Thursday, December 19, 2013

Osteoporosis

O S T E O P O R O S I S
I.                   Introduction
"porous bones", from Greek: οστούν/ostoun meaning "bone" and πόρος/poros meaning "pore"
One of the most common metabolic bone skeletal disorder is osteoporosis. Osteoporosis is a condition that affects bone strength (the word osteoporosis literally means "porous bones"). Bone is made of collagen fibres (tough, elastic fibres) and minerals (gritty, hard material). It is a living tissue and contains cells that make, mould and resorb bone. Initially, in the early years, bone formation exceeds bone resorption. But, as a person gets older, this reverses and, after about the age of 45, a person loses a certain amount of bone material. The bones become less dense and less strong. The amount of bone loss can vary. If you have osteoporosis, your bones can break more easily than normal, especially if you have an injury such as a fall.
II.                Anatomy & Physiology
The adult human skeleton usually consists of 206 named bones. The human skeletal system consists of bones, cartilage, ligaments and tendons and accounts for about 20 percent of the body weight. Bones provide a rigid framework, known as the skeleton,that support and protect the soft organs of the body. The skeleton supports the body against the pull of gravity. The large bones of the lower limbs support the trunk when standing. It also protects the soft body parts. The fused bones of the cranium surround the brain to make it less vulnerable to injury. Vertebrae surround and protect the spinal cord and bones of the rib cage help protect the heart and lungs of the thorax. Bones work together with muscles as simple mechanical lever systems to produce body movement. They contain more calcium than any other organ. The intercellular matrix of bone contains large amounts of calcium salts, the most important being calcium phosphate.
Structure of Bone Tissue
There are two types of bone tissue: compact and spongy. The names imply that the two types differ in density, or how tightly the tissue is packed together. There are three types of cells that contribute to bone homeostasis. Osteoblasts are bone-forming cell, osteoclasts resorb or break down bone, and osteocytes are mature bone cells. An equilibrium between osteoblasts and osteoclasts maintains bone tissue.
a.      Compact Bone
Compact bone consists of closely packed osteons or haversian systems. The osteon consists of a central canal called the osteonic (haversian) canal, which is surrounded by concentric rings (lamellae) of matrix. Between the rings of matrix, the bone cells (osteocytes) are located in spaces called lacunae. Small channels (canaliculi) radiate from the lacunae to the osteonic (haversian) canal to provide passageways through the hard matrix. In compact bone, the haversian systems are packed tightly together to form what appears to be a solid mass. The osteonic canals contain blood vessels that are parallel to the long axis of the bone. These blood vessels interconnect, by way of perforating canals, with vessels on the surface of the bone.
b.      Spongy (Cancellous) Bone
Spongy (cancellous) bone is lighter and less dense than compact bone. Spongy bone consists of plates (trabeculae) and bars of bone adjacent to small, irregular cavities that contain red bone marrow. The canaliculi connect to the adjacent cavities, instead of a central haversian canal, to receive their blood supply. It may appear that the trabeculae are arranged in a haphazard manner, but they are organized to provide maximum strength similar to braces that are used to support a building. The trabeculae of spongy bone follow the lines of stress and can realign if the direction of stress changes.
Classification of Bones
a.      Long Bones
The bones of the body come in a variety of sizes and shapes. The four principal types of bones are long, short, flat and irregular. Bones that are longer than they are wide are called long bones. They consist of a long shaft with two bulky ends or extremities. They are primarily compact bone but may have a large amount of spongy bone at the ends or extremities. Long bones include bones of the thigh, leg, arm, and forearm.
b.      Short Bones
Short bones are roughly cube shaped with vertical and horizontal dimensions approximately equal. They consist primarily of spongy bone, which is covered by a thin layer of compact bone. Short bones include the bones of the wrist and ankle.
c.       Flat Bones
Flat bones are thin, flattened, and usually curved. Most of the bones of the cranium are flat bones.
d.      Irregular Bones
Bones that are not in any of the above three categories are classified as irregular bones. They are primarily spongy bone that is covered with a thin layer of compact bone. The vertebrae and some of the bones in the skull are irregular bones.
