1 / 43

HYPOCALCEMIA

HYPOCALCEMIA. Hasan AYDIN , MD Yeditepe University Medical Faculty Department of Endocrinology and Metabolism. Overview of Calcium Balance. Etiolog y. Decreased GI Absorption Poor dietary intake of calcium Impaired absorption of calcium Vitamin D deficiency

nixie
Download Presentation

HYPOCALCEMIA

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. HYPOCALCEMIA Hasan AYDIN, MD Yeditepe UniversityMedicalFaculty Department of EndocrinologyandMetabolism

  2. Overview of Calcium Balance

  3. Etiology Decreased GI Absorption Poor dietary intake of calcium Impaired absorption of calcium Vitamin D deficiency Poor dietary intake of vitamin D Malabsorption syndromes Decreased conversion of vit. D to calcitriol Liver failure Renal failure Low PTH Hyperphosphatemia Decreased Bone Resorption/Increased Mineralization Low PTH ( hypoparathyroidism) PTH resistance ( pseudohypoparathyroidism) Vitamin D deficiency / low calcitriol Hungry bones syndrome Osteoblastic metastases Increased Urinary Excretion Low PTH Thyroidectomy I131 treatment Autoimmune hypoparathyroidism PTH resistance Vitamin D deficiency / low calcitriol

  4. Parathyroid Related Disorders • Absence of the parathyroid glands or of PTH • Congenital • DiGeorge’s syndrome • X-linked or autosomally inherited hypoparathyroidism • Autoimmune polyglandular syndrome type I • PTH gene mutations • Postsurgical hypoparathyroidism • Infiltrative disorders • Hemachromatosis • Wilson’s disease • Metastases • Hypoparathyroidism following radioactive iodine thyroid ablation • Impaired secretion of PTH • Hypomagnesemia • Respiratory alkalosis • Activating mutations of the calcium sensor • Target organ resistance • Hypomagnesemia • Pseudohypoparathyroidism (Type I and II)

  5. Vitamin D Related Disorders • Vitamin D deficiency • Dietary absence • Malabsorbtion • Accelerated loss • Impaired enterohepatic recirculation • Anticonvulsant medications • Impaired 25-hydroxylation • Liver disease • Isoniazid • Impaired 1α-hydroxylation • Renal failure • Vitamin D dependent rickets type I • Oncogenic osteomalcia • Target organ resistance • Vitamin D dependent rickets type II • Phenytoin

  6. Other Causes • Excessive deposition in to the skeleton • Osteoblastic malignancies • Hungry bone syndrome • Chelation • Foscarnet • Phosphate infusion • Infusion of citrated blood products • Infusion of EDTA containing contrast agents • Fluoride • Neonatal hypocalcemia • Prematurity • Asphyxia • Diabetic mother • Hyperparathyroid mother • HIV infection • Drug therapy • Vitamin D deficiency • Impaired PTH responsiveness • Critical illness • Pancreatitis • Toxic shock syndrome • Intensive care unit patients

  7. Clinical Features • Signs and symptoms depend on • Level of serum calcium • Age at onset and duration • Level of serum magnesium and potassium • Accompanying disturbances in acid-base homeostasis • Sometimes only symptoms of underlying disorder

  8. Symptoms and Signs • Systemic • Confusion • Weakness • Mental retardation • Behavioral changes

  9. Symptoms and Signs • Neuromuscular • Parestesias • Psychosis • Seizure • Carpopedal spasm • Chvostek’s and Trousseau’s signs • Depression • Muscle cramps • Parkinsonism • Irritability • Basal ganglia calcifications

  10. Syptoms and Signs • Cardiac • Prolonged QT interval • T wave changes • Congestive heart failure • Ocular • Cataracts

  11. Syptoms and Signs • Dental • Enamel hypoplasia of teeth • Defective root formation • Failure of adult tooth to erupt • Respiratory • Laryngospasm • Bronchspasm • Stridor

