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LCRS Pharma > Adverse Drug Reactions > Flashcards

Adverse Drug Reactions Flashcards

1
Q

simple definition of adverse drug effect

A

preventable or unpredicted medication events with harm to the patient.

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2
Q

describe the epidemiology of ADRs

A

o 4th-6th leading cause of death amongst patients.
o 6.7% incidence of serious ADRs.
o 0.3%-7% of all hospital admissions and costs a lot of money.
o 30-60% are preventable.

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3
Q

what are ADRS classed based on?

A
  • onset
  • severity
  • type
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4
Q

what are the different onsets of ADRs?

A

o Acute <1 hour.
o Sub-acute 1-24 hours.
o Latent >2 days.

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5
Q

what are the different severities of ADRs? what changes should take place following?

A

o Mild
-no change in therapy required.
o Moderate
- change in therapy required, additional treatment and hospitalisation.
o Severe
- disabling, life-threatening, prolongs hospitalisation, causes congenital abnormalities,
requires intervention to prevent further injury.

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6
Q

what are the different types of ADRs?

A
  • Type A: Augment/extend the pharmacological effect.
  • Type B: Bizarre – Idiosyncratic or Immunologic reactions.
  • Type C: Chronic – Long-term use side effects.
  • Type D: Delayed – Delayed effects.
  • Type E: End of treatment side effects.
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7
Q

what is Type A?

A

Augmented effect:

  • 60-70% of ADRs
  • can be expected from the pharmacology
  • Usually predictable and dose-dependent
  • the pharmacology of the drug is not necessarily fully understood

e.g. 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.

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8
Q

what is Type B?

A

Bizarre:
Unpredictable, rare (totally unexpected)
and include allergy and “pseudo-allergy”.

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9
Q

name drugs with their Type A reactions

A

Augmented reactions:
Atenolol–> heart block
NSAIDs–>peptic ulcers.

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10
Q

name drugs with Type B reactions

A

Bizarre/Idiosyncratic reactions:
Chloramphenicol–>aplastic anaemia
ACE inhibitors–>angioedema
Herceptin–> cardiac toxicity

  • new cancer drugs are tested for cardiac toxicity pre-clincially
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11
Q

what is Type C?

A

Chronic:

Involves dose accumulation over time associated with chronic use

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12
Q

name drugs with Type C reactions

A

chronic use reactions:
Methotrexate –> liver fibrosis
antimalarial–> ocular toxicity

methotrexate is immunosuppressive for IBD

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13
Q

what is Type D?

A

Delayed effects of drugs

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14
Q

name drugs and their Type D reactions

A

delayed reaction:
 Carcinogenicity – e.g. immunosuppressants.
 Teratogenicity – e.g. thalidomide.

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15
Q

what is 3 reactions make up Type E?

A

End of treatment side effects consists of 3 reactions:
1) Withdrawal reactions
– patient cannot make endogenous supply

2) Rebound reactions
– disease gets worse when drugs stopped

3) “Adaptive” reactions
– adapted body reactions to drugs

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16
Q

name drugs that cause a withdrawal reaction?

A

opiates
corticosteroids
benzodiazepines

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17
Q

name drugs that cause a rebound reaction

A
  • clonidine (BP increases again after stoppage but higher to how it worse before treatment)
  • beta-blockers
  • corticosteroids

Type E (due to stoppage)

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18
Q

name drugs that cause an “adaptive reaction”

A

Type E

neuroleptics (tranquilisers) used in schiz

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19
Q

what is the effect of stopping clonidine treatment?

A

BP increases again after stoppage but higher to how it worse before treatment

Clonidine hydrochloride is an anti hypertensive

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20
Q

classification overview of ADR types

A 
o	A – augmented pharmacological effect.
o	B – bizarre.
o	C – chronic.
o	D – delayed.
o	E – end-of-treatment.
21
Q

what are the types of allergic reactions (hypersensitivity)

A

 Type 1 – immediate, anaphylactic
 Type 2 – cytotoxic antibody.
 Type 3 – serum sickness (antibody-antigen complex)
 Type 4 – delayed-type hypersensitivity

22
Q

what are the mediators of the different allergic reaction types?

A
  • type 1–> IgE
  • type 2–> IgG, IgM
  • type 3–> IgG, IgM
  • type 4–> T-cell
23
Q

Type B ADR involves allergic reactions:

types of allergic reaction (hypersensitivities) and examples of drugs that cause them?

A

type 1: anaphylaxes with penicillin
type 2: methyldopa and HA.
type 3: procainamide-induced lupus.
type 4: contact dermatitis

type 1 is immediate and anaphylactic (IgE)
type 2 is mediated by cytotoxic antibody (IgG, IgM)
type 3 involves immune complexes (IgG, IgM)
type 4 is delayed type (T cell)

24
Q

what are pseudo-allergies?

A

they are not allergies because they have no associated immune response
they are pharmacological reactions

25
Q

what is the pseudo-allergic reaction to aspirin and NSAIDs in general?

A

bronchospasm :
Aspirin/NSAIDs inhibit COX so less prostaglandin synthesis and more leukotrienes made.

some asthmatics need to avoid NSAIDs

26
Q

what is the pseudo-allergic reaction to ACEis?