III.             Assessment of the Patient
            Assessment of the patient with osteoporosis includes history and physical examination, laboratory testing, and imaging studies. Information gathered during this assessment assists clinicians in targeting strategies to prevent fractures. The medical history should contain items such as personal and family history of fractures, lifestyle, intake of substances such as vitamin D, calcium, corticosteroids, and other medications. The physical examination can reveal relevant information such as height loss and risk of falls. Bone mineral density (BMD), most commonly determined by dual-energy x-ray absorptiometry (DEXA), best predicts fracture risk in patients without previous fracture. BMD testing is most efficient in women over 65 years old but is also helpful for men and women with risk factors. Serial BMD tests can identify individuals losing bone mass, but clinicians should be aware of what constitutes a significant change. Laboratory testing can detect other risk factors and can provide clues to etiology. Selection of laboratory tests should be individualized, as there is no consensus regarding which tests are optimal. Biochemical markers of bone turnover have a potential role in fracture risk assessment and in gauging response to therapy, but are not widely used at present. Clinicians should be aware of problems with vitamin D measurement, including seasonal variation, variability among laboratories, and the desirable therapeutic range. Careful assessment of the osteoporotic patient is essential in developing a comprehensive plan that reduces fracture risk and improves quality of life.
a.      History & Physical Examination
Age, risk factors, history of fractures, smoking history, alcohol intake, medications, usual diet, menstrual history including menopause, usual exercise/activity level, low back pain
b.      Physical Assessment
            Height, spinal curves
c.       Diagnostic Tests
*      Dual-Energy X-Ray Absorptiometry (DEXA) - DEXA measures bone density in the lumbar spine or hip and is considered to be highly accurate.
*      Ultrasound – transmits painless sound waves through the heel of the foot to measure bone density. This 1-minute test is not as sensitive as DEXA, but is accurate enough for screening purposes.
*      Alkaline phosphatase (AST) – elevates following a fracture, and serum bone Glaprotein (osteocalcin), which can be used as a marker of osteoclastic activity and therefore is an indicator of the rate of bone turnover. This test is most useful to evaluate the effects of treatment, rather than as indicator of the severity of the disease.
IV.             Pathophysiology
Incidence
            The National Osteoporosis Foundation (2006) has found that 10 million people have osteoporosis and 34 million have low bone mass, increasing their risk for the disease. Although osteoporosis can occur at any age and in both men and women, 80% of those with osteoporosis are women. One in two women and one in four men over age 50 will have an osteoporosis-related fracture in his or her lifetime.
Risk Factors
a.      Unmodifiable Risk Factors
*      Gender
            Both men and women are susceptible to osteoporosis as they age, because the osteoblasts and osteoclasts undergo alterations that diminish their activity. But women have a significantly higher risk for manifestations and complications of osteoporosis because their peak bone mass is 10% to 15% less than that of men. Estrogen in women and testosterone in men appear to help prevent bone loss; decreasing levels of these hormones associate with aging contribute to bone loss. Estrogen promotes the activity of osteoblasts, increasing new bone formation. In addition, estrogen enhances calcium absorption and stimulates the thyroid gland to secrete calcitonin, a hormone that suppresses osteoclast activity and increases osteoblast activity.
*      Age
            Age-related bone loss in men occurs 15 to 20 years later than n women and at a slower rate. In addition, age-related bone loss begins earlier and proceeds more rapidly in women, beginning in their early 30s and before menopause.
*      Race
            European Americans and Asians are at a higher risk for osteoporosis than African Americans, who have greater bone density.
*      Endocrine Disorders
            Clients who have an endocrine disorder such as hyperthyroidism, hyperparathyroidism, hyperparathyroidism, Cushing’s syndrome, or Diabetes Mellitus are at high risk for osteoporosis. These disorders affect the metabolism, in turn affecting nutritional status and bone mineralization.
b.      Modifiable Risk Factors
*      Lifestyle
            Premature osteoporosis is increasing in female athletes, who have greater incidence of eating disorders and amenorrhea. Poor nutrition and intense physical training can result in a deficient production of estrogen. Decreased estrogen, combined with a lack of calcium and vitamin D, results in a loss of bone density.
