Acute Inflammation Flashcards Preview

ESA 2- Mechanisms of Disease > Acute Inflammation > Flashcards

Flashcards in Acute Inflammation Deck (205):
1

What is acute inflammation?

The response of living tissue to injury

2

What is acute inflammation initiated to do?

Limit tissue damage

3

What is the purpose of acute inflammation?

It is a protective reposponse

4

What are the features of acute inflammation?

Innate 
Immediate and early
Stereotyped
Short duration

5

What is meant by acute inflammation being innate?

You are both with it

6

What is meant by acute inflammation being stereotyped?

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

7

What is the duration of acute inflammation?

Minutes/hours/few days, depending on process

8

What type of reactions occur in acute inflammation?

Vascular
Cellular

9

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

Accumulation of fluid exudate
Neutrophils in tissues

10

What is acute inflammation controlled by?

A variety of chemical mediators

11

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

Plasma cells

12

Why is control of acute inflammation very strict?

Don’t want it to get out of control

13

When is acute inflammation a good thing?

Nearly all the time

14

When is acute inflammation not a good thing?

It can lead to local complications and systemic effects

15

What causes acute inflammation?

Microbial infections 
Hypersensitivity reactions
Physical agents
Chemicals
Tissue necrosis

16

What type of microbial infections particularly cause acute inflammation?

Bacteria

17

What are pyogenic organisms?

Pus forming

18

What are hypersensitivity reactions?

Immunological reactions

19

What part of hypersensitivity reactions causes acute inflammation?

Acute phase

20

What physical agents cause acute inflammation?

Heat
Other forms of energy

21

What are the clinical features of acute inflammation?

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

22

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

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

23

What changes does acute inflammation cause in tissues?

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

24

What is required for each step of acute inflammation?

Inflammatory mediators

25

What happens in the vascular phase of acute inflammation?

Changes in blood flow

26

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

- 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

27

How long does transient vasoconstriction of arterioles take?

A few seconds

28

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

Causes heat and redness

29

What does the increased permeability of blood vessels lead to?

Exudation of protein rich fluid from plasma into tissues
Slowing of circulation

30

Why does increased permeability of blood vessels slow the circulation?

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

31

What does slowing of circulation lead to?

Swelling

32

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

Histamine

33

What kind of molecule is histamine?

Protein

34

Where is histamine released from?

Mast cells, basophils, platelets

35

What is histamine released in response to?

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

36

What does histamine cause?

Vascular dilation
Transient increase in vascular permeability 
Pain

37

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

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

38

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

They are incompletely understood

39

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

Leukotrienes
Bradykinin

40

What are leukotrienes derived from?

Arachidonic acid

41

What is significant about leukotrienes?

They are the most important chemical mediator

42

What law does fluid loss from vessels follow?

Starling’s Law

43

What is Starling’s Law?

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

44

What is hydrostatic pressure?

The blood pressure- force with which the blood flows

45

What is colloid osmotic pressure?

The protein level between plasma and interstitial fluid

46

What does increased hydrostatic pressure lead to?

Increased fluid flow out of the vessel

47

Why is hydrostatic pressure increased in acute inflammation?

Because of the increased flow

48

What does increased colloid osmotic pressure of the interstitium cause?

An increase in fluid flow out of the vessel

49

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

Because it sucks fluid out to balance the levels

50

What does exudation of fluid cause in inflammation?

Protein levels to increase

51

Why does exudation of fluid occur in acute inflammation?

Arteriolar dilatation 
Increased permeability of vessel walls

52

Why does arteriolar dilatation cause exudation of fluid?

Because it causes an increase in hydrostatic pressure

53

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

Because it leads to loss of protein to the interstitium

54

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

Oedema

55

What is oedema?

Increase fluid in tissue spaces

56

What can fluid be?

Transudate or exudate

57

What does oedema lead to?

Increased lymphatic drainage

58

Why does oedema lead to increased lymphatic drainage?

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

59

What is exudate?

Fluid loss in inflammation

60

What is the protein content of exudate?

High

61

What is transudate?

Fluid loss due to hydrostatic pressure imbalance

62

What is the protein content of transudate?

Low- the same as plasma

63

When does transudate formation occur?

When there is cardiac failure or venous outflow obstruction

64

What are the mechanisms of vascular leakage?

Endothelial contraction
Cytoskeletal reorganisation 
Direct injury
Leukocyte dependent injury
Increased transcytosis

65

Why does endothelial contraction cause vascular leakage?

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

66

What is endothelial contraction mediated by?

Histamine 
Leukotrienes

67

Why does cytoskeletal reorganisation lead to vascular leakage?

Leads to formation of gaps

68

What is cytoskeletal reorganisation mediated by?

