Lifetime risk in general population: 2% (1 in 50)
• Mean age of presentation: 64 years; rare under 35 (only 3%)
• More prevalent in high-income countries
• Ethnic variation: White women ~18/100,000; Asian ~12/100,000; Black ~9/100,000
• Women with hereditary cancer present earlier: mean age 54 years

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Classification

• Krukenberg tumours = ovarian metastases from primary cancers of the colon, stomach, or breast

Epithelial Tumour Subtypes:

• High-grade serous (~75% of all epithelial ovarian cancers) — worst prognosis; characterized by psammoma bodies (concentric calcification rings)
• Endometrioid — resembles endometrial cancer histologically; associated with endometriosis (~10%) and synchronous endometrial cancer (10–15%); better survival
• Clear cell — arises from endometriosis; cells have abundant clear cytoplasm (like renal cancer)
• Mucinous — large, multiloculated; associated with pseudomyxoma peritonei
• Low-grade serous — distinct biology, slower progression
• Borderline (BOTs) — ~10% of epithelial tumours; well-differentiated, features of malignancy but do not invade basement membrane; spread to peritoneum/omentum but rarely recur after surgery; most are serous

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Aetiology & Risk Factors

High-Grade Pelvic Serous Carcinomas

• Often impossible to establish site of origin (ovary vs tube vs peritoneum) — all grouped as "high-grade pelvic serous carcinoma"
• Precursor lesion: serous tubal intraepithelial carcinoma (STIC) — TP53 mutations in secretory cells of the distal fallopian tube
• ~30% associated with somatic or germline BRCA mutations

Other Epithelial Subtypes

• Arise from inclusion cysts and endometriosis
• Driver mutations: KRAS, PTEN, BRAF, ARID1A (not TP53)

Risk Factor Table:

• "Incessant ovulation" theory: repeated damage to ovarian epithelium at ovulation → increased cancer risk
• Excess gonadotrophins → oestrogen-stimulated proliferation → malignant transformation

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Genetic Factors

• ≥10–15% of epithelial ovarian cancers have hereditary predisposition
• General population lifetime risk: 1 in 50 (2%)
• 1 affected family member: rises to 1 in 20 (5%)
• 2 first-degree relatives affected: rises to 40–50%

BRCA1/2 (Breast-Ovarian Cancer Syndrome)

• Most common hereditary predisposition — 90% of hereditary ovarian cancers
• BRCA1 (80%), BRCA2 (15%) — tumour suppressor genes
• BRCA-associated ovarian cancers: usually high-grade serous or grade 3 endometrioid, present at advanced stage, poor prognosis
• BUT: BRCA-associated cancers are particularly sensitive to platinum-based chemotherapy
• Hereditary cancers occur ~10 years earlier than sporadic; associated with breast, colon, rectum cancers

Lynch Syndrome

• Pathogenic variants in MMR genes: MLH1, MSH2, MSH6, PMS2
• 10–17% lifetime risk of ovarian cancer (usually endometrioid or clear cell)
• Lynch-associated ovarian tumours: present at earlier stages, better prognosis than BRCA-associated

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Prevention

For BRCA Carriers:

• Offered risk-reducing prophylactic bilateral salpingo-oophorectomy (BSO) after completing family
• Reduces ovarian cancer risk by 90% (does not completely eliminate primary peritoneal cancer risk)
• Timing: prior to age-related surge — BRCA1: mid-to-late 30s; BRCA2: mid-to-late 40s
• Alternative strategy being explored: bilateral salpingectomy in 30s → delayed oophorectomy later (offsets surgical menopause morbidity) — efficacy not yet proven

General Population:

• Opportunistic salpingectomy during hysterectomy for benign disease reduces ovarian cancer risk
• Tubal ligation and hysterectomy with ovarian conservation also reduce risk
• Combined oral contraceptive pill (COCP): reduces risk by up to 50% in both BRCA carriers and average-risk women

Screening:

• No screening programme is effective — neither TVUSS nor CA125 measurement improves survival in average-risk or familial predisposition groups
• High-grade serous tumours (most lethal) develop rapidly → already advanced before screening detects them

