Module 10 - The Musculoskeletal System Flashcards

1
Q

Describe 4 functions of the skeleton.

A

The skeleton acts as a framework for our bodies; it serves as a site for muscle attachment; it protects vital organs and soft tissue structures; it stores calcium and other minerals; it is the site where blood cells are produced.

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2
Q

Name the 2 major skeletal divisions and the bones that comprise each.

A

The axial skeleton is made up of the bones of the skull, thorax, and the vertebral column. The appendicular skeleton is made up of the bones of the upper and lower extremities as well as the pectoral and pelvic girdles.

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3
Q

Compare and contrast cortical bone and cancellous bone.

A

Cortical bone is compact, it forms the outer shell of the bone, and the bone tissue is densely packed extracellular matrix making it rigid.

Cancellous bone is the interior aspect and trabeculae, or columns of connective tissue, form a grid like pattern that is lined with bone forming cells and filled with red or yellow bone marrow. The composition of cancellous bone gives it its weight bearing properties and allows it to be highly resistant to tensile or torsional stresses.

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4
Q

List the 4 shapes of bone and give an example of each.

A

Long bones - appendicular skeleton; humerus or femur.

Short bones - wrist and hand

Flat bones - axial skeleton for underlying soft tissue and large surface area for muscle attachment; skull, ribcage.

Irregular bones - don’t fit into the other categories; vertebrae.

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5
Q

Describe the structure and function of the extracellular matrix of osseous tissue.

A

The extracellular matrix of osseous or bone tissue is calcified or hardened. This feature gives bone its ability to support the weight of the body and provide protection to the soft tissue structures that lie beneath it. The extracellular matrix can be divided into the organic matrix and the inorganic matrix. The organic matrix (of bone and other connective tissue types) is composed of collagen fibers and ground substance. Ground substance, composed of proteins and polysaccharides, plays an important role in metabolic functions required for bone growth and repair. The inorganic matrix is composed mostly of calcium phosphate. It also contains carbonate, magnesium, sodium, and other heavy metals, such as lead, that may have been removed from circulation.

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6
Q

Be able to name and describe the function of the 4 bones cells.

A

Osteoprogenitor cells - undifferentiated cells in the periosteum, endosteum, and epiphysial plates of growing bones. When they are stimulated by bone morphogenic proteins (BMPs) they will differentiate into osteoblasts which contribute to normal bone growth and replacing worn bone.

Osteoblasts - bone building cells, responsible for the formation of bone matrix.

Osteocytes - mature bone cells; maintain the integrity of the bony matrix and have channels that allow for the exchange of nutrients between osteocytes and vessels.

Osteoclasts - “bone chewing cells” that resorb bone by removing mineral content and organic matrix.

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7
Q

Describe the function of PTH – include details about where it is produced and what triggers its secretion.

A

Parathyroid hormone (PTH) is secreted by the parathyroid glands and serves to maintain blood calcium and phosphate levels. If blood calcium levels are low, the parathyroid glands will secrete PTH to return levels to normal. Negative feedback will cause the release of PTH to stop once normal levels are reached or there are increased levels of blood calcium. PTH will regulate calcium levels in one of four ways: (1) It will stimulate the release of calcium from bone; (2) it will increase renal reabsorption of calcium while simultaneously increasing renal excretion of phosphate; (3) it will activate vitamin D in turn increasing intestinal absorption of calcium, and finally (4) it will reduce blood phosphate levels.

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8
Q

Describe the function of Calcitonin – include details about where it is produced and what triggers its secretion.

A

Calcitonin is secreted by the parafollicular cells of the thyroid gland. It acts in opposition to PTH by decreasing blood calcium levels. Calcitonin acts to inhibit the release of calcium from bone and reduces the tubular reabsorption of calcium and phosphate. The primary stimulus for the synthesis and secretion of calcitonin is an increase in blood calcium levels.

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9
Q

Be familiar with Figure 10.5 and be able to describe the activation pathways of Vitamin D.

A

Vitamin D in its inactive form is taken in by food or sunlight, it is absorbed by the liver and then transported to the kidneys, where it is converted to tis active form.

