Inflammation and repair Flashcards

1
Q

List the causes of inflammation

A

Infections, microbial toxins
Tissue necrosis
Foreign bodies and endogenous substances (urate crystals)
Hypersensitivity

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2
Q

What components recognise microbes and damaged cells?

A

Cellular receptors for microbes, such as TLRs
Sensors of cell damage, such as NLRs
Receptors for Fc tails of antibodies
Complement

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3
Q

What is the inflammasome?

A

Receptors for cell damage (NLRs) activate the inflammasome, which is multiprotein cytosolic complex. The inflammasome recruits IL-1

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4
Q

How does IL-1 induce inflammation?

A

IL-1 is recruited by the inflammasone, and IL-1 recruits leukocytes

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5
Q

In which inflammatory diseases is the inflammasone implicated?

A

Gout/uric acid, metabolic syndrome and obesity-associated T2DM/lipids, aterosclerosis/cholesterol crystals, AD/amyloid

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6
Q

What are the key components of inflammation?

A

Vascular reaction and cellular response

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7
Q

What are the 5 steps of inflammation?

A

Recognition
Recruitments of leukocytes
Removal of agent
Regulation of inflammation and
Repair

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8
Q

What are the three major components of acute inflammation?

A

Vasodilation and increased blood flow
Increased microvascular permeability
Leukocytes arrival and activation

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9
Q

Define exudate

A

Extravascular fluid that has high protein concentration and contains cellular debris. Its presence implies inflammation and increased vessel permeability

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10
Q

Define transudate

A

Fluid with low protein content, little cellular debris and low specific gravity. It is produced from osmotic or hydrostatic imbalance without increase in vascular permeability

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11
Q

Is oedema transudate or exudate?

A

Can be either

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12
Q

Describe vasodilation in inflammation

A

Early manifestation
Caused by histamine
Involves arterioles and then opening of new capillaries
Increases blood flow, heat and erythema

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13
Q

What is the results of vasodilation and increased vessel permeability?

A

Slow flow, concentration of red cells and increased viscosity of blood.
Small vessels engorge, leading to stasis, vascular congestion and localised erythema

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14
Q

How are leukocytes recruited to inflammation?

A

With stasis, leukocytes accumulate along the vascular endothelium. Mediators activate endothelial cells to increase expression of adhesion molecules. Leukocytes adhere to endothelium and then migrate through the vessel wall.

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15
Q

How is increased vascular permeability achieved?

A

Contraction of endothelial cells
Endothelial injury causing necrosis and detachment, enhanced by leukocyte binding

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16
Q

What causes endothelial contraction?

A

Histamine, bradykinin, leukotrienes and other chemical mediators

17
Q

What is the immediate transient response in acute inflammation?

A

Endothelial cell contraction
Rapid and short-lived, up to 30 mins

18
Q

In which cases doe late vascular leakage occur?

A

Mild injury such as burns, irradiation, UV radiation and some bacterial toxins