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Medicine Year 2 5 > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What does ESR stand for?

A

Erythrocyte sedimentation rate

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2
Q

Give 2 circumstances where there are false positives of ESR

A
  • ) Age
  • ) Female
  • ) Obesity
  • ) Ethnicity
  • ) Hypercholesterolaemia
  • ) Anaemia
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3
Q

What does CRP stand for?

A

C-reactive protein

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4
Q

Where is CRP released, and in response to what?

A

Liver, IL-6

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5
Q

What type of joint disease is osteoarthritis?

A

Degenerative

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6
Q

Give 2 things osteoarthritis can be secondary to

A
  • ) Obesity
  • ) Occupational factors
  • ) Haemochromatosis
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7
Q

What is the process of osteoarthritis mediated by?

A

Cytokines

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8
Q

What are the main pathological features of osteoarthritis? (2)

A
  • ) Loss of cartilage

- ) Disordered bone repair

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9
Q

Give 4 risk factors for osteoarthritis

A
  • ) Age
  • ) Gender (F more after menopause)
  • ) Genetic predisposition
  • ) Obesity (low grade inflammatory state)
  • ) Occupation (manual labour)
  • ) Local trauma, inflammatory arthritis, abnormal biomechanics
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10
Q

Give 3 main symptoms that differentiate osteoarthritis from rheumatoid arthritis

A
  • ) Stiffness after rest for <30 minutes
  • ) Pain worse on exertion
  • ) Worse pain at end of day
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11
Q

Give 3 commonly affected joints in osteoarthritis

A
  • ) DIP
  • ) Thumb CMP
  • ) Knees
  • ) Hip
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12
Q

Give 3 symptoms of osteoarthritis

A
  • ) Pain and crepitus on movement
  • ) Background ache at rest
  • ) Worse with activity
  • ) Joint tenderness, derangement, bony swelling
  • ) Reduced range of movement
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13
Q

What are the 2 types of nodes in osteoarthritis?

A

Heberden’s - DIP

Bouchard’s - PIP

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14
Q

What do plain radiographs show in OA?

A 
LOSS
Loss of joint space
Osteophytes
Subarticular sclerosis
Subchondral cysts
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15
Q

Give 4 treatment options for OA

A
  • ) Exercise
  • ) Analgesia
  • ) Intra-articular steroid injections
  • ) Heat/cold packs
  • ) Walking aids
  • ) Joint replacement
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16
Q

Where do the majority of septic arthritis cases occur?

A

Knee

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17
Q

Give 3 risk factors for septic arthritis

A
  • ) Pre-existing joint disease (esp. RA)
  • ) DM
  • ) Immunosuppression
  • ) Chronic renal failure
  • ) Recent joint surgery
  • ) Prosthetic joints
  • ) IVDU
  • ) Age >80
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18
Q

What is the main differential diagnosis for septic arthritis?

A

Crystal arthropathies

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19
Q

What is the main investigation for septic arthritis?

A

Urgent joint aspiration for synovial fluid microscopy and culture

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20
Q

What must we do prior to giving antibiotics in septic arthritis?

A

Blood cultures

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21
Q

Give 3 causative organisms for septic arthritis

A
  • ) Staph aureus
  • ) Streptococci
  • ) Neisseria gonococcus
  • ) Gram negative bacilli
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22
Q

What is the treatment for septic arthritis?

A
  • ) Empirical IV antibiotics (flucloxacillin)
  • ) Vancomycin if MRSA risk
  • ) Cefotaxine if gram negative, gonococcus
  • ) Possible washout and debridement
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23
Q

What do we give instead of flucloxacillin if the patient is penicillin allergic?

A

Clindamycin

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24
Q

What is osteomyelitis?

A

Infection and inflammation of the bone and bone marrow

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25
Q

What are the 2 classifications of osteomyelitis?

A
  • ) Acute/chronic suppurative osteomyelitis

- ) Diffuse/focal sclerosing

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26
Q

Give 3 of the most common causative organisms for osteomyelitis

A
  • ) Staph aureus
  • ) Enterobacter species
  • ) Streptococcal species
  • ) H. influenzae
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27
Q

Which infection in osteomyelitis is more common in sickle cell disease?

A

Salmonella

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28
Q

Give 3 risk factors for osteomyelitis

A
  • ) Behavioural factors (risk of trauma)
  • ) Vascular supply
  • ) Pre-existing bone/joint problem
  • ) Immune deficiency
  • ) IVDU
  • ) TB
  • ) Injury
  • ) Surgery
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29
Q

What bones are usually affected in osteomyelitis? (2)

A

Adult - vertebrae and pelvis

Children - long bones

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30
Q

What type of osteomyelitis usually occurs in children?

A

Acute haematogenous osteomyelitis (blood to bone)

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31
Q

What is the pathogenesis of osteomyelitis in children?

A

1) Blood flow slower in metaphysis (shaft)
2) Endothelial basement membranes absent
3) Capillaries lack/have inactive phagocytic cells
4) High blood flow in developing bones (to carry infection)

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32
Q

What type of osteomyelitis usually occurs in adults?

A

Contiguous osteomyelitis (infection to bone)

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33
Q

What is the pathogenesis of osteomyelitis in adults?

A

1) Vertebrae become more vascular with age
2) Bacterial seeding of vertebral endplate more likely
3) Lumbar > thoracic > cervical

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34
Q

Give 2 key histopathological changes that occur in osteomyelitis

A
  • ) Necrotic bone - sequestra

- ) New bone formation - involucrum

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35
Q

Why do sequestra and involucrum occur in osteomyelitis?

A

Interruption of periosteal blood supply due to inflammatory exudate extending through periosteum

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36
Q

Give 2 symptoms of osteomyelitis

A
  • ) Several day onset
  • ) Dull pain at site of OM
  • ) May be aggravated by movement
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37
Q

Give 3 signs of osteomyelitis

A
  • ) Fevers, riggers, sweats, malaise
  • ) Tenderness, warmth, erythema, swelling
  • ) Draining sinus tract
  • ) Deep/large ulcers failing to heal despite several weeks treatment
  • ) Non-healing fractures
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38
Q

What can osteomyelitis also present as?

A

Septic arthritis

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39
Q

Give 3 tests we do to diagnose osteomyelitis

A
  • ) Radiographs and CT
  • ) MRI
  • ) Bloods
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40
Q

What do radiographs and CTs show in osteomyelitis?

A
  • ) Cortical destruction in advanced disease
  • ) Soft tissue swelling
  • ) Sclerosis
  • ) Sequestra
  • ) Periosteal reaction
  • ) Takes 1-2 weeks to show changes
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41
Q

What does an MRI show in osteomyelitis?

A
  • ) Marrow oedema
  • ) Delineates cortical, bone marrow and soft tissue inflammation
  • ) Takes 3-5 days to show cahnges
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42
Q

What is the treatment for osteomyelitis?

A

Prolonged specific antibiotic therapy

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43
Q

What are crystals?