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Clinical Features

• Symptoms are non-specific and vague → main reason 66% present with stage III or greater
• Most common symptoms:
  • Increased abdominal girth / bloating
  • Persistent pelvic and abdominal pain
  • Difficulty eating / feeling full quickly
• Other: change in bowel habit, urinary symptoms, backache, irregular bleeding, fatigue
• Any woman with persistence of these symptoms should be assessed by her GP
• Examination findings: fixed, hard pelvic mass ± ascites; pleural effusion; enlarged lymph nodes
• Fewer than 20% of adnexal masses in premenopausal women are malignant; rises to ~50% postmenopausally

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Investigations

1. TVUSS — first-line imaging; characterizes mass (size, solid elements, bilaterality, ascites, extraovarian disease)
2. Tumour markers:

• CA125 elevated in >80% of epithelial ovarian cancers; only ~50% of early-stage disease; also raised in benign conditions (pregnancy, endometriosis, alcoholic liver disease)
• Risk of Malignancy Index (RMI): calculated from menopausal status + ultrasound features + CA125 → triages masses as low/intermediate/high risk

1. CT scan — extrapelvic disease, staging
2. MRI — tissue planes, operability
3. Other pre-op: CXR, ECG, FBC, U&E, LFTs
4. Paracentesis / pleural aspiration — symptom relief + cytological diagnosis if gross ascites/effusion
5. Biopsy (laparoscopic or CT/US-guided, usually omentum) — required before primary chemotherapy

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Staging (FIGO)

• Stage I: 25% | Stage II: 10% | Stage III: 50% | Stage IV: 15%

• Early-stage (I–II): up to 20% have occult nodal disease
• Advanced (III–IV): up to 60%

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Management

Surgery

• Mainstay — needed for diagnosis, staging, AND treatment
• Should be performed by a gynaecological oncologist at a cancer centre (proven to improve outcomes)
• Objective: complete removal of all visible tumour — the most important prognostic factor is no residual disease
• Approach: vertical (midline) incision → access all abdominal areas
• Procedure: ascites/washings sampled → total abdominal hysterectomy + BSO + omentectomy + further debulking (bowel resection, peritoneal stripping, splenectomy as needed)
• Complete debulking achievable in 40–80% of advanced cases
• Restaging (laparoscopic) offered if initial surgery performed outside a cancer centre

• Unilateral salpingo-oophorectomy + omentectomy + peritoneal biopsies + pelvic/para-aortic node dissection + endometrial sampling
• Also appropriate for borderline tumours if fertility is desired

• Offered if complete debulking is unlikely or patient is unfit for surgery
• 3 cycles neoadjuvant chemotherapy → restaging CT → interval debulking surgery → 3 more cycles
• Not inferior to upfront surgery; associated with less morbidity but does not influence survival

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Chemotherapy

• Platinum compound → DNA strand cross-linkage → arrests cell replication
• Dose calculated by GFR (area under the curve)
• Less nephrotoxic and less nausea than cisplatin, equally effective
• BRCA-associated cancers are particularly sensitive to platinum

• Derived from Pacific yew bark
• Causes microtubular damage → prevents replication
• Pre-emptive steroids required (high-sensitivity reactions)
• Side effects: peripheral neuropathy, neutropenia, myalgia, total body hair loss (dose-independent)

• Bevacizumab side effects: hypertension, delayed wound healing, GI perforation, arterial thromboembolic events
• Olaparib side effects: nausea, loss of appetite, fatigue; rarely serious neutropenia, acute myeloid leukaemia

• Remission >6 months → carboplatin again
• Otherwise: paclitaxel (taxol), topotecan, or liposomal doxorubicin
• Treatment is largely palliative at recurrence

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Prognosis

• Overall UK 5-year survival: 46%
• Outcomes have improved with widespread MDT care

1. Stage of disease
2. Volume of residual disease after surgery
3. Histological type and grade
4. Age at presentation

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Primary Peritoneal Carcinoma

• High-grade pelvic serous carcinoma; histologically indistinct from fallopian tube/ovarian tumours
• Criteria for diagnosis:
  • Normal-sized or slightly bulky ovaries
  • More extra-ovarian than ovarian disease
  • Low-volume peritoneal disease
• Same clinical behaviour, prognosis, and treatment as other high-grade pelvic serous carcinomas
• Trend toward primary chemotherapy (complete surgical debulking is difficult)

