Lecture 19: Rheumatology Flashcards

1
Q

What is arthritis?

A

Inflammation w/in a joint that can have many causes. It is associated w/ pain, stiffness, edema/swelling.
-May appear as acute episodes w/ periods of remission or chronic symptoms.

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2
Q

What are the common rheumatic/arthritic conditions?

A
  • Rheumatoid Arthritis
  • Osteoarthritis
  • Juvenile Idiopathic Arthritis
  • Diffuse Connective Tissue Diseases: Systematic Lupus Erythematous, scleroderma, polymyositis and dermatomyositis.
  • Crystal-induced arthritis: Gout
  • Spondyloarthropathies: ankylosing spondylitis, Reiter’s syndrome, psoriatic arthritis.
  • Fibromyalgia
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3
Q

What is Raynaud’s Phenomenon?

A
  • Episodic vasoconstriction of the arteries of the hands or feet leading to cyanosis or blanching, burning or tingling.
  • Usually associated w/ cold or stress.
  • Erythema (redness of the skin) can be seen after vasospasm as a result of vasodilation.
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4
Q
  1. What is RA?
  2. Epidemiology of RA.
  3. Etiology
A
  1. Chronic, systemic, inflammatory disorder. Inflammation of joints w/ associated damage. Often progressive.
    No cure, medication slows progress of the disease.
  2. 1% population. Women>men. Age onset 25-50yo.
  3. Cause=unknown, combination of factors.
    - Genetics (HLA-D)
    - Environment
    - Multiple cell types involved
    - Auto-immune involvement: Immune system attacks healthy tissue of the body especially joints and periarticular surfaces.
    - High levels of autoantibodies.
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5
Q

What is the clinical course of RA?

A

Typically manifests in small joints of the hand and feet.

Insidious or sudden onset. 
Type 1: Self-limited 
Type 2: Minimally progressive
Type 3: Progressive 
-Flare ups and remission common
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6
Q

What are symptoms of RA?

A
  • Fatigue
  • General malaise
  • Low grade fever during active phase
  • Anemia
  • Weakness
  • Depression
  • Weight loss
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7
Q

What are the articular manifestations of RA?

A
  • Symmetrical pattern
  • Pain
  • Swelling
  • Stiffness (usually after periods of inactivity)
  • Joint deformities
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8
Q

What are common hand and wrist deformities?

Neck?

A
  • Swan neck
  • Boutonniere
  • ZigZag deformity thumb
  • UD MCPs
  • ZigZag wrist and fingers (RD of wrist w/ UD MCPs)
  • Synovitis

-C1-2 subluxation

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9
Q

What are common feet and toe deformities?

Knees?

A
  • Mallet Toe
  • Hammer Toe*
  • Hallux Valgus*
  • Claw Toes
  • Most common
    Genu Valgus or Varum
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10
Q

Must look at different factors to confirm RA diagnosis, not one single test:

  1. Who should be tested for RA?
  2. What is the diagnosis based on?
  3. What are the criteria for diagnosis of RA?
  4. Why is early diagnosis important?
A
    • 1 joint w/ clinical synovitis.
    • Synovitis is not better explained by another disease.

2.
-Joint involvement: Large joints, small joints.
-Lab Tests:
Serology: RF and ACPA
Acute Phase Reactants: CRP, ESR (general swelling/inflammation factors)
-Duration (< or > than 6 wks)
See table in slides

  1. New (acute) pts: > 6 points
    Pt w/ erosive disease typical of RA and hx of prior fulfillment of criteria (>6pts)- including pts whose disease is inactive.
  2. To get medication early, slow the disease process. To minimize inflammation causing joint deformity and laxity.
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11
Q

What are the differences b/w RA and OA

A

Systemic: RA-Yes OA-No

Morning Stiffness Duration: RA- longer >30 min OA-Shorter as when the move it gets better <30 min

Extra-Articular Manifestation: RA-Yes (Rash, Raynaud) OA-No

Symmetrical: RA-Usually OA-No (sometimes can have symmetry w/ wb joints)

Joint involvement: RA- Mainly small hands, wrists, elbow, shoulders, hip, knees, neck and feet.
OA- hip, knee WB joint, Usually DIP, PIP, 1st IP, MCP, 1st CMC.

