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Phase 2a > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What is osteoarthritis?

A

Non-inflammatory wear and tear of joints resulting from loss of cartilage

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2
Q

Describe the epidemiology of osteoarthritis

A
  • Most common type of arthritis
  • More common in females
  • More common in elderly
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3
Q

What are 6 risk factors for osteoarthritis?

A
  1. Obesity
  2. Age
  3. Female
  4. Family history
  5. Trauma
  6. Occupations associated with manual labour
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4
Q

Describe the pathophysiology of osteoarthritis

A
  • Imbalance between cartilage being worn down and the chondrocytes replacing it
  • Usually occurs in larger, weight-bearing synovial joints e.g. hips and knees
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5
Q

What are 3 common symptoms of osteoarthritis?

A
  1. Joint pain exacerbated by exercise
  2. Joint stiffness after rest (transient in morning)
  3. Reduced functionality (limited joint movement)
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6
Q

What are 2 additional symptoms of osteoarthritis?

A

Bone swellings in fingers:
- Herberden’s node (in distal interphalangeal joints)
- Bouchard’s node (in proximal interphalangeal joints)

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7
Q

What is the investigation for patients with osteoarthritis and the 4 most common findings?

A

X ray (LOSS):
- L - loss of joint space
- O - osteophytes formation
- S - subchondral sclerosis (increased density of bone along joint)
- S - subchondral cysts (fluid-filled holes in bone)

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8
Q

What is the treatment for osteoarthritis?

A
  • Pain relief (start with paracetamol and work up analgesics ladder)
  • Cortisol injections
  • Physiotherapy
  • Weight loss
  • Joint replacement (must lose weight)
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9
Q

What is the difference between pain in patients with osteoarthritis vs rheumatoid arthritis?

A

Osteoarthritis - worse during/after exercise
Rheumatoid arthritis - better during/after exercise

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10
Q

What is rheumatoid arthritis?

A

Autoimmune inflammation of synovial joints - symmetrical polyarthritis

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11
Q

Describe the epidemiology of rheumatoid arthritis

A
  • More common in females (3:1)
  • Most often develops younger/middle age
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12
Q

What are 4 risk factors for rheumatoid arthritis?

A
  1. Genetics - HLA DR4 gene (often present in RF positive patients)
  2. Genetics - HLA DR1 (often present in RA patients)
  3. Rheumatoid factor (RF)
  4. Cyclic citrullinated peptide antibodies (anti-CCP)
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13
Q

What does rheumatoid factor (RF) do?

A

Autoantibody that targets Fc portion of IgG antibody, triggering activation of the immune system

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14
Q

Describe the pathophysiology of rheumatoid arthritis

A
  • Autoimmune destruction of synovium
  • Inflammation causes damage to bone cartilage, tendons and ligaments
  • Most common joints affected are PIP joints and MCP joints (HARDLY EVER DIP JOINTS - if these are affected, it is usually always osteoarthritis)
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15
Q

What are 5 signs of rheumatoid arthritis?

A
  1. ‘Boggy’ feeling when palpating synovium around joints
  2. Z-shaped deformity of thumb
  3. Swan neck deformity (hyperextended PIP with flexed DIP)
  4. Boutonnieres deformity (hyperextended DIP with flexed PIP)
  5. Ulnar deviation of fingers at knuckle
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16
Q

What are 5 symptoms of rheumatoid arthritis?

A
  1. Joint pain/swelling/stiffness (pain worse after rest/in the mornings and improves with activity)
  2. Fatigue
  3. Weight loss
  4. Flu-like illness
  5. Muscle aches/weakness
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17
Q

What is palindromic rheumatism?

A
  • Self-limiting short episodes of inflammatory arthritis with joint pain/stiffness/swelling
  • Lasts 1-2 days and then completely resolves itself
  • May progress to full RA (greater risk if have RF and anti-CCP antibodies)
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18
Q

What are 2 investigations for patients with rheumatoid arthritis?

A
  1. X-ray
  2. Bloods
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19
Q

What does an x-ray show in patients with rheumatoid arthritis?

A

LOES:
- L - lost joint space
- O - osteopenia (reduced bone density)
- E - erosion
- S - soft tissue swelling

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20
Q

What do bloods show in patients with rheumatoid arthritis?

A
  • Anti-CCP antibodies (more sensitive and specific than RF)
  • RF
  • Raised ESR/CRP
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21
Q

What is the treatment for rheumatoid arthritis?

A
  • Physiotherapy
  • Ibuprofen/NSAIDs
  • Steroids
  • Methotrexate
  • Rituximab (if others not working)
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22
Q

What are 3 complications of rheumatoid arthritis?

A
  1. Atlantoaxial subluxation –> cervical spinal cord compression
  2. Inflammation of tendons increases risk of tendon rupture
  3. Lung involvement e.g. interstitial lung disease, fibrosis etc.
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23
Q

Describe atlantoaxial subluxation

A
  • Local synovitis and damage to ligaments and bursa around odontoid peg of axis (C2) and atlas (C1)
  • This causes the axis (C2) and odontoid peg to shift within the atlas (C1)
  • Subluxation causes cervical spinal cord compression (weakness/loss of sensation) and is an EMERGENCY
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24
Q

What must be excluded when investigating patients with gout/pseudogout?

A

Septic arthritis (life threatening - medical emergency)

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25
Q

What is the difference between gout and pseudogout?

A

Both crystal arthropathies
Gout - deposition of monosodium urate crystals within joints
Pseudogout - deposition of calcium pyrophosphate crystals within joints

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26
Q

What is crystal arthropathy/arthritis?

A

Joint disorder caused by deposits of crystals in joints and soft tissues around them

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27
Q

Describe the difference in epidemiology between gout and pseudogout

A

Gout - more common in males
Pseudogout - more common in females

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28
Q

What are 7 risk factors for gout?

A
  1. Male
  2. Obesity
  3. High purine diet (meat/seafood)
  4. Alcohol
  5. Diuretics
  6. Existing CVD/kidney disease
  7. Family history
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29
Q

What are 4 risk factors for pseudogout?

A
  1. Hyperthyroidism
  2. Hyperparathyroidism
  3. Excess iron/calcium
  4. Female
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30
Q

Describe the pathophysiology of gout

A
  • Deposition of monosodium urate crystals within joints
  • Most affected joints are metatarsophalangeal/carpometacarpal joints and wrists
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31
Q

Describe the pathophysiology of pseudogout

A
  • Damage to joints causes deposition of calcium pyrophosphate crystals within joints
  • Most affected joints are knees, shoulders, wrists and hips
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32
Q

What is the main sign of gout?

A

Gouty tophi:
- Subcutaneous deposits of uric acid
- Most commonly in small joints (DIP joints) and connective tissue of hands, elbows and ears

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33
Q

What is the main symptom of gout and pseudogout?

A

Hot, swollen, painful, stiff joint (gout - 1st metatarsal/DIP joint, pseudogout - knee)

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34
Q

What are 3 investigations for patients with gout and pseudogout?

