Musculoskeletal Flashcards

1
Q

What is amyloidosis?

A

A (heterogenous) group of diseases characterised by extracellular deposition of insoluble amyloid fibrils

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2
Q

What are the two types of amyloidosis?

A
  1. AL amyloid = primary, immunoglobulin light chain amyloidosis, associated with Myeloma
  2. AA amyloid = secondary, non-familial and familial
    2a. Non- familial AA = Inflammatory polyarthropathies account for 60% of cases, then chronic infections, IBD
    2b. Familial AA = familial periodic Mediterranean fever syndrome
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3
Q

What are the risk factors for amyloidosis?

A

PMH of inflammatory conditions (AA)
Chronic infections (AA)
Positive FH

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4
Q

What are the features of primary amyloidosis (AL)?

A

Dependent on organ involvement:
1. Kidneys: glomerular lesions—proteinuria and nephrotic syndrome
2. Heart: restrictive cardiomyopathy (looks ‘sparkling’ on echo), arrhythmias, angina
3. Nerves: peripheral and autonomic neuropathy; carpal tunnel syndrome
4. GI: macroglossia (big tongue), malabsorption/weight, perforation, haemorrhage, obstruction, and hepatomegaly
5. Vascular: purpura, especially periorbital—a characteristic feature

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5
Q

What are the features of secondary non-familial amyloidosis (AA)?

A

PMH of chronic inflammation (e.g. RA/ IBD) or chronic infection (e.g. TB)
Affects the kidneys, liver, and spleen, and may present with proteinuria, nephrotic syndrome, or hepatosplenomegaly
Macroglossia is not seen; cardiac involvement is rare

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6
Q

What are the appropriate investigations for amyloidosis?

A

Diagnosis made with biopsy of affected tissue: positive Congo Red staining with apple-green birefringence under polarized light microscopy
The rectum or subcutaneous fat are relatively non-invasive sites for biopsy and are positive in 80%
Can also use serum amyloid precursor (SAP) scan

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7
Q

What is the management of amyloidosis?

A

AL: optimize nutrition; PO melphalan + prednisolone extends survival
High-dose IV melphalan with autologous stem cell transplantation may be better
AA: manage the underlying condition optimally

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8
Q

What is the prognosis of patients with amyloidosis?

A

Median survival is 1–2 years
Patients with myeloma and amyloidosis have a shorter survival than those with myeloma alone

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9
Q

What are the articulating surfaces of the ankle?

A

Tibia + fibula + talus

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10
Q

What are the two ligaments involved in the ankle joint?

A

Medial and lateral ligament (originating from the corresponding malleolus)

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11
Q

What are the muscle groups and movements of the ankle joint?

A

Plantarflexion: muscles in posterior compartment of leg (gastrocnemius, soleus, plantaris and posterior tibialis)
Dorsiflexion: muscles in anterior compartment of leg (tibialis anterior, extensor hallucis longus and extensor digitorum longus)

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12
Q

What is the neurovascular supply of the ankle?

A

Aterial supply = Malleolar branches of anterior tibial, posterior tibial and fibular arteries
Innervation is provided by tibial, superficial fibular and deep fibular nerves

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13
Q

What are the most common causes of posterior heel pain?

A

Achilles tendon disorders

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14
Q

What are the common achilles tendon disorders?

A
  1. Tendinopathy (tendinitis)
  2. Partial tear
  3. Complete rupture of the Achilles tendon
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15
Q

What are some risk factors for Achilles tendon disorders?

A

Quinolone use (e.g. ciprofloxacin) is associated
Hypercholesterolaemia → predisposes to tendon xanthomata

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16
Q

What are the features of achilles tendinopathy (tendinitis)?

A
  1. Gradual onset of posterior heel pain that is worse following activity
  2. Morning pain and stiffness are common
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17
Q

What is the management of achilles tendinopathy (tendinitis)?

A

Typically supportive
1. Simple analgesia
2. Reduction in precipitating activities
3. Calf muscle eccentric exercises (self-directed or through physiotherapy)

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18
Q

What are the features of Achilles tendon rupture?

A

Suspected if the patient reports the following whilst playing a sport or running:
1. An audible ‘pop’ in the ankle
2. Sudden onset significant pain in the calf
2. Inability to walk or continue the sport

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19
Q

What is the examination for Achilles tendon rupture?

A

Simmond’s triad
1. Ask the patient to lie prone with their feet over the bed
2. Look for an abnormal angle of declination - there will be a greater dorsiflexion of the injured foot compared to the other
3. Feel for a gap in the tendon and gently squeeze the calf muscles: if there is a rupture the achilles tendon injured foot will stay in a neutral position

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20
Q

What is the imaging modality of choice for Achilles tendon rupture?

A

Ultrasound

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21
Q

What is the Thompson test?

A

Lack of plantar flexion when calf is squeezed

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22
Q

What is the management for Achilles tendon rupture?

A

Acute referral to orthopaedic specialist
1. Non-operative : functional bracing/ casting in resting equinus
2. Operative: open end-to-end achilles tendon repair (for acute ruptures < 6 weeks) or percutaneous repair

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23
Q

What are some complications of Achilles tendon rupture?

A
  1. Re-rupture: higher with non-operative management
  2. Wound healing complications
  3. Sural nerve injury (percutaneous repair)
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24
Q

What is hallux valgus/ bunions?

A
  1. When the great toe deviates laterally to the metatarsophalangeal (MTP) joint
  2. The pressure of the MTP joint against a tight shoe results in a bunion
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25
Q

What is the aetiology of bunions?

A

Wearing pointed shoes or high heels

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26
Q

What is the management of bunions?

A
  1. Conservative: bunion pads, comfortable shoes, plastic wedge between the first and second toes
  2. Surgical: metatarsal osteotomy
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27
Q

What are ankle fractures?

A

Very common injuries which generally occur due to a twisting mechanism

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28
Q

What are the locations of ankle fractures?

A

Breakdown by fracture type:
1. Isolated malleolus fracture = 70%
2. Bimalleolar = 20%
3. Trimalleolar = 7%

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29
Q

What are the risk factors for ankle fractures?

A

Male
Younger age (mainly 15-24 years)
Obesity
Smoking
Alcohol consumption

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30
Q

What is the main mechanism of injury for ankle fractures?

A

Twisting injuries

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31
Q

What are the three ligament complexes that stabilise the ankle?

A
  1. Deltoid
  2. Lateral ligament complex
  3. Syndesmosis
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32
Q

What are the two tendons which stabilise the ankle?

A
  1. Peroneal tendons: peroneus longus and brevis
  2. Posterior tibial tendon
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33
Q

What are the neurovascular structures surrounding the ankle?

A
  1. Anterior tibial artery and depot peroneal nerve
  2. Posterior tibial artery and tibial nerve
  3. Superficial peroneal nerve
  4. Sural nerve
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34
Q

What are the features of an ankle fracture?

A

Severe ankle pain
Difficulty or inability to walk

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35
Q

What are the findings of an ankle fracture of a physical exam?

A

Ecchymosis and swelling
Deformity
Limited ankle motion

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36
Q

What are the Ottawa ankle rules for an ankle fracture?

A

State that x-rays are only necessary if there is pain in the malleolar zone and:
1. Inability to weight bear for 4 steps
2. Tenderness over the distal tibia
3. Bone tenderness over the distal fibula

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37
Q

What is the Weber system in ankle fractures?

