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Phase 2A revision > rheumatology to work on > Flashcards

rheumatology to work on Flashcards

1
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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2
Q

what is the clinical presentation of ankylosing spondylitis

A
  • Lower back pain + stiffness → worse with rest + improves with movement
  • Sacroiliac pain - radiates to hips
  • Flares of worsening symptoms
  • loss of lumbar lordosis and increased kyphosis
  • progressive loss of spinal movement
  • anterior uveitis
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3
Q

What is the treatment for ankylosing spondylitis?

A

NSAIDs
corticosteroids
anti-TNF drugs infliximab

Physio, lifestyle advice
Surgery for deformities

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4
Q

what are the clinical features of psoriatic arthritis

A
  • Asymmetrical oligoarthritis (60%)
  • Large joint arthritis (15%)
  • Enthesitis - inflammation of entheses
  • Dactylitis - inflammation of full finger
  • Nail changes (pitting, onycholysis)
  • inflammatory joint pain
  • plaques of psoriasis
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5
Q

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

A

X-ray

- Erosion in DIPJ + periarticular new-bone formation  - Osteolysis  - Pencil-in-cup deformity

Bloods

  • ESR + CRP - normal or raised
  • Rheumatoid factor -ve
  • anti-CCP - negative

Joint aspiration - no bacteria or crystals

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6
Q

What is reactive arthritis?

A

● A sterile synovitis which occurs following GI infection or STI
● Typically affects lower limb

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7
Q

What GI infections are associated with causing reactive arthritis?

A 
Salmonella
Shigella
Yersinia 
enterocolitica
campylobacter
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8
Q

What GU infections are associated with causing reactive arthritis?

A

Chlamydia
Ureaplasma
urealyticum

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9
Q

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

A 
ESR + CRP - raised
ANA - negative
RF - negative
X-ray - sacroiliitis or enthesopathy
Joint aspirate - negative (exclude septic arthritis + gout)
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10
Q

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

A

Enteropathic arthritis

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11
Q

Psoriatic arthritis commonly involved swelling of what joint?

A

DIP joint

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12
Q

Give 4 properties of bone that contribute to bone strength

A
  1. Bone mineral density
  2. Bone size
  3. Bone turnover
  4. Bone micro-architecture
  5. Mineralisation
  6. Geometry
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13
Q

Give 5 risk factors for osteoporosis

A
  • old age, women, FHx, previous fracture, smoking, alcohol, Asian/Caucasian

‘SHATTERED’

  • Steroid use
  • Hyperthyroidism, hyperparathyroidism, hypercalciuria
  • Alcohol + tobacco use
  • Thin (BMI < 18.5)
  • Testosterone (low)
  • Early menopause
  • Renal or liver failure
  • Erosive/inflammatory bone disease (e.g. myeloma or RA)
  • Dietary low calcium /malabsorption or Diabetes type 1
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14
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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15
Q

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

A

Neutrophils

Giant cells

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16
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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17
Q

Describe the pathophysiology of giant cell arteritis

A

Arteries become inflamed, thicken and can obstruct blood flow

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18
Q

what are is the clinical presentation of giant cell arteritis?

A
  1. Headache, typically unilateral over temporal area
  2. Temporal artery/scalp tenderness
  3. Jaw claudication
  4. Visual symptoms - vision loss (painless)
  5. Systemic symptoms - fever, malaise, lethargy
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19
Q

What are the investigations for giant cell arteritis?

A
  • ↑ESR and/or CRP (=highly sensitive) ESR >50 mm/hr
  • Halo sign on US of temporal and axillary artery
  • Temporal artery biopsy = gold standard for Dx (show giant cells, granulomatous inflammation)
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20
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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21
Q

Describe the treatment for giant cell arteritis

A
  1. High dose corticosteroids - prednisolone ASAP
  2. DMARDs - methotrexate (sometimes)
  3. Osteoporosis prophylaxis is important - lansoprazole, alendronate, Ca2+, vit D
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22
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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23
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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24
Q

What is the affect of Wegener’s granulomatosis on the Upper respiratory tract?

A
  1. Sinusitis
  2. Otitis
  3. Cough
  4. Haemoptysis
  5. Saddle nose deformity
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25
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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26
Q

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

A

Glomerulonephritis –> haem/proteinuria

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27
Q

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

A

Ulcers Pulpura

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28
Q

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

A

Uveitits
Scleritis
Episcleritis

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29
Q

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

A

ANCA testing - c-ANCA
Tissue biopsy - (renal biopsy best) - shows granulomas
CT - assessment of organ involvement
FBC - high eosinophils

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30
Q

What is the treatment for Wegener’s Granulomatosis?

