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FMS > MSCT Week 3: Pharmacotherapy for RA and Gout > Flashcards

MSCT Week 3: Pharmacotherapy for RA and Gout Flashcards

1
Q

Drug classes commonly used to treat rheumatoid arthritis

5 Listed

A
  • NSAIDs
  • Disease-modifying antirheumatic drugs (DMARDs)
  • Biologics/cytokine blockers
  • Inhibitors of T cell activation
  • Inhibitors of B cell function
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2
Q

DMARDs AKA

A

Disease-modifying antirheumatic drugs

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3
Q

Non-selective COX inhibitors vs selective COX-2 inhibitors in RA

A

COX-2 inhibitors reduce the incidences of these side-effects by 50% (GI perforations, ulcers, bleeds)

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4
Q

Disease-Modifying Antirheumatic Drugs Classes

5 Listed

A
  • Antineoplastic agents
  • Antimalarial agents
  • Chelating Agent
  • Immunosuppressives
  • Mechanism-targeted inhibitors
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5
Q

Disease-Modifying Antirheumatic Drugs: Antineoplastic Agents

A

Methotrexate

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6
Q

Disease-Modifying Antirheumatic Drugs: Antimalarial agents

A

Hydroxychloroquine

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7
Q

Disease-Modifying Antirheumatic Drugs: Chelating Agents

A

Penicillamine

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8
Q

Disease-Modifying Antirheumatic Drugs: Immunosuppressives

10 listed

A
  • cyclosporin
  • glucocorticoids
  • etanercept
  • infliximab
  • anakinra
  • abatacept
  • rituximab
  • leflunomide
  • gold salts
  • azathioprine
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9
Q

Methotrexate drug class

A

Antineoplastic agents

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10
Q

Methotrexate mechanism and mechanism in RA

A
  • Folate antagonist
  • exerts cytotoxic effects
  • mechanism of anti-inflammatory activity in RA is uncertain; it may inhibit T cell activation and/or suppress the expression of adhesion molecules on T cells
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11
Q

Methotrexate Excretion

A
  • 80-90% excreted unchanged in the urine
  • t1/2 is influenced by the glomerular filtration rate
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12
Q

Methotrexate common side effects for doses to treat RA

6 listed

A
  • N/V
  • mouth sores
  • headache
  • fatigue
  • alopecia
  • rash
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13
Q

Methotrexate Severe Side Effects

3 listed

A
  • Life-threatening hepatotoxicity
  • pulmonary damage
  • myelosuppression
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14
Q

Hydrochloroquine Drug Class

A

Antimalarial Agents

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15
Q

Hydrochloroquine MOA

2 listed

A

Mechanism in treating RA is uncertain but possibilities are;

  • Inhibition of Toll-like Receptors (esp. TLR-9)
  • Block antigen processing in macrophages and presentation of antigen-MHC complex to CD4+ T cells
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16
Q

Hydroxychloroquine efficacy in RA

3 listed

A
  • Relatively low efficacy as an antirheumatic agent
  • commonly combined with other therapies
  • onset of therapeutic effects is relatively slow
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17
Q

identify proinflammatory cytokines and anti-inflammatory

A
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18
Q
  • Infliximab
  • Adalimumab
  • etanercept
  • anakinra
  • ustekinumab
  • guselkumab
  • secukinumab
  • ixekizumab

Drug class

A

Cytokine blockers

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19
Q

Inhibitors of TNF-α

3 listed

A
  • Infliximab
  • adalimumab
  • etanercept
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20
Q

Inhibitor of IL-1 Function

A

Anakinra

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21
Q

Inhibitor of IL-12 and IL-23

A

Ustekinumab

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22
Q

Inhibitor of IL-23

A

Guselkumab

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23
Q

Inhibitor of IL-17A

2 listed

A
  • Secukinumab
  • ixekzumab
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24
Q

Biosimilar Examples

6 listed

A

Etanercept-szzs

Adalimumab-atto

adalimumab-adbm

infliximab-dyyb

infliximab-qbtx

infliximab-abda

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25
Q

A biosimilar product is?