A

Describe ankle fractures related to the level of the fibular fracture:
Type A = below the syndesmosis
Type B = fractures start at the level of the tibial plafond and may extend proximally to the syndesmosis
Type C = above the syndesmosis which may itself be damaged

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38
Q

How is the Weber system for ankle fractures classified?

A

Type A: infrasyndesmotic
Type B: transsyndesmotic
Type C: Suprasyndesmotic

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39
Q

What are some differentials for an ankle fracture?

A

Ankle sprain
Syndesmotic injury
Achilles tendon rupture

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40
Q

What are some features of an ankle sprain?

A

May be able to weight bear
Positive anterior drawer or talar tilt test
Radiographs without fracture

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41
Q

What are the principles of management for ankle fractures?

A

Depends on the stability of the ankle joint and patient’s comorbidities
1. All fractures should be promptly reduced to remove pressure on the overlying skin and subsequent necrosis
2. Young patients = usually require surgical repair often using a compression plate
3. Elderly patients = usually fare better with conservative management as their thin bones do not hold metalwork well

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42
Q

What are some of the non-operative management options for ankle fractures?

A

Short-leg AO splint
Short-leg cast
CAM boot
(for stable ankle fractures and those unfit for surgery)

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43
Q

What are some of the operative management options for ankle fractures?

A

Open reduction internal fixation
External fixation

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44
Q

What are the Ottawa rules (ankle fractures)?

A

An x-ray is only required if there is any pain in the malleolar zone and one of the following:
1. Bony tenderness at the lateral malleolar zone
2. Bony tenderness at the medial malleolar zone
3. Inability to walk 4 weight bearing steps immediately after the injury

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45
Q

What is the management of ankle fractures according the Weber classification?

A

Type A: Usually stable → reduction and cast →ORIF occasionally needed
Type B: Stability variable → may require ORIF
Type C: Unstable fracture → ORIF

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46
Q

What is a lisfranc injury?

A

When bones in the midfoot are broken or ligaments that support the midfoot are torn

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47
Q

What is a metatarsal stress fracture?

A

Stress fracture = tiny cracks in the bone caused by repetitive force often from overuse
A hairline fracture in one of the long metatarsal bones in the foot from overly stressing the foot when using it in the same way repeatedly

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48
Q

What is Morton’s Neuroma?

A
  1. Pain from pressure on an interdigital neuroma (thickening of tissue around a nerve) between the metatarsals
  2. Pain radiates to the medial side of one toe and lateral side of another, can cause pain and tingling on the ball of the foot (plantar)
  3. Management includes:
    a. activity modification
    b. NSAIDs
    c. Avoid narrow shoes or high heels
    d. If severe: neuroma excision
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49
Q

What is plantar fasciitis?

A
  1. The most common cause of heel pain seen in adults
  2. Caused by inflammation of the plantar fascia aponeurosis at its origin on the calcaneus
  3. Pain is usually worse around the medial calcaneal tuberosity
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50
Q

What are the risk factors for plantar fasciitis?

A
  1. Obesity (high BMI)
  2. Weight bearing endurance activity e.g. dancing, running
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51
Q

What is the pathophysiology of plantar fasciitis?

A
  1. Chronic overuse leads to micro tears in the plantar fascia
  2. Repetitive trauma leads to recurrent inflammation and periostitis
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52
Q

What are the features of plantar fasciitis?

A
  1. Sharp heel pain
  2. Insidious onset of heel pain, often when first getting out of bed (may prefer to walk on toes initially)
  3. Worse at the end of the day after prolonged standing
  4. Relieved by ambulation (walking)?
  5. Common to have symptoms bilaterally
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53
Q

What are the signs of plantar fasciitis on examination?

A
  1. Tender to palpation at medial tuberosity of calcaneus
  2. Dorsiflexion of the toes and foot increases tenderness with palpation
  3. Limited ankle dorsiflexion due to a tight Achilles tendon
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54
Q

Where is the pain usually worse in plantar fasciitis?

A

Medical calcaneal tuberosity (heel)

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55
Q

What are the investigations for plantar fasciitis?

A
  1. Usually made clinically with tenderness to palpation at the medial tuberosity of the calcaneus that worsens with dorsiflexion of the toes and foot
  2. Can consider imaging to exclude stress fractures e.g. bone scan
  3. Lab tests not indicated unless concerned of other causes of heel pain e.g. infection, inflammatory arthritis
  4. EMG: exclude entrapment
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56
Q

What is the management of plantar fasciitis?

A
  1. Conservative (first line): pain control, splinting and therapy (stretching)
    a. Rest feet where possible
    b. Wear shoes with good arch support and cushioned heels
    c. Insoles and heel pads may be helpful
  2. Shock wave: for chronic heel pain lasting longer than 6 months when other treatments have failed
  3. Surgical release with plantar fasciotomy: for persistent pain after 9 months of failed conservative measures (complications common including lateral plantar nerve injury and chronic pain)
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57
Q

What is Ankylosing spondylitis?

A

A HLA-B27 associated spondyloparthlopathy (chronic progressive inflammatory arthropathy)

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58
Q

What is the epidemiology of ankylosing spondylitis?

A

Typically presents in males (3:1) aged 20-30 years old

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59
Q

What are the features of ankylosing spondylitis?

A
  1. Typically a young man who presents with lower back pain and stiffness of insidious onset
  2. Stiffness is usually worse in the morning and improves with exercise
  3. Patient may experience pain at night which improves on getting up
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60
Q

What are the clinical signs of ankylosing spondylitis on examination?

A
  1. Reduced lateral flexion
  2. Reduced forward flexion: Schober’s test
  3. Reduced chest expansion
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61
Q

What is Schober’s test for ankylosing spondylitis?

A
  1. A line is drawn 10cm above and 5 cm below the back dimples (dimples of Venus)
  2. The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as normal
    Reduced lumbar spine flexion (due to vertebral fusion) in AS: < 5cm
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62
Q

What are the other features of ankylosing spondylitis?

A
  1. Apical fibrosis
  2. Anterior uveitis
  3. Aortic regurgitation
  4. Achilles tendonitis
  5. AVN block
  6. Amyloidosis
  7. Cauda equina syndrome
  8. Peripheral arthritis (more common in females)
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63
Q

What are the investigations of ankylosing spondylitis?

A
  1. Bloods: laboratory markers, HLA-B27 (limited use)
  2. Plain x-ray of the sacroiliac joints = most useful investigation
  3. If x-ray negative but suspicion is high = MRI
  4. Spirometry: restrictive
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64
Q

Why is HLA-B27 testing of limited use in the investigation of ankylosing spondylitis?

A

Positive in 90% of AS patients, but also in 10% of normal patients

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65
Q

What is the most useful investigation in establishing the diagnosis of ankylosing spondylitis?

A

Plain x-ray of the sacroiliac joints

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66
Q

What are the features of ankylosing spondylitis on plain x-ray of the sacroiliac joints?

A

May be normal in early disease. Later changes include:
1. Sacroiliitis: subchondral erosions and sclerosis
2. Squaring of lumbar vertebrae
3. ‘Bamboo spine’ - late and uncommon
4. Syndesmophytes: due to ossification of outer fibres of annulus fibrosus

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67
Q

What might be found on a chest x-ray in a patient with ankylosing spondylitis?