  12. Chvostek’s Sign • Elicited by tapping over facial nerve causing twitching of ipsilateral facial muscles

  13. Trousseau’s Sign • Carpal spasm in response to inflation of BP cuff to 20 mm Hg above SBP for 3 min

  14. Differential Diagnosis

  15. Evaluation of Hypocalcemia • History: • Paresthesias/ cramping • Tetany • Carpopedal spasm • Laryngospasm • Seizures

  16. PhysicalExamination • Signs of hypocalcemia: • Chvostek sign • Trousseau sign • Hyper-reflexia • Dysmorphism (Di George Syndrome, PHP) • Dental abnormalities • Chronic mucocutaneous candidiasis • Rickets

  17. Investigations • Serum calcium (ionic), phosphate, magnesium • Ionized Ca is physiologically active • 0.1 increase in pH increases iCa by 3-8% • 10 g/L decrease in albumin increases iCa by 0.2 • iPTH • Serum urea and creatinine levels • Vitamin D levels (if available) • Genetic studies (if necessary)

  18. Approach to low serum calcium PTH Level Low High Mg level Phosphate Low High High Low Hypo magnesemia Hypo parathyroid Creatinine 25 OH Vit D High Normal Low Normal Renal Failure PHP 1,25 OH Vit D Nutrition Malabsorption Liver disease Vit D Dep Rickets Vit D Res Rickets

  19. Treatment • Symptomatic: • Parenteral Ca • 10% CaCl2: 10 cc ampoules contains 360 mg of elemental Ca • 10% Ca gluconate: 10 cc ampoules contains 93 mg of elemental Ca • Recommended dose: 100-300 mg of elemental Ca over 10-20 min followed by an infusion of 0.5-2 mg/kg/h

  20. Treatment • Side effects: • Nausea • Vomiting • Flushing • Hypertension • Bradycardia, heart block (patients should be monitored)

  21. Treatment • Asymptomatic • Oral Ca supplementation • 1-4 g/day in divided doses • If patient has concurrent hypomagnesemia, Careplacement alone will not correct hypocalcemia unless Mg is also replaced (2-4 g IV for symptomatic patients)

  22. Acute Management Of Hypocalcemia • Frank Tetany • 10-20 ml calcium gluconate (93 mgf elemental Ca/10 ml) for 10 min. • Ongoing severe hypercalcemia • 10 ampul of 10 ml calcium gluconate infused over 8-10 hours (in saline or dextrose) • When due to hypomagnesemia • 1-2 gram of magnesium sulfate (8-16 mEq) q6h, for several days

  23. SPECIFIC CAUSES OF HYPOCALCEMIA

  24. DevelopmentalAbnormalities • DiGeorge Syndrome • Parathyroid dysplasia, thymic hypoplasia, immune deficiency, cardiac defects, craniofacial malformations, mental retardation • Deletion on long arm of chromosome 22 • Kenny Caffey Syndrome • Parathyroid aplasia, medullary stenosis of long bones, growth retardation • Barakat syndrome • Hypoparathyroidism, nerve deafness, renal dysplasia

  25. Disorders of 25-OH D Metabolism • Hepatic and hepatobiliary disease • Impairement of synthesis • Particularly in biliary cirrhosis • Gastrointestinal disorders • Malabsorption and disruption of enterohepatic circulation of vitamin D • Protein wasting syndrome • Drugs • Increased conversion of 25 OH D to inactive metabolites

  26. Disorders of 1,25-OH D Metabolism • Vitamin D dependent rickets type I • Vitamin D dependent rickets type II • Vitamin D resistant rickets and osteomalacia • Hypercalciuric hypophosphatemic rickets • Tumor induced osteomalacia

  27. Vitamin D Dependent Rickets Type I • Autosomal recessive • Inactivating mutations on chromosome 12 • Circulating levels of 1,25 (OH) D are low • Treatment with calcitriol 0,5-3 mcg/day

