Risk Factors, Clinical Presentation And Outcome

One of these symptoms is jaundice, which is characterized by yellowish skin and eyes because of an inability of the liver to remove bilirubin from the blood. Patient with cirrhosis also suffering from itching, due to deposited bile's products in the skin. This patient also suffers from accumulation of fluid in legs that is called edema. As a result of the blockage of blood flow via the liver, fluid accumulation in abdomen which is worsen by the decrease in protein production. Other symptoms include fatigue, weakness, loss of appetite, weight loss and nausea. As the disease progress, complications may develop ,such as varices that happens with cirrhosis patient when the blood flow through the liver slows, so the blood from intestine go back to the vessels of the stomach and esophagus, these vessels are not meant to carry this much of blood so they dilate (varices), with increasing

Portal Hypertension is known as an increase in the pressure of the portal venous system (Lewis, Heitkemper, Dirksen, & Bucher, 2014). Portal Hypertension puts an individual at risk of damage to the vessels that lead to the liver, resulting in poor blood circulation (Lewis et al., 2014). As portal hypertension

This case study is about Abdul Chidiac, a 51 year old male, married with 4 children. He had a medical history of hypertension, hypercholesterolaemia and cirrhosis with two admissions in the last six months. He is a smoker and drinks beer, 5-6 bottles per day. As Carithers & McClain (2010) explained the patient’s medical history is another indicator of the risk for cirrhosis; the progression to cirrhosis is adaptable and may take time over weeks or many years. Cirrhosis is a liver disease characterized by permanent scarring of the

Cirrhosis is a consequence of chronic liver disease characterized by replacement of normal, healthy liver tissue by fibrotic scar tissue, blocking the flow of blood through the organ and preventing it from working as it should, as well as regenerative nodules leading to progressive loss of liver function. The liver, the largest organ in the body, is vital in keeping the body functioning properly. It removes or neutralizes poisons from the blood, produces immune agents to control infection, and removes germs and bacteria from the blood. It

Pamela B., a 52-year-old female, presented to the emergency department complaining of abdominal distention that worsened over a two week period. She noted black, tarry stools several days after the onset of her abdominal distention, and decided to seek medical attention after experiencing three large incidences of frank hematemesis, vomiting consisting of bright red blood. She has a past medical history of cirrhosis of the liver, which is the deposition of connective tissue, collagen fibers, in the liver, resulting in the formation of nodules. These nodules can alter blood flow, and liver function (1). Additionally, she has hepatitis C, a viral infection most commonly associated with the liver, that is transmissible by blood (1). Her

Alcohol abuse and hepatitis B and C are the most common causes of cirrhosis. Cirrhosis can cause weakness, loss of appetite, jaundice, itching, and fatigue, and can be diagnosed by blood tests, physical examinations, and a liver biopsy. There are many complications of cirrhosis, such as edema and ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal vein hypertension, hepatorenal and hepatopulmonary syndrome, hypersplenism, and liver cancer. One of the most common treatments of cirrhosis is a liver transplant. However, alcoholics have to be sober for six months to prove that they are serious about taking care of their new liver and staying sober after the

A sudden and dramatic liver transaminase elevation in relation to cardiogenic shock correlates extensive hepatocellular necrosis called ischemic hepatitis (Crespo- Leiro et al., 2008).

The general public and even some medical professionals lacks in depth information on Necrotizing Fasciitis. Most Americans have not heard of it or do not have enough information about it to know what to do. It is commonly misdiagnosed and is often fatal because it is not caught in time. I will discuss what it is, what causes it, describe clinical presentation, treatment options, and the prognosis of this disease. In hopes that more people can be made aware of this deadly disease.

Characterized by progressive tissue injury and scarring, cirrhosis is among the leading causes of chronic liver failure in the United States. Recent research conducted by the National Institutes of Health indicated that the prevalence of cirrhosis, especially in clients diagnosed with Hepatitis C, has increased steadily throughout the past decade and will likely continue to increase in the future (Kanwal et al., 2011). Caused by recurrent tissue damage and inflammation, cirrhosis occurs as healthy hepatocytes (liver cells) are replaced by fibrotic and non-functional scar tissue through natural healing processes. Although liver tissue is normally very resilient, sustained injury eventually

