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      Proton Pump Inhibition in the Management of Hypokalemia in Anorexia Nervosa with Self-Induced Vomiting

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      Canadian Journal of General Internal Medicine
      Dougmar Publishing Group, Inc.

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          Abstract

          Hypokalaemia is a dangerous complication in severe cases of eating disorders with self-induced vomiting and can result in rhabdomyolysis, cardiac arrhythmias, and death. Self-induced vomiting leads to hypokalaemia through two pathways.  First, loss of gastric acid causes hypochloraemic metabolic alkalosis, which increases filtered bicarbonate load in the nephron (exceeding the tubular resorptive threshold), and subsequently increases distal sodium bicarbonate delivery.  Secondly, hypovolaemia causes activation of the renin-angiotensin-aldosterone axis. Increased distal sodium delivery and mineralocorticoid activity together cause urinary potassium wasting.  Standard management of severe hypokalaemia in patients with anorexia or bulimia nervosa and persistent self-induced vomiting includes intravenous replacement of potassium and correction of hypovolaemia. However, hypokalaemia is often refractory in eating disorder outpatients who have ongoing self-induced vomiting after discharge. We present a case of hypokalaemia due to anorexia nervosa, binge-purge subtype with self-induced vomiting successfully treated with a proton pump inhibitor (PPI) in addition to standard therapy.

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          25 Years of Proton Pump Inhibitors: A Comprehensive Review

          Proton pump inhibitors (PPIs) were clinically introduced more than 25 years ago and have since proven to be invaluable, safe, and effective agents for the management of a variety of acid-related disorders. Although all members in this class act in a similar fashion, inhibiting active parietal cell acid secretion, there are slight differences among PPIs relating to their pharmacokinetic properties, metabolism, and Food and Drug Administration (FDA)-approved clinical indications. Nevertheless, each is effective in managing gastroesophageal reflux disease and uncomplicated or complicated peptic ulcer disease. Despite their overall efficacy, PPIs do have some limitations related to their short plasma half-lives and requirement for meal-associated dosing, which can lead to breakthrough symptoms in some individuals, especially at night. Longer-acting PPIs and technology to prolong conventional PPI activity have been developed to specifically address these limitations and may improve clinical outcomes.
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            Pathophysiology and management of hypokalemia: a clinical perspective.

            Potassium (K(+)) ions are the predominant intracellular cations. K(+) homeostasis depends on external balance (dietary intake [typically 100 mmol per day] versus excretion [95% via the kidney; 5% via the colon]) and internal balance (the distribution of K(+) between intracellular and extracellular fluid compartments). The uneven distribution of K(+) across cell membranes means that a mere 1% shift in its distribution can cause a 50% change in plasma K(+) concentration. Hormonal mechanisms (involving insulin, β-adrenergic agonists and aldosterone) modulate K(+) distribution by promoting rapid transfer of K(+) across the plasma membrane. Extrarenal K(+) losses from the body are usually small, but can be marked in individuals with chronic diarrhea, severe burns or prolonged sweating. Under normal circumstances, the kidney's distal nephron secretes K(+) and determines final urinary excretion. In patients with hypokalemia (plasma K(+) concentration <3.5 mmol/l), after the exclusion of extrarenal causes, alterations in sodium ion delivery to the distal nephron, mineralocorticoid status, or a specific inherited or acquired defect in distal nephron function (each of which affects distal nephron K(+) secretion), should be considered. Clinical management of hypokalemia should establish the underlying cause and alleviate the primary disorder. This Review aims to inform clinicians about the pathophysiology and appropriate treatment for hypokalemia.
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              Use of a Proton-Pump Inhibitor for Metabolic Disturbances Associated with Anorexia Nervosa

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                Author and article information

                Journal
                Canadian Journal of General Internal Medicine
                Can Journ Gen Int Med
                Dougmar Publishing Group, Inc.
                2369-1778
                1911-1606
                August 27 2018
                August 27 2018
                : 13
                : 3
                : 35-38
                Article
                10.22374/cjgim.v13i3.255
                da03c531-0cf1-41fa-91d7-a232df0ace96
                © 2018

                Copyright of articles published in all DPG titles is retained by the author. The author grants DPG the rights to publish the article and identify itself as the original publisher. The author grants DPG exclusive commercial rights to the article. The author grants any non-commercial third party the rights to use the article freely provided original author(s) and citation details are cited. To view a copy of this license, visit https://creativecommons.org/licenses/by-nc/4.0/


                General medicine,Geriatric medicine,Neurology,Internal medicine
                General medicine, Geriatric medicine, Neurology, Internal medicine

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