osteoporosis, Spondylolysis, spinal stenosis, excessive thoracic kyphosis, excessive lumbar lordosis and scoliosis., Adolescent idiopathic scoliosis, back strains, sprains and spasms, Flashcards

1
Q

What is osteoporosis, and how is it characterized in terms of bone density and porosity?

A

Osteoporosis is a quantitative bone defect characterized by reduced bone mineral density and increased porosity.

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2
Q

What are the differences between Type I and Type II osteoporosis in terms of onset, risk factors, and associated fractures?

A

Type I osteoporosis involves exacerbated bone loss post-menopause, influenced by early menopause, familial factors, and environmental risks. It often leads to Colles fractures and vertebral insufficiency fractures. Type II osteoporosis occurs in old age with a significant decline in bone density, and factors like chronic diseases, inactivity, and reduced sunlight exposure contribute. This type is associated with femoral neck and vertebral fractures.

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3
Q

Name the various secondary causes of osteoporosis.

A

Secondary causes of osteoporosis include drugs (corticosteroids, aromatase inhibitors), alcohol abuse, malnutrition, GI disorders, chronic diseases (CKD, malignancy, rheumatoid arthritis), endocrine disorders (Cushing?s, hyperthyroidism, hyperparathyroidism), and immobilization.

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4
Q

Explain the pathophysiology of osteoporosis, including factors influencing peak bone mass and the changes that occur with aging.

A

Peak bone mass is determined by hereditary and environmental factors. After reaching peak bone mass, there’s an average annual bone loss of 0.7%. Aging reduces osteoblast function, response to growth factors, and physical activity, leading to increased porosity and reduced density, which heightens fracture risk.

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5
Q

How does osteoporosis increase the risk of fractures, and what are the implications of reduced density and increased porosity in bones?

A

Osteoporosis increases the fragility of bones, raising the risk of fractures even with minimal trauma. Reduced density and increased porosity amplify bone fragility, leading to conditions like vertebral compression fractures.

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6
Q

What are the direct effects of corticosteroids on bones?

A

Corticosteroids directly affect bones by reducing osteoblast activity and lifespan, suppressing replication of osteoblast precursors, and reducing calcium absorption.

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7
Q

List the common sites for osteoporotic fractures.

A

Common sites for osteoporotic fractures include the neck of the femur, vertebral bodies, distal radius, and humeral neck.

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8
Q

What risk assessment tools are used in osteoporosis evaluation, and who should undergo a DEXA scan?

A

Risk assessment tools for osteoporosis include a 10-year osteoporotic fracture risk calculator. DEXA scans are recommended for individuals over 50 years with risk factors, and for those under 50 years with very strong clinical risk factors (e.g., early menopause, glucocorticoid use).

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9
Q

How is osteoporosis diagnosed using DEXA scanning, and what are the definitions for osteoporosis and severe osteoporosis?

A

Osteoporosis is diagnosed when bone density is 2.5 standard deviations below the mean peak value of young adults of the same race and sex. Severe osteoporosis is defined as bone density 2.5 standard deviations below the mean peak value of young adults, combined with a fragility fracture.

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10
Q

What are some additional investigations recommended for assessing decreased bone density, and why are they conducted?

A

Additional investigations for assessing decreased bone density include U+Es, LFTs, FBC, PV, TSH, protein electrophoresis/Bence Jones proteins, coeliac antibodies, testosterone, 25OH vitamin D, and PTH. These tests aim to ensure safety in treatment and rule out underlying conditions contributing to decreased bone density.

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11
Q

Explain the goal of osteoporosis management and outline the lifestyle advice recommended for managing the condition.

A

Osteoporosis management aims to slow further deterioration and decrease the risk of subsequent fractures. Lifestyle advice includes increasing calcium intake, high-intensity strength training, low-impact weight-bearing exercises, avoiding excess alcohol and smoking, and focusing on fall prevention.

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12
Q

What pharmacological management options are available for osteoporosis, and what are the primary considerations for their usage?

