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HIV - 01-02-08 13:05
A 49-year-old man with a long history of alcohol abuse is brought to the physician by his wife because of gradually increasing confusion. He had been working as an apartment building superintendent until approximately 2 weeks ago, when he began feeling drowsy throughout the day and had difficulty sleeping at night. Since then, he has become confused and occasionally disoriented as to time and day. He can recognize his wife and neighbors, but cannot maintain casual conversations. He denies any fever, chills, or abdominal pain. Six months ago, he was admitted to the hospital with an upper gastrointestinal bleed, which was due to bleeding esophageal varices. His medications include ranitidine, spironolactone, furosemide, and propranolol. On physical examination, he is lethargic and disheveled. His temperature is 36.9 C (98.4 F), blood pressure is 112/64 mm Hg, pulse is 62/min, and respirations are 18/min. He has mildly icteric sclera and bitemporal wasting. His oral mucous membranes are dry. There is no jugulovenous distension. His lungs are clear, and he has a regular heart rhythm. His abdomen reveals a firm liver edge with a liver span of 7 cm in the midclavicular line. There is no shifting dullness, and a spleen tip is not palpable. He has no peripheral edema. On a mental status examination he recognizes the physician but cannot name the date, the reason for his visit, or his home address. Neurologic examination is nonfocal, and asterixis is present. Which of the following laboratory abnormalities will most likely be found?
A. BUN of 53 mg/dL
B. Glucose of 192 mg/dL
C. Potassium of 5.7 mEq/L
D. Serum bicarbonate of 16 mEq/L
E. Serum calcium of 14.2 mEq/L
HIV - 01-02-08 13:05
A 49-year-old man with a long history of alcohol abuse is brought to the physician by his wife because of gradually increasing confusion. He had been working as an apartment building superintendent until approximately 2 weeks ago, when he began feeling drowsy throughout the day and had difficulty sleeping at night. Since then, he has become confused and occasionally disoriented as to time and day. He can recognize his wife and neighbors, but cannot maintain casual conversations. He denies any fever, chills, or abdominal pain. Six months ago, he was admitted to the hospital with an upper gastrointestinal bleed, which was due to bleeding esophageal varices. His medications include ranitidine, spironolactone, furosemide, and propranolol. On physical examination, he is lethargic and disheveled. His temperature is 36.9 C (98.4 F), blood pressure is 112/64 mm Hg, pulse is 62/min, and respirations are 18/min. He has mildly icteric sclera and bitemporal wasting. His oral mucous membranes are dry. There is no jugulovenous distension. His lungs are clear, and he has a regular heart rhythm. His abdomen reveals a firm liver edge with a liver span of 7 cm in the midclavicular line. There is no shifting dullness, and a spleen tip is not palpable. He has no peripheral edema. On a mental status examination he recognizes the physician but cannot name the date, the reason for his visit, or his home address. Neurologic examination is nonfocal, and asterixis is present. Which of the following laboratory abnormalities will most likely be found?
A. BUN of 53 mg/dL
B. Glucose of 192 mg/dL
C. Potassium of 5.7 mEq/L
D. Serum bicarbonate of 16 mEq/L
E. Serum calcium of 14.2 mEq/L
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#3
Re: im funtonic - 01-08-08 17:50 He is using furosemide, so I don' think it is C, most probably A.
#4
Re: im 8401glacieres - 01-11-08 07:45 A-BUN raised.
Past history of uppergi bleed and this time he may be having that. So degraded RBC will add further to BUN and can potentiate hepatic encephalopathy. He is for sure accoding t history having hepatic encephalopathy. A search should be made for any reversible cause.His histo doesn;t tell any thing about chronic hepatic failure, but he may have some underlying hepatic pahology, which can be made surface by running some serology tests, like Hep B/C surface antigens.
An elevated blood ammonia level is the classic laboratory abnormality reported in patients with hepatic encephalopathy. This finding may aid in correctly diagnosing patients with cirrhosis who present with altered mental status. However, serial ammonia measurements are inferior to clinical assessment in gauging improvement or deterioration in a patient under therapy for hepatic encephalopathy. Checking the ammonia level in a patient with cirrhosis who does not have hepatic encephalopathy has no utility. Only arterial or free venous blood specimens must be assayed when checking the ammonia level. Blood drawn from an extremity to which a tourniquet has been applied may provide a falsely elevated ammonia level when analyzed.
The reason why I am not picking up raised potassium is because renal failur is caused by infections in any hepatic encephalopathy patient and this patient is not having any signs of infection.
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