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MSK/Rheumatology Flashcards

1
Q

OSTEOARTHRITIS
What is osteoarthritis (OA)?
What causes it?

A
  • Degenerative joint disorder with loss of hyaline cartilage “wear and tear”
  • Primary (no underlying cause) or secondary to joint trauma or obesity
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2
Q

OSTEOARTHRITIS
What joints does OA tend to affect?
What symptoms might a patient complain of?

A
  • Large weight bearing (hip, knee), also carpometocarpal joints, DIP/PIPJs
  • Morning stiffness <30m + stiffness after rest
  • Joint pain which is exacerbated on movement
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3
Q

OSTEOARTHRITIS

What are some examination signs of OA?

A
  • Deformity = squaring of thumb (carpometacarpal joint of thumb), Bouchard nodes (PIPJ swelling) + Heberden nodes (DIPJ swelling)
  • Decreased range of movement
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4
Q

OSTEOARTHRITIS

What investigation would you do in suspected OA and what would you expect to see?

A

Joint x-ray shows LOSS –

  • Loss of joint space
  • Osteophytes
  • Subchondral cysts
  • Subchondral sclerosis
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5
Q

OSTEOARTHRITIS

What is the conservative management of OA?

A
  • Weight loss
  • Aerobic exercises for muscle strengthening (avoid weight-bearing)
  • Physio/OT
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6
Q

OSTEOARTHRITIS

What is the stepwise medical management of OA?

A
  • First line = paracetamol + topical NSAID gel
  • Second line = PO NSAIDs (+ PPI) or weak then stronger opioids
  • Intra-articular steroid injections
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7
Q

OSTEOARTHRITIS

After medical management, how might you manage OA?

A
  • Surgical = arthroplasty (joint replacement), arthroscopy (loose bodies), fusion
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8
Q

RHEUMATOID ARTHRITIS
What is rheumatoid arthritis (RA)?
What is the epidemiology?

A
  • Autoimmune inflammatory synovial joint disease commonly presenting with a symmetrical distal polyarthropathy affecting small joints
  • F>M, peak onset 40–60s
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9
Q

RHEUMATOID ARTHRITIS
What joints does RA tend to affect?
What symptoms might a patient complain of?

A
  • Small joints in hands + feet, almost NEVER DIPJs
  • Early morning stiffness >30m which improves with use
  • Swollen, painful joints in hands + feet
  • Systemically unwell (fatigue, flu-like illness)
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10
Q

RHEUMATOID ARTHRITIS

What are some examination signs of RA?

A
  • Swollen, red, warm + tender joints
  • Ulnar deviation of fingers at the MCPJs
  • Z-shaped deformity of thumb
  • Boutonnière thumb = hyperextended DIPJ, flexed PIPJ
  • Swan-neck deformity = hyperextended PIPJ, flexed DIPJ
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11
Q

RHEUMATOID ARTHRITIS

What are some extra-articular manifestations of RA?

A
  • Eyes = keratoconjunctivitis sicca #1, (epi)scleritis, corneal ulceration
  • Neuro = carpal tunnel syndrome
  • Resp = pulmonary fibrosis, pleural effusion, nodules
  • Cardio = pericardial effusion, IHD
  • Felty syndrome = RA + splenomegaly + low WCC
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12
Q

RHEUMATOID ARTHRITIS

A patient with known RA presents with neck pain, weakness and loss of sensation in the arms. What has happened?

A
  • Atlanto-axial joint subluxation
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13
Q

RHEUMATOID ARTHRITIS

What investigations would you do in RA?

A
  • FBC = anaemia of chronic disease
  • Raised CRP/ESR
  • Serum Ab = rheumatoid factor (IgM) first-line but anti-CCP if negative as more specific
  • XR of hands + feet
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14
Q

RHEUMATOID ARTHRITIS

What does an xray show in RA?

A

LESS –

  • Loss of joint space
  • Erosions (periarticular)
  • Soft tissue swelling
  • Soft bone (periarticular osteoporosis) + Subluxation
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15
Q

RHEUMATOID ARTHRITIS

What are some poor prognostic markers in RA?

A
  • RF
  • Anti-CCP
  • XR showing early erosions
  • Extra-articular signs
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16
Q

RHEUMATOID ARTHRITIS
What is the mainstay of management for RA?
Give some examples

A
  • Disease modifying antirheumatic drugs (DMARDs)

- Methotrexate, leflunomide, sulfasalazine + hydroxychloroquine

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17
Q 
RHEUMATOID ARTHRITIS
How is methotrexate prescribed?
Does it require monitoring?
What drugs should be avoided and why?
What are some side effects?
A
  • Once weekly, 5mg folic acid on separate day
  • Regular FBC, U&E, LFTs baseline, weekly, 3/12
  • Trimethoprim + co-trimoxazole as risk of marrow aplasia
  • Myelosuppression, liver/pulmonary fibrosis, teratogenic (M+F stop 6m prior to conception)
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18
Q

RHEUMATOID ARTHRITIS
What are some side effects of…

i) leflunomide?
ii) sulfasalazine?
iii) hydroxychloroquine?

A

i) HTN, peripheral neuropathy
ii) Rashes, oligospermia
iii) Retinopathy (reduced vision), nightmares

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19
Q

RHEUMATOID ARTHRITIS

What more advanced treatments may be used in RA management and what are some side effects of them?

A
  • TNF-alpha inhibitors (infliximab, adalimumab, etanercept) = severe infections, reactivation of TB
  • Rituximab (monoclonal Ab to CD20) = night sweats + thrombocytopaenia
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20
Q

RHEUMATOID ARTHRITIS

What is the stepwise management of RA?

A
  • 1st = DMARD monotherapy ± short course of bridging prednisolone
  • 2nd = 2 DMARDs in combination
  • 3rd = Methotrexate PLUS TNF-alpha inhibitor
  • 4th = Methotrexate PLUS rituximab
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21
Q

RHEUMATOID ARTHRITIS
How do you manage a flare of RA?
How does NICE recommend you assess response to RA management?
What other options might you consider in RA management?

A
  • PO/IM corticosteroids
  • CRP + disease activity (DAS28 score)
  • Analgesia (NSAIDs), physiotherapy + surgery
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22
Q

GOUT

What is gout?

A
  • Inflammatory arthritis caused by hyperuricaemia (>0.45) + intra-articular deposition of monosodium urate crystals
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23
Q

GOUT

What are the two broad aetiologies of gout and some examples for each?

A
  • Increased uric acid production = myelo- + lymphoproliferative disorders, chemotherapy, severe psoriasis
  • Decreased uric acid excretion = diuretics, renal impairment, alcohol excess
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24
Q

GOUT
What are some potential triggers of a gout episode?
What are some risk factors for gout?

A
  • Seafood/protein binges, chemo, trauma + surgery

- Men, obesity, CKD, DM, medications (diuretics, ACEi)

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25
Q

GOUT
What joints are typically affected in gout?
What is the clinical presentation of gout?

A
  • Classically 1st metatarsophalangeal joint, also wrists + CMCJ of thumb
  • Acute hot, swollen, red + painful joint
  • Reduced ROM
  • Mild fever
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26
Q

GOUT

What are two potential sequelae from gout?

