Week 3- Inflammation Flashcards

1
Q

What is inflammation?

A

A non specific response to injury designed to remove the cause and consequence

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2
Q

What are the 4 signs of acute inflammation? (Give the english AND latin)

A

Color/rubor
Pain/dolor
Swelling/tumor
Heat/calor

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3
Q

What are some causes of acute inflammation?

A

Allergens, non apoptotic cell injury, physical damage, temperature

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4
Q

What are the 3 steps of acute inflammation? Briefly describe each one

A
  1. Steady state
  2. Damage: inflammatory signals, vasodialators eg histamine released, vascular changes eg increased permeability, plasma leakage, reduced flow, dilatation
  3. Immune cell recruitment: chemokines produced at injury site and diffuse out in a gradient, leukocytes w complementary receptors migrate to chemokine source
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5
Q

What is exudate?

A

When fluid, proteins and cells leak out of blood vessels

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6
Q

What are some soluble mediators that may be released at the site of injury?

A

Histamine, chemokines, cytokines, complements

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7
Q

Describe the process of neutrophil extravasion

A
  1. Cytokines cause endothelial upregulation of adhesion molecules called selectin
  2. Carbohydrate ligands on neutrophils bind to selectins
  3. Chemokines encourage tight adhesion by stimulating a low to high affinity switch
  4. Transmigration occurs where the cytoskeleton is rearranged to allow the neutrophil to enter the cell without cell death
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8
Q

What do neutrophils do once they have reached the sight of inflammation?

A
  1. Pathogen recognition (via polysaccarides)
  2. Pathogen destruction (via phagocytosis or netosis where the neutrophil releases its DNA and traps the pathogen in a DNA net)
  3. Cytokine secretion (more immune cells are recruited)
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9
Q

What is netosis?

A

When at the sight of inflammation, the neutrophil releases its DNA and traps the pathogen in a DNA net

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10
Q

How is acute inflammation resolved?

A
  1. Neutrophils have a short half life
  2. Macrophages clear apoptotic cells and produce anti inflammatory mediators
  3. ECM is deposited at the site for repair
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11
Q

What is chronic inflammation?

A

Chronic inflammation is persistent/ongoing due to constant stimuli
Macrophages, T cells etc are recruited instead of neutrophils
The agent is not cleared

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12
Q

How are macrophages involved in inflammation?

A

Recruited as monocytes
Tissue resident
Phagocytic, cytotoxic, anti inflammatory
Cons: can be pro fibrotic, cytotoxicity kills good cells

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13
Q

How are lymphocytes involved in inflammation?

A

Innate and adaptive cells work together, T cells (cytotoxic, regulatory) and B cells (produce antibodies and can operate remotely or locally)

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14
Q

What is granulomatous inflammation?

A

Chronic inflammation w formation of granules (these are accumulations of activated macrophages)
Triggered by strong T cell responses

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15
Q

Describe the differences between acute and chronic inflammation in terms of: onset, molecules that dominate, molecules that are released and what happens after

A

Onset: immediate vs delayed
Molecules that dominate: neutrophils vs monocytes
Molecules that are released: histamine vs cytokines
Aftermath: necrosis vs scarring

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16
Q

How are wounds healed?

A

Neutrophils are recruited, macrophages cause fibroblasts to form myofibroblasts, ECM secreted, network is remodeled

17
Q

What are some consequences of inflammation?

A

Scarring, loss of tissue function, respiratory infections