Bone-Related Disorders: Calcium Functions and Requirements

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To better understand metabolic bone disease and its pharmacotherapy, you need basic knowledge of calciums role in normal body functions. Calcium is necessary for maintaining the health of the:

Musculoskeletal systemmuscle contraction and health of bones and teeth Nervous systemconduction of nerve impulses Cardiovascular systemblood coagulation

More than 99% of the bodys total amount of calcium is found in the bones; most of the remaining calcium is in the blood. About half of this serum calcium is in the active form (ionized), which plays a vital role in intracellular functions.1 The normal range of serum calcium is 4.55.5 mEq/L. Levels outside this range cause:2

Hypercalcemia (more than 5.5 mEq/L)very high levels can lead to kidney stones or kidney failure, dysrhythmias, dementia, and coma Hypocalcemia (less than 4.5 mEq/L)very low levels can lead to dysrhythmias, severe seizures and muscle spasms, hypotension, tetany, and bone fractures (if chronic)

To maintain homeostasis, the body must obtain an adequate amount of calcium from the diet or supplements. Otherwise, calcium is taken from the bones. Over time, low calcium intake causes bones to become weak, prone to fractures and breaks. Adults need to take in between 800 and 1200 mg of calcium per day.3 Women who are pregnant, breastfeeding, or postmenopausal typically need higher amounts. The amount of calcium absorbed is influenced by certain body conditions:

Absorption increases with:

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Moderate fat intake High protein intake High gastric acidity Hormonal conditions causing low serum calcium Vitamin D deficiency High-fat diet Decreased gastric acidity

Absorption decreases with:

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Increased GI motility Hormonal conditions causing high serum calcium

Bone-Related Disorders: How Calcium Balance Is Maintained

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The balance of calcium in the body is maintained through the actions of three substances:

Parathyroid hormone (PTH)produced by the parathyroid glands when serum calcium levels drop too low, resulting in:
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Increased bone resorption (demineralization), which is the process of breaking down bone into calcium and other minerals Increased calcium reabsorption in the kidneys Increased formation of activated vitamin D

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Calcitoninhormone produced by the thyroid gland when serum calcium levels rise too high, resulting in:
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Increased bone deposition, which is the process of moving calcium from blood into bone Increased excretion of calcium by the kidneys The only vitamin the body can synthesize Increases absorption of calcium in the small intestine

Vitamin D
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The process by which vitamin D is made and activated is as follows: 1. The inactive form of vitamin D, cholecalciferol, is synthesized from cholesterol. Serum levels of cholecalciferol are increased:
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By skin exposure to sunlight or ultraviolet light From dietary sources, such as milk or other substances fortified with vitamin D

2. Cholecalciferol is then converted to calcifediol, the intermediate form of vitamin D. 3. Calcifediol is metabolized in the kidneys and becomes the active form of vitamin D, called calcitriol. The primary role of calcitriol is to aid the absorption of calcium in the GI tract. From there, calcium is transported to bone, muscle, and other tissues. Because the kidneys have an active role in the formation of calcitriol, clients with severe renal disease may exhibit both calcium and vitamin D abnormalities.

Bone-Related Disorders: Hypocalcemia

A client is considered hypocalcemic if his/her serum calcium level drops below 4.5 mEq/L. Even though hypocalcemia is not a bone disease process, it is a sign of an underlying

problem that could greatly weaken the bones. Finding that underlying cause is essential for proper therapy. Many factors may contribute to hypocalcemia:

Lack of dietary intake of calcium or vitamin D Excessive vomiting Malabsorption disorders Chronic renal disease Decreased secretion of PTH due to disease or surgical removal of the thyroid or parathyroid Drug therapy:
o o o o o

Phenytoin (Dilantin) Furosemide (Lasix) Phosphate therapy Bisphosphonates Long-term corticosteroid therapy

Blood transfusions

Often, hypocalcemia occurs without symptoms. However, a client with this condition may exhibit:

Hyperactive reflexes Twitching muscles (for example, a positive Chvostek signcontraction of facial muscles when the facial nerve is tapped) Tremors Abdominal cramping Numbness and tingling of extremities Confusion

Bone-Related Disorders: Osteomalacia

Metabolic bone disease (MBD) is a term used to describe disorders that cause defects in the structure of bone. MBDs are caused by abnormal amounts of vitamins/minerals