A

Pharmacological management for osteoporosis includes calcium and/or vitamin D supplements for individuals with poor dietary intake or limited sunlight exposure. Oral bisphosphonates such as alendronic acid, risedronate, and etidronate are used to reduce osteoclastic resorption, typically as a first-line treatment, especially when the T score is equal to or less than -2.5.

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13
Q

Explain the function and application of oral bisphosphonates in osteoporosis management.

A

Oral bisphosphonates reduce osteoclastic resorption and are considered first-line treatments for most patients. Consider treatment when the T score is less than or equal to -2.5. For those with an ongoing steroid requirement of 7.5mg prednisolone for three months or longer or those with a prevalent vertebral fracture, treatment should be considered when the T score is less than -1.5.

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14
Q

What is the purpose and recommended use of Zoledronic acid in osteoporosis treatment?

A

Zoledronic acid is an annual intravenous bisphosphonate and is considered a second-line treatment for many patients, particularly those who experience side effects with oral bisphosphonates.

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15
Q

Describe the mechanism of action of Teriparatide and its specific recommendation in osteoporosis treatment.

A

Teriparatide, a recombinant parathyroid hormone, stimulates bone growth (anabolic) rather than reducing bone loss. It’s recommended to reduce the risk of vertebral and non-vertebral fractures in postmenopausal women with severe osteoporosis. It’s also recommended over oral bisphosphonates for postmenopausal women with at least two moderate or one severe low trauma vertebral fracture to prevent vertebral fracture.

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16
Q

What is Romosozumab, and for which patient group is it recommended in osteoporosis management?

A

Romosozumab is a monoclonal antibody that binds to and inhibits sclerostin to increase bone formation and reduce bone resorption. It’s recommended for postmenopausal women with severe osteoporosis who have had a fragility fracture and are at imminent risk of further fracture within 24 months.

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17
Q

How can peak bone mineral density be influenced to prevent osteoporosis, and what lifestyle measures are recommended for prevention?

A

Peak bone mineral density can be influenced by exercise, a good diet, and healthy sunlight exposure before the decline in bone density begins, thereby potentially reducing the risk of osteoporosis.

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18
Q

What is osteoporosis?

A

Osteoporosis involves a significant reduction in bone density, making bones weaker and more susceptible to fractures.

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19
Q

What does osteopenia refer to?

A

Osteopenia refers to a less severe decrease in bone density compared to osteoporosis.

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20
Q

How does the World Health Organization (WHO) define bone conditions based on the T-score at the femoral neck from a DEXA scan?

A

WHO defines normal bone density with a T-score greater than -1, osteopenia with a T-score between -1 and -2.5, osteoporosis with a T-score less than -2.5, and severe osteoporosis with a T-score less than -2.5 along with a fracture.

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21
Q

How is bone mineral density (BMD) measured, and what method is commonly used for this measurement?

A

BMD is measured using a DEXA scan (dual-energy x-ray absorptiometry), which measures bone density by analyzing the radiation absorption of bones.

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22
Q

Which areas of the skeleton are assessed for bone mineral density, and which is considered most important?

A

Bone mineral density can be measured in various parts of the skeleton, but the femoral neck reading is considered most crucial for assessment.

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23
Q

How are the Z-score and T-score different in bone mineral density evaluation?

A

The Z-score measures standard deviations from the average bone density for the patient’s age, sex, and ethnicity, whereas the T-score measures deviations from an average healthy young adult and is primarily used for diagnosis.

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24
Q

What does a T-score of -1 signify?

A

A T-score of -1 indicates that the bone mineral density is one standard deviation below the average for healthy young adults.

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25
Q

How are diagnoses for normal, osteopenia, osteoporosis, and severe osteoporosis made based on the T-score?

A

Normal diagnosis corresponds to a T-score greater than -1, osteopenia is between -1 and -2.5, osteoporosis is less than -2.5, and severe osteoporosis is below -2.5 accompanied by a fracture.

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26
Q

What are the common risk factors associated with osteoporosis?

