MALABSORPTIONGROUP A

MALABSORPTION SYNDROME Diminished intestinal absorption of one or

more dietary nutrients Not an adequate final diagnosis Most are associated with steatorrhea

Increase in stool fat excretion of >6% dietary fat intake

APPROACH TO THE PATIENTMalabsorption

HISTORY, SYMPTOMS AND INITIAL PRELIMINARY OBSERVATION Extensive small-intestinal resection for

mesenteric ischemia Short bowel syndrome

Steatorrhea with chronic alcohol intake and chronic pancreatitis Pancreatic exocrine dysfunction

ACTIVE TRANSPORT OF SITE-SPECIFIC DIETARY NUTRIENT ABSORPTION Throughout SI (Proximal>Distal)

Glucose, amino acids, lipids Proximal SI (esp. duodenum)

Calcium IronFolate

IleumCobalaminBile acids

ADAPTATION Morphologic and functional Due to segmental resection Secondary to the presence of luminal

nutrients and hormonal stimuli Critical for survival

STEATORRHEA Quantitative stool fat determination (72

hours)Gold standard

Qualitative Sudan III stainDoes not establish degree of fat

malabsorptionFor preliminary screening studies

Blood, breath, and isotropic testDo not directly measure fat absorptionExcellent sensitivity only with obvious

steatorrheaNot survived transition from research

laboratory to commercial application

LABORATORY TESTING Vitamin D malabsorption

Evidence of metabolic bone disease Elevated serum ALP Reduced serum calcium

Vitamin K malabsorption Elevated prothrombin time Without liver disease No intake of anti-coagulants

LABORATORY TESTING Cobalamin/Folate malabsorption

Macrocytic anemia Iron malabsorption

Iron deficiency anemia No occult bleeding from GIT Non-menstruating female Exclusion of celiac sprue

Iron is absorbed in the proximal SI

DIAGNOSTIC PROCEDURESMalabsorption

DIAGNOSIS OF MALABSORPTION Effect of prolonged (>24h) fasting on stool

output Osmotic diarrhea

Decrease in stool output: Presumptive evidence that diarrhea is related to malabsorption

Secretory diarrhea Persistence of stool output: Not due to nutrient

deficiency

STOOL OSMOTIC GAP

Normal: 290-300 mosmol/kg H20 Significant osmotic gap

Suggests the presence of anions other than Na and K are present in the stool, presumably the cause of diarrhea

Diff >50: osmotic gap present, dietary nutrient is not absorbed

Diff <25: dietary nutrient is not responsible for the diarrhea

Useful in differentiating secretory from osmotic diarrhea

2 x (stool [Na+] + [stool K+]) ≤ stool osmolality

Schilling Test Urinary D-Xylose Test

Radiologic Examination

Use

-determine the cause for cobalamin malabsorption-assess the integrity of stomach, pancreas, and colon

-test for carbohydrate absorption-assessment of proximal small-intestinal mucosal function

-evaluation of the patient with presumed or suspected malabsorption

Procedure-performed by administering 58Co-labeled cobalamin orally and collecting urine for 24 h

- performed by giving 25 g D-xylose and collecting urine for 5 h

-performed with the examination of the esophagus to duodenal bulb-insufficient barium is given to the patient

AbnormalFindings

<10% excretion in 24 h <4.5 g excretion

Ex. strictures & fistulas (Crohn’s disease),

Disadvantage

- infrequently performed because of the unavailability of human intrinsic factor

- diminished use due to ease of obtaining a mucosal biopsy by endoscopy and false-negative rate

-abnormalities are rarely seen with current barium suspensions, skilled personnel required

COBALAMIN ABSORPTION

SCHILLING TEST Pernicious Anemia

Atrophy of gastric parietal cells lead to absence of gastric acid and intrinsic factor secretion

Chronic Pancreatitis Deficiency of pancreatic proteases to split the

cobalamin-R binder complex Achlorydia

Absence of another factor secreted with acid that is responsible for splitting cobalamin from the proteins in food

Bacterial Overgrowth syndromes Bacterial utilization of cobalamin

Ileal dysfunction Impaired cobalamin – intrinsic factor uptake

SCHILLING TEST58Co-Cbl 

With Intrinsic Factor

With Pancreatic Enzymes

After 5 Days of Antibiotics

Pernicious anemia Reduced Normal Reduced Reduced

Chronic pancreatitis Reduced Reduced Normal Reduced

Bacterialovergrowth Reduced Reduced Reduced Normal

Ileal disease Reduced Reduced Reduced Reduced

BIOPSY OF SMALL-INTESTINAL MUCOSA Essential in the evaluation of a patient with

documented steatorrhea or chronic diarrhea

Preferred method to obtain histologic material of proximal small-intestinal mucosa

Indications: Evaluation of a patient either with documented

or suspected steatorrhea or with chronic diarrhea

Diffuse or focal abnormalities of the small intestine defined on a small-intestinal series

BIOPSY LESIONS AND FINDINGS

RESULTS OF DIAGNOSTIC STUDIES IN DIFFERENT CAUSES OF STEATORRHEA

D-Xylose Test  Schilling Test Duodenal Mucosal Biopsy

Chronic pancreatitis Normal 50% abnormal; if abnormal, normal with pancreatic enzymes

