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MSK Flashcards

1
Q

What is osteoarthritis?

A

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

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2
Q

What joint tissue is most affected in OA?

A

Articular cartilage is the most affected

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3
Q

What are the main pathological features of OA?

A

o Loss of cartilage

o Disordered bone repair

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4
Q

What are the chemical mediators in OA?

A

Cytokines – IL-1, TNF-α, NO

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5
Q

What the risk factors for OA?

A
  • Age - >45 years
  • Gender - F>M
  • Genetics
  • Obesity
  • Occupation - manual labour, sport, farming etc.
  • Inflammatory arthritis
  • Trauma/abnormal biomechanics
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6
Q

Symptoms of OA

A
  • Pain – evening, exercise
  • Morning stiffness <30mins
  • Functional impairment – walking, ADL’s
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7
Q

Signs of OA

A 
•   Alteration in gait
•   Joint swelling – bony enlargement, effusion
•   Other joint abnormalities:
       o   Limited ROM
       o   Crepitus
       o   Tenderness
       o   Deformities
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8
Q

Radiological features in OA

A
  1. Joint space narrowing
  2. Osteocyte formation
  3. Subchondral sclerosis
  4. Subchondral cysts
  5. Abnormalities of bone contour
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9
Q

What joints are involved in hand OA?

A

DIP, PIP, CMC joints

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10
Q

What are the signs of hand OA?

A
  • Heberden’s nodes at DIP joints

* Bouchard’s nodes at PIP joints

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11
Q

Non-pharmacological management of OA

A 
o	Activity and exercise
o	Weight loss
o	Physiotherapy
o	Occupational therapy
o	Footwear
o	Orthoses
o	Walking aids
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12
Q

Pharmacological management of OA

A

o Topical – NSAIDs, capsaicin
o Oral – paracetamol
o Transdermal patches – lignocaine
o Intra-articular steroid injections

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13
Q

What is rheumatoid arthritis?

A

A chronic systemic inflammatory disease, characterized by a symmetrical, deforming, peripheral polyarthritis

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14
Q

Epidemiology of RA

A
  • 40-60yrs old
  • HLA DR4/DR1 linked
  • Smokers
  • 3x more women
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15
Q

Pathology of RA

A

Inflammatory cells infiltrate synovium -> angiogenic cytokines form new synovial blood vessels -> synovium proliferates and grows out over surface of cartilage producing a pannus -> pannus destroys cartilage and subchondral bone -> bony lesions

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16
Q

Main symptoms of RA

A 
o   Early morning stiffness/pain 
     >60 mins, eases with use
o   Loss of function
o   Deformity 
o   Pattern – symmetrical, most commonly wrists and 
     feet, rarely DIP's
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17
Q

Signs of RA

A 
o   Ulnar deviation 
o   Swan neck deformity 
o   Boutonnieres deformity
o   Z thumb
o   Rheumatoid nodules 
o   Joint inflammation
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18
Q

What are the 4 features of inflammation?

A

Red, heat, swelling, pain

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19
Q

Symptoms of extra-articular involvement in RA

A 
o   Eyes – dry eyes, scleritis
o   Neurological – Carpal tunnel 
o   Haematological – anaemia, splenomegaly 
o   Lungs – plural effusion 
o   Heart – pericarditis 
o   Kidneys – amyloidosis 
o   Skin – vasculitis
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20
Q

Investigations for suspected RA

A
  • RhF positive in approx. 70%
  • Anti-CCP is more sensitive and specific
  • Anaemia if chronic, raised inflammatory markers
  • X-rays
  • Use criteria – diagnostic ≥6
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21
Q

Features of RA on x-ray

A

o Soft tissue swelling
o Osteopenia (soft bones)
o Loss of joint space
o Erosion

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22
Q

Non-pharmacological management of RA

A
  • Physiotherapy, occupational therapy

* Surgery

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23
Q

Disease modifying drugs for RA

A
  • DMARDs (methotrexate) - 1st line
  • TNF-α inhibitor (infliximab) -2nd line
  • Rituximab - 3rd line
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24
Q

What drugs can be used for symptomatic relief in RA?

A

Steroids, NSAIDs

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25
Q

Epidemiology of gout

A

o Men >40yrs
o Rises in post-menopausal women
o Chinese, Polynesian, Filipino – if westernised diet

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26
Q

What is uric acid a product of?

