Hypersensitivity 1 Flashcards

(29 cards)

1
Q

How many types of hypersensitivity are there?

A

4

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2
Q

Type I hypersensitivity?

A

Allergy

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3
Q

Type II-IV hypersensitivity?

A

Autoimmunity

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4
Q

Type II hypersensitivity?

A

Autoantibodies

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5
Q

Type III hypersensitivity?

A

Deposition of immune complexes

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6
Q

Type IV hypersensitivity?

A

T cell mediated tissue injury

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7
Q

What do allergens do to the innate immune response?

A

“skip it”

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8
Q

How does an allergen cause a reaction?

A

It crosslinks IgE antibodies, degranulating the MAST cell

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9
Q

How do mast cells exist normally?

A

“pre-primed” with IgE bound to the surface via FC receptors

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10
Q

What happens when a MAST cell is degranulated?

A

Histamine release, cytokine release

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11
Q

What can MAST cell mediators cause?

A

Increased vascular permeability
Vasodilation
Bronchial and smooth Muscle con
Local inflammation

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12
Q

Why do allergic reactions increase over time?

A

formation of memory b cells forming after the first time

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13
Q

What are allergies treated with?

A

Anti-histamines e.g. cetirizine

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14
Q

What do allergens require before the substance triggers an immune response?

A

Repeated exposure

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15
Q

Characteristics of many allergens?

A

small, glycosylated molecules w/ high solubility in body fluids

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16
Q

Why is there no TH1 or macrophage activation in allergies?

A

They don’t trigger the innate response

17
Q

Why do allergens need repeating units?

A

They need to cross link IgE antibodies on MAST cell surface–> bind to more than one antibody at once

18
Q

Why do allergens not trigger the innate response?

A

Dont have anything that would trigger pattern recognition receptors–> LPS, etc

19
Q

How many mechanisms can autoantibodies act by?

20
Q

First way of autoantibodies acting (complement)?

A

Autoantibody activating complement and stimulating phagocytosis

21
Q

Second way of autoantibodies acting (neutrophils)?

A

Autoantibodies recruiting neutrophils which cause tissue damage

22
Q

What is graves disease?

A

Producing antibodies against thyroid stimulating hormone receptor

23
Q

Mechanism of myasthenia gravis?

A

Antibodies block the nicotinic ACh receptors on muscle

24
Q

Outcome of myasthenia gravis?

A

muscle weakness especially in eyelids

25
Myasthenia gravis treatment?
Acetycholineesterases--> keeps ACh levels in synapse high
26
Thirway of autoantibodies acting (receptor)?
Can bind to receptor and stimulate or inhibit function
27
Example of complement activation and phagocytosis stimulation in autoantibodies?
Mothers can produce antibodies against foetal blood--> leads to haemolytic anaemia
28
Example of neutrophil recruitment in autoantibodies?
Activation in smaller vessels--> leads to glomerulus damage as an example
29