joint disease Flashcards

1
Q

what is osteoporosis?

A

Osteoporosis is becoming more prevalent as we are getting an ageing population, it is a disease of age but it does start early in life.
There are things we can do in school years to prevent the affects of osteoporosis.
 osteoporosis is a generalized skeletal disorder of low bone mass (thinning of the bone) and deterioration in its architecture, causing susceptibility to fracture.

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2
Q

what is the epidemiology of OP?

A

> 30,000 fractures a year
£3 billion to NHS a year
- 1 in 2 women over 50 years will have OP
- 1 in 5 men over 50 will

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3
Q

what is the pathogenesis/

A

• Thick outer shell of bone = cortex
• Meshwork of bone inside cortex = trabecular bone this is what becomes weaker as you develop it which means it is more likely to fracture
• Bone constantly turned over/ remodeled
o Takes around 3 months to remodel
• Osteoblasts build new bone
• Osteoclasts break down old bone (resorption)

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4
Q

what cayses OP?

A

o increased osteoclast activity this means bone is being broken down quicker than it can be remodeled, so we want to try and rebalance this to make sure you have bone less likely to fracture
o low peak bone mass – 25-40 years old and after this you lose about 1% of bone mass a year

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5
Q

what are the signs and symptoms of OP/

A
  • Fracture- usually first presentation
  • Reduced bone density on DXA scan - high intensity scan calculates to determine if the bone is weaker. Very expensive and don’t have them everywhere. Only scan the high risk patients
  • Pain
  • Reduced mobility
  • Kyphosis- in vertebral fractures. Spine starts to curve and this is the first indication they have it. Can cause loss of height and indigestion – this is because there is an increase of pressure
  • Reduction in height
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6
Q

what are vertebral fractures?

A
  • Can result in height reduction of 10-20cm
  • Often underdiagnosed
  • Can cause problems with indigestion, neck weakness, back pain, loss of mobility
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7
Q

what is bone density?

A

changes throughout life with a peak around 25-40 years.

post maturity you lose 0.5-1% a year

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8
Q

what are DXA scans?

A

onlu used for high risk patients or those with OP

usually measure bone density at hip or lower spine

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9
Q

what is a T score/

A

measure the risk of chance of developing OP

T score<2.5

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10
Q

what are the risk factors of OP?

A
history
smoking
low body weight
female
oestogren defiency
coricosteroid use
low calcium intake
excess alcohol
lack of excerise
dementia
recurrent falls
impaired eyesight
white race
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11
Q

what is primary prevention of OP?

A
–	Adequate Ca and Vit D
–	Weight bearing exercise
–	Reduced alcohol intake
–	Stop smoking
–	Reduce risk of falls esp in elderly
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12
Q

what is secondary prevention of OP?

A
–	Calcium
–	Vit D
–	Calcitriol
–	HRT
–	SERMS
–	Bisphosphonates
–	Calcitonin
–	Strontium
–	PTH
–	Denosumab
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13
Q

what is osteoarthritis?

A

disease of wear and tear and is usually limited to 1-2 joints and associated with increased use and abuse of the joint

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14
Q

what is the epidemoilogy of OA?

A
  • Overall affects 2%
  • > 65yrs – affects 12%
  • Onset most common at 40-60yrs
  • More common in women
  • Obesity increases risk
  • Unknown aetiology
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15
Q

what are the clinical features of OA?

A
  • Joint pain, worsened on movement and at end of day
  • May be accompanied by swelling
  • Most common in knee, hands, lumbar & cervical spine
  • EMS up to 30 mins
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16
Q

what is the pathogenesis of OA?

A
  • Cartilage gradually roughens and becomes thin
  • Thickening of underlying bone
  • Formation of osteophytes
  • Thickening & inflammation of synovium
  • Thickening and contraction of ligament
  • Some joints repair themselves, others don’t
17
Q

what is severe OA?

A

two bones move closr together - sometimes even touch and this is very painful.
there is no synovial fluid to lubricate the joint and help it move and this is when you can have a life long permeant deformity

18
Q

what are the goals of management of OA?

A
  • Reduce pain
  • Don’t always want to use painkillers as don’t want them dependant on opiods
  • Optimise mobility
  • Minimise joint deformity
  • Patient education
  • Multidisciplinary approach
  • Physio, drs, pharmacists
19
Q

what are the non-pharmacological managements of OA?

A
  • Weight reduction
  • Physiotherapy
  • Exercise plan
  • Heat packs / cold packs – on affected area
  • Occupational therapy review – help with advice on how to manage at home
  • Psychological support
  • Surgery
20
Q

what is pharmacological management of OA?

A
  • Simple analgesics
  • NSAIDs – if we know there is inflammation of the joint as they don’t always have it
  • Corticosteroids – into the joint
  • Chondroprotective agents
21
Q

wnat is rheumatoid arthritis?

