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etiology cause of disease pathogenesis mechanism of disease development hypertrophy physiologic example increased muscle mass by lifting weight hypertorphy pathologic example increased heart size because of hypertension cell response to injury adaptation (4) hyperplasia, hypertrophy, atrophy, metaplasia Hyperplasia increase in number of cells (due to hormones or growth factors) hypertrophy increased size of cells hyperplasia physiology example uterus grows during pregnancy, liver regenerates after resection hyperplasia pathologic endometrial hyperplasia or benign prostatic hyperplasia (increased risk for developing malignancy atrophy decreased size of cells or organ (decreased organells) and/or loss of cells atrophy physiology example disuse: muscles atrophy from lack of use, loss of innervation, decreased blood, inadequate nutrition, loss of endocrine stimulation, aging atrophy pathologic example pressure atrophy (bedsores) metaplasia change of one cell type to another (due to chronic irritation (reversible) metaplasia pathologic example smoking causes respiratory epithelium to change to squamous, distal esophagus changes to columnar epithelium (intestinal metaplasia or barrett esophagus) due to acid reflux; increased risk of malignancy reversible injury causes (biggie) decreased ox phos, decreased ATP reversible injury morphology cell swelling, fatty change causes of injury (7) hypoxia, physcial agents, chemicals/durgs, infectious agents, immunologic rxns, genetic defects, nutritional deficiency Cell Death necrosis always pathologic, many cells, nuclear changes (pyknosis, karyorrhexis, karyolysis), inflammation cell death apoptosis pathologic or physiologic, single cell, nuclear/cytoplasmic fragmentation (apoptotic bodies), no inflammation irreversible injury point of no return, severe mitochondrial damange (amorphous densities), loss of membrane functions, cell death hallmark of irreversible injury flocculent densities necrosis patterns in tissue (5) coagulation, liquifactive, caseation, fat, fibrinoid mechanism of cell injury (7) decreases atp, mitochondrial damage, entry of calicum, increased ROS, membrane damage, protein misfolding, DNA damage ATP depletion causes... loss of Na pump, increased anaerobic glycolysis, and detachment of ribosomes loss of na pump causes influx of calium, sodium, and water, efflux of K+--> er swelling, cellular swelling, loss of microvilli, blebs anaerobic glycolysis decreased pH, glycogen, and increased lactic acid--> clumping of nuclear chromatin detachment of ribosomes decreased protein synthesis, lipid deposition Mitochondrial damage get formation of mitochondrial mem permeability transition pore (loss of potential, can't generate ATP), leak of cytochrome c into cytosol (no apoptosis) increased ca 2+ opens mitochondrial transition pore, destructive enzyme activation Free radical damange oxidative stress--> lipid perox (mem damage), protein oxidation and cross links (enzyme damage), DNA breaks and cross linking membrane damage mechanisms (5) atp depletion, free radicals, decreased phospholipid synthesis, increased phospholipid breakdown, cytoskeletal abnormalities cell membrane damage results loss of osmotic balance, calcium influx, leakage of enzymes mitochondrial membrane damage opens membrane transition pore, decreased ATP Point of no return 2 mechanisms inability to reverse mitochondrial dysfunction, severe injury to membranes abnormal intracellular accumulations sources coal dust, tattoo (exogenous), lipids, proteins, glycogen, lipofuscin, melanin, hemosiderin (endogenous) endogenous accumulate due to faulty transport or inability to degrade (abnormal alpha 1 antitrypsin) or no transport mechanism exists normal endogenous accumulate due to over production or under metbolized (triglycerides in fatty liver), storage disease dystrophic calcification normal process in dying or dead tissues or in other path processes psammoma bodies in papillary thyroid or ovarian cancer metastatic calcification occurs in normal tissues due to hypercalcemia, primary due to hyperparathyroidism (affects GI, kidney, lung, systemic arteries and pulmonary veins cell aging mechanism decreased replication, telomere shortening, progressive metabolic and genetic damage by oxidative mechanisms, failure of repair mechanisms, visible indictor- accumulation of lipofuscin pigment, indivative of lipid peroxidation