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Pharmacology (5th year) > Drug Hypersensitivity > Flashcards

Drug Hypersensitivity Flashcards

1
Q

Examples of Type 1 reactions

A
  • allergic rhinitis
  • asthma
  • systemic anaphylaxis
    (mast cell activation)
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2
Q

Examples of Type 2 reactions

A

Some drug allergies (penicillin)

FcR cells

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3
Q

Examples of Type 3 reactions

A

Serum sickness

FcR cells, complement

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4
Q

Examples of Type 4a reactions

A
  • Tuberculin reaction
  • contact dermatitis
    (macrophage activation
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5
Q

Examples of Type 4 b reactions

A
  • chronic asthma
  • maculopapular exanthema
    (eosinophils)
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6
Q

Examples of Type 4c reactions

A
  • contact dermatitis
  • maculopapular and bullous exanthema
  • hepatitis
    (T cells)
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7
Q

Examples of Type 4 d reactions

A
  • acute generalised exanthematous pustulosis
  • Behcet disease
    (neutrophils)
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8
Q

Mechanism and examples of Type 1 drugs

A

(IgE- mediated, immediate reaction)

  • beta-lactam antibiotics
  • neuromuscular blockers
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9
Q

Mechanism and examples of Type 2 drugs

A

(IgG/M- mediated cytotoxic)

  • heparin
  • methyldopa
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10
Q

Mechanism and examples of Type 3 drugs

A

(IgG/M-mediated immune complexes)

  • beta-lactams
  • quinidine
  • procainamide
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11
Q

Mechanism and examples of Type 4a drugs

A

(Th1 cells activate monocytes via IGN-G and TNF-a)

  • topical antibiotics and antihistamines
  • local anaesthetics
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12
Q

Mechanism and examples of Type 4b drugs

A

(Th2 cells drive eosinophilic inflammation - IL-5,4,13)

  • Rifampicin
  • pyrazinamide
  • INH
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13
Q

Mechanism and examples of Type 4c

A

(CD41/81 cytotoxic T cells kill targets with perforin)

  • Neviropine
  • abacavir
  • rifampicin
  • pyrazinamide
  • INH
  • carbamazepine
  • sulfonamides
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14
Q

Mechanism and examples of Type 4d

A

(T cells recruit and activate neurophils)

  • sulfonamides
  • tetracyclines
  • cephalosporins
  • penicillins
  • hydroxychloroquine
  • NSAIDs
  • azoles
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15
Q

How does a small molecule induce an immune reaction?

A

Stimulate innate immune system
- bind to proteins and stimulate cells of IIS

Stimulate specific immune system

  • couple to carrier protein to form hapten-protein complex
  • complex is precessed by APCs
  • modified proteins can induce a humoral immune system by stimulating B cells
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16
Q

Drugs that cause majority of adverse reactions

A
  • antibiotics
  • general anaesthesia
  • ACE-I
  • asprin/ NSAIDS
  • local anaesthetics
  • radio-contrast media
17
Q

Classification of NSAID hypersensitivity

A
  • asprin-exacerbated respiratory disease
  • urticaria exacerbated cutaneous disease
  • multiple NSAIDS-induced urticaria/ angioedema
  • Single NSIADS IgE allergy
  • Single NSAIDS T cell reaction (Non-immediate)
18
Q

Discuss ACE-I associated angioedema

A
  • vasodilatory effect due to bradykinin

- not immune-related

19
Q

SCAR reactions

severe cutaneous adverse drug reactions

A
  • mobilliform eruptions
  • SJS and TEN
  • drug rash with eosinophilia and systemic symptoms
  • Lichenoid drug eruptions
  • AGEP
20
Q

Reactions with Rif

A
  • DRESS, LDE, SJS/TEN
  • DILI
  • AIN
  • anaphlyactoid urticaria/ angioedema
21
Q

Reactions with INH

A
  • DRESS, LDE, SJS/TEN

- DILI

22
Q

Reactions with pyrazinamide

A
  • SJS/TEN, DRESS

- DILI

23
Q

Reactions with ethambutol

A
  • DRESS, SJS/TEN
24
Q

Reactions with fluoroquinolones

A

Anaphylactoid

25
Q

Reactions with ethionamide

A

DRESS, SJS/TEN

26
Q

Agents responsible for DILI

A
  • antimicrobials
  • dietary supplements
  • lipid lowering agents
  • antineoplastic drugs
  • NSAIDS
  • psychotropics
  • immunosuppressants
27
Q

Common antimicrobials causing DILI

A
  • amoxil/ calvulanate
  • INH
  • nitrofurantoin
  • Co-trimox
  • minocycline
  • ciproflox
  • azithro
28
Q

How do genetics play a role in DILI?

A
  • N-acetyltransferase 2 and CYP2E polymorphisms associ with anti-TB DILI
  • cytokine polymorphisms associ with diclofenac DILI
  • HLA associations with Co-amoxyclav DILI
29
Q

Main categories of acute renal failure

A
  • tubular necrosis
  • interstitial nephritis
  • acute glomerulonephritis
30
Q

Causes of AIN

A
  • antibiotics
  • Rif
  • herbal/traditional meds
  • NSAIDS
  • duiretics
  • allopurinol
  • phenytoin
31
Q

Histological findings in AIN

A
  • intersitial oedema

- diffuse interstitial infiltrate of inflammatory cells (T-cells and eosinophils)

32
Q

AIN pathogenesis

A

Immunologically mediated hypersensitivity reaction to an antigen

33
Q

Clinical manifestations for drug induced AIN

A
  • rash
  • joint pain
  • eosinophilia
  • eosinophiliuria
34
Q

Features of Rif-induced AIN

A
  • occurs when reintroduced
  • not associated with eosinophilia
  • flu-like symptoms, flank pain, hypertension, oliguria, ARF
  • can also see acute tubular necrosis
35
Q

Treatment of drug-related AIN

A
  • cessation of drug (usually resolves in a few days)
  • if not:
  • renal biopsy
  • high dose prednisone

Pharmacology (5th year) (15 decks)

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