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Year 2 - Pharm Lectures 11+ > ADR > Flashcards

ADR Flashcards

1
Q

Define adverse drug event

A

Preventable or unpredicted medication events with harm to the patient

Involves
• medication errors AND adverse drug reactions

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2
Q

What are ADRs classified based upon?

A

(1) Onset
(2) Severity
(3) Type

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3
Q

Describe the classification of ADRs in relation to (1)

A

Onset

  1. Acute
    • <1 hour
  2. Sub-acute
    • 1-24hour
  3. Latent
    • >2days
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4
Q

Describe the classification of ADRs in relation to (2)

A

Severity

  1. Mild
    • requires no change in therapy
  2. Moderate
    • change in therapy required
    • additional treatment & hospitalisation
3. Severe
 • disabling, life-threatening
 • prolongs hospitalisation
 • causes congential abnormalities
 • requires intervention to prevent further injury
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5
Q

Explain the classification of ADRs in relation to (3)

A

Type

Type A-E

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6
Q

ADR Type A classification?

A

Augment/extend the pharmacological effect!

Usually predictable and dose-dependent
• represents 2/3rds of ADRs

Paracetamol has a threshold below which it has minimal side effects (and then exceeding this, side effects rapidly increase).

Digoxin just has a dose-dependent line with constant increasing SEs

E.G.
• Atenolol + heart block
• Anticholinergics + dry mouth
• NSAIDs + peptic ulcers

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7
Q

ADR Type B classification?

A

Bizarre – Idiosyncratic or Immunologic reactions!

Unpredictable, rare,
• includes allergy and “pseudo-allergy”.

E.G.
• Chloramphenicol + aplastic anaemia
• ACE inhibitors + angioedema

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8
Q

ADR Type C classification?

A

Chronic – Long-term use side effects!

Involves dose accumulation

E.G.
• Methotrexate + liver fibrosis
• Antimalarials + ocular toxicity

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9
Q

ADR Type D classification?

A

Delayed – Delayed effects!

 Carcinogenicity
– e.g. immunosuppressants

 Teratogenicity
– e.g. thalidomide.

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10
Q

ADR Type E classification?

A

End of treatment side effects!

 Withdrawal reactions
– patient cannot make endogenous supply
– opiates, corticosteroids, BDPs

 Rebound reactions
– disease gets worse when drugs stopped
– clonidine, beta-blockers, corticosteroids
 “Adaptive” reactions
– adapted body reactions to drugs
– neuroleptics (tranquilisers)

BDP = benzodiazepines.

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11
Q

Explain the ‘Withdrawal Reactions’ seen in ADR Type E classification

A

Clonidine example:

• after stopping the drug, the patients BP ends up WORSE than it was to begin with

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12
Q

Give and overview of the ADR classification by type

A

A - Augemented pharmacological effect

B - Bizzare

C - Chronic

D - Delayed

E - End-of-treatment

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13
Q

Explain the classification of allergies

A

Type B - Immunological

 Type 1 – immediate, anaphylactic.
• IgE
• E.G. anaphylaxes with penicillin

 Type 2 – cytotoxic antibody
• IgG, IgM
• E.G. methyldopa and HA

 Type 3 – serum sickness (antibody-antigen complex)
• IgG, IgM
• E.G. procainamide-induced lupus

 Type 4 – delayed-type hypersensitivity
• T-Cell
• E.G. contact dermatitis

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14
Q

Explain the classification of ‘pseudoallergies’

A

Type B - Immunological ‘pseudo-allergies’

Aspirin/NSAIDs = bronchospasm:
• Aspirin/NSAIDs inhibit COX so LESS prostaglandin synthesis & MORE leukotrienes made

ACE inhibitors = cough/angioedema:
• ACEi inhibit production of AngII and stop the breakdown of inflammatory mediators such as bradykinin which stimulate the cough receptors in the lungs

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15
Q

Common causes of ADRs?

A 
These 4 account for 2/3 of fatal ADRs:
	Antineoplastics – cytotoxic drugs	
	Cardiovascular drugs.				
	NSAIDs/analgesics.
	CNS drugs

 Antibiotics.
 Anticoagulants
 Hypoglycaemics
 Antihypertensives

Note that ADR frequency increases with increased individual drug use.

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16
Q

How is ADR detected?

