Gastrointestinal tract potassium

The primary routes of entry for animal exposure to chromium compounds are inhalation, ingestion, and, for hexavalent compounds, skin penetration. This last route is more important in industrial exposures. Most hexavalent chromium compounds are readily absorbed, are more soluble than trivalent chromium in the pH range 5 to 7, and react with cell membranes. Although hexavalent compounds are more toxic than those of Cr(III), an overexposure to compounds of either oxidation state may lead to inflammation and irritation of the eyes, skin, and the mucous membranes associated with the respiratory and gastrointestinal tracts. Skin ulcers and perforations of nasal septa have been observed in some industrial workers after prolonged exposure to certain hexavalent chromium compounds (108—110), ie, to chromic acid mist or sodium and potassium dichromate. 

Information regarding the rapid lethal effects following oral intake of cyanide in humans indicates that cyanide is rapidly absorbed from the gastrointestinal tract. In a case study, an 80-kg male ingested an estimated 15-25 mg CNVkg as potassium cyanide in a suicide attempt (Liebowitz and Schwartz 1948). 

Ingestion of large doses can cause irritation of the gastrointestinal tract and nausea. Potassium chloride can stop the heart beat and is a component of lethal injections. 

Sustained release preparations of potassium chloride have been widely used to overcome the gastrointestinal side effects following medication with enteric coated tablets. Such formulation techniques delay the rate of absorption and produce a slow release of potassium chloride during the passage through the gastrointestinal tract [1,2]. 

An inhibition of the voltage-dependent potassium channels located in presy-naptic terminals can be expected to lead to spike broadening, an increase in calcium influx, and facilitation of neurotransmitter release (19). Thus, one potential functional role for 5-HT4 receptors could be the facilitation of synaptic transmission in the CNS. Although evidence for such an effect remains equivocal in CNS neurons, activation of 5-HT4 receptors has been reported to increase synaptic transmission in the myenteric nervous system (20). Such an effect might contribute to the prokinetic activity of benzamide 5-HT4 receptor agonists in the gastrointestinal tract. 

Elimination of Tl is mainly through the gastrointestinal tract but elimination also occurs through the kidneys, saliva, hair, skin, sweat, and breast milk. Relative amounts excreted by each route vary by species. Thallium is likely excreted through intestinal and gastric secretions associated with potassium loss or excretion. Likewise, reabsorption of Tl also occurs, mainly from the colon. The estimated biological half-life of Tl is 10 days but values up to 1 month have been reported (WHO, 1996). 

Osmosin, a formulation that contains potassium bicarbonate and releases indometacin osmoticaUy, was withdrawn because of reports of intestinal irritation, bleeding, perforation, and even death. These adverse effects were most probably caused by the very high local concentrations of indometacin and potassium in the lower part of the gastrointestinal tract produced by the tablet, which shifted the adverse reactions from the stomach to the intestine (SEDA-8,103) (26). 

Potassium chloride is irritating to the gastrointestinal tract, even to the extent of causing perforation (4). In a retrospective study at surgical clinics in Stockholm County there were 22 cases of small-bowel ulceration in which a connection with slow-release potassium chloride tablets was probable (5). Most of the ulcers had caused stenosis of 1-2 cm of gut, and in four cases there was also perforation of the bowel wall. Five patients had perforation without signs of stenosis. Mortality was 27%. The pathology of the ulcers was similar to that described after use of enteric-coated potassium chloride tablets. The frequency of potassium-induced ulceration is low (about 3 cases per 100 000 patient-years of slow-release tablet use), but this complication can be serious. 

Therapeutically, potassium bicarbonate is used as an alternative to sodium bicarbonate in the treatment of certain types of metabolic acidosis. It is also used as an antacid to neutralize acid secretions in the gastrointestinal tract and as a potassium supplement. 

High localized concentrations of potassium chloride in the gastrointestinal tract can cause ulceration, hence the development of the many enteric-coated and wax matrix sustained-release preparations that are available.Although it is claimed that some formulations cause less ulceration than others, it is often preferred to administer potassium chloride as an aqueous solution. However, solutions have also been associated with problems, mainly due to their unpleasant taste. 

Chemical interactions in the gastrointestinal tract between nutrients and drugs may considerably reduce the absorption of some drugs calcium ions from dairy products form insoluble and therefore nonabsorbable complexes with the antibiotic tetracycline. On the other hand, certain drugs are irritants to the gastrointestinal tract (nonsteroidal antiinflammatory drugs and potassium chloride tablets) and must be ingested with food. 

Clostridium perfringens has at least six serotypes and produces over 20 toxins. Epsilon toxin, along with alpha, beta, and iota toxins, is dermonecrotic and lethal. It is produced by some strains of type B and especially type D as a protoxin that is then converted to an active, mature, heat-labile toxin. The resulting toxin binds to cell membranes and forms a membrane complex that promotes the efflux of intracellular potassium. Because the usual route of entry is the gastrointestinal tract, the resulting pathology is an increase in intestinal permeability that enhances absorption of more toxin and ensures systemic toxemia. In animals, increased vascular permeability leads to enterotoxemia, pulpy kidney , altered hepatic function, and cerebral edema and necrosis. 

Reghkemmer G (1992) Absorption and secretion of K in the gastrointestinal tract. In Anonymous, ed. Potassium in Ecosystems, 23rd Colloquium of the International Potash Institute, Basel, Switzerland, pp. 205-210. 

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