A
  • Chronic tophaceous gout = large smooth white deposits (tophi, urate crystals) in skin + joints (DIPJ, elbows, ears)
  • Chronic polyarticular gout = painful erythematous swelling
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27
Q

GOUT

What investigations would you do in gout and why?

A
  • Serum urate (2w after attack as can be low/falsely normal)
  • Joint fluid aspiration MC&S to rule out septic arthritis
  • Joint XR
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28
Q

GOUT

What would joint fluid aspiration MC&S show in gout?

A
  • NO bacterial growth = excludes septic arthritis
  • Needle shaped crystals
  • Negative birefringence under polarised light
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29
Q

GOUT

What would a joint xray show in gout?

A
  • NORMAL joint space
  • Soft tissue swelling
  • Periarticular erosions
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30
Q

GOUT

What lifestyle advice would you recommend in gout?

A
  • Reduce alcohol + avoid in acute
  • Lose weight
  • Avoid purine rich food = liver, kidney, seafood, oily fish
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31
Q

GOUT
How do you manage an acute flare of gout?
What is a side effect to be aware of?

A
  • NSAIDs first line (unless C/I) if not colchicine
  • Colchicine = slower onset + can cause diarrhoea
  • Steroids may be considered
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32
Q

GOUT
What is the prophylaxis for gout and it’s mechanism?
When is it started?
What drug should you be cautious of?

A
  • Allopurinol = xanthine oxidase inhibitor > reduces uric acid levels
  • After acute attack (2w) + cover with colchicine or NSAID
  • Azathioprine toxicity due to 6-mercaptopurine build up
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33
Q

PSEUDOGOUT
What is pseudogout?
What are some associations with it?

A
  • Microcrystal synovitis caused by deposition of calcium pyrophosphate crystals on joint surfaces
  • Hyperparathyroidism, hypothyroidism, haemochromatosis + hypophosphataemia
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34
Q

PSEUDOGOUT
What joints are typically affected in pseudogout?
What is the clinical presentation of pseudogout?

A
  • Knee, wrists + shoulder
  • Acute hot, swollen, red, painful joint
  • Reduced ROM
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35
Q

PSEUDOGOUT

What investigations would you do in pseudogout and what would you find?

A
  • Joint fluid aspiration MC&S = no bacterial growth (excludes septic arthritis), rhomboid-shaped crystals, Positive birefringence under polarised light
  • XR = chondrocalcinosis (calcium deposition in cartilage of joints)
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36
Q

PSEUDOGOUT

What is the management of pseudogout?

A
  • NSAIDs or colchicine if C/I

- PO/intra-articular corticosteroids if both above C/I

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37
Q

ANKYLOSING SPONDYLITIS

What is ankylosing spondylitis?

A
  • Seronegative spondyloarthropathy = HLA B27 associated typically affecting the sacroiliac joints + joints of the vertebral column
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38
Q

ANKYLOSING SPONDYLITIS

What is the clinical presentation of ankylosing spondylitis?

A
  • Insidious onset lower back pain + stiffness in a young man
  • Stiffness worse in the morning + improves with exercise
  • Night pain which improves with movement
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39
Q

ANKYLOSING SPONDYLITIS

What are some examination signs of ankylosing spondylitis

A
  • Reduced lateral + forward flexion (Schober’s test <20cm)
  • Loss of lumbar lordosis + progressive thoracic kyphosis
  • Reduced chest expansion
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40
Q

ANKYLOSING SPONDYLITIS

What are some extra-articular features of ankylosing spondylitis?

A
  • As = Apical fibrosis, Anterior uveitis, Aortic regurg, Achilles tendonitis (enthesitis), AV node block, Amyloidosis
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41
Q

ANKYLOSING SPONDYLITIS
What investigations may you do in ankylosing spondylitis?
What investigation is most useful?

A
  • FBC, CRP/ESR elevated, HLA B27 +ve
  • CXR = apical fibrosis
  • Restrictive spirometry
  • Plain x-ray of sacroiliac joints/spine most useful
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42
Q

ANKYLOSING SPONDYLITIS

What features may be present on x-ray in ankylosing spondylitis?

A
  • Sacroiliitis = subchondral erosions, sclerosis
  • Squaring of lumbar vertebrae
  • Syndesmophytes = ossification of outer fibres of annulus fibrosus
  • Bamboo spine (fusion) is late finding
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43
Q

ANKYLOSING SPONDYLITIS

What is the management of ankylosing spondylitis?

A
  • Encourage regular exercise, physio input
  • NSAIDs = first line
  • DMARDs only useful if peripheral joint involvement
  • Anti-TNF therapy if persistently high disease activity despite treatments
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44
Q

PSORIATIC ARTHRITIS
What is psoriatic arthritis?
What are the 5 different types?

A
  • Seronegative spondyloarthropathy = HLA-B27 associated
  • Symmetrical polyarthritis (>5 joints)
  • Asymmetrical oligoarthritis (<5 joints)
  • Spondylitic pattern
  • Distal interphalangeal joint arthritis
  • Arthritis mutilans
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45
Q

PSORIATIC ARTHRITIS
What are some features of…

i) symmetrical polyarthritis?
ii) asymmetrical oligoarthritis?
iii) spondylitic pattern?
iv) arthritis mutilans?

A

i) Like RA but DIPJ affected and MCPJ less affected in comparison
ii) Mainly affects digits
iii) Back stiffness + sacroiliitis, more common in men
iv) Severe deformity with destruction of bone in digits > telescoping

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46
Q

PSORIATIC ARTHRITIS
What is the clinical presentation of psoriatic arthritis?
What are some extra-articular findings?

A
  • Joint pain, swelling + stiffness

- Anterior uveitis, aortitis, amyloidosis

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47
Q

PSORIATIC ARTHRITIS

What are some clinical signs seen in psoriatic arthritis?

A
  • Psoriatic plaques (check scalp, behind ears, umbilicus, natal cleft)
  • Nail changes = onycholysis, pitting, subungual hyperkeratosis
  • Enthesitis = Achilles’ tendonitis, plantar fasciitis
  • Tenosynovitis
  • Dactylitis
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48
Q

PSORIATIC ARTHRITIS

What investigation might you do in psoriatic arthritis and what might you see?

A
  • XR = erosive changes + new bone formation, periostitis, ‘pencil-in-cup’ appearance
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49
Q

PSORIATIC ARTHRITIS

What is the management of psoriatic arthritis?

A
  • Guided by rheumatologist > mild peripheral arthritis = NSAIDs, some may be on monoclonal antibodies
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50
Q

REACTIVE ARTHRITIS

What is reactive arthritis?

A
  • Seronegative spondyloarthropathy = HLA-B27 with sterile inflammation of the synovial membrane due to autoimmune reaction to infection elsewhere
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51
Q

REACTIVE ARTHRITIS

What causes reactive arthritis?

A
  • Post-dysenteric illness = Shigella, Salmonella, Campylobacter
  • Post-STI = chlamydia (more common in men)
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52
Q

REACTIVE ARTHRITIS

What is the clinical presentation of reactive arthritis?

