ADR + Interactions Flashcards

1
Q

What is ADR

A

preventable or unpredicted medication event with harm to the patient.

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2
Q

Classification of ADRs - 3 sections

A

Onset
Severity
Type

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3
Q

Types of onset classification

A

Acute - within 1 hour
Sub-acute - 1-24hrs
Latent >2days

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4
Q

Types of severity classification

A

Mild - requires no change in therapy

Moderate - requires change in therapy, additional treatment, hospitalisation

Severe - disabling/life-threatening. Can result in death, prolongs hospitalisation, causes congenital abnormalities, requires intervention

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5
Q

How many types of ADRs are there?

A

5
ABCDE

Augmented
Bizarre
Chronic
Delayed 
Endoftreatment
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6
Q

What happens in Type A ADR

A

Extension of pharmacologic effect
Dose dependent
Most ADRs

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7
Q

Examples of Type A ADR

A

o Atenolol (beta blocker) will slow the heart down but if you give too much of it, it may cause complete heart block
o Chronic use of NSAIDs can cause peptic ulcers
o Anticholinergics can lead to dry mouth

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8
Q

What happens in Type B ADR

A

Idiosyncratic/immunologic reactions
Allergy
Rare + unpredictable

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9
Q

Examples of Type B ADR

A
  • Chloramphenicol can cause aplastic anaemia (1 in 10,000)- it is usually irreversible than fatal
  • ACE inhibitors can cause angioedema
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10
Q

What happens in Type C ADR

A

More common
Assoc w long term use of drug
Dose accumulation over long period

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11
Q

Examples of Type C ADR

A
  • Methotrexate – leads to liver fibrosis/ toxicity

* Antimalarials - ocular toxicity (can damage the optic nerve and retina)

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12
Q

What happens in Type D ADR

A

Delayed effects - sometimes dose independent

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13
Q

Examples of Type D ADR

A

o Carcinogenicity - e.g. immunosuppression

o Teratogenicity - e.g. thalidomide

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14
Q

What happens in Type E ADR

A

End of dosing/treatment reactions
o Withdrawal reactions (opiates, benzodiazepines, corticosteroids)
o Rebound reactions
o Adaptive reactions

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15
Q

What happens when u stop taking clonidine

A

Withdrawl - rebound reactions
It used to be antihypertensive- is an alpha2 agonist so it reduces release of NA from S neurones.
This leads to drop in BP. Without clonidine, can lead to large rise in BP = stroke/death. Long term use = compensatory upregulation in adrenergic receptors on post-synaptic neuron. Thus when inhibition of NA release by clonidine is removed, NA starts being produced again and more receptors = cause great affect = rise in BP

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16
Q

How many classifications of allergy are there

A

4

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17
Q

What is Type I alergy

A

Immediate - anaphylactic (IgE)
Lifethreatening + rapid onset
Treated as emergency

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18
Q

What is Type 2 allergy

A

Cytotoxic Antibody (IgG + IgM)

19
Q

What is Type 3 allergy

A
Serum Sickness (IgG + IgM)
Antigen-antibody complex
20
Q

What is Type 4 allergy

A
Delayed hypersensitivity (T cell)
Common
21
Q

What pseudoallergy does aspirin/NSAIDs cause

A

Bronchospasm
- Inhibiting production of prostanoids + prostaglandings via COX pathway which are bronchodilators
- Arachidonic acid is diverted to make leukotrienes (proinflamm + bronchoconstriction = bronchospasm + mucus secretion in airways)
Thus giving these to asthmatics = caution

22
Q

What pseudoallergy does ACE inhibitor cause

A

Cough/Angioedema

ACE inhibitor stops production of AT2, stops breakdwon of bradykinins (inflamm peptides). Thus these accumulate = triggers coughing as it acts on sensory nerves of lungs.

Angioedema - leads to bronchospasm, swelling of mouth + lips

23
Q

Another way of classifying ADRs - DoTS

A

Dose
Time
Susceptibility

24
Q

4 common causes of fatal ADRs

A

Antineoplastics
CV drugs
NSAIDs/analgesics
CNS drugs

25
Q

4 common causes of nonfatal ADRs

A
  • Antibiotics
  • Anticoagulants
  • Hypoglycaemics
  • Anti-hypertensives
26
Q

What affects frequency of ADRs

A

polypharmacy - number of drugs pt taking

27
Q

What is the Yellow Card Scheme

A

This is a system for reporting adverse drug reactions.

28
Q

3 types of pharmacodynamic drug interactions

A
  • Additive effects - two drugs add together
  • Synergistic effects - two drugs potentiate each other’s actions to get a greater2 effect than expected
  • Antagonist effects - drugs that antagonise each other’s actions
29
Q

2 types of pharmacokinetic drug interactions

A
  • Alteration in absorption

* Protein binding effects

30
Q

How can there be alteration in absorption

A

Chelation - irreversible binding of drugs in GIT making it difficult to absorb

31
Q

How can protein binding effects occur as a drug interaction

A

o Competition between drugs for protein or tissue binding sites- two drugs may have the same binding site on the protein circulating in the blood which means that one drug may displace the other.

32
Q

Over half of drug metabolism is done by….

A

CYP2D6/CYP3A4

these are CYP450 isoenzymes

33
Q

CYP450 Inhibitors

A

Erythryomycin + related abx
Ciproflaxin + related abx
Ritonavir + HIV drugs
Grapefruit juice

34
Q

How long does inhibition of CYP450 take

A

rapid - within hours

35
Q

How long does induction of CYP450 take

A

hours/days - need to produce new gene products/proteins

36
Q

CYP450 Inducers

A
  • Rifampicin
  • Carbamazepine
  • (Phenobarbitone)- anti-convulsants
  • (Phenytoin)
  • St. John’s Wort (hypericin is the compound that induces CYP450)
37
Q

Where do drug elimination interactions occur

A

renal tubule

38
Q

what is used to stop penicillin being excreted (thus use less + have substantial effects

A

 Probenecid

39
Q

What stops lithium being cleared thus it accumulates + is toxic

A

thiazides/NSAIDs

40
Q

Why are Levodopa + carbidopa used together

A

Carbidopa prevents Levodopa from being broken down in the periphery so more can act in the brain, thus lower doses of Levodopa can be used.

41
Q

Which 2 drugs enhance each others antiHTN effects so are used together

A

ACE inhibitors + Thiazides

42
Q

Which 2 drugs used in pt w severe Staph A infection

A

• Penicillins + Gentamycin

43
Q

why are salbutamol + ipratropium used together

A

beta-agonists and anti-muscarinic inhalers are used in the treatment of COPD and asthma