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
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.
The 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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