RANZCR Pathology cheat sheet

Pathology: General and Systemic Pathology Relevant to Clinical Radiology

• Cell injury: reversible injury shows cellular swelling and fatty change; irreversible injury is marked by mitochondrial membrane rupture and plasma membrane loss, with necrosis or apoptosis as the endpoint.

• Necrosis subtypes: coagulative (preserved architecture, ischemic solid organs), liquefactive (brain, abscess), caseous (TB, granulomas), fat (pancreatitis, lipase-mediated), fibrinoid (vasculitis, immune-complex vessel injury).

• Acute inflammation: vasodilation and increased permeability produce protein-rich exudate; neutrophils dominate the first 6-24 hours, then macrophages after 24-48 hours.

• Chronic inflammation: lymphocytes, plasma cells, and macrophages with fibrosis and angiogenesis; granulomas are collections of epithelioid histiocytes with or without caseation (caseating in TB, non-caseating in sarcoidosis).

• Neoplasia nomenclature: benign tumors use -oma (adenoma, lipoma); malignant epithelial tumors are carcinomas, malignant mesenchymal tumors are sarcomas; mixed germ-layer tumors are teratomas.

• Metastasis routes: carcinomas spread via lymphatics first; sarcomas spread hematogenously, most often to lung; portal drainage sends GI tumors to liver; prostatic carcinoma favors vertebral bone via Batson plexus.

• Tumor grading describes differentiation and mitotic activity; staging describes anatomic extent (TNM). Stage correlates better with prognosis than grade for most solid tumors.

• Carcinogenesis: oncogenes (RAS, MYC, HER2) gain function; tumor suppressors (TP53, RB, APC, BRCA1/2) lose function; two-hit hypothesis requires biallelic inactivation of a suppressor gene.

• Paraneoplastic and tumor markers: AFP (hepatocellular, yolk sac), CEA (colorectal), CA-125 (ovarian), CA 19-9 (pancreatic), PSA (prostate), calcitonin (medullary thyroid), beta-hCG (trophoblastic).