Milk-alkali syndrome pathophysiology: Difference between revisions

Jump to navigation Jump to search
No edit summary
m (Robot: Changing Category:Diseases to Category:Disease)
Line 13: Line 13:
{{WH}}
{{WH}}
{{WS}}
{{WS}}
[[Category:Needs content]]
[[Category:Needs content]]
[[Category:Electrolyte disturbances]]
[[Category:Electrolyte disturbances]]
[[Category:Calcium]]
[[Category:Calcium]]
[[Category:Urinary system]]
[[Category:Urinary system]]
[[Category:Diseases]]
[[Category:Disease]]
[[Category:Kidney diseases]]
[[Category:Kidney diseases]]
[[Category:Urology]]
[[Category:Urology]]

Revision as of 19:31, 28 December 2012

Milk-alkali syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Milk-alkali syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

Ecocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Milk-alkali syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Milk-alkali syndrome pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Milk-alkali syndrome pathophysiology

CDC on Milk-alkali syndrome pathophysiology

Milk-alkali syndrome pathophysiology in the news

Blogs on Milk-alkali syndrome pathophysiology

Directions to Hospitals Treating Milk-alkali syndrome

Risk calculators and risk factors for Milk-alkali syndrome pathophysiology

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 overingestion 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.

References

Template:WH Template:WS