Introduction to joint disease Flashcards

1
Q

When does osteoporosis increase in prevalence?

A

as age increases - starts very early on in life, lots of intervention available

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2
Q

What group of people does osteoporosis primarily affect?

A

Women after the menopause (decrease in oestrogen)

*can also affect men

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3
Q

What fractures are most common in osteoporosis?

A

Hip, wrist and spine (hip fractures are main problem - high bed occupancy and mortality)

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4
Q

What is the thick outer shell of bone called?

A

cortex

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5
Q

What is the meshwork of bone inside cortex called?

A

trabecular bone

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6
Q

What happens to the trabecular bone in osteoporosis?

A

Becomes more holey and weaker

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7
Q

What builds new bone?

A

Osteoblasts

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8
Q

What breaks down old bone? (resorption)

A

Osteoclasts

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9
Q

What is Osteoporosis caused by?

A

Reduced osteoBLAST activity and increased osteoCLAST activity (bone is being broken down quicker than its being remodelled )

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10
Q

What peak bone mass do patients with osteoporosis have?

A

low peak bone mass between 25 and 40 yrs and then 1% lost per year

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11
Q

What is the WHO definition for osteoporosis?

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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12
Q

How long does it take for bone to be remodelled?

A

100 days

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13
Q

What is bone turnover influenced by?

A

Hormones (oestrogen/testosterone), cytokines and prostaglandins

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14
Q

What are the phases in bone remodelling?

A
Resorption 
Reversal Phase 
Formation
Resting Phase 
Activation
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15
Q

What are the signs and symptoms of osteoporosis?

A
  • Fracture (usually first presentation)
  • Reduced bone density on DXA scan
  • Pain
  • Reduced mobility
  • Kyphosis - in vertebral fractures, curving of the spine
  • Reduction in height
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16
Q

What are the problems that come with vertebral fractures?

A
  • can result in height reduction of 10-20cm
  • often undiagnosed
  • can cause problems with indigestion, neck weakness, back pain, loss of mobility
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17
Q

How is Bone Mass Density determined?

A

by DEXA scan

18
Q

When do you have peak bone mass?

A

Between 25 and 40 yrs and then Post maturity bone loss of 0.5-1% / year

19
Q

What do women in menopause have regarding bone mass?

A

Accelerated bone loss around menopause due to loss of protective effect of oestrogens - important to have a diet rich in calcium and vitamin D

20
Q

When are DXA scans used?

A

Only for high risk patients / those with established OP

21
Q

What do DXA scans measure?

A

Usually measures bone density at hip/lower spine to get a “T score”

22
Q

What T score indicated Osteoporosis?

A

Less than or equal to -2.5

23
Q

What can portable DXA scanners scan?

A

ankle - not as reliable

24
Q

What are the risks factors for OP?

A
  • History of fracture (and/or in 1st degree relative)
  • Smoking
  • Low body weight (bone density is reduced)
  • Female
  • Oestrogen deficiency
  • Corticosteroid use (prednisolone ≥ 7.5mg daily for 3/12 or more)
  • White race
  • Increase age
  • Low calcium intake
  • Excess alcohol
  • Lack of exercise
  • Recurrent falls
  • Dementia
  • Impaired eyesight
  • Poor health/fraility - especially RA, renal disease, liver disease, IBD
25
Q

What is included in the 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
26
Q

What is included in the secondary prevention of OP?

A
Pharmacological management:
 - Calcium
 - Vit D
 - Calcitriol
 - HRT
 - SERMS
 - Bisphosphonates
 - Calcitonin
 - Strontium
 - PTH
 - Denosumab
In addition to lifestyle changes
27
Q

What is Osteoarthritis?

A

Disease of wear and tear - usually limited to one or two joints (differs from rheumatoid arthritis)

28
Q

What groups of people are affected by Osteoarthritis?

A
  • Over 65s
  • Onset most common at 40-60 yrs
  • More common in women
  • Common in obesity
29
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 (early morning stiffness) up to 30 mins
30
Q

What happens in OA (pathogenesis)?

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
31
Q

What is the difference between a normal joint and a joint with mild OA?

A
  • Normal: bone and cartilage protecting bone, meniscus is extra protection. Synovium is membrane
  • Mild OA: bone underneath becomes thicker and starts to wear away cartilage. Inflammation occurs
32
Q

What happens to a joint with severe OA?

A

Bone can touch opposing bone and is very painful, needs joint replacement

33
Q

What are the goals for management of OA?

A
  • Reduce pain
  • Optimise mobility (encourage weight loss and exercise)
  • Minimise joint deformity
  • Patient education
  • Multidisciplinary approach
34
Q

What non-pharmacological management is there for OA?

A
  • Weight reduction
  • Physiotherapy
  • Exercise plan
  • Heat or cold packs
  • Occupational therapy review
  • Psychological support
  • Surgery
35
Q

What is some pharmacological management for OA?

A
  • Simple analgesics
  • NSAIDs – only if inflammation present
  • Corticosteroids – not oral, only injections
  • Chondroprotective agents
36
Q

What is Rheumatoid arthritis?

A
  • Systemic condition that can affect many joints in many ages
  • Onset most common at 30-50 yrs
  • Reduced life expectancy
  • Female:Male = 3:1
37
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
  • Pain tends to decrease as day progresses
38
Q

What are the Extra-articular symptoms of RA?

A
  • Sjorgen’s syndrome – drying of secretions e.g. dry eyes/mouth
  • Vasculitis – inflammatory condition of blood vessels
  • Neuropathy
  • Subcutaneous nodules
  • Lymphadenopathy
  • Cardiovascular disease
  • Depression
  • Respiratory disease
39
Q

What is the pathogenesis of RA?

A
  • Lymphocytes infiltrate synovial membrane, causing inflammation & thickening
  • Formation of pannus over cartilage causes erosion into bone
  • Eventual degeneration of cartilage & joint
40
Q

What are the goals of management for RA?

A
  • Relief of pain & inflammation
  • Prevention of joint damage
  • Preservation/improvement of functional ability
  • Maintenance of lifestyle
  • Multidisciplinary approach
41
Q

What is the pharmacological management of RA?

A
  • Analgesics
  • NSAIDs
  • Conventional DMARDs – methotrexate, sulfasalazine
  • Biological DMARDs – injection, much better at managing condition
  • Steroids