Ch. 43 Flashcards
osteoarthritis
- most common arthritis type
- progressive loss of cartilage
- joint pain, loss of function characterized by progressive deterioration
- osteophytes (bone spurs)
- cartilage disintegrates, bone and cartilage “float” into joint causing crepitus
osteoarthritis primary etiology (causes)
aging
genetic factors
osteoarthritis secondary etiology
- joint injury
- obesity
- repetitive stress to joints
most common joints affected by osteoarthritis
weight-bearing joints mostly
- knees
- hips
osteoarthritis incidence and prevalence
33 million in US
- 5th most common cause of disability worldwide
people > 60 years old: higher risk
F>M: higher risk
osteoarthritis health promotion
maintain proper nutrition
avoid injuries
stay active
take work breaks: think construction workers who bend their joints all day at work
joint changes in degenerative joint disease
- bone hypertrophy (bone spurs)
- cartilage particles
- loss of cartilage
joint thickens, decrease in synovial fluid: think bone on bone
osteoarthritis assessment: history
- joint pain: localized, unilateral
- may be secondary to another dx
- age: usually older than 60 years old
osteoarthritis assessment: physical assessment/ s/sx
Persistent joint pain and stiffness
Crepitus: grating sound from bone on bone
Joint effusions
Heberden’s nodes (in hand)
Bouchard’s nodes (in hand)
Atrophy of skeletal muscle
osteoarthritis assessment: psychosocial assessment
lifestyle changes
- can’t walk as well
- not socializing or going out as much
osteoarthritis assessment: labs
- aspirated joint fluid: analyzed under microscope
- ESR: generic blood level showing inflammation in the body, may be elevated
- hsCRP: generic blood level showing inflammation in the body, may be elevated
osteoarthritis assessment: imaging
X-ray: arthritic changes in the joints
MRI
hebern’s nodes
bony nodules at the distal interphalangeal joints (closer to end of the fingers/nail beds)
bouchard’s nodes
bony nodules at the proximal interphalangeal (closer to the hand)
priority problems for patients with osteoarthritis
- persistent pain (once you have arthritic, it does not go away- unless you have a joint replacement)
- potential for decreased mobility
(arthritis) chronic pain: non-surgical management
Drug therapy
- most commonly: Acetaminophen (arthritis 500mg)
- OTC NSAID like ibuprofen
Rest, immobilization
Positioning
Thermal modalities: heating pad or ice
Weight control: getting weight stable, nutrition/diet
Integrative therapies
- Glucosamine, chondroitin (let PCP know! interactions!)
chronic joint pain: surgical management
total joint arthroplasty (TJA)/total joint replacement (TJR)
- knees: outpatient
- hip: inpatient
arthroscopy: osteotomy
- less invasive, use scope to clean up cartilage
osteoarthritis care coordination and transition management
- home care management
- health care resources
- self-management education
post-op care for TJR
- abductor position (triangle foam pillow) while in bed: prevent dislocation of hip
- watch for VTE, leg exercises, use of compression devices/socks
- assess signs of infection: redness, edema, inflammation, drainage
- monitor Hgb, Hct (normal for slight decrease), watch for need of blood transfusion
- check limb for: color, pulses, temperature, sensation
post-op complications for TJR
Collaborate with patient/family to become safety partners to prevent complications
- Hip dislocation
- VTE** (very common w/ ortho surgeries)
- Infection
- Anemia
- Neurovascular compromise
exercise after THR
hip flexion no greater than 90° (want < 90°)
- leg exercises
continuous passive motion machine
- patient comes up from OR with
- computerized iPad with settings: compare with computer to ensure that they match
- used after THR
osteoarthritis evaluation
- Achieves pain control to a pain intensity level of 2 to 3 on a scale of 0 to 10 or at a level that is acceptable to the patient
- Does not experience complications associated with total joint arthroplasty (if performed)
- Moves and functions in own environment independently with or without assistive devices
rheumatoid arthritis (RA)
- Common connective tissue disease, destructive to joints
- Chronic, progressive, systemic inflammatory autoimmune disease
- affects primarily synovial joints; affects joints throughout the body (not just one, not unilateral)
- Characterized by remissions and exacerbations
- Transformed autoantibodies (rheumatoid factors) form, attack healthy tissue causing inflammation
RA: causes
- combination of environmental and genetic factors
- physical and emotional stressors are linked to exacerbations
RA pathology
bone erosion
decreased synovial fluid
- may be unilateral, single joint
- affects weight-beating joints and hands, spine
- metacarpophalangeal joints spared
- systemic autoimmune inflammatory d/o
RA incidence and prevalence
- 1.5 million people
- more common in Euro-Americans
- women 2-3x more likely to have RA than men
