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ENGR 1 > Type 1 immunopath > Flashcards

Type 1 immunopath Flashcards

1
Q

Hypersensitivity

A

excessive/damaging reaction produced by normal immune system

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2
Q

hypersensitivity reactions require __ state of the host

A

a pre-sensitized

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3
Q

Cellular component of hypersensitivity

A

main cell = mast cell/basophil

amplified by platelets, neutrophils, eosinophils

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4
Q

mechanism of hypersensitivity

A

production of IgE in response to allergens

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5
Q

why are some people allergic?

A

produce more Th2 cells that secrete IL-4, IL-5, IL-13 –> IgE class switch

IgE high affinity for Fce, CD23 receptor

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6
Q

Atopic

A

individuals with predisposition to certain allergic hypersensitivity reactions through life

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7
Q

Allergy/Allergen

A

Atypical response to enviorn antigen mediated by IgE and mast cell

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8
Q

Anaphylaxis

A

life-threatening type 1 rxn

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9
Q

Asthma

A

reversible bronchoconstrictive disease with progressive inflammation –> fibrosis

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10
Q

wheal and flare

A

develop hives after intradermal injection of allergen

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11
Q

Incidence of atopic disease in general popn

A

15%

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12
Q

incidence of atopic diseae with 1 allergic parent?

2 allergic parent?

A

35%

65%

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13
Q

Mechanism of IgE hypersensitivity

A

1) Th2-like Tfh –> B cells –> IgE
2) IgE binds mast cell/basophil IgE receptor (FceRI)
3) Mast cell releases granules when 2 IgE molec cross-linked by allergen
4) Degranulation –> release histamine, heparin, enzymes, TNF (15 min) (itch, redness, leakiness)

5) Mast cell converts membrane phospholipids –> PGs/LTs (ECF-A)
(ECF-A) ==> inflammation, bronchoconstriction, attract eosinophil (4-10hrs)

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14
Q

Common features of Atopic diseases

A

Abnormal IgE response to environ antigen

Mediated by Th2 cells

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15
Q

Why use glucocorticoid?

A

Treat inflammation caused by late-phase reactants/Th2 in lung

Prevents chronic inflamm/irrev fibrosis

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16
Q

Why glucocorticoids over steroids?

A

steroids not easily absorbed

more side effects

17
Q

Procedure of intradermsal skin test

A

1) drop allergen on forearm
2) prick epidermis
3) diameter of wheel/flare

codeine = control (histamine-releaser)

18
Q

Safety of intradermal skin test

A

dangerous for severe allergies

19
Q

Specificity of intradermal skin test

A

many false positives due to cross reactions and subclinical sensitivities

20
Q

Time of immediate vs. late phase

A

w/n 15 min vs. 4-10 hrs

21
Q

Mediators of immediate allergic rxn

A

Histamine
Heparin
enzymes
TNF

22
Q

Mediators of late phase rxn

A

PGs,
LTs
cytokines

23
Q

Therapy: Avoidance

A

cornerstone of treatment

24
Q

Therapy: antihistamines

A

early, acute symptoms

25
Q

epinephrine

A

first line in emergencies

26
Q

cromolyn sodium

A

stabilizes mast cell

limit histamine release

27
Q

theophylline

A

incr cAMP, bronchial smooth muscle relaxation

28
Q

glucocorticoids

A

block PG/LT synthesis

induce eosinophil apoptosis

29
Q

leukotriene inhibitors

A

addition to asthma tx

30
Q

IgE monoclonal antibody

A

mops up IgE in blood

31
Q

immunotherapy

A

allergy shots with incr allergen concentration

32
Q

Mechanism of IgG, IgE, M2 macrophage, eosinophil in helminth immunity

A

1) worms induce strong Th2
2) Th2 cells stim B cells to produce IgG/IgE
3) IgG binds worm/ova (attract neutrophils that can’t destroy worm)
4) antigens from worm diffuse to IgE that is bound to mast cell
5) IgE cross-linked by bound antigen and causes mast cells to degranulate
6. Released histamine causes peristalsis!
7. Mast cells are also activated to produce PGs and LTs that attract eosinophils!
8. eosinophil have receptor for IgG coating worm so bind receptor and release MBP that destroy worm
9) Th2 release lymphokines that attract and activ M2 macrophage
10) M2 macrophage heal damage/wall off worm

ENGR 1 (29 decks)

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