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PHASE 2A > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Define rheumatology

A

Medical management of musculoskeletal disease

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2
Q

Give 3 causes of inflammatory joint pain?

A
  1. Autoimmune (RA, connective tissue disease, spondyloarthropathy, vasculitis)
  2. Crystal arthritis
  3. Infection
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3
Q

Give 2 causes of non-inflammatory joint pain?

A
  1. Degenerative (OA)

2. Non-degenerative (fibromyalgia)

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4
Q

What are the 5 main signs of inflammation?

A
  1. Red (rubor)
  2. Heat (calor)
  3. Pain (dolor)
  4. Swelling (tumour)
  5. Loss of function
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5
Q

How does inflammatory pain differ from degenerative non-inflammatory pain?

A

Inflammatory pain eases with use

Degenerative pain increases with use

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6
Q

Are you more likely to see swelling in inflammatory or degenerative pain?

A

In inflammatory pain = synovial swelling

Often no swelling in degenerative

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7
Q

What is bone pain?

A

Pain at rest and at night

Can be due to tumour, infection, fracture

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8
Q

What is inflammatory joint pain?

A

Pain and stiffness in joints in the morning, at rest and with use
Can be inflammatory or infective

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9
Q

Name 2 inflammatory markers that can be detected in blood tests

A
  1. ESR (erythrocyte sedimentation rate)

2. CRP

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10
Q

Explain why ESR levels are raised in someone with inflammatory joint pain

A

Inflammation leads to increased fibrinogen –> RBC’s clump together –> RBC’s fall faster = increased ESR

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11
Q

Explain why CRP levels are raised in someone with inflammatory joint pain

A

Inflammation leads to increased IL-6 levels –> CRP produced in response to IL-6 –> CRP raised

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12
Q

Describe the ESR and CRP levels in someone with lupus

A

ESR raised

CRP low

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13
Q

What else might be seen in blood tests for joint pain?

A

Auto-antibodies = immunoglobulins that bind to self antigens

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14
Q

With what tissue type are all spondyloarthropathies conditions associated?

A

HLA B27 tissue type

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15
Q

Give 5 conditions that fall under the term spondyloarthritis

A
  1. Ankylosing spondylitis
  2. Reactive arthritis
  3. Psoriatic arthritis
  4. Enteropathic arthritis
  5. Juvenile idiopathic arthritis
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16
Q

What is the function of HLA B27?

A

Class 1 surface antigen that interacts with MHC and antigen presenting cell

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17
Q

Name 3 theories that can explain why HLAB27 is associated with spondyloarthritis

A
  1. Molecular mimicry
  2. Mis-folding theory
  3. HLAB27 heavy chain hypothesis
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18
Q

Describe the ‘molecular mimicry’ theory for explaining why HLAB27 is associated with spondyloarthritis

A

Infection –> immune response –> infectious agent has peptides very similar to HLAB27 –> autoimmune response triggered against HLAB27

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19
Q

Give the 3 main clinical features of spondyloarthritis

A
  1. Seronegative and HLAB27 association
  2. Axial arthritis
  3. Asymmetrical large joint arthritis
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20
Q

Give 6 signs of spondyloarthritis

A

SPINE ACHE

  1. Sausage digits = dactylics
  2. Psoriasis
  3. Inflammatory back pain
  4. NSAID responsive
  5. Enthesitis
  6. Arthritis
  7. Crohn’s/UC
  8. HLAB27
  9. Eye - uveitis
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21
Q

What is the general treatment for all spondyloarthritis?

A

Initially DMARDs and then biological agents if DMARDS fail (TNF blockers)

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22
Q

Describe the pathophysiology of ankylosing spondylitis

A

Inflammation of spine –> erosive damage –> repair/new bone formation –> irreversible fusion of spine (syndesmophytes)

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23
Q

When does ankylosing spondylitis usually present?

A

In young adults (16-30)

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24
Q

Give 5 signs and symptoms of ankylosing spondylitis

A
  1. Syndesmophytes - vertical vertebral bone growth
  2. Sacroililitis - joint fusion/los of joint space
  3. Kyphosis - spine curved downwards
  4. Enthesitis
  5. Anterior uveitis
  6. BACK PAIN
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25
Q

What investigations might you do in someone who you suspect to have ankylosing spondylitis?

A
  1. X-ray –> sacroilitis and syndesmophytes (bamboo spine)
  2. MRI
  3. HLAB27 test
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26
Q

What is the diagnostic criteria for ankylosing spondylitis?

A
  1. > 3 months back pain
  2. Aged <45 at onset
  3. Plus one of the SPINE ACHE symptoms
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27
Q

What is the treatment for ankylosing spondylitis?

A

Exercise
Long term NSAIDS
TNF inhibitors (infliximab)
Surgery - spinal/hip replacement

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28
Q

Give 3 locations that psoriasis commonly occurs at

A
  1. Elbows
  2. Knees
  3. Fingers
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29
Q

Give 4 clinical features of psoriatic arthritis

A
  1. Asymmetrical oligoarthritis (60%)
  2. Large joint arthritis (15%)
  3. Enthesitis
  4. Dactylitis
  5. Nail changes (pitting, onycholysis)
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30
Q

What investigations might you do in someone you suspect to have psoriatic arthritis?

A

X-ray = pencil cup deformity (erosion) in IPJs

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31
Q

How do you treat psoriatic arthritis?

A

NSAIDs
DMARDS (methotrexate, sulfasalazine)
TNFa inhibitor (infliximab)

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32
Q

What is reactive arthritis?

A

Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually GI or genital

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33
Q

What GI infections are associated with reactive arthritis?

A

Salmonella
Shigella
Yersinia enterocolitica

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34
Q

What GU infections are associated with reactive arthritis?

A

Chlamydia

Ureaplasma urealyticum

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35
Q

What is the triad of symptoms for reactive arthritis?

A
  1. Arthritis
  2. Conjunctivitis
  3. Urethritis
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36
Q

What investigations might you do in someone you suspect to have reactive arthritis?

A

Inflammatory markers - ESR and CRP raised
Stool culture
Infectious serology

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37
Q

How is reactive arthritis treated?

A

Antibiotics to treat infections

NSAIDs and corticosteroids

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38
Q

What type of spondyloarthritis occurs in 20% of patients with IBD?

A

Enteropathic arthritis

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39
Q

What is the criteria for making a clinical diagnosis of juvenile idiopathic arthritis?

A

Joint swelling/stiffness >6 weeks in children <16 and no other cause is identified

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40
Q

What is the aetiology of JIA?

A

Unknown - idiopathic

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41
Q

Why is it important to check the eyes in JIA?

A

Children with JIA are at high risk of developing uveitis

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42
Q

Describe the treatment for JIA

A
  1. Steroid joint injections
  2. NSAIDs
  3. Methotrexate
  4. Systemic steroids
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43
Q

Psoriatic arthritis commonly involved swelling of what joint?

