Malabsorption

6/10/2016 add footer here (go to view menu and choose header) 2 Malabsorption Clinical syndrome associated with diminished intestinal absorption of one or more dietary nutrients

Malabsorption Pathophysiology Premucosal (luminal) factors Mucosal factors Postmucosal (lymphatic obstruction) 6/10/2016 add footer here (go to view menu and choose header) 3

Malabsorption causes Intraluminal maldigestion pancreatic exocrine insufficiency Chronic pancreatitis Cancer of pancreas Cystic fibrosis bacterial overgrowth bariatric surgery biliary disease 6/10/2016 add footer here (go to view menu and choose header) 4

Malabsorption Mucosal malabsorption Enteropathy Coeliac disease Tropical sprue Lymphoma Whipple's disease infection (giardiasis) radiation hypogammaglobulinaemia eosinophilic gastroenteritis chronic ischemia 6/10/2016 add footer here (go to view menu and choose header) 5

Malabsorption Post-mucosal obstruction (1° or 2° lymphatic obstruction ) congenital intestinal lymphangiectasia acquired lymphatic obstruction trauma Tumor infection 6/10/2016 add footer here (go to view menu and choose header) 6

Malabsorption Clinical features Normal bowel habit Diarrhoea watery and voluminous. Bulky pale and offensive stools (steatorrhoea) Abdominal distension Borborygmi, cramps Weight loss Undigested food in the stool Symptoms related to deficiencies of specific vitamins, trace elements 6/10/2016 add footer here (go to view menu and choose header) 7

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Malabsorption Approach to the Patient History and examination limit extensive, ill-focused, and expensive laboratory and imaging studies 6/10/2016 add footer here (go to view menu and choose header) 9

Malabsorption Investigations Test to confirm malabsorption Routine tests Haematology Microcytic anaemia (iron deficiency) Macrocytic anaemia (folate or B 12 deficiency) Increased prothrombin time (vitamin K deficiency) Biochemistry Hypoalbuminaemia Hypocalcaemia Hypomagnesaemia Deficiencies of phosphate, zinc 6/10/2016 add footer here (go to view menu and choose header) 10

Malabsorption Specific tests Fat malabsorption Stool fat collection (24 hr > 7 g) sudan black test ( qualitative test) 6/10/2016 add footer here (go to view menu and choose header) 11

Malabsorption Carbohydrate malabsorption (Urinary D-Xylose Test) D-Xylose, is disaccharide 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) 6/10/2016 add footer here (go to view menu and choose header) 12

Malabsorption B12 absorption (Schilling Test) 58 Co-labeled cobalamin orally and collecting urine for 24 h. Urinary excretion of cobalamin assessed. 1 mg cobalamin is administered intramuscularly 1 h following ingestion of the radiolabeled cobalamin. The Schilling test may be abnormal (usually defined as <10% excretion in 24 h) in : – pernicious anemia – chronic pancreatitis, – blind loop syndrome – ileal disease 6/10/2016 add footer here (go to view menu and choose header) 13

Malabsorption Radiologic Examination –flocculation –segmentation –mucosal abnormality –dilation of intestine –anatomical abnormalities strictures and fistulas (Crohn's disease) blind loop syndrome (jejun. diverticula ) 6/10/2016 add footer here (go to view menu and choose header) 14

Malabsorption Determine the cause Small bowel biopsy Barium follow-through Pancreatic exocrine assessment Ultrasound, CT and MRCP EUS (endoscopic US) 6/10/2016 add footer here (go to view menu and choose header) 15

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Malabsorption Nonspecific Diffuse: Celiac sprue Short or absent villi mononuclear infiltrate epithelial cell damage hypertrophy of crypts Tropical sprue Similar to celiac sprue Patchy: Bac. overgrowth Patchy damage to villi lymphocyte infiltration

Malabsorption Specific: Intestinal lymphomaMalignant cells in lamina propria and submucosa Intestinal lymphangiectasia Dilated lymphatics Eosinophilic gastroenteritis Eosinophil infiltration mucosa Infection by microorganisms as giardiasis

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malabsorption CBC, Ca, Ph Albumin, immunogl. Celiac serology Barium image Fat collection D-xylose test Duodenal BX Aspirate culture Pancreatic function test CT abdomen normal

Malabsorption Coeliac disease is an immunologically mediated inflammatory disorder of the small bowel occurring in genetically susceptible individuals and resulting from intolerance to wheat gluten and similar proteins found in, barley, rye and, to a lesser extent, oats The prevalence is approximately 1%

Malabsorption Pathophysiology The precise mechanism of mucosal damage is unclear but immunological responses to gluten play a key role.

