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42 Cards in this Set
- Front
- Back
inflammation is characterized by what (what is in it, where does it go first, second)
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interstital accumulation of fluid
accumulation of leukocytes - first around injury then within injury |
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characteristics of acute inflammation
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short duration
increases vascular permeability neutrophil infiltration |
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characteristics of chronic inflammation
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long duration
mononuclear cell infiltration (monocyte, macrophage, lymphocyte) associated with tissue REPAIR (fibrosis) |
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what are the cells involved in acute inflammation? chronic?
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acute- neutrophil infiltration
chronic- monocyte, macrophage, lymphocyte |
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what are the cardinal signs of inflammation
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rubor- redness (erythema)
tumor- swelling (edema) calor- heat (pyrexia) dolor- pain (hyperalgesia) functio laesa- tissue injury/dysfunction |
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what does ITIS mean
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inflammation!
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what are the UNDERLYING settings of ACUTE inflammation
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tissue necrosis (trauma)
bacterial infection immune (type 1 2 and 3 hypersensititvites) |
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acute inflammation- hemodynamic alterations?
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blood flow/pressure increase = erythema
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acute inflammation- effects on venules?
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increase in vascular permeability
(leaky postcapillary venules) = edema |
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what causes erythema?
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vasodilation of PREcapillary arterioles
swelling= edema or accumulation of water in tissues |
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acute inflammation- what cells infiltrate? where do they emigrate through?
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neutrophil infiltration (PMN)
emigrate through POSTcapillary venules *pmn= polymorphonuclear leukocyte |
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what are the underlying settings of chronic inflammation
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persistent tissue insult or injury
repeated bouts of acute inflammation infection by intracellular parasites immune- type 4 hypersensitivity, autoimmunity foreign bodies |
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what cells are in the interstitial fluid of chronic inflammation
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lymphocytes, monocytes/macrophages and possible plasma cells
maybe diffuse or focal with perivascular cuffing (around the venule) *eosinophils= parasitic infection |
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what is a granuloma?
what is granulomatous? |
granuloma- filled with mononucleated giant cells, epitheliod histeocytes and lymphocytes
granulomatous- adj. describing a granuloma |
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chronic inflammation- describe granulomatous
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spherical mononuclear cells, central necrosis
epitheliod histeocytes (macrophages) in center multinucleated ginat cells outer rim contains lymphocytes, plasma cells and fibrosis |
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what are the morphologic patterns of inflammation
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serous
fibrinous suppurative hemorrhagic ulcerative mixed |
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what are the steps (pathophysiology) of inflammation
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injury
mediator release target cell receptors signal transduction target cell activation target cell response pathophys respons cardinal signs of inflammation |
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what types of injuries are leukocyte mediated
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apoptosis
necrosis |
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inflammatory tissue injury/dysfunction includes
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obstruction
leukocyte injury systemic fibrosis |
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hemodynamic response involves
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erythema and increases vascular permeability
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define 4 modes of target cell activation
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autocrine- same target cell
paracrine- different target cells in immediate proximity endocrine- different target cells at distant locations juxtacrine- two target cells after their adherence to each other |
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what are the sources of inflammatory mediators
cell derived- 7 plasma derived- 4 |
cell- PMN, lymphocytes, monocyte/macrophage, platelets, endothelial cells, mast cells, parenchymal cells
plasma- complement, kallikrein-kinin, coagulation, fibrinolytic |
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describe bradykinin formation
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activators-> prekallikrein-->kallikrein-->kininogen-->bradykinin
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describe characteristics of bradykinin
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vasodilation
increased vascular permeability pain endothelial cell stimulation |
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c3b, c3bi--->opsonins
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c3b, c3bi--> opsonins
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what are cyclooxygenase AA (arachidonic acid) products
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PGE2, PGI2, TXA2
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what are effects of PGE2
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vasodilation, hyperalgesia (pain), fever, potentiates edema
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how do NSAIDS work (in regards to AA, COX1,2)
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nsaids block COX1,2 which blocks PGE2 and all the other pg's
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how do steroids work?
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they block PLA2 and AA and cut off allll the stuff
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what are the cell classifications in regards to proliferative capacity
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permanent cells- dont divide
stable cells- not continuously dividing but can be stimulated to do so labile cells- continuously cycling stem cells- pluripotent precurosrs |
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give examples of different types of proliferating cells
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labile- epithelial
stable- hepatocytes permanent- neuron, cardiac |
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what is the difference between cell necrosis and apoptosis
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necrosis- breakdown of plasma membrane organelles and nucleus, leakage of contents
apoptosis- cell is fragmented into apoptotic bodies and phagocytosized |
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describe the steps of apoptosis
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cell shrinkage
chromatin condensation cytoplasmic blebbing apoptotic body formation phagocytosis of bodies = cell death with no inflammation |
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in what instances would be see cell apoptosis (or programmed cell death)
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morphogenesis/metamorphosis
normal cell aging hormone growth factor stimulation or withdrawal mitochondrial cytochrom c release failed dna repair tumor regression cytotoxic ddrugs, ionizing radiation |
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what are some leukocyte responses to inflammation
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margination and pavementing on vascular endothelium
transendothelial migration (diapedesis, emigration) chemotaxis through interstitium phagocytosis, intracellular killing and digestion |
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define tissue regeneration
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replacement of lost tissue by tissue of same type
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define tissue REPAIR
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replacement of lost tissue bye FIBROUS CONNECTIVE TISSUE SCAR
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examples of growth cells
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labile- epithelial and hematopoietic cells
stable cells- liver and connective tissue permanent- neurons cardiac skeletal |
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what are the requisite factors of tissue regeneration
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must be comprised of labile and or stable cells
must be preservation of at least some portion of original tissue must be preservation of scaffolding of original tissue (extracell matrix) |
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what are the requisite factors of tissue repair
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always in necrotic tissue containing permanent cells
when there has been extensive tissue necrosis tissue scaffolding destroyed chronic inflammation |
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what is granulation tissue
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highly vascularized loose connective tissue formed during tissue repair that produces typ1 collagen scar
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what is the sequence of scar formation by granulation tissue
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type 1 collagen biosynthesis by fibroblasts
extracell secretion of collagen and formation of collagen fibrils resoprtion of granulation tissue by apoptosis covalent cross linking of type 1 collagen froming the mature scar |