Carbon dioxide gastric

Magnesium oxide is an effective nonsystemic antacid, ie, it is converted to the hydroxide. It does not neutralize gastric acid excessively nor does it hberate carbon dioxide. The light form is preferable to the heavy for adininistration in Hquids because it is suspended more readily. One gram of magnesium oxide neutralizes 87 mL of 0.1 NUCl in 10 min, and 305 mL in 2 h. 

Baldini F., Falai A., De Gaudio A.R., Landi D., Lueger A., Mencaglia A., Scherr D., Trettnak W., Continuous monitoring of gastric carbon dioxide with optical fibres, Sensors and Actuators B 2003 90 132-138. 

Carbon dioxide Sulfur dioxide Aliphatic hydrocarbons Aromatic hydrocarbons Cholinesterase inhibitors Paraquat Lead Arsenic Mercury Removal from exposure and administer oxygen Removal from exposure Removal from exposure Removal from exposure Atropine, pralidoxime Gastric lavage and dialysis Dimercaprol, penicillamine Dimercaprol, penicillamine Dimercaprol (elemental), penicillamine, dimercaprol (inorganic salts)... 

Table 2 gives details of some conventional regimes (see British National Formulary, 2008). The efficacy of therapy can be checked by Radiocarbon-labelled urea breath testing (which depends upon release of labelled carbon dioxide by bacterial urease) or by testing gastric biopsy material for persistence of gastric urease, but should only be done after eradication therapy has been discontinued for at least a month, and whilst any anti-secretory treatment has been discontinued (because it tends to suppress but does not eradicate the organism). 

Sodium bicarbonate (eg, baking soda, Alka Seltzer) reacts rapidly with HC1 to produce carbon dioxide and NaCl. Formation of carbon dioxide results in gastric distention and belching. Unreacted alkali is readily absorbed, potentially causing metabolic alkalosis when given in high doses or to patients with renal insufficiency. Sodium chloride absorption may exacerbate fluid retention in patients with heart failure, hypertension, and renal insufficiency. 

This Gram-negative, microaerophilic bacterium infects areas of the stomach and duodenum it can result in peptic ulcers, gastritis, duodenitis and cancers. H. pylori s hehcal shape and flagella favour its motility in the mucus layer. Adhesins are produced by the bacterium, which binds to membrane-associated lipids and carbohydrates to maintain its attachment to epithelial cells. Large amounts of the enzyme urease are produced, both inside and outside of the bacterium. Urease metabolises urea (which is normally secreted into the stomach) to carbon dioxide and ammonia (which neutralises gastric acid), and is instrumental in the survival of the bacterium in the acidic environment. 

Indirect calorimetry provides the ability to measure the relative contribution of macronutrients toward energy use. The measurements of expired carbon dioxide and consumed oxygen are used to calculate respiratory quotient (RQ). An RQ of 1.0 indicates use of carbohydrate solely, an RQ of 0.7 indicates use of fat solely, whereas an RQ of 0.85 indicates mixed use of macronutrients. Data in rats demonstrates a significant increase in using fat as an energy substrate following DAG oil infusion (gastric) as observed by a decreased respiratory quotient value between 3-5 hours post-infusion (15). 

The enzyme carbonic anhydrase facilitates the reaction between carbon dioxide and water to form carbonic acid, which then breaks down to hydrogen (H" ) and bicarbonate (HCOj") ions. This process is fundamental to the production of either acid or alkaline secretions and high concentrations of carbonic anhydrase are present in the gastric mucosa, pancreas, eye and kidney. Because the number of available to exchange with Na" in the proximal tubule is reduced, sodium loss and diuresis occur. But HCOg reabsorption from the tubule is also reduced, and its loss in the urine leads within days to metabolic acidosis, which attenuates the diuretic... 

The mechanism presented for gastric acid production did not reveal the source of protons and chloride ions. Continued production of gastric acid by this mechanism would result in depletion of the chloride ions in the cell and alkalinization of the cell because of the loss of protons. Figure 2.27 shows that the source of chloride ions is the bloodstream and the source of protons is carbonic add, H COj. As detailed in a later section, carbonic acid is produced by the action of carbonic anhydrase, the enzyme that catalyzes the reversible condensation of a molecule of water with a molecule of carbon dioxide. Carbonic acid ionizes to produce a... 

With sodium bicarbonate, gastric rupture due to massive carbon dioxide release has been described, though it is very rare (12). 

Treatment begins with supportive care, and enteric suction is useful only if recent ingestion or retained gastric methanol is suspected. To prevent formation of toxic metabolites, fomepizole (4-methyl pyrazole or 4-MP) or ethanol to inhibit ADH should be administered. Fomepizole is preferred over ethanol if available [93]. It is well tolerated and may improve initial visual defects [94]. Mild methanol poisoning with levels below 20 mg/ dL can likely be treated with fomepizole only and bicarbonate however a methanol elimination half-life of over 50 hours with fomepizole requires prolonged infusion and monitoring [95]. Folic or folinic acid should be administered to promote conversion of formate to water and carbon dioxide [96]. 

On contact with gastric acid, magnesium carbonate reacts in the stomach to form soluble magnesium chloride and carbon dioxide. Magnesium carbonate should therefore not be used as an antacid by those individuals whose stomachs cannot tolerate the evolution of carbon dioxide. Some magnesium is absorbed but is usually excreted in the urine. As with other magnesium salts, magnesium carbonate has a laxative effect and may cause diarrhea. 

As an excipient, potassium bicarbonate is generally used in formulations as a source of carbon dioxide in effervescent preparations, at concentrations of 25-50% w/w. It is of particular use in formulations where sodium bicarbonate is unsuitable, for example, when the presence of sodium ions in a formulation needs to be limited or is undesirable. Potassium bicarbonate is often formulated with citric acid or tartaric acid in effervescent tablets or granules on contact with water, carbon dioxide is released through chemical reaction, and the product disintegrates. On occasion, the presence of potassium bicarbonate alone may be sufficient in tablet formulations, as reaction with gastric acid can be sufficient to cause effervescence and product disintegration. 

Orally ingested sodium bicarbonate neutralizes gastric acid with the evolution of carbon dioxide and may cause stomach cramps and flatulence. 

The gastric glands of the stomach secrete enough hydrochloric acid to give the stomach juices a hydrochloric acid concentration of over 0.01 M. Some of this stomach acid can be neutralized by an antacid that contains calcium carbonate. The CaC03 reacts with FICl in the stomach to form aqueous calcium chloride, carbon dioxide gas, and water. A regular antacid tablet will react with about 80 mL of 0.050 M HCl. How many milliliters of CO2 gas at 37 °C and 1.02 atm will form from the complete reaction of 80 mL of 0.050 M HCl ... 

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