Feces

Most bile salts excreted in the feces are of the secondary type. Their formation is discussed in Section VII. The daily fecal excretion of bile salts in healthy subjects is highly variable and easily influenced by dietary alterations. Values from several studies are given in Table VIII. Bile salts virtually disappear from the stools during prolonged fasting, and turnover nearly ceases (19). Primary bile salts appear in the stools of patients with diarrhea (1). Patients taking cholestyramine excrete the usual pattern of secondary bile salts (57), so that apparently bacterial dehydroxylation of bile salts can occur in the presence of this resin. Patients with total external bile fistulas have no bile salts in the feces (2) this does not exclude transintestinal excretion of bile salts but makes it unlikely. As mentioned earlier, the predominance of chenodeoxycholic acid in blood and bile is often reflected in a predominance of lithocholate over deoxycholate in the feces (27). 

TABLE Vm. Daily Fecal Excretion of Bile Acids in Man 

Subjects and conditions Fecal bile acid excretion (mg/day) References 

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Problems involving routine calculations are solved much faster and more reliably by computers than by humans. Nevertheless, there are tasks in which humans perform better, such as those in which the procedure is not strictly determined and problems which are not strictly algorithmic. One of these tasks is the recognition of patterns such as feces. For several decades people have been trying to develop methods which enable computers to achieve better results in these fields. One approach, artificial neural networks, which model the functionality of the brain, is explained in this section. 

With the permission of your instructor, carry out the following experiment. In a beaker, mix equal volumes of 0.001 M NH4SCN and 0.001 M FeCE (the latter solution must be acidified with concentrated HNO3 at a ratio of 4 drops/L to prevent the precipitation of Fe(OH)3). Divide solution in half, and add solid KNO3 to one portion at a ratio of 4 g per 100 mL. Compare the colors of the two solutions (see Color Plate 3), and explain why they are different. The relevant reaction is... 

Other than the biofilter and culture chambers, recirculating systems typically also employ one or more settling chambers or mechanical filters to remove soHds such as unconsumed feed, feces, and mats of bacteria that slough from the bio filter into the water. Each recirculating system requires a mechanical means of moving water from component to component. That usually means mechanical pumping, though air-lifts can also be used. 

Fibers and Fiber Sources. Fibers are present ia varyiag amounts ia food iagredients and are also added separately (see Dietary fiber). Some fibers, including beet pulp, apple pomace, citms pulp, wheat bran, com bran, and celluloses are added to improve droppiags (feces) form by providing a matrix that absorbs water. Some calorie-controUed foods iaclude fibers, such as peanut hulls, to provide gastroiatestinal bulk and reduce food iatake. Peanut hulls normally have a high level of aflatoxias. They must be assayed for aflatoxia and levels restricted to prevent food rejection and undesirable effects of mycotoxias. 

Laxatives faciUtate the passage and elimination of feces. These agents are used most commonly as self-treatment and are rarely prescribed by physicians. 

Lead enters the body through inhalation and ingestion, is absorbed into the circulatory system from the lungs and digestive tract, and excreted via the urine and feces. Normally, intake of lead approximately equals output. However, excessive exposure and intake can cause tissue concentrations to increase to the point where illness can result. 

Usually some fraction of the mineral nutrient ingested is not absorbed and passes into the feces. Modes of excretions bsted pertain only to the fraction of ... 

Odors are measured by their intensity. The threshold value of one odor to another, however, can vary greatly. Detection threshold is the minimum physical intensity necessary for detection by a subject where the person is not required to identify the stimulus, but just detect the existence of the stimulus. Accordingly, threshold deterrninations are used to evaluate the effectiveness of different treatments and to estabflsh the level of odor control necessary to make a product acceptable (8). Concentration can also produce different odors for the same matenal. For example, indole (qv) in low concentrations has the smell of jasmine and a low threshold of perception. In high concentrations, it has a strong odor of feces and CX-naphthyl amine as well as a considerably higher threshold of perception. 

Excretion factors are often related to lipophilicity. More lipophilic compounds tend to be excreted by the Hver into the bile, resulting in elimination ultimately in the feces. As this is a relatively slow process, much of the radioactivity having a shorter half-life decays before being eliminated. Polar compounds are more likely to be excreted by the kidneys. 

The dermal adsorption of DEBT in humans has been studied in the Netherlands by appHcation of DEBT as undiluted technical material or as 15% solutions in alcohol. Labeled material was recovered from the skin, and absorption of DEBT was indicated by the appearance of label in urine after two hours of skin exposure. About 5—8% of the appHed treatments was recovered as metaboHtes from urine, and excretion of metaboHtes in the urine came to an end four hours after exposure ended. DEBT did not accumulate in the skin, and only a small (less than 0.08%) amount ended up in feces. Curiously, less has been absorbed through skin from 100% DEBT appHcation (3—8%, mean of 5.6%) than from 15% alcohol appHcation (4—14%, mean of 8.4%). These results have been described as consistent with previous absorption/metaboHsm studies using guinea pigs, rats, and hairless dogs. Other pubHcations on DEBT toxicology have been cited (92). 