Inflammatory process:
RA- Primary (auto-immune) Inflammation then jt degradation and laxity.
Secondary- Jt degeneration then inflammation, crepitus, osteophytes.

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12
Q

What are the general management strategies for rheumatic conditions?

A
  • Interdisciplinary approach
  • Early intervention (delay deformity)
  • Ongoing care
  • Systemic reassessment
  • Pt and family involvement
  • Ecosystem approach (home/work eval)

PT sees pt over a long period of time, especially during periods of flare up or after jt replacement.

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13
Q

What is involved in the medical management of RA?

A

Drug Therapy:

  • NSAIDS
  • Corticosteroids
  • Disease-modifying anti rheumatic drugs (DMARDs): Traditional, biologics and biosimilars.

Surgery: Jt replacement.

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14
Q

What are the components of a PT evaluation for RA?

A

Hx: Can be extensive depending on how long they have had the disease. Current/past illness, surgeries, rehab services, medication, appt w/ a rheumatologist, social hx.

Disease activity and damage:

1) Inflammation: duration morning stiffness, grip strength, active joint count, VAS, ES rate, RF, X-ray.
2) Damage: Damage jt count
3) Extra-articular features (Raynaud’s)

Physical and functional status: ROM, strength, endurance, transfers, gait, posture, balance, neuro.

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15
Q

What are the goals of PT Rx for RA?

A
  • Educate pt and caregiver (disease process and self-management)
  • Control inflammation
  • Decrease pain and stiffness
  • Decrease rate of damage and preserve jt integrity
  • Increase and maintain jt mobility and ms strength. It is a progressive disease so there will be deterioration over time-try to maintain as much as possible.
  • Preserve or restore function.
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16
Q

What PT interventions are used for RA?

A

1) Education: Dx, ice/heat, Jt protection (ex: use splints, avoid maintaining same position for prolonged periods), energy conservation, exercise, body mechanics, links other info, self-management, footwear/insoles.
2) Exercise: ROM, stretching, balance, land and water based CV, HEP.

3) Thermal modalities: Use ice during flare-up, do not use heat this will increase inflammation.
May use hot and cold same time at different joints.
Active-cold
non-Active-hot to help w/ pain

4) Electrotherapy
5) Manual therapy: limited role b/c of jt instability especially spine.

6) Walking aids
7) Referral

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17
Q

What are the ACSM guidelines for RA?

What is the goal of ACSM guidelines?

Special Consideration?

A

ROM/Flexibility: Daily all major ms groups

Resistance: 2-3d/wk , light to high, if jt damage lower intensity recommended.

Aerobic: 3-5 d/wk, light to mod, >150 min. Activities low jt stress.

Generally these guidelines are similar as for healthy adults, just have to consider pain and status- during active flare up activity may be contraindicated.

Goal: Minimize pain but gradually progress towards a level that provide health benefits.

Special Consideration:

  • Functional Ex
  • Adequate WU/CD to min pain
  • Avoid strenuous Ex during acute flare-up (ROM are appropriate- parameters for acute/irritable condition 5-10 reps no hold 2-5 times per day).
18
Q

What are the recommended clinical practice guidelines for RA?

Cochrane?

A
  1. Ex therapy
  2. Education
  3. US, Estim, LLT, thermotherapy
  4. Message, manual therapy, balneotherapy.