A

DIP joint

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44
Q

Describe a psoriatic plaque

A

Pink, scaling lesion

Occurs on extensor surfaces of limbs

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45
Q

Give 3 differences between RA and psoriatic arthritis

A 
Psoriatic = psoriatic lesions, sausage like swelling around DIP joint, pencil in cup erosion on XR, HLAB27 associated.
RA = hands and wrists typically affected, peri-articular erosion on XR, rheumatoid nodules
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46
Q

Defne osteoporosis

A

A systemic skeletal disease characterised by low bone mass and micro architectural deterioration of bone tissue
Increase in bone fragility and fracture susceptibility

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47
Q

Describe the epidemiology of osteoporosis

A

50% of women and 20% of men over 50 are affected

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48
Q

What 2 factors are important for determining the likelihood of osteoporotic fracture?

A
  1. Propensity to fall –> trauma

2. Bone strength

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49
Q

Give 4 properties of bone that contribute to bone strength

A
  1. Bone mineral density
  2. Bone size
  3. Bone turnover
  4. Bone mice-architecture
  5. Mineralisation
  6. Geometry
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50
Q

Name a hormone that can control osteoclast action and so bone turnover

A

Oestrogen

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51
Q

Why are so many women over 50 affected by osteoporosis?

A

Likely to post-menopausal –> less oestrogen –> osteoclast action isn’t inhibited
High rate of bone turnover –> bone loss and deterioration –> increased fracture risk

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52
Q

What happens to bone micro-architecture as we get older that leads to a reduction intone strength?

A

Trabecular thickness decreases and horizontal connection decrease –> lowers trabecular strength –> increase risk of fracture

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53
Q

Why can RA cause osteoporosis?

A

RA is an inflammatory disease

High levels of IL-6 and TNF –> increase bone resorption

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54
Q

What is the affect of high cortisol levels on bone turnover?

A

Cortisol increases bone turnover –> increase bone resorption and induces osteoblast apoptosis

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55
Q

Give 5 risk factors for osteoporosis

A
  1. Age
  2. Women
  3. Previous fracture
  4. Family history of osteoporosis or fracture
  5. Alcohol
  6. Smoking
  7. Medications
  8. Immobility
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56
Q

Name 3 endocrine disease that can be responsible for causing osteoporosis

A
  1. Hyperthyroidism and primary hyperparathyroidism - TH and PTH increase bone turnover
  2. Cushing’s syndrome - cortisol leads to increase bone resorption and osteoblast apoptosis
  3. Early menopause, male hypogonadism - less oestrogen/testosterone to control bone turnover
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57
Q

Name 2 medications that can cause osteoporosis

A
  1. Glucocorticoids
  2. Depo-povera
  3. GnRH analogues
  4. Androgen deprivation
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58
Q

Give the clinical presentation of osteoporosis

A
  1. Asymptomatic development
  2. Fragile bones
  3. Pathological fractures (femur neck)
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59
Q

What investigations might you do in someone who you suspect to have osteoporosis

A

DEXA scan = bone mineral density scan - gives you a T score

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60
Q

Name 2 areas of the skeleton commonly affected by osteoporosis that the DEXA scan focuses on

A
  1. Lumbar spine

2. Hip

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61
Q

What is a T score?

A

Is a standard deviation that is compared to a gender-matched young adult mean

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62
Q

What is a normal T score?

A

> -1.0

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63
Q

What T score signifies that a patient has osteopenia?

A

-2.5 < t < -1

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64
Q

What T score signifies that a patient has osteoporosis?

A

T < -2.5

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65
Q

What tool can be used to assess someones risk of osteoporotic fracture?

A

FRAX = predicts 10 year fracture chance

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66
Q

Give 2 examples of anti-resorptive treatments used in the management of osteoporosis

A

Decrease osteoclast activity and bone turnover

  1. Bisphosphonates - alendronate, risedronate
  2. HRT - oestrogen
  3. Denosumab
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67
Q

Give an example of an anabolic treatment used in the management of osteoporosis

A

Increase osteoblast activity and bone formation

1. Teriparatide = PTH analogue

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68
Q

Give 3 advantages of HRT

A
  1. Reduces fracture risk
  2. Stops bone loss
  3. Prevent menopausal symptoms
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69
Q

Give 3 disadvantages of HRT

A
  1. Increased risk of breast cancer
  2. Increased risk of stroke and CV disease
  3. Increased risk of thrombo-embolism
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70
Q

How do bisphosphonates work?

A

Inhibit cholesterol formation –> osteoclast apoptosis

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71
Q

Define osteopenia

A

Pre-cursor to osteoporosis characterised by low bone density

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72
Q

Define osteomalacia

A

Poor bone mineralisation leading to soft bone due to lack of Ca2+

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73
Q

What is vasculitis?

A

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

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74
Q

What cells might you see on a histological slide taken form someone with vasculitis?

A

Neutrophils

Giant cells

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75
Q

Describe the pathophysiology of of vasculitis

A

Vessel wall destruction –> perforation and haemorrhage

Endothelial injury –> thrombosis and infarction

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76
Q

Give an example of large vessel vasculitis

A

Giant cell arteritis

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77
Q

Give an example of medium/small vessel vasculitis

A

Wegner’s granulomatosis (Granulomatosis polyangitis)

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78
Q

What is Giant cell arteritis?

A

Granulomatous inflammation of large cerebral arteries as well as other large vessels (aorta) which occurs in association with Polymyalgia rheumatica

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79
Q

Describe the epidemiology of giant cell arteritis

A

Affects those > 50 years old
Incidence increase age
Twice as common in women

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80
Q

Describe the pathophysiology of giant cell arteritis

A

Arteries become inflamed, thicken and can obstruct blood flow

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81
Q

Give 5 symptoms of giant cell arteritis

A
  1. Headache
  2. Temporal artery/scalp tenderness
  3. Jaw claudication
  4. Visual symptoms - vision loss
  5. Systemic symptoms - fever, malaise
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82
Q

How does giant cell arteritis present in a medical emergency?

A

Stroke and blindness

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83
Q

What might you find on clinical investigation in someone with giant cell arteritis?

A
  1. Palpable and tender temporal arteries with reduced pulsation
  2. Sudden monocular visual loss, optic disc is pale and swollen
  3. High ESR
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84
Q

What is the diagnostic criteria for giant cell arteritis?

A
  1. Age >50
  2. New headache
  3. Temporal artery tenderness
  4. Abnormal artery biopsies
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85
Q

What investigations might you do in someone who you suspect has giant cell arteritis?

A
  1. Bloods - high ESR, CRP

2. Temporal artery biopsy

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86
Q

Describe the treatment for giant cell arteritis

A
  1. Corticosteroids - prednisolone
  2. DMARDs - methotrexate (sometimes)
  3. Osteoporosis prophylaxis is important
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87
Q

Give 2 complications of giant cell arteritis

A
  1. Increased CVA risk

2. Visual loss

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88
Q

What does ANCA stand for?

A

Anti-neutrophil cytoplasmic antibodies

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89
Q

What is the pathophysiology of Wegener’s granulomatosis?

A

Necrotising granulomatous vasculitis affecting arterioles and venules
ANCAs can activate primed circulating neutrophils which leads to fibrin deposition in vessel walls and deposition of destructive inflammatory mediators

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90
Q

What organ systems can be affected Wegener’s granulomatosis?

A
  1. URT
  2. Lungs
  3. Kidneys
  4. Skin
  5. Eyes
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91
Q

What is the affect of Wegener’s granulomatosis on the URT?

