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Derm Pharm 2020 > 1 - CYCLOSPORINE > Flashcards

1 - CYCLOSPORINE Flashcards

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Dermatology Board Prep flashcards
1
Q

Cyclosporine is also known as cyclosporine A (CsA)

A

True

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2
Q

CsA was originally discovered and isolated from the soil fungus Tolypocladium inflatum gams

A

True

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3
Q

Sandimmune and Neoral are both formulations of CsA

A

True (only Neoral is approved for the treatment of psoriasis)

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4
Q

Neoral is a more bioavailable and more consistently absorbed microemulsion formulation of CsA

A

True (only Neoral is approved for the treatment of psoriasis)

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5
Q

CsA is not cytotoxic

A

True (in contrast to other drugs used to treat psoriasis I.e. MTX)

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6
Q

CsA is not immunosuppressive

A

True (in contrast to other drugs used to treat psoriasis I.e. MTX)

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7
Q

CsA is not teratogenic

A

True (in contrast to other drugs used to treat psoriasis I.e. MTX and Acitretin)

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8
Q

CsA is nephrotoxic

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout)

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9
Q

CsA may cause lymphoproliferative malignancies

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout)

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10
Q

CsA is a neutral cyclic peptide available in oral solution or in capsules

A

True

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11
Q

Concomitant intake of Grapefruit juice with CsA should be avoided as Grapefruit juice affects the metabolism of CsA through inhibiting the CYP 450 enzyme system

A

True (to make the oral solution more palatable, Neoral should be diluted with Apple juice or orange juice instead)

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12
Q

Neoral has a 10-50% higher bioavailability than Sandimmune

A

True

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13
Q

Neoral is less dependent on bile, food, diet and the GI environment for proper absorption

A

True

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14
Q

CsA is excreted in breast milk and breastfeeding should be avoided while on CsA

A

True

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15
Q

CsA is extensively metabolised by the CYP3A4 enzyme in the liver

A

True

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16
Q

CsA is excreted mainly in the bile and faeces

A

True

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17
Q

Only 6% of CsA and its metabolites are excreted in urine

A

True (mainly excreted in bile and faeces)

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18
Q

Hepatic insufficiency may prolong the half life of CsA

A

True (CYP3A4 metabolism in the liver)

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19
Q

CsA dose needs to be adjusted in hepatic insufficiency

A

True (metabolised in the liver through CYP3A4)

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20
Q

Dialysis and renal failure does not significantly alter CsA’s clearance

A

True (mainly metabolised in the liver and excreted in the bile and faeces)

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21
Q

90% of CsA is protein bound

A

True

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22
Q

The exact mechanism of action of CsA is not fully understood although there is an effect on T lymphocytes in psoriasis

A

True

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23
Q

CsA inhibits T cell secretion of cytokines (IL-2, IFN-gamma, ICAM-1), lymphocyte infiltration and inflammation

A

True

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24
Q

CsA inhibits production of IL-2 by inhibiting calcineurin that results in decreased T cell proliferation

A

True

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25
Q

CsA inhibits IFN-gamma production by T lymphocytes that results in reduced keratinocyte proliferation

A

True

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26
Q

Neoral has a more complete and more predictable absorption than Sandimmune

A

True

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27
Q

CsA is effective in patients who present with widespread, intensely inflammatory psoriasis

A

True

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28
Q

CsA is effective in patients who present with a sudden severe flare of their psoriasis

A

True

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29
Q

CsA may be used in patients with moderate to severe or disabling psoriasis who are unable to tolerate, have contraindications to or have failed other systemic therapies

A

True

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30
Q

CsA may be useful in psoriasis patients experiencing major life events where substantial clearing of psoriasis for a short period of time is important

A

True

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31
Q

CsA may also be strongly considered for erythrodermic psoriasis

A

True

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32
Q

CsA may also be strongly considered for pustular psoriasis

A

True

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33
Q

CsA is generally effective for all forms of psoriasis

A

True

34
Q

CsA may be used for Severe atopic dermatitis

A

True

35
Q

CsA is ideally given for 3-6 months and 12 months at the most due to risk of nephrotoxicity

A

True

36
Q

CsA, tacrolimus and pimecrolimus are calcineurin inhibitors

A

True

37
Q

Significantly decreased renal function is a contraindication for CsA

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout)

38
Q

Uncontrolled hypertension is a contraindication for CsA

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout)

39
Q

Clinically cured or persistent malignancy (except NMSCs) is a contraindication for CsA

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout)

40
Q

Cutaneous T-cell lymphoma is a contraindication for CsA

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout)

41
Q

Patients with cutaneous T cell lymphoma progressed after treatment with CsA

A

True

42
Q

The risk of nephrotoxicity and hypertension from CsA increase with increasing dose and duration of therapy

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout)

43
Q

Neurological effects I.e. Tremor, headaches, paraesthesia and hyperesthesia are the most common adverse effects noted in patients using CsA for 2 months or less

