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Microbiology BDS1 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

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1
Q

what is hypersensitivity?

A

a state of altered reactivity in which the body reacts with an exaggerated immune response to a foreign agent

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2
Q

what is an allergen?

A

an antigen that causes an allergic reaction

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3
Q

what is the Gell and Coombs’s classification?

A

the 4 types of hypersensitivity

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4
Q

what is the most common and rapid hypersensitivity?

A

type 1

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5
Q

what is type 1 hypersensitivity in response to?

A

allergen (antigen) so sometimes called immediate hypersensitivity

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6
Q

what is type 1 hypersensitivity mediated by?

A

IgE so sometimes called IgE mediated hypersensitivity

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7
Q

what is atopy?

A

a genetic predisposition for allergy

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8
Q

what is anaphylaxis?

A

acute serious allergic response

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9
Q

what are the 2 types of allergens

A

proteins and haptens

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10
Q

what is a hapten?

A

any small molecule that can be recognised by a specific antibody but cannot elicit an immune response

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11
Q

how do haptens elicit an immune response?

A

they must be chemically linked to a protein molecule (carrier) to elicit antibody and/or T-cell responses

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12
Q

what does a protein allergen have the ability to do?

A

elicit an immune response

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13
Q

what is the mechanism of type 1 hypersensitivity?

A

IgE producing B cells activated during sensitisation, IgE binds to Fc receptor on mast cells or CD63 on basophils (APCs), IgE recognises allergen and next exposure binds rapidly and causes immediate degranulation resulting in allergy symptoms

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14
Q

what is the main role of hypersensitivity 1

A

immune cell recruitment, neurotransmitter, vasodilator, endothelial constriction, bronchoconstrictor

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15
Q

what are the examples of type 1 hypersensitivity?

A

cutaneous atopy, systemic anaphylaxis

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16
Q

what does cutaneous atopy cover?

A

allergic rhinitis (hay fever), atopic dermatitis (allergic eczema), asthma (lower respiratory tract)

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17
Q

what is systemic anaphylaxis?

A

anaphylactic shock throughout the body

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18
Q

how does systemic anaphylaxis arise?

A

from mast cell degranulation

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19
Q

what are anaphylatoxins produced by?

A

the complement cascade

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20
Q

what are the ways to test for allergies?

A

skin prick test and patch test, blood test, food challenge

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21
Q

what is a skin prick test and patch test used for?

A

a skin reaction and are done to identify suspected allergen

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22
Q

what do blood tests measure?

A

IgE levels in blood

23
Q

what does a food challenge do?

A

diagnoses food allergy

24
Q

what are the different anti-allergy methods?

A

avoid allergen, drugs, immunological treatment

25
Q

what drugs are used for anti-allergy purposes?

A

anti-histamines, hydrocortison, cromoglycate, epinephrine

26
Q

what does anti-histamines do?

A

compete with histamine for receptors and can be inverse agonists or antagonists

27
Q

what does hydrocortisone do?

A

block histamine synthesis

28
Q

what does cromoglycate do?

A

stabilises mast cells and stops histamine release

29
Q

what does epinephrine do?

A

stimulation of adrenoreceptors (for anaphylactic shock), increases peripheral vascular resistance, improves blood pressure, reverses peripheral vasodilation, causes bronchodilation, reduces inflammatory mediator release

30
Q

what types of immunological treatment are available for anti-allergy purposes?

A

hypo- or de- sensitisation (repeat injections of allergen) and IgE to IgG production

31
Q

what type of response is atpoy?

A

localised

32
Q

what type of response is anaphylaxis?

A

systemic

33
Q

what does type 2 hypersensitivity involve

A

activation of complement by IgG or IgM binding to an antigenic cell (cell surface auto-antigens or haptens/allergens)

34
Q

in type 2 hypersensitivity how are the cells destroyed?

A

either by membrane attack complex formation (complement) or by antibody dependent cell mediated cytotoxicity (natural killer cells or CD8+ T cells)

35
Q

give a common example of hypersensitivity 2

A

transfusion reactions/autoimmune hemolytic anaemia (mismatched blood type)

36
Q

what does type 3 hypersensitivity involve?

A

reactions against soluble antigens circulating in serum

37
Q

what happens in type 3 hypersensitivity?

A

antibody-antigen immune complexes are deposited in organs which leads to complement activation, neutrophil recruitment, inflammation-mediated damage

38
Q

what are the examples of type 3 hypersensitivity?

A

Arthus reaction, serum sickness, oral erythema multiforme

39
Q

what is arthus reaction and what does it arise from?

A

localised hypersensitivity reaction, antibody-antigen complexes are localised e.g. blood vessel walls and can arise from injected particles (vaccinations) or from inhaled or ingested allergens (farmers lung and coeliac disease)

40
Q

what is serum sickness?

A

a systemic form of arthus reaction, antibody-antigen complexes circulate and lodge in many different tissues

41
Q

what is oral erythema multiforme characterised by?

A

crusty blistering of oral mucosa

42
Q

what is oral EM caused by?

A

deposition of immune complexes (IgM-bound immune complexes) in the microvasculature of the oral mucous membrane

43
Q

what type of inflammatory response is oral EM?

A

can be an acute inflammatory response to viral infections e.g. HSV

44
Q

what drug can cause oral EM?

A

trimethoprimsulfamethoxazole which is widely administered to treat urinary or lower respiratory tract infections

45
Q

what is type 4 hypersensitivity

A

T-cell mediated hypersensitivity (no antibodies)

46
Q

why is type 4 hypersensitivity sometimes called delayed hypersensitivity

A

it takes time to recruit T cells (adaptive immune cells)

47
Q

what occurs in type 4 hypersensitivity?

A

localised T cell reaction at site of antigen exposure e.g. contact dermatitis

48
Q

what cells does type 4 hypersensitivity involve?

A

CD4+ (inflammation induced damage via macrophages) and CD8+ (direct damage of cells -cytotoxicity) T cells

49
Q

what are the examples of type 4 hypersensitivity?

A

contact dermatitis, tissue graft rejection, OFG, response to intracellular pathogens e.g. TB characterised by the formation of granulomas in lung tissue

50
Q

what mediates type 1 hypersensitivity

A

IgE (mast cells and antibodies)

51
Q

what mediates type 2 hypersensitivity?

A

IgG or IgM leading to complement activation and/or antibody dependent cell mediate cytotoxicity

52
Q

what mediates type 3 hypersensitivity?

A

antibody-allergen

53
Q

what mediates type 4 hypersensitivity?

A

T cells (no antibodies required)

Microbiology BDS1 (20 decks)

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