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Phase 2a > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

Which cancers are most likely to metastasise to bone?

A
  • prostate
  • breast
  • lung
  • kidney
  • thyroid
  • myeloma
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2
Q

What are some side effects of bisphosphonates?

A
  • fever / flu-like symptoms
  • hypocalcaemia
  • bone & joint pain
  • constipation / diarrhoea
  • oesophagitis / oesophageal irritation
  • osteonecrosis of the jaw
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3
Q

Examples of bisphosphonates?

A
  • alendronic acid
  • zoledronic acid

(-dronic acid / -dronate)

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4
Q

Bisphosphonates mechanism of action?

A
  • pyrophosphate analogues
  • bind to hydroxyapatite crystals
  • promote osteoclast apoptosis and disrupt cholesterol synthesis pathway (to decrease osteoclast function)
  • decreased bone resorption
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5
Q

X ray features of osteoarthritis?

A
  • joint space narrowing
  • osteophyte formation
  • subchondral cysts
  • subchondral sclerosis
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6
Q

Investigation to diagnose Sjögren’s syndrome?

A

Schirmer’s test - strip of paper in eye to measure tear production.
Tear production is decreased in Sjögren’s syndrome.

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7
Q

What does a pencil-in-cup X ray deformity signify?

A
  • arthritis mutilans

- may indicate psoriatic arthritis

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8
Q

What does a bamboo spine deformity signify?

A

Advanced ankylosing spondylitis

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9
Q

First-line management of ankylosing spondylitis?

A

Ibuprofen

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10
Q

Preventative gout medication?

A

Allopurinol

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11
Q

Allopurinol mechanism of action?

A

Reduces production of uric acid by inhibiting xanthine oxidase.

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12
Q

T score for osteoporosis?

A

< -2.5

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13
Q

T score for osteopenia?

A

-1 to -2.5

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14
Q

What autoantibodies are found in granulomatosis with polyangiitis?

A

cANCA (antis neutrophil cytoplasmic antibodies)

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15
Q

What was granulomatosis with polyangiitis formerly known as?

A

Wegener’s granulomatosis

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16
Q

What are some clinical manifestations of granulomatosis with polyangiitis?

A
  • sinusitis
  • nose bleeds
  • saddle shaped nose (perforated septum)
  • cough, wheeze, haemoptysis
  • glomerulonephritis
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17
Q

Investigations for Sjögren’s syndrome?

A

Blood tests - ANA, anti-Ro, anti-La, rheumatoid factor

Schirmer test

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18
Q

What type of arthritis does Sjögren’s syndrome cause?

A
  • chronic (there may be acute flares)
  • systemic
  • inflammatory
  • symmetric
  • autoimmune
  • non-erosive
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19
Q

Management of Sjögren’s syndrome?

A
  • artificial saliva / tears
  • vaginal lubricants
  • pilocarpine (muscarinic agonist)
  • corticosteroids
  • methotrexate / azathioprine / cyclophosphamide
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20
Q

What is Sjögren’s syndrome?

A

Lymphocyte-mediated autoimmune disease characterised by destruction of the minor salivary glands, lacrimal glands and joints.

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21
Q

Clinical triad found in Sjögren’s syndrome?

A
  • xerostomia (dry mouth)
  • xerophthalmia (dry eyes)
  • inflammatory arthritis
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22
Q

What diseases might Sjögren’s syndrome occur secondary to?

A
  • rheumatoid arthritis
  • SLE
  • other autoimmune conditions
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23
Q

What autoantibodies are found in patients with SLE?

A
  • ANA

- anti-dsDNA

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24
Q

What gene is associated with ankylosing spondylitis?

A

HLA B27

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25
Q

X ray findings in ankylosing spondylitis?

A
  • bamboo spine
  • vertebral body squaring
  • subchondral sclerosis and erosions
  • syndesmophytes
  • ossification of ligaments, discs and joints
  • fusion of costovertebral & sacroiliac joints
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26
Q

Anti-TNF drug examples?