A

Nucleic acid/purine metabolism

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27
Q

Pathology of gout

A

Hyperuricaemia -> formation of sharp urate crystals in joints -> phagocyte activation -> inflammatory arthritis

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28
Q

Causes of gout

A 
o   Under-excretion:
       - Dehydration
       - Alcohol
       - Aspirin, diuretics 
       - HTN 
       - Obesity, DM
o   Over-production:
       - Hyperlipidaemia
       - Alcohol 
       - Psoriasis  
       - Excess meat, shellfish, offal, gravy, yeast
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29
Q

Signs and symptoms of gout

A

o First metatarsal joint of big toe most common
o Inflammation – hot, red, swollen
o Podagra:
- Wakes up feeling like big toe on fire
- Pain most severe in hours after attack
- Can last days-weeks

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30
Q

Management of gout

A

o Anti-inflammatories – NSAID, colchicine
o Prevention – allopurinol
o Diet modification, stay active

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31
Q

Complications of gout

A

Repeated gouty attacks -> chronic gout – arthritis, tissue destruction, tophi, kidney stones

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32
Q

What is gout?

A

Joint inflammation caused by uric acid crystal deposits in the joint space

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33
Q

What is pseudogout?

A

Inflammation of a joint caused by deposits of calcium pyrophosphate crystals

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34
Q

Investigations for suspected crystal arthropathy

A

o Polarised light microscopy of synovial fluid
o Bloods
o X-ray

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35
Q

Management of pseudogout

A

o Acute attacks - cool packs, rest, aspiration, intra-
articular steroids
o Prevention - NSAIDs and colchicine may prevent
o Methotrexate if chronic

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36
Q

What is osteoporosis?

A

A skeletal disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility and increased risk of fractures

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37
Q

List 9 risk factors for osteoporosis

A
  • Steroids
  • Hyperthyroidism, hyperparathyroidism, hypercalciuria
  • Alcohol and tobacco
  • Thin
  • Testosterone low
  • Early menopause/female
  • Renal/liver failure
  • Erosive/inflammatory bone disease
  • Dietary low calcium/malabsorption
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38
Q

Why does incidence of osteoporosis in women increase after menopause?

A

Lack of oestrogen increases bone resorption and decreases bone deposition

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39
Q

Why does calcium deficiency cause osteoporosis?

A

Deficiency of calcium -> increased bone resorption through PTH

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40
Q

Pathology of osteoporosis

A

Peak bone mass inadequate due to excessive bone resorption and inadequate formation of new bone during remodelling

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41
Q

Signs and symptoms of osteoporosis

A
  • Asymptomatic

* Bone fragility -> fracture

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42
Q

What is the main investigation used to diagnose osteoporosis?

A

DEXA Bone Densitometry

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43
Q

How is a DEXA score interpreted?

A

o Produces ‘T score’:
T > -1 = normal
-1 < T > -2.5 = osteopenia
T < -2.5 = osteoporosis

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44
Q

What tool can be used to assess fracture risk in osteoporosis?

A

FRAX

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45
Q

Pharmacological management of osteoporosis

A 
•   Anti-resorptive drugs:
       o   Bisphosphates – alendronic acid
       o   HRT – RF’s breast cancer, CVD
       o   Denosumab - SC 2x yearly
•   Anabolic drugs – teriparatide
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46
Q

Non-pharmacological management of osteoporosis

A

• Lifestyle:
o Quite smoking and reduce alcohol
o Weight-bearing and balance exercise
o Calcium and vit D-rich diet/supplements
o Occupational health – fall prevention

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47
Q

List the 7 shared clinical features of spondyloarthropathies

A
  1. Rheumatoid factor negative
  2. HLA B27 association
  3. Axial arthritis
  4. Asymmetrical large-joint arthritis
  5. Enthesitis – inflammed of insertion site of
    tendon/ligament into bone
  6. ‘Sausage digit’
  7. Extra-articular manifestations – iritis, psoriaform
    rashes, oral ulcers, aortic valve incompetence, IBD
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48
Q

What is ankylosing spondylitis?

