Portal Vein Thrombosis On Patients With Liver Cirrhosis

Functional studies showed decreased LES function with a low amplitude of acid clearance and primary esophageal peristalsis in cirrhotics with large varices [9]. These phenomena could also be due to a mechanical effect of the varices. Cirrhotic patients without EV have also esophageal motor disorders and mixed acid and bile reflux as the main pattern whereas the cirrhosis itself was an important causative factor. It is unclear whether this might contribute to bleeding from varices [8]. Data on management of GERD in cirrhosis are few, however, the indications of use for PPIs may remain exactly the same also in patient with cirrhosis of the liver as general population for the treatment of erosive esophagitis or in general the pathology secondary to gastroesophageal reflux acid (10)

Cirrhosis is a condition that results in development of fibrosis in liver, resulting in decrease in

There are associations between cardiovascular disease (CVD) and liver cirrhosis. The effect of cardiovascular diseases on the underlying liver disease is well-recognized. The management is vital in the long term care of patients with liver cirrhosis, particularly whom considered for liver transplantation. CVD in cirrhotics may happen as a part of a systemic disease that incorporates the liver e.g.: Wilson 's disease, or a systemic disease which does not include the liver e.g.: atherosclerosis and coronary artery disease, or as a limited cardiovascular disease without related hepatic or systemic affiliation (Karasu et al., 2004).

Extra-hepatic portal vein obstruction (EHPVO), i.e., in the absence of liver cirrhosis or abdominal cancer, is a rare manifestation of venous thrombosis that often leads to portal hypertension1.After prothrombin, factor V, next most common cause of thrombophilia is high plasma levels of coagulation factor VIII, which are present in approximately 20% of patients with deep vein thrombosis (DVT) of the lower limbs and increase the risk of the disease in a dose-dependent manner 2. Like fibrinogen, factor VIII is an acute phase reactant whose concentration rises in plasma in the presence of inflammation. However, high factor VIII levels are associated with an increased risk of DVT independently of the acute phase reaction3.

As cirrhosis progresses, the hardened tissues being formed stop the liver from functioning properly. The buildup of scar tissue prevents blood flow through the liver and slows down toxin and nutrient processing. The production of substances made by the liver is also delayed (WebMD, 2014). As stated in WebMD, 2014, symptoms of cirrhosis include: loss of appetite, lack of energy (fatigue), weight loss or weight gain, bruises, yellowing of skin or the whites of eyes (jaundice), itchy skin, fluid retention (edema) and swelling, a brownish or orange tint to the urine, light colored stools, confusion, disorientation, personality changes, blood in the stool, and

Cirrhosis with types I or II HRS on top of chronic kidney disease or acute kidney injury.

Liver cirrhosis is a problem that can be caused by many liver diseases. It is a progressive disease itself, developing slowly over many years. It is characterized as scarring to the normal liver tissue which keeps this organ from working as it should and causes it to take on an abnormal structure. The diseases that lead to cirrhosis injure and kill liver cells. Scar tissue that has formed due to inflammation and repair, prevents the cells that have not died to properly replace the dead cells which result in newly formed cell clusters forming within the scar tissue.

HRS is the most advanced stage of different pathophysiologic derangements that occur in individuals with cirrhosis. Intense renal vasoconstriction that begins at an early time point and progresses with worsening of liver disease are the hallmark of HRS. The underlying mechanisms that are involved in HRS are incompletely understood but may include both increased vasoconstrictor and decreased vasodilator factors acting on the renal circulation. Type 2 HRS is gradually progressive and arises in association with the progression of cirrhosis, whereas type 1 is an acute deterioration in kidney function associated with severe renal vasoconstriction and failure of compensatory mechanisms that are responsible for maintenance of renal perfusion [Wadei

