ABSTRACT
Constipation is a common complaint that can be a symptom of serious disease. Awareness of the potential etiologies can help direct the history, physical exam and subsequent work-up for the presenting individual. This article details the differential diagnosis and pathophysiology of constipation based on a review of the literature. The article is also designed to be useful as a guide to the work-up of constipation. Key elements of the history, physical exam and testing are outlined. Included is a detailed flow diagram to guide the work-up of constipation. Testing methods and their value in the evaluation of chronic idiopathic constipation are discussed. Finally, although the focus of this article is the evaluation of constipation, a section on the treatment of constipation is included.
Subject(s)
Constipation/diagnosis , Constipation/etiology , Adult , Central Nervous System Diseases/complications , Constipation/therapy , Diagnosis, Differential , Diagnostic Techniques, Digestive System , Endocrine System Diseases/complications , Gastrointestinal Diseases/complications , Humans , Medical History Taking/methods , Metabolic Diseases/complications , Physical Examination/methodsABSTRACT
Previous work from this laboratory and others has shown that neurotransmitters can activate phospholipase D. Unlike the phospholipase C that specifically hydrolyzes inositol-containing phospholipids, phospholipase D in neuronal tissue specifically hydrolyzes phosphatidylcholine. One route for the synthesis of phosphatidylcholine, is via methylation of phosphatidylethanolamine. Using an in vitro assay, we have previously shown that methylated intermediates are also good substrates for phospholipase D (1). In this manuscript we demonstrate that these intermediates are also substrates in the intact PC12 cells. Cells incubated with methyl and dimethylethanolamine incorporate more [3H]palmitic acid into the corresponding phospholipid, phosphatidyl-N-methylethanolamine and phosphatidyl-N,N-dimethylethanolamine. In these cells bradykinin causes a greater increase in [3H]phosphatidylethanol production. Elevated levels of [3H]phosphatidylcholine do not enhance bradykinin-stimulated [3H]phosphatidylethanol production, therefore, this effect is specific for the methylated intermediates. Finally, this effect is not due to some generalized enhancement of receptor coupling because incubation of the cells with methylethanolamine does not lead to an increase in bradykinin stimulated inositol phosphate production.
