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59 Cards in this Set
- Front
- Back
What are the 4 classifications of disease?
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1. Developmental
2. Inflammatory 3. Neoplasmic 4. Degenerative |
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Pathognomonic
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a sign or symptom that is unique for a particular disease
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Syndrome
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a group of signs and symptoms that characterize a particular disease or disorder
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Prevalence
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number of individuals in a specific location currently having a particular disease
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Incidence
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Number of new cases of a disease (usually on an annual basis) in a given population
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stagnant hypoxia
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reduced venous drainage interfering with oxygenation
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histotoxic hypoxia
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failure of the ETC system (cyanide poisoning)
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How do cells differ in their response to anoxia?
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1. neurons die after 3-5 minutes
2. Myocardial cells may survive 30-60 mins under ideal conditions 3. Hepatic and renal tubular cells 1-2 hrs 4. a leg may last for many hours |
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What are the 2 classes of toxic substances/chemical agents?
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1. Those that directly interact w/ cells w/out requiring metabolic activation
2. those that are not toxic themselves, but are metabolized to yield a toxin |
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Examples of Toxic substances that directly interact w/ cells w/out requiring metabolic activation
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1. Heavy metals and cyanide--> mito
2. Phalloidin and taxol --> cytoskeleton 3. Chemo alkylating agents --> DNA |
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Carbon tetrachloride
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-metabolized in the liver--> chloride ion and a highly toxic free radical (trichloromethyl) which damages hepatocytes
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Acetaminophen
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-an important constituent of many analgesics, detoxified in the liver
-however, large doses can overwhelm the detox mechanism and toxic products of the process accumulate--> destroy hepatocytes |
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Examples of Secondary nutritional deficiencies:
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1. Increased requirement
2. Defective absorption 3. Defective utilization (liver disease) |
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epigenetics
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-genetic function is changed w/out changing the genes themselves
-ex DNA methylation |
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Mitochondrial permeability transition: MPT
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-a nonselective inner membrane channel that disrupts the proton gradient required for oxidative phosphorylation, allows Ca and other substances to leak into the cytosol
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Summary of damage to Mitochondrias
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-can result in cell damage and death (cytochrome c --> apoptosis) by compromising ATP production, disrupting Ca homeostasis, increasing oxidative stress and activating apoptotic pathways
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4 important O2 derived free radicals
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1. hydroxyl radical
2. superoxide anion 3. hydrogen peroxide 4. hypoclorite ion |
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What are 4 sources of free radicals?
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1. Oxidation-reduction rxns
2. Nitric oxide 3. Radiation 4. metabolism of exogenous chemicals (carbon tetrachloride) |
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Lipid peroxidation of membranes
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-oxidative degradation of lipids, free radicals react w/ lipids in cell membranes--> cell damage
-most often affects polyunsat FA b/c they have multiple double bonds |
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What is a common 1st rxn of lipid peroxidation?
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hydroxyl ion abstracts a hydrogen to make water and FA radical
-this leads to chain rxn--> increased # of FA radicals formed--> cell memb destruction |
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Oxidative modification of proteins
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free radicals promote:
1. oxidation of AA side chains of prots 2. formation of prot-prot cross linking 3. oxidation of the protein backbone--> fragmentation -distrupt enz activity and structural architecture of the cell |
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Superoxide dismutases
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enzymes found in the cytosol and mito that catalyzes the conversion of superoxide to hydrogen peroxide and O2
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Catalase
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present in peroxisomes, catalzyes the breakdown of H2O2 to water and O2
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Glutathione peroxidase
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catalyzes the conversion of the hydroxyl radical to water and the glutathione homodimer (GSSG)
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Antioxidants
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vitamins A, E, C and B-carotene may block the formation of free rads or scavenge them once formed
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Primary lysosomes
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IC organelles containing catabolic enzymes, fuse w/ vacuoles containing material to be digested
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Phagolysosome (secondary lysosome)
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here digestion and the killing of microorganisms takes place
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Lysosomal storage diseases
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inherited lack of certain catabolic lysosomal enzymes result in the abnormal accumulation of the substrates of those enzymes
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Xanthomas
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accumulations of foam cells that form masses beneath the skin, happens in diseases involving high levels of serum choleterol
-foam cells may contain debris such as triglycerides, cholesterol and cholesterol esters |
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Russell Bodies
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accumulation of immunoglobulins in plasma cells result in rounded eosinophilic structures
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Mallory bodies
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accumulation of proteins in liver cells as a result of alcoholism form characteristic eosinophilic deposits
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Hemosiderin
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golden yellow to brown deposits derived from breakdwon of hemoglobin in cells and tissues when there is a local or systemic excess of iron
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Hemosiderosis
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a condition in which hemosiderin is confined mainly to macrophages and is not associated w/ tissue or organ damage
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Hemochromatosis
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an extensive accumulation of hemosiderin often involving parenchymal cells and tissue damage
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Dystrophic calcification
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deposition of Ca phosphate in necrotic tissues
-serum levels of Ca and P can be normal |
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Metastic calcification
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deposition of Ca-Phosphate in normal tissues when Ca and/or phosphate serum levels are high
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Major causes of hypercalcemia
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1. Primary hyperparathyroidism
2. Increased destruction of bone 3. Vit D toxicity 4. Renal failure -secondary hyperparathyroidism |
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Major causes of hyperphospatemia
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1. Primary hypoparathyroidism
2. Renal insufficiency |
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What are the 5 basic types of cellular adaptation?
