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MSK Flashcards

1
Q

Joints most commonly affected in septic arthritis?

Organisms?

A

Joints = knee and hip

Organisms = Staph, Strep, gram -ve cocci (neisseria gonococcus), gram -ve bacilli

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2
Q

Risk factors for septic arthritis?

A
  • Joint disease (RA)
  • Immunosuppression
  • Recent joint surgery
  • IV drug abuse
  • DM
  • CKD
  • Prosthetic joints
  • Age >80 yrs
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3
Q

Investigations in septic arthritis?

A
  1. Bloods
    • FBC (WCC), CRP, ESR, cultures
  2. Joint aspiraiton
    • Yellow, purulent synovial fluid - MC+S
    • Raised WCC, organisms on gram stain, +ve culture
  3. X-Ray
    • As baseline - may show joint destruction later
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4
Q

Management of septic arthritis?

A

Urgent orthopaedic referral

  • Joint aspiration until dry - rest joint
  • May need arthrocentesis, lavage and debridement.
  • Analgesia – NSAIDs
  • High dose IV abx – local guidelines. (~2 weeks then 4 weeks PO) after diagnostic joint aspiration.
    • Typical - Flucloxacillin (1g/6h IV) – Clindamycin if pen allergic.
    • Gonococcal or Gram –ve - Cefotaxime (1g/8h IV)
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5
Q

What happens in GCA?

A

Caused by immune response to undefined stimulus causing vasculitis à vascular stenosis and occlusion

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6
Q

Symptoms and signs of GCA?

A

Symptoms

  • >50, headache, jaw claudication, visual problems, aching muscles, weight loss, night sweats, scalp tendernes
  • Extracranial symptoms = dyspnoea, morning stiffness, unequal or weak pulses

Signs

  • Temporal artery and scalp tenderness, pulseless or nodular temporal artery

.

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7
Q

Complications of GCA?

A

Blindness (10-50%), TIA/stroke, scalp necrosis, lingual infarction, aortic dissection/aneurysm, complications of high-dose steroids

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8
Q

Investigations in GCA?

A

Bloods - ↑↑ESR (50mm/h), ↑CRP, ↑plts, ↓Hb all suggestive

Biopsy – within 7 days of starting steroids

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9
Q

Management of GCA?

A
  • Prednisolone 60mg/day PO immediately (+ PPI/bisphosphonate protection)
  • Urgent ESR
  • IV methylprednisolone if visual involvement (consult ophthalmology)

Two year course of steroids à complete remission.

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10
Q

Causes of spinal cord compression?

A

Secondary malignancy = commonest cause (PB KTL)

  • Infection (epidural abscess)
  • Cervical disc prolapse
  • Haematoma (warfarin)
  • Intrinsic cord tumour
  • Atlanto-axial subluxation
  • Myeloma
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11
Q

Signs of cord compression?

A
  • Weakness
  • Numbness (+/- pain) below lesion
  • Incontinence
  • Dermatomal distribution; UMN below lesion, LMN at lesion (tone + reflexes can be reduced in acute compression)
    • Spastic and hyper-reflexic
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12
Q

Signs in cauda equina?

A
  • Leg weakness and pain (often bilateral)
  • Urinary and/or faecal incontinence (retention –> overflow incontinence).
  • ↓Perianal sensation
  • ↓Anal tone
  • ↓Leg power, sensation and reflexes
    • Flaccid and areflexic - not spastic and hyper-reflexic
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13
Q

Investigations in cord compression/cauda equina?

A
  • PR examination
  • Bloods
    • FBC, ESR, B12, syphilis serology, U+E, LFT, PSA, serum electrophoresis/bence jones protein
  • URGENT MRI whole spine
  • CXR (rule out malignancy)
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14
Q

Differentials for sudden onset leg weakness?

A
  • Transverse myelitis/MS
  • Spinal artery thrombosis
  • Trauma
  • Dissecting aneurysm
  • Guillain-Barré
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15
Q

Management of cord compression?