A

Older age, post-menopausal women, reduced mobility and activity, low BMI (under 19 kg/m^2), low calcium or vitamin D intake, alcohol and smoking, personal or family history of fractures, chronic diseases (e.g., chronic kidney disease, hyperthyroidism, and rheumatoid arthritis), long-term corticosteroids (e.g., 7.5mg or more of prednisolone daily for longer than 3 months), certain medications (e.g., SSRIs, PPIs, anti-epileptics, and anti-oestrogens).

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27
Q

Why are post-menopausal women specifically at risk for osteoporosis?

A

Post-menopausal women are at increased risk due to a significant drop in protective estrogen levels after menopause. Hormone replacement therapy (HRT) is protective against osteoporosis due to its estrogen content.

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28
Q

How are risk assessments recommended for osteoporosis?

A

Assessments are recommended for individuals on long-term oral corticosteroids, those with a previous fragility fracture, anyone 50 and over with risk factors, all women 65 and over, and all men 75 and over.

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29
Q

What tools can be used to calculate the 10-year risk of osteoporotic fractures?

A

The QFracture tool and the FRAX tool are used to calculate the 10-year risk of major osteoporotic and hip fractures.

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30
Q

How are patients categorized based on risk assessment tools?

A

Patients are categorized as low, intermediate, or high risk based on the risk calculator output. For QFracture, patients above 10% risk are considered for a DEXA scan, while FRAX’s categorization is guided by the NOGG guideline chart.

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31
Q

Are there exceptions to the assessment recommendations?

A

Yes, for instance, a DEXA may be arranged without calculating the risk in patients over 50 with a fragility fracture. Treatment might start without a DEXA in patients with a vertebral fracture.

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32
Q

What is the initial approach in managing osteoporosis concerning reversible risk factors?

A

The first step involves addressing reversible risk factors, such as increasing physical activity, maintaining a healthy weight, quitting smoking, and reducing alcohol consumption.

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33
Q

How is insufficient intake of calcium and inadequate vitamin D corrected in osteoporosis management?

A

For insufficient calcium intake (less than 700mg per day) and inadequate vitamin D due to limited sun exposure, additional calcium (at least 1000mg) and vitamin D (400-800 IU) are recommended.

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34
Q

What is the primary or first-line treatment for osteoporosis?

A

Bisphosphonates are the main recommended treatment for osteoporosis. They work by interfering with osteoclasts’ attachment to bone, reducing their activity and bone reabsorption.

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35
Q

What are the side effects associated with Bisphosphonates in osteoporosis treatment?

A

Bisphosphonates may lead to reflux, esophageal erosions, atypical fractures (e.g., atypical femoral fractures), osteonecrosis of the jaw, and external auditory canal issues. Regular dental check-ups are advised during treatment.

36
Q

How are oral Bisphosphonates typically administered for osteoporosis management?

A

Oral Bisphosphonates are taken on an empty stomach with a full glass of water. Patients should remain upright for 30 minutes to minimize the risk of reflux and esophageal erosions.

37
Q

Can you provide examples of Bisphosphonates used in osteoporosis treatment?

A

Examples of Bisphosphonates include Alendronate 70 mg once weekly (oral), Risedronate 35 mg once weekly (oral), and Zoledronic acid 5?mg once yearly (intravenous).

38
Q

According to NICE CKS (2023), when should Bisphosphonate treatment be reassessed?

A

Treatment should be reassessed after 3-5 years. It may be stopped if the T-score improves to better than -2.5 but continued in high-risk patients.

39
Q

What are some specialist treatment options for osteoporosis when Bisphosphonates are unsuitable?

A

Specialist treatment alternatives include Denosumab, Romosozumab, Teriparatide, Hormone Replacement Therapy (HRT), Raloxifene, and Strontium ranelate.

40
Q

What are the concerns associated with Strontium ranelate and Raloxifene in osteoporosis treatment?

A

Strontium ranelate increases the risk of venous thromboembolism and myocardial infarction, whereas Raloxifene, although stimulating estrogen receptors in bones, increases the risk of venous thromboembolism but not in the uterus or breast.

