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2 major joint disorders
osteoarthritis (OA): primarily noninflammatory/degenerative
rheumatoid arthritis (RA): inflammatory autoimmune
musculoskeletal basis
ligaments: bone to bone
tendons: muscle to bone
joint types:
synovial: freely moveable
joint cavity
synovial membrane
synovial fluid: lubricates joint (smooth movement)
articular cartilage
ligaments
bursa: fluid-filled sacs that reduce friction (muscles/tendons glide over bone)
nonsynovial: immovable/slightly movable
osteoarthritis
chronic, progressive, primarily noninflammatory degeneration of articular cartilage in synovial joints, especially weight-bearing joints
primary/idiopathic OA: no prior joint injury/systemic dz
women (post-menopausal)
secondary OA: joint trauma, repetitive occupational/sports injury, previous inflammatory dz, other joint abnormalities
men
OA common sites
Hips
Knees
Cervical/lumbar spine
Fingers: DIP + PIP
Foot: MTP
OA patho
articular cartilage degenerates → body attempts repair → new cartilage softer + less elastic → cartilage fissures/erodes → bone-on-bone contact → osteophytes/bone spurs form
osteophytes: bone growths/bone spurs that develop at joint margins
OA risk factors
Age
Female sex/hormonal changes
Obesity: greater weight places greater mechanical stress on joints (knees and hips)
Genetics
Joint abnormalities
Weak supporting muscles
Trauma
Repetitive joint use
Occupational stress
Inactivity
OA sxs
Usually asymmetrical/unilateral
Localized rather than systemic
Pain worsens with activity/use
Crepitus (grinding/crunching/grating sensation or sound during joint movement d/t roughed surfaces/cartilage loss)
Limited ROM
Joint stiffness (<30 minutes and improves w/ movement)
joint that locks/gives way: more advanced OA in weight-bearing joint
Possible instability/locking
heberden vs bouchard nodes
Heberden nodes → DIP joints
Bouchard nodes → PIP joints
Both are osteophyte/bony enlargements associated with OA
OA diagnosis
H&P (main)
X-ray
Joint-space narrowing
Osteophytes
Cartilage loss-related changes
Labs mainly used to rule out inflammatory arthritis, infection, gout
OA synovial fluid: clear/yellow, noninflammatory, WBC <2,000
OA treatment goals
goals
Manage pain/inflammation
Prevent disability
Maintain/improve joint function
Preserve independence/QOL
OA pain medications
Acetaminophen (1000 mg Q6h; 4g/day max) → liver toxicity
NSAIDs
GI irritation/bleeding (abd pain, tarry stools, hematemesis)
Renal toxicity
Cardiovascular effects
COX-2 inhibitors: celecoxib (Celebrex)
Opioids
Cymbalta
Lyrica
Topical/counter-irritants
Intra-articular injections:
hyaluronan/viscosupplementation: knee OA to improve lubrication and help reduce pain
corticosteroid joint injections: temp reduce pain/inflammation
excessive → accelerate cartilage deterioration
OA nonpharmacologic treatment
Weight reduction if appropriate
PT
Aerobic exercise
ROM
Strengthening
Flexibility
Balance training
Low-impact exercise
Assistive devices
Heat/cold
Tai chi
Water exercise
low impact exercise for OA
Helps:
Maintain ROM
Strengthen supporting muscles
Improve stability
Support weight management
examples:
Walking
Water exercise
Tai chi
Cycling
OA surgery
considered for:
Significant loss of joint function
Severe/unrelieved pain
Conservative treatment failure
Reduced ability to perform self-care independently
types
Repair
Fusion
Total hip replacement
Total knee replacement Joint Disorders_UNRS314_VJS
rheumatoid arthritis
chronic systemic autoimmune inflammatory disease causing symmetrical, erosive inflammation of synovial joints, usually with periods of remission and exacerbation
RA risk factors
Female sex
Genetic component
Viral/bacterial/hormonal factors
Smoking
Environmental factors
Stress
Comorbidities
Possible periodontal/gut bacterial associations
