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Semester 2-PP > Session 2-Acute Inflammation > Flashcards

Session 2-Acute Inflammation Flashcards

1
Q

What are the causes of acute inflammation? (5)

A
  • microbial infections
  • hypersensitivity reactions
  • physical agents such as heat, light and radiation
  • chemicals
  • tissue necrosis
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2
Q

What are the clinical signs of acute inflammation? (5)

A

1) rubor=redness
2) tumor=swelling
3) calor=heat
4) dolor=pain
5) loss of function

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3
Q

Which changes occur in tissues in acute inflammation? (3)

A

1) changes in blood flow
2) exudation of fluid into tissues
3) infiltration of inflammatory cells

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4
Q

What are the steps of the vascular phase of acute inflammation? (3)

A

1) Transient vasoconstriction of arterioles
2) Vasodilation of arterioles and then capillaries (increased blood flow -> heat and redness)
3) Increased permeability of blood vessels

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5
Q

What is stasis?

A

Increased viscosity of blood

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6
Q

Which chemical mediator is responsible for the immediate early response?

A

Histamine

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7
Q

Which cells release histamine? (3)

A

Mast cells
Basophils
Platelets

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8
Q

What does the release of histamine cause? (3)

A

1) Vascular dilatation
2) Transient increase in vascular permeability
3) Pain

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9
Q

Histamine is released in response to which stimuli?

A

1) physical damage
2) immunologic reactions
3) Complement (C3a, C5a)

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10
Q

What determines fluid flow across vessel walls?

A

Balance of hydrostatic and colloid osmotic pressure

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11
Q

Complete the sentence:

Increased hydrostatic pressure leads to __________ fluid flow out of the vessel

A

Increased

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12
Q

Complete the sentence:

Increased colloid osmotic pressure of interstitium leads to __________ fluid flow out of vessel

A

Increased

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13
Q

Complete the sentences:

Arteriolar dilatation leads to ____________ hydrostatic pressure. Increased permeability of vessel walls leads to _______ of protein into interstitium therefore net flow of fluid out of cell leads to ___________.

A

Increased
Loss
Oedema

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14
Q

True or false: oedema can be transudate or exudate

A

TRUE

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15
Q

Define transudate

A

Oedema has the same protein content as plasma

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16
Q

Define exudate

A

Oedema has more protein than plasma

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17
Q

What does oedema lead to?

A

Increased lymphatic drainage

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18
Q

What is fluid loss in inflammation called?

A

Exudate (high protein content)

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19
Q

Fluid loss due to hydrostatic pressure imbalance is called what?

A

Transudate

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20
Q

What are the mechanisms of vascular leakage? (5)

A

1) endothelial contraction (gaps)
2) cytoskeletal reorganisation (gaps)
3) direct injury - toxic burns, chemicals
4) leukocyte dependent injury
5) increased transcytosis

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21
Q

What is transcytosis?

A

Fluid moves across wall of non-leaky blood vessel

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22
Q

Which plasma protein is good at localising inflammation?

A

Fibrin

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23
Q

Which is the primary type of WBC involved in inflammation?

A

Neutrophil

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24
Q

What is another name for neutrophil?

A

Polymorph

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25
Q

What are the steps of neutrophil infiltration? (4)

A

1) Margination
2) Rolling
3) Adhesion
4) Emigration

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26
Q

Describe the first step of neutrophil infiltration

A

Margination-stasis causes neutrophils to line up at the edge of blood vessels along the endothelium

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27
Q

Describe the second step of neutrophil infiltration

A

Rolling-Neutrophils roll along the endothelium, sticking to it

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28
Q

Describe the third step of neutrophil infiltration

A

Adhesion-Neutrophils stick avidly to the endothelium

29
Q

Describe the fourth step of neutrophil infiltration

A

Emigration-neutrophils emigrate through blood vessel wall

30
Q

How do neutrophils escape from vessels? (3)

A

1) Relaxation of inter-endothelial cell junctions
2) Digestion of vascular basement membrane
3) Movement

31
Q

What is chemotaxis?

A

Movement along concentration gradients of chemoattractants

32
Q

What are the three simple steps of phagocytosis?

A

1) contact
2) recognition
3) internalisation

33
Q

What happens in opsonisation?

