Hepatic parenchyma

BaP alone produced glycogen depletion in liver cadmium alone caused hepatic perivascular fibrosis. Mixture produced complete disorganization of the hepatic parenchyma, including nuclear degeneration higher increase in EROD activity (by 19-fold), BaP hydroxylase activity (by 71-fold), and cytochrome P-450 microsomal content by 2-fold... 

Recently, there has been success in generating cocultures that more faithfully reproduce in vivo metastatic microenvironments. An ex vivo microscale liver perfusion bioreactor was used to assess metastatic seeding, mimicking the salient features of fluid dynamics and functionality of hepatic parenchyma. Invasion and subsequent growth of breast and prostate carcinoma cells were detected by two-photon microscopy of fluorescently labeled cells. Tumors... 

Hepatic lobule and hepatic acinus are relatively well-accepted models to describe the structure and functional aspects of the liver. Histologically, the hepatic lobule is a hexagonal region of the liver parenchyma around the central vein. Typically, six portal triads, consisting of branches from the portal vein and hepatic artery as well as bile ductules, border the edge of the lobule. Cords of hepa-tocytes are arranged radially around the central vein and blood sinusoids form between them. The hepatic parenchyma is divided into three zones based on the proximity to... 

Steatohepatitis is the accumulation of lipids and the presence of inflammatory cells within hepatic parenchyma. Steatohepatitis is usually the next stage of steatosis if untreated (Bautista, 2002 French, 2003 Lieber, 1994). The inflammatory cells are usually neutrophils and mononuclear leukocytes. Conditions usually associated with steatohepatitis are alcoholic liver disease, NAFLD, and endotoxemia secondary to intestinal disease. Any toxic compounds that cause steatosis can also result in steatohepatitis if the condition is left untreated. Steatohepatitis may progress to flbrosis/cirrhosis and hepatocellular carcinoma if the inciting cause is not removed or treated (Diehl, 2002). 

Fig. 6.4 Structural changes in the hepatic parenchyma with regard to reflex density and reflex distribution...

Mikami, N., Ebara, M., Yoshikawa, M., Ohto, M. Relationship between ultrasound-findings of low-echoic nodule of hepatic parenchyma in liver cirrhosis and development of hepatocellular carcinoma. (Japan.) Japon. J. Gastroenterol. 1990 87 1010-1019... 

This form of cholestasis is derived from a temporary or permanent obstruction of the intrahepatic bile ducts. Diffuse processes of disease can act as mechanical obstacles in the hepatic parenchyma, or major bile ducts may be subject to regional obstruction, (s. tab. 13.3)... 

In cases of severe fatty liver, there is indeed a risk of fat embolism occurring in the lungs, brain and kidneys. In view of the considerable fat masses stored in the hepatic parenchyma due to this condition, R. Virchow suspected the manifestation of fat embolism as early as 1886. (s. tab. 31.9) Blunt traumatism of the (enlarged) liver with subsequent mobilization of fat is thought to be the cause of this condition. It is not clear at present whether this so-called inundation theory offers sufficient explanation or whether it needs to be amended or even replaced by the so-called segregation theory (high lipaemia, deemulsification of blood fats, etc.). While hepatic fat embolism may be rare, it is nevertheless clinically relevant. 

In the course of massive subacute liver necrosis (or hepatic dystrophy), large parts of the hepatic parenchyma can be destroyed within a few months. Extensive regenerative nodes form from the remaining epithelium. Within these regenerations, the lobular architecture is either still maintained or has been partially restored. Areas of parenchymal loss are converted into fibre-dense scar tissue with embedded pseudoductuli and duct proliferations as well as irregularly located residual hepatocytes. This course is extremely rare. In the literature, it is also called incomplete postnecrotic cirrhosis. 

The electroporation-mediated in vivo gene transfer had been successfully used for hepatic parenchyma (70, 71), hepatocellular carcinoma (72), skin (73,74), skeletal muscle (69, 75,761, mouse testes (77), melanoma (65), human primary myoblast (78), glomeruli (79), brain (80), human primary hematopoietic stem cells (81), human esophageal tumor (82), and rat skeletal muscle for correcting anemia of renal failure (83). 

