Encyclopedia > Diabetes mellitus
Diabetes mellitus
As of 2002, about 17 million United States nationals suffer from diabetes. For at least 20 years, diabetes rates in North America have been increasing substantially. The Centers for Disease Control has termed the changes an epidemic. This is a medically and economically important disease, well in the top 10 and perhaps in the top 5, and is becoming rapidly more so (see big killers[?]).
Long-term diabetes can have detrimental effects on numerous organs of the body. A prolonged high blood glucose level leads to endothelial[?] damage - manifesting as micro- and macrovasular damage. This blood vessel damage leads to retinopathy, nephropathy, peripheral neuropathy, microangiopathy and macroangiopathy.
In severe cases, this can lead to blindness, such poor blood circulation in the feet that cause ulcers leading to gangrene and eventually requiring amputation and chronic renal failure requiring dialysis or transplantation (diabetes mellitus is the most common cause of renal failure worldwide). Heart disease, stroke and nerve damage are other possible consequences.
While diabetes cannot currently be cured (except experimentally in some Type I patients), it can be treated very effectively.
Traditionally the goal of treatment was prevention of either hyperglycemic or hypoglycemic coma or, mostly for Type I diabetics, keto-acidosis. Since (relatively inexpensive) blood glucose measurement became possible in the last generation or so, and since portable blood glucose meters became available in the last 2 decades, treatment goals have also included 'reasonable' levels of blood glucose. Since some large studies were completed in the last decade, it has become absolutely clear that the effort needed to keep blood glucose levels as close to normal as possible is well worth while. Damage from complications is directly reduced in proportion to how normal glucose levels are kept. More recent studies of Type 2 diabetes stress the need for more stringent blood pressure control.
The aim today is to avoid or minimize chronic diabetic complications as well as to avoid acute problems due to too high or too low blood glucose. For Type I diabetics, the chief tool is external insulin (in one or more types), usually injected. For Type II diabetics, treatment usually begins with diet, exercise, and weight reduction. Many Type IIs require some form of oral hypoglycaemic agents but a substantial fraction of Type IIs eventually require insulin as well since there is a considerable fraction of patients who eventually fail to respond to the currently available oral hypoglycemic agents. In all cases, patient monitoring of blood glucose levels is desirable. Because diabetes, and its treatment(s), is usually a major continuing influence on patients' lives and activities, the general well-being of the person affected with diabetes is important.
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"Diabetes" is a Greek word meaning "a passer through; a siphon". "Mellitus" comes from the Greek word "sweet". Apparently, the Greeks named it thus because the excessive amounts of urine that a diabetic (when in a hyperglycemic state) would excrete attracted flies and bees because of the glucose content. The ancient Chinese would test for diabetes by observing whether ants were attracted to a person's urine.
Passing abnormal amounts of urine can be a symptom of several diseases (most commonly of the kidneys), and the word diabetes is connected with many diseases. The most common are diabetes insipidus and diabetes mellitus.
Insulin is a hormone that enables blood glucose molecules to enter about 2/3 of the cells of the body. It also controls many other body mechanisms, from fat processing (in liver and fat cells), protein synthesis (by controlling amino acid uptake in cells), and electrolyte balance (by controlling potassium uptake in cells). It is the central hormone involved in controlling Metabolism]. It is produced in the endocrine part of the pancreas, which consists of clumps of specialised cells scattered throughout that organ (the 'Islets of Langerhans'). Hyperglycemia (too high blood glucose levels) results if the amount of insulin is not sufficient to cause the cells to take up the glucose from the blood, or if those body cells which require insulin to absorb glucose no longer respond adequately to it. This can have two major causes, which may occur together:
- not enough insulin is produced by the pancreas (Type I, and some Type II)
- the cells of the body have become resistant to insulin action (Type II)
There are several types of diabetes mellitus:
- Type 1, most commonly first diagnosed in children and adolescents, an autoimmune disorder in which the body's own immune system attacks the hormone producing beta cells of the islets of Langerhans in the pancreas, preventing it from producing enough (or any) insulin. The auto-immune attack is generally triggered by an infection, often by one of the Coxsackie virus family. Some types of poisoning work by selectively destroying the beta cells, producing Type I diabetes. Pancreatic trauma or tumor can do so as well. Type I is almost always treated with insulin injections, usually at least once daily. About 5-10% of all North American cases of diabetes are type 1. The fraction of Type I's in other parts of the world varies. formerly called 'childhood' or 'juvenile' diabetes.
- Type 2, in which the body's cells become resistant to insulin. Eventually, internal insulin is insufficient to cause enough absorption of blood glucose, resulting in hyperglycemia and finally in glucose being dumped by the kidneys into the urine. Type II often develops late in life, and is often accompanied by overweight. There is a strong genetic connection to Type II diabetes. Relatives with Type II are a considerable risk factor. Type II can be treated with drugs, diet and/or exercise. Several drugs, and other conditions, can also cause Type II. Diabetes is a common side effect of long-term steroid use, and is often the result of untreated hemochromatosis (a defect in handling of body iron stores, often inherited and the most common genetic disease among Northern Europeans). About 90-95% of all North American cases of diabetes are type 2, and 20% of the population over the age of 65 suffer from it. See also Diabetes mellitus type 2. The fraction of Type II's in other parts of the world varies. Formerly called 'adult-onset' or 'obesity-related' diabetes.