The activation process of Vitamin D begins in the liver where the inactive form of Vitamin D is hydroxylated to form 25-hydroxyvitamin D From here it is transported to the kidneys where it is converted to the active forms of either 1,25-dihydroxyvitamin D3 or 24,25-dihydroxyvitamin D3. Vitamin D can be taken into the body in one of two ways. It can be absorbed through the intestines by dietary intake (best sources include fatty fish, cheese, beef liver, and egg yolks), or it can be absorbed through the skin by way of ultraviolet radiation from the sun.

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10
Q

Be able to describe Synarthroses and Synovial joints. List and describe the types of joints that would fall into each category.

A

Synarthroses do not have a joint cavity and allow little to no movement. They include:

Synostoses - joints that allow no movement between them and are jointed by dense connective tissue or bone; e.g. bones of the skull

Synchondroses - joints that allow limited movement and are connected by hyaline cartilage; e.g. ribs connected to the sternum

Syndesmoses - permit a small degree of movement and separated by a fibrous disc and joined by interosseous ligaments; e.g. pubic symphysis and the intervertebral joints.

Synovial joints are freely moving:

Pivot joints - rotational movement; between the cervical vertebrae.

Hinge joints - will flex toward or away from one another; knee or elbow.

Saddle joints - similar to hinge joints that allow flexion and extension, but also medial and lateral movement; carpometacarpal joint of the thumb.

Plane joints - glide for movement in multiple directions; intercarpal and intertarsal joints

Condyloid joints - similar to plane joints, gliding occurs between the bones of the joint but hte surfaces of the bones are irregular; radio-carpal joint

Ball and socket - will allow movement through all degrees of freedom; shoulder and hip.

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11
Q

If the synovial membrane were damaged, would the healing process be quick or prolonged? Explain your answer.

A

Healing to the synovial membrane would occur quickly because the synovial membrane has a rich vascular supply. There are capillaries near the surface of the synovium which allow blood to escape into the synovial fluid with minor injuries.

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12
Q

List the risk factors associated with developing OA.

A

Age (>70s), gender (males younger women older), excess weight, joint trauma, heredity.

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13
Q

Describe the role of articular cartilage within a joint.

A

Articular cartilage works in conjunction with the synovial fluid to decrease friction between articulating bones within a joint and it works to spread forces evenly across the surface of the joint and down into the bone.

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14
Q

What is the role of chondrocytes within the extracellular matrix or cartilage?

A

Chondrocytes contribute to matrix breakdown by producing matrix-degrading enzymes; they also synthesize the new matrix.

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15
Q

Describe the role of Interleukin -1beta and Tumor Necrosis Factor-Alpha in the OA disease process.

A

They are cytokines that promote the destruction of the joint which makes the chondrocytes more susceptible to damage, impairing their ability to produce new collagen and proteoglycans.

Interleukin -1beta and Tumor Necrosis Factor-Alpha work to promote the destruction of the joint. This interruption to the integrity of the joint makes the chondrocytes more susceptible to damage impairing their ability to produce new collagen and proteoglycans.

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16
Q

Describe the various structural changes that occur in OA and how they come to be.

A

The enlargement and reorganization of chondrocytes in the superficial layer of the articular cartilage is followed by edema within the cartilaginous matrix. At this point the cartilage is no longer a smooth surface. Microfractures begin to form. Synovial fluid will fill these surface cracks, and they will continue to widen. Eventually these microfractures will extend through the articular surface and into the subchondral bone. Portions of the articular cartilage will erode over time leaving the subchondral bone exposed. The exposed bone will thicken. Small fragments of the remaining cartilage will break off and become free-floating in the joint cavity. The trabecular bone will harden decreasing its ability to absorb shock. Small bony growths called osteophytes or spurs will begin to form around the joint margins.

17
Q

Be able to differentiate between OA and RA.

A

OA is a degenerative disease typically isolated to a single joint.

Rheumatoid arthritis is an autoimmune disease which is systemic and characterized by joint inflammation caused by an immune response that leads to synovial inflammation and destruction of the joint architecture. There is a genetic factor to it - IgRF. RA has symmetrical or bilateral presentations. Average onset age for RA is younger than OA. And RA is a chronic disease that is progressive and has periods of flare ups and remissions. RA patients will complain of morning stiffness in affected joints that lasts longer than 30 minutes. RA joints loosen with movement and range of motion.

