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(I) Symposium: Science Underpinning Practice, High Yield > High Risk Drugs > Flashcards

High Risk Drugs Flashcards

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1
Q

Therapeutic range for for Gentamicin and Amikacin

A

One-hour (peak) serum concentration should be 5 to 10 mg/L, pre-dose trough level should be < 2mg/L.

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2
Q

Indication for Gentamicin and Amikacin

A

Endocarditis.
Meningitis
Severe diabetic foot infection

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3
Q

Activity against gram (-)/gram (+) for Gentamicin and Amikacin

A

Very good gram negative coverage.
P.aeruginosa + K.pneumonia.

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4
Q

Mechanism of action for Gentamicin and Amikacin

A

Irreversible 30s ribosome inhibitor.

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5
Q

Elimination route for Gentamicin and Amikacin

A

70% renal excreted.

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6
Q

Monitoring for for Gentamicin and Amikacin: safety and efficacy.

A

Serum concentration: taken at trough level.
Renal function.
Auditory and vestibular function.
{ treatment efficacy: temperature, CRP, WBC).

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7
Q

Caution/Contraindication for Gentamicin and Amikacin

A

Renal failure.

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8
Q

Renal/Liver for Gentamicin and Amikacin

A

Creatinine clearance <20 mL/min.

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9
Q

Adverse effects for for Gentamicin and Amikacin + why.

A

Ototoxicity: generates free radicals within the ear causing permanent damage to sensory cells and neurons.
Nephrotoxicity: Direct damage tissue. 70% is cleared here so accumulation can lead to this.

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10
Q

Lithium indication.

A

Treatment and prophylaxis bipolar disorder.

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11
Q

Therapeutic range for Lithium

A

0.6-1 mmol/L.

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12
Q

Lithium main route of elimination.

A

Renal; 80% reabsorbed.

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13
Q

When do you not prescribe lithium

A

Cardiac disease associate with rhythm disorders.
Significant renal impairment.
Untreatable hypothyroidism + Addisons disease.

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14
Q

How does lithium cause hypo/hyperthyroidism.

A

Lithium concentrates by the thyroid and inhibits thyroidal iodine up-take.

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15
Q

How does lithium cause hypercalcaemia and what are the potential clinical implications.

A

Increase circulation of calcium due to increase reabsorption at the loop of Henle —> Increase circulation parathyroid hormone (PTH) which can lead to bone thinning and kidney stones.

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16
Q

How does lithium cause hyponatremia

A

Competitively taken up by sodium re-uptake (more than Na+) via the Na+/H+ co-transporters in the proximal tubules and then accumulates in the renal tubules. Also competitively taken up by the Na+ channels located in the loop of Henle.

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17
Q

Fill in the diagram.

A
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18
Q

How does lithium cause Nephrogenic diabetes insipidus.

A

By inhibiting arginine vasopressin from increase the reabsorption of water through the AQ2 channel.

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19
Q

What are the formulation considerations that need to take place when using lithium.

A

Lithium available in two salts: lithium carbonate and lithium citrate. They are not dose equivalent.
Always prescribe by brand name.

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20
Q

Increase lithium concentration is more likely with
(a) Thiazide diuretics
(b) Loop diuretics
(c) Spironolactone

A

(a) More likely with thiazide diuretics, loop diuretics are less likely to result in lithium toxicity.

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21
Q

Which agent when combined with lithium is likely to cause neurotoxicity.
(a) Ibuprofen
(b) ACE-inhibitor
(c) Dapagliflozin
(d) Duloxetine
(e) Carbamazepine

A

(e) Carbamazepine, SSRI/duloxetine have been linked rarely to CNS toxicity.

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22
Q

Which agent when combined with lithium is likely to decrease lithium levels due to increase lithium renal clearance.
(a) Ibuprofen
(b) ACE-inhibitor
(c) Dapagliflozin
(d) Duloxetine
(e) Carbamazepine

A

(c) SGLT-2 inhibitor because sodium is not being reabsorbed via the SGLT2 pump.

