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Fundamentals Of Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is inflammation?

A

A defensive reaction of a macro organism mechanism against injury

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2
Q

How long does acute inflammation take to develop?

A

Minutes/ hours

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3
Q

How long does acute inflammation last for?

A

Hours or days

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4
Q

What are the 5 (general) triggers for inflammation?

A 
- Infections
Tissue damage due to:
- physical agents
- Chemical agents
- mechanical injury and ischemia
- foreign bodies
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5
Q

What are the 5 responses inflammation induces?

A
  • alerts and initiates appropriate immune response
  • limits the spread of infection or injury
  • protects site from infection
  • eliminates dead cells/ tissue
  • makes conditions right for healing
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6
Q

Is acute inflammation beneficial?

A

Yes

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7
Q

Name the 5Rs

A 
Recognition of injury
Recruitment of leukocytes
Removal of injurious agents 
Regulation (closure of inflammatory response)
Resolution/ repair of affected tissue
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8
Q

What are the 5 signs of acute inflammation?

A 
Heat
Redness
Swelling
Pain
Loss of function
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9
Q

Why does the area heat up when inflamed?

A

Increased blood flow and metabolic activity

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10
Q

Why does the area go red when inflamed?

A

Increased blood flow to injured area

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11
Q

What is hyperaemia?

A

Increased blood flow

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12
Q

Why does the area swell up when inflamed?

A

Fluid accumulation due to permeability of vessels

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13
Q

Why does the area become painful when inflamed?

A

Release of pain mediators; pressure on nerve ends

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14
Q

Why does the area (sometimes) lose function when inflamed?

A

Damage to the area

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15
Q

What are the 3 systemic changes that happen when an area is inflamed?

A

Fever
Neurophilia
Acute phase reactions are released

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16
Q

What does an increase in fibrinogen mean?

A

Makes the RBCs sticky -> stacking of RBCs -> faster sedimentation rate

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17
Q

Give some examples of acute phase reactants

A
  • C reactive proteins
  • fibrinogen
  • complement
  • serum amyloid A protein
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18
Q

Are there complications of the acute inflammation response?

A

Very rarely, it causes a severe systemic inflammatory reaction called sepsis or a form of inflammatory response syndromes (SIRS)

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19
Q

What happens to the vasculature in the acute inflammatory response?

A

Local reaction. Vasodilation, plasma exudation and oedema

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20
Q

What happens to the cells in the acute inflammatory response?

A

Infiltration of inflammatory cells. Cell recruitment, phagocytosis and NETosis

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21
Q

What happens to the humor in the acute inflammatory response?

A

Release of inflammatory mediators

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22
Q

What inflammatory mediators are released in the acute inflammatory response (5)?

A

Complement, plasma factors, clotting cascade, chemokines and cytokines

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23
Q

What happens in the resolution of the acute inflammatory response?

A

Inflammation is controlled and self-limiting. Healing, regeneration and repair of tissue

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24
Q

What is vasodilation induced by?

A

Histamine and seratonin released by injured cells, mast cells and macrophages

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25
Q

What does increased vascular permeability lead to?

A

Leakage of fluids into the tissues (swelling)

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26
Q

What happens as exudate accumulates at the inflamed site?

A

Pressure increases, and nerve endings are stimulated by the excess fluid and inflammatory mediators (pain)

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27
Q

What does the activation of endothelial cells lead to?

A

Increasing their expression of adhesion molecules

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28
Q

What is the overall effect of increased vascular permeability?

A

Leukocytes and plasma proteins exit vessels and enter the inflammation site to deal with infection

29
Q

What does endothelial cell constriction lead to?

A

Loss of proteins and cell movement

30
Q

What happens when the proteins are lost into the tissue in acute inflammation?

A

Increases the osmotic pressure/ gradient, leading to fluid leakage to the area, causing oedema

31
Q

What is in inflammatory exudate?

