By Vikas Bhushan
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Increased serum lactate; hvpei phosphatcmia. 27); bicarbonate 14 mEq/L (low). Increased anion gap (19) with no ketoacids; BUN and creatinine normal. 2. Treat shock. Discussion A state of increased levels of lactic acid in blood (LACTIC ACIDOSIS) may be due to a number of causes, including shock and sepsis (both of which increase lactic acid production due to hypoxia), methanol poisoning, metformin toxicity, and liver failure (due to failure of lactic acid to be removed from blood by its transformation to glucose).
CRIGLER-NAJJAR SYNDROME ID/CC A 21-year-old female college student visits her gastroenterologist for an evaluation of fatigability and intermittent right upper quadrant and epigastric pain. " PE VS: normal. PE: mild jaundice in conjunctiva and underneath tongue; well hydrated and in no acute distress; no hepatosplenomegaly on abdominal exam; no signs of hepatic failure. Labs Increased direct bilirubin (vs. Gilbert's syndrome, in which hyperbilirubinemia is indirect) and indirect bilirubin; liver enzymes mildly elevated.
IV calcium gluconate. HYPOCALCEMIA FROM PANCREATITIS ID/CC HPI PE Labs A 73-year-old female complains of weakness, painful muscle cramps, and constipation. She suffers from chronic congestive heart failure (CHF) that has been treated with digoxin and furosemide. She was also on oral potassium tablets but has discontinued them because of gasuic upset. VS: irregularly irregular pulse (atrial fibrillation); hypertension (BP 145/90); no fever. PE: well hydrated; conjunctiva normal; jugular venous pulse slightly increased, S3 heard; mild hepatomegaly and pitting edema of lower legs (all due to CHF) ; deep tendon reflexes hypoactive.
Blackwell's underground clinical vignettes. Biochemistry by Vikas Bhushan