1/11
Major causes of cell injury include hypoxia/ischemia, chemicals, infections, immune reactions, genetic defects, nutritional problems, physical injury, and aging. Reversible injury results in swelling and fatty changes, while irreversible injury results in necrotic or apoptotic changes.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai | Chat |
|---|
No analytics yet
Send a link to your students to track their progress
oxygen deprivation
hypoxia — tissue does not receive adequate oxygen
examples:
pneumonia → fluid within alveoli impairs oxygen exchange
CO poisoning → CO interferes with oxygen transport by hemoglobin
ischemia — blood supply is inadequate
blood delivers oxygen, so ischemia commonly produces hypoxia
caused by impaired arterial flow or impaired venous drainage
chemical agents
damage cells through many mechanisms
poisons → alter membrane permeability
innocuous substances → harmful at abnormal concentrations
example — excess salt can disrupt osmotic environment across cell membrane
infectious agents
viruses
bacteria
fungi
protozoa
helminths
immunologic injury
immune system can injure the body’s own tissues
inflammatory reactions
autoimmunity
hypersensitivity
genetic defects
genetic abnormalities can cause:
deficient proteins
abnormal proteins
dysfunctional cellular pathways
nutritional imbalance
deficiencies and excesses can injure cells
deficiency → inadequate nutritional access
excess → contribute to disorders like type 2 diabetes and obesity-related disease
physical agents
trauma
temperature extremes
radiation
changes in atmospheric pressure
aging
contributes to cellular vulnerability and accumulated injury
morphology of cell injury
morphology is structural changes that can be observed in an injured cell or tissue
biochemical dysfunction → ultrastructural changes → light microscopic changes → gross changes
functional/biochemical abnormalities occur before obvious structural abnormalities
reversible injury morphology
cellular swelling:
decreased ATP → failure of energy-dependent pumps → Na+ accumulates inside → water follows Na+ → cell swells
inability to maintain ionic and fluid homeostasis
fatty change
fat accumulates inside injured cells that cannot properly metabolize lipid
microscopically → lipid vacuoles appear within cytoplasm
common in tissues involving fat metabolism, including liver and myocardium
necrosis morphology
major hallmark — loss of plasma membrane integrity
increased eosinophilia → denatured cytoplasmic proteins bind more eosin and loss of RNA
myelin figures → remnants of damaged cellular membranes
calcification → calcium deposits in dead or damaged tissues, saponification of phospholipids
nuclear changes to nucleus:
pyknosis → nuclear shrinkage and increased basophilia
karyorrhexis → fragmentation of pyknotic nucleus
karyolysis → fading of nuclear basophilia due to DNA degradation
apoptosis morphology
contents remain packaged, so inflammation is minimized
chromatin condenses
cell fragments into membrane-bound pieces
apoptotic bodies form