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Semester 2 > MoD Session 2 > Flashcards

MoD Session 2 Flashcards

0
Q

Why is acute inflammation initiated?

A

To limit tissue damage

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1
Q

What is acute inflammation?

A

Response of living tissue to injury

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2
Q

What characterises acute inflammation?

A

Innate
Immediate
Early
Stereotyped

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3
Q

How long does acute inflammation last?

A

Mins to a few days

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4
Q

How does the reaction of acute inflammation to a stimulus vary?

A

It does not, it is the same irrespective of frequency

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5
Q

What causes the accumulation of fluid exudate and neutrophils in tissues in acute inflammation?

A

Vascular and cellular reactions

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6
Q

What controls acute inflammation and is derived mostly from plasma cells?

A

Variety of chemical mediators

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7
Q

Even though acute inflammation is protective, what can it lead to?

A

Local complications

Systemic effects

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8
Q

What can cause acute inflammation?

A

Chemicals
Any tissue damage
Microbial infections by pyogenic organisms
Acute phase of hypersensitivity reactions
Physical agents

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9
Q

What are the five cardinal signs of acute inflammation?

A 
Redness
Swelling
Heat
Pain
Loss of function
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10
Q

Why is function lost in acute inflammation?

A

To prevent further damage

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11
Q

What are the 3 changes to tissues seen in acute inflammation?

A

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

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12
Q

What controls each of the three changes to tissues in acute inflammation?

A

Mediators for each step

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13
Q

How is blood flow increased in the vascular phase of acute inflammation?

A

Transient vasoconstriction of arterioles followed by vasodilatation of arterioles then capillaries

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14
Q

What changes do the increase in bloodflow seen in acute inflammation cause?

A

Heat

Redness

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15
Q

What are the effects of increasing BV permeability in the vascular phase of acute inflammation?

A

Exudation of protein-rich fluid into tissues

Slowing of circulation due to thicker blood from fluid loss to tissues

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16
Q

Why is stasis of blood seen in the vascular phase of acute inflammation?

A

Increased concentration of RBC in small vessels

Increased blood viscosity

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17
Q

What type of granulocyte/polymorphonuclear leucocyte is the primary type of WBCS involved in inflammation?

A

Neutrophils leucocytes

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18
Q

How is tissue oedema seen histiologically?

A

Pale neutrophils due to high fluid content

Margination and emigration of neutrophils visible

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19
Q

What determines the exudation of fluid into tissues?

A

Balance of hydrostatic and colloid osmotic pressure

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20
Q

What two pressure changes cause fluid to move out of the BV?

A

Increase hydrostatic pressure

Increase oncotic pressure of intersticium

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21
Q

Why does arteriolar dilatation increase hydrostatic pressure?

A

Lack of resistance to blood flow

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22
Q

What can cause pathological exudation of fluid into tissues?

A

Heart failure

Inflammation

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23
Q

What mechanisms of vascular leakage can be used?

A 
Endothelial contraction
Cytoskeletal reorganisation 
Direct injury
Leukocyte dependent injury
Increased transcytosis
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24
Q

What causes endothelial contraction?

A

Histamine and leukotrienes

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25
Q

What mediators are used in cytoskeletal reorganisation?

A

IL-1

TNF

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26
Q

What is leukocyte dependent injury?

A

When inflammatory response causes tissue injury itself

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27
Q

What causes damage in leukocyte dependent injury?

A

Toxic oxygen species

Leucocyte enzymes

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28
Q

What is transcytosis?

A

Channels across endothelial cytoplasm not visible by light microscopy

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29
Q

What increases transcytosis?

A

Vascular endothelial growth factor - VEGF

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30
Q

Why are plasma proteins delivered to the site of injury in the vascular phase of acute inflammation?

A

Fibrin localises injury and prevents fluid loss

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31
Q

How is delivery of plasma proteins to site of injury in acute inflammation mediated?

