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PT2 Neuro 10-11 and Pain 1-4 > RA pharmacology > Flashcards

RA pharmacology Flashcards

1
Q

rheumatoid arthritis definition

A

autoimmune disease that results in chronic inflammation of the lining of the joints

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2
Q

drugs for symptomatic relief of RA

A

NSAIDs

glucocorticoids

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3
Q

disease modifying antirheumatic drugs (DMARDs)

A 
methotrexate
leflunomide
sulfasalazine
hydroxychloroquine
minocycline
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4
Q

NSAID use in RA

A

-for pain and inflammation only by reducing prostanoid production

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5
Q

glucocorticoid use in RA

A
  • provides rapid relief from symptoms

- more potent than NSAIDs

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6
Q

NSAID side effects

A

GI upset

bleeding

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7
Q

glucocorticoids acute adverse effects

A
  • GI ulceration and hemorrhage

- impaired resistance to infection

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8
Q

glucocorticoids chronic adverse effects

A
  • adrenal suppression
  • Cushing’s syndrome
  • weight gain
  • facial puffiness
  • osteoporosis
  • much more
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9
Q

DMARD use in RA

A
  • slow or stop progression

- do not provide symptomatic relief

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10
Q

cytotoxic DMARD

A

methotrexate

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11
Q

methotrexate MOA

A
  • inhibits replication and function of T and B lymphocytes

- suppress secretion of inflammatory cytokines

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12
Q

first line agent in RA

A

methotrexate

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13
Q

methotrexate adverse effects

A
  • N/D
  • rashes
  • alopecia
  • folic acid antagonism
  • teratogenic
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14
Q

notable ADME of methotrexate

A
  • gets polyglutamated which retains it in the cell

- 3-10 hr half life depending on kidney function

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15
Q

leflunomide MOA

A
  • inhibits dihydroorotate dehydrogenase

- inhibits pyrimidine biosynthesis which has cytostatic effect on B and T cells

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16
Q

leflunomide use in RA

A

can be used as additive agent due to its unique MoA

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17
Q

leflunomide adverse effects

A
  • hepatotoxicity
  • GI
  • diarrhea
  • alopecia
  • teratogen
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18
Q

leflunomide notable ADME

A

half life of 14-18 hours

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19
Q

sulfasalazine adverse effects

A
  • GI

- sulfa allergies

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20
Q

hydroxychloroquine adverse effects

A
  • ocular problems
  • retinopathy
  • irreversible visual loss
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21
Q

minocycline adverse effects

A
  • autoimmune syndromes
  • CNS effects
  • superinfection
  • teratogen
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22
Q

gold products used in RA

A

start with aura(o)

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23
Q

the two biologic response modifiers we want to target

A

IL-6

TNF-alpha

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24
Q

IL-6

A

pro-inflammatory cytokine

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25
Q

TNF-alpha

A

responsible for inflammation

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26
Q

biologics that target TNF-alpha

A

infliximab

adalimumab

27
Q

recombinant human TNF-alpha receptor

A

etanercept

28
Q

infliximab and adalimumab adverse effects

A
  • TB risk

- cancer risk

29
Q

etanercept adverse effects

A

-rare myocardial and CNS toxicities

30
Q

abatacept MoA

A

-inhibits T-cell activation by binding CD80 and CD86

31
Q

abatacept adverse effects

A
  • headache
  • nausea
  • infections (especially respiratory)
32
Q

do not mix abatacept with

A

TNF therapy (infliximab, adalimumab)

33
Q

rituximab MOA

A

-targets CD20 of B cells

34
Q

rituximab use in RA

A

when other nonbiologic DMARDs fail

35
Q

rituximab adverse effects

A
  • hematopeoetic toxicities
  • CNS effects
  • GI toxicities
36
Q

tocilizumab MOA

A

targets IL-6 receptor

37
Q

tocilizumab adverse reactions

A
  • increase infection susceptibility

- GI perforations

38
Q

gout

A

metabolic disease characterized by chronic hyperuricemia caused by urate crystals deposits in joints and cartilage

39
Q

potential causes of gout

A
  • increased urate production

- decreased urate excretion

40
Q

3 aspects of gout therapy

A
  • inhibit inflammatory response
  • decrease uric acid production
  • enhance uric acid clearance
41
Q

drugs for acute therapy of gout

A
  • colchicine
  • NSAIDs
  • glucocorticoids
42
Q

drugs for chronic therapy of gout

A
  • probenecid
  • allopurinol
  • febuxostat
  • sulfinpyrazone
43
Q

colchicine MOA

A

inhibit microtuble function which decreases leukocyte migration

44
Q

colchicine use in gout

A

combination therapy with allopurinol and probenecid

45
Q

colchicine adverse effects

A
  • GI

- hematopoetic toxicities

46
Q

NSAIDs used in gout

A

-indomethacine, naproxen, ibuprofen (more COX-1 selective)

47
Q

glucocorticoid use in gout

A

only used in patients unable to take NSAIDs or colchicine

48
Q

allopurinol MOA

A
  • inhibits xanthine oxidase which prevents formation of uric acid
  • leads to increased excretion
49
Q

allopurinol adverse effects

A
  • increased risk of kidney stones
  • GI
  • peripheral neuritis
  • skin reactions
  • bone marrow depression
50
Q

febuxostat MOA

A

inhibits xanthine oxidase

51
Q

febuxostat adverse effects

A

similar to allopurinol

52
Q

allopurinol and renal impairment

A

must adjust dosage

53
Q

febuxostat and renal impariment

A

may not require dose adjustment

54
Q

uricosuric agents ultimately work by

A

reducing uric acid reabsorption or increasing excretion

55
Q

probenecid MOA

A

decreased reabsorption of uric acid in proximal tubule

56
Q

probenecid adverse reactions

A
  • GI irritation
  • allergic dermatitis
  • aplastic anemia
57
Q

problem with probenecid initiation

A

may trigger acute gouty attack

58
Q

uricosuric agents

A

probenecid

sulfinpyrazone

59
Q

sulfinpyrazone MOA

A
  • decreased reabsorption of uric acid in proximal tubule

- more potent than probenecid, but has platelet inhibition

60
Q

sulfinpyrazone adverse effects

A

-GI problems

61
Q

rasburicase MOA

A

catalyses the breakdown of uric acid to allantoin

62
Q

problem with rasburicase

A

its a recombinant enzyme so you will develop an immune response to it

63
Q

tofacitinib MOA

A

JAK inhibitor – inhibits phosphorylation of STATs and prevents transcription

PT2 Neuro 10-11 and Pain 1-4 (5 decks)

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