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Module 2 vet med > Inflammatory response > Flashcards

Inflammatory response Flashcards

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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
Transudate fluid colour
Clear
26
Exudate fluid colour
Yellow Red
27
Fibrinogen is a
Plasma protein
28
How does fibrinogen form fibrin
It polymerises in extravascular tissue
29
The fibrin net does what
Confines stimuli to isolated area provides well defined target for migrating inflammatory cells
30
Fibrin also has what factors
Has chemotactic properties Instrumental in blood clot formation Forms framework for fibroblast and endothelial cell migration in healing
31
What forms the framework for fibroblast
Fibrin
32
Cell in inflammation
Polymorphonuclear Leukocytes Granulcytes Neutrophils Eosinophils Basophils Mononuclear leukocytes- mast cells
33
What are examples of special B cells
Lymphocytes Plasma cells
34
Neutrophils features
Main cells for acute inflammation First cells to enter exudate
35
What are the first cells to enter exudate
Neutrophils
36
Pus is
Dead neutrophils and liquified exudate
37
What is the purpose of cells of inflammation
Kill pathogen Tumour cells Degrade foreign material
38
What is the function of inflammatory fells
Phagocytosis of microbes and foreign material
39
Eosinophils
Typical in allergic and parasitic disease
40
Basophils
Often occur with eosinophils, granules contain histamine
41
What do mast cells do
Important in triggering acute inflammation
42
Neutrophils are first to respond in response. True and false
True
43
Where are neutrophils produced
Bone marrow
44
How long are neutrophils in the blood and tissue for
Blood- 10ths Tissue- 1-4days
45
Purpose of neutrophils
Kill pathogens and tumour cells Degrade foreign material
46
Function of neutrophils
Phagocytosis of microbes and foreign material Secretion and release of granule content to enhance inflammatory response
47
Stimuli of neutrophils
Infectious agents- bacteria Non infectious tissue damage
48
Non degenerate neutrophils
Segmented nucleus Condensed chromatin
49
Degenerate neutrophils
Swollen Smooth Paler basophilic chromatin Indicated presence of bacterial endotoxins
50
Eosinophils commonly at transition from
Acute to chronic inflammation
51
Where are eosinophils typical in
Allergic and parasitic disease
52
Where are eosinophils produced
Bone marrow
53
How long do eosinophils stay in the blood and tissues
Blood- 4hrs Tissue- 2wks
54
Rule outs of eosinophils should include
Allergy Parasitic disease Fungal disease Eosinophilia granuloma Paraneopstic disease
55
Where are basophils produced
Bone marrow
56
How long do basophils circulate
In blood- 12hrs Tissue- 2wks
57
Basophils often occur with
Eosinophils
58
Granules contain
Histamine Cytokines
59
Rules outs for basophils should include
Allergy Parasites
60
Basophils have what colour of granules
Pink granules
61
Eosinophils have what colour of granules
Blue
62
Leukocyte recruitment full name of steps
Leukocyte adhesion cascade
63
Leukocyte recruitment 5 steps
Margination Rolling Adhesion Transmigration Chemotaxis
64
In its normal state, vascular endothelium does not bind
Circulating cells or allow passage of circulating cells
65
In inflammation what type of cells are activated and thus bind leukocytes to help them exit vessels
Endothelial cells
66
What is firm adhesion mediated by
Integrins on leukocyte surfaces and ligands on endothelial cell surfaces
67
In firm adhesion what happens
Leukocyte stops rolling and is spread out on endothelial surface
68
Firm adhesion is induced by what
Chemokines
69
Margination is enhanced by
Inflammatory processes Ie. Dilated vessels with reduced hydrostatic pressure and slowed blood flow- stasis
70
In margination
Leukocytes move towards periphery of vascular lumen
71
Rolling
Leukocytes tumble along the endothelial surface. Undergo weak and transient adhesion to endothelial cells
72
Transmigration is equal to
Diapedesis
73
Transmigration is when
Leukocytes squeeze between endothelial cells at intercellular junctions
74
Transmigration is driven by
Chemokines which stimulate leukocytes to migrate to site of injury or infection
75
Chemotaxis definition
Migration/ locomotion along a chemical gradient
76
What happens in Chemotaxis
Migrate to site of injury
77
Exogenous and endogenous substances can be
Chemotactic
78
Neutrophils dominate what period in inflammatory response
First 2 days
79
Monocytes dominate in
24-48hrs
80
Inherited defects
Chediak- higashi syndrome Inherited disease Autosomal recessive Defective lysosomes
81
Function of inherited defects
Hyperpigmentation Bleeding tendency
82
Acute inflammation features
Vascular changes- vasodilation and oedema Leukocyte migration Short duration
83
Chronic inflammation features
Macrophages, lymphocytes, plasma cells Angiogenesis Fibrosis Long duration
84
What are phagocytic cells
Neutrophils Macrophages
85
What are the 3 steps of phagocytosis
Recognition and attachment Engulfment Killing and degradation
86
Opsosins can be
Antibodies Complement Circulating proteins
87
Recognition and attachment of particle stage
Specific cell surface receptors Receptors for opsonins
88
Opsonins are
Flags on cells that tell other cells that it needs destroyed
89
Engulfment stage
Extension of the cytoplasm to form a vesicle
90
Killing and degradation stage
Lysosome- with enzymes-fuses with the phagosome Formation of phagolysosome Killing of microbes by ROS and nitrogen species
91
Septic inflammation is
Intracellular bacteria required
92
Septicaemia
Organisms circulating in the bloodstream
93
Sepsis
Septic shock
94
Macrophages also
Produce growth factors that initiate the subsequent process of repair
95
Chronic inflammation
Prolonged inflammation May follow acute inflammation Causes- Persistent infection by certain organisms Autoimmunity
96
Components on the resolution of inflammation
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
Morphological features
Mainly mononuclear cells Lymphocytes Tissue damage Angiogenesis Fibrosis

Module 2 vet med (16 decks)

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