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Ortho/ Rheumatology Flashcards

1
Q

What is osteoarthritis and who might it affect?

A
  • = Degenerative joint disorder in which there is progressive loss of hyaline cartilage and bone remodelling.
  • Typically affects people >50y. “Wear and tear”
  • Risk factors: Age, obesity, previous injury, joint abnormality, haemachromatosis.
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2
Q

Presentation of osteoarthritis

A
  • Pattern= asymmetrical. Large weight bearing joints.
  • Hand signs:
    • Deformity
    • Periarticular tenderness
    • Muscle wasting/ weakness
    • Heberden’s and Bouchard’s nodes.
    • Joint instability.
    • Fixed flexion deformity.
    • Thumb squaring.
  • Bony osteophytes. No oedema, erythema or synovitis.
  • Limited to joint involvement.
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3
Q

Ix of Osteoarthritis

A
  • Bedside- SHx and ADLs
  • Bloods- no change.
  • Imaging- x-ray:
    • Loss of joint space
    • Osteophytes
    • Subchondral cysts
    • Subchondral sclerosis
  • Special - ?joint aspirate –> WCC <2000
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4
Q

Tx of osteoarthritis

A
  • Conservative- physio, OT, hydrotherapy, walking aids, home modification, weight loss, hot and cold packs
  • Med- analgesia (paracetamol, NSAIDs, tramadol). Joint injections- local anaesthetic, steroids, synthetic synovial fluid.
  • Surg- arthroscopic arthroplasy or washout. Osteotomy.
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5
Q

What is Rheumatoid Arthritis? Who might present with it?

A
  • = Chronic systemic inflammatory disease. Characterised by symmetrical deforming peripheral polyarthritis. Inflamed synovial membranes.
  • Associations:
    • AI disease - female, post-partum, genetics, smoking. Eg thyroid, DM.
    • Female : Male 3:1
    • Any age
    • Genetics- Rh Factor, HLA-DR4
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6
Q

Presentation of RA

A
  • Symmetrical
  • Small joints - MCP, MTP, DIP sparing
  • Limited movement due to pain and stiffness (>1h morning). Stiffness improves with exercise.
  • Boggy swelling. Red + hot.
  • Joint signs:
    • Deformity + ulnar deviation
    • Warm and tender joints
    • Muscle weakness
    • Synovitis/ effusion
    • Swan neck / Boutonierre deformity
    • Z deformity
    • Subluxation
    • RA nodules - Firm. Elbows, hands, feet, lungs
  • MULTISYSTEMIC!
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7
Q

Extra-articular features of RA

A
  • Lungs- interstitial lung disease, pulmonary fibrosis, pleurisy, fibrosing alveolitis, nodules (Caplan syndrome = RA + pneumoconiosis esp coal miner)
  • Skin - nodules. Firm, non-tender.
  • Neuro - Cervical myelopathy, carpal tunnel
  • Eyes - Sjogren’s, uveitis, iritis, scleritis
  • CVS - vasculitis, pericarditis, Reynaud’s
  • Weight loss (inflammation)
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8
Q

Ix of RA

A
  • Bloods:
    • FBC- normocytic, normochromic anaemia
    • Rh factor +ve in 70%
    • Imflammation- raised CRP, ESR, platelets
    • Anti-CCP
    • ANA
  • Imaging:
    • X-ray: loss of jointn space, erosions, soft tissue swelling, osteopoenia.
    • ?USS
    • ?MRI
  • Special- joint aspirate WCC >2000
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9
Q

Diagnosis of RA

A
  • 4/7 of:
    • Morning stiffness >1h for 6 weeks
    • Arthritis in >3 joints
    • Arthritis of hand joints
    • Symmetrical
    • Rheumatoid nodules
    • +ve Rh factor
    • Radiographic changes
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10
Q

Tx of RA

A
  • Conservative- Physio, OT, reg exercise, education, safety netting.
  • Med:
    • Analgesia- paracetamol, NSAIDs (+PPI), opiates
    • Steroids - IM, PO, intra-articular. For exacerbations.
    • Manage CVS risk
    • ?Bisphosphonates to prevent osteoporosis
    • DMARDs = 1st line
    • Biologics if 2 DMARDs failed
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11
Q

Examples of DMARDs and SE

A
  • All can cause myelosuppression –> pancytopoenia
  • Methotrexate - SE: low folate, teratogenic, hepatotoxic, pulm oedema. Reg bloods.
  • Hydroxychloraquin - SE: retinopathy, seizures. Safer in preg.
  • Sulfasalazine - ABx + aspirin. SE: hepatotoxic, SJS, orange urine, low sperm count
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12
Q

What are biologics? Examples + SEs

A
  • = Monoclonal Abs used in refractory RA.
  • NB to screen for a Tx TB 1st
  • Anti-TNFalpha: Infliximab, adalimubab. SE: infection, AI disease, cancer.
  • Anti-CD20: rituximab.
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13
Q

What screening tool is used to monitoro RA?

