Other bone diseases Flashcards
Paget’s disease
localized bone disease characterized be uncontrolled bone resorption w/ secondary increase of bone formation, new bone is poorly organized, irregularly shaped and poor mineralization, bones are thick and brittle
Paget’s affects how many
3-4% of all Americans over the age of 50, second bost prevalent bone remodeling disease second only osteoporosis
Clinical presention of Paget’s
often asymptomatic, deep aching sensation worsens w/ wt bearing, pain is mild to severe unrelated to activity, may have deformities, loss of ht
Complication of Paget’s
often occur when bony overgrowth presses against other structures- lead to blindness, vertigo, hearing loss, tinnitus, increased calcification can lead to CHF, gout, arthritic changes
Treatment of Paget’s
Asymptomatic- monitor pt, education, symptomatic- bisphosphonates- DOC for their activity on osteoclasts to slow bone turnover, NSAIDs, Calcitonin- relieve bone pain, used if bisphosphonates cannot be used, PT, surgical intervention
Rickets
associated with softening and weakening of bones in children, usually related to an extreme vit d deficit, can be genetic
Rickets presents with
delayed growth, pain, muscle weakness, bowed legs, thickened wrists/ankles, breastbone projection
Rickets risk factors
age, dark skin, prematurity, exclusively breast-fed infants
Rickets etiology
nutritional, vit D resistant rickets, vit D dependent rickets type 1, vit D dependent rickets type II, renal osteodystrophy
Vit D analog
Calcitriol (Rocaltrol), Cholecalciferol, Doxercalciferol (Hectoral), Ergocalciferol (Drisdol), Paricalcitol (Zemplar)
Vit D MOA
Vit D analog bind to the Vit D receptors in kidneys, PTH gland, intestines and bone, doing so reduces PTH levels and improves Ca and Phos homeostasis
Vit D PEARLs
decreased renal conversion of vit D to its primary active metabolite in chronic renal failure leads to reduced activation of vit D receptor, removes suppression of PTH release, increased serum PTH reduces calcium excretion and enhances bone resorption
Calcitriol (Rocaltrol) MOA
active form of Vit D works via several pathways to increase [Ca], once daily, IV 1-2 per month, adequate dietary Ca necessary for effect
Calcitriol (Rocaltrol) clinical uses
rickets, hypocalcemia related to renal disease, management of hyperparathyroidism in pts w/ chronic kidney disease
Calcitriol (Rocaltrol) ADRs
well tolerated, GI intolerance only
Cholecalciferol (Vit D3) MOA
synthetic vit D3 derivative, products available OTC, often in combo w/ calcium, given PO once daily
Cholecalciferol (Vit D3) clinical uses
rickets, vit D deficiency, osteoporosis prevention, hypocalcemia
Ergocalciferol (Drisdol) MOA
Active form of Vit D works via several pathways to increase [Ca], given once daily, once weekly or monthly
Ergocalciferol (Drisdol) clinical uses
vit d deficiency, osteoporosis prevention, hypoparathyroidism, osteomalcia, rickets
Doxercalciferol (Hectoral) MOA
metabolized to the active form of vit D, given IV and PO, usually 3 x weekly, monitor and adjust dose based on PTH levels
Docercalciferol (Hectoral) clinical uses
secondary hyperparathyroidism in pts with CKD
Docercalciferol (Hectoral) ADRs
edema, GI intolerance
Paricalcitol (Zemplar) MOA
synthetic vit D analog, IV every 2-4 weeks, titrated to goal PTH, PO 3x weekly
Paricalcitol (Zemplar) caution use
hypercalcemia, excessive vit D can lead to over suppression of PTH
Two types of hyperparathyroidism
Primary- unknown cause, prob familial and characterized by excessive secretion of PTH, Secondary- usually due to disease state such as renal failure, cuases decrease in ionized serum calcium levels (Thyroiditis, medications)
Effects of hyperparathyroidism
bone looses density, hypercalcinuria, anorexia, N/V, ab pain, agitation, nervousness, anxiety, fatigue
Treatment of hyperparathyroidism
focuses on correcting hypertrophy of the parathyroid, vit D therapy and renal replacement therapy for pt w/ renal failure, adequate hydration, diuretics, drugs that decrease resorption of Ca, surgery
