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Phase2a > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is rheumatology?

A

The medical management of musculoskeletal disease.

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2
Q

Give two rough categories that joint pain can be divided into.

A
  • Inflammatory

- Non-inflammatory

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3
Q

Give three examples of inflammatory joint problems.

A
  • Autoimmune
  • Crystal arthritis
  • Infection
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4
Q

Give three examples of autoimmune rheumatological diseases.

A
  • Rheumatoid arthritis
  • Spondyloarthropathy
  • Connective tissue disease
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5
Q

Give an example of a degenerative rheumatoid condition.

A

Osteoarthritis

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6
Q

Give an example of a non-degenerative, non-inflammatory rheumatoid condition.

A

Fibromyalgia

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7
Q

Compare the pain in inflammatory and degenerative rheumatological conditions.

A 
INFLAMMATORY = eases with use
DEGENERATIVE = increases with use, clicks/clunks
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8
Q

Compare the stiffness in inflammatory and degenerative rheumatological conditions.

A 
INFLAMMATORY = Significant (>60mins), early morning, at rest (evening)
DEGENERATIVE = Not prolonged (<30mins), morning/evening
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9
Q

Compare the swelling in inflammatory and degenerative rheumatological conditions.

A 
INFLAMMATORY = Synovial +/- bony
DEGENERATIVE = No synovial, bony
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10
Q

Compare the inflammation in inflammatory and degenerative rheumatological conditions.

A 
INFLAMMATORY = may be hot and red
DEGENERATIVE = Not clinically inflamed
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11
Q

Compare the patient demographics in inflammatory and degenerative rheumatological conditions.

A 
INFLAMMATORY = young, psoriasis, family history
DEGENERATIVE = older, prior occupation, sport
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12
Q

Compare the joint distribution in inflammatory and degenerative rheumatological conditions.

A 
INFLAMMATORY = hands and feet
DEGENERATIVE = 1st CMCJ, DIPJ, knees
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13
Q

Compare the NSAID response in inflammatory and degenerative rheumatological conditions.

A 
INFLAMMATORY = good response
DEGENERATIVE = Less convincing
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14
Q

Describe the pattern of pain in bone pain.

A

Pain at rest and at night.

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15
Q

Give three things that can cause bone pain.

A
  • Tumour
  • Infection
  • Fracture
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16
Q

Describe the pattern of pain in inflammatory joint pain.

A

Pain and stiffness in joints in the morning, at rest, and with use.

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17
Q

Give two things that can cause inflammatory joint pain.

A
  • Inflammatory

- Infective

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18
Q

Describe the pattern of pain in osteoarthritis.

A

Pain on use and at the end of the day.

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19
Q

Describe the pattern of pain in neuralgic pain.

A

Pain and paraesthesia in dermatomal distribution worsened by specific activity.

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20
Q

What causes neuralgic pain?

A

Root or peripheral nerve compression

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21
Q

Describe the pattern of pain in referred pain.

A

Pain unaffected by local movement.

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22
Q

If the distal interphalangeal joint is involved in a rheumatological disorder, what are the two potential diagnoses?

A
  • Psoriatic arthritis

- Osteoarthritis

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23
Q

How quickly does ESR rise and fall?

A

Slowly (days to weeks)

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24
Q

How quickly does CRP rise and fall?

A

Rapidly

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25
Q

Define spondyloarthritis.

A

Spondyloarthritis is an umbrella term encompassing several forms of arthritis.

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26
Q

Give seven forms of spondyloarthritis.

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
  • Enteropathic arthritis
  • Acute anterior uveiits (iritis)
  • Enthesis related juvenile idiopathic arthritis
  • Undifferentiated spondyloarthritis
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27
Q

Give a genetic factor which all of the spondyloarthropathies are related to.

A

HLA B27

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28
Q

Give three theories as to how HLA B27 causes disease.

A
  • Molecular mimicry (previous infectious agent has peptides similar to HLA)
  • Mis-folding of HLA B27 stimulates cytokines
  • Heavy chain homodimer activates T cells
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29
Q

What are the clinical features of spondyloarthritis?

A

SPINEACHE

  • Sausage digits (dactylitis)
  • Psoriasis
  • Inflammatory back pain
  • NSAIDs (good response)
  • Enthesitis (heel)
  • Arthritis (may be asymmetrical oligoarthritis)
  • Crohn’s/Colitis/CRP elevated
  • HLA B27
  • Eye (uveitis)
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30
Q

What is ankylosing spondylitis?

A

Inflammatory arthritis of the spine and rib cage.

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31
Q

Describe what happens to the vertebra in ankylosing spondylitis.

A

Patients lay down new bone in spine due to inflammation and this forms sheets of calcified ligaments.

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32
Q

In what age group does ankylosing spondylitis usually present?

A

Late teenage years/20s

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33
Q

What are the six characteristics of inflammatory back pain associated with ankylosing spondylitis?

A
  • Onset below 40yrs
  • Insidious onset
  • Lasting >3months
  • Morning stiffness
  • Improvement with exercise
  • Pain at night
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34
Q

Give two signs of ankylosing spondylitis which can be seen on an XRay.

A
  • Syndesmophytes

- Sacroiliitis

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35
Q

What are syndesmophytes?

A

New bone formation and vertical growth from anterior vertebral corners.

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36
Q

What is sacroiliitis?

A

Sclerosis, erosions, loss of joint space, and fusion of the sacroiliac joint.

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37
Q

How can ankylosing spondylitis be diagnosed earlier than just using XR?

A

Inflammation and bone marrow oedema in the sacroiliac joints show up earlier on MRI.

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38
Q

Give three treatment options for ankylosing spondylitis.

A
  • Exercise
  • NSAIDs
  • Anti-TNF and Anti-IL17 drugs
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39
Q

Give a complication of ankylosing spondylitis.

A

Fusing of the spine (severe kyphosis of thoracic and vertebral spine).

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40
Q

Give the five patterns of psoriatic arthritis.

A
  • DIPJ only
  • RA like (symmetrical small joint)
  • Large joint oligoarthritis
  • Axial
  • Arthritis mutilans
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41
Q

Give two radiological changes that occur in psoriatic arthritis.

A
  • Erosive changes

- ‘Pencil in cup’ deformity in severe cases

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42
Q

Give three treatment options of psoriatic arthritis.

A
  • DMARDs (salfasalazine)
  • Anti TNF drugs (infliximab)
  • IL12/IL23/IL17 blockers
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43
Q

What is reactive arthritis?

A

Sterile inflammation of the synovial membrane, tendons, and fascia, triggered by an infection at a distant site (usually gastrointestinal or genital).

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44
Q

Give four gut infections that are associated with reactive arthritis.

A
  • Salmonella
  • Shigella
  • Yersinia
  • Campylobacter
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45
Q

Give two sexually acquired infections which are associated with reactive arthritis.

A
  • Chlamydia

- Ureaplasma urealyticum

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46
Q

Give the three classical features of reactive arthritis (also known as Reiter’s syndrome).

A
  • Arthritis (typically 2 days to 2 weeks post infection)
  • Conjunctivitis
  • (Sterile) urethritis
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47
Q

Give two signs/features associated with reactive arthritis.

A
  • Keratoderma blenorrhagica (brown raised plaques on palms and soles)
  • Circinate balanitis (painless penile ulceration, secondary to chlamydia)
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48
Q

Give three investigations that should be carried out in reactive arthritis.

A
  • Raised ESR/CRP
  • Aspirate joint to exclude infection/crystals
  • Urethral swab/stool culture
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49
Q

Give two differential diagnoses that must be excluded in reactive arthritis.

A
  • Septic arthritis

- Gout

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50
Q

What is enteropathic arthritis?

A

Episodic peripheral synovitis which occurs in up to 20% of patients with IBD.

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51
Q

What is the most common pattern of enteropathic arthritis?

A

Asymmetric lower limb arthritis

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52
Q

How is enteropathic arthritis related to the inflammatory bowel disease?

A

Arthritis usually reflects disease activity, and remission is generally related to suppression of the bowel disease.

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53
Q

Which gender is rheumatoid arthritis more common in?

A

Women

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54
Q

What is the most common age to develop rheumatoid arthritis?

A

40-60years

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55
Q

What percentage of the population does rheumatoid arthritis affect?

A

1%

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56
Q

Describe the pathology behind rheumatoid arthritis.

A
  • Tissue inflamed due to infiltration of lymphocytes, macrophages, and plasma cells
  • Synovium proliferates to form pannus, which grows over the articular cartilage
  • Pannus invades and erodes the bone
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57
Q

How do autoantibodies contribute to the development of rheumatoid arthritis?

A

Autoantibodies form immune complexes, which results in immunoglobulins and cytokines present in synovial fluid.

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58
Q

Give three methods of bone loss in rheumatoid arthritis.

A
  • Focal erosion
  • Periarticular osteoporosis
  • Generalised osteoporosis in skeleton may result from RA
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59
Q

Give two things that contribute to cartilage loss in rheumatoid arthritis.

A
  • Neutrophils release enzymes

- Pannus releases pro-inflammatory cytokines

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60
Q

What enzymes do neutrophils release which contribute to cartilage destruction in rheumatoid arthritis?

A

Matrix metalloproteinases

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61
Q

Describe the classical presenting joint pattern in rheumatoid arthritis.

A

Symmetrical, deforming, polyarthropathy

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62
Q

In >80% of cases, which parts of the body does rheumatoid arthritis affect?

A

Hands and feet

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63
Q

Describe the rate of onset in rheumatoid arthritis.

