Osteoarthritis, Crystal arthritis and Soft Tissue Rheumatism Flashcards

1
Q

What is osteoarthritis?

A

Articular cartilage thinning or loss

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2
Q

Is osteoarthritis a consequence of aging?

A

Yes

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3
Q

What are some risk factors for osteoarthritis?

A
Age
Female
Obesity
Previous injury
Muscle weakness
Proprioceptive deficits
Genetic elements
Acromegaly
Joint inflammation
Crystal deposition in cartilage
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4
Q

What is the pathogenesis of OA?

A
  1. Normal joint - healthy cartilage is lubricated by synovial fluid
  2. OA causes the cartilage to begin breaking down, making it thinner and then creating cracks in the surface
  3. Gaps in the cartilage can expand until they reach the bone
  4. Synovial fluid leaks into cracks which form in the bones surface when the replacement cartilage wears away. This causes further damage and can lead to cysts or bone deformities
  5. If not treated, damage can progress to the point where the bones in the joint become permanently deformed
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5
Q

What are the two types of OA?

A

Idiopathic

Secondary

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6
Q

What can OA be secondary to?

A

Previous injury
Calcium crystal deposition disease
Rheumatoid arthritis

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7
Q

At what sites is OA likely to occur?

A
Hip
Knee
Foot (mtp joints)
Cervical spine
Lumbar spiner
Hand - DIP, PIP, IP, MCP, CMC
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8
Q

What are the symptoms of OA?

A

Pain - worse on activity, relieved by rest (mechanical pain)

Stiffness - Morning usually lasts less than 30 minutes

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9
Q

What would be seen on examination of OA?

A

Crepitus
Joint swelling - bony enlargements due to osteophytes
Joint tenderness
Joint effusion

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10
Q

What are bony enlargements at the DIPs called?

A

Heberdens nodes

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11
Q

What are bony enlargements at the PIPs called?

A

Bouchards nodes

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12
Q

What else may be seen in the hands of an OA patient?

A

Squaring of the hand

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13
Q

What may be seen in the knee of an OA patient?

A
Osteophytes 
Effusions
Crepitus
Restriction of movement
Genu varus 
Valgus deformities
Bakers cyst
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14
Q

What may be seen in the hip of an OA patient?

A

Pain in groin or radiating to knee
Pain in hip from lower back
Restricted hip movements

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15
Q

What may be seen in the spine of an OA patient?

A

Cervical - pain and restriction of neck movement
Lumbar - Pain on standing or walking for some time
Spinal stenosis

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16
Q

How is OA diagnosed?

A

Clinical + Radiological

  • Loss of joint space
  • Subchondral sclerosis
  • Subchondral cysts
  • Osteophytes
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17
Q

What are the categories for the Kellgren-Lawrence Radiographic grading scale of osteoarthritis?

A

Grade 0 - No radiographic findings of OA
Grade 1 - Minute osteophytes of doubtful significance
Grade 2 - Definitive osteophytes with unimpaired joint space
Grade 3 - Definitive osteophytes with moderate joint space narrowing
Grade 4 - Definitive osteophytes with severe joint space narrowing and subchondral sclerosis

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18
Q

Do symptoms of OA tend to improve?

A

Yes - not fully however

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19
Q

What is the non-pharmacological management of OA?

A

Explanation - not because of normal use
Physiotherapy - Muscle strengthening
Common sense measures - weight loss, exercise, trainers, walking stick, insoles

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20
Q

What is the pharmacological management of OA?

A

Analgesia - Paracetamol, compound analgesics, topical analgesia
NSAIDs - topical/systemic, may give additional symptomatic relief, consider risk/benefit ratio
Pain modulators - Tricyclics (amitriptyline, anti-convulsants)
Intra-articular - steroids

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21
Q

What is the surgical management of OA?

A

Arthroscopic washout, loose body, soft tissue trimming

Joint replacement

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22
Q

What is gout?

A

Inflammation in the joint triggered by uric acid crystals

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23
Q

What two factors contribute to purine levels?

A

Diet

DNA/RNA

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24
Q

What can lead to increased uric acid levels?

A

Excess consumption
Over production
Under excretion

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25
Q

What is the clinical level for hyperuricaemia?

A

> 0.42mmol/l

26
Q

What are some reasons for increased urate production?

A
Inherited enzyme defects
Psoriasis
Haemolytic disorders
Alcohol
High dietry intake
27
Q

What are some reasons for reduced urate excretion?