A
  1. Sinusitis
  2. Otitis
  3. Cough
  4. Haemoptysis
  5. Saddle nose deformity
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92
Q

What is the affect of Wegener’s granulomatosis on the lungs?

A
  1. Pulmonary haemorrhage/nodules

2. Inflammatory infiltrates are seen on X-ray

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93
Q

What is the affect of Wegener’s granulomatosis on the Kidney?

A

Glomerulonephritis –> haem/proteinuria

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94
Q

What is the affect of Wegener’s granulomatosis on the skin?

A

Ulcers

Pulpura

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95
Q

What is the affect of Wegener’s granulomatosis on the eyes?

A

Uveitits
Scleritis
Episcleritis

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96
Q

What investigations might you do in someone you suspect to have Wegener’s Granulomatosis?

A

ANCA testing
Tissue biopsy - (renal biopsy best)
CT - assessment of organ involvement

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97
Q

What is the treatment for Wegener’s Granulomatosis?

A

Glucocorticoids (prednisolone) AND Immunosuppresive drugs (cyclophosphamide OR rituximab) AND plasma exchange for specific complications

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98
Q

Define osteoarthritis

A

A non-inflammatory degenerative disorder of moveable joints characterised by the deterioration of articular cartilage and the formation of new bone

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99
Q

Why does the prevalence of OA increase with age?

A

Due to the cumulative effect of trauma and a decrease in neuromuscular function

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100
Q

Give 5 risk factors for developing OA

A
  1. Genetic predisposition - females, FHx
  2. Trauma
  3. Abnormal biomechanics (e.g. hypermobility)
  4. Occupation (e..g manual labor)
  5. Obesity = pro-inflammatory state
  6. Old age
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101
Q

What are the most important cells responsible for OA?

A

Chondrocytes

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102
Q

Describe the pathophysiology of osteoarthritis

A

Mechanical stress –> cytokine mediated TNF/IL/NO involved

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103
Q

Name the 2 main pathological features of osteoarthritis

A
  1. Cartilage loss

2. Disordered bone repair

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104
Q

Name the 3 joints of the hand that are commonly affected in osteoarthritis

A
  1. Distal interphalangeal joint
  2. Proximal interphalangeal joint
  3. Carpal metacarpal joint
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105
Q

Which surface of the knee is most commonly affected by OA?

A

Medial surface

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106
Q

Give 5 symptoms of OA

A
  1. Morning stiffness (<30 minutes)
  2. Pain - aggravated by activity
  3. Tendernes
  4. Walking and ADLs affected
  5. Joint swelling and bony enlargement
  6. Deformities
  7. Crepitus
  8. Synovitis and effusion
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107
Q

What is the primary investigation used to make a diagnosis of OA?

A

X-ray

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108
Q

Give 5 radiological features associated with OA

A

LOSS

  1. Loss of joint space - articular cartilage destruction
  2. Osteophyte formation - calcified cartilaginous destruction
  3. Subarticular sclerosis - exposed
  4. Subchondral cysts
  5. Abnormalities of bone contour
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109
Q

Describe the non-medical management of osteoarthritis

A
  1. Eduction
  2. Weight loss
  3. Activity and exercise
  4. Physiotherapy and occupational therapy
  5. Walking aids/podiatry
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110
Q

Describe the pharmacological management of OA

A
  1. Pain relief - paracetamol and NSAIDs –> opioids if needed
  2. Intra-articular steroid injections
  3. DMARDs - in inflammatory OA
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111
Q

Describe the surgical management for OA

A

Arthroscopy for loose bodies
Osteotomy (changing bone length)
Arthroplasty (joint replacement)
Fusion (ankle/foot)

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112
Q

Give 3 indications for surgery in OA

A
  1. Significant limitation of function
  2. Uncontrolled pain
  3. Waking at night from pain
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113
Q

A patient complains of ‘locking’, what is the most likely cause?

A

A loose body - bone or cartilage fragment

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114
Q

Nodal osteoarthritis can affect the DIP and PIP joints. What are the 2 terms sued for nodes on these joints?

A
  1. PIP = Bouchard’s nodes

2. DIP = Heberden’s nodes

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115
Q

Give an example of an inherited connective tissue disease

A
  1. Marfan’s syndrome = abnormal fibrillar production

2. Ehler Dnalos syndrome = abnormal collagen production

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116
Q

Give 3 features of Marfan’s syndrome

A
  1. Long limbs
  2. Lens dislocation
  3. Abnormal sternum (pectus excavatum)
  4. Aortic root enlargement
  5. Arachnodactyly - long fingers
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117
Q

Give 2 features of Ehler Danlos syndrome

A
  1. Stretchy skin

2. Joint hypermobility

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118
Q

Give an example of an autoimmune connective tissue disease

A
  1. SLE
  2. Systemic sclerosis (scleroderma)
  3. Sjogren’s syndrome
  4. Dermatomyositis/Polymyositis
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119
Q

What is SLE?

A

Systemic lupus erythematous = inflammatory multi-system disease characterised by the presence of serum anti-nuclear antibodies (ANA)

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120
Q

Describe the epidemiology of SLE

A
  1. 90% of cases are in young women
  2. More common in afro-caribbean
  3. Genetic association
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121
Q

Describe the pathogenesis of SLE

A

Type 3 hypersensitivity reaction = immune complex mediated

Autoantibodies to a variety of auto antigens result in formation and deposition of immune complexes

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122
Q

What can cause thrombosis in SLE?

A

The presence of antiphospholipid antibodies

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123
Q

What autoantibody is specific to SLE?

A

Anti-double stranded DNA

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124
Q

Give 5 symptoms of SLE

A
  1. Rash - photosensitive vs diced vs malar (butterfly rash)
  2. Mouth ulcers
  3. Raynaud’s phenomenon
  4. General - fever, malaise, fatigue
  5. Depression
  6. Lupus nephritis –> proteinuria, renal failure and renal hypertension
  7. Arthritis - symmetrical
  8. Serositis - pleurisy/pleural effusion
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125
Q

What investigations might you do in someone who you suspect has SLE?

A
  1. Blood tests = anaemia, neutropenia, thrombocytopenia, RAISED ESR and NORMAL CRP
  2. Serum autoantibodies - ANA, anti-dsDNA
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126
Q

Describe the non medical treatment for SLE

A

Patient eduction and support
UV protection
Screening for end organ damage
Reduce CV risk factors - smoking cessation

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127
Q

Describe the pharmacological treatment for SLE

A

Corticosteroids
NSAIDs
Antimalarials
Immumnosuppresives/DMARDs
Anticoagulants (for those with antiphospholipid antibodies)
Biological therapy targeting B cells - rituximab

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128
Q

What is systemic sclerosis (scleroderma)?

