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PR3154 > IC16 Management of osteoarthritis and rheumatoid arthritis > Flashcards

IC16 Management of osteoarthritis and rheumatoid arthritis Flashcards

1
Q

What is Osteoarthritis (OA)?

A

OA is a degenerative disease with inflammation of bone & joint cartilage.

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2
Q

What are the risk factors of OA?

A
  1. Age
  2. Gender
  3. Weight - Obesity
  4. Genetics
  5. Joint injury
  6. Anatomy - misalignment of joints
       -  - At younger age (<50yo), OA is more likely in men as compared to women
   - At older age (>50yo), OA is more common in women than men.
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3
Q

What is the process of OA?

A
  1. Cartilage damage occurs
  2. Chondrocytes help to remove/repair damage
    - Chondrocytes are the cells responsible for cartilage formation
  3. Abnormal chondrocytes results in more cartilage breakdown
  4. There is cartilage loss and apoptosis of chondrocytes
  5. Cartilage shards are formed, causing inflammation of the synovial joints
  6. Bones rub against each other, causing the formation of osteophytes triggering pain.
    - a compensatory structure to stabilise osteoarthritic joints
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4
Q

Based on the process of OA, what are the 3 main pathophysiology of OA?

A
  1. Cartilage degeneration
  2. Bone remodeling & osteophyte formation
  3. Synovial inflammation
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5
Q

What are the 7 symptoms that a patient w OA presents?

A
  1. *Pain
  2. *Swelling
  3. *Erythematous & warm
  4. Morning stiffness <30mins
  5. Limited joint movement
  6. Functional limitation
  7. Asymmetrical polyarthritis - typically on weight bearing joints
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6
Q

What are the distinguishing factors between OA and RA?

A

OA starts off unilaterally
RA starts of bilaterally.

Erythema of OA is not as obvious or bad as RA.

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7
Q

What are the pain characteristics of OA?

A
  1. Pain gets worse w joint use, relieved by rest
  2. Worse in late afternoon / early evening
  3. May be associated w anxiety, depression, sleep disturbances
  4. Severe OA can severely limit functions
  5. Pain is most severe over the joint line
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8
Q

How to diagnose a pt w OA?

A

Pt can be diagnosed with OA if they present w typical S&S in the at-risk age group.

E.g of S&S:
- ≥ 45yo
- Activity related joint pain
- Morning stiffness ≤ 30mins

Diagnosis can be done without radiography or lab investigations, if pt has presenting S&S and is of at-risk age group.

Younger pts that do not fall in the at-risk age group require additional testing.

We will have to assess for:
- History of recent trauma
- Rapidly or worsening symptom or deformity
- Concerns of infection or malignancy

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9
Q

What are the goals of therapy of OA?

A
  1. Relieve pain
  2. Improve / preserve rang of motion & joint function
  3. Improve QoL
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10
Q

What are pharmacological treatments for OA?

A
  1. Topical NSAIDs
  2. Oral NSAIDs + PPIs
  3. Opioids (tramadol 25-50mg TDS) / Paracetamol
  4. Glucocorticoids

Do not give glucosamine, chondroitin, fish oil, vitamin D and etc.

To be used at the lowest effective dose, for the shortest possible time.

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11
Q

What are non-pharmacological treatments for OA?

A
  1. Low impact exercises - Tai Chi, walking, aquatic aerobics
  2. Weight loss
  3. Educate, provide information & support
  4. Acupuncture
  5. Walking w a cane
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12
Q

What are some GI concerns with PO NSAIDs?

A

Prolonged use of PO NSAIDs can cause GI ADRs such as:
- GI bleeding
- GI ulceration
- GI perforation

Common SE:
- Nausea
- Dyspepsia
- Anorexia
- Abdominal pain

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13
Q

What are the risk factors that puts a pt at increased risk of having NSAIDs induced GI ulcer/bleed?

