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Immunology > Allergic disease > Flashcards

Allergic disease Flashcards

1
Q

Mechanism of desensitisation

A

Instead of allergen stimulating Th1 and IL4, IL5 release, we swing the reaction to stimulation of Treg cells

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2
Q

Duration of desensitisation

A

3 years

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3
Q

How do we do desensitisation?

A

Subcutaneous or sublingual

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4
Q

If allergic to latex, what foods to avoid?

A

Avocado and kiwi

Due to allergy to shared epitope

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5
Q

If allergy to burch pollen, what food to avoid?

A

Apple

Due to allergy to shared epitope

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6
Q

If allergic to lupine (flower plant), what food are they potentially allergic to?

A

Peanut

Due to allergy to shared epitope

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7
Q

Definition of anaphylaxis

A

Criterion 1
Skin/mucosal reaction + at least 1 of
- Respiratory, hypotension, GI symptoms

Criterion 2
2 or more of the following after suspected allergen
- Skin/mucosal reaction
- Respiratory
- Hypotension
- GI symptoms

Criterion 3
- SBP <100 or a >30% decrease in SBP after suspected allergen

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8
Q

Diagnosis of anaphylaxis

A

Clinical diagnosis

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9
Q

Investigations to do in anaphylaxis

A

Serum tryptase

  • Peaks 60-90 minutes, persists up to 5 hours
  • Beware of false negatives especially in food anaphylaxis and anaesthetic reactions. Timing very important!
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10
Q

Is plasma histamine useful in anaphylaxis?

A

No

Peaks in 5 minutes, back to baseline in 1 hour

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11
Q

What potential allergies should you NOT do intradermal skin prick testing?

A

Food!
Dangerous

Also aeroallergens like dust mites, pollen. Generally can just do surface testing cause its very sensitive.

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12
Q

What potential allergies would you do intradermal skin prick testing?

A

Venom (bees)
Drug allergy
- Immediate (IgE) penicillin allergy has NPV 99%
- Less sensitive for immediate (IgE) cephalosporin allergy. NPV 30-72%

To increase sensitivity

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13
Q

Management of anaphylaxis to insect stings

A

Desensitisation is particularly important!

Large local reaction - nothing recommended apart from local therapy, anti H+, steroids

Anaphylaxis - desensitisation is the treatment of choice

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14
Q

What’s mastocytosis?

A

Proliferative abnormal disorder of hemopoietic mast cell progenitors –> proliferation of mast cells in BM

Due to mutation in TK receptor

Present with recurrent anaphylaxis

Persistently high tryptase despite no anaphylaxis reaction

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15
Q

Investigations for drug allergy

A

1) Skin prick testing - intradermal (IgE mediated)

2) Drug provocation test
- To exclude hypersensitivity when history not suggestive
- To confirm diagnosis when SPT and SpIgE negative (penicillin)

IgE not helpful

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16
Q

How soon do you have to do tryptase within an allergic reaction?

A

Within 60-90 minutes

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17
Q

Management of drug allergy

A

Avoid the drug
Watch out for cross-reactivity

Consider desensitisation

  • Requires life long therapy or recurrent desensitisation everytime you use the drug
  • Can’t be done for type 4 reactions e.g. SJS, TEN; haemolytic anaemias; interstitial nephritis, hepatitis
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18
Q

What do we do in reported penicillin allergy?

A

1) Skin prick testing (intradermal)
- Very good sensitivity 90%+ and NPV 99% (especially if testing with major and minor determinants)

2) Specific IgE ab
- Only available for some beta-lactams
- Very specific but not sensitive

If negative/inconclusive, 3) do oral challenge

  • High specificity but poor sensitivity`
  • Reserve oral challenge for when skin test or specific IgE is not available/inconclusive
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19
Q

What does penicillin allergy cross react with?

A

Cephalosporins esp 1st and 2nd generation

<1% with imipenem/meropenem

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20
Q

If someone is very allergic to amoxycillin, which other abx should you avoid?

