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PHAR255 > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is rheumatoid arthritis?

A

an autoimmune condition leading to inappropriate immune system activity causing synovial and connective tissue inflammation
-chronic inflammation–>growth of tissue (pannus)–>cartilage and bone loss
-triggered by genetics and a “stochastic” event

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2
Q

What are the consequences of inflammation due to rheumatoid arthritis?

A

loss of cartilage
formation of scar tissue
ligament laxity
tendon contractures

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3
Q

Which sex is rheumatoid arthritis more common in?

A

women (earlier onset as well)
-occurs at any age
-no difference with ethnicity

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4
Q

What are the symptoms of rheumatoid arthritis?

A

symmetrical joint pain and stiffness > 6 weeks
muscle pain
may have fatigue, low-grade fever, decreased appetite, weakness
joint tenderness with warmth + swelling
rheumatoid nodules may develop

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5
Q

What is the typical presentation of a new case of rheumatoid arthritis?

A

rapid onset starting in peripheral joints

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6
Q

Differentiate OA and RA.

A

age of onset:
-RA: any
-OA: later in life
speed of onset:
-RA: fast
-OA: slow
joint symptoms:
-RA: painful, swollen, stiff
-OA: painful; little swelling
systemic symptoms:
-RA: yes, especially during flares
-OA: none
affected joints:
-RA: symmetrical
-OA: often starts unilateral, weight bearing joints mainly
duration of morning stiffness:
-RA: >1hr duration
-OA: <1hr duration, stiffness returns end of day or activity

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7
Q

Describe the joint damage caused by rheumatoid arthritis.

A

occurs early in the course of RA
30% have bone erosion at time of diagnosis
damage is irreversible
functional loss follows

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8
Q

What is the extraarticular sequelae of rheumatoid arthritis?

A

blood vessels
eyes
lungs
heart
skin
hematologic
muscle
bone

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9
Q

Describe the impacts that rheumatoid arthritis can have on blood vessels.

A

rheumatoid vasculitis (autoimmune)
can affect any blood vessel (sx depend on affected vessel)
occurs with severe, long-standing RA
substantial morbidity
only tx: aggressive tx of RA

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10
Q

Describe the impacts that rheumatoid arthritis can have on the lungs.

A

pleuritis, pleural effusion, fibrosis, pulmonary nodules
drugs used to treat RA can impact lung function

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11
Q

Describe the impacts that rheumatoid arthritis can have on the eyes.

A

periscleritis, scleritis, uveitis, iritis
painful, visual acuity loss

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12
Q

Describe the impacts that rheumatoid arthritis can have on the heart.

A

pericarditis, myocarditis
increased risk of CAD, HF, afib

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13
Q

Describe the impacts that rheumatoid arthritis can have on muscle.

A

generalized muscle weakness and pain
from synovial inflammation, myositis, vasculitis
steroid-induced

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14
Q

Describe the impacts that rheumatoid arthritis can have on the bone.

A

osteopenia is common
local bone loss around affected joints

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15
Q

Describe the impacts that rheumatoid arthritis can have on the skin.

A

rheumatoid nodules
ulcers
steroid-induced

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16
Q

Describe the impacts that rheumatoid arthritis can have on hematology.

A

anemia of chronic disease

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17
Q

How is rheumatoid arthritis diagnosed?

A

cannot be established by a single lab test or procedure
established diagnostic criteria/scoring system:
-joint involvement
-lab tests: rheumatoid factors, elevated ESR + CRP, anti-CCP
-duration of symptoms

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18
Q

What are the goals of therapy for rheumatoid arthritis?

A

prevent and control joint damage
improve QoL
prevent loss of function
decrease pain
achieve remission or low disease activity
-tender/swollen joint count < 1
-measure function based on HAQ
-physical global assessment < 2
-CRP score < 1
-PtGA < 2 **

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19
Q

What are the principles of management for rheumatoid arthritis?

