Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

YR2 LCRS Pharmacology > 22. Adverse drug reactions > Flashcards

22. Adverse drug reactions Flashcards

1
Q

why are adverse drug reactions an issue?

A
  • they cause substantial morbidity and mortality
  • they are one of the leading causes of death amongst hospitalised patients
  • they are responsible for many hospital admissions and cost a lot of money
  • 30-60% of events are preventable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how is the onset of adverse drug reactions classified?

A

ACUTE: within 1hr
SUB-ACUTE: 1-24hrs
LATENT: more than 2 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is the severity of adverse drug reactions classified?

A

MILD: requires no change in therapy
MODERATE: requires a change in therapy, may require additional treatment and possibly hospitalisation
SEVERE: disabling, life-threatening, requires prolonged hospitalisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how is the type of reaction of adverse drug reactions classified?

A 
TYPE A: Augmented pharmacological effect
TYPE B: Bizarre
TYPE C: Chronic
TYPE D: Delayed 
TYPE E: End-of-treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the characteristics of type A reactions?

A
  • an extension of the pharmacologic effect of the drug that we already know about
  • usually predictable and dose dependent
  • responsible for at least 2/3 ADRs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

give some examples of type A reactions

A
  • atenolol and heart block
  • anticholinergics and dry mouth
  • NSAIDS and peptic ulcer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the characteristics of type B reactions?

A
  • more dramatic
  • particular to given individuals/immunological reactions (e.g. allergy and “pseudo-allergy”)
  • rare and unpredictable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

give some examples of type B reactions

A
  • chloramphenicol and aplastic anemia

- ACE inhibitors and angioedema (pseudo-allergy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the characteristics of type C reactions?

A
  • associated with long-term drug use

- involve dose accumulation (total dose someone is exposed to over a period of time)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

give some examples of type C reactions

A
  • methotrexate and liver fibrosis

- anti-malarial drugs and ocular toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the characteristics of type D reactions?

A
  • delayed effects

- not strongly linked to dose - may happen at very low doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

give some examples of type D reactions

A
  • carcinogenicity (e.g. immunosuppressants)

- teratogenicity (e.g. thalidomide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the characteristics of type E reactions?

A
  • withdrawal reactions: opiates, benzodiazepines, corticosteroids
  • rebound reactions: clonidine, beta-blockers, corticosteroids
  • “adaptive” reactions: neuroleptics (major tranquillisers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is clonidine?

A
  • an alpha 2 agonist which reduces the release of noradrenaline from sympathetic neurones
  • the reduction in sympathetic outflow leads to a drop in blood pressure
  • clonidine used to be an anti-hypertensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why does clonidine withdrawal occur and what does it result in?

A
  • long-term use of clonidine causes long-term suppression of peripheral noradrenaline production which leads to compensatory upregulation in adrenergic receptors on post-synaptic neurones
  • the upregulation in receptors means that when the inhibition of NA release by clonidine is removed, NA starts being produced again and has more receptors to act on so causes a greater effect –> substantial rise in blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how are allergies classified?

A

TYPE 1: immediate, anaphylactic (IgE) e.g. anaphylaxis with penicillin

TYPE 2: cytotoxic antibody (IgG, IgM) e.g. methyldopa and hemolytic anaemia

TYPE 3: serum sickness (IgG, IgM) antigen-antibody complexes e.g. procainamide-induced lupus

TYPE 4: delayed hypersensitivity (T cell) e.g. contact dermatitis

17
Q

describe the example of aspirin/NSAIDS and bronchospasm as a pseudoallergy

A
  • 5% of people that take the drug get bronchospasm
  • this is because these drugs inhibit COX enzymes
  • blocking COX results in reduced prostanoid/prostaglandin synthesis (bronchodilators)
  • instead the body makes more leukotrienes (pro-inflammatory and bronchoconstrictors)
18
Q

what are pseudoallergies?

A

pseudoallergies have nothing to do with the immune system

19
Q

describe the example of ACE inhibitors and cough/angioedema as a pseudoallergy

A
  • 10-20% of people taking ACE inhibitors suffer from chronic, dry cough
  • this is due to the accumulation of inflammatory peptides in the lung
  • bradykinin triggers cough through sensory receptors in the lung
  • less than 1% of patients may suffer from angioedema (many of the same signs and symptoms of anaphylaxis but less severe)
20
Q

what are common causes of ADRs?

A
  • antibiotics
  • antineoplastic drugs
  • anticoagulants
  • cardiovascular drugs
  • hypoglycemic drugs
  • antihypertensive drugs
  • NAID/analgesics
  • CNS drugs
21
Q

how are ADRs detected?

