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MSK Flashcards

1
Q

List three features seen in tendinopathy.

A
  • degeneration, disorganisation of collagen fibres
  • increased cellularity
  • little inflammation
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2
Q

List some risk factors of tendinopathy.

A

age, chronic disease, DM, RA, adverse biomechanics, repetitive exercise, quinolone antibiotics

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3
Q

Describe the pathology of tendinopathy. (4 points)

A
  • deranged collagen fibres/degeneration with a scarcity of inflammatory cells
  • increased vascularity around tendon
  • failed healing response to micro tears
  • inflammatory mediators released IL-1, NO, PG’s - cause apoptosis, pain and provoke degeneration through release of MMPs
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4
Q

Lateral epicondylitis is commonly known as?

A

tennis elbow

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5
Q

What is another name for medial epicondylitis?

A

golfers elbow

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6
Q

What are the clinical features of tendinopathy?

A

pain, swelling, thickening, tenderness, provocative tests

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7
Q

List some non-operative treatment options for tendinopathy.

A

NSAIDS, physiotherapy, GTN patches, extra corporeal shockwave therapy - common ones

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8
Q

Discuss how physiotherapy is beneficial in tendinopathy.

A

eccentric loading - contraction of the musculotendinous unit whilst it elongates - beneficial in 80%

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9
Q

Discuss the operative treatment options for tendinopathy.

A
  • debridement
  • excision
  • tendon transfers
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10
Q

What is compartment syndrome?

A

elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise

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11
Q

What are the common sites of compartment syndrome?

A

leg, forearm, thigh

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12
Q

What causes compartment syndrome?

A
  • increased internal pressure e.g. bleeding, swelling, iatrogenic infiltration
  • increased external compression e.g. casts/bandages, full thickness burns
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13
Q

Describe the pathophysiology of compartment syndrome.

A

continuous cycle of increased pressure, increased venous pressure, reduced blood flow, ischaemia, muscle swelling, increased permeability

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14
Q

Over time, what are the effects of ischaemia in compartment syndrome?

A

irreversible nerve and muscle damage

ischaemia

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15
Q

List some clinical features of compartment syndrome.

A
  • pain - out of proportion to that expected from the injury
  • pain on passive stretching of the compartment
  • pallor
  • parasthesia
  • paralysis
  • pulselessness
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16
Q

How might you use compartment pressure measurement in the diagnosis of compartment syndrome?

A

A pressure higher than 30 mmHg of the diastolic pressure in conscious or unconscious person is associated with compartment syndrome

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17
Q

How might you treat compartment syndrome?

A
  • open any constricting dressings/bandages
  • reassess
  • surgical release
  • later wound closure
  • skin grafting/plastic surgery input
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18
Q

What is the commonest form of primary bone tumour?

A

myeloma

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19
Q

Where do secondary tumours in bone usually arise?

A

bronchus, breast, prostate, kidney, thyroid

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20
Q

Name two childhood secondary bone tumour origins.

A

neuroblastoma, rhabdomysosarcoma

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21
Q

What are the effects of metastases on bone?

A
  • often asymptomatic
  • bone pain
  • bone destruction
  • long bones - pathological fracture
  • hypercalcaemia
  • spinal metastatic effects
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22
Q

List some effects of spinal metastases.

A
  • vertebral collapse
  • spinal cord compression
  • nerve root compression
  • back pain
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23
Q

What is the best imaging technique for metastatic bone disease?

A

PET CT

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24
Q

What is the mechanism of destruction in bone tumours?

A
  • osteoclasts, not tumour cells
  • stimulated by cytokines from tumour cells
  • inhibited by bisphosphonates
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25
Q

Where do sclerotic metastases of bone originate from?

A
  • prostatic carcinoma
  • breast carcinoma
  • carcinoid tumour
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26
Q

Renal and thyroid carcinomas typically lead to which type of bone metastases?

A

solitary

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27
Q

Monoclonal proliferation of which type of cell leads to myeloma?

A

plasma cells

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28
Q

Discuss the impact of renal impairment caused by myeloma.

A
  • precipitated light chains in renal tubules - Bence Jones protein in urine
  • hypercalcaemia
  • amyloidosis
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29
Q

Discuss the impact of marrow replacement caused by myeloma

A
  • pancytopenia
  • anaemia
  • leukopenia: infections
  • thrombocytopenia: haemorrhage
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30
Q

Name 3 benign primary bone tumours.

A
  • osteoid osteoma
  • chondroma
  • giant cell tumour
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31
Q

Name 3 malignant primary bone tumours.

A
  • osteosarcoma
  • chondrosarcoma
  • Ewing’s tumour
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32
Q

List four clinical features of osteoid osteoma.

A
  • M:F 2:1
  • any bone, especially long bones
  • pain - worse at night, relieved by aspirin
  • sympathetic synovitis - juxta-articular tumours
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33
Q

What is an osteoid osteoma?

A

a small, benign osteoblastic proliferation

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34
Q

What is an osteosarcoma?

A

a malignant tumour whose cells form osteoid or bone

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35
Q

What are the two commonest sites of osteosarcoma?

A

metaphysis of long bones e.g. around knee

early lung metastases

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36
Q

Define Paget’s disease.

A
  • disorder of excessive bone turnover
  • increased osteoclasis, increased bone formation, structurally weak bone
  • disorganised bone architecture
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37
Q

Where is Paget’s disease common?

