Ess portal phg

ess portal phg

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Welcome to ESS Global ESS Global is a leading education consultant in India that has been serving aspiring students since 2007 to study abroad. We have a team of devoted, competent, and knowledgeable professionals, who are highly experienced and well-acquainted with the industry requirements. With years of experience, every member of our team is committed and provides personalized counselling as per client requirements. Studying abroad has created a new wave in the minds of the students.

Keeping this in mind, we have been consistently providing the apt overseas consultancy to turn their dreams into reality.
At Ess portal phg Public Schools, you can access two different user-interfaces of our Employee Self-Service (ESS) system. Both user-interfaces work with the same back-end system, so any changes made using either interface will save and be sent to Payroll.

The enhanced version, also referred to as Neptune ESS, offers a new and improved user experience which enables you to access the ESS system from your mobile device, which means you can now do things like record your time, view your paychecks, and view time off statements right from your phone!

Which Version of ESS Do you need TRAINING FOR? Clinically significant portal hypertension (CSPH) is one of the main prognostic factors in cirrhotic patients and the main trigger for the development of esophageal and gastric variceal bleeding.

The prevalence varies from around 30% in compensated to 60% in decompensated cirrhosis. The incidence rate of new varices is 9% per year and the progression rate from small to medium/large varices is 10% per year. The rate of bleeding from small esophageal varices is around 10% at 2 year while for medium/large varices it increases to 30% also depending on the Child-Pugh score. Without secondary prophylaxis, after an initial episode of bleeding, the 6-week risk of rebleeding is 15–20% and increases to 60% within the first year.

The 6-week mortality rate is 20–25%, mainly due to recurrence of bleeding (40%) and the development of liver complications.

ess portal phg

After endoscopic treatment, varices recur with a rate of 50% at 2 years, without pharmacological therapy. Gastric varices are less frequent (prevalence 10–20%); and bleed less frequently than esophageal varices (25% vs. 64%) but usually more severely with a 6-week mortality rate of 45%. In this chapter, we discuss selected issues on the epidemiology of varices and variceal bleeding. Portal hypertension patients with or without cirrhosis commonly experience two distinct forms of gastric mucosal abnormalities: portal hypertensive gastropathy (PHG) and gastric vascular antral ectasia (GAVE).

The morbidity and mortality risks associated with PHG are highly underestimated.

ess portal phg

Variceal bleeding is correlated with 39.1% mortality rate while PHG is associated with 12.5% mortality rate; neither is considered benign. These mortality and morbidity rates are significantly associated with two main factors: chronic blood loss anemia and repeated hospitalizations for insignificant small bleeding.

Clinical features of PHG and GAVE, such as gastrointestinal hemorrhage, can result in sudden death and therefore require significant attention.

It is imperative to precisely identify the timing of the first initial screening used to identify high-risk individuals. Several tools are available to assess the presence, severity, and complexity of PHG. Additionally, treatment options are available to prevent secondary bleeding and control of blood loss anemia.

ess portal phg

The mainstay therapy for chronic bleeding is nonselective β-blockers, while vasopressin, somatostatin, and their derivatives are used in cases of acute bleeding.

Large portosystemic venous collaterals pathways can be found in any part of the gastrointestinal tract, but when these veins are not in the gastroesophageal region they are denominated ectopic varices (EcV).

Ess portal phg addition, dilated veins in the abdominal wall and retroperitoneum are also classified as EcV. These veins can cause up to 5% of all variceal bleeding in patients with liver cirrhosis and even more in extrahepatic portal hypertension. When compared with esophageal varices, EcV tend to be larger, leading to significant hemorrhage and requiring more time to find the bleeding source during the endoscopic approach. Despite the advances in diagnostic modalities, the management of EcV is still under debate, requiring skilled doctors on a multidisciplinary team.

ess portal phg

The initial clinical support for treating gastroesophageal variceal hemorrhage can be extrapolated to EcV bleeding. EcV sites, stigmata of high risk of bleeding, hemodynamic profile, local expertise and resources, the patient’s conditions, and underlying diseases can influence the indication of the therapeutic modality. Endoscopic interventions, such as injection of thrombin, cyanoacrylate, sclerotherapy, and rubber band ligation, should be attempted before radiologic or surgical interventions.

Portal hypertension is a common clinical syndrome, defined by a pathologic increase in the portal venous pressure. Increased resistance to portal blood flow, the primary factor in the pathophysiology of portal hypertension, is in part due to morphological changes occurring in chronic liver diseases.

This results in rerouting of blood flow away from the liver through collateral pathways to low-pressure systemic veins. Through a variety of computed tomographic, sonographic, magnetic resonance imaging and angiographic examples, this article discusses the appearances and prevalence of both common and less common portosystemic collateral channels in the thorax and abdomen.

