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Books on the topic 'Radiation induced liver disease'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

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1

Farrell, Geoffrey C. Drug-induced liver disease. Edinburgh: Churchill Livingstone, 1994.

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2

Second primary cancers and cardiovascular disease after radiation therapy. Bethesda, Md: National Council on Radiation Protection and Measurements, 2011.

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3

Gofman, John W. Preventing breast cancer: The story of a major, proven, preventable cause of this disease. San Francisco, Calif., U.S.A: C.N.R. Book Division, Committee for Nuclear Responsibility, 1995.

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4

Gofman, John W. Preventing breast cancer: The story of a major, proven, preventable cause of this disease. 2nd ed. San Francisco, Calif., U.S.A: C.N.R. Book Division, Committee for Nuclear Responsibility, Inc., 1996.

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5

Drug-Induced Liver Disease. Elsevier Science & Technology Books, 2013.

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6

Neil, Kaplowitz, and DeLeve Laurie D. 1955-, eds. Drug-induced liver disease. 2nd ed. New York: Informa Healthcare USA, 2007.

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7

(Editor), Neil Kaplowitz, and Laurie D. DeLeve (Editor), eds. Drug-Induced Liver Disease. Informa Healthcare, 2002.

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8

Neil, Kaplowitz, and DeLeve Laurie D. 1955-, eds. Drug-induced liver disease. New York: Marcel Dekker, 2003.

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9

Kaplowitz, Neil. Drug-Induced Liver Disease. Edited by Neil Kaplowitz and Laurie D. DeLeve. CRC Press, 2007. http://dx.doi.org/10.3109/9781420021141.

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10

Keshav, Satish, and Palak Trivedi. Drug-induced liver disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0215.

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Drugs are an important and common cause of hepatic injury. This is unsurprising, as the liver is a major site for drug clearance, biotransformation, and excretion. A careful history of drugs taken (prescribed, over the counter, herbal, or illicit) is vital when assessing anyone with abnormal liver function tests. Although toxic or idiosyncratic adverse reactions may occur with many therapeutic agents, drug-induced jaundice is not so common.
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11

Drug-Induced Liver Disease. Elsevier, 2013. http://dx.doi.org/10.1016/c2010-0-68917-6.

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12

Kaplowitz, Neil. Drug-Induced Liver Disease. CRC Press, 2002. http://dx.doi.org/10.1201/b15279.

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13

Neil, Kaplowitz, and DeLeve Laurie D. 1955-, eds. Drug-induced liver disease. New York: Marcel Dekker, 2003.

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14

(Editor), Neil Kaplowitz, and Laurie D. DeLeve (Editor), eds. Drug-Induced Liver Disease, Second Edition. 2nd ed. Informa Healthcare, 2007.

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15

Kaplowitiz, Neil, and Laurie DeLeve, eds. Drug-Induced Liver Disease, Second Edition. Informa Healthcare, 2002. http://dx.doi.org/10.1201/9780203909126.

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16

Keshav, Satish, and Alexandra Kent. Alcoholic liver disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0211.

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Alcoholic liver disease develops in excessive drinkers and can manifest in three forms: alcoholic fatty liver (steatosis; >80%), alcoholic hepatitis (10%–35%), and cirrhosis (10%). The more alcohol consumed, the greater the risk of alcoholic liver disease, although other factors may also be involved. Alcohol can cause significant damage without producing any symptoms, and many patients will only have liver dysfunction detected on routine blood tests. Many patients report non-specific symptoms, such as anorexia, morning nausea, diarrhoea, and vague right upper quadrant abdominal pain. The underlying pathogenesis of alcohol-induced injury is not fully understood but is thought to involve various mechanisms. This chapter discusses alcoholic liver disease, focusing on its etiology, symptoms, demographics, natural history, complications, diagnosis, prognosis, and treatment.
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17

Zimmerman, Hyman J. Hepatotoxicity: The Adverse Effects of Drugs and Other Chemicals on the Liver. 2nd ed. Lippincott Williams & Wilkins, 1999.

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18

National Academy of Sciences (U.S.), ed. Review of the Hanford thyroid disease study draft final report. Washington, D.C: National Academy Press, 2000.

