Joint disease Flashcards

1
Q

Epidemiology of osteoporosis?

A
  • In UK, OP results in > 300,000 fractures/year
  • Cost to NHS=>3 billion/ year
  • Hip fractures main problem- high bed occupancy and mortality
  • Of 230,00 fractures / year: 70,000 hip, 120,000 spine (largely go unnoticed so don’t get admitted), 50,000 wrist
  • 1 in 2 women>50yrs – may not develop a fracture but will have the disease
  • 1 in 5 men>50yrs
  • 3 million in UK
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2
Q

Hip fracture epidemiology?

A

Hip fractures: associated with prolonged hospital admission- 20% die within 6/12 from complications such as hospital acquired infection / VTE
Over half of the people with have serious mobility issues and this may mean they need to adapt there way of life such as move to a care home

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3
Q

Pathogenesis of OP:

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
  • Takes around 3 months to remodel
  • Osteoblasts build new bone
  • Osteoclasts break down old bone (resorption)
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4
Q

OP caused by?

A

OP caused by: reduced osteoblast activity 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

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5
Q

Peak bone mass?

A

Peak bone mass – 25-40 years old and after this you lose about 1% of bone mass a year

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6
Q

WHO definition of OP?

A

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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7
Q

Bone turnover influenced by ________:

A

Hormones ( oestrogen/ testosterone), cytokines, prostaglandins

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8
Q

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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9
Q

Vertebral fractures factors:

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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10
Q

Notes on trends in bone density?

A
  • Peak bone mass at around 25 years
  • After 40 yrs, loss of 0.5-1% bone density / year
  • Women have accelerated bone loss around menopause due to loss of protective effect of oestrogens
  • Important to have healthy balanced diet / weight bearing exercise early on in life to optimise peak bone mass
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11
Q

What are DXA scans?

A
  • Only for high risk patients / those with established OP
    Usually measures bone density at hip / lower spine to get a “T score”
  • T score of ≤ -2.5 = osteoporosis
  • Portable DXA scanners scan ankle- not as reliable as scanning hip / lower spine
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12
Q

Risk factors for OP?

A
  • Hx of fracture
  • Hx of fracture in 1st degree relative
  • Smoking
  • Low body weight – eating disorders increase the risk of - OP as bone density reduces
  • Female
  • Oestrogen deficiency
  • Corticosteroid use- prednisolone ≥ 7.5mg daily for 3/12 or more
  • White race
  • Increase age
  • Low calcium intake
  • XS alcohol
  • Lack of exercise
  • Recurrent falls
  • Dementia
  • Impaired eyesight
  • Poor health/ frailty- especially RA, renal disease, liver disease, IBD
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13
Q

Primary prevention of OP?

A

Lifestyle changes:

  • Adequate Ca and Vit D
  • Weight bearing exercise
  • Reduced alcohol intake
  • Stop smoking

Reduce risk of falls esp in elderly

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14
Q

Secondary prevention of OP?

A

Pharmacological management:

  • Calcium
  • Vit D
  • Calcitriol
  • HRT
  • SERMS
  • Bisphosphonates
  • Calcitonin
  • Strontium
  • PTH
  • Denosumab
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15
Q

Osteoarthritis (OA) epid.?

A
  • Overall affects 2%
  • > 65yrs – affects 12%
  • Onset most common at 40-60yrs
  • More common in women
  • Obesity increases risk
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16
Q

Aetiology of OA?

A

Unknown

17
Q

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 (early morning stiffness) up to 30 mins
18
Q

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
19
Q

What is the synovial and synovial fluid?

A

Synovium = membrane that encases everything

Synovial fluid= lubricant

20
Q

What is severe OA?

A

Two bones move closer together – you can get the bone touch and this will be very painful - no lubricant to help the joint move well and at this point you can have deformity of the joint which can be permeant

21
Q

Goals of management : 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)
22
Q

Non-pharmacological management 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
23
Q

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 – injected into the joint
  • Chondroprotective agents
24
Q

Rheumatoid Arthritis(RA) epide.?