A ess portal phg overview of established interventional radiologic techniques for treatment of portal hypertension will also be provided. Awareness of the various imaging manifestations of portal hypertension can be helpful for assessing overall prognosis and planning proper management.

Background Gastrointestinal bleeding and anemia in patients with liver cirrhosis are common problems caused by various etiologies such as bleeding esophageal and gastric varices, bleeding peptic ulcer whether Helicobacter pylori or non-H.

pylori related, portal hypertensive gastropathy (PHG), and other causes. Impairment of the gastric protective barriers and production of inflammatory cytokines such as tumor necrosis factor-α and interleukins, which occur because of colonization of gastric mucosa by H.

pylori, may make the stomach more susceptible to the effects of portal hypertension. Aim of work The aim of this study was to investigate the prevalence of H. pylori infection and its association with PHG in patients with liver cirrhosis. Patients and methods Overall, 50 patients with liver cirrhosis and PHG (cases) and 50 patients with cirrhosis without PHG (controls) were enrolled in this study. H. pylori stool antigen rapid bedside test and upper endoscopy were done for patients in both groups to diagnose PHG and H.

pylori infection. Results The prevalence of H. pylori infection among patients with PHG was higher than those without PHG (34 vs. 10%, respectively; P=0.031), and prevalence of H.

pylori infection was 22% among the whole of the studied groups. There was no correlation between H. pylori infection and severity of PHG (P=0.381), Child score, Model for End-Stage Liver Disease score, or serum albumin level.

However, our study showed a significant correlation between splenic size and portal vein diameter in patients with cirrhosis and PHG (P=0.002). Conclusion There ess portal phg significant association between H. pylori infection and PHG, but there is no significant correlation between H. pylori infection and the severity of PHG or the severity of liver cirrhosis.

Also, there is significant correlation between splenic size and portal vein diameter in patients with cirrhosis and PHG. Aim: To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy (PHG) based on a systematic literature review.

Methods: Computerized search of the literature was performed via PubMed using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy".

The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. Results: PHG is diagnosed by characteristic endoscopic findings of small polygonal areas ess portal phg variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal ess portal phg.

Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance.

The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG. PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration.

PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow.

ess portal phg

Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse.

Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding.

Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepatic-portosystemic-shunt and liver transplantation are highly successful ultimate therapies because they reduce the underlying portal hypertension. Conclusion: PHG is important to recognize in patients with cirrhotic or non-cirrhotic portal hypertension because it can cause acute or chronic GI bleeding that often requires pharmacologic therapy.

The purpose of the present study was to characterize uncommon portosystemic collateral circulation in hepatic cirrhosis. Portosystemic uncommon collateral circulation (UCC) was detected, characterized and evaluated by a combination of spiral computed tomography angiography, three-dimensional imaging angiography and electronic gastroscopy in patients ess portal phg with hepatic cirrhosis.

ess portal phg

In total, 118 cases with UCC were detected from a pool of 700 hepatic cirrhosis patients with portal hypertension. The incidence was 16.86% and included cases with splenic-renal, gastro-renal, paravertebral, retroperitoneal, gastric-splenic and cardio-phrenic angle vein shunts. The occurrence rate of UCC formation increased with the Child-Pugh grade. Compared with common collateral circulations, the incidence of severe esophageal or gastric ess portal phg varicose veins, severe portal hypertensive gastropathy and the incidence of a large quantity ess portal phg ascites was much lower in the patients with UCC (P<0.01), whereas the incidence of hepatic encephalopathy and chronic elevated blood ammonia levels was significantly higher (P<0.01).

The incidence of uncommon portosystemic collateral circulation is extremely common in patients with liver cirrhosis and is associated with the Child-Pugh grades of hepatic function. UCC can aid in the relief of the complications derived from portal hypertension, but it may increase the incidence of hepatic encephalopathy and chronic elevated blood ammonia levels. Objectives: Evaluation of the outcome and experience in 2 years of management of portal hypertensive gastropathy (PHG) by argon plasma coagulation (APC) in a cohort of Egyptian cirrhotic patients.

Methods: This study was conducted over a 2-year period from January 2011 to February 2013. Upper gastrointestinal endoscopy was performed to evaluate the degree and site of PHG. APC was applied to areas with mucosal vascular lesions.

ess portal phg

Ess portal phg In total, 200 cirrhotic patients were enrolled; 12 patients were excluded due to death (n = 6) caused by hepatic encephalopathy (n = 3), hepatorenal syndrome (n = 2), or chronic lymphatic leukemia (n = 1), or did not complete the treatment sessions (n = 6), so 188 patients completed the study. PHG was mainly fundic in 73 patients (38.8 %), corporeal in 66 patients (35.1 %), and pangastric in 49 patients (26.1 %) (P = 0.026).