            On the other hand, sedentary lifestyle is another factor that can cause osteoporosis. Weight bearing exercise, such as walking, influences bone metabolism in several ways. The stress of this exercise causes an increase in osteoblast growth and activity. Without this, there will be minimal growth promoting nutrients to stimulate bone resorption.
*      Calcium Deficiency
            Calcium is an essential mineral in the process of bone formation and other significant body functions. When there is an insufficient intake of calcium in the diet, the body compensates by removinf calcium from the skeleton, weakening bone tissue.
*      High-protein/High-phosphate Diet
            Acidosis, which usually results from a high-protein diet, contributes to osteoporosis in two ways: Calcium is withdrawn from the bone as the kidneys attempt to buffer the excess acid. Acidosis also may directly stimulate osteoclast function. A high intake of diet soda with a high phosphate content depletes calcium stores.
*      Smoking
            Smoking decreases the blood supply to bones. Nicotine slows the production of osteoblasts and impairs the absorption of calcium, contributing to decreased bone density.
*      Alcohol Intake
            Alcohol has a direct toxic effect on osteoblast activity, suppressing bone formation during periods of alcohol intoxication. In addition, heavy alcohol use may be associated with nutritional deficiencies that contribute to osteoporosis. Interestingly, moderate alcohol consumption in postmenopausal women may actually increase bone mineral content, possibly by increasing levels of estrogen and calcitonin.
*      Medication Therapy
            Prolonged use of medications that increase calcium excretion, such as aluminium-containing antacids and anticonvulsants, increase the risk of developing osteoporosis. Heparin therapy increases bone resorption, and its prolonged use is associated with osteoporosis. Antiretroviral therapy for people with AIDS or HIV infection may cause decreased bone density and osteoporosis.
            Anyone who takes a glucocorticoid medication for more than 3 months is at risk for glucocorticoid-induced osteoporosis. These medications, often prescribed to control many rheumatic diseases, include prednisone, prednisolone, dexamethasone, and cortisone, These medications can directly affect bone cells, slowing the rate of bone formation. They also interfere with how the body uses calcium and affect levels of sex hormones, leading to bone loss. Problems that result, such as an increased possibility of fractures, can be prevented by taking a daily regimen of calcium supplements with added vitamin D and one multivitamin.
Pathophysiology
            Although the exact pathophysiology of osteoporosis is unclear, it is known to involve an imbalance of the activity of osteoblasts that form new bone and osteoclasts that resorb bone. Until age 35, when peak bone mass occurs, formation occurs more rapidly than does reabsorption. After peak bone mass is achieved, slightly more is lost than is gained. This loss is accelerated if the diet is deficient in vitamin D and calcium. In women, bone loss increases after menopause (with loss of estrogen), then slows but does not stop at about age 60. Older women may have lost between 35% and 50% of their bone mass, older men may have lost between 20% and 35%. Osteoporosis affects the diaphysis and the metaphysis. The diameter of the bone increases  thinning the outer supporting cortex. As osteoporosis progresses, trabeculae are lost from calcellous bone, and the outer cortex thins to the poingt that even minimal stress will fracture the bone
What is Osteoporosis?
Clinical manifestations
            The most common manifestations of osteoporosis are loss of height, progressive curvature of the spine, low back pain, and fractures of the forearm, spine or hip. Osteoporosis is often called the ‘silent disease’ because bone loss occurs without symptoms.
http://www.elderlyelder.com/images/osteoporosis.jpgThe loss of height occurs as vertebral bodies collapse. Acute episodes generally are painful, with radiation of the pain around the flank into the abdomen. Vertebral collapse can occur with little or no stress; minimal movements such as bending, lifting, or jumping may precipitate pain. In some clients, vertebral collapse may occur slowly, accompanied by little discomfort. Along with loss of height, characteristic dorsal kyphosis and cervical lordosis develop, accounting for the “dowager’s hump” often associated with aging. The abdomen tends to protrude and knees and hips flex as the body attempts to maintain its center of gravity.
