22 - Osteoarthritis Flashcards
Definition of OA
- 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
Difference between primary and secondary OA
- Primary OA = idiopathic (often in the elderly)
- Secondary OA:
- Joint insults (trauma, infection)
- RA, gout
- Congenital joint abnormalities
- Hematological genetic abnormalities (leukemia)
What protects the joint?
- 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
Pathophysiology of OA
- 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
Risk factors for OA
- Ethnicity, age
- Gender and hormonal status
- Bone density, joint injury, joint biomechanics
- Nutritional factors
- Obesity (most modifiable risk factor), occupation
- Physical activity
- Muscle weakness
Sx of OA
- 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
Signs of OA
- Often unilateral, occasionally symmetrical
- Joints not usually tender or inflamed
- Joint instability may be present
- No systemic sx
What causes the pain of OA?
- 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
Diagnosis of OA
- 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)
Physical exam of OA
- 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)
X-ray for OA
- 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
Assessment of severity of OA
- 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)
Goals of therapy for OA
- *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
Stepwise approach to OA tx
- 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
Non pharms for hand OA based on ACR 2012 guidelines
- 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
Pharm options for hand OA based on ACR 2012 guidelines
- Topical capsaicin, topical NSAIDs
- Oral NSAIDs, including COX-2 selective inhibitors
- Tramadol
Non pharms for knee OA based on ACR 2012 guidelines
- Participate in CV (aerobic) and/or resistance land-based exercise
- Participate in aquatic exercise
- Lose weight (for persons who are overweight)
Pharm options for knee OA based on ACR 2012 guidelines
- Acetaminophen
- Topical NSAIDs
- Oral NSAIDs
- Tramadol
- IA corticosteroid injections
Non pharms for hip OA based on ACR 2012 guidelines
- Participate in CV and/or resistance land-based exercise
- Participate in aquatic exercise
- Lose weight (for persons who are overweight)
Pharm options for hip OA based on ACR 2012 guidelines
- Acetaminophen
- IA corticosteroid injections
- Oral NSAIDs
- Tramadol
General non-pharms for OA
- 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
Acetaminophen for OA (dose, role in OA, efficacy, and safety)
- 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
Capsaicin for OA (dose, role in OA, and safety)
- 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)
Topical diclofenac for OA (dose, role in OA, and safety)
- 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
NSAIDs for OA (dose, role in OA, and safety)
- 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
NSAID options for those w/ high GI and/or CV risk
- 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
IA steroids for OA (dose, role in OA, efficacy, and safety)
- 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
IA hyaluronic acids for OA (dose, role in OA, efficacy, and safety)
- 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
Duloxetine for OA (dose, role in OA, efficacy, and safety)
- 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)
Tramadol for OA (dose, role in OA, efficacy, and safety)
- 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
NSAID harms
- 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)
Topical therapy for OA (advantage and efficacy)
- 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
Monitoring drug effect – what and who/when
- What = decrease in pain
- Who/when
- Pt = daily
- HCP = day 7, 14
Monitoring pain relief – what and who/when
- What = improvement or elimination as determined by pre-defined goals
- Who/when
- Pt = daily
- HCP = day 3, 7, 14, 28
Monitoring N, dyspepsia, abdominal discomfort – what and who/when
- What = minimal or none
- Who/when
- Pt = daily
- HCP = day 3, 7
Pt education for OA
- 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)