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Module 2 vet med > Inflammatory response > Flashcards

Inflammatory response Flashcards

1
Q

Inflammation is typically denoted by the suffix

A

Itis

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2
Q

Benefits of inflammation

A

Dilution/ inactivation of pathogens and toxins
Killing foreign material, necrotic tissue and neoplastic cells
Provide wound healing factors
Restricting movement allowing time for repair
Increasing temp to induce vasodilation and inhibit replication of pathogens

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3
Q

Disadvantages of inflammation

A

Collateral damage
Excessive or prolonged inflammatory response can be harmful eg.ibd, Johnes disease, pemiphigus
Anti inflammatory medication

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4
Q

Inflammatory stimuli

A

Agents and microbial toxins- bacteria, virus, fungi, parasites
Tissue damage- hypoxia, trauma, physical and chemical damage
Foreign material
Immune reaction- hypersensitivity

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5
Q

Components of acute inflammation

A

Inflammatory stimulus
Vascular response
Recruitment of leukocytes
Removal of injurious agent due to leukocytes

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6
Q

What is leukocyte activation

A

Response in leukocytes following recognition of microbes or dead cells

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7
Q

Leukocyte activation includes the process of

A

Stimuli for activation
Sensed by various receptors
Result- enhanced function like recruitment of leukocytes, removal of injurious agent by phagocytosis

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8
Q

Mediators of inflammation

A

Plasma protein derived mediators
Cell derived mediators

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9
Q

Plasma protein derived features

A

Complement system
Coagulation system
Vasodilation

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10
Q

Cell derived mediators features

A

Vasoactive amines
Arachidonic acid metabolites
Cytokines
Chemokines

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11
Q

Increased vascular permeability factors

A

Endothelial cells
Endothelial cell contraction
Endothelial cell retraction
Endothelial cell injury
Leukocyte mediated endothelial cell injury
Increased transcytosis

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12
Q

Endothelial cells are key factor to increased vascular permeability- why?

A

Contraction
Retraction
Injury
Leukocyte mediated injury
Transcytosis

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13
Q

Endothelial cell contraction factors

A

Actin and myosin concentration
Chemical mediators
Immediate transient response

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14
Q

Endothelial cell retraction- why?

A

Sunburn- persists longer due to longer period of leakage
Mediated by cytokines

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15
Q

Endothelial cell injury- why?

A

Loosing cells by cell necrosis and is rapid onset and persists longer

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16
Q

Leukocyte mediated endothelial cell injury- why?

A

Neutrophils release toxic mediators, long lived

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17
Q

Increase transcytosis

A

Movement through endothelial cells, high permeability of new vessels but repair of tissues is not as impermeable and are more leaky

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18
Q

Consequence of increased vascular permeability

A

Extravasation of fluid and leukocytes

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19
Q

Transudate- hydro-oedema

A

Leakage of fluid containing water and electrolytes but low protein

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20
Q

Oedema has

A

Decreased oncotic pressure
Increased hydrostatic pressure
Decreased lymphatic drainage

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21
Q

Exudate-pyo-leakage

A

Leakage if fluid containing water and electrolytes with high protein contents

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22
Q

Exudate features

A

Opaque
Viscous
Increased vascular permeability

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23
Q

Examples of transudate

A

Liver disease
Kidney disease
Increased protein loss

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24
Q

If there is more oncotic pressure what happens to fluid

A

Leaves vessels to places with more plasma proteins

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25
Q

Transudate fluid colour

A

Clear

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26
Q

Exudate fluid colour

A

Yellow
Red

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27
Q

Fibrinogen is a

A

Plasma protein

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28
Q

How does fibrinogen form fibrin

A

It polymerises in extravascular tissue

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29
Q

The fibrin net does what

A

Confines stimuli to isolated area provides well defined target for migrating inflammatory cells

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30
Q

Fibrin also has what factors

A

Has chemotactic properties
Instrumental in blood clot formation
Forms framework for fibroblast and endothelial cell migration in healing

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31
Q

What forms the framework for fibroblast

A

Fibrin

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32
Q

Cell in inflammation

A

Polymorphonuclear
Leukocytes
Granulcytes
Neutrophils
Eosinophils
Basophils
Mononuclear leukocytes- mast cells

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33
Q

What are examples of special B cells

A

Lymphocytes
Plasma cells

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34
Q

Neutrophils features

A

Main cells for acute inflammation
First cells to enter exudate

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35
Q

What are the first cells to enter exudate

A

Neutrophils

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36
Q

Pus is

A

Dead neutrophils and liquified exudate

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37
Q

What is the purpose of cells of inflammation

A

Kill pathogen
Tumour cells
Degrade foreign material

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38
Q

What is the function of inflammatory fells

A

Phagocytosis of microbes and foreign material

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39
Q

Eosinophils

A

Typical in allergic and parasitic disease

40
Q

Basophils

A

Often occur with eosinophils, granules contain histamine

41
Q

What do mast cells do

A

Important in triggering acute inflammation

42
Q

Neutrophils are first to respond in response. True and false

A

True

43
Q

Where are neutrophils produced

A

Bone marrow

44
Q

How long are neutrophils in the blood and tissue for

A

Blood- 10ths
Tissue- 1-4days

45
Q

Purpose of neutrophils

A

Kill pathogens and tumour cells
Degrade foreign material

46
Q

Function of neutrophils

A

Phagocytosis of microbes and foreign material
Secretion and release of granule content to enhance inflammatory response