A
  • DAS28: Disease Activity Score
    • Tender joints (28)
    • Swollen joints (28)
    • ERP/ CRP
    • Patient’s VAS score (Patient’s global assessment of their health)
  • –> guides management. >5.1= active disease
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14
Q

Psoriatic Arthirits - patterns of joint involvement

A
  1. Asymmetrical oligoarthritis (60%)
  2. Distal arthritis of DIPs
  3. Symmetrical polyarthritis (inc. DIPs)
  4. Arthritis mutilans
  5. Psoriatic spondylitis
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15
Q

Presentation, Ix and Tx of psoriatic arthritis

A
  • Asymmetrical arthritis including DIPs
  • Extra-articular:
    • Nail changes
    • Synovitis –> dactylitis
    • Plaques
    • Achilles tendonitis, plantar fasciitis
  • Ix- X-ray= ‘pencil in cup’ and ‘plantar spur’
  • Tx:
    • NSAIDs
    • DMARDs
    • Biologics
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16
Q

What is enteropathic arthritis? Presentation, Tx

A
  • = Chronic inflammatory arthritis in those with IBD (1/5)
  • Presentation:
    • Arthritis- asymmetrical, commonly peripheral limbs (esp legs). May have sacroilitis.
    • Abdo pain
    • Change in bowel habit
  • Tx: Tx the IBD!
    • Self-limiting 6w
    • Acute- NSAIDs, intra-articular joint injections
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17
Q

Reactive arthritis - presentation, Ix, Tx

A
  • = Sterile arthritis 1-4w after urethritis (chlamydia) or dysentry (campylobacter, salmonella, shigella)
  • Reiter= can’t see, can’t pee, can’t climb tree
  • Presentation:
    • Asymmetrical lower limb oligoarthritis esp knee
    • Eyes- iritis, conjunctivitis
    • Keratoderma blenorrhagia (plaques on soles and palms)
    • Circinate balanitis (painless penile ulceration)
  • Ix- stool sample, swabs/ urine. bloods (raised CRP/ESR), x-ray
  • Tx- splint, NSAIDs, local analgesia. DMARDS if >6w.
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18
Q

Septic arthritis - RF, organism, presentation, DDx

A
  • Source= local or haematogenous.
  • Organism- Staph. A, gonococcus, streps
  • RF: Overlying infection, prosthesis, age, immunosuppression
  • Presentation:
    • V. quick onset
    • Triad: Fever, pain, reduced ROM
    • Hip + knee = most common. Knee > hip > ankle
    • Severe pain, swelling, redness, heat
    • Systemically unwell
  • DDx - gout, reactive arthritis
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19
Q

Ix, Tx and complications of septic arthritis

A
  • Ix:
    • Bloods- cultures, FBC, ESR, CRP (raised)
    • X-ray
    • Joint aspiration - ++WCC
  • Tx:
    • Cons- splint, rest. Physio once resolved. Mobilise to avoid deformity
    • Med- IV ABx- fluclox/ clindamycin
    • Surg- washout, arthroscopic drainage
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20
Q

What is Gout? + RF/ causes

A
  • = Monoarthropathy (or polyarthropathy) due to accumulation of monosodium urate crystals in and around joint –> erosive arthritis.
  • RF:
    • Dietary purines (red meat), ++ alcohol
    • FHx
    • Male
    • Renal failure/ dehydration
    • DM
    • Obesity
    • Psoriasis
    • Haemolysis
  • Preciptants- surgery, infection, fasting, diuretics
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21
Q

Presentation of Gout

A
  • Usually monoarthropathy with severe joing inflammation (red, hot, swollen)
  • Site- 60% MTP. Also ankle, foot, hand, wrist, elbow, knee
  • Tophi - urate deposits
  • Renal disease- stones, interstitial nephritis
  • Associations to check for- IHD, HTN, metabolic syndrome
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22
Q

Ix of Gout

A
  • Bloods- serum urate
  • X-ray- early= soft tissue swelling. late= loss of joint space, punched out periarticular
  • Synovial fluid LM- -vely birefringent needle shaped crystals
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23
Q

Gout Tx

A
  • Acute- NSAIDs + colchicine. (Steroids if renal impairment), rest.
  • Prevention:
    • Cons- lose weight, no alcohol
    • Med- allopurinol if recurrent attacks, tophi or renal stones. Sx free 4w.
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24
Q

What is pseudogout? Presentation, Ix and Tx

A
  • = Calcium pyrophosphate deposition
  • Presentation- usually spont. Acute monoarthropathy, typically in elderly
  • Ix= synovial fluid LM. +ve birefringent rhomboid crystals
  • Tx= cool packs, rest, NSAIDs +/- colchicine
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25
Q

What is ankylosing spondylitis and who is likely to get it?

A
  • Chronic disease of unknown aetiology characterised by stiffening and inflammation of the spine and sacroiliac joints.
  • Epidemiology:
    • M:F 6:1
    • Men present earlier (teens-20s)
    • 90% HLA B27 positive
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26
Q

Conditions associated with HLA B27

A

PAIR

  • Psoriasis
  • Ankylosing spondylitis
  • IBD
  • Reactive arthritis
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27
Q

Presentation of Ankylosing Spondylitis

A
  • Gradual onset
  • Lower back pain. Worse at night, relieved by exercise. Can radiated into buttocks.
  • Spinal stiffness + progressive loss of movement
  • ? mark posture/ bamboo back
  • Eyes- acute ititis/ uveitis
  • Osteoporosis
  • Costochondritis
  • Apical pulmonary fibrosis + reduced thoracic expansion
  • Aortic valve incompetence
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28
Q

Ix and Tx of Ankylosing Spondylitis

A
  • Dx= clinical with Schrober’s test and occipital wall distance.
  • Bloods- CRP, ESR, HLA
  • Imaging- X-ray signs are late:
    • Sacroilitis (blurring and narrowing)
    • Squaring of vertebra
    • Bamboo spine- calcification of ligaments
  • Tx:
    • Cons- EXERCISE, physio
    • Med- NSAIDs, local steroid injections, bisphosphonates, anti-TNFalpha if severe
    • Surg- hip replacement
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29
Q

What is osteoporosis and it’s RF?