A
  • 4w post-infection triad of “can’t see, can’t pee, can’t climb a tree” = conjunctivitis, urethritis + arthritis
  • Usually asymmetrical oligoarthritis of lower limbs
  • Systemically unwell
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53
Q

REACTIVE ARTHRITIS

What are the extra-articular manifestations of reactive arthritis?

A
  • Anterior uveitis
  • Circinate balanitis (painless vesicles on prepuce)
  • Keratoderma blenorrhagica = waxy yellow/brown papules on palms/soles
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54
Q

REACTIVE ARTHRITIS

What investigations would you do in reactive arthritis?

A
  • Raised CRP/ESR
  • HLA-B27 +ve
  • Joint MC&S to exclude septic arthritis = sterile with high neutrophils
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55
Q

REACTIVE ARTHRITIS

What is the management of reactive arthritis?

A
  • Analgesia (NSAIDs), ?intra-articular steroids

- DMARDs (methotrexate/sulfasalazine) if Sx >6m

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56
Q

SEPTIC ARTHRITIS
What is septic arthritis?
How does it occur?
What can cause it?

A
  • Acute joint infection which can cause damaging inflammation + joint loss <24h
  • Commonly haematogenous spread
  • # 1 overall = staphylococcus aureus
  • # 1 in young, sexually active = neisseria gonorrhoea
  • In infants, think about group B strep
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57
Q

SEPTIC ARTHRITIS

What are some risk factors for developing septic arthritis?

A
  • Pre-existing joint disease (especially RA)
  • Prosthetic joints
  • IVDU
  • Immunosuppression (DM/HIV)
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58
Q

SEPTIC ARTHRITIS
What is the clinical presentation of septic arthritis?
Additional features in paeds?

A
  • Acute red, hot, swollen joint (commonly knee)
  • Pain on movement + reduced ROM
  • Systemically unwell (fever)
  • Paeds = may present with limb + refusal to weight bear
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59
Q

SEPTIC ARTHRITIS

What investigations would you do for septic arthritis?

A
  • Blood cultures, FBC (raised WCC), CRP/ESR raised
  • Joint aspiration for MC&S crucial
  • XR joint
  • Kocher criteria ≥3 = temp>38.5, non-weight bearing, raised ESR + WCC
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60
Q

SEPTIC ARTHRITIS

What is the management of septic arthritis?

A
  • IV Abx often flucloxacillin (clindamycin if pen allergic) before sensitivities back
  • Arthroscopic lavage may be required, analgesia
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61
Q

OSTEOMYELITIS
What is osteomyelitis?
What are the two ways it can occur?

A
  • Infection in the bone + bone marrow, often in metaphysis of long bones
  • Haematogenous from bacteraemia (#1 paeds) or non-haematogenous from spread from adjacent soft tissues (#1 adults)
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62
Q

OSTEOMYELITIS
What are some risk factors for haematogenous spread osteomyelitis?
What are some risk factors for non-haematogenous spread osteomyelitis?

A
  • Sickle cell anaemia, IVDU, immunosuppression

- PVD, DM + diabetic foot ulcers

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63
Q

OSTEOMYELITIS

What are some common organisms that can cause osteomyelitis?

A
  • Staph. aureus #1, H. influenzae

- Most common in sickle cell anaemia = Salmonella

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64
Q

OSTEOMYELITIS

What is the clinical presentation of osteomyelitis?

A
  • Local pain, swelling + erythema
  • Refusal to weight bear + reduced ROM
  • Systemically unwell (fever)
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65
Q

OSTEOMYELITIS

What are some investigations for osteomyelitis?

A
  • FBC (raised WCC), raised ESR/CRP, blood cultures

- XR may be normal so MRI is best diagnostic imaging

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66
Q

OSTEOMYELITIS

What is the management of osteomyelitis?

A
  • IV empirical Abx (flucloxacillin or clindamycin if pen allergic) until sensitivities back
  • Surgical debridement mainstay for chronic
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67
Q

SLE
What is the pathophysiology of systemic lupus erythematosus (SLE)?
What is the epidemiology?

A
  • Multi-system autoimmune disease where immune system dysregulation leads to immune complex formation + deposition (T3HR)
  • More common in females, Afro-Caribbean + Asian communities + onset 20–40y
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68
Q

SLE
What are some drugs that may cause SLE?
What are some potential triggers of SLE?

A
  • SHIPP = Sulfonamides, Hydralazine, Isoniazid, Phenytoin, Procainamide
  • Oestrogen containing contraception, sunlight overexposure, infections + stress
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69
Q

SLE

What is the clinical presentation of SLE?

A

DOPAMINE RASH –

  • Discoid lupus (erythematous raised patches with keratotic scales)
  • Oral ulcers
  • Photosensitivity
  • Arthritis
  • Malar rash (spares nasolabial folds)
  • Immunological
  • Neuro (psychosis, depression, seizures)
  • ESR raised
  • Raynaud’s/renal involvement (proteinuria, HTN)
  • ANA +ve
  • Serositis (pleurisy, pericarditis)
  • Haem (anaemia of chronic disease, low WCC + plts)
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70
Q

SLE

What are some investigations you might do in SLE?

A
  • FBC (anaemia of chronic disease, low WCC + plts)
  • Antibodies = 99% ANA +ve (not specific), anti-dsDNA (specific) and anti-Smith (specific), anti-histone in drug induced lupus
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71
Q

SLE

How would you monitor SLE disease activity?

A
  • ESR as CRP can be normal so raised CRP ?infection
  • Complement levels (C3/4) LOW in active disease
  • Urinalysis + urine ACR to monitor for proteinuria
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72
Q

SLE
What is the leading cause of death in SLE?
What are some other complications?

A
  • CVD
  • Infections, pericarditis, pleurisy
  • Lupus nephritis > nephrotic syndrome > ESRF
  • Antiphospholipid syndrome
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73
Q

SLE

What is antiphospholipid syndrome?

A
  • Acquired disorder leading to predisposition to venous + arterial thromboses, recurrent foetal loss + thrombocytopaenia
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74
Q

SLE

What is the clinical presentation of antiphospholipid syndrome?

A

CLOTS

  • Coagulation defect (raised APTT)
  • Livedo reticularis
  • Obstetric (Recurrent miscarriage)
  • Thrombocytopaenia
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75
Q

SLE
What markers in the blood would you look for in antiphospholipid syndrome?
What is the primary thromboprophylaxis of antiphospholipid syndrome?

A
  • Anticardiolipin + lupus anticoagulant antibodies

- Low dose aspirin

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76
Q

SLE

How do you manage VTE in antiphospholipid syndrome?

A
  • First = lifelong warfarin with INR target 2–3

- Subsequent on warfarin = INR target 3–4

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77
Q

SLE

What is the management of SLE?

A
  • Conservative = sun block
  • Mainstay = DMARD hydroxychloroquine + NSAIDs
  • Consider pred or cyclophosphamide if internal organ involvement
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78
Q

GIANT CELL ARTERITIS
What is giant cell arteritis (GCA)?
What is it associated with?