A

Apical fibrosis

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68
Q

When is an MRI used in ankylosing spondylitis?

A
  1. If an x-ray is negative for sacroiliac joint involvement but the suspicion remains high
  2. Will see signs of early inflammation involving sacroiliac joints (bone marrow oedema
  3. Confirms the diagnosis and prompts further treatment
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69
Q

What might be seen on spirometry in a patient with ankylosing spondylitis?

A

Restrictive defect due to a combination of pulmonary fibrosis, kyphosis and ankylosis of costovertebral joints

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70
Q

What is the management of ankylosing spondylitis?

A
  1. Encourage regular exercise such as swimming
  2. NSAIDs are first line (with gastric protection)
  3. Physiotherapy
  4. DMARDs e.g. sulphasalazine are only really useful if there is peripheral joint involvement
  5. Anti-TNF therapy should be given if there is persistently high disease activity despite conventional treatments
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71
Q

What is the first line drug treatment for ankylosing spondylitis?

A

NSAIDs e.g. naproxen 500mg BD

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72
Q

What is arthroplasty?

A

Joint replacement e.g. total hip replacement, hemiarthroplasty

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73
Q

What is a hip fracture?

A

Fracture of the hip, which a common site especially in osteoporotic elderly females

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74
Q

What is the risk of neck of femur fractures?

A

Avascular necrosis: the blood supply to the femoral head runs up the neck of the femur
Risk is greater in displaced fractures

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75
Q

What are the features of hip fractures?

A
  1. Pain
  2. Shortened and externally rotated leg
  3. Patient with non-displaced or incomplete neck of femur fractures may be able to weight bear
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76
Q

How can hip fractures/ neck of femur fractures be classified?

A
  1. Location
  2. Garden system
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77
Q

What is the location classification for neck of femur fractures?

A
  1. Intracapsular: from the edge of the femoral head to the insertion of the capsule of the hip joint
    Lesser trochanter is the dividing line
  2. Extracapsular: these can either be trochanteric or subtrochanteric
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78
Q

What is the Garden system for hip fractures?

A

Type 1: Stable fracture with impaction in valgus
Type 2: Complete fracture but undisplaced
Type 3: Displaced fracture, usually rooted and angulated but still has boney contact
Type 4: Complete boney disruption

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79
Q

What Garden types most commonly have blood supply disruption and so greater risk of avascular necrosis?

A

Types 3 and 4

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80
Q

What is the management of an intracapsular hip fracture?

A

Depends if it is displaced or undisplaced:
1. Undisplaced = internal fixation or hermiarthroplasty if unfit
2. Displaced = replacement arthroplasty (either THR or hemirthroplasty), THR is favoured if:
a. Patients were able to walk independently with no more than the use of a stick
b. Not cognitively impaired
c. Medically fit for anaesthesia and procedure

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81
Q

What is the management for an extra capsular hip fracture?

A
  1. Stable intertrochanteric fracture = dynamic hip screw
  2. Reverse oblique, transverse or subtrochanteric features = intramedullary device
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82
Q

What advice should be given to patients who have had a hip replacement to minimise the risk of dislocation?

A
  1. Avoid flexing the hip > 90 degrees
  2. Avoid low chairs
  3. Do not cross your legs
  4. Sleep on their back for the first 6 weeks
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83
Q

What are the different surgical techniques in hip arthroplasty?

A
  1. Cemented hip replacement (most common): metal femoral component is cemented into the femoral shaft
  2. Uncemented hip: increasingly popular in younger and more active patients but more expensive
  3. Hip resurfacing: metal cap over the femoral head (advantage of preserving femoral neck in case conventional arthroplasty is needed later in life)
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84
Q

What is involved in post-arthroplasty recovery?

A
  1. Physiotherapy and a course of home exercises
  2. Walking sticks or crutches for up to 6 weeks after replacement surgery
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85
Q

What are some of the complications of arthroplasty?

A
  1. Wound and joint infection
  2. Thromboembolism: require low dose molecular weight heparin for 4 weeks after surgery
  3. Risk of dislocation
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86
Q

What does arthroplasty mean?

A

Joint replacement

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87
Q

What sign is seen in pelvic fracture?

A

Positive Trendelenburg sign from superior gluteal nerve dysfunction

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88
Q

What is arthroscopy?

A
  1. A type of keyhole surgery for checking or repairing your joints (most commonly the knees)
  2. Minimally invasive
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89
Q

What is gout?

A
  1. A form of inflammatory arthritis
  2. Microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium
  3. Around 70% of first presentations affect the 1st metatarsophalangeal (MTP) joint
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90
Q

What is the aetiology of gout?

A

Underlying metabolic disturbance is chronic hyperuricaemia (uric acid > 0.45 mmol/l) which may be caused by:
1. Increased urate intake or production: dietary, lymphoma, leukaemia
2. Decreased renal excretion: idiopathic, drugs, renal dysfunction

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91
Q

What drugs can cause decreased renal excretion?

A

CANT LEAP’:
Ciclosporin
Alcohol
Nicotinic acid
Thiazides
Loop diuretics
Ethambutol (AB for TB)
Aspirin
Pyrizinamide (AB for TB)

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92
Q

What are the predisposing factors for an acute attack of gout?

A
  1. Decreased excretion of uric acid:
    a. drugs*: diuretics
    b. chronic kidney disease
    c. lead toxicity
  2. Increased production of uric acid:
    a. myeloproliferative/lymphoproliferative disorder
    b. cytotoxic drugs
    c. severe psoriasis
  3. Lesch-Nyhan syndrome
    hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency: only seen in boys, other features: renal failure, neurological deficits, learning difficulties, self-mutilation
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93
Q

What are the features of gout?

A
  1. Acute episodes: typically develop maximal intensity with 12 hours
  2. Pain: this is often very significant
  3. Swelling
  4. Erythema
94
Q

What are the common joints affected in gout?

A
  1. 1st metatarsophalangeal (MTP) joint (70%)
  2. Ankle
  3. Wrist
  4. Knee
95
Q

What are the presenting symptoms of gout?

A
  1. Acute attacks: sudden excruciating monoarticular pain, the symptoms peak at 12 h and resolve in 7–10 days
  2. Foot joint distribution: most commonly involved are joints in the feet, especially the first metatarsophalangeal
  3. Joint stiffness: morning stiffness is prominent
  4. Attacks are often recurrent, but the patient is symptom free between attacks
96
Q

What are the signs of gout on physical examination?

A
  1. Foot joint distribution
  2. Swelling and joint effusion
  3. Tenderness
  4. Erythema and warm
  5. Painful tophi (urate deposits)- best seen on tendons and the pinna of the ear
97
Q

What are the investigations for gout?

A
  1. Synovial fluid analysis: needle shaped negatively birefringent monosodium urate crystals under polarised light
  2. Uric acid: should be checked once the acute episode has settled down (typically 2 weeks later) as may be high, normal or low during the acute attack
  3. X-ray of affected joint:
    a. joint effusion is an early sign
    b. well-defined ‘punched-out’ erosions with sclerotic margins in a juxta-articular distribution with overhanging edges
    c. relative preservation of joint space until late disease
    d. eccentric erosions
    e. no periarticular osteopenia (in contrast to rheumatoid arthritis)
    f. Soft tissue swelling/ tophi
98
Q

What is the first line management of an acute attack of gout?

