RA Flashcards

1
Q

Non-pharmacologic tx for RA

A

patient education, psychosocial intervention, rest, exercise, therapy, nutrition/dietary counseling, risk reduction intervention (CV disorders, smoking, osteoporosis), immunizations

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2
Q

pretreatment evaluation of RA

A

baseline labs, serologic testing for hepatitis (B/C), opthamalogic screening, latent TB

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3
Q

baseline labs for RA

A

CBC, serum creatinine, LFT, ESR, CRP

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4
Q

treatment option choices for RA based on what

A

level of disease, stage of therapy, outside decision maker (insurance), patient preference (cost, frequency, ROA)

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5
Q

NSAID use for RA

A

pain and inflammatino

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6
Q

corticosteroid use and administratino in RA

A

antiinflammation - intraarticular, systemic

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7
Q

non-biologic DMARDS

A

methotrexate, leflunomide, hydroxychloroquine, sulfasalazine

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8
Q

biologic DMARDS

A

infliximab, etanercept

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9
Q

DMARD

A

disease modifying anti-rheumatic drugs

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10
Q

how to treat mild active RA

A

antiinflammatory with NSAID, DMARD (methotrexate)

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11
Q

how to treat moderate to severe RA

A

antiinflammatory (NSAID or corticosteroid), DMARD (methotrexate at first then add hydroxychloroquine + sulfasazine)

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12
Q

monitoring of RA

A

see pt on a regular basis: clinical evaluation (sxs improvement, better QOL), lab test reevaluation, drug toxicity detection

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13
Q

how long does it take drugs for RA to work?

A

wekks-months

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14
Q

true or false: early treatment of RA is best

A

true - 90 day window, start with DMARDs

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15
Q

uses for hydroxychloroquine

A

RA, SLE, malaria preventino/treatment

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16
Q

RA drug that it ototoxic

A

hydroxychloroquine

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17
Q

how fast is the response to hydroxychloroquine?

A

slow-acting, 4-6 weeks for response time, 3-6 months to see response

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18
Q

kinetics of hydroxychloroquine

A

rapid, 50% plasma protein binding, extended half life

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19
Q

ototoxic effects of hydroxychloroquine

A

depigmentation around the fovea (dose related retinopathy) from any dose that can be temproary or permanent

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20
Q

ADR of hydroxychloroquine

A

GI (n/v, abd pain, dyspepsia), CNS (HA, irritability, psychosis, nightmares, seizures), hemolytic anemia (G6PD deficiency (AA, mediterranean, middle eastern))

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21
Q

uses for sulfasalazine

A

RA, ulcerative colitis, crohn’s disease

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22
Q

ADR of sulfasalazine

A

GI (nausea/dyspepsia), skin rash, Headache, hematologic (leukopenia, throbocytopenia, neutropenia)

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23
Q

True or false: 30% of pts stop sulfasalazine d/t ADR

A

true

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24
Q

max dose of sulfasalazine

A

3g/day

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25
Q

what should be given along with methotrexate to ensure it doesn’t get depleted?

A

folic acid - look very similar

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26
Q

MOA of methotrexate

A

increases AMP with increases adenosine (anti-inflammatory)

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27
Q

true or false: methotrexate is a prodrug

A

true - takes up to 28 weeks to change

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28
Q

uses of methotrexate

A

RA, psoriasis, juvenile idiopathic arthritis, oncology indications (NHL, lymphoma, osteolymphomas)

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29
Q

ADR of methotrexate

A

minor GI side effects, stomatitis, minor transaminase elevations, leukopenia, thrombocytopenia, hepatotoxicity, interstitial pneumonitis

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30
Q

how often is methotrexate given?

A

once a week

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31
Q

uses for leflunomide

A

RA (unlabeled for CMV disease)

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32
Q

do you need to dose adjust leflunomide for renal/hepatic disease?

A

no but check labs anyway

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33
Q

if a pt had previous problems with hematoglogic disorders, is leflunomide a risk?

A

slight risk for this

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34
Q

ADR of leflunomide

A

hepatotoxicity, infections, pulmonary (rare ILD), peripheral neuropathy, cancer (lymphoma?)

35
Q

good combo therapy for leflunamide

A

MTX, TNF blockers

36
Q

risks of taking immune modulators

A

risk of infection, malignancy (similar rate seen with DMARDs or RA)

37
Q

ADR of immune modulators

A

local injectino site reaction, CNS (fever, fatigue, chills, HA), GI (nausea, diarrhea, abd pain), hematologic (neurtopenia, thrombocytopenia, positive ANA titer)

38
Q

administration of immune modulators

A

subQ/IV

39
Q

goals of therapy for RA

A

control pain and swelling, minimize disability, improved QOL, educate on disease management

40
Q

important inflammatory cytokines in RA

A

TNF, IL, PGE, IGF

41
Q

what type of joints does RA affect?