Cirrhosis involves a complication in the liver which cause the loss of liver cells and irreversible scarring of the liver. Some of the common causes of the Cirrhosis is the abuse of alcohol fatty liver disease, viral hepatitis B and C. Other possible causes that cause Cirrhosis are Iron buildup in the body, Cystic fibrosis, Copper accumulated in the liver, poorly formed bile ducts, inherited disorders of sugar metabolism and Infection such as Schistosomiasis. Cirrhosis does not show very often signs or symptoms until the liver is damaged extensive. When signs and symptoms do occur According to Mayo clinic

This case study examines the development of Portal Vein Thrombosis (“PVT”) in two patients, M.W. and R.C., diagnosed with adenocarcinoma of the pancreas. In both cases the patients had low volume local disease which responded to treatment over time. Both experienced a longer survival length than typical pancreatic cancer patients, but ultimately experienced thombosis of the portal vein and the superior mesenteric vein. Extrinsic compression of the celiac axis by the tumor further exacerbated the disease. Both patients died as a result of liver failure caused by PVT. New research in this field gives additional insight into prevention, diagnosis, and recognition of this disease. To prevent PVT, low-molecular weight heparin administration reduces

Patients with cirrhosis are susceptible to bacterial infections that frequently result in acute-on-chronic liver failure (9-11). Cirrhosis is thought to be the most common immunodeficiency syndrome worldwide with an occurrence of bacterial infections in 30 to 50% of hospitalized patients (12,13). The overall median mortality rate of infected cirrhotic patients is 38% (14). In cirrhosis, sepsis is frequently accompanied by an imbalanced cytokine response leading to excessive inflammation. Bacterial infections develop as a consequence of immune dysfunction that occurs progressively during the course of cirrhosis. (15,16). During severe bacterial infections, disruption of the integrity of the endothelial barrier markedly increases permeability to fluids, solutes and inflammatory cells. The activation status of leukocytes has been shown to be associated with increased morbidity and mortality (17-19). Of particular interest, many of these studies demonstrated activation rather than a depression of peripheral mononuclear cells in cirrhosis (20-23). Given that the liver plays an essential role in several stages of lipid synthesis, transportation and metabolism, hypocholesterolemia is frequently found in patients with decompensated cirrhosis (24). Interestingly, low circulating cholesterol levels show a strong correlation with survival

The excellent marker for the resolution of HCV infection is sustained virological response (SVR), defined as undetectable HCV RNA in blood 24 weeks after finishing the treatment (Desmond et al., 2006). SVR is accompanied by reduction in hepatic inflammation and regression of fibrosis in patients without cirrhosis; but in patients with cirrhosis remain at risk of life-threatening complications as hepatic failure and portal hypertension (Younossi et al., 2007). The risk of HCC is reduced but not eliminated in patients who achieve SVR, and therefore screening for HCC must continue (Bruno et al., 2007).

Liver has many haemostatic functions including the synthesis of most coagulation factors and inhibitors as well as fibrinolytic factors. The balance between procoagulant and anticoagulant factors is essential to prevent excessive blood loss from injured vessels and to prevent spontaneous thrombosis (11).The global effect of liver disease with regard to hemostasis is therefore complex, so that patients with advanced liver disease can experience severe bleeding or even thrombotic complications (12).

ISSN 2320-5407 International Journal of Advanced Research (2015), Volume 3, Issue 12, 1539 –15481546INR levels were less in PVT group than control group but in patients with early stages of liver cirrhosis, no differences in their levels was found between the 2 groups. Therefore, patients with advanced liver cirrhosis and less prolonged coagulation parameters appear to carry a higher risk of PVT compared with patients with advanced liver cirrhosis and markedly prolonged coagulation parameters. These findings were also reported by Weber et al. (19)in their study on cirrhotic patients with PVT. The platelet levels were also lower with advanced stages of liver disease possibly from hypersplenism, immune mechanisms and/or decreased production of thrombopoietin synthesis in the liver (23).Our study demonstrated that platelet count inversely proportionate with degree of liver decompensation. In patients with Child 's class C, the decrease in platelet count in PVT group was less than that of control group. These results werein agreement with Francoz et al. (24)and Donglei et al. (21)who reported that cirrhotic patients with PVT had higher platelet level in comparison with cirrhotic patients without PVT and advanced stages of liver disease. From the previous results we can conclude that, in cirrhotic patients the impact of portal hypertension and deficiency of natural