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ESA 2- Mechanisms of Disease > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is acute inflammation?

A

The response of living tissue to injury

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2
Q

What is acute inflammation initiated to do?

A

Limit tissue damage

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3
Q

What is the purpose of acute inflammation?

A

It is a protective reposponse

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4
Q

What are the features of acute inflammation?

A

Innate
Immediate and early
Stereotyped
Short duration

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5
Q

What is meant by acute inflammation being innate?

A

You are both with it

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6
Q

What is meant by acute inflammation being stereotyped?

A

It is the same every time it happens, and doesn’t get better or worse

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7
Q

What is the duration of acute inflammation?

A

Minutes/hours/few days, depending on process

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8
Q

What type of reactions occur in acute inflammation?

A

Vascular

Cellular

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9
Q

What is the result of vascular and cellular reactions in acute inflammation?

A

Accumulation of fluid exudate

Neutrophils in tissues

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10
Q

What is acute inflammation controlled by?

A

A variety of chemical mediators

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11
Q

What are the chemical mediators that control acute inflammation derived from?

A

Plasma cells

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12
Q

Why is control of acute inflammation very strict?

A

Don’t want it to get out of control

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13
Q

When is acute inflammation a good thing?

A

Nearly all the time

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14
Q

When is acute inflammation not a good thing?

A

It can lead to local complications and systemic effects

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15
Q

What causes acute inflammation?

A 
Microbial infections
 Hypersensitivity reactions
 Physical agents
 Chemicals
 Tissue necrosis
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16
Q

What type of microbial infections particularly cause acute inflammation?

A

Bacteria

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17
Q

What are pyogenic organisms?

A

Pus forming

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18
Q

What are hypersensitivity reactions?

A

Immunological reactions

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19
Q

What part of hypersensitivity reactions causes acute inflammation?

A

Acute phase

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20
Q

What physical agents cause acute inflammation?

A

Heat

Other forms of energy

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21
Q

What are the clinical features of acute inflammation?

A 
Rubor (redness)
 Tumour (swelling)
 Calor (heat)
 Dolour (pain)
 Loss of function
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22
Q

Why isn’t loss of function independent from the other clinical features?

A

Because it occurs partly because whatever is inflamed is sore, swollen, hot and red

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23
Q

What changes does acute inflammation cause in tissues?

A

Changes in blood flow
Exudation of fluid into tissues
Infiltration of inflammatory cells

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24
Q

What is required for each step of acute inflammation?

A

Inflammatory mediators

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25
Q

What happens in the vascular phase of acute inflammation?

A

Changes in blood flow

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26
Q

What are the stages of the vascular phase of acute inflammation?

A
  • Transient vasoconstriction of arterioles
  • Vasodilation of arterioles and then capillaries cause increase in blood flow to injured tissue
  • Increased permeability of blood vessels
  • Concentration of red blood cells in small vessels and the increased viscosity of blood leads to stasis
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27
Q

How long does transient vasoconstriction of arterioles take?

A

A few seconds

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28
Q

What is the result of increased blood flow to injured tissue?

A

Causes heat and redness

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29
Q

What does the increased permeability of blood vessels lead to?

A

Exudation of protein rich fluid from plasma into tissues

Slowing of circulation

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30
Q

Why does increased permeability of blood vessels slow the circulation?

A

If liquid leaves the blood, left with cells, so slows

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31
Q

What does slowing of circulation lead to?

A

Swelling

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32
Q

What is the chemical mediator of the immediate early response of the vascular phase of acute inflammation?

A

Histamine

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33
Q

What kind of molecule is histamine?

A

Protein

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34
Q

Where is histamine released from?

A

Mast cells, basophils, platelets

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35
Q

What is histamine released in response to?

A 
Many stimuli, including-
 Physical damage
 Immunological reactions
 C3a
 C5a
 IL-1
 Factors form neutrophils and platelets
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36
Q

What does histamine cause?

A

Vascular dilation
Transient increase in vascular permeability
Pain

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37
Q

What are the chemical mediators of the persistent response in the vascular phase of acute inflammation?

A

Many and varied chemical mediators, which are interlinked and of varying importance

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38
Q

What is the problem with studying the chemical mediators of the persistent response of the vascular phase of acute inflammation?

A

They are incompletely understood

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39
Q

Give two examples of chemical mediators of the persistent response of the vascular phase of acute inflammation?

A

Leukotrienes

Bradykinin

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40
Q

What are leukotrienes derived from?

A

Arachidonic acid

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41
Q

What is significant about leukotrienes?

