10. Overview of Immunological diseases Flashcards

1
Q

Type I Hypersensitivity Reaction

-Examples

A

-IgE antibody directed against allergen triggers mast cell degranulation- release of histamines

E.g. Seasonal rhinitis
Cat allergy

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2
Q

Type II Hypersensitivity Reaction

-Examples

A

-A pathogenic antibody directly causes diseases

antibody mediated disease

E.g. Autoimmune haemolysis- lyses of red blood cells

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3
Q

Type III Hypersensitivity Reaction

-Examples

A

Antibody-antigen complex-mediated disease
- enlarged complex that is not removed as they should be

Eg. Serum sickness
Systemic lupus erythematosis

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4
Q

Type IV Hypersensitivity Reaction

-Examples

A

Inflammation directly mediated by T cells

E.g.
Delayed type hypersensitivity

Contact dermatitis (form of eczema)
Tuberculin reaction

-takes time for allergy to appear(hours)

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5
Q

Autoimmune Haemolysis

A

Type 2 hypersensitivity

Autoantibodies develop against rbcs:
igG anti-red cell response produced de novo
can be destroyed by phagocytes (extracellular hamoysis)
or intravascularly in the spleen

clinical presentation- Anaemia , and jaundice due to release of bilirubin

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6
Q

Hypersensitivity pneumonitis

A

Type III reaction

clinically presents with pts exposed to airbourne (like hay) antigen then develops sudden breathlessness

  • produce IgG antibodies
  • eventual lung scarring and fibrosis
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7
Q

Tuberculin skin test (TST)

A

Type IV hypersensitivity reaction

  • Used to determine previous exposure to TB
  • Tuberculin injected intradermally
  • Local inflammatory response evolves over 24-72 hours if prev exposed

Antigen is injected sc and processed by local APC

  • TH1 recognizes antigen and releases cytokines
  • Recruitment of phagocytes and plasma to site of antigen -Injection causes visible lesion
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8
Q

Universal recipients belong to which blood group

A

Group AB

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9
Q

Universal blood donors belong to which blood group

A

Blood Group O

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10
Q

Haemolytic disease of the newborn

A
  • ‘D’ antigen (Rhesus) is a secondary classification
  • Majority of the population are D+
  • IgG antibodies produced by the mother move through placenta

Rhesus-negative mothers with rhesus+ partner are given anti-D IgG during pregnancy

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11
Q

Local immune complex disease

A

Type III reaction

deposition of circulating immune complexes

causing painful lesions

also seen in SLE

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12
Q

Serum sickness

A

Type III reaction

injection of certain immunogenic drugs or anti-sera produced in animals

Presentation: Rash
Fever
Arthritis
Glomerulonephritis

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13
Q

Contact dermatitis: sensitisation

A

Type IV reaction

In the skin:
Highly reactive, small molecule breaks the skin and forms protein-hapten 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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14
Q

Interferon gamma release assay (IGRA)

A

Previous Tb exposure:
Th1 cells recognise antigen. Because this is a secondary immune response, they are ‘primed’ and release cytokines within this short timeframe

No previous Tb exposure:
No primed memory T cells specific for MTB. No interferon gamma produced in such a short timeframe

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15
Q

Gell and Coombes

Pros and Cons

A

useful framework

  • oversimplifies immunology
  • not particularly used
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