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204: Theme 3 > Disease of the Musculoskeletal system > Flashcards

Disease of the Musculoskeletal system Flashcards

1
Q

What is Bursitis?

A
  • Inflammation of bursa.
  • Bursae are synovial membrane lined pockets that serve to allow free movement of adjacent structures where otherwise, there could be friction.
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2
Q

What is Enthesitis?

  • example
A
  • Inflammation of an enthesis. Entheses are the points where tendons, ligaments or joint capsules insert into bone.
  • The largest site is the Achilles insertion.
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3
Q

Define the following:

Osteoporosis –

Osteomalacia –

Osteomyelitis –

Osteosarcoma –

A
  • Osteoporosis – Reduced bone density
  • Osteomalacia – Poor bone mineralisation
  • Osteomyelitis – Bone infection
  • Osteosarcoma – An example of malignant bone tumour
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4
Q

What are the following muscle conditions?

  • Myalgia
  • Myositis
A
  • Myalgia - Pain in muscles.
    • Very common.
    • Commonly associated with viral infections.
    • Can be drug-induced (eg by statins).
  • Myositis - Inflammation of the muscles.
    • Far less common than myalgia and can be autoimmune
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5
Q

What are some points to consider when someone presents with joint pain?

A
  • Is it Articular or
    • Non-articular/ periarticular
  • Inflammatory or
    • Non inflammatory/ degenerative/ mechanical
  • How many joints are affected
    • monoarthritis
    • oligoarthritis 2-5
    • polyarthritis 5+
  • Duration of onset
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6
Q

Review this flow chart

A
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7
Q

What are likely differential diagnosis based on the number of joints affected?

  • Monoarticular (1)
  • Oligoarticular (2-4)
  • Polyarticular (≥5)
A
  • Monoarticular (1)
    • Trauma, hemarthrosis, spondyloarthropathy
    • Septic, crystal-induced
  • Oligoarticular (2-4)
    • Spondyloarthropathy, crystal-induced, infection
  • Polyarticular (≥5)
    • RA, SLE, crystal-induced, infectious
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8
Q

You are asked to review a patient presenting with thenar eminence atrophy. Which nerve do you think is affected?

A

Median

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9
Q

Which epicondyle is affected in tennis elbow?

1) Medial
2) Lateral

A

Lateral

(medial is golfer)

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10
Q

What are the key differences between Inflammatory and Non-Inflammatory pain?

Morning stiffness

Activity

Rest

Worst time of day

Fatigue

Steroids

A
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11
Q

50 year old ex-rugby player presents with 3 years of painful swollen right knee and painful left hip. He works as builder and by the end of the day the pain is worse. Rest and elevation of the knee helps the pain. EMS lasts 30 minutes.

is this Inflammatory or non-inflammatory

A

Non-Inflammatory

50 year old ex-rugby player presents with 3 years of painful swollen right knee and painful left hip. He works as builder and by the end of the day the pain is worse. Rest and elevation of the knee helps the pain. EMS lasts 30 minutes.

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12
Q

30 year old female, who presents with a three-month history of painful, swollen MCPs and wrists. The pain is worse in the mornings and EMS lasts 3 hours. Heat and movement help the pain but when she stops moving her hands the pain returns.

is this Inflammatory or non-inflammatory

A

Inflammatory

30 year old female, who presents with a three month history of painful, swollen MCPs and wrists. The pain is worse in the mornings and EMS lasts 3 hours. Heat and movement help the pain but when she stops moving her hands the pain returns.

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13
Q

You are asked to review a 35 year old male, who presents with a 2 days history of a painful, swollen right knee. What are your differential diagnosis?

1) Post-traumatic hemarthrosis
2) Gout
3) Septic arthritis
4) All of the above

A

All the above

  • if a joint is hot and swollen always do a joint aspiration
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14
Q

What needs to be identified when a Joint Aspiration is done when septic arthritis is a differential?

