Week 3 - Inflammation Flashcards

1
Q

Goal of inflammation

A

respond to stimuli -> restore balance

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2
Q

What are the 5 cardinal signs of inflammation

A
  1. pain
  2. heat
  3. redness
  4. swelling
  5. loss of function
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3
Q

Sequence of events during an acute inflammatory response

A
  • damaged cells and immune cells at the site of injury release chemical mediators
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4
Q

Action of chemical mediators in acute inflammatory response

A
  • Pain response: bind to nearby nociceptors
  • Vascular response: vasodilation and increased capillary permeability
  • cellular response: attract immune cells to the site of injury (chemotaxis)
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5
Q

Role of Platelets in inflammatory response

A

release blood-clotting proteins at the wound site (if needed)

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6
Q

Role of mast cells in inflammatory response

A

secrete chemical mediators

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7
Q

Role of neutrophils in inflammatory response

A

migrate to the site and secrete factors that kill pathogens, phagocytosis to remove pathogens and debris

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8
Q

Role of macrophages in inflammatory response

A

secrete cytokines, phagocytosis to remove pathogens and debris

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9
Q

Role of fibroblasts in inflammatory response

A

build connective tissue as part of the healing process

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10
Q

Mast cell chemical mediators

A
  • histamine
  • prostaglandins
  • Leukotrienes
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11
Q

Macrophages chemical mediators

A
  • cytokines (interleukins and lymphokines)
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12
Q

Platelets chemical mediator

A
  • platelet activating factor
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13
Q

Plasma proteins - chemical mediators

A
  • bradykinin
  • complement system
  • prothrombin & fibrinogen
  • C-reactive protein (CRP)
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14
Q

Histamine role

A

vasodilation and increased capillary permeability

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15
Q

Prostaglandins role

A

vasodilation and increased capillary permeability, fever, pain

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16
Q

Leukotrienes role

A

vasodilation and increased capillary permeability, chemotaxis

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17
Q

Cytokines (interleukins & lymphokines) role

A

fever, chemotaxis, leukocytosis

18
Q

Platelet-activating factor role

A

platelet aggregation

19
Q

Bradykinin role

A

vasodilation and increased capillary permeability, pain, chemotaxis

20
Q

Complement system role

A

vasodilation and increased capillary permeability, chemotaxis, potentiate histamine release

21
Q

What is exudate?

A

interstitial fluid collected in the area of inflammation

22
Q

Serous exudate characteristics

A

watery, fluid + small amounts of protein and white blood cells

23
Q

Fibrinous exudate characteristics

A

thick and sticky, higher cell and fibrin content

24
Q

Purulent exudate characteristics

A

thick and yellow-green colour, higher white blood cells and cell debris
- may also contain microorganisms
- suggests bacterial infection

25
Hemorrhagic exudate characteristics
blood vessels damaged
26
What is an abscess
pocket of purulent exudate in a solid tissue
27
Changes in the blood with inflammation: Leukocytosis
increased numbers of white blood cells, especially neutrophiles
28
Changes in the blood with inflammation: differential count
proportion of each type of white blood cells altered, depending on the cause
29
Changes in the blood with inflammation: Plasma proteins
increased fibrinogen and prothrombin
30
Changes in the blood with inflammation: C-reactive protein and other cytokines
a protein not normally found in the blood, but appears with acute inflammation and necrosis within 24-48 hours
31
Changes in the blood with inflammation: Increased erythrocyte sedimentation rate (ESR)
elevated plasma proteins increase the rate at which red blood cells settle in a sample
32
Changes in the blood with inflammation: Cell enzymes
released from necrotic cells and enter tissues fluids and blood: may indicate the site of inflammation
33
Non-pharmaceutical treatments for inflammation
- compression - cold - hot - elevation - rest/avoid further trauma in acute phase
34
What are the potential healing fates for inflammation?
- resolution - regeneration - replacement
35
Inflammatory fate - resolution
damaged cells recover
36
inflammatory fate - regeneration
damaged cells are a cell type that can divide by mitosis and can therefore be replaced by an identical type
37
Inflammatory fate - replacement
damaged cells replaced by connective tissue (scar tissue) loss of function in this area
38
What immune cells infiltrate in acute inflammation
mainly neutrophils
39
What immune cells infiltrate in chronic inflammation?
monocytes, macrophages, lymphocytes
40
Chronic inflammation etiology
- acute inflammation that is unable to resolve - low level exposure to an irritant or foreign material - autoimmune disorders - defect in cells responsible for mediating inflammation - inflammatory and biochemical inducers causing oxidative stress and mitochondrial dysfunction
41
Non pharmaceutical treatment of chronic inflammation
- nutrition - aerobic and resistance exercise - sleep quality and quantity - stress reduction