Robbins Pathology: Cell Injury, Cell Death, and Adaptations

Vocabulary flashcards covering key terms, cellular adaptations, mechanisms of injury, and pathways of cell death from Chapter 2 of Robbins Basic Pathology.

Etiology

Refers to the underlying causes and modifying factors responsible for the initiation and progression of disease.

Pathogenesis

Refers to the mechanisms of development and progression of disease, accounting for the cellular and molecular changes that give rise to specific functional and structural abnormalities.

Homeostasis

The tightly regulated state in which the intracellular milieu of cells remains fairly constant despite changing demands and extracellular stresses.

Hypoxia

Oxygen deficiency that deprives tissues of oxygen, leading to failure of energy-dependent metabolic pathways and cellular injury or necrosis.

Ischemia

Reduced blood supply to a tissue that deprives it of oxygen and essential nutrients while causing a accumulation of toxic metabolites.

Cellular Swelling

A pattern of nonlethal reversible cell injury, also called hydropic change or vacuolar degeneration, characterized by cell enlargement due to failure of energy-dependent plasma membrane ion pumps.

Fatty Change

A form of reversible cell injury manifested by the appearance of triglyceride-containing lipid vacuoles in the cytoplasm, principally encountered in organs involved in lipid metabolism such as the liver.

Pyknosis

A pattern of nuclear damage in necrotic cells characterized by nuclear shrinkage and increased basophilia, where DNA condenses into a dark mass.

Karyorrhexis

A pattern of nuclear damage in necrotic cells in which the pyknotic nucleus undergoes fragmentation.

Karyolysis

A pattern of nuclear damage in necrotic cells in which nuclear basophilia fades because of DNA digestion by deoxyribonuclease ($\text{DNase}$) activity.

Coagulative Necrosis

A form of tissue necrosis in which the underlying tissue architecture is preserved for at least several days due to denaturation of structural proteins and enzymes, characteristic of infarcts in solid organs except the brain.

Liquefactive Necrosis

A form of tissue necrosis characterized by complete digestion of dead cells, transforming tissue into a viscous liquid mass, typical of focal bacterial or fungal infections and hypoxic death in the central nervous system.

Caseous Necrosis

A friable, yellow-white, cheeselike pattern of tissue necrosis characteristic of tuberculous infection, in which tissue architecture is completely obliterated.

Fat Necrosis

Focal areas of fat destruction typically resulting from the release of activated pancreatic lipases, producing released fatty acids that combine with calcium to form grossly visible chalky white areas (saponification).

Fibrinoid Necrosis

A special form of necrosis occurring in vascular immune reactions where antigen-antibody complexes and leaked plasma proteins produce a bright pink, amorphous appearance in vessel walls.

Apoptosis

A pathway of regulated cell death in which cells activate enzymes that degrade their own nuclear DNA and proteins, forming apoptotic bodies that are cleared by phagocytes without eliciting an inflammatory reaction.

Mitochondrial Pathway of Apoptosis

The intrinsic apoptotic pathway triggered by loss of survival signals or cell stress, causing cytochrome c to leak into the cytosol and activate caspase-9.

Death Receptor Pathway of Apoptosis

The extrinsic apoptotic pathway initiated by engagement of surface death receptors (such as type I TNF receptor or Fas/CD95) by their ligands, recruiting adaptor proteins to recruit and activate caspase-8.

Necroptosis

A form of regulated cell death initiated by TNF receptors or other triggers that involves receptor-interacting protein (RIP) kinases, resulting in cell dissolution similar to necrosis.

Pyroptosis

A form of cell death associated with activation of the cytosolic inflammasome, leading to caspase activation, production of pro-inflammatory cytokines, fever, and coexisting apoptosis.

Autophagy

A cellular survival mechanism in times of nutrient deprivation involving lysosomal digestion of the cell's own components sequestered within autophagic vacuoles.

Respiratory Burst

The rapid oxidative reaction in phagocytic leukocytes catalyzed by phagocyte oxidase ($\text{NADPH}$ oxidase) that converts oxygen into superoxide anion ($O_2^{\bullet-}$) within phagolysosomes.

Unfolded Protein Response

An adaptive cellular pathway triggered by the accumulation of misfolded proteins in the ER that activates signaling pathways to increase chaperone production and decrease protein translation.

Hypertrophy

An increase in the size of cells resulting in an increase in organ size, occurring in tissues with a limited capacity for cell division in response to increased workload or hormonal stimulation.

Hyperplasia

An increase in the number of cells in an organ or tissue stemming from increased proliferation of differentiated or progenitor cells.

Atrophy

Shrinkage in the size of cells caused by loss of cell substance, representing an adaptive retreat to a smaller cell size at which survival remains possible.

Metaplasia

A reversible cellular adaptation in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type better able to withstand an adverse environment.

Lipofuscin

An insoluble brownish-yellow granular intracellular pigment ('wear-and-tear pigment') representing complexes of lipid and protein produced by free radical-catalyzed peroxidation of membrane polyunsaturated lipids.

Hemosiderin

A hemoglobin-derived golden-yellow to brown granular pigment that forms large aggregates of ferritin micelles in tissues during local or systemic excesses of iron.

Dystrophic Calcification

Pathologic deposition of calcium salts occurring in injured or dead tissues despite normal serum calcium levels and normal calcium metabolism.

Metastatic Calcification

Pathologic deposition of calcium salts in normal tissues throughout the body, resulting almost exclusively from hypercalcemia secondary to derangements in calcium metabolism.

Replicative Senescence

The terminal nondividing state that normal somatic cells enter after a fixed number of divisions due to progressive shortening of chromosomal ends (telomeres).