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PTRS 746 > Arthritis > Flashcards

Arthritis Flashcards

1
Q

What are 4 things to consider with arthritis?

A

It’s complicated
It’s highly prevalent
It’s not just for old people
It’s getting worse

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2
Q

What are two major forms of arthritis?

A

Rheumatoid: systemic inflammatory disease primarily affecting joint synovium

Osteoarthritis or Degenerative Joint Disease: localized process involving destruction of cartilage tissue

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3
Q

What does OA and DJD look like on x-ray?

A

Joint space collapse

bright white spots are sclerosis

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4
Q

What does RA look like on x-ray?

A

inflammation, joint space narrowing, joint erosion
overall washed out appearance
articular surfaces eaten away

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5
Q

What is RA?

A

Chronic systemic inflammatory process with spontaneous exacerbation and remission.
Closely related to other rheumatologic conditions
Diagnostic criteria continually reevaluated

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6
Q

What is diagnostic criteria for RA?

A

Must meet 4/7 criteria, 1-4 must be > 6 weeks duration

Morning stiffness: at least an hour
Arthritis of 3 or more joint areas: 14 areas (L/R), PIP, MCP, wrist, elbow, knee, ankle, MTP
Arthritis of hand joints: wrist, PIP, MCP
Symmetry
Rheumatoid nodules
Positive serum rheumatoid factor
Radiographic evidence or erosion, bony decalcification

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7
Q

What are epidemiology of RA?

A

Affects 1.5 million people
Women>men
Peak occurrence 60-70
Lower prevalence in African americans, japanes, and Chinese vs. Caucasian, increased in native americans

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8
Q

What is etiology of RA?

A

Considered autoimmune disorder
Specific etiology unknown
Maybe genetic
Potential bacterial or viral component, smoking may contribute
Rheumatoid factor: autoantibody against IgGFc in about 70% of patients

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9
Q

What is pathophysiology of RA?

A

Infiltration of synovium by CD4, T cells, B cells, and monocytes
Production of inflammatory cytokines and chemokines
Hyperplastic synovium (pannus) invades and erodes cartilage, bone, articular capsule, and ligaments
Neutrophil infiltration of synovial fluid, venous distension, capillary obstruction, thrombus, and hemorrhage

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10
Q

What is simple pathophysiology statement of RA?

A

Hyperplastic granulation (pannus) invades joint, releasing inflammatory factors which erode cartilage and subchondral bone

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11
Q

What is diagnostic criteria for RA?

A

No single diagnostic test

Based on: exclusion of other diagnoses, clinical presentation over time, lab and radiographic findings

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12
Q

What are differential diagnosis for RA?

A

OA, reactive arthritis, inflammatory bowel disease, gout, psoriatic arthritis, polymyalgia rheumatica, infection, fibromyalgia, SLE, sarcoidosis

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13
Q

What is clinical presentation of RA?

A 
usually insidious onset
Symmetrical morning stiffness (> 60 min)
Generalized fatigue and malaise
Low-grade fever
Anorexia and weight loss
Depression
Progression most rapid in first 6 years
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14
Q

What are the 3 different disease courses of RA?

A

Monocyclic (20%): one episode abates within 2 years of initial presentation
Polycyclic (70%): fluctuating level of disease activity
Progressive and Unremitting (10%)

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15
Q

What are patterns of joint involvement for RA?

A

Bilateral/symmetrical
Hands and wrists most common
Join inflammation
Crepitus
80% develop joint abnormalities within 10 years of diagnosis
Axial skeleton and DIP joints rarely involved
Cervical spine sometimes affected
May be accompanied by joint ankylosis or ankylosing spondylitis

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16
Q

What occurs in wrist during RA?

A

Volar (palmar) subluxation and ulnar displacement of carpals in relation to radius
Frequent development of flexion contractures
De Quervain’s and CTS are common due to synovitis

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17
Q

How is hand involved in RA?

A

Symmetric MCP and PIP joint involvement is fist clinical feature of RA

MCPs: volar subluxation and ulnar drift
PIPs: swan neck and boutonniere deformities with osteophyte formation, Bouchard’s nodes
Thumb: IP hyperextension and MCP flexion, with progressive CMC involvement
DIPs: Usually uninvolved

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18
Q

What is Mutilans deformity?

A

severe deformity with profound instability and functional impairment
loss of joint integrity

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19
Q

Can hip be involved with RA?

A 
More common in OA
Characteristic joint space narrowing with intact articular cortex
No sclerosis (bone doesn't light up)
Consider treatments that reduce risk of hip joint degeneration
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20
Q

Is knee involved in people with RA?