A

Water, salts, small plasma proteins, inflammatory cells and RBCs

32
Q

What is transudate?

A

When the fluid leaks due to altered osmotic/hydrostatic pressure; vessel permeability stays normal

33
Q

What are the cellular mediators of inflammation (4)?

A

Macrophages
Neutrophils
Mast cells
Platelets

34
Q

What do mast cells in the tissues secrete?

A

Histamine

35
Q

What is needed for clotting to begin?

A

Fluid, anti microbial proteins and clotting factors

36
Q

What do chemokines do?

A

Attract more phagocyte cells from the blood to the injury site

37
Q

Why are neutrophils recruited?

A

To kill pathogens and remove cell debris at the site

38
Q

What is regulation and tissue repair promoted by?

A

The release of immunoregulatory factors (TGFbeta)

39
Q

What are the 5 steps in neutrophil recruitment?

A 
Margination and rolling
Integrin activation 
Firm adhesion to endothelium 
Cell movement through endothelium into tissue
Chemotaxis
40
Q

What is rolling mediated by?

A

Selectins

41
Q

What is arrest and adhesion in inflammation mediated by?

A

Integrins and cell adhesion molecules

42
Q

What is margination in neutrophil recruitment of acute inflammation?

A

Leukocytes and stem cells move towards the edges of the vessels

43
Q

What molecules are involved in neutrophil recruitment?

A

Selectins
Integrins
Immunoglobulin superfamily cell adhesion molecules (CAMs)

44
Q

What are selectins expressed by?

A

Activated endothelium

45
Q

What are p-selectins?

A

Preformed granules

46
Q

What are e-selectins?

A

Cytokines produced by macrophages, mast cells and endothelial cells at site of inflammation

47
Q

What do leukocytes express?

A

selectin

48
Q

What do neutrophils express?

A

Integrins

49
Q

What configuration are integrins in if there is no binding to ligands?

A

Low affinity

50
Q

What do activated endothelial cells produce?

A

Chemokines

51
Q

What do integrins bind to?

A

Ligands on the endothelium

52
Q

What does integrin binding result in?

A

Firm adhesion to the neutrophil

53
Q

Where do neutrophils migrate through?

A

Interendothelial spaces

54
Q

What is neutrophil chemotaxis?

A

Movement of cells towards tissue towards inflamed sites

55
Q

What is chemotaxis guided by?

A

Chemoattractants

56
Q

Where are chemoattractants produced?

A

At the site of infection/ damage

57
Q

What mechanisms are involved in pathogen destruction?

A
  • Release of granule content
  • Phagocytosis
  • generation of reactive oxygen/nitrogen species
  • formation of NETs
58
Q

What are NETs?

A

Mesh of chromatin that traps microbes

59
Q

What are the two types of neutrophil granules and which one is small and which is large?

A 
Specific granules (small)
Azureophil granules (large)
60
Q

What can granule content cause?

A

Healthy tissue damage

61
Q

What are monocytes recruited to do?

A

Fight infection and differentiation into macrophages that promote dead cell clearance and tissue repair

62
Q

What are the short lived cells at inflammation sites?

A

Neutrophils

63
Q

What are the longer surviving cells at inflammation sites?

A

Monocytes

64
Q

Do inflammatory mediators naturally damage the tissue?

A

Yes

65
Q

Why is termination of acute inflammatory reaction important?

A

To avoid extensive bystander damage

66
Q

Why do inflammatory mediators degrade?

A

Short lived or are used up

67
Q

What does apoptosis of neutrophils and their subsequent clearance drive?

A

Potent anti-inflammatory and tissue-restoring mechanisms

68
Q

Why are macrophages so critical?

A

They secrete anti-inflammatory and reparative mediators and orchestrate the reparative processes

69
Q

What happens if the inflammatory response doesnt reach a critical threshold?

A

The mechanisms of regulation are not effectively promoted

Fundamentals Of Pathology (20 decks)

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