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MSK II Exam 2 > Lanigan Osteoarthritis > Flashcards

Lanigan Osteoarthritis Flashcards

1
Q

Epidemiology

A

Osteoarthritis is the most common type of joint disease.
It affects >30 million patients in the U.S.
Leading cause of chronic disability.

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2
Q

Osteoarthritis

A 
Most common arthropathy
Primary pathology involves cartilage, subchondral bone, and synovium
Non-inflammatory joint fluid
Involves active cytokines
Multifactorial etiology
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3
Q

OA – Multifactorial etiology

A

Progressive deterioration & loss of articular cartilage, leading to loss of normal joint structure & function.

Primary

  • Aging or Idiopathic
  • Hands: DIP, PIP, first CMP.

Secondary
Due to disorders that damage articular cartilage, subchondral bone, or synovium

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4
Q

Causes of OA

“VINDICATE”

A

Vascular
- Sickle cell, thalassemia, avascular necrosis

Infectious/Inflammatory/Infiltrative
- Staphylococcus, sarcoid, hemophilia

Neoplastic/Neuromuscular
- Acromegaly, muscle weakness, diabetic/Charcot joint

Degenerative/Deficiency
- Menopause

Idiopathic

Congenital
- Developmental hip dysplasia, slipped capital femoral epiphysis, genetic

Autoimmune
- Rheumatoid arthritis

Traumatic
- Repetitive squatting, stairs, surgery

Endocrine/metabolic
- Obesity, gout, pseudogout, hemochromatosis

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5
Q

Osteoarthritis is thought to be a(n):

A – Noninflammatory process
B – Inflammatory process
C – Neurodegenerative process

A

noninflammatory

some cytokines going on but only local

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6
Q

Pathology

A 
Altered chondrocyte function
Loss/thinning of cartilage
Subchondral bone thickening/sclerosis
Bone remodeling
Osteophytes
Cystic changes in subchondral bone
Mild reactive synovitis
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7
Q

Early osteoarthritis:

A

External events & forces alter the synovium, articular cartilage, and/or subchondral bone.
IL-17 and metalloproteases are released into joint.
→ Synovial cell stimulation to repair cartilage.
↑ synthesis of proteoglycans.
This leads to cartilage swelling (mediated by IL-1).
This stage may last for years or decades, with hypertrophic repair of the articular cartilage.

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8
Q

later pathophysiology

A

Eventually proteoglycans become exhausted.
Cartilage softens & loses elasticity.
Microscopic flaking and fibrillations (vertical clefts) develop along the normally smooth articular cartilage on the joint surface.

Loss of cartilage leads to narrowed joint spaces & further trauma from adjoining bone, with more destruction in high load areas. Eventually underlying bone is exposed.

Subchondral bone responds with vascular invasion and cell proliferation, becoming thickened and dense (aka eburnation) at areas of pressure.

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9
Q

Eburnation

A

A change in exposed subchondral bone in degenerative joint disease in which it is converted into a dense substance with a smooth surface like ivory.
Synonym: bone sclerosis

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10
Q

Vascularization with osseous metaplasia eventually produces

A

ossifying cartilagenous protrusions referred to as spurs or osteophytes.

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11
Q

osteoarthritic cysts (subchondral cysts)- where do they come from?

A

Chronic impaction with osseous necrosis or intrusion of synovial fluid leads to osteoarthritic cysts (subchondral cysts).

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12
Q

Which of the following is a joint commonly affected by osteoarthritis?

A – Elbow
B – Sacroiliac
C – Distal interphylangeal (DIP)
D – Metacarpophylangeal (MCP)

A

DIP

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13
Q

Osteoarthritis presentations

A 
Common:
Cervical spine
Lumbar spine
1st CMC
PIP
DIP
Hip
Knee
1st MTP
Uncommon:
Shoulder
Thoracic spine
Elbow
Wrist
MCP
Ankle
Subtalar
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14
Q

Symptoms of OA

A

Insidious onset
Deep, achy joint pain associated with movement
Minimal stiffness – usually lasting <30 minutes

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15
Q

Physical Exam Signs of OA

A 
Limited ROM
Crepitus
Joint line tenderness
Cool effusions
Spasm or atrophy of adjacent muscles
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16
Q

Diagnostic Tests

A 
No specific diagnostic tests
Synovial fluid:  class 1 (non-inflammatory) – clear, yellow, WBC < 2000, <25% neutrophils
X-rays
- Cartilage loss/joint space narrowing
- Osteophytes at joint margins
- Subchondral sclerosis
- Subchondral cysts
17
Q

Subsets of OA

A 
Nodal osteoarthritis – hands
Erosive (inflammatory) osteoarthritis
Primary osteoarthritis
Secondary osteoarthritis – knees, hip, spine
Patellofemoral arthritis
Spondylosis
18
Q

What type of OA?

52-year-old man with hemachromatosis and joint pain

A

Secondary osteoarthritis

19
Q

What type of OA?

52-year-old women with acute onset of pain in several DIP and PIP joints

A

Erosive osteoarthritis

20
Q

What type of OA?