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Malabsorption Clinical features In infancy presents diarrhoea failure to thrive In children present delayed growth mild abdominal distension present. short stature

Malabsorption In adults The presentation is highly variable florid malabsorption non-specific symptoms iron deficiency anaemia with or without folate deficiency weight loss atypical presentation oral ulceration dyspepsia and bloating

Malabsorption Diagnosis Haematology microcytic hypochromic macrocytic anaemia dimorphic anaemia hyposplenism (target cells, spherocytes and Howell-Jolly bodies). Biochemical tests calcium, phosphate vitamin D total s. protein, albumin

Malabsorption serology Antigliadin Ab (IgG, IgA) Antiendomysial Ab (IgA) Anti tissue transglutaminase Ab (IgA, IgG)

Malabsorption Endoscopic finding flat doudenal folds or thin Serrated doudenal folds Duodenal biopsy The histological features are characteristic Short or absent villi hypertrophy of crypts mononuclear infiltrate

Malabsorption Important causes of villous atrophy Coeliac disease Tropical sprue Dermatitis herpetiformis Lymphoma AIDS enteropathy Giardiasis Hypogammaglobulinaemia Radiation Whipple's disease Zollinger-Ellison syndrome

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Malabsorption

Disease associations of coeliacdisease Insulin-dependent diabetes mellitus (2-8%) Thyroid disease (5%) Primary biliary cirrhosis (3%) Sjögren's syndrome (3%) IgA deficiency (2%) Pernicious anaemia Inflammatory bowel disease Sarcoidosis Myasthenia gravis Dermatitis herpetiformis Down's syndrome Squamous carcinoma of oesophagus Microscopic colitis Splenic atrophy pancreatic insufficiency

Malabsorption Management Exclusion of wheat, barley, rye Life-long gluten-free diet Correct existing deficiencies Frequent dietary counseling Mineral and vitamin supplements Regular monitoring of symptoms, weight and nutrition is essential

Malabsorption Complications Ulcerative jejuno -ileitis 'refractory' celiac Enteropathy -associated T-cell lymphoma Wt loss abdominal pain anorexia fever Small bowel carcinoma

Malabsorption Poor response  Dietary compliance should be assessed  Exclusion of the other conditions pancreatic insufficiency microscopic colitis complications ulcerative jejunitis T-cell lymphoma.

Malabsorption 'refractory' celiac Persistent symptom and villous atrophy despite GFD  Wt loss  Diarrhea  Abdominal pain  Bleeding  anaemia Dx need more extensive Ix There is role  corticosteroids  immunosuppressive

Malabsorption Tropical sprue Chronic malabsorption in a patient from the tropics, associated with abnormalities of small intestinal structure and function. 5-10% of tropical area popu affected.

Malabsorption Etiology pathogenesis of tropical sprue are uncertain Infective agent often begins after an acute diarrhoeal illness. Isolation of Escherichia coli, Enterobacter and Klebsiella Response to Abs Folic acid deficiency

Malabsorption Clinical features chronic diarrhoea abdominal distension anorexia, fatigue and weight loss features of malabsorption megaloblastic anaemia (folic acid malabsorption) other deficiencies

Malabsorption The course of the disease Remissions and relapses may occur. The differential diagnosis infective cause of diarrhea. giardiasis

Malabsorption Diagnosis  chronic diarrhea plus malabsorption  patient in tropics  small-intestinal mucosal biopsy partial villous atrophy  No response to GFD Management Tetracycline 250 mg 6-hourly with folic acid (5 mg daily) for 28 days is the treatment of choice

Malabsorption Small bowel bacterial overgrowth (blind loop syndrome) group of disorders with diarrhea, steatorrhea, and macrocytic anemia due to the proliferation of colonic-type bacteria within the small intestine The normal duodenum and jejunum contain less than 104/mL organisms

Malabsorption Pathophysiology Disorders which impair the normal physiological mechanisms controlling bacterial proliferation in the intestine causing:  deconjugation of bile acids  bacterial utilisation of vitamin B12.

