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Immunology > Inflammation > Flashcards

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
Q

Integrins

A

heterodimers that bind to Ig-CAMs. Leukocyte integrin = CD18. Mutated CD18 = LAD

26
Q

Ig-CAMs

A

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
Q

Steps of leukocyte extravasation

A

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
Q

Neutrophil extravasation molecules

A
  1. Selectin L binds PSGL-1 (rolling)
  2. IL-8, MIP-1beta (activation)
  3. CD18 responsible for adhesion
  4. chemokine gradient (diapedesis)
29
Q

Monocyte extravasation molecules

A
  1. CD62L for rolling
  2. MCP-1 for activation
  3. PECAM-1 for diapedesis
    Complement receptors involved in extravasation
30
Q

Chemokines that activate lymphocytes in HEV

A

CCL19, CCL21, CXCL12

31
Q

Manifestations of systemic inflammation

A

Acute phase response, alterations in WBC counts, high fever, sepsis and SIRS

32
Q

Acute phase response

A

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
Q

APP in Cat

A

SAA

34
Q

APP in Dog

A

CRP, SAA

35
Q

APP in Horse

A

SAA

36
Q

APP in Cow

A

Hp, SAA

37
Q

APP in Pig

A

CRP, Pig-MAP

38
Q

Systemic effects of inflammation

A

loss of appetite, altered sleep, lethargy, muscle wasting, metabolic acidosis

39
Q

Inflammation resolution

A

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
Q

Outcomes of inflammation

A

resolution, fibrosis (tissue destruction), abscess formation, chronic inflammation

Immunology (11 decks)

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