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Books on the topic 'Hepatic Toxicity and CCl4'

Author: Grafiati

Published: 4 June 2025

Last updated: 1 August 2025

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Consult the top 17 books for your research on the topic 'Hepatic Toxicity and CCl4.'

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1

Felipo, Vicente, and Santiago Grisolia, eds. Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity. Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1989-8.

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2

Grisolía, Santiago, Vicente Felipo, and María-Dolores Miñana, eds. Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5826-8.

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3

International Symposium on Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity, Molecular Basis and Clinical Aspects (1989 Valencia, Spain). Cirrhosis, hepatic encephalopathy, and ammonium toxicity. Plenum Press, 1990.

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4

Vicente, Felipo, and Grisolía Santiago 1923-, eds. Hepatic encephalopathy, hyperammonemia, and ammonia toxicity. Plenum Press, 1994.

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5

Redegeld, Franciscus Antonius Maria. Hepatic and renal toxicity of xenobiotics: The role of metabolism and transport. s.n.], 1989.

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6

Felipo, Vicente, Santiago Grisolía, and Maria-Dolores Miñana. Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity. Springer London, Limited, 2013.

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7

Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity. Island Press, 1995.

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8

Felipo, Vicente, and Santiago Grisolía. Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity. Springer London, Limited, 2012.

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9

Felipo, Vicente, and Santiago Grisolía. Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity. Springer, 2012.

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10

Felipo, Vicente, Santiago Grisolía, and Maria-Dolores Miñana. Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity. Springer, 2012.

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11

Minana, Maria-Dolores. Cirrhosis, Hepatic Encephalopathy, and Ammonium Toxicity. Island Press, 1991.

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12

(Editor), Vicente Felipo, and Santiago Grisolía (Editor), eds. Hepatic Encephalopathy, Hyperammonemia and Toxicity (Advances in Experimental Medicine and Biology). Springer, 1995.

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13

(Editor), Santiago Grisolía, Vicente Felipo (Editor), and Maria-Dolores Miñana (Editor), eds. Cirrhosis, Hepatic Encephalopathy and Ammonium Toxicity (Advances in Experimental Medicine and Biology). Springer, 1991.

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14

Padmakumar, Anand D., and Mark C. Bellamy. Pathophysiology and causes of jaundice in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0192.

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Critically-ill patients develop jaundice for a variety of reasons. A good understanding of bilirubin metabolism can help the clinician to diagnose and treat jaundice. Intensive care unit (ICU) physicians commonly encounter elevated serum bilirubin in severely-ill patients, which can be associated with increased morbidity and mortality. A complex interaction of enzymatic pathways leads to safe excretion of bilirubin. This fine homeostasis is often disturbed and leads jaundice, which can be broadly classified into three main categories—prehepatic, hepatic, and post-hepatic. Common examples inclu

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15

MacCallum, Niall S. Management of oncological complications in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0376.

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Important treatment complications relevant to critical care are discussed. Cancer-related pain is complex and requires multidisciplinary care, particularly in the peri-operative setting. Chemotherapeutic complications include pancytopenia, cardiac, pulmonary, renal, gastrointestinal, hepatic, and neurotoxicity. Radiotherapy complications include cardiac, pulmonary, and gastrointestinal toxicity. In general, management includes assessing the risk-benefit to cytotoxic therapy withdrawal and supportive care. There is a paucity of proven treatment options for most complications, althoughcertain th

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16

Columb, Malachy O. Local anaesthetic agents. Edited by Michel M. R. F. Struys. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0017.

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Local anaesthetic agents cause a pharmacologically induced reversible neuropathy characterized by axonal conduction blockade. They act by blocking the sodium ionophore and exhibit membrane stabilizing activity by inhibiting initiation and propagation of action potentials. They are weak bases consisting of three components: a lipophilic aromatic ring, a link, and a hydrophilic amine. The chemical link classifies them as esters or amides. Local anaesthetics diffuse through the axolemma as unionized free-base and block the ionophore in the quaternary ammonium ionized form. The speed of onset of b

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17

Al-Darraji, Haider A., and Frederick L. Altice. The Perfect Storm. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199374847.003.0008.

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Globally, tuberculosis (TB) is a major cause of morbidity and mortality among people who use drugs (PWUD), particularly those co-infected with HIV. This chapter describes how TB is prevalent in several prison systems by virtue of the concentration of PWUD and people living with HIV. TB is further amplified within this system through overcrowding, poor ventilation, and delayed access to quality prevention and treatment services. In many countries, individuals cycling through prisons are inadequately screened and treated for TB, and affected individuals may have frequent treatment interruptions.

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