Lecture 7 and 19 - OA and RA Flashcards
What is the definition of osteoarthritis?
progressive loss of articular cartilage
accompanied by
- attempted repair of articular cartilage,
- remodelling, and
- sclerosis of subchondral bone, and
in many instances the formation of
- subchondral bone cysts and
- marginal osteophytes.
T/F Secondary OA: A. can come from a neurological disorder B. Is idiopathic C. Is the most common D. Is explain by age-related dynamic reaction pattern E. joint injuries can be identified
Secondary OA:
A. can come from a neurological disorder - T
B. Is idiopathic - F
C. Is the most common - F
D. Is explain by age-related dynamic reaction pattern - F
E. joint injuries can be identified - T
What can influence the pathogenesis of OA?
- susceptibility of joint damage, repair failure (6)
- site and severity of OA (6)
(name as much as you can)
Age, gender, menopause, genetics, nutrition, bone density
- susceptibility of joint damage, repair failure
Mechanical factors: obesity, injury, surgery, m.weakness
Joint deformity: repetitive joint loading, elite athletics
- site and severity of OA
What are signs and symptoms of OA (5)?
Tips:
type of e/f, subjective, observations (2), sound
joint pain restriction of motion (capsular vs. bony) crepitus with motion joint effusions deformity
What is the typical progression of OA?
- slow or rapid?
- Improvement expected or degeneration until the end of time?
Typically slow, over many years: Occasionally rapid
May spontaneously stabilize or even improve
partial restoration of the articular surface
decrease in symptoms
T/F
In OA, the patients undergoing 2nd non cognate total joint replacement are most likely ipsilateral
Patients undergoing a 2nd total joint replacement of a hip or knee due to OA or RA
RA: 2nd joint “random”
OA: Non-random
Highest: contralateral cognate joint
Non-cognate joint
contralateral more than 2x as likely
Explain a common problem among OA population pre and post op, often leading to deterioration and poor prognosis of the joint?
Patients pre-op for total hip replacement -> Peak knee adduction moment and peak medial compartment load: contralateral > ipsilateral
Patients post-op for total hip replacement-> Persistent asymmetry of knee kinetics
High knee adduction moment during gait is associated with:
- Radiographic severity of knee OA
- Radiographic deterioration of symptomatic knee OA
- Poor surgical prognosis for high tibial osteotomy (repair of varus deformity)
Easy one: Name good exercises to give OA patients
Low impact aerobic exercise, ex: cycling (land-based), quidditch (air-based), aqua-water-based exs.
Individualized
- ROM & flexibility
- Ms endurance and str exs
Describe some modalities that are recommended for OA? Not recommended?
Recommended
- Thermal: hand, knee, hip
- TENS and other electrical
- Acupuncture, balneotherapy
- Manual therapy
Not recommended
- Ultrasound
T/F in OA
1- Joint replacement is recommended for appropriate patients with knee and hip OA
2- Arthroscopy with debridement is recommended for the management of symptomatic knee OA
3- Intra-articular corticosteroids are recommended for knee and hip OA
4- Intra-articular hyaluronans are recommended for knee and hip OA
1- Joint replacement is recommended for appropriate patients with knee and hip OA (T)
2- Arthroscopy with debridement is recommended for the management of symptomatic knee OA (F)
3- Intra-articular corticosteroids are recommended for knee and hip OA (T)
4- Intra-articular hyaluronans are recommended for knee and hip OA (F: not enough evidence)
Pharmacologically in OA, what is recommended
- 1st line
- 2nd line
- Refractory symptoms
- Others
- 1st line: acetaminophen
- 2nd line: topical: capsaicin, topical NSAIDs
- Refractory symptoms: tramadol
- Others: opioids, duloxetine
For obesity-induced OA, what is
- the minimum physical activity recommended
- The recommended phys.activ (extra recommended… like more than minimal)
- Why?
- Minimum ≥150 min/wk of moderate-intensity PA
- ~250 to 300 min/wk (approximately 2000 kcal/wk)
- Why minimal?
o prevent significant weight gain
o reduce associated chronic disease risk factors
o elicit modest reductions in body weight in overweight and obese individuals
Why extra?
o likely to promote greater weight loss and enhanced prevention of weight regained
When patients should be tested for RA?
they have at least 1 joint with definite clinical synovitis (swelling)
the synovitis is not better explained by another disease (e.g. systemic lupus erythematosus, psoriatic arthritis, gout)
What is the RA diagnosis based on?