A

Homogenous solids that act to remove excess ions by surface binding

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44
Q

What is a crystal arthropathy?

A

Arthritis caused by crystal deposition in the joint lining

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45
Q

What type of crystals occur in gout?

A

Monosodium urate crystals

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46
Q

What type of crystals occur in pseudogout?

A

Calcium pyrophosphate crystals

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47
Q

Where does the majority of gout present?

A

Metatarsophalangeal joint of big toe

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48
Q

Give 3 things gout attacks may be precipitated by

A
  • ) Trauma
  • ) Surgery
  • ) Starvation
  • ) Infection
  • ) Diuretics
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49
Q

What are long term urate deposits known as?

A

Tophi

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50
Q

What does severe joint inflammation present as?

A

Hot, red, swollen joints

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51
Q

What is uric acid produced from, and what is a key enzyme in this pathway?

A

Purine metabolism, xanthine oxidase

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52
Q

Give 3 causes of under excretion of uric acid

A
  • ) Drugs (aspirin), alcohol
  • ) Renal impairment
  • ) HTN/ anti-HTNs
  • ) Metabolic syndrome
  • ) Diuretics
  • ) Age
  • ) Male
  • ) Post menopause
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53
Q

Give 3 causes of over production of uric acid

A
  • ) Diet (alcohol, meat, fructose)
  • ) Hyperlipidaemia
  • ) Psoriasis
  • ) Chemotherapy
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54
Q

What is the amplification loop hypothesis?

A

The more crystals you have, there more likely you are to get more

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55
Q

Give 2 locations of tophi

A
  • ) Pinna ear cartilage
  • ) Joints
  • ) Tendons
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56
Q

Give 3 associations of diseases with gout

A
  • ) DM
  • ) CVD
  • ) HTN
  • ) Chronic renal failure
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57
Q

What is tophaceous gout?

A

Long term deposition without treatment

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58
Q

What is the main test for gout?

A

Polarised light microscopy of synovial fluid

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59
Q

What does a polarised light microscopy of synovial fluid show in gout?

A

Negatively birefringent urate crystals, needle shaped

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60
Q

What do radiographs show in gout?

A
  • ) Soft tissue swelling early

- ) Well defined punched out erosions in juxta-articular bone later

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61
Q

What is the treatment of gout? (3)

A
  • ) High dose NSAID or colchicine
  • ) Steroids
  • ) Rest and elevate joint
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62
Q

Give 3 lifestyle changes for the prevention of gout

A
  • ) Lose weight
  • ) Avoid prolonged fasts
  • ) Avoid alcohol excess
  • ) Avoid purine-rich meats
  • ) Avoid low dose aspirin
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63
Q

When should we start prophylaxis for gout and what is it?

A
  • ) >1 attack a year, tophi, renal stones
  • ) Allopurinol
  • ) Titrate and increase until plasma urate <0.3mmol/L
  • ) Wait until 3 weeks after acute episode
  • ) Cover with NSAID/colchicine
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64
Q

What is allopurinol?

A

Xanthine oxidase inhibitor

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65
Q

Give 3 risk factors for pseudogout

A
  • ) Hyperparathyroidism
  • ) Haemochromatosis
  • ) Hypophosphataemia
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66
Q

Which joints are affected in pseudogout?

A

Knee > wrist > shoulder > ankle > elbow

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67
Q

What does a polarised light microscopy of synovial fluid show in pseudogout?

A

Weakly positive birefringent crystals, rhomboid shaped

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68
Q

What is pseudogout associated with on an XR?

A

Soft tissue calcium deposition

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69
Q

What is the management of pseudogout?

A
  • ) Cool packs, rest
  • ) Aspiration
  • ) Intra-articular steroids
  • ) NSAIDs (+PPI) +/- colchicine may prevent acute attacks
  • ) Methotrexate and hydroxychloroquine for chronic
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70
Q

What should we check for if the pseudogout is early onset (<55), polyarticular, or frequent?

A

Metabolic disease

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71
Q

What is osteoporosis?

A

Reduced bone mass and micro-architectural deterioration in bone tissue

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72
Q

What can occur if trabecular bone is affected in osteoporosis?

A

Crushing fractures of vertebrae

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73
Q

What can occur if cortical bone is affected in osteoporosis?

A

Long bone fractures more likely (femoral neck)

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74
Q

Does osteoporosis occur more in men or women >50, and why?

A

Women, lose trabecular with age

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75
Q

Give 3 risk factors for primary osteoporosis

A
  • ) Parental history
  • ) Alcohol
  • ) RA
  • ) Low BMI
  • ) Prolonged immobility
  • ) Untreated menopause
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76
Q

Give 9 other risk factors for osteoporosis (acronym)

A 
SHATTERED
Steroid use
Hyperthyroidism, hyperparathyroidism, hypercalciuria
Alcohol and tobacco
Thin (low BMI <18.5)
Testosterone decreased
Early menopause
Renal/liver failure
Erosive/inflammatory bone disease (RA)
Dietary calcium low, DM
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77
Q

What % of women will have a fracture due to osteoporosis in their lifetime?

A

50%

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78
Q

What is the Eular buckling theory? (osteoporosis)

A

Connections between horizontal trabeculae decrease, therefore decrease in overall strength

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79
Q

What are the 2 tests for osteoporosis?

A

XR, DEXA

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80
Q

What does DEXA stand for?

A

Dual energy XR absorptiometry

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81
Q

Where do we scan with DEXA?

A

Hip

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82
Q

What is the T-score in a DEXA scan?

A

The number of standard deviations the bone mineral density is from the young healthy adult average (25)

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83
Q

What does each decrease of 1SD in bone mineral density give?

A

2.6 times increased risk of hip fracture

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84
Q

What do the T-scores mean in osteoporosis? (5)

A
  • ) >0, better than normal
  • ) 0 to -1, normal
  • ) -1 to -2.5, osteopenia
  • ) >-2.5, osteoporosis
  • ) >-2.5 plus fracture, severe osteoporosis
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85
Q

What is a risk assessment tool for estimating 10 year risk of osteoporotic fracture in untreated patients?

A

FRAX

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86
Q

Give 3 lifestyle changes to make in osteoporosis

A
  • ) Quit smoking
  • ) Reduce alcohol
  • ) Weight bearing exercise
  • ) Balance exercises
  • ) Cacium and vitamin D diet
  • ) Home based fall prevention
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87
Q

How should a patient take bisphosphonates?

A

Plenty of water, upright for >30 minutes, wait 30 mins before eating/other drugs

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88
Q

What is denosumab and when should it be given?

A

Monoclonal antibody to RANK ligand, given SC twice yearly, has fast offset

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89
Q

What does RANK stand for?

A

Receptor Activator of Nuclear factor-Kappa B

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90
Q

What does anti-resorptive treatment do in osteoporosis?

A

Decreases osteoclast activity and bone turnover (allows osteoblasts to catch up)

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91
Q

What does anabolic treatment do in osteoporosis?

