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Metabolic Bone Disorders Objectives Differentiate metabolic bone disorders by etiology, treatment and outcome. Outline common nursing diagnoses, outcome criteria and interventions for common metabolic bone disorders. Bone Cell Types Osteoblast Forms bone & mineralization of matrix Osteocyte Transformed osteoblast Maintains bone found in matrix Osteoclast Breaks down bone salts Responsible for bone reabsorption Bone Cell Mnemonics Osteoblasts “Baby bone cells” “Building Blocks” Osteoclasts “Clean up” cells Osteocytes “Cycle” of bone Question #1: Which statement is true of osteoblasts? a. They transform osteocytes into osteoblasts. b. They maintain cells within the bone matrix. c. Osteoblasts form bone cells within matrix. d. Osteoblasts break down bone salts. Answer #1. Which statement is true of Osteoblasts? c. Osteoblasts form bone cells within matrix. Rationale: Osteoblasts are “bone builders”; the other responses are related to functions of other bone cell types. Bone Remodeling Process PHASE I PHASE II PHASE III Hormonal, Biochemical Physiological Indicators Osteoclasts Resorb Bone Osteoblasts Form Bone Activate Precursors Creates Cavities in Cortical & Cancellous Bone Create New Bone In Formed Cavities Osteoclast Formation Hormonal Regulation of Bone Metabolism Thyroid gland Thyroxine, triodothronine & calcitonin Regulated by TSH / TRH & calcitonin by plasma levels of calcium Parathyroid gland Parathormone PTH (protein hormone) Regulated by serum ionized calcium levels Hormonal Regulation of Bone Metabolism Anterior pituitary gland ACTH / TSH / FSH / LH / Prolactin Regulated by hypothalamus Adrenal cortex Glucocortcoids / mineralcorticoids & androgens Estrogen Increased osteoblast activity Retention of calcium and phosphate Question #2: Which hormone is the most important for regulating serum calcium levels because it acts directly on bone and kidneys? a. Parathyroid hormone. b. Growth hormone. c. Calcitonin. d. Adrenal corticosteroids. Answer #2: Which hormone is the most important for regulating serum calcium levels because it acts directly on bone and kidneys? a. Parathyroid Hormone. Rationale: As noted earlier, this hormone acts directly on bone and kidneys Hyperparathyroidism Mainly two types Primary- cause unknown but thought to be familial and characterized by excessive secretion of PTH Secondary-usually due to disease state such as renal failure which causes decrease in ionized serum calcium levels Excess Secretion of PTH Interrupts metabolism of calcium / phosphate / Bone Hyperparathyroidism- Pathophysiology Although primary/secondary cause either hypo or hypercalcemia, end result remains elevated levels of PTH which causes eventual hypercalcemia and multisystem problems Hyperparathyroidism Primary Secondary Results in: Hypercalcemia Causes Adenoma / Carcinoma Genetic / Multiple Endocrine Disorder Results in initial hypocalcemia followed by hypercalcemia Causes Chronic Renal Failure / Malabsorption Syndromes / Vitamin D Deficiency Hyperparathyroidism Clinical manifestations •Bones – Demineralization due to excessive osteoclast and osteocyte activity •Kidneys – renal calculi, UTI •GI– Anorexia / NV, pancreatitis, peptic ulcers, constipation, hypergastrinemia •Psychiatric issues •Muscle weakness, myalgias Hyperparathyroidism Diagnostics All other causes of hypercalcemia must be eliminated first 6 month history of symptoms of hypercalcemia Kidney stones, hypophosphatemia, hypochloremia Serum Calcium Levels - >10mg/dl PTH Assay – ↑1° Radioactive Iodine Uptake Test - ↓ Subclinical / Post- Partum / Acute Thyroiditis Urinary Calcium – ↑(24 Hr Specimen) DEXA Bone Density - ↓ Hyperparathyroidism Clinical Management Adequate Hydration Increase urinary excretion of Ca++ with diuretics Drugs that decrease resorption of Ca++ by bone-biphosphates, calcitonin Surgery Parathyroidectomy – NOT Often Recommended Leaves ½ of one Lobe of the Parathyroid Remove Adenoma Question #3: Ms. Jones is a 60-year-old female who presents in the Clinic with a 6 month history of frequent renal stones, abdominal pain, muscle aches and several fractures of her