Summary Med Surg - Exam 4 Study Guide

Med Surg Exam 4

Chronic Musculoskeletal Disorders: Osteoarthritis

Evolution of osteoarthritis
 Bone
 Cartilage
 Thinning of cartilage
 Cartilage remnants
 Destruction of cartilage

Osteoarthritis
 Slowly progressive noninflammatory disorder of diarthrodial (synovial) joints
o Diarthrodial joint: most common and movable joint which is characterized by the
presence of a layer of fibrocartilage or hyaline cartilage that lines the opposing
bony surfaces, as well as a lubricating synovial fluid within the synovial cavity
 Inflammation is not a characteristic of OA, but secondary synovitis may result when
phagocyticic cells try to rid the joint of small pieces of cartilage torn from the joint
surface
o Inflammation causes initial pain and joint stiffness of OA
o Pain later in disease is due to contact between exposed bony joint surfaces after
articular cartilage has deteriorated completely
 Most common form of joint
 21 million Americans affected
o Expected to greatly increase as population ages
 Not considered a normal part of aging process
 Growing older is a risk factor
 Cartilage destruction can begin between ages 20 and 30
 Majority of adults affected by age 40
 Usually affects joints asymmetrically
 Most commonly affected joints
o Spine, hip, hand, foot, knee
 Etiology unknown
 Modifiable risk factors
o Obesity
o Anterior cruciate ligament (ACL) injury
 ACL injury r/t quick stops and pivoting as in football and soccer
o Occupations that require kneeling and stooping

Most commonly affected joints
 Distal interphalangeal (DIP) and proximal interphalangeal (PIP) of fingers
 Metacarpophalangeal (MCP) joint of thumb
 Weight-bearing joints hips and knees

,  Cervical and lumbar vertebrae
 Spine, hips, hand, foot, knee

OA: Pathophysiology
 In a normal joint, healthy cartilage, lubricated by synovial fluid, cushions the bones and
allows them to move easily
 OA causes the cartilage to begin breaking down, first making it thinner and then creating
cracks in its surface
 Gaps in the cartilage can expand until they reach the bone itself
 Synovial fluid leaks into cracks which can form in the bones surface when this
replacement cartilage wears away
o This causes further damage and in some cases can lead to cysts in the bone or
other deformities
 If not treated, damage can progress to the point where the bones in the joint becomes
seriously and permanently deformed
 Early stages of disease
o Degeneration of cartilage
o Reactive new bone
 Late stages of disease
o Cartilage particles
o Loss of cartilage
o Bone hypertrophy

OA: Clinical Manifestations
 Joint pain
o Predominant symptom ranging from mild discomfort to significant disability
o Pain worsens with joint use
 Early stages: relieved with rest
 Later stages: pain with rest and sleep is disturbed because of pain and
increased joint discomfort
 As OA progresses, increasing pain can contribute significantly to disability and loss of
function
o Sitting down becomes difficult, as does rising from a chair when hips and knees
are involved
 Joint stiffness
o Worse after rest or inactivity
 Unlike pain that is worse with activity
o Morning stiffness is common; generally resolves in 30 minutes
 Crepitation
o Grafting sensation caused by loose particles of cartilage in the joint cavity
 Indicates loss of cartilage integrity
 Presents in >90% of patients with OA of knee
 Deformity of the involved joints

,  Herberden’s Nodes
o Occur in DIP joints
o Indicates osteophyte formation and loss of joint space
o Swollen knuckles on fingers
 Bouchard’s Nodes
o Occur in PIP joints
o Herberden’s and Bouchard’s nodes are often red, swollen, and tender
o Nodes do not often cause significant loss of function
o Patient may be distressed by visible disfigurement
o Distorted fingers (bent)
 Knee OA
o Leads to joint malalignment
o Bowlegged appearance
o Altered gait
 Hip OA
o One leg shorter from loss of joint space
 Spine OA
o Pain and muscle spasm in extremity innervated by the area of the spine involved

OA: Medical Management
 No known cure
 Goals
o Managing pain and inflammation
o Maintaining and improving joint function
o Preventing disability
 Includes
o Non-pharmacologic
o Drug therapy
o Surgery

Non-pharmacologic Management of OA
 Rest and joint protection
 Heat and cold applications
 Nutrition
o Weight reduction
 Exercise
 Complementary and alternative therapies
o Acupuncture
o Yoga, massage, guided imagery, therapeutic touch
o Glucosamine and chondroitin
 Balance rest and activity
o Rested during periods of inflammation
o Maintained in functional position with splints or braces

, o Immobilization should not exceed 1 week
 May need to modify usual activities to decrease stress on affected joints
o OA of knee should avoid prolonged periods of standing, kneeling, or squatting
o Using assistive devices: canes, walkers, or crutches
 May help decrease stress on affected joints
 Heat used most often
o Helps for stiffness
o Hot packs, whirlpool baths, ultrasound, paraffin wax baths
 Cold may be helpful with acute inflammation

Drug Therapy for Management of OA
 Based on severity of symptoms
 Mild to moderate joint pain
o Tylenol
 Up to 1,000 mg every 6 hours
 Not to exceed 4 gm/day
 Limit to 2 gm/day in alcoholic patients
o Topical agent
 Capsaicin (Zostrix)
 Blocks pain by locally interfering with substance P, which is
reversible for transmission of pain impulses
o OTC products
 Contain camphor, eucalyptus oil, and menthol
 BenGay, Arthricare
o Topical salicylates
 Can be absorbed into the blood Aspercreme
 Fail to obtain relief with Tylenol or moderate to severe pain
o NSAIDs
 Initiated with low dose OTC strengths ibuprofen (Motrin, Advil, Nuprin)
 200 mg up to 4x/day
 Dose increases as symptoms progress
 COX-2 inhibitors (Celebrex)
 Block production of prostaglandins from arachidonic acid by inhibiting the
production of COX-1 and COX-2, therefor increased risk of GI erosion and
bleeding is increased
 Affect platelet aggregation leading to prolonged bleeding
o COX-2 Inhibitors
 Less GI irritation
 Increased MI and stroke risk
o Aspirin may be preferred by some patients
 No longer recommended treatment
 Should not be used with NSAIDs both prolong bleeding time
o Intra-articular injections of corticosteroids/anesthetics