Hypersensitivity Flashcards

1
Q

What is the immune reactant in type II hypersensitivity?

A

IgG

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2
Q

What is the immune reactant in type III hypersensitivity?

A

IgG

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3
Q

What is the immune reactant in type IV hypersensitivity?

A

Th1 cells, Th2 cells, CTL

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4
Q

What is the antigen associated with type II hypersensitivity?

A

Cell or matrix associated

Cell surface receptor

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5
Q

What are the properties of the antigens in type III sensitivity?

A

soluble

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6
Q

What are the properties of the antigens in type VI sensitivity?

A

Soluble

cell-associated antigen

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7
Q

What is the effector mechanism in type II hypersensitivity?

A

Complement

FcR and cell

Ab alters signalling

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8
Q

What is the effector mechanism in type III hypersensitivity?

A

complement

phagocytes

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9
Q

What is the effector mechanism in type VI hypersensitivity?

A

Macrophage activation

Eosinophil activation

cytotoxicity

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10
Q

Example of type II sensitivity

A

Drugs

Chronic urticaria

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11
Q

Example of type III sensitivity

A

Arthus reaction

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12
Q

Example of type IV sensitivity

A

contact dermatitis

tuberculin reaction

chronic asthma

allergic rhinitis

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13
Q

What are type II reactions a result of?

A

antibodies, usually IgG, binding to componenets of cell membranes or extracellular matrix

Can be self-components, or exogenous

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14
Q

What is a presentation of self-type II sensitivity?

A

Goodpasture’s syndrome

  • antibodies bind to basemement membrane of collage type IV
  • glomerulophritis in kidney
  • haemorrhage in lung
  • auditory canal and ears
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15
Q

What is haemolytic anaemia and what can it be caused by?

A

antibodies to substances bound to host cell surface

penicillin

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16
Q

Describe penicillin allergey

A
  1. penicillin modifies proteins on human RBC to create a foreign apltopose
  2. complement caoted penicillin modified RBCs are phagocytosed by macrophages using their complement receptors
  3. macrophages present peptides from penicillin-protein conjugate and activate specific CD4 T cells to become Th2 cells
  4. B cells are activate by antigen and by help from Th2 cells
  5. Plasma cells secrete penicillin specific IgG which binds to modified RBC
  6. Penicillin specific IgG binds to penicillin modified proteins on RBC
  7. Actuvation of complement causes lysis or phagocytosis of RBC
17
Q

What antibodies cause type II hypersenstivity? And what is it?

A

IgG but sometimes IgM

directed to soluble antigen

excess immune complex deposition

18
Q

What are the main sites of immune compelx deposition?

A

no necessarily from where the anitgen is derived

  • glomeruli
  • blood vessel walls
  • synvoial membranes
  • skin
  • systemic sites
19
Q

What is type IV hypersensitivty mediated by?

A

cell mediated

complement does not play a role

20
Q

What are most type IV reactions caused by?

A

CD4+ delayed type hypersensitivyt (DTH) reactions

21
Q

“delayed” =

A

2 - 4 days after exposure after antigen exposure

22
Q

Examples of contact sensitivites

A

Chemical that binds to cell surface

  • heavy metal sensitivity
  • Poison ivy - reaction in the skin to catechols
23
Q

Examples of type II hypersensitivty reactions

A
  • autoimmune haemolytic anaemia - destruction of RBC
  • Autoimmune thrombocytopenic purpure; platelet integrin, GpIIb:IIIa - abnormal bleeding
  • Goodpasture’s syndrome; collagen type IV - glomerulonephritis, pulmonary haemorrhage
  • Pemphigus vulagris; epidermal caherin - skin blisters
  • acute rheumatic fever; strep cell wall - arthritis, myocarditis, valve scarring
24
Q

Examples of type III hypersensitivity syndromes?

A
  • mixed essential cryoglobulinemia - systemic vasculitis
  • SLE - glomerulnephritis
  • Rheumatoid arthritis - arthritis
25
Q

Example of type IV sensitivity syndrome

A
  • insulin dependent diabetes = beta cell destruction
  • rheumatoid arthritis = joint destruction and inflammation
  • MS = nervous system damage
26
Q

Summary of each type of hypersensitivity

A
  • Type II reactions: antibody mediated, cell membranes, drugs bound to cell membranes
  • Type III: antibody mediated, immune complex formation to soluble antigens, deposits at key sites, kidney, vessels, joints, skin
  • Type IV: cell mediated, DTH reactions to infectious organisms, granuloma. Contact sensitivity to reactive chemicals.