A
  1. > 65yo
  2. History of ulcers
  3. Use of high dose NSAID OR Use of NSAID long term
  4. Concurrent use of glucocorticoids, antiplatelets, anticoagulants

If pt presents with ≥ 3 of these 4 risk factors, use -coxibs OR give pt PPI.

Coxibs have lesser propensity to cause GI toxicity as compared to non-selective.

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14
Q

If a pt is suspected to have NSAID-induced GI complications:
- Fatigue
- Severe dyspepsia
- Signs of GI bleed
- Unexplained blood loss anaemia
- Iron deficiency

What should you do?

A

Refer the patient immediately.

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15
Q

Apart from GI safety concerns, what other concerns are there with regards to PO NSAIDs?

A

PO NSAIDs can increase the risk of CV events and renal toxicity.

Examples of CV events:
- MI
- Stroke
- Vascular death

Renal toxicity can lead to acute kidney injury.
- *Avoid use of NSAIDs in eGFR <15
- If pt is on diuretics or ACEi/ARBs, avoid PO NSAIDs, or use topical NSAIDs.
- Avoid use tgt w aminoglycosides, amphotericin B, radiocontrast material

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16
Q

What should we do if a patient has an allergy or pseudoallergy to PO NSAIDs?

A
  1. Avoid giving all NSAIDs, including coxibs, to pts with allergy
  2. Avoid giving NSAIDs to pseudoallergic pts. However, Coxibs may still be used w caution.
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17
Q

Can you list out the 9 special populations we should avoid giving PO NSAIDs to?

A
  1. Hypersensitivity
  2. Asthmatic pts
  3. Pregnant women
  4. Pt w PUD or GI bleed
  5. Pt on anticoagulants, antiplatelets, PO glucocorticoids
  6. Severe renal impairment
  7. Pt at CVS risk
  8. Pts w bleeding disorders
  9. On other NSAIDs already
18
Q

What is the last resort for treating OA?

A

Total knee replacement surgery.

Total knee replacement surgery is often used when non-surgical treatment have proven to be ineffective for the pt.

Post rehab is essential for successful outcome.

19
Q

What is Rheumatoid Arthritis (RA)?

A

RA is a chronic autoimmune inflammatory systemic disease.

20
Q

What are risk factors of RA?

A
  1. Family history - 3x more at risk is 1st degree relative has RA.
  2. Genetics - pt w HLA-DRB1 gene have increased likelihood for RA
  3. Smoking
21
Q

What is the pathophysiology of RA?

A

It is the destruction of articular cartilage & underlying bone due to proteases and inflammatory cytokines.

Some examples of inflammatory cytokines involved are:
- TNF
- IL-1
- IL-6
- IL-17

22
Q

What are some clinical presentation of RA?

A
  1. Pain (much more than OA)
  2. Swelling (much more than OA)
  3. Erythematous & warm
  4. Early morning stiffness > 30mins
  5. Symmetrical polyarthritis
  6. Joint deformities in severe RA - e.g swan neck, can impair activities of daily living
23
Q

What are some systemic symptoms of RA?

A
  1. Generalized aching/stiffness
  2. Fatigue
  3. Fever
  4. Weight loss
  5. Depression
24
Q

What are some lab test that are affected in RA pt?

A
  1. Rheumatoid factor, RF
  2. Anti-CCP
  3. Erythrocyte sedimentation rate, ESR
  4. C-reactive protein
  5. FBC

Note that not all RA pt presents w RF or Anti-CCP. These test may show changes in value but they are not indicative for RA.

25
Q

How do we diagnose a pt w RA?

A

There is a scoring system developed by the 2010 American College of Rheumatology. It list the S&S of RA and if a pt scores more than ≥6/10, pt is then diagnosed w RA.

26
Q

What are the goals of therapy for RA pt?

A
  1. Achieve remission or low disease activity
  2. Achieve maximal functional improvement
  3. Stop disease progression
  4. Prevent joint damage
  5. Control pain
27
Q

What does achieving remission mean in RA pt?