A
  1. Joint aspiration (both)
  2. X-ray (both)
  3. Bloods (gout)
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35
Q

Describe the difference in joint aspiration results between gout and pseudogout

A
  • No bacterial growth (both)
  • Monosodium crystals (gout)/calcium pyrophosphate crystals (pseudogout)
  • Crystals are needle shaped (gout)/rhomboid shaped (pseudogout)
  • Birefringence (under polarised light) = negative (gout), positive (pseudogout)
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36
Q

What do bloods show in patients with gout?

A

Hyperuricaemia

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37
Q

What does an x-ray look like in patients with gout?

A
  • Space between joint is typically maintained
  • Lytic lesions in bone
  • Punched out erosions (which may have sclerotic borders with overhanging edges)
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38
Q

What does an x-ray look like in patients with pseudogout?

A
  • Chondrocalcinosis (thin white line in the middle of the joint space due to calcium deposition)
  • LOSS (loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts)
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39
Q

What is the treatment for gout?

A
  • Lifestyle changes (e.g. losing weight, staying hydrated, reducing alcohol/purine-based food intake)
  • NSAIDs (first line)
  • Colchicine
  • Allopurinol
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40
Q

What is the treatment for pseudogout?

A

Symptoms usually resolve spontaneously over several weeks
Symptomatic management:
- NSAIDs
- Colchicine
- Joint aspiration
- Steroid injections/oral steroids
- Joint washout (arthrocentesis - in severe cases)

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41
Q

When is colchicine used in patients with gout/pseudogout?

A

Used in patients that cannot have NSAIDs e.g. patients with renal impairment or significant heart disease

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42
Q

What is allopurinol and what does it do?

A

Xanthine oxidase inhibitor - reduces uric acid production

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43
Q

What are 2 complications of gout?

A
  1. Infection in gouty tophi
  2. Destruction of joint
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44
Q

What is osteoporosis/osteopenia?

A

Osteoporosis - reduction in bone density
Osteopenia - less severe reduction in bone density than osteoporosis

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45
Q

Describe the epidemiology of osteoporosis/osteopenia

A
  • More common in females
  • More common in elderly
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46
Q

What are 9 risk factors for osteoporosis/osteopenia?

A

SHATTERED:
S - steroid use
H - hyperthyroidism, hyperparathyroidism, hypercalciuria
A - alcohol/tobacco use
T - thin (BMI <18.5)
T - testosterone low
E - early menopause
R - renal/liver failure
E - erosive/inflammatory bone disease
D - dietary low calcium/malabsorption & Diabetes type I

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47
Q

What are 4 other groups of medications that can increase the risk of osteoporosis/osteopenia?

A
  1. SSRIs
  2. PPIs
  3. Anti-epileptics
  4. Anti-oestrogens
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48
Q

Describe the pathophysiology of osteoporosis/osteopenia

A
  • Decreased bone mass/density and micro-architectural deterioration
  • Increase in bone fragility and susceptibility to fracture
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49
Q

What are 2 investigations for patients with osteoporosis/osteopenia?

A
  1. FRAX score
  2. Bone mineral density (BMD) using DEXA (dual-energy x-ray absorptiometry) scan
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50
Q

What does a FRAX score tell us?

A

Predicts the risk of a major osteoporotic or hip fracture over the next 10 years

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51
Q

DEXA scans look at BMD and calculate a Z score and a T score, what is a Z score?

A

Tells us the number of standard deviations that a patient’s bone density falls below the mean for their age

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52
Q

DEXA scans look at BMD and calculate a Z score and a T score, what is a T score?

A

Tells us the number of standard deviations that a patient’s bone density falls below the mean for a healthy young adult
T score at hip:
- >-1 = normal
- -1 to -2.5 = osteopenia
- <-2.5 = osteoporosis

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53
Q

What is the treatment for osteoporosis/osteopenia?

A
  • Lifestyle changes (exercise, maintain healthy weight, avoid falls, smoking cessation, reducing alcohol consumption)
  • Vitamin D and calcium supplements
  • Bisphosphonates e.g. alendronate, risendronate, zolendronic acid
  • Denosumab (alternative to bisphosphonates)
  • HRT
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54
Q

What do bisphosphonates do?

A

Interfere with osteoclasts and reduce their activity which slows down the breakdown of bone (slows down bone reabsorption)

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55
Q

What are 4 key side effects of bisphosphonates?

A
  1. Reflux and oesophageal erosions
  2. Atypical fractures
  3. Osteonecrosis of jaw
  4. Osteonecrosis of external auditory canal
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56
Q

How are reflux and oesophageal erosions prevented in patients taking bisphosphonates?

A

Patients advised to take them on an empty stomach, sitting upright for 30 minutes before moving/eating

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57
Q

What is fibromyalgia?

A

Chronic persistent musculoskeletal pain with unknown cause (non-specific muscular disorder)

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58
Q

Describe the epidemiology of fibromyalgia

A
  • More common in women
  • Usually presents around ages 20-50
  • More common in people with poorer socioeconomic statuses
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59
Q

What are 8 risk factors/associations for fibromyalgia?

A
  1. Female
  2. Middle aged
  3. Low household income
  4. Divorced
  5. IBS
  6. Chronic headache
  7. Depression
  8. Chronic fatigue syndrome
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60
Q

What are 4 symptoms of fibromyalgia?

A
  1. Fatigue
  2. Brain fog
  3. Pain (worse with stress and cold weather)
  4. Morning stiffness
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61
Q

What are 2 investigations for patients with fibromyalgia?

A
  1. Exclude all other differentials with bloods and imaging
  2. 11 tender points in 9 pairs of sites for >6 months
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62
Q

What is the treatment for fibromyalgia?

A
  • Exercise
  • Relaxation
  • Analgesia e.g. paracetamol, tramadol, codeine
  • CBT
  • TCAs e.g. amitriptyline
  • Pregabalin (anti-convulsant)
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63
Q

What are 4 complications of fibromyalgia?

A
  1. Worse quality of life
  2. Anxiety/depression
  3. Insomnia
  4. Opiate addiction
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64
Q

What is Sjogren’s syndrome?

A

Autoimmune destruction of exocrine glands (especially lacrimal and salivary glands)

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65
Q

Describe the epidemiology of Sjogren’s syndrome

A

More common in females

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66
Q

What are 3 causes of Sjogren’s syndrome?

A

Primary = idiopathic
Secondary = develops as a complication of SLE or RA

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67
Q

What are 3 risk factors for Sjogren’s syndrome?

A
  1. Family history (first degree relative = 7x increased risk)
  2. Female
  3. > 40 years
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68
Q

What is the main symptom of Sjogren’s syndrome?

A

Dry mucous membranes i.e. dry mouth/eyes/vagina

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69
Q

What are 2 investigations for patients with Sjogren’s syndrome?

A
  1. Anti-Ro and anti-La antibodies
  2. Schirmer test (tears travel <10mm on filter paper = lack of tears)
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70
Q

What is the treatment for Sjogren’s syndrome?

A
  • Artificial tears/saliva
  • Vaginal lubricants
  • Hydroxychloroquine (used to halt progression)
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71
Q

What are 3 common complications of Sjogren’s syndrome?

A
  1. Eye infections (conjunctivitis, corneal ulcers)
  2. Oral problems (dental cavities, candida infections)
  3. Vaginal problems (candidiasis, sexual dysfunction)
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72
Q

What are 5 rare complications of Sjogren’s syndrome?

