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MI1 > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

What is osetoarthritis (OA)?

A

A condition characterised by damage to the articular cartilage of joints & the underlying bone

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2
Q

What are the functional properties of articular cartilage?

A
  • Joint lubrication
  • Stability
  • Deformation & congruence
  • Loading: Static vs dynamic (cyclic)
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3
Q

What type of loading is good for joints and why?

A

Dynamic

  • Delivers nutrients to the joint
  • Improves movement of fluid through the joint
  • Improves amount of water in the articular cartilage
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4
Q

What load factors contribute to degree of joint lubrication?

A
  • Manner of loading
  • Exercise increases synovial fluid viscosity & lymphatic clearance
  • Cartilage deteriorates when unloaded
  • Potential for wear increases when joint goes from static to high loads
  • Repetitive impulse (sudden) loading is detrimental to HAC & subchondral bone
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5
Q

What are some of the more recently proven facts about OA (former myths)?

A
  • Not wear & tear
  • Joints are not worn out
  • Not increased by exercise (except in mechanical stress/exceptionally repetitive)
  • Cartilage needs movement
  • OA is a failure of repair
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6
Q

What are the two types of OA?

A

Primary

  • Genetic
  • Bilateral
  • Symmetrical
  • Inverse to osteoporosis

Secondary

  • Mechanical stress (injury, alignment, affects specific joint)
  • Metabolic, chemical or inflammatory (affects multiple joints)
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7
Q

What joints are commonly associated with primary OA?

A

Weight-bearing joints

  • Fingers (IPs, not CMCs)
  • Knees
  • Hips
  • Lumbar spine
  • 1st MTP
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8
Q

What are examples of diseases that may cause secondary metabolic OA?

A
  • Rheumatoid arthritis
  • Haemophilia
  • Gout
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9
Q

What are the subjective clinical features of OA?

A
  • Middle-aged or elderly
  • Insidious onset or aggravated by an event
  • Intermittent, local pain
  • Morning stiffness >30 mins
  • Stiffness after rest lasts few minutes
  • Worse with activity, better with rest
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10
Q

What are the objective clinical features of OA?

A
  • Tenderness
  • Limited ROM
  • Crepitus
  • Occasional effusion
  • Bony enlargement
  • Narrow joint lines
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11
Q

What are the x-ray clinical features of OA?

A
  • Osteophytes (bony spurs)
  • Joint space narrowing
  • Flattened condyles
  • Subchondral sclerosis
  • Malalignment (can be cause or effect, i.e. not diagnostic feature)
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12
Q

How do the articular cartilage cells change as they get deeper into the tissue?

A

Change from being flat to much more columnar

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13
Q

What does the tide line of articular cartilage divide?

A
  • Uncalcified cartilage (top layer)
  • Calcified cartilage (middle layer)
  • Subchondral bone (bottom layer)
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14
Q

What is cartilage chemistry made up of?

A

Proteoglycans (hydrophilic)

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15
Q

What occurs in the very early to moderate stages of OA?

A
  • V early OA: Cartilage swells, superficial layer loss, structural changes
  • Early OA: Loss of superficial laminar layer, bone starts growing
  • Moderate OA: Loss of organisation & hypertrophy
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16
Q

What occurs in the late to end stages of OA?

A
  • Late OA: Cartilage loss, growth of bone

- End stage OA: Sclerosis

17
Q

What stages of OA are reversible?

A

Up to moderate

18
Q

What are the main differences between the chemical and mechanical pathways of OA?

A
  • Mechanical pathway progresses much slower
  • Chemical pathway progresses much faster
  • Chemical pathway much more painful (inflammation)
19
Q

What are the inflammatory markers?

A
  • Interleukin-1 (IL-1)
  • Interleukin-6 (IL-6)
  • Tumour necrosis factor-alpha (TNF-alpha)
20
Q

What are the cartilage breakdown biomarkers in OA?

A

Early OA: Agrecanase (ADAMTS)

Late OA: Matrix metalloproteinase (MMP)

21
Q

What are the bony changes associated with OA?

A
  • Subchondral bone fractures
  • Increased osteoblast activity
  • Increased subchondral bone density
  • Reduced flexibility
  • Osteophytes (bone spurs)
22
Q

What does the reversibility of OA depend on?

A
  • The number of chondrocytes left
  • Stages of damage
  • Kinds of healing
  • Patient’s QOL
23
Q

What are the predictors of progression of medial OA?

A
  • Adduction moment (varus thrust/bow legs)
  • Gender
  • Mechanical axis (varus knee)
  • BMI (obesity = cytokines)
  • Pain
  • Age/presence of OA in other joints
  • Not physical activity (joint motion is good for cartilage)
24
Q

What are the principles of treatment for OA?

A
  • Find cause of mechanical stress
  • Relieve extra loading
  • Protect joint from shearing damage
  • Improve joint nutrition (exercise)
  • Relieve pain to enable exercise
25
Q

What are the core treatments for OA according to the OARSI guidelines?

A
  • Land-based exercise
  • Water-based exercise
  • Weight management
  • Self-management & education
  • Strength training

MI1 (18 decks)

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