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PHA 332 > OSTEOARTHRITIS THERAPEUTICS > Flashcards

OSTEOARTHRITIS THERAPEUTICS Flashcards

1
Q

what is osteoarthritis?

A

it means bone joint inflammation

it is primarily a degenerative disease

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2
Q

how is OA charactersied?

A

by the progressive degeneration, destruction and

erosion of articular cartilage

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3
Q

what joints are usually affected in OA?

A

large-weight bearing joints

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4
Q

what occurs in OA?

A

loss of articular cartilage
bone ends rub together
pain and limitation of movement

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5
Q

what is the difference between RA and OA?

A

RA- swollen and inflamed synovial membrane
erosion of bone
autoimmune disease
symmetrical

OA- loss of articular cartilage
bone’s end rub together
degenerative disease
asymmetrical

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6
Q

how do the symptoms of RA and OA differ?

A

RA- pain, stiffness and INFLAMATION
morning stiffness lasting MORE than 30 min

OA- pain and stiffness in movement
morning stiffness lasting less than 30 min

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7
Q

who is OA most common in?

A

mainly in mid 40s and older

more common in women

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8
Q

what are the most common joints affected in OA?

A

knee
hip
hand/wrist

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9
Q

does the risk of devleoping OA increase with age?

A

yes

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10
Q

what is the occupational risk that poses OA?

A

occupations such as- coal miners- elbow joints
golfer- foot
footballers-knee
rugby- everything

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11
Q

how would a certain occupation increase your risk of OA?

A 
Bending of the knee
•Kneeling 
•Squatting
•Standing for long hours (≥ 2 hour per day)
•Walking ≥ 3 km/day
•Regular stair climbing
•Heavy lifting (≥ 10 kg)
•Vibration
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12
Q

what are the OA risk factors?

A

growing old- heart disease/ cancer/ OA

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13
Q

how do you acquire OA?

A

biochemical
genetic
biological

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14
Q

what is thought to be the most common consistant genetic linkage for OA?

A

in the chromosome 2q13-32
•This particular region includes the IL-1 (interleukin-1) gene cluster,
•Frizzled related protein 3 (FRZB)
•cartilage structural protein matrilin-3 (MATN3)

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15
Q

how does OA differ from early to late stage pathophysology?

A

•In the early stages of disease, cartilage develops irregularities at the surface
where it becomes fibrillated
•As the condition progresses, deep clefts form in the cartilage, with loss of
aggrecan and type II collagen within the cartilage extracellular matrix

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16
Q

what do chondrocytes do?

A

Chondrocytes also clump within cartilage, surrounded by regions of intense
staining material indicating increased proteoglycan

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17
Q

how does the breakdown of cartlidge occur?

A

Fibrillation and erosion of the cartilage surface.
Release of breakdown products into synovial fluid.
Synovial cells ingest the breakdown products
Synovial cells release proteinases and
proinflammatory cytokines, which upregulate
catabolic processes in synovial membrane and
cartilage.

18
Q

what do osteophytes do in OA?

A

osteophytes are ‘bone spurs’ formed in OA

they can limit space in the joint

19
Q

where can bone spurs occur in?

A
  • Neck
  • Shoulder
  • Knee
  • Lower back
  • Fingers or big toe
  • Foot or heel
20
Q

what are the osteoarthritis symptoms?

A 
clicking or cracking sounds
slow onset of symptoms
mild swelling
asymmetry
stiffness
pain in joint
bone spurs
reduced flexibility
21
Q

how do you diagnise OA?

A
  • Medical History
  • Physical Examination
  • X-Ray
  • MRI
  • Fluid aspiration – infection / crystals in the joint
22
Q

what is the difference between primary and secondary OA?

A

1-•No known “cause”
•Known as Idiopathic Osteoarthritis
•Seen in elderly patients
•Most common form

secondary-•Linked to existing disease
•Gout, hemochromatosis
•Congenital abnormality
•Hormonal / Inflammatory disorders
•Acromegaly or Paget’s
•Joint injuries
•Seen in younger patients
•Less common
23
Q

what is the aim of treatment and management?

A

•Reduce pain/stiffness, prevent further joint damage, Improve QoL –
combined approach

24
Q

what is the types of non-pharmacological treatment for OA?

A
  • Exercise and manual Therapy
  • Joint aids/supports
  • TENS
  • Surgical joint replacement and arthroscopic lavage
  • Nutraceuticals
25
Q

what is the pharmacological management of OA?

A
  • Paracetamol
  • NSAIDs
  • Capsaicin
  • Corticosteroids
  • Disease-Modifying Osteoarthritis Drugs (DMOADs).
26
Q

what sort of exercise and manual therapy can be done? why s this done?

A

aerobic, low impact exercise
swimming/ yoga
for weight loss and muscle strengthening

27
Q

why do you want to reduce a persons weight in OA?

A

to lessen impact on the joints

consider gastric bypass if extreme

28
Q

what joint support can be given and why?

A 
•Balance/shift load from affected 
joints - lessen impact
•Joint Supports
•Knee Braces
•Shoe Wedges
•Insoles
•Walking aids – Frames, Crutches, 
Stick
29
Q

what is a TENS machine?

A

it is a transcutaneous electrical nerve stimulation
- use as an adjunct to core treatments for pain relief
pain signals can be blocked by electrical impulses
non-invasive, fast and drug free

30
Q

when would one consider surgery for OA?

A
  • Constant or high Pain levels
  • Lack of Joint movement
  • Joint destruction
  • Impacting QoL
31
Q

what are the options for surgery?

A
  • Joint Fusing – fixed joint
  • Osteotomy – addition/removal of small bones
  • Whole Joint replacement
  • Prosthesis
  • Hip, Knee
32
Q

what are nutraceuticals?

A

Dietary supplements, particularly glucosamine, chondroitin and S-
adenosylmethionine remain both popular and controversial.

33
Q

what is the possible mechanism of neutraceuticals?

A

possibly by stimulation of chondrocytes

they produce structual components of cartliage

34
Q

how does hyaluronic acid help in the treatment of OA?

A

•Aids synovial fluid
•NOT recommended for treatment of OA
by NICE
used to be given as injections

35
Q

what is the first line treatment for OA?

A

Paracetamol as the first line treatment –
debatable effects..!!
•Prescribe ahead of NSAIDs

36
Q

what is 3rd line treatment when pain relief with paracetamol is insufficent?

A

consider opioids in combination
- co-codamol
must consider risk benefit- addiction/ withdrawl strategy

37
Q

what NSAIDS are typcially used for treatment?

A

•COX-2 inhibitors (see Mark Gray Lecture)
•Consider Topical NSAIDs over oral (long term use)
•Typically Ibuprofen/Naproxen
lowest dose for shortest time

38
Q

why is naproxen favoured?

A

•Vascular and cardiovascular events on the increase with coxib,
diclofenac, ibuprofen
•Naproxen associated with less vascular risk than other NSAIDs

39
Q

why is topical capsaicin found useful?

A 
Repetitive administrations of 
capsaicin produces a desensitization 
and an inactivation of sensory 
neurons. 
•Transient receptor potential vanilloid 
1 (TRPV1) is a ligand-gated cation 
channel selectively expressed in nerve 
fibres,
40
Q

what is capsaicin?

A

Capsaicin is an active component of

chili peppers, analgesic properties

41
Q

when are corticosteroids used as OA treatment?

A

Intra-articular injections for moderate to severe pain

42
Q

what drug is used for corticosteroid injections and how often are they given?

A
  • Hydrocortisone
  • Dexamethasone
  • Prednisolone
  • Injected once every 3 months

PHA 332 (42 decks)

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