A
  • Affects 1-3% population
  • Onset most common at 30-50yrs but can affect any age.
  • Reduced life expectancy
  • Increased risk of heart problems and liver problems
  • Female:male=3:1
  • Unknown aetiology
25
Q

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
26
Q

Extra-articular symptoms of RA?

A
  • Sjorgen’s syndrome - dry eyes and mouth
  • 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
27
Q

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
28
Q

Goals of management : RA?

A
  • Relief of pain & inflammation
  • Prevention of joint damage
  • Preservation/improvement of functional ability
  • Maintenance of lifestyle
  • Multidisciplinary approach
29
Q

Pharmacological management of RA?

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
30
Q

Summary: OA vs. 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
31
Q

Outline the key counselling points that should be discussed with Mrs RF before starting methotrexate and hydroxychloroquine?

A

HCQ = can damage retina therefore, need regular eye checks (you get referred to the eye hospital to get an eye review annually if you are on HCQ long term). Eye damage is reversible.

  • One tablet twice a day (can be dropped down to OD)
  • Up to 3 weeks to take effect

MT = once a week (same day). Folic acid needed because it helps reduce some of the side effects of MT but must be taken a couple of days after MT as it can reduce effectiveness of MT.

  • SE’s – sickness, lower RBC and WBC count, alcohol intake reduced
  • Vaccinations may be needed (avoid live due to immunocompromisation)
  • Should not become pregnant whilst on MTX, need adequate contraception, Need to wait 3 months between stopping and trying for pregnancy.
  • Avoid – aspirin, trimethoprim, and septrin.
  • Monitoring: FBC, LFT’s, U&E’s
32
Q

Outline the key counselling points that should be discussed with Mrs RF before starting sulfasalazine?

A
  • Increased risk of infection (not as much as MTX)
  • Stains contact lenses
  • Orange urine (almost to the point it looks like passing blood)
  • Regular blood checks
  • Explain how it works, explain that it isn’t a pain killer
  • Up to 3 months to take effect
  • Indigestion
  • Rash – stop immediately and contact rheum team
  • Safe to conceive
33
Q

Possible treatment options for sulfasalazine is ineffective?

A
  • Biologic is DAS score adequate

- Entanacept (works on TNF)

34
Q

Describe two advantages and two disadvantages of biologic DMARD’s compared with non-biologic DMARDS.

A

Adv:

  • Work quicker (within 2 weeks you can see improvement)
  • More specific
  • Generally better tolerated

Disadv:

  • More expensive
  • Can increase risk of skin cancer and blood borne cancers.
  • Only been around for 10-15 years, long term side effects aren’t clear
  • Self admin – patient acceptability
35
Q

Outline pre-screening checks that must be completed before starting biologic treatment for RA:

A
  • TB vaccination
  • Hep B
  • Hep C
  • HIV
  • LFT’s
  • Cancer pre-screening: history and if up to date with mammograms and cervical screening
  • Recent travel abroad
  • History of heart disease
  • Exclude pregnancy
36
Q

How would etanercept be administered?

A
  • Subcutaneous injection. Once or twice a week
  • Can be done at home – injections supplied via specialist through a home care company who are a third party who will receive Rx’s from specialist centres which are checked and dispensed and delivered to the patient. Will also organise a nurse to go out and train the person on self admin.
37
Q

2) What options are available to Mr CP if etanercept becomes ineffective?

A
  • Depends on the patient/cost etc
  • Rituximab – acts on B cells – given by intravenous infusion, has to be done in hospital, one dose every two weeks
  • Infliximab
  • Rituximab in combination with methotrexate is recommended as an option for the treatment of adults with severe active rheumatoid arthritis who have had an inadequate response to, or are intolerant of, other DMARDs, including at least one TNF inhibitor.
  • Treatment with rituximab should be given no more frequently than every 6 months.