Acute and chronic inflammation Flashcards

(80 cards)

1
Q

Aetiology definition

A

cause of a disease/condition (pathology). Can be genetic +/ environmental

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2
Q

Pathogenesis definition

A

progressive changes as the disease develops (morphological cellular changes and macroscopic)

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3
Q

Sequalae definition

A

what happens next e.g. an intervention

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4
Q

What is inflammation?

A

an immune response aimed at eliminating the inciting cause

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5
Q

What are the possible inciting causes?

A

microorganisms, particulate materials (allergens or prostheses), altered self cells (disorders or injury) and transformed malignant cells (neoplasia)

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6
Q

What are the stages of inflammation?

A

initiation (response to harmful agent), progression (containment), amplification (modulation of immune response), resolution (healing or failure to resolve)

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7
Q

What is the resolution of acute inflammation?

A

healing (complete restoration of tissues)

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8
Q

What is the resolution of chronic inflammation?

A

failure to resolve (leads to loss of function)

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9
Q

Which parts of the immune system are involved in acute inflammation?

A

innate immune system only (e.g. neutrophils)

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10
Q

Characteristics of acute inflammation

A

rapid onset, short-term, localised response

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11
Q

In which type of inflammation may an abscess form?

A

acute inflammation

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12
Q

What tends to precede chronic inflammation?

A

Acute inflammation

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13
Q

How long can chronic inflammation last?

A

long-term, years, entire lifetime (persistent inflammation)

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14
Q

Which parts of the immune system are involved in chronic inflammation?

A

Innate and adaptive immune system

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15
Q

What is fibrosis?

A

formation of scar tissue

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16
Q

In which type of inflammation may fibrosis occur?

A

chronic inflammation

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17
Q

What are the 5 cardinal signs of inflammation?

A

redness (rubor), swelling (tumor), heat (calor), pain (dolor), loss of function (functio laesa)

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18
Q

What causes redness (rubor) and heat (calor)?

A

dilation of small blood vessels adjacent to site of damage

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19
Q

What happens to endothelial cells during inflammation?

A

endothelial cells swell and retract. Become activated to promote diapedesis (migration of immune cells to site of damage)

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20
Q

Exudation definition

A

vessels become leaky and allow passage of fluids

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21
Q

What substances drive dilation, exudation and endothelial activation?

A

soluble mediators

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22
Q

What causes swelling (tumor)?

A

Exudation leads to oedema and there is an increased blood and lymph flow

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23
Q

Oedema definition

A

excess of watery fluid collecting in tissues of body

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24
Q

What does inflammatory exudate consist of?

A

fluids (lymph) and salts, glucose and oxygen (for immune cells), immune cells and soluble mediators, fibrin