A

NSAIDs (plus PPI) or colchicine

99
Q

What is colchicine in the management of an acute attack of gout?

A
  1. Inhibits microtubule polymerization by binding to tubulin, interfering with mitosis
  2. Also inhibits neutrophil motility and activity
  3. Has a slower onset of action
  4. ay be used with caution in renal impairment: the BNF advises to reduce the dose if eGFR is 10-50 ml/min and to avoid if eGFR < 10 ml/min REF
  5. Main side-effect is diarrhoea
100
Q

What is the second line management of an acute attack of gout?

A
  1. Oral steroids if NSAIDs and colchicine are contraindicated (prednisolone 15mg/day)
  2. Another option is intra-articular steroid injection
  3. If the patient is already taking allopurinol it should be continued*
101
Q

What should be offered to all patients following an acute attack of gout?

A

Urate-lowering therapy (ULT):
1. First line: Allopurinol:
a. initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 300 µmol/l
b. Consider colchicine cover when starting (up to 6 months)
2. Second line: Febuxostat (also a xanthine oxidase inhibitor)

102
Q

What is the lifestyle management of gout?

A
  1. Reduce alcohol intake and avoid during an acute attack
  2. Lose weight if obese
  3. Avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products
  4. Consideration should be given to stopping precipitating drugs (such as thiazides)
103
Q

What is psuedogout?

A

A form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium

104
Q

What is the aetiology of psuedogout?

A
  1. Strongly associated with increasing age
  2. Patients who develop pseudogout at a younger age (e.g. < 60 years) usually have some underlying risk factor:
    a. haemochromatosis
    b. hyperparathyroidism
    c. low magnesium, low phosphate
    d. acromegaly
    e. Wilson’s disease
105
Q

What are the features of psuedogout?

A
  1. Most commonly affect the knee, wrist and shoulders
  2. Joint aspiration: weakly-positively birefringent rhomboid-shaped crystals
  3. X-ray: chondrocalcinosis: in the knee this can be seen as linear calcifications of the meniscus and articular cartilage
106
Q

What is the management of psuedogout?

A
  1. Aspiration of joint fluid, to exclude septic arthritis
  2. NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
107
Q

What is fibromyalgia?

A

A syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites

108
Q

What is the epidemiology of fibromyalgia?

A
  1. Women are around 5 times more likely to be affected
  2. Typically presents between 30-50 years old
109
Q

What are the features of fibromyalgia?

A
  1. Chronic pain: at multiple site, sometimes ‘pain all over’
  2. Lethargy
  3. Cognitive impairment: ‘fibro fog’
  4. Sleep disturbance, headaches, dizziness are also common
110
Q

How is fibromyalagia diagnosed?

A
  1. Clinical: American College of Rheumatology
    classification criteria
  2. Lists 9 pairs of tender points on the body
  3. If a patient is tender in at least 11 of these 18 points it makes a diagnosis of fibromyalgia more likely
111
Q

What is the management of fibromyalgia?

A
  1. Often difficult and needs to be tailored to the individual patient
  2. A psychosocial and multidisciplinary approach is helpful
  3. Combination of:
    a. Full explanation to patient
    b. Aerobic exercise (strongest evidence base)
    c. Cognitive behavioural therapy
    d. Medication: pregabalin, duloxetine, amitriptyline
112
Q

What is polymyositis?

A
  1. Inflammatory disorder causing symmetrical, proximal muscle weakness
  2. Thought to be a T-cell mediated cytotoxic process directed against muscle fibres
  3. May be idiopathic or associated with connective tissue disorders
  4. Associated with malignancy
113
Q

What is the epidemiology of polymyositis?

A
  1. Typically affects middle-aged women
  2. Female:male 3:1
114
Q

What are the features of polymyositis?

A
  1. Proximal muscle weakness ± tenderness
  2. Raynaud’s
  3. Respiratory muscle weakness
  4. Interstitial lung disease
    e.g. fibrosing alveolitis or organising pneumonia (indicates a poor prognosis)
  5. Dysphagia, dysphonia
115
Q

What are the investigations for polymyositis?

A
  1. Muscle enzymes:
    a. Elevated creatine kinase
    b. Lactate dehydrogenase, aldolase, AST and ALT are also elevated in 85-95% of patients
  2. EMG
  3. Muscle biopsy
  4. Anti-synthetase antibodies:
    anti-Jo-1 antibodies are seen in pattern of disease associated with lung involvement, Raynaud’s and fever
116
Q

What is the management of polymyositis?

A
  1. High-dose corticosteroids tapered as symptoms improve
  2. Azathioprine may be used as a steroid-sparing agent
117
Q

What is dermatomyositis?

A
  1. An inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions
  2. May be idiopathic or associated with connective tissue disorders or underlying malignancy (typically ovarian, breast and lung cancer): screening for underlying malignancy should occur at presentation
118
Q

What are the skin manifestations of dermatomyositis?

A
  1. Photosensitive
    macular rash over back and shoulder
  2. Heliotrope rash in the periorbital region
  3. Gottron’s papules - roughened red papules over extensor surfaces of fingers
  4. ‘mechanic’s hands’: extremely dry and scaly hands with linear ‘cracks’ on the palmar and lateral aspects of the fingers
  5. Nail fold capillary dilatation
119
Q

What are the investigations for dermatomyositis?

A
  1. Majority of patients (around 80%) are ANA positive
  2. 30% are positive for anti-synthetase antibodies:
    a. Antibodies against histidine-tRNA ligase (also called Jo-1)
120
Q

What is transient synovitis?

A
  1. Sometimes referred to as irritable hip
  2. It generally presents as acute hip pain following a recent viral infection
  3. It is the commonest cause of hip pain in children: typical age group is 3-8 years
121
Q

What are the features of transient synovitis?

A
  1. Limp/refusal to weight bear
  2. Groin or hip pain
  3. Low-grade fever is present in a minority of patients
    a. If high fever: raise the suspicion of other causes such as septic arthritis
122
Q

What is the management of transient synovitis?

A

Self-limiting, requiring only rest and analgesia

123
Q

What is Ehler-Danlos syndrome?

A
  1. An autosomal dominant connective tissue disorder that mostly affects type III collagen
  2. This results in the tissue being more elastic than normal: leading to joint hypermobility and increased elasticity of the skin
124
Q

What are the features and complications of Ehler-Danlos syndrome?

A
  1. Elastic, fragile skin
  2. Joint hypermobility: recurrent joint dislocation
  3. Easy bruising
  4. Aortic regurgitation, mitral valve prolapse and aortic dissection
  5. Subarachnoid haemorrhage
  6. Angioid retinal streaks
125
Q

What is Marfan’s syndrome?

A
  1. An autosomal dominant connective tissue disorder
  2. It is caused by a defect in the FBN1 gene on chromosome 15 that codes for the protein fibrillin-1
  3. Typical presentation in men with tall stature with dilation of the aortic sinuses: could lead to aortic dissection/ aneurysm
126
Q

What are the features of Marfan’s syndrome?