A

Cephalexin and cefaclor

Similar 7 side chain

Should do skin prick testing and oral challenge before prescribing

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21
Q

Sulphonamides causes which reactions?

A

Type 1 and 4

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22
Q

If someone has an allergy to Bactrim, can they have other non-antibiotic sulphonamide based medications e.g. frusemide, celecoxib, sulphasalazine, HCT?

A

Yes
No cross reactivity with other non-antibiotic sulfonamide based medications
Except dapsone!

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23
Q

Radiocontrast media

Are people allergic to seafood more likely to be allergic to radiocontrast media?

A

No

They’re allergic to the protein, not iodine

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24
Q

How to reduce the likelihood of Radiocontrast media

allergy?

A

Low osmolar, non-ionic
Gadolinium is usually ok when people report allergy to contrast for CT scan

Pre-medication - prednisolone and diphenhydramine before and after (for suspected IgE mediated reactions only)

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25
Q

Mechanism of angioedema

A

Build up of bradykinin (e.g. ACEI) –> binds bradykinin receptor –> releases NO –> vascular permeability –> angioedema

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26
Q

Treatment of angioedema

A

Icatibant

Works quickly
Binds to bradykinin receptor and blocks it

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27
Q

Explain mechanism of aspirin/NSAIDs allergy

A

Inhibit COX 1 and 2 –> preferentially shunt arachidonic acid metabolism towards leukotriene production

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28
Q

4 types of aspirin/NSAID reactions

A

1) Aspirin exacerbated respiratory disease
- Samter’s triad - asthma, nasal polyps

2) NSAID exacerbated urticaria/angioedema
3) Multiple NSAID-induced urticaria/angioedema - often facial oedema
4) Single NSAID-induced urticaria/angioedema (possibly IgE)

29
Q

Investigation for possible aspirin/NSAID allergy

A

Skin prick testing is not useful as its a metabolism problem

Diagnosis with provocation challenge
- Challenge with a structurally distinct NSAID e.g. COX2. If tolerant, use that.

30
Q

What can you do if you’re allergic to aspirin but you still want to use it?

A

If anaphylaxis, nothing. Use something else like clopidogrel.

If non-anaphylactic, desensitisation is useful.

31
Q

Indications of drug desensitisation

A

No alterative drug e.g. syphilis in pregnancy

No history of anaphylaxis to medication. May need to do it in anaphylaxis if no other alternatives.

32
Q

What drug to omit before performing desensitisation?

A

B blocker in well controlled asthma

33
Q

Chronic idiopathic urticaria minimum duration

A

6 weeks

34
Q

Chronic idiopathic urticaria possible MOA

A

IgG against Fc epsilon receptors –> stimulate complement production –> mast cell degranulation –> histamine release

Not exogenous cause

35
Q

Diagnosis of Chronic idiopathic urticaria

A

Clinical diagnosis

Itchy, hive like lesions, unprovoked, lasting <24h before moving to another area, doesn’t leave a mark
Intermittent for >6 weeks

36
Q

Investigations of Chronic idiopathic urticaria

A

To exclude autoimmunity (often normal) - ANA, complement
e.g. occult lupus, urticarial vasculitis

Associated with thyroid antibody (not pathogenic)

Skin biopsy not usually necessary

37
Q

How to monitor Chronic idiopathic urticaria?

A

Urticaria activity score

Patient reports intensity of pruritis and number of wheals

38
Q

Treatment Chronic idiopathic urticaria

A

Non-sedating antihistamines up to QID (50% refractory)

Omalizumab

  • Downregulates Fc receptors so IgG can’t bind. In small proportion of patients, binds to IgE if there is an allergic component (but usually not main MOA)
  • Well tolerated
  • High urticaria activity score or associated angioedema
  • Very efficacious
  • Effects in 3-4 weeks
  • Subcut 300mg every 4 weeks
  • Continue for 6-8/12

Cyclosporin

  • Very few require this, despite 3-4 injections of omalizumab
  • AEs+++

Limit prolonged oral steroids to short term flares

39
Q

Skin prick testing works for type 4 sensitivity reactions e.g. TEN, SJS

A

No don’t do it - will be falsely negative

40
Q

SJS/TEN prevention?

