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Inflammation Flashcards

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1
Q

4 causes of inflammation

A

Pathogenic organisms

Poisons/toxins

Mechanical/thermal injury

Immune reactions and hypersensitivities

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2
Q

Cardinal signs of inflammation

A

Rubor (redness)

Calor (heat)

Dolor (pain)

Tumor (swelling)

Loss of function (function laesa)

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3
Q

Steps of vascular response to inflammation

A
  1. Vasodilation
  2. Increased vascular permeability
  3. Change in rate of blood flow
  4. WBC margination, rolling, adhesion
  5. Transmigration
  6. Emigration of WBCs
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4
Q

With mild injury, what do you expect to become more permeable

A

Post-capillary venules

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5
Q

With Moderate to severe injury, what becomes more permeable

A

Capillaries to small venules

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6
Q

With very severe injury - what becomes more permeable

A

Arterioles, capillaries, venules

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7
Q

Why does blood stasis occur (3)

A

1) Increased viscosity: blood loses plasma (increased vascular permeability) and there is accumulation of larger WBCs and protein to inflammatory site
2) Histamine: swelling of endothelial cells results in mechanical resistance
3) Passive congestion and stasis of lymph flow

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8
Q

Why does leukocyte margination, rolling and adhesion occur

A

1) Slowed blood flow means leukocytes move to peripheral Plasmatic Zone
2) They roll along endothelium
3) They adhere to Cell Adhesion Molecules (upregulated by inflammation)

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9
Q

How does transmigration occur

A

WBCs insert pseudopodia into junctions between cells to squeeze through

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10
Q

How does emigration occur

A

Along chemical gradient (chemotaxis)

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11
Q

What are some chemotaxins

A

Soluble bacterial products

Complement proteins (C5a)

Lipoxgenase pathway products

Platelet activating factor

Chemokines

Interleukins

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12
Q

Properties of neutrophils at site of infection

A

Amoeboid movement

Strong phagocytic activity

Ability to digest particulate matter

Release granules to kill microbes and tumors

Form Neutrophil Extracellular Traps - nets that ensnare bacteria

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13
Q

What are primary and secondary granules in neutrophils

A

Primary: proteins and enzymes that break down and kill bacteria

Secondary: contain toxic oxygen compounds and lactoferrin that bind iron

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14
Q

Whats an important role of neutrophils in sepsis

A

Formation of neutrophil extracellular traps in blood vessels to trap bacteria

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15
Q

Migration of neutrophils stimulates the release of what? What does this cause?

A

Colony stimulating factor

CSF stimulates granulopoesis and release of neuts from bone marrow

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16
Q

What’s left shift

A

Presence of banded neutrophils in blood

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17
Q

Regenerative left sift

A

Mature and bands are increased

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18
Q

Degenerative left shift

A

Matures normal or decreased. Bands increased

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19
Q

What does a degenerative left shift mean in most species

A

Poor prognosis :(

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20
Q

What does a degenerative left shift mean in cows

A

Common - they dont have large neutrophil reserves in bone marrow!

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21
Q

Should you expect to find a lot of eosinophils in blood

A

No - they only spend 30 min in blood before moving to tissues, where they spend 12 days

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22
Q

Functions of eosinophils

A

Cytotoxicity of parasites and fungi

Augmentation of inflammatory reaction during immediate hypersensitivity reaction

Phagocytic activity (more limited than neutrophils)

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23
Q

Eosinophilia is common in…..