metatarsals. The nurse would suspect: a. Gout. b. Hyperparathyroidism. c. Hypoparathyroidism. d. Paget’s Disease. Answer # 3: Ms. Jones is a 60-year-old female who presents in the Clinic with a 6 month history of frequent renal stones, abdominal pain, muscle aches and several fractures of her metatarsals. The nurse would suspect: b. Hyperparathyroidism. Rationale: As defined earlier, these are common s/s of hyperparathyroidism Question #4: In order to confirm this diagnosis, diagnostic testing needs to be performed. As the Nurse you know: a. That you can rely on one blood sample to give complete results. b. The patient will need blood work, DEXA scans, and 24 hour urine samples c. That you can rely on urine testing alone. d. The tests will most likely be inconclusive. Answer #4: In order to confirm this diagnosis, diagnostic testing needs to be performed. As the Nurse you know: b. You will need to have results of serum Ca++, phosphate, magnesium, bicarbonate levels as well as a DEXA scan and a 24 hour urine for excreted Ca++ Rationale: DEXA scan shows demineralization of bone, 24 hour urine shows excess Ca++, and abnormal serum levels of trace elements Question #5: Mrs. Jones is diagnosed with hyperparathyroidism. As the nurse doing the patient teaching, you are aware that adequate hydration is essential in preventing: a. Constipation. b. Hypercalcemia. c. Alteration in fluid balance. d. All of the above. Answer #5: Mrs. Jones is diagnosed with Hyperparathyroidism. As the nurse doing the patient teaching, You are aware that adequate hydration is essential in preventing: d. All of the above. Rationale: Adequate hydrationhelps to prevent constipation, hypercalcemia and fluid balance alterations Hypoparathyroidism Decreased Secretion of PTH Most commonly caused by injury to parathyroid gland during surgery Can also be caused by hypomagnesemia Pathophysiology Bones – Mineralization Bone Resorption Hypocalcemia / Intestinal Ca+ Absorption Metabolic Alkalosis (Mild) Parkinson-like Symptoms Hypoparathyroidism Clinical Presentation Mental Fatigue Abdominal Pain Patient History of Alcoholism Physical Examination Muscle Spasm / Tetany / Excitability Deep Tendon Reflexes Dry Skin / Hair Loss / Weakened Tooth Enamel Hypoparathyroidism Diagnostics Serum Calcium Levels – DECREASED Serum Phosphorus – INCREASED Low Vitamin D Levels Urinary Calcium –DECREASED X-Rays Increased Bone Density Hypoparathyroidism Clinical Management Acute condition MEDICAL EMERGENCY Prevent larygneal spasms- administer IV Ca++ gluconate/carbonate STAT! Chronic condition Lifetime Vitamin D therapy Calcium supplementation- 1 to 3 gm/day Muscle relaxants to control muscular spasms Drugs to reduce GI absorption of phosphorous Osteomalacia (Adult Rickets) Inadequate and delayed mineralization of osteoid in mature compact and spongy bone Major deficit is in Vitamin D , which is required for Ca++ uptake in intestines Decreased Ca++ stimulates PTH, which does increase Ca++, but also increases phosphate excretion by kidney When phosphate levels too low, mineralization cannot occur Osteomalacia (Adult Rickets) con’t Etiology More prevalent in extreme preemies, elderly, those following strict macrobiotic vegetarian diets and persons on anticonvulsant Rx Pancreatic insufficiency Hepatobiliary diseases Lack of bile salts decreases absorption of Vit D Malabsorption syndromes Hyperthyroidism Rare in US due to fortification of foods Common in GB and Middle Eastern Countries Osteomalacia Clinical Presentation Generalized body aches /LBP as well as hip pain Lower extremity pain & deformity Physical examination Scoliosis / kyphosis of spine Deformities of weight bearing bones Muscle weakness leading to classic waddling gait Generalized Malaise Osteomalacia Diagnostics Serum Ca++ –↓ or Normal Serum inorganic Phosphate ↑> 5.5 Vitamin D ↓ BUN & creatinine ↑ Alkaline Phosphatase & PTH ↑ Bone bx to determine aluminum levels X-Rays Demineralization Pseudofractures Bowing of long bones Osteomalacia Clinical Management Correcting serum Ca++ & phosphorous Chelating bone aluminum if needed Suppressing hyperthyroidism Supplement with Vitamin D Administer Ca++ carbonate to ↓ hyperphosphatemia Renal dialysis/transplant for renal osteodystrophy Correction of associated intestinal disorders Question #6: X-rays of a patient with Osteomalacia would reveal: a. Increased bone density. b. Stress fractures. c. Normal joint alignment. d. Demineralization. Answer #6: X-rays of a patient with Osteomalacia would reveal: d. Demineralization. Rationale: As calcium and phosphorus levels are decreased, demineralization can be noted on x-ray Osteoporosis Most common metabolic bone disease Reduction of bone mass density (BMD) fractures Estrogen deficiency leads to a rapid in BMD Rapid bone loss may occur Up to 20% during the first 5-7 years post-menopause Surgically induced menopause Results in severe decrease in BMD regardless of age Osteoporosis Type I - Postmenopausal Type II - Senile Secondary Predominantly in Females Affects Males & Females Affects Males & Females 10-15 Years Postmenopause Common After Age 70 Occurs At Any Age Decreased Levels of Estrogen Related to Nutrition Decreased Physical Activity Result of Disease Process Or Medical Treatment Loss of Trabecular Bone Loss of Cortical & Trabecular Bone Loss of Cortical & Trabecular Bone Accelerated Bone Loss Non-Accelerated Bone Loss Osteoporosis – Risk Factors Inherited Gender / Ethnicity Body composition Gyn considerations Family History Hx. Of osteoporosis Medical Conditions Rheumatoid arthritis Thyroid / Liver Dz Spinal cord injury Behavioral Physical activity level Nutritional status Lifestyle habits Medications Thyroid replacement Corticosteroid use Antacids Long term anticonvulsant use Osteoporosis Clinical Presentation Attire Height Spine (Posture) Chest/ Abdomen Gait Ill fitting clothes Recent loss of height Kyphosis Chest resting on protruding abdomen Slow reciprocal – Wide base stance Osteoporosis Differential Diagnosis Urinary calcium - ↑ in secondary osteoporosis Biochemical markers of bone resorption Urinary pyridinoline- ↑ for a variety of metabolic bone diseases X-Rays ↑ density often not seen until 50% loss DEXA Hip / Lumbosacral spine -↑ Osteoporosis – Fracture Risk • Essential to ALL groups Post-menopausal & elderly MOST at risk for fracture • Bone strength depends on Mass Architecture Bone Quality • BMD Testing Bone Mass Measurement Act Osteoporosis Nutritional support Calcium intake levels RDA based on age Co-Factors Vitamin D Serum 1,25-dihydroxyvitamin D3 Exercise Weight bearing exercise 2-3 x week Recommended Daily Calcium Intake 1600 1400 1200 1000 800 600 400 200 RDA Suggested 0 0-6 mos. 6-12 1-5 yrs mos. 5-10 yrs 11-24 yrs 25-50 yrs +65 yrs Anti-Resorptive Medication Estrogen Prevents bone resorption Most commonly used Start within 3 Yrs of menopause Positive effect of calcium absorption & calcitonin risk of endometrial cancer – progesterone MUST be added if no hysterectomy Oral / Transdermal New data shows no change in CV risk Anti-Resorptive Medication Calcitonin Inhibits osteoclasts – prevents bone resorption Tx. postmenopausal osteoporosis Males & females In conjunction with calcium & Vitamin D Analgesic properties Intranasal administration Anti-Resorptive Medication Bisphosphonates Non-Hormonal agent Highly selective osteoclast inhibitor Indicated for treatment & prevention & osteoporosis in men BMD 2 standard dev. below norm for young adults SE – GI disorders / Esophageal & gastric ulcers Anti-Resorptive Medication SERM - Selective Estrogen Receptor Modulator Indicated for prevention Enhances beneficial effects of estrogen without increasing risks to breast / uterus Caution use in patients at risk for DVT Bone Forming Agents Slow-Release calcium fluoride Stimulate osteoblast activity New bone matrix remains brittle Not effective with severe demineralization Must have adequate calcium intake See Handout for medications Osteoporosis Surgical intervention for vertebral fractures Vertebroplasty High pressure injection of bone cement through pedicles to vertebral body Contraindicated in severe vertebral body collapse Osteoporosis Surgical intervention for vertebral fractures Kyphoplasty Bone tamp through cortical window Inflation of bladder in vertebral body Injection of bone cement