Ischemia and hypoxia
Explication
Ischemia and hypoxia are among the principal mechanisms of cell injury, along with free-radical, toxic, and immune-mediated injury.
Necrosis is injury-related cell death, whereas apoptosis is programmed cell death
Explication
Necrosis is cell death caused by injury, while apoptosis is a form of programmed cell death.
Intracellular accumulation of water, proteins, fats, carbohydrates, or pigments
Explication
Reversible parenchymal changes include intracellular accumulation of water, proteins, fats, carbohydrates, and pigments. The defining feature of reversibility is that the cell can recover.
Cell swelling, hydropic change, and vacuolar change
Explication
Intracellular water accumulation appears as cell swelling, hydropic changes, and vacuolar changes. Hyaline droplets and Russell bodies instead represent protein accumulation.
Distended and detached fragments of the endoplasmic reticulum
Explication
Cell swelling is a reversible injury in which small cytoplasmic vacuoles represent distended and detached fragments of the endoplasmic reticulum, with loss of fine structures and blurred cell borders.
Vacuolar change
Explication
Vacuolar changes consist of fluid-filled cytoplasmic vacuoles and can occur in the liver during acute viral hepatitis. Hyaline droplets and Russell bodies are protein accumulations.
Reduced organ function, such as impaired myocardial contractility
Explication
Reversible cell injury can reduce organ function; impaired myocardial contractility is an example of this clinical consequence.
Hyaline-droplet change caused by increased glomerular protein permeability
Explication
Hyaline-droplet changes are microscopic protein droplets in proximal convoluted tubules and occur when the glomerular filter becomes more permeable to protein, including in nephrotic syndrome.
Accumulation of hydrophilic glycosaminoglycans in the interstitial substance with entry of plasma proteins and glycoproteins
Explication
Mucoid edema results from the accumulation of hydrophilic glycosaminoglycans in the interstitial substance, accompanied by penetration of plasma proteins and glycoproteins. Marked collagen destruction is characteristic of fibrinoid swelling instead.
Accumulation of chromotropic substances causing metachromasia
Explication
Accumulated chromotropic substances make the ground substance metachromatic, so toluidine blue produces a reddish color rather than its usual blue. This staining change reflects the altered glycosaminoglycan-rich matrix.
Immune-complex injury to the microcirculatory bed and connective tissue
Explication
Fibrinoid swelling is associated with immune-complex injury involving the microcirculatory bed and connective tissue. Glycosaminoglycan accumulation and related staining changes are characteristic of mucoid edema.
Marked collagen destruction with penetration of plasma globulins and fibrinogen
Explication
Fibrinoid swelling involves marked destruction of collagen fibers and penetration of plasma proteins, especially globulins and fibrinogen, into connective tissue. Mucoid edema primarily alters glycosaminoglycans rather than causing major collagen destruction.
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What are the possible types of cell injury?
Cell injury may be reversible, irreversible, programmed, or residual.
Name some consequences of cell injury.
Consequences include degeneration, necrosis, apoptosis, subcellular injury, intracellular accumulation, gangrene, and pathological calcification.
What are the principal mechanisms of cell injury?
Ischemia and hypoxia, free-radical injury, toxic injury, and immune-mediated injury.
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