A

– Systemic condition which can affect many joints and all ages.
– Juvenile arthritis – younger affected
– Need to approach to management very differently as you have a lot more options as it is an autoimmune condition

22
Q

what is the epideimology of RA?

A

• Affects 1-3% population
• Onset most common at 30-50yrs but can affect any age.
• Reduced life expectancy
o Increased risk of heart problems and liver problems
• Female:male=3:1
• Unknown aetiology

23
Q

what are the clinical features of RA?

A
  • Slow progressive symmetrical polyarthritis
  • Pain & stiffness in small joints of hands & feet
  • Involvement of wrists, shoulders, elbows, knees & ankles
  • Early morning stiffness (EMS) – can progress throughout the day can take them to lunch time to get moving
  • The pain usually gets better throughout the day but stiffness increases
24
Q

what are extra-articular symptoms of RA?

A
  • Sjorgen’s syndrome
  • Vasculitis – inflammatory conditions of blood vessels
  • Neuropathy – circulation problems
  • Subcutaneous nodules – painful build up of tissues
  • Lymphadenopathy – wide spread
  • Cardiovascular disease
  • Depression – chronic codnition
  • Respiratory disease
25
Q

what is the pathogenesis of RA?

A
  • Lymphocytes infiltrate synovial membrane, causing inflammation & thickening
  • Formation of pannus over cartilage causes erosion into bone – permeant joint damage
  • Eventual degeneration of cartilage & joint
26
Q

what is severe RA?

A
  • Reduction in the amount of fluid – so reduced lubrication of the joints
  • Drs are looking for erosions as if they already have these there is nothing you can do to reverse this
  • You want to get to spot it before erosion so you can prevent it
27
Q

what are the goals of management of RA?

A
  • Relief of pain & inflammation
  • Prevention of joint damage
  • Preservation/improvement of functional ability
  • Maintenance of lifestyle
  • Multidisciplinary approach
28
Q

what are the pharmacological management?

A
  • Analgesics
  • NSAIDs
  • Conventional DMARDs – methotrexate and sulphsalzamine
  • Biological DMARDs – these are changed the way the condition has been managed. Injection control the condition – but have a lot more issues
  • Steroids – tablet, injection into joint to help when people have flare ups
29
Q

what is the summary of OA and RA?

A
OA
•	Restricted to joints
•	Occasional warm,tender,swollen joints
•	?raised inflammatory markers
•	Rarely severe joint deformities
•	Affects 50yrs onwards
RA
•	Systemic disease
•	Multiple joint involvement
•	Usually warm,tender,swollen joints
•	Raised inflammatory markers
•	Often joint deformities
•	Many extra-articular symptoms
•	Affects any age
30
Q

what are the 3 main treatments for RA?

A
  • hydrocholoroquine
  • methotrexate gold standard best treatment first line if they are postiive for RA
  • sulfasalazine
31
Q

what are the counselling points for methotrexate?

A

only taken once a week due to its toxic in high doses

  • PPP must not be pregnant or get pregnant when on this
  • usually 10mg a week bought up to 20mg
  • takes around 12 weeks to kick in
  • can affect eyesight
  • blood check needed
  • may cause a skin rash
32
Q

what are the counselling points for hydrochloroquinine?

A
  • can cause a skin rash and make your skin more sensitive
  • dont take with indigestion remedies as it stops absoroption
  • can affect eyesight
33
Q

what are the key counselling points for sulfasalzine?

A

good as methotrexate but jsut isnt a first line - usually after a failed course

  • oral with a dose increase over a few weeks so you tolerate the doses
  • can cause GI disturbances
  • take with a meal so you have protection on stomach
  • causes urine discolouration
  • can stain contact lenses
  • need regular blood checks
  • rash - if you see this stop treatment immediately
  • takes around 12 weeks to start
  • can be taken with pregancny
34
Q

what do you use if you have two failed treatments?

A

biologics

35
Q

what does a DAS score need to be over to be able to start treatment?

A

5.1

36
Q

what is an advantage of a biologic DMARD?

A
  • quicker treatment
  • more effective
  • reverse joint damage
  • can be an injection given at home
37
Q

what are disadvantages of biologic DMARDs?

A
  • expensive
  • increase risk of cancer
  • increase risk of neurological disease
  • increase infection risk
38
Q

what screening must be done before you start a biologic DMARD?

A
  • chest x-ray
  • infection check
  • WBC count
  • signs of malignancy
  • screen for pregnancy
  • recent travel abroad
  • histroy of heart disease
39
Q

what are examples of biologic DMARD?

A
  • etanercept
  • infliximab
  • adalimumab
  • rituximab