IPLab:Lab 12:Alcoholic Cirrhosis - Revision history

Peter Anderson: /* Clinical Summary */

2020-07-09T21:10:19Z

‎Clinical Summary

Peter Anderson: /* Journal Articles */

2016-08-25T13:47:20Z

‎Journal Articles

Peter Anderson: /* Journal Articles */

2016-08-25T13:44:48Z

‎Journal Articles

Seung Park: /* Images */

2013-08-30T01:47:31Z

‎Images

Seung Park: /* Related IPLab Cases */

2013-08-26T14:52:13Z

‎Related IPLab Cases

Seung Park: /* Images */

2013-08-26T14:51:43Z

‎Images

Seung Park: /* Journal Articles */

2013-08-26T14:50:30Z

‎Journal Articles

Seung Park: /* Reference */

2013-08-26T14:49:45Z

‎Reference

Seung Park at 04:26, 23 August 2013

2013-08-23T04:26:31Z

Peter Anderson at 16:21, 21 August 2013

2013-08-21T16:21:54Z

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 == Clinical Summary ==
-This 56-year-old white male came to the emergency room because of weakness, lack of appetite, shortness of breath, abdominal distention, and an altered mental status. He was a known alcoholic who drank approximately one pint of whiskey per day. Physical examination revealed a wasted appearance, icterus, a protuberant abdomen, bilateral gynecomastia, sparse axillary hair, and spider angiomata on his chest. Liver and spleen were not palpable, the testes were atrophic, and the legs showed petechial hemorrhages and 3+ edema. Admission laboratory values revealed a hemoglobin of 9.5 g/dL, an MCV of 106 fL, a platelet count of 97,000/mL, and a prothrombin time of 19.2 seconds. In addition, his albumin was 2.3 g/dL, bilirubin, total 6.5 mg/dL, AST 21.0 U/L, ALT 56 U/L, alkaline phosphatase 180 U/L, and GGT 320 U/L. The patient was treated with thiamine, folate, multivitamins, and vitamin K and an intravenous line was placed to infuse 5% dextrose. An esophagogastroduodenoscopy (EGD) was performed which demonstrated large esophageal varices with evidence of previous bleeding sites. Two days after admission the patient developed a massive hematemesis and his hematocrit dropped to 17%. Emergency EGD showed ruptured esophageal varices. Despite successful sclerotherapy and supportive transfusions, the patient lapsed into coma and died the next day.
+The patient was given thiamine, folate, multivitamins, and vitamin K and an intravenous line was placed to infuse 5% dextrose. An esophagogastroduodenoscopy (EGD) demonstrated large esophageal varices. Two days after admission the patient developed a massive hematemesis due to rupture of an esophageal varices and despite successful sclerotherapy and supportive transfusions, the patient died the next day.
 == Images ==

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 === Journal Articles ===
 * Fujimoto J.  [http://www.ncbi.nlm.nih.gov/pubmed/10759218 Gene therapy for liver cirrhosis].  ''J Gastroenterol Hepatol'' 2000 Mar;15 Suppl:D33-6.
-* Ge PS and Runyon BA  [http://http://www.nejm.org/doi/pdf/10.1056/NEJMra1504367 Treatment of Patients with Cirrhosis].  ''NEJM'' 2016 Aug 25 375(8):767.
+* Ge PS and Runyon BA  [http://www.nejm.org/doi/pdf/10.1056/NEJMra1504367 Treatment of Patients with Cirrhosis].  ''NEJM'' 2016 Aug 25 375(8):767.
 === Images ===

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 === Journal Articles ===
 * Fujimoto J.  [http://www.ncbi.nlm.nih.gov/pubmed/10759218 Gene therapy for liver cirrhosis].  ''J Gastroenterol Hepatol'' 2000 Mar;15 Suppl:D33-6.
 === Images ===

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 === Images ===
-* [http://peir.path.uab.edu/library/index.php?/tags/128-cirrhosis PEIR Digital Library: Cirrhosis Images]
+* [{{SERVER}}/library/index.php?/tags/128-cirrhosis PEIR Digital Library: Cirrhosis Images]
 * [http://library.med.utah.edu/WebPath/LIVEHTML/LIVERIDX.html WebPath: Hepatic Pathology]

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 == Related IPLab Cases ==
+* [[IPLab:Lab 2:Fatty Change and Cirrhosis|Lab 2: Liver: Fatty Change and Cirrhosis]]
 {{IPLab 12}}
 [[Category: IPLab:Lab 12]]

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 == Additional Resources ==
 === Reference ===
+* [http://emedicine.medscape.com/article/185856-overview eMedicine Medical Library: Cirrhosis]
 === Journal Articles ===

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 Increased portal pressure also leads to increased pressure in the inferior hemorrhoidal veins and can lead to the formation of anorectal varices.</spoiler>
 * <spoiler text="What is the pathogenesis of Wernicke's encephalopathy?">Wernicke's encephalopathy is caused by thiamine (Vitamin B1) deficiency. Chronic alcoholics often have poor diets and alcohol inhibits intestinal absorption of thiamine. Thus, some chronic alcoholics can develop Wernicke's encephalopathy which consists of foci of symmetric discoloration, softening, and punctate hemorrhages in the paraventricular regions of the thalamus and hypothalamus, in the mamillary bodies, around the aqueduct in the midbrain, in the floor of the fourth ventricle and in the anterior cerebellum. There is demyelinization and loss of neuropil. Even after treatment with thiamine, there is significant memory deficit.</spoiler>
 {{IPLab 12}}
 [[Category: IPLab:Lab 12]]

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 File:IPLab12Alcoholic14.jpg|This is another photograph of the cerebellum from this patient demonstrating the marked thinning of the anterior portion of the cerebellum (arrows). This pattern of cerebellar damage is consistent with Wernicke's encephalopathy.
 </gallery>
 {{IPLab 12}}
 [[Category: IPLab:Lab 12]]