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Inflammation I Flashcards

1
Q

what are the principal mediators of vasodilation

A
  1. histamine

2. prostaglandins

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2
Q

what are the principal mediators of increased vascular permeability

A
  1. histamine and serotonin
  2. C3a and C5a (liberate vasoactive amines from mast cells)
  3. leukotrienes C4, D4, E4
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3
Q

what are the principal mediators of chemotaxis, leukocyte recruitment and activation?

A
  1. TNF, IL-1
  2. chemokines
  3. C3a, C5a
  4. leukotriene B4
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4
Q

what are the principal mediators of fever?

A
  1. IL-1, TNF

2. prostaglandins

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5
Q

what are the principal mediators of pain

A
  1. prostaglandins

2. bradykinin

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6
Q

what are the principal mediators of tissue damage?

A
  1. lysosomal enzymes of leukocytes

2. ROS

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7
Q

what cells release histamine?

A
  1. mast cells
  2. basophils
  3. platelets
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8
Q

function of histamine

A

vasodilation, increased vascular permeability, endothelial activation

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9
Q

what cells release prostaglandins?

A
  1. mast cells

2. leukocytes

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10
Q

function of prostaglandins

A

vasodilation, pain, fever

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11
Q

what cells release leukotrienes?

A
  1. mast cells

2. leukocytes

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12
Q

function of leukotrienes

A

increased vascular permeability, chemotaxis, leukocyte adhesion and activation, primary for wheezing

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13
Q

what cells release cytokines like TNF, IL-1, IL-6

A
  1. macrophages
  2. endothelial cells
  3. mast cells
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14
Q

local function of cytokines

A

endothelial activation to express adhesion molecules

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15
Q

systemic function of cytokines

A

fever, metabolic abnormalities, hypotension, shock

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16
Q

what cells release PAF (platelet activating factor)

A
  1. leukocytes

2. mast cells

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17
Q

function of PAF

A

vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

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18
Q

what cells release chemokines?

A
  1. leukocytes

2. activated macrophages

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19
Q

function of chemokines

A

chemotaxis, leukocyte activation

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20
Q

what cells release complement?

A

plasma cells in the liver

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21
Q

function of complement

A

leukocyte chemotaxis and activation, direct target killing via MAC, vasodilation via mast cell stimulation

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22
Q

what cells release kinins?

A

plasma cells in the liver

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23
Q

function of kinins?