Cochrane:

  • Exercise
  • Thermotherapy
  • US
  • TENS
  • E-stim
  • LLLT
  • Split and orthoses
  • Tai-chi
19
Q

Systemic Lupus Erythematosis (SLE)

  1. Epidemiology
  2. General Presentation
  3. Clinical Course
  4. System involvement
  5. Lab tests
  6. Medical Management
A
  1. 1 per 2000, women>men b/w age 15-40yo.
  2. Chronic, systemic, inflammatory auto-immune disorder with multi-organ involvement. Genetics factors play a role. Antibodies attack healthy tissue resulting in inflammation of many tissues in body.
  3. No characteristic pattern. Initial presentation can be linked to fever, weakness, fatiguability and weight loss. Usually periods of active flare-ups and remission.
  4. Joints:
    -Symmetric
    -Inflammatory but non-erosive. Deformities are rare and ca be reversible
    -Small>larger joints
    -mainly capsule/supporting structures.
    Sling: photosensitivity rash, butterfly rash, ulcers.
    Muscles: myositis.
    Kidneys, lungs, Gi, cardiac, vascular, neuro and neuropsych also involved.
  5. Antinuclear Antibodies (ANA)
    Hematological abnormalities: low WBC, RBC, platelets or combination
    High ERS
  6. Drugs: NSAIDs, Glucocovrticosteroids and DMARDs.
20
Q

PT evaluation and treatment for SLE?

A

Eval: Similar to RA, but more close examination of all systems. Heart/lung->endurance
Neurological->balance

Treatment: Advice for skin rash (avoid sun, sun block and protective clothing)

21
Q

Scleroderma:

  1. Epidemiology
  2. General Presentation
  3. Types
  4. System involvement
  5. Specific Changes
A
  1. Rare 5-15 per 1 million. Female>male 30-50
  2. Genetic and environmental causes.

Systemic, auto-immune, connective tissue disease characterized by fibrosis of the skin and internal organs.
Inflammation, vasculopathy and fibrosis (collagen deposits).
Sclera=Hardening Derma=Skin Fibrotic changes in the skin characteristic feature.

Early symptoms: muscle pain and stiffness.

3. 
Limite Scleroderma 
C-Calcium deposits
R-Raynaud
E-Esophageal dismotility
S-Thickening skin toes and fingers
T-small dilated blood vessels

-Skin involved distal to elbow and knees. Less organ involvement. Neck and face are not involved. Better prognosis.

Diffuse Scleroderma

  • Trunk and proximal limbs
  • Sever organ involvement
  • Peak after 5-6 hrs then regression
  1. Skin: Thickening/rigidity of skin and ca deposits
    MSK: Erosive arthritis and myositis.
    GI, Lung, Cardiac, Renal
  2. Hand Involvement: Edema (sausage fingers), Thickening of skin, bonds resorption, contractors, Ca deposits. Raynaud common 90%.

Mauskopf Facial Change: Contractors and hardening of facial tissue: muscle atrophy, absence skin folds, pursed lips, poor oral aperture, expressionless.

22
Q

PT interventions for Scleredoma

A
  • ROM for affected jts
  • Facial and mouth ex
  • Strengthening
  • Hot pack or wax bath
  • Monitor skin integrity w/ ROM/stretching
  • Education re cold exposure, monitor w/ heat

Mouth Exercises:
2X/day, 15 min each over 18 wk improve mouth opening 10 mm.
Improve eating, speaking, oral hygiene and insertion dentures.
1) Finger exercise
2) Splint

23
Q

Gout (Crystal-Induced Arthritis)

  1. Epidemiology
  2. Etiology
  3. Most commonly affected joint
  4. Clinical presentation
  5. Medical Management
A
  1. 1% population, male>female, peak 40-50 yo.
  2. Acute inflammatory condition resulting from hyperuricemia: excess of uric acid in the blood, leading to the formation of hard uric acid crystals in one joint which can lead to joint degeneration.
  3. 1st MTP, may also affect heels, ankles and knees. (Kidneys as well).
  4. Rapid onset of swelling and redness of a joint, combined w/ pain. Feet or LE involvement and inability to WB. Fever and chills. Flare-up lasts 1-2 wks.
  5. NSAIDs for acute attack and Allopurinol to reduce uric acid production.
24
Q

Role of PT for Gout?

A

Similar to other rheumatic conditions.

Possibly assistive devices if walking is affected.

Fairly rare.

