Acute Inflammation 1 Flashcards

0
Q

Triple response

A
  1. Reddening = vasodilation
  2. Flare (red halo) = hyperaemia
  3. Wheal (swelling)= oedema
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1
Q

Vascular Response: Key Processes

A
1.Transient vasoconstriction
–neurogenic – occurs within seconds
2.Arteriolar dilation
–axon reflex arc  capillary beds open: red & hot
–histamine, nitric oxide
3.Increased blood viscosity
–blood stasis
–impedes outflow
4.Increased vascular permeability
–fluid enters interstitial space (transudate)
–hallmark feature of AI
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2
Q

Increased vascular permeability: transudate vs exudate

A

Transudate: low protein ( albumin) less than 30g/L, low cells ( less than 1500 cells per micro/L) NON- INFLAMMATORY RESPONSE

Exudate: high protein ( greater than 30g/L), high cells ( greater than 5000 per micro/L) INFLAMMATORY EFFUSION

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3
Q

Oedema

A

Increase in interstitial fluid

Usually classifies as a transudate ( NON- INFLAMMATORY)

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4
Q

Increased Vascular Permeability

A
  1. Gaps between endothelial cells
    •Vasoactive mediators (histamine, leukotrienes)
    •VEGF-induced channels
  2. Direct endothelial injury
    •Toxins, burns, chemicals
  3. Leukocyte-mediated injury to endothelium
    •Leukocyte products (ROS, enzymes)
  4. Angiogenesis
    •Leakage from new vessels
  5. Radiation damage
    •Sunburn, x-rays, UV radiation damage to endothelial cells
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5
Q

Inducers of Acute Inflammation

A
  • Infections
  • Trauma (+/- sterile)
  • Physical and chemical agents
  • Foreign bodies
  • Tissue necrosis (“bad death”)
  • Hypersensitivity reaction
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6
Q

Components of Acute Inflammation

A

•Vascular Response
–Changes to blood flow and vessel permeability

•Cellular Response
–Recruitment of leukocytes

•Soluble mediators
–Co-ordinators of the tissue response

•Molecular “sensors”
–Control the type of inflammation

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7
Q

Acute Inflammation

A

•Immediate response to tissue damage
•Primarily an innate response
–Cells and molecules of the innate immune system: non-specific
•Local response to limit tissue damage
•Characterised by:
–Leakage of blood proteins (fibrinogen > fibrin)
–Recruitment of leukocytes from the blood
•Inflammatory exudate
–hallmark feature of AI

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8
Q

Cardinal Signs of Acute inflammation

A
  1. Heat (calor)
  2. Pain (dolor)
  3. Redness (rubor)
  4. Swelling (tumor)
  5. Loss of function (functio laesa)
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9
Q

Leukocyte activation

People sometimes say money counts

A

Production of arachidonic acid metabolites
Secretion/ degranulation of lysosomal enzymes
Secretion of cytokines
Modulation of leukocyte
Cell division induction

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10
Q

What are the three types of soluble mediators

A

Vasoactive amines
Cytokines
Arachidonic acid metabolites

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11
Q

What is the arachidonic acid metabolites pathway

A

Phospholipase forms 5-lipoxygenase and cyclooxygenase

5-lipoxygenase forms 12-lipoxygenase

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12
Q

What are cytokines

A

Activate leukocyte
IL-1, IL-2, TNF-a
Induce acute phase response

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13
Q

Tissue necrotic factor are produced by what type of cells?

A

Macrophages

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14
Q

What are interleukins?

A

Produced by leukocytes
Act of leukocytes
Activate T-cells and neutrophils ( phagocytic cells)

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15
Q

What are chemokines?

A

Activators and chemoattractants for leukocytes

16
Q

Two branches of CHEMOTAXIS

A

Exogenous- bacterial

Endogenous- chemokines, cytokines

17
Q

Process of phagocytosis

A
  1. Recognition and attachment
  2. Engulfment- forming a phagosome
  3. Killing and degradation- lysosomes secrete into phagosome
    Oxygen dependent and oxygen independent
18
Q

What do mast cells and basophils produce when they degranulation?

A

Heparin: prevents thrombosis
Histamine: increases vascular permeability
Leukotrienes: increases vascular permeability

19
Q

Difference between mast cells and basophils

A

Basophils are short lives, mast cells are long lives

20
Q

What do eosinophils produce when they degranulate?

A
Enzymes
Toxic proteins
Cytokines
Chemokines
Leukotrienes
21
Q

Leukocytes extravasation

A
1. Extravasation
Leukocytes move from blood to injury
2. Margination
Leukocytes adhere to endothelial wall
3. Transmigration
Leukocytes move through endothelium
4. Migration 
Leukocytes move into interstitial fluid
22
Q

Types of plasma proteins in exudates

A
Albumin: Ca, Cu, Zn
Interferrin: Fe
Heptoglobin: haemoglobin
Ceruloplasmin: Fe mechanism
Immunoglobulins: binding antigens
23
Q

Neutrophils produce

A

Bacteriocidal and oxygen free radicals

24
Q

What is a modified transudate?

A

High proteins

Low cells

25
Q

Triple response

A

Redness- vasodilation
Flare- hyperaemia
Wheal- oedema

26
Q

Increased vascular permeability: mechanisms

A
  1. Gaps between endothelial cells
  2. Direct endothelial injury
  3. Leukocyte- mediated injury to endothelial wall
  4. Angiogenesis- leakage from new vessel
  5. Radiation
27
Q

Vascular changes to acute inflammation

A

Transient vasoconstriction: neurogenic
Arteriolar dilation: histamine and nitric oxide
Increased vascular permeability: fluid enters interstitial fluid
Increased blood viscosity: blood stasis, impedes outflow