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121 Cards in this Set
- Front
- Back
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acute inflammation
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rapid onset, short duration
edema and neutrophils |
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chronic inflammation
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long duration
lymphocytes and macro's proliferation of blood vessels, fibrosis and tissue necrosis |
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features if inflammation
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increased blood flow, vascular permeability, accumulation of leukocytes
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two main components of inflammatory response
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vascular-dilation, permeability, stasis, endothelial gaps
cellular- leukocyte migration, chemotaxis, phagocytosis |
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diapedesis
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leukocyte adhesion and transmigration
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chemotaxis
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locomotion along a chemical gradient
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stimuli for acute inflammation
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infections and toxins
trauma physical and chemical agents tissue necrosis foreign bodies immune reactions |
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vascular changes in acute inflammation
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1 changes in flow and caliber-vasodilation, stasis, increased permeability and leukocyte accum.
2 increased permeability- endothelial gaps, leakage, transcytosis |
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cellular events in acute inflammation
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diapedesis in venules
chemotaxis-bacterial products and attractants leukocyte activation-cytokines, arachidonic acid, adhesion moleculs, degranulation phagocytosis- killing and degradation resulting in release of leukocyte products(injury) |
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termination of acute response
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short half-lives, degradation, stimulus release, anti-inflammatory mediators
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vasoactive amines
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histamine, serotonin
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stimulation of histamine release
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injury, immune rxns, C3a and C5a, substance P and IL1 and 8
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action of histamine
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vasodilation and increased permeability of venules
vasoconstriction of large arteries |
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where does histamine come from
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preformed in mast cells, basophils and platelets
principal in transient phase |
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where does serotonin come from
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preformed in platelets and enterochromaffin cells
actions similar to histamine |
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actions of bradykinins
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increase permeability, smooth mm. contraction, vasodilation, pain
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actions of thrombin
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mobilization of P selectin, production of chemokines, induction of cyclooxygenase 2, production of NO and platelet-activating factor, endo. adhesion molecules
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actions of plasmin
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activates complement, fibrin-split products, activates Hageman factor
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C345a
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histamine release
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C5a
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chemotaxis
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C3b
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phagocytosis
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C5-9
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membrane attack complex
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autocoids
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short range hormones-rapid formation and decay
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action of phospholipase A2
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arachadonic acid release
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actions of PG's
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vasodilation
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actions of LT's
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vasoconstriction, increased permeability and chemotaxis
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where is PAF found
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platelets, basophils,mast cells, neutrophils,macro's, mono's, endo's
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actions of PAF
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vaso and bronchoconstriction, leukocyte adhesioin, chemotaxis, degranulation, greater action than histamine
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actions of TNF and IL-1
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endothelial activation, neutro priming, induction of acute phase reactants,
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where are TNF and IL-1 found
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activated macros stimulated by endotoxin, immune complexes or injury
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what happens from sustained TNF
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cachexia-illness with emaciation
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chemokines
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chemoattractant for leukocytes
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where does NO come from
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endothelium, macro's and neurons
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actions of NO
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smooth mm relaxation,vasodilation, reduces inflammation
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action of alpha1 antitrypsin and alpha2 macroglobulin(antiproteases)
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control release of lysosomal contents
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action of low level free radicals
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increased chemokines, cytokines and adhesion molecules
destruction of phagocytosed microbes |
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action of high level free radicals
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endothelial damage, antiprotease inactivation, parenchymal and red cell injury
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where is substance P formed
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nerve fibers in lung and GI tract
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action of substance P
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pain signal transmission, BP regulation, endocrine secretion stim., permeability
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outcomes of acute inflammation
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1 complete resolution- ability of parenchyma to regenerate
2 fibrosis- inability to regenerate, tissue damage 3 progression to chronic- unresolved |
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patterns of acute inflammation
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1 serous
2 fibrinous 3 suppurative 4 ulcers |
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charac. of serous inflamm.
