Goljan High Yield Inflammation and Repair EC Flashcards
Histamine
key chemical in acute inflammation: mast cell
Arteriole vasodilation
Increased venular permeability
Rubor acute inflammation
Redness Arteriole vasodilation (histamine)
Calor acute inflammation
Heat Arteriole vasodilation (histamine)q
Tumor acute inflammation
Swelling
Increased vessel permeability (histamine)
Dolor acute inflammation
Pain
bradykinin and PGE
Acute inflammation
Neutrophil dominant
Increased IgM
Initial vessel events in inflammation
Neutrophil dominant
Increased IgM
Neutrophil rolling acute inflammation
Due to selectins
Integrins
Neutrophil adhesion molecules
C5a and LTB4
Activate neutrophil margination
CD11/CD18
Markers for integrins
Endothelial cell adhesion molecules
activated by IL-1 and TNF
ICAM
Intercellular adhesion molecule
VCAM
vascular cell adhesion molecule
Leukocyte adhesion molecule defect
failure of umbilical cord to separate
Poor wound healing
Decreased neutrophil adhesion molecules
Neutrophilic leukocytosis
Due to corticosteroids and catecholamines
Increased neutrophil adhesion molecules
Neutropenia
Endotoxins
Chemotaxis
Directed movement
C5a and LTB4
Opsonizing agents
IgG
C3b
Enhance phagocytosis
Receptors for IgG, C3b
PMNs
Monocytes
Macrophages
Most potent microbicidal system
O2 dependent MPO system
in PMNs and monocytes but NOT macrophages
Production of superoxide from O2
NADPH oxidase with PADPH cofactor
Produces respiratory burst
Test for respiratory burst
Nitroblue tetrazolium (NBT)
Converts superoxide to peroxide
Superoxide dismutase
Lysosomal enzyme that combines peroxide + Cl to form bleach (HOCl)
Myeloperoxidase
Microbicidal defects
Chronic granulomatous disease of childhood (XR) Myeloperoxidase deficiency (AR)
Absent NADPH oxidase, no respiratory burst
Chronic granulomatous disease
Catalase + organisms (ie S aureus) not killed, but strep killed
Chronic granulomatous disease
Respiratory burst present
No bleach produced
Myeloperoxidase deficiency (AR)
Opsonization defect
Bruton’s agammaglobulinemia (XR)
Decreased IgG
Phagocytosis defect
Chediak-Higashi
Also has defect in microtubule polymerization
COX inhibitors
NSAIDS (non-selective)
COX-2 inhibitors
Vasodilation, fever
PGE2
Vasodilator, prevent platelet aggregation
PGI2
Vasodilator, FR gas from conversion of Arginine to Citrulline
NO
Fever, synthesis of acute phase reactants in liver, leukocytosis
IL-1 and TNF