A
  • infliximab
  • adalimumab
  • etanercept
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27
Q

Pathophysiology of osteoarthritis?

A

Imbalance between cartilage being worn down and chondrocytes repairing it.

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28
Q

What is Paget’s disease of bone?

A

Excessive uncoordinated bone turnover, with increased activity of both osteoblasts and osteoclasts.
Particularly affects the axial skeleton.

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29
Q

How does the skull appear in Paget’s disease of bone?

A

Cotton wool appearance due to patches of increased and decreased density.

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30
Q

Which antibody is most specific for rheumatoid arthritis?

A

anti-cyclic citrullinated peptide antibody

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31
Q

Management of rheumatoid arthritis?

A
  1. DMARD monotherapy (methotrexate / leflunomide / sulfasalazine)
  2. DMARDs x 2
  3. methotrexate + anti-TNF
  4. methotrexate + rituximab
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32
Q

What is Felty’s syndrome?

A

Complication of rheumatoid arthritis.

  • rheumatoid arthritis
  • neutropenia
  • splenomegaly
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33
Q

What is polymyalgia rheumatica?

A

Immune-mediated inflammatory disorder causing pain, stiffness and inflammation in the shoulders, neck, and hip muscles.

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34
Q

What is dermatomyositis?

A

Chronic inflammation of the skin and muscles.

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35
Q

What is polymyositis?

A

Chronic inflammation of the muscles.

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36
Q

What are some blood markers for dermato- / polymyositis?

A
  • raised creatinine kinase
  • anti-Jo-1
  • anti-Mi-2 (dermatomyositis only)
  • ANA (dermatomyositis only)
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37
Q

What are the muscle symptoms of dermato- / polymyositis?

A
  • muscle pain, fatigue, and weakness
  • bilateral
  • typically proximal muscles affected
  • shoulder and pelvic girdle
  • develops over weeks
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38
Q

What are the skin symptoms of dermatomyositis?

A
  • Gottron lesions (erythematous plaques)
  • photosensitive erythematous rash on back, shoulders, and neck
  • purple rash on face & eyelids
  • periorbital oedema
  • subcutaneous calcinosis
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39
Q

What is the function of 1-alpha-hydroxylase?

A

Hormone secreted by the proximal convoluted tubule, activates vitamin D to form calcitriol.

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40
Q

What condition causes brittle bones in adults due to a lack of vitamin D?

A

osteomalacia

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41
Q

What condition occurs in children due to a lack of vitamin D?

A

Ricketts

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42
Q

Why does Ricketts not occur in adulthood?

A

Ricketts occurs due to impaired bone mineralisation PRIOR to epiphyseal closure.

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43
Q

How is giant cell arteritis diagnosed?

A

Multinucleated giant cells seen on temporal artery biopsy.

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44
Q

Management of giant cell arteritis?

A

Steroids

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45
Q

Gout microscopy appearance?

A
  • negatively birefringent on polarised light microscopy

- needle-shaped monosodium urate crystals

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46
Q

Pseudogout microscopy appearance?

A
  • positively birefringent on polarised light microscopy

- rhomboid crystals of calcium pyrophosphate

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47
Q

Classic X ray change in pseudogout?

A

chondrocalcinosis - thin white line in joint space due to calcium deposition

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48
Q

Most common joint affected in pseudogout?

A

knee

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49
Q

What is fibromyalgia?

A

Disorder characterised by widespread musculoskeletal pain accompanied by fatigue, sleep, memory and mood issues.

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50
Q

What are some risk factors for developing fibromyalgia?

A
  • depression, anxiety, stress
  • dissatisfaction at work
  • middle age
  • low income
  • divorced
  • low educational status
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51
Q

What empirical antibiotics are first line for septic arthritis?

A

Flucloxacillin + rifampicin for the first two weeks.

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52
Q

OA vs RA pattern of joint involvement?

A

OA - asymmetrical

RA - symmetrical

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53
Q

OA vs RA most common joints affected?

A

OA - DIPJs, knees, hips

RA - PIPJs (rarely DIPJs), wrists, feet

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54
Q

OA vs RA joint stiffness?

