trastornos del calcio magnecio y fosforo
DESCRIPTION
Trastornos de Metabolismo del Calcio, Magnecio y del fosforoTRANSCRIPT
Director Dr. Humberto Fernán Mandirola Brieux
Calcio, Magnesio y Fósforo
Ca
Mg P
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Cuhigh: Copper toxicity · Wilson's disease
deficiency: Copper deficiency · Menkes disease/Occipital horn syndrome
Fe
high: Primary iron overload disorder: Hemochromatosis/HFE1 · Juvenile/HFE2 · HFE3 · African iron overload/HFE4 · Aceruloplasminemia · Atransferrinemia · Hemosiderosis
deficiency: Iron deficiency
Znhigh: Zinc toxicity
deficiency: Acrodermatitis enteropathica
PO43−
high: Hyperphosphatemia
deficiency: Hypophosphatemia · alkaline phosphatase (Hypophosphatasia)
Mg2+
high: Hypermagnesemia
deficiency: Hypomagnesemia
Ca2+
high: Hypercalcaemia · Milk-alkali syndrome (Burnett's) · Calcinosis (Calciphylaxis, Calcinosis cutis) · Calcification (Metastatic calcification, Dystrophic calcification)
deficiency: Hypocalcaemia · Osteomalacia · Pseudohypoparathyroidism (Albright's hereditary osteodystrophy) · Pseudopseudohypoparathyroidism
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sarcomere (Greek sárx = "flesh", méros = "part")
Tetania
Estado de excitabilidad neuromuscular generalizada
Normo-Ca2+ y Normo-Mg2+
Alcalosis (> respiratoria)HipopotasemiaHipernatremiaTóxicos
HipocalcémicasCa total < 8,5 mg/dLCa iónico < 1,1 mMol/L
HipomagnesémicasMg total < 1,6 mg/dL
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Tetania
Sintomática(manifiesta) Latente
Convulsión (tónica) Laringoespasmo
Espasmo carpopedal Laringoespasmo Convulsión (tónica) Parestesias
SIGNOS CLÍNICOS S. de Chevostek S. de Trousseau... Hiperreflexia tendinosa
ELECTRODIAGNÓSTICO Electromiografía (E.M.G.)
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Causas de hipocalcemia
Recién nacido
Lactantes y Niños> 3 años
Precoz (< 72 h) Asfixia Hijo de madre diabética Hiperparatirodismo materno
Tardía (> 72 h) Aporte excesivo de P Hipoparatiroidismo
Hipoparatiroidismo Congénito Adquir ido
AutoinmuneResistencia a la PTH
Raquit ismo Deficiencia de vit . DDefectos del met. Vit D
Hiperfosfatemia IntoxicacionesInsuficiencia renal
Enfermedad grave Shock séptico 30/01/15 15
HipocalcemiaInvestigación en Urgencias
• SANGRE– Calcio iónico– Hemograma– Ionograma y EAB– Prot. totales / albúmina– Urea / Creatinina– Mg, P, F. alcalina
• ORINA– Urianálisis con densidad– Ionograma y osmolaridad– Amilasa
• ECG – Alargamiento QTc
• Considerar– Orina 24 h: RTP, Ca– Rx carpo, rodillas– PTH– 25-(OH), 1,25-(OH)2D3
• Calcio iónico– Acidosis (↑)– Alcalosis (↓) (> respiratoria)– Transfusiones (citrato)– Lisis tumoral (↑ fosfato)
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Hipocalcemia. Tratamiento
Asintomática–Suplementos orales
• Gluconato cálcico 10 % (Calcium Sandoz®)–Vial 10 ml = 2,2 mmol de Ca ≈ 90 mg de Ca.
• Acetato cálcico (Royen®)–Cápsulas 500 mg = 3,2 mmol de Ca ≈ 125 mg de Ca.
• Carbonato cálcico (Mastical®)–Comprimidos 1,26 g = 12,5 mmol de Ca ≈ 500 mg de Ca.
• Pidolato cálcico (Ibercal®)–Solución: 5 ml = 1,7 mmol de Ca ≈ 70 mg de Ca.
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Hipocalcemia. Tratamiento
Sintomática:–Gluconato cálcico 10 % (94 mg/ml de Ca elemental)
• Vía intravenosa lenta (< 1 ml/min). Auscultación continua de los tonos cardiacos durante la administración.
• Añadido a fluidos i.v. (asegurar que no llevan HCO3Na).
• Dosis: 0,5-1,0 ml/kg cada 4-6 horas ≈ 200-500 mg/kg/día.
