RA Flashcards

1
Q

What is RA?

A

An autoimmune dz that involves the joints, mostly

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2
Q

Describe the dz process of RA

A

Immune sys attacks synovial and connective tissues > inflammation > chronic inflammation leads to growth of tissue called pannus > leads to loss of bone and cartilage

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3
Q

Main affect site in RA?

A

Joints (synovial tissues)

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4
Q

T or F: RA is more likely to affect older inds than younger inds

A

F (anyone is susceptible since this is an autoimmune dz)

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5
Q

Signs and sx’s of RA

A

a. SYMMETRICAL joint pain/stiffness for >6 weeks
b. muscle pain
c. systemic sx’s (fatigue, fever, loss of appetite) (late dz)
d. joint tenderness, warmth, swelling
e. rheumatoid nodules (unctrled dz)

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6
Q

Joint consequences of RA

A

Joint consequences:

a. Joint damage and bone erosion
b. ulnar drift in hands

There’re extraarticular consequences (blood vessels, eyes, lungs, bone, etc.)

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7
Q

What single lab test can definitively establish RA?

A

None exists > must be diagnosed using certain criteria

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8
Q

What body part must be involved to consider a dx of RA?

A

JOINTS

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9
Q

Ultimate goal of tx?

A

Remission

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10
Q

Sig damage occurs in the first __ years of RA.

A

Sig damage occurs in the first 2 years of RA.

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11
Q

T or F: DMARDs should be started v. slowly in the beginning to reduce AEs.

A

F

Tx aggressively to get early remission

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12
Q

T or F: Rheumatoid factor must be present for a dx of RA.

A

F (only 60-70% of pts have this)

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13
Q

Main classes of meds used to tx RA?

A
  1. Traditional DMARDs
  2. Biologic DMARDs
  3. Synthetic DMARDs (Janus Kinase inhibitor)
  4. CS’s
  5. NSAIDs (analgesia)
  6. Combo
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14
Q

Are traditional DMARDs good for flares? Why or why not?

A

No b/c they have a SLOW ONSET

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15
Q

What classes of drugs are used for maintenance tx?

A

Traditional DMARDs, biologic DMARDs, synthetic DMARDs

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16
Q

What classes of drugs are used for flare tx?

A

NSAIDs, CS’s

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17
Q

List the traditional DMARDs

A

methotrexate (MTX), leflunomide (LEF), hydroxychloroquine (HCQ), sulfasalazine (SSZ)

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18
Q

Which trad DMARDs inhibit the immune sys more upstream?

A

MTX and LEF

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19
Q

What do HCQ and SSZ ultimately do (MOA-wise)?

A

Reduce inflammation

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20
Q

Important dosing point of methotrexate?

A

Must be TITRATED

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21
Q

Very common AE of methotrexate?

A

Fatigue

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22
Q

A patient has a cold. Should we put him on MTX? Why or why not?

A

No bc MTX suppress the immune response, which would prevent the body from dealing w/ the infection

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23
Q

Is there bone healing with MTX?

A

Yes

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24
Q

MTX’s place in tx?

A

FIRST LINE/Backbone of tx

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25
Q

Common LEF A/E’s?

A

N/D

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26
Q

T or F: LEF is safe in pregnancy, whereas MTX is not.

A

F

They’re BOTH CI in pregnancy (and lactation for that matter)

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27
Q

When is LEF used?

A

Either

  1. added to MTX when RA isn’t well-ctrled
  2. monotx when MTX is not tolerated
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28
Q

Is there bone healing with LEF?

A

Yes

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29
Q

Best tolerated trad DMARD?

A

HCQ (hydroxychloroquinone)

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30
Q

Most important AE assoc w/ HCQ?

A

Ocular tox

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31
Q

How long does it take for ocular toxicity to show up when taking HCQ?

A

≥7 years

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32
Q

A patient has retinopathy. Which trad DMARD are we gonna avoid giving him?

A

HCQ (it causes ocular tox)

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33
Q

HCQ - place in tx

A

Almost always added on to other DMARDs
OR
Used for early, mild RA

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34
Q

Important DI with sulfasalazine (SSZ)?

A

Warfarin (it causes an increased INR)

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35
Q

Name the biologic DMARDs

A

TNF-alpha inhibitors, IL-1/6 inhibitors, T-cell co-stimulation inhibitors, B-cell depletors

36
Q

TNF-alpha drugs:

A
adalimumab
certolizumab
etanercept
golimumab
infliximab
37
Q

Which TNF-alpha inhibitor(s) is/are always given with MTX?

A

golimumab and infliximab

38
Q

Which TNA-alpha inhibitors are safe during pregnancy?

A

adalimumab, etanercept > both are safe up to the 3rd trimester

certolizumab > safe in all trimesters

39
Q

Why might TNF-alpha inhibitor efficacy drop over time?

A

Ab development

40
Q

Initial biologic DMARD of choice?

A

TNA-alpha

41
Q

IL-1/IL-6 inhibitor drugs:

A

IL-1 blocker: anakinra

IL-6 blockers: tocilzumab, sarilumab

42
Q

T or F: IL-1/IL-6 experience Ab development.

A

T (but there’s no reduced efficacy, interestingly)

43
Q

Why is simvastatin CI’ed with tocilumab (IL-6 blocker)?

