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MSK Summative > Pharmacology of Gout and DMARDS > Flashcards

Pharmacology of Gout and DMARDS Flashcards

1
Q

How can gout be managed without taking medication?

A
  • Lower urate levels with lifestyle modification/risk reduction
    • dietary changes
    • weight loss
    • reduce alcohol intake
    • examine medication list
      • (salicylates, diuretics etc.)
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2
Q

What are 3 drugs used to treat acute gout attacks?

A

Mainly want to suppress inflammation and try and decrease symptoms (pain)

  1. NSAIDs
  2. Colchicine (if NSAID C/I)
  3. Glucocorticoids
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3
Q
  • Which NSAIDs are recommended to treat acute gout?
    • MOA?
  • Why wouldn’t you use aspirin?
A
  • Naproxen or indomethacin
  • NO ASPIRIN (at low doses)
    • because it is a salicyate so it will retain uric acid; so uric acid levels increase

MOA:

  • Reversibly inhibit COX1 and COX2
    • block prostoglandin synthesis (anti-inflammatory)
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4
Q

Main side effects of NSAIDs?

A
  • Cardiovascular events
  • GI toxicity
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5
Q
  • Colchicine used to treat?
    • MOA?
    • Major Side effects?
A
  • Used to treat:
    • acute gout (2nd line after NSAIDs)
    • prophylactic value
  • MOA:
    • binds and stabilizes tubulin to inhibit microtubule polymerization (G1 arrest)
      • impair neutrophil chemotaxis (adhesion) and degranulation
  • Side effects:
    • GI (diarrhea)
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6
Q
  • What are two glucocoticoids that can be used to treat acute gout?
    • Administered?
A
  • Prednisone, triamicnolone
  • Administered:
    • oral, intra-articular or parenteral
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7
Q

MOA of glucocorticoids?

A
  • Metabolic, catabolic, anti-inflammatory and immunosuppressive effects
    • mediated by interaction with:
      • glucocorticoid response elements
      • inhibition of phospholipase A2
      • inhibition of transcription factors like NF-kB
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8
Q
  • Chronic gout is due to what two scenarios?
    • What can occur during treatment of chronic gout?
    • What is recommended for this?
A
  • Due to either:
    • uric acid overproduction
    • uric acid under-excretion (mostly)
  • Possibility of:
    • acute gout flares during treatment initiation
      • crystals can be broken down in the joint they are in and lead to an inflammatory response
  • Recommended:
    • prophylactic colchicine/NSAIDs
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9
Q

What two drugs inhibit xanthine oxidase in chronic gout treatment?

A
  1. Allopurinal
  2. Febuxostat
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10
Q
  • MOA of Allopurinal?
  • Used to treat?
    • What does it increase the concentration of?
A
  • MOA:
    • competitive inhibitor of xanthine oxidase
      • decreases conversion of hypoxanthine and xanthene to urate
        • deals with both excretion and production issues
  • Used for:
    • Chronic gout
  • Increases concentration of:
    • azathioprine and 6-MP
      • used in chemo; both normally metabolized by xanthine oxidase
      • can increase risk of toxicity
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11
Q
  • Probenecid is a uricosuric drug.
    • Used to treat?
    • MOA?
    • What else does it have an effect on?
    • Side effect?
A
  • Used for:
    • chronic gout
      • 2nd line agents for under excreters
  • MOA:
    • inhibits reabsorption of uric acid in proximal convoluted tubule in kidney
      • competitively inhibits URAT-1 transporter
  • Drug interactions:
    • competes with same transporter as penicillins, MTX
      • can delay/inhibit excretion of penicillins
  • Side effects:
    • exacerbate gouty attack
    • uric acid stone formation
      • ​need to stay hydrated because excreting lots of uric acid
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12
Q
  • What is Pegloticase and Rasburicase(MOA)?
    • What is it used to treat?
    • When is it used?
A
  • Used for:
    • Rasburicase: hyperuricemia associated with malignancy
    • Pegloticase: chronic gout
  • MOA:
    • recombinant uricase that catalyzes metabolism of uric acid to allantoin
      • more water soluble product
      • promotes excretion
  • 3rd line treatment (IV)
    • if other treatments fail; severe cases
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13
Q

Treatment of pseudogout?

A
  • Due to pyrophosphate crystal deposition
    • in large joint, like knee
  • Treatment similar to gout:
    • NSAIDs
    • Glucocorticoids
    • Colchicine (if necessary)
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14
Q
  • What are the 5 non biological DMARD drugs?
    • First line treatment?
A
  1. Methotrexate (MTX)
  2. Hydroxychloroquine (HCQ)
  3. Sulfasalazine (SSZ)
  4. Leflunomide
  5. Azathioprine, cyclophosphamide (less common)
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15
Q

4 biological DMARDs

A
  1. TNFa inhibitors
  2. IL receptor antagonists
  3. Co-stimulation inhibitors
  4. JK inhibitor (small molecule)
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16
Q

What are the RA recommendation for treatments of early disease?