• Precauciones:–Bradicardia/asistolia si administración i.v. rápida (> 1 ml/min).–Vena bien canalizada: necrosis de partes blandas si hay extravasación.–No administrar simultáneamente o inmediatamente antes o después de
HCO3Na, puede cristalizar (lavar vía con ClNa 0,9%)
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El factor IV de la cadena de coagulación es el CalcioRecuerden también que el Citrato Trisódico (C6H5O7Na3) actúa impidiendo que el calcio se ionice, evitando así la coagulación.El citrato lo usan en Hemoterapia para evitar que la sangre de banco se coagule por lo tanto tener presente que por cada 3 unidades de sangre total transfundida, se debe administrar 1 g de cloruro cálcico o 4 g de gluconato de calcio. ...
Hipercalcemia
• Asintomática (< 13 mg/dl)• Sintomática (> 14 mg/dl)
– Anorexia, náuseas, vómitos– Estreñimiento, dolor abdominal– Pancreatitis– Letargia Coma– Si nefrocalcinosis poliuria, nicturia– Arritmia cardiaca
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HipercalcemiaInvestigación en Urgencias
• SANGRE– Calcio iónico– Hemograma– Ionograma y EAB– Prot. totales / albúmina– Urea / Creatinina– Amilasa
• ORINA– Urianálisis con densidad– Ionograma y osmolaridad– Amilasa
• ECG – Acortamiento QTc– Bloqueo A-V
• Ecografía abdominal• Considerar
– TAC craneal– Ecocardiografía– Fondo de ojo
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Hipercalcemia. Tratamiento
Ca < 14 mg/dl ó asintomática Observación
Ca > 14 mg/dl ó sintomática: Expansión volumen
• Solución salina: ClNa 0,9 %
Diuréticos: Furosemida
Glucocorticoides: inicio de acción días
Otros: calcitonina, difosfonatos
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Hipomagnesemia
• Definición
– Lactante Mg2+ < 1,6 mg/dl < 0,7 mmol/L
– Niños y adultos Mg2+ < 1,4 mg/dl < 0,6 mmol/L
• Hipomagnesemia sintomática
– Mg2+ plasmático < 1,2 mg/dl < 0,5 mmol/L
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Causas de Hipomagnesemia
Ingesta disminuida Ayuno prolongadoNutrición parenteral total prolongada
Malabsorción intestinal Diarrea crónicaCeliaquía
Pérdidas renales Hereditaria (tubulopatías) Síndrome de Gitelman
S. de hipo-Mg+ con hipercalciuria S. de BartterFármacos (furosemida, anfotericina
B, aminoglucósidos, cisplat ino)
Endocrinopatía Hiperparatiroidismo, diabetes mell i tus
hipermineralcort icismo
Otros Sepsis, quemaduras
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HipomagnesemiaManifestaciones clínicas
• Neuromuscular– Hiperreflexia, parestesias– Tetania– Debilidad muscular– Ataxia– Depresión, psicosis
• Digestivo– Disfagia
• Cardiovascular– Arritmia– HTA– Sensibilidad a digital
• Sistema endocrino– Resistencia a PTH– Hiperreninemia– Hiperaldosteronismo
• Hematológico– Anemia
• Bioquímica– Hipocalcemia
Secreción ↓ de PTHResistencia a la PTHResistencia a la vit. D
– HipopotasemiaPérdida renal de K
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Hipomagnesemia. Tratamiento
Síntomática: Sulfato magnésico Dosis: 25-50 mg/kg, cada 4-6 h, vía i.m./i.v. Solución 50 % (500 mg/ml)
– 0,1-0,2 ml/kg, i.m. o i.v. Solución 15 % (Hospital)
– Ampollas 10 ml = 1,5 g (150 mg/ml)– Dosis: 0,2-0,6 ml/kg, i.m. o i.v.
