4. Acute phase reaction Flashcards

1
Q

Acute inflammation

A

A healthy reaction by the body to virtually any trauma

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2
Q

Acute phase reaction

A

= sysinflammation
It’s a protective response of connective tissue to injury
Aim: eliminate injury + start repair process

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3
Q

Classification of inflammation

A

1) Local
- Acute
- Chronic
2) Systemic
- Acute phase reaction

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4
Q

Steps of local inflammation

A

1) Vasodilation (minutes)
2) Increased capillary permeability (plasma exudation) (minutes)
3) Inflammatory cells (hours)

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5
Q

Components of local immune response

A
  • Dendritic cell w/TLR
  • Macrophage
  • Neutrophil granulocyte
  • Mast cell
  • Platelets
  • Cytokines
  • Complement system
  • Coagulation system
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6
Q

Vascular changes in inflammation

A
  • Blood stasis

- Increased vascular permeability

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7
Q

Innate immunity characteristics

A
  • Non-antigen-specific
  • Immediate action
  • No memory
  • Linear amplification
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8
Q

Adaptive immunity characteristics

A
  • Antigen-specific
  • Latency
  • Memory
  • Exponential amplification
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9
Q

Causes of acute phase reaction

A
Exogenous:
- Infection
- Chemical
- Radioactive irradiation, active radicals
- Necrosis
Endogenous
- Tumor
- Intense local immune reaction
- Major metabolic disturbance
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10
Q

Components in blood clotting

A
  • PAF (platelet activating factor)
  • TXA2
  • MCP (macrophage chemoattractant protein)
  • TGF (transforming growth factor)
  • IL
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11
Q

Initiation of acute phase reaction

A
  • Bleeding and blood clotting -> platelet activation-> IL-1
  • Infectious agent -> complement activation-> C5a + C3a
  • Immune complex -> same as above
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12
Q

Small complement fragments and their role

A

C3a, C4a, C5a (“anaphylatoxins”)

  • Mast cell degranulation
  • Chemotaxis
  • Leukocyte recruitment
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13
Q

Anaphylatoxins

A

C3a, C4a, C5a

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14
Q

Middle stage of acute phase reaction (“alarm”)

A

Increased levels of IL-6, IL-1, TNFα and IFNγ throughout the body, caused by:

  • Macrophage
  • Endothel cells
  • Fibroblasts
  • Keratinocytes
  • T cells
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15
Q

The two “fire departments” (anti-inflammatory)

A

1) Hypothalamic-pituitary-adrenal axis
- Activated by IL-6
- Cortisol anti-inflammatory effector
2) Liver
- Activated by IL-6, IL-1 and TNF
- Effector molecules:
- > Serum amyloid protein
- > C reactive protein
- > Mannose binding protein
- > Fibrinogen

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16
Q

Acute phase proteins: protease inhibitors

A

α2-macroglobulin and α1-antitrypsin

17
Q

Acute phase proteins: complement

A

C3, factor B and C1 inhibitor

18
Q

Acute phase proteins: coagulation

A

Fibrinogen

19
Q

Acute phase proteins: opsonins

A

C3, CRP, SAA, SAP, mannose binding lectin

20
Q

Acute phase proteins: immune response modifiers

A

C3, SAP, protein inhibitor

21
Q

Acute phase proteins: radical-cathing

A

Albumin, SAA, coeruloplasmine

22
Q

Acute phase proteins that increase

A

1,5-2X: C3, Bf, coeruloplasmine
2-4X: α1-antitrypsin, haptoglobulin, fibrinogen
6-8X: C1 inhibitor
100-1000X: CRP, SAA !!

23
Q

Acute phase proteins that decrease

A

0,4-0,6X: transferrin, albumin, fibronectin

24
Q

Function of acute phase proteins

A
  • Coagulation
  • Opsonisation
  • Protease inhibitors
  • Radical cathing
  • Immuno modulation
  • Carrier proteins
25
Q

CRP

A

Opsonization APP

  • Bind to phosphocholine on surface of dead cells and pathogens
  • Enhances phagocytosis of particularily bacteria and autoantigens