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Magnesium imbalances
• Magnesium is the fourth most abundant
cation.
• Magnesium balance is maintained by renal
regulation of magnesium reabsorption.
• Magnesium deficiency and
hypomagnesaemia can result from a variety of
causes including gastrointestinal and renal
losses.
• Magnesium deficiency can cause a wide
variety of features including hypocalcaemia,
hypokalaemia and cardiac and neurological
manifestations.
• Chronic low magnesium state has been
associated with a number of chronic diseases
including diabetes, hypertension, coronary
heart disease, and osteoporosis
• Hypermagnesaemia is less frequent than
hypomagnesaemia and results from failure of
excretion or increased intake.
• Hypermagnesaemia can lead to hypotension
and other cardiovascular effects as well as
neuromuscular manifestations
Mg metabolism
• Plasma magnesium concentration/magnesium status
• Glomerular filtration rate
• Volume status
• Hormones
• PTH
• Calcitonin
• Antidiuretic hormone
• Glucagon
• Insulin
• Phosphate depletion
• Acid base status
• Hypercalcaemia
• Diuretics
• Miscellaneous factors
Factors affecting tubular reabsorption of magnesium
Tests used in assessing magnesium
status
Serum Magnesium Concentration
Total magnesium
Ultrafiltrable magnesium
Ionised magnesium
Intracellular Magnesium content
Red cells
Mononuclear blood cells
Skeletal muscle
Physiological tests
Metabolic balance studies
24 h urinary excretion of magnesium
Magnesium loading test
Intracellular free magnesium ion concentration
Fluorescent dye
Nuclear magnetic resonance spectroscopy
Magnesium Deficiency and Hypomagnesaemia
• Hypomagnesaemia is frequently undetected.
• In patients with other electrolyte
abnormalities hypomagnesaemia is more
frequent, 40% in hypokalaemic patients, 30%
in hypophosphataemic patients, 23% in
hyponatraemic patients and 22–32% in
hypocalcaemia patients
Aetiology and pathogenesis
Redistribution of magnesium
Refeeding and insulin therapy
Correction of acidosis
Massive blood transfusion
Gastrointestinal causes
Reduced intake
Mg free intravenous fluids
Dietary deficiency
low oxalate diet
Reduced absorption
Malabsorption syndrome
Chronic diarrhoea
Intestinal resection
Renal loss
Reduced sodium reabsorption
Saline infusion
Diuretics
Renal disease
Post renal transplantation
Dialysis
Diuretic phase of acute renal failure
Endocrine causes
Hypercalcaemia
Hyperthyroidism
Hyperaldosteronism
Diabetes mellitus
Alcoholism
Drugs
Clinical Features
Electrolyte disturbance
Hypokalaemia
Hypocalcaemia
Neuromuscular and central nervous system
Carpopedal spasm
Convulsations
Muscle cramps
Muscle weakness, fasciculations, tremors
Vertigo
Nystagmus
Depression, psychosis
Athetoid movements & choreform movements
Cardiovascular
Atrial tachycardias, fibrillation
Supraventricular arrhythmias
Ventricular arrhythmias
Digoxin sensitivity
Complications of magnesium deficiency
Altered glucose homeostasis
Atherosclerotic vascular disease
Hypertension
Myocardial infarction
Osteoporosis
Management
• Manage hypoventilation and respiratory
depression.
• ECG monitoring
• Monitor K+and Ca 2+ levels
• IV MgSO4 oral also can be used.
• Mg rich foods-whole grains,meat sea food
green leafy vegetables
Hypermagnesemia
• ECF Mg level> 2.5mEq/L
ETIOLOGY
Less common
Underlying chronic renal diasease
abnormla retension- renal failure,adrenal
insufficiency,and Rx with Mg salts
Pathopohysiology
• occurs as a result of decreased GFR
• May occur with laxatives compromised renal
function
Clinical manifestation
• Peripheral vasodilation
• nausea,vomiting,paralysis
• hypotension
• decreased DTRs
• Resp depression,C arrest also
Management
• treat underlying cause
• Ca Gluconate/ salts antagonizes Mg reverses
cardiac manifestations
• IV hydration for renal clearance
• dialysis may be indicated.
• monitor vitals , LOC
PHOSPHATE IMBALANCE
• In the body, almost all phosphorus is combined
with oxygen to form phosphate. Phosphate is
used as a building block for many substances
such as DNA, cell membranes, etc.
• The body obtains phosphate from food and
excretes it in urine and sometimes stool.
• Foods that are phosphate rich are milk, egg yolks,
chocolate and soft drinks. Imbalances in
phosphate may be too high
(Hyperphosphatemia) or too low
(Hypophosphatemia).