A
  1. Pneumonia and bronchiectasis
  2. Non-Hodgkin’s lymphoma
  3. Peripheral neuropathy
  4. Vasculitis
  5. Renal impairment
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73
Q

What is vasculitis?

A

Autoimmune disease that causes inflammation of the blood vessel walls

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74
Q

What are the 4 types of small vessel vasculitis?

A
  1. Henoch-Schonlein Purpura (HSP)
  2. Microscopic polyangiitis
  3. Granulomatosis with polyangiitis (Wegner’s granulomatosis)
  4. Eosinophilic granulomatosis with polyangiitis (Churg-Straus syndrome)
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75
Q

What are the 3 types of medium vessel vasculitis?

A
  1. Eosinophilic granulomatosis with polyangiitis (Churg-Straus syndrome)
  2. Polyarteritis nodosa
  3. Kawasaki disease
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76
Q

What are the 2 types of large vessel vasculitis?

A
  1. Giant cell arteritis
  2. Takayasu’s arteritis
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77
Q

What are 3 general signs of vasculitis?

A
  1. Renal impairment
  2. Anterior uveitis and scleritis
  3. Hypertension
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78
Q

What are 4 general symptoms of vasculitis?

A
  1. Purpura
  2. Joint/muscle pain
  3. Peripheral neuropathy
  4. GI disturbances (diarrhoea, bleeding, abdominal pain)
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79
Q

What are 5 systemic presentations of vasculitis?

A
  1. Fever
  2. Malaise
  3. Fatigue
  4. Weight loss/anorexia
  5. Anaemia
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80
Q

What investigation is usually done for all types of vasculitis?

A

Bloods = inflammatory markers ESR and CRP = raised

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81
Q

What is the standard treatment for vasculitis?

A

Corticosteroids and immunosuppressants e.g. prednisolone + cyclophosphamide

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82
Q

What are the main steroid options for vasculitis?

A
  • Oral e.g. prednisolone
  • IV e.g. hydrocortisone
  • Nasal spray for nasal symptoms
  • Inhaled for lung involvement
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83
Q

What are the main immunosuppressant options for vasculitis?

A
  • Cyclophosphamide
  • Methotrexate
  • Azathioprine
  • Rituximab (and other monoclonal antibodies)
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84
Q

Which 2 types of vasculitis are usually treated differently and why?

A

Henoch-Schonlein Purpura (HSP) and Kawasaki disease –> most often affects children

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85
Q

What is Henoch-Schonlein Purpura (HSP)?

A

Small vessel vasculitis that occurs due to IgA deposits in blood vessels

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86
Q

Describe the epidemiology of HSP

A

Commonly presents in children <10 years

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87
Q

Describe the pathophysiology of HSP

A
  • IgA deposits in the blood vessels of organs e.g. skin, kidneys, GI tract
  • Often triggered by gastroenteritis or an upper airway infection (e.g. tonsilitis)
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88
Q

What are 4 clinical presentations of HSP?

A
  1. Symmetrical purpura on lower limbs/buttocks
  2. Joint pain
  3. Abdominal pain
  4. Renal involvement (HTN)
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89
Q

What is the treatment for HSP?

A
  • Typically supportive e.g. analgesia, rest, hydration
  • Patients without kidney involvement usually recover within 4-6 weeks
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90
Q

What are 2 complications of HSP?

A
  1. 1/3 of patients have a recurrence within 6 months
  2. 1% of patients go on to develop end stage renal failure
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91
Q

What is microscopic polyangiitis?

A

A type of small vessel vasculitis

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92
Q

What are 3 clinical presentations of microscopic polyangiitis?

A
  1. Renal failure (main feature)
  2. Shortness of breath
  3. Haemoptysis
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93
Q

What are 2 investigations for microscopic polyangiitis?

A
  1. Perinuclear anti-neutrophil cytoplasmic antibodies (p-ANCA) blood tests (a.k.a anti-MPO antibodies)
  2. No granulomas on histology
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94
Q

What is granulomatosis with polyangiitis?

A

Small vessel vasculitis that affects the respiratory tract and kidneys

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95
Q

What is granulomatosis with polyangiitis also known as?

A

Wegener’s Granulomatosis

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96
Q

What are 5 clinical presentations of granulomatosis with polyangiitis in the upper respiratory tract?

A
  1. Saddle-shaped nose (due to perforated nasal septum - MAIN SIGN)
  2. Epistaxis
  3. Crusty nasal secretions
  4. Hearing loss
  5. Sinusitis
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97
Q

What are 4 clinical presentations of granulomatosis with polyangiitis in the lungs/kidneys?

A
  1. Cough
  2. Wheezing
  3. Haemoptysis
  4. Rapidly progressing glomerulonephritis
    (Often misdiagnosed as pneumonia in lungs)
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98
Q

What are 2 investigations for granulomatosis with polyangiitis?

A
  1. Anti-neutrophil cytoplasmic antibodies antibodies (c-ANCA) blood tests (a.k.a anti-PR3 antibodies)
  2. Histology shows granulomas
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99
Q

What is eosinophilic granulomatosis with polyangiitis?

A

Small and medium vessel vasculitis most often associated with lung and skin problems (can also affect kidneys)

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100
Q

What is eosinophilic granulomatosis with polyangiitis also known as?

A

Churg-Straus syndrome

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101
Q

Describe the epidemiology of eosinophilic granulomatosis with polyangiitis

A

Usually presents in late teenage years/early adulthood

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102
Q

What is a clinical presentation of eosinophilic granulomatosis with polyangiitis?

A

Severe asthma

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103
Q

What are 2 investigations for eosinophilic granulomatosis with polyangiitis?

A
  1. Anti-neutrophil cytoplasmic antibodies (p-ANCA) blood tests (a.k.a anti-MPO antibodies)
  2. FBC = elevated eosinophil levels
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104
Q

What is polyarteritis nodosa?

A

Medium vessel vasculitis that affects the skin, GI tract, kidneys and heart

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105
Q

Describe the epidemiology of polyarteritis nodosa

A
  • Associated with hepatitis B (also Hep C/HIV)
  • More common in developing countries
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106
Q

What are 5 clinical presentations of polyarteritis nodosa?

A
  1. Livedo reticularis (mottled purple rash)
  2. Cutaneous/subcut nodules
  3. Unilateral orchitis
  4. Abdominal pain
  5. Hypertension
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107
Q

What are 2 investigations for polyarteritis nodosa?

A
  1. HbsAg
  2. Biopsy = shows transmural fibrinoid necrosis
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108
Q

What is the treatment for polyarteritis nodosa?

A
  • Hep B negative = usual vasculitis treatment
  • Hep B positive = antiviral agent, plasma exchange and corticosteroids
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109
Q

What are 5 complications of polyarteritis nodosa?

A
  1. Renal impairment
  2. Stroke
  3. Myocardial infarction
  4. GI perforation and haemorrhages
  5. Arthritis
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110
Q

What is Kawasaki Disease?

A

Medium vessel vasculitis (arteritis) associated with mucocutaneous lymph nodes

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111
Q

Describe the epidemiology of Kawasaki Disease

A
  1. Commonly presents ages <5 years
  2. 1.5 x more common in males
  3. More common in children of Japanese descent
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112
Q

What are 2 risk factors for Kawasaki Disease?