A

Usually insidious onset

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64
Q

Describe the articular symptoms in rheumatoid arthritis.

A

Early morning stiffness and pain, which may improve with activity but lasts several hours.
Loss of function, especially fine motor movements.

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65
Q

Give two systemic symptoms of rheumatoid arthritis.

A
  • Fatigue

- Malaise

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66
Q

Give five consequences of lung involvement in RA.

A
  • Pleural effusion
  • Fibrosing alveolitis
  • Rheumatoid nodules
  • Caplan’s syndrome
  • Small airways disease
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67
Q

Give three consequences of cardiac involvement in RA.

A
  • Pericardial rub
  • Pericarditis
  • Pericardial effusion
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68
Q

Give four consequences of skin involvement in RA.

A
  • Vasculitis
  • Small digital infarcts along nail beds
  • Ischaemic mononeuropathy
  • Raynaud’s phenomenon
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69
Q

Give four consequences of eye involvement in RA.

A
  • Sicca (dry eyes)
  • Seconday Sjogren’s
  • Episcleritis
  • Scleritis
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70
Q

Give two consequences of renal involvement in RA.

A
  • Amyloidosis

- Analgesic neuropathy

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71
Q

Give three consequences of nervous system involvement in RA.

A
  • Sensory peripheral neuropathy
  • Entrapment neuropathies
  • Cervical instability
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72
Q

Give four consequences of soft tissue involvement in RA.

A
  • Nodules
  • Bursitis
  • Tenosynovitis
  • Muscle wasting
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73
Q

Give three consequences of haematological involvement in RA.

A
  • Palpable lymph nodes
  • Enlarged spleen
  • Anaemia
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74
Q

What are the three aspects of Felty’s Syndrome?

A
  • Seropositive rheumatoid arthritis
  • Splenomegaly
  • Neutropenia
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75
Q

What would blood tests show in RA?

A
  • Anaemia

- High ESR/CRP

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76
Q

Give three antibodies that may appear in the serum of people with RA.

A
  • Rheumatoid factor
  • Anti-cyclic citrullinated peptide antibody
  • Anti-nuclear antibody
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77
Q

What percentage of people with RA test positive for RF?

A

70%

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78
Q

What percentage of people with RA test positive for anti-cyclic citrullinated peptide antibody?

A

80%

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79
Q

What percentage of people with RA test positive for ANA?

A

<50%

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80
Q

What percentage of people with RA are sero-negative?

A

20%

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81
Q

Which antibody is specific for RA?

A

Anti-cyclic citrullinated peptide antibody

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82
Q

What does rheumatoid factor bind to?

A

The Fc portion of IgG

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83
Q

Give the four factors that are taken into account when making a diagnosis of RA.

A
  • Joint involvement
  • Serology
  • Acute phase reactants
  • Duration of symptoms
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84
Q

Give three DMARDs that can be used to treat rheumatoid arthritis.

A
  • Methotrexate
  • Sulfasalazine
  • Hydroxychloroquine
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85
Q

Give two TNF-a inhibitors that can be used to treat RA.

A
  • Infliximab

- Enteracept

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86
Q

Give a biological agent which is used to deplete B cells in RA.

A

Rituximab

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87
Q

Give a biological agent which inhibits IL-1/IL-6 in RA.

A

Tocilizumab

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88
Q

Gives a biological agent which disrupts T cell function in RA.

A

Abatacept

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89
Q

What can be used in acute inflammation in RA?

A

Steroids (prednisolone)

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90
Q

What drugs can relieve symptoms in RA?

A

NSAIDs

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91
Q

Give two non-pharmacological management techniques for RA.

A
  • Physiotherapy

- Occupational therapy

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92
Q

Define osteoarthritis.

A

An age-related, dynamic reaction pattern of a joint in response to insult or injury.

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93
Q

Which tissue/s of the joint are involved in osteoarthritis?

A

All tissues are involved, but articular cartilage is the most affected.

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94
Q

Briefly describe the pathogenesis of osteoarthritis.

A

Metabolically active and dynamic process mediated by cytokines, and driven by mechanical forces.

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95
Q

Give three cytokines which are involved in osteoarthritis.

A
  • IL-1
  • TNF-a
  • NO
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96
Q

Give the two main pathological features of osteoarthritis.

A
  • Loss of cartilage

- Disordered bone repair

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97
Q

Name eight risk factors for osteoarthritis.

A
  • Age
  • Gender
  • Genetic predisposition
  • Obesity
  • Occupation
  • Local trauma
  • Inflammatory arthritis
  • Abnormal biomechanics
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98
Q

Why is age a risk factor for osteoarthritis?

A

Due to cumulative effect of traumatic insult and decline in neuromuscular function.

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99
Q

Describe the age distribution of osteoarthritis.

A
  • Uncommon under 45yrs

- Common over 65yrs

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100
Q

Describe how gender is a risk factor for osteoarthritis.

A
  • Affects more females, with increased prevalence after menopause
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101
Q

Give two ethnic groups that have a lower prevalence of OA hip.

A
  • Afro-Caribbean

- Asian

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102
Q

Give two ethnic groups which have a lower prevalence of OA hand.

A
  • Black African

- Malaysian

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103
Q

Describe why obesity is a risk factor for osteoarthritis.

A

Obesity is a low grade inflammatory state (release of IL-1, TNF, adipokines).
*Not thought to be due to mechanical factors

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104
Q

Give three examples of how occupation acts as a risk factor for osteoarthritis.

A
  • Manual labour associated with OA of small hand joints
  • Farming associated with OA of hips
  • Football associated with OA of knees
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105
Q

Give three examples of abnormal mechanics which can cause osteoarthritis.

A
  • Joint hypermobility
  • Congenital hip dysplasia
  • Neuropathic conditions
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106
Q

Describe the symptoms of OA.

A
  • Pain worse with use and at end of day
  • Morning stiffness <30mins
  • Functional impairment (walking, activities of daily living)
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107
Q

Give some signs of OA.

A
  • Alteration in gait
  • Joint swelling (bony enlargement, effusion, very occasionally synovitis)
  • Crepitus
  • Limited range of movement
  • Tenderness
  • Deformities
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108
Q

Give the five radiological features of osteoarthritis.

A
  • Joint space narrowing
  • Osteophyte formation
  • Subchondral sclerosis
  • Subchondral cysts
  • Abnormalities of bone contour
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109
Q

Describe the inflammatory phase in OA of hands.

A

Occurs early, as nodes are forming.

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110
Q

Which joints are involved in OA of the hands?

A
  • DIP
  • PIP
  • CMC
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111
Q

What causes reduced hand function in OA hand?

A

Bony swelling and cyst formation.

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112
Q

Which form of hand OA has a strong genetic component (especially in women)?

A

Nodal form

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113
Q

Describe the nodes in hand OA.

A
  • Heberden’s Nodes at DIP joints

- Bouchard’s Nodes at PIP joints

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114
Q

What are the three patterns of knee OA?

(Which is the commonest)?

A
  • Medial (commonest)
  • Lateral
  • Patellofemoral
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115
Q

Describe the evolution of OA of the knee (without significant trauma).

A

Evolution may be slow.

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116
Q

What is meant by ‘loose bodies’ in the knee?

A

Bone or cartilage fragment present in the joint.

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117
Q

What is the main symptom of loose bodies in the knee?

A

Locking of the knee

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118
Q

What is the main presentation of OA hip?

A

Groin pain

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119
Q

What is erosive/inflammatory OA, and how is it treated differently to OA?

A
  • A subset of OA with a strong inflammatory component

- DMARD therapy used in addition to standard management

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120
Q

Give some non-medical management methods for OA.

A
  • Patient education
  • Activity/exercise
  • Weight loss
  • Physiotherapy
  • Occupational therapy
  • Footwear
  • Walking aids
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121
Q

What is the role of intra-articular steroid injections in OA?

A

The role remains unclear.

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122
Q

Give some forms of pain relief used in OA.

A
  • NSAIDs
  • Capsaicin (topical)
  • Paracetamol
  • Opioids
  • Buprenorphine
  • Lignocaine
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123
Q

Give four surgical treatments for OA.

A
  • Arthroscopy
  • Osteotomy (cutting bone)
  • Arthroplasty
  • Fusion
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124
Q

When is arthroscopy used in OA?

A

ONLY for loose bodies

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125
Q

When is osteotomy used in OA?

A

Mostly in young people with knee OA.

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126
Q

When is arthroplasty used in OA?

A

For uncontrolled pain (particularly at night) and significant limitation of function.

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127
Q

On which joint would fusion usually be used in OA, and what is the down side of this treatment?

A
  • Usually used in ankle and foot

- However results in a limited range of movement

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128
Q

Define vasculitis.

A

Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow.

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129
Q

Give two consequences of vessel wall destruction in vasculitis.

A
  • Perforation

- Haemorrhage into tissues

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130
Q

Give two consequences of endothelial injury in vasculitis.

A
  • Thrombosis

- Ischaemia/infarction of dependent tissues

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131
Q

Give three histological features of vasculitis.

A
  • Vessel wall infiltration by neutrophils, mononuclear cells, +/- giant cells
  • Fibrinoid necrosis inside vessel wall
  • Leukocytoclasis (dissolution of leukocytes)
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132
Q

Give four ways of classifying vasculitis.

A
  • Size of vessel
  • Target organ
  • Anti-neutrophil cytoplasmic antibodies (ANCA) involvement
  • Primary vs secondary
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133
Q

In which types of vasculitis can anti-neutrophil cytoplasmic antibodies be present?

