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Vocabulary flashcards covering cellular adaptation, cellular injury mechanisms, and modes of cell and tissue death from the lecture notes.
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Etiology
The cause of a disease process, which can involve intrinsic (genetic) or acquired (infectious, nutritional, chemical, physical) factors.
Pathogenesis
The sequence of events from the initial stimulus to the ultimate expression of a disease.
Cellular Adaptation
A change in cell structure or function in response to environmental changes, categorized into physiological and pathological types.
Atrophy
A decrease in cell size (shrinkage) accompanied by fewer mitochondria, less endoplasmic reticulum, and an increase in autophagic vesicles.
Hypertrophy
An increase in cell size occurring in nondividing cells, driven by mechanical stretch or trophic signals such as growth factors and hormones.
Hyperplasia
An increase in the number of cells resulting from cell division through multi-step cell cycle processes.
Dysplasia
Abnormal changes in cell size, shape, and organization, commonly found in epithelial cells adjacent to cancerous tissue.
Metaplasia
The reversible replacement of one mature cell type by another, usually less mature or less differentiated cell type.
Hypoxia
A cellular state characterized by a lack of oxygen, resulting from decreased environmental oxygen, loss of hemoglobin, decreased red blood cells, or cardiovascular/respiratory disease.
Ischemia
A specific type of hypoxia caused by decreased blood flow to tissues.
Anoxia
A complete absence of blood flow to tissues.
Free Radical
An electrically uncharged atom or group of atoms possessing an unpaired electron that induces oxidative stress and cellular damage.
Apoptosis
Type I programmed cell death characterized by cell shrinkage, maintenance of membrane integrity, chromatin margination, non-random DNA cleavage, and absence of inflammation.
Caspases
A family of cysteine proteases divided into initiators, executioners, and cytokine processors that mediate apoptotic pathways.
p53
A tumor suppressor protein regulating cell cycle, growth, and death, which is mutated in over 50% of human cancers.
Autophagy
Type II cell death characterized by cytoplasmic vacuolization and the formation of double-membrane autophagosomes that fuse with lysosomes.
Beclin-1
A BH-3 domain-containing protein that regulates human class III PI3K to facilitate autophagosome formation and serves as a potential switch between autophagy and apoptosis.
Necrosis
Type III cell death characterized by cell and organelle swelling, early loss of plasma membrane integrity, random DNA fragmentation, and secondary inflammation.
Pyknosis
A nuclear morphologic change during necrosis characterized by nuclear shrinkage and chromatin condensation.
Karyolysis
A nuclear change in necrotic cells characterized by nuclear fading and dissolution.
Karyorrhexis
A nuclear change during cell death characterized by the fragmentation of the nucleus.
Mixed Lineage Kinase Domain-Like Protein (MLKL)
A kinase phosphorylated by RIPK3 during regulated necrosis whose activation leads directly to rupture of the plasma membrane.
Inflammasome
Multi-protein complexes that process and convert interleukin-1β and interleukin-18 into active forms, acting as drivers of pyroptosis.
Coagulative Necrosis
A pattern of necrosis occurring primarily in the kidney and heart due to severe hypoxia, leading to protein denaturation and a firm, opaque appearance.
Liquefactive Necrosis
A pattern of tissue death affecting brain neurons and glial cells or resulting from bacterial infections, where hydrolytic enzymes turn tissue into a soft liquid mass.
Caseous Necrosis
A combination of coagulative and liquefactive necrosis characteristic of tuberculous pulmonary infection, resulting in soft, granular, clumped cheese-like cellular debris.
Fat Necrosis
Tissue death occurring in the breast, pancreas, and abdominal organs where lipases break down triglycerides into fatty acids that combine with Ca2+, Mg2+, and Na+ to form chalk-white soaps.
Gangrenous Necrosis
Death of tissue resulting from severe hypoxia, clinically described as dry (coagulative), wet (liquefactive), or gas gangrene.