The pathology of inflammatory responses Flashcards
features of acute inflammation (2)
short lived
neutrophil rich
features of chronic inflammation (4)
long lived
lymphocytes
plasma cells
macrophages
cardinal signs of acute inflammation
redness heat swelling pain (loss of function)
microvascular changes of acute inflammation
inflammatory exudate
oedema
pus
what complement would a pathogen bind
C3
what does binding of C3 cause
- activation of complement cascade,
- release of histamine and chemoattractants
- altered permeability of vessels
- altered adhesiveness of endothelium (cellular migration)
- phagocyte recognition of C3b-opsonised pathogen
2 systems that mediators for acute inflammation come from
cellular
plasma
4 cell-derived inflammatory mediators
platelets
mast cells
basophils
inflammatory cells
3 plasma derived systems for acute inflammation
- kinin system
- coagulation and fibrinolytic system
- complement system
2 pathways originating from arachidonic acid
cyclo-oxygenase pathway
lipo-oxygenase pathway
Which out of the COX and LOX pathway has a greater effect on platelets
COX
LOX or COX for effect on phagocytes
shared across both
COX pathway uses_____
prostaglandins
LOX pathway uses_____
leukotrienes
PAF=
platelet aggregation factor
systemic effect of acute inflammation (4)
- acute phase reactions
- Fever
- Altered liver metabolism
- HPA axis change
what can bacteria produce to cause fever
exogenous pyrogens (LPS)
what are cytokines involved in acute inflammation called
endogenous pyrogens
E.g of endogenous pyrogens
IL-1
IL-6
what happens in the liver in acute inflammation
acute phase proteins produced
whats a good early test for inflammatory response
acute phase proteins
4 stages of streptococcus pneumoniae infection
- congestion
- consolidation
- Grey hepatisation
- Resolution or Organisation
what is congestion
accumulation of fluid causing loss of function
what is consolidation
fluid and cells spread leading to solidification,
also called red hepatisation= dense texture like liver