module 2 Musculoskeletal disorders

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What is the skeletal system critical for?

maintenance of blood calcium and phosphate levels. The inorganic matrix comprising bone stores around 99% of the body’s calcium and a significant proportion of phosphates and provides structural support to the body.

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why is calcium important

critical ion in the cardiac action potential is essential for homeostasis, and phosphates are needed for muscle contraction, nervous function, and repair of bony tissue

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what happens when there are disorders in the skeletal system?

Disorders of the skeletal system can lead to bone deformities, fractures, impaired mobility, and disruptions in calcium and phosphate balance, affecting overall health and function.

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Describe the causes and characteristics of the main types of bone fractures


Fractures are caused by trauma and accidents, repeated minor trauma (stress fractures) or underlying pathology where bones are weakened by pre-existing disease. Fractures can be:

  • Greenstick: a fracture extending only partially through the bone. Common in infants due to soft bones.

  • Comminuted: the bone is fragmented

  • Oblique or spiral: the fracture is at an angle

  • Displaced: the ends of the bones at the fracture site are misaligned

  • Stress: a slowly developing fracture that occurs due to repeated physical overloading


<p><span>Fractures are caused by trauma and accidents, repeated minor trauma (stress fractures) or underlying pathology where bones are weakened by pre-existing disease. Fractures can be:</span></p><ul><li><p><span>Greenstick: a fracture extending only partially through the bone. Common in infants due to soft bones.</span></p></li><li><p><span>Comminuted: the bone is fragmented</span></p></li><li><p><span>Oblique or spiral: the fracture is at an angle</span></p></li><li><p><span>Displaced: the ends of the bones at the fracture site are misaligned</span></p></li><li><p><span>Stress: a slowly developing fracture that occurs due to repeated physical overloading </span></p></li></ul><p></p>
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Outline the steps involved in fracture healing


  1. Inflammatory phase (hours to days): The initial stage of healing involves formation of a haematoma due to bleeding from damaged blood vessels. The haematoma provides a framework of healing. 

  2. Reparative phase (days to weeks): Soft (cartilaginous) and then a hard (ossified) fracture callus forms around the haematoma as bone forming cells (osteoblasts) are recruited to the site. Soft callus is pliable and can deform or bend if the fracture is not adequately supported. Hard callus is weaker than normal bone but is capable of withstanding external forces.

  3. Remodelling phase (months to years): The bone is remodelled to replace the normal architecture of trabecular bone as bones are loaded and grow.


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Identify the main types of tumours that occur in the skeleton


  • Primary bone tumours are rare, and often result in significant disfigurement as a consequence of the tumour and surgical management of the malignancy.

  • Metastatic bone tumours are more common than primary bone tumours and arise secondary to tumours originating at other anatomical sites (e.g. of the haematopoietic tissue in cases of leukaemia or myeloma) metastasising to the bone.

  • Malignant bone tumours (osteosarcomas - bone; and chondrosarcomas - cartilage), are cancer and have a high mortality rate (50%).

  • Benign bone tumours are more common than malignant bone tumours and include osteochondromas, endochondroma and osteoclastomas.


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Describe the causes and possible consequences of skeletal muscle atrophy


skeletal muscle atrophy can occur in many ways:

Loss of innervation; The nerve supplying the muscle is damaged, so the muscle no longer receives normal signals to contract. It gradually wastes away. E.g due to a Spinal cord injury or peripheral nerve damage.

disuse; The muscle isn't being used enough, so the body reduces muscle protein and the fibres shrink. Being bedridden or having a leg in a cast

cachexia; Severe muscle wasting associated with chronic illnesses, driven by inflammation and altered metabolism. Advance: Diseases that directly affect muscle fibres, causing damage, weakness and sometimes progressive wasting. cancer, heart failure or COPD

old age/sarcopenia: Age-related loss of muscle mass, strength and function due to changes in muscle fibres, hormones and activity.

primary myopathies

Depending on severity and location, symptoms can include postural, balance and coordination problems which may lead to a higher risk of falls leading to fractures.


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In disuse atrophy patients that are bedbound can lose up to what percentage of muscle mass per day?

2-5%

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What are contractures

Contractures can be briefly defined as a reduction to the functional range of motion of a joint due to either muscle shortening or scar tissue formation.

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Describe the causes and possible consequences of contractures


causes or either neural or non-neural in origin: Neural conditions that result in contractures are injury to the CNS like spinal cord or traumatic brain injuries, stroke and cerebral palsy, there is also a link between Alzheimer’s disease and contractures. Non-neural origins can be due to muscular dystrophy and thermal burns.

Contractures result in decreased motor performance, joint deformities, and mobility limitations. This may lead to loss of function, and undesirable positioning. Can lead to pressure injuries/bed sores. Causes pain due to replacement of elastic and flexible skeletal muscles and tendons with inflexible fibrotic tissue. 