A
  • Glucocorticoids (prednisolone)
  • Immunosuppresive drugs (cyclophosphamide OR rituximab)
  • plasma exchange for specific complications
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31
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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32
Q

What are the most important cells responsible for OA?

A

Chondrocytes

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33
Q

Describe the pathophysiology of osteoarthritis

A

Mechanical stress –> progressive destruction and loss of articular cartilage
exposed subchondral bone becomes sclerotic
cytokine mediated TNF/IL/NO involved
deficiency in growth factors

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34
Q

Name the 2 main pathological features of osteoarthritis

A
  1. Cartilage loss

2. Disordered bone repair

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35
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. Subchondral sclerosis - exposed
  4. Subchondral cysts
  5. Abnormalities of bone contour
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36
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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37
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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38
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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39
Q

what are the clinical features of SLE?

A

Symptoms:
butterfly rash, wt loss, fever, fatigue, joint pain, mouth ulcers

Signs: correctable ulnar deviation

  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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40
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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41
Q

Describe the non medical treatment for SLE

A

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

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42
Q

Describe the pharmacological treatment for SLE

A 
● Avoid excessive sunlight and reduce CVS risk factors 
● NSAIDs - ibuprofen
● Chloroquine and hydroxychloroquine 
● Corticosteroids - prednisolone
● cyclophosphamide
● methotrexate
● Topical steroids
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43
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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44
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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45
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
Pulmonary arterial hypertension

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46
Q

Give 4 signs of diffuse scleroderma

A

Skin changes develop more rapidly and are more widespread than inlimited cutaneous scleroderma/CREST

  1. Proximal scleroderma
  2. Pulmonary fibrosis
  3. Bowel involvement
  4. Myositis
  5. Renal crisis
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47
Q

What is a diagnostic test for scleroderma?

A

Limited - ACAs

Diffuse - 
Anti-topoisomerase, 
Anti scl-70
ANAs
ESR (normal)

If renal involvement, there may be anemia

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48
Q

Describe the management of scleroderma

A

avoid smoking, handwarmers

GI - PPIs, Antibiotics
Renal - ACEi
Pulmonary fibrosis - cyclophosphamide

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49
Q

Give 5 symptoms of sjögren’s syndrome

A
  1. Dry eyes and dry mouth
  2. dry skin and dry vagina
  3. Inflammatory arthritis
  4. Rash
  5. Neuropathies
  6. Vasculitis
  7. fatigue
  8. salivary and parotid gland enlargement
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50
Q

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

A

Serum auto-antibodies –> anti-RO, anti-La, RF, ANA

Raised immunoglobulins and ESR

Schirmer’s test
- ability for eyes to self-hydrate - <10mm in 5 minutes

Rose bengal staining and slit lamp exam

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51
Q

What is the treatment for sjögren’s syndrome?

A
  • Artificial tears, artificial saliva, vaginal lubricants
  • Hydroxychloroquine
  • NSAID
  • M3 agonist - pilocarpine
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52
Q

What is dermatomyositis?

A

A rare disorder of unknown aetiology

Inflammation and necrosis of skeletal muscle fibres and skin

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53
Q

Give 3 symptoms of dermatomyositis

A
  1. Rash
  2. Muscle weakness
  3. Lungs are often affected too (e.g. interstitial lung disease)
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54
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
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55
Q

What is the treatment for dermatomyositis?

A

Steroids - prednisolone

Immunosuppressants

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56
Q

What are the 3 phases of Raynaud’s?

A

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

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57
Q

which organisms can cause septic arthritis?

A
  1. Staphylococcus aureus
  2. Streptococci
  3. Neisseria Gonorrhoea
  4. Gram negative = E. coli, pseudomonas aeruginosa
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58
Q

what are the risk factors for septic arthritis?

A 
Pre-existing joint disease (OA or RA)
Joint prostheses
IVDU
Immunosuppression
Alcohol misuse
Diabetes
Intra-articular corticosteroid injection
Recent joint surgery
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59
Q

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

A

Aspirate joint → MC+S
Blood culture
WCC → may be raised
ESR + CRP → raised

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60
Q

Describe the treatment for septic arthritis

A 
Aspirate joint 
Empirical Abx - flucloxacillin 
- if allergic to penicilin = clindamycin
- if MRSA = vancomycin
- if gram negative = cefotaxime
Analgesia - NSAIDS
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61
Q

What organisms can cause osteomyelitis?

