A 32-year-old smoker with high-risk HPV infection asks how cigarette smoking increases her risk of cervical cancer. The most accurate explanation is:
- A Tobacco carcinogens and their metabolites concentrate in cervical mucus and act synergistically with HPV, with depletion of local Langerhans cells ✓
- B Smoking directly induces mutations in the p53 gene of cervical epithelium independent of any viral cofactor
- C Nicotine accelerates clearance of HPV, paradoxically selecting out more virulent integrated strains
- D Smoking causes cervical ectopy, exposing columnar epithelium that is intrinsically malignant
Explanation
Cotinine and other tobacco metabolites are measurable in cervical mucus at levels higher than in serum. They act as a cofactor with persistent high-risk HPV infection and reduce local immune surveillance by depleting Langerhans cells, roughly doubling squamous carcinoma risk. The effect is synergistic with HPV rather than independent, which rules out option B, and smoking does not accelerate viral clearance.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.