Clinical Approach- Joint Pain I Flashcards by Allison Zarnke

What type of disease process is osteoarthritis?

Degenerative-

It is characterized by degeneration of articular cartilege

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In osteoarthritis, chondrocytes of articular cartilage respond to which two types of stress?

Biomechanical

Biologic stresses

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In what joints do we most commonly see symptomatic osteoarthritis?

Knee

Hip

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What is the strongest risk factor for developing osteoarthritis?

Age

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List the four components of the specialized connective tissue of joints

collagen, proteoglycans, water, chondrocytes

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What is the role of collagen (type II) in the joints?

Distributes compressive forces
Tethers cartilage to subchondral bone
Dissipates weight bearing force, protects soft tissue and subchondral bone

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What is the role of proteoglycans in the joints?

High negative charge –> retention of water

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What is the role of chondrocytes in joints?

Mediate turnover of matrix components

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Describe the growth patterns of chondrocytes in osteoarthritis

Chondrocytes, which are normally isolated cells, now proliferate and cluster

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What happens to the water content of joints early in the process of osteoarthritis?

It increases –> cartilage swelling

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What imbalance leads to cartilage destruction?

Increase in catabolic&raquo_space; anabolic activity

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Is the pain in osteoarthritis worse following weight bearing activity or after rest?

After weight bearing activity

Better with rest

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Describe the changes in the joints themselves in someone with osteoarthritis

Bony enlargements
Joint crepitus

Swelling is NOT common

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How do x-ray findings correlate to pain?

They don’t necessarily

xray findings may not be proportionate to pain

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What are some useful labs to order for osteoarthritis?

There are none. Xrays and physical exam help you the most

OA is not an inflammatory process, so there aren’t really good biologic markers to measures

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What is the most prominent finding on x-ray of a joint with OA?

loss of joint space

also spurs/osteophytes

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What is the general management strategy for OA?

Manage risk factors- physical therapy, exercise, weight loss, dietary measures…

NSAIDS for pain

Surgery as a last resort (joint replacement)

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Other than joints, what other organs can be affected by rheumatoid arthritis?

Lungs
Anemia of chronic disease
Eyes
Skin
Heart 
CNS/peripheral neuropathy

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What is the genetic risk factor for RA

HLA-DRB-1

Class II MHC

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What antibody is looked for when diagnosing RA?

anti-CCP

Cyclic citrullinated peptide

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What habit is associated with RA?

Smoking

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Differentiate morning stiffness in RA vs OA

RA: prolonged morning stiffness
OA: no morning stiffness

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Compare joints of the hand involved RA vs OA

RA: PIPs, MCPs, wrists
OA: DIPs, PIPs, CMCs

Compre lumbar spine involvement in RA vs OA

RA: Lumbar spine not involved
OA: Lumbar spine commonly involved

Compare areas of joint involvement in RA vs OA

RA: more on the edges- inflammation comes from the synovium OA: Distributed throughout

Which inflammatory cells are activated in RA?

CD4+ helper T cells

What are the top three upregulated cytokines in RA?

IL1, IL6, TNFalpha

What activation process leads to ultimate destruction of the bone in the joints in RA?

Increased expression of RANKL (by cytokines) --> increased osteoclast activation --> breakdown/erosion of bone

Can bone destruction be reversed in RA?

No- goal is to prevent destruction in the first place

What is the initiating factor in pannus formation?

Chronic papillary synovitis

What causes thickening of the synovium?

Synovial cell hyperplasia and proliferation

What causes the synovium to become dense?

Inflammatory cell infiltrates (CD4+ cells, plasma cells, macrophages)

Is the synovium usually vascular?

No - angiogenesis occurs in RA and the synovium becomes vascularized

Describe the layering that occurs in the synovium during the formation of a pannus

Neutrophils and organizing fibrin on the synovial surface --> layering

What causes erosion of the bone at the synovium?

Osteoclast activation

How many joints need to be involved for the diagnosis of RA?

4+ Polyarticular

What factor do we look for in the blood in someone with RA?

Rheumatoid factor: auto-antibody against Fc portion of normal polyclonal IgG Highest levels are IgM

What lab change do we see in the synovial fluid of someone with RA?

High inflammatory cells, low glucose Other nonspecific changes

Describe the histology of a rheumatoid nodule

area of fibrinoid necrosis surrounding by palisading histiocytes

What is the mainstay long-term treatment for RA?

DMARDS- disease modifying anti-rheumatic drugs They are mostly immunosuppressive

Name two non-biologic DMARDS

Methotrexate --- most commonly used, replaces steroids | Leflunomide

Anti-inflammatories against which cytokines are the most effective?

TNF-alpha Also IL1 and iL6

Compare OA vs spondyloarthropathy in terms of pain being relieved by rest

OA: improves with rest, worse with exercise Spondyloarthropathy: does not improve with rest because it is an inflammatory process. Does improve with exercise

Compare pattern of joint involvement between RA and spondyloarthropathy

RA: Not much lower back involvement, polyarthropathy Spondyloarthropathy: Involves lower back, oligoarticular (<3), asymmetric, more large joints are involved. More axial involvement

What is enthesitis?

Inflammation where tendon inserts into the joint - seen in spondyloarthropathy

Spondyloarthritis is a generic term that covers which four specific arthropathies?

Psoriatic arthritis Ankylosing spondylitis (spine fusion- bamboo spine) Inflammatory Bowel Disease related Reactive Arthritis (Formerly known as Reiter's Syndrome) (Can't see, can't pee, can't climb a tree) ...+ undifferentiated spondyloarthropathy

Which is the gene marker for increased risk with spondyloarthropathy?

HLA-B27 (MHC Class I)

What is the age of onset for spondyloarthropathies?

16-30

What is the relationship between infections with yersinia, shigella, salmonella, campylobacter and chlamydia and spondyloarthropathies?

Molecular mimicry theory Infection --> antibodies produced attack self-antigen (synovium, collagen etc) --> auto immunity

Which are the key cytokines upregulated in spondyloarthropathy?

IL17, IL23 TH17 cells IL23 --> increased Th17 cells --> increased IL17 --> increased pathways that leads to inflammation, cartilage damage and bone erosion

What is the initial step in the pathogenesis of ankylosis?

Granulation tissue erodes through the bone and cartilage into the joint cavity

Following inflammation, erosion, caritlage fusion etc., what is the final step that leads to ankylosis?

Osteoblast activity: leads to replacement of cartilage by bone --> fusion of bones

What are syndesmophytes?

sclerosis and squaring of vertebral corners --> bridging/ossification between vertebral discs

What are a few features of spondyloarthropathies that differentiate it from RA?

INflammatory back/buttock pain Chest wall pain Dactylitis (involvement of whole finger) Extra-articular involvement (uveitis) Sacroiliitis

What are treatments unique for spondyloarthropathies?

+ anti IL-23/IL12 | Also anti TNF alpha are useful