A
  1. Staph. aureus
  2. Coagulase negative staph (s. epidermidis)
  3. Aerobic gram negate bacilli (salmonella)
  4. haemophilus influenza
  5. Mycobacterium TB
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62
Q

Name 2 predisposing conditions for osteomyelitis

A
  1. Diabetes

2. PVD

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63
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

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64
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
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65
Q

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

A
  1. Inflammatory cells
  2. Oedema
  3. Vascular congestion
  4. Small vessel thrombosis
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66
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
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67
Q

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

A
  • Inflammation in BM increase intramedullary pressure exudate into bone cortex which rupture through periosteum
  • this causes interruption of periosteum blood supply which results in necrosis and sequestra
  • therefore new bone forms
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68
Q

What is acute osteomyelitis associated with?

A

Associated with inflammatory bone changes caused by pathogenic bacteria

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69
Q

What is chronic osteomyelitis associated with?

A

Involves bone necrosis

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70
Q

what is the clinical presentation of osteomyelitis?

A
  1. Slow onset
  2. Dull pain at OM site, aggravated by movement
  3. Systemic = fever, rigors, sweating, malaise
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71
Q

what are the signs of acute osteomyelitis?

A
  1. Tender
  2. Warm
  3. Red swollen area around OM
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72
Q

what are the signs of chronic osteomyelitis?

A
  1. Acute OM signs
  2. Draining sinus tract
  3. Non-healing ulcers/fracture
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73
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
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74
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 - gold standard
  4. Blood cultures
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75
Q

Describe the usual treatment for osteomyelitis

A

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

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76
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
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77
Q

Why is osteomyelitis difficult to treat?

A

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

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78
Q

Name 3 risk factors of RA

A
  1. Smoking
  2. Women
  3. family history
  4. Other AI conditions
  5. genetic factors - HLA-DR4 and HLA-DRB1
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79
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
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80
Q

what are the 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
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81
Q

what are the signs of RA?

A
  1. Symmetrical polyarthorpathy
  2. Deforming –> ulnar deviation, swan neck deformity, boutonniere deformity
  3. Erosion on X-ray
  4. 80% = RF positive
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82
Q

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

A

Nodules
Bursitis
Muscle wasting

83
Q

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

A

Dry eyes
Scleritis
Episcleritis

84
Q

RA extra-articular involvement: describe the neurological effects

A

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

85
Q

RA extra-articular involvement: describe the haematological effects

A

Felty’s syndrome (RA + splenomegaly + neutropenia) Anaemia

86
Q

RA extra-articular involvement: describe the pulmonary effects

A

Pleural effusion

Fibrosing alveolitis

87
Q

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

A

Pericardial rub

Pericardial effusion

88
Q

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

A

Amyloidosis

89
Q

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

A

Vasculitis - infarcts in nail bed

90
Q

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

A
  • Blood for inflammatory markers
  • ESR and CRP raised
  • RF and Anti-CCP

X-ray- Synovial fluid is sterile with high neutrophil count

91
Q

What is rheumatoid factor?

A

An antibody against the Fc portion of IgG

92
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
93
Q

What joints tend to be affects in RA?

A

MCP
PIP
Wrist (DIP often spared)

94
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

Overproduction/under excretions of uric acid causes build up and precipitated out in joints

95
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
96
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
97
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
98
Q

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

A

first line = bloods

  • U&E and eGFR - renal failure
  • Uric acid levels - 4-6 weeks after to confirm hyperuricaemia
  • gold standard = joint aspiration
99
Q

What is the aim of treatment for gout?

A

To get urate levels < 300 mol/L

100
Q

How would you treat acute gout?

A

1st line = NSAID or colchicine

2nd line = intra-articular steroid injection

lifestyle advice - wt loss, exercise, diet, alcohol and fluid intake

101
Q

what is the management for chronic gout?

A

1st line = allopurinol - inhibits xanthine oxidase

2nd line = febuxostat

consider co-prescribing colchicine with allopurinol for 6 months

102
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

103
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
104
Q

Describe the pathophysiology of pseudogout

A

Calcium pyrophosphate crystals are deposited on joint surfaces - produces the radiological appearance of chondrocalcinosis
Crystals elicit an acute inflammatory response

105
Q

What can cause pseudogout?