Joint involvement
- Large joints = shoulders, elbows, hips, knees, ankles
Small joints = MCP, PIP, thumb IP, wrists, 2nd – 5th MTP
Lab testing
Duration
What are the joints affected by OA AND RA and not taken into account in the diagnosis of RA?
1st CMC and 1st MTP
With the ACR & EULAR collaborative criteria, how does the RA gets diagnosed?
New (acute) patients: ≥ 6 points
or
Patients with erosive disease typical of RA and Hx of prior fulfillment of criteria (i.e. ≥ 6 points)
including pts whose disease is inactive (with or without treatment)
What are the elements of comprehensive management in RA (4)?
Interdisciplinary approach
Early intervention, ongoing care and systemic reassessment (follow-up)
Pt and family involvement
Ecosystemic approach (Home/work evaluation; recommendations when possible)
What are the drug therapy for RA?
NSAIDs
Glucocorticosteroids (Corticosteroids)
Disease-modifying antirheumatic drugs (DMARDs): Traditional DMARDs, Biologics, Biosimilars
What are the 3 MAIN steps in RA PT evaluation?
- Take hx
- Assess disease activity and damage
- Assess physical and functional status
In the RA PT evaluation, what is assessed concerning the disease activity and damage?
Inflammation - Duration of morning stiffness - Grip strength - Active joint count - VAS for pain and fatigue - Tests: Erythrocyte Sedimentation rate (N = <15 mm/hr ♂, <20 mm/hr ♀), RF+, x-rays, etc Damage (deformities) - Damaged joint count Extra-articular features - Raynaud’s - Eye and mouth dryness, etc,…
Give some example of what is assessed when evaluating physical and functional status in RA (tot:8).
ROM & MMT Neurological exam Posture Balance Endurance Transfers Gait Stairs, etc…
What are some goals in the PT treatment in RA (6)?
Educate pts and caregivers
disease processes
self-management
Control inflammation ↓ pain and stiffness ↓ rate of damage and preserve jt integrity ↑ & maintain jt mobility and ms strength Preserve or restore function
Give some PT interventions for RA (tot:10)?
Dx Jt protection techniques Energy conservation techniques: 4 “P”s: plan, posture, prioritize, pace Body mechanics & postural (positioning) hygiene Exercises Use of ice/heat Proper footwear/insoles Self-management strategies
Links to further information : e.g. The Arthritis Society information line, Arthritis Self Management Program, education and support groups, local programs
Give some joint protection technique principles in RA (tot:13)
Respect pain
Alternate b/w rest and work periods
↓ the qty of effort necessary to accomplish a task
Use stronger & larger jts to accomplish the task
Avoid maintaining the same position for a long time period
Avoid any activities that cannot be stopped
Use splints to protect your jts
Use adaptations to protect your jts
Maintain adequate postural hygiene (sitting position, lying, standing or during leisure activities and work)
Maintain adequate body mechanic
Keep a healthy weight
Maintain strong ms around the jts
Maintain jt alignment
RA - PT interventions.
Give some examples (tot:4)
Exercises
ROM, strengthening ex’s, stretching, balance, whirlpool, land-based CV, water-based CV, HEP
Thermal modalities (Hot/cold packs, wax bath) Electrotherapy as needed
Manual therapy Limited role because of jt instability \+/- gentle accessory mobs (gr I-II) for “inactive” jt C-spine traction rarely used Manipulation techniques not indicated
Walking aids & gait training
Other assistive device, splinting/ bracing (OT)
Referrals: Rheumatologist, OT, Psychology, Social worker
What should you consider when giving exs during RA flare up
Avoid strenuous ex’s during acute flare-ups/ inflammation
ROM ex’s are appropriate
Parameters for acute/painful/irritable condition
Adequate warm-up and cool-down are important to minimize pain
Suggest that they exercise at the moment during the day that their pain is typically less severe or during peak activity of pain meds
In the PT valuation of SLE, what changes compared to RA?