A

Parasitic infections

Allergic conditions

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24
Q

What is eotaxin

A

IL-5 - mast cell tumors and lymphomas release it, evoking eosinophilia

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25
Important enzymes of eosinophils
Perioxidase | Phosphotase
26
Idiopathic eosinophilic lesions of animals
1) Feline eosinophilic granuloma complex 2) Equine collagenolytic granulomes 3) Eosinophilic myositis in dogs, cows, sheep
27
Feline eosinophilic granuloma complexes
Eosinophilic plaque: pruritic lesion in skin of cats. Usually abdomen, inner thigh. Round/ovoid, ooze serum - Can see eosinophils microscopically Eosinophilic granuloma: linear granuloma on thighs. Pink to yellow elevated area --- Microscopically look like granulomas Eosinophilic ulcers (rat ulcer): oral cavity, ulcerated
28
Location of eosinophilic granulomas in dogs
Usually in oral cavity and lips
29
Location of equine collagenolytic granulomas
Saddle area
30
Eosinophilic myositis in dogs
Affects masticatory muscles -- attack their myosin
31
Eosinophilic myositis in ruminants
Affects skeletal and cardiac muscle -- sudden death! Believed to be due to allergy to muscle
32
Where are mast cells found
Organs rich in connective tissue at environment-host junction (skin, GI, respiratory tract)
33
Where are basophils found
Mainly in blood, and then emigrate to sites of inflammation
34
Which live longer in tissues: mast cells or basophils
Mast cells (1-3 months vs 3 days)
35
Mast cells and basophils have high affinity for which antibody
IgE
36
T/F - mast cells are phagocytic
No- mast cells and basophils are not
37
Are mast cells and basophils mobile?
Not really
38
What do mast cells and basophils contain
``` Histamine Serotonin Heparin Eotaxin (IL-5) Chemokines ```
39
Are lymphocytes acute or chronic
Chronic
40
Which WBCs constitute majority in peripheral blood
Lymphocytes
41
How long do lymphocytes live
Several months
42
Do lymphocytes respond to free antigens
No - must be presented to T-cell with MHC
43
CD4+ T cells are
Helper
44
CD 8+ T cells are
Cytotoxic
45
Types of B cells
Memory | Plasma
46
How long does transformation to plasma cell take? How long does it live for?
4-5 days Lives for 12 hours
47
Which cell represents 15% of lymphocytes
NK cells
48
Do naive NK cells express T-cell receptors
No
49
Can NK cells form memory
Yes
50
How do NK cells kill other cells
Secrete granules containing potent cytoxic molecules (perforin, granzyme)
51
Functions of blood monocytes (4)
1) Phagocytosis 2) Antigen presentation --> initiate cell-mediate immunity 3) Produce pro-inflammatory substances that kill and remove dead tissue 4) Iron sequestration (less for bacteria)
52
Which 'system' do macrophages engage in
Reticuloendothelial system ---> they live in certain organs
53
Mechanism of phagocytosis
1. Makes contact with particle 2. Psuedopodia sent out around particle 3. Psuedopodia fuse so that particle lays in vacuole 4. Phagosome fuses with lysosomes that contain oxygen radicals and other toxins 5. Intracellular killing 6. Exocytosis, antigen presentation
54
What type of macrophage might you seen in Johne's disease
(Chronic inflammation) Giant multinucleated cells
55
Where do lipid mediators come from
Cell membranes
56
Pathways from which lipid mediators are produced
Arachidonic Acid Pathway Platelet Activating Factor Pathway
57
What do COX-1 and COX-2 produce
COX-1 and COX -2 produce prostaglandins COX-1 (alone) produces thromboxane
58
Which COX is only in inflammation
COX-2
59
Which COX has good effects, like cytoprotection of mucosal cells
COX-1
60
Why do NSAIDs run the risk of causing ulcers
Because they also inhibit good effects of COX-1 (mucosal protection)
61
What are three enzymes from Arachidonic acid pathway
COX-1 COX-2 5-Lipoxygenase
62
What does 5-lipoxygenase do
Produces leukotrienes
63
What C/S do prostaglandins cause
``` Fever Pain Vasodilation Increased permeability Leukocyte adhesion/chemotaxis ```
64
What does thromboxane cause (2)
Vasoconstriction | Platelet aggregation
65
What do leukotrienes cause