47
Q

Stimuli of neutrophils

A

Infectious agents- bacteria
Non infectious tissue damage

48
Q

Non degenerate neutrophils

A

Segmented nucleus
Condensed chromatin

49
Q

Degenerate neutrophils

A

Swollen
Smooth
Paler basophilic chromatin
Indicated presence of bacterial endotoxins

50
Q

Eosinophils commonly at transition from

A

Acute to chronic inflammation

51
Q

Where are eosinophils typical in

A

Allergic and parasitic disease

52
Q

Where are eosinophils produced

A

Bone marrow

53
Q

How long do eosinophils stay in the blood and tissues

A

Blood- 4hrs
Tissue- 2wks

54
Q

Rule outs of eosinophils should include

A

Allergy
Parasitic disease
Fungal disease
Eosinophilia granuloma
Paraneopstic disease

55
Q

Where are basophils produced

A

Bone marrow

56
Q

How long do basophils circulate

A

In blood- 12hrs
Tissue- 2wks

57
Q

Basophils often occur with

A

Eosinophils

58
Q

Granules contain

A

Histamine
Cytokines

59
Q

Rules outs for basophils should include

A

Allergy
Parasites

60
Q

Basophils have what colour of granules

A

Pink granules

61
Q

Eosinophils have what colour of granules

A

Blue

62
Q

Leukocyte recruitment full name of steps

A

Leukocyte adhesion cascade

63
Q

Leukocyte recruitment 5 steps

A

Margination
Rolling
Adhesion
Transmigration
Chemotaxis

64
Q

In its normal state, vascular endothelium does not bind

A

Circulating cells or allow passage of circulating cells

65
Q

In inflammation what type of cells are activated and thus bind leukocytes to help them exit vessels

A

Endothelial cells

66
Q

What is firm adhesion mediated by

A

Integrins on leukocyte surfaces and ligands on endothelial cell surfaces

67
Q

In firm adhesion what happens

A

Leukocyte stops rolling and is spread out on endothelial surface

68
Q

Firm adhesion is induced by what

A

Chemokines

69
Q

Margination is enhanced by

A

Inflammatory processes
Ie. Dilated vessels with reduced hydrostatic pressure and slowed blood flow- stasis

70
Q

In margination

A

Leukocytes move towards periphery of vascular lumen

71
Q

Rolling

A

Leukocytes tumble along the endothelial surface.
Undergo weak and transient adhesion to endothelial cells

72
Q

Transmigration is equal to

A

Diapedesis

73
Q

Transmigration is when

A

Leukocytes squeeze between endothelial cells at intercellular junctions

74
Q

Transmigration is driven by

A

Chemokines which stimulate leukocytes to migrate to site of injury or infection

75
Q

Chemotaxis definition

A

Migration/ locomotion along a chemical gradient

76
Q

What happens in Chemotaxis

A

Migrate to site of injury

77
Q

Exogenous and endogenous substances can be

A

Chemotactic

78
Q

Neutrophils dominate what period in inflammatory response

A

First 2 days

79
Q

Monocytes dominate in

A

24-48hrs

80
Q

Inherited defects

A

Chediak- higashi syndrome
Inherited disease
Autosomal recessive
Defective lysosomes

81
Q

Function of inherited defects

A

Hyperpigmentation
Bleeding tendency

82
Q

Acute inflammation features

A

Vascular changes- vasodilation and oedema
Leukocyte migration
Short duration

83
Q

Chronic inflammation features

A

Macrophages, lymphocytes, plasma cells
Angiogenesis
Fibrosis
Long duration

84
Q

What are phagocytic cells

A

Neutrophils
Macrophages

85
Q

What are the 3 steps of phagocytosis

A

Recognition and attachment
Engulfment
Killing and degradation

86
Q

Opsosins can be

A

Antibodies
Complement
Circulating proteins

87
Q

Recognition and attachment of particle stage

A

Specific cell surface receptors
Receptors for opsonins

88
Q

Opsonins are

A

Flags on cells that tell other cells that it needs destroyed

89
Q

Engulfment stage

A

Extension of the cytoplasm to form a vesicle

90
Q

Killing and degradation stage

A

Lysosome- with enzymes-fuses with the phagosome
Formation of phagolysosome
Killing of microbes by ROS and nitrogen species

91
Q

Septic inflammation is

A

Intracellular bacteria required

92
Q

Septicaemia

A

Organisms circulating in the bloodstream

93
Q

Sepsis

A

Septic shock

94
Q

Macrophages also

A

Produce growth factors that initiate the subsequent process of repair

95
Q

Chronic inflammation

A

Prolonged inflammation
May follow acute inflammation
Causes-
Persistent infection by certain organisms
Autoimmunity

96
Q

Components on the resolution of inflammation

A

Return to normal vascular permeability
Drainage of edema fluid and proteins into lymphatic or by pinocytosis into macrophages
Phagocytosis of apoptotic neutrophils and of necrosis debris into macrophages
Disposal of macrophages

97
Q

Morphological features

A

Mainly mononuclear cells
Lymphocytes
Tissue damage
Angiogenesis
Fibrosis

Module 2 vet med (16 decks)

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