Cancer-related fatigue and depression: What is the relationship? How safe are disposable cuffs? Using abdominal massage to reduce residual gastric volumes in critically ill patients. Helping stroke patients regain their motor functions. provide a thesis statement. This is your argument that will feature in every part of the paper Sep 30, · Kaempferia parviflora or Krachaidum (in Thai), also known as “Thai ginseng,” is a medicinal plant in the family Zingiberaceae. It is found in tropical areas such as Malaysia, Sumatra, Borneo Island, and Thailand. Its rhizome has been long used as folk medicine for many centuries. 1 Among the Hmong hill tribe, Krachaidum is widely believed to reduce perceived effort, improve Oct 28, · Core tip: Features of gut dysfunction are common in patients with cirrhosis and may have an impact on quality of life and nutritional status as well as contribute to the development of cirrhosis complications. Cirrhotic patients often report gastrointestinal symptoms. Their pathophysiology is complex, probably involving factors related to liver disease severity, psychological distress, and
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Try out PMC Labs and tell us what you think. Learn More. Correspondence to: Evangelos Kalaitzakis, MD, PhD, FEBGH, gastric cancer phd thesis, Associate Professor, Department of Gastroenterology, Skåne University Hospital, University of Lund, Lund, Sweden.
enicidem sikaztialak. Patients with liver cirrhosis exhibit several features of gut dysfunction which may contribute to the development of cirrhosis complications as well as have an impact on nutritional status and health-related quality of life.
Gastrointestinal symptoms are common in cirrhosis and their pathophysiology probably involves factors related to liver disease severity, psychological distress, and gut dysfunction e. They may lead to reduced food intake and, thus, may contribute to the nutritional status deterioration in cirrhotic patients. Although tense ascites appears to have gastric cancer phd thesis negative impact on meal-induced accommodation of the stomach, published data on gastric accommodation in cirrhotics without significant ascites are not unanimous.
Gastric emptying and small bowel gastric cancer phd thesis have generally been shown to be prolonged. This may be related to disturbances in postprandial glucose, insulin, and ghrelin levels, gastric cancer phd thesis, which, in turn, appear to gastric cancer phd thesis associated to insulin resistance, a common finding in cirrhosis. Furthermore, small bowel manometry disturbances and delayed gut transit may be associated with the development of small bowel bacterial overgrowth.
Finally, several studies have reported intestinal barrier dysfunction in patients with cirrhosis especially those with portal hypertensionwhich is related to bacterial translocation and permeation of intestinal bacterial products, e.
Core tip: Features of gut dysfunction are common in patients with cirrhosis and may have an impact on quality of life and nutritional status as well as contribute to the development of cirrhosis complications. Cirrhotic patients often report gastrointestinal symptoms. Their pathophysiology is complex, probably involving factors related to liver disease severity, psychological distress, and increased gastric sensitivity to distension as well as delayed gut transit. The latter is common in cirrhosis and may be related to postprandial glucose and hormone disturbances due to insulin resistance.
Intestinal barrier dysfunction, potentially leading to bacterial translocation and permeation of bacterial products, gastric cancer phd thesis, has been frequently reported in cirrhotic patients, especially those with portal hypertension. In recent years it has become widely recognized that liver cirrhosis may affect several organ systems such as the cardiovascular system[ 12 ], the respiratory system[ 3 ], the kidneys[ 45 ], and the skeletal system[ 67 ].
Cirrhosis has gastric cancer phd thesis been associated with varying degrees of malnutrition[ 8 ] and with alterations in the gastrointestinal GI tract[ 9 ]. Apart from the presence of structural changes in the GI tract, gastric cancer phd thesis as esophageal varices and portal hypertensive gastropathy, that may be the cause of GI bleeding and anemia, there have also been described abnormalities in the sensorimotor and barrier function gastric cancer phd thesis the gut in liver cirrhosis.
These changes are of importance as they might contribute to malnutrition and health-related quality of life impairment in these patients, gastric cancer phd thesis, while impaired gut barrier function may also contribute to the development of cirrhosis complications, in particular bacterial infections. It is associated with increased morbidity and mortality[ 8 ] and it can compromise liver transplantation results[ 11 ]. Lean-mass depletion is also related to hepatic encephalopathy in liver transplant candidates with cirrhosis[ 17 ].
