Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hilary week 5 > allergy 1 and IV hypersensitivity > Flashcards

allergy 1 and IV hypersensitivity Flashcards

1
Q

What is atopy?

A

genetic predisposition to allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Do you have allergy symptoms in sensitisation?

A

nope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what two systems does anaphylaxis affect?

A

circulation (hypotension) and respiration (bronchoconstriction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is anaphylactoid reactions driven by?

A

Non-IgE mediated mast cell degranulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why kind of Th responses are induced in allergy and what cytokines involved in IgE production?

A

Th2, cytokines Il4 Il and Il13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What factors cause immediate allergic reactions?

A

contents of granules in mast cells which are released: histamine, TNFa, heparin and proteases.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are mid and late responses to mast cell activation?

A

leukotrienes, prostaglandins and then cytokine production e.g. IL-4, IL-13 (requires transcription)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

effects of histamine on blood vessels?

A

vasodilation and increased vasopermeabiliyt leading to liquid extravasation- swelling- and hypotension (anaphylaxis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

effects of histamine on smooth muscles?

A

Stimulates smooth muscle contraction in bronchi and gut.
Also stimulates mucus secretion in these areas as well as in the nose.
Neural stimulation causes itching and sneezing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

effects of late release of leukotrienes and cytokines responsible?

A

chemotaxis of eosinophils, epithelial damage and shedding.

can cause a biphasic reaction- initiating anaphylactoid reactoins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can chronic mast cell stimulation and leukotriene and cytokine release lead to?

A

T cell inflammation, collagen deposition and smooth muscle hypertrophy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What sort of questions are asked when diagnosing allergies?

A

time since exposure (needs to be less than an hour for immediate reaction)

reproducible?

where do you have symptoms (different antigens)

seasonal or perennial?

food is cooked or raw?

reaciton in exercise (wheat associated exercise dependent anaphylaxis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How long after anaphylaxis would you test for specific IgE levels?

A

3-4 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are positive and negative controls for skin prick tests?

A

positive (is nettle antigen/ histamine)

negative control is just saline (just to test for non specific redness).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How to treat anaphylaxis?

A

adrenalin, bronchodilators salbutamol/ oxgyen

antihistmaines/steroids.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

why would you measure tryptase levels?

A

released at the same time as histamine, but much longer half life than short histamine half life.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Condition where tryptase can remain high even after 24 hrs?

A

systemic mastocytosis.

18
Q

How does venom immunotherapy work?

A

weekly small doses which are built up. Moves to every 8 weeks.

induces Treg responses, IL-10 and TGF-B dampen down the Th2 response.

Also generates inert IgG4 antibody production which competes with IgE for the environmental Ag.

19
Q

When may you not give venom immunotherapy?

A

severe asthma, autoimmune disease, or patients on immunosuppressive or modulatory drugs.
cancer patients and during pregnancy.

20
Q

What else could someone be allergic to if they have allergic rhinitis against birch pollen?

A

apples (but not cooked form)

21
Q

What progression is often seen from early onset of eczema?

A

eczema to allergic rhinitis and then asthma.

22
Q

examples of allergens in allergic rhinitis?

A

pollen, animal dander and dust mite debris.

23
Q

Early and late symptoms of allergic rhinitis?

A

sneezing, itching, watery eye and itchy chest.

late: congested nose and inflamed and swollen eyes.

24
Q

what cytokines recruit and promote the survival of eosinophils and basophils?

A

IL3 and Il-5

25
Q

What other Late cytokines in allergic rhinitis?

A

EPO, ECP, EDN-MBP

26
Q

what cells can be recruited in late stage of allergic rhinitis?

A

Th2 cells and esoniphils- contribute towards inflammation and congestion.

27
Q

What treatment can inhibit cytokine produciton in allergic rhinitis (late phase response?)

A

steroid nasal sprays - immunotherapy only for severe cases.

28
Q

Can you eat raw or cooked food in a) oral allergy syndrome?

A

allergic to raw foods, with common antigens in to pollen e.g. birch pollen and apple.

29
Q

Common Antigens in pollen and food in oral allergy sydnrome?

A

PR-10 protein and profilins.

30
Q

Antigens in pollen and food causing systemic reactions? Which isn’t safe to eat when cooked?

A

lipid transfer proteins and storage proteins.

Storage proteins are resistant to changes when cooking- unsafe to eat cooked food as well as raw food (includes a lot of nuts)

31
Q

What are some examples of delayed sensitivity?

A

atopic dermatitis and contact dermatitis.

32
Q

What sorts of defects contribute to atopic dermatitis?

A

barrier skin dysfunctions e.g. fillagrin, increased epidermal water loss and decreased ceramides.

33
Q

Pathogenesis of atopic dermatitis?

A

Barrier defects may mean antigen uptake is increased,
Taken up by LCs and DCs triggering a Th2 response.

Contact with allergen causes allergic reaction and itchiness, scratching then causes damanage and cytokine release and a Th1/ Th17 response.

eosinophils and macrophages also implicated in chronic response.

34
Q

What cytokines can drive Th2 response in atopic dermatitis?

A

IL-4 Il-10 TSLP

35
Q

how is NFAT triggered and what can prevent this?

A

ca2+ influx in T cell activation leads to calmodulin binding and activation of calcineurin. Calcineurin will dephosphorylate NFAT- NFAT translocation.

tacrolimus will bind to FKBP to prevent calcineurin activation.

36
Q

what does dupilumab inhibit and what condition?

A

inhibits IL-4, IL-13 ni atopic dermatitis to imporve pruritus.

37
Q

What test is done for contact dermatitis?

A

patch test- affixed to back for 48-72 hours.

38
Q

What can allergens do that cause contact dermatitis?

A

lipophilic and can cross epidermis, can haptenate proteins e.g. albumin.

39
Q

Mechanism of contact dermatitis sensitisation

A

lipophilic antigen adsorbed across epidermis, binds to host protein e,.g albumin to create a neoepitope that can be taken up by LCs.

Activation of e.g TLR4 by Ni or other danger signals triggered by hapten.

uptake and presentation of hapten on cell surface.

Also primes CD8 response ( which can have keratinocyte cytotoxicity).

40
Q

What can be a non -IgE mediated response?

A

Asthma and contact dermatitis.

41
Q

Genetic factors for allergy?

A

filaggrin (in keratinocytes- nnull mutations Atopic dermatitis)

ADAM 33 metalloprotease has a role in asthma.

IL-4 Il13 MHC FcER1.

Hilary week 5 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions