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Pharm 3 Flashcards

1
Q

What’s the first line of treatment in RA?

A

methotrexate

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2
Q

How does methotrexate work?

A

inhibits dihydrofolate reductase leading to decreased folic acid supplies

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3
Q

Methotrexate MOA

A

decreases cell proliferation; increases apoptosis of T cells; increases adenosine release; alters expression of CAM; inhibits pro-inflammatory cytokies

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4
Q

SE of methotrexate

A

mucosal ulcers, stomatitis, nausea, diarrhea, alopecia, anemia

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5
Q

When is methotrexate contraindicated?

A

pregnancy

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6
Q

Dose for leflunomide?

A

10-20 mg qd after LD of 100 mg for 3 days

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7
Q

LD or leflunomide is associated with?

A

severe diarrhea and may be skipped

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8
Q

Leflunomide mechanism

A

inhibits mitochondrial dihydroorotate dehydrogenase (DHODH) ultimately resulting in decreased DNA and RNA in rapidly dividing cells

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9
Q

Leflunomide is approved for?

A

RA

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10
Q

SE of Leflunomide?

A

diarrhea, alopecia, elevated liver enzymes, weight gain, increased BP

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11
Q

Sulfasalazine dose

A

maintenance dose 1 gram bid-tid

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12
Q

SE of Sulfasalazine

A

N/V, HA, rash, rarely anemia and methemoglobinemia and neutropenia; reversible infertility in men but not women

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13
Q

Is Sulfasalazine ok in pregnancy?

A

yes

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14
Q

Hydroxychloroquine dosing

A

200 mg bid

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15
Q

What type of drug is Hydroxychloroquine

A

anti-malarial

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16
Q

How long is it to see an effect on Hydroxychloroquine

A

3-6 months

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17
Q

Does Hydroxychloroquine impact bone changes in RA?

A

no

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18
Q

SE of Hydroxychloroquine

A

retinal damage if doses exceed 6 mg/kg/day, GI issues, rash, nightmares

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19
Q

Is Hydroxychloroquine safe in pregnancy?

A

Yes

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20
Q

Hydroxychloroquine and diabetes?

A

may improve glucose profiles in diabetic patients and lower A1c

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21
Q

Hydroxychloroquine and cardiac risk?

A

LDL, HDL, TG improvement

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22
Q

Ultimately how does Hydroxychloroquine help RA?

A

helps symptomatically, but not with bone changes

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23
Q

Tofacitinib dose

A

5 mg bid

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24
Q

What type of drug is Tofacitinib

A

Janus Kinase Inhibitor–suppresses immune response

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25
Q

When is Tofacitinib used?

A

in combo with MTX or alone in moderate to severe disease where MTX failed or cannot be used

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26
Q

When does Tofacitinib dose need to be decreased to 5 mg qd?

A

if patient is on a CYP3A4 or CYP2C9 inhibitors or has moderate to severe renal or liver impairment

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27
Q

Does Tofacitinib decrease joint damage?

A

no

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28
Q

Avoid Tofacitinib in conjunction with?

A

immunosuppressants and live vaccines

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29
Q

Tofacitinib SE?

A

HA, diarrhea, URI, rarely GI perforation

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30
Q

Examples of anti-TNF agents

A

etanercept, infliximab, adalimumab, certolizumab, golimumab

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31
Q

Examples of non-TNF agents

A

abatacept, rituximab, tocilizumab

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32
Q

SE of TNF-alpha inhibitors

A

injection site reaction, infection, new onset psoriasis, increased risk of leukemia and lymphoma

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33
Q

Contraindications for TNF-alpha inhibitors

A

presence of serious or recurrent infections

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34
Q

TNF-alpha inhibitors should be avoided in?

A

patients with class III or higher HF and EF less than 50% as well as patients with demyelinating diseases

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35
Q

What happens if a patient needs TNF-alpha inhibitor therapy?

A

meds must be held for duration of treatment

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36
Q

What should patients be tested for prior to starting a TNF-alpha inhibitor?

A

TB

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37
Q

Types of non-TNF agents

A

B cell depleters, t cell co-stimulation inhibitors, IL-6 inhibitors

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38
Q

SE of B cell depleters

A

infusion reactions, rash (30%) with first infusion then decreases with subsequent infusions

39
Q

Contraindications of B cell depleaters

A

presence of serious or recurrent infection, type 1 allergic reactions to murine proteins

40
Q

T cell co-stimulation inhibitors SE

A

infusion, reactions, increased risk of lymphoma

41
Q

Contraindications of T cell co-stimulation inhibitors

A

presence of serious or recurrent infection

42
Q

IL-6 inhibitors SE

A

infusion reactions, infection, increased lipids, URI, HA, HTN, elevated liver enzymes, decreased neutrophils, decreased platelets, GI perforation (esp in diverticulitis and on corticosteroids)

43
Q

What should patients be screened for before staring an IL-6 inhibitors?

44
Q

Which two drugs may decrease risk of diabetes?

A

hydroxychloroquine and TNF inhibitors

45
Q

Pregnancy is a contraindication for which two drugs?

A

MTX and leflunomide

46
Q

When are biologics recommended?