- Type 3 All other specific forms, accounting for up to 5% of all diagnosed cases of diabetes:
- Type 3A: genetical defect in beta cells.
- Type 3B: genetically caused insulin resistance.
- Type 3C: diseases of the pancrease.
- Type 3D: caused by hormonal defects.
- Type 3E: caused by chemicals or drugs.
- Type 3F...3H other causes.
- Type 4 or Gestational diabetes mellitus appears in about 2-5% of all pregnancies. About 20-50% of the women go on to develop type 2 diabetes later.
The older names, juvenile or insulin-dependent (IDDM) for Type 1, and adult-onset or non-insulin dependent (NIDDM) for Type 2 diabetes, are discouraged as they are misleading. Type 2 diabetes sometimes requires treatment with insulin, and is increasingly diagnosed among juveniles. Some Type I diabetics become Type II's later in life.
There have been claims that a form of diabetes can be caused by malnutrition or protein deficiency, but there is considerable controversy about this among researchers and any conclusion awaits further review.
Both type 1 and type 2 diabetes are genetically linked. Type 1 diabetes may be triggered by infection, stress, or poisons in the environment. There is clearly a genetic element in the susceptibility of individuals to some of these triggers; it has been traced to a particular HLA genotype. There is an even stronger genetic link in Type 2 diabetes. It is also often connected to obesity, which is found in approximately 85% of (North American) patients diagnosed with that form of the disease. Age is also thought to be a contributing factor, though the exact reason for this is unknown.
The brain requires many things to function correctly, but two things are critically important at all times: oxygen and glucose. Breathing (lungs) and blood circulation (heart and blood vessels) supply the oxygen, without which brain cells very quickly (minutes) die. Blood circulation also supplies glucose, without which brain cells starve (they maintain no internal glucose stores) and brain function is immediately (also minutes) impaired. The level of consciousness is altered, physiological functions are impaired, and ultimately, the patient with hypoglycemia (too little glucose) will die if untreated.
Patients with hyperglycemia (too much glucose) also will eventually (months, up to a few years) die without treatment for the same basic reason: cell starvation as glucose (fuel) cannot get into about 2/3 of the cells. Muscle cells are prominently affected and muscle wasting follows.
However, with hyperglycemia, death is the result of little or no glucose in most cells (because insulin is missing or not responded to), whereas in hypoglycemia there is no little or no glucose in the blood to be absorbed and used in any cell.
Acute hypoglycemia and hyperglycemia can both cause a diabetic coma. Though from different reasons. In acute hypoglycemia, there is so little glucose that the brain, starving, malfunctions sufficiently to cause loss of consciousness. In acute hyperglycemia, general metabolic maladjustment (ie, ketosis) or blood electrolyte imbalances (caused by hyperglycemic osmosis), or both, cause brain malfunction sufficient to cause loss of consciousness. The treatment in one case is to raise blood glucose levels, and in the other to adjust blood chemistry values back to something more nearly normal, including lowering glucose levels. In hypoglycemia if patient is conscious, feeding with some simple carbohydrate may be sufficient to normalize blood glucose. In severe hyperglycemia, medical treatment is generally required due to its complex, interconnected, and quite dangerous biochemical disturbances.
Presentation (signs and symptoms)
In Type 2 diabetes there is almost always a slow onset (years), but in Type 1, particularly in children, onset may be quite fast (weeks or months).
Early symptoms of Type 1 diabetes are often polyuria (frequent urination) and polydipsia[?] (increased thirst and concomitant increased fluid intake). There may also be weight loss, increased appetite and fatigue.
Thirst develops because of osmotic effects - excess glucose is excreted by the kidneys but this causes water to follow, water that must be replaced.
Dangerous signs to watch out for include the smell of ketones in the patient's breath (a sign of ketosis), Kussmaul breathing[?] (rapid, deep breathing) and an altered state of consciousness in the patient, the worst form of which is the so-called "diabetic coma".
Diabetic ketoacidosis
Diabetic ketoacidosis[?] is a complication of diabetes, particularly of Type I diabetes and is a medical emergency. It arises from a lack of insulin in the system, leading to reduced glucose absorption in most body cells. It is more common in Type I diabetics because they do not secrete any significant amounts of their own insulin whereas Type II diabetics often do. In addition, it is uncommon even in Type II diabetics who require insulin due to failure of their beta cells.
