Liver & GIT
Which of the following parasitic infestation can lead to malabsorption syndrome? (LQ)
Malabsorption of Lipids –
Physiology of the digestion and absorption of lipids have 3 phases –
1. Intraluminal phase 2. Mucosal phase 3. Post absorptive phase
1. Intraluminal phase-It has two components-lipolysis and micellar formation. Lipolysis is done in stomach(20-30%) by gastric lipase and in duodenum and proximal jejunum by pancreatic lipase.
Impaired lipolysis occur due to pancreatic insufficiency ( decrease pancreatic lipase )
Or due to inactivation of pancreatic lipase which is inactivated at pH<7 in patient with gastrinoma.
Micelles formation occur in duodenum and jejunum with the help of bile acids. Impaired micelles formation occur when there is decreased intra duodenal bile acids. The causes of decreased intra duodenal bile acids are –
a. Decreased synthesis –e.g. cirrhosis
b. Decreased biliary secretion – e.g. Primary biliary cirrhosis.
c. Decreased conjugated bile acids e.g. Bacterial overgrowth syndrome.
d. Decreased reabsorption e.g. ileal disease, Crohn’s disease.
2. Mucosal phase- It involve the mucosal uptake and re esterification of fatty acids and monoglycerides to form triglycerides. Impaired uptake and esterification occur in mucosal inflammation ( e.g. coeliac sprue ) and intestinal resection.
3. Post-absorptive phase-It involve the formation of chylomicrons in the small intestine epithelial cell and their transportation to the liver via the lymphatic.
Impaired chylomicron formation occur in abetalipoproteinemia while impaired delivery from intestine occur in intestinal lymphangiectasia.
Malabsorption of Carbohydrates –
1. Lactose malabsorption-It occur due to lactase deficiency.
a. Primary lactase deficiency- Genetically absent / decrease lactase. Other enzymes are normal.
b. Secondary lactase deficiency- occur in association with small-intestine mucosal disease with abnormalities in structure and function of other brush border enzymes and transport process e.g. celiac sprue.
2. Monosaccharide malabsorption – It is due to congenital absence of SGLT. Diarrhea occur due to ingestion of glucose, galactose ( as these are activity transported monosaccharide ) and not due to fructose
( which is not actively transported ).
Malabsorption of proteins –
The proteolysis occur in both the stomach and small intestine by pepsin and trypsinogen respectively.
The disorders of protein absorption are mainly genetic including.
a. Enterokinase deficiency– Due to absence of brush border enzyme that convert proenzyme trypsinogen to trypsin and is associated with diarrhea, growth retardation and hypoproteinemia.
b. Hartnup syndrome- It is due to defect in neutral amino-acid transport and is associated with pellagra like rash and neuropsychiatric symptoms.
c. Cystinuria- It is due to defect in dibasic amino acid transport and is associated with renal calculi and chronic pancreatitis
Test for malabsorption –
Mal absorbed nutrient Laboratory finding
(1) Fat Quantitative -72 hr stool fat on a defined diet ( >6% of fat intake )
Qualitative – Sudan III stain
(2) Carbohydrate (a) D-Xylose test -25 gram D-xylose given orally, and urine is collected for
5 hrs. It is abnormal when there is <4.5 gm excretion.
(b) Lactose tolerance test- Oral lactose is given which is followed by a little
rise in blood glucose level. Also abdominal discomfort and diarrhea occur.
(3) Protein (a) Decreased serum albumin
(b) Fecal nitrogen –False–ve due to bacteria
(c) Measuring focal radioactivity after giving radioactive protein.
(d) α1 antitrypsin clearance-Increased fecal loss of α1- antitrypsin.
(As it is resistant to proteolysis).
Serum α1antitryspin concentration.
(4) Vitamin B12 (a) Macrocytosis Q
(b) Decreased serum vitamin B12level. Q
(c )Schilling test- Q
Nutrients Site of absorption
(1) Calcium, Iron Folic acid a. Proximal small intestine
(2) Cobalamin, bile acids b. Ileum
(3) Glucose, amino acid, lipids c. Both proximal and distal small intestine