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Diarrhea and Malabsorption

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Diarrhea and Malabsorption 7/20/12 PPY 222 Gastrointestinal Pathophysiology, Spring 2007 - Tufts OpenCourseWare S e a r c h Diarrhea and Malabsorption Author: Laurence Scott Bailen, M.D. 1. Objectives: Pathophysiology of Diarrhea Color Key Important key words or phrases. 1. To be able to describe five major categories of causes of diarrhea Important concepts or main ideas. 2. To understand that there is considerable overlap in the pathophysiology of diarrhea in clinical conditions 3. Understand the fecal osmotic gap in evaluating patients with chronic diarrhea 4. Understand how small intestinal bacterial overgrowth syndrome results in malabsorption 5. Understand the epidemiology, clinical presentation, and diagnosis of celiac disease 6. Understand the current hypothesis for the pathogenesis of celiac disease 7. Understand the mechanism of diarrhea in the two more common causes of secretory diarrhea due to excess secretion of a hormone: Zollinger­Ellison syndrome (gastrinoma) and carcinoid syndrome (serotonin, bradykinin and others) 8. Understand the diagnostic tests used to evaluate patients with chronic diarrhea with attention to the tests for malabsorption such as the d­xylose test 2. Pathophysiology of Diarrhea and Malabsorption 2.1. Introduction Diarrhea may best be defined as doctors Roux and Ryle did in 1924: “Diarrhea is the too rapid evacuation of too fluid stools." Normal stooling varies from three bowel movements per week to three bowel movements per day. Patients may report diarrhea when their own normal pattern of bowel movements is altered. Loosening of the stool occurs when daily fecal water output increases by only 50­60mL. An increase of fecal water excretion of 100mL is sufficient to increase daily stool weight by 200grams/24 hours, the upper limit of normal. The major causes of diarrhea, outlined in Table 1 , may be classified into five broad categories related to their pathophysiology: 1. Osmotic diarrhea, 2. Malabsorption /maldigestion/fatty diarrhea (steatorrhea), 3. Inflammatory diarrhea, 4. Secretory diarrhea, or 5. Altered motility. This section will review the pathophysiology of some of the more common and important causes of diarrhea in these categories. It should be remembered, though, that these categories are not absolute and that in any one individual disease or syndrome one or more pathophysiologic processes may be the mechanism behind the development of diarrhea. For example, Crohn’s disease may cause diarrhea based on an inflammatory, malabsorptive, and secretory pathophysiology. In addition, some causes of malabsorption or maldigestion may not necessarily be associated with diarrhea. Diarrhea may also be divided into acute diarrhea and chronic diarrhea . Acute diarrheal states (diarrhea lasting less than 4 weeks) are most commonly due to infectious causes. However, many different medications or ischemia to the intestines can cause acute diarrhea. Chronic diarrhea is diarrhea which lasts for longer than 4 weeks. This section will not only discuss the pathophysiology of diarrhea, but also the evaluation and treatment of patients with diarrhea. This section will NOT focus on inflammatory bowel disease or infectious diarrhea, as these entities are covered elsewhere. Table 1. Major Causes of Diarrhea Osmotic diarrhea : Osmotic laxative abuse Mg(OH)2), MgSO4, Na2SO4, Lactulose, Polyethylene glycol Carbohydrate malabsorption Lactose intolerance ocw.tufts.edu/Content/48/lecturenotes/571075 1/8 7/20/12 PPY 222 Gastrointestinal Pathophysiology, Spring 2007 - Tufts OpenCourseWare Malabsorption/Maldigestion/Fatty Diarrhea Malabsorption syndromes Mucosal diseases of small intestine (e.g. Celiac sprue) Short bowel syndrome (after multiple surgical resections) Small bowel bacterial overgrowth Mesenteric ischemia Maldigestion Pancreatic insufficiency (chronic pancreatitis, cystic fibrosis) Reduced luminal bile acid Inflammatory diarrhea Inflammatory bowel disease Ulcerative colitis Crohn’s disease Lymphocytic or collagenous colitis Ulcerative jejunoileitis (rare complication of celiac sprue) Infections Invasive bacterial infection (Clostridium difficile, E.Coli 0157:H7 and others) Phenolphthalein, anthraquinones, bisacodyl, senna, aloe, ricinoleic acid (castor oil), dioctyl sodium sulfosuccinate Ischemic Colitis Radiation enterocolitis Neoplasia: colon carcinoma, lymphoma Secretory diarrhea Non­osmotic laxative use Phenolphthalein, anthraquinones, bisacodyl, senna, aloe, ricinoleic acid (castor oil), dioctyl sodium sulfosuccinate Congential chloridorrhea Infectious diarrhea: liberation of bacterial toxins Ileal bile acid malabsorption Vasculitis Drugs Neuroendocrine tumors Gastrinoma VIPoma Somatostatinomas Mastocytosis Carcinoid syndrome Medullary carcinoma of thyroid