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Year 3 ICSM 2 > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

Learning objectives

A

Answer

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2
Q

Define amyloidosis

A

• Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils

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3
Q

Explain the aetiology / risk factors of amyloidosis

A

• Amyloid fibrils are polymers of low-molecular-weight subunit proteins
• These are derived from proteins that undergo conformational changes to adopt an anti-parallel beta-pleated sheet configuration
• Their deposition progressively disrupts the structure and function of normal tissue
• Amyloidosis is classified according to the fibril subunit proteins
o Type AA - serum amyloid A protein
o Type AL - monoclonal immunoglobulin light chains
o Type ATTR (familial amyloid polyneuropathy) - genetic-variant transthyretin

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4
Q

Summarise the epidemiology of amyloidosis

A
  • AA - incidence of 1-5% amongst patients with chronic inflammatory diseases
  • AL - 300-600 cases in the UK per year
  • Hereditary Amyloidosis - accounts for 5% of patients with amyloidosis
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5
Q

Recognise the presenting symptoms & signs of amyloidosis

A
  • Renal - proteinuria, nephrotic syndrome, renal failure
  • Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina
  • GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding
  • Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome
  • Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules
  • Joints - painful asymmetrical large joints, enlargement of anterior shoulder
  • Haematological - bleeding tendency
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6
Q

Identify appropriate investigations for amyloidosis and interpret the results

A 
•	Tissue Biopsy
•	Urine - check for proteinuria, free immunoglobulin light chains (in AL)
•	Bloods
o	CRP/ESR 
o	Rheumatoid factor 
o	Immunoglobulin levels 
o	Serum protein electrophoresis 
o	LFTs 
o	U&Es 
•	SAP Scan - radiolabelled SAP will localise the deposits of amyloid
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7
Q

Define ankylosing spondylitis

A

• Seronegative inflammatory arthropathy affecting preferentially the axial skeletal and large proximal joints+A10:B10

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8
Q

Explain the aetiology/risk factors of ankylosing spondylitis

A

• UNKNOWN
• Strong association with the HA10:B12LA-B27 gene (> 90% of cases are HLA-B27 positive)
• Infective triggers and antigen cross-reactivity with self-peptides have been hypothesised
• Pathophysiology
o Inflammation starts at the entheses (where ligaments attach to vertebral bodies)
o Persistent inflammation leads to reactive new bone formation
o Changes begin in the lumbar vertebrae and progress superiorly
o Vertebral bodies become more square
o Syndesmophytes (vertical ossifications bridging the margins between adjacent vertebrae)

o Fusion of syndesmophytes and facet joints
o Calcification of anterior and lateral spinal ligaments

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9
Q

Summarise the epidemiology of ankylosing spondylitis

A
  • COMMON

* Earlier presentation in males

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10
Q

Recognise the presenting symptoms of ankylosing spondylitis

A

• Lower back and sacroiliac pain
• Disturbed sleep
• Pain pattern
o Worse in the morning
o Better with activity
o Worse when resting
• Progressive loss of spinal movement
• Symptoms of asymmetrical peripheral arthritis
• Pleuritic chest pain (due to costovertebral joint involvement)
• Heel pain (due to plantar fasciitis)
• Non-specific symptoms (e.g. malaise, fatigue)

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11
Q

Recognise the signs of ankylosing spondylitis on physical examination

A
  • Reduced range of spinal movement (particularly hip rotation)
  • Reduced lateral spinal flexion
  • Schober’s Test

o Two fingers are placed on the patients back about 10 cm apart
o The patient is asked to bend over
o The distance between the two fingers should increase by > 5 cm on forward flexion
o Reduced movement would suggest ankylosing spondylitis
• Tenderness over the sacroiliac joints
• LATER STAGES:
o Thoracic kyphosis
o Spinal fusion
o Question mark posture

•	Signs of Extra-Articular Disease: 5 As
o	Anterior uveitis 
o	Apical lung fibrosis 
o	Achilles tendinitis 
o	Amyloidosis
o	Aortic regurgitation
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12
Q

Identify appropriate investigations for ankylosing spondylitis

A 
•	Bloods
o	FBC - anaemia of chronic disease 
o	Rheumatoid factor - negative 
o	ESR/CRP - high 
•	Radiographs
o	Anteroposterior and lateral radiographs of the spine 
•	May show Bamboo spine

o Anteroposterior radiograph of sacroiliac joints
• Shows symmetrical blurring of joint margins

o	LATER STAGES:
•	Erosions 
•	Sclerosis 
•	Sacroiliac joint fusion 
o	CXR - check for apical lung fibrosis 
•	Lung Function Tests
o	Assess mechanical ventilatory impairment due to kyphosis
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13
Q

Define gout

A

• A disorder of uric acid metabolism causing recurrent bouts of acute arthritis caused by deposition of monosodium urate crystals in joints, and also soft tissues and kidneys

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14
Q

Explain the aetiology/risk factors of gout

A

• The main metabolic disturbance is hyperuricaemia
• This may be caused by:
o Increased urate intake or production
• Increased dietary intake
• Increased nucleic acid turnover (e.g. lymphoma, leukaemia, psoriasis)
• Increased synthesis of urate (e.g. Lesch-Nyhan syndrome)
o Decreased Renal Excretion
• Idiopathic
• Drugs (e.g. ciclosporin, alcohol, loop diuretics)
• Renal dysfunction

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15
Q

Summarise the epidemiology of gout

A
  • 10 x more common in MALES
  • Very rare pre-puberty
  • Rare in pre-menopausal women
  • More common in HIGHER social classes
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16
Q

