Hypersensitivity and Allergy Flashcards

(27 cards)

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

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
Mechanism of Type III Hypersensitivity
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
Extrinsic Allergic Alveolitis
Example of Type III Hypersensitivity Immune complexes deposit into the alveoli and cause fibrosis and inflammation
27
Mechanism of Type IV Hypersensitivity
e.g. Contact Dermatitis T cells activate macrophages that lead to tissue damage