A
  1. early recognition + diagnosis
    -significant damage in first two years of disease
  2. early use of DMARDs
    -start within 3 months of diagnosis
    -depending on severity, treat aggressively
  3. concept of “tight control”
    -treat until remission or low disease severity
    -quickly treat exacerbations
    -add DMARDs or early switch
    -adjunct NSAIDs/steroids
  4. responsible NSAID and steroid use
    -reduce/dc as disease enters remission
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20
Q

What are the non-pharmacological therapies for rheumatoid arthritis?

A

education
rest is important, balance with activity
reduce joint stress with RA friendly tools
occupational and physical therapy
diet/weight loss
surgery

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21
Q

What are the classes of treatment for rheumatoid arthritis?

A

maintenance:
-tDMARDs
-biologic DMARDs
-synthetic DMARDs
flares:
-steroids
-NSAIDs/analgesia

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22
Q

What are examples of tDMARDs?

A

hydroxychloroquine
sulfasalazine
methotrexate
leflunomide

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23
Q

What are the benefits of tDMARDs?

A

controls symptoms
delay or stop progression of disease

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24
Q

True or false: tDMARDs do not require regular monitoring

A

false

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25
Q

What is the MOA of the different tDMARDs?

A

hydroxychloroquine:
-inhibits neutrophils and chemotaxis
-impairs complement system
sulfasalazine:
-prodrug metabolized into 5-ASA and sulfapyridine
-modulates inflammatory mediators
methotrexate:
-anti folate=less DNA synthesis, repair, replication and immune respinse
leflunomide:
-inhibits pyrimidine synthesis = anti-inflamm.

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26
Q

What is the onset of the tDMARDs?

A

hydroxychloroquine: 2-6 months
sulfasalazine: 2-3 months
methotrexate: 1-2 months
leflunomide: 1-3 months

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27
Q

What is the dosing of methotrexate?

A

7.5-25mg po weekly
-titrate to target in most cases
-renal dosing: 10-50ml
-may initiate at target dose in select pts

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28
Q

What are the common adverse effects of hydroxycholoroquine?

A

best tolerated DMARD
NVD, cramps
skin/allergic reactions
HA, dizziness

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29
Q

What are the common adverse effects of sulfasalazine?

A

HA
NVD
photosensitivity

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30
Q

What are the common adverse effects of leflunomide?

A

nausea, diarrhea
rash and HTN
reversible alopecia

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31
Q

What are the common adverse effects of methotrexate?

A

NV
fatigue
stomatitis
photosensitivity
hair loss
skin itch/burning/rash

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32
Q

What some strategies to manage the adverse effects of methotrexate?

A

folic acid 1-5mg/d or 5-10mg once weekly
split dosing on the same day
SC for GI side effects
add a PPI for 3 days

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33
Q

What are the serious adverse effects of the tDMARDs?

A

hydroxychloroquine:
-myopathy, ocular toxicity
sulfasalazine:
-hematologic
methotrexate:
-hepatotoxicity, hematologic, pulmonary toxicity, infection increase, reversible sterility in men
leflunomide:
-hepatotoxicity, infection increase, weight loss

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34
Q

What are the contraindications to the tDMARDs?

A

hydroxychloroquine:
-pre-existing retinopathy
sulfasalazine:
-hypersensitivity to salicylates or sulfonamides, asthma attack precipitated by ASA or NSAID, GI ulcer, severe renal/hepatic impairment
methotrexate:
-caution in lung dysfunction, pregnancy/breastfeeding, hematologic abnorm, severe hepatic impairment
leflunomide:
-mod to severe renal/hepatic impairment, pregnant/breastfeeding, hematologic abnorm, infection

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35
Q

What are the drug interactions of the tDMARDs?
-not including MTX

A

hydroxychloroquine:
-no CYP interactions, high risk of QT prolongation
sulfasalazine:
-nausea with MTX, warfarin
leflunomide:
-bile acid sequestrants (elimination), immunosuppression, live vaccines

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36
Q

What are the drug interactions of methotrexate?

