1. Disorders of Absorption

2. INTRODUCTION Broad spectrum of conditions with multiple etiologies and varied clinical manifestations. Almost all of these clinical problems are associated with diminished intestinal absorption of one or more dietary nutrients and are often referred to as the malabsorption syndrome

3. Classification of Malabsorption Syndrome A. Inadequate digestion: Postgastrectomy steatorrhea. Exocrine Pancreatic insufficiency. Reduced bile salt concentration in intestine: I.) Liver Disease II.) Cholestasis III.) Bacterial over growth IV.) Interruption of enterohepatic circulation of bile salt.

4. B. Inadequate absorptive surface: Resection Diseased intestine C. Lymphatic obstruction. e.g Lymphoma D. Primary mucosal defects. Crohn ’ s disease Coeliac disease Tropical Sprue Disaccharide Deficiency Lymphoma TB

5. Signs & symptoms Calori Weight loss with normal appetite Fat Pale,voluminous,greasy offensive diarrhea Protein Edema, muscle atrophy, amenorrhea carbohydrate Abdominal bloating, flatus, w. diarrhea B12 Macrocytic anemia Subacut combined degeneration of sp.cord Folic acid Macrocytic anemia Vit B (general) Cheliosis, glossitis,A.stomatitis, Acrodermatitis Iron Microcytic anemia Ca & Vit D Osteomalacea (bone pain,pathologic#), Tetany Vit A Follicular hyperkeratosis, Night blindness VIt K Bleeding diathesis, Hematoma

6. Approach to the Patient with Malabsorption

7. Clinical Evaluation Diarrhea- duration, consistency, frequency Weight loss Bloating & flatulence Abdominal pain Previous abdominal surgery Medication Alcohol intake DM

8. Clinical Examination Evidence of weight loss Signs of anaemia Features of specific nutrient deficiency.

9. Angular Cheilosis Deficiencies: Vitamin B-12 Iron Folate B vitamins

10. Glossitis Deficiencies of: Vitamin B-12 Iron Folate Niacin

11. Red tongue with burning sensation B-12 deficiency with hypersegmented PMNs

12. Zinc Deficiency Acrodermatitis

13. Initial Lab Finding Serum albumin Stool fat Serum carotene Serum ca, alk.phos. Mineralization of bone Prothrombin time Serum folate or vit B 12 Serum iron

14. Urinary D-Xylose Test The urinary D-xylose test for carbohydrate absorption provides an assessment of proximal small-intestinal mucosal function. D-Xylose, a pentose, is absorbed almost exclusively in the proximal small intestine. The D-xylose test is usually performed by giving 25 g D-xylose and collecting urine for 5 h. An abnormal test (<4.5 g excretion) primarily reflects the presence of duodenal/jejunal mucosal disease.

16. EPIDEMIOLOGY Epidemiological studies using these tests with biopsy verification established higher prevalences of 1:300 to 1:500 in most countries.

17. Etiology An immunologic component to etiology is suspected. Serum antibodies—IgA antigliadin, IgA antiendomysial, and IgA anti-tTG antibodies—are present, but it is not known whether such antibodies are primary or secondary to the tissue damage

18. Clinical Manifestations of Coeliac Disease Weight loss Abdominal discomort Bloating Diarrhea Steatorrhea Anemia symptoms malabsorption Osteopenic bone disease

20. WHO SHOULD BE TESTED

21. Gastrointestinal symptoms: chronic diarrhea, malabsorption, weight loss, and abdominal distension. Unexplanations signs and symptoms : persistent elevation in serum aminotransferases, short stature, delayed puberty, iron-deficiency anemia, recurrent fetal loss, and infertility.

22. Positive predictive value of serum tests for celiac disease based upon 4615 adults in Northern Italy Serum test : IgAantiendomysium IgG antigliadin IgA antigliadin IgG and IgA antigliadin Probability*, percent 100 2 12 33

24. Stereomicroscopic view of small bowel biopsies: Normal (below) Celiac sprue (right)

25. Normal Small Bowel Biopsies Celiac Sprue Villi and mature enterocytes destroyed Deep crypts (arrows) Inflammation

26. Tropical Sprue Affects both expatriates and natives in certain but not all tropical areas and is manifested by chronic diarrhea, steatorrhea, weight loss, and nutritional deficiencies, including those of both folate and cobalamin. This disease affects 5–10% of the population in some tropical areas.

