Hypersensitivity Flashcards

1
Q

Which type of hypersensitivity reaction is responsible for most allergic reactions?

A

Type I Hypersensitivity

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2
Q

Give five examples of clinical manifestations of type I hypersensitivity

A
Allergic rhinoconjunctivitis 
Asthma
Eczema/urticaria
Food allergy
Anaphylaxis
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3
Q

What mediates type I hypersensitivity?

A

IgE antibodies

Also: mast cells, basophils, eosinophils, T-helper2 cells

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4
Q

Which type of hypersensitivity reaction is responsible for most tissue-specific cytotoxic reactions?

A

Type II Hypersensitivity

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5
Q

Give four examples of type II hypersensitivity reactions

A

Haemolytic reaction following blood transfusion (ABO, Rhesus incompatibility)
Haemolytic disease of the newborn
Hyperacute graft rejection
Organ-specific autoimmune disease

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6
Q

Give four autoimmune diseases that are caused by type II hypersensitivity reaction

A

Graves disease
Myasthenia gravis
Goodpasture’s syndrome
Pemphigus (skin blisters)

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7
Q

What mediates type II hypersensitivity reactions?

A

IgG or IgM antibodies

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8
Q

Which type of hypersensitivity reaction involves the abnormal deposition of formed antibody-antigen complexes in tissues?

A

Type III Hypersensitivity

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9
Q

Give six examples of diseases caused by type III hypersensitivity

A

Systemic Lupus Erythematosus
Serum sickness
Extrinsic allergic alveolitis (e.g. farmer’s lung)
Chronic infection (e.g. leprosy, malaria)
Post-strep glomerulonephritis
Tumours

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10
Q

What are the main mediators of type III hypersensitivity?

A

Antibodies

- immune complexes involving soluble antigens

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11
Q

Which type of hypersensitivity reaction takes at least 48 hours to manifest itself?

A

Type IV Hypersensitivity

- aka delayed hypersensitivity

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12
Q

Give five examples of diseases caused by type IV hypersensitivity

A
Mycobacteria infection (tuberculosis)
Type 1 Diabetes Mellitus
Multiple sclerosis
Rheumatoid arthritis
Contact dermatitis
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13
Q

What mediates type IV hypersensitivity?

A

T-helper cells Th1 and Th17

Also the cytokines secreted by Th cells

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14
Q

What type of antigens trigger type IV hypersensitivity reactions?

A

Haptens (low molecular weight agent)

+ Carrier (host protein that attaches to the hapten to provide sufficient antigenic bulk)

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15
Q

What are the three phases of a type I hypersensitivity reaction?

A
  1. sensitisation
    2a. early phase response
    2b. late phase response
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16
Q

Describe the sensitisation process in type I hypersensitivity

A

Phagocyte in periphery picks up an unrecognised allergen, becomes an APC and goes to the lymph node
Th2 cell in lymph node does not recognise the antigen
Th2 cell activated against the allergen and produces interleukins
IL-4 activates B-cells which produce IgE against the allergen
- IgE primes mast cells against the allergen
IL-5 activates eosinophils

17
Q

Which mediators are involved in the response phases of type I hypersensitivity?

A
Early response: 
 - preformed mast cell mediators (histamine, proteases)
Late response:
 - newly synthesised mediators 
 - Th2 cytokines
 - eosinophil mediators
18
Q

Describe the pathophysiology of type II hypersensitivity

A

B-cells are pathologically self-reactive - produce IgG/IgM antibodies which bind to antigens on host cell surfaces
Antigen-antibody complex activates complement
Degranulation of neutrophils and formation of MAC cause cell lysis

19
Q

What is the MAC?

A

Membrane Attack Complex

- forms transmembrane channels which disrupt the cell membrane of target cells, leading to cell lysis and death

20
Q

Describe the pathophysiology of type III hypersensitivity

A

Excessive/abnormal immune complex formation (due to problems with the antigens and/or host response)
Complement activation and recruitment/activation of inflammatory cells by immune complexes
Inflammation causes tissue damage

21
Q

What antigen and host-response factors contribute towards type III hypersensitivity?

A

Antigen

  • chronic persistence of antigen
  • abnormal Ag/Ab ration
  • abnormal rate of Ag/Ab formation

Host response

  • Antibody defects
  • Complement defects
  • Fc or phagocyte defects
22
Q

How does the pathophysiology of type IV hypersensitivity differ to that of type I?

A

Different ligand bonds form during sensitisation
- CD28 and B7 ligand bonds form in type IV
T-helper1 cells involved in type IV, T-helper2 cells involved in type I
Type IV also involves cytotoxic T cells

23
Q

How to Tc cells cause cell death in type IV hypersensitivity?

A

Release perforin which damages the cell surface

24
Q

Describe the pathophysiology of type IV hypersensitivity

A

Macrophages become APCs and secrete IL-12, which stimulates the proliferation of further CD4+ Th1 cells.
CD4+ T cells secrete IL-2 and interferon gamma,
- IL-2 induces the further release of other Th1 cytokines
- IFN-gamma stimulates macrophages

25
Q

How is type I hypersensitivity diagnosed?

A

History/examination
Skin-prick test
RAST test (IgE level)
Other lab tests

26
Q

What are the treatment options for type I hypersensitivity?

A
Education and allergen avoidance
Antihistamines
Sodium cromoglycate
Steroids
Leukotriene antagonists
Desensitisation immunoglobulins
Adrenaline for anaphylaxis
27
Q

How is type II hypersensitivity managed?

A
Prevention:
 - cross match blood
 - tissue typing
 - detection of RhD in pregnancy
Immune suppression in autoimmune disease and transplant rejection
28
Q

How is type III hypersensitivity diagnosed?

A

Clinical features
Tissue biopsy
Circulating immune complex tests
Precipitating antibody tests

29
Q

What are the treatment options for type III hypersensitivity?

A

Antigen elimination (infection, tumour)
Removal of immune complexes
Immunosuppressive therapy

30
Q

What are the management options for type IV hypersensitivity?

A

Prevention/avoidance of contact with allergen
Antimicrobial therapy (if required)
Anti-inflammatory drugs e.g. corticosteroids
Immunosuppressive drugs
Other immune modifiers e.g. monoclonal antibodies

31
Q

Describe the pathophysiology of contact dermatitis

A

Type IV hypersensitivity reaction:
Haptens cross stratum corneum
Langerhans cells present to TH1 cells
TNF alfa and IL 1, 13 and 18 produced by TH1
LCs become differentiated Dendritic cells presenting allergenic epitope and multiply
More aggressive response 2nd time