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21. H Conditions And Diseases Health English
Encephalopathy ? Hepatitis English Health Conditions and Diseases DigestiveDisorders Liver Hepatitis ? hepatocerebral encephalopathy English Health
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    Hemorrhagic Fevers @; Hemorrhoids @; Hepatic Encephalopathy @; Hepatitis@; hepatocerebral encephalopathy @. Hepatolenticular Degeneration
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    35. Hepatocerebral Degeneration
    Acquired (non Wilsonian) hepatocerebral degeneration is an uncommon complication of chronic the acute transient form of hepatic encephalopathy and the hepatocerebral syndrome
    http://www.neuro.nwu.edu/meded/MOVEMENT/hepato.html
    Please read our . This material is indended for use of third year medical students in the Neurology clerkship.
    Wilson's Disease
    Wilson's disease is an autosomal-recessive inherited disease caused by a defect on chromosome 143 encording copper transport. All patients with Wilsons have a fundemental defect in the hepatobiliar system and present with a combination of neurologic, psychiatric and musculoskeletal manifestations. Clinical findings include a dementia, a characteristic "wing beating" tremor, and ocular findings (deposition of copper in the cornea, the so-called Kayser-Fleisher ring). There can be a variety of other eye findings including oculogyric crises (Lee et al, 1999). Serum ceruloplasmin levels may be abnormal as is serum copper and urinary copper excretion. Treatment is with copper chelaters (D-penicillamine).
    Hepatocerebral Degeneration
    Acquired (non Wilsonian) hepatocerebral degeneration is an uncommon complication of chronic hepatic cirrhosis with spontaneous or surgical portosystemic shunting. It is characterized by a fluctuating but generally progressive course over one to nine years, often punctuated by bouts of acute hepatic encephalopathy. Examination post-mortem reveals foci of destruction of nerve cells and other parenchymal elements and widespread transformation of astrocytes, changes that are very similar to those of Wilson's disease. Pathologic: Portosystemic shunts are always present. The cerebral lesion is localized more regularly in the cortex than in Wilson's Disease. There is a predilection for the parietal and occipital regions and the lenticular nuclei may appear shrunken and discolored. Lesions resembling hypoxic zones are concentrated in vascular border zones. There is usually a sparing of the hippocampus, globus pallidus, and the deep folia of the cerebellar cortex (sites of predilection for anoxic encephalopathy). Microscopically there is widespread hyperplasia of protoplasmic astrocytes in the deep layers of the cerebral cortex, cerebellar cortex, thalamic, lenticular nuclei and other nuclei of the brainstem.

    36. Hepatic Encephalopathy
    Hepatic encephalopathy is a syndrome seen in progressive hepatocerebral degeneration, the latter a clinical variant of hepatic encephalopathy characterized by
    http://www.geocities.com/twisted_artist/Medecine/hepatic_encephalopathy.htm
    More Medical Pages Hepatic Encephalopathy Pancreatic Cancer Acute Pancreatitis Chronic Pancreatitis ... Anal Incontinence Hepatic Encephalopathy
    DEFINITION: Hepatic encephalopathy is a syndrome seen in patients with cirrhosis of the liver. It is characterized by personality changes, intellectual impairment, and a depressed level of consciousness , fluctuating neurologic signs, asterixis or "flapping tremor," and distinctive electroencephalographic changes. An important prerequisite for the syndrome is diversion of portal blood into the systemic circulation through porto-systemic collateral vessels. Indeed, hepatic encephalopathy may develop in non-cirrhotic patients who have undergone portocaval shunt surgery. The development of hepatic encephalopathy is explained to some extent by the effect of neurotoxic substances, which occurs in the setting of cirrhosis and portal hypertension. Subtle signs of hepatic encephalopathy are seen in nearly 70% of patients with cirrhosis. Symptoms may be debilitating in a significant number of patients and are seen in 24-53% of patients who undergo portosystemic shunt surgery. About 30% patients dying of end-stage liver disease will experience significant encephalopathy, approaching coma. Encephalopathy may be acute and reversible or chronic and progressive . In severe cases, irreversible coma and death may occur. Acute episodes may recur with variable frequency

    37. Hepatic Encephalopathy
    encephalopathy. encephalopathy, Hepatic; Portosystemic encephalopathy; encephalopathy, hepatocerebral; encephalopathy, PortalSystemic; encephalopathy
    http://medical.webends.com/index.php?id=5662