A
  • = reduction in bone mass –> fragility fractures
  • RF= SHATTERED + female, age
    • Steroids
    • Hyperthyroid/hyperparathyroid
    • Alcohol/ tobacco
    • Thin (BMI <22)
    • Testosterone
    • Early menopause
    • Renal/liver disease
    • Erosive/ inflammatory joint disease
    • Diet- malabsorption, low calcium
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30
Q

Presentation and Ix of osteoporosis

A
  • Presentation- usually ASx. Present with fragility fracture - NOF, vertebral crush fracture, distal radius
  • Ix:
    • qFracture score - 30-99y
    • FRAX score (40-90y)= 10y risk of fragility fracture. ?Education + repeat 2-3y. ?BMD scan? Risk >20% –> treat!
    • Bloods- FBC, ESR/CRP, U+Es, calcium testosterone, immunoglobulins, albumin, Mg, phosphate, ALP. (Bone profile, rule out DDx)
    • Imaging- X-ray fracture, DEXA scan
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31
Q

What bloods are in a bone profile?

A
  • Calcium
  • Albumin
  • Phosphate
  • Magnesium
  • ALP
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32
Q

Indications and meaning of DEXA scan results

A
  • Indications- Low impact fracture, women >65y with 2 or more RF, long term steroids, PTH disorder, myeloma, HIV, early menopause
  • T score= no. SD away from youthful average.
  • Z score= age matched
  • Results:
    • -1 - +1= Normal
    • -1 - -2.5= Osteopoenia
    • <-2.5= Ostoporosis
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33
Q

Tx of osteoporosis

A
  • Cons- quit smoking and alcohol, weight bearing, calcium/ vit D in diet, falls prevention.
  • Med:
    • Bisphosphonates= 1st line. Eg alendronic acid. (Take with ++ water, sitting up). SE: GO, oesophageal erosis, MSK pain, osteonecrosis of jaw
    • Strontium ranelate
    • Calcium + vit D supplement
    • Calcitonin
    • HRT
  • Surg- fix fracture
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34
Q

What is osteomalacia and how might it present?

A
  • = Loss of bone mineral content. Uncalcified osteoid/ cartilage. Normal bone mass, lower quality.
  • Presentation:
    • Children= Rickets. Knock-kneed/ bow-legged, bone pain, craniotabes, growth retardation, Harrison’s sulcus, rachitic rosary
    • Adults= Osteomalacia. Bone pain, fractures, proximal myopathy (low phosphate)
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35
Q

Causes of osteomalacia

A
  • Vit D deficiency
  • Liver/ renal failure (Vit D hyroxylation)
  • Inherited Vit D resistance
  • AEDs
  • Malignancy- hypophosphataemia
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36
Q

Ix and Tx of osteomalacia

A
  • Ix:
    • Bloods - low calcium, PO4, vit D. High ALP, PTH
    • X-ray- loss of cortical bone. Cupped mataphyses in rikets. Looser’s zones (pseudofractures)
  • Tx:
    • Cons- dietary Calcium D3
    • Med- Vitamin D replacement. Monitor Calcium
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37
Q

What is fibromyalgia + its RF

A
  • = chronic disease with widespread MSK of medically unexplained cause
  • RF:
    • Female (x10)
    • Middle aged
    • Depression/ anxiety/ stress
    • Marital probs
    • Low income/ work satisfaction
  • Associations: Chronic fatigue, IBS, chronic headache
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38
Q

Presentation and Tx of fibromyalgia

A
  • Presentation:
    • Chronic widespread MSK pain
    • Mornign stiffness
    • Fatigue
    • Low mood
    • Sleep disturbance
    • Poor concentration
  • Tx:
    • Cons- education, CBT, graded exercise prog
    • Med- amitryptiline, pregabalin, venlafaxine
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39
Q

What is Sjogren’s syndrome and what is it associated with?

A
  • = Keratoconjunctivitis sicca
  • Classification:
    • Primary. F:M 9:1. 4th-5th decade
    • Secondary: RA< SLE, systemic sclerosis
  • Associations:
    • AI- thyroid, AIH, PBC
    • MALT lymphoma
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40
Q

Presentation of Sjogren’s syndrome

A
  • Xerostomia (dry mouth)
  • Dry eyes
  • Bilat. parotid swelling
  • Vaginal dryness and dyspareunia
  • Systemic- polyarthritis, Raynaud’s, pulm. fibrosis, vasculitis, myositis
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41
Q

Ix and Tx of Sjogren’s syndrome

A
  • Ix:
    • Bedside- schirmer test
    • Bloods- ANA Ro + La, Rh factor, hypergammaglobulinaemia
    • Special- Parotid biopsy
  • Tx:
    • Cons- artificial tears, saliva replacement
    • Med- NSAIDs/ hydroxychloraquin for arthralgia. Severe- immunosuppression
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42
Q

What is Raynaud’s phenomenon and how is it classified?