41
Q

What is spondylolysis?

A

Spondylolysis is a condition typically affecting the lower lumbar vertebrae, characterized by a defect in the vertebral arch in the vertebral pars interarticularis.

42
Q

How does spondylolisthesis differ from spondylolysis?

A

Spondylolisthesis occurs when the vertebral defect in spondylolysis is bilateral, causing the affected vertebra to shift anteriorly relative to the vertebra below it.

43
Q

How does spondylolysis of L5 lead to spondylolisthesis?

A

Spondylolysis of L5 can cause the L5 vertebral body to move anteriorly relative to the S1 vertebra, potentially overlapping the sacral promontory.

44
Q

What symptoms are associated with spondylolisthesis?

A

Spondylolisthesis can result in lower back pain and lower limb pain due to compression of spinal nerves.

45
Q

What characterizes spinal stenosis?

A

Spinal stenosis is caused by
* degenerating intervertebral discs, resulting in a disproportionate load on the posterior aspect of the spinal column and
* subsequent osteophyte formation, leading to narrowing of the spinal canal.

46
Q

How does spinal stenosis lead to symptoms?

A

The narrowing of the spinal canal can compress spinal nerve roots, causing symptoms such as back pain, difficulty walking, and tingling/numbness in the legs. Severe cases can involve poor control of bowel movements and urination.

47
Q

What is neurogenic claudication, and how does it differ from vascular claudication?

A

Neurogenic claudication, due to spinal stenosis, is the compression of spinal nerves that worsens with an erect posture but improves when leaning forward or assuming a forward-leaning position. Vascular claudication is caused by decreased arterial blood flow and patients find relief when standing upright.

48
Q

What is the posture dependence in neurogenic claudication?

A

Walking and standing in an upright position exacerbate spinal canal narrowing, worsening symptoms, whereas leaning forward, like leaning over a shopping cart or walking uphill, relieves symptoms.

49
Q

How does symptom relief differ in vascular claudication compared to neurogenic claudication?

A

Patients with vascular claudication find relief when standing upright, contrasting the relief experienced by those with neurogenic claudication when leaning forward or assuming a forward-leaning posture.

50
Q

What is spondylolysis, and which part of the vertebral arch does it affect?

A

Spondylolysis is a condition that usually affects the lower lumbar vertebrae. It involves a unilateral or bilateral defect of the vertebral arch in the vertebral pars interarticularis, causing the posterior part of the arch to separate from the rest of the vertebrae.

51
Q

What is spondylolisthesis, and when does it occur in the context of spondylolysis?

A

Spondylolisthesis occurs when the defect in spondylolysis is bilateral, leading to the anterior slipping of one vertebra relative to the vertebra below it. For example, spondylolysis of L5 can cause the L5 vertebral body to move anterior relative to the S1 vertebra.

52
Q

What are the potential consequences of spondylolisthesis?

A

Spondylolisthesis can lead to the compression of spinal nerves, resulting in symptoms such as lower back pain and lower limb pain.

53
Q

What is spinal stenosis, and what contributes to its development?

A

Spinal stenosis is caused by the narrowing of the vertebral canal due to degeneration of intervertebral discs, leading to osteophyte formation. This narrowing can result from disproportionate loading on the posterior aspect of the spinal column.

54
Q

How does spinal stenosis affect spinal nerve roots, and what are the associated symptoms?

A

Spinal stenosis can compress one or more spinal nerve roots within the vertebral canal, potentially causing symptoms like back pain, difficulty walking, tingling, numbness in the legs, and, in severe cases, poor control of bowel and urinary functions.

55
Q

What is neurogenic claudication, and how does it differ from vascular claudication?

A

Neurogenic claudication is the term used to describe the compression of spinal nerves due to spinal stenosis. It differs from vascular claudication, which is caused by decreased arterial blood flow. Symptoms of neurogenic claudication are more posture-dependent, worsening with walking and standing in an erect position and improving when leaning forward or walking uphill. In contrast, vascular claudication symptoms improve when standing upright.

