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MCM Test 1 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A

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

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2
Q

What are 4 main causes of inflammation?

A

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

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3
Q

What is the onset and duration of acute inflammation?

A

develops within minutes to hours, short duration

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4
Q

What are local features of acute inflammation?

A

redness, heat, swelling/edema

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5
Q

What cells are involved in acute inflammation?

A

neutrophils and other phagocytes (innate immunity cells)

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6
Q

What are the 3 possible outcomes of acute inflammation?

A

resolution, resolution w fibrosis, or progression to chronic inflammation

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7
Q

What is the onset and duration of chronic inflammation?

A

develops over days to months, long duration

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8
Q

What cells are involved with chronic inflammation?

A

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

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9
Q

What is the outcome of chronic inflammation?

A

progressive and sometimes severe tissue damage with fibrosis

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10
Q

What effect does fibrosis have on tissue?

A

limits function

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11
Q

What blood vessel changes occur in acute inflammation?

A

increased flow due to vasodilation, increased permeability

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12
Q

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

A

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)

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13
Q

What two forces balance vessel pressure?

A

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

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14
Q

What are the two types of fluid leakage?

A

exudate and transudate

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15
Q

Describe an exudate vessel.

A

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

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16
Q

Describe a transudate vessel.

A

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

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17
Q

What is margination?

A

leukocyte movement to peripheral region of blood flow

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18
Q

What receptors mediate margination?

A

selectins

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19
Q

What receptors mediate leukocyte adhesion to endothelial cells?

A

integrin ligands

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20
Q

What is diapedesis?

A

leukocytes traversing the endothelium

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21
Q

Which process follows diapedesis?

A

chemotaxis

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22
Q

What is chemotaxis?

A

migration along chemical gradient due to chemoattractants

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23
Q

What are the two classes of chemoattractants?

A

exogenous (bacterial products) and endogenous (chemical mediators)

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24
Q

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

A

neutrophils

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25
Q

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

A

monocytes (macrophages)

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26
Q

What are the steps in the process of phagocytosis?

A
  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
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27
Q

What are 3 pathways for microbial killing?

A

ROS, NO, lysosomal enzymes/proteins

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28
Q

What is the killing agent formed in the ROS pathway?

A

hypochlorite OCl2-

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29
Q

What is the killing agent formed in the NO pathway?

A

peroxynitrite ONOO-

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30
Q

What are the 2 steps in the ROS pathway?

A

NADPH oxidase generates superoxide anion

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

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31
Q

What are the 2 steps in the NO pathway?

A

inducible nitric oxide synthase (iNOS) generates NO

works with superoxide anion to generate peroxynitrate ONOO-

32
Q

What 4 lysosomal enzymes are responsible for microbial killing?

A

lysozyme, collagenase, elastase, acid hydrolase

33
Q

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

A

location, antioxidants, antiproteases

34
Q

What is the function of an antioxidant?

A

get rid of excess ROS in body

35
Q

What to antiproteases act against?

A

elastases and collagenases

36
Q

What are 4 primary antioxidants?

A

superoxide dismutase, catalase, glutathione peroxidase, ceruplasmin/transferrin

37
Q

What are the 2 primary antiproteases?

A

alpha-1-antitrypsin and alpha-2-macroglobulin

38
Q

What are the 4 classes of mediators of acute inflammation?

A

vasoactive amines
arachidonic acid metabolites
cytokines/chemokines
complement system

39
Q

What are the vasoactive amines?

A

histamine and serotonin

40
Q

What are AA metabolites derived from?

A

cell membrane phospholipids

41
Q

Which two enzymes create different AA metabolite pathways?

A

cyclooxygenase or lipoxygenase

42
Q

What inhibits the formation of AA?

A

steroids

43
Q

What inhibits the function of cyclooxygenase?

A

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

44
Q

Which 4 AA metabolites are derived from the cyclooxygenase pathway?

A

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

45
Q

Which 7 AA metabolites are derived from the lipoxygenase pathway?

A

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

46
Q

PGI2

A

causes vasodilation, inhibits platelet aggregation

47
Q

TXA2

A

causes vasoconstriction, promotes platelet aggregation

48
Q

PDG2, PGE2

A

causes vasodilation, increased vascular permeability

49
Q

HETE, LTB4

A

chemotaxis

50
Q

LTC4, D4, E4

A

bronchospasm, increased vascular permeability

51
Q

LXA4,B4

A

inhibition of inflammation

52
Q

What are the primary cytokines in acute inflammation?

A

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

53
Q

How do cytokines affect the endothelium?

A

increase permeability and expression of adhesion molecules

54
Q

How do cytokines affect the brain?

A

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

55
Q

How do cytokines affect the liver?

A

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

56
Q

How do cytokines affect bone marrow?

A

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

57
Q

How does TNF affect the heart?

A

low output

58
Q

How does TNF affect thrombosis?

A

increases risk

59
Q

How do cytokines affect muscles?

A

insulin resistance (TNF, IL-1)

60
Q

What are chemokines?

A

small chemoattractant proteins

61
Q

Where do chemokines bind?

A

bind to 7 transmembrane G-protein coupled receptors

62
Q

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

A

C3

63
Q

What cleaves C3 and into what parts?

A

C3 convertase, C3a and C3b

64
Q

What is a MAC?

A

membrane attack complex

65
Q

What makes up a MAC?

A

C5b, C6-C9

66
Q

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

A

C5a and C3a

67
Q

Which complement system mediator is involved in phagocytosis?

A

C3b

68
Q

What is pus?

A

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

69
Q

What are 3 causes of chronic inflammation?

A

persistent infections, hypersensitivity diseases, prolong exposure to toxins

70
Q

What are 3 morphologic feature of chronic inflammation?

A

mononuclear cell infiltration, tissue destruction, attempts at healing

71
Q

What are cellular features of granulomatous inflammation?

A

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

72
Q

What are some causes of granulomatous inflammation?

A

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

73
Q

How do acute phase protein levels change during inflammation?

A

increase

74
Q

How do white blood cell levels change during inflammation?

A

increase (leukocytosis)

75
Q

What are the acute phase proteins?

A

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

MCM Test 1 (23 decks)

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