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Pathology > Inflammation > Flashcards

Inflammation Flashcards

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
Q

Important enzymes of eosinophils

A

Perioxidase

Phosphotase

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26
Q

Idiopathic eosinophilic lesions of animals

A

1) Feline eosinophilic granuloma complex
2) Equine collagenolytic granulomes
3) Eosinophilic myositis in dogs, cows, sheep

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27
Q

Feline eosinophilic granuloma complexes

A

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

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28
Q

Location of eosinophilic granulomas in dogs

A

Usually in oral cavity and lips

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29
Q

Location of equine collagenolytic granulomas

A

Saddle area

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30
Q

Eosinophilic myositis in dogs

A

Affects masticatory muscles – attack their myosin

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31
Q

Eosinophilic myositis in ruminants

A

Affects skeletal and cardiac muscle – sudden death!

Believed to be due to allergy to muscle

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32
Q

Where are mast cells found

A

Organs rich in connective tissue at environment-host junction (skin, GI, respiratory tract)

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33
Q

Where are basophils found

A

Mainly in blood, and then emigrate to sites of inflammation

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34
Q

Which live longer in tissues: mast cells or basophils

A

Mast cells (1-3 months vs 3 days)

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35
Q

Mast cells and basophils have high affinity for which antibody

A

IgE

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36
Q

T/F - mast cells are phagocytic

A

No- mast cells and basophils are not

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37
Q

Are mast cells and basophils mobile?

A

Not really

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38
Q

What do mast cells and basophils contain

A 
Histamine
Serotonin
Heparin
Eotaxin (IL-5)
Chemokines
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39
Q

Are lymphocytes acute or chronic

A

Chronic

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40
Q

Which WBCs constitute majority in peripheral blood

A

Lymphocytes

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41
Q

How long do lymphocytes live

A

Several months

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42
Q

Do lymphocytes respond to free antigens

A

No - must be presented to T-cell with MHC

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43
Q

CD4+ T cells are

A

Helper

44
Q

CD 8+ T cells are

A

Cytotoxic

45
Q

Types of B cells

A

Memory

Plasma

46
Q

How long does transformation to plasma cell take? How long does it live for?

A

4-5 days

Lives for 12 hours

47
Q

Which cell represents 15% of lymphocytes

A

NK cells

48
Q

Do naive NK cells express T-cell receptors

A

No

49
Q

Can NK cells form memory

A

Yes

50
Q

How do NK cells kill other cells

A

Secrete granules containing potent cytoxic molecules (perforin, granzyme)

51
Q

Functions of blood monocytes (4)

A

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
Q

Which ‘system’ do macrophages engage in

A

Reticuloendothelial system —> they live in certain organs

53
Q

Mechanism of phagocytosis

A
  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
Q

What type of macrophage might you seen in Johne’s disease

A

(Chronic inflammation)

Giant multinucleated cells

55
Q

Where do lipid mediators come from

A

Cell membranes

56
Q

Pathways from which lipid mediators are produced

A

Arachidonic Acid Pathway

Platelet Activating Factor Pathway

57
Q

What do COX-1 and COX-2 produce

A

COX-1 and COX -2 produce prostaglandins

COX-1 (alone) produces thromboxane

58
Q

Which COX is only in inflammation

A

COX-2

59
Q

Which COX has good effects, like cytoprotection of mucosal cells

A

COX-1

60
Q

Why do NSAIDs run the risk of causing ulcers

A

Because they also inhibit good effects of COX-1 (mucosal protection)

61
Q

What are three enzymes from Arachidonic acid pathway

A

COX-1
COX-2

5-Lipoxygenase

62
Q

What does 5-lipoxygenase do

A

Produces leukotrienes

63
Q

What C/S do prostaglandins cause

A 
Fever
Pain
Vasodilation
Increased permeability
Leukocyte adhesion/chemotaxis
64
Q

What does thromboxane cause (2)

A

Vasoconstriction

Platelet aggregation

65
Q

What do leukotrienes cause

A

1) Smooth muscle contraciton
2) Vasodilation
3) Neutrophil adhesion and chemotaxis
4) Mucous secretion
5) More potent than histamine, less rapid response

66
Q

What does platelet activating factor do

A

Potent increase in permeability (1000x potent than histamine and leukotrienes)

Also: chemotaxis, activation and adhesion, platelet activation, mediator release from WBCs

