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PHA223 > osteoarthritis (Steve Darby) > Flashcards

osteoarthritis (Steve Darby) Flashcards

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
Q

joint supports and examples

A 
balance/shift load from affected joint/lessen impact
knee braces
shoe wedges
insoles
walking aids - frames, crutches, stick
26
Q

What does TENS stand for?

A

transcutaneous electrical nerve stimulation

27
Q

How do TENS work?

A

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
Q

When would surgery be done?

A
  • treatments are ineffective
  • constant/high pain levels
  • lack of joint movement
  • joint destruction
  • impacting QoL
29
Q

3 types of surgery options

A
  1. joint fusing - make a joint fixed
  2. osteotomy - addition/removal of small bones
  3. whole joint replacement - prosthesis (hip/knee)
30
Q

What are nutraceuticals?

A

dietary supplements

  • glucosamine
  • chondroitin
  • S-adenosylmethionine
31
Q

possible MOA of nutraceuticals

A

possibly stimulate chondrocytes

may inhibit cartilage enzyme activity (glucosamine sulfate)

32
Q

What do chondrocytes do in healthy cartilage?

A
  • produce structural components of cartilage
  • > like collagen, proteoglycans, glycosaminoglycans
  • structural component lossed in OA
33
Q

What does NICE say about glucosamine or chondroitin products?

A

don’t offer them for OA management

34
Q

hyaluronic acid for OA

A

injection
not recommended
-> thought to support elasticity of joints and help synovial fluid

35
Q

1st line analgesics

A

paracetamol

ahead of NSAIDs

36
Q

What to give if pain relief not sufficient with paracetamol?

A

combination with opiods

- co-codamol (codeine and paracetamol)

37
Q

problems with giving opioids

A

additction potential

-> withdrawal strategies in place

38
Q

2nd line drug therapy

A

NSAIDs

- topical considered over oral (ibuprofen or naproxen)

39
Q

What to give if paracetamol/topical NSAIDs ineffective?

A

oral NSAID/COX-2 inhibitors

oral NSAID at lowest possible dose for shortedt period of time

40
Q

considerations before starting on oral NSAIDs

A

CV risk
GI risk
renal risk
if thye’re on low dose aspirin (CV)

41
Q

Treatment for gastric problems with NSAIDs

A

co-prescribe PPI

  • omeprazole
  • lansoprazole
  • pantoprazole
  • esomeprazole
42
Q

What NSAID has lowest vascular risk?

A

naproxen

43
Q

1st/2nd/3rd/4th line management of OA

A

1st - paracetamol
2nd - paracetamol with opioids
3rd - topical NSAIDs
4th - oral NSAIDs (PPI if GI problems)

44
Q

What treatment can be given adjunct to NSAIDs esp for knee/hand OA?

A

capsaicin

45
Q

What is capsaicin from?

A

chili peppers (analgesic properties)

46
Q

How deos capsaicin work?

A
  • 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
Q

What is TRPV1?

A

transient receptor potential vanilloid 1
ligand gates cation channel
selectively expressed in nerve fibres

48
Q

When are intra-articular injections of corticosteroids given?

A

moderate to severe pain

49
Q

examples of steroid used for intra-articular injections

A

hydrocortisone (most used)
dexamethasone
prednisolone

50
Q

How often are intra-articular steroids given?

A

every 3 months

51
Q

What injection is not recommended in UK?

A

hyaluronic acid

PHA223 (43 decks)

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