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BDS1 > Acute and chronic inflammation > Flashcards

Acute and chronic inflammation Flashcards

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
Q

What causes pain (dolor) during inflammation?

A

stretching of tissues (due to excess fluid build up) and due to soluble mediators)

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26
Q

What are the main types of soluble mediators?

A

AMPs, enzymes, cytokines and chemokines, complement proteins, prostaglandins and leukotrienes, immunoglobulins, growth factors, matrix metalloproteinases (MMPs)

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27
Q

What are prostaglandins and leukotrienes?

A

chemical mediators

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28
Q

Which cells produce prostaglandins and leukotrienes?

A

macrophages and neutrophils

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29
Q

How are prostaglandins and leukotrienes produced?

A

By the metabolism of the fatty acid, arachidonic acid (found in neutrophils and macrophages)

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30
Q

Which enzyme converts arachidonic acid into leukotrienes?

A

lipoxygenase

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31
Q

Which enzyme converts arachidonic acid into prostaglandins?

A

cyclooxygenase

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32
Q

How does ibuprofen work?

A

targets cyclooxygenase (enzyme) to inhibit prostaglandins production. This reduces inflammation

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33
Q

What roles do prostaglandins and leukotrienes play in inflammation?

A

cause vascular dilation, act on nerve fibres (itching), involved in chemotaxis, tissue remodelling

34
Q

What is the largest component of human blood?

A

plasma (55%)

35
Q

What are the 4 plasma factor systems?

A

complement, kinins, coagulation factors, fibrinolytic system

36
Q

What is the name of the protein that can activate all 4 plasma factor systems?

A

Hageman factor (coagulation factor XII)

37
Q

What is the Hageman factor?

A

A serine protease (enzyme) that is circulating inactive in blood

38
Q

How is the Hageman factor activated?

A

When it circulates in inflamed tissue

39
Q

What is the complement system made up of?

A

A collection of soluble proteins present in circulation

40
Q

Where are complement proteins produced?

A

in the liver and by immune cells

41
Q

What 3 processes are driven by complement proteins?

A

opsonisation (tagging microorganisms for removal), forming membrane attack complexes (pores) and as pro-inflammatory proteins

42
Q

What are the 3 pathways of complement?

A

classical, lectin and alternative pathway

43
Q

Which complement pathway does the Hageman factor activate?

A

classical pathway

44
Q

What is the kinin system made up of?

A

collection of different inactivated proteins circulating in the blood waiting to be activated

45
Q

What does the kinin system ultimately lead to the production of?

A

bradykinins

46
Q

What is the main protein within the kinin system?

A

Kallikrein

47
Q

How is kallikrein activated?

A

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
Q

Function of kallikrein

A

kallikrein converts kininogens to kinins

49
Q

Example of kinin

A

bradykinin

50
Q

Function of kinins/bradykinin

A

has widespread effects (like complement proteins/anaphylatoxins) e.g. driving diapedesis, swell and retract endothelial cells making blood vessels leaky.

51
Q

Outline the kinin system pathway

A

pre-kallikrein is converted to kallikrein by Hageman factor/neutrophils. Kallikrein converts kininogens to kinins (e.g. bradykinins)

52
Q

Function of the coagulation system

A

form blood clots

53
Q

What are the 2 pathways that activate the coagulation system?

A

intrinsic and extrinsic pathway

54
Q

How is the intrinsic pathway of the coagulation system activated?

A

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
Q

How is the extrinsic pathway of the coagulation system activated?

A

External injury leading to bleeding (e.g. cut)

56
Q

What is common about the intrinsic and extrinsic pathways?

A

Both involve a cascade of clotting factors (plasma proteins) e.g. starting with the activation of the Hageman factor

57
Q

What do both the intrinsic and extrinsic pathways diverge into?

A

common pathway

58
Q

What does the common pathway of the coagulation system involve?

A

formation of a stable blood clot (fibrin) through the action of thrombin and the support of platelets

59
Q

What is a stable blood clot made up of?

A

fibrin and activated platelets (have projections)

60
Q

What happens to the blood vessel during the formation of a platelet plug?

A

vasoconstriction

61
Q

Which clotting factor converts fibrinogen into fibrin?

62
Q

What is the name of inactivated thrombin?

A

prothrombin

63
Q

Which plasma factor systems can activate the complement system?

A

kinin system and fibrinolytic system

64
Q

What is the main protein in the kinin system?

A

kallikrein

65
Q

What is the main protein in the coagulation system?

66
Q

What is the main protein in the fibrinolytic system?

67
Q

Function of the fibrinolytic system

A

breaks down fibrin to prevent excess clotting and (plasmin) can activate the complement system

68
Q

What is the precursor to plasmin?

A

plasminogen

69
Q

How is plasminogen converted to plasmin in the fibrinolytic system?

A

By the Hageman factor or kallikrein

70
Q

Function of plasmin

A

breaks down fibrin and activates the complement system

71
Q

How does activate the complement system?

A

Plasmin can cleave the C3 complement protein (drives opsonisation, inflammation, membrane attack complex)

72
Q

Name of disease caused by excess blood clotting in circulatory system

A

thrombosis

73
Q

Name of disease caused by excessive bleeding into tissues

A

haemorrhage

74
Q

How may thrombosis or haemorrhage arise?

A

imbalance between the coagulation and fibrinolytic system

75
Q

What is maintaining the balance between the coagulation and fibrinolytic systems known as?

A

haemostasis

76
Q

Why is it important to maintain haemostasis?

A

to prevent thrombosis and haemorrhage

77
Q

How can haemostasis be maintained in people with disorders of the plasma factor system?

A

by sequalae (interventions)

78
Q

Examples of disorders of the plasma factor systems

A

Von Willebrand disease, Haemophilia A and B

79
Q

What causes Von Willebrand disease, Haemophilia A and Haemophilia B?

A

mutations in genes that code for clotting factor proteins (specifically in coagulation system)

80
Q

What medications inhibit blood clotting?

A

Warfarin and Heparin

BDS1 (71 decks)

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