Term
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Definition
| branch of bioscience dealing with the study of the form and structure of organisms & their specific structural features |
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Term
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Definition
| underlying mechanisms of disease |
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Term
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Definition
| increase in the size of cells resulting in increase in the size of the organ |
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Term
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Definition
| reduced reduced blood flow |
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Term
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Definition
| increased cell numbers in response to hormones; occurs in tissues whose cells are able to divide |
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Term
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Definition
| shrinkage in the size of the cell by the loss of cell substance; result of decreased nutrient supply or disuse |
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Term
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Definition
| reversible change in which one adult cell type is replaced by another adult cell type |
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Term
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Definition
| cell death in which cell is enlarged; nucleus goes through pyknosis-> karyorrhexis-> karyolysis; cellular contents enzymatically digested and may leak out thru cell membrane; invariably pathologic |
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Term
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Definition
| regulated mechanism of cell death; serves to eliminate unwanted and irreparably damaged cells; cell size reduced, nucleus fragments, cell membrane remains intact |
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Term
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Definition
oxygen deprivation (ischemia most common)
chemical agents
infectious agents
immunologic reactions
genetic defects
nutritional imbalances
physical agents (trauma, electric shock, etc)
aging |
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Term
| reversible injury to cells |
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Definition
| cell injury that does not result in cell death: includes cellular swelling and fatty change, also loss of microvilli, plasma membrane blebbing, mitochondrial swelling, dilation of ER, eosiniphilia,ribosomal dispersal, chromatin clumping |
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Term
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Definition
| in nutrient-deprived cells, organelles can be digested by lysosomal enzymes (occurs inside vacuoles) |
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Term
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Definition
| compensatory mechanism to maximize removal of toxins |
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Term
| Mechanisms of cell injury |
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Definition
ATP depletion
mitochondrial damage
influx of calcium
accumulation of reactive oxygen species
increased permeability of cellular membranes
accumulation of damaged DNA & misfolded proteins |
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Term
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Definition
| refers to causes of diseases or pathologies |
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Term
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Definition
| body's ability to physiologically regulate its inner environment to ensure stability in response to fluctuations |
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Term
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Definition
| he reversible replacement of one differentiated cell type with another mature differentiated cell type, generally caused by some sort of abnormal stimulus |
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Term
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Definition
| caused by excessive hormonal or growth factor stimulation |
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Term
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Definition
| step-by-step development of a disease and the chain of events leading to that disease; due to series of changes in structure/function caused by a microbial, chemical, or physical agent |
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Term
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Definition
| reversible changes in the number, size, phenotype, metabolic activity, or functions of cells in response to changes in their environment |
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Term
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Definition
| decrease in cellular size due to pressure on the cells (eg- atrophy in brain cells after a tumor) |
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Term
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Definition
| abnormality of development; generally consists of an expansion of immature cells, with corresponding decrease in number & location of mature cells |
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Term
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Definition
| includes hormonal hyperplasia and compensatory hyperplasia |
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Term
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Definition
| lit. "blood movement"; study of blood flow or circulation |
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Term
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Definition
| formation of a blood clot inside a blood vessel, obstructing flow thru the circulatory system |
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Term
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Definition
| thrombus that has broken free and travels through vascular system |
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Term
