ABSTRACT
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Subject(s)
Chloride Channel Agonists/administration & dosage , Constipation/drug therapy , Defecation/drug effects , Gastric Mucins/metabolism , Gastric Mucosa/drug effects , Lubiprostone/administration & dosage , Mucus/metabolism , Chloride Channel Agonists/adverse effects , Chronic Disease , Constipation/diagnosis , Constipation/metabolism , Constipation/physiopathology , Double-Blind Method , Gastric Mucosa/metabolism , Humans , Kansas , Lubiprostone/adverse effects , Treatment OutcomeABSTRACT
BACKGROUND: The creation of no interruption zones (NIZs) reduces medical errors by reducing distraction levels on hospital wards. To date, the effect of a NIZ during colonoscopy has not been evaluated. AIMS: Assess the effects of a NIZ during colonoscopy, on distraction levels, withdrawal times, and adenoma detection rates (ADRs). METHODS: This was a non-randomized prospective study of screening colonoscopies at a teaching hospital. The intervention, a NIZ, was created by limiting conversations to the care of the patient undergoing the procedure and posting a "do not disturb" sign during the withdrawal phase of colonoscopy. Distraction levels, withdrawal times, and ADRs were analyzed at baseline and after the NIZ. RESULTS: The implementation of the NIZ leads to a significant reduction of high-distraction-level environments (13.1 vs. 5.1 %; p < 0.0001). There was a significant decrease in withdrawal time with NIZs; (10.6 vs. 9.9 min, p = 0.0038). There was no significant difference in ADRs (38 % baseline vs. 36 % NIZs, respectively; p = 0.33). CONCLUSIONS: Creation of a NIZ was associated with a significant decrease in high-distraction environments and shorter withdrawal times with no significant change in ADRs. Further studies are needed to evaluate whether lower distraction levels in an endoscopy suite translate to improved quality measures.
Subject(s)
Adenoma/diagnosis , Attention , Colonic Neoplasms/diagnosis , Colonoscopy/standards , Operative Time , Aged , Colonoscopy/psychology , Colonoscopy/statistics & numerical data , Female , Gastroenterology/standards , Gastroenterology/statistics & numerical data , Humans , Male , Middle Aged , Prospective StudiesABSTRACT
The liver has the amazing capacity to repair itself after injury; however, the same processes that are involved in liver regeneration after acute injury can cause serious consequences during chronic liver injury. In an effort to repair damage, activated hepatic stellate cells trigger a cascade of events that lead to deposition and accumulation of extracellular matrix components causing the progressive replacement of the liver parenchyma by scar tissue, thus resulting in fibrosis. Although fibrosis occurs as a result of many chronic liver diseases, the molecular mechanisms involved depend on the underlying etiology. Since studying liver fibrosis in human subjects is complicated by many factors, mouse models of liver fibrosis that mimic the human conditions fill this void. This review summarizes the general mouse models of liver fibrosis and mouse models that mimic specific human disease conditions that result in liver fibrosis. Additionally, recent progress that has been made in understanding the molecular mechanisms involved in the fibrogenic processes of each of the human disease conditions is highlighted.