  • Check
  • Send for
A

Check:

  • Clarity
  • Colour - straw-coloured/ clear
  • Viscosity - easily retractable

Send for:

  • Gram stain (TB)
  • Bacterial Culture
  • Crystals
  • White cell differential
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15
Q

What are important points about how septic arthritis presents and how it is managed

A
  • Mortality rates are of 11%. This increases to 50% in polyarticular disease with sepsis.
  • The commonest organisms are staph and strep
  • Always think about it in a patient with a (usually) single, hot and swollen joint.
  • They do not have to be systemically unwell and they may be able to weight bear.
  • Seek senior advice. Do not delay antibiotic therapy.
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16
Q

Take? Give?

What is the Sepsis 6

A

Take

  • Cultures
  • Lactate
  • Urine output

Give

  • High flow oxygen
  • IV antibiotics
  • Fluids
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17
Q

What is Gout?

A
  • when the serum urate levels are > physiological saturation point
  • leads to monosodium urate crystal formation and deposit in
    • cartilage (ear)
    • bone
    • periarticular tissues or peripheral joints (toe)
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18
Q

Who gets Gout?

A
  • Men aged 40 years and over
  • Women over 65 years
  • It increases with age, affecting 15% of men aged over 75 in the United Kingdom
  • Metabolic syndrome and its components (insulin resistance, obesity, hyperlipidaemia, and hypertension) are strongly associated with gout
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19
Q

What are risk factors for Gout?

A
  • Male sex/ Older age
  • Genetic factors (mainly reduced excretion of urate)
  • Chronic kidney disease (reduced excretion of urate)
  • Metabolic syndrome
    • Obesity
    • Hypertension
    • Hyperlipidaemia
  • Loop and thiazide diuretics (reduce excretion of urate)
  • Osteoarthritis (enhanced crystal formation)
  • Dietary factors (increased production of uric acid)
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20
Q

What crystals are you expecting to find in the knee fluid aspirated from our previous patient if you suspect clinically that he has gout?

A

Monosodium urate

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21
Q

How is Gout managed?

  • Conservative (2)
  • Acute (3)
  • Long term (2)
A

Conservative:

  • Reduce alcohol and high purine foods
  • Diabetic control

Acute attacks:

  • NSAIDs e.g. naproxen
  • Colchicine
  • Steroids

Long term:

  • Urate-lowering therapy e.g. allopurinol or febuxostat or benzbromarone
  • Anakinra (IL-1 antagonist)
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22
Q

55 year old with sudden pain and swelling right knee. You are waiting for aspiration results to return but his observations are normal. Bloods come back and uric acid is normal but calcium is high.

  • What is the main differential diagnosis
    1) Septic
    2) Gout
    3) Calcium Pyrophosphate Deposition
A

Calcium Pyrophosphate Deposition

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23
Q

How do Calcium Pyrophosphate crystals appear under a microscope?

A

Positively birefringent

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24
Q

What pathology is seen in this X-ray?

  • wat indicates this?
A

Chondrocalcinosis

  • it should be a solid black line between the joints,
  • however you can see shadowing as you have some crystal deposition
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25
Q

What is the management of Calcium Pyrophosphate Deposition (CPPD)?

  • conservative
  • acute
  • long term
A

Conservative:

  • Hot / cold pack
  • Immobilisation

Acute attacks:

  • NSAIDs e.g. naproxen
  • Colchicine
  • Steroids

Long term:

  • Colchicine prophylaxis
  • Anakinra (IL-1 antagonist)
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26
Q

How does Osteoarthritis commonly present?

A
  • common in older age
  • most commonly clinically affects the
    • knees
    • hips
    • small joints of the hands (DIP, PIP 1st CMCJ)
  • commonly characterised by joint pain and very variable degrees of functional limitation
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27
Q

What are radiological signs of Osteoarthritis?

A
  • osteophyte
  • reduced joint space
  • sclerosis
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28
Q

What radiological signs are commonly seen in Osteoarthritis of the hand?

