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What is osteoarthritis?
Slow and progressive non-inflammatory disorder of diarthrodial joints - it is not a part of the normal aging process
What is the pathophysiology of OA?
Gradual loss of articular cartilage. The central cartilage becomes thinner, the edges become thicker, and osteophytes form, resulting in uneven weight distribution. In later stages, the bones rub together, leading to increasing pain.
What are the RF for OA?
Age
menopause
obesity
ACL injury
frequent kneeling/stooping
What are the s/s of OA?
Primary s/s ranges from mild discomfort to significant disability
Joint and pain stiffness
Sitting becomes difficult (and getting up from chair when hips are lower than knees)
Intervertebral joints affected - local pain and stiffness
Crepitation
Affects joints asymmetrically
Deformity
How does pain change in OA?
Early stages - relieved with rest
Later stages - occurs with rest
may worsen with lower barometric pressure
pain may be referred to groin/buttock/outside of thigh/knee
main worsen with joint use
how does joint stiffness change in OA?
occurs after periods of rest/unchanged position
early morning stiffness usually resolved w/in 30mins
overactivity may increase stiffness
What deformities may occur with OA?
Heberden’s nodes - bony growths on DIP joints (closest to knuckle)
Bouchard’s nodes - bony growths on PIP joints (closest to finger tip)
Bowlegged (varus deformity)
Knock-kneed (lateral knee)
One leg shorter than the other
What is the tx for OA? Rest and joint protection
Rest and joint protection
Balance rest/activity
Rest during acute inflammation (limiting immobility to <1wk)
Modify activities to decrease joint stress
Avoid prolonged standing/kneeling/squatting
Assistive devices PRN
what is the tx for OA? Heat and cold
Heat and cold
Ice for acute inflammation
heat therapy for stiffness
hot pacs, whirlpool baths, US, paraffin wax
What is the tx for OA? Nutrition/therapy/exercise
Weight loss (only if overweight)
Dietary changes
Supplements w/anti-inflammatory effects
Fish oil
Ginger
SAM-E
Exercise
Aerobic
ROM
Muscle strengthening
What is the drug therapy for OA? mild-moderate joint pain
For mild-moderate joint pain
Acetaminophen
Topical agents, OTC creams containing camphor, eucalyptus oil, menthol
Topical salicylates
Capsaicin creams
What is the drug therapy for moderate-sever joint pain in OA?
Moderate-severe pain
NSAIDs (start low-dose, increase as needed)
Ibuprofen 200mg (up to 4x/day)
Misoprostol to decrease GI effects
Arthrotect (misoprostol + diclofenac)
Avoid topical + PO NSAIDs together
COX-2 inhibitors - Celebrex
What are the other drugs used for OA?
Intra-articular corticosteroid injections
Not recommended anymore - has long term effects
Hyaluronic acid injections - for knees
No longer recommended
DMOADs
What is the surgical tx for OA?
Arthroscopic surgery
For pts w/loss of function/unmanaged pain/decreased independence
Hip and knee replacement
What other tx can be used for OA?
Acupuncture
Massage
Tai-chi
What is the pt teaching for OA?
Pain management (different meds for mild-moderate and moderate-severe)
Body mechanics + correct use of assistive devices
Canes, walkers
Elevated toilet seats
Grab bars
tx options
If knee OA - avoid standing, kneeling, or squatting for long periods of time
Environment modification
Eliminate scatter rugs
Use railings and night-lights
Wear well-fitted supporting shoes
what is rheumatoid arthritis?
Chronic, systemic autoimmune disease where inflammation of connective tissue in synovial joints occurs.
what is the pathophysiology of RA?
Rheumatoid factor combines w/IgG to form immune complexes which deposit on synovial membranes or cartilage in joints, leading to activation of complement and inflammatory response
Neutrophils become attracted to site of inflammation and release proteolytic enzymes that dmg cartilage and thicken synovial lining
T-helper cells are activated, and they stimulate monocytes, macrophages, and synovial fibroblasts to secrete proinflammatory cytokines. (interleukin-1,6 and TNF)
What are the joint manifestations of RA?
Localized stiffness with progression, limited motion
increases with inactivity
Morning stiffness last 60mins or hours
Pain that may increase with motion
Signs of inflammation
s/s occur symmetrically
Subluxation - muscle atrophy and tendon destruction
Tenosynovitis affecting wrists may lead to CTS s/s
Inflammation and fibrosis may cause deformity and disability
Issues with walking
Deformities of hands
What s/s of inflammation may be present in the joints w/RA?
MCP and PIP joints swollen
Spindle shaped fingers
Joints tender, painful, and warm to touch
What are the extra-articular clinical manifestations in RA?
Rheumatoid nodules
Firm and nontender masses found on bony areas exposed to pressure
Cataracts, vision loss
Atherosclerosis - risk of MI increases
Nodular myositis
Pleurisy, pleural effusion
Pericarditis, pericardial effusion, cardiomyopathy
Sjorgen’s syndrome, Felty Syndrome
Flexion fractures and deformities - cause decrease grasp strength and affect ability to perform self care
Depression
Due to pain and disability
May have increased CRP levels
What is Sjorgen’s syndrome?
Dry gritty eyes, photosensitivity
What is Felty syndrome?
enlarged spleen and low wbc
increased risk for infection and lymphoma
What is the RA deformity ulnar drift?