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23
Q

Monitoring for lithium

A

One week after treatment lithium levels are taken 12 hours post-dose.
BMI, U&E, TFT, eGFR, Ca2+ then every 6 months.

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24
Q

What are the signs of lithium toxicity

A

CNS disturbances: Lethargy, dizziness, lack of coordination, tinnitus
GI: diarrhoea, vomiting, anorexia
PNS: Muscle hyper irritability.

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25
Q

Lithium toxicity occurs at:
(a) 1.2 mmol/L
(b) 1.5 mmol/L
(c) 0.8 mmol/L
(d) 1.0 mmol/L

A

(b) 1.5 mmol/L

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26
Q

What advise should people taking lithium be given.

A

Carry lithium card.
Regular blood test.
Adverse effects to effect.
Maintain fluid intake.
Avoid OTC NSAIDs.

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27
Q

Valproate mechanism of action.

A

Inhibition of sodium gated channels.

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28
Q

MHRA warning concerning Valproate.

A

Valproate should not be prescribed in girls, female adolescents, women who are pregnant or of childbearing age.

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29
Q

What supplementation is added during valproate regime.

A

Folic acid supplementation 5 mg daily 


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30
Q

What is the most effective primary pregnancy prevention intervention when patient is on valproate.

(a)Levonorgestrel-releasing intrauterine system.
(b)Combined hormal contraceptive
(c) Progesterone only pill
(d) progestogen implant

A

(d) and (a) most effective with a failure rate less than 1%.
Others recommend with barrier protection.

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31
Q

What are the adverse effects associated with valproate (vALPROate).

A

Anemia
Liver dysfunction
Pancreatitis
Spino bifida
Weight gain
Thrombocytopenia

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32
Q

What % protein binding seen with valproate.

A
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33
Q

Which drug when co- administered with valproate is displaced.

(A) Aspirin
(B) Simvastatin
(C) Warfarin
(D) Nifidipine

A

(C) Warfarin is less bound to protein and valproate can displace it easily.

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34
Q

Which drug when co- administered with valproate is able to DISPLACE valproate.

(A) Aspirin
(B) Simvastatin
(C) Warfarin
(D) Nifidipine

A

(A) Aspirin

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35
Q

What are the key monitoring for someone who is taking valproate.

A
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36
Q

Indication for methotrexate.

A

2nd line: Maintenance of Crohn’s disease or inducing remission for CD.
Rheumatoid arthritis.

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37
Q

Mechanism of action for Methotrexate

A

Inhibit dihydrofolate reductase, which catalase the conversion of dihydrofolate into tetrahydrofolate, the active form folic acid. Cause increase adenosine which has anti-inflammatory effect —> repress T-cell activation, down-regulation B cells.

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38
Q

Dosing and Prescribing practice for Methotrexate

A

Orally or SC once WEEKLY. 25 mg for 16/52 weeks.
Prescribe 5 mg Folic acid taken on a separate day.

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39
Q

Adverse drug reaction with Methotrexate

A

Nausea + vomiting.
Mouth ulcers
Rash
Bone marrow suppression.
Liver disease: jaundice.

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40
Q

What should patients avoid during flu season. ( who are on methotrexate)

A

Live vaccines.

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41
Q

Warning signs when on Methotrexate

A

GI toxicity.
Sore throat—> infection.
Pulmonary toxicity—> cough, dyspnoea —> methotrexate can induce hypersensitivity pneumonitis.
Renal injury—> direct tubular damage

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42
Q

Patient comes to your pharmacy and tells you that they have had a sore throat so they would like to have some lozenges. You ask them about their medication history and you find out the following:
- Methotrexate SC 25 mg
- Diltiazem 5 mg OD for AF
- Folic acid 5 mg once a week
What are you concerned about.

A

Patient may be have blood disorder due to bone marrow suppression therefore stop methotrexate and advise them to go urgently go hospital.

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43
Q

Monitoring for Methotrexate

A

FBC, renal and LFTs: every 1-2 weeks until therapy stabilised then every 2-3 months.
Warn Tx about symptoms sore throat.

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44
Q

Why would you advise patient on Methotrexate to avoid buying OTC NSAIDs or be cautious of penicillin.