A
  1. Male
  2. Japanese
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113
Q

What does Kawasaki Disease most commonly affect?

A

Coronary arteries

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114
Q

What are 4 clinical presentations of Kawasaki Disease?

A
  1. Fever for >5 days
  2. Non-purulent bilateral conjunctivitis
  3. Strawberry tongue
  4. Erythema and desquamation (skin peeling) of palms and soles
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115
Q

What is an investigation for Kawasaki Disease?

A

Echo

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116
Q

What is the treatment for Kawasaki Disease?

A

Aspirin and IV immunoglobulins

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117
Q

What is a complication of Kawasaki Disease?

A

Coronary artery aneurysm

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118
Q

What is giant cell arteritis?

A

Large vessel vasculitis (arteritis) that affects the aorta and/or its major branches (carotid and vertebral arteries)

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119
Q

What is Takayasu’s arteritis?

A

Large vessel vasculitis (arteritis) that mainly affects the aorta and its branches (also pulmonary arteries - a.k.a pulseless disease)

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120
Q

What is the difference between giant cell arteritis and Takayasu’s arteritis?

A

Very similar - Takayasu’s arteritis usually affects younger patients (<40 years) than giant cell arteritis (>50 years)

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121
Q

Describe the epidemiology of giant cell arteritis

A
  • 2-3 x more common in females
  • More common in people of Northern European descent
  • Often presents in patients >50 years
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122
Q

What are 3 risk factors for giant cell arteritis?

A
  1. Female
  2. Northern European
  3. Family history of polymyalgia rheumatica
123
Q

What are 6 clinical presentations of giant cell arteritis?

A
  1. Headache over temporal area (typically unilateral)
  2. Scalp tenderness
  3. Jaw claudication
  4. Blurred vision
  5. Diplopia (double vision)
  6. Amaurosis fugax (blindness in one/both eyes)
124
Q

What are 2 investigations for giant cell arteritis?

A
  1. Temporal artery biopsy (GOLD standard) = shows giant cells and granulomatous inflammation
  2. Halo sign of temporal and axillary arteries
125
Q

What is the treatment for giant cell arteritis?

A

High dose glucocorticoid ASAP (usually prednisolone 40mg-60mg)

126
Q

What are 2 complications of giant cell arteritis?

A
  1. Blindness
  2. Irreversible neuropathy
127
Q

Describe the epidemiology of Takayasu’s arteritis

A

Usually presents before the age of 40

128
Q

What are 2 specific symptoms of Takayasu’s arteritis?

A
  1. Arm claudication
  2. Syncope
129
Q

What are 3 non-specific symptoms of Takayasu’s arteritis?

A
  1. Fever
  2. Malaise
  3. Muscle aches
130
Q

What are 3 investigations for Takayasu’s arteritis?

A
  1. CT/MRI angiography (GOLD STANDARD)
  2. Granulomatous inflammation on histology
  3. Doppler ultrasound of carotids (used to detect carotid disease)
131
Q

What is a complication of Takayasu’s arteritis?

A

Aortic aneurysm

132
Q

What is Paget’s disease?

A

Disorder of bone turnover

133
Q

Describe the epidemiology of Paget’s disease

A

Affects up to 10% of individuals by the age of 90

134
Q

Describe the pathophysiology of Paget’s disease

A
  • Excessive bone formation and resorption due to excessive osteoblast and osteoclast activity
  • Leads to patchy areas of high density (sclerosis) and low density (lysis)
  • Causes enlarged, misshapen, weak bones
  • Particularly affects axial skeleton (bones of head/spine)
135
Q

What are 5 clinical presentations of Paget’s disease?

A

60-80% are asymptomatic
1. Bone deformity e.g. bowed tibia, skull changes
2. Fractures
3. Hydrocephalus (due to blockage of aqueduct of sylvius)
4. Bone pain
5. Hearing loss (due to nerve compressive of 8th cranial nerve)

136
Q

What are 2 investigations for patients with Paget’s disease?

A
  1. X-ray
  2. Bloods
137
Q

What does an x-ray look like in patients with Paget’s disease?

A
  • Bone enlargement and deformity
  • Osteoporosis circumscripta (well defined osteolytic lesions)
  • Cotton wool appearance of skull (poorly defined areas of sclerosis and lysis)
  • V-shaped defects in long bones
138
Q

What are the results of bloods in patients with Paget’s disease?

A
  • Raised ALP (alkaline phosphate)
  • Normal calcium and phosphate
139
Q

What is the treatment for Paget’s disease?

A
  • Bisphosphonates
  • NSAIDs for bone pain
  • Calcium and vitamin D supplements
140
Q

What are 2 complications of Paget’s disease?

A
  1. Osteosarcoma
  2. Spinal stenosis and cord compression
141
Q

What are spondyloarthropathies?

A

Chronic inflammatory diseases that most commonly affect the sacroiliac (SI) joints and axial skeleton

142
Q

Describe the epidemiology of spondyloarthropathies

A
  • All conditions associated with HLA-B27 gene
  • Seronegative (RF -ve)
143
Q

What are the 5 types of spondyloarthropathies?

A
  1. Ankylosing arthritis
  2. Psoriatic arthritis
  3. Reactive arthritis
  4. Enteropathic arthritis (a.k.a IBD associated arthritis)
  5. Juvenile idiopathic arthritis
144
Q

What are the features of spondyloarthropathies?

A

SPINEACHE
S - sausage digits
P - psoriasis
I - inflammatory back pain
N - NSAIDs (good response)
E - enthesitis (heel)
A - arthritis
C - crohn’s/colitis/elevated CRP
H - HLA-B27
E - eye (uveitis)

145
Q

What is ankylosing spondylitis?

A

Inflammatory condition that mainly affects the sacroiliac joints and axial skeleton

146
Q

Describe the epidemiology of ankylosing spondylitis

A
  • Typically presents in late teens/20s
  • Used to think it was 3 x more common in males but now seem to think it affects both equally
147
Q

What is a risk factor for ankylosing spondylitis?

A
  1. HLA-B27 gene
  2. Male?
148
Q

Describe the pathophysiology of ankylosing spondylitis

A
  • Inflammatory arthritis of spine and rib cage
  • Leads to new bone formation and fusion of joints
149
Q

What are 3 symptoms of ankylosing spondylitis?

A
  1. Lower back pain and stiffness - worse with rest and improves with movement
  2. Sacroiliac pain
  3. Flares of worsening symptoms
150
Q

What are 6 investigations for patients with ankylosing spondylitis?

A
  1. X-ray
  2. HLA-B27 genetic test
  3. Rheumatoid factor -ve
  4. CRP and ESR = raised
  5. MRI of spine (bone marrow oedema)
  6. Schober’s test
151
Q

What does an x-ray look like in patients with ankylosing spondylitis?

A
  • Bamboo spine
  • Squaring of vertebral
  • Subchondral sclerosis and erosions
  • Syndesmophytes (bony outgrowths from spinal ligaments)
  • Ossification of ligaments, discs and joints
  • Fusion of facet, sacroiliac and costovertebral joints
152
Q

What is Schober’s test?