A
  • Large vessel vasculitis

- PMR, those >60y/o

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79
Q

GIANT CELL ARTERITIS

What is the clinical presentation of GCA?

A
  • Severe unilateral temporal headache
  • Scalp tenderness (brushing hair)
  • Jaw claudication
  • Blurred, double vision, amaurosis fugax
  • Systemic = fever, fatigue, weight loss
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80
Q

GIANT CELL ARTERITIS

What signs might be present in GCA?

A
  • Tender, thickened, pulseless temporal artery
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81
Q

GIANT CELL ARTERITIS

What initial investigations would you do in GCA?

A
  • FBC = normocytic anaemia + thrombocytosis
  • LFTs = raised ALP
  • CRP/ESR (ESR >60mm/h in >60y/o)
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82
Q

GIANT CELL ARTERITIS
What other investigations would you do in GCA?
What investigation is diagnostic?

A
  • Duplex USS temporal artery = hypoechoic halo sign

- Vascular for temporal artery biopsy Dx = multinucleated giant cells, ?skip lesions

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83
Q

GIANT CELL ARTERITIS

What are some potential complications of GCA and how are they managed?

A
  • Stroke
  • Permanent monocular blindness due to anterior ischaemic optic neuropathy
  • Ophthalmology for emergency same day appt if visual Sx
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84
Q

GIANT CELL ARTERITIS

What is the management of GCA?

A
  • Stat high dose corticosteroids before biopsy = IV methyl pred (visual loss), PO pred (no visual loss) + gradually taper
  • Bisphosphonate + PPI cover whilst on steroids
  • Aspirin 75mg OD to decrease vision loss + stroke risk
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85
Q

POLYMYALGIA RHEUMATICA
What is polymyalgia rheumatica?
How does it usually present?

A
  • Inflammatory condition strongly associated to GCA causing muscle stiffness
  • Rapid onset <1m in a white woman >60y/o
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86
Q

POLYMYALGIA RHEUMATICA

What is the clinical presentation of polymyalgia rheumatica?

A
  • Bilateral shoulder + pelvic girdle pain
  • Aching + morning stiffness in proximal limb muscles but NO weakness
  • Systemic = low-grade fever, fatigue
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87
Q

POLYMYALGIA RHEUMATICA
What investigations would you do in polymyalgia rheumatica?
What is the management?

A
  • ESR/CRP raised, creatinine kinase + EMG normal

- PO prednisolone shows dramatic response (diagnostic)

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88
Q

SJOGREN’S SYNDROME

What is the pathophysiology of Sjogren’s syndrome?

A
  • Autoimmune lymphocytic infiltration of exocrine glands (type 4 hypersensitivity reaction) > dry mucosal surfaces
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89
Q

SJOGREN’S SYNDROME
What causes Sjogren’s syndrome?
What is the epidemiology and what are patients with Sjogren’s syndrome at risk of?

A
  • Primary or secondary to RA, SLE or other connective tissue disorders
  • Much more common in females
  • Increased risk of lymphoid malignancy
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90
Q

SJOGREN’S SYNDROME

What is the clinical presentation of Sjogren’s syndrome?

A
  • Reduced tear secretion (keratoconjunctivitis sicca) = dry, gritty eyes
  • Reduced saliva = dry mouth + dysphagia
  • Recurrent episodes of parotitis
  • Vaginal dryness = dyspareunia
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91
Q

SJOGREN’S SYNDROME

What are some extra-glandular features of Sjogren’s syndrome?

A
  • Raynaud’s
  • Arthritis
  • Systemic upset (fever, fatigue)
92
Q

SJOGREN’S SYNDROME

What investigations would you do in Sjogren’s syndrome?

A
  • Schirmer’s test = filter paper near conjunctival sac to measure tear formation
  • Specific Ab = anti-Ro + anti-La
  • Non-specific Ab = RF + ANA
93
Q

SJOGREN’S SYNDROME

What is the management of Sjogren’s syndrome?

A
  • Artificial saliva + tears

- Pilocarpine may stimulate saliva production

94
Q

RAYNAUD’S
What is Raynaud’s?
What causes it?

A
  • Exaggerated vasoconstrictive response of digital arteries + cutaneous arterioles to the cold or emotional stress
  • Primary (Raynaud’s disease) or secondary (phenomenon) = RA, SLE, Sjogren’s
95
Q

RAYNAUD’S
What is the classic clinical presentation of Raynaud’s?
How can you clinically differentiate between Raynaud’s disease and phenomenon?

A
  • Colour change of fingertips white > blue > red
  • Disease = young women, bilateral
  • Phenomenon = unilateral, rashes, onset after 40y/o
96
Q

RAYNAUD’S

What is the management of Raynaud’s

A
  • All referred to secondary care
  • First line = CCB nifedipine
  • IV prostacyclin infusion may be used
97
Q

SYSTEMIC SCLEROSIS
What is systemic sclerosis?
Who does it normally affect?
What general antibodies are associated with it?

A
  • Disease characterised by hardened, sclerotic skin + other connective tissues
  • Females
  • ANA + RF but not specific
98
Q

SYSTEMIC SCLEROSIS

What are the three subtypes in systemic sclerosis and the antibodies associated?

A
  • Limited cutaneous systemic sclerosis = anti-centromere
  • Diffuse cutaneous systemic sclerosis = anti-scl-70
  • Scleroderma
99
Q

SYSTEMIC SCLEROSIS
Where is affected in limited cutaneous systemic sclerosis?
What is the clinical presentation?

A
  • Scleroderma affects face + distal limbs mainly

- Subtype CREST syndrome = Calcinosis, Raynaud’s, oEsophageal dysmotility, Sclerodactyly, Telangiectasia

100
Q

SYSTEMIC SCLEROSIS
Where is affected in diffuse cutaneous systemic sclerosis?
What are some complications?

A
  • Diffuse (may affect many internal organs) scleroderma affects trunk + proximal limbs mainly
  • # 1 cause of death resp involvement (ILD, pulmonary HTN), renal disease + HTN
101
Q

SYSTEMIC SCLEROSIS

How does scleroderma present?

A
  • Tightening and fibrosis of skin without internal organ involvement
102
Q

POLYMYOSITIS
What is polymyositis?
What is a variant?
What causes it?

A
  • Autoimmune inflammatory disorder causing symmetrical, proximal myopathy
  • Dermatomyositis with prominent skin manifestations
  • Idiopathic or associated with connective tissue disorders or malignancy (lung, ovarian, breast)
103
Q

POLYMYOSITIS

What is the clinical presentation of polymyositis?

A
  • Progressive symmetrical proximal muscle weakness (shoulder + pelvic girdle), F>M
  • Dysphagia, dysphonia + resp muscle weakness
104
Q

POLYMYOSITIS

How does dermatomyositis present?

A
  • Photosensitive rash
  • Grotton’s papules = rough red papules on finger extensors
  • Heliotrope (purple) periorbital rash
105
Q

POLYMYOSITIS
What are some investigations you might do in polymyositis?
What investigation is diagnostic?
What antibodies might you find?

A
  • Muscle enzymes raised (CK, LDH), EMG
  • Muscle biopsy Dx
  • Anti-Jo-1 (specific), also ANA
106
Q

POLYMYOSITIS

What is the management of polymyositis?