A

A chronic inflammatory disease of the spine and sacroiliac joints

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49
Q

Cause of ankylosing spondylitis

A

Unknown, HLA B27 association

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50
Q

Epidemiology of ankylosing spondylitis

A

M>F, <30yrs

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51
Q

Signs and symptoms of ankylosing spondylitis

A

o Low back pain – gradual onset, worse at night,
radiates to hips/buttocks
o Spinal morning stiffness relieved by exercise
o Progressive loss of spinal movement -> decreased
thoracic expansion
o Kyphosis, neck hyperextension, spino-cranial
ankylosis
o Osteoporosis
o Iritis -> blindness

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52
Q

Investigations for suspected ankylosing spondylitis

A

o Clinical examination
o MRI – inflammation and destructive changes
o X-ray
o Bloods - RF -ve

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53
Q

Management of ankylosing spondylitis

A

o Exercise, physio
o Drugs – NSAIDS, TNF α-blockers, steroid injections,
bisphosphonates
o Surgery – hip replacements ect.

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54
Q

What is psoriatic arthritis?

A

joint inflammation associated with psoriasis - about 10% of those with psoriasis

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55
Q

What are the 5 patterns of psoriatic arthritis?

A

DIPJ only, RA like, large joint oligoarthritis, axial, arthritis mutilans

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56
Q

Signs and symptoms of psoriatic arthritis

A

o Nail changes
o Synovitis
o Acneiform rashes
o Joint inflammation

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57
Q

What changes would you see on x-ray for psoriatic arthritis?

A

Erosive changes, ‘Pencil in cup’ deformity

58
Q

Management of psoriatic arthritis

A

NSAIDS, DMARD, methotrexate, anti-TNF agents

59
Q

Name a DMARD

A

Sulfasalazine

60
Q

What is reactive arthritis?

A

Arthritis and other clinical manifestations that occur as an autoimmune response to infection elsewhere in the body

61
Q

Signs and symptoms of psoriatic arthritis

A 
o	Nail changes 
o	Arthritis
o	Conjunctivitis 
o	Psoriatic-like skin lesions
o	Circinate Balanitis
62
Q

Investigations for suspected psoriatic arthritis

A

o Bloods – raised inflammatory markers, RF -ve
o Culture stool, sexual health check
o X-ray

63
Q

Management of psoriatic arthritis

A

o NSAIDS, local steroid injections, DMARDs,
methotrexate
o Splint affected joints

64
Q

What is osteomyelitis?

A

Inflammation of the bone or bone marrow - usually from infection

65
Q

What are the three main mechanisms of getting osteomyelitis?

A

o Direct inoculation of infection into bone - surgery
o Contiguous spread of infection to bone from
adjacent soft tissues and joints
o Haematogenous seeding

66
Q

Where is the most common site for osteomyelitis in adults?

A

Vertebrae

67
Q

Where is the most common site for osteomyelitis in children?

A

Long bones

68
Q

What is the most common cause of osteomyelitis?

A

Staph. Aureus

69
Q

Pathology of osteomyelitis, and difference between acute and chronic

A

Bacteria reaches bone -> proliferate -> alert immune cells -> immune cells break down bone -> immune system destroys all bacteria:
o Acute – osteoblasts and osteoclasts repair
damage over a number of weeks
o Chronic – affected bone becomes necrotic and
separates (‘sequestrum’)

70
Q

Symptoms of osteomyelitis

A

o Dull pain at site – may be aggravated by movement

o Fever, rigors, sweats, malaise

71
Q

Signs of osteomyelitis

A

Tenderness, warmth, redness, swelling

72
Q

Investigations for suspected osteomyelitis

A

o Bloods – raised WCC, ESR, CRP
o Imaging:
- X-ray – thickening of cortical bone and
periosteum, osteopenia
- MRI/CT/bone scan – diagnostic, abscesses
o Bone biopsy and cultures

73
Q

Management of osteomyelitis

A

o Surgical – abscess,

o Antimicrobial therapy – tailored to cause

74
Q

What is septic arthritis?

A

Invasion of a joint by an infectious agent resulting in joint inflammation

75
Q

Causes of septic arthritis

A

Staph. Aureus, streptococci, Neisseria gonococcus

76
Q

Risk factors for septic arthritis

A

RA, DM, immunosuppression, CKD, prosthetic joints, IVDU, >80yrs

77
Q

Signs and symptoms of septic arthritis

A

o Painful, red, swollen, hot joint - usually monoarthritis
o Fever
o Knee > hip > shoulder

78
Q

Investigations for suspected septic arthritis

A

o Joint aspiration
o X-ray
o Blood cultures BEFORE antibiotics

79
Q

Give a differential diagnosis for septic arthritis

A

Crystal arthropathies

80
Q

Management of septic arthritis

A

o Surgical – washout

o Antimicrobial therapy – tailored to cause

81
Q

What empirical antibiotics should be given for an MSK infection

A

Flucloxacillin

82
Q

What is SLE?

