Pathophysiology of liver disease:
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
Philadelphia [u.a.]
Saunders
2000
|
| Schriftenreihe: | Clinics in liver disease
4,2 |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XII S., S. 295 - 512 |
Internformat
MARC
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| 245 | 1 | 0 | |a Pathophysiology of liver disease |c Jorge L. Herrera |
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Datensatz im Suchindex
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| adam_text | PATHOPHYSIOLOGY OF LIVER DISEASE
CONTENTS
Preface xi
Jorge L. Herrera
Apoptosis in Hepatic Pathophysiology 295
Tushar Patel
Apoptosis is a fundamental biologic process involved in hepatic
physiology and pathophysiology. This article provides an over¬
view of the cellular mechanisms of apoptosis as related to liver
diseases, and the role of apoptosis in pathophysiologic processes
and specific diseases of the liver is discussed. Further research
into the mechanisms of hepatic apoptosis eventually will enhance
our understanding of disease pathophysiology and may provide
novel therapeutic strategies for the treatment of a wide range of
human liver diseases.
The Cell and Molecular Biology of Hepatic
Fibrogenesis: Clinical and Therapeutic Implications 319
Don C. Rockey
Extensive investigation over the past two decades has yielded
significant new information about the cellular and molecular
mechanisms underlying hepatic fibrogenesis. This work has been
important to understanding the pathophysiologic basis of hepatic
fibrogenesis and has provided an important conceptual frame¬
work with which to base therapy. The central event in fibrogen¬
esis is activation of resident perisinusoidal cells, termed hepatic
stellate cells. Stellate cell activation is characterized by a number
of important features including enhanced extracellular matrix
synthesis and a prominent contractile phenotype. Substantial ef¬
fort has been directed at understanding the basic mechanisms
underlying activation; indeed, given the central role of stellate
CLINICS IN LIVER DISEASE
VOLUME 4 • NUMBER 2 • MAY 2000 V
cell activation in hepatic fibrogenesis, effective therapy for hepatic
fibrogenesis will most likely be directed at this event. Finally,
available and potential therapies, in the context of the pathogene
sis of fibrogenesis are highlighted.
Mechanisms of Cholestasis 357
Gerd A. Kullak Ublick and Peter J. Meier
Cholestasis describes the disruption of bile flow or bile produc¬
tion. The site of injury can be intrahepatic, extrahepatic, or both.
Generic intrahepatic cholestasis syndromes are caused by dys¬
function of individual hepatocellular transport systems, by inborn
errors of bile salt synthesis secondary to specific enzymopathies,
or by autoimmune disease. Acquired intrahepatic cholestasis syn¬
dromes are caused by drugs, inflammation, or sex steroids. Recent
insights into the molecular mechanisms underlying the patho
physiology of disturbed bile production may facilitate the devel¬
opment of specific therapies for patients with cholestatic liver
disease.
Liver Injury in Alphai Antitrypsin Deficiency 387
David H. Perlmutter
Alpharantitrypsin deficiency is the most common genetic cause
of liver disease in children. It is also associated with chronic liver
disease, hepatocellular carcinoma, and pulmonary emphysema in
adults. Liver injury is caused by hepatotoxic effects of retention
of the mutant alphai antitrypsin molecule within the endoplasmic
reticulum of liver cells, and emphysema is caused by uninhibited
proteolytic damage to elastic tissue in the lung parenchyma. Re¬
cent studies of the biochemistry and cell biology of the mutant
alpharantitrypsin molecule have led to advances in understand¬
ing susceptibility to liver injury and in developing new strategies
for prevention of both liver and lung disease.
Iron Induced Liver Injury 409
Herbert L. Bonkovsky and Richard W. Lambrecht
Iron, either in the form of heme or non heme compounds, is
essential to life, but it can also pose serious health risks. The liver
is a principal target for iron toxicity because it is chiefly responsi¬
ble for taking up and storing excessive amounts of iron. The
major hepatic toxicities of iron overload include damage to multi¬
ple cell types (hepatocytes, Kupffer cells, hepatic stellate cells)
and to multiple subcellular organelles (mitochondria, lysosomes,
and smooth endoplasmic reticulum). Heavy iron overload, as
occurs in primary (hereditary) or secondary forms of hemochro
matosis, may cause cirrhosis, liver failure, and hepatocellular
carcinoma. In addition, iron has been shown to be a contributory
factor in the development or progression of alcoholic liver dis
Vi CONTENTS
ease, nonalcoholic liver steatohepatitis, chronic viral hepatitis,
porphyria cutanea tarda, and, perhaps, in alpharantitrypsin defi¬
ciency and end stage liver disease, regardless of cause.
