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Cells to systems > Lecture 11 - acute inflammation > Flashcards

Lecture 11 - acute inflammation Flashcards

1
Q

What is Rubor

A

Redness, Vessel dilation and increased blood flow

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2
Q

What is Calor

A

Heat, Vessel dilation and increased blood flow

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3
Q

What is tumor

A

Tumor (Swelling)

– Accumulation of exudate fluid

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4
Q

What is Dolor

A

Dolor (Pain)
– Chemical mediators,
– Pressure on nerve endings

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5
Q

What are the cardinal signs of inflammation

A
  • Rubor
  • Calor
  • Tumor
  • Dolor
  • Functio Laesa
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6
Q

Whatis functio Laesa

A

Loss of function

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7
Q

What are the inflammatory mediators

A

Autacoids
Eicosanoids
Cytokines

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8
Q

What are Autocoid

A

(fast, short-acting, hormone-like factors)
• Histamine
• Bradykinin
• Substance P

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9
Q

What is eicosanoid

A

(arachidonic acid metabolites)
• Prostaglandins
• Leukotrienes

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10
Q

What is cytokines

A

(cell-signalling molecules)
• Tumour-necrosis factor (TNF)
• IL-1

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11
Q

Where is histamine released?

A

Mostly released from mast cells (also basophils)

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12
Q

What stimulate histamine release?

A

Wide range of stimuli for release: heat, cold, trauma, IgE

antibodies, cytokines, bacterial components, nerve signalling…

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13
Q

What are histamine

A

autocoids

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14
Q

What are bradykinin

A

autocoids

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15
Q

What substance P

A

autocoids

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16
Q

What are prostagladins

A

eicosanoids

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17
Q

What are Leukotrienes

A

eicosanoids

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18
Q

What are Tumour-necrosis factor (TNF)

A

cytokines

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19
Q

What are IL-1

A

cytokines

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20
Q

What are the effects of autacoid

A

• Vasodilation (reddening/hyperaemia)
• Increased vascular permeability (swelling/oedema)
• Pain/itching
Other effects:
• Histamine and bradykinin causes bronchoconstriction
• Histamine causes increased mucus secretion
• Substance P activates leukocytes

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21
Q

What are effects of eicosanoids

A 
Metabolites of arachidonic acid from cell membrane
Synthesized on demand, slower action
Two major types:
• Prostaglandins
• Leukotrienes
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22
Q

What are prostagladins

A

Eicosanoids

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23
Q

What are the inflammtory prostagladins

A

Prostaglandin D2
(PGD2)
Prostaglandin E2
(PGE2)

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24
Q

What produce prostagladin D2

A

mast cells

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25
Q

What are the effect of prostagladin D2

A

Causes vasodilation and increased vascular permeability

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26
Q

What are the effects of prostagladin E2 (PGE2)

A

Causes vasodilation and increased vascular permeability

• Also causes pain and fever

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27
Q

What produces prostagladins E2 (PGE2)

A

Produced by epithelium, fibroblasts and smooth muscle

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28
Q

What are the coagulation mediators

A

– Prostacyclin (PGI2
)
– Thromboxane A2 (TxA2
)

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29
Q

What are the effects of prostacyclin (PGI2)

A

Vasodilation and prevention of coagulation

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30
Q

What are the effects of thromboxane A2 (TxA2)

A

Vasoconstriction and promotion of coagulation

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31
Q

What are prostagladins synthesized by

A

arachidonic acid by cyclooxygenase 2 (COX-2)

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32
Q

What does cyclooxygenase 1 regulate

A

many important physiological effects

• Renal and gastrointestinal homeostasis

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33
Q

What synthesized leukotrienes

A

arachidonic acid by lipoxygenases (LOX)

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34
Q

What are the leukotrienes

A

Leukotriene B4
Leukotrienes C4
, D4 and E4

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35
Q

What produces leukotriene B4

A

– Produced by neutrophils

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36
Q

What are the effects of leukotriene B4

A

Attracts and activates neutrophils

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37
Q

What are the effects of C4, D4, E4

A

– Cause vasoconstriction and increased vascular permeability

– Cause bronchoconstriction

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38
Q

What produces leukotrienes C4, D4 and E4

A

mast cells and eosinophils

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39
Q

What is does corticosteroids do

A

inhibits the production of arachidonic acid, blocks phospholipid A

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40
Q

What is the function of non-steroidal antiinflammatories

A

prevents the production of prostagladin H2, blocks cyclooxgenases (COX)

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41
Q

What is the function of lipooxygenase

A

prevent the production of leukotriene A4, blocks LOX

42
Q

What happens during the acute-phase cytokines

A

Mediators of inflammation secreted by leukocytes

43
Q

What mediators of inflammation are secreted by leukocytes

A
  • Tumour necrosis factor (TNF)

* Interleukin 1 (IL-1)

