Acute inflammatory response part 2 Flashcards
Drops that block chemical mediators of inflammation
Zatidor: anti-histamine / mast cell stabilizers
Prolensa: NSAID
Predforte: steroid
cell-derived mediators: Histamine
produced by mast cells, basophils, and platelets
- stimuli, and immune reactions
- actions: vasodilation, increased vascular permeability
cell-derived mediators: Arachidonic Acid Metabolites
- prostaglandins, leukotrienes, lipoxins
- produced by leukocytes, mast cells, endothelial cells, platelets
- released via phospholipase
AA metabolite 2 enzymatic pathways
cyclooxygenase: prostaglandins and thromboxanes
lipooxygenase: leukotrienes and lipoxins
what blocks different enzymatic pathways?
- steroids inhibit phospholipases, blocking both enzymatic pathways
- NSAIDS inhibit cyclooxygenases, which blocks prostaglandins and thromboxanes
acetaminophen vs ibuprofen
- acetaminophen: reduces pain and fever
- ibuprofen: reduces pain, fever, and inflammation. don’t use for GIT diseases, ulcers, and anti-coagulants
AA metabolite actions
- vasodilation: prostaglandins
- increased vascular permeability: prostaglandins, leukotrienes
- chemotaxis, leukocyte adhesion: leukotrienes, and HETE
- pain and fever: prostaglandin
NSAIDS
- COX-1 and COX-2 inhibitors
- COX-1: produced in response to inflammation: most tissues
- COX-2: produced in response to inflammation: absent from most tissues
steroids (glucocorticoids)
- presidone, pred forte, prednisolone acetate
- inhibit activity of phospholipase –> inhibit release of AA from membrane lipids
pro-inflammatory drugs
- increases uveoscleral outflow, used to treat glaucoma
cell-derived mediator: platelet-activating factor
all-inclusive mediator of acute inflammation
cell-derived mediator: cytokines
- immune and inflammatory messengers
- include interleukins, tumor necrosis factor (TNF) and chemokines
cell-derived mediator: TNF and IL-1
from macrophages, mast cells, and endothelial cells
- activates endothelial cell in immunity and inflammation
cell-derived mediator: chemokine
recruit leukocytes to inflamed area
cell-derived mediator: reactive oxygen species and nitric oxide
kill microbes and can potentiate tissue injury
plasma protein-derived mediators
complement, kinin, and coagulation
mechanism of complement
- activated by antigens
- opsonization (coating) of microbe
- phagocytosis / destruction
- inflammatory response
what does complement lead to?
generation of anaphylatoxins, which causes degranulation of mast cells
what 3 pathways activate C3?
- classical: antigen-antibody complex + C1
- alternative: microbial cell wall components + properdin + factors B & D
- lectin: lectin in plasma binds to microbes
Activation of C3
- C3 convertase separates C3 into C3a and C3b
activation of C5
- C3b + microbe surface, uses C5 convertase to split C5 into C5a and C5b
final product of complement pathway
C5b leads to MAC (membrane attack complex) generation
important complement information
- mediators of inflammation
- generation of anaphylatoxins (C3a and C5a)
- phagocytosis by C3b
- MAC and C9
anaphylatoxins (C3a and C5a) functions
- cause release of histamine from mast cells
- leukocyte activation, causing adhesion and chemotaxis
