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Pathological Processes > PP 2 Acute Inflammation > Flashcards

PP 2 Acute Inflammation Flashcards

1
Q

Inflammation definition

A

Response of living tissue to injury

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2
Q

Features of acute inflammation

A

Immediate
Short duration
Innate/normal
Stereotyped - same regardless
Limits damage

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3
Q

Causes of acute inflammation

A

Trauma/foreign body
Micro organisms/infections
Hypersensitivity - allergies
Other illnesses e.g. cancer, necrosis

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4
Q

Clinical signs of acute inflammation

A

Rubor: redness
Tumour: swelling
Calor: heat
Dolor: pain
Loss of function

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5
Q

How long does vasoconstriction last and what is it?

A

Decreased diameter for a few seconds

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6
Q

How does calor arise?

A

Vasodilation
Increased diameter
More blood

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7
Q

How does rubor arise?

A

Vasodilation
Increased diameter
More blood

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8
Q

What occurs in vasodilatation?

A

1- arterioles dilate
2- flow accelerates into capillaries
3- capillary pressure increases
4- increases delivery of fluids tend leukocytes to injury site

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9
Q

What does increased permeability of walls cause?

A
  • Fluid + cells to move out of vessel
  • causing oedema
  • increase the viscosity of blood > stasis
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10
Q

Stasis meaning

A

Reduced blood flow in vessels

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11
Q

Where does interstitial fluid drain to?

A

Lymph nodes
Stimulates adaptive immune response

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12
Q

Types of interstitial fluid

A

Exudate
Transudate

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13
Q

Difference between exudate and transudate

A

Exudate - protein rich that develops in inflammation
Transudate - lacks proteins + occurs in normal vessels

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14
Q

How does exudate form?

A
  • Tissue injury > release of vasoactive mediators
  • arteriolar dilation > ^ capillary hydrostatic pressure
  • inflammatory mediators cause ^ permeability of walls
  • fluid + plasma proteins diffuse into interstitial space
  • osmotic pressure increase = holds fluid in the interesitial spae
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15
Q

Examples of proteins in exudate

A

Fibrin- mesh limits spread of toxin
Immunoglobulin- from adaptive immune response

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16
Q

What does exudate formation occur in?

A

Inflammation

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17
Q

Vascular permeability in exudate formation

A

Increased permeability

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18
Q

Vascular permeability in transudate formation

A

Unchanged

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19
Q

How does transudate form?

A

Fluid moves out due to:
Increased hydrostatic pressure
Decreased oncotic pressure

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20
Q

What does transudate formation occur in?

A

Hepatic failure
Heart failure
Renal failure

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21
Q

Causes of increased wall permeability

A
  • Retraction of endothelial cells
  • Direct injury e.g. burns, toxins, trauma
  • Leukocyte dependent injury
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22
Q

What are the primary WBC in acute inflammation?

A

Neutrophil

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23
Q

How do neutrophils escape vessels

A

1- migration: cells pushed to vessel wall
2- rolling
3- adhesion
4- emigration/diapedesis: cells move out of vessel

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24
Q

What are responsible for rolling in the cellular phase?

A

Selectins

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25
Q

Where are selectins found?

A

On activated endothelial cells

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26
Q

What are activated endothelial cells?

A

Endothelial cells which are actively doing something

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27
Q

What are selectins activated by?

A

Chemical mediators

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28
Q

What is responsible for adhesion in the cellular phase?

A

Integrins

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29
Q

Where are integrins found?

A

On neutrophil surface

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30
Q

Chemotaxis meaning

A

Directional movements towards a chemical attractant

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31
Q

How do neutrophils move through the intersisitum?

