Session 2: Acute Inflammation Flashcards

1
Q

When and why does acute inflammation occur?

A
  • Response of living tissue to injury

- Initiated to limit the tissue damage

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2
Q

What are some characteristics of acute inflammation? (4)

A
  1. innate
  2. immediate
  3. stereotyped
  4. Short duration - mins/hrs/few days
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3
Q

What tissue changes are brought about by acute inflammation? (3)

A
  1. Vascular flow
  2. Formation of a fluid exudate
  3. Neutrophil emigration
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4
Q

What are the causes of acute inflammation? (5)

A
  1. Microbial infections
  2. Acute phase hypersensitivity reactions
  3. Physical agents
  4. Chemicals
  5. Tissue necrosis
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5
Q

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

A
  1. Rubor
  2. Tumour
  3. Calor
  4. Dolor
  5. Loss of function
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6
Q

What are the 3 stages of the vascular phase of acute inflammation?

A
  1. Changes in blood flow
  2. Exudation of fluid into tissues
  3. Infiltration of inflammatory cells
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7
Q

What changes to blood flow occur in the vascular phase? (4)

A
  1. Initial few secs vasoconstriction of arterioles
  2. Vasodilation of arterioles and then capillaries
  3. Increased permeability of blood vessels
  4. Stasis - Concentration of RBCs in small vessels and increased viscosity of blood
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8
Q

What is the effect of increased permeability of blood vessels? (2)

A
  1. Exudation of protein-rich fluid into interstitium

2. Slowing of circulation (swelling)

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9
Q

Which chemical mediator in vessels is involved in the immediate early response?

A

Histamine

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10
Q

Which cells release histamine? (3)

A

Mast cells
Basophils
Platelets

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11
Q

What stimulates the release of histamine? (5)

A
  1. Physical damage
  2. Immunologic reaction
  3. Complement factors C3a and C5a
  4. IL-1
  5. Factors from neutrophils and platelets
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12
Q

What effects does histamine bring about? (3)

A
  1. Vascular dilatation
  2. Transient increase in vascular permeability
  3. Pain
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13
Q

What chemical mediators are involved in the persistent response? (Incompletely understood) (2)

A

Leukotrienes

Bradykinin

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14
Q

What determines fluid loss from vessels? (2)

A
  1. Increased hydrostatic pressure

2. Increased colloid osmotic pressure of interstitium

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15
Q

What causes an increase in hydrostatic pressure resulting in fluid exudation?

A

Arteriolar dilatation

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16
Q

What are the consequences of vascular leakage?

17
Q

What are the 2 types of fluid that could accumulate in the interstitium in oedema?

A

Transudate or exudate

18
Q

What is transudate?

What is exudate?

A

Transudate - low protein content (fluid loss due to hydrostatic pressure imbalance only)
Exudate - more protein content than plasma (inflammation)

19
Q

How can fluid extracted from pleural effusion help in diagnosis?

A

High protein content (exudate) - inflammation

Low protein content - heart failure or venous outflow obstruction

20
Q

What are the mechanisms of vascular leakage? (5)

A
  1. Endothelial contraction - gaps
  2. Cytoskeletal reorganisation - gaps
  3. Direct injury of vessel walls - toxic burns, chemicals
  4. Leukocyte-dependent injury
  5. Increased transcytosis - channels across endothelial cytoplasm
21
Q

Which chemical mediators are involved in endothelial contraction?

A

Histamine

Leukotrienes

22
Q

Which chemical mediators are involved in cytoskeletal reorganisation?

A

Cytokines

  • IL-1
  • TNF
23
Q

How do leukocytes trigger leukocyte-dependent injury?

A

Toxic oxygen species and enzymes released

24
Q

Which signal protein is responsible for transcytosis?

A

VEGF - vascular endothelial growth factor

25
Which plasma proteins are delivered to area of injury though exudation of fluid? (3)
1. Immunoglobulins 2. Inflammatory mediators (complement factors) 3. Fibrinogen
26
Why is fibrinogen delivered to the site of injury?
- gets converted to insoluble fibrin - part of the haemostatic cascade - localises inflammation - prevents spreading to serosal lining
27
What is the primary type of WBC involved in acute inflammation?
Neutrophils
28
What are the four stages of infiltration of neutrophils? What happens in each stage?
1. Margination - stasis causes neutrophils to line up at the edge of blood vessels along endothelium 2. Rolling - neutrophils roll along endothelium, sticking to it intermittently 3. Adhesion - cells stick more avidly 4. Emigration - movement through blood vessel wall
29
What is stasis?
Sludging of RS in the middle of the blood vessel due to slower blood flow