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Phase 2a > MSK > Flashcards

MSK Flashcards

1
Q

What are degenerative MSK disorders?

A

Disorders involving progressive impairment of both the structure and function of part of the body e.g. osteoarthritis

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2
Q

What are inflammatory MSK disorders?

A

Disorders involving a local response to cellular injury that is marked by redness, heat, pain, swelling and often loss of function e.g. rheumatoid arthritis

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3
Q

What are seronegative/seropositive MSK disorders testing for?

A

Rheumatoid factor

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4
Q

Name 2 differences between inflammatory and degenerative disorders

A

Inflammatory pain eases with use, degenerative pain increases with use
Inflammatory is significantly stiff for >60mins in the morning, degenerative is not prolonged <30mins

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5
Q

What are the 4 pillars of inflammation?

A

Red (rubor), painful (dolor), hot (calor), swollen (tumour)

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6
Q

What are the 2 markers of inflammation?

A

ESR and CRP

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7
Q

What is osteoarthritis?

A

A group of diseases characterised by joint degeneration. It is an age-related, dynamic reaction pattern of a joint in response to insult or injury

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8
Q

What are the features of osteoarthritis?

A

Affects synovial joints
All tissues of the joint are involved
Articular cartilage is the most affected

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9
Q

Describe the pathology of osteoarthritis

A

Insult to joint tissue initiating a cycle of cellular events, including low-grade chronic inflammation of the synovium, release of metalloproteinases, and degradation of articular cartilage matrix

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10
Q

What are the main pathological features of osteoarthritis?

A

Loss of cartilage, disordered bone repair

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11
Q

What are the risk factors for osteoarthritis?

A

Age, female gender, genetic predisposition, obesity, occupation

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12
Q

How does osteoarthritis present?

A

Joint pain, tenderness, swelling of small joints, stiffness, symptoms typically worsen during the day with activity

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13
Q

How is osteoarthritis diagnosed?

A 
Radiographs show LOSS;
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts
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14
Q

How is osteoarthritis managed?

A

Activity and exercise, weight loss
Analgesia, NSAIDs, DMARDs
Joint replacement/ arthroplasty

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15
Q

What is rheumatoid arthritis?

A

A multisystem autoimmune disease in which the brunt of disease activity falls upon the synovial joints

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16
Q

How does rheumatoid arthritis present?

A

Symmetrical, swollen, painful, stiff, small joints of hands and feet
Symptoms typically worse in morning

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17
Q

Where are rheumatoid nodules commonly found?

A

Pressure points e.g. olecranon

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18
Q

How is rheumatoid arthritis diagnosed?

A

Rheumatoid factor is positive
X-rays show soft tissue swelling, juxta-articular osteopenia and decrease joint space
US and MRI can identify synovitis

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19
Q

How is rheumatoid arthritis managed?

A

DMARDs
Steroids reduce symptoms and inflammation
Surgery may relieve pain, improve function, prevent deformity

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20
Q

What are the different patterns of fractures?

A

Transverse, oblique, spiral, butterfly, comminution, segmental, greenstick

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21
Q

How are fractures managed?

A

Analgesia, reduce, immobilise, rehabilitate

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22
Q

What are the risk factors for fractures?

A

Osteoporosis, metabolic bone disease e.g. osteomalacia, Paget’s disease, bone infiltrated by malignant tumours

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23
Q

Briefly describe how fractures heal

A

Haematoma organised and dead bone removed, callus formed, then replaced by trabecular bone, and finally remodelled into lamellar bone
Fracture healing delayed if bone ends are mobile, infected very badly, misaligned or avascular

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24
Q

What is osteoporosis?

A

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

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25
Q

What is the primary cause of osteoporosis?

A

Post-menopausal and age related (70+)

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26
Q

What are the secondary causes of osteoporosis?

A

Cushing’s, hyperparathyroidism, hypogonadism, coeliac disease, IBD, poor nutrition

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27
Q

What are the risk factors for osteoporosis?

A

SHATTERED;
Steroid use, hyperthyroidism, alcohol, thin, testosterone low, early menopause, renal failure, erosive bone disease, dietary low calcium

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28
Q

Why are women more likely to develop osteoporosis after menopause?

A

Oestrogen deficiency accelerates bone loss

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29
Q

What increases bone loss with increasing age?

A

Decreased bone turnover, decreased physical activity, reduce sex hormones and reduced calcium absorption from the gut

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30
Q

How can post-menopausal osteoporosis be prevented?

