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A final year of medicine > Prescribing Safety Assessment: Drug Monitoring & ADRs > Flashcards

Prescribing Safety Assessment: Drug Monitoring & ADRs Flashcards

1
Q

Which patients are statins associated with myopathy in?

A

Personal or family history of muscular disorders, previous history of muscular toxicity, renal impairment, high alcohol intake, hypothyroidism, elderly. Check CK at baseline in these patients only.

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2
Q

What monitoring level is done for phenytoin?

A

Pre-dose (trough)

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3
Q

Checking ALT when starting statin?

A

Should be done in all patients. If ALT/AST are 3* normal, statins are contraindicated (or if have active liver disease). Should be checked at 3 and 12 months after starting treatment.

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4
Q

Normal range for lithium?

A

0.4-0.8mmol/L

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5
Q

When to monitor lithium?

A

12 hours post dose

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6
Q

When should routine lithium monitoring be done?

A

Weekly after initiation, after each dose change until stable, and every 3 months thereafter

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7
Q

Sodium and lithium?

A

Sodium depletion is known to increase the risk of lithium toxicity and patients are advised to avoid making dietary changes that increase/decrease sodium intake

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8
Q

What parameters need monitoring for lithium?

A

Serum concentration, U&E, TFTs, ECG, BMI/weight

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9
Q

When to monitor methotrexate?

A

FBC regularly, but can be 2-3 months when established

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10
Q

Starting methotrexate if LFTs abnormal?

A

Should not be done!

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11
Q

Key parameter at baseline when starting APS?

A

Fasting blood glucose; ECG only indicated in those with CVD or RFs

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12
Q

Key parameter when starting COCP?

A

Cardiovascular e.g. blood pressure.

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13
Q

What thyroid bloods need monitoring for amiodarone?

A

Full panel e.g. T3/T4/TSH

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14
Q

Key baseline investigation in amiodarone?

A

CXR (risk of pulmonary toxicity), LFTs, U&E (K+), TFTs

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15
Q

Amiodarone and potassium?

A

Should be used with caution when hypokalaemic (risk of arrhythmia)

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16
Q

Which doses need checking for multiple daily dose regimen in gentamicin?

A

Pre-dose (trough) and peak dose

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17
Q

When is plasma digoxin concentration measured?

A

Not routinely done! Only if toxicity/ non-compliance or inadequate effect suspected

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18
Q

Key blood to monitor in digoxin?

A

U&E (renally excreted)

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19
Q

One advantage of digoxin over CCBs and B-blockers?

A

Does not cause hypotension so may be better for hypotensive patients

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20
Q

Monitoring valproate?

A

Should do baseline LFTs and regular monitoring, and FBC.

21
Q

Clozapine dose if leukocyte and neutrophil counts drop below normal?

A

Should STOP it, not adjust it

22
Q

Who needs to register with clozapine monitoring service?

A

All patients!

23
Q

Type A and B drug reactions?

A

Type A = common, predictable, dose-related. Type B = idiosyncratic, bizarre, unexpected

24
Q

ADRs of CCBs?

A

Hypotension, bradycardia, peripheral oedema, flushing

25
Q

ADRs of diuretics?

A

Hypotension, electrolyte abnormalities, AKI, sub-class specific e.g. gynaecomastia

26
Q

ADRs of B-blockers?

A

Hypotension, bradycardia, wheeze in asthmatics, worsens acute heart failure

27
Q

ADRs of heparins?

A

Haemorrhage (especially if renal failure or <50kg), thrombocytopenia

28
Q

ADRs of aspirin?

A

Haemorrhage, PUD, gastritis, tinnitus in large doses

29
Q

ADRs of warfarin?

A

Haemorrhage, obviously. Initially pro-thrombotic hence why need LMWH alongside warfarin for the first few days

30
Q

ADRs of digoxin?

A

Nausea, V&D, blurred vision, confusion, drowsiness, xanthopsia (yellow/green vision inc. ‘halo’ vision)

31
Q

Digoxin and potassium?

A

As digoxin competes with K+ at Na+/K+ ATPase, low K+ augments digoxin effect

32
Q

Amiodarone ADRs?

A

Pulmonary fibrosis, thyroid disease (hypo and hyper), skin greying, corneal deposits

33
Q

Lithium ADRs?

A

Early = tremor, int. = tiredness, late = arrhythmias, seizures, coma, renal failure, diabetes insipidus

34
Q

ADRs of haloperidol?

A

Dyskinesias e.g. acute dystonic reactions, drowsiness

35
Q

ADRs of fludrocortisone?

A

Hypertension/sodium and water retention

36
Q

ADRs of statins?

A

Myalgia, abdominal pain, increased ALT/AST, rhabdomyolysis (or just mildly increased CK)

37
Q

Inhibition and induction time-scales?

A

Inhibition only takes hours-days, while inductions takes days-weeks

38
Q

Drugs interacting with alcohol to cause GI bleeding?

A

NSAIDs

39
Q

Drugs interacting with alcohol to cause increased anti-coagulation?

A

Warfarin (with acute alcohol due to its enzyme inhibition, while chronic alcohol excess causes enzyme induction thus reducing antiocoagulant effect)

40
Q

Drugs interacting with alcohol to cause sweating, flushing, nausea and vomiting?

A

Metronidazole, disulfiram

41
Q

Drugs interacting with alcohol to cause lactic acidosis?

A

Metformin!

42
Q

Drugs interacting with alcohol to cause hypertensive crisis?

A

MAOIs

43
Q

Drugs interacting with alcohol to cause sedation?

A

Barbiturates, opiods and benzos

44
Q

Co-prescribing NSAIDs and ACEI?

A

Bad; NSAIDs constrict the afferent vessels, while ACEI dilate the efferent, leading to fall in renal perfusion and so the GFR tails off

45
Q

What type of drug is amiloride?

A

K+ sparing diuretic

46
Q

Key to finding which interactant is important?

A

Look for the “potentially serious interaction” (shown by black dot)

47
Q

What is protamine used to treat?

A

Effects of heparin

48
Q

Where should drug-induced hypoglycaemia be managed?

A

In hospital, as the effects can persist for hours

49
Q

Why does metformin cause lactic acidosis?

A

Metformin inhibits hepatic gluconeogenesis. Normally, lactate is taken up in this process, so it can accumulate.

A final year of medicine (20 decks)

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