A

Commonly involved due to large amount of joint synovium
Flexion contractures are common due to pain, muscle guarding
On X-ray there is osteopenia, joint collapse, and absence of osteophytes

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21
Q

Can foot and ankle be involved with RA?

A

Pronated hindfoot
Collapse of longitudinal and transverse arches
Hallux valgus
MTP joint subluxation
Hammer or claw toes
On x-ray: hallux valgus, PIP erosions, claw toes

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22
Q

What is involvement of muscle in RA?

A

Primary or Secondary?
Muscle involvement at affected joints
Disuse atrophy, myositis, steroid induced myopathy, and or peripheral neuropathy

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23
Q

Can tendon and ligaments be involved in RA?

A

Altered biomechanics due to chronic inflammatory process
Tenosynovitis interrupts gliding at tendon sheath, causing damage and potential for rupture
Flexor tenosynovitis is considered poor prognosis factor

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24
Q

What are radiographic stages of RA?

A

Early
Moderate
Severe
Terminal

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25
Q

What does radiograph look like in early stage?

A

no radiographic evidence, possible osteoporosis

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26
Q

What does radiography look like in moderate stage of RA?

A

OP with slight cartilage destruction, muscle atrophy, and no joint deformity

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27
Q

What does radiograph look like in severe stage?

A

OP and destruction of cartilage and bone, joint deformity without ankylosis, extensive atrophy

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28
Q

What does radiograph look like in terminal stage?

A

Stage 3 + fibrosis or bony ankylosis

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29
Q

What are laboratory tests for RA?

A 
Rheumatoid factor
Erythrocyte sedimentation rate
C-reactive protein
Complete blood count
Synovial fluid analysis
30
Q

What are possible complications of RA?

A 
Functional impairments
Deconditioning
Rheumatoid nodules
Vascular complications
Neurological complications
Cardiopulmonary complications
Ocular complications
31
Q

What happens with functional impairment an deconditioning in people with RA?

A 
Functional problems: graded from class 1-4
Deconditioning: may not be due to disease process, (drug side effects), loss of lean body mass, elevated resting energy expenditure
32
Q

What are rheumatoid nodules?

A

most common extra-articular manifestation
can be subcutaneous or deep
usually located in areas subjected to mechanical pressure

33
Q

What are vascular complications of RA?

A

relatively rare
most are asymptomatic
Can result in infection, CHF, GI bleeding, hemorrhage

34
Q

What are neurological, cardiopulmonary, ocular complications?

A

Neuro: associated with compression/entrapment
Heart: impaired fitness, pericarditis and pleuropulmonary complications occur rarely
Ocular: sjogren’s syndrome- inflammatory disorder of lacrimal and salivary glands

35
Q

What is pharmalogical therapy for RA?

A

NSAIDS: both analgesic and anti-inflammatory action, tradition COX inhibitors
DMARD (disease modifying anti-rheumatic drugs): for early and prolonged use, methotrexate, gold products
BRM (biological response modifiers): enbril, humira

36
Q

What is prognosis for RA?

A

mortality 1.5-1.6 fold higher than general population
Elevated risk of death from infection, renal, respiratory, and GI disease
Early aggressive disease or poor functional status= poor prognosis
50% develop marked disability

37
Q

What are characteristics of OA?

A

localized process that is confined to the affected joints
Characterized by 2 features: progressive destruction of articular cartilage, formation of bone (osteophytes) at the margins of the joint

38
Q

What is diagnostic criteria for OA?

A

Based on signs, symptoms, and distribution of involvement.
Asymmetrical joint involvement
Lack of generalized symptoms
Morning or post inactivity stiffness of shorter duration than RA
Pain is variable and occurs/worsens with motion
Radiographic tests

39
Q

What is epidemiology of OA?

A 
affects more than 27 million people
Common over age 40
widespread over age 65
Men>women until 5th decade and then reverses
Knee>hip
40
Q

What is etiology of OA?

A 
Primary idiopathic: unknown etiology
Secondary: identifiable trauma, congenital malformation, or other musculoskeletal disease
1) increased age
2) trauma
3) occupational/functional tasks
4) obesity
5) infection
41
Q

What is pathophysiology of OA?

A

Initial increase in articular cartilage H2O content
Proteoglycan and collagen synthesis increase
Later proteoglycan loss reduces compressive stiffness and elasticity (increased friction, decreased shock absorption)
Subchondral bone and periarticular structures

42
Q

What is the clinical diagnostic criteria for OA?

A

symptomology

radiographic criteria: kellgren and Lawrence, grade 0-4, presence of osteophytes, joint space narrowing, deformity

43
Q

What is differential diagnosis for OA?

