Pathology: Cell Death and Necrosis Overview

Study Notes

Pathology is the scientific study of disease.
The word "pathology" comes from Latin words "patho" (disease) and "logy" (study).

Excess fluid enters the cell, causing swelling and rupture of the membrane.
Enzymes for cell digestion come from dying cells or leukocytes.
Mechanisms include hypoxia, free radical-induced injury, cell membrane damage, and increased intracellular calcium level.
Common causes include ischemic injury (reduced blood flow), chemical injury (like mercury chloride poisoning), infections (viral, bacterial, fungal), immune reactions, or genetic defects.

Coagulative necrosis: Often from sudden loss of blood supply, especially to the heart.
Liquefactive necrosis: Tissue digestion and softening; occurs in suppurative infections (pus formation).
Fat necrosis: Trauma to tissues with high fat content (e.g., breast).
Caseous necrosis: Cheese-like appearance; typical of tuberculosis.
Gangrenous necrosis: Due to vascular occlusion (blocked blood vessels), frequently affects lower extremities and bowel. Can be "wet" (complications of bacterial infection with liquefactive necrosis) or "dry" (coagulative necrosis without liquefactive).

Apoptosis is the death of individual cells within clusters of other cells (unlike necrosis which affects clusters of cells).
Cells shrink and show increased acidophilic staining.
Fragmentation of cells into apoptotic bodies occurs.
A normal physiological process for removing cells during development (embryogenesis), menstruation, etc. Also seen in response to mild injurious stimuli.
Apoptosis does not usually cause inflammation or calcification.

Cytoplasmic changes: Increased eosinophilia (pink staining).
Nuclear changes: Karyolysis (chromatin fading), pyknosis (nuclear shrinkage), and karyorrhexis (fragmentation). The nucleus may disappear completely one to two days after cell death.