Over time the liver is unable to metabolize the alcohol and leads the liver to form fibrous tissue, develop nodules, and the liver shrinks and has a nodular uneven appearance (Pearson, 2015). Biliary cirrhosis is another type of liver disease that is characterized by the inability of bile to be excreted, causing build up within the liver which eventually destroys the cells within the liver. The third type of cirrhosis is known as posthepatic cirrhosis and is the result of a patient having hepatitis B or C resulting from an unknown cause. This type of cirrhosis causes the liver to shrink and become nodular and fibrous resulting in destruction of the liver cells. Risk factors for all three types of cirrhosis include high risk behaviors such as consuming excessive amounts of alcohol, drug use (primarily IV), unsafe sexual behaviors leading to the development of hepatitis B or C. Clinical manifestations of cirrhosis include portal hypertension, which is caused by the portal vein becoming inflamed and casing blood to be rerouted to adjoining lower pressure vessels, splenomegaly, ascites which is the enlargement of the stomach due to a collection of fluid in the abdominal cavity, esophageal varices, which are enlarged, thin walled veins that form in the esophagus, portal, systemic encephalopathy, which is due to neurotoxins being rerouted into the blood, hepatorenal syndrome caused by imbalanced blood flow, and spontaneous bacterial peritonitis, which is a contamination of the peritoneal cavity (Pearson,

Throughout the years, many diseases have had significant effects on the world such as HIV/AIDS, Ebola, and the plague. Hepatitis is one of them. Hepatitis is the irritation and inflammation of the liver caused by the hepatitis virus that attacks the liver. The liver is a large organ in the right side of the body. Its functions are to filter blood, detoxify chemicals, metabolize drugs, secrete bile, and it also makes proteins. There are 6 types of hepatitis that have already been discovered; hepatitis A, B, C, D, E, and G, but the most important cases of hepatitis deal with hepatitis A, B, and C (Berkman, 2000).

Description of acute liver failure (ALF) is the sudden loss of function of liver cells in a patient with formerly normal liver function, which includes blood clots and hepatic encephalopathy disease. However, the causes of pathological and the clinical causes of acute liver failure are variables, these causes are recognized as the severe acute Wilson, activated (illuminated) of hepatitis B and hepatitis autoimmune usually be chronic liver disease instead of the acute liver failure Foundation. (2)

The viral hepatitis B and Hepatitis C, alcoholic liver disease (ALD), non alcoholic fatty liver disease (FLD), cirrhosis and hepatocellular cancer [1,2] are known to cause most morbidity and mortality among

In decompensated cirrhosis, patient can develop jaundice, ascites or encephalopaty (Bedossa and Poynard, 1996). The risk for decompensation is estimated to be 5% per year in cirrhotics (Poynard et al., 1997). Once patient developed decompensation, the 5-year survival rate is reaching upto 50% (Planas et al., 2004). Hepatocellular carcinoma (HCC) developed in patients with cirrhosis and liver transplantation is then the only effective therapy (Kim, 2002).

Portal hypertension is abnormal high blood pressure in the hepatic portal system. The Hepatic venous system is a significant role of supplying blood to the liver. The portal vein carries blood from the intestine, stomach, spleen, pancreas, and gallbladder and coursing through the liver. If the vessels in the liver are blocked due to hepatocellular diseases, blood cannot flow throughout the liver properly. As a result, the blood in the portal vein slows down and increases hepatic resistance. High resistance causes pressure increased, resulting in varices or dilation of the vessels.Normally, the portal venous pressure should not above 10 mmHg or the hepatic venous gradient is not more than 5 mmHg. If one of them is detected, that is a positive

Hepatic fibrosis and cirrhosis are potentially reversible with timely intervention. [1] To achieve the best possible outcome, treatment must be initiated in the early stages of liver fibrosis.[1] Another benefit of timely treatment of fibrosis and cirrhosis is the prevention of hepato-cellular carcinoma.[3, 6] Additionally, in patients with chronic hepatitis C,anti-viral treatment is indicated with severe fibrosis. [3, 6]Therefore, clinicians must serially monitor the level and severity of fibrotic tissue, to ensure timely treatment and to determine the patient’s risk of liver-related morbidity, mortality and hepatic comorbidities, for example, portal hypertension or hepatic carcinoma.[7-10]