Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic gastropathy is a term that encompasses a number of neuromuscular dysfunctions of the stomach, including abnormalities of gastric contractility, tone, and myoelectrical activity in patients with diabetes. These abnormalities range from tachygastrias to antral hypomotility and frank gastroparesis. Diabetic gastropathies may be acutely produced during hyperglycemia. Symptoms of chronic diabetic gastropathy include chronic nausea, vague epigastric discomfort, postprandial fullness, early satiety, and vomiting. Because these symptoms are nonspecific, other disorders such as mechanical obstruction of the gastrointestinal tract, gastroesophageal reflux disease, cholecystitis, pancreatitis, mesenteric ischemia, and drug effects should be considered. Neuromuscular abnormalities of the stomach may be assessed noninvasively with gastric emptying tests, electrogastrography, and ultrasound. Gastrokinetic agents such as metoclopramide, cisapride, domperidone, and erythromycin increase fundic or antral contractions and/or eradicate gastric dysrhythmias. Diet and glucose control also are important in the management of diabetic gastropathy. As the pathophysiology of diabetic gastropathy is better understood, more specific and improved treatments will evolve.
 ...
PMID:Diabetic gastropathy: gastric neuromuscular dysfunction in diabetes mellitus: a review of symptoms, pathophysiology, and treatment. 1038 75

Severe acute pancreatitis is a two-phase systemic disease. The first phase is a clinical response resulting from systemic effects of proinflammatory mediators called SIRS (systemic inflammatory response syndrome), that may lead to multiple organ failure and death. The second phase, if the process is not reversed by natural defences or treatment, may be accompanied by local complications such as infected pancreatic necrosis. The severity of the disease must be established early to identify patients requiring intensive monitoring and support. The clinico-biochemical score (Ranson score) is about 80% accurate at 48 hours but is not accurate before this time; the APACHE II system has the sensitivity to predict severe pancreatitis in 61% of patients on admission. Although not perfect, the prognostic systems of severity remain better than clinical judgement. SIRS followed by local complications is accompanied by increased energy requirements and, with the absence of oral intake, a persistently negative nitrogen balance and mineral and micronutrient deficiencies. Thus, early nutritional support is indicated. Formerly, total parenteral nutrition was the standard practice for providing exogenous nutrients avoiding pancreatic stimulation. The use of early enteral feeding has recently been evaluated. Gastric atony and obstruction of the duodenum by pancreatic oedema or necrosis have been overcome by delivering enteral nutrition to the jejunum, distal to the ligament of Treitz; in this position, regular diets do not stimulate pancreatic secretions. The efficacy, tolerance, clinical outcome and cost of enteral nutrition suggest that this feeding route should be preferred in patients with severe acute pancreatitis.
 ...
PMID:[Nutrition in acute pancreatitis]. 1058 62

In veterinary patients, postgastric feeding is indicated for uncontrollable gastric vomiting, gastroparesis, biliary tract disease, pancreatitis, and for patients at increased risk for aspirating secondary to decreased mentation, prolonged recumbency, or an unprotected airway. Postgastric feeding may be implemented via the placement of a jejunal feeding tube. These tubes can be placed surgically (jejunostomy tubes) or with fluoroscopic or endoscopic guidance. This article will focus on methods of jejunal feeding-tube placement, advantages and disadvantages of the methods described, and complications associated with jejunal feeding.
 ...
PMID:Placement of jejunal feeding tubes for post-gastric feeding. 1502 95

Sphincter of Oddi dysfunction (SOD) is a poorly-understood disorder, typically presenting as postcholecystectomy, "biliary-type," right-sided abdominal and/or chest wall pain. Most patients referred to specialist clinics for work-up of presumed SOD do not, in fact, have anything wrong with their bile ducts or biliary sphincter mechanisms. A careful history and focused physical examination will often identify the true source of the pain syndrome, ranging from chest wall costochondritis and nerve injury at surgical trochar sites, to gastroparesis and visceral hypersensitivity ("irritable bowel"). The Rome III classification of functional gallbladder and biliary disorders defines SOD as episodic (not daily) pain lasting more than 30 min, which is disruptive of normal activities and not associated with bowel upset. It is not relieved by gastric acid suppression or antispasmodics. Other causes of abdominal pain must be excluded. Standard work-up includes endoscopic retrograde cholangiopancreatography (ERCP) with biliary manometry, which risks post-ERCP pancreatitis, especially in young women with normal bile ducts and liver serology. Noninvasive tests for SOD, such as timed ("gated") cholecystokinin (CCK)-stimulated hepatobiliary iminodiacetic acid (HIDA) scans and secretin-stimulated magnetic resonance cholangiopancreatography, are imperfect and still evolving. Although many doubt the very existence of SOD, a multidisciplinary approach to the management of pre- and postcholecystectomy abdominal pain syndromes is long overdue.
 ...
PMID:Sphincter of Oddi dysfunction. 2042 85