Malabsorption Etiology Hypo- or achlorhydria Pernicious anaemia Partial gastrectomy Long-term PPI therapy Impaired intestinal motility Scleroderma Diabetic autonomic neuropathy Chronic intestinal pseudo-obstruction Structural abnormalities Gastric surgery (blind loop after Billroth II operation) Jejunal diverticulosis Enterocolic fistulas (e.g. Crohn's disease) Strictures (e.g. Crohn's disease) Impaired immune function Hypogammaglobulinaemia

Malabsorption Clinical features  watery diarrhoea and/or steatorrhoea  anemia due to B12 deficiency  symptoms from the underlying intestinal cause.

Malabsorption Investigations  Barium follow-through may reveal blind loops or fistulas.  Endoscopic duodenal biopsies exclude mucosal disease such as coeliac disease.  Jejunal contents for bacteriological examination can be aspirated at endoscopy  Schilling test abnormal  Serum vitamin B12 concentration is low.

Malabsorption Management  Surgical treatment of the underlying cause  B12 supplementation is needed in chronic cases.  Antibiotics (2-3 weeks)  Tetracycline 250 mg 6-hourly  Metronidazole 400 mg 8-hourly or  ciprofloxacin 250 mg 12-hourly

Malabsorption Short bowel syndrome Short bowel syndrome is defined as malabsorption resulting from resection of various length intestinal small

Malabsorption Features depend on (1) the segment resected (jejunum vs ileum) (2) the length of the resected segment (3) the integrity of the ileocecal valve (4) whether any large intestine has also been removed (5) residual disease in the remaining small and/or large intestine (e.g., Crohn's disease (6) the degree of adaptation in the remaining intestine

Malabsorption Etiology Children Congenital anomalies (e.g. mid-gut volvulus, atresia) Necrotising enterocolitis Adults Mesenteric infarction Crohn's disease Radiation enteritis Volvulus jejunoileal bypass for obesity

Malabsorption Clinical features Diarrhea Steatorrhoea Dehydration and hypovolaemia Weight loss, malnutrition No intestinal symptoms renal calcium oxalate calculi cholesterol gallstones

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Malabsorption Treatment  Enteral feeding can be cautiously introduced after 1-2 weeks under careful supervision  PPI therapy is given to reduce gastric secretions.  Replacement therapy ( VITAMINS)  Rx of the bacterial overgrowth  TPN is needed less than 100 cm of jejunum remains.  Intestinal transplantation

Malabsorption The principles of long-term management Nutritional assessments at regular intervals. Monitoring of fluid and electrolyte balance. Fats are.Medium-chain triglyceride Antidiarrhoeal agents, e.g. loperamide or codeine phosphate low-fat and high-carbohydrate

Protein-Losing Enteropathy group of gastrointestinal and nongastrointestinal disorders with hypoproteinemia and edema in the absence of either proteinuria or defects in protein synthesis in the liver, e.g., chronic liver disease

Protein-Losing Enteropathy Causes With mucosal ulceration Crohn's disease Ulcerative colitis Radiation damage Oesophageal, gastric or colonic cancer Lymphoma

Protein-Losing Enteropathy Without mucosal ulceration Ménétrier's disease Bacterial overgrowth Coeliac disease Tropical sprue Eosinophilic gastroenteritis

Protein-Losing Enteropathy With lymphatic obstruction Intestinal lymphangiectasia Constrictive pericarditis Lymphoma Whipple's disease

Protein-Losing Enteropathy Clinical features Peripheral edema low serum albumin and globulin levels lymphatic obstruction often have steatorrhea and diarrhea and lymphopenia

Protein-Losing Enteropathy Treatment treatment the underlying disease in intestinal lymphangiectasia Treatment of the hypoproteinemia is accomplished by a low-fat diet and the administration of MCTs.