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Body Defence > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is inflammation?

A

A complex reaction of vascularised connective tissue to local injury

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2
Q

What are the purposes of inflammation? (3)

A

1) Contain/isolate injurious stimulus
2) Destroy/dilute/wall off agents to neutralise toxins
1 + 2 = LIMIT DAMAGE
3) Repair damage caused

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3
Q

What is inflammation classified according to?

A

Time course

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4
Q

What are the two types of inflammation?

A
  • Chronic

- Acute

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5
Q

What is acute inflammation?

A

Inflammation of relatively short duration. Quick response

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6
Q

What is chronic inflammation?

A

Inflammation of relatively long duration

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7
Q

What does acute inflammation response time depend on? (2)

A
  • Pathogen causing injury

- Body ability to respond to injury

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8
Q

What are the two parts that make up the name given to an infection?

A
  • Name of organ/tissue

- Suffix “itis”

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9
Q

What are the 5 signs of acute inflammation?

A
  • Heat
  • Redness
  • Swelling
  • Pain
  • Loss of function
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10
Q

What is heat and redness caused by in acute inflammation?

A

Hyperaemia (increased blood flow)

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11
Q

What is swelling caused by in acute inflammation?

A

Increased amount of fluid in tissue (exudate)

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12
Q

What 2 things is pain caused by in acute inflammation?

A
  • Neural damage

- Chemical mediators e.g across gland

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13
Q

Why is pain important in acute inflammation?

A

For awareness of event

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14
Q

What can loss of function be caused by in acute inflammation?

A

Pain

-

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15
Q

What does loss of function be caused in acute inflammation depend on?

A

Specific part affected by inflammation e.g reduced mobility in joint

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16
Q

What are the 3 processes an injury triggers in acute inflammation?

A
  • Vascular changes
  • Cellular events
  • Chemical mediators
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17
Q

What is the first immediate vascular reaction in acute inflammation?

A

Rapid transient vasoconstriction of arterioles to reduce blood flow

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18
Q

Why is there an initial rapid transient vasoconstriction of arterioles to limit blood flow in acute inflammation?

A

Limit pathogenic spread

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19
Q

What is the change in vascular calibre after the initial transient vasoconstriction in acute inflammation?

A

Vasodilation to increase blood flow to capillaries

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20
Q

What activates the vasodilation after initial transient vasoconstriction in acute inflammation?

A

Chemical mediators activated
Causes damaged tissues releasing INF and interleukins
- Nitric oxide released
- Dilates vessels

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21
Q

What activates the vasodilation after initial transient vasoconstriction in acute inflammation? (4)

A
  • Chemical mediators activated
  • Causes damaged tissues releasing INF and interleukins
  • Nitric oxide released
  • Dilates vessels
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22
Q

Why is there vasodilation after initial transient vasoconstriction in acute inflammation? (2)

A
  • Dilute pathogenic agent

- Increases WBCS locally

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23
Q

What changes occur in vascular calibre during acute inflammation?

A

Rapid transient vasoconstriction of arterioles followed by vasodilation

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24
Q

What changes occur in blood flow during acute inflammation?

A

Initial reduction of blood flow followed by increased blood flow to capillaries

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25
Q

What changes occur in vascular permeability during acute inflammation?

A

Increased permeability of microvasculature

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26
Q

What is the purpose of increased permeability of microvasculature during acute inflammation? (4)

A
  • Blood vessels leak fluid and protein
  • Losing protein reduces oncotic pressure in vessels
  • Favours fluid movement to interstitium
  • Allows migration of WBCs from vessel to interstitium
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27
Q

What is exudate? (3)

A
  • Protein rich fluid from plasma (similar protein levels)
  • Inflammatory
  • Extravascular
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28
Q

What is tissue swelling/oedema caused by in acute inflammation? (3)

A
  • Increased hydrostatic pressure
  • Decreased osmotic gradient
  • Increased fluid in interstitium
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29
Q

Is swelling always a sign of inflammation?

A

No

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30
Q

What is the colour of exudate the same colour as?

A

Plasma

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31
Q

What is inflammatory swelling caused by?

A

Oedema due to accumulation of exudate

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32
Q

What is the specific gravity of exudate?

A

More than 1.020

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33
Q

What is non inflammatory swelling caused by?