A

Chemotactic FDPs

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32
Q

How long do chemical mediators take before they mount a response in the vascular phase of acute inflammation?

A

1/2 hour

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33
Q

What mediates the very early steps of acute inflammation and causes its symptoms?

A

Histamine

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34
Q

Where is histamine released from?

A

Mast cells
Basophils
Platelets

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35
Q

What stimuli can cause histamine release?

A 
Trauma
Immunologic reactions
C3a, C5a
IL-1
Neutrophils and platelet factors
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36
Q

What action does histamine have?

A

Acts in receptors in BV wall to cause vascular dilation causing transient increase in vascular permeability and pain

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37
Q

What effect does persistent response have on mediators (which is incompletely understood)?

A

Interlinks mediators

Histamine thought to interlink w/leukotrienes and bradykinin

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38
Q

What is neutrophil margination?

A

Neutrophils line up at the edge of the BV along the endothelium

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39
Q

How is neutrophil rolling achieved?

A

Neutrophils intermittently stick to endothelium whilst rolling

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40
Q

What is the name given to different receptors allowing neutrophils to stick during their infiltration?

A

Adhesion

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41
Q

What is neutrophil emigration?

A

Movement through BV wall

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42
Q

How does cell movement alter when blood velocity decreases?

A

Cells move towards endothelial edge

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43
Q

What do surface ligands bind to in the rolling phase of neutrophils migration?

A

Endothelial receptors
Selectins
sLc^x

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44
Q

What do neutrophils bind to in primary adhesion in neutrophil migration?

A

Integrins
lCAM1
VAM
MAdCAM

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45
Q

Which molecules are used in stable adhesion and aggregation in neutrophil migration?

A

Integrins
PECAMI
lCAM1

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46
Q

How are neutrophils found outside BV in neutrophil migration?

A

Transendothelial migration –> extravasation

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47
Q

How do neutrophils escape from vessels in the cellular phase of acute inflammation?

A

Relaxation of endothelial cell junctions
Enzymatic digestion of vascular BM
Neutrophils change shape to fit through vessels

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48
Q

How do neutrophils move?

A

Diapedesis and emigration by chemotaxis

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49
Q

What is chemotaxis?

A

Movement along a concentration gradient of chemoattractants

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50
Q

What attract receptor-binding ligands causing a rearrangement of the cytoskeleton leading to the production of a pseudopod?

A

Chemotaxins:
C5a
LTB4
Bacterial peptides

51
Q

Describe the process of phagocytosis in the cellular phase of acute inflammation.

A

Contact –> recognition –> internalisation

52
Q

What is phagocytosis facilitated by?

A

Opsonins
Non-specific fixed component of antibodies
C3b

53
Q

How are secondary lysosomes formed in phagocytosis?

A

Cytoskeletal changes occur allowing phagosomes to fuse with lysosomes

54
Q

What is oedema?

A

Increase in fluid in intersticium of any cause

55
Q

What change does oedema cause to the lymphatic system?

A

Increases drainage

56
Q

What are the two types of oedema?

A

Transudate

Exudate

57
Q

What causes transudate oedema?

A

Cardiac failure
Venous outflow obstruction
Arterial dilation removing resistance
Sluggish flow at venules –> high hydrostatic pressure

58
Q

What characterises exudate oedema?

A

High protein content

59
Q

What mechanism causes exudate oedema?

A

Leaky membrane –> increase capillary hydrostatic pressure due to arterial dilatation and oncotic pressure

60
Q

What pathology can cause exudate formation?

A

Cancers

Inflammation

61
Q

Which type of killing mechanism is the most efficient?

A

Oxygen dependent

62
Q

What do oxygen dependent killing mechanisms produce?

A

Superoxide

Hydrogen peroxide

63
Q

Which proteins are used in oxygen independent killing mechanisms?

A

Lysozyme
Cationic proteins - defensins
Bactericidal permeability increasing protein (BPI)
Hydrolases

64
Q

How do neutrophils cause host tissue damage?

