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Year 4 > MSK > Flashcards

MSK Flashcards

1
Q

Epidemiology and risk factors for RA

A

Increased in women (2-4x)
Peak age is 40s

RFs
Smoking
Genetics - HLA DR4 and 1
Winter
Others - increased birth weight, silica exposure, alcohol abstention, obesity, diabetes,
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2
Q

Presentation of RA

A

ARTHRITIS
Insidious symmetrical polyarthritis
Small joints of hands or feet
Morning stiffness >30 minutes
PIP, MCP, wrist, MTP, ankle, knee, cervical spine (SPARES DIP)
Hand deformities - ulnar deviation, swan neck, Boutonnieres, Z deformity of thumb, piano key deformity of wrist

SYSTEMIC SIGNS
- Eyes: scleritis, episcleritis
- Skin: leg ulcers, rashes, raynauds
- Rheumatoid nodules
- Neuro: carpal tunnel, polyneuropathy
- Resp: pleuritic, pulmonary fibrosis
- CV: pericardial involvement, vasculitis, increased MI
- Kidneys: RARE
- Liver: mild hepatomegaly, raised transaminases
Thyroid disorders, osteoporosis, depression, splenomegaly, lymphadenopathy

Pain, fatigue, myalgia, weight loss

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3
Q

Investigations for RA

A
  • ESR, CRP, plasma viscosity - usually raised (can be normal)
  • FBC - normochromic normocytic anaemia, thrombocytosis, raised ferritin
  • LFTs - mildly raised ALP and GGT
  • Antinuclear antibody in 30% +

Rheumatoid factor - positive in 60-70% (and 10% normal population)

Anti-CCP

X-ray - soft tissue swelling, periarticular osteopaenia, decreased joint space, erosions, deformity

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4
Q

Management of RA

A

Start within 3 months
Simple analgesia + NSAIDs

DAS28 - number of joints and ESR. For active disease >5.1, remission <2.6

  1. Methotrexate + alt DMARD + short course steroid (min 6 months)
  2. different mono/combined DMARD therapy (min 6 month)
  3. TNF alpha inhibitors (adalimumab, etancercept, infliximab)
  4. Rituximab (anti CD20) + methotrexate
  5. Toclizumab (anti IL6)

Surgery if persistent pain, worsening joint function, progressive deformity, nerve entrapment, stress fracture

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5
Q

Complications of RA

A

Decrease mobility, restricted ADLs
Inability to work
Depression
Vasculitis
Systemic effects - pleuracy, heart complications, lymphadenopathy, neuropathy, anaemia, dry eye syndrome, anaemia, carpal tunnel, tendon rupture
Osteoporosis
Felty’s syndrome - enlarged spleen, decreased WCC + RA

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6
Q

Prognosis of RA

A

40% disabled in 10 years

Worse prognosis if: <30, male, insidious onset, persistent anaemia, increased number of joints, raised anti-CCP, early Xray changes

Pregnancy beneficial for RA

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7
Q

Criteria for RA

A

4 or more of:

  • morning stiffness >1 hour >6 weeks
  • at least 3 joints
  • hand joints
  • symmetrical
  • rheumatoid nodules
  • positive for rheumatoid factor
  • radiological changes
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8
Q

Epidemiology and risk factors for osteoarthritis

A

24% adults - knee, 11% hips

RFs
Genetic
Female
Obesity
High or low bone density
joint injury
decrease muscle strength
joint laxity or misalignment
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9
Q

Presentation of OA

A

Clinical without investigation if over 45, pain activity related and no morning stiffness

  • Pain exacerbated by exercise, relieved by rest
  • Stiffness after rest
  • Decreased function and range of movement
  • Swelling, tenderness
  • Crepitus
  • No systemic features
  • Heberdens DIP, Bouchards PIP
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10
Q

Investigations for OA

A

X-ray: osteophytes, decreased joint space, bone cysts, subarticular sclerosis

  • MRI for other causes of joint pain
  • Blood tests will be normal, should do baseline prior to starting NSAIDs
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11
Q

Management of OA

A
  • Promote function, physio, OT
  • Annual review if pain, multiple joints or regular meds
  • Encourage exercise
  • Encourage weight loss
  • Paracetamol +/- topical NSAIDs
  • Oral NSAIDs or COX2 inhibitors + PPI
  • Intra-articular corticosteroids

NO glucosamine, no arthroscopic lavage or debridement

  • Surgery if there is substantial limits on life
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12
Q

Xray changes in OA

A 
Joint space narrowing
Subarticular sclerosis 
Subchondral cysts
Bone collapse
Osseous loose bodies
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13
Q

Epidemiology and RFs for septic arthritis

A

1-2% of prosthetic joint replacements
20% of joint surgery revisions
Most commonly staph aureus

RFs
Increasing age
Prior joint damage
Diabetes
Joint surgery - hip or knee
Immunodeficiency
Recent Steroid injection
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14
Q

Presentation of septic arthritis

A 
Single/few joints - acute, very painful
Fever
Bacteraemia
Swollen, warm, tender
Effusion

TRIAD - fever, pain, impaired range of motion

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15
Q

Causes of septic arthritis

A

Staph aureus
Gonococcal
Group B Strep
Lyme disease

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16
Q

Investigations for septic arthritis

A

FBC - raised WCC, CRP

Synovial fluid examination - raised leukocytes, culture (also exclude crystal arthropathy)

Blood cultures

Imaging - US or MRI/CT

Have a higher index of suspicion if prosthetic joint

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17
Q

Treatment for septic arthritis

A

Surgical drainage + Lavage + High dose IV antibiotics

Antibiotics
- Start empirically before cultures, cover staph and strep as minimum, for minimum of 2-3 weeks

Flucloxacillin (if staph) - allergy to penicillin = clindamycin
Vancomycin = if MRSA
Cefotaxime - gonococcal

Corticosteroids may decrease extent of cartilage destruction

Splint in position of function

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18
Q

Prognosis of septic arthritis

A

10-20% mortality

Worse prognosis - over 65, shoulder, elbow or multiple sites

Staph - 50% get back to baseline

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19
Q

Referral for joint replacement

A

Should have tried all basic treatments (weight loss, pain relief)

If New Zealand score
<39 - primary care
40-69 - non-surgical
70+ then refer for surgery

Patient age, sex, smoking status or BMI should not be a barrier for referral

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20
Q

Complications for joint replacement

A 
Joint infection
DVT/PE
Stiffness
Implant loosening/failure
Hip dislocation
Time span - need replacement after 10-15 years
Bleeding
Haemotoma
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21
Q

Classifications of gout

A

Deposition of monosodium urate monohydrate crystals

  • asymptomatic
  • hyperuricaemia
  • acute gout
  • chronic tophaceous gout

PRIMARY - in men 30-60 with acute attacks
SECONDARY - due to chronic diuretic therapy and associated with OA

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22
Q

Epidemiology and RF for gout

A

Increased in men 9:1
Increased in Asians and South Pacific

High meat diet
Diabetes
Seafood
Alcohol 
Chronic renal failure
Diuretic therapy
Obesity
High cholesterol
HTN
CHD
Psoriasis
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23
Q

Presentation of gout

A

First MTP joint (knee, tarsals, wrists, ankles, hands)
Acute pain in swollen joint that reaches crescendo in 6-12 hours

Florid synovitis
Will resolve in 5-15 days

If tophaceous gout - irregular firm nodules with chalky appearance beneath skin

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24
Q

Investigations for gout

A

Synovial fluid - MSU crystals
Gram staining and culture as infection and gout can co-exist

Serum uric acid - can be raised
Testing fasting lipids and glucose for hyperglycaemia

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25
Q

Management of gout

A

ACUTE

  • NSAIDs and pain relief
  • Colchicine
  • Systemic corticosteroids
  • (continue allopurinol)

ADVICE

  • stop alcohol, red meat, reduce protein
  • avoid purines - liver, kidney, seafood
  • avoid dehydration
  • increase exercise, stop smoking

CHRONIC

  • Allopurinol
  • Canakinumab - if more than 3 attacks per year
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26
Q

Complications of gout

A 
Renal disease from deposition of crystals
Severe degenerative arthritis
secondary infections
carpal tunnel
Nerve impingment
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27
Q

Prevention of gout

A

Manage RFs - HTN, diet, medications

Start treatment if tophi, renal insufficiency, uric acid stones or diuretics.

