Pancreatitis Leading to Severe Malabsorption. Report of Three Cases
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Nutritional Disturbances in Crohn's Disease ANTHONY D
Postgrad Med J: first published as 10.1136/pgmj.59.697.690 on 1 November 1983. Downloaded from Postgraduate Medical Journal (November 1983) 59, 690-697 Nutritional disturbances in Crohn's disease ANTHONY D. HARRIES RICHARD V. HEATLEY* M.A., M.R.C.P. M.D., M.R.C.P. Department of Gastroenterology, University Hospital of Wales, Cardiffand *Department ofMedicine, St James's University Hospital, Leeds LS9 7TF Summary deficiency in the same patient. The most important A wide range of nutritional disturbances may be causes of malnutrition are probably reduced food found in patients with Crohn's disease. As more intake, active inflammation and enteric loss of sophisticated tests become available to measure nutrients (Dawson, 1972). vitamin and trace element deficiencies, so these are being recognized as complications ofCrohn's disease. TABLE 1. Pathogenesis of malnutrition It is important to recognize nutritional deficiencies at an early stage and initiate appropriate treatment. Reduced food intake Anorexia Otherwise many patients, experiencing what can be a Fear of eating from abdominal pain chronic and debilitating illness, may suffer unneces- Active inflammation Mechanisms unknown Protected by copyright. sarily from the consequences of deprivation of vital Enteric loss of nutrients Exudation from intestinal mucosa nutrients. Interrupted entero-hepatic circulation Malabsorption Loss of absorptive surface from disease, resection or by-pass KEY WORDS: growth disturbance, Crohn's disease, anaemia, vitamin deficiency. Stagnant loop syndrome from strictures, fistulae or surgically created blind loops Introduction Miscellaneous Rapid gastrointestinal transit Effects of medical therapy Crohn's disease is a chronic inflammatory condi- Effects of parenteral nutrition tion ofunknown aetiology that may affect any part of without trace element supplements the gastrointestinal tract from mouth to anus. -
Diverticular Disease 1
WGO Practice Guidelines Diverticular disease 1 World Gastroenterology Organisation Practice Guidelines: Diverticular Disease Core review team: Dr. T. Murphy Prof. R.H. Hunt Prof. M. Fried Dr. J.H. Krabshuis Contents 1 Definitions 2 Epidemiology 3 Etiology 4 Pathophysiology 5 Medical and surgical management 6 Other forms of diverticular disease 7 Global aspects 8 References 9 Useful web sites 10 WGO Practice Guidelines Committee members who contributed to this guideline 11 Queries and feedback 1 Definitions Diverticulum: • A sac-like protrusion of mucosa through the muscular colonic wall [1]. • Protrusion occurs in weak areas of the bowel wall through which blood vessels can penetrate. • Typically 5–10 mm in size. • Diverticula are really pseudodiverticular (false diverticula), as they contain only mucosa and submucosa covered by serosa. Diverticular disease consists of: • Diverticulosis: the presence of diverticula within the colon • Diverticulitis: inflammation of a diverticulum • Diverticular bleeding Types of diverticular disease: © World Gastroenterology Organisation, 2007 WGO Practice Guidelines Diverticular disease 2 • Simple (75%), with no complications • Complicated (25%), with abscesses, fistula, obstruction, peritonitis, and sepsis 2 Epidemiology Prevalence by age [1]: • Age 40: 5% • Age 60: 30% • Age 80: 65% Prevalence by sex: • Age < 50: more common in males • Age 50–70: slight preponderance in women • Age > 70: more common in women Diverticular disease in the young (< 40) Diverticular disease is far more frequent in older people, with only 2–5% of cases occurring in those under 40 years of age. In this younger age group, diverticular disease occurs more frequently in males, with obesity being a major risk factor (present in 84–96% of cases) [2,3]. -
Does Your Patient Have Bile Acid Malabsorption?
