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POD Exam 3 > Hypersensitivity I > Flashcards

Hypersensitivity I Flashcards

1
Q

When is hypersensitivity seen?

A

second exposure

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2
Q

Type I

A

Ab mediated - IgE

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3
Q

Type II

A

Ab mediated

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4
Q

Type III

A

Immune complex mediated

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5
Q

Type IV

A

T cells/Macs

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6
Q

Components of Type I

A 
IgE - allergen specific
Mast cells 
Allergen
Eosinophils
CD4+ Th2 cells
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7
Q

another word for allergy

A

atopy

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8
Q

how is allergen introduced into the body

A

inhaled
eaten
administered as drugs

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9
Q

Sensitization

A

first expo to allergen

activate Th2 cells and stimulation of IgE class switching in B cells

– IgE produced by plasma cell –> binds to FceRI on mast cells

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10
Q

which cytokine induces class switch to IgE

A

IL-4

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11
Q

Activation of mast cells

A

repeat expo to allergen: Ag crosslinked with IgE/FceRI – activation – PREFORMED mediators released

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12
Q

what is released to induce immediate hypersenstivity reaction in Type I

A

Vasoactive amines, synthesis of lipid mediators

acts on vascular smooth muscle

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13
Q

what is released to induce late-phase hypersenstivity reaction in Type I

A

cytokines

inflammation

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14
Q

what is also activated via cross linking in addition to mast cells?

A

basophils

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15
Q

Biologic effects of mast cells mediators:

Biogenic amines: histamines

A

vasodilation

vascular leak

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16
Q

Biologic effects of mast cells mediators:

lipid mediators

A

bronchoconstriction
intestinal hypermotility
inflammation

17
Q

Biologic effects of mast cells mediators:

IL-5

A

inflammation

18
Q

Biologic effects of mast cells mediators:

enzymes

A

tissue damage

19
Q

Late phase reaction

A

IL-5 (from mast cells and Th2 cells): recruit and activate eosinophils

4-8 hrs later, lasts 1-2 days

20
Q

What does eosinophil help with?

A

Killing of parasites/host cells

tissue modeling

21
Q

What characterizes immediate reaction? Late phase?

A

Mast cell degranulation – wheel and flare

Eosinophils

22
Q

Local reactions - Type I, immediate

A

allergic rhinitis/sinusitis (hay fever)
food allergies
bronchial asthma
anaphylaxis

23
Q

Systemic anaphylaxis

A

Ag in blood –> tissue and activates CT mast cells throughout the body–> degranulation and mediators released

  • Heart and vascular sys: inc permeability/fluid entry, anaphylactic shock
  • respiratory tract: SM contraction, constriction of airways
  • GI tract: contraction of muscle/diarrhea
24
Q

Progression of allergic sx with age

A

atopic dermatitis (eczema) and GI disorders —> rhinitis –> asthma –> adult asthma

IgE!

Allergy March

25
Q

Skin test

A

intro of Ag into skin

Wheal and Flare

w/in 20 min

26
Q

what is occuring in wheal

A

bump

vasodilation and congestion

27
Q

Allergen-specific IgE testing

A
  • kids afraid of skin test
  • ptns with skin conditions
  • don’t want to stop taking anti-histamines

NOT a screening test

28
Q

How is Allergen-specific IgE test done?

A

Plate coated with allergen - allergen specific

then patients serum is added and labeled with anti-e

29
Q

How are the IgE levels with Allergen-specific IgE test?

A

wide variability
inc in variety of disease states
age-related standards need to be used

30
Q

Serum IgE levels

A

ELISA method

TOTAL serum IgE

31
Q

Total serum IgE testing

A

solid surface with anti-IgE antibody

then patient’s serum added and labeled with anti-e

32
Q

whats the problem with total serum IgE test?

A

not specific enough

33
Q

Therapy for Type I

A

avoid allergen, drugs

Immunotherapy

34
Q

What is immunotherapy

A

increasing doses of allergens are injected subcutaneously

rise in IgG – blocking seasonal rise in IgE Abs and a slow decline in the level of specific IgE . IgG binds Ag instead!

35
Q

What is immunotherapy not very effective against?

A

asthma

36
Q

What is occuring during immunotherapy?

A

Desensitization

Rise in IgG and IgG4, decline in IgE

over the course of about 2 years

POD Exam 3 (6 decks)

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