Recognise the presenting symptoms and signs of gout

A

• Acute Attack
o Precipitating factors:
• Trauma
• Infection
• Alcohol
• Starvation
• Introduction or withdrawal of hypouricaemic agents
o Symptoms:
• Sudden excruciating monoarticular pain
 Usually affecting the metatarsophalangeal joint of the great toe (podagra)

• Symptoms peak at 24 hrs
• They resolve over 7-10 days
• Sometimes, acute attacks can present with cellulitis, polyarticular or periarticular involvement
• Attacks are often recurrent
• Patients are symptom-free between attacks
• Intercritical Gout
o DEFINITION: asymptomatic period between acute attacks
• Chronic Tophaceous Gout
o Follow repeated acute attacks
o Symptoms:
• Persistent low-grade fever
• Polyarticular pain with painful tophi (urate deposits)
 Best seen on tendons and the pinna of the ear

• Symptoms of urate urolithiasis (renal calculi symptoms)

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17
Q

Identify appropriate investigations for gout

A

• Synovial Fluid Aspirate
o Monosodium urate crystals will be seen

o	They are:
•	Needle-shaped 
•	NEGATIVE birefringence under polarised light microscopy 
o	Microscopy and culture will also be performed to exclude septic arthritis
•	Bloods
o	FBC - raised WCC
o	U&Es
o	Raised urate 
o	Raised ESR 
•	AXR/KUB Film
o	Uric acid renal stones may be seen
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18
Q

Define fibromyalgia

A

• A chronic pain disorder with an unknown cause.

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19
Q

Explain the aetiology/risk factors of fibromyalgia

A
  • UKNOWN aetiology

* Thought to be something to do with altered pain perception

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20
Q

Summarise the epidemiology of fibromyalgia

A
  • COMMON
  • 10 x more common in WOMEN
  • Usual age of presentation: 20-50 yrs
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21
Q

Recognise the presenting symptoms and signs of fibromyalgia

A
  • Pain at multiple sites (MAIN SYMPTOM)
  • Fatigue
  • Sleep disturbance
  • Morning stiffness
  • Paraesthesia
  • Feeling of swollen joints
  • Problems with cognition
  • Headaches
  • Light headedness
  • Anxiety
  • Depression
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22
Q

Identify appropriate investigations for fibromyalgia

A

• CLINICAL diagnosis
• Key features of fibromyalgia:
o Widespread pain involving both sides of the body, above and below the waist for at least 3 months
o Presence of 11 tender points among the 9 pairs of specific sites shown in the diagram below

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23
Q

Define giant cell arteritis

A

• Granulomatous inflammation of large arteries, particularly branches of the external carotid artery, most commonly the TEMPORAL ARTERY

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24
Q

Explain the aetiology/risk factors of giant cell arteritis

A
  • UNKNOWN
  • More common with increasing age
  • Some associations with ethnic background and infections
  • Associated with HLA-DR4 and HLA-DRB1
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25
Q

Summarise the epidemiology of giant cell arteritis

A
  • More common in FEMALES

* Peak age of onset: 65-70 yrs

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26
Q

Recognise the presenting symptoms of giant cell arteritis

A

• Subacute onset (usually over a few weeks)
• Headache
• Scalp tenderness
• Jaw claudication
• Blurred vision
• Sudden blindness in one eye
• Systemic: malaise, low-grade fever, lethargy, weight loss, depression
• Symptoms of polymyalgia rheumatica - early morning pain and stiffness of muscles of the shoulder and pelvic girdle
o NOTE: 40-60% of GCA has polymyalgia rheumatica

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27
Q

Recognise the signs of giant cell arteritis on physical examination

A
  • Swelling and erythema overlying the temporal artery
  • Scalp and temporal tenderness
  • Thickened non-pulsatile temporal artery
  • Reduced visual acuity
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28
Q

Identify appropriate investigations for giant cell arteritis

A

• Bloods
o High ESR
o FBC - normocytic anaemia of chronic disease
• Temporal Artery Biopsy
o Must be performed within 48 hrs of starting corticosteroids
o Negative biopsy doesn’t necessarily rule out GCA

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29
Q

Generate a management plan for giant cell arteritis

A
  • High dose oral prednisolone IMMEDIATELY to prevent visual loss
  • Reduce the dose of prednisolone gradually
  • Many patients will need to be kept on a maintenance dose of prednisolone for 1-2 yrs
  • Low dose aspirin (with PPIs and gastroprotection) - reduces risk of visual loss, TIAs and stroke
  • Annual CXR for up to 10 yrs to look for thoracic aortic aneurysms
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30
Q

Identify possible complications of giant cell arteritis

A
  • Carotid artery aneurysms
  • Aortic aneurysms
  • Thrombosis
  • Embolism to the ophthalmic artery leading to visual disturbance and loss of vision
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31
Q

Summarise the prognosis for patients with giant cell arteritis

A

• In most cases the condition will last for around 2 years before complete remission
o Can detect osteoarthritic change
o Rarely diagnostic if non-traumatic
• MRI
o Allows assessment of root and cord compression
o Helps exclude spinal cord tumour and nerve root infiltration by granulomatous tissue
• Needle Electromyography (EMG)

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32
Q

Define polymyositis and dermatomyositis

A

• Connective tissue diseases characterised by inflammation of muscles.

