Absorption GI tract

Completely absorbed from the GI tract (absorption decreased in CHF and nephrotic syndrome). Protein binding 94%-96%. Partially metabolized in the liver. Primarily excreted in urine. Not removed by hemodialysis. Half-life 1-1.5 hr. 

Rapidly and almost completely absorbed from the GI tract (absorption not affected by food). Protein binding 93%. Undergoes low first-pass metabolism not extensively metabolized. Primarily excreted in urine (more than 80% as unchanged drug). Half-life 6.5-10 hr. 

Pharmacokinetics Poorly absorbed from GI tract (absorption increases with food). Metabolized in liver. Primarily eliminated in feces. Half-life 2.5-9 hr (half life increased with impaired renal function. 

Pharmacokinetics Readily absorbed from the GI tract (absorption decreased by food). Protein binding less than 4%. Undergoes phosphorylat ion i nt racellularly to the active metabolite. Primarilyexcreted in urine. Removed by hemodialysis. HaJf-Hfe 1-3 hr metabolite, 2.6-10 hr (increased in impaired renal function). 

Ethanol Toxicosis. Absorption of ethanol by the GI tract absorption is rapid. Peak levels can be reached 30 to 60 minutes after ingestion. As a rule of thumb, 1 ml of absolute ethanol per kilogram weight results in a level of 100 mg/100 ml (0.1%) in 1 hour. Supportive treatment is directed toward the control of acidosis and hypoglycemia. 

Absorption of cystine and dibasic amino acids in renal tubule and GI tract Absorption of lysine and cationic amino acids in renal tubule and GI tract... 

Oral 7-15% of ingested dose of HgCl2 absorbed from the GI tract absorption proportional to water solubility of mercuric salt uptake by neonates greater than adults... 

ABSORPTION, FATE, AND EXCRETION Quaternary ammonium neuromuscular blocking agents are poorly and irregularly absorbed from the gastrointestinal (GI) tract. Absorption is adequate from intramuscular sites. Rapid onset is achieved with intravenous administration. The more potent agents must be given in lower concentrations, and diffusional requirements slow their rate of onset. 

Absorption In general, the opioids are absorbed readily from the GI tract absorption through the rectal mucosa is adequate, and a few agents e.g., morphine, hydromorphone) are available in suppositories. The more lipophilic opioids also are absorbed readily through the nasal or buccal... 

Figure 9.9 Human GI tract absorption of a set of 32 drugs versus HDM log Pg values for the best permeability in the range of pH 4-8. (Reprinted with permission from, J. Med. Chem. 2001, 44, 923-930, copyright 2001, American Chemical Society).

Torres-Lugo, M., Garcia, M., Record, R., Peppas, N.A. pH sensitive hydrogels as GI tract absorption enhancers Transport mechanism of salmon calcitonin and other model molecules using caco-2 cell model. Biotech. Prog., 18, 612, 2002. 

In other applications of CT, orally administered barium sulfate or a water-soluble iodinated CM is used to opacify the GI tract. Xenon, atomic number 54, exhibits similar x-ray absorption properties to those of iodine. It rapidly diffuses across the blood brain barrier after inhalation to saturate different tissues of brain as a function of its lipid solubility. In preliminary investigations (99), xenon gas inhalation prior to brain CT has provided useful information for evaluations of local cerebral blood flow and cerebral tissue abnormalities. Xenon exhibits an anesthetic effect at high concentrations but otherwise is free of physiological effects because of its nonreactive nature. 

Tocainide is rapidly and well absorbed from the GI tract and undergoes very fitde hepatic first-pass metabolism. Unlike lidocaine which is - 30% bioavailable, tocainide s availability approaches 100% of the administered dose. Eood delays absorption and decreases plasma levels but does not affect bio availability. Less than 10% of the dmg is bound to plasma proteins. Therapeutic plasma concentrations are 3—9 jig/mL. Toxic plasma levels are >10 fig/mL. Peak plasma concentrations are achieved in 0.5—2 h. About 30—40% of tocainide is metabolized in the fiver by deamination and glucuronidation to inactive metabolites. The metabolism is stereoselective and the steady-state plasma concentration of the (3)-(—) enantiomer is about four times that of the (R)-(+) enantiomer. About 50% of the tocainide dose is efirninated by the kidneys unchanged, and the rest is efirninated as metabolites. The elimination half-life of tocainide is about 15 h, and is prolonged in patients with renal disease (1,2,23). 

