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
Q

what is pain in inflammation due to

A
  • Increase in tissue pressure due to oedema

- Inflammatory mediators

26
Q

outcomes of acute inflammaton

A

1 complete resolution
2 healing by fibrosis
3 progression to chronic inflammation

27
Q

healing by fibrosis result of acute inflammation

A

body cannot regenerate itsel

leads to granulation tissue maturing into scar tissue

28
Q

granulation tissue

A

fibroblasts and endothelial cells

29
Q

scar tisseu

A

increase in collagen

decrease in vessels

30
Q

chronic inflammation

A
  • Inflammation, repair and continued tissue destruction occur simultaneously
  • Lasts weeks/months/years
31
Q

how do you progress to chronic inflammtion

A

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
Q

causes of chronic inflammation

A
  • certain microorganisms such as mycobacteria
  • prolonged exposure to toxins
  • autoimmune disease
  • failure of acute inflammation to resolve cause
33
Q

chronic inflammatory cells

A

macrophages
plasma
lymphocyetes

34
Q

what type of response is greater in chronic

A

cellular repsince

35
Q

what do plasma cells do

A

produce antuboides

36
Q

features of chronic inflammation

A
  • Minimal vascular changes
  • Infiltration by chronic inflammatory cells
  • Repair which may mature to give scarring
  • Continued tissue destruction (inflammatory agent or inflammatory cells)