18
Q

List and Describe the 3 treatment interventions for OA.

A

Physical rehab (manage progression with strengthening exercises), oral medications (NSAIDs, corticosteroids to reduce pain and inflammation), surgical intervention (arthroscopic debridement to improve joint alignment and reduce osteophytes, knee and hip replacements).

19
Q

What is Bone Mass Density and how does it relate to the risk for developing osteoporosis?

A

Bone Mass Density (BMD) is a measure of the amount of minerals (mainly calcium and phosphorus) contained within a certain volume of bone. BMD will increase steadily through childhood and adolescence. Peak BMD is reached in the young adult years. This peak value can determine one’s risk for later developing osteoporosis.

20
Q

How does estrogen contribute to BMD?

A

Estrogen increases the production of OPG and in turn lowers the rate at which osteoclasts are formed. The decline in estrogen levels that occurs with menopause leads to a higher rate of osteoclast activity as OPG levels also decline.

21
Q

What is the relationship between physical activity and senile osteoporosis?

A

There is often a decline in physical activity that comes with aging. Decreased weight bearing and loading of the joint will contribute to lower bone density as weight bearing activity contributes to bone remodeling.

22
Q

Be able to determine whether a T-score is normal, indicative of osteopenia, or indicative of osteoporosis.

A
  • 1.0 and above is normal
  • 1.0 - -2.5 is low bone density; osteopenia
  • 2.5 or lower is osteoporosis
23
Q

Be able to identify risk factors for osteoporosis and how they contribute to diagnostic testing.

A

Screenings should be done in women (65+), men (70+), those with a broken bone after 50, people of menopausal age with risk factors, postmenopausal under age 65 with risk factors, men age 50-69 with risk factors.

Also people with a history, small bone structure, sedentary lifestyle, calcium deficiency, excessive alcohol/caffeine intake and smoking, or take drugs or have disease that relate.

24
Q

List the pharmacologic treatments for osteoporosis and describe their mechanism of action.

A

(1) Estrogen and SERMs (selective estrogen receptor modulators) (2) Bisphosphonates and (3) Calcitonin. Estrogen is very effective at reducing the progression of osteoporosis; however, risk/benefit analysis is necessary due to secondary health problems that can arise with the use of hormone therapy. Raloxifene is a SERM that has shown to be effective in the prevention and treatment of osteoporosis in postmenopausal women. Bisphosphonates including alendronate, risedronate, and ibandronate, are the most commonly prescribed drugs used to treat osteoporosis. They work to inhibit bone resorption by reducing osteoclast activity. They are effective at reducing the risk of fracture. Calcitonin works to inhibit osteoclast activity. Teriparatide is a form of parathyroid hormone used to treat osteoporosis. It stimulates bone remodeling by increasing osteoblast activity.

25
Q

Differentiate between primary and secondary gout.

A

Primary gout is characterized by the overproduction or the underexcretion of uric acid. The cause is unknown but is often associated with diet and/or alcohol overuse or a metabolic syndrome. Secondary gout is typically caused by medications or certain conditions that result in hyperuricemia.

26
Q

If a patient has a uric acid serum level of 7.2 mg/dL, are they given a diagnosis of gout?

A

No because not all people with hyperuricemia have gout (20%). They would have to do an analysis of synovial fluid for urate crystals.

27
Q

Be familiar with the 4 pathways leading to elevated serum uric acid levels.

A

There can be an overproduction of purines, a decrease in the salvage of free purine bases, an increase of cell turn over resulting in the break down of nucleic acids, and a decrease in the amount of uric acid excreted from the body.

28
Q

Be familiar with the 4 phases of gout and the progression from one phase to another.

A

Asymptomatic hyperuricemia. Acute gout arthritis which includes pain that may last days to weeks. When the attacks subside they are in the inter-critical phase of gout. They may have more attacks and with more frequency, that’s when permanent joint changes occur and they are in the chronic tophaceous gout phase.

29
Q

List 2 ways that a definitive diagnosis of gout is made.

A

A diagnosis can only be made by determining the presence of urate crystals in the synovial fluid or in tissue sections of tophi if present and through the collection of a 24-hour urine specimen to measure whether uric acid is being overproduced or under-excreted.