A
  1. Hypo/hyperthyroidism
  2. Haemochromatosis
  3. Diabetes
  4. Magnesium levels
106
Q

what is the clinical presentation of pseudogout?

A

SYMPTOM
hot, swollen, tender joint, usually knees

SIGNS
recent injury to the joint in the history
Typically the wrists and knees

107
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

108
Q

What is the most likely differential diagnosis for pseudogout?

109
Q

Describe the treatment for pseudogout

A
  • high dose NSAIDs - ibuprofen
  • Colchicine - anti-gout
  • IM prednisolone
  • Aspiration, intra-articular steroid injections
110
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

111
Q

What kind of crystals do you see in pseudogout?

A

Positive birefringent calcium pyrophosphate rhomboid crystals

112
Q

What kind of crystals do you see in gout?

A

Monosodium urate crystals = negatively birefringent

113
Q

What kind of crystals fo you see in pseudogout?

A

Calcium pyrophosphate crystals = positively birefringent

114
Q

Name 4 diseases that fibromyalgia is commonly associated with

A
  1. Depression
  2. Choric fatigue
  3. IBS
  4. Chronic headache
115
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
  7. poor concentration, brain fog
116
Q

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

A
  1. Hypothyroidism
  2. SLE
  3. Low vitamin D
117
Q

Define sarcoma

A

A rare tumour of mesenchymal origin

A malignant connective tissue neoplasm

118
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
119
Q

What are secondary bone tumours?

A

Metastases from:

  1. Lungs
  2. Breast
  3. Prostate
  4. Thyroid
  5. Kidney
120
Q

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

A

1st line → x-ray
Gold standard → biopsy
Bloods → FBC, ESR, ALP, lactate dehydrogenase, Ca, U+E
CT chest/abdo/pelvis

121
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

122
Q

What staging is used for bone cancers?

A

Enneking grading

123
Q

How are malignant bone cancers staged using Enneking grading?

A 
G1 = Histologically benign
G2 = Low grade
G3 = High grade
A = intracompartmental
B = extracompartmental
124
Q

How are benign bone cancers staged using Enneking grading?

A 
G1 = Latent
G2 = Active 
G3 = Aggressive
125
Q

How are bone cancers treated?

A 
MDT management 
Benign 
- NSAIDS
- Bisphosphonates (alendronate) 
- symptomatic help

Malignancy = surgical excision –> limb sparing/amputation
radio/chemotherapy

126
Q

Give 4 local complications with surgery for bone cancers

A
  1. Haematoma
  2. Loss of function
  3. Infection
  4. Local recurrence
127
Q

Where do osteosarcomas usually present?

A

Knee - distal femur, proximal humerus

128
Q

What is an osteosarcoma?

A

Malignant tumour of bone
Spindle cell neoplasm that produce osteoid
rapidly metastases to the lung

129
Q

Give 3 features of osteosarcoma

A
  1. Fast growing
  2. Aggressive - Destroys bone and spreads into surrounding tissues, rapidly metastasises to lung
  3. Typically affects 15-19 year olds
  4. often relatively painless
130
Q

Name a boney sarcoma that responds well to chemotherapy

A

Ewings sarcoma

131
Q

Where does Ewings sarcoma arise from?

A

mesenchymal stem cells

132
Q

Give 3 side effects of NSAIDs

A
  1. Peptic ulcer disease
  2. Renal failure
  3. Increased risk of MI and CV disease
133
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

134
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
135
Q

How do DMARDs work?

A

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

136
Q

Give 3 potential side effects of methotrexate

A
  1. Bone marrow suppression
  2. Abnormal liver enzymes
  3. Nausea
  4. Diarrhoea
  5. Teratogenic
137
Q

What are cytokines?

A

Short acting hormones

138
Q

Describe the mechanism of action of infliximab

A

Inhibits T cell activation

139
Q

How does alendronate work?

A

Reduces bone turnover by inhibiting osteoclast mediated bone resorption

140
Q

what are the signs of osteoarthritis?

A

● Deformity and bony enlargement of the joints
● Limited joint movement
● Muscle wasting of surrounding muscle groups
● Crepitus (grafting) due to disruption of normally smooth articulating surfaces of joints
● May be joint effusion
● Heberden’s nodes are bony swellings at DIPJs
● Bouchard’s nodes occur at proximal interphalangeal joints

141
Q

what are the investigations for osteoarthritis?