A
  • = Peripheral digital ischaemia precipiated by cold/ emotion.
  • Classification:
    • Primary- Idiopathic Raynaud’s disease
    • Secondary- Systemic sclerosis, SLE, RA, Sjogren’s, thrombocytosis, beta blockers
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43
Q

Presentation and Tx of Raynaud’s

A
  • Presentation:
    • Digital pain + triphasic colour change: white –> blue –> crimson
    • Digital ulceration + gangrene
  • Tx:
    • Cons- wear gloves
    • Med- ACEi, CCB eg nifedipine, IV prostacyclin.
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44
Q

Bone mets- common primaries + presentation + Ix + Tx

A
  • Primaries: Breast, lung, prostate, thryroid
  • Presentation:
    • Bone pain
    • Pathological fracture
    • Hypercalcaemia
    • SC compression
  • Ix- urinalysis, bone profile (high calcium, alk phos and phosphate), x-ray, bone scan, CT, MRI, PET
  • Tx- Physio, OT, hormone therapy, chemo/ radio, bisphosphonates, surgery
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45
Q

Types of primary bone cancer

A
  • Osteosarcoma- teens. More in hip/ leg/ shoulder/ humerus
  • Ewing’s Sarcoma- Teens. Normally starts pelvis/ fermur/ tibia. + CT tumours
  • Chondrosarcoma- 30-60y. Cartilage
  • Spindle cell sarcome
  • Chordoma
46
Q

Presentation + Tx of achilles tendon rupture

A
  • Presentation:
    • Sudden severe pain in ankle when running/ jumping. “kick”
    • Limp
    • Inability to raise heel from floor when standing on leg
    • O/E- palpable gap, Simmond’s +ve: kneel on chair and squeeze both calves, less plantar flexion on affected side.
  • Tx:
    • Conservative- cast 6-8w. Equinous position –> neutral
    • Surg- surgical tendon repair. Young athletic/ late presentation
47
Q

Rotator cuff presentation, Ix and Tx

A
  • = Damage to supr/infraspinatus, subscapularis.
  • Causes- age related, trauama
  • Presentation:
    • Shoulder weakness and pain
    • –> impingement syndrome –> painful arch
    • Night pain
  • Ix- USS, MRI
  • Tx- arthroscopic repair
48
Q

Adhesive capsulitis- associations, presentation, Tx

A
  • = Frozen shoulder
  • Associations: cervical spondylitis, DM, thyroid.
  • Presentation:
    • Severe pain in shoulder, ++ at night
    • Reduced ROM in shoulder
    • Phases:
      1. Freezing (<1y) ++ pain, reduction in acitve + passive movement. Abduction +/- external rotation
      2. Frozen (6-12m) Stiff. Less pain.
      3. Thawing phase (1-3y). Slowly regain movement
  • Tx:
    • Cons- physio
    • Med- NSAIDs, steroid joint injections
    • Surg- Release, arthroscopic arthrolysis
49
Q

What is Dupuytren’s contracture? RF + Tx

A
  • = Progressive, painless fibrotic thickening of plamar fascia w/ skin thethering –> MCP joint flexion.
  • More little/ ring finger. Often bilat.
  • Causes: Genetic, smoking, DM, antiepileptics
  • Tx:
    • Med- injectable clostridium histolyticum
    • Surg- fasciotomy
50
Q

What is a ganglion cyst and how may it be treated?

A
  • = Smooth, multilocular swelling containing jelly like fluid. In communication with joint capsule/ tendon sheaths.
  • Tx:
    • Cons- go spont/ under pressure
    • Surg- aspiration/ surgical dissection if pain/ pressure
51
Q

What is trigger finger? How does it present? Tx

A
  • Caused by swelling of flexore tendon or tightening of sheath –> A1 pulley catches –> locked in flexion –> can sometimes ‘trigger’ back into place.
  • More common in DM
  • Presentation:
    • Pain of MCP
    • Locking
  • Tx:
    • Cons- rest, splinting
    • Med0 steroid injections
    • Surgery
52
Q

What is osteomyelitis? Types and common RF/ organisms

A
  • = Infection of bone. Organisms: Staph A., pseudomonas, E. coli, strep.
  • RF: Prosthesis, recent ortho surgery, fracture, Immunosuppression esp DM, neuropathy
  • Types:
    • Acute haematogenous
    • Secondary to local infection
    • Direct innoculation - trauma/ surgery
53
Q

Presentation of osteomyelitis

A
  • Common site:
    • Vertebra (adults)
    • Long bones of leg (children)
    • Humerus
    • Pelvis
  • Presentation:
    • Pain, gradual onset
    • Lump/ red/ warm over site
    • Pus into joint/ skin
    • Systemic- fever, malaise
    • ?fracture
54
Q

Ix and Tx of osteomyelitis

A
  • Ix:
    • Bedside- swabs
    • Bloods- CRP, ESR, WCC, culture
    • Imaging
      • X-ray (after 10-14d), haziness, loss of density, necrotic bone fragments
      • MRI
    • Special- bone biopsy= gold standard
  • Tx:
    • Cons- physio, supportive
    • Med- 6w IV ABx: vancomycin, cefotaxime
    • Surg- Bone debridement of sequestra and graft. Indications: abscess, spread to other structures.
55
Q

What is Polymyalgia Rheumatica and how might it present?

A
  • = inflammatory condition of unknown cause.
  • Shares demographics with GCA- F>M, >50y.
  • Presentation:
    • Subacute (<2w) onset of bilateral aching/ tenderness with morning stiffness <45 mins in shoulders and proximal limb muscles.
    • ** Not weaknes **
    • +/- Mild polyarthritis, tenosynonvitis, carpal tunnel
    • +/- systemic: fatigue, fever, weight loss, anorexia, depression
56
Q

Ix and Tx of PMR

A
  • Ix= Bloods:
    • ++ CRP/ ESR. ESR usually >40
    • Raised ALP in 30%
    • CK normal
  • Tx:
    • Physio, educate on risk of GCA!
    • Med- prednisolone 15mg/d PO. Massive improvement 1w. Wean down 1mg/ week.
    • Gastric and bone protection
57
Q

