40 terms

Cell adaptation, cell injury, cell death

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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