Cirrhosis is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrous scar tissue as well as regenerative nodules (lumps that occur as a result of a process in which damaged tissue is regenerated. Cirrhosis is most commonly caused by alcoholism and hepatitis C, Cirrhosis causes GI bleeding due to the development of gastro-esophageal varices as a consequence of portal hypertension Portal hypertension is an increase in the pressure within the portal vein (the vein that carries blood from the digestive organs to the liver). The increase in pressure is caused by a blockage in the blood flow through the liver.
In the normal person the blood from the digestive organs is carried through the portal vein in to the liver and then the IVC. But following scarring in the lever, there is a physical barrier to the transport of blood through the liver. Thus blood gets accumulated in the draining tributaries. Thus the oesophageal veins at the GE junctions dilate in response to back pressure. These channels get dilated, and tortuous, and extremely thin walled. And bleed massively and easily. These are known as gastro-osephageal varices. What neurological changes would you expect in Mr. S that are related to his alcoholic cirrhosis?
What causes these changes? Hepatic encephalopathy is the term given to the series of neurological changes that occur in alcoholic cirrhosis. One of the earliest manifestations of hepatic encephalopathy is “day-night reversal. ” In other words, affected individuals tend to sleep during the day and stay awake at night. Another early manifestation is impairment in spatial perception. This can be made apparent by noting the patient’s poor ability to copy or draw various simple images, In addition to changed level of consciousness, the hallmark of hepatic encephalopathy on the physical examination is the presence of asterixis.
in cirrhosis and other forms of liver disease, the damaged liver will not be able to get rid of all the metabolic load, with poor detoxification of metabolic some of these toxic substances that accumulate in the setting of liver failure and affect the brain are thought to include ammonia (NH3) and mercaptans. Ammonia is normally converted to urea by the liver and, as with mercaptans, is produced by the bacterial breakdown of protein in the intestines. Ammonia can cross the blood-brain barrier, where it causes the support cells of the brain (astrocytes) to swell.
The swelling of the brain tissue increases intracranial pressure, and can lead to coma or death via herniation of the brainstem. What is the effect of alcoholic cirrhosis on renal function? Why is blood urea nitrogen not an accurate indicator of renal function in Mr. S.? Hepatorenal syndrome (HRS) is the development of renal failure in patients with advanced chronic liver disease, occasionally fulminant hepatitis, who have portal hypertension and ascites. The hallmark of HRS is renal vasoconstriction.
Multiple mechanisms are probably involved and include interplay between disturbances in systemic hemodynamics, activation of vasoconstrictor systems, and a reduction in activity of the vasodilator systems. There is activation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, and profound vasoconstriction of the kidneys Blood urea is a poor indicator of renal function here, because it is as it raised in liver failure due to poor detoxification