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Parasite Versus Host: Pathology and Disease
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
A granuloma represents the host’s attempt to isolate an antigenic source and mitigate the damage caused by this source. In schistosomiasis, the source of antigens is the egg itself (Figure 5.19). Granulomas result in considerable pathology. Once granulomas have initially formed, the excess collagen and other extracellular matrix material deposited around them cause scarring. In the liver, such scarring disrupts liver function. In severe cases, it can occlude branches of the portal vein, causing portal hypertension. Ultimately, ascites, the buildup of tissue fluid in the mesenteries and abdominal cavity, can result. Nevertheless, things would be much worse if granulomas did not form. Rampant inflammation in response to egg antigens would result in progressive tissue necrosis and ultimately organ failure. It’s worth noting that the granulomatous response is good for the parasite as well. Recent evidence has shown that it is vital in helping eggs transit into the intestinal lumen.
Paper 3
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Sonographic features of portal hypertension include loss of the normal triphasic portal vein Doppler waveform, reduced portal vein flow (<10 cm/sec) and reversal of flow. Normal portal vein flow should be hepatopetal (towards the liver); however, in portal hypertension this can eventually reverse causing hepatofugal flow, and collaterals form, such as oesophageal and splenic varices.
Liver Blood Flow
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The portal vein is a valveless vein and drains blood from the large and small intestines, spleen, stomach, pancreas and gall bladder to the liver. The hepatic portal vein contributes 70% of total liver blood flow and 50%–60% of basal oxygen supply. In the fasting state, the oxygen saturation of portal venous blood is approximately 85%, but this decreases with increased gut activity. The higher O2 saturation in portal venous blood at resting conditions, compared with mixed venous O2 saturation, is due to the high mesenteric arterial shunting through the intestinal capillaries draining into the portal system. The velocity of blood flow in the portal system is 9 cm/s – approximately half that in the hepatic artery. Thus, the hepatic portal system is a low-pressure (5–10 mmHg), low-resistance and low-velocity system. The portal venous pressure depends on the state of constriction/dilatation of mesenteric arterioles and on intrahepatic resistance. The resistance in the portal system is approximately 6%–12% of that in the hepatic artery.
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].
Evening primrose oil attenuates oxidative stress, inflammation, fibrosis, apoptosis, and ultrastructural alterations induced by metanil yellow in the liver of rat: a histological, immunohistochemical, and biochemical study
Published in Ultrastructural Pathology, 2023
Amany Mohamed Shalaby, Rania H. Shalaby, Mohamed Ali Alabiad, Doaa I. Abdelrahman, Mohammed Alorini, Fatima A. Jaber, Shaimaa Mohamed Abdelfattah Hassan
The liver architecture in the control and EPO groups was normal. It was formed of the classical hepatic lobule with a central vein in the middle. Hepatocyte cords appear to spread from the central vein, with blood sinusoids in between (Figure 4a). The portal tract is located at the periphery of the classical hepatic lobule and is formed of a terminal branch of the hepatic artery, a small branch of portal vein, and a bile ductule (Figure 4b). Regarding the hepatocytes, they were polygonal in shape with eosinophilic cytoplasm and had rounded euchromatic nuclei and prominent nucleoli. Binucleated hepatocytes were also demonstrated. Kupffer cells and flat endothelial cells bordered the blood sinusoids (Figure 4c). Myl caused severe changes in the liver. The central veins were dilated, congested, and surrounded by cellular infiltration (Figure 4d). The portal tracts showed dilated congested portal veins with cellular infiltrations around their components. As well as proliferation of bile ductules was also detected (Figure 4e). The hepatocytes revealed vacuolations of their cytoplasm (Figure 4f). Concurrent treatment with EPO and Myl helps to protect the structure of the liver. Nevertheless, mild infiltration around central veins and portal tracts, as well as small vacuolation within a few hepatocytes were demonstrated (Figures. 4g-i).
Two-year free of complications during antiviral therapy predicts stable re-compensation in immediate-treatment HBV-related decompensated cirrhosis
Published in Scandinavian Journal of Gastroenterology, 2023
Zhiying He, Jialing Zhou, Yu Tian, Shanshan Wu, Yameng Sun, Xiaojuan Ou, Jidong Jia, Bingqiong Wang, Xiaoning Wu, Hong You
In this retrospective, single-center cohort study, a total of 1704 liver cirrhotic patients who occurred decompensated complications and were hospitalized at Beijing Friendship Hospital from Mar 2013 to May 2018, were consecutively screened according to the following criteria: (1) age ≥18 years; (2) hepatitis B surface (HBsAg) positive for more than six months; (3) clinical evidence for liver cirrhosis, including any of: a) esophageal gastric varices confirmed by endoscopy; b) features of cirrhotic portal hypertension confirmed by imaging assessment, including liver surface nodularity, splenomegaly or portal vein ≥ 1.3 cm; c) laboratory test showed PLT < 100 × 109/L and ALB < 35 g/L; (4) presence of ascites or VH as the first episode of decompensated complications, and clinical material about first event was available; (5) follow-up time duration from the first decompensated event was more than 12 months.