MALABSORPTION
GROUP 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 PATIENT
Malabsorption
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

Glucose, amino acids, lipids
 Proximal



SI (esp. duodenum)
Calcium
Iron
Folate
 Ileum
Cobalamin
 Bile acids

SI (Proximal>Distal)
ADAPTATION
Morphologic and functional
 Due to segmental resection
 Secondary to the presence of luminal nutrients
and hormonal stimuli
 Critical for survival

STEATORRHEA
 Quantitative
hours)

Gold standard
 Qualitative



Sudan III stain
Does not establish degree of fat malabsorption
For preliminary screening studies
 Blood,


stool fat determination (72
breath, and isotropic test
Do not directly measure fat absorption
Excellent sensitivity only with obvious
steatorrhea
Not 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 PROCEDURES
Malabsorption
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
Useful in differentiating secretory from osmotic diarrhea
2 x (stool [Na+] + [stool K+]) ≤ stool
osmolality
 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
Schilling Test
Radiologic
Examination
-test for carbohydrate
absorption
-assessment of proximal
small-intestinal mucosal
function
-evaluation of the
patient with presumed
or suspected
malabsorption
Procedure
-performed by
administering 58Colabeled 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
Abnormal
Findings
<10% excretion in 24 h
<4.5 g excretion
Ex. strictures & fistulas
(Crohn’s disease),
- diminished use due to
ease of obtaining a
mucosal biopsy by
endoscopy and falsenegative rate
-abnormalities are
rarely seen with current
barium suspensions,
skilled personnel
required
Use
-determine the cause
for cobalamin
malabsorption
-assess the integrity of
stomach, pancreas, and
colon
Urinary D-Xylose
Test
- infrequently
performed because of
Disadvantage the unavailability of
human intrinsic factor
COBALAMIN ABSORPTION
Dietary
cobalamin
in meat
Bound to
R-binder
protein in
stomach
Complex
bound in
acid milieu
in the
stomach
Uptake of
cobalamin
in
receptors
in brush
border of
ileal
enterocytes
Pancreatic
protease
enzymes
split
cobalamin
and
binding
protein
Cobalamin
enters the
proximal
small
intestine
and binds
to intrinsic
factor
SCHILLING TEST

Pernicious Anemia


Chronic Pancreatitis


Absence of another factor secreted with acid that is
responsible for splitting cobalamin from the proteins in
food
Bacterial Overgrowth syndromes


Deficiency of pancreatic proteases to split the cobalamin-R
binder complex
Achlorydia


Atrophy of gastric parietal cells lead to absence of gastric
acid and intrinsic factor secretion
Bacterial utilization of cobalamin
Ileal dysfunction

Impaired cobalamin – intrinsic factor uptake
SCHILLING TEST
58Co-Cbl
With
Intrinsic
Factor
With
Pancreatic
Enzymes
After 5
Days of
Antibiotics
Pernicious
anemia
Reduced Normal
Reduced
Reduced
Chronic
pancreatitis
Reduced Reduced
Normal
Reduced
Bacterial
overgrowth
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
Chronic pancreatitis Normal
Bacterial
overgrowth
syndrome
Ileal disease
Celiac sprue
Normal or only
modestly
abnormal
Normal
Decreased
Intestinal
lymphangiectasia
Normal
Schilling Test
Duodenal
Mucosal
Biopsy
Normal
50% abnormal; if
abnormal, normal
with pancreatic
enzymes
Often abnormal; if Usually normal
abnormal, normal
after antibiotics
Abnormal
Normal
Normal
Abnormal:
probably "flat"
Normal
Abnormal:
"dilated
lymphatics"
DIFFERENTIAL DIAGNOSIS FOR CHRONIC
DIARRHEA: APPROACH TO A PATIENT WITH
MALABSORPTION
CC: Diarrhea 1
month duration
Prolonged fast
(>24h)
Osmotic Diarrhea (>50
osmotic gap difference)
Secretory Diarrhea (<25
osmotic gap difference)
Diagnostic Procedures
i.e. biopsy of SI, Schilling
test
Diagnosis: Cause of
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
Clinical Presentation
Diarrhea
 Steatorrhea
 Possibility of
hyperoxaluria
 Increase in gallstone risk
 Increase in gastrin levels

Pathophysiology

Removal of Ileum



Removal of ileocecal valve



Bile unabsorbed
Stimulates colonic fluid and
electrolyte secretion
Bacterial overgrowth
Decrease in intestinal time
Removal of intestinal
mucosa


Lactose intolerance
Lipid, fluid and electrolytes
are not absorbed
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
Diarrhea
 Steatorrhea
 Macrocytic anemia

BACTERIAL OVERGROWTH SYNDROME
Pathogenesis
Macrocytic
Anemia
Steatorrhea
Etiology
•Cobalamin deficiency
•Increased bacteria =
use more B12
•Impaired micelle
formation
Anatomical
Stasis
Direct
Communication
between SI and
LI
Functional
Stasis
Bacterial
Overgrowth
Diarrhea
•Due to steatorrhea
•Due to bacterial
enterotoxins
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 causes
 Clinical Manifestation






Diarrhea
Steatorrhea
Weight loss
Abdominal pain
Arthralgia
CNS/ cardiac problems
WHIPPLE’S DISEASE
Epidemiology

More common in men


Etiology and Pathogenesis

Middle aged caucasian
men
T. whipplei
Gram negative
 Rod shaped
 Presence of PAS (+)
macrophages in SI
lamina propria

Fatal if left untreated

Steatorrhea caused by
SI mucosal injury
 Lymphatic obstruction

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
Pathogenesis

Etiology
Excess protein loss in
the GI tract

Exceeds the normal
10% protein
catabolism
Non ulcerated
mucosa
group; altered
permeability
Mucosal
Ulceration
Group
Lymphatic
dysfunction
Protein
Losing
enteropathy
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
Treatment
Celiac Sprue
Complete dietary gluten restriction
Dietary lactose and fat restriction for more severe cases
Tropical Sprue
Broad spectrum antibiotics and folic acid
Tetracycline for 6 months
Short Bowel Syndrome
Opiates (codeine),
Low fat high, high carbohydrate diet
Fat soluble vitamins, folate, cobalamin, calcium, iron,
magnesium, zinc
Bacterial Overgrowth Syndrome
Surgical correction on the anatomical blind loop
Broad- spectrum antibiotics: Tetracycline, metronidazole,
amoxicillin/clavulanic acid and cephalosporins
Whipple’s disease
Double strength trimethoprin/sulfamethoxazole for 1 year
Alt: chloramphenicol
Protein losing enteropathy
Treat the underlying disease process
Low fat diet and MCT’s for the treatment of hypoproteinemia