A

OA - less than 30 minutes morning stiffness

RA - more than 30 minutes morning stiffness

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55
Q

OA vs RA effect of movement?

A

OA - pain worsens with movement

RA - pain improves with movement

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56
Q

Osteoarthritis hand signs?

A

Bouchard’s nodes (PIPJ)
Heberden’s nodes (DIPJ)
B comes before H

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57
Q

Genetic associations of RA?

A

HLA DR4 / HLA DR2

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58
Q

RA X ray signs?

A

LESS

  • loss of joint space
  • erosions
  • soft tissue swelling
  • soft bones
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59
Q

RA hand signs?

A
  • Boutonniere deformity
  • swan neck deformity
  • ulnar deviation
  • Z shaped thumb deformity
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60
Q

Side effects of methotrexate?

A
  • pulmonary fibrosis

- teratogenic

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61
Q

What is taken with methotrexate?

A

Folic acid (on a DIFFERENT day)

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62
Q

What is Caplan’s syndrome?

A

Rheumatoid pneumoconiosis - occurs in people with RA who have inhaled coal dust / silica.
Pulmonary fibrosis with pulmonary nodules.

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63
Q

What is osteoporosis?

A

Skeletal disease characterised by low bone density and micro-architectural defects in bone tissue, resulting in increased bone fragility and susceptibility to fracture.

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64
Q

Risk factors for osteoporosis?

A
  • steroid use
  • hyperthyroidism / hyperparathyroidism
  • low BMI
  • early menopause
  • malabsorption
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65
Q

Protective factor for oestoporosis?

A

Oestrogen

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66
Q

Investigations for osteoporosis?

A
  • x-ray shows fragility fractures
  • DEXA scan
  • FRAX score
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67
Q

What is the FRAX score?

A

Risk of a fragility fracture over the next 10 years.

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68
Q

Classic triad of symptoms of reactive arthritis?

A

Can’t see, can’t pee, can’t climb a tree.

conjunctivitis, urethritis, arthritis

69
Q

Most common cause of native joint septic arthritis?

A

Staph aureus

70
Q

Cause of septic arthritis in young & sexually active patients?

A

Neisseria gonorrhoea

71
Q

Cause of septic arthritis in joint replacement patients?

A

Staph epidermidis

72
Q

Cause of septic arthritis in IVDU / immunocompromised?

A
  • E. coli

- pseudomonas aeruginosa

73
Q

Antibodies associated with SLE?

A
  • ANA (non-specific)

- anti-dsDNA (highly specific)

74
Q

Syndromes associated with SLE?

A
  • antiphospholipid syndrome

- Raynaud’s

75
Q

First line for mild SLE?

A

Hydroxychloroquine

76
Q

Bone tumour symptoms?

A
  • persistent bone pain
  • nocturnal bone pain
  • rest pain
  • unexplained fractures
  • fatigue / weight loss / fever
  • swelling / lump
77
Q

What group of patients does osteosarcoma most commonly affect?

A

More common in males than females.

Peak incidence 13-16 years.

78
Q

Distinguishing features of osteosarcoma?

A
  • childhood and adolescence
  • overlying skin ulceration
  • affects the distal femur, proximal tibia (bones around the knee)
79
Q

Distinguishing features of Ewing’s sarcoma?

A
  • childhood and adolescence
  • may affect pelvis, femur, humerus, ribs
  • onion skin x ray appearance
80
Q

Distinguishing features of chondrosarcoma?

A
  • affects adults over 40
  • femur, pelvis, arm, knee
  • ring and arcs calcification
81
Q

What is pANCA?

A

perinuclear ANCA (targets MPO inside neutrophils)

82
Q

What is cANCA?

A

cytoplasmic ANCA

83
Q

What type of hypersensitivity reaction is SLE?

84
Q

Rheumatological condition associated with miscarriage?

85
Q

What is Raynaud’s associated with?