A

● FBC and ESR normal
● Rheumatoid factor is negative but positive low titre tests may occur incidentally in elderly
● XRs abnormal in advanced disease

142
Q

what are the complications of rheumatoid arthritis?

A

Cervical spinal cord compression- weakness and loss of sensation
Lung involvement- interstitial lung disease, fibrosis.

143
Q

what is the difference between the presentation of early and late septic arthritis

A

● Early infection presents with inflammation, discharge, joint effusion, loss of function and pain
● Late disease presents with pain or mechanical dysfunction

144
Q

what are the risk factors for gout?

A

Middle age overweight males.
high purine diet,
increased cell turnover

145
Q

what are the complications of gout?

A

Infection in the tophi

Destruction of the joint

146
Q

what are the risk factors for osteomyelitis?

A 
Previous osteomyelitis
Penetrating injury
IVDU
Diabetes
HIV
Recent surgery
Distant or local infection
Sickle cell disease
RACKD
Children → upper resp tract  or varicella infection
147
Q

what are the risk factors for ankylosing spondylitis?

A

HLA-B27

environment - klebsiella, salmonella, shigella

148
Q

what is arthritis mutilans?

A

Most severe form of psoriatic arthritis
Occurs in phalanxes
Osteolysis of bones around joints in digits → leads to progressive shortening
Skin then folds as digit shortens → telescopic finger

149
Q

what are the different types of psoriatic arthritis?

A

● Distal interphalangeal arthritis – most typical pattern of joint involvement – dactylitis is characteristic
● Mono- or oligoarthiritis
● Symmetrical seronegative polyarthritis – resembling RA
● Arthritis mutilans – a severe form with destruction of the small bones in the hands and feet
● Sacroiliitis – uni- or bilateral

150
Q

what treatment should be used if reactive arthritis relapses?

A

methotrexate or sulfasalazine

151
Q

what is the pathophysiology of reactive arthritis?

A

● Bacterial antigens or DNA have been found in the inflamed synovium of affected joints – suggests persistent antigenic material is driving the inflammatory response

152
Q

what are the complications for SLE?

A

Cardiac, lung, kidney involvement. Widespread inflammation causing damage.

153
Q

what is the the pathophysiology of fibromyalgia?

A

Unknown, possibly pain perception/hyper excitability of pain fibres

154
Q

what are the complications of fibromyalgia?

A
  • can really affect quality of life
  • anxiety, depression, insomnia
  • opiate addiction
155
Q

what is rickets?

A

Rickets: inadequate mineralization of the bone and epiphyseal cartilage in the growing skeleton of CHILDREN.

156
Q

what are the complications of Sjogren’s syndrome?

A
  • eye infections- oral problems (dental cavities, candida infections)
  • vaginal problems (candidiasis, sexual dysfunction)

RARE

  • pneumonia and bronchiectasis
  • non-hodgkin’s
  • vasculitis
  • renal impairment
  • peripheral neuropathy
157
Q

which arteries are particularly affected by giant cell arteritis?

A
  • aorta and vertebral arteries
  • Cerebral arteries affected in particular e.g. temporal artery
  • Opthalmic artery can also be affected potentially resulting in permanent ortemporary vision loss
158
Q

what is found on physical examination of giant cell arteritis?

A

temporal arteries may be tender on palpation and thickened. Pulses may be diminished.

159
Q

what is antiphospholipid syndrome?

A
  • Syndrome characterised by thrombosis (arterial or venous) and/or recurrentmiscarriages with positive blood tests for antiphospholipid antibodies (aPL) - hypercoagulable state
160
Q

what are the risk factors for antiphospholipid syndrome?

A
  • diabetes
  • hypertension
  • obesity
  • female
  • underlying autoimmune condition
  • smoking
  • oestrogen therapy
161
Q

what is the clinical presentation of antiphospholipid syndrome?

A
  • thrombosis
  • miscarriage
  • livedo reticularis - purple lace rash
  • ischaemic stroke, TIA, MI
  • DVT, budd-chiari syndrome
  • thrombocytopenia
  • valvular heart disease, migraines, epilepsy
162
Q

what is the pathophysiology of antiphospholipid syndrome?

