6: acute inflammation I Flashcards
define inflammation
local reaction of vascularized tissue to injury
0-2 days
acute
2-14 days
subacute
> 14 days
chronic
PMNs
acute inflammatory
PMNs, monocytes, lymphocytes, plasma cells, fibroblastic elements, angioblastic elements
subacute inflammation
monocytes, lymphocytes, plasma cells, macrophages, granuloma cells (epitheliod cells and giant cells)
chronic inflammation
> 5% eosinophil (predominant inflammatory cell) indicates what type of infection
allergic reaction or parasitic infection
immune system
Ab
C3
C5fragments
plasma derived
kinin system (bradykinin)
plasma derived
clotting system (thrombin)
plasma derived
fibrinolytic system (pllasmin)
plasma derived
acute phase proteins (c-reactive prtn, ceruloplasmin, haptoglobin)
plasma derived
vasoactive amines (histamin, serotonin)
tissue derived
acidic lipids (prostaglandins, leukotrienes, lipoxins)
tissue derived
cytokines (IL-1, TNF)
tissue derived
chemokines (IL-8, MCP-1, MIP-1alpha, lymphotactin)
tissue derived
PAF, NO, ROS, lysosomal enzymes
tissue derived
6 cardinal signs of inflammation
1) Heat
2) Redness
3) Swelling
4) Pain
5) Loss of function
6) Systemic changes
serous acute inflammation
watery fluid
skin blister from burn or viral infection inflammation
serous
increased vascular permeability allows leakage of larger molecules such as fibrinogen
fibrinous inflammation
characteristic of inflammation of body cavities
fibrinous
manifested by large amounts of pus
suppurative inflammation
focal collection of pus; central necrotic region surrounded by layer of preserved PMN
abscesses
more likely to cause suppurative inflammation
pyogenic bacteria
local defect, excavation produced by sloughing of inflammatory necrotic tissue
ulceration
can only occur on or near a surface
ulceration
Key events of acute inflammation
- increased blood flow
- structural changes in microvasculature
- emigration of leukocytes and their accumulation/activation
when does vasoconstriction occur during inflammatory process
immediate
transient
variable
cutaneous arterioles
when does vasodilation occure in inflammation
arteriolar
results in increased capillary blood flow
open precapillary sphincters
acute inflammation (closed in normal state)
transudation v. exudation
trans: just fluid
exudate: protein and fluid due to widened intraepithelial junctions
at what vascular level does increased permeability occur?
at the level of capillaries and postcapillary venules as endothelial cells contract thus widening their intercellular junctions
how does local blood viscosity change in inflammation
stasis of circulation resulting in increased blood viscosity
leukocytes, mostly PMNs line up along endothelial cell surface
margination
steps to leukocyte extravasation
1) margination
2) adhesion
3) emigration
4) chemotaxis
migration between EC and across basement membrane to interstitial space
emigration
directed movement along chemical gradient towards injury
chemotaxis
what are CAM cell adhesion molecules
selectins
immunoglobulin
integrins
membrane proteins that promote leukocyte attachment and participation in the inflammatory response
selectin
rolling
slow down
- not involved in firm adhesion
where are selectins located?
on surface of endothelium, platelets and leukocytes
ICAM-1 is expressed where
on surface of cytokine stimulated endothelium
what does ICAM-1 bind to
itnerins LFA-1 and Mac-1
where are integrins LFA-1 and Mac-1 located
on cell membranes of neutrophils and macrophages
what and where does VCAM-1 bind
VCAM-1 binds to integrin VLA-4 on WBCs
PECAM-1 binds what and where
PECAM-1 binds CD-31 and plays and impotant role in the diapedesis step of leukocyte emiration
VLA-4 binds what
VLA-4 (only on WBCs) binds to VCAM-1 on endothelium
what increases the surface expression of B2 integrins (CD11/18)
activation of phagocytic cells by chemotactic stimuli
what assists in localization of phagocytes to injury sites and subsequent extravasation
LFA-1 and CR3/4 bind to ICAM-1