  • Allopurinol - wait 1-2 weeks after attack to start
  • Febuxostat
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28
Q

Epidemiology of psoriatic arthritis

A 
5-25% of people with arthritis
In 80% psoriasis precedes arthritis
Increased in Caucasians
35-55 years old
Autoimmune mediated - HLA B27
Women have more rheumatoid pattern, men with spondylitic subtype
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29
Q

Presentation of psoriatic arthritis

A 
Joint stiffness, pain, swelling
Relapsing and remitting
Enthesopathy - Achilles tendon and plantar fascia common
Tenosynovitis - affects flexors
20-30% conjunctivitis

Rheumatoid pattern - symmetrical polyarthritis. Hands, wrists, feet DIP not MCP. FEMALES

Spondylytic pattern - morning stiffness, limitation of back movement, asymmetrical vertebral involvement

Asymmetrical oligoarticular arthritis - dactylitis (sausage fingers)
Lone DIP - hammer blow appearance
Juvenile onset - 20% of childhood arthritis

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30
Q

Investigations for psoriatic arthritis

A

Raised ESR and CRP
Raised IgA
Raised neutrophils in synovial aspirate, no crystals

X-ray changes - mild bony erosion, asymmetric erosive changes of small joints, DIP and PIP, erosion of distal tuft of distal phalanx

Can do MRI or CT

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31
Q

Management of psoriatic arthritis

A

Refer to rheumatology

  • NSAIDs
  • Local corticosteroid injections (never oral due to rebound worsening of psoriasis)
  • DMARDs
    Methotrexate/sulfasalazine/leflunomide
    (not hydroxychloroquine)
  • TNF inhibitors (adalimumab/etanercept/golimumab/infliximab) if not responding to DMARD
  • Cytokine modulator (ustekinumab) if others failed
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32
Q

Complications of psoriatic arthritis

A 
joint destruction
Deformity
Eye disease
Aortitis (rare)
Decreased QOL
Increased risk of CVD
ARTHRITIS MUTILANS - severe deformity (telescopic fingers)
Radiological damage in 50%
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33
Q

Complementary therapies for MSK pains

A

Capsacin -5/5
Fishoil, evening primrose oild for RA
Acupuncture for OA

Glucosamine does not work or chondritin or chiropractors

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34
Q

Epidemiology of SLE

A

Increased in females 5:1
Peak age - 50-54 for women, 70-74 for adults
Increased in Chinese, SE Asian and afro-Caribbean

RFs
HLA DRB1
Defective complement C4 gene
UV light
EBV
Drugs - chlorpromazine, hydralazine, methyldopa
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35
Q

Presentation of SLE

A

Relapsing remitting
Fatigue and malaise
Arthralgia - early morning stiffness, non-erosive, peripheral, symmetrical
Photosensitive rash - malar rash
Discoid (without systemic features)
Pulmonary - pleurisy, fibrosing alveolitis
APLS - PE
CV - pericarditis, HTN, increased CV risk
Renal - nephritis
Anxiety and depression
Any neurological presentation

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36
Q

Diagnostic criteria for SLE

A

4 or more from list (not at the same time)

Malar rash
Discoid lupus
Photosensitivity
Oral ulcers
Non-erosive arthritis in 2+ joints
Pleuritis/pericarditis
Renal involvement
Seizures/psychosis
Positive ANA
Haematological disorder
Immunological disorder
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37
Q

Investigations for SLE

A

FBC - Raised ESR, normocytic anaemia, normal CRP, leukopaenia, thrombocytopaenia

Antibodies

  • ANA (95% sens)
  • Anti-dsDNA - 70% sens but more specific - levels reflect disease process
  • Anti-Sm - most specific but 30% sens
  • Anti0 SSA(Ro), Anti- SSB(La) in 15% and other connective tissue disease

Check for antiphospholipid antibodies for APLS

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38
Q

Management of SLE

A
  • Avoid sun exposure
  • Regular exercise
  • NSAIDs
  • Hydroxychloroquine for skin, arthralgia and myalgia
  • Cyclophosphomide - in life threatening disease
  • Mycophenolate mofetil
  • Azathioprine
  • Methotrexate or ciclosporin
  • IV gammaglobulin and granulocyte colony stimulating factor (if resistant)
  • BELIMUMAB as adjunct if active and antibody positive
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39
Q

Conditions associated with SLE

A 
APLS
scleroderma
RA
Sjorgen's 
thyroiditis
Drug allergies
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40
Q

Epidemiology of ankylosing spondylitis

A 
0.1% of the population
Increased in Northern European
Peak onset 20-30
Increased in males (3:1)
STRONG FHx - HLA B27
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41
Q

Presentation of ankylosing spondylitis

A

Insidious onset under 30 years old
Can be mild chronic or intermittent flares
Systemic features - weight loss, fever, fatigue
Morning stiffness
Inflammatory back pain
Pain improves with activity
Early morning wakening
Peripheral enthesis - 33% (Achilles tendonitis, plantar fasciitis)
Peripheral arthritis - 33% - asymmetrical - hips, shoulders, chest wall, TMJ

Tenderness of sacroiliac joints
Limited range of spinal motion
Lumbar lordosis, thoracic kyphosis, buttock atrophy

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42
Q

Extra-articular findings in ankylosing spondylitis

A

Acute anterior uveitis
Aortitis
Restrictive lung disease - pulmonary fibrosis in upper lobes
Amyloidosis (rare) can cause renal dysfunction
Neuro - C1/C2 subluxation leading to cervical myelopathy
Osteoporosis or osteopaenia
Cauda equina

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43
Q

Diagnostic criteria of ankylosing spondylitis

A

Radiological findings + 1 clinical finding

Radiological - sacroilitis on X-ray

Clinical

  • Lower back pain > 3 months, improves with exercise, not relieved by rest
  • Limitation of lumbar movement in both planes
  • Limit of chest expansion
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44
Q

Investigations for ankylosing spondylitis

A

FBC and CRP (can have normocytic anaemia)
LFTs - ALP often raised
Xray - may be normal in early disease, “bamboo spine”, sacroilitis, enthesititis. Spinal osteopaenia common
MRI
SEXA scan
US in enthesitis

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45
Q

Management of ankylosing spondylitis

A
  • No DMARDs
  • NSAIDs + PPI
  • Local corticosteroid injections
  • Oral steroids - short term only
  • TNF alpha inhibitors e.g. etanercept or adalimumab]
  • Surgery: spinal fixation, vertebral osteotomy
  • Bisphosphonates for osteoporosis
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46
Q

Prognosis of ankylosing spondylitis

A

Increased risk of fractures
Frozen thorax
Blindness from recurrent uveitis
70-90% fully independent

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47
Q

Aetiology of lower back pain

A

Mechanical - hypermobility, arthritis, disc disease, scoliosis, spinal stenosis, sacroilitis
- Bone disease, osteoporosis, osteomalacia, Paget’s

Non-mechanical:

  • Inflammation: Ankylosing spondylitis
  • Infection: osteomyelitis
  • Cancer: bony mets, myeloma

Referred

  • Renal disease
  • Sickle cell crisis
  • Gynae
  • Fibromyalgia
  • Dissecting aortic aneurysm
  • Posterior duodenal ulcer
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48
Q

Epidemiology of back pain

A

60-80% have back pain at some point
1% have chronic back pain

RFs

  • prolonged standing
  • awkward lifting
  • demanding jobs
  • obesity
  • stress
  • FHx
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49
Q

Red flags for back pain

A

Cauda equina syndrome - saddle anaesthesia, urinary/faecal symptoms

Spinal fracture - sudden onset severe pain, relieved by lying down

Cancer or infection - unrelenting pain, worse on lying

Spondyloarthropathy

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50
Q

Investigations for back pain

A

Do not routinely offer imaging, imaging only if red flag symptoms

  • Lumbar X-ray if suspected fracture, mets, collapse from osteoporosis, Paget’s

CT or MRI

FBC, ESR and CRP
LFTs - ALP may be raised
Urine - for infection

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51
Q

Appearance of cancer on X-ray

A

Prostate - sclerotic

Lung, thyroid, kidney = osteolytic

Breast – either (most commonly osteolytic)

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52
Q

Management of back pain

A
  • Information, reassurance, advice
  • Be active, no bed rest
  • Regular pain relief (NSAIDs, Paracetamol)
  • WHO pain ladder
  • Short course muscle relaxant if spams
  • Massage, MDT approach and exercise
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53
Q

Yellow flags for back pain

A 
Belief that pain and activity are harmful
Sickness behaviours - extended bed rest
Social withdrawal
Low mood, depression, anxiety, stress
Problems at work
Over protective family, no support
Inappropriate expectations of treatment
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54
Q

When to refer for back pain

A
  • Red flags, 2WW or urgent if CES
  • Progressive, persistant, or severe neurological deficit when neuro/ortho in 1 week
  • Pain/disability problematic >1-2 weeks - physio
  • > 6 weeks sciatica - see within 3 weeks
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55
Q

Red flag symptoms: cauda equina syndrome

A

Severe or progressive bilateral neurological deficit
Recent onset urinary retention or incontinence
Recent onset faecal incontinence
Perianal or perineal sensory loss
Laxity of anal sphincter

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56
Q

Red flag symptoms - spinal fracture

A 
Sudden onset severe central pain
Relieved by lying down
History of major or minor trauma
Strucutral deformity of spine
Point tenderness over vertebral body
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57
Q

Red flag symptoms - cancer or infection

A 
>50, <20
Pain remains when supine, aching night pain, disturbs sleep
Hx of cancer
Fever, chills and weight loss
Recent infection
IV drug user
Immunocompromised
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58
Q

Red flag symptoms - spondyloarthropathy

A

Early morning stiffness > 45 minutes
Night pain
“gelling”
Improves with movement, worse after rest

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59
Q

Most common location for sciatica due to disc prolapse

A

L5-S1

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60
Q

Presentation of prolapsed disc

A 
Unilateral leg pain
Radiates below the knee, into feet
Leg pain > back pain
Positive straight less raise
Pain relieved by lying down
Exacerbated by long walks and prolonged sitting
Single dermatome

cauda equina syndrome

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61
Q

Investigation for prolapse disc

A

None if symptoms settle in < 6 weeks
MRI is very sensitive
X-ray and CT limited

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62
Q

Management of prolapsed disc

A
  1. Analgesia
    - Paracetamol/NSAIDs
    - Add weak opiod/tramadol
    - Consider benzo, TCA or gabapentin
    - Pain clinic
  • Keep active, encourage swimming
  • Heat and massage
  • Avoid aggravating activities e.g. lifting
  1. Physiotherapy
  2. Surgery
    - Discectomy or spinal fusion
    - Prosthetic disc replacement
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63
Q

Measurement of bone density

A

Measured with DEXA scan

It is expressed in relation to a reference population

T-score - SD in relation to healthy population

Z-score - comparison of density for normal age. <2 is below normal

Normal T>1
Osteopaenia T between -1 and -2.5
Osteoporosis T < -2.5
Severe osteoporosis T

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64
Q

Epidemiology and RF for osteoporosis

A

Increase in women (post-menopause)
Increased with age - 25% at 80 years
2 million women in the UK

RFs

  • Parental history of RF
  • PMH of fragility fracture
  • Low BMI/anorexia
  • Corticosteroid > 3 months
  • Cushing’s
  • Smoking
  • Alcohol
  • Falls = visual or hearing impairment, decreased strength, cognitive impairment, sedatives,
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65
Q

Secondary causes of osteoporosis

A 
RA/inflammatory arthritis
Prolonged immobilisation/sedentary lifestyle
Primary hypogonadism
Primary hyperparathyroidism
Hyperthyroidism
Post-transplantation
CKD
Crohn's, UC, Coeliac
Untreated premature menopause
Type 1 diabetes
COPD
Chronic liver disease
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66
Q

Drugs that can contribute to osteoporosis

A 
PPIs
Anticonvulsants
Depot medroxyprogesterone
Antidepressants
Thiazolidinediones
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67
Q

Who should be assessed for osteoporosis?

