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PR3154 > IC 16: Approach to the Management of Osteoarthritis and Rheumatoid Arthritis > Flashcards

IC 16: Approach to the Management of Osteoarthritis and Rheumatoid Arthritis Flashcards

1
Q

What are the differentials when patients present with joint pain?

A
  • OA
  • RA
  • Gout
  • Pseudogout
  • Infection
  • Trauma
  • Tumours
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2
Q

What are the investigations required to differentiate gout, RA, septic arthritis, pseudogout

A
  • Haematologic tests
  • Erythrocyte sedimentation rate
  • C-reactive protein
  • Rheumatoid factor
  • Anti-CCP
  • Joint aspiration
  • X-ray/MRI
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3
Q

What is OA?

A

Degenerative disease (with inflammation) of bone and joint cartilage

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4
Q

What are the risk factors for OA?

A
  • Genetic predisposition
  • Anatomic factors (varus alignment, valgus alignment)
  • Joint injury
  • Obesity (increase load on weight-bearing joints)
  • Aging (change in ECM)
  • Gender
  • Occupation
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5
Q

What is the pathophysiology of OA?

A
  1. Articular cartilage damage
  2. Chondrocyte activity to remove/repair damage
  3. Aberrant chondrocyte function and more breakdown
  4. Subchondral bone release of vasoactive peptides and matrix metalloproteinases (increase break down of collagen)
  5. Cartilage loss and apoptosis of chondrocytes
  6. Formation of fibrillations in cartilage and cartilage “shards” (cartilage “shards” cause inflammatory and pathologic changes)
  7. Subchondral bones rub against each other
  8. Formation of osteophytes (a compensatory structure to stabilise osteoarthritis joints)
  9. Effusion and synovial thickening
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6
Q

What leads to pain in OA?

A
  • Activation of nociceptive nerve endings within the joint by mechanical and chemical irritants
  • Distension of synovial capsule from increase joint fluid, microfracture, periosteal irritation or damage to ligament, synovium or meniscus
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7
Q

What contributes to inflammation in OA?

A
  • Formation of cartilage “shards”
  • Meiscal damage (release of inflammatory cytokines)
  • Ligament tears (release of inflammatory cytokines)
  • Synovitis (release of inflammatory cytokines)
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8
Q

What leads to cartilage degradation in OA?

A
  1. Articular cartilage daamge
  2. Chondrocytes proliferate and undergo phenotypic switch
  3. Produce improperly mineralised collagen
  4. Weakening and degradation of collagen matrix in synovium
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9
Q

How does bone remodeling and osteophyte formation occur in OA?

A
  1. Weakened collagen matrix causes thickening of subchondral bone
  2. Sclerosis and formation of bone spurs (osteophytes)
  3. Widening of joints
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10
Q

How does synovial inflammation occur in OA?

A
  1. Weakening and degradation of collagen matrix
  2. Cartilage flakes off forming cartilage shards
  3. Lymphocytes and macrophages get recruited by synovial membrane
  4. Proinflammatory cytokines produced
  5. Synovitis
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11
Q

What are the key features of OA?

A
  • Pain
  • Swelling
  • Erythematous and warm
  • Morning stiffness < 30 mins (resolves with motion, recurs with rest)
  • Limited joint movement
  • Functional limitation/instability (falls)
  • Asymmetrical polyarthritis (hand, knee, hip)
  • Symptoms related to weather
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12
Q

How is the pain like for OA?

A
  • Slow progression over years
  • Worse with joint use and relieved by rest
  • Worse in late afternoon/early evening
  • For knees it is worse going down the stairs/slope
  • Most severe over joint line
  • May also have anxiety, depression, sleep disturbance
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13
Q

What are the various stages of OA?

A
  • Stage 1: predictable sharp pain with mechanical insult, only modest effect on function
  • Stage 2: pain becomes more constant, with unpredictable episodes of stiffness, daily activities to be affected
  • Stage 3: constant dull/aching pain and often unpredictable intense, exhausting pain, severe limitations in function
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14
Q

What may be found on physical exam of an OA patient?

A
  • Asymmetric monoarticular or oligoarticular
  • Crepitus on motion (popping of joint)
  • Reduced range of motion
  • Transient joint effusion
  • Palpable warmth
  • Bone tenderness
  • Bone enlargement
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15
Q

What may be found when doing an X-ray on a OA patient (done in advanced disease)?