A

NSAIDs: decrease clearance of MTX
-<15mg/week: likely no risk
-15-25mg/week: very low risk
-risk increases with renal dysfunction
trimethoprim: contraindicated
PPIs: issue if MTX > 500mg/wk
loop diuretics: decrease clearance of MTX, issue if high dose
live vaccines

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37
Q

How can we monitor tDMARDs for efficacy?

A

disease activity (ESR, CRP) q1-3 months initially
radiographs q6-12 months
patient assessment

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38
Q

How can we monitor tDMARDs for safety?

A

hydroxychloroquine:
-no labs, ophthalmic exam baseline and q5yrs
sulfasalazine:
-CBC, LFT, SCr
methotrexate:
-CBC, LFT, SCr, CXR (baseline)
leflunomide:
-CBC, LFT, SCr

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39
Q

What is the relative potencies of the tDMARDs?

A

MTX=leflunomide > SSZ > HCQ

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40
Q

Which tDMARDs show “healing” of bone?

A

methotrexate
leflunomide

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41
Q

Which tDMARDs are considered less effective?

A

hydroxychloroquine and sulfasalazine
less effective vs other DMARDs

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42
Q

What is the place in therapy for each tDMARD?

A

hydroxychloroquine:
-mild + early RA, best tolerated, combo
sulfasalazine:
-not tolerating others, most effective earlier, combo
methotrexate: standard therapy
-highly effective in mod-severe dx, increase efficacy with biologics
leflunomide:
-MTX not tolerated, added in low doses to MTX

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43
Q

What is central to the inflammatory process of rheumatoid arthritis?

A

monocytes, macrophages, and fibroblasts within the synovium which produce cytokines: TNF-a and IL
-over time these damage soft tissue and bone
-B and T cells also a target

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44
Q

What are the main classes of biologic DMARDs?

A

TNF-a inhibitors
IL 1 or 6 inhibitors
T-cell co-stimulation inhibitors
B-cell depletors

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45
Q

What are the common adverse effects of all biologics?

A

nausea
diarrhea
headache
malaise

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46
Q

What are concerns for all biologics?

A

injection site rxn
infection rate increase
neutropenia
malignant disease
antibody development

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47
Q

Describe the concern regarding infection rate with biologics.

A

age and dose related
common: URTI, fungal, pneumonia
serious: Hep B/C, zoster, TB, etc
risk highest early in therapy

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48
Q

How can we mitigate the increased infection rate associated with biologics?

A

screen for serious infections prior to therapy
up to date on vaccinations
use biologics with shorter dosing interval if high risk
educate on signs of infection
never combine two biologics

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49
Q

Which biologic might be the safest option in patients at high risk of infection?

A

abatecept

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50
Q

What should be done if infection occurs while on a biologic?

A

consider temporary d/c

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51
Q

Describe the risk of neutropenia that is common with all biologics.

A

~20% will experience a decrease
increases severity of infections
monitoring important
not a reason to d/c therapy

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52
Q

Describe the risk of malignancy that is common with all biologics.

A

overall: no cancer risk increases except for: skin and lymphomas
avoid biologics in those active malignancies
preferentially avoid if previous skin cancer
use rituximab if previous lymphoma

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53
Q

What occurs when there is antibody development to a biologic?

A

clearance of drug increased by body’s defenses
-usually occurs within 2-6 months of starting

54
Q

Which TNF-a inhibitor has the highest risk of antibody development? Which have lower risk?

A

higher risk: infliximab
lower risk: etanercept, adalimumab

55
Q

Which drug can lower formation of antibodies to biologics?

A

methotrexate

56
Q

True or false: antibody development does not occur with Il-6 inhibitors

A

true

57
Q

What is the risk of antibody development with B and T cell inhibitors?

A

possible risk, less than TNF-inhibitors

58
Q

What are examples of TNF-a inhibitors?

A

adalimumab
golimumab
certolizumab
infliximab
etanercept

59
Q

Why is TNF-a one of the targets in rheumatoid arthritis with biologic drugs?

A

high TNF-a in RA patients –> bone erosion

60
Q

What is the onset for TNF-a inhibitors?

A

within weeks

61
Q

Describe the efficacy of TNF-a inhibitors?

