6. Osteoarthritis Flashcards

(35 cards)

1
Q

when do molecular changes begin prior to onset

A

20 years before clinical symptoms appear

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2
Q

what are the two forms of osteoarthritis

A

primary and secondary

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3
Q

what is the difference between primary and secondary OA

A

Primary OA is the gradual degeneration of a joint without any particular reason, found mainly in the knee joint

secondary OA is often caused by trauma and can occur in any joint

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4
Q

what percentage of the UKs population live with a musculoskeletal condition

A

28.9%

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5
Q

is there a gender bias in the number of people suffering with musculoskeletal conditions

A

yes : 10.1 million females to 7.7 million males

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6
Q

what is the cost per minute to the economy of treating OA and RA

A

19K a minute

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7
Q

genetic factors account for how much of hand and hip OA

A

60%

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8
Q

people who are overweight or obese are how many times more likely to develop knee OA

A

2.5-4.6 times

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9
Q

what occupation is likely to exacerbate OA

A

desk-based jobs

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10
Q

what molecules is cartilage composed of

A

water
collagen II
proteoglycans (aggrecan)
small proteoglycans

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11
Q

what is the most abundant

A

proteoglycan

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12
Q

what is the structure of aggregcan

A

it has a protein core attached to glycosaminoglycans (which can hold the water)

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13
Q

what two properties define cartilage

A

aneural and avascular

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14
Q

cartilage is aneural and avascular, what does this mean

A

it has no neurons and no blood supply

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15
Q

cartilage is constantly undergoing a slow remodelling process, why is it so slow?

A

all processes happen by diffusion - this is why the remodelling process is so slow

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16
Q

what happens to the cartilage in the knee joint when u stand

A

pushes the water in the cartilage out into the synovial gap

17
Q

what happens when pressure is no longer applied to the knee joint

A

cartilage soaks the water back up

18
Q

what happens when the water is lost

A

loss of functionality

19
Q

how is aggrecan and collagen attacked

A

matrix metalloproteinases and aggrecanase

20
Q

how else can we run out of functional collagen

A

there is an imbalance between the degradation and anabolic synthetic processes

(degrading it quicker than we are resynthesising it)

21
Q

what holds the water in collagen

22
Q

describe the structure of the cartilage in OA

A

thinner than normal, the surface is rough and the meniscus is damaged or missing

23
Q

where is the meniscus located

A

between the tibial plateau and the femoral condyl

24
Q

what is the role of the meniscus

A

involved in load transmission, shock absorption and lubrication

25
what does meniscal damage correlat ewith
an increased incidence of osteoarthritic disease
26
name 2 inflammatory cytokines
IL1 and TNF-alpha
27
name 2 anti-inflammatory cytokines
IL-4 and IL-10
28
what do inflammatory cytokines do
inhibit anabolic processes and promote catabolic processes by stimulating the activity of proteases
29
what do anti-inflammatory cytokines do
promote anabolic processes and inhibit catabolic processes by increasing protease inhibitor production
30
name a protease inhibitor
tissue inhibitors of metalloproteinase (TIMP)
31
what are some symptomatic treatments available for OA
NASIDs - inhibit COX enzymes - e.g. ibuprofen
32
what is the issue with NASIDs and COX2 inhibitors
produce unwanted outcomes - gastrointestinal issues
33
what surgical options are there for managing OA
resurfacing joint replacement
34
how could infliximab therapy be used to treat OA
inhibit the effects of TNF-alpha and up-regulate anti-inflammatory cytokines (IL-10)
35
what is the problem with prospective treatments for OA, what needs to be further researched
by the time symptoms appear it may be too late research needs to look for biomarkers of acicular cartilage breakdown as an early sign of OA