70-year-old man with gradual development of DIP and PIP pain & swelling

A

Nodal osteoarthritis

21
Q

Heberden’s vs Bouchard’s

A

DIP- heberden’s

PIP- Bouchard’s

22
Q

Hand (Nodal) Osteoarthritis

A

Heberden’s Nodes: DIP
Bouchard’s Nodes: PIP
1st CMC Joint: base of thumb

23
Q

Erosive Osteoarthritis

A

A subset of hand osteoarthritis

  • Affects 5-15% of pts. with hand OA
  • Heberden’s & Bouchard’s nodes may be seen

Acute onset of pain

Greater amount of inflammation than OA

Presence of erosions on x-ray

Subluxations, flexion contractures, ankylosis may also be seen

Most common in postmenopausal women
- Typical onset age 50-55

Feet may be affected also

24
Q

Erosive Osteoarthritis

Diagnosis

A

OA of hands.
Subchondral erosions in at least 2 IP joints, with 1 a DIP.
Negative RF, anti-CCP, ESR, CRP.
No psoriasis, gout, or pseudogout.

*Essential for diagnosis.

25
Q

Erosive Osteoarthritis

players

A 
Inflammatory cytokines (may be related to obesity):  
↑ IL-2, IL-4 receptors, adiponectin;

↓ IL-4, IL-1, TNF-α.

26
Q

Primary OA

A

Idiopathic / “wear and tear” OA
May be related to aging, obesity, and/or hx of significant but non-injurious joint use
May be local (a few joints) or generalized
Develops around age 55

Knees
- Most common location
Hips
Hands
Spine
- Cervical, thoracic, lumbar, spinal canal stenosis
Feet - 1st MTP
27
Q

Secondary OA

A

Joint degeneration in a joint with preexisting abnormality.

Due to trauma, genetics, inactivity, congenital anomalies, inflammatory/infectious arthritis, hemachromatosis, etc.
- Osteoarthritis susceptibility genes: ADAM12, CLIP, COL11A2, IL10, MMP3, MCF2L, others…

Develops earlier than primary OA, around age 45.

28
Q

OA and trauma

A

Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.

29
Q

Patellofemoral arthritis

A

Isolated patellofemoral arthritis may cause anterior knee pain that worsens with climbing stairs or rising from a seated position. As it worsens, it interferes with walking and running.

~5% of pts. with OA of the knee have patellofemoral arthritis without tibiofemoral arthritis. The etiology of knee arthritis is divided equally between patellar dislocation, fracture, and primary osteoarthritis.

M (closest distance between articular ridge & medial condyle)
L (closest distance between lateral facet & condyle)
On exam, compress patella as pt. flexes the knee. Pain is elicited if arthritis is present. Resisted knee extension may also reproduce symptoms.

30
Q

Spondylosis Arthritis

A

The degeneration in spine osteoarthritis affects vertebral bodies, neural foramina and facet joints.
This is spondylosis (ie, age-related degeneration) & is asymptomatic.

In degenerative spondylolisthesis, intersegmental instability is present as a result of spondylosis. The slip occurs from progressive spondylosis within this three-joint motion complex.

Most commonly occurs at L4-5 interspace.

31
Q

Management of OA

A 
Education
Heat and cold
Weight reduction
Conditioning
Proper footwear / Orthotics
Physical Therapy
Occupational Therapy
Topical Agents 
- capsaicin, diclofenac
Acetaminophen
NSAIDs
Intra-articular steroids
Tramadol
Duloxetine (Cymbalta)
Viscosupplementation hyaluronic acid (?)
Surgery
Hydroxychloroquine (esp. in erosive OA)
Colchicine
32
Q

Lumber spinal stenosis from facet joint osteoarthritis

A

> age 70
Neurogenic claudication – worse with prolonged standing or walking, relieved by sitting or lumbar flexion
Radicular pain – one or both buttocks or legs

33
Q

Diffuse Idiopathic Skeletal Hyperostosis

A

(DISH/Forestier’s disease)

M > F. Incidence increases with age.

“Flowing osteophytes” in ≥ 4 contiguous vertebrae. (can also see Candle Wax Pattern)

Ossification of anterior longitudinal ligament.
- Posterior longitudinal ligament occasionally involved.

Preservation of joint and disc spaces.

No systemic inflammation.

Usually asymptomatic. Symptomatic pts. may have pain, stiffness, dysphagia.

Associated with Type 2 DM, obesity, hyperuricemia.

34
Q

Patients with obesity or Type 2 diabetes have hyperinsulinemia following glucose challenge…

A

It is hypothesized that insulin at prolonged and high physiologic levels promotes new bone growth in the entheseal regions.

35
Q

IGF-1 causes

A

differentiation of progenitor cells into osteoblasts, with resultant ossification of ligaments and entheseal areas.

36
Q

Cervical Involvement in DISH

A

Anterior ligament ossification - may cause dysphagia

Rare posterior ligament ossification – potential for cord compression

37
Q

Osteophyte vs. Syndesmophyte

A

DISH - clear space between ossified ligament and vertebral body.

Ankylosing spondylitis has involvement of SI joints & syndesmophytes. Syndesmophytes bridge across the joint as compared to osteophytes which are non-bridging.

38
Q

Characteristic of DISH

A

Ligementous Calcification at Entheses are Characteristic of DISH

Ligamentous calcification of iliolumbar, sacrotuberous, & acetabular ligaments suggests DISH.

Isolated bony spurs in the calcaneum, patella, & olecranon, especially if symmetric, can lead to early diagnosis of DISH.

may see whiskering calcifications

MSK II Exam 2 (16 decks)

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