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This document outlines some of the key pathophysiological factors involved in non-alcoholic fatty liver disease (NAFLD). It identifies several non-modifiable risk factors like genetic predisposition, gender, ethnicity, and age. It also discusses modifiable risk factors like obesity, dietary habits, high blood pressure, and alcohol consumption. The document then describes how fatty acids are absorbed into the liver and accumulate in hepatocytes, leading to liver enlargement and dysfunction that can cause symptoms like abdominal pain, nausea, vomiting, and jaundice.
This document outlines some of the key pathophysiological factors involved in non-alcoholic fatty liver disease (NAFLD). It identifies several non-modifiable risk factors like genetic predisposition, gender, ethnicity, and age. It also discusses modifiable risk factors like obesity, dietary habits, high blood pressure, and alcohol consumption. The document then describes how fatty acids are absorbed into the liver and accumulate in hepatocytes, leading to liver enlargement and dysfunction that can cause symptoms like abdominal pain, nausea, vomiting, and jaundice.
This document outlines some of the key pathophysiological factors involved in non-alcoholic fatty liver disease (NAFLD). It identifies several non-modifiable risk factors like genetic predisposition, gender, ethnicity, and age. It also discusses modifiable risk factors like obesity, dietary habits, high blood pressure, and alcohol consumption. The document then describes how fatty acids are absorbed into the liver and accumulate in hepatocytes, leading to liver enlargement and dysfunction that can cause symptoms like abdominal pain, nausea, vomiting, and jaundice.
Genetic Increase delivery of fatty Obesity and dietary
predisposition acid habits (Hypertension and Obesity DM) Have high blood Female gender Absorption of fatty acid to pressure Hispanic ethnicity adipose tissue Prolonged and heavy Hepatitis C alcohol consumption Age 40 years old Cigarette smoking above Fatty acids transported into hepatocytes
Accumulation of Fats in cells
Enlargement of the liver Decreased Decreased Decreased Decreased
liver cell conversion of synthesis of conversion of ammonia into urea clotting factor bilirubin to Increased pressure for excretion conjugated exerted on the abdomen Decreased bilirubin plasma albumin Blood in vomit production Accumulation of and stools RUQ pain ammonia in CNS Decreased bilirubin Decreased Bleeding and excretion Nausea and vomiting intravascular bruising more Trouble sleeping easily oncotic pressure (insomnia) Jaundice