Malnutrition in Patients with Liver Cirrhosis
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Indigestion, Antacids, Achlorhydria and H. Pylori. by Michael T
FEATURE ARTICLE Indigestion, antacids, achlorhydria and H. pylori. by Michael T. Murray, N.D. digestive aids include hydrochloric Perhaps the most effective treatment of used to describe a feeling of acid and pancreatic enzyme prepara- chronic reflux esophagitis is to utilize Thegaseousness term "indigestion" or fullness is in often the tions. This article will take a critical look gravity. The standard recommendation abdomen. It can also be used to describe at the use of these agents and contrast is to simply place four-inch blocks "heartburn." Indigestion can be attributed their use with natural digestive aids. The under the bedposts at the head of the to a great many causes, including not topic of H. pylori will also be addressed. bed. This elevation of the head is very only increased secretion of acid but also effective in many cases. decreased secretion of acid and other General considerations Another recommendation to heal digestive factors and enzymes. The A 1983 article in the American the esophagus is using deglycyrrhizinated dominant treatment of indigestion is the Journal of Gastroenterology asked the licorice (DGL). Although DGL is primarily use of over-the-counter preparations. question "Why do apparently healthy used for treating peptic ulcers, I have These preparations include antacids people use antacids?"1 The answer: used it clinically in cases of heartburn which work by binding free acid, and reflux esophagitis, the medical term with success. DGL is further discussed drugs like Tagamet, Zantac, and Pepcid for heartburn. Reflux esophagitis is below. which inhibit the release of antacids by most often caused by the flow of gastric blocking histamine (H2) receptors juices up the esophagus leading to a Common antacid medications including antacids. -
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. -
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. -
Primary Biliary Cholangitis: a Brief Overview Justin S
REVIEW Primary Biliary Cholangitis: A Brief Overview Justin S. Louie,* Sirisha Grandhe,* Karen Matsukuma,† and Christopher L. Bowlus* Primary biliary cholangitis (PBC), previously referred to supported by the higher concordance of PBC in monozy- as primary biliary cirrhosis, is the most common chronic gotic compared with dizygotic twins.4 In addition, certain cholestatic autoimmune disease affecting adults in the human leukocyte antigen haplotypes have been associ- United States.1 It is characterized by a hallmark serologic ated with PBC, as well as variants at loci along the inter- signature, antimitochondrial antibody (AMA), and specific leukin-12 (IL-12) immunoregulatory pathway (IL-12A and bile duct pathology with progressive intrahepatic duct de- IL-12RB2 loci).5 struction leading to cholestasis. PBC is potentially fatal and can have both intrahepatic and extrahepatic complications. PATHOGENESIS EPIDEMIOLOGY The primary disease mechanism in PBC is thought to be T cell lymphocyte–mediated injury against intralobu- PBC affects all races and ethnicities; however, it is best lar biliary epithelial cells. This causes progressive destruc- studied in the Caucasian population. The condition pre- tion and eventual disappearance of the intralobular bile dominantly affects women older than 40 years, with a ducts. Molecular mimicry has been proposed as the ini- female/male ratio of 9:1.2 Although the incidence of PBC tiating event in the loss of tolerance primarily to mito- appears to be stable, the overall prevalence of the disease chondrial pyruvate dehydrogenase complex, E2, during is increasing.3 An individual’s genetic susceptibility, epige- which exogenous antigens evoke an immune response netic factors, and certain environmental triggers seem to that recognizes an endogenous (self) antigen inciting an play important roles. -
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. -
Infectious Diarrhea
Michael Yin Infectious Diarrhea A. Introduction Acute gastrointestinal illnesses rank second only to acute respiratory illnesses as the most common disease worldwide. In children less than 5 years old, attack rates range from 2-3 illnesses per child per year in developed countries to 10-18 illnesses per child per year in developing countries. In Asia, Africa, and Latin America, acute diarrheal illnesses are a leading cause of morbidity (1 billion cases per year), and mortality (4-6 million deaths per year, or 12,600 deaths per day) in children. Most cases of acute infectious gastroenteritis are caused by viruses (Rotavirus, Calicivirus, Adenovirus). Only 1-6% of stool cultures in patients with acute diarrhea are positive for bacterial pathogens; however, higher rates of detection have been described in certain settings, such as foodborne outbreaks (17%) and in patients with severe or bloody diarrhea (87%). This syllabus will focus on bacterial