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Discuss compartment syndrome and complications


Compartment syndrome can be acute or chronic and is defined by an increased pressure within a muscle compartment that leads to ischaemia and tissue necrosis. If not relieved this can lead to loss of the affected limb or life.

Most often, acute compartment syndrome is the result of trauma or fracture which leads to muscle swelling, but it can also be caused by restrictive dressings, casts etc. which decrease the compartment size. As the fascia surrounding the muscle compartment is inelastic, swelling within the compartment leads to increased pressure. This has two detrimental effects: 1) it can lead to pressure building up in the associated venous system, leading to oedema (increased hydrostatic pressure), and 2) reduce blood flow through the muscle resulting in tissue ischaemia and necrosis.

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compartment syndrome clinical features/manifestations and management/treatment

Prompt recognition of the signs and symptoms are necessary to avoid tissue death. Signs and symptoms may present immediately or be delayed by several hours or days. The cardinal sign of compartment syndrome is pain that is not relieved with opioids and increases upon passive stretch.

6ps:

Paraesthesia (numbness, tingling), pain (On passive stretch, not relieved by medication),pressure (increasing in the compartment), pallor (pale and cool skin), paralysis (loss of function), pulselessness ( Decreased or no detectable peripheral pulse in affected limb)

Monitoring is required to assess compartment syndrome and prevention is best. If the cause is restrictive dressing, this may be loosened. Surgical intervention may be required to relieve pressure. This is called a decompressive fasciotomy, and involves cutting the skin and fascia to release pressure, the wound may kept open for several days and complications can include infection.


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Describe the risk factors, pathophysiology and clinical manifestations of rheumatoid arthritis


Rheumatoid arthritis is a chronic systemic autoimmune disorder that principally targets the joints producing inflammatory synovitis. Dysregulated T-helper cells (CD4+) trigger production of auto-antibody (from plasma cells) called rheumatoid factor, that is deposited in joints as immune complexes.

The pathophysiology of rheumatoid arthritis is complex and characterised by the following changes:

  1. Synovial cell hyperplasia and proliferation.

  2. Dense inflammatory cell infiltrate, destruction of cartilage and bone, formation of scar tissue (pannus) that grows over the articular cartilage causing erosion of the deeper bone.

  3. The pannus bridges the opposing bones to form a fibrous and then bony ankylosis of the joint.

Early clinical manifestations include swelling of the joints, which over time will become visibly deformed.

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Describe osteoarthritis, the risk factors, pathophysiology and clinical manifestations.

Osteoarthritis is a degenerative joint disease characterised by structural and functional failure of synovial joints as a consequence of cartilage degeneration. Osteoarthritis is the most common joint disease.

Risk factors for development include:

  • Increasing age

  • Obesity

  • Joint injury and misalignment

  • Repetitive mechanical stress

  • Inflammation Chondrocyte (connective tissue cells) changes in osteoarthritis:

  1. Chondrocyte injury leads to damage and erosion of articular cartilage, which covers the ends of the bones forming the joint.

  2. Chondrocytes proliferate and secrete inflammatory mediators to remodel the cartilagenous matrix leading to further inflammation and changes in the synovial membrane and subchondral bone.

  3. Repetitive injury and chronic inflammation lead to loss of chondrocytes, cartilage and extensive subchondral bone changes (sclerotic bone and osteophytes/bone spurs). Clinical manifestations and complications

    Signs and symptoms usually start appearing after 50 years. Usually the first sign is pain that is initially relieved by rest, and gradually worsens. Some people experience worsening pain with poor weather and also early morning stiffness. Pain also contributes to loss of mobility in the joint. Osteoarthritis in some joints can lead to deformity or shortening of stature. It is loss of movement and chronic pain that can prevent people from social or occupational activities. Depression is known to co-occur with osteoarthritis (co-morbidity).


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Osteoarthritis Management

Osteoarthritis is progressive, there is no cure. Management centres around pain management and maintaining mobility. There are a number of different strategies:

  • rest whilst inflammation present,

  • use of walkers, wheelers to reduce weight bearing on joints

  • weight loss (where indicated)

  • application of heat and cold

  • guided exercise

  • pain medication

  • anti-inflammatory medication

  • nutrition (mixed evidence for effectiveness of some supplements, e.g. glucosamine)


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Contrast the pathophysiology of osteoarthritis and rheumatoid arthritis


Characteristic

Osteoarthritis

Rheumatoid arthritis

Onset of symptoms

Usually >50 years

30-50 years

Sex

Before 55 years of age higher in males, after 55 years higher in females

More likely in females

Affected joints

Weight bearing joints, often asymmetrical joint involvement (one sided).

