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Fluid and Electrolyte Absorption

If the intestinal contents become hyperosmolar, water enters the lumen to produce iso-osmolarity, and fluid and electrolyte loss occur. This condition is seen in lactose intolerance, ingestion of nonabsorbable laxatives such as magnesium salts, and ingestion of sugars such as lactulose. Bile acids inhibit the absorption of Na+ in the colon. Under normal circumstances, bile acids do not reach the [Pg.222]

Shiga toxin produced by Shigella dysenteriae has similar structural features. The toxin binds to a glycolipid (Gb3), undergoes endocytosis, and the enzymatie Ai fragment, which is a specific N-glycosidase, removes adenine from one particular adenosine residue in the 28S RNA of the 60S ribosomal subunit. Removal of the adenine inactivates the 60S ribosome, blocking protein synthesis. Ricin, abrin, and a number of related plant proteins inhibit eukaryotic protein synthesis in a similar manner (Chapter 25). [Pg.223]

Several E. coli strains also elaborate heat-labile entero-toxins that cause diarrheal disease ( traveller s diarrhea) by similar mechanisms. In V. cholerae, the same enterotoxin is produced by all pathogenic strains and is chro-mosomally determined, whereas in E. coli, different en-terotoxins are produced and the toxin genes are carried on plasmids. [Pg.223]

The actions of diphtheria and pertussis toxins are also mediated by ADP-ribosylation. Diphtheria toxin inhibits eukaryotic protein synthesis by ADP ribosylation of elongation factor II (Chapter 23). Pertussis toxin inactivates Gi by ADP ribosylation of its A-subunit and causes an increase in cAMP production. Unlike cholera toxin, pertussis and diphtheria toxins gain access to many tissues to produce diverse biological effects. Severe watery diarrhea [Pg.223]


Mechanism of Action-. An antidiarrheal and growth hormone suppressant that suppresses the secretion of serotonin and gastroenteropancreatic peptides and enhances fluid and electrolyte absorption from the G1 tract Therapeutic Effect Prolongs intestinal transit time. [Pg.893]

Stimulant laxatives Bisacodyl, 5-15 mg daily. Senna, dosage varies, consult product labeling Correctol, Dulcolax, Ex-Lax, Senokot, various generic Stimulant laxative actions include direct irritation of intestinal mucosa or stimulation of the myenteric plexus, resulting in peristalsis. These agents may also cause alteration of fluid and electrolyte absorption, resulting in luminal fluid accumulation and bowel evacuation. [Pg.1347]

Bismuth subsalicylate (BSS) is used widely in humans for treatment of diarrhea and is specifically recommended for the prevention of traveler s diarrhea. The precise mechanism of action remains undetermined and although the end result of treatment with BSS is reduction in diarrhea (Figueroa-Quintanilla et al 1993), its effect is probably not related to a direct antisecretory mechanism. Salicylates have been shown to stimulate intestinal fluid and electrolyte absorption per se but it is likely that, in many cases of colitis, resolution of inflammation and restoration of a normal surface epithelium is required to restore mucosal function. When used as pretreatment or coadministered, BSS significantly reduced the fluid secretory response to E. coli LT enterotoxin and cholera toxin in intestinal loops of rabbits and pigs (Ericsson et al 1990). However, when administered even 5 min after the enterotoxins, BSS had no significant effect on enterotoxin-stimulated intestinal secretion. These results suggest that BSS adsorbs or neutralizes bacterial enterotoxins but does not alter the effect of enterotoxins once they have bound to intestinal mucosa. BSS also modulates normal... [Pg.94]

In addition to its role in surfactant production, the type II cell also has a progenitor function, acting as the stem cell of the alveolar epithelium. The alveolar type I cells are highly susceptible to injury by oxygen and a variety of noxious substances. In such situations, type II cells can differentiate into type I cells and thus regenerate the gas-exchanging alveolar surface. Other functions of the type II cell are also believed to be the metabolism of foreign compounds (xenobiotic metabolism) and fluid and electrolyte absorption from the alveolar sacs into the interstitial matrix that surrounds the alveoli. [Pg.304]

The goal is to transition the patient to enteral or oral nutrition and taper off PN as soon as feasible clinically. When initiating enteral or oral nutrition, monitor the patient for glucose, fluid, and electrolyte abnormalities. Perform calorie counts to determine the adequacy of nutrition via the oral or enteral route. When the patient is tolerating more than 50% of total estimated daily calorie and protein requirements via the oral or enteral route, wean PN by about 50%. PN can be stopped once the patient is tolerating more than 75% of total estimated daily calorie and protein requirements via the oral or enteral route, assuming that intestinal absorption is maintained. [Pg.1504]

No specific antidote has been shown to be effective in treating 1,2-dibromoethane intoxication once absorption into the bloodstream has occurred (Ellenhorn and Barceloux 1988). Intravenous infusions of glucose may limit the hepatotoxicity of 1,2-dibromoethane (ERA 1989b). During the recovery phase, a diet rich in vitamin B and carbohydrates may limit liver damage (Dreisbach and Robertson 1987 Lawrence and Michaels 1984). Hemodialysis may be needed to regulate extracellular fluid and electrolyte balance and to remove metabolic waste products if renal failure occurs (ERA 1989b). [Pg.72]

Mechanism of Action A laxative prepared from the bean of the castor plant but the exact mechanism of acfion is unknown. Acts primarily in the small intestine. Maybe hydrolyzed to ricinoleicacid which reduces net absorption of fluid and electrolytes and stimulates peristalsis. Therapeutic Effect Increases peristalsis, promotes laxative effect. [Pg.202]

