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302 SBM: Infection & Immunity > Drug Allergy > Flashcards

Drug Allergy Flashcards

1
Q

How many people does drug hypersensitivity affect?

A
  • 50000 UK hospital admissions/ year
  • 10% of population report penicillin allergy
  • In anaesthetics 1/10000-20000
  • Majority, had a known reaction to drug already
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2
Q

What is a type A adverse drug reaction?

A
  • related to the pharamcology of drug
  • predictable
  • usually dose dependent
  • high morbidity, low mortality
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3
Q

Give an example of a type A adverse drug reaction

A

Drowsiness with 1st gen anti histamines
Liver failure with paracetamol overdose
Nausea + constipation with opiates
Dry mouth with TCAs

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4
Q

What is a type B adverse drug reaction?

A
  • not directly related to pharmacology
  • unpredictable
  • (often) dose independent
  • high mortality
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5
Q

Give an example of a type B adverse drug reaction

A
  • anything that resembles “allergy”
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6
Q

Describe an IMMEDIATE DHR

Timing, symptoms
Mechanism

A
  • occurs within 1 hour of first dose

Clinical features of mast cell degranulation!

  • Skin: urticaria, angioedema
  • Respiratory: rhinitis, bronchospasm, laryngeal oedema
  • Gut: diarrhoea
  • CV collapse
  • May be IgE mediated, or a form of non-allergic immediate DHR
  • Recedes rapidly after drug cessation
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7
Q

State 3 drugs that can cause non-IgE mediated immediate DHR

A
  • Non- specific mast cell activators: opiates, myorelaxants, radiocontrast media
  • ACEi
  • NSAIDs
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8
Q

What is a common side effect of non-specific mast cells activators?

A
  • Itching
  • A patient who recieves opiates, myorelaxants and radiocontrast media can appear to. be in anaphylactic shock due to summation
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9
Q

Describe the events the follow mast cell IgE ligation

A
  • IgE binds to its specific allergen
  • Cross linking of IgE antibodies by allergen leads to clustering of FcεR1 receptors
  • The intracellular portion of the receptor becomes phosphorylated
  • Resulting in intracellular cascade which leads to cellular activation
  • Mast cell “degranulates” releasing histamine, tryptase and other pre-formed mediators
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10
Q

In which situations may the onset of symptoms vary in immediate DHR

A
  • IV treatments often have a quicker onset

- NSAIDs may be a little delayed, still within an hour

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11
Q

What questions should you make sure you ask in Hx?

A
  • Which drug?
  • When?
  • Nature of symptoms
  • At what stage in the course did it happen?
  • What was the time between LAST dose and symptoms onset?
  • How long did it last once drug was stopped?
  • Has it been subsequently tolerated?
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12
Q

How long does it take for IgE response

A
  • IgE drug allergies take a few weeks as you need to make the antibodies
  • About 14 days
  • May vary if already sensitised
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13
Q

Generally speaking what kind of drugs cause IgE allergy

A
  • Naturally occuring protein derived drugs stimulate IgE

- Biggest category: antimicrobials, myorelaxants, taxene based chemo

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14
Q

How does atopy affect drug allergy?

A
  • DHR is not part of the “atopic” phenotype of asthma, eczema, rhinitis and food allergy
  • The risk is similar in atopic and non-atopic patients
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15
Q

What questions should you ask if you’re considering an immediate DHR as a differential?

A
  • What was the drug? What was the timing? What were the symptoms? How did they resolves?
  • Does the Hx sound like an immediate reaction?
  • Does it change what medication you would use going forward?
  • Do i need advice?
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16
Q

How might a patient who has improved from a DHR following iV treatment appear?

A
  • Hypotensive
  • Resp compromise
  • May not have skin signs
17
Q

What is adrenaline treatment effective?

A
  • if it could be a drug allergy, do not delay adrenaline
  • Adrenaline should be given promptly
  • If patient arrests
18
Q

How would you know if your patient has arrested?

A

Pulseless electrical activity (PEA) is characteristic

19
Q

How is mast cell tryptase used in the diagnosis of anaphylaxis?

When might this be helpful?

A
  • Serum tryptase easier to meaure in lab than histamine
  • Take blood 1-2 hours after symptoms onset and after 24 hours
  • Increase followed by normalisation confirms
  • 70% sensitive
  • To confirm anaphylaxis in sedated patient
20
Q

How does an allergist approach immediate DHR

A
  • The HISTORY is everything
  • Diagnostic test rare, other than drug challenges which are expensive and dangerous
  • Pragmatic approach vs definitive (should challenge patients at high risk or low risk for confirmation)
21
Q

B Lactam allergies are reported by 10% of population however the true prevalence is closer to 1-2%. Why is it so over-reported?