Need to look more closely at all the systems during the evaluation.
Heart/lung involvement
Can limit ability to work on improving endurance
Neurological involvement
Balance can be affected
Is there any change in the PT treatment of SLE compared to RA?
Similar to RA
Advices specific for skin rash
Avoid exposure to sun
Use sun block & protective clothing
What are the PT interventions in sceroderma?
Mainly supportive interdisciplinary approach
ROM ex’s for the affected jts (gentle) Facial and mouth exercises Strengthening ex’s Hot pack or wax bath Close monitoring of skin integrity with ROM/ stretching necessary
Education
Avoid exposure to cold, monitor closely with heat (Raynaud’s phenomenon )
Give an example of mouth exercise parameters.
What improvements are expected?
Exercises done 2X/day, 15 min each, over 18 wks
Mean improvement in mouth opening
10.7±2.06 mm
Improvements in eating, speaking, oral hygiene, and the insertion of their dentures was easier
What is the joint most affected with gout?
1st MTP
What are the 5 screening questions in AS?
T/F
If more than 50% are positive, the sensitivity and sensibility are high enough to suggest AS
Is there morning stiffness?
Is there improvement in discomfort with exercise?
Was the onset of back pain before age 40 years?
Did the problem begin slowly?
Has the pain persisted for at least 3 months?
F: 4/5 positive questions
What postural effect is expected in AS?
Loss of Lx lordosis, ↑ Tx kyphosis, compensatory ext of Cx spine
What are the spinal mobilit test done in PT with AS?
Finger-to-floor Occiput-to-wall Cx spine: all mvts T1-to-wall, T7-to-wall Lx spine: Modified Schober’s test
What does the PT evaluate in AS?
- duration of morning stifness
- posture
- spinal mobility
- chest expansion at xiphoid process
- active joint count
The PT do an active joint count in AS if ….?
if peripheral jt involved
Name one specific disease battery tests in AS and what does it include.
(or all 4, if motivation is still existing somehow)
BASDAI
Bath Ankylosing Spondylitis Disease Activity Index
Measures fatigue, spinal pain, joint pain, swelling, areas of local tenderness, morning stiffness
Self-administration, uses VAS
BASMI (Metrology Index)
Measures spinal mobility: tragus to wall, Lx flex, Cx rot, Lx SF, Intermalleolar distance
BASFI (Functional Index)
10 questions on function and ability to cope with everyday life
Self-administration, uses VAS
BASGI (Global Index)
2 questions on the effect of the disease in the last wk and the last 6 mths
Self-administration, uses VAS
What are the goals in PT management of AS (6)
Maintain a good posture and avoid stiffening in a flexed position
Optimize spinal and chest mobility
Optimize general ms strength
Optimize CV function
Maintain and improve general functioning and HR-QOL
Design lifelong health and rehabilitation programs with the patient
What are the component of education in AS (9)?
Dx (spinal & CV components)
Smoking reduction or cessation
Nutrition, weight control, hydration
Cold and flu prevention
Benefits of aerobic, mobility and strengthening exercises
Self-management
Pacing and energy conservation
Posture
Keeping the spine as straight as possible while walking or sitting
Avoid prolonged stooping or bending.
Sleeping on back on a firm mattress using the thinnest possible pillow
Name 4 exercise to give to a patient suffering from AS (6 listed).
Postural correction exercises / Global postural reeducation
Spine & Chest wall mobility exercises
Should include all planes of movement with a rotational component
General trunk stretching
Soft tissue mobilization
Deep breathing exercises & breathing control, incentive spirometry, coughing maneuvers
ROM exercises
Strengthening exercises
Gait reeducation
Aerobic exercise
T/F
- A secondary effect of corticosteroids AND NSAIDs is to bruise easily
- With corticostroids and patients suffering from Osteoporosis -> be careful for potential risk of #
- With biologics and biosimilars, GI discomfort may interfere with rehab
- A secondary effect of corticosteroids AND NSAIDs is to bruise easily - TRUE
- With corticosteroids and patients suffering from Osteoporosis -> be careful for potential risk of # - TRUE
- With biologics and biosimilars, GI discomfort may interfere with rehab - NO thats with NSAIDS
With which medication these sides effects are expected (nsaids, corticosteroids, biological/biosimilar):
- increased risk of infection
- Hyperglycemia
- Dizziness
- GI discomfort
- skin fragility
- Stiffness
- ms rigidity
- impaired vision
- increased risk of infection - bio/bio
- Hyperglycemia - cortico
- Dizziness - cortico
- GI discomfort - NSAIDs
- skin fragility - cortico
- Stiffness - bio/bio
- ms rigidity - bio/bio
- impaired vision - cortico
Compare RA and OA
- is it systemic?
