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MSK > Red PTS STUFF > Flashcards

Red PTS STUFF Flashcards

1
Q

What is Polymyalgia rheumatica

A

common systemic inflammatory disease that is one of the most common indications for long-term steroids. It is characterised by myalgia and muscles stiffness with preponderance to the neck, shoulder and pelvic girdle.

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2
Q

Who is affected by polymyalgia rheumatica

A

PMR is predominantly a disease of older adults and rarely presents before 50 years old. The peak prevalence is estimated between 70-80 years. Women are 2-3 times more likely to be affected than men.

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3
Q

Aetiology of PMR

A

there appears to be a pro-inflammatory response with elevated levels of IL-6, an increase in certain T-cell subsets and subclinical arterial inflammation in some patients.

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4
Q

Genetic and environmental factors for aetiology of PMR

A

Genetic: PMR, like GCA, has been associated with several human leucocyte antigen (HLA) alleles (e.g. HLA-DR4).

Environmental: the cyclical pattern of cases and peak incidence in winter months suggests an infectious trigger.

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5
Q

Predominant sites of inflammation for PMR

A

proximal articular and periarticular structures.

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6
Q

Pathophysiology of PMR

A

predominant site of inflammation includes bursae and tendons. Bursae are fluid-filled sacs that counteract the friction associated with tendons.

Despite the site of inflammation, patients still present with generalised muscle stiffness and pain, particularly in the shoulder and pelvic girdles.

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7
Q

Characteristic sites in the upper and lower extremities associated with PMR:

A

Shoulder girdle: subdeltoid/subacromial bursitis and biceps tenosynovitis.

Pelvic girdle: bursae around the greater trochanters and ischial processes. liopectineal and iliopsoas bursitis. Hamstring tendinitis and hip synovitis.

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8
Q

Symptoms of PMR

A

Bilateral shoulder and/or hip girdle pain
Stiffness and upper limb tenderness: particularly mornings
Systemic features: low-grade fever, fatigue, weight loss
Low mood
Peripheral symptoms

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9
Q

Signs of PMR

A

Reduced range of movement: shoulder, cervical spine, and hips
Inability to abduct shoulders past 90º
Synovitis and swelling
Motor exam:

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10
Q

GCA and PMR

A

10% of patients with PMR will develop GCA. Therefore, it is essential to assess for features of GCA including unilateral headache, visual changes, jaw claudication, temporal artery tenderness, scalp pain and constitutional symptoms.

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11
Q

Diagnosis of PMR

A

Age: 50 years or older at disease onset
Typical symptoms: bilateral, symmetrical shoulder and/or hip girdle pain associated with stiffness
Duration: > 2 weeks and lasting > 45 minutes at a time
Elevated inflammatory markers (ESR/CRP): supportive, but diagnosis can be made if normal
Rapid resolution of symptoms with corticosteroids: patient-reported global improvement of 70% or more within a week

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12
Q

Atypical features

A

Younger age of onset
Significant weight loss
Night pain
Neurological findings
Absence of core symptoms
Normal, or markedly elevated, inflammatory markers
Chronic onset

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13
Q

Investigations

A

FBC
UE
LFT
Autoimmune screen
Chest and shoulder x ray

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14
Q

Management of PMR

A

Start on oral prednisolone 15mg daily
After initiation - prednisolone should be reduced once symptoms are fully controlled - usually after a period of 3-4 weeks

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15
Q

Steroid - related complications

A

teroid-induced hyperglycaemia, mood changes, insomnia, gastrointestinal bleeding, immunosuppression, weight gain, cushingoid appearance, osteoporosis and adrenal cortex suppression.

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16
Q

Prognosis of PMR

A

Up to 45% of patients may not respond to steroids within the first 3-4 weeks of treatment and a more extended course of steroids may be needed.

Thankfully, there is no increased mortality associated with PMR, but relapse is common and patients may develop morbidity associated with side-effects from corticosteroids.

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17
Q

What is Pagets?

A

A chronic bone disorder that is characterised by focal areas of increased bone remodelling, resulting in overgrowth of poorly organised bone.

