6. Osteoarthritis Flashcards

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

A

aggrecan

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
Q

what does meniscal damage correlat ewith

A

an increased incidence of osteoarthritic disease

26
Q

name 2 inflammatory cytokines

A

IL1 and TNF-alpha

27
Q

name 2 anti-inflammatory cytokines

A

IL-4 and IL-10

28
Q

what do inflammatory cytokines do

A

inhibit anabolic processes and promote catabolic processes

by stimulating the activity of proteases

29
Q

what do anti-inflammatory cytokines do

A

promote anabolic processes and inhibit catabolic processes

by increasing protease inhibitor production

30
Q

name a protease inhibitor

A

tissue inhibitors of metalloproteinase (TIMP)

31
Q

what are some symptomatic treatments available for OA

A

NASIDs - inhibit COX enzymes - e.g. ibuprofen

32
Q

what is the issue with NASIDs and COX2 inhibitors

A

produce unwanted outcomes - gastrointestinal issues

33
Q

what surgical options are there for managing OA

A

resurfacing joint replacement

34
Q

how could infliximab therapy be used to treat OA

A

inhibit the effects of TNF-alpha and up-regulate anti-inflammatory cytokines (IL-10)

35
Q

what is the problem with prospective treatments for OA, what needs to be further researched

A

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