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These flashcards cover key vocabulary terms related to cell injury, aging, and death as discussed in the lecture.
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Cell Injury
Damage to cells caused by various environmental factors or internal dysfunction.
Necrosis
Pathological cell death due to external injury characterized by cell rupture and inflammation.
Apoptosis
Programmed cell death, a physiological process that eliminates unnecessary or damaged cells without causing inflammation.
Reversible Injury
Cell injury that allows the cell to recover and return to its normal function.
Irreversible Injury
Damage to cells that leads to cell death and cannot be reversed.
Hydropic Swelling
A primary manifestation of reversible cell injury characterized by excessive water accumulation in cells.
Atrophy
Decrease in cell size and function due to various factors including decreased workload and inadequate nutrition.
Hypertrophy
Increase in cell size and organ size, often as a response to increased workload or hormonal stimulation.
Hyperplasia
Increase in the number of cells in a tissue or organ, often in response to physiological demand.
Metaplasia
Reversible change in which one adult cell type is replaced by another, usually in response to chronic irritation.
Dysplasia
Disordered growth of cells characterized by variations in size, shape, and arrangement; potential precursor to cancer.
Somatic Death
Death of the entire organism, characterized by the cessation of all biological functions.
Hypoxia
Low oxygen levels that impair ATP production; the most common cause of cell injury.
Ischemia
Reduced blood flow leading to oxygen and nutrient deprivation.
Free Radical Injury
Cell damage caused by reactive oxygen species (ROS) that attacks lipids, proteins, and DNA.
Oxidative Stress
An imbalance between ROS production and the cell’s ability to detoxify them.
Intracellular Accumulations
Build-up of abnormal amounts of substances such as lipids, proteins, pigments, or calcium within cells.
Fatty Change (Steatosis)
Accumulation of lipids within cells, commonly seen in livers cells.
Coagulative Necrosis
Preservation of tissue architecture; commonly due to ischemia.
Liquefactive Necrosis
Formation of liquid mass; typical in brain infarcts and abscesses.
Caseous Necrosis
Cheese-like appearance; associated with tuberculosis.
Fat Necrosis
Destruction of fat cells often due to pancreatitis or trauma.
Gangrenous Necrosis
Large area of necrosis due to ischemia.
Dry Gangrene
Coagulative necrosis with dry, shriveled tissue; mainly from arterial obstruction.
Wet Gangrene
Liquefactive necrosis with bacterial infection; tissue appears wet and swollen.
Gas Gangrene
Caused by Clostridium infection producing gas bubbles in tissue.
Intrinsic Apoptosis Pathway
Triggered by internal signals such as DNA damage or mitochondrial dysfunction.
Extrinsic Apoptosis Pathway
Triggered by external signals such as death receptors on the cell surface.
Cellular Aging
Progressive decline in cell function due to accumulated damage and decreased replication capacity.
Telomere Shortening
Reduction in telomere length with each cell division, limiting replicative lifespan.
Autophagy
Cellular “self-eating” process that removes damaged components to maintain survival.
Etiology of Cellular Injury
Cell injury may result from physical, chemical, infectious, immunologic, nutritional, or mechanical factors.
Reperfusion Injury
Cell injury that occurs after blood flow is restored, caused by reactive oxygen species and inflammation.
Chaperone Proteins
Proteins that assist with normal protein folding and prevent accumulation of misfolded proteins.
Ubiquitin-Proteasome System
A pathway that tags abnormal or misfolded proteins for degradation.
Indicators of Cell Death
Pain, inflammation, fever, elevated WBC count, increased serum enzymes, and loss of function.
Physiologic Hypertrophy
Normal increase in cell size due to hormonal or functional demand (e.g., uterus in pregnancy).
Pathologic Hypertrophy
Abnormal increase in cell size due to disease (e.g., hypertrophic heart in hypertension).
Postmortem Changes
Include rigor mortis, body fluid settling, and tissue breakdown from autolysis.