Sutures are required to hold tissues together until the tissues can heal adequately to support the tensions exerted on the wound duting normal activity. Sutures can be used ia skin, muscle, fat, organs, and vessels. Nonabsorbable sutures are designed to remain ia the body for the life of the patient, and are iadicated where permanent wound support is required. Absorbable sutures are designed to lose strength gradually over time by chemical reactions such as hydrolysis. These sutures are ultimately converted to soluble components that are then metabolized and excreted ia urine or feces, or as carbon dioxide ia expired air. Absorbable sutures are iadicated only where temporary wound support is needed. 

The unusual physical complaints and findings in workers overexposed to teUurium include somnolence, anorexia, nausea, perspiration, a metallic taste in the mouth and garlic-like odor on the breath (48). The unpleasant odor, attributed to the formation of dimethyl teUuride, has not been associated with any adverse health symptoms. Tellurium compounds and metaboUc products have been identified in exhaled breath, sweat, urine, and feces. Elimination is relatively slow and continuous exposure may result in some accumulation. No definite pathological effects have been observed beyond the physical complaints outlined. Unlike selenium, teUurium has not been proved to be an essential biological trace element. 

Tb allium, which does not occur naturaHy in normal tissue, is not essential to mammals but does accumulate in the human body. Levels as low as 0.5 mg/100 g of tissue suggest thallium intoxication. Based on industrial experience, 0.10 mg /m of thallium in air is considered safe for a 40-h work week (37). The lethal dose for humans is not definitely known, but 1 g of absorbed thallium is considered sufficient to kHl an adult and 10 mg/kg body weight has been fatal to children. In severe cases of poisoning, death does not occur earlier than 8—10 d but most frequently in 10—12 d. Tb allium excretion is slow and prolonged. For example, tb allium is present in the feces 35 d after exposure and persists in the urine for up to three months. 

Only the small amounts of T and T that are free in the circulation can be metabolized. The main route is deiodination of T to T and i-T, and from these to other inactive thyronines (21). Most of the Hberated iodide is reabsorbed in the kidney. Another route is the formation of glucuronide and sulfate conjugates at the 4 -OH in the Hver. These are then secreted in the bile and excreted in the feces as free phenols after hydrolysis in the lower gut. 

Pharmaceuticals. Examples of trace and ultratrace analyses of various dmgs and pharmaceuticals have been provided throughout. The purity of the active ingredient, its content and availabiUty in dosage form, therapeutic blood levels, deflvery to target areas, elimination (urine, feces, and metabohtes), and toxicity are always of importance. 

Studies show that the main sites of uranium deposition ate the renal cortex and the Hvet (8). Uranium is also stored in bones deposition in soft tissues is almost negligible. Utanium(VI) is deposited mostly in the kidneys and eliminated with the urine whereas, tetravalent uranium is preferentially deposited in the Hvet and eliminated in the feces. The elimination of uranium absorbed into the blood occurs via the kidneys in urine, and most, - 84%, of it is cleared within 4 to 24 hours (8). 

Ascorbic acid is very soluble in water and mainly excreted in the urine. No ascorbic acid is excreted during vitamin C deficiency. A minimum amount is lost in the feces, even after intake of gram dosages (154). 

Antibacterial activity of clindamycin is found both in urine and feces after adrninistration of clindamycin. This activity is a consequence of the presence of both clindamycin and its metaboUte, de- /V-methy1c1indamycin [22431-45-4] (6, R = R = H). Unlike de-/V-methy11incomycin, the de-Ai-methyl analogue is as active in vitro as clindamycin. The analogue has been isolated from the urine of humans who had received clindamycin, and its presence in semm has been detected (65). 

Whipworm (Trichuris trichiurd) adult females are 5 cm long. These worms thread their entire body into the epithelium of the colon, where they feed on tissue juice and small amounts of blood. Infections of several hundred worms may cause irritation and inflammation of the mucosa, with abdominal pain, diarrhea, and gas. Eggs are discharged and passed into the feces. Infections result from the swallowing of eggs that are obtained directly from contaminated soil. Untreated adult worms Hve for years. 

Since about 85% of the administered dose is passed unchanged in the feces of the patient, selective toxicity of the dmg can be attributed primarily to poor absorption. Side effects include abdominal pain, nausea, vomiting, diarrhea, loss of appetite, headaches, and vertigo or drowsiness. Skin rashes can also develop. Pyrantel pamoate is produced by Pfi2er, Inc., New York, New York. 

Balantidiasis (balantidiosis, balantidial dysentery), an intestinal disease seen almost worldwide, is caused by the large ciUated protozoan, balantidium coll The organism is usually found in the lumen of the large intestine of humans and animals. Cysts formed in the lumen of the colon or in freshly evacuated feces of humans or domesticated and wild animals, can colonize the colon and terminal ileum of new hosts by the latter s ingestion of contaminated food or water. The hog has been found to be the most heavily parasitized host. Its association with the rat may be a means for maintaining a reservoir infection in the two animals. 