A
  • SLE
  • systemic sclerosis
  • RA
  • dermatomyositis
86
Q

Medication for Raynaud’s?

87
Q

What is systemic sclerosis?

A

Multisystem autoimmune disease in which there is increased fibroblast activity, and therefore increased collagen deposition. This results in abnormal growth of connective tissue.

88
Q

Signs and symptoms of systemic sclerosis?

A
  • beak-like nose and small mouth
  • calcinosis (deposition in subcutaneous tissues)
  • raynauds
  • oesophageal dysmotility or strictures
  • sclerodactyly (thickening of skin on fingers / toes)
  • telangiectasia
    (CREST)
89
Q

Organ involvement in systemic sclerosis?

A
  • GI
  • renal
  • lung
90
Q

Management of systemic sclerosis?

A

Manage symptoms:

  • GI - PPIs
  • renal - ACEi
  • pulmonary fibrosis - cyclophosphamide
  • Raynaud’s - handwarmers
91
Q

Investigations for Paget’s disease?

A
  • ALP elevated
  • calcium and phosphate normal
  • X rays show osteoarthritis, cotton wool skull appearance
92
Q

Management of Paget’s disease?

A
  • bisphosphonates

- NSAIDs

93
Q

What is osteomalacia?

A

Defective bone mineralisation due to inadequate phosphate / calcium or due to increased bone resorption (hyperparathyroidism).

94
Q

What is osteomyelitis?

A

Infection of bone marrow.

95
Q

Routes of infection in osteomyelitis?

A
  • haematogenous
  • open wound
  • contiguous from skin
96
Q

Gold standard for osteomyelitis diagnosis?

A

Bone biopsy

97
Q

What is osteoarthritis?

A

Degenerative synovial joint disorder, characterised by progressive loss of articular cartilage and remodelling of the underlying bone.

98
Q

Risk factors for OA?

A
  • older age
  • female
  • obesity
  • previous trauma
  • manual occupation
99
Q

What is an osteophytes?

A

Boney spur growing around a joint.

100
Q

What is a subchondral cyst?

A

Sac of fluid formed inside a joint.

101
Q

Investigations for OA?

A

Diagnosis can be made clinically if patient is over 45 with typical OA presentation.

  • x-rays
  • CRP / ESR (normal)
102
Q

Management of OA?

A
  • exercise (muscle strengthening and aerobic fitness)
  • physiotherapy
  • weight loss
  • step-wise approach to pain management
  • arthroplasty
103
Q

Risk factors for RA?

A
  • family Hx
  • smoking
  • female
104
Q

How does RF cause disease?

A
  • targets Fc portion of the IgG antibody

- results in recruitment of inflammatory cells and complement activation

105
Q

Investigations for RA?

A
  • RF, anti-CCP
  • CRP / ESR
  • FBC (anaemia)
  • x-ray
  • MRI
106
Q

Summary of RA management?

A
  • DMARDs
  • corticosteroids & NSAIDs (adjuncts)
  • biological therapies
  • arthroplasty / arthroscopy
  • analgesia
  • physiotherapy
107
Q

Drug for mild RA?

A

Hydroxychloroquine

108
Q

Pharmacological management of RA?

A
  1. Methotrexate / leflunomide / sulfasalazine monotherapy.
  2. Combination of DMARDs.
  3. Methotrexate + anti-TNF (infliximab).
  4. Methotrexate + rituximab.
109
Q

Mechanism of action of methotrexate?

A

Disrupts folate metabolism and suppresses components of the immune system.

110
Q

Side effects of anti-TNF drugs?

A

Reactivation of TB and hep B.

111
Q

Side effects of rituximab?

A
  • night sweats

- thrombocytopenia

112
Q

Complications of RA?

A
  • Felty syndrome
  • pericarditis
  • pleural effusions
113
Q

What are tophi?

A

Subcutaneous deposits of uric acid. Typically affect the small joints and connective tissues of the hands (DIPJs), elbows and ears.

114
Q

Risk factors for gout?

