Acute Inflammation Flashcards

1
Q

What is inflammation and why is it important?

A

A response of living tissue to injury

It delivers defensive materials to the site of injury, clears damaged tissues and initiates repair

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2
Q

What is acute inflammation?

A

The rapid response to an injury to tissue that aims to deliver mediators of host defences

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3
Q

What kinds of things cause acute inflammation?

A
Foreign bodies 
Infections 
Immune reactions 
Trauma 
Tissue necrosis
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4
Q

What are the three essential components that make up acute inflammation?

A

Vascular and cellular reactions
Chemical mediators
Protective functions

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5
Q

What vascular reactions occur in tissue during acute inflammation?

A

Changes in blood flow: vasoconstriction (secs), vasodilation, increased blood flow, increased permeability, increase in haematocrit, stasis

Exudation of fluid into tissues: increased hydrostatic pressure, loss of protein, increased oncotic pressure, fluid moves out of vessels and causes oedema

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6
Q

What is the difference between exudate and transudate?

A

Exudate is protein rich and is formed as a result of inflammation
Transudate is protein poor and occurs in normal vessels when the hydrostatic pressure is increase in the capillary (e.g. in heart failure)

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7
Q

What cellular reactions occur in tissues during acute inflammation?

A

Neutrophils and other inflammatory cells migrate to the site of inflammation

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8
Q

How do neutrophils migrate to sites of inflammation?

A

Summoned by chemotaxis, activated to higher metabolic state then:
Margination - stick to endothelial surface
Rolling - roll along the endothelial surface
Adhesion - bind to adhesion molecules and stop rolling
Emigration (Diapedesis) - dig themselves out of venules by digesting the cell BM

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9
Q

What chemical mediators of acute inflammation are there and what do they do?

A

Histamine - increases vascular permeability
Leukotrines - increase vascular permeability
Bradykinin - dilation of blood vessels
Cytokines/chemokines- chemoattraction
Clotting cascades- generate inflammatory mediators
Complement components- C3a, C5a, opsonin C3b

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10
Q

What protective components of acute inflammation are there and what do they do?

A

Delivery of plasma proteins- dilution of toxins and increased lymphatic drainage to clear the site of inflammation
Infiltration of cells- remove debris
Pain and loss of function- reenforce rest and reduce further damage (bradykinin)

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11
Q

Give some local complications of acute inflammation

A
Swelling- blockage 
Exudate- compression 
Loss of fluid e.g.burns- dehydration 
Pain
Loss of function
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12
Q

Give some systemic complications of acute inflammation

A
Fever 
Leukocytosis 
APP - CRP, fibrinogen 
Decreased appetite 
Increased pulse 
Shock- circulatory failure (bad)
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13
Q

What are the sequelae for acute inflammation, best outcome to worst?

A
  • Complete resolution
  • Continued acute inflammation with chronic inflammation (abscess)
  • Chronic inflammation and fibrous repair, probably with tissue regeneration
  • Death
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14
Q

Give examples of 4 types of exudate that can be seen in inflammation

A
  1. Pus/abscess
  2. Haemorrhagic exudate - destructive infection/malignancy
  3. Serous exudate - blisters
  4. Fibrinous exudate
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