27. Short Bowel Syndrome The factors that determine both the type and degree of symptoms include: the specific segment (jejunum vs ileum) resected the length of the resected segment residual disease in the remaining small (e.g., Crohn's disease, mesenteric artery disease) the degree of adaptation in the remaining intestine

28. Treatment Treatment of short bowel syndrome depends on the severity of symptoms and whether the individual is able to maintain caloric and electrolyte balance with oral intake alone. Initial treatment includes judicious use of opiates (including codeine) to reduce stool output and to establish an effective diet. An initial diet should be low-fat and high- carbohydrate to minimize the diarrhea from fatty acid stimulation of colonic fluid secretion.

29. Bacterial Overgrowth Syndrome Bacterial proliferation is due to stasis caused by impaired peristalsis (functional stasis) Changes in intestinal anatomy (anatomic stasis), direct communication between the small and large intestine. These conditions have also been referred to as stagnant bowel syndrome or blind loop syndrome

30. Features Macrocytic anemia is due to cobalamin, not folate, deficiency. Most bacteria require cobalamin for growth, and increasing concentrations of bacteria use up the relatively small amounts of dietary cobalamin. Steatorrhea is due to impaired micelle formation as a consequence of a reduced intraduodenal concentration of conjugated bile acids and the presence of unconjugated bile acids.Certain bacteria, e.g., Bacteroides, deconjugate conjugated bile acids to unconjugated bile acids

31. Diagnosis Bacterial overgrowth is best established by a Schilling test, which should be abnormal following the administration of 58 Co- labeled cobalamin, with or without the administration of intrinsic factor. Following the administration of tetracycline for 5 days, the Schilling test will become normal, confirming the diagnosis of bacterial overgrowth.

32. Diagnosis Breath hydrogen testing or lactulose (nondigestible disaccharide) administration has also been used to detect bacterial overgrowth.

33. Treatment bacterial overgrowth secondary to strictures, one or more diverticula, or a proximal afferent loop can potentially be cured by surgical correction of the anatomical state. In contrast, the functional stasis of scleroderma or certain anatomical stasis states (e.g., multiple jejunal diverticula), cannot be corrected surgically, and these conditions should be treated with broad-spectrum antibiotics

34. Chronic Pancreatitis Often due to long-standing alcohol use

35. Chronic Pancreatitis: Manifestations Weight loss Abdominal pain Bulky, oily stool Fat soluble vitamin deficiency may occur in long-standing severe cases

36. Bile duct Pancreatic duct

37. ERCP view of Chronic Pancreatitis Endoscopic Retrograde CholangioPancreatography Single arrow points to bile duct compressed by fibrotic pancreas Double arrow points to dilated pancreatic duct with short stubby side branches

38. Tests for steatorrhea Fecal elastase test 72hr stool fat collection > 6gm/day – pathologic Patients with steatorrhea - >20gm/day

39. Whipple's Disease Whipple's disease is a chronic multisystem disease associated with diarrhea, steatorrhea, weight loss, arthralgia, and central nervous system (CNS) and cardiac problems

40. Whipple's Disease It is caused by the bacteria Tropheryma whipplei. Until the identification of T. whipplei by polymerase chain reaction, the hallmark of Whipple's disease had been the presence of PAS-positive macrophages in the small intestine and other organs with evidence of disease

41. Whipple's Disease: Treatment The current drug of choice is double-strength trimethoprim/sulfamethoxazole for approximately 1 year.

42. Protein-Losing Enteropathy These diseases are characterized by excess protein loss into the gastrointestinal tract. Normally, about 10% of total protein catabolism occurs via the gastrointestinal tract

43. Protein-Losing Enteropathy Mucosal ulceration, such that the protein loss primarily represents exudation across damaged mucosa, e.g., ulcerative colitis, gastrointestinal carcinomas, and peptic ulcer; Non ulcerated mucosa, but with evidence of mucosal damage so that the protein loss represents loss across epithelia with altered permeability, e.g., celiac disease

44. Protein-Losing 3) lymphatic dysfunction, representing either primary lymphatic disease or secondary to partial lymphatic obstruction that may occur as a result of enlarged lymph nodes or cardiac disease

45. Diagnosis The diagnosis of protein-losing enteropathy is suggested by the presence of peripheral edema and low serum albumin and globulin levels in the absence of renal and hepatic disease. It is extremely rare for an individual with protein- losing enteropathy to have selective loss of only albumin or only globulins

46. Protein-Losing Enteropathy: Treatment Treatment should be directed primarily to the underlying disease process and not to the hypoproteinemia.