overview of inflammation:) Flashcards
what is inflammation
response of a vascular tissue to injury
what does inflammation do
bring the cells and molecules of host defence from circulation to the sites where they are needed
- protective
- gets rid of harmful/unwanted substances
- initiate repair
features of inflammation
red hot swollen pain loss of function
causes of inflammation
infection trauma physical and chemical agents tissue nercrosis forgein bodies immune reactions
tooth abcess
tooth may have caries and become non vital and necrotic
bacteria leak out of periodical area
Acute respocne
acute vs chronic
acute rapid mainly neutrophils usually mild tissue injury prominent local/systemic signs
chronic slow macrophages and lympocytes severe and progressive tissue injury less local/systemic signs
2 main events in acute inflammation
vascular resource - immediate cellular response - hours - neutrophils then macrophages
vascular events for acute inflammtion
1- vasocontrisction arterioles
2- arteriolar capillary and venue dilation
3 - increased vascular permeability
4- vascular stasis
vasoconstriction in vascular events of acute
prevent blood loss
affected area become white
arteriolar, capillary and venue dilation in vascular events of acute
to increase blood flow to an area to bring WBCs and plasma proteins
- affected area red and wam
increased vascular permeability in vascular events of acute
endothelial cells contract to increase spaces between cells
allows leakage of WBCs through blood vessel wall to damaged area
- swelling due to oedema
vascular stasis in vascular events of acute
WBCs can adhere to endothelial cells to move from blood vessel to tissue
- loss of fluid slows blood Flow
what is oedema
swelling of the tissue
what does oedema do
dilute bacterial toxins and other toxins
promotes and regulates inflammatory responce
attraction of phagocytes
initiates repair
opsonin
can bind to an injurious agent and help a macrophage or neutrophil bind to it
- allows body to recognise bacteria easier
(antibodies or complement proteins act as opsonin)
explain the process of opsonin
1) Macrophage approaches bacterial
2) Bacteria is able to evade the macrophage
3) Opsonin on the bacteria (binds) helps the macrophage recognise the antibody now on the bacteria
- Binds more easily
what happens normally to leukocytes and erthrocytes
flow within the middle of the vessel and quickly
what happens to the cellular response during inflammation
1) Margination (due to vascular stasis)
2) Pavementation
3) Emigration/extravasation between endothelial cells
4) Aggregate around inflammatory sites
5) Phagocytose micro organisms and cellular debris
what is margination in the cellular response during inflammation
leukocytes move from the middle to the edge of the blood vessel
pavementation in the cellular response during inflammation
adhere to the endothelial cells of the blood vessel
use integrins and ?prolactin?
increase in these receptors during inflamation
emigration/extravastion between endothelial cells in the cellular response during inflammation
endothelial cells contract to increase permabilityof the wall
leukocytes can move between cells
aggregate around inflammatory sites in the cellular response during inflammation
chemokines attach WBCs
function of neutrophils in cellular repsocne
1) Phagocytosis
2) Kill microbes by antimicrobial peptides
3) Production of NETS (neutrophil extracellular traps)
- Neutrophils die in the process
- Releases its DNA, inthe DNA it attracts the antimicrobial peptides in DNA meshwork, traps bacteria inside it
steps of phagocytosis
- Recognition and attachment (use of pseudopodia which are extensions of cell membrane)
- Engulfment (to form a phagosome, binds to a lysosome to form a phagolysosome)
- Killing and degradation of material
what is pain in inflammation due to
- Increase in tissue pressure due to oedema
- Inflammatory mediators
outcomes of acute inflammaton
1 complete resolution
2 healing by fibrosis
3 progression to chronic inflammation
healing by fibrosis result of acute inflammation
body cannot regenerate itsel
leads to granulation tissue maturing into scar tissue
granulation tissue
fibroblasts and endothelial cells
scar tisseu
increase in collagen
decrease in vessels
chronic inflammation
- Inflammation, repair and continued tissue destruction occur simultaneously
- Lasts weeks/months/years
how do you progress to chronic inflammtion
1) Acute inflammatory response fails to get rid of injurious agent
- Grit in wound, retention of sutures, continued infection at root apex
2) Interference with normal process of healing
- e.g. poor blood supply
causes of chronic inflammation
- certain microorganisms such as mycobacteria
- prolonged exposure to toxins
- autoimmune disease
- failure of acute inflammation to resolve cause
chronic inflammatory cells
macrophages
plasma
lymphocyetes
what type of response is greater in chronic
cellular repsince
what do plasma cells do
produce antuboides
features of chronic inflammation
- Minimal vascular changes
- Infiltration by chronic inflammatory cells
- Repair which may mature to give scarring
- Continued tissue destruction (inflammatory agent or inflammatory cells)
