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acute inflammation Flashcards

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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
process for neutrophil extravasation
Neutrophil line up along endothelium (margination) Roll along endothelium (rolling) Stick to endothelium (adhesion) Emigrate through endothelium (diapedesis)
26
What is the oxygen independant killing mechanism of neutrophils
Enzymes such as lysozymes and proteases from neutrophil granules form holes in microbes
27
What is the deficiency in hereditory angioedema
C1 esterase inhibitor
28
What is the complement system activated by(4)
proteolytic enzymes from necrotic cells antigen-antibody complexes gram negative bacteria products of kinin and fibrinolytic systems
29
What is the apperance of purulent exudate
thick, opaque drainage that is tan, yellow, green, or brown
30
What is starling's law in relation to capillaries
Movement of fluid across vessel wall due to balance between hydrostatic and osmotic pressure between intravascular and extravascular space
31
What is serous exudate
clear, thin, watery plasma drainage
32
What is sequence after acute inflammation
resolution of inflammation Suppuration (excess exudate formation) chronic inflammation death
33
What is purulent exudate
inflammatory exudate with a high concentration of leukocytes - predominantly neutrophils
34
What is indirect endothelial cell injury
Damage to endothelial cell as a side effect of another action Reactive oxygen species production Proteolytic enzymes released from neutrophils
35
What is haemorrhagic exudate
drainage of a thin, watery, pink coloured fluid composed of blood and serum.
36
What is fibrinous exudate
exudate containing large amount of fibrinogen and fibrin
37
What is exudate fluid
high protein content fluid
38
What is expressed by neutrophils during adhesion phase of neutrophil extravastion
integrins
39
What is expressed by endothelial cells during the rolling phase of neutrophil extravasation
Selectins
40
What is direct endothelial cell injury
Injury due to trauma,chemicals of toxins released from microbes
41
What is chemotaxis
movement along concentration gradients
42
What is bradykinin produced from
Plasma precursor kininogen
43
What is an example of a vasoactive peptide
bradykinin
44
What is alpha antitrypsin
Protease inhibitor which deactivates enzymes released from neutrophils during inflammation
45
What is acute inflammation
Protective rapid response of living tissue to injury
46
What increases expression of integrin production by neutrophils
C5a LTB4 IL-1 TNF
47
What does oedema elicit in acute inflammation
Increased lymphatic drainage deliver antigen to immune system
48
What does exudation of fluid deliver to area of injury
Plasma proteins immunoglobulins inflammatory mediators
49
What do selectins expressed by endothelial cells in neutrophil extravasation bind to
Carbohydrate ligands on neutrophils
50
What do pyrogenic cytokines act on
Anterior hypothalamus
51
what do integrin expressed by neutrophils during adhesion phase of neutrophil extravasation bind to
integrin ligands on endothelium
52
What cytokines accelerate release of leucocytes from bone marrow
IL-1 TNFa
53
What cell is serotonin produced from
Platelets
54
What can trigger pyrexia in acute inflammation
Bacterial endotoxins pyrogenic cytokines
55
What can cause acute inflammation(4)
Microbial infections physical and chemical agents tissue necrosis hypersensitivity reactions
56
What are the types of exudate(4)
Purulent Haemorrhagic serous fibrinous
57
What are the mechanisms of vascular leakage in vascular phase of acute inflammation
Endothelial cell contraction Endothelial cell injury structural re-organisation of cytoskeleton Transcytosis
58
What are the hallmarks of acute inflammation
Exudate of fluid Infiltrate of cells
59
What are the clinical signs of acute inflammation
Redness - rubor swelling - tumor heat - calor pain - dolor loss of function
60
What are the 4 main systemic effects of acute inflammation
pyrexia leucocytosis acute phase response in liver Shock
61
What are the 3 enzymatic cascade systems used to produce endogenous inflammatory mediators
Coagulation system Kinin system Complement system
62
What are the 2 types of endothelial cell injury
Direct indirect
63
What are the 2 phases in acute inflammation
Vascular and cellular phase
64
What are the 2 different killing mechanisms of neutrophils
Oxygen dependent and oxygen-indepedent
65
What are the 2 categories of extravascular fluid
Transudate Exudate
66
What are some features of acute inflammation
Immediate short duration innate immune system involved
67
What are some examples of vasoactive amines
Histamine Serotonin
68
What are some examples of pyrogenic cytokines
IL-2 TNF
69
What are some examples of local complications that can occur in acute inflammtion
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
What are some clinical features of acute inflammation(3)
Involves vascular and cellular reactions controlled by chemical mediators that are inactive It is a protective mechanism that can lead to complications
71
What are some acute phase proteins produced during acute phase response in liver
Fibrinogen CRP (C-reactive protein) Alpha 1 antitrypsin
72
What are prostaglandins produced from
Phospholipids by cyclo-oxygenase
73
What are MMP's
Matrix metallopeptidases degrade both matrix and non-matrix proteins
74
What are leukotrienes
family of eicosanoid inflammatory mediators produced by leukocytes
75
What are leukotrienes
family of eicosanoid inflammatory mediators produced by leukocytes
76
What are features of chemical mediators
Short lived Can be endogenous or exogenous has an inhibitor
77
What are examples of endogenous chemical mediators
Vasoactive amines Vasoactive peptides Chemokines Arachidonic acid metabolites Nitric oxide
78
What are examples of arachidonic acid metabolites
Prostaglandins Leukotrienes
79
How is hydrostatic pressure increased in capillaries in acute inflammation
Arteriolar dilation
80
How does vasodilation combat injury in acute inflammation
Increases delivery and temperature
81
How does pain and loss of function combat injury in acute inflammation
Enforces rest and reduce chance of further injury
82
How does infiltration of inflammatory cells combat injury
Remove pathogenic organisms and necrotic debris
83
How does body stimulate leucocytosis
macrophages and endothelial cells release colony stimulating factors so bone marrow produces more leucocytes
84
How does blood flow change in vascular phase of acute inflammation
Transient vasoconstriction of arterioles Vasodilation of arterioles to increase blood flow Increased vascular permeability Vascular stasis
85
How do pyrogenic cytokines cause pyrexia
Increase synthesis of prostaglandin E2
86
How do neutrophils escape from vessels
Intracellular junctions relax Collagenase released and breaks down capillary basement membrane MT-MMP and MMP produced
87
what does the complement cascade generate?
C3 - functions as opsonin c5a - attracts neutrophils c5-9 complex - attach to cell cause lysis
88
examples of anti-inflammatories
aspirin/NSAIDs antihistamines TNF alpha antagonists - infliximab corticosteroids

MoD (8 decks)

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