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255B > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is RA

A

an autoimmune condition leading to inappropriate immune system activity causing synovial and connective tissue inflammation

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2
Q

What is the pathophysiology of RA?

A

chronic inflammation -> growth tissue (pannus) -> loss of bone and cartilage

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3
Q

Sx of RA

A

Symmetrical joint pain and stiffness >6 weeks
Muscle pain
May have fatigue, weakness, low-grade fever, appetite decrease

Joint tenderness with warmth and swelling over affected joints
Rheumatoid nodules may develop

most commonly a rapid onset starting in peripheral joints

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4
Q

List some key differences b/w OA and RA?

A

Affected joints
OA - Symmetrical
RA - often starts unilateral and on weight bearing joints
Duration of Morning Stiffness
OA - > 1 duration
RA - <1 hours duration - stiffness returns end of day or after activity
Presence of Systemic Sx
OA - yes, especially during flares
RA - none

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5
Q

List all of the extra articular sequelae affected by RA

A

Blood vessels
Lungs
Eyes
Heart
Muscle
Bone
Skin
Hematologic abnormalities

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6
Q

How to diagnosis RA?

A

Cannot be established by a single lab test or procedure

Established diagnostic criteria / scoring system
Joint involvement
Lab test findings
Rheumatoid factor in 60-70% of patients
Elevated ESR and CRP
Anti-cyclic citrullinated peptide antibody (anti-CCP)
Duration of symptoms

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7
Q

What is the goal of RA tx

A

prevent and control joint damage
prevent loss of function
maintain QoL
decrease pain

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8
Q

Achieve remission or low disease activity

A

Tender/swollen joint count <1
A measure of function based on the Health Assessment Questionnaire (HAQ)
CRP score <1
A physician global assessment <2
A patient assessment of global disease activity (PtGA) <2

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9
Q

List some general principles of management

A

1) Early recognition and diagnosis
Significant damage occurs in first two years of disease
2) Early use of DMARDs
Start within 3m of diagnosis
Depending on severity, treat aggressively
3) Concept of “tight control”
Treat until remission or low disease activity
Quickly treat exacerbations
Aggressively add DMARDs or early switch
Adjunct NSAID / steroids
Frequent reassessment
4) Responsible NSAID and glucocorticoid use
Reduce / discontinue as disease enters remission

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10
Q

List non pharmacologic therapy for RA

A

Patient education

Rest important, but balance with activity

Reduce joint stress with RA friendly tools

Occupational and physical therapy

Diet / weight loss

Surgery

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11
Q

Main classes of tx

A

Maintenance
- tDMARDs
-biologic DMARDs
-synthetic DMARDs
Flares
-corticosteroids
-NSAIDs/Analgesia

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12
Q

What should you know about tDMARDs

A

Slow onset of action
Controls symptoms
May delay or stop progression of disease
Requires regular monitoring

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13
Q

List the different tDMARDs

A

Hydroxychloroquine
Sulfasalazine
Methotrexate
Leflunomide

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14
Q

MOA of hydroxychloroquine

A

inhibits neutrophils and chemotaxis
impairs complement system

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15
Q

MOA of sulfasalazine

A

prodrug metabolized into 5-ASA and sulfapyridine
modulates mediators of inflammatory response
may inhibit TNF

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16
Q

MOA of methotrexate

A

anti-folate –> less DNA synthesis, repair, cellular replication and immune response

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17
Q

MOA of leflunomide

A

inhibits pyrimidine synthesis, leading to anti-inflammatory effects
modulates many signaling pathways

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18
Q

Onset of hydroxychloroquine

A

2-6 months

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19
Q

Onset of sulfasalazine

A

2-3 months

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20
Q

Onset of methotrexate

A

1-2 months

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21
Q

Onset of leflunomide

A

1-3 months

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22
Q

Dosing for Methotrexate

A

7.5 mg to 25 mg PO weekly
titrate to target in most cases
renal dosing for GFR 10-50 ml
may initiate at target dose in select patients

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23
Q

S/E for hydroxychloroquine

A

best tolerated of the DMARDs
NVD. stomach cramps
skin / allergies lesions (10%)
H/A
dizziness

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24
Q

S/E for sulfasalazine

A

H/A
photosensitivity
NVD

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25
Q

S/E for leflunomide

A

N,D
rash and HTN
reversible alopecia

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26
Q

S/E for Methotrexate

A

N/V
fatigue
stomatitis

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27
Q

A/E for hydroxychloroquine

A

myopathy
ocular toxicity

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28
Q

A/E for sulfasalazine

A

hematologic abnormalities

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29
Q

A/E for methotrexate

A

Hepatotoxicity
Hematologic abnormalities
Pulmonary toxicity
Reversible sterility in men
Infection increase

