Trastornos de Metabolismo del Calcio, Magnecio y del fosforo

1. Director Dr. Humberto Fernán Mandirola Brieux

2. Calcio, Magnesio y Fósforo
Ca
M
g P
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Cu
high: 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
Zn
high: Zinc toxicity
deficiency: Acrodermatitis enteropathica
PO4
3−
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")

5. Tetania
Estado de excitabilidad neuromuscular generalizada
Normo-Ca2+
y Normo-Mg2+
Alcalosis (> respiratoria)
Hipopotasemia
Hipernatremia
Tóxicos
Hipocalcémicas
Ca total < 8,5 mg/dL
Ca iónico < 1,1 mMol/L
Hipomagnesémicas
Mg total < 1,6 mg/dL
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6. 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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Rickets

14. HipoCalcemias
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15. 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
Adquirido
Autoinmune
Resistencia a la PTH
Raquitismo Deficiencia de vit. D
Defectos del met. Vit D
Hiperfosfatemia Intoxicaciones
Insuficiencia renal
Enfermedad grave Shock séptico
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16. Hipocalcemia
Investigación 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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17. 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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18. 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 Calcio
Recuerden 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. ...

20. HiperCalcemias
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21. 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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22. Hipercalcemia
Investigación 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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23. 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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24. HipoMagnesemia
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25. 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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26. Causas de Hipomagnesemia
Ingesta disminuida Ayuno prolongado
Nutrición parenteral total prolongada
Malabsorción intestinal Diarrea crónica
Celiaquía
Pérdidas renales Hereditaria (tubulopatías)
Síndrome de Gitelman
S. de hipo-Mg+
con hipercalciuria
S. de Bartter
Fármacos (furosemida, anfotericina
B, aminoglucósidos,
cisplatino)
Endocrinopatía Hiperparatiroidismo, diabetes
mellitus
hipermineralcorticismo
Otros Sepsis, quemaduras
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27. Hipomagnesemia
Manifestaciones 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 PTH
Resistencia a la PTH
Resistencia a la vit. D
– Hipopotasemia
Pérdida renal de K
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28. 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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29. HiperMagnesemia
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30. Síntomas de HiperMagnesemia
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Weakness, nausea and
vomiting
Impaired breathing
Hypotension
Hypocalcemia
Arrhythmia and Asystole

31. 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 reflex
10.0-13.0 mEq/L - respiratory depression
15.0-25.0 mEq/L - altered atrioventricular conduction and (further)
complete heart block
>25.0 mEq/L - cardiac arrest

32. 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.

33. 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 function
Dialysis, when kidney function is impaired and the patient is
symptomatic from hypermagnesemia

34. HipoPosfatemia
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35. 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.

36. 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 infections
Instability of cell membranes due to low ATP levels: this may cause
rhabdomyolysis with increased CPK, and also hemolytic anemia.

37. 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.

38. HiperFosfatemia
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39. 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

40. Sintomatología
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Signs and symptoms include :
•ectopic calcification, secondary
•hyperparathyroidism, and
•renal osteodystrophy.

41. Tratamiento de la Hiperfosfatemia
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High phosphate levels can be avoided with phosphate binders and dietary
restriction of phosphate.

42. Fin
La presentación la pueden bajar de
http://f1.grp.yahoofs.com/v1/MM15TJbeDibsLxgCSRNBpobQiHG58C5oLjcSOfCldb7PP8EPtbSlbM
TX15Srxl2cltaJh1x9vACzlXTIsbqzkQ/Presentaciones%20en%20PPT/04%20Calcio
%20Magnecio%20%20Fosforo.pdf
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