A

rule out RA and other rheumatic conditions
Joint distribution/symmetry
Radiographic findings: RA had bone erosion, OA has bone formation
Laboratory findings: RF, CBC, etc

44
Q

What are patterns of joint involvement for OA in UE?

A

DIP, PIP, thumb CMC

Herberden’s nodes: osteophyte formation at the DIP (may also be in RA but most common in OA)

45
Q

What are patterns of joint involvement for OA in spine?

A

Degenerative disc disease of cervical and lumbar spine

46
Q

What are patterns of joint involvement in the hip in OA?

A

Protective position: hip flexion, abduction, and ER

Decreased hip ROM correlated to decreased walking speed and functional limitations

47
Q

What are the patterns of knee involvement in OA?

A

Most prevalent form of OA
Functional impact similar to CHF, COPD
Joint collapse, osteophytes, and sclerosis of bone

48
Q

What is the Kellgren and Lawrence grading system?

A

Grade 0: normal
Grade 1: possible osteophytes, questionable joint narrowing
Grade 2: Definite osteophyte formation
Grade 3: Moderate osteophytes, narrowing, possible deformity
Grade 4: large osteophytes, marked narrowing, severe sclerosis, definite deformity

49
Q

What is pharmacologic treatment for OA?

A

Goal is pain control, traditional drugs do not affect disease progression

50
Q

What does pain control include for treating OA?

A

medication, patient education, joint protection, exercise

51
Q

What is medication people can take to help with OA?

A

Oral analgesics/NSAIDs
Corticosteroid injections
Viscosupplementation: hyaluronic acid
Topical analgesics: creams, distract brain from pain

52
Q

What are possible pharmacologic therapy that has little evidence behind them

A

Nutraceuticals: glucosamine sulfate, chondroitin sulfate
Magnets
acupuncture

53
Q

What are 3 indications for surgery for OA?

A

intractable pain
loss of function
progression of deformity

54
Q

What are soft tissue procedures for OA?

A

Synovectomy
Soft tissue release
Tendon transfer

55
Q

What are bone and joint procedures for OA?

A

Osteotomy
Arthroplasty
Arthodesis

56
Q

What are red flags when doing your ortho exam?

A

Recent trauma, unusual pain or weakness, constitutional signs (fatigue, malaise, etc)

57
Q

What do you look at in ortho exam?

A

History, pain characteristics, vocation, current activity level, past medical history, patient goals, ROM, strength, joint stability, endurance, gait, mobility, functional assessment, sensation, psychological status, environmental factors

58
Q

What are things to look at when assessing ROM?

A

goniometric assessments
Functional ROM
Influence on ADLs
Biomechanical impact on surrounding joints

59
Q

What precautions should you take with MMT?

A

procede with caution

modify or use functional tests

60
Q

What are goals and outcome for PT interventions?

A

Decrease pain, increase or maintain ROM, increase of maintain strength, improve joint stability, decrease mechanical joint stress, increase functional endurance, maximize independence of ADLs, improve gait efficacy and safety, establish exercise and conditioning programs, education to increase capacity for self management

61
Q

What directs the evaluation and intervention with arthritis patients?

A

stage of inflammation

62
Q

What is rehab management in acute phase?

A

Reduce pain and inflammation
Rest affected joints
Modalities
Maintain ROM, strength, endurance, functional independence

63
Q

What should you focus on in sub acute phase of arthritis rehab?

A

Progress ROM, strength, endurance, and functional training
Improve performance and range of ADLs
Joint protection

64
Q

What are goals during chronic stage of arthritis rehab?

A

Independence in ADLs
Return to vocation, recreation
Patient education

65
Q

What are modalities used for with arthritis?

A

Reduce pain and facilitate activity

66
Q

What are possible modalities to use for your intervention?

A

Superficial heat
Deep heat: contraindicated for acute inflammation, efficacy in arthritis is questionable
Cold modalities: indicated for acute edema
TENS

67
Q

What are interventions for joint mobility with arthritis?

A

positioning and self ROM
lengthen shortened muscle groups
Manual therapy not indicated for RA

68
Q

What are interventions for strengthening with arthritis?

A

isometric or sub maximal
add dynamic, concentric, eccentric
Use resistance with caution: pain free range, monitor for exacerbation, incorporate functional activities
Exercise induced discomfort should subside within one hour

69
Q

What are joint protection interventions?

A

splints/orthoses
maintain ROM
biomechanical support
reduce pain

70
Q

What are interventions for gait training and endurance training?

A

Gait: improve walking speed and normalize gait, assistive device selection , cane may unload hip by up to 60%
Endurance: consider NWB modes, if possible

71
Q

What are education interventions for patients?

A

disease process
joint protection
pain management
resources

PTRS 746 (15 decks)

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