A

Increases osteoblast activity and bone formation

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92
Q

Give 3 examples of anti-resorptive treatment in osteoporosis (5)

A
  • ) Bisphosphonates - alendronic acid
  • ) Strontium ranelate - only in severe intolerance and without CVD
  • ) HRT
  • ) Raloxifene - selective osterogen receptor modulator
  • ) Denosumab
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93
Q

Give an example of anabolic treatment in osteoporosis

A

Teriparatide - recombinant PTH

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94
Q

Give 3 differences between osteomalacia and osteoporosis

A
  • ) OM serum calcium low, OP no biochemical changes
  • ) OM has decreased mineralisation of bone, OP no defect in mineralisation
  • ) OM ache and weakness, OP no symptoms
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95
Q

What is Raynaud’s syndrome?

A

Peripheral digital ischaemia due to paroxysmal vasospasm

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96
Q

What is Raynaud’s syndrome precipitated by?

A

Cold, emotion

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97
Q

What occurs to the fingers or toes in Raynaud’s syndrome? (4)

A
  • ) Ache and change colour
  • ) Pale (ischamia)
  • ) Blue (deoxygenation)
  • ) Red (reactive hyperaemia)
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98
Q

What is idiopathic Raynaud’s syndrome?

A

Raynaud’s disease

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99
Q

What is Raynaud’s syndrome with an underlying cause?

A

Raynaud’s phenomenon

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100
Q

Give 3 conditions in which Raynaud’s phenomenon may be exhibited

A
  • ) Systemic sclerosis
  • ) SLE
  • ) RA
  • ) Occupational, vibrating tools
  • ) Obstructive conditions
  • ) Thrombocytosis
  • ) Beta-blockers
  • ) Hypothyroidism
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101
Q

What is the treatment for Raynaud’s?

A
  • ) Keep warm
  • ) Stop smoking
  • ) Nifedipine
  • ) Possible sympathectomy (sympathetic nerve trunk resection)
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102
Q

What is fibromyalgia?

A

Syndrome with symptoms of fatigue and widespread pain

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103
Q

Give 4 risk factors for fibromyalgia

A
  • ) Female
  • ) Middle age
  • ) Low income
  • ) Divorced
  • ) Low educational status
  • ) Problems at work/family
  • ) Anxiety
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104
Q

Give 4 psychosocial risk factor yellow flags for developing persisting chronic pain and long term disability

A
  • ) Belief that pain and activity are harmful
  • ) Sickness behaviours such as extended rest
  • ) Social withdrawal
  • ) Emotional problems such as low mood, anxiety, stress
  • ) Problems/dissatisfaction at work
  • ) Problems with claims for compensation/time off work
  • ) Overprotective family/lack of support
  • ) Inappropriate expectations of treatment
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105
Q

Give 3 conditions fibromyalgia is associated with

A
  • ) Chronic fatigue syndrome
  • ) IBS
  • ) Chronic headaches
  • ) RA
  • ) AS
  • ) SLE
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106
Q

Give 3 diagnostic features of fibromyalgia

A
  • ) Chronic pain >3 months
  • ) Widespread pain (L, R, above, below was it, axial skeleton)
  • ) Profound fatigue
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107
Q

Give 3 additional features of fibromyalgia

A
  • ) Morning stiffness
  • ) Paraesthesiae
  • ) Headaches
  • ) Poor concentration
  • ) Low mood
  • ) Sleep disturbance
  • ) Widespread and severe tender points
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108
Q

What is the treatment of fibromyalgia?

A
  • ) Remain active
  • ) Keep working
  • ) Exclude alternative diagnosis
  • ) Exercise
  • ) Pacing of activity
  • ) Relaxation
  • ) Rehabilitation
  • ) Physiotherapy
  • ) CBT for coping strategies and achievable goals
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109
Q

What medications can we give in fibromyalgia?

A
  • ) Low dose amitriptyline - pain and sleep

- ) Duloxetine or SSRI - anxiety and depression

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110
Q

What is vasculitis?

A

Inflammatory disorder of blood vessel walls

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111
Q

Give 3 things vasculitis can be secondary to

A
  • ) SLE
  • ) RA
  • ) Hepatitis B, C
  • ) HIV
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112
Q

How is vasculitis categorised?

A

By the size of the vessel affected

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113
Q

What does vasculitis cause?

A

Destruction (aneurysm/rupture) or stenosis

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114
Q

Give 2 examples of each of large and medium vasculitis

A

Large - giant cell arteritis, Takayasu’s arteritis

Medium - polyarteritis nodosa, Kawasaki disease

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115
Q

Give 4 examples of small vessel vasculitis

A 
ANCA associated:
-) Microscopic polyangiitis
-) Granulomatosis with polyangiitis
ANCA negative:
-) Goodpasture's disease
-) IgA vasculitis
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116
Q

What is the main symptom of vasculitis?

A

Overwhelming fatigue with increased ESR/CRP

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117
Q

Give 10 symptoms of vasculitis (think systems)

A

-) Systemic - fever, malaise, weight loss, etc
-) Skin - purpura, ulcers etc
-) Eyes - episcleritis
-) ENT - epistaxis, stridor
-) Pulmonary - haemoptysis and dyspnoea
-) Cardiac - angina, MI, HF
-) GI - pain, perforation
-) Renal - HTN, renal failure
-) Neuro - stroke, fits, confusion
-) GU - testicular pain
NOT EXHAUSTIVE LIST

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118
Q

What does ANCA stand for?

A

Anti-neutrophil cytoplasmic antibodies

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119
Q

What is c-ANCA?

A

Cytoplasmic ANCA

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120
Q

What is p-ANCA?

A

Perinuclear ANCA

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121
Q

What test do we do to diagnose vasculitis?

A

Angiography +/- biopsy

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122
Q

How do we treat vasculitis?

A

Large - steroids

Medium/small - immunosuppression with steroids +/- cyclophosphamide or methotrexate/azathioprine

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123
Q

What is giant cell arteritis also known as?

A

Temportal arteritis

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124
Q

What is giant cell arteritis associated with in 50%?

A

Polymyalgia rheumatic

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125
Q

What type of arteritis is giant cell?

A

Granulomatous

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126
Q

Give 4 symptoms for giant cell arteritis

A
  • ) Headache
  • ) Temporal artery and scalp tenderness
  • ) Tongue/jaw claudication
  • ) Amaurosis fungax/sudden unilateral blindness
  • ) Dyspnoea, weight loss, morning stiffness, unequal/weak pulses
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127
Q

What do blood tests show in giant cell arteritis?

A
  • ) Very increased ESR and CRP
  • ) Increased platelets
  • ) Increased ALP
  • ) Decreased Hb
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128
Q

Is giant cell arteritis ANCA positive or negative?

A

Negative

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129
Q

What is the gold standard of diagnosis in giant cell arteritis?

