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Finals > Orthopaedics and Rheumatology > Flashcards

Orthopaedics and Rheumatology Flashcards

1
Q

Presentation of rheumatoid arthritis

A
  • swollen, painful joints in the hands and feet
  • stiffness worse in the morning
  • gradually gets worse with larger joints becoming involved
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2
Q

What are the poor prognostic factors for rheumatoid arthritis?

A
  • anti CCP
  • rheumatoid factor
  • early erosions on X ray (<2 years)
  • HLA DR4
  • Extra articular features
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3
Q

Management of rheumatoid arthritis

A
  • dMARD with a bridging course of prednisolone
  • methotrexate/sulfasalazine
  • hydroxychloroquine if mild or palinodromic
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4
Q

How can you monitor response to treatment of rheumatoid arthritis?

A
  • crp
  • disease activity score e.g. DAS28
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5
Q

Management of flare of rheumatoid

A

corticosteroid

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6
Q

Indication for TNF-a in rheumatoid arthritis

A

Failed response to at least two dMARDs

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7
Q
A
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8
Q

Name 3 TNFa inhibitors

A
  • etanercept
  • infliximab
  • adalimumab
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8
Q

X ray findings of rheumatoid arthritis

A
  • loss of joint space
  • juxta-articular osteoporosis
  • soft tissue swelling
  • periarticular erosion
  • subluxation
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9
Q

methotrexate side effects

A
  • myelosuppression
  • pneumonitis
  • liver cirrhosis
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10
Q

Side effects of sulfasalazine

A
  • rashes
  • oligospermia
  • heinz body anaemia
  • interstitial lung disease
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11
Q

hydroxychloroquine side effects

A
  • retinopathy
  • corneal deposits
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12
Q

What are the patterns of psoriatic arthritis?

A
  • symmetric
  • asymmetrical
  • sacroillitis
  • DIP joint disease
  • arthritis mutilans
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13
Q

Signs of psoriatic arthritis

A
  • psoriatic skin lesions
  • periarticular disease: enthesitis, tenosynovitis, dactylitis
  • nail changes: pitting, onycholysis
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14
Q

X ray psoriatic arthritis

A
  • pencil in cup appearance
  • periostitis
  • erosive changes, new bone formation
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15
Q

Management of psoriatic arthritis

A
  • NSAID if mild
  • dMARD (methotrexate) if moderate or severe
  • monoclonal antibodies such as ustekinumab (targets both IL-12 and IL-23) and secukinumab (targets IL-17)
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16
Q

Pseudogout

A

deposition of calcium pyrophosphate dihydrate crystals in the synovium

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17
Q

Risk factors of pseudogout

A
  • haemochromotosis
  • wilsons
  • hyperparathyroidism
  • acromegaly
  • low magnesium, low phosphate
    -age
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18
Q

Features of pseudogout

A
  • knee, wrist, shoulder
  • joint aspiration: weakly-positively birefringent rhomboid-shaped crystals
  • x-ray: chondrocalcinosis
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19
Q
A
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20
Q

What are the main features of gout?

A
  • pain
  • swelling
  • erythema
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21
Q

commonly affected joints in gout

A
  • most commonly the 1st MTP joint
  • others: ankle, wrist, knee
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22
Q

Investigations for gout

A
  • measure the uric acid level if >360 supports the diagnosis, if under and symptoms still suggest gout then repeat in 2 weeks
  • synovial fluid analysis (needle shaped negatively birefringent monosodium urate crystals)
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23
Q

What is the management of an acute flare of gout?

A
  • NSAIDs
  • Colchicine
  • if the patient is already taking allopurinol they should continue taking it
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24
Q

What is the main side effect of colchicine?

A

Diarrhoea

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25
Q

Who should be started on urate lowering therapy and when?

A

Anyone who has had an attack of gout, two weeks after the attack

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26
Q

Management of gout to prevent an attack

A
  • allopurinol
  • lifestyle advice: avoid alcohol, lose weight if obese, avoid food high in purines: liver, oily fish, seafood, yeast products
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27
Q

When is urate lowering therapy particularly recommended?