organisms, since viral and parasitic (Giardia, Entamoeba, Cryptosporidium, Isospora, Microspora, Cyclospora) causes of gastroenteritis are covered elsewhere. Clostridium difficile colitis will be covered in the lecture and syllabus on Anaerobes. Diarrhea is an alteration in bowel movements characterized by an increase in the water content, volume, or frequency of stools. A decrease in consistency and an increase in frequency in bowel movements to > 3 stools per day have often been used as a definition for epidemiological investigations. “Infectious diarrhea” is diarrhea due to an infectious etiology. “Acute diarrhea” is an episode of diarrhea of < 14 days in duration. “Persistent diarrhea” is an episode of diarrhea > 14 days in duration, and “chronic diarrhea” is diarrhea that last for >30 days duration. -
Non-Alcoholic Fatty Liver Disease
Non-alcoholic fatty liver disease Description Non-alcoholic fatty liver disease (NAFLD) is a buildup of excessive fat in the liver that can lead to liver damage resembling the damage caused by alcohol abuse, but that occurs in people who do not drink heavily. The liver is a part of the digestive system that helps break down food, store energy, and remove waste products, including toxins. The liver normally contains some fat; an individual is considered to have a fatty liver (hepatic steatosis) if the liver contains more than 5 to 10 percent fat. The fat deposits in the liver associated with NAFLD usually cause no symptoms, although they may cause increased levels of liver enzymes that are detected in routine blood tests. Some affected individuals have abdominal pain or fatigue. During a physical examination, the liver may be found to be slightly enlarged. Between 7 and 30 percent of people with NAFLD develop inflammation of the liver (non- alcoholic steatohepatitis, also known as NASH), leading to liver damage. Minor damage to the liver can be repaired by the body. However, severe or long-term damage can lead to the replacement of normal liver tissue with scar tissue (fibrosis), resulting in irreversible liver disease (cirrhosis) that causes the liver to stop working properly. Signs and symptoms of cirrhosis, which get worse as fibrosis affects more of the liver, include fatigue, weakness, loss of appetite, weight loss, nausea, swelling (edema), and yellowing of the skin and whites of the eyes (jaundice). Scarring in the vein that carries blood into the liver from the other digestive organs (the portal vein) can lead to increased pressure in that blood vessel (portal hypertension), resulting in swollen blood vessels (varices) within the digestive system. -
Achlorhydria and Anæmia
Jan., 1942] ACHLORHYDRIA AND ANAEMIA: BHENDE 13 Table I ACHLORHYDRIA AND ANJEMIA 84 cases An analysis of 79 cases Diagnosis Number of By Y. M. BHENDE, m.d. (Bom.) cases (From the Department of Pathology, P. G. Singhanee Anaemia 79 Hindu Hospital, Bombay) Chronic gastritis 2 Chronic 1 ' appendicitis inormal gastric juice contains hydrochloric Dyspepsia' 2 acid, pepsin, rennin and the intrinsic factor of Castle. The secreting function of the stomach It is seen at once that the, bulk of the cases may be investigated by means of a fractional is formed by the anaemia group; in fact, it was test meal. As ordinarily performed, the the anaemic state of these patients that neces- examination gives information only as to the sitated their admission to the hospital for hydrochloric-acid formation; the presence of investigation. A detailed analysis of these pepsin and rennin can be recognized by in vitro 79 cases of anaemia, with special reference to test, but for the detection of the intrinsic the state of their gastric secretion, forms the factor in vivo tests are necessary. basis of this communication. each case a detailed Davis (1931) by using the histamine test Procedure.?In clinical was taken. The blood was meal was able to demonstrate that the failure history scrutinized of all the absolute a the stomach function was probably progres- minutely, recording indices, van den and the red cell sive; his investigations (confirmed by many Bergh reaction, fragi- Wassermann or Kahn tests were done others) established the fact that, as a general lity test; rule, the ferment factors of the stomach fail as a routine and, wherever indicated, other A marrow after the hydrochloric acid; and whenever there bio-chemical studies. -
Vaccinations for Adults with Chronic Liver Disease Or Infection
