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Derm Pharm 2020 > 1 - METHOTREXATE > Flashcards

1 - METHOTREXATE Flashcards

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Dermatology Board Prep flashcards
1
Q

Methotrexate is a chemotherapeutic agent

A

True (cytotoxic and teratogenic)

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2
Q

Methotrexate is an immunosuppressive agent

A

True

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3
Q

MTX is often used with TNF-alpha antagonists

A

True (FDA approved in patients with arthritis)

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4
Q

Methotrexate is a potential competitive antagonist and inhibitor of dihydrofolate reductase

A

True

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5
Q

Methotrexate is structurally similar to folic acid

A

True

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6
Q

Folic acid is the natural substrate for the enzyme dihydropteroate synthetase and dihydrofolate reductase

A

True

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7
Q

Methotrexate can be administered orally

A

True

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8
Q

Methotrexate can be administered intravenously

A

True

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9
Q

Methotrexate can be administered intramuscularly

A

True

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10
Q

Methotrexate can be administered subcutaneously

A

True

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11
Q

Methotrexate is rapidly absorbed through the GI tract

A

True

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12
Q

Peak plasma levels of orally administered Methotrexate are reached more slowly than intravenous or subcutaneous/intramuscular route

A

True

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13
Q

The oral route of Methotrexate provides more reliable blood levels than parenteral administration even though the absorption of oral methotrexate may be incomplete and variable with doses > 15mg

A

True

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14
Q

Concurrent food intake, particularly milk-based meals may reduce bioavailability in children

A

True (though bioavailability in adults is not affected by concurrent food ingestion)

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15
Q

The bioavailability of methotrexate in adults is not affected by concurrent food ingestion

A

True

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16
Q

The absorption of methotrexate may be reduced by non-absorbable antibiotics such as neomycin

A

True

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17
Q

Methotrexate does not penetrate the blood brain barrier well

A

True (the reason why intrathecal methotrexate is needed in some chemotherapy regimens)

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18
Q

The level of plasma Methotrexate once absorbed, has a triphasic reduction

A

True

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19
Q

The first phase of the triphasic reduction of plasma methotrexate occurs rapidly over 0.75 hours and reflects distribution of the drug throughout the body

A

True

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20
Q

The second phase of the triphasic reduction of plasma methotrexate occurs over 2-4 hours and reflects renal excretion

A

True

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21
Q

The third phase of the triphasic reduction of plasma methotrexate occurs between 10 and 27 hours and reflects the terminal half life and slow release of methotrexate primarily bound to dihydrofolate reductase from the tissues

A

True

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22
Q

Methotrexate is a weak organic acid and is excreted through the kidneys

A

True

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23
Q

Methotrexate is a weak organic acid predominately excreted through the kidneys; MTX glomerular filtration and active tubular secretion are susceptible to drug interactions with other weak acids I.e. Salicylates, probenecid, and sulfonamides

A

True

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24
Q

Approx 50% of methotrexate is bound to plasma proteins and 50% is the unbound free fraction/active portion of the drug

A

True

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25
Q

The beneficial effects and potential for toxicity is increased when the unbound free fraction of methotrexate is increased by certain drugs I.e. Salicylates, sulfonamides, probenecid

A

True

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26
Q

Methotrexate is metabolised intracellularly in all cells that it is actively transported into, including the liver

A

True

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27
Q

Methotrexate is metabolised intracellularly to polyglutamated forms/metabolites which are potent inhibitors of dihydrofolate reductase and play a key role in methotrexate toxicity

A

True

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28
Q

The polyglutamated metabolites of intracellular methotrexate metabolism contributes toward methotrexate toxicity

A

True (the metabolites are also dihydrofolate reductase inhibitors)

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29
Q

Methotrexate has a greater affinity to dihydrofolate reductase than the enzyme’s natural substrate folic acid

A

True

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30
Q

Folic acid (natural substrate of dihydrofolate reductase) is converted to tetrahydrofolate by dihydrofolate reductase

A

True

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31
Q

Tetrahydrofolate is converted to DNA by thymidylate synthetase

A

True

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32
Q

Methotrexate competitively and irreversibly binds to dihydrofolate reductase with a greater affinity than folic acid

A

True (prevents conversion of dihydrofolate to tetrahydrofolate)

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33
Q

Methotrexate prevents the conversion of dihydrofolate to tetrahydrofolate by competitively and irreversibly binding to dihydrofolate reductase

A

True

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34
Q

Methotrexate also competitively and partially reversibly inhibits thymidylate synthetase within 24 hours of methotrexate administration to prevent thymidine and purine nucleotide synthesis to take place from tetrahydrofolate

A

True (affects DNA synthesis)

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35
Q

The overall effect of methotrexate is inhibition of DNA synthesis/cell division which takes place during the S phase of the cell cycle

