Acute Inflammation Flashcards

1
Q

What are the causes for acute inflammation?

A

Micro-organisms, mechanical trauma to tissue, chemical changes, extreme physical conditions, dead tissue and hypersensitivity

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2
Q

What are the benefits of acute inflammation?

A

Rapid and non-specific response

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3
Q

How is the inflamed site protected?

A

Cardinal signals and a loss of function at the site

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4
Q

How are pathogens destroyed?

A

Neutrophils

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5
Q

What is the function of neutrophils?

A

They destroy pathogens and denature antigens for macrophages

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6
Q

What is the function of plasma proteins?

A

They localise the process

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7
Q

What does resolution mean?

A

Returns to normal

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8
Q

What are neutrophils?

A

Mobile phagocytes

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9
Q

What are the 3 sequences of microvascular change?

A

Change in vessel radius (flow), change in vessel permeability and movement of neutrophils

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10
Q

How is the vessel radius changed?

A

Transient arterioles constrict and local arterioles dilate, while the surrounding smooth muscle relaxes

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11
Q

What occurs when the vessel radius dilates?

A

Increase in blood flow which causes Rubor and Calor

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12
Q

How is vessel permeability changed?

A

It is a localised vascular response. It is changed by endothelial leak, exudation and oedema

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13
Q

What causes endothelial leak?

A

Local chemical mediators

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14
Q

What is exudation?

A

Plasma and proteins (e.g. fibrinogen and immunoglobulin) are excreted from the organism

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15
Q

What does oedema cause?

A

Swelling, which reduces function and causes pain

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16
Q

Where do neutrophils move?

A

From vessels to the extravascular space

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17
Q

What are the 3 process by which neutrophils move?

A

Margination, Pavementing and Emigration

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18
Q

What is the process of margination?

A

Neutrophils move into the endothelial aspect of lumen

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19
Q

What is pavementing?

A

Neutrophils adhere to endothelia

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20
Q

What is the endothelia?

A

The epithelium that lines the interior side of BVs

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21
Q

What is emigration?

A

Neutrophils move outside of the tissues by squeezing between endothelia

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22
Q

What is an exudate?

A

Plasma which is fluid in protein e.g. fibrinogen and immunoglobulin

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23
Q

How is an exudate formed?

24
Q

Where does an exudate move from?

A

Lumen to tissue

25
What causes exudation?
An increase in capillary permeability
26
What is exudation?
Net movement of plasma form the capillaries to the extravascular space
27
What can exudation form?
An oedema
28
What is an oedema?
An accumulation of fluid in the extravascular space
29
What are the systematic effects?
Pyrexia, Malaise, Neutrophilia, Septic shock, Lymph node enlargement, weight loss, Anaemia and Suppuration
30
What is pyrexia?
Increased body temperature
31
What is malaise?
General discomfort, it is the first indication of disease
32
What is Neutrophilia?
Too many neutrophils due to leucocytosis
33
What is septic shock?
Very low BP due to sepsis which causes an inability to perfuse and can lead to a haemorrhage. It is rapidly fatal as it causes tissue hypoxia
34
What type of process is weight loss?
Catabolic
35
What is Anaemia?
Blood loss
36
What is suppuration?
Pus formation, which leads to an abscess
37
How does an abscess discharge?
By pointing first
38
What is a multiloculated abscess?
Pus bursts through membrane but not the epithelial surface and forms new cavities
39
What is pus surrounded by?
Pyogenic membrane
40
What occurs as a result of tissue hypoxia?
Cell death
41
What is systematic vascular resistance (SVR)?
Index of arteriolar constriction calculated by BP/CO
42
How do you calculate cardiac output (CO)?
CO= SV x HR
43
What does inflammation lead to?
The formation of granulation tissue and scar formation
44
How does it result in healing and repair?
The abscess is collapsed and granulation tissue forms collagen
45
What is the process of scar formation?
Fibrosis
46
What are the negative effects?
Sepsis, Bacteraemia, Septicaemia and Toxaemia
47
What is Bacteraemia?
Bacteria in blood
48
What is Septicaemia?
Growth of bacteria in blood
49
What is Toxaemia?
Toxic products in the blood
50
How is granulation tissue formed?
Capillaries grow in into an inflammatory mass which allows access of plasma proteins, macrophages and fibroblasts which lay down collagen to repair the damage
51
When does granulation formation occur?
After a large amount of damage or an inability to remove dirt from a wound
52
What are the mediators of acute inflammation?
Vasodilation and constriction
53
What is the function of mediators?
Altered permeability, neutrophil adhesion, chemotaxis and pain
54
What are the effects of mediators?
They result in a dynamic steady state and favour or inhabit acute inflammation
55
What are mediators relative to?
Need
56
What is chemotaxis?
Movement of an organism along the gradient of increasing/decreasing concentration