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MBBS II MSS > L03 - Introduction to Degenerative Joint Disorders > Flashcards

L03 - Introduction to Degenerative Joint Disorders Flashcards

1
Q

Define OA?

A

■ progressive loss of articular cartilage

■ accompanied by attempted repair of the cartilage, remodelling and sclerosis of subchondral bone, formation of subchondral bone cyst and marginal osteophytes

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2
Q

Epidemiology of OA?

A

common, age-related, heterogeneous

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3
Q

Why can’t articular cartilage fully repair?

A

Articular cartilage is avascular, aneural, alymphatic

Relies on diffusion for nutrients… etc

does not have the capacity to repair structural damage

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4
Q

What are the components of articular cartilage?

A

■ Chondrocytes
■ Water
■ Structural macromoleules:
– type II collagen (60 % of dry weight)
– Proteoglycans = protein core and one or more glycosaminoglycan (hyaluronic acid, chondroitin sulfate, keratan sulfate, dermatan sulfate) chains
– Non-collagenous proteins & glycoproteins

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5
Q

Describe the interaction between the matrix and the chondrocytes in articular cartilage?

A

– Matrix protects chondrocytes from mechanical damage … transduce and transmits signals with loading …

– Chondrocytes degrade and synthesize matrix macromolecules … synthesize and release cytokines

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6
Q

Compare the structural changes between normal aging articular cartilage and OA?

A 
Aging = stable structure 
OA = progressive structural changes
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7
Q

Compare between aging articular cartilage and OA: Water content?

A

Aging = Decrease water content

OA = Increase water content

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8
Q

Compare between aging articular cartilage and OA: collagen structure?

A

Aging = Increase cross-linking between collagen

OA = Change in arrangement & size of collagen fibres + progressive loss of proteoglycans

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9
Q

What are some causes of secondary OA?

A
  • Trauma - High-intensity-impact joint-loading**
  • Injury – ligament injury**
  • Infection – septic arthritis**
  • Hereditary – ochronosis
  • Endocrine – acromegaly, hypothyroidism
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10
Q

Which parts of the body is affected by primary OA?

A

Hips & Knee

Distal interphalangeal joints of hands

Many Synovial joints

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11
Q

What is found in the joints of the hands in primary OA?

A

Heberdon’s nodes in DIP

Bouchard’s nodes in PIP

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12
Q

List some synovial joints that are affected in primary OA?

A

Mainly:
Hip and knee + DIP, PIP in hand

Others:
• carpometacarpal joint of thumb 
• metatarsophalangeal joint of the great toe 
• facet joints of the spine 
• elbows 
• shoudlers
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13
Q

What causes OA?

A 
Systemic factors that predispose to OA
\+
Local mechanical factors that dictate its distribution and severity 
\+/-
Various genetic abnormalities 
= 
Joint damage
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14
Q

What are some systemic factors that predispose to OA?

A 
Old  
Female 
Low Bone density 
Hormonal status - e.g. postmenopausal 
Nutrition and metabolic factors
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15
Q

What are some Local mechanical factors that dictate the distribution and severity of OA?

A

– Joint deformity/malalignment
– Joint injury
– Muscle weakness
– Obesity

– Occupational factors
– Sports

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16
Q

What are the 2 types of lower limb misalignment?

A

Genu valgum = knock knee

Genu varum = bow leg

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17
Q

How do local mechanical factors affect the progression of OA?

A

Create uneven loading of the joints = exacerbate damage to joint = increase attempt to heal and worsening pathology

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18
Q

Compare the prevalence of OA hip in Chinese and White ethnicities?

A

– 43 / 100,000 in Whites
– 1.3 / 100,000 in Chinese population

OA hip was rare in Hong Kong Chinese age > 50

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19
Q

What is the EULAR guideline on clinical features of OA?

A

3 symptoms, 3 signs

– Persistent pain
– Limited morning stiffness
– Reduced function

– Crepitus*
– Restricted ROM
– Bony enlargement

20
Q

Describe the clinical feature of pain due to OA?

A

Triphasic pain: increase when starts to walk, decrease after a while, increase again with long walk

21
Q

What is the range of severity of OA pain?

A

Increasing severity:

• at rest • at night • need of pain killers • walking distance and walking aids • effect on daily activities, occupation, hobbies

22
Q

Describe the clinical feature of stiffness due to OA?

A
  • Gelling after waking up or prolonged immobility
  • Effect on daily activities (i.e. cannot put on socks, cut toe nails, squat)
  • Limited passive ROM in physical exam
23
Q

What causes crepitus in OA knee?

A

Grating, crackling or popping sounds and sensations experienced under the skin and joints

due to loss of articular cartilage that creates lots of friction

24
Q

Describe grade 0 to grade 4 of Articular cartilage damage in OA?

