Steatorrhea pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sunny Kumar MD [2]

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.

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.

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

• 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.

The development of steatorrhea is the result of multiple genetic mutations. Common genetic conditions associated with steatorrhea include:

• Cystic fibrosis
• Crohn’s disease
• Ulcerative colitis
• Abetalipoproteinemia 

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.

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.

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