A
  1. Tall stature with arm span to height ratio > 1.05
  2. High-arched palate
  3. Arachnodactyly: fingers long and slender
  4. Pectus excavatum
  5. Pes planus: flat feet
  6. Scoliosis of > 20 degrees
  7. Heart:
    a. dilation of the aortic sinuses (seen in 90%) which may lead to aortic aneurysm, aortic dissection, aortic regurgitation
    b. mitral valve prolapse (75%),
  8. Lungs: repeated pneumothoraces
  9. Eyes:
    a. upwards lens dislocation (superotemporal ectopia lentis)
    b. blue sclera
    c. myopia
  10. Dural ectasia (ballooning of the dural sac at the lumbosacral level)
127
Q

What is the leading cause of death in Marfan’s syndrome?

A

Aortic dissection and other cardiovascular problems

128
Q

What is the prognosis of Marfan’s syndrome?

A

With the advent of regular echocardiography monitoring and beta-blocker/ACE-inhibitor therapy life expectancy has improved significantly over recent years

129
Q

What is osteoarthritis?

A

Age-related degenerative synovial joint disease when cartilage destruction exceeds repair: causing pain and disability

130
Q

What is the aetiology of osteoarthritis?

A
  1. No single cause
  2. Primary: Aetiology unknown- likely to be multifactorial; wear and tear concept
  3. Secondary: other diseases can cause altered joint architecture and stability e.g. inflammatory (RA, gout), metabolic (acromegaly)
131
Q

What are the risk factors for osteoarthritis?

A
  1. Age > 50 years
  2. Women are affected more than men
  3. Obesity
  4. Genetic factors
  5. Strong association with manual workers
132
Q

What is the epidemiology for osteoarthritis?

A

1/Common, with 25% of those > 60 years symptomatic
2. More common in females, Caucasians and Asians

133
Q

What are the presenting symptoms of osteoarthritis?

A
  1. Joint pain or discomfort, usually use-related, stiffness or gelling after inactivity
  2. Difficulty with certain movements or feelings of instability
  3. Restriction walking, climbing stairs, manual tasks
  4. *Systemic features are typically absent
134
Q

What are the signs of osteoarthritis on physical examination?

A
  1. Local joint tenderness
  2. Bony swellings along joint margins, e.g. Heberden’ s nodes (at distal interphalangeal joints), Bouchard’s nodes (at proximal interphalangeal joints)
  3. Crepitus and pain during joint movement, joint effusion
  4. Restriction of range of joint movement
135
Q

What is a relieving factor in osteoarthritis?

A

Rest - pain is worse on activity
(although joints can grow stiffer on rest)

136
Q

What is osteoarthritis of the hand?

A
  1. Results from the loss of cartilage at synovial joints and is often accompanied by the degeneration of underlying bone
  2. More common in women
  3. Rare to present before 55 years of age
137
Q

What does osteoarthritis of the hand increase the risk of?

A

Increases the risk of future hip and knee OA (higher for hip OA than for knee OA)

138
Q

What are the risk factors for osteoarthritis of the hand?

A
  1. Previous trauma of a joint increases the risk of having OA in that joint
  2. Obesity
  3. Hypermobility of a joint increases the risk of OA in that joint
  4. Occupation e.g. cotton workers and farmers are more susceptible to hand OA
  5. Osteoporosis reduces the risk of OA
139
Q

What are the features of osteoarthritis of the hand?

A
  1. Usually bilateral: Usually one joint at a time is affected over a period of several years
  2. Episodic joint pain: An intermittent ache: provoked by movement and relieved by resting the joint
  3. Stiffness: worse after long periods of inactivity e.g. waking up in the morning (lasts only a few minutes compared to the morning joint stiffness seen in RA)
  4. Painless nodes (bony swellings):
    a. Heberden’s nodes at the DIP joints
    b. Bouchard’s Nodes at the PIP joints
    c. Result from osteophyte formation
  5. Squaring of the thumbs: Deformity of the carpometacarpal joint of the thumb resulting in fixed adduction of the thumb
  6. Functionally patients do not usually have any problems: severe involvement of the DIPJs, there may be reduced grip strength (from disuse atrophy)
140
Q

What are the investigations for osteoarthritis?

A
  1. Joint x-ray of involved joints typically show four classic features:
    a. Narrowing of joint spaces (resulting from cartilage loss)
    b. Subchondral cysts
    c. Subchondral sclerosis
    d. Osteophytes
    Others: inflammatory markers (ESR and CRP) to exclude differentials, RF/ anti-CCP antibodies
    MRI of affected joints (cartilage loss, bone marrow lesions, and meniscal tears)
141
Q

What are the LOSS x-ray findings of oestoarthritis?

A

L- loss of joint space
O- osteophyte formation at joint margins
S- Subchondral cysts
S- Subchondral sclerosis

142
Q

What is the management of osteoarthritis?

A
  1. All patients should be offered help with weight loss, given advice about local muscle strengthening exercises and general aerobic fitness
  2. Paracetamol and topical NSAIDs are first-line analgesics
    a. Topical NSAIDs are indicated only for OA of the knee or hand
  3. Second-line treatment is oral NSAIDs/COX-2 inhibitors (plus PPI), opioids, capsaicin cream and intra-articular corticosteroids
  4. Non-pharmacological treatment options include supports and braces, TENS and shock-absorbing insoles or shoes
  5. If conservative treatment fails: refer for consideration of joint replacement
143
Q

What is osteoarthritis of the hip?

A

The second most common presentation of OA after the knee

144
Q

What are the risk factors for OA of the hip?

A
  1. Increasing age
  2. Female gender (twice as common)
  3. Obesity
  4. Developmental dysplasia of the hip
145
Q

What are the features of OA of the hip?

A
  1. Chronic history of groin ache following exercise and relieved by rest
  2. Red flag features suggesting an alternative cause include rest pain, night pain and morning stiffness > 2 hours (RA)
  3. The Oxford Hip Score is widely used to assess severity
146
Q

What are the investigations for OA of the hip?

A
  1. NICE recommends that if the features are typical then a clinical diagnosis can be made
  2. Otherwise plain x-rays are the first-line investigation
147
Q

What is the management of OA?

A
  1. Oral analgesia
  2. Intra-articular injections: provide short-term benefit
  3. Total hip replacement: remains the definitive treatment (arthroplasty)
148
Q

What are the complications of a THR in osteoarthritis of the hip?

A
  1. Perioperative:
    a. VTE
    b. Intraoperative fracture
    c. Nerve injury
    d. Surgical site infection
  2. Leg length discrepancy
  3. Posterior dislocation:
    a. May occur during extremes of hip flexion
    b. Typically presents acutely with a ‘clunk’, pain and inability to weight bear
    c. On examination there is internal rotation and shortening of the affected leg
  4. Aseptic loosening (most common reason for revision): prosthetic joint infection
149
Q

What can be seen in OA of the Knee?

A

Baker’s cysts (also known as a popliteal cyst):
a. are not true cysts but rather a distension of the gastrocnemius-semimembranosus bursa
b. Primary (children), secondary(adults, from OA)
c. Present as swellings in the popliteal fossa behind the knee
d. Rupture may occur resulting in similar symptoms to a deep vein thrombosis, e.g. pain, redness and swelling in the calf (most are asymptomatic though)

150
Q

What is polymyalgia rheuamtica?

A
  1. A relatively common condition seen in older people characterised by muscle stiffness and raised inflammatory marker
  2. Association with temporal arteritis
151
Q

What are the features of PMR?

A
  1. Typically patient > 60 years old (female)
  2. Usually rapid onset (e.g. < 1 month)
  3. Aching, morning stiffness in proximal limb muscles (not always weakness)
  4. Also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
152
Q

What are the investigations for PMR?