A
  • subjective report (complaint)

- objective report (observation and abnormal findings) –> physical examination, lab testing, diagnostic procedure

22
Q

what is the yellow card system?

A
  • a public way of detecting adverse reactions
  • it can be used by doctors, dentists, nurses, coroners, pharmacists and members of the public
  • includes blood products, vaccines, contrast media
  • for established drugs only report SERIOUS ADRs (fatal disabling)
  • for “black triangle” drugs (newly licensed) report ANY SUSPECTED ADRs
  • ADR suspected –> ADR confirmed –> frequency estimated –> prescribers informed
23
Q

what is the problem with drug-drug interactions?

A
  • there are no proper databases to find this out
  • people take over-the-counter medicines
  • difficulty assessing herbal drug therapy use
  • difficulty determining the contribution of drug interaction in complicated patients
24
Q

what are the 3 varieties of drug interactions?

A

PHARMACODYNAMIC INTERACTIONS: related to the drug’s effects in the body (receptor site occupancy)

PHARMACOKINETIC INTERACTIONS: related to the body’s effects on the drug (absorption, distribution, metabolism, elimination)

PHARMACEUTICAL INTERACTIONS: drugs interacting outside the body (mostly IV infusions)

25
Q

in terms of pharmacodynamic drug interactions, what does additive mean?

A

if you put 2 drugs together they produce an effect that is the sum of the drugs

26
Q

in terms of pharmacodynamic drug interactions, what does synergistic action of antibiotics mean?

A

two drugs potentiate each others’ actions to get a greater effect than expected

27
Q

in terms of pharmacodynamic drug interactions, what does antagonistic effects mean?

A

drugs that antagonise each others’ actions

28
Q

in terms of pharmacokinetic drug interactions, what does alterations of absorption (chelation) mean? give an example

A

irreversible binding of drugs in the GI tract

e.g. tetracylines and quinolone antibiotics can be involved in chelation

they may be given together with ferrous sulfate, antacids, dairy products

they form a stable chelate so you don’t absorb the mineral ion but also don’t absorb the antiobiotic

29
Q

in terms of pharmacokinetic drug interactions, what does protein binding interactions mean? give an example of a clinically significant PBI

A
  • competition between drugs for protein or tissue binding sites
  • increase in free (unbound) concentration due to displacement –> enhanced pharmacological effect

e.g. warfarin is tightly bound to proteins, so even displacing a small amount can have drastic effects

30
Q

in terms of pharmacokinetic drug interactions, what does drug metabolism and elimination mean?

A
  1. a drug may be excreted completely unchanged by the kidney
  2. you may get a phase I reaction after which the drug can be excreted in its changed form by the liver/kidney
  3. you can get a phase II reaction so the kidney clears the drug after being changed
31
Q

what is the relevance of CYP450 substrates?

A

CYP450 isozymes metabolise potentially toxic compounds, including drugs (substrates)

  • some drugs undergo metabolism by a single isozyme
  • most drugs undergo metabolism by multiple isozymes
  • if we inhibit metabolism via 1 pathway we get metabolism redundancy
  • if co-administered with a CYP450 inhibitor, some isozymes “pick up slack” for the inhibited isozyme
32
Q

what proportion of drugs are metabolised by CYP450 isozymes?

A
  • over half of drug metabolism is by CYP2D6 and CYP3A4

- 2D6 shows a great degree of variability

33
Q

list some CYP450 inhibitors

A
  • cimetidine
  • erythromycin and related antibiotics
  • ketoconazole
  • ciprofloxacin
  • ritonavir
  • grapefruit juice
34
Q

list some CYP450 inducers

A
  • rifampicin
  • carbamazepine
  • phenobarbitone
  • phenytoin
35
Q

compare how long inhibition and induction take

A

inhibition: rapid - minutes
induction: slower - hours/days as you wait for new CYP450 to be synthesised

36
Q

where do drug elimination interactions take place?

A

in the renal tubule

37
Q

give some examples of drug elimination interactions

A
  • probenecid and penicillin (good) - reduces elimination of penicillin so it lasts longer
  • lithium and thiazides (bad) - thiazides reduce clearance of lithium which can lead to toxicity
38
Q

what deliberate interactions are commonly prescribed?

A
  • levodopa and carbidopa (inhibitor of decarboxylase in peripheral tissues)
  • ACE inhibitors and thiazides (reduce BP)
  • penicillins and gentamicin (antibiotics)
  • salbutamol and ipratropium (b2-antagonist and anti-cholinergic used in asthma to bronchodilate)

YR2 LCRS Pharmacology (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions