acute inflammation Flashcards
inflammation
repsonce of vasuclar living tissue to injury
- protective
- destroy, wall off or dilute injurious agent
- initiate repair
features of acute inflammtion
1) red
2) hot
3) swollen
4) pain
5) loss of function
actue vs chronic
- immediate onset
- short lived
- usually single episode
- neutrophils and other granulocytes
eg dental abcess - usually vascular responce
Chronic - gradual onset
- prolonged
- frustrated healing (repair and destruction occurring simultaneously)
- macrophages and lymphocytes
- usually cellular reponce
causes of infection
bacteria viruses parasites trauma phsycial/chemcial agents tissue necrosis forign bodies immune reactions
examples of acute in the OC
abcess acute pulpitis lacterations aute herpetic gingivostomatitis parotitis reactions to piercings
steps of acute inflammation
vascualr
cellular
events that occur acute vascular response
vasoconstriciton arterioes
arterioolar capillary and venule dilation
increased vascialr permeabilty
vascular stasis
what casues vascular permeabiloty
histamine
C3a and C5a
leukotrines
vasoilation
1) trauma and complement can cause mast cells to release histamine
2) causes vasodilation
3) platelet aggregation causes release of serotonin
4) factors from WBCs and Nitric oxide and prostaglandins can cause vasodilation
increased vascualr permeability occurs by
retraction of endothelail cells
endothelial injuries
increased transport of fluid and proteins through endothelail cells (transcytosis)
oedema
excess of fluid in tissues
types od oedema
exudate
transudate
exudate
- extravascular fluid with a high protein content
- seen in inflammation
- high protein content caused by plasma protein’s and WBC
- only get it when we have increased vascular permeability, to allow movement from vessels to the tissues
transulate
- extravascular fluid with low protein content
- occurs in situations without increased permeability
- only fluid can move into tissues, not the protiens ect
role of oedema
4) contains clotting cascade
- fibrin forms a barrier to spread of infection (fibrinogen converted to fibrin by thrombin
- coagulation may also promote inflammation
5) contains kininogens
- these are converted to kinins by proteases eg thrombin
- bradykinin – similar effect to histamine vascular dilation
6) dilutes bacterial and other toxins
pathways to acitvate complement
classical
alternative
lectin
classical pathway
- antibodies bound to antigen
- C1 detects this and triggers pathway
alternative pathway
- C1 direct binding to pathogen via microbial surface molecules
lectin pathwat
- plasma manose binding lectin? binds to microbes and directly activates c1
degradation of C3
C3a can affect vascular permeability
C3b stays on the cell, along with previously generated fragments forms C5 convertase
splitting C5 into C5a and b
C5a affects VP
C5b remains attached, then attracts C6-9 and eventually forms membrane attack complex (drill hole in cell wall, allows fluids to come into cell and cause destruction of the cell)
opsonisaiton is caused by
- C3b can also bind to pathogens and phagocytes have a C3b receptor with which to bind to this
what does c3a c3b and c5a do
- dilation and increased vascular permeability C3a
- stimulate histamine release (C3a and C5a)
- promote formation of leukotrienes (attracts neutrophils) and prostaglandins (vasodilation)
- attracts phagocytes (C3a and C5a)
membrane attack complex
C5-9 membrane attack complex (MAC)
- destroys microorganisms
MAC forms transmembrane channels
these disrupt the phospholipid bilayer = cell lysis and death
cellular repsonce steps
1) Margination
- due to vascular stasis
- white blood cells drop to the edge of the blood vessel
2) Pavmentation
- neutrophils adhere using adhesion molecules on vessels walls known as selectins
- neutrophils then bind more strongly using integrins on their cell surface to ICAM on enodthemliall cells (promoted by IL-1, TNF alpha)
- ensure they only stop and stick to parts where there is inflammation
3) emigration
- movement of neutrophils between endothelial cells via chemotaxis via chemotactic gradient eg IL 8. C5a)
- move in between the endothelial cells
- neutrophils attracted by cytokines and parts of the complement system, aggregate around the area needed
4) Phagocytosis
- neutrophils and macrophages engulf and destroy microorganisms/necrotic tissue
- pseudopodia (projection) surrounds microorganism to form phagosome and destroyed by reactive oxygen species and hydrolytic enzymes (from lysosome)
- - lysosome binds with the phagosome within cytoplasm
