Your SlideShare is downloading. ×
0
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Trastornos del  calcio magnecio y  fosforo
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Trastornos del calcio magnecio y fosforo

2,444

Published on

Trastornos de Metabolismo del Calcio, Magnecio y del fosforo

Trastornos de Metabolismo del Calcio, Magnecio y del fosforo

Published in: Health & Medicine, Technology
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total Views
2,444
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
112
Comments
0
Likes
0
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. Director Dr. Humberto Fernán Mandirola Brieux
  • 2. Calcio, Magnesio y Fósforo Ca M g P 30/01/15 2
  • 3. 30/01/15 3 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
  • 4. 30/01/15 4 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 30/01/15 5
  • 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.) 30/01/15 6
  • 7. 30/01/15 7
  • 8. 30/01/15 8
  • 9. 30/01/15 9
  • 10. 30/01/15 10
  • 11. 30/01/15 11
  • 12. 30/01/15 12
  • 13. 30/01/15 13 Rickets
  • 14. HipoCalcemias 30/01/15 14
  • 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 30/01/15 15
  • 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) 30/01/15 16
  • 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. 30/01/15 17
  • 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%) 30/01/15 18
  • 19. 30/01/15 19 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 30/01/15 20
  • 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 30/01/15 21
  • 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 30/01/15 22
  • 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 30/01/15 23
  • 24. HipoMagnesemia 30/01/15 24
  • 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 30/01/15 25
  • 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 30/01/15 26
  • 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 30/01/15 27
  • 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 30/01/15 28
  • 29. HiperMagnesemia 30/01/15 29
  • 30. Síntomas de HiperMagnesemia 30/01/15 30 Weakness, nausea and vomiting Impaired breathing Hypotension Hypocalcemia Arrhythmia and Asystole
  • 31. Clínica de HiperMagnesemia 30/01/15 31 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 30/01/15 32 •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 30/01/15 33 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 30/01/15 34
  • 35. HipoFosfatemia Causas 30/01/15 35 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 30/01/15 36 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 30/01/15 37 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 30/01/15 38
  • 39. Causas de HiperFosfatemia 30/01/15 39 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 30/01/15 40 Signs and symptoms include : •ectopic calcification, secondary •hyperparathyroidism, and •renal osteodystrophy.
  • 41. Tratamiento de la Hiperfosfatemia 30/01/15 41 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 30/01/15 42

×