A

They are the most important chemical mediator

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42
Q

What law does fluid loss from vessels follow?

A

Starling’s Law

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43
Q

What is Starling’s Law?

A

Fluid flow across vessel walls is determined by the balance of hydrostatic and colloid osmotic pressure comparing plasma and interstital fluid

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44
Q

What is hydrostatic pressure?

A

The blood pressure- force with which the blood flows

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45
Q

What is colloid osmotic pressure?

A

The protein level between plasma and interstitial fluid

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46
Q

What does increased hydrostatic pressure lead to?

A

Increased fluid flow out of the vessel

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47
Q

Why is hydrostatic pressure increased in acute inflammation?

A

Because of the increased flow

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48
Q

What does increased colloid osmotic pressure of the interstitium cause?

A

An increase in fluid flow out of the vessel

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49
Q

Why does in increased colloid osmotic pressure cause an increase in fluid flow out of the vessel?

A

Because it sucks fluid out to balance the levels

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50
Q

What does exudation of fluid cause in inflammation?

A

Protein levels to increase

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51
Q

Why does exudation of fluid occur in acute inflammation?

A

Arteriolar dilatation

Increased permeability of vessel walls

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52
Q

Why does arteriolar dilatation cause exudation of fluid?

A

Because it causes an increase in hydrostatic pressure

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53
Q

Why does increased permeability of vessel walls cause exudation of fluid?

A

Because it leads to loss of protein to the interstitium

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54
Q

What does net flow of fluid out of vessels lead to?

A

Oedema

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55
Q

What is oedema?

A

Increase fluid in tissue spaces

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56
Q

What can fluid be?

A

Transudate or exudate

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57
Q

What does oedema lead to?

A

Increased lymphatic drainage

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58
Q

Why does oedema lead to increased lymphatic drainage?

A

Because if fluid gets into tissue space by leaking out of vessels, there has to be a means for it to get away again, and therefore it is drained out of the lymphatic system

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59
Q

What is exudate?

A

Fluid loss in inflammation

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60
Q

What is the protein content of exudate?

A

High

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61
Q

What is transudate?

A

Fluid loss due to hydrostatic pressure imbalance

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62
Q

What is the protein content of transudate?

A

Low- the same as plasma

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63
Q

When does transudate formation occur?

A

When there is cardiac failure or venous outflow obstruction

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64
Q

What are the mechanisms of vascular leakage?

A 
Endothelial contraction
 Cytoskeletal reorganisation
 Direct injury
 Leukocyte dependent injury
 Increased transcytosis
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65
Q

Why does endothelial contraction cause vascular leakage?

A

Because it leads to the formation of gaps, which are leaky

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66
Q

What is endothelial contraction mediated by?

A

Histamine

Leukotrienes

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67
Q

Why does cytoskeletal reorganisation lead to vascular leakage?

A

Leads to formation of gaps

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68
Q

What is cytoskeletal reorganisation mediated by?

A

Cytokines
IL-1
TNF

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69
Q

What kinds of direct injury can cause vascular leakage?

A

Toxic burns

Chemicals

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70
Q

What can cause leukocyte dependent injury?

A

Toxic oxygen species

Enzymes from leukocytes

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71
Q

What causes transcytosis?

A

Channels across endothelial cytoplasm, where fluid moves along normally for a lot of physiological systems

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72
Q

What mediates an increase in transcytosis in inflammation?

A

VEGF

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73
Q

What is exudate rich in?

A

Fibrin

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74
Q

Where is fibrin an important component?

A

The acute inflammatory process

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75
Q

What is fibrin good at?

A

Making stuff sticky, and keeping it together

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76
Q

What is the purpose of fibrin?

A

To localise area of inflammation around injured tissue

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77
Q

Where is fibrins role in acute inflammation important?

A

If get inflammation in an organ that has a serosal surface

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78
Q

Give 3 examples of organs with serosal surfaces?

A

Lungs
Appendix
Heart

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79
Q

Why is fibrin important if you get inflammation in an organ that has a serosal surface?

A

Because where there is acute inflammatory infiltrate on a serosal surface, you run the risk that you’ll exudate all of the blood volume into the cavity. Fibrin is good at preventing this.

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80
Q

What is a neutrophil leucocyte?

A

A primary type of white blood cell involved in inflammation

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81
Q

What kind of cell is a leucocyte?

A

A type of granulocyte, also known as a polymorphonuclear leucocyte. This means that they are myeloid cells.

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82
Q

What are the characteristics of myeloid cells?