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33
Q

Explain the aetiology/risk factors of polymyositis and dermatomyositis

A
  • Autoimmune basis

* Viral infection has been implicated in its pathogenesis

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34
Q

Summarise the epidemiology of polymyositis and dermatomyositis

A
  • Polymyositis presents between 30-60 yrs
  • Dermatomyositis can occur at any age (peak onset: 5-10 (children) and 50 (adults))
  • Both diseases are 2 x more common in FEMALES
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35
Q

Recognise the presenting symptoms of polymyositis and dermatomyositis

A

• Polymyositis
o Inflammatory myopathy with onset over weeks or months
o Steady progression of symptoms
o Diffuse weakness in proximal muscles
• Causing difficulty rising from a low chair, climbing steps, lifting objects and combing hair
• Also fatigue, myalgia and muscle cramps
o Distal muscles are spared - so fine motor coordination tends to be preserved in the early stages
o Pharyngeal weakness –> dysphagia
o NO rash
• Dermatomyositis
o Inflammatory myopathy with onset over weeks or months
o RASH
o Systemic upset with fever, arthralgia, malaise and weight loss
o Possible cardiac disease (e.g. conduction blocks, tachyarrhythmia)
o GI ulcers and infections
o Interstitial lung disease (30-50%)
o Children have more non-muscular features (e.g. GI ulcers and infections)

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36
Q

Recognise the signs of polymyositis and dermatomyositis on physical examinations

A 
•	Polymyositis
o	Muscle weakness 
o	NOT painful in most patients
o	Proximal myopathy 
o	Extraocular muscles and distal muscles are spared 
o	Weak forced flexion of the neck 
o	Muscular atrophy 
o	Muscles may be tender on palpation 
•	Dermatomyositis
o	RASH characteristics

• Blue-purple discolouration of the upper eyelids with periorbital oedema
• Flat red rash involving the face and upper trunk
• Raised purple-red scaly patches over the extensor surfaces of joints and fingers
o Rash may affect knees, shoulders, back and upper arms
o Rash may be exacerbated by sunlight
o Proximal myopathy
o Muscle pain and tenderness in early disease

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37
Q

Identify appropriate investigations for polymyositis and dermatomyositis

A

• Polymyositis
o Creatine kinase - up to 50 x higher than normal
o Electromyography (EMG)
o Muscle biopsy - DEFINITIVE TEST
o Autoantibodies (e.g. myositis specific antibody, anti-Jo-1 antibody)
o Enzymes (e.g. SGOT, SGPT, LDH)
• Dermatomyositis
o Creatine kinase - not as reliable as in polymyositis
o Enzymes (SGOT, SGPT and LDH may be raised)
o Autoantibodies
• ANA
• Anti-Mi-2
• Anti-Jo-1 (more common in polymyositis)
o EMG - may be helpful but can be normal as well
o Muscle biopsy

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38
Q

Define pseudogout

A

• Arthritis associated with deposition of calcium pyrophosphate dihydrate (CPPD) crystals in the joint cartilage

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39
Q

Explain the aetiology/risk factors for pseudogout

A

• CPPD crystal formation is initiated in cartilage located near the surface of chondrocytes
• It is linked with excessive calcium pyrophosphate production
• This abundance of calcium pyrophoshpate leads to the formation of CPPD crystals
• Shedding of crystals in to the joint cavity leads to acute arthritis
• Most causes of joint damage predispose to pseudogout (e.g. osteoarthritis, trauma)
• Rarer conditions that increase the risk of pseudogout:
o Haemochromatosis
o Hyperparathyroidism
o Hypomagnesaemia
o Hypophosphatasia
• Precipitating factors:
o Intercurrent illness
o Surgery
o Local trauma

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40
Q

Summarise the epidemiology of pseudogout

A
  • 2 x more common in WOMEN

* More common in the ELDERLY

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41
Q

Recognise the presenting symptoms of pseudogout

A 
•	Acute Arthritis
o	Painful
o	Swollen Joint (e.g. knee, ankle, shoulder, elbow, wrist)
•	Chronic Arthropathy
o	Pain 
o	Stiffness 
o	Functional impairment
•	Uncommon Presentations
o	Tendonitis 
o	Tenosynovitis 
o	Bursitis
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42
Q

Recognise the signs of pseudogout on physical examination

A

• Acute Arthritis

o	Red 
o	Hot 
o	Tender 
o	Restricted range of movement 
o	Fever 
•	Chronic Arthropathy
o	Similar to osteoarthritis
o	Bony swelling 
o	Crepitus 
o	Deformity
o	Restriction of movement
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43
Q

Identify appropriate investigations for pseudogout

A 
•	Bloods
o	High WCC in acute attacks 
o	High ESR 
o	Blood culture - to exclude septic arthritis 
•	Joint Aspiration
o	Rhomboid, brick-shaped crystals 
o	POSITIVE birefringence 
o	Culture or Gram-staining to exclude septic arthritis 
•	Plain Radiograph of the Joint
o	Chondrocalcinosis

o Signs of osteoarthritis:

  • Loss of joint space
  • Osteophytes
  • Subchondral cysts
  • Sclerosis
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44
Q

Define osteoarthritis

A

• Age-related degenerative joint disease when cartilage destruction exceeds repair, causing pain and disability

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45
Q

Explain the aetiology/risk factors of osteoarthritis

A

• Can be classified according to the distribution of affected joints
• Pathogenesis
o Synovial joint cartilage destruction
o Eventually, there is loss of joint volume due to altered chondrocyte activity
o Patchy chronic synovial inflammation
o Fibrotic thickening of joint capsules
• Primary Osteoarthritis
o UNKNOWN aetiology
o Multifactorial causes
• Secondary Osteoarthritis
o Other diseases lead to altered joint architecture and stability
o Commonly associated diseases include:
• Developmental abnormalities (e.g. hip dysplasia)
• Trauma (e.g. previous fractures)
• Inflammatory (e.g. rheumatoid arthritis, gout, septic arthritis)
• Metabolic (e.g. haemochromatosis, acromegaly)

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46
Q

Summarise the epidemiology of osteoarthritis

A
  • COMMON
  • 25% of those > 60 yrs
  • More common in FEMALES, CAUCASIANS and ASIANS
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47
Q

