RA, OA and others Flashcards

1
Q

What is rheumatoid arthritis?

A
Autoimmune disease (chronic, systemic, inflammatory disorder affecting whole body and not just joints)
Primarily synovial joints tho
Has extraarticular manifestations
More women (35-50 YO)
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2
Q

Etiology of rheumatoid arthritis

A

Interaction betwwen genes (HLA) and environment

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3
Q

Progression of RA

A

External trigger causing autoimmune rxn and inflammatory process
Synovial hypetrophy and chronic joint inflammation
Destruction of joints (bones and cartilage are eroded)
Joint deformity

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4
Q

Clinical features of RA

A

Symmetrical polyarthritis
Progresses from periphery to more proximal
Usually spare axial skeleton (except C1/2)
Gradual onset with difficulty performing ADLs
May have constitutional features

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5
Q

Predominant sxs of RA

A

Pain, stiffness and swelling of mostly small joints of hands, wrists and forefoot (can be elbows, shoulders, ankles and knees)
Morning stiffness OVER 1 HOUR (gets better with movement)

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6
Q

What is spared in RA?

A

DIP joints

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7
Q

Physical findings in RA

A

TTP or movement of joint
Squeeze tenderness of MCP and MTP joints
Palpable synovial thickening (boggy)
Effusion (fluctuance)

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8
Q

What do the hands look like in RA?

A

Symmetrical inflammation of MCP and PIP
Flexor tendon tenosynovitis (decreased ROM/grip strength, trigger finger)
Swan neck and boutonniere deformities
Ulnar deviation/drift

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9
Q

What do the wrists look like in RA?

A

Loss of extension

Carpal tunnel syndrome (entrapment of nerve due to inflammation)

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10
Q

What do the elbows look like in RA?

A

Loss of extension
Ulnar nerve compression
Rheumatoid nodules most common here

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11
Q

What do the shoulders look like in RA?

A

Seen late in disease (because disease moves distal to proximal)
Frozen shoulder

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12
Q

What do the LEs look like in RA?

A

Feet/ankles: callus formation, hallux valgus (bunion), hammer toes, compensated flexion
Knees: effusion, limited ROM (flexion), Baker’s cyst
Hips: in longstanding disease there is restriction of movement

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13
Q

When is the cervical spine affected in RA?

A

Atlantoaxial joint instability (C1/2) due to chronic inflammation
Cervical subluxation causes neck pain, stiffness and radicular pain (radiating numbness/tingling associated with spinal nerves) that can lead to cervical myelopathy (pinch spinal cord)

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14
Q

What is the significance of extraarticular manifestations in RA?

A

Marker of disease severity (associated with increased morbidity and premature mortality)
Pts more likely to see this: hx of smoking, early onset of physical disability, test + for serum RF

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15
Q

Where can you see extraarticular manifestations in RA?

A

Skin (subcutaneous nodules), eye, pulmonary, cardiovascular (CAD), MSK, hematologic (anemia), CNS (aseptic meningitis)

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16
Q

Felty syndrome

A

Triad of RA, splenomegaly and neutropenia

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17
Q

What is seen in radiography for RA?

A

Preferred INITIAL imaging study

Soft tissue swelling around joint, periarticular osteopenia, joint space narrowing, bony erosions, subluxation

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18
Q

What is the use of MRI and US in RA?

A

More sensitive at detecting changes resulting from synovitis

MRI is valuable for assessing cervical spine

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19
Q

What lab studies do you do for RA?

A

RF, anti-cyclic citrullinated peptide antibodies, ANA (30%), CBC, ESR/CRP, synovial fluid analysis

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20
Q

What is RF?

A

First autoantibody associated with RA
Seen in 75-80% of RA pts (some point in disease)
Moderate specificity
Prognostic value

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21
Q

What are anti-CCP antibodies?

A

Autoantibody most specific for RA
Present in 60-70% pts
Specificity for RA is high
Correlate strongly with erosive disease

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22
Q

CBC in RA

A

See anemia of any chronic disease, thrombocytosis or mild leukocytosis (indicative of an inflammatory process)

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23
Q

Why would ESR/CRP be elevated in RA?

A

Parallels the activity of the disease so it would be high in an active flare

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24
Q

Why is an arthrocentesis used in RA?