A

A multi system disease characterised by excess production and accumulation of collagen –> inflammation and vasculopathy

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129
Q

Describe the pathophysiology of scleroderma

A

Various factors cause endothelial lesion and vasculopathy

Excessive collagen deposition –> inflammation and auto-antibody production

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130
Q

Give 5 signs of limited scleroderma

A

CREST

  1. Calcinosis - skin calcium deposits
  2. Raynauds
  3. Esophageal reflux/stricture
  4. Sclerodactyly - thick tight skin on fingers/toes
  5. Telangiectasia - dilated facial spider veins
  6. Pulmonary arterial hypertension
131
Q

Give 4 signs of diffuse scleroderma

A
  1. Proximal scleroderma
  2. Pulmonary fibrosis
  3. Bowel involvement
  4. Myositis
  5. Renal crisis
132
Q

What is a diagnostic test for scleroderma?

A

Centromere autoantibody = diagnostic

133
Q

Describe the management of scleroderma

A
  1. Raynauds = physical protection and vasodilators (nifedipine -CCB)
  2. GORD = PPI (omeprazole) for life
  3. Annual echo and pulmonary function tests to monitor arterial pulmonary pressure
  4. ACEi to prevent renal crisi
134
Q

What is the pathophysiology of sjögren’s syndrome?

A

Lymphatic infiltration of exocrine glands - especially lacrimal and salivary

135
Q

What does sjögren’s syndrome often occur secondary to?

A

Other autoimmune disease –> SLE, RA, scleroderma, primary biliary cirrhosis

136
Q

Give 5 symptoms of sjögren’s syndrome

A
  1. Dry eyes and dry mouth
  2. Inflammatory arthritis
  3. Rash
  4. Neuropathies
  5. Vasculitis
137
Q

Why does someone with sjögren’s syndrome have dry eyes and a dry mouth?

A

There is immunologically mediated destruction of epithelial exocrine glands meaning the lacrimal and salivary glands produce fewer secretions

138
Q

What investigations might you do in someone who you suspect to have sjögren’s syndrome?

A

Serum auto-antibodies –> anti-RO, RF, ANA
Raised immunoglobulins and ESR
Schirmer’s test - ability for eyes to self-hydrate

139
Q

What is the treatment for sjögren’s syndrome?

A

Tear and saliva replacement

Immunosuppression/corticosteroids for systemic complications

140
Q

What is dermatomyositis?

A

A rare disorder of unknown aetiology

Inflammation and necrosis of skeletal muscle fibres and skin

141
Q

Give 3 symptoms of dermatomyositis

A
  1. Rash
  2. Muscle weakness
  3. Lungs are often affected too (e.g. interstitial lung disease)
142
Q

What investigations might you do in someone who you suspect has dermatomyositis?

A
  1. Muscle enzymes raised
  2. Electromyography (EMG)
  3. Muscle/skin biopsy
  4. Screen for malignancy
  5. CXR
143
Q

What is the treatment for dermatomyositis?

A

Steroids - prednisolone

Immunosuppressants

144
Q

What is the name given to inflammation of an entire digit?

A

Dactylitis

145
Q

What class of drugs can cause Raynaud’s?

A

Beta blockers

146
Q

What are the 3 phases of Raynaud’s?

A

White (vasoconstriction) –> Blue (tissue hypoxia) –> red (vasodilation)

147
Q

What class of drugs does Nifedipine fall into and why can is be used to treat Raynaud’s?

A

Nifedipine - CCB

Relaxes blood vessels and stops vasospasm

148
Q

Describe the pathophysiology of septic arthritis

A

Infection produces inflammation in joints

Knee > Hip > Shoulder

149
Q

Give 3 causes of septic arthritis

A
  1. Staphylococcus aureus
  2. Streptococci
  3. Neisseria Gonorrhoea
  4. Gram negative = E. coli, pseudomonas aeruginosa
150
Q

Give 5 risk factors for septic arthritis

A
  1. Prosthetic joints
  2. Old age
  3. IVDU
  4. Immunocompromised
  5. Rheumatoid arthritis
  6. DM
151
Q

Give 4 symptoms of septic arthritis

A
  1. Painful
  2. Red
  3. Swollen
  4. Hot
  5. Fever
152
Q

What investigation would you do to someone you suspect has septic arthritis?

A

Joint fluid aspiration –> culture and microbiology

153
Q

Describe the treatment for septic arthritis

A 
Antibiotics guided by aspirate cultures 
Joint aspiration/drainage 
Splinting and physiotherapy 
Analgesia
Prosthetic joints - debridement --> arthroplasty
154
Q

Define osteomyelitis

A

Bone inflammation secondary to infection

155
Q

Describe the epidemiology of osteomyelitis

A

Increasing incidence of chronic OM

Bimodal age distribution (children and elderly)

156
Q

What can cause osteomyelitis?

A
  1. Staph. aureus
  2. Coagulase negative staph (s. epidermidis)
  3. Aerobic gram negate bacilli (salmonella)
  4. Mycobacterium TB
157
Q

Name 2 predisposing conditions for osteomyelitis

A
  1. Diabetes

2. PVD

158
Q

Osteomyelitis: Describe the 3 routes of infection into bone

A
  1. Direct inoculation of infection to bone (trauma, surgery)
  2. Contagious spread of infection from adjacent tissues to bone
  3. Hematogenous seeding (e.g. due to cannula infection)
159
Q

Osteomyelitis: Who is most likely to be effected by contagious spread of infection?

A

Affects older adults, those with DM, chronic ulcers, vascular disease, arthroplasties

160
Q

What bones are likely to be affected by hematogenous seeding in adults?

A

Vertebrae

161
Q

What bones are likely to be affected by hematogenous seeding in children?

A

Long bones

162
Q

Why do vertebrae tend to be affected by hematogenous seeding in adults?

A

With age, the vertebrae become more vascular meaning bacterial seeding is more likely

163
Q

Why do long bones tend to be affected by hematogenous seeding in children?

A

In children the metaphysis of long bones has a high but slow blood flow and basement membrane are absent meaning bacteria can move from the blood to bone

164
Q

Name a group of people who are at risk of hematogenous osteomyelitis

A

IVDU and other groups at risk from bacteraemia

165
Q

Give 4 host factors that affect the pathogenesis of osteomyelitis

A
  1. Behavioural (risk of trauma)
  2. Vascular supply (arterial disease, DM)
  3. Pre-existing bone/joint problems (RA)
  4. Immune deficiency
166
Q

Acute osteomyelitis: what changes to bone might you see histologically?

A
  1. Inflammatory cells
  2. Oedema
  3. Vascular congestion
  4. Small vessel thrombosis
167
Q

Chronic osteomyelitis: what changes to bone might you see histologically?

A
  1. Necrotic bone - ‘squestra’
  2. New bone formation ‘involucrum’
  3. Neutrophil exudates
  4. Lymphocytes and histiocytes
168
Q

Why does chronic osteomyelitis lead to sequestra and new bone formation?

A

Inflammation in BM increase intramedullary pressure –> exudate into bone cortex –> rupture through periosteum –> interruption of periosteum blood supply –> necrosis –> sequestra –> new bone forms

169
Q

What is acute osteomyelitis associated with?

A

Associated with inflammatory bone changes caused by pathogenic bacteria

170
Q

What is chronic osteomyelitis associated with?