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outpouring of thin fluid
skin blisters serosal cavity effusions |
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charac. of fibrinous inflamm.
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large vascular leaks with fibrin
cavity inflamm. |
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charac. of suppurative inflamm.
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a lot of pus-neutrophils, necrotic cells, edema fluid, bacteria
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charac. of ulcers
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local defect of surface organ or tissue by sloughing of necrotic inflamm. tissue
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causes of chronic inflammation
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persistent infx., prolonged toxin exposure, autoimmunity
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morphologic features of chronic inflammation
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cell infiltrate of macro's, lymphocytes and plasma cells
tissue destruction attempted tissue replacement-angiogenesis and fibrosis |
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cellular component of chronic inflammation
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macro's- tissue injury
lymphocytes- IL12 and IFN gamma plasma cells- from B's, immuno production eosinophils- IgE inflamm. and parasites, major basic protein mast cells- IgE receptor, histamine and arachidonic release, anaphylactic rxns |
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granulomatous inflammation
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chronic inflammation with accumulation of activated macrophages, develop epithelioid appearance
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causes of granulomatous inflamm.
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tuberculosis, sarcoidosis, cat-scratch fever,leprosy, syphilis, berylliosis
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charac. of granulomatous inflammation
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aggregate of activated macro's surrounded by collar of lymphocytes and plasma cells-histiocytes, giant cells,
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systemic effects of inflammation
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fever-
pyrogens, acute phase reactants( C protein, fibrinogen and amyloid A) leukocytosis tachacardia and hypertension rigors and chills anorexia, malaise sepsis |
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exudate
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inflammatory extravascular fluid high in proteins
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transudate
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fluid with low protein content
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is edema due to exudate or transudate?
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can be either
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what cytokines increase vascularization by reorganizing the cytoskeleton?
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IFN gamma, TNF, IL-1
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margination
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process of leukocyte accumulation on endothelial surface in inflammation
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which adhesion molecules are involved in rolling?
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P and E selectin
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which adhesion molecules are involved in adhesion?
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ICAM-1 and VCAM-1
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which adhesion molecule is involved in lymphocyte homing?
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GlyCam-1
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which adhesion molecule is involved in leukocyte migration through endothelium?
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CD31(PECAM)
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what helps bind leukocytes to the extracellular matrix?
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beta-1 integrins and CD44
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what is the first type of leukocyte to reach the site of inflammation usually?
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neutrophils
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what is the most common exogenous chemoattractant?
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bacterial products
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what is the major macrophage activating cytokine?
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IFN gamma
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why don't the mannose receptors lead to phagocytosis of host cells?
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they recognize terminal mannose and fucose residues of microbes, not sialic acid or n-acetyl-galactosamine of mammals
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what are the major opsonins?
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IgG antibodies, C3 products and MBL
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what is responsible for the generation of reactive oxygen intermediates in phagocytosis killing?
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NADPH oxidase
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what is the problem in leukocyte adhesion deficiency 1?
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defect in beta 2 chain shared by LFA-1 and Mac-1 integrins
bacterial infection and poor wound healing |
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what is the problem in leukocyte adhesion deficiency 2?
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absence of sialyl-Lewis X, a ligand for E-selectin
bacterial infection |
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what goes on in Chediak-Hegashi syndrome?
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low neutro's, defective degranulation, delayed killing
large granules, albinism, bleeding disorders |
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what goes on in chronic granulomatous disease?
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defect in NADPH oxidase genes
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where is histamine found?
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mast cells, basophils and platelets
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where does histamine bind to endothelial cells?
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the H1 receptors
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where is serotonin located?
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platelets and enterochromaffin cells
NOT mast cells |
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how is bradykinin formed?
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Hageman factor(XII) produces XIIa from negative surface, converts prekallikrein to kallikrein, cleaves kininogen to bradykinin
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what cleaves fibrinogen to fibrin?
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thrombin
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what lyses fibrin clots?
