Transcript Disorders of Absorption: Introduction

Disorders of Absorption
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
Classification of Malabsorption Syndrome
Inadequate digestion:
A.
•
•
•
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.
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
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
Approach to the Patient with
Malabsorption
Clinical Evaluation
Diarrhea- duration, consistency, frequency
Weight loss
Bloating & flatulence
Abdominal pain
Previous abdominal surgery
Medication
Alcohol intake
DM
Clinical Examination
Evidence of weight loss
Signs of anaemia
Features of specific nutrient deficiency.
Angular Cheilosis
Deficiencies:
Vitamin B-12
Iron
Folate
B vitamins
Glossitis
Deficiencies of:
Vitamin B-12
Iron
Folate
Niacin
Red tongue with burning sensation
B-12 deficiency with hypersegmented PMNs
Zinc Deficiency
Acrodermatitis
Initial Lab Finding
Serum albumin
Stool fat
Serum carotene
Serum ca, alk.phos.
Mineralization of bone
Prothrombin time
Serum folate or vit B12
Serum iron
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.
EPIDEMIOLOGY
 Epidemiological studies using these tests with
biopsy verification established higher prevalences
of 1:300 to 1:500 in most countries.
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
Clinical Manifestations of Coeliac
Disease
Weight loss
Abdominal discomort
Bloating
Diarrhea
Steatorrhea
Anemia symptoms
malabsorption
Osteopenic bone disease
WHO SHOULD BE TESTED
 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.
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
Stereomicroscopic view of
small bowel biopsies:
Normal (below)
Celiac sprue (right)
Small Bowel Biopsies
Normal
Celiac Sprue
Villi and mature enterocytes destroyed
Deep crypts (arrows)
Inflammation
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.
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
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 highcarbohydrate to minimize the diarrhea from fatty
acid stimulation of colonic fluid secretion.
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
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
Diagnosis
 Bacterial overgrowth is best established by
a Schilling test, which should be abnormal
following the administration of 58Colabeled 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.
Diagnosis
 Breath hydrogen testing or lactulose
(nondigestible disaccharide) administration
has also been used to detect bacterial
overgrowth.
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
Chronic Pancreatitis
Often due to long-standing alcohol use
Chronic Pancreatitis: Manifestations
Weight loss
Abdominal pain
Bulky, oily stool
Fat soluble vitamin deficiency may occur in long-standing
severe cases
Bile duct
Pancreatic duct
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
Tests for steatorrhea
Fecal elastase test
72hr stool fat collection
> 6gm/day – pathologic
Patients with steatorrhea - >20gm/day
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
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
Whipple's Disease: Treatment

 The current drug of choice is double-strength
trimethoprim/sulfamethoxazole for approximately 1 year.
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
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
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
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
Protein-Losing Enteropathy: Treatment
 Treatment should be directed primarily to the
underlying disease process and not to the
hypoproteinemia.