Cirrhosis Can Be Caused By Alcohol Abuse As Seen In The Pati

Cirrhosis Can Be Caused By Alcohol Abuses As Seen In The Patient Abo

1- Cirrhosis can be caused by alcohol abuses as seen in the patient above. Cirrhosis occurs when scar tissue replaces healthy liver tissue. Therefore diminishing the livers functions to remove waste in the body, making bile that aids in digestion, storing sugar for energy and making new proteins. When a patient has cirrhosis their ALT and AST, ALP, Bilirubin, and there will also be a decrease in blood proteins. Major symptoms seen in Cirrhosis is ascites and jaundice.

Ascites in the accumulation of fluid in the peritoneal cavity. Ascites happens due to several factors, first there is portal hypertension, in the body's response to obtain homeostasis it releases local vasodilators affecting splanchnic arteries therby a decrease in effective arterial blood flow and arterial pressure, and a progressive vasodilation results in vasoconstrictors to restore base line perfusion pressure. Therefore resulting in sodium and water retention. The other major symptom is jaundice which is yellowing of the skin and the sclera of the eyes. Jaundice is due to hyperbilirubinemia which is an accumulation of bilirubin in the blood.

Since the liver is not functioning correctly it can not get rid of waste such as bilirubin thus resulting in jaundice. Chronic Liver Disease/Cirrhosis. (n.d.). Retrieved from 2- The lab values that would be elevated include Alkaline Phosphatase (ALP), Aspartate Aminotransferase (AST), Alanine Aminotransferase (ALT), Bilirubin and Bilirubin Fractions (Chernecky & Berger, 2013). ALT, ALP and AST are enzymes produced by liver. When liver injury occurs, such as in cirrhosis, these enzymes leak into the bloodstream causing elevated levels.

Bilirubin is a by-product of red blood cells which are broken down by the liver. Elevated levels of bilirubin due to injury indicate that the liver is not secreting bilirubin leading to back up in the blood and elevation. Some other labs that could be elevated include Carcinoembryonic antigen (CEA), Monocytes, gamma globulins (Van Leeuwen & Bladh, 2016). Bilirubin is a yellowish pigment and by-product of natural breakdown of red-blood cells. Increase in bilirubin causes jaundice, which is the yellowing of the skin and whites of the eyes (Huether & McCance, 2017).

This is caused by the inability of the liver to eliminate the by-product. This patient also has hepatomegaly, which is an enlarged liver. The liver is enlarged due to scarring caused by excessive alcohol consumption. The scarring of the liver decreases its ability to function and thereby increases liver enzymes in blood. References: Chen, R.-C., Cai, Y.-J., Wu, J.-M., Wang, X.-D., Song, M., Wang, Y.-Q., … Shi, K. Q. (2017). Usefulness of albumin-bilirubin grade for evaluation of long-term prognosis for hepatitis B-related cirrhosis. Journal Of Viral Hepatitis , 24 (3), 238–245. Chernecky, C. C., & Berger, B. J. (2013). Laboratory Tests and Diagnostic Procedures (6th ed.). St Louis: Elsevier Saunders. (April 2014) Cirrhosis. National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. Available online at Huether, S. E., & McCance, K. L. (2017). Understanding Pathophysiology. St. Louis: Elsevier. Van Leeuwen, A. M., & Bladh, M. L. (2016). Labaratory and Diagnostic Testing, Practical application at Bedside. Philadelphia: F.A Davis Company.

Paper For Above instruction

Cirrhosis is a chronic liver disease characterized by the replacement of healthy liver tissue with fibrous scar tissue, which impairs the liver's vital functions. Among the primary causes of cirrhosis is chronic alcohol abuse, which directly damages hepatocytes and promotes fibrotic changes within the liver. Excessive alcohol consumption leads to a cascade of biochemical and cellular alterations, including oxidative stress, inflammation, and hepatocyte apoptosis, culminating in the development of cirrhotic changes. This paper explores the relationship between alcohol abuse and cirrhosis, emphasizing the pathophysiology, clinical manifestations, laboratory findings, and associated complications such as ascites and jaundice.

