Steatorrhea pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sunny Kumar MD [2]
Overview
Steatrorhea can be defined as loss of undigested fat in stools. The processes can be invoked by either defect of the normal architecture of digestive tract or it may involve defect of synthesis or secretion of enzymes of GI tract which are needed to metabolize fatty content of food.
Pathophysiology
Normal Fat absorption
To understand the pathophysiology of fat malabsoption we need to understand normal physiology of fat metabolization:[1][2][3][4][5][6][7][8]
- Absorption of fat requires a complex interaction of
- Digestive enzymes
- Bile salts
- An intact intestinal mucosa
- Ingested fats are initially emulsified in the stomach.
- By the action of digestive enzymes emulsified lipids are hydrolyzed subsequently.
- Once hydrolyzed, they aggregate to form micelles with the help of bile salts.
- These micelles are absorbed across the intact intestinal villi of proximal small intestine.
- After absorption, micelles are packaged into chylomicrons within intestinal epithelial cells and transported to the circulation via the lymphatic system.
Pathogenesis
Any disturbance in the normal physiology results in decreased absorption of the fats.
- Disturbance in intact intestinal mucosa
- Marked acceleration of intestinal transit can increase nutrient malabsorption and induce symptoms due to:
- High osmotic load
- Increased bacterial metabolism in the colon
- Delayed intestinal transit may promote small intestinal bacterial overgrowth.
- This bacterial overgrowth also causes malnutrition by consuming ingested nutrients.
- In addition, de-conjugation of bile acids also sets in by the action of bacterial enzymes
- Compromises bile acid absorption in the terminal ileum
- Depletes the bile acid pool
- Disturb lipid absorption
- Marked acceleration of intestinal transit can increase nutrient malabsorption and induce symptoms due to:
- Impaired Bile Acid Synthesis and Secretion
- Bile acids support the emulsification of triglycerides and form micelles with fatty acids and monoglycerides to enable absorption from the intestinal lumen.
- Thus, decreased luminal availability may result in or contribute to steatorrhea.
- While there are rare inborn errors of bile acid synthesis and transport
- Interruption of the enterohepatic circulation is the clinically most important pathomechanism which leads to decreased luminal availability of bile acids and lipid malabsorption.
Genetics:
The development of steatorrhea is the result of multiple genetic mutations. Common genetic conditions associated with steatorrhea include:
Gross pathology
On gross pathology the gastro-intestinal tract looks normal in conditions which involves enzyme deficiencies. However in condition which involves obstruction of ducts involved in secretion of enzymes will look narrowed. The luminal causes which damage the luman of GIT and does not allow the absoption of faty products will also look ulcerated.
Microscopic pathology
On microscopy the GIT looks normal in conditions which involves enzyme deficiencies. However in condition which involves obstruction of ducts involved in secretion of enzymes will look narrowed. The luminal causes which damage the luman of GIT and does not allow the absoption of faty products will also look ulcerated.
References
- ↑ Kumar R, Bhargava A, Jaiswal G (2017). "A case report on total pancreatic lipomatosis: An unusual entity". Int J Health Sci (Qassim). 11 (4): 71–73. PMC 5654180. PMID 29085272.
- ↑ Previti E, Salinari S, Bertuzzi A, Capristo E, Bornstein S, Mingrone G (2017). "Glycemic control after metabolic surgery: a Granger causality and graph analysis". Am J Physiol Endocrinol Metab. 313 (5): E622–E630. doi:10.1152/ajpendo.00042.2017. PMID 28698280.
- ↑ Vakhrushev YM, Lukashevich AP (2017). "[Specific features of impaired intestinal digestion, absorption, and microbiocenosis in patients with cholelithiasis]". Ter Arkh. 89 (2): 28–32. doi:10.17116/terarkh201789228-32. PMID 28281512.
- ↑ Scarpignato C, Gatta L, Zullo A, Blandizzi C, SIF-AIGO-FIMMG Group. Italian Society of Pharmacology, the Italian Association of Hospital Gastroenterologists, and the Italian Federation of General Practitioners (2016). "Effective and safe proton pump inhibitor therapy in acid-related diseases - A position paper addressing benefits and potential harms of acid suppression". BMC Med. 14 (1): 179. doi:10.1186/s12916-016-0718-z. PMC 5101793. PMID 27825371.
- ↑ Podboy A, Anderson BW, Sweetser S (2016). "61-Year-Old Man With Chronic Diarrhea". Mayo Clin Proc. 91 (2): e23–8. doi:10.1016/j.mayocp.2015.07.033. PMID 26769182.
- ↑ Burnett JR, Hooper AJ (2015). "Vitamin E and oxidative stress in abetalipoproteinemia and familial hypobetalipoproteinemia". Free Radic Biol Med. 88 (Pt A): 59–62. doi:10.1016/j.freeradbiomed.2015.05.044. PMID 26086616.
- ↑ Valenzise M, Alessi L, Bruno E, Cama V, Costanzo D, Genovese C; et al. (2016). "APECED syndrome in childhood: clinical spectrum is enlarging". Minerva Pediatr. 68 (3): 226–9. PMID 25502918.
- ↑ Wilcox C, Turner J, Green J (2014). "Systematic review: the management of chronic diarrhoea due to bile acid malabsorption". Aliment Pharmacol Ther. 39 (9): 923–39. doi:10.1111/apt.12684. PMID 24602022.