A

Small/medium vessel vasculitis.

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134
Q

What are anti-neutrophil cytoplasmic antibodies?

A

Specific antibodies for antigens in cytoplasmic granules of neutrophils and monocyte lysosomes.

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135
Q

How are ANCAs detected?

A

Using indirect immunofluorescence microscopy.

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136
Q

Give the two different types of ANCA.

A
  • cytoplasmic ANCA

- peri-nuclear ANCA

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137
Q

What are the two potential targets for ANCA?

A
  • Proteinase 3

- Myeloperoxidase

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138
Q

How do ANCA contribute to the disease process in vasculitis?

A

They contribute to blood vessel damage.

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139
Q

Why is vasculitis so hard to diagnose?

A

There is no single typical presentation, as vasculitis can affect any vessel or organ.

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140
Q

Give some general signs/symptoms of vasculitis.

A
  • Systemically unwell
  • Fever
  • Arthralgia/arthritis
  • Rash
  • Weight loss
  • Headache
  • Footdrop
  • Major event (stroke, bowel infarction)
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141
Q

Give two differential diagnoses of vasculitis.

A
  • Sepsis

- Malignancy

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142
Q

Give a type of large vessel vasculitis.

A

Giant cell (temporal arteritis)

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143
Q

What is giant cell (temporal) arteritis?

A

Granulomatous arteritis of the aorta and larger extracranial branches of carotid arteries.

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144
Q

What age range does giant cell (temporal) arteritis affect?

A

> 50yrs (incidence increases with age)

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145
Q

Give two groups of patients in which giant cell (temporal) arteritis is more common.

A
  • Women

- Caucasians

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146
Q

What does giant cell (temporal) arteritis increase the risk of?

A

Stroke

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147
Q

Describe the symptoms of giant cell (temporal) arteritis.

A
  • Headache
  • Scalp tenderness
  • Jaw claudication
  • Acute blindness (medical emergency)
  • Non-specific malaise
  • Associated symptoms of polymyalgia rheumatica
  • Anterior ischaemic optic neuropathy
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148
Q

Give three signs of giant cell (temporal) arteritis.

A

Temporal arteries palpable, tender, and reduced pulsation.

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149
Q

Describe anterior ischaemic optic neuropathy.

What disease is it a feature of?

A

Sudden, painless, monocular and severe visual loss, may be preceded by transient visual loss (curtains coming over eyes).
It is a feature of giant cell (temporal) arteritis.

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150
Q

What is the gold standard investigation for giant cell (temporal) arteritis?

A

Temporal artery biopsy

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151
Q

To diagnose giant cell (temporal) arteritis, three or more of the following 5 criteria must be present:

A
  • Age >50
  • New headache
  • Temporal artery tenderness or decreased pulsation
  • ESR>50
  • Abnormal artery biopsies
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152
Q

What is the treatment for giant cell (temporal) arteritis?

A

Prompt corticosteroids (prednisolone)

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153
Q

How quick is the usual response to treatment in giant cell (temporal) arteritis?

A

48hrs

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154
Q

In giant cell (temporal) arteritis, how long does treatment usually last?

A

50% are off steroids at two years.

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155
Q

What other type of drug can be used in giant cell (temporal) arteritis?

A

Steroid sparing agents (azathioprine/methotrexate/biologics)

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156
Q

What prophylaxis treatment must be given in giant cell (temporal) arteritis?

A

Prophylaxis of osteoporosis from the steroids.

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157
Q

Give an example of small vessel vasculitis.

A

Granulomatosis with polyangiitis (Wegener’s Granulomatosis, GPA)

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158
Q

Describe the pathology in GPA.

A
  • Necrotizing, granulomatous vasculitis of arterioles, capillaries, and post capillary venules
  • Associated with anti-neutrophil cytoplasmic antibodies (c-ANCA)
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159
Q

What age does GPA usually affect?

A

25-60yrs (but can affect any age)

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160
Q

What is the classic triad of affected organs in GPA?

A
  • Upper respiratory tract
  • Lungs
  • Kidney
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161
Q

How is GPA described if there is no renal involvement?

A

It is limited

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162
Q

What are the consequences of GPA affecting the upper respiratory tract?

A
  • Sinusitis
  • Otitis
  • Nasal crusting
  • Bleeding
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163
Q

What are the consequences of GPA affecting the lungs?

A
  • Pulmonary nodules

- Haemorrhage

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164
Q

What are the consequences of GPA affecting the kindey?

A

Glomerulonephritis

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165
Q

What are the consequences of GPA affecting the skin?

A
  • Purpura

- Ulcers

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166
Q

What are the consequences of GPA affecting the nervous system?

A
  • Mononeuritis multiplex

- CNS vasculitis

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167
Q

What are the consequences of GPA affecting the eyes?

A
  • Proptosis
  • Scleritis
  • Episcleritis
  • Uveitis
  • Swelling of muscles behind the eye
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168
Q

What are the consequences of GPA affecting the nose, how common is it?

A

Saddle nose deformity.

Rare now due to better treatments.

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169
Q

Give four ‘miscellaneous’ consequences of GPA.

A
  • Synovitis
  • Pericarditis
  • GI
  • GU
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170
Q

What is the treatment for severe (organ-threatening) GPA?

A

High does steroids/cyclophosphamide/biologics

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171
Q

What is the treatment for non-end organ threatening GPA?

A

Moderate dose steroids + methotrexate/mycophenolate/azathioprine

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172
Q

What is the commonest autoimmune connective tissue disease?

A

Systemic lupus erythematosus

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173
Q

Give an ethnic group in which SLE is more common?

A

Afro-Caribbeans

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174
Q

Is SLE more common in men or women?

A

90% patients are women

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175
Q

What is the typical age range for development of SLE?

A

14-64yrs

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176
Q

Describe the pathogenesis of SLE.

A

Inflammation and immune reactions against self antigens lead to immune complex mediated tissue damage.

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177
Q

What causes increased risk of thrombosis in SLE?

A

Phospholipid antibodies.

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178
Q

Give some clinical features of SLE.

A
  • Fatigue
  • Arthritis
  • Skin rashes
  • Mucosal ulceration
  • Alopecia
  • Pleurisy
  • Pericarditis
  • Raynaud’s phenomenon
  • Glomerulonephritis
  • Venous/arterial thrombosis
  • Recurrent abortion
  • Vasculitis
  • Depression
  • Psychosis
  • Lymphadenopathy
  • Neuro-psychiatric features
  • Anaemia
  • Throbocytopenia
  • Neutropenia
  • Lymphopenia
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179
Q

Describe the arthritis in SLE.

A
  • Symmetrical
  • Less proliferative than RA
  • Can be deforming
  • Non-erosive
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180
Q

Give four types of rash that can occur in SLE.

A
  • Discoid rash
  • Photosensitive rash
  • Subacute lupus rash
  • Butterfly rash
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181
Q

Give the three features of glomerulonephritis in SLE.

A
  • Hypertension
  • Proteinuria
  • Renal failure
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182
Q

Describe the anaemia in SLE.

A

Coombs positive haemolytic anaemia

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183
Q

Give the three main antibodies in SLE.

A
  • Anti-nuclear antibody
  • Double stranded DNA antibody
  • Anti-phospholipid antibody
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184
Q

Which antibody is specific for lupus?

A

Double stranded DNA antibody

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185
Q

How does anti-nuclear antibody help to diagnose lupus?

A

It is sensitive (95%) but not specific.

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186
Q

Give six other antibodies that may be detected in lupus.

A
  • Rheumatoid factor
  • Cardiolipin antibodies
  • Anti Ro/La/Sm/RNP
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187
Q

A diagnosis of SLE is made if 4 out of this 11 criteria are met…

A
  • Malar rash (Butterfly rash)
  • Discoid rash
  • Photosensitivity
  • Oral ulcers
  • Non-erosive arthritis
  • Serositis (pleuritis, pericarditis)
  • Renal disorder (persistent proteinuria, cellular casts)
  • CNS disorder (seizures, psychosis)
  • Haematological disorder (haemolytic anaemia, leukopaenia, lymphopaenia, thrombocytopaenia)
  • Immunological disorder (presence of specific antibodies)
  • Antinuclear antibodies
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188
Q

Describe the non-pharmacological management for SLE.

A
  • Patient education and support
  • UV protection
  • Assessment of lupus activity (clinical/immunological)
  • Screening for major organ involvement
  • Assessment of damage
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189
Q

Give some methods of drug treatment for SLE.

A
  • No treatment
  • Topical (sunscreens, steroids, cytotoxic)
  • NSAIDs
  • Antimalarial (hydroxychloroquine)
  • Steroids
  • Cytotoxic
  • Anticoagulants
  • Biological
  • Plasmapheresis
  • Stem cell transplant
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190
Q

Give five cytotoxic treatments that can be used in SLE.

A
  • Azathioprine
  • Mycophenolate
  • Ciclosporin
  • Methotrexate
  • Cyclophosphamide
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191
Q

Describe the ESR and CRP in lupus.

A

ESR tends to be high but CRP tends to be normal.

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192
Q

Is primary or secondary Raynaud’s phenomenon more common?

A

Primary

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193
Q

Give three things that can cause secondary Raynaud’s phenomenon.

A
  • Connective tissue disease
  • Drugs
  • Vascular damage
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194
Q

Give three connective tissue diseases that can cause Raynaud’s phenomenon.

A
  • Systemic sclerosis
  • Mixed connective tissue disease
  • SLE
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195
Q

Give three factors which can cause vascular damage, which can result in Raynaud’s phenomenon.