  • what signs would be seen in the actual hand and where(2)
A
  • Gullwing deformities
  • Heberden’s nodes (PIP)
  • Bouchard’s nodes (DIP)
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29
Q

What does this image show and what do the arrows point to?

A
  • Osteoarthritis of the hands

Bouchard’s nodes (PIPs)

Heberden’s nodes (DIPs)

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30
Q

What is the pathophysiology of Osteoarthritis?

A
  • Metabolically active, dynamic process involving all joint tissues (cartilage, bone, synovium, capsule, ligaments/muscles)
  • Focal destruction of articular cartilage
  • Remodelling of adjacent bone = hypertrophic reaction at joint margins (osteophytes)
  • Remodelling and repair process (efficient but SLOW)
  • Secondary synovial inflammation and crystal deposition
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31
Q

What are the clinical features of Osteoarthritis?

A
  • Age > 50 years
  • Morning stiffness < 30 minutes
  • Persistent joint pain aggravated on use
  • Crepitus
  • NO INFLAMMATION
  • Bony enlargement and/or tenderness (not bogginess like synovial inflammation)
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32
Q

Review the treatment of Osteoarthritis

A
33
Q

What are the differences between RA and OA? (review)

A
34
Q

What are Spondyloarthpathies?

  • types
A
  • arthritis of the spine
    • can be seronegative: rheumatoid factors and anti CCP are negative

Types: they all overlap and get Sacrolittis and uveitis

  • Ankylosing spondylitis (most common)
  • Juvenile Ankylosing spondylitis
  • Intestinal Arthropathy
    • linked with UC and Chrons
  • Psoriatic Arthropathies
  • Reactive Arthropathy
    • Reiter Syndrome
35
Q

What are the clinical features of Spondyloarthropathies?

A

● Pattern of peripheral arthritis: predominantly lower limb, asymmetric

● Enthesitis (tennis/ golfers elbow)

● Tendency to radiographic sacroiliitis

● Absence of rheumatoid factor / anti-CCP

● Extra-articular features characteristic of the group (such as anterior uveitis)

● Significant familial aggregation

● Association with HLA-B27

36
Q

What is Ankylosing Spondylitis and when does it present?

A
  • Greek ‘ankylos‘- bent/crooked (fused)
    • ‘spondylos‘-a spinal vertebra
  • Characteristically affects young adults
  • Peak onset between 20-30 yrs
  • Male:female - approximately 3:1*
37
Q

How do you test for Sacroiliac joint pain?

  • what would pain in this area indicate?
A
  • would indicate Ankylosing spondylitis or some spondyloarthropathy
38
Q

What tests would you do if you suspected of Ankylosing Spondylitis?

A
  • Sacroiliac assessment
  • Wall test: see how far the occiput is from the wall
    • question mark spin
  • Schober’s test
    • put a tape measure on the lumbar region standing up, it should extend to 15 cms
39
Q

How does Ankylosing Spondylitis present radiologically in the spine?

A
  • with a bamboo spine as there is bone deposition between the vertebrae
40
Q

How does Ankylosing present radiologically in the pelvis?

A
  • more white areas on the x-ray due to fusion
41
Q

What are the Clinical features of Ankylosis Spindolytis?

A
  • Low back pain - Often the first symptom (in ~ 75%).
  • Buttock pain - indicative of SI involvement. Often poorly localised and may be referred to the posterior thigh.
  • Limited spinal mobility
  • Hip and Shoulder pain- girdle arthritis
  • Peripheral arthritis -Acute monoarthritis or oligoarthritis Mostly non-erosive and non-destructive.
  • Enthesitis.
  • Constitutional features- fatigue and malaise. Disturbed sleep, caused by back or joint pain at night, may contribute to fatigue
42
Q

What are other organ involvements in Seronegative Spondylarthpathies?

(All the As) (6)

A
  • Anterior uveitis (iritis) – 40%
  • Achillies tendonitis (enthesitis)
  • Aortic regurgitation (4%)
  • Apical lung fibrosis (1.5%)
  • A-V conduction defects (rare)
  • Amyloidosis (rare)
43
Q

What can positive HLA-B27 be associated with?

