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PATH300 > inflammation and repair > Flashcards

inflammation and repair Flashcards

1
Q

4 major signs of inflammation

A

heat, redness, swelling, pain

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2
Q

name immunes cells in circulation

A

monocytes, leukocytes (neutrophils, basophils, eosinophils), platelets, lymphocytes

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3
Q

name 3 cells that recognize infection and produce inflammatory mediators

A

macrophages, dendritic cells, mast cells

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4
Q

what inflammatory mediators are released by macrophages, DCs, mast cells?

A

amines, cytokines (IL-1, IL-6, IL-12, IL-18)

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5
Q

what is different about capillaries in normal vs inflammation?

A

normal: most capillaries are empty
inflamation: vasodilation -> blood flows through most capillaries (hyperemia)

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6
Q

what is hyperemia?

A

increased blood flow

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7
Q

what is transudate? exudate?

A

transudate: Fluid that exits the capillaries under normal circumstances.
exudate: fluid containing metabolites and proteins

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8
Q

what changes in pressure happen during acute inflammation?

A

increase in hydrostatic pressure in all areas of microcirculation, and decrease in colloidal osmotic pressure

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9
Q

what is edema? (part of inflammation)

A

local swelling at the site of injury

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10
Q

what is histamine’s role?

A

increases vasodilation in arterioles and endothelial contraction in venules (leaky venules)

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11
Q

give an example of a delayed prolonged response?

A

sunburn

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12
Q

what is margination?

A

during inflammation when RBCs are clustered at the center and larger leukocytes become pressed against the venule wall

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13
Q

what protein is responsible for leukocytes slowing down? and stopping?

A

slow down = selectins
adhesion = integrins

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14
Q

what induces selectins?

A

cytokines and histamine

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15
Q

what is PECAM-1 (CD31)?

A

adhesion molecule found on the neutrophil and the endothelial cell wall that helps pull neutrophil through the gap between the endothelium wall

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16
Q

what kind of receptors on leukocytes sense chemokines

A

G-protein coupled receptors

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17
Q

what cells are recruited by chemokines?

A

TH1 and TH2

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18
Q

what cells are the first to arrive at site of inflammation

A

neutrophils

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19
Q

where do neutrophils come from? how long do they last?

A

bone marrow; die after a few days

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20
Q

what do NETs do?

A

Traps the microbe and stops the bacteria from travelling to other tissues

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21
Q

what are the precursors of macrophages?

A

monocytes

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22
Q

what are macrophage’s roles?

A

phagocytose bacteria, produce inflammatory mediators,
synthesize molecules for blood clotting, cell growth, tumor growth, collagen production, antibacterial defenses… ,
initiation of the immune response,
cleanup operations,
induction of general effects like fever, acute phase reaction, cachexia, loss of appetite

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23
Q

what are other names for macrophages?

A

microglial cells in CNS, interstitial dendritic cells, alveolar macrophages in lungs, kupffer cells in liver, osteoblasts in bones

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24
Q

what immune cells are involved in allergic and immune reactions

A

eosinophils and basophils

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25
Q

name 3 macrophages types and their role

A

classically activated macrophage: attack microbes
wound-healing macrophages: tissue repair
regulation macrophages: anti-inflammatory

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26
Q

steps of inflammatory reactions from day to day

A

day 1: edema
day 2: neutrophils
day 3: monocytes/macrophages

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27
Q

what do TLRs detect? what do they trigger?

A

detect pathogens, trigger inflammation

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28
Q

what do lectins detect?

A

fungal polysaccharides

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29
Q

describe the steps of phagocytosis

A
  1. recognition: PRRs recognize PAMPs (ex IgG, C3b), complement components
  2. engulfment: by phagosome
  3. killing and digestion: through lysosomal enzymes with free radicals
  4. extrusion
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30
Q

what are vasoactive mediator’s role?