A
  • Atherosclerosis
  • Frost bite
  • Vibrating tools
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196
Q

Describe the colour changes in Raynaud’s phenomenon.

A

White in cold
Then blue (lack of oxygen)
Red on warmth (vasodilation)

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197
Q

What is dermatomyositis/polymyositis?

A

Inflammation of muscle and skin, causing rash and muscle weakness.

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198
Q

What is the consequence of lung involvement in dermatomyositis/polymyositis?

A

Interstitial lung disease

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199
Q

As well as a ‘primary’ disease, how else can dermatomyositis/polymyositis present?

A

As a paraneoplastic syndrome.

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200
Q

What are the clinical features of dermatomyositis/polymyositis?

A
  • Myalgia
  • Arthralgia
  • Rash
  • Dysphagia
  • Dysphonia
  • Respiratory weakness
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201
Q

What investigations should be carried out in dermatomyositis/polymyositis?

A
  • Muscle enzymes
  • EMG
  • Muscle/skin biopsy
  • Screen for malignancy
  • Antibody screen
  • Chest XR, PFTs, high resolution CT lungs
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202
Q

What will the muscle enzymes show in dermatomyositis/polymyositis?

A

High creatine kinase

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203
Q

What is the management of dermatomyositis/polymyositis?

A
  • Steroids

- Immunosuppressive drugs

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204
Q

Give four clinical subsets of systemic sclerosis.

A
  • Limited cutaneous
  • Diffuse cutaneous
  • Sine (without) scleroderma
  • Overlap syndromes/mixed connective tissue disease
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205
Q

Is systemic sclerosis more common in men or women?

A

Women

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206
Q

What is the most common age for systemic sclerosis to present?

A

30-40yrs

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207
Q

Give three elements of the pathogenesis of systemic sclerosis.

A
  • Vasculopathy
  • Inflammation and excessive collagen deposition by fibroblasts
  • Auto-antibody production
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208
Q

Give three antibodies that may appear in systemic sclerosis.

A
  • Anti-nuclear antibodies
  • Anti-centromere antibodies
  • Anti-topoisomerase antibodies
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209
Q

What percentage of patients with systemic sclerosis test positive for ANA?

A

65%

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210
Q

In which type of systemic sclerosis might anti-centromere antibodies appear, and in what percentage of patients?

A

70-80% of patients with limited SSc

211
Q

In which type of systemic sclerosis might anti-topoisomerase antibodies appear, and in what percentage of patients?

A

40% of patients with diffuse SSc

212
Q

What are five features of limited cutaneous SSc?

A

CREST

  • Calcinosis (subcutaneous tissue)
  • Raynaud’s (long history)
  • Esophageal and gut dysmotility
  • Sclerodactyly (hard fingers)
  • Telangiectasia (spider veins)
213
Q

Describe the skin involvement in limited cutaneous SSc.

A

Limited to face, hands, and feet.

214
Q

What is a late feature of limited cutaneous SSc?

A

Pulmonary hypertension

215
Q

Give five clinical features of diffuse cutaneous SSc.

A
  • Proximal scleroderma and trunk involvement (diffuse skin involvement)
  • Short history of Raynaud’s
  • Increased risk of renal crisis
  • Increased risk of cardiac involvement
  • Increased risk of interstitial lung disease
216
Q

What is the treatment for systemic sclerosis?

A
  • Treat Raynaud’s (physical protection, vasodilators)
  • PPIs for life (for GORD)
  • ACEi to inhibit renal crisis
  • Early detection of pulmonary arterial hypertension
  • Treatment of skin oedema (cytotoxic drugs, autologous stem cell transplant)
  • Treatment of pulmonary fibrosis (cyclophosphamide)
217
Q

Give five things that may cause secondary Sjogren’s syndrome.

A
  • SLE
  • Rheumatoid arthritis
  • Scleroderma
  • Primary biliary cirrhosis
  • Other auto-immune diseases
218
Q

Briefly describe the pathology of Sjogren’s syndrome.

A

Lymphocytic infiltration and fibrosis of exocrine glands.

219
Q

What are the clinical features of sjogren’s syndrome?

A
  • Dry eyes
  • Dry mouth
  • Arthritis
  • Rash
  • Neurological features
  • Vasculitis
  • Interstitial lung disease
  • Renal tubular acidosis
220
Q

Give a condition which is strongly associated with Sjogren’s syndrome.

A

Gluten sensitivity

221
Q

Sjogren’s syndrome increases the risk of which condition?

A

Lymphoma

222
Q

Give the laboratory features of Sjogren’s syndrome.

A
  • Positive ANA
  • Positive RF
  • Positive Ro and La
  • Negative DS DNA
  • Raised immunoglobulins
  • Abnormal salivary glands on ultrasound
  • Sialadenitis on lip biopsy (infection of salivary glands)
223
Q

What is the treatment for Sjogren’s syndrome?

A
  • Tear and saliva replacement

- Immune-suppression for systemic complications

224
Q

Give two features of both crystal arthritis and infection.

A
  • Rapid onset

- Very red and hot joints

225
Q

How can crystal disease and infection be differentiated?

A
  • Clinical history

- Joint aspirate

226
Q

Give five differential diagnoses of systemic diseases.

A
  • Infection
  • Auto-immune diseases
  • Malignancy
  • Endocrine diseases
  • Metabolic diseases
227
Q

Give two inherited connective tissue diseases.

A
  • Marfan’s Syndrome

- Ehler Danlos Syndrome

228
Q

Give the pattern of inheritance for Marfan’s syndrome.

A

Autosomal dominant

229
Q

Give five features of Marfan’s syndrome.

A
  • Tall/long arms
  • Lens dislocation
  • Aortic valve incompetence/dilated aortic root
  • High arched palate
  • Sunken chest
230
Q

Give two features of Ehler Danlos syndrome.

A
  • Stretchy skin

- Joint hypermobility

231
Q

What is the prevalence of fibromyalgia?

A

0.5-4%

232
Q

Is fibromyalgia more common in men or women?

A

Women

233
Q

Give five risk factors for fibromyalgia.

A
  • Female sex
  • Middle age
  • Low household income
  • Divorced
  • Low educational status
234
Q

Give three other conditions that are associated with fibromyalgia.

A
  • Chronic fatigue syndrome
  • Irritable bowel syndrome
  • Chronic headaches syndrome
235
Q

Describe the clinical features of fibromyalgia.

A
  • Chronic pain (>3months)
  • Pain is widespread
  • Absence of inflammation
  • Presence of pain on palpation of at lease 11/18 specified ‘tender points’
  • Morning stiffness
  • Fatigue
  • Poor concentration
  • Low mood
  • Sleep disturbance
236
Q

What do the investigations show in fibromyalgia?

A

All are normal

237
Q

Describe the principles of management of fibromyalgia.

A
  • Education of patient and family
  • Explanation and reassurance
  • Cognitive behavioural therapy
  • Antidepressants may help to relieve pain
238
Q

What is another name for Paget’s disease?

A

Osteitis deformans

239
Q

What age group is Paget’s disease more common in?

A

Over 40s

240
Q

Briefly describe the pathology of Paget’s disease.

A
  • Increased numbers of osteoblasts and osteoclasts
  • Increased bone turnover and remodelling
  • Resulting in bone enlargement, deformity and weakness
241
Q

Describe the clinical features of Paget’s disease.

A
  • Asymptomatic in about 70%
  • Deep, boring pain
  • Bony deformity and enlargement
242
Q

Give five sites where Paget’s disease commonly manifests.

A
  • Pelvis
  • Lumbar spine
  • Skull
  • Femur
  • Tibia
243
Q

Give six complications of Paget’s disease.

A
  • Pathological fractures
  • Osteoarthritis
  • Hypercalcaemia
  • Nerve compression due to bone overgrowth
  • High output congestive heart failure
  • Osteosarcoma
244
Q

Give two consequences of nerve compression in Paget’s disease.

A
  • Deafness

- Root compression

245
Q

Give two radiological features of Paget’s disease.

A
  • Localised enlargement of bone

- Patchy cortical thickening with sclerosis, osteolysis, and deformity

246
Q

Describe the calcium, phosphate, and alkaline phosphate levels in Paget’s disease.

A
  • Calcium normal
  • Phosphate normal
  • Alkaline phosphate raised
247
Q

Describe the treatment for Paget’s disease.

A
  • Analgesia

- Alendronate (to reduce pain/deformity if analgesia fails)

248
Q

What is ‘osteomalacia’ called if it occurs during the period of bone growth?

A

Rickets

249
Q

Briefly describe the pathophysiology of osteomalacia.

A
  • Normal bone amount but low mineral content

- Excess uncalcified osteoid and cartilage

250
Q

Give six causes of osteomalacia.

A
  • Vitamin D deficiency
  • Renal osteodystrophy (renal failure)
  • Drug-induced
  • Vitamin D resistance
  • Liver disease
  • Tumour-induced osteomalacia
251
Q

What are the signs/symptoms of rickets?

A
  • Growth retardation
  • Hypotonia
  • Apathy in infants
  • Knock-kneed
  • Bow-legged
  • Deformities of metaphyseal-epiphyseal junction
  • Features of hypocalcaemia (usually mild)
252
Q

Give the signs/symptoms of osteomalacia.

A
  • Bone pain and tenderness
  • Fractures (especially femoral neck)
  • Proximal myopathy
  • Low phosphate and vitamin D
253
Q

What would plasma investigations show in osteomalacia?