A

only after nonbiologic failure in patient with poor prognosis or failure of two nonbiologic regimens in patients without poor prognosis; given with MTX

47
Q

What are our four drugs for acute gout treatment?

A

fast-acting NSAIDs, Cox-2 inhibitors, corticosteroids, colchicine

48
Q

First line therapy for acute gout?

A

Fast-acting NSAIDs

49
Q

Fast-acting NSAID examples

A

indomethacin, naproxen, sulindac

50
Q

When do you begin fast-acting NSAIDs during an acute gout attack?

A

first 24 hours

51
Q

Dosing for fast-acting NSAID for gout

A

High dose for 2-3 days then step down over 2 weeks and continue for 2 days after resolution

52
Q

Issue with cox-2 inhibitors?

A

increased CV risk

53
Q

How are corticosteroids administered in acute gout?

A

Intra-articular injection is highly effective in large joints and when limited to one or two locations; could do oral for small joints

54
Q

Issue with indomethacin?

A

can cause CNS issues in the elderly

55
Q

Colchicine MOA

A

binds intracellular tubulin ultimately leading to inhibition of leukocyte migration and phagocytosis -> anti-inflammatory effects

56
Q

Common colchicine dose?

A

0.6 mg qd-bid

57
Q

What are our two xanthine oxidase inhibitors?

A

allopurinol, febuxostat

58
Q

What is the standard of care for chronic gout?

A

allopurinol

59
Q

allopurinol dose

A

100 mg qd then increase 100 mg qd every 1-4 weeks until goal serum level is reached (lower dose for renal disease)

60
Q

When do you start allopurinol for gout?

A

Give with NSAID or colchicine initially until uric acid levels are less than 6 mg/dl then slowly D/C (over months)

61
Q

SE of allopurinol?

A

GI disturbance, HA, rash, rarely cataracts, aplastic anemia, peripheral neuritis

62
Q

Does allopurinol work in an acute attack?

63
Q

Febuxostat dosage

A

40-80 mg qd; in clinical trials, 80-120 mg was more effective at lowering uric acid than 300 mg allopurinol regardless of overproduction or underexcretion

64
Q

What should you use febuxostat with?

A

NSAID or colchicine

65
Q

SE of febuxostat

A

elevated LFTs, diarrhea, HA, nausea

66
Q

What’s the concern with febuxostat

A

cardiovascular events in higher doses

67
Q

Metabolism of febuxostat

A

liver, so no need for renal adjustment

68
Q

urate oxidase enzyme example

A

pegloticase

69
Q

What is pegloticase?

A

recombinant mammalian uricase attached to PEG

70
Q

MOA of pegloticase

A

Catalyzes oxidation of uric acid to allantoin (inert and soluble)

71
Q

Dosing of pegloticase

A

Given as IV infusion every 2 weeks; optimal length of treatment not established

72
Q

what should be given with pegloticase?

A

NSAID or colchicine prophylaxis needed for first 6 months of treatment

73
Q

SE of pegloticase

A

infusion reactions (premed with antihistamine and corticosteroid), gout flares, nausea, bruising

74
Q

You should not use pegloticase in who?

A

Do not use in G6PD deficiency; screening of patients of African and Mediterranean decent recommended

75
Q

What happens with the immune system and pegloticase?

A

Patients will develop immune response to pegloticase (92%) – increased risk of infusion reactions seen as well as decreased efficacy

76
Q

Drugs that cause gout

A

thiazides, niacin, levodopa, cyclosporine, aspirin

77
Q

Lupus drugs

A

hydroxychloroquine, NSAIDs, immunosuppressants and corticosteroids, biologics

78
Q

Hydroxychloroquine does what for lupus

A

decreases flare ups

79
Q

Efficacy of hydroxychloroquine decreases with

80
Q

When are immunosuppressants and corticosteroids used for in lupus?

A

serious or life threatening lupus

81
Q

Examples of lupus biologics

A

belimumab, rituximab

82
Q

Which biologic is useful in decreasing symptoms in mild lupus

83
Q

which biologic is useful in resistant lupus

84
Q

What % of lupus is drug induced lupus

85
Q

Does drug-induced lupus resolve?

A

Typically resolves after drug d/c but may take weeks to months

86
Q

Common drug induced lupus agents

A

hydralazine, procainamide, isoniazid, methyldopa, quinidine, minocycline, chlorpromazine

87
Q

Age differences in SLE vs DILE

A

SLE age 20-40; DILE 50

88
Q

sex differences in SLE vs DILE

A

SLE: women DILE: both

89
Q

onset differences in SLE vs DILE

A

SLE: gradual; DILE: sudden

90
Q

severity differences in SLE vs DILE

A

SLE: can be severe; DILE: remains mild

91
Q

Hepatomegaly differences in SLE vs DILE

A

SLE: hepatomegaly less common; DILE: hepatomegaly common

92
Q

anti-double strand DNA antibody differences in SLE vs DILE

A

SLE: 50-70%; DILE: rare

93
Q

anti-smith differences in SLE vs DILE

A

SLE: 20-30%; DILE: rare

94
Q

hypocomplimentemia differences in SLE vs DILE

A

SLE: 50-60%; DILE: rare

Clinical Medicine (13 decks)

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