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File:IPLab12Alcoholic14.jpg|This is another photograph of the cerebellum from this patient demonstrating the marked thinning of the anterior portion of the cerebellum (arrows). This pattern of cerebellar damage is consistent with Wernicke's encephalopathy.
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== Study Questions ==
* <spoiler text="How does alcohol cause liver damage?">Initial changes include hepatocellular steatosis. This is caused by altered metabolism with high levels of NADH from lactate dehydrogenase resulting in increased lipid biosynthesis. Mobilization of lipids from peripheral fat stores and decreased lipid acceptor protein synthesis leads to insufficient lipoprotein production.
Alcohol induces free radical production as it is broken down by the microsomal ethanol oxidizing system. Alcohol also impairs microtubular and mitochondrial function and membrane fluidity.
Acetaldehyde, the major ethanol metabolite, can cause lipid peroxidation and acetaldehyde-protein complexes that further inhibit the microtubular system.
Finally, alcohol also induces an immunologic reaction in the liver. This immune-mediated liver damage is thought to result from the expression of neoantigens on hepatocytes possibly due to alcohol-induced alterations in membranes or acetaldehyde binding to proteins leading to neoantigen formation.</spoiler>
* <spoiler text="Why did this patient have a prolonged prothrombin time?">Since most of the clotting factors are produced by the liver, chronic liver damage with loss of liver parenchyma will lead to a reduction in clotting factors. In addition, this patient had bleeding esophageal varices and ascites which could both use up or sequester clotting factors, respectively.</spoiler>
* <spoiler text="What causes esophageal varices in a patient with hepatic cirrhosis?">Hepatic cirrhosis with extensive parenchymal damage and fibrosis results in an increased resistance to portal blood flow. The increased portal pressure leads to increased pressure in the coronary veins of the stomach. This results in increased pressure in the esophageal plexus in the terminal portion of the esophagus as the blood travels through this plexus to empty into the azygous vein. The increased pressure and increased flow of blood through this plexus of thin-walled veins leads to dilation and formation of varices. These varices can then rupture and lead to life-threatening hemorrhage as was seen in this case.
Increased portal pressure also leads to increased pressure in the inferior hemorrhoidal veins and can lead to the formation of anorectal varices.</spoiler>
* <spoiler text="What is the pathogenesis of Wernicke's encephalopathy?">Wernicke's encephalopathy is caused by thiamine (Vitamin B1) deficiency. Chronic alcoholics often have poor diets and alcohol inhibits intestinal absorption of thiamine. Thus, some chronic alcoholics can develop Wernicke's encephalopathy which consists of foci of symmetric discoloration, softening, and punctate hemorrhages in the paraventricular regions of the thalamus and hypothalamus, in the mamillary bodies, around the aqueduct in the midbrain, in the floor of the fourth ventricle and in the anterior cerebellum. There is demyelinization and loss of neuropil. Even after treatment with thiamine, there is significant memory deficit.</spoiler>
{{IPLab 12}}
[[Category: IPLab:Lab 12]]