under LOW PRESSURE Osteoporosis Physiological Decreased respiratory function Kyphotic deformity GI/Bowel alteration Protrusion of abdomen Medications Self-care deficits Osteoporosis Psychological Low self-esteem Depression Social isolation Retreat from activities Sleep disturbances Physical/Psychological component Ms. Rice Is a 56 year old woman. She presents to the GYN for her annual check-up. A detailed nursing history reveals the following: Ht: 5’5” (5’6” last yr) Wt: 126 lbs. Race: Caucasian Medical History LMP 4 years earlier Thyroidectomy 10 yrs Mild OA rt. knee Current Meds/Supplements Synthroid Calcium 1000 mgs. Case Study con’t Social History Non-smoker Infrequent Exercise Family History: Mother Osteoporosis Question #7: Of the identified risk factors, which would be considered to be modifiable? a. Use of thyroid replacement medications. b. Exercise level. c. Family history of osteoporosis. d. Loss of height. Answer #7: Of the identified risk factors, which would be considered to be modifiable? b. Exercise level. Rationale: While Ms. Rice can control amount of exercise, she cannot modify other factors. Question #8: The nurse should assess Ms. Rice’s dietary intake of calcium to be sure she is getting a suggested daily intake of: a. 800 mgs. Daily. b. 1000 mgs. Daily. c. 1500 mgs. Daily. d. Calcium is not required as she is post-menopausal. Answer #8: The nurse should assess Ms. Rice’s dietary intake of calcium to be sure she is getting a suggested daily intake of: c. 1500 mgs. daily. Rationale: Noting age and history, Ms. Rice’s dietary intake of calcium should be the same as an adolescent Question # 9: Ms. Rice has a DEXA Test. It demonstrates BMD 2.5 St. Dev. She has been advised to start taking medication. As part of the patient education, the nurse understands that: a. Estrogen can be started at any time postmenopause and retain the same level of effectiveness. b. Calcium alone is effective in increasing BMD. c. SERMs risk of breast & uterine cancer. d. Bisphosphonates are osteoclast inhibitors & are effective anti-resorptive agents. Answer #9: Ms. Rice has a DEXA test. It demonstrates BMD 2.5 St. Dev. She has been advised to start taking medication. As part of the patient education, the nurse understands that: d. Bisphosphonates are osteoclast inhibitors & are effective anti-resorptive agents. Rationale: As per previous discussion, other statements are incorrect Paget’s Disease Osteitis Deformas Bone resorption bone formation develop large irregularly shaped bones with poor mineralization thick brittle bones Etiology Slow progressing disease Often occurs between 50-70 years Familial tendency in males Usually asymptomatic Paget’s Disease Clinical Presentation Deep aching sensation with weight bearing Pain - mild to severe unrelated to activity May have bony deformities – skull Loss of height Physical Examination Kyphosis / Bowing of long bones Conductive hearing loss Fracture healing is impaired Complications – CHF / Paget’s sarcoma Paget’s Disease Diagnostics Serum alkaline phosphatase -↑ Urinary hydroxyproline - ↑ Serum/ urinary citrate – ↑ Serum uric acid – ↑in < 50% X-Rays Early localized demineralization Later bony overgrowth – irregular Mosaic pattern Bone scan Metabolic activity- ↑ Paget’s Disease Clinical Management Asymptomatic Monitor patient Symptomatic NSAIDs Calcitonin – relieve bone pain Bisphosphonates Ambulation with assistive devices Surgical Intervention Correction of malalignment / fractures Question #10: Paget’s Disease is characterized by: a. Decreased bone formation. b. Decreased bone resorption. c. Mosaic patterned bone growth. d. Accelerated bone healing. Answer #10: Paget’s Disease is characterized by: c. Mosaic patterned bone growth. Rationale: Decreased bone formation, bone resorption and accelerated bone healing produce a mosaic pattern of growth Summary Bone cell types Hormonal regulation of bone formation Causes & consequences of / levels of hormones Solutions Dietary considerations (note: cause & solution) Exercise patterns (note: cause & solution) Medications Hormonal / Non-hormonal / vitamins Surgical intervention (note: rx. for effect / cause)