A

True

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36
Q

The competitive and irreversible inhibition of dihydrofolate reductase by methotrexate can be bypassed by Leucovorin (folinic acid)

A

True (thus folinic rescue may reverse the acute haematologic toxicity secondary to methotrexate)

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37
Q

Leucovorin (folinic acid) may reverse the acute haematologic toxicity secondary to methotrexate

A

True

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38
Q

Methotrexate acts via an immunosuppressive mechanism by affecting the proliferation of lymphocytes

A

True

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39
Q

Methotrexate affects the proliferation of lymphocytes

A

True

40
Q

Methotrexate blocks migration of activated T cells

A

True

41
Q

The anti-inflammatory effects of methotrexate are predominately mediated by adenosine

A

True

42
Q

There is decrease methotrexate efficacy with concomitant folic acid

A

True (folic acid is no longer routinely recommended unless adverse effects arise I.e. GI upset or haematologic toxicity

43
Q

The use of folic acid as a method of inhibiting Methotrexate induced GI adverse effects and pancytopenia is controversial

A

True

44
Q

Salicylates increase methotrexate levels and toxicity due to decreased renal excretion and displacement from plasma proteins

A

True

45
Q

NSAIDS increase methotrexate levels and toxicity due to decreased renal excretion and displacement from plasma proteins

A

True

46
Q

Sulfonamides increase methotrexate levels and toxicity due to decreased renal excretion, displacement from plasma proteins and inhibition of dihydropteroate synthetase (converts folic acid to dihydrofolate)

A

True

47
Q

Probenecid increase methotrexate levels and toxicity due to increased intracellular accumulation and decreased renal excretion

A

True

48
Q

Dipyridamole increase methotrexate levels and toxicity due to increased intracellular accumulation

A

True

49
Q

Chloramphenicol increase methotrexate levels and toxicity due to displacement from plasma proteins

A

True

50
Q

Phenothiazines increase methotrexate levels and toxicity due to displacement from plasma proteins

A

True

51
Q

Phenytoin increase methotrexate levels and toxicity due to displacement from plasma proteins

A

True

52
Q

Tetracyclines increase methotrexate levels and toxicity due to displacement from plasma proteins

A

True

53
Q

Trimethoprim inhibits dihydrofolate reductase (coverts dihydrofolate to tetrahydrofolate) in the folate pathway resulting in increased haematologic toxicity

A

True (methotrexate and trimethoprim are competitive inhibitors of dihydrofolate reductase)

54
Q

Folic acid is also converted to dihydrofolate by dihydropteroate synthetase

A

True (and folic acid can be converted to tetrahydrofolate by dihydrofolate reductase)

55
Q

Dapsone and sulfonamides inhibit dihydropteroate synthetase (coverts folic acid to dihydrofolate) and thus can amplify the inhibition of dihydrofolate reductase by methotrexate due to less dihydrofolate being available to the enzyme, resulting in increased haematologic toxicity

A

True

56
Q

Therapeutic doses of folic acid competes with methotrexate for dihydrofolate reductase to decrease the adverse effects of methotrexate by increasing tetrahydrofolate production

A

True

57
Q

Systemic retinoids may synergistically increase hepatotoxicity if given concomitantly with methotrexate due to the liver being the common target organ for toxicity in both drugs

A

True

58
Q

Alcohol may synergistically increase hepatotoxicity if given concomitantly with methotrexate due to the liver being the common target organ for toxicity in both drugs

A

True

59
Q

Trimethoprim and sulphamethoxazole in combination markedly increase the risk of haematologic toxicity when used with methotrexate due to a more complete inhibition of 2 step folate pathway

A

True (trimethoprim inhibits dihydrofolate reductase, and sulphamethoxazole being a sulfonamide inhibits dihydropteroate synthetase)

60
Q

Methotrexate is absolutely contraindicated in pregnancy

A

True (category X)

61
Q

Methotrexate may cause hepatotoxicity in the form of liver fibrosis

A 
True (procollagen type III peptide non-invasive test) 
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
62
Q

Methotrexate may cause infections

A 
True
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
63
Q

Methotrexate may cause idiosyncratic acute pneumonitis and pulmonary fibrosis with small doses of methotrexate

A 
True (CXR only if patient develops symptoms suggesting penumonitis)
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
64
Q

Methotrexate may cause pancytopenia

A 
True (risk significantly reduced by folic acid supplementation, consider supplementation regardless of whether patient is experiencing GI side effects)
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
65
Q

Poor renal function may precipitate haematologic toxicity associated with methotrexate

A

True (due to increased free methotrexate in plasma) - avoid combining trimethoprim/sulphamethoxazole and NSAIDS with methotrexate and consider folic acid supplementation regardless of whether the patient is experiencing GI side effects

66
Q

Folic acid supplementation is usually given to improve the GI side effects associated with methotrexate