A

Involves bone necrosis

171
Q

Give 3 symptoms of osteomyelitis

A
  1. Slow onset
  2. Dull pain at OM site, aggravated by movement
  3. Systemic = fever, rigors, sweating, malaise
172
Q

Give 3 signs of acute osteomyelitis

A
  1. Tender
  2. Warm
  3. Red swollen area around OM
173
Q

Give 3 signs of chronic osteomyelitis

A
  1. Acute OM signs
  2. Draining sinus tract
  3. Non-healing ulcers/fracture
174
Q

What is the differential diagnosis of osteomyelitis?

A
  1. Cellulitis
  2. Charcot’s joints (sensation loss –> degeneration)
  3. Gout
  4. Fracture
  5. Malignancy
  6. Avascular bone necrosis
175
Q

What investigations might you do on someone who you suspect may have osteomyelitis?

A
  1. Bloods - raised inflammatory markers (CRP, ESR) and WCC
  2. X-rays (cortical erosion, sequestra, sclerosis) and MRI (delineates inflammatory layers, marrow oedema)
  3. Bone biopsy
  4. Blood cultures
176
Q

Describe the usual treatment for osteomyelitis

A

Large dose IV antibiotics tailored to culture findings (S. aureus = flucloxacillin)
Surgical treatment = debridement +/- arthroplasty of joint involved

177
Q

How is the stopping of antibiotics determined in osteomyelitis?

A

Guided by ESR and CRP

178
Q

Give 4 ways in which TB osteomyelitis is different to other osteomyelitis

A
  1. Slower onset
  2. Epidemiology is different
  3. Biopsy is essential - caseating granuloma
  4. Longer Treatment = 12 months
179
Q

Why is osteomyelitis difficult to treat?

A

Antibiotics struggle to penetrate bone and bone has a poor blood supply

180
Q

What is bacteraemia?

A

Bacteria in the blood

181
Q

What is debridement?

A

The removal of damaged tissue

182
Q

What is the most serious complication of arthroplasty surgery?

A

Prosthetic joint infection

183
Q

Give 2 ways in which prosthetic joint infections can be prevented

A
  1. Aseptic environment and laminar air flow

2. Systemic prophylactic antibiotics

184
Q

What investigations might you do on someone who you suspect might have a prosthetic joint infection?

A
  1. Aspirate –> microbiology
  2. Bloods for inflammatory markers and FBC
  3. X-rays
185
Q

What must you never do before aspirating a joint?

A

Never give antibiotics before aspiration

For at least 2 weeks

186
Q

What are the 3 aims of treatment for prosthetic joint infections?

A
  1. Eradicate sepsis
  2. Relieve pain
  3. Restore function
187
Q

What treatment you choose for a patient who has a prosthetic joint infection that is unfit for surgery?

A

Antibiotic suppression

188
Q

What is the gold standard treatment for prosthetic joint infections?

A

Exchange arthroplasty

  • radical debridement of all infected and dead tissue
  • systemic and local antibiotic cover
  • sufficient joint and soft tissue reconstruction
189
Q

What condition must always be rules out in an acutely inflamed joint?

A

Septic arthritis –> aspirate the joint

190
Q

What is rheumatoid arthritis?

A

An auto-inflammatory synovial joint disease

191
Q

Name 3 risk factors of RA

A
  1. Smoking
  2. Women
  3. Other AI conditions
192
Q

Describe the pathophysiology of RA

A
  1. Chronic inflammation - B/T cells and neutrophils infiltrate
  2. Proliferation –> pannus formation (synovium grows out and over cartilage)
  3. Pro-inflammatory cytokines –> proteinases –> cartilage destruction
193
Q

Give 5 symptoms of RA

A
  1. Early morning stiffness (>60 mins)
  2. Pain eases with use
  3. Swelling
  4. General fatigue, malaise
  5. Extra-articular involvment
194
Q

Give 4 signs of RA

A
  1. Symmetrical polyarthorpathy
  2. Deforming –> ulnar deviation, swan neck
  3. Erosion on X-ray
  4. 80% = RF positive
195
Q

RA extra-articular involvement: describe the effect on soft tissues

A

Nodules
Bursitis
Muscle wasting

196
Q

RA extra-articular involvement: describe the effect on the eyes

A

Dry eyes
Scleritis
Episcleritis

197
Q

RA extra-articular involvement: describe the neurological effects

A

Sensory peripheral neuropathy
Entrapment neuropathies (carpal tunnel syndrome)
Instability of cervical spine

198
Q

RA extra-articular involvement: describe the haematological effects

A

Felty’s syndrome (RA + splenomegaly + neutropenia)

Anaemia

199
Q

RA extra-articular involvement: describe the pulmonary effects

A

Pleural effusion

Fibrosing alveolitis

200
Q

RA extra-articular involvement: describe the effects on the heart

A

Pericardial rub

Pericardial effusion

201
Q

RA extra-articular involvement: describe the effects on the kidney

A

Amyloidosis

202
Q

RA extra-articular involvement: describe the effects on the skin

A

Vasculitis - infarcts in nail bed

203
Q

What investigations might you do in someone you suspect has rheumatoid arthritis?

A

Blood for inflammatory markers - ESR and CRP raised
Test for anaemia
Test for RF and Anti-CCP
X-ray

204
Q

What is rheumatoid factor?

A

An antibody against the Fc portion of IgG

205
Q

What is seen on an X-ray of someone with RA?

A

LESS:

  • Loss of joint space (due to cartilage loss)
  • Erosion
  • Soft tissue swelling
  • Soft bones = osteopenia
206
Q

Describe the treatment for rheumatoid arthritis

A
  • NSAIDS and paracetamol
  • Corticosteroids - intra-articular glucocorticoid injections
  • DMARDs (methotrexate)
  • Biological agents (TNF inhibitor - infliximab)
  • Physio and OT
  • Synovectomy
207
Q

What joints tend to be affects in RA?

A

MCP
PIP
Wrist
(DIP often spared)

208
Q

What is gout?

A

Crystal arthritis

209
Q

Describe the epidemiology of gout?

A

Gout is most common in men over 75

Rise in post-menopausal women

210
Q

What joint does gout most commonly affect?

A

Big toe metatarsophalangeal joint

211
Q

Describe the pathophysiology of gout

A

Purine –> (by xanthine oxidase) xanthine –> uric acid –> monosodium rate crystals OR excreted by kidneys
Urate blood/tissue imbalance –> rate crystal formation –> inflammatory response through phagocytic activation

212
Q

Give 3 causes of gout

A

= Hyperuricaemia

  1. Impaired excretion - CKD, diuretics, hypertension
  2. Increased production - hyperlipidaemia
  3. Increased intake - high purine diet = red meat, seafood, fructose, alcohol
213
Q

Name 3 common precipitants of a gout attack

A
  1. Aggressive introduction of hypouricaemic therapy
  2. Alcohol or shellfish binges
  3. Sepsis, MI, acute severe illness
  4. Trauma
214
Q

Name 4 diseases that someone with gout might have an increased risk of developing

A
  1. Hypertension
  2. CV disease - e.g. stroke
  3. Renal disease
  4. Type 2 diabetes
215
Q

Give a symptom of gout

A

Very red, hot, swollen, tender joint (shiny/taut skin)
Tophi
Urate renal stone formation

216
Q

What are tophi?

A

Onion like aggregates of urate crystals with inflammatory cells. Proteolytic enzymes are released –> erosion

217
Q

What investigations might you do in a patient you think has gout?