A 
Women > 65, Men > 75
Or under that age, if any RF
- Previous fragility fracture
- Frequent oral corticosteroids
- Hx of falls
- FHx of hip fracture
- Causes of 2y osteoporosis
- BMI <18.5
- Alcohol > 14 units per week
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68
Q

How is osteoporosis risk assessed?

A

FRAX or QFracture - gives 10 year fracture risk

Green - no treatment or DEXA
Amber - DEXA. Use result to determine if treatment required
Red - treat, no necessity for DEXA

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69
Q

Primary prevention for osteoporosis

A

Bisphosphonates - ALENDRONATE

  • Must have adequate calcium and vitamin D
  • Do not take with food
  • Cause oesophageal ulcers - drink ++ water and sit up
  • 2nd line: risedronate, etidronate
  • Denosumab (monoclonal antibody that decreased osteoclasts)
  • Strontium ranelate - only to be prescribed by specialists
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70
Q

Secondary prevention for osteoporosis

A

Bisphosphonates +/- vitamin D/calcium supplements
Raloxifene
Denosumab/strontium

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71
Q

Describe osteomyelitis

A

Infection of the bone marrow which can spread to the bone cortex and periosteum

  • Dead bone can detach causing sequestrum
  • Most common distal femur, proximal tibia

2 types

  • Haematogenous from remote source
  • Direct (from contact with infected tissue)
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72
Q

Pathogens responsible for osteomyelitis

A

S. aureus (most common)
Haemophilus influenza
Streptococcus
E.coli/Proteus/Pseudomonas/mycobacteria/fungi

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73
Q

Epidemiology and risk factors for osteomyelitis

A 
Increasing incidence (due to increased diabetes and peripheral arterial disease)
Bimodal age - children or adults
RFs
Trauma/open fracture
Prosthetic joint
Diabetes
Peripheral arterial disease
Chronic joint disease
Alcoholism
IV drug abuse
Chronic steroid use
Immunosuppression
TB
Sickle cell
HIV/AIDS
Catheter use
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74
Q

Presentation of osteomyelitis

A 
Acutely febrile
Bacteraemic
Painful, immobile limb
Swelling
Extreme tenderness
Exacerbated by movement

If vertebral - unremitting pain, worse at rest, night pain

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75
Q

What is Pott’s disease

A

Osteomyelitis in the spine with TB

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76
Q

Investigations for osteomyelitis

A 
FBC - raised WCC and CRP
Blood cultures
Expressed fluid should be cultured
Urine dipstick 
Bone cultures - GOLD STANDARD
MRI = imaging of choice
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77
Q

Management of osteomyelitis

A

4-6 weeks minimum antibiotics - Flucloxacillin, clindamycin if penicillin allergy
MRSA - vancomycin
If chronic infection - 12 weeks

Surgical debridement

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78
Q

Spinal fracture - epidemiology and risk factors

A

50% of white females will have osteoporotic fracture
Increased in females

RFs as osteoporosis
Increased age
Low BMI
Parental history of fracture
Corticosteroids > 3 months
Cushing syndrome
Smoking
Alcohol
Falls
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79
Q

Classification of spinal fractures

A

Wedge compression - isolated anterior column failure
Stable burst - anterior and middle column compression failure, posterior intact
Unstable burst - disruption of anterior, middle and posterior
Flexion-distraction - wedge + tensile failure of posterior and centre of rotation is posterior and anterior
Chance fracture = through spinous process, pedicles and vertebral bodies
Translational fractures = disruption of canal alignment in transverse plane

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80
Q

Presentation of spinal fractures

A 
Central spinal pain
Non-radiating
Disturbing sleep
Can give weakness, numbness and tingling
Kyphotic deformity
Loss of balance
Loss of standing height
Usually T7-T8, T12-L2
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81
Q

Investigations for spinal fractures

A 
Lateral view, plain X-ray - wedging, spinal process misalignment
FBC, CRP
ALP, calcium
Blood cultures
DEXA scan CT/MRI
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82
Q

Management of spinal fractures

A

Anterior column only

  • 24-48 hours bed rest and analgesia
  • Pain will gradually improve over 6-12 weeks
  • Naproxen or diclofenac with Paracetamol
  • early mobilisation and orthosis
  • osteoporosis prophylaxis
  • Vertebroplasty/kyphoplasty/surgical stabilisation
  • if severe unrelenting pain, stabilising joint fracture by infecting cement
  • Pain clinic referral

Multiple column involvement

  • STRICT bed rest
  • Analgesia
  • Open surgical reconstruction +/- decompression
  • osteoporosis prophy`laxis
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83
Q

Epidemiology and RFs for osteomalacia

A

50% adults have insufficient vitamin D
Increased in non-Caucasians
Increased in children and over 65s
FHx has a component

RFs
Pregnancy
Obesity
Housebound/institutionalised
Routine covering of face and body
Poverty
Exclusive breast feeding >6 months
Vegetarianism
Living at high altitude
Alcoholism
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84
Q

Aetiology of osteomalacia

A

GI malabsorption - surgery, short bowel, chronic pancreatitis, CF, Crohn’s, coeliac, biliary disease

Liver disease - cirrhosis
Renal disease - defective 1,25-D3
Drugs - anticonvulsants, rifampicin, HAART,
Severe calcium deficiency

RARE
Hypophosphataemia
Systemic acidosis
Intoxication with fluoride or aluminium
Hyperparathyroidism
Mesenchymal tumour

Genetic rare causes

  • Fanconi’s syndrome
  • Vitamin D dependent rickets (failure to convert 25 to 1,25)
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85
Q

Presentation of osteomalacia in children

A 
Hypocalcaemic seizures or tetany
Bone deformity - genu varum 
Anterior bowing of femur
Internal rotation at ankle
Irritable and reluctant to weight bear
Impaired growth
Increased susceptibility o infections
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86
Q

Presentation of osteomalacia in adults

A 
Pain in hip, pelvis, thigh
Proximal muscle weakness
General lack of well being
Diffuse muscle aches and weakness
Diffuse muscle aches and weakness
Lethargy
Waddling gait
Costochondral swelling
Signs of hypocalcaemia

Bilateral symmetrical multiple fractures - femoral neck, scapula, pelvis

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87
Q

Investigations for osteomalacia

A 
BCP - U&amp;Es including calcium and phosphate
LFTs - raised ALP
PTH - raised
FBC - anaemia if malabsorption
Urine for CKD
Vitamin D <25nmol/L

Radiograph of long bone - cupping, splaying, fraying metaphysis

DEXA scan for decreased bone density

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88
Q

Management of osteomalacia

A

Calceferol 10,000IU for 8-12 weeks (use IM if problems with absorption)

  • Monitor calcium or a few weeks
  • Monitor VitD, PTH, calcium after 3-4 months and every 6-12 months
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89
Q

Mechanism of shoulder dislocation

A

95% are anterior - traumatic.
Generally a fall with combination of abduction and extension - FOOSH

Posterior - fall with arm in internal rotation and adduction e.g. epileptic fit or electricution

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90
Q

Epidemiology of shoulder dislocation

A

One of the most commonly dislocated joints
Increased in males due to increased contact sports
Peak at 20-30 and again at 60-80
If multiple dislocations - consider Ehlers-Danlos

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91
Q

Presentation of shoulder dislocation

A

ANTERIOR

  • Holds arm in external rotation
  • Humeral head palpable anteriorly
  • Abduction and internal rotation are resisted
  • CHECK RADIAL PULSE, DELTOID SENSATION (AXILLARY NERVE), RADIAL NERVE FUNCTION

Posterior

  • Present with arm adducted and internally rotated
  • Abduction and external rotation painful-
  • May resemble frozen shoulder
  • Vascular and nerve problems not associated generally
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92
Q

Complications of shoulder dislocation

A 
Axillary nerve or artery damage
Brachial plexus damage
Radial nerve damage
Recurrent shoulder dislocation
Rotator cuff injury

Bankart lesion - rupture of joint capsule and interior glenohumeral ligament

HillSachs lesion - posterolateral head indentation fracture

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93
Q

Investigations for shoulder dislocation

A

Xray - AP + axillary

Anterior - head under coracoid on AP, humeral head anterior to glenoid

Posterior - may be normal on AP, may have lightbulb sign due to rotation . Head posterior to glenoid on rotation

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94
Q

Management of shoulder dislocation

A

Opioid
Benzos for muscle spasms
No fracture - closed reduction
If fracture = surgery

Multiple number of reduction methods

Post reduction re-check neurovascular assessment
Post-reduction xray
Immobilise the shoulder for 3-6 weeks
Analgesia and physiotherapy

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95
Q

Fracture healing stages

A
  1. Fracture haematoma
  2. Fibrovascular tissue replaces clot - collagen fibres laid
  3. Subperiosteal bone formed at ends beneath periosteum
  4. Primary callus response (few weeks)
  5. Bridging external callus
  6. Endosteoal new bone formation
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96
Q

Common wrist fractures

A

Colles- distal radius with dorsal displacement of fragments

Smiths - distal radius with volar displacement of fragments

Scaphoid

Bartons - fracture dislocation of radiocarpal joint

Chauffeur’s - radial styloid fracture

Greenstick - children

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97
Q

Colles fracture

A

Fracture through distal metaphysis of radius within 2-3cm of articular surface - dorsal displacement of fractures

Common in elderly with osteoporosis

From FOOSH - forced dorsiflexion of wrist

Dinner fork deformity = backwards and laterally

CHECK MEDIAN NERVE FOR DAMAGE

Manage with anaesthesia, redaction and back slab. Surgical reduction only if intra-articular.

