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Year 3 - Clinical (Winter) > 22 - Osteoarthritis > Flashcards

22 - Osteoarthritis Flashcards

1
Q

Definition of OA

A
  • ACR (American College of Rheumatology) -> joint pain that occurs for most days of the prior month plus radiographic changes in the symptomatic joint
  • Impacts any joint, but typically in spine (cervical or lumbar), hands, hips, and knees
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2
Q

Difference between primary and secondary OA

A
  • Primary OA = idiopathic (often in the elderly)
  • Secondary OA:
    • Joint insults (trauma, infection)
    • RA, gout
    • Congenital joint abnormalities
    • Hematological genetic abnormalities (leukemia)
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3
Q

What protects the joint?

A
  • Synovial fluid -> reduces friction between articulating cartilage surfaces (physical protectant)
  • Ligaments & tendons -> via mechanoreceptor sensory afferent nerves fire during movement; allows for the right tension in joints for maximal protection
  • Bone -> shock-absorbing effects
  • Cartilage:
    • 2-3 mm thin coating of tissue at the ends of 2 opposing bones
    • Lubricated by synovial fluid to create frictionless surface for the opposing bones
    • Compressible characteristics yields impact-absorbing quality
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4
Q

Pathophysiology of OA

A
  • Involves a complex interaction of many extracellular and intracellular molecules (metalloproteinases (MMPs), cytokines (IL-1, TNF-alpha), and growth factors)
  • Cartilage destruction occurs faster than cartilage formation
  • IL-1 and metalloproteases have been found to play an important role in cartilage destruction
  • Local growth factors, especially transforming growth factor (TGF) are involved in formation of osteophytes
    • Osteophyte = compensatory mechanism of new bone formation to stabilize the joint
    • Characterized by joint pain, loss of motion, weakness, disability
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5
Q

Risk factors for OA

A
  • Ethnicity, age
  • Gender and hormonal status
  • Bone density, joint injury, joint biomechanics
  • Nutritional factors
  • Obesity (most modifiable risk factor), occupation
  • Physical activity
  • Muscle weakness
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6
Q

Sx of OA

A
  • Stiffness – morning or after periods of inactivity; lasts less than 30 mins
  • Sx localized to affected joint
  • Pain worse w/ activity (especially weight bearing) or prolonged use
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7
Q

Signs of OA

A
  • Often unilateral, occasionally symmetrical
  • Joints not usually tender or inflamed
  • Joint instability may be present
  • No systemic sx
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8
Q

What causes the pain of OA?

A
  • Not related to destruction of cartilage
  • From activation of nociceptive nerve endings within the joint by mechanical and chemical irritants
  • May be due to distention of synovial capsule by increased joint fluid, microfracture, periosteal irritation, or damage to ligaments, synovium, or the meniscus
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9
Q

Diagnosis of OA

A
  • Clinical diagnosis = no further tests if -> > 45 y/o + activity-related joint pain + no morning joint-related stiffness or morning stiffness lasting < 30 mins
  • Lab tests useful to rule out other causes of the sx
  • Radiographs and joint aspiration (useful for red, hot, swollen joints)
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10
Q

Physical exam of OA

A
  • Pain, stiffness, and limitation of both passive and active movement of the joint
  • Crepitus (grating, popping of joints), deformity, muscle atrophy, ligament tenderness in 1 or more of the affected joints
  • Ligament and capsular laxity (looseness) + muscle atrophy = joint instability (later leading to deformity)
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11
Q

X-ray for OA

A
  • Imaging may not directly correlate w/ the clinical picture
  • 2017 EULAR recommendations -> X-rays not needed for initial usual presentation of OA or follow-up
  • Can help identify narrowing of joint space (due to loss of cartilage), osteophytes, and bone cysts
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12
Q

Assessment of severity of OA

A
  • No lab monitoring
  • Assessment scales:
    • Western Ontario and McMaster Universities (WOMAC) questionnaire has been widely used to assess pain, stiffness, and physical function in px w/ hip and/or knee OA
    • Visual analog scale (VAS)
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13
Q

Goals of therapy for OA

A
  • *Relieve or eliminate pain (and stiffness)
  • Improve or restore joint function and mobility
  • Improve muscle strength to protect cartilage, ligaments, and joint capsule
  • Prevent and reduce damage to the joint cartilage, bone, ligaments, muscles, and nerves
  • Maximize QOL
  • Educate the pt/caregiver to promote adherence
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14
Q