(such as calcium, phosphate, or vitamin D) or hormones (such as PTH or calcitonin) that play a role in bone homeostasis. Osteomalacia is an MBD that is also known as rickets when it occurs in children. In this condition, the bones become softened without disturbing the basic bone structure. As a result, skeletal deformities can occur from weight-bearing stress. The main cause of osteomalacia is a deficiency of calcium and vitamin D. Although this MBD is very rare in the United States, those most at risk are premature infants, vegans (vegetarians who do not eat dairy products), and older adults. Other risk factors may include:

Malabsorption disorders of the small intestine Damage to the kidneys tubules Adverse effects of antiseizure therapy Liver impairment Limited exposure to sunlight

Symptoms of osteomalacia include:

Hypocalcemia Muscle weakness and/or spasms Scattered bone painparticularly in the hip area but also in the spine, arms, or legs Bowed legs and pigeon breast (typical in children)

Diagnostic testing includes:

X-rays and biopsy of bones CT scans of the spine Serum levels of vitamin D, calcium, and phosphate

Bone-Related Disorders: Osteoporosis

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Osteoporosis, the most common MBD in the United States, is distinguished by:

Bone demineralization Decreased bone density Bone fractures

The exact cause of osteoporosis is not known. However, two main theories of pathogenesis are:

Slow bone deposition caused by the presence of defective bone cells, which have a very short life span and are less efficient Increased rate of bone resorption caused by bone cells that have an increased level of activity

Risk factors for osteoporosis include:

Onset of menopause (most common association) Age over 60 History of osteoporosis in the family Asian or Caucasian racial heritage Anorexia nervosa Low level of dietary calcium Vitamin D deficiency Hormonal deficiencies (estrogen or androgen) Lack of exercise High consumption of alcohol History of smoking

Because osteoporosis is usually asymptomatic, diagnostic testing is important in identifying this MBD:

Bone mineral density (BMD) testing Dual-energy x-ray absorbtiometry (DEXA) scan

Bone-Related Disorders: Paget Disease

Paget disease is a chronic progressive disorder that causes enlarged and weakened bones, especially in the:

Spinal column Skull Sternum

Pelvis Femur and tibia

Other characteristics of Paget disease:

The cause is unknown, but genetic and viral factors may play a role. Bone loss and new bone formation occur concurrently at an abnormally fast rate. Bone changes lead to fractures and deformities. This MBD occurs in both genders aged over 40.

Most people with Paget disease have no symptoms. A few clients report:

Headaches Joint inflammation Pain in the hips, femurs, face, and spine Hearing loss

Paget disease is diagnosed by:

X-ray Elevated serum level of the enzyme alkaline phosphatase (ALP) Elevated serum level of calcium

Successful treatment of Paget disease depends largely on an early diagnosis. Kidney stones, arthritis, permanent bone abnormalities, and heart disease may result if a diagnosis is not made until late in the disease process.

Pharmacotherapy of Bone-Related Disorders: Calcium

In mild cases of hypocalcemia, foods rich in calcium should first be added to or increased in the clients diet. Good sources include:

Dairy products Orange juice fortified with calcium

Cereals Dark green leafy vegetables such as spinach, broccoli, and kale Seafood such as salmon, clams, and oysters

If dietary changes fail to correct the hypocalcemia, over-the-counter calcium supplements, many of which also contain vitamin D, will likely be recommended by the health care provider. Severe hypocalcemia may require an emergency IV infusion of calcium salts, such as calcium chloride or calcium gluconate. Calcium supplements/salts may also be prescribed for clients who are diagnosed with MBDs.

Pharmacotherapy of Bone-Related Disorders: Vitamin D

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Vitamin D is required for intestinal absorption of calcium. When providing vitamin D therapy, keep the following in mind:

Client needs will vary based on sunlight exposure. Daily requirement increases from 400 to 600 units after age 70.4

Between 50,000 and 100,000 units per day may be administered in cases of severe malabsorption.5 Vitamin D is available as a medication in three forms: active, intermediate, and inactive. Many calcium supplements contain vitamin D. Overdoses can occur, because vitamin D is fat-soluble. Watch for signs of hypercalcemia such as vomiting, fatigue, loss of appetite, and excessive thirst.

