Cell Injury and Cell Death pt. 1

Homeostasis

The state of balance that cells maintain.

Reversible Cell Injury

A type of cell injury in which the cell can recover its normal structure and function once the damaging stimulus is removed.

ATP Depletion

A hallmark of reversible cell injury, resulting from reduced oxidative phosphorylation.

Cellular Swelling

A hallmark of reversible cell injury, resulting from the failure of energy-dependent ion pumps in the plasma membrane; it is the first manifestation of almost all forms of cell injury.

Hydropic Change (Vacuolar Degeneration)

The microscopic appearance of small clear vacuoles within the cytoplasm due to cellular swelling.

Fatty Change

Abnormal accumulation of lipid vacuoles in the cytoplasm, especially in cells involved in fat metabolism (e.g., liver, heart); associated with hypoxia, toxins, and metabolic derangements.

Irreversible Cell Injury

Cell injury characterized by the inability to reverse mitochondrial dysfunction and profound disturbances in membrane function.

Necrosis

An "accidental," unregulated form of cell death resulting from damage to cell membranes and loss of ion homeostasis, leading to cellular contents leaking out and eliciting an inflammatory reaction; it is always a pathologic process.

Apoptosis

A highly regulated process of "programmed cell death" characterized by nuclear dissolution, cell fragmentation without complete loss of membrane integrity, rapid removal of cellular debris, and no inflammatory reaction.

Pyknosis

A nuclear change seen in necrosis (and apoptotic cell death) characterized by nuclear shrinkage and increased basophilia.

Karyorrhexis

Fragmentation of the pyknotic nucleus.

Karyolysis

Fading of the chromatin basophilia.

Hypoxia

Deficiency of oxygen, which reduces aerobic oxidative respiration.

Ischemia

Reduced blood flow, a cause of hypoxia.

Free Radicals

Highly reactive molecules with unpaired electrons that can damage lipids, proteins, and DNA, contributing to cell injury and apoptosis.

Reactive Oxygen Species (ROS)

A subset of free radicals derived from oxygen, including superoxide and hydrogen peroxide, involved in oxidative damage.

Oxidative Stress

An imbalance between ROS production and antioxidant defenses, resulting in cellular damage.

Coagulative Necrosis

A pattern of necrosis where the architecture of dead tissues is preserved for a span of at least some days, typically caused by ischemia in all organs except the brain.

Infarct

A localized area of coagulative necrosis.

Liquefactive Necrosis

A pattern of necrosis characterized by digestion of the dead cells, transforming the tissue into a liquid viscous mass; commonly seen in focal bacterial or fungal infections and hypoxic death of cells within the CNS.

Gangrenous Necrosis

A term for extensive coagulative necrosis of a limb due to loss of blood supply, often involving multiple tissue layers.

Wet Gangrene

Gangrenous necrosis where bacterial infection is superimposed, leading to more liquefactive necrosis due to the actions of degradative enzymes in the bacteria and attracted leukocytes.

Caseous Necrosis

A pattern of necrosis encountered most often in foci of tuberculous infection, characterized by a friable white, "cheese-like" appearance.

Fat Necrosis

Focal areas of fat destruction resulting from the release of activated pancreatic lipases, commonly seen in acute pancreatitis.

Fat Saponification

Grossly visible chalky-white areas resulting from the combination of fatty acids (derived from triglycerides by lipase) and calcium in fat necrosis.

Fibrinoid Necrosis

A necrotic pattern seen in immune-mediated vascular injury, with deposition of immune complexes and fibrin producing a bright pink, fibrin-like appearance histologically.

Plasma Membrane Alterations (Reversible Injury)

Ultrastructural changes in reversible cell injury that include blebbing, blunting, and loss of microvilli.

Mitochondrial Changes (Reversible Injury)

Ultrastructural changes in reversible cell injury characterized by swelling and the appearance of amorphous densities.

Dilation of the ER (Reversible Injury)

Ultrastructural change in reversible cell injury involving the endoplasmic reticulum, often with detachment of polysomes and the possible presence of intracytoplasmic myelin figures.

Nuclear Alterations (Reversible Injury)

Ultrastructural changes in reversible cell injury including disaggregation of granular and fibrillary elements.

Denaturation of Intracellular Proteins

A key process in necrosis that, along with enzymatic digestion, leads to the morphological features of necrotic cells.

Enzymatic Digestion

The breakdown of lethally injured cells by enzymes, contributing to the morphological appearance of necrosis.

Increased Eosinophilia (Necrosis)

A morphological feature of necrotic cells, partly due to the loss of cytoplasmic RNA and partly to denatured cytoplasmic proteins.

Moth-Eaten Cytoplasm (Necrosis)

The appearance of vacuolated cytoplasm in necrotic cells after enzymes have digested the cytoplasmic organelles.

Calcification (Necrosis)

The ultimate fate of some dead cells, where they may become calcified.

Inflammation (Necrosis)

A host reaction that occurs when cellular contents leak out of the damaged plasma membrane in necrosis.

Oxygen at High Concentrations

A chemical agent that can cause cell injury.

Anemia

A condition of decreased oxygen-carrying capacity of the blood, which can lead to hypoxia.

Misfolded Proteins

Proteins that may accumulate due to prolonged ATP depletion or genetic derangements, potentially triggering cell death.

Phagocytosis of Debris

The process by which necrotic cells and their contents disappear from the body, carried out by leukocytes.

Transition Metals

Elements like iron and copper that can catalyze free radical formation during intracellular reactions.

Nitric Oxide (NO)

A molecule that can act as a free radical and be converted to other highly reactive species like peroxynitrite anion.

Antioxidants

Substances that either block free radical formation or inactivate existing free radicals.

Catalase

An enzyme found in peroxisomes that breaks down hydrogen peroxide, reducing oxidative stress.

Glutathione Peroxidase

A selenium-containing enzyme that reduces peroxides using glutathione, protecting cells from oxidative damage.

Lesions in DNA

DNA strand breaks and cross-linking caused by free radicals, contributing to mutations and cell death.

Decreased Phospholipid Synthesis

A consequence of mitochondrial damage that impairs membrane repair and contributes to cell injury.

Increased Phospholipid Breakdown

Excessive degradation of membrane phospholipids by activated enzymes, producing toxic byproducts.

Cytoskeletal Abnormalities

Damage to elements of the cytoskeleton caused by activation of proteases, contributing to membrane damage.

Acute Pancreatitis

An abdominal emergency where pancreatic enzymes leak out of acinar cells and liquefy the membranes of fat cells in the peritoneum, leading to fat necrosis.