Immediate hypersensitivity Flashcards

1
Q

5 contribution to rise in allergic disease

A
  1. genes
  2. env.
  3. lifestyle
  4. occupational exposires
  5. some meds.
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2
Q

3 peices of evidence for genes

A
  1. family history common
  2. 70-75% chance of dev. asthma if both parents atopic
  3. early dermatitis predicts later asthma
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3
Q

5 potential lifestyle involvments

A
  1. hygene - no shift to Th1 type from Th2
  2. resp viruses may risk asthma
  3. less fruit and veg mean less antioxidants
  4. fatty foods may shift to allergic susceptibility
  5. food preservative amy affect gut flora
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4
Q

what is link with nutrition

A

good nutrition leads to a better immune system and allergies are a hyperactive immune system

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5
Q

how is urban lifestyle involved

A

more hygienic and thus more of a Th2 env

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6
Q

what is a medication involved

A

Proton pumpis - less acid and don’t degrade allergens as well so they get in

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7
Q

3 types of immediate hypersens. reactions

A
  1. Immunologic - IgE mediated
  2. immunologic - non-IgE mediated
  3. non-immunologic
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8
Q

what is non-IgE mechanism

A
  1. substances act directly on mast cells to activate mediator release
    - no need for prior exposure
    - no need for specific IgE
    - often drugs
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9
Q

feature of non-immunologic reactions

A
  • complement mediated C3a and C5a

- reactions to blood products and dialysis membranes

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10
Q

what is IgE isotype switch

A

change of one class to another

  • constant region changes but the variable region stays the same
  • antigen spec. the same, but interacts with different molecules/cells
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11
Q

what is outcome of the IgE isotype switch

A

this becomes the high affinity molecule on mast cells

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12
Q

features of IgE mediated rxns

A
  1. requires previous exposure
  2. allergen specific IgE produced by plasma cells and released into body
  3. IgE binds to mast cells and they release mediators
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13
Q

2 important things for reaction to IgE

A
  1. dose - high is worse

2. route of exposure - skin, IV, mouth

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14
Q

what are outcomes for IV, subcut, inhal., ingestion

A
  1. IV - systemic histamine release -anaphylaxis
    Subcut -local hist. release - wheal and flare
    inhaled - allergic rhinitis and bronchoconstriction
    ingestion - smooth muscle causes diarrhea and vomiting
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15
Q

what happens the next time an allergen is encountered

A

allergen cross-links with the IgE bound to mast cell and causes it to degranulate

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16
Q

where does mast cell bind to the IgE

A

high affinity receptor

17
Q

what are 3 classes of mediators released from mast cells

A
  1. immediate (stored) - less dangerous - hist., TNF, proteases
  2. newly synthesized - lipid mediators, prostaglandins,
  3. cytokines - basophils, IL3,4,5, chemokines
18
Q

what is different about late phase

A

actually inflammatory

19
Q

what is effect of hist

A

non-lofe threatenening

- wheal, sneeze, conjunctivitis, bronchospasm

20
Q

what is effect of late phase reactants

A

attract and activate neutrophils - inflamation

21
Q

what is uniphasic anaphylaxis

A

initial Sx are treated and go away

22
Q

what is biphasic anaphylaxis

A

after treatment is latent for a period and then returns

23
Q

what is protracted anaphylaxis

A

keeps coming back after treatment and is associated with increase mortality

24
Q

what should be given in a reaction

A

anti-inflammatory, because due to the inflammatory late phase reactants