Recognise the presenting symptoms of osteoarthritis

A 
•	Joint pain and discomfort 
o	Use-related 
•	Stiffness or gelling after inactivity 
•	Difficulty with certain movements 
•	Feelings of instability 
•	Restriction walking, climbing stairs and doing manual tasks
•	Systemic features are usually absent
48
Q

Recognise the signs of osteoarthritis on physical examination

A
  • Local joint tenderness
  • Bony swellings along joint margins

o Heberden’s Nodes - DISTAL interphalangeal joint
o Bouchard’s Nodes - PROXIMAL interphalangeal joint
• Crepitus and pain during joint movement
• Joint effusion
• Restriction of range of joint movement

49
Q

Identify appropriate investigations for osteoarthritis

A

• Joint X-Ray of the affected joint will show FOUR classic features:

o Loss of joint space (narrowing)
o Osteophytes
o Subchondral cysts
o Subchondral sclerosis

50
Q

Define osteomyelitis

A

• Infection of the bone leading to inflammation, necrosis and new bone formation. Can be acute, subacute or chronic.
• Causative organisms:
o Staphylococcus aureus
o Group A Streptococcus

51
Q

Explain the aetiology/risk factors of osteomyelitis

A 
•	Bacterial infection from indirect inoculation from skin (e.g. trauma, operative, chronic skin ulcers, haematogenous spread)
•	Risk Factors
o	Diabetes 
o	Immunosuppression 
o	IV drug use 
o	Prostheses 
o	Sickle-cell anaemia
52
Q

Summarise the epidemiology of osteomyelitis

A
  • Mostly in YOUNG CHILDREN

* < 20% of cases are in adults

53
Q

Recognise the presenting symptoms of osteomyelitis

A
  • Pain in the affected area
  • Fever
  • Malaise
  • Rigors
  • History of preceding skin lesion, sore throat, trauma or operation
  • NOTE: infants may not show localising signs
54
Q

Recognise the signs of osteomyelitis on physical examination

A
  • Localised erythema
  • Tenderness
  • Swelling
  • Warmth
  • Painful/limited movement of affected limb
  • Seropurulent discharge from an associated wound or ulcer
55
Q

Identify appropriate investigations for osteomyelitis

A 
•	Bloods
o	FBC 
o	Blood culture 
o	ESR 
o	CRP 
•	Swabs of wound or discharge 
•	Radiographs
•	Radioisotope bone scan - shows areas of increased activity
56
Q

Define polymyalgia rheumatica

A

• An inflammatory condition of unknown cause, which is characterised by severe bilateral pain and morning stiffness of the shoulder, neck and pelvic girdle.
o NOTE: polymyalgia rheumatica does NOT cause weakness

57
Q

Explain the aetiology/risk factors of polymyalgia rheumatica

A

• UNKNOWN
• Genetic and environmental factors
• Associations
o Temporal Arteritis
• 40-50% of people with temporal arteritis have polymyalgia rheumatica
• 15% of people with polymyalgia rheumatica will go on to develop temporal arteritis
• Both conditions respond to corticosteroids

58
Q

Summarise the epidemiology of polymyalgia rheumatica

A
  • Relatively common
  • Occurs in people aged > 50 yrs
  • Peak age of onset: 73 yrs
  • 3 x more common in FEMALES
59
Q

Recognise the presenting symptoms and signs of polymyalgia rheumatica

A

• Tend to be relatively non-specific
• Usual inclusion criteria for polymyalgia rheumatica:
o Age > 50 yrs
o Duration of symptoms > 2 weeks
o Bilateral shoulder or pelvic girdle aching, or both
o Morning stiffness lasting > 45 mins
o High ESR/CRP
• The characteristic clinical picture of polymyalgia rheumatica: bilateral shoulder pain and stiffness of acute or subacute onset with bilateral arm tenderness
• NO WEAKNESS
• Symptoms are worst when walking
• Morning stiffness may be so bad that they find it difficult to get out of bed, or raise their arms enough to brush their hair
• May be flu-like symptoms at onset

60
Q

Identify appropriate investigations for polymyalgia rheumatica

A
  • ESR/CRP - raised in polymyalgia rheumatica
  • FBC
  • U&Es
  • LFTs
  • Bone profile
  • Protein electrophoresis
  • TFTs
  • Creatine kinase
  • Others: urinary Bence Jones proteins, autoantibodies (e.g. anti-CCP antibodies)
61
Q

Generate a management plan for polymyalgia rheumatica

A
  • CORTICOSTEROIDS
  • Steroid-sparing agents (e.g. methotrexate) are sometimes used
  • Assistance from physiotherapy and occupational therapy
  • Monitor for adverse effects of steroids (e.g. osteoporosis)
62
Q

Identify possible complications of polymyalgia rheumatica

A
  • Temporal arteritis
  • Relapse of disease
  • Complications of steroid use (e.g. fracture risk)
63
Q

Summarise the prognosis for patients with polymyalgia rheumatica

A
  • 15% risk of getting temporal arteritis
  • Variable course and prognosis
  • Usually responds rapidly to steroid treatment
  • Relapse is common
64
Q

Define reactive arthritis

A

• Characterised by a sterile arthritis occurring after an extra-articular infection (commonly GI or urogenital).
• Reiter’s Syndrome is defined as a TRIAD of:
o Reactive arthritis
o Urethritis
o Conjunctivitis

65
Q

Explain the aetiology/risk factors for reactive arthritis

A 
•	Associated with infections:
o	GI
•	Salmonella
•	Shigella 
•	Yersinia
•	Campylobacter
o	Urogenital
•	Chlamydia trachomatis (60%)
•	It is thought that initial activation of the immune system by a microbial antigen is followed by an autoimmune reaction that involves the skin, eyes and joints 
•	HLA-B27 allele is identified in 70-80% of patients
66
Q