A

Joint fluid aspirate and microscopy = -ve birefringent needle rate crystals
X-ray = rat bite erosions

218
Q

What is the aim of treatment for gout?

A

To get urate levels < 300 mol/L

219
Q

How would you treat acute gout?

A

Ice packs and rest
NSAIDS
Colchicine = anti-gout medication
Corticosteroids - IM or IA

220
Q

Name 3 treatment options for gout

A
  1. Lifestyle modifications - diet, weight loss, reduce alcohol
  2. Allopurinol (xanthine oxidase inhibitor)
  3. Colchicine or NSAIDs
221
Q

You see a patient with gout who is taking bendroflumethiazide. What drug might you replace this with to help treat their gout?

A

You would switch bendroflumethiazide to cosartan as bendroflumethiazide is a diuretic and so impairs urate excretion

222
Q

Name 6 factors that can cause an acute attack of gout

A
  1. Sudden overload
  2. Cold
  3. Trauma
  4. Sepsis
  5. Dehydration
  6. Drugs
223
Q

A patient presents with an acute mono-arthropathy of their big toe. What are the two main differential diagnoses?

A
  1. Gout

2. Septic arthritis

224
Q

A patient presents with an acute mono-arthropathy of their big toe. What investigations might you do?

A

Joint aspirate
If septic arthritis - high WCC and neutrophilia and bacteria on gram stain
If gout - urate crystals

225
Q

Describe the pathophysiology of pseudogout

A

Calcium pyrophosphate crystals are deposited on joint surfaces
Crystals elicit an acute inflammatory response

226
Q

What can cause pseudogout?

A
  1. Hypo/hyperthyroidism
  2. Haemochromatosis
  3. Diabetes
  4. Magnesium levels
227
Q

Give a symptom of pseudogout

A

Acute, hot and swollen joints

Typically the wrists and knees

228
Q

What investigations might you do in someone you suspect might have pseudogout?

A

Aspiration –> fluid for crystals and blood cultures = positive birefringent rhomboid crystals
X-rays –> can show chondrocalcinosis

229
Q

What is the most likely differential diagnosis for pseudogout?

A

Infection

230
Q

Describe the treatment for pseudogout

A

Colchicine - anti-gout
Aspiration, intra-articular steroid injections
Methotrexate - for inflammation
Surgery if really bad - synovectomy

231
Q

How can you distinguish OA from pseudogout?

A

Pattern of involvement –> Pseudo = wrists, shoulders, ankle, elbows
Marked inflammatory component –> Elevated CRP and ESR
Superimposition of acute attacks

232
Q

What kind of crystals do you see in pseudogout?

A

Positive birefringent calcium pyrophosphate rhomboid crystals

233
Q

What kind of crystals do you see in gout?

A

Monosodium urate crystals = negatively birefringent

234
Q

What kind of crystals fo you see in pseudogout?

A

Calcium pyrophosphate crystals = positively birefringent

235
Q

What is the diagnostic criteria for fibromyalgia?

A

Chronic widespread pain lasting for > 3 months with other causes excluded
Pain is at 11/18 tender point sites

236
Q

Name 4 diseases that fibromyalgia is commonly associated with

A
  1. Depression
  2. Choric fatigue
  3. IBS
  4. Chronic headache
237
Q

Give 4 symptoms of fibromyalgia

A
  1. Neck and back pain
  2. Pain is aggravated by stress, cold and activity
  3. Generalised morning stiffness
  4. Paraesthesia of hands and feet
  5. Profound fatigue
  6. Unrefreshing sleep
238
Q

Give 3 disease that might be included in the differential diagnosis for fibromyalgia

A
  1. Hypothyroidism
  2. SLE
  3. Low vitamin D
239
Q

How is fibromyalgia diagnosed?

A

Everything seems normal
11/18 trigger points
Exclude other diagnoses

240
Q

Describe the management of fibromyalgia

A 
Educate the patient and family 
CBT and exercise programmes
Acupuncture 
Analgesics 
Low dose antidepressants (amitriptyline) and anticonvulsants (pregabalin)
241
Q

What is mechanical back pain?

A

Back pain resulting from physical wear and tear

242
Q

Name 3 causes of mechanical back pain

A
  1. Disc herniation
  2. Cauda equina syndrome
  3. Osteoarhtritis
  4. Fibromyalgia
  5. Osteomyelitis
243
Q

Name 3 risk factors of mechanical back pain

A
  1. Psychological distress
  2. Smoking
  3. Dissatisfaction with work
244
Q

Give 3 symptoms of mechanical back pain

A
  1. Lumbosacral pain
  2. Muscle spasm
  3. Cauda equina syndrome –> sharp localised pain with paraesthesia and related bladder/bowel dysfunction
245
Q

Describe the management of mechanical back pain

A

Prevention = education, exercise
Analgesic ladder = paracetamol –> NSAIDS –> codeine –> low dose amitriptyline
Adjuvant procedures –> physio, acupuncture, CBT

246
Q

Define fracture

A

Soft tissue injury with discontinuity of the bone

247
Q

Describe the 3 initial steps in the management of fractures

A
  1. Reduce the fracture –> restore length, alignment and rotation
  2. Immobilisation
  3. Rehabilitation
248
Q

What are the 4 main stages of fractures healing?

A
  1. Haematoma formation
  2. Fibrocatilaganeous callus formation
  3. Bony callus formation
  4. Bone remodelling
249
Q

Name 4 types of fracture

A
  1. Transverse
  2. Linear
  3. Oblique, non-displaced
  4. Oblique, displaced
  5. Spiral
  6. Greenstick (specific to children)
  7. Comminuted
250
Q

Give 5 potential complications of fractures

A
  1. Contamination (infection)
  2. Compartment syndrome
  3. Damage to surrounding structures
  4. Mal union = bone heals wit deformity
  5. Non union = bone fails to heal
  6. Avascular necrosis
  7. Crush syndrome
  8. Cast problems
251
Q

Why is a neck of femur fracture considered so bad?

A

Cuts off the blood supply to the head of the femur = avascular necrosis of head of femur

252
Q

How does a NOF fracture present?

A

Fall
Groin pain
Inability to weight bare
Externally rotated and short leg (on side of fracture)

253
Q

What is the treatment for a NOF fracture?

A 
ANALGESIA = morphine and regional nerve block 
Intracapsular = Total hip replacement or hemi arthroplasty 
Extracapsular = DHS or cannulated hip screws
254
Q

How are ankle fracture classified?

A

By Weber classification
A = fracture below syndesmosis
B = fracture at level of syndesmosis
C = fracture above level of syndesmosis (worst)

255
Q

What is the treatment for an ankle sprain?

A 
Analgesia
Ice 
Elevation
Early mobilisation
Build up strength around anklet to prevent recurrence
256
Q

How do you treat an open fracture?

A 
Tetanus vaccination 
Antibiotic s
Cover with saline soaked gauge 
Stabilise 
Debridement 
Surgery as soon as X-ray has been done
257
Q

What is compartment syndrome?

A

Increase in intra-compartmental pressure due to build up of fluid –> pressure on veins causing collapse –> collapse of nerves –> pressure on arteries

258
Q

How does compartment syndrome present?

