Hypersensitivity Part 2 Flashcards

1
Q

What is Goodpasture’s Syndrome?

A
  • when IgG binds to a self-component causing a type II hypersensitivity reaction
  • antibodies bind to basement membrane collagen type IV
  • causes glomerulonephritis in the kidney and pulmonary haemorrhage in the lung
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2
Q

Describe what can happen to a person with a penicillin allergy

A
  • type II hypersensitivity reaction
  • penicillin binds to components of RBC membrane
  • can form a complex which is taken up by macrophages
  • complex can form neo-antigen which activates T cells that interact with B cells and antigen presenting cells to drive forward antibodies that recognise penicillin RBC complex
  • immunoglobulins bind to RBC when penicillin is bound resulting in complement activation causing:
  • lysis of RBCs
  • binds to Fc receptor on macrophage to cause phagocytosis
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3
Q

What is responsible for clearing type III hypersensitivity reactions and what causes pathology?

A
  • cleared by reticuloendothelial system (macrophages, neutrophils in liver spleen and bone marrow that ingest and degrade immune complexes)
  • pathology is caused by excess immune complex deposition in tissues
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4
Q

Describe the progression of a type III hypersensitivity reaction

A
  • locally injected antigen in immune individual with IgG antibody
  • local immune-complex formation
  • activation of complement release inflammatory mediators and induces mast cell degranulation
  • causes local inflammation, movement of fluid and protein into tissue and blood vessel occlusion
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5
Q

What are the sites of type III immune complex depositon?

A
  • glomeruli of kidney
  • blood vessel walls: accumulates on veins and arteries causing vasculitis
  • synovial membranes: RA can develop (when IgG of immune complexes becomes antigen itselg)
  • skin: causes rashes
  • systemic sites: if systemic lupus erythematosus it deposits in kidney, joints, skin, vasculature, muscle and other organs
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6
Q

What causes the majority of type IV hypersensitivity reactions?

A
  • delayed type hypersensitivity reactions (DTH)
  • some can be prolonged and damaging (eg. listerial and TB)
  • can lead to walling off infectious sites, granuloma
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7
Q

Describe the progression of a type IV hypersensitivity reaction

A
  • antigen introduced into subcutaneous tissue and processed by local antigen-presenting cells
  • a TH1 effector cell recognises antigen and releases cytokines which act on vascular endothelium
  • results in recruitment of T cells, phagocytes, fluid and proteins to site of antigen injections to cause lesion
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8
Q

What are contact sensitivities?

A
  • a special category of DTH reaction in which antigen is not infectious but a chemical that binds to cell surface
  • eg. heavy metal sensitivity and poison Ivy
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9
Q

Describe examples of autoimmune diseases that can be classified according to type II hypersensitivity reactions

A
  • haemolytic anaemia: caused by blood group antigens resulting in destruction of rbc causing anaemia
  • acute rheumatic fever caused by strep cell wall autoantigen (Ab x-react to cardiac muscle) causing arthritis, myocarditis and valve scarring
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10
Q

Describe examples of autoimmune diseases that can be classified according to type III hypersensitivity reactions

A
  • SLE caused by DNA/histones/ribosome autoantigens resulting in glomerulonephritis, vasculitis and rash
  • RA caused by rheumatoid factor IgG complexes resulting in arthritis
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11
Q

Describe examples of autoimmune diseases that can be classified according to type IV hypersensitivity reactions

A
  • insulin dependent diabetes mellitus: caused by pancreatic B-cell antigen causing B-cell destruction
  • RA: caused by synovial joint antigen resulting in joint inflammation and destruction
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