A
  • ≥2 attacks in the last 3 months
  • tophi
  • renal disease
  • uric acid renal stones
  • if on cytotoxics or diuretics
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28
Q

Typical joints osteoarthrtitis

A
  • larger joints
  • knee
  • hip
  • carpometocarpal
  • DIP, PIP joints
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29
Q

X ray findings osteoarthritis

A
  • loss of joint space
  • subchondral sclerosis
  • subchondral cysts
  • osteophytes
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30
Q

What is the management of osteoarthritis

A
  • weight loss, local muscle strengthening, general aerobic fitness advice
  • topical NSAIDs
  • second line: oral NSAIDs and PPI
  • intra-articular steroid injections if analgesia not effective (pain relief only lasts 2-10 weeks)
  • consideration of joint replacement
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31
Q

What are the most common causes of septic arthritis in adults?

A
  • staph aureus
  • n. gonnorhoeae in young adults who are sexually active
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32
Q

Features of septic arthritis

A
  • acute, swollen joint
  • warm to touch/fluctuant
  • restricted movement
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33
Q

Investigations septic arthritis

A
  • synovial fluid aspiration
  • blood cultures
  • joint imaging
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34
Q

Management of septic arthritis

A
  • IV antibiotics
  • flucloxacillin
  • switch to oral antibiotics after 2 weeks
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35
Q

What is reactive arthritis

A

Arthritis that develops following an infection in which the organism cannot be recovered from the joint

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36
Q

STI reactive arthritis

A
  • chlamydia
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37
Q

post dysenteric arthritis

A
  • shigella
  • salmonella
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38
Q

What is the management of reactive arthritis?

A
  • analgesia, NSAIDs, intra-articular steroids
  • sulfasalazine or methotrexate if continuing disease
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39
Q

Features of reactive arthritis

A
  • typically develops within 4-6 weeks post infection
  • asymmetrical oligoarthritis
  • dactylitis
  • urethritis
  • conjunctivitis or anterior uveitis
  • circinate balanitis (painless vesicles on the coronal margin of the prepuce)
    keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
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40
Q

What are the common features of the seronegative spondyloarthropathies?

A
  • rheumatoid factor negative
  • peripheral arthritis and usually asymmetrical
  • sacroillitis
  • enthesopathy
  • extra- articular manifestations (uveitis, pulmonary fibrosis (upper zone), amyloidosis, aortic regurgitation)
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41
Q

What are the sero-negative spondyloarthropathies?

A
  • ankylosing spondylitis
  • psoriatic arthritis
  • reactive arthritis
  • enteropathic arthritis
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42
Q

Features of ankylosing spondylitis

A
  • typically a young man with lower back pain and stiffness of insidious onset
  • stiffness worse in the morning, better with exercise
  • may experience pain at night which gets better on getting up
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43
Q

clinical exam ankylosing spondylitis

A
  • reduced lateral flexion
  • reduced forward flexion (schober’s test)
  • reduced chest expansion
  • the A’s: apical fibrosis, AV node block, anterior uveitis, aortic regurgitation, achilles tendonitis, amyloidosis
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44
Q

Investigation ankylosing spondylitis

A
  • X ray of sacroiliac joints
  • ESR and CRP may be raised
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45
Q

X ray ankylosing spondylitis

A
  • sacroilitis: subchondral erosions, sclerosis
  • sparing of lumbar vertebrae
  • bamboo spine
  • syndesmophytes
  • chest x ray: apical fibrosis
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46
Q

Early sign of ankylosing spondylitis if X ray is negative

A
  • bone marrow oedema on MRI
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47
Q

Management of ankylosing spondylitis

A
  • regular exercise e.g. swimming
  • NSAIDs are first line treatment
  • physiotherapy
  • disease modifying drugs can be used if there is peripheral arthritis
  • anti- TNF if high level disease activity despite conventional treatments e.g. etanercept
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48
Q

Onset SLE

A

20-40

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49
Q

ethnicity SLE more common

A

Afro-Caribbean, asian

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50
Q

sensitivity reaction SLE

A

Type 3

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51
Q

Genes SLE

A

HLA B8, DR2, DR3

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52
Q

General features of SLE

A
  • fatigue
  • fever
  • mouth ulcers
  • lymphadenopathy
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53
Q