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Definition
| a serious, life-threatening medical condition defined as an insufficient perfusion which cannot meet cellular metabolism needs |
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Term
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Definition
| occurs when a portion of tissue is removed or diseased (as in regrowth of partially removed liver) |
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Term
Distinguish the concepts of etiology, pathogenesis, morphological consequences and
clinical significance in context of a specific condition such as heart failure due to myocardial infarction |
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Definition
| Etiology would be the formation of a thrombus. Pathogenesis would be ischemia due to the thrombus blocking an artery. Morphological consequences would be necrosis of cardiomyocytes due to ischemia of the downstream cells that aren’t receiving oxygenated blood flow. Clinical significance would be a disruption in heart function due to an area of necrotic tissue. |
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Term
| Distinguish atrophy, hypertrophy, hyperplasia and metaplasia |
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Definition
| atrophy is a decrease in cell size, hypertrophy is an increase in cell size, hyperplasia is an increase in cellular number, metaplasia is a uniform change in cellular morphology |
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Term
| Provide one specific example of atrophy, hypertrophy and hyperplasia |
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Definition
| atrophy of myocytes due to lack of nervous stimulation, hypertrophy of myocytes due to exercise, hyperplasia of breast tissue due to hormonal input during puberty |
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Term
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Definition
| lack of oxygenation to tissues |
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Term
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Definition
| injury to tissues because of the restoration of blood flow following ischemia; may be due to increased ROS or influx of leukocytes |
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Term
| Distiguish necrosis and apoptosis by causes and morphological features |
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Definition
| Necrosis is cellular death that is not initiated by the cells- cell swelling, inflammatory response, blebbing, degradative enzymes, karyolysis, disrupted cellular membrane; pathologic; apoptosis is a form of programmed cellular death- cell shrinkage, lack of inflammatory response, apoptotic bodies, non-disrupted cellular membrane, usually physiologic, nuclear fragmentation |
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Term
| Distinguish ischemia and hypoxia |
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Definition
| schemia is a lack of blood flow to the tissues resulting in decreased oxygen and glucose, hypoxia is a lack of oxygenation of the tissues; there can be hypoxia without ischemia, but not ischemia without hypoxia- the common feature is oxygenation |
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Term
| Identify 4 distinct causes of cellular injury |
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Definition
oxygen deprivation,
chemical agents,
infectious agents,
phagolysosome |
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Term
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Definition
| chemicals with an unpaired electron |
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Term
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Definition
| excess free radical accumulation |
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Term
| mitochondrial permeability transition |
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Definition
| loss of proton gradient generated in the oxidative phosphorylization |
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Term
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Definition
| enzyme responsible for oxidative burst, geneartes ROS, present in the o Ca influx and activation of degradative enzymes, cytC is released from the mito membrane leading to apoptosis |
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Term
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Definition
| tissue architecture is maintained because necrosis occurs rapidly; typical of ischemic injury, heart, kidneys |
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Term
| oxidative phosphorylation |
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Definition
| electrochemical process in the inner mitochondrial membrane that generates ATP |
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Term
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Definition
| ox phos enxyme that triggers apoptosis when released from the mitochondria |
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Term
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Definition
| SER oxidative enzyme, generates ROS |
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Term
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Definition
| reactive oxygen species; oxygen-deprived free radical that is generated by the mitochondria and peroxisome |
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Term
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Definition
| converts superoxide anion to hydrogen peroxide |
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Term
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Definition
| molecular oxygen with an unpaired electron, highly reactive |
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Term
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Definition
| reduces oxidative species by oxidizing itself |
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Term
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Definition
| converts hydrogen peroxide to water and oxygen |
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Term