A

chemically similar to FDA-approved biological product and is clinically similar to the approved product in terms of safety, purity and effectiveness

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26
Q

The pharmacokinetic properties of a biosimilar product…

A

Must be similar to those of the approved product

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27
Q

An important consideration of the clinical immunogenicity

A

incidence and severity of human immune response of the biosimilar product

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28
Q

Anti-TNF agents

3 listed

A

Infliximab

etanercept

adalimumab

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29
Q

Infliximab

A
  • biosimilar
  • a chimeric (human constant regions and mouse variable regions) anti-TNF-α monoclonal antibody
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30
Q

Infliximab drug class

A

Anti-TNF Agents

biosimilar

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31
Q

Etanercept description

A

Human TNF receptor linked to the Fc portion of human IgG1

Biosimilar

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32
Q

Etanercept drug class

A
  • Anti-TNF agents
  • biosimilar
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33
Q

Adalimumab description

A

Human monoclonal Ab specific for TNF-α

biosimilar

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34
Q

Adalimumab Drug class

A
  • Anti-TNF agents
  • Biosimilar
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35
Q

Infliximab Pharmacokinetics

A
  • IV
  • administer at 0, 2 and 6 weeks, then every 8 weeks
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36
Q

Entanercept Pharmacokinetics

A

Given 2X/week, SC

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37
Q

Adalimumab Pharmacokinetics

A
  • Given 1X every other week
  • peak plasma concentration 131+-56 hrs after administration
  • t1/2 = 14 days
  • methotrexate reduces clearance
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38
Q

Adalimumab clearance is reduced by?

A

Methotrexate

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39
Q

Untoward effects of Anti-TNF therapy

6 considerations

A
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40
Q

Autoimmune diseases successfully treated with Anti-TNF therapy

A

7 listed

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41
Q

ACR50 vs 20 in Anti-TNF therapy

A
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42
Q

Anakinra description

A

A recombinant nonglycosylated synthetic form of the human IL-1 receptor antagonist (IL-1Ra) an endogenous regulator of IL-1 action

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43
Q

Anakinra Indications

A
  • FDA approved to treat RA and neonatal-onset multisystem inflammatory disease (NOMID)
  • Not FDA approved but sometimes used for systemic juvenile idiopathic arthritis, adult-onset Still’s Disease, Gout, Calcium pyrophosphate deposition (Pseudogout), Behcet’s disease, ankylosing spondylitis, Uveitis, auto-inflammatory syndromes
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44
Q

Ustekinumab description

A

Inhibitor of IL-12 and IL-23

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45
Q

Ustekinumab Indications

A
  • Indicated for the treatment of psoriatic arthritis in adults
  • administered alone or in combination with methotrexate
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46
Q

Ustekinumab Adverse effects

A

upper respiratory infection

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47
Q

Abatacept description

A
  • Fusion protein of the extracellular domain of the CTLA4 molecule and the Fc domain of human IgG1
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48
Q

Abatacept MOA

A

Blocks the costimulatory signal required for T cell activation

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49
Q

Abatacept Indications

A

approved for patients who do not respond well to methotrexate and for patients who do not respond to or cannot tolerate TNF antagonists

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50
Q

Abatacept Dosage

A
  • 30-minute infusion given at 2 and 4 weeks after the first infusion, then every 4 weeks thereafter
  • Fixed-dose approximately 10 mg/kg based on weight range throughout the course of treatment
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51
Q

Abatacept Mechanism Diagram

A
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52
Q

Rituximab Description

A
  • Inhibitor of B cell function
  • A chimeric murine/human mAb against the CD20 antigen found on the surface of normal and malignant B lymphocytes
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53
Q

Rituximab MOA

A

Include complement-mediated cytotoxicity and antibody-dependent cell-mediated cytotoxicity

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54
Q

Rituximab indications

A
  • Approved only for patients that fail to respond to anti-TNF-α therapy.
  • Also approved for the treatment of non-Hodgkin’s Lymphoma
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55
Q

Rituximab Dosage

A
  • Two-1000 mg IV infusions separated by 2 weeks
  • Administration of a glucocorticoid prior to each infusion is recommended in order to reduce the incidence and severity of infusion reactions
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56
Q

Rituximab MOA Diagram

A
57
Q

Tofacitinib Description

A

JAK inhibitor (Janus Kinase Inhibitor) blocks JAK 3 and JAK 1, to a lesser degree blocks JAK 2

58
Q

Tofacitinib Indications

A

FDA approved for moderately-to-severely active RA in patients who do not respond adequately to (or are intolerant of) methotrexate

59
Q

Tofacitinib Side Effects

4 listed

A
  • Inflammation of nasal passages and upper pharynx
  • upper respiratory tract infections
  • ^ risk of TB and Lymphoma
  • Headache
60
Q

Tofacitinib Metabolized by?

A

CYP3A4

61
Q

Tofacitinib MOA Diagram

A
62
Q

Apremilast Effects

2 listed

A
  • increases intracell cAMP
  • decreases TNF-α production
63
Q

Apremilast Indications

A

For moderate-to-severe plaque psoriasis and for psoriatic arthritis

64
Q

Apremilast Adverse Effects

4 listed

A
  • diarrhea
  • nausea
  • nasopharyngitis
  • upper respiratory tract infection
65
Q

Apremilast Metabolized by

A

CYP3A4 and later non-CYP mediated hydrolysis

66
Q

Apremilast Excretion

A

58% urine

39% feces

severe renal impairment need to reduce dose

67
Q

Apremilast is associated with?