Principles of fracture management

A
  • Reduce
  • Hold
  • Rehabilitate
58
Q

How to describe a fracture

A
  • Type of fracture- spiral, oblique, transverse, segmental, wedge, comminuted
  • Impacted/ compressed
  • Displaced vs undisplaced - Describe DISTAL segment in relation to proximal
    • Shifted
    • Angulated (describe apex)
    • Rotated
    • Overlapped
    • Distracted
  • Dislocated/ subluxed
  • Open/ compound
59
Q

Complications of fracture

A
  • Early:
    • General- other injuries, VTE, fat embolism
    • Bone- infection, neurovascular injury
    • Soft tissue- Infection, plaster injuries, compartment syndrome
  • Late:
    • General- chest infection, UTI, pressure sore
    • Bone- Non-union/ malunion/ delayed union, avascular necrosis
    • Soft tissue- tendon rupture, nerve compression, complex regional pain, contracture
60
Q

Most common sites of avascular necrosis

A
  • Anatomically at risk- talus, scaphoid
  • Most common- head of humerus, head of femur (NOF, SUFE)
61
Q

Non-traumatic causes of avascular necrosis

A
  • Radiotherapy
  • Chemotherapy
  • Steroid use
  • Drug addicts
  • Alcoholism
62
Q

What is compartment syndrome, how might it present and how would you treat it?

A
  • Muscles in compartments surrounded by fibrous septa.
  • Fracture or soft tissue injury –> increased pressure –> loss of venous return –> more pressure –> loss of arterial supply –> necrosis –> renal failure (UO and K+) and death
  • Presentation: Dx= clinical!
    • ++ Pain, out of proportion
    • Pain on passive muscle stretching
    • Looks and feels tight/ swollen
    • 6Ps= late sign
    • Intracompartmental pressure= >30
  • Tx:
    • Cons- loosen tight dressings
    • Surg- Fasciotomy
63
Q

Spinal Fractures: Causes, types, Ix and Tx

A
  • Causes
    • Low energy- osteoporosis, malignancy
    • High energy- trauma
  • Types:
    • Compression- osteoporosis, tumour
    • Axial burst- fall from height
    • Chance- seat belt injury
  • Ix= Xray
  • Tx:
    • Minor- cervical bracing
    • Complex- traction/ surgery
64
Q

Humerus fractures - mechanism, Ix, Tx

A
  • Shaft fracture:
    • Mechanism- fall with direct blow/ torsional force
    • Ix- X-ray. Rule out radial n. damage
    • Tx: Cast. Or surival ORIF with plate and screws
  • Condylar fracture:
    • Mechanism- Impaction. Condyle splits into T/ Y.
    • Types= intracondylar/ supracondylar
    • Tx:
      • Intracondylar- reduction + cast. ?replacement if elderly
      • Extracondylar- cast. ORIF if displaced.
65
Q

What is a monteggia fracture?

A

Ulnar fracture with dislocation of proximal radioulnar joint

66
Q

Scaphoid fracture- mechanism, presentation, Ix, Tx

A
  • Mechanism- Fall onto outstretched hand
  • O/E- fullness in anatomical snuffbox. Tender volar surface
  • Ix- scaphoid series
  • Tx- below elbow in neutral position
67
Q

Distal radius fracture- mechanism, types, Ix, Tx

A
  • Mechanism= Fall onto outstretched hand
  • Types:
    • Colles’ = extra-articular fracture of DR with dorsal diplacement and angulation. ‘Dinner fork’
    • Smith’s = Extra-articular fracture of DR with volar displacement and angulation
    • Barton’s= intra-articular fracture with dislocation of radio-carpal joint
  • Ix- neurovascular assessment, x-ray
  • Tx:
    • Cons- closed reduction, backslab, physio
    • Surgery- K-wire fixation
  • Complications= medican n. damage, malunion.
68
Q

Pelvis fracture- mechanism, presentation, Tx and complications

A
  • Mechanism- <60y= RTA/ high impact. >60y= fall from standing
  • 1 break= stable. 2 breaks= unstable
  • O/E- neuro/ GI/ GU injury? Risk of massive haemorrhage
  • Ix: X-ray of inlet and outlet
  • Tx:
    • Single fracture- mobilise early.
    • Multiple fracture= unstable –> ex-fix –> pelvic stabilisation with ORIF and screws.
  • Complications- Haemorrhage, shock. ST injury, VTE, OA, neuro damage
69
Q

Classification of fractured NOF

A
  • Intracapsular- subcapital, basocervical
  • Extracapsular- intertrochanteric, subtrochanteric
  • Garden Classification I-IV
70
Q

Presentation of fractured NOF

A
  • Cause- low energy (eg fall in elderly/ osteoporotic), high energy eg RTA
  • Presentation:
    • Pain in groin/ hip
    • Bruising/ swelling
    • Inability to weight bear
    • Shortened and externally rotated
    • Unable to straight leg raise
    • ** full neurovascular exam **
71
Q

Ix and Tx of fractured NOF

A
  • Ix:
    • Bedside- delirium screen, urine dip
    • Bloods- FBC, U+Es, coags, G+S, ?CK
    • X-ray- 2 views. Disruption of Shenton’s line?
  • Tx:
    • Cons- falls prevention, physio, OT, good basic care, early mobilisation
    • Med- DVT prophylaxis, analgesia, IVT
    • Surg:
      • Intracapsular- hemiarthroplasty/ complete hip replacement
      • Extracapsular- DHS
72
Q

