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Pathology Short Answers

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Q1. Discuss the etiology, risk factors, morphology, clinical features, and complications of cervix carcinoma

• High-risk HPV (types 16, 18) is the dominant cause; HPV E6 protein inactivates p53 and E7 inactivates RB
• Risk factors: early first intercourse, multiple sexual partners, persistent high-risk HPV infection, immunosuppression
• Transformation zone (squamocolumnar junction) is the site of origin where immature metaplastic cells are vulnerable

• Squamous cell carcinoma (80%) - most common; precursor = SIL (LSIL/CIN I → HSIL/CIN II-III)
• Adenocarcinoma & mixed adenosquamous (15%) - arising from endocervical glands
• Small cell neuroendocrine carcinoma (<5%)
• LSIL: dysplasia in lower 1/3 of epithelium + koilocytic change
• HSIL (CIN II): lower 2/3 involved; CIN III: full-thickness atypia

• Early stage: asymptomatic, detected by abnormal Pap smear
• Later: postcoital/irregular vaginal bleeding, vaginal discharge, pelvic pain

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Q2. Classify gestational trophoblastic disease (GTD) - CF, pathology, morphology, and collo carcinoma (choriocarcinoma)

1. Hydatidiform Mole - Complete and Partial
2. Invasive Mole
3. Choriocarcinoma
4. Placental Site Trophoblastic Tumor (PSTT)
5. Epithelioid Trophoblastic Tumor

• Gross: grape-like translucent cystic structures (swollen hydropic villi) filling uterine cavity
• Micro: hydropic villi with loose myxomatous stroma, central cisterns, proliferation of both cytotrophoblasts and syncytiotrophoblasts

• Highly malignant, aggressive trophoblastic tumor
• Arises after any type of pregnancy (mole 50%, term pregnancy 25%, abortion 25%)
• Consists of sheets of anaplastic cytotrophoblasts and syncytiotrophoblasts - no villous structures
• Early hematogenous spread: lungs, brain, liver, kidneys
• Very chemosensitive (methotrexate, actinomycin D) - cure rate >90%
• Diagnosis: markedly elevated serum hCG

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Q3. Describe the classification, etiology, pathology, morphology & clinical features of endometrial hyperplasia and carcinoma. Add risk factors of endometrial carcinoma.

• Caused by unopposed estrogen (endogenous or exogenous)
• Classified by presence/absence of cytologic atypia:
  • Without atypia - low risk of progression (~1-3%)
  • With atypia (EIN - Endometrial Intraepithelial Neoplasia) - high risk (~25-30%) of progression to carcinoma

• Obesity, anovulatory cycles (PCOS), estrogen-secreting ovarian tumors, exogenous estrogen without progestin, nulliparity, late menopause, diabetes, hypertension, Lynch syndrome (Type II)

• Endometrioid: glandular structures resembling normal endometrium; polypoid/fungating mass; grades I-III based on glandular architecture and solid growth
• Serous: papillary architecture; psammoma bodies; pleomorphic cells; high-grade

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Q4. Describe the pathology, morphology, clinical features, and tumor markers of epithelial ovarian tumors (carcinoma)

1. Epithelial tumors (most common, >40 yr) - serous, mucinous, endometrioid, clear cell, transitional (Brenner)
2. Sex cord-stromal tumors - granulosa cell, Sertoli-Leydig, thecoma-fibroma
3. Germ cell tumors - dysgerminoma, yolk sac tumor, teratoma, embryonal carcinoma

• Serous carcinoma - most common malignant; many arise in the distal fallopian tube (BRCA1/2 mutation); psammoma bodies; bilateral; spreads to peritoneum
• Mucinous tumors - typically benign; large multilocular cysts; filled with mucin; pseudomyxoma peritonei if rupture
• Endometrioid carcinoma - associated with endometriosis; concurrent endometrial carcinoma in 15-30%

• CA-125 - serous carcinoma (elevated in ~80%)
• CEA - mucinous tumors
• AFP + hCG - germ cell tumors (yolk sac, choriocarcinoma component)
• Inhibin - granulosa cell tumor (sex cord-stromal)
• LDH - dysgerminoma

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Q5. Explain the gross and microscopic features, clinical presentation, complications, and differences between leiomyoma and leiomyosarcoma

• Most common uterine tumor; benign smooth muscle tumor; estrogen-dependent
• Locations: intramural (most common), submucosal, subserosal, pedunculated
• Gross: well-circumscribed, firm, whorled white-grey nodule; sharply demarcated from myometrium; may undergo hyaline, cystic, calcific, red (carneous - in pregnancy) degeneration
• Micro: interlacing bundles of bland spindle-shaped smooth muscle cells with cigar-shaped nuclei, no/rare mitoses, no atypia, no necrosis
• Clinical: often asymptomatic; abnormal uterine bleeding (submucosal), pressure effects (urinary frequency, constipation), infertility, pregnancy complications (preterm labor, malpresentation, PPH)

• Malignant smooth muscle tumor; arises de novo (NOT from malignant transformation of leiomyoma)
• Gross: soft, fleshy, poorly circumscribed; areas of necrosis and hemorrhage; irregular infiltrating borders
• Micro: high cellularity, marked cytologic atypia, coagulative tumor cell necrosis, >10 mitoses per 10 HPF; infiltrates myometrium
• Clinical: postmenopausal bleeding, rapidly enlarging uterine mass, pelvic pain; poor prognosis (5-year survival ~50% for Stage I, worse for higher stages); hematogenous spread to lungs