Milk-alkali syndrome pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
==Pathophysiology== | ==Pathophysiology== | ||
The name "milk-alkali syndrome" derives from when patients would take in excessive amounts of milk and antacids to control their dyspepsia, leading to | The name "milk-alkali syndrome" derives from when patients would take in excessive amounts of milk and antacids to control their dyspepsia, leading to over ingestion of two key ingredients that lead to the disorder, excess calcium and excess base. Ingesting over two grams of elemental [[calcium]] per day produces this disorder in susceptible individuals. [[Gastrointestinal tract|Gastrointestinal]] absorption of such a large amount of calcium leads to [[hypercalcemia]]. This inhibits [[parathyroid hormone]] secretion by the [[parathyroid gland]] and may also lead to [[diabetes insipidus]]. The body's attempt to rid itself of the excess base in the urine may cause bicarbonaturia and subsequent hypovolemia due to transport of sodium ions to accompany the bicarbonate. | ||
Hypovolemia may increase the reabsorption of calcium and [[bicarbonate]] in the [[proximal convoluted tubule]]s of the kidney. Elevated bicarbonate levels in the blood raises the [[pH]], producing an alkalemia. In this state, excess bicarbonate eventually begins to reach the [[distal convoluted tubule]], leading to sodium retention in the lumen, an effect similar to the action of [[thiazide]] diuretics, hence increasing lumen positivity and driving calcium through the passive calcium channels to bind intracellular [[calbindin]]. Finally, because of the decreased intracellular sodium, there is an increased driving force for the basolateral Na+/Ca++ antiporter, thus facilitating calcium reabsorption. Basically, hypovolemia is the culprit that prevents correction of the hypercalcemia. | Hypovolemia may increase the reabsorption of calcium and [[bicarbonate]] in the [[proximal convoluted tubule]]s of the kidney. Elevated bicarbonate levels in the blood raises the [[pH]], producing an alkalemia. In this state, excess bicarbonate eventually begins to reach the [[distal convoluted tubule]], leading to sodium retention in the lumen, an effect similar to the action of [[thiazide]] diuretics, hence increasing lumen positivity and driving calcium through the passive calcium channels to bind intracellular [[calbindin]]. Finally, because of the decreased intracellular sodium, there is an increased driving force for the basolateral Na+/Ca++ antiporter, thus facilitating calcium reabsorption. Basically, hypovolemia is the culprit that prevents correction of the hypercalcemia. | ||
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The understanding of this mechanism led to the development of a simple yet elegant treatment for hypercalcemia. The first and most important step is [[Route of administration#Parenteral by injection or infusion|intravenous infusion]] of [[Saline (medicine)|normal saline]] to restore the intravascular volume, which reverses the calcium and bicarbonate retention in the PCT. Then a [[loop diuretic]] is used, but only after the volume replacement is complete, otherwise volume contraction would result, which would further exacerbate the hypercalcemia. The loop diuretics inhibit the [[Na-K-2Cl symporter]] and hence eliminate passive diffusion of potassium into the lumen via the [[ROMK]] channel. This effectively removes the net positive charge from the lumen, one of the main driving forces for calcium reabsorption via the paracellular pathway. In addition, loop diuretics increase the flow of luminal contents, which helps flush the calcium to the distal nephron. | The understanding of this mechanism led to the development of a simple yet elegant treatment for hypercalcemia. The first and most important step is [[Route of administration#Parenteral by injection or infusion|intravenous infusion]] of [[Saline (medicine)|normal saline]] to restore the intravascular volume, which reverses the calcium and bicarbonate retention in the PCT. Then a [[loop diuretic]] is used, but only after the volume replacement is complete, otherwise volume contraction would result, which would further exacerbate the hypercalcemia. The loop diuretics inhibit the [[Na-K-2Cl symporter]] and hence eliminate passive diffusion of potassium into the lumen via the [[ROMK]] channel. This effectively removes the net positive charge from the lumen, one of the main driving forces for calcium reabsorption via the paracellular pathway. In addition, loop diuretics increase the flow of luminal contents, which helps flush the calcium to the distal nephron. | ||
== | ==Referen== | ||
{{reflist|2}} | {{reflist|2}} | ||
[[Category:Needs content]] | [[Category:Needs content]] | ||
[[Category:Electrolyte disturbances]] | [[Category:Electrolyte disturbances]] | ||
Revision as of 21:50, 22 April 2019
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
The name "milk-alkali syndrome" derives from when patients would take in excessive amounts of milk and antacids to control their dyspepsia, leading to over ingestion of two key ingredients that lead to the disorder, excess calcium and excess base. Ingesting over two grams of elemental calcium per day produces this disorder in susceptible individuals. Gastrointestinal absorption of such a large amount of calcium leads to hypercalcemia. This inhibits parathyroid hormone secretion by the parathyroid gland and may also lead to diabetes insipidus. The body's attempt to rid itself of the excess base in the urine may cause bicarbonaturia and subsequent hypovolemia due to transport of sodium ions to accompany the bicarbonate.
Hypovolemia may increase the reabsorption of calcium and bicarbonate in the proximal convoluted tubules of the kidney. Elevated bicarbonate levels in the blood raises the pH, producing an alkalemia. In this state, excess bicarbonate eventually begins to reach the distal convoluted tubule, leading to sodium retention in the lumen, an effect similar to the action of thiazide diuretics, hence increasing lumen positivity and driving calcium through the passive calcium channels to bind intracellular calbindin. Finally, because of the decreased intracellular sodium, there is an increased driving force for the basolateral Na+/Ca++ antiporter, thus facilitating calcium reabsorption. Basically, hypovolemia is the culprit that prevents correction of the hypercalcemia.
The understanding of this mechanism led to the development of a simple yet elegant treatment for hypercalcemia. The first and most important step is intravenous infusion of normal saline to restore the intravascular volume, which reverses the calcium and bicarbonate retention in the PCT. Then a loop diuretic is used, but only after the volume replacement is complete, otherwise volume contraction would result, which would further exacerbate the hypercalcemia. The loop diuretics inhibit the Na-K-2Cl symporter and hence eliminate passive diffusion of potassium into the lumen via the ROMK channel. This effectively removes the net positive charge from the lumen, one of the main driving forces for calcium reabsorption via the paracellular pathway. In addition, loop diuretics increase the flow of luminal contents, which helps flush the calcium to the distal nephron.