RA common sites
MCP
PIP
Wrists
Feet/MTP
Knees
Elbows
Shoulders
(DIP joint spared)
RA patho
RF antibodies develop against immunoglobulin
↓
Antigen-antibody immune complexes form
↓
Complexes deposit in synovium
↓
Joint becomes swollen/inflamed
↓
Synovium hypertrophies
↓
PANNUS forms (thick, proliferative, invasive inflamed synovial tissue that destroys cartilage and eventually bone)
↓
Pannus erodes cartilage + tendons + ligaments + bone
RA sxs
Morning stiffness that improves with activity (≥60 minutes to several hours)
Symmetric swelling
Warmth
Tenderness
Pain
Small joints first
Reduced ROM
systemic RA sxs
Fatigue
Malaise
Muscle aches
Anorexia
Weight loss
Low-grade fever
Anemia
Possible lymphadenopathy
RA deformities
Swan-neck deformity: PIP hyperextends, DIP flexes, MCP may flex
Boutonniere deformity: PIP flexes, DIP hyperextends
ulnar deviation: fingers drift toward ulnar side due to joint capsule stretching and muscle imbalance
rheumatoid nodules: firm, usually nontender subcutaneous nodules, often near extensor surfaces such as the elbow
hallux valgus: lateral deviation of the great toe with bunion formation; can occur with chronic RA

RA diagnosis
Rheumatoid factor (positive ~80%)
not only specific to RA
Anti-CCP (most specific)
ESR/CRP → active inflammation
ANA
Synovial fluid: inflammatory and cloudy with elevated WBC; >20,000-25,000/µL
X-ray/imaging
RA treatment goals
Decrease pain/swelling
Prevent structural joint damage
Preserve joint function
Slow progression
Reduce systemic disease activity
RA medications (NSAIDs + glucocorticoids)
NSAIDs: pain, inflammation, swelling (does not stop progression/prevent joint destruction)
Glucocorticoids: rapid tx pain, swelling, stiffness, acute inflammatory activity (bridge for slower DMARDs)
SE: infection, hyperglycemia, osteoporosis/fractures, weight gain, thin skin, GI problems, mood changes
RA medications (DMARDs + biologics)
DMARDs: slow disease progression and prevent permanent joint destruction (early RA)
first-line: methotrexate (MTX)
SE: bone marrow suppression, hepatotoxicity (monitor CBC/LFTs)
Hydroxychloroquine/Plaquenil: report vision changes/eye exams
Leflunomide/Arava: liver injury, diarrhea, teratogenicity (no pregnancy)
Sulfasalazine
Methotrexate
Biologic agents
Etanercept — Enbrel
Infliximab — Remicade: TB testing/chest imaging before therapy
Adalimumab — Humira
Rituximab — Rituxan
Abatacept — Orencia
IMMUNOSUPPRESION → INFECTION RISK
TB testing, hepatitis testing, avoid infection exposure/crowds, no live vaccines, monitor fever/nfection
RA nursing management
Pain control
Maintain ROM
Preserve mobility
Prevent deformity
Rest during flares
Exercise when inflammation controlled
Coping/body image
Sleep
Medication education
Infection precautions
Nutrition/spiritual support
RA exercises
ROM
Strengthening
Low-intensity aerobic activity
Water exercise
PT/OT
During severe acute inflammation→ limit exercise intensity/repetitions
OA vs RA
OA | RA | |
|---|---|---|
Main problem | Cartilage degeneration | Autoimmune inflammation |
Pattern | Often asymmetrical | Symmetrical |
Inflammation | Minimal/noninflammatory | Inflammatory |
Pain | Worse with activity/later day | Morning stiffness |
Systemic symptoms | No | Yes |
Common finger joints | DIP + PIP | PIP + MCP; DIP spared |
postop joint replacement priorities
Neurovascular status Q4h
Pain, Pulse, Pressure, Paresthesia, Pallor, Paralysis
DVT/PE prevention: early ambulation, anticoag (Lovenox)
Infection
Pain
Mobility
Dislocation prevention
Skin integrity
Education
hip replacement precautions
AVOID:
Hip flexion >90°
Adduction (use abduction wedge/pillow)
Excessive internal rotation
Crossing legs
Twisting
home devices:
Elevated toilet seat
Reacher/grabber
Long-handled shoehorn
Sock aid
signs of dislocation:
Pain
Loss of function
