Female & Male Genital Pathology: Ulcers, OmpathStudy

FEMALE GENITAL SYSTEM — ADDITIONAL ESSAYS Q23. State the aetiology of any 5 genital ulcer diseases. Syphilis — Treponema pallidum (painless, indurated ulcer/chancre) Chancroid — Haemophilus ducreyi (painful, ragged-edged ulcer) Genital herpes — Herpes simplex virus type 2 (multiple painful vesicles/ulcers) Lymphogranuloma venereum (LGV) — Chlamydia trachomatis serovars L1-L3 (small ulcer + painful inguinal lymphadenopathy) Granuloma inguinale (Donovanosis) — Klebsiella granulomatis (beefy-red, painless, progressive ulcer, Donovan bodies) Q24. Explain the pathogenesis of cervical squamous cell carcinoma. Persistent infection with high-risk HPV (16, 18) is the essential cause Viral oncoproteins E6 degrades p53 (loses apoptosis/DNA repair control); E7 degrades RB (loses G1/S checkpoint control) Result: unchecked proliferation of cervical squamous cells at the transformation zone Progression: normal epithelium → low-grade CIN I → high-grade CIN II/III (carcinoma in situ) → invasion through basement membrane → invasive SCC Cofactors that promote progression: smoking, multiple sexual partners, early coitarche, immunosuppression (HIV), multiparity, long-term OCP use Without HPV clearance/screening (Pap smear detects dysplasia early), progression to invasive cancer can take 10-20 years Q25. State 5 theories in the pathogenesis of endometriosis. Retrograde menstruation (Sampson's theory) — menstrual endometrium flows backward through fallopian tubes and implants on pelvic peritoneum/ovaries Coelomic metaplasia — peritoneal mesothelium undergoes metaplastic transformation into endometrial-type tissue Vascular/lymphatic dissemination — endometrial cells spread via blood or lymphatics to distant sites (explains rare extrapelvic endometriosis, e.g. lung) Direct implantation — surgical transplantation of endometrial tissue (e.g. into a caesarean scar) Induction theory — hormonal/immune factors induce undifferentiated peritoneal cells to differentiate into endometrial tissue (Bonus) Stem cell theory — bone-marrow-derived stem cells differentiate into ectopic endometrial tissue Q26. State 5 degenerative changes uterine leiomyomas can undergo. Hyaline degeneration — most common, homogenous pink hyaline change Cystic degeneration — liquefaction creating cystic spaces Calcification — especially in postmenopausal, poorly vascularized fibroids Red (carneous) degeneration — haemorrhagic infarction, classically in pregnancy Myxoid degeneration — gelatinous, mucoid change (Bonus) Fatty change and necrosis (in rapidly growing or twisted pedunculated fibroids) Q27. Classify ovarian neoplasms with examples. Surface epithelial tumours (most common category overall) — Serous (cystadenoma, cystadenocarcinoma) — Mucinous (cystadenoma, cystadenocarcinoma) — Endometrioid carcinoma — Clear cell carcinoma — Brenner tumour Germ cell tumours (mostly in young women) — Mature cystic teratoma (benign, commonest germ cell tumour) — Dysgerminoma — Yolk sac (endodermal sinus) tumour — Choriocarcinoma — Embryonal carcinoma Sex cord-stromal tumours — Granulosa cell tumour (oestrogen-secreting, Call-Exner bodies) — Thecoma / Fibroma — Sertoli-Leydig tumour (androgen-secreting, virilizing) Metastatic tumours — Krukenberg tumour (bilateral, signet-ring cells, usually from gastric primary) Q28. Discuss the pathogenesis of toxaemia of pregnancy (pre-eclampsia/eclampsia). Root cause: abnormal trophoblastic invasion of maternal spiral arteries — cytotrophoblasts fail to remodel the spiral arteries into low-resistance vessels Result: persistently high-resistance, narrow spiral arteries → placental hypoperfusion/ischemia Ischemic placenta releases anti-angiogenic factors: increased sFlt-1 (soluble Flt-1, a VEGF/PlGF antagonist) and decreased PlGF (placental growth factor) These circulate systemically → widespread endothelial dysfunction Endothelial dysfunction → vasospasm, increased vascular permeability, activation of coagulation Clinical result: maternal hypertension, proteinuria, oedema (pre-eclampsia); severe cases → seizures (eclampsia), HELLP syndrome (Haemolysis, Elevated Liver enzymes, Low Platelets) Q29. Write short notes on Uterine Endometriosis. Definition: presence of endometrial glands and stroma outside the uterine cavity, most commonly ovaries, uterosacral ligaments, and pelvic peritoneum Pathogenesis: see Q25 theories (retrograde menstruation most widely accepted) Morphology: blue-black "powder-burn" lesions; ovarian involvement forms "chocolate cysts" (endometriomas) from cyclic bleeding of trapped old blood Clinical features: chronic pelvic pain, dysmenorrhea, dyspareunia, infertility Diagnosis: laparoscopy with biopsy showing endometrial glands + stroma + haemosiderin-laden macrophages Complications: infertility, adhesions, rarely malignant transformation (endometrioid or clear cell carcinoma) Q30. Outline the classification of Primary Malignant Ovarian neoplasms. Malignant epithelial tumours — Serous cystadenocarcinoma (most common malignan