Skin features of SLE

A
  • malar rash (butterfly)
  • discoid rash
  • photosensitivity
  • raynauds
  • livedo reticularis
  • non scarring alopecia
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54
Q

msk features of SLE

A
  • arthralgia
  • non erosive arthritis
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55
Q

cardiovascular features of SLE

A
  • pericarditis
  • myocarditis
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56
Q

Respiratory features of SLE

A
  • pleurisy
  • fibrosing alveolitis
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57
Q

Renal features of SLE

A
  • proteinuria
  • glomerulonephritis
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58
Q

Neuropsychiatric features of SLE

A
  • anxiety and depression
  • psychosis
  • seizures
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59
Q

Antibodies in SLE

A
  • 99% are ANA positive (high sensitivity, low specificity
  • anti- dsDNA (high specificity, sensitivity 70%)
  • 20% rheumatoid factor positive
  • anti-smith
  • anti- Ro, anti-La
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60
Q

monitoring of SLE

A
  • Inflammatory markers: ESR, crp
  • complement C3/4 are low during activity of disease
  • anti-ds DNA can be used
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61
Q

management of SLE

A
  • NSAIDs
  • sun block
  • hydroxychloroquine
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62
Q

What are the 3 types of systemic sclerosis

A
  • limited cutaneous
  • diffuse cutaneous
  • scleroderma (without internal organ involvement)
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63
Q

limited cutaneous sclerosis

A
  • raynauds
  • scleroderma affecting the face and distal limbs
  • subtype= CREST: calcinosis, raynauds, esophageal dysmotility, sclerodactyly, telangiectasia
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64
Q

antibodies limited cutaneous sclerosis

A

anti-centromere antibodies

(ANA also positive in cutaneous sclerosis)

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65
Q

Diffuse cutaneous sclerosis

A
  • scleroderma affecting the trunk and proximal limbs
  • respiratory: ILD/pulmonary arterial hypertension
  • renal disease and hypertension
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66
Q

What is scleroderma?

A

Thickening and tightening of the skin

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67
Q

What is sjogrens?

A

autoimmune disorder affecting the exocrine glands resulting in dry mucosal surfaces

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68
Q

Features of sjogrens

A
  • dry eyes, mouth, vagina
    -arthralgia
  • raynauds
  • myalgia
  • sensory polyneuropathy
  • parotitis
  • renal tubular acidosis
  • increased lymphoid malignancy
69
Q

investigations for sjogrens

A
  • rheumatoid factor positive in 50%
  • Anti Ro positive in 70%
  • Anti La positive in 30%
  • ANA positive in 70%
  • schirmers test to measure tear formation
70
Q

Management of sjogrens

A
  • artificial tears and saliva
  • pilocarpine may stimulate saliva production
71
Q

What is polymyositis?

A

inflammatory disorder causing symmetrical, proximal muscle weakness, thought to be t cell mediated.

72
Q

Associations of polymyositis

A
  • malignancy
  • connective tissue disorders
73
Q

Features of polymyositis

A
  • proximal muscle weakness/tenderness
  • raynauds
  • respiratory muscle weakness
  • interstitial lung disease
  • dysphagia, dysphonia
74
Q

Investigation polymyositis

A
  • elevated creatine kinase
  • elevated muscle enzymes (LDH, AST, ALT)
  • EMG
  • Muscle biopsy
  • anti-jo-1 Antibodies (anti-synthetase antibodies)
75
Q

Management of polymyositis

A
  • high dose steroids, tapered down
  • azathioprine as steroid sparing therapy
76
Q

What is dermomyositis

A
  • inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions
  • idiopathic, related to connective tissue disorders, or malignancy
77
Q

What should be done prior to a diagnosis of dermomyositis?

A

Malignancy screen

78
Q

skin features dermomyositis

A
  • photosensitivity
  • macular rash over back and shoulder
  • helitrope rash in the orbital area
  • gottron’s papule
  • mechanic’s hands’: extremely dry and scaly hands with linear ‘cracks’ on the palmar and lateral aspects of the fingers
  • nail fold capillary dilatation
79
Q

histidine tRNA ligase

A

Anti -jo-1

80
Q

anti - RNP

A

SLE/mixed CTD

81
Q

anti sm

A

SLE

82
Q

Antiphospholipid syndrome antibodies

A

anticardiolipin antibodies

83
Q

What is antiphospholipid syndrome?