V.                Nursing diagnosis
*      Acute pain of the lower spine related to vertebral compression
*      Imbalanced nutrition: less than body requirements related to inadequate calcium intake
*      Risk for injury related to the effects of change in bone structure secondary to osteoporosis.
VI.             Treatment
*      Lifestyle
            Lifestyle prevention of osteoporosis is in many aspects the inverse of the potentially modifiable risk factors. As tobacco smoking and high alcohol intake have been linked with osteoporosis, smoking cessation and moderation of alcohol intake are commonly recommended as ways to help prevent it.
            Weight-bearing endurance exercise and/or exercises to strengthen muscles improve bone strength in those with osteoporosis. Aerobics, weight bearing, and resistance exercises all maintain or increase BMD in postmenopausal women. Fall prevention can help prevent osteoporosis complications. There is some evidence for hip protectors specifically among those who are in care homes.
*      Nutrition
            As of 2013 there is insufficient evidence to determine if supplementation with calcium and vitamin D results in greater harm or benefit in men and premenopausal women. Low dose supplementation (less than 1 gm of calcium and 400 IU of vitamin D) is not recommended in postmenopausal women as there does not appear to be a difference in fracture risk. It is unknown what effect higher doses have. There however may be some benefit for the frail elderly living in care homes. While vitamin D supplementation alone does not prevent fractures, combined with calcium it might. There however is an increased risk of myocardial infarctions and kidney stones. Vitamin K supplementation may reduce the risk of fractures in post menopausal women; however there is no evidence for men.
*      Medications
            Bisphosphonates are useful in decreasing the risk of future fractures in those who have already sustained a fracture due to osteoporosis. This benefit is present when taken for three to four years. They have not been compared directly to each other, though, so it is not known if one is better. With evidence of little benefit when used for more than three to five years and in light of the potential adverse events, it may be appropriate to stop treatment after this time in some.
            For those with osteoporosis but who have not had any fractures evidence does not support a reduction of in fracture risk with risedronate or etidronate. Alendronate may decrease fractures of the spine but does not have any effect on other types of fractures. Half stop their medications within a year.
            Teriparatide (a recombinant parathyroid hormone) has been shown to be effective in treatment of women with postmenopausal osteoporosis. Some evidence also indicates strontium ranelate is effective in decreasing the risk of vertebral and nonvertebral fractures in postmenopausal women with osteoporosis. Hormone replacement therapy, while effective for osteoporosis, is only recommended in women who also have menopausal symptoms. Raloxifene, while effective in decreasing vertebral fractures, does not affect the risk of nonvertebral fracture. And while it reduces the risk of breast cancer, it increases the risk of blood clots and strokes. Denosumab is also effective for preventing osteoporotic fractures.

VII.          References
*      Black JM, Hawks JH. (2009). Medical-Surgical Nursing, Clinical Management for Positive Outcomes 8th Edition. Elsevier PTE LTD.
*      National Osteoporosis Foundation (2002). America’s Bone Health: The State of Osteoporosis and Low Bone Mass in Our Nation. Washington, DC: National Osteoporosis Foundation.
*      Nettina, S.M. (2006). Lippincott Manual of Nursing Practice, 8th Edition. USAL: Lippincott Williams & Wilkins.
*      Porth CM. (2007). Essentials of Pathophysiology, Concepts of Altered Health States 2nd Edition. Lippincott Williams and Wilkins.
*      Seeley Et Al., Essentials of Anatomy & Physiology, Sixth Ed., McGraw-Hill International Edition, 2007, Asia
*      Smeltzer S.H., et.al (2008). Brunner and Suddarth’s Textbook of Medical Surgical Nursing 11th Edition. Lippincott Williams and Wilkins.
*      Udan, J.Q. (2002). Medical-Surgical Nursing: Concepts and Clinical Application: A Reference Book and Study Guide. Manila: Educational Pub. House.


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