A
  • Used to assess how much mobility there is in the spine
  • Patient stands straight
  • Find L5 vertebrae and mark a point 10cm above and 5cm below
  • Ask the patient to bend forward as far as they can and measure the distance between the points
  • Distance <20cm = indicates restriction in lumbar movement
153
Q

What is the treatment for ankylosing spondylitis?

A
  • NSAIDs
  • Steroids
  • Anti-TNF drugs e.g. etanercept
  • Monoclonal antibodies against TNF e.g. infliximab, adalimumab
  • Physiotherapy and lifestyle advice
  • Surgery for deformities
154
Q

What is a complication of ankylosing spondylitis?

A

Vertebral fractures

155
Q

What is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis

156
Q

Describe the epidemiology of psoriatic arthritis

A

1 in 5 patients with psoriasis have psoriatic arthritis

157
Q

What is a risk factor for psoriatic arthritis?

A

HLA-B27 gene

158
Q

What are 5 clinical presentations of psoriatic arthritis?

A
  1. Inflammatory joint pain
  2. Plaques of psoriasis
  3. Onycholysis (separation of nail from nail bed)
  4. Dactylitis (inflammation of full finger)
  5. Enthesitis (inflammation of entheses - point of insertion of tendons into bone)
159
Q

What are 3 patterns of psoriatic arthritis?

A
  1. Symmetrical polyarthritis
  2. Asymmetrical polyarthritis
  3. Spondylitic pattern
160
Q

Describe symmetrical polyarthritis

A
  • Presents similarly to rheumatoid arthritis
  • More common in women
  • Most affected = hands, wrists, ankles and DIP joints
  • MCP joints less commonly affected
161
Q

Describe asymmetrical polyarthritis

A

Mainly affects the digits and feet

162
Q

Describe spondylitic pattern

A
  • More common in men
  • Back stiffness
  • Sacroiliitis
  • Atlanto-axial joint involvement
163
Q

What are 6 investigations for patients with psoriatic arthritis?

A
  1. X-ray
  2. ESR and CRP = raised
  3. HLA-B27 genetic test
  4. Rheumatoid factor -ve
  5. Negative for anti-CCP
  6. Joint aspiration (no bacteria/crystals)
164
Q

What does an x-ray look like in patients with psoriatic arthritis?

A
  • Erosion in distal interphalangeal (DIP) joint
  • Periarticular new bone formation
  • Osteolysis
  • Pencil-in-cup deformity
165
Q

What is the treatment for psoriatic arthritis?

A
  • NSAIDs
  • Physiotherapy
  • Steroid injection
  • DMARDs (disease-modifying anti-rheumatic drugs) e.g. methotrexate, sulfasalazine
  • TNF inhibitors/monoclonal antibodies e.g. etanercept, infliximab, adalimumab
  • Ustekinumab (last line - monoclonal antibody that targets interleukins 12 and 23)
166
Q

What is the main complication of psoriatic arthritis?

A

Arthritis mutilans:
- Severe form of psoriatic arthritis (joint is completed destroyed)
- Occurs in phalanxes
- Osteolysis of bones around the joints in the digits
- Leads to progressive shortening of the digit
- Skin then folds as the digit shortens, giving an appearance of ‘telescopic finger’

167
Q

What is reactive arthritis?

A

Inflammatory arthritis (synovitis) that occurs after exposure to certain GI or GU infections (used to be known as Reiter syndrome)

168
Q

What are 5 common causes of reactive arthritis?

A
  1. Chlamydia
  2. Gastroenteritis
  3. Campylobacter jejuni
  4. Salmonella enteritidis
  5. Shigella
169
Q

What is a risk factor for reactive arthritis?

A

HLA-B27 gene

170
Q

What are 5 clinical presentations of reactive arthritis?

A
  1. Often mistaken for septic arthritis as present similarly
  2. Begins 1-4 weeks after onset of infection
  3. Asymmetrical oligoarthritis
  4. Painful, swollen, warm, red and stiff joints
  5. Dactylitis (inflammation of full finger)
171
Q

What is the classic triad of clinical presentation for reactive arthritis?

A

“Can’t see, can’t pee, can’t climb a tree”
- Conjunctivitis
- Urethritis
- Arthritis

172
Q

What are 6 investigations for patients with reactive arthritis?

A
  1. X-ray (sacroiliitis or enthesopathy)
  2. Joint aspiration (negative - exclude septic arthritis and gout)
  3. ESR and CRP = raised
  4. HLA-B27 genetic test
  5. Rheumatoid factor -ve
  6. Negative for ANA
173
Q

What is the treatment for reactive arthritis?

A
  • NSAIDs
  • Corticosteroids
  • DMARDs e.g. methotrexate (for chronic)
174
Q

What is septic arthritis?

A

Infection of one or more joints causes by pathogenic inoculation of microbes

175
Q

Describe the epidemiology of septic arthritis

A

Common complication of joint replacement - occurs in around 1% of straight forward hip or knee replacements

176
Q

What are 5 causes of septic arthritis?

A
  1. Staphylococcus aureus (most common)
  2. Neisseria gonorrhoea
  3. Streptococcus pyogenes (Group A streptococcus)
  4. Haemophilus influenza
  5. Escherichia coli (E. Coli)
177
Q

How is septic arthritis spread?

A

Via direct inoculation or via haematogenous spread

178
Q

What are 8 risk factors for septic arthritis?

A
  1. Pre-existing joint disease e.g. OA/RA
  2. Joint prostheses
  3. IVDU
  4. Immunosuppression
  5. Alcohol misuse
  6. Diabetes
  7. Intra-articular corticosteroid injection
  8. Recent joint surgery
179
Q

What does septic arthritis most commonly affect?

A

Usually only affects a single joint - most common is knee

180
Q

What are 5 symptoms of septic arthritis?

A

1 Hot, red, swollen and painful joint
2. Stiffness and reduced range of motion
Systemic symptoms:
3. Fever
4. Lethargy
5. Sepsis

181
Q

What are 3 investigations for septic arthritis?

A
  1. Joint aspiration (fluid may be purulent)
  2. Blood culture
  3. Bloods (WCC, ESR, CRP = raised)
182
Q

What are joint aspiration samples sent for in patients with septic arthritis?

A
  • Gram staining
  • Crystal microscopy
  • Culture
  • Antibiotic sensitives
183
Q

What is the treatment for septic arthritis?

A
  • IV antibiotics for 3-6 weeks
  • Aspirate joint
  • Analgesia
184
Q

What are 3 antibiotic options for septic arthritis?

A
  1. First line = flucloxacillin + rifampicin
  2. Vancomycin = vancomycin + rifampicin (if allergic to penicillin, MRSA or prosthetic joint)
  3. Clindamycin
185
Q

What is osteomyelitis?

A

Infection in the bone and bone marrow

186
Q

Describe the epidemiology of osteomyelitis

A
  • More common in males
  • Commonly presents in children <10 years
187
Q

What are the 2 most common causes of osteomyelitis?

A
  1. Staphylococcus aureus
  2. Salmonella (if the patient has sickle cell anaemia)
188
Q

What are 7 risk factors for osteomyelitis?

A
  1. Male
  2. Open bone fracture
  3. Orthopaedic surgery
  4. Immunocompromised
  5. Sickle cell anaemia
  6. HIV
  7. TB
189
Q

What are 3 ways of entry for osteomyelitis?

