General Pathological Anatomy: Apoptosis and Necrosis

Comprehensive vocabulary flashcards covering the biological concepts, genetic regulation, morphogenesis, microscopic features, and etiological classifications of apoptosis and necrosis.

Apoptosis

Cell death in a living organism occurring through the activation of a predetermined genetic program ('cell suicide'), not preceded by damage, which maintains tissue homeostasis by balancing proliferation and the death of physiologically exhausted cells.

J. Kerr (1972)

The scientist who introduced the term 'apoptosis' (from Greek apo — separation, and ptosis — falling) and characterized it as cell suicide via the sequential activation of 'death genes' and a 'suicidal biochemical pathway,' analogizing it to the 'falling of withered leaves from a tree.'

Inducers of Apoptosis

Extracellular factors initiating the apoptotic cascade, which include death signals such as Tumor Necrosis Factor (TNF / ФНО) or Transforming Growth Factor-β (TGF-β / ТФР-β) binding to specific cell surface receptors, or the cessation of essential growth factors and survival hormones.

Functional Gene Groups of Apoptosis

The four stages of genetic regulation in apoptosis: genes transmitting the signal from the cell membrane into the cell, genes transmitting the signal intracellularly, genes directly executing apoptosis, and genes regulating the phagocytosis of formed apoptotic bodies.

Apoptogenic Signal Genes

Key regulatory genes involved in transmitting pro-apoptotic signals, notably members of the bcl- and bax-gene families, p53, Rb, c-vec, c-fos, and c-jun.

Apaf-1

A Bcl-2-binding protein that, alongside members of its family, functions to inhibit and prevent the development of apoptosis.

Caspases

A family of cysteine proteinases that execute apoptosis by cleaving the cellular matrix and nuclear proteins, leading to biochemical alterations in the cytolemma that ensure rapid phagocytic clearance without releasing biologically active substances.

Duration of Apoptosis

A rapid physiological process that completes on average within $30\,\text{min}$, preventing the release of cellular contents into the extracellular environment and averting an inflammatory response.

Morphogenesis of Apoptosis

The sequence of morphological alterations during apoptosis: cell dehydration via selective enzyme transport systems regulating $K^+$, $Na^+$, $Cl^-$, and water; condensation of organelles; cytolemma invagination; and fragmentation of the cytoplasm and nucleus into membrane-bound bodies.

Apoptotic Bodies

Fragments of cytoplasm and nucleus enclosed by an intact cytomembrane that express surface adhesive molecules binding to receptors and lectins of adjacent cells for immediate phagocytosis, or removal via glandular secretions, lymph, and blood.

Pathological Categories of Apoptosis

Three clinically recognized forms of dysregulated apoptosis: excessive (observed in viral infections), insufficient (seen in hyperplastic processes and autoimmune diseases), and incomplete (occurring in certain malignant tumors).

Necrosis

The death and mortification of cells and tissues in a living organism (from Greek nekros — dead), accompanied by the complete and irreversible cessation of their vital functioning.

Paranecrosis

The initial stage in the morphogenesis of necrosis that resembles necrotic alterations morphologically but remains entirely reversible.

Necrobiosis

The second stage in the morphogenesis of necrosis, consisting of irreversible dystrophic changes characterized by the predominance of catabolic reactions over anabolic reactions.

Autolysis

The final stage of necrosis involving the enzymatic decomposition and dissolution of dead substrate by hydrolytic enzymes derived from dead cells and macrophages.

Karyopyknosis

The initial nuclear alteration of necrosis involving shrinkage of the nucleus, loss of visible nucleoli, and condensation (compaction) of chromatin into a dense, hyperchromatic mass.

Karyorrhexis

The intermediate stage of nuclear necrosis in which the condensed chromatin disintegrates and breaks apart into discrete fragments and clumps due to endonuclease activity.

Karyolysis

The complete dissolution and disappearance of the cell nucleus caused by the hydrolytic activity of ribonucleases and deoxyribonucleases, which cleave phosphate groups and depolymerize nucleic acids.

Plasmorrhexis

The stage of cytoplasmic necrosis following protein coagulation and denaturation, characterized by the breakdown and fragmentation of the cytoplasm into clumpy aggregates.

Plasmolysis

The concluding stage of cytoplasmic necrosis involving the hydrolytic melting and liquefaction of the cytoplasm following membrane disintegration and cellular hydration.

Cytolysis

Complete hydrolytic liquefaction and melting that encompasses the entire cell, driven by the activation of lysosomal hydrolytic enzymes.

Focal Coagulative Necrosis

A circumscribed form of necrosis limited to only a portion of the cell, which coagulates and is sloughed off, permitting the potential full restoration of the outer cell membrane.

Elastolysis

The destructive alteration of elastic fibers in vascular walls and connective tissue during necrosis, manifesting as swelling, basophilia, fragmentation, and enzymatic lysis via elastases.

Adipose Tissue Necrosis

A type of necrosis driven by lipolytic enzymes that split neutral fats into fatty acids and soaps, triggering reactive inflammation and the formation of lipogranulomas.

Demarcation Inflammation

A reactive inflammatory zone that develops around a focus of necrotic tissue detritus to separate non-viable tissue from adjacent living structures.

Mummification

A gross manifestation of necrosis where the affected non-viable tissue becomes dehydrated, dense, firm, and dry.

Myomalacia and Encephalomalacia

Gross presentations of colliquative necrosis marked by flaccid softening and liquefactive melting of necrotic tissue in muscle (myomalacia) or brain parenchyma (encephalomalacia).

Traumatic Necrosis

Necrosis caused by direct injury from physical or chemical factors, such as ionizing radiation, frostbite (low temperature), burns (high temperature), wound canal margins, or electric shock.

Toxic Necrosis

Necrosis produced by bacterial or non-bacterial toxins and chemicals (acids, alkalis, ethanol, therapeutic agents), such as proximal renal tubular necrosis in sublimate poisoning or cardiomyocyte necrosis from diphtheria exotoxin.

Trophoneurotic Necrosis

Necrosis resulting from severe disruption of tissue innervation and neural trophism, leading to circulatory and necrobiotic disorders; classic examples include non-healing trophic ulcers and decubitus ulcers (bedsores).

Allergic Necrosis

Necrosis occurring in a sensitized organism as an expression of immediate-type hypersensitivity, typically presenting as fibrinoid necrosis in autoimmune or infectious-allergic diseases, with the Arthus phenomenon being the classical prototype.

Vascular Necrosis (Infarction)

Ischemic necrosis resulting from critical reduction or cessation of arterial blood flow due to thrombosis, embolism, or prolonged spasm (angiogenic necrosis), often provoked by functional strain in organs with compromised collateral circulation.