1) Smooth muscle contraciton 2) Vasodilation 3) Neutrophil adhesion and chemotaxis 4) Mucous secretion 5) More potent than histamine, less rapid response
66
What does platelet activating factor do
Potent increase in permeability (1000x potent than histamine and leukotrienes) Also: chemotaxis, activation and adhesion, platelet activation, mediator release from WBCs
67
What do vasoactive amines do
Immediate, short lived responses in inflammation - Vasodilation - Increased permeability - Smooth muscle contraction
68
What are the most prevalent vasoactive amines
Histamine | Serotonin
69
What does nitric oxide do
Vasodilation (can also react with oxygen-derived radicals to form nitrogen-derived radicals that are both antimicrobial and damaging to tissue)
70
What is nitric oxide produced by
Endothelial cells | Macrophages
71
Main cytokines
IL-1 TNF-a INF-gamma IL-10
72
What does IL-1 do
Fever, neutrophilia Activates: - Endothelial cells - Membrane phospholipase A2 Stimulates acute phase proteins
73
What does TNF-a do
Shock Activates: - Neutrophils - Endothelial cells Stimulates production of other cytokines
74
What does INF-gamma do
Shifts to chronic inflammation Activates macrophages and lymphocytes
75
What does IL-10 do
Immune system suppression
76
Which cytokines are acute
IL-1 | TNF-alpha
77
Which cytokines are chronic
INF-gamma
78
Which cytokines are immunosuppressive
IL-10
79
What are the chemokines
1) IL-8 2) Eotaxin 3) CCL1, CCL2, CCL17, CCL22 4) MCP-1, CCL2
80
What do lysosomal enzymes do
Break down pathogens But also cause damage to host
81
What is Classical Path activated by
IgG and IgM antigen attack complexes
82
What is Lectin Path activated by
Sugar residues
83
What is Alternative Path activated by
Bacterial surface structures (ie LPS)
84
Whats the end result of all three complement pathways
Membrane Attack Complex -- punctures foreign cells
85
What is a very important mediator of complement
C3
86
What does C3 produce when its cleaved
1) C3a - anaphylatoxin (constricts smooth muscle and acts on mast cells to produce histamine) 2) C3b - opsonin (enhances macrophage and neutrophil phagocytosis)
87
What does C5 produce
C5a and C5b They are powerful chemotactic agents for neutrophils and (kinda) macrophages. Also increase vasodilation, mast cell activity and interleukin production
88
Your dog is deficient in C5 proteins. Will this be an issue?
Major issue as it is used in all three complement pathways
89
Your dog is deficient in C2 proteins. Will this be an issue
Yes, but you can still use Alternative pathway
90
Your cat is decicient in C4 proteins. Is this bad?
Yes, but you can still use Alternative pathway
91
Which proteins does Classical Path use
C1, C4, C2, C3, C5
92
Which protiens does Lectin path use
C4, C2, C3, C5
93
Which proteins does Alternative path use
C3 C5
94
Intrinsic clotting cascade triggered by
Damage to vessel
95
Extrinsic clotting cascade triggered by
Damage to tissue
96
Which factor starts intrinsic path
XII
97
Which factor starts extrinsic path
VII and Tissue Factor
98
Which factor is first step of Common Path
X
99
What is final common pathway
Prothrombin --> Thrombin Fibrinogen ---> Fibrin
100
What happens in fibrinolytic system
Plasminogen --> Plasmin which lyses fibrin into FDPs Also cleaves C3 of complement cascade, generating C3b and C3a Can also generate Bradykinin
101
What is Kinin System activated by
Coagulation Factor XII (Hagemen Factor), microbes, and proteases
102
What does kinin system do and what is most known kinin
Releases Kinins that activate pain, vasodilation, increase permeability, chemotaxis (BRADYKININ!)
103
Can factors from clotting, complement and kinin system activate each other
Yes!
104
What does Plasmin come from and what can it activate
From fibrinolytic system Can activate both Complement and Kinin system
105
What does factor XII come from and what can it activate
Its step 1 of intrinsic pathway but also initiates Kinin System
106
Examples of Vasoactive Amines
Histamine | Serotonin

Pathology (8 decks)

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