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Psychology- Pharm > Drugs to treat RA/Gout > Flashcards

Drugs to treat RA/Gout Flashcards

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1
Q

What three types of drugs are used to treat the acute joint pain in RA?

A

NSAIDS
Analgesics
Glucocorticoids

Provides symptomatic relief only

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2
Q

What two class of drugs used in the treatment of RA inhibit the progression of the disease?

A

Disease modifying anti-rheumatic drugs (DMARDS)

Biologic Response Modifiers (BRM)

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3
Q

What is the purpose of using NSAIDS, analgesics, and glucocorticoids in RA?

A

Minimize symptomatic effects while waiting for clinical effects of slow acting DMARDS and BRMs.

Used for ACUTE joint pain

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4
Q

List three analgesics used in the treatment of acute RA

A

Acetaminophen
Capsaicin
Opioids

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5
Q

List the four DMARDS.

A

hydroxychloroquine
sulfasalazine
methotrexate
leflunomide

Nonspecific inhibitors of the immune system

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6
Q

Name three anti-TNF drugs used in the treatment of RA

A

Etanercept
Adalimumab
Infliximab

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7
Q

Name two anti-cytokine drugs used in the treatment of RA

A

anakinra

tocilizumab

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8
Q

Name a drug used in the treatment of RA that inhibits T cells

A

abatacept

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9
Q

Name a drug used in the treatment of RA that inhibits B cells

A

Rituximab

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10
Q

Name a chemical inhibitor of cytokine signaling used in the treatment of RA

A

Tofacitinib

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11
Q

How long does it take before DMARDs are effective against RA?

A

slow acting

Takes weeks to months to show efficacy

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12
Q

What is the most commonly used DMARD?

A

Methotrexate

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13
Q

Name 5 of the less frequently used DMARDS in the treatment of RA

A 
Azathioprine
D-Penicillinamine
Gold Salts
Cyclosporine
Cyclophosphamide
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14
Q

What type of RA may be treated with hydroxycholoquine

A

Mild arthritis

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15
Q

Is hydroxychloroquine safe in pregnancy and lactation?

A

Yes

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16
Q

List a rare/serious side effect of hydroxychloroquine

A

Ocular toxicity–> can result in total blindness

Increased risk with age > 60, treatment > 5 years and high doses

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17
Q

Is sulfasalazine safe to use during pregnancy

A

Yes

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18
Q

What are adverse effects associated with sulfasalazine?

A

Agranulocytosis within 2 weeks (very rare)

Hepatotoxicity (fully reversible)

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19
Q

What is the time to effect of hydroxychloroquine?

A

3-6 months

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20
Q

What is the time to effect of sulfasalazine?

A

1-3 months

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21
Q

What is the MOA of sulfasalazine?

A

Unclear- thought to interfere with immune system activation through NF-kappa B

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22
Q

What is the active component of sulfasalazine?

A

sulfapyridine

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23
Q

Is sulfasalazine administrated as a monotherapy?

A

NO- generally given with hydroxychloraquine

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24
Q

What is the drug of choice for patients with active/severe RA?

A

Methotrexate

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25
Q

What is the effect of methotrexate in RA?

A

Reduces the rate of new bone erosions

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26
Q

How long does it take for the effects of methotrexate to begin?

A

4-6 months

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27
Q

What is the low dose MOA of methotrexate (as opposed to high dose MOA for cancer tx)

A

indirectly increases production of adenosine –> immunosuppressive properties

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28
Q

Why do patients on methotrexate need to avoid alcohol?

A

Methotrexate commonly causes dose-related hepatotoxicity

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29
Q

List three rare side effects of methotrexate that requires clinical monitering

A

Pulmonary toxicity
Bone marrow suppression
Risk of lymphoma

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30
Q

What is the metabolism of methotrexate?

A

80-90% excreted renally

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31
Q

Is methotrexate safe in pregnancy?

A

NO- it is actually used an as abortifactant

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32
Q

Methotrexate is contraindicated in patients with which two underlying diseases?

A

Liver disease

Renal impairment

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33
Q

What is the efficacy of leflunomide?

A

as effective as either sulfasalazine or methotrexate

Used as an alternative to methotrexate

34
Q

What is the time to onset for leflunomide?

A

1-2 months

35
Q

What is the MOA of leflunomide?

A

Inhibits dihydroorotate dehydrogenase –> inhibits uridine synthesis –> inhibits both T-cell proliferation and production of autoantibodies by B cells

36
Q

Which side effect of leflunomide requires monitoring?

A

Hepatotoxicity

Also associated with GI upset and HTN

37
Q

Is leflunomide safe during pregnancy?

A

No

38
Q

In general, how to BRMs work?

A

Specific inhibition of cytokines or B-cells/T-cells

39
Q

How do etanercept, infliximab and adalimumab work?

A

They are all antibodies against the TNF-alpha receptor

40
Q

What is the time to effect for Etanercept?

A

1-4 weeks

41
Q

Are the anti-TNF alpha drugs used as a monotherapy or in tandem with other drugs?

A

Used either as a monotherapy or combined with methotrexate

It is often added to patients who are not responding adequately to methotrexate

42
Q

List the adverse effects associated with the anti-TNFalpha drugs

A

Increased risk for bacterial and fungal infections
Reactivation of latent TB and latent HBV
Cannot be used for patients with a chronic infection

43
Q

List three rare but serious side effects of the anti-TNF alpha drugs

A

Exacerbation of heart disease
Onset of MS
Onset of lymphoma

44
Q

What is the MOA of abatacept?