A

Tense compartment with pain disproportionate to injury and the 5 P’s

  1. Pain
  2. Pallor
  3. Perishingly cold
  4. Pulselessness
  5. Paraesthesia
259
Q

What is the treatment of compartment syndrome?

A

Fasciotomy = relieves pressure

260
Q

Why is the ACL so important?

A

Important stabiliser of the knee joint, limits anterior translation of the tibia and also contributes to knee rotational starbility

261
Q

How does cauda equina syndrome present?

A

Bilateral sciatica
Severe or progressive bilateral neurological deficit of legs
Bowel/bladder dysfunction

262
Q

How can you treat cauda equina syndrome?

A

Decompression and discectomy

263
Q

Name the 4 rotator cuff muscles

A

Subscapularis
Supraspinatus
Infraspinatus
Teres minor

264
Q

Define sarcoma

A

A rare tumour of mesenchymal origin

A malignant connective tissue neoplasm

265
Q

What are the red flag symptoms for bone malignancy?

A 
Rest pain
Night pain
Loss of function
Neurological problems 
Weight loss
Growing lump 
Deformity
266
Q

Who are primary bone tumours seen in?

A

Only seen in the young - rare

267
Q

Give 3 primary bone tumours

A
  1. Osteosarcoma
  2. Fibrosarcoma
  3. Chondromas
  4. Ewings tumour
268
Q

What are secondary bone tumours?

A

Metastases from:

  1. Lungs
  2. Breast
  3. Prostate
  4. Thyroid
  5. Kidney
269
Q

What investigations might you do in someone you suspect has bone cancer?

A 
Bloods --> FBC, U/E's, Hypercalcaemia, raised alkaline phosphate
X-ray --> bone-lesion interaction
MRI --> soft tissue/bone marrow change
CT --> bone quality and staging
PET
Bone scan --> skeletal masses
USS --> Soft tissue masses 
Biopsy 
Skeletal isotope scan
270
Q

What might you seen on an X-ray of someone with bone cancer?

A

Onion skin/sunburst appearance = Ewings

Colman’s triangle = osteosarcoma, Ewings, GCT, Osteomyelitis, metastasis

271
Q

What staging is used for bone cancers?

A

Enneking grading

272
Q

How are malignant bone cancers staged using Enneking grading?

A 
G1 = Histologically benign
G2 = Low grade
G3 = High grade
A = intracompartmental
B = extracompartmental
273
Q

How are benign bone cancers staged using Enneking grading?

A 
G1 = Latent
G2 = Active 
G3 = Agressive
274
Q

How are bone cancers treated?

A

MDT management
Benign = NSAIDS
Bisphosphonates (alendronate) - symptomatic help
Malignancy = surgical excision –> radio/chemotherapy

275
Q

Give 4 local complications with surgery for bone cancers

A
  1. Haematoma
  2. Loss of function
  3. Infection
  4. Local recurrence
276
Q

Where do osteosarcomas usually present?

A

Knee - distal femur, proximal tibia

277
Q

What is an osteosarcoma?

A

Malignant tumour of bone

Spindle cell neoplasm that produce osteoid

278
Q

Give 3 features of osteosarcoma

A
  1. Fast growing
  2. Aggressive
  3. Typically affects 15-19 year olds
279
Q

What is a chondrosarcoma?

A

A malignant neoplasm of cartilage

280
Q

Where does a chondrosarcoma usually present?

A

Pelvis

281
Q

Name a boney sarcoma that responds well to chemotherapy

A

Ewings sarcoma

282
Q

Where does Ewings sarcoma arise from?

A

Neural crest cells

283
Q

Boney sarcomas make up what percentage of overall sarcomas?

A 
20% = boney 
80% = soft tissue
284
Q

Name 3 soft tissue sarcomas

A
  1. Liposarcoma = malignant neoplasm of adipose tissue
  2. Leiomyosarcoma = malignant neoplasm of smooth muscle
  3. Rhabdomyosarcoma = malignant neoplasm of skeletal muscle
285
Q

If it not possible to get a wide margin when resecting a sarcoma what might you do?

A

Give adjuvant radiotherapy

286
Q

Name 2 NSAIDs

A
  1. Ibuprofen

2. Naproxen

287
Q

Give 3 side effects of NSAIDs

A
  1. Peptic ulcer disease
  2. Renal failure
  3. Increased risk of MI and CV disease
288
Q

What can you do to reduce the risk of gastric ulcers and bleeding in someone taking NSAIDs?

A
  1. Co-prescribe PPI

2. Prescribe low doses and short courses

289
Q

Give 5 potential side effects of steroids

A
  1. Diabetes
  2. Muscle wasting
  3. Osteoporosis
  4. Fat redistribution
  5. Skin atrophy
  6. Hypertension
  7. Acne
  8. Infection risk
290
Q

How do DMARDs work?

A

Non-specific inhibition of inflammatory cytokines cascade = reduces joint pain, stiffness and swelling

291
Q

Give an example of a DMARD

A

Methotrexate = gold standard
Hydroxycholoquine
Sulfasalazine

292
Q

How often should methotrexate be taken?

A

Once weekly

293
Q

Give 3 potential side effects of methotrexate

A
  1. Bone marrow suppression
  2. Abnormal liver enzymes
  3. Nausea
  4. Diarrhoea
  5. Teratogenic
294
Q

What can be co-prescribed with methotrexate to reduce the risk of side effects?

A

Folic acid

295
Q

What are cytokines?

A

Short acting hormones

296
Q

Name a TNF blocker

A

Infliximab

Adalimumab

297
Q

Name a monoclonal antibody that binds to CD20 on B cells

A

Rituximab - binds to CD 20 –> B cell depletion

298
Q

Describe the mechanism of action of infliximab

A

Inhibits T cell activation

299
Q

How does alendronate work?

A

Reduces bone turnover by inhibiting osteoclast mediated bone resorption

300
Q

What class of drug is alendronate?

A

Bisphosphonate

301
Q

Name 2 drugs that act on the HMGcoA pathway

A
  1. Bisphosphonates - alendronate

2. Statins - simvistatin

302
Q

Which of the following is a typical clinical feature of osteoarthritis?

a. 60 minutes of early morning stiffness
b. Painful, swelling across the metacarpophalangeal joints and PIP joints
c. Pain in 1st carpometacarpal joints
d. Mobile subcutaneous nodules and points of pressure
e. Alternating buttock pain

A

c. Pain in 1st carpometacarpal joints

Morning stiffness is only 15 mins ish in OA
OA = CMC and DIP joints

303
Q

Which of the following is an extra-articular manifestation of rheumatoid arthritis?

a. Subcutaneous nodules
b. Episcleritis
c. Peripheral sensory neuropathy
d. Pericardial effusion
e. All of the above

A

e. All of the above

304
Q

Which of the following is a classical feature of rheumatoid arthritis on X-ray?

a. Peri-articular sclerosis
b. Sub-chondral cysts
c. Osteophytes
d. Peri-articular erosions
e. New bone formation

A

d. Peri-articular erosions Inflammatory cytokines causing lysis of bone causing joint damage

Peri-articular sclerosis = OA
Sub-chondral cysts = OA
Osteophytes = OA
New bone formation = SpAs)