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98
Q

Complication of colles fracture

A 
Median and ulnar nerve damage
Compartment syndrome
Deformity on healing
Chronic pain
Mal-union
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99
Q

Scaphoid fracture

A

Increased in males 20-30 years
Vulnerable blood supply - high risk of avascular necrosis

From FOOSH or RTA from steering wheel impact
Tenderness in anatomical snuffbox

20% not seen on x-ray - need 4 views: PA, true lateral, semi-pronated oblique, PA and ulnar deviation
Presumptive casting - 10 degrees of flexion with thumb and forefinger able to oppose.
Repeat xray after 2 weeks

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100
Q

Smiths fracture

A

Reverse colles
Fracture of distal radius with anterior displacement of fragments
Caused by falling backwards
Generally closed reduction

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101
Q

Bartons fracture

A

Distal radius fracture with additional dislocation at radiocarpal joint
Colles or Smiths + dislocation
May be entrapment of tendons of ulnar nerve or artery
Operative reduction required

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102
Q

Nerve distribution in the hand

A

Ulnar - pinky side little and half of ring finger both sides

Median - palm side of thumb, first, middle and half of ring finer

Radial - back of hand, thumb, first, middle and half of ring finger. Not finger tips

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103
Q

Most common sites for radial nerve damage

A

Proximal forearm
Humeral fractures
Radial aspects of wrist

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104
Q

Causes of radial nerve damage

A

Axilla compression - shoulder dislocation OR Saturday night syndrome

Upper arm - triceps and brachioradialis spared - usually due to fracture of humerous

Elbow - tenderness over radial tunnel

Wrist - radial fracture, elbow deformity, finger drop with intact sensation

Superficial - pain and sensory loss, normal motor. Ruptured synovial effusion at elbow OR handcuffs, wristbands, plastercasts

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105
Q

Muscles supplied by radial nerve that needs testing if suspecting damage

A 
Triceps
Brachioradialis
Externsor carpi radialis longus
Supinator 
Extensor digitorum
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106
Q

Muscles supplied by ulnar nerve

A

Hypothenar muscles
Adductor pollicis
3rd and 4th lumbricals
Dorsal and palmar interorssei

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107
Q

Causes of ulnar nerve damage

A

ELBOW
Cubital tunnel syndrome, medical epicondylitis (golfer’s elbow), supracondylar fracture, osteophytic encroachment in OA
Claw hand deformity, unable to flex terminal phalanges or abduct little finger

Wrist - cutaneous sensation usually spared
Positive Tinel’s and Phalen’s sign

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108
Q

RF for carpal tunnel syndrome

A 
Late 50s
Female
Obesity
FHx
Post-colles fracture
Short stature
Injury
Thyroid disorders
Diabetes
Acromegaly
Inflammatory arthritis
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109
Q

Presentation of carpal tunnel syndrome

A 
Tingling, numbness, pain
Worse at night
Causes wakening
Handing hand out of the bed
Weakness in hand grip

Positive Phalen’s Test
Positive Tinel’s Test

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110
Q

Phalen’s test

A

60s of flexion at the wrist causes pain or paraesthesia

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111
Q

Tinel’s test

A

Tapping over median nerve causes pain or paraesthesia

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112
Q

Investigations and management of carpal tunnel

A

ENG - median nerve stimulation to detect muscle action potential over thenar eminence
US
MRI if ENG ambiguous

Minimise aggravating factors
Local steroid injections are diagnostic and therapeutic
Surgical decompression - return to work in 12-19 days

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113
Q

What runs through the carpal tunnel

A

Flexor digitorum superficialis and profundus
Flexor pollicis longus
Flexor carpi radialis
Median nerve

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114
Q

Attachment and function of FDP and FDS

A

FDS - attaches to middle phalanges.
Flexes PIP, MCP and wrist

FDP - attaches to distal phalanges
Flexes DIP, MCP and wrist

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115
Q

Presentation of extensor tendon damage

A

Mallet dinger - fixed flexion of DIP
Boutonniere deformity - fixed flexion of PIP

Inability to extend finger

116
Q

Epidemiology of polymyalgia rheumatica

A

84 per 100,000
Mean age 73. Exclusively over 50s
Increase in females (3:1)
Increased in North European

117
Q

Presentation of polymyalgia rheumatica

A 
Morning stiffness > 45 minutes
Bilateral shoulder or pelvic girdle aching
For over 2 weeks in over 50s
Symptoms worse on waking
Flu like features at onset
Sudden onset over 1-2 weeks

No lymphadenopathy
No active infection
No cancer
No temporal arteritis

118
Q

Investigations for polymyalgia rheumatica

A

Raised inflammatory markers - CRP (more sensitive than ESR)

CHECK
FBCs, U&amp;Es, LFTs
Protein electrophoresis
Urinalysis
Bence Jones protein,

Consider temporal arteritis in all with PMR

119
Q

Management for polymyalgia rheumatica

A

Glucocorticoids
Referral to physio or OT

15mg prednisolone for weeks then drop very slowly
Treatment for 1-2 years. Maintenance dose usually 2.5-5mg

DEXA scan
Calcium and vitamin D therapy +/- bisphosphonates

Monitor - 15% get temporal arteritis

120
Q

Epidemiology of temporal arteritis

A

2.2 per 10,000
Increased in northern European
increased in females (3:1)
Common after 60

121
Q

Presentation of temporal artertitis

A 
Recent onset temporal headache
Worse at night
Myalgia
Malaise
Fever
Scalp tenderness
Transient visual symptoms - diplopia, ischaemic optic neuritis, blurred vision, visual loss, amarousis fugax
Jaw claudication
Anoexia, weight loss, 
Thoracic aorta often involve
122
Q

Diagnostic criteria for temporal arteritis

A

3 out of 5 needs

Over 50
New headache
Temporal artery abnormality - tenderness, pulsation
Increased ESR
Abnormal artery biopsy
123
Q

Investigations for temporal arteritis

A

Urgent referral for temporal artery biopsy
Increased ESR or CRP
FBC - normocytic normochromic anaemia, thrombocytosis
LFTs - raised ALP
Biopsy - 87% sensitivity
Colour duplex ultrasonography

124
Q

Management of temporal arteritis

A

Urgent referral - should not delay treatment
Steroids - 40g OD prednisolone, 60g if claudication
If visual symptoms then IV prednisolone
Lower once symptoms resolved or test results normal

Start aspirin and PPI
Osteoporosis prophylaxis

125
Q

Complications and prognosis of temporal arteritis

A

Permanent visual loss
Aneurysms, dissections, stenotic lesions of aorta
CNS disease - seizures, strokes
Steroid related complications - osteoporosis, myopathy, bruising, diabetes, HTN

Relief with treatment but relapses are common
Often need steroids for 2 years

126
Q

Describe radial head and neck fractures

A

Radial head fractures are the most common elbow fractures in adults
In children - radial neck

Swelling over lateral elbow.
Limited motion and point tenderness
Neurovascular assessment

Investigations - AP and lateral. Fat pad sign

Urgent surgical treatment

127
Q

Describe olecranon fractures

A

Often low energy fractures causes by sudden pull of triceps or brachioradialis
Swelling and tenderness over olecranon
Inability to extend against gravity

Should be seen clearly on lateral xray

Immobilise in split at 60-90 degrees of flexion

128
Q

Elbow dislocation

A

2nd most common dislocation

Terrible triad -

  • Elbow dislocation
  • Coronoid process fracture
  • Radial head fracture

Associated with injury to brachial artery and nerve
Prompt reduction essential

129
Q

Types of hip fracture / classification

A

Femoral neck #
Femoral shaft #
Femoral stress #

Intracapsular - between edge of femoral head and insertion of joint capsule into the hip (intertrochanteric line)
Assume vascular compromise

Extracapsular - distal to intertrochanteric line
Can be due to avulsion fractures from gluteus medius
Assume vascular system spared

Can use Garden’s classification if intracapsular
- Garden 1 - inferior cortex intact, no significant displacement
2 = trabeculae in line, fracture visible from superior to inferior cortex
3 = obvious complete #, slight displacement or rotation
4 = gross and often complete displacement

130
Q

Risk factors for hip fracture

A

Increased age
Osteoporosis
Family history of hip fracture (maternal)
osteomalacia
Falls = instability, decreased core strength, gait disturbance, sensory impairment

131
Q

Presentation of hip fracture

A

Pain in outer upper thigh or groin
Pain may radiate to the knee
Inability to weight bear
Pain aggravated by flexion and rotation of the leg

shortened, adducted and externally rotated leg

132
Q

Diagnosis of hip fracture

A

AP and lateral x-ray
Disruption of trabecular, inferior or superior cortices and abnormality of pelvic contours
Broken Shenton’s line
MRI should be performed if suspected but not seen on x-ray

133
Q

Shenton’s line

A

Curved line formed by top of obturator foramen and inner side of neck of femur

Line broken in hip #

134
Q

Management of hip #

A

Intracapsular

  • surgery within 24 hours
  • reduction and internal fixation
  • if young patient then dynamic hip screw where possible
  • if poor prognosis hemi-arthroplasty
  • if otherwise fit full hip-replacement

Extra-capsular

  • Dynamic hip screw if trochanteric
  • Sub trochanteric = screws, nails and pins
135
Q

