Synthesis Of Most Coagulation Factors And Inhibitors

The dabigatran etexilate (DE) is a prodrug that directly competes for the active site of thrombin.1 This direct inhibition inactivates both fibrin-bound and free form of thrombin. Because of its rapid onset and offset of action, there is no need for the initial parenteral anticoagulant treatment in patients with acute thrombosis.1 On the other hand, the enoxaparin indirectly inhibits factor Xa.2 It has a shorter duration of action (12h vs 24h) and a shorter half-life (4.5-7h vs 12-14h) in comparison to DE. The DE and the enoxaparin have no interaction with diet and alcohol. There is no routine monitoring required

Oppositely; chronic liver disease per se may influence heart functions and electrophysiology in the absence of other cardiac disease. These abnormalities are collectively called cirrhotic cardiomyopathy that affects the patient prognosis and exacerbates the course during invasive procedures as insertion of a trans jugular intrahepatic porto systemic shunt (TIPS), surgery and orthotropic liver transplantation (OLT) (Moller and Bernardi, 2013).

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.

Hemostasis is a process which causes bleeding to stop. Thrombin is a proteolytic enzyme that is formed from prothrombin and facilitates the clotting of blood by catalyzing conversion of fibrinogen to fibrin as well as catalyzing many coagulation related reactions.

A detailed medical history was taken about other systemic and/ or CVD. Macrovascular disease was defined as a history of MI, presence of angina, revascularization procedures or stenosis >50% of the coronary artery, a history of cerebrovascular diseases or PAD based on a previous L.L Doppler U/S examination [13]. DM was defined according to American Diabetes Association (ADA) criteria [14]. Hypertension was defined as blood pressure above 140/90 mmHg or taking antihypertensive

Dr. L. Vijaya Mohan Rao, an internationally recognized investigator in the field cardiovascular diseases, has been awarded 1.45 million dollar R01 grant from National Institute of the Health to continue and expand his research program in blood diseases. Cardiovascular diseases constitute the major cause of morbidity and mortality in US and other Western countries. More people die from these diseases than cancer. Thrombus (clot) formation in major blood vessels occludes blood supply to vital organs, including to heart and brain, that results in heart attack and stroke. It is not entirely clear what triggers unwanted clots in blood vessels. In the healthy condition, the cells that come in contact with blood are quiescent and not capable of generating the clot. However, in disease conditions, such as atherosclerosis, infection and cancer, the cells are activated to express a potent procoagulant factor that triggers the clot formation. Dr. Rao’s research focuses on identifying factors that elaborate in diseases that transform the cryptic and non-functional clotting factor on blood cells to highly thrombogenic clotting factor. Identifying these factors

Factors such as female gender, normal liver serology/liver function test, nondilated bile ducts, and obesity increase the risk of PEP

The assessment of hepatic vein morphology has been shown to be a good indicator of cirrhosis. Examination of hepatic vein wall is recommended to be performed in segment 5 or 6 (Vessal et al., 2009). Also, changes in the dynamics of portal venous circulation correlate with progression of cirrhosis in ultrasound. Portal hypertension occurs once portal pressure reaches 5-10 mmHg above normal as a complication of cirrhosis, with recognized effects as development of splenomegaly and collateral portal venous anastomoses (Taylor et al.,

Hemostasis is the process of blood coagulation. The first thing that happens is the contraction of the smooth muscles in the blood vessel wall. next is the formation of the platelet plug, which become sticky and adhere to the defect to form a temporary plug. Formation of a blood clot then happens. The substance needed for coagulation are normally inactive in the bloodstream. some substances in clotting are ones such as, calcium ion, enzyme precursors, vitamin k, fibrinogen, calcium. After these substances are obtained then the final steps begin. First substance released from the damaged tissue and sticky platelets initiate a reaction that leads to the formation of prothrombinase. Next the prothrombinase converts prothrombin in the blood to

Chronic liver failure from an inability for the organ to repair itself from repeated injury and scarring that remains permanent. Alcoholic liver disease is the 2nd most common diagnoses for liver transplant, however many candidates must abstain from alcohol for a required period in addition to adhering to an abuse program. Metabolic liver disease is a non- alcoholic steatohepatitis where inflammation and scarring can occur from a development of fatty liver not related to alcohol but rather obesity or disorders such as diabetes and hyperlipidemia. Autoimmune liver disease or (AIH) autoimmune hepatitis where the patient’s own immune needs to be suppressed to prevent destruction of the liver (Tan, 730). Vascular liver disease results in poor blood flow or clotting of hepatic veins and hepatocellular carcinoma (HCC) in which liver transplantation will unquestionably cure HCC so long that the cancer does not spread beyond the liver (Bryce,

It is important to rule out common causes of liver injury, such as alcohol, drug use, and viral hepatitis as well as other co-existing etiologies for chronic liver disease including alpha-1 antitrypsin deficiency, hemochromatosis, autoimmune liver disease (types 1 and 2), chronic viral hepatitis, and Wilson’s disease

“Qualitative or quantitative abnormalities interfere with or prevent enzymatic reactions that transform clotting factors, circulating as plasma proteins into a stable fibrin clot” (Huether and McCance 544). Some defects are caused by a single factor, these would be hemophilias and von Willebrand disease and some are acquired and result from “deficient synthesis of clotting factors by the liver” which is caused by liver disease and vitamin K deficiency (Huether and McCance 544). Other abnormalities in coagulation disorders are caused by “pathologic conditions” such as a cardiovascular abnormality that alters blood flow. An example of this is thromboembolic disease where blood clots block vessels (Huether and McCance 544). Vasculitis and damage to vessels activates platelets which activates coagulation (Huether and McCance 544). Prolonged vasculitis leads to clogging of the

The main blood component engaged in hemostasis, and subsequently in thrombosis too, are the platelets. Platelets during hemostasis adhere to the injured vessel wall creating a barrier that blocks the blood loss. The initial platelet adhesion is followed by platelet aggregation and platelet-platelet adhesion which are induced by cytokines released by the activated platelets. As a final step in hemostasis, the coagulation cascade is stimulated with final result thrombin and fibrin formation at the site of damage. 1,2

ISSN 2320-5407 International Journal of Advanced Research (2015), Volume 3, Issue 12, 1539 – 1548

ISSN 2320-5407 International Journal of Advanced Research (2015), Volume 3, Issue 12, 1539 –15481539Journal homepage:http://www.journalijar.comINTERNATIONAL JOURNALOF ADVANCED RESEARCHRESEARCH ARTICLEPortal vein thrombosis in patients with liver cirrhosis:insights to risk factors, clinical presentation and outcomeAfifi F. Afifi 1, Osama M. Basha 1, Fady M. Wadea 1, Abdelaziz E. Samack 2, Raghda Abd-elatif Hafez31-GIT and hepatology unit, Internal Medicine department, Faculty of Medicine, Zagazig University.2-Radiology department, Faculty of Medicine, Zagazig University.3-Microbiology&Immunologydepartment, Faculty of Medicine, Zagazig University. EGYPTManuscriptInfoAbstract Manuscript History:Received:14 October 2015Final Accepted: 22 November 2015Published Online: December 2015Key words: Portal vein,