A 19-year-old man is brought to the emergency department due to weakness and confusion. Family members report that for the last 2 weeks he has experienced polyuria, polydipsia, and increased appetite. Medical history is remarkable for an appendectomy at age 12. The patient does not use tobacco, alcohol, or illicit drugs. Family history is significant for hypothyroidism in his brother. Temperature is 36.7 C (98 F), blood pressure is 90/60 mm Hg, pulse is 97/min, and respirations are 22/min. On physical examination, the patient is lethargic but follows simple commands. His breath has a fruity odor. This patient is most likely deficient in a hormone that normally performs which of the following actions?

Question

A 19-year-old man is brought to the emergency department due to weakness and confusion.  Family members report that for the last 2 weeks he has experienced polyuria, polydipsia, and increased appetite.  Medical history is remarkable for an appendectomy at age 12.  The patient does not use tobacco, alcohol, or illicit drugs.  Family history is significant for hypothyroidism in his brother.  Temperature is 36.7 C (98 F), blood pressure is 90/60 mm Hg, pulse is 97/min, and respirations are 22/min.  On physical examination, the patient is lethargic but follows simple commands.  His breath has a fruity odor.  This patient is most likely deficient in a hormone that normally performs which of the following actions?

Quizplus · Accepted Answer

11ec160b_3caa_cb2b_9249_fdd38a426d3a_MD0001_00 This patient has undiagnosed type 1 diabetes mellitus and is now presenting with diabetic ketoacidosis (polyuria, polydipsia, altered mental status, fruity breath [exhaled ketones]). Diabetic ketoacidosis results from a deficiency of insulin coupled with an excess of counterregulatory hormones (ie, glucagon, epinephrine). Blood glucose levels are normally maintained within a tight range by the opposing effects of insulin (secreted by beta cells) and glucagon (secreted by alpha cells). In the fasting state, low blood glucose levels stimulate secretion of glucagon, which increases blood glucose levels by upregulating glycogenolysis and gluconeogenesis in the liver. In contrast, insulin is released in response to high glucose levels and functions to decrease hepatic glucose production (Choice D) and increase glucose uptake by insulin-responsive tissues. Insulin also suppresses glucagon by directly acting on the alpha cells, enhancing the metabolic effects of insulin. In type 1 diabetes mellitus, unsuppressed glucagon secretion due to insulin deficiency contributes to excess blood glucose levels. (Choice A) In adipose tissue, hormone-sensitive lipase hydrolyzes intracellular triglycerides to release free fatty acids. Hormone-sensitive lipase is activated by ACTH and epinephrine in the fasting state and is downregulated by insulin in the fed state. In untreated type 1 diabetes, the lack of insulin induces a catabolic state, resulting in increased lipolysis; patients typically lose weight despite a normal or increased appetite. (Choice C) In skeletal muscle, insulin increases glucose uptake and synthesis of glycogen, which is then available for energy production during exercise. Insulin also increases amino acid transport and ribosomal translation efficiency in muscle tissue, leading to an overall increase in protein synthesis. Insulin deficiency in type 1 diabetes leads to decreased muscle glycogen synthesis and muscle wasting. (Choice E) In the renal tubules, glucose is actively taken up from the tubular lumen by sodium-glucose co-transporter 2 (SGLT2) and then passed across the basolateral membrane. This occurs independent of insulin levels and leads to near-complete reabsorption of filtered glucose (unless severe hyperglycemia overwhelms the reabsorptive capacity, leading to osmotic diuresis and polyuria). Educational objective: Normal blood glucose levels are maintained by the opposing effects of insulin and glucagon. Glucagon stimulates hepatic glycogenolysis and gluconeogenesis, whereas insulin increases peripheral glucose uptake and inhibits lipolysis and ketoacid formation. Insulin also suppresses glucagon release. __________ References: Minireview: glucagon in the pathogenesis of hypoglycemia and hyperglycemia in diabetes. (http://www.ncbi.nlm.nih.gov/pubmed/22166985)

A 19-Year-Old Man Is Brought to the Emergency Department Due