mechanisms of inflammation Flashcards

0
Q

Acute inflammation

A

from tissue damage and/or infection
immediate response beginning within minutes of tissue insult
predominant infiltrating cell type - neutrophil

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1
Q

Inflammation

A

complex rxn following infection, trauma or noxious agents involving vascular alterations and migration of leukocytes
eliminates microbes and repairs damaged tissues
Excessive tissue damage can occur

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2
Q

Chronic inflammation

A

often follows unresolved acute inflammation
days after acute inflammation
infiltrating cell type: mononuclear - monocyte derived macs, T cells, rarely B cells

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3
Q

Allergic inflammation

A

allergens
follows allergen mediated degranulation of mast cells
infiltrating cells - Eosinophils and mononuclear cells - T cells and Macs

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4
Q

Examples of autoimmune diseases

A

Rheumatoid arthirits
Lupus
Type 1 diabetes

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5
Q

Inflammatory diseases that are not autoimmune or infectious

A

Asthma
Alzheimer’s
Psoriasis
Atherosclerosis

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6
Q

where are Mast cells found?

A

Mucosal sub epithelia

Skin

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7
Q

General process of Inflammation

A
Stimulus 
Release of inflammatory mediators 
Increased vascular permeability 
upregulation of adhesion molecules on endothelial cells and leukocytes 
attraction and activation of leukocytes 
Phagocytosis or other effector functions
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8
Q

Cardinal signs of inflammation

A
Cellulitis 
Rubor - redness
Tumor - swelling 
Calor - Heat 
Dolor - Pain
Functio - loss of function
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9
Q

Causes of cardinal signs of inflammation

A

Vascular dilation - slows and increases blood flow
Extravasion of plasma - Edema, swelling
Leukocyte accumulation at site of injury
Kinin stimulation of nerve fibers - pain

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10
Q

molecular basis of inflam stimuli

A

Microbial PAMP are detected by PRR (TLR) on resident tissue cells.
these cells release pro-inflammatory cytokines

Damaged cells release “warning” chemicals (damage associated molecular patterns) detected by DRR on tissue Macs, DCs and other tissue cells

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11
Q

Where are PRRs?

A

On the surface of cells and inside cells as well

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12
Q

Vasodilation and increased vascular permeability happen

A

together

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13
Q

Upon vasodilation, proteins leak out, name some

A

cytokines
antibodies
complement
clotting factors

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14
Q

Increased vascular permeability

A

Endothelial cell constriction allows gaps to open up so plasma, proteins and cells can enter tissues

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15
Q

Briefly describe the process of Leukocyte migration through blood vessels

A
Activation and attraction by inflammatory cytokines of lymphocytes 
Rolling of lymphocytes 
Adhesion of lymphocytes 
Arrest 
Transmigration
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16
Q

P-selection

A

Rolling of neutrophils, monocytes, lymphocytes

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17
Q

E-selectin

A

Rolling, adhesion to activated endothelium - neutrophils, monocytes, T cells

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18
Q

ICAM-1

A

Adhesion, arrest, transmigration - all leukocytes

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19
Q

VCAM-1

A

adhesion of eosinophils, monocytes and lymphocytes

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20
Q

CD31(PECAM)

A

Leukocyte migration through endothelium

21
Q

What mediators does the Liver contribute to the inflammatory response?

A

Factor XII - Kinin and coagulation system

Complements

22
Q

Activation of Hageman Factor (FActor XII) leads to

A

activation of the Kinin, complement and clotting cascade

23
Q

IL-1 and TNF-a

A

Activate endothelial cells to constrict and up regulate adhesion moleucles

24
Q

Eicosanoids for vasoconstriction

A

Thromboxane A2

Leukotrienes C4, D4, E4

25
Q

IL-6

A

induces release of acute phase proteins from liver

26
Q

CC chemokines

A

recruitment of mononuclear cells and eosinophils

MIP, MCP, RANTES eotactin

27
Q

CXC chemokines

A

involved in neutrophil recruitment

IL8

28
Q

IL-17

A

leads to neutrophil production from bone marrow and neutrophil activation

29
Q

IL-2

A

activation of T cells, T cell proliferation

30
Q

IFN-gamma

A

from Th1 cells

activates Macs

31
Q

Mononuclear cells

A

Monocyte/Macs and lymphocytes

33
Q

Type of Chronic inflammation

A

Granuloma formation
seen in TB
Histologically, see Multinucleated Giant cells
round in appearance

34
Q

What are some sources for inflammatory mediators?

A

Tissue macrophages, dendritic cells
Mast cells
Leukocytes
Endothelial cells

35
Q

What stimulates the alternative pathway to inflammation?

A

C5a, C3a

36
Q

What stimulates the classic pathway to phagocytosis?

A

C3b

37
Q

What stimulates the lectin pathway to lysis of the cell?

A

MAC formation

38
Q

What are the three interaction cascades of plasma protein systems?

A

Clotting
Kinin
Complement

39
Q

What do all three plasma protein cascades lead to?

A

Inflammation

40
Q

What eicosanoids cause vasoconstriction?

A

Thromboxane A2, leukotrienes C4, D4, E4

41
Q

What eicosanoids cause vasodilation?

A

PGI2, PGE1 and 2, PGD2

42
Q

What eicosanoids cause inc vascular permeability?

A

Leukotriene B4, HETE, lipoxin

43
Q

What eicosanoids cause chemotaxis, leukocyte adhesion?

A

Leukotriene B4, HETE, lipoxin

44
Q

What are the events for inflammatory mediators?

A
Fever
Pain
Vasodilation
Inc vascular permeability
Attraction of leukocytes
Activation of endothelium
45
Q

What are the chemokines involved in recruitment of monouclear cells into sites of inflammation?

A

CCL2 (MCP-1)
CCL3 (MIP-1a)
CCL4 (MIP-1b)
CCL5 (RANTES)

46
Q

Eosinophils and mononuclear cells characterize the;

A

Infiltrate in allergic inflammation

47
Q

What are the steps of the inflammatory process in allergic reactions?

A

Stimulus
Secretion from inflammatory mediators (mast cells)
Vasodilation (histamine)
Inc vascular permeability (TNF and arachidonic acid)
Up-regulation of adhesion molecules to VLA-4
Diapedesis, chemotoxis and activation of leukocytes

48
Q

What are acute inflammatory disease?

A
ARDS
Acute transplant rejection
Acute asthma attack
Glomerulonephritis 
Septic shock
Vasculitis
49
Q

What are chronic inflammation diseases?

A

Arthritis
Atherosclerosis
Chronic lung disease
Chronic transplant rejection

50
Q

What are allergic inflammation diseases?

A

Asthma

Atopic dermatitis