25
Q

Ankylosing Spondylitis (AS):

  1. Epidemiology
  2. Etiology
  3. Pathology
  4. Clinical Presentation
  5. Criteria diagnosis
  6. Medical Tests
  7. Lab Tests
  8. Medical Management
A
  1. Men>Women, 20-40 yrs
  2. Unknown (genetics HLA-B27 antigen). Association w/ inflammatory bowel disease.
  3. Idiopathic progressive, inflammatory disorder. Immune system attacks healthy tissue causing inflammation. Axial skeleton most commonly involved: SI joint, costovertebral and constotransverse joints and larger peripheral joints (hip, knee, shoulder)
    - Ankylosis: pathology leads to new bone formation, reduced joint mobility due to fusion of bones.
    - Spine and chest wall rigidity can affect breathing.
    - Ocular, pulmonary, cardiac and synovitis.
  4. 20-40 yo, insidious onset > 3 maths of pain and stiffness (back)
    - Pain increase w/ rest and decreased w/ activity (night pain)
    - Flattening lower spine (loss lordosis)
    - Loss spinal mobility
    - Limited chest expansion
  5. Hx inflammatory lower back pain, loss spinal mobility, radiological evidence of sacroiliacitis.
  6. X-Ray
    Early changes: sacroiliacitis, squaring vertebral bodies.
    Late changes: Bamboo spine appearance, joint fusion (z-joints Cx spine most common)
  7. Systemic inflammation (negative for RF, positive ESR and CRP, HLA-B27)
  8. Med: NSAIDS, DMARDs (not effective spondylitis, peripheral arthritis only), biologics or biosimilars , glucocorticosteroids.
    Surgical: spinal osteotomy, joint arthroplasty (hip).
26
Q

What are the screening questions for AS and what are their significance?

A
  1. Is there morning stiffness?
  2. Is there improvement in discomfort w/ exercise?
  3. Was the onset of back pain before age 40?
  4. Did the problem begin slowly?
  5. Has the pain persisted for at least 3 months.

4/5 positive answer has high sensitivity and specificity. PPV=0.04 bc AS is rare.

27
Q

What evaluations should PT do for AS?

A
  • Duration morning stiffness
  • Posture (loss of lumbar lordosis, increase Tx kyphosis, compensatory ext of Cx spine)
  • Spinal Mobility (tape measure): finger-to-floor, occiput-to-wall, Cx spine: all movements, T1 or T7 to wall, Lx spine: Modified Schober’s Test
  • Chest expansion at xiphoid process
  • Active jt count as needed for peripheral jts
28
Q

What are 2 tests for spinal mobility and how are they done?

A

Occiput-to-wall: Distance b/w occipital protuberance and wall.

Modified Schober’s Test: Midway btwn 2 PSIS, mark 10 cm & 5cm above and bellow in neutral. Measure distance when fully flexed. Normal > 4cm difference.

29
Q

What are some disease specific tests for AS?

A

BASDAI: Measures fatigue, spinal pain, joint pain, swelling, areas of local tenderness, morning stiffness. (VAS)

BASMI (Metrology Index): Measures spinal mobility

BASFI (Functional Index): Functional and ability to cope w/ everyday life.

BASGI (Global Index): 2 questions about effect of disease in the last week and 6 months.

30
Q

What are the goals of PT management for AS?

A
  • Maintain a good posture and avoid stiffening in a flexed position
  • Optimize spinal and chest mobility
  • MS strength
  • CV function
  • Maintain and improve general functioning and HR-QOL
  • Design lifelong health and rehab programs w/ pt.
31
Q

What are the components of education for a pt w/ AS?

A
  • Dx (spinal and CV components)
  • Smoking cessation
  • Nutrition, weight, hydration
  • Cold and flu prevention (b/c medication for AS immunosuppressive effects)
  • Benefits of aerobic, strength and mobility ex
  • Self-management
  • Pacing and energy conservation
  • Posture: spine as straight as possible while walking or sitting, avoid prolonged stooping or bending.
  • Sleep on back on a firm mattress, thin pillow
32
Q

What are the other PT management strategies for AS?