A

Oestrogen replacement

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31
Q

What changes to trabecular architecture occur with osteoporosis due to ageing?

A

Decreases in trabecular thickness, more pronounced for non-load bearing horizontal trabeculae
Decrease in connections between horizontal trabeculae
Decrease in trabecular strength and increased susceptibility to fracture

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32
Q

How does osteoporosis present?

A

Usually clinically silent until fragility fractures occur

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33
Q

What fractures are common when trabecular bone is affected?

A

Crush fractures of vertebrae

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34
Q

What fractures are common when cortical bone is affected?

A

Long bone fractures e.g. femoral neck

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35
Q

How is osteoporosis diagnosed?

A

X-ray: after a fracture
Bone densitometry DEXA scan: T score is number of standard deviations the bone mineral density is from the youthful average

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36
Q

What T score is osteopenia?

A

-1 to -2.5

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37
Q

What T score is osteoporosis?

A

-2.5 or worse

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38
Q

What questionnaire is used to evaluate the fracture risk of patients?

A

FRAX questionnaire - gives a 10 year probability of a fracture

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39
Q

How is osteoporosis managed through lifestyle measures?

A

Quit smoking and reduce alcohol consumption
Weight-bearing exercise may increase bone mineral density
Balance exercises such as tai chi reduce risk of falls
Calcium and vitamin D rich diet

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40
Q

How is osteoporosis managed pharmacologically?

A

1st line - bisphosphonates e.g. alendronic acid - decreases osteoclast activity and bone turnover
HRT - post-menopausal women

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41
Q

What is systemic sclerosis?

A

Condition featuring scleroderma (skin fibrosis), internal organ fibrosis and microvascular abnormalities

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42
Q

What are the features of systemic sclerosis?

A

Skin disease is limited (involves face/hands/feet) or diffuse (whole body).
No cure, immunosuppression required with BP monitoring

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43
Q

What are polymyositis and dermatomyositis?

A

Rare conditions characterised by insidious onset of progressive symmetrical proximal muscle weakness and autoimmune-mediated striated muscle inflammation

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44
Q

What is systemic lupus erythematosus?

A

A multisystem autoimmune disease characterised by autoantibody production against a number of nuclear and cytoplasmic autoantigens

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45
Q

Describe the pathology of SLE

A

Circulating immune complexes become deposited in tissues such as the skin, joints and kidneys where they stimulate inflammation and tissue damage

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46
Q

How does SLE present?

A

Fatigue, weight loss, low-grade fever, arthralgia (joint involvement), scaly red lesions on sun-exposed sites (skin involvement)

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47
Q

How is SLE diagnosed?

A

Clinical criteria
Acute - Malar rash
Chronic - Discoid rash
Synovitis, serositis, presence of proteinuria, thrombocytopenia

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48
Q

How is SLE managed?

A

Prednisolone for flares
NSAIDs, advance to methotrexate for maintenance
High-factor sun cream

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49
Q

What is Sjogren’s syndrome?

A

A chronic inflammatory autoimmune disorder, which may be primary or secondary, associated with connective tissue disease

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50
Q

What can Sjogren’s syndrome be secondary to?

A

SLE, rheumatoid arthritis, scleroderma, primary biliary cirrhosis

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51
Q

What are the features of Sjogren’s syndrome?

A

Decreased tear production, decreased salivation, parotid swelling, systemic signs such as Raynaud’s phenomenon

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52
Q

How is Sjogren’s syndrome diagnosed?

A

Schirmer’s test to measure conjunctival dryness
Rose Bengal stain may show keratitis
Biopsy shows focal lymphocytic aggregation

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53
Q

How is Sjogren’s syndrome managed?

A

Treat symptoms e.g. hypromellose (artificial tears), frequent drinks
NSAIDs for arthralgia

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54
Q

What is Raynaud’s phenomenon?

A

Peripheral digital ischaemia due to paroxysmal vasospasm, precipitated by cold or emotion

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55
Q

What do the colours of the fingers/toes in Raynaud’s indicate?

A

Pale -> ischaemia
Blue -> deoxygenation
Red -> reactive hyperaemia

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56
Q

How is Raynaud’s phenomenon managed?

A

Keep warm e.g. hand warmers
Stop smoking
Chemical or surgical (lumbar or digital) sympathectomy may help in those with severe disease

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57
Q

What are seronegative spondyloarthropathies?

A

A group of inflammatory joint diseases characterised by arthritis affecting the spinal column and peripheral joints, and enthesitis

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58
Q

What does seronegative mean?

