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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
What are the steps of neutrophil infiltration? (4)
1) Margination 2) Rolling 3) Adhesion 4) Emigration
26
Describe the first step of neutrophil infiltration
Margination-stasis causes neutrophils to line up at the edge of blood vessels along the endothelium
27
Describe the second step of neutrophil infiltration
Rolling-Neutrophils roll along the endothelium, sticking to it
28
Describe the third step of neutrophil infiltration
Adhesion-Neutrophils stick avidly to the endothelium
29
Describe the fourth step of neutrophil infiltration
Emigration-neutrophils emigrate through blood vessel wall
30
How do neutrophils escape from vessels? (3)
1) Relaxation of inter-endothelial cell junctions 2) Digestion of vascular basement membrane 3) Movement
31
What is chemotaxis?
Movement along concentration gradients of chemoattractants
32
What are the three simple steps of phagocytosis?
1) contact 2) recognition 3) internalisation
33
What happens in opsonisation?
Substances are coated by immunoglobulins or complement to make them recognisable by neutrophils
34
Give an example of an opsonin
C3b
35
What do phagosomes fuse with?
Lysosomes, to produce secondary lysosomes
36
What are the two killing mechanisms?
1) oxygen dependent | 2) oxygen independent
37
What is produced in the oxygen dependent killing mechanism?
Produces superoxide and hydrogen peroxide
38
Which killing mechanism is more effective?
Oxygen dependent
39
How do neutrophils migrate to a site of injury?
Chemotaxis
40
Why are neutrophils not 100% reliable?
Activated neutrophils may release toxic metabolites and enzymes, causing damage to host tissue
41
What are the three main classes of chemical mediators in acute inflammation?
1) proteases 2) prostaglandins/leukotrienes 3) cytokines/chemokines
42
Give examples of proteases (chemical meditators in acute inflammation)
Kinins Complement system (C3a, C5a) Coagulation system
43
True or false: cytokines are small proteins and chemokines are large proteins
FALSE - other way round
44
Which chemical mediators are responsible for increased blood flow in acute inflammation?
Histamine | Prostaglandins
45
Which chemical mediators are responsible for vascular permeability in acute inflammation?
Histamine | Leukotrienes
46
Which chemical mediators are responsible for neutrophil chemotaxis in acute inflammation?
C5a LTB4 Bacterial peptides
47
Which chemical mediator is responsible for phagocytosis in acute inflammation?
C3b
48
How does exudation of fluid combat injury? (3)
1) delivers plasma proteins to area of injury 2) dilutes toxins 3) increases lymphatic drainage
49
How does infiltration of cells combat injury?
Removes phagocytic organisms (mostly polymorphs but also macrophages) and necrotic debris
50
How does vasodilation combat injury?
Increases delivery | Increases temperature
51
How does pain and loss of function combat injury?
Enforces rest | Reduces chance of further traumatic damage
52
True or false: acute inflammation can be local or systemic
TRUE
53
What are the local complications of acute inflammation? (4)
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
What are the systemic effects of acute inflammation? (3)
1) fever 2) leukocytosis 3) acute phase response-decreased appetite, raised pulse, altered sleep patterns
55
The acute phase response leads to changes in plasma concentrations of what?
Acute phase proteins: - CRP - alpha-1 antitrypsin - fibrinogen
56
Define shock
Clinical syndrome of systemic circulatory failure
57
What may happen after the development of acute inflammation? (4)
1) complete resolution 2) continued acute inflammation with chronic inflammation=abscess 3) chronic inflammation and fibrous repair 4) death
58
True or false: all mediators of acute inflammation have long half-lives
FALSE - have short half-lives
59
Give an example of a chemical mediator which is unstable and can break down by itself?
Prostaglandins
60
What can acute inflammation in the meninges cause?
Vascular thrombosis and reduced cerebral perfusion
61
What are the symptoms of lobar pneumonia?
``` Worsening fever Prostration Hypoxaemia Dry cough Breathlessness ```
62
Name some examples of causes of skin blisters
Heat Sunlight Chemical
63
What are the predominant features of skin blisters?
Pain | Profuse exudate
64
What type of necrosis occurs at the centre of an abscess?
Liquefactive
65
True or false: abscesses can cause high pressure and therefore lots of pain
TRUE (sadly)
66
What happens in acute inflammation in serous cavities?
Exudate pours into cavity
67
What is ascites?
Oedema in peritoneal cavity
68
What is the inflammation in pericarditis described as?
Bread and butter pericarditis
69
Give some examples of disorders of acute inflammation
Alpha-1 antitrypsin deficiency Inherited Complement deficiencies Defects in neutrophil function and numbers

Semester 2-PP (13 decks)

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