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Sex Cord Stromal Tumours (~10% of ovarian tumours)

• Almost 90% of all functional (hormone-producing) ovarian tumours
• Generally low malignant potential, good long-term prognosis
• Hormone production → precocious puberty, abnormal menstrual bleeding, endometrial cancer risk (oestrogen-producing) or virilization (androgen-producing)

Subtypes:

• Granulosa cell tumours — most common (>70% of sex cord stromal); peak incidence at menopause; juvenile form presents under age 10 with precocious puberty
  • Produce inhibin → used as tumour marker for follow-up; rises before clinical recurrence
  • Can recur many years after initial treatment → long-term follow-up required
  • No effective chemotherapy for recurrence → surgery is mainstay
• Sertoli–Leydig cell tumours — produce androgens in >50%; present with pelvic mass + virilization (amenorrhoea, deep voice, hirsutism); rarely produce oestrogen or renin (→ hypertension)

Clinical features:

• Irregular menstrual bleeding, postmenopausal bleeding, precocious puberty
• Usually unilateral ovarian mass up to 15 cm; solid with areas of haemorrhage; yellow cut surface (steroid production)

Treatment:

• Young patients (early-stage): unilateral salpingo-oophorectomy + endometrial sampling + staging
• Older patients: full surgical staging

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Germ Cell Tumours (~10% of ovarian tumours)

• Mainly affect young women; derived from primordial germ cells → can contain any cell type
• 70% are stage I at diagnosis
• Spread: lymphatic or haematogenous
• Most common presenting symptom: pelvic mass; 10% present acutely with torsion/haemorrhage; some present during pregnancy

Subtypes:

Investigations:

• Pre-operative tumour markers (AFP, hCG) — influence post-operative chemotherapy decisions
• MRI for teratoma morphology; CT abdomen for lymph nodes/liver; CXR for pulmonary metastases

Treatment:

• Emphasis on fertility-preserving surgery + chemotherapy
• Exploratory laparotomy → remove tumour → assess contralateral ovary (20% spread in dysgerminoma) → peritoneal biopsies + pelvic/para-aortic node sampling → debulk metastatic disease
• Stage I dysgerminoma and low-grade teratoma: surgery alone → 5-year survival >90%
• Disease outside ovary: chemotherapy
• BEP regimen (Bleomycin + Etoposide + Cisplatin): 3–4 cycles, 3-weekly → >90% long-term cure, fertility preserved
• Recurrent disease: 90% present within first year; salvage chemotherapy has very good success rates

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Key Learning Points Summary

1. Ovarian cancer presents late with non-specific symptoms — high index of suspicion is essential
2. Screening (CA125 + TVUSS) has not proven effective
3. Treatment: remove all tumour surgically + platinum-based chemotherapy
4. Prognosis is stage-dependent: Stage I → 80–90% survival; Stage III → 30% survival
5. Sex cord stromal tumours present with endocrine effects (excess oestrogen or androgens)
6. Germ cell tumours affect young women and are often cured with fertility-preserving surgery + BEP chemotherapy

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Ectropion — Key Points

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Part 1: Cervical Ectropion (Cervical Ectopy)

Definition

• Also called cervical ectopy or ectropion
• Occurs when columnar epithelium (which normally lines the endocervical canal) extends onto the ectocervix, appearing as a red zone surrounding the external os
• It is a normal physiological variant, not a disease or STI

Anatomy Background

• The cervix has two epithelial types:
  • Ectocervix = smooth, pale pink squamous epithelium (extension of vaginal epithelium)
  • Endocervical canal = columnar/glandular epithelium (forms frond-like "grape" structures visible at colposcopy)
• The junction between the two is the squamocolumnar junction (SCJ)
• In younger women, the SCJ sits on the ectocervix (visible) — this is ectropion
• The transformation zone (TZ) = area between mature squamous epithelium distally and columnar epithelium proximally; site of active squamous metaplasia and the area most vulnerable to HPV

When It Occurs

• Physiologically in:
  • Young women (especially adolescents)
  • Pregnancy
  • Women on the combined oral contraceptive pill (COCP) — COCs cause broadening of the area on the ectocervix covered by columnar cells
• Not considered pathological