Hepatic Effects. Intentional ingestion of formaldehyde in a suicide attempt has been associated with hepatomegaly, icterus, and congestion of the hepatic parenchyma (Koppel et al. 1990). Some reports of human ingestion of formaldehyde include hepatotoxicity and increased liver enzymes (Freestone and Bentley 1989), although other reports do not indicate hepatic effects (Eells et al. 1981). 

FIGURE 8.4 Transitional cell carcinoma of the kidney is immu-nostained by CK7 (A) and CK20 (B). Metastatic gastrointestinal-derived carcinoma demonstrates strong CK20 reactivity, but hepatic parenchyma is CK20 negative (C). 

Extensive and progressive fibrosis of the hepatic parenchyma leads to cirrhosis of the liver, a process that has many canses. The development of fibrosis requires the activities of hepatic stellate cells, cytokines, proteases, and protease inhibitors. 

Focal nodular hyperplasia (FNH) arises in utero as an overgrowth of the hepatic parenchyma secondary to an arteriovenous malformation of the liver (SwiSCHUK 2005 SoMECH et al. 2001). Although it commonly presents in the adult population, some children with FNH have also been reported with a presentation peak in the pediatric age group between 6-10 years of age (39% of cases) (Somech et al. 2001). 

Sulfur-colloid liver scintigraphy may show large filling defects in the hepatic parenchyma, with prominent tracer avidity at the site of the tumor within a few seconds of the appearance of the bolus in the abdominal aorta. This increased activity persists into the venous phase. Hepatoblastomas may demonstrate increased uptake on delayed imaging, but this is rare (Suchy 2003). 

HCC can be represented on US as a hypo- or hyperechogenic mass depending on the amount of fat, or even as a heterogeneous mass with ill-defined borders located in the hepatic parenchyma. It may look identical to a hepatoblastoma. The presence of shadowing fod within the tumor will suggest intra-tumor calcifications. Evaluation of vascular invasion and dilatation of the portal vein will be seen with color Doppler with conventional gray-scale US (Siegel 2000) (Fig. 4.10a). 

The gallbladder blood supply comes not only from the cystic artery, but also from perforators to the body of the gallbladder from the hepatic parenchyma and the GDA. This is important from a practical viewpoint as, if the cystic artery is small, then this alternative route of blood supply to the gallbladder may be assumed to be present and prophylactic occlusion may be considered when avoiding microsphere flow into the cystic artery becomes impossible. 

Hepatic arterial bland and chemo-embolization have also been utilized. This therapy is based on the anatomic vascular distribution of the blood supply for hepatic tumors. The hepatic artery serves tumors in the liver almost exclusively while the portal vein serves normal hepatic parenchyma. There is some crossover but it is only approximately 10%. Bland embolization uses particles placed in the hepatic artery only while chemoembolization mixes these particles with a variety of chemotherapeutic agents and lipiodol, an iodinated poppy seed oil, which has been shown to increase the uptake into the cell via a pump in the cell wall. This therapy has been utilized for the last 20 years but eventual re-growth and recurrence have also uniformly occurred. Repeated embolizations are necessary to keep the disease in check and to palliate the patient s symptoms. The mean response to embolization is approximately 12-18 months with eventual occlusion of the hepatic arterial supply to the tumor after multiple embolizations. Response to embolotherapy has been dramatic for palliation of symptoms, with 63% of patients reporting a reduction in symptoms and an objective response seen on CT to be 76% either partial or minimal response, with an additional 16% reporting stable disease [4]. The embolotherapy will rid the patient of much of their tumor burden but isolated islets of viable tumor will remain after the procedure, accounting for the resurgence of disease. 

The basic assumption of Y infusion and dosimetry is the homogeneous distribution of microspheres, throughout the hepatic parenchyma resulting in the same radiation dose to the volume targeted for treatment. Some arteriovenous shunting within tumor is inevitable. Since tumors are fed almost exclusively by hepatic vasculature and are hypervascular rela-... 

Within the hepatic parenchyma, the uptake and storage of copper occurs in hepatocytes, which regulate the excretion of this metal into the bile. Copper appears in the bile as an unabsorbable complex, and as a result, there is no enterohepatic circulation of this metal. 

Figure 7. Electrophoretic-polarographic examination (a) top graph, healthy subject (6) middle graph, patient with lipoid nephrosis (c) bottom graph, patient with severe lesion of hepatic parenchyma.

Figure 11. Electrophoretic-polarographic denaturation examination of patient with less severe lesion of hepatic parenchyma.

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