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Definition
| enzyme mediators of apoptosis that have to activated by cleavage |
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Term
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Definition
| cofactor with cytC to fully activate caspases |
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Term
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Definition
| inhibits the release of cytC from the mitochondria and inhibits cytC interaction with Apaf-1 |
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Term
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Definition
| free radical interaction with double bonds of unsaturated fatty acids in membranes |
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Term
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Definition
| condensation of the nucleus |
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Term
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Definition
| destruction of the nuclear material |
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Term
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Definition
| fragmentation of the nuclear material |
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Term
| unfolded protein response |
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Definition
| subcellular response to ER stress that leads to the degradation of unfolded proteins; may ultimately lead to apoptosis |
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Term
| Distinguish oxidative stress from oxidative phosphorylation |
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Definition
| n ox stress there is an accumulation of ROS, in ox phos oxygen is coupled to hydrogen and electrons from the ETC to form water, ox phos generates ATP; free radicals attack the double bonds in unsaturated fatty acids that sets off autocatalytic oxidative reactions |
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Term
| Identify 4 (types of) enzymes affected by disruption of calcium homeostasis |
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Definition
ATPases,
proteases,
phospholipases,
endonucleases |
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Term
| Identify 3 enzymes that promote free radical production |
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Definition
| NADPH oxidase, cytochrome p450, ox phos enzymes |
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Term
Identify 3 enzymes that protect against
excessive free radical production |
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Definition
| atalase, glutathione peroxidase, superoxide dismutase |
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Term
| characteristic markers of irreversible cell injury |
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Definition
| autophagy, loss of plasma membrane integrity, loss of mitochondrial membrane integrity, loss of nuclear integrity (pyknosis, karyolysis, karyorrhexis) |
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Term
| injurious effects of cyanide |
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Definition
| binds to cytC and inhibits oxidative phosphorylation |
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Term
| injurious effects of acetaminophen |
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Definition
| ctive metabolite that interacts with and depletes antioxidant enzymes |
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Term
| injurious effects of mercuric chloride |
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Definition
| binds to cystein residues and disrupts disulfide bonds |
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Term
| injurious effects of carbon tetrachloride |
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Definition
| onverted to reactive species (CCl3 with unpaired electron) by P450 enzymes |
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Term
| Identify the cell processes affected by plasma and mitochondrial membrane permeability disruptions |
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Definition
| Plasma membrane permeability disruptions affect osmotic maintenance leading to cellular swelling; mitochondrial membrane permeability disruptions result in dissipation of the proton gradient and a loss of ATP production; selectivity of the plasma membrane leads to immunologic reactions |
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Term
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Definition
| enzymatic digestion that destroys cell architecture; may be purulent, common in brain (example: CVA) |
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Term
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Definition
| combination of coagulative and liqufactive, appears cheesy (example: TB) |
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Term
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Definition
| pancreatic lipases break down fat that mixes with calcium to form calcium soaps, may undergo saponification to dystrophic calcification (example: pancreatitis) |
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Term
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Definition
| misnomer: usually applied to a limb that has lost blood supply; actually a form of coagulative necrosis (with liquefactive = "wet gangrene"); gas gangrene is due to clostridium |
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Term
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Definition
| membrane-bound vesicles of cytosol and organelles |
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Term
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Definition
| extracellular ligand that binds to TNFR and activates the extrinsic pathway |
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Term
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Definition
| trimerization of death receptors following ligand binding |
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Term
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Definition
| ligand expressed on the surface of activated T-lymphocytes that can interact with FasR expressed on other cell surfaces |
