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Inflammation > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What do diseases which cause inflammation end in?

A

itis

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2
Q

How does inflammation help stop infection: Delivery system?

A

Deliver effector molecules, drugs and cells to infection site or injury

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3
Q

How does inflammation help stop infection: clotting

A

Induce local blood clotting

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4
Q

How does inflammation help stop infection: immune response?

A

stimulate adaptive immune response

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5
Q

How does inflammation help stop infection: repair?

A

Promote repair of injured tissue

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6
Q

What injuries do the host respond to e.g. catagory?

A

Infection

Trauma/overuse

Exposure to noxious chemicals or allergens

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7
Q

What are common signs of inflammation?

A

Redness

Swelling

Heat

Pain

Loss of function

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8
Q

What is the initial sign of inflammation?

A

vasodilation and nitric oxide flow

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9
Q

Where does nitric oxide flow and what does it do?

A

flow from arterioles into capillary beds close to the site of injury. This is responsible for the heat and redness

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10
Q

What does vasodilation do to blood flow?

A

blood rate to slow

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11
Q

What is margination?

A

Vasodilation causes blood rate to slow meaning the white blood cells can move towards the walls of the cell

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12
Q

What happens after margination of white blood cells to endothelial walls?

A

Chemical signals are released causing changes to endothelial wall

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13
Q

What do chemicals cause the cell wall to do?

A

causing them to contract and allow fluid into surrounding tissues causing swelling

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14
Q

What surface proteins are increased in the endothelial cells by chemical signals caused by margination?

A

selectin and ICAM

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15
Q

What does selectin bind to?

A

Selectins bind to glycoproteins on the surface of passingcells

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16
Q

What does ICAM bind to?

A

ICAM binds to integrin which is expressed on leukocytes

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17
Q

What does binding of selectin and ICAM do to leukocytes?

A

slowly roll along vessel wall as the binding is not strong

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18
Q

What binds to leukocytes to change the structure of integrin on them?

A

Chemokines

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19
Q

What does change of Integrin structure do to the leukocyte?

A

binds to ICAM strongly so stops rolling and flattens against cell wall

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20
Q

How does the leukocyte get through the cell wall after flattening and what is this called?

A

extending pseudoposa through the gaps and pull themselves through into the extravascular space – this is diapedesis

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21
Q

Once in the extravascular space how does the leukocytes get to the site of injury? (chemotaxis)

A

following a chemical gradient (C5A or the complement system)

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22
Q

is C5A high at site of injury?

A

yes

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23
Q

What does the leukocyte do at the site of injury?

A

clears or prevents infection by releasing cytokines or phagocytosing material

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24
Q

What is the key leukocyte here which acts through phagocytosis?

A

Neutrophils

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25
Q

What are inducers of inflammation? list :(

A

Cell lysis,
virulence factors (LPS, exotoxins ect.),
PAMPS,
cellular necrosis and release of intracellular contents, degradation of basement membrane
loss of epithelial/endothelial integrity

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26
Q

what does vasodilation lead to?

A

increased blood supply and increased vascular permeability (entry of plasma proteins)

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27
Q

When does loss of function occur?

A

if inflammation is severe

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28
Q

What are mast cells and what do they do?

A

release granulaes of inflammatory mediators

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29
Q

What do mononuclear phagocytes (macrophages) do?

A

Phagocytose and produce pro-inflammatory cytokines

30
Q

What so neutrophils do?

A

Phagocytes which release proteases

31
Q

What are main components of inflammatory response?

A

Fibroblasts, epithelial and endothelial cells
Platelets
NK cells

32
Q

What are vasoactive inflammatory mediators?

A

Histamine, kinins

33
Q

What are lipid inflammatory mediators?

A

Eicosanoids - Leuko tire service and prostaglandins

34
Q

What are some protein inflammatory mediators?

A

Complement components and cytokines (TNF-alpha, IL-1, IL-6) and chemokines (IL-8)

35
Q

How do mast cell’s activate and work?

