PP A > Session 2 Lecture 1 > Flashcards

Session 2 Lecture 1 Flashcards

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1
Q

Define acute inflammation

A
  • Response of living tissue to injury
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2
Q

Describe some features of acute inflammation

A

Innate, immediate, early, stereotypes (always the same) and has a short duration (minutes/hours/few days).

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3
Q

What is the purpose of acute inflammation?

A
  • Protect the body against infection
  • Clear tissue damage
  • Initiate tissue repair
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4
Q

What controls acute inflammation?

A

Chemical mediators

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5
Q

What are the causes of acute inflammation?

A
  • Foreign bodies
  • Immune reaction
  • Infection
  • Tissue necrosis
  • Trauma
  • Physical and chemical agents
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6
Q

What are the clinical signs of acute inflammation in Latin?

A

Rubor, tumor, calor, dolor and loss of function

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7
Q

Rubor

A

Redness

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8
Q

Tumor

A

Swelling

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9
Q

Calor

A

Heat

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10
Q

Dolor

A

Pain

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11
Q

What are the phases of acute inflammation

A
  1. Vascular phase

2. Cellular phase

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12
Q

What are the tissue level changes that occur in acute inflammation?

A
  1. Changes in blood flow
  2. Exudation of fluid into tissues
  3. Infiltration of inflammatory cells
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13
Q

What is the first part of vascular phase of inflammation?

A

Changes in blood flow

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14
Q

What is the second part of the vascular phase of inflammation?

A

Exudation of fluid into tissues

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15
Q

Give an overview of what happens in acute inflammation

A
  1. Transient vasoconstriction of arterioles
  2. Vasodilation of arterioles and then capillaries
  3. Increased permeability of blood vessels
  4. Conc of RBC in the small vessels increases
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16
Q

What is a chemical mediator that is important in acute inflammation?

A

Histamine - responsible for the immediate early response

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17
Q

Where is histamine released from?

A

Mast cells, basophils and platelets

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18
Q

When is histamine released?

A

IN response to many stimuli: physical damage; immunological reactions; C3a, C5a, IL-1; factors from neutrophils and platelets.

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19
Q

What does histamine cause?

A
  • Vascular dilatation
  • Transient increases in vascular permeability
  • Pain
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20
Q

What is Starling’s law?

A

Fluid flow across vessel walls is determines by the balance of hydrostatic and colloid osmotic pressure comparing plasma ad interstitial fluid.

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21
Q

What happens with increased hydrostatic pressure?

A

Increase fluid out of the vessel

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22
Q

What happens with increased colloid osmotic pressure on interstitium?

A

Increased fluid flow out of vessel

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23
Q

Explain/ describe how you can get oedema in acute inflammation?

A
  • Arteriolar dilatation leads to inc hydrostatic pressure
  • Inc permeability of vessel walls leads to loss of protein into interstitium
  • Net flow of fluid out of the vessel leads to oedema
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24
Q

Define oedema

A

Excess fluid in interstitium

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25
What are the two different types of oedema?
- Transudate | - Exudate
26
Transudate oedema
Oedema has a lower protein content than the plasma. | - Caused when the fluid loss is due to hydrostatic pressure imbalance only
27
Exudate oedema
Oedema has a higher protein content than plasma | - caused when you have fluid loss due to inflammation
28
What causes endothelial contraction?
Histamine and leukotrienes
29
What causes cytoskeleton reoganisation?
Cytokines, IL-1 and TNF
30
What causes increased transcytosis?
VEGF
31
What are the different mechanisms of vascular leakage?
- Endothelial contraction - Cytoskeletal reorganisation - Direct injury - Leukocyte dependent injury - Increased transcytosis
32
What delivers plasma proteins to the site of injury?
Fibrin
33
What is fibrin?
- Part of the haemostatic cascade | - Crucial to blood clotting because it causes a sticky meshwork to form. Good way to localise inflammation.
34
What is the primary type of white blood cell that is involved in inflammation?
Neutrophils
35
What are neutrophils?
Type of granulocyte
36
What part of inflammation are neutrophils involved in?
Cellular phase
37
What are the different steps to the infiltration of neutrophils?
Margination, Rolling, Adhesion and Emigration
38
How do neutrophils escape from vessels?
- Relaxation of inter-endothelial cells junctions - Digestion of vascular basement membrane - Movement
39
How do neutrophils move?
Chemotaxis
40
What is chemotaxis?
The movements along concentration gradients of chemoattractants.
41
What do neutrophils do?
Phagocytosis
42
What are the different stages of phagocytosis?
Contact, recognition and internalisation
43
What facilitates the process of recognition?
Opsonisation
44
What are the two main killing mechanisms?
- Oxygen dependent | - Oxygen independent
45
What are the main groups of chemical mediators involved in acute inflammation?
- Proteases - Protaglandins/leukotrienes - Cytokines/chemokines
46
What are the different types of proteases?
- Kinins - Complement system C3a, C5a - Coagulation/fibrinolytic system
47
Which chemical mediators increase blood flow?
Histamine and prostaglandins
48
Which chemical mediators cause vascular permeability?
Histamine and leukotrienes
49
Which chemical mediators cause neutrophil chemotaxis?
C5a, LTB4, bacterial peptides
50
Which chemical mediators cause phagocytosis?
C3b
51
What is the hallmark of acute inflammation?
1. Exudate of oedema fluid | - Infiltrate of inflammatory cells
52
How does exudation of fluid combat injury?
- Delivers plasma proteins to area of injury - Dilutes toxins - Increases lymphatic drainage
53
How does infiltration of cells combat injury?
Removes pathogenic organisms, necrotic debris
54
How does vasodilation help combat injury?
Increases delivery and increases temperature
55
How does pain and loss of function help combat injury?
Enforces rest, reduces chance of further traumatic damage
56
What are the local complications of acute inflammation?
- Swelling - blockage of tubes eg bile duct - Exudate - compression - Loss of fluid - burns
57
What are the systemic effects of acute inflammation?
- Fever | - Leukocytosis
58
Define shock
A clinical syndrome of circulatory failure
59
What might happen after the development of acute inflammation?
- Complete resolution - Continued acute inflammation - Chronic inflammation and fibrous repair - Death
60
What are the mechanisms of resolution?
- All mediators of acute inflammation have short half lives - May be inactivated by degredation - Inhibitors may bind
PP A
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