Mechanisms of Autoimmune Liver Disease 431
Christopher L. Mabee and Dwain L. Thiele
Several lines of evidence suggest that autoimmune hepatitis and
primary biliary cirrhosis are autoimmune diseases. This article
discusses both the immunologic mechanisms of liver injury and
the mechanisms of cell injury mediated by lymphocytes. This
article also reviews the proposed immunopathogenesis of autoim¬
mune hepatitis and primary biliary cirrhosis.
Mechanisms of Ascites Formation 447
Andres Cardenas, Ramon Bataller, and Vicente Arroyo
This article reviews the current knowledge of the pathophysiol
ogy of ascites formation in cirrhosis. A detailed description of the
local factors (portal hypertension and lymph production), the
renal functional abnormalities, and the deranged systemic and
splanchnic hemodynamics involved in ascites formation is pro¬
vided. Finally, the recently proposed Forward Theory of ascites
formation is discussed.
Pathogenesis of Hepatic Encephalopathy 467
E. Anthony Jones
Hepatic encephalopathy (HE) is considered to be a reversible
metabolic encephalopathy that occurs as a complication of hepa
tocellular failure and is associated with increased portal systemic
shunting of gut derived nitrogenous compounds. Its manifesta¬
tions are most consistent with a global depression of central
nervous system function, which could arise as a consequence
of a net increase in inhibitory neurotransmission, owing to an
imbalance between the functional status of inhibitory (e.g.,
GABA) and excitatory (e.g., glutamate) neurotransmitter systems.
In liver failure, factors that contribute to increased GABAergic
tone include increased synaptic levels of GABA and increased
brain levels of natural central benzodiazepine (BZ) receptor ago¬
nists. Ammonia, present in modestly elevated levels, may also
augment GABAergic tone by direct interaction with the GABAA
receptor, synergistic interactions with natural central BZ receptor
agonists, and stimulation of astrocytic synthesis and release of
neurosteroid agonists of the GABAA receptor. Thus, there is ratio¬
nale for therapies of HE that lower ammonia levels and incremen¬
tally reduce increased GABAergic tone towards the physiologic
norm.
CONTENTS Vii
Hepatorenal Syndrome 487
Ramon Bataller, Pere Gines, Vicente Arroyo, and
Juan Rodes
Hepatorenal syndrome (HRS) is a functional renal failure charac¬
terized by a striking renal vasoconstriction that complicates cir
rhotic patients with advanced liver disease and ascites. The re¬
cently revised diagnostic criteria and clinical types of this
syndrome are discussed. The factors acting on renal circulation
leading to renal vasoconstriction and the link between systematic
circulatory abnormalities and renal hypoperfusion are specially
reviewed. The development of new and promising treatments
(transjugular intrahepatic portosystemic shunts and systemic va¬
soconstrictors) that are capable of prolonging survival in some
patients with HRS, is reviewed. Finally this article discusses the
low likelihood of timely liver transplantation in these patients
and the need to prevent the development of HRS in cirrhotic
patients with ascites.
Index 509
Subscription Information Inside back cover
Vlii CONTENTS
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| physical | XII S., S. 295 - 512 |
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| series | Clinics in liver disease |
| series2 | Clinics in liver disease |
| spelling | Pathophysiology of liver disease Jorge L. Herrera Philadelphia [u.a.] Saunders 2000 XII S., S. 295 - 512 txt rdacontent n rdamedia nc rdacarrier Clinics in liver disease 4,2 Foie, maladies - Physiopathologie Liver Diseases Pathophysiologie (DE-588)4044898-8 gnd rswk-swf Leberkrankheit (DE-588)4034937-8 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Leberkrankheit (DE-588)4034937-8 s Pathophysiologie (DE-588)4044898-8 s DE-604 Herrera, Jorge L. Sonstige oth Clinics in liver disease 4,2 (DE-604)BV011603500 4,2 HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=008986110&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Pathophysiology of liver disease Clinics in liver disease Foie, maladies - Physiopathologie Liver Diseases Pathophysiologie (DE-588)4044898-8 gnd Leberkrankheit (DE-588)4034937-8 gnd |
| subject_GND | (DE-588)4044898-8 (DE-588)4034937-8 (DE-588)4143413-4 |
| title | Pathophysiology of liver disease |
| title_auth | Pathophysiology of liver disease |
| title_exact_search | Pathophysiology of liver disease |
| title_full | Pathophysiology of liver disease Jorge L. Herrera |
| title_fullStr | Pathophysiology of liver disease Jorge L. Herrera |
| title_full_unstemmed | Pathophysiology of liver disease Jorge L. Herrera |
| title_short | Pathophysiology of liver disease |
| title_sort | pathophysiology of liver disease |
| topic | Foie, maladies - Physiopathologie Liver Diseases Pathophysiologie (DE-588)4044898-8 gnd Leberkrankheit (DE-588)4034937-8 gnd |
| topic_facet | Foie, maladies - Physiopathologie Liver Diseases Pathophysiologie Leberkrankheit Aufsatzsammlung |
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