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Term
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Definition
| prototypic death receptor (CD95), recognizes FasL |
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Term
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Definition
| prototypic death receptor that recognizes TNF |
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Term
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Definition
| TNF receptor-activated death domain, adapter protein |
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Term
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Definition
| transcription factor that gets activated after TNF binding |
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Term
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Definition
| pro-apoptotic transcription factor |
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Term
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Definition
| SER enzyme involved in detoxification |
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Term
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Definition
| decrease in the size of myocytes due to lack of somatic motor simulation |
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Term
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Definition
| inactive form of the NfKB transcription factor; IkB is an inhibitory molecule |
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Term
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Definition
| link death domains to enzymes |
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Term
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Definition
| DNA is broken apart; characteristic of apoptosis |
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Term
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Definition
| pathway of apoptosis that is triggered by an extracellular molecule |
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Term
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Definition
| pathway of apoptosis that is triggered by cytC release |
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Term
| Distinguish apoptosis from necrosis |
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Definition
| ecrosis is usually pathological, apoptosis can be pathological but is usually physiological |
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Term
| Describe the mechanisms of apoptosis and distinguish the intrinsic and extrinsic pathways of programmed cell death |
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Definition
intrinsic-withdrawal of growth factor or hormones or damage to DNA (radiation, chemicals, free radicals) lead to MPT and release of cytC and activation of caspases;
extrinsic- death receptor formed by ligand binding, adapter molecules mediate activation of caspase 8 |
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Term
| Describe the sequence of events in TNF mediated cell survivial or cell death |
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Definition
the outcome of TNF binding is determined by cell type and adapter proteins;
survival mechanism-activation of NfKB leading to transcriptional changes, TNF-TNFR-TRADD-adapter-kinase cascade-NfKB activation by release of IkB; apoptosis- TNF activates TNFR activates TRADD activates FADD activates procaspase 8 |
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Term
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Definition
| cell eating, large volume |
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Term
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Definition
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Term
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Definition
| methods of bringing things into the cell |
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Term
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Definition
| self-digestion; destruction of a cell thru the action of its own enzymes |
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Term
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Definition
| the taking into a cell of exogenous material by phagocytosis or pinocytosis and the digestion of the ingested material after fusion of the newly formed vacuole with a lysosome |
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Term
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Definition
| a catabolic process involving the degradation of a cell's own components through the lysosomal machinery |
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Term
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Definition
| inclusions of intermediate filaments, AKA alcoholic hyalin |
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Term
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Definition
| inclusions of filaments; hallmark of Alzheimer's |
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Term
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Definition
| abnormal condition of fat accumulation |
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Term
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Definition
| smooth muscle cells and macrophages are filled with cholesterol and cholesterol esters |
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Term
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Definition
| intracellular accumulation of glycogen; enzymatic defects in synthesis or breakdown |
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Term
| lysosomal storage disorder |
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Definition
| excess accumulation of material in lysosomes due to enzyme affect |
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Term
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Definition
| defective mitochondrial metabolism associated with increased numbers of abnormally large mitochondria in the skeletal muscles |
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Term
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Definition