Summarise the epidemiology of reactive arthritis

A
  • 20 x more common in MALES
  • Age of onset: 20-40 yrs
  • Seen in 2% of patients with non-specific urethritis
67
Q

Recognise the presenting symptoms of reactive arthritis

A
  • Symptoms can develop 3-30 days after infection
  • Burning or stinging when passing urine (due to urethritis)
  • Arthritis
  • Low back pain (due to sacroiliitis)
  • Painful heels (due to enthesitis and plantar fasciitis)
  • Conjunctivitis
68
Q

Recognise the signs of reactive arthritis on physical examination

A

• Signs of Arthritis

o Asymmetrical oligoarthritis
o Often affects the lower extremities
o Sausage-shaped digits
• Signs of Conjunctivitis

o Anterior uveitis - painful red eye
• Oral Ulceration
• Circinate Balanitis

o Scaling red patches on the glans
• Keratoderma Blenorrhagica

o	Brownish-red macules 
o	Vesicopustules 
o	Yellowish-brown scales 
o	Found on the SOLES and PALMS
•	Others
o	Nail dystrophy
o	Hyperkeratosis 
o	Onycholysis
69
Q

Identify appropriate investigations for reactive arthritis

A 
•	Bloods
o	FBC 
o	High ESR and CRP 
o	HLA-B27 testing 
•	Stool or Urethral Swabs and Cultures
o	May be negative by the time the arthritis develops (because the arthritis occurs post-infection)
•	Urine
o	Screen for Chlamydia trachomatis
•	Plain X-Rays
o	Useful in chronic cases 
o	Erosions seen at the entheses (insertion of tendons into bone) 
•	Joint Aspiration
o	To exclude septic or crystal arthritis
70
Q

Define rheumatoid arthritis

A

• Chronic inflammatory systemic disease characterised by symmetrical deforming polyarthritis and extra-articular manifestations

71
Q

Explain the aetiology/risk factors of rheumatoid arthritis

A 
•	AUTOIMMUNE disease 
•	UNKNOWN cause 
•	Associated with other autoimmune diseases (e.g. Sjogren's syndrome)
•	HLA associations:
o	HLA-DR1
o	HLA-DR4
72
Q

Summarise the epidemiology of rheumatoid arthritis

A
  • COMMON
  • 1% of general population
  • 3 x more common in FEMALES
  • Peak incidence: 30-50 yrs
73
Q

Recognise the presenting symptoms of rheumatoid arthritis

A 
•	GRADUAL onset 
•	Joint pain 
•	Swelling 
•	Morning stiffness
•	Impaired function 
•	Usually affects peripheral joints symmetrically
•	Systemic Symptoms:
o	Fever 
o	Fatigue 
o	Weight loss
74
Q

Recognise the signs of rheumatoid arthritis on physical examination

A 
•	Arthritis - most common in the HANDS 
•	Early Signs
o	Spindling of fingers 
o	Swelling of MCP and PIP joints 
o	Warm, tender joints 
o	Reduction in range of movement 
•	Late Signs
o	Symmetrical deforming arthropathy
o	Ulnar deviation of fingers as a result of subluxation (partial dislocation) of the MCP joints

o Radial deviation of the wrist

o Swan neck deformity

o Boutonniere deformity

o Z deformity of the thumb
o Trigger finger (inability to straighten the finger, tendon nodule palpable)
o Tendon rupture
o Wasting of small muscles of the hand
o Palmar erythema
• Rheumatoid Nodules - firm subcutaneous nodules (usually found on the elbows, ulnar margin, palms and over extensor tendons)

• Signs of complications

75
Q

Identify appropriate investigations for rheumatoid arthritis

A

• Bloods
o FBC - low Hb, high platelets
o High ESR and CRP
o Rheumatoid factor (found in 70% of RhA patients)
• The presence of rheumatoid factor is associated with rheumatoid nodules and extra-articular manifestations
o Antinuclear antibodies (30%)
• Joint Aspiration
o May be performed in the acute setting to rule out septic arthritis
• Joint X-Ray

o Deformity
o Osteopaenia
o Narrowing of joint space
o Soft tissue swelling

76
Q

Define sarcoidosis

A

• Multisystem granulomatous inflammatory disorder

77
Q

Explain the aetiology/risk factors of sarcoidosis

A

• UNKNOWN
• Transmissible agents (e.g. viruses), environmental triggers and genetic factors have all been suggested
• Pathogenesis
o An UNKNOWN antigen is presented on MHC class 2 complexes on macrophages to CD4+ T-lymphocytes
o These accumulate and release cytokines
o This leads to the formation of non-caseating granulomas in organs

78
Q

Summarise the epidemiology of sarcoidosis

A
  • Most common in AFRICANS and SCANDINAVIANS

* Can occur at any age but tends to be in adults > 50 yrs

79
Q

Recognise the presenting symptoms and the signs of sarcoidosis

A 
•	General Symptoms
o	Fever 
o	Malaise 
o	Weight loss 
o	Bilateral parotid swelling 
o	Lymphadenopathy
o	Hepatosplenomegaly
•	Pulmonary Symptoms
o	Breathlessness
o	Dry cough
o	Chest discomfort 
o	Minimal clinical signs 
•	Musculoskeletal Symptoms
o	Bone cysts (e.g. dactylitis) 
o	Polyarthralgia 
o	Myopathy
•	Eye Symptoms
o	Keratoconjunctivitis sicca (inflammation of the conjunctivitis and surrounding tissues due to the eyes being dry)

o Uveitis
o Papilloedema
• Skin Symptoms
o Lupus pernio (red-blue infiltrations of the nose, cheeks, ears and terminal phalanges)

o	Erythema nodosum 
o	Maculopapular eruptions
•	Neurological Symptoms
o	Lymphocytic meningitis 
o	Space-occupying lesions 
o	Pituitary infiltration 
o	Cerebellar ataxia 
o	Cranial nerve palsies 
o	Peripheral neuropathy
•	Cardiac Symptoms
o	Arrhythmia
o	Bundle branch block 
o	Pericarditis 
o	Cardiomyopathy
o	Congestive cardiac failure
80
Q

