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Vertebral Column > Growth Pathologies of the Vertebral Column > Flashcards

Growth Pathologies of the Vertebral Column Flashcards

1
Q

Where is the most common location for MSK TB?

A

Vertebral column

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2
Q

What is Pott’s disease?

A

Vertebral column TB

2 or more vertebrae affected

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3
Q

What is the average number of vertebrae affected in Pott’s disease? (Reference?)

A

2.6 vertebrae

Hugar et al., 2013

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4
Q

When and by who was spinal TB first reported?

A

5000 years ago

Ancient Egyptians

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5
Q

How much of the world population was affected by TB according to WHO in 1997?

A

More than 1/3

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6
Q

What percentage of TB cases are spinal in HIV- individuals?

A

3-5%

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7
Q

What percentage of TB cases are spinal in HIV+ individuals?

A

60%

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8
Q

Why are more TB cases spinal in HIV+ individuals?

A

Lower CD4+ count

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9
Q

Is spinal TB usually primary TB or secondary to extraspinal TB?

A

Secondary to extraspinal TB

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10
Q

What can spinal TB result in in children?

A

Severe kyphosis due to vertebral body destruction

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11
Q

What is the most common pattern of spinal TB?

A

Spondylodiscitis:

  • > =2 vertebrae
  • Infection spreads anteriorly across disc space
  • Relative sparing of disc space
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12
Q

What are the risk factors for spinal TB?

A 
Poverty
Overcrowding
Malnutrition
Alcoholism
Diabetes
HIV infection
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13
Q

What did Zhang et al., (2010) suggest predisposes an individual to spinal TB?

A

Polymorphism in Vit. D receptor gene:

- Investigated by PCR

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14
Q

What are the sequelae of spinal TB?

A
  1. Destruction of vertebral bodies and IV discs
  2. Formation of abscesses/lesions
  3. Anterior wedging
  4. Functional disability
  5. Spinal cord compression
  6. Back pain
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15
Q

What cells are involved in the pre-pus inflammatory reaction in the spread of TB?

A

Langerhans giant cells
Epitheloid cells
Lymphocytes

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16
Q

What causes a paraspinal abscess in the spread of TB?

A

Tissue necrosis and inflammatory cell breakdown

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17
Q

What are the steps of TB spread to the spine?

A
  1. Haematogenous spread from primary Po./GU infection
  2. Pre-pus inflammatory reaction
  3. Granulation tissue proliferates and vessel thrombosis
  4. TIssue necrosis and inflammatory cell breakdown
  5. Continued necrosis = Kyphosis
  6. Spread to other VBs by longitudinal ligaments
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18
Q

What treatments may be prescribed if spinal TB is confused for other pathologies?

A

Anti-inflammatory drugs
Physical therapy
Posture-correcting corsets

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19
Q

What imaging techniques are used to diagnose spinal TB?

A

CT for guidance
MRI:
- High sensitivity for early diagnosis
- Good for measuring extent of disease and soft tissue involvement

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20
Q

What diagnostic technique is essential for diagnosing spinal TB?

A

Histopathological diagnosis

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21
Q

How are the IV discs involved in spinal TB in children?

A

IV discs are vascularised:

- Infection can spread and start there

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22
Q

How are the IV discs involved in spinal TB in adults?

A

Disc involvement is secondary:

- Via spread from adjacent vertebral body

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23
Q

How can MRI affect prognosis of spinal TB?

A

May aid in early diagnosis and reduce risk of neurological deficits due to compression of surrounding neural structures

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24
Q

When should anti-TB treatment be started for spinal TB?

A

Immediately

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25
Q

What is the drug treatment protocol for TB?

A 
Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
All four for 2 months
Then rifampicin and isoniazid for minimum of 4-8 months
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26
Q

What does early use of anti-TB drugs reduce the risk of?

A

Neurological deficits

Paraplegia

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27
Q

What happens in drug-resistant spinal TB?

A

Surgery is only option for cure

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28
Q

What surgical procedures can be used for spinal TB?

A 
Screw insertion to correct deformity
Bone grafts (spinal fusion)
Abscess draining with needles
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29
Q

How is the correct area of spinal TB identified prior to surgery?

A

MRI

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30
Q

What surgical approaches can be used for spinal TB?

A

Anterior
Posterior
Combined

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31
Q

What are the risk of surgery for spinal TB?

A

Secondary post-op deformity if:

  • Incorrect fixation
  • Fusion of unsuitable segments
  • Poor balance
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32
Q

What are the potential positive outcomes of spinal TB?