A

vertebrae, pelvis, skull, femur

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38
Q

List some clinical features of Paget’s disease.

A
  • bone pain
  • bowing of long bones
  • pathological fracture
  • osteoarthritis
  • deafness
  • spinal cord compression
  • high cardiac output
  • Paget’s sarcoma - lytic
  • age > 40
  • M > F
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39
Q

Name 3 cartilaginous tumours.

A
  • enchondroma
  • osteocartilaginous exostosis
  • chondrosarcoma
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40
Q

What is an enchondroma?

A

lobulated mass of cartilage within medulla

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41
Q

Where does enchondroma affect? And what are the symptomatic features?

A

hands - swelling, pathological fracture
feet
long bones - often asymptomatic

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42
Q

What is an osteocartilaginous exostosis?

A

benign outgrowth of cartilage with endochondral ossification, probably derived from growth plate (metaphysis of long bones)

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43
Q

When is osteocartilaginous exostosis common?

A

adolescence

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44
Q

Is chondrosarcoma primary or secondary?

A

Both
primary - de novo
secondary - pre-existing enchondroma or exostosis

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45
Q

What sites are chondrosarcomas usually found?

A

axial skeleton, pelvis, ribs, shoulder girdle, proximal femur and humerus

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46
Q

What is a chondrosarcoma?

A

a cancer composed of cells derived from transformed cells that produce cartilage

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47
Q

What is Ewing’s sarcoma?

A

a malignant small, round, blue cell tumour. It is a rare disease in which cancer cells are found in the bone or in soft tissue

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48
Q

At what age does Ewing’s sarcoma peak?

A

5-15 years

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49
Q

Where does Ewing’s sarcoma affect?

A 
long bones (diaphysis or metaphysis)
flat bones of limb girdles
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50
Q

Name 3 common sites for Ewing’s sarcoma to metastases to.

A

lung, bone marrow, bone

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51
Q

What are the three basic steps in indirect fracture healing?

A

inflammation
repair
remodeling

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52
Q

Define indirect fracture healing.

A

formation of bone via a process of differential tissue formation until skeletal continuity is restored

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53
Q

Give more detail about the inflammatory process in indirect fracture healing.

A
  • fracture haematoma forms from broken vessels
  • 6-8 hours after injury
  • swelling and inflammation to dead bone cells
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54
Q

Describe fibrocartilage callus formation in fracture healing.

A
  • lasts about 3 weeks
  • new capillaries organise fracture haematoma into granulation tissue - ‘procallus’
  • fibroblasts and osteogenic cells invade procallus
  • make collagen fibres which connect ends together
  • chondrocytes begin to produce fibrocartilage
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55
Q

Describe bony callus formation in fracture healing.

A
  • after 3 weeks and lasts about 3-4 months

- osteoblasts make woven bone

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56
Q

Discuss bone remodeling in relation to indirect fracture healing.

A
  • osteoclats remodel woven bone into compact bone and trabecular bone
  • often no trace of fracture line on X-rays
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57
Q

Define direct fracture healing.

A

‘direct formation of bone via osteoclastic absorption and osteoblastic formation, without the process of callus formation, to restore skeletal continuity’

  • unique ‘artificial’ surgical situation
  • relies upon compression of bone ends
  • cutting cones cross fracture site
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58
Q

Briefly describe the blood supply of bone.

A
  • endosteal - inner 2/3rds

- periosteal - outer 1/3rds

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59
Q

Which fractures are prone to problems with union or necrosis because of problems with blood supply?

A
  • proximal pole of scaphoid fractures
  • talar neck fractures
  • intracapsular hip fractures
  • surgical neck of humerus fractures
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60
Q

List some patient factors which inhibit fracture healing.

A

increasing age, diabetes, anaemia, malnutrition, peripheral vascular disease, hypothyroidism, smoking, alcohol

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61
Q

Name some medications which inhibit fracture healing.

A

NSAIDs, steroids, bisphosphonates

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62
Q

Describe how NSAIDs inhibit fracture healing.

A
  • reduce local vascularity at fracture site
  • additional reduction in healing effect independent of blood flow
  • specifically COX-2 inhibitors
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63
Q

Describe how bisphosphonates inhibit fracture healing.

A
  • inhibit osteoclastic activity

- delay fracture healing as a result

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64
Q

List potential fractures of the femoral neck.

A
  • subcapital
  • transcervical
  • intertrochanteric
  • subtrochanteric
  • fracture of greater trochanter
  • fracture of less trochanter
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65
Q

What is the hallmark sign of degenerative bone disease?

A

bone production

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66
Q

What is the hallmark sign of inflammatory joint disease?

A

periarticular erosions

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67
Q

What is the hallmark of depositional bone disease?

A

periarticular soft tissue masses

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68
Q

On X-ray how can you tell the difference between an active and old bone erosion?

A 
active = ill-defined
old = well-defined
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69
Q

What are the X-ray features of primary degenerative arthritis?

A
  • narrowed joint space
  • osteophytes
  • subchondral sclerosis/cysts
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70
Q

Where is excessive wear and tear most common?

A

hips and knees

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71
Q

List the common causes of secondary degenerative arthritis.

A

trauma, infection, avascular necrosis, calcium pyrophosphate dihydrate deposition (CPDD) disease, RA, haemophilia

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72
Q

What causes CPDD disease?

