Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-specific abdominal complaints are a very frequent cause of discomfort. Even if only comparatively few are brought to the attention of the physician, they account for a considerable portion of the reasons for seeking medical care, both in acute and chronic conditions. On the other hand, few drugs are free of the suspicion of causing abdominal complaints, which make up between one-tenth and one-third of reported adverse reactions. A wide variety of possible alternative or concomitant causes makes a clear causative attribution to suspected drugs very difficult. This holds especially true for the ill-defined conditions of indigestion and anorexia. For nausea and vomiting, specific scales have been developed which facilitate differentiation between drugs causing these effects most frequently and most intensively. They have been applied in cytostatic therapy, where this is one of the most frequently encountered problems, but nausea and vomiting can seriously affect compliance in many other treatments. Somatic abdominal pain results in most instances from the irritation of the parietal peritoneum and is usually the effect of a lesion. This may or may not be caused by a drug, but this cause should be the first consideration. Visceral pain may result from functional disturbance of secretory glands or of the muscular coat, from drug action on bowel content or from irritation of the mucosa, all of which are frequently interrelated. Most frequently suspected pharmacological causes are drugs with anticholinergic action, antibiotics, potassium supplements and non-steroidal, anti-inflammatory agents. Drug-induced hyperinsulinism and porphyria are rare cases. Abuse of laxatives should always be considered because of its prevalence. A great number of other untoward drug effects have been described in the literature, but rarely merit first consideration. With the exception of promptly occurring or persistent emesis, gastrointestinal symptoms usually are not pathognomonic for drug effects and are the result of several factors. The usual approach to identifying an adverse drug effect is to delineate the functional or structural disorder, and to associate this diagnosis with possible pharmacodynamic aetiologies.
 ...
PMID:Abdominal pain, indigestion, anorexia, nausea and vomiting. 304 63

It is widely appreciated that visceral pain differs significantly from pain that arises from cutaneous structures. Visceral pain is difficult for both the patient and physician to localize because it is diffuse in character and is typically referred to cutaneous structures. Further, there are differences between acute, post-operative visceral pain and the altered sensations associated with the so-called functional bowel disorders (e.g. non-ulcer dyspepsia, non-cardiac chest pain and irritable bowel syndrome). A variety of considerations suggests that sensory inputs from the fiscera, like nociceptive inputs from the skin, can be sensitized. Accordingly, inputs from the viscera that are not typically perceived may give rise to discomfort and pain if either visceral afferent fibres are sensitized or central neurones undergo a change in excitability ('central sensitization') after persistent visceral input. The anatomy and potential mechanisms associated with visceral hyperalgesia will be considered as will new information about opioid modulation of visceral inputs to the spinal cord.
 ...
PMID:Visceral nociception: consequences, modulation and the future. 764 39

Visceral pain is characterized by a subjectively painful perception located in the abdominal area. Distinct structural lesions or biochemical abnormalities which could serve as explanation for these painful sensations can be only detected in a proportion of patients. In the absence of precise causes for visceral pain, the symptoms are attributed to functional disorders. The two major single entities among functional disorders of the gut are functional dyspepsia and irritable bowel syndrome. Patients with functional dyspepsia characteristically localize the symptoms in the upper abdomen. Functional gastrointestinal disturbances which are localized in the lower abdomen are summarized as irritable bowel syndrome. Interestingly,both functional dyspepsia and irritable bowel syndrome may overlap.
 ...
PMID:[Epidemiology and clinical phenomenology of visceral pain]. 1247 30

Defective colonic and gastric accommodations have been related to altered viscerosensitivity in irritable bowel syndrome and to functional dyspepsia, respectively. We assessed colonic accommodation in rats with impaired gastric accommodation to determine if altered accommodation can be regarded as a widespread pathophysiological alteration within the gastrointestinal (GI) tract. Colonic accommodation during colorectal distension (CRD) was assessed in Wistar Kyoto rats (WKY), an animal model of impaired gastric accommodation, and in Sprague-Dawley (SD) and Wistar rats, considered normal. CRD (10-80 mmHg)-induced visceral pain responses were also evaluated in the same strains of rats. During gastric distension, WKY rats had lower intra-gastric volume (0.96 +/- 0.22 ml) than SD (1.85 +/- 0.19 ml, P < 0.05) or Wistar rats (2.80 +/- 0.26 ml, P < 0.05), indicating impaired gastric accommodation. In the same animals, pressure-volume curves were constructed during CRD as a measure of colonic accommodation. During short-lasting (1 min) phasic CRD (2-20 mmHg), the pressure-volume curve in WKY rats was displaced to the right compared with SD or Wistar rats, indicative of reduced colonic accommodation (maximal volume: SD, 1.22 +/- 0.05 ml; Wistar, 1.07 +/- 0.04 ml; WKY, 0.87 +/- 0.07 ml; P < 0.01). Pre-treatment with atropine normalised the pressure-volume responses in WKY rats. No differences among strains were observed during the 2-min phasic or ramp-tonic CRD. Visceral pain responses during CRD (10-80 mmHg) were, overall, similar in the three strains, although WKY rats showed lower thresholds for pain (28.0 +/- 4.9 mmHg) than SD (42.3 +/- 6.6 mmHg, P = 0.072) or Wistar rats (48.3 +/- 6.0 mmHg, P < 0.05). WKY rats, although having impaired gastric accommodation, have the ability to fully accommodate the colon to increasing pressures. In WKY rats, impaired accommodation of the smooth muscle might not be a widespread phenomenon along the GI tract but rather a local disturbance.
 ...
PMID:Characterisation of colonic accommodation in Wistar Kyoto rats with impaired gastric accommodation. 1790 48