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plasmin
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what four systems of inflammation does Hageman factor induce?
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1 kinin system
2 clotting system 3 fibrinolytic system 4 complement system |
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where does arachidonic acid come from?
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dietary sources of linoleic acid
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what does PGE2 do?
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makes skin hypersensitive to pain
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what does PGD2 do?
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vasodilation and increase in permeability
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difference between COX 1 and 2?
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1 is present in most tissues regardless of inflammation
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what does LTB4 do?
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chemotaxis of neutrophils and leukocyte adhesion
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what cells are involved in lipoxin generation?
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neutrophils and platelets
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what are the actions of lipoxins?
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inhibit leukocyte recruitment and components of inflammation
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what do cyclooxygenase inhibitors act on?
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inhibit prostaglandin synthesis
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how is asthma treated?
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lipoxygenase inhibitors
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how do glucocorticoids work?
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down-regulate target genes involved in inflammation
up-regulate genes for anti-inflammatory proteins |
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what does PAF do to vessels?
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at low concentrations it dilates, but at increased levels it constricts
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what produces the acute-phase responses?
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IL-1 and TNF
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what happens with sustained production of TNF?
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cachexia-weight loss through lipid and protein mobilization and anorexia
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what does IL-8(CXC) do?
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activation and chemotaxis of neutrophils
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what do CC chemokines do?
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attractant for monocytes, eosinophils, basophils and lymphocytes
NOT neutrophils |
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what do the C chemokines do?
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lyphocyte attractant
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how does NO target cells?
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via GMP
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how are the constitutively expresses eNOS and nNOS activated?
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increase in cytoplasmic Ca
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how is the inducible iNOS activated?
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cytokines
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main functions of NO?
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vasodilation, reduced leukocyte recruitment and platelet aggregation
host defense against infection |
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what are some major antiproteases?
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alpha1-antitrypsin and alpha2-macroglobulin
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what are some important anti-oxidants?
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ceruloplasmin
transferrin superoxide dismutase catalase glutathione peroxidase |
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where is substance P released from?
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neurons in the lung and GI tract
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action of substance P?
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pain signal transmission
BP regulation endocrine cell secretion increase in vascular permeability |
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what is a common example of acute suppurative inflammation?
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acute appendicitis
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where does fibrinous inflammation usually occur?
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lining of body cavities
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where are ulcers most commonly found?
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mucosa of mouth,stomach,intestines or genitourinary tract
subq inflammation of the lower extremities |
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what is the dominant cell in chronic inflammation?
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macrophage
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what do eosinophil granules contain to control parasite infection?
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major basic protein
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difference between Langhans and foreign body-type giant cells?
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the nuclei of the Langhans are arranged peripherally and haphazardly in the foreign
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what is the prototype of the immune granuloma?
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tuberculosis
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what produces fever?
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response to pyrogens that stimulate prostaglandin synthesis which act in the hypothalamus to reset the temperature set point higher
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what does serum amyloid A protein do?
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replaces apolipoprotein A and alters the targeting of high density lipoproteins from liver cells to macro's
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what does fibrinogen due as an acute-phase protein?
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causes erythrocytes to form stacks that sediment more rapidly
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what is CRP used for as an acute-phase protein?
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marker for increased risk of myocardial infarction
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what produces neutrophilia?
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bacterial infection
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what produces lymphocytosis?
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viral infections
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what produces eosinophilia?
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asthma, hay fever and parasitic infection
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what produces leukopenia?
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typhoid, protazoa, cancer or tuberculosis
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what happens in sepsis?
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enormous amounts of cytokines
intravascular coagulation thrombosis impaired liver function abnormal glucose levels |
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what is the triad of septic shock?
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disseminated intravascular coagulation
hypoglycemia cardiovascular failure |
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what causes adult respiratory distress syndrome?
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neutrophil-mediated endothelial injury allows fluid to escape from the blood into the airspace
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