Significance

• The zone of ectopy is friable — bleeds easily when touched (e.g. with a cotton swab/spatula) → explains postcoital bleeding and contact bleeding
• May produce a mucoid vaginal discharge due to the exposed glandular epithelium
• Increases vulnerability to STIs, especially Chlamydia trachomatis (which infects only glandular epithelium — COC-related ectopy may therefore increase chlamydia susceptibility)
• N. gonorrhoeae also infects only glandular epithelium

Colposcopic Appearance

• Red area surrounding os due to exposed columnar epithelium
• After applying 3% acetic acid: dysplastic cells appear white (acetowhite) — helps distinguish ectropion from dysplasia
• After Lugol's iodine (Schiller's test): normal squamous epithelium turns dark brown; columnar epithelium (ectropion), CIN, metaplasia, and inflammation do not stain (Lugol's negative)

Clinical Assessment

• Diagnosis is clinical — direct inspection at speculum examination
• Ectropion itself requires no biopsy unless there is concern for cervical dysplasia/cancer
• Used during evaluation of cervicitis: touching the ectropion with a swab assesses friability; mucopus in the endocervical canal indicates true cervicitis

Management

• No treatment required if asymptomatic — it is a normal finding
• If causing troublesome discharge or recurrent contact bleeding:
  • Cryotherapy or cold coagulation (thermal ablation) to destroy the columnar epithelium → prompts squamous metaplasia
• Avoid unnecessary treatment — the transformation zone is best left alone unless symptoms are significant

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Part 2: Eyelid Ectropion (Ophthalmology)

Definition

• Eversion (outward turning) of the eyelid margin away from the globe, most commonly the lower lid
• Exposes the palpebral conjunctiva

Types

1. Involutional (Age-Related) Ectropion — Most Common

• Affects the lower lid of elderly individuals
• Symptoms:
  • Epiphora (tear overflow) — due to malposition of the inferior lacrimal punctum
  • Exacerbates ocular surface disease
  • Red, unsightly exposed conjunctiva
  • Long-standing cases → tarsal conjunctiva becomes chronically inflamed, thickened, and keratinized
• Causes (aetiological factors):
  • Horizontal lid laxity — lid pulls >8 mm from globe and fails to snap back without blinking
  • Lateral canthal tendon laxity — rounded lateral canthus; lid can be pulled >2 mm medially
  • Medial canthal tendon laxity — inferior punctum displaced >1–2 mm on lateral traction (mild = punctum reaches limbus; severe = punctum reaches pupil)
• Treatment:
  • Generalized ectropion → repair of horizontal lid laxity via lateral tarsal strip procedure (lower canthal tendon shortened and reattached to lateral orbital rim)
  • Alternative: excision of a tarsoconjunctival pentagon (useful for misdirected lashes or keratinized conjunctiva)
  • Medial ectropion (mild) → medial conjunctival diamond excision (medial spindle procedure) ± tarsal strip or lateral canthal sling
  • Medial canthal tendon laxity (marked) → stabilization before horizontal shortening (to avoid excessive lateral dragging of the punctum)
  • Punctal ectropion alone → managed separately

2. Cicatricial Ectropion

• Caused by scarring or contracture of skin and underlying tissues pulling the lid away from the globe
• Test: pushing skin up over the orbital margin with a finger relieves the ectropion; opening the mouth accentuates the eversion
• Both lids may be involved; defect may be local (trauma) or generalized (burns, dermatitis, ichthyosis, Stevens-Johnson, severe atopic disease)
• Treatment:
  • Mild localized cases: excision of scar tissue + vertical skin lengthening procedure (e.g. Z-plasty)
  • Severe generalized cases: transposition flaps or free skin grafts (from upper lids, posterior auricular, preauricular, or supraclavicular areas)
  • In ichthyosis: systemic retinoids can reduce thick periocular scale and decrease tendency to develop ectropion; severe cases require careful eye maintenance (lids may fail to close fully)