A
  • Antiphospholipid antibodies (aPL) play a role in thrombosis by binding tophospholipid on the surface of cells such as endothelial cells, platelets andmonocytes
  • Once bound, this change alters the functioning of those cells leading tothrombosis and/or miscarriage
  • Antiphospholipid antibodies (aPL) cause CLOTs:
    • Coagulation defect
    • Livedo reticularis - lace-like purplish discolouration of skin
    • Obstetric issues i.e. miscarriage
    • Thrombocytopenia (low platelets)
163
Q

what are the investigations for antiphospholipid syndrome?

A

Hx of thrombosis/ pregnancy complications + Antibody screen with raised:

  - anticardiolipin antibodies
 - lupus anticoagulant
 - anti-beta-2 glycoprotein I antibodies
164
Q

what is the treatment for antiphospholipid syndrome?

A
  • long term warfarin
  • Pregnant women on low molecular weight heparin (e.g. enoxaparin) + aspirin
  • lifestyle - smoking cessation, exercise, healthy diet
165
Q

what are the complications of antiphospholipid syndrome?

A
  • Venous thromboembolisms (e.g. DVT, pulmonary embolism)
  • Arterial thrombosis (stroke, MI, renal thrombosis)
  • Pregnancy complications (recurrent miscarriage, pre-eclampsia,…)
166
Q

what is the clinical presentation of wegener’s granulomatosis?

A

Classic sign on exams: saddle shaped nose

Epistaxis - nosebleed

Crusty nasal/ ear secretions 🡪 hearing loss

Sinusitis

Cough, wheeze, haemoptysis

167
Q

what are the complications of wegener’s granulomatosis?

A

Glomerulonephritis

168
Q

what is the most common primary bone malignancy in children?

A

osteosarcoma

169
Q

what condition is osteosarcoma associated with?

A

Paget’s disease

170
Q

what is the appearance of osteosarcoma on x-rays?

A

bone destruction and formation,

soft tissue calcification produces a sunburst appearance

171
Q

what is the clinical presentation of ewing’s sarcoma?

A

● Presents with mass/swelling, most commonly in long bones of the
o Arms, legs, pelvis, chest
o Occasionally skull and flat bones of the trunk

● Painful swelling, redness in surrounding area, malaise, anorexia, weight loss, fever, paralysis and/or incontinence if affecting the spine, numbness in affected limb

172
Q

where is Ewing’s sarcoma commonly found?

A

Presents with mass/swelling, most commonly in long bones of the
o Arms, legs, pelvis, chest
o Occasionally skull and flat bones of the trunk

173
Q

where does chrondosarcoma commonly present?

A

Common sites are pelvis, femur, humerus, scapula and ribs

174
Q

what is the clinical presentation of chrondrosarcoma?

A

Associated with dull, deep pain and affected area is swollen and tender

175
Q

which is the most common sarcoma in adults?

A

chondrosarcoma

176
Q

which types of malignancy cause bone pain?

A
  • multiple myeloma
  • lymphoma
  • primary bone tumours
  • metastases - secondary bone tumour
177
Q

other than bone pain, what other symptoms can indicate bone tumours?

A
  • Mobility issues → unexplained limp, joint stiffness, reduced ROM
  • Inflammation + tenderness over bone
  • Systemic symptoms
178
Q

what is the prophylactic treatment for antiphospholipid syndrome?

A

aspirin or clopidogrel for people with aPL

179
Q

what are the risk factors for scleroderma?

A
  • exposure to vinyl chloride, silica dust, rapeseed oil, trichloroethylene
  • bleomycin
  • genetic
180
Q

what is polymyositis?

A

a rare muscle disorder of unknown aetiology in which there is inflammation and necrosis of skeletal muscle fibres

181
Q

what is dermatomyositis?

A

polymyositis with skin involvement

182
Q

what is the clinical presentation of polymyositis?

A
  • symmetrical progressive muscle weakness and wasting - affects proximal muscles of shoulder and pelvic girdle
  • difficulty squatting, going upstairs, rising from chair and raising hands above head
  • involvement of pharyngeal, laryngeal and respiratory muscles = dysphagia, dysphonia and respiratory failure
  • pain and tenderness = uncommon
183
Q

what is the clinical presentation of dermatomyositis?

A
  • heliotrope (purple) discolouration of eyelids
  • scaly erythematous plaques over knuckles (Gotton’s papules)
  • arthralgia, dysphagia and raynauds
184
Q

what are the investigations for polymyositis/dermatomyositis?