A

Oedema due to accumulation of transudate

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34
Q

What is transudate? (3)

A
  • Ultrafiltrate of blood
  • Low protein
  • No inflammatory cells
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35
Q

What is the specific gravity of transudate?

A

Less than 1.012

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36
Q

What is transudate swelling often found in and why?

A

Pregnancy due to increased BP

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37
Q

List the cellular events that occur in acute inflammation (3)

A
  • Leucocyte transmigration
  • Leucocyte degranulation
  • Phagocytosis
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38
Q

Why is leucocyte transmigration necessary in acute inflammation?

A

Leucocytes need to move from circulation to damage site

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39
Q

What are the two steps to leucocyte transmigration and degranulation in acute inflammation?

A
  • Extravasation

- Migration

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40
Q

What occurs in extravasation during leucocyte transmigration and degranulation in acute inflammation?

A

Endothelial cells and leuocytes express mutually recognising adhesion molecules

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41
Q

How do leucocytes migrate during leucocyte transmigration and degranulation in acute inflammation? (2)

A

Leuocytes “roll” from one adhesion molecule to another on endothelium
- Until eventually reach molecule enabling transmembrane WBC movement

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42
Q

What allows leucocytes to “roll” loosely during leucocyte transmigration and degranulation in acute inflammation?

A

Bonds to adhesion molecules are not very strong

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43
Q

What ensures leucocytes migrate towards the wound site in leucocyte transmigration and degranulation in acute inflammation? (2)

A
  • More adhesion proteins closer to wound site

- Follow conc. gradients of chemicals and inflammatory mediators (chemotaxis)

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44
Q

Define chemotaxis

A

Movement of a cell in direction due to gradient of increasing or decreasing concentration of a particular substance

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45
Q

What is phagocytosis?

A

Phagocytes binding to material to ingest in multistep process

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46
Q

Give 2 examples of material ingested in phagocytosis

A
  • Bacteria

- Necrotic tissue

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47
Q

What are the steps of phagocytosis? (3)

A
  • Recognition and attachment
  • Engulfment
  • Killing/degradation
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48
Q

How does recognition and attachment occur in phagocytosis? (2)

A
  • Through own cell receptor

- Molecules released by other cells bound to agent to eliminate

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49
Q

How does engulfment occur in phagocytosis?

A

Pseudopodia surrounds agent producing a vacuole

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50
Q

What is the vacuole produced in phagocytosis engulfment called?

A

Phagosome

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51
Q

How does killing/degradation occur in phagocytosis? (2)

A
  • Lysosomal granules fuse with phagosome

- Activates destruction by releasing chemicals

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52
Q

What chemicals are released to activate killing/degradation in phagocytosis?

A
  • Lysozymes
  • Proteases
  • Hydrolase (oxygen independent)
  • Toxic superoxides (oxygen dependant)
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53
Q

What are the two types of chemical mediators released in acute inflammation?

A
  • Plasma mediators

- Cell mediators

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54
Q

What occurs when leucocytes reach the inflammation site after transmigration?

A

Release cytokines (degranulation)

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55
Q

What are plasma mediators?

A

Present in precursor form and need to be activated

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56
Q

What are the 3 types of plasma mediator?

A
  • Cogulation system
  • Kinin system
  • Complement system
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57
Q

What are cell mediators?

A
  • Normally sequestered in intracellular granules (released from cells in inflammatory process)
  • Synthesised de novo
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58
Q

What is the life length of chemical mediators once released from cells and why?

A

Short lived because inflammatory process should be self contained

59
Q

What are the 3 types of cell mediators?

A
  • Mast cells
  • Basophils
  • Platelets
60
Q

What is the coagulation system activated by?

A

Tissue damage

61
Q

What is the end product of the coagulation system?

62
Q

What is the purpose of fibrin in the coagulation system? (2)

A
  • Mesh limiting site of infection in coagulation cascade

- Provides clot to stop bleeding

63
Q

What is the purpose of thrombin in the coagulation system? (2)

A
  • Increases leukocyte adhesion

- Increases fibroblast proliferation

64
Q

What reaction does thrombin catalyse?

A

Degradation of fibrinogen into fibrin

65
Q

What is the purpose of factor Xa in the coagulation system? (3)

A
  • Increases vascular permeability
  • Increases leukocyte exudation
  • Modulates ability of WBCs to migrate externally
66
Q

What is fibrin degraded to?

