Nutritional Aspects in Inflammatory Bowel Diseases
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Intro to Gallbladder & Pancreas Pathology
Cholecystitis acute chronic Gallbladder tumors Adenomyoma (benign) Intro to Adenocarcinoma Gallbladder & Pancreatitis Pancreas acute Pathology chronic Pancreatic tumors Helen Remotti M.D. Case 1 70 year old male came to the ER. CC: 5 hours of right –sided abdominal pain that had awakened him from sleep ; also pain in the right shoulder and scapula. Previous episodes mild right sided abdominal pain lasting 1- 2 hours. 1 Case 1 Febrile with T 100.7 F, pulse 100, BP 150/90 Abdomen: RUQ and epigastric tenderness to light palpation, with inspiratory arrest and increased pain on deep palpation. (Murphy’s sign) Labs: WBC 12,500; (normal bilirubin, Alk phos, AST, ALT). Ultrasound shows normal liver, normal pancreas without duct dilatation and a distended thickened gallbladder with a stone in cystic duct. DIAGNOSIS??? 2 Acute Cholecystitis Epigastric, RUQ pain Radiate to shoulder Fever, chills Nausea, vomiting Mild Jaundice RUQ guarding, tenderness Tender Mass (50%) Acute Cholecystitis Stone obstructs cystic duct G.B. distended Mucosa disrupted Chemical Irritation: Conc. Bile Bacterial Infection 50 - 70% + culture: Lumen 90 - 95% + culture: Wall Bowel Organisms E. Coli, S. Fecalis 3 Culture Normal Biliary Tree: No Bacteria Bacteria Normally Cleared In G.B. with cholelithiasis Bacteria cling to stones If stone obstructs cystic duct orifice G.B. distended Mucosa Disrupted Bacteria invade G.B. Wall 4 Gallstones (Cholelithiasis) • 10 - 20% Adults • 35% Autopsy: Over 65 • Over 20 Million • 600,000 Cholecystectomies • #2 reason for abdominal operations -
Inflammatory Bowel Disease Irritable Bowel Syndrome
Inflammatory Bowel Disease and Irritable Bowel Syndrome Similarities and Differences 2 www.ccfa.org IBD Help Center: 888.MY.GUT.PAIN 888.694.8872 Important Differences Between IBD and IBS Many diseases and conditions can affect the gastrointestinal (GI) tract, which is part of the digestive system and includes the esophagus, stomach, small intestine and large intestine. These diseases and conditions include inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). IBD Help Center: 888.MY.GUT.PAIN 888.694.8872 www.ccfa.org 3 Inflammatory bowel diseases are a group of inflammatory conditions in which the body’s own immune system attacks parts of the digestive system. Inflammatory Bowel Disease Inflammatory bowel diseases are a group of inflamma- Causes tory conditions in which the body’s own immune system attacks parts of the digestive system. The two most com- The exact cause of IBD remains unknown. Researchers mon inflammatory bowel diseases are Crohn’s disease believe that a combination of four factors lead to IBD: a (CD) and ulcerative colitis (UC). IBD affects as many as 1.4 genetic component, an environmental trigger, an imbal- million Americans, most of whom are diagnosed before ance of intestinal bacteria and an inappropriate reaction age 35. There is no cure for IBD but there are treatments to from the immune system. Immune cells normally protect reduce and control the symptoms of the disease. the body from infection, but in people with IBD, the immune system mistakes harmless substances in the CD and UC cause chronic inflammation of the GI tract. CD intestine for foreign substances and launches an attack, can affect any part of the GI tract, but frequently affects the resulting in inflammation. -
General Signs and Symptoms of Abdominal Diseases
General signs and symptoms of abdominal diseases Dr. Förhécz Zsolt Semmelweis University 3rd Department of Internal Medicine Faculty of Medicine, 3rd Year 2018/2019 1st Semester • For descriptive purposes, the abdomen is divided by imaginary lines crossing at the umbilicus, forming the right upper, right lower, left upper, and left lower quadrants. • Another system divides the abdomen into nine sections. Terms for three of them are commonly used: epigastric, umbilical, and hypogastric, or suprapubic Common or Concerning Symptoms • Indigestion or anorexia • Nausea, vomiting, or hematemesis • Abdominal pain • Dysphagia and/or odynophagia • Change in bowel function • Constipation or diarrhea • Jaundice “How is your appetite?” • Anorexia, nausea, vomiting in many gastrointestinal disorders; and – also in pregnancy, – diabetic ketoacidosis, – adrenal insufficiency, – hypercalcemia, – uremia, – liver disease, – emotional states, – adverse drug reactions – Induced but without nausea in anorexia/ bulimia. • Anorexia is a loss or lack of appetite. • Some patients may not actually vomit but raise esophageal or gastric contents in the absence of nausea or retching, called regurgitation. – in esophageal narrowing from stricture or cancer; also with incompetent gastroesophageal sphincter • Ask about any vomitus or regurgitated material and inspect it yourself if possible!!!! – What color is it? – What does the vomitus smell like? – How much has there been? – Ask specifically if it contains any blood and try to determine how much? • Fecal odor – in small bowel obstruction – or gastrocolic fistula • Gastric juice is clear or mucoid. Small amounts of yellowish or greenish bile are common and have no special significance. • Brownish or blackish vomitus with a “coffee- grounds” appearance suggests blood altered by gastric acid. -