Stepwise approach to OA tx

A
  • Step 1 -> non-pharm (education, exercise, physiotherapy, assistive devices); acetaminophen
  • Step 2 -> add topical diclofenac; advise on other topical therapies
  • Step 3 -> assess risk of adverse GI events
    • Low (no risk factors) = low dose nonselective NSAIDs
    • Moderate (1-2 risk factors) = low dose nonselective NSAID + gastroprotection OR low dose COX-2 inhibitor
    • High (multiple risk factors) = alternative therapy (ex: local injections, duloxetine, opioids) OR low dose COX-2 inhibitor + gastroprotection
  • Step 4 -> if not adequate pain relief, full-dose nonselective NSAID or COX-2 inhibitor +/- gastroprotection
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15
Q

Non pharms for hand OA based on ACR 2012 guidelines

A
  • Evaluate ability to perform activities of daily living (ADLs) and provide assist devices
  • Instruct in joint protection techniques
  • Instruct in use of thermal modalities
  • Provide splints for px w/ trapeziometacarpal joint OA
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16
Q

Pharm options for hand OA based on ACR 2012 guidelines

A
  • Topical capsaicin, topical NSAIDs
  • Oral NSAIDs, including COX-2 selective inhibitors
  • Tramadol
17
Q

Non pharms for knee OA based on ACR 2012 guidelines

A
  • Participate in CV (aerobic) and/or resistance land-based exercise
  • Participate in aquatic exercise
  • Lose weight (for persons who are overweight)
18
Q

Pharm options for knee OA based on ACR 2012 guidelines

A
  • Acetaminophen
  • Topical NSAIDs
  • Oral NSAIDs
  • Tramadol
  • IA corticosteroid injections
19
Q

Non pharms for hip OA based on ACR 2012 guidelines

A
  • Participate in CV and/or resistance land-based exercise
  • Participate in aquatic exercise
  • Lose weight (for persons who are overweight)
20
Q

Pharm options for hip OA based on ACR 2012 guidelines

A
  • Acetaminophen
  • IA corticosteroid injections
  • Oral NSAIDs
  • Tramadol
21
Q

General non-pharms for OA

A
  • Strength training and aerobic exercises (land/aquatic)
  • Weight loss of at least 5% in those overweight or obese
  • Joint protection (splints, taping, braces)
  • Supportive footwear
  • Use of ambulation aids (ex: cane, walkers)
  • Social support (telephone follow-up, caregiver education)
  • Acupuncture
  • Heat or cold therapy
  • Massage
  • Surgery
22
Q

Acetaminophen for OA (dose, role in OA, efficacy, and safety)

A
  • Dose -> 325-1000 mg q4-6h or SR 650 mg q8h x 2 weeks before assessing effect
    • Max 4 g/day
  • Role in OA -> 1st line especially for non-inflammatory OA
  • Efficacy -> equal to NSAIDs for mild, non-inflammatory OA; less effective than NSAIDs in inflammatory/advanced OA
  • Safety -> considered safe; consider 3.2 g/day max in px > 75 y/o; avoid in those w/ > 3-4 drinks/day
    • Enhanced hepatotoxicity w/ other hepatotoxic medications
23
Q

Capsaicin for OA (dose, role in OA, and safety)

A
  • Dose -> apply sparingly TID-QID x 3-4 weeks to achieve maximum therapeutic effect
  • Role in OA -> 1st line, especially for non-inflammatory OA
  • Safety -> tingling, burning, or redness (majority of px)
24
Q

Topical diclofenac for OA (dose, role in OA, and safety)

A
  • Dose -> OTC up to 2%; Rx up to 10%
  • Role in OA -> 2nd line in OA due to safety; can be used first-line if inflammatory component to OA
  • Safety -> minimal systemic safety concerns w/ limited systemic BA
25
Q

NSAIDs for OA (dose, role in OA, and safety)

A
  • Dose -> depends on the NSAID
  • Role in OA -> alternative first line tx for hand OA for those who can’t tolerate local skin reactions or inadequate relief from topical NSAIDs; in knee and hip OA after failure or CI to acetaminophen
  • Safety:
    • Common AE = N, dyspepsia, anorexia, abdominal pain, flatulence & diarrhea in 10-60% of px
    • Serious AE = ulcer, GI bleeding, kidney disease, hepatitis, CNS effects, many serious drug interactions
26
Q

NSAID options for those w/ high GI and/or CV risk

A
  • If high GI risk and high CV risk (on ASA) -> avoid NSAID if possible
    • If can’t avoid NSAID, if very high CV risk is primary concern -> naproxen + PPI; if very high GI risk is primary concern -> COX-2 + PPI
  • If high GI risk and low CV risk -> COX-2 alone or traditional NSAIDs + PPI
  • If low GI risk and high CV risk (on ASA) -> naproxen + PPI
  • If low GI risk and low CV risk -> traditional NSAID
  • *High CV risk = CV secondary px w/ ASA or high 10 year CV risk
27
Q

IA steroids for OA (dose, role in OA, efficacy, and safety)

