Sandbox:ajay: Difference between revisions

Jump to navigation Jump to search
← Older editNewer edit →
VisualWikitext
Ajay Gade (talk | contribs)
nocaptcha
1,722 edits
Ajay Gade (talk | contribs)
nocaptcha
1,722 edits
No edit summary
Line 1: Line 1:
==Pathophysiology==
*The pathogenesis of functional dyspepsia is obscure, but a postinfectious or inflammatory origin has been suggested for irritable bowel syndrome.103
*The initial research of esophageal acid clearance in patients with reflux esophagitis cautioned that acid clearance time become nearly continuously longer within the patients than in regular patients.
*Moreover, gastroparesis has been reported after a viral infection.104 Using a questionnaire in 400 consecutive patients with functional dyspepsia, we found that 17% had a history with acute onset, suggestive of a postinfectious origin.10
*Subsequent research, but, demonstrated that enormous overlap in acid clearance times took place among patients and controls.
*These patients had a particularly high prevalence of impaired accommodation. Because the proximal stomach in these patients relaxed to administration of a nitric oxide donor but did not respond to sumatriptan, which releases nitric oxide through activation of 5-hydroxytryptamine (5-HT)1 receptors on nitrergic neurones, the abnormality is attributable to a dysfunction at the level of gastric nitrergic neurons.10
*As a consequence, some patients with reflux signs and symptoms exhibit normal esophageal acid clearance times whereas in other patients acid clearance is abnormally long.
*As previously mentioned, whether psychological factors have a pathogenetic role in functional dyspepsia, especially in patients with hypersensitivity to gastric distention, or whether they are disease modulators determining health care seeking, perception of symptoms, and the outcome of the disorder is not known.  
*Abnormal esophageal motility is generally associated with extended acid clearance, not all individuals with delayed acid clearance, but, have the overt peristaltic disorder.
*There are several sources of evidence for a role of the central nervous system in visceral hypersensitivity.  
*Unfortunately, the challenge of esophageal-body motor function in patients with reflux esophagitis has received negligible attention.
*Studies in experimental animals indicate that acute psychological stress facilitates increased sensitivity to visceral stimuli.105 In line with such a finding, rats genetically predisposed to anxiety have been shown to display an increased visceral sensitivity.106
*Earlier reports primarily based on manometry with non-infused catheters recommended that most of the people of sufferers show up the disordered esophageal motor hobby after deglutition.
*Similarly, in humans, the perception of gut distention has been found to be reduced during periods of distraction and increased during periods of attentiveness or during mental stress associated with anxiety.107
*The major motor abnormality appeared to be an increased incidence of nonperistaltic contractions, often repetitive, inside the distal esophagus.
*However, the role of central factors and stress in visceral hypersensitivity and symptom generation in functional dyspepsia remains to be established.
these contractions were believed to cause ineffective esophageal emptying in recumbent patients.
*Finally, an association between dyspeptic symptoms and a functional polymorphism in a G-protein subunit was reported.108
*Subsequent studies the use of infused-catheter manometry suggests that many, if not the majority, of patients with reflux esophagitis, have overtly regular primary peristalsis.
*It remains to be established whether this genotype is associated with any specific pathophysiologic mechanism, the likelihood of postinfectious functional disorders, or altered psychosocial features.
*The latest study indicates that that patients with reflux esophagitis and controls have a similar excessive frequency of swallowing in the conscious nation and occasional frequency whilst asleep.
*Extra statistics are wished, however, approximately swallowing frequency and occurrence of intact primary peristaltic sequences in the esophagitis patients.
*Even much less is understood approximately secondary peristalsis in patients with reflux esophagitis.
*In patients with reflux esophagitis followed via esophageal-body motor dysfunction, the motor abnormality may both antedate the reflux esophagitis or be as a result of the esophagitis. again, the choice wants no longer be "either-or." we've got located each variety of circumstances.
*In some patients, esophageal motor abnormalities improve or disappear after recuperation of reflux esophagitis.
*This collection argues that the motor abnormality became secondary.
*In different patients, esophageal motor dysfunction persists after complete resolution of reflux esophagitis.
*This finding indicates that the motor disorder either preceded reflux esophagitis or the esophagitis turned into sufficiently intense to motive permanent damage to esophageal muscle or nerves.
*regardless of whether or not the esophageal motor disorder is number one or secondary, this option, as soon as the present, may also create a vicious cycle wherein esophageal motor disorder leads to increasingly severe reflux esophagitis that during turn similarly impairs esophageal motor function.
 
* A 2nd factor that could cause delayed acid clearance is abnormal salivation.
* diminished salivation would decrease: (a) swallowing frequency and (b) the quantity of saliva available to dilute, neutralize, and washout esophageal acid.
 
