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Applied Pathophysiology > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

What is osteoarthritis?

A

A progressie joint disease when damaged joint tissues are unable to normally repair themselves, resulting in breakdown of cartilage and bone

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2
Q

What is the prevalence of OA in Canada?

A

1 in 10 people

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3
Q

Give three reasons why OA is so prevalent in Canada.

A

1) Aging baby boomer population
2) Increased life expectancy
3) Increased obesity rates

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4
Q

What are the 3 main risk factors for OA?

A

1) Obesity
2) Occupation, sports, trauma
3) Genetics, age, gender

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5
Q

What types of occupations make people susceptible to OA?

A

Hard labourers typically with frequent, repetitive motions or those including heavy lifting

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6
Q

What joints does obesity typically affect?

A

knee
hip
hand

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7
Q

What kind of disorders can increase your risk for OA?

A

joint malalignment disorders

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8
Q

How much is your risk of OA reduced if you lose 5kg?

A

50% risk reduction

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9
Q

Why is obesity a risk factor for OA?

A

Increased stress on joints and sedentary lifestyle leads to decreased cartilage health

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10
Q

What groups of people would most likely have OA in the knee?

A

carpenters
miners
dockers
athletes

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11
Q

What groups of people would most likely have OA in the ankle?

A

ballet dancers

soccer players

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12
Q

What age group is most at risk for OA?

A

Older people

older you get, higher your risk

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13
Q

What races are usually at a lower risk for OA? Why?

A

Asian and Indian populations

Usually not obese

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14
Q

Name 4 reasons why older people are at higher risk of getting OA.

A

1) Blunted chondrocyte repair potential
2) Weakened muscles (joint protection)
3) Slower sensory nerve input (less effective muscle/tendon response)
4) Ligament stretch with age (less effective force absorption)

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15
Q

What are the two main types of OA?

A

Primary OA

Secondary OA

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16
Q

Which OA is more common, primary or secondary?

A

Primary

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17
Q

What is the difference between primary and secondary OA?

A

Primary - idiopathic

Secondary - known cause/trigger

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18
Q

Name 4 components of the joint protective mechanisms?

A

1) joint capsules/ligaments
2) synovial fluid
3) mechanoreceptor sensory afferent nerves
4) Muscles/tendons

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19
Q

How do joint capsules/ligaments protect the joints?

A

provide a limit of excursion thereby fixing the range of joint motion
ligaments - give strength and stability to the joint

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20
Q

How does the synovial fluid help protect the joints?

A

Fills joint space to reduce friction between cartilage surfaces

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21
Q

How do the mechanoreceptor sensory afferent nerves protect the joints?

A

Provides feedback so muscles and tendons assume the right tension at appropriate points

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22
Q

How do muscles and tendons help protect the joints?

A

Bridge the joint and contract at appropriate times to minimize the focal stress across the joint
Tendons - joint stabilization
muscles - support

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23
Q

What is cartilage?

A

Thin rim of tissue at the ends of two opposing bones

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24
Q

What lubricates cartilage? What is its function?

