UKYNIJ

1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
ALTERATIONS OF
PHOSPHORUS AND
MAGNESIUM
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018

2. ALTERATIONS OF PHOSPHORUS AND MAGNESIUM
HYPERPHOSPHOREMIA
Concept.- The urinary excretion of phosphate regulates the plasma concentration
of phosphorus, which is regulated in turn by FGF-23 and PTH. The normal
phosphorus values in adults are 2.5-4.5 mg / dL (0.8-1.45 mmol / L) and in
children and adolescents it is 6 mg / dL (1.9 mmol / L). ).
Etiology.- Caused by decreased phosphorus renal excretion, acute exogenous
phosphorus overload, and transcellular phosphorus movement.
Clinical picture.- Hypocalcemia, with risk of tetani, red eye syndrome, and blood
vessels.
Treatment.- Acute hyperphosphatemia is treated by forcing diuresis with 0.9%
saline (3-6 L / day) and acetazolamide (15 mg / kg body weight every 3-4 h),
while chronic hyperphosphatemia is deals with phosphorus restriction of the diet
and administration of oral phosphorus binders.
HYPOPHOSPHOREMIA
It occurs in 10% -15% of hospitalized patients, although the severe form (less than
1 mg / dL [0.32 mmol / L]) is less frequent.
Etiology.- Caused by redistribution of extracellular phosphorus, intracellular
phosphofructokinase is stimulated in respiratory alkalosis, which in turn
stimulates glycolysis, phosphorus depletion due to decreased intestinal absorption:
the consumption of antacids containing aluminum or magnesium binds
phosphorus in the intestine and its abuse can produce hypophosphatemia and
osteomalacia, in steatorrhea and in chronic diarrhea the hypophosphoremia, is due
not only to a lower absorption of phosphorus but to the coexistence of a deficit of
vitamin D, depletion due to renal loss: Phosphaturic effect of PTH can produce
hypophosphatemia in primary hyperparathyroidism. Something similar occurs in
hyperparathyroidism secondary to situations of vitamin D deficiency, imatinib
mesylate used in the treatment of chronic myeloid leukemia, the most frequent
causes of deep hypophosphatemia are alcohol deprivation, nutritional repletion,
diabetic ketoacidosis and alkalosis respiratory

3. Differential diagnosis: Calcemia, phosphaturia. A phosphaturia above 100 mg /
day (32.2 mmol / L) or a percentage of tubular reabsorption of phosphorus lower
than 95% in the presence of hypophosphoremia point to a renal loss.
Clinical picture.- It appears when there are less than 2 mg / dL (0.64 mmol / L)
and chronic phosphorus depletion coexist, there may be decreased cardiac output
and cause congestive heart failure, as well as respiratory failure due to muscular
disease, in general when phosphorus is less than 1 mg / dL (0.32 mmol / L). In the
skeletal muscle, proximal myopathy and even rhabdomyolysis are frequent in
severe cases in alcoholic patients, hemolysis may occur when the phosphorus
values are below 0.5 mg / dL (0.16 mmol / L).
Treatment.- It does not need treatment when the phosphorus is higher than 2 mg /
dL (0.64 mmol / L), with lower figures should preferably be tried the oral
supplement of 1 to 2 g / day of phosphorus, element such as sodium phosphate
and potassium neutral in divided doses (1 mmol of phosphate = 31 mg of
phosphorus element), it is useful to increase the intake of dairy products, because
each liter of milk contains approximately 1 g of phosphorus. When the oral route
is not possible or the hypophosphoremia is severe, it is necessary to resort to the
intravenous route. The phosphate dose ranges from 2.5-5 mg / kg in 500 mL of
saline, every 4-6 h (ampoules of 1 M monosodium phosphate 10 mL = 130 mg)
depending on the severity of the hypophosphoraemia. Prophylactic treatment with
phosphate i.v. only parenteral nutrition is indicated; 450 mg of phosphate per
1000 kcal perfused are recommended.
HYPERMAGNESEMIA
Concept.- It is a plasma concentration of magnesium higher than 2.5 mg / dL (1
mmol / L).
Etiology.- The most frequent is renal failure, so should not receive antacids or
laxatives containing magnesium, treatment with magnesium sulfate in eclampsia
can also produce transient hypermagnesemia, the administration of enemas
containing magnesium in subjects with function Normal renal function can also
cause hypermagnesemia. Familial hypocalciuric hypercalcemia, tumor lysis
syndrome, diabetic ketoacidosis and adrenal insufficiency are other causes of
hypermagnesemia.

