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Intro to path > Hypersensitivity 8 20 14 > Flashcards

Hypersensitivity 8 20 14 Flashcards

1
Q

sensitization vs effector stages

A

sensitization is clinically silent, is primary immune response

effector is secondary immune response

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2
Q

hypersensitivity def

A

an excessive or abnormal secondary immune response to a sensitizing agent

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3
Q

Type I hypersensitivity rxn

A

formation of IgE antibody

basophils and mast cells release vasoactive mediators

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4
Q

ex of type I hypersensitivity rxn

A

ANAPHYLAXIS, allergies, some forms of bronchial asthma

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5
Q

Type II hypersensitivity rxn

A

formation of IgM and IgG binding to antigen that’s cell/matrix based

phagocytosis or lysis of target cell by complement or antibody-dependent cellular cytotoxicity

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6
Q

Type III hypersen rxn

A

SOLUBLE antigen

antigen-antibody (IgG) complexes, activated complement, attracts neutrophils

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7
Q

type IV hypersen rxn

A

sensitized T lymphocytes

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8
Q

Th2 helper T cells generated as a result of what? in type I hypersen

A

IL-4

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9
Q

what do Th2 helper T cells make? in type I hypersen

A

IL4, IL5

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10
Q

how long does sensitization take for allergic disease?

A

4 weeks

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11
Q

what occurs during sensitization in allergic disease

A

allergen is presented by antigen presenting cell to Th2 cell, which releases IL4 and IL6 to stimulate B cells to make IgE

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12
Q

early phase of Type I hypersensitivity response

A

under 15 minutes

allergen cross-links with IgE on mast cell

mast cell releases: histamine, tryptase, leukotrienes, PGD2, IL-4, other cytokines

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13
Q

can basophils be involved in early phase of type I hypersen response?

A

yes

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14
Q

late phase response in type I hypersen

A

4-6 hours after exposure (due to time needed to make cytokines)

eosinophils make leukotrienes and other products

damage to epithelium, cellular recruitment

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15
Q

allergens vs irritants

A

allergens: IgE mediated, require sensitization, affects only those sensitized to allergen, not usually dose-dependent
irritant: not mediated through IgE, dose dependent response, will affect everyone at high enough dose

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16
Q

ex of allergens

A

pollen, house dust mite, furred animals, fungi or mold

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17
Q

ex of irritants

A

tobacco smoke
exhaust fumes
perfumes

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18
Q

what things are release immediately from mast cells due to preformed stores?

A

histamine
heparin (works like histamine)
enzymes like tryptase

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19
Q

how are basophils diff from mast cells in type I hypersen rxn?

A

basophils don’t release tryptase or PGD2

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20
Q

what remains identifiable in the serum for up to 4 hours after release from mast cell in type I hypersen rxn?

A

tryptase

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21
Q

role of tryptase in type I hypersen rxn

A

remodeling of connective tissue

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22
Q

effects of mast cell activation? (or basophil) in type I hypersen rxn

A

vascular permeability is increased
bronchoconstriction
intestinal hypermotility

inflammation

tissue dammage

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23
Q

how are cytokines and chemokines different from histamine when released from mast cells in activation in type I hypersen rxn?

A

cyotkines must be made with activation, so release is delayed 4 to 6 hrs after degranulation of preformed things like histamine

24
Q

Il 4 and IL13 role in type I hypersensitivity rxn

A

associated with Th2 cells and lead to Ig class switching in B cells to produce IgE

25
Q

what cytokines in type I hypsensitivity rxn promote survival and activation of eosinophils?

A

IL3, IL5, GM CSF

26
Q

role of TNF in type I hypersen rxn

A

activates endothelium and leads to adhesion molecules expression

27
Q

what lipid mediators are release from mast cells in type I hypersen rnx in immediate reaction?

A

leukotrienes C4, D4, E4-lead to eosionphil migration, sm musc contrac, vascular permeability, mucus hypersecretion

platelet activating factor-attracts eosinophils, activates eosinophils and neutrophils and platelets

28
Q

late phase of type I hypser response in mast cells has mostly what type of cells responding?

A

eosinophils

29
Q

you get elevated eosinophil count in what conditions? (mneumonic)

A 
NAACP:
neoplasia
asthma
allergy
connective tissue disease
parasitic disease
30
Q

what kind of receptor does eosinophil have?

A

CCR3

31
Q

corticosteroids’ effect on eosinophils

A

apoptosis of eosinophils

reduce IL-5 production

32
Q

what is IL-5 made by

A

Th2 lymphocytes

33
Q

IL-5 has what effects in vivo?

A

eosinophilia

34
Q

what do eosinophils secrete?

A

IL5

Leukotrienes B4, C4, C5

35
Q

what role do eosinophils play?

A

kill parasites and host cells

tissue damage

36
Q

clinical aspects of type I hypersen

A

allergic rhinitis
asthma
anaphylaxis
urticaria

37
Q

allergic rhinitis

A

cross-linking of IgE in nasal mucosa and ocular conjunctiva with specific antigen exposure

38
Q

asthma

A

IgE mediated disease in lower airways

leads to wheezing, shortness of breath due to airway contriction (prevents exhalation), increased mucus secretion and production

39
Q

immediately after anaphylaxic event, can you skin test?

A

no, b/c all the IgE would be used up in the response

40
Q

H1 in anaphylaxis has what effect?

A

smooth muscle contrac

vascular permeab

41
Q

H2 in anaphylaxis has what effect?

A

vascular permeab

42
Q

H1 & H2 in anaphylaxis have what effect?

A

vasodilatation, pruritis

43
Q

ex of type II hypersen rxn

A 
Goodpasture syndrome
bulloud pemphigoid
pernicious anemia
vasculitides
thrombotic phenomena
acute rheumatic fever
44
Q

how do immune complexes cause damage in type III hypersen?

A

BOTH by activating FcgammaR expressing cells and activating complement at sites of deposition

45
Q

where is type III hypersen damage usually found?

A

kidney, vessels, joints, skin

46
Q

where do small complexes in type III hypersen usually precipitate?

A

blood vessel walls

47
Q

ex of type III hypersen rxn

A

Arthus rxn
serum sickness (large quantities of foreign protein injected)
Farmer’s lung (hay dust, mold spores)
systemic antigen excess (autoimmune disease, infections with antigen production)

48
Q

why in serum sickness, does it take 7-10 days to get symptoms?

A

b/c this is the time needed to switch from IgM to IgG (IgG actually fixes complement and causes the symptoms you see)

then when you have too much IgG, no longer get complement deposition so no longer get symptoms

49
Q

how can type IV hypersen by distinguished from other types of hypersen rxns?

A

no antibodies

50
Q

what is the usual target organ for type IV hypersen rxn?

A

skin

51
Q

how long does it take for Type IV hypersen rxn to develop?

A

24-72 hours

52
Q

ex of type IV hypersen rxn

A

tuberculin response

contact hypersensitivity

53
Q

What makes IL4, IL5, IL13 in type I hypersen?

A

mast cells

54
Q

what makes eotaxin and RANTES in type I hypersen?

A

mast cells

55
Q

what makes MBP, EDN, ECP in type I hypersen?

A

eosinophils

56
Q

where do you see symptoms in Type I hypersen?

A

early phase and late phase response

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