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Flashcards in Inflammation Deck (75):
1

What is inflammation?

a host defense response to infection and tissue damage intended to eliminate the offending agents

2

What are 4 main causes of inflammation?

infections (bacterial, viral, fungal, parasitic), tissue necrosis (ischemia, trauma, injury), foreign bodies (exogenous or endogenous), immune reactions (hypersensitivity)

3

What is the onset and duration of acute inflammation?

develops within minutes to hours, short duration

4

What are local features of acute inflammation?

redness, heat, swelling/edema

5

What cells are involved in acute inflammation?

neutrophils and other phagocytes (innate immunity cells)

6

What are the 3 possible outcomes of acute inflammation?

resolution, resolution w fibrosis, or progression to chronic inflammation

7

What is the onset and duration of chronic inflammation?

develops over days to months, long duration

8

What cells are involved with chronic inflammation?

lymphocytes, plasma cells, monocytes, macrophages, fibroblasts (adaptive immunity cells)

9

What is the outcome of chronic inflammation?

progressive and sometimes severe tissue damage with fibrosis

10

What effect does fibrosis have on tissue?

limits function

11

What blood vessel changes occur in acute inflammation?

increased flow due to vasodilation, increased permeability

12

What is the difference between endothelial cell retraction vs. injury?

retraction is induced by mediators and is rapid, short lived, and reversible
injury is caused by burns or toxins and can be rapid but long lived (resulting in edema)

13

What two forces balance vessel pressure?

colloid osmotic pressure (water in) and hydrostatic pressure (water out)

14

What are the two types of fluid leakage?

exudate and transudate

15

Describe an exudate vessel.

fluid and protein leakage, vasodilation and increased permeability, characteristic feature of inflammation

16

Describe a transudate vessel.

fluid but no protein leakage, not a feature of inflammation, usually associated with CHF and edema

17

What is margination?

leukocyte movement to peripheral region of blood flow

18

What receptors mediate margination?

selectins

19

What receptors mediate leukocyte adhesion to endothelial cells?

integrin ligands

20

What is diapedesis?

leukocytes traversing the endothelium

21

Which process follows diapedesis?

chemotaxis

22

What is chemotaxis?

migration along chemical gradient due to chemoattractants

23

What are the two classes of chemoattractants?

exogenous (bacterial products) and endogenous (chemical mediators)

24

What is the primary component of cellular infiltrate 6-24 hours after inflammation begins?

neutrophils

25

What is the primary component of cellular infiltrate 24-48 hours after inflammation begins?

monocytes (macrophages)

26

What are the steps in the process of phagocytosis?

1. recognition and attachment
2. engulfment of microbe and creation of phagosome
3. fusion of phagosome with lysosome to form phagolysosome
4. killing and degradation

27

What are 3 pathways for microbial killing?

ROS, NO, lysosomal enzymes/proteins

28

What is the killing agent formed in the ROS pathway?

hypochlorite OCl2-

29

What is the killing agent formed in the NO pathway?

peroxynitrite ONOO-

30

What are the 2 steps in the ROS pathway?

NADPH oxidase generates superoxide anion
superoxide anion generated H2O2 which works with myeloperoxidase and Cl to generate hypochlorite

31

What are the 2 steps in the NO pathway?

inducible nitric oxide synthase (iNOS) generates NO
works with superoxide anion to generate peroxynitrate ONOO-

32

What 4 lysosomal enzymes are responsible for microbial killing?

lysozyme, collagenase, elastase, acid hydrolase

33

What are 3 protective mechanisms against unwanted tissue damage by killing pathways?

location, antioxidants, antiproteases

34

What is the function of an antioxidant?

get rid of excess ROS in body

35

What to antiproteases act against?

elastases and collagenases

36

What are 4 primary antioxidants?

superoxide dismutase, catalase, glutathione peroxidase, ceruplasmin/transferrin

37

What are the 2 primary antiproteases?

alpha-1-antitrypsin and alpha-2-macroglobulin

38

What are the 4 classes of mediators of acute inflammation?

vasoactive amines
arachidonic acid metabolites
cytokines/chemokines
complement system

39

What are the vasoactive amines?

histamine and serotonin

40

What are AA metabolites derived from?

cell membrane phospholipids

41

Which two enzymes create different AA metabolite pathways?

cyclooxygenase or lipoxygenase

42

What inhibits the formation of AA?

steroids

43

What inhibits the function of cyclooxygenase?

COX-1 and COX-2 inhibitors, aspirin, indomethacin

44

Which 4 AA metabolites are derived from the cyclooxygenase pathway?

prostacyclin (PGI2), thromboxane A2 (TXA2), PGD2, and PGE2

45

Which 7 AA metabolites are derived from the lipoxygenase pathway?

HETE, Leukotriene (LTB4, C4, D4, E4), Lipoxin (LXA4, B4)

46

PGI2

causes vasodilation, inhibits platelet aggregation

47

TXA2

causes vasoconstriction, promotes platelet aggregation

48

PDG2, PGE2

causes vasodilation, increased vascular permeability

49

HETE, LTB4

chemotaxis

50

LTC4, D4, E4

bronchospasm, increased vascular permeability

51

LXA4,B4

inhibition of inflammation

52

What are the primary cytokines in acute inflammation?

TNF, IL-1, IL-6, chemokines, IL-17

53

How do cytokines affect the endothelium?

increase permeability and expression of adhesion molecules

54

How do cytokines affect the brain?

fever (TNF,IL-1,IL-6)

55

How do cytokines affect the liver?

acute phase protein production increase (IL-1, IL-6)

56

How do cytokines affect bone marrow?

Stimulate leukocyte production (TNF, IL-1, IL-6)

57

How does TNF affect the heart?

low output

58

How does TNF affect thrombosis?

increases risk

59

How do cytokines affect muscles?

insulin resistance (TNF, IL-1)

60

What are chemokines?

small chemoattractant proteins

61

Where do chemokines bind?

bind to 7 transmembrane G-protein coupled receptors

62

Which mediator is at the central part of the complement system?

C3

63

What cleaves C3 and into what parts?

C3 convertase, C3a and C3b

64

What is a MAC?

membrane attack complex

65

What makes up a MAC?

C5b, C6-C9

66

Which complement system mediators are involved in recruitment and activation of leukocytes?

C5a and C3a

67

Which complement system mediator is involved in phagocytosis?

C3b

68

What is pus?

collection of dead cells and cellular debris (both regular tissue and microbes)

69

What are 3 causes of chronic inflammation?

persistent infections, hypersensitivity diseases, prolong exposure to toxins

70

What are 3 morphologic feature of chronic inflammation?

mononuclear cell infiltration, tissue destruction, attempts at healing

71

What are cellular features of granulomatous inflammation?

macrophages with abundant cytoplasm, giant cells, T lymphocytes, and variable necrosis

72

What are some causes of granulomatous inflammation?

foreign material, mycobacterial or fungal infection, and certain immune reactions

73

How do acute phase protein levels change during inflammation?

increase

74

How do white blood cell levels change during inflammation?

increase (leukocytosis)

75

What are the acute phase proteins?

C-reactive protein, fibrinogen, serum amyloid A, hepcidin