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30
Q

A/E for leflunomide

A

Hepatotoxicity
Significant weight loss
infection increase

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31
Q

CI for hydroxychloroquine

A

pre-existing retinopathy

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32
Q

CI for sulfasalazine

A

Hypersensitivity to salicylates or sulfonamides
Asthma attacks precipitated by ASA or NSAIDs
Severe renal / hepatic impairment
Existing gastric or duodenal ulcer

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33
Q

Precautions and CI for methotrexate

A

Precaution
Caution in lung dysfunction
CI
Severe hepatic impairment
Current hematologic abnormalities
Pregnancy / breastfeeding
Catergory X

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34
Q

Precautions and CI for Leflunomide

A

CI
Moderate-severe renal (<60ml/min) / hepatic impairment
Increase chance of toxicity
Current hematologic abnormalities or serious infection
Pregnancy / breastfeeding

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35
Q

DDI for hydroxychloroquine

A

no CYP interactions
high risk QT-prolongation

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36
Q

DDI for Sulfasalazine

A

additive N if used with MTX
possible issue with warfarin

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37
Q

DDI for leflunomide

A

Bile-acid sequestrants cause rapid elimination – can use to help remove (if they want to get pregnancy 6 months (without this process is 2 years)
Additive immunosuppression – will flag but it common to use both
Live vaccines – coadministration is when we are cautious

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38
Q

DDI for MTX

A

Many drug interactions only significant based on cancer doses (e.g. 500 - 2000mg weekly)

NSAIDs
Decreases clearance of MTX, increased toxicity potential
MTX <15mg/week – likely no risk
MTX 15-25mg/week – very low risk
Risk increases with concomitant renal dysfunction
Trimethoprim (mono agent or in combination with sulfamethoxazole)
Significantly increases risk of pancytopenia at any MTX dose, consider contraindicated
PPIs
Only an issue if MTX >500mg/week
Loop diuretics
Decreases clearance of MTX, may increase nephrotoxicity potential
Likely only an issue on high doses
Live vaccines

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39
Q

Monitoring for DMARDs for Efficacy

A

disease activity (ESR,CRP) every 1-3 months initially
radiographs q1-3m

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40
Q

Monitoring for Hydroxychloroquine for safety

A

no lab tests required
ocular toxicity - ophthalmic exam baseline and annually after 5 years

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41
Q

Monitoring for sulfasalazine for safety

A

CBCs and LFTs, creatinine

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42
Q

Monitoring for MTX for safety

A

CBCs and LFTs, creatinine
chest x-ray (baseline)

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43
Q

Monitoring for leflunomide for safety

A

CBCs and LFTs, creatinine

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44
Q

Where is the place in therapy for hydroxychloroquine?

A

Useful for early, mild RA
Best tolerated of the DMARDs
Combined with other DMARDs – monotherapy generally rare

45
Q

Where is the place in therapy for sulfasalazine

A

Use if other options not tolerated
Most effective the earlier used
Combined with other DMARDs – monotherapy generally rare

46
Q

Where is the place in therapy for methotrexate

A

Highly effective in mod-severe disease
Significantly improves efficacy when combined with biologics
Standard therapy – “backbone”

47
Q

Where is the place in therapy for leflunomide

A

Replacement for MTX if not tolerated
May be added in low doses to MTX

48
Q

List the main classes for Biologic DMARDs

A

TNF – α inhibitors
Interleukin – 1 or 6 inhibitors
T-Cell Co-stimulation inhibitors
B-Cell depletors

49
Q

Common S/E for biologics DMARDs

A

Common side effects
Nausea
Headache
Diarrhea
Malaise

50
Q

Concerns for all biologics

A

Injection site reactions
SC  minor redness and itching, swelling, pain.
Lasts 3-5 days each injection
Severity declines over time
IV  headache and nausea, rash, hives, fever, chills, fatigue

Hypersensitivity
Anaphylaxis uncommon
Often pre-treat: acetaminophen + antihistamine + steroid ~90 min prior

51
Q

What factors increase the infection rate for biologics?