A
  • Mild hypocalcaemia (but may be severe)
  • Low phosphate
  • High alkaline phosphatase
  • High PTH
  • Low vitamin D (except in Vitamin D resistance)
254
Q

What would the bone biopsy show in osteomalacia?

A

Incomplete mineralisation

255
Q

What would the muscle biopsy show in osteomalacia?

A

Normal

256
Q

Give two radiological features of osteomalacia.

A
  • Loss of cortical bone

- Apparent partial fractures without displacement

257
Q

Give a radiological feature of Rickets.

A

Cupped, ragged metaphyseal surfaces

258
Q

What would the treatment be for osteomalacia caused by vitamin D deficiency?

A

Vitamin D

259
Q

What treatment would be given in vitamin D resistant osteomalacia or renal disease?

A
  • Alfacalcidiol

- Calcitriol

260
Q

What is type I vitamin D resistance rickets?

A

Low renal 1a-hydroxylase activity

261
Q

What is type II vitamin D resistance rickets?

A

End-organ resistance to 1,25-dihydroxycholecalciferol

262
Q

How are both type I and type II vitamin D resistance rickets treated?

A

Large doses of calcitriol

263
Q

Describe the inheritance pattern of X-linked hypophosphataemic rickets.

A

Dominant X linked

264
Q

Briefly describe the pathology in X-linked hypophosphataemic rickets.

A

Defect in renal phosphate handling

265
Q

How is X-linked hypophosphataemic rickets treated?

A

High doses of oral phosphate and calcitriol

266
Q

Give eight things associated with developing carpel tunnel syndrome.

A
  • Obesity
  • Short stature
  • Pregnancy
  • Oral contraceptive pill
  • Diabetes
  • Hypothyroidism
  • Rheumatoid arthritis
  • Acromegaly
267
Q

Give two work-related causes of carpel tunnel syndrome.

A
  • Forceful and repetitive work (painters, meat processors)

- Hand-transmitted vibration

268
Q

Give two special tests that can be used to diagnose carpal tunnel syndrome.

A
  • Tinel’s test

- Phalen’s test

269
Q

Describe Tinel’s test.

A

Tap lightly over the median nerve and see if patient feels paresthesia distally.

270
Q

Describe Phalen’s test.

A

Patient fully flexes elbows and wrists (upside down prayer position) and if symptoms occur the test is positive.

271
Q

What causes hand-arm vibration syndrome?

A

Excessive exposure to hand-transmitted vibration (chain saws, angle grinders, jack hammers, drills)

272
Q

Describe the presentation of hand-arm vibration syndrome.

A
  • Vascular (blanching)

- Neural (tingling, numbness, loss of dexterity)

273
Q

Hand-arm vibration syndrome is a secondary cause of what condition?

A

Raynaud’s phenomenon

274
Q

Briefly describe hypothenar hammer syndrome.

A

Occlusion of ulnar artery and superficial palmar arch.

275
Q

What is the most common cause of tenosynovitis?

A

Inflammation of abductor pollicis longus and extensor pollicis brevis tendon sheath.

276
Q

Give an occupational risk of developing tenosynovitis.

A

Job requires forceful and repetitive hand movements.

277
Q

Give a special test used to diagnose tenosynovitis.

A

Finkelstein’s test

278
Q

Describe Finkelstein’s test.

A

The examiner pulls the thumb of the patient in ulnar deviation and if there is pain in the radial styloid process the test is positive.

279
Q

Give four methods of treatment for tenosynovitis.

A
  • NSAIDs
  • Steroid injection
  • Rest
  • Change job
280
Q

What is another name for lateral epicondylitis.

A

Tennis elbow

281
Q

What is another name for medial epicondylitis?

A

Golfer’s elbow

282
Q

What causes epicondylitis?

A

Forceful flexion-extension of the wrist or forceful pronation-supination.

283
Q

Give a special test used to diagnose lateral epicondylitis.

A

Cozen’s test

284
Q

Describe Cozen’s test.

A

Patient’s elbow in 90degree flexion, hand in radial deviation, forearm pronation.
Patient extends wrist against resistance.
Pain = positive.

285
Q

Give five methods of treatment for epicondylitis.

A
  • NSAIDs
  • Steroid injection
  • Clasp
  • Rest
  • Surgery
286
Q

What is repetitive strain disorder?

A

Non-specific pain in the hand

287
Q

Give four treatment methods for repetitive strain disorder.

A
  • Rest breaks
  • Job rotation
  • Reduced force
  • Ergonomically neutral working postures
288
Q

Describe briefly what causes writers cramp.

A

A focal dystonia (neurological condition affecting the nerves).

289
Q

Briefly describe usual rotator cuff problems.

A

Tendonitis or a tear, usually affecting the supraspinatus tendon.

290
Q

Give two occupational associations with rotator cuff problems.

A
  • Shoulder impingement

- OA of acromioclavicular joint

291
Q

Describe the presentation of rotator cuff problems.

A

Painful arc

292
Q

Give a special sign used to diagnose rotator cuff problems.

A

Hawkin’s sign

293
Q

Describe Hawkin’s sign.

A

Shoulder flexed to 90degrees.
Elbow flexed to 90degrees.
Quickly rotate arm internally.
Pain below acromioclavicular joint is positive.

294
Q

Give three high risk activities that can increase likelihood of developing rotator cuff problems.

A
  • Heavy manual lifting
  • Lifting above shoulder height
  • Throwing
295
Q

Describe thoracic outlet syndrome.

A

Pain or tingling down arm or blanching of fingers related to posture of arm.

296
Q

Describe what causes thoracic outlet syndrome.

A

Compression of brachial plexus trunks or subclavian artery in neck under clavicle.
May be due to anatomical abnormalities in the neck.

297
Q

Give two occupational associations with thoracic outlet syndrome.

A
  • Poor posture

- Loading of shoulders

298
Q

Give three things (including a special test) that can be used to diagnose thoracic outlet syndrome.

A
  • Roos sign
  • X-ray neck
  • MRI
299
Q

Describe Roos sign.

A

Patient has both arms in 90degree abduction-external rotation position.
Patients opens and closes hands slowly over 3 minute period.
Normal if only forearm muscles fatigue, other signs are positive.

300
Q

What is the treatment for thoracic outlet syndrome?

A

Surgery

301
Q

Describe Dupytren’s contracture.

A

Thickening of palm fascia caused by vibrating tools, resulting in flexion of one or more fingers.

302
Q

What is Seamstress’ finger?

A

Heberden’s nodes at distal interphalangeal joints.

303
Q

Give a classical feature of rheumatoid arthritis on X ray.

A

Peri-articular erosions

304
Q

As well as in the back, where else might pain be felt in inflammatory back pain?

A

Across the costochondral joints.

305
Q

What antibody is usually positive in all autoimmune connective tissue disorders?

A

Anti-nuclear antibody

306
Q

What type of arthritis (deforming or erosive) is associated with systemic lupus erythematosus?

A

Deforming

307
Q

Give a rheumatological condition in which thrombocytosis may be a feature.

A

Rheumatoid arthritis

308
Q

What is osteomyelitis?

A

An infection localised to bone.

309
Q

Why is there increasing incidence of chronic osteomyelitis?

A

There is increasing risk of pre-disposing conditions.

310
Q

Give two age groups in which osteomyelitis is more common?

A

Children and elderly

311
Q

Give seven risk factors for osteomyelitis.

A
  • Non-native joint
  • Diabetes mellitus
  • Inflammatory arthritis
  • Immune deficiency
  • Peripheral vascular disease
  • Sickle cell disease
  • (Behavioural) risk of trauma
312
Q

Briefly describe the pathology of osteomyelitis.

A
  • Inflammatory cells, oedema, vascular congestion, and small vessel thrombosis increase intramedullary pressure
  • This causes periosteum to rupture and periosteal blood supply is interrupted, causing necrosis
  • Necrotic bone is left behind (sequestra)
  • New bone formation occurs (involucrum)
313
Q

What is sequestra in osteomyelitis?

A

Necrotic bone which is left behind

314
Q

What is involucrum in osteomyelitis?

A

New bone formation

315
Q

Give three methods of infection in osteomyelitis.

A
  • Direct inoculation
  • Contiguous spread
  • Haematogenous seeding
316
Q

In osteomyelitis, is direct inoculation usually monomicrobial or polymicrobial?

A

Can be either

317
Q

In osteomyelitis, is contiguous spread monomicrobial or polymicrobial?

A

Can be either

318
Q

In osteomyelitis, is haematogenous seeding usually monomicrobial or polymicrobial?

A

Monomicrobial

319
Q

Give two ways that bones can be infected by direct inoculation.

A
  • Trauma

- Surgery

320
Q

Describe contiguous spread in osteomyelitis.

A

Spread of infection from adjacent tissue.

321
Q

Give four ‘conditions’ that increase likelihood of contiguous spread in osteomyelitis.

A
  • Diabetes mellitus
  • Chronic ulcers
  • Vascular disease
  • Arthroplasties
322
Q

In which bone/s is osteomyelitis more likely to occur by haematogenous seeding in adults and why?

A

Vertebra.

Because vertebrae become more vascular with age.

323
Q

In which bone/s is osteomyelitis more likely to occur by haematogenous seeding in children and why?

A

Long bones.
Because in metaphyses blood flow is easier, basement membrane is absent, capillaries lack phagocytic lining, and there is high blood flow to developing bones.

324
Q

Give two risk factors for contracting osteomyelitis via haematogenous seeding.