A

Predisposition to arterial and venous thromboses, fetal loss, and thrombocytopenia

84
Q

What are the features of antiphospholipid syndrome

A
  • venous/arterial thromboses
  • recurrent miscarriages
  • livedo reticualris
85
Q

Investigations antiphospholipid syndrome

A
  • anticardiolipin antibodies
  • thrombocytopenia
  • prolonged APTT
86
Q

Management of antiphospholipid syndrome

A
  • Primary thromboprophylaxis: low dose aspirin
  • Secondary venous thrombophylaxis: warfarin, target INR 2-3
87
Q

comminuted fracture

A

> 2 fragments

88
Q

segmental fracture

A

More than one fracture along a bone

89
Q

Grade 1 open fracture

A

low energy wound <1cm

90
Q

grade 2 open fracture

A

greater than 1cm with moderate soft tissue damage

91
Q

Grade 3 open fracture

A

high energy wound >1cm with extensive soft tissue damage

a- adequate soft tissue coverage
b- inadequate soft tissue coverage
c- associated arterial injury

92
Q

Management of open fracture

A
  • removal of gross debris,
  • debridement and irrigation
  • IV broad spectrum antibiotics
  • immobilise (internal fixation should be avoided)
  • monitor the neurovascular function
93
Q

What are the two main fractures that risk compartment syndrome?

A
  • supracondylar fracture
  • tibial shaft
94
Q

Features of compartment syndrome

A
  • pain, especially on movement (including passive)
  • paraesthesia
  • pallor
  • arterial pulsation
  • paralysis of the muscle group
95
Q

Diagnosis of compartment syndrome

A
  • intracompartmental pressure measurement >20 is abnormal, >40 is diagnostic
96
Q

Compartment syndrome x ray

A

Will probably not show anything

97
Q

What is the management of compartment syndrome

A
  • extensive fasciotomies
  • debridement
  • consider amputation
98
Q

What may occur after a fasciotomy?

A

myglobinuria resulting in renal failure - give aggressive IV fluids

99
Q

What level does the spinal cord end?

A

L1-2

100
Q

What are the features of cauda equina?

A
  • lower back pain
  • bilateral sciatica
  • saddle anaesthesia
  • decreased anal tone
  • urinary dysfunction
101
Q

Investigation for cauda equina

A

urgent MRI

102
Q

What is the management of cauda equina syndrome?

A

surgical decompression

103
Q

What are the causes of cauda equina syndrome?

A
  • herniated disc
  • tumour, metastases
  • spondylolisthesis
  • abscess
  • trauma
104
Q

What is the management of metastatic spinal cord compression syndrome?

A
  • high dose dexamethasone
  • analgesia
  • radiotherapy
  • surgery
105
Q

What are the complications of cauda equina syndrome?

A
  • bladder dynsfunction
  • bowel dysfunction
  • sexual dysfunction
  • leg weakness
  • sensory impairment
106
Q

What are the red flags for back pain?

A
  • age<20, >50
  • history of previous malignancy
  • night pain
  • history of trauma
  • systemically unwell
107
Q

Features of spinal stenosis

A
  • gradual onset
  • uni or bi lateral leg pain
  • numbness
  • weakness
  • symptoms worse on walking, resolves when sitting, leaning forwards or crouching
108
Q

What are the causes of mechanical back pain?

A
  • muscle or ligament sprain
  • facet joint dysfunction
  • sacroiliac joint dysfunction
  • herniated disc
  • spondylolisthesis
  • scoliosis
  • degnereative changes
109
Q

Which cancers metastasise to the bones?

A
  • prostate
  • renal
  • thyroid
  • breast lung
110
Q

What are the ottawa ankle rules?

A

An ankle X ray is only required if there is any pain in the malleolar zone and one of the following:
- bony tenderness at the lateral malleolar zone (lateral malleolus to lower 6cm of the posterior border of the fibula)
- bony tenderness at the medial malleolar zone (from tip of the medial malleolus to the lower 6cm of the posterior border of the tibia)
- inability to walk four weight bearing steps immediately after the injury and in the emergency department

111
Q

Syndesmosis of the ankle

A
  • joins the distal tibia and fibula together
  • anterior inferior tibiofibular ligament
  • posterior inferior tibiofibular ligament
  • interosseous ligament
  • interosseous membrane
112
Q

How is the distal tibia secured to the talus?