A

idiopathic or associated with hyperparathyroidism and haemochromatosis

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73
Q

What impact does CPDD have on articular cartilage? And which bones does it most commonly affect?

A

calcification

  • triangular fibrocartilage of wrist
  • knee, hip, shoulder
  • symphysis pubis
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74
Q

Describe the clinical features of CPDD.

A
  • sudden onset of pain/fever
  • tender, swollen, red joint
  • may mimic septic arthritis
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75
Q

Which organisms commonly cause infectious arthritis?

A

staph, strep, TB

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76
Q

Which joints does infectious arthritis commonly affect?

A
  • fingers from bites
  • feet in diabetes
  • hips in total hip replacements
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77
Q

Describe the clinical features of a infectious arthritis joint.

A
  • soft tissue swelling
  • destruction of cartilage/bone
  • rapid loss of joint space
  • +/- periosteal reaction
  • osteoporosis
  • later subluxation, OA, fusion
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78
Q

What are the radiographic findings in discitis?

A
  • normal 1-3 weeks
  • end-plate erosion
  • disc space narrowing
  • bone destruction
  • paravertebral mass
  • late - sclerosis
  • ankylosis
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79
Q

What is the newest classification for RA?

A

presence of bilateral wrist, MCP or PIP joint enhancement on MRI and leads to a more accurate diagnosis of early RA

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80
Q

Describe a RA joint.

A
  • soft tissue swelling
  • synovitis
  • effusion
  • erosions and cysts
  • joint space narrowing
  • secondary degenerative changes
  • bone marrow oedema
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81
Q

How do sero-negative inflammatory arthropathies differ from RA?

A
  • negative rheumatoid factor
  • normal bone density
  • periostitis
  • ankylosis (fusion)
  • asymmetrical pattern
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82
Q

What gene is positive in sero-negative inflammatory arthropathies?

A

HLA-B27

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83
Q

List 4 causes of sero-negative inflammatory arthropathy.

A

Psoriatic arthritis
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis

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84
Q

Discuss the clinical features of psoriatic arthritis.

A
  • usually skin and nail changes
  • DIP joints of hands > feet
  • pencil in cup deformity
  • resorption of distal phalanges
  • M=F, young adults
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85
Q

What is the other name for reactive arthritis?

A

Reiter’s syndrome

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86
Q

Discuss the clinical features of reactive arthritis including extra-articular manifestations.

A
  • M > F
  • 20-40 yrs
  • asymmetrical oligoarthritis
  • lower limb and sacroiliac joint
  • dactylitis, enthesitis, bursitis
  • circinate balanitis
  • keratoderma blennorrhagicum
  • mouth ulcers
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87
Q

What organisms cause reactive arthritis?

A

chlamydia, salmonella, shigella

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88
Q

What illnesses go in hand with reactive arthritis to form a triad?

A
  • urethritis

- conjuncitivitis

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89
Q

Who does ankylosing spondylitis commonly affect?

A
  • M:F 3:1
  • 20-40 yrs
  • HLA B27 +ve
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90
Q

Describe the clinical features of AS?

A
  • low back pain
  • stiffness
  • bilateral sacro-illiitis
  • squaring of vertebral bodies
  • peripheral large joint arthritis
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91
Q

What is gout?

A

sodium urate crystal induced synovial inflammation

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92
Q

Who does gout usually affect?

A

elderly males, hereditary, young age suspect renal disease or myeloproliferative disorder

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93
Q

What are the radiographic features seen in gout?

A
  • para-articular erosions
  • sharply marginated with sclerotic rims
  • overhanging edges
  • no joint space narrowing till late
  • little or no osteoporosis
  • soft tissue swelling
  • tophi not usually calcified
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94
Q

What is osteonecrosis?

A

avascular necrosis - refers to bone infarction near a joint

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95
Q

Where is osteonecrosis most common?

A

hip and shoulder

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96
Q

What are the consequences of osteonecrosis?

A
  • pain from infarction

- death of subchondral bone can lead to collapse of the joint surface and end stage arthritis

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97
Q

Describe how osteonecrosis present with particular focus on femoral head.

A
  • often asymptomatic and found on imaging
  • pain - either from infarction or arthritis
  • groin pain that worsens with weight-bearing and motion
  • rest pain 2/3
  • night pain 1/3
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98
Q

Osteonecrosis accounts for what percent of total hip replacement?

A

10

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99
Q

What is the peak age of prevalence for avascular necrosis?

A

40-50

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100
Q

What is the prevalence of osteonecrosis in sickle cell anaemia?

A

10

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101
Q

Discuss the pathophysiology of osteonecrosis.

A
  • decreased intraosseous blood flow
  • ischaemia
  • bone necrosis
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102
Q

What can cause decreased blood flow in osteonecrosis? (4 points)

A
  1. Blood vessel disruption e.g. trauma
  2. Intraluminal obliteration e.g. fat microemboli and thrombosis
  3. Increased marrow pressure e.g. adipocyte hypertrophy and bone oedema
  4. Cytotoxicity
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103
Q

List factors which lead to poor outcome of osteonecrosis.

A
  • extensive

- heavy loads

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104
Q

What happens to cause the necrotic cancellous bone to collapse?

A
  • osteoclasts resorb the necrotic trabeculae while remaining ones serve as scaffolding for deposition of new bone
  • ‘creeping substitution’ may not be fast enough
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105
Q

What is the crescent sign seen in osteonecrosis?