Small joints, wrists, elbow, shoulders. Symmetrical joint involvement (both sides).



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What percentage of Australians have arthiritis

15%

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what are the numbers on a t-score for normal and low bone density and OP

T-score

Classification

−1.0 or higher

Normal

Between −1.0 and −2.5

Low bone mass (osteopenia)

−2.5 or lower

Osteoporosis


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Describe the key characteristics of osteopenia and osteoporosis including risk factors, and factors that contribute to attaining peak bone mass


Osteoporosis is defined as osteopaenia that causes a loss of bone mass severe enough to increase fracture risk. Osteoporosis can be localised if the precipitating factor is disuse of a limb, or can involve the entire skeleton if metabolic in origin. Osteoporosis occurs more commonly in women over 80-years of age. Peak bone mass occurs during young adulthood and is influenced by genetics, physical activity, muscle strength, diet, and hormones. The most common forms of osteoporosis are senile and postmenopausal.



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Describe the characteristics of osteomalacia and rickets


Both conditions involve impaired bone mineralisation, usually due to vitamin D or calcium deficiency, resulting in soft, weakened bones.

  • Osteomalacia (adults): Causes bone pain, weakness and increased fracture risk.

  • Rickets (children): Affects growing bones and growth plates, causing bowed legs and short stature.

Key difference: Osteomalacia affects adults, while rickets affects children whose growth plates are still open.

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Discuss the role of renal osteodystrophy in osteoporosis and other bone disorders


Chronic kidney disease causes renal osteodystrophy by lowering active vitamin D and calcium, raising PTH, which weakens bones and may overlap with osteoporosis and osteomalacia.

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Define osteomyelitis and list some causes and complications of osteomyelitis


Osteomyelitis is a condition associated with inflammation of the bone and bone marrow, almost always secondary to infection.steomyelitis may be secondary to a systemic infection or can manifest as primary focal disease.

The most common infectious agents that causes osteomyelitis are bacteria, but fungi, parasites and viruses are also responsible. Infectious agents reach the bone.Initial clinical manifestations include signs and symptoms associated with inflammation - pain, swelling, heat, loss of function.If acute osteomyelitis progresses to chronic osteomyelitis, this may require surgical removal of the affected bone. The complications include bone death (necrosis) as a result of ischaemia. In children, a complication can occur where an abscess forms under the periosteum, depriving underlying tissues of blood supply. This occurs as the periosteum is not as firmly attached as in adulthood.

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what is the difference between: Cartilage, ligaments and tendons

Cartilage is a flexible connective tissue that provides support and cushioning in joints, ligaments connect bones to other bones at joints, and tendons attach muscles to bones, enabling movement.

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what do these bone cells do: Osteoblasts, osteocytes and osteoclasts

Osteoblasts — BUILD bone

Produce osteoid (mainly type I collagen) and promote mineralisation.

Osteocytes — MAINTAIN bone

Mature osteoblasts embedded in bone; detect mechanical stress and regulate remodelling.

Osteoclasts — BREAK DOWN bone

Resorb bone using acid and enzymes, releasing calcium and phosphate

BLAST builds, CLAST crushes, CYTE maintains.

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Explain the difference between fibrous, cartilaginous and synovial joints

Joint

Movement

Example

Fibrous

Little or none

Skull sutures

Cartilaginous

Limited

Intervertebral discs

Synovial

Freely movable

Knee, shoulder, hip


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What is the parathyroid hormone (PTH) and bone

PTH is released by the parathyroid glands when blood calcium is LOW. PTH acts on:

Bone: Increases osteoclast-mediated resorption indirectly through osteoblast-lineage cells

Kidneys: Increase calcium reabsorption and activate vitamin D

Intestines: Increase calcium absorption indirectly via calcitriol = blood calcium increases. Important: Chronically elevated PTH can cause excessive bone resorption and weakened bones.

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calcitonin vs calcitriol

  • Calcitonin = lowers blood calcium (minor physiological role in adults).

  • Calcitriol = raises blood calcium by increasing absorption from the gut.


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long bones in children vs adults

Children

Open epiphyseal growth plate (cartilage), allowing longitudinal bone growth.

Adults

Growth plate ossified into an epiphyseal line; longitudinal growth has stopped.

Clinical significance: Growth plate fractures in children can disrupt future bone growth, causing limb length differences or deformity.

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Fracture complications of fractures

Fracture of the femur or pelvic bones, particularly of the elderly, can lead to life threatening blood loss (hypovolaemia) or embolus formation. Another complication occurs when bones remain misaligned as the healing process begins, this can lead to limb deformity and may require re fracturing the bone to obtain correct alignment.

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how likely is it that osteosarcoma develops in the long bones (Arms and legs)?

94% very likely

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