A

Relieves spinal nerve compression
Regaining spinal stability
Correcting spinal deformity
Eliminating sites of TB

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33
Q

What is a reference for surgery for spinal TB?

A

Long et al., 2015

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34
Q

Regarding anti-TB drugs and surgery for spinal TB, what did Rasouli et al., (2012) find?

A

6-9 months drug therapy plus surgery is equivalent to 18 months drug therapy
4-6 weeks of drug therapy = Pain and symptom improvement
Combined approach (drugs and surgery) is best
CT often used for needle guidance

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35
Q

What is Scheuermann’s Disease characterised by?

A

Juvenile thoracic kyphosis

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36
Q

When does Scheuermann’s Disease develop?

A

Prior to puberty

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37
Q

When does Scheuermann’s Disease become more pronounced?

A

During adolescent growth spurt (aged 10-16 years)

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38
Q

What type of kyphosis does Scheuermann’s Disease cause?

A

Primary kyphosis:

  • Concave anteriorly
  • Convex posteriorly
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39
Q

In what ages is Scheuermann’s Disease most common?

A

12-15 years

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40
Q

What is the prevalence of Scheuermann’s Disease?

A

0.4-8.3%

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41
Q

What are the typical locations of Scheuermann’s Disease?

A

Mid-thoracic
Lower thoracic
Thoracolumbar junction

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42
Q

What is atypical Scheuermann’s Disease?

A

Scheuermann’s Disease in the lumbar spine

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43
Q

Are there variations in sex and geographical location for Scheuermann’s Disease?

A

Sex - No

Geographical location - Yes

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44
Q

What is the most common presentation of Scheuermann’s Disease?

A

Painless kyphotic deformity

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45
Q

How do more severe cases of Scheuermann’s Disease present?

A

Painful kyphosis

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46
Q

What can worsen back pain in Scheuermann’s Disease?

A

Physical effort

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47
Q

What compensatory features can be seen in Scheuermann’s Disease?

A

Cervical and lumbar lordosis

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48
Q

Why can cutaneous pigmentation arise in Scheuermann’s Disease?

A

Continual friction at apex of deformity

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49
Q

Where are flexion contractures present in Scheuermann’s Disease?

A

Hip

Shoulder

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50
Q

What muscles can spasm in Scheuermann’s Disease?

A

Hamstrings

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51
Q

How was Scheuermann’s Disease described by Sachs et al., (1987)?

A

Kyphosis >45 degrees

At least 1 wedge-shaped vertebra - Minimum of 5 degrees

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52
Q

What are the six characteristics of Scheuermann’s Disease according to Bezalel and Kalichman, (2015)?

A
  1. Vertebral body wedging
  2. Irregularity in vertebral end plate
  3. Reduced anterior vertebral growth
  4. Schmorl’s nodes
  5. Narrowing of IV disc space
  6. Premature IV disc degeneration
53
Q

What is vertebral body wedging?

A

When ventral height > dorsal height (or vice versa)
Overall decrease in height ventrally
Entire vertebral body can appear flattened

54
Q

What is vertebral body wedging also a key feature of?

55
Q

What are the three broad categories of scoliosis?

A
  1. Idiopathic
  2. Congenital
  3. Neuromuscular
56
Q

What is the most common category of scoliosis?

A

Idiopathic (75-85%)

57
Q

In regards to scoliosis, what is Scheuermann’s Disease a common cause of?

A

Hyperkyphosis following idiopathic scoliosis

58
Q

What is premature IV disc degeneration in Scheuermann’s Disease linked to?

A

Slow loss of water in nucleus pulposus
Reduced proteoglycan content
Increased keratin sulfate to chondroitin sulfate ratio

59
Q

In regards to IV disc degeneration in Scheuermann’s Disease, what did Paajanin et al., (1989) find?

A

55%+ of IV discs were degenerate in 20 year old Scheuermann’s Disease patients (5x more than the asymptomatic group)
(MRI study)

60
Q

What are the two components of the vertebral endplate?

A

Cartilaginous

Bony

61
Q

What do the vertebral endplates predispose to and why?

A

Mechanical failure:

- Weakest part of disc and vertebral body interface

62
Q

What is the function of the vertebral endplate?

A

Physical shield between IV disc and adjacent VBs
IV disc nutrient supply:
- Capillaries from vertebral arteries through endplate

63
Q

What are the sequelae of vertebral endplate irregularities?

A

Reduced nutrients reaching IV disc

64
Q

What can end plate irregularities mimic?