A

Bc toci increases simvastatin levels by 4-10x

44
Q

Is there bone healing with IL-1/6 inhibitors?

A

Yes

45
Q

Which biologic would be considered if the pt has liver tox?

A

abatacept (T-cell co-stimulation inhibitor) > only biologic known for this

46
Q

What unique A/E is assoc w/ abatacept (T-cell co-stim inhibitor)?

A

It worsens COPD

47
Q

Name the B-cell depletor drug:

A

rituximab

48
Q

In what kind of pts is rituximab more effective?

A

In rheumatoid factor-positive pts

49
Q

T or F: rituximab (B-cell depletor) is not affected by Ab development

A

F

50
Q

What is the initial biologic DMARD attempted?

A

TNF-inhibitors

51
Q

What initial biologic DMARD is tried if TNF-alpha blockers are not tolerated?

A

IL-1/6 blockers

52
Q

When are T-cell co-stim inhibitors indicated?

A

When trad DMARDs and TNF blockers have failed

53
Q

Last line biologic DMARD?

A

B-cell depletor (rituximab) > when ALL ELSE has failed

54
Q

Another name for synthetic DMARD?

A

Janus kinase inhibitor

55
Q

How do janus kinase inhibitors work (MOA)?

A

they inhibit JK enzymes > reduces IL signalling > reduces inflammation

56
Q

Name the janus kinase inhibitor drugs (synthetic DMARDs):

A
  1. tofacitinib

2. baricitinib

57
Q

Ab development with synthetic DMARDs?

A

No

58
Q

Which DMARDs lose their efficacy due to Ab development?

A
  1. TNF-alpha blockers (biologic DMARD)
  2. T-cell co-stim inhibitors (??) (biologic DMARD)
  3. B-cell depletors (biologic DMARD)
59
Q

Which DMARDs DO NOT lose their efficacy due to Ab development?

A
  1. IL-1/6 inhibitors (biologic DMARD)
  2. Synthetic DMARDs
  3. All traditional DMARDs
60
Q

When are Synthetic DMARDs considered?

A

When pt has failed on 3 other biologics

61
Q

When are CS’s used in RA pts?

A

During flares

62
Q

How are CS’s usually used to tx flares?

A

10-15 mg prednisone equivalent/day for 2-3 months (yes, MONTHS for short-term use) > taper afterwards

63
Q

T or F: It’s safe to use CS’s as monotx during RA flares.

A

F (a DMARD should always be on board)

64
Q

How are NSAIDs dosed for RA flares?

A

High doses at initial RA dx > used for 2 weeks for max effect

65
Q

Common combinations seen in RA tx:

A
  1. NSAID’s/CS’s can be added to any regimen
  2. MTX can be added to any biologic
  3. Trad DMARD combos: a. any 2 of the 4 trad DMARDs (double tx) b. MTX + SSZ + HCQ (triple tx)
66
Q

Which RA tx combos are avoided or questionable?

A
  1. Multiple biologics = avoided

2. Biologic + 2 DMARDs = questionable efficacy

67
Q

T or F: Intra-articular CS’s are NEVER used in RA.

A

F

They are s.times used, esp. during flares that affect 1 or a few joints only

68
Q

Why are NSAIDs used in RA?

A

To treat the PAIN assoc w/ RA flares.

69
Q

Live, attenuated vaccines are CI’ed with what kind of tx?

A

biologic DMARD tx

70
Q

Which DMARDs should be stopped before thinking about pregnancy?

A

MTX and LEF

71
Q

Safest trad DMARDs during pregnancy?

A

HCQ and SSZ

72
Q

Which biologics are safe during pregnancy?

A

TNF-alpha blockers:

  1. adalimumab (up to the 3rd trimester)
  2. atanercept (up to the 3rd trimester)
  3. certolizumab (safe for all trimesters)
73
Q

How much folic acid should be used during preg in RA pts?

A

0.4-1 mg usually

5 mg if previous MTX use

74
Q

Safest options for maintenance drugs during lactation?

A

HCQ, SSZ, TNF-alpha inhibitors

75
Q

Systemic JRA (juvenile rheumatoid arthritis) tx’s:

A
  1. NSAIDs + physical tx
  2. CS’s (cautiously and sparingly)
  3. Biologic (if indicated) - tocilzumab (IL-6 blocker)
76
Q

Pauciarticular/Polyarticular JRA tx

A

MTX or TNF-alpha blocker = 1st line

77
Q

What kind of drug is anakinra?

A

IL-1 inhibitor

78
Q

What kind of drug is certolizumab?

A

TNF-alpha blocker

79
Q

What kind of drug is etanercept?

A

TNF-alpha blocker

80
Q

What kind of drug is abatacept?

A

T-cell co-stimulation inhibitor

81
Q

What kind of drug is rituximab?

A

B-cell depletor

82
Q

What kind of drug is baricinib?

A

Janus kinase inhibitor

83
Q

What kind of drug is sarilumab?

A

IL-6 inhibitor

84
Q

What kind of drug is tofacitinib?

A

Janus kinase inhibitor

85
Q

What kind of drug is golimumab?

A

TNF-alpha blocker

86
Q

What kind of drug is infliximab?

A

TNF-alpha blocker