Encainide is almost completely absorbed from the GI tract. Eood may delay absorption without altering its bioavailabiUty. The dmg is rapidly metabolized in 90% of the patients to two principal metaboUtes, 0-demethylencainide (ODE) and 3-methoxy-O-demethylencainide (MODE), while the other 10% metabolize encainide slowly with Htde or no ODE or MODE formed. Encainide, ODE, and MODE are extensively protein bound 75—80% for encainide and ODE and 92% for MODE. Peak plasma concentrations are achieved in 30—90 min. Therapeutic plasma concentrations are very low the concentrations of ODE and MODE are approximately five times those of encainide. The findings with the metaboUtes are significant because ODE is 2—10 times and MODE, 1—4 times more effective than encainide as antiarrhythmics. The half-Hves for encainide in fast and slow metabolizers is 1—2 h and 6—12 h, respectively. The elimination half-life for ODE is 3—4 h and for MODE 6—12 h in fast metabolizers. Excretion occurs through the Hver and kidneys (1,2). 

Because digitoxin is a nonpolar, lipophilic glycoside, absorption from the GI tract is complete. About 90% of the dmg in plasma is tightly bound to protein. It is metabolized in the Hver to many metaboHtes, including digoxin which is the only pharmacologically active metaboHte. The dmg is excreted via the bile into feces. The elimination half-life of digitoxin is seven to nine days (87). 

With few exceptions, small particles of vegetable foods are generally stripped of their more accessible nutrients during digestion in the GI tract. In this way starch, protein, fat and water-soluble small components (sugars, minerals) are usually well absorbed. This is not always the case, however, for larger food particles or for molecules that cannot diffuse out of the celF tissue. Neither is it the case for the lipid-soluble components. These need to be dissolved in lipid before they can be physically removed from the cell to the absorptive surface, since the cell wall is unlikely to be permeable to lipid emulsions or micelles, and the presence of lipases will strip away the solvating lipid. 

Stimulating activation of vitamin D by 1-a-hydroxylase to cal-citriol (1,25-dihydroxyvitmin D3) to promote calcium absorption in the GI tract and increased calcium mobilization from bone... 

All of these actions are directed at increasing serum calcium levels and decreasing serum phosphorus levels, although the activity of calcitriol also increases phosphorus absorption in the GI tract and mobilization from the bone, which can worsen hyperphosphatemia. Calcitriol also decreases PTH levels through a negative feedback loop. These measures are sufficient to correct serum calcium levels in the earlier stages of CKD. 

Phosphate-Binding Agents When serum phosphorus levels cannot be controlled by restriction of dietary intake, phosphate-binding agents are used to bind dietary phosphate in the GI tract to form an insoluble complex that is excreted in the feces. Phosphorus absorption is decreased, thereby... 

Solutions that contain sodium citrate/citric acid (Shohl s solution and Bicitra) provide 1 mEq/L (1 mmol/L) each of sodium and bicarbonate. Polycitra is a sodium/potassium citrate solution that provides 2 mEq/L (2 mmol/L) of bicarbonate, but contains 1 mEq/L (1 mmol/L) each of sodium and potassium, which can promote hyperkalemia in patients with severe CKD. The citrate portion of these preparations is metabolized in the liver to bicarbonate, while the citric acid portion is metabolized to C02 and water, increasing tolerability compared to sodium bicarbonate. Sodium retention is also decreased with these preparations. However, these products are liquid preparations, which may not be palatable to some patients. Citrate can also promote aluminum toxicity by augmenting aluminum absorption in the GI tract. 

Around 99% of calcium is contained in the bones, whereas the other 1% resides in the extracellular fluid. Of this extracellular calcium, approximately 40% is bound to albumin, and the remainder is in the ionized, physiologically active form. Normal calcium levels are maintained by three primary factors parathyroid hormone, 1,25-dihydroxyvitamin D, and calcitonin. Parathyroid hormone increases renal tubular calcium resorption and promotes bone resorption. The active form of vitamin D, 1,25-dihydroxyvitamin D, regulates absorption of calcium from the GI tract. Calcitonin serves as an inhibitory factor by suppressing osteoclast activity and stimulating calcium deposition into the bones. 

The location of the tip of the feeding tube is important when considering medication administration down a feeding tube. This is particularly true if the medication acts locally in the GI tract itself. For example, sucralfate and antacids act locally in the stomach. Therefore, administration of these medications through a duodenal or jejunal tube is not logical. Likewise, for medications such as itraconazole that require acid for best absorption, administration directly into the duodenum or jejunum would be expected to result in suboptimal absorption. Absorption of drugs when administered directly into the small bowel, especially the jejunum, rather than into the stomach is another area where more research would be useful. 

Parenteral administration of drugs by intravenous (IV), intramuscular (IM), or subcutaneous (SC) routes is now an established and essential part of medical practice. Advantages for parenterally administered drugs include the following rapid onset, predictable effect, predictable and nearly complete bioavailability, and avoidance of the gastrointestinal (GI) tract and, hence, the problems of variable absorption, drug inactivation, and GI distress. In addition, the parenteral route provides reliable drug administration in very ill or comatose patients. 

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