Exam 2 - 508: Osteoarthritis

Learning Objectives

• Describe the etiology, pathogenesis, and clinical manifestations of OA

• Learn goals of therapy and general treatment strategies

• Review medications used for treatment

  • Focus on dose, potential adverse effects, monitoring parameters, contraindications, and patient education

• Understand how to monitor for efficacy/safety

• Apply knowledge gained to optimize care for OA patients

What is defined as osteoarthritis?

• Characterized by cartilage deterioration, synovial thickening, local pathologic bone changes inflammation, and pathologic bone changes

• Most commonly affects weight bearing joints (knees, hips, spine) and hands

• Causes pain, limitation of motion, deformity, progressive disability, and decreased QOL

Is osteoarthritis inflammatory or noninflammatory?

Generally thought of as non-inflammatory

• Synonymous with degenerative joint disease (DJD)

• Not just an“age-related disease”

  • Results from a complex interplay of multiple factors including: joint integrity, genetic predisposition, local inflammation, mechanical forces, and cellular and biochemical processes

  • Involves the entire joint, not only degeneration of cartilage

What is the presentation/characterization of osteoarthritis?

• Characterized by cartilage deterioration, synovial thickening, local inflammation, and pathologic bone changes

• Most commonly affects weight-bearing joints (knees, hips, spine) and hands

• Causes pain, limitation of motion, deformity, progressive disability, and decreased QoL

What are risk factors for osteoarthritis?

• Age OA: Risk Factors

• Obesity ***most important preventable risk factor!!!

• Gender

  • Age <45 → more common in men

  • Age >45 → more common in women

• Occupation

  • Excessive mechanical stress (kneeling, squatting, lifting— esp. heavy objects, and prolonged standing)

  • Repetitive motion (hand OA)

• Participation in certain sports (wrestling, boxing, cycling, football, baseball pitching)

• Hx of joint injury or surgery

• Quadriceps muscle weakness - important for joint stability

• Genetic predisposition—many genes involved

Pathophysiology of OA

What are signs/symptoms of OA?

• Pain/Tenderness

• Stiffness - especially after inactivity

• Crepitus

  • Grating, crackling or popping sounds and sensations experienced in joints

• Bone spurs/osteophytes

  • Bony projections that develop on bone edges

• Effusions

  • Increased fluid in joint cavity

• Radiographic changes

  • Joint space narrowing, bone sclerosis, osteophytes

What are the two main classifications of OA?

• 1) Primary (idiopathic) OA → most common, no identifiable cause

• 2) Secondary OA

  • Associated with a known cause such as RA or other inflammatory arthritis, trauma, metabolic or endocrine disorders, and congenital factors

• Other terms

  • Localized: 1 or 2 sites affected

  • Generalized: 3 or more sites affected

  • Erosive: erosions present on X-ray

What tx/therapy is the only available method shown to delay the progression of OA?

NON-PHARM THERAPY

• Exercise/Education/Weight loss

What are non-pharmacologic therapies we use in OA?

• Education → disease process, the extent of OA, the prognosis, and treatment options

• Weight loss → ↓ weight by at least 10%

• Exercise

  • Aerobic (low impact)

  • Muscle strengthening

  • PhysicalTherapy (PT)

  • Occupational Therapy (OT)

Recommendations for OA in different body parts

What are common medications used to treat OA?

• Acetaminophen

• OralNSAIDs

• Opioid analgesics

  • Tramadol

  • Hydrocodoneproducts

• Duloxetine

• Glucosamine/Chondroitin

• TopicalAnalgesics

  • Trolamine salicylate

  • apsaicin

  • NSAIDs

• Intra-articular corticosteroid injections (CSI)

  • INJ only, no topical or PO

• Intra-articular hyaluronates

Medications should be scheduled

What are clinical pearls of acetaminophen?

• Analgesic and antipyretic effects

• Conjugated in the liver into inactive metabolites eliminated by the kidneys

• Generally well-tolerated

  • Occasional N/V, Constipation, Headache, pruritis

What serious ADR is associated with acetaminophen?

• Serious: hepatotoxicity

  • Dose dependent

  • May be fatal

  • Increased risk w/ concomitant EtOH, pre-existing liver disease and/or other medications (isoniazid)

• Caution with combination proucts/OTCs

Therefore, we MONITOR FOR LFTs

How do we dose APAP? Who gets lower doses?

• Dose: 650 - 1000mg q4-6 hrs, MAX 4g/d

• Lower MAX doses (2-3g/d) –

  • Elderly

  • Pre-existing liver disease

  • EtOH abuse (not recommended for those who drink ≥ 3 drinks daily)

  • Those who have long-term use

What are clinical pearls of NSAIDs?

• Has analgesic, anti-inflammatory, antipyretic

• Relieve pain and fever quickly (min-hrs)

  • Lower doses

• As effective as ASA, less GI AEs

• Individual variability in response

• Does NOT alter the progression of OA

How long do you take NSAIDs until you reach peak anti-inflammatory effect?

2-3 weeks for peak anti-inflammatory response using HIGH or MAX doses

Which NSAIDs are more COX-2 selective?

Meloxicam (Mobic) and Celecoxib (Celebrex)

Which AEs can be seen with NSAID use?

• HA/dizziness

• Tinnitis

• Rash

• GI upset (take with food)

  • Nausea, dyspepsia, Abd pain

  • Ulceration

  • Bleeding

• Asthma exacerbations

• Cardiovascular

  • MI, stroke

  • HTN

  • CHF

• Coagulation issues PLT effects

  • Reversible inhibition (effects last 1-3 days)

  • DI with anticoagulants

• Hepatotoxicity

• Renal toxicity

What should we monitor with long term NSAID use?

MONITOR

• BP

• CBC

• sCr

• LFTs

What should we consider adding to NSAIDs to reduce upper GI events?

Add PPIs when NSAID is used for chronic management of knee/hip

How do we use NSAIDs in hx of GI ulcer with no bleeding?

Recommend using either a COX-2 inhibitor or a nonselective NSAID + PPI

How do we use NSAIDs in hx of GI bleeds?

Recommend using a COX-2 inhibitor with a PPI

At what stage of CKD should NSAIDs not be used?

CKD Stage IV or V (eGFR < 30mL/min)

If a patient is taken baby aspirin for cardioprotection, how do we use NSAIDs?

Use a nonselective NSAID (other than ibuprofen) + PPI

How can aspirin cause asthma exacerbations?

Aspirin-induced hypersensitivity