56
Q

What is the primary cause of spinal stenosis?

A

Spinal stenosis is primarily caused by degenerative joint disease, commonly observed in middle-aged to elderly individuals. It often results from spondylosis, bulging discs, bulging ligamentum flavum, and osteophytosis, collectively leading to reduced space for the cauda equina in the lumbar spine.

57
Q

What are the typical clinical features of spinal stenosis?

A

Spinal stenosis usually affects patients over the age of 60 and commonly manifests as claudication, resulting in leg pain upon walking.

58
Q

How does neurogenic claudication due to spinal stenosis differ from claudication arising from peripheral vascular disease (PVD)?

A

Neurogenic claudication, distinct from PVD-related claudication, is characterized by inconsistent claudication distances, a burning type of pain (as opposed to cramping), exacerbated symptoms during spinal extension (standing or walking downhill), and alleviation of symptoms during back flexion (sitting or walking uphill). Additionally, pedal pulses remain preserved in neurogenic claudication.

59
Q

What investigations are commonly employed to diagnose spinal stenosis?

A

The diagnosis of spinal stenosis is primarily based on clinical assessment, with no specific tests required for diagnosis.

60
Q

What treatment approaches are utilized for spinal stenosis management?

A

Conservative management strategies include analgesia, physiotherapy, and weight loss if indicated. In cases where conservative measures fail to alleviate symptoms and MRI evidence confirms stenosis, surgical intervention, involving decompression to create more space for the cauda equina, may be recommended to alleviate symptoms.

61
Q

What is spinal stenosis and its common locations in the spine?

A

Spinal stenosis refers to the narrowing of a part of the spinal canal, leading to the compression of the spinal cord or nerve roots. It commonly affects the cervical or lumbar spine.

62
Q

What are the three types of spinal stenosis?

A

The three types are: Central stenosis (narrowing of the central spinal canal), Lateral stenosis (narrowing of the nerve root canals), and Foramina stenosis (narrowing of the intervertebral foramina).

63
Q

What are the causes of spinal stenosis?

A

Various conditions such as congenital spinal stenosis, degenerative changes, herniated discs, ligament thickening, spinal fractures, spondylolisthesis, and tumors can lead to the narrowing of the spinal canal.

64
Q

What are the key symptoms and characteristics associated with lumbar spinal stenosis?

A

Lumbar spinal stenosis often presents with intermittent neurogenic claudication. Symptoms include lower back pain, buttock and leg pain, leg weakness, which worsen upon standing and walking and improve when bending forward. Severe cases may show features of cauda equina syndrome.

65
Q

How does neurogenic claudication in spinal stenosis differ from peripheral arterial disease (PAD)?

A

Neurogenic claudication symptoms are similar to PAD but can be differentiated by normal peripheral pulses and ankle-brachial pressure index (ABPI) in spinal stenosis. Moreover, back pain is more characteristic of spinal stenosis rather than PAD.

66
Q

What is radiculopathy and what causes it in the context of spinal stenosis?

A

Radiculopathy refers to the compression of nerve roots as they exit the spinal cord and column. It is caused by the narrowing of the spinal canal, leading to motor and sensory symptoms.

67
Q

What is the primary imaging technique used to diagnose spinal stenosis?

A

The primary imaging investigation for diagnosing spinal stenosis is MRI (Magnetic Resonance Imaging).

68
Q

In cases where symptoms of intermittent claudication are present, what investigations might be necessary to exclude other conditions?

A

Investigations to exclude peripheral arterial disease, such as ankle-brachial pressure index and CT angiogram, may be appropriate when symptoms of intermittent claudication are present.

69
Q

What are the possible management options for spinal stenosis?

A

Management options may include exercise and weight loss if suitable, analgesia, physiotherapy, and, if conservative treatment fails, decompression surgery.

70
Q

What does a laminectomy involve, and what part of the vertebra is affected?

A

A laminectomy involves the removal of part or all of the lamina from the affected vertebra. The lamina is the bony part that forms the posterior part of the vertebral foramen, creating the spinal canal and attaches to the spinous process.