A

Multiple compression fractures

65
Q

How does reduced anterior vertebral growth occur in Scheuermann’s Disease?

A

Increased stress on anterior part of growth plate
Greater weight = Greater compressive force
Uneven force distribution:
- Faster growth in posterior column

66
Q

How are mild cases of Scheuermann’s Disease managed?

A

Left alone

67
Q

What sports must be avoided in Scheuermann’s Disease?

A

Those involving excessive spinal load bearing:

  • Rugby
  • Weightlifting
68
Q

The first line treatment of Scheuermann’s Disease is rehabilitation. What are the aims of this?

A

Relieve pain
Improve sagittal balance:
- Re-establish posture
- Promote muscle balances

69
Q

What are the gold standard methods of rehabilitation of Scheuermann’s Disease?

A

Physiotherapy

Bracing

70
Q

What are the purposes of exercise techniques in the treatment of Scheuermann’s Disease?

A

Strengthen and stretch the trunk
Postural control
Musculotendinous stretching

71
Q

The second line treatment of Scheuermann’s Disease is orthopaedics. In what regions is it most effective?

A

Lower thoracic

Lumbar

72
Q

What are the purposes of orthopaedics in Scheuermann’s Disease?

A

Reduce pressure on anterior endplate
Reduce pain
Reduce coronal deviation
Limit rotation

73
Q

What does a static brace do?

A

Provides constant pressure

It is rigid

74
Q

What does a dynamic brace do?

A

Movement opposes spinal movement using flexible bands

75
Q

How often do braces need worn in Scheuermann’s Disease?

A

Depends on severity
Can be:
- Full time
- At intervals

76
Q

What does the selection of a brace in Scheuermann’s Disease depend on?

A

Location of curve
Severity of curve
Patient cooperation

77
Q

What is surgery reserved for in Scheuermann’s Disease?

A

Severe kyphosis (>70 degrees)

78
Q

What is the surgical procedure for Scheuermann’s Disease?

A 
Spinal fusion (bony graft) WITH
Instrumentation (metal implants or support)
79
Q

In spinal fusion for Scheuermann’s Disease, where is the fusion carried out?

A

Fusion extends just above and just below kyphosis

80
Q

When is posterior spinal fusion carried out in Scheuermann’s Disease?

A

Curvatures less than 55 degrees

81
Q

What are the complications of surgery for Scheuermann’s Disease?

A

Neurological injury

Infection

82
Q

What diseases is ankylosing spondylitis related to?

A 
Rheumatoid arthritis
Other spondyloarthropathies:
- Reactive arthritis
- Enteropathic arthropathy
- Psoriatic arthritis
83
Q

What is the incidence of ankylosing spondylitis in caucasian populations?

84
Q

In what group is ankylosing spondylitis more common?

85
Q

What are the symptoms of ankylosing spondylitis?

A 
Chronic pain:
- Lower back
- Buttocks
Increased stiffening of spine
As disease progresses:
- Stooped/hunchback posture
- Difficulty expanding chest
86
Q

Why does ankylosing spondylitis cause stooped posture and difficult expanding the chest as it progresses?

A

Fusion affects:

  • Costovertebral joints
  • Costosternal joints
87
Q

How else does ankylosing spondylitis manifest?

A 
Hip/Shoulder arthritis (33.3%)
Peripheral joint arthritis (50%)
Acute anterior uveitis (25-40%)
Aortic regurg (2-10%)
Conducting system disturbances
Secondary amyloidosis
Nerve subluxation and cauda equina
IBD
88
Q

What HLA is ankylosing spondylitis associated with?

89
Q

What is HLA?

A

Proteins derived from HLA complex consisting of 200 genes on chromosome 6
3 classes:
- Class 1 expresses HLA on surface of almost all cells

90
Q

What percentage of ankylosing spondylitis are HLA-B27 negative?

91
Q

What percentage of HLA-B27 positive individuals develop ankylosing spondylitis?

92
Q

Using gene mapping, how many loci are associated with ankylosing spondylitis and what percentage of risk do these contribute?

A

114

Contribute another 7% of risk

93
Q

How can infection result in ankylosing spondylitis?

A

Gut infection if genetically predisposed can cause ankylosing spondylitis

94
Q

What is the molecular mimicry theory?

A

Different HLA-B27 subtypes have small differences in binding sites:
- May allow bacterial protein binding (Chlamydia trachomatis or other arthritogenic bacteria)

95
Q

What subtypes of HLA are affected by the molecular mimicry theory?