A

Synovial fluid

Provides an almost frictionless surface across which these two bones move

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25
What is the main function of cartilage?
Absorbs shock
26
Is cartilage innervated or vascularized?
Nope
27
What are two major macromolecules that make up cartilage? What type of cell produces these macromolecules?
Type 2 collagen Aggrecan Produced by chondrocytes
28
What is the function of type 2 collagen?
provide cartilage strength with its tensile strength
29
what is aggrecan?
proteoglycan linked with hyaluronic acid, highly -ively charged glycosaminoglycans
30
What are the 2 functions of aggrecan?
keeps sponginess of cartilage | prevents contact of DDR-2 receptor (collagen receptor) with collagen
31
What gives cartilage its compressive stiffness?
electrostatic repulsion of aggrecan molecules being forced together by tightly woven type 2 collagen
32
What are the three types of cartilage? Which one is found in joints?
1) Elastic 2) Hyaline (joint) 3) Fibrocartilage
33
What two enzymes does the chondrocyte produce? What do they do?
``` Matrix metalloproteinases (MMP-13): breaks down type 2 collagen ADAMTS-4 and -5: breaks down aggrecan ```
34
What is the first step in cartilage breakdown?
Increase in chondrocyte activity due to cartilage damage
35
What is the second step in cartilage breakdown?
Cartilage damage and increased chondrocyte activity leads to activation of ADAMTS-5
36
What is the 3rd step in cartilage breakdown?
ADAMTS-5 destroys aggrecan on chondrocyte, leading to collagen exposure to DDR-2 receptor
37
What is the 4th step in cartilage breakdown?
Exposed DDR-2 receptor activates MMP-13 (inhibitors overwhelmed - balance shifts toward degradation) destroys collagen and proteoglycans
38
How do pro-inflammatory cytokines drive cartilage breakdown and amplify MMP? (4 pts)
1) modulating chondrocyte metabolism to increase MMP synthesis 2) Inhibit synthesis of MMP inhibitor molecules (alpha2 macroglobulin) 3) inhibit synthesis of collagen and proteoglycans 4) induce chondrocyte to increase prostaglandin E2, NO, and bone morphogenic protein 2 (BMP-2) synthesis (effects matrix synthesis/degradation)
39
What are 3 results of cartilage breakdown?
1) changes in sub-chondral bone 2) osteophytes form at joint margin 3) synovium becomes edematous and inflamed
40
what are osteoclasts? osteoblasts? what activates them?
osteoclasts - break down bone osteoblasts - make bone cytokines, GFs
41
what are osteophytes?
outgrowths of new cartilage that eventually becomes ossified (turned into bone)
42
Does OA typically present symmetrically or asymmetrically?
asymmetrically
43
what joints are typically affected by OA?
``` Neck Lumbar spine hip Fingers Knee ```
44
What is erythrocyte sedimentation rate? what is its purpose?
A measure of the settling of RBCs in a tube of blood during one hr Detects inflammation, rules out RA
45
What are the physical findings for OA? (7pts)
``` Tenderness Crepitus (crackling) with joint motion Bony enlargement of joint Restricted range of motion Pain on passive range of motion Deformity (bowed legs) Joint instability ```
46
What clinical history points indicate OA? (4pts)
Joint stiffness upon waking up (less than 30min) Pain often worse with exercise Pain improvement with rest (more than 1hr leas to stiffness) Chronic, progressive, worsening symptoms
47
What are Heberden and Bouchard nodes?
Heberden - node at DIP | Bouchard - node at PIP
48
What is the diagnostic definition of OA?
joint pain that occurs for most days of the prior month plus radiographic changes in the symptomatic joint
49
What are the 4 goals of therapy for OA?
Reduce joint pain Improve joint function and mobility Maintain normal articular and peri-articular structures Prevent (and possibly reverse) joint cartilage damage
50
Is cartilage loss associated with OA pain?
NO
51
What structures are associated with OA pain?
``` Synovium Joint capsule Muscle Subchondral bone Osteophytes ```
52
What are the 5 pain mediators of OA?
``` VIP - vasoactive interstinal peptide TRPVI - transient receptor potential cation channel subfamily V member I (aka vanilloid receptor I or capsaicin receptor) NO - nitric oxide NGF - neural growth factor Prostaglandins ```
53
What three sources cause pain in OA?
Synovial inflammation Joint effusions (abnormal fluid build up) Bone marrow edema
54
What are 6 non-pharm treatment options for OA?
1) patient education 2) wt loss 3) exercise 4) physical therapy 5) braces 6) physical modalities
55
how will weight loss help with OA?
reduce load on joints
56
how will exercise help with OA?
strengthen supportive muscles around joints
57
how will braces help with OA?
help reduce load and provide structural support for joint space and surrounding ligament/muscles
58
what is the primary use for lab tests for OA?
exclude other types of arthritis and monitor the disease
59
What 6 pharm methods to treat OA?
1) Acetaminophen 2) NSAIDs 3) Cox 2 inhibitors 4) capsaicin cream 5) intra-articular glucocorticoids 6) intra-articular sodium hyaluronate
60
how does acetaminophen help with OA?
block pain impulse from PNS and inhibit CNS PG synthesis
61
how do NSAIDs help with OA?
inhibit cox-1 and cox-2
62
how do capsaicin cream help with OA?
deplete substance P from neurons
63
How do intra-articular glucocorticoids help with OA?
inhibit inflammatory cells and mediators
64
how do intra-articular sodium hyaluronate?
may restore viscoelasticity of synovial fluid and normalize HA synthesis and/or inhibit degradation

Applied Pathophysiology (11 decks)

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