A

subchondral radiolucency which precedes subchondral collapse

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106
Q

Discuss what is seen in imaging in late stages of AVN.

A
  • loss of sphericity and collapse of femoral head
  • joint space narrowing
  • bone remodelling
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107
Q

List RF’s of AVN.

A
  • trauma
  • corticosteroids
  • alcohol abuse
  • sickle cell disease
  • bisphosphonates
108
Q

What are the treatment option for AVN?

A
  • partial weight bearing
  • bisphosphates (undergoing trial)
  • core decompression with or without bone graft in early stages
  • replacement if bone collapse
109
Q

What is RA?

A

a chronic autoimmune multisystem disease affecting any synovial joint
hallmark is synovial but multiple extra-articular manifestations

110
Q

Discuss the aetiology of RA.

A
  • HLA-DR4
  • smoking
  • infection
  • hormonal
111
Q

Describe the pathophysiology of RA.

A
  • synovitis = immune cells invading a normally acellular synovium in the form a of pannus
  • release of TNF, IL-1 and IL-6 causing inflammation and destruction
112
Q

What is a pannus in relation to RA?

A

hyperplastic, invasive tissue leading to cartilage breakdown, erosions and reduced function

113
Q

Name some clinical features of RA.

A
  • synovitis
  • symmetrical
  • early = MCPs/PIPs/wrists
  • inflammatory = pain, erythema, swelling
  • fatigue, weakness, fever, weight loss, anoxeria
114
Q

What are the classic joint features seen in late stage RA?

A
  • boutonniere
  • swan neck
  • Z thumb
  • volar subluxation of wrist
  • ulnar deviation digits
  • radial deviation wrists
  • piano key ulnar head
115
Q

Describe some of the extra-articular manifestations of RA.

A
  • pleural effusions
  • mononeuritis multiplex
  • anaemia
  • thrombocytosis
  • lung fibrosis and nodules
  • muscle wasting
116
Q

Which investigations would you undertake in a patient with suspected RA?

A

FBC, U&Es, LFT, ESR/CRP, RF, ACPA, ANA

117
Q

What is rheumatoid factor? What is its role in investigating RA?

A
  • autoantibody against Fc portion of IgG

- part of assessment, not diagnostic

118
Q

What is ACPA?

A

Anti–citrullinated protein antibody - linked with smoking (increases citrullination) - predictor of worse prognosis, more erosions and resistant disease

119
Q

Discuss the imaging techniques useful in RA and what they show.

A
  • XR: Loss of joint space, Erosions, Soft tissue swelling, Soft bones (osteopenia)
  • USS: synovitis and erosions
  • MRI: bone marrow oedema
120
Q

What non-pharmacological treatments are available for RA?

A

OT, PT, podiatrists, dietitians

121
Q

Discuss the pharmacological medications available in RA including symptomatic and disease modifying.

A
  • symptomatic: NSAIDs, analgesia

- DMARDs: glucocorticoids, methotrexate, sulfasalazine, anti-TNF (infliximab), anti-CD20, anti-IL6

122
Q

Which DMARD is a dihydrofolate reductase inhibitor?

A

methotrexate

123
Q

What must be given alongside MTX?

A

folic acid

124
Q

What is MTX contraindicated?

A

pregnancy, infection, on antibiotics

125
Q

What are common side effects of sulfasalazine?

A

GI, rashes, BM

126
Q

In what case is sulfasalazine indicated over MTX?

127
Q

Etanercept, inflixumab and adalimumab are examples of which type of biologic therapy?

128
Q

What are the side effects of anti-TNF therapy?

A

TB, infection, MS, CHF

129
Q

What is the mechanism of rituximab?

130
Q

List 3 side effects of rituximab.

A

infection, PML, hypogammaglobulinaemia

131
Q

Name an anti-IL6 therapy.

A

tocilizumab

132
Q

In which populations is SLE most common?

A

afro-caribbean, south asian, mexican

133
Q

List the clinical SLICC criteria used in diagnosis of SLE.

A
  • acute cutaneous lupus e.g. malar rash
  • chronic cutaneous lupus e.g. classic discoid rash
  • oral ulcers
  • non-scarring alopecia
  • synovitis
  • serositis
  • renal dysfunction
  • neurological: seizures, pyschosis
  • haemolytic anaemia
  • leucopenia
  • thrombocytopenia
134
Q

List the immunological SLICC criteria used in diagnosis of SLE.

A
  • high ANA
  • > x2 anti-asDNA
  • antiphospholipid (lupus anticoagulant)
  • low complement
  • +ve direct Coomb’s test
135
Q

How is SLE diagnosed from SLICC? (2 points)

A
  • 4 of criteria including one from each section

- biopsy proven nephritis compatible with SLE and with ANA or anti-dsDNA antibodies

136
Q

Describe the common features in the clinical presentation of SLE.

A
  • constitutional symptoms
  • cutaneous manifestations
  • arthralgia and arthritis
137
Q

Name 3 MSK manifestations of SLE.

A
  • AVN
  • fibromyalgia
  • osteoporosis
138
Q

What % of people with SLE will develop ESFR in 10 years?

139
Q

List some pulmonary manifestations of SLE.

