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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
S/E for leflunomide
N,D rash and HTN reversible alopecia
26
S/E for Methotrexate
N/V fatigue stomatitis
27
A/E for hydroxychloroquine
myopathy ocular toxicity
28
A/E for sulfasalazine
hematologic abnormalities
29
A/E for methotrexate
Hepatotoxicity Hematologic abnormalities Pulmonary toxicity Reversible sterility in men Infection increase
30
A/E for leflunomide
Hepatotoxicity Significant weight loss infection increase
31
CI for hydroxychloroquine
pre-existing retinopathy
32
CI for sulfasalazine
Hypersensitivity to salicylates or sulfonamides Asthma attacks precipitated by ASA or NSAIDs Severe renal / hepatic impairment Existing gastric or duodenal ulcer
33
Precautions and CI for methotrexate
Precaution Caution in lung dysfunction CI Severe hepatic impairment Current hematologic abnormalities Pregnancy / breastfeeding Catergory X
34
Precautions and CI for Leflunomide
CI Moderate-severe renal (<60ml/min) / hepatic impairment Increase chance of toxicity Current hematologic abnormalities or serious infection Pregnancy / breastfeeding
35
DDI for hydroxychloroquine
no CYP interactions high risk QT-prolongation
36
DDI for Sulfasalazine
additive N if used with MTX possible issue with warfarin
37
DDI for leflunomide
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
38
DDI for MTX
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
39
Monitoring for DMARDs for Efficacy
disease activity (ESR,CRP) every 1-3 months initially radiographs q1-3m
40
Monitoring for Hydroxychloroquine for safety
no lab tests required ocular toxicity - ophthalmic exam baseline and annually after 5 years
41
Monitoring for sulfasalazine for safety
CBCs and LFTs, creatinine
42
Monitoring for MTX for safety
CBCs and LFTs, creatinine chest x-ray (baseline)
43
Monitoring for leflunomide for safety
CBCs and LFTs, creatinine
44
Where is the place in therapy for hydroxychloroquine?
Useful for early, mild RA Best tolerated of the DMARDs Combined with other DMARDs -- monotherapy generally rare
45
Where is the place in therapy for sulfasalazine
Use if other options not tolerated Most effective the earlier used Combined with other DMARDs -- monotherapy generally rare
46
Where is the place in therapy for methotrexate
Highly effective in mod-severe disease Significantly improves efficacy when combined with biologics Standard therapy – “backbone”
47
Where is the place in therapy for leflunomide
Replacement for MTX if not tolerated May be added in low doses to MTX
48
List the main classes for Biologic DMARDs
TNF – α inhibitors Interleukin – 1 or 6 inhibitors T-Cell Co-stimulation inhibitors B-Cell depletors
49
Common S/E for biologics DMARDs
Common side effects Nausea Headache Diarrhea Malaise
50
Concerns for all biologics
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
What factors increase the infection rate for biologics?
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
A/E for biologics
Neutropenia malignant disease increase infection risk such as TB, Hep C, HIV antibody development
53
Monitoring Plan for Biologics (infection risk)
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
List the TNF a inhibitors
Adalimumab Certolizumab Etanercept Golimumab Infliximab
55
Which TNF a inhibitors are indicated in combination with MTX?
infliximab golimumab
56
CI for TNF a inhibitors
active severe infection moderate to severe HF
57
DDI for TNF a inhibitors
live vaccines additive immunosuppression with other drugs
58
List some of the serious A/E for TNF a inhibitor
Liver enzyme elevation heart failure cutaneous autoimmune disease seizure risk
59
Monitoring plan for TNF a inhibitor
TB, HIV, Hep B/C screening CBCs LFTs Signs of infection Ensure vaccinated
60
What should be considered when choosing b/w TNF a inhibitor?
frequency of dosing and route cost -> considered those with a biosimilar rheumatologist preference
61
How does IL-1 or 6 inhibitors work?