A
  • Lie flat to minimise spine movement
  • Urgent MRI spine
  • Analgesia
  • Dex IV 16mg + PPI cover (if malignancy)
  • Refer to neurosurgery/onc for palliative radiotherapy
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16
Q

Symptoms of OA?

A

Pain on movement and crepitus, worse at end of day; background pain at rest; joint gelling; joint instability

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17
Q

Complications of OA?

A

Assess effect of symptoms on occupation, family duties, hobbies and lifestyle

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18
Q

Investigations in OA?

A

X-Ray (LOSS)

  • Loss of joint space
  • Osteophytes
  • Subarticular sclerosis
  • Subchondral cysts

Bloods – CRP may be slightly elevated

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19
Q

Management of OA?

A

Conservative

  • Exercise to improve muscle strength and general fitness
  • Weight loss if overweight
  • MDT approach – physios and OT
  • Heat/cold packs at site of pain, walking aids, stretching/manipulation or TENS

Medical

  • Regular paracetamol and topical NSAIDs
  • Codeine or short-term oral NSAID (+PPI) if ineffective
  • Intra-articular steroid injection – temporary relief in severe symptoms

Surgical

  • Joint replacement (hips/knees)
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20
Q

Definition of osteoporosis and osteopenia?

A
  • Defined as BMD >2.5 SDs bellow the young adult mean (T-score of -2.5).
  • Osteopenia is diagnosed if T-score between -1 and -2.5
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21
Q

Factors contributing to osteoporosis?

A

Endocrine

Hypogonadism (prem menopause, anorexia, androgen blockade, aromatase inhibitors), hyperthyroidism, hyperparathyroidism, hyperprolactinaemia, Cushing’s disease, T1DM, steroid use

GI

Coeliac disease/other malabsorption, IBD, chronic liver disease, chronic pancreatitis

Rheumatological

RA, other inflammatory arthropathies

Other

Immobility, multiple myeloma, haemoglobinopathy, systemic mastocytosis, CF, COPD, CKD, homocystinuria

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22
Q

What is a fragility fracture?

A
  • Fracture sustained from falling from < standing height
  • Common fractures = hip, wrist (Colle’s), osteoporotic vertebral collapse
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23
Q

Investigations in osteoporosis?

A

Fracture Risk Prediction

  • FRAX or QFracture – provide info on 10 year probability of hip or other osteoporotic fracture.

DEXA

  • Gold standard for diagnosis – measures bone mineral density (BMD).

Bloods (identify underlying causes and rule out differentials – osteomalacia, myeloma)

  • FBC, ESR/CRP
  • U+E, LFT, TFT, serum calcium
  • Testosterone/gonadotrophins in men
  • Serum immunoglobulins and paraproteins, urinary Bence-Jones’ proteins
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24
Q

Management of osteoporosis?

A

Conservative

  • Nutrition (Normal BMI, adequate intake of calcium and vitamin D)
  • Regular Exercise
  • Stop Smoking
  • Reduce Alcohol

Medical

  • Alendronate 10mg OD or 70mg once weekly, or risedronate 5mg OD or 35mg once weekly
  • Vitamin D/calcium supplements (higher doses for housebound/elderly)
  • HRT for women with premature menopause
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25
Q

Prevention of osteoporosis?

A

For patients taking oral/high-dose inhaled steroids for >3 months, or frequent courses, in addition:

  • Add bone protection (bisphosphonates) for patients >65y or with history of fragility fracture, or
  • Refer patients <65y without history of fragility fracture for DEXA scan, and add bone protection agent if T-score is <1.5.
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26
Q

Early and late signs of RA?

A

Early

  • Swollen MCP, PIP, wrist or MTP joints (symmetrical)

Later

  • Ulnar deviation of fingers and dorsal wrist subluxation.
  • Boutonniére and swan-neck deformities of fingers, or Z-deformity of thumbs
  • Hand extensor tendon rupture
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27
Q

Symptoms of RA?

A
  • Peripheral joints affected – symmetrical joint pain, effusions, soft tissue swelling, early morning stiffness.
  • ↓Grip strength and function –> disability
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28
Q

Non-articular signs of RA?

