Drugs & Toxicology Flashcards

1
Q

Reasons for TDM (drug factors) (5)

A
  • overdose s/s similar to disease being treated
  • very toxic in overdose
  • narrow therapeutic index
  • wide variation of therapeutic index (e.g. by variable pharmacokinetics, underlying conditions, DDI)
  • ensure efficacy of the drug
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2
Q

Indications to start TDM (patient factors) (5)

A
  • initiation / change of dosage
  • suboptimal response despite compliance
  • loss of control in previously stable patient
  • additional drugs are given / polypharmacy
  • confirm clinical diagnosis of toxicity
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3
Q

How many half-lives are required for a drug to reach steady-state concentration?

A

5 (so blood sampling should be taken afterwards)

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4
Q

Factors leading to a high / abnormal drug level (5)

A
  • change in the form of medication –> affect bioavailability
  • wrong dosage
  • wrong sampling
  • impaired excretion (e.g. renal impairment)
  • DDI
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5
Q

Reasons for TDM for gentamicin (2)

A
  • half-life is prolonged in renal impairment (2~3h to up to 100h)
  • nephrotoxicity similar to GN septicaemia
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6
Q

TDM inclusion criteria for gentamicin (4)

A
  • abnormal RFT
  • > 60y
  • concurrent use of nephrotoxic medication / contrast medium
  • duration of planned therapy >5~7d
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7
Q

Sampling time for TDM of gentamicin

A

6~14h post-dose

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8
Q

What is the graph used to determine dosing interval of gentamicin?

A

Hartford nomogram

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9
Q

Reasons for TDM of phenytoin (3)

A
  • non-linear dose-concentration curve (narrow therapeutic index)
  • variable pharmacokinetics
    (a) CYP substrate
    (b) highly protein binding
  • CNS toxicity
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10
Q

Why TDM of phenytoin is indicated in pregnancy?

A

pregnancy –> ↑ protein level –> ↓ pheytoin conc. as it is highly protein bound

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11
Q

Sampling time for TDM of cyclosporine (what sample is taken?)

A
  1. C0 (pre-dose)
  2. C2 (2h post-dose)
    (whole blood)
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12
Q

Therapeutic range of digoxin (HF and arrhythmia)

A

HF: 0.6~1.3
Arrhythmia: 1.2~2.6

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13
Q

When is digoxin effect potentiated? (4)

A

hypoK, hyperCa, hypoMg, hypothyroidism

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14
Q

DDI between digoxin and…
(a) Amiodarone
(b) Antibiotics

A

amiodarone –> ↓ elimination of digoxin
antibiotics –> ↓ gut metabolism of digoxin –> ↑ oral availability

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15
Q

Reasons for TDM of cyclosporine (4)

A
  • narrow therapeutic index
  • therapeutic index varying with organ transplanted and time from transplantation
  • renal & hepatic toxicity mimic graft rejection
  • ensure efficacy of drug
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16
Q

Reasons for TDM of digoxin (4)

A
  • narrow therapeutic index
  • conc. greatly varied by electrolytes
  • toxicity (n/v, anorexia, colour vision distortion, arrhythmia) mimics chronic HF
  • DDI (amiodarone, antibiotics)
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17
Q

Sampling time for digoxin

A

6h post-dose

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18
Q

Management of digoxin overdose (2)

A

digibind
correct electrolyte disturbance

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19
Q

Management of lithium overdose (2)

A

haemodialysis
correct water & sodium deficits

20
Q

Comprehensive drug screening
(a) Indications (2)
(b) Sample
(c) Lab method

A

(a) poisoning of unknown cause / unexplained hypoK or hypoglycaemia
(b) urine
(c) mass spectrometry

21
Q

Toxic metabolite of paracetamol (how is it detoxified in human body?)

A

NAPQI
(by glutathione conjugation in liver)

22
Q

Toxic dose of paracetamol (lower threshold for which patients?)

A

> 150 mg/kg
(malnutrition, chronic alcoholics, CYP450 inducers)

23
Q

Antidote for paracetamol poisoning (mechanism?)

A

IV N-acetylcysteine
(provide cysteine for glutathione synthesis / combine directly with NAPQI)

24
Q

What is the graph that predict hepatotoxicity in acute paracetamol overdose? (sampling time?)

A

Rumack-Matthew nomogram
(>4h from intake)

4m in the name lolll

25
Q

What is the usual acid-base disturbance in salicylate overdose?

A

respiratory alkalosis + metabolic acidosis

26
Q

Treatment for salicylate poisoning

A

alkalinisation of urine

27
Q

Metabolism of methanol (which metabolic is toxic?)

A

methanol –> formaldehyde –> formic acid (toxic) –> CO2

28
Q

Osmolar gap abnormal range

A

> 10 mOsm/L

29
Q

Management for methanol overdose (4)

A
  • ethanol / fomepizole
    –> inhibit alcohol dehydrogenase –> ↓ metabolism of methanol into formic acid
  • NaHCO3 (correct metabolic acidosis)
  • Folic acid (↑ metabolism of formic acid)
  • haemodialysis
30
Q

Acute toxicity of Fe

A

corrosion to GI tract

31
Q

Deficiency of which trace element gives impaired hair and nail growth?

A

Cu

32
Q

Deficiency of which trace element gives impaired insulin effect?

A

Cr(III)

33
Q

Deficiency of which trace element gives Keshan syndrome & Kashin-Beck disease?

A

Se

34
Q

Deficiency of which trace element gives Acrodermatitis enteropathica?

A

Zn

35
Q

Toxicity of which essential trace element gives pneumonitis?

A

Zn

36
Q

What does most essential element toxicity present with?

A

dermatitis

37
Q

Which heavy metals readily pass through the placenta? (2)

A

Pb, Cd

38
Q

Management of heavy metal toxicity

A

remove from further exposure
chelation by penicillamine, BAL **except Cd

39
Q

Forms of mercury (which is most selective to lipid-rich tissues like neurons?)

A

elemental (vapour), inorganic, organic

(organic)

40
Q

Which heavy metal gives Mad hatter’s disease / Erethism?

A

Hg

41
Q

Which heavy metal gives Pink disease / acrodynia?

A

Hg

42
Q

Which heavy metal gives Itai-Itai disease? (what is it?)

A

Cd (disturbed Ca metabolism –> bone pain)

43
Q

Which heavy metal is commonly found in seafood?

A

As (organic form)

44
Q

Which form of As is toxic?

A

Inorganic

45
Q

Which heavy metal gives peripheral neuropathy, intra-vascular haemolysis and renal toxicity?

A

As