Complications of hip #

A 
Mortality high - 10% at 1 month, 33% at 1 year
Infection
Haemorrhage
Avascular necrosis
Delayed union, malunion, non-union
Pneumonia
MI
Stroke
DVT/PE
Pressure ulcers
136
Q

Femoral saft #

A

Severe pain, tense, swollen thigh
Inability to weight bear
X-ray AP and lateral - include bilateral hip and knee for comparison

Management 
- Cross match
- Analgesia
- Monitor pulses and sensation
- Reduce and surgery - nails most common
Early mobilisation

4-6 months healing time

Be aware:

  • Acute compartment damage
  • Vessel or nerve damage
  • Large potential blood loss
137
Q

Blood supply to femoral head

A

Most comes from upwards extending branch of profunda femoris which forms lateral and medial circumflex which then forms sub synovial ring

Very small from ligamentum teres - branching from obturator artery

138
Q

Pelvic #

A

High energy trauma
Tenderness, bruising, swelling, crepitus
Haematuria and rectal bleeding
Neuro and vascular abnormality in legs

Can be due to lateral compression causing sacral # and sacroiliac disruption (side swipe car accidents)

Can be due to AP compression - head on collisions = open book fracture, springs open hinging on sacroiliac joints

CT, PV and PR for bleeding
ATLS!
Leg length discrepancy
Perineal bruising
Pelvic binder at greater trochanter to tamponade bleeding
139
Q

Patella #

A

2 ways to fracture

  • Direct fall onto flexed knee - stellate shape
  • Sudden contraction of quadriceps to prevent fall = transverse #

Check extensor mechanism = can patient lift heel from bed (if in tact then they can)

Management

  • Undisplaced = conservative cylinder cast
  • Displaced or extensor mechanism affected = surgery
  • Tension batwing wiring
  • repair extensor retinaculum,
140
Q

Define compartment syndrome

A

Caused by increased pressure in a closed anatomical space

Compromises circulation and function of tissues within the space.
Can damage muscles and nerves

Can be acute or chronic
Acute is caused by trauma or intense exercise
Chronic is caused by exercise

141
Q

Common sites for compartment syndrome

What can they damage

A

FOREARM

  • Ventral: median and ulnar nerves. Radial and ulnar artery
  • Dorsal: posterior interosseous nerve. No vessels

LOWER LIMB

  • Anterior tibial: deep peroneal nerve. Anterior tibial artery.
  • Superficial posterior: none
  • Deep posterior: posterior tibial nerves and vessels. Peroneal artery
  • Peroneal: deep and superficial peroneal nerves

GLUTEAL
- uncommon. often have muscle necrosis and sciatic nerve palsy due to late diagnosis

ABDOMINAL

  • in multiple trauma patient in profound shock
  • AKI, cardiac dysfunction, raised central venous pressure
  • Sudden release can cause ischaemia reperfusion injury, acidosis and cardiac arrest
142
Q

Aetiology of acute compartment syndrome

A 
Fractures especially distal limbs
Crush injury
Burns
Infection
Prolonged limb compression
Vascular - ischaemic, haemorrhage, phlegmasia caerulea dolens
Iatrogenic - IM injections, vascular puncture (if anti-coagulated) 
Muscle hypertrophy in adults
143
Q

Presentation of acute compartment syndrome

A

Within 48 hours of injury
Increase pain despite immobilisation of fracture
Sensory deficit in nerves passing through compartment
Muscle tenderness and swelling
Excessive pain on movement
May have peripheral pulses until late stages - pallor, pulselessness

144
Q

Investigations for acute compartment syndrome

A

CLINCIAL diagnosis
Can measure pressure
- Wick catheter, pressure transducer and site ported needles
- MRI if ambiguous

145
Q

Management of acute compartment syndrome

A

Urgent decompression to reduce ischaemia
Remove all dressings
Urgent orthopaedic referral

open FASCIOTOMY

  • skin and deep fascia divided along length of compartment, leave would open
  • debride any muscle necrosis

Complication- tissue necrosis

146
Q

RF for chronic compartment syndrome

A 
athletes
under 40
repetitive motion
exercise - tennis, running, gymnastics, cycling
excessive training
147
Q

Presentation of chronic compartment syndrome

A

severe pain and tightness triggered by exercise
Resolves with rest
May have tinging and weakness
May have abnormal gait

148
Q

Management of chronic compartment syndrome

A

Deep massage
Limit offending activity
Decompressive fasciotomy - used in athletes that refuse to modify activity

149
Q

Early complications of lower limb #

A 
LOCAL
vascular injury
visceral injury e.g. bladder, bowel
damage to nerves, tissue or skin
haemoarthrosis
compartment syndrome
wound infection
fracture blisters
SYSTEMIC
fat embolism
shock
vte, PE, DVT
exacerbation of underlying disease e.g. COPD
pneumonia
150
Q

Late complications of lower limb #

A 
LOCAL
delayed union
malunion
joint stiffness
non-union
contractures
myositis ossificans
avascular necrosis
algodystrophy
osteomyelitis
growth disturbance/deformity

SYSTEMIC
gangrene, tetanus, septicaemia
fear of mobilising

151
Q

RF for delayed union

A 
severe soft tissue damage
inadequate blood supply
infection
insufficient splinting
excessive traction
increased age
severe anaemia
diabetes
low vitamin D
hypothyroid
NSAIDs
steroids 
complicated fracture
osteoporosis
152
Q

presentation and management of non-union

A 
pain at site, tenderness, swelling
non-use of limb
movement at the # site
palpable gap
absence of callus
weight bearing and casting
bone stimulation - teriparatide
debridement
bone grafting
internal fixation
153
Q

Myositis ossificans

A

calcifications and bony formation in muscles

increased risk after humeral supracondylar fracture

154
Q

Algodystrophy

A 
"Sudeck's atrophy"
Reflex sympathetic dystrophy
Hand or foot
Continuous burning pain
Accompanied initially with swelling, warmth and redness
Then pallor and atrophy

Manage with analgesia and physio

155
Q

Complications of casts

A

malunion if misplaced

Cast disease - circulatory disturbance, inflammation, bone disease

  • Osteoporosis
  • Chronic oedema
  • Tissue atrophy
  • Joint stiffness
thermal ulcers during hardening
pressure ulcers
thrombophlebitis
infection if wet skin
decreased bone density
156
Q

Complciations of traction

A 
pressure ulcers
pneumonia/UTI
permanent foot drop contractures
peroneal nerve palsy
pin tract infection
Thromboembolism
157
Q

Complications of external fixation

A 
Pin tract infection
Pin loosening or breaking
Interference with joint movement
Neurovascular damage
Misalignment if misplaced
Psychological - visible deformity and disability
158
Q

Rehab post #

A 
Prompt surgery
MDT
Physio
OT
Social workers
Orthopaedics
\+/- geriatrics

EXERCISE ASAP

Decreased motivation = decreased recovery
Exercise is important

159
Q

Impact of amputation

A 
PHYSICAL
decreased mobility and dexterity
stump or phantom limb pain
infection
increased care requirements
muscle contractures therefore require regular stretching
DVT/PE
EMOTIONAL
traumatic/PTSD
depression
adapting psychologically to the loss
body image issues
decreased social activities
social isolation

Prosthetic limbs require skin desensitisation with compression bandaging

160
Q

Ankle joint

A

Involves tibia, fibular and talus

Syndesmosis joint between tibia and fibular

Tibiotalar joint allows dorsi and plantar flexion

Subtalar joint between talus and calcaneous allows inversion and eversion

161
Q

Presentation of ankle #

A 
immediate severe pain which can extend to foot and knee
swelling
bruising
tenderness
joint deformity
inability to weight bear
162
Q

Ottawa rules for ankle #

A

X-ray is recommended if:

  • over 55
  • unable to weight bear for 5 steps either at time of accident or evaluation
  • bone tenderness at posterior edge or tip of medial malleolus
  • bone tenderness at posterior edge or tip of lateral malleolus
  • tender 5th metatarsal, cuboid or navicular
163
Q

Investigations for ankle #

A

x-ray (Ottawa rules)
AP, lateral and oblique views
If one injury is seen, look for a second
CT or MRI if soft tissue or intra articular joint

164
Q

Classification for ankle #

A

Danis-Weber classification

A - fibular # below syndesmosis
B - fibular # at the level syndesmosis
C - fibular # above syndesmosis indicating rupture

Operative if type C or some type B

165
Q

Pott’s #

A

and # dislocation of distal tibia and fibular involving 2 elements of ankle ring, very unstable

166
Q

Pilon #

A

fracture of distal tibia and disruption of talar dome

Due to falling from a height

167
Q

Management of ankle #

A

ABCDE
If neurovascular compromise reduce immediately (before XR)
Analgesia

If not displaced or type A then conservative (or if not fit for surgery)
4-6 weeks in cast
Repeat x-ray regularly to ensure reduction and healing
if displaces then surgery

If type C or some type B then operative
Also if dislocation, bimalleolar #, joint incongruity
Open reduction and internal fixation

Early remobilisation and weight bearing

168
Q

Epidemiology of burns

A

0.3 per 1000
300 deaths per year

Increased in under 5s or over 75
50% occur in kitchens

169
Q

What is the rule of 9s

A

Body split into different areas that either have 9% SA or 18%SA to estimate area of burns

9% for head and each upper limb
18% for torso front, torso back and each lower limb

Use Lund and Bower chart for children as not equal

170
Q

Depth of burns

A

Epidermal/ Superficial partial thickness

Superficial dermal

Deep dermal

Full thickness (3rd degree)

4th degree

171
Q

Describe an epidermal/ superficial partial dermal burn

A 
Red
Glistening
Painful
Brisk cap refill
Heals in 1 week with no scarring
172
Q