    38. Hepatic Encephalopathy
    encephalopathy, Hepatic; Portosystemic encephalopathy; encephalopathy, hepatocerebral;encephalopathy, PortalSystemic; encephalopathy, Portosystemic
    http://medical.webends.com/kw/Hepatic Encephalopathy
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    Hepatic Encephalopathy
    Encephalopathy, Hepatic; Portosystemic Encephalopathy; Encephalopathy, Hepatocerebral; Encephalopathy, Portal-Systemic; Encephalopathy, Portosystemic; Fulminant Hepatic Failure with Cerebral Edema; Hepatic Coma; Hepatic Stupor A syndrome characterized by central nervous system dysfunction in association with LIVER FAILURE , including portal-systemic shunts. Clinical features include lethargy and CONFUSION (frequently progressing to COMA ); asterixis; NYSTAGMUS; brisk oculovestibular reflex es; decorticate and decerebrate posturing; MUSCLE SPASTICITY ; and bilateral extensor plantar reflex es (see REFLEX , BABINSKI ELECTROENCEPHALOGRAPHY may demonstrate triphasic waves. (From Adams et al., Principles of Neurology Diagnosis of Stupor and Coma , 3rd ed, p222-5)
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    39. Chapter 14 - Section 13: First Principles Of Gastroenterology
    acute recurrent, chronic recurrent and chronic permanent encephalopathy (the lastoften forms part of the spectrum of acquired hepatocerebral degeneration).
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    - Select a chapter - 1. Symptoms and Signs 2. Nutrition 3. Ethics 4. Research/Clinical Trials 5. Esophagus 6. Stomach and Duodenum 7. Small Intestine 8. Intestinal Ischemia 9. H.I.V. 10. Inflammatory Bowel 11. Colon 12. Pancreas 13. Biliary System 14. Liver 15. Paediatrics 16. Video Endoscopic Images Search
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    13. Hepatic Encephalopathy / L.J. Worobetz page 537 Hepatic encephalopathy (HE) is a complex, potentially reversible neuropsychiatric condition that occurs as a consequence of acute or chronic liver disease. It is characterized by changes of personality, consciousness, behavior and neuromuscular function ( Table 20 ). Early features include reversal of sleep pattern, apathy, hypersomnia, irritability and personal neglect. In later stages, delirium and coma may occur. Neurologic signs may include hyperreflexia, rigidity, myoclonus and asterixis. Asterixis is not specific to hepatic encephalopathy and may be present in other causes of metabolic encephalopathy. Seizures and lateralizing signs are uncommon and are more commonly seen in acute than chronic liver failure. Clinically, a number of encephalopathic patterns can be observed: acute, acute recurrent, chronic recurrent and chronic permanent encephalopathy (the last often forms part of the spectrum of acquired hepatocerebral degeneration).

    40. Hepatic Encephalopathy
    Hepatic encephalopathy is a syndrome seen in progressive hepatocerebral degeneration, the latter a clinical variant of hepatic encephalopathy characterized by
    http://www.meverett.com/hepatic/encephalopathy1.html
    Hepatic Encephalopathy
    DEFINITION: Hepatic encephalopathy is a syndrome seen in patients with cirrhosis of the liver. It is characterized by personality changes, intellectual impairment, and a depressed level of consciousness , fluctuating neurologic signs, asterixis or "flapping tremor," and distinctive electroencephalographic changes. An important prerequisite for the syndrome is diversion of portal into the systemic circulation through porto-systemic collateral vessels. Indeed, hepatic encephalopathy may develop in non-cirrhotic patients who have undergone portocaval shunt surgery. The development of hepatic encephalopathy is explained to some extent by the effect of neurotoxic substances, which occurs in the setting of cirrhosis and portal hypertension. Subtle signs of hepatic encephalopathy are seen in nearly 70% of patients with cirrhosis. Symptoms may be debilitating in a significant number of patients and are seen in 24-53% of patients who undergo portosystemic shunt surgery. About 30% patients dying of end-stage liver disease will experience significant encephalopathy, approaching coma. Encephalopathy may be acute and reversible or chronic and progressive . In severe cases, irreversible coma and may occur. Acute episodes may recur with variable frequency

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