Pathology
Injury, inflammation, and neoplasia
Pathology questions test mechanisms. Know reversible versus irreversible cell injury, necrosis subtypes, apoptosis, and the consequences of ischemia and reperfusion. Inflammation requires familiarity with acute mediators, neutrophil recruitment, chronic inflammation, granulomas, and wound healing. Hemodynamics includes thrombosis, embolism, infarction, edema, and shock. Neoplasia tests benign versus malignant features, dysplasia, invasion, metastasis, tumor suppressor genes, oncogenes, and paraneoplastic syndromes.
Traps and distinctions
A frequent trap is equating all cell death with necrosis. Apoptosis is energy-dependent, caspase-mediated, and typically lacks inflammation; necrosis often releases contents and provokes inflammation. Another trap is calling a tumor benign solely because it is slow-growing. Malignancy is defined by invasion and metastatic potential, not speed alone. For infarcts, red infarcts occur in loose tissues or with dual blood supply; pale infarcts occur in solid organs with end-arterial supply.
Worked example
A lung infarct is typically red because the lung has dual blood supply and spongy tissue that permits hemorrhage. A kidney infarct is typically pale because the kidney is solid with end-arterial circulation. The rule of thumb: red infarct = loose tissue or dual supply; pale infarct = solid organ with end-arterial supply. This illustrates why organ architecture changes the gross appearance of ischemia.