- is there morning stifness?
- is there extra-articular manifestation?
- is it symmetrical?
RA/OA
- Y/N
- Y/N
- Y/N
What joints are involved in
- OA?
- RA?
- OA: DIP, PIP, 1st IP, MCP, CMC’ joints & WB joints
2. RA: typically small joints of hands and feet, but also wrists, ellbows, shld, hips, knees, neck
What is the difference in the inflammation process in
- OA
- RA
- OA: changes in synovium are secondary
2. RA: primarily auto-immune, primary changes in synovium
What is a pannus formation?
an abnormal layer of fibrovascular tissue
presenting as a thickening of synovial membrane that appears as a result of the inflammatory process.
what is the overall result of the pathology and inflammatory process of RA
The overall result of the pathology and inflammatory process is:
• Joint degeneration
• Ligamentous laxity
• Joint deformities
What are some general and systemic RA symptoms (7)
Fatigue General malaise Low grade fever (during active phase of the disease) Anemia Weakness Depression Weight loss
What are some RA articular manifestation (5)
Typically, symmetrical pattern Pain in the affected joints Swelling of the joints Stiffness - commonly following periods of sitting, inactivity, and sleep (morning stiffness) Joint deformities
Describe a swan neck deformity
o MCP flexion
o PIP extension
o DIP flexion
Describe a boutonnière deformity
o MCP Extension
o PIP flexion
o DIP extension
Describe a zig zag deformity
Zig-zag deformity of wrist & fingers (RD of wrist combined with UD of MCPs)
Describe a hammer toe
MTP hyperext; PIP flex; DIP ext
Describe a claw toe
MTP hyperext; PIP & DIP flex
What are the most common deformities in toes?
Hallux valgus
hammer toe
What deformities can be observed in the knee
Genu varum
Genu valgum
What deformity can be observed in the neck?
C1-2 subluxation (due to laxity of transverse ligament)
What are rheumatoid nodules and with what are they associated with?
Rheumatoid nodules – hard fibrous tissue nodules, generally in
the subcutaneous tissue
o Occur in up to 50% of pts with RA at some point
o Associated with +ve rheumatoid factor (RF+)
o Often over pressure areas (e.g. dorsal surface of F/A)
but can present in any location and can also be internal
(e.g. in the lungs)
What are some extra-articular manifestation of RA
- Rheumatoid nodules
- vascular (vasculitis and raynaud synd.
- sjogren synd
- Resp: nodules, fibrosis, pleurisy ±effusion
- cardiac: pericardial eff, pericarditis
- Neuro: carpal tunnel synd, ulnar n entrapement, neuropathy, spinal cord compression
- GI, renal, hemato
(more info: p5 of the RA reading document)
T/F
X-rays are helpful for the RA dx?
F
X-rays are generally not helpful for the purpose of diagnosis
of RA but they can be helpful in assessing its severity and prognosis.
What is bone scintigraphy useful for?
Assessment of increased bone remodelling at joints
T/F
SLE is an acute, localized, inflammatory, auto-immune disease.
F
SLE is a chronic, systemic, inflammatory, auto-immune disease with multi-organ involvement.
What is the typical patter at onset of SLE
Sorry… my bad for this one
SLE does not have any clear, characteristic pattern at onset of disease, nor any consistency in the course
of disease.
Does SLE have a systemic involvement?
Yes…. it touches litteraly EVERYTHING, (p8 for more info)
What’s the lab test for SLE?