44
Q

What are tumour necrosis factor (TNF) produced by

A

Produced by leukocytes (especially macrophages)

45
Q

What aree interleukin 1 (IL-1) produced by

A

leukocytes (especially macrophages) and epithelial cells

46
Q

Wjhat are the effects of the Mediators of inflammation secreted by leukocytes

A
  • Increase vascular permeability
  • Promote leukocyte release and activation
  • Promote leukocyte extravasation
  • Increase production of inflammatory mediators (autacoids, eicosanoids)
  • Induce fever
  • Promote coagulation
47
Q

What are the key response from acute inflammatory

A
  1. Vasodilation
  2. Increased vascular permeability
  3. Emigration of leukocytes
48
Q

What is vasodilation mediated by

A 
• Autacoids (histamine/bradykinin)
• Prostaglandins (PGD2
, PGE2
, PGI2
)
• Nitric oxide
49
Q

What are the effects of vasodilation

A

Perfuses tissue with inflammatory mediators and leukocytes

• Slows blood flow to allow leukocyte margination

50
Q

What causes Increased vascular permeability during accute inflammation

A

Leaking due to disruption of endothelial barrie

51
Q

What does vacular permeability do

A

Allows release of plasma proteins and leukocytes from blood vessels

52
Q

What mechanism does vascular permeability have

A

Endothelial cell retraction

Endothelial injury

53
Q

What does endothelial cell retraction do

A

– Increased intercellular gaps mostly in venules
– Immediate response due to histamine
– Delayed (approx. 2-8 hours) due to eicosanoids, bradykinin,
complement and cytokines

54
Q

What happens when there is endothelial injury

A

– Damage leads to prolonged leakage until repair

– Can result from initial injury or damage by leukocytes

55
Q

What are the effects of increased vascular permeability

A
  • Transudate
  • Modified transudate
  • Exudate
56
Q

What does the fluid produced depend on

A

degree of

permeability

57
Q

What is the effect of transudate

A

– Mild increase in permeability for fluid only
– Low protein, few cells
– Often non-inflammatory (eg. heart failure)

58
Q

What is the effect of modified transudate

A

– Moderate increase in permeability
– Leakage of fluid and protein
– Higher protein, but still few cells

59
Q

What are the effect of exudate

A

– Large increase in permeability
– Leakage of fluid and protein with cell migration
– High protein, many cells
– Typically inflammatory

60
Q

What are the steps for emigration of leukocytes

A
  1. Endothelial activation
  2. Leukocyte rolling
  3. Adhesion
  4. Transmigration
61
Q

What is Endothelial activation in emigration of leukocytes

A
  • Expression of adhesion molecules (selectins, integrins)

* Induced by TNF, IL-1, tissue damage

62
Q

What does leukocyte rolling do

A
  • Allows loose attachment of leukocytes via selectins

* Gradual slowing of leukocyte

63
Q

What does adhesion of leukocyte do

A

Firm attachment via integrins

64
Q

What does transmigration do

A
  • Migration (chemotaxis) between endothelial cells into interstitium
  • Attracted by chemical signals (chemokines)
65
Q

What in an exudate

A

Fluid
Plasma proteins
Leukocytes

66
Q

What are in the fluid in an exudate

A
  • Water containing mixture of salts to dilute toxins and pathogens
  • Drains via lymphatics and lymph nodes for immune surveillance
67
Q

What plasma proteins are in an exudate

A

• Inflammatory mediators and antimicrobial molecules
• Antibodies
• Clotting factors
• Fibrin
– Formed from circulating precursor protein, fibrinogen
– Polymerises via blood coagulation cascade
– Forms clot composed of filamentous, insoluble protein
– Meshwork blocks migration of bacteria and aids migration of leukocytes

68
Q

What leukocytes are in an exudate

A
  • Neutrophils

* Other leukocytes

69
Q

What the role of neutrophil in an exudate

A

Neutrophils
– First-line immune defence
– Phagocytose and degrade foreign material
– Produce enzymes, free radicals, cytokines and other inflammatory
mediators

70
Q

What is the role of other leukocyte in an exudate

A

• Other leukocytes

– Sometimes macrophages and lymphocytes (chronic changes)

71
Q

What is does the classification of acute inflammation, serous mean

A

– Least severe; mild inflammation
– Only water and low MW solutes pass out of plasma
– Formation of transudate

72
Q

What is does the classification of acute inflammation, catarrhal mean

A

– Exudate formed on mucosal surfaces
– Hypersecretion of mucus intermixed with serous fluid
plus cell debris and inflammatory cells

73
Q

What is does the classification of acute inflammation, fibrinous mean

A

Fibrinous
– Leakage of fibrin from vessels
– Fibrinogen converted to fibrin
– Yellow gel which gradually becomes more solid over time
– Typically coats serosal or mucosal surfaces
– ‘Ground glass’ (mild) or ‘bread and butter’ appearance