A

Rheumatoid factor is negative

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59
Q

What are the shared clinical features of the spondyloarthropathies?

A

Seronegativity, HLA B27 association, axial arthritis, enthesitis, dactylitis

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60
Q

What is ankylosing spondylitis?

A

A chronic inflammatory disease of the spine and sacroiliac joints

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61
Q

How does ankylosing spondylitis present?

A

Lower back pain, typical case worse during the night with morning stiffness relieved by exercise.
Extra-articular manifestations - iritis, pulmonary fibrosis, aortitis

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62
Q

How is ankylosing spondylitis diagnosed?

A

Clinical - supported by imaging
MRI shows active inflammation
X-rays can show joint space narrowing

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63
Q

What are the patterns of psoriatic arthritis?

A

Symmetrical polyarthritis, DIP joints, asymmetrical oligoarthritis, spinal

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64
Q

How does psoriatic arthritis present?

A

Affects the interphalangeal joints and may lead to severe deformation

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65
Q

How is psoriatic arthritis diagnosed?

A

Radiology: erosive changes

Nail changes, synovitis, acneiform rashes

66
Q

How is psoriatic arthritis managed?

A

NSAIDs (methotrexate)

Anti-TNF agents

67
Q

What is reactive arthritis?

A

A condition in which arthritis and other clinical manifestations occur as an autoimmune response to infection elsewhere in the body

68
Q

What infections are related to reactive arthritis?

A

Chlamydia, shigella, salmonella, campylobacter

69
Q

How does reactive arthritis present?

A

Pain and stiffness in the lower back, knees, ankles and feet
Enthesitis.
Triad: urethritis, arthritis, conjunctivitis

70
Q

What is enthesitis?

A

Inflammation at the insertion site of tendons and ligament to bone

71
Q

How is reactive arthritis diagnosed?

A

Increased ESR and CRP, culture stool if diarrhoea, infectious serology
X-ray may show enthesitis

72
Q

How is reactive arthritis managed?

A

No cure. Splint affected joints - treat with NSAIDs or local steroid injections.
Methotrexate if >6 months

73
Q

What are crystal arthropathies?

A

A group of joints diseases caused by deposition of crystals in joints

74
Q

Describe the pathology of crystal arthropathies

A

Crystals are deposited in joints, neutrophils ingest the crystals and degranulate, releasing enzymes that damage the joint

75
Q

What causes gout?

A

Deposition of monosodium urate crystals in joint

76
Q

How does gout present?

A

Acute, painful, swollen, red joint - typically first metatarsophalangeal joint

77
Q

What is chronic tophaceous gout?

A

Large deposits of urate occur in the skin and around joints

78
Q

What are the risk factors for gout?

A

Reduced urate excretion (impaired renal function, hypertension, elderly)
Excess urate production (dietary, genetic disorders, psoriasis)

79
Q

How is gout diagnosed?

A

Polarised light microscopy of synovial fluid shows negatively birefringent urate crystals
Serum urate raised

80
Q

How is gout managed?

A

High-dose NSAID

Rest and elevate joint.

81
Q

How is gout prevented?

A

Lose weight, avoid prolonged fasts, alcohol excess, low-dose aspirin

82
Q

What is pseudogout?

A

Calcium pyrophosphate deposition

83
Q

What causes pseudogout?

A

Deposition of calcium pyrophosphate crystals in a joint

84
Q

How does pseudogout present?

A

Acute gout attack, pain in knee/wrist, low-grade fever, stiffness, swelling

85
Q

What is an acute gout attack?

A

Crystals break loose from their locations and move into a joint space. This causes sudden pain in the joint along with redness, warmth and inflammation

86
Q

How is pseudogout diagnosed?

A

Polarised light microscopy of synovial fluid shows weakly urate positive birefringent crystals.
X-ray: soft tissue calcium deposition

87
Q

How is psuedogout managed?

A

Acute attacks: cool packs, rest, aspiration

NSAIDs may prevent acute attacks

88
Q

What is vasculitis?

A

A group of conditions in which inflammation and damage to blood vessels is the primary underlying pathology

89
Q

Name an example of a small, medium and large vessel vasculitis

A

Large - Giant cell arteritis
Medium - Polyarteritis nodosa
Small - Goodpasture’s disease

90
Q

What are the features of vasculitis?

A

Fever, malaise, weight loss, purpura, ulcers, angina, pericarditis, malabsorption, hypertension

91
Q

How is vasculitis managed?

A

Large-vessel: steroids

Medium/small: immunosuppression - steroids

92
Q

What is giant cell arteritis?