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #198 Carol Rees Parrish, MS, RDN, Series Editor Does Your Patient Have Bile Acid Malabsorption? John K. DiBaise Bile acid malabsorption is a common but underrecognized cause of chronic watery diarrhea, resulting in an incorrect diagnosis in many patients and interfering and delaying proper treatment. In this review, the synthesis, enterohepatic circulation, and function of bile acids are briefly reviewed followed by a discussion of bile acid malabsorption. Diagnostic and treatment options are also provided. INTRODUCTION n 1967, diarrhea caused by bile acids was We will first describe bile acid synthesis and first recognized and described as cholerhetic enterohepatic circulation, followed by a discussion (‘promoting bile secretion by the liver’) of disorders causing bile acid malabsorption I 1 enteropathy. Despite more than 50 years since (BAM) including their diagnosis and treatment. the initial report, bile acid diarrhea remains an underrecognized and underappreciated cause of Bile Acid Synthesis chronic diarrhea. One report found that only 6% Bile acids are produced in the liver as end products of of British gastroenterologists investigate for bile cholesterol metabolism. Bile acid synthesis occurs acid malabsorption (BAM) as part of the first-line by two pathways: the classical (neutral) pathway testing in patients with chronic diarrhea, while 61% via microsomal cholesterol 7α-hydroxylase consider the diagnosis only in selected patients (CYP7A1), or the alternative (acidic) pathway via or not at all.2 As a consequence, many patients mitochondrial sterol 27-hydroxylase (CYP27A1). are diagnosed with other causes of diarrhea or The classical pathway, which is responsible for are considered to have irritable bowel syndrome 90-95% of bile acid synthesis in humans, begins (IBS) or functional diarrhea by exclusion, thereby with 7α-hydroxylation of cholesterol catalyzed interfering with and delaying proper treatment. -
Malabsorption and Exocrine Pancreatic Insuffiecienty (Pi)
MALABSORPTION AND EXOCRINE PANCREATIC INSUFFIECIENTY (PI) Pancreatic Insufficiency is a condition in which a person does not have enough enzymes and bicarbonate being delivered from the pancreas to the intestine for digestion. This causes mal- absorption of nutrients, failure to gain weight and grow, weight loss, vitamin and mineral deficiency, and gastrointestinal symptoms. Most people with CF have mal-absorption due to PI. Onset usually occurs in the first one to two years of life, often in early infancy, but can start at anytime. Symptoms of mal-absorption -Change in number of stools -Large, bulky stools -Stools may be bulky and soft -Greasy, oily or floating stools, oil in toilet water -Stools may smell worse than usual or normal -Rectal prolapse -Mal-absorption of calorie providing nutrients and poor weight gain or weight loss Fat …………………………………………….9 calories/gram Protein………………………………..…….4 calories/gram Complex Carbohydrate ……………..4 calories/gram -Results in poor weight gain, weight loss, poor growth, decreased immune function and decreased lung health. -Mal-absorption of FAT SOLUBLE VITAMIN and deficiency: Vitamin A, Vitamin D, Vitamin E, Vitamin K -Mineral deficiencies: Calcium, Zinc, Sodium, Chloride Learn more about vitamins and minerals at: http://www.cff.org/treatments/Therapies/Nutrition/Vitamins/ Tests to Diagnose PI and Mal-absorption -72 hr fecal fat test -Pancreatic Fecal Elastase Treatment of PI and Mal-absorption Pancreatic Enzyme Replacement Therapy (PERT) Pancreatic enzymes are taken with each meal, snack, breast feed, bottle , and drink that contains fat protein and or complex carbohydrate. Antacid and acid blocking medicines can be added to make enzymes work better Fat Soluble Vitamin Supplementation with special supplements made for mal-absorption are prescribed Each enzyme company offers programs that provide free nutritional support and/or CF therapy support High Calorie, high protein diet Even with PERT, not all calories and nutrients from food are absorbed as expected and calories and nutrients are lost and need replacement. -
Jejunoileal Diverticulitis: Big Trouble in Small Bowel