Examples of vitamin D analogs are:

Generic Names calcitriol

Trade Names Calcijex, Rocaltrol

Nursing Considerations Used to manage hypocalcemia and parathyroid dysfunction Elevates serum calcium levels by promoting absorption of calcium in the intestines and renal retention of calcium Pregnancy category C Routes of administration are PO and IV Treatment for osteomalacia, osteoporosis, familial hypophosphatemia (vitamin Dresistant rickets), hypocalcemia associated with hypoparathyroidism Prophylaxis for nutritional rickets Regulates levels of serum calcium and phosphate ions by enhancing absorption in the intestines Pregnancy category C Route of administration is PO

ergocalciferol

Activated Ergosterol, Drisdol, DViSol

Click to review more details on the prototype drug calcitriol.

Pharmacotherapy of Bone-Related Disorders: Bisphosphonates

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Bisphosphonates are bone metabolism regulators. In general, they slow the rate of bone resorption, which results in increased bone mass and decreased incidences of fractures. Medications in this classification include:

Generic Names alendronate sodium etidronate disodium ibandronate sodium pamidronate disodium risedronate sodium tiludronate disodium zoledronic acid

Trade Names Fosamax Didronel, EHDP Boniva Aredia Actonel Skelid Reclast, Zometa

Routes of Administration PO PO PO IV PO PO IV

Click to review more information on alendronate sodium. Bisphosphonates are frequently the drugs of choice for treating Paget disease and osteoporosis. Indications for these medications include:

Osteoporosis in postmenopausal womenalendronate, ibandronate, risedronate, zoledronic acid (Reclast) Osteoporosis in menalendronate, risedronate Corticosteroid-induced osteoporosisalendronate, risedronate, zoledronic acid (Reclast) Paget diseasealendronate, etidronate, pamidronate, risedronate, tiludronate, zoledronic acid (Reclast) Bone metastasespamidronate, zoledronic acid (Zometa) Malignant hypercalcemiapamidronate, zoledronic acid (Zometa)

Nursing considerations include:

Depending on the specific bisphosphonate, contraindications and reasons for cautious use may include: hypocalcemia, fever or infection, active upper GI problems, difficulty swallowing or narrowed esophagus, liver disease, renal impairment, hyperphosphatemia, congestive heart failure, osteomalacia, pregnancy, or lactation.

Some of the adverse effects frequently associated with bisphosphonates are nausea, vomiting, dyspepsia, and esophageal irritation. These medications should be taken on an empty stomach, 3060 minutes before eating. After administration, clients should remain upright for 3060 minutes. In the case of etidronate, clients should avoid eating for 2 hours after taking it.6

Antacids and other drugs containing calcium, as well as foods and beverages high in calcium, should be avoided for at least 2 hours before and after taking bisphosphonates.7

Pharmacotherapy of Bone-Related Disorders: Bisphosphonates

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Bisphosphonates are bone metabolism regulators. In general, they slow the rate of bone resorption, which results in increased bone mass and decreased incidences of fractures. Medications in this classification include:

Generic Names alendronate sodium etidronate disodium ibandronate sodium pamidronate disodium risedronate sodium tiludronate disodium zoledronic acid

Trade Names Fosamax Didronel, EHDP Boniva Aredia Actonel Skelid Reclast, Zometa

Routes of Administration PO PO PO IV PO PO IV

Click to review more information on alendronate sodium. Bisphosphonates are frequently the drugs of choice for treating Paget disease and osteoporosis. Indications for these medications include:

Osteoporosis in postmenopausal womenalendronate, ibandronate, risedronate, zoledronic acid (Reclast) Osteoporosis in menalendronate, risedronate Corticosteroid-induced osteoporosisalendronate, risedronate, zoledronic acid (Reclast) Paget diseasealendronate, etidronate, pamidronate, risedronate, tiludronate, zoledronic acid (Reclast) Bone metastasespamidronate, zoledronic acid (Zometa) Malignant hypercalcemiapamidronate, zoledronic acid (Zometa)

Nursing considerations include:

Depending on the specific bisphosphonate, contraindications and reasons for cautious use may include: hypocalcemia, fever or infection, active upper GI problems, difficulty swallowing or narrowed esophagus, liver disease, renal impairment, hyperphosphatemia, congestive heart failure, osteomalacia, pregnancy, or lactation.

