Acute Inflammation Flashcards

(16 cards)

1
Q

Acute Inflammation and its functions

A

Rapid Response of vascularised tissue to injury

  • Eradicates cause of injury
  • Remove damaged cellular material
  • Initiates repair process

(Think of out of control house party and the cleanup the morning afterwards; kicking out people who are still there, tidy up the mess, call somebody repair broken windows and such)

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2
Q

What can trigger acute inflammation

A
Infection
Trauma
Necrosis
Immune Reactions
Foreign bodies
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3
Q

What happens during acute inflammation

A
  1. Vasodilation - Local blood vessels briefly contract then dilate to slow blood flow to the area (within seconds, mediated by mast cells and NO2 from endothelial cells); this slowing allows neutrophils to come into contact with endothelium
  2. Increased vascular permeability - Tight junctions between capillary endothelial cells loosen and leak fluid rich in mediators to surrounding tissue (contains neutrophils, come macrophages and lymphocytes, plasma and proteins - lots of fibrinogen), causes swelling
  3. Cellular Activation/Migration - [Neutrophils are made to adhere to endothelium, increased motility allows emigration from blood vessels to surrounding tissue]
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4
Q

How do cells roll across blood vessels

A

Cell adhesion molecules (e.g. selectins and integrins) on the endothelial cells enable macrophages to adhere to them and slip out of the vessel then migrate to the wound and do their shit

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5
Q

Phagocytosis in inflammation

A

WBCs (neutrophils and macrophages but less so) in large numbers leave the blood and engluf/neutralise foreign particles; the activation of the WBCs makes it easier for them to leave the blood and be more efficient at phagocytosis

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6
Q

Describe the life span of neutrophils during activity

A

Clearing cellular debris then getting full up and dying - short lived

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7
Q

Phagosome

A

Vesicle formed around a particle engulfed by a phagocyte via phagocytosis

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8
Q

Compare phagocytosis by macrophages and neutrophils

A

Phagocytosis by macrophages is slower and less of a burst so they can keep going back. They become more and more useful the longer that the inflammation lasts

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9
Q

Suffix -itis

A

Acute inflammation of x

e.g. gastritis - inflammation of stomach

pleurisy (exception) - inflammation of gas around lungs

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10
Q

Examples of bad inflammation

A

Autoimmune disorders like rheumatoid arthritis, allergies, strong response to a severe infection

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11
Q

What does bradykinin mediate

A

It mediates pain

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12
Q
A
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13
Q

Systemic (full body) effects of acute inflammation

A
Neutrophilia
Fever
Fatigue
Loss of Appetite
Increased acute phase proteins in blood
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14
Q

Where do systemic effects of acute inflammation come from

A

They are mediated by cytokines (mainly from activated macrophages) which act on the brain in the acute inflammatory response as well as on the bone marrow to increase neutrophil production

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15
Q

How long does acute phase response take and what are the 3 acute phase proteins

A

Onset within hours - days

Fibrinogen
C Reactive Protein (CRP)
Serum Amyloid A (SAA)

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16
Q

Which cytokines upregulate acute phase proteins the most; where do they come from

A

TNFα, IL-1 (increases SAA), IL-6 (increases CRP and fibrinogen)

They come from macrophages