Jejunoileal Diverticulitis: Big Trouble in Small Bowel MICHAEL CARUSO DO, HAO LO MD EMERGENCY RADIOLOGY, UMASS MEMORIAL MEDICAL CENTER, WORCESTER, MA LEARNING OBJECTIVES: After excluding Meckel’s diverticulum, less than 30% of reported diverticula occurred in the CASE 1 1. Be aware of the relatively rare diagnoses of jejunoileal jejunum and ileum. HISTORY: 52 year old female with left upper quadrant pain. diverticulosis (non-Meckelian) and diverticulitis. Duodenal diverticula are approximately five times more common than jejunoileal diverticula. FINDINGS: 2.2 cm diverticulum extending from the distal ileum with adjacent induration of the mesenteric fat, consistent with an ileal diverticulitis. 2. Learn the epidemiology, pathophysiology, imaging findings and differential diagnosis of jejunoileal diverticulitis. Diverticulaare sac-like protrusions of the bowel wall, which may be composed of mucosa and submucosa only (pseudodiverticula) or of all CT Findings (2) layers of the bowel wall (true . Usually presents as a focal area of bowel wall thickening most prominent on the mesenteric side of AXIAL AXIAL CORONAL diverticula) the bowel with adjacent inflammation and/or abscess formation . Diverticulitis is the result of When abscess is present, CT findings may include relatively smooth margins, areas of low CASE 2 obstruction of the neck of the attenuation within the mass, rim enhancement after IV contrast administration, gas within the HISTORY: 62 year old female with epigastric and left upper quadrant pain. diverticulum, with subsequent mass, displacement of the surrounding structures, and edema of thickening of the surrounding fat inflammation, perforation and or fascial planes FINDINGS: 4.7 cm diameter out pouching seen arising from the proximal small bowel and associated with adjacent inflammatory stranding. -
Digestive Health Center Nutrition Services Nutrition Guidelines for Chronic Pancreatitis Patient Education
Digestive Health Center Nutrition Services Nutrition Guidelines for Chronic Pancreatitis Patient Education The pancreas is an organ that: Produces pancreatic enzymes to help digest (break down) food in the small intestine for absorption Makes hormones (such as insulin) to help control blood sugars Chronic pancreatitis is ongoing inflammation of the pancreas. Symptoms can be worse after eating. Symptoms include: Abdominal pain Nausea Vomiting Weight loss Fatty stools (stools may also float and/or have a foul odor) Malabsorption of nutrients can occur from poor digestion of food (due to reduced pancreatic enzyme activity), which will result in nutrients passing into the stools. This is seen especially with fat and fat soluble vitamins (A, D, E) as digestion of fat is highly dependent on pancreatic enzymes. In some cases, diabetes can develop if the pancreas is not able to make enough insulin to help control blood sugars, so blood sugars stay high. Nutritional Guidelines Follow a low fat diet, which for chronic pancreatitis is often restricted to 50 grams of fat, but could also range between 30-50 grams of fat depending on tolerance. If you have diabetes, eat recommended serving sizes of low fat carbohydrates to help control blood sugars (low fat/non fat dairy, fruits, vegetables, whole grains, beans, lentils etc). Information on serving sizes is available. Take pancreatic enzymes as prescribed by your doctor to treat malabsorption. Take the enzymes before each meal and snack. They will not work if taken at the end of the meal. 1 Low Fat Diet Tips Eat 4-6 small meals throughout the day Spread out your fat intake throughout the day Use butter, margarine and cooking oils sparingly Bake, grill, roast and/or steam foods. -
Brief Reports Enteroliths in a Meckel's Diverticulum Mimicking Gallstone
brief reports Enteroliths in a Meckel’s Diverticulum Mimicking Gallstone Ileus Peter G. Justus, MD, James J. Bergman, MD, and Thomas R. Reagan, MD Redmond, W ashington allstone ileus is a form of mechanical obstruction of pain. The recurring symptoms had a duration of several G the small intestine caused by a large gallstone that hours, each time culminating in severe distress lasting 10 has passed from the gallbladder to the intestine through to 15 minutes. Progressive fatigue and episodic anorexia acholecystoenteral fistula.1 This diagnosis is suspected in pursued. He denied fatty food intolerance, jaundice, vom patients with gallstones and symptoms or signs of inter iting, or a past history of gastrointestinal disease. The mittent small-bowel obstruction. family history and other personal history were unremark Meckel’s diverticulum, the most common malformation able. of the gastrointestinal tract, is found in about 2 percent On examination the patient was well nourished and in of individuals.2 Its rare clinical manifestations include in no acute distress. He was normotensive, afebrile, and testinal obstruction, ulceration, hemorrhage, intussus nonicteric. The abdomen was mildly distended, and there ception, and neoplasm. Such phenomena usually are not was mild tenderness to deep palpation of the right upper diagnosed preoperatively.3 Some 50 cases of enteroliths quadrant. No rebound or guarding was elicited, nor were occurring in a Meckel’s diverticulum have been reported.4 there masses noted. Rectal examination was negative, al This unusual finding occurs most often in men and can though some brown, guaiac-positive stool was recovered. present with lower abdominal pain, vomiting,5 rectal The remainder of the physical examination was within bleeding,6 anemia,7 or bowel obstruction.8 Radiographs normal limits. -
