Sandbox: nima: Difference between revisions
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*Chronic alcohol use | *Chronic alcohol use | ||
*History of drug and toxin use | *History of drug and toxin use | ||
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**Aphlatoxin | **Aphlatoxin | ||
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Revision as of 17:45, 16 November 2018
Overview
The hallmark of Hepatic Encephalopathy is accumulation of ammonia and toxic substances in the blood that are normally detoxified in the liver. A positive history of and is suggestive of . The most common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3]. Common symptoms of [disease] include [symptom 1], [symptom 2], and [symptom 3]. Less common symptoms of [disease name] include [symptom 1], [symptom 2], and [symptom 3].
History and Symptoms
Hepatic encephalopathy or portosystemic encephalopathy is a syndrome of largely reversible impairment of brain function occurring in patients with acute or chronic liver failure or when the liver is bypassed by portosystemic shunts.[1]Hepatic encephalopathy (HE) is a common problem in liver cirrhosis and is associated with typical changes of cerebral metabolite pattern observed by proton magnetic resonance spectroscopy (MRS).[2][3]
A positive history of Alcohol use and viral Hepatitis is suggestive of HE. The most common symptoms of Hepatic encephalopathy include:
History
Patients with hepatic encephalopathy may have a positive history of:[5]
- Viral hepatitis
- Chronic alcohol use
- History of drug and toxin use
- Halothane
- Acetaminophen
- Aphlatoxin
Common Symptoms
Common symptoms of hepatic encephalopathy include:
- Memory impairment
- Personality changes
- Coma
- Jaundice
Hepatic encephalopathy (HE) is a common problem in liver cirrhosis and is associated with typical changes of cerebral metabolite pattern observed by proton magnetic resonance spectroscopy (MRS).[2]
Hepatic encephalopathy (HE) is a common problem in liver cirrhosis and is associated with typical changes of cerebral metabolite pattern observed by proton magnetic resonance spectroscopy (MRS).
Less Common Symptoms
Less common symptoms of [disease name] include
- [Symptom 2]
- [Symptom 3]
References
- ↑ Schulz C, Schütte K, Vilchez-Vargas R, Vasapolli R, Malfertheiner P (November 2018). "Long-Term Effect of Rifaximin with and without Lactulose on the Active Bacterial Assemblages in the Proximal Small Bowel and Faeces in Patients with Minimal Hepatic Encephalopathy". Dig Dis: 1–9. doi:10.1159/000494216. PMID 30428474.
- ↑ 2.0 2.1 . PMID 30427626. Missing or empty
|title=(help) - ↑ Rimar D, Kruzel-Davila E, Dori G, Baron E, Bitterman H (April 2007). "Hyperammonemic coma--barking up the wrong tree". J Gen Intern Med. 22 (4): 549–52. doi:10.1007/s11606-007-0131-6. PMC 1829435. PMID 17372808.
- ↑ Shawcross DL, Dunk AA, Jalan R, Kircheis G, de Knegt RJ, Laleman W, Ramage JK, Wedemeyer H, Morgan IE (February 2016). "How to diagnose and manage hepatic encephalopathy: a consensus statement on roles and responsibilities beyond the liver specialist". Eur J Gastroenterol Hepatol. 28 (2): 146–52. doi:10.1097/MEG.0000000000000529. PMC 4885589. PMID 26600154.
- ↑ Hoffmann V, Jones K, Leroy J (December 2015). "Mitigating aflatoxin exposure to improve child growth in Eastern Kenya: study protocol for a randomized controlled trial". Trials. 16: 552. doi:10.1186/s13063-015-1064-8. PMC 4669614. PMID 26634701.