A
  • Dose:
    • Methylprednisolone acetate (Depo-Medrol) -> 10-20 mg/joint; 20-80 mg/large joint (knee, hip, shoulder)
    • Triamcinolone acetonide (Kenalog) -> 5-15 mg/joint; 10-40 mg/large joint
  • Role in OA -> alternative first-line tx for both knee and hip OA when pain control w/ acetaminophen or NSAIDs is suboptimal or offered concomitantly w/ oral analgesics
  • Efficacy -> superior to placebo in alleviating knee pain and stiffness caused by OA but w/ a relatively short duration; benefit lasts 4-6 weeks
  • Safety -> inexpensive, safe, and effective therapy for individual joints (especially hips/knees)
    • AE = hyperglycemia, edema, elevated BP, flushing, dyspepsia
28
Q

IA hyaluronic acids for OA (dose, role in OA, efficacy, and safety)

A
  • Dose -> sodium hyaluronate 1 injection into involved joint; may be given once only, or weekly x 3-5 weeks depending on affected joint & product used
  • OA role -> 2nd line
  • Efficacy -> limited efficacy and risks of serious events limit the routine use
  • Safety -> no general systemic effect
    • Serious AE = increased pain, joint swelling, and stiffness
29
Q

Duloxetine for OA (dose, role in OA, efficacy, and safety)

A
  • Dose -> 60 mg once daily (max. dose of 120 mg per day)
  • OA role -> adjunctive tx in px w/ a partial response to first-line analgesics; may be preferred 2nd line med in px w/ both neuropathic and MSK OA pain
  • Efficacy -> demonstrated efficacy primarily as add-on therapy when there has been less than optimal response to acetaminophen or oral NSAIDs
    • Reduction in pain occurs at about 4 weeks after initiation
  • Safety -> don’t use w/ potent CYP1A2 inhibitors or MAOI
    • Caution w/ other serotonergic drugs (dextro, trazadone, triptans)
    • Common AE = GI w/ N, V, constipation
    • CI in liver disease, severe renal impairment (ie: CrCl < 30 mL/min)
30
Q

Tramadol for OA (dose, role in OA, efficacy, and safety)

A
  • Dose -> 25 mg AM, titrate dose in 25 mg increments to reach maintenance of 50-100 mg TID (max dose 200-300 mg/day)
  • OA role:
    • Recommended as alternative first-line tx of knee/hip pain in OA in px who have failed tx w/ acetaminophen, topical NSAIDs, and who aren’t appropriate candidates for oral NSAIDs and IA corticosteroids
    • Can be safe add-on therapy to partially effective acetaminophen or oral NSAID therapy
  • Efficacy -> demonstrated efficacy (moderate pain improvement when compared to placebo), primarily as add-on therapy when there has been less than optimal response to acetaminophen or oral NSAIDs
    • Reduction in pain occurs at ~4 weeks after initiation
  • Safety; common AEs = N/V, dizziness, constipation, headache, somnolence
    • Don’t use if CrCl < 30 mL/min
    • May need to taper dose upon d/c to prevent withdrawal sx
31
Q

NSAID harms

A
  • GI
  • Renal (ie: AKI)
    • Any NSAID better than the others? Not likely
    • Increases risk by 1.6-2.2X, depending on volume depletion, CHF, ACEI/ARB use, renal disease, cirrhosis, 70 years and older
  • Cardiac
    • Diclofenac and high-dose celecoxib increase risk by 2-4X
    • Low-dose naproxen, ibuprofen, and celecoxib appear CV “neutral”
    • Absolute risk depends on other risks (CHF, CAD/ high risk for CVD)
32
Q

Topical therapy for OA (advantage and efficacy)

A
  • Advantage -> major adverse effects comparable to placebo (systemic availability = 2-15% vs. oral NSAIDs)
  • Efficacy:
    • vs. oral NSAIDs for OA of hands and knees is equal
    • vs. placebo for OA, tendonitis -> superior in week 1 and 2 but equal after week 4
33
Q

Monitoring drug effect – what and who/when

A
  • What = decrease in pain
  • Who/when
    • Pt = daily
    • HCP = day 7, 14
34
Q

Monitoring pain relief – what and who/when

A
  • What = improvement or elimination as determined by pre-defined goals
  • Who/when
    • Pt = daily
    • HCP = day 3, 7, 14, 28
35
Q

Monitoring N, dyspepsia, abdominal discomfort – what and who/when

A
  • What = minimal or none
  • Who/when
    • Pt = daily
    • HCP = day 3, 7
36
Q

Pt education for OA

A
  • Expected outcomes and response times
  • Self-monitoring for safety and efficacy
  • Importance of adherence to non-pharm therapy and pharm therapy
  • Set goals w/ px (for all types of pain)

Year 3 - Clinical (Winter) (30 decks)

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