Patients were exposed to APC and received proton pump inhibitors together with propranolol at a dose sufficient to reduce the heart rate by 25 % or down to 55 beats/min. The mean (± standard deviation) number of sessions was 1.65 ± 0.8; six patients needed four sessions (3.2 %), 19 patients needed three sessions (10.1 %), 74 patients needed two sessions (39.4 %), and 89 patients needed one session (47.3 %). Patients with fundic and corporeal PHG required the lowest number of sessions (P = 0.000).

Patients were followed up every 2 months for up to 1 year; the end point was a complete response with improved anemia and blood transfusion requirement which was achieved after ess portal phg session in 89 patients (75.4 %), two sessions in 24 patients (20.3 %) and three sessions in five patients (4.3 %). A complete response was more prevalent in patients with corporeal and fundic PHG (P = 0.04).

Conclusions: After 2 years’ experience in managing PHG, we found that a combination of APC and non-selective beta blockers was highly efficacious and safe in controlling bleeding from PHG. In addition, APC alone is rapid, and effective in the control of PHG induced bleeding, especially when beta blockers are contraindicated. In this review the updated information concerning the influence of portal hypertension on gastric mucosa is presented.

ess portal phg

The term portal hypertensive gastropathy [PHG] defines a wide spectrum of endoscopic lesions that appear in the gastric mucosa of cirrhotic patients and which should be differentiated from gastric antral vascular ectasia.

These endoscopic findings correspond to dilated mucosal and submucosal vessels in the absence of inflammation. There is wide variation in the prevalence of PHG, but its natural history in not clearly documented. Endoscopic variceal obliteration may contribute to the development or aggravation of these lesions. Similar influence of portal hypertension seems to be extended in the lower gastrointestinal tract.

With regard to gastric mucosal hemodynamics. it is mot known whether active congestion or passive congestion causes gastric mucosal hyerthemia.

ess portal phg

The pathogenesis of PHG in not well known, but both venous congestion related to raised portal pressure and increased gastric blood flow seem to be crucial factors for its development. Gastric mucosal defense mechanisms are impaired in PHG.

Bleeding is its unique clinical manifestation and occurs in patients with severe lesions. Pharmacological, surgical and interventional radiological procedures ess portal phg available for the treatment of bleeding PHG, but the treatment needs to be improved. Portal hypertensive gastropathy (PHG) is a painless condition of gastric mucosal ectasia and impaired mucosal defense, commonly seen in patients with elevated portal pressures.

While it is typically asymptomatic and incidentally discovered on upper endoscopy, acute and chronic bleeding may occur. There are no definitive recommendations for treatment of asymptomatic PHG. Non-selective β-blockers represent the mainstay of therapy for chronic bleeding, while somatostatin and vasopressin and their derivatives may be used in conjunction with supportive measures ess portal phg acute bleeding.

Salvage therapy with transjugular intrahepatic portosystemic shunt or rarely surgical shunt is appropriate when medical management fails. The role of endoscopic therapy for PHG is controversial. Liver transplantation should be considered as a final resort in cases of refractory bleeding due to PHG. Objective: Information is lacking on portal hypertensive gastropathy (PHG) in cirrhotics without varices; our aim it is to evaluate whether clinical and sonographic parameters are associated with PHG and may provide information suitable for the management of these patients.

Patients and methods: After endoscopic selection of 145 cirrhotics without varices, 75 with PHG and 70 without PHG, clinical and sonographic characteristics were assessed. Results: Forty portosystemic shunts were present in 27 patients. The mean Child-Pugh score was 6.3±1.4 and 5.6±0.5 in patients with severe and mild PHG, respectively (P=0.004).

The mean portal vein diameter was 10.4±1.7 and 11.6±2.0 mm in cirrhotics without and with PHG, respectively (P=0.0002). Conclusion: A link between the presence of PHG and a more advanced phase of cirrhosis was found. Duplex Doppler sonography was confirmed to be a valuable diagnostic method in monitoring cirrhosis.

Management of these patients cannot be performed on the basis of a single diagnostic method, and a multimodal diagnostic approach is required. Transjugular intrahepatic portosystemic shunt is an effective accepted treatment in the management of portal hypertension complications in a hepatic cirrhosis patient. Transjugular intrahepatic portosystemic shunt placement is a safe technique that improves the quality of life of these patients and of those suffering from refractory ascites and gastrointestinal bleedings.

This procedure emerged . [Show full abstract] over 20 years ago; however no reports on Cuban literature about the implementation of this technique are found. This article described the placement of a covered portosystemic stent graft performed in a 52 years-old male patient who presented with upper digestive bleeding resulting from enolic cirrhosis diagnosed 6 years before.