| helper proteins that aid in protein folding |
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Term
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Definition
| protein used to target other proteins for degradation |
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Term
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Definition
| degrades ubiquinated proteins |
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Term
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Definition
| "wear and tear" pigment; results from aging process and is indicative of past free radical damage |
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Term
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Definition
| pink pigment that arises from a pinocytic vesicle that contains albumin and has fused with a lysosome |
|
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Term
| Distinguish steatosis from atherosclerosis, and identify the organs in which fatty changes or fatty streaks are typically observed |
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Definition
steatosis is accumulation of TAG in vesicles in the liver;
atherosclerosis is accumulation of cholesterol and cholesteryl esters in smooth muscle cells and macrophages in arteries |
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Term
| Provide 2 examples of a pathology caused by an alteration in protein folding |
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Definition
1. cystic fibrosis
2. a1-antitrypsin deficiency |
|
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Term
| Provide 2 examples of a pathology caused by an alteration in cytoskeletal elements |
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Definition
1. hypertrophic cardiomyopathy
2. immotile cilia syndrome (Kartagener) |
|
|
Term
| provide 2 examples of pathologies caused by an alteration in cellular metabolism |
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Definition
1. Tay-Sach’s
2. Niemann-Pick |
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Term
| Distinguish heterophagy from autophagy |
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Definition
heterophagy is ingestion and degradation of material from outside the cell;
autophagy is material from inside the cell |
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Term
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Definition
| calcium deposition in dead or dying cells |
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Term
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Definition
| calcium deposition in viable tissues, usually involves Ca derangement (eg hypercalcemia) |
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Term
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Definition
| increased concentration of Ca in the blood |
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Term
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Definition
| point at which cells stop dividing; cell cycle arrest |
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Term
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Definition
| short repeated sequences of DNA found at the linear ends of chromosomes |
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Term
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Definition
| enzyme responsible for maintaining telomeres in actively dividing cells |
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Term
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Definition
| accumulation of damage over time due to ROS |
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Term
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Definition
| DNA damage as a result of normal replication and increased free radicals |
|
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Term
| Distinguish the principal causes of dystrophic and metastatic calcifications |
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Definition
| dystrophic is Ca accumulation on necrotic tissues; metastatic is Ca accumulation on viable tissues due to Ca derangement |
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Term
| Identify the role of the telomere and its suspected association in aging |
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Definition
| hortened telomeres signal cellular senescence |
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Term
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Definition
| does not retain memory; provides generalized response |
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Term
| adaptive (acquired) immune system |
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Definition
| retains memory of specific antigens; specific attacks directed at recognized markers or pathogen qualitites |
|
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Term
| name 5 defensive barriers of innate immune system (and examples) |
|
Definition
epithelial (skin, gi tract, resp tract)
mechanical (cilia, eyelashes, nasal/otic hairs)
phagocytic leukocytes (neutrophils & macrophages)
natural killer cells
complement system
inflammation (WBC influx) |
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Term
| what are the key cell-types of innate immunity? |
|
Definition
| epithelial, mucosal, neutrophils, macrophages (monocytes), mast cells (basophils) |
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Term
| What might be the outcome(s) of defects within innate immunity? |
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Definition
a. The body’s first line defense against all invasion is required for normal life/function; any defect compromises the body and puts it at increased risk
b. Defects with mechanical barriers such as wounds in or compromise of epithelial tissue would mean penetration of pathogens into the rest of the body
c. Innate immunity is the immediate response to invasion, programmed response is much slower and specific. Since the body is not programmed for all potential antigens, innate response must be intact to eliminate and protect the body from the broadest spectrum of pathogens.