3. Paralytic Ectropion / Facial Nerve Palsy

• Caused by ipsilateral facial nerve (VII) palsy
• Associated with: retraction of upper and lower lids, brow ptosis (may mimic narrowed palpebral aperture), lagophthalmos
• Complications:
  • Exposure keratopathy (cornea exposed during attempted blink — assessed by Bell phenomenon)
  • Epiphora — due to punctal malposition + failed lacrimal pump + increased tear production from corneal exposure
• Treatment:
  • Temporary (awaiting spontaneous recovery):
    • High-viscosity tear substitutes (day) + ointment + lid taping (sleep)
    • Botulinum toxin into levator muscle → induces temporary ptosis to protect cornea
    • Temporary tarsorrhaphy — lateral upper/lower lids sutured together (especially if poor Bell phenomenon)
  • Permanent (irreversible nerve damage, or no improvement after 6–12 months in Bell palsy):
    • Medial canthoplasty (if medial canthal tendon intact) — lids sutured medial to lacrimal puncta
    • Horizontal lid shortening
    • Gold weight implantation in upper lid
    • Lower lid tightening procedures

4. Mechanical Ectropion

• Caused by a mass, tumour, or oedema mechanically pulling/pushing the lid away from the globe
• Treat the underlying cause

Complications of All Eyelid Ectropion (Untreated)

• Chronic conjunctival inflammation, thickening, and keratinization of exposed conjunctiva
• Exposure keratopathy → corneal ulceration
• Epiphora from punctal malposition and lacrimal pump failure
• Cosmetic disfigurement

Post-surgical Ectropion (Important Complication)

• Can occur after blepharoplasty (overaggressive lower lid skin resection or failure to address lower lid laxity)
• Can occur after periorbital laser skin resurfacing (especially in patients with prior blepharoplasty)
• After haemorrhoidectomy: anal ectropion (Whitehead's deformity) — a distinct complication involving eversion of the anorectal mucosa, different from eyelid ectropion

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Summary Comparison

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Obstructed Labour — Key Points

Definition

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Causes — "The 3 Ps"

1. Passenger (Fetal Factors)

• Cephalopelvic disproportion (CPD) — most common cause; fetal head too large relative to the pelvis
• Malpresentation:
  • Brow presentation (largest presenting diameter — mentovertical)
  • Face presentation (mentoposterior)
  • Shoulder presentation / transverse lie
• Malposition: persistent occipitoposterior (OP), deep transverse arrest
• Fetal abnormalities: hydrocephalus, conjoined twins, fetal tumours (sacrococcygeal teratoma)
• Macrosomia / shoulder dystocia

2. Passage (Maternal Pelvic Factors)

• Contracted pelvis: rickets, childhood malnutrition, trauma
• Android or platypelloid pelvis (abnormal pelvic shapes)
• Pelvic tumours: fibroids (lower segment), ovarian cysts
• Cervical stenosis (rare)
• Vaginal septum or obstruction

3. Powers (rarely primary cause here)

• Obstructed labour is distinct from prolonged labour due to poor contractions (dystocia) — in obstruction, contractions are often vigorous

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Diagnosis

Symptoms

• Prolonged, painful labour (>12 hours in active first stage, or >2 hours in second stage without progress)
• Severe, continuous lower abdominal pain
• Inability to pass urine (bladder compression)
• Exhaustion, distress, dehydration

Signs

Abdominal Examination

• Bandl's retraction ring — a visible/palpable transverse groove across the abdomen between the upper (thickened, contracted) and lower (thinned, overstretched) uterine segments; marks imminent uterine rupture — a critical warning sign
• Uterus may be constantly contracted (tetanic) and tender
• Fetal parts difficult to palpate due to tense uterus

Vaginal Examination

• Caput succedaneum — oedematous swelling on fetal presenting part (scalp/face); large caput = prolonged obstruction
• Moulding — overriding of fetal skull bones (graded 0–3+); 3+ moulding = severe obstruction
• Presenting part high/not engaged despite contractions
• Cervix oedematous and swollen (may not dilate further)
• Dry vagina (reduced liquor)

Maternal Signs of Deterioration

• Dehydration, ketosis, tachycardia
• Haematuria — from pressure necrosis of bladder (vesicovaginal fistula risk)
• Fever — suggests infection/sepsis (chorioamnionitis)
• Signs of uterine rupture (see below)

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Complications

Maternal Complications

Fetal/Neonatal Complications

• Fetal distress / asphyxia → hypoxic-ischaemic encephalopathy (HIE)
• Perinatal death (stillbirth or early neonatal death)
• Intracranial haemorrhage / skull fracture — from moulding, instrumental delivery
• Brachial plexus injury (if shoulder dystocia)
• Neonatal infection