4. Clinical picture.- Presents muscle weakness and paralysis, quadriplegia and
ventilatory failure, bradyarrhythmias, which can lead to complete atrioventricular
block and cardiac arrest. The vasodilatory effect of Mg has a peripheral
vasodilatory effect, which results in hypotension. Hypermagnesemia also
decreases calcemia by decreasing PTH secretion. In the most severe cases,
arreactive mydriasis due to parasympathetic blockade, which simulates a
herniated trunk.
Treatment.- Calcium gluconate administration, hemodialysis. Moderate and
asymptomatic chronic hypermagnesemia usually does not require treatment.
HYPOMAGNESEMIA
Concept.- It is defined as a decrease in the plasma concentration of magnesium
below 1.7 mg / dL (0.7 mmol / L).
Etiology.- It may be due to:
 Intestinal losses: occur in syndromes of malabsorption, acute or chronic
diarrhea and surgery of the small intestine, the most frequent cause is
alcoholism, acute poisoning with ethanol increases the urinary elimination
of magnesium, other factors such as the reduction of intake , vomiting,
diarrhea and malabsorption due to chronic pancreatitis are also important,
 By redistribution: acute pancreatitis can also produce hypomagnesemia
by saponification of magnesium in necrotic fat, in polytransfusions
hypomagnesemia can be produced by the binding effect of citrate, and in
the syndrome of bone hungry after parathyroidectomy, by its deposit in the
bone .
Mainly two factors intervene:
1) Osmotic diuresis
2) Urinary elimination of organic acids
Renal losses: they are identified by a high magnesiuria in the presence of
hypomagnesemia, a magnesiuria higher than 20 mg / day (8.2 mmol / day) in the
presence of hypomagnesemia suggests renal losses.
Renal magnesium losses can occur through two major mechanisms:
a) Inhibition of the passive reabsorption of magnesium secondary to that of
sodium

5. b) Due to a primary tubular defect, in volume expansion, as in the case of
primary hyperaldosteronism, or with the use of loop or thiazide diuretics,
the decrease in magnesium reabsorption follows that of sodium.
In hypercalcemic conditions such as primary hyperparathyroidism, the excessive
filtered calcium load competes with magnesium in the ascending loop of Henle
for its resorption, with the possible appearance of hypomagnesemia. Numerous
nephrotoxic agents can produce hypomagnesemia; These include
aminoglycosides, cyclosporine and tacrolimus, cisplatin, amphotericin B and
pentamidine. Nephrotoxic hypomagnesemia may be important, even to produce
secondary hypocalcemia.
Hypomagnesemias due to a primary tubular defect are usually observed in the
postobstructive polyuric phase or after kidney transplantation. Finally,
hypomagnesemia is also seen in familial hypercalciuric hypomagnesemia with
nephrocalcinosis that is due to a mutation of claudin 16 and usually progresses to
renal failure.
Clinical picture.- In many patients, the decrease in serum magnesium does not
cause clinical manifestations. When symptoms appear (usually with magnesium
concentrations less than 1.5 mg / dL [0.61 mmol / L]) they are located mainly in
the neuromuscular system, with asthenia, muscle hyperexcitability manifested in
the form of fasciculations, myoclonias, signs of Chvostek and Trousseau positive
or even tetany frank. When hypomagnesemia exists, the release of acetylcholine
in the motor plate is facilitated and the clinical picture of neuromuscular
hyperexcitability is produced. There may also be metabolic encephalopathy, with
disorientation, convulsions and obtundation. Although hypomagnesemia is
capable of causing tetany by itself, the vast majority of cases of tetany that appear
during the course of magnesium reduction are due to hypocalcemia.
The decrease in magnesium favors the appearance of severe ventricular
arrhythmias, which also limits the renal capacity of potassium preservation, so it
is very common to observe hypokalemia together with hypomagnesemia.
Treatment.- Correct the base disorder. Oral contributions, such as chloride or
magnesium lactate (500 mg / day of magnesium in divided doses) are sufficient in
asymptomatic subjects. In contrast, patients with tetany and associated

6. hypocalcemia, and those with hypomagnesemia and hypokalemia with ventricular
arrhythmias, should receive intravenous magnesium sulfate, as detailed in the
treatment of hypocalcemia.
BIBLIOGRAPHICAL REFERENCE:
A. Torres Ramírez "Alterations of calcium, phosphorus and magnesium
metabolism" Farreras Valenti, Rozman Ciril "Internal Medicine", Barcelona
Spain, Elsiever, 2016, p. 793-795.