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Paper 2
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
The description is typical for PSC. This condition typically affects males aged 20–40 years. It is an idiopathic, progressive, fibrosing inflammatory disorder of the biliary tree. Associated with ulcerative colitis (UC), Riedel thyroiditis, Sjögren syndrome, cystic fibrosis (CF) and retroperitoneal fibrosis. Imaging features include both intra- and extrahepatic duct strictures with alternating segments of dilatation and stenosis (the ‘string of beads’ appearance on MRCP). On ultrasound there is increased echogenicity of the portal triads. MRCP can demonstrate a ‘pruned tree’ appearance with obliteration of the peripheral ducts.
Status of Nonoperative Management of Blunt Hepatic Injuries in 1995: A Multicenter Experience with 404 Patients
Published in Stephen M Cohn, Ara J. Feinstein, 50 Landmark Papers every Trauma Surgeon Should Know, 2019
HL Pachter, MM Knudson, B Esrig, S Ross, D Hoyt, T Cogbill, H Sherman, T Scalea, P Harrison, S Shackford, J Trauma
Some of the surgical techniques described in this paper have survived the test of time and are still critical to achieving hemostasis in patients with complex liver injuries. These include the use of portal triad occlusion (Pringle maneuver) and the finger fracture technique. Over time, we have learned that direct suture liga-tion of the parenchymal bleeding vessel, perihepatic packing, repair of venous injury under total vascular isolation, and damage control surgery with the utilization of preoperative and/or postoperative angioembolization are the preferred methods, compared to anatomical resection of the liver and use of the atriocaval shunt. In addition, a better understanding of the pathophysiology of liver trauma has allowed us to move from a prolonged continuous occlusion of the portal triad to a shorter intermittent clamping leading to improved liver ischemia tolerance.
The accessory organs: Pancreas, liver and gallbladder
Published in Paul Ong, Rachel Skittrall, Gastrointestinal Nursing, 2017
Blood leaving the small intestine is rich in absorbed nutrients. It travels via the superior mesenteric vein to the hepatic portal vein where it then enters the liver. And 75% of the blood entering the liver is venous blood which enters via the hepatic portal vein. The remaining 25% of blood is arterial blood and this enters the liver via the hepatic artery. Blood enters the liver at the porta hepatis (doorway to the liver) via the hepatic artery and the hepatic portal vein. The blood enters the liver lobules via portal triads (Figure 6.10). There are six portal triads, one for each corner of the hexagonal-shaped lobule. A portal triad consists of a branch of the hepatic artery, the hepatic portal vein and the bile duct. When blood enters the lobule via the portal triad, venous and arterial blood becomes mixed as it drains into sinusoids. Sinusoids are ducts in the liver tissue which function like ‘canals’ transporting the blood to the hepatocytes. As blood flows through the sinusoids it comes into contact with hepatocytes which then absorb nutrients and secrete synthesised molecules. If there is an excess of nutrients these are removed and stored and if there is a deficiency of nutrients these are released or synthesised by the hepatocytes. From sinusoids blood then flows into the central vein, hepatic vein and then into the vena cava.
Chebulagic acid attenuates HFD/streptozotocin induced impaired glucose metabolism and insulin resistance via up regulations of PPAR γ and GLUT 4 in type 2 diabetic rats
Published in Toxicology Mechanisms and Methods, 2022
Ganesh Vasu, Ramalingam Sundaram, Karuppiah Muthu
Figure 8 portrays hematoxylin and eosin staining of the liver of control and experimental rats. Pathologically, the liver of normal control rats showed no dilated blood sinusoids with red blood cells and congestion of the area around the central vein (Figure 8(A)). Section of hepatic tissues of diabetic rat showed dilated blood sinusoids with red blood cells and congestion of the area around the central vein. Hepatocytes were found to be swollen with fatty deposits. These features are the characteristic of a diabetic liver. There was the distortion of the lumen of the sinusoids. Inflammatory changes were observed in the region of the portal triad with the polymorph nuclear cells infiltrating the area of the portal triad. The features of necrosis were characteristically observed in the region around the portal triad. Collagen deposits were also observed in the region of the portal triad (Figure 8(B)). The liver of the diabetic rats treated with chebulagic acid and metformin did not reveal any infiltration of the portal triad. Blood sinusoids were normal and no congestion was observed in the region near the central vein and the portal triad. The microstructure resembled a normal liver (Figure 8(C,D)).
Induction of hepatic portal fibrosis, mitochondria damage, and extracellular vesicle formation in Sprague-Dawley rats exposed to copper, manganese, and mercury, alone and in combination
Published in Ultrastructural Pathology, 2020
Priyanka Dhanraj, Chantelle Venter, Megan Jean Bester, Hester Magdalena Oberholzer
The general morphology of the liver tissue for the control and the single, double, and triple metal-exposed groups (Figures 1 and 2) was evaluated. In the control group (Figure 1(a and b)), the typical arrangement of hepatocytes with no hydropic swelling was observed. None to minimal sinusoidal dilation with the presence of erythrocytes and hydropic swelling (black arrows) of hepatocytes was observed in all the metal-exposed groups (Figure 1(c–p)). Binucleated hepatocytes (Bi) were also observed in the exposed groups, particularly in the area surrounding the central vein. Figure 2 illustrates the general structure of the portal triad consisting of a branch of the portal vein (PV), a branch of the hepatic artery (HA) and bile ductules (B), in loose stromal connective tissue. In contrast to the control (Figure 2(a)), accumulation of inflammatory cells (white arrows) in the exposed groups (Figure 2(b–h)) was observed.
Neonatal hemochromatosis in a newborn with Down syndrome
Published in Fetal and Pediatric Pathology, 2020
Rasheeda M, Suvendu Purkait, Amit Kumar Satapathy, Joseph John, Susama Patra, Suvradeep Mitra
The hematological and the biochemical parameters are tabulated in Table 1. There were anemia, thrombocytopenia and neutrophilic leukocytosis. This time, the peripheral blood smear did not show any atypical cells. There was unconjugated hyperbilirubinemia with low total protein and hypoalbuminemia. Alkaline phosphatase was normal with 10 times elevated aspartate aminotransferase (AST). However, alanine aminotransferase (ALT) levels remained close to 100 IU/L. Thyroid profile of the child was normal. HIV and HBsAg were non-reactive. TORCH screening and screening for inborn errors of metabolism were negative. Gas chromatography/mass spectrometry was negative and did not highlight any metabolic disorder. Karyotyping of the child showed trisomy 21 (Fig. 1a). An ultrasound of the abdomen showed mildly heterogeneous echotexture of the liver with prominent portal triads along with mild splenomegaly and gross ascites. A HIDA scan could not be performed due to the severity of the sickness. A possibility of Down syndrome-associated neonatal cholestasis secondary to transient myeloproliferative disorder or sepsis-induced secondary hemophagocytic lymphohistiocytosis was considered.