A
  • Patients may have reaction in childhood but sensitisation is lost at a rate of 10%/yr, label persists
  • “Rash” result of infection not drug
  • Different drugs caused the rash
22
Q

Give 3 examples of different antibiotic groups which may trigger B Lactam allergy

A
  • Penicillins: natural (G) and synthetic (V)
  • Penicillinase-resistant (fluclox)
  • Aminopenicillins (Amoxicillin)
  • Monobactams
  • Carbopenems
  • Cephalosporins
23
Q

If a patient has a history of immediate DHR to penicillin what must you consider?

A

Potential cross reactivity between B Lactam groups, include this in risk management

24
Q

What is guidance on choosing an alternative to penicillin in the context of a known DHR ?

A
  • If B lactam is needed and clinical risk is low, cephalosporin is reasonable
  • cross reactivity with 2nd/3rd gen cephs is very low
  • if clinical risk is high, seek advice
  • oral test dose may be possible (safer than IV), seek advice from seniours
25
Q

Give an example of a delayed DHR

A
  • Delayed urticaria
  • Maculo-papular eruptions
  • Fixed drug eruptions
26
Q

Give an example of a non-immediate systemic DHR

A
  • Toxic epidermal necrosis= TEN
  • Steven-Johnsons syndrom= SJS
  • Drug rash with eosinophilia and systemic symptoms = DRESS
  • Vasculitis
27
Q

What are the key features of non-immediate DHR

A
  • not directly related to drug dose, may appear so
  • Onset: 3-5 if treated with drug before, 5-8 if first exposure
  • Clinical features not in keeping with mast cell degranulation
  • Continue for some time after drug cessation
  • Biggest culprits= antimicrobials
28
Q

What are the most dangerous non-immediate DHR

A
  • Steven Johnsons syndrome (SJS)

- Toxic epirdermal necrolysis spectrum

29
Q

Describe the presentation and causes of SJS/TENS

A
  • Fever, cough, conjunctivitis, mucositis
  • M> W, <30
  • Present 3-8 days after dose
  • Causes: antibiotics, anticonvulsants
  • Also infection-induced

VERY HIGH MORTALITY, GETS WORSE WITH EACH EXPOSURE

30
Q

How does the presentation of SJS/TENS change in its mild to severe form?

Can you continue to give the drug causing it after?

A

Erythema multiforme- target lesions on skin

Most severe = epidermal necrolysis

Never give drug again, a mild episode can be succeeded by a severe episode. Theres no test

31
Q

Describe a standard type 4 hypersensitivity

Timing, presentation,

A
  • Onset 3-8 days
  • Dry inflamed skin/
  • Maculo-papular: flat red rash
  • Gradually fades over days-weeks
  • No systemic upset
32
Q

How can you help your patient understand and manage non-immediate DHR?

A
  • Patient advice and written details
  • Alert GP
  • Flag DHR in hospital records
  • MedicAlert Device, not adrenaline pen
  • Consider referral to immunology
33
Q

When is referral to immunology needed?

A
  • if drug will be needed again
  • Choice of drugs is restricted
  • Cross reactivity questions
  • Diagnostic doubt

NOT
- if drug wont be used again, only minor reaction (maculo-papular rash), alternatives available, nothing more to add as in TENS

34
Q

How come B Lactam allergy testing is available?
Comment on its accuracy?
Who should be tested?
What happens if positive?

A
  • The antigens and known
  • It has a high negative predictive value. Confirm with a challenge test
  • Only select few tested: no good alternatives, high Abx use, multiple allergies
  • If positive, perform challenge with alternatives to demonstrate tolerance
35
Q

Consider allergy to local anaesthesia

  • How does the “reaction” usually present?
  • Can testing be used for confirmation?
  • Can the drug be used again?
  • Is the reaction reproducible?
A
  • Local swelling, syncope, sensitivity to adrenaline
  • Skin testing unhelpful; challenge test of 0.1/1/3ml of non-adrenalised product given subcut by Immunology
  • Generally avoid drug unless tolerability proved
  • Not reproducible
36
Q

How does DHR to NSAIDs present?

Diagnosis? Management?

A
  • Cutaneous: urticaria, angioedema, often in a background of spontaneous urticaria
  • True anaphylaxis
  • Aspirin sensitive asthma/rhinitis
  • 10% react to paracetamol as well
  • Clinical diagnosis
  • Avoid all NSAIDs, refer in specific situations (e.g. elective PCI)

302 SBM: Infection & Immunity (4 decks)

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