A
  1. Raised inflammatory markers e.g. ESR > 40 mm/hr
  2. Note creatine kinase and EMG normal
153
Q

What is the management of PMR?

A

Prednisolone e.g. 15mg/od:
patients typically respond dramatically to steroids, failure to do so should prompt consideration of an alternative diagnosis

154
Q

What is Porphyria cutanea tarda?

A
  1. The most common hepatic porphyria
  2. It is due to an inherited defect in uroporphyrinogen decarboxylase or caused by hepatocyte damage e.g. alcohol, hepatitis C, oestrogen
155
Q

What are the features of porphyria cutanea tarda?

A
  1. Classically presents with photosensitive rash with blistering and skin fragility on the face and dorsal aspect of hands (most common feature)
  2. Hypertrichosis: excessive hair growth
  3. Hyperpigmentation
156
Q

What are the investigations for porphyria cutanea tarda?

A
  1. Urine: elevated uroporphyrinogen and pink fluorescence of urine under Wood’s lamp
  2. Serum iron ferritin level is used to guide therapy
157
Q

What is the management of porphyria cutanea tarda?

A
  1. Chloroquine
  2. Venesection: preferred if iron ferritin is above 600 ng/ml
158
Q

What is Acute intermittent porphyria (AIP)?

A
  1. Rare autosomal dominant condition caused by a defect in porphobilinogen deaminase, an enzyme involved in the biosynthesis of haem
  2. This results in the toxic accumulation of delta aminolaevulinic acid and porphobilinogen
  3. It characteristically presents with abdominal and neuropsychiatric symptoms in 20-40-year-olds
  4. More common in females (5:1)
159
Q

What is the presentation of Acute intermittent porphyria?

A

Combination of abdominal, neurological and psychiatric symptoms:
1. Abdominal: abdominal pain, vomiting
2. Neurological: motor neuropathy
3. Psychiatric: e.g. depression
4. Hypertension and tachycardia common

160
Q

What are the investigations for Acute intermittent porphyria?

A
  1. Classically urine turns deep red on standing
  2. Raised urinary porphobilinogen (elevated between attacks and to a greater extent during acute attacks)
  3. Assay of red cells for porphobilinogen deaminase
  4. Raised serum levels of delta aminolaevulinic acid and porphobilinogen
161
Q

What is the management of acute intermittent porphyria?

A
  1. Avoiding triggers
  2. Acute attacks:
    a. IV haematin/haem arginate
    b. IV glucose should be used if haematin/haem arginate is not immediately available
162
Q

What is Psoriatic arthritis?

A
  1. An inflammatory arthritis associated with psoriasis and is classed as one of the seronegative spondyloarthropathies
  2. It correlates poorly with cutaneous psoriasis and often precedes the development of skin lesions
163
Q

What is the epidemiology of psoriatic arhtirits?

A

Around 10-20% of patients with skin lesions develop an arthropathy with males and females being equally affected

164
Q

What is the pattern of arthritis in psoriatic arthritis?

A
  1. Symmetric polyarthritis:
    a. Very similar to RA
    b. Most common type
  2. Asymmetrical oligoarthritis: typically affects hands and feet (20-30%)
  3. Sacroiliitis
  4. DIP joint disease (10%)
  5. Arthritis mutilans (severe deformity fingers/hand, ‘telescoping fingers’)
165
Q

What are the other features of psoriatic arthritis?

A
  1. Psoriatic skin lesions
  2. Periarticular disease: tenosynovitis and soft tissue inflammation resulting in:
    a. Enthesitis: inflammation at the site of tendon and ligament insertion e.g. Achilles tendonitis, plantar fascitis
    b. Tenosynovitis: typically of the flexor tendons of the hands
    c. Dactylitis: diffuse swelling of a finger or toe
  3. Nail changes: pitting, onycholysis
166
Q

What are the investigations for psoriatic arthritis?

A
  1. Often have the unusual combination of coexistence of erosive changes and new bone formation
  2. Periostitis
  3. ‘pencil-in-cup’ appearance
167
Q

What is the management of Psoriatic arthirtis?

A
  1. Should be managed by a rheumatologist
  2. Treatment is similar to that of rheumatoid arthritis (RA)
  3. Mild peripheral arthritis/mild axial disease may be treated with ‘just’ an NSAID
  4. Use of monoclonal antibodies such as ustekinumab (targets both IL-12 and IL-23) and secukinumab (targets IL-17)
  5. Apremilast: phosphodiesterase type-4 (PDE4) inhibitor → suppression of pro-inflammatory mediator synthesis and promotion of anti-inflammatory mediators
168
Q

Which has a better prognosis, psoriatic arthritis or rheumatoid arthritis?

A

Psoriatic arthritis

169
Q

What are the seronegative spondyloarthropathies?

A
  1. Associated with HLA-B27
  2. Rheumatoid factor negative
  3. Usually peripheral and asymptomatic arthritis
  4. Ankylosing spondylitis
  5. Psoriatic arthritis
  6. Reactive arthritis
  7. Enteropathic arthritis (associated with IBD)
  8. Enthesopathy: e.g. Achilles tendonitis, plantar fasciitis
  9. Extra-articular manifestations: uveitis, pulmonary fibrosis (upper zone), amyloidosis, aortic regurgitation
170
Q

What is reactive arthritis?

A

Defined as an arthritis that develops following an infection where the organism cannot be recovered from the joint (usually GI or GU infection)

171
Q

What is the aetiology and epidemiology of reactive arthritis?

A
  1. Post-STI form much more common in men (e.g. 10:1): Chlamydia trachomatis
  2. Post-dysenteric form equal sex incidence:
    a. Shigella flexneri
    b. Salmonella typhimurium
    c. Salmonella enteritidis
    d. Yersinia enterocolitica
    e. Campylobacter
172
Q

What is the triad sometimes seen in reactive arthritis?

A

Urethritis, conjunctivitis and arthritis (following a recent GI or GU infection)

173
Q

What are the investigations for reactive arthritis?

A
  1. Bloods:
    a. Raised ESR and CRP
    b. FBC: anaemia indicates extent of systemic disease
  2. Stool culture: may be negative by the time arthritis develops
  3. Urine/ Swabs: Screening for Chlamydia trachomatis
  4. Plain X-ray radiographs (chronic cases): Erosions at insertions of tendons (entheses) e.g. Achilles tendon, sacroiliitis (HLA-B27 association)
174
Q

What is the management of reactive arthritis?

A
  1. Treat STI if present
  2. Symptomatic: analgesia, NSAIDS, intra-articular steroids
  3. Sulfasalazine and methotrexate are sometimes used for persistent disease
  4. Symptoms rarely last more than 12 months
175
Q

What is rheumatoid arthritis?

A

Chronic inflammatory systemic disease characterized by symmetrical deforming polyarthritis and extra-articular manifestations

176
Q

What joints are usually affected in rheumatoid arthritis?

A

Small joints of the hands and feet

177
Q

What is the HLA associated with rheumatoid arthritis?

A

HLA DR-4 (and DR-1)

178
Q

What are the associated autoimmune conditions associated with rheumatoid arthritis?