A

increased vascular permeability, smooth muscle contraction, vasodilation, pain

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24
Q

onset of acute inflammation

A

fast: minutes or hours

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25
cellular infiltrate associated with acute inflammation
neutrophils
26
what tissue injury or fibrosis is associated with acute inflammation?
usually mild and self-limited
27
what are the/ local and systemic signs of acute inflammation
usually prominent signs
28
onset of chronic inflammation
slow: days
29
cellular infiltrate associated with chronic inflammation
monocytes/macrophages/lymphocytes
30
what tissue injury or fibrosis is associated with chronic inflammation
severe and progressive injury/fibrosis
31
what are the local and systemic signs of chronic inflammation
less prominent signs
32
common causes of acute inflammation
1. infections 2. tissue necrosis from ischemia, trauma, physical/chemical injury 3. foreign bodies 4. immune or hypersensitivity reactions
33
what is the first step of inflammatory reaction
recognition of microbes and damaged cells
34
what are cellular mechanisms of recognition
1. TLR 2. cytosol receptors that recognize molecules that are released with cell damage 3. circulating proteins (complement)
35
what is the sequence of events in an inflammatory reaction?
macrophages and other cells in tissues recognize microbes and damaged cells. this liberates mediators that trigger vascular and cellular reactions of inflammation
36
cardinal 5 signs of inflammation
1. redness 2. swelling 3. heat 4. pain 5. loss of function
37
3 major local manifestations of acute inflammation
1. vascular dilation and increased blood flow (erythema and warmth) 2. extravasation and extravascular deposition of plasma fluid and proteins (edema) 3. leukocyte emigration and acumulation in the site of injury
38
what are the vascular changes in acute inflammation
1. vasodilation 2. increased permeability 3. stasis of blood flow 4. neutrophils marginate and adhere to endothelium and then migrate through vessel into the interstitium
39
describe the vasodilation that occurs with acute inflammation
transient constriction of arterioles may occur first, then dilation of arterioles and opening of capillary beds (retraction of endothelia due to histamine)
40
describe the impact of increased microvascular permeability
excess of interstitial fluid or cavity fluid (edema)
41
describe why vascular congestion occurs
loss of fluid into the intersitium and the increased diameter of the blood vessel leads to increased concentration of RBC in the vessel, increased viscosity and slower blood flow
42
what induces retraction of endothelial cells?
histamine and other mediators (
43
what are the 2 principal causes of increased vascular permeability?
1. retraction of endothelial cells (rapid and short lived) | 2. endothelial injury (rapid and longer lived)
44
what is exudate?
fluid leaking out of vessels that is high in protein and cellular content associated with acute inflammation and pus
45
what is transudate
fluid leaking out of vessel is low in protein and cellular content
46
what is transudate usually associated with
1. low serum albumin (low osmotic pull) | 2. increased hydrostatic pressure (heart failure)
47
what could cause increased hydrostatic pressure
venous outflow obstruction (congestive heart failure)
48
what could cause decreased colloid osmotic pressure
decreased protein synthesis due to liver disease or increased protein loss due to kidney disease
49
what is lymphangitis
inflammation of lymphatic vessels
50
what is lymphadenitis
inflammation of draining lymph node
51
what do lymphatics drain
they drain increased interstitial fluid that has accumulated due to increased vascular permeability
52
what cell types drain into lymph?
microbes, leukocytes, cellular debris
53
steps of extravasation
1. adhesion of leukocytes to vascular endothelium 2. transmigration across endothelium (diapedesis) 3. chemotaxis 4. leukocyte activation 5. phagocytosis
54
what mediates rolling of leukocyte
E selectin and P selectin
55
what activates integrins (ICAM) to tightly bind to rolling leukocyte
chemokines
56
what makes a stable adhesion between leukocytes and endothelial cell
ICAM-1
57
what mediates diapedesis?
PECAM-1
58
how does leukocyte rolling start?
redistribution of P selectin from within the endothelial cytoplasm to the cell surface induced by histamine and thrombin
59
what induces redistribution of P selectin
histamine and thrombin
60
what acitvates P selectin?
cytokines, histamines, thrombin
61
order of induction of rolling
1. redistribution of adhesion molecule P selectin 2. induction of adhesion molecule synthesis of E selectin and ligands for ICAM/VCAM 3. increase in binding affinity of leukocyte integrins
62
when does induction of adhesion molecule synthesis occur?
2-3 hours after induction
63
what induces adhesion molecule synthesis of E electin and ICAM/VCAM?
IL-1 | TNF
64
what increases binding affinity of leukocyte integrins?
chemokines
65
how do leukocytes migrate through endothelium?
leukocyte squeezes through endothelial gaps assisted by PECAM-1/CD31
66
how do leukocytes pierce the basement membrane?
secrete collagenases
67
what cells primarily transmigrate during acute inflammation
neutrophils
68
how does chemotaxis work
leukocytes move within tissue along increasing chemoattractant gradient toward site of injury
69
what are important exogenous chemotactic factors for neutrophils?
factors originating from source of inflammation like bacterial products like peptides with N formyl methionine terminal amino acid and lipids
70
what are endogenous chemotactic factors for neutrophils?
factors produced by the injured host
71
what are the important endogenous chemotactic factors?
1. complement (C5a) 2. leukotriene B4 (LTB4) 3. chemokines (IL-8)
72
how do chemoattractants induce leukocyte movement?
1. chemoattractant binds to specific receptor on leukocyte membrane 2. binding activates intracellular phospholipase C 3. phospholipase C causes increase in intracellular Ca within leukocyte 4. intracellular Ca triggers crosslinking of actin within focal area of leukocyte cytoskeleton 5. crosslinking makes a pseudopod form in the direction of the increasing density gradient of chemoattractant
73
how are leukocytes activated
1. recognition of offending agents which deliver signals that 2. activate the leukocytes to ingest and destroy the offending agents and 3. amplify inflammatory reaction
74
stimulation of leukocyte produces what responses? (4)
1. amplification of inflammatory reaction 2. degranulation and release of lysosomal enzymes 3. phagocytosis and activation of oxidative burst within leukocyte 4. increase in binding affinity of adhesion molecules
75
how do leukocytes amplify inflammatory reaction?
1. production of arachidonic acid metabolites by leukocyte | 2. secretion of cytokines by leukocyte
76
what is superoxide dismutase
makes ROS into hydrogen peroxide and water
77
how does extracellular release damage the host?
1. damage to endothelial cells causes increased vascular permeability 2. inactivation of antiproteases (like alpha 1 antitrypsin)
78
how does alpha 1 antitrypsin damage tissue
inactivation of alpha 1 antitrypsin leads to unopposed protease activity with increased tissue destruction
79
what is catalase
detoxifies hydrogen peroxide
80
what is ceruloplasmin
copper containing serum protein (carries copper)
81
what are the antioxidant mechanisms
1. superoxide dismutase 2. catalase 3 ceruloplasmin 4. iron free fraction of serum transferrin
82
what produces NO?
endothelial cells and macrophages
83
action of NO
1. potent vasodilator | 2. kills microorganisms
84
how does NO kill microorganisms
interacts with oxygen derived free radicals to produce antimicrobial substances which can kill microorganisms within macrophage phagolysosomes
85
what are neutrophils primary/azurophillic granules
1. myeloperoxidase (MPO) 2. bactericidal factors (lysozyme, defensins) 3. acid hydrolases 4. neutral proteases (elastase, collagenases, proteinases)
86
what are neutrophil's secondary/specific granules
1. lysozyme 2. collagenase 3. gelatinase 4. lactoferrin 5. plasminogen activator 6. histaminase 7. alkaline phosphatase
87
what are monocytes/macrophages lysosomal constituents?
1. acid hydrolase 2. collagenase 3. elastase 4. phospholipase 5. plasminogen activator
88
what holds extracellular release of lysosomal enzymes in check?
antiproteases like alpha-1-antitrypsin and alpha2 macroglobulin
89
what are NETS
fibrillary networks containing antimicrobial substances produced by neutrophils
90
what do NETS fibrillary network consist of?
1. nuclear chromatin | 2. contents of cytoplasmic granules (antimicrobial proteins and enzymes)
91
where are inflammatory mediators derived?
cells or plasma proteins in response to various stimuli like substances from microbes and necrotic cells, complement and other proteins

MFMII (29 decks)

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