Hypersensitivity and Allergy Flashcards

1
Q

What does an exaggerated response cause

A

Tissue damage (hypersensitibity)

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2
Q

Allergy Hypersensitivity vs Autoimmunity Hypersensitivity

A

Allergy - foreign material recognised but self material damaged

Autoimmunity - Self material recognised and self material damaged

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3
Q

Type 1 hypersensitivity

A

Immediate hypersensitivity or atopic allergy

Caused by IgE being cross linked on the surface of mast cells

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4
Q

What are type 2,3 and 4 hypersensitivities referred to as

A

Type 2 Hypersensivity - Antibody dependent hypersensitivity

Type 3 Hypersensitivity - Immune complex hypersensitvity

Type 4 Hypersensitivity - Delayed time hypersensitvity
*note that type 4 is mediated by cells not antibodies

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5
Q

What 3 factors mediate type I hypersensitivity

A

Mast Cells
IgE
Allergens

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6
Q

Examples of Type I Allergies

A
Allergic rhinitis (hayfever)
Allergic Asthma
Eczema
Food Allergies
Anaphylaxis

(don’t memorise just be vaguely aware)

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7
Q

What does the mast cell cause during type I allergy

A

Release of mediators causing oedema and smooth muscle contraction

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8
Q

Sensitisation

A

Allergen crosses the mucosal surfaces and enters body

Phagocytosed into APC

Does the same for allergen as it would for antigen; presents on MHC complex II

Peptide of that protein is presented to a TH2 cell

TH2 cell causes class switching in B cells to produce IgE antibodies against that allergen that sit on the surface of the mast cell via their Fc receptors

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9
Q

Which interleukins are released by Th2 cells during type I hypersensitivity and what do they each do

A

IL10: inhibits Th1 activity and activates mast cells

IL4: Activates B cells and causes class switching

IL5: Activates Eosinophils

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10
Q

What happens on subsequent exposure to the same allergen (Elicitation)

A

Mast cell degranulates as the IgE antibodies are bound - releases inflammatory mediators which lead to the allergic reaction

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11
Q

Atopic subject

A

Person predisoposed to having high levels of IgE

thus predisposed to allergies
such as hay fever, perennial rhinitis, asthma and atopic eczema

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12
Q

What are some mediators released during reactions of type I hypersensitivity

A
Histamine
Heparin
Tryptase
Arachidonic Acid
Leukotrienes-D4
Prostaglandin-D2
TNFa
IL-4
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13
Q

Would there be an anaphalactic response to a bee sting on the first time? Why/Why not?

A

No IgE antibodies against phospholipase A (protein causing reaction) have been made that are bound to mast cells

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14
Q

Why do dust-mites cause allergy

A

We do not have an allergic response to the mites themselves; instead we have a response to their faecal matter

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15
Q

Route of Entry and Bodily Response for Systemic Anaphylaxis

A

Route of Entry:
Intravenous either directly or through absorption of food into blood

Reponse:
Full body mast cell degranulation
Oedema
Increased Vascular Permeability
Tracheal Occlusion
Circulatory Collapse
Death
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16
Q

Route of Entry and Bodily Response for Acute Uticaria

A

Subcutaneously

Local increase in blood flow and vascular permeability

17
Q

Route of Entry and Bodily Response for ALlergic Rhinitis

A

Inhalation

Oedema and Irritation of nasal mucosa

18
Q

Route of Entry and Bodily Response for Asthma

A

Inhalation

Bronchial Constriction, Increased mucous production, Airway Inflammation

19
Q

Route of Entry and Bodily Response for Food Allergy

A

Oral

Vomiting
Diarrhea
Pruritus
Uticaria
Anaphylaxis
20
Q

Urticaria

A

Hives

21
Q

Allergic Response in Asthma

A

Allergen enters the airways and causes IgE to crosslink on mast cell surface; causing the acute and chronic responses:

Acute Phase: Vasodilation, increased vascular permeability and cellular recruitment causing tissue damage

Chronic Phase: Eosinophils are recruited into airways; they release cytotoxic mediators to attack airways like they would do to a parasite

22
Q

How to detect an allergy

A

Skin tests where a tiny amount of the allergen is pricked into the skin to prompt an immune response

23
Q

Mechanism II of hypersensitivity

A

e.g. Allergic Haemolytic Anaemia

Mediated by antibodies;

  • IgG
  • IgA
  • IgM

Caused by neutrophils releasing their mediators and antibody binding to a target leading to tissue damage

24
Q

Rhesus Haemolytic disease of a newborn

A

Example of Type II Hypersensitivity

IgG goes through the placenta of the SECOND foetus of RhD+ blood type when mother is RhD- (first foetus familiarises the mother’s body with the allergen) and causes damage to the unborn foetus by attacking the RhD protein

25
Q

Mechanism of Type III Hypersensitivity

A

e.g. Dermatitis

Immune complex formation; too many are formed so the immune system cannot effectovely clear them leading to their deposition in the skin which causes damage and necrosis

26
Q

Extrinsic Allergic Alveolitis

A

Example of Type III Hypersensitivity

Immune complexes deposit into the alveoli and cause fibrosis and inflammation

27
Q

Mechanism of Type IV Hypersensitivity

A

e.g. Contact Dermatitis

T cells activate macrophages that lead to tissue damage