Rheumatoid Arthritis Treatment 4 Flashcards

1
Q

why are NSAIDS used in RA treatment

A
  1. useful as a background antiinfllamatory
    - there I sinter patient variability between response to each NSAID
  2. beware of potential side effects- consider risk vs benefit
    - CV risk
    - GI risk
    - renal risk
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2
Q

describe the kinetics and mechanism of action of NSAIDS

A
  1. well absorbed
  2. highly protein bound
  3. metabolised by liver
  4. excreted by GF or TS
  5. peak plasma of 1-4hrs
  6. accumulate at site
  7. short half lives
  8. they lead to the inhibition of COX
    - Cyclooxygenase is required to convert arachidonic acid into thromboxanes, prostaglandins, and prostacyclins
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3
Q

describe the efficacy between NSAIDS and COX 2 inhibition

A
  1. no difference between NSAIDS and COX 2
  2. particularly useful in acute inflammation
  3. choice varies between patients
  4. if no effect in 2 weeks, witch to an alternative
  5. no rationale for combination therapy
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4
Q

give an example of the GI effects that NSAIDS can cause

A
  • serious upper GI bleeding/perforation
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5
Q

describe how systemic glucocorticoids are used in rheumatology

A
  1. various systemic effects that have an effect on disease modification
  2. they decrease proinflammatory cytokines and enzymes
  3. inhibit transcription factors, decrease T cell function and Fc receptor expression
  4. adverse events common, short courses only
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6
Q

describe how dose timing affects outcome

A
  1. clearance varies by time of day because of the distribution of normal cortisol production
  2. very early morning administration results in more profound reduction of inflammation
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7
Q

what are the practical recommendations of using glucocorticoids

A
  1. use the lowest dose for the shortest time
  2. discuss risk vs benefit
  3. use in combination with a DMARD
  4. offer adequate bone protection
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8
Q

describe the ACR response rates

A
  1. ACR reported as % improvement, comparing disease activity at 2 discrete time points
    - usually baseline and post baseline
  2. ACR20 is > 20% improvement
    - clinically significant
  3. ACR50 is >50% improvement
  4. ACR70 is >70% improvement
    - ACR70 responders include ACR20 and ACR50 responders
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9
Q

give examples of non immunosuppressive disease modifying antirheumatic drugs

A
  1. old school drugs but still useful
  2. gold
  3. sufasalazine
  4. hydroxychloroquine
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10
Q

describe the properties of parenteral gold and how it can be used as treatment in RA

A
  1. rapidly absorbed and highly protein bound
  2. very slowly eliminated by kidney
  3. MOA unknown
    - probably reduces oxidative stress and affects macrophages and cytokines
  4. IM gold is as effective as oral methotrexate
  5. high ADR rate than methotrexate
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11
Q

give examples of adverse drug reactions of gold

A
  • acute renal failure
  • metallic taste
  • diarrhoea
  • rash
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12
Q

describe the properties of sulfasalazine and how it can be used in treatment of RA

A
  1. prodrug metabolised by bacteria to 5ASA and sulfapyridine
  2. MOA unclear- probably reduces oxidative damage
  3. effective as lower doses of methotrexate
  4. generally well tolerated
  5. can cause oligospermia
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13
Q

describe the properties of hydroxychloroquine and how it can be used in treatment of RA

A
  1. antimalarial found by chance to improve RA
  2. half life is 40 days but LDs not normally used as increases ADRs
  3. Cpss takes 3 months- slow acting
  4. often used in SLE as its anchor drug
  5. inhibits Toll like receptors affecting cytokine signalling
  6. moderate effects alone, but better in combination
  7. can cause retinal changes
    - must have regular eye testing
    - if it occurs, stop drug and switch to alternative DMARD
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