A
  • IV drug users

- People with risk factor for bacteraemia

325
Q

What is the most common causative organism in osteomyelitis?

A

Staphylococcus aureus

326
Q

Why is Staph.aureus good at infecting bones?

A

It binds host proteins and can survive in macrophages.

327
Q

Give the three usual organisms which can cause osteomyelitis.

A
  • Staphylococcus aureus
  • Coagulase -ve staph
  • Aerobic gram -ve bacilli
328
Q

Give five less common organisms which can cause osteomyelitis.

A
  • Streptococci
  • Enterococci
  • Anaerobes
  • Fungi
  • Mycobacteria
329
Q

Which organism commonly causes osteomyelitis in sickle cell disease?

A

Salmonella

330
Q

Give two organisms which cause osteomyelitis in IV drug users.

A
  • Pseudomonas aeruginosa

- Serratia marcescens

331
Q

Describe the symptoms of osteomyelitis.

A

Dull pain at site of infection, may be aggravated by movement.

332
Q

Describe the rate of onset of osteomyelitis symptoms.

A

Onset over several days

333
Q

Give four systemic signs of osteomyelitis.

A
  • Fever
  • Rigors
  • Sweats
  • Malaise
334
Q

Give four local acute signs of osteomyelitis.

A
  • Tenderness
  • Warmth
  • Swelling
  • Erythema
335
Q

Give seven local chronic signs of osteomyelitis.

A
  • Tenderness
  • Warmth
  • Swelling
  • Erythema
  • Draining sinus tract
  • Deep/large ulcers that fail to heal
  • Non-healing fractures
336
Q

Give three findings on a blood test in oesteomyelitis.

A
  • High WCC (chronic can have normal)
  • Raised CRP
  • Raised ESR
337
Q

What type of imaging can be carried out to diagnose acute osteomyelitis.

A

MRI (or CT/nuclear bone scan)

338
Q

Why aren’t X-rays that sensitive to acute osteomyelitis?

A

They take about 2 weeks for changes to appear

339
Q

Give two investigations to identify the causative organism in osteomyelitis.

A
  • Bone biopsy (sample to microbiology and histology)

- Blood cultures

340
Q

Give six signs of chronic osteomyelitis on X-ray.

A
  • Cortical erosion
  • Periosteal reaction
  • Mixed lucency
  • Sclerosis
  • Sequestra
  • Soft tissue swelling
341
Q

Give two features of osteomyelitis on MRI.

A
  • Marrow oedema

- Delineation on cortical, bone marrow, and soft tissue inflammation

342
Q

Give seven differential diagnoses of osteomyelitis.

A
  • Soft tissue infection (cellulitis, erysipelas)
  • Charcot joint
  • Avascular necrosis of bone
  • Gout
  • Fracture
  • Bursitis
  • Malignancy
343
Q

Give the two steps in the management of osteomyelitis.

A
  • Surgery

- Antimicrobial therapy

344
Q

What does surgery for osteomyelitis involve?

A

Debridement and hardware replacement/removal

345
Q

Give two things that choice of antimicrobial therapy in osteomyelitis depends on.

A
  • Infective organism

- Bone penetration of drug

346
Q

How long should antibiotics be given for in osteomyelitis?

A

6 weeks minimum, treatment length guided by ESR/CRP

347
Q

How does the presentation of mycobacterial osteomyelitis differ from other forms of osteomyelitis?

A
  • Slower onset

- More systemic symptoms

348
Q

What investigation is essential to diagnose mycobacterial osteomyelitis?

A

Biopsy

349
Q

How long is the typical treatment for mycobacterial osteomyelitis?

A

12 months

350
Q

Is septic arthritis more common in males or females?

A

They are equal

351
Q

What percentage of septic arthritis cases occur in patients over 65yrs?

A

45%

352
Q

Give nine risk factors for septic arthritis.

A
  • Prosthetic joint
  • Rheumatoid arthritis
  • Immunosuppression
  • Elderly
  • Diabetes
  • Any cause for bacteraemia
  • Trauma
  • Local skin breaks/ulcers
  • Damages joints
353
Q

What is the main causative organism in septic arthritis (native joints)?

A

Staphylococcus aureus

354
Q

Give six less common causative organisms of septic arthritis.

A
  • Streptococci
  • Neisseria gonorrhoea
  • Gram -ve bacilli
  • Anaerobes
  • Mycobacterium
  • Fungi
355
Q

What used to be a major cause of septic arthritis in children, but now isn’t due to immunisation?

A

Haemophilus influenzae

356
Q

Give four features of gonococcal septic arthritis.

A
  • Fever
  • Arthritis (polyarticular)
  • Tenosynovitis
  • Rash
357
Q

Give three presenting features of septic arthritis.

A
  • Painful, red, swollen, hot joint
  • Disuse (especially in children)
  • Fever
358
Q

Is septic arthritis usually monoarthritis or polyarthritis?

A

90% monoarthritis, but polyarthritis can occur (eg. In gonorrhoea)

359
Q

Give the relative frequencies of septic arthritis the hip, knee, and shoulder.

A

Knee>hip>shoulder

360
Q

Give two investigations to carry out in suspected septic arthritis.

A
  • Joint aspirate

- Blood cultures

361
Q

Give three features of joint aspirate that would suggest septic arthritis.

A
  • Turgid fluid
  • High leukocyte content
  • Gram stain (+ve cocci)
362
Q

What additional investigation may be required if mycobacterial septic arthritis is suspected?

A

Synovial biopsy

363
Q

Give seven management strategies for septic arthritis.

A
  • Aspiration
  • Stop DMARDs and biologics
  • High dose/long course antibiotics (6 weeks minimum)
  • Double dose steroids
  • Analgesia
  • Splinting/rest
  • Joint aspiration and washout
364
Q

What should be done first: blood cultures or antibiotics?

And why?

A

Blood cultures, because antibiotics may eradicate the bacteria in the sample to give a false negative.

365
Q

How is a prosthetic joint infection caught after surgery?

A

Haematogenous spread

366
Q

What is the most common causative organism of prosthetic joint infections?

A

Coagulase -ve staphylococci

367
Q

Give three causative organisms of prosthetic joint infections.

A
  • Coagulase -ve staphylococci
  • Staphylococcus aureus
  • Enterobacteria
368
Q

Give four preventative techniques that orthopaedic surgeons can use to prevent infections in prosthetic joints.

A
  • Double glove
  • Air filters
  • Separation between surgeons and anaesthetists in theatre
  • Prophylactic antibiotics
369
Q

Give three X ray features that may suggest an infection in a prosthetic joint.

A
  • Prosthetic loosening
  • Periosteal thickening
  • Ectopic bone formation
370
Q

Give a highly sensitive/specific inflammatory marker that can be used to diagnose prosthetic joint infections.

A

Alpha defensin

371
Q

When would antibiotic suppression be used to treat prosthetic joint infection?

A

If the patient is unfit for surgery

372
Q

When would debridement and retention of prosthesis be used to treat prosthetic joint infection?

A

If it is an early postoperative infection or in an acute haematogenous infection.

373
Q

When would excision arthroplasty be used to treat prosthetic joint infection?

A

If at higher risk.

374
Q

What is the consequence of an excision arthroplasty being used to treat prosthetic joint infection?

A

Poor functional outcome

375
Q

What does a one stage exchange arthroplasty to treat prosthetic joint infections involve?

A

Debridement of all infected/dead tissues, soft tissue cover/reconstruction, and new prosthesis (all in one).

376
Q

What does two stage exchange arthroplasty to treat prosthetic joint infection involve?

A

Debridement, then wait before inserting new prosthesis.

377
Q

Describe the presentation of bone tumours.

A
  • Vague symptoms
  • Pain
  • Swelling
  • Erythema
  • Limp or disuse
  • Failure to thrive/meet milestones (children)
  • Unremitting pain
  • Night pain
  • Pain on mobilising
  • Altered neurology
  • Symptoms from primary tumour (if metastatic)
378
Q

What lab tests can be carried out in a suspected bone tumour?

A
  • PSA
  • Serum/urine electrophoresis
  • ESR
  • CRP
  • Calcium
  • Alkaline phosphatase
379
Q

What imaging can be carried out to assess bone tumours?

A
  • Plain X ray

- Potentially CT/MRI/Bone scan

380
Q

Give three things that can be determined from imaging of a bone tumour.

A
  • Location of tumour
  • Tumour-bone/Bone-tumour interaction
  • Look at matrix (medullary cavity)
381
Q

Describe how biopsies are carried out in bone tumours.

A

Performed by the surgeon who will be operation, as tract must be excised along with tumour as it will contain tumour cells.

382
Q

Give three features that can be looked at to determine if a bone tumour is benign or malignant.

A
  • Zone of transition
  • Periosteal reaction
  • Cortical destruction
383
Q

What does a narrow zone of transition suggest about the malignancy of a bone tumour?

A

It is likely to be benign

384
Q

What does a wide zone of transition suggest about the malignancy of a bone tumour?

A

It is likely to be a more aggressive disease

385
Q

What does a solid periosteal reaction suggest about the malignancy of a bone tumour?

A

The tumour is less malignant

386
Q

What does a lamellated periosteal reaction suggest about the malignancy of a bone tumour?

A

It is more malignant than a solid periosteal reaction but still not too aggressive.

387
Q

What does a sunburst periosteal reaction suggest about the malignancy of a bone tumour?

A

The tumour is malignant, but not the most malignant it can be.

388
Q

What does a Codman’s triangle periosteal reaction suggest about the malignancy of a bone tumour?

