Response needed to following discussion post from classmate:
“Pathophysiology of Alcoholic and Nonalcoholic Liver Disease
The liver suffers from two forms of diseases known as Alcoholic Liver Disease (ALD) and Nonalcoholic Fatty Liver Disease (NAFLD). Although they are different forms, they still have some similarities. Accurate diagnosis and the development of multitherapeutic treatments depend on our ability to understand the similarities and differences of this illness.
Pathophysiology of Alcoholic Liver Disease (ALD)
In alcoholic liver disease, the disorder arises as a result of prolonged and chronic alcohol use, leading to liver inflammation and damage. Primary ethanol metabolism occurs in the liver, where alcohol dehydrogenase oxidizes ethanol to acetaldehyde, which is then transformed to acetate by aldehyde dehydrogenase (Osna et al., 2017). This procedure initiates a disruption that generates reactive oxygen species (ROS) and induces oxidative stress; and lipid peroxidation, the mechanism accountable for hepatocellular damage (Osna et al., 2017). Furthermore, by its impact on lipid metabolism, alcohol induces fat storage in hepatocytes, a precursor to cirrhosis and inflammation of the liver (steatohepatitis). This recurring cycle of events culminates in the development of hepatocellular carcinoma (Osna et al., 2017).
Pathophysiology of Nonalcoholic Fatty Liver Disease (NAFLD)
The pathophysiology of nonalcoholic fatty liver disease (NAFLD) is a two-step process. Which begins with abnormal hepatic lipid accumulation that increases insulin resistance in the first phase. Following this, lipolysis ensues due to the increased insulin resistance, facilitating the discharge of fatty acids into the circulatory system. De novo lipogenesis (DNL) is the hepatic process by which it transforms free fatty acids from the bloodstream into triglycerides (Guo et al., 2022). Due to the inhibition of free fatty acid oxidation by this mechanism, these fatty acids accumulate in the hepatocytes. An overabundance of hepatocyte triglycerides induces oxidative stress in the second phase. Reactive oxygen species (ROS) generation is responsible for instigating inflammatory reactions and inducing cellular damage (Guo et al., 2022). Inflammatory cells such as neutrophils and monocytes, liver macrophages, and activated kupffer cells cause chronic inflammation that progresses NAFLD to nonalcoholic steatohepatitis (NASH), a severe form of NAFLD.
Comparison and Contrast
Nonalcoholic fatty liver disease (NAFLD) and alcohol-associated liver disease (ALD) share a key characteristic: the accumulation of adipose tissue in the liver. The etiology of alcoholic fatty liver disease is often associated with the direct hepatotoxic impacts of alcohol and its metabolites, while nonalcoholic liver disease is frequently linked to impairments such as type 2 diabetes, metabolic syndrome, and obesity (Idalsoaga et al., 2020). If the illness advances, fibrosis, cirrhosis, and hepatocellular carcinoma are potential complications that may develop over time.
In conclusion, the pathophysiology of alcoholic and nonalcoholic liver disease might be different, there is a similarity in the pathogenic mechanisms depending on the hepatic fat deposition, inflammation, and oxidative stress. Understanding these similarities and differences is critical for correct diagnosis and the development of multitherapeutic treatments to reduce liver damage, therefore improving patient outcomes.”
