Alkalosis

To present a cogent and practical review of the medical complications and their treatment in patients with bulimia nervosa. Thorough review of the medical literature from 1990 to current in regards to the medical complications of bulimia nervosa and the therapeutic intervention that are effective to treat them. Extensive and detailed review of the medical complications of bulimia nervosa.

Antacids are chemical substances which neutralizing the acid that causes heartburn. By reducing the
acidity, the acid is less able to irritate the esophagus. The effect of antacids on the stomach is due to
partial neutralisation of gastric hydrochloric acid and inhibition of the proteolytic enzyme, pepsin. There
are commonly used self-prescribed medications. Antacids are available many forms such as suspensions,
chewable tablets and liquid gels. They consist of calcium carbonate and magnesium and aluminum salts
in various compounds or combinations. Antacids are used for gastric and duodenal ulcers, gastrooesophageal
reflux disease, stress gastritis, pancreatic insufficiency, non-ulcer dyspepsia, biliary reflux,
bile acid mediated diarrhoea, constipation, osteoporosis, urinary alkalinisation and chronic renal failure
as a dietary phosphate binder.

Generalised paresis, severe hypokalaemia and kaliuresis, metabolic alkalosis and hypertension, characteristic of mineralocorticoid excess, were identified in a dog with hyperadrenocorticism due to a functional adrenocortical carcinoma. Aldosterone concentration was decreased and deoxycorticosterone concentration increased in the presence of hypokalaemia. These metabolic abnormalities resolved with resection of the carcinoma. Mineralocorticoid excess in dogs with hyperadrenocorticism is generally considered to be of little clinical significance but resulted in the acute presentation of this patient. The possible pathogenesis of mineralocorticoid excess in this case of canine hyperadrenocorticism is discussed.

Abstract:  Plasmapheresis (PP) is widely known as the standard therapy for thrombotic thrombocytopenic purpura (TTP). Citrate is used as an anticoagulant in fresh frozen plasma, and the large amount of citrate infused during PP induces metabolic alkalosis. A 29-year-old woman was diagnosed with TTP associated with systemic lupus erythematosus, and was treated by daily PP in addition to a steroid, an immunosuppressant, vincristine, and cyclophosphamide. Uncompensated alkalosis caused by a combination of metabolic and respiratory alkalosis developed after artificial ventilation was discontinued. Her metabolic status improved after controlling her respiratory status and the activity of the TTP. Metabolic alkalosis is a common complication in TTP patients treated by frequent PP, but several factors that affect metabolic status may aggravate the alkalosis and induce uncompensated alkalosis.

Since the initial description in the 1960s of patients with seemingly inherited disorders characterized by hypokalemia and metabolic alkalosis, the pathophysiologic processes underlying Bartter and Gitelman syndromes have generated tremendous study and speculation. Recently described mutations in genes encoding transport proteins important in sodium and chloride reabsorption in the thick ascending limb of Henle and distal convoluted tubule have confirmed these processes as the proximate defects in Bartter and Gitelman syndromes, respectively. Basic understanding of the role of these proteins in normal sodium and chloride homeostasis, and review of the secondary mediators stimulated by loss of their function provide insight into the clinical manifestations and response to treatment observed in these disorders.

The urinary bladder of 10 clinically normal dogs was excised and the ureters were implanted into an isolated, vagotomized gastric segment derived from the fundic region of the stomach. The gastric segment was closed to form a conduit. Continence was maintained with a modified Kock "nipple valve" created from an isolated segment of ileum. Four dogs were euthanatized by day 30 because of complications related to the early onset of renal failure and electrolyte alterations. Six dogs were euthanatized on day 150. Ureteral dilatation, hydronephrosis, and decreased endogenous creatinine clearance rates were measured in all dogs at the end of the survival period. Pyelonephritis was diagnosed histologically in seven dogs. Positive renal cultures were obtained from seven dogs at necropsy. It was concluded that gastric conduit urinary diversion is unsatisfactory for long-term or short-term clinical use in dogs.

Delta F508 mutation is recognized as the most common genotype of cystic fibrosis (CF) however, there are small numbers of CF patients having Delta F508/F311L. In the present study, the authors report a 2-year-old Thai boy, originating from North India, presenting with recurrent episodes of febrile illness, hyponatremia, hypokalemia, and metabolic alkalosis since 4 months of age. He was transferred to our hospital for further investigation. Blood chemistry revealed the following serum electrolytes, sodium 122, potassium 3.69, chloride 79.7, and bicarbonate 33.8 mEq/L, and the following urine electrolytes, sodium < 10, potassium 45.7 and chloride < 10 mEq/L. After intravenous fluid administration, hyponatremia and metabolic alkalosis improved DNA sequencing analysis of his blood demonstrates compound mutation for Delta F508 and F311L in CFTR gene. In conclusion, the authors report a rare case of CF with Delta F508/F311L genotype presented with recurrent hyponatremia and metaboli...

The increased concentration of protons during fatiguing exercise may contribute to increased activation of group III and IV afferents and subsequently reduced central drive, however this has yet to be confirmed in exercising humans. Here we determined whether inducing metabolic alkalosis differentially effects descending central drive following fatiguing exercise, and whether this effect may, in part, be explained by attenuating group III and IV afferent firing. 11 males performed a maximal 2 min voluntary knee extension (MVC) followed by a 2 min rest and subsequent 1 min MVC with an occlusive cuff either under placebo (PLA; 0.3 g·kg(-1) BW calcium carbonate) or alkalosis (ALK; 0.3 g·kg(-1) BW sodium bicarbonate) condition. Femoral nerve stimulation was applied prior to exercise, after the 2 min MVC and then at 40 to 60 s intervals throughout the remainder of the protocol to explore central and peripheral mechanisms associated with reductions in maximum force and rate of torque deve...

Collecting ducts (CD) not only constitute the final site for regulating urine concentration by increasing apical membrane Aquaporin-2 (AQP2) expression, but are also essential for the control of acid–base status. The aim of this work was to examine, in renal cells, the effects of chronic alkalosis on cell growth/death as well as to define whether AQP2 expression plays any role during this adaptation. Two CD cell lines were used: WT- (not expressing AQPs) and AQP2-RCCD1 (expressing apical AQP2). Our results showed that AQP2 expression per se accelerates cell proliferation by an increase in cell cycle progression. Chronic alkalosis induced, in both cells lines, a time-dependent reduction in cell growth. Even more, cell cycle movement, assessed by 5-bromodeoxyuridine pulse-chase and propidium iodide analyses, revealed a G2/M phase cell accumulation associated with longer S- and G2/M-transit times. This G2/M arrest is paralleled with changes consistent with apoptosis. All these effects appeared 24 h before and were always more pronounced in cells expressing AQP2. Moreover, in AQP2-expressing cells, part of the observed alkalosis cell growth decrease is explained by AQP2 protein down-regulation. We conclude that in CD cells alkalosis causes a reduction in cell growth by cell cycle delay that triggers apoptosis as an adaptive reaction to this environment stress. Since cell volume changes are prerequisite for the initiation of cell proliferation or apoptosis, we propose that AQP2 expression facilitates cell swelling or shrinkage leading to the activation of channels necessary to the control of these processes. J. Cell. Physiol. 224: 405–413, 2010. © 2010 Wiley-Liss, Inc.