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25
What causes pain (dolor) during inflammation?
stretching of tissues (due to excess fluid build up) and due to soluble mediators)
26
What are the main types of soluble mediators?
AMPs, enzymes, cytokines and chemokines, complement proteins, prostaglandins and leukotrienes, immunoglobulins, growth factors, matrix metalloproteinases (MMPs)
27
What are prostaglandins and leukotrienes?
chemical mediators
28
Which cells produce prostaglandins and leukotrienes?
macrophages and neutrophils
29
How are prostaglandins and leukotrienes produced?
By the metabolism of the fatty acid, arachidonic acid (found in neutrophils and macrophages)
30
Which enzyme converts arachidonic acid into leukotrienes?
lipoxygenase
31
Which enzyme converts arachidonic acid into prostaglandins?
cyclooxygenase
32
How does ibuprofen work?
targets cyclooxygenase (enzyme) to inhibit prostaglandins production. This reduces inflammation
33
What roles do prostaglandins and leukotrienes play in inflammation?
cause vascular dilation, act on nerve fibres (itching), involved in chemotaxis, tissue remodelling
34
What is the largest component of human blood?
plasma (55%)
35
What are the 4 plasma factor systems?
complement, kinins, coagulation factors, fibrinolytic system
36
What is the name of the protein that can activate all 4 plasma factor systems?
Hageman factor (coagulation factor XII)
37
What is the Hageman factor?
A serine protease (enzyme) that is circulating inactive in blood
38
How is the Hageman factor activated?
When it circulates in inflamed tissue
39
What is the complement system made up of?
A collection of soluble proteins present in circulation
40
Where are complement proteins produced?
in the liver and by immune cells
41
What 3 processes are driven by complement proteins?
opsonisation (tagging microorganisms for removal), forming membrane attack complexes (pores) and as pro-inflammatory proteins
42
What are the 3 pathways of complement?
classical, lectin and alternative pathway
43
Which complement pathway does the Hageman factor activate?
classical pathway
44
What is the kinin system made up of?
collection of different inactivated proteins circulating in the blood waiting to be activated
45
What does the kinin system ultimately lead to the production of?
bradykinins
46
What is the main protein within the kinin system?
Kallikrein
47
How is kallikrein activated?
Hageman factor cleaves the precursor of kallikrein (pre-kallikrein) to convert it into kallikrein (active). Neutrophils also can produce enzymes to convert pre-kallikrein into kallikrein.
48
Function of kallikrein
kallikrein converts kininogens to kinins
49
Example of kinin
bradykinin
50
Function of kinins/bradykinin
has widespread effects (like complement proteins/anaphylatoxins) e.g. driving diapedesis, swell and retract endothelial cells making blood vessels leaky.
51
Outline the kinin system pathway
pre-kallikrein is converted to kallikrein by Hageman factor/neutrophils. Kallikrein converts kininogens to kinins (e.g. bradykinins)
52
Function of the coagulation system
form blood clots
53
What are the 2 pathways that activate the coagulation system?
intrinsic and extrinsic pathway
54
How is the intrinsic pathway of the coagulation system activated?
By internal vasculature injury (blood vessel rupture) which results in the Hageman factor (coagulation factor XII) becoming activated as it comes into contact with abnormal/activating surfaces
55
How is the extrinsic pathway of the coagulation system activated?
External injury leading to bleeding (e.g. cut)
56
What is common about the intrinsic and extrinsic pathways?
Both involve a cascade of clotting factors (plasma proteins) e.g. starting with the activation of the Hageman factor
57
What do both the intrinsic and extrinsic pathways diverge into?
common pathway
58
What does the common pathway of the coagulation system involve?
formation of a stable blood clot (fibrin) through the action of thrombin and the support of platelets
59
What is a stable blood clot made up of?
fibrin and activated platelets (have projections)
60
What happens to the blood vessel during the formation of a platelet plug?
vasoconstriction
61
Which clotting factor converts fibrinogen into fibrin?
thrombin
62
What is the name of inactivated thrombin?
prothrombin
63
Which plasma factor systems can activate the complement system?
kinin system and fibrinolytic system
64
What is the main protein in the kinin system?
kallikrein
65
What is the main protein in the coagulation system?
fibrin
66
What is the main protein in the fibrinolytic system?
plasmin
67
Function of the fibrinolytic system
breaks down fibrin to prevent excess clotting and (plasmin) can activate the complement system
68
What is the precursor to plasmin?
plasminogen
69
How is plasminogen converted to plasmin in the fibrinolytic system?
By the Hageman factor or kallikrein
70
Function of plasmin
breaks down fibrin and activates the complement system
71
How does plasmin activate the complement system?
Plasmin can cleave the C3 complement protein (drives opsonisation, inflammation, membrane attack complex)
72
Name of disease caused by excess blood clotting in circulatory system
thrombosis
73
Name of disease caused by excessive bleeding into tissues
haemorrhage
74
How may thrombosis or haemorrhage arise?
imbalance between the coagulation and fibrinolytic system
75
What is maintaining the balance between the coagulation and fibrinolytic systems known as?
haemostasis
76
Why is it important to maintain haemostasis?
to prevent thrombosis and haemorrhage
77
How can haemostasis be maintained in people with disorders of the plasma factor system?
by sequalae (interventions)
78
Examples of disorders of the plasma factor systems
Von Willebrand disease, Haemophilia A and B
79
What causes Von Willebrand disease, Haemophilia A and Haemophilia B?
mutations in genes that code for clotting factor proteins (specifically in coagulation system)
80
What medications inhibit blood clotting?
Warfarin and Heparin