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Chronic Liver Disease
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Julia M. Boster, Kelly A. Klaczkiewicz, Shikha S. Sundaram
In patients with cirrhosis, a careful physical exam can identify the presence and progression of portal hypertension. In addition to a firm and nodular liver, patients may develop ascites and splenomegaly. Thrombocytopenia due to hypersplenism may lead to petechiae and easy bruising or bleeding. Dilated blood vessels on the abdomen (“caput medusae”) and telangiectasias (tiny spider-like skin lesions caused by dilated capillaries) may also be apparent, including on the face.
Questions 1–20
Published in Anna Kowalewski, SBAs and EMQs in Surgery for Medical Students, 2021
Where a child presents with massive haematemesis and accompanying splenomegaly, oesophageal varices should always be very high up on the differential. The child is likely to be suffering from portal hypertension (i.e. the portal venous pressure is 10–12 mmHg higher than in the inferior vena cava). If the patient is known to suffer from oesophageal varices, prophylactic sclerotherapy may be offered. The successful treatment of the portal hypertension depends upon the cause.
The liver, gallbladder and pancreas
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Dina G. Tiniakos, Alastair D. Burt
This is increased blood pressure in the portal vein, >1 kPa (7 mm Hg), reflecting the resistance to blood flow through grossly disturbed liver structure, as occurs in cirrhosis. It is further compounded by intrahepatic arteriovenous shunting of blood. Portal hypertension is caused by a variety of other conditions (Table 11.5). It leads to splenic enlargement and this may result in excessive removal of red cells and platelets from the blood – the syndrome of hypersplenism. There is also dilatation of the plexus of venous channels around the gastric fundus and oesophagus to form varices. These varices are thin walled and bleed readily, causing torrential and life-threatening haematemesis. Portal hypertension also contributes to the development of ascites.
Decompensation as initial presentation in patients with liver cirrhosis is associated with an increased risk of future decompensation and mortality
Published in Scandinavian Journal of Gastroenterology, 2023
Koos de Wit, Thijs Kuipers, Koen Van der Ploeg, Lubbertus C. Baak, Ulrich Beuers, R. Bart Takkenberg
Liver cirrhosis is a pathophysiologic entity resulting from chronic liver injury. The development of cirrhosis is characterized by chronic inflammation leading to fibrosis in the liver [1]. As fibrosis progresses, increased structural and functional hepatic vascular resistance is observed. As a result, cirrhosis is associated with impaired liver function and hyperdynamic circulation and splanchnic vasodilation. Subsequently increased inflow in the portal vein leads to portal hypertension. Furthermore, the risk of development of hepatocellular carcinoma (HCC) is increased [2]. Chronic alcohol misuse and chronic hepatitis C (CHC) are still the main underlying causes of liver cirrhosis in developed countries [2]. But due to effective therapeutic options in CHC on the one hand and the obesity epidemic on the other hand, the incidence of cirrhosis due to non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) is rising alarmingly [3].
Oxidative stress and histopathological changes in several organs of mice injected with biogenic silver nanoparticles
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2022
Shushanik Kazaryan, Lilit Farsiyan, Juleta Tumoyan, Gayane Kirakosyan, Naira Ayvazyan, Hrachik Gasparyan, Sona Buloyan, Lilit Arshakyan, Ara Kirakosyan, Ashkhen Hovhannisyan
A different morphological picture was observed in the liver with extract stabilized AgNPs. Examination revealed that AgNPs induced acute venous congestion with hyperaemia of portal veins, and dilation of sinusoids compared to the control group. The observed pathological alterations confirm the development of severe portal hypertension. In addition, there is periportal infiltration of lymphocytes in some triads. These phenomena indicate the toxic effect of nanoparticles, which causes inflammatory processes in the liver tissue. Along with inflammation, few foci of metastases were observed in some areas around the portal triads and central veins. The process of focal necrosis of hepatocytes was clearly observed (Figure 10). Statistical analysis of the liver tissue in this group indicated that only the parameter of inflammation in portal tracts was significantly higher compared with the control group (p < .05), while other parameters were not significantly different.
Pulmonary arterial hypertension in adults with congenital heart disease: markers of disease severity, management of advanced heart failure and transplantation
Published in Expert Review of Cardiovascular Therapy, 2021
Katrijn Jansen, Andrew Constantine, Robin Condliffe, Robert Tulloh, Paul Clift, Shahin Moledina, S John Wort, Konstantinos Dimopoulos
Transplant assessment involves a multidisciplinary approach and can be time-consuming, often requiring more than one admission, another reason why timely referral is crucial. Objective assessment of exercise capability is needed not only for risk stratification, but also to tailor the pre- and post-operative rehabilitation program to the individual patient’s needs. Co-morbidities are a major risk factor around transplantation and their severity and response to therapy should be carefully documented. Renal and liver dysfunction are common in PAH-CHD and are related to a low cardiac output state, chronic congestion, and cyanosis, previous insult due to surgery, interventions or investigations (e.g. use of radiological contrast medium) [8]. Further investigations typically include 24-hour urine collection, renal and liver ultrasound and/or cross-sectional imaging (triple phase CT or MRI) to assess liver architecture and the severity of portal hypertension. A liver biopsy, though not without risk, might be required to exclude severe liver fibrosis/cirrhosis and a gastroscopy to assess presence of esophageal varices.