A

ACR50 ~40%
combo with MTX = more effective
slow/stop radiographic progression

62
Q

Which TNF-a inhibitors are only indicated in combination with MTX?

A

infliximab
golimumab

63
Q

Which TNF-a inhibitor is administered IV?

A

infliximab (maybe golimumab)
-rest are SC

64
Q

How frequently are TNF-a inhibitors administered?

A

mainly q2wks

65
Q

What is an area that TNF-a inhibitors lack data in and therefore should be avoided?

A

renal impairment

66
Q

True or false: TNF-a inhibitors are safe in pregnancy/breastfeeding

A

true

67
Q

What are the contraindications to TNF-a inhibitors?

A

active severe infection
mod-severe HF

68
Q

What are the drug interactions of TNF-a inhibitors?

A

live vaccines
additive immunosuppression

69
Q

What are the adverse effects of TNF-a inhibitors?

A

liver enzyme elevations
HF (unique concern)
cutaneous (unique concern + rituximab)
autoimmune disease (unique concern)
seizure risk (unique concern)

70
Q

When are we concerned about liver enzyme elevations with TNF-a inhibitors?

A

> 5x ULN (monitor periodically)

71
Q

Describe HF as a unique concern for TNF-a inhibitors.

A

evidence is not conclusive
may cause or worsen HF
use cautiously if needed
utilize low doses

72
Q

Describe cutaneous AEs as a unique concern for TNF-a inhibitors and rituximab.

A

increased risk of:
-cellulitis
-autoimmune skin disease
-malignancy

73
Q

True or false: TNF-a inhibitors are an appropriate therapy if the patient has a seizure disorder

A

false

74
Q

What are some monitoring parameters for TNF-a inhibitors?

A

TB, HIV, Hep B/C screening
CBCs
LFTs
signs of infection
ensure vaccinated

75
Q

What is the MOA of IL inhibitors?

A

antagonize interleukin receptors –> decreased cytokine activity

76
Q

What are examples of IL inhibitors?

A

anakinra (IL-1)
tocilizumab (Il-6)
sarilumab (IL-6)

77
Q

What is the onset of IL inhibitors?

A

weeks but peak at 5-6 months

78
Q

What are the contraindications to IL inhibitors?

A

anakinra: none
tocilizumab: active infection
sarilumab: none

79
Q

What is the efficacy of the IL inhibitors?

A

anakinra:
-less anti-inflammatory than other biologics
-likely less effective than other biologics
-40% achieve ACR20
tocilizumab/sarilumab:
-~40% achieve ACR50
-similar or potentially more effective than TNF inhibitors

80
Q

What is the route and admin and dosing frequency of the IL inhibitors?

A

anakinra: SC daily
tocilizumab: IV q4wks
sarilumab: SC q2wks

81
Q

Which class of biologics has the robust data for renal impairment?

A

IL inhibitors

82
Q

What are the adverse effects of the IL inhibitors?

A

anakinra:
-injection site rxns and infection
-serious AE risk similar to placebo
tocilizumab/sarilumab:
-GI perforation (unique + rituximab): caution if GI risk
-dyslipidemia (unique): increased TC/TG and decreased HDL
-HTN
-Ab development not linked to decreased efficacy (unique)
-others similar to TNF-a inhibitors

83
Q

What are the drug interactions of IL inhibitors?

A

all:
-decreased IL-1/6 = increased CYP activity
-live vaccines
-additive immunosuppression
tocilizumab:
-increased simvastatin 4-10x

84
Q

What are the monitoring parameters for the IL inhibitors?

A

anakinra:
-baseline CBCs, LFTs, SCr then q3-6mo
tocilizumab/sarilumab:
-baseline CBCs, LFTs, SCr then 4-8wks then q3-6mo
-lipids
-BP
-latent/active TB, HepB/C screening

85
Q

What is the MOA of T cell co-stimulation inhibitors?

A

inhibit T cell activity

86
Q

What is the use for T cell co-stimulation inhibitors?