A

Chemotaxis

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32
Q

Examples of chemoattractants

A

Bacterial peptides
Inflammatory mediators - C5a, LTB4
Rearrangement of neutrophil cytoskeleton

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33
Q

Opsonisation meaning

A

Adding opsonin to pathogen to make it visible to neutrophil for phagocytosis

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34
Q

Examples of opsonin

A

C3b
C4b
IgG antibody
IgM antibody
CRP
Collectins

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35
Q

List the order of events that neutrophil follow to capture and kill bacterium

A

Chemotaxis
Activation
Margination
Diapedesis
Recognition attachment
Phagocytosis

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36
Q

List the stages of acute inflammation

A

1- stimulus
2- vascular phase
3- cellular phase
4- resolution or persistence

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37
Q

Steps in the vascular phase

A

1- vasoconstriction of arterioles
2- vasodilation of arterioles, then capillaries
3- increased permeability of blood vessels
4- increased viscosity > stasis

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38
Q

How does Tumor arise?

A

Increased permeability in vessel walls
Increased fluid in interstitial space - exudate

39
Q

Function of exudate

A
  • to deliver fibrin, inflammatory mediators and immunoglobulins to site of damage
  • dilutes toxins: reduces damage to tissues
  • ^ lymphatic drainage > delivers antigens + pathogens to lymph nodes > initiates immune response
40
Q

Types of exudate

A

Pus/purulent
Haemorrhagic
Serous
Fibrinous

41
Q

What colour is pus and why?

A

White/creamy
Rich in neutrophils

42
Q

What is pus typical in?

A

Pyogenic bacterial infectoin

43
Q

What colour is haemorrhagic exudate and why?

A

Red
Lots of RBCs

44
Q

What does haemorrhagic exudate indicate?

A

Significant vascular damage
RBCs are normally too big to leave

45
Q

What colour is serous exudate and what does this indicate?

A

Clear
No micro organisms

46
Q

What is serous exudate produced in?

A

Blisters and burns

47
Q

What sound does fibrinous exudate make and why?

A

Rubbing sound
Deposition of fibrin causes friction between serosal surfaces

48
Q

Local complications of acute inflammation

A
  • Swellling - compression of tubes
  • Compression of organs e.g cardiac tamponae
  • Loss of fluid
  • Pain
  • Loss of function
49
Q

Systemic complications of acute inflammation

A

Fever
Acute phase response
Leucocytosis
Acute phase proteins
Septic shock

50
Q

What is a pyrogen?
Examples

A

A substance which produces a fever when in the blood
e.g. prostaglandins, IL-1, IL-6 and TNF-a

51
Q

How does leucocytosis occur in acute inflammation?

A

Inflammatory mediators act on bone marrow to produce more leucocytes

52
Q

What WBCs are measure in FBC in bacterial infections?

A

Neutrophil

53
Q

What WBCs are measure in FBC in viral infections?

A

Lymphocytes

54
Q

Acute phase proteins present in acute inflammation

A

C-reactive protein - marker of severity
Fibrinogen
Alpha-1 antitrypsin

55
Q

What is the acute phase response?

A

A change in the level of plasma proteins as liver changes its levels of protein synthesis

56
Q

What does the acute phase response cause?

A

Decreased appetite
Tachycardia
Altered sleep
Change in plasma proteins
Malaise

57
Q

Malaise meaning

A

Feeling of discomfort

58
Q

What occurs in septic shock?

A

Huge release of chemical mediators
Widespread vasodilatation
Hypotension
Tachycardia
Multi-organ failure

59
Q

What can happen after acute inflammation?

A
  • Complete resolution
  • Repair with connective tissue - fibrosis
  • Progression to chronic inflammation
60
Q

What occurs in complete resolution of acute inflammation?

A
  • Neutrophils stop marginating
  • Vessel permeability returns to normal
  • Exudate drained via lymphatics
  • Neutrophils undergo apoptosis + get phagocytosed
  • regeneration - if tissue architecture is preserved
  • inflammatory mediators degrade
61
Q

Clinical examples of acute inflammation

A

Bacterial meningitis
Pneumonia
Acute appendicitis
Abscess
Inflammation off serous cavities

62
Q

What causes inflammation in serous cavities?

A

When exudate pours into cavity

63
Q

What is an abscess?

A

Accumulation pf dead + dying neutrophils

64
Q

What can an abscess cause?

A

Compression of surrounding structures
Pain
Blockage of ducts

65
Q

What is diapedesis?

