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71 Cards in this Set
- Front
- Back
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pathology
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study of suffering
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disease
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an alteration in the state of the body or it's organs interrupting or disturbing the performance of vital organs
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health
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state of well being
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etiology
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cause of disease
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pathogenesis
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mechanisms of disease development
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morphology
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structural alterations induced in the cell and organs
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clinical significance
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functional consequences of morphologic changes
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iatrogenic
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cause induced by physicians procedure or therapy
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idiopathic
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etiology undetermined
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the four aspects of the disease process
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etiology, pathogenesis, morphology and clinical significance
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classes of etiology
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intrinsic, extrinsic, idiopathic and multifactorial
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classification of disease
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etiologic, pathogenetic mechanisms, organ systems and pathology course
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most common causes of death
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1 heart disease
2 cancer 3 stroke 4 lung disease 5 trauma 6 diabetes |
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cytopathology
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evaluation of cells removed from organ or fluid
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hyperplasia
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increase in the number of cells
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hypertrophy
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increase in the size of cells
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atrophy
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decrease in cell size due to loss of cell substance
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metaplasia
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reversible change replacing one adult cell type with another
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ischemia
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decrease in blood flow leading to O2 deprivation
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hypoxia
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decrease in tension resulting in O2 deprivation
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reversible cell injury
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cellular swelling due to vacuolar degeneration
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irreversible cell injury
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due to membrane breakdown
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necrosis
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morphologic changes due to death in vivo
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apoptosis
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form of cell death designed to eliminate unwanted host cells through activation of coordinated internally programmed series of events
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intracellular accumulations
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accumulation of abnormal amounts of either normal cellular substances, exogenous substances or metabolites or pigment due to metabolic derangement
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steatosis
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fatty change in liver caused by toxins, obesity, diabetes, viral infection or alcohol abuse
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physiologic causes of hyperplasia
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hormone induced-female breast
compensatory-regeneration of liver |
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pathologic causes of hyperplasia
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due to excessive hormone or growth factor stim.-endometrial proliferation due to estrogen
increase cancer risk |
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causes of hypertrophy
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physiologic-uterine growth during pregnancy
pathologic |
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physiologic causes of atrophy
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notochord, thyroglossal duct, uterine resumption after pregnancy
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pathologic causes of atrophy
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disuse, de-innervation, loss of blood supply, malnutrition, loss of endocrine function, pressure
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cause of metaplasia
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cellular response to adverse environment
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major causes of cellular injury
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O2 deprivation, physical agents, chemical agents and drugs, infections agents, immune reactions, genetic defects, nutritional factors
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major mechanisms of cellular injury
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1 ATP depletion
2 loss of Ca homeostasis 3 oxidative stress and free radical injury 4 defects in membrane permeability |
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features of reversible injury
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Na-K pump inactivation-Na accumulation and K loss, cellular swelling
switch to anaerobic glycolysis- decrease pH protein synthesis disruption cytoskeletal element dispersion |
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features of irreversible injury
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mit. membrane function loss-Ca accum.
plasma membrane damage-loss of enzymes and proteins lysosomal membrane leakage-release of acid |
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features of reperfusion injury
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O2 free radical generation
cytokine and adhesion molecule production-inflamm. cell recruitment |
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initiation of free radicals
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radiation or ultraviolet light
chemicals or drugs O2 metabolism metal reactions NO |
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how do free radicals cause cellular damage
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peroxidation of lipids
cross-linking and oxidation of amino acid residues TT breaks in DNA |
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how are free radicals controlled
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anti-oxidants(A and E)
sequestration of metals by transferrin and ceruloplasmin enzyme degradation by catalase, glutathione and superoxide dismutase |
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mechanisms of chemical injury
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direct
conversion to toxic metabolites-acetaminophen depletes glutathione |
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coagulative necrosis
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preservation of basic cell outline, loss of nucleus, glassy
due to ischemia or hypoxia in cardiac or kidney |
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liquefactive necrosis
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in CNS due to hypoxia
liquid viscous mass from bacteria or fungus |
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caseous necrosis
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tuberculosis
granulomatous inflammation |
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fat necrosis
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type of coagulative
fat saponification by Ca and fatty acids acute pancreatitis |
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causes of apoptosis
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embryogenesis
homeostasis-obstruction, hormones, proliferating cell population immune defense-neutrophil death, B and T lymphocytes damaged cell removal-viral disease, radiation, hypoxia aging |
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changes due to apoptosis
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cell shrinkage
chromatin condensation blebs and apoptotic bodies phagocytosis WITHOUT inflammation |
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biochemical features of apoptosis
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protein cleavage-caspases
protein cross-linking DNA breakdown phagocytic recognition-phosphatidylserine, thrombospondin |
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mechanisms of apoptosis
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signaling pathways-TNF and Fas, intracellular
promoters-Bax, Bad, p53 inhibitors- Bcl-2 execution-caspases, granzyme B, perforin phagocytosis |
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major subcellular responses to cell injury
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lysosome catabolism
hypertrophy of SER mit. changes cytoskeletal changes |
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disorders leading to lipid accumulation
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atherosclerotic plaques-foam cells in arterial intima
xanthomas-cholesterol in macro's in soft tissue and tendons cholesterolosis-foamy macro's in gallbladder lamina propria |
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disorders leading to protein accumulation
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proteinuria- reabsorption in renal tubular cells
Russell bodies-plasma cells filled with immunoglobulins alpha 1 antitrypsin def., huntingtons, alzheimers and parkinsons- folding problems |
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disorders leading to glycogen accumulation
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diabetes
glycogen storage disease pompe's disease |
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what are common intracellular pigments
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bilirubin, hemosiderin, homogentisic acid, melanin, lipofuscin, anthracosis,
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anthracosis
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carbon deposits in lung and lymph nodes
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tattooing
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pigment phagocytized by dermal macro's
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lipofuscin
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oxidized lipids in perinuclear lysosomes in heart and liver
yelloq-brown, granular |
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melanin
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brown-black
endogenous |
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homogentisic acid
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alkaptonuria, ochronosis
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hemosiderin
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tissue storage form of iron
yellow-brown, granular or crystalline prussian blue stain |
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hemosiderosis
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due to systemic iron overload
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hemochromatosis
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disease of iron overload associated with liver, pancreas and heart damage
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bilirubin
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hemoglobin metabolite, no iron
jaundice |
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staining charac. of lipids
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stainable with Sudan IV or Oil Red O
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staining of glycogen
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PAS stain positive
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staining of iron
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Prussian blue
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dystrophic calcification
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deposition of calcium salts in nonviable or dying tissues despite of normal Ca levels
necrosis, atheromas or heart valves |
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metastatic calcification
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deposition of calcium salts in normal tissue during hypercalcemia
hyperparathyroidism, bone destruction, Vitamin D disorders, renal failure |
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hyaline change
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smooth, glassy and pink
intracellular accum.-reabsorption droplets, mallory hyalin, russell bodies extracellular-collagen in scars, arteriolar walls, amyloid |
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staining of amyloid
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congo red-apple green color
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theories of cellular aging
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1 clock mechanism-telomere shortening or clock genes
2 accumulated damage- oxidative stress, glycation end-products, chromosome damage |
