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
coagulation and kinin systems produce what?
produce bradykinin, which increases vascular permeability, arteriolar dilation, and pain
vasodilation contributors
prostaglandin, and histamine
increased vascular permeability contributors
histamine, prostaglandin, anaphylatoxins, and leukotrienes
chemotaxis and leukocyte activation contributors
TNF, IL-1, chemokines, anaphylatoxins, and leukotrienes
fever contributors
IL-1, TNF, and prostaglandins
pain contributors
prostaglandins, and bradykinin
tissue damage contributors
lysosomal enzymes, and ROS