A
  • Weight loss, fever, malaise.
  • Rheumatoid nodules (extensor forearm)
  • Vasculitis – digital infarction, skin ulcers, mononeuritis
  • Eye – Sjogren’s syndrome, episcleritis, scleritis
  • Lungs – pleural effusions, fibrosing alveolitis, nodules
  • Heart – pericarditis, mitral valve disease, conduction defects
  • Skin – palmar erythema, vasculitis, rashes
  • Neurological – nerve entrapment (carpal tunnel, mononeuropathy)
  • Felty’s syndrome – RA, splenomegaly and leucopenia
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29
Q

Complications of RA?

A

Physical disability, depression, osteoporosis, infections, lymphoma, cardiovascular disease, amyloidosis, side effects of treatment

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30
Q

Investigations in RA?

A

Bloods

  • FBC (anaemia of chronic disease), ↑ESR/CRP, ↑platelets
  • Rheumatoid factor (RhF) is +ve in the majority (associated with severe disease)
  • ACPA/anti-CCP = highly specific for RA.

Imaging

  • X-rays = soft tissue swelling, juxta-articular osteopenia, ↓joint space.
  • Later may show bony erosions, subluxation or complete carpal destruction.
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31
Q

Medical Management of RA?

A

Analgesia

  • NSAIDs/PCM - alter as necessary

Steroids

  • Intra-articular injections (triamcinolone) can settle local flares and can be used up to 3x/year in any one joint.
  • Daily low-dose oral steroids – can help symptoms and modify disease progression, but have adverse side-effects.

DMARDs

  • Methotrexate, gold, sulfasalazine, penicillamine, azathioprine, leflunomide, hydroxychloroquine, ciclosporin, cyclophosphamide
  • Biologic therapies = rituximab, infliximab, etanercept, adalimumab
    • Can take months to show any effect
    • Before starting, baseline bloods: U+E, creatinine, eGFR, LFTs, FBC, urinalysis
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32
Q

Surgical management of RA?

A

Aims to relieve pain and improve function – joint fusion, replacement or excision, tendon transfer and repair, nerve decompression

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33
Q

Who gets PMR?

A
  • Elderly
  • Female
    • 50% of GCA have PMR, 15% of PMR have GCA
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34
Q

Non-specific signs/symptoms of PMR - same as GCA?

A

Malaise, anorexia, fever, night sweats, weight loss and depression.

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35
Q

Diganostic criteria for PMR?

A
  1. Age >50y; duration >2 wks
  2. Bilateral shoulder or pelvic girdle aching, or both
  3. Morning stiffness duration >45 min
  4. Evidence of acute phase response (↑ESR or CRP)

Can make diagnosis without inflammatory markers if classical clinical picture and rapid response to steroid treatment

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36
Q

Investigations in PMR?

A

Bloods

  • ESR/CRP
  • FBC, U+E, eGFR, LFT, TFT, CK

Others

  • Bone profile (Ca2+, phosphate, PTH, albumin, alk phos)
  • Protein electrophoresis (urinary Bence-Jones protein)
  • Rheumatoid factor

Imaging

  • Consider CXR and/or hip/pelvis/shoulder/cervical spine x-ray (rule out malignancy)
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37
Q

Differentials for PMR?

A
  • Inflammatory arthritis (RA)
  • OA
  • Neoplasia (myeloma)
  • Fibromyalgia
  • Connective tissue/vaculitis (SLE)
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38
Q

Management of PMR?

A

Steroids

  • Prednisolone 15mg OD – rapid response (within 1 week) – ESR/CRP should normalise within 4 weeks. Continue for 3 weeks.
    • ↓Dose to 12.5mg OD for 3 weeks
    • Then 10mg OD for 4-6 weeks,
    • Then reduce by 1mg every 4-8 weeks (1-2y of treatment usually needed)
  • Give osteoporosis prophylaxis and supply with steroid card.
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39
Q

What is gout associated with? What does this mean?

A
  • CV disease, HTN, DM and CKD
  • Patients with gout should be screened for these
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40
Q

Predisposing factors for gout?