Also known as osteitis deformans.

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18
Q

Epidemiology of Pagets

A
  • Typically affects older people (rare in under-40s)
  • Commoner in temperate climates and anglo-saxons
  • UK has highest prevalence in the world
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19
Q

Aetiology of Pagets

A
  • Can be triggered by infections e.g. measles virus
  • Linked to genetic mutations e.g. SQSTM1
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20
Q

RF for Pagets

A
  • Family history
  • Age >50 years
  • Infection
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21
Q

Pathophysiology of Pagets

A
  • Phase 1 - lytic phase
    • Osteoclasts which have up to 100 nuclei aggressively demineralise the bone (x20 more than normal).
  • Phase 2 - mixed phase (lytic and blastic)
    • Blastic phase - rapid, disorganised proliferation of new bone tissue by a large number of osteoblasts. Collagen deposited in a haphazard way.
  • Phase 3 - sclerotic phase
    • New bone formation exceeds bone resorption. The bone is structurally disorganised and weak.
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22
Q

clinical manifestations of Pagets

A

Pain
Hearing loss
VIsion loss
Kyphosis - curved spine
Pelvic assymetry
Bowlegs

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23
Q

Investigation for Pagets

A

Biochemisty - ALP elevated, calcium and phosphate normal
X- ray - bone enlargement and deformity,
Bone biopsy

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24
Q

Management for Pagets

A
  • Pain relief
    • NSAIDs
  • Anti-resorptive medication - Biphosphonates e.g. alendronic acid
    • Along with calcium and vit D supplementation
  • Surgery -
    • Correct bone deformities
    • Decompress impinged nerve
    • Decrease fracture risk
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25
Q

Monitoring Pagets

A

Check the serum alkaline phosphatase (ALP) and review symptoms. Effective treatment should normalise the ALP and eliminate symptoms.

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26
Q

Complications for Pagets

A

Paget’s sarcoma (osteosarcoma)
Spinal stenosis and spinal cord compression
- Fractures
- Vision loss
- Hearing loss
- Arthritis - if any joint involvement

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27
Q

Definition of osteomalacia

A

Osteomalacia is a metabolic bone disease characterised by incomplete mineralisation of the underlying mature organic bone matrix (osteoid) following growth plate closure in adults.

This results in softening of the bones.
Results in rickets in children and osteomalacia in adults

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28
Q

Epidemiology of osteomalacia

A
  • In the developed world, it is estimated that 40% of individuals over the age of 50 years are vitamin D deficient; this is the most common cause of osteomalacia.
  • Fortification of foods with vitamin D and the use of vitamin supplements has greatly reduced the incidence of osteomalacia in the Western world.
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29
Q

Aetiology of osteomalacia

A
  • Vitamin D
  • Calcium
  • Phosphate
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30
Q

RFs for osteomalacia

A
  • Limited exposure to sunlight
  • Dark skin
  • Dietary vitamin D deficiency
    CKD
    Vit D resistance
    Liver dysfunction
    Malabsorption
    Tumour induced
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31
Q

Vit D activation

A

itamin D requires activation by the liver (25-hydroxylation) and then by the kidney (1-alpha-hydroxylation/ calcitriol). Active vitamin D raises serum calcium and phosphate by increasing intestinal absorption, as well as resorption from the bone and kidney. These electrolytes then contribute to bone mineralisation.

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32
Q

What does parathyroid hormone do

A

Stimulates resorption of Ca2+ and phosphate from bone, increases Ca2+ reabsorbtion and phosphate excretion from kidneys and also boosts 1-alpha-hydroxylase activity causing increased levels of vit D.

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33
Q

Pathophysiology of osteomalacia

A

Osteomalacia is primarily caused byvitamin D deficiencywhich can be due to reduced sunlight exposure, poor nutrition, malabsorption, liver failure, and renal failure. Occasionally osteomalacia can be caused by hypophosphataemia due to inborn errors in metabolism.

