Cell Injury, Cell Death, and Adaptations

Comprehensive vocabulary flashcards covering the fundamental concepts of pathology, cellular adaptations, mechanisms of cell injury, pathways of cell death, and cellular aging as discussed in Chapter 2.

Pathology

The study of the structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease.

Etiology

The initiating cause of a disease, which can be grouped into two broad classes: genetic and environmental.

Pathogenesis

The sequence of molecular, biochemical, and cellular events that lead to the development of disease.

Morphologic Changes

The structural alterations in cells or tissues that are characteristic of a disease and diagnostic of an etiologic process.

Homeostasis

A healthy steady state in which a normal cell is able to handle physiologic demands.

Adaptations

Reversible functional and structural responses to changes in physiologic states or pathologic stimuli, leading to new but altered steady states.

Hypertrophy

An increase in the size of cells resulting in an increase in the size of the affected organ, without the creation of new cells.

Hyperplasia

An increase in the number of cells in an organ or tissue in response to a stimulus, occurring only in tissues capable of division.

Atrophy

A reduction in the size of an organ or tissue due to a decrease in cell size and number.

Metaplasia

A reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type better able to withstand a particular stress.

Hypoxia

A deficiency of oxygen that causes cell injury by reducing aerobic oxidative respiration.

Ischemia

Reduced blood flow, which compromises the delivery of substrates for glycolysis and causes more rapid and severe tissue injury than hypoxia alone.

Integrated Stress Response (ISR)

An evolutionarily conserved network of intracellular signaling pathways that modulate gene expression and protein synthesis via the phosphorylation of $eIF2\alpha$ to help cells adapt to injury.

Unfolded Protein Response (UPR)

A series of alterations triggered by the accumulation of misfolded proteins in the endoplasmic reticulum ($ER$) to restore protein homeostasis.

ER Stress

A state in which the intracellular accumulation of misfolded proteins exceeds the cell's cytoprotective response, triggering apoptosis via caspases.

Autophagy

A process in which a cell delivers its own cytoplasmic materials to the lysosome for degradation, often acting as a survival mechanism during nutrient deprivation.

Necrosis

A pathologic process of cell death resulting from severe injury, characterized by denaturation of cellular proteins, leakage of cellular contents, and local inflammation.

Apoptosis

A type of regulated cell death induced by a tightly regulated suicide program where cells activate intrinsic enzymes to degrade their own $DNA$ and proteins.

Coagulative Necrosis

A form of necrosis in which the architecture of dead tissue is preserved for several days and the affected tissue identifies with a firm texture.

Liquefactive Necrosis

A type of necrosis characterized by the digestion of dead cells into a viscous liquid, commonly seen in focal bacterial or fungal infections and hypoxic death of cells within the central nervous system.

Gangrenous Necrosis

A clinical term usually applied to a limb that has lost its blood supply and undergone necrosis (typically coagulative) involving multiple tissue planes.

Caseous Necrosis

A cheeselike form of necrosis often found in tuberculous infection, characterized by a structureless collection of fragmented cells enclosed within a granuloma.

Fat Necrosis

Focal areas of fat destruction resulting from the release of activated pancreatic lipases, leading to the formation of chalky-white areas through fat saponification.

Fibrinoid Necrosis

A special form of vascular damage seen in immune reactions where complexes of antigens and antibodies are deposited in artery walls, appearing bright pink and amorphous in H&E stains.

Damage-Associated Molecular Patterns (DAMPs)

Molecules released from injured cells, such as $ATP$ and uric acid, that trigger phagocytosis and the production of cytokines that induce inflammation.

Necroptosis

A hybrid form of cell death that resembles necrosis morphologically but is mechanically triggered by genetically controlled signal transduction pathways involving $RIPK1$ and $RIPK3$.

Pyroptosis

A lytic form of cell death accompanied by the release of inflammatory mediators like $IL-1$, typically occurring in cells infected by microbes.

Ferroptosis

An iron-dependent form of cell death triggered by excessive membrane lipid peroxidation when antioxidant defenses are overwhelmed.

Reactive Oxygen Species (ROS)

Oxygen-derived free radicals produced normally during mitochondrial respiration that can cause oxidative stress when produced in excess, damaging lipids, proteins, and $DNA$.

Steatosis

Abnormal accumulations of triglycerides within parenchymal cells, also known as fatty change.

Lipofuscin

An insoluble, brownish-yellow 'wear-and-tear' pigment composed of lipid-protein polymers, serving as a telltale sign of free radical injury and lipid peroxidation.

Hemosiderin

A hemoglobin-derived, golden yellow-to-brown granular pigment that serves as a major storage form of iron.

Dystrophic Calcification

The abnormal deposition of calcium salts in areas of necrosis or dying tissues, occurring despite normal serum levels of calcium.

Metastatic Calcification

The deposition of calcium salts in normal tissues, almost always resulting from hypercalcemia secondary to disturbances in calcium metabolism.

Cellular Senescence

A terminally nondividing state where a cell has a limited capacity for replication, often associated with telomere shortening.

Sirtuins

A family of $NAD$-dependent protein deacetylases that promote health and longevity by adapting bodily functions to environmental stresses and promoting genomic integrity.