A

True

67
Q

Regardless of whether GI side effects are present, consider folic acid supplementation to reduce the risk of pancytopenia associated with methotrexate

A

True

68
Q

Should significant myelosuppression develop from methotrexate, Leucovorin (folinic acid) can be given promptly to treat this

A

True

69
Q

Patients who inadvertently take methotrexate daily are at a greater risk for pancytopenia

A

True

70
Q

A high MCV without anaemia is common in dermatologic dosage levels of methotrexate

A

True (not a cause for concern)

71
Q

Lymphoma has been reported in patients with psoriasis on methotrexate

A 
True (although EBV has been found within these lymphomas and demonstrated regression of the lymphoma with cessation of methotrexate, there is no statistical evidence that methotrexate increases the risk of developing a subsequent malignancy in psoriasis patients)
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
72
Q

The subject of folic acid compromising efficacy of methotrexate remains contradictory due to mixed reports

A

True

73
Q

Nausea and anorexia are common adverse reactions to methotrexate

A 
True
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
74
Q

Diarrhoea, vomiting and ulcerative stomatitis are less frequent adverse effects of methotrexate

A 
True 
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
75
Q

Methotrexate should be ceased if diarrhoea and ulcerative stomatitis is observed

A 
True
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
76
Q

Men on methotrexate should be counselled with regard to possible reversible oligospermia

A

True

77
Q

Men on methotrexate should avoid impregnating a woman

A

True (although a recent study did not reveal any congenital malformations or spontaneous abortions associated with these men)

78
Q

In dermatological doses, methotrexate is not likely to cause renal toxicity

A 
True (encountered in the higher doses used in chemotherapy secondary to precipitation of methotrexate in renal tubules)
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
79
Q

Methotrexate is phototoxic

A 
True (may cause phototoxicity and sunburn recall)
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
80
Q

Methotrexate may cause sunburn recall

A 
True 
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
81
Q

Deaths due to methotrexate induced cirrhosis have occurred in patients with psoriasis

A 
True 
L - Liver toxicity
I - Infections
M - Marrow suppression/Malignancy
I - Idiopathic pulmonary fibrosis
T - Teratogenecity
G - GI effects 
P - Phototoxicity
S - Sunburn recall
82
Q

Patients with diabetes or obesity are presumed to be at greater risk for liver toxicity

A

True (increased incidence of non-alcoholic steatohepatitis in this group) - avoid prescribing methotrexate

83
Q

Patients with history of exposure to hepatotoxins I.e. Alcohol or IV drugs are presumed to be at greater risk for liver toxicity

A

True (avoid prescribing methotrexate)

84
Q

Avoid prescribing methotrexate in patients with personal or family history of liver disease

A

True (higher risk of hepatoxicity)

85
Q

Patients with abnormal baseline LFTs or hepatitis serology are presumed to be at greater risk for liver toxicity

A

True (avoid prescribing methotrexate)

86
Q

The need for repeated liver biopsies is based on the total dose of methotrexate - generally after every 1.5g total dose

A

True

87
Q

Patients with grade I (normal vs mild fatty infiltration) or II (moderate to severe fatty infiltration) liver histology findings may continue methotrexate

A

True

88
Q

Patients with grade IIIa (mild fibrosis) liver histology findings may continue methotrexate but should have a repeat liver biopsy in 6 months

A

True

89
Q

Patients with grade IIIb (moderate to severe liver fibrosis) or IV (cirrhosis) liver histology findings need to stop methotrexate

A

True (also needs careful follow up of liver biopsies)

90
Q

If the WBC count is <3500/mm3, discontinue or reduce the dose of methotrexate

A

True (methotrexate may be restarted at a lower dose if the lab abnormality has resolved after 2-3 weeks)

91
Q

If the platelet count is <100,000 /mm3, discontinue or reduce the dose of methotrexate

A

True (methotrexate may be restarted at a lower dose if the lab abnormality has resolved after 2-3 weeks)

92
Q

If the liver transaminases increase over twice the upper normal value, discontinue or reduce the dose of methotrexate

A

True (methotrexate may be restarted at a lower dose if the lab abnormality has resolved after 2-3 weeks)

93
Q

Methotrexate is usually given as a single weekly dose

A

True

94
Q

Methotrexate may be given in 3 divided doses over a 24 hour period each week I.e. Day 1 8am and 8pm followed by Day 2 8am

A

True (equally effective with similar toxicity to the once weekly dose)

95
Q

Intramuscular methotrexate may be considered in patients non-compliant to the oral dose or patients who develop nausea from the oral dose

A

True

96
Q

A methotrexate test dose of 5-10mg is generally given followed by a FBC and LFTs 6-7 days later

A

True

97
Q

Patients receiving IM or IV methotrexate are able to tolerate higher doses due to more rapid renal clearance

A

True

Derm Pharm 2020 (47 decks)

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