A

By the deltoid ligament

113
Q

How is the distal fibula secured to the talus?

A
  • anterior and posterior talofibular liaments
114
Q

How is the distal fibula secured to the calcaneus?

A

Calcaneofibular ligament

115
Q

What is a sprain

A

stretching, partial, or complete tear of a ligament

116
Q

High ankle sprain

A

syndesmosis

117
Q

Low ankle sprain

A

lateral colateral ligaments (anterior and posterior talofibular ligaments and calcaneofibular ligament)

118
Q

Presentation of a low ankle sprain

A
  • anterior talofibular ligament most commonly affected
  • inversion injury is the most common
  • pain, swelling and tenderness over the affected ligaments, sometimes bruising
  • patients usually able to weight bear unless severe
119
Q

Investigation for low ankle sprain

A
  • Follow ottowa rules for x ray
  • MRI if persistent pain
120
Q

Management of low ankle sprains

A
  • Rest, ice, compression and elevation
  • cast and/or crutches for short term symptom relief
  • MRI and surgical intervention can be considered in extreme cases
121
Q

Presentation of high ankle sprain

A
  • external rotation of the foot causing the talus to push fibula laterally
  • weight bearing painful
  • pain when the tibia and fibula are squeezed together at the level of the mid calf (hopkins squeeze test)
122
Q

What are the causes of avascular necrosis of the hip?

A
  • long term steroid use
  • chemotherapy
  • alcohol excess
  • trauma
123
Q

Investigation avascular necrosis of the hip

A
  • plain film x-ray may be normal initially (osteopenia/microfractures, crescent sign (collapse of articular surface))
  • MRI is the investigation of choice
124
Q

Management of avascular necrosis of the hip

A

Joint replacement

125
Q

What is a baker’s cyst?

A

Distension of the gastrocnemius-semimembranous bursa. Can be primary (no underlying pathology), or secondary e.g. due to osteoarthritis

  • swelling in the popliteal fossa
126
Q

Presentation of a biceps rupture

A
  • sudden pop or tear either at the shoulder (long tendon) or at the antecubital fossa (distal tendon) followed by pain, bruising and swelling
  • popeye deformity
  • weakness in the shoulder and elbow, including supination
127
Q

Investigation biceps rupture

A
  • biceps squeeze test (supination seen in arm)
  • ultrasound scan
  • for distal tendon rupture MRI urgently, can consider in long tenson
128
Q

What does paget’s affect?

A
  • spine
  • skull
  • pelvis
  • femur
129
Q

Bloods pagets

A
  • ALP raised
  • other normal
130
Q

Pagets on x ray

A
  • thickened sclerotic bone
131
Q

treatment of pagets

A

bisphosphonates

132
Q

what happens in pagets?

A

Focal bone resorption followed by excessive and chaotic bone deposition

133
Q

osteoporosis bloods

A
  • ALP normal
  • calcium normal
134
Q

Nerve carpal tunnel

A

Median nerve

135
Q

Presentation of carpal tunnel

A
  • pain/pin sand needles in the thumb, index and middle finger
  • symptoms ascend proximally
  • patient may shake their hand to relieve symptoms, classically at night
136
Q

Examination carpal tunnel

A
  • weakness of thumb abduction (abductor pollicis brevis)
  • wasting of the thenar eminence (not hypothenar)
  • tinel’s sign: tapping causes paraesthesia
  • phalens: flexion of the wrist causes symptoms
137
Q

What are the causes of carpal tunnel syndrome?

A
  • idiopathic
  • pregnancy
  • oedema e.g. heart failure
  • lunate fracture
  • rheumatoid arthritis
138
Q

Electrophysiology of carpal tunnel

A

motor and sensory prolongation of the action potential

139
Q

Treatment of carpal tunnel

A
  • 6 week trial of conservative treatment: corticosteroid injection, wrist splint at night (particularly useful if transient factors present)
  • severe or symptoms persist: surgical decompression: flexor retinaculum division
140
Q

What is a charcot joint?