A

Methotrexate + (HCQ or SSZ)

17
Q

Methotrexate for RA: (non biological drug)

  • MOA?
  • Adverse effects?
A
  • MOA:
    • Inhibits production of folic acid by competitively inhibiting dihydrofolate reductase (decrease DNA synthesis)
    • Inhbits DHFR and AICR transformylase
      • cause accumulation of extracellular adenosine
      • suppress B and T- cells
  • Adverse effects:
    • hepatotoxic
18
Q
  • How is hydroxychloroquine (nonbiological; HCQ) used in RA treatment?
  • Major side effect?
A
  • Not first line (made for malaria)
    • approved for people who haven’t responded to other drugs
    • usually combined with MTX
  • Side effects:
    • Retinal toxicity
    • GI
19
Q
  • Mechanism of Sulfasalazine (SSZ; nonbiological) in treatment of RA?
    • activated by?
A
  • Combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory)
    • activated by colonic bacteria
  • Sulfa drug to salicylate
20
Q
  • Leflunomide (nonbiological DMARD) is used to treat?
  • MOA?
  • Adverse effects?
A
  • Used for:
    • rheumatoid arthritis only
  • MOA:
    • reversibly inhibits dihydroorotate dehydrogenase, preventing pyrimidine synthesis
      • suppress T cell proliferation
  • Side effects:
    • Hepatotoxicity
    • Respiratory tract infections
    • Diarrhea
21
Q
  • Azathioprine (non biological DMARD) is used to treat?
    • MOA?
    • Drug interactions?
A
  • Used for:
    • RA
  • MOA:
    • antimetabolite precursor of 6-mercaptopurine (6-MP)
      • inhibits lymphocyte proliferation by blocking nucleotide synthesis
  • Drug interactions:
    • 6-MP is degraded by xanthine oxidase
      • toxicity is increased by allopurinal (inhibits XO)
22
Q

What are common side effects of the non biological DMARDs?

A
  • GI effects,
  • infection
  • malignancy

(MTX, HCQ, SSZ, Leflunomide, Azathioprine)

23
Q
  • What are the 5 TNFa inhibitor (biological DMARD) used to treat RA?
    • all of them are?
A
  1. Etanercept
  2. Infliximab
  3. Adalimumab
  4. Certolizumab
  5. Golimumab

All monoclonal antibodies

24
Q

All TNFa inhibitors predispose patients to getting?

A
  • infection; including reactivation of latent TB
    • since TNF is important in granuloma formation and stabilization
25
Q
  • Etanercept is a TNFa inhibitor used to treat?
  • MOA?
A
  • Used for:
    • RA
  • Fusion protein
    • receptor for TNFa + IgG Fc)
    • produced by recombinant DNA
  • MOA:
    • TNF decoy receptor
26
Q

General MOA for TNFa inhibitors? (Infliximab, adalimumab)

A
  • Anti-TNFa monoclonal antibodies
  • MOA:
    • decrease TNFa receptor activation so decrease inflammatory and immune response
    • decrease macrophage and T cell function
      • decrease joint inflammation, cartilage degredation and bone erosion
27
Q
  • What are two IL receptor inhibitors used to treat RA? (biologic)
    • side effects for each?
A
  1. Anakinra: anti IL-1 receptor
    • injection site reaction (IV)
  2. Tocilizumab: anti IL-6 receptor
    • hyerlipidemia
    • TB (infections)
28
Q
  • Co-stimulatory inhibitor (biological DMARD) to treat RA?
    • MOA?
A
  • Abatacept
  • MOA:
    • binds to CD80/86 to prevent co-stimulatory signal on T cells
29
Q
  • Rituximab can be used as biological DMARD to treat RA.
    • MOA?
    • Side effect?
A
  • MOA:
    • anti-CD20 monoclonal antibody
    • induce apoptosis of B-cell
  • Side effect:
    • infusion reaction
    • infection
    • myelosuppression
30
Q

Side effects of Allopurinal?

A
  • Steven Johnson Syndrome (drug reaction)
    • rash
  • Can cause drug reaction with eosinophilia and systemic symptoms
31
Q
  • Side effect of Pegloticase?
  • Administered?
A
  • Need to be administered IV
  • Side effects:
    • anaphylaxis
    • can cause hemolysis in G6PD deficiency (bite cells when spleen removes Heinz bodies)

MSK Summative (8 decks)

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