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1. Atrophy
2. Hypertrophy 3. Hyperplasia 4. Metaplasia 5. Dysplacia |
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Metaplasia
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the replacement of one adult cell type with another adult cell type
eg response to irritation resulting in a change from columnar to squamous cells in the RT |
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Dysplasia
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-abnormal but non-neoplastic tissue development
-characterized by: 1. pleomorphism 2. hyperchromasia 3. increase in mitotic activity 4. loss of normal orientation |
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pleomorphism
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range of sizes and shapes of the cells and their nuclei
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cloudy swelling
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-common first manifestation of injury in which cells swell w/ course granules in the cytoplasm
-loss of Na/K ATPase |
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What are the 3 nuclear changes in necrosis?
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1. pyknosis
2. Karyolysis 3. Karyorrhexis -cell death by necrosis invariably results in an inflamm response |
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Pyknosis
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darkly stained and shrunken nuclei
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Karyolysis
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swollen and abnormally pale nuclei
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Karyorrhexis
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rupture and fragmentation of the nuclei
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Coagulative necrosis
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-basic architecture of the tissue is maintained
-tissue may appear fixed with a loss of cellular detail -characteristic of hypoxic death in most tissues |
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What are the 6 types of necroses?
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1. Coagulative necrosis
2. Liquifactive necrosis 3. Caseous necrosis 4. Fat necrosis 5. Gangrenous necrosis 6. Fibrinoid necrosis |
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Liquifactive necrosis
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destruction of cells by hydrolytic enzyme digestion either from cells own lysosomes or exogenously from phagocytic cells
-occurs in abscesses in the brain |
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Caseous necrosis
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-loss of tissue architecture w/out liqification
-tissue is replaced w/ a granular, soft, cheesy (caseous) material -seen in TB |
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Fat necrosis
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-not a specific pattern of necrosis
-focal areas of fat destruction from lipases released from acinar cells of the pancreas |
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Gangrenous necrosis
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Not a specific pattern of necrosis
-describes ischemic necrosis of a limb -basically coagulative necrosis w/ a liquefactive component |
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Fibrinoid necrosis
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-Not a specific pattern of necrosis
-morphologic change in dead cells in which the tissue stains deeply eosinophilic, homogenous , refractile, resembling fibrin -limited to small arteries, arterioles, venules, and glomerular vessels |
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4 types of apoptosis in disease
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1. Cells infx w/ viruses (By T-lymphocytes and NK cells)
2. Modulation of CMI responses 3. Cells w/ DNA damage (increase production of p53 inducer of apop) 4. Radiation and chemicals used in cancer therapy |
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What are 3 external signals (negative signals) that trigger apoptosis when activated?
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1. TNF-A binding to TNF receptor
2. Lymphotoxin (TNF-B) binding to TNF receptor 3. Fas ligand (Fas L) binding to Fas receptor |
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The intrinsic or mitochondrial pathway of apoptosis
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-relative [] of 2 mito membrane proteins Bax and Bcl-2
-Bcl-2 inhibs the action of Bax--> cellular damage leads to an increase in [Bax]--> increase in permeability of the mito membrane allowing cytochrome c to leak out |
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The intrinsic or mitochondrial pathway of apoptosis...Part 2
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released cytochrome c binds to protein Apaf-1--> aggregate to form apoptosomes--> bind to and activate a protease designated caspase-9-->activation of proteolytic enzymes that are involved in degradation of nuclear and cytoplasmi contents of cell
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Extrensis or death receptor pathway of apoptosis
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-Fas and TNF receptor activation transmits a signal to that cytoplasm that results in the activation of caspase-8--> initiates a cascade of caspases that activate enzymes--> cell degradation
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