Some of the adverse effects frequently associated with bisphosphonates are nausea, vomiting, dyspepsia, and esophageal irritation. These medications should be taken on an empty stomach, 3060 minutes before eating. After administration, clients should remain upright for 3060 minutes. In the case of etidronate, clients should avoid eating for 2 hours after taking it.6

Antacids and other drugs containing calcium, as well as foods and beverages high in calcium, should be avoided for at least 2 hours before and after taking bisphosphonates.7

Pharmacotherapy of Bone-Related Disorders: Raloxifene

Raloxifene hydrochloride (Evista) belongs to the class of drugs called selective estrogen receptor modulators (SERMs). It is used to prevent and treat osteoporosis in postmenopausal women.

Raloxifene works by reducing bone loss, thereby increasing bone density. As a result, the probability of fractures is decreased. Nursing considerations for raloxifene include: Contraindications

Other Considerations

Pregnancy and lactation (pregnancy category X) History of deep vein thrombosis (active or past)

Hot flashes are a common adverse effect. Others may include leg cramps and weight gain. This drug should not be given at the same time as cholestyramine (Questran, Prevalite), or any drugs that contain estrogen. Calcium and vitamin D supplements are recommended with raloxifene.

Immobilized clients (due to risk for thrombosis) Severe liver impairment Children Hypersensitivity to raloxifene

Click to review more details on raloxifene hydrochloride.

Pharmacotherapy of Bone-Related Disorders: Miscellaneous Drugs

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Two miscellaneous drugs used to treat MBDs are:

Drug Names calcitoninsalmon (Fortical, Miacalcin)

Descriptions Salmon form of the hormone calcitonin Classified as a bone metabolism regulator Inhibits bone resorption and promotes excretion of calcium by the kidneys Treatment for Paget disease and postmenopausal osteoporosis Calcitonin salmon is administered SC, IM, or intranasal spray (calcitonin human is administered SC only)

teriparatide (Forteo)

Human form of PTH produced by genetic engineering technology Classified as a parathyroid hormone agonist Increases new bone formation Treatment of osteoporosis in men and postmenopausal women Usually given to clients at high risk for fractures Administered SC daily

Joint Disorders: Osteoarthritis

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Arthritis can be categorized as inflammatory or noninflammatory. The video on this screen provides an overview and examples of both types. Osteoarthritis (OA), a noninflammatory joint disorder, is the most common form of arthritis and a major cause of disability in the United States. OA is a progressive degenerative condition in which articular cartilage is broken down. The disease process typically involves these changes:

Joint use and the bearing of weight may cause joint cartilage to thin.

Bone is eventually exposed, causing bone spurs and bone cysts to form, and the joint space becomes narrowed. Lubricating (synovial) fluid is also lost. All of these factors combine to cause inflammation, pain, destruction of the joint lining, and instability of the joint. The hips, knees, and spine are affected most often because they are the primary weight-bearing joints. The hands are also affected because of repetitive use.

The two types of OA are:

Idiopathicmost common type; no known cause but associated with the aging process Secondarymay be caused by joint inflammation and instability resulting from:
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Trauma or mechanical stress Neurologic disorders

People at risk for OA include:

Overweight individuals Postmenopausal women, due to a lower production of estrogen Those who have an overproduction of either growth hormone or PTH

X-rays, physical exams, and clients medical histories are used to diagnose OA. Symptoms include:

Initial joint pain (mild to severe) and stiffness Deep, aching joint pain that feels worse when moving, but is alleviated by rest Numbness or tingling with pain at night Reduced range of motion (ROM) and increased pain, as the condition progresses Increased size of joints, which usually feel hard and cool to the touch

Joint Disorders: Pharmacotherapy of OA

Both pharmacotherapy and nonpharmacologic therapy are used to manage OA. Nonpharmacologic therapy includes exercise that minimizes joint stress, such as walking, swimming, bicycling, yoga, or passive ROM exercise. The goals of pharmacotherapy are reduced pain and swelling of the joints, and minimized disability. Medications used to achieve these goals include:

Generic Names acetaminophen

Trade Names Tylenol

Descriptions Nonnarcotic analgesic Drug of choice for initial treatment of OA For severe OA pain, products that combine acetaminophen and codeine may be prescribed

capsaicin celecoxib ibuprofen naproxen sodium tramadol hydrochloride

Capsin, Zostrix Celebrex Advil, Motrin Aleve, Anaprox Rybix, Ultram

Topical analgesic Nonsteroidal anti-inflammatory drugs (NSAIDs) Treatment for OA pain unrelieved by acetaminophen

Narcotic analgesic For moderate to moderately severe pain

Other examples of OTC topical preparations for pain relief include salicylates such as Aspercreme, and counterirritants such as Ben-Gay and Icy Hot. Some drugs, such as corticosteroids, are injected directly into a joint for acute pain. This pharmacotherapy often provides several months of pain relief.

