Inflammation Flashcards

1
Q

Bovine acute mastitis

A

inflammation of mammary gland. Common diagnostic: leukocytes in milk.

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2
Q

Inflammation definition

A

defence reaction of living tissue against damage, aimed at removing the cause of injury and repairing the tissue

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3
Q

Acute inflammation

A

fights early stage of infection, prepares tissue repair process

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4
Q

Chronic inflammation

A

continuous presence of macrophages in injured tissue, mostly when cause of inflammation is not removed

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5
Q

Exogenous causes of inflammation

A

physical agents (fractures, foreign objects, burns, freezing)
Chemical agents: toxic gases, acids/bases
Biological agents: bacteria, viruses, parasites, fungi

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6
Q

Endogenous causes of inflammation

A
Circulation disorders (thrombosis)
Metabolic products (uric acid, urea)
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7
Q

hallmarks of inflammation!

A

redness, pain, swelling, heat, loss of function

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8
Q

What causes “heat” in inflammation?

A

vasodilation to the injured tissue bringing lots of blood flow

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9
Q

What causes “redness” in inflammation?

A

increased blood flow to tissue!

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10
Q

What causes “swelling” in inflammation?

A

fluid leakage into the tissues due to increased vascular permeability

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11
Q

What causes “pain” in inflammation?

A

inflammatory mediators released by leukocytes in the damaged tissue

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12
Q

Pro-inflammatory cytokines that mediate inflammation

A

TNF-alpha and IL-1 –> fever, stress hormones, production of IL-6, IL-8, IFN-gamma
IL-6 –> release of CRPs
IL-1, 6, 8 –> promote chemotaxis, induce extravasation, degranulation of neutrophils

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13
Q

Complement components mediation of inflammation

A

C3a, C5a –> increase vascular permeability

All –> Stimulate chemotaxis of granulocytes

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14
Q

Prostaglandins mediation of inflammation

A

contribute to vasodilation, capillary permeability, pain, fever
lower BP, potentiate effects of histamine
TXA2 –> promote platelet aggregation

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15
Q

Vasoactive amines in inflammation

A

found at high concentrations in mast cells, platelets. Cause dilation and increased permeability of capillaries. Act through histamine and serotonin receptors

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16
Q

Platelet activating factor in inflammation

A

induces platelet aggregation, activates neutrophils, attracts eosinophils, contributes to edema

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17
Q

Plasma proteases in inflammation

A

kinins - increase capillary permeability and pain

clotting factors - help final clotting stages

18
Q

Phase 1 of vascular response

A

momentary vasoconstriction

19
Q

Phase 2 of vascular response

A

active vasodilation!

Increased blood flow to area, active hyperemia

20
Q

Phase 3 of vascular response

A

passive vasodilation
blood vessels stop reacting to nervous/humoral stimuli
increase in vascular permeability causing swelling, loss of function

21
Q

Cellular response of inflammation

A

movement of leukocytes to damaged tissue

22
Q

Types of CAMs

A

Selectins
Mucins
Integrins
Ig-CAMs

23
Q

Selectins

A

Selectin L (on leukocytes) binds selectin P/E on endothelium.

24
Q

Mucins

A

Bind to selectins

25
Integrins
heterodimers that bind to Ig-CAMs. Leukocyte integrin = CD18. Mutated CD18 = LAD
26
Ig-CAMs
Bind to integrins. Expressed on endothelial cells. Some Ig-CAMs have a mucin domain so they can bind to selectins as well. MAdCAM-1 responsible for binding leukocytes to the mucosa
27
Steps of leukocyte extravasation
Rolling - leukocyte mucins bind to selectins E and P Activation - increase in cytokine release activates Adhesion - integrins on leukocytes bind to endothelial Ig-CAMs Diapedesis - due to binding of PECAM-1
28
Neutrophil extravasation molecules
1. Selectin L binds PSGL-1 (rolling) 2. IL-8, MIP-1beta (activation) 3. CD18 responsible for adhesion 4. chemokine gradient (diapedesis)
29
Monocyte extravasation molecules
1. CD62L for rolling 2. MCP-1 for activation 3. PECAM-1 for diapedesis Complement receptors involved in extravasation
30
Chemokines that activate lymphocytes in HEV
CCL19, CCL21, CXCL12
31
Manifestations of systemic inflammation
Acute phase response, alterations in WBC counts, high fever, sepsis and SIRS
32
Acute phase response
change in serum proteins during inflammation APP - proteins whose concentrations change during this response Synthesis (in liver) induced by pro-inflammatory cytokines like TNF-alpha, IL-1, IL-6
33
APP in Cat
SAA
34
APP in Dog
CRP, SAA
35
APP in Horse
SAA
36
APP in Cow
Hp, SAA
37
APP in Pig
CRP, Pig-MAP
38
Systemic effects of inflammation
loss of appetite, altered sleep, lethargy, muscle wasting, metabolic acidosis
39
Inflammation resolution
Must be done to prevent damage. TGF-beta, IL-4 and IL-10 used to downregulate response. Anti-inflammatory molecules will be upregulated, apoptosis of pro-inflammatory cells, production of anti-inflammatory lipoxins
40
Outcomes of inflammation
resolution, fibrosis (tissue destruction), abscess formation, chronic inflammation