A

Increased risk of depression, asses patient risk for depression and suicidal thoughts or behavior

68
Q

Gout description

A

deposition of monosodium urate monohydrate crystals (MSU)

69
Q

Pseudogout description

A

associated with the deposition of Calcium Pyrophosphate (CPP) crystals and is sometimes referred to as calcium pyrophosphate disease (CPPD)

70
Q

CPP AKA

A

Calcium Pyrophosphate

71
Q

MSU AKA

A

Monosodium urate monohydrate crystals

72
Q

If gout or pseudogout remains untreated

A

these disorders can lead to joint destruction and renal damage

73
Q

What are Gout and Pseudogout?

A

Recurrent Episodes of pain and joint inflammation due to the formation of crystals within the joint space and deposition of crystals in soft tissue

74
Q

Humans lack _________ and cannot convert _______ to soluble _______ as the end product of _________ metabolism

A
  • uricase
  • urate
  • allantoin
  • purine metabolism
75
Q

90% of individuals with gout have?

A

Hyperuricemia with serum urate level >6.8 mg/dL

76
Q

Hyperuricemia can be found in patients taking certain drugs

A
  • Thiazide diuretics
  • cyclosporine
  • low doses of aspirin
77
Q

Uric acid levels and gout

A

Uric acid levels by itself do not precipitate gout; rather, acute changes in the level of uric acid cause gout

78
Q

Primary gout

A

is related to renal urate underexcretion or overproduction of uric acid

79
Q

Secondary gout

A

Is related to myeloproliferative disease or their treatment, therapeutic regimens producing hyperuricemia, renal failure, renal tubular disorders, lead poisoning, hyperproliferative skin disorders, enzymatic defects (e.g. deficient hypoxanthine-guanine phosphoribosyl transferase, and glycogen storage diseases)

80
Q

Gout and ______ Metabolism

A
81
Q

How many Clinical Phases of Gout

A

Gout has two clinical phases

82
Q

The first clinical phase of gout?

A

The first phase is characterized by intermittent acute attacks that spontaneously resolve, typically over a period of 7 to 10 days with asymptomatic periods between attacks

83
Q

The second clinical phase of gout

A

With inadequately treated hyperuricemia, the transition to the second phase can occur, manifested as chronic tophaceous gout, which often involves polyarticular attacks, symptoms between attacks, and crystal deposition (tophi) in soft tissues or joints

84
Q

Tophi AKA

A

Crystal Deposition

85
Q

3/4 of patients who had gout for 20 years or more had?

A

Tophaceous gout

86
Q

Gout recurrence

A

Recurrent attacks are common

87
Q

Complications of gout

7 listed

A
88
Q

Acute Gout Treatment options

A
  • NSAIDs
  • Colchicine
  • Glucocorticoids
  • Corticotropin
89
Q

Acute Pseudogout Treatment

A
  • NSAIDs
  • Colchicine
  • Glucocorticoids
  • Corticotropin
90
Q

Gout and Pseudogout prophylaxis

A

Colchicine and Hydroxychloroquine are effective for prophylaxis

91
Q

Aspirin in Gout Treatment

A
  • Aspirin is not indicated for treating acute gout
  • at lower doses aspirin causes uric acid retention by the kidney
  • at higher doses aspirin has a uricosuric effect
92
Q

Acute Gout Treatment First-line Agents

A

NSAIDs and Colchicine

93
Q

Acute Gout Treatment when NSAIDs or Colchicine is poorly tolerated or contraindicated

A

glucocorticoids or corticotropin may be used

94
Q

Acute Gout NSAID and Colchicine treatment timeline

A

7-10 days of treatment may be necessary to ensure resolution of symptoms

95
Q

Dosages of NSAIDs in Acute Gout

A

Increased doses of anti-inflammatories are typically initially prescribed and reduced as symptoms improve

96
Q

Urate-lowering drugs in the treatment of acute gout

A
  • Urate-lowering drugs are of no benefit in the treatment of acute gout
  • in general therapy with these agents should not be initiated during an acute attack
  • for patients already being treated with a urate-lowering agent, therapy should be continued
97
Q

CV Aspirin Patients in Gout

A

Low-dose aspirin for its protective CV effects does NOT need to be discontinued in MOST individuals