Describe a superficial dermal burn

A 
Pale pink/ mottled skin
Swelling
Small blisters
Hypersensitive
Wet/weeping
Brisk cap refill
Heals in 2-3 weeks 
Minimal scarring
173
Q

Describe a deep dermal burn

A 
Blistering
Dry
Blotchy, cherry red
Does not blanch
No cap refill
Decreased or absent sensation
Heals in 3-8 weeks
Scarring
May require surgery
174
Q

Describe a full thickness burn

A 
Old 3rd degree burn
Dry
White / Black
No blisters
No cap refill
Absent sensation
Requires surgical repair/grafting
175
Q

Describe 4th degree burn

A

Includes subcutaneous tissue, muscle or bone

Requires reconstruction and often amputation

176
Q

Initial baseline investigation in burns patient

A

Bloods - FBC, group and save, carboxyhaemoglobin, glucose, U&Es, pregnancy test

ABG(s)
CXR
Cardiac monitoring
Hourly urine outputs / catheter

177
Q

Management of minor burns

A

Stop burning

  • remove all clothing. any adherent clothing cool with water. remove all jewellery
  • rinse with tap water for at least 20 minutes
  • NOT ICED WATER as this causes vasoconstriction and can further tissue damage
  • brush off any dry chemicals first

Minor

  • wash with soap and water
  • is blister >1cm then aspirate aseptically, if <1cm then leave
  • non-adhesive dressings with gauze padding, change after 3-5 days
  • if infection develops: flucloxacillin / erythromycin
178
Q

Management of major burns

A

ABCDE

A - check for inhalation injury
- endotracheal intubation if required

B - ABGs and 100% O2, presume CO poisoning

  • elevate head and chest by 20-30 degrees to decrease neck and chest oedema
  • RARE: escharotomies to release chest tightness

C - fluid replacement - IV line ASAP
If burns >15% then start fluid replacement for minimum 24 hours
4ml Hartmann’s per kg per % affected

Strong opiate
Sedation
Prevent hypothermia

Other

  • fasciotomy
  • gastric tube insertion
  • antibiotics if infection
  • grafts (must be within 3 weeks)
179
Q

When to refer to burns unit

A

Under 5, over 60
Burns to face, hands, neck, perineum or full thickness to large area
Inhalation injury
Chemical burn / ionising radiation / high pressure steam injury or electrical injury
>10% SA in adults, >5% in child
Pregnancy

180
Q

Complications of burns

A 
Respiratory distress
Fluid loss, hypovolaemia, shock
infection
raised metabolic rate
increased plasma viscosity
muscle damage (if electrical) - rhabdomylysis
Poisoning
Haemoglobinuria and renal damage
Scarring
181
Q

Indications of inhalation injury

A

Can be subtle and present over 24 hours after incident

  • face/neck burns
  • singed eyebrows
  • carbon deposits in oropharynx/ sputum
  • acute inflammation of oropharynx
  • explosion in enclosed space
  • hoarseness
  • carboxyhaemoglobin >10%
  • history of impaired awareness

Intubate and mechanical ventilation
Transfer to burns unit

182
Q

Signs of non-accidental burns

A 
Delayed or avoidance of treatment
Incident not witnessed
No explanation
Implausible mechanism of injury
Details change with time
Lack of concern from accompanying adult
Abnormal demeanour - withdrawn

Sharply demarcated
Glove and stocking injury
Uniform depth of burn
Donut sparing of buttocks on bottom of tub

183
Q

Epidemiology of chronic pain

A

23% worldwide
Increases with age, over 45s
Increased in females
Most common locations: back pain, headache, joint pain

Risk factors
Pregnancy
Hx of trauma or chronic pain
Fhx
smoking
high risk occupation
co-morbid personality
184
Q

Aetiology of chronic pain

A

MSK - OA, RA, osteomyelitis, osteoporosis, AS, myofascial disease, PMR, fractures, strains

Neurological - diabetic neuropathy, spinal stenosis, brachial plexus traction injury, thoracic outlet syndrome, trigeminal neuralgia, alcoholism, thyroid disease, pernicious anaemia

headache - migraine, temporal arteritis, glaucoma,

Psychological - depression, anxiety, personality disorder, sleep disturbance

Cancer = mets, myeloma, paraneoplastic syndrome

Systemic diseases = SLE, Sjorgen’s, diabetes, hypothyroid, hyperparathyroidism, HIV, Hep C

185
Q

Management of MSK chronic pain

A

Physiotherapy
Paracetamol and/or NSAIDs
OT
Pain management psychology = relaxation techniques, stress management, coping skills, CBT

186
Q

Management of neuropathic pain

A 
Gabapentin/pregabalin/amitryptiline/duloxetine
Capsacin/topic lidocaine
oxycodone
physio/OT
Pain management psychology
TENS
Pain clinic referral
187
Q

Alternative therapies used for pain management

A

Capsacin

Acupuncture OA 5/5, LBP 5/5 GREEN

Chiropractor 2/5 for OA and LBP AMBER

Massage 5/5 LBP FM, 2/5 OA

Relaxation therapy

Tai chi
Yoga

188
Q

Why would people use alternative therapies for pain relief?

A 
Want more natural treatments
Want to feel in control 
Persistent pain
Pain not relieved by conventional treatment
Concerns about medication side effects
189
Q

Benefits of CBT for pain

A

encourages problem solving attitude
patients are pro=active
involves homework
provides coping mechanisms

small improvement in pain and disability
moderate increase on mood

190
Q

epidemiology of fibromyalgia

A 
Increase in females (x10)
20-50 years most commonly
low income
being divorced
failing to complete education
5% of population
191
Q

Presentation of fibromyalgia

A 
chronic widespread pain
unrefreshing sleep/tiredness
fatigue
sleep disturbance
morning stiffness
paraesthesia
feeling of swollen joints
problems with cognition
headaches
light headedness
anxiety/depression
192
Q

Management of fibromyalgia

A 
MDT approach
EXERCISE - swimming, aerobic exercise, resistance training
CBT
Relaxation/physio
Paracetamol/weak opioids/ tramadol
Antidepressants
Pregabalin/gabapentin

Take care not to over investigate

193
Q

What is O’Donohue’s Triad

A

Knee injury triad
ACL
MCL
Meniscus tear

194
Q

Most common to least common knee injury mechanisms

A 
Valgus
Twist
Hyperextension
Hyperflexion
Varus
195
Q

Morton’s neuroma

A

Interdigital neuritis in the feet
Repeated trauma from walking causes irritation leading to neuroma
Causes anaesthesia of interdigital sides of connecting toes
Treated with surgical removal
Pain on squeezing feet

196
Q

Jone’s fracture

A

fracture at the base of the 5th metatarsal

avulsion fracture

197
Q

Achilles tendon rupture

A

Describe it as if kicked from behind and then fell
Use Thompson’s test
Decrease recurrence with surgery for management
Place wedges inside a boot for 2-4 weeks

198
Q

Plantar fascitiis

A 
Heel pain worse on a morning
Tenderness over calcaneus
Gets better with walking
Self-limiting
Treat with stretching exercises
199
Q

Risk factors for congential dysplasia of hip

A

Female
Oligohydramnios
FHx
Multiple pregnancies

200
Q

management of congenital dysplasia of the hip

A

Use US for diagnosis as the femur head is cartilage for 3 moinths

Use calipers/splinting to keep hips externally rotated and abducted
At 3months do x-ray.
Hip spiker
Muscle release
Osteotomy if others fail = if need surgery then they will need a hip replacement in their 30s

201
Q

Perthe’s disease

A

Increased in 6-9 year olds
Males
Pain, limping, no history of trauma

Due to avascular necrosis of epiphyseal plates
Head develops asymmetrically - mushroom shapes. Increased subluxation

202
Q

Slipped capital femoral epiphysis

A 
Hypogonadism
occurs in puberty
Large hips
Males
passed off as "growing pains"
3 stages depending on angle of slip 
1 = 10 degrees, 2 = 30, 3=45
1&amp;2 fixed with pinning
3 = open fixation, but 20% risk of damaging blood supply
Most around knees
203
Q

Osteogenesis imperfecta

A 
Defect in gene for collagen
Increased in females
Most die in utero/labour
If mild form then multiple breaks
Blue sclera
Heal very quickly
Treat as you would normally treat the fracture
Number of fractures decreases with age
204
Q

Congential talipes equinovarus

A 
Club foot
1%
Increased in males or FHx
Increased in breech and oligohydramnios
5-10% bilateral

Treat with stretching and manipulation
Serial splinting to minimise surgical intervention
No limitations in life with treatment

205
Q

Epidemiology of DDH

A 
Developmental dysplasia of the hip
1-3% of newborns
Left hip more commonly affected 
Increased in female babies
Increased in countries that swaddle babies
RFs
Sibling with DDH
First born
Vaginal delivery for breech (x17)
C-section for breech (x7)
Oligohydramnios
Multiple pregnancy
Prematurity
Neuromuscular disorders - CP, meningocoele

20% are bilateral

206
Q

Screening for DDH

A 
Screened at birth and 6-8 week baby check
US at 6 weeks ONLY if:
- 1st degree FHx of DDH
- Breech after 36 weeks
- If breech < 36 weeks scan at birth
207
Q

Examination for DDH

A

At 3 months or under

  • Look for asymmetry of skin folds, leg length
  • Orlani and Barlow tests
  • Orlani - forward pressure on femoral head
  • Barlow - back pressure on femoral head. If movement then dislocating.