A

It is a very malignant tumour

389
Q

How useful is cortical destruction in determining whether a bone tumour is benign or malignant?

A

Not very useful, as some benign lesions can cause destruction.

390
Q

What does complete cortical destruction suggest about the malignancy of a bone tumour?

A

It is an aggressive disease

391
Q

Give four radiographic features of a benign bone tumour.

A
  • Well defined, sclerotic border
  • Lack of soft tissue mass
  • Solid periosteal reaction
  • Geographic bone destruction
392
Q

Give four radiographic features of a malignant bone tumour.

A
  • Interrupted periosteal reaction
  • Moth-eaten or permeative bone destruction
  • Soft tissue mass
  • Wide zone of transition
393
Q

What is a major complicating factor in bone tumours?

A

Fracture

394
Q

What is Mirel’s scoring system in bone tumours?

A

A score given to determine a patient’s risk of fractures.

395
Q

What four factors are considered when calculating Mirel’s score in bone tumours?

A
  • Site
  • Pain
  • Lesion type (blastic/mixed/lytic)
  • Lesion size
396
Q

Is it more common for a bone tumour to be primary or secondary?

A

Secondary

397
Q

How do patients with primary bone tumours commonly present?

A

Constant, non-mechanical pain.

398
Q

Give an example of a primary bone tumour that typically occurs in patients aged between 10 and 19 years.

A

Osteosarcoma

399
Q

Give an example of a primary bone tumour which typically occurs in patients <18yrs of age.

A

Ewing’s sarcoma

400
Q

Give an example of a primary bone tumour which is usually found in people >40yrs, and with Paget’s disease.

A

Chondrosarcoma

401
Q

Describe the bone lesions in metastatic bone tumours.

A

They are lytic

402
Q

Describe developmental dysplasia of the hip.

A

Hip socket too shallow and femoral head not held tightly in place.

403
Q

Give two treatment options for developmental dysplasia of the hip.

A
  • Harness

- Surgery

404
Q

Describe slipped capital femoral epiphysis.

A

The epiphyseal growth plate slips and the femur moves superiorly compared to the epiphysis.

405
Q

How does sepsis in a joint lead to arthritis?

A

It causes chondrolysis

406
Q

What three aspects of an orthopaedic history are ‘most important’/

A
  • SOCRATES
  • Occupation
  • Handedness (left/right)
407
Q

Briefly describe the blood supply to the femoral head.

A

The profunda femoris artery gives rise to the lateral and medial circumflex arteries.

408
Q

Which type of hip fracture can cut off the blood supply to the femoral head?

A

Intracapsular fracture

409
Q

Describe a type 1 intracapsular hip fracture.

A

Incomplete, doesn’t affect blood supply to head

410
Q

Describe a type 2 intracapsular hip fracture.

A

Complete, not displaced, doesn’t cut off blood supply to head

411
Q

Describe a type 3 and type 4 hip fracture.

A

Displaced, interrupted blood supply to femoral head

412
Q

How are type 1 and type 2 hip fractures fixed?

A

Using screws

413
Q

How are type 3 and type 4 hip fractures fixed?

A

Hemiarthroplasty or full arthroplasty

414
Q

Describe an extracapsular hip fracture in terms of blood supply.

A

The blood supply to the femoral head is maintained.

415
Q

How are extracapsular hip fractures fixed?

A

Screws

416
Q

Give the three principles of management of orthopaedic trauma.

A
  • Reduce (put back in line)
  • Stabilise (nails)
  • Rehabilitate (walk)
417
Q

Give the four stages of fracture healing.

A
  1. Haematoma formation
  2. Fibrocartilagenous callus formation
  3. Bony callous formation
  4. Bone remodelling
418
Q

Give six cytokines/molecules requires for haematoma formation after a fracture.

A
  • IL-1
  • IL-6
  • IL-12
  • TNF-a
  • PDGF
  • COX2 (required for osteoblasts)
419
Q

What is cauda equina syndrome?

A

Compression or damage of the cauda equina below the spinal cord.

420
Q

Describe and explain the typical urinary symptoms experienced in cauda quina syndrome.

A
  • Pudendal nerve compression
  • Can’t relax external sphincter
  • Overflow incontinence
421
Q

Give five signs/symptoms of cauda equina syndrome.

A
  • Uni/bilateral leg pain
  • Perineal numbness
  • Back pain
  • Urinary symptoms
  • May have faecal problems
422
Q

What is the treatment for cauda equina syndrome?

A

Decompression

423
Q

What is contained within hyaline cartilage which attracts water to it?

A

Proteoglycans (hyaluronic acid)

424
Q

What is crystal arthritis?

A

Arthritis caused by crystal deposition in the joint lining.

425
Q

What is a crystal?

A

A homogenous solid formed of ions bonded closely in ordered, repeating, symmetric arrangement.

426
Q

Give two reasons why crystals are necessary in animals.

A
  • To strengthen exoskeleton and endoskeleton

- Remove excess ions by surface binding

427
Q

What does crystal deposition in the body lead to?

A

Local inflammatory response and tissue damage.

428
Q

What is the condition called when crystals are deposited in the gallbladder or kidney.

A

Nephrolithiasis

429
Q

Give four types of crystal that can be deposited in joints to cause crystal arthritis.

A
  • Monosodium urate
  • Calcium pyrophosphate
  • Calcium hydroxyapatite
  • Cholesterol
430
Q

What is the medical condition which results from monosodium urate crystal deposition in the joints?

A

Gout

431
Q

Is gout more common in men or women?

A

Men

432
Q

When does the incidence of gout rise in women?

A

Postmenopause (often related to identifiable trigger)

433
Q

What is the commonest arthritis in men >40yrs?

A

Gout

434
Q

Give some causes of under-excretion of urate.

A
  • Alcohol
  • Renal impairment
  • Hypertension
  • Inherited metabolic
  • Hypothyroidism
  • Hyperparathyroidism
  • Obesity
  • Diabetes
  • Low dose aspirin
  • Diuretics
  • Cyclosporine/tacrolimus
  • Ethambutol/pyrazinamide
435
Q

Give some causes for over-production of urate.

A
  • Diet
  • Metabolic syndrome (hyperlipidaemia)
  • Proliferative (myeloproliferative, cytotoxic drugs)
  • Psoriasis
  • Lesch-Nyhan syndrome
436
Q

Give nine dietary factors which may increase urate levels in the body.

A
  • Red meat
  • Fizzy drinks
  • Sugar
  • Alcohol
  • Shellfish
  • Offal
  • Gravy
  • Yeast
  • Fructose
437
Q

Give a dietary factor that may be protective against gout.

A

Dairy products

438
Q

Give nine factors that may cause a sudden alteration in uric acid concentration, leading to acute attacks of gout.

A
  • Aggressive hypouricaemic therapy
  • Alcohol/shellfish binge
  • Sepsis
  • MI
  • Acute severe illness
  • Sudden cessation of hypouricaemic therapy
  • Trauma
  • Surgery
  • Dehydration
439
Q

How is uric acid produced in the body?

A

Purine metabolism by xanthine oxidase.

440
Q

What is the concentration of uric acid at which the serum is saturated?

A

0.3mmol/L

441
Q

At what serum level of uric acid is a patient at risk of crystal deposition?

A

> 0.36mmol/L

442
Q

At what serum level of uric acid does supersaturation occur, making crystal deposition very likely?

A

> 0.42mmol/L

443
Q

Give the steps in purine metabolism leading to uric acid.

A

Purine -> hypoxanthine -> xanthine -> uric acid

444
Q

Describe the acute presentation of gout.

A
  • Hot, swollen, painful joint
  • Often affects first metatarso-phalangeal joint
  • Systemically unwell
445
Q

How does chronic gout usually present?

A

Longer term joint damage and tophi under the skin.

446
Q

What are tophi?

A

Onion-like aggregates of urate crystals with inflammatory cells.

447
Q

How long does it take to control attacks of tophaceous gout?

A

6-9months

448
Q

How long can it take for tophi to resolve?

A

Up to 2 years

449
Q

Give three investigations that should be carried out in gout.

A
  • Joint aspiration
  • Blood tests
  • X rays
450
Q

What would you expect the serum urate level to be in gout?

A

May be high, but may be normal or low in acute attacks.

451
Q

Give two features of gout that may be seen on an xray.

A
  • Punched out bone lesions

- Narrow joint space

452
Q

How would the crystals appear under a microscope in gout?

A

Negatively birefringent needles

453
Q

How would the crystals appear under the microscope in pseudogout?

A

Weakly positive birefringent rhomboids

454
Q

Give four things that can be used to treat acute attacks of gout.

A
  • Anti-inflammatories
  • NSAIDs
  • Colchicine
  • Steroids
455
Q

Describe the longer term treatment for prevention of gout.

A
  • Xanthine oxidase inhibitors (allopurinol or febuxostat)

- Cover with colchicine or NSAID at start (otherwise gouty flare may be induced)

456
Q

What is the disease called when calcium pyrophosphate crystals are deposited on a joint surface?

A

Pseudogout

457
Q

Give two groups of patients in whom pseudogout is more common.

A
  • Elderly

- Females

458
Q

What other rheumatological condition often occurs with pseudogout?

A

Osteoarthritis

459
Q

Give four places that pseudogout typically affects.

A
  • Knees
  • Wrists
  • Shoulders
  • Hips
460
Q

Give some triggers of acute pseudogout attacks.