Nutritional Considerations in Inflammatory Bowel Disease
NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #5 Series Editor: Carol Rees Parrish, M.S., R.D., CNSD Nutritional Considerations in Inflammatory Bowel Disease by Kelly Anne Eiden, M.S., R.D., CNSD Nutrient alterations are commonplace in patients with inflammatory bowel disease. The etiology for these alterations is multifactorial. Nutrition assessment is the first step in successful nutrition management of any patient with gastrointestinal disease. Nutritional goals include assisting with nutrition risk, identifying macronutrient and micronutrient needs and implementing a nutrition plan to meet those needs. This article addresses many of the nutrition issues currently facing clinicians including: oral, enteral and parenteral nutrition, common vitamin/mineral deficiencies, medium chain triglycerides and nutrition as primary and supportive therapy. INTRODUCTION and supportive treatment in both Crohn’s and UC. The nflammatory bowel disease (IBD), encompassing following article will provide guidelines to help the both Crohn’s disease and ulcerative colitis (UC), is clinician determine nutritional risk, review specialized Ia chronic inflammatory intestinal disorder of nutrient needs and discuss nutrition as a treatment unknown etiology. A multitude of factors, including modality in the patient with IBD. drug-nutrient interactions, disease location, symp- toms, and dietary restrictions can lead to protein NUTRITION ASSESSMENT IN INFLAMMATORY energy malnutrition and specific nutritional deficien- BOWEL DISEASE cies. It is estimated that up to 85% of hospitalized IBD patients have protein energy malnutrition, based on Factors Affecting Nutritional Status abnormal anthropometric and biochemical parameters in the Patient with IBD (1,2). As Crohn’s disease can occur anywhere from There are many factors that alter nutrient intake in the mouth to anus (80% of cases in the terminal ileum), it patient with IBD. -
Chronic Pancreatitis. 2
Module "Fundamentals of diagnostics, treatment and prevention of major diseases of the digestive system" Practical training: "Chronic pancreatitis (CP)" Topicality The incidence of chronic pancreatitis is 4.8 new cases per 100 000 of population per year. Prevalence is 25 to 30 cases per 100 000 of population. Total number of patients with CP increased in the world by 2 times for the last 30 years. In Ukraine, the prevalence of diseases of the pancreas (CP) increased by 10.3%, and the incidence increased by 5.9%. True prevalence rate of CP is difficult to establish, because diagnosis is difficult, especially in initial stages. The average time of CP diagnosis ranges from 30 to 60 months depending on the etiology of the disease. Learning objectives: to teach students to recognize the main symptoms and syndromes of CP; to familiarize students with physical examination methods of CP; to familiarize students with study methods used for the diagnosis of CP, the determination of incretory and excretory pancreatic insufficiency, indications and contraindications for their use, methods of their execution, the diagnostic value of each of them; to teach students to interpret the results of conducted study; to teach students how to recognize and diagnose complications of CP; to teach students how to prescribe treatment for CP. What should a student know? Frequency of CP; Etiological factors of CP; Pathogenesis of CP; Main clinical syndromes of CP, CP classification; General and alarm symptoms of CP; Physical symptoms of CP; Methods of -
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. -
Intro to Gallbladder & Pancreas Pathology Gallstones Chronic
Cholecystitis Choledocholithiasis acute chronic (Stones in the common bile duct) Gallbladder tumors Pain: Epigastric, RUQ-stones may be passed Adenomyoma (benign) Intro to Obstructive Jaundice-may be intermittent Adenocarcinoma Gallbladder & Ascending Cholangitis- Infection: to liver 20%: No pain; 25% no jaundice Pancreatitis Pancreas acute Pathology chronic Pancreatic tumors Helen Remotti M.D. Gallstones (Cholelithiasis) • 10 - 20% Adults • 35% Autopsy: Over 65 • Over 20 Million • 600,000 Cholecystectomies • #2 reason for abdominal operations Acute cholecystitis = ischemic injury Cholesterol/mixed stones Chronic Cholecystitis • Associated with calculi in 95% of cases. • Multiples episodes of inflammation cause GB thickening with chronic inflammation/ fibrosis and muscular hypertrop hy . • Rokitansky - Aschoff Sinuses (mucosa herniates through the muscularis mucosae) • With longstanding inflammation GB becomes fibrotic and calcified “porcelain GB” 1 Chronic Cholecystitis • Fibrosis • Chronic Inflammation • Rokitansky - Aschoff Sinuses • Hypertrophy: Muscularis Chronic cholecystitis Cholesterolosis Focal accumulation of cholesterol-laden macrophages in lamina propria of gallbladder (incidental finding). Rokitansky-Aschoff sinuses Adenomyoma of Gall Bladder 2 Carcinoma: Gall Bladder Uncommon: 5,000 cases / year Fewer than 1% resected G.B. Sx: same as with stones 5 yr. survival: Less than 5% (survival relates to stage) 90%: Stones Long Hx: symptomatic stones Stones: predispose to CA., but uncommon complication 3 Gallbladder carcinoma Acute pancreatitis Case 1 56 year old woman presents to ER in shock, following rapid onset of severe upper abdominal pain, developing over the previous day. Hx: heavy alcohol use. LABs: Elevated serum amylase and elevated peritoneal fluid lipase Acute Pancreatitis Patient developed rapid onset of respiratory failure necessitating intubation and mechanical ventilation. Over 48 hours, she was increasingly unstable, with evolution to multi-organ failure, and she expired 82 hours after admission. -
Chronic Viral Hepatitis in a Cohort of Inflammatory Bowel Disease
pathogens Article Chronic Viral Hepatitis in a Cohort of Inflammatory Bowel Disease Patients from Southern Italy: A Case-Control Study Giuseppe Losurdo 1,2 , Andrea Iannone 1, Antonella Contaldo 1, Michele Barone 1 , Enzo Ierardi 1 , Alfredo Di Leo 1,* and Mariabeatrice Principi 1 1 Section of Gastroenterology, Department of Emergency and Organ Transplantation, University “Aldo Moro” of Bari, 70124 Bari, Italy; [email protected] (G.L.); [email protected] (A.I.); [email protected] (A.C.); [email protected] (M.B.); [email protected] (E.I.); [email protected] (M.P.) 2 Ph.D. Course in Organs and Tissues Transplantation and Cellular Therapies, Department of Emergency and Organ Transplantation, University “Aldo Moro” of Bari, 70124 Bari, Italy * Correspondence: [email protected]; Tel.: +39-080-559-2925 Received: 14 September 2020; Accepted: 21 October 2020; Published: 23 October 2020 Abstract: We performed an epidemiologic study to assess the prevalence of chronic viral hepatitis in inflammatory bowel disease (IBD) and to detect their possible relationships. Methods: It was a single centre cohort cross-sectional study, during October 2016 and October 2017. Consecutive IBD adult patients and a control group of non-IBD subjects were recruited. All patients underwent laboratory investigations to detect chronic hepatitis B (HBV) and C (HCV) infection. Parameters of liver function, elastography and IBD features were collected. Univariate analysis was performed by Student’s t or chi-square test. Multivariate analysis was performed by binomial logistic regression and odds ratios (ORs) were calculated. We enrolled 807 IBD patients and 189 controls. Thirty-five (4.3%) had chronic viral hepatitis: 28 HCV (3.4%, versus 5.3% in controls, p = 0.24) and 7 HBV (0.9% versus 0.5% in controls, p = 0.64). -
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. -
Liver Disease in Ulcerative Colitis: an Epidemiological and Follow up Study
84 Gut 1994; 35:84-89 Liver disease in ulcerative colitis: an epidemiological and follow up study in the county of Stockholm Gut: first published as 10.1136/gut.35.1.84 on 1 January 1994. Downloaded from U Broome, H Glaumann, G Hellers, B Nilsson, J Sorstad, R Hultcrantz Abstract sclerosing cholangitis (PSC) are said to be more In an epidemiological study ofthe incidence of common in patients with UC.47 The incidence of ulcerative colitis (UC) in the county of Stock- these complications varies in different studies holm between 1955 and 1979, 1274 patients depending on selection criteria and on the with UC were discovered. Almost all these definition of hepatobiliary disease.89 The true patients had regularly been investigated with incidence of hepatobiliary dysfunction in UC, liver function tests; 142 (11%) of them showed however, can only be obtained by tests of liver signs of hepatobiliary disease. A follow up function tests such as transaminases, alkaline study on all 142 patients with abnormal liver phosphatases, and bilirubin made routinely in function and UC was made between 1989 and unselected groups of patients with UC. Because 1991 to evaluate the cause of the liver abnor- the cause of hepatic involvement in UC is mality and to find out if the liver disease had enigmatic it is important to find out if the rate affected the survival rates. At follow up, eight of this complication is increasing, because of patients were reclassified as having Crohn's factors unrelated to UC, or if it mirrors the disease, 60 had developed normal liver func- incidence ofUC in itself. -
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. -
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.