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
List the IL-1 and 6 inhibitors
Anakinra (IL-1)* Tocilizumab (IL-6) Sarilumab (IL-6)
63
CI for IL1 and 6 inhibitors
none for anakinra and sarilumab active infections for tocilizumab
64
Onset of action for IL 1 and 6 inhibitors
weeks but peak at 5-6 months
65
S/E for anakinra
Injection-site reactions and infections Overall serious adverse effects similar to placebo rate
66
S/E for tocilizumab / sarilumab
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
DDI for IL 1 and 6 inhibitors
all - decreased IL-1 and 6 activity =increased CYP activity additive immunosuppression live vaccines
68
Specific DDI for tocilizumab
simvastatin increased 4-10x
69
Monitoring plan for anakinra
Baseline CBC, LFTs, creatinine; then every 3-6 months
70
Monitoring plan for tocilizumab & sarilumab
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
What do you need to know about T-cell co-stimulation inhibitor?
Inhibits T-cell activation Used if inadequate response to DMARDs or TNF inhibitors Monotherapy or combination with traditional DMARDs (MTX)
72
List the T cell Co-stimulation inhibitor
Abatacept
73
S/E for abatacept
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
Monitoring for T cell Co stimulation inhibitor
Signs and symptoms of infection TB and hepatitis screening CBCs, creatinine Blood pressure Blood glucose
75
What do you need to know about B cell depletor
B-cells central to immune memory and the production of auto-antibodies B-cell depletors bind to B-cells to cause lysis
76
List the B cell depletor
rituximab
77
What is the place in therapy for b cell depletor
only studied in combination with MTX AND failure on a TNF inhibitor
78
Onset for b cell depletor
may be delayed up to 6 months
79
A/E for B cell depletor
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
Monitoring for B cell depletor
Baseline CBC, LFTs, creatinine TB, Hepatitis B/C screening
81
Which biologic has no antibody resistance
IL 6 inhibitor
82
Which biologic should be avoided in HF
TNF a inhibitor
83
Which biologic should be used in liver injury?
T cell co-stimulation inhibitor
84
Which biologics have high risk for GI perforation, HTN, and increase lipid levels?
IL 6 inhibitors
85
Which biologic should be avoided with seizures?
TNF a inhibitors
86
Which biologic has increase risk of glucose changes and COPD exacerbation?
T cell Costimulator inhibitors
87
What is the place of therapy for IL 1
for those risk averse or who cannot tolerate other DMARDs
88
What is the place of therapy for TNF a inhibitor
initial biologic of choice for most
89
What is the place of therapy for IL 6
for moderate to severe RA often in combination with MTX
90
What is the place of therapy for T cell Co-stimulation inhibitors
when traditional DMARDs or TNF inhibitors have failed
91
What is the place of therapy for B cell depletors
combo with MTX when others have failed use if history of lymphoma
92
What should you know about janus kinase inhibitor
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
What is the place in therapy for janus kinase inhibitor
last line option
94
List the janus kinase inhibitor
tofacitinib baricitinib upadacitinib
95
A/E for Janus Kinase Inhibitors
Similar to TNF inhibitors and other biologics, including: HTN Infections / cytopenia LFTs / hepatotoxicity Bradycardia GI perforation No concern about antibody development
96
CI for Janus Kinase Inhibitor
use during severe infections
97
Warning for Janus Kinase Inhibitor
*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
DDI for Janus Kinase Inhibitors
Tofactinib / upadacitinib are major 3A4 substrates; baricitinib is a minor 3A4 substrate Live vaccines Additive immunosuppression
99
Monitoring Plan for Janus Kinase Inhibitor
Latent TB testing Lipid profile CBCs every 3-6m months LFTs
100
What are the three treatment modalities used for RA with corticosteroids
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
Monitoring plan for Steroids for RA
Cataracts Dyslipidemia Hyperglycemia Osteoporosis Weight gain
102
What do you need to know about intra articular injections with steroids for RA?
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
What is the potential issues for steroids intra-articular injections
tendon rupture acute synovitis acute synovitis localized skin hypopigmentation septic arthritis
104
What is the guideline approach for steroids for RA?
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
What should you know about NSAIDs use in RA?
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
List factors of flare management
Intra articular glucocorticoid if few joints Initiate / increase glucocorticoid Consider increasing DMARD doses Add new DMARDs if frequent flares
107
What is the order of preference for initial of DMARDs
HCQ > SSZ > MTX > LEF
108
When should therapy be escalated?
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

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