The pathogenesis of malnutrition in liver cirrhosis is not fully understood but poor dietary intake[ 818 ], gastric cancer phd thesis, increased energy expenditure[ 1119 - 21 ], malabsorption[ 822 ] and poor synthetic capacity of the cirrhotic liver may be involved. Potential reasons for low energy intake include reduced appetite possibly associated with increased brain tryptophan availability[ 23 ], gastric cancer phd thesis, satiety due to ascites[ 24 ], poor palatability of low-sodium gastric cancer phd thesis, and hepatic encephalopathy[ 8 ], GI symptoms[ 2526 ], and gut dysfunction[ 27 ].
Increased glucose and lower ghrelin levels postprandially have also been suggested to be related to poor food intake and weight loss in cirrhosis[ 28 ]. Postprandial glucose and ghrelin alterations are probably associated with insulin resistance which is common in these patients[ 28 ].
Increased energy expenditure, although not a constant feature of cirrhosis, has also been reported to contribute to a negative energy balance[ 81119 - 2129 - 31 ]. Last, fat malabsorption has been reported to be frequent especially in those with evidence of malnutrition [ 22 ]. This may be related to the cholestasis often present in cirrhosis, but a reduction in the area of the intestinal absorptive surface has also been proposed in cirrhotics[ 32 ].
However, not all studies have found defective active absorption in these patients[ 22gastric cancer phd thesis, 33 ]. The most common GI symptoms reported include abdominal bloating in GI symptom severity appears to be related to liver disease severity[ 25 ], lactulose use[ 25 ], the presence of ascites[ 25 ], and psychological distress[ 2634 ] as well as low serum testosterone levels[ 26 ]. The pathophysiology of GI symptoms, however, appears to be complex, and to also involve abnormalities in gut motility function as outlined later in this review.
Although they improve following liver transplantation, GI symptoms remain of concern post-transplant, mainly due to diarrhea[ 26 ]. The higher the score in gastrointestinal symptom rating scale GSRS the higher the severity of gastrointestinal symptoms. Adapted from the reference [25]. GI symptoms in cirrhosis are related to recent weight loss[ 25gastric cancer phd thesis, 26 ]. Thus, GI symptoms appear to have an impact on meal induced gastric cancer phd thesis which may limit food intake.
Last but not least, GI symptoms are associated with impaired physical and mental health-related quality of life in cirrhosis[ 25 ]. In a caloric satiation drinking test, gastric cancer phd thesis are asked to consume a liquid caloric meal at a constant rate, scoring their satiation level at 5-min intervals. The test is terminated when gastric cancer phd thesis subject reaches maximal satiation.
Adapted from the reference [26]. The structural effects of liver cirrhosis on the GI tract have been considered to be mainly associated with portal hypertension.
Esophageal varices develop in the majority of patients with cirrhosis, provided a long enough follow-up period[ 3637 ]. They can be the site of GI bleeding, a potentially lethal complication[ 3637 ]. Mucosal changes are also frequently encountered upon endoscopic examination of the GI tract in patients with cirrhosis[ 938 ].
Portal hypertensive intestinal vasculopathy is a term used to describe changes in the intestinal microcirculation secondary to longstanding portal hypertension[ 9 ].
Signs of portal hypertensive intestinal vasculopathy may be observed in all parts of the GI tract[ 9 ]. Among patients with cirrhosis without a history of variceal bleeding, medium or large esophageal varices, previous endoscopic therapy, or propranolol treatment, the prevalence of portal hypertensive gastropathy was reported to be Major predictors of portal hypertensive gastropathy are the presence of esophageal varices and increased severity of cirrhosis[ 40 ], and it has been found to be associated to poor prognosis in gastric cancer phd thesis patients[ 41 ].