A

Fibrinopeptide

67
Q

What is the purpose of fibrinopeptide? (2)

A
  • Acts as a chemotactic factor for leucocytes

- Increases endothelial permeability

68
Q

What is a chemotatic factor?

A

Acts as a chemical stimulus along a concentration gradient, attracting cells to a site of inflammation

69
Q

What overall effect does fibrinopeptide/degradation of fibrin have? (2)

A
  • More cells to damaged site

- More blood flow to damaged site

70
Q

What is the kinin system activated through?

A

Coagulation factor XII

71
Q

What is the end product of the kinin system?

A

Bradykinin

72
Q

What does kinin system cause? (2)

A
  • Vasodilation

- Triggers pain

73
Q

What is the purpose of the complement system?

A
  • Triggers expression of adhesion molecules on leucocytes
  • Components accumulate on surface of pathogenic agent to promote recognition = phagocytosis
  • Triggers other cells = intercellular mediator release e.g histamine
74
Q

How many components are there in the complement system?

75
Q

What is the complement system activated by?

A

Foreign substances

76
Q

What are the 3 parts of the complement system?

A
  • Opsonisation
  • Binding
  • Phagocytosis
77
Q

What is opsonisation?

A

Invading particle e.g bacteria is identified to the phagocyte

78
Q

List the chemical mediators involved in lysis of microbes (6)

A
  • Membrane attack complex (MAC)
  • C5
  • C6
  • C7
  • C8
  • C9
79
Q

What chemical mediator acts as an opsonin?

80
Q

What chemical mediator is a powerful chemotactic agent?

81
Q

What chemical mediators increase permeability and cause vasodilation through histamine? (3)

A
  • C3a
  • C5a
  • Anaphylatoxins
82
Q

What hormone causes vasodilation with the aid of chemical mediators?

83
Q

What is histamine produced by? (3)

A
  • Mast cells
  • Basophils
  • Platelets
84
Q

What is histamine released in response to? (4)

A
  • Physical injury
  • Trauma
  • Cold/heat
  • Immune reaction
85
Q

What does histamine increase? (3)

A
  • Arteriole dilation
  • Venule vascular permeability
  • Activation of inflammatory cascade
86
Q

What are the vasoactive amine chemical mediators of inflammation? (2)

A
  • Histamine

- Serotonin

87
Q

What is serotonin produced by in inflammation? (2)

A
  • Platelets

- Enterochromaffin cells

88
Q

What are the actions of serotonin similar to?

89
Q

List the chemical cell mediators of inflammation (7)

A
  • Arachidonic acid metabolites
  • Cytokines and chemokines
  • Nitric oxide
  • Platelet activating factor
  • Lysosomal constituents of leukocytes
  • Oxygen derived free radicals
  • Neuropeptides
90
Q

What are arachidonic acid metabolites also known as?

A

Prostaglandins

91
Q

What is the purpose of arachidonic acid metabolites? (2)

A
  • Arterior dilatation

- Pain

92
Q

What is the purpose of cytokines and chemokines? (2)

A
  • Increase vascular permeability

- Chemotaxis

93
Q

What are cytokines and chemokines released by?

A

Blood cells

94
Q

What does nitric oxide cause?

A

Vasodilation

95
Q

What is the purpose of platelet activating factor? ()

A
  • Platelet aggregation
  • Increased vascular permeability
  • Leucoyte activation (+adhesion molecules)
  • Chemotaxis
96
Q

What is the purpose of lysosomal constituents of leukocytes?

A

Phagocytosis

97
Q

What is the purpose of neuropeptides?

98
Q

List the systemic effects of acute inflammation (7)

A
  • Fever
  • Malaise/lethargy/sleppiness
  • Pain
  • Leucocytosis
  • Tissue damage
  • Hyperpyrexia
  • Shock/Death
99
Q

What 3 chemical mediators released by damaged tissue cause fever in acute inflammation?

A
  • IL1
  • IL6
  • TNF
100
Q

How do Il1, IL6 and TNF cause fever in acute inflammation?

A

Release prostaglandins resetting hypothalmic thermostat to increase set point temp

101
Q

What is the purpose of fever in acute inflammation?

A

Destroys bacteria/virus

102
Q

Why can acute inflammation fever be damaging?

A

Can increase risk of seizures

103
Q

What drugs are needed to bring down fever in acute inflammation?