A

Diagnosis of exclusion of gout, psuedogout or infection

Synovial fluid analysis can reveal an inflammatory effusion

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25
Who should be tested for RA?
People who have at least 1 joint with definite clinical synovitis and they have synovitis that is not better explained by another disease
26
What is seronegative RA?
When people lack both RF and anti-CCP antibodies Can be diagnosed upon findings characteristic of RA if everything else is excluded Refer to rheum
27
Main goals of RA tx
Early DMARDs, treat-to-target strategy to get remission of low disease activity, prevent joint injury, maintain muscle strength and joint mobility
28
Most important non-pharmacoloigc tx or RA
Smoking cessation
29
Pharmacologic tx of RA
Antiinflammatory agents to control pain and inflammation used in conjunction with DMARDs (disease modifying antirheumatic drugs)
30
What are DMARDs?
Slow/halt disease progression to preserve joint function | Start early
31
What is the pretreatment evaluation for before you can use DMARDs?
Baseline serology (CBC, creatinine, ESR/CRP, hep b or c) Ophthalmologic screening for hydroxychloroquine use TB test Vaccines
32
Types of DMARDs
Nonbiologic (methotrexate) | Biologic (TNF inhibitors etc)
33
Prevalence of osteoarthritis
Increases over 50 | More women over 55
34
Primary sx of OA
Joint pain and functional impairment
35
Most common joints involved in OA
Knees, hips, DIP/PIP/1st CMC joint, spine (cervical/lumbar), 1st MTP joints
36
Pathogenesis of OA
Involves all the joint tissues (cartilage, bone, ligaments, synovium) due to many factors
37
What happens to the joint in OA?
Progressive loss and destruction of cartilage (joint space narrows) Bony changes to joint: thinking of subchondral bone (bone sclerosis), subchondral cysts, osteophytes (bone spurs) Synovial inflammation May see soft tissue components affected
38
What is pathognomonic of OA?
Osteophytes (bone spurs)
39
Factors thought to lead to OA
Aging, joint injury, obesity, genetics, anatomic factors, females
40
Clinical presentation of OA
Joint pain worse with use and relieved by rest Stiffness is worse after effort (so seen in evening) If there is morning stiffness, it is less than 30 min
41
Physical findings of OA
TTP, reduced ROM, bony enlargement/swelling, joint deformity, joint instability
42
What do the hands look like in OA?
Bilateral Heberdens and Bouchards nodes (classic) First carpometacarpal joint is squared off
43
What do the knees and hips look like in OA?
Knees: bilateral, swelling, joint line tenderness, crepitus, limited ROM Hips: unilateral, restricted internal ROM, pain around hip/groin, may refer to knee (if you see hip problems on an xray that is advanced disease)
44
What is seen on an Xray in OA?
Joint space narrowing, osteophyte fomration, subchondral sclerosis, subchondral cysts
45
Pharmacologic tx of OA
Oral and topical NSAIDs used most Topical capsaicin Cymbalta (Duloxetine)- SSRI and NE inhibitors And others
46
When do you do surgery for OA?
When they have failed the less invasive modes of therapy
47
Main presentation of polymyalgia rheumatica
Proximal aching and stiffness (pelvic girdle, shoulder and neck) Worse in the morning over an hour because inflammatory
48
Prevalence of PMR
Mostly over 50 Peak between 70 and 80 Females Northern European descent
49
What is PMR associated with?
Giant cell (temporal) arteritis
50
What causes the sxs of PMR?
Nonerosive synovitis and tenosynovitis
51
Clinical presentation of PMR
Recent, discrete change in sx Bilateral Shoulder and pelvic girdle pain Morning stiffness and gel phenomenon (stiffness with inactivity)
52
What is seen on the physical exam with PMR?
Limited ROM (common to see limitation of active abduction) Normal strength but subjective weakness Synovitis
53
Diagnositc studies in PMR
Elevated ESR and/or CRP (ESR often over 50 mm/hr) May see normocytic anemia Normal and negative for other tests/antibodies
54
When is there the most rapid resolution of PMR?
With low dose glucocorticoids (10-20 mg/day)
55
What is fibromyalgia?
Chronic widespread musculoskeletal pain and tenderness often with fatigue, cognitive disturbances etc More in women (20-50) Often occurs with RA and SLE
56
Pathophysiology of fibromyalgis
Central pain processing (heightened/altered sensation of pain) Strong genetic predisposition
57
Clinical presentation of fibromyalgia
Widespread MSK pain Fatigue and poor sleep Cognitive disturbances (fibro fog) Psychiatric disturbances
58
Other sxs/disorders seen in fibromyalgis
Headache, pelvic pain, IBS, interstitial cystitis/painful bladder syndrome, obstructive sleep apnea, restless legs syndrome
59
History seen with fibromyalgia
Widespread MSK pain and tenderness (muscles and joints) for over 3 months Achiness
60
What abnormalities are seen in labs with fibromyalgia?
None
61
Pharmacologic tx of fibromyalgia
Tricyclic antidepressants (amitriptyline) Serotonin and NE reuptake inhibitors (SNRIs) like Cymbalta or Savella Anticonvulsants (Lyrics or Neurontin) NO OPIOID NARCOTICS