Abduction < 60 degrees at 90 degrees of hip flexion

Over 3 months

  • Unilateral limitation and symmetry of hip abduction
  • Galeazzi sign: unilateral femoral shortening when supine at hip flexed to 90 degrees
208
Q

Investigations for DDH

A

Dynamic US for hip stability and acetabular development
US is better under 4 months
After 4 months, pelvic X-ray better as the femoral ossification centre has developed

Arthrography peri-operatively to determine if open or closed reduction

209
Q

Management of DDH

A

Early diagnosis gives better outcome
Most self-stabilise by 2-6 weeks

Non-surgical

  • Dynamic flexion-abduction orthosis (Pavlik harness) from the time of diagnosis
  • adjust as the child grows, remains in place at all times
  • Risk of avascular necrosis or temporary femoral nerve palsy
  • contraindicated once over 4.5 months

Surgical

  • If don’t respond or late diagnosis
  • Closed reduction with adductor or psoas tenotomy
  • THEN 3-4 months in abduction brace
  • If over 18 months then may need osteotomy
210
Q

Epidemiology of pes planus

A 
20% of adults
45% of children, but generally resolves before 10 years
Common in young children 
Increased in Africans
only pathological in 1%
Increased in males
Increased with obesity
211
Q

Foot findings in pes planus

A

Collapse of medial longitudinal arch
Foot PRONATES
VALGUS position of heel and forefoot

212
Q

Aetiology of pes planus

A

CHILDREN

  • Normal in 3-6 years
  • Neurological problems; CP or polio
  • Bony abnormalities: tarsal coalition, accessory navicular bone
  • Ligament laxity: Ehler’s-Danlos, Marfan’s

ADULTS

  • Physiological in 20%
  • Decreased arch strength - dysfunction of tibilias posterior tendon, ligament tear, neuropathic foot (diabetes, polio), arthropathy, OA
  • Increased load - shoes limiting movement, tight Achilles tendon, obesity, pregnancy
213
Q

Symptoms of tibialis posterior dysfunction

A

Pain or swelling behind medial malleolus and along instep
Change in foot shape (pes planus)
Decreased walking ability and balance
Ache on walking long distances

214
Q

Management of pes planus

A

CHILDREN

  • treatment often unnecessary
  • generic foot orthoses
  • surgery only if rigid

ADULTS

  • exercise and barefoot walking
  • heel cord stretching to lengthen Achilles tendon
  • orthtics: heel wedge and arch support
  • Advice: shows with low heel and wide toes. weight reduction

Surgical - if rigid, progressive or CP with equinovarus foot

  • Soft tissue reconstruction e.g. tibialis posterior or Achilles
  • Arthoeresis
  • Reconstructive osteotomy for realignment
  • Arthrodesis
215
Q

Complications of pes planus

A 
Tibialis posterior dysfunction
Hallux valgus
Metatarsalgia
Plantar fasciitis
Knee pain
216
Q

Causes of in-toeing

A

Metatarsus varus

  • From birth, inward twisting of forefoot
  • Observe, 85% resolve
  • If persistent, splinting then surgery
  • Associated with DDH

Tibial torsion

  • Presents at 1-3 years
  • Resolves spontaneously

Internal femoral torsion

  • 3-10 years
  • Abnormal anteversion of femoral neck
  • At birth 40 degrees, 15 as adult, Slow transition causes intoeing
  • most have spontaneous resolution
  • Some require rotational osteotomy
217
Q

Genu Varum

A

Lateral bowing
“bow legged)
Normal in children under 2
Associated with out-toeing

218
Q

Causes of genu varum

A 
Ricket's
Scurvy
Blout disease
Paget's disease
OA (in elderly)
219
Q

Pathological features of genu varum

A

Inter-malleolar distance >10cm
FHx of skeletal abnormality
Asymmetry of knees
Abnormally short stature

220
Q

Genu valgum

A 
Knock kneed
Common between 2-4 years
If symmetrical usually benign 
Measure intermalleolar gap
Associated with intoeing

Causes:
Rickets
Scurvy
RA/OA

221
Q

Epidemiology of scoliosis

A

Increased in FEMALES
2-3%
More common to curve to right

RF
Trauma
Neuromuscular imbalance
Congenital
Most are idiopathic
222
Q

Types of scoliosis

A

Infantile - before 3 years. Increased in boys. Many resolve spontaneously. Some get severe deformity

Juvenile - 3-10 years. increase in girls. high risk of progression. often require surgical intervention

Adolescent idiopathic scoliosis (AIS) - 10 years to maturity. Occurs at onset or during puberty. Increase in females. Need surgery

223
Q

Presentation of scoliosis

A

Increasing pain with increasing deformity
Unlevel shoulders
Waistline asymmetry
Rib prominence

Scoliometer to measure
Can place a wedge under one foot to see improvement, if improvement then may be due to a shorter leg.

224
Q

Aetiology of scoliosis

A

Idiopathic (80%)
Congenital malformation of vertebrae (10%) - usually have GU deformity
Neuromuscular - CP, spina bifida, polio
Metabolic - Hunter’s
Crush # from trauma, osteoporosis, TB, malignancy
Dysmorphic syndromes - neurofibromatosis, Marfan’s, osteogenesis imperfect

225
Q

Causes of anterior bowing of legs

A

ALWAYS insignificant

  • Congenital absence of fibula
  • Neurfibromatosis type 1
  • Osteogensis imperfecta
226
Q

Investigations for scoliosis

A

PA and lateral spine x-rays
Cobb’s angle is used to measure degree of scoliosis, needs to be >10
CT/MRI if required

227
Q

Management of scoliosis

A

Infantile - generally no surgery
Juvenile - generally require surgery
AIS - surgery depends on size of curve

Bracing - where still growing, trying to prevent worsening
Exercises
Surgery - in 25%, if Cobb’s angle >45, solid fusion
Magnetic expansion control growth rods

228
Q

Complications of scoliosis

A

Decreased exercise capacity and weak respiratory muscles
Compression of abdominal contents
Severe = damage to spinal cord
Psychological problems

Cardiopulmonary problems at 60 degrees, myelopathy at 90 degrees

229
Q

Scheuermann’s disease

A

thoracic kyphosis > 40 degrees
Painless
Surgery not required

230
Q

Define cerebral palsy

A

Group of permanent disorders of the development of movement and posture causing activity limitation that are attributed to disturbances in development of foetal or infant brain

231
Q

Classification of cerebral palsy

A

Spastic types = intermittent increase tone and pathological reflexes

Athetoid - hyperkinesia

Ataxic = loss of muscular co-ordination

Mixed

Other classficiations:

  • pre-natal, natal or post-natal
  • monoplegia, diplegia, hemiplegia
  • congenital or acquired
232
Q

TORCH infections

A 
Toxoplasmosis
Other
Rubella
Cytomegalovirus
Herpes Simplex
233
Q

Epidemiology of cerebral palsy

A 
1 per 1000 live normal weight births
16 per 1000 underweight live births
Increasing maternal age
Increased in black population
Increase in IUGR

In those severely injures, the lighter the birth the longer the life expectancy

234
Q

Presentation of cerebral palsy

A

Delayed developmental milestones
Definitive diagnosis is hard under 18 months
Abnormal posture and movement

Most common = bilateral spastic cerebral palsy

commonly associated symptoms:

  • Epilepsy
  • Failure to thrive
  • Bladder incontinence or increased infection
  • Constipation for decrerased mobility and intake
  • Drooling
  • Sleep disturbance
  • orthopaedics: joint contractures, hip/foot deformity, shortened muscles, scoliosis, #
235
Q

Investigations for cerebral palsy

A

Clinical examination and parental observation

Exclude other causes:

  • Thyroid studies
  • Chromosomal analysis
  • Pyruvate and lactate levels
  • Amino acid levels for metabolism errors
  • CSF for hypoxia

Imaging - US or MRI may be helpful
Evoked potentials to check vision and hearing
EEG - to detect damage post hypoxia

236
Q

Diseases associated with cerebral palsy

A 
Intrauterine infections: TORCH, HIV
Congenital malformation
Toxic or teratogenic agents = alcohol, smoking, cocaine
Maternal abdo trauma
Maternal thyroid illness
Intracranial haemorrhage
Trauma
Infection
Hyperbilirubinaemia
Seizures
237
Q

Management of CP

A

Physio, OT, speech therapy, recreational therapy, paediatrics, orthopaedics

  • Baclofen for muscle spasm
  • Alternatives: tizanidine, botulinum A
  • Diazepam or gabapentin
  • Surgery for fixed contractures
  • Mobility aids
  • Heat, cold, vibration to decrease spasticity
  • Splinting to increase range of movement at a joint
238
Q

Complications of CP

A 
Moderate to severe learning difficulties
Hearing loss
Contractures
Failure to thrive
Osteoporosis
Aspiration pneumonia
Dental problems

Decreased life expectancy with severe forms

239
Q

Define Perthe’s disease

A

Self-limiting hip disorder caused by ischaemia and subsequent necrosis of femoral head

240
Q

Epidemiology of Perthe’s disease

A

4-8 years
Increased in males (4:1)
Increased in obesity
Increased in Caucasians

241
Q

Pathogenesis of Perthe’s disease

A

Avascular necrosis of femoral epiphysis
Delayed ossific nucleus
Articular cartilage is nourished by synovial fluid and continues to grow
Cartilage columns distort
Do not undergo normal ossification - excess calcified cartilage in bone
Symptoms are due to # and subchondral collapse

242
Q

Presentation of Perthe’s disease

A 
Pain in hip or knee causing limp
4-8 years old
Effusion due to synovitis
10-15% bilateral (but asymmetrical stages)
All hip movements limited
Antalgic gait
Trendelenburg gait in late stages
No history of trauma
Roll test: roll leg in internal and external rotation when supine will produce guarding
243
Q

Investigations for Perthe’s disease

A

FBC, ESR
X-ray
- Early: widening of joint space or normal
- Later: decrease size of femoral head with patchy deformity
- Later: collapse and deformity of femoral head (increased arthritis)