Normal

Bacterial overgrowth syndrome

Normal or only modestly abnormal

Often abnormal; if abnormal, normal after antibiotics

Usually normal

Ileal disease Normal Abnormal NormalCeliac sprue Decreased Normal Abnormal:

probably "flat"Intestinal lymphangiectasia

Normal Normal Abnormal: "dilated lymphatics"

DIFFERENTIAL DIAGNOSIS FOR CHRONIC DIARRHEA: APPROACH TO A PATIENT WITH MALABSORPTION

DISEASE ENTITIES CAUSING MALABSORPTION

CELIAC SPRUE Other names:

Nontropical sprue, Celiac disease, gluten-sensitive enteropathy

Etiology is not known Environmental – gliadin-associated Immunologic – IgA antigliadin, IgA antiendomysial, IgA

anti-tTg antibodies Genetic – HLA-DQ2 allele

Protean manifestations most of which are secondary to nutrient malabsorption

Onset of symptoms occur at ages ranging from first year of life to eighth decade

Clinical manifestations: Appear with the introduction of cereals in an infants

diet ranges from significant malabsorption to multiple

nutrients, diarrhea, steatorrhea, weight loss, consequences of nutrient depletion to absence of any GI symptoms but with evidence of a single nutrient depletion

Hallmark: malabsorption and histologic changes

Mechanism of diarrhea: Steatorrhea Secondary lactase deficiency Bile acid malabsorption Endogenous fluid secretion

Associated diseases: Dermatitis herpetiformis (DH) DM type 1 IgA deficiency

Complications: GI and non GI neoplasms Intestinal ulceration Refractory sprue Collagenous sprue

TROPICAL SPRUE Affects 5-10% of population in some tropical

area Etiology and pathogenesis is uncertain Clinical manifestations:

Chronic diarrhea Steatorrhea Weight loss Folate and cobalamin deficiencies

SHORT BOWEL SYNDROME General term for

digestive problems that occur after a resection

Depends on Segment resected Length of segment Presence of ileocecal

valve Extent of colon removal Residual disease

Generally, need to lose 2/3 of intestine

Usually acquired Can be congenital in

children Congenital short bowel

After resection, intestine undergoes adaptation.

SHORT BOWEL SYNDROME

Diarrhea Steatorrhea Possibility of

hyperoxaluria Increase in gallstone

risk Increase in gastrin

levels

Removal of Ileum Bile unabsorbed Stimulates colonic fluid and

electrolyte secretion Removal of ileocecal valve

Bacterial overgrowth Decrease in intestinal time

Removal of intestinal mucosa Lactose intolerance Lipid, fluid and electrolytes

are not absorbed

Clinical Presentation Pathophysiology

SHORT BOWEL SYNDROME KEY POINTS Follows resection of intestines Generally inadequacy in absorbing food and

fluids because of lack of surface area

BACTERIAL OVERGROWTH SYNDROME Proliferation of colonic type bacteria within

small intestine Clinical Manifestation

DiarrheaSteatorrheaMacrocytic anemia

BACTERIAL OVERGROWTH SYNDROMEPathogenesis Etiology

BACTERIAL OVERGROWTH SYNDROME KEY POINTS

Macrocytic anemia Because of lack of B12

Stasis = allows bacteria to multiply

WHIPPLE’S DISEASE Insidious in presentation Chronic multisystem disease Usually causesClinical Manifestation

DiarrheaSteatorrheaWeight lossAbdominal painArthralgiaCNS/ cardiac problems

WHIPPLE’S DISEASE

More common in men Middle aged caucasian

men Fatal if left untreated

T. whipplei Gram negative Rod shaped Presence of PAS (+)

macrophages in SI lamina propria

Steatorrhea caused by SI mucosal injury Lymphatic obstruction

Epidemiology Etiology and Pathogenesis

WHIPPLE’S DISEASE KEY POINTS Rare, SYSTEMIC disease Insidious CNS and cardiac symptoms

Dementia = POOR prognosis Caused by damage to mucosa and lymphatic

obstruction

PROTEIN LOSING ENTEROPATHY Group of diseases with Hypoproteinemia and

edema WITHOUT Proteinuria/ kidney problems Protein synthesis defects/ liver problems

Clinical Manifestation Peripheral edema Diarrhea Steatorrhea

PROTEIN LOSING ENTEROPATHY

Excess protein loss in the GI tract Exceeds the normal

10% protein catabolism

Pathogenesis Etiology

PROTEIN LOSING ENTEROPATHY KEY POINTS Peripheral edema, hypoproteinemia More than >10% total protein breakdown Proteins lost through exudates, altered

permeability, lymphatic obstruction

TREATMENT

Disease Entity TreatmentCeliac Sprue Complete dietary gluten restriction

Dietary lactose and fat restriction for more severe cases

Tropical Sprue Broad spectrum antibiotics and folic acidTetracycline for 6 months

Short Bowel Syndrome Opiates (codeine), Low fat high, high carbohydrate dietFat soluble vitamins, folate, cobalamin, calcium, iron, magnesium, zinc

Bacterial Overgrowth Syndrome Surgical correction on the anatomical blind loopBroad- spectrum antibiotics: Tetracycline, metronidazole, amoxicillin/clavulanic acid and cephalosporins

Whipple’s disease Double strength trimethoprin/sulfamethoxazole for 1 yearAlt: chloramphenicol

Protein losing enteropathy Treat the underlying disease processLow fat diet and MCT’s for the treatment of hypoproteinemia