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Block 6 - MSK > Patho-4-OA > Flashcards

Patho-4-OA Flashcards

1
Q

What 5 changes would you expect to find in an osteoarthrtic synovial joint?

A
  1. irregular thickening & remodelling of sub-chondral bone with sclerosis & cysts
  2. thickening, distortion & fibrosis of capsule
  3. fibrillation, loss of volume & degradation of articular cartilage
  4. modest, patchy, chronic synovitis
  5. osteophytes & soft tissue growth at joint margin
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2
Q

T/F Most people >75 have OA changes in at least 1 joint

A

True

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3
Q

T/F: OA is more common in men than women

A

False

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4
Q

T/F Obesity does not correlate with OA

A

false - correlates best with knee OA

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5
Q

T/F OA is commonest form of arthritis

A

True

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6
Q

Prevalence of radiographic OA in men & women wrt joints commonly affected

A

Men - DIP > kneee - eak around 70

Women - DIP > knee > hip - peak around 70

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7
Q

Risk factors for OA

A
  • trauma
  • inflammatory arthritis, crystal arthropahy
  • metabolic D/O (haemochromatosis, ochronosis)
  • endocrine D/O (acromegaly)
  • other bone & joint D/O (congential hip dysplasias, slipped capital femoral epiphyses, Paget’s, AVN)

Susceptibility - body bulid, hereditary, reproductive variables, osteoporosis, hypermobility, smoking, other diseases

Mechanical factors - trauma, joint shape, repetitive use (occupational, leisure)

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8
Q

What is OA?

A
  • OA results from articular cartilage failure - complex interplay between genetics, metabolic, biochemical, biomechanical factors with secondary inflammation
  • process - mismatched interaction between degradation & repair processes of cartilage, bone & synovium
  • initiation process involves abnormalities in biomechanical forces &/or less often in cartilage
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9
Q

What is the hallmark feature of OA?

A

Degradation and loss of articular cartilage, with synovial inflammation

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10
Q

What cells are considered the most important for development of OA?

A

chondrocytes

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11
Q

Pathology of OA

A
  • cartilage irregularity (fibrillation, clefts) –> ulceration of cartilage surface –> frank/rapid cartilage loss
  • biochemically - reduced glycosaminoglycan content, increased water & increased MMP activity
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12
Q

Discuss early pathogenesis of OA

A

chrondrocytes exhibit transient proliferative response undergoing cloncal growth –> production of cytokines (TNF-alpha, IL1), growth factors, matrix-degrading enzymes

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13
Q

Major collagen type involved?

A

2

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14
Q

Discuss later pathogenesis of OA

A

initiating event attributed to mechanical stress –> altered chondrocyte metabolism & production of proteolytic enzymes & disruption of matrix properties

  • first pathologic event may be multiple microfractures
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15
Q

What is arachindonic acid (AA)?

A

Omega 6 fatty acid precursor of pro-inflammatory prostaglandins and leukotrienes

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16
Q

What is the relationship between AA and OA?

A

Availability of AA for production of inflammatory eicosanoids could be a predisposing factor for synovitis

17
Q

Why are omega 3 fats important?

A
  • EPA and DHA are homologues of AA
  • Makes for competitive inhibition of AA metabolism thus reducing inflammation, pain and synovitis
18
Q

What joints is OA commonly found in?

A
  • DIP
  • PIP
  • 1st CMC
  • C & L spine
  • 1st MTP of feet
  • knee
  • hip
19
Q

Generalised OA?

A

3 or more joint groups involved/considered

20
Q

What is generalised OA commonly associated with?

A

Herberden’s & Bouchard’s nodes

21
Q

What joints are considered atypical for OA?

A
  • MCPs
  • wrist
  • elbows
  • shoulders
  • ankles
22
Q

Distribution of OA of hip joints x3

A
  • Superolateral - most common (60%; M > F)
  • Medial pole (25%, F > M)
  • Concentric (15%, F > M)
23
Q

Clinical Symptoms of OA

A
  • Morning stiffness (Common <30mins)
  • Worse in cold weather
  • Insidious onset of pain (improves with rest or nocturnal pain in severe disease)
  • Instability or buckling of joint (knee)
  • growin pain, giat problems (hip)
  • Problems with manual dexterity (CMC)
  • nerve problems in lower C & L spine facet joints (osteophytes can narrow foramen & compress nerve roots)
24
Q

Examination signs of OA

A
  • Bony enlargement and bony tenderness at joints
  • Jt instability
  • Limited ROM
  • Locking
  • Crepitus
  • Malalignment
  • Pain in motion
  • Joint effusion
  • signs of inflammation in IP jts of hands with erosive OA
25
Q

Radiographic features of OA

A

X-ray: - clinical dx confirmation

  • osteophytes at margin
  • assymetric jt space narrowing
  • subchondral bone sclerosis
  • subchondral cysts

Erosive OA - central erosions & cortical collapse in DIPs +/- PIPs of hands

26
Q

Filli in this table

A
27
Q

Goals of therapy for pts with OA

A
  • control pain & sweling
  • minimise disability
  • improve QoL
  • education on disease management
28
Q

Examples of Non-pharm management

A
  • Education
  • Physio
  • OT
  • Social support
  • Exercise
29
Q

Examples of Pharm management

A
  • Topical - capsaicin
  • Oral - non-opioid analgesics (paracetamol, tramadol), NSAIDs/COX2 inhibitors, opiods, glucosamine & chrondoitin, fish oil
  • Systemic
  • Intra-articular (Corticosteroids)
30
Q

Using a table discuss clinical difference between RA and OA in terms of primary joints affected, Heberden’s nodes, joint characteristics, stiffness, lab findings

A

Block 6 - MSK (5 decks)

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