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19

Colvin, Lesley A., and Marie Fallon. Cancer-induced bone pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0132.

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Bone is the third most common site of metastatic disease, after liver and lung, with approximately 75% of these patients suffering from related pain. Cancer-induced bone pain (CIBP) is a major clinical problem, with limited options for predictable, rapid, and effective treatment for some of the elements without unacceptable adverse effects. Our understanding of how current therapy acts is based mainly on studies in non-cancer pain syndromes, which are likely to be quite different, not only in clinical presentation, but also in terms of pathophysiology. It can be difficult to study the specific neurobiological changes associated with CIBP, although development of laboratory models of isolated bone metastases has allowed more specific study of pain mechanisms in this syndrome. In order to evaluate our current therapies properly and direct the development of new therapies logically, it is important to understand the underlying mechanisms of CIBP. This chapter discusses pain processing and the mechanisms and management of CIBP.
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20

Izzedine, Hassan, and Victor Gueutin. Drug-induced chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0087.

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The chronic form of drug-induced tubulointerstitial nephritis (CTIN) is an insidious disease and most probably represents the common final response pattern of the kidney to a variety of agents (including analgesics, lithium, antineoplastic chemotherapeutic agents, like cisplatin and nitrosoureas, and immunosuppressive drugs, such as ciclosporin and tacrolimus). Drug-induced CTIN is usually asymptomatic, presenting with slowly progressive renal impairment. Because of its insidious nature, CTIN is often diagnosed incidentally on routine laboratory screening or evaluation of CKD. The diagnosis of drug-induced CTIN largely depends on the history of exposure to a nephrotoxic drug. Clinical investigations may show modest elevation in serum creatinine, evidence of tubular dysfunction (e.g. renal tubular acidosis), or Fanconi syndrome (i.e. aminoaciduria, glycosuria, hypophosphataemia, and hypouricaemia). Urinalysis may be normal or show low-grade proteinuria (< 1.5 g/day) and/or pyuria. Diagnosis depends on renal biopsy, which reveals variable cellular infiltration of the interstitium, tubular atrophy, and fibrosis. Analgesic nephropathy is possibly still the most common category of CTIN worldwide. The amount of phenacetin-acetaminophen combination required to cause CTIN has been estimated to be at least 2–3 kg over many years. Lithium-induced CTIN occurs in a small subset of patients receiving long-term lithium therapy, who have had repeated episodes of lithium toxicity, with high serum drug levels. CTIN induced by ciclosporin or tacrolimus is common among patients receiving kidney, heart, liver, and pancreas transplants. The mechanism appears to be dependent largely on the potent vasoconstrictive effects of these drugs. The recognition of a potential association between a patient’s renal disease and exposure to a drug is crucial, because, unlike many other forms of renal disease, drug-induced CTIN can be prevented and even reversed, by avoiding additional drug exposure.
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21

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Gastroenterology and hepatology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0009.

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Chapter 9 covers the basic science and clinical topics relating to gastroenterology and hepatology which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers basic science, gastrointestinal investigation, malabsorption and malnutrition, inflammatory bowel disease, acute upper gastrointestinal haemorrhage, lower gastrointestinal bleeding and related disorders, gastrointestinal infections, gastrointestinal cancer, miscellaneous gastrointestinal problems, normal liver and biliary function, variceal disease, hepatic tumours, acute (fulminant) liver failure, haemochromatosis, Wilson disease (hepatolenticular degeneration), Alpha-1 antitrypsin deficiency, alcohol-induced liver disease, hepatitis, biliary diseases, and non-alcoholic fatty liver disease.
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22

(Contributor), WHO, ed. Ionizing Radiation, Part II: Some Internally Deposited Radionuclides (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans). World Health Organisation, 2001.

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23

Patel, Sameer, and Julia Wendon. Pathophysiology and causes of acute hepatic failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0194.

