Flashcards in Cell Injury, Death, And Adaptations Deck (51):
Cell getting bigger
Always bad, never normal, only pathological
Why would a cell undergo atrophy?
Disuse, inadequate nutrients, lack of endocrine stimulus, poor blood supply, denervation, aging
When would a cell undergo hypertrophy or hyperplasia?
Increased work demand, metabolic demand, excess endocrine stimulus, persisting injury
When would a cell undergo metaplasia?
Increased capacity to enable tissue survival - persisting injury
What determines obesity?
What determines adipocytes number?
Gestational birth weight
In utero toxin exposure
Causes of cell injury (10)
Most common type of cell injury
Little oxygen to tissues
little oxygen to cells = decrease ATP
No oxygen to cells = decrease ATP
What happens to a cell under oxygen depravation?
Decrease in ATP
= failure of sodium potassium and calcium pump
= cell swelling
= reduce pH
Under extreme conditions, cell can burst
What happens to the ETS under oxidative stress?
Electron buildup and the production of a superoxide
Super oxidase dismutase
Will convert superoxide radical into hydrogen peroxide
What can hydrogen peroxide do in a cell?
Can turn into a hydroxyl radical and could cause lipid peroxidation, and alter proteins or DNA
Can be turned into water with catalase or glutathione
When can mitochondrial swelling occur?
Asphyxial cell injuries
Suffocation, strangulation, chemical asphyxiates, drowning
Chemical agents that can cause cell injury
Lead, carbon monoxide, ethanol, Mercury, drugs
Immunologic reactions to cell injury
Immune and inflammatory substances
Slows cell metabolic processes
Heat cramps, heat exhaustion, heat stroke
Radiation can affect what type of cells
Gastrointestinal cells, fetus, bone marrow (lymph nodes)
How can intercellular ca2+ increase?
Mitochondria, injurious agent, smooth ER
What can happen with increased intracellular ca2+?
Activate enzymes like phospholipase, protease, endonuclease, and atpase that can cause membrane damage, nuclear damage, and decreased ATP
What can cause cell aging?
DNA damage, decreased cell replication, decreased functional proteins, and altered transcription due to environmental stress
Features of a reversible injury
Altered ion flux
Sings of an irreversible injury
Everything like reversible, as well as
Greater nuclear changes
Manifestations of cell injury include cell accumulations like
Cell death due to loss of memb integrity and leakage of cell contents leading to local damage via inflammation
Cell death where cells activate enzymes that degrade the cells own DNA and nuc/cytoplasmic proteins. Plasma memb stays intact and the cell is phagocytosed.
Necrosis stage when chromatin condenses
Necrosis stage when chromatin fragments
Necrosis when cell bursts/ nucleus dissolves
Sign of cytoplasmic changes during necrosis
Will take up eosin (h&e stain)
Calcification during necrosis
Dead cells can be degraded into FA that bind calcium
Protein denaturation - albumin turns opaque
Kidneys, heart, spleen, adrenal glands
Neurons and glial cells of the brain
Combo of coagulation and liquefactive
Enclosed within inflammatory border (granuloma)
Pancreas, breast, abdominal organs
Activation of lipases
Free FA and calcium
Antigens and antibodies are in walls of arteries
Result of hypoxia, affects limbs
Dry - not enough to blood, coagulation, dry, crusty, black
Wet - infection, liquefactive, cold, swollen, black, smelly
Pathological causes of apoptosis
End of usefulness
Elimination of wbcs
Pathological causes of apoptosis
Accrual of misfolded proteins
Injury from infections
BCL2 (apoptosis inhibitor) controlled
Cyt c release= activate apoptosis
Death receptor apoptosis
Death receptors activated, will activate capsases
Lysosomal digestion of cells own components. A survival mechanism in times of nutrient depravation