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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
What is the effect of methotrexate in RA?
Reduces the rate of new bone erosions
26
How long does it take for the effects of methotrexate to begin?
4-6 months
27
What is the low dose MOA of methotrexate (as opposed to high dose MOA for cancer tx)
indirectly increases production of adenosine --> immunosuppressive properties
28
Why do patients on methotrexate need to avoid alcohol?
Methotrexate commonly causes dose-related hepatotoxicity
29
List three rare side effects of methotrexate that requires clinical monitering
Pulmonary toxicity Bone marrow suppression Risk of lymphoma
30
What is the metabolism of methotrexate?
80-90% excreted renally
31
Is methotrexate safe in pregnancy?
NO- it is actually used an as abortifactant
32
Methotrexate is contraindicated in patients with which two underlying diseases?
Liver disease | Renal impairment
33
What is the efficacy of leflunomide?
as effective as either sulfasalazine or methotrexate Used as an alternative to methotrexate
34
What is the time to onset for leflunomide?
1-2 months
35
What is the MOA of leflunomide?
Inhibits dihydroorotate dehydrogenase --> inhibits uridine synthesis --> inhibits both T-cell proliferation and production of autoantibodies by B cells
36
Which side effect of leflunomide requires monitoring?
Hepatotoxicity Also associated with GI upset and HTN
37
Is leflunomide safe during pregnancy?
No
38
In general, how to BRMs work?
Specific inhibition of cytokines or B-cells/T-cells
39
How do etanercept, infliximab and adalimumab work?
They are all antibodies against the TNF-alpha receptor
40
What is the time to effect for Etanercept?
1-4 weeks
41
Are the anti-TNF alpha drugs used as a monotherapy or in tandem with other drugs?
Used either as a monotherapy or combined with methotrexate It is often added to patients who are not responding adequately to methotrexate
42
List the adverse effects associated with the anti-TNFalpha drugs
Increased risk for bacterial and fungal infections Reactivation of latent TB and latent HBV Cannot be used for patients with a chronic infection
43
List three rare but serious side effects of the anti-TNF alpha drugs
Exacerbation of heart disease Onset of MS Onset of lymphoma
44
What is the MOA of abatacept?
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
WHen are patients given abatacept?
Patients who are non-responsive to TNF-alpha inhibitors
46
What are the adverse effects associated with abatacept?
REactivation of latent TB and HBV screen before administration
47
Can any of the BRMs be combined with each other?
NO Can only be given in combo with DMARD drugs
48
What is the MOA of rituximab?
Binds CD20 on human B cells --> depletes B cells from the blood
49
How long do effects from a rituximab injection last?
Although onset of benefit is not seen for 3 months, the effect can last for up to 2 years with a single infusion
50
Which patients receive rituximab?
Patients who are unresponsive to TNF alpha inhibitors
51
Which is a rare adverse effect associated with rituximab?
PML (demyelinating disease associated with reactivation of the JC virus)
52
What is the MOA of anakinra?
Inhibits IL-1 (decreases pro-inflammatory effects)
53
What is the relative efficacy of IL-1 inhibitors (anakinra?)
Decreased efficacy as compared to anti- TNF alpha agents Also must be given subQ daily
54
Who should not receive anti-IL-1 (anakinra)/
patients with acute/chronic infections Increased risk of infections/neutropenia
55
What is MOA of tocilizumab?
IL-6 cytokine receptor antagonist
56
Who receives tocilizumab?
Patients unresponsive to TNF inhibitors May be used in combo with methotrexate
57
What are unique adverse effects associated with Tocilizumab?
Bone marrow suppression | Increased hypercholesterolemia
58
What is the MOA of Tofacitinib?
inhibits Jak tyrosine kinase | involved in immune cell cytokine signaling
59
List the tx strategies for mild, moderate and severe RA
Mild: hydroxychloroquine or sulfasalazine or combo Moderate: methotrexate (alt, leflunomide) or combo therapy of DMARDS + TNF alpha inhibitors Severe: Switch to biologics
60
Are tophi present in acute gout?
No- they form in chronic gout
61
Which two drugs are used to relieve the symptoms of an acute gouty attack?
Colchicine | NSAIDS
62
list two drugs that increase uric acid excretion
Probenecid | Lesinurad (newly approved)
63
List two drugs that lower uric acid synthesis
Allopurinol | Febuxostat
64
List a drug that directly degrades uric acid
Pegloticase
65
Which two NSAIDS can induce gout?
Aspirin and salicylates -- they inhibit uric acid secretion
66
Is colchicine an analgesic?
No- antiinflammatory but no analgesic properties
67
When is colchicine effective?
When given within the first 24-48 hours of an attack Limited used due to side effects (GI upset)
68
What is the MOA of colchacine?
Inhibits microtubule rearrangements --> inhibits leukocyte migration and phagocytosis
69
What is the therapeutic window of colchicine?
Very narrow- leads to GI upset
70
What is the MOA of probenecid?
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
When should probenecid NOT be administered?
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
In what type of patients is probenecid contraindicated?
In patients with increased uric acid synthesis Probenecid will increase the risk of kidney stones
73
What is the MOA of allopurinol and Febuxostat
Inhibitors of xanthine oxidase Hypoxanthine cannot be converted to uric acid
74
Patients with tophi should be treated with which drug?
Allopurinol (or febuxostat)
75
What is the rare but potentially deadly side effect of allopurinol?
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
What race is more susceptible to the life threatening allopurinol side effect?
Thai, Korean, Han Chinese
77
Allopurinol has a DDI with which two other drugs?
6-mercaptopurine and azathioprine
78
What is the goal of treating chronic gout?
Reduce uric acid levels to <6 mg/dl
79
How long do you treat someone with gout?
Life long - goal to prevent acute gouty attacks
80
What is the MOA of pegloticase?
Pig enzyme that converts uric acid to allanatoin which can be readily excreted
81
What are the downsides of pegloticase?
It must be administered by IV every two weeks, requires NSAID/colchicine prophylaxis Self-limited as anti-drug antibodies may develop

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