67
Q

What do vasoactive amines do

A

Immediate, short lived responses in inflammation

  • Vasodilation
  • Increased permeability
  • Smooth muscle contraction
68
Q

What are the most prevalent vasoactive amines

A

Histamine

Serotonin

69
Q

What does nitric oxide do

A

Vasodilation

(can also react with oxygen-derived radicals to form nitrogen-derived radicals that are both antimicrobial and damaging to tissue)

70
Q

What is nitric oxide produced by

A

Endothelial cells

Macrophages

71
Q

Main cytokines

A

IL-1
TNF-a
INF-gamma
IL-10

72
Q

What does IL-1 do

A

Fever, neutrophilia

Activates:

  • Endothelial cells
  • Membrane phospholipase A2

Stimulates acute phase proteins

73
Q

What does TNF-a do

A

Shock
Activates:
- Neutrophils
- Endothelial cells

Stimulates production of other cytokines

74
Q

What does INF-gamma do

A

Shifts to chronic inflammation

Activates macrophages and lymphocytes

75
Q

What does IL-10 do

A

Immune system suppression

76
Q

Which cytokines are acute

A

IL-1

TNF-alpha

77
Q

Which cytokines are chronic

A

INF-gamma

78
Q

Which cytokines are immunosuppressive

A

IL-10

79
Q

What are the chemokines

A

1) IL-8
2) Eotaxin
3) CCL1, CCL2, CCL17, CCL22
4) MCP-1, CCL2

80
Q

What do lysosomal enzymes do

A

Break down pathogens

But also cause damage to host

81
Q

What is Classical Path activated by

A

IgG and IgM antigen attack complexes

82
Q

What is Lectin Path activated by

A

Sugar residues

83
Q

What is Alternative Path activated by

A

Bacterial surface structures (ie LPS)

84
Q

Whats the end result of all three complement pathways

A

Membrane Attack Complex – punctures foreign cells

85
Q

What is a very important mediator of complement

A

C3

86
Q

What does C3 produce when its cleaved

A

1) C3a - anaphylatoxin (constricts smooth muscle and acts on mast cells to produce histamine)
2) C3b - opsonin (enhances macrophage and neutrophil phagocytosis)

87
Q

What does C5 produce

A

C5a and C5b

They are powerful chemotactic agents for neutrophils and (kinda) macrophages. Also increase vasodilation, mast cell activity and interleukin production

88
Q

Your dog is deficient in C5 proteins. Will this be an issue?

A

Major issue as it is used in all three complement pathways

89
Q

Your dog is deficient in C2 proteins. Will this be an issue

A

Yes, but you can still use Alternative pathway

90
Q

Your cat is decicient in C4 proteins. Is this bad?

A

Yes, but you can still use Alternative pathway

91
Q

Which proteins does Classical Path use

A

C1, C4, C2, C3, C5

92
Q

Which protiens does Lectin path use

A

C4, C2, C3, C5

93
Q

Which proteins does Alternative path use

A

C3 C5

94
Q

Intrinsic clotting cascade triggered by

A

Damage to vessel

95
Q

Extrinsic clotting cascade triggered by

A

Damage to tissue

96
Q

Which factor starts intrinsic path

A

XII

97
Q

Which factor starts extrinsic path

A

VII and Tissue Factor

98
Q

Which factor is first step of Common Path

A

X

99
Q

What is final common pathway

A

Prothrombin –> Thrombin

Fibrinogen —> Fibrin

100
Q

What happens in fibrinolytic system

A

Plasminogen –> Plasmin which lyses fibrin into FDPs

Also cleaves C3 of complement cascade, generating C3b and C3a

Can also generate Bradykinin

101
Q

What is Kinin System activated by

A

Coagulation Factor XII (Hagemen Factor), microbes, and proteases

102
Q

What does kinin system do and what is most known kinin

A

Releases Kinins that activate pain, vasodilation, increase permeability, chemotaxis

(BRADYKININ!)

103
Q

Can factors from clotting, complement and kinin system activate each other

A

Yes!

104
Q

What does Plasmin come from and what can it activate

A

From fibrinolytic system

Can activate both Complement and Kinin system

105
Q

What does factor XII come from and what can it activate

A

Its step 1 of intrinsic pathway but also initiates Kinin System

106
Q

Examples of Vasoactive Amines

A

Histamine

Serotonin

Pathology (8 decks)

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