Principles of Inflammation 2 Flashcards
what can apmplify a reaction?
mediators
what induces cell necrosis?
C5 - 9 MAC (membrane attack complex)
what effects are > than C3a
C5a, chemotactic for polys
Hageman factor
triggers kinin system cascade
plasmin
activates hageman factor, cleaves c3 + c5
what increases vascular permeability
when fibrin split products
fibrin is formed –>
vascular occlusion which may lead to ischemia
IL-6 fever
^ CRP production by liver
Endothelial damage
during wbc adhesion to endothelium
anti-oxidants
superoxide dismutase
catalase
sources of free radical
radition
phagocytosis, inflammation
mitochondria
free radicals especially bind to
thymine –> DNA breaks
free radicals on protein cross-linking
leads to enhanced degradation
managment system to deal with free raidcals
SOD converts
O2 ->H2O2 + O2
what can purines bind to?
receptors of platelets for activation and aggregation
what can be released from polys?
purines ATP and ADP
what reverses inflammtion? (5)
chalones hemostasis reducing swelling (lymphatics drain edema fluid from site) mediators anti-oxidants
eNO reduces?
rollng + adhesion
Lipoxins (reverse of inflammation)
part of lipo-oxygenase pathway
what stops IL-1 production
pyrin (marenostrin)
what triggers formation of inflammasome
bacterial endotoxins, cell necrosis and cytkines
what activates IL-1
caspase 1
what blocks activation of caspase1
pyrin
antiinflammatory drugs
antihistamins
corticosteroids
nsaids
leukotreine drugs
vasoactive amines (histamine)
released from mast cells
induced by injury
reorient WP bodies (p-selection
lysomal constiuents (enz)
released from polys, macrophage
tissue destruction and permeabiltiy
IL-8
chemotaxis for polys
acute-short duration of inflammation
polys predominate
subacute-intermiedaite duration of inflammation
polys, granulation tissue + round cells
chornic-long duration of inflammation
no polys, –>healing with collagen
lympcotes, macrophages and plasma cells
chronic-granuomatous
features:
localized, replaces normal tissue
giant cells, necrosis
chronic-granulomatous
general causes:
delated hypersensivity, foriegn material
chronic-granulomatous
specific causes:
TB, fungus, syphilis, sutures
what is a ganuloma
macrophages fused together forming giant cells
what influences grnaulomas
IL-4 made by Th2 cells
what does granuloma cause?
E-caderin expression on cell surface and fusion
serous
watery blister
effusion
serous fluid in body cavity
catarrhal
water + mucous
fibrinous
fibrin on surfaces
purulent
pus with polys abcess
hemorrhagic
vascular damage-bacteria
pseudomembranous
dead cells + polys
increased pmns in blood
leukocytosis
Esoinophilic leukocytosis
allergic reactions, parasiic infections
acute phase reactants include
fibrinogen, glibulins, C-reactive protein and protein SAA
Elevated CRP
post op, after acute MI, infections, inflammatory disease
CRP rises in serum after
4-6 hours
stimulant of increased hapatic CRP production
IL-6
ESR elevated in patients with inflammation
system inflammatory disease, infection
