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MSK Conditions & Treatment > IC16: Management of RA > Flashcards

IC16: Management of RA Flashcards

1
Q

State the peak incidence of RA and which gender is it most common in

A

Peak: 40-50yo
Most common in females (~3x)

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2
Q

State 3 risk factors for RA

A

Family history 3x higher in 1st degree relative, 2x higher is 2nd deg relative
Genetic predisposition: HLA-DRB1 gene
Smoking

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3
Q

RA increases the risk of developing other chronic diseases such as…

A
  1. CVD
  2. Lung disease
  3. Psychiatric disorders
  4. osteoporosis
  5. Malignancies
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4
Q

List 4 inflammatory cytokines involved in RA pathophysiology

A
  • IL-1
  • IL-6
  • IL-17
  • TNF-a
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5
Q

List the clinical presentations of RA

A
  1. Pain, swelling, erythematous (red) & warm
  2. Early morning stiffness > 30min
  3. Symmetrical polyarthritis (may be unilateral at first)
  4. Systemic symptoms (fatigue, fever, weight loss, depression, generalised aching/stiffness)
  5. Extra-articular complications
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6
Q

List 2 complications of **chronic RA **

A
  1. Deformities- swan neck, boutonneire, Z-shaped thumb etc…
  2. Loss of physical function & ability to carry out ADL
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7
Q

List the extra articular complications of RA. State the organ and type(s) of complications

A
  • Eye: Sjogren’s syndrome
  • Heart: Coronary Artery Disease
  • Haematology: Felty’s syndrome
  • Lungs: pleural effusion, interstitial lung disease
  • Renal: glumorulonephritis
  • Skin: Rheumatoid nodules
  • Vascular: Rheumatoid vasculitis, peripheral vascular disease
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8
Q

List the laboratory findings found in a patient with RA

A
  1. Autoantibodies: RF+, anti-ccp +ve
  2. Acute phase response: Elevated ESR, CRP
  3. FBC: decreased Hct, elevated platelets &WBC
  4. Radiologic(X-ray/MRI): Narrowing of joint space, erosion (around joint margin), hypertrophic synovial tissue (due to pannus formation)
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9
Q

Is radiologic imaging required for the diagnosis of RA?

A

No. Usually done at baseline for monitoring disease progression than diagnosis. Early onset damage usually not observable

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10
Q

Describe the criteria for RA diagnosis

A
  • RA is diagnosed using history, PE, labs, radiographs
    & Must fulfill at least 4 of the following:
  • Early Morning Stiffness > 1 hour x > 6 weeks
  • Swelling of > 3 joints x > 6 weeks
  • Swelling of wrist/ MCP/ PIP joints x > 6 weeks
  • Rheumatoid nodules
  • +ve RF and/or anti-CCP tests
  • Radiographic changes
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11
Q

List the goals of treatment for RA

A
  1. Achieve remission or low disease activity
    * for at least 6mths, using:
    * Boolean 2.0 criteria (remission)
    * Index based definition of SDAI/CDAI/DAS 28
  2. Achieve maximal functional improvement
  3. Stop disease progression
  4. Prevent joint damage
  5. Control pain
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12
Q

List the drugs used to treat RA

A
  1. NSAIDs
  2. Glucocorticoids
  3. DMARDs
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13
Q

List 4 csDMARDs

A

Methotrexate, sulfasalazine, leflunomide, hydroxychloroquine

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14
Q

List 3 TNF-a inhibitors

A

Infliximab, etanercept, adalimumab

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15
Q

List an IL-6 receptor antagonist

A

Tocilizumab

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16
Q

State 2 tsDMARDs

A

Tofacitinib, baricitinib

tsDMARDs = JAK inhibitors

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17
Q

Describe the place in therapy of NSAIDs for the treatment of RA

A
  1. Does not alter course of diseaes
  2. Used as adjunct to DMARDs to relieve pain & minor inflammation
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18
Q

Describe the place in therapy of glucocorticoids for the treatment of RA

A
  1. Used as bridging therapy with DMARDs
  2. Used as continuous low-dose therapy for difficult to control patients, **but not recommended due to SE ** of many DMARDs
  3. IA injections used to control flares
19
Q

List at least 5 adverse effects of glucocorticoids

A
  1. Increased CV risk
  2. Cataract glaucoma
  3. Gastric ulcer (+ nsaids)

Endocrine
4. hyperglycemiaImpaired glucose metabolism, insulin resistance, b-cell dysfunction
5. Weight gain/obesity
6. Fluid retention, edema
7. Cushing syndrome

Osteoporosis/osteonecrosis

20
Q

Which of the RA drug classes alter disease progression, and which does not?