A

– Grade 0: Normal cartilage

– Grade I: cartilage becomes soft and swells

– Grade II: partial-thickness defect with fibrillation (shredded appearance) or fissures (depressions)

– Grade III: increased amount of damage to the level of subchondral bone

– Grade IV: exposed subchondral bone, “eburnation” ( bone in contact with joint surface = smooth marble-like appearance)

25
Q

What are the pathoanatomical features of OA?

A

■ Articular cartilage damage
■ Osteophyte formation
■ Subchondral sclerosis
■ Subcondral cysts

26
Q

Osteophyte formation causes pain in patients with OA knee and forms due to aberrant growth of damaged bone. True or False?

A

False

Osteophyte formation is attempted repair of loss of cartilage

Formed to increase surface area of the bone and relieve pressure from loading of body weight

Not a cause of pain in most patients

27
Q

Explain why subchondral cysts occur in OA?

A

Loss of cartilage (bare bone)

> > high pressure from joint pushes synovial fluid into subchondral area

> > form cyst in bone where pressure is lower

28
Q

What forces act on the hip when walking?

A

Weight of body part +
forces created by muscle contraction

3 times body weight during single-legged stance

29
Q

What increases the loading force on the knee joint in OA?

A

Varus malalignment and increased knee adduction movement

30
Q

What is the loading force on the knee during walking?

A

3X Body Weight during level ground walking
4X Body Weight with stair walking

60-70% force on the medial side of knee

31
Q

What increases the forces on the Patellofemoral joint surface in OA?

A

Increase deep knee bend due to abnormal gait

Abnormal patellar height and abnormal tracking movement

32
Q

What is the magnitude of forces on the patellofemoral joint surface when descending stairs?

A

2-3X Body Weight while descending stairs

33
Q

What are the investigative tests for OA?

A

■ Imaging (common)
– Plain radiographs
– Magnetic resonance imaging

■ Blood tests (rare)
■ Joint aspiration (rare)

34
Q

What is the classification used to assess Xray of OA hip or knee?

A

Kellgren Lawrence Classification

35
Q

What are the grades in Kellgren Lawrence Classification?

A

Grade 0 = normal
Grade 1 = Doubtful narrowing of joint space and possible osteophtic lipping
Grade 2 = Definite osteophyte and possible narrowing of joint space
Grade 3 = Moderate multiple osteophytes, definite narrowing of joint space + sclerosis
Grade 4 = Large osteophytes, marked narrowing of joint space, severe sclerosis, definite deformity of bone ends

36
Q

What are the pathological features of MRI in OA?

A
  • Meniscal tear due to trauma and degeneration
  • Loose bodies (fragments of cartilage or bone that freely float inside the knee joint space)
  • Bakers cysts (fluid-filled cyst that causes a bulge and a feeling of tightness behind your knee)
37
Q

What does increase in ESR AND CRP signify when investigating OA?

A

Normally degenerative OA = normal ESR and normal CRP

Severe inflammatory cause = Increased ESR and CRP

38
Q

What is the normal blood test result for OA?

A

Normal WBC
Normal ESR and CRP
Normal bone profiles (ions i.e. calcium, phosphate, alkaline phosphatase)

39
Q

What is the normal joint fluid aspiration result for degenerative OA?

A

– Clear
– Total cell count <1000/mm3
– Gram smear –ve & culture –ve
– Crystals -ve

40
Q

What is the normal joint fluid aspiration result for gouty OA?

A

Increased WBC

Increased urate crystals

41
Q

What are some physical treatments and risk factor modifications for OA?

A
  • Weight loss, walking aid
  • Muscle strengthening, ROM exercise, Muscle stretching, Aerobic exercises
  • Knee brace and shoe insoles
42
Q

What are some pharmacological treatments for OA?

A

■ Acetaminophen

■ Non-steroidal anti-inflammatory drugs (NSAID) : Non-selective + COX-2-specific inhibitor

■ Topical agents

■ Others
– Narcotic analgesics
– Anticonvulsants
– Antidepressants

43
Q

What supplements can be taken for OA?

A

Glucosamine – Substrate for synthesis of proteoglycans

44
Q

How does Hyaluronate intra-articular injections help OA?

A

Hyaluronate/ Glycosaminoglycan

Injected to act as visco-supplementation: Supplement viscosity of joint fluid for lubrication & cushioning & Pain relief

45
Q

What are the 4 intra-articular injections for OA?

A

■ Hyaluronate (common)
■ Steroid (common)
■ Platelet rich plasma (PRP)
■ Stem cells

46
Q

What surgery can be done for OA?

A

1) Arthroscopy – Loose bodies, meniscal tear with locking symptoms in the knee

> > Arthroscopic “lavage” or “debridement”: washout debris, synovial fluid and remove damaged cartilage or bone

2) Realignment osteotomy
» Redistribute stress to normal part of the joint

3) Joint replacement (for end stage OA)

MBBS II MSS (31 decks)

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