A

Substances are coated by immunoglobulins or complement to make them recognisable by neutrophils

34
Q

Give an example of an opsonin

A

C3b

35
Q

What do phagosomes fuse with?

A

Lysosomes, to produce secondary lysosomes

36
Q

What are the two killing mechanisms?

A

1) oxygen dependent

2) oxygen independent

37
Q

What is produced in the oxygen dependent killing mechanism?

A

Produces superoxide and hydrogen peroxide

38
Q

Which killing mechanism is more effective?

A

Oxygen dependent

39
Q

How do neutrophils migrate to a site of injury?

A

Chemotaxis

40
Q

Why are neutrophils not 100% reliable?

A

Activated neutrophils may release toxic metabolites and enzymes, causing damage to host tissue

41
Q

What are the three main classes of chemical mediators in acute inflammation?

A

1) proteases
2) prostaglandins/leukotrienes
3) cytokines/chemokines

42
Q

Give examples of proteases (chemical meditators in acute inflammation)

A

Kinins
Complement system (C3a, C5a)
Coagulation system

43
Q

True or false: cytokines are small proteins and chemokines are large proteins

A

FALSE - other way round

44
Q

Which chemical mediators are responsible for increased blood flow in acute inflammation?

A

Histamine

Prostaglandins

45
Q

Which chemical mediators are responsible for vascular permeability in acute inflammation?

A

Histamine

Leukotrienes

46
Q

Which chemical mediators are responsible for neutrophil chemotaxis in acute inflammation?

A

C5a
LTB4
Bacterial peptides

47
Q

Which chemical mediator is responsible for phagocytosis in acute inflammation?

A

C3b

48
Q

How does exudation of fluid combat injury? (3)

A

1) delivers plasma proteins to area of injury
2) dilutes toxins
3) increases lymphatic drainage

49
Q

How does infiltration of cells combat injury?

A

Removes phagocytic organisms (mostly polymorphs but also macrophages) and necrotic debris

50
Q

How does vasodilation combat injury?

A

Increases delivery

Increases temperature

51
Q

How does pain and loss of function combat injury?

A

Enforces rest

Reduces chance of further traumatic damage

52
Q

True or false: acute inflammation can be local or systemic

A

TRUE

53
Q

What are the local complications of acute inflammation? (4)

A

1) swelling-blockage of tubes
2) exudate-compression (eg cardiac tamponade), serositis
3) loss of fluid eg burns
4) pain and loss of function

54
Q

What are the systemic effects of acute inflammation? (3)

A

1) fever
2) leukocytosis
3) acute phase response-decreased appetite, raised pulse, altered sleep patterns

55
Q

The acute phase response leads to changes in plasma concentrations of what?

A

Acute phase proteins:

  • CRP
  • alpha-1 antitrypsin
  • fibrinogen
56
Q

Define shock

A

Clinical syndrome of systemic circulatory failure

57
Q

What may happen after the development of acute inflammation? (4)

A

1) complete resolution
2) continued acute inflammation with chronic inflammation=abscess
3) chronic inflammation and fibrous repair
4) death

58
Q

True or false: all mediators of acute inflammation have long half-lives

A

FALSE - have short half-lives

59
Q

Give an example of a chemical mediator which is unstable and can break down by itself?

A

Prostaglandins

60
Q

What can acute inflammation in the meninges cause?

A

Vascular thrombosis and reduced cerebral perfusion

61
Q

What are the symptoms of lobar pneumonia?

A 
Worsening fever
Prostration 
Hypoxaemia 
Dry cough 
Breathlessness
62
Q

Name some examples of causes of skin blisters

A

Heat
Sunlight
Chemical

63
Q

What are the predominant features of skin blisters?

A

Pain

Profuse exudate

64
Q

What type of necrosis occurs at the centre of an abscess?

A

Liquefactive

65
Q

True or false: abscesses can cause high pressure and therefore lots of pain

A

TRUE (sadly)

66
Q

What happens in acute inflammation in serous cavities?

A

Exudate pours into cavity

67
Q

What is ascites?

A

Oedema in peritoneal cavity

68
Q

What is the inflammation in pericarditis described as?

A

Bread and butter pericarditis

69
Q

Give some examples of disorders of acute inflammation

A

Alpha-1 antitrypsin deficiency
Inherited Complement deficiencies
Defects in neutrophil function and numbers

Semester 2-PP (13 decks)

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