A

Migrate to site of injury by chemotaxis –> phagocytose microorganisms –> may release toxic metabolites and enzymes

65
Q

What molecules are chemical mediators of acute inflammation?

A

Cytokines/chemokines
Prostaglandins/leukotrienes
Proteases

66
Q

How do cytokines/chemokines mediate acute inflammation?

A

TNF-alpha and interleukins are produced by WBCs for communication

67
Q

Which chemical mediators act on neutrophil chemotaxis?

A

Bacterial peptides
C5a
Leukotriene B4

68
Q

Which chemical mediators of acute inflammation act on phagocytosis?

69
Q

Which chemical mediators of acute inflammation act to increase blood flow?

A

Prostaglandins

Histamine

70
Q

Which chemical mediators of acute inflammation act on vascular permeability?

A

Histamine

Leukotrienes

71
Q

Which proteases mediate acute inflammation?

A

Kinins
Complement system - C3a/C5a
Generally plasma proteins produced in liver
Coagulation/fibrinolytic system

72
Q

How are prostaglandins/leukotrienes formed?

A

Metabolites of arachidonic acid formed from tissue phospholipids

73
Q

What does leukotriene B4 do to mediate acute inflammation?

A

Recruits and activates neutrophils, monocytes and eosinophils
Can prolong inflammation

74
Q

What is the hallmark of acute inflammation?

A

Exudate of fluid and infiltration of cells

75
Q

How does exudation of fluid combat injury in acute inflammation?

A

Delivers plasma proteins, immunoglobulins, inflammatory mediators and fibrinogen to site of injury
Dilutes toxins, increases lymphatic drainage, delivers microorganisms to phagocytes and antigens to lymph nodes

76
Q

How does infiltration of cells combat injury in acute inflammation?

A

Removes pathogenic organisms and necrotic debris

77
Q

What order do cells infiltrate in acute inflammation?

A

Neutrophils followed by macrophages

78
Q

How does vasodilatation combat injury in acute inflammation?

A

Increases delivery and temperature to give a more efficient response

79
Q

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

A

Enforces rest and reduces the chance of further traumatic damage

80
Q

What are local complications of acute inflammation?

A

Swelling
Exudate
Loss of fluid
Pain and loss of function

81
Q

How does swelling caused by acute inflammation cause complication?

A

Blockage of tube e.g. Bile duct, intestine, epiglottis in children

82
Q

What determines the significance of response in exudate formation in acute inflammation?

83
Q

At what point does appendix inflammation need rapid treatment?

A

When perforation of the appendix causes peritonitis which will be fatal if not treated

84
Q

When can exudate production be dangerous to the heart?

A

If it causes compression e.g. in cardiac tamponade

85
Q

What causes circulatory failure due to lack of fluid in vessels from vasodilation and exudation?

A

Failure of initial inflammatory reaction to localise cause leading to acute phase response and subsequent spread of micro-organisms and toxins

86
Q

What are systemic effects of acute inflammation?

A

Fever
Leukocytosis
Acute phase response

87
Q

What causes fever in acute inflammation?

A

Endogenous pyrogens IL-1, TNF-alpha, and prostaglandins turn up thermostat in hypothalamus

88
Q

How does acute inflammation cause leukocytosis?

A

IL-1 and TNF-alpha stimulate WBC release –> macrophages and T-lymphocytes produce CSF

89
Q

How are viral and bacterial leukocytosis differentiated?

A 
Bacterial = neutrophils
Viral = lymphocytes
90
Q

What is the acute phase response?

A

Decreased appetite
Increased pulse
Altered sleep patterns
Changes in plasma concentration of: CRP, alpha 1-antitrypsin, haptoglobin, fibrinogen, serum amyloid A protein

91
Q

What are the four acute inflammation sequelae?

