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Vertebral Column > Gross Pathologies of the Vertebral Column > Flashcards

Gross Pathologies of the Vertebral Column Flashcards

1
Q

Describe spinal tuberculosis

A
  • Vertebral column is the most common loaction for musculoskeletal tuberculosis.
  • Spinal TB = Mycobacterium TB
  • Accounts for 11% of extra-pulmonary TB
  • Affects 2 or more adjacent vertebral bodies
  • Average number of vertebrae affected = 2.6
  • Progression of disease is slow
  • Can be associated with HIV:
    • TB in HIV negative patients = 3-5% spinal
    • TB in HIV positive patients = 60% spinal
  • Usually secondary to an extraspinal source of infection
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2
Q

What spinal deformity can be caused by spinal tuberculosis and why?

A
  • Severe kyphosis
  • Due to vertebral body destruction during childhood
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3
Q

Where does spinal tuberculosis most commonly start?

A

Usually begins in anterior spine and surrounding soft tissue structures then proceeds posteriorly.

Relatively sparing of the disc space.

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4
Q

What are the causes of spinal tuberculosis?

A
  • Poverty
  • Overcrowding
  • Malnutrition
  • Alcoholism
  • Diabetes
  • HIV infection
  • Genetic
    • Zhang et al. (2010) found that polymorphism in the vitamin-D receptor gene was related to spinal TB.
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5
Q

List the effects of spinal tuberculosis

A
  • Destruction of vertebral bodies and IV discs
  • Formation of abscesses / lesion
  • Anterior wedging
  • Functional disability
  • Spinal cord compression
  • Back pain
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6
Q

What is stage 1 in the spread of spinal tuberculosis?

A

Hematogenous spread via arterial / venous route from a pulmonary lesion or a genitourinary infection.

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7
Q

What is stage 2 in the spread of spinal tuberculosis?

A

Pre-pus inflammatory reaction with Langerhans giant cells, epitheloid cells and lymphocytes.

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8
Q

What is stage 3 in the spread of spinal tuberculosis?

A

Granulation tissue proliferates, and thrombosis of blood vessels occurs.

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9
Q

What is stage 4 in the spread of spinal tuberculosis?

A

Tissue necrosis and / or breakdown of inflammatory cells = paraspinal abscess. Produces pus.

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10
Q

What is stage 5 in the spread of spinal tuberculosis?

A

Continued necrosis leads to kyphosis.

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11
Q

What is stage 6 in the spread of spinal tuberculosis?

A

Spread to other vertebral bodies via longitudinal ligaments.

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12
Q

What does hematogenous mean?

A

To spread via blood

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13
Q

Describe the process of diagnosis of spinal TB

A
  • Patients are often wrongly prescribed anti-inflammatories and physical therapy.
    • Slow disease progression so difficult to diagnose initially.
  • MRI and CT used for diagnosis.
  • BUT, histopathological diagnosis is ESSENTIAL.
  • Adults and children differ (primary and secondary)
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14
Q

Explain the difference between spinal tuberculosis in adults and spinal tuberculosis in children

A
  • As intervertebral discs are vascularised in children, infection can spread to the discs and start there as a primary infection.
  • In adults, disc involvement is secondary following spread of infection from adjacent vertebrae.
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15
Q

What are the 2 main treatment options for spinal tubrculosis?

A
  • Antituberculosis drugs
  • Surgery
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16
Q

Describe drug treatmnt of spinal tuberculosis

A
  • Chemotherapy remains the gold standard for spinal TB treatment.
  • 3 main treatment drugs:
    • Rifampin
    • Isoniazid
    • Pyrazinamide
  • Early onset chemotherapy can minimise further risks
  • All 3 drugs are typically administered every day for 2 months.
  • Then, switch to only Rifampin and Isoniazid for a minimum of 4-8 months.
  • Potential problems - drug resistance.
17
Q

Describe the surgical treatment of spinal tuberculosis

A
  • Can be anterior, posterior or combined
  • First, use MRI to identify affected area(s)
  • Insertion of screws to correct deformity
  • Bone grafts (spinal fusion)
  • Draining of abscess using needle

Secondary postoperative deformity can develop from incorrect choice of method to fixate the affected area, fusing unsuitable segments or a resultant poor balance following surgery.

18
Q

What are the outcomes of treating spinal TB (one hopes)?

A
  • Relieving spinal nerve compression
  • Regaining spinal stability
  • Correcting spinal deformity
  • Eliminating sites of tuberculosis
19
Q

Describe Scheuermann’s disease

A
  • Characterised by juvenile thoracic kyphosis
  • Usually occurs at 10-16 years
  • Reported prevalence between 0.4 and 8.3%
  • Typically seen at mid-thoracic level, lower thoracic level or at the thoracolumbar junction.
  • No sex difference
  • Geographical variations
  • Common reason for hyperkyphosis following idiopathic scoliosis.
20
Q

Describe the clinical presentation of Scheuermann’s disease

A
  • Painless kyphotic deformity = most common symptom
  • Painful kyphosis = more severe symptoms
  • Compensatory cervical and lumbar lordosis
  • Cutaneous pigmentation
  • Hip and shoulder flexion contractures
  • Hamstring spasm
21
Q

What is a flexion contracture?

