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Psychology- MHD > Clinical Approach- Joint Pain I > Flashcards

Clinical Approach- Joint Pain I Flashcards

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1
Q

What type of disease process is osteoarthritis?

A

Degenerative-

It is characterized by degeneration of articular cartilege

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2
Q

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

A

Biomechanical

Biologic stresses

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3
Q

In what joints do we most commonly see symptomatic osteoarthritis?

A

Knee

Hip

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4
Q

What is the strongest risk factor for developing osteoarthritis?

A

Age

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5
Q

List the four components of the specialized connective tissue of joints

A

collagen, proteoglycans, water, chondrocytes

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6
Q

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

A

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

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7
Q

What is the role of proteoglycans in the joints?

A

High negative charge –> retention of water

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8
Q

What is the role of chondrocytes in joints?

A

Mediate turnover of matrix components

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9
Q

Describe the growth patterns of chondrocytes in osteoarthritis

A

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

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10
Q

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

A

It increases –> cartilage swelling

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11
Q

What imbalance leads to cartilage destruction?

A

Increase in catabolic&raquo_space; anabolic activity

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12
Q

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

A

After weight bearing activity

Better with rest

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13
Q

Describe the changes in the joints themselves in someone with osteoarthritis

A

Bony enlargements
Joint crepitus

Swelling is NOT common

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14
Q

How do x-ray findings correlate to pain?

A

They don’t necessarily

xray findings may not be proportionate to pain

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15
Q

What are some useful labs to order for osteoarthritis?

A

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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16
Q

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

A

loss of joint space

also spurs/osteophytes

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17
Q

What is the general management strategy for OA?

A

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

NSAIDS for pain

Surgery as a last resort (joint replacement)

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18
Q

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

A 
Lungs
Anemia of chronic disease
Eyes
Skin
Heart 
CNS/peripheral neuropathy
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19
Q

What is the genetic risk factor for RA

A

HLA-DRB-1

Class II MHC

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20
Q

What antibody is looked for when diagnosing RA?

A

anti-CCP

Cyclic citrullinated peptide

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21
Q

What habit is associated with RA?

A

Smoking

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22
Q

Differentiate morning stiffness in RA vs OA

A

RA: prolonged morning stiffness
OA: no morning stiffness

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23
Q

Compare joints of the hand involved RA vs OA

A

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

24
Q

Compre lumbar spine involvement in RA vs OA

A

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

25
Q

Compare areas of joint involvement in RA vs OA

A

RA: more on the edges- inflammation comes from the synovium

OA: Distributed throughout

26
Q

Which inflammatory cells are activated in RA?

A

CD4+ helper T cells

27
Q

What are the top three upregulated cytokines in RA?

A

IL1, IL6, TNFalpha

28
Q

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

A

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

29
Q

Can bone destruction be reversed in RA?

A

No- goal is to prevent destruction in the first place

30
Q

What is the initiating factor in pannus formation?

A

Chronic papillary synovitis

31
Q

What causes thickening of the synovium?

A

Synovial cell hyperplasia and proliferation

32
Q

What causes the synovium to become dense?

A

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

33
Q

Is the synovium usually vascular?

A

No - angiogenesis occurs in RA and the synovium becomes vascularized

34
Q

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

A

Neutrophils and organizing fibrin on the synovial surface –> layering

35
Q

What causes erosion of the bone at the synovium?

A

Osteoclast activation

36
Q

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

A

4+

Polyarticular

37
Q

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

A

Rheumatoid factor: auto-antibody against Fc portion of normal polyclonal IgG

Highest levels are IgM

38
Q

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

A

High inflammatory cells, low glucose

Other nonspecific changes

39
Q

Describe the histology of a rheumatoid nodule

A

area of fibrinoid necrosis surrounding by palisading histiocytes

40
Q

What is the mainstay long-term treatment for RA?

A

DMARDS- disease modifying anti-rheumatic drugs

They are mostly immunosuppressive

41
Q

Name two non-biologic DMARDS

A

Methotrexate — most commonly used, replaces steroids

Leflunomide

42
Q

Anti-inflammatories against which cytokines are the most effective?

A

TNF-alpha

Also IL1 and iL6

43
Q

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

A

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

44
Q

Compare pattern of joint involvement between RA and spondyloarthropathy

A

RA: Not much lower back involvement, polyarthropathy

Spondyloarthropathy: Involves lower back, oligoarticular (<3), asymmetric, more large joints are involved. More axial involvement

45
Q

What is enthesitis?

A

Inflammation where tendon inserts into the joint - seen in spondyloarthropathy

46
Q

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

A

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

47
Q

Which is the gene marker for increased risk with spondyloarthropathy?

A

HLA-B27 (MHC Class I)

48
Q

What is the age of onset for spondyloarthropathies?

A

16-30

49
Q

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

A

Molecular mimicry theory

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

50
Q

Which are the key cytokines upregulated in spondyloarthropathy?

A

IL17, IL23

TH17 cells

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

51
Q

What is the initial step in the pathogenesis of ankylosis?

A

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

52
Q

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

A

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

53
Q

What are syndesmophytes?

A

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

54
Q

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

A

INflammatory back/buttock pain

Chest wall pain
Dactylitis (involvement of whole finger)
Extra-articular involvement (uveitis)
Sacroiliitis

55
Q

What are treatments unique for spondyloarthropathies?

A

+ anti IL-23/IL12

Also anti TNF alpha are useful

Psychology- MHD (14 decks)

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