-IBIS-1.5.0-
tx
endocrine system
hypoglycemia
diagnoses

definition and etiology

definition: An abnormally low blood glucose, below 50 mg/dl.

etiology: There are two types of hypoglycemia: reactive (after a meal or drugs) or spontaneous (during a fast). Reactive hypoglycemia is the most common of the two and typically occurs 2-4 hours post-prandially.

If termed "alimentary or postgastrectomy hypoglycemia" the hypoglycemia is due to a rapid absorption of glucose into the circulation from the intestinal tract followed by a marked release of insulin. It is frequently seen after gastrectomy, gastrojejunostomy, pyloroplasty, or vagotomy.

In functional reactive hypoglycemia, the reaction comes after a carbohydrate load and the mechanism is less known, although it is presumably similar to the alimentary type. Reactive hypoglycemia is called "true hypoglycemia" when a low blood glucose is measurable and "nonhypoglycemic hypoglycemia" when patients experience symptoms 2-5 hours after eating but a measurable low blood sugar is not found. Spontaneous hypoglycemia from fasting occurs in liver disease or other causes that are less common (e.g. a large tumor consuming available glucose).

• Functional reactive hypoglycemia (FRHG)is probably the most common of all the hypoglycemias, even though its existence is still doubted by many conservative conventional physicians.
When complex carbohydrates are eaten, the body breaks them down slowly and the basic sugars are gradually released into the bloodstream, where they circulate as energy for the brain (which uses up to 80% of all circulating blood sugar) and other body organs and systems.
Chronic ingestion of simple carbohydrates (refined sugar and flour products) is the main causative factor for the development of FRHG. When simple carbohydrates are ingested, the body quickly digests them and floods the bloodstream with glucose. The body quickly responds to this excessive level by having the pancreatic beta-cells release insulin, which brings the sugar into the cells (with the aid of GTF chromium and oxygen).
Excess sugar in the bloodstream is taken into the liver (where it is stored as glycogen), fat cells (where it is converted to adipose), and the muscles (where it is converted to muscle glycogen). The blood sugar level therefore falls severely, causing feedback to the hypothalamus and the pituitary and thyroid glands.
During this time the patient can experience the symptoms of hypoglycemia (see below in "signs and symptoms").
The pituitary releases growth hormone, which causes the liver to change glycogen back into sugar and release it; growth hormone also causes the adrenals to release cortisol (which also tells the liver to make sugar, increases amino acid release from the muscle tissues, and cause cells in the body to use less sugar) and epinephrine (which also tells the liver to promote gluconeogenesis).
The thyroid gland increases the metabolic rate to help the liver make more sugar quickly while increasing the rate of carbohydrate oxidation in all the tissues. Thus the body strives to replace the needed blood sugar.
It is interesting to note that the brain does not use insulin for its supply of sugar energy, as insulin does not pass the blood-brain barrier. Therefore, when a lot of insulin is needed following a simple carbohydrate meal, there is essentially less energy for the brain (as the insulin will bring the sugar into the other body cells), which may account for post-prandial fatigue and lethargy.
Unfortunately, if the body must constantly send out a lot of insulin to balance the effect of a meal of simple carbohydrates, the pancreas and other organs will begin to suffer; then the load falls on other organs (adrenals, pituitary, liver) which in turn will begin to falter.
In this way, after the insulin reaction, the blood will remain low in FRHG patients. The patient will then begin to suffer from the array of signs and symptoms associated with low blood sugar. This is the proposed pathogenesis of functional reactive hypoglycemia.

• It has been suggested that the most common form of hypoglycemia exists in individuals whose liver does not use lithium properly in the process of releasing stored glycogen. They experience a chronic low energy state until lack of food or increased stress elicits a massive glycogen-dumping episode, leaving them more drained than ever. It is further observed that the second most common type of hypoglycemic is that where the patient experiences extreme moodiness from amino-acid glycogen-storage dysfunction; a third suggested etiology relates to nickel and diminished capacity to store sugar as glycogen (Easley).

signs and symptoms

signs and symptoms:
• Epinephrine release: palpitation,tremors, perspiration, tachycardia,
anxiety/nervousness, hunger.
• CNS symptoms: irritability, dizziness, headache. If marked and serious: confusion, vision problems, palsy, ataxia, personality disturbances, loss of consciousness, convulsions, and coma.
• Better eating.
• Chronic low energy
• Bipolar episodes of feeling energetic then feeling even worse the next day (Easley)
• Feeling extremely moody, better eating, then worse 30 min. to 2 hr. later (Easley)
• Needing to eat sugar all day long (Easley)

lab findings:
• Blood sugar < 50 mg/dl (fasting).
• Impaired glucose tolerance test, even if not clearly diagnostic of hypoglycemia.
• Reactive hypoglycemia usually shows a normal fasting glucose.
• 2 hour post-prandial glucose test is more useful.

course and prognosis

The prognosis for functional hypoglycemia is good once the patient is helped with nutrition counseling and stress management, if necessary.
Severe hypoglycemia may approach insulin shock and is a medical emergency.

differential diagnosis

• Diabetes mellitus.
• Addison's disease.
• Anorexia nervosa.
• Anxiety.
• Bulimia.
• Islet cell tumor.
• Hypothyroidism.


footnotes