Acute bleeding from portal hypertensive gastropathy has been reported to occur infrequently but may be severe[ 4042 ], while chronic bleeding resulting in anemia may be a concern[ 4042 ]. Cirrhotics compared to healthy controls, have been shown to have higher plasma gastrin[ 43 ] and higher prevalence of peptic ulcers[ 4445 ]. In an endoscopic study, the annual incidence rate of peptic ulcers observed in patients undergoing endoscopic follow-up was 4. In a meta-analysis, the prevalence of helicobacter pylori infection has been found to be higher in cirrhotics with compared to those without peptic ulcer disease[ 48 ], but its role in the pathogenesis of peptic ulcers in these patients has been questioned[ 49 ] with alcohol consumtion and portal hypertension being hypothsized as major contributing factors[ 50 ].
Cirrhotic patients have a significantly increased risk of peptic ulcer bleeding and re-bleeding compared to the general population[ 5152 ]. However, their prognosis during an ulcer bleeding episode may not differ drastically from that of non-cirrhotic patients[ 50 ].
In the fasting state, the proximal stomach smooth muscle maintains a tonic contractile activity[ 53 - 55 ]. During and after food ingestion, a relaxation of the proximal stomach occurs, providing the meal with a reservoir and enabling a volume increase without a rise in pressure gastric accommodation reflex [ 535456 - 59 ].
Impaired gastric accommodation has been associated with upper GI symptoms, such as early satiety, bloating, and epigastric pain, in patients with functional dyspepsia[ 6061 ], gastric cancer phd thesis, diabetes[ 62 ], prior fundoplication surgery[ 63 ], vagotomy and partial gastrectomy[ 64 ].
Gastric barostat studies, gastric cancer phd thesis, using a polyethylene balloon placed in the fundus of the stomach, are generally considered to be the gold standard for the evaluation of gastric accommodation[ 59 ]. However, other types of tests such as abdominal ultrasound, magnetic resonance imaging, and single-photon emission computed tomography SPECT are also commonly used[ 59 ]. Thus far, three studies have assessed gastric accommodation in cirrhosis.
Not unexpectedly, accommodation improved following large-volume paracentesis, resulting in an increase in caloric intake[ 66 ]. Thus, gastric cancer phd thesis it appears reasonable that meal-induced accommodation is impaired in the presence of tense ascites[ 66 ], to date, it remains unclear gastric cancer phd thesis it is affected in patients with cirrhosis of different etiologies without significant ascites.
Gut stimuli, specifically gastric distension by food ingestion, may induce GI symptoms. It has been reported that gastric tone is important in determining gastric sensitivity to distension[ 5567 ] and that in particular gastric wall tension determines perception of gastric distension, at least below nociception levels[ 68 ]. Hypersensitivity to gastric distension, defined as enhanced sensitivity to balloon distension of the proximal stomach, is present in a subset of functional dyspepsia patients[ 6970 ] and it is associated with weight loss[ 69 ].
However, sensory thresholds were related to gastrointestinal symptom severity and liver disease severity, expressed as the Child-Pugh and MELD scores lower threshold with increasing symptom and liver disease severity [ 27 ]. Another way of assessing gastric motor function is measurement of gastric emptying. Delayed gastric emptying has traditionally been considered a mechanism that contributes to symptom generation in patients with GI motility disorders and systemic diseases affecting the GI tract[ 71 ].
Most studies in cirrhosis have found gastric emptying to be delayed[ 72 - 76 ], but some controversy exists with other studies reporting normal[ 77 - 80 ], or accelerated[ 81 ] gastric emptying. Several factors may account for the divergence of results hitherto published, including selection of patient groups with different characteristics, selection of small patient groups or small control groups and use of different measurement methods. Delayed gastric emptying was also related to postprandial hyperglycemia, hyperinsulinemia, and hypoghrelinemia[ gastric cancer phd thesis ].
The latter abnormalities appear to be associated to insulin resistance, which is frequent in cirrhosis. These findings are in accordance with published data showing that induced hyperglycemia is associated with reduced gut motility[ 82 ], delayed gastric emptying, decreased hunger[ 83 ], and increased postprandial symptoms[ 84 ] in healthy subjects.