A

Lead to vasodilation and increase the vascular permeability

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31
Q

name 2 vasoactive amines and their origin

A

histamines: released by degranulation of mast cells, basophils, platelets
serotonin: released by platelets

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32
Q

what are plasma proteases (type of vasoactive mediators) role?

A

increase permeability and edema

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33
Q

what are C reactive proteins and what do they do

A

involved in inflammatory processes and play an important role in various disease states

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34
Q

3 roles of complement?

A

lysis of bacteria,
chemotaxis,
opsonization

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35
Q

briefly describe the complement activation pathways

A

classical pathway: C1 binding to antibodies -> triggers vasodilation, edema, MAC
lectin pathway: triggered by microbe; use of mannose-binding lectin
alternative pathway: triggered by microbe; generates C3b

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36
Q

what is the outcome of all the complement pathways?

A

C3 is cleaved, C3a and C5a are released, C3b opsonin and C5a chemoattractant are also released, C5b-C9 form the MAC

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37
Q

what are kinin and role?

A

coagulation proteins made in the liver involved in pain signaling

38
Q

name kinins. what receptors do they act on?

A

bradykinin, prostaglandin, 5-HT, histamine. act on free nociceptor nerve ending

39
Q

what are prostaglandins made from?

A

plasma membrane component called arachidonic acid. made bvy enzyme COX-1

40
Q

what do anti-inflammatory drugs act on?

A

inhibit COX-1 and COX-2 or lipoxygonase

41
Q

most common anti-inflammatories

A

NSAIDs: aspirin and ibuprofen

42
Q

what do prostaglandins do?

A

cause vasodilation, inhibit platelet aggregation and increase vascular permeability

43
Q

name the chemokines receptors on leukocytes

A

CXCR, CCR

44
Q

what cytokines cause fever

A

IL-1, IL-6, TNF

45
Q

on what brain region do prostaglandin act to cause fever?

A

vasomotor center of the hypothalamus

46
Q

why do we have fever?

A

increased temperature speed up leukocyte migration and reduces virulency of microbes

47
Q

what effect can interleukins have on the liver?

A

induction of acute phase protein synthesis

48
Q

what effect do interleukins and TNF have on the bone marrow?

A

increase production of leukocytes in a prolonged immune response

49
Q

what is acute-phase reaction? what triggers it?

A

systemic reaction: fever, change in sleep, decreased appetite, decreased blood pressure, neutrophilia. triggered by IL-1 and TNF

50
Q

what are IL-1 and TNF endothelial effects?

A

increase adhesion molecules, increase coagulation

51
Q

what are IL-1 and TNF fibroblast effects?

A

increased fibroblast proliferation, increased collagen synthesis, increased collagenase

52
Q

what are IL-1 and TNF leukocyte effects?

A

increase cytokine secretion

53
Q

what is PAF and its effect?

A

platelet-activating factor: increase permeability, platelet aggregation, vasoconstriction, chemotaxis, GFs, clotting, fibrinogen

54
Q

what are nitric oxide’s effect?

A

released by macrophages, reduces adhesion, increases vasodilation

55
Q

where does the fluid escaped from vasculature during inflammation go after?

A

reabsorbed by lymphatic system

56
Q

which cells clean-up after inflammatory process?

A

macrophages

57
Q

4 things caused by acute inflammation

A

infarction, bacterial infections, toxins, trauma

58
Q

what are the features of acute inflammation?

A

vascular changes, increased permeability & vasodilation, increased expression of adhesion molecules, neutrophils recruitment, mediators

59
Q

what can cause scarred tissue after acute inflammation?

A

excess pus formation

60
Q

what are the causes of chronic inflammation

A

viral infections, chronic infections, persistent injury, autoimmune disease, progression from an acute inflammation

61
Q

what type of cells play an important role in chronic inflammation?

A

macrophages and lymphocytes

62
Q

what are features of chronic inflammation?