A
  • Most commonly associated with Ankylosing spondylitis
  • can be positive with the health implications
44
Q

What is the treatment for Ankylosing Spondylitis?

A
  • Physiotherapy & exercise
  • Pain relief: simple analgesics & Anti-inflammatory (NSAIDs)
  • DMARDs (if peripheral joints affected)
  • Steroids-oral/intra-muscular/intra-venous
  • Anti-TNF agents (only for treating peripheral signs)
  • Surgery e.g. hip replacement
  • DEXA-Osteoporosis prophylaxis
  • Osteopathy, Chiropractic (any form of spinal manipulation) is not recommended.
45
Q

What is the aim of Ankylosing Spondylitis treatment?

(5)

A
  • Symptomatic relief -Eliminate/reduce pain and stiffness.
  • Restore/preserve function
  • Prevent joint damage
  • Prevent spinal fusion - to maintain spinal mobility, and prevent development of spinal deformities
  • Minimise extra-spinal and extra-articular manifestations
46
Q

What is the Reactive Arthritis Triad?

A
  • Conjunctivitis: discharge, erythema, burning, photophobia
  • Urethritis: dysuria, urgency, frequency, discharge
  • Arthritis: Knees, ankles, feet
  • can’t see, can’t pee, can’t climb a tree
47
Q

What is the common cause of Reactive Arthritis?

A
  • Chlamydia / Gonorrhoea
  • Shigella / Salmonella / Yersinia / Campylobacter / C.Difficile
  • Flu
48
Q

What are other symptoms of Reactive Arthritis?

A
  • Dactylitis
  • Swollen knees
  • Keratoderma blenorrgaicum
  • Ballanitis
49
Q

What investigations are done for Reactive Arthritis?

A
  • ESR, C-Reactive protein, FBC, Liver and Renal function, RF
  • Urine analysis, Radiograph of affected joints
  • Ophthalmologic examination if eye symptoms present
  • Joint fluid Aspiration-Cell count, crystals, Gram stain & culture
  • Bacterial culture of:
    • Faeces, Urine or urethral swab, Cervical sample, Throat
    • Blood culture (not always necessary)
50
Q

What is the treatment for Reactive Arthritis?

A
  • Rest
  • Antibiotics if infection is still present
  • NSAIDs
  • Intra-articular/Systemic corticosteroids
  • Disease modifying anti-rheumatic drugs in some cases
51
Q

How does Psoartic Arthritis present?

A
  • nail changes
  • Sacroiliac joint involvement can be symmetrical or asymmetrical
  • largely arthritis with DIP joint involvement
  • Arthritis mutilans
  • Symmetric polyarthritis – indistinguishable from RA
  • Asymmetric oligoarticular arthritis
  • Predominant spondylitis (Axial)
52
Q

What changes are seen in this x-ray?

  • what is the disease?
A
  • ‘Pencil in a cup’ changes
    • periarticular erosions and bone resorption gives this presentation
  • Psoriatic Arthritis
53
Q

Review the treatment pathway for Psoriatic arthritis?

  • anti-TNF therapy?
A
54
Q

Review the areas of the body that Vasculitis can effect

A
55
Q

How is Vasculitis Classified? (3)

  • what do they include
A
  • Large Vessel
    • Takayasu’s, Giant Cell
  • Medium Vessel
    • Polyarteritis nodosa, Kawasaki’s
  • Small
    • Henoch Schonlein purpura, EGPA and GPA, MPA
56
Q

What is small vessel Vasculitis divided into?

