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
What is included in the primary prevention of OP?
Lifestyle changes: - Adequate Ca and Vit D - Weight bearing exercise - Reduced alcohol intake - Stop smoking - Reduce risk of falls esp in elderly
26
What is included in the secondary prevention of OP?
``` Pharmacological management: - Calcium - Vit D - Calcitriol - HRT - SERMS - Bisphosphonates - Calcitonin - Strontium - PTH - Denosumab In addition to lifestyle changes ```
27
What is Osteoarthritis?
Disease of wear and tear - usually limited to one or two joints (differs from rheumatoid arthritis)
28
What groups of people are affected by Osteoarthritis?
- Over 65s - Onset most common at 40-60 yrs - More common in women - Common in obesity
29
What are the clinical features of OA?
- 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
What happens in OA (pathogenesis)?
- 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
What is the difference between a normal joint and a joint with mild OA?
- 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
What happens to a joint with severe OA?
Bone can touch opposing bone and is very painful, needs joint replacement
33
What are the goals for management of OA?
- Reduce pain - Optimise mobility (encourage weight loss and exercise) - Minimise joint deformity - Patient education - Multidisciplinary approach
34
What non-pharmacological management is there for OA?
- Weight reduction - Physiotherapy - Exercise plan - Heat or cold packs - Occupational therapy review - Psychological support - Surgery
35
What is some pharmacological management for OA?
- Simple analgesics - NSAIDs – only if inflammation present - Corticosteroids – not oral, only injections - Chondroprotective agents
36
What is Rheumatoid arthritis?
- 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
What are the clinical features of RA?
- 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
What are the Extra-articular symptoms of RA?
- 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
What is the pathogenesis of RA?
- Lymphocytes infiltrate synovial membrane, causing inflammation & thickening - Formation of pannus over cartilage causes erosion into bone - Eventual degeneration of cartilage & joint
40
What are the goals of management for RA?
- Relief of pain & inflammation - Prevention of joint damage - Preservation/improvement of functional ability - Maintenance of lifestyle - Multidisciplinary approach
41
What is the pharmacological management of RA?
- Analgesics - NSAIDs - Conventional DMARDs – methotrexate, sulfasalazine - Biological DMARDs – injection, much better at managing condition - Steroids