A
  1. Raynaud’s phenomenon: An exaggerated vascular response to cold temperature or emotional stress characterized by episodic color changes of blanching, cyanosis, and hyperemia
  2. Sjögren’s syndrome
179
Q

What is the epidemiology of rheumatoid arthritis?

A
  1. Common- prevalence is 1% of general population
  2. Three times more common in females, peak incidence at 30–50 years
180
Q

What are the typical features of rheumatoid arthritis?

A
  1. Swollen, painful joints in hands and feet
  2. Stiffness worse in the morning
  3. Gradually gets worse with larger joints becoming involved
  4. Presentation usually insidiously develops over a few months
  5. Positive ‘squeeze test’ - discomfort on squeezing across the metacarpal or metatarsal joints
181
Q

What are the late features of rheumatoid arthritis?

A
  1. Symmetrical deforming arthropathy:
    a. Swan neck deformity (MCP and DIP fixed flexion, PIP extension)
    b. Boutonniere deformity (MCP and DIP joint extension, PIP flexion)
    c. Ulnar deviation of fingers at MCP joints
  2. Extra-articular features, such as rheumatoid nodules over the extensor surfaces of tendons
182
Q

What are the ocular manifestiations of rheumatoid arthritis?

A
  1. Are common, with 25% of patients having eye problems
  2. Dry eye: keratoconjunctivitis sicca (most common)
  3. Episcleritis (erythema)
  4. Scleritis (erythema and pain)
  5. Corneal ulceration
  6. Keratitis
  7. Iatrogenic: steroid-induced cataracts
183
Q

What are the appropriate investigations for rheumatoid arthritis?

A
  1. Rheumatoid Factor: positive
  2. Anti-cyclic citrullinated protein: positive (best marker)
  3. Elevated CRP and ESR
  4. Joint X-ray radiography:
    a. Soft tissue swelling
    b. Angular deformity
    c. Periarticular erosions and osteoporosis
  5. ?Consider joint aspiration to exclude septic arthritis
184
Q

What percentage of patients with rheumatoid arthritis are RF positive?

A

70-80%: therefore even if RF negative, patients with symptoms should be tested for Anti-cyclic citrullinated peptide antibody (anti-CCP)

185
Q

What are the x-ray changes of rheumatoid arthritis?

A
  1. Early:
    a. Loss of joint space
    b. Juxta-articular osteoporosis
    c. Soft-tissue swelling
  2. Late:
    a. Periarticular erosions
    b. Subluxation (incomplete/ partial dislocation)
186
Q

What is the initial management of rheumatoid arthritis?

A

DMARD monotherapy ± a short-course of bridging prednisolone

187
Q

How is rheumatoid arthritis response to treatment monitored?

A

Combination of CRP and disease activity (using a composite score such as DAS28)

188
Q

How are flares in rheumatoid arthritis managed?

A

Corticosteroids - oral or intramuscular

189
Q

What are DMARDs in the management of rheumatoid arthritis?

A
  1. Disease-modifying drugs
  2. Monitoring of FBC & LFTs is essential due to the risk of myelosuppression and liver cirrhosis. Other side-effect: pneumonitis
  3. Methotrexate is most widely used
  4. Others:
    a. sulfasalazine
    b. leflunomide
    c. hydroxychloroquine
190
Q

When would patients with rheumatoid arthritis be managed with a TNF inhibitor?

A

If there is an inadequate response to at least two DMARDs including methotrexate

191
Q

What are TNF-inhibitors in the management of rheumatoid arthritis?

A
  1. Etanercept: recombinant human protein, acts as a decoy receptor for TNF-α, s/c administration, can cause demyelination, risks include reactivation of TB
  2. Infliximab: monoclonal antibody, binds to TNF-α and prevents it from binding with TNF receptors, intravenous administration, risks include reactivation of TB
  3. Adalimumab: monoclonal antibody, subcutaneous administration
192
Q

What is Rituximab in the management of rheumatoid arthritis?

A
  1. Anti-CD20 monoclonal antibody, results in B-cell depletion
  2. Two 1g IV infusions are given two weeks apart
  3. Infusion reactions are common
193
Q

What are the side effects of methotrexate and corticosteroids in the management of rheumatoid arthritis?

A
  1. Methotrexate:
    a. Myelosuppression
    b. Liver cirrhosis
    c. Pneumonitis
  2. Prednisolone:
    a. Cushingoid features
    b. Osteoporosis
    c. Impaired glucose tolerance
    d. Hypertension
    e. Cataracts
194
Q

What are the different extra-articular complications of rheumatoid arthritis?

A
  1. Respiratory: pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy
  2. Ocular: keratoconjunctivitis sicca (most common), chloroquine retinopathy
  3. Osteoporosis
  4. Ischaemic heart disease: RA carries a similar risk to type 2 diabetes mellitus
  5. Increased risk of infections
  6. Depression
195
Q

What are poor prognostic factors of rheumatoid arthritis?

A
  1. Rheumatoid factor positive
  2. anti-CCP antibodies
  3. Poor functional status at presentation
  4. X-ray: early erosions (e.g. after < 2 years)
  5. Extra articular features e.g. nodules
  6. HLA DR4
  7. Insidious onset
  8. Maybe female gender
196
Q

What is the difference between spondylolysis and spondylolisthesis?

A
  1. Spondylolysis:
    a. Congenital or acquired deficiency of the pars interarticularis of a particular vertebral body, usually affects L4/ L5
    b. May be asymptomatic
    c. Affects 5% of population
    d. The commonest cause of spondylolisthesis in children
    e. Asymptomatic cases do not require treatment
  2. Spondylolisthesis:
    a. Occurs when one vertebra is displaced relative to its immediate inferior vertebral body
    b. May occur as a result of stress fracture or spondylolysis
    c. Traumatic cases may show the classic ‘Scotty Dog’ on plain films
    d. Treatment depends upon the extent of deformity and associated neurological symptoms
    e. Minor cases: actively monitored
    f. Individuals with radicular symptoms or signs will usually require spinal decompression and stabilisation
197
Q

What is carpal tunnel syndrome?

A

Caused by compression of median nerve in the carpal tunnel

198
Q

What are the symptoms of carpal tunnel syndrome in the history?

A
  1. Pain/pins and needles in thumb, index, middle finger
  2. Unusually the symptoms may ‘ascend’ proximally
  3. Patient shakes their hand to obtain relief, classically at night
199
Q

What are the signs of carpal tunnel syndrome on examination?

A
  1. Weakness of thumb abduction (abductor pollicis brevis)
  2. Wasting of thenar eminence (NOT hypothenar)
  3. Tinel’s sign: tapping causes paraesthesia
  4. Phalen’s sign: flexion of wrist causes symptoms
200
Q

What are the causes of carpal tunnel syndrome?

A
  1. Idiopathic
  2. Pregnancy
  3. Oedema e.g. heart failure
  4. Lunate fracture
  5. Rheumatoid arthritis
201
Q

What is seen on EMG in carpal tunnel syndrome?

A

Motor + sensory: prolongation of the action potential

202
Q

What is the management of carpal tunnel syndrome?

A
  1. 6-week trial of conservative treatments if the symptoms are mild-moderate:
    a. corticosteroid injection
    b. wrist splints at night
  2. If there are severe symptoms or symptoms persist with conservative management:
    surgical decompression (flexor retinaculum division)
203
Q

What is Dupuytren’s contracture?

