Chapter 53-care of patients with musculoskeletal problems Flashcards
Osteoporosis pathophysiology
Chronic metabolic disease in which bone loss causes decreased density and possible fracture. Also known as the silent disease because the first sign maybe a fracture. Spine, hip,, wrist, and forearm are most common. There is a loss of height, progressive curvature of the spine and low back.
Osteoclastic activity is greater than osteoblastic activity resulting in a decrease bone mineral density. BMD peaks between 25 and 30 years of age. After that age bone resorption exceeds rebuilding. Estrogen does not build bone, but helps prevent loss.
Generalized
Primary in post menopausal women or men in 70-80s
Secondary due to medical condition such as
Hyperparathyroidism, long-term drug therapy, prolonged immobility.
Regional: This is secondary disease that occurs when limb is immobilized related to a fracture, injury, or paralysis. Immobility for longer than 8 to 12 weeks can cause this. Can also occur in astronauts.
The risk depends on how much bonemass is achieved and how much is later lost. Women lose about 2% of their bone mass every year in the first five years after menopause. For women of any age that do not take estrogen replacement the risk increases. Men also get it after 50 because testosterone decreases which is responsible for building bone tissue.
Osteoporosis: Nonmodifiable risk factors
Older age
parental history especially the mother
history of low trauma fracture after 50 years,
being female, especially Caucasian and Asian (bone mass corresponds to amount of skin pigmentation, thats why africans have lower risk)
Low bodyweight/thin built
Endocrine disorders such as hyperthyroidism,
hyperparathyroidism, Cushing’s syndrome, or DM
Osteoporosis: modifiable risk factors
chronic low calcium and or vitamin D intake.
Estrogen and testosterone deficiency.
Current smoking.
High alcohol intake over three drinks.
Lack of physical exercise or prolonged immobility.
Medications: aluminum containing antacids, anticonvulsants,
heparin, antiretrovirals, and glucocorticoids
Osteoporosis: diet/nutrition
Excess caffeine can cause calcium loss.
A diet lacking calcium and vitamin D stimulates the parathyroid to release PTH which causes release of calcium from the bone.
Calcium loss increases when phosphorus intake is high. High amounts of carbonated beverages put you at high risk.
Protein deficiency can reduce bone density as 50% of serum calcium is protein-bound. Too much protein can increase calcium lost in the urine.
Excessive alcohol and tobacco use that a person at risk. Excessive exercise, weight loss dieting, eating disorders.
Activated vitamin D is needed for calcium uptake in the body.
Malabsorption of nutrients in the G.I. tract contribute to a low serum calcium level. Patients who are not exposed to sunlight maybe at a higher risk because they do not receive adequate vitamin D for metabolism of calcium
Osteoporosis: ACCESS
Alcohol Corticosteroid Calcium low Estrogen low Smoking Sedentary lifestyle
Osteoporosis: health promotion
Teaching should begin with young women are at 30 years old.
Prevention to decrease modifiable risk factors.
Ensure adequate calcium intake: including food such as dairy, dark green leafy vegetables, and calcium supplements. Divide calcium into to three doses. Get sun exposure for vitamin D and also vitamin D supplements. Limit carbonated beverages. Avoid sedentary lifestyle. Continue weight-bearing exercises.
Tests for osteoporosis
No lab test, but some biochemical markers. Other metabolic diseases may have change in calcium, vitamin D, phosphorus, serum protein, thyroid function tests.
DXA/dual x-ray absorptiometry of the spine and hip. Women in 40s should have a baseline done, less radiation than a chest x-ray. Best for a definitive dx
QCT-Quantitative computed tomography can measure bone density using either central or peripheral technique. Analyzes trabecular cortical bone separately and sensitive to changes in the vertebral column. More expensive
QUS-Quantitative ultrasound. Heel, tibia, and patella tested. No preparation or radiation exposure.
Intervention for osteoporosis
Nutrition therapy. Same as preventions. Get adequate amounts of protein, magnesium, vitamin K, and trace minerals. Increase calcium and vitamin D. Avoid excess alcohol and caffeine. You must increase all nutrients not just one. Have exercising program that includes strengthening and weight-bearing. Walk for 30 minutes 3 to 5 times a week is most effective for prevention. Avoid high-impact activities. Avoid tobacco. Prevent falls to reduce your risk of fractures.