A

Temporal artery, be aware of skip lesions

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130
Q

What is the treatment of giant cell arteritis? (4)

A
  • ) Immediate prednisolone/IV methylprednisolone
  • ) Reduce when symptoms resolve and ESR down
  • ) Balance risks of long term steroid treatment
  • ) PPI, bisphosphonate, calcium with colecalciferol
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131
Q

What is polyarteritis nodosa? (PAN)

A

Necrotising vasculitis that causes aneurysms and thrombosis in medium sized arteries

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132
Q

What does PAN lead to?

A

Infarction in the affected organs with severe systemic symptoms

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133
Q

What gender is giant cell arteritis more common in?

A

Females

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134
Q

What gender is PAN more common in?

A

Males

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135
Q

Give 3 symptoms of PAN

A
  • ) Systemic features

- ) Skin, renal, cardiac, GI, GU, neuro problems

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136
Q

Is PAN ANCA positive or negative?

A

Negative

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137
Q

What tests are diagnostic for PAN?

A
  • ) Renal/mesenteric angiography

- ) Renal biopsy

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138
Q

What is the treatment for PAN?

A
  • ) Control BP
  • ) Steroids for mild
  • ) Steroid sparing agent for severe
139
Q

What is PAN associated with?

A

Hep B

140
Q

What is polymyalgia rheumatic?

A

Not a true vasculitis, frequently occurs with GCA

141
Q

How does polymyalgia rheumatic present?

A

Subacute onset of bilateral aching, tenderness, morning stiffness in shoulders and proximal limb muscles

142
Q

What are other symptoms of polymyalgia rheumatic?

A
  • ) Mild polyarthritis
  • ) Tenosynovitis
  • ) Carpal tunnel syndrome
  • ) Systemic features
143
Q

What is the treatment for polymyalgia rheumatic?

A

Prednisolone with gastric and bone protection

144
Q

What is granulomatosis with polyangiitis also known as?

A

Wegener’s granulomatosis

145
Q

What is granulomatosis with polyangiitis?

A

Necrotising granulomatous vasculitis of arterioles, capillaries and post capillary venues

146
Q

What is granulomatosis with polyangiitis associated with?

A

Anti-neutophil cytoplasmic antibodies (c-ANCA)

147
Q

What is the classic triad that granulomatosis with polyangiitis affects?

A

Upper respiratory tract, lungs, kidney

148
Q

What are the skin signs of granulomatosis with polyangiitis?

A

Red spots on legs and feet

149
Q

What is the treatment for granulomatosis with polyangiitis?

A
  • ) Corticosteroids and cyclophosphamide (or rituximab) for remission
  • ) Azathioprine and methotrexate for maintenance
  • ) Possible plasma exchange
  • ) Co-trimoxazole as prophylaxis
150
Q

Give 5 red flags for back pain

A
  • ) Aged <20 or >55
  • ) Acute onset in elderly
  • ) Constant/progressive/nocturnal pain
  • ) Worse pain when supine
  • ) Fever, night sweats, weight loss
  • ) History of malignancy, abdominal mass
  • ) Thoracic back pain
  • ) Morning stiffness
  • ) Bilateral/alternating leg pain, leg claudication, exercise related leg pain
  • ) Neuro, sphincter disturbance
  • ) Current/recent infection
  • ) Immunosuppression
151
Q

If someone was lifting something heavy, and they describe a ‘popping’ sensation in their back, this is what?

A

A slipped disc

152
Q

What are the most likely causes of back pain according to age? (15-30)

A
  • ) Prolapsed disc
  • ) Trauma
  • ) Fractures
  • ) Ankylosing spondylitis
  • ) Pregnancy
153
Q

What are the most likely causes of back pain according to age? (30-50)

A
  • ) Degenerative spinal disease
  • ) Prolapsed disc
  • ) Malignancy
154
Q

What are the most likely causes of back pain according to age? (>50)

A
  • ) Degererative
  • ) Osteoporotic vertebral colapse
  • ) Paget’s disease
  • ) Malignancy
  • ) Myeloma
  • ) Spinal stenosis
155
Q

Give 2 rarer causes of back pain

A
  • ) Cauda equina tumours
  • ) Psoas abscess
  • ) Spinal infection
156
Q

What is the best imaging tool for back pain, and what can it detect?

A

MRI, can detect disc prolapse, cord compression, cancer, infection, inflammation

157
Q

What is the treatment for back pain?

A
  • ) Stay active
  • ) Paracetamol +/- NSAIDs +/- codeine
  • ) Consider low dose amitriptyline if these fail
  • ) Physiotherapy, acupuncture, exercise programme
  • ) Psychosocial issues
158
Q

What are the spondyloarthropathies? (SpA)

A

Group of related chronic inflammatory conditions

159
Q

Give the 7 shared clinical features of SpA

A

1) Seronegativity (RF -ve)
2) HLA B27 association
3) Axial arthritis - pathology in spine and sacroiliacs
4) Asymmetrical arge joint oligo/monoarthritis
5) Enthesitis - inflammation of site of insertion of tendon/ligament into bone
6) Dactylitis - inflammation of entire digit
7) Extra-articular - iritis, psoriaform past, oral ulcers, IBD, aortic valve incompetence

160
Q

What are the features of SpA? (acronym)

A 
SPINEACHE
Sausage digit (dactylitis)
Psoriasis
Inflammatory back pain
NSAID good response
Enthesitis (heel)
Arthritis
Crohn's/colitis/elevated CRP
HLA B27
Eye (uveitis)
161
Q

What is ankylosing spondylitis? (AS)

A

Chronic inflammatory disease of spine and sacroiliac joints

162
Q

In which gender is AS more common?

A

Men

163
Q

What is the typical patient in AS?

A

<30 man with gradual onset of low back pain that is worse at night with spinal morning stiffness relieved by exercise

164
Q

Where does the pain radiate from/to in AS?

A

Pain radiates from sacroiliac joints to hips/buttocks, usually improves towards end of day

165
Q

What is AS associated with? (3)

A

Osteoporosis, aortic valve incompetence, pulmonary apical fibrosis

166
Q

Give 3 other symptoms of AS

A
  • ) Progressive loss of spinal movement
  • ) Enthesitis in achilles tendonitis, plantar fasciitis
  • ) Anterior mechanical chest pain
  • ) Fatigue
167
Q

What are the pathological steps of bamboo spine in AS?

A

1) Bony proliferations due to enthesitis between ligaments and vertebra (vertebral syndesmophytes)
2) These fuse with vertebral body above, causing ankylosis
3) Calcification of ligaments with ankylosis leads to bamboo spine

168
Q

What is the delayed damage theory in AS?

A

The sequence of structural damage is

1) Inflammation
2) Erosive damage repair
3) New bone formation

169
Q

What does an MRI show in AS?

A
  • ) Detection of active inflammation (bone marrow oedema)
  • ) Erosions
  • ) Sclerosis
  • ) Ankylosis
170
Q

What does an XR show in AS?