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34
Q

Signs of osteomalacia

A

Osteomalacia is primarily caused byvitamin D deficiencywhich can be due to reduced sunlight exposure, poor nutrition, malabsorption, liver failure, and renal failure. Occasionally osteomalacia can be caused by hypophosphataemia due to inborn errors in metabolism.

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35
Q

Symptoms of osteomalacia

A
  • Generalised bone pain: rib, hip, pelvis, thigh and foot pain are typical
  • Proximal muscle weakness
  • Difficulty walking upstairs
  • Muscle spasms and numbness due to hypocalcaemia
  • Fracture: often secondary to mild trauma, most commonly affecting the long bones
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36
Q

Primary investigation for osteomalacia

A

Serum calcium and phosphate
Serum 25-hydroxy vitamin D
pth LEVEL
Serum ALP

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37
Q

GS investigation for osteomalacia

A

Iliac bone biopsy with double tetracycline labelling

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38
Q

DD for osteomalacia

A
  • Osteoporosis
  • Paget’s disease
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39
Q

tREATMENT OF OSTEOMALACIA

A

Treat underlying cause
Calcium D3 given if dietary insufficiency

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40
Q

If there is malabsorption or hepatic disease what do you do?

A

itamin D2 (ergocalciferol) or IM calcitriol. If renal disease of vitamin D resistance, then give alfacalcidol or calcitriol

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41
Q

Monitoring osteomalacia

A

Monitor plasma Ca2+, initially weekly, and nausea and vomiting.

42
Q

Consequences of osteomalacia

A
  • Insufficiency fracture
  • Complications of treatment:hypercalcaemia, hyperphosphataemia
  • Secondary hyperparathyroidism
43
Q

Prognosis of osteomalacia

A

The prognosis of patients with osteomalacia is generally very good but is dependent on the underlying cause.

Rickets and osteomalacia normally respond rapidly to vitamin D replacement, which manifests as increased mobility and muscle strength

44
Q

What is Ehlers-Danlos Syndrome

A

group of connective tissue disorders caused by mutations of connective tissue proteins, with collagen being the most commonly affected.

45
Q

Rf for EDS

A

fAMILY HISTORY - AUTOSOMAL dominant is the most common subytype

46
Q

What does EDS lead to

A

eakened connective tissue in the skin, bones, blood vessels, and organs, which accounts for the numerous features of the disorder.

47
Q

Classical Ehlers-Danlos syndrome

A
  • Classical Ehlers-Danlos syndrome
    • Caused by mutation in COL5A1 and COL5A2 genes
    • Passed on by autosomal dominant inheritance
48
Q

Vascular Ehlers-Danlos syndrome

A
  • Mutation in COL3A1
  • Decrease in type III collagen weakens blood vessels
  • Most dangerous due to risk of aneurysms and aortic and organ rupture
49
Q

Autosomal recessive EDS

A
  • Classical-like Ehlers-Danlos Syndrome
    • Mutation in gene that encodes TNXB (causes defect in protein called tenascin X)
      • Tenascin-X provides flexibility and also plays a role in regulating production and assembly of certain types of collagen
  • Kyphoscoliotic Ehlers-Danlos syndrome
    • Insufficient lysyl hydroxylase
  • Musculocontractural Ehlers-Danlos syndrome
    • Defect in collagen peptidase
50
Q

Clinical manifestations of EDS

A

Musculoskeletal

  • Joint hypermobility and pain
  • Recurrent dislocation
  • Scoliosis and spinal pain

Skin

  • Hyperelasticity
  • Easy bruising
  • Atrophic skin
51
Q

Investigations

A
  • Examine joints and skin
  • Genetic testing to identify mutation
  • Echocardiogram:assess for mitral valve prolapse and aortic root dilatation
  • Spine X-ray:evidence of scoliosis or spondylolisthesis (vertebral misalignment); usually required in patients with spinal pain or scoliosis on examination
52
Q

Management for EDS

A
  • Physiotherapy
  • Orthopaedic instrument e.g. bracing, wheelchair and casting
  • Lifestyle advice: avoid contact sports and heavy labour to reduce the risk of tissue damage and joint dislocation
  • Analgesia
  • Psychological input: due to chronic pain and the impact on quality of life, patients may develop mental illness
53
Q

Complications

A

Mitral valve prolapse: mid-systolic click and late-systolic murmur

Aortic dissection

Abdominal aortic aneurysms

Organ rupture
Subarachnoid haemorrhage

Angioid retinal streaks

Abdominal hernia

Gastro-oesophageal reflux disease

Degenerative arthritis due to recurrent joint dislocation

Depression and anxiety

54
Q

What is Marfans syndrome

A

genetic disorder that results in defective connective tissue. This can affect the skeleton, heart, blood vessels, eyes and lungs.