Cytokines
IL-1
TNF

69

What kinds of direct injury can cause vascular leakage?

Toxic burns
Chemicals

70

What can cause leukocyte dependent injury?

Toxic oxygen species
Enzymes from leukocytes

71

What causes transcytosis?

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

72

What mediates an increase in transcytosis in inflammation?

VEGF

73

What is exudate rich in?

Fibrin

74

Where is fibrin an important component?

The acute inflammatory process

75

What is fibrin good at?

Making stuff sticky, and keeping it together

76

What is the purpose of fibrin?

To localise area of inflammation around injured tissue

77

Where is fibrins role in acute inflammation important?

If get inflammation in an organ that has a serosal surface

78

Give 3 examples of organs with serosal surfaces?

Lungs
Appendix 
Heart

79

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

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.

80

What is a neutrophil leucocyte?

A primary type of white blood cell involved in inflammation

81

What kind of cell is a leucocyte?

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

82

What are the characteristics of myeloid cells?

Granular cytoplasm with lots of cells in it

83

What is the predominant purpose of neutrophil leucocytes?

Acute inflammation

84

What are the stages of infiltration of neutrophils?

- 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

Why does stasis occur?

Due to laminar flow

86

Why does laminar flow cause stasis?

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

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

Rolling

88

What is the process of more avid neutrophil sticking called?

Adhesion

89

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

White cells and endothelial ligands have different receptors

90

How do neutrophils escape from vessels?

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

91

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

It creates gaps, and the cells move into the gaps

92

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

It is rebuilt

93

What is chemotaxis?

Movement along concentration gradients of chemoattractants

94

Why is chemotaxis important?

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

What can chemotaxis occur due too?

Chemotaxins
Receptor-ligand binding

96

Give 3 examples of chemotaxins

C5a
LTB4
Bacterial peptides

97

What is C5a?

An activated component of complement

98

Where is lTB4 from?

Cell membranes

99

What are bacterial peptides?

Stuff from outside the body that are very potent chemotaxins

100

Where are the receptors for receptor-ligand binding?

On the surface of white cells

101

What happens in receptor-ligand binding?

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

102

What are pseudopods important for?

They are how cells move

103

What is the main function of white cells?

Phagocytosis

104

What are the three stages of phagocytosis?

Contact
Recognition
Internalisation

105

What happens once internalisation has happened?

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

106

What is phagocytosis facilitated by?

Opsonins

107

Give two examples of opsonins?

Fc
C3b

108

What is Fc?

A fixed component of immunoglobulin

109

What is C3b?

A complement component

110

What changes does phagocytosis involve?

Cytoskeletal

111

What is produced when phagosomes fuse with lysosomes?

Secondary lysosomes

112

What are the two classes of phagocytitic killing mechanisms?

Oxygen dependent
Oxygen independent

113

What are the oxygen dependent killing mechanisms?

Production of superoxide and hydrogen peroxide
Hydrogen peroxide-myeloperoxidase-halide system

114

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

HOCl -

115

What are the oxygen independent killing mechanisms?

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

116

What are the stages of neutrophil chemotaxis and phagocytosis?

#NAME?

117

What are the chemical mediators of acute inflammation?

Proteases
Prostaglandins/leukotrienes
Cytokines/chemokines

118

Where are proteases produced?

Liver

119

Where are proteases found?

Plasma

120

What is the function of proteases in acute inflammation?

Kinins
Complement system
Coagulation system

121

What proteases are involved in the complement system?

C3a, C5

122

Why are proteases important in the complement system?

In producing chemotaxins and opsonins

123

What are prostaglandins/leukotrienes?

Metabolites of arachidonic acid, produced by different enzymatic reactions

124

Where are cytokines/chemokines produced by?

White blood cells

125

Give two examples of cytokines/chemokines?

Interleukins
TNF α

126

What do the chemical mediators of acute inflammation cause?

Increased blood flow 
Vascular permeability
Neutrophil chemotaxis
Phagocytosis

127

What chemical mediators cause increased blood flow?

Histamine
Prostaglandins

128

What chemical mediators cause vascular permeability?

Histamine
Leukotrienes

129

What chemical mediators cause neutrophil chemotaxis?

C5a
LTB4
Bacterial peptides

130

What chemical mediators cause phagocytosis?

C3b

131

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

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

132

What is the hallmark of acute inflammation?

Exudate of fluid
Infiltrate of inflammatory cells

133

What is the purpose of the exudation of fluid?

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

134

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

Immunoglobulins
Inflammatory mediators 
Fibrinogen

135

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

Delivers microorganisms to phagocytes and antigens to the immune system

136

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

Removes pathogenic organisms and necrotic debris

137

What is the purpose of vasodilation in acute inflammation?