Complications of fractured NOF

A
  • Mortality= 30% at 1y
  • Avascular necrosis - primary blood supply from medial femoral circumflex artery
  • Dislocation
  • Future falls
  • Infection
  • UTI/ pneumonia
  • Pressure sores
  • DVT
  • Peri-prosthetic fracture
73
Q

Femoral shaft fracture- mechanism, Tx and complications

A
  • Mechanism- high energy eg RTA, osteoporosis, mets
  • Ix/ Tx:
    • ABCDE, access, IVT
    • Bloods- FBC, U+Es, G+S
    • Realign and splint with Thomas splint
    • Open- IV ABx
    • Surg- intramedullary nailing, plate and screw
  • Complications- compartment syndrome + general complications of fracture
74
Q

Goalsl for fractures NOF management

A
  • Seen by orthogeriatricians
  • Early surgery <36h
  • Early mobilisation
  • Assessment of delirium
  • Basic care eg feeding, preventing pressure sores
  • FRAX score and falls prevention
75
Q

Ankle fracture - mechanism, presentation, and classification

A
  • Mechanism- low energy rotational force
  • Presentation:
    • Fracture of proximal fibula = ankle fracture or dislocation until proven otherwise
    • Bruising/ swelling
    • Deformity
    • ?Open
    • Examine whole fibula for tenderness
  • Weber classification: A= below syndesmosis, B= at syndesmosis, C= above syndesmosis
  • Tibia + fibular = paired bones. If one fractured, other must be or damaged syndesmosis
76
Q

Tx of ankle fracture

A
  • Displaced/ dislocation= Emergency. Reduce ASAP –> backslab
  • Stable- lat. malleolus only + no medial tenderness –> below knee cast for 6w.
  • Unstable - Weber B/C with no medial tenderness –> backslab + elevate + ICE –> ORIF and cast
77
Q

What’s involved of pre-op assessment for arthroplasty?

A
  • 6w before. ?co-morbidities and ability to cope?
  • Exam- CVS, resp, GI, MSK, airway
  • Bloods- FBC, U+Es, G+S, cross-match
  • Urinalysis
  • Others- ?CXR, ?spirometry, ECG
  • Explain complications and give written info
78
Q

Indications for hip/knee arthoplasty

A
  • Pain (esp at night)
  • Disability
  • Mod-severe RA/ OA
  • Avascular necrosis
  • Congenital dislocation
79
Q

Types of hip arthroplasty + lifespan

A
  • Total- head of femur and acetabulum. Metal-on-plastic (or metal)
  • Hemiarthroplasty- only head of femur replaced
  • +/- cement
  • Lifespan 9-10y
80
Q

Types of knee replacement

A
  • Unicompartmental
  • Unconstrained bicompartment
  • Contrained (less bone)
81
Q

Post-op care of arthroplasty

A
  • Early mobilisation
  • Involve physio and OT
  • Optimise care
  • DVT and PE prophylaxis
  • Follow up
  • Falls prevention
82
Q

Complications of knee/ hip arthroplasty

A
  • Dislocation - esp after revision
  • Prosthetic loosening - esp metal-on-metal
  • Periprosthetic fracture
  • Infection - fever, pain, reduced ROM. Esp strep. Tx- earlyl debridement, ABx. Prophylaxis with gentamicin impregnated cement
  • Joint stiffening
  • General- DVT, PE, infection etc
  • Damage to surrounding structures?
83
Q

What is systemic sclerosis? Who might get it? What are the 2 different types?

A
  • = Multisystemic. Excessive deposition of collagen in skin and internal organs
  • Demographics: F>M, usually 30-40s
  • Types:
    • Limited- upto elbows, knees + face
    • Diffuse- beyond elbows
84
Q

Features of diffuse systemic sclerosis

A
  • Ab= Scl-70, RNA, polymerase III
  • Presentation:
    • Raynaud’s
    • Digital ulceration
    • Diffuse skin thickening - morphea= thick and waxy. (also morphea linear, en coup de sabre)
    • Systemic (early)- ILD, GI, renal, cardiac
  • Tx= vascular and immunosuppression
85
Q

Features of limited systemic sclerosis

A
  • Ab= Anti-centromere
  • Presentation= CREST
    • Calcinosis - Ca2+ deposits in finger clubs
    • Raynaud’s
    • oEsophageal- GI in general
    • Sclerodactyly
    • Telangectasia
    • Other- scleroderma of face and neck, fibrotic lung disease, HTN, GI disease
  • Tx= vascular- sildenafil, bosentan
86
Q

Ix and Tx of systemic sclerosis

A
  • Ix: **monitor renal and lung function**
    • Bedside- urine dip, BP, weight, nailfold capillaroscopy, PFTs
    • Bloods- U+Es, FBC
    • Imaging- CXR, HRCT, ECHO every 2y, OGD/colonoscopy/ barium swallow
  • Tx:
    • Cons- keep hands warm, skin lubricants
    • Med- Tx complications. ACEi (BP), immunosuppression- cyclophosphamide
    • Raynaud’s- CCB
    • Oesophageal- PPI
87
Q

What is myositis and its types? Who might get it?

