Inflammation Flashcards
This is a protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces
Inflammation
name the 4 cells/molecules involved in inflammation
1) leukocytes
2) endothelial cells
3) cells & extracellular matrix of the surrounding tissue
4) plasma cells/proteins
these are mediators released by platelets,inflammatory cells, endothelial cells
plasma cells/proteins
what releases plasma cells/proteins
1) platelets
2) inflammatory cells
3) endothelial cells
types of inflammation
acute inflammation
chronic inflammation
rapid onset & short duration (hours to few days)
acute inflammation
characterized by:
1) exudation of of fluid & plasma proteins (edema) &
2) the emigration of leukocytes, predominantly neutrophils (PMN)
acute inflammation
longer time course (days to years)
chronic inflammation
involves different cell types compared to acute inflammation
chronic inflammation
cell types involved in chronic inflammation
lymphocytes
macrophages
cell types involved in acute inflammation
plasma cells/proteins
leukocytes (neutrophils/PMN)
when tissue repair coexists with tissue destruction
chronic inflammation
cardinal signs of acute inflammation
- calor (heat)
- rubor (redness)
- tumor (swelling)
- dolor(pain)
- loss of motion
causes of acute inflammation
- infection
- trauma
- physical & chemical agents
- necrosis (Myocardial Infarction)
- foreign bodies
- immune reaction (2ndary to allergic rxn; endogenous & exogenous)
stages of acute inflammation
1) vasodilation
2) increased vascular permeability
3) movement of WBCs from blood vessels into soft tissue at the site of inflammation
occurs through a release of mediators
vasodilation
happens after a transient vasoconstriction
vasodilation
mediators released during vasodilation
1) histamine
2) prostaglandin i2 (resp. for fever)
3) nitric oxide
what mediator is responsible for fever
prostaglandin
vasodilation first involves the?
arterioles
vasodilation= arterioles –> leading to ______
opening of new capillary beds in the area
increased blood flow caused by __-
heat
increased blood flow caused by heat results to?
erythema/redness
vasodilation increases the ___?
hydrostatic pressure
increase in hydrostatic pressure due to vasodilation causes what?
slowing/sludging of blood flow
slowing of blood flow causes ?
migration of leukocytes along the wall of blood vessels
increased leakiness of blood vessels
stage 2= increased vascular permeabilty
outpouring of protein-rich fluid into the extravascular tissues (edema)
increased vascular permeability
the hallmark of acute inflammation
increased vascular permeability
allows fluid to cross into the interstitial tissue
increased vascular permeability
fluid crossing into the interstitial tissue due to increased vascular permeability causes
increased protein levels in the interstitial tissue
increased interstitial protein levels in interstitial tissue, causes an ______ osmotic pressure in the interstitial tissue
decreased!!!
this causes fluid to flow out of the vessel resulting to edema to interstitial fluid
increased vascular permeability
mediators of increased vascular permeability
1) histamine
2) bradykinn
3) leukotrienes (C4, D4, E4)
name the 4 mechanisms of increased vascular permeability
1) endothelial cell contraction
2) endothelial cell retraction
3) direct endothelial injury
4) delayed prolonged response
these are physiologic mechanisms and are due to mediators
referring to the type of mechanism of increased vascular permeability
endothelial contraction & retraction
these are pathologic mechanisms due to damaging agents not under the body’s control
(referring to the type of mechanism of increased vascular permeability)
direct endothelial injury
contraction of endothelial cells result to
increase in ___? spaces
mediators of endothelial cell contraction
1) histamine
2) bradykinin
3) leukotrienes
time course of endothelial cell contraction
immediate;short (30 minutes)
mediators of endothelial cell retraction
1) TNF
2) interleukins
occurs due to structural rearrangement of cytoskeleton
endothelial cell retraction
time course of endothelial cell retraction
4-6 hours; delayed response
mediators of direct endothelial injury
bacterial enzyme
occurs due to endothelial cell necrosis
direct endothelial injury
time course of direct endothelial injury
immediate; immediate sustained response
occurs due to UV light, xray, and mild termal injury
delayed prolonged response
uncertain mechanism
delayed prolonged response
pushes fluid from vessel to tissue
HP
attract fluid back to blood vessels
albumin
takes care of remaining fluid in interstitium
lymphatics
fluid only
filtrate
components of protein-rich fluid
fluid + albumin
what is the fist stage of acute inflammation
vasodilation
what is the 2nd stage of acute inflammation
increased vascular permeability
what is the 3rd stage of acute inflammation
movement of WBCs from blood vessels into soft tissue @ site of inflammation
steps in the 3rd stage of acute inflammation
“RPT”
1) rolling
2) pavementing
3) transmigration
the process by which WBCs are drawn to the site of acute inflammation
CHEMOTAXIS
loose, intermittent contact of WBCs with endothelium
rolling
partially due to margination of WBC from stages? of blood
rolling
tight, constant contact of WBC with endothelium
pavementing
WBC crossing through the endothelial layer
transmigration
particles that bind to foreign materials & signals leukocytes to remove it
opsonin
types of opsonins
1) IgG
2) C3b
3) Collectins
type of opsonin that is recognized by Fc receptor of WBC
IgG
type of opsonin that is recognized by Cr 1, 2 &3 of leukocyte
C3b
type of opsonin that is recognized by C2q on leukocyte
collectins