A
  • FH
  • Obesity
  • Alcohol
  • High-purine diet
  • Plaque psoriasis
  • Diuretics
  • Acute infection
  • Surgery
  • Renal failure
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41
Q

Complications of gout?

A

Chronic gout –> recurrent attacks, tophi (urate deposits) in pinna, tendons and joints, and joint damage. Refer to rheumatology.

42
Q

Investigations in Gout?

A

Bloods

  • WCC, ESR, blood urate (all raised but may be normal)

Microscopy of Synovial Fluid

  • Polarised light microscopy of synovial fluid –> negatively bi-refringent urate crystals.

X-Rays

  • Show soft tissue swelling only.
43
Q

Management of acute gout?

A

Conservative

  • Exclude infection
  • Rest and elevate joint - apply ice pack

Pharmacological

  • NSAIDs – naproxen 500mg BD
  • Colchicine - 500 mcg BD, increased slowly to QDS until pain relieved.
    • NO NSAIDs OR COLCHICINE IN RENAL IMPAIRMENT
  • Steroids – joint injection or IM steroids
44
Q

Gout prevention?

A

Conservative

  • Lose weight; avoid purine-rich foods (offal, red meat, yeast extracts, pulses, mussels)
  • Avoid thiazide diuretics and aspirin

Medical

  • Allopurinol 100-300mg daily – wait until 1mo after acute attack and co-prescribed colchicine or NSAID for first 1-3mo to avoid precipitation of another acute attack
  • Febuxostat is alternative
45
Q

Most common joints for gout?

A

big toe, feet, ankles most commonly

46
Q

What is pseudogout?

A

Calcium Pyrophosphate Deposition Disease (CPPD)

  • Inflammatory arthritis due to deposition of pyrophosphate crystals.
  • Associated with OA, hyperparathyroidism and haemochromatosis.
  • Attacks are less severe than gout. Knee, wrist and shoulder are most commonly affected. Acute attacks can be triggered by intercurrent illness and metabolic disturbance.

Rhomboid-shaped calcium pyrophosphate dihydrate crystals – Pseudogout = Positive birefringence in polarised light

  • Treat acute attacks like gout
47
Q
A
48
Q

Red flags for back pain?

A
49
Q

Differentials for back pain?

A

Serious – cord compression, cauda equina, metastases, myeloma, infection, fracture, aortic aneurysm

Common – mechanical back pain, renal colic, prolapsed disc, postural, trauma

50
Q

Investigations in back pain?

A

If suspect mechanical back pain and no worrying features, no investigations required.

Bloods – FBC, ESR, CRP, Ca2+, ALP, PSA

CXR - +/- spinal X-ray if post-trauma or risk of pathological fracture

MRI spine – as emergency if cord compression or cauda equina suspected; urgent if suspect malignancy, infection or fracture; routine if suspect inflammatory disorder.

DEXA

Do not X-ray for back pain routinely

51
Q

Management of mechanical back pain?

A
  • Early mobilisation, avoid lifting, maintain good posture
  • Analgesia (consider tricyclic or strong opioids if paracetamol, NSAIDs and weak opioids ineffective)
  • Diazepam 2mg/8h PO for muscular spasm
  • Safety-net – if bilateral symptoms or incontinence

Cord Compression/Cauda Equina

  • Neurological emergencies
52
Q

What is ank spond?

A

Chronic inflammatory disease of the spine and sacroiliac joints (HLA-B27 +ve)

53
Q

Conditions associated with HLA-B27?

A

PAIR

  • Psoriaiss
  • Ank spond
  • IBD
  • Reactive arthritis
54
Q

Who gets ank spond?

A

♀:♂ = 1:6 at 16 years old, 2:1 at 30 years old

men present earlier

55
Q

Symptoms of ank spond?

A
  • Gradual onset low back pain, worse at night, spinal morning stiffness relieved by exercise.
  • Pain radiates from sacroiliac joints to hips/buttocks, usually improves towards end of day.
  • Progressive loss of spinal movement (all directions) –> ↓thoracic expansion.
56
Q

Signs of ank spond?

A

Spinal kyphosis, sacroiliac joint fusion, neck hyperextension, neck rotation.