A

Non-steroidal anti-inflammatory drugs (NSAIDs)

104
Q

What is malaise caused by in acute inflammation?

A

Cytokines affecting brain to reduce counterproductive behaviour

105
Q

What 2 chemical mediators cause pain in acute inflammation?

A
  • Prostaglandins

- Bradykinin

106
Q

Other than chemical mediators, what causes pain in acute inflammation?

A

Localised nerve damage

107
Q

What is one of the first signs of acute inflammation?

A

Leucocytosis

108
Q

What is leucocytosis? (2)

A
  • Colony stimulating factors stimulate release of leucocytes from bone marrow
  • Big increase in WBC in blood systemically
109
Q

What 3 chemicals released in acute inflammation cause tissue damage?

A
  • Neutrophil and macrophage lysosomal enzymes
  • Oxygen metabolites
  • Nitric oxide
110
Q

Why is there often brain damage in acute inflammation?

A

Swelling in a confined space

111
Q

What causes hyperpyrexia/shock/death in acute inflammation?

A

Too many cytokines

112
Q

What is hyperpyrexia?

A

Extreme elevation in body temp (+40c)

113
Q

What are the 4 types of acute inflammation?

A
  • Serous inflammation
  • Fibrinous inflammation
  • Suppurative inflammation
  • Ulcer
114
Q

What does the type of inflammatory response depend on?

115
Q

What is serous inflammation?

A

Exudation of transudate into space caused by

  • Tissue damage (skin blister)
  • Body cavities (effusion)
116
Q

What are the causes of serous inflammation? (3)

A
  • Increased BP
  • Reduced oncotic pressure
  • Mechanical trauma
117
Q

What is exudation?

A

Fluid being emitted by organism through wound/pores

118
Q

What is fibrinous inflammation?

A

Fibrinogen exits blood and accumulates as fibrin in extracellular space

119
Q

What are the 2 causes of fibrinous inflammation?

A
  • Increased vascular permeability

- Procoagulant stimuli (tumours)

120
Q

What occurs if fibrinolysis is not complete?

121
Q

What is purulent inflammation?

A

Production of pus

122
Q

What does pus in purulent inflammation contain? (4)

A
  • Neutrophils (dead/alive)
  • Cellular debris
  • Oedema
  • Sometimes microorganisms
123
Q

What common infection involves purulent inflammation?

A

Appendicitus

124
Q

How does appendicitus progress to peritonitus?

A

If purulent exodate reaches the serosa

125
Q

What is purulent exodate a type of?

A

Inflammatory infiltrate

126
Q

Label the histology picture of appendicitus

A

See notes for diagram

127
Q

What is pus a type of?

A

Inflammatory exudate

128
Q

What is abscess?

A

Localised collection of pus surrounded by fibrous tissue, confined so can’t be drained

129
Q

What is the advantage of abscess?

A

Normally physiologically protective - contains infection

130
Q

What is the disadvantage of abscess?

A

Doesn’t allow antibiotics to permeate

131
Q

How is abscess treated?

A

Surgery for drainage and debriment

132
Q

What is debriment?

A

Removal of damaged tissue/foreign objects from a wound

133
Q

What is empyema?

A

Pus (exudate) formation in existing body cavity

134
Q

Give 4 examples of body cavities that empyema could occur in

A
  • Pleura
  • Joints
  • Uterus
  • Pericardium
135
Q

Where is pus often found in the skin?

A

Acne - localised accumulation of pus in the skin

136
Q

When is pus found in the gall bladder?

A

Cholecystitis (esp. after gall stones)

137
Q

What does the outcome of acute inflammation depend on?

A
  • Type of injury

- Ability of body to respond

138
Q

What are the 4 non death outcomes of acute inflammation?

A
  • Complete resolution
  • Healing by fibrosis
  • Abscess formation
  • Chronic inflammation
139
Q

What is the advantage of healing by fibrosis?

A

Puts connective tissue patch on damage, resists further damage

140
Q

What is the disadvantage of healing by fibrosis?

A

Area no longer functioning

141
Q

In what 2 ways can acute inflammation cause death?

A
  • Severe local damage

- Uncontrolled infection

142
Q

Give 2 conditions where severe local damage caused by acute inflammation leads to death

A
  • Meningitus

- Endocarditus

143
Q

How does uncontrolled infection in acute inflammation lead to death?

A
  • Sepsis

- Shock

Body Defence (11 decks)

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