• Hypophosphatemia is a short-term or chronic
condition that happens when you have a low
level of phosphate in your blood.
• While mild hypophosphatemia is somewhat
common and usually isn’t a cause for concern,
severe hypophosphatemia can be life-
threatening and requires medical treatment.
• MAINLY IN BONES REST IN ECF
• ALSO FOUND IN TEETH SOFT TISSUES
• NORMAL LEVEL 2.5-4.5MG/DL
HYPOPHOSPHATEMIA
• LEVEL BELOW 3 MG/DL
• BELOW 1 MG/DL IS LIFE THREATENING
ETIOLOGY
LIMTED INTAKE
SHIFT INTO ICF
REDUCED ABSORPTION FROM GI TRACT
INCREASED RENAL ECRETION
PATHOPHYSIOLOGY
LIMITED INATKE R/T VOMITING, LONG TERM STARVATION
CELLULAR SHIFT DURING RAPID GROWTH,, HYPERMTABOLIC
STATE
EXCESSIVE USE OF ANTACIDS BINDING OCCURS
MALABSORPTION- IN CROHN’S DISEASE
HEMOLYTIC ANEMIA- ATP DEFICIENCY ( MAINTAIN RED CELL
MEMBRANE)
CLINICAL MANIFESTATION
IRRITABILITY, DISORIENTATION, TREMORS,
SEIZURES, RESPIRATORY FAILURE
POTENTIAL COMA
MANAGEMENT
• IDENTIFY CAUSE
• SLOW REPLACEMENT
• ENTERAL PHOSPHATE INFUSION OVER 6 HRS
HYPERPHOSPHATEMIA
• LEVEL> 4.5MG/DL
ETIOLOGY
• CHRONIC RENAL FAILURE( ABSORPTION
CONTINUES DESPITE GI ABSORPTION)
• RAPID CELL CATABOLISM –RELEASES PHOPSHATE
• VIT D INCREASES Ph ABSORPTION
CLINICAL MANIFESTATIONS
TACHYCARDIA
HYPERREFLEXIA
ABDOMINAL CRAMPS
NAUSEA
DIARRHOEA
MUSCLE TETANY
MANAGEMENT
• TREAT UNDERLYING CAUSE
• DIETARY RESTRICTION
• ALUMINIUM ANTACIDS
• ADEQUATE HYDRATION AND CORRECTION OF
HYPOCALCEMIA
• NaHCO3 ADMINISTRATION ENHANCES RENAL
EXCRETION OF PHOSPHORUS
• DIALYSIS

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Magnesium imbalances HYPO AND HYPERPHOSPHATEMIA.pptx

  • 2. • Magnesium is the fourth most abundant cation. • Magnesium balance is maintained by renal regulation of magnesium reabsorption. • Magnesium deficiency and hypomagnesaemia can result from a variety of causes including gastrointestinal and renal losses.
  • 3. • Magnesium deficiency can cause a wide variety of features including hypocalcaemia, hypokalaemia and cardiac and neurological manifestations. • Chronic low magnesium state has been associated with a number of chronic diseases including diabetes, hypertension, coronary heart disease, and osteoporosis
  • 4. • Hypermagnesaemia is less frequent than hypomagnesaemia and results from failure of excretion or increased intake. • Hypermagnesaemia can lead to hypotension and other cardiovascular effects as well as neuromuscular manifestations
  • 6. • Plasma magnesium concentration/magnesium status • Glomerular filtration rate • Volume status • Hormones • PTH • Calcitonin • Antidiuretic hormone • Glucagon • Insulin • Phosphate depletion • Acid base status • Hypercalcaemia • Diuretics • Miscellaneous factors Factors affecting tubular reabsorption of magnesium
  • 7. Tests used in assessing magnesium status Serum Magnesium Concentration Total magnesium Ultrafiltrable magnesium Ionised magnesium Intracellular Magnesium content Red cells Mononuclear blood cells Skeletal muscle Physiological tests Metabolic balance studies 24 h urinary excretion of magnesium Magnesium loading test Intracellular free magnesium ion concentration Fluorescent dye Nuclear magnetic resonance spectroscopy
  • 8. Magnesium Deficiency and Hypomagnesaemia • Hypomagnesaemia is frequently undetected. • In patients with other electrolyte abnormalities hypomagnesaemia is more frequent, 40% in hypokalaemic patients, 30% in hypophosphataemic patients, 23% in hyponatraemic patients and 22–32% in hypocalcaemia patients
