2) Osteoarthritis Flashcards

1
Q

What is osteoarthritis?

A

The most prevalent of the arthritis’ occurring when damaged joint tissues are unable to
normally repair themselves resulting in a
breakdown of cartilage and bone

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2
Q

The ratio of people who have osteoarthritis?

A

1 in 10 (3 million Canadians)

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3
Q

Modifiable and Non-Modifiable Risk Factors for Osteoarthritis.

A

Modifiable: obesity, occupation, sports, and trauma

Non-modifiable: genetics, age, and gender

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4
Q

How does obesity affect osteoarthritis?

A

Most important preventable risk factor.

It’s is predictor of prosthetic joint replacement. With the loss of 5kg results in 50% risk reduction.

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5
Q

How does overuse and trauma affect osteoarthritis?

A

Repetitive motion causing wear and trauma to joint, similar to the results of injury

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6
Q

What gender is more commonly affected by osteoarthritis?

A

Females

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7
Q

Why does age affect the risk of getting osteoarthritis?

A
  • Blunted chondrocyte repair potential
  • Weakened muscles (joint protection)
  • Slower sensory nerve input: less effective muscle and tendon response
  • Ligaments stretch with increasing age: less effective absorption of force
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8
Q

Primary vs Secondary causesOsteoarthritis

A

Primary: idopathic, with no identifiable causes
Secondary: rheumatoid arthritis, trauma, obesity and disease

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9
Q

Name 4 joint protective mechanisms

A
Joint capsule and ligament (fixes range of motion)
Synovial fluid (fills joint space to reduce friction btwn cartilage)
Mechanoreceptor sensory afferent nerve (provide feedback for muscles and tendons for positioning) 
Muscles and tendons (minimize focal stress across the joint)
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10
Q

Osteoarthritis is what kind of disease?

A

Progressive, “wear and tear”, large joint disease

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11
Q

What is cartilage and what is its function?

A

Thin rim of tissue on either end of two bones lubricated by synovial fluid with no vascular supply or nerve innervation.
It is to absorb shock.

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12
Q

What are Chrondrocytes?

A

They produce the two major macromolecules that make up cartilage and also the enzymes that break down cartilage.

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13
Q

What are the two major macromolecules that make up cartilage?

A

Type II Collagen: provides strength
Aggrecan: proteoglycan linked with hyaluronic acid. Negatively charged.
Work together to give compressive stiffness through electrostatic repulsion.

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14
Q

What are the enzymes involved in cartilage breakdown?

A
  • Matrix metalloproteinases (MMP-13) : breaks down Type II Collagen
  • ADAMTS-4 and ADAMTS-5: breaks down Aggrecan
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15
Q

True or Flase: Actual cartilage damage is a chemically-mediated disease process?

A

True

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16
Q

Describe the basic steps of osteoarthritis in cartilage.

A

1) Damage to Cartilage
2) Chondrocyte activity increases
3) Balance of breakdown vs re-synthesis lost
4) Vicious cycle of increasing breakdown leading to further cartilage loss

17
Q

Describe the cycle of cartilage breakdown.

A

Cartilage damage occurs which activates ADAMTS-5. ADAMTS-5 triggers aggrecan destruction exposing the DDR-2 receptor to collagen, activating it. DDR-2 then increases MMP-13 which destroys collagen.

18
Q

The enzymes are overexpressed when injury occurs to cartilage, shifting balance towards degradation resulting in loss of collagen and proteoglycans

A

Cartilage matrix degrading enzymes also known as Matrix Metalloproteases

19
Q

Where is proteoglycan protein found and what is it a major component of?

A

Found in connective tissue and cartilage; Major component of extracellular matrix and has lubricating functions which is inhibited in cartilage breakdown.

20
Q

Name 4 pro-inflammatory cytokines.

A

TNF-α, IF gamma, IL-1 and IL-6

21
Q

How do pro inflammatory cytokines drive the breakdown of cartilage and amplify MMP?

A
  1. Modulate chondrocyte metabolism to ↑ MMP
    synthesis
  2. Inhibit synthesis of MMP inhibitor molecules
  3. Inhibit synthesis of collagen & proteoglycans
  4. Induce chondrocyte to ↑ prostaglandin which effect matrix synthesis and degradation
22
Q

Does the sub chondral plate thicken or thin during cartilage breakdown?

A

Thicken, due to the activation of osteoclasts and osteoblasts by cytokines and GFs

23
Q

What do osteophytes form at the joint margin after cartilage damage?

A

Causes outgrowths of new cartilage which become ossified.

24
Q

What can occur to the synovium upon cartilage breakdown?

A

Can develop synovitis (becomes edematous and inflamed), which stretches the capsule possibly causing it to become fibrotic.

25
Q

Is osteoarthritis symmetrical or non-symmetrical

A

Can be non-symmetrical.

26
Q

Where are the most common sites of osteoarthritis?

A

Neck, Lumbar Spine, Hips, Fingers and Knees

27
Q

Common signs of OA

A

Large joints that have cracking and stiffness that is relieved with movement.

28
Q

7 physical presentation of OA

A
• Tenderness 
• Crepitus with joint motion 
• Bony enlargement of joint
Ex) Heberden (DIP) or Bouchard (PIP)
• Restricted range on motion 
• Pain on passive range of motion 
• Deformity
Ex)bowed legs
• Joint instability and stiffness that decreases with movement
29
Q

Are osteoarthritis symptoms chronic or acute?

A

Chronic with progressively worsening symptoms

30
Q

What are bone spurs?

A

Osteophytes that have a parrot beak appearances that fill in the space between the joints where cartilage used to be.

31
Q

What are the lab tests that can be done to diagnose for OA

A

There are no lab tests specific to OA, just tests that exclude other types of athritis.
These tests are:
ANA,ESR/C Reactive Protein: identifies general non-specific inflammation if +ve.
Followed by RF and anti-CCP to confirm RA with anti-CCP (more specific than RF)

32
Q

Because cartilage has no nerves to transmit pain, the nerves of their structures associates with the joint send pain signals in the form of these 5 pain mediators:

A
  • VIP= vasoactive intestinal peptide
  • TRPV1= Transient receptor potential cation channel subfamily V member 1 (AKA, vanilloid receptor 1 or, the capsaicin receptor)
  • NO = Nitric oxide
  • NGF = nerve growth factor
  • Prostanoids- example: prostaglandins
33
Q

What are the 5 non-pharrmalogical methods of management for osteoarthritis?

A
Weight loss
Exercise
Physical therapy
Braces
Physical modalities (TENS, Acupuncture)
34
Q

Name the three main pharmacological treatments of OA.

A

Acetaminophen (Block pain-impulse from PNS and inhibit CNS PG synthesis)
Capsaicin cream (depletes substance P from neurons)
Intra-articular sodium hyaluronate (May restore viscoelasticity of synovial fluid and normalize HA synthesis and/or inhibit degradation)