A
  • Direct trauma
  • Intercurrent illness
  • Surgery (parathyroidectomy)
  • Blood transfusion
  • IV fluid
  • T4 replacement
  • Joint lavage
  • Most are spontaneous
461
Q

Describe the presentation of pseudogout.

A
  • Acute synovitis
  • Acute monoarthritis in elderly
  • Severe pain, stiffness, swelling
  • Fever
462
Q

Give a classical joint distribution which suggests pseudogout instead of osteoarthritis.

A

2nd and 3rd metacarpo-phalangeal joint swelling

463
Q

What would the X ray show in pseudogout?

A

Chondrocalcinosis

464
Q

Describe the treatment for pseudogout.

A

Usually resolves in 1-3 weeks.

Drugs not very effective.

465
Q

What can be used to treat the symptoms of pseudogout?

A
  • NSAIDs
  • Analgesia
  • Aspiration
  • Injection
  • Physiotherapy
466
Q

What treatment may be tried if there are continued inflammatory changes in pseudogout?

A
  • Anti-rheumatic treatment
  • Synovectomy
  • Surgery
467
Q

Give the typical patient demographic for calcium hydroxyapatite crystal arthropathy.

A

Elderly females

468
Q

Describe the damage that occurs in calcium hydroxyapatite crystal arthropathy.

A

Destructive attacks on the shoulders

469
Q

Give eight metabolic diseases which are associated with gout.

A
  • Haemochromatosis
  • Hyperparathyroidism
  • Hypophosphatasia
  • Hypomagnesaemia
  • Hypothyroidism
  • Acromegaly
  • Familial hypocalciuric hypercalcaemia
  • X-linked hypophosphataemic rickets
470
Q

Give four indications to screen for a metabolic disease when someone presents with gout.

A
  • Early onset (<55)
  • Polyarticular
  • Frequent recurrent attack
  • Additional clinical or radiographic clues
471
Q

Define osteoporosis.

A

A metabolic bone disease characterised by a generalised reduction in bone mass, increased bone fragility, and predisposition to fracture.

472
Q

What is the likely consequence if trabecular bone is affected by osteoporosis?

A

Crush fractures of the vertebrae

473
Q

What is the likely consequence if cortical bone is affected by osteoporosis?

A

Long bone fractures

474
Q

What is the prevalence of osteoporosis in men over 50 years?

A

6%

475
Q

What is the prevalence of osteoporosis in women over 50 years?

A

18%

476
Q

What are the risk factors for developing osteoporosis?

A

SHATTERED FeMur

  • Steroid use
  • Hyperthyroidism, hyperparathyroidism, hypercalciuria
  • Alcohol and tobacco use
  • Thin (BMI<22)
  • Testosterone low
  • Early menopause (or low oestrogen)
  • Renal or liver failure
  • Erosive/inflammatory bone or bowel disease (myeloma/RA)
  • Dietary (low calcium, malabsorption, Type 1 DM)
  • Family history
  • Mobility low
477
Q

Briefly describe the pathology of osteoporosis.

A
  • Peak bone mass and rate of bone loss affect bone mineral density
  • Bone turnover and architecture affect bone quality
  • Bone quality and density affect strength, and reduced strength leads to fractures
478
Q

Describe what causes post-menopausal osteoporosis, and its features.

A
  • Loss of restraining effects of oestrogen on bone turnover

- Characterised by high bone turnover, predominantly cancellous bone affected, and microarchitectural disruption

479
Q

Give three ways that osteoporosis develops with age.

A
  • Decrease in trabecular thickness
  • Decrease in connections between horizontal trabeculae
  • Decrease in trabecular strength and increased susceptibility to fracture
480
Q

Why aren’t Xrays usually used to diagnose osteoporosis?

A

They have low sensitivity and specificity

481
Q

What would blood tests usually show in osteoporosis?

A

Normal calcium, phosphate, and alkaline phosphatase

482
Q

What test is used to diagnose osteoporosis?

A

DEXA

483
Q

What does DEXA stand for?

A

Dual energy X-ray absorptiometry

484
Q

Which bones are used for a DEXA scan?

A
  • lumbar spine
  • proximal femur
  • distal radius
485
Q

What does DEXA measure?

A

Bone mineral density (g/cm2) compared to a young healthy adult

486
Q

What is meant by the DEXA T-score?

A

The number of standard deviations away from the bone mineral density of a young adult.

487
Q

What does a DEXA T-score >0 mean?

A

BMD better than the reference

488
Q

What does a DEXA T-score 0 to -1 mean?

A

BMD in the top 84%, no evidence of osteoporosis

489
Q

What does a DEXA T-score of -1 to -2.5 mean?

A

Osteopenia

490
Q

What action should be taken for a DEXA T-score of -1 to -2.5?

A

Give lifestyle advice

491
Q

What does a DEXA T-score of -2.5 or worse mean?

A

Osteoporosis

492
Q

What action should be taken for a DEXA T-score worse than 2.5?

A

Lifestyle advice and treatment

493
Q

What risk assessment tool can estimate the 10yr risk of an osteoporotic fracture?

A

FRAX

494
Q

Give six lifestyle advice treatments for osteoporosis.

A
  • Quit smoking
  • Reduce alcohol consumption
  • Weight-bearing exercise may increase BMD
  • Balance exercise reduces risk of falls
  • Calcium and vitamin D rich diet
  • Home-based fall prevention programme
495
Q

How do anti-resorptive pharmacological treatments for osteoporosis work in general?

A

Decrease osteoclast activity and bone turnover.

496
Q

Give three anti-resorptive pharmacological treatments for osteoporosis.

A
  • Bisphoshonates
  • Hormone replacement therapy
  • Denosumab
497
Q

Name a bisphosphonate used to treat osteoporosis.

A

Alendronate

498
Q

How do bisphosphonates work to treat osteoporosis?

A

Inhibit an enzyme in the cholesterol synthesis pathway (farnesyl pyrophosphate synthase) to cause apoptosis of osteoclasts.

499
Q

How does denosumab work to treat osteoporosis?

A

Monoclonal antibody to RANK-L

500
Q

How do anabolic pharmacological treatments for osteoporosis work in general?

A

Increase osteoblast activity and bone formation.

501
Q

Give an anabolic pharmacological treatment for osteoporosis.

A

Teriparatide (recombinant PTH)

502
Q

How is strontium ranelate used to treat osteoporosis?

A

It reduces fracture rates and can be an alternative to bisphosphonates.

503
Q

How does raloxifine work to treat osteoporosis?

A

It is a selective oestrogen receptor modulator

504
Q

How is calcitonin beneficial in osteoporosis?

A

It may reduce pain after a vertebral fracture

505
Q

What is implied by the term ‘mechanical’, when applied to lower back pain?

A

The pathology lies within the spinal joints, discs, vertebrae, or soft tissues.

506
Q

Give six associations with mechanical lower back pain.

A
  • Heavy manual handling
  • Stooping and twisting whilst lifting
  • Exposure to whole body vibration
  • Psychosocial distress
  • Smoking
  • Dissatisfaction with work
507
Q

Where might the pathology lie if the patient experiences pain on bending forwards?

A

Intervertebral discs

508
Q

Where might the pathology lie if the patient experiences pain on bending backwards?

A

Facet joints

509
Q

Give two normal findings on an MRI scan in mechanical lower back pain.

A
  • Disc degeneration

- Bulging discs

510
Q

Give five management points for mechanical lower back pain.

A
  • Avoid prolonged inactivity
  • Maintain normal activities within limits of back pain
  • Simple analgesics or NSAIDs
  • Spinal manipulative therapy
  • Spinal exercises, behavioural therapy, and workplace adaptations (to return patient to work)
511
Q

How early do vertebral discs undergo degeneration compared to other connective tissues in the body?

A

They are the earliest connective tissue to undergo degeneration.

512
Q

Give three strong associations with vertebral disc degeneration.

A
  • Back pain
  • Sciatica
  • Disc herniation or prolapse
513
Q

What is a Schmorl’s node?

A

Formed when the nucleus pulposus of a vertebral disc herniates vertically into an adjacent vertebral body.

514
Q

Give three pathological steps in vertebral disc degeneration.

A
  • Disc becomes more disorganised
  • Nerves and blood vessels increasingly found
  • Cell death by necrosis
515
Q

What percentage of women will have a fracture due to osteoporosis in their lifetime?

A

50%

516
Q

Why do cortisol and steroids cause osteoporosis?

A

Cortisol increases bone resorption and induces osteoblast apoptosis.

517
Q

Why does ageing cause degeneration of the horizontal bone trabeculae before vertical trabeculae?

A

Vertebral trabeculae are preserved because most skeletal strain is vertical.

518
Q

Give three deformities that may be seen in the hand in Rheumatoid Arthritis.

A
  • Ulnar deviation
  • Boutonniere deformity
  • Swan neck deformity
519
Q

Describe Boutonniere deformity.

A

Proximal interphalangeal joint flexion and distal interphalangeal joint extension.

520
Q

Describe swan neck deformity.

A

Proximal interphalangeal joint extension and distal interphalangeal joint flexion.

521
Q

Give another name for the popliteal cyst which may appear in Rheumatoid arthritis.

A

Baker’s cyst

522
Q

Describe what causes a Baker’s cyst in Rheumatoid Arthritis.

A

The synovial sack of the knee joint bulges posteriorly.

523
Q

Give an antibody found in the antiphospholipid syndrome.

A

Anti-cardiolipin

524
Q

Give three features of antiphospholipid syndrome.

A
  • Arterial thrombosis
  • Venous thrombosis
  • Recurrent abortion

Phase2a (12 decks)

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