A
  • Joint motion limitation
  • Results from muscle shortening / fibrosis
  • Named for the opposite action, so flexion contracture lacks full extension and vice versa.
22
Q

List the pathologies caused by Scheuermann’s disease

A
  • Vertebral body wedging (>5°) - sometimes whole body can appear flattened.
  • Premature degeneration of IV discs - linked to loss of water in nucleus pulposus, proteoglycan content decrease.
  • Vertebral endplate irregularity - main gateway for nutrient supply to IV disc so irregularities = less nutrients reach disc.
  • Schmorl’s nodes
  • Narrowing of space between IV discs
  • Reduced anterior vertebral growth - increased stress on anterior part of growth plate. Greater weight = greater compressive force (also uneven distribution of force).
23
Q

What are the 3 types of treatment for Scheuermann’s disease?

A
  • Rehabilitation
  • Orthopaedic treatment
  • Surgical treatment

Mild cases can be left alone and unmanaged.

Patients should avoid all sports involving excess spinal load bearing.

24
Q

Describe the rehabilitation of patients with Scheuermann’s disease

A
  • Physiotherapy and bracing - gold standard.
  • Exercise techniques include:
    • Strengthening and stretching the trunk
    • Postural control
    • Musculotendinous stretching
25
Q

Describe orthopaedic treatment of Scheuermann’s disease

A
  • Most effective for lower thoracic and lumbar regions
  • 42-92% success in stabilisation (depends on compliance)
  • Reduction of coronal deviating / limiting rotation
  • 2 main types of brace:
    • Static - constant pressure; rigid
    • Dynamic - movement opposes spinal movement; uses flexible bands
26
Q

Describe the surgical treatment of Scheuermann’s disease

A
  • Very uncommon in this disease
  • Only for very severe kyphosis (>70°)
  • Spinal fusion with instrumentation (use of bone graft to joint 2 opposing bony surfaces)
  • Fusion typically extends from just above to just below kyphosis
  • Curves of 55° or less treated with posterior spinal fusion
27
Q

Describe ankylosing spondylitis

A
  • Chronic inflammatory disease related to rheumatoid arthritis and the spondylopathies disease family.
  • Incidence at 0.2-0.8% in Caucasian populations.
  • More common in males than females.
28
Q

What are the symptoms of ankylosing spondylitis?

A
  • Chronic back pain
  • Increased stiffening of the spine
  • Stooped or hunchback posture
  • Difficulty expanding chest
29
Q

What are the conditions which often manifest in conjunction with ankylosing spondylitis (AS)?

A
  • 1/3 of patients will also experience arthritis in the hip or shoulder.
  • 1/2 of patients will also experience peripheral joint synovitis.
  • 25-40% of AS patients will also develop acute anterior uveitis (inflammation of the iris and ciliary body) at some point in their lifetime.
  • 2-10% of AS patients will develop aortic regurgitation caused by weakening heart valves; the valve may need to be replaced.
  • Long life (prolonged AS) increases the risk of conduction system disturbances in the heart. It occurs in 3% of patients who’ve had AS for 15 years and 9% of patients who’ve had it for 30 years. It is corrected by fitting a pacemaker.
  • 2-3% of patients with AS may develop secondary amyloiditis (accumulation of amyloid protein in the kidney).
  • Nerve subluxation and caud equina syndrome.
  • Inflammatory bowel disease (6%).
30
Q

Describe peripheral synovitis

A
  • Inflammation similar to rheumatoid arthritis found in hips, knees, ankles, fingers and toes.
  • Unlike rhumatoid arthritis it affects the joint capsule, enthesis attachments and even bone lining, not just the synovial membrane.
  • Can also affect an entire digit, not just one joint.
31
Q

Describe cauda equina syndrome

A
  • Fibrous tissue constricts the cauda equina and can result in loss of:
    • Continence
    • Sensation to the lower body
    • Motor function to the lower body
32
Q

Which genes are associated with the aetiology of ankylosing spondylitis?

A
  • Human leukocyte antigens (HLA)
    • HLAs are a family of proteins derived from the HLA complex which consists of around 200 genes on chromosome 6.
  • Particularly HLA-B27
33
Q

Describe HLA-B27 misfolding

A
  • Subtypes of HLA-B27 have different binding specificities.
  • Insufficient binding of peptides and interaction with the chaperone protein results in misfolding.
  • Results in endoplasmic reticulum associated protein degradation and autophagy, but also cytokine production which promotes inflammation.
34
Q

What results from abnormal HLA-B27 and KIR3DL2 interaction?

A
  • Cytokine production
  • Helper T cell proliferation
35
Q

Describe sacroiliitis secondary to ankylosing spondylitis

A
  • SI joint is usually the first area affected by AS.
  • Pathology:
    • Inflammation
    • Cartilage and subchondral bone degradation
    • Remodelling and osteoproliferation leading to joint fusion
36
Q

Describe facet joint fusion secondary to ankylosing spondylitis

A
  • Inflammation and joint space narrowing
  • Cartilage and subchondral bone degradation
  • Articular cartilage fusion
  • Remodelling and osteoproliferation - bone fusion
  • Restricted motion

Thought to occur before syndesmophyte formation.

37
Q

Describe syndesmophytes secondary to ankylosing spondylitis

A
  • Inflammation where the vertebrae meets the annulus fibrosus.
  • Syndesmophytes begin as inflammation which leads to a build-up of granulose tissue at the point where the annulus fibrosus meets the vertebral body.
  • Remodelling and osteoproliferation causes bony bridges to form between vertebrae - fibrous tissue forms over the affected area, repairing the lesions.
  • Restricted motion.
38
Q

What are the treatments for ankylosing spondylitis?

A
  • Physiotherapy and exercise
  • Non-steroidal anti-inflammatory drugs
  • Tumour necrosis factor antagonists
  • Bisphosphonates
  • Disease-modifying antirheumatic drugs

Vertebral Column (13 decks)

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