Acute Inflammation Flashcards

1
Q

What is acute inflammation

A

Response of living tissue to injury. It is innate, immediate, stereotypes and short lived

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2
Q

Give 5 causes of acute inflammation

A
  1. Microbial infections
  2. Hypersensitivity reactions
  3. Physical agents
  4. Chemicals
  5. Tissue necrosis
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3
Q

What are the clinical signs of acute inflammation

A
Rubor (redness)
Tumour (swelling)
Dolor (pain)
Calor (heat)
Loss of function
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4
Q

What changes in the tissue occur as a result of inflammation

A
  1. Changes in blood flow
  2. Exudation of fluid into tissues
  3. Infiltration of inflammatory cells
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5
Q

What is exudation of fluid

A

Fluid that filters from the circulatory system into lesions (areas of tissue suffering from damage) or areas of inflammation

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6
Q

What are the changes in the changes of blood flow

A
  1. Vasoconstriction of arterioles occurs for a few seconds
  2. Vasodilation then occurs
    There is an increased permeability of blood vessels
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7
Q

How does the blood flow change in acute inflammation

A

It increases due to vasodilation

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8
Q

What does an increase in permeability of blood vessels cause

A

Exudation of protein rich fluid

Slowing down of the circulation

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9
Q

What are the 2 types of chemical mediators of acute inflammation

A

Immediate response mediators

Mediators giving a persistent response

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10
Q

Give an example of an immediate chemical mediator

A

Histamine, cytokines and chemokines

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11
Q

What cells release histamine

A

Mast cells, basophils and platelets

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12
Q

When is histamine released

A

In response to physical damage, complementary factors C3a and C5a, interleukin and neutrophils

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13
Q

What does histamine cause

A

Vasodilation, increased permeability of blood vessels and pain

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14
Q

Give an example of a persistent chemical mediator of acute inflammation

A

Leukotriene and Proteases (bradykinin, complement proteins C3a and C5a, fibrin)

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15
Q

What 2 pressure determine fluid flow across vessel walls

A

Hydrostatic and oncotic pressure

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16
Q

If there is an increased oncotic pressure in the interstitum what happens to fluid in the vessels

A

It will move out of the vessels in to the interstitium

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17
Q

What is oedema

A

Increased fluid in the tissues

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18
Q

True or false: arteriolar dilation leads to an increase in hydrostatic pressure

A

True as there is more blood flow through the capillaries increasing the pressure. This forces more fluid out

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19
Q

What does transudate mean

A

The fluid outside of the vessels has the same protein content as the plasma

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20
Q

What is the protein content like in an exudate

A

Greater than in the plasma

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21
Q

True or false: fluid loss in inflammation is a transudate

A

False - it is an exudate

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22
Q

What are the 5 mechanisms of increasing vessel permeability

A
  1. Endothelial contraction
  2. Cytoskeleton reorganisation
  3. Direct injury
  4. Leukocyte dependant injury
  5. Increased transcytosis
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23
Q

What is transcytosis

A

When fluid moves across the endothelial cytoplasm through cells and not between cells