55
Q

What is Marfans Syndrome

A

A genetic disorder that results in defective connective tissue. This can affect the skeleton, heart, blood vessels, eyes and lungs. aq

56
Q

Epidemiology of Marfans

A

he incidence in the European population is estimated to be 3 in 10,000.

57
Q

Pathophysiology if Marfan’s

A

Marfan syndrome is caused by mutations in a gene called FBN1 (fibrillin 1) on chromosome 15. This is autosomal dominant.

BN1 gene encodes fibrillin 1 protein. In Marfan syndrome, fibrillin 1 is either dysfunctional or less abundant, which results in fewer functional microfibrils. This also means there is less tissue integrity and elasticity.

Additionally, TGF-beta doesnt get successfully sequestered so TGF-beta signalling is excessive in these tissues = more growth

58
Q

Clinical features of Marfans

A

Features might not always be there
- Tall stature, long arms and long legs due to excessive long bone growth
- Arachnodactyly - long fingers and toes
- Pectus excavatum (chest sinks in) or pectus carinatum (chest points out)
- Scoliosis
- Inability to extend elbows to 180 degrees
- Flexible joints (hypermobility)
- Downward slant of the eyes
- Narrow high-arch palate - crowds teeth
- Stretch marks

59
Q

Investigations for Marfans

A

Diagnosis is based on clinical features (diagnose if >2 features)

  • Lens dislocation
  • Aortic dissection/ dilation
  • Dural ectasia - widening of the dural sac
  • Skeletal features e.g. long arms, arachnodactyly
  • Pectus deformity
  • Scoliosis
  • Pes planus - flat feet
    MRI
60
Q

DDs of MARFANS

A
  • Ehlers-Danlos syndrome
  • Erdheim’s deformity - presents with dilation of aortic root
  • Homocystinuria - body cannot process amino acids properly. Presents similar to Marfan syndrome
61
Q

General Management for Marfans

A
  • Physiotherapy can be helpful in strengthening joints and reducing symptoms arising from hypermobility.
  • Genetic counselling is important in considering the implications of having children that may be affected by the condition
62
Q

Eye and CVD related management for Marfans

A

Eye-related

  • Replacement of dislocated lens with artificial lens

Cardiovascular-related

  • Lifestyle changes, such as avoiding intense exercise and avoiding caffeine and other stimulants - minimise stress to help cardiac complications
  • Beta blockers can also be used to stop aortic dilation
  • Angiotensin receptor blocker e.g. losartan - decreases tgf-beta signalling and can also decrease aortic dilation
  • Surgical repair of wide aorta.
63
Q

Complications for Marfans

A
  • Retinal detachment and lens dislocation
  • Joint dislocations and pain due to hypermobility
  • Bulla formation on lungs - leading to pneumothorax
  • Cardiovascular:
    • Aortic dilation causing aortic valve insufficiency
    • Cystic medial necrosis (tunica media of aortic wall degenerates)
    • Increased risk of aortic dissection, aneurysm and rupture
    • Mitral valve prolapse
    • Aortic valve prolapse
64
Q

Prognosis of Marfans

A

The average life expectancy used to be only 32 years but, due to early surgery, it is now approaching that of the general population.

Long-term survival is excellent with beta-blocker control and surgery when indicated. **Once aortic dissection occurs, survival is considerably reduced to between 50% and 70% at 5 years.

65
Q

What do we mean by mechanical

A

Mechanical means that the source of the pain may be in your spinal joints, discs, vertebrae, or soft tissues.