Vaccinations for Adults with Chronic Liver Disease or Infection This table shows which vaccinations you should have to protect your health if you have chronic hepatitis B or C infection or chronic liver disease (e.g., cirrhosis). Make sure you and your healthcare provider keep your vaccinations up to date. Vaccine Do you need it? Hepatitis A Yes! Your chronic liver disease or infection puts you at risk for serious complications if you get infected with the (HepA) hepatitis A virus. If you’ve never been vaccinated against hepatitis A, you need 2 doses of this vaccine, usually spaced 6–18 months apart. Hepatitis B Yes! If you already have chronic hepatitis B infection, you won’t need hepatitis B vaccine. However, if you have (HepB) hepatitis C or other causes of chronic liver disease, you do need hepatitis B vaccine. The vaccine is given in 2 or 3 doses, depending on the brand. Ask your healthcare provider if you need screening blood tests for hepatitis B. Hib (Haemophilus Maybe. Some adults with certain high-risk conditions, for example, lack of a functioning spleen, need vaccination influenzae type b) with Hib. Talk to your healthcare provider to find out if you need this vaccine. Human Yes! You should get this vaccine if you are age 26 years or younger. Adults age 27 through 45 may also be vacci- papillomavirus nated against HPV after a discussion with their healthcare provider. The vaccine is usually given in 3 doses over a (HPV) 6-month period. Influenza Yes! You need a dose every fall (or winter) for your protection and for the protection of others around you. -
Symptomatic Approach to Gas, Belching and Bloating 21
20 Osteopathic Family Physician (2019) 20 - 25 Osteopathic Family Physician | Volume 11, No. 2 | March/April, 2019 Gennaro, Larsen Symptomatic Approach to Gas, Belching and Bloating 21 Review ARTICLE to escape. This mechanism prevents the stomach from becoming IRRITABLE BOWEL SYNDROME (IBS) Symptomatic Approach to Gas, Belching and Bloating damaged by excessive dilation.2 IBS is abdominal pain or discomfort associated with altered with OMT Treatment Options Many patients with GERD report increased belching. Transient bowel habits. It is the most commonly diagnosed GI disorder lower esophageal sphincter (LES) relaxation is the major and accounts for about 30% of all GI referrals.7 Criteria for IBS is recurrent abdominal pain at least one day per week in the Carly Gennaro, DO1; Helaine Larsen, DO1 mechanism for both belching and GERD. Recent studies have shown that the number of belches is related to the number of last three months associated with at least two of the following: times someone swallows air. These studies have concluded that 1) association with defecation, 2) change in stool frequency, 1 Good Samaritan Hospital Medical Center, West Islip, NY patients with GERD swallow more air in response to heartburn and 3) change in stool form. Diagnosis should be made using these therefore belch more frequently.3 There is no specific treatment clinical criteria and limited testing. Common symptoms are for belching in GERD patients, so for now, physicians continue to abdominal pain, bloating, alternating diarrhea and constipation, treat GERD with proton pump inhibitors (PPIs) and histamine-2 and pain relief after defecation. Pain can be present anywhere receptor antagonists with the goal of suppressing heartburn and in the abdomen, but the lower abdomen is the most common KEYWORDS: ABSTRACT: Intestinal gas production is a normal physiologic progress. -
Hypochlorhydric Stomach: a Risk Condition for Calcium Malabsorption and Osteoporosis?
Scandinavian Journal of Gastroenterology, 2010; 45: 133–138 REVIEW ARTICLE Hypochlorhydric stomach: a risk condition for calcium malabsorption and osteoporosis? PENTTI SIPPONEN1 & MATTI HÄRKÖNEN2 1Repolar Oy, Espoo, Finland, and 2Department of Clinical Chemistry, University of Helsinki, Helsinki, Finland Abstract Malabsorption of dietary calcium is a cause of osteoporosis. Dissolution of calcium salts (e.g. calcium carbonate) in the stomach is one step in the proper active and passive absorption of calcium as a calcium ion (Ca2+) in the proximal small intestine. Stomach acid markedly increases dissolution and ionization of poorly soluble calcium salts. If acid is not properly secreted, calcium salts are minimally dissolved (ionized) and, subsequently, may not be properly and effectively absorbed. Atrophic gastritis, gastric surgery, and high-dose, long-term use of antisecretory drugs markedly reduce acid secretion and may, therefore, be risk conditions for malabsorption of dietary and supplementary calcium, and may thereby increase the risk of osteoporosis in the long term. Key Words: Achlorhydria, atrophic gastritis, calcium carbonate, calcium salt, hypochlorhydria, malabsorption, osteoporosis, proton-pump inhibitor, stomach acid For personal use only. Introduction acid for calcium absorption and emphasize that the in vitro water solubility of calcium salts is not associated Malabsorption of dietary calcium is a risk factor for with their in vivo absorbability [1–3]. This may cer- osteoporosis. Acid induces dissolution of the calcium tainly be true in subjects with a healthy stomach and in the stomach as a calcium ion (Ca2+). If the stomach normal acid secretion. However, in subjects with an does not secrete acid, calcium salts may not be effec- hypochlorhydric stomach, and with failure of the tively dissolved and ionized, and may be poorly “gastric acid machine”, this may no longer be the absorbed in the proximal small intestine.