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24
Q

What causes endothelial contraction

A

Histamine and leukotrienes

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25
What does endothelial contraction causes
Gaps inbetween the endothelial making the vessels more leaky
26
What causes cytoskeleton reorganisation
Cytokines interleukin and TNF
27
What does cytoskeleton reorganisation cause
Gaps in the vessel walls
28
How can leukocyte dependant injury occur
When neutrophils release toxic oxygen species and enzymes
29
What causes an increase in transcytosis
VEGF
30
What is the primary type of white blood cell involved in inflammation
Neutrophils
31
Describe the appearance of a neutrophil
Granular, multi-lobed nucleus
32
What are the 4 stages in neutrophil infiltration
1. Margination 2. Rolling 3. Adhesion 4. Emigration
33
What occurs in migration in the infiltration of neutrophils
Neutrophils line up at the edge of the blood vessel along the endothelium
34
What is rolling in the infiltration of neutrophils
Neutrophils roll along the endothelium, sticking to it loosely
35
What is the adhesion stage of the infiltration of neutrophils into blood vessels
When neutrophils tightly adhere to the endothelial lining the blood vessel
36
What occurs in the emigration stage of the infiltration of neutrophils into the blood vessels
Neutrophils move through the blood vessel wall
37
What allows neutrophils to bind onto the endothelial wall of the blood vessel
Inflammatory mediators cause a change to the endothelial receptors which allows the neutrophils to bind
38
How to the neutrophils move through the endothelial wall
There is relaxation of inter-endothelial cell junction, digestion of the vascular basement membrane which then allows the neutrophil to move across
39
What is chemotaxis
Movement along concentration gradients of chemoattractants
40
What process do neutrophils do
Phagocytosis
41
What facilitates phagocytosis by neutrophils
Opsonins (C3b)
42
What happens during phagocytosis
Opsonins allows the neutrophil to recognise and make contact with the particle. The cytoskeleton then changes to allow endocytosis of the particle. Lysosomes fuse
43
What are the 2 mechanisms of phagocytosis
Oxygen dependant and independant
44
What occurs in oxygen dependant phagocytosis
Enzymes produce superoxide and hydrogen peroxide
45
Which type of phagocytosis is particularly good for killing bacteria
Oxygen dependant
46
What occurs in oxygen independant phagocytosis
Lysozymes and hydrolases break down the particle
47
Why is the response by neutrophils not always 100% reliable
Neutrophils may release toxic metabolites and enzymes causing damage to host tissue
48
Give 2 examples of cytokines
Interleukin and TNF alpha
49
What chemicals mediators cause increased blood flow
Histamine
50
What chemicals mediators cause vascular permeability
Histamine and leukotrienes
51
What chemicals mediators cause neutrophil chemotaxis
C5a, bacterial peptides, lnterleukin
52
What chemicals mediators cause phagocytosis
C3b
53
How does the exudation of fluid combat injury?
1. Delivers plasma proteins, immunoglobulins, inflammatory mediators and fibrinogen to area of injury 2. Dilutes toxins 3. Increases lymphatic drainages
54
Why is an increased lymphatic drainage advantageous in an inflammatory response
Delivers microorganisms to phagocytes and antigens in the immune system through the lymph nodes
55
How does the infiltration of cells combat injury
Removes pathogenic organisms and debris
56
How does vasodilation help combat injury
1. Increases delivery of helping components (plasma proteins, immunoglobin, fibrinogen, mediators) 2. Increases temperature
57
How does an increased temperature help combat injury
The cells work more efficiently at higher temperatures
58
How does pain and loss of function help combat injury
Reduces chance of further damage
59
What complications can occur due to local inflammation
1. Swelling can block tubes 2. Exudate can cause compression 3. Pain and loss of function
60
What is serositis
Inflammation of serous membranes
61
What are systemic effects of inflammation
1. Fever | 2. Leukocytosis
62
What causes a fever
Endogenous pyrogens
63
Give 2 examples of endogenous pyrogens
Interleukin 1 and TNF alpha
64
What chemical mediators are found in aspirin to reduce fever
Prostaglandins
65
What is leukocytosis
An increase in the number of white cells in the blood normally as a response to infections
66
What type of white cell increases in the blood due to bacterial infections
Neutrophils
67
What type of white cell increases in the blood due to viral infection
Lymphocytes
68
What are acute phase proteins
Plasma proteins that increase in infections
69
Give 3 examples of acute phase proteins
C reactive protein Alpha 1 antitrypsin Fibrinogen
70
What is the acute phase physiological responses of acute inflammation
Decreased appetite, raised pulse rate, altered sleep pattern and changes in plasma concentrations of acute plasma proteins
71
What does it mean by acute
Rapid onset
72
What is shock
Clinical syndrome of systemic circulatory failure
73
What are the 4 outcomes of acute inflammation
1. Complete resolution 2. Continued acute inflammation with chronic inflammation (abscess) 3. Chronic inflammation and fibrous repair giving scarring 4. Death
74
How is the plasma levels of fibrin reduced
Degraded by plasmin and proteases
75
How is the exudate reduced
Drained to the lymphatics
76
When is complete resolution not possible
If cell architecture is destroyed
77
True or false: mediators of acute inflammation have short half lives
True
78
How are the amount of mediators reduced when resolving inflammation
- short half lives - inactivated by degradation - inhibited - diluted in exudate
79
What is lobar pneumonia
Inflammation of the pulmonary lobe
80
What organism causes lobar pneumonia
Streptococcus pneumoniae (pneumococci)
81
What systems are seen with lobar pneumonia
Fever, hypoxaemia, dry cough and breathlessness
82
What is bacteria meningitis
Acute inflammation of the meninges (membrane outlining the brain and spinal cord) causing vascular thrombosis and reduced cerebral perfusion
83
What causes bacterial meningitis
Streptococcus pneumoniae
84
What is an abscess
Collection of pus (inflammatory exudate) in the tissues due to bacterial infection. This causes high pressure giving pain and can damage adjacent tissue
85
What type of necrosis is associated with an abscess
Liquefactive in the centre
86
What occurs if the inflammatory exudate pours into serous cavities
Ascites, pleural or pericardial effusion
87
What is pericarditis
Swelling of the pericardium with fibrin deposits there
88
List 4 examples of inflammation disorders
1. Hereditary angiotensin-oedema (attacks of swelling) 2. Alpha-1 antitrypsin deficiency 3. Inherited complementary deficiencies 4. Defects in neutrophil number and size
89
What is diapedesis
Passage of blood cells through the capillary walls