Hypersensitivity 8 20 14

Question 1

sensitization vs effector stages

Answer 1

sensitization is clinically silent, is primary immune response

effector is secondary immune response

Question 2

hypersensitivity def

Answer 2

an excessive or abnormal secondary immune response to a sensitizing agent

Question 3

Type I hypersensitivity rxn

Answer 3

formation of IgE antibody

basophils and mast cells release vasoactive mediators

Question 4

ex of type I hypersensitivity rxn

Answer 4

ANAPHYLAXIS, allergies, some forms of bronchial asthma

Question 5

Type II hypersensitivity rxn

Answer 5

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

Question 6

Type III hypersen rxn

Answer 6

SOLUBLE antigen

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

Question 7

type IV hypersen rxn

Answer 7

sensitized T lymphocytes

Question 8

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

Answer 8

IL-4

Question 9

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

Answer 9

IL4, IL5

Question 10

how long does sensitization take for allergic disease?

Answer 10

4 weeks

Question 11

what occurs during sensitization in allergic disease

Answer 11

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

Question 12

early phase of Type I hypersensitivity response

Answer 12

under 15 minutes

allergen cross-links with IgE on mast cell

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

Question 13

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

Answer 13

yes

Question 14

late phase response in type I hypersen

Answer 14

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

eosinophils make leukotrienes and other products

damage to epithelium, cellular recruitment

Question 15

allergens vs irritants

Answer 15

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

Question 16

ex of allergens

Answer 16

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

Question 17

ex of irritants

Answer 17

tobacco smoke
exhaust fumes
perfumes

Question 18

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

Answer 18

histamine
heparin (works like histamine)
enzymes like tryptase

Question 19

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

Answer 19

basophils don’t release tryptase or PGD2

Question 20

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

Answer 20

tryptase

Question 21

role of tryptase in type I hypersen rxn

Answer 21

remodeling of connective tissue

Question 22

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

Answer 22

vascular permeability is increased
bronchoconstriction
intestinal hypermotility

inflammation

tissue dammage

Question 23

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

Answer 23

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

Question 24

Il 4 and IL13 role in type I hypersensitivity rxn

Answer 24

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

Question 25

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

Answer 25

IL3, IL5, GM CSF

Question 26

role of TNF in type I hypersen rxn

Answer 26

activates endothelium and leads to adhesion molecules expression

Question 27

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

Answer 27

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

Question 28

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

Answer 28

eosinophils

Question 29

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

Answer 29

``` NAACP: neoplasia asthma allergy connective tissue disease parasitic disease ```

Question 30

what kind of receptor does eosinophil have?

Answer 30

CCR3

Question 31

corticosteroids' effect on eosinophils

Answer 31

apoptosis of eosinophils | reduce IL-5 production

Question 32

what is IL-5 made by

Answer 32

Th2 lymphocytes

Question 33

IL-5 has what effects in vivo?

Answer 33

eosinophilia

Question 34

what do eosinophils secrete?

Answer 34

IL5 Leukotrienes B4, C4, C5

Question 35

what role do eosinophils play?

Answer 35

kill parasites and host cells tissue damage

Question 36

clinical aspects of type I hypersen

Answer 36

allergic rhinitis asthma anaphylaxis urticaria

Question 37

allergic rhinitis

Answer 37

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

Question 38

asthma

Answer 38

IgE mediated disease in lower airways leads to wheezing, shortness of breath due to airway contriction (prevents exhalation), increased mucus secretion and production

Question 39

immediately after anaphylaxic event, can you skin test?

Answer 39

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

Question 40

H1 in anaphylaxis has what effect?

Answer 40

smooth muscle contrac | vascular permeab

Question 41

H2 in anaphylaxis has what effect?

Answer 41

vascular permeab

Question 42

H1 & H2 in anaphylaxis have what effect?

Answer 42

vasodilatation, pruritis

Question 43

ex of type II hypersen rxn

Answer 43

``` Goodpasture syndrome bulloud pemphigoid pernicious anemia vasculitides thrombotic phenomena acute rheumatic fever ```

Question 44

how do immune complexes cause damage in type III hypersen?

Answer 44

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

Question 45

where is type III hypersen damage usually found?

Answer 45

kidney, vessels, joints, skin

Question 46

where do small complexes in type III hypersen usually precipitate?

Answer 46

blood vessel walls

Question 47

ex of type III hypersen rxn

Answer 47

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)

Question 48

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

Answer 48

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

Question 49

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

Answer 49

no antibodies

Question 50

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

Answer 50

skin

Question 51

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

Answer 51

24-72 hours

Question 52

ex of type IV hypersen rxn

Answer 52

tuberculin response | contact hypersensitivity

Question 53

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

Answer 53

mast cells

Question 54

what makes eotaxin and RANTES in type I hypersen?

Answer 54

mast cells

Question 55

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

Answer 55

eosinophils

Question 56

where do you see symptoms in Type I hypersen?

Answer 56

early phase and late phase response