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Adverse reactions to drugs Flashcards

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1
Q

Define adverse drugs event

A

preventable or unpredicted medication event—with harm to patient

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2
Q

ADR can be classified according to what

A

Onset
Severity
Type

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3
Q

Classify ADR according to onset of event

A 
Acute 
Within 1 hour
Sub-acute 
1 to 24 hours
Latent 
>  2 days
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4
Q

Classify ADR according to severity

A 
Severity of reaction:
Mild
requires no change in therapy
Moderate
requires change in therapy, additional treatment, hospitalisation 
Severe
disabling or life-threatening
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5
Q

What might be the consequences of a sever ADR

A

Results in death

Life-threatening

Requires or prolongs hospitalisation

Causes disability

Causes congenital anomalies

Requires intervention to prevent permanent injury

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6
Q

Outline type A ADR

A

extension of pharmacologic effect

usually predictable and dose dependent

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7
Q

Give examples of type A ADR

A

e.g., atenolol and heart block, anticholinergics and dry mouth, NSAIDS and peptic ulcer

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8
Q

Differentiate the ADR with paracetemol and digoxin

A

Digoxin the ADR steadily increases, throughout the therapeutic window

With paracetemol, there is low ADR throughout the therapeutic window, but dramatically increases following even a small amount over the therapeutic dose

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9
Q

Outline type B ADR

A

idiosyncratic or immunologic reactions

includes allergy and “pseudoallergy”

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10
Q

Give examples of type B ADR, including pseudoallergy

A

e.g., chloramphenicol and aplastic anemia,

PSEUDOALLERGY: ACE inhibitors and angioedema

Aspirin/NSAIDs – bronchospasm

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11
Q

Differentiate the commonality of type A and type B ADR

A

A- 2/3 of ADR

B- very rare and unpredictable

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12
Q

Outline type C ADR

A

associated with long-term use

involves dose accumulation

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13
Q

Example of type C ADR

A

e.g., methotrexate and liver fibrosis, antimalarials and ocular toxicity

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14
Q

Give an example of acute onset ADR

A

Anaphylaxis

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15
Q

Outline type D classification of ADR

A

delayed effects (sometimes dose independent)

carcinogenicity

teratogenicity

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16
Q

Type D. What is carcinogenecity. Give an example

A

Cancer causing (immunosuppressant)

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17
Q

Type D what is teratogenecity. Give an example

A

Damage to foetus… thalidomide

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18
Q

Outline type E reactions

A

Withdrawal reactions

Rebound reactions

“Adaptive” reactions
`

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19
Q

Give examples of withdrawal reaction (type E)

A

Opiates (cold turkey), benzodiazepines (can lead to fitting), corticosteroids

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20
Q

Give examples of rebound reactions (type E)

A

Clonidine, beta-blockers, corticosteroids

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21
Q

Give example of adaptive reactions

A

Neuroleptics (major tranquillisers)

Movement reactions (i.e. the EPS)

