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ANAT2012 > Joints, Articular cartilage and Synovial fluid L2: Hyaline cartilage & synovial joint pathology > Flashcards

Joints, Articular cartilage and Synovial fluid L2: Hyaline cartilage & synovial joint pathology Flashcards

1
Q

Hyaline cartilage is vascular/avascular

A

Avascular

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2
Q

When is hyaline cartilage highly vulnerable?

A

Excessive, impulsive high loading

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3
Q

Hyaline cartilage health depends on ______.

A

Loading patterns.

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4
Q

Alterated loading patterns (for hyaline cartilage) such as ____, _____ and _____ can lead to altered compositional properties.

A

Excessive, Prolonged and Absence

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5
Q

The _______ contributes directly to interstitial fluid pressurization –> attract H2O and offer______ resistance to interstitial fluid flow.

A

proteoglycan network strong

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6
Q

Most curved surfaces compressed by ____ forces (eg. compression)

A

external

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7
Q

What 2 types of loading alter chondrocytes metabolism?

A
  1. Increased intermittent hydrostatic pressure
  2. Shear stress
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8
Q

How does increased intermittent hydrostatic pressure alter chondrocytes metabolism?

A
  • Aggrecan
  • Type II collagen
  • macromolecule
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9
Q

How does shear stress alter chondrocytes metabolism?

A
  • increased the release of the proinflammatory mediator,
  • decreased aggrecan and Type II collagen expression, and
  • induced molecular changes associated with apoptosis (self-destruction, pre-programmed cell-death)
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10
Q

What are the 5 changes that occur in ECM during ageing?

A
  1. hypertrophic changes in chondrocytes
    • chondrocytes hypertrophy before they die- aging chondrocytes hypertrophy
  2. loss of glycosaminoglycans (associated with aging and OA)
  3. calcification of the ECM
  4. increased number of tidemarks > 60 years age
  5. movement of the tide mark to the cartilage surface = replacement of the lower calcified cartilage by bone
    • Tide mark = the line marking the border between the calcified cartilage and the non-calcified cartilage
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11
Q

What are the 4 causes of hyaline cartilage patholgy?

A
  1. Acute trauma
    • Impulsive high rate of application
  2. Altered kinematics
  3. Prolonged overloading
    • Obesity ( body weight)
  4. Prolonged immobilization
    • Lack of stimulus
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12
Q

How are ACL ruptures associated with primary cartilage damage & development of OA?

A
  • Mechanism = simultaneously valgus + rotation = dynamic loading in multiple planes
  • Often associated with
    • Meniscal damage (non-contact, rapid deceleration, valgus force rapid change of direction)
      • Primary or secondary
      • Medial meniscus (most common injury)
  • Direct articular cartilage lesion
    • Usually femoral condyles (split, impact lesion on femoral condyle = change in ECM)
  • Collateral ligament tears (MCL)
  • Bone marrow lesion (change in stiffness)
  • Haemarthosis
    • Bleeding, rapid swelling –> 2nd reaction –> irritation of inflammatory mediators (eg. synovial)
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13
Q

What are the 2 changes (in proteogylcans) that occur in hyaline cartilage during immobilisation?

A
  1. • Significant ↓ Proteoglycans ipsilateral side
  2. Significant ↑ Proteoglycans contralateral side
    • Increase in loading of contralateral side
  • Even after 50 weeks, ipsilateral side did not fully recover
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14
Q

What are the 4 reasons why hyaline cartilage is unable to spontaneously repair?

A

*not normal post-inflammatory response

  1. avascular & aneural
  2. low cellular density
    • less cells to maintain
  3. low metabolic activity
  4. inability to migrate to the site of injury (chondrocytes can’t move around)
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15
Q

Why is OA a ‘whole joint disease’?

A

It affects:

  • Cartilage
  • Bone
  • Intra-articular & periarticular structures
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16
Q

What causes OA?

A

A result of excessive mechanical stress applied in the context of systemic susceptibility

17
Q

What are 6 factors that can increase the risk of OA?

A
  1. Age
    • Thinning of cartilage
    • Poor proteoglycan
    • Changes in synovial fluid
  2. Obesity
  3. Previous injury
  4. Female gender
    • hormonal, biomechanics- pelvis, strength
  5. Genetic inheritance
  6. Nutritional factors
18
Q

What are 4 various theories of pathological changes due to previous injury or disease (sequelae)/

A
  1. Mechanical wear &tear
    • Bearing surface failure under repeated high loads
    • Altered lubrication
      • Change in quality of synovial fluid
      • Loss of fluid film between articular surface
  2. Alteration in chondrocyte activity
  3. Alteration in ECM
  4. Altered subchondral bone stiffness
19
Q

What is the chondrocytes theory?