The procedure was performed with no immediate complicatios and instant reduction of portal pressure from 24 to 12 %. We consider that the transjugular intrahepatic portosystemic shunt could be technically placed by the interventionist radiologist. The ess portal phg will depend to a great extent on the experience of the staff.

ess portal phg

This procedure, which gains more reliability among physicians and patients because of its high rate of success and resolute capacity, may be implemented in Cuba on a systematic basis. Taking this initial experience as a starting point, the procedure may be extended to other hospitals in the country for the benefit of the patients. Read more Refractory esophageal variceal hemorrhage (EVH) remains a formidable problem in patients awaiting liver transplantations.

Transjugular intrahepatic portosystemic shunts (TIPS) ess portal phg provided an alternative approach for managing EVH that may obviate the need for portosystemic shunt surgery.

Experience with TIPS placement and subsequent successful hepatic transplantation in patients without previous . [Show full abstract] portosystemic shunt surgery has not been previously reported. Two patients are reported who underwent TIPS placement and subsequent successful hepatic transplantation without previous portosystemic shunt surgery.

ess portal phg

This experience indicates that (1) TIPS can provide effective control of EVH for at least several weeks, (2) TIPS placement decreases portal hypertension, thus facilitating technical performance of the transplant procedure and minimizing blood loss, (3) TIPS may undergo vascular incorporation, thus requiring that they be accurately positioned so that the lengths of suprahepatic inferior vena cava and portal vein are not compromised at the time of transplantation, (4) TIPS thrombosis can be effectively treated and prolonged patency may be observed, and (5) deterioration in hepatic function and exacerbation of hepatic encephalopathy were not observed after TIPS placement.

In summary, TIPS provide an attractive, effective means for managing refractory EVH in patients awaiting liver transplantation. Read more Liver cirrhosis as a stage in chronic diffuse liver diseases development manifests itself in structural remodeling of parenchyma and appearance of the main syndrome--portal hypertension. In turn it leads to hemorrhage in 54,3% with death rate of 30-50%. In the article research of hemodynamics in abdominal vessels by the means of modified sonographic Doppler flowmetry and prognosis of high risk .

[Show full abstract] esophageal varices are described. On the basis of statistical dependency between degree of esophageal varices, cirrhotic gastropathy and results of modified protocol close correlation is shown, which allow to recommend them as alternative in non-invasive diagnosis of liver cirrhosis complications. Read more Knowledge of the normal anatomy, most frequent variants, and congenital and acquired anomalies of the portal venous system is of great importance for liver surgery and interventional procedures such as creation of ess portal phg intrahepatic portosystemic shunts.

Radiologic studies of the portal venous system include color Doppler ultrasonography (US), computed tomography (CT), magnetic resonance . [Show full abstract] imaging, and arterial or direct portography. Among the most common branching variants of the portal vein are trifurcation, right anterior portal branch arising from the left portal vein, and right posterior portal branch arising from the main portal vein.

Agenesis of the right or left portal vein is the most frequently reported congenital anomaly. Venous collateral vessels due to portal hypertension and cavernous transformation of the portal vein are best evaluated with cross-sectional imaging. Intrahepatic portosystemic, arterioportal, and arteriosystemic fistulas and associated perfusion anomalies have characteristic features at dual-phase helical CT.

Color Doppler US is the single most useful tool for demonstration of aneurysms of the portal venous system and bland or neoplastic portal vein thrombosis. CT is also the best means of evaluating gas in the portal venous system, which is no longer an ominous sign and must be differentiated from aerobilia.

View full-text Disease-related changes in prostaglandin (PG) levels ess portal phg contribute to a bleeding tendency and local vasodilation in the portal circulation in patients with liver cirrhosis.

We measured the plasma and tissue PG metabolite levels (6-keto Ess portal phg and thromboxane TXB2) in the systemic and portal circulation in 12 rats with CCl4-induced liver cirrhosis (LC rats) and ten with portal hypertension induced .

[Show full abstract] by 2 weeks of partial portal ligation (PH rats) and compared them with normal control rats (n=10). We also compared the plasma PG metabolite levels in the systemic and portal circulations in 11 cirrhotic patients with hepatocellular carcinoma (HCC) and five patient controls without liver disease.

In the animal study, LC rats had significantly higher portal blood 6-keto PGF1α (P Read more
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For over 45 years Elizabeth Seton School has been a bastion for quality education guided by a noble mission of contributing to the integral growth ess portal phg development of our Filipino youth by cultivating them to be authentic Christians, responsible Filipino citizens and life-long learners in constant pursuit of excellence.

ess portal phg

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