A

mononuclear cell infiltration (monocytes), angiogenesis, fibrosis

63
Q

what is the outcome of chronic inflammation?

A

scarred tissue

64
Q

what are classically vs alternatively activated macrophages involved in?

A

classically: microbial actions and inflammation
alternatively: tissue repair and anti-inflammatory effects

65
Q

explain the positive feedback loop involving macrophages and lymphocytes

A

macrophages release cytokines at the site of injury which activates lymphocytes, which in turn can release cytokines to activate macrophages

66
Q

in chronic inflammation, what causes tissue injury and fibrosis?

A

activated macrophages

67
Q

what effects does TNF-alpha have?

A

endothelial activation, angiogenesis, chondrocyte and osteoblast activation, prostaglandin formation, increase the release of proinflammatory cytokines

68
Q

what is a granuloma?

A

ball of lymphoid cells containing macrophages and a giant cell in the center and T cells and fibroblasts in the shell surrounding

69
Q

when are granulomas formed? what is their role?

A

when there is a foreign body that the immune system cannot get rid of during chronic inflammation.
to prevent the microbe from replicating and spreading in the rest of the body.

70
Q

what happens in the middle of a granuloma once the macrophages kill the bacteria?

A

caseous necrosis

71
Q

what cytokine promotes formation of granulomas?

A

IL-1

72
Q

what is serous inflammation?

A

blisters; it self resolves and doesn’t have fibrin

73
Q

in what disease is fibrinous inflammation often seen?

A

pneumonia

74
Q

why does fibrin develop in alveoli during pneumonia?

A

to trap the bacteria in the alveolus, preventing it from spreading

75
Q

in pneumonia, what cells lyse the fibrin strands trapping the bacteria?

A

macrophages

76
Q

what is an abscess? how does it resolve? what causes it?

A

a hole with liquefactive necrosis (pus made of white blood cells). usually heals but scarred tissue remains. caused by bacteria infection.

77
Q

what is an ulcer? what causes them?

A

erosion on the surface of the skin or organ. superficial caused by inadequate blood flow

78
Q

what is an example of membranous inflammation?

A

diphtheria infection in the back of the troat causing formation of a thick membrane which can impair breathing

79
Q

describe the 4 outcomes of inflammation

A
  1. resolution (usual)
  2. disharge of pus from excessive exudate and increased neutrophils
  3. chronic inflammation from persistent causal agent
  4. repair and organization (from excessive necrosis
80
Q

how does repair work?

A

Fibroblasts fill the site of injury and lay down connective tissue, forming a scar

81
Q

what is regeneration?

A

when the injured or dead cell can be replaced by a cell of the same type.

82
Q

what is a labile cell?

A

cell that is continuously cycling. constant turnover of cells like in the epidermis

83
Q

what is a stable cell? name an example

A

not in constant turnover, but there can be turnover if necessary, however, can’t fix extensive damage. ex: hepatocytes

84
Q

what is a permanent cell? give an example

A

cells that can’t be replaced when they die. ex: neurons: only axons can be regenerated or other neurons can grow to compensate for loss of innervation

85
Q

what is replacement?

A

when the damaged tissue cannot be repaired or regenerated

86
Q

what is healing by primary intension? what cells does it involve?

A

small wounds; leads to no scar or hairline scar.
macrophages, angiogenesis, endothelial precursor, fibroblasts (secrete collagen)

87
Q

what is healing by secondary intention?

A

A greater wound will cause the granulation of the tissue and will leave a larger scar

88
Q

what is granulation and how does it form?

A

new blood vessels and fibroblasts grow and secrete collagen and elastin fibres into granulation tissue.

89
Q

what is a keloid and how is it formed?

A

overactive collagen deposition

90
Q

what are differentiated myofibroblasts? in what process do they participate?

A

fibroblast precursor. is contractile. important for tissue remodelling ex wound contraction

PATH300 (10 decks)

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