A
  • pleural effusions
  • acute pneumonitis
  • diffuse alveolar haemorrhage
  • pulmonary hypertension
140
Q

List some CV manifestations of SLE.

A
  • pericarditis
  • myocarditis
  • valvular abnormalities
  • coronary heart disease
  • risk of MI x50
141
Q

Name some neuropsychiatrc manifestations of SLE.

A

headache, anxiety, seizures, demyelinations, GBS, mononeuritis

142
Q

List some haematological manifestations of SLE.

A
  • anaemia of chronic disease
  • autoimmune haemolytic anaemia
  • thrombotic thrombocytopenic purpura
  • leucopenia
  • thrombocytopenia
143
Q

What is the significance of ANA?

A

anti-nuclear antibody, often diagnostic of SLE

144
Q

What are the three medications licensed as treatment for SLE in UK?

A
  • steroids
  • hydroxychloroquine
  • belimumab
145
Q

What is belimumab?

A

human monoclonal antibody that inhibits B-cell activating factor (BAFF)

146
Q

What is the treatment for mild cutaneous SLE disease?

A

topical therapies, UVA/UVB sunblock

147
Q

What is the treatment for mild MSK SLE disease?

A

NSAIDs, IA/IM steroid, low dose oral prednisolone

148
Q

What is the treatment for mild serositis SLE disease?

A

NSAIDs, MTX

149
Q

Discuss the treatment of moderate SLE.

A

treatment as per mild plus:

  • oral prednisolone
  • MTX
  • immunosuppressants e.g. Azathioprine, Mycophenolic acid, ciclosporin, tacrolimus
  • belimumab
150
Q

Discuss the treatment of severe SLE disease.

A

treatment as per mild and moderate plus:

  • high dose steroid
  • DMARDs
  • cyclophosphamide
  • IV immunoglobulin therapy
  • plasmapheresis
151
Q

What are the primary vasculitides?

A

a group of autoimmune conditions characterised by inflammation of blood vessels

152
Q

What systems can be affected by inflammation of blood vessels?

A

joints, skin, nerves, kidneys, lungs, ENT

153
Q

What are the different types of vasculitis?

A
  • large vessel vasculitis: giant cell arteritis, Takayasu’s arteritis
  • medium vessel vasculitis: polyarteritis nodosa, Kawasaski disease
  • small: ANCA-associated (microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis), immune complex (HSP-IgA vasculitis, Goodpasture’s disease)
154
Q

Define giant cell arteritis.

A

systemic vasculitis that affects the aorta and its major branches

155
Q

Describe the clinical presentation of giant cell arteritis.

A
  • headache - temporal with tenderness, subacute onset, constant
  • visual symptoms
  • jaw claudication
  • polymyalgia rheumatica symptoms
156
Q

What are polymyalgia rheumatica symptoms?

A

subacute onset of shoulder and pelvic gridle stiffness and pain

157
Q

What are the three main complications of temporal arteritis?

A
  • visual loss
  • large vessel vasculitis
  • CVA
158
Q

How is GCA typically diagnosed?

A
  • clinical presentation
  • clinical examination findings
  • acute phase response: ESR/CRP
159
Q

What are the clinical exam findings in GCA?

A

temporal artery assymetry, thickening, loss of pulsatility

160
Q

Describe the gold standard diagnostic tool in GCA.

A

temporal artery biopsy:

- positive if interruption of internal elastic lamina with infiltration of mononuclear cells in vessel

161
Q

What are the treatment options for GCA?

A
  • prednisolone 60mg for 1 month
  • taper to 15mg by 12 weeks
  • discontinue by 12-18 months
162
Q

What is the DDx of cutaneous vasculitis?

A

idiopathic, drugs, infection, secondary RA/CTD/PBC, malignancy, manifestation of ANCA vasculitis

163
Q

Describe the clinical features of Henoch Schonlein Purpura.

A
  • classic purpuric rash esp. buttocks, thigh
  • hives, confluent petechiae, ecchymoses, ulcers
  • arthralgia/arthritis
164
Q

List some complications of Henoch Schonlein Purpura.

A
  • GI: pain, bleeding, diarrhoea
  • renal: IgA nephropathy
  • orchitis (inflammation of testicles)
165
Q

Discuss the approach to management of HSP.

A
  1. Exclude secondary causes
  2. Assess extent of involvement - urinalysis
  3. Often no treatment required - frequently self-limiting up to 16 weeks
166
Q

Streptococcal sore throat can occasionally trigger which vasculitis?

167
Q

Which group of vasculides have the most morbidity and mortality associated with it?

A

ANCA- associated small vessel vasculitis

168
Q

Define granulomatosis with polyangiitis.

A

vasculitis characterised by granulomatous necrotising inflammatory lesions of the upper and lower respiratory tract and often a pauci-immune glomerulonephritis

169
Q

Describe the triad of GPA disease.

A
  1. Upper airway/ENT - rhinitis, sinusitis, chronic otitis media
  2. Renal - pauci-immune glomerulonephritis
  3. Lower respiratory - parenchymal nodules, alveolar haemorrhage
170
Q

List some constitutional symptoms of GPA.

A

fatigue, weight loss, fever, sweats, myalgia, arthralgia, failure to thrive in elderly

171
Q

What are ANCAs?

A

autoantibodies directed against the cytoplasmic constituents of neutrophils and monocytes

172
Q

What are the two methods for testing ANCA?