A

Painless condition in which there is abnormal thickening of the fascia causing the fingers to bend toward palm of the hand (usually ring finger and little finger)

204
Q

What is the epidemiology of Dupuytren’s contracture?

A
  1. Prevalence of about 5%
  2. It is more common in older male patients
  3. Around 60-70% have a positive family history
205
Q

What are the specific causes of Dupuytren’s contracture?

A
  1. Manual labour
  2. Phenytoin treatment
  3. Alcoholic liver disease
  4. Diabetes mellitus
  5. Trauma to the hand
206
Q

What is the management of Dupuytren’s contracture?

A

Consider surgical treatment of Dupuytren’s contracture when the metacarpophalangeal joints cannot be straightened and thus the hand cannot be placed flat on the table

207
Q

What is a scaphoid fracture?

A

A type of wrist fracture, typically arises as a result of a fall onto an outstretched hand

208
Q

What is the aetiology of scaphoid fractures?

A
  1. Falling onto an outstretched hand (FOOSH)
  2. Contact sports: The peak incidence during the autumn is thought to correlate with the start of football and rugby activities at school
  3. Results in axial compression of the scaphoid, with the wrist hyperextended, and radially deviated
209
Q

What are the presenting symptoms of scaphoid fractures?

A
  1. Pain along the radial aspect of the wrist, at the base of the thumb
  2. Loss of grip / pinch strength
210
Q

What are the signs of a scaphoid fracture on examination?

A
  1. Point of maximal tenderness over the anatomical snuffbox -highly sensitive (around 90-95%)
  2. Wrist joint effusion
    a. Hyperacute injuries (<4hrs old), and delayed presentations (>4days old) may not present with joint effusions
  3. Pain elicited by telescoping of the thumb (pain on longitudinal compression)
  4. Tenderness of the scaphoid tubercle (on the volar aspect of the wrist)
  5. Pain on ulnar deviation of the wrist
211
Q

What are the investigations for a scaphoid fracture?

A
  1. Clinical examination has a high diagnostic probability
  2. Plain film: wrist in the anterior-posterior view, and lateral view (‘scaphoid views’)
  3. MRI is considered the definite investigation to confirm or exclude a diagnosis:
    a. NICE: first-line imaging following clinical examination
    b. Often used second line after plain films
212
Q

What are the scaphoid views on plain film x-ray for scaphoid fracture?

A

Posterioranterior (PA), lateral, oblique (with wrist pronated at 45º) and Ziter view (PA view with the wrist in ulnar deviation and beam angulated at 20º)

213
Q

What is the initial management of suspected or confirmed scaphoid fracture?

A
  1. Immobilisation with a Futuro splint or standard below-elbow backslab
  2. Referral to orthopaedics
    clinical review with further imaging should be arranged for7-10 days later when initial radiographs are inconclusive
214
Q

What is the orthopaedic management of scaphoid fractures?

A
  1. Dependent on the patient and type of fracture
  2. Undisplaced fractures of the scaphoid waist:
    a. cast for 6-8 weeks
    b. union is achieved in > 95%
    c. certain groups e.g. professional sports people may benefit from early surgical intervention
  3. Displaced scaphoid waist fractures: requires surgical fixation
  4. Proximal scaphoid pole fractures: require surgical fixation
215
Q

What are the complications of scaphoid fractures?

A
  1. Non-union → pain and early osteoarthritis
  2. Avascular necrosis: dorsal carpal branch (branch of the radial artery)
216
Q

What is a Colles’ fracture?

A
  1. Distal radius fracture with dorsal displacement of fragments
  2. Described as a dinner fork type deformity
217
Q

What is the aetiology of a Colles’ fracture?

A

Classically follows a fall onto an outstretched hand (known as a FOOSH)

218
Q

What are the three features of a Colles’ fracture?

A
  1. Transverse fracture of the radius
  2. 1 inch proximal to the radio-carpal joint
  3. Dorsal displacement and angulation
219
Q

What are the complications of a colles’ fracture?

A
  1. Early:
    a. Median nerve injury: acute carpal tunnel syndrome presenting with weakness or loss of thumb or index finger flexion
    b. Compartment syndrome
    c. Vascular compromise
    d. Malunion
    e. Rupture of the extensor pollicis longus tendon
  2. Late:
    a. Osteoarthritis
    b. Complex regional pain syndrome
220
Q

What is Smith’s fracture (reverse Colles’ fracture)?

A
  1. Volar angulation of distal radius fragment (Garden spade deformity)
  2. Caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed
221
Q

What is a Galeazzi fracture?

A
  1. Radial shaft fracture with associated dislocation of the distal radioulnar joint
  2. Occur after a fall on the hand with a rotational force superimposed on it
  3. On examination, there is bruising, swelling and tenderness over the lower end of the forearm
  4. X Rays reveal the displaced fracture of the radius and a prominent ulnar head due to dislocation of the inferior radio-ulnar joint
222
Q

What is a Radial head fracture?

A
  1. Common in young adults
  2. It is usually caused by a fall on the outstretched hand
  3. On examination, there is marked local tenderness over the head of the radius, impaired movements at the elbow, and a sharp pain at the lateral side of the elbow at the extremes of rotation (pronation and supination)
223
Q

What is a ganglion cyst?

A
  1. A ganglion presents as a ‘cyst’ arising from a joint or tendon sheath
  2. They are most commonly seen around the dorsal aspect of the wrist and are 3 times more common in women
  3. A firm and well-circumscribed mass that transilluminates
224
Q

What is the management of a ganglion cyst?

A
  1. Ganglions often disappear spontaneously after several months
  2. Surgical excision is indicated for cysts associated with severe symptoms or neurovascular manifestations
225
Q

What is De Quervain’s tenosynovitis?

A
  1. When the sheath containing the extensor pollicis brevis and abductor pollicis longus tendons is inflamed
  2. It typically affects females aged 30 - 50 years old
226
Q

What are the features of De Quervain’s tenosynovitis?

A
  1. Pain on the radial side of the wrist
  2. Tenderness over the radial styloid process
  3. Abduction of the thumb against resistance is painful
  4. Finkelstein’s test: the examiner pulls the thumb of the patient in ulnar deviation and longitudinal traction: in a patient with tenosynovitis this action causes pain over the radial styloid process and along the length of extensor pollisis brevis and abductor pollicis longus
227
Q

What is the management of De Quervain’s tenosynovitis?

A
  1. Analgesia
  2. Steroid injection
  3. Immobilisation with a thumb splint (spica) may be effective
  4. Surgical treatment is sometimes required
228
Q

What is trigger finger?

A
  1. A common condition associated with abnormal flexion of the digits
  2. It is thought to be caused by a disparity between the size of the tendon and pulleys through which they pass (tendon becomes ‘stuck’ and cannot pass smoothly)
  3. Majority of cases are idiopathic
  4. More common in women
229
Q

What conditions are associated with trigger finger?

A
  1. Rheumatoid arthritis
  2. Diabetes mellitus
230
Q

What are the features of a trigger finger?

A
  1. More common in the thumb, middle, or ring finger
  2. Initially stiffness and snapping (‘trigger’) when extending a flexed digit
  3. A nodule may be felt at the base of the affected finger
231
Q

What is the management of a trigger finger?

A
  1. Steroid injection is successful in the majority of patients
    a. A finger splint may be applied afterwards
  2. Surgery should be reserved for patients who have not responded to steroid injections