A
  • Postural correction exercises
  • Spine and chest wall mobility exercise: all planes of movement w/ rotational component. General trunk stretching, soft tissue mobilization, deep breathing ex and breathing control (spirometry, coughing maneuvers)
  • ROM
  • Strength
  • Gait
  • Aerobic
33
Q

What does the evidence show for PT for AS?

A

Individual or supervise program better than no intervention.

  • Supervised PT better than home
  • Spa followed by group PT, better than group PT alone.
  • PT is important Rx to maintain and improvement movement of spine, improve fitness and reduce pain in pt w/ AS.
34
Q

What are the pharmacological agents used in rheumatological conditions?

A

NSAIDs
Glucocorticosteroids

Disease-Modifying Antirheumatic Drugs (DMARDs)

  • Traditional
  • Biologics
  • Biosimilars
35
Q

What is the role of NSAIDs for rheumatological conditions?

  1. What are the implication of NSAIDS for Rehab?
A
  • Pain and inflammation reduction (symptom management) during early stage of the conditions
  • Do not alter course of disease (joint damage)
  • Use early in disease b/c DMARDs take weeks to months to kick in.
  1. Therapy session conducted w/ pain relief, do not push pts too much. Avoid aggressive mobilizations at peak analgesic.
    -High doses ASA may bruise easily
    -GI discomfort may interfere w/ rehab.
36
Q
  1. Glucocorticosteroids have what effect on the body?
  2. What are they used for in RC?
  3. Max # intra-articular injections/year
  4. Short Term and Long Term side effects.
  5. Implication of Corticosteroids for rehab?
A
  1. Anti-inflammatory and immunosuppressive. Inhibit production of pro-inflammatory substances and increase production of anti-inflammatory proteins.
  2. Slow disease process. Decrease WBC. However, numerous side effects w/ long term use or high doses, so only used early in disease while DMARDs kick in.
  3. 2-3 per year
  4. Catabolic effect on all supportive tissues.
    ST: hypertension, edema, increase glucose, GI

LT: Increased susceptibility infection, osteoporosis…

  1. Osteoporosis, be careful for potential risk #
    - Watch signs hypoglycaemia
    - Dizziness and impaired vision may affect balance
    - Monitor skin condition when using ex equipment (fragility and bruising).
    - Post-injection implications
37
Q
  1. What are DMARDs?
  2. When are they prescribed?
  3. What is the most common DMARD?
  4. What do DMARDs increase the risk of?
A
  1. Drugs used in autoimmune disorders to slow the disease progression via immunosuppressive effects. Many also have anti-inflammatory effects. Do not generally induce a complete remission.
  2. Usually prescribed along w/ NSAIDs b/c they are slow-acting an may take 1-6 months to have effect.
  3. Methotrexate. Effective and safe.
    - usually prescribed folic acid
    - Headache, nausea, vomiting, diarrhea, dizziness may affect rehab
  • Some pts may take a combination of DMARDs.
    4. Infection because of immunosuppressive effect.
38
Q

What are Biologics?

A
  • Agents that slow down disease progression in autoimmune conditions.
  • Produced through genetic manipulation of living organisms
  • Inhibit TNF-alpha and IL-1
  • Administered by injection
  • Expensive

Side effects:
-Allergic rxn, infections, cancer, demyelinating disorders, changes in mental status.

39
Q

What are biosimilars?

A

Made by other manufactures of the original biologic agents once the patent of the original biological agent has expired.

  • Slow down disease progression
  • Reduced health care cost
  • Studies still exploring whether it is safe to switch from biological to biosimilar.
  • Pt already on biologic should not switch to biosimilar.
  • Initial prescription for new diagnosis can be biosimilar.
40
Q

What are the implications for rehab if a pt is on biologics or biosimilars?

A
  • Increase risk infection: Should be considered when scheduling PT treatment, careful about cleaning therapy equipment appropriately before use, refer to MD if signs infection
  • Be aware of unusual ms stiffness or rigidity (demyelinating disorders side effect possible)
  • Refer to MD if fever, difficulty breathing or chest pain.