A
  • Myositis= Inflammatory myopathies of striated muscle. –> weakness and elevated muscle enzymes
  • 2 types- polymyositis, dermatomyositis
  • RF:
    • Female
    • Paraneoplastic- lung, pancrease, ovaries, bowel
88
Q

Presentation of polymyositis and dermatomyositis

A
  • Progressive symmetrical muscle weakness (sparing distal and occular muscles)
  • Wasting of shoulders and pelvic girdle
  • Dysphagia, dysphonia, resp weakness. LIFE THREATENING.
  • Associated with: myalgia, arthralgia, arthritis, fever, pulm. fibrosis, Raynaud’s, myocarditis, arrhythmias
  • Dermatomyositis= + skin signs:
    • Helitrope rash on eyelids w/ oedema
    • Macular rash- photosensitive. Shawl sign.
    • Nail fold erythema
    • Gottren’s papulse - knuckles, elbows, knees
    • Painful rough skin, cracking
    • Retinopathy- haemorrhages, cotton wool spots
89
Q

Polymyositis/ Dermatomyositis- Ix and Tx

A
  • Ix:
    • Bedside- PFTs, EMG
    • Bloods- CK, Anti-Jo1, raised AST/ALT/LDH, tumour markers
    • Imaging- screen for malignancy- CXR, mammogram, pelvic/ abdo USS, CT
    • Special- muscle biopsy (CD4 infiltrate)
  • Tx:
    • Cons- screen for malignancy
    • Med- Immunosuppression: steroids, cytotoxics (azathioprine, methotrexate).
90
Q

What is Marfan’s and how might it present?

A
  • = Inherited CT disease. Autosomal dominant (spont in 25%). Mutation in FBN1 gene –> fibrillin 1 –> elastin
  • Presentation:
    • Cardiac- aortic root dilatation –> regurg, aortic aneurysm + dissection, mitral valve prolapse/regurg
    • Ocular- lens dislocation
    • MSK- high arched palate, arachnodactyly, arm span>height, pectus excavatum, scoliosis, joint hypermobility
  • Dx= 2/3 organ systems
91
Q

Ix and Tx of Marfan’s

A
  • Ix:
    • Bedside- slit lamp, ECG
    • Imaging:
      • CXR- wide mediastinum, scoliosis, pneumothorax
      • ECHO- aortic root dilatation
      • MRI
    • Special- genetic testing
  • Tx: (ortho, cardio, ophthalmology)
    • Cons- less cardiotensive sports
    • Med- beta blockers
    • Reg ECHO –> surg when >5cm
92
Q

What is Ehlers Danlos syndrome and how might it present?

A
  • = Group of collagen disorders.
  • Presentation:
    • Hyperelastic skin
    • Hypermobile joints
    • Fragile BVs
    • Poor healing
    • Cardiac- MVP, AR, MR, aneurysms
93
Q

What is anti-phospholipid syndrome and what are it’s key features? + Tx

A
  • = Mostly primary disease. 30% related to SLE.
  • Anti-cardiolipin + lupus anticoagulant –> CLOTS (esp renal and cerebral)
    • Coagulation defect
    • Livedo reticularis
    • Obstetric - miscarriage and eclampsia
    • Thrombocytopoenia
  • Tx- Good obstetric advice/ care. Low dose aspirin/ warfarin.
94
Q

Diagnostic criteria of anti-phospholipid syndrome

A
  • At least 1 clinical and 1 lab
  • Clinical:
    • Vascular thormbosis confirmed by scan
    • Pregnancy morbidity- spont abortion, prem birth, >2 unexplained consecutive spont abortions
  • Lab:
    • High anticardiolipin
    • High lupus anticoagulant
    • +ve on 2 occasions 12w apart
95
Q

What is SLE and who might it affect?

A
  • = Systemic Lupus Erythematous
  • AI disease - autoAb to a variety of autoantigens –> formation and deposition of immune complexes.
  • Epidemiology:
    • Females of child bearing age
    • Afro-Caribbeans and Asians
    • Genetic- HLA DR2/3
    • Environmental trigger- infection, UV radiation
96
Q

Multisystemic signs and Sx of Lupus

A
  • Constitutional- Malaise, myalgia, fever, weight loss
  • Eyes- Sjogren’s, conjunctivitis
  • Mucocutaneous- Malar/ discoid rash, ulcers, Raynaud’s, lymphadenopathy, vasculitis
  • MSK- Arthralgia, mornign stiffness, arthritis, synovitis, Jaccoud’s deformity
  • Cardiopulm- Pericarditis, pleuritis, lupus pneumonitis
  • Reproductive- stillbirth/ miscarriage
  • Nervous- Headaches, psych, seizures, neuropathy
  • GI- Abdo pain, loss of appetite
  • Renal- “lupus nephritis”. HTN, GN, nephritis, nephrotic syndrome
97
Q

Lupus Ix

A
  • Bedside- urine dip, BP, ECG, o2 sats
  • Bloods:
    • FBC- macrocytic anaemia (–> direct Coomb’s), low lymphocytes, low platelets
    • U+Es
    • LFTs
    • CRP (?norm), ESR ++
    • Complement C3/4 low
    • Autoantibodies- ANA, dsDNA, ENA Ro/La, Antiphospholipids (cardiolipid/lupus anticoagulant), anti-histone (drug-induced)
    • Monitoring disease activity- Anti-dsDNA, complement, ESR
  • Imaging- CXR may show complications
98
Q

Diagnostic criteria of Lupus

A

4 or more (at least 1 clinical and 1 lab) or biopsy proven lupus nephritis

  • Clinical criteria:
    • Acute cutaneous lupus
    • Oral/nasal ulcers
    • Non-scarring alopecia
    • Arthritis
    • Serositis
    • Renal
    • Immunologic
    • Haemolytic anaemia
    • Leukopenia
    • Thrombocytopoenia
  • Immunologic:
    • ANA
    • Anti-dsDNA
    • Anti-Sm
    • Antiphospholipid Ab
    • Low complement
99
Q

Causes and presentation of drug-induced lupus

A
  • Causes- phenytoin, hydralazine, isoniazid
  • Mostly skin and lung signs
  • Ix- anti-histone Ab
  • Usually remits once drug removed
100
Q

Management of SLE

A
  • Specialist SLE and nephritis clinics
  • Cutaneous Sx- prevention with suncream, Tx with topical steroids
  • Maintenance of skin and joint Sx- NSAIDs, hydroxychloraquin +/- low dose steroids
  • Lupus nephritis- ACEi for proteinuria, GN –> immunosuppression
  • Tx complications- OP, CVS disease
101
Q

What is vasculitis and what might cause it?

