Cell Injury & Death Atlas: Hypertrophy, Hyperplasia, Atrophy, Metaplasia, Ubiquitin, Autophagy, Apoptosis, Necrosis, Coagulative, Liquefactive, Caseous, Fibrinoid, Fat Necrosis, Dry vs Wet Gangrene, Lipofuscin, Hemosiderin, Neoplasia, Benign vs Malignant,

Cell Injury & Death Atlas: Hypertrophy, Hyperplasia, Atrophy, Metaplasia, Ubiquitin, Autophagy, Apoptosis, Necrosis, Coagulative, Liquefactive, Caseous, Fibrinoid, Fat Necrosis, Dry vs Wet Gangrene, Lipofuscin, Hemosiderin, Neoplasia, Benign vs Malignant, Papilloma, Hamartoma, Choristoma, Carcinoma, Sarcoma, Dysplasia, Differentiation, Low/High Grade, Anaplasia, Lymphatic Metastasis Exam Questions Verified and Complete with A+ Graded Rationales Latest Updated 2026 hypertrophy increase in cell size Hyperplasia increase in number of cells atrophy decrease in cell size and number metaplasia Mature cell type is replaced by a different mature cell type - response to stress EX: respiratory cells shifting from simply columnar to stratified squamous cells mechanisms of atrophy ubiquitin autophagy apoptosis cell injury when adaptive responsive to cell stresses are inadequate - injury and cell death can occur Reversible cell injury the injury to the cell may be reversible if the damaging stimulus is removed **swelling, fatty change, membrane blebs, mitochondria swelling** Irreversible cell injury necrosis and apoptosis - results in cell death - increase in eosinophilia increase in eosinophilia = irreversible injury to the cell Necrosis Cell membrane is leaking contents Lots of inflammatory cells with neutrophils Injured mitochondria via dilation **really pink cells** Apoptosis programmed cell death - involution of organs **shrink up and die** - then macrophages eat them **NO INFLAMMATION/NEUTROPHILS** Coagulative necrosis ischemic injury - architecture of tissue is preserved liquefactive necrosis liquid mixed with neutrophils - "viscous liquid" EX: abscesses EX: stroke caseous necrosis