A
  • Screen for malignancy

- Immunosuppression with PO pred

107
Q

OSTEOMALACIA

What is osteomalacia?

A
  • Softening of bones secondary to low vitamin D levels + other minerals > decreased bone mineral content (but normal bone mass density)
108
Q

OSTEOMALACIA

What are some causes of osteomalacia?

A
  • Vitamin D deficiency = malabsorption (IBD/coeliac), lack of sunlight, CKD, cirrhosis
  • Drugs = anticonvulsants (carbamazepine, phenytoin)
  • Inherited = hypophosphataemic rickets
109
Q

OSTEOMALACIA

What is the clinical presentation of osteomalacia?

A
  • Bone pain + tenderness
  • Fractures (especially NOF)
  • Proximal myopathy > waddling gait
110
Q

OSTEOMALACIA

What would investigations show in osteomalacia?

A
  • Low = vitamin D, calcium + phosphate
  • Raised = ALP, PTH
  • XR may show translucent bands (Looser’s zones)
111
Q

OSTEOMALACIA

What is the management of osteomalacia?

A
  • Vitamin D (colecalciferol) if 25–50nmol/L (loading dose if <25)
  • Renal disease = alfacalcidol as needs activated
  • Calcium supplementation if dietary calcium inadequate
112
Q

COMPARTMENT SYNDROME

What is the pathophysiology of compartment syndrome?

A
  • Oedema within a closed anatomical space leads to increased compartment pressure more than the venous pressure so no venous blood leaves
  • This leads to further pressure rise + so prevents entry of arterial blood leading to rapid ischaemia, muscle necrosis, rhabdomyolysis + acute renal failure
113
Q

COMPARTMENT SYNDROME

What are some causes of compartment syndrome?

A
  • Tight plaster cast, burns

- # = especially supracondylar + tibial shaft (anterior leg compartment #1)

114
Q

COMPARTMENT SYNDROME

What is the clinical presentation of compartment syndrome?

A
  • Increasing pain + pain on passive flexion
  • Loss of function + opiate analgesia does not control pain
  • Pulseless (may be present), paralysis, pallor
115
Q

COMPARTMENT SYNDROME

What investigations would you do in compartment syndrome and what might they show?

A
  • Typically XR normal

- Compartment pressure >20mmHg abnormal, >40mmHg diagnostic

116
Q

COMPARTMENT SYNDROME

What is the management of compartment syndrome?

A
  • Remove all pressure + emergency fasciotomy
  • May require debridement
  • Aggressive IV fluids due to myoglobinuria from rhabdomyolysis
117
Q

SHOULDER DISLOCATION
What happens in a shoulder dislocation?
What is the most common type?
What causes it?

A
  • Humeral head dislodges from glenoid cavity of scapula, often 2º to trauma
  • Anterior 95% = antero-inferior dislocation
  • Posterior = sustained muscle contraction like epilepsy, electric shocks
118
Q

SHOULDER DISLOCATION
What is a key complication of shoulder dislocation?
How might it present?

A
  • Axillary nerve damage
  • Sensory loss in regimental badge area over lateral deltoid
  • Motor loss in deltoid (shoulder abduction)
119
Q

SHOULDER DISLOCATION
How does shoulder dislocation present?
How is it diagnosed?
How is it managed?

A
  • Pain, reduced ROM + joint deformity
  • AP + lateral shoulder x-ray
  • Anterior = manual reduction (without sedation if recent) + sling immobilisation
  • Posterior = orthopaedic input for closed reduction
120
Q

ADHESIVE CAPSULITIS
What is adhesive capsulitis?
What is the epidemiology?

A
  • Reactive inflammation within the capsule causing adhesions (frozen shoulder)
  • Middle aged females + DM
121
Q

ADHESIVE CAPSULITIS

What is the clinical presentation of adhesive capsulitis?

A
  • Gradual onset pain + stiffness
  • EXTERNAL ROTATION is most affected, also abduction
  • BOTH active + passive movement affected
122
Q

ADHESIVE CAPSULITIS

What is the management of adhesive capsulitis?

A
  • Conservative = rest + physio

- Medical = NSAIDs or steroid injections

123
Q

ROTATOR CUFF PATHOLOGY

What are the 4 rotator cuff muscles and their action?

A

SITS –

  • Supraspinatus = abducts arm (first 20º then deltoids)
  • Infraspinatus = externally rotates arm
  • Teres minor = externally rotates arm
  • Subscapularis = internally rotates arm
124
Q

ROTATOR CUFF PATHOLOGY

What is subacromial impingement?

A
  • Entrapment of supraspinatus tendon + subacromial bursa between humeral head + acromion = subacromial bursitis + supraspinatus tendinitis
125
Q

ROTATOR CUFF PATHOLOGY

What is the clinical presentation of subacromial impingement?

A
  • Painful arc = pain between 60–120º
  • Passive abduction is painless
  • Weakness + decreased ROM (especially with overhead)
126
Q

ROTATOR CUFF PATHOLOGY

How would you investigate and manage subacromial impingement?

A
  • XR to evaluate acromiohumeral joint space
  • Conservative (rest + physio)
  • Medical (NSAIDs or steroid injection)
  • Surgical = arthroscopic acromioplasty
127
Q

ROTATOR CUFF PATHOLOGY
What causes rotator cuff tears?
How do they present?

A
  • Traumatic or secondary to repetitive activity
  • Supraspinatus = painful arc
  • Pain on movement
  • Decreased ROM depending on site of tear
128
Q

ROTATOR CUFF PATHOLOGY

How would you investigate and manage rotator cuff tears?

A
  • USS + MRI for imaging

- Rest + physio, may need open or arthroscopic repair

129
Q

EPICONDYLITIS
What are the two types of epicondylitis?
How do they present similarly?

A
  • Lateral = Tennis elbow > exTensor mechanism (of wrist)
  • Medial = Golfer’s elbow > flexor mechanism (of wrist)
  • Hx of elbow related activity
130
Q

EPICONDYLITIS
What is the clinical presentation of tennis elbow?
What is the clinical presentation of golfer’s elbow?

A
  • Pain + tenderness on lateral epicondyle, pain worse on wrist extension
  • Pain + tenderness on medial epicondyle, pain worse on wrist flexion
131
Q

EPICONDYLITIS
What signs may you elicit in tennis elbow?
What signs may you elicit in golfer’s elbow?

A
  • Pain worse on resisted wrist extension/forearm supination with elbow extended
  • Medial pain reproduced on resisted wrist flexion
132
Q

EPICONDYLITIS

What is the management of epicondylitis?

A
  • Avoid muscle overload
  • Simple analgesia (NSAIDs)
  • Physiotherapy
133
Q

OLECRANON BURSITIS

What is olecranon bursitis?

A
  • Inflammation of the bursa (fluid filled sac of synovial membrane which reduces friction between bones + soft tissues during movement) in the elbow
134
Q

OLECRANON BURSITIS

What can cause olecranon bursitis?

