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Principles of Disease > Adverse Drug reactions > Flashcards

Adverse Drug reactions Flashcards

1
Q

Define adverse drug reactions

A

Any response to a drug which is noxious, unintended and occurs at doses used in man for prophylaxis, diagnosis or treatment.

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2
Q

How frequent are adverse reactions and consequences ?

A
  • 4th leading cause of death
  • 60% of ADRs are preventable
  • primary care ADRs leads to hospital admission
  • secondary care ADRs lead to longer hospital stay
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3
Q

What causes avoidable ADRs and what is their frequency?

A
  • non-steroidal drugs
  • anti-inflammatory drugs
  • anti coagulants
  • antiplatelets

-they cause a third of admissions

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4
Q

What are the top 5 contributors to adverse drug reactions?

A
  • surgery
  • medication errors
  • medical errors (nonsurgical)
  • patient falls
  • nosocomial infections
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5
Q

What is the classification of onset of adverse drug reactions?

A
  • Acute
  • Sub acute
  • Latent
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6
Q

In what cases are ADRs not preventable?

A

nausea in chemo treatment for cancer

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7
Q

What is the classification of acute ADRs?

A
  • occurs within 60 minutes

- bronchoconsitrction

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8
Q

What is the classification of sub-acute ADRs?

A
  • 1-24 hours

- rash, serum sickness

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9
Q

What is the classification of latent ADRs?

A
  • 2 days

- excematous eruptions

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10
Q

Classification of severity of ADRs?

A

-Mild
-Moderate
Severe

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11
Q

Classification of mild ADRs?

A
  • Bothers some but requires no change in therapy

- Metallic taste with metronidazole

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12
Q

Classification of moderate ADRs?

A
  • Requires change in therapy, additional treatment or hospitalization
  • Diuretic induced hypokalemia
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13
Q

Classification of severe ADRs?

A
  • Disabling or life-threatening

- Kidney failure

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14
Q

How do we classify the different types of ADRs?

A 
Type A- Augmented 
Type B- Bizarre
-	Idiosyncratic and unpredictable 
Type C-Chronic
Type D- Delayed
Type E- End of treatment
Type F- Failure of treatment
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15
Q

What are predisposing factors for ADRs?

A
  • multiple drug therapy
  • inter-current disease (renal and hepatic impairment)
  • race and genetic polymorphisms
  • age (elderly and neonates)
  • sex
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16
Q

What gender is ADRs most common in and why?

A

Women due to different liver functions and pharmacokinetics

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17
Q

Describe Type A ADRs

A
  • Augmented response to the pharmacological actions of a drug
  • Dose dependent
  • Entirely Predictable
  • not usually life threatening
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18
Q

What are the 2 types of ADRs?

A

o Augmentation of the primary effect

o Secondary effect

19
Q

Examples of Type A ADRs.

A
  • Due to excess pharmacological action
    o Bradycardia with beta-blockers
    o Hypoglycaemia with sulphonylureas or insulin
20
Q

Describe the secondary effect of type A ADRs

A
  • Due to the secondary pharmacology of a drug unrelated to the therapeutic effect.
  • Still rationalizable form the known pharmacology of the drug.
21
Q

Examples of secondary effect of Type A ADRs

A
  • Galactorrhoea with domperidone

- Dry mouth with tricyclic antidepressants

22
Q

Causes for Type A ADRs?

A
  • Too high a dose
  • Pharmaceutical variation
    o Pharmacokinetic variation
     Absorption
    • Dose
    • Formulation
    • GI motility
    • First pass metabolism
    o Pharmacodynamic variation
23
Q

Describe Type B ADRs.

A
  • Bizarre, unpredictable, rare, cause serious illness or death
  • Unidentified for months or years
  • Unrelated to the dose or concentration
  • Not readily reversed
24
Q

What factors increase the chances of Type B ADRs?

A
  • More common with macromolecules
    o Proteins
    o Vaccines
    o Polypeptides
  • Patients with history of asthma, excema
  • HLA status
    o Presence of particular HLA increases risk of a Type B reaction
25
Q

What are the mechanisms of type B ADRs?

A
  • Idiosyncratic

- Drug allergy or hypersensitivity

26
Q

Describe the idiosyncratic mechanism of Type B ADRs.

A
  • inherent abnormal response to a drug

- occurs due to genetic abnormality to a drug or abnormal receptor activity

27
Q

Describe the drug allergy or hypersensitivity mechanisms of Type B ADRs.
How does it manifest?

A
  • immunological
  • has no relation to the pharmacological action of the drug
  • delay been exposure and ADR
  • manifests as rash, asthma, serum sickness
28
Q

Describe Type C Chronic ADRs.

A
  • Related to the duration of treatments and the dose
  • Does not occur with a single dose
  • semi predictable
29
Q

Examples of tYPE C chronic disease

A

o Latrogenic Cushings disease
o Opiate dependence
o Steroid induced osteoporosis

30
Q

Describe Type D Delayed ADRs

A
  • adverse effects occur a long time after treatment
  • teratogenesis
  • carcinogenesis
31
Q

What is teratogenesis?

A

seen in type d delayed ADRs
o Children of treated patients
o Abnormal congenital malformations in the fetus following in utero exposure due to maternal medication use during 1st trimester of pregnancy

32
Q

Example of teratogenesis?

A

o Craniofacial malformaitons in childrens whose mothers were treated with isotretinoin

33
Q

What are teratogenic agents?

A

 Cytotoxics
 Vitamin A
 Antithyroid drugs
 Steroids

34
Q

How to prevent teratogensis

A

o All drugs should be avoided during pregnancy unless they are safe or the benefit out-weigh potential risk.

35
Q

What is carcinogenesis in Type D ADRs?

A

o In treated patients years after treatment has stopped

36
Q

What is Type E End of treatment ADRs?

A
  • Occurs when a drug treatment is stopped especially suddenly following long term use
37
Q

Examples of Type E End of treatment ADRs?

A

o Unstable angina and MI - when beta blockers are stopped
o Alcohol
o Withdrawal seizures when anti-epileptics are stopped
o Addisonian crisis when long term steroids are suddenly stopped

38
Q

When does rebound phenomena occur?

A

When a drug is suddenly withdrawn.

  • Alcohols
  • Benzodiazepines
  • Beta-blockers
  • Corticosteroids
39
Q

What is Type F ADRs?

A
  • Failure of therapy
  • Frequently caused by drug interactions
  • Common
  • Dose related
  • Most worrying- failure of the OCP when administered with hepatic enzyme inducers/antibiotics
40
Q

How do we diagnosis ADRs?

A
  1. Differential diagnosis- be suspicious
  2. Medication history (past and present)
  3. Assess time of onset and dose relationship
  4. Laboratory investigations
    o Plasma concentration measurement
    o Allergy tests
41
Q

Who is most at risk of ADRs?

A
  • Age (children and elderly)
  • Multiple medications
  • Multiple co-morbid conditions
  • Inappropiate medication prescribing, use or monitoring
  • End-organ dysfunction
  • Altered physiology
  • Prior history of ADRs
  • Extent (dose) and duration of exposure
  • Genetic predisposition
42
Q

What are drugs commonly involved?

A

Drugs that we are very used to.

  • Antibiotics
  • Painkillers- NSAID, Opiates
  • Cardiovascular drugs
  • Hypogycemics
43
Q

Surveilance methods for ADRs

A

Anecdotal reporting

Most common is using yellow card scheme

Principles of Disease (53 decks)

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