74
Q

What is does the classification of acute inflammation, suppurative mean

A

– Purulent exudate (pus)
– Contains
• Large numbers of neutrophils
• Dead cell debris

75
Q

What is does the classification of acute inflammation, Abscess mean

A

– Localised collection of pus caused by suppurative inflammation
– Response to pyogenic bacteria
– Confined by wall of fibrous tissue when chronic

76
Q

What is does the classification of acute inflammation, phlegmon

A

– Spreading diffuse suppurative inflammation
– Within loose connective tissue
– Margins poorly defined
– In soft tissue referred to as cellulitis

77
Q

What is does the classification of acute inflammation, Empyema mean

A

Accumulation of pus within a body cavity

78
Q

What are the other features of inflammation

A

Pain, itch, Fever (pyrexia; febrile response)

79
Q

What do pain usually caused by?

A

– Damage/injury to peripheral nerve endings
– Effect of inflammatory mediators on nerve endings (nociceptors)
– Pressure on nerve endings from tissue swelling

80
Q

What caused Heightened pain sensitivity in inflammation

A

– Hypersensitivity of nerve endings
– Amplification of pain pathways in the spinal cord
– Caused by mediators such as prostaglandin E2
, IL-1b

81
Q

What is neurogenic inflammation

A

– Inflammatory mediators such as substance P released from

nerve endings

82
Q

What does itch usually accompanied with?

A

local skin inflammation

83
Q

What does itch usually caused by

A

– Effect of inflammatory mediators on nerve endings
(puriceptors)
• e.g. histamine, serotonin, prostaglandins
– Substance P releases histamine from mast cells

84
Q

Where does Unmyelinated nerve fibers for itch and pain originate from

A

in the skin

85
Q

What is the purpose of Fever (pyrexia; febrile response)

A

– Increases motility of leukocytes, phagocytosis
– Increases proliferation of T cells
– Impairs growth of temperature-sensitive pathogens

86
Q

What is the mechanism behind Fever (pyrexia; febrile response)

A

– Induced by pyrogens
• Endogenous: cytokines, such as interleukin 1 (α and β), IL-6, TNF-α
• Exogenous: e.g. bacterial toxin, lipopolysaccharide (endotoxin)
– Pyrogen causes a release of PGE2
– PGE2 acts on the hypothalamus in the brain:
• Increases physiological “thermostat”
• Results in systemic responses to increase temperature
– Shivering
– Peripheral vasoconstriction

87
Q

What is fever pyrexia induced by?

A
  • Endogenous: cytokines, such as interleukin 1 (α and β), IL-6, TNF-α
  • Exogenous: e.g. bacterial toxin, lipopolysaccharide (endotoxin)
88
Q

What does pyrogen cause

A

release of PGE2

89
Q

What does PGE2 do?

A 
acts on the hypothalamus in the brain:
• Increases physiological “thermostat”
• Results in systemic responses to increase temperature
– Shivering
– Peripheral vasoconstriction
90
Q

What is the resolution of inflammation

A

• Reduced stimulus for leukocyte migration
• Apoptosis of neutrophils in tissue
• Lipoxins
– Alternative arachidonic acid metabolism
– “Stop signal” to suppress neutrophil activity
• Anti-inflammatory cytokines
– IL-10 from regulatory T cells
– TGF-β from anti-inflammatory macrophages

91
Q

What is the ideal outcome of acute inflammation

A

Resolution (ideal outcome)
• Damaged area replaced by organised tissue with
normal structure and function

92
Q

What are the outcome of acute inflammation

A

Resolution
Fibrous repair
Chronic inflammation

93
Q

What is Fibrous repair outcome

A

Scar tissue, • Tissue architecture destroyed; original cell types
cannot re-grow
• Usual response to substantial tissue damage (nonspecialised)

94
Q

What is a chronic inflammation

A
  • Damaging agent and tissue destruction persists
  • Ongoing attempts to heal by fibrous repair
  • Ongoing immune responses
95
Q

Which one is mostly responsible for asthma

A

leukotrienes

96
Q

What is the difference between selectins and integrins

A

Selectin specialise in sticky and not sticky attachment. Where integrins specialises in firm attachment to the endothelial

97
Q

What causes Septic shock and multiple organ dysfunction from inflammation

A

Coagulopathies
Haemodynamic disturbances
Tissue damage

98
Q

What Pro-inflammatory
cytokines: IL-1, TNF
Eicosanoids: PGE2
, PGI2 do

A

Endothelial activation

Leukocyte activation

99
Q

What is inflammation

A

The body’s response to infection, irritation or injury

100
Q

What is acute inflammation

A
  • Rapid response to injury, onset in seconds to minutes

* Non-specific response – innate immune mechanisms

101
Q

What is the function of inflammation

A

– Delivery of biological mediators and leukocytes to site of inflammation
– Destruction of pathogens
– Breakdown and removal of damaged tissue and debris

Cells to systems (25 decks)

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