A
  • indirect immunofluorescence which gives p/cANCA staining patterns
  • ELISA for PR3/MPO
173
Q

How useful is ANCA?

A
  • diagnosis
  • prognostic information
  • assess response to treatment
  • monitoring for early signs of relapse
174
Q

Which ANCA result is suggestive of GPA?

A

cANCA with PR3

175
Q

Which ANCA result is suggestive of MPA?

A

pANCA with MPO

176
Q

How is vasculitis treated?

A
  1. Remission induction - prednisolone + MTX (if moderate)/rituximab or cyclophosphamide (if severe) i.e. IMMUNOSUPPRESSION
  2. Remission maintenance - prevent relapse, lower drug toxicites, more prolonged therapy: azathioprine, MTX
177
Q

List some side effects of corticosteroids.

A
  • weight gain and fluid retention
  • glaucoma
  • osteoporosis
  • infection
  • hypertension and hypokalaemia
  • peptic ulcer, GI bleed
  • psychological symptoms
178
Q

What is the mechanism of action of corticosteroids?

A

Bind to glucocorticoid receptors. This causes up-regulation of a variety of anti-inflammatory mediators and down regulation of pro-inflammatory mediators. This provides immunosupression.

179
Q

What is the mechanism of action of methotrexate?

A

Stops the action of the enzyme dihydrofolate needed for production of DNA.

180
Q

List some adverse effects of methotrexate.

A
  • GI: N&V, diarrhoea, hepatitis, stomatitis
  • haematological: leukopenia
  • others: frequent infection, PF
181
Q

What are the main indications for MTX use?

A
  • RA
  • psoriasis and psoriatric arthropathy
  • steroid sparing agent in GCA
182
Q

Discuss the mechanism of action of azathioprine.

A

Disrupt DNA synthesis. Blocks purine synthesis mainly in lymphocytes.

183
Q

What are some adverse effects of azathioprine?

A
  • GI: N&V, diarrhoea, hepatitis, cholestasis
  • haematological: leucopenia, thrombocytopenia
  • frequent infections
184
Q

How can toxicity develop when using azathioprine?

A

some individuals lack TPMP enzyme which is vital in reducing active drug in cells

185
Q

When is azathioprine used in clinical practice?

A
  • IBD e.g. ulcerative colitis, Crohn’s disease
  • myaesthenia gravis
  • eczema
186
Q

How does cyclosporin work?

A
  • small molecule inhibitor of calcineurin
  • effect of inhibiting signal transduction from activated TCR complex
  • profound inhibition of T cell activation
187
Q

List some adverse effects of cyclosporin.

A

nephrotoxicity, hypertension, hepatotoxicity, anorexia, lethargy, hirsutism, paraesthesia

188
Q

What are the indications for cyclosporin use?

A
  • usually given for organ transplantation
  • inflammatory conditions
  • used topically i.e. skin, eyes
189
Q

What are the disadvantages of immunosuppressants?

A
  • often insufficient to control inflammatory disease with subsequent progression
  • significant toxicities
  • bone marrow suppression
  • frequent infections
190
Q

What are some side effects of biologic therapies?

A

hypersensitivity reaction, infusion reactions, mild GI toxicity

191
Q

There is an increased risk of TB infection with which biologic therapy?

A

anti-TNF - need to screen for latent TB before prescribing

192
Q

Which therapies increase risk of pneumonia and respiratory tract infection?

A

abatacept (anti-CD86) and anti-IL1

193
Q

Rituximab increased the risk of which infections?

A
  • generalised increased risk of serious infection

- hepatitis B reactivation

194
Q

85% of Ewing’s sarcoma are associated with translocation of which chromosomes?

195
Q

In AVN of femoral head, which movements are particularly limited?

A

internal rotation and abduction

196
Q

What is the name given to the disease causing avascular necrosis and collapse of the lunate bone in the wrist?

A

Kienbock’s disease

197
Q

What are the three key imaging findings in osteonecrosis?

A

1 subchondral collapse
2 bone remodelling
3 crescent sign

198
Q

What are some of the risk factors to developing septic arthritis?

A
  • RA and OA
  • joint prosthesis/surgery
  • IV drug abuse
  • ALD
  • diabetes
  • cutaneous infections/ulcers
  • chronic renal failure
199
Q

What are the differentials of an acute hot, swollen, tender joint?

A
  • septic arthritis
  • crystal arthropathy
  • trauma
  • early presentation of polyarthropathy
200
Q

What investigations should be carried out if septic arthritis is suspected?

A

joint aspirate, blood cultures, CRP, X-ray

201
Q

How long should an antibiotic regimen be carried out in septic arthritis?

A
  • 2 weeks IV

- 4 weeks oral

202
Q

Which joint is most commonly affected with gout?

A

MTP joint of big toe

203
Q

List some factors which may precipitate an attack of gout.

A

trauma, surgery, infection, starvation, diuretics

204
Q

What are the risk factors for developing gout?

A
  • reduced urate excretion: elderly, impaired renal function, hypertension, metabolic syndrome
  • excess urate production: diet, genetics, myelo/lympho-proliferative disorders, psoriosis
205
Q

Polarised light microscopy is used to investigate synovial fluid. What is the main difference seen between gout and CPPD?

A
  • gout = negatively birefringent crystals

- CPPD = positively birefringent crystals

206
Q

What are some of the risk factors to developing septic arthritis?

