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The incidence of hypoglycemia due to complex drug interactions, especially involving oral hypoglycemic agents and insulin for diabetes, rises with age. Though much rarer, the incidence of insulin-producing tumors also rises with advancing age. Most tumors causing hypoglycemia by mechanisms other than insulin excess occur in adults. [citation ...
Inborn errors of metabolism may cause infant hypoglycemia, and much less commonly adult hypoglycemia. [25] Disorders that are related to the breakdown of glycogen, called glycogen storage diseases, may cause hypoglycemia. [3] [25] Normally, breakdown of glycogen leads to increased glucose levels, particularly in a fasting state. [3]
In the elderly, hypoglycemia can produce focal stroke-like effects or a hard-to-define malaise. [medical citation needed] The symptoms of a single person do tend to be similar from episode to episode. In the large majority of cases, hypoglycemia severe enough to cause seizures or unconsciousness can be reversed without obvious harm to the brain.
Management of hypoglycemia due to treatment of type 2 diabetes is similar, and the dose of the oral hypoglycemic agent may need to be reduced. Reversal and prevention of hypoglycemia is a major aspect of the management of type 1 diabetes. Hypoglycemia due to drug overdose or effect is supported with extra glucose until the drugs have been ...
A non-exhaustive list of causes of pathologic ketotic hypoglycemia is listed below: [2] Growth hormone deficiency; Glycogen storage diseases. Glycogen storage disease type IX is a particularly common cause of ketotic hypoglycemia, with the subtype IXa mainly affecting male children [6] Maple syrup urine disease; Prader-Willi syndrome
Hypoglycemia can also be caused by sulfonylureas in people with type 2 diabetes, although it is far less common because glucose counterregulation generally remains intact in people with type 2 diabetes. Severe hypoglycemia rarely, if ever, occurs in people with diabetes treated only with diet, exercise, or insulin sensitizers.
Fasting hypoglycemia is often the most significant problem in GSD I, and typically the problem that leads to the diagnosis. Chronic hypoglycemia produces secondary metabolic adaptations, including chronically low insulin levels and high levels of glucagon and cortisol. Lactic acidosis arises from impairment of gluconeogenesis.
In a healthy adult male of 75 kg (165 lb) with a blood volume of 5 L, a blood glucose level of 5.5 mmol/L (100 mg/dL) amounts to 5 g, equivalent to about a teaspoonful of sugar. [14] Part of the reason why this amount is so small is that, to maintain an influx of glucose into cells, enzymes modify glucose by adding phosphate or other groups to it.
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