Principles of inflammation 1 Flashcards
causes of inflammation
physical:
trauma, surgery
causes of inflammation
chemical:
mediical drugs
causes of inflammation
infection
bacteria, fungi, virsus
causes of inflammaion
immune reaction
allergy, auto-immune
inflammation signs
red, warm, swelling, pain –or loss of function
inflamamtion events (1-3)
vasoconstriction, vasodialation, statis-capillaries + venules
vasodialation
increased blood flow
leads to erthema and heat
statis-caillaries and venules
hemonconcentration -> ^ viscosisty
margination of leukocytes
Permeability mechanisms
endothelial gaps
rapid/short lived
reversible
due to endothelial contraction
mediated by histamine
permeability mechanism
direct injruy
arterioles, capillaries
toxins, burn, chemicals
rapid/long lived
Permeabilty mechanism
leukocyte-dependent injury
ppolys cause injury when adhere to endothelim
–>release of free radicals
Permeability mechanism
Transcytosis
early response
transport endothelim via cytoplasmic vesicles
mediated by VEGF–> new vessels forming
Results in early acute inflammtion
edema (Extracellular h2o)
hemoconcentration (intravascular) from fluid loss
pain from press within tissues
transudate
fluid clear and mostly water
exudate
fluid, protein, cells
inflammation events 4-9
margination rolling * adhesion * transmigration * chemotaxis phagocytosis
what is margination based on
slow flow, not adhesion
molecules : rolling –> adhesion
selections
molecules: adhesion –>transmigration
integrins
selectins
transmembrane proteins
lectin domain binds to carbs
* binds to addressins with Lewis X
*weak
intergrins (30 protein family)
bind to endothelium
immunoglobin superfamily
bind to intergrins on WBCs
importance of P-Selection
binds to Lewis X (all wbcs)
primes cells for rolling
improtance of ELAM-1 (E-selections)
binds to Lew X (poly, mono)
invlved in rolling
importance of ICAM -1
binds to an integrin CD18 (all wbcs)
involed in adhesion
why dont endothelium and wbcs sick together all the time?
weibel-palade bodies
what is used by all wbcs to migrate between endo cells
PeCAM (homotypic) –>pierces membrane using collagenases
transmigration
wbcs move through vessel wall
poly after 24
mon after 48
chemotaxis
wbcs attracted to injury
mediators like c5a, LTB4, IL-8
chemotaxis mechanism
c5a binds–>activates phos lipase –>PIP2 –>IP3—>increased Ca++–>Assembly of contracile proteins–>cell motility
what regulates cell traficking?
chemotactic factors
where do cell move toward during chemotaxis
toward high concenration of chemokines
phagocytosis
pmns-sloppy eats
macro-polite eater