Nutrition Management in the Adult Patient with Crohn's Disease
Review Article: Nutrition management in the adult patient with Crohn’s disease Nutrition management in the adult patient with Crohn’s disease Basson A, MS RD(USA)(SA) Lecturer and Hospital Student Internship Supervisor, University of the Western Cape Correspondence to: Abigail Basson, email: [email protected] Keywords: inflammatory bowel disease, nutrition therapy, Crohn’s disease Abstract Malnutrition, nutrient deficiencies and osteoporosis are common in patients with Crohn’s disease, regardless of disease activity. While the role of diet in the pathogenesis of the disease remains inconclusive, upon diagnosis, nutrition therapy plays an integral role in patient care. Successful nutrition intervention involves appropriate nutritional assessment, supplemental nutrition and individualised counselling and support. Peer reviewed. (Submitted: 2012-05-08. Accepted: 2012-11-04.) © SAJCN S Afr J Clin Nutr 2012;25(4):164-172 Introduction Low-fibre, high-fat and high-sugar intakes have been implicated as some of the environmental triggers in disease development, Crohn’s disease (CD) is a chronic and recurrent immune-mediated although the role of a pre-illness diet in the pathogenesis of CD inflammatory disorder of the gastrointestinal tract.1,2 Typically, pa- remains inconclusive.16-18 However, upon diagnosis, nutrition therapy tients suffer from chronic intestinal inflammation that follows a plays an integral role in patient care, regardless of disea se activity. relapse-remitting pattern, as well as from a variety of complications 3,4 (Table I) that may or may not involve the gut. Disease activity can Malnutrition be classified by the Crohn’s Disease Activity Index5 (CDAI) (Table II), and usually, treatment includes various combinations of corticoste- Weight loss, low body mass index (BMI) and nutrient deficiencies roid, anti-inflammatory (aminosalicylates), immune-modulating or have been well documented in patients with CD, especially during biological therapy.4 While the exact cause of CD is not known, it is active disease. -
Jejunal Diverticula Causing a Life-Threatening Lower
Available online at www.ijmrhs.com cal R edi ese M ar of c l h a & n r H u e o a J l l t h International Journal of Medical Research & a S n ISSN No: 2319-5886 o c i t i Health Sciences, 2019, 8(4): 196-200 e a n n c r e e t s n I • • IJ M R H S Jejunal Diverticula Causing a Life-Threatening Lower Gastrointestinal Bleeding: A Case Report Abdelmoniem MM Makkawi* and Mohammed Eltoum Hamid Azoz Department of Surgery, University of Elimam Elmahadi, Kosti, Sudan *Corresponding e-mail: [email protected] ABSTRACT A jejunal diverticulum is a rare and usually asymptomatic disease. More commonly it is usually seen as incidental findings on radiological studies or during surgery. Complications such as bleeding, perforation, abscess formation, obstruction, malabsorption, blind loop syndrome, volvulus, and intussusception may warrant surgical intervention. Herein, we report a case of a 62-year old woman presenting with massive lower gastrointestinal bleeding, she was pale, clammy and hemodynamically unstable, she was initially resuscitated with IV fluids and whole blood, urgent upper endoscopy was normal, colonoscopy revealed sigmoid colon ulcerative lesion with histopathological evidence of adenocarcinoma, there was bleeding coming from upwards. After staging of the tumor, the decision was then made to proceed to exploratory laparotomy with a pre-operative plan of segmental colectomy. Intra-operatively segmental sigmoid colectomy was performed with end to end anastomosis, during formal laparotomy we found 2 giant diverticula in the proximal jejunum, small bowel resection and end to end anastomosis was done with the good postoperative outcome. -
Low Fructose Diet
Low Fructose Diet What is fructose? Fructose is a simple sugar found naturally in certain fruits, vegetables, and sweeteners. It is also added to some processed foods and is a component of regular table sugar (sucrose). What is fructose malabsorption? Some people cannot completely absorb fructose in the small intestine. When fructose is not absorbed it is quickly consumed by the bacteria that normally live in the gut. The result is abdominal bloating, cramping, gas, diarrhea, and/or constipation. Fructose malabsorption can occur in people with Irritable Bowel Syndrome (IBS) and other gastrointestinal (GI) disorders. It is diagnosed with a fructose hydrogen breath test and the treatment is a low fructose diet. What foods should I avoid? You do not have to avoid all foods that contain fructose, only those that are high in excess fructose listed below. Excess fructose means