RA assessment: history
Acute and severe, or slow and progressive
RA assessment: physical assessment/ s/sx
Joint and systemic symptoms
Generalized weakness and fatigue: malaise
Morning stiffness
Advanced disease symptoms
RA assessment: psychosocial assessment
body changes
mobility changes
- go out less/ less social
RA assessment: labs
Rheumatoid Factor
Anti-CCP
ANA: can be elevated due to inflammation in the body
ESR: can be elevated due to inflammation in the body
hsCRP: can be elevated due to inflammation in the body
Serum complement (C3 & C4)
Serum protein electrophoresis
Serum immunoglobulins
Thrombocytosis can occur with late RA
RA assessment: diagnostic tests
X-rays
CT scan
Arthrocentesis (fluid analysis in the lab)
Bone Scan
RA joint involvement progression (s/sx early vs late)
Early—joint stiffness, swelling, pain, fatigue, generalized weakness, low-grade fever (99°)
Late—joints become progressively inflamed and quite painful, SQ nodules; OT involvement, assistive devices
priority problems for patients with RA
- Chronic inflammation and persistent pain
- Potential for decreased mobility
- Potential for decreased self-esteem
RA plan/interventions
Managing chronic inflammation and pain
- Drug therapy
Promoting mobility
Enhancing self-esteem
RA systemic complications
Weight loss, fever, extreme fatigue
- Exacerbations
Subcutaneous nodules
Respiratory, cardiac complications
Vasculitis: inflammation of the blood vessels- pulmonary and cardiac problems
Periungual lesions
Paresthesias: numbness and tingling to extremities
RA- associated syndromes
Sjögren’s syndrome
Felty’s syndrome
Caplan’s syndrome
Sjögren’s syndrome: triad of sx
triad of sx
- dry eyes, dry mouth, vaginal dryness
Felty’s syndrome
associated with RA
triad of disorders/diagnoses
RA, splenomegaly: enlarged spleen, elevated WBC
Caplan’s syndrome
a combination of rheumatoid arthritis and pneumoconiosis that manifests as intrapulmonary nodules, which appear well-defined and homogenous on chest x-ray.
It is defined as lung nodules in dust-exposed personnel, either with a history of rheumatoid arthritis or develops RA after 5-10 year
RA nonpharmacologic interventions
Adequate rest
Proper positioning
Ice and heat application
Plasmapheresis (not common): machine takes plasma out of body and removes rheumatoid antibodies and then puts plasma back into body
Complementary and alternative therapies
Promotion of self-management
Management of fatigue
Enhance body image
RA drug therapy
DMARDs (disease modifying antirheumatic drugs)
- methotrexate: decrease inflammation, immunosuppressive agent: decrease immune system/low platelet/low WBC- stay out of public places, stay away from sick people; teratogenic agent: pregnancy test before using, need to be on strict birth control
- hydroxychloroquine: decrease inflammation, immunosuppressive agent: decrease immune system/low platelet/low WBC- stay out of public places, stay away from sick people; retinal vessel damage- regular eye exams needed, look behind retina for damage
NSAIDs
BRMs (biological response modifiers)
- affects immune system: look for s/sx of infection, call PCP if develop a sx of infection (ie cough)
Other:
- Glucocorticoids (taper off, don’t stop suddenly)
- Immunosuppressive agents (prednisone- hyperglycemia sugar levels)
- E788 awaiting approval
gout
aka gouty arthritis
- urate crystals deposit in joints and other body tissues, causing inflammation
- primary or secondary
- M > F higher risk
- men > 50 years at higher risk
primary gout
related to underexcretion or overproduction of uric acid, often associated with a mix of dietary excesses or alcohol overuse and metabolic syndrome
secondary gout
hyperuricemia: high levels of uric acid
- causative diet: steak, wine, red meats
- use of diuretics: thiazide
gout assessment: phase 1
asymptomatic hyperuricemia
high levels of uric acid levels in the blood
gout assessment: phase 2
acute gouty arthritis
- painful attack
- affects 1 joint; usually the great toe but can affect any joint
- severe pain, swollen, red (no sheet on feet so painful)
gout assessment: phase 3
tophaceous arthritis (aka tophi)
gout interventions
Maintain serum uric acid level less than 6 mg/dL
Drug Therapy
- Colchicine
Nutrition therapy
- Limit proteins
- Avoid trigger foods: seafood, red meat, alcohol
- Plenty of fluids
- pH increased with alkaline foods
- Low purine diet
tophi
stage 3 gout
- most common in great toe
- can affect hand
- swollen nodule-type things
hip flexion after THR
- don’t want hip flexion > 90°: causes dislocation
- use abductor pillow
- can do leg exercises
- stand up with leg extended out and support with hands on either side to push off
- slide on shoes/ have someone that can help with putting them on
- no crossing legs: hip dislocation
gout drug therapy: acute attack
- NSAIDs
- colchicine
*pain treatment, but no uric acid treatment
gout drug therapy: chronic attack
- allopurinol
- finoxbasat
*decrease uric acid levels