A
  • RA and OA
  • joint prosthesis/surgery
  • IV drug abuse
  • ALD
  • diabetes
  • cutaneous infections/ulcers
  • chronic renal failure
207
Q

What are the differentials of an acute hot, swollen, tender joint?

A
  • septic arthritis
  • crystal arthropathy
  • trauma
  • early presentation of polyarthropathy
208
Q

What investigations should be carried out if septic arthritis is suspected?

A

joint aspirate, blood cultures, CRP, X-ray

209
Q

How long should an antibiotic regimen be carried out in septic arthritis?

A
  • 2 weeks IV

- 4 weeks oral

210
Q

Which joint is most commonly affected with gout?

A

MTP joint of big toe

211
Q

List some factors which may precipitate an attack of gout.

A

trauma, surgery, infection, starvation, diuretics

212
Q

What are the risk factors for developing gout?

A
  • reduced urate excretion: elderly, impaired renal function, hypertension, metabolic syndrome
  • excess urate production: diet, genetics, myelo/lympho-proliferative disorders, psoriosis
213
Q

Polarised light microscopy is used to investigate synovial fluid. What is the main difference seen between gout and CPPD?

A
  • gout = negatively birefringent crystals

- CPPD = positively birefringent crystals

214
Q

What medications are currently available for acute gout attack?

A
  • NSAIDs
  • colchicine
  • steroids
  • RICE
215
Q

How might an acute attack of gout be prevented?

A
  • lifestyle changes
  • allopurinol
  • febuxostat (use in renal failure)
216
Q

When should prophylaxis for acute gout attacks be considered?

A

> 1 attack in 12 months, tophi, renal stones

217
Q

Describe the mechanism of action of allopurinol.

A

xanthine oxidase inhibitor

Reduces synthesis of uric acid by competitively inhibiting xanthine oxidase. Reduces serum uric acid level.

218
Q

What side effects are associated with allopurinol?

A

SJS/TEN, hepatitis, vasculitis, AKI

219
Q

Describe the clinical criteria for diagnosis of rheumatoid arthritis.

A 
A: Joint involvement
- 1 large joint = 0
- 2-10 large joints = 1
- 1-3 small joints = 2
- 4-10 small joints = 3
- >10 joints = 5
B: Serology
- -ve RF and -ve anti-CCP = 0
- low +ve RF or low +ve anti-CCP = 2
- high +ve RF or high +ve anti-CCP = 3
C: Acute phase reactants
- normal CRP and ESR = 0
- abnormal CRP or ESR = 1
D: Duration of symptoms
- <6 weeks = 0
- >6 weeks = 1

Scores =/> 6 are diagnostic

220
Q

What is Sjogren’s syndrome?

A

chronic inflammatory autoimmune disorder involving lymphocytic infiltration and fibrosis of exocrine glands

221
Q

List some of the clinical features of Sjogren’s syndrome.

A
  • decreased tear production
  • decreased salivation
  • parotid swelling
  • dry cough and dysphagia
222
Q

What are some of the systemic signs of Sjogren’s syndrome?

A

polyarthritis, Raynaud’s, lymphadenopathy, vasculitis, peripheral neuropathy

223
Q

Which other autoimmune conditions is Sjogren’s syndrome associated with?

A

thyroid disease, autoimmune hepatitis, PBC

224
Q

What investigations should you carry out in Sjogren’s syndrome?

A
  • Schirmer’s test = conjunctival dryness

- antibodies = anti-RO, anti-La, ANA, RF

225
Q

What treatment is available for Sjogren’s syndrome?

A
  • hypromellose (artificial tears)
  • frequent drinks
  • NSAIDs for arthralgia
226
Q

Describe the three main features of systemic sclerosis.

A
  1. Scleroderma
  2. Internal organ fibrosis
  3. Microvascular abnormalities
227
Q

Which plasma autoantibodies are present in limited systemic sclerosis?

A

ANA, anticentromere antibodies

228
Q

Describe the skin distribution of both limited and diffuse systemic sclerosis.

A
  • limited: face, hands, feet

- diffuse: whole body

229
Q

Which plasma autoantibodies may be positive in diffuse systemic sclerosis?

A

ANA, antitopoisomerase-1, anti-RNA polymerase

230
Q

What is myositis?

A

rare conditions characterised by insidious onset of progressive symmetrical proximal muscle weakness and autoimmune mediated striated muscle inflammation, associated with myalgia +/- arthralgia.

231
Q

What are some of the consequences of muscle weakness in myositis?

A

dysphagia, dysphonia, respiratory weakness

232
Q

List the skin signs seen in dermatomyositis.

A
  • macular rash
  • lilac-purple rash on eyelids often with oedema
  • nailfold erythema
  • Gottron’s papules
233
Q

Name the tests that you would carry out in myositis.

A
  • muscle enzymes in plasma: increased
  • MRI: muscle oedema
  • autoantibodies: anti-Mi2, anti-Jo1
234
Q

What treatment is available for myositis?

A
  • prednisolone

- skin: hydroxychloroquine/topical tacrolimus

235
Q

Define juvenile idiopathic arthritis.

A

disease of childhood onset characterised primarily by arthritis persisting for at least 6 weeks and currently having no known cause

236
Q

Which eye disease often co-exists with oligoarthritis in children?