  28. Vitamin D Dependent Rickets Type II • Target organ resistance to calcitriol • Markedly elevated plasma levels of 1,25 (OH) D • Sporadic and autosomal recessive • Alopecia, epidermal cysts, oligodentia • Low 24,25 (OH)2D3 and 24 (OH)-25-hydroxylase • Treatment with massive doses of vitamin D (10-20 mg/day) or 1,25 (OH)D (6 mcg/kg/day)

  29. Vitamin D Resistant Rickets and Osteomalacia • Sporadic or familial • X-linked hypophosphatemic VDRR • Hypophosphatemia, normocalcemia, normal PTH, hyperphophaturia • 25 (OH)D normal, 1,25 (OH)D low/normal • Treatment with administration of phosphorus supplements and vitamin D

  30. Tumor Induced Osteomalacia • Release of humoral factors affecting renal phosphate reabsorption, and formation of 1,25 (OH)2D • Bone pain, muscle weakness, recurrent pathological fractures, pseudofractures • Hypophosphatemia, hypocalcemia, elevated ALP, PTH vary • Surgery of tumor • Treatment with phosphorus + vitamin D

  31. Hypoparathyroidism • Clinically • Symptomsof neuromuscular hyperactivity • Biochemically • hypocalcemia, • hyperphosphatemia, • diminished to absent circulating iPTH.

  32. Etiology • Surgical hypoparathyroidism(most common) • Familial hypoparathyroidism • Idiopathichypoparathyroidism • Functionalhypoparathyroidism

  33. Functional Hypoparathyroidism • long periods of hypomagnesemia • selective gastrointestinal magnesium absorption defects • generalized gastrointestinal malabsorption • alcoholism. • Serum PTH low • Hypocalcemia • Mg is required for PTH release • Mgis probably also required for the peripheral action of PTH

  34. Classification • 5 categories based primarily on the concentration of serum calcium. • Grades 1  with no hypocalcemia, • Grades 2 inconstant hypocalcemia • Grades 3  serum calcium is below 8.5 mg/dl • Grades 4  serum calcium is below 7.5 mg/dl • Grades 5 serum calcium is below 6.5 mg/dl • Clinical manifestations of hypoparathyroidism depend upon the severity and chronicity of the hypocalcemia.

  35. Treatment • Physiologic replacement of PTH. • Pharmacologic doses of vitamin D • (ergocalciferol or its more potent analog dihydrotachysterol, in combination with oral calcium administration) • Diets low in phosphate (restriction of dairy products and meat) and oral aluminum hydroxide gels

  36. PTH Resistance Syndromes

  37. Etiology of Pseudohypoparathyroidism • abnormal target tissue responses • receptor binding of the hormone • final expression of the cellular actions of PTH • resistance to several other hormones (vasopressin, glucagon). • secretion of a biologically inert form of PTH, • circulating inhibitors of PTH action, • an intrinsic abnormality of PTH receptors, • autoantibodies to the PTH receptor, 

  38. Pseudohypoparathyroidism • Rare familial disorder • Target tissue resistance to PTH, • Hypocalcemia, hyperphosphatemia • Increased parathyroid gland function, • Short stature and short metacarpal and metatarsal bones.

  39. PsHP Type Ia (Albright Syndrome) • Hypoparatrhyroidism, short stature, round facies, obesity, brachydactily, neck webbing, sc calcifications • Defect in the function of Gs protein • TSH, Glucagon, Gonadotropin resintance • Autosomal dominant • Intermittant hypocalcemia, elevated PTH, low urine Ca

  40. Pseudopseudohypoparathyroidism • developmental defects • without the biochemical abnormalities of pseudohypoparathyroidism. • lack evidence of PTH resistance • 50% reduction in Gs alpha function • Autosomal dominant

  41. Pseudoidiopathic hypoparathyroidism • Structurally abnormal form of PTH present • Fail to respond to own PTH • Normal response to exogenous PTH

More Related