osteoarthritis (Steve Darby) Flashcards

(51 cards)

1
Q

What is osteoarthritis?

A

degenerative disease
characterised by the progressive degeneration, destruction and erosion of articular cartilage
bone ends rub together

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2
Q

difference between OA and RA

A
OA is a degenerative disease
-> RA is an autoimmune disease
OA inflammation is minimal
-> RA has imflammed synovial membrane
OA is erosion of cartilage
-> RA erosion of bone
OA bone ends rub together
-> RA they don't
OA asymmetrical
-> RA symmetrical
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3
Q

When is stiffness with OA?

A

morning stiffness lasting less than 30mins

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4
Q

joints most affected

A

knee
hip
hand/wrist

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5
Q

risk factors for OA

A
occupation (coal miners, golfers, footballers, rugby)
bending of the knee
kneeling
squatting
standing for long hrs (>2 per day)
walking >3km per day
regular stair climbing
heavy lifting
vibration
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6
Q

What chromosome is important for genetic linkage of OA?

A

chromosome 2q13-32

  • includes the IL-1 gene cluster
  • frizzles related protein (FRZB)
  • cartilage structural protein matrilin-3 (MATN3)
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7
Q

What happens in early stages of OA?

A

cartilage develops irregularities at the surface where it becomes fibrillated

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8
Q

What happens as OA progresses?

A
  • deep clefts form in cartilage
  • loss aggrecan and type II collagen within the cartilage extracellular matrix (structural proteins)
  • chondrocytes clump within cartilage surrounded by regions of intense staining material indicating increased proteoglycan
  • ongoing cartilage damage, articular joint surface damaged, loss of joint fxn
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9
Q

MMPs

A

matrix metallo proteases

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10
Q

What leads to MMP production?

A
  • increased mechanical insult (yrs of damage)
  • chondrocytes release cytokines (IL1, TNF alpha)
  • increases MMP production
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11
Q

What do MMPs do?

A

degrading enzymes

  • breakdown extracellular matrix in tissues
  • collagen destruction
  • synovial cell irritation
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12
Q

Where do cartilage breakdown products go?

A

into synovial fluid

synovial cells ingest the breakdown products

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13
Q

What do synovial cells release?

A

proteinases and proinflammatory cytokines

these upregulate catabolic processes in synovial membrane and cartilage

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14
Q

What structural proteins are broken down in the cartilage?

A

collagen

proteoglycan

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15
Q

What are osteophytes?

A

bony spurs formed in OA
can limit space in the joint
pinch nerves

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16
Q

Where can osteophytes occur?

A
neck
shoulder
knee
lower back
fingers
big toe
foot/heel
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17
Q

OA symptoms

A
  • clicking/cracking sounds in joints
  • slow onset of symptoms
  • mild swelling
  • asymmetry
  • stiffness
  • pain in a joint (hip/knee/hands most common)
  • bone spurs
  • reduced flexibility (bending/stairs)
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18
Q

OA diagnosis

A

medical Hx
physical examination
x-ray/MRI
fluid aspiration (oculd be joint infection, crystals-gout)

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19
Q

primary OA

A
  • no known cause (onset over time)
  • idiopathic OA
  • elderly
  • most common
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20
Q

secondary OA

A
  • linked to an existing disease (gout, haemochronatosis)
  • congenital abnormality
  • hormonal/inflammatory disorder (Acromegaly/Paget’s)
  • joint injuries (not repaired correctly)
  • younger patients
  • less common
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21
Q

What approach is used for management of OA?

A

combined approach of

  • non-pharmacological
  • pharmacological
22
Q

non-pharmacological management

A
exercise and manual therapy
joint aids/supports
TENS
surgical joint replacement and arthroscopic lavage
nutraceuticals
23
Q

pharmacological management

A
  • paracetamol
  • NSAIDs
  • capsaicin
  • corticosteroids
  • DMOADs (not on market)
24
Q

main non-pharmacological management

A
weight loss
- aerobic exercise
- low impact
- swimming/yoga
muscle strengthening
- joints
- ligaments/tendons
- stretching/physiotherapy
25
joint supports and examples
``` balance/shift load from affected joint/lessen impact knee braces shoe wedges insoles walking aids - frames, crutches, stick ```
26
What does TENS stand for?
transcutaneous electrical nerve stimulation
27
How do TENS work?
pads placed around the joint pain signals can be blocked by electrical impulses from a TENS machine non-invasive, fast acting and drug free
28
When would surgery be done?
- treatments are ineffective - constant/high pain levels - lack of joint movement - joint destruction - impacting QoL
29
3 types of surgery options
1. joint fusing - make a joint fixed 2. osteotomy - addition/removal of small bones 3. whole joint replacement - prosthesis (hip/knee)
30
What are nutraceuticals?
dietary supplements - glucosamine - chondroitin - S-adenosylmethionine
31
possible MOA of nutraceuticals
possibly stimulate chondrocytes may inhibit cartilage enzyme activity (glucosamine sulfate)
32
What do chondrocytes do in healthy cartilage?
- produce structural components of cartilage - > like collagen, proteoglycans, glycosaminoglycans - structural component lossed in OA
33
What does NICE say about glucosamine or chondroitin products?
don't offer them for OA management
34
hyaluronic acid for OA
injection not recommended -> thought to support elasticity of joints and help synovial fluid
35
1st line analgesics
paracetamol | ahead of NSAIDs
36
What to give if pain relief not sufficient with paracetamol?
combination with opiods | - co-codamol (codeine and paracetamol)
37
problems with giving opioids
additction potential | -> withdrawal strategies in place
38
2nd line drug therapy
NSAIDs | - topical considered over oral (ibuprofen or naproxen)
39
What to give if paracetamol/topical NSAIDs ineffective?
oral NSAID/COX-2 inhibitors | oral NSAID at lowest possible dose for shortedt period of time
40
considerations before starting on oral NSAIDs
CV risk GI risk renal risk if thye're on low dose aspirin (CV)
41
Treatment for gastric problems with NSAIDs
co-prescribe PPI - omeprazole - lansoprazole - pantoprazole - esomeprazole
42
What NSAID has lowest vascular risk?
naproxen
43
1st/2nd/3rd/4th line management of OA
1st - paracetamol 2nd - paracetamol with opioids 3rd - topical NSAIDs 4th - oral NSAIDs (PPI if GI problems)
44
What treatment can be given adjunct to NSAIDs esp for knee/hand OA?
capsaicin
45
What is capsaicin from?
chili peppers (analgesic properties)
46
How deos capsaicin work?
- repeated administration produces a desensitisation and an inactivation of sensory neurons - binds to TRPV1 - transient receptor potential vanilloid 1 - NTs released when body feels heat - use capsaicin, will feel burning/stinging sensation - gives relief from pain of OA
47
What is TRPV1?
transient receptor potential vanilloid 1 ligand gates cation channel selectively expressed in nerve fibres
48
When are intra-articular injections of corticosteroids given?
moderate to severe pain
49
examples of steroid used for intra-articular injections
hydrocortisone (most used) dexamethasone prednisolone
50
How often are intra-articular steroids given?
every 3 months
51
What injection is not recommended in UK?
hyaluronic acid