A

NOT desensitisation

Just avoidance

41
Q

SJS/TEN MOA

A

Related to T cells and NK cells

IFN, TNF, FASL, granzyme, perforin

42
Q

Treatment SJS/TEN

A 
Supportive care
Transfer to burns unit
Remove inciting agents
Steroids +/- IVIG
Some benefit from cyclosporin if severe
43
Q

Potential medications that can cause SJS/TEN

A 
Abavacir - check HLA B5701
Anti-infective sulphonamides 
AEDs - carbamazepine, phenytoin
Allopurinol
Checkpoint inhibitors
44
Q

Gold standard in diagnosis of atopic food disease

A

Double-blind placebo controlled food challenge (DBPCFC) is the gold standard diagnostic test in food allergy

But this may not always be safe especially when drug allergies

Make sure you have safety equipment around

45
Q

Class I ADR

1) Mechanism
2) Onset
3) Clinical manifestation
4) Commonly involved abx
5) Testing
6) Desensitisation?

A

1) IgE mediated
2) Quick onset <30 minutes-1 hr
3) Pruiritis/urticaria, angioedema, bronchospasm, laryngeal oedema, anaphylaxis
4) Beta-lactams
5) Can be severe. Needs skin testing before oral challenge.
6) Desensitisation helpful (but not for anaphylaxis).

46
Q

Class II ADR

1) Mechanism
2) Onset
3) Clinical manifestation
4) Commonly involved abx
5) Testing
6) Desensitisation?

A

1) Cytotoxic; IgG mediated
2) Accelerated or delayed (5 to >72hr)
3) Haemolytic anaemia, thrombocytopenia
4) Sulfa abx, rifampicin, beta lactams, vancomycin, dapsone
5) No testing available. Avoid drug.
6) Desensitisation unhelpful.

47
Q

Class III ADR

1) Mechanism
2) Onset
3) Clinical manifestation
4) Commonly involved abx
5) Testing
6) Desensitisation?

A

1) Immune complex; IgG mediated
2) Accelerated or delayed (3 to >72hr)
3) Serum sickness, small vessel vasculitis
4) Ceclor, beta lactams, minocycline, sulfa abx
5) No testing available. Avoid drug.
6) Desensitisation unhelpful.

48
Q

Class IV ADR

1) Mechanism
2) Onset
3) Clinical manifestation
4) Commonly involved drugs
5) Testing
6) Desensitisation?

A

1) T cell mediated
2) Delayed (24 to >72 hr)
3) Contact dermatitis, SCAR (DRESS, SJS, TEN), AGEP
4) Beta lactams, sulfa antimicrobials, abacavir, carbamazepine, phenytoin, vancomycin
5) If mild reaction, may be ok for oral challenge. With severe cutaneous adverse reactions (SCAR), need specialist testing. May be able to do HLA testing (abacavir, carbamazepine)
6) Desensitisation unhelpful.

49
Q

What’s AGEP?

Hint: ADR

A

Acute generalised erythematous pustulosis

Small red pustules

Vancomycin > amoxycillin

Typically not unwell. Resolves quickly

50
Q

What’s DRESS?

Hint: ADR

A

Drug reaction with eosinophilia and systemic symptoms

Vanc > sulfonamides > beta lactams

Rash and fever

> 50% body involvement, facial oedema, renal and liver involvement

51
Q

Immediate severe penicillin hypersensitivity (anaphylaxis)

Can we use penicillin and cephalosporins?