A

Alter: DMARDs
Does not: NSAIDs, glucocorticoids

21
Q

Describe the benefits of DMARDs

A

DMARDs alter disese progression via:
* Slow/prevent radiographic joint dmg
* Improve physical function
* Lower ESR/CRP

22
Q

When should DMARDs be initiated after a diagnosis of RA?

A

Start ASAP after diagnosis

23
Q

State the first-line DMARD used for RA treatment

A

Methotrexate (Sulfasalazine/leflunomide if MTX is CI or not tolerated)

24
Q

Which class of medication is commonly given when initating/changing DMARDs?

A

MTX + Glucocorticoids (short term), taper & discontinue ASAP to avoid long term SE)

25
Q

How often should RA treatment be monitored in active disease?

A

If no improvement by 3mth or target not reached by 6 mth

26
Q

According to ACR 2021,

Which DMARD is preferred in moderate to high disease activity for DMARD-naive patients

A

Moderate to high disease activity

27
Q

According to ACR 2021,

Which DMARD(s) are preferred in low disease activity for DMARD-naive patients?

A
  1. Hydroxychloroquine (better tolerated)
  2. Sulfasalazine (less immunosuppressive vs MTX)
  3. MTX > leflunomide (greater dosing flexibility & lower cost)
28
Q

State the dosing for MTX monotherapy

Initiation, dose increment, target dose, max dose

A
  1. Initiation dose: 7.5 mg ONCE weekly
  2. Dose increment 2.5 – 5 mg/week every 4-12 weeks based on response
  3. Target dose: 15 mg/week within 4-6 weeks of initiation
  4. Max 25 mg/week
29
Q

State the dosing for short term glucocorticoid therapy to MTX

Initiation dose, duration, when to discontinue?

A

Prednisolone ≤7.5mg/d x 3mths.
Taper & discontinue: within 3 months OR
Discontinue if bDMARD/tsDMARD started

30
Q

Compare & contrast between the csDMARDs

MOA, PK, dose adjustment, CI, DDI, SE, pregnancy, monitoring, labs

A

Refer to IC16 RA, slide 21

31
Q

Which DMARD(s) should be avoided in pregnancy? Which can be used in pregnancy?

A

Avoid: MTX & Leflunomide
Can use: Sulfasalazine, hydroxychloroquine

32
Q

For patients on MTX but not at target, what should be done?

A
  • Add bDMARD or tsDMARD (bMARD > tsDMARD)
  • Add hydroxychloroquine & sulfasalazine (triple therapy; less risk of adverse events & lower cost)
33
Q

For patients on bDMARD/tsDMARD but not at target, what should be done?

A

Switch to bDMARD or tsDMARD of a different class

34
Q

Compare & contrast between bDMARDs and tsDMARDs

1) ROA, 2) MOA

A

bDMARD:
* ROA: SC injection/IV infusion
* MOA: bind to cytokines or their receptorrs to downregulate/inhibit fxn, this reduces immune & inflammatory response

tsDMARD:
* ROA: Oral
* MOA: binds to JAK proteins inside cells, prevent JAKs from transphosphorylating the associated cytokine & growth factor receptor

