Twenty Seven

Question 1

What is osteoarthritis? Where does it affect? Risk factors?

Answer 1

Progressive degenerative disorder that affects joints of the hands, spine and weight-bearing joints
D. Affects a limited numbe r of joints (oligoarticular); hips, lower lumbar spine, knees,
and the distal interphalangeal joints (DIP) and proximal int^rphalangeal joints (PIP)
of fingers are commo n sites.

Most common articular disorder

Accounts for more disability among elderly than any other disease

No systemic symptoms; inflammation when present, is mild

Risk Factors: obesity, heredity, age, previous joint trauma, smoking, certain occupations

Question 2

What are some clinical features of OA? Lab findings?

Answer 2

Clinical:

AM stiffness < 30 min
Gel phenomenon (stiffness after rest)

Joint pain and tenderness, worse with activity, better with rest

Crepitus

Bony swelling-Heberden’s nodes/Bouchard’s nodes

Functional impairment

Periarticular muscle atrophy

Lab:

Noninflammatory synovial fluid, high viscosity, clear and yellow, wbc <1-2k

Question 3

What will be seen on radiographs?

Answer 3

A. Radiographs:

 Osteophytes

Nonuniform joint space narrowing

Subchondral cysts, sclerosis and erosions

malalignment

Question 4

What is the pathology/pathogenesis?

Answer 4

F. Pathologic features include
1 . Disruption of the cartilage that lines the articular surface (Fig. 18.7); fragments of cartilage floating in the joint space are called ‘joint mice. ‘
2. Eburnatio n (polishing) of the subchondral bone
3 . Osteophyte formation (reactive bony outgrowths) ; classically arises in the DIP (Heberden nodes) and PIP (Bouchard nodes) joints of the lingers
4. Synovial fluid forced into underlying bonecysts

Question 5

How is OA treated?

Answer 5

No medication has been shown to stop or reverse the disease process

Alleviate symptoms, increase function

NSAIDs, ASA, acetaminophen

Glucosamine chondroitin

Viscosupplementation

Joint replacement surgery

PT for MS, ROM, medial unloader brace, assistive devices

Topical capsaicin, diclofenace patches, lidocaine patches

Narcotics, steroid injections

Weight reduction, exercise

Question 6

What is RA? Epidemiology? What HLA is it associated with? What is the pathophys?

Answer 6

A. Chronic, systemic autoimmune disease
1 . Classically arises in women of late childhearing age
2. Associated with HLA-DR4

B. Characterized by involvement of joints
L Hallmark is synovitis leading to formatio n of a pannus (inflamed granulation tissue).
2. Leads to destruction of cartilage and ankylosis (fusion) of the joint, osteoporosis near joint, deviations/malalignment of the joint (myofibrils in granulation tissue pull the bone a different direction.

Question 7

What are the joint clinical features of RA? Which joints? What is seen on xray?

Answer 7

C. Clinical features
1 . Arthritis with morning stiffness that improves with activity.
i. Symmetri c involvement of PIP joints of the fingers (swan-neck deformity), wrists (ulnar deviation), elbows, ankles, and knees is characteristic (Fig.
18.8); DIP is usually spared (unlike osteoarthritis).
Claw toe, or hammer toe deformity
Flattening of the arch
Hind foot valgus deformity

ii. Joint-space narrowing, loss of cartilage, and osteopenia are seen on X0ray.
Abnormal alignment

Periarticular osteoporosis

Symmetric (uniform) joint space narrowing

Deformities

Marginal erosions

Soft tissue swelling

Synovial enhancement or tenosynovitis on MRI or US

Question 8

What non-joint clinical features are seen in RA?

Answer 8

2. Fever, malaise, weight loss, and myalgias
   3 . Rheumatoi d nodules—central zone of necrosis surrounde d by epithelioid histiocytes; arise in skin and visceral organs
3. Vasculitis—Multiple organs may be involved.
   5 . Baker cyst—swelling of bursa behind the kne e
   ti. Pleura! effusions, lymphadenopathy, and interstitial lung fibrosis

Question 9

What lab findings are there in RA? What are some systemic complications?

Answer 9

1 . IgM autoantibody against Fc portion oflg G (rheumatoid factor} ; marker of tissue damage and disease activity
2. Neutrophils and high protein in synovial fluid
E. Complications include anemia of chronic disease and secondary amyloidosis.

Normochromic, normocytic anemia 
Positive RF (80-90%)
Anti-CCP Ab (70%) 
Elevated ESR and CRP 
25% have +ANA 
Normal urinalysis 
Normal renal, hepatic, and metabolic functions

Question 10

How is RA treated?

Answer 10

NSAIDs

Corticosteroids-oral or intraarticular

Disease Modifying Anti-rheumatic Drugs (DMARDS)

Biologic agents

New class of therapies of cytokine blockade that have drastically changed outcomes and morbidity of RA

Anti-TNFs: etanercept, adalimumab, infliximab, certolizumab, golimumab

Anti-IL1: anakinra

Anti-IL6: tocilizumab

Anti-CD 20: rituximab

CTLA-4 modulator(inhibits costimulation of T-cells): abatacept

JAK kinase inhibitor-tofacitinib