scholarly journals Passive Congestion

2020 ◽  
Author(s):  
Keyword(s):  
2021 ◽  
Vol 91 (4) ◽  
pp. 359-378
Author(s):  
Yanad Abou Monsef ◽  
◽  
Osman Kutsal

The objective of this study was to investigate pathological disorders of the hepatobiliary system in dogs and cats in Ankara using pathomorphological methods, and to determine the types and frequency of the observed lesions. Furthermore, we aimed to evaluate hepatic reparation as a reaction of the liver to injury with different hepatobiliary lesions using immunohistochemical methods. Livers obtained from 56 cats and 74 dogs submitted for post-mortem investigation were examined macroscopically and microscopically. Samples with hepatic fibrosis were stained immunohistochemically with an α-SMA antibody. Lesions were found in 98% of the livers of the examined dogs and cats. The most common histopathological diagnoses were hepatitis (39.28%), hepatocellular lipidosis (16.07%), and cholangitis/cholangiohepatitis (14.28%) in cats. In dogs they were hepatitis (28.38%), passive congestion (25.68%) and proliferative lesions (21.62%). For some hepatobiliary lesions, breed, age and gender predispositions were observed. Immunohistochemically, the α-SMA antibody positively stained parenchymal, portal and septal myofibroblasts. A positive correlation was verified between immunohistochemical α-SMA scores and histochemical fibrosis scores. This is the first study in Turkey documenting both the incidence of hepatobiliary lesions among feline and canine species, and their pathomorphological features. In terms of reparation, the major role of the hepatic myofibroblasts in liver fibrosis was observed. There were variations in the intensity and location of positively stained cells according to the type of lesion. The conclusion of this research indicates the need to pay attention to certain hepatic lesions in dogs and cats, and provides a reference standard for further clinical and histopathological studies.


2020 ◽  
Vol 21 (24) ◽  
pp. 9420
Author(s):  
José Ignacio Fortea ◽  
Ángela Puente ◽  
Antonio Cuadrado ◽  
Patricia Huelin ◽  
Raúl Pellón ◽  
...  

Liver disease resulting from heart failure (HF) has generally been referred as “cardiac hepatopathy”. One of its main forms is congestive hepatopathy (CH), which results from passive venous congestion in the setting of chronic right-sided HF. The current spectrum of CH differs from earlier reports with HF, due to ischemic cardiomyopathy and congenital heart disease having surpassed rheumatic valvular disease. The chronic passive congestion leads to sinusoidal hypertension, centrilobular fibrosis, and ultimately, cirrhosis (“cardiac cirrhosis”) and hepatocellular carcinoma after several decades of ongoing injury. Contrary to primary liver diseases, in CH, inflammation seems to play no role in the progression of liver fibrosis, bridging fibrosis occurs between central veins to produce a “reversed lobulation” pattern and the performance of non-invasive diagnostic tests of liver fibrosis is poor. Although the clinical picture and prognosis is usually dominated by the underlying heart condition, the improved long-term survival of cardiac patients due to advances in medical and surgical treatments are responsible for the increased number of liver complications in this setting. Eventually, liver disease could become as clinically relevant as cardiac disease and further complicate its management.


1915 ◽  
Vol 21 (3) ◽  
pp. 203-212 ◽  
Author(s):  
G. H. Whipple ◽  
J. S. Speed

It has been established that specific liver poisons (chloroform, phosphorus) which cause histological changes in the liver cells, decrease the liver excretion of phenoltetrachlorphthalein. Also vascular disturbances (Eck fistula, passive congestion) with or without histological evidence may cause a fall in the output of phthalein through the liver. Sufficient evidence has been brought forward to show that the phenoltetrachlorphthalein excretion is a valuable index concerning the functional capacity of the liver. Ether anesthesia for a period of two hours usually causes a depression in the phthalein curve during the twenty-four hours following the anesthesia. Paraldehyde in doses sufficient to give anesthesia and stupor for a few hours will give adefinite fall in phthalein excretion. Chloral and urethane usually cause a decrease in phthalein output when given in considerable amounts. Alcohol causes a drop in the phthalein curve when given in large doses sufficient to cause stupor for a few hours. The drop in phenoltetrachlorphthalein excretion is demonstrated in the twenty-four hours following administration of the drug. A drop in the phthalein curve to two-thirds or one-half of normal indicates a definite liver injury and temporary impairment of function.


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