A
  1. Hematogenously (through blood)
  2. Open wound
  3. Contiguously (skin into blood)
190
Q

What are 6 symptoms of osteomyelitis?

A
  1. Afebrile/low grade fever
  2. Pain
  3. Swelling
  4. Tenderness
  5. Malaise/fatigue
  6. Refusal to use limb or weight bear
191
Q

What are 5 investigations for patients with osteomyelitis?

A
  1. X-ray
  2. MRI
  3. Bloods (WCC, ESR, CRP = raised)
  4. Blood culture
  5. Bone marrow aspiration/bone biopsy with histology and culture
192
Q

What is the treatment for osteomyelitis?

A
  • Extensive and prolonged antibiotic therapy
  • Surgery for drainage and debridement of infected bone
193
Q

What is systemic lupus erythematosus (SLE)?

A

Inflammatory multisystem autoimmune connective tissue disease

194
Q

Describe the epidemiology of SLE

A
  • More common in women
  • More common in Asian people
  • Commonly presents in 20s-40s
195
Q

Describe the pathophysiology of SLE

A

Type III hypersensitivity reaction
- Anti-nuclear antibodies and anti double stranded DNA antibodies trigger inflammatory response

196
Q

What is the most specific symptom of SLE?

A

Photosensitive malar rash across face (‘butterfly’ shaped)

197
Q

What are 6 non-specific symptoms of SLE?

A
  1. Fatigue
  2. Weight loss
  3. Fever
  4. SOB
  5. Mouth ulcers
  6. Hair loss
198
Q

What are 6 investigations for patients with SLE?

A
  1. Antibodies (ANA, anti-dsDNA)
  2. FBC (normocytic anaemia in chronic)
  3. C3 and C4 = decreased
  4. Raised ESR but normal (or slightly elevated) CRP
  5. Immunoglobulins = raised
  6. Urinalysis = proteinuria
199
Q

What is the treatment for SLE?

A
  • Hydroxychloroquine (first line for mild)
  • NSAIDs
  • Steroids e.g. prednisolone
  • Immunosuppressants e.g. methotrexate, azathioprine, cyclosporin
  • Monoclonal antibodies e.g. rituximab
  • Suncream and sun avoidance for rash
200
Q

What are 9 complications of SLE?

A
  1. CVD
  2. Infection
  3. Anaemia of chronic disease
  4. Pericarditis
  5. Pleuritis
  6. Interstitial lung disease
  7. Lupus nephritis
  8. Venous thromboembolism
  9. Recurrent miscarriage
201
Q

What is antiphospholipid syndrome?

A

Autoimmune disease associated with antiphospholipid antibodies causing the blood to become more prone to clotting

202
Q

Describe the epidemiology of antiphospholipid syndrome

A

More common in females

203
Q

What are the causes of antiphospholipid syndrome?

A

Can occur on its own or secondary to an autoimmune condition, especially SLE

204
Q

What are 7 risk factors for antiphospholipid syndrome?

A
  1. Diabetes
  2. HTN
  3. Obesity
  4. Female
  5. Smoking
  6. Oestrogen therapy for menopause
  7. Underlying systemic autoimmune disease
205
Q

Describe the pathophysiology of antiphospholipid syndrome

A
  • Associated with antiphospholipid antibodies
  • These interfere with coagulation and create a hypercoagulable state where the blood is more prone to clotting
206
Q

What are the 3 antiphospholipid antibodies?

A
  1. Lupus anticoagulant
  2. Anticardiolipin antibodies
  3. Anti-beta-2 glycoprotein I antibodies
207
Q

What are 4 clinical presentations of antiphospholipid syndrome?

A
  1. Thrombosis
  2. Recurrent miscarriage
  3. Livedo reticularis (purple rash)
  4. Thrombocytopenia
208
Q

How is antiphospholipid syndrome diagnosed?

A

History of thrombosis/pregnancy complication + persistent antiphospholipid antibodies

209
Q

What is the treatment for antiphospholipid syndrome?

A
  • Long-term warfarin
  • Low molecular weight heparin + aspirin (in pregnancy)
210
Q

What are 3 complications of antiphospholipid syndrome?

A
  1. Venous thromboembolism e.g. DVT, PE
  2. Arterial thrombosis e.g. stroke, MI, renal thrombosis
  3. Pregnancy complications e.g. recurrent miscarriages, pre-eclampsia, stillbrith
211
Q

What is Raynaud’s phenomenon?

A

Intermittent spasm in the arteries supplying the fingers and toes usually precipitated by cold and relieved by heat

212
Q

What 4 conditions are most commonly associated with Raynaud’s phenomenon?

A
  1. SLE
  2. Systemic sclerosis
  3. Rheumatoid arthritis
  4. Dermatomyositis
213
Q

What is dermatomyositis?

A

Autoimmune connective tissue disorder involving chronic inflammation of the skin and muscles

214
Q

What is polymyositis?

A

Autoimmune disorder involving chronic inflammation of the muscles

215
Q

What are causes of dermatomyositis/polymyositis?

A

Usually as a result of underlying malignancy - paraneoplastic syndrome
Commonly associated with cancers:
- Lung
- Breast
- Ovarian
- Gastric

216
Q

What are 2 symptoms of both dermatomyositis and polymyositis?

A

Symptoms develop over weeks
1. Bilateral muscle pain, mostly affecting proximal muscles in shoulder and pelvic girdle
2. Fatigue/weakness

217
Q

What are 5 skin involvement symptoms of dermatomyositis?

A
  1. Gottron lesions
  2. Photosensitive erythematous rash on back, shoulders and neck
  3. Purple rash on face/eyelids
  4. Periorbital oedema
  5. Subcutaneous calcinosis
218
Q

What are 2 investigations for patients with dermatomyositis/polymyositis?

A
  1. Creatine kinase blood test (<300U/L)
  2. Autoantibodies
219
Q

Which autoantibodies are usually present in patients with dermatomyositis?

A
  1. Anti-Jo-1 antibodies
  2. Anti-Mi-2 antibodies
  3. Anti-nuclear antibodies
220
Q

Which autoantibodies are usually present in patients with polymyositis?

A

Anti-Jo-1 antibodies

221
Q

What is the treatment for dermatomyositis/polymyositis?

A
  • Corticosteroids
  • Immunosuppressants e.g. azathioprine
  • IV immunoglobulins
  • Biological therapy e.g. infliximab, etanercept
222
Q

What is scleroderma/systemic sclerosis?

A

Autoimmune inflammatory and fibrotic connective tissue disease causing hardening of the skin

223
Q

Describe the pathophysiology of scleroderma/systemic sclerosis

A
  • Increased fibroblast activity
  • Leads to increased collagen deposition
  • Results in abnormal growth of connective tissue
224
Q

What is the characteristic presentation of scleroderma/systemic sclerosis?

A

‘Beak’-like nose and small mouth

225
Q

What are the 2 main patterns of disease for scleroderma/systemic sclerosis?