A

Granular cytoplasm with lots of cells in it

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83
Q

What is the predominant purpose of neutrophil leucocytes?

A

Acute inflammation

84
Q

What are the stages of infiltration of neutrophils?

A
  • Stasis causes neutrophils to line up at the edge of blood vessels
  • Neutrophils roll along endothelium, becoming loosely adherent, sticking to it intermittently
  • They then stick more avidly
  • Followed my emigration of neutrophils along the blood vessel wall
85
Q

Why does stasis occur?

A

Due to laminar flow

86
Q

Why does laminar flow cause stasis?

A

Blood cells tend to flow down the middle of the vessel, not the edges, however, when the blood gets static, the blood cells go to the periphery

87
Q

What is the process of neutrophils sticking intermittently to the endothelium called?

A

Rolling

88
Q

What is the process of more avid neutrophil sticking called?

A

Adhesion

89
Q

What is responsible for each of the different stages of neutrophil infiltration?

A

White cells and endothelial ligands have different receptors

90
Q

How do neutrophils escape from vessels?

A

Relaxation of inter-endothelial cell junctions
Digestion of vascular basement membrane
Movement of white cells

91
Q

Why does the digestion of the vascular basement membrane allow neutrophils to escape from vessels?

A

It creates gaps, and the cells move into the gaps

92
Q

What happens to the digested vascular basement membrane at the end of inflammation?

A

It is rebuilt

93
Q

What is chemotaxis?

A

Movement along concentration gradients of chemoattractants

94
Q

Why is chemotaxis important?

A

Because it’s how, once a polymorph gets out of a capillary, it knows where to go and what to do, as it needs to get to the bit of tissue thats most injured

95
Q

What can chemotaxis occur due too?

A

Chemotaxins

Receptor-ligand binding

96
Q

Give 3 examples of chemotaxins

A

C5a
LTB4
Bacterial peptides

97
Q

What is C5a?

A

An activated component of complement

98
Q

Where is lTB4 from?

A

Cell membranes

99
Q

What are bacterial peptides?

A

Stuff from outside the body that are very potent chemotaxins

100
Q

Where are the receptors for receptor-ligand binding?

A

On the surface of white cells

101
Q

What happens in receptor-ligand binding?

A

Once the receptor has bound to the ligand on a neutrophil, it rearranges the cytoskeleton and produces a pseudopod

102
Q

What are pseudopods important for?

A

They are how cells move

103
Q

What is the main function of white cells?

A

Phagocytosis

104
Q

What are the three stages of phagocytosis?

A

Contact
Recognition
Internalisation

105
Q

What happens once internalisation has happened?

A

It means all things that sit inside lysosomes and the cytoplasm can do their job

106
Q

What is phagocytosis facilitated by?

A

Opsonins

107
Q

Give two examples of opsonins?

A

Fc

C3b

108
Q

What is Fc?

A

A fixed component of immunoglobulin

109
Q

What is C3b?

A

A complement component

110
Q

What changes does phagocytosis involve?

A

Cytoskeletal

111
Q

What is produced when phagosomes fuse with lysosomes?

A

Secondary lysosomes

112
Q

What are the two classes of phagocytitic killing mechanisms?

A

Oxygen dependent

Oxygen independent

113
Q

What are the oxygen dependent killing mechanisms?

A

Production of superoxide and hydrogen peroxide

Hydrogen peroxide-myeloperoxidase-halide system

114
Q

What is produced in the hydrogen peroxide-myeloperoxidase-halide system?

A

HOCl -

115
Q

What are the oxygen independent killing mechanisms?

A

Lysosome and hydrolases
Bacterial Permeability Increasing Protein (BPI)
Cationic proteins (defensins)

116
Q

What are the stages of neutrophil chemotaxis and phagocytosis?

A

NAME?

117
Q

What are the chemical mediators of acute inflammation?

A

Proteases
Prostaglandins/leukotrienes
Cytokines/chemokines

118
Q

Where are proteases produced?

A

Liver

119
Q

Where are proteases found?

A

Plasma

120
Q

What is the function of proteases in acute inflammation?

A

Kinins
Complement system
Coagulation system

121
Q

What proteases are involved in the complement system?

A

C3a, C5

122
Q

Why are proteases important in the complement system?

A

In producing chemotaxins and opsonins

123
Q

What are prostaglandins/leukotrienes?

A

Metabolites of arachidonic acid, produced by different enzymatic reactions

124
Q

Where are cytokines/chemokines produced by?

A

White blood cells

125
Q

Give two examples of cytokines/chemokines?