A

Movement of blood cells through intact blood vessel wall

66
Q

What is an opsonin?

A

Substate which coats pathogen and makes them easier to phagocytose

67
Q

What is a free radial?

A

Molecule with a single unpaired electron in outer orbit

68
Q

Examples of protection against free radicals

A

Antioxidant scavengers e.g. vitamin A,C + E
Enzymes e.g. superoxide dismutase + catalase and glutathione peroxidase

69
Q

How do anti-oxidant scavengers protect against free radicals?

A

Donate an electron to the free radical and neutralise it

70
Q

Examples of chemoattractants

A

Thrombin
Endotoxin
Fibrin degradation products
C3a
C4a
C5a
Leukotriene B4
Interleukin 8

71
Q

What mechanisms do neutrophils use to destroy pathogens?

A

Oxygen independent
Oxygen dependent

72
Q

How do neutrophils kill pathogens (oxygen independent)?

A

Lysozyme
Hydrologic enzymes
Defensins

73
Q

How do neutrophils kill pathogens (oxygen dependent)?

A
  • ROS e.g. hydrogen peroxide, OH radical, superoxide anion
  • RNS e.g nitric oxide, nitrogen dioxide
74
Q

Where do chemical messengers originate from?

A

Activated inflammatory cells
Platelets
Endothelial cells
Toxins

75
Q

What do chemical messengers do?

A

Control and coordinate the inflammatory response

76
Q

Inflammatory mediators which bring about vasodilatation

A

Histamine
Serotonin
Prostaglandins
Nitric oxide

77
Q

Inflammatory mediators which increase permeability

A

Histamine
Bradykinin
Leukotrienes
C3a
C5a

78
Q

Inflammatory mediators which bring about Chemotaxis

A

Interleukin 1
C5a
TNF-a
Bacterial peptides

79
Q

Inflammatory mediators which bring about fevers

A

Prostaglandins
Interleukin 1
Interleukin 6
TNF-a

80
Q

What is TNF?

A

Tumour necrosis factor
Inflammatory mediators

81
Q

Inflammatory mediators which bring about pain

A

Bradykinin
Substance P
Prostaglandins

82
Q

Outline the cellular phase

A

1- neutrophils leak out
Margination, rolling, adhesion, diapedesis
2- release inflammatory mediators > chemotaxis
3- phagocytosis
4- opsonisation

83
Q

What is alpha-1 antitrypsin deficiency?

A

Autosomal recessive disorder where there are low levels of alpha-1 antitrypsin

84
Q

What is seen in alpha-1 antitrypsin deficiency?

A

Emphysema
Hepatocyte damage&raquo_space; cirrhosis

85
Q

What is hereditary angio-oedema?

A

Autosomal dominant condition
Inherited deficiency of C1-esterase inhibitor

86
Q

What is seen in hereditary angio-oedema?

A

Non-itchy cutaneous angio-oedema
Recurrent abdominal pain

87
Q

What is chronic granulomatous disease?

A

Condition where phagocytes are unable to generate superoxide
Phagocytes cannot kill bacteria as they cant generate an oxygen burst

88
Q

What is seen in chronic granulomatous disease?

A

Recurrent infections
Skin abscesses

89
Q

What are prostaglandins and what do they cause?

A

Substances produced in inflammation from cell membrane phospholipids
Cause vasodilation, fever + increased pain sensitivity

90
Q

What is seroma?

A

A tissue space filled with clear, sterile fluid that occurs as a post-operative complications

91
Q

What are the complications following lobar pneumonia? (5)

A
  • bacteraemia
  • lung abscesses
  • empyema
  • pleural effusion
  • lung fibrosis
92
Q

What distinguishes acute and chronic inflmmation at a cellular level?

A

Acute inflammation involves a rapid response with neutrophils
Chronic inflammation features lymphocytes + macrophages

93
Q

How can NSAIDs affect acute inflammation?

A

NSAIDs inhibit COX enzymes > reduces production of pro-inflammatory mediators like prostaglandins

Pathological Processes (14 decks)

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