Flashcards in Acute Inflammation 8-4-15 Deck (16):
1
DAMPS/PAMPS + TLRs on monocytes form what? What does this do?
Inflammasome
-Activates Caspase-1
-Cleaves IL1 to active form which sets inflammatory cytokines in action
2
What do IL-1 and TNF alpha do?
increase adhesion molecules
3
What happens once you have chemokines?
marginal flow of neutrophils-->lectins and proteoglycans cause stick and roll
4
What do chemoattractants do?
activate membrane receptors on the innate cells that then activate cytoskeleton *actin
changes that move the cell along the gradient to the site of inflammation
5
What promotes monocyte chemotaxis? What happens once monocytes come?
neutrophil degranulation
-monocytes send signal to stop neutrophils from coming
6
What is Left shift?
Marrow starts sending out slightly immature cells-band form
7
What is the half life of a neutrophil?
12 feet in blood
1-2 inches at inflammatory site
8
How do neutrophils kill and degrade?
-degraunlation
-oxidative burst
-activation of NADPH generated H202
-lysosomal enzyme donate MPO
-MPO+halide = HOCl
9
How do NETs work?
PMN sacrifice nucleus by casting its chromatin laden with killer granules out of the cell as a net to trap bacteria and fungi
10
What happens when there is no TLR or phagocytic receptor activation?
-decreased pro-inflammatory mediator synthesis and release
-macrophages sense this as they clean up dying neutrophils
-predominant cytokines TGF b and IL10
11
TGF b and IL 10
anti-inflammatory cytokines
set up for healing and wound repair
12
What are the types of acute inflammation from least severe to most severe?
1. serous (transudate)
2. fibrinous
3. suppurative/abscess(exudate)
Special category. ulcerative
13
Serous (transudate)
protein poor
from space peritoneal to pericardial or pleural
14
Fibrinous
Fluid with larger molecules dominated by fibrinogen which converts to fibrin and potential scarring
15
Supperative/abscess
protein rich fluid with inflammatory cell, alive and dead necrotic debris
16