that the food has more than half of its natural sugar as fructose. Glucose is the other simple sugar found in these foods which helps absorb fructose in the small intestine. The more glucose than fructose in a food, the more “gut-friendly” it is. Avoid these high fructose foods: Fruit: apple, pear, Asian pear, watermelon, fig, mango, cherries Vegetables: artichokes, sugar snap peas, asparagus Sweeteners: honey, agave, high fructose corn syrup (HFCS), fruit juice concentrate of the above fruits, and large amounts of sucrose (white or brown sugar) UMHS Division of Gastroenterology - 1 - Beverages: juices of the fruit listed above, regular soda and drinks that are sweetened with fructose or HFCS, rum General guidelines: Read labels and avoid products that contain fructose, crystalline fructose, HFCS, honey, agave, and fruit juice concentrates (i.e. -
Zenker's Diverticulum and Squamous Esophageal Cancer
Journal of Mind and Medical Sciences Volume 4 | Issue 2 Article 15 2017 Zenker’s diverticulum and squamous esophageal cancer: a case report Ion Dina Carol Davila University, St. Ioan Clinical Hospital, Department of Gastroenterology, Bucharest, Romania Octav Ginghina Carol Davila University, St. Ioan Clinical Hospital, Department of Surgery, Bucharest, Romania Corina D. Toderescu Vasile Goldis Western University of Arad, Faculty of General Medicine, Arad, Romania Cristian Bălălău Carol Davila University, St. Pantelimon Hospital, Department of Surgery, Bucharest, Romania, [email protected] Bianca Galateanu University of Bucharest, Department of Biochemistry and Molecular Biology, Bucharest, Romania See next page for additional authors Follow this and additional works at: http://scholar.valpo.edu/jmms Part of the Medical Sciences Commons, and the Surgery Commons Recommended Citation Dina, Ion; Ginghina, Octav; Toderescu, Corina D.; Bălălău, Cristian; Galateanu, Bianca; Negrei, Carolina; and Iacobescu, Claudia (2017) "Zenker’s diverticulum and squamous esophageal cancer: a case report," Journal of Mind and Medical Sciences: Vol. 4 : Iss. 2 , Article 15. DOI: 10.22543/7674.42.P193197 Available at: http://scholar.valpo.edu/jmms/vol4/iss2/15 This Case Presentation is brought to you for free and open access by ValpoScholar. It has been accepted for inclusion in Journal of Mind and Medical Sciences by an authorized administrator of ValpoScholar. For more information, please contact a ValpoScholar staff member at [email protected]. Zenker’s diverticulum and squamous esophageal cancer: a case report Authors Ion Dina, Octav Ginghina, Corina D. Toderescu, Cristian Bălălău, Bianca Galateanu, Carolina Negrei, and Claudia Iacobescu This case presentation is available in Journal of Mind and Medical Sciences: http://scholar.valpo.edu/jmms/vol4/iss2/15 J Mind Med Sci. -
University of Cincinnati
UNIVERSITY OF CINCINNATI Date:___________________ I, _________________________________________________________, hereby submit this work as part of the requirements for the degree of: in: It is entitled: This work and its defense approved by: Chair: _______________________________ _______________________________ _______________________________ _______________________________ _______________________________ Prevalence of Subclinical Vitamin K Deficiency in Cholestatic Liver Disease A thesis submitted to the Division of Research and Advanced Studies of the University of Cincinnati In partial fulfillment of the Requirements for the degree of MASTER OF SCIENCE In the Division of Epidemiology and Biostatistics, Department of Environmental Health of the College of Medicine 2004 by Jennifer A. Strople, M.D. B.A., University of Virginia, 1994 M.D., University of Alabama at Birmingham School of Medicine, 1998 Thesis committee: James E. Heubi, M.D. (Chair and Advisor) Paul Succop, Ph.D. Abstract Current practice is to monitor prothrombin time as an indicator of vitamin K sufficiency in cholestatic liver disease. Since prothrombin time is a surrogate marker, it may underestimate the actual prevalence of vitamin K deficiency in this population. This study investigates the frequency of vitamin K deficiency among a convenience sample of children and adults with cholestatic liver disease by determining plasma levels of protein induced in vitamin K absence II (PIVKA-II), and assesses the relationship between PIVKA-II levels and markers of cholestasis, measured prothrombin time, and vitamin A, E and 25-hydroxyvitamin D levels. Methods: Subjects with cholestatic liver disease were recruited from the Cincinnati referral area. Subjects with decompensated cirrhosis, malignancy, concurrent disease that results in fat malabsorption and AIDS were excluded. All subjects had blood collected for liver function tests, prothrombin time (PT), INR, bile acids, 25-hydroxyvitamin D, vitamin A, vitamin E and PIVKA-II levels.