d. Natural killer cells are programmed to recognize normal cells from within the body; if deficient, could attack normal cells (autoimmune disorders)
e. Phagocytic cells are required for destruction and discarding of pathogens and degenerated cells; deficient function here leads to accumulation of such things which can create additional pathologies |
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Term
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Definition
| family of adhesion molecules that mediates weak/transient adhesions involved in rolling; stick lightly to leukocytes |
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Term
|
Definition
| leukocytes tumbling along endothelial surface |
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Term
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Definition
| intercellular adhesion molecules; structurally related members on the immunoglobulin supergene family; ligands for the beta2 integrin molecules on leukocytes |
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Term
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Definition
| transmembrane heterodimeric glycoproteins that adhere to appropriate ligands when leukocytes are activated by chemokines; cluster together, increase affinity, create stable attachement of leukocytes to endothelial cells |
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Term
|
Definition
| increase in number of leukocytes (WBCs); common feature of inflammatory reactions, especially to bacteria |
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Term
|
Definition
| process of leukocyte accumulation at periphery of vessels; smaller RBCs move quickly in center of lumen while larger WBCs accumulate at edges |
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Term
|
Definition
| movement of leukocytes between epithelial cells out of venules or capillary walls to site of infection/damage |
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Term
|
Definition
| chemical gradient created that aids helper cells to find site of injury |
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Term
|
Definition
| enzyme that helps create superoxidases that aid in pathogenic microbe destruction |
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Term
|
Definition
| a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cell and tissues resulting from original insult; accomplished by diluting, destroying, or otherwise neutralizing harmful agents |
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Term
| 4 classic signs of inflammation |
|
Definition
1. heat (calor)
2. redness (rubor)
3. swelling (tumor)
4. pain (dolor)
(5. loss of function, or function laesa) |
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Term
|
Definition
infection (bacterial, viral, fungal, parasitic)
trauma (blunt or penetrating)
physical and chemical agents (thermal injury, sunburn, environmental chemicals)
tissue necrosis (ischemia, MI)
foreign bodies (splinters, dirt, sutures)
immune reactions (hypersensitivity reaction) |
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Term
|
Definition
| rapid response to injury or microbes or other foreign substance that is designed to deliver leukocytes and plasma proteins to sites of injury; vasodilation & cellular recruitment/activation |
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Term
|
Definition
| inflammation of prolonged duration (weeks -> years); infiltration with mononuclear cells (macrophages, leukocytes, plasma cells), tissue destruction largely induced by products of inflammatory cells, repair involving angiogenesis and fibrosis |
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Term
|
Definition
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Term
|
Definition
| formed when fluid leaks out because of increased hydrostatic pressure or decreased osmotic pressure |
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Term
|
Definition
| abnormal collection of fluid in a body cavity or space |
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Term
|
Definition
| alternation in vessel caliber resulting in increased blood flow |
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Term
|
Definition
| early symptom that might occur start of a disease before specific symptoms occur |
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Term
|
Definition
| redness caused by vascular expansion |
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Term
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Definition
| a state in which the normal flow of a body liquid stops |
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Term
|
Definition
| inflammation of the lymphatic channels |
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Term
|
Definition
| disease of the lymph nodes; swollen/enlarged lymph nodes |
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Term
|
Definition
| hormone-like molecules that act in a paracrine fashion to regulate immune responses. examples: TNF & IL-1 |
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|
Term
| Effects of TNF and IL-1 on endothelial cells |
|
Definition
| increased leukocyte adherence, increased PGI2 synthesis, increased procoagulant activity, decreased anticoagulant activity, increased IL-1, IL-8, IL-6, PDGF |
|
|
Term
| systemic effects of TNF and IL-1 |
|
Definition
| fever, increased sleep, decreased appetite, increased acute-phase proteins, shock, neutrophilia |
|
|
Term
| Effects of TNF and IL-1 on fibroblasts |
|
Definition
| increased proliferation, increased collagen synthesis, increased collagenase, increased protease, increased PGE synthesis |
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|
Term
| Effects of TNF and IL-1 on WBCs |
|
Definition
| increased cytokine secretion (IL-1, IL-6) |
|
|
Term
| what is the purpose of a fever? |
|
Definition
| allows the body to reach high temperatures, causing an unbearable environment for some pathogens. White blood cells also rapidly proliferate due to the suitable environment and can also help fight off the harmful pathogens and microbes that invaded the body |
|
|
Term
| what is a major inducer of fever? |
|
Definition