A

HLA-B2705
HLA-B2702
HLA-B27*04

96
Q

What does insufficient peptide binding and interaction with chaperone protein of HLA-B27 result in?

A

Misfolding and accumulation in ER

97
Q

What does HLA-B27 misfolding result in?

A

Acute ER stress:

  • Protein degradation and autophagy = Increased expression of XBP1 promotes autophagy in AS lesions
  • Cytokine production = Inflammation
98
Q

What receptors, used by NK and T-cells, are used more in ankylosing spondylitis? What does this receptor do?

A

KIR3DL2:
Binds HLA-B27:
- Expression of RORy
- Th17 proliferation

99
Q

What do abnormal reactions at the KIR3DL2 receptor cause?

A

IL-17 production:

- Promotes inflammation in AS

100
Q

What does inflammation in ankylosing spondylitis begin with?

A

Enthesitis:

- Inflammation of ligament insertion into bone

101
Q

Where is inflammation found in ankylosing spondylitis?

A

IV disc surface
SIJ
Costovertebral joint
Sternum

102
Q

When the inflammation in ankylosing spondylitis moves to subchondral bone, what cells are responsible for the resulting osteitis?

A

Lymphocytes
Plasma cells
Macrophages
Chondrocytes

103
Q

What do the invading cells in ankylosing spondylitis cause?

A

Erosion of cartilage

Erosion of subchondral bone

104
Q

What forms over areas of degradation in ankylosing spondylitis?

A

Fibrous tissue

105
Q

What do remodelling and osteoproliferation result in in ankylosing spondylitis?

A

SIJ:
- Obliteration
- Fusion
Entheses of ligaments to ossify = Hyperostosis

106
Q

When does facet joint fusion in ankylosing spondylitis occur?

A

Before syndesmophyte formation

107
Q

What are the stages of facet joint fusion in ankylosing spondylitis?

A
  1. Reduced joint space (due to inflammation)
  2. Articular cartilage fusion
  3. Bone fusion
108
Q

Where do fibroblasts and osteoblasts accumulate in the facet joints in ankylosing spondylitis?

A

At join borders

109
Q

What causes facet joint articular cartilage degeneration in ankylosing spondylitis?

A

Increased chondrocyte apoptosis

Matrix degeneration

110
Q

What happens once subchondral bone is thinned by osteoblasts in the facet joints in ankylosing spondylitis?

A

Allows fibrous tissue to invade bone marrow

Fibrous tissue replaces 20-30% of subchondral bone

111
Q

What do chondrocytes lose from the matrix in ankylosing spondylitis?

A

Proteoglycan

112
Q

How do syndesmophytes form in ankylosing spondylitis?

A
  1. Inflammation
  2. Build up of granulation tissue where annulus fibrosus meets VB
  3. Remodelling and osteoproliferation
  4. Bony bridge up sides of annulus fibrosus connecting adjacent vertebrae = Syndesmophytes
113
Q

What do syndesmophytes cause?

A

Restrictions of spinal movements

114
Q

What do physiotherapy and exercise improve in ankylosing spondylitis?

A

Posture
Pain
Chest expansion
Lung capacity

115
Q

What is the first line treatment for ankylosing spondylitis if physiotherapy doesn’t work?

116
Q

What is the second line drug treatment for ankylosing spondylitis?

A

TNF antagonists

117
Q

What effects do NSAIDs have in ankylosing spondylitis?

A

Reduce pain

Reduce inflammation

118
Q

What are the side effects of NSAID therapy?

A

10-60% have GI issues

CVS and renal-relted hypertension

119
Q

How do NSAIDs affect disease progression in ankylosing spondylitis?

A

Do not halt it

120
Q

When are TNF antagonists used in ankylosing spondylitis?

A

If NSAIDs fail to relieve symptoms

121
Q

What effect do TNF antagonists have in ankylosing spondylitis?

A

Improve pain and functionality

122
Q

What effect do TNF antagonists have on disease progression of ankylosing spondylitis?

123
Q

Give examples of TNF antagonists?

A

Etanercept

Infliximab

124
Q

What are bisphosphonates used for in ankylosing spondylitis?

A

Osteoporosis

125
Q

Give examples of bisphosphonates?

A

Pamidronate

Alendronic acid

126
Q

What are DMARDs used for in ankylosing spondylitis?

A

To treat peripheral arthritides

127
Q

Do DMARDs treat ankylosing spondylitis?

128
Q

Give examples of DMARDs?

A

Methotrexate
HCQ
Sulfasalazine

Vertebral Column (14 decks)

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