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
Q

Hemorrhagic exudate characteristics

A

blood vessels damaged

26
Q

What is an abscess

A

pocket of purulent exudate in a solid tissue

27
Q

Changes in the blood with inflammation: Leukocytosis

A

increased numbers of white blood cells, especially neutrophiles

28
Q

Changes in the blood with inflammation: differential count

A

proportion of each type of white blood cells altered, depending on the cause

29
Q

Changes in the blood with inflammation: Plasma proteins

A

increased fibrinogen and prothrombin

30
Q

Changes in the blood with inflammation: C-reactive protein and other cytokines

A

a protein not normally found in the blood, but appears with acute inflammation and necrosis within 24-48 hours

31
Q

Changes in the blood with inflammation: Increased erythrocyte sedimentation rate (ESR)

A

elevated plasma proteins increase the rate at which red blood cells settle in a sample

32
Q

Changes in the blood with inflammation: Cell enzymes

A

released from necrotic cells and enter tissues fluids and blood: may indicate the site of inflammation

33
Q

Non-pharmaceutical treatments for inflammation

A
  • compression
  • cold
  • hot
  • elevation
  • rest/avoid further trauma in acute phase
34
Q

What are the potential healing fates for inflammation?

A
  • resolution
  • regeneration
  • replacement
35
Q

Inflammatory fate - resolution

A

damaged cells recover

36
Q

inflammatory fate - regeneration

A

damaged cells are a cell type that can divide by mitosis and can therefore be replaced by an identical type

37
Q

Inflammatory fate - replacement

A

damaged cells replaced by connective tissue (scar tissue) loss of function in this area

38
Q

What immune cells infiltrate in acute inflammation

A

mainly neutrophils

39
Q

What immune cells infiltrate in chronic inflammation?

A

monocytes, macrophages, lymphocytes

40
Q

Chronic inflammation etiology

A
  • 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
Q

Non pharmaceutical treatment of chronic inflammation

A
  • nutrition
  • aerobic and resistance exercise
  • sleep quality and quantity
  • stress reduction