A

Muscle Biopsy

Bloods
- serum creatine kinase, aminotransferases, lactate dehydrogenase (LDH) and aldolase all raised

Immunology
ANA, Anti jo1, anti mi2

185
Q

what is the treatment for polymyositis/dermatomyositis?

A
  • bed rest + exercise plan
  • oral prednisolone
  • steroid sparing immunosuppressive - azathioprine, methotrexate, ciclosporin
  • hydroxychloroquine for skin disease
186
Q

what factors are used in the FRAX score calculation?

A
  • age
  • sex
  • height and weight
  • previous fractures
  • smoking
  • parent fractured hip (FHx)
  • steroid (glucocorticoid use)
  • RA
  • secondary osteoporosis
  • alcohol consumption (>3 units)
  • femoral neck bone mineral density
187
Q

what is the diagnostic criteria for RA?

A

RF RISES - >6 weeks and >4 of following:

  • RF positive
  • Finger/hand/wrist involvement
  • Rheumatoid nodules present
  • Involvement of >3 joints
  • Stiffness in morning >1 hr
  • Erosions on x-ray
  • Symmetrical involvement
188
Q

what is the treatment for raynauds phenomenon?

A

Lifestyle - protect the hands, stop smoking

Medications - CCB

189
Q

what is limited scleroderma?

A
  • skin involvement limited to hands, face, feet and forearms
  • characteristic ‘beak’-like nose and small mouth
  • Microstomia - small mouth
190
Q

what is diffuse scleroderma?

A

skin changes develop more rapidly and are more widespread
Raynaud’s phenomenon coincident with skin involvement
GI, Renal, Lung involvement

191
Q

what is paget’s disease?

A

localized disorder of bone remodelling
↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
Leads to structurally disorganized mosaic of bone (woven bone)

192
Q

what is the pathophysiology of paget’s disease?

A

↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
Leads to structurally disorganized mosaic of bone (woven bone)

193
Q

what are the clinical features of paget’s disease?

A

60-80% are asymptomatic

  • bone pain
  • joint pain
  • deformities -> bowed tibia and skull enlargement
  • neurological complications
  • CN8 compression -> deafness
  • blockage of aqueduct of sylvius causing hydrocephalus
194
Q

what are the investigations for paget’s disease?

A

Bloods - Increased ALP, normal calcium and phosphate

Urinary hydroxyproline increase

X-rays - Findings of osteoarthritis, sclerotic changes, bone loss and reduced density

isotope bone scan

195
Q

what is the management for paget’s disease?

A

Bisphosphonates,

NSAIDS

196
Q

what is osteomalacia?

A

Defective mineralization of newly formed bone matrix or osteoid in adults, due to inadequate phosphate or calcium, or due to ↑ bone resorption (hyperPTH)

197
Q

what are the causes of osteomalacia?

A

malnutrition (most common)
drug induced
defective 1-alpha hydroxylation
Liver disease

198
Q

what is the clincial presentation of osteomalacia?

A 
Osteomalacia
widespread bone pain and tenderness
gradual onset and persistent fatigue
muscle weakness, parasthesia, waddling gait
fractures
199
Q

what is the clincial presentation of rickets?

A

leg-bowing and knock knees
- tender swollen joints
- growth retardation
- bone and joint pain
dental deformities – delayed formation of teeth, enamel hypoplasia
- enlargement of end of ribs (‘rachitic rosary’)

200
Q

what are the investigations for Osteomalacia / rickets?

A

Bloods - U&Es, Serum ALP, Vit D

X-rays - defective mineralisation, rachitic rosary

201
Q

what is the management for osteomalacia/rickets?

A

Lifestyle - nutrition, sunlight
Medications - Vit D replacement
Malabsorption/Renal disease - IM calcitriol

202
Q

what is the sepsis 6?

A
  1. administer O2
  2. take blood cultures
  3. give IV antibiotics
  4. give IV fluids
  5. check serial lactates
  6. measure urine output
203
Q

what are the common sites for bone changes in paget’s disease?

A

pelvis
vertebrae - thoracic + lumbar
femur
skull tibia

204
Q

what are the complications of Paget’s?

A

nerve compression - deafness and paraparesis
hydrocephalus
oestosarcoma
high output cardiac failure and myocardial hypertrophy

Phase 2A revision (38 decks)

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