Neoplasia: villous adenoma, colon cancer, lymphoma Idiopathic secretory diarrhea Disordered motility Post­vagotomy Post­sympathectomy Diabetic neuropathy ocw.tufts.edu/Content/48/lecturenotes/571075 2/8 7/20/12 PPY 222 Gastrointestinal Pathophysiology, Spring 2007 - Tufts OpenCourseWare Hyperthyroidism Addison’s disease (adrenal insufficiency) Irritable bowel syndrome 2.2. Osmotic Diarrhea Excess amounts of poorly absorbed substances that remain in the intestinal lumen may cause osmotic diarrhea. Large amounts of these substances (e.g. lactose, lactulose, magnesium) contain osmotically active solutes which obligate retention of water in the lumen of the intestine by virtue of their osmotic effects. + + ­ ­ Electrolyte absorption (Na , K , Cl , HCO3 ) is unaffected by these osmotically­active substances therefore stool water contains very little unabsorbed sodium and potassium. This is the basis for the measurement and calculation of the fecal osmotic gap , a diagnostic test in the evaluation of patients with chronic diarrhea. The fecal osmotic gap estimates the difference between luminal osmolality and the osmolality of luminal contents contributed by fecal electrolytes. Luminal osmolality is approximately equal to body fluid osmolality (290 mosm/kg H2O) since the colon cannot maintain an osmotic gradient against plasma. Furthermore, fecal osmolality may be measured directly but this measurement should NOT be used in the calculation of the fecal osmotic gap: fecal osmolality begins to rise almost immediately as it sits in the collection container. This rise is due to monosaccharide conversion by bacterial fermentation to several osmotically active organic acids. The osmolality of luminal contents contributed by fecal electrolytes is calculated by multiplying the sum of the Na+ and K+ concentrations measured in a stool sample by 2 (to account for the anions that accompany these cations). Therefore: + + Fecal osmotic gap = 290 mosm/kg H2O – 2 ([Na ] + [K ]) mmol/L In patients with pure osmotic diarrhea the fecal osmotic gap should be large (> 125 mosm/kg H2O). In patients with secretory diarrhea (see Table 1) the osmotic gap should be small (<50 mosm/kg H2O). Measurement of the pH of feces may also be helpful in assessing osmotic diarrhea. Carbohydrate induced diarrhea, such as lactase deficiency, typically has a low pH whereas magnesium induced diarrhea has a high pH. The hydrogen breath test (also occasionally utilized in the assessment of bacterial overgrowth syndrome, discussed below) may be used to detect lactose intolerance. A oral dose of lactose is administered and, in patients with lactase deficiency, excess H2 is produced by colonic bacterial fermentation of the unabsorbed carbohydrate. H2 diffuses into the general circulation and is liberated in expired air. In general, a rise of over 20 ppm (parts per million) in exhaled hydrogen at 3­6 hours after ingestion of the substrate is abnormal. Important examples of osmotic diarrhea include lactose malabsorption and ingestion of excess magnesium as in magnesium hydroxide. Lactose intolerance is due to congenital or, more commonly, acquired deficiency in the brush border disaccharidase lactase. This leads to malabsorption of lactose – the sugar contained in dairy products. Lactose remains in the intestinal lumen and acts as a strong osmotic substance. This leads to symptoms of flatulence, bloating, and diarrhea. Lactase deficiency is particularly common in Asians, African­ Americans, Native Americans, Jews, Hispanics, Southern Europeans, and Mediterraneans. Over one­half of the world's population is affected. Lactose intolerance is treated by avoidance of lactose containing foods and/or supplementing oral intake of dairy products with liquid or tablet form of the lactase enzyme. 2.3. Malabsorption, Maldigestion, and Fatty Diarrhea Abnormalities of absorption may have several pathophysiologic mechanisms as outlined below. Although all three major nutrients (fat, carbohydrate, and protein) may be malabsorbed, clinical symptoms usually only develop with carbohydrate and fat malabsorption. Some disorders that cause fat, carbohydrate, and protein malabsorption may not cause diarrhea. The student is directed to the review section on normal physiology of digestion and absorption prior to studying this section. 1. Luminal Phase 1. Reduced nutrient availability 1. Cofactor deficiency 2. Nutrient consumption 2. Impaired fat solubilization 1. Reduced bile salt 2. Impaired bile salt secretion 3. Bile salt inactivation 4. Impaired CCK release 5. Increased bile salt losses 3. Defective nutrient hydrolysis 1. Lipase ocw.tufts.edu/Content/48/lecturenotes/571075 3/8 7/20/12 PPY 222 Gastrointestinal Pathophysiology, Spring 2007 - Tufts OpenCourseWare 2. Enzyme deficiency 3. Improper mixing or rapid transit 2. Mucosal Phase 1. Extensive
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