71
Q

Are epidural injections commonly utilized in the management of spinal stenosis?

A

The benefits of epidural injections with local anesthetic and corticosteroids are unclear, and they are generally not used in the management of spinal stenosis.

72
Q

What are the four normal curvatures of the vertebral column seen on a lateral view?

A

The normal curvatures are thoracic and sacral kyphosis, which are concave in the anterior direction, and cervical and lumbar lordosis, which are concave in the posterior direction.

73
Q

How are abnormal curvatures of the vertebral column identified?

A

Abnormal curvatures are identified by examining the profile of the vertebral column from the side and posterior aspect in an anatomical position. They may result from developmental anomalies or pathological processes like osteoporosis.

74
Q

What are some causes and effects of excessive thoracic kyphosis?

A

Excessive thoracic kyphosis, often caused by osteoporosis, results in an abnormal increase in the curvature of the thoracic spine. It can decrease the anteroposterior diameter of the thorax, reducing pulmonary capacity.

75
Q

What is excessive lumbar lordosis, and what can cause it?

A

Excessive lumbar lordosis occurs when the pelvis tilts anteriorly, leading to increased extension of the lumbar vertebrae. Causes include weakened trunk musculature, late pregnancy, or obesity leading to lower back pain due to increased abdominal weight.

76
Q

What is scoliosis, and when does it most commonly occur?

A

Scoliosis is an abnormal lateral curvature of the vertebral column often accompanied by vertebral rotation. It most commonly occurs in adolescents during growth periods and, in many cases, is idiopathic.

77
Q

How is adolescent idiopathic scoliosis diagnosed, and what are the management approaches based on the degree of curvature?

A

Adolescent idiopathic scoliosis is identified by a Cobb angle over 10 degrees and is usually asymptomatic. The management depends on the Cobb angle: mild scoliosis (10-30 degrees) is monitored every 6 months, a Cobb angle over 30 degrees may require a spinal brace, and over 40 degrees might necessitate surgery in children with remaining growth potential.

78
Q

What are the factors that contribute to back strains?

A

Back strains commonly occur due to heavy lifting or participating in sports. Improper lifting techniques, especially using the back as a lever instead of employing the lower limb and gluteal muscles, increase the likelihood of back strains.

79
Q

How does lifting improperly contribute to back strains?

A

Lifting awkwardly can cause an imbalance in weight distribution on the vertebral column, straining specific back muscles. It’s crucial to use the legs rather than the back as the primary force for lifting heavy objects.

80
Q

What characterizes a back sprain?

A

A back sprain is an injury affecting ligaments or their connection to bones. It usually results from excessively strong contractions during movements like extension or rotation of the vertebral column.

81
Q

What defines a muscle spasm of the back, and what triggers it?

A

A muscle spasm in the back is a protective mechanism that involves sudden, involuntary contractions of one or more muscle groups, often occurring after an injury or due to inflammation. These spasms are accompanied by cramps and pain.

82
Q

What preventive measures can help avoid back strains, sprains, and spasms?

A

Warming up, stretching before exercising, and focusing on strengthening core muscles, particularly the transverse abdominis muscle involved in lumbar stabilization, can assist in preventing back strains, sprains, and spasms.

83
Q

What is a Jefferson fracture?

A

A Jefferson fracture involves fractures in one or both of the anterior or posterior arches of the C1 vertebra (atlas), which occur due to compressive forces driving the lateral masses apart, usually caused by vertical forces between the occipital condyles and C2 (axis).

84
Q

What is the most common mechanism that causes a Jefferson fracture?

A

A classic example is hitting the bottom of the pool with the top of the head while diving, which leads to vertical forces compressing the lateral masses between the occipital condyles and C2 (axis).

85
Q

Why is the C1 vertebra called the Atlas?

A

The C1 vertebra is called the Atlas because, similar to the God Atlas of Greek mythology, it carries or sustains the weight of the cranium, much like how Atlas bore the weight of the world on his shoulders.