  • 9. Aetiology and pathogenesis Redistribution of magnesium Refeeding and insulin therapy Correction of acidosis Massive blood transfusion Gastrointestinal causes Reduced intake Mg free intravenous fluids Dietary deficiency low oxalate diet Reduced absorption Malabsorption syndrome Chronic diarrhoea Intestinal resection Renal loss Reduced sodium reabsorption Saline infusion Diuretics Renal disease Post renal transplantation Dialysis Diuretic phase of acute renal failure Endocrine causes Hypercalcaemia Hyperthyroidism Hyperaldosteronism Diabetes mellitus Alcoholism Drugs
  • 10. Clinical Features Electrolyte disturbance Hypokalaemia Hypocalcaemia Neuromuscular and central nervous system Carpopedal spasm Convulsations Muscle cramps Muscle weakness, fasciculations, tremors Vertigo Nystagmus Depression, psychosis Athetoid movements & choreform movements Cardiovascular Atrial tachycardias, fibrillation Supraventricular arrhythmias Ventricular arrhythmias Digoxin sensitivity Complications of magnesium deficiency Altered glucose homeostasis Atherosclerotic vascular disease Hypertension Myocardial infarction Osteoporosis
  • 11. Management • Manage hypoventilation and respiratory depression. • ECG monitoring • Monitor K+and Ca 2+ levels • IV MgSO4 oral also can be used. • Mg rich foods-whole grains,meat sea food green leafy vegetables
  • 12. Hypermagnesemia • ECF Mg level> 2.5mEq/L ETIOLOGY Less common Underlying chronic renal diasease abnormla retension- renal failure,adrenal insufficiency,and Rx with Mg salts
  • 13. Pathopohysiology • occurs as a result of decreased GFR • May occur with laxatives compromised renal function Clinical manifestation • Peripheral vasodilation • nausea,vomiting,paralysis • hypotension • decreased DTRs • Resp depression,C arrest also
  • 14. Management • treat underlying cause • Ca Gluconate/ salts antagonizes Mg reverses cardiac manifestations • IV hydration for renal clearance • dialysis may be indicated. • monitor vitals , LOC
  • 15. PHOSPHATE IMBALANCE • In the body, almost all phosphorus is combined with oxygen to form phosphate. Phosphate is used as a building block for many substances such as DNA, cell membranes, etc. • The body obtains phosphate from food and excretes it in urine and sometimes stool. • Foods that are phosphate rich are milk, egg yolks, chocolate and soft drinks. Imbalances in phosphate may be too high (Hyperphosphatemia) or too low (Hypophosphatemia).
  • 16. • Hypophosphatemia is a short-term or chronic condition that happens when you have a low level of phosphate in your blood. • While mild hypophosphatemia is somewhat common and usually isn’t a cause for concern, severe hypophosphatemia can be life- threatening and requires medical treatment.
  • 17. • MAINLY IN BONES REST IN ECF • ALSO FOUND IN TEETH SOFT TISSUES • NORMAL LEVEL 2.5-4.5MG/DL
  • 18. HYPOPHOSPHATEMIA • LEVEL BELOW 3 MG/DL • BELOW 1 MG/DL IS LIFE THREATENING ETIOLOGY LIMTED INTAKE SHIFT INTO ICF REDUCED ABSORPTION FROM GI TRACT INCREASED RENAL ECRETION
  • 19. PATHOPHYSIOLOGY LIMITED INATKE R/T VOMITING, LONG TERM STARVATION CELLULAR SHIFT DURING RAPID GROWTH,, HYPERMTABOLIC STATE EXCESSIVE USE OF ANTACIDS BINDING OCCURS MALABSORPTION- IN CROHN’S DISEASE HEMOLYTIC ANEMIA- ATP DEFICIENCY ( MAINTAIN RED CELL MEMBRANE) CLINICAL MANIFESTATION IRRITABILITY, DISORIENTATION, TREMORS, SEIZURES, RESPIRATORY FAILURE POTENTIAL COMA
  • 20. MANAGEMENT • IDENTIFY CAUSE • SLOW REPLACEMENT • ENTERAL PHOSPHATE INFUSION OVER 6 HRS
  • 21. HYPERPHOSPHATEMIA • LEVEL> 4.5MG/DL ETIOLOGY • CHRONIC RENAL FAILURE( ABSORPTION CONTINUES DESPITE GI ABSORPTION) • RAPID CELL CATABOLISM –RELEASES PHOPSHATE • VIT D INCREASES Ph ABSORPTION
  • 23. MANAGEMENT • TREAT UNDERLYING CAUSE • DIETARY RESTRICTION • ALUMINIUM ANTACIDS • ADEQUATE HYDRATION AND CORRECTION OF HYPOCALCEMIA • NaHCO3 ADMINISTRATION ENHANCES RENAL EXCRETION OF PHOSPHORUS • DIALYSIS