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Fundamentals Of Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

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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
What does increased vascular permeability lead to?
Leakage of fluids into the tissues (swelling)
26
What happens as exudate accumulates at the inflamed site?
Pressure increases, and nerve endings are stimulated by the excess fluid and inflammatory mediators (pain)
27
What does the activation of endothelial cells lead to?
Increasing their expression of adhesion molecules
28
What is the overall effect of increased vascular permeability?
Leukocytes and plasma proteins exit vessels and enter the inflammation site to deal with infection
29
What does endothelial cell constriction lead to?
Loss of proteins and cell movement
30
What happens when the proteins are lost into the tissue in acute inflammation?
Increases the osmotic pressure/ gradient, leading to fluid leakage to the area, causing oedema
31
What is in inflammatory exudate?
Water, salts, small plasma proteins, inflammatory cells and RBCs
32
What is transudate?
When the fluid leaks due to altered osmotic/hydrostatic pressure; vessel permeability stays normal
33
What are the cellular mediators of inflammation (4)?
Macrophages Neutrophils Mast cells Platelets
34
What do mast cells in the tissues secrete?
Histamine
35
What is needed for clotting to begin?
Fluid, anti microbial proteins and clotting factors
36
What do chemokines do?
Attract more phagocyte cells from the blood to the injury site
37
Why are neutrophils recruited?
To kill pathogens and remove cell debris at the site
38
What is regulation and tissue repair promoted by?
The release of immunoregulatory factors (TGFbeta)
39
What are the 5 steps in neutrophil recruitment?
``` Margination and rolling Integrin activation Firm adhesion to endothelium Cell movement through endothelium into tissue Chemotaxis ```
40
What is rolling mediated by?
Selectins
41
What is arrest and adhesion in inflammation mediated by?
Integrins and cell adhesion molecules
42
What is margination in neutrophil recruitment of acute inflammation?
Leukocytes and stem cells move towards the edges of the vessels
43
What molecules are involved in neutrophil recruitment?
Selectins Integrins Immunoglobulin superfamily cell adhesion molecules (CAMs)
44
What are selectins expressed by?
Activated endothelium
45
What are p-selectins?
Preformed granules
46
What are e-selectins?
Cytokines produced by macrophages, mast cells and endothelial cells at site of inflammation
47
What do leukocytes express?
selectin
48
What do neutrophils express?
Integrins
49
What configuration are integrins in if there is no binding to ligands?
Low affinity
50
What do activated endothelial cells produce?
Chemokines
51
What do integrins bind to?
Ligands on the endothelium
52
What does integrin binding result in?
Firm adhesion to the neutrophil
53
Where do neutrophils migrate through?
Interendothelial spaces
54
What is neutrophil chemotaxis?
Movement of cells towards tissue towards inflamed sites
55
What is chemotaxis guided by?
Chemoattractants
56
Where are chemoattractants produced?
At the site of infection/ damage
57
What mechanisms are involved in pathogen destruction?
- Release of granule content - Phagocytosis - generation of reactive oxygen/nitrogen species - formation of NETs
58
What are NETs?
Mesh of chromatin that traps microbes
59
What are the two types of neutrophil granules and which one is small and which is large?
``` Specific granules (small) Azureophil granules (large) ```
60
What can granule content cause?
Healthy tissue damage
61
What are monocytes recruited to do?
Fight infection and differentiation into macrophages that promote dead cell clearance and tissue repair
62
What are the short lived cells at inflammation sites?
Neutrophils
63
What are the longer surviving cells at inflammation sites?
Monocytes
64
Do inflammatory mediators naturally damage the tissue?
Yes
65
Why is termination of acute inflammatory reaction important?
To avoid extensive bystander damage
66
Why do inflammatory mediators degrade?
Short lived or are used up
67
What does apoptosis of neutrophils and their subsequent clearance drive?
Potent anti-inflammatory and tissue-restoring mechanisms
68
Why are macrophages so critical?
They secrete anti-inflammatory and reparative mediators and orchestrate the reparative processes
69
What happens if the inflammatory response doesnt reach a critical threshold?
The mechanisms of regulation are not effectively promoted

Fundamentals Of Pathology (20 decks)

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