Ch. 11 Hypersensitivity

Question 1

Type 1 - Immediate hypersensitivity

Answer 1

• 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

Question 2

Th2 response in Immediate

Answer 2

• 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

Question 3

sensitization

Answer 3

• coating mast cells with IgE on first exposure

Question 4

3 results of Mast cell activation by cross linking of IgE

Answer 4

• 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

Question 5

treatments of immediate hypersensitivity

Answer 5

• 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

Question 6

Type II Antibody mediated

Answer 6

• 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

Question 7

type III immune complex mediated

Answer 7

• 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

Question 8

Mechanism for II/III damage

Answer 8

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

Question 9

Autoimmune hemolytic anemia

Answer 9

• Antibodies against RBC - opsonization and phagocytosis

Question 10

Autoimmune thrombocytopenic purpura

Answer 10

• autoantibodies against platelets - opsonization and phagocytosis

Question 11

pemphigus vulgaris

Answer 11

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

Question 12

Goodpasture’s syndrome

Answer 12

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

Question 13

rheumatic fever

Answer 13

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

Question 14

Myasthenia gravis

Answer 14

antibody against Ach receptor - inhibits Ach signalling

- muscle weakness and paralysis

Question 15

Grave’s disease

Answer 15

antibody against TSH receptor

- hyperthyroidism

Question 16

Treatment of II/III

Answer 16

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

Question 17

Type IV delayed hypersensitivity

Answer 17

• 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