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acute inflammation Flashcards

1
Q

Why does redness occur in acute inflammation?

A

Vessels are dilated

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2
Q

Why does osmotic pressure in capillaries decrease during acute inflammation?

A

Increased hydrostatic pressure means more fluid and proteins forced out and venular permeability is increased and gradient for reabsorption is reduced

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3
Q

Where is histamine produced in

A

Mast cells
Basophils
Platelets

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4
Q

What type of genetic condition is hereditory angioedema

A

Autosomal dominant

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5
Q

what type of genetic condition is alpha antitrypsin deficiency

A

Autosomal recessive

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6
Q

What stimulates increased selectin expression by endothelial cells in neutrophil extravasation

A

IL-1
TNF

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7
Q

What stimulates diapedesis (extravasation)?

A

C3a
Leukotriene B4
Bacterial peptides

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8
Q

What opsonins does neutrophils coat pathogens in

A

C3b and IgG

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9
Q

What occurs to arterioles in vascular phase of acute inflammation

A

Transient vasoconstriction and vasodilatation

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10
Q

What occurs in vascular phase of acute inflammation

A

Changes in blood flow - increased

Movement of fluid into tissue

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11
Q

What occurs in the cellular phase of acute inflammation

A

Infiltration of inflammatory cells

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12
Q

What occurs in suppuration

A

formation of pus

becomes walled off and abscess forms

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13
Q

What occurs in resolution of acute inflammation

A

mediators have short half lives and degrade
exudate drains into lymphatics
fibrin broken down by thrombolytic process

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14
Q

What occurs in oxygen-dependant killing mechanisms with neutrophils

A

Oxygen free radicals released into phagosome

Hypochlorite produced

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15
Q

What occurs in chronic granulomatous disease

A

neutrophil unable to generate free radicals superoxide hence cannot kill bacteria

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16
Q

What mediates structural re-organisation of cytoskeleton in vascular leakage

A

IL-1
TNF

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17
Q

What mediates endothelial cell contraction in vascular leakage

A

Histamines
C5a
NO(nitric oxide)

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18
Q

What is VEGF(Vascular endothelial growth factor)

A

Signalling protein that promotes growth of new vessels

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19
Q

What is vascular stasis

A

Blood becoming more viscous due to increased concentration of red cells in vessels

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20
Q

What is transudate fluid

A

low protein content fluid

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21
Q

What is transcytosis

A

molecules captured in vesicles at one side and ejected at other side

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22
Q

What is the role of exudation of fluid in acute inflammation

A

Dilute toxins and reduce impact

deliver plasma proteins, IGs and mediators to injure site

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23
Q

What is the role of chemical meditators

A

Modulate inflammatory response

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24
Q

process for neutrophil extravasation

A

Neutrophil line up along endothelium (margination)
Roll along endothelium (rolling)
Stick to endothelium (adhesion)
Emigrate through endothelium (diapedesis)

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25
Q

process for neutrophil extravasation

A

Neutrophil line up along endothelium (margination)
Roll along endothelium (rolling)
Stick to endothelium (adhesion)
Emigrate through endothelium (diapedesis)

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26
Q

What is the oxygen independant killing mechanism of neutrophils

A

Enzymes such as lysozymes and proteases from neutrophil granules form holes in microbes

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27
Q

What is the deficiency in hereditory angioedema

A

C1 esterase inhibitor

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28
Q

What is the complement system activated by(4)

A

proteolytic enzymes from necrotic cells
antigen-antibody complexes
gram negative bacteria
products of kinin and fibrinolytic systems

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29
Q

What is the apperance of purulent exudate

A

thick, opaque drainage that is tan, yellow, green, or brown

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30
Q

What is starling’s law in relation to capillaries

A

Movement of fluid across vessel wall due to balance between hydrostatic and osmotic pressure between intravascular and extravascular space

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31
Q

What is serous exudate

A

clear, thin, watery plasma drainage

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32
Q

What is sequence after acute inflammation

A

resolution of inflammation
Suppuration (excess exudate formation)
chronic inflammation
death

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33
Q

What is purulent exudate

A

inflammatory exudate with a high concentration of leukocytes - predominantly neutrophils

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34
Q

What is indirect endothelial cell injury

A

Damage to endothelial cell as a side effect of another action
Reactive oxygen species production
Proteolytic enzymes released from neutrophils

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35
Q

What is haemorrhagic exudate

A

drainage of a thin, watery, pink coloured fluid composed of blood and serum.

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36
Q

What is fibrinous exudate

A

exudate containing large amount of fibrinogen and fibrin

37
Q

What is exudate fluid

A

high protein content fluid

38
Q

What is expressed by neutrophils during adhesion phase of neutrophil extravastion

A

integrins

39
Q

What is expressed by endothelial cells during the rolling phase of neutrophil extravasation

A

Selectins

40
Q

What is direct endothelial cell injury

A

Injury due to trauma,chemicals of toxins released from microbes

41
Q

What is chemotaxis

A

movement along concentration gradients

42
Q

What is bradykinin produced from

A

Plasma precursor kininogen

43
Q

What is an example of a vasoactive peptide

A

bradykinin

44
Q

What is alpha antitrypsin

A

Protease inhibitor which deactivates enzymes released from neutrophils during inflammation

