Cell injury and repair

What is atrophy?

Decrease in tissue mass due to decrease in size or number of cells after normal growth is reached.

What is hyperplasia?

Increase in tissue mass due to increase in the number of cells.

What is hypertrophy?

Increase in tissue mass due to increase in individual cell size.

What is metaplasia?

Altered differentiation of cells, change from one adult cell type to another.

Two main types of cell death

Necrosis and Apoptosis.

Key features of necrosis

Membrane rupture, protein denaturation, inflammation.

Key features of apoptosis

Cell shrinkage, fragmentation, no inflammation, apoptotic bodies.

Intrinsic apoptosis pathway

Mitochondrial pathway.

Extrinsic apoptosis pathway

Death receptor–initiated pathway.

What is oxidative stress?

Cellular damage caused by free radicals with unpaired electrons.

Examples of reactive oxygen species (ROS)

Superoxide anion, hydrogen peroxide, hydroxyl radical.

Endogenous sources of free radicals

Metabolic enzyme reactions, metal cations, inflammatory disease, neoplasia.

Exogenous sources of free radicals

Chemicals, drugs, toxins, radiation, tissue trauma.

Antioxidant defenses against oxidative stress

Vitamin E, Vitamin C, Vitamin A, Selenium, Beta-carotene, Ceruloplasmin, Transferrin.

Nuclear changes in necrosis

Pyknosis, Karyorrhexis, Karyolysis.

Morphology of apoptosis

Chromatin condensation, cytoplasm condensation, apoptotic bodies.

Types of necrosis

Coagulative, Caseous, Liquefactive, Gangrenous, Fat necrosis.

Causes of coagulative necrosis

Ischemia, free radicals, toxins, burns, X-rays.

Gross appearance of coagulative necrosis

Gray/white, depressed tissue compared to surrounding.

Histology of coagulative necrosis

Preserved tissue outline, hypereosinophilia, nuclear changes.

Cause of caseous necrosis

Toxins of certain microorganisms (e.g., Mycobacterium).

Gross appearance of caseous necrosis

Cheese-like, dry, greasy, friable tissue.

Histology of caseous necrosis

Loss of tissue architecture, granular purple staining.

Liquefactive necrosis—common sites

Central nervous system, abscesses.

Reason for liquefaction in CNS

High lipid content and poor connective tissue.

Reason for liquefaction in abscesses

Bacterial toxins and leukocyte hydrolytic enzymes.

Classifications of fat necrosis

Enzymatic, traumatic, nutritional, idiopathic.

Gross appearance of fat necrosis

White, opaque, firm, granular.

Histology of fat necrosis

Shadowy cell outlines, calcification, saponification of fat.

Gangrenous necrosis

Occurs in distal extremities/organs; dry or wet form.

Dry gangrene

Coagulative necrosis with mummification, no bacteria, dry leathery tissue.

Wet gangrene

Coagulative plus liquefactive necrosis with bacterial infection.

Healing by regeneration

Dead cells replaced by identical cell type, restoring homeostasis.

Healing by repair

Dead cells replaced by fibrous scar tissue when progenitor/supportive cells are lost.

Labile cells

High regenerative capacity; examples: skin, GI mucosa, respiratory, urogenital epithelium, bone marrow.

Stable cells

Regenerate when stimulated; examples: liver, kidney tubules, pancreas, adrenal gland, bone, tendon, smooth muscle.

Permanent cells

No regenerative capacity; examples: skeletal muscle, cardiac muscle, neurons of CNS.

Healing in permanent cells

Occurs by repair with fibrous scar tissue or glial scar in CNS.