Disorders of immune system Flashcards

1
Q

Give 5 examples of things that could cause a type 1 hypersensitivity reaction

A
  • Pollen
  • Animal hair
  • house dust mite
  • moulds
  • insect bites
  • food - peanuts
  • latex
  • medicine - penicillin
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2
Q

What is the process of a pollen allergy?

A
  • First exposure - B cells recognise the Ag, internalise it and present to Th2 cells, which secrete IL-4, starting class-switching - B cells make IgE
  • IgE produced from previous allergen exposure diffuses through body
  • IgE binds to mast cells by its Fc region into mast cell Fc receptors

Second exposure to pollen

  • Pollen enters and binds to the Ig, if pollen cross-links the IgE on the mast cell, it will release Histamine
  • Mast cells generate other cytokines, encouraging Th cells to also produce cytokines - prolongs allergic reaction
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3
Q

What causes a type II reaction?

A

Ag and Ab interaction of IgM

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4
Q

Gives some examples of type II reactions

A
  • Myasthenia gravis
  • Rhesus isoimmunisation
  • HDN
  • Graves
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5
Q

What happens in myasthenia gravis?

A
  • In healthy individuals, nerve impulses trigger release of Ach from nerve endings, binds to AchR on muscle cells triggering contraction
  • In MG, autoantibodies to AchR are produced. These block the AchR at the postsynaptic NMJ, diminishing muscle contraction
  • Causes muscle atrophy
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6
Q

What happens in Rhesus isoimmunisation?

A
  • RhD Ag is carried on RBCs
  • If RhD-ve mother has baby with RhD+ve father, mother will become sensitised to RhD and make Abs
  • In the second pregnancy, if the foetus is Rh+ve, small amounts of RBCs crossing placenta stimulate memory cells
  • This causes production of more anti-RhD Abs, which cross the placenta and cause HDN
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7
Q

What happens in Grave’s disease?

A
  • Autoantibodies are made that act on TSHR on thyroid

- Causes lots of TH to be made

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8
Q

What happens in myasthenia gravis?

A
  • In healthy individuals, nerve impulses trigger release of Ach from nerve endings, binds to AchR on muscle cells triggering contraction
  • In MG, autoantibodies to AchR are produced. These block the AchR at the postsynaptic NMJ, diminishing muscle contraction
  • Causes muscle atrophy
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9
Q

What causes a type II reaction?

A

Ag and Ab interaction of IgM

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10
Q

What is a type IV reaction?

A
  • Delayed hypersensitivity
  • T-cell mediated but DCs, macrophages and cytokines contribute to process
  • e.g. Mantoux test, Type 1, coeliac, IBD, Crohns, psoriasis
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11
Q

What happens in myasthenia gravis?

A
  • In healthy individuals, nerve impulses trigger release of Ach from nerve endings, binds to AchR on muscle cells triggering contraction
  • In MG, autoantibodies to AchR are produced. These block the AchR at the postsynaptic NMJ, diminishing muscle contraction
  • Causes muscle atrophy
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12
Q

Define a type III reaction

A
  • Type III target is soluble circulating Ag
  • Ag can be own tissue or foreign material
  • e.g. SLE
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13
Q

What happens in SLE?

A
  • Aetiology unknown, but familial pattern
  • Make autoantibody directed against self molecules including DNA and nuclear ribonucleoproteins
  • Forms immune complexes - get trapped in kidney and cause glomerulonephritis
  • The Abs can fix complement - tissue injury
  • Abnormal activation of B cells - more sensitive to stimulatory cytokines
  • Reduced Th1 response
  • probs with phagocytes mean that they cant clear immune complexes
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14
Q

What is a type IV reaction?

A
  • Delayed hypersensitivity
  • T-cell mediated but DCs, macrophages and cytokines contribute to process
  • e.g. Mantoux test, Type 1, coeliac, IBD, Crohns, psoriasis
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15
Q

What is the mantoux test?

A
  • TB vaccine test
  • Inject pt with extract of mycobacterial Ag in skin
  • Macrophages present ag to activate Th cells - release cytokines to activate macrophages, which release cytokines
  • Red swelling of skin
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16
Q

What components can lead to immundeficiency?

A
  • complement - C1q inhibitor deficiency -> hereditary angioedema (continuous complement activation)
  • C3 deficiency -> infection
  • Phagocytes - Chediak-Higashi (failure of phagolysosome formation and lysosome degranulation)
  • B cell deficiencies - SCID (lack of development of stem cells into B or T cells)
  • Hyper IgM (increased IgM but little or no IgG)
  • Common variable immunodeficiency (IgG/A deficiency - B cells unable to mature into plasma cells)
  • T cell deficiencies
  • Lack of thymus -> DiGeorge
17
Q

What happens in coeliac?

A
  • Small intestine disease
  • HLA type imortant
  • Patients have IgA anti-gliadin, antiendomysium and antireticulin Abs
  • T cells present in intestine
  • Causes villous atrophy
  • Leads to malbsorption
18
Q

What causes psoriasis?

A
  • Chronic skin disease - red plaque with silvery scales
  • Genetic and environmental factors
  • lots of CD4+ cells in skin
  • Immunosuppressive treatment is effective
19
Q

What factors contribute to development of autoimmune disease?

A
  • Age and gender (autoantibodies more common in elderly, SLE and Grave more common in women)
  • Drugs
  • Immunodeficiency
20
Q

What components can lead to immundeficiency?

A
  • complement - C1q inhibitor deficiency -> hereditary angioedema (continuous complement activation)
  • C3 deficiency -> infection
  • Phagocytes - Chediak-Higashi (failure of phagolysosome formation and lysosome degranulation)
  • B cell deficiencies - SCID (lack of developmnt of stem cells into B or T cells)
21
Q

What can cause secondary immunodeficiency?

A
  • HIV infection - AIDS
  • Malnutrition
  • Tumours - cancerous cells can release immunosuppressive factors
  • Cytotoxic drugs/ radiation