A

Complete resolution
Continued acute inflammation w/chronic inflammation causing abcess - effectively walled off and needs extra input to overcome
Chronic inflammation and fibrous repair probably w/tissue regeneration
Death

92
Q

What happens to changes that have occurred gradually during acute inflammation?

A

They reverse

93
Q

What takes place during resolution of acute inflammation?

A

Vascular changes stop
Neutrophils no longer marginate
Vessel permeability returns to normal
Vessel calibre returns to normal

94
Q

What happens to exudate formed by acute inflammation upon resolution?

A

Drains into lympahtics

95
Q

What thrombolytic process occurs during resolution of acute inflammation?

A

Fibrin degraded by plasmin and proteases

96
Q

What happens to neutrophils upon resolution of acute inflammation?

A

Die –> break up –> carried away/phagocytosed

97
Q

What must happen for damaged tissue to be regenerated in resolution of acute inflammation?

A

Tissue architecture not destroyed

98
Q

Which acute inflammation resolution mechanisms may be unstable?

A

Some arachidonic acid derivatives, esp. prostaglandins

99
Q

Which inhibitors may bind to allow resolution of acute inflammation?

A

Various anti-proteases

100
Q

Which specific inhibitors of acute inflammatory changes are used in acute inflammation resolution?

A

Endothelin

Lipoxins

101
Q

What may inactivate mechanisms to resolve acute inflammation?

A

Degradation e.g. by heparhase

102
Q

What common feature do all mediators of acute inflammation resolution share?

A

Short half life

103
Q

What mechanism of acute inflammation resolution may be diluted in the exudate?

A

Fibrin degradation products

104
Q

Give four clinical examples of acute inflammation.

A

Bacterial meningitis
Lobar pneumonia
Skin blister
Abscess

105
Q

Why can bacterial meningitis cause vascular thrombosis and reduce cerebral perfusion?

A

All BV to the brain transverse meninges so can be compromised by inflammation

106
Q

What accumulates in bacterial meningitis?

107
Q

What causes lobar pneumonia?

A

Streptococcus pneumoniae (pneumococcus) causes alveoli to contain exudate instead of air

108
Q

What are the S/S of lobar pneumonia?

A 
Worsening fever
Prostration
Hypoxaemia over a few days
Dry cough
Breathlessness
109
Q

What is prostration?

A

No energy to get up

110
Q

What can cause a skin blister?

A

Heat
Sunlight
Chemicals

111
Q

What are the predominant features of a skin blister?

A

Pain due to high sensory function

Profuse exudate which can lead to large loss of fluid

112
Q

What causes the overlying epithelium in a skin blister to strip off?

A

Collection of fluid

113
Q

In what circumstance would the exudate of a skin blister not appear clear?

A

If bacterial infection develops due to few inflammatory cells

114
Q

What are the sequelae of skin blisters?

A

Resolved

Scarring

115
Q

Where are abscesses usually found?

A

In solid tissues

116
Q

How do abscesses form?

A

Inflammatory exudate forces tissues apart w/liquefactive necrosis in the centre forming pus

117
Q

Why do abscesses cause lots of pain?

A

They can cause high pressure

118
Q

What can abscesses do to surrounding tissue?

A

Cause damage

Squash adjacent structures

119
Q

What alternative treatment can be better than antibiotics in some cases when treating an abscess?

120
Q

How does acute inflammation in serous cavities cause ascites, pleural or pericardial effusion?

A

Exudate pours into the cavity

121
Q

What can acute inflammation in serous cavities cause?

A

Respiratory of cardiac impairment

Localised fibrin deposition –> ‘bread and butter’ pericarditis

122
Q

Why are disorders of acute inflammation rare?

A

Natural selection

123
Q

Give four examples of acute inflammation disorders.

A

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

124
Q

What does hereditary angio-oedema predispose patients to?

A

Airway swelling

125
Q

Which disorder of acute inflammation causes repeated infections?

A

Alpha-1 antitrypsin deficiency

Semester 2 (45 decks)

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