Summary
Summary Nur 323 Exam 4 Study Guide
- Course
- NUR 323
- Institution
- University Of Rhode Island
This is a comprehensive and detailed study guide on Exam 4 for Nur 323. *Essential Study Material!!
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Med Surg Exam 4Chronic 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
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