66
Q

Epidemiology of mechanical back pain

A

Common in young people: 20-55 years

67
Q

Aetiology of mechanical back pain

A
  • Strain
  • Heavy manual handling
  • Stooping and twisting whilst lifting
  • Pregnancy
  • Trauma
  • Lumbar disc prolapse
  • Spondylolisthesis (one vertebrae slips out of place causing back pain)
  • Osteoarthritis
  • Fractures
  • Exposure to whole body vibration
68
Q

RF for mechanical back pain

A
  • Female
  • Increasing age
  • Pre-existing chronic widespread pain - fibromyalgia
  • Psychosocial factors e.g. high levels of psychological distress, poor self-rated health, smoking and dissatisfaction with work
69
Q

Physiology of mechanical back pain

A

Spinal movement occurs at the disc and the posterior facet joints - stability is normally achieved by a complex mechanism of spinal ligaments and muscles. Any of these structures may be a source of pain.

70
Q

Where do the main lesions occur

A

in an intervertebral disc - a fibrous structure whose tough capsule inserts into the the rime of the adjacent vertebra. This capsule encloses a fibrous outer zone and a gel-like inner zone

Disc allows rotation and bending

71
Q

When do changes in discs start?

A
  • occasionally start in teenage years or early twenties and often increase with age
  • The gel changes chemically, breaks up, shrinks and loses its compliance
  • The surrounding fibrous zone develop circumferential or radial issues
72
Q

What happens when discs become thinner and less compliant

A
  • These changes cause circumferential bulging of the intervertebral ligaments
  • Reactive changes develop in adjacent vertebrae; the bone becomes sclerotic and osteophytes form around the rim of the vertebra
73
Q

Most common site for lumbar spondylosis

A

L5/S1 & L4/L5

74
Q

Spondylosis (mostly symptomless) but can cause

A
  • Episodic spinal pain
  • Progressive spinal stiffening
  • Facet joint pain
  • Acute disc prolapse, with or without nerve irritation
  • Spinal stenosis
75
Q

Facet Joint Syndrome

A
  • Lumbar spondylosis causes secondary osteoarthritis of the misaligned facet joints
  • Pain is typically worse on bending backwards and when straightening from flexion - it is lumbar in site, unilateral or bilateral and radiates to the buttock
  • Facet joints are well seen on MRI and may show osteoarthritis, an effusion or a ganglion cyst
    • Treatment consists of direct corticosteroid injections under imaging
    • Physiotherapy and help to reduce weight may also be offered
76
Q

Fibrositic nodulosis

A
  • There are tender nodules in the upper buttock and along the iliac crest
  • This condition causes unilateral or bilateral lower back and buttock pain
    • Local intralesional corticosteroid injections may help
77
Q

Clinical manifestations of mechanical lower back pain

A

Stiff back
Scoliosis
Muscular spasm
Pain worse in the evening

78
Q

Investigations for mechanical lower back pain

A
  • MRI - imagine modality of choice. Can see disc prolapse, cord compression, cancer, infection or inflammation.
  • Bone scans
  • Examine patient to exclude pathologies e.g. nerve root lesions affecting reflexes
  • Spinal X-rays
79
Q

Differential diagnossi for mechanical lower back pain

A
  • Polymyalgia rheumatica (PMR): in elderly, ESR and CRP will distinguish this from mechanical back pain
  • Sinister causes of back pain e.g. malignancy, infection or inflammatory causes. Must be excluded with spinal x-ray.
80
Q

Management for mechanical lower back pain

A

Analgesics - NSAIDs paracetamol, codeine
Acupuncture
Avoid excessive rest
Comfortable sleeping postions

81
Q

What is intervertebral disc disease?

A

common condition characterised by the breakdown (degeneration) of one or more of the discs that separate the bones of the spine (vertebrae), causing pain in the back or neck and frequently in the legs and arms.