A
  1. Limited cutaneous systemic sclerosis
  2. Diffuse cutaneous systemic sclerosis
226
Q

Describe limited cutaneous systemic sclerosis

A

Used to be called CREST syndrome
C - calcinosis (calcium deposits under skin in fingertips)
R - Raynaud’s phenomenon (white/blue fingertips in response to cold)
E - oEsophageal dysmotility (swallowing difficulties, acid reflux, oesophagitis)
S - sclerodactyly (shiny, tight skin without normal folds in hands)
T - telangiectasia (dilated small blood vessels in skin))

227
Q

Describe diffuse cutaneous systemic sclerosis

A

Features of CREST syndrome plus:
- Cardiovascular problems e.g. HTN, CAD
- Lung problems e.g. pulmonary hypertension, pulmonary fibrosis
- Kidney problems e.g. glomerulonephritis, scleroderma renal crisis

228
Q

What are 2 investigations for scleroderma/systemic sclerosis?

A
  1. Autoantibodies
  2. Nailfold capillaroscopy
229
Q

Which autoantibodies are found in patients with limited cutaneous systemic sclerosis?

A
  • Anti-nuclear antibodies
  • Anti-centromere antibodies
230
Q

Which autoantibodies are found in patients with diffuse cutaneous systemic sclerosis?

A
  • Anti-nuclear antibodies
  • Anti-Scl-70 antibodies
231
Q

What is nailfold capillaroscopy?

A
  • Magnify and examine area where the skin meets the fingernails
  • Allows us to examine the health of peripheral capillaries
  • Indications of scleroderma/systemic sclerosis = abnormal capillaries, avascular areas and micro-haemorrhages
232
Q

What is the treatment for scleroderma/systemic sclerosis?

A
  • Steroids and immunosuppressants
  • Avoid smoking
  • Gentle skin stretching to maintain range of motion
  • Emollients
  • Treat symptoms e.g. nifedipine for symptoms of Raymaud’s phenomenon
233
Q

What is polymyalgia rheumatica?

A

Inflammatory condition causing pain and stiffness in the shoulders, pelvic girdle and neck

234
Q

Describe the epidemiology of polymyalgia rheumatica

A
  • Strong association with giant cell arteritis
  • More common in women
  • More common in Caucasians
  • Usually affects older adults >50 years
235
Q

What are 4 systemic symptoms of polymyalgia rheumatica?

A
  1. Weight loss
  2. Fatigue
  3. Fever
  4. Low mood
236
Q

What are 3 other clinical presentations of polymyalgia rheumatica?

A
  1. Upper arm tenderness
  2. Carpel tunnel syndrome
  3. Pitting oedema
237
Q

What are 5 main clinical presentations of polymyalgia rheumatica?

A
  1. Bilateral shoulder pain that may radiate to elbow
  2. Bilateral pelvic girdle pain
  3. Worse with movement
  4. Interferes with sleep
  5. Stiffness for at least 45 minutes in the morning
238
Q

What are 2 investigations for patients with polymyalgia rheumatica?

A
  1. ESR and CRP = raised
  2. Exclude other conditions (FBC, urinalysis, LFTs etc.)
239
Q

What is the treatment for polymyalgia rheumatica?

A

Steroids - initially 15mg prednisolone

240
Q

How is a diagnosis of polymyalgia rheumatica confirmed?

A

After 3-4 weeks of steroids, should expect to see a 70% improvement in symptoms and inflammatory markers to return to normal

241
Q

How are patients with polymyalgia rheumatica typically weaned off steroids?

A
  • 15mg prednisolone until symptoms are fully controlled
  • 12.5 mg for 3 weeks
  • 10mg for 4-6 weeks
  • reduce by 1mg every 4-8 weeks
  • Can take 1-2 years to fully wean off
242
Q

What is mechanical lower back pain?

A

Pain related to movements of the lumbar and sacral regions of the spine associated with no specific disease

243
Q

Describe the epidemiology of mechanical lower back pain

A
  • Most common form of back pain
  • More common in females
244
Q

What are 7 causes of mechanical lower back pain?

A
  1. Muscle/ligament sprain
  2. Facet joint dysfunction
  3. Sacroiliac joint dysfunction
  4. Herniated disc
  5. Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
  6. Scoliosis
  7. Degenerative changes e.g. arthritis
245
Q

What are 7 risk factors for mechanical lower back pain?

A
  1. Manual labour
  2. Smoking
  3. Low socioeconomic status
  4. Poor working conditions
  5. Female
  6. Psychological disorder
  7. Pre-existing chronic widespread pain
246
Q

What are 2 signs for serious pathology in patients with mechanical lower back pain?

A
  1. Elderly (myeloma)
  2. Neuropathic pain (spinal cord compression)
247
Q

What are 2 symptoms of mechanical lower back pain?

A
  1. Unilateral back pain often helped by rest, worse in evenings and aggregated by exercise
  2. Muscular spasm causing local pain and tenderness
248
Q

What are red flag symptoms in patients with mechanical lower back pain?

A

TUNAFISH
T - trauma
U - unexplained weight loss and night sweats
N - neurological deficits, bowel/bladder incontinence
A - age <20 or >55
F - fever
I - IVDU
S - steroid use/immunosuppression
H - history of cancer

249
Q

What are 2 investigations for patients with mechanical lower back pain?

A
  1. Bloods (ESR, CRP, FBC, ALP)
  2. Imaging e.g. DEXA scan/MRI
250
Q

What is the treatment for mechanical lower back pain?

A
  • Often self-limiting
  • Analgesia ladder
  • Lifestyle advice
  • Physiotherapy
251
Q

What is lumbar spondylosis?

A

Degeneration of the intervertebral disc due to it losing its compliance and thinning over time

252
Q

Describe the epidemiology of lumbar spondylosis

A

Affects older patients

253
Q

What are the symptoms of lumbar spondylosis?

A

Initially asymptomatic and progressively worsens:
- Pain in lower back/buttocks/thighs
- Numbness/tingling spreading from lower back down a leg (sciatica)
- L4/L5 most common

254
Q

What is the treatment for lumbar spondylosis?

A
  • Analgesia
  • Physiotherapy
255
Q

What is osteomalacia?

A

Defective bone mineralisation leading to soft bone due to a lack of Ca2+

256
Q

What is Rickets?

A

Inadequate mineralisation of bone and epiphyseal cartilage in the growing skeleton of children

257
Q

What are 4 causes of osteomalacia/rickets?

A
  1. Malnutrition
  2. Drug induced
  3. Defective 1-alpha hydroxylation
  4. Liver/kidney disease
258
Q

Describe the pathophysiology of osteomalacia

A
  • Vitamin D deficiency
  • Lack of vitamin D reduces calcium and phosphate absorption from the intestines and kidneys
  • Lack of calcium and phosphate in the blood
  • = defective bone mineralisation
259
Q

What are 4 symptoms of osteomalacia?

A
  1. Fatigue
  2. Bone pain
  3. Muscle weakness/aches
  4. Pathological or abnormal fractures
260
Q

What are 6 symptoms of Ricket’s?

A
  1. Leg bowing and knock knees
  2. Tender swollen joints
  3. Growth retardation
  4. Bone and joint pain
  5. Dental deformities (delayed formation of teeth, enamel hypoplasia)
  6. Enlargement of end of ribs (rachitic rosary)
261
Q

What are 4 investigations for patients with osteomalacia?

A
  1. Serum 25-hydroxyvitamin D (insufficiency = 25-50nmol/L, deficiency = <25nmol/L)
  2. Low serum calcium and phosphate
  3. DEXA = low BMD
  4. X-ray = loss of cortical bone
262
Q

What is the treatment for osteomalacia?

