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General Pathology > Mediators of Inflammation > Flashcards

Mediators of Inflammation Flashcards

1
Q

What are the main mediators

A

Cytokines

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2
Q

Who mediates acute inflammation

A

TNF
IL-1
IL-17
Chemokines

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3
Q

Where does TNF come from

A

Macrophages, mast cells, T cells

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4
Q

What doe TNF do?

A

Expression of endothelial adhesion molc, release of other cytokines, systemic effects

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5
Q

Where does IL-1 come from

A

Macrophages, endothelial, some epithelial

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6
Q

Where do chemokines come from

A

macrophages, endothelial cells, T-cells, mast cells

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7
Q

Where does IL-17 come from

A

T-cells

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8
Q

Who mediates chronic inflammation

A

IL-12
IFN-gamma
IL-17

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9
Q

Where does IL-12 come from

A

dendritic cells, macrophages

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10
Q

Where does IFN gamma come from

A

T-cells, NK cells

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11
Q

What are arachidonic acid metabolites derived from

A

cell membranes, then cleaved by phospholipids

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12
Q

What is the name for the class of enzymes made from AA metabolites

A

eicosanoids

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13
Q

What are the types of eicosanoids

A

cyclooxygenase
lipoxygenase

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14
Q

What do cyclooxygenases produce

A

prostaglandins

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15
Q

What do lipooxygenases produce

A

leukotrienes and lipoxins

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16
Q

Why are AA metabolites so important

A

They produce and mediate almost every step of inflammation

17
Q

How are steroids and AAs related

A

Steroids act on phospholipases and prevent AA creation

18
Q

Pyrogens:

A

substances that induce fever

19
Q

How are fevers caused

A

IL-1 + TNF –> upregulate cyclooxygenases –> produce prostaglandins –> released into hypothalamus –> release neurotransmitters that increase body temp

20
Q

What are elevated acute-phase proteins

A

Plasma proteins synthesized in the liver

21
Q

What are the acute phase proteins

A

C-reactive protein
Fibrinogen
SAA

22
Q

What are some negative effects of inflammation

A

Septic shock
Secondary amyloidosis

23
Q

What causes septic shock

A

High levels of bacteria lead to large amounts of TNF and IL-1 being released
Eventually leads to DIC

24
Q

What causes secondary amyloidosis

A

Prolonged SAA production –> deposits of misfolded SAA
Can lead to tissue dysfunction

25
Q

What does TNF do

A

Stimulates the release of other cytokines
Stimulates endothelial adhesion molecules
Upregulates cyclooxygenase
Mediates granulocyte release
Septic shock
SAA production

26
Q

What do lipoxins do

A

Inhibit neutrophil adhesion

27
Q

What do leukotrienes do

A

Vasoconstriction
Increase vascular permeability
Leukocyte adhesion

General Pathology (19 decks)

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