57
Q

Complications and extra-articular signs of ank spond?

A
  • ↓Chest Expansion
  • Chest Pain
  • Hip/Knee Arthritis
  • Plantar fasciitis
  • Iritis
  • Crohn’s/UC
  • Heart disease – carditis, aortic regurg, conduction defects
  • Osteoporosis
  • Psoriaform rashes
58
Q

Investigations in ank spond?

A

Bloods

  • FBC – normochromic or microcytic hypochromic anaemia.
  • ESR – may be normal
  • RF – usually -ve

X-Ray

  • Initial – widening of SI joints and marginal sclerosis
  • Later – SI joint fusion and bamboo spine (vertebral squaring/fusion)
59
Q

Management of ank spond?

A

Conservative

  • Exercise for backache – regimens to maintain posture and mobility.

Pharmacological

  • NSAIDs – relieve pain and slow progression
  • TNF-a blockers – indicated if NSAIDs fail
  • Local steroid injections – temporary relief
  • Bisphosphonates due to increased risk of osteoporotic spinal fractures.

Surgery

Hip replacement if hips involved – sometimes spinal osteotomy.

60
Q

Large vessel vasculitis?

A
  1. GCA
  2. Takayasu’s Arteritis
  3. Buerger’s Disease
61
Q

Medium vessel vasculitis?

A
  1. Polyarteritis Nodosa
  2. Kawasaki’s Disease
62
Q

Small vessel vasculitis?

A

pANCA

  • Churg-Strauss Syndrome

cANCA

  • Wegener’s Granulomatosis
  • Microscopic Polyangiitis

ANCA -ve

  • HSP
  • Goodpasture’s Disease
63
Q

Takayasu’s Arteritis?

A

Epidemiology

  • Rare outside Japan
  • F>M
  • 20-40 yrs

Features

  • Constitutional symptoms (Fever, fatigue, weight loss)
  • Weak pulses in upper limbs
  • Visual disturbance
  • HTN
64
Q

Beurger’s Disease?

A

Strongly associated with smoking

  • Extremity ischaemia: intermittent claudication, ischaemic ulcers etc.
  • Superficial thrombophlebitis
  • Raynaud’s phenomenon
65
Q
A
66
Q

Polyarteritis nodosa?

A

Epidemiology

  • Rare in UK
  • M>F
  • Young adults

Features

  • Associated with hep B
  • Constitutional symptoms
  • Rash
  • Renal –> HTN
  • GI –> melena and abdo pain

Management

  • Prednisolone and cyclophosphamide
67
Q

Kawasaki’s Disease?

A

Childhood PAN variant

Features

FEVER AND CREAM

  • 5-day fever
  • Conjunctivitis (bilateral)
  • Rash (polymorophic, trunk)
  • Extremity changes (erythema, desquamation)
  • Adenopathy (cervical)
  • Mucositis (oral)

Complication = coronary artery aneurysms

Management

  • IV Ig and aspirin
68
Q

Churg Strauss Syndrome?

A
  • Late-onset asthma
  • Eosinophilia
  • Paranasal sinusitis
  • Heart disease, skin lesions/ nasal polyps
  • Granulomatous small-vessel vasculitis
    • Rapidly progressing glomerulonephritis
    • Palpable purpura
    • GI bleeding

May be associated with montelukast

69
Q

Microscopic polyangiitis?

A
  • Rapidly progressing glomerulonephritis
  • Haemoptysis
  • Palpable purpura
70
Q

Wegener’s Granulomatosis (Granulomatosis with Polyangiits - GPA)?

A

Necrotising granulomatous inflammation and small vessel vasculitis –> URT, LRT and kidneys

URT

  • Chronic sinusitis
  • Epistaxis
  • Saddle-nose deformity

LRT

  • Cough
  • Haemoptysis
  • Pleuritis

Renal

  • Rapidly progressing glomerulonephritis
  • Haematuria/proteinuria

Other

  • Palpable purpura
  • Ocular: conjunctivitis, keratitis, uveitis
71
Q

Investigations in Wegener’s?