305
Q

A 53-year-old man presents to you with a 3-day history of pain in his lower ache. The pain started spontaneously, and he first noticed it at work. He works as a builder and has been unable to go to work for the last 3 days and is keen to have a sick note. Physical examination reveals him to be slightly overweight with a BMI of 29, but there are no neurological deficits or spinal deformity and the pain is not easily localised on examination. Which of the following describe the best management?

a. Given his age, he should be referred to a specialist
b. He should be sent for an x-ray to look for any pathological changes in his spine
c. He should not be given a sick note, and advised to return to work straight away
d. He should be reassured and advised to take simple analgesics and return to normal activity as soon as he can manage
e. He should be advised to seek other employment

A

d. He should be reassured and advised to take simple analgesics and return to normal activity as soon as he can manage

306
Q

For a lytic tumour to be visible on X-ray, it must have lost:

a. Greater than 6% bone density
b. Greater than 16% bone density
c. Greater than 60% bone density
d. Greater than 90% bone density
e. 100% bone density

A

c. Greater than 60% bone density

307
Q

A 57-year-old man presents with a 3-day history of a painful 1st MTP joint. ON examination the area is red and very warm. He has a BMI of 32 and hypertension and has had identical episodes before. Which of the following dietary changes would reduce his risk of future similar episodes?

a. Diet with a high red meat content
b. A diet rich in dairy products
c. Drinking >5 cans of non-diet fizzy drinks per day
d. A diet rich in sugary foodstuffs
e. Switching form drinking beer to drinking larger

A

b. A diet rich in dairy products

= GOUT

308
Q

Which of the following is not an autoimmune connective tissue disease?

a. Systemic lupus erythematosus
b. Ehler Danlos syndrome
c. Primary Sjogren’s syndrome
d. Systemic sclerosis
e. Dermatomyositis

A

b. Ehler Danlos syndrome (inherited connective tissue disease)

309
Q

A 23-year-old woman presents with mouth ulcers, fever, painful white fingers and pleuritic chest pain. She is antinuclear antibody (ANA) positive, her ESR is 52 (0-15), and her WCC is low (leucopenic). Which of the following features would you not expect to be associate with her illness?

a. Deforming arthritis
b. Photosensitive rash
c. Seizures
d. Pulmonary embolism
e. Thrombocytosis

A

e. Thrombocytosis

= SLE so would be thrombocytopenia

310
Q

Which of the following is used in the treatment of SLE?

a. Anti-TNF
b. Anti-malarials
c. Ustekinumab (IL12/23 blocker)
d. Sulfasalazine
e. Allopurinol

A

b. Anti-malarials (hydroxycloroquinine)

Others
Ustekinumab (IL12/23 blocker) = SpAs
Sulfasalazine = RA
Allopurinol = Gout

311
Q

An adult male present with a 6-week history of right sided headache. General malaise, early morning stiffness, and pain in his jaw when eating. His CRP is 63 (0-5), ESR 78 (0-15). Which of the following is true about his underlying disease?

a. It is associated with ANCA positivity
b. It typically affects those between 50 and 60 years old
c. It can present with acute sight loss
d. It rarely responds to corticosteroids
e. It is a vasculitis affecting small blood vessels

A

c. It can present with acute sight loss

GIANT CELL ARTERITIS (VASCULITIS)

ANCA = small vessel vasculitis
Giant cell arteritis = patients 70-75 years old

312
Q

Which of the following is now a rare cause for joint infections in infants, due to the standard childhood immunisation schedule in the UK?

a. Staphylococcus Aureus
b. Gp A (B haemolytic) streptococcus
c. Varicella Zoster
d. Rubella
e. Haemophilus Influenzae

A

e. Haemophilus Influenzae

313
Q

A 64-year-old women with T2DM has been struggling with cellulitis of her right forefoot for 4 weeks. After making no progress with oral antibiotics, she has now had 14 days of IV flucloxacillin and co-amoxiclavulanic acid but then pain and erythema persist, and her CRP has only fallen to 47 from its peak of 91. What is the next most appropriate investigation?

a. Blood cultures
b. MRI right forefoot
c. Plain x-ray right forefoot
d. Skin biopsy of right forefoot
e. USS of right forefoot

A

c. Plain x-ray right forefoot

314
Q

Which of the following is a non-inflammatory cause of joint pain?

a. RA
b. Septic arthritis
c. SpAs
d. Fibromyalgia
e. Gout

A

d. Fibromyalgia

315
Q

Which of these is not a feature of RA?

a. NSAIDs help
b. Pain eases with use
c. Effects the DIP joints
d. Pain lasts for an hour or so in the morning
e. Ulnar deviation

A

c. Effects the DIP joints

Symptom of OA

316
Q

Alendronic acid is a bisphosphate used in treatment of osteoporosis. What is the MOA?

a. Cause increased bone deposition
b. Cause reactivation of the metaphysis and epiphysis
c. Inhibit osteoclast activity and cause osteoclast apoptosis
d. Reduce the signalling pathway between osteoblasts and clasts by increasing RANK ligand
e. Increase removal of calcium into the haversian canal within bone

A

c. Inhibit osteoclast activity and cause osteoclast apoptosis

317
Q

Pain big toe = gout. Joint aspiration – what is seen to confirm diagnosis?

a. Tophi
b. Needle shaped crystals which are +ve birefringent
c. Needle shaped crystals which are -ve birefringent
d. Rhomboid shaped crystals which are +ve birefringent
e. Rhomboid shaped crystals which are -ve birefringent

A

c. Needle shaped crystals which are -ve birefringent = Gout

PSEUDOGOUT = Rhomboid shaped crystals which are +ve birefringent

318
Q

3 weeks stiff and painful knee, urethritis and conjunctivitis. What is the most likely cause?

a. Staphylococcus aureus
b. E. coli
c. Streptococcus pneumonia
d. Haemophilus influenzae
e. Chlamydia

A

e. Chlamydia

Reactive arthritis symptoms –> often caused by STI

319
Q

Aching hand arm and pins and needles in thumb, index and middle fingers. Shaking his hand seems to help. What is it?

a. Cervical spine fracture
b. Compression of median
c. Compression of radial
d. C8-T1 lesion
e. Compression of ulnar

A

b. Compression of median = Carpal tunnel syndrome

320
Q

Ankylosing spondylitis, what tissue type is associate with this condition?

a. HLA DQ2
b. HLA B27
c. HLA DR3
d. HLA DR2
e. HLA AD6

A

b. HLA B27

321
Q

Which is most common cause of osteomyelitis?

a. Strep pneumonia
b. Staph aureus
c. Strep pyogens
d. Mycobacterium TB
e. Haemophilus influenzae

A

b. Staph aureus

322
Q

Lupus –> blood test reveal what?

a. Anti-DsRNA positive
b. Raised ESR and CRP
c. Raised ESR but normal CRP
d. ANCA positive
e. ANA negative

A

c. Raised ESR but normal CRP

323
Q

DEXA scan with T score -1.6, what does this mean?

a. Normal
b. Osteopenia
c. Osteoporosis
d. Severe osteoporosis
e. Paget’s disease

A

b. Osteopenia

PHASE 2A (16 decks)

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