Drug therapy for osteoporosis
Calcium and vitamin D supplements. Intake of calcium alone is not a treatment that is important for prevention. Calcium carbonate over-the-counter is good for people with G.I. upset. Take it with food and drink 6 to 8 ounces of water to prevent urinary or renal calculi. Be careful for hypercalcemia.
Estrogen or hormone therapy. It reduces bone loss, increases bone density and reduces the risk of fractures in postmenopausal women.
Biphosphonate: drug of choice for preventing and treating. they are potent inhibitors of bone resorption that preserve bone mass and increased density such as Fosamax, Boniva, intestinal. Side effects include heartburn, difficulty swallowing, jaw pain. Report them. Prior to beginning having oral assessment and preventative dentistry. Tell any dentist that you are taking these. Take early in the morning with 8 ounces of water and remain upright for 30 to 60 minutes before eating. Discontinue if chest discomfort. Do not take if you have decreased renal function, hypocalcemia, or GERD.
Hypocalcemia may occur and you need to maintain adequate intake of calcium and vitamin D. Calcium interferes with the drug and should be taken at a different time.
Reclast and Aredia Are given IV. Reclast is given once a year and Aredia is given every 3 to 6 months. Both have a complication of jaw osteonecrosis. Have dentistry prior to beginning drug.
Zometa IV once a year, but contraindicated with aspirin sensitivity. Check creatinine prior because of renal problems.
Selective Estrogen Receptor modulators: SERMs prevent bone loss by mimicking estrogen. Reduces risk of breast cancer. Evista, Nolvadex, Tamofen
Calcitonin is a thyroid hormone that inhibit osteoclastic activity. Have analgesic effect after vertebral fracture.
Osteomalacia: pathophysiology
Osteomalacia is the loss of bone related to Vitamin D deficiency. Causes softening of the bone. Calcification doesn’t occur. Called rickets in children. It is more common in poor and famine countries. Older adults most at risk. Vegans, homeless, and alcoholics also at risk. Dark skin is more at risk than light skin
Osteomalacia causes
Vitamin D disturbances can come from inadequate production, lack of sunlight, dietary deficiency, abnormal metabolism, drug therapy with Dilantin, fluoride, or barbiturates, liver disease, renal disease, post gastrectomy, malabsorption, inflammatory bowel.
Kidney disease including acidosis and hypophosphatemia
Osteomalacia prevention, teaching, and treatment:
Increase vitamin D through the diet, and exposure, entrance supplements. Foods with vitamin D include milk and food that has vitamin D added, eggs, swordfish, chicken, liver, enriched cereals and bread. Cheese and yogurt do not normally have vitamin D in it. Read food labels to find out. At least five minutes a day of sunlight for homebound.
400 to 800 units Vitamin D needed
Osteomalacia Assessment
Take a thorough nutritional and sun exposure assessment. Include any history of chronic diseases of the G.I. tract and renal disease. Medication history. They may have hypophosphatemia leading to muscle weakness and hypocalcemia leading to muscle cramping. The muscle strength and gait. If the patient has pain it’s usually aggravated by activity and gets worse at night.
Osteomalacia diagnosis
X-rays show decrease in cancellous bone and lack of osteoid sharpness. The classic diagnostic finding is the presence of radiolucent band called losers lines or zones. They represent stress fractures that are not mineralized. They appear in the neck, ribs, and pelvis. Bone biopsy may be needed. DXA scan may help
Paget’s disease pathophysiology
AKA osteitis deformans
Metabolic disorder in which bone is excessively broken down and reformed. The bones are weak with increased risk for bowing and fractures. It can be familial or sporadic.
Active phase: Rapid increase in osteoclast that breakdown bone and cause destruction and deformity.
Mixed phase: osteoblasts form new bone causing it to be vascular, structurally weak, and deformed.
Inactive phase: When osteoblast exceed osteoclast activity. The newly formed bone becomes sclerotic and hard
Most common areas include the vertebrae, fever, skull, clavicle, humerus, and pelvis.
It is possibly a result of a viral respiratory infection or an autosomal dominant pattern (identical twins). Offer genetic counseling
Men over 50, Europeans are at risk