Malabsorption protein losing enteropathy

Malabsorption

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* Malabsorption
Clinical syndrome associated with diminished intestinal absorption of one or more dietary nutrients

Malabsorption

Pathophysiology Premucosal (luminal) factors Mucosal factors Postmucosal (lymphatic obstruction)
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Malabsorption

causes Intraluminal maldigestion pancreatic exocrine insufficiency Chronic pancreatitis Cancer of pancreas Cystic fibrosis bacterial overgrowth bariatric surgery biliary disease
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Malabsorption

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Malabsorption

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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
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Malabsorption
Approach to the Patient History and examination limit extensive, ill-focused, and expensive laboratory and imaging studies
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Malabsorption

Investigations Test to confirm malabsorption Routine tests Haematology Microcytic anaemia (iron deficiency) Macrocytic anaemia (folate or B12 deficiency) Increased prothrombin time (vitamin K deficiency) Biochemistry Hypoalbuminaemia Hypocalcaemia Hypomagnesaemia Deficiencies of phosphate, zinc
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Malabsorption
Specific tests Fat malabsorption Stool fat collection (24 hr > 7 g) sudan black test ( qualitative test)
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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)
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Malabsorption

B12 absorption (Schilling Test) 58Co-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
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Malabsorption

Radiologic Examination flocculation segmentation mucosal abnormality dilation of intestine anatomical abnormalities strictures and fistulas (Crohn's disease) blind loop syndrome (jejun. diverticula)
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Malabsorption

Determine the cause Small bowel biopsy Barium follow-through Pancreatic exocrine assessment Ultrasound, CT and MRCP EUS (endoscopic US)


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Malabsorption

Malabsorption

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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

Malabsorption

Malabsorption

Malabsorption

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 anaemiaPartial gastrectomyLong-term PPI therapy Impaired intestinal motility SclerodermaDiabetic autonomic neuropathyChronic intestinal pseudo-obstruction Structural abnormalities Gastric surgery (blind loop after Billroth II operation)Jejunal diverticulosisEnterocolic 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

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.