A
  • Inflammation of BVs –> swelling, necrosis, stenosis, occlusion, aneurysms.
  • Usually AI
  • Primary or secondary: SLE, RA, Hep B/C, HIV, Sjogren’s, malignancy, infection, drugs (allopurinol, sulfasalazine)
102
Q

Classification of vasculitis

A
  • Large vessel- GCA, Takayasu’s. Claudication, absent pulses, bruits, asymmetric BP
  • Medium vessel- Polyarteritis nodosa, Kawasaki. Livedo, gangrene, ulceration, mononeuritis multiplex, microaneurysms
  • Small vessel- purpura, GN, alveolar haemorrhage, eye involvement
    • ANCA +ve: pANCA= EGPA, microscopic polyangitis. cANCA= GPA
    • ANCA -ve: HSP, Goodpasture’s, cryoglobulinaemia
103
Q

Ix of vasculitis

A
  • Bedside- urinalysis, BP, ECG
  • Bloods- FBC, U+Es, LFTs, bone profile, CRP, ESR, ANCA, autoAb, complement
  • Imaging- ECHO, CXR, USS, MRI, angiography
  • Special- Biopsy
104
Q

Key features of Takayasu’s

A
  • = Pulseless disease
  • Japan. F>M. 20-40y
  • Clinical phases:
    1. Inflammatory- fever, flu-like Sx
    2. Ischaemic pulseless phase- aorta and branches
    3. Burnout + remission
  • Features- fever, fatigue, weight loss, HTN, weak pulses in upper extremities, claudication, visual disturbance
  • Ix- stenotic lesions
  • Tx- Immunosuppression, CVS management, surg in remission
105
Q

Key features of polyarteritis nodosa

A
  • Rare in Uk. M>F. Young adults.
  • Associated with Hep B
  • Presentation:
    • Skin- purpura, ulcers, livedo
    • Constitutional
    • Renal impairment
    • GI –> abdo pain + melaena
    • Neuopathy
  • Ix: HbSAg, angio (aneurysms, stenosis)
  • Tx: Pred, cyclophosphamide
106
Q

Key features of Kawasaki Disease

A
  • = childhood PAN variant, esp Japan
  • Features:
    • 5d fever
    • Conjunctivitis
    • Oral mucositis - strawberry tongue
    • Cervical lymphadenopathy
    • Coronary artery aneurysms –> CVS complications
    • Polymorphic rash - macularpapular. Palms and soles.
  • Tx= IV immunoglobulin, aspirin
107
Q

Key features of Microscopic Polyangitis

A
  • pANCA +ve
  • Presentation:
    • Constitutional
    • Abdo pain and bleeding
    • GN + nephritic syndrome
    • Haemoptysis
    • Mononeuritis multiplex
    • Palpable purpura
  • Tx- Steroids, cyclophosphamide
108
Q

What is EGPA and its core features? + Ix and Tx

A
  • = Eosinophilic Granulomatosis with Polyangitis
  • “Churg-Strauss”
  • Features:
    • Triad of adult onset asthma, eosinophilia and vasculitis
    • Skin lesions
    • Neuropathy- mono/poly
    • GI Sx - bleeding
    • Rapidly progressive GN
  • Ix:
    • Bedside- urine, BP
    • Blood - pANCA, eosinophilia
    • Imaging- Pulm. infiltrates
    • Biopsy
109
Q

Key features of GPA

A
  • = Granulomatosis with Polyangitis
  • Presentation:
    • Systemic- Fever, weight loss, arthralgia, ulcers, rash, myalgia
    • URT- sinusitis, epistaxis, saddle nose deformity
    • LRT- cough, haemoptysis, pleuritis
    • Renal- RPGN, haematuria, proteinuria
    • Ocular- conjunctivitis, keratisis, uveitis
  • Ix:
    • Bedside- urine dip, BP
    • Bloods- cANCA
    • Imaging- CXR, CT head/ sinus
    • Biopsy
  • Tx: steroids +/- methotrexate/ cyclophosphamide/ rituximab
110
Q

What is Behcet’s Disease? Features + Tx

A
  • = Systemic inflammatory disease targetting venules. HLA-B5
  • Features- oral/ genital ulcers, uveitis, skin lesions, arthritis, vasculitis
  • Tx- colchicine (ulcers), azathioprine/ cyclophosphamide
111
Q

Key features of HSP

A
  • = Henoch-Schonlein Purpura. Childhood IgA nephropathy variant.
  • Presentation:
    • Follows URTI
    • Deposition of IgA in skin/kidney/bowel
    • Palpable purpura on buttocks
    • Colicky abdo pain
    • Arthralgia
    • Haematuria
  • Ix= BP, urinalysis, ANCA -ve, biopsy of BV/skin/kidney- IgA. RPGN, crescents
  • Tx- supportive. ?NSAIDs
112
Q

What is mixed connective tissue disease?

A
  • Mixture of RA, SLE, myositis, scleroderma
  • Features- Raynaud’s, arthritis, ILD, skin changes
  • Antibody= Anti-RNP

Finals!!! (19 decks)

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