A
  • Repetitive damage like manual workers (e.g., carpet layers)
  • Associated with RA + gout
135
Q

OLECRANON BURSITIS

What is the clinical presentation of olecranon bursitis?

A
  • Fluctuant swelling around posterior elbow
  • May be pain, warmth + erythema
  • Infected = systemically unwell, hot to touch, spreading erythema
136
Q

OLECRANON BURSITIS

What is the management of olecranon bursitis?

A
  • Exclude septic arthritis if unwell > aspirate for joint fluid MC&S + treat empirically
  • Conservative (ice, NSAIDs), PO flucloxacillin if infected but not too unwell
137
Q

CUBITAL TUNNEL SYNDROME

What is cubital tunnel syndrome

A
  • Compression of ulnar nerve as it passes through the cubital tunnel
138
Q

CUBITAL TUNNEL SYNDROME

What is the clinical presentation of cubital tunnel syndrome?

A
  • Intermittent paraesthesia + numbness in 4/5th digit > constant
  • Over time weakness + muscle wasting
  • Pain worse when leaning on affected elbow
139
Q

CUBITAL TUNNEL SYNDROME

What signs may be present in cubital tunnel syndrome?

A
  • Claw hand

- +ve Froment’s = thumb bent when holding paper (weak adductor pollicis)

140
Q

CUBITAL TUNNEL SYNDROME

What is the management of cubital tunnel syndrome?

A
  • Avoid aggravating activity
  • Elbow splint
  • Physio
  • Steroid injections
141
Q

DE QUERVAIN’S TENOSYNOVITIS
What is De Quervain’s tenosynovitis?
What’s the epidemiology?

A
  • Sheath inflammation containing extensor pollicis brevis + abductor pollicis longus
  • Females 30–50y
142
Q

DE QUERVAIN’S TENOSYNOVITIS

What is the clinical presentation of De Quervain’s tenosynovitis?

A
  • Pain + swelling in anatomical snuffbox
  • Radial styloid process tenderness
  • Finkelstein’s test = pain reproduced by bending thumb into palm
143
Q

DE QUERVAIN’S TENOSYNOVITIS

What is the management of De Quervain’s tenosynovitis?

A
  • Rest, NSAIDs, steroid injections, thumb splint

- Surgical decompression may be required

144
Q

TRIGGER FINGER

What is trigger finger?

A
  • Thickening of flexor tendon or tendon sheath with tendon nodules at entry of tendon sheath > prevents tendon passing through sheath = trapped in flexion
145
Q

TRIGGER FINGER
What is the clinical presentation of trigger finger?
How is it managed?

A
  • Fixed flexion deformity in thumb, middle + ring finger
  • Forced extension = painful click
  • Steroid injection ± finger splint or surgery
146
Q

DUPUYTREN’S CONTRACTURE
What is a dupuytren’s contracture?
What causes it?
What is the management?

A
  • Painless fibrotic thickening of palmar fascia, commonly ring + little fingers
  • Manual labour, phenytoin, alcoholic liver disease, DM
  • Physio, fasciectomy if MCPJ cannot be straightened (hand can’t be flat on table)
147
Q

UPPER LIMB FRACTURES
What is a key feature of a proximal humerus fracture?
What is a key complication?

A
  • Children = #1 greenstick fracture (breaks on 1 side) through surgical neck
  • Axillary nerve damage = sensory loss regimental badge area over deltoid, motor loss in deltoid (shoulder abduction
148
Q

UPPER LIMB FRACTURES
What causes a supracondylar fracture of the humerus?
How does it present?

A
  • Children fall onto outstretched arm

- Elbow in semi-flexed position with tenderness + swelling

149
Q

UPPER LIMB FRACTURES
What is a potential consequence of a supracondylar fracture?
What is the management?

A
  • Damage to brachial artery, median or radial nerve + compartment syndrome
  • Non-displaced = collar + cuff, displaced = anaesthetic manipulation
150
Q

UPPER LIMB FRACTURES

What is a Colles’ fracture?

A
  • Transverse radial # within 2.5cm of distal end of radius with dorsal (upwards) angulation of distal fragment
151
Q

UPPER LIMB FRACTURES

What are some clinical features of a Colles’ fracture?

A
  • Falling onto outstretched hand
  • Females >50y with osteoporosis
  • Dinner fork deformity
152
Q

UPPER LIMB FRACTURES

What is the management of a Colles’ fracture?

A
  • Manipulation for reduction if not open reduction + internal fixation
153
Q

UPPER LIMB FRACTURES
What causes a scaphoid fracture?
What are the clinical features?

A
  • Fall onto outstretched hand
  • Tender, swollen anatomical snuffbox
  • Pain on wrist movements + thumb compression
154
Q

UPPER LIMB FRACTURES

What is a key complication with scaphoid fractures?

A
  • Retrograde blood supply so complete # = avascular necrosis + non-union
155
Q

UPPER LIMB FRACTURES
How are scaphoid fractures diagnosed?
What is the management of scaphoid fractures?

A
  • Scaphoid XRs
  • Treat if high suspicion even if no initial radiological evidence
  • Wrist in scaphoid plaster
156
Q

UPPER LIMB FRACTURES

What is a smith’s fracture?

A
  • Reverse Colles’ with anterior (volar) angulation of distal fragment
157
Q

UPPER LIMB FRACTURES
What is a boxer’s fracture?
How does it present?

A
  • # neck of 4th or 5th metacarpal due to punching a hard object
  • Pain + swelling over MCPJ of 4th/5th fingers
158
Q

UPPER LIMB FRACTURES
What is a Bennett’s fracture?
How does it appear on XR?

A
  • Intra-articular # at base of thumb metacarpal from fist fights
  • Triangular fragment at base of metacarpal
159
Q

UPPER LIMB FRACTURES

What is a Barton’s fracture?

A
  • Colles/Smith’s with associated radiocarpal dislocation
160
Q

UPPER LIMB FRACTURES

What is the difference between a Monteggia + Galeazzi fracture?

A

MUGGER –
- MonteggiA = PROXIMAL Ulnar # with dislocation of PROXIMAL radial head
- GaleazZi = DISTAL Radial # with dislocation of DISTAL radio-ulnar joint
(A is proximal, Z is distal)

161
Q

HIP FRACTURE

What are the two types of hip fracture?

A
  • Intracapsular = break in femoral neck, within the capsule of the hip joint
  • Extracapsular = trochanteric or subtrochanteric (lesser trochanter divides)
162
Q

HIP FRACTURE

How can intracapsular hip fractures be classified?

A

Garden system –

  • Type I = incomplete #, not displaced
  • Type II = complete #, not displaced
  • Type III = partial displacement (trabeculae are at an angle)
  • Type IV = full displacement = (trabeculae are parallel)
163
Q

HIP FRACTURE

What are some risk factors for hip fractures?

A
  • Increasing age
  • Osteoporosis
  • Female
164
Q

HIP FRACTURE

What is the clinical presentation of a hip fracture?

A
  • Painful hip with a shortened + externally rotated leg

- Nondisplaced/incomplete NOF # may be able to weight bear

165
Q

HIP FRACTURE
What investigations would you do in hip fracture?
What would indicate a hip fracture?

