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22 Cards in this Set

  • Front
  • Back
Major portion of Ca absorption is:
- proximal segment of the small intestine.
How does hypocalcemia result from?
1. Inadequate intake of Ca or vit. D.
2. Failure to absorb Ca
3. Hypoparathyroidism
4. Renal Failure

5. Tetany, paresthesias, increased neuromuscular excitability, laryngospasm, muscle cramps, and convulsions
Treatment of hypocalcemia.
1. Ca Salts --> immediate therapy.
2. Ca gluconate, Ca Choride and Ca gluceptate for I.V. use.
Ca gluconate is less irritating.
1. Calcitrol
2. Milder problems --> CaCl, Carbonaate, Citrate
1. constipation
2. CNS abnormalities.
3. Renal Ca decomposition (nephrocalcinosis)
4. Cardiac arrthymias
5. Bone cysts, osteoporsis, fracturers
What are the causes of HYPERCALCEMIA:
1. Hypervitaminosis D
2. Hyperparathyroidism
3. Hyperthyroidism
4. Milk-alkali syndrome
5. Malignancy
6. Thiazide Therapy
Treatment of Hypercalcemia:
1. Saline plus loop diuretic.
2. Bisphosphonates
3. Steriods: if hypercalcemia is due to sarcoid, tumors or hypervitaminosis D.
4. Mithramycin/Plicamycin
More Tx of Hypercalcemia:
1. Calcitonin: high fall in ca but only lasts several day.
2. Gallium Nitrate (Ganite) inhibits bone resportion --> appears to be superior to calcitonin in lowering serum ca in hyperca of maliganccy, can cuase nephrotoxicity.
Zoledronic Acid (ZOMETA)
- can cause nephrotoxicity.
Bone Resorption =
Bone Renewal =
Regulation of Ca is by:
Ca = into the body via the intestine

Exit of Ca = via kidney

Deposition and resorption of Ca from skeleton.
Effect on Ca:

1. PTH
2. Calcitonin
1. increase conc. of free ionized plasma Ca.
2. decrease conc. of free ionized plasma Ca.
Parathyroid Hormone (PTH)
- when plasma conc. of Ca is low, PTH secretion increases.
vice versa.

- prolonged hypocal causes hypertrophy and hyperplasia of the parathyriods.
Function of PTH:
1. increases bone resorption and mobilizes bone Ca
2. Increases renal reabsorption of Ca
3. Decreases renal reabsorption of Phosphate
4. Increass synthesis of calcitroil.

NET effect: increase Ca and Decreased phosphate plasma conc.
Teriparatide (FORTEO):
recombinant DNA orgin is the 34-N terminaL A.A. of PTH.

- FOR tx of osteoporsis in postmenopausal women and in men

Activation of Vitamin D
1. by PTH.
2. regulated by a negative- feedback system controlled by Ca AND phosphate conc.
Vitamin D feedback regulation;
1. Low plasma phosphate = activates the 1a-OHase
2. Low Plasma Ca stimulates teh PT gland to secrete PTH, which in turn stimulates the 1a-OHase
Vitamin D functions:
- Calcitrol Effects
- Decreases urinary excretion of CA and P.
- Increases intestinal absorption of Ca and P.
- Stimulates Bone resorption.

NET EFFECT: INCREASE the plasma conc. of Ca and P.
Osteomalacia is caused by:
- vitamin D deficiency
- by phosphate depeletion due to abuse of Al- containing antacids.
Vitamin D is generally given orally and GI absorption is adequate.
- Vitamin D2 and D3 are absorbed from small intestine.
- Bile is essential for adequate absorption and excretion.
Excess Vitamin D =
stored in adipose tissue and liver.

IN PLASMA = Vitamin D tightly bound to an a-globulin carrier protein.
Drug interactions w/ Vitamin D =
1. Phenytoin and Phenobarbital = decrease plasma level

2. Cholestyramine, colestipol & mineral oil -->
decrease intestinal absorption.

3. Thiazide Diuretics --> increase risk of hypercal.

4. Orlistat --> decrease GI absorption.

5. Digoxin w/Vit D. tx CAUSE cardiac arrthymias.
Nutritional Rickets ->