A

IgE antibodies are inserted into the mast cells membrane and cross links of antibodies by antigens signal the release of inflammatory mediators.

36
Q

What activates mass cells?

A

C3a and C5a, cytokines or direct mechanical damage

37
Q

What do mast cells release?

A

TNF-alpha

38
Q

What does the TNF-alpha secreted by mast cells do?

A

Activate macrophages, increase proteins which triggers clotting, endothelial cells increase adhering surface, induce IL-8, induce contraction and gap formation making it more permeable

39
Q

What two molecules to mast cells secrete?

A

prostaglandins and leukotrienes

40
Q

What enzyme converts prostaglandins from arachidonic acid?

A

COX1 and COX2

41
Q

What do prostaglandins do?

A

Increase body temp and cause vasodilation

42
Q

What molecule is a potent potentiators of the activity of histamine and kinins?

A

posteglandins

43
Q

What enzyme drives the formation of Leukotrienes from arachidonic acid?

A

5-lipo-oxygenase

44
Q

What do Leukotrienes do?

A

upregulate the expression of adhesion molecules on neutrophils, increase their toxic oxygen properties proliferation, cytokine release of macrophages, are chemotaxins factors for neutrophils and macrophages.

45
Q

What do macrophages secrete?

A

TNF-alpha, IL-8, IL-6 and IL-1

46
Q

What is IL-8?

A

chemotaxis agent

47
Q

What does IL-1 and IL-6 help the macrophages do?

A

secrete IL-8 and upregulate cell adhesion molecules on the surface of the endothelial cells.

48
Q

What are kinins derived from?

A

precursors proteins

49
Q

what enzyme converts precursor proteins into kinins?

A

kallikrein

50
Q

what triggers kallikrein to convert?

A

clotting cascade and tissue damage

51
Q

What 2 molecules are made by Kallikrein from precursor protiens?

A

bradykinin and kalidin

52
Q

What do bradykinin and kalidin do?

A

increase vascular permeability, dilate venules and cause contraction on smooth muscles in airways

53
Q

What does bradykinn do specifically?

A

directly on pain nerve endings

54
Q

What is ICAM1’s ligand?

A

LFA-1

55
Q

What concentration gradient does neutrophils follow to the site of injury?

A

IL-8

56
Q

What three ways does pain develop?

A

Inflammatory mediators affect nocioceptors, Bradykinin and exudation of plasma increases tissue pressure.

57
Q

Why is it good you get a fever?

A

defenses work better, faster lymphocyte division, increases cell migration, inhibits microbial replication

58
Q

What mediates the resolution of inflammation?

A

strict temporal and spatial synthesis

59
Q

What is M1?

A

pro-inflammatory

60
Q

What is M2?

A

anti-inflammatory

61
Q

How do macrophages reduce actute inflammation?

A

they take on different phenotypes

62
Q

How do neutrophils resolve inflammation?

A

apoptose

63
Q

What are the sepcific molecules for resolution of inflammation?

A

lipoxins and resolvins

64
Q

what secretes lipoxins and resolvins?

A

macrophages, neutrophils and structural cells

65
Q

what needs to be reduced in inflammation?

A

diapedesis, neutrophil chemotaxis, production of pro-inflammatory cytokines and vascular permeability

66
Q

what does the resolution mediator TGF-beta do?

A

mediates wound healing, angiogenesis, fibroblast proliferation, collagen synthesis and deposition, remodelling of ECM.

67
Q

what is Efferocytosis?

A

Is the clearance of apoptotic cells by phagocytes.

68
Q

What are the three signals neutraphils show?

A

find me - attract macrophages
Kepp-out - deter other neutrophils
Eat-me/do no eat-me - help phagocytes distinguish viable/apoptotic cells

69
Q
A

genetic predisposition to developing these allergies

70
Q

What does histamine secreted by mast cells

A

Inflammation (2 decks)

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