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout

44
Q

CsA may cause hypertrichosis

A

True

45
Q

CsA may cause gingival hyperplasia

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout)

46
Q

CsA may cause GI side effects I.e. Nausea, diarrhoea, abdominal discomfort

A

True
N - Neoplasm
E - Epilepsy
O - Oral (gingival hyperplasia)
R - Renal Toxicity leading to Hypertension
A - Anorexia due to GI effects
L - Lab abnormalities (hyperkalaemia, hyperlipidaemia, hypomagnesaemia, hyperuricaemia leading to Gout)

47
Q

A reduction of CsA dose is recommended when there is a 30% increase from the baseline creatinine value

A

True

48
Q

The development of hypertension due to CsA is not a contraindication to continuing therapy with CsA

A

True (CsA can be continued as long as the hypertension can be controlled using the calcium channel blocker nifedipine)

49
Q

The risk of NMSCs is probably increased in psoriasis patients undergoing long term treatment with CsA

A

True

50
Q

Hyperlipidaemia is a common adverse effect of CsA

A

True

51
Q

The hyperlipidaemia from CsA may be treated using a lipid lowering agent

A

True

52
Q

Fluvastatin (lipid lowering agent) is suitable to be used for CsA induced hyperlipidaemia as it is not a substrate of CYP3A4 and does not interact with CsA

A

True (CsA is metabolised by CYP3A4)

53
Q

Rosuvastatin (lipid lowering agent) is suitable to be used for CsA induced hyperlipidaemia as it is not a substrate of CYP3A4 and does not interact with CsA

A

True (CsA is metabolised by CYP3A4)

54
Q

Pravastatin (lipid lowering agent) is suitable to be used for CsA induced hyperlipidaemia as it is not a substrate of CYP3A4 and does not interact with CsA

A

True (CsA is metabolised by CYP3A4)

55
Q

Lovastatin (lipid lowering agent) should not be used for CsA induced hyperlipidaemia as similar to CsA, it is also a substrate of CYP3A4 and interacts with CsA

A

True

56
Q

Simvastatin (lipid lowering agent) should not be used for CsA induced hyperlipidaemia as similar to CsA, it is also a substrate of CYP3A4 and interacts with CsA

A

True

57
Q

Atorvastatin (lipid lowering agent) should not be used for CsA induced hyperlipidaemia as similar to CsA, it is also a substrate of CYP3A4 and interacts with CsA

A

True

58
Q

CsA may cause hypomagnesaemia

A

True

59
Q

CsA may cause hyperuricaemia and potentially gout

A

True

60
Q

Macrolide antibiotics (erythromycin, clarithromycin, azithromycin) may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4)

61
Q

Fluoroquinolones antibiotics (Ciprofloxacin) may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4)

62
Q

Cephalosporins may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4)

63
Q

Doxycycline may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4)

64
Q

Azole antifungals (ketoconazole, itraconazole, fluconazole) may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4)

65
Q

HIV-1 protease inhibitors (Ritonavir, Idinavir) may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4)

66
Q

Calcium channel blockers (Diltiazem, Verapamil) may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4) - but not nifedipine

67
Q

H2 antihistamines (cimetidine) may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4)

68
Q

Diuretics (thiazides, frusemide) may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4)

69
Q

Grapefruit juice may increase CsA levels due to CYP3A4 inhibition

A

True (CsA is metabolised by CYP3A4)

70
Q

Rifampicin may reduce CsA levels due to CYP3A4 induction

A

True (CsA is metabolised by CYP3A4)

71
Q

Carbamazepine may reduce CsA levels due to CYP3A4 induction

A

True (CsA is metabolised by CYP3A4)

72
Q

Phenytoin may reduce CsA levels due to CYP3A4 induction

A

True (CsA is metabolised by CYP3A4)

73
Q

Nephrotoxic drugs should be used with caution with CsA as this may potentiate renal toxicity

A

True

74
Q

ACE-inhibitors may increase the CsA risk of hyperkalaemia when used concurrently with CsA

A

True

75
Q

Potassium sparing diuretics may increase the CsA risk of hyperkalaemia when used concurrently with CsA

A

True

76
Q

Discontinuation of CsA should be gradual while an alternative therapy is instituted to reduce the risk of rebound in psoriasis disease activity

A

True (cases of pustular psoriasis when CsA stopped cold turkey)

77
Q

CsA is a very good clearing agent for psoriasis

A

True (The ideal sequential therapy approach is to use CsA first to induce clearing, followed by Acitretin with a slow onset of action as maintenance therapy)

78
Q

When converting Sandimmune to Neoral, a 1:1 dose conversion strategy is recommended even though Neoral is more readily absorbed than Sandimmune

A

True

79
Q

Warfarin may increase CsA levels due to competitive binding to CYP3A4 (both warfarin and CsA are CYP3A4 substrates)

A

True (CsA is also metabolised by CYP3A4)

80
Q

The overall ratio of bioavailability between Sandimmune and Neoral is 5:4

A

True

Derm Pharm 2020 (47 decks)

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