Absorption altered gastrointestinal function

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. 

Electrolytes are involved in many metabolic and homeostatic functions, including enzymatic and biochemical reactions, maintenance of cell membrane structure and function, neurotransmission, hormone function, muscle contraction, cardiovascular function, bone composition, and fluid homeostasis. The causes of electrolyte abnormalities in patients receiving PN may be multifactorial, including altered absorption and distribution excessive or inadequate intake altered hormonal, neurologic, and homeostatic mechanisms altered excretion via gastrointestinal and renal losses changes in fluid status and fluid shifts and medications. 

The rate and extent of absorption of drug Y will be a function of its solubility, intestinal permeability, and stability in the gastrointestinal fluids and dissolution rate. Differences in the absorption of two phannaceutically equivalent products should then primarily be a function of their in vivo dissolution rate differences, assuming the excipients used do not alter bioavailability [38]. Therefore, the key question here is Does an in vitro dissolution test emulate in vivo drug dissolution ... 

Gastrointestinal Tract Absorption. The structure and function of this tract is varied and complex. The structure of the pesticide may be altered within the G.I. tract due to changes in pH in the stomach and intestine, or due to enzymatic action within the gut before it is absorbed into the lacteals and eventually into the hepatic portal system or lymphatic system. 

In addition to steatorrhea and nutritional deficiencies, patients with pancreatic exocrine insufficiency also develop symptoms such as postprandial pain, cramps, bloating, and distention. These are caused by profound alterations of upper gastrointestinal secretory and motor functions in response to increased nutrient delivery to the distal small intestine, particularly the ileum. In the first 5-10 years of chronic pancreatitis, overt malabsorption is usually neither detected nor a major clinical problem, although enzyme output may decrease by 60%-90%. Still, there is evidence that, even in the early stages of chronic pancreatitis, the site of maximal nutrient digestion and absorption is shifted from the duodenum to the more distal small intestine. 

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