A

No
If a penicillin is essential, perform desensitisation
In non-urgent situations, consider allergy testing and drug provocation
Consider carbapenem

52
Q

Immediate non-severe penicillin hypersensitivity (rash)

Can we use penicillin and cephalosporins?

A

Avoid penicillin
Can have most cephalosporins. Avoid cephalexin and cefaclor in amoxycillin/ampicillin allergy.
Can have carbapenem.
If a penicillin is essential, perform desensitisation
In non-urgent situations, consider allergy testing and drug provocation

53
Q

Delayed severe penicillin hypersensitivity (e.g. SCAR) or significant organ involvement such as acute interstitial nephritis
Can we use penicillin and cephalosporins?

A

No
Can consider carbapenem
Can’t do desensitisation cause further drug exposure may be fatal

54
Q

Delayed non-severe penicillin hypersensitivity (rash)

Can we use penicillin and cephalosporins?

A

Avoid penicillin
In a non-urgent situation and under specialist guidance, can consider a single dose of a penicillin followed by a prolonged (5-7 days) provocation test

Can have cephalosporin, carbapenem

55
Q

History of non-immune mediated effect to penicillin (GI upset)
Can we use penicillin and cephalosporins?

A

Yes

Remove the allergy!

56
Q

What is the major cause of cross reactivity between penicillins?

A

R1 side chain

57
Q

What is the true rate of cross reactivity between penicillin and cephalosprins?

A

<2%

58
Q

Where is IgE located?

A

Most IgE are bound to receptors of mast cells and eosinophils in the tissues. As soon as a familiar antigen comes (after desensitisation), it binds quickly to the IgE causing degranulation of mast cells and eosinophils.
Hence what is measured in serum is small %.

59
Q

What’s the hygiene hypothesis?

A

Early life exposure (first 2 years) to microbes prime immune response to Th1 predominant phenotype and there tends to be less of an allergy response. If less of these exposure in early life, tend to shift towards predominant Th2 (allergic type response) –> atopy (reaction to common things in the environment that is not pathogenic e.g. mould, dust)

60
Q

Mechanism of immunotherapy

A

Shift Th2 response (allergic response) to Th1/Th0 response

Promotes generation of IL10, TGF-beta

  • Promotes Treg cells = inhibits Th2 response
  • Class switch B cells to IgG, IgG4, IgA (from IgE) = downregulation of IgE-dependent Th2 response
61
Q

What’s the difference between type 2 low and type 2 high asthma?

A

Type 2 low

  • Low Th2 response
  • Non-allergic, non-atopic
  • Low IgE, non-eosinophilic

Type 2 high

  • High Th2 response
  • Allergic, atopic
  • High IgE or eosinophilic or both
62
Q

Omalizumab in asthma MOA

A

Anti-IgE antibody

63
Q

Mepolizumab in asthma MOA

A

Anti-IL5 antibody = stops recruitment of eosinophils

64
Q

Benralizumab in asthma MOA

A

Anti-IL5 receptor antibody = stops recruitment of eosinophils

65
Q

Mechanism of allergy response

A

Allergen –> APC –> Presents to Th2 cell –> secretes IL4 –> activates B cells –> turn into plasma cells –> make IgE –> IgE binds to mast cell –> when activated, release cytokines and mediators

Th2 cell also secretes IL5 –> recruits eosinophils

66
Q

What’s considered an immediate reaction, non-immediate reaction and delayed reaction?

A

Immediate: <1hr (IgE mediated event caused by preformed IgE antibodies)
Non-immediate: 1-72hr (T cell mediated)
Delayed: >72hr (T cell mediated)

67
Q

How useful is testing specific serum IgE antibodies for allergy testing?

A

Only available from some beta lactam antibiotics (very limited use)

Poor NPV but better PPV than skin testing (good specificity but poor sensitivity)

68
Q

List possible triggers of non-immunological anaphylaxis (direct mast cell activation)

A

Exercise, cold, heat, sunlight
ETOH
Medications e.g. opioids

Immunology (6 decks)

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