Adaptation
A reversible response involving structural or functional modifications to accommodate both physiologic (normal) demands and pathologic (adverse) conditions.
Atrophy
Decrease in cell size.
Hypertrophy
Increase in cell size.
Hyperplasia
Increase in cell number.
Metaplasia
Reversible replacement of one mature cell type by another, less mature cell type or a change in cell phenotype.
Dysplasia
Deranged cellular growth, not considered a true cellular adaptation, but rather atypical hyperplasia
Hypoxia
Lack of sufficient oxygen within cells, most common cause of cellular injury
Ischemia
Reduced supply of blood, and therefore oxygen as well; MOST COMMON CAUSE OF HYPOXIA
Ischemia-reperfusion injury
Additional cell injury after blood flow restoration, can cause cell death
ROS
Reactive molecules from molecular oxygen formed as a natural oxidation species in cells during mitochondrial respiration and energy generation
Free radical
Electrically uncharged atom/group which has an unpaired electron
Xenobiotics
Compounds + chemicals that have a toxic, mutagenic, or carcinogenic property (ex: fungal mycotoxin)
Biotransformation
Process where enzymatic reactions convert 1 chemical into a less toxic or nontoxic compound
Antioxidants
Molecules that inhibit the oxidation of other molecules, preventing the formation of free radicals; terminate the chain of reaction (can be endogenous or exogenous)
Endogenous antioxidants
Produced by the body; SOD, ALA, CoQ10, GPX
Exogenous antioxidants
From outside the body, like dietary sources; vitamin C
Cellular swelling
Most common degenerative change, results from extracellular water going into the cells
Oncosis
Progressive vacuolation results in cytoplasmic swelling; hydropic degeneration
Necrosis
Cellular death, dissolution of cellular components, sum of cellular changes after local cell death, INFLAMMATORY RESPONSE (pain, swelling), karyolysis and sometimes karyorrhexis
Coagulative necrosis
Occurs as result of protein denaturation, albumin is turned into a firm opaque substance, *COMMON, caused by an infarct from ischemia, happens in all organs except the brain
Liquefactive necrosis
Results from ischemic injury to the brain, often triggered by bacterial infection/fungal
Caseous necrosis
Results from tuberculosis (lungs only); Dead cells not entirely hydrolyzed; causes a granuloma formation
Fatty necrosis
Cellular dissolution caused by lipases, found in breast, abdominal, and pancreas, saponification
Gangrenous necrosis
Tissue death from severe hypoxic injury; dry, wet, and gas; Ischemia -> infarct
Dry gangrene necrosis
Coagulative necrosis from loss of blood supply, skin becomes dry and shriveled
Wet gangrene necrosis
More lethal form, infection from gram-positive cocci, gram-negative rods; especially Clostridium spp.
Gas gangrene necrosis
Wet gangrene caused by Clostridium from deep puncture wounds with soil contaminated objects, Hydrolytic enzymes destroy tissue and cause gas bubbles, death within 12 hours
Apoptosis
Programmed cell death, "dropping off", NO inflammatory response, no pain; NOT pathologic, cell size shrinks
Mitochondrial (intrinsic) pathway
Inside the cell, cell becomes injured internally and signals apoptosis
Death receptor (extrinsic) pathway
Signal from outside the cells to initiate apoptosis
Autophagy
Self-destructive process that delivers cytoplasmic contents to the lysosome for degradation, NOT apoptosis, Eats self, recycling factory, occurs when cell has no nutritional support