A
  • male
  • obesity
  • high purine diet (meat and seafood)
  • excessive alcohol
  • diuretics
  • renal impairment
  • older age
115
Q

Pathophysiology of gout?

A
  • hyperuricaemia results in super-saturation and crystal formation (monosodium urate)
  • urate crystals trigger an acute inflammatory response, activating cytokines and signalling pathways
  • influx of neutrophils into the joint
116
Q

How does gout resolve (spontaneously)?

A

Clearance of urate crystals by macrophages.

117
Q

Gold standard investigation for gout?

A

Joint fluid aspiration with synovial fluid analysis.

118
Q

Differentials for gout?

A
  • pseudogout

- septic arthritis

119
Q

Treatment of acute gout?

A
  1. NSAIDs
  2. colchicine
  3. corticosteroids
120
Q

Long term gout prevention?

A
  • allopurinol (xanthine oxidase inhibitor)

- dietary modifications and weight loss

121
Q

Pathophysiology of pseudogout?

A
  • chondrocytes deposit calcium pyrophosphate
  • local CPP supersaturation (due to excess production) leads to crystal formation
  • crystals stimulate a pro-inflammatory response with activation of phagocytes and neutrophils
122
Q

Gold standard investigation for pseudogout?

A

Joint aspiration and synovial fluid analysis.

123
Q

Management of pseudogout?

A 
Conservative: ice packs, rest joint.
Pharmacological: NSAIDs, colchicine, corticosteroids.
Joint injection (corticosteroid + lidocaine).
124
Q

What gene are spondyloarthropathies associated with?

125
Q

What is ankylosing spondylitis?

A

Seronegative inflammatory arthritis characterised by inflammation of the sacroiliac joints and the axial skeleton.

126
Q

Risk factors for AS?

A
  • male
  • family Hx
  • HLA-B27
127
Q

Pathophysiology of AS?

A
  • inflammation between vertebrae and intervertebral discs results in ossification and syndesmophyte formation
  • syndesmophyte bridging across multiple vertebrae leads to ‘bamboo spine’
128
Q

What are syndesmophytes?

A

Ossified spinal ligaments

129
Q

Typical presentation of AS?

A

Young male with chronic lower back pain and morning stiffness.
May have achilles tendon enthesitis and anterior uveitis.

130
Q

7 As of AS?

A
  • aortitis
  • anterior uveitis
  • AV block
  • atlanto-axial instability
  • apical lung fibrosis
  • amyloidosis
  • IgA nephropathy
131
Q

Schober test?

A

Test of spinal movement limitation in AS.

Increase of less than 5cm during flexion is a positive result.

132
Q

X ray signs in AS?

A
  • dagger sign (central radiodense line due to ligament ossification)
  • bamboo spine
  • squaring of vertebral bodies
  • syndesmophytes
  • vertebral body fusion
133
Q

Investigations for AS?

A
  • x-rays
  • genetic testing (HLA-B27)
  • CRP / ESR elevated
134
Q

Management of AS?

A
  1. Non-pharmacological (physiotherapy).
  2. NSAIDs (+ PPIs).
  3. Methoxtrexate
  4. Anti-TNF agents.
135
Q

Complications of AS?

A
  • limited mobility (due to spinal fusion)
  • osteoporosis
  • spinal cord injury
  • restrictive lung disease (fibrosis)
136
Q

What is psoriatic arthritis?

A

Seronegative inflammatory spondyloarthritis associated with psoriasis.

137
Q

Pattern of joint involvement in psoriatic arthritis?

A
  • symmetrical polyarthritis (similar to RA)

- spondylitic pattern (similar to AS)

138
Q

Signs and symptoms of psoriatic arthritis?

A
  • psoriatic plaques
  • nail pitting and onycholysis
  • dactylitis
  • enthesitis
  • inflammatory eye disease
  • arthritis mutilans
139
Q

What is onycholysis?

A

Separation of the nail from the nail bed.

140
Q

X ray findings in psoriatic arthritis?

A
  • pencil-in-cup deformities (erosions)
  • soft tissue swelling
  • osteolysis
  • syndesmophytes (advanced spinal involvement)
141
Q

Management of psoriatic arthritis?