A

Supplementary vitamin D (cholecalciferol)

263
Q

Describe the epidemiology of primary bone tumours

A
  • More common in males
  • More common in children
264
Q

Describe the epidemiology of osteosarcomas

A
  • Most sarcoma
  • Usually presents in adolescents and younger adults 10-20 years
265
Q

Describe the epidemiology of ewing sarcomas

A
  • Very rare
  • Usually presents in teens
266
Q

Describe the epidemiology of osteochondroma

A

Common in males <25 years

267
Q

What are 4 risk factors for primary bone tumours?

A
  1. Previous radiotherapy
  2. Previous cancer
  3. Paget’s disease (associated with osteosarcoma)
  4. Benign bone lesions
268
Q

Describe the pathophysiology of osteosarcomas

A

Originates from metaphysis of long bones - most commonly affects femur, tibia and humerus

269
Q

Describe the pathophysiology of ewing sarcomas

A

Originates from mesenchymal stem cells in long bones

270
Q

Describe the pathophysiology of osteochondromas/chondrosarcoma

A

Originates from cartilage - overproduction of bone which deposits on metaphysis

271
Q

What is the difference between osteochondromas/chondrosarcomas?

A

Osteochondroma = benign
Chondrosarcoma = malignant

272
Q

Where are primary bone tumours most common?

A

Long bones

273
Q

What are 5 clinical presentations of primary bone tumours?

A
  1. Persistent bone pain, worse at night
  2. Bone swelling
  3. Palpable mass
  4. Easy bruising
  5. Mobility issues e.g. limp, joint stiffness, reduced range of movement
274
Q

What are 3 investigations of primary bone tumours?

A
  1. Biopsy (gold standard)
  2. X-ray (first line)
  3. Bloods (raised ALP)
275
Q

What does an x-ray look like in patients with primary bone tumours?

A
  • Poorly defined lesion in the bone
  • Destruction of normal bone
  • ‘Fluffy’ bone
  • ‘Sunburst’ appearance
276
Q

What is the treatment for primary bone tumours?

A
  • Surgical resection of lesion, often with limb amputation
  • Chemotherapy
  • Radiotherapy
277
Q

What are 2 complications of primary bone tumours?

A
  1. Pathological bone fractures
  2. Metastasis
278
Q

Describe the epidemiology of secondary bone tumours

A

More common than primary bone tumours

279
Q

Tumours where are most likely to metastasise to bone?

A

PBKTL (lead kettle):
- Prostate
- Breast
- Kidney
- Thyroid
- Lungs

280
Q

What are 5 clinical presentations of secondary bone tumours?

A
  1. Severe bone pain, worse at night
  2. Weight loss
  3. Fatigue
  4. Fever
  5. Malaise
281
Q

What are 2 investigations for secondary bone tumours?

A
  1. X-ray = lytic lesions
  2. CT scans = metastases
282
Q

What is the treatment of secondary bone tumours?

A
  • Chemotherapy
  • Radiotherapy
  • Surgery
  • Bisphosphonates
283
Q

What is Marfan’s syndrome?

A

Autosomal dominant condition affecting the gene responsible for creating fibrillin

284
Q

What is a risk factor for Marfan’s syndrome?

A

Family history

285
Q

Describe the pathophysiology of Marfan’s syndrome

A
  • Fibrillin is an important component of connective tissue
  • People with Marfan’s syndrome lack this and so have features resulting from abnormal connective tissue
286
Q

What are 8 clinical presentations of Marfan’s syndrome?

A
  1. Tall stature
  2. Long neck
  3. Long limbs
  4. Long fingers (arachnodactyly)
  5. High arch palate
  6. Hypermobility
  7. Pectus carinatum or pectus excavatum
  8. Downward sloping palpable fissures
287
Q

What are 2 investigations for patients with Marfan’s syndrome?

A
  1. Ask patients to cross their thumb across their palm (thumb tip goes past opposite edges of hand = indicates arachnodactyly)
  2. Ask patients to wrap the thumb and fingers of one hand around the other wrist (thumb and fingers overlap = indicates arachnodactyly)
288
Q

What is the treatment for Marfan’s syndrome?

A
  • Lifestyle changes (avoid intense exercise, caffeine, stimulants)
  • Drugs e.g. beta blockers, angiotensin II receptor antagonists
  • Physiotherapy
  • Yearly echo and ophthalmologist review
289
Q

What is the main aim of treatment for Marfan’s syndrome?

A

Minimise blood pressure and heart rate

290
Q

What are 6 complications of Marfan’s syndrome?

A
  1. Valve prolapse
  2. Aortic aneurysms
  3. Lens dislocation
  4. Pneumothorax
  5. GORD
  6. Scoliosis
291
Q

What is Ehlers-Danlos Syndrome (EDS)?

A

Group of autosomal dominant conditions that cause defects in collagen

292
Q

Describe the epidemiology of Ehlers-Danlos Syndrome (EDS)

A

Hypermobile EDS = most common and least severe type of EDS
Vascular EDS = most dangerous type

293
Q

What is a risk factor for Ehlers-Danlos Syndrome (EDS)?

A

Family history

294
Q

What are 5 clinical presentations of Ehlers-Danlos Syndrome (EDS)?

A
  1. Hypermobility of joints
  2. Easily stretched skin (hyperextensibility)
  3. Easy bruising
  4. Chronic joint pain
  5. Re-occurring dislocations
295
Q

What are 3 clinical presentations of classical Ehlers-Danlos Syndrome (EDS)?

A
  1. Joint pain
  2. Abnormal wound healing
  3. Lumps over pressure points
296
Q

What is a clinical presentation of vascular Ehlers-Danlos Syndrome (EDS)?

A

Thin, translucent skin

297
Q

What is the investigation for Ehlers-Danlos Syndrome (EDS)?

A

Beighton score (used to assess extent of hypermobility)

298
Q

What is the Beighton score?

A

One point scored for each side of the body:
- Palms flat on floor with straight legs (score 1)
- Elbows hyperextend
- Knees hyperextend
- Thumb can bend to touch forearm
- Little finger hyperextends past 90 degrees

299
Q

What is the treatment for Ehlers-Danlos Syndrome (EDS)?

A
  • Physiotherapy
  • Occupational therapy
  • Psychological support
300
Q

What are 4 complications of classical Ehlers-Danlos Syndrome (EDS)?

A
  1. Hernias
  2. Prolapse
  3. Aortic root dilation
  4. Mitral regurgitation
301
Q

What is a complication of vascular Ehlers-Danlos Syndrome (EDS)?

A

Skin, internal organs and vessels prone to rupture

302
Q

What is a complication of hypermobile Ehlers-Danlos Syndrome (EDS)?

A

Postural orthostatic tachycardia syndrome (POTS)

303
Q

What is postural orthostatic tachycardia syndrome (POTS)?

A

Result of autonomic dysfunction that causes appropriate tachycardia on sitting or standing up

304
Q

What are 6 symptoms of postural orthostatic tachycardia syndrome (POTS)?

A
  1. Pre syncope
  2. Syncope
  3. Headaches
  4. Disorientation
  5. Nausea
  6. Tremor

Phase 2a (29 decks)

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