A

inadequate response to DMARDs or TNF inhibitors
-monotherapy or combo with DMARD (MTX)

87
Q

What is an example of a T cell co-stimulation inhibitor?

A

abatecept

88
Q

What is the route of administration and frequency for abatecept?

A

optional IV loading dose
then SC once weekly

89
Q

What are the adverse effects of abatecept?

A

similar to TNF inhibitors
COPD exacerbations (unique)
no impact on liver function (unique)
HTN
increased blood glucose
unknown if Ab impact efficacy or safety

90
Q

What are the monitoring parameters for abatecept?

A

signs and symptoms of infection
TB and hepatitis
SCr, CBCs
blood pressure
blood glucose

91
Q

What is the MOA of B-cell depletors?

A

bind B-cells and cause lysis
-B cells central to immune memory and Ab production

92
Q

What is an example of a B-cell depletor?

A

rituximab

93
Q

What is the efficacy of rituximab?

A

ACR50 of 43%
does not work well in RF-negative pts
no halt of radiographic progression

94
Q

What is the route of admin and frequency for rituximab?

A

2 dose course: 1g IV 2 wks apart
-pretreat: methyprednisolone, dph, acet
-retreat when needed (~6 months)
-withhold HTN meds the morning of infusion

95
Q

What are the adverse effects of rituximab?

A

infusion rxn more rapid, but mild + brief
initial infection rate non-existent, increases with rpt course
HTN
increased BG
GI perforation
cutaneous rxn (more common than other biologics)
Ab formation = increased rxns, decreased efficacy1

96
Q

What are the monitoring parameters for rituximab?

A

CBC, SCr, LFT
TB, Hep B/C screening

97
Q

What is the place in therapy for the biologic DMARDs?

A

considered once other options have been tried
-exception: initial severe RA
TNF inhibitors:
-initial biologic of choice for most
IL-1/6 inhibitors:
-anakinra: risk averse or cannot tolerate other DMARDs
-tocilizumab/sarilumab: mod-severe RA, combo with MTX
-both: Ab develop to other biologics
T-cell co-stimulation inhibitors:
-tDMARDs or TNF inhibitors failed
B-cell depletors:
-combo with MTX when others failed
-history of lymphoma

98
Q

What is the MOA of JAK inhibitors?

A

JAK is a group of enzymes responsible for IL signaling

99
Q

How should JAK inhibitors be taken?

A

preferably in combo with MTX
-may be used alone if MTX intolerance
-no other combos recommended

100
Q

What is the place in therapy for JAK inhibitors?

A

last line

101
Q

What are examples of JAK inhibitors?

A

tofacitinib
upadacitinib
baracitinib

102
Q

What is the route of admin and frequency for JAK inhibitors?

A

po
OD or BID

103
Q

What is the efficacy of JAK inhibitors?

A

combo: ACR50 46%
alone: ACR50 38%

104
Q

What are the adverse effects of JAK inhibitors?

A

similar to TNF-inhibitors and other biologics:
-HTN
-LFTs/hepatotoxicity
-infections
-bradycardia
-GI perforation
no concern about Ab development

105
Q

What is a contraindication to JAK inhibitors?

A

severe infection

105
Q

What is the main drawback of JAK inhibitors?

A

CV risk (MI, clots)
malignancy

106
Q

What are the drug interactions of JAK inhibitors?

A

tofacitinib/upadacitinib: major 3A4 substrate
live vaccines
immunosuppression

107
Q

What are the monitoring parameters for JAK inhibitors?

A

CBC
LFT
lipids
TB testing

108
Q

True or false: there is lots of data supporting JAK inhibitor use in pregnancy/breastfeeding

A

false
lacking data

109
Q

What is an important tool in rheumatoid arthritis treatment?

A

corticosteroids
-most will use in course of disease
-likely has DMARD properties, and decreases early progression of RA

110
Q

What are the three treatment modalities with corticosteroids for rheumatoid arthritis?

