P8 - Inflammation Part 3 Flashcards
types of chemical mediators of inflammation (2)
- cellular derived
- plasma derived
cellular derived chemical mediators of inflammation
- pre-made released from cells after stimulation or lysis
- inflammatory cells, vascular endothelium, platelets
plasma derived chemical mediators of inflammation
- soluble and interconnected cascade systems
types of cell-derived chemical mediators (4)
- lipid mediators
- vasoactive amines
- cytokines and chemokines
- lysosomal contents from phagocytic cells
arachidonic acid pathway (4)
- COX-1
- COX-2
- leukotrienes
- platelet activating factor (PAF)
COX-1 is expressed in, role and increased during
- healthy animals
- role in cytoprotection of mucosal cells and renal function
- increased during inflammation
COX-2 is induced
secondary to inflammation
thromboxanes expressed during and cause
- inflammation
- vasoconstriction and platelet aggregation
prostaglandins expressed during and cause
- inflammation
- fever, pain, vasodilation, increased vascular permeability, leukocyte adhesion and chemotaxis
NSAIDs inhibit
- Cox 1 and Cox 2 enzymes
- given too long can decrease renal function and mucosal protection
leukotrienes associated with
- hypersensitivities and allergies
leukotrienes cause (5)
- smooth muscle contraction
- vasodilation
- leukocyte adhesion and chemotaxis
- mucous secretion
- more potent than histamine but lass rapid response
most potent activator of vascular permeability
platelet activating factor
glucocorticosteroids inhibits
- phospholipase A2
glucocorticosteroids cause (3)
- prevent leukocyte adhesion
- create immune suppression
- decrease mucosal protection and renal function
vasoactive amines (3)
- histamine
- serotonin
- nitric oxide
histamine is produced by (3)
- mast cells
- basophils
- platelets
serotonin produced by
- platelets
nitric oxide secreted by
- endothelial cells and macrophages
nitric oxide causes
- vasodilation and regulates recruitment of leukocytes to site of inflammation
- reacts with oxygen radicals to produce reactive metabolites
cytokine and chemokines produced by
- many cells including WBCs, endothelial cells and fibroblasts
important cytokines (4)
- IL-1
- TNF-alpha
- INF-gamma
- IL-10
IL-1 cellular target (5)
- fever
- neutrophilia
- activation of endothelial cells
- activation of membrane phospholipase A2
- stimulates acute phase proteins
TNF-alpha cellular targets (4)
- shock
- activation of neutrophils
- activation of endothelial cells
- stimulates production of other cytokines
INF-gamma cellular targets (2)
- fosters shift from acute to chronic inflammation
- activates macrophages and lymphocytes
IL-10 cellular targets (1)
- immune suppression
important chemokines (4)
- IL-8
- Eotaxin
- CCL1, CCL2, CCL17, CCL22
- monocyte chemoattractant protein 1
IL-8 cellular target
- neutrophils
eotaxin cellular target
- eosinophils
CCL1, CCL2, CCL17, CCL22 cellular target
- lymphocytes
monocyte chemoattractant protein 1 cellular target
- monocytes
lysosomal components (3)
- reactive oxygen metabolites (free radicals)
- antimicrobial peptides
- enzymes (proteases, esterases, nucleases)
lysosomal components reactive oxygen metabolites (free radicals) are highly reactive to
- pathogens and host cells
lysosomal components antimicrobial peptides include
- defensins (neutrophils) and major basic protein (eosinophils)
lysosomal components enzymes (proteases, esterases, neucleases) function
- break down of cellular structures
anaphylatoxins (C3a and C5a) role in inflammation
- mast cell degranulation
- vascular changes (edema)
- leukocyte adhesion and chemotaxis
opsonization (C3b) role in inflammation
- enhanced phagocytosis by neutrophils and macrophages
role of complement in inflammation (4)
- anaphylatoxins (C3a and C5a)
- opsonization (C3b)
- membrane attack complex with cell lysis
- removal of antibody-antigen complexes
kinin system results in (4)
- pain
- vasodilation and increased vascular permeability
- stimulates complement system
- chemotaxis
fibrinolytic system degrades
- fibrin and blood clots
fibrinolytic system cleaves
- C3 - initiates complement system (initiate more clotting factors)
disseminated intravascular coagulation (DIC)
- overactivity of inflammatory mediators cause widespread consumption of clotting factors along with microvasculature thrombosis
clinical relevance of link between inflammation and coagulation
- disseminated intravascular coagulation (DIC)