A

NSAIDs (ACE-I) and penicillin all reduce renal perfusion and subsequently excretion of methotrexate which could increase risk of methotrexate toxicity.

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45
Q

What agent when combined with Methotrexate increase risk of haematological toxicity

A

Co-trimoxazole due to additive bone marrow suppression. Both of these drugs are antimetabolite which cause suppression of DNA nucleotides.
Thymines and purines

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46
Q

Indication for Ciclosprin

A

Acute steroid resistance sever UC including toxic megacolon.

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47
Q

Form Cyclosporin is given in.

A

IV infusion

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48
Q

Cyclosporin main metabolism pathway.

A

CYP3A4

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49
Q

Cyclosporin monitoring

A

U&E (magnesium, K+), blood lipids, renal function, liver function, blood pressure, dermatological and physical examination.
Cyclosporine concentration at trough level.

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50
Q

What are the warning signs associated with cyclosporine

A

Neurotoxicity: tremor, headache, encephalopathy.
Blood disorders: fever, sore throat.
Liver toxicity: jaundice
Hypertension.

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51
Q

Cyclosporin affects on electrolytes and why.

A

In distal consulted tubule. Cyclosporin inhabits Mg2+ channels reabsorbing magnesium: hypomagnesia. It inhibits the RAAS system causing retention of K+ hyperkalemia and reduction in sodium and water reabsorption.

52
Q

In sever liver impairment how would you manage the dosing of ciclosporin.

A

Dose reduction.

53
Q

Which agent is likely to reduce cyclosporin levels.
(a) Grapefruit
(b) John’s Wart
(c) Smoking
(d) Carbamazepine
(e) Itraconazole

A

(d) + (b) CYP3A4 inducers.

54
Q

Which agent is likely to increase cyclosporin levels.
(a) Grapefruit
(b) John’s Wart
(c) Smoking
(d) Carbamazepine
(e) Itraconazole

A

(a) + (e) are inhibitors of CYP3A4.

55
Q

Patient presents with new onset confusion and tremor. You are on the ward and have taken a drug history, you find that the patient is on:
- Ciclosporin 120 mg IV
- Ibuprofen OTC for headache 2 days ago.
What is the likely explanation for her presentation.

A

Ciclosprorin toxicity due to decreased renal perfusion owing to NSAID administration leading to accumulation of cyclosporin.

56
Q

Warfarin MAO

A

Inhibits Vit K dependent epoxide reductase activity, which modifies FVII, FIX, FX, and prothrombin (FII) during synthesis in liver.

57
Q

Warfarin: Inhibits the intrinsic coagulation cascade…
True Or False

A

True

58
Q

Warfarin Pharmacokinetic parameter and cautions

A

99% albumin bound, taking 1-3 days to see full effect.
Metabolised by CYP2C9 and CYP3A4.
Elimination is 20-60 hours but varies due to high patient inter-variability (CYP2C9 deficient).

59
Q

What type of PK interaction does warfarin experience.

A

PK interaction involves albumin displacement and CYP enzymes.

60
Q

Which drug from this list increase the INR when on Warfarin.
(a) Alcohol
(b) Carbamazepine
(c) Phenytoin
(d) Erythromycin

A

(d) Macrolide are inhibitors of CYP3A4.

61
Q

Which drug from this list decreases the INR of warfarin.
(a) Amiodarone
(b) Phenytoin
(c) Clarithromycin
(d) Vancomycin

A

(b) Phenytoin.

62
Q

Which drug from this list decreases the INR of warfarin due to albumin displacement.
(a) Amiodarone
(b) Phenytoin
(c) Aspirin
(d) Vancomycin

A

(C) Aspirin has a high ability to displace as well as its ability to increase bleeding risk.

63
Q

Which drug should be avoided due to Antiplatelet effect when on warfarin
(a) prednisolone
(b) methotrexate
(c) Venlafaxine
(d) Miconazole

A

(c) Venlafaxine: SNRI

64
Q

Which antidepressant should be avoided when used with warfarin due to anticoagulant effect.
(a) prednisolone
(b) Mirtazapine
(c) Venlafaxine
(d) Miconazole

A

(b) Mirtazapine (TCA and mirtazapine enhance anticoagulant effect).

