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Path > mediators of local/systemic inflammation- week 2 > Flashcards

mediators of local/systemic inflammation- week 2 Flashcards

1
Q

what are cytokines

A

proteins produced by many types of cells that mediate immune and inflammatory reactions

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2
Q

what cytokines are in acute inflammation

A

TNF, IL-1, Chemokines, IL-17

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3
Q

What cytokines are in chronic inflammation

A

IL-12, IFN-gamma, IL-17

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4
Q

what are principle sources of TNF

A

macrophages, mast cells, T cells

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5
Q

what are principle sources of IL-1

A

macrophages, endothelial cells, some epithelial cells

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6
Q

what are principle sources of chemokines

A

macrophages, endothelial cells, T cells, mast cells

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7
Q

what are principle sources of IL-17

A

T cells

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8
Q

what is the action of TNF

A

stimulated expression of endothelial adhesion molecules, release of other chemokines, has systemic effects

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9
Q

what are principle actions of IL-1

A

similar to TNF

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10
Q

what are principle actions of chemokines

A

leukocyte recruitment

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11
Q

what are principle actions of IL-17

A

neutrophil, and monocyte recruitment

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12
Q

what are cytokines of chronic inflammation

A

IL-12, IFN-gamma, IL-17

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13
Q

what are principle sources of IL-12

A

dendritic cells, macrophages

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14
Q

what are principle sources of IFN-gamma

A

T cells, NK cells

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15
Q

what are principle sources of IL-17

A

T cells

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16
Q

what are principle actions of IL-12

A

increased production of IFN-gamma

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17
Q

what are principle actions of IFN-gamma

A

increased ability of macrophages to kill microbes and tumor cells

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18
Q

what are principle actions of IL-17

A

neutrophil and monocyte recruitment

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19
Q

other ________ of inflammation work in concert with cytokines

A

mediators

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20
Q

arachidonic acid is derived from_______

A

cell membranes

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21
Q

___________ or release of other mediators causes release of AA from cell membrane

A

injury/irritation

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22
Q

active AA is released via _________

A

cleavage by phospholipases

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23
Q

AA is further metabolized to create 2 classes of enzymes

A

cyclooxygenase
lipoxygenase

24
Q

what does cyclooxygenase generate

A

prostaglandin

25
Q

what does lipoxygenase produce

A

leukotrienes and lipoxins

26
Q

drugs that inhibit enzymes that are responsible for creating AA metabolites are used to treat________

A

inflammation

27
Q

_______ act on phospholipases

A

steroids

28
Q

AA metabolites have what response

A

vascular reactions, leukocyte chemotaxis
(vasodilation/vasoconstriction/leukocyte adhesion, inhibition of neutrophil adhesion, CHEMOTAXIS)

29
Q

systemic effects aka

A

acute phase response

30
Q

examples of systemic effects

A

fever
elevated levels of acute phase proteins
leukocytosis

31
Q

which molecules are involved in systemic inflammation effects?

A

AA metabolites: leukotrienes, prostaglandins
Cytokines (IL-6, IL-12, TNF)

32
Q

Cytokines (IL-1, IL-6, TNF) mediate _______

A

leukocyte recruitment and migration

33
Q

substances that induce fever:

A

exogenous substances (LPS)
endogenous substances (IL-1, TNF)

34
Q

exogenous substances that cause fever cause cells to release _______

A

endogenous substances (IL-1, TNF)

35
Q

IL-1 and TNF upregulate

A

cyclooxygenases

36
Q

cyclooxygenases synthesize

A

prostaglandin

37
Q

prostaglandins are released by ______ and stimulate the release of neurotransmitters that reset the body’s temp to a higher level

A

hypothalamus

38
Q

in fever, temp reset is via _________ and by increasing heat production via _________

A

vasoconstriction (reduce heat loss)
effect on brown fat and skeletal muscle

39
Q

most plasma proteins are synthesized in the

A

liver

40
Q

examples of plasma proteins

A

C reactive protein
fibroinogen
serum amyloid A

41
Q

CRP is simulated by

A

IL-6

42
Q

fibrinogen is stimulated by

A

IL-6

43
Q

SAA is stimulated by

A

IL-1 or TNF

44
Q

SAA and CRP may act as opsonins by

A

binding to bacterial walls or interact with complement
-may bind chromatin (helps clear necrotic cells)
-CRP levels measured to detect inflammation

45
Q

fibrinogen binds to RBC and causes them to form ______ which causes blood to _________

A

stacks
sediment faster

46
Q

leukocytosis initially occurs because of

A

increased release of granulocytes from bone marrow

47
Q

fast mobilization causes

A

increased immature cells - left shift

48
Q

neutrophilia means

A

bacterial infections

49
Q

lymphocytophilia means

A

viral infections

50
Q

eosinophilia menas

A

allergies and parasitic infections

51
Q

other systemic effects besides fever

A

inc. HR and BP
decreased heat loss
shiver, chills, anorexia, sleepiness

52
Q

what causes septic shock

A

high levels of bacterial products induce large amounts of cytokines (TNF, IL-1)
this causes hypotensive shock, blood clot disorders

53
Q

what is secondary amyloidosis

A

prolonged production of SAA leads to deposits of misfolded SAA proteins
causes tissue disfunction

54
Q

AA metabolites can be pro or anti inflammatory

A

true

55
Q

IL-17 is important in neutrophil recruitment

A

true

56
Q

T cells are the principle source of all but which mediator

A

IL-1

57
Q

the production of CRP is stimulated by IL-1

A

false

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