A
  • ) SI joint space narrowing/widening
  • ) Sclerosis
  • ) Erosions
  • ) Ankylosis/fusion
171
Q

What is the treatment for AS?

A
  • ) Exercise
  • ) NSAIDs
  • ) TNF alpha blockers
  • ) Local steroid injections for pain
  • ) Surgery - replacement
  • ) Bisphosphonates
172
Q

Give an example of a TNF alpha blocer

A

Etanercept, adalimumab

173
Q

What is psoriatic arthritis?

A

Can occur with psoriasis and present before skin changes

174
Q

What are the 5 patterns psoriatic arthritis can present with?

A

1) Symmetrical polyarthritis (like RA)
2) DIP joints only
3) Asymmetrical oligoarthritis
4) Spinal (similar to AS)
- ) Psoriatic arthritis mutilans (rare, severe)

175
Q

What radiological changes are seen in psoriatic arthritis?

A

Erosive changes, ‘pencil in cup’ deformity

176
Q

Give 3 features of psoriatic arthritis

A
  • ) Nail changes
  • ) Synovitis (dactylitis)
  • ) Acneiform rashes
  • ) Palmo-plantar pustulosis
177
Q

What is the management of psoriatic arthritis?

A
  • ) NSAIDs
  • ) Suldasalazine
  • ) Methotrexate
  • ) Anti TNF agents
  • ) Possible IL 12/23 blockers
178
Q

What does DMARD stand for?

A

Disease modifying anti rheumatic drugs

179
Q

What is reactive arthritis?

A

A condition in which arthritis and other clinical manifestations occur as an autoimmune response to infection elsewhere in the body (may have resolved)

180
Q

What infections does reactive arthritis occur after?

A
  • ) Urethritis (chlamydia/ureaplasma)

- ) Dysentery (campylobacter/salmonella)

181
Q

Give 3 symptoms of reactive arthritis

A
  • ) Iritis
  • ) Keratoderma blenorrhagica (brown raised plaques on soles and palms)
  • ) Mouth ulcers
  • ) Circinate balanitis (penile ulceration)
  • ) Enthesitis
182
Q

What is Reiter’s syndrome?

A

Triad of urethritis, arthritis, conjunctivitis

183
Q

What does an XR in reactive arthritis show?

A

Enthesitis with periosteal reaction

184
Q

What is the management of reactive arthritis?

A
  • ) Splnit affected joints
  • ) NSAIDs/local steroid injections
  • ) Sulfasalazine or methotrexate if >6 months
185
Q

What is enteropathic/enteric arthritis associated with?

A

IBC, GI bypass, coeliac and Whipple’s disease

186
Q

How do we treat enteropathic arthritis?

A

Treatment of bowel symptoms, DMARDs

187
Q

What is rheumatoid arthritis?

A

A chronic systemic inflammatory disease characterised by a symmetrical, deforming, peripheral polyarthris

188
Q

What does RA increase the risk of?

A

CVD

189
Q

What is the typical presentation of RA?

A

Symmetrical, swollen, painful and stiff small joints of hands and feet

190
Q

What are the 3 types of bone loss in RA?

A
  • ) Focal erosion
  • ) Periarticular osteoporosis
  • ) Generalised osteoporosis in skeleton
191
Q

Is the prevalence of RA increased or decreased in smokers?

A

Increased

192
Q

What is RA linked to? (genetically)

A

HLA DR4/DR1

193
Q

How long does stiffness last in RA?

A

> 60 minutes

194
Q

Is RA better or worse with use?

A

Better

195
Q

Give 3 less common presentations of RA

A
  • ) Sudden onset, widespread arthritis
  • ) Recurrent mono/polyarthritis of joints
  • ) Persistant monoarthritis
  • ) Systemic illness with extra articular symptoms
  • ) Polymyalgic onset
  • ) Recurrent soft tissue problems
196
Q

Give 2 signs of early RA

A
  • ) Inflammation
  • ) Swollen MCP, PIP, wrist, MTP (often symmetrical)
  • ) Tenosynovitis/bursitis
197
Q

Give 2 signs of late RA

A
  • ) Joint damage, deformities
  • ) Ulnar deviation
  • ) Subluxation of wrist and fingers
  • ) Boutonniere and swan neck of fingers
  • ) Z-deformity of thumbs
  • ) Hand extensor tendon rupture
198
Q

Give 4 extra-articular manifestations of RA

A

-) Nodules (elbows, lungs, etc)
-) Lungs (pleural disease, interstitial fibrosis etc)
-) Cardiac (IHD, pericarditis, pericardial effusion etc)
-) Eye (episcleritis, scleritis etc)
-) Osteoporosis
NOT COMPREHENSIVE

199
Q

What is Felty’s syndrome?

A

RA and splenomegaly and neutropenia

200
Q

What 2 things are usually positive in RA?

A

RF and anti CCP (very specific)

201
Q

What does anti CCP stand for?

A

Anticyclic citrullinated peptide antibodies

202
Q

What does an XR show in RA?

A

Soft tissue swelling, juxta-articular osteopenia, decreased joint space

203
Q

What are better at identifying synovitis and bone erosions than XRs in RA?

A

MRI and US

204
Q

What 4 things can be found with a blood test in RA?

A
  • ) Anaemia of chronic disease
  • ) Increased platelets
  • ) Increased ESR
  • ) Increased CRP
205
Q

What is the management of RA?

A
  • ) Treat to target
  • ) DMARDs and biological agents
  • ) Steroids
  • ) NSAIDs
  • ) Physio and occupational therapy
  • ) Surgery
  • ) Manage risk factors (CVD and cerebrovascular disease)
206
Q

Give 2 examples of a biological DMARD used for RA

A
  • ) TNF alpha blocker
  • ) IL-1 receptor blocker (anakinra)
  • ) Rituximab (lysis of B cells)
  • ) Tocilizumab (IL-6 receptor antibody)
  • ) Abatacept (T cell function disruption)
207
Q

Give 2 examples of a non-biological DMARD used for RA

A
  • ) Sulfasalazine
  • ) Methotrexate (CI pregnancy)
  • ) Leflunomide
208
Q

Give 4 autoimmune connective tissue disorders

A
  • ) SLE
  • ) Systemic sclerosis
  • ) Sjogren’s syndrome
  • ) Polymyositis
  • ) Dermatomyositis
209
Q

What is Sjogren’s syndrome?

A

A chronic inflammatory autoimmune disorder

210
Q

What is the pathology in Sjogren’s?

A

Lymphocytic infiltration and fibrosis of exocrine glands (especially lacrimal/salivary)

211
Q

Give 3 clinical features of Sjogren’s

A
  • ) Decreased tear production
  • ) Decreased salivation
  • ) Parotid swelling
212
Q

Give 3 other features of Sjogren’s

A

-) Vaginal dryness
-) Dyspareunia (painful sex)
-) Dry cough
-) Dysphagia
-) Polyarthritis
-) Raynaud’s
-) Lymphadenopathy
-) Vasculitis
-) Fatigue
-) Peripheral neuropathy
ETC

213
Q

Give 2 things decreased tear production in Sjogren’s causes

A
  • ) Dry eyes

- ) Keratoconjunctivitis sicca

214
Q

How do we measure conjunctival dryness in Sjogren’s?