A
  • Joint space narrowing
  • Marginal osteophytes
  • Subchondral bone sclerosis
  • Abnormal alignment of joint
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16
Q

Can diagnosis for OA be done without radiography? If yes when?

A

Yes.
* It can be done for patients >= 45 years old
* With activity-related joint pain
* Morning stiffness <= 30 mins

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17
Q

What are the non-pharm treatment for OA?

A
  • Exercise (reduce pain and improve function) (strengthening, low-impact aerobic, mind-body exercise, neuromuscular training) (PT) (about 30 mins, 3 times a week)
  • Weight management
  • Information and support
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18
Q

What are the drugs that can be considered for OA?

A
  • Topical NSAIDs (first) (for knee, less feasible for hand, unlikely to benefit for hip)
  • Oral NSAIDs / coxib ( + PPI)
  • Oral paracetamol / tramadol (if contraindicated to NSAIDs)
  • Intraarticular glucocorticoid injections for short-term symptom relief
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19
Q

What are the common GI side effects of oral NSAIDs?

A
  • Nausea
  • Dyspepsia
  • Anorexia
  • Abdominal pain
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20
Q

What are the risk factors for NSAID-induced GI ulcer/bleed?

A
  • > 65 y/o
  • History of ulcer
  • Use of high dose/chronic NSAID
  • Concurrent glucocorticoids/antiplatelets/anticoagulants
  • High risk is more those with >= 3 of 4 risk factors
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21
Q

What are signs of NSAID-induced GI complications?

A
  • Fatigue
  • Severe dyspepsia
  • Signs of GI bleeding
  • Unexplained blood loss anemia
  • Iron deficiency
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22
Q

What NSAIDs should be given for patients with high risk of GI bleed or ulcers?

A
  • Ibuprofen can be used instead of naproxen
  • Give coxibs like celecoxib or etoricoxib
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23
Q

What is the CVS safety concerns of oral NSAIDs?

A
  • There is a risk of cardiovascular events like MI, stroke, vascular death
  • Use celecoxib at doses < 400 mg/day
  • Use of high-dose systemic diclofenac is contraindicated in patients with established CV disease, can be used if <= 100mg/day if treatment for > 4 weeks
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24
Q

What are the renal safety concerns for use of NSAIDs?

A
  • AKI
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25
Q

What are the risk factors for NSAID-induced AKI?

A
  • CKD (can use if < 5-7 days in eGFR < 60, not in eGFR < 15)
  • Volume depletion (emesis, diarrhea, sepsis, hemorrhage)
  • Effective arterial volume depletion (HF, nephrotic syndrome, cirrhosis)
  • Severe hypercalcemia/renal artery stenosis
  • Aminoglycosides, amphotericin B, radiocontrast material
  • Diuretics and ACEi/ARB
  • more than 65 y/o
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26
Q

What are concerns for NSAIDs in terms of allergic reactions?

A
  • Ig-E mediated allergic reactions
  • Pseudoallergic reactions (related to COX-1 inhibition) (can use coxib with caution)
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27
Q

What side effects are associated with oral NSAIDs use?

A
  • GI bleeds/ulcers
  • AKI
  • Allergic reactions
  • Effects on BP and hypertension
  • Hematologic effects (inhibit platelet function)
  • CNS: drowsiness, dizziness, headaches, tinnitus
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28
Q

What are the contraindications to intraarticular glucocorticoid injection use?

A
  • Periarticular infection
  • Septic arthritis
  • Joint instability
  • Juxaarticular osteoporosis
29
Q

What are further pharmacotherapy that can be considered?

A

Duloxetine
Topical capsaicin

30
Q

When is surgical treatment considered for OA patients?

A
  • If non surgical treatment is ineffective or unsuitable
31
Q

What are some contraindications to total knee replacement surgery?

A
  • Active infection
  • Chronic lower extremity ischemia
  • Skeletal immaturity
32
Q

What is the difference between primary and secondary OA?

A
  • Primary OA: no preceding injury
  • Secondary OA: due to congenital abnormality, trauma, inflammatory arthropathy
33
Q

What is RA?

