pediatrics
Diabetes Mellitus in Children and Adolescents
Pathophysiology of Diabetes in Children and Adolescents
 causes hyperglycemia and impaired glucose utilization in skeletal muscle. Muscle and fat are then broken down to provide energy. Fat breakdown produces ketones, which cause acidemia and sometimes a significant, life-threatening acidosis ( Diabetic Ketoacidosis (DKA) [DKA]). function to prevent DKA at diagnosis, but children can sometimes present with DKA (up to 25%) or, less commonly, Hyperosmolar Hyperglycemic State (HHS) (HHS), also referred to as hyperosmolar hyperglycemic nonketotic syndrome (HHNK), in which severe hyperosmolar dehydration occurs. HHS most often occurs during a period of stress or infection, with nonadherence to treatment regimens, or when glucose metabolism is further impaired by drugs (eg, corticosteroids). Other metabolic derangements associated with Dyslipidemia (leading to Atherosclerosis ) Hypertension None Polycystic Ovary Syndrome (PCOS) None Obstructive Sleep Apnea (OSA) None Metabolic Dysfunction–Associated Liver Disease (MASLD) (fatty liver) Atherosclerosis begins in childhood and adolescence and markedly increases risk of cardiovascular disease. Inmonogenic forms of diabetes,the underlying defect depends on the type. The most common types are caused by defects in transcription factors that regulate pancreatic beta-cell function (eg, hepatic nuclear factor 4-alpha [HNF-4-α], hepatic nuclear factor 1-alpha [HNF-1-α]). In these types,insulinsecretion is impaired but not absent, there is noinsulinresistance, and hyperglycemia worsens with age. Another type of monogenic diabetes is caused by a defect in the glucose sensor, glucokinase. With glucokinase defects,insulinsecretion is normal but glucose levels are regulated at a higher set point, causing fasting hyperglycemia that worsens minimally with age. Despite the common misconception, diabetic ketoacidosis can occur in children with type 2 diabetes. 