tommyk
04-08-2006, 11:10 PM
Hy 2107
A 50-year-old man named Robert Redford with a long history of alcohol drinking 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?
1-High glucose over 200
2-B.U.N. of 60
3-K+ of 6.0
4-pH under 7.0
5-Bicarbonate
6-Lithium levels in toxic range
7-Calcium of 18
8-Hepatic adenomas
a) Answer is #2!!! This patient with alcoholic cirrhosis and portal hypertension has signs and symptoms consistent with hepatic encephalopathy.
The one possible explanation in the absence of any obvious infection or gastrointestinal bleeding is dehydration related to his diuretic use. Although the diuretics may have been appropriately prescribed for ascites, at present he has multiple physical findings suggesting that he is dehydrated: dry mucous membranes and absence of jugulovenous distention, ascites, and peripheral edema. His pulse does not demonstrate a reflex tachycardia because of the propranolol, which is being used to reduce his portal pressure. In the setting of dehydration, the patient's BUN would be expected to be elevated and is a frequent exacerbating factor for hepatic encephalopathy.
There is no history of diabetes in this patient, so a glucose of 200 mg/dL would not be expected, and this degree of relatively mild hyperglycemia would not explain his mental status.
Although the patient is on spironolactone, he is also on furosemide, so it would not be likely that he would be hyperkalemic. Since Lasix is known by First Aid to LOSE ions.
There is nothing to suggest that the patient has a metabolic acidosis so it is unlikely that he would have a low serum bicarbonate. Remember, the kidneys SHOULD compensate.
There is nothing in the history to suggest the possibility of developing hypercalcemia. No history of cancer or hypothyroidism. Furthermore, the patient's furosemide would tend to decrease, not increase, serum calcium as mentioned
There is nothing to suggest his condition is due to Lithium
A 50-year-old man named Robert Redford with a long history of alcohol drinking 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?
1-High glucose over 200
2-B.U.N. of 60
3-K+ of 6.0
4-pH under 7.0
5-Bicarbonate
6-Lithium levels in toxic range
7-Calcium of 18
8-Hepatic adenomas
a) Answer is #2!!! This patient with alcoholic cirrhosis and portal hypertension has signs and symptoms consistent with hepatic encephalopathy.
The one possible explanation in the absence of any obvious infection or gastrointestinal bleeding is dehydration related to his diuretic use. Although the diuretics may have been appropriately prescribed for ascites, at present he has multiple physical findings suggesting that he is dehydrated: dry mucous membranes and absence of jugulovenous distention, ascites, and peripheral edema. His pulse does not demonstrate a reflex tachycardia because of the propranolol, which is being used to reduce his portal pressure. In the setting of dehydration, the patient's BUN would be expected to be elevated and is a frequent exacerbating factor for hepatic encephalopathy.
There is no history of diabetes in this patient, so a glucose of 200 mg/dL would not be expected, and this degree of relatively mild hyperglycemia would not explain his mental status.
Although the patient is on spironolactone, he is also on furosemide, so it would not be likely that he would be hyperkalemic. Since Lasix is known by First Aid to LOSE ions.
There is nothing to suggest that the patient has a metabolic acidosis so it is unlikely that he would have a low serum bicarbonate. Remember, the kidneys SHOULD compensate.
There is nothing in the history to suggest the possibility of developing hypercalcemia. No history of cancer or hypothyroidism. Furthermore, the patient's furosemide would tend to decrease, not increase, serum calcium as mentioned
There is nothing to suggest his condition is due to Lithium