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Acute liver failure (ALF) is a rare, life-threatening clinical syndrome, resulting in loss of hepatic metabolic and immunological function, in a person with no prior history of liver disease. Mortality can still exceed 50%. ALF is characterized by hepatic encephalopathy (HE) and coagulopathy, occurring within days or weeks. Establishing aetiology is essential for treatment, prognostication, and liver transplantation consideration. Viral hepatitis and drug-induced liver failure are the two commonest causes worldwide. Aetiology and time of onset of encephalopathy determines prognosis. Disease progression can rapidly result in multi-organ failure. Ammonia has been postulated in the development of HE, cerebral oedema and intracranial hypertension. Coagulopathy can be highly variable, with some patients prothrombotic, or exhibiting balanced coagulation disorders. Systemic inflammatory response syndrome (SIRS) and associated infection are frequently observed. Significant haemodynamic changes are common while renal failure is an independent risk factor for mortality. Respiratory failure is less common. Deranged homeostasis results in severe hypoglycaemia, and metabolic disturbance.
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24

Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Haemostasis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0010.

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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
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25

Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Angela Theodoulou. Haemostasis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0010_update_001.

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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
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26

Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Red cell disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0002.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia - β thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
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27

Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, Banu Kaya, and Angela Theodoulou. Red cell disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0002_update_001.

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The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α‎ thalassaemia - β‎ thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
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28

Newell-Price, John, Alia Munir, and Miguel Debono. Obesity: differential diagnosis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0081.

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This topic addresses the causes and consequences of obesity, defined as a body mass index (BMI) of 30 or above. While BMI is the most commonly used measure of obesity, the waist-to-height ratio correlates better with visceral obesity. At least 1.1 billion adults are overweight worldwide, but a medical cause for obesity is found in less than 1 out of every 100 cases. The health consequences of obesity are diverse and serious. Approximately 50% of all hypertension is secondary to obesity, and the heart may also be harmed by obesity-induced chronic volume overload and ischaemic heart disease. Obesity contributes strongly to the pathophysiology of type II diabetes and its consequences. Obese patients have higher rates of stroke, osteoarthritis, obstructive sleep apnoea, gastro-oesophageal reflux, chronic liver disease, and infertility. In addition, obesity increases the incidence of some cancers (e.g. breast, prostate, and colorectal). The psychological and social effects of obesity include higher rates of depression and anxiety, and reduced employment.
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29

Muche, Marion, and Seema Baid-Agrawal. Hepatitis B. Edited by Vivekanand Jha. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0185_update_001.

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Hepatitis B virus (HBV) has been causally linked to a variety of renal diseases, the most common being glomerular diseases and systemic autoimmune disease. Membranous nephropathy (MN) is the commonest HBV-associated glomerulonephritis (HBV-GN), followed by membranoproliferative glomerulonephritis (MPGN), mesangial proliferative glomerulonephritis, immunoglobulin (Ig)-A nephropathy, and focal segmental glomerulosclerosis (FSGS). Polyarteritis nodosa is a rare manifestation. The incidence of HBV-associated renal diseases seems to be decreasing with the introduction of vaccination programmes.HBV-MN is the most frequent cause of nephrotic syndrome in children in countries with high endemicity of HBV infection. The clinical course is usually benign in children with high rates of spontaneous remission rates and low risk of progression to renal failure. The prognosis is worse in adults. Of the systemic autoimmune disorders associated with HBV infection that involve the kidneys, the strongest link has been found with polyarteritis nodosa (PAN), a lesion that causes arteritis of medium-sized renal vessels. HBV-associated PAN (HBV-PAN) usually manifests in the first year after infection, and is clinically indistinguishable from classic PAN.Diagnosis of HBV-GN or -PAN is based on the clinical picture, histological findings, evidence of viral replication in serum and/or liver and detection of HBV antigens or DNA in the tissue. Besides deposition of immune complexes, other mechanisms such as virus-induced cytopathic damage have been proposed to explain the pathogenesis.HBV-GN and HBV-PAN appear to respond to antiviral treatment. Both show remission after HBeAg seroconversion. The available studies predominantly employed first-generation agents like interferon alpha and lamivudine, which showed suppression of viral replication and clinical remission of HBV-associated renal disease. Immunosuppressive therapy appears to be inevitable for the control of severe HBV-PAN and could be helpful in addition to antiviral treatment for cases of HBV-GN not responding clinically to antiviral treatment.
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