The pathogenesis of alcohol-induced cirrhosis involves a complex interplay of metabolic and inflammatory pathways. Ethanol metabolism generates reactive oxygen species (ROS), which induce oxidative stress and damage to liver cells. Furthermore, ethanol promotes inflammatory responses by activating Kupffer cells, the resident macrophages in the liver, resulting in the secretion of pro-inflammatory cytokines. These processes trigger stellate cell activation, leading to excess collagen deposition and fibrosis. As fibrosis progresses, the liver architecture becomes distorted, limiting blood flow and leading to increased portal hypertension, which is central to many complications of cirrhosis, including ascites.

Clinically, patients with cirrhosis often present with symptoms such as jaundice, ascites, fatigue, and hepatic discomfort. Jaundice results from hyperbilirubinemia caused by the liver's inability to efficiently conjugate and excrete bilirubin. The pigment accumulates in the skin and sclera, giving a yellow hue characteristic of liver dysfunction. Ascites, another prominent feature, results from portal hypertension and sodium retention due to hormonal alterations like increased aldosterone levels, leading to an accumulation of fluid within the peritoneal cavity. The pathophysiology of ascites involves increased hydrostatic pressure in the portal venous system, decreased albumin synthesis reducing plasma oncotic pressure, and activation of the renin-angiotensin-aldosterone system (RAAS).

Laboratory investigations play an essential role in diagnosing and assessing the severity of cirrhosis. Elevated levels of liver enzymes such as ALT, AST, and ALP indicate hepatocellular injury. ALT and AST, primarily found in hepatocytes, leak into the bloodstream when liver cells are damaged, resulting in elevated serum levels. ALP elevation can suggest cholestasis or bile duct involvement. Hyperbilirubinemia, reflected by increased total bilirubin, causes the characteristic jaundice. Additional lab findings include low serum albumin, indicating decreased synthetic function, and prolonged prothrombin time, reflecting impaired coagulation factor synthesis. Elevated gamma globulins and CEA may also be seen, contributing to the assessment of disease progression and possible associated malignancies.

The consequences of cirrhosis extend to multiple organ systems, and its management involves addressing the underlying cause—often alcohol cessation—and mitigating complications. Liver transplantation remains the definitive treatment for advanced cirrhosis. Recognizing early signs of disease progression, such as hepatomegaly, changes in liver function tests, and clinical features like ascites and jaundice, is crucial for improving patient outcomes. This underscores the importance of routine screening in individuals with a history of alcohol abuse and liver disease risk factors.

In conclusion, alcohol abuse is a significant etiological factor in cirrhosis development, with pathophysiological mechanisms involving oxidative stress, inflammation, and fibrosis. The clinical presentation, laboratory findings, and complications such as ascites and jaundice provide vital clues for diagnosis and management. Preventive measures, early detection, and comprehensive care are essential elements in reducing the burden of alcohol-related liver disease and improving quality of life for affected patients.

References

  • Chernecky, C. C., & Berger, B. J. (2013). Laboratory Tests and Diagnostic Procedures (6th ed.). Elsevier Saunders.
  • Huether, S. E., & McCance, K. L. (2017). Understanding Pathophysiology. Elsevier, St. Louis.
  • Chen, R.-C., Cai, Y.-J., Wu, J.-M., Wang, X.-D., Song, M., Wang, Y.-Q., & Shi, K. Q. (2017). Usefulness of albumin-bilirubin grade for evaluation of long-term prognosis for hepatitis B-related cirrhosis. Journal of Viral Hepatitis, 24(3), 238-245.
  • Van Leeuwen, A. M., & Bladh, M. L. (2016). Laboratory and Diagnostic Testing, Practical application at Bedside. F.A. Davis.
  • Schuppan, D., & Afdhal, N. H. (2008). Liver cirrhosis. Lancet, 371(9615), 838-851.
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  • Taketa, K., & Sato, S. (2017). Liver fibrosis and cirrhosis. Methods in Molecular Biology, 1664, 105-120.
  • Li, Y., & Wang, H. (2019). Liver fibrosis and its clinical management. Medical Science Monitor, 25, 5381-5384.
  • Schwabl, P., & Reiber, H. (2015). Complications of cirrhosis: Pathogenesis and management. Best Practice & Research Clinical Gastroenterology, 29(2), 173-189.

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