A

synovial membranes of multiple joints - can also affect many other body systems

42
Q

how often should you get BW for RA?

A

every 2-3 weeks for 3 months then every 2-3 months for 6 months, then every 3 months once stabilized

43
Q

SAARDs

A

slow acting anti-rheumatic drugs (same as DMARDs)

44
Q

hydroxychloroquine is a derivative of?

A

quinine (used for malaria)

45
Q

MOA of hydroxychloroquine

A

decreases T lymphocyte response, blockade of toll-like receptors, trap free radicals

46
Q

MOA of sulfasalazine

A

enters the GI system, leaves the GI system and comes back then is worked on by azoreductase and turned into sulfapyridine (goes to CV, hepatic, and renal systems) and 5-aminosalicylic acid

47
Q

Onset of action for sulfasalazine

A

slightly faster than hydroxychloroquine, variable between 1-4 months

48
Q

pts with G6P insufficiency are at risk for developing

A

hemolytic anemia (sulfasalazine)

49
Q

with methotrexate, as oral dose rises?

A

bioavailability decfreases

50
Q

best ROA for methotrexate

A

subQ, IV

51
Q

what does MTX bind to in the blood?

A

plasma proteins - this is good! If displaced by NSAIDs or other drugs, could be too much MTX!

52
Q

does MTX need dosed differently for renal impairment?

A

yes, NSAIDs also reduce renal clearance so if using both need to dose adjust!

53
Q

max dose of MTX

A

20mg/week

54
Q

is it OK to use ASA with MTX?

A

no!

55
Q

lower doses of MTX are required in?

A

DM, renal failure, obese pts

56
Q

is it ok to drink EtOH with MTX?

A

no

57
Q

when should folic acid be administered with MTX use?

A

every day except the day you give the first dose of MTX

58
Q

MOA of leflunomide

A

pro-drug, RUMP inhibitor

59
Q

Selective T cell costimulation blocker

A

abatacept

60
Q

TNF blocker

A

humira, enbrel, remicade

61
Q

IL3 receptor agonist

A

anakira

62
Q

IL6 receptor agonist

A

Actemra

63
Q

JAK inhibitor

A

Xeljanz

64
Q

B cell depletion

A

rituxan

65
Q

what are cytokines

A

mediators that influence activation and migration of leukocytes

66
Q

primary cytokines

A

IL1 and TNFalpha

67
Q

how to cytokines signal leukocytes?

A

NF-B, Jak/STAT signlaing pathway

68
Q

what exactly is RA caused by?

A

abnormal response of cytokines to increase migration of macrophages

69
Q

MOA of immune modulators

A

inhibit the second signal required for T cell activation, deplete B cells

70
Q

what are the Th1 cytokines?

A

TNF, IL-1beta

71
Q

how do Th cells contribute to RA?

A

stimulate synovial cells to proliferate and synthesize collagenase (breaks down bone, stimulates bone resorption, decreased proteoglycans which lubricates joints)

72
Q

cept immune modulators

A

fusion of receptor to the Fc part of human IgG1

73
Q

mab immune modulators

A

monoclonal antibodies

74
Q

ximab immune modulators

A

chimeric monoclonal antibodies

75
Q

umab immune modulators

A

humanized monoclonal antibody

76
Q

how do soluble receptor antagonists work?

A

bind the target cytokine thus inhibiting interaction with cell surface receptors

77
Q

how do monoclonal antibodies work?

A

higher affinity for certain sytokines than soluble receptor antagonists, bind target cytokine not only when in serum but also when bound to cell surface

78
Q

how do cell surface receptor antagonists work?

A

biologically inactive protein that complexes with the cytokine at the cell surface receptor

79
Q

how does costimulation blockade work?

A

activation of T cells needs binding of T cell receptor to peptide and peptide to MHC complex II, binding of CD28 and/or CTLA-4 or CD40. This regulates t-cell activation and T-cell dependent B-cell function

80
Q

indications of etanercept

A

RA. Psoriatic arthritis, plaque psoriasis, ankylosing spondylitis, polyarticular juvenile idiopathic arthritis

81
Q

indications for adalimumab and infliximab

A

same as etanercept plus crohns and ulcerative colitis

82
Q

indications for tofacitinib

A

RA

83
Q

why is tofacitinib called two faced?

A

head and tail look the same

84
Q

MOA of tofacitinib

A

works intracellularly as an immune modulator