HBB - acute inflammation Flashcards

1
Q

What are the cardinal signs of inflammation?

A
Redness
Swelling
Pain
Heat 
Loss of function
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2
Q

What is the mechanism of each of the cardinal signs of inflammation?

A

Redness - capillary dilation
Swelling - exudation, capillary dilation and congregation of cells
Pain - exudation, cellular degranulation effects of mediators
Heat - capillary dilation
Loss of function - pain and exudation

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3
Q

Why is apoptosis associated with little or no inflammation?

A

The fragment is enclosed within cell membrane. So is not recognised as foreign.

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4
Q

What is the endogenous trigger of acute inflammation?

A

DAMPs - Damage Associated Molecular Patterns. These are derived from the host. They initiate and perpetuate an inflammatory response.

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5
Q

What is the exogenous trigger of acute inflammation?

A

PAMPs - Pathogen Associated Molecular Patterns. These are from pathogens. Release cytokines, which initiates inflammation.

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6
Q

What are the 3 main phases of acute inflammation?

A

Vascular phase
Exudative phase
Cellular phase

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7
Q

What are the mediators of the vascular phase of acute inflammation and what is their function?

A

Bradykinin and vasoactive amines - capillary sphincters dilate in order to increase blood flow.
Vasoactive amines, direct damage and leukocyte activity - junctional complexes between endothelial cells open in venules.

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8
Q

What is the exudative phase of acute inflammation?

A

Exudate = pus
Caused by the increased permeability of the capillary bed.
Protein-rich and cell-rich

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9
Q

Which cells are involved in the cellular phase of acute inflammation?

A

Neutrophils
Cells that release enzymes
Phagocytes

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10
Q

What are the steps of the leukocyte adhesion cascade?

A

Cells marginate

Transient weak binding allows for the cell to roll along the endothelium. Mediated by selectin receptors from the endothelial cells. Occurs in capillaries and venules.

Firm adhesion. Cytokines activate the neutrophils and endothelial cells. Cells bind to integrins that are expressed by the cell membrane. This causes the cell to move to the endothelial junction.

Neutrophil transmigrates through the endothelial junction through using leukocyte adhesion molecules found on the endothelial membrane.

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11
Q

What are the 4 mediators of acute inflammation?

A

Histamine
Arachidonic acid metabolites
Free radicals
Cytokines

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12
Q

How does histamine mediate acute inflammation?

A

Causes vasodilation, increase permeability, itching and pain.

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13
Q

Which cells preform and store histamine?

A

Mast cells.

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14
Q

How do arachidonic metabolites mediate acute inflammation?

A

Produces pro-inflammatory factors such as leukotrienes, prostaglandins and thromboxanes.
Produces anti-inflammatory factors such as lipoxin

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15
Q

How do free radicals mediate acute inflammation?

A

Pro-inflammatory function: activates endothelial cells (bradykinin), enhances cytokine production, inactivates antiproteases, injures endothelial cells, chemotactic factors and NO production.
Also has an antioxidant role.

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16
Q

How do cytokines mediate acute inflammation?

A

Modulates other cell types that cause inflammation.
Hematopoietin - GF for cell colonies
Interferons - Antiviral, cell growth, immune activation
Chemokines - Chemoattractants
Tumour necrosis factor - activates cell signalling, pathways for cell survival, death and differentiation
Interleukins - promotes leukocyte development and differentiation

17
Q

How is acute inflammation resolved?

A
  • Remove the stimulus
  • Degradation of pro-inflammatory cytokines
  • Down-regulation of receptors
  • Dephosphorylation signalling molecules
  • Anti-inflammatory mediators
  • Death of inflammatory cells
    May progress to chronic inflammation