that is all about calcium which we use clinically.

1.  Distribution:
 Most abundant cation(1.2-1.4kg)
 99% in bone and 1% in cells of soft tissues,
ECF
 Serum calcium:
 Normal value: 10 +/- 0.5mg/dl
 50-55% ionized form, 40% bound to albumin,
5-10% complexed with anions of organic
acids (such as phosphate, bicarbonate,
citrate, lactate,sulphate

2.  Ionized (free) calcium
 Physiologically active
 Total serum calcium level does not always reflect
ionized calcium. e.g. hypoproteinemia -
reduction of protein bound and total calcium
but ionized calcium remais
unchanged(pseudohypocalcemia)
 Correction of total serum calcium in
pseudohypocalcemia: add 1 mg/dl to serum
calcium for each 1 mg/dl reduction in serum
albumin

3.  Regulation
 PTH and calcitriol (active form of vitamin D) are main
factors that maintain normal serum ionised calcium
 PTH: increase serum calcium by
1. Stimulating bone reabsorption
2. Increase synthesis of calcitriol in kidney
 Hypocalcemia stimulates and hypercalcemia suppresses
PTH secretion by negative feedback
 Calcitriol: increase serum calcium by
1. Stimulating bone reabsorption
2. Promoting intestinal calcium reabsorption
 Regulates synthesis of PTH by negative feedback
 Hypophosphatemia and PTH both stimulates and
hyperphosphatemia suppresses synthesis of calcitriol

4.  Causes
A. Low parathyroid hormone level
1. Parathyroid agenesis
 Isolated
 Digeorge’s syndrome
2. Parathyroid destruction
 Surgical
 Radiation
 Infiltration by metastasis or systemic disease
 Autoimmune
3. Reduced parathyroid hormone function
 Hypomagnesemia
 Activating CaSR or G protein mutations

5. B. High parathyroid hormone level(secondary hyperparathyroidism)
1. Vitamin D deficiency or impaired calcitriol production/action
 Nutritional
 Renal insufficiency
 Vitamin D resistance
2. Parathyroid hormone resistance syndromes
 PTH receptor mutation
 Pseudohypoparathyroidism (G protein mutations)
3. Drugs
 Calcium chelators
 Inhibitors of bone resorption (bisphosphonates, plicamycin)
 Altered vitamin D metabolism (phenytoin, ketoconazole)
4. Miscellaneous
 Acute pancreatitis
 Acute rhabdomyolysis
 Hungry bone syndrome after parathyroidectomy
 Osteoblastic metastasis with marked stimulation of bone formation(prostate
cancer)
 Massive transfusion of citrated blood

6.  clinical features
 Mild: asymptomatic
 Moderate:
 Paresthesias over fingers, toes, circumoral regions
 Chvostek’s sign: twitching of circumoral muscles in
response to gentle tapping of fascial nerve just ant to ear)
 Trousseau’s sign: carpal spasm indused by inflation of BP
cuff to 20 mmHg above pt’s SBP for 3 min
 Severe:
 Seizures
 Carpopedal spasm
 Bronchospasm
 Laryngospasm
 Prolongation of QT interval

7. Diagnosis
 S.calcium
 S. PTH
 S. albumin
 S. phosphorus
 S. magnesium

8. Management
 Depends on
 Severity
 Rapidity with which it develops
 Associatede
complications(seizures,laryngospasm)

9.  Acute
 Calcium gluconate: 1 amp of 10 ml 10%
wt/vol(90 mg) in 50 ml D5% or NS iv over 5
min -10 amp in 1 L D5% or NS over 24 hr
 Correct associated hypomagnesemia
 In tratment of metabolic acidosis with
hypocalcemia(e.g.CRF) correct hypocalcemia
before correction of hypocalcemia
 After 4 citrated BT 1 amp

10.  Chronic
 Calcium supplements: 1-1.5 g/d elemental
calciumin divided doses
 Vitamin D supplements: 25000-100000 U/d

11.  Etiology
 Excessive PTH production
 Primary hyperparathyroidism(adenoma,hyperplasia ,rarely
carcinoma)
 Tertiary(long term stimulation of PTH secretion in renal
insufficiency)
 Ectopic PTH secretion (very rare)
 Familial hypocalciuric hypercalcemia(inactivating mutations in
CaSR or in Gproteins
 Lithium therapy(alteration in CaSR function)hypercalcemia of
malignancy
 Overproduction of PTHrP(many solid tumors)
 Lytic skeletal metastasis(breast, myeloma)

12.  Excessive calcitriol production
 Granulomatous diseases(sarcoidosis,TB, silicosis)
 Lymphoma
 Intoxication
 Primary increase bone resorption
 Hyperthyroidism
 Immmobilization
 Excessive calcium intake
 Milk alkali syndrome
 TPN
 Others
 Endocrine disorders(adrenal insufficiency, pheochromocytoma,VIPoma
 Medications(thiazides, vit A, antiestrogens)

13.  Clinical features
 Mild(11-11.5mg/dl):asymptomatic
 Moderate(11.5-13):
 Vague neuropsychitry symptoms including trouble concentrating,
personality changes or depression
 Peptic ulcer disease
 Nephrolithiasis
 Increase fracture risk
 Severe(>13):
 Lethargy,stupor or coma
 GI symptoms: nausea,anorexia, constipation, pancreatitis
 Decrease renal concentrating ability: polyuria, polydipsia
 Bone pain or pathological fractures
 ECG: bradycardia, AV block, short QT interval

14. Diagnosis
 S. calcium
 S. PTH
 S. phosphate
 S. creat
 S. HCO3
 S.calcitriol

15.  Management
 Volume expansion
 4-6 L with loop diuretics
 Drugs that inhibit bone resorption(esp in severe hyperparathyroidism or
malignancy)
 IV Bisphosponates (e.g. zolendronic 4mg over 30 min ,ibandronate 2mg
over 2 hr ,pamidronate 60-90 mg over2-4 hr): may cause extensive organ
damage by calcium phosphate complexes
 Gallium nitrate 200mg/m2/d iv for 5 days: may cause nephrotoxicity
 Drugs that decrease calcitriol production
 Glucocorticoids (hydrocortisone 100-300mg /d for 3-7 d, prednisolone 40-
60mg/d for 3-7 d)
 Ketoconazole
 Chloroquine, HCQ