Phenytoin s absorption is slow and variable yet almost complete absorption eventually occurs after po dosing. More than 90% of the dmg is bound to plasma protein. Peak plasma concentrations are achieved in 1.5—3 h. Therapeutic plasma concentrations are 10—20 lg/mL but using fixed po doses, steady-state levels are achieved in 7—10 days. Phenytoin is metabolized in the fiver to inactive metabolites. The plasma half-life is approximately 22 h. Phenytoin is excreted primarily in the urine as inactive metabolites and <5% as unchanged dmg. It is also eliminated in the feces and in breast milk (1,2). Prolonged po use of phenytoin may result in hirsutism, gingival hyperplasia, and hypersensitivity reactions evidenced by skin rashes, blood dyscrasias, etc... 

Elecainide is weU absorbed and 90% of the po dose is bioavailable. Binding to plasma protein is only 40% and peak plasma concentrations are attained in about 1—6 h. Three to five days may be requited to attain steady-state plasma concentrations when multiple doses are used. Therapeutic plasma concentrations are 0.2—1.0 lg/mL. Elecainide has an elimination half-life of 12—27 h, allowing twice a day dosing. The plasma half-life is increased in patients with renal failure or low cardiac outputs. About 70% of the flecainide in plasma is metabolized by the Hver to two principal metaboUtes. The antiarrhythmic potency of the meta-O-dealkylated metaboUte and the meta-O-dealkylated lactam, relative to that of flecainide is 50 and 10%, respectively. The plasma concentrations of the two metaboUtes relative to that of flecainide are 3—25%. Elecainide is mainly excreted by the kidneys, 30% unchanged, the rest as metaboUtes or conjugates about 5% is excreted in the feces (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). 

Sotalol is rapidly and almost completely (>90%) absorbed. Bioavahabhity of absorbed dmg is 89—100%. Peak plasma levels are achieved in 2—4 h. Sotalol is 50% bound to plasma proteins. Plasma half-life of the compound is about 5.2 h. No metabolites of sotalol have been identified indicating littie metabolism. The dmg is excreted mainly by the kidneys (80—90%) and about 10% is eliminated in the feces. The plasma half-life is prolonged in patients having renal failure. Kinetics of the compound are not affected by changes in liver function (1,2). Sotalol has ah the adverse effects of -adrenoceptor blockers including myocardial depression, bradycardia, transient hypotension, and proarrhythmic effects (1,2). 

After po dosing, verapamil s absorption is rapid and almost complete (>90%). There is extensive first-pass hepatic metabolism and only 10—35% of the po dose is bioavahable. About 90% of the dmg is bound to plasma proteins. Peak plasma concentrations are achieved in 1—2 h, although effects on AV nodal conduction may be apparent in 30 min (1—2 min after iv adrninistration). Therapeutic plasma concentrations are 0.125—0.400 p.g/mL. Verapamil is metabolized in the liver and 12 metabolites have been identified. The principal metabolite, norverapamil, has about 20% of the antiarrhythmic activity of verapamil (3). The plasma half-life after iv infusion is 2—5 h whereas after repeated po doses it is 4.5—12 h. In patients with liver disease the elimination half-life may be increased to 13 h. Approximately 50% of a po dose is excreted as metabolites in the urine in 24 h and 70% within five days. About 16% is excreted in the feces and about 3—4% is excreted as unchanged dmg (1,2). 

Po adrninistered nifedipine is almost completely absorbed. The onset of action is 20 min and peak effects occur at 1—2 h. The principal route of elimination is through hepatic metaboHsm by oxidation to hydroxycarboxyHc acid and the corresponding lactone. These metaboHtes are pharmacologically inactive. Almost 70—80% of dmg is eliminated in the urine during the first 24 h. About 15% is excreted in the feces. The elimination half-life of nifedipine is about 1—2.5 h (1,98,99). Frequency of occurrence of side effects in patients is about 17% with about 5% requiring discontinuation of therapy (1,98,99). 

Nicardipine is almost completely absorbed after po adrninistration. Administration of food decreases absorption. It undergoes extensive first-pass metaboHsm in the Hver. Systemic availabiHty is dose-dependent because of saturation of hepatic metaboHc pathways. A 30 mg dose is - 35% bioavailable. Nicardipine is highly protein bound (>95%). Peak plasma concentrations are achieved in 0.5—2.0 h. The principal path of elimination is by hepatic metaboHsm by hydrolysis and oxidation. The metaboHtes are relatively inactive and exert no pharmacological activity. The elimination half-life is 8.6 h. About 60% of the dose is excreted in the urine as metaboHtes (<1% as intact dmg) and 35% as metaboHtes in the feces (1,2,98,99). 

After po doses, atenolol is rapidly but incompletely absorbed ( 50%) from the GI tract, and 50% is excreted unchanged in the feces. Six to 16% of the plasma concentration is bound to protein. Atenolol undergoes Httie first-pass metaboHsm. Peak plasma concentrations occur in 2—4 h after po doses. The elimination half-hfe of atenolol is 6—7 h. Excretion of absorbed dmg is mainly by the kidneys and elimination can be impaired in patients having renal failure. The adverse effects of atenolol are similar to those seen for propranolol therapy (98,99,108). 

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