A

Subjective reports
• patients complaint (yellow-card system)

Objective reports
• direct observations of events
• abnormal findings - physical examination, lab tests, diagnostic procedures

17
Q

Fact about rare events seen after drug use?

A

Rare events will probably NOT be detected before drug is marketed

18
Q

Yellow-card scheme?

A

Voluntary

  • Established drugs –> only report serious adverse reactions
  • “Black triangle” drugs (newly licensed) –> report ANY suspected adverse reactions.
19
Q

Why is drug-drug interaction incidence difficult to ascertain?

A

o Data for drug-related hospital admissions do not differentiate out drug interactions, only ADRs

o There is a lack of available comprehensive databases

o Difficulty in assessing OTC drug use

o Difficulty in determining drug contribution to interactions in complicated patients

o Sometimes the principal causes of ADRs is with specific drugs – e.g. statins

20
Q

Explain drug interactions in regards to pharmacodynamics

A

Pharmacodynamics
• drug’s effect on the body (i.e. receptor site dynamics)

Can have additive, synergistic or antagonistic effects from co-administrations
• Synergistic actions of antibiotics – use of two ABs will increase the effect more than their separate contributions (i.e. 2+2=5) OR they antagonise each other
• Overlapping toxicity – ethanol and benzodiazepines.
• Antagonistic effects – anticholinergic medications

21
Q

Explain drug interactions in relation to pharmacokinetics

A

Pharmacokinetics - body’s effects on the drug (ADME)

 Alteration in absorption – CHELATION:
• Irreversible binding in the GI-tract, for example, antibiotics to metal ions or calcium to form chelates that prevent absorption of the antibiotic

 Protein-binding interactions – not usually clinically significant but some are (e.g. warfarin).
• Warfarin is 99% albumin-bound so anything to decrease that will increase the free warfarin so there is more anti-coagulative effects

 Drug metabolism and excretion:
• Drugs can either be (1) directly excreted, (2) undergo Ph1 metabolism and be excreted, (3) undergo Ph1 and Ph2 and then be excreted or (4) only undergo Ph2 and then be excreted.

22
Q

Explain drug interactions in relation to pharmaceutical

A

Pharmaceutical - drug interactions OUTSIDE the body

e.g. in IV infusions

23
Q

Phase I vs. II metabolism?

A

Phase I - OXIDATION
• oxidation
• reduction
• hydrolysis

Phase II - CONJUGATION
 • glucuronidation
 • sulphation
 • acetylation
 • methylation
24
Q

In regards to metabolism, explain the effect of co-administration on it using an example

A

Drug metabolism can be enhanced or inhibited by co-administration

CYP450 system has been most extensively studied as family of drug metabolism enzymes:

• metabolism by a single isoenzyme – few examples

  • metabolism by multiple isoenzymes – most drugs
  • thus, co-administration of a CYP450 inhibitor may not affect metabolism rate as some isoenzymes can pick-up the slack for the inhibited isoenzyme
25
Q

Examples of CYP450 inhibitors

A

Inhibition is very RAPID

o Cimetidine (H2 antagonist)

o Erythromycin (and related ABs)

o Ketoconazole

o Ciprofloxacin (and related ABs)

o Ritonavir (and other HIV drugs)

o Grapefruit juice

o Fluoxetine (and other SSRIs)

26
Q

Examples of CYP450 inducers?

A

Induction takes HOURS/DAYS

o Rifampicin

o Carbamazepine

o St John’s wort (hypericin in the compound that induces CYP450)

o Phenobarbitone

o Phenytoin

27
Q

Drug elimination interactions almost always occur where and give a good/bad example

A

In RENAL TUBULES

GOOD:
• Probenecid + penicillin
• probenecid REDUCED penicillin excretion (penicillin used to be ££)

BAD:
• Lithium + thiazides
• thiazides lead to toxic accumulations of lithium

28
Q

State some deliberate drug interactions

A

 Levodopa + carbidopa
• can use lower doses of levodopa as carbidopa reduced peripheral metabolism

 ACEi + thiazides
• treat HF

 Penicillin’s + gentamycin
• treat severe staph. infections

 Salbutamol + ipratropium
• beta-agonists and anti-muscarinics used in inhalers to treat asthma

Year 2 - Pharm Lectures 11+ (23 decks)

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