A

Multisystemic autoimmune disease characterised by presence of antinuclear antibodies

83
Q

Epidemiology of SLE

A

Women of child-bearing age, Afro-Caribbean’s, HLA DR2/3

84
Q

Causes of SLE

A

Genetics and environment, drug induced

85
Q

What complement factors are lacking in SLE?

A

C3 and C4

86
Q

Pathophysiology of SLE

A

Environmental trigger damages cells -> apoptosis -> release of nuclear antigens -> genetic factors mean individual cannot clear these effectively -> immune system recognises nuclear antigens as foreign -> ANA produced -> deposited in tissues -> inflammation

87
Q

What type of hypersensitivity reaction is SLE?

A

Type 3

88
Q

Signs and symptoms of SLE

A 
•   Fever 
•   Joint pain 
•   Weight loss 
•   Malaise, fatigue, myalgia 
•   Butterfly rash – UV triggered 
•   Alopecia
•   Haematological disorders – anaemia, 
    thrombocytopenia etc.
89
Q

Investigations for suspected SLE

A
  • Bloods - ESR raised, anti-dsDNA antibodies

* Urinalysis – proteinuria

90
Q

Management of SLE

A

• Non-medical:
o UV protection
o Screen for comorbidities
• Pharmacological:
o NSAIDs – joint and skin symptoms
o Severe – high dose steroids and rituximab

91
Q

What are primary bone tumours?

A

Tumours that form from bone tissue and can be malignant

92
Q

What are secondary bone tumours?

A

Tumours from metastatic disease

93
Q

Signs and symptoms of bone tumours

A
  • Rest pain
  • Night pain
  • Lump present
  • Loss of function
  • Neurological symptoms
  • Weight loss
94
Q

Investigations for suspected bone tumour

A
  • Blood tests – FBC, U+E, Ca2+, Alk Phos
  • Plain x-rays
  • Ultrasound
  • CT Scan
  • MRI Scan
  • Bone Scan
  • Biopsy
95
Q

What are the 3 special signs sometimes seen on a plain x-ray that can signify bone cancer?

A

o Codman’s Triangle
o Sunburst appearance
o Onion-skin appearance

96
Q

What system is used to grade bone tumours?

A

Enneking system

97
Q

What is fibromyalgia?

A

A long-term condition that causes pain all over the body

98
Q

Risk factors for fibromyalgia

A
  • Female
  • Middle age
  • Low socioeconomic status
  • Life dissatisfaction
99
Q

What other conditions are associated with fibromyalgia?

A

• Somatic syndromes – chronic fatigue, IBS, chronic
headaches
• RA, SLE

100
Q

Features of fibromyalgia

A
  • Chronic pain, >3 months, widespread
  • Profound fatigue
  • Morning stiffness
  • Paraesthesiae
  • Headaches
  • Poor concentration and low mood
101
Q

Investigations for suspected fibromyalgia

A

All normal, diagnosis clinical

102
Q

Management of fibromyalgia

A
  • Encourage activity and staying in work if possible
  • CBT
  • Relaxation, rehabilitation and physiotherapy
  • Medications - mitriptyline/pregabalin
103
Q

Associations with mechanical back pain

A

Heavy manual handling, stooping and twisting whilst lifting, exposure to whole body vibration, psychosocial distress, smoking and dissatisfaction with work

104
Q

High risk activities for mechanical back pain

A
  • Heavy manual handling (>20Kg)
  • Lifting above shoulder height
  • Lifting from below knee height
  • Incorrect manual handling technique
  • Forceful movements
  • Fast repetitive work; poor postures; poor grip
105
Q

Management of mechanical back pain

A 
•   Analgesics or NSAIDs
•   Spinal manipulative therapy
•   Spinal injections 
•   Spinal exercises, behavioural therapy and workplace 
    adaptations
106
Q

What is osteomalacia?

A

Normal amount of bone but its mineral content is low -> excess uncalcified osteoid and cartilage

107
Q

How does Rickets occur?