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Management

Immediate General Measures

1. IV access — large-bore cannula; send bloods (FBC, group & save, clotting)
2. IV fluids — rehydration + correction of electrolyte imbalance
3. Urinary catheter — to monitor urine output and decompress bladder; observe for haematuria
4. Analgesia — adequate pain relief
5. Antibiotics — if signs of infection or prolonged membrane rupture
6. Oxygen — if maternal or fetal compromise
7. Senior obstetric review IMMEDIATELY

Definitive Treatment: Emergency Caesarean Section (CS)

• Cephalopelvic disproportion
• Brow / shoulder / transverse presentation
• Any case with Bandl's ring, fetal distress, or poor progress despite measures

• The lower segment may be markedly thinned and oedematous — risk of extension of uterine incision
• Baby may be deeply impacted in the pelvis — requires "push" manoeuvre from below (assistant's hand per vaginum) or reverse breech extraction
• High risk of PPH — anticipate and prepare for

Destructive (Operative) Delivery — Low-Resource Settings Only

• Craniotomy and cranioclast (for hydrocephalus or impacted head)
• Decapitation (for transverse lie with dead fetus)
• Evisceration / cleidotomy
• These procedures are performed only by skilled practitioners when CS is unavailable and the fetus is confirmed dead

Symphysiotomy — Rarely Used

• Partial division of the pubic symphysis to widen the pelvic outlet
• Historically used in low-resource settings; largely replaced by CS
• Risk: long-term pelvic instability, urological injury

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Uterine Rupture — Critical Complication

Signs:

• Threatened rupture: Bandl's ring, severe abdominal pain, maternal tachycardia, fetal distress
• Actual rupture:
  • Sudden cessation of contractions ("relief" of pain)
  • Fetal parts easily palpable abdominally (fetus extruded into peritoneal cavity)
  • Maternal shock (rapid deterioration, hypotension, tachycardia)
  • Vaginal bleeding (may be concealed)
  • Fetal heart sounds absent

Management of Rupture:

• Emergency laparotomy — immediate
• Repair or hysterectomy depending on extent of rupture and haemostasis
• Aggressive resuscitation, blood transfusion

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Vesicovaginal Fistula (VVF) — Long-term Consequence

• Develops 3–7 days after delivery from pressure necrosis
• Presents as continuous uncontrollable urinary leakage
• Major public health issue in sub-Saharan Africa and South Asia
• Prevention = timely CS for obstructed labour
• Treatment: surgical repair (after 3 months to allow oedema resolution), usually transvaginal or transabdominal

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Partograph — Key Monitoring Tool

• A graphical record of labour progress (cervical dilation, fetal descent, contractions, maternal vitals, fetal heart rate)
• Alert line: crosses at 1 cm/hour — if labour falls to the right of this, action needed
• Action line: 4 hours to the right of alert line — crossing this requires intervention
• Early identification of slow progress → prevents obstructed labour
• WHO recommends universal use of the partograph in all labours

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Prevention

• Skilled birth attendance at all deliveries
• Universal use of the partograph to detect poor progress early
• Antenatal pelvic assessment — identify at-risk women (small stature, history of rickets, previous CS for CPD)
• Timely referral from primary/community care to hospital
• Adequate nutrition in childhood (prevention of rachitic pelvis)
• Reduction of teenage pregnancy (immature pelvis)
• Early recognition and action when labour is not progressing

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Key Learning Points Summary

1. Obstructed labour = mechanical obstruction preventing descent despite adequate contractions — most commonly due to CPD or malpresentation
2. Bandl's ring on abdominal examination = warning sign of imminent uterine rupture — act immediately
3. 3+ moulding on VE = severe obstruction
4. Emergency caesarean section is the definitive treatment in nearly all cases
5. Complications include uterine rupture, VVF, PPH, sepsis, and perinatal death
6. Haematuria = bladder compression/necrosis → risk of VVF
7. The partograph is the cornerstone of prevention — identifies abnormal labour progress before obstruction occurs
8. VVF is a devastating long-term consequence, largely preventable with timely CS
9. In low-resource settings, obstructed labour remains a leading cause of maternal and neonatal death