A
  • ANCA associated and Non-ANCA associated
    • need to send blood tests to identify the difference
57
Q

A 64 year old man complains of general malaise and has lost 6kg in weight over six months. Severe haemoptysis 9 days ago. Purpuric (non-blanching ) rash on his legs

  • what investigations would you do
  • what are the differentials
A
  • General obvs (BP, urinalysis)
  • Creatinine, Hb
  • Serology
    • ANCA (came back positive)
      • likely GPA as haemoptysis is more classically linked with it
    • Anti GBM abs
    • Antiphospholipid screen
    • ANA/ENA
    • dsDNA / Complement
    • Anti streptococcal abs
    • RF / Anti CCP
58
Q

What other illnesses/ drugs can mimic vasculitis?

A
  • Infections: Hep B/C, N. Meningitidis
  • Drug: Cocaine, Amphetamines
  • Medications: NSAIDs, Abx, Thiazide Diuretics, Warfarin
  • Malignancy: Lymphomas, Myeloma
  • Inflammatory: RA / SLE
59
Q

What is the treatment/ management for Vasculitis?

A
  • Corticosteroids (3 days IV Methylpred 1g)
  • Cyclophosphamide / Rituximab
  • Azathioprine / Methotrexate
  • Full systems review
60
Q

55 year old lady presents with Proximal myalgia

Complaining of pain and difficulty turning over in bed and combing her hair

  • what investigations would you carry out
  • assuming they are positive what type of disease does this suggest?
A
  • Inflammatory investigations
    • ESR- 60
    • CRP- 45
  • Polymyalgia Rheumatica - Giant cell artheritis
61
Q

How do you screen for Giant Cell Myalgia and Polymyalgia Rheumatica?

A
  • Age > 50
  • Scalp tenderness and headache (temporal and unilateral)
  • Jaw or limb claudication
    • pain, when they chew and resolves when they stop
  • Blindness or diplopia
  • Weight loss, anorexia, fever, night sweats, malaise
  • Raised ESR and CRP
  • Biopsy or USS
  • Proximal muscle pain and stiffness
62
Q

What are the examination features of Giant Cell Arteries and Polymyalgia Rheumatica?

A
  • Abnormal Superficial Temporal Artery
    • Tender
    • Thickened (can’t feel the pulse)
    • Reduced/ Absent Pulsation
  • Scalp Tenderness
  • Cranial Nerve Palsies
  • Vascular Bruits
  • Asymmetric Pulses
63
Q

What is the visual effect seen in Giant Cell Arteries and Polymyalgia Rheumatica?

A
  • Field Defect
  • Afferent Pupillary Defect
  • Anterior Ischaemic Optic Neuritis
  • Central Retinal Artery Occlusion
  • Diplopia
64
Q

What investigations are done for Giant Cell Arteries?

A
  • FBC, U&Es, LFTs, CRP, ESR.
  • CXR
  • Urinalysis
  • Temporal Artery biopsy
  • USS Temporal Arteries
65
Q

What is the importance of Biopsy and USS in Giant Cell Arteries?

A
  • Temporal artery biopsy (TAB) should be considered whenever a diagnosis of GCA is suspected.
    • This should not delay glucocorticosteroid therapy
  • TAB may be negative in some patients (Skip lesions)
  • Imaging techniques show promise for the diagnosis and monitoring of GCA. High sensitivity.
  • These do not replace TAB for cranial GCA.
    • USS limited as it requires a high level of experience and training.
  • PET and MRI currently reserved for investigation of suspected large-vessel GCA.
66
Q

What is the treatment for Giant cell arteries?

  • uncomplicated GCA
  • evolving visual loss
  • established visual loss
A
  • Steroids – immediately (tapering regimen)
  • Uncomplicated GCA (no jaw claudication or visual disturbance)
    • 40mg prednisolone daily.
  • Evolving visual loss or amaurosis fugax (complicated GCA):
    • 500 mg to 1 g of i.v. methylprednisolone for 3 days before oral glucocorticosteroids.
      • high dose to spare the contralateral eye
  • Established visual loss
    • 60 mg prednisolone daily to protect the contralateral eye.
  • bone protection is needed
67
Q

How does SLE present?