A

Age and dose related
Incidence in trials was 5-10%/yr (common) or 2-4%/yr (serious)
Common infections: sinusitis, pharyngitis, candidiasis, pneumonia, UTIs
Serious infections: TB, mycobacterial, PCP, CMV, zoster, Hep B/C
Risk highest early in therapy

52
Q

A/E for biologics

A

Neutropenia
malignant disease
increase infection risk such as TB, Hep C, HIV
antibody development

53
Q

Monitoring Plan for Biologics (infection risk)

A

Screen for TB, Hep C, Hep B, HIV prior to therapy
Up to date on vaccinations (esp. influenza / COVID)
Use biologics with a shorter dosing interval in high-risk patients
Educate patient on signs of infection (moderate fever/malaise)
Abatacept may be safest option in high-risk patients
Never use two biologics in combination

54
Q

List the TNF a inhibitors

A

Adalimumab
Certolizumab
Etanercept
Golimumab
Infliximab

55
Q

Which TNF a inhibitors are indicated in combination with MTX?

A

infliximab
golimumab

56
Q

CI for TNF a inhibitors

A

active severe infection
moderate to severe HF

57
Q

DDI for TNF a inhibitors

A

live vaccines
additive immunosuppression with other drugs

58
Q

List some of the serious A/E for TNF a inhibitor

A

Liver enzyme elevation
heart failure
cutaneous
autoimmune disease
seizure risk

59
Q

Monitoring plan for TNF a inhibitor

A

TB, HIV, Hep B/C screening
CBCs
LFTs
Signs of infection
Ensure vaccinated

60
Q

What should be considered when choosing b/w TNF a inhibitor?

A

frequency of dosing and route
cost -> considered those with a biosimilar
rheumatologist preference

61
Q

How does IL-1 or 6 inhibitors work?

A

Endogenous interleukins bind to interleukin receptors  mediates many immunological responses  cartilage damage

IL-1 and 6 inhibitors antagonize the receptors  reduction in cytokine activity

62
Q

List the IL-1 and 6 inhibitors

A

Anakinra (IL-1)*
Tocilizumab (IL-6)
Sarilumab (IL-6)

63
Q

CI for IL1 and 6 inhibitors

A

none for anakinra and sarilumab

active infections for tocilizumab

64
Q

Onset of action for IL 1 and 6 inhibitors

A

weeks but peak at 5-6 months

65
Q

S/E for anakinra

A

Injection-site reactions and infections
Overall serious adverse effects similar to placebo rate

66
Q

S/E for tocilizumab / sarilumab

A

GI perforation (unique + rituximab)
Rare
Caution if at risk of GI issues

Dyslipidemia (unique): ↑ TC / TG and ↓HDL

Antibody development not linked to decreased effect (unique)

Hypertension

Other concerns similar to TNF inhibitors (common ADRs, LFTs, infections, malignancy, neutropenia)

67
Q

DDI for IL 1 and 6 inhibitors

A

all
- decreased IL-1 and 6 activity =increased CYP activity
additive immunosuppression
live vaccines

68
Q

Specific DDI for tocilizumab

A

simvastatin increased 4-10x

69
Q

Monitoring plan for anakinra

A

Baseline CBC, LFTs, creatinine; then every 3-6 months

70
Q

Monitoring plan for tocilizumab & sarilumab

A

Baseline CBC, LFTs, creatinine; repeating in 4-8 weeks after starting, then every 3-6 months
Lipid panel
Blood pressure
Latent / active TB, Hep B/C screening

71
Q

What do you need to know about T-cell co-stimulation inhibitor?

A

Inhibits T-cell activation

Used if inadequate response to DMARDs or TNF inhibitors

Monotherapy or combination with traditional DMARDs (MTX)

72
Q

List the T cell Co-stimulation inhibitor

A

Abatacept

73
Q

S/E for abatacept

A

Similar to TNF inhibitor – infections (likely lower risk), neutropenia, common ADRs
COPD exacerbations (unique)

No impact on liver function (unique)
Hypertension
Blood glucose increased
Unknown if antibodies impact efficacy or safety

74
Q

Monitoring for T cell Co stimulation inhibitor

A

Signs and symptoms of infection
TB and hepatitis screening
CBCs, creatinine
Blood pressure
Blood glucose

75
Q

What do you need to know about B cell depletor

A

B-cells central to immune memory and the production of auto-antibodies

B-cell depletors bind to B-cells to cause lysis

76
Q

List the B cell depletor

A

rituximab

77
Q

What is the place in therapy for b cell depletor

A

only studied in combination with MTX AND failure on a TNF inhibitor

78
Q

Onset for b cell depletor

A

may be delayed up to 6 months

79
Q

A/E for B cell depletor

A

Infusion reactions tend to be more rapid, but mild and brief

Serious infection rate is non-existent initially; then increases on repeat courses

Hypertension
GI perforation
Blood glucose increase

Mucocutaneous reactions (SJS, TEN) – reported, more common than other biologics

Antibody formation likely leads to increased infusion reactions and decreased efficacy

80
Q

Monitoring for B cell depletor

A

Baseline CBC, LFTs, creatinine
TB, Hepatitis B/C screening

81
Q

Which biologic has no antibody resistance

A

IL 6 inhibitor

82
Q

Which biologic should be avoided in HF

A

TNF a inhibitor

83
Q

Which biologic should be used in liver injury?