A

Schirmer’s test - <5mm in 5mins is positive

215
Q

What 4 things may be present in blood tests in Sjogren’s?

A
  • ) Anti Ro antibody
  • ) Anti La antibody
  • ) RF
  • ) ANA
216
Q

What does a biopsy show in Sjogren’s?

A

Focal lymphocytic aggregation

217
Q

What does Rose Bengal staining show in Sjogren’s?

A

Keratitis

218
Q

How do we treat Sjogren’s?

A
  • ) Treat sicca (artificial tears, frequent drinks)
  • ) NSAIDs and hydroxycholoroquine for arthralgia
  • ) Immunosuppressants for severe
219
Q

What 3 things does systemic sclerosis feature?

A
  • ) Scleroderma (skin fibrosis)
  • ) Internal organ fibrosis
  • ) Microvascular abnormalities
220
Q

What was limited systemic sclerosis formally known as?

A

CREST syndrome

221
Q

What is limited systemic sclerosis associated with?

A

Anticentromere antibodies (75%)

222
Q

What parts of the body does limited systemic sclerosis involve?

A

Face, hands, feet

223
Q

Give 5 features of limited systemic sclerosis

A
  • ) Calcinosis of subcutaneous tissues
  • ) Raynaud’s syndrome
  • ) Oesophageal and gut dysmotility
  • ) Sclerodactyly (digit inflammation)
  • ) Telangiectasia (spider veins)
224
Q

What do we treat pulmonary HTN with in limited systemic sclerosis? (2)

A

Sildenafil, bosentan

225
Q

What parts of the body does diffuse systemic sclerosis involve?

A

Whole body

226
Q

What are 2 antibodies found in diffuse systemic sclerosis?

A
  • ) Antitopoisomerase-1 (SCL-70, 40%)

- ) Anti-RNA polymerase (20%)

227
Q

What 4 systems are potentially fibrosed in systemic sclerosis?

A

Lung, cardiac, GI, renal

228
Q

What is the treatment for systemic sclerosis?

A
  • ) Immunosuppression (cyclophosphamide)
  • ) Monitor BP and renal function
  • ) ACEI/ARBs (+PPIs)
  • ) Treat Raynaud’s
  • ) Annual echocardiograms and spirometry
229
Q

What can antiphospholipid syndrome cause? (4)

A 
CLOTs
Coagulation defect
Livedo reticularis
Obstetric problems
Thrombocytopaenia
230
Q

How do we treat antiphospholipid syndrome?

A

Aspirin/warfarin if recurrent

231
Q

What are polymyositis and dermatomyositis?

A

Rare conditions characterised by the insidious onset of progressive symmetrical proximal muscle weakness and autoimmune mediate striated muscle inflammation (myositis)

232
Q

What are poly/dermatomyositis associated with?

A

Myalgia +/- arthralgia

233
Q

What may muscle weakness cause in poly/dermatomyositis?

A
  • ) Dysphagia
  • ) Dysphonia
  • ) Respiratory weakness
234
Q

Dermatomyositis features myositis plus what 3 skin signs

A
  • ) Macular rash
  • ) Lilac-purple (heliotrope) rash on eyelids
  • ) Mailfold erythema
  • ) Gottron’s papules (red papules over knickers)
235
Q

What do we need to screen for in poly/dermatomyositis?

A

Cancers

236
Q

Give 3 extra-muscular signs of poly/dermatomyositis

A
  • ) Fever
  • ) Arthralgia
  • ) Raynaud’s
  • ) Interstitial lung fibrosis
  • ) Myocardial involvement
237
Q

Give 2 antibodies associated with poly/dermatomyositis

A

Anti-Mi2, anti-Jo1

238
Q

What do we test for in poly/dermatomyositis? (4)

A
  • ) Increased muscle enzymes
  • ) EMG shows characteristic fibrillation potentials
  • ) Muscle biopsy
  • ) MRI shows muscle oedema in acute myositis
239
Q

Give 4 muscle enzymes

A
  • ) ALT (alanine transaminase)
  • ) AST (aspartate transaminase)
  • ) LDH (lactate dehydrogenase)
  • ) CK (creatinine kinase)
  • ) Aldolase
240
Q

What is the treatment for poly/dermatomyositis?

A
  • ) Prednisolone
  • ) Immunosuppressives and cytotoxic if resistance
  • ) Hydroxychloroquine/topical tacrolimus for skin disease
241
Q

What is systemic lupus erythematous? (SLE)

A

Mutisystemic autoimmnue disease

242
Q

What are the pathogenic steps of SLE? (4)

A
  • ) Autoantibodies made against variety of autoantigens
  • ) Form immune complexes
  • ) Inadequate clearance of immune complexes
  • ) Host of immune responses which cause tissue inflammation and damage
243
Q

Which gender is SLE more common in?

A

Women

244
Q

Which ethnicities is SLE more common in?

A

Afro-Caribbean, Asia

245
Q

What 3 genetic associations are there in SLE?

A

HLA B8
HLA DR2
HLA DR3

246
Q

Give 3 non-specific symptoms of SLE

A
  • ) Malaise
  • ) Fatigue
  • ) Myalgia
  • ) Fever
247
Q

What type of presentation does SLE have?

A

Remitting and relapsing illness of variable presentation and course

248
Q

Give 5 clinical criteria of SLE

A
  • ) Acute cutaneous lupus (malaria rash/butterfly, photosensitive rash)
  • ) Chronic cutaneous lupus (discoid rash)
  • ) Non scarring alopecia
  • ) Oral/nasal ulcers
  • ) Synovitis (2 or more joints)
  • ) Serositis (lung/pericardial pain)
  • ) Urinanalysis (proteinuria)
  • ) Neuro features (seizures, psychosis)
  • ) Haemolytic anaemia
  • ) Leucopenia
  • ) Thrombocytopenia
249
Q

Give 3 other features of SLE

A
  • ) Lymphadenopathy
  • ) Weight loss
  • ) Alopecia
  • ) Nail fold infarcts
  • ) Raynaud’s
  • ) Non infective endocarditis
  • ) Stroke
  • ) Retinate exudates
250
Q

Give 3 laboratory criteria for SLE

A
  • ) +ve ANA
  • ) Anti-dsDNA
  • ) Anti-Smith antibodies
  • ) Antiphospholipid Abs
  • ) Low complement (C3, C4)
  • ) +ve Direct Coombs
251
Q

What are ESR and CRP like in SLE?