Increases delivery
Increases temperature

138

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

Enforces rest
Reduces chance of further traumatic damage

139

What are the local complications of acute inflammation?

Swelling
Exudate 
Loss of fluid 
Pain and loss of function

140

What can swelling in acute inflammation lead to?

Blockage of tubes

141

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

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

142

What can a blocked bile duct cause?

Jaundice

143

What problems can exudate cause?

Compression 
Serositis

144

Give an example of when compression can be problematic

Cardiac tamponade

145

What happens in cardiac tamponade?

Fluid splints the heart, stopping it from beating

146

What is serositis?

Inflammation of a serosal surface

147

When my loss of fluid be a problem?

In burns, when plasma can be lost through the skin

148

When can pain and loss of function be particularly problematic?

If prolonged

149

What are the systemic complications of acute inflammation?

Fever
Leukocytosis
Acute phase response

150

Why does acute inflammation cause fever?

‘Endogenous pyrogens’ produced
Prostaglandins produced

151

Give two examples of endogenous pyrogens

IL-1
TNF α

152

How can aspirin reduce temperature

It inhibits the production of prostaglandins

153

What is leukocytosis?

An increased number of WBC in blood

154

What do IL-1 and TNF α produce?

Accelerated release from marrow

155

What do macrophages and T lymphocytes produce?

Colony-stimulating factors

156

What do bacterial infections recruit?

Neutrophils

157

What do viral infections recruit?

Lymphocytes

158

What happens when there is severe acute inflammation?

There is a big area of infarcted tissue

159

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

Appendicitis

160

What can severe acute inflammation lead to?

Systemic pathological symptoms

161

What systemic pathological systems will severe acute inflammation lead to?

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

162

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

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

163

How can Cr-reaction protein be useful?

Can help tell if a patient has had an infarction

164

What happens if inflammation doesn’t work?

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

165

What is shock?

Clinical syndrome of circulatory failure

166

What kind of shock is inflammatory shock?

Septic shock

167

What can happen after development of acute inflammation?

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

168

What outcome of acute inflammation happens most of the time?

Complete resolution

169

What happens in complete resolution of acute inflammation?

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

What happens when vascular changes stop in complete resolution?

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

171

Can damaged tissue regenerate in acute inflammation?

May be able too

172

When is complete resolution not possible?

If tissue architecture has been destroyed

173

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

Abscess

174

What are the mechanisms of resolution of acute inflammation?

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

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

Heparinase

176

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

Various anti-proteases

177

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

Some arachidonic acid derivatives

178

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

Fibrin degradation produces

179

Give two examples of specific inhibits of acute inflammatory changes

Lipoxins
Endothelin

180

What happens in bacterial meningitis?

Bacterial infection in the meninges causes acute inflammation in them

181

What are meninges?

Spaces surrounding the brain

182

What can acute inflammation in meninges cause?

Vascular thrombosis and reduced perfusion

183

What is the outcome of bacterial meningitis?

If recognised and treated quickly, fine. 
If don’t, death

184

What causes death in bacterial meningitis?

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

185

What can acute inflammation in meninges damage?

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

186

What happens in lobar pneumonia?

Inflammatory exudate and infiltrate into alveolar space

187

What can happen if lobar pneumonia is severe?

Can kill

188

What causes lobar pneumonia?

Streptococcus pneumoniae

189

What are the symptoms of lobar pneumonia?

Worsening fever
Prostration 
Hypoxaemia
Dry cough
Breathlessness

190

What is the outcome of lobar pneumonia if treated?

Can resolve completely

191

What can skin blisters be due to?

Heat
Sunlight
Chemicals

192

What are the predominant features of skin blisters?

Pain 
Profuse exudate

193

What causes the skin blister?

Collection of fluid strips off overlying epithelium

194

Why is the exudate clear in a skin blister?

Because inflammatory cells are relatively flew

195

Why is bacterial infection a problem in burns?

There is no skin, so no protection

196

What is the outcome of skin blisters?

Either resolves or scars

197

What are abscesses?

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

198

When do abscesses occur?

When acute inflammation can’t get out 
When there are pus forming organisms that the body can localise, but not deal with

199

What can abscesses cause?

Pain 
Tissue damage
Squash adjacent structures

200

Why do abscesses cause pain?

Because causes high pressure

201

What happens when you get acute inflammation in serous cavities?

Exudate pours into the cavity

202

What can acute inflammation in serous cavities cause?

Ascities
Pleural or pericardial effusion

203

What can pleural or pericardial effusion cause?

Respiratory or cardiac impairment

204

How is acute inflammation in serous cavities dealt with?

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

205

Give 5 disorders of acute inflammation

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