A
  • AP and lateral (frog leg) XR = first line (Shenton’s line disruption from medial edge of femoral neck + inferior edge of superior pubic ramus)
  • MRI second line if clinically hip # but normal XR
166
Q

HIP FRACTURE
What is a key complication of hip fractures?
Explain the process of this

A
  • Avascular necrosis
  • Branches of medial + lateral circumflex femoral arteries run along surface of femoral neck, within the capsule + only supply femoral head
  • Intracapsular hip # (especially displaced III/IV) can disrupt supply so femoral head removed + replaced, nondisplaced may have intact blood supply
167
Q

HIP FRACTURE

What is the management of intracapsular hip fractures?

A
  • Not displaced (I/II) = ORIF (open reduction + internal fixation) with cannulated screws OR hemiarthroplasty if unfit
  • Displaced (III/IV) = arthroplasty to all patients
168
Q

HIP FRACTURE

How do you determine what arthroplasty to do in displaced intracapsular hip fractures?

A
  • THR favoured to hemiarthroplasty (just femoral head replaced, not acetabulum) if pt able to walk independently with no more than stick, not cognitively impaired + med fit for anaesthesia + procedure
169
Q

HIP FRACTURE

What is the management of extracapsular hip fractures?

A
  • Intertrochanteric = ORIF with dynamic hip screws

- Sub-trochanteric = intramedullary device

170
Q

HIP FRACTURE
What is a key differential of hip fracture?
How would it present?
What are the risks?

A
  • Hip dislocation 2º to trauma (posterior dislocation #1)
  • Affected leg shortened, adducted + INTERNALLY rotated
  • Risk of sciatic nerve injury + avascular necrosis
171
Q

TROCHANTERIC BURSITIS
What is trochanteric bursitis?
What are some causes?

A
  • Inflammation of bursa overlying the greater trochanter of the femur
  • Friction from repetitive movements, trauma, inflammatory RA
172
Q

TROCHANTERIC BURSITIS

How might trochanteric bursitis present?

A
  • Tenderness on palpation of greater trochanter

- Pain over lateral side of hip > worse at night + exacerbated by activity

173
Q

TROCHANTERIC BURSITIS

What signs might you elicit on clinical examination in trochanteric bursitis?

A
  • +ve Trendelenburg (foot falls to side with foot off ground) = weak hip abductors on contralateral side
  • Pain on resisted abduction, internal + external rotation
174
Q

TROCHANTERIC BURSITIS

What is the management of trochanteric bursitis?

A
  • Analgesia ± steroid injections
  • Physio
  • Rarely bursectomy
175
Q

KNEE INJURIES
What is the mechanism of an ACL injury?
How might it present?
What signs may be present?

A
  • High twisting force applied to a bent knee, sport injury
  • Loud crack, feel it give way + rapid joint swelling (haemoarthrosis)
  • +ve anterior draw + Lachman’s test
176
Q

KNEE INJURIES
What investigations would you do in ACL injury?
How would you manage an ACL injury?

A
  • MRI

- NSAIDs, physio or arthroscopic surgery

177
Q

KNEE INJURIES
What is the mechanism of a PCL injury?
How might it present?

A
  • Hyperextension injuries > tibia lies back on the femur

- Paradoxical anterior draw test, +ve posterior sag test

178
Q

KNEE INJURIES
What is the mechanism of an MCL injury?
How does it present?
What is the management?

A
  • Leg forced into valgus via force outside the leg
  • Knee unstable when put into valgus position
  • Immobilisation cast + surgical reconstruction
179
Q

KNEE INJURIES

What is the mechanism of a meniscal tear?

A
  • Rotational sporting injury, often minor trauma
180
Q

KNEE INJURIES
How might a meniscal tear present?
What sign may you elicit?

A
  • Delayed knee swelling, knee locking (medial more common)

- Thessaly’s test +ve = weight bearing at 20º knee flexion = pain on twisting

181
Q

KNEE INJURIES
How would you investigate a meniscal tear?
What is the management of a meniscal tear?

A
  • MRI

- NSAIDs, physio, arthroscopy ± meniscectomy

182
Q

KNEE INJURIES
What cause a patella fracture?
Who is it commonly seen in?
What is the management?

A
  • Fall onto a flexed knee or car crash dashboard injury
  • Adolescent girls = dislocates laterally
  • Non-displaced = cast, displaced = ORIF, comminuted = patellectomy
183
Q

KNEE INJURIES

What is a Baker’s cyst?

A
  • Popliteal swelling due to herniation from joint synovium often 2º to OA
184
Q

KNEE INJURIES

How might a Baker’s cyst present?

A
  • Acute calf pain + swelling

- Foucher’s sign = increased tension of cyst on extension of knee (standing)

185
Q

KNEE INJURIES
How might you investigate a Baker’s cyst?
What’s the management?

A
  • USS

- NSAIDs, physio, steroid injections, aspiration

186
Q

ACHILLES’ TENDINOPATHY

What are some risk factors for Achilles’ tendinopathy?

A
  • Quinolone use such as ciprofloxacin

- Hypercholesterolaemia predisposes to tendon xanthomata

187
Q

ACHILLES’ TENDINOPATHY

What is Achilles’ tendon rupture?

A
  • Loss of connection between calf muscles (gastrocnemius + soleus) + calcaneus
188
Q

ACHILLES’ TENDINOPATHY

What is the clinical presentation of Achilles’ tendon rupture?

A
  • Often during sport
  • Audible ‘pop’ in ankle
  • Sudden onset significant pain in calf or ankle
  • Inability to walk or continue sport
189
Q

ACHILLES’ TENDINOPATHY

What might examination reveal in Achilles’ tendon rupture?

A
  • Greater dorsiflexion of injured foot compared to uninjured
  • Palpable gap in tendon
  • Simmonds test = squeeze calf muscles as acute rupture > no plantar flexion response
190
Q

ACHILLES’ TENDINOPATHY
How would you investigate Achilles’ tendon rupture?
What is the management of Achilles’ tendon rupture?

A
  • USS initial choice

- Acute referral to orthopaedics for either boot immobilisation or surgical reattachment

191
Q

ACHILLES’ TENDINOPATHY

How would Achilles’ tendinitis present?

A
  • Gradual onset of posterior heel pain that is worse following activity
  • Morning pain + stiffness
192
Q

ACHILLES’ TENDINOPATHY
What is the management of Achilles’ tendinitis?
What would you avoid?

A
  • NSAIDs, reduce precipitating activities, calf muscle exercises (self-directed or physio guided)
  • Steroid injections as risk of tendon rupture
193
Q

PLANTAR FASCIITIS

What is plantar fasciitis?

A
  • Strain on attachment of plantar fascia to calcaneus
194
Q

PLANTAR FASCIITIS

How does plantar fasciitis present?

A
  • Pain when heel strikes ground on walking

- Tender point on heel

195
Q

PLANTAR FASCIITIS

What is the management of plantar fasciitis?

A
  • Firm pad in shoes
  • Analgesia
  • Steroid injections
196
Q

MORTON’S NEUROMA
What is Morton’s neuroma?
Where is commonly affected?
Who is commonly affected?