A

When osteomalacia is present during growth

108
Q

Causes of osteomalacia

A
  • Vitamin D deficiency
  • Renal osteodystrophy
  • Drug-induced – anticonvulsants
  • Vitamin D resistance
  • Liver disease – cirrhosis
  • Tumour-induced
109
Q

Signs and symptoms of Rickets

A

Growth retardation, hypotonia, knock-kneed, bow-legged

110
Q

Signs and symptoms of osteomalacia

A

Bone pain, tenderness, fractures, waddling gait

111
Q

Investigations for suspected osteomalacia

A

• Plasma – hypocalcaemia, hypophosphataemia, high
PTH, low vit D (except resistance)
• Bone biopsy – incomplete mineralisation
• X-ray – loss of cortical bone

112
Q

Management of osteomalacia

A

Oral calciferol

113
Q

Cause of vertebral disc degeneration

A

Disease of aging

114
Q

Pathology of vertebral disc degeneration

A

• Degenerative fibrocartilage and clusters of
chondrocytes present
• Fibrocartilage replaces the material of the nucleus
pulposus as the disc changes with age

115
Q

Presentation of vertebral disc degeneration

A

Chronic low back pain, sometimes radiating to the hips, or the buttocks

116
Q

Investigations for suspected vertebral disc degeneration

A

CT, MRI

117
Q

Management of vertebral disc degeneration

A
  • Physical therapy
  • NSAIDs
  • Epidural steroids
  • Surgery
118
Q

Complications of vertebral disc degeneration

A

Sciatica, alkylosis

119
Q

What is vasculitis?

A

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

120
Q

How is vasculitis categorised?

A

By size of the vessels affected

121
Q

Give an example of a large cell vasculitis

A

Giant cell arteritis

122
Q

Give and example of a medium cell vasculitis

A

Polyarteritis nodosa

123
Q

Give and example of a small cell arteritis

A

Granulomatosis with polyangiitis (GPA)

124
Q

Is GPA ANCA positive or negative?

A

Positive

125
Q

Signs and symtoms of GPA

A

Upper airways disease, sinusitis, pulmonary haemorrhage, glomerulonephritis, skin ulcers, CNS vasculitis, scleritis, pericarditis, saddle nose deformity

126
Q

Management of GPA

A

o Severe – high dose steroids
o Mild/moderate – moderate dose steroids +
methotrexate

127
Q

Is giant cell arteritis ANCA positive or negative?

A

Negative

128
Q

Epidemiology of giant cell arteritis

A

o >50yrs old

o F>M

129
Q

Symptoms of giant cell arteritis

A 
o   Headache
o   Scalp tenderness – hurts to brush hair 
o   Jaw claudication
o   Acute blindness 
o   Malaise
130
Q

What is the diagnostic criteria for giant cell arteritis?

A 
o   >50yrs
o   New headache
o   Temporal artery tenderness or decreased pulsation
o   High ESR,  >50mm/h
o   Abnormal artery biopsies
131
Q

Management of giant cell arteritis

A

o Prompt prednisolone – dramatic response in 48 hr
o Steroid sparing agents – methotrexate
o Prophylaxis of osteoporosis

132
Q

What is Padget’s disease?

A

Increased bone turnover associated with increased osteoblasts and osteoclasts with resultant remodelling, bone enlargement, deformity and weakness

133
Q

Signs and symptoms of Padget’s disease

A 
o   Usually asymptomatic 
o   Deep, boring pain 
o   Bony deformation and enlargement
o   Pathological fractures
o   Osteoarthritis 
o   Nerve compression -> hearing loss, vision loss 
o   Hypercalcaemia
134
Q

Epidemiology of Padget’s disease

A

> 40yrs

135
Q

Which nerve is compressed in carpal tunnel syndrome?

A

Median nerve

136
Q

What would be seen on joint fluid microscopy of a patient with Pseudogout?

A

Positively Birefringent Rhomboid Shaped Crystals

137
Q

What would be seen on joint fluid microscopy of a patient with gout?

A

Negatively Birefringent Needle Shaped Crystals

138
Q

What does anti-CCP stand for?

A

Anti-cyclic citrullinated peptide

139
Q

Why is methotrexate contraindicated in pregnancy?

A

Folate antagonist

140
Q

What is the most common composition of renal stones?

A

Calcium oxalate

Phase 2a (9 decks)

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