Other bone diseases

Question 1

Paget’s disease

Answer 1

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

Question 2

Paget’s affects how many

Answer 2

3-4% of all Americans over the age of 50, second bost prevalent bone remodeling disease second only osteoporosis

Question 3

Clinical presention of Paget’s

Answer 3

often asymptomatic, deep aching sensation worsens w/ wt bearing, pain is mild to severe unrelated to activity, may have deformities, loss of ht

Question 4

Complication of Paget’s

Answer 4

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

Question 5

Treatment of Paget’s

Answer 5

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

Question 6

Rickets

Answer 6

associated with softening and weakening of bones in children, usually related to an extreme vit d deficit, can be genetic

Question 7

Rickets presents with

Answer 7

delayed growth, pain, muscle weakness, bowed legs, thickened wrists/ankles, breastbone projection

Question 8

Rickets risk factors

Answer 8

age, dark skin, prematurity, exclusively breast-fed infants

Question 9

Rickets etiology

Answer 9

nutritional, vit D resistant rickets, vit D dependent rickets type 1, vit D dependent rickets type II, renal osteodystrophy

Question 10

Vit D analog

Answer 10

Calcitriol (Rocaltrol), Cholecalciferol, Doxercalciferol (Hectoral), Ergocalciferol (Drisdol), Paricalcitol (Zemplar)

Question 11

Vit D MOA

Answer 11

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

Question 12

Vit D PEARLs

Answer 12

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

Question 13

Calcitriol (Rocaltrol) MOA

Answer 13

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

Question 14

Calcitriol (Rocaltrol) clinical uses

Answer 14

rickets, hypocalcemia related to renal disease, management of hyperparathyroidism in pts w/ chronic kidney disease

Question 15

Calcitriol (Rocaltrol) ADRs

Answer 15

well tolerated, GI intolerance only

Question 16

Cholecalciferol (Vit D3) MOA

Answer 16

synthetic vit D3 derivative, products available OTC, often in combo w/ calcium, given PO once daily

Question 17

Cholecalciferol (Vit D3) clinical uses

Answer 17

rickets, vit D deficiency, osteoporosis prevention, hypocalcemia

Question 18

Ergocalciferol (Drisdol) MOA

Answer 18

Active form of Vit D works via several pathways to increase [Ca], given once daily, once weekly or monthly

Question 19

Ergocalciferol (Drisdol) clinical uses

Answer 19

vit d deficiency, osteoporosis prevention, hypoparathyroidism, osteomalcia, rickets

Question 20

Doxercalciferol (Hectoral) MOA

Answer 20

metabolized to the active form of vit D, given IV and PO, usually 3 x weekly, monitor and adjust dose based on PTH levels

Question 21

Docercalciferol (Hectoral) clinical uses

Answer 21

secondary hyperparathyroidism in pts with CKD

Question 22

Docercalciferol (Hectoral) ADRs

Answer 22

edema, GI intolerance

Question 23

Paricalcitol (Zemplar) MOA

Answer 23

synthetic vit D analog, IV every 2-4 weeks, titrated to goal PTH, PO 3x weekly

Question 24

Paricalcitol (Zemplar) caution use

Answer 24

hypercalcemia, excessive vit D can lead to over suppression of PTH

Question 25

Two types of hyperparathyroidism

Answer 25

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)

Question 26

Effects of hyperparathyroidism

Answer 26

bone looses density, hypercalcinuria, anorexia, N/V, ab pain, agitation, nervousness, anxiety, fatigue

Question 27

Treatment of hyperparathyroidism

Answer 27

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