The aim of this study was to examine differences in presentation and outcome in pancreaticoduodenectomy for benign and malignant processes. Pancreaticoduodenectomies performed for pancreatic adenocarcinoma or chronic pancreatitis from 2000 to 2008 were identified from a prospectively maintained database and compared. Pancreaticoduodenectomy revealed adenocarcinoma in 220 patients and benign chronic pancreatitis in 40 patients. Patients with adenocarcinoma were older (64 +/- 10.6 years and 47.6 +/- 10.8 years, respectively, P < 0.001) and more likely to demonstrate jaundice (92 and 13%, respectively, P < 0.001), weight loss (76 and 58%, respectively, P = 0.01), and discrete masses (72 and 55%, respectively, P = 0.03). By contrast, chronic pancreatitis presented with increased pain (98 and 49%, respectively, P < 0.001) and nausea (68 and 32%, respectively, P < 0.001). Patients with pancreatitis experienced reduced blood loss (227 +/- 156 and 571 +/- 626 mL, respectively, P = 0.05) and transfusion (10 and 42%, respectively, P < 0.001). Postoperatively, the groups were similar in risk of fistula, gastroparesis, overall morbidity, and mortality. Infection rates were higher in adenocarcinoma (42 and 20%, respectively, P = 0.01). Forty-nine patients underwent pancreaticoduodenectomy for presumptive chronic pancreatitis, of which nine had adenocarcinoma; logistic regression identified increasing age and jaundice as predictors of malignancy. Compared with patients with adenocarcinoma, those who undergo pancreaticoduodenectomy for chronic pancreatitis are less likely to require preoperative biliary drainage and perioperative transfusion. Infectious complication risk is higher in patients with adenocarcinoma. Increased age and jaundice should raise suspicion of cancer in patients with chronic pancreatitis undergoing evaluation for surgical treatment.
 ...
PMID:Differences in presentation and perioperative outcome after pancreaticoduodenectomy for cancer and benign pancreatitis. 2058 16

Gastrointestinal disorders are common complications of diabetes mellitus and include gastroparesis, nonalcoholic fatty liver disease, gastroesophageal reflux disease, and chronic diarrhea. Symptoms of gastroparesis include early satiety, postprandial fullness, nausea, vomiting of undigested food, bloating, and abdominal pain. Gastroparesis is diagnosed based on clinical symptoms and a delay in gastric emptying in the absence of mechanical obstruction. Gastric emptying scintigraphy is the preferred diagnostic test. Treatment involves glucose control, dietary changes, and prokinetic medications when needed. Nonalcoholic fatty liver disease and its more severe variant, nonalcoholic steatohepatitis, are becoming increasingly prevalent in persons with diabetes. Screening for nonalcoholic fatty liver disease is not recommended, and most cases are diagnosed when steatosis is found incidentally on imaging or from liver function testing followed by diagnostic ultrasonography. Liver biopsy is the preferred diagnostic test for nonalcoholic steatohepatitis. Clinical scoring systems are being developed that, when used in conjunction with less invasive imaging, can more accurately predict which patients have severe fibrosis requiring biopsy. Treatment of nonalcoholic fatty liver disease involves weight loss and improved glycemic control; no medications have been approved for treatment of this condition. Diabetes is also a risk factor for gastroesophageal reflux disease. Patients may be asymptomatic or present with atypical symptoms, including globus sensation and dysphagia. Diabetes also may exacerbate hepatitis C and pancreatitis, resulting in more severe complications. Glycemic control improves or reverses most gastrointestinal complications of diabetes.
 ...
PMID:Diabetes Mellitus: Management of Gastrointestinal Complications. 2807 92

Mitochondrial disorders (MIDs) due to respiratory-chain defects or nonrespiratory chain defects are usually multisystem conditions [mitochondrial multiorgan disorder syndrome (MIMODS)] affecting the central nervous system (CNS), peripheral nervous system, eyes, ears, endocrine organs, heart, kidneys, bone marrow, lungs, arteries, and also the intestinal tract. Frequent gastrointestinal (GI) manifestations of MIDs include poor appetite, gastroesophageal sphincter dysfunction, constipation, dysphagia, vomiting, gastroparesis, GI pseudo-obstruction, diarrhea, or pancreatitis and hepatopathy. Rare GI manifestations of MIDs include dry mouth, paradontosis, tracheoesophageal fistula, stenosis of the duodeno-jejunal junction, atresia or imperforate anus, liver cysts, pancreas lipomatosis, pancreatic cysts, congenital stenosis or obstruction of the GI tract, recurrent bowel perforations with intra-abdominal abscesses, postprandial abdominal pain, diverticulosis, or pneumatosis coli. Diagnosing GI involvement in MIDs is not at variance from diagnosing GI disorders due to other causes. Treatment of mitochondrial GI disease includes noninvasive or invasive measures. Therapy is usually symptomatic. Only for myo-neuro-gastro-intestinal encephalopathy is a causal therapy with autologous stem-cell transplantation available. It is concluded that GI manifestations of MIDs are more widespread than so far anticipated and that they must be recognized as early as possible to initiate appropriate diagnostic work-up and avoid any mitochondrion-toxic treatment.
 ...
PMID:Gastrointestinal manifestations of mitochondrial disorders: a systematic review. 2828 66

Post-pancreatitis diabetes mellitus (PPDM) is a sub-type of diabetes of the exocrine pancreas that develops after acute or chronic inflammation of the pancreas. While pro-inflammatory milieu, glucose metabolism, and lipid metabolism in PPDM have been investigated, little is known about gastrointestinal function in the post-pancreatitis setting. This article overviews studies on epidemiology and impact of gastroparesis in the setting of type 1 and type 2 diabetes, with a view to estimating the possible burden of gastrointestinal dysfunction in PPDM. Further, the usefulness of quantifying gastrointestinal dysmotility is discussed. The gastroparesis cardinal symptom index has emerged as a standardized gastrointestinal dysmotility endpoint and its use in individuals after pancreatitis is justified.
 ...
PMID:Post-pancreatitis diabetes mellitus: towards understanding the role of gastrointestinal motility. 2991 34