A
  • cANCA
  • Dipstick
  • CXR - bilateral nodular and cavity infiltrates
72
Q

HSP?

A

Childhood IgA nephropathy variant - 3-8 yrs

  • Post URTI
  • Palpable purpura on buttocks
  • Colicky abdo pain
  • Arthralgia
  • Haematuria

Self-limiting - need to dip urine for a year after.

73
Q

Goodpasture’s syndrome?

A
  • Rapidly progressive glomerulonephritis
  • Haemoptysis
    • Anti-GBM Ab
    • CXR –> bilateral lower zone infiltrates (haemorrhage)

Rx = Immunosuppression and plasmapheresis

74
Q

Differences between GPA and Churg-Strauss?

A
75
Q

Investigations in vasculitis?

A

Bedside

  • Urine Dip

Bloods

  • FBC, U+E, LFT, CRP, ESR, ANCA

Imaging

  • Depends on syndrome - CXR, renal USS, doppler, angiogram of large vessels

Other

  • Angiography/biopsy may be diagnostic
76
Q

Causes of reactive arthritis? When does it present?

A

1-4 weeks after...

  • Urethritis (chlamydia)
  • Dysentery (campylobacter, salmonella, shigella)
77
Q

Signs in reactive arthitits?

A
  • Iritis
  • Keratoderma blenorrhagica (brown, raised plaques on soles and palms)
  • Circinate balanitis (painless penile ulceration secondary to Chlamydia)
  • Mouth ulcers
  • Enthesitis
78
Q

Investigations in reactive arthritis?

A

Bloods

  • Raised ESR and CRP

Others

  • Stool MC+S if diarrhoea
  • Infectious serology
  • Sexual health review
79
Q

Management of reactive arthritis?

A

General

  • Splint affected joints acutely

Pharmacological

  • NSAIDs
  • Local steroid injections
  • Consider sulfalazine or methotrexate if symptoms >6 months
80
Q

What is Paget’s disease?

A

Increased bone turnover with resultant remodelling, bone enlargement, deformity and weakness.

81
Q

Who gets Paget’s?

A

>40yrs, incidence increases with age

82
Q

Symptoms of Paget’s? Complications?

A
  • Usually asymptomatic
  • Deep, boring pain
  • Bony deformities and enlargement
    • Pelvis, lumbar spine, skull, femur, tibia (bowed sabre tibia

Complications

  • Pathological fractures, OA, hypercalcaemia, nerve compression, high output CCF, osteosarcoma
83
Q

Investigations in Paget’s disease?

A

Bloods

  • Ca2+ and PO43- normal
  • Alk phos VERY raised

Imaging

  • Localised enlargement of bone; patchy cortical thickening with sclerosis, osteolysis and deformity
  • Cotton wool skull appearance
84
Q

What is osteomalacia/rickets?

A

Normal amount of bone but mineral content low (opposite of osteoporosis)

  • Rickets = this process during bone growth
  • OM = after fusion of the epiphyses
85
Q

Causes of osteomalacia?

A
  • Vitamin D deficiency
  • Renal osteodystrophy
  • Drug induced
  • Vitamin D resistance
  • Liver disease
  • Tumour induced
86
Q

Presentation of osteomalacia/rickets?

A

Rickets

  • Growth retardation, hypotonia, apathy
  • Knock-knee/bow-leg and deformitites of metaphyseal-epiphyseal junction

Osteomalacia

  • Bone pain, tenderness, fractures (especially femoral neck), proximal myopathy
87
Q

Investigations in osteomalacia?

A

Bloods

  • Mild ↓Ca2+, ↓PO43-, ↑alk phos, PTH high, ↓25(OH)-vitamin D

Imaging

  • Cortical bone loss (lucency)
  • Looser’s zone = apparent partial fractures without displacement – esp on lateral border of scapula, inferior femoral neck and medial femoral shaft.

​

88
Q

What is SLE?