Identify appropriate investigations for sarcoidosis

A 
•	Bloods
o	High serum ACE 
o	High calcium 
o	High ESR 
o	FBC - WCC may be low due to lymphocyte sequestration in the lungs 
o	Immunoglobulins - polyclonal hyperglobulinaemia 
o	LFTs - high ALP + GGT 
•	24 hr Urine Collection
o	Hypercalciuria
•	CXR
o	Stage 0 - may be clear 
o	Stage 1 - bilateral hilar lymphadenopathy

o Stage 2 - stage 1 with pulmonary infiltration and paratracheal node enlargement
o Stage 3 - pulmonary infiltration and fibrosis
• High-Resolution CT Scan
o Check for diffuse lung involvement
• Gallium Scan - shows areas of inflammation
• Pulmonary Function Tests
o Low FEV1
o FVC shows restrictive picture
• Bronchoscopy and Bronchoalveolar Lavage
o High lymphocytes
o High CD4: CD8 ratio
• Transbronchial Lung Biopsy (or lymph node biopsy)

o Shows non-caseating granulomas consisting of:
• Epithelioid cells (activated macrophages)
• Multinucleate Langerhans cells
• Mononuclear cells (lymphocytes)

81
Q

Define Sjogren’s syndrome

A

• Characterised by inflammation and destruction of exocrine glands (usually salivary and lacrimal glands).
o NOTE: when associated with other autoimmune diseases, Sjogren’s syndrome is termed secondary

82
Q

Explain the aetiology/risk factors of Sjogren’s syndrome

A 
•	UNKNOWN
•	Genetic associations:
o	HLA-B8
o	HLA-DR3
•	Associated autoimmune diseases:
o	Rheumatoid arthritis 
o	Scleroderma
o	SLE 
o	Polymyositis 
o	Organ-specific autoimmune diseases (e.g. PBC, autoimmune hepatitis, myasthenia gravis)
83
Q

Recognise the presenting symptoms of Sjogren’s syndrome

A
  • Fatigue
  • Fever
  • Weight loss
  • Depression
  • Dry eyes (keratoconjunctivitis sicca) - they will be gritty and sore
  • Dry mouth - leads to secondary dysphagia
  • Dry upper airways - leads to a dry cough and recurrent sinusitis
  • Dry skin or hair
  • Dry vagina - may cause dyspareunia
  • Reduced GI mucus secretions leads to reflux oesophagitis, gastritis and constipation
84
Q

Recognise the signs of Sjogren’s syndrome on physical examination

A
  • Parotid or salivary gland enlargement
  • Dry eyes
  • Dry mouth or tongue
  • Signs of associated conditions
85
Q

Identify appropriate investigations for Sjogren’s syndrome

A 
•	Bloods
o	High ESR 
o	High amylase (if salivary glands involved)
•	Autoantibodies
o	Rheumatoid factor 
o	ANA 
o	Anti-ENA (extractable nuclear antigens)
•	Schirmer's Test

o A strip of filter paper is placed under the eyelid
o Positive for Sjogren’s syndrome if < 10 mm of the strip is wet after 5 mins
• Fluorescein/Rose Bengal Stains
o May show punctate or filamentary keratitis
• Other Investigations
o Reduced parotid salivary flow rate
o Reduced uptake or clearance on isotope scan
• Biopsy - of salivary or labial glands

86
Q

Define sciatica

A

• Pain, tingling and numbness that arise from nerve root compression or irritation in the lumbosacral spine.

87
Q

Explain the aetiology/risk factors of sciatica

A

• Most commonly caused by a disc herniation
• Other causes:
o Spinal stenosis
o Spondylolisthesis
o Spinal injury or infection
o Tumour
o Cauda equina syndrome
• Risk Factors
o Age - older people are more like to get slipped discs
o Job that requires regular heavy lifting

88
Q

Summarise the epidemiology of sciatica

A
  • Relatively COMMON

* More common in MALES

89
Q

Recognise the presenting symptoms and signs of sciatica

A
  • Pain (usually affects the buttocks and the legs more than the back)
  • Numbness
  • Tingling sensation that radiates from the lower back down one of the legs
  • Weakness in the calf muscles or the muscles that move the foot or ankle
90
Q

Identify appropriate investigations for sciatica

A
  • CLINICAL diagnosis
  • Straight Leg Raise

o If pain in the distribution of the sciatic nerve is reproduced on passive flexion of the straight leg at the hip between 30-70 degrees then it is considered a positive sign (Lasegue’s sign)
o This test is sensitive but not very specific
• CT/MRI - helps visualise a lumbar disc herniation

91
Q

Define cervical spondylosis

A

• Progressive degenerative process affecting the cervical vertebral bodies and intervertebral discs, and causing compression of the spinal cord and/or nerve roots

92
Q

Explain the aetiology/risk factors of cervical spondylosis

A

• Osteoarthritic degeneration of the vertebral bodies leads to the formation of osteophytes
• These osteophytes protrude on to the foramina and spinal canal
• This leads to compression of:
o Nerve roots - radiculopathy
o Anterior spinal cord - myelopathy

93
Q

Summarise the epidemiology of cervical spondylosis

A
  • Mean age at diagnosis = 48 yrs

* More common in MALES

94
Q

Recognise the presenting symptoms of cervical spondylosis

A
  • Neck pain/stiffness
  • Arm pain (stabbing or dull ache)
  • Paraesthesia
  • Weakness
  • Clumsiness in the hands
  • Weak and stiff legs
  • Gait disturbance
  • Atypical chest pain
  • Breast pain
  • Pain in the face
95
Q