65
Q

Which drug should be avoided due to increased bleeding risk.
(a) prednisolone
(b) methotrexate
(c) Venlafaxine
(d) Clopidogrel

A
66
Q

Warfarin: What is significance of reducing INR?

A

Increased risk of thrombotic event.

67
Q

Warfarin: What is the significance of increasing the INR?

A

Risk of hemorrhagic event.

68
Q

What key considerations are made when dosing individual on warfarin?

A

Age
Ethnicity

Other disease states e.g. liver disease.
Life-style: Drinker, Smoker?
Diet: High vitamin K diet (e.g. binge brocoli).

69
Q

Warfarin: Caution/C/I

A

Teratogenic: Avoid in pregnancy
Significant bleeding.

70
Q

Warfarin adverse effect:

A

Bleeding: spontaneous epistaxis and retroperineal bleeding, Alopecia.

71
Q

Warfarin: Monitoring before and during

A

★ Before: Baseline prothrombin time.
★ At start: daily or alternate days determine the INR , then longer intervals depending on response, then up to every 12 weeks.

72
Q

What is the maximum time between monitoring INR for patient with good response on Warfarin.
(a) 12 weeks
(b) 6 weeks
(c) 4 weeks
(d) 2 months
(e) 3 months

A

(a) 12 weeks.

73
Q

Warfarin: Key counselling to patient.

A

★ Discuss patient warfarin treatment is balance between benefits (preventing clots) and risk (bleeding).
★ Educate patient on food, drug, alcohol interactions and to call doctor/pharmacist if see bruises and signs of bleed (e.g. blood in stool-dark colour).
★ Mention the yellow book is essential as regular blood test are required to ensure safety whilst on treatment. Explain rat poison issue.

74
Q

What dietary advice with warfarin

A

☆ Green leafy vegetables: don’t binge, but keep it consistent.
☆ Cranberry juice.
☆ Don’t take garlic supplements: Increase INR.

75
Q

Garlic interacts with warfarin
a. True
b. False

A

a. True advice patient to stop taking it because it increase bleeding risk.

76
Q

How is warfarin introduced in AF.

A

Slow-loading regimen is done over 3-4 weeks with Warfarin 1 mg or 2 mg daily is generally an acceptable starting dose. The average daily maintenance dose is usually around 5 mg daily.

77
Q

How is warfarin introduced in acute VTE

A

Heparin or a low molecular weight heparin is given concurrently — this is done in secondary care.Warfarin is inducted at 5 mg titrated according to patient response 2-15 mg daily.

78
Q

Warfarin INR range: VTE and AF

A
79
Q

Warfarin INR: mechanical valves

A
80
Q

Antidote for warfarin: dose and onset of action

A

Vitamin K injection

81
Q

Digoxin indication

A

Atrial fibrillation or flutter.
Heart failure
Emergency loading dose for atrial fibrillation or flutter.

82
Q

Digoxin Therapeutic Range

A

0.7 to 2 ng/mL (wide inter-individual variations).

83
Q

How do you start digoxin (dose)

A

Loading dose of 250 micrograms to 750 micrograms for 7 days followed by maintenance dose 125 micrograms-250 micrograms adjusted according to renal function and heart rate response.

84
Q

What is max maintenance dose of digoxin.
(a) 250 micrograms
(b) 125 micrograms
(c) 300 micrograms
(d) 150 micrograms

A

(a) 250 micrograms daily

85
Q

When would you suspect DigToxicity.
(a) 0.5 nanogram/mL
(b) 3.0 nanograms/mL
(c) 3.0 nanograms/L
(d)1.5 nanogram/mL in presence of hypokalemia
(e) 0.8 nanograms.
(f) 1.8 nanograms/L nanograms

A

(b) 3.0 nanograms/mL + (d) 1.5 nanogram/mL in presence of hypokalemia because dig toxicity is more pronounced in hypokalemia due to less competition to bind to sodium potassium pump.