A

Chronic autoimmune inflammatory systemic disease

34
Q

What is the genetic predisposition for RA?

A
  • HLA typing HLA-DR4 and/or HLA-DR1
  • More likely if parents are RF positive
  • Twins
35
Q

What is the pathophysiology of RA?

A
  1. Genetic predisposition + immunologic trigger (citrullinated antigens picked up by an antigen-presenting cell)
  2. T-cell mediated immune response (produce inflammatory cytokines IL-17, TNF, IL-1, IL-6)
  3. Inflammatory response (angiogenesis in synovium and synovial cell proliferation, pannus invasion)
  4. Recruitment of inflammatory cells
  5. Release of proteases and prostaglandins
  6. Destruction of articular cartilage and underlying bone (increased RANKL on T-cells)
36
Q

What is the clinical presentation of RA?

A
  • Pain
  • Swelling
  • Erythematous and warm
  • Early morning stiffness > 30 mins
  • Symmetrical polyarthritis (both small and large joints)
  • Systemic symptoms (generalised aching/stiffness, fatigue, fever, weight loss, depression) (especially in those with disease onset > 60 y/o)
  • Extra-articular complications
37
Q

What are some examples of extra-articular complications for RA?

A
  • Eye: episcleritis, scleritis
  • Heart: pericarditis, myocarditis, coronary artery disease, atrial fibrillation, heart failure, nodules
  • Hematology: anemia, felty’s syndrome, lymphoproliferative disease
  • Lung: pleural effusion, interstitial lung disease
  • Renal: glomerulonephritis, amyloidosis
  • Skin: rheumatoid nodules, neutrophilic dermatoses, skin ulcers
  • Vascular: rheumatoid vasculitis, peripheral vascular disease
38
Q

What are the deformities that can result in RA?

A
  • Swan neck
  • Boutonneire
  • Z-shaped thumb
  • MCP subluxation
  • Ulnar deviation
  • Rheumatoid nodules (elbow)
  • Popliteal cyst (knee)
  • MTP subluxation (toes)
39
Q

What lab finding would be significant in RA?

A
  • Rheumatoid factor positive
  • anti citrullinated peptides antibodies positive
  • Erythrocyte sedimentation rate increase
  • C-reactive protein increase
  • Hematocrit decrease
  • Platelets increase
  • WBC increase
40
Q

What would be observed in X-ray/MRI (late in course of disease) for RA?

A
  • Narrowing of joint space
  • Erosion (around margin of joint)
  • Hypertrophic synovial tissue
41
Q

What symptoms must be present to make a diagnosis for RA?

A

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

42
Q

What is the MOA of glucocorticoids?

A
  • Anti-inflammatory
  • Immunosuppressive
43
Q

What is the place in therapy of glucocorticoids for RA?

A
  • Low-dose bridging therapy when initiating DMARDs
  • Control flare (intraarticular injections) (q3 monthly but not more than 2-3 times per year per joint)
44
Q

What is are the adverse effects associated with glucocorticoid use?

A
  • Osteonecrosis
  • Osteporosis
  • Impaired glucose metabolism
  • Insulin resistance
  • betacell-dysfunction
  • Gastric ulcer
  • Cataract glaucoma
  • Increase cardiovascular risk
45
Q

What is the first line therapy for DMARDs?

A
  • Methotrexate
46
Q

What can be considered if methotrexate is contraindicated or not tolerated?

A
  • Sulfasalazine
  • Leflunomide
47
Q

What can be given concurrently when initiating methotrexate?

A

Short-term glucocorticoids but should be tapered and discontinued as rapidly as clinically feasible

48
Q

After what duration of treatment should it be adjusted if there is no response?

A

By 3 months

49
Q

What is the management of RA for DMARD naive patients?

A
  • Moderate-to-high disease activity: start methotrexate, short-term low-dose glucocorticoid
  • Low disease activity: hydroxychloroquine preferred, sulfasalazine > methotrexate > leflunomide
50
Q

What is the dose for methotrexate?

A
  • Initiation: 7.5 mg ONCE weekly
  • Dose increment: 2.5-5mg/week every 4-12 weeks based on response
  • Target dose: 15mg/week within 4-6 weeks of initiation
  • Max 25mg/week
51
Q

When should glucocorticoids be discontinued for RA?