Recognise the signs of cervical spondylosis on physical examination

A

• ARMS
o Atrophy of the forearm and hand muscles
o Segmental muscle weakness in a nerve root distribution (e.g. C5 –> shoulder abduction and elbow flexion weakness)
o Hyporeflexia
o Sensory loss (mainly pain and temperature)
o Pseudoathetosis (writhing finger movements when hands are outstretched, fingers spread and eyes closed)
• LEGS - if cervical cord compression
o Increased tone
o Weakness
o Hyper-reflexia
o Extensor plantar response
o Reduced vibration and joint position sense
• Lhermitte’s Sign - neck flexion causes crepitus (grating sound) and/or paraesthesia down the spine

96
Q

Identify appropriate investigations for cervical spondylosis

A

• Spinal X-Ray (lateral)

97
Q

Define SLE

A

• Multi-system inflammatory autoimmune disorder
• 4/11 of the diagnostic criteria of the American College of Rheumatology provides high sensitivity and specificity for the diagnosis of SLE: SOAP BRAIN MD
o Serositis
o Oral ulcers
o Arthritis (non-erosive)
o Photosensitivity
o Bloods (haemolytic anaemia/leukopaenia/thrombocytopaenia)
o Renal disease (urine casts/proteinuria)
o ANA
o Immunological disorder (anti-dsDNA/anti-Sm/anti-phospholipid)
o Neurological disease (psychosis/seizures)
o Malar rash
o Discoid rash

98
Q

Explain the aetiology/risk factors of SLE

A
  • UNKNOWN
  • Tissue damage may be caused by vascular immune complex deposition
  • Could be due to a combination of hormonal, genetic and exogenous factors
99
Q

Summarise the epidemiology of SLE

A
  • COMMON
  • 1-2/1000
  • More common in the YOUNG
  • More common in AFRO-CARIBBEAN and CHINESE
  • 9 x more common in FEMALES
100
Q

Recognise the presenting symptoms and signs of SLE

A 
•	General Symptoms
o	Fever 
o	Fatigue 
o	Weight loss 
o	Lymphadenopathy
o	Splenomegaly
•	Raynaud's phenomenon
•	Oral ulcers 
•	Skin Rash
o	Malar rash 
o	Discoid lupus (red scaly patches)
o	Atypical rashes (e.g. photosensitivity, vasculitis, urticaria, purpura)

• Systemic Involvement
o Musculoskeletal - arthritis, tendonitis, myopathy
o Heart - pericarditis, myocarditis, arrhythmias, Libman-Sacks endocarditis
o Lung - pleurisy, pleural effusion, basal atelectasis, restrictive lung defects
o Neurological - headache, stroke, cranial nerve palsies, confusion, chorea
o Psychiatric - depression, psychosis
o Renal - glomerulonephritis

101
Q

Identify appropriate investigations for SLE

A 
•	Bloods
o	FBC
o	U&amp;E
o	LFT 
o	Raised ESR 
o	Normal CRP
o	Clotting 
o	Complement 
•	Autoantibodies
o	Anti-dsDNA (60%)
o	Rheumatoid factor (30-50%)
o	Anti-ENA
o	Anti-RNP
o	Anti-SM
o	Anti-Ro
o	Anti-La
o	Anti-histone
o	Anti-cardiolipin
•	Urine - haematuria, proteinuria, red cell casts 
•	Joints - plain radiographs 
•	Heart and Lungs - CXR, ECG, echocardiogram, CT 
•	Kidneys - renal biopsy (if glomerulonephritis suspected)
•	CNS - MRI scan, lumbar puncture
102
Q

Define systemic sclerosis

A 
•	Rare connective tissue disease characterised by widespread small blood vessel damage and fibrosis in skin and internal organs
•	Also known as scleroderma
•	It is a spectrum of diseases:
o	Pre-Scleroderma
•	Raynaud's phenomenon
•	Nail-fold capillary changes 
•	Antinuclear antibodies 
o	Diffuse Cutaneous Systemic Sclerosis (40%)
•	Raynaud's phenomenon
•	Followed by skin changes with truncal involvement 
•	Tendon friction 
•	Joint contracture 
•	Early lung disease 
•	Heart, GI and renal disease 
•	Nail-fold capillary dilatation
o	Limited Cutaneous Systemic Sclerosis (60%)
•	Previously known as CREST Syndrome because of its FIVE characteristic features:
	Calcinosis 
	Raynaud's phenomenon
	(O)esophageal dysmotility
	Sclerodactyly
	Telangiectasia
o	Scleroderma sine Scleroderma
•	Internal organ disease with NO skin changes
103
Q

Explain the aetiology/risk factors of systemic sclerosis

A

• UNKNOWN
• Genetic and environmental factors
• Pathogenesis is unclear
• Activated monocytes, macrophages and lymphocytes may interact with:
o Endothelial cells –> endothelial cell damage, platelet activation, narrowing of blood vessels
o Fibroblasts –> lay down collagen in the dermis

104
Q

Summarise the epidemiology of systemic sclerosis

A
  • Age of onset: 30-60 yrs

* 3 x more common in FEMALES

105
Q

Recognise the presenting symptoms and signs of systemic sclerosis

A
  • Skin - Raynaud’s phenomenon
  • Hands

o Initially swollen painful fingers
o Later, they become thickened, tight, shiny and bound to underlying structures
o Changes in pigmentation
o Finger ulcers
• Face
o Microstomia (puckering of the skin around the mouth)

o Telangiectasia
• Lung - pulmonary fibrosis —> pulmonary hypertension
• Heart - pericarditis or pericardial effusion, myocardial fibrosis, heart failure, arrhythmias
• GI - dry mouth, oesophageal dysmotility, reflux oesophagitis, gastric paresis
• Kidneys - hypertensive renal crisis, chronic renal failure
• Neuromuscular - trigeminal neuralgia, muscular wasting, weakness
• Others - hypothyroidism, impotence