A
  1. NSAIDs
  2. Methotrexate
  3. Anti-TNF agents
142
Q

What is reactive arthritis?

A

Seronegative inflammatory arthritis causing sterile joint inflammation post-infection.

143
Q

What infections commonly precede reactive arthritis?

A

Urogenital (chlamydia, neisseria gonorrhoeae).

GI (campylobacter, shigella, salmonella).

144
Q

What is Poncet’s disease?

A

Reactive arthritis caused by mycobacterial infection.

145
Q

Pathophysiology of reactive arthritis?

A

Molecular mimicry - cross reaction of pathogen antigens with self antigens.

146
Q

Investigations for reactive arthritis?

A
  • joint aspiration and synovial fluid analysis
  • blood cultures
  • x-rays
  • mid-stream urine MC&S
147
Q

Management of reactive arthritis?

A
  • treat precipitating infection
  • NSAIDs
  • corticosteroids
  • steroid joint injection
148
Q

What is SLE?

A

Inflammatory autoimmune connective tissue disease, affecting multiple organs and systems.

149
Q

Risk factors for SLE?

A
  • female
  • Black ethnicity
  • family history
150
Q

Signs and symptoms of SLE?

A
  • fatigue, weight loss
  • arthralgia and myalgia (non-erosive arthritis)
  • photosensitive malar rash / discoid rash
  • dyspnoea & pleuritic chest pain
  • mouth ulcers
  • hair loss
  • Raynaud’s
  • thrombosis
151
Q

Investigations for SLE?

A
  • ANA and anti-dsDNA antibodies
  • prothrombin time & anti-phospholipid antibodies
  • CXR
  • chest CT
  • X-rays of joints
  • renal biopsy (for lupus nephritis)
152
Q

Management of SLE?

A
  • hydroxychloroquine
  • corticosteroids
  • methotrexate
  • rituximab
  • sun protection
153
Q

Complications of SLE?

A
  • anaemia
  • pericarditis
  • pleural effusion
  • lupus nephritis
  • thrombosis
  • susceptible to infection
  • corticosteroid-related complications
154
Q

Most common cause of back pain?

A

Mechanical

155
Q

Differentials for back pain?

A
  • mechanical
  • spondyloarthritis
  • osteomyelitis
  • malignancy
  • fracture
  • osteoarthritis
  • pyelonephritis
156
Q

Treatment of fibromyalgia?

A

Neuropathic pain relief - tricyclic antidepressants (amitriptyline), gabapentin, pregabalin.
Opiates

157
Q

What is fibromyalgia?

A

Chronic pain syndrome characterised by the presence of widespread body pain (neuropathic). Often co-morbid symptoms - fatigue, memory and mood problems, sleep disturbance.

158
Q

Criteria for fibromyalgia diagnosis?

A

11 out of 18 tender point sites.

Pain history of at least 3 months.

159
Q

Inheritance of Marfan syndrome?

A

Autosomal dominant

160
Q

What is Marfan syndrome?

A

Autosomal dominant connective tissue disorder characterised by loss of elastic tissue.

161
Q

Complications of Marfan syndrome?

A
  • aortic dissection

- heart failure

162
Q

Signs and symptoms of Marfan syndrome?

A
  • tall stature
  • wide arm span
  • arachnodactyly
  • pectus excavatum
  • joint hypermobility
163
Q

Treatment of antiphospholipid syndrome?

164
Q

Most common cause of osteomyelitis in sickle cell anaemia patients?

A

salmonella

165
Q

Does alcohol cause osteoporosis or osteomalacia?

A

Osteoporosis

166
Q

Antibodies in anti-phospholipid syndrome?

A
  • lupus anticoagulant
  • anti-cardiolipin
  • anti-beta2 GP1
167
Q

Risk factors for osteomalacia?

A
  • reduced sun exposure

- low dietary vitamin D

168
Q

Age range in fibromyalgia?

Phase 2a (10 decks)

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