Asintomática: Suplemento oral Lactato Mg
– MagnesioBoi®: Comprimidos 500 mg
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Síntomas de HiperMagnesemia
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Weakness, nausea and vomitingImpaired breathingHypotensionHypocalcemiaArrhythmia and Asystole
Clínica de HiperMagnesemia
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Clinical consequences related to serum concentration:4.0 mEq/l hyporeflexia>5.0 mEq/l Prolonged atrioventricular conduction>10.0 mEq/l Complete heart block>13.0 mEq/l Cardiac arrest
7.0-10.0 mEq/L - loss of patellar reflex10.0-13.0 mEq/L - respiratory depression15.0-25.0 mEq/L - altered atrioventricular conduction and (further) complete heart block>25.0 mEq/L - cardiac arrest
Causas de HiperMagnesemia
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•Hemolysis, magnesium concentration in erythrocytes is approximately three times greater than in serum, therefore hemolysis can increase plasma magnesium. Hypermagnesemia is expected only in massive hemolysis.•Renal insufficiency, excretion of magnesium becomes impaired when creatinine clearance falls below 30 ml/min. However, hypermagnesemia is not a prominent feature of renal insufficiency unless magnesium intake is increased.•Other conditions that can predispose to mild hypermagnesemia are diabetic ketoacidosis, adrenal insufficiency, hyperparathyroidism and lithium intoxication.
Tratamiento
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Prevention of hypermagnesemia usually is possible. In mild cases, withdrawing magnesium suppletion is often sufficient. In more severe cases the following treatments are used:Intravenous calcium gluconate, because the actions of magnesium in neuromuscular and cardiac function are antagonized by calcium.Definitive treatment of hypermagnesemia requires increasing renal magnesium excretion through:Intravenous diuretics, in the presence of normal renal functionDialysis, when kidney function is impaired and the patient is symptomatic from hypermagnesemia
HipoFosfatemia Causas
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Refeeding syndrome This causes a demand for phosphate in cells due to the action of phosphofructokinase, an enzyme that attaches phosphate to glucose to begin metabolism of this. Also, production of ATP when cells are fed and recharge their energy supplies, requires phosphate.Respiratory alkalosis Any alkalemic condition moves phosphate out of the blood into cells. This includes most common respiratory alkalemia (a higher than normal blood pH from low carbon dioxide levels in the blood), which in turn is caused by any hyperventilation (such as may result from sepsis, fever, pain, anxiety, drug withdrawal, and many other causes).Alcohol abuse Alcohol impairs phosphate absorption. Alcoholics are usually also malnourished with regard to minerals. In addition, alcohol treatment is associated with refeeding, and the stress of alcohol withdrawal may create respiratory alkalosis, which exacerbates hypophosphatemia (see above).Malabsorption This includes GI damage, and also failure to absorb phosphate due to lack of vitamin D, or chronic use of phosphate binders such as sucralfate, aluminum-containing antacids, and (more rarely) calcium-containing antacids.Phosphaturia or hyperexcretion of phosphate in the urine. This condition is divided into primary and secondary types. Primary hypophosphatemia is characterized by direct excess excretion of phosphate by the kidneys, as from primary renal dysfunction, and also the direct action of many classes of diuretics on the kidneys. Additionally, secondary causes, including both types of hyperparathyroidism cause hyperexcretion of phosphate in the urine.
HipoFosfatemia Síntomas
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Muscle dysfunction and weakness. This occurs in major muscles, but also may manifest as: diplopia, low cardiac output, dysphagia, and respiratory depression due to respiratory muscle weakness.Mental status changes. This may range from irritability to gross confusion, delirium, and coma.White cell dysfunction, causing worsening of infectionsInstability of cell membranes due to low ATP levels: this may cause rhabdomyolysis with increased CPK, and also hemolytic anemia.
Tratamiento de HipoFosfatemia
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Standard intravenous preparations of potassium phosphate are available and are routinely used in malnourished patients and alcoholics. Oral supplementation also is useful where no intravenous treatment is available. Historically one of the first demonstrations of this was in concentration camp victims who died soon after being re-fed: it was observed that those given milk (high in phosphate) had a higher survival rate than those who did not get milk.
HiperFosfatemia
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Causas de HiperFosfatemia
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Hypoparathyroidism: In this situation, there are low levels of Parathyroid hormone (PTH). PTH normally inhibits renal reabsorption of phosphate, and so without enough PTH there is more reabsorption of the phosphate.Chronic renal failure: When the kidneys aren't working well, there will be increased phosphate retention.Drugs: hyperphosphatemia can also be caused by taking oral sodium phosphate solutions prescribed for bowel preparation for colonoscopy in children
Sintomatología
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Signs and symptoms include :•ectopic calcification, secondary•hyperparathyroidism, and •renal osteodystrophy.
Tratamiento de la Hiperfosfatemia
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High phosphate levels can be avoided with phosphate binders and dietary restriction of phosphate.
Fin
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TX15Srxl2cltaJh1x9vACzlXTIsbqzkQ/Presentaciones%20en%20PPT/04%20Calcio%20Magnecio%20%20Fosforo.pdf
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