A

A vasculitis of medium and large vessels which preferentially affects head and neck arteries.

93
Q

How does giant cell arteritis present?

A

Fever, anorexia, weight loss
Temporal artery - headache, scalp tenderness, jaw claudication
Occular vessels - blindness

94
Q

How is giant cell arteritis diagnosed?

A

Positive temporal artery biopsies show lymphohistiocytic infiltrate
Raised ESR and CRP

95
Q

How is giant cell arteritis managed?

A

Start prednisolone PO immediately or IV methylprednisolone if evolving visual loss

96
Q

What is the prefix for bone tumours?

A

Osteo

97
Q

What is the prefix for cartilage tumours?

A

Chondro

98
Q

What is the prefix for skeletal muscle tumours?

A

Rhabdomyo

99
Q

What is the prefix for fat tumours?

A

Lipo

100
Q

What does the suffix ‘Oma’ tell us?

A

Benign tumour

101
Q

What is a sarcoma?

A

Malignant connective tissue tumour

102
Q

What is a carcinoma?

A

Malignant epithelial/ endothelial tumour

103
Q

What is a blastoma?

A

Malignant tumour of embryonic cells

104
Q

What are secondary bone tumours?

A

Tumours that have metastasised to bone

105
Q

How are most MSK tumours managed?

A

Chemo/radiotherapy
Surgery
Local recurrence increases risk of amputation

106
Q

What is an osteochondroma?

A

Benign cartilaginous-forming tumour of bone

107
Q

What are osteoid osteomas?

A

Benign bone-forming tumours of bone - long bones

108
Q

What are osteoblastomas?

A

Benign bone-forming tumours of bone - axial skeleton

109
Q

What are endochondromas?

A

Benign cartilaginous-forming tumour of bone that occur in small bones

110
Q

What are the 5 most common tumours to metastasise to bone?

A

Lung, breast, kidney, thyroid, prostate

111
Q

What are osteosarcomas?

A

Malignant bone-forming tumours

112
Q

What are giant cell tumours?

A

Benign, locally aggressive neoplasms of bone that arise in the ends of long bones

113
Q

What is Ewing’s sarcoma?

A

A malignant round cell tumour of bone of neuroectodermal origin (neural crest cells)

114
Q

What is fibromyalgia?

A

A long term condition that causes pain all over the body. Very similar to chronic fatigue syndrome

115
Q

What are the risk factors for fibromyalgia?

A

Female, middle age, low household income, divorced, low educational status

116
Q

How does fibromyalgia present?

A

Allodynia, hyperaesthesia, profound fatigue, complaint of unrefreshing sleep, morning stiffness, headaches, poor concentration

117
Q

How is fibromyalgia diagnosed?

A

Diagnosis is clinical

118
Q

How is fibromyalgia managed?

A

Encourage patient to stay active and continue with work
Cognitive behavioural therapy
Pharmacotherapy - low-dose amitriptyline relieves pain and improves sleep

119
Q

What are the red flags of back pain?

A 
Constant/ progressive pain
Nocturnal pain
Fever, night sweats, weight loss
Abdominal mass
Morning stiffness
Neurological disturbance
120
Q

What are the most common causes of back pain in 15-30 year olds?

A

Prolapsed disc, trauma, fractures, ankylosing spondylitis, pregnancy

121
Q

How is mechanical back pain investigated?

A

MRI - can detect disc prolapse, cord compression, cancer, infection or inflammation
X-ray - fractures/abnormalities

122
Q

How is mechanical back pain managed?

A

Low-dose amitriptyline
Physiotherapy, acupuncture, exercise programme
Education and active
Urgent neurosurgical referral if any neurological deficit

123
Q

What is septic arthritis?

A

Infection within a joint

124
Q

What are the risk factors for septic arthritis?

A

Pre-existing joint disease, diabetes mellitus, immunosuppression, CKD, recent joint surgery

125
Q

How does septic arthritis present?

A

Extremely painful, hot, red, swollen joint
Fever
Knee > hip > shoulder

126
Q

How is septic arthritis diagnosed?

A

Microbiology: Staphylococcus aureus/
Urgent joint aspiration for fluid microscopy - no crystals
Culture for causative organism

127
Q

How is septic arthritis managed?

A

Empirical IV antibiotics (after aspiration - until sensitivities known)
Flucloxacillin
Analgesia
Ceftriaxone for gonococcus

128
Q

What are common causative organisms of septic arthritis?

