Immunological disease classifications Flashcards

1
Q

Gell and Coombes hypersensitivity reactions

A

Classification of immunologically-mediated diseases.

- Where the immune system is inappropriately activated.

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2
Q

Type 1 hypersensitivity reaction

  • Mechanism
  • Examples
A

IgE antibody is directed against allergens
- mast cell degranulation

Examples

  • Seasonal arthritis
  • Cat allergies
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3
Q

Ig-E mediated allergy

A

Believed to assist parasite immunity.

Secreted IgE from B cells binds to mast cells/ basophils.

Allergen specific to IgE on mast cell binds and causes cross linking of the receptors.

Mast cell degranulates- releases histamine, tryptase and other mediators
- Leads to symptoms of the affected organ

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4
Q

Type 2 hypersensitivity reaction

  • Mechanism
  • Examples
A

Pathology directly caused by antibodies.

Examples

  • Autoimmune haemolysis
  • Haemolytic disease of the newborn
  • Mismatch blood transfusion
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5
Q

Type 2 hypersensitivity reaction: Mismatch blood transfusion

A

Isoantibodies (IgM) developed against surface antigens of gut bacteria are produced against AB antigens of red blood cells.

Hence why:
- Rbc A antigen--> B ab
- Rbc B antigen--> A ab
- Rbc AB antigen--> No ab
Universal recipient
  • Rbc no antigen–> AB antibody
    Universal donor

Mismatch of blood= Type 2 hypersensitivity

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6
Q

Haemolytic disease of the newborn

A

T2 reaction.

Mother Rh-, father Rh+ (can have Rh+ baby)

Mother can be exposed to D antigens during trauma/ parturition, if baby is D+.
- Causes mother to produce Ab against D antigens which can cross placenta in later pregnancies.

Ab binds to fetal red cells=haemolysis

  • Growth retardation
  • CVS failure
  • High bilirubin neurotoxicity
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7
Q

Haemolytic disease of the newborn management

A

If mother is Rh- and partner is Rh+, anti-D IgG is given at 28 weeks routinely.
- IgG blocks fetal rbcs, prevents sensitisation

Reduces risk from 16% to 0.1%

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8
Q

Autoimmune haemolysis

A

T2 reaction

Autoantibodies develop against rbcs
- auto-Ab-RBC complex is either destroyed via phagocytosis (intersitium) or complement activation (intravascular haemolysis)

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9
Q

Type 3 reactions

A

Caused by Ab-Ag complexes that become insoluble and cause disease

Due to:

  • Large amounts of Ab or Ag
  • Very strong affinity between Ab and Ag
  • Larger complexes

Examples

  • Local immune complex disease
  • Serum sickness
  • Hypersensitivity pneumonitis
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10
Q

Local immune complex disease

A

T3 reaction

Deposits of circulating immune complexes in the fingertip pulp

Seen in infective endocarditis (Olser’s nodes), SLE

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11
Q

Serum sickness

A

T3 reaction

Injection from certain immunogenic drug/ anti-sera from animals causes a transient immune complex disease.

Signs

  • Rash
  • fever
  • Arthritis
  • Glomerulonephritis
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12
Q

Hypersensitivity pneumonitis

A

T3 reaction

Repeated exposure to environmental antigen leads to a large production of IgG ab.

  • Mould spores in hay
  • Pigeon feathers and still.

IgG forms complexes in the lung

Presentation

  • Shortness of breath
  • Cough
  • Initially transient then scarring when repeated.
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13
Q

Type IV hypersensitivity

A

Caused by antigen-specific T effector Cells.

Tend to present at least 24 hrs after exposure to antigen
- Takes time to process and present antigen

Example
- Contact dermatitis

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14
Q

Contact dermatitis

  • Mechanism of sensitisation
  • Examples
A

T4 reaction

In the skin:

  • Highly reactive, small molecule breaks the skin and forms protein-happen complex
  • Complex is taken up by langerhan cells which migrates to lymph nodes
  • Antigen is processed and presented via MHC II in langerhan cells–> recognised as foreign by T cells
  • T cells migrate to dermis= inflammation (IFN-gamma, cytokines)

Examples

  • Nickel
  • Perfume/ cosmetic molecules
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15
Q

Tuberculin skin test

A

Type 4 hypersensitivity reaction
- Determines previous exposure to TB

Tuberculin injected intradermally
- Causes local inflammation if previously exposed

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16
Q

Tuberculin skin test mechanism

A

Tuberculin is processed by local APCs.

Th1 cells (from previous exposure) recognises it and releases cytokines on vascular endothelium
- Recruits phagocytes and plasma cells to site of injection= lesion
17
Q

Inteferon gamma release assay

A

Method of detecting TB-specific Th1 cells in vitro.

MTB peptides are added to patient’s blood sample.
- APCs will present the peptides (MHC 2) and secrete IL-12

IFN-gamma secreted if there was previous exposure.

18
Q

Gell and Coombes pros

A
  • The only successful attempt to classify disease by mechanism.
  • Useful in describing & understanding various diseases.
19
Q

Cons of Gell and Coombes

A

Not useful in clinical practice

Oversimplifies immunology
- I.e in autoimmune haemolysis, many components of the immune system are involved.

Many diseases are more complex, esp. chronic inflammatory disease

  • RA
  • Chronic asthma
  • IBD