Limb shortening
Malalignment
knee replacement device for early knee ROM:
continuous passive motion (CPM) machine
main indications for amputations
Peripheral arterial disease
Diabetes
Nonhealing ischemic wounds
Gangrene
Severe trauma/crush (MVA, workplace injury, sports, military)
Burns/frostbite
Cancer
Severe/recurrent infection/sepsis
Severe loss of function
PAD/amputation risk factors
Smoking
Diabetes: neuropathy, foot ulceration, poor healing, PAD, repeat amputation risk (foot ulcer)
Obesity
Hypertension
Hyperlipidemia
Increasing age
Family history of PAD/CAD/stroke
6 P’s of limb ischemia/neurovascular compromise
Paresthesia: tingling/numbeness/loss of normal sensation
Pain: sudden increasing distal pain or pain not relieved by medication
Pressure
Pallor: arterial insufficiency
Paralysis: serious neurovascular injury/ischemia
Pulselessness: severe arterial compromise → report urgently
intermittent claudication
leg: pain, numbness, aching, heaviness
occurs w/ exercise/activity (impaired arterial blood flow)
compartment syndrome
dangerous pressure buildup in a closed muscle compartment → ↓ blood flow → tissue/nerve ischemia → permanent injury
sxs: tightness, severe pain, tingling/burning, neurovascular changes
causes: fracture, crush injury, severe muscle bruise, excessive exercise/overstretching, tight cast/bandage
geriatric amputation considerations
Cognitive changes
Lower cardiopulmonary reserve
Reduced coordination
Visual/hearing impairment
Weakness/deconditioning
Gait/balance problems
Limited ROM/arthritis
Reduced independence
Multiple comorbidities
Social determinants
4 M’s: what matters, medications, mobility, mentation
pediatric amputation considerations
Often related to congenital limb differences
Parents also experience grief
Rehab must educate both child + parents
Repeated prosthetic evaluation/refitting is needed with growth
psychological response to amputation
Grief: not just limb
also body part, function, independence, roles/routines, body image, future expectations
Anger
Crying
Denial
Withdrawal
Anxiety
Depression
Body-image changes
Fear of intimacy
Reduced self-esteem/isolation
FAMILY NEEDS SUPPORT TOO
interdisciplinary rehab team
Patient/family
Nursing
Rehab physician
Psychologist/psychiatrist
PT
OT
Social worker
Case manager
Dietitian
Prosthetist
Chaplain
goal: restore and maintain optimal function and quality of life
residual limb care
Promote wound healing
wound care: mild soap/water, soft dressing, avoid adhesive directly on fragile skin, inspect skin regularly
Prevent infection
Manage edema
Shape limb for prosthesis
Prevent contractures/deformity
Maintain alignment
Preserve ROM/strength
Prepare for prosthetic use
residual-limb edema management
Soft dressing
Ace wrap
Residual-limb shrinker/sock
Semi-rigid/rigid dressing when indicated
goal: promote healing, shape limb, prepare for prosthetic fitting, improve comfort
limb wrapping
figure-8 wrapping
Control edema
Shape limb
Promote healing
Prepare for prosthesis
positioning/contracture prevention
prevent: malalignment, contracture/deformity, loss of ROM
contractures make transfers, ambulation, prosthetic fitting/use more difficult
prosthesis preparation
Wound healing
Edema reduction
Residual limb shaping
Adequate ROM/strength
Skin integrity
Functional training
prosthetist: helps evaluate, fit, and adjust the patient’s prosthetic limb
pain after amputation
residual limb pain: originating from remaining tissue/surgical site
phantom limb pain: perceived in limb that is no longer physically present
phantom sensation: feeling that missing limb is still there
amputation care plan priorities
Knowledge deficit
Self-care needs
Impaired mobility
Residual pain
Body image/change in routine
Psychosocial stress
Spiritual distress
Social determinants affecting outcomes