35
Q

State the adverse effects of bDMARDS & tsDMARDs

A
  • Injection site / infusion reactions: acute vs delayed (not seen in JAK-i due to PO adm)
  • Myelosuppression: need to monitor CBC with WBC differentials & platelet count
  • Infections: URTI, TB, hepatitis, opportunistic infections -> pre-DMARD screening & Tx needed
  • Malignancy risk: similar risks between bDMARD & tsDMARD? -> shared decision-making needed
  • Autoimmune diseases: SLE or lupus-like syndromes, demyelinating peripheral neuropathies
  • Cardiovascular diseases: HF (avoid TNF-a, inhibitors in NYHA class III & IV), HTN,
  • Hepatic effects: Increased aminotransferase -> monitor LFT
  • Metabolic effects: Hyperlipidemia -> monitor lipid panel
  • Pulmonary diseases: Pulmonary toxicity -> use with caution in interstitial disease
  • Gastrointestinal perforation: esp with IL-6 inhibitors & JAK inhibitors (risk factors: diverticulitis, > 65yo, GC use, NSAID use) / also reported in Rituximab (ave onset ~ 6 days, range 1-77 days) -> evaluate abdo pain or repeated vomiting
  • Thrombosis: esp with JAK inhibitors & IL-6 inhibitors (avoid in patients w Hx of thrombotic events)
36
Q

State the principles for the selection of bMARD/tsDMARDs

A
  1. Do not use > 1 bDMARD/tsDMARD at the same time
  2. Consider contraindications during selection
    * Hypersensitivity to components of the formulation
    * Severe infections e.g. sepsis, TB, opportunistic infections -> consider vaccination against diseases with vaccination before initiating DMARDs
    * HF (for TNF-a inhibitors)
  3. Anti-drug antibodies (ADA) may occur with TNF-a inhibitors –> loss of efficacy
  4. Switch to a bDMARD w a different MOA when one fails
37
Q

List 4 DMARDs to be avoided in heart failure

A

To avoid TNF-a inhibitors (IGAE)
- Infliximab, golimumab, adalimumab, etanercept

38
Q

Explain if bDMARDs or tsDMARDs are preferred. Explain why

A

bDMARDs are preferred. tsDMARDs eg. tofacitinib has higher risk for MACE & Malignancy compared to TNF-a inhibitors

39
Q

State the risk factors that contribute to MACE & malignancy when using a JAK-inhibitor/tsDMARD

A

1. Cardiovascular risk factors: > 65 yo, Hx for past/current smoking, Obesity
2. PMH of DM, HTN: Risk factors for malignancy, Hx for past/current malignancy
3. Risk factors for thromboembolic events: PMH of MI, HF, Inherited blood clotting disorders, blood clots, Use of CHC, HRT, Undergoing major surger, Immobility

40
Q

List 3 screening parameters that should be performed before initiating bDMARDs/tsDMARDs

A

1. Pre-treatment screening
* Tuberculosis (latent/active): start after completing anti-TB Tx
* Hepatitis B & C: avoid if untreated disease detected

2. Vaccination required before initiation
* Pneumococcal
* Influenza
* Hepatitis B
* Varicella zoster / Herpes zoster

3.Laboratory screening/monitoring
* CBC w differential white count & platelet count
* LFT (ALT, AST, bilirubin, ALP)
* Lipid panel
* SCr

41
Q

How should DMARDs be discontinued after patients are at target for ≥ 6mths?

For monotherapy, triple therapy & MTX + bDMARD/tsDMARD

A

Mono: Dose reduction gradually
Triple: Gradual discontinuation of sulfasalazine recommended over hydroxychloroquine (for lower adverse events & better tx persistence)
MTX + bDMARD/tsDMARD: gradual discontinuation of MTX is recommennded for better disease control

Abrupt discontinuation can lead to flares

42
Q

State 3 nonpharmacological interventions for RA

A

1. Rest inflamed joint/use splints to support joints & reduce pain- do not promote rest when there is no ongoing active disease as this can lead to acute flares
2. Physical activity & exercise- ROM exercises, exercises to incr muscle strength, aerobic exercise, avoid high intensity weight bearing exercises
3. PT/OT referral- supervised/tailored exercise
4.Nutritional & dietary counselling
5. Psychosocial interventions: CBT for enhancing self efficacy % QOL
6. Patient education- evidence based info abt diseaes & Tx; expectations of tx; correct misconceptions

43
Q
A

MSK Conditions & Treatment (6 decks)

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