Antinuclear Antibodies (ANA) are present in the serum (ANA +) of ~95% of patients with SLE
• Hematological abnormalities: Leukopenia (low white blood cells); Thrombocytopenia (low levels of
platelets); Anemia (low levels of red blood cells); Pancytopenia (low levels of RBC, WBC, platelets)
• Elevated Erythrocyte Sedimentation Rate
Scleroderma is characterized by what?
characterized by inflammation, vasculopathy involving small blood vessels,
and fibrosis: collagen deposits (often quite large) cause a build-up of tough, scar-like, fibrous tissue.
What are the 2 types of scleroderma?
Limited scleroderma (CREST) and diffuse scleroderma are the two types.
Limited scleroderma is characterized by what?
C = Calcinosis (Ca + deposits in soft tissue) R = Raynaud’s phenomenon E = Esophageal dysmotility (including acid reflux) S = Sclerodactyly (localized thickening and tightness of skin of fingers or toes) T = Telangiectasia (small dilated blood vessels near surface of skin or mucous membranes)
Limited or diffused scleroderma?
1. the skin involvement is distal to the elbows and knees
2. Permanent organ damage
3. trunk and proximal limbs (upper arms and thighs) are commonly affected
4.neck and face are not affected
5.The disease often
peaks after 5-6 years, followed by regression and softening of the skin
6.Prognosis more favorable
Lim/diff
1. the skin involvement is distal to the elbows and knees - lim
2. Permanent organ damage - diff
3. trunk and proximal limbs (upper arms and thighs) are commonly affected - diff
4.neck and face are not affected - lim
5.The disease often
peaks after 5-6 years, followed by regression and softening of the skin -diff
6.Prognosis more favorable - lim
Scleroderma:
What signs on the hand you can observe
- early
- later
Early
Edema (sausage digits)
Later
Thickening / tightening of skin (sclerodactyly)
Bony resorption: distal phalanges shortened & nails deformed
Contractures: MCP ext & PIP flex
Calcium deposits: sometimes open areas oozing chalky material
Describe Mauskopf facial changes
Contraction and hardening of tissues of the face (most common in diffuse scleroderma) can lead to characteristic changes known as “Mauskopf”:
• Muscles atrophy at the temple, face and neck • Absence of normal skin folds • Thin pursed lips c̅ radial furrowing • Expressionless face • Narrowing of the oral aperture o poor dentition o difficulty eating
Where hard crystal of acid uric can deposit in gout?
- 1st MTP
- heels, ankles and knees
- kidneys, causing kidney stones and renal damage
Which joint are more commonly affected in AS?
- axial skelton
- sacroiliac joint
- costovertebral, costotransvers joints
- hip, knee, shld
What can be affected with ankylosis
Spine and
chest wall rigidity may also affect thoracic expansion, which can affect breathing and exercise capacity
What’s the onset of AS
20-40 years
What are the dx criteria for AS
- History of inflammatory low back pain (LBP)
- Loss of spinal mobility
- Radiological evidence of sacroiliitis
This description describe what disease
- inability to WB
- May not tolerate LT of affected joint
Gout
T/F
The DMARDs
1- have a immunostimulation effect
2- do not generally induce a complete remission
3- The disease activity may persist and joint damage may continue to progress
4- NSAIDS are prescribed for 6-12 months until the patient gets symptomatic relief from DMARDs
The DMARDs
1- have a immunostimulation effect- F
2- do not generally induce a complete remission - T
3- The disease activity may persist and joint damage may continue to progress - T
4- NSAIDS are prescribed for 6-12 months until the patient gets symptomatic relief from DMARDs - F (for 1-6 months)
What is the most common DMARDs
Methotrexate
How should PTs decreased infection risks when treating a patient ender DMARDs/bio/bio
Should be considered when scheduling PT treatment
Should be careful about cleaning therapy equipment appropriately before use with these patients
Refer to MD if signs of infections
The RA diagnosis is based on which lab test A. Hb B. white blood cell count C. RF and anti-citrullinated protein antibody D. midichlorians E. CRP F. B lymphocytes count E. T lymphocyte count
Serology: rheumatoid factor (RF) & anti–citrullinated protein antibody (ACPA)
Acute Phase Reactants: C-reactive protein (CRP)& erythrocyte sedimentation rate (ESR)
