• Like
  • Save
Calcium Metabolism
Upcoming SlideShare
Loading in...5

Calcium Metabolism



Calcium Metabolism

Calcium Metabolism



Total Views
Views on SlideShare
Embed Views



0 Embeds 0

No embeds


Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

    Calcium Metabolism Calcium Metabolism Presentation Transcript

    • 10
    • 13
    • ETIOLOGIES OF HYPERCALCEMIAIncreased GI Absorption Decreased Bone Milk-alkali syndrome Mineralization Elevated calcitriol Vitamin D excess Elevated PTH Excessive dietary intake Aluminum toxicity Granuomatous diseases Elevated PTH Hypophosphatemia Decreased Urinary ExcretionIncreased Loss From Bone Thiazide diuretics Increased net bone resorption Elevated calcitriol Elevated PTH Hyperparathyroidism Elevated PTH Malignancy Osteolytic metastases Increased bone turnover Paget’s disease of bone Hyperthyroidism
    • 15 CAUSES Approx. 80% of all cases are caused by Malignancy or Primary Hyperpathyroidism• V Vitamins  T Thiazide,• I Immobilization other drugs - Lithium• T Thyrotoxicosis  R Rabdomyolysis• A Addison’s disease  A AIDS• M Milk-alkali syndrome  P Paget’s disease,• I Inflammatory disorders Parental nutrition, Pheochromocytoma,• N Neoplastic related Parathyroid disease disease• S Sarcoidosis
    • 17
    • SIGNS AND SYMPTOMS Bones, stones, abdominal groans, and psychic moans. • Malaise, fatigue, headaches, diffuse aches and pains, constipation. • Patients are often dehydrated • Lethargy and psychosis when hypercalcemia is severe. • Calcifications in skin, cornea, conjunctiva, and kidneys. 18
    • CLINICAL1. Renal ; , stone, nephrocalcinosis2. GI ;, Constipation, PU, Pancratitis3. Neuro ; Weakness, Drowsiness, Apnea4. Cardio ; Short QT <0.3 ,Broad T, Heart Block, Vent arrhythmia,Asystole, Sense to digoxin5. Musculo ; Cramp, Bone pain, Pathologic Fx6. Others ; Band Keratopathy 19
    • 20
    • DIAGNOSIS Detailed history and physical examination… PTH level Vitamin D level Serum calcium levels Urine evaluation Ultrasound X-RAYS,MRI,CT scan PET(Positron Emission Tomography
    • MANAGEMENT HYPERCALCEMIA General  Hydration 2-4L/day Keep urine output > 1-2 ml/kg/hr onset 12-24 hr  Lasix 10-20 mg iv. q 6-12 hr * only after adequate hydration *  Mobilization  Dialysis 22
    • MANAGEMENT HYPERCALCEMIA Specific  Calcitonin  Bishosphonates  Galliumnitrite  Plicamycin, Mithramycin  Hydrocortisone 23
    • ETIOLOGIES OF HYPOCALCEMIADecreased GI Absorption Poor dietary intake of calcium Impaired absorption of calcium Vitamin D deficiency Increased Urinary Excretion Poor dietary intake of vitamin D Malabsorption syndromes Low PTH Decreased conversion of vit. D to thyroidectomy calcitriol Liver failure I131 treatment Renal failure Autoimmune hypoparathyroidism Low PTH PTH resistance Hyperphosphatemia Vitamin D deficiency / low calcitriolDecreased Bone Resorption/Increased Mineralization Low PTH PTH resistance pseudohypoparathyroidism) Vitamin D deficiency / low calcitriol Hungry bones syndrome Osteoblastic metastases
    • SYMPTOMS AND SIGNS OF HYPOCALCEMIA Neuromuscular irritability Paresthesias Laryngospasm / Bronchospasm Tetany Seizures Chvostek sign Trousseau sign Prolonged QTc time on ECG
    • Trousseau sign: (very uncomfortable and painful) A blood pressure cuff is inflated to a pressure above the patients systolic level. Pressure is continued for several minutes. Carpopedal spasm: * flexion at the wrist * flexion at the MP joints * extension of the IP joints * adduction thumbs/fingers
    •  Long QT interval with normal T waves Prolongation of the ST segment with little shift from the baseline
    • TREATMENT HYPOCALCEMIA  Symptomatic hypocalcemia needs IV calcium and continuous monitoring for arrhythmias.  Once serum Ca is in safe range ( >7 mg/dl) IV Ca can be stopped, and oral Ca started.  Oral Ca and vit D are initiated as soon as possible when patient is tolerating oral feed.  Active form of vit D is preferred in treatment of HPH and hyperphosphatemia because both impair activation of 25 OH vit D by one alpha hydroxylase.  Diet, no specific diet is required but adequate Ca and vit D intake is recommended.
    • Thank you