A
  • Dysfunction of a nerve in intermetatarsal space towards top of foot
  • 3rd/4th metatarsal
  • F>M, high heels
197
Q

MORTON’S NEUROMA

What is the clinical presentation of Morton’s neuroma?

A
  • Pain at front of foot + sensation of lump in shoe
  • Burning, numbness or paraesthesia in distal toes
  • Mulder’s sign = painful click when metatarsal heads rub neuroma
198
Q

MORTON’S NEUROMA
How is Morton’s neuroma diagnosed?
What is the management of Morton’s neuroma?

A
  • Clinical Dx but USS can confirm

- Shoe padding (metatarsal pads) ± steroid injections or neuroma excision

199
Q

BUNION
What is a bunion?
How does it present?

A
  • Bony lump created by deformity at MTP joint at base of big toe
  • Big toe = hallux valgus (deviates laterally to other toes), can be painful
200
Q

BUNION
How is bunion diagnosed?
What is the management of a bunion?

A
  • Weight bearing radiograph
  • Conservative = comfortable shoes + bunion pads
  • Surgical = bunionectomy + treat hallux valgus deformity
201
Q

LOWER LIMB FRACTURES

How can fibular fractures in the ankle be classified and subsequently managed?

A

Weber system

  • A: # below joint line + syndesmosis = closed reduction
  • B: # at level of joint line + syndesmosis = ?closed, ?ORIF
  • C: # above joint line + syndesmosis = very unstable, ORIF
202
Q

LOWER LIMB FRACTURES

When considering whether to order an x-ray in ankle fractures, what must be satisfied?

A

1 of Ottawa ankle rules –

  • Bony tenderness at lateral malleolar zone
  • Bony tenderness at medial malleolar zone
  • Inability to walk 4 steps directly after injury + in ED
203
Q

LOWER LIMB FRACTURES
How are ankle fractures managed?
What is a key differential and how does it present?

A
  • Prompt reduction due to pressure on overlying skin > necrosis
  • Ankle sprain, low more common 2º to inversion injury
204
Q 
LOWER LIMB FRACTURES
What is a tibial plateau fracture?
How are they classified?
Who does it occur in?
How do you manage it?
A
  • Tibia # which subsequent breaks the knee joint itself
  • Schatzker classification
  • Elderly or young high energy impact
  • Immobilisation + brace or surgical fixation if displaced/open
205
Q

LOWER LIMB FRACTURES
What is a stress fracture?
What are the features?
What is the management?

A
  • 2nd metatarsal # common in athletes
  • Gradual pain related to activity, direct palpation causes pain
  • Rest + analgesia, physio
206
Q

LOWER LIMB FRACTURES
What is a type of foot fracture?
What causes it?
What is the management?

A
  • Avulsion # of 5th metatarsal base
  • Common due to inversion with plantar flexion
  • Below knee plaster cast
207
Q

LOWER LIMB FRACTURES
What is an open fracture?
What fractures are most at risk?

A
  • Bone breaches the skin + communicates directly with external environment
  • # of tibia + phalanges
208
Q

LOWER LIMB FRACTURES

What is the management of an open fracture?

A
  • Increased infection risk so As = Analgesia, prompt Abx, Assess (neurovascular), Antisepsis (irrigate, cover), Alignment (reduction + fixation)
209
Q

BONE CANCER

What are the most common bone tumours?

A
  • Secondary bone tumours e.g., metastases = Breast, Bronchus, Bidney, Byroid, Brostate
210
Q

BONE CANCER
What are some benign bone tumours?
What is the most common?

A
  • Osteochondroma (exotosis) #1 = males,

- Osteoma = benign overgrowth of bone, often skull

211
Q

BONE CANCER
What is the most common primary bone tumour?
Where does it normally present and who in?

A
  • Osteosarcoma

- Knee in adolescent males

212
Q

BONE CANCER

What is the clinical presentation of osteosarcoma?

A
  • Persistent, localised bone pain often worse at night

- Warm painful swelling

213
Q

BONE CANCER

How might an osteosarcoma appear on xray?

A
  • Sunburst appearance

- Codman’s triangle = periosteal elevation

214
Q

BONE CANCER
What is another type of primary bone cancer?
Where does it normally present and who in?

A
  • Ewing’s sarcoma

- Long bone diaphysis (e.g., femoral), males <20

215
Q

BONE CANCER
How does Ewing’s sarcoma present?
How might it present on xray?

A
  • Painful, warm, enlarging mass, fever, raised WCC + ESR

- Lytic tumour, onion skin periosteal reaction

216
Q

BONE CANCER
What other type of bone cancer is there?
Where does it normally present and who in?

A
  • Chondrosarcoma = malignant tumour of cartilage
  • Axial skeleton
  • Middle age >40y
217
Q

PAGET’S DISEASE (BONE)
What is Paget’s disease of the bone?
Where is commonly affected?

A
  • Uncontrolled bone turnover with excessive osteoclastic resorption then chaotic bone deposition by osteoblasts
  • Skull, spine/pelvis + lower extremity long bones
218
Q

PAGET’S DISEASE (BONE)
What is the clinical presentation of Paget’s disease of the bone?
If left untreated, what can happen?

A
  • Older male with bone pain and isolated raised ALP (normal calcium + phopshate)
  • Bowing of tibia + bossing of skull, hearing loss, OA
219
Q

PAGET’S DISEASE (BONE)
What investigation might you do?
What is the management of Paget’s disease of the bone?

A
  • XR = osteolysis, osteoporosis circumscripta on skull XR (lytic skull lesions)
  • Bisphosphonate
220
Q

POLYARTERITIS NODOSA
What is polyarteritis nodosa?
What is the epidemiology?

A
  • Medium-sized vasculitis with necrotising inflammation > aneurysms
  • Middle-aged men + associated with hepatitis B
221
Q

POLYARTERITIS NODOSA

What are some clinical features of polyarteritis nodosa?

A
  • Systemic = fever, weight loss, arthralgia
  • Cardio = aneurysms, thrombosis + HTN
  • Renal = haematuria, renal failure
  • Does NOT affect pulmonary vessels
222
Q

FIBROMYALGIA
What is fibromyalgia?
What is the epidemiology?

A
  • Widespread pain throughout the body with tender points at specific anatomical sites
  • F>M, 30–50y
223
Q

FIBROMYALGIA

What is the clinical presentation of fibromyalgia?

A
  • Chronic pain at multiple sites, sometimes all over
  • Lethargy, cognitive impairment (fibro fog)
  • Sleep disturbance, headaches, dizziness
224
Q

FIBROMYALGIA
How is fibromyalgia diagnosed?
What is the management of fibromyalgia?

A
  • Diagnosis likely = tender in 11/18 tender points (9 pairs) in body
  • MDT approach = CBT, aerobic exercise, meds (amitriptyline, pregabalin)
225
Q

GANGLION
What is a ganglion?
What are some features?
How are they managed?

A
  • Smooth fluid filled swelling near a joint or tendon
  • 90% dorsum of wrist, F>M, may limit movement, cause pain or nerve pressure Sx
  • Resolves spontaneously

FINALS (20 decks)

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