Joint Disorders: Rheumatoid Arthritis

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Rheumatoid arthritis (RA) is an inflammatory joint disorder. This chronic, progressive autoimmune disease is less common than OA. RA causes joint inflammation and disfigurement of the affected joints. The disease process includes:

Autoantibodies, known as rheumatoid factors, combine with immunoglobulin G in response to the inflammatory process of RA. Over time, chronic inflammation in the joints results in damage of the articular cartilage and nearby bone structures. Eventually, scar tissue formed from the damage prevents joints from moving.

The exact cause of RA is unknown, but genetic, environmental, and viral factors may play a role. Symptoms of RA may include:

Initial stagejoint stiffness in the morning, joint swelling and pain, general fatigue; joints may feel warm to the touch and appear reddened As the disease progressesdegree of joint stiffness increases, deformities of the joints and supporting tissues appear, muscle weakness occurs, ROM decreases Advanced stagelow fever, anemia, weight loss, extreme fatigue

Diagnosis is determined by:

Medical history and physical exam Elevated rheumatoid factor Elevated erythrocyte sedimentation rate (ESR) Elevated antinuclear antibody titers Elevated serum immunoglobulin levels

Joint Disorders: Pharmacotherapy of RA

The main goals of pharmacotherapy for RA are:

Controlled inflammation Reduced pain Maximized tolerance of physical activity

Although the pharmacotherapy goals for RA and OA have things in common, the treatment approach and many of the drugs used are different:

Therapy for RA is begun with NSAIDs because they reduce both pain and inflammation. These NSAIDs are given in higher doses than those for OA treatment.

Corticosteroids are prescribed for moderate to severe pain because of their antiinflammatory properties. However, they are not used for long-term therapy, due to adverse effects.

Tissue damage that results from RA can be treated with a group of medications called disease-modifying antirheumatic drugs (DMARDs):
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Types of DMARDs include gold salts, antimalarial drugs, D-penicillamine, and drugs that alter immune and anti-inflammatory responses. The choice of DMARD depends on the health care provider and the particular client. More than one DMARD may be prescribed concurrently, or with analgesics.

Examples of DMARDs include:

Generic Names adalimumab anakinra etanercept hydroxychloroquine infliximab leflunomide methotrexate sodium sulfasalazine

Trade Names Humira Kineret Enbrel Plaquenil Sulfate Remicade Arava MTX Azulfidine

Click to review more information on hydroxychloroquine.

Joint Disorders: Gout

Gout is a type of inflammatory arthritis caused by uric acid crystals gathering in joint spaces and other tissues. There are two types of gout:

Primaryresults from the bodys inability to handle uric acid; caused by genetic problems affecting purine metabolism Secondarycaused by diseases or drugs that increase the metabolism of nucleic acids, or affect the excretion of uric acid:
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Examples of drugsthiazide diuretics, aspirin (Bayer, Ecotrin, Empirin), cyclosporine (Gengraf, Neoral, Sandimmune), chronic alcohol use

Examples of disordersdiabetic ketoacidosis, kidney impairment, multiple myeloma, hypothyroidism, leukemia, hemolytic anemia

Symptoms of acute gouty arthritis may include:

Swollen, painful joints, especially in toes, heels, ankles, wrists, fingers, knees, elbows Red inflamed tissue Elevated body temperature Hyperuricemia (increased level of uric acid in the blood)

Risk factors or triggers of acute gouty arthritis may include:

Alcohol intake Dehydration Stress Joint injury Fever

Factors in the diagnosis of gout:

When completing a medical history and physical exam, be aware that initial signs may be vague. Many clients have normal uric acid levels even during an acute attack of gouty arthritis. A definitive diagnosis can be made by analyzing the synovial fluid.