A

High ESR, normal CRP

252
Q

Give 3 causes of drug induced lupus

A
  • ) Isoniazid
  • ) Hydralazine
  • ) Quinidine
  • ) Anti-TNF agents
253
Q

What is the general treatment for SLE?

A
  • ) Sunblock
  • ) Hydroxychloroquine
  • ) Screen for co-morbidities
  • ) Topical steroids for skin flares
254
Q

How do we maintain SLE? (3)

A
  • ) NSAIDs and hydroxychloroquine for joint and skin
  • ) Azathioprine, methotrexate, mycophendlate as steroid-sparing agents
  • ) Belimumab for autoantibody positive disease
255
Q

What do we give for moderate flares in SLE?

A

DMARDs or mycophenolate

256
Q

What do we give for severe flares in SLE? (4)

A
  • ) Urgent high dose steroids
  • ) Mycophenolate
  • ) Rituximab
  • ) Cyclophosphamide
257
Q

What do we give for lupus nephritis?

A
  • ) Intensive immunosuppression with steroids and cyclophosphamide
  • ) BP control vital
  • ) Possible renal replacement therapy
258
Q

What is the most common causative organism of infections?

A

Coagulase negative staph, then staph aureus

259
Q

Give 3 mechanisms of infection

A
  • ) Transient bacteraemia (e.g. from gut)
  • ) Pets and wounds
  • ) Dental work, already coloniser
  • ) Index surgery infection
260
Q

What is propionibacteria?

A

A skin commensal involvement in upper limb (real) and lower limb (contaminant) infections

261
Q

Give 3 risk factors for a joint prosthesis infection

A
  • ) Male sex
  • ) Hybrid fixation
  • ) Cement without antibiotics
  • ) Inflammatory disease
  • ) Hip fracture
  • ) Femoral head necrosis
262
Q

What infection is extra bone formation associated with?

A

Staph infection

263
Q

Give 3 treatment options for infection of a joint prosthesis

A
  • ) Antibiotic suppression
  • ) Debridement and retention of prosthesis
  • ) Excision/exchange arthroplasty
  • ) One/two stage exchange
  • ) Amputation
264
Q

What can we do to make the likelihood of detecting an infection when using CRP and ESR?

A

Multiple sasmples

265
Q

What is the gold standard for the diagnosis of a joint infection?

A

Aspiration

266
Q

What is the limitation to aspiration when detecting an infection?

A

Cannot do if patient has had antibiotics in last 2 weeks

267
Q

What inflammatory marker has a sensitivity/specificity of 95% for a joint infection?

A

Alpha defensin

268
Q

What does gonococcal arthritis occur with?

A

Disseminated gonococcal infection

269
Q

Give 3 features of gonococcal arthritis presentation

A
  • ) Fever
  • ) Arthritis
  • ) Tenosynovitis
  • ) Polyarticular
  • ) Maculopapular pustular rash common in peripheries (palms, sole, painful before visible)
270
Q

How do we detect the organism in gonococcal arthritis?

A

Mucosal swabs and blood cultures

271
Q

What is a sunburst appearance on an XR indicative of? (2)

A

Osteosarcoma, Ewing’s

272
Q

What is a onion skin appearance on an XR indicative of?

A

Ewing’s

273
Q

What is the appearance of Codman’s triangle on an XR indicative of? (5)

A

Osteosarcoma, Ewing’s, OM, GCT, metastasis

274
Q

What 3 things can a bone scan tell us?

A
  • ) How fast blood is flowing to lesion
  • ) Inflammation
  • ) Uptake within bone (turnover rate)
275
Q

What 4 imaging tools can we use to detect a bone tumour?

A

US, CT, MRI, XR

276
Q

What system do we use to stage malignant and benign bone tumours?

A

Enneking

277
Q

What are the 3 grades for a malignant tumour?

A

G0 - histologically benign, well differentiated, low mitotic count
G1 - low grade malignant, moderate diff, local spread only, few mitoses
G2 - high grade malignant, poorly diff, frequent mitoses, high risk of mets

278
Q

What are the 3 grades for a benign tumour?

A

Grade 1 - latent, well defined, stops growing, may heal
Grade 2 - active, growth limited by natural barriers, may expand
Grade 3 - aggressive, not limited by natural barriers, mets present in 5%, high recurrence

279
Q

What does the prefix ‘osteo’ relate to?

A

Bone

280
Q

What does the prefix ‘chondro’ relate to?

A

Cartilage

281
Q

What does the prefix ‘rhabdomyo’ relate to?

A

Skeletal muslce

282
Q

What does the prefix ‘lipo’ relate to?

A

Fat

283
Q

What does the suffix ‘oma’ relate to?

A

Benign tumour

284
Q

What does the suffix ‘sarcoma’ relate to?

A

Malignant connective tissue tumour

285
Q

What does the suffix ‘carcinoma’ relate to?

A

Malignant epithelial/endothelial tumour

286
Q

What does the suffix ‘blastoma’ relate to?

A

Malignant tumour of embryonic cells

287
Q

What does a pleomorphic soft tissue sarcoma mean?

A

It doesn’t have a clear tissue of origin

288
Q

Give 4 things we describe when looking at an XR with a suspected tumour

A
  • ) Radiographic view, anatomical location
  • ) Epi/meta/diaphysis
  • ) Bone/cartilage forming
  • ) Bone destruction/reaction
  • ) Zone of transition
  • ) Benign/malignant
289
Q

What mutation is osteosarcoma associated with?

A

p53

290
Q

What do XRs show in osteosarcoma?

A

Bone formation with bone destruction

291
Q

What is the most common type of osteosarcoma?

A

High grade intramedullary osteosarcoma

292
Q

What is the treatment for osteosarcoma?

A

Multi-agent chemo pre-op

293
Q

Give 3 different types of osteosarcoma

A
  • ) Intramedullary
  • ) Parosteal
  • ) Periosteal
  • ) Telangiectatic
294
Q

What does Ewing’s sarcoma arise from?

A

Neural crest cells (neuroectodermal origin)

295
Q

What is the genetic element of Ewing’s sarcoma?

A

Balanced translocation t(11,22)

296
Q

What type of lesion occurs in Ewing’s sarcoma?

A

Diaphyseal, destructive lytic lesion

297
Q

How do we diagnose Ewing’s sarcoma?

A

Bone marrow biopsy (carefully!)

298
Q

How do we treat Ewing’s sarcoma?

A

Chemo, radio, excision/reconstruction

299
Q

How does multiple myeloma present? (3)

A
  • ) Bone pain
  • ) Pathological fractures
  • ) Fatigue (anaemia)
300
Q

What proteins are seen in the urine in multiple myeloma?

A

Bence-Jones proteins

301
Q

What does an XR show in multiple myeloma?

A

Punched out lytic lesions (pepper pot skull)

302
Q

What does blood serum electrophoresis show in multiple myeloma?

A

Monoclonal bands

303
Q

What is the treatment for multiple myeloma?

A

Surgical stabilisation and radiotherapy

304
Q

What does histology show in multiple myeloma?