Fingers of hand bend/shift towards pinky
What is swan neck in RA?
a deformity where the PIP joint is hyperextended and the DIP joint is flexed
What is boutonniere’s deformity?
deformity where the PIP joint is permanently bending downward while the DIP joint id hyperextended
What criteria must be met for diagnosis of RA?
Joint involvement - at least 1 joint w/clinical synovitis
Serology
Acute phase reactants
Duration of s/s
What labs are used to diagnose RA?
CBC
ESR, CRP - indicate activate inflammation
RF (positive in 80% of people)
Anti-CCP - antibody specific to RA
ANA(antinuclear antibodies) - indicates autoimmune reaction
What scans/tests are used to diagnose RA?
Bone scans - identify early joint changes
X-ray to check for progression
Synovial fluid analysis - cloudy, straw-colored fluid w/fibrin freckles and MMP-3
What are the main drug classes for treating RA?
Disease-modifying anti-rheumatic drugs (DMARDs)
Slow progression and decrease risk of joint deformity and erosion
Biologic response modifiers (BRMs/Biologics/Immunotherapy)
Slow progression
Corticosteroid therapy (IAI or low-dose oral for limited time)
NSAIDs and salicylates
Celebrex (COX-2 inhibitor)
Other drugs: Immunosuppressants, pencillamine, gold preparations
What are the complications of RA?
Ulnar drift, Swan neck, Boutonniere
Hallux valgus
Pericarditis
Accelerated CAD risk
What is the patient teaching for RA? balancing rest and activity
Alternate rest periods with activity (may help with pain and fatigue)
Amount of rest varies
No total bed rest
8-10hrs of sleep + daytime rest ideal
Work simplification
Pacing and organizing
Use of carts
Delegation of tasks
what is the pt teaching for RA regarding heat/cold application?
May relieve pain, stiffness, and muscle spasm
Cold is especially beneficial during periods of disease activity
Should not exceed 10-15mins at a time
Moist heat relieves chronic stiffness
Should not exceed 20mins at a time
Use heating pads, moist hot packs, paraffin baths, warm baths, or showers
No topical heat producing cream
What is the pt teaching for RA regarding exercise?
To improve flexibility, and strength
Increase overall endurance
Avoid overly aggressive exercise
Gentle ROM daily
Aquatic exercises in warm water beneficial
Limit to 1-2 reps during acute inflammation
what is the pt teaching for RA regarding joint protecting?
Firm mattress/bed board
Positions of extension when resting, avoid flexion positions
No pillows under knees, but a small and flat pillow under head and shoulders
Modify tasks for less stress on joints
Joint protective devices
What other pt teaching for RA should someone get?
home management
s/s of infection
use of relaxation techniques
biofeedback and tens are effect non-drug therapy ideas
What is gout?
Type of arthritis characterized by hyperuricemia and deposition of uric acid crystals in one or more joints. It has remissions and exacurbations.
What is the patho of gout?
Kidneys cannot excrete enough uric acid or too much is being produced, leading to a build up of it. Two process must occur for gout to develop - crystallization and inflammation.
What are the diagnostic studies/labs + results for gout?
Serum uric acid - >6
24-hr urine for uric acid
Synovial fluid aspiration - the gold standard, shows needle shaped crystals
Clinical symptoms
X-ray of affected joints - tophi may appear as eroded areas in the bone
what are the causes of gout?
Primary hyperuricemia is genetic
Secondary hyperuricemia is due to increased production/decreased excretion/drugs that inhibit uric acid excretion
Caused by interaction of factors: metabolic syndrome, increased intake of high purine foods, prolonged fasting, excessive alc
What are the s/s of Gout? joint manifestations
Affects one or more joints (usually <4)
Most commonly affected joint is great toe
Skin becomes dusky or cyanotic
The area becomes very tender
What are the s/s of gout at onset?
Sudden swelling and severe pain
Sensitive to light touch
Low-grade fever
Lasts 2-10 days w or w/o treatment
Redness
What are the s/s of chronic gout?
Multiple joint involvement
Tophi develop (deposits of crystals in subq tissue, synovial membranes, tendons, and soft tissues)
Typically develop years after onset
what are other s/s of gout?
Severity of gout is variable
Can involve frequent, mild attacks or multiple severe attacks
Slow progressive disability
High serum uric acid causes increase in episodes/tophi
Chronic inflammation leads to deformity, cartilage destruction, secondary OA
Large crystals may pierce skin, draining sinuses and causing infection
What is the drug therapy for acute gout attacks?
PO colchicine for acute attacks
Anti-inflammatory
NSAIDs - aspirin should be avoided as it can increase uric acid levels
Ibuprofen is better option
Corticosteroids - PO or IA for prevention
Adrenocorticotropic hormone - in pts where NSAIDs, colchicine, or steroids are problematic
What is the drug therapy for chronic gout?
Xanthine oxidase inhibitors (Allopurinol, febuxostat)
Decreases uric acid production (Includes allopurinol, febuxostat)
Uricosuric (Probenecid, Zurampic, Duzallo (combo of probenecid/zurampic)
Increase urinary excretion of uric acid
PT:
AVOID ASA, Take with food and water (2L/day)
How is gout managed outside of drugs?
Monitor serum uric acid regularly
Dietary restrictions
Limit alc and food high in purine
Limit Organ meats, sardines, aspirin
Increase fluid intake
DASH diet
Weight reduction
Teach about factors that may increase risk of acute attack
Fasting, drug use (diuretics), and major medical events