Lecture 3: Inflammation II Flashcards

1
Q

3 possible outcomes from acute inflammation

A
  1. Regeneration
  2. Scarring/fibrosis
  3. Progression to chronic inflammation
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2
Q

Causes of chronic inflammation

A
  1. Prolonged injury/irritant exposure
  2. Immune-mediated disease
  3. Persistent infection
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3
Q

Cells of chronic inflammation

A
  • Monocytes/macrophages
  • Lymphocytes
  • Eosinophils
    Not PMNs (acute)
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4
Q

T helper subtypes and their cytokines

A

Th1: pro-inflam. TNF, IL-1, IFNγ
Th2: IL-4, -5, -13
Th17: IL-17, PMN recruitment

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5
Q

Neutrophils vs macrophages (both phagocytes)

A

PMNs: much shorter life span, respiratory burst, low iNOS levels, prominent degranulation, NETs, lysosomal enzyme release

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6
Q

Chronic inflammation process

A

Persistent tissue injury -> inflam./T cell/macrophage cytokines -> fibroblast recruitment/differentiation -> scarring/fibrosis

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7
Q

Layers of chronic inflammation wounds

A

Occurs w/ deeper, more severe wounds
1. Fibrinopurulent exudate (fibrin/PMNs)
2. Granulation tissue (capillary network w/ fibroconnective tissue/ECM)
3. Scarring

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8
Q

TNF

A

Works in local concentrations; drives chronic inflammation by increasing inflam. cell recruitment and MMP, PG secretion by synovial cells. Inhib. as treatment for many diseases

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9
Q

IL-6

A

Synthesized by many different cells. Triggers:
- Acute phase reactant synth. by liver
- Systemic fever
- B cell growth

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10
Q

Acute Phase Proteins

A

Induced by cytokines, synth. in liver. Plasma proteins that are an inflammatory marker e.g. CRP. Measured w/ ESR

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11
Q

Granulomatous inflammation

A

Assoc. w/ specific pathologic conditions; formation of granuloma in attempt to eliminate/contain insult too large for a single cell

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12
Q

Granuloma

A

Macrophage + other cells aggregate around large pathogen/irritant (epitheliod macrophages, lymphocytes, fibroblasts, multinucleated giant cells

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