reactions don’t go away when you remove the drug, and can get worse

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22
Q

When are antimalarial drugs given

A

In some rheumatic disease

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23
Q

Outline rebound reactions with clonidine

A

BP reduces during

But missing a couple of doses results in rebound

You end up worse than before you started

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24
Q

Memoire for dverse drug reactions

A 
A     Augmented pharmacological effect
B	Bizarre
C	Chronic
D	Delayed
E	End-of-treatment
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25
Classify the 4 hypersensitivity reactions
I- Immediate, anaphylactic II- cytotoxic antibody (IgG, IgM) III- serum sickness (IgG, IgM) IV- delayed hypersensitivity (T cell)
26
Give an example of a drug allergy associated with each hypersensitivity type
I- anaphylaxis with penicillins II- methylopa and haemolytic anaemia III- procainamide-induced lupus IV- contact dermatitis
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30
Give examples of pseuoallergies
Aspirin/NSAIDs – bronchospasm Block COX and thus prostanoids..... more leukotrienes produced. They are pro-inflammatory and bronchoconstrictor Only happens in a minority of patients, but NSAIDs not used ACE inhibitors – cough/angioedema Pharmacoloical... due to build of bradykinin which causes cough, swelling of tongue, lips, etc. Bradykinin is pro-inflammatory. Not in everyone (ethnic differences) THESE ARE PHARMACOLOGICAL NOT ALLERGIC
31
Which drugs are most common cause of ADRs
Antineoplastic, CVS, NSAIDs/Analgesics, CNS drugs account for 2/3 of fatal ADRs ``` Also: ABs, Anticonvulsants, Hypoglycaemics, Antihypertensives ``` are common causes of ADRs
32
All cuases of ADR
``` Antibiotics Antineoplastics* Anticoagulants Cardiovascular drugs* Hypoglycemics Antihypertensives NSAID/Analgesics* CNS drugs* ```
33
Why is there lots of ADR with CVS and CNS drugs
Cos so many take them
34
What causes increase in ADR
Giving more drugs
35
How are ADR detected
Subjective report -patient complaint Objective report: - direct observation of event - abnormal findings
36
What abnormal findings might help with ADR
physical examination laboratory test diagnostic procedure
37
What is the problem with ADR detection
Stastically, large numbers needed to detect rare events 1 in 100 needs 300 to detect 1 in 100 X 3 needs 650 people to detect ie rare events will probably not be detected before drug is marketed
38
What is the yellow card scheme
for established drugs only report serious adverse reactions (fatal, life-threatening, needing hospital admission, disabling) for “black triangle “ drugs (newly licensed, usually <2 years) report any suspected adverse reaction
39
Who can yellow card scheme be used by
can be used by doctors, dentists, nurses, coroners and pharmacists, and members of the public voluntary
40
What should happen if ADR is suspected
Should be confirmed (high probability) Estimate frequency Inform prescribers
41
Why is it hard to work out drug drug interactin
Data for drug-related hospital admissions do not separate out drug interactions, focus on ADRs Lack of availability of comprehensive databases Difficulty in assessing OTC and herbal drug therapy use Difficulty in determining contribution of drug interaction in complicated patients Sometimes principal cause of ADRs with specific drugs eg statins
42
Outline the three types of drug interactios
Pharmacodynamic Related to the drug’s effects in the body Pharmacokinetic Related to the body’s effects on the drug Pharmaceutical - drugs interacting outside the body (mostly IV infusions)
43
What does pharmacodynaic drug interaction relate to
Related to the drug’s effects in the body | Receptor site occupancy
44
What does pharmacokinetic drug interaction relate to
Related to the body’s effects on the drug | Absorption, distribution, metabolism, elimination
45
Outline pharmacodynamic drug interactions give examples
Additive, synergistic, or antagonistic effects from co-administration of two or more drugs Synergistic actions of antibiotics Overlapping toxicities - ethanol & benzodiazepines Antagonistic effects - anticholinergic medications (amitriptyline and acetylcholinesterase inhibitors)
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48
What are the pharmacokinetic drug interactions
Alteration in absorption Protein binding effects Changes in drug metabolism Alteration in elimination
49
Give an example of alterations in absorptions as a cuase of drug drug interactions
Chelation Irreversible binding of drugs in the GI tract Tetracyclines, quinolone antibiotics (i.e. those used for COMPLICATED gastric ulcer!!!) can bind to: - ferrous sulfate (Fe+2), - antacids (Al+3, Ca+2, Mg+2), - dairy products (Ca+2) So that you absorb less of these ions and you absorb NO antibiotic!
50
Outline protein binding interactions
Competition between drugs for protein or tissue binding sites Increase in free (unbound) concentration may lead to enhanced pharmacological effect
51
Why have protein binding interactiosn been overestimated
Many interactions previously thought to be PB interactions were found to be primarily metabolism interactions PB interactions are not usually clinically significant but a few are
52
Give an example of a clinically significant protein binding interactions
PB interactions are not usually clinically significant | but a few are (mostly with warfarin)
53
How can a drug be handled by the kidney
1. Excreted unchanged by kidney (furesomide) 2. Phase 1 reaction in liver / kidney. Excreted OR in kidney: 3. Phase 2 reaction (with or without previous phase 1) nand excreted by kidney
54
Examples of phase 1 metabolism
Oxidation Reduction Hydrolysis
55
T/F Phase I must happen before Phase II
F
56
Examples of phase II metabolism
Conjugation: Glucoronidation Sulphation Acetyation
57
Outline drug metaboism interactions
Drug metabolism inhibited or enhanced by coadministration of other drugs Phase 2 metabolic interactions (glucuronidation, etc.) occur, research in this area is increasing
58
T.f most drugs are metabolised by a single isoenzyme predominantly
Few examples of clinically used drugs Examples of drugs used primarily in research on drug interactions Most drugs metabolized by more than one isozyme
59
What is the problem with targeting CYP 450
If co-administered with CYP450 inhibitor, some isozymes may “pick up slack” for inhibited isozyme
60
Give examples fof CYP 450 inhibitors
Cimetidine Erythromycin and related antibiotics Ketoconazole etc Ciprofloxacin and related antibiotics Ritonavir and other HIV drugs Fluoxetine and other SSRIs Grapefruit juice
61
Give examples of CYP 450 inducers
The “usual suspects” Rifampicin Carbamazepine (Phenobarbitone) (Phenytoin) St John’s wort (hypericin)
62
Differentiate change in CYP450 activity
Inhibition is very rapid... due to enzyme inhibiton Induction takes hours/days (new enzyme synthesis and protein making etc.)
63
Outline the drug elimintation interactions with examples
Almost always in renal tubule - probenecid and penicillin (good), - lithium and thiazides (bad)
64
Explain - probenecid and penicillin (good)
Good Giving probenecid with penicillin allows you to give smaller doses of penicillin as the probenecid reduces elimintation of the penecillin
65
Exmplain - lithium and thiazides (bad)
the thiazide will increase the excretion of sodium at the expense of the lithium Lithium retained and circulating levels increased
66
Give examples of deliberate drug interactions
levodopa + carbidopa salbutamol + ipratropium ACE inhibitors + thiazides penicillins + gentamicin (particulary staphylococcal)

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