Ch. 11 Hypersensitivity Flashcards

1
Q

Type 1 - Immediate hypersensitivity

A
  • aka allergy
  • mediated by eosinophils and mast cells
  • first exposure IgE cells are produced and bind to mast cells
  • next exposure antigens crosslink IgE on mast cell and lead to degranulation
    • leads to vascular dilation and smooth muscle construiction
    • production of cytokines to recruit neutrophils and eosinophils
      • TNF - neutrophil, IL-4 IgE
      • IL-5 activates eosinophil
    • inflammation causes tissue damage
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2
Q

Th2 response in Immediate

A
  • Interactions with some antigens stimulates Th2 response leading to creation of IgE and eosinophil activation (only certain individuals)
  • IgE binds to the mast cells via Fc receptor
  • leads to immediate hypersensitivity next time there is an exposure
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3
Q

sensitization

A
  • coating mast cells with IgE on first exposure
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4
Q

3 results of Mast cell activation by cross linking of IgE

A
  • Degranulation:
    • Vasoactive amines (histamine) - vascular dilation, smooth muscle contraction
    • proteases - tissue damage
  • Lipid mediator synth. and secretion (arachidonic acid metabs)
    • prostaglandins - vascular dilation
    • leukotrines - smooth muscle contraction
  • Cytokines - late phase attracts leukocytes
    • TNF and IL-4 - neutrophil and eosinophil rich inflammation
    • Th2 recruited, secretes more cytokines - IL-5 activates more eosinophils
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5
Q

treatments of immediate hypersensitivity

A
  • allergic sinusitis (hay fever) and food allergies
    • desensitization, Anti-IgE antibody, antihistamines
  • Bronchial Asthma - smooth muscle contraction of airways
    • corticosteroids
  • Anaphylaxis Shock - airway obstruction edema in larynx (widespread mast cell degranulation), fall in bp
    • Epinephrine
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6
Q

Type II Antibody mediated

A
  • Antibodies (IgM or IgG) bind to tissues and target them for damage - autoantibodies
  • usually target a specific tissue type
  • promote phagocytosis of cells and activate complement and inflammation
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7
Q

type III immune complex mediated

A
  • They tend to deposit in high bp areas - kidney and turbulence - blood vessel split
  • widespread vasculitis, arthritis, nephritis
  • auto-antibodies
  • vasculitis - inflammation and damage in blood vessels where the complement and antibodies depsosit
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8
Q

Mechanism for II/III damage

A
  • inflammation
    • IgG - neutrophil and macrophage recruitment
    • IgM - complement activation
  • opsonization
  • interfering with normal function
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9
Q

Autoimmune hemolytic anemia

A
  • Antibodies against RBC - opsonization and phagocytosis
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10
Q

Autoimmune thrombocytopenic purpura

A
  • autoantibodies against platelets - opsonization and phagocytosis
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11
Q

pemphigus vulgaris

A
  • autoantibodies against epidermal cadherin in junction
    • skin bullae and vesicles
    • disrupts intracellular adhesion
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12
Q

Goodpasture’s syndrome

A
  • antibodies against proteins in basement membrane of kidney glomerulus and lung aveoli
  • nephritis and lung hemorrhages
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13
Q

rheumatic fever

A

antibodies against strept bacteria cross reacts with an antigen in the heart
- myocarditis

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14
Q

Myasthenia gravis

A

antibody against Ach receptor - inhibits Ach signalling

- muscle weakness and paralysis

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15
Q

Grave’s disease

A

antibody against TSH receptor

- hyperthyroidism

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16
Q

Treatment of II/III

A
  • corticosteroids- reduce inflammation and tissue damage
  • plasmapheresis - filter out the antibodies
  • inhibit production of autoantibodies by attacking B-cells with antibodies against CD20
17
Q

Type IV delayed hypersensitivity

A
  • Normal CD4 and CD8 responses causes tissue damage
  • often autoimmune
  • but also foreign like contact poison Ivy
  • peak takes 24-48 hrs
  • treat with immune suppressors - cyclosporin, inflammation decreasers - corticosteroids and anti-TNF