106
Q

Identify appropriate investigations for systemic sclerosis

A

• Autoantibodies
o Antinuclear
o Anti-centromere (70% of limited cutaneous systemic sclerosis cases)
o Anti-topoisomerase II (anti-Scl-70) - 30% of diffuse cutaneous systemic sclerosis cases
o Anti-nucleolar
o Anti-RNA polymerase
• Lungs - CXR, pulmonary function tests, CT scan
• Heart - ECG, echocardiography
• GI - endoscopy, barium studies
• Kidneys - U&Es, creatinine clearance
• Neuromuscular - electromyography, biopsy
• Joints - radiography
• Skin - biopsy (rarely needed)

107
Q

Define vasculitis

A 
o	Primary vasculitides are classified based on the MAIN VESSEL SIZE affected:
•	LARGE
	Giant cell arteritis 
	Takayasu's aortitis 
•	MEDIUM
	Polyarteritis nodosa
	Kawasaki's disease 
•	SMALL
	Churg-Strauss syndrome 
	Microscopic polyangiitis 
	Wegner's granulomatosis 
	Henoch-Schonlein purpura
	Mixed essential cryoglobulinaemia (MEC)
	Relapsing polychondritis
108
Q

Explain the aetiology/risk factors of vasculitides

A

• UNKNOWN
• Suggested autoimmune origin
• Immune complex deposition in the walls of blood vessels leads to inflammation
• Risk Factors
o Hepatitis B - polyarteritis nodosa
o Hepatitis C - mixed essential cryoglobulinaemia
o pANCA - microscopic polyangiitis + Churg-Strauss
o c-ANCA - Wegner’s granulomatosis

109
Q

Summarise the epidemiology of vasculitides

A
  • RARE

* Takayasu’s arteritis is most common in JAPANESE FEMALES

110
Q

Recognise the presenting symptoms and signs of vasculitides

A

Large vessel vasculitides have classic clinical patterns based on the vessels affected (e.g. GCA and loss of vision/headache)
Medium and small vessel vasculitides are characterised by multiorgan involvement and have less specific clinical features
• Possible Features of ALL Vasculitides
o General: fever, malaise, night sweats, weight loss
o Skin: rash
o Joint: arthralgia, arthritis
o GI: abdominal pain, haemorrhage, diarrhoea
o Kidneys: glomerulonephritis, renal failure
o Lungs: dyspnoea, cough ,chest pain, haemoptysis, haemorrhage
o CVS: pericarditis, coronary arteritis, myocarditis
o CNS: mononeuritis multiplex, infarctions
o Eyes: retinal haemorrhage, cotton wool spots
• Features Characteristics of Specific Vasculitides
o GCA: loss of vision, jaw claudication, headache, scalp tenderness

o Polyarteritis Nodosa: microaneurysms, thrombosis, infarctions, hypertension, testicular pain
o Henoch-Schonlein Purpura: purpura, arthritis, gut symptoms, glomerulonephritis, IgA deposition

o Wegner’s Granulomatosis: granulomatous vasculitis of upper and lower respiratory tract, nasal discharge, ulceration and deformity, haemoptysis, sinusitis, glomerulonephritis, saddle nose

111
Q

Identify appropriate investigations for vasculitides

A

• Bloods
o FBC - normocytic anaemia, high platelets, high neutrophils
o High ESR/CRP
• Autoantibodies - e.g. cANCA in Wegner’s
• Urine - haematuria, proteinuria, red cell casts (if glomerulonephritis)
• CXR - diffuse, nodular or flitting shadows, atelectasis
• Biopsy - renal, lung, temporal artery (in GCA)
• Angiography - to identify aneurysms (in PAN

112
Q

Define carpal tunnel syndrome

A

• Carpal tunnel syndrome refers to the symptom complex brought on by compression of the median nerve in the carpal tunnel

113
Q

Explain the aetiology/risk factors of carpal tunnel syndrome

A

• Symptoms are caused by compression of the median nerve as it runs through the carpal tunnel
• Usually IDIOPATHIC
• May be SECONDARY to:
o Tenosynovitis (e.g. in rheumatoid arthritis)
o Infiltrative diseases of the canal/increased soft tissue (e.g. amyloidosis, acromegaly)
o Bone involvement in the wrist (e.g. osteoarthritis, fracture)
o Fluid retention states (e.g. pregnancy, nephrotic syndrome)
o Other (e.g. obesity , menopause, diabetes)

114
Q

Summarise the epidemiology of carpal tunnel syndrome

A
  • Prevalence: 2.7%

* Lifetime risk of 10%

115
Q

Recognise the presenting symptoms of carpal tunnel syndrome

A
  • Tingling and pain in the hand and fingers

* Weakness and clumsiness of the hand

116
Q

Recognise the signs of carpal tunnel syndrome on physical examination

A
  • Sensory impairment in the median nerve distribution
  • Weakness and wasting of thenar eminence
  • Tinel’s Sign - tapping the carpal tunnel causes symptoms
  • Phalen’s Test - flexion of the wrist for 1 min may cause symptoms

• Look out for signs of the underlying cause (e.g. acromegaly, hypothyroidism)

117
Q

Identify appropriate investigations for carpal tunnel syndrome

A

• Bloods
o TFTs
o ESR
• Nerve Conduction Study (not usually necessary)
o Shows impaired median nerve conduction across the carpal tunnel

Year 3 ICSM 2 (16 decks)

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