A

binds with high affinity to CD80/CD86 (recombinant fusion protein of CTLA4)

–> inhibits T-cell activation by blocking CD28 co-stimulatory signals essential for T-cell activation

45
Q

WHen are patients given abatacept?

A

Patients who are non-responsive to TNF-alpha inhibitors

46
Q

What are the adverse effects associated with abatacept?

A

REactivation of latent TB and HBV

screen before administration

47
Q

Can any of the BRMs be combined with each other?

A

NO

Can only be given in combo with DMARD drugs

48
Q

What is the MOA of rituximab?

A

Binds CD20 on human B cells

–> depletes B cells from the blood

49
Q

How long do effects from a rituximab injection last?

A

Although onset of benefit is not seen for 3 months, the effect can last for up to 2 years with a single infusion

50
Q

Which patients receive rituximab?

A

Patients who are unresponsive to TNF alpha inhibitors

51
Q

Which is a rare adverse effect associated with rituximab?

A

PML (demyelinating disease associated with reactivation of the JC virus)

52
Q

What is the MOA of anakinra?

A

Inhibits IL-1 (decreases pro-inflammatory effects)

53
Q

What is the relative efficacy of IL-1 inhibitors (anakinra?)

A

Decreased efficacy as compared to anti- TNF alpha agents

Also must be given subQ daily

54
Q

Who should not receive anti-IL-1 (anakinra)/

A

patients with acute/chronic infections

Increased risk of infections/neutropenia

55
Q

What is MOA of tocilizumab?

A

IL-6 cytokine receptor antagonist

56
Q

Who receives tocilizumab?

A

Patients unresponsive to TNF inhibitors

May be used in combo with methotrexate

57
Q

What are unique adverse effects associated with Tocilizumab?

A

Bone marrow suppression

Increased hypercholesterolemia

58
Q

What is the MOA of Tofacitinib?

A

inhibits Jak tyrosine kinase

involved in immune cell cytokine signaling

59
Q

List the tx strategies for mild, moderate and severe RA

A

Mild: hydroxychloroquine or sulfasalazine or combo

Moderate: methotrexate (alt, leflunomide) or combo therapy of DMARDS + TNF alpha inhibitors

Severe: Switch to biologics

60
Q

Are tophi present in acute gout?

A

No- they form in chronic gout

61
Q

Which two drugs are used to relieve the symptoms of an acute gouty attack?

A

Colchicine

NSAIDS

62
Q

list two drugs that increase uric acid excretion

A

Probenecid

Lesinurad (newly approved)

63
Q

List two drugs that lower uric acid synthesis

A

Allopurinol

Febuxostat

64
Q

List a drug that directly degrades uric acid

A

Pegloticase

65
Q

Which two NSAIDS can induce gout?

A

Aspirin and salicylates – they inhibit uric acid secretion

66
Q

Is colchicine an analgesic?

A

No- antiinflammatory but no analgesic properties

67
Q

When is colchicine effective?

A

When given within the first 24-48 hours of an attack

Limited used due to side effects (GI upset)

68
Q

What is the MOA of colchacine?

A

Inhibits microtubule rearrangements –> inhibits leukocyte migration and phagocytosis

69
Q

What is the therapeutic window of colchicine?

A

Very narrow- leads to GI upset

70
Q

What is the MOA of probenecid?

A

Blocks the URATE1 ion transporter in the renal tubules –> decreased reabsorption and increased uric acid excretion

Most gout is due to underexcretion of uric acid

71
Q

When should probenecid NOT be administered?

A

Within 2-3 weeks following an acute gouty attack.

The drug will disrupt uric acid homeostasis and can increase risk of a second attack

Administer with prophylactic colchicine or NSAID

72
Q

In what type of patients is probenecid contraindicated?

A

In patients with increased uric acid synthesis

Probenecid will increase the risk of kidney stones

73
Q

What is the MOA of allopurinol and Febuxostat

A

Inhibitors of xanthine oxidase

Hypoxanthine cannot be converted to uric acid

74
Q

Patients with tophi should be treated with which drug?

A

Allopurinol (or febuxostat)

75
Q

What is the rare but potentially deadly side effect of allopurinol?

A

Rash, fever, hepatitis, eosinophilia and acute renal failure

Occurs in patients with pre-existing renal failure, patients taking excessive doses

NOT induced by febuxostat (which is 50% hepatic elimination)

76
Q

What race is more susceptible to the life threatening allopurinol side effect?

A

Thai, Korean, Han Chinese

77
Q

Allopurinol has a DDI with which two other drugs?

A

6-mercaptopurine and azathioprine

78
Q

What is the goal of treating chronic gout?

A

Reduce uric acid levels to <6 mg/dl

79
Q

How long do you treat someone with gout?

A

Life long - goal to prevent acute gouty attacks

80
Q

What is the MOA of pegloticase?

A

Pig enzyme that converts uric acid to allanatoin which can be readily excreted

81
Q

What are the downsides of pegloticase?

A

It must be administered by IV every two weeks, requires NSAID/colchicine prophylaxis

Self-limited as anti-drug antibodies may develop

Psychology- Pharm (7 decks)

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