98
Q

Chronic treatment of Gout

2 considerations

A
  • in patients with hyperuricemia who have at least two gout attacks per year or tophi (as determined by either clinical or radiographic methods) urate-lowering therapy is used
  • The severity and frequency of flares, the presence of coexisting illnesses and patient preference are additional considerations
99
Q

When should Urate-lowering therapy by initiated

A

Urate-lowering therapy (ULT) should not be initiated during acute attacks but rather started 2 to 4 weeks after flare resolution

100
Q

ULT AKA

A

Urate-Lowering Therapy

101
Q

How is ULT managed

3 considerations

A
  • Start with a low initial dose and increase as needed over a period of weeks to months
  • Adjust dose to maintain a serum urate level < 6 mg/dL, which is associated with a reduced risk of recurrent attacks and tophi; often the target is <5mg/dL
  • Therapy is generally continued indefinitely
102
Q

Urate-Lowering Agent Classes

3 listed

A
  • Xanthine Oxidase Inhibitors
  • Uricosuric Agents
  • Uricase Agents
103
Q

Safety of combinational urate-lowering therapies

A

Data is limited

104
Q

When is urate-lowering combination therapy appropriate?

A

When the target serum urate has not been reached with a xanthine oxidase inhibitor (first-line therapy) alone

105
Q

Xanthine Oxidase inhibitors MOA

A

Block the synthesis of uric acid

106
Q

Xanthine Oxidase inhibitors Treatment line

A

First-line pharmacologic ULT

107
Q

Xanthine Oxidase inhibitors indication when there is overproduction of urate

A

Can be used regardless of whether there is an overproduction of urate

108
Q

Xanthine Oxidase inhibitors: Allopurinol side effects

A

A mild rash in 2% of patients

109
Q

Severe allopurinol hypersensitivity

A

much less common but can be life-threatening

110
Q

Xanthine Oxidase inhibitors examples

2 listed

A
  • Allopurinol
  • Febuxostat
111
Q

Xanthine Oxidase Inhibitors Function

A

Block the synthesis of Uric Acid

112
Q

Xanthine Oxidase Inhibitors line of treatment of gout

A

First-line treatment of ULT of Gout

113
Q

Uricosuric drugs examples

A
  • Probenecid
  • Lesinurad
114
Q

Uricosuric drugs Function

A

Block renal tubular urate reabsorption

115
Q

Uricosuric drugs Indications

A
  • can be used in patients with an underexcretion of urate (90% of patients with gout) they are used less frequently than xanthine oxidase inhibitors

and

  • are contraindicated in patients with a history of nephrolithiasis
116
Q

Uricosuric drugs contraindicated in?

A

patients with a history of nephrolithiasis

117
Q

Uricosuric drugs in renal impaired patients

A

In general, these drugs are ineffective in patients with renal impairment

118
Q

Probenecid and lesinurad are

A

Uricosuric drugs

119
Q

Duzallo is?

A

A fixed-dose oral combination of lesinurad and allopurinol for treatment of hyperuricemia associated with gout who serum uric acid levels have not been achieved by allopurinol alone

120
Q

Uricase Agents Examples

A

Pegloticase

121
Q

Pegloticase drug class

A

Uricase Agents

122
Q

Uricase Agents MOA

A

Converts uric acid into soluble allantoin

123
Q

Pegloticase properties

A

a polyethylene glycolated (pegylated) modified porcine recombinant uricase approved for chronic gout that is intolerant of conventional treatments

124
Q

Pegloticase administration and issues

A

can be administered intravenously and infusion reactions are common

125
Q

Non-pharmacologic approach to gout

A
  • Avoiding alcohol
  • modifying diet
126
Q

DASH diet

A
  • lowers uric acid by 1.3 mg/dL
  • consumption of less red meat, lowers purine levels
  • high intake of fruits and vegetables
  • increase vitamin C
127
Q

Case 1

A
128
Q

Case 2

A
129
Q

Case 3

A
130
Q

differences in gout and pseudogout

  • Men:Women
  • Age group affected
  • Serum Urate
  • Joints affected
  • Involvement of first MTP (Podagra)
  • Tophi
  • Radiographic findings
  • Crystals
A
131
Q

Describe the prevalence of gout

A
132
Q

Describe the mechanisms of inflammation in gout

A
133
Q

Explain how gout is diagnosed

A
134
Q

Describe criteria for an acute gout attack

A
135
Q

Describe a clinical presentation of gout or pseudogout

A
136
Q

What are Tophi?

4 listed

A
137
Q

What does Tophi look like?

A
138
Q

What does a radiograph of the hands look like in gout?

A
139
Q

What does a radiograph of the feet look like with gout?

A

FMS (34 decks)

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