A

T cell co-stimulation inhibitor

84
Q

Which biologics have high risk for GI perforation, HTN, and increase lipid levels?

A

IL 6 inhibitors

85
Q

Which biologic should be avoided with seizures?

A

TNF a inhibitors

86
Q

Which biologic has increase risk of glucose changes and COPD exacerbation?

A

T cell Costimulator inhibitors

87
Q

What is the place of therapy for IL 1

A

for those risk averse or who cannot tolerate other DMARDs

88
Q

What is the place of therapy for TNF a inhibitor

A

initial biologic of choice for most

89
Q

What is the place of therapy for IL 6

A

for moderate to severe RA often in combination with MTX

90
Q

What is the place of therapy for T cell Co-stimulation inhibitors

A

when traditional DMARDs or TNF inhibitors have failed

91
Q

What is the place of therapy for B cell depletors

A

combo with MTX when others have failed
use if history of lymphoma

92
Q

What should you know about janus kinase inhibitor

A

Janus Kinase are a group of enzymes responsible for enabling interleukin signalling

Indicated preferably in combination with MTX
May be used as monotherapy if MTX intolerance
Other combinations not recommended

93
Q

What is the place in therapy for janus kinase inhibitor

A

last line option

94
Q

List the janus kinase inhibitor

A

tofacitinib
baricitinib
upadacitinib

95
Q

A/E for Janus Kinase Inhibitors

A

Similar to TNF inhibitors and other biologics, including:
HTN
Infections / cytopenia
LFTs / hepatotoxicity
Bradycardia
GI perforation

No concern about antibody development

96
Q

CI for Janus Kinase Inhibitor

A

use during severe infections

97
Q

Warning for Janus Kinase Inhibitor

A

New data - CV risk (MI, clots) - NNH 113/5yrs
New data - Malignancy (lung cancer, lymphoma) – NNH 55/5 yrs
GI perforations
Bradycardia
Dyslipidemia

*these are reasons why they are last line

98
Q

DDI for Janus Kinase Inhibitors

A

Tofactinib / upadacitinib are major 3A4 substrates; baricitinib is a minor 3A4 substrate
Live vaccines
Additive immunosuppression

99
Q

Monitoring Plan for Janus Kinase Inhibitor

A

Latent TB testing
Lipid profile
CBCs every 3-6m months
LFTs

100
Q

What are the three treatment modalities used for RA with corticosteroids

A

Short term use - doses of 10-15 mg per day about 2 months with titration
taper and d/c as sxm improve

chronic use - 5-10 mg per day indefinitely
long term steroid safety issues become apparent
increases need for monitoring and adjunctive tx

Pulse Therapy - high dose for a few days
- safety issues is CV collapse, hypokalemia, MI
considered last resort option in RA

101
Q

Monitoring plan for Steroids for RA

A

Cataracts
Dyslipidemia
Hyperglycemia
Osteoporosis
Weight gain

102
Q

What do you need to know about intra articular injections with steroids for RA?

A

Safe and effective when done by experienced MD
Effects dramatic, but temporary
Same joint should not be done more than once per 3 months
Considered “palliative”
Rest joint for 3 days after injection

103
Q

What is the potential issues for steroids intra-articular injections

A

tendon rupture
acute synovitis
acute synovitis
localized skin hypopigmentation
septic arthritis

104
Q

What is the guideline approach for steroids for RA?

A

Consider for flares or as “bridging”
Aim for a max dose of 10mg/d
Never use as monotherapy
Find minimum dose/duration

Consider avoiding in those more at risk of steroid side effects

105
Q

What should you know about NSAIDs use in RA?

A

Provide high dose NSAIDs at initial diagnosis

Use for at least 2 weeks for maximum benefit

Cautiously combined with other treatments

Consider providing GI protection

Should not need to use chronically

mainly uses celoxib

106
Q

List factors of flare management

A

Intra articular glucocorticoid if few joints
Initiate / increase glucocorticoid
Consider increasing DMARD doses
Add new DMARDs if frequent flares

107
Q

What is the order of preference for initial of DMARDs

A

HCQ > SSZ > MTX > LEF

108
Q

When should therapy be escalated?

A

Failure to achieve remission or acceptable disease activity after 3-6 months at optimal doses
Inability to taper steroids
Recurrent flares
Disease progression on Xray

109
Q
A

255B (5 decks)

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