GI motility

Induces dyskinesia/vasodilatation, schizophrenia/4- coordination Vaso constriction/cell proliferation/aldosterone secretion Vaso constriction/cell proliferation/bronchoconstriction 4-memory, sedation/vasodilatation/4 GI motility A blood pressure/4- GI secretion Vagal effects/A blood pressure/tachycardia... 

Antidiarrheal medications that reduce GI motility, such as loperamide, diphenoxylate/atropine, or codeine should be avoided in patients with active IBD due to the risk of precipitating acute colonic dilation (toxic megacolon). 

Patients who have had multiple intestinal resections due to CD may have diarrhea related to the inability to reabsorb bile salts. Cholestyramine has been demonstrated to improve diarrheal symptoms in this population.8,15 NSAIDs should be avoided for pain management due to their ability to worsen IBD symptoms. Narcotic analgesics should be used with caution, as they may significantly reduce GI motility. 

An additional important component of therapy is nutrition. Intraabdominal infections often involve the GI tract directly or disrupt its function (paralytic ileus). The return of GI motility may take days, weeks, and occasionally, months. In the interim, enteral or parenteral nutrition as indicated facilitates improved immune function and wound healing to ensure recovery. 

Other patient variables may affect GI motility and, thereby, the extent or rate of availability of a drug from a delivery system. As illustrated in Chapter 2, the degree of physical activity, age, disease state, and emotional condition of a patient may increase or de-... 

Thus, drugs that alter GI motility may increase or decrease the rate of availability of another drug. In addition, concurrent therapy may increase, decrease,... 

The pharmacist, as a drug therapist, should advise both the physician and the patient of the potential problems involved in either initiating or discontinuing concurrent therapy of drugs known to alter GI motility. The pharmacist can also advise the physician... 

Although it is possible to control the dissolution rate of a drug by controlling its particle size and solubility, the pharmaceutical manufacturer has very little, if any, control over the D/h term in the Nernst-Brunner equation, Eq. (1). In deriving the equation it was assumed that h, the thickness of the stationary diffusion layer, was independent of particle size. In fact, this is not necessarily true. The diffusion layer probably increases as particle size increases. Furthermore, h decreases as the stirring rate increases. In vivo, as GI motility increases or decreases, h would be expected to decrease or increase. In deriving the Nernst-Brunner equation, it was also assumed that all the particles were... 

A predictable delivery rate independent of environmental factors such as viscosity, pH, water content, and stirring rate (i.e., GI motility) Controllable release rates during the delivery period Delivery characteristics independent of the properties of the drug (e.g., aqueous solubility)... 

Analogs 11-13 are representative of new morphinan-derived zwitter-ions. The orally active 14-substituted ether (11) is 10-fold more potent than 2 in reversing morphine-induced decrease in GI motility in rat [41]. 

FGIDs present with variable combinations of chronic or recurring GI symptoms not explained by overt biochemical or structural abnormalities and encompass conditions like functional dyspepsia (FD), irritable bowel syndrome (IBS) and chronic idiopathic constipation [1], A variety of mechanisms that could explain the etiology of FGIDs are currently under investigation and include, but are not limited to altered GI motility, visceral hypersensitivity and post-infectious abnormalities [2],... 

Muscarinic M3 receptor Antagonist Acute (gastrointestinal system) Reduced GI motility Darifenacin26... 

Developmental differences in drug absorption between neonates, infants and older children are summarized in Table 1. It must be recognized that the data contained therein reflect developmental differences which might be expected in healthy pediatric patients. Certain conditions and disease states might modify the function and/or structure of the absorptive surface area(s). GI motility and/or systemic blood flow can further impact upon either the rate or extent of absorption for drugs administered by ex-travascular routes in pediatric patients. 

Difenoxin is a metabolite of diphenoxylate with antidiarrheal effects similar to the parent drug. Loperamide Imodium) is a piperidine derivative of diphenoxylate, which acts both at the level of the gut and also in the CNS to reduce GI motility. Its use as an antidiarrheal and its potency are similar to those of diphenoxylate. 

Drugs that enhance GI motility are often called prokinetics. Their goal is to increase contractile force and accelerate intraluminal transit. Most of these drugs act either by enhancing the effect of acetylcholine or by blocking the effect of an inhibitory neurotransmitter such as dopamine. The prokinetics discussed in this chapter are metoclopramide, cisapride and tegaserod, and erythromycin. 

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