A

Interleukins

TNF α

126
Q

What do the chemical mediators of acute inflammation cause?

A

Increased blood flow
Vascular permeability
Neutrophil chemotaxis
Phagocytosis

127
Q

What chemical mediators cause increased blood flow?

A

Histamine

Prostaglandins

128
Q

What chemical mediators cause vascular permeability?

A

Histamine

Leukotrienes

129
Q

What chemical mediators cause neutrophil chemotaxis?

A

C5a
LTB4
Bacterial peptides

130
Q

What chemical mediators cause phagocytosis?

A

C3b

131
Q

Why are the immune system and the inflammatory response said to by symbiotic?

A

They work together, and both as defence mechanisms, but are different

132
Q

What is the hallmark of acute inflammation?

A

Exudate of fluid

Infiltrate of inflammatory cells

133
Q

What is the purpose of the exudation of fluid?

A

Delivers plasma proteins to area of injury
Dilutes toxins
Increases lymphatic drainage

134
Q

What plasma proteins need to be delivered to the site of injury?

A

Immunoglobulins
Inflammatory mediators
Fibrinogen

135
Q

What is the advantage of the increase in lymphatic drainage in acute inflammation?

A

Delivers microorganisms to phagocytes and antigens to the immune system

136
Q

What is the purpose of infiltration of cells in acute inflammation?

A

Removes pathogenic organisms and necrotic debris

137
Q

What is the purpose of vasodilation in acute inflammation?

A

Increases delivery

Increases temperature

138
Q

What is the purpose of pain and loss of function in acute inflammation?

A

Enforces rest

Reduces chance of further traumatic damage

139
Q

What are the local complications of acute inflammation?

A

Swelling
Exudate
Loss of fluid
Pain and loss of function

140
Q

What can swelling in acute inflammation lead to?

A

Blockage of tubes

141
Q

When is swelling causing blockage of tubes likely to be problematic?

A

If you have acute inflammation in a small tube with a narrow lumen

142
Q

What can a blocked bile duct cause?

A

Jaundice

143
Q

What problems can exudate cause?

A

Compression

Serositis

144
Q

Give an example of when compression can be problematic

A

Cardiac tamponade

145
Q

What happens in cardiac tamponade?

A

Fluid splints the heart, stopping it from beating

146
Q

What is serositis?

A

Inflammation of a serosal surface

147
Q

When my loss of fluid be a problem?

A

In burns, when plasma can be lost through the skin

148
Q

When can pain and loss of function be particularly problematic?

A

If prolonged

149
Q

What are the systemic complications of acute inflammation?

A

Fever
Leukocytosis
Acute phase response

150
Q

Why does acute inflammation cause fever?

A

‘Endogenous pyrogens’ produced

Prostaglandins produced

151
Q

Give two examples of endogenous pyrogens

A

IL-1

TNF α

152
Q

How can aspirin reduce temperature

A

It inhibits the production of prostaglandins

153
Q

What is leukocytosis?

A

An increased number of WBC in blood

154
Q

What do IL-1 and TNF α produce?

A

Accelerated release from marrow

155
Q

What do macrophages and T lymphocytes produce?

A

Colony-stimulating factors

156
Q

What do bacterial infections recruit?

A

Neutrophils

157
Q

What do viral infections recruit?

A

Lymphocytes

158
Q

What happens when there is severe acute inflammation?

A

There is a big area of infarcted tissue

159
Q

Give an example of where they will be severe acute inflammation?

A

Appendicitis

160
Q

What can severe acute inflammation lead to?

A

Systemic pathological symptoms

161
Q

What systemic pathological systems will severe acute inflammation lead to?

A

Decreased appetite
Raised pulse rate
Altered sleep patterns
Change in plasma concentrations of acute phase proteins

162
Q

What acute phase protein concentrations are changed when there is severe acute inflammation?

A 
C-reaction protein
 α-1 antitrypsin
 Haptoglobin
 Fibrinogen
 Serum amyloid A protein
163
Q

How can Cr-reaction protein be useful?

A

Can help tell if a patient has had an infarction

164
Q

What happens if inflammation doesn’t work?

A

It doesn’t rapidly localise and deal with infection, so can get spread of microrganisms and toxins

165
Q

What is shock?

A

Clinical syndrome of circulatory failure

166
Q

What kind of shock is inflammatory shock?

A

Septic shock

167
Q

What can happen after development of acute inflammation?