*Some other possible abnormality of saliva is a decreased capability for acid neutralization. Even though salivation is known to be defective in certain disease entities which includes Sjogren's syndrome, salivary flow and content remain to be comprehensively analyzed in patients with reflux esophagitis.
*Irrespective of the underlying purpose, not on time esophageal clearance promotes esophageal exposure to the refluxed fabric.
*A few patients with reflux esophagitis may additionally have the same frequency of GE reflux as healthy patients, but sustain an immoderate esophageal exposure to acid because of an abnormality in esophageal acid clearance.
 
==Natural history==
*Rex et al and Palmer produced follow up studies showing that 35-39% of oesophagitis patients improved with time. While some more recent studies similarly suggested that a significant proportion of oesophagitis or GORD patients do very well, others have reported the reverse.
*Follow up periods were very variable, however, and few of these studies concentrated on the clearly defined group of GORD patients with oesophagitis.  
*It shows the natural history of the condition more than 10 years after diagnosis. One of the most striking findings relates to the frequency of heartburn among responders.
*More than half had heartburn at least weekly despite the fact that 55% of these symptomatic patients were taking daily acid suppression treatment, and in total over three quarters either had frequent symptoms or took regular antireflux medication.  
*This suggests a worse prognosis than previous reports,23 24 27 but the discrepancies probably result from their inclusion of patients with less severe GORD or a hiatus hernia alone. The rate of stricture formation (2%) in this study is lower than that quoted by others.
*This may be explained by the fact that previous studies investigating complications have concentrated on those patients with resistant disease, whereas we followed up consecutive, non-complicated cases, most of whom had been discharged from hospital follow up years previously.  
*This would suggest that our lower figure more accurately represents the natural history of all oesophagitis patients. However, not all patients with dysphagia weekly or more often, or daily heartburn, agreed to repeat endoscopy, so it is possible that strictures may have been missed in our study.
*It could also be argued that our incidence of one patient developing Barrett's mucosa is too low, again because of the low uptake of repeat endoscopy.
*The finding that grade of oesophagitis did not influence the level of symptoms or quality of life scores at a review is in keeping with the findings of others who have reported that oesophagitis grade is not a useful predictor of long-term outcome.
*However, those with more severe esophagitis did have significantly higher consumption of both H2RAs and proton pump inhibitors.  
*Our finding that age at the time of diagnosis is the only independent predictor of outcome after diagnosis of oesophagitis has not been previously reported.  
*Hiatus hernia and complications of oesophagitis (Barrett's mucosa and stricture) are more common over the age of 50 years,8 which may explain' why those with a worse outcome in this study were older than the comparatively asymptomatic group receiving no treatment.

Revision as of 22:24, 29 January 2018

  • The pathogenesis of functional dyspepsia is obscure, but a postinfectious or inflammatory origin has been suggested for irritable bowel syndrome.103
  • Moreover, gastroparesis has been reported after a viral infection.104 Using a questionnaire in 400 consecutive patients with functional dyspepsia, we found that 17% had a history with acute onset, suggestive of a postinfectious origin.10
  • These patients had a particularly high prevalence of impaired accommodation. Because the proximal stomach in these patients relaxed to administration of a nitric oxide donor but did not respond to sumatriptan, which releases nitric oxide through activation of 5-hydroxytryptamine (5-HT)1 receptors on nitrergic neurones, the abnormality is attributable to a dysfunction at the level of gastric nitrergic neurons.10
  • As previously mentioned, whether psychological factors have a pathogenetic role in functional dyspepsia, especially in patients with hypersensitivity to gastric distention, or whether they are disease modulators determining health care seeking, perception of symptoms, and the outcome of the disorder is not known.
  • There are several sources of evidence for a role of the central nervous system in visceral hypersensitivity.
  • Studies in experimental animals indicate that acute psychological stress facilitates increased sensitivity to visceral stimuli.105 In line with such a finding, rats genetically predisposed to anxiety have been shown to display an increased visceral sensitivity.106
  • Similarly, in humans, the perception of gut distention has been found to be reduced during periods of distraction and increased during periods of attentiveness or during mental stress associated with anxiety.107
  • However, the role of central factors and stress in visceral hypersensitivity and symptom generation in functional dyspepsia remains to be established.
  • Finally, an association between dyspeptic symptoms and a functional polymorphism in a G-protein subunit was reported.108
  • It remains to be established whether this genotype is associated with any specific pathophysiologic mechanism, the likelihood of postinfectious functional disorders, or altered psychosocial features.
Retrieved from "https://www.wikidoc.org/index.php?title=Sandbox:ajay&oldid=1434657"