A

Based on the Boolean 2.0 criteria, remission means:
- Tender Joint Count (TJC) ≤ 1, for 6 months
- Swollen Joint Count (SJC) ≤ 1, for 6 months
- CRP ≤ 1mg/dL, for 6 mths

Based on the index based definition (more commonly used)
- Disease Activity Score (DAS) 28 is the more commonly used target for remission

28
Q

What are some pharmacological therapies given for RA patients?

A
  1. Glucocorticoids
  2. csDMARDs - MTX, sulfasalasine, hydroxychloroquine, leflunomide
  3. bDMARDs - infliximab, etanercept, adalimumab
  4. tsDMARDs - tofacitinib

NSAIDs are not really effective in RA, as it does not alter the course of the disease like the DMARDs. However, NSAIDs can still be used as adjunctive therapy.

29
Q

How are glucocorticoids used in RA pt?

A

Glucocorticoids are used as:
- *Low-dose bridging therapy when initiating DMARDs

It is NOT recommended to use continuous low-dose therapy due to SE.

30
Q

When should we initiate DMARDs in RA pt?

A
  1. DMARDs should be initiated immediately after a diagnosis is made.
    - MTX is 1st line for moderate to severe RA pt.
       - Sulfasalazine and leflunomide are used if MTX is contraindicated, not tolerated.

   - Sulfasalazine & hydroxychloroquine are preferred for patients w mild RA.
  2. Short-term glucocorticoids should be considered when initiating DMARDs. It is then tapered & discontinued.
31
Q

How often should we monitor an RA pt after initiating DMARDs?

A

We should monitor a RA pt every 1-3 months

32
Q

What is the dosing for MTX?

A

7.5mg Methotrexate once weekly.

MTX to be given with Folic acid 5mg.
Folic acid to be taken the day after MTX dosing

33
Q

What is the dose of prednisolone to give for bridging in newly initiated DMARD pt?

A

When started DMARD for moderate-high RA disease activity, give:

≤7.5mg/day prednisolone for up to 3 months.

Prednisolone to be tapered and discontinued within 3 months.

Prednisolone is also to be discontinued if bDMARD or tsDMARD are started.

34
Q

What should we do if a pt does not respond sufficiently to csDMARD?

A
  1. For pts w MTX but not at target, add bDMARD or tsDMARD. Avoid adding a second csDMARD.
  2. For pt already on bDMARD / tsDMARD but not at target, switch to a bDMARD or tsDMARD of a different class.
35
Q

What must we do before initiating bDMARD or tsDMARD?

A
  1. Pre-treatment screening
  2. Vaccinations are required before screening
  3. Lab test / monitoring
36
Q

What is the main MOA of bDMARDs?

A

To bind to inflammatory cytokines, or their receptors & downregulate their functions.

This will help to reduce immune & inflammatory responses.

37
Q

What is the main MOA of tsDMARDs - JAK inhibitor?

A

JAK inhibitors bind to JAK proteins inside the cells.
This prevents JAK from transphosphorylating the cytokine & growth factor receptor.

38
Q

What should we not do when using bDMARDs or tsDMARDs?

A

Do not use >1 bDMARDs/tsDMARDs at the same time.

39
Q

Why is bDMARDs preferred over tsDMARDs?

A

bDMARD is preferred over tsDMARDs as tofacitinib carries higher risk for MACE & malignancy.

tsDMARDs are associated w - increased CV risk, malignancy and thromboembolic events.

JAK inhibitors are often the last resort.

40
Q

When do we stop DMARDs in RA patients?

A

We discontinue DMARDs when RA pt has been at target levels for ≥6 months.

However, we do NOT discontinue abruptly. There must be gradual discontinuation.

41
Q

What are some non-pharmacological management interventions for RA?

A
  1. Avoid high-intensity weight bearing exercises / activities
  2. Do range of motion exercises
  3. Do exercises to increase muscle strength
  4. Do aerobic exercises

Caution against resting too much as it can lead to sedentary lifestyle.

PR3154 (19 decks)

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