MEDizzy
MEDizzy
USMLE
Mix questions 2
A 21-year-old woman with a history of type 1 diabetes mellitus is brought to the emergency department with nausea, vomiting, lethargy, and dehydration. Her mother notes that she stopped taking insulin 1 day before presentation. She is lethargic, has dry mucous membranes, and is obtunded. Blood pressure is 80/40 mmHg, and heart rate is 112 bpm. Heart sounds are normal. Lungs are clear. The abdomen is soft, and there is no organomegaly. She is responsive and oriented × 3 but difusely weak. Serum sodium is 126 mEq/L, potassium is 4.3 mEq/L, magnesium is 1.2 mEq/L, blood urea nitrogen is 76 mg/dL, creatinine is 2.2 mg/dL, bicarbonate is 10 mEq/L, and chloride is 88 mEq/L. Serum glucose is 720 mg/dL. All the following are appropriate management steps EXCEPT:
Explanation
ExplanationDiabetic ketoacidosis is an acute complication of diabetes mellitus. It results from a relative or absolute defciency of insulin combined with a counterregulatory hormone excess. In particular, a decrease in the ratio of insulin to glucagons promotes gluconeogenesis, glycogenolysis, and the formation of ketone bodies in the liver. Ketosis results from an increase in the release of free fatty acids from adipocytes, with a resultant shift toward ketone body synthesis in the liver. This is mediated by the relationship between insulin and the enzyme carnitine palmitoyltransferase I. At physiologic pH, ketone bodies exist as ketoacids, which are neutralized by bicarbonate. As bicarbonate stores are depleted, acidosis develops. Clinically, these patients have nausea, vomiting, and abdominal pain. They are dehydrated and may be hypotensive. Lethargy and severe central nervous system depression may occur. The treatment centers on replacement of the body’s insulin, which will result in cessation of the formation of ketoacids and improvement of the acidotic state. Assessment of the level of acidosis may be done with an arterial blood gas. These patients have an anion gap acidosis and often a concomitant metabolic alkalosis resulting from volume depletion. Volume resuscitation with intravenous f uids is critical. Many electrolyte abnormalities may occur. Total-body sodium, potassium, and magnesium are depleted in these patients. As a result of the acidosis, intracellular potassium may shift out of cells and cause a normal or even elevated potassium level. However, with improvement in the acidosis, the serum potassium rapidly falls. Therefore, potassium repletion is critical despite the presence of a “normal” level. Because of the osmolar efects of glucose, fuid is drawn into the intravascular space. This results in a drop in the measured serum sodium. There is a drop of 1.6 mEq/L in serum sodium for each rise of 100 mg/dL in serum glucose. In this case, the serum sodium will improve with hydration alone. The use of 3% saline is not indicated because the patient has no neurologic defcits, and the expectation is for rapid resolution with IV fuids alone.
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