Inflamation Flashcards

1
Q

What are the symptoms of acute inflammation?

A
  • swelling and redness
  • heat and fever
  • pain
  • loss of function
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2
Q

What are the major cell mediators of acute inflammation?

A
  • Neutrophils
  • Macrophages
  • Mast cells
  • Endothelial cells
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3
Q

What are the major secreted mediators of inflammation?

A

-TNF -a
- IL-6
- IL-1
- Acute phase proteins

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4
Q

What prostaglandins are important with acute inflammatory?

A
  • PGE2 (can sensitise nerves to pain)
  • PGE2PGI2 (involved in vasodilation)
  • PGE2 (involved in fever)
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5
Q

What PAMP/PRRs are involved as apart of recognition?

A
  • innate cell recognition of pathogens
    -macrophages and neutrophils
    -mast cells
    -TLRs and other PRRS
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6
Q

What do DAMPS do at recognition?

A
  • innate cell recognition of damage
  • damage associated molecular protein
  • immune system should only see them when damage has occurred
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7
Q

How does redness and heat occur?

A
  • IL-1 and TNF-a
  • capillaries closer to the surface ( increase in redness and heat)
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8
Q

How does swelling occur?

A
  • chemokines
    -cellular infiltration of infection/damage
  • upregulation of adhesion molecules on endothelia (IL-4)
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9
Q

What happens at the acute phase response of acute inflamation?

A
  • pro-inflammatory cytokines (IL-6) lead to downregulation and upregulation of hundreds of proteins
  • release of acute-phase protiens from liver
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10
Q

How does complement effect inflamation?

A
  • C3a (mast cell activation/degranulation)
  • C4a (mast cell activation)
  • C5 a (chemotaxis/ vasodilation/ neutrophil and mast cell activation/degranulation)
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11
Q

What acute phase proteins are released during inflamation?

A
  • haptoglobin (binds to haemoglobin/ prevents bacteria requiring iron from gaining it)
  • fibrinogen (potential damage to tissues/ generates fibrin threads/ clot can block pathogen)
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12
Q

How is pain caused during inflamation?

A
  • serotonin and bradykinin stimulate nerve endings causing pain
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13
Q

What does the hypersecretion of cytokines during sepsis and toxic shock create?

A

positive feedback loop

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14
Q

What causes chronic inflammation?

A
  • T cells important
  • Pathogens or non-pathogens
  • can be Th1/ Th2/Th17
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15
Q

How is acute inflammation resolved?

A
  • short-half life proinflammatory mediatory
  • production of pro-inflammatory prostaglandin and chemokines stops
    -stops neutrophil migration
  • existing neutrophils are phagocytosed by macrophages
  • major change in cell types (Tregs - CD4+ produce anti-inflammatory cytokines)
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16
Q

What does CD4+ cells secrete to have an anti-inflammatory effect?

A
  • Downregulation of Th1 cytokine production
  • Downregulation of MHC class 11
  • Downregulation of co-stimulatory molecules
    SECREATION OF IL-10 AND/OR TGF-B