A
  • Autoantibodies are made against a variety of autoantigens.
  • Immunopathology –> polyclonal B-cell secretion of pathogenic autoantibodies causing tissue damage
    • Immune complex formation/deposition, complement activation, other direct effects

Anitbodies = ANA, RhF (others = Anti-Ro, Anti-La, Anti-RNP)

89
Q

General presentation of SLE? Specific features?

A
  • Non-specific constitutional symptoms (malaise, fatigue, myalgia and fever)
  • 95% = ANA +ve
  • Increased risk of CV disease/osteoporosis
  • Antiphospholipid syndrome associated with SLE
    • Malar rash (butterfly rash)
    • Discoid rash
    • Photosensitivity
    • Oral ulcers
    • Non-erosive arthritis
    • Serositis
    • Renal disorder
    • CNS disorder (seizures/psychosis)
    • Haematological disorder
    • Immunological disorder
    • ANA +ve
90
Q

Limited cutaneous sclerosis?

A
  • More common type of SSc.
  • Only the face, forearms and lower legs up to the knee.
  • AKA CREST syndrome

Antibodies = ANA (anti-centromere), RhF

91
Q

What does CREST stand for?

A
  • Calcinosis
  • Raynaud’s disease
  • Esophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
92
Q

Diffuse systemic sclerosis? (dcSSc)

A
  • Less common
  • Also upper arms, thighs or trunk
  • Higher risk of mortality – early organ fibrosis (lung, cardiac, GI, renal).

Anti-Scl70

93
Q

Cardinal features of systemic sclerosis?

A
  • Excessive collagen production and deposition
  • Vascular damage
  • Immune system activation via autoantibody production and cell-mediated autoimmune mechanisms
94
Q

Rotator cuff tear?

A

Tears in supraspinatus tendon (or adjacent subscapularis and infraspinatus)

  • Can present insidiously from degeneration in elderly or after trauma in younger patients (more rare)
  • Shoulder weakness and pain
  • Night pain may affect sleep as patient is unable to keep arm in comfortable position.

Imaging –> US/MRI

Management –> surgery (arthroscopic)

95
Q

What is impingement syndrome?

A

Painful arc –> occurs as supraspinatus tendon catches under the acromion during abduction (70-140)

96
Q

Frozen Shoulder (Adhesive Capsulitis)?

A

No obvious triggers. Pain may be severe and worse at night. Natural history can be divided into:

  1. Painful phase (up to 1 year) – active and passive movement range reduced
  2. Frozen phase (6-12 months) – pain usually settles but shoulder remains stiff
  3. Thawing phase (1-3 years) – shoulder slowly regains range of movement.

Can be associated with cervical spondylosis, diabetes and thyroid disease.

Management = early physio and NSAIDs. Steroid injections may reduce pain in early phases. Surgical release is most effective treatment.

97
Q

Lateral epicondylitis (Tennis elbow)?

A

Inflammation where forearm extensor tendon arises from lateral epicondyle.

  • Usually clear history of repetitive strain
  • Pain is felt at the front of the lateral condyle, and is exacerbated when the tendon is most stretched (wrist and finger flexion with hand pronated).
  • Ask the patient to extend the wrist, and then to resist extension of the middle finger: is pain elicited?

Management –> Restriction of activities that overload the tendons à usually lasts 6-24 months; 90% recover in 1 year.

98
Q

Medial Epicondylitis (golfer’s elbow)?

A

Inflammation of forearm flexor muscles at insertion on medial epicondyle

  • Most common cause of medial elbow pain, but 1⁄5 as common as tennis elbow.
  • Pain is exacerbated by pronation and forearm flexion.
  • Occasionally associated with ulnar neuropathy as the ulnar nerve runs behind the epicondyle.

Same treatment and prognosis as LE

99
Q

Differentials for limping child at different ages?

A
100
Q

Investigations for limping child?

A
  • Temperature
  • Bloods - FBC, CRP, ESR, Blood cultures, RF, ANA, ASOT – anti streptolysin titre, HLA B27
  • Urine
    • Dipstick + MSU
  • X-rays
    • AP/ Lateral frog imaging
  • USS
    • Can demonstrate effusion
  • MRI/bone scan
    • May aid diagnosis

- FINALS (24 decks)

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