45
Q

What is acute inflammation

A

Protective rapid response of living tissue to injury

46
Q

What increases expression of integrin production by neutrophils

A

C5a
LTB4
IL-1
TNF

47
Q

What does oedema elicit in acute inflammation

A

Increased lymphatic drainage

deliver antigen to immune system

48
Q

What does exudation of fluid deliver to area of injury

A

Plasma proteins
immunoglobulins
inflammatory mediators

49
Q

What do selectins expressed by endothelial cells in neutrophil extravasation bind to

A

Carbohydrate ligands on neutrophils

50
Q

What do pyrogenic cytokines act on

A

Anterior hypothalamus

51
Q

what do integrin expressed by neutrophils during adhesion phase of neutrophil extravasation bind to

A

integrin ligands on endothelium

52
Q

What cytokines accelerate release of leucocytes from bone marrow

A

IL-1
TNFa

53
Q

What cell is serotonin produced from

A

Platelets

54
Q

What can trigger pyrexia in acute inflammation

A

Bacterial endotoxins
pyrogenic cytokines

55
Q

What can cause acute inflammation(4)

A

Microbial infections
physical and chemical agents
tissue necrosis
hypersensitivity reactions

56
Q

What are the types of exudate(4)

A

Purulent
Haemorrhagic
serous
fibrinous

57
Q

What are the mechanisms of vascular leakage in vascular phase of acute inflammation

A

Endothelial cell contraction
Endothelial cell injury
structural re-organisation of cytoskeleton
Transcytosis

58
Q

What are the hallmarks of acute inflammation

A

Exudate of fluid

Infiltrate of cells

59
Q

What are the clinical signs of acute inflammation

A

Redness - rubor
swelling - tumor
heat - calor
pain - dolor
loss of function

60
Q

What are the 4 main systemic effects of acute inflammation

A

pyrexia
leucocytosis
acute phase response in liver
Shock

61
Q

What are the 3 enzymatic cascade systems used to produce endogenous inflammatory mediators

A

Coagulation system
Kinin system
Complement system

62
Q

What are the 2 types of endothelial cell injury

A

Direct
indirect

63
Q

What are the 2 phases in acute inflammation

A

Vascular and cellular phase

64
Q

What are the 2 different killing mechanisms of neutrophils

A

Oxygen dependent and oxygen-indepedent

65
Q

What are the 2 categories of extravascular fluid

A

Transudate
Exudate

66
Q

What are some features of acute inflammation

A

Immediate
short duration
innate immune system involved

67
Q

What are some examples of vasoactive amines

A

Histamine
Serotonin

68
Q

What are some examples of pyrogenic cytokines

A

IL-2
TNF

69
Q

What are some examples of local complications that can occur in acute inflammtion

A

Swelling
Inappropriate inflammation
Exudation of fluid
Loss of fluid
Prolonged pain and loss of function
Digestion of host tissue by enzymes released by neutrophils

70
Q

What are some clinical features of acute inflammation(3)

A

Involves vascular and cellular reactions

controlled by chemical mediators that are inactive

It is a protective mechanism that can lead to complications

71
Q

What are some acute phase proteins produced during acute phase response in liver

A

Fibrinogen
CRP (C-reactive protein)
Alpha 1 antitrypsin

72
Q

What are prostaglandins produced from

A

Phospholipids by cyclo-oxygenase

73
Q

What are MMP’s

A

Matrix metallopeptidases
degrade both matrix and non-matrix proteins

74
Q

What are leukotrienes

A

family of eicosanoid inflammatory mediators produced by leukocytes

75
Q

What are leukotrienes

A

family of eicosanoid inflammatory mediators produced by leukocytes

76
Q

What are features of chemical mediators

A

Short lived

Can be endogenous or exogenous

has an inhibitor

77
Q

What are examples of endogenous chemical mediators

A

Vasoactive amines
Vasoactive peptides
Chemokines
Arachidonic acid metabolites
Nitric oxide

78
Q

What are examples of arachidonic acid metabolites

A

Prostaglandins
Leukotrienes

79
Q

How is hydrostatic pressure increased in capillaries in acute inflammation

A

Arteriolar dilation

80
Q

How does vasodilation combat injury in acute inflammation

A

Increases delivery and temperature

81
Q

How does pain and loss of function combat injury in acute inflammation

A

Enforces rest and reduce chance of further injury

82
Q

How does infiltration of inflammatory cells combat injury

A

Remove pathogenic organisms and necrotic debris

83
Q

How does body stimulate leucocytosis

A

macrophages and endothelial cells release colony stimulating factors so bone marrow produces more leucocytes

84
Q

How does blood flow change in vascular phase of acute inflammation

A

Transient vasoconstriction of arterioles
Vasodilation of arterioles to increase blood flow
Increased vascular permeability
Vascular stasis

85
Q

How do pyrogenic cytokines cause pyrexia

A

Increase synthesis of prostaglandin E2

86
Q

How do neutrophils escape from vessels

A

Intracellular junctions relax
Collagenase released and breaks down capillary basement membrane
MT-MMP and MMP produced

87
Q

what does the complement cascade generate?

A

C3 - functions as opsonin

c5a - attracts neutrophils

c5-9 complex - attach to cell cause lysis

88
Q

examples of anti-inflammatories

A

aspirin/NSAIDs

antihistamines

TNF alpha antagonists - infliximab

corticosteroids

MoD (8 decks)

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