A
  • Malar rash
  • Discoid rash
  • Serositis – Pleuritis / Pericarditis
    • released sitting forward
  • Oral ulcers
  • Arthritis – non-erosive
  • Photosensitivity (rashes, burn easily)
  • Blood disorders
  • Renal disorders
  • ANA + anti Smith / dsDNA / antiphospholipid abs
  • Neurologic symptoms
68
Q

Review the systems that SLE effect

A
69
Q

where does SLE effect

What investigations are done for SLE?

(8)

A
  • Urinalysis – urinary protein: creatinine ratio
  • Full blood count
  • Urea and electrolytes
  • ESR
  • CRP
  • Liver function test
  • Antibodies: ANA; ENA; Anti –dsDNA; Lupus anticoagulant; ANTI C1q;
  • C3, C4
70
Q

Review the management of SLE

A
71
Q

What is Sjogren’s Syndrome?

  • how does it present
A
  • Lymphocytic infiltration of exocrine glands
  • Sicca: Dry eyes (lacrimal gland involvement) and xerostomia (salivary gland involvement)
  • Extra-glandular disease: joint pain, skin disease and pulmonary disease
  • Fatigue, myalgia
72
Q

What are the complications of Sjogren’s syndrome?

A
  • Non-Hodgkins Lymphoma
  • Chronic dry eyes —> corneal and conjunctival damage
  • Chronic dry mouth —> dental caries
  • Congenital heart block in off-spring
73
Q

How is Sjogren’s Syndrome Diagnosed?

(6)

A

presents with 4/6 criteria including one underlined

  • Dry eyes >3 months/using artificial tears TDS
  • Dry mouth >3 months/need liquids to swallow dry foods / recurrent swollen salivary glands
  • Shirmer’s test <5mm/5 mins / positive vital dye staining
  • Abnormal parotid sialography or salivary scintigraphy or unstimulated whole salivary flow (<1.5ml/15mins)
  • Focal lymphocytic sialoadenditis on lip biopsy
  • Anti-Ro / Anti La positive
74
Q

What is the treatment for Sjogren’s Syndrome?

  • conservative/ medications
A

Conservative:

  • Stop smoking / oral hygiene /
  • Artificial tears and saliva

Medications:

  • Cholinergic agents: pilocarpine / cevimeline
  • NSAIDs / Steroids
  • Immunosuppressants eg. hydroxychloroquine / methotrexate / rituximab
75
Q

What is Systemic Sclerosis

  • Types? (4)
A
  • Immune activation, vascular damage and excessive deposition of collagen
    • more frequent in ages 30-50
    • 5: 1 females
  • Limited: CREST (calcinosis, Raynaud’s, Esophageal dysmotility, sclerodactyly, telangiectasias)
  • Diffuse: scleroderma beyond the elbows
  • Overlap syndromes with SLE / Sjogren’s
  • Sine scleroderma: no skin presentations
76
Q

What antibodies are associated with Systemic Sclerosis?

(4)

A
  • anti topoisomerase (anti-Scl-70)
  • Anti centromere (ACA)
  • anti-RNA polymerase III
  • ANA
77
Q

What are the clinical features of Systemic Sclerosis?

A
  • Sclerodactyly
  • Raynaud’s phenomenon
  • Heartburn
  • Abnormal nailfold capillaries
  • Telangiectasia: Telangiectasia is a condition in which widened venules (tiny blood vessels) cause threadlike red lines or patterns on the ski
  • Pulmonary arterial hypertension
  • Interstitial lung disease
  • Lower bowel: distension / diarrhea / constipation
  • Renal failure / proteinuria
  • Erectile dysfunction
78
Q

What is the treatment for Systemic Sclerosis?

  • conservative/ medication
A

Conservative

  • Stop smoking
  • Controlled exercise
  • Wear gloves
  • Warm wax baths

Medications

  • Raynaud’s – amlodipine / losartan / fluoxetine / sildenafil
  • Reflux - omeprazole
  • Immunosuppressants- mycophenolate, methotrexate, cyclophosphamide, steroids, rituximab, IV immunoglobulins

204: Theme 3 (6 decks)

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