A

uveitis - screening by paediatric opthalmologist

237
Q

What are the childhood equivalents of RA and AS?

A
  • RA = rheumatoid factor positive polyarthritis

- AS = enthesitis related arthritis

238
Q

What is an enthesis?

A

insertion of tendon, ligaments, joint capsule, fascia to bone

239
Q

How does Kawasaki disease present in young children and babies?

A

aneurysm formation in medium to large sized arteries, high fever, mucositis, conjunctivitis, arthritis, red palms

240
Q

What are some of the causes of non-specific low back pain?

A
  • lumbar strain/sprain
  • degenerative discs/facet joints
  • disc prolapse, spinal stenosis
  • compression fractures
241
Q

What is a vertebral disc prolapse and how might it present clinically?

A
  • herniated nucleus pulposus
  • acute lower back pain
  • worse when coughing
  • leg > back pain ‘sciatica’
  • leg pain = dermatomal distribution
242
Q

In which cause of back pain is the straight leg test positive?

A

disc prolapse

243
Q

What is spinal stenosis and how does it present?

A
  • anatomical narrowing of spinal canal

- ‘claudication’ in legs/calves - worse walking, rest in flexed position

244
Q

What are the red flag symptoms of cauda equina syndrome?

A
  • bilateral sciatica
  • saddle anaesthesia
  • bladder or bowel dysfunction
  • reduced anal tone on PR
245
Q

What is spondylolisthesis?

A

when one of the vertebrae slips out of place

246
Q

Where does pain from a vertebral compression fracture usually radiate?

A

in ‘belt’ around chest/abdomen

247
Q

What treatments are available for vertebral compression fractures?

A
  • analgesia
  • vertebroplasty
  • kyphoplasty
248
Q

Describe sources of referred pain to the back.

A
  • aortic aneurysm
  • acute pancreatitis
  • peptic ulcer disease
  • acute pyelonephritis/renal colic
  • endometriosis
249
Q

What are the symptoms of infective discitis?

A

constant back pain, fever, weight loss

250
Q

What investigations should you carry out if suspecting infective discitis?

A
  • FBC, ESR, CRP
  • blood cultures
  • radiology-guided aspiration
251
Q

What is the most common pathogen to cause infective discitis?

A

staph aureus

252
Q

What is the distinguishing feature between vertebral infection and malignancy on X ray?

A
  • infection = damage to both sides

- malignancy = only one side

253
Q

What are the classical features of inflammatory back pain?

A
  • onset < 45 years
  • early morning stiffness >30 mins
  • back stuff after rest and improves with movement
  • waking during night with buttock pain
254
Q

What are the red flag symptoms of back pain?

A

new onset age <16 or >50, trauma, previous malignancy, fever/rigors, malaise, weight loss, previous steroid use, IV drug use, HIV, immunosuppression, recent infection, urinary retention, non-mechanical pain

255
Q

What are the red flag signs of back pain?

A

saddle anaesthesia, reduced anal tone, hip or knee weakness, generalised neurological deficit, progressive spinal deformity

256
Q

What is the criteria for diagnosis of ankylosing spondylitis?

A
  1. Clinical criteria
    a) low back pain and stiffness > 3 months which improves with exercise, but is not relieved by rest
    b) limitationof motion of the lumbar spine
    c) limitation of chest expansion relative to normal
  2. Radiological criterion
    - sacroiliitis grade =/> 2 bilaterally or grade 3-4 unilaterally

Definite AS if radiological criterion is associated with at least 1 clinical criterion.

257
Q

What is ankylosing spondylitis and which gene mutation is commonly associated with it?

A
  • chronic inflammatory condition of the spine and sacroiliac joints of unknown aetiology
  • HLA B27
258
Q

What is the difference between radiography axSpA and AS?

A
  • radio: X-ray +ve sacro-ilitis

- AS: X-ray +ve sacro-ilitis and/or spinal changes

259
Q

What are some of the features of spondyloarthritis?

A
  • axial arthritis - inflammatory back pain
  • fatigue
  • enthesitis
  • dactylitis
  • ankylosis/new bone formation
  • osteoporosis
  • extra-articular: psoriasis, uveitis, IBD, aortic valve incompetence, oral ulcers
260
Q

Discuss the ASAS classification criteria for axial SpA.

A
  1. Sacroilitis on imaging plus >/= 1 SpA feature
    OR
  2. HLA-B27 plus >/= other SpA features
261
Q

In which people groups are axSpA and AS most common?

A
  • onset < 45 years
  • mainly 15-35
  • AS = mainly male
  • axSpA = equal gender
262
Q

Discuss what is seen in MRI and X-ray in AS.

A
  • MRI: inflammation (bone marrow oedema), erosions, sclerosis, ankylosis
  • X-ray: joint space narrowing, sclerosis, erosion, ankylosis, syndesmophytes
263
Q

Which cytokines are associated with enthesitis and axSpA?

A

IL-23, IL-17

264
Q

What are the treatment options for axSpA?

A
  • exercise, physiotherapy
  • NSAIDs
  • TNFa inhibitors
  • IL17 inhibitors
  • surgery
265
Q

Differentiate between the X-ray signs seen in RA and OA.

A

RA: Loss of joint space, Erosions, Soft tissue swelling, Soft bone (osteopenia)
OA: Loss of joint space, Osteophytes, Subchondral sclerosis, Subchondral cysts

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