Joint Disorders: Pharmacotherapy of Gout

The goals of pharmacotherapy for gout are:

Stop acute attacks

Prevent future incidences from occurring Avoid complications such as kidney stones and formations of tophi

Preventative measures should include:

Changes in dietavoiding alcohol and foods such as mushrooms, oatmeal, legumes Avoiding thiazide diuretics, aspirin (Bayer, Ecotrin), cyclosporine (Gengraf, Neoral)

Although NSAIDs or corticosteroids may be used to treat the pain and inflammation caused by gout, the drugs of choice are uric acid inhibitors and antigout medications. Uric acid inhibitors block the accumulation of uric acid in the blood and uric acid crystals in the joints. Examples of drugs used to treat gout are:

Generic Names Trade Names allopurinol Alloprin, Lopurin, Zyloprim

Descriptions Lowers both urinary and serum uric acid levels For managing primary hyperuricemia and prevention of acute gouty attacks Routes of administration are IV and PO Inhibits inflammation and decreases pain and swelling in acute attacks of gouty arthritis (given every hour until symptoms subside) Prophylactic for recurring gouty arthritis Has common adverse effects on GI system, such as nausea, vomiting, and diarrhea Route of administration is PO Prevents formation of new tophi and buildup of uric acid in the blood and tissues Treats tophaceous gout and chronic gouty arthritis Route of administration is PO Promotes excretion of uric acid in the urine and inhibits reabsorption of uric acid in the kidneys Maintenance therapy for tophaceous gout

colchicine

Colcyrus

probenecid

Benemid, Probalan

sulfinpyrazone

Anturane

and chronic gouty arthritis Route of administration is PO

Nursing Role: Assessment and Planning

During the assessment stage of the nursing process, you, as the nurse, are responsible for obtaining a baseline assessment that may include:

Vital signs, height, and weight

Pain assessment (onset, location, intensity, duration, character, precipitation, or alleviating factors) Health and medication history, including drug allergies and history of fractures Physical examination, which may include:
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Assessment for signs of hypercalcemia and hypocalcemia Assessment of tissue surrounding joints (presence or level of swelling, tenderness, warmth, redness; ROM)

Checking for any contraindications to prescribed medication(s) Laboratory data, as ordered by health care provider
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X-rays of bones or joints For bone-related disorders, may include complete blood count (CBC), electrolyte (calcium, phosphate, magnesium) and vitamin D serum levels, renal function studies, bone mineral density

For RA, may include rheumatoid factor, erythrocyte sedimentation rate, antinuclear antibody titers, serum immunoglobulin levels For gout, may include CBC, urinalysis, renal and liver function studies, uric acid level

In the planning stage, your role as a nurse includes doing what is necessary to ensure that the client can:

Experience the desired therapeutic effects of the medication(s) with minimal to no adverse effects Verbalize an understanding of new medication(s), including use, adverse effects, and precautions Demonstrate accurate self-administration of medication(s) Verbalize when to notify the health care provider

One of the ways to help achieve these goals is to make sure you understand the reasons why particular medications have been prescribed, before they are administered.

Nursing Role: Implementation

Your role, as the nurse, in the implementation phase of administering medications for bone and joint disorders may include:

Ensuring therapeutic effects by frequent client assessment and monitoring Minimizing adverse effects by:
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Frequent vital sign assessment Verification of medications taken at home (medication reconciliation) Medication use, adverse effects, and precautions Self-administration of medications and importance of compliance When to contact the health care provider Importance of periodic testing and follow-up appointments with the health care provider

Client education regarding:

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How to recognize symptoms of hypercalcemia, including nausea and vomiting, increased thirst and fatigue, loss of appetite How to recognize symptoms of hypocalcemia, including twitching muscles, abdominal cramping, numbness and tingling of extremities, confusion Safety precautions for avoiding injuries and preventing fractures Lifestyle modifications

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Dietary changes in cases of hypocalcemia (increasing intake of calcium-rich foods) Dietary changes in cases of gout (avoiding alcohol and high-purine foods) Exercise that minimizes joint stress, for clients with OA

Nursing Role: Evaluation

Your role in the evaluation phase of administering medications for bone and joint disorders may include:

Evaluating the effectiveness of the medication(s) for:

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Relief of pain Ability to perform activities of daily living Improved or maintained ROM Improved activity tolerance due to less pain Decreased progression of disease In the case of gout, fewer or no incidences of recurring attacks In the case of osteoporosis, improved bone density and absence of bone fractures

Evaluating the effectiveness of client education:

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Client is able to verbalize an understanding of the education provided, including self-administration of medications, adverse drug effects, and when to contact the health care provider.

Client demonstrates compliance with the drug regimen and recommended lifestyle changes. Client has kept follow-up appointments for lab work and appointments with the health care provider.