82
Q

Which discs are most commonly affected

A

Discs in the lower lumbar spine

83
Q

What is acute disc diseae

A

Progressive intervertebral disc breakdown leading to prolapse of the intervertebral disc resulting in acute back pain (lumbago)

84
Q

Epidemiology of Acute disc disease

A
  • Disease of younger people (20-40 yrs) - the disc degenerates with age
    and in the elderly it is no longer able to prolapse
    • In older patients, sciatica is more likely to result (as opposed to prolapse) - due to compression of the nerve root by osteophytes in the lateral recess of
      the spinal canal
85
Q

Aetiology of Acute disc disease

A
  • Accumulation of natural stress, minor injury throughout life
  • Genetic predisposition
86
Q

RF for acute disc disease

A

– Genetic predisposition
- Advanced age
- Menopause
- Repeated spinal trauma

87
Q

Pathophysiology of acute disc disease

A

Intervertebral disc’s nucleus pulposus (mostly water) dehydration → decreased proteoglycan and collagen → decreased padding between vertebrae → unable to absorb shock → disc collapse → annular tears, herniation of disc contents into spinal canal → nerve impingement → pain

88
Q

Clinical manifestations acute disc injury

A
  • Sudden onset of severe back pain - often following a strenuous activity
  • Decreased range of motion
  • Tingling, paresthesia and numbness
  • Muscle weakness and atrophy
  • Muscle spasm leads to a sideways tilt when standing
  • Decreased tendon reflexes
  • The radiation of the pain and the clinical findings depend on the disc
    affected - the lower three disks are more commonly affected
89
Q

Investigation of acute disc

A
  • X-rays are often normal - can detect fracture
  • MRI
    • Evaluates spinal canal
    • Detects annular tears
    • Increased signal may indicate disc dehydration
    • If surgery is being considered
90
Q

Management for acute disc disease

A

Bed rest on firm mattress
Analgesics - NSAIDs
Surgery only for severe or increasing neurological impairment
- Nerve root injection
- Corpectomy

91
Q

Complications of Acute Disc disease

A
  • Spine collapse
  • Disc herniation
  • Compression fracture
  • Bony spur growth
  • Neurological deficit
  • Myelopathy
  • Vertebral artery compression
92
Q

Chronic Disc Disease definition

A

Associated with degenerative changes in the lower lumbar discs and facet joints (joining the vertebral bones together)

93
Q

Clinical manifestations of chronic disc disease

A
  • Pain is usually of the mechanical type i.e. aggravated by movement
  • Sciatic radiation may occur with pain in the buttocks radiating into the posterior
    thigh
  • Usually the pain is long-standing and there is no cure
94
Q

Management of Chronic disc disease

A
  • NSAIDs, physiotherapy and weight reduction can be useful
  • Surgery can be done when pain arises from a single identifiable level -
    fusion at this level with decompression of the affected nerve roots
95
Q

Cervical spondylosis definition

A

Osteoarthritis of the spine, which includes the spontaneous degeneration of either disc or facet joints.

96
Q

Pathophysiology of cervical spondylosis

A

Degeneration of annulus fibrosus (the tough outer coating of the intervertebral discs), combined with osteophyte formation on the adjacent vertebra leads to narrowing of the spinal canal and intervertebral foramina.

As the neck flexes and extends, the cord is dragged over these osteophytes and is indented by the thickened ligamentum flavum posteriorly.

97
Q

Signs of cervical spondylosis

A
  • Limited neck movement
  • Neck flexion may produce tingling down spine (Lhermitte’s sign) - does not differentiate between a cord or root issue.
  • Root compression presents with:
    • Pain in arms or fingers at the level of compression, with numbness and dull reflexes
    • Lower motor neuron weakness and wasting of muscles innervated by the affected root
    • Weak clumsy hands
    • Gait disturbance
98
Q

Symptoms of cervical spondylosis

A
  • Neck stiffness
  • Crepitis (crunching) on moving neck
  • Stabbing or dull arm pain
  • Forearm/ wrist pain
99
Q

Investigations of cervical spondylosis

A

MRI

100
Q

Management for cervical spondylosis

A
  • Analgesia
  • Encourage gentle activity
  • Cervical collars for brief painful episodes
  • If no improvement consider:
    • Epidural
    • Surgical decompression

MSK (20 decks)

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