86
Q

What are the symptoms of DigToxicity.

A

Confusion, nausea, anorexia, visual colour disturbances.

87
Q

What is the antidote for DigToxicity

A

DigiFab antibody

88
Q

Monitoring for Digoxin
(a) Routine monitoring
(b) Monitoring when patient presents with confusion and visual colour disturbances
(c) Monitoring when patient is on amiodarone or diltiazem
(d) Monitoring when patient comes in for regular blood pressure and heat rate monitoring.

A

(b) and (c)

89
Q

Lithium indication.

A

Treatment and prophylaxis bipolar disorder.

90
Q

Therapeutic range for Lithium

A

0.6-1 mmol/L.

91
Q

Lithium main route of elimination.

A

Renal; 80% reabsorbed.

92
Q

When do you not prescribe lithium

A

Cardiac disease associate with rhythm disorders.
Significant renal impairment.
Untreatable hypothyroidism + Addisons disease.

93
Q

How does lithium cause hypo/hyperthyroidism.

A

Lithium concentrates by the thyroid and inhibits thyroidal iodine up-take.

94
Q

How does lithium cause hypercalcaemia and what are the potential clinical implications.

A

Increase circulation of calcium due to increase reabsorption at the loop of Henle —> Increase circulation parathyroid hormone (PTH) which can lead to bone thinning and kidney stones.

95
Q

How does lithium cause hyponatremia

A

Competitively taken up by sodium re-uptake (more than Na+) via the Na+/H+ co-transporters in the proximal tubules and then accumulates in the renal tubules. Also competitively taken up by the Na+ channels located in the loop of Henle.

96
Q

How does lithium cause Nephrogenic diabetes insipidus.

A

By inhibiting arginine vasopressin from increase the reabsorption of water through the AQ2 channel.

97
Q

What are the formulation considerations that need to take place when using lithium.

A

Lithium available in two salts: lithium carbonate and lithium citrate. They are not dose equivalent.

Always prescribe by brand name.

98
Q

Increase lithium concentration is more likely with
(a) Thiazide diuretics
(b) Loop diuretics
(c) Spironolactone

A

(a) More likely with thiazide diuretics, loop diuretics are less likely to result in lithium toxicity.

99
Q

Which agent when combined with lithium is likely to cause neurotoxicity.
(a) Ibuprofen
(b) ACE-inhibitor
(c) Dapagliflozin
(d) Duloxetine
(e) Carbamazepine

A

(e) Carbamazepine, SSRI/duloxetine have been linked rarely to CNS toxicity.

100
Q

Which agent when combined with lithium is likely to decrease lithium levels due to increase lithium renal clearance.
(a) Ibuprofen
(b) ACE-inhibitor
(c) Dapagliflozin
(d) Duloxetine
(e) Carbamazepine

A

(c) SGLT-2 inhibitor because sodium is not being reabsorbed via the SGLT2 pump.

101
Q

Monitoring for lithium

A

One week after treatment lithium levels are taken 12 hours post-dose.
BMI, U&E, TFT, eGFR, Ca2+ then every 6 months.

102
Q

What are the signs of lithium toxicity

A

CNS disturbances: Lethargy, dizziness, lack of coordination, tinnitus
GI: diarrhoea, vomiting, anorexia
PNS: Muscle hyper irritability.

103
Q

Lithium toxicity occurs at:
(a) 1.2 mmol/L
(b) 1.5 mmol/L
(c) 0.8 mmol/L
(d) 1.0 mmol/L

A

(b) 1.5 mmol/L

104
Q

What advise should patient receiving lithium be given.

A

Carry lithium card.
Regular blood test.
Adverse effects.

Maintain fluid intake.
Avoid OTC NSAIDs.

105
Q

Indication for Ciclosprin

A

Acute steroid resistance sever UC including toxic megacolon.

106
Q

Form Cyclosporin is given in.

A

IV infusion

107
Q

Cyclosporin main metabolism pathway.

A

CYP3A4

108
Q

Cyclosporin monitoring

A

U&E (magnesium, K+), blood lipids, renal function, liver function, blood pressure, dermatological and physical examination.