A

1) angioedema:
ACEi inhibit production of AngII (in Afro-Carribean patients particularly)

2) cough:
stop the breakdown of inflammatory mediators such as bradykinin which stimulate the cough receptors in the lungs.

the drug needs to be removed in this case

27
Q

what drugs are the most common causes of ADRS?

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

 Antibiotics.
 Anticoagulants.
 Hypoglycaemics.
 Antihypertensives.

ADR frequency increased with increased individual use

28
Q

how can ADRs be detected and recorded?

A

subjective and objective reports:

1) Subjective reports:
o Patient complaints – yellow-card system.

2) Objective reports:
o Direct observations of events.
o Abnormal findings – physical examination, lab tests, diagnostic procedures.

Rare events will probably NOT be detected before a drug is marketed.

29
Q

what is the Yellow Card Scheme? how should it be used?

A

Reporting of adverse effects:
This was a scheme introduced after the 1964 incident with thalidomide and is run by the Committee on Safety of Medicines (branch of medicines control agency).

Voluntary, can be used by any healthcare professional, and includes blood products, vaccines and contrast media.

Established drugs should only report serious adverse reactions.

“Black triangle” drugs (newly licensed) should report ANY suspected adverse reactions.

30
Q

why is it difficult to ascertain the incidence of drug-drug interaction?

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 which enhances toxicity of other drugs with co-administration

31
Q

what are the 3 classifications of drug interactions?

A

pharmacodynamic
pharmacokinetic
pharmaceutical

32
Q

what are pharmacodynamic drug interactions?

A

drug’s effects on the body
– e.g. receptor site dynamics.
Additive, synergistic, or antagonistic effects from co-administration (looks at drug’s properties)

33
Q

give examples of pharmacodynamic drug interactions

A

• 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.

34
Q

what are pharmacokinetic drug interactions?

A

body’s effects on the drug

– e.g. absorption, distribution, metabolism, excretion

35
Q

give examples of pharmacokinetic drug interactions?

A

Involves aspects of ADME (pharmokinetics)

1) Alteration in absorption 
– chelation 
2) Protein-binding interactions 
– e.g. warfarin
3) Drug metabolism and excretion
36
Q

what is the effect of chelation on drug absorption?

A

Irreversible binding in the GI-tract, for example, antibiotics to metal ions or calcium to form chelates that prevent absorption of the antibiotic.

e.g. drugs with milk

37
Q

what is the significance of PPB in the effects of warfarin?

A

Warfarin is 99% albumin-bound so anything to decrease that (competing drug) will increase the free warfarin so there is more anti-coagulative effects.

38
Q

how can drugs be excreted after going through the phases of metabolism?

A

Drugs can be

(1) directly excreted
(2) undergo Ph1 metabolism and be excreted,
(3) undergo Ph1 and Ph2 and then be excreted
(4) only undergo Ph2 and then be excreted.

39
Q

what are pharmaceutical drug interactions?

A

drug interactions outside the body – e.g. in IV infusions.

40
Q

what are the reactions that occur in phase 1 metabolism?

A

oxidation
reduction
hydrolysis

41
Q

what are the reactions that occur in phase 2 metabolism?

A 
conjugation (glutathione, amino-acid)
glucuronidation
sulphation
acetylation
methylation.

produce polar, water soluble excretable product

42
Q

how are most drugs metabolised in the CYP450 system?

A

by multiple isoenzymes

Thus, co-administration of a CYP450 inhibitor may not affect metabolism rate as some isoenzymes can pick-up the slack for the inhibited isoenzyme.

43
Q

name inhibitors of CYP450

A
  • Cimetidine [H2 receptor antagonist used in peptic ulcer]
  • Erythromycin (and related ABs)
  • Ketoconazole [anti fungal and Cushing’s]
  • Ciprofloxacin (and related ABs)
  • Ritonavir (and other HIV drugs).
  • Grapefruit juice.
  • Fluoxetine (and other SSRIs).

the inhibition effect is very rapid

44
Q

name inducers of CYP450

A
  • Rifampicin
  • Carbamazepine
  • St John’s wort (hypericin)
  • Phenobarbitone.
  • Phenytoin.

the induction take hours/days

45
Q

compare the onset of effects of inhibitors and inducers of CYP450 enzymes

A

inhibitors are rapid

inducers take hours/days

46
Q

where do drug elimination interactions almost always occur?

A

renal tubules

47
Q

name a good elimination interaction? why was this good?

A

GOOD: Probenecid + penicillin

Probenecid reduced excretion of penicillin and penicillin used to be expensive.

48
Q

example of bad elimination interaction

why is this bad?

A

BAD: Lithium and thiazides

thiazides lead to toxic accumulations of lithium

49
Q

name some deliberate drug interactions

A

Levodopa + carbidopa
- can use lower doses of levodopa as carbidopa reduced peripheral metabolism of levodopa so more can cross BBB

ACEi + thiazides
- treat HF.

Penicillin’s + gentamycin
- treat severe staph. infections.

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

LCRS Pharma (32 decks)

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