A

Complete resolution
Continued acute inflammation with chronic inflammation
Chronic inflammation and fibrous repair
Death

168
Q

What outcome of acute inflammation happens most of the time?

A

Complete resolution

169
Q

What happens in complete resolution of acute inflammation?

A

Changes gradually reverse
Vascular changes stop
Exudate drains to lymphatics
Fibrin is degraded by plasmin and other proteases
Neutrophils die, break up and are carried away, or are phagocytosed

170
Q

What happens when vascular changes stop in complete resolution?

A

Neutrophils no longer marginate
Vessel permeability returns to normal
Vessel calibre returns to normal

171
Q

Can damaged tissue regenerate in acute inflammation?

A

May be able too

172
Q

When is complete resolution not possible?

A

If tissue architecture has been destroyed

173
Q

What does continued acute inflammation with chronic inflammation lead to when there is a pus forming microorganism?

A

Abscess

174
Q

What are the mechanisms of resolution of acute inflammation?

A

All mediators of acute inflammation have short half lives
May be inactivated by degradation
Inhibitors may bind
May be unstable
May be diluted in exudate
Specific inhibitors of acute inflammatory changes

175
Q

Give an example of a mediator of acute inflammation that is inactivated by degradation

A

Heparinase

176
Q

Give an example of a mediator of acute inflammation that is stopped by a binding inhibitor

A

Various anti-proteases

177
Q

Give an example of a mediator of acute inflammation that is unstable

A

Some arachidonic acid derivatives

178
Q

Give an example of a mediator of acute inflammation that is diluted in the exudate

A

Fibrin degradation produces

179
Q

Give two examples of specific inhibits of acute inflammatory changes

A

Lipoxins

Endothelin

180
Q

What happens in bacterial meningitis?

A

Bacterial infection in the meninges causes acute inflammation in them

181
Q

What are meninges?

A

Spaces surrounding the brain

182
Q

What can acute inflammation in meninges cause?

A

Vascular thrombosis and reduced perfusion

183
Q

What is the outcome of bacterial meningitis?

A

If recognised and treated quickly, fine.

If don’t, death

184
Q

What causes death in bacterial meningitis?

A

Because the acute inflammatory exudate in meningeal space in the hard skull results in a raised intracranial pressure.

185
Q

What can acute inflammation in meninges damage?

A

Things that cross in the meningeal space- blood vessels, cranial nerve

186
Q

What happens in lobar pneumonia?

A

Inflammatory exudate and infiltrate into alveolar space

187
Q

What can happen if lobar pneumonia is severe?

A

Can kill

188
Q

What causes lobar pneumonia?

A

Streptococcus pneumoniae

189
Q

What are the symptoms of lobar pneumonia?

A 
Worsening fever
 Prostration
 Hypoxaemia
 Dry cough
 Breathlessness
190
Q

What is the outcome of lobar pneumonia if treated?

A

Can resolve completely

191
Q

What can skin blisters be due to?

A

Heat
Sunlight
Chemicals

192
Q

What are the predominant features of skin blisters?

A

Pain

Profuse exudate

193
Q

What causes the skin blister?

A

Collection of fluid strips off overlying epithelium

194
Q

Why is the exudate clear in a skin blister?

A

Because inflammatory cells are relatively flew

195
Q

Why is bacterial infection a problem in burns?

A

There is no skin, so no protection

196
Q

What is the outcome of skin blisters?

A

Either resolves or scars

197
Q

What are abscesses?

A

Solid tissues that occur when inflammatory exudate forces tissue apart, with liquefactive necrosis in the centre

198
Q

When do abscesses occur?

A

When acute inflammation can’t get out

When there are pus forming organisms that the body can localise, but not deal with

199
Q

What can abscesses cause?

A

Pain
Tissue damage
Squash adjacent structures

200
Q

Why do abscesses cause pain?

A

Because causes high pressure

201
Q

What happens when you get acute inflammation in serous cavities?

A

Exudate pours into the cavity

202
Q

What can acute inflammation in serous cavities cause?

A

Ascities

Pleural or pericardial effusion

203
Q

What can pleural or pericardial effusion cause?

A

Respiratory or cardiac impairment

204
Q

How is acute inflammation in serous cavities dealt with?

A

Localised fibrin deposition, which helps localise the inflammation, favouring resolution rather than continuation of inflammation

205
Q

Give 5 disorders of acute inflammation

A

Hereditary angio-oedema Alpha-1 antitrypsin deficiency Inherited complement deficiencies Defects in neutrophil function Defects in neutrophil numbers

ESA 2- Mechanisms of Disease (11 decks)

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