A
  • Within 3 months of initiation
  • If bDMARD/tsDMARD started
52
Q

What is the dose of glucocorticoids for RA?

A

<= 7.5 mg/day up to 3 months

53
Q

What dose adjustment is required for methotrexate use in renal impairment?

A

CrCl < 30 to avoid use

54
Q

In what patients are the first line therapies contraindicated?

Methotrexate, hydroxychloroquine, sulfasalazine, leflunomids

A

Methotrexate: preexisting liver disease, immunodeficient syndrome, blood dyscrasias
Sulfasalazine: sulfonamide allergies, caution in G5PD deficiency
Hydroxychloroquine: preexisting retinopathy, caution in C5PD deficiency
Leflunomids: preexisting liver disease, immunodef states

55
Q

What are some important side effects for the first line drugs for RA?

Methotrexate, hydroxychloroquine, sulfasalazine, leflunomids

A
  • Methotrexate: increase transaminases, myelosuppression, TENS, SJS
  • Hydroxychloroquine: retinopathy
  • Leflunomids: increase transaminases, alopecia, myelosuppression
56
Q

Which of the first line drugs for RA is contraindicated for pregnancy?

Methotrexate, hydroxychloroquine, sulfasalazine, leflunomids

A

Methotrexate and leflunomids

57
Q

What can be done to adjust therapy for patients that symptoms are not at target for RA?

A
  • For patients on MTX: add bDMARD or tsDMARD, add hydroxychloroquine and sulfasalazine
  • For patients on bDMARD/tsDMARD: switch to bDMARD or tsDMARD of a different class
58
Q

What is the MOA of the bDMARD and tsDMARD?

A
  • bDMARD: bind to cytokines or their receptors to downregulate or inhibit their function, which reduces immune and inflammatory responses
  • tsDMARD: bind to JAK proteins inside cells to prevent JAKs from transphosphorylating the associated cytokine and growth factor receptor
59
Q

What are the safety concerns of bDMARDs and tsDMARDs?

A
  • Injection site/infusion reactions
  • Myelosuppression
  • Infections
  • Malignancy risk
  • Autoimmune disease
  • Cardiovascular disease
  • Hepatic (increased aminotransferase)
  • Metabolic (hyperlipidemia)
  • Pulmonary diseases (pulmonary toxicitiy)
  • GI perforation
  • Thrombosis
60
Q

Which is preferred: bDMARDs or tsDMARDs?

A

bDMARDs as tofacitinib (tsDMARD) carries higher risk for major adverse cardiovascular events and malignancy

61
Q

What are the cardiovascular risk factors when using DMARDs?

A
  • > 65 y/o
  • History for past/current smoking
  • Obesity
  • PMH of DM, htn
62
Q

What are the risk factors for malignancy when using DMARDs?

A
  • History for past/current malignancy
63
Q

What are the risk factors for thromboembolic events when using DMARDs?

A
  • PMH of MI, HF, inherited blood clotting disorders, blood clots
  • Use of CHC, HRT
  • Undergoing major surgery
  • Immobility
64
Q

What vaccination is required before initiation of bDMARD or tsDMARD?

A
  • Pneumococcal
  • Influenza
  • Hep B
  • Varicella zoster
65
Q

What lab monitoring is required before initiating bDMARD or tsDMARD?

A
  • CBC with differential white count and platelet count
  • LFT
  • Lipid panel
  • SCr
66
Q

How is management done after low disease activity or remission is achieved?

A
  • Continuation of all DMARDs
  • If on triple therapy, gradual discontinuation of sulfasalazine over hydroxychloroquine is recommended
  • If on MTX + bDMARD/tsDMARD: gradual discontinuation of MTX is recommended
67
Q

What are the non-pharm interventions for RA?

A
  • Psychosocial interventions
  • Rest inflamed joint/use of splints to support joints and reduce pain
  • Physical activity and exercise (avoid high-intensity weight-bearing exercises)
  • PT/OT
  • Nutritional and dietary counselling (weight maangement if obese, dietary interventions)
68
Q

What are the important cytokines involved in RA?

A
  • TNF-alpha, IL-1 and IL-6
  • Produced by macropahes
  • Stimulated synovial cells to proliferate

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