A

Staph. aureus, streptococci, Neisseria gonococcus, and gram -ve bacilli

129
Q

What is osteomyelitis?

A

Infection of a bone

130
Q

How can infection occur in a bone?

A

Haematogenous spread
Penetrating trauma e.g. open fracture
Iatrogenic e.g. following joint replacement
Direct spread from an adjacent infection e.g. complication of a diabetic foot ulcer

131
Q

Describe the pathology of osteomyelitis

A

Infection leads to influx of acute inflammatory cells into bone
Destruction of bone leads to necrotic bone (sequestrum)

132
Q

How does osteomyelitis present?

A

Fever and pain in the affected bone
Aggravated by movement
Tenderness, warmth, erythema, swelling

133
Q

How is osteomyelitis diagnosed?

A

Microbiology - most caused by staphylococcus aureus
Bloods: high WCC
Raised inflammatory markers

134
Q

How is osteomyelitis managed?

A

IV antibiotics and surgical debridement of any necrotic bone

135
Q

What is osteomalacia?

A

A metabolic bone disease characterised by inadequate mineralisation of bone in the mature skeleton

136
Q

What is rickets?

A

A metabolic bone disease characterised by inadequate mineralisation of bone and epiphyseal cartilage in the growing skeleton of children

137
Q

Describe the pathology of osteomalacia and rickets

A

There is inadequate mineralisation of bone matrix (osteoid) due to lack of calcium and occasionally phosphate
Bone becomes soft and prone to deformity and fracture

138
Q

How does osteomalacia present?

A

Bone pain and tenderness, fractures, proximal myopathy

139
Q

How are rickets and osteomalacia diagnosed?

A

Bone biopsies: incomplete mineralisation
X-ray: loss of cortical bone
Plasma: mildly reduced calcium

140
Q

How are rickets and osteomalacia managed?

A

Vitamin D supplementation results in rapid mineralisation of bone and resolution of symptoms
Renal disease - alfacalcidol

141
Q

What is Paget’s disease?

A

A metabolic bone disease characterised by excessive chaotic bone turnover in localised parts of the skeleton

142
Q

How does Paget’s disease present?

A

Asymptomatic - diagnosis made incidentally on radiology

Symptomatic disease usually presents with bony pain and deformity

143
Q

How is Paget’s disease diagnosed?

A

X-ray: localised enlargement of bone. Patchy cortical thickening with sclerosis, osteolysis and deformity

144
Q

How is Paget’s disease managed?

A

Bisphosphonates - block osteoclasts from resorbing bone

Analgesia for pain

145
Q

When is capsaicin used?

A

Symptomatic relief in osteoarthritis

146
Q

What are the side effects of capsaicin?

A

Cough, sneezing, watering eye, asthma exacerbated

147
Q

When is paracetamol used?

A

For mild to moderate pain

148
Q

What are the side effects of paracetamol?

A

Thrombocytopenia, bronchospasm, rash, hepatic function abnormal

149
Q

When are NSAIDs used?

A

Rheumatoid/ osteoarthritis

150
Q

Give an example of an NSAID

A

Diclofenac, aceclofenac

151
Q

What are the side effects of NSAIDs?

A

Diarrhoea, dizziness, GI discomfort/ nausea

152
Q

Give an example of a bisphosphonate

A

Alendronic acid

153
Q

How do bisphosphonates work?

A

Bisphosphonates are adsorbed onto hydroxyapatite crystals in bone, slowing both their rate of growth and dissolution, and therefore reducing the rate of bone turnover

154
Q

What are the side effects of bisphosphonates?

A

Alopecia, anaemia, constipation, diarrhoea, headache, fever, malaise

155
Q

What does DMARD stand for?

A

Disease-modifying antirheumatic drugs

156
Q

Give an example of a DMARD

A

Methotrexate, hydroxychloroquine

157
Q

How does methotrexate work?

A

Methotrexate inhibits the enzyme dihydrofolate reductase, essential for the synthesis of purines and pyrimidines

158
Q

When is methotrexate used?

A

Used to treat moderate to severe active rheumatoid arthritis by mouth, and severe RA by IM/SC injection

159
Q

What are the side effects of methotrexate?

A

Fever, headache, nausea, vomiting, anemia, diarrhoea, fatigue, drowsiness

160
Q

When is hydroxychloroquine used?

A

Active rheumatoid arthritis

161
Q

What are the side effects of hydroxychloroquine?

A

Abdominal pain, diarrhoea, vomiting, vision disorders, headache

Phase 2a (16 decks)

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