Non-Alcoholic Fatty Liver Disease: Pathogenesis and clinical findings Diagnosis of Metabolic Syndrome when ≥ 3 out of the 5 preceding risk factors are present
Authors: Stephanie Happ Reviewers: Obesity Hypertension Diabetes Hypertriglyceridemia Hypercholesterolemia Iffat Naeem Sunawer Aujla Edwin Cheng* * MD at time of publication
Insulin resistance develops in adipose tissue and hepatocytes
↓ Ability of insulin to suppress lipolysis of adipose tissue
↑ Delivery of free fatty acids from adipocytes to the liver
↑ De-novo lipogenesis in the liver
Hepatic Steatosis: accumulation of fat in the liver (in the absence of alcohol consumption, termed Non-Alcoholic Fatty Liver (NAFL))
Steatohepatitis: chronic inflammatory and apoptotic climate in the hepatocytes (in the absence of alcohol consumption, termed Non-Alcoholic Steatohepatitis (NASH))
Fibrosis of the Liver: excessive scarring of liver tissue resulting from chronic inflammation, although liver architecture is largely intact
Fat droplets form and grow in the hepatocytes
Hepatic mitochondria increase their workload in attempt to break down the excess free fatty acids through beta-oxidation
↑ in cellular workload creates more reactive oxygen speciesà Inflammation and apoptosis of hepatocytes
On-going inflammation damages hepatic stellate cells (the primary extracellular matrix–producing cells of the liver) causing the release of fibrinogenic cytokines
Cirrhosis of the liver: normal lobular structure distorts and is replaced by regenerating nodules and bridging septa, disrupting normal liver blood flow
Deposition of fibrotic
material and collagen within the perisinusoidal spaces of the liver
Decompensated Cirrhosis Hepatocellular carcinoma
Legend:
Pathophysiology
Mechanism
Sign/Symptom/Lab Finding
Complications
Published November 25, 2023 on www.thecalgaryguide.com