A

Joint that has become badly disrupted and damaged secondary to a loss of sensation e.g. diabetes

141
Q

What is a colles fracture?

A
  • distal radius fracture with dorsal displacement of the fragments
  • described as a dinner fork deformity
142
Q

early complications of colles fracture

A
  • median nerve injury: acute carpal tunnel with weakness or loss of thumb or index finger flexion
  • compartment syndrome
  • vascular compromise
  • malunion
143
Q

Late complications of a colles fracture

A
  • osteoarthritis
  • complex regional pain syndrome
144
Q

compression of what nerve causes cubital tunnel syndrome

A

Ulnar nerve

145
Q

Features of cubital tunnel syndrome

A
  • tingling and numbness of the 4th and 5th finger
  • weakness and muscle wasting
  • pain worse on leaning on the affected elbow
  • often a history of osteoarthritis or prior trauma to the area
146
Q

Management of cubital tunnel syndrome

A
  • avoid aggravating activity
  • physiotherapy
  • steroid injections
  • surgery in resistant cases
147
Q

What is the most common cause of discitis?

A

staphylococcus aureus

148
Q

complications of discitis

A
  • sepsis
  • epidural abscess
149
Q

Treatment of discitis

A
  • 6 to 8 weeks of IV antibiotics
  • blood culture or CT guided biopsy
  • assess for endocarditis with a transthoracic echo or transoesophageal echo
150
Q

Presentation of discitis

A
  • back pan
  • pyrexia, rigors, sepsis
  • neurological features: changing lower limb neurology if an epidural absecess develops
151
Q

Causes of dupuytrens contracture

A
  • manual labour
  • phenytoin treatment
  • alcoholic liver disease
  • diabetes
  • trauma to the hand
152
Q

Management of dupuytrens contracture

A

Metacarpophalangeal joints cannot be straightened and hand cannot be placed flat on the table

153
Q

Greater trochanteric pain syndrome

A
  • pain over the lateral side of the hip/thigh
  • tenderness on palpation fo the greater trochanter
  • also called trochanteric bursitis
154
Q

Which type of hip dislocation is most common?

A

Posterior

155
Q

Presentation of posterior hip dislocation

A
  • affected leg is shortened, adducted and internally rotated
156
Q

Presentation of anterior hip dislocation

A
  • affected leg is usually abducted and externally roated
  • no leg shortening
157
Q

Management of hip dislocation

A
  • ABCDE
  • analgesia
  • reduction under GA within 4 hours
  • physio
158
Q

Complications of hip dislocation

A
  • sciatic or femoral nerve injury
  • avascular necrosis
  • osteoarthritis
  • recurrent dislocation due to the damage of supporting ligaments
159
Q

Presentation of hip fracture

A

Shortned, externally rotated leg

160
Q

Intracapsular hip fracture

A

from edge of the femoral head to the insertion of the capsule of the hip joint

161
Q

extracapsular hip fracture

A

either trochanteric or subtrochanteric (divided by the lesser trochanter)

162
Q

Classification for hip fracture

A

Garden system

163
Q

Explain the garden system

A
  • type 1: stable fracture with impaction in valgus
  • type 2: complete fracture but undisplaced
  • type 3: displaced fracture, usually rotated and angulated but still has boney contact
  • type 4: complete boney disruption
164
Q

Management of an undisplaced hip fracture

A
  • internal fixation
  • hemiarthroplasty if unfit
165
Q

Management of displaced intracapsular hip fracture

A

arthroplasty (total hip replacement or hemiarthroplasty) to all patient with a desplaced intracapsular hip fracture

166
Q

Which patients with a displaced intracapsular hip fracture should get total hip replacement over a hemiarthroplasty

A
  • able to walk independently out of doors with no more than the use of a stick and
  • are not cognitively impaired and
  • medically fit for anaesthesia and the procedure
167
Q

Management of an extracapsular hip fracture

A
  • if stbale intertrochanteric fractures: dynamic hip screw
  • if reverse oblique, transverse or subtrochanteric: intramedullary device
168
Q

Nerve humeral shaft fracture

A

Radial nerve

169
Q
A

Finals (37 decks)

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