Hip aspiration if ?septic
Arthrogram or MRI

244
Q

Management of Perthe’s disease

A

Under 6s respond better
Over 6s tend to need surgery
Physio to increase muscle strength and range of motion
Surgery - proximal varus osteotomy

245
Q

Define slipped capital femoral epiphysis

A

Often atraumatic or associated with a minor injury.
Most common adolescent hip disorders
Instability of proximal femur growth plate

  • Preslip
  • Acute (10-15%)
  • Chronic (85%)

Stable in 90%, unstable in 10%

246
Q

Epidemiology of slipped capital femoral epiphysis

A 
I per 10,000
13 year old boys
11.5 year old girls
Most common hip disorder
Bilateral in 20%
Left>right
Increased in males
Incidence rising
RF
Obesity
Local trauma 
Neglected septic arthritis
Short stature
Hypothyroid
Hypopituitarism
Past radiation of pelvis
247
Q

Presentation of slipped capital femoral epiphysis

A 
Discomfort in hip, groin, medial thigh during walking
Pain worsens with running or jumping
Acute <3 weeks, chronic > 3 weeks
External rotation of leg on walking
Hip motion is limited

Drehmann’s sign - supine, passively flex the hip, leg falls into external rotation and abduction

If chronic - atrophy of thigh and shortening of affected leg

248
Q

Investigations for Perthe’s disease

A

AP and frog leg lateral x-ray

- widening of epiphyseal line or displacement of femoral head

249
Q

Management of Perthe’s disease

A

Analgesia and immediate orthopaedic referral
Avoid moving or rotating leg
Surgery is mainstay of treatment
- Prevents further slops
- Prevent femeroactabular impingement
- Centre to centre screw fixation across plate
- OR open reduction and osteotomy of femoral neck

250
Q

Define transient synovitis

A

Irritable hip
Common between 2 and 12
Acute onset of hip pain and a limp that gradually resolves
Child otherwise well

251
Q

Clinical features of transient synovitis

A 
Acute onset of hip pain or limp
Between 2 and 12
Increased in boys (2:1)
Inability to weight bear
Leg held in flexion, adduction with slight external rotation
Extension limited
Child otherwise well
persists for 1-2 weeks
Resolves spontaneously
252
Q

Investigations for transient synovitis

A 
Exclude other diagnoses
FBC, CRP and ESR
X-rays
US - for effusion 
Aspirate fluid

ALL are normal

253
Q

Management for transient synovitis

A

Rest and analgesia

254
Q

Pathophysiology

Duchenne’s muscular dystrophy

A

Most common muscular dystrophy
X linked recessive
Mutations in dystrophin gene - NO DYSTROPHIN PRODUCED
Progressive muscle degeneration

255
Q

Presentation of Duchenne’s

A

Progressive proximal muscular dystrophy
Characteristic pseudohypertrophy of calves
All have symptoms by 3 years
Delayed motor milestones
Waddling gait on running
Gower’s sign = climbing up with hands when getting off floor
Failure to thrive
Speech delay
Raised LFTs
Anaesthetic complications - rhabdomyolysis, malignant hyperthermia
Fatigue

** Lose independent mobility by 8-11 years**

256
Q

Investigations for Duchenne’s

A

Raised CK (x10-100x normal) from birth
Normal CK rules out Duchenne’s
Muscle biopsy looking for dystrophin
Genetic analysis

257
Q

Management of Duchenne’s

A

Physio and orthoses may increase walking time
Corticosteroids can increase walking by 6-24 months
Bone protection
After loss of mobility (8 to 11) then supportive and orthopaedic care
Monitor cardiac and respiratory function

258
Q

Complications of Duchenne’s

A

Joint contractures
Resp failure (most common cause of death)
Cardiomyopathy and cardiac failure
learning difficulty (10-20%)
Immobility - constipation, osteoporosis, obesity, HTN
Weight loss

259
Q

Differences between Duchenne’s and Becker’s

A

Very similar
Both x-linked recessive
Dystrophin gene - fully gone in Duchenne’s, partially functional in Becker’s
Walking ability lost at 40-60, in Duchennes 8-11
Presentation of Becker’s is the same but slower
- Difficultly climbing stairs and heavy lifting in teenage years

260
Q

Epidemiology of Osgood-Schlater’s disease

A 
Common cause of knee pain
Boys between 12-15
Girls between 8 and 12
Common in athletes
Increased in males
261
Q

Pathogenesis of Osgood-Schlater’s

A

Possibly caused by small avulsion fractures from contraction of quadriceps muscles at insertion on proximal tibial apophysis

Usually occurs during growth spurt before tibial tuberosity has finished ossification
Strength of quadriceps exceeds force

As avulsed # heal and grow the tibial tuberosity enlarges

262
Q

Presentation of Osgood-Schlater’s

A

Gradual onset of pain and swelling below the knee
Relieved by rest
Made worse by extending the knee against resistance
Tenderness and swelling at tibial tuberosity

263
Q

Management of Osgood-Schlater’s

A 
Rest from painful activities
Ice
Physio and stretching exercises
Simple analgesia - Paracetamol and ibuprofen
No corticosteroid injections 
Surgery rarely required

Most return to normal in 2-3 weeks

264
Q

Pathophysiology of Sever’s disease

A

Line of ossification in calcaneal apophysis is thought to develop microfractures due to recurrent heel stresses combined with growth spurt of puberty

265
Q

Presentation of Sever’s disease

A 
8 and 14 years old
Heel pain in physically active individuals
Gradual onset, worse on exercise
Relieved by rest
Often bilateral
tenderness on palpation of heel at Achilles tendon insertion
pain or dorsiflexion
May have swelling at calcaneous
266
Q

Investigations and management of Sever’s

A

X-ray to exclude tumour or fracture
It is a clinical diagnosis

Management with stretching, strengthening, heel lift
Correct alignment with orthoses

267
Q

Antalgic gait

A

OA/Trauma

  • Avoids certain movements due to pain
  • limited joint range of motion
  • inability to fully weight bear
  • limp with slow and short steps
268
Q

Ataxic gait

A

Cerebellar disease

  • Arrhythmic steps
  • wide based
  • unsteady
  • highly impaired tandem gait
  • difficulty walking straight and turning
269
Q

Festinated gait

A

Parkinson’s

  • Short steps (petit pas)
  • Decreased arm swinging
  • Stooped posture
  • Festination (hasty but short steps)
  • Centre of gravity behind or in front of feet
270
Q

Hemiparetic gait

A

Stroke

  • Limb extended and circumducted
  • Spastic quads and gluts
  • Extensors are stronger than flexors in legs
  • Foot plantar flexed causes dragging
271
Q

Scissor gait

A

Cerebral palsy

  • legs flexed slightly at hips and knees
  • Spastic gait, stiff, foot dragging
  • tiptoe walking
  • thighs and knees rub together
272
Q

Trendelenburg gait

A

Dropping of contralateral hip as ipsilateral adductors can’t stabilise the pelvis.
Body swings to other side to compensate

273
Q

Clavicle #

A

Most commonly middle 1/3
Then lateral 1/3
Then medial 1/3

Complications:

  • pneumothorax
  • brachial plexus damage
  • subclavian vessel damage

Place in figure of 8 bandage and sling for 3 weeks

274
Q

Bankart lesion

A

Injury of the anterior glenoid labrum of the shoulder due to anterior shoulder dislocation

275
Q

Hill Sachs lesion

A

Damage to the posterior humeral head (reciprocal of Bankart lesion)

276
Q

How would a patient hold their arm in anterior dislocation?

A

Holds arm externally rotated and slightly abducted

277
Q

Damage that can occur in anterior dislocation?

A

Axillary artery
Axillary nerve (37%)
Suprascapular nerve
Radial nerve

278
Q

Treatment of anterior shoulder dislocation

A

Disimpaction
External rotation
Abduction
Internal rotation

279
Q

Salter Harris classification

A

Classification of fractures through the epiphyseal growth plate of the bone

1 - S Slip (separated or straight across)
2 - A Above fracture lies above the epiphysis or away from the joint
3 - L Lower - # below the physis in the epiphysis
4 - TE Through Everything - # through metaphysis, physis, epiphysis
5 - R Rammed - crushed physis 9rare)

SALTER mneumonic

280
Q

Upper motor neuron signs

A 
Upgoing plantar
Increased tone
Weakness
Increased reflexes
Sustained clonus
281
Q

Lower motor neuron signs

A 
Decreased tone
Weakness
Wasting (atrophy)
Arreflexia
Muscle fasciculation's
282
Q

Spinal stenosis

A

Abnormal narrowing of the spinal canal that can occur in any of the regions of the spine

Most commonly cervical spinal stenosis
Lumbar spinal stenosis is next common
Rare in thoracic

Results in neurological deficit

  • Standing discomfort
  • Bilateral symptoms
  • Numbness
  • Weakness

Intermittent neurogenic claudication - lower limb numbness, weakness, diffuse or radicular leg pain with paraesthesia
Weakness of heaviness in buttocks radiating into lower extremities
- Will resolve at rest, takes longer than vascular claudication

283
Q

Causes of spinal stenosis

A 
Herniated intervertebral discs
Compression #
OA
RA - less common
Hereditary - too small at birth
Spondylolisthesis - vertebra slips forward on one another
Trauma
Tumours of the spine
284
Q

Neurofibromatosis

A

Group of 3 conditions in which tumours grow in the nervous system

NF1 - neurofibromas
NF2 - schwann cells
Schwannomatosis

BENIGN

285
Q

Symptoms of neurofibromatosis 1

A

Light brown spots on skin - café au lait
Freckles in arm pit and groin
Small mumps within nerves and scoliosis

286
Q

Symptoms of neurofibromatosis 2

A 
Hearing loss 
Cataracts
Balance problems
Flesh coloured skin flaps
Muscle wasting
Bilateral acoustic neuromas

Year 4 (7 decks)

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