109
Q

What are the warning signs associated with cyclosporine

A

Neurotoxicity: tremor, headache, encephalopathy.
Blood disorders: fever, sore throat.
Liver toxicity: jaundice
Hypertension.

110
Q

Cyclosporin affects on electrolytes and why.

A

In distal consulted tubule. Cyclosporin inhibits Mg2+ channels reabsorbing magnesium: hypomagnesemia. It inhibits the RAAS system causing retention of K+ hyperkalemia and reduction in sodium and water reabsorption.

111
Q

In sever liver impairment how would you manage the dosing of ciclosporin.

A

Dose reduction.

112
Q

Which agents is likely to reduce cyclosporin levels.
(a) Grapefruit
(b) John’s Wart
(c) Smoking
(d) Carbamazepine
(e) Itraconazole

A

(d) + (b) CYP3A4 inducers.

113
Q

Which agent is likely to increase cyclosporin levels.
(a) Grapefruit
(b) John’s Wart
(c) Smoking
(d) Carbamazepine
(e) Itraconazole

A
114
Q

Patient presents with new onset confusion and tremor. You are on the ward and have taken a drug history, you find that the patient is on:
- Ciclosporin 120 mg IV
- Ibuprofen OTC for headache 2 days ago.
What is the likely explanation for her presentation.

A

Ciclosprorin toxicity due to decreased renal perfusion owing to NSAID administration leading to accumulation of cyclosporin.

115
Q

Theophylline (aminophylline) therapeutic range.

A

10-20 mg/L

116
Q

Theophylline mechanism of action.

A

Main action is through inhibition of PDE4 that results in reduced inflammatory response mediated by alveolar macrophages.

117
Q

Theophylline undesirable side effects.

A

Seizure
Tachycardia
Headaches
Nausea

118
Q

Major route of elimination for theophylline

A

Liver metabolism.

119
Q

Major enzyme metabolising theophylline.

A

CYP1A2.

120
Q

Major lifestyle interaction with theophylline.

A

Cigarette smoking induces CYP1A2 enzymes reducing theophylline concentration.

121
Q

Major pharmacodynamic interaction with theophylline.
(a) Beta-2-agonist +theophylline
(b) Phenytoin + theophylline
(c) Allopurinol + theophylline
(d) erythromycin+ theophylline
(e) cigarette + theophylline

A

(a) major pharmacodynamic interaction they both increase risk of hypokalemia.

122
Q

Drug-disease interaction where theophylline concentration increases.
(a) Asthma + theophylline
(b) Heart failure + theophylline
(c) Chronic renal disease +theophylline
(e) Hypothyroidism +theophylline.

A

(b) Heart failure decreases the flow of blood to the liver therefore there is increased concentration of theophylline.

123
Q

Which drug increases the plasma concentration of theophylline.
(a) carbamazepine
(b) ritonavir
(c) erythromycin
(d)corticosteroids.

A

(c) Macrolide increases the plasma concentration of theophylline.

124
Q

Which drug increases the risk of convulsions with theophylline.
(a) Ciprofloxacin
(b) Cimetidine
(c) Carbamazepine
(d)Primidone

A

(a) Ciprofloxacin has seizure potential.

125
Q

Which drugs decreases the concentration of theophylline.
(a) ciprofloxacin
(b) diltiazem
(c)phenytoin
(d)oestrogen

A

(c) phenytoin, is an inducer therefore decreases theophylline concentration.

126
Q

What are the monitoring requirements for initiating Theophylline.

A

Before starting:
LFTs
Urea and electrolytes [K+]
Smoking status

After:
Take plasma concentration of theophylline 5 days after treatment then 3 days after any dose adjustment.
Once stable: when signs toxicity, adherence issue or drug-drug interaction.

127
Q

What are the symptoms of theophylline toxicity.

A

CNS/cardiac/GI
Nausea
Vomiting
Tremor
Sinus tachycardia.
Dilated pupils

(I) Symposium: Science Underpinning Practice, High Yield (12 decks)

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