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Flashcards in MoD Session 2 Deck (126):
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What is acute inflammation?

Response of living tissue to injury

1

Why is acute inflammation initiated?

To limit tissue damage

2

What characterises acute inflammation?

Innate
Immediate
Early
Stereotyped

3

How long does acute inflammation last?

Mins to a few days

4

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

It does not, it is the same irrespective of frequency

5

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

Vascular and cellular reactions

6

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

Variety of chemical mediators

7

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

Local complications
Systemic effects

8

What can cause acute inflammation?

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

9

What are the five cardinal signs of acute inflammation?

Redness
Swelling
Heat
Pain
Loss of function

10

Why is function lost in acute inflammation?

To prevent further damage

11

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

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

12

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

Mediators for each step

13

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

Transient vasoconstriction of arterioles followed by vasodilatation of arterioles then capillaries

14

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

Heat
Redness

15

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

Exudation of protein-rich fluid into tissues
Slowing of circulation due to thicker blood from fluid loss to tissues

16

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

Increased concentration of RBC in small vessels
Increased blood viscosity

17

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

Neutrophils leucocytes

18

How is tissue oedema seen histiologically?

Pale neutrophils due to high fluid content
Margination and emigration of neutrophils visible

19

What determines the exudation of fluid into tissues?

Balance of hydrostatic and colloid osmotic pressure

20

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

Increase hydrostatic pressure
Increase oncotic pressure of intersticium

21

Why does arteriolar dilatation increase hydrostatic pressure?

Lack of resistance to blood flow

22

What can cause pathological exudation of fluid into tissues?

Heart failure
Inflammation

23

What mechanisms of vascular leakage can be used?

Endothelial contraction
Cytoskeletal reorganisation
Direct injury
Leukocyte dependent injury
Increased transcytosis

24

What causes endothelial contraction?

Histamine and leukotrienes

25

What mediators are used in cytoskeletal reorganisation?

IL-1
TNF

26

What is leukocyte dependent injury?

When inflammatory response causes tissue injury itself

27

What causes damage in leukocyte dependent injury?

Toxic oxygen species
Leucocyte enzymes

28

What is transcytosis?

Channels across endothelial cytoplasm not visible by light microscopy

29

What increases transcytosis?

Vascular endothelial growth factor - VEGF

30

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

Fibrin localises injury and prevents fluid loss

31

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

Chemotactic FDPs

32

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

1/2 hour

33

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

Histamine

34

Where is histamine released from?

Mast cells
Basophils
Platelets

35

What stimuli can cause histamine release?

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

36

What action does histamine have?

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

37

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

Interlinks mediators
Histamine thought to interlink w/leukotrienes and bradykinin

38

What is neutrophil margination?

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

39

How is neutrophil rolling achieved?

Neutrophils intermittently stick to endothelium whilst rolling

40

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

Adhesion

41

What is neutrophil emigration?

Movement through BV wall

42

How does cell movement alter when blood velocity decreases?

Cells move towards endothelial edge

43

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

Endothelial receptors
Selectins
sLc^x

44

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

Integrins
lCAM1
VAM
MAdCAM

45

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

Integrins
PECAMI
lCAM1

46

How are neutrophils found outside BV in neutrophil migration?

Transendothelial migration --> extravasation

47

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

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

48

How do neutrophils move?

Diapedesis and emigration by chemotaxis

49

What is chemotaxis?

Movement along a concentration gradient of chemoattractants

50

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

Chemotaxins:
C5a
LTB4
Bacterial peptides

51

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

Contact --> recognition --> internalisation

52

What is phagocytosis facilitated by?

Opsonins
Non-specific fixed component of antibodies
C3b

53

How are secondary lysosomes formed in phagocytosis?

Cytoskeletal changes occur allowing phagosomes to fuse with lysosomes

54

What is oedema?

Increase in fluid in intersticium of any cause

55

What change does oedema cause to the lymphatic system?

Increases drainage

56

What are the two types of oedema?

Transudate
Exudate

57

What causes transudate oedema?

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

58

What characterises exudate oedema?

High protein content

59

What mechanism causes exudate oedema?

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

60

What pathology can cause exudate formation?

Cancers
Inflammation

61

Which type of killing mechanism is the most efficient?

Oxygen dependent

62

What do oxygen dependent killing mechanisms produce?

Superoxide
Hydrogen peroxide

63

Which proteins are used in oxygen independent killing mechanisms?

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

64

How do neutrophils cause host tissue damage?

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

65

What molecules are chemical mediators of acute inflammation?

