Clinically, hypoglycemia is defined as a plasma glucose concentration less than 50 mg/dL (3.8 mmol/l), that may be asymptomatic. Two categories of hypoglycemia exist: postprandial (reactive) hypoglycemia and fasting hypoglycemia.
Postprandial hypoglycemia generally generates symptoms of adrenergic stimulation including diaphoresis, anxiety, irritability, palpitations, tremor, and hunger. Occurs 2 to 4 hours postprandially, occurs suddenly and generally subsides in 15 to 20 minutes. Caused by stimulation of epinephrine release. Postprandial hypoglycemia is often idiopathic but may be caused by:
Diagnosis is carried out by means of a 5 hour 75 g GTT. Little knowledge has been achieved about the last two; idiopathic means so much as unknown.
Patients suffering from fasting hypoglycemia generally have symptoms of neuroglycopenia, including headache, mental dullness, and fatigue. If hypoglycemiais more severe, may progress to confusion, visual blurring, loss of consciousness, and seizures. Occurs with fasting greater than 4 hours. Possible causes are:
Diagnosis is carried out by measuring plasma glucose after
an overnight fast. If the overnight value is normal (greater than
50mg/dL) an observed 72-hour fast should be tried.
Malnutrition, as with marasmus and kwashiorkor, is a common cause of hypoglycemia in third world countries. No storage energy from fats or proteins is available, and one is prone to low blood sugar values when not eating.
Metabolic diseases, where hypoglycemia often is the main symptom, are the following:
With no disease the liversize is so big as with glycogenose diseases. Patients have a swollen belly and a typical body build. Blood and urine lactose levels are strongly increased.
Patients with decreased gluconeogenesis are difficult to recognise. Patients often show neurological disorders, like balancing and eye problems, and a strongly increased lactose concentration in the blood.
Also called galactose intolerance or fructose intolerance are the only metabolic diseases where hypoglycemia occurs *after* ingestion of these sugars. Patients often have a natural dislike of these particular sugars. The sugars can be found in the urine.
With breakdown disorders of the amino acids leucine, isoleucine and valine the person sometimes have a particular body and urine smell. When an infection is present, severe auto-intoxication will develop due to increase of certain organic acids in the blood.
Cases differ from light hypoglycemia to a state with severe liver disorders, looking similar to Reye disease. Symptoms can occur after infection, fasting and sometimes a high fat eating pattern. The disorder can be diagnosed by investigating the disability of these patients to produce ketons during fasting and overproduction of abnormal fatty acids (dicarbon acids), which are release in the urine.
Hormonal causes of hypoglycemia are quite rare. The most notorious cause is hyperinsulinism. The overload of insuline cause severe hypoglycemia. In addition, the fatty acid oxidation is being suppressed. So at the same time there is both a fatty acid oxidation and glucose shortage, having an energy crisis as a result.
The combination of low blood sugar values, low concentration of free fatty acids and the lack of ketosis is highly characteric for hyperinsulinism. This is the case with overgrowth of insulin-producing beta-cells in the pancreas and as a side-effect of medications, e.g. by a high insulin-dosis with a diabetic patient.
Hypoglycemia can be an caused by hypothyroid too.
With liver diseases with a strong decay of liver cells the
production and release of glucose is disturbed, but the hypoglycemia
as a result of this is part of a much more serious disturbance
of other metabolic processes. Glycogenoses and gluconeogenesis
defects (see above) are liver-related metabolic diseases which
may lead to hypoglycemia. Alcohol abuse may cause hypoglycemia
too.
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Hypoglycemia
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