Physiological hyperglycemia has been shown to slow gastric emptying in diabetes mellitus[ 85 ] and healthy volunteers[ 86 ]. Experimental euglycemic hyperinsulinemia also impairs stomach and duodenal motility[ 87 ] and prolongs gastric emptying[ 8788 ]. Gastric emptying time in cirrhosis has not been found to be related to portal pressure expressed as variceal pressure, as measured with a small pressure-sensitive capsule attached to a gastroscope[ 72 ] or as hepatic venous pressure gradient[ 80 ].
Finally, a role for autonomic dysfunction in the pathophysiology of delayed gastric emptying has also been proposed in these patients[ 89 ]. Adapted from the gastric cancer phd thesis [76].
Manometry studies have shown disturbed gut motility in liver cirrhosis[ 90 - 93 ]. An abnormal propagation pattern of pressure waves with a high number of long clusters and frequent waves propagating in a retrograde fashion have been reported in cirrhotics, in particular those with portal hypertension[ 93 ]. Gastric cancer phd thesis bowel manometry disturbances have, anecdotally, been reported to improve following liver transplantation[ 94 ]. However, similar to investigations on gastric cancer phd thesis emptying, gut transit studies have shown contradictory results[ 7277798095 - 97 ] in these patients, with most reporting prolonged small bowel transit times.
These findings are in accordance with data from non-cirrhotic patients with unexplained GI symptoms whose small bowel transit was frequently slow in unexplained diarrheal disease[ 98 ]. Small bowel bacterial overgrowth is also common in cirrhosis[ 92gastric cancer phd thesis, 99 ] and appears to be related to liver disease severity[ ], although it was only observed in patients with portal hypertension in one study[ 93 ].
Interestingly, patients with small bowel bacterial overgrowth have been also shown to have slower small bowel transit[ 72 ]. It is thus possible that delayed small bowel transit in cirrhosis may lead to the development of small bacterial overgrowth, which could contribute to the symptoms of abdominal pain and diarrhea.
More importantly, small bacterial overgrowth has been speculated to be related to bacterial translocation and infectious complications, such as spontaneous bacterial peritonitis[ 92 ]. Intestinal permeability: The gut barrier includes immunogenic factors such as mucosal lymphocytes and immunoglobulins and the epithelial barrier i.
Central to the role of barrier function of the epithelial cells are the tight junctions and adherens junctions regulating paracellular transport[ ].
As a barrier, the gut prevents the permeation of microorganisms or substances, such as luminal gastric cancer phd thesis and proinflammatory factors. At the same time it allows for selective permeation of certain substances such as nutrients[]. Non-invasive methods have been used to assess gut barrier function by measuring the urinary excretion of orally administered test substances such as monosaccharides, gastric cancer phd thesis, disaccharides, gastric cancer phd thesis 51 Cr-EDTA[].
To address the complexity of factors affecting the results of gut permeability tests, the principle of differential urinary excretion of several test substances administered at the same time has been developed[ ], gastric cancer phd thesis. Bacterial infections are of concern in patients with cirrhosis, with spontaneous bacterial peritonitis being the most relevant[]. They may occur as a consequence of repeated access of bacteria from the lumen to the mesenteric lymph nodes translocationand thereby to the ascitic fluid[ ].
Intestinal permeability in liver cirrhosis has been variably reported as increased or normal[ 3233- ].
Stanford Doctor on Increased Risk of Gastric Cancer in Asians
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Snehasikta Swarnakar (born ) is an Indian chemical biologist and the senior principal scientist at the Division of Cancer Biology and Inflammatory Disorder of the Indian Institute of Chemical blogger.com for her studies in the field of gastric, ovarian, head and neck cancers, Swarnakar is an elected fellow of the National Academy of Sciences, India and the West Bengal Academy of Science We would like to show you a description here but the site won’t allow blogger.com more Sep 30, · Kaempferia parviflora or Krachaidum (in Thai), also known as “Thai ginseng,” is a medicinal plant in the family Zingiberaceae. It is found in tropical areas such as Malaysia, Sumatra, Borneo Island, and Thailand. Its rhizome has been long used as folk medicine for many centuries. 1 Among the Hmong hill tribe, Krachaidum is widely believed to reduce perceived effort, improve
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