A
Chronic renal impairment 
Volume depletion
Hypothyroidism
Diuretics
Cytotoxics
28
Q

What gender does gout affect more?

A

Men

29
Q

How many joints does Acute gout usually affect?

A

Just one

30
Q

What are the three most commonly affected joints by acute gout?

A

MTP
Ankle
Knee

31
Q

How long does acute gout take to settle?

A

10 days without treatment

3 Days with treatment

32
Q

What are the characteristics of acute gout?

A

Abrupt onset
Often overnight
May have normal uric acid

33
Q

What is chronic tophaceous gout?

A

Chronic joint inflammation

34
Q

What is chronic tophaceous gout associated with?

A

Diuretics
High serum uric acid
Tophi
May have acute attacks

35
Q

What are the investigations for chronic tophaceous gout?

A
Raised inflammatory markers
Serum uric acid raised
Synovial fluid 
Renal impairment
X-ray
36
Q

What will polarising microscopy show in gout synovial fluid?

A

Needle shaped negatively birefringent crystals

37
Q

What is the acute treatment for chronic tophaceous gout?

A

NSAIDs
Colchicine
Steroids

38
Q

What is the prophylaxis treatment for chronic tophaceous gout?

A

Allopurinol

Febuxostat

39
Q

When should prophylaxis be started for chronic tophaceous gout?

A

2-4 weeks after acute attack

40
Q

What are the two types of calcium pyrophophate deposition disease?

A

Calcium pyrophosphate

Calcium hydroxyappatite crystals

41
Q

What age group is CPPD common in?

A

The elderly

42
Q

Where does CPPD affect?

A

Fibrocartilage

  • Knees
  • Wrists
  • Ankles
43
Q

What happens to chondrocalcinosis with age?

A

Increases with age

44
Q

What are acute attacks of CPPD caused by?

A

Calcium pyrophosphate crystals (pseudogout)

45
Q

What shape are calcium pyrophosphate crystals?

A

Envelope shaped

Mildly positive birefringent

46
Q

What happens to the inflammatory markers in CPPD?

A

Marked rise

47
Q

What are the associations in CPPD?

A
Hyperparathyroidism
Hypercalcaemia
Haemochromotosis
Hypomagnesia
Hypothyroidism
Gout
Neuropathic joints
Aging
Amyloidosis
Trauma
48
Q

What is the treatment for CPPD?

A

NSAIDs
Colchicine
Steroids
Rehydration

49
Q

What does hydroxyapatite cause?

A

Milwaukee shoulder

50
Q

What are the characteristics of hydroxyapatite deposition?

A

Release of collagenases, serine proteinases and IL-1
Acute and rapid deterioration
Females
50-60 years

51
Q

What is the treatment for hydroxyapatite deposition/

A

NSAIDs
Intra-articular steroid injection
Physiotherapy
Partial or total arthroplasty

52
Q

What is soft tissue rheumatism the general term to describe?

A

Pain that is caused by inflammation/damage to the ligaments, tendons, muscles or nerve near a joint

53
Q

Is the pain in STR localised or general?

A

Localised

54
Q

What should you consider with generalised soft tissue pain?

A

Fibromyalgia

55
Q

What should be considered with neck pain?

A

Muscular
Self-limiting
OA of cervical spine
Occipital migrane

56
Q

Where is the commonest area for soft tissue pain?

A

Shoulder

57
Q

What are causes of shoulder pain?

A
Adhesive capsulitis
Rotator capsulitis
Calcific tendonitis 
Impingement
Partial rotator cuff tears
Full rotator cuff tears
58
Q

What are possible diagnoses for Elbow, wrist, pelvis and foot pain?

A

Elbow - medial and lateral epicondylitis
Wrist - De-Quervains tenosynovitis
Pelvis - Trochanteric, iliopsoas, ischiogluteal bursitis and stress enthesopathies
Foot - plantar fascitis

59
Q

What are the investigations and treatment for STR?

A
X-ray
MRI
Pain control
Rest and Ice
PT
Steroid injections
Surgery
60
Q

What gender and age does joint hypermobility syndrome usually affect?

A

Females

Childhood

61
Q

What is the modified brighton score?

A

Testing hypermobility

62
Q

What are features of hypermobility?

A

Arthralgia
Premature osteoarthritis
Normal investigations