Malabsorption syndromes occur when nutrients are not properly absorbed in the small intestine, leading to deficiencies. Common symptoms include chronic diarrhea and steatorrhea, or excess fat in stool. Malabsorption can result from problems with intraluminal digestion by pancreatic enzymes or bile acids, defects in brush border enzymes, or issues with transcellular transport. Treatment focuses on correcting nutritional deficiencies through supplementation or parenteral nutrition, as well as treating any underlying diseases causing the malabsorption.
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Malabsorption syndromes
1. Malabsorption Syndromes
Definition: defective absorption of fats, vitamins,
proteins, carbohydrates, electrolytes and minerals, and water.
*The most common presentation is chronic diarrhea
*The hallmark of malabsorption syndromes is steatorrhea
Steatorrhea: increase fat in stool-bulky-greasy and yellow or grey in color
Pathophysiology: Malabsorption is the result of disturbance of:
1-Intraluminal digestion: where enzymes break down the nutrients for absorption
due to : *pancreatic insufficiency
*cholestatic liver disease
*intestinal bacterial overgrowth
*Extensive ileal resection
*inflammatory bowel disease
Diarrhea: is a result of:
1-unabsorbed substance osmotic defect
2- or increase in intestinal execration
Steatorrhea: is a result of:
1- absence or defect in bile
2- or defect in pancreatic lipase
2-Terminal digestion: the hydrolysis of carbs and peptide by disaccharidase
and peptidase in brush border of small intestine mucosa.
When there is a defect this lead to lactose intolerance.
1- Small intestine doesn't produce enough lactase to digest lactose.
2-Lactose in food moves into the colon instead of being processed
and absorbed.
3-In the colon, normal bacteria interact with undigested lactose,
causing the signs and symptoms ((diarrhea - bloating and flatulence).
There are three types of lactose intolerance:
1-primary: Normally the number of the enzyme will
reduced in number when the baby start eating but here it will reduce in
abnormal way.
2-secondry: result of intestinal illness or injury or procedure.
3- Congenital or developmental: complete absence – autosomal recessive – most
serious ( diarrhea - lose of weight).
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2. 3-Transepithelial transport: where the fat be absorbed, if it is:
1- short chain blood
2-long chain transporter protein called (fatty acid binding protein) Smooth
endoplasmic reticulum and it will be triglyceride Golgi apparatus will be
chylomicrons lymphatic.
When there is a defect (mutation in the Microsomal Triglyceride
Transfer Protein (MTP) gene) it leads to rare autosomal recessive disease
characterized by an inability to secrete triglyceride-rich lipoproteins (beta
lipoproteins) triglycerides accumulate within the epithelial cells.
presents in infancy and the clinical pictures is: failure to thrive, diarrhea and
steatorrhea.
Failure to absorb essential fatty acids leads to:
*Deficiencies of fat-soluble vitamins
*There are systemic lipid membrane abnormalities
4-Lymphatic transport of absorbed lipids: the defect is complete absence of
lymphatics because of:
1- congenital.
2- secondary TB.
3- retroperitoneal fibrosis.
Management of Malabsorption Syndromes:
Two basic principles underlie the management of patients with malabsorption:
(1) the correction of nutritional deficiencies
(2) when possible, the treatment of causative diseases.
Nutritional support:
o Supplementing various minerals, such as calcium, magnesium, iron, and
vitamins.
o Caloric and protein replacement.
o Medium-chain triglycerides can be used as fat substitutes because they do
not require micelle formation for absorption and their route of transport is
portal rather than lymphatic.
o In severe intestinal disease, such as massive resection and extensive
regional enteritis, parenteral nutrition may become necessary.
Treatment of causative diseases:
o A gluten-free diet helps treat celiac disease.
o Similarly, a lactose-free diet helps correct lactose intolerance.
o lipase supplements are the therapy for pancreatic insufficiency.
o Antibiotics are the therapy for bacterial overgrowth.
References:
* Robbins basic pathology book.
*Medscape.com.
Norah alfayez
436019528