overview of inflammation:) Flashcards

1
Q

what is inflammation

A

response of a vascular tissue to injury

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2
Q

what does inflammation do

A

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
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3
Q

features of inflammation

A
red 
hot
swollen
pain
loss of function
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4
Q

causes of inflammation

A
infection
trauma
physical and chemical agents
tissue nercrosis
forgein bodies
immune reactions
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5
Q

tooth abcess

A

tooth may have caries and become non vital and necrotic
bacteria leak out of periodical area
Acute respocne

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6
Q

acute vs chronic

A
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
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7
Q

2 main events in acute inflammation

A
vascular resource 
- immediate 
cellular response 
- hours
- neutrophils then macrophages
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8
Q

vascular events for acute inflammtion

A

1- vasocontrisction arterioles
2- arteriolar capillary and venue dilation
3 - increased vascular permeability
4- vascular stasis

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9
Q

vasoconstriction in vascular events of acute

A

prevent blood loss

affected area become white

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10
Q

arteriolar, capillary and venue dilation in vascular events of acute

A

to increase blood flow to an area to bring WBCs and plasma proteins
- affected area red and wam

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11
Q

increased vascular permeability in vascular events of acute

A

endothelial cells contract to increase spaces between cells
allows leakage of WBCs through blood vessel wall to damaged area
- swelling due to oedema

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12
Q

vascular stasis in vascular events of acute

A

WBCs can adhere to endothelial cells to move from blood vessel to tissue
- loss of fluid slows blood Flow

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13
Q

what is oedema

A

swelling of the tissue

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14
Q

what does oedema do

A

dilute bacterial toxins and other toxins
promotes and regulates inflammatory responce
attraction of phagocytes
initiates repair

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15
Q

opsonin

A

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)

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16
Q

explain the process of opsonin

A

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

17
Q

what happens normally to leukocytes and erthrocytes

A

flow within the middle of the vessel and quickly

18
Q

what happens to the cellular response during inflammation

A

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

19
Q

what is margination in the cellular response during inflammation

A

leukocytes move from the middle to the edge of the blood vessel

20
Q

pavementation in the cellular response during inflammation

A

adhere to the endothelial cells of the blood vessel
use integrins and ?prolactin?
increase in these receptors during inflamation

21
Q

emigration/extravastion between endothelial cells in the cellular response during inflammation

A

endothelial cells contract to increase permabilityof the wall
leukocytes can move between cells

22
Q

aggregate around inflammatory sites in the cellular response during inflammation

A

chemokines attach WBCs

23
Q

function of neutrophils in cellular repsocne

A

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

24
Q

steps of phagocytosis

A
  • 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
25
what is pain in inflammation due to
- Increase in tissue pressure due to oedema | - Inflammatory mediators
26
outcomes of acute inflammaton
1 complete resolution 2 healing by fibrosis 3 progression to chronic inflammation
27
healing by fibrosis result of acute inflammation
body cannot regenerate itsel | leads to granulation tissue maturing into scar tissue
28
granulation tissue
fibroblasts and endothelial cells
29
scar tisseu
increase in collagen | decrease in vessels
30
chronic inflammation
- Inflammation, repair and continued tissue destruction occur simultaneously - Lasts weeks/months/years
31
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
32
causes of chronic inflammation
- certain microorganisms such as mycobacteria - prolonged exposure to toxins - autoimmune disease - failure of acute inflammation to resolve cause
33
chronic inflammatory cells
macrophages plasma lymphocyetes
34
what type of response is greater in chronic
cellular repsince
35
what do plasma cells do
produce antuboides
36
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)