| pyrogen, causes a release of prostaglandin E2 (PGE2). PGE2 then in turn acts on the hypothalamus, which generates a systemic response back to the rest of the body, causing heat-creating effects to match a new temperature level |
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Term
|
Definition
| type of cytokine that mediates communication between leukocytes |
|
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Term
|
Definition
| tumor necrosis factor; type of cytokine involved in systemic inflammation and is a member of a group of cytokines that stimulate the acute phase reaction; The primary role of TNF is in the regulation of immune cells. TNF is able to induce apoptotic cell death, to induce inflammation, and to inhibit tumorigenesis and viral replication |
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|
Term
|
Definition
| weight loss caused by cytokines; loss of body mass that cannot be reversed nutritionally |
|
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Term
|
Definition
| chemicals secreted by leukocytes and macrophages exposed to bacteria and other foreign substances |
|
|
Term
| what is a common precursor lipid for Eicosanoids? |
|
Definition
| a 20 carbon essential fatty acid (Omega-3s and Omega-6s) |
|
|
Term
| what are the 2 major classes of Eicosanoids? |
|
Definition
1. Prostanoids (prostaglandins, thromboxanes, and prostacyclins)
2. Leukotrines (leukotrines and lipoxins) |
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Term
|
Definition
| cyclooxygenase; generates prostanoids from AA |
|
|
Term
|
Definition
|
|
Term
| what are potential effects of blocking COX? |
|
Definition
inhibition of COX-1, expressed in gastric mucosa, can lead to increased incidence of gastric ulceration, since the mucosal PGs are protective against acid induced damage
COX-2 inhibition affects PGI2 synthesis more than TXA2 synthesis, which can induce a prothrombic state and increased risk of acute coronary artery disease |
|
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Term
|
Definition
| prostacyclin; produced by COX2 pathway, responsible for vasodilation and inhibition of platelet aggregation |
|
|
Term
|
Definition
| thromboxane; produced by COX2 pathway, responsible for vasoconstriction and platelet recruitment and aggregation |
|
|
Term
| what are the potential effects of blocking LOX? |
|
Definition
| inhibition results in inflammation |
|
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Term
|
Definition
| lipooxygenase; the predominate AA-metabolizing enzyme in neutrophils. major products are leukotrines and lipoxins |
|
|
Term
|
Definition
| chemotactic agents for neutrophils; vasoconstriction, bronchospasm, increased vasopermeability |
|
|
Term
|
Definition
| inhibit inflammation by inhibiting neutrophil chemotaxis and adhesion to the endothelium |
|
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Term
|
Definition
| non-steroidal anti inflammatory drugs; inhibit COX activity and all PG synthesis, making them efficient for treating pain, fever, and inflammation |
|
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Term
|
Definition
| presence of bacteria in the blood |
|
|
Term
|
Definition
| lipopolysaccharides; stimulate leukocytes to produce cytokines; intial event in cytokine cascade of sepsis |
|
|
Term
|
Definition
| systemic hypoperfusion, cellular hypoxia, possible eventual death |
|
|
Term
|
Definition
| systemic activation of inflammation, including complement activation, cytokines, histamine, serotonin, leukotrines, clotting cascade (can lead to systemic leakiness and subsequent shock, systemic clotting and organ failure or systemic tissue damage) |
|
|
Term
| 5 forms that chronic inflammation can take |
|
Definition
1. Granuloma (TB, leprosy, silicosis, chronic granulomatous disease)
2. Serous (fluid accumulation; soreness and pain that leads to blister, possible arthritis)
3. Fibrinous (exudate contains clotting proteins, cell debris, eventual pleurisy)
4. Suppurative (abcess: pus surrounded by fibrin)
5. Fibrous (scar tissue: stiffness, slow healing) |
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|
Term
| clinical signs that point to cause and/or extent of inflammation |
|
Definition
| fever, drop in BP, prodromal symptoms (aches, nausea, fatigue), leukocytosis, acute phase proteins (C-reactive protein, complement, fibrinogen, prothrombin, & other clotting factors), cachexia, lymphadenitis/lymphangitis |
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|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
bacterial infection, burns, trauma, MI
Normal is >2000/mm3 |
|
|
Term
|
Definition
|
|
Term
|
Definition
| allergic reactions, asthma, several autoimmune diseases (pemphigus, SLE, lymphoma); normal is <350 cells/mm3 |
|
|
Term
|
Definition
| chronic infections (TB, bacterial endocarditis, rickettsias, malaria), systemic lupus erythematosus, inflammatory bowel disease (ulcerative colitis); normal is <800 cells/mm3 |
|
|
Term
|
Definition
| viral infections (hepatitis, CMV, infectious mono), lymphocytic leukemias |
|
|
Term
|
Definition
| increase in fibroblasts; extensive deposition of collagen that occurs in the lungs, liver, kidney, and other organs as a consequence of chronic inflammation, or in the myocardium after extensive ischemic necrosis (infarction) |
|
|
Term
|
Definition
| neovascularization; preexisting vessels send out capillary sprouts to produce new vessels |
|
|
Term
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Definition
| the process by which Some tissues are able to replace the damaged components and essentially return to a normal state |
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| The key processes in the proliferation of cells are DNA replication and mitosis |
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| cells that have the capacity for self-renewal and asymmetric replication |
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| cells that are quiescent and can re-enter the cell cycle (eg hepatocytes) |
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| portion of most solid tissues that is made up of stable cells (eg hepatocytes) |
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| regulate progression of the cell cycle through G1 phase |