A
  1. short-term use
    -10-15mg prednisone equivalent/day
    -taper and dc as sx improve
    -limited safety issues if dose/duration kept low
  2. chronic use
    -5-10mg prednisone equivalent/day
    -safety issues become apparent
    -increased need for monitoring and adjunct treatment
  3. pulse therapy
    -high doses for a few days
    -safety: CV collapse, hypokalemia, MI, severe infection
    -last resort in RA
110
Q

What is the onset of corticosteroids?

A

within days

110
Q

What is the efficacy of corticosteroids for rheumatoid arthritis?

A

reduces joint tenderness more than NSAIDs and placebo
reduces pain more than NSAIDs
improves QoL measures
small radiographic progression decrease
main benefit: subjective symptomatic improvement

111
Q

What are the monitoring parameters for corticosteroids?

A

long-term AEs
-glaucoma
-hyperglycemia
-dyslipidemia
-osteoporosis
-weight gain

112
Q

Describe intra-articular corticosteroid injections for rheumatoid arthritis.

A

safe and effective when done by MD
effects are dramatic but temporary
same joint should not be done more than 3 months
rest joint x 3 days post-injection
issues: tendon rupture, synovitis, septic arthritis

113
Q

What is the guideline approach to corticosteroid use in rheumatoid arthritis?

A

consider for flares or bridging
aim for max dose of 10mg/d
never use as monotherapy
consider avoiding if risk of steroid AE

114
Q

What is the use of NSAIDs for rheumatoid arthritis?

A

provide high dose NSAIDs at initial diagnosis
use for at least 2 wks for maximum benefit
cautiously combine with other tx
consider providing GI protection
should not need to use chronically

115
Q

What is the role of acetaminophen in rheumatoid arthritis?

A

sometimes added
-poor efficacy

116
Q

What is the role of opioids in rheumatoid arthritis?

A

avoid
-limited evidence
-proper DMARD and non-pharm = greater benefit

117
Q

What is tDMARD double therapy? Triple therapy?

A

double therapy: any two of MTX, SSZ, HCQ, SSZ
triple therapy: MTX + SSZ + HCQ

118
Q

In general, how can we manage a rheumatoid arthritis flare?

A

intraarticular glucocorticoid if few joints
initiate/increase glucocorticoid
consider increasing DMARD dose
add new DMARD if frequent flares

119
Q

As per the 2023 CRA guidelines, what is recommended regarding biologic or synthetic DMARDs for patients in remission or low disease activity?

A

remission: 6 months
reduce dose in stepwise manner but dont d/c

120
Q

As per the 2023 CRA guidelines, what is recommended for people who fail to respond to TNF inhibitors?

A

different TNF inhibitor
non-TNF inhibitor biologic
JAK inhibitor

121
Q

What is the recommendation from the ACR regarding DMARD tapering/dc?

A

recommend staying on DMARDs at current doses
-only consider taper if pt will remain on therapeutic dose of at least 1 DMARD, AND has been in remission x 6 months

122
Q

When should therapy be escalated for rheumatoid arthritis?

A

failure to achieve remission or acceptable disease activity after 3-6 months at optimal dose
inability to taper steroids
recurrent flares
disease progression on xray

123
Q

What are the recommendations for pre-conception in rheumatoid arthritis?

A

must dc unsafe meds
-MTX: male and female - stop 3 months prior
-leflunomide: male and female
achieve remission on safe options
-HCG and SSZ
-all biologics except: rituximab
-certolizumab has most robust data

124
Q

What are the recommendations for peri-pregnancy in rheumatoid arthritis?

A

steroids can be used sparingly
ensure folic acid 5mg/d if previous MTX use
cautious use of NSAIDs

125
Q

What are the recommendations for post-partum in rheumatoid arthritis?

A

flares are common
return to pre-pregnancy dose if compatible with breastfeeding

126
Q

Which agents can be used for rheumatoid arthritis during lactation?

A

NSAIDs (ibuprofen preferred)
low dose steroids (<20mg prednisone per day)
SSZ and HCQ
TNF and IL-6 inhibitors

127
Q

Which rheumatoid arthritis agents should be avoided during lactation?

A

MTX and LEF

PHAR255 (24 decks)

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