The constipating effects of morphine and certain other opioid derivatives have been recognized for some time. These drugs produce a general decrease in GI motility, and they may also reduce fluid loss by increasing the absorption of salt and water or by decreasing fluid and electrolyte excretion from the GI tract.44 The exact manner in which opioids exert these effects, however, is not known. As indicated in Chap-... [Pg.394]

Bismuth salicylate has a number of properties contributing to its antidiarrheal effects. This drug may stimulate water and electrolyte absorption from the lower GI tract, thus decreasing fecal fluid loss. In addition, the bismuth component of this compound may have antibacterial effects, and the salicylate component may inhibit the production of prostaglandins that irritate the intestinal lining. The combination of these properties makes this drug fairly effective in... [Pg.395]

Increased motility of the gastrointestinal tract and decreased absorption of fluid are major factors in diarrhea. Antidiarrheal drugs include antimotility agents, adsorbents, and drugs that modify fluid and electrolyte transport (Figure 24.8). [Pg.254]

Q6 Loperamide hydrochloride is an opioid. The starting dose will be 4 mg, which can be reduced to 2 mg, three times a day for five days if necessary. Opioids act on // opiate receptors in the myenteric plexus of the intestine and may modulate acetylcholine release to reduce peristalsis. They trigger mucosal transport of ions and water out of the lumen and cause a reduction in secretion. The absorption of fluid and electrolytes is increased since the stool remains in the colon for a longer period. Loperamide does not produce sedation or other central effects associated with opiates, since it does not cross the blood-brain barrier. [Pg.267]

Diarrhoea results from an imbalance between secretion and reabsorption of fluid and electrolytes it has numerous causes, including infections with enteric organisms (which may stimulate secretion or damage absorption), inflammatory bowel disease and nutrient malabsorption due to disease. It also commonly occurs as a manifestation of disordered gut motility in the absence of demonstrable disease (see below). Rarely it is due to secretory tumours of the alimentary tract, e.g. carcinoid tumour or vipoma (a tumour which secretes VIP, vasoactive intestinal peptide). [Pg.643]

Disorders that cause increased secretion of fluid and electrolytes into the small intestine of the horse are characterized by abdominal discomfort, distension of the small intestine and enterogastric reflux. In young foals with small intestinal secretory disorders, diarrhea may occur. Increased intestinal secretion can result from the active secretion of electrolytes and water, for example the cyclic nucleotide-stimulated secretion that results from exposure to bacterial enterotoxins. Passive secretion of water can result from increased permeability of the intestine, such as in enteritis, distension or ischemia, or decreased absorption of osmoti-caUy active substances, such as with lactose intolerance in foals. Disorders in which there is decreased secretion of fluid into the small intestine are not appreciated, although impactions of ingesta in segments of the small intestine can occur. [Pg.113]

Only symptomatic treatment is available. Adequate measures should be taken to maintain fluid and electrolyte balance and keep the body temperature within tolerable limits. Measures should be taken to remove the poison from the body through gastric lavage and saline cathartic. Gastrointestinal absorption may be... [Pg.871]

General supportive care is the focus of therapy. There is no antidote. Administration of activated charcoal may decrease absorption of the plant if given within an hour of the ingestion. Intravenous fluid and electrolyte replacement should be administrated as needed. Symptomatic patients should have continuous cardiac monitoring. Symptomatic bradycardia may be treated with atropine. For patients whose blood pressure does not respond to fluid replacement, vasopressors may be needed. Recovery can occur within hours to days. [Pg.2457]

Minerals require a suitable mucosal surface across which to enter the body. Resection or diversion of a large portion of small bowel obviously affects mineral absorption. Extensive mucosal damage due to mesenteric infarction or inflamatory bowel disease or major diversion by jejunoileal bypass procedures reduces the available surface area. Minerals whose absorption occurs primarily in the proximal intestine, e.g., copper or iron, are affected differently than those absorbed more distally, e.g., zinc. In addition, the integrity of the epithelium, the uptake of fluids and electrolytes, the intracellular protein synthesis, the energy-dependent pumps, and the hormone receptors must be intact. [Pg.55]

Fluid turnover of about 9 L occurs daily in the GI tract. Ingested water contributes about 2 L, and the remainder arises from secretions of the GI tract mucosa and associated glands. Nearly all of this water is reabsorbed, and about 200 mL (2%) or less is excreted (Table 12-8). If the amount of water excreted in feces exceeds 500 mL, diarrhea results. Similarly, only 2% of Na+ and 10% of K+ in gastrointestinal fluids appear in the feces. Most absorption of fluid and electrolytes occurs in the small intestine. [Pg.222]

The mechanism by which cholera toxin causes secretory diarrhea is through continuous stimulation of the CFTR-regulated CL channel (Figure 12-15). In cystic fibrosis, CFTR defects cause the abolition of intestinal chloride secretion without affecting the absorptive capacity. In homozygous CF patients, the disease is eventually lethal (discussed earlier). In cholera infections, however, CFTR is overactivated with fluid and electrolyte losses that lead to... [Pg.223]

Brown, D.R. and Miller, R.J. (1991) Neurohormonal control of fluid and electrolyte transport in intestinal mucosa, in Handout of Physiology, The Gastrointestinal System IV, Gastrointestinal Physiology Absorptive and Secretory Process of the Intestine, M. Field and R.A. Frizzel, Eds. pp. 527-589. Bethesda, MD American Physiological Society. [Pg.414]


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