Immediate hypersensitivity Flashcards

1
Q

What is immediate hypersensitivity?

A

A type I hypersensitivity reaction caused by IgE production and mast cell activation

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2
Q

What is atopy?

A

A genetic predisposition to produce IgE antibodies in response to environmental allergens and develop strong hypersensitivity reactions

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3
Q

What are common IgE-mediated allergic diseases?

A

Hay fever asthma eczema urticaria and allergic conjunctivitis

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4
Q

What is asthma in the context of hypersensitivity?

A

An immediate hypersensitivity reaction in the lungs causing reversible airway obstruction and bronchial inflammation

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5
Q

What are the symptoms of immediate hypersensitivity reactions?

A

Itchy skin rashes sneezing runny nose coughing wheezing red eyes swelling vomiting and diarrhea

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6
Q

What is anaphylaxis?

A

A systemic immediate hypersensitivity reaction characterized by edema bronchoconstriction and hypotension

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7
Q

What are common allergens in immediate hypersensitivity?

A

Dust mites tree and grass pollen food proteins such as peanuts animal dander and drugs

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8
Q

What is the mechanism of immediate hypersensitivity?

A

Allergen exposure activates Th2 cells leading to B cell class switching to IgE IgE binds to mast cells and re-exposure triggers mast cell degranulation

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9
Q

What cytokines are involved in IgE class switching?

A

IL4 and IL13 secreted by Th2 cells promote IgE production by B cells

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10
Q

What mediators are released by mast cells in hypersensitivity?

A

Histamine platelet-activating factor leukotrienes prostaglandins and cytokines

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11
Q

What are the early and late-phase responses in immediate hypersensitivity?

A

The early phase includes vasodilation edema and bronchospasm while the late phase involves cellular recruitment and inflammation

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12
Q

What is the role of eosinophils in immediate hypersensitivity?

A

Eosinophils are recruited by IL5 and release toxic proteins such as major basic protein causing tissue damage

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13
Q

What are the effects of histamine in hypersensitivity?

A

Bronchoconstriction vasodilation increased vascular permeability and stimulation of nerve endings causing itching

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14
Q

What is the hygiene hypothesis in allergy development?

A

A lack of early exposure to infectious agents and parasites increases susceptibility to allergies by suppressing immune development

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15
Q

How is anaphylaxis treated?

A

With adrenaline to reverse bronchoconstriction and vasodilation and antihistamines to block histamine receptors

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16
Q

What are common treatments for asthma in hypersensitivity?

A

Corticosteroids to block inflammatory cytokines and sodium cromolyn to inhibit mast cell mediator release

17
Q

What is the role of Th2 cells in immediate hypersensitivity?

A

Th2 cells secrete IL4 IL13 IL5 and eotaxin promoting IgE production and eosinophil recruitment

18
Q

What is the genetic basis of atopy and IgE production?

A

Atopy is influenced by multiple genes including those encoding IL4 IL5 IL13 and Fc receptors

19
Q

What is the role of eotaxin in hypersensitivity?

A

Eotaxin attracts eosinophils to sites of inflammation

20
Q

How does dust mite allergen trigger hypersensitivity?

A

Dust mites produce proteins that can penetrate mucosal barriers and trigger IgE production

21
Q

What cytokines are involved in the late-phase response of hypersensitivity?

A

IL3 promotes mast cell proliferation TNF-alpha promotes inflammation and IL5 recruits eosinophils

22
Q

How do mast cells contribute to hypersensitivity reactions?

A

Mast cells release pre-formed mediators synthesize new mediators and produce cytokines during allergic responses

23
Q

What is the clinical course of immediate hypersensitivity reactions?

A

The immediate phase occurs within minutes while the late-phase reaction peaks hours after allergen exposure

24
Q

What is the focus of drug therapy for immediate hypersensitivity?

A

Blocking mast cell degranulation and the effects of mediators and cytokines