A

There are 2 types of hyaline cartilage:Temporary and permanent

20
Q

How does the chondrocytes theory affect endochondral ossification (default pathway)?

A
  • Mesenchymal cells differentiate into chondrocytes
  • Chondrocytes undergo terminal differentiation
  • Hypertrophy & apoptosis
  • Cartilage –> bone
21
Q

How does the chondrocytes theory affect the normal articular hyaline cartilage?

A

the terminal differentiation of chondrocytes is halted

22
Q

What are the 2 types of inflammatory theories?

A
  1. Local
  2. Systemic
23
Q

What is the local inflammatory theory?

A
  • Synovium irritated by cartilage fragments
    • inflammatory response
    • Inflammatory markers in synovial fluid
    • activate superficial chondrocytes
    • Proteases
    • Cartilage breakdown
  • Abnormal mechanical stress / increase in shear stress
  • Mechanotransduction
  • synthesis of inflammatory mediators by chondrocytes & subchondral osteocytes
24
Q

What is the systemic inflammatory theory?

A
  • Metabolic syndrome
  • Age
25
Q

75% of knee OA affects the ______ compartment.

A

Medial

26
Q

How does the hip-knee-angle alignment affect OA/

A
  • contributes to the load distribution across the knee articular surface
  • proportionately divides load between the medial and lateral compartments The load-bearing mechanical axis = a line from the centre of femoral head to the center of the talus
27
Q

What occurs in varus knee? Is there a higher or lower progression of OA?

A
  • mechanical axis passes medial to the knee
  • creates a moment arm
  • further increases load on the medial compartment.

Higher tibiofemoral adduction moment –> OA progression

28
Q

What is the role of muscles in knee OA?

A

To balance external adduction (varus) moment

29
Q

Which muscles help to balance the external adduction (varus) moment of the knee?

A
  • quadriceps *rectus femoris, (early stance)
  • sartorius,
  • long head biceps femoris,
  • lateral gastrocnemius (late stance)

Decrease varus force = decreased progression of OA

30
Q

What muscles control eccentric knee flexion @ HS to control loading rate?

A

Quadriceps

31
Q

What muscles ensure pelvic control? Why is this important?

A
  • hip abductors - gluteus medius & minimus
  • Contralateral hip drop moves CoM toward swing limb i.e. further from centre of stance knee –> increases moment arm of ground reaction force
32
Q

Stance limb hip _______ eccentrically control the femur. Why is this important?

A

Adductors

  • “lift” medial femoral condyle to resist varus
33
Q

What are 4 possible articular cartilage repair procedures ?

A
  1. Arthroscopic lavage and debridement
    • cleaning out and evening up the joint surface
    • short-term relief
  2. Marrow stimulating techniques
  3. Osteochondral autografts and allografts
  4. Autologous chondrocyte implantation
34
Q

How does the marrow stimulating techniques work in repairing cartilage?

A
  • removing damaged cartilage – drilling holes in the underlying bone to cause bleeding
    • natural replacement of hyaline cartilage with fibrocartilage
    • quick recovery time
    • effective articulating surface than hyaline cartilage
35
Q

How does the osteochondral autografts and allografts work in repairing cartilage? What are the advantages and disadvantages?

A
  • Remove injured cartilage and the underlying bone
  • Replace with cartilage & bone from another site
    • within the joint (autograft)
    • a tissue donor (allograft)
  • The replacement core is gently tapped into place until it lines up with the surrounding tissue.
    • No screws or other devices are typically needed to hold the replacement core in place since it fits tightly.
  • start to weight-bear within 4-6 weeks of surgery
  • gradually activity
  • return to sport typically after 6-9 months
  • advantage = the ability to replace both cartilage and bone with similar tissue.
  • limitation = amount of tissue that can be taken from within a patient’s own joint
36
Q

What is the advantage of using osteochondral autografts and allografts to repair cartilage?

A

the ability to replace both cartilage and bone with similar tissue.

37
Q

What is the disadvantage of using osteochondral autografts and allografts to repair cartilage?

A

amount of tissue that can be taken from within a patient’s own joint

ANAT2012 (31 decks)

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