Cytokines/chemokines
Prostaglandins/leukotrienes
Proteases

66

How do cytokines/chemokines mediate acute inflammation?

TNF-alpha and interleukins are produced by WBCs for communication

67

Which chemical mediators act on neutrophil chemotaxis?

Bacterial peptides
C5a
Leukotriene B4

68

Which chemical mediators of acute inflammation act on phagocytosis?

C3b

69

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

Prostaglandins
Histamine

70

Which chemical mediators of acute inflammation act on vascular permeability?

Histamine
Leukotrienes

71

Which proteases mediate acute inflammation?

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

72

How are prostaglandins/leukotrienes formed?

Metabolites of arachidonic acid formed from tissue phospholipids

73

What does leukotriene B4 do to mediate acute inflammation?

Recruits and activates neutrophils, monocytes and eosinophils
Can prolong inflammation

74

What is the hallmark of acute inflammation?

Exudate of fluid and infiltration of cells

75

How does exudation of fluid combat injury in acute inflammation?

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

How does infiltration of cells combat injury in acute inflammation?

Removes pathogenic organisms and necrotic debris

77

What order do cells infiltrate in acute inflammation?

Neutrophils followed by macrophages

78

How does vasodilatation combat injury in acute inflammation?

Increases delivery and temperature to give a more efficient response

79

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

Enforces rest and reduces the chance of further traumatic damage

80

What are local complications of acute inflammation?

Swelling
Exudate
Loss of fluid
Pain and loss of function

81

How does swelling caused by acute inflammation cause complication?

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

82

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

Site

83

At what point does appendix inflammation need rapid treatment?

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

84

When can exudate production be dangerous to the heart?

If it causes compression e.g. in cardiac tamponade

85

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

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

86

What are systemic effects of acute inflammation?

Fever
Leukocytosis
Acute phase response

87

What causes fever in acute inflammation?

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

88

How does acute inflammation cause leukocytosis?

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

89

How are viral and bacterial leukocytosis differentiated?

Bacterial = neutrophils
Viral = lymphocytes

90

What is the acute phase response?

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

91

What are the four acute inflammation sequelae?

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

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

They reverse

93

What takes place during resolution of acute inflammation?

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

94

What happens to exudate formed by acute inflammation upon resolution?

Drains into lympahtics

95

What thrombolytic process occurs during resolution of acute inflammation?

Fibrin degraded by plasmin and proteases

96

What happens to neutrophils upon resolution of acute inflammation?

Die --> break up --> carried away/phagocytosed

97

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

Tissue architecture not destroyed

98

Which acute inflammation resolution mechanisms may be unstable?

Some arachidonic acid derivatives, esp. prostaglandins

99

Which inhibitors may bind to allow resolution of acute inflammation?

Various anti-proteases

100

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

Endothelin
Lipoxins

101

What may inactivate mechanisms to resolve acute inflammation?

Degradation e.g. by heparhase

102

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

Short half life

103

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

Fibrin degradation products

104

Give four clinical examples of acute inflammation.

Bacterial meningitis
Lobar pneumonia
Skin blister
Abscess

105

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

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

106

What accumulates in bacterial meningitis?

Pus

107

What causes lobar pneumonia?

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

108

What are the S/S of lobar pneumonia?

Worsening fever
Prostration
Hypoxaemia over a few days
Dry cough
Breathlessness

109

What is prostration?

No energy to get up

110

What can cause a skin blister?

Heat
Sunlight
Chemicals

111

What are the predominant features of a skin blister?

Pain due to high sensory function
Profuse exudate which can lead to large loss of fluid

112

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

Collection of fluid

113

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

If bacterial infection develops due to few inflammatory cells

114

What are the sequelae of skin blisters?

Resolved
Scarring

115

Where are abscesses usually found?

In solid tissues

116

How do abscesses form?

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

117

Why do abscesses cause lots of pain?

They can cause high pressure

118

What can abscesses do to surrounding tissue?

Cause damage
Squash adjacent structures

119

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

Surgery

120

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

Exudate pours into the cavity

121

What can acute inflammation in serous cavities cause?

Respiratory of cardiac impairment
Localised fibrin deposition --> 'bread and butter' pericarditis

122

Why are disorders of acute inflammation rare?

Natural selection

123

Give four examples of acute inflammation disorders.

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

124

What does hereditary angio-oedema predispose patients to?

Airway swelling

125

Which disorder of acute inflammation causes repeated infections?

Alpha-1 antitrypsin deficiency