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| synthesis: DNA replication |
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| Growth phase 1: premitotic phase; progression controlled by cyclins |
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| growth phase 2: premitotic phase |
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| replacement of injured tissue with connective fibrous tissue and formation of a scar |
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| process of stem cells changing to phenotypically resemble specific tissue cells; a process of maturation |
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| continuously dividing, continually being lost and replaced by maturation from stem cells and proliferation of mature cells (eg GI tract, epithelial cells, hematapoietic cells) |
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| terminally differentiated tissues that are unable to proliferate (eg cardiomyocytes and neurons) |
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| proteins that promote cell survival and proliferation; important in regeneration and healing; pleiotropic effects (migration, differentiation, contractility) |
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| form complexes with cyclins to regulate the cell cycle |
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| mitosis: prophase, metaphase, anaphase, telophase; parent cell divides into 2 daughter cells |
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| a phase outside the cell cycle where cells can persist and not actively proliferate |
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| fter each cell division, some progeny enter a differentiation pathway while others remain undifferentiated, retaining their self-renewal capacity (characteristic of stem cells) |
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| production of fibrous tissue, usually implying an abnormal increase of nonneoplastic fibrous tissue |
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| basic fibroplast growth factor: action of heparan sulfate-degrading enzymes activates bFGF, thus mediating angiogenesis |
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| vascular endothelial cell growth factor (A-D): causes increase in vascular permeability and is mitogenic for endothelial cells |
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| a dynamic constantly remodeling macromolecular complex synthesized locally which assembles into a network that surrounds cells; sequesters water, providing turgor presser to soft tissues and minerals and giving rigidity to bone; regulates proliferation, movement, and differentiation of the cells living within it |
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| 3 polypeptide chains braided, made up of hydroxyproline and hydroxylysine; for tensile strength |
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| histological appearance (pink, soft, granular) is characterized by proliferation of fibroblasts and new thin-walled delicate capillaries in a loose ECM; progressively accumulates connective tissue matrix, eventually resulting in formation of a scar |
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| highly organized ECM around epithelial, endothelial and smooth muscle cells; in between epithelial and mesenchymal cells |
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| responsible for degradation of collagens and other ECM components; depend on zinc ions, breakdown collagen; contain enzymes: interstitial collagenases, gelatinases, and stromelysins |
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| tissue inhibitors of metalloproteinases; one method to help tightly control MMPs (collagenases); play an important role in debridement of the injured site and in remodeling of the ECM - inhibits scar formation |
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| Identify the major steps in new blood vessel formation. Identify 2 distinct functions of VEGF Vascular endothelial growth factor |
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Definition
Vasodilation in response to NO and increased permeability of the preexisting vessel induced by vascular endothelial growth factor (VEGF)
Migration of endothelia cells toward the area of tissue injury
Proliferation of endothelial cells just behind the leading front of migrating cells
Inhibition of endothelial cell proliferation and remodeling into capillary tubes – not to overstimulate
Recruitment of peri-endothelial cells to mature vessel
VEGF stimulates both proliferation and motility of endothelial cells, and increase permeable of the preexisting vessel |
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| Identify 3 major events underlying fibrosis. Describe the role of TIMPs in scar remodeling |
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Definition
Migration and proliferation of fibroblasts (come to the site and divide): Macrophages not only play an important role in granulation tissue they also elaborate a host of mediators that induce fibroblast proliferation and ECM production
Collagen synthesis – scar formation
Connective tissue remodeling- TIMPS (but not too much) help here by working with the MMP’s to break down and build up the ECM doe scar formation. |
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Term
| Identify the possible outcomes, or resolution, of tissue injury and inflammation |
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Definition
| Healing with little organization or healing with exudative organization; Also restoration via regeneration and the second option being healing by the formation of scar tissue |
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| Distinguish the outcomes of necrosis in proliferative versus permanent tissue |
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Definition
Proliferative tissue is dividing; complete regeneration and/or caseous granuloma i.e. abcess
Permanent tissue lacks cell cycle and is not coming back. The organization is with loss of function. ex. brain, myocardium |
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