A

Plasma cells and perinuclear halo

305
Q

What is a soft tissue sarcoma?

A

Malignant tumour of connective tissue

306
Q

Give 4 factors where we would consider masses to be malignant in soft tissue sarcoma

A
  • ) >5cm
  • ) Deep to fascia
  • ) Enlarging in size
  • ) Painful
307
Q

What 5 tumours most commonly metastasise to bone?

A
  • ) Breast
  • ) Lung
  • ) Prostate
  • ) Kidney
  • ) Thyoid
308
Q

How is RANK-L involved in bone resorption?

A

Activation of osteoclasts by tumour cells, RANK-L binds to RANK receptor on osteoclasts

309
Q

Give 3 presentations of bony mets

A
  • ) Bone pain
  • ) General malaise
  • ) Pathological fractures
310
Q

Give 3 management principles for bony mets

A
  • ) Correct metabolic abnormalities (CALCIUM)
  • ) XRs
  • ) Mirel’s score
  • ) Possible primary disease
  • ) Treat met as primary
  • ) If widespread, lease with oncology
311
Q

What is Mirel’s scoring system used for?

A

Diagnosing impending pathological fractures

312
Q

What are the 4 parameters for Mirel’s score?

A

-) Site of lesion
-) Pain
-) Nature of lesion
-) Width of cortical destruction
3 points a parameter

313
Q

What score gives a 33% chance of fracture?

A

9, give prophylactic stabilisation

314
Q

Give 3 local complications of surgery

A
  • ) Haematoma
  • ) LOF
  • ) Infection (silver coating of implant reduces risk)
  • ) Local recurrence
315
Q

Where does the blood supply of the hip come from?

A

Medial and lateral femoral arteries

316
Q

What is a significant trauma defined as?

A

> 20mph or >20ft fall

317
Q

Give 4 things a fracture can be

A
  • ) Intra/extra articular
  • ) Associated with dislocation
  • ) Transverse/oblique/spiral/butterfly/comminution/segmental
  • ) Broken skin
318
Q

What is the management of a fracture?

A

Analgesia, reduce, immboilise, rehabilitate

319
Q

What is Paget’s disease of bone?

A

Focal disorder of bone remodelling

320
Q

What are the pathogenic steps of Paget’s disease? (6)

A

1) Increase in osteoclastic bone reabsorption
2) Compensatory increase in bone formation
3) Increased local bone blood flow
4) Increased fibrous tissue deposition in adjacent bone marrow
5) Bone formation exceeds bone resorption
6) New bone is weaker and more likely to fracture

321
Q

What is a genetic mutation that can cause Paget’s?

A

Mutation of the gene that codes for the osteoclast mediator protein p62

322
Q

How is Paget’s often found?

A

Incidental finding of elevated serum alkaline phosphatase

323
Q

Give 3 of the most commonly affected sites of Paget’s disease

A

Pelvis, femur, lumbar spine, skull, fibia

324
Q

Give 3 symptoms of Paget’s disease

A
  • ) Bone and joint pain
  • ) Deformities (e.g. bowed tibia)
  • ) Neurological complications
  • ) High output HF
  • ) Hypercalcaemia
  • ) Pathological fractures
  • ) Osteoarthritis, osteosarcoma
325
Q

What is the treatment for Paget’s?

A

Bisphosphonates, analgesia/alendronic acid

326
Q

What is osteomalacia?

A

Defective mineralisation of newly formed bone matrix (osteoid)

327
Q

What is the difference between osteomalacia and osteoporosis?

A

OM - normal amount of bone, low mineral content

OP - Mineralisation unchanged, overall bone loss

328
Q

What is the difference between rickets and OM?

A

Rickets - during period of bone growth

OM - after fusion of epiphyses

329
Q

Give 3 symptoms of rickets

A
  • ) Growth retardation
  • ) Hypotonia
  • ) Apathy in infants
  • ) Knock-kneed
  • ) Bow-legged
  • ) Deformities of metaphyseal-epiphyseal junction
  • ) Ill
330
Q

Give 3 symptoms of OM

A
  • ) Bone pain and tenderness
  • ) Fractures (esp. femoral neck)
  • ) Proximal myopathy (waddling gait)
331
Q

What does an XR show in Paget’s disease? (4)

A
  • ) Localised enlargement of bone
  • ) Patchy cortical thickening
  • ) Sclerosis, osteolysis, deformity
  • ) Hot spots
332
Q

Give 5 causes of osteomalacia

A
  • ) Vitamin D deficiency
  • ) Renal osteodystrophy (renal failure)
  • ) Drug induced (anticonvulsants)
  • ) Vitamin D resistance
  • ) Liver disease
  • ) Tumour induced osteomalacia (oncogenic hypophosphataemia)
333
Q

Give 2 causes of vitamin D deficiency

A
  • ) Malabsorption
  • ) Poor diet
  • ) Lack of sunlight
334
Q

Give 4 findings in the plasma in OM

A
  • ) Decreased Ca
  • ) Decreased PO4
  • ) Increased ALP
  • ) Increased PTH
  • ) Decreased 25(OH)-vitamin D (except in resistance)
335
Q

What does an XR show in OM?

A
  • ) Loss of cortical bone

- ) Partical fractures, especially at Looser’s zones (scapula, inferior femoral neck, medial femoral shaft)

336
Q

What does an XR show in rickets?

A

Cupped, ragged metaphyseal surfaces

337
Q

What is the treatment for OM?

A
  • ) Diet - vitamin D
  • ) Malabsoprtion/hepatic disease - Vitamin D2 (ergocalciferol)
  • ) Renal/resistance - Alfacalcidol/calcitriol
338
Q

What risk is there with aldacalcidol and calcitriol?

A

Hypercalcaemia! - monitor

339
Q

What are the steps of the conversion of vitamin D into its active form? (4)

A

1) 7-dehydrocholestrol (from sun)
2) Cholecalciferol (vitamin D3, or from diet)
3) 25-hydroxyvitamin D3 (in liver)
4) 1,25-dihydroxyvitamin D3 (in kidneys)

340
Q

Give 4 symptoms of granulomatosis with polyangiitis

A

-) Nasal obstruction, ulcers, epistaxis, destruction of nasal septum
-) Sinusitis
-) Glomeruloneprhtis, proteinuria, haematuria
-) Cough, haemopysis, pleuritis
-) Skin purpura, nodules, peripheral neuropathy, arthritis/arthralgia
-) Keratitis, conjunctivitis, scleritis, episcleritis, uveitis
ETC

341
Q

What is a specific test for granulomatosis with polyangiitis?

A

cANCA directed against PR3

342
Q

What does a CXR show in granulomatosis with polyangiitis?

A

Nodules +/- fluffy infiltrates of pulmonary haemorrhage

343
Q

What may a CT show in granulomatosis with polyangiitis?

A

Diffuse alveolar haemorrhage

Medicine Year 2 5 (17 decks)

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