DKA arises due to the breakdown of fatty acids[?] to provide glucose for most body cells. In the absence of glucose, fatty acid metabolism produces ketone bodies as end products, and any more than small quantities cause changes in the acid/base balance of the blood. These changes are fatal if not reversed carefully, and promptly. The brain continues to use glucose from the blood (nerve cells do not require insulin to absorb glucose) but is unable to survive the acidosis if it continues too long. In diabetic ketoacidosis, the ketone bodies produced are acetone, acetoacetic acid and beta-hydroxybutyric acid[?]. Oddly, only two are, chemically, ketones. The marked hyperglycaemia[?] also causes osmotic diuresis[?], leading to excessive losses of water, sodium and potassium.
Signs of ketoacidosis include lethargy[?], lowered level of consciousness[?], an increased respiratory rate[?] (Kussmaul breathing[?]) and the smell of ketones[?] (ie, acetone which is found in many nail polish remover preparations) on the patient's breath. Early symptoms are polyuria, nausea, vomiting and abdominal pain[?], with lethargy[?] and somnolence[?] a later development, progressing to unconsciousness and coma if untreated.
A patient with DKA is almost always dehydrated, acidotic, and hyperglycaemic. The patient urgently requires IV fluids[?] and insulin. A bicarbonate infusion may be necessary if the pH of the blood is less than 7. DKA is an urgent medical emergency.
There are several different ways of delivering drugs for treating Type II diabetes: insulin injections, insulin pumps, pills, and implants. Common drugs in pill form (for Type IIs ONLY) include metformin, and the sulfonylureas (eg, Orinase, Diabinase, and Tolinase among many others).
Major studies have shown clearly and convincingly that keeping blood glucose levels as close as possible to the normal, nondiabetic, range really does prevent, slow, and delay chronic diabetic complications -- damage to the eyes, kidneys, blood vessels, and nerves. Close control should be undertaken with care, as keeping blood glucose levels 'normally' low leaves less room for error and increases the possibility of a (dangerous) hypoglycemic episode.
Hypoglycemia means an excessively low blood glucose level. It arises in diabetics who inject too much insulin for the amount of food they eat and exercise they get. On days when, for whatever reason, less food is taken, less insulin will be required. When more exercise is gotten, less insulin will be required. And vice versa. Since there are many different types of insulin, since foods vary in their effect on blood glucose levels (even if the same amount of calories is taken), and since exercise varies depending on many things, getting the amount and timing of the insulin needed is not trivial. In most diabetics, it takes some time and effort to 'get the hang of it'. Adjusting insulin and other drugs is hardly impossible, but it is not simple, nor trivially safe either. The consequences of making a error include death (from coma or accident or ...), and so great caution, and useful expert advice, are both mandatory. Especially early in one's diabetic experience, medication changes should be done only in consultation wtih at physician.
Illness, surgery, and stress also affect glucose levels, so all diabetics should be aware that their insulin and other drug routines may have to change. Previously prepared "sick day rules" may be a reasonable approach, but must actually be suitable to the diabetic situation during illness, stress, ....
Sensible treatment of diabetes depends on blood glucose testing, and since blood glucose levels change regularly and rapidly (hours or so), portable meters are a very good choice. Testing only in a clinic, doctor's office, or hospital is entirely inadequate as a basis for decisions about food exercise and drug dosage and timing. Urine glucose testing is also less than useful, except perhaps in an emergency. It reflects glucose levels since the last urination, not what they are now. How often to test, and what to do with the results are closely connected with insulin schedules, food, and exercise. There are multiple suppliers of these meters, all of which must be approved (by the FDA in the US). Differences among them include size of the blood droplet required, whether the blood sample may be applied to a test strip before or after it is inserted in the meter, length of delay until results are available, size and packaging of the disposable test strips, compatibility with computer programs for keeping records of readings and other information, etc. Test strip cost varies substantially, and probably should be the single largest factor in choosing a meter since cumulative strip costs over even short periods completely swamp all meter cost variation.
A useful laboratory investigation for long term diabetic glycemic control is to measure the patient's serum level of glycosylated haemoglobin (HbA1c). Non-diabetics have a HbA1c level of less than 7% and 7% is a good target for diabetics to reach. A HbA1c level of more than 10% indicates very poor glycemic control.
Long term complications of diabetes mellitus include damage to the the small blood vessels (microangiopathy[?]), larger blood vessels (macroangiopathy[?]), kidneys nephropathy[?], and to the peripheral and autonomous nervous system[?] (diabetic neuropathy[?]). Distinct forms of microangiopathy are damage to the retina of the eye (diabetic retinopathy) and damage to the kidneys (nephropathy[?]). The damage seems to be primarily due to high glucose levels, probably to assorted reactions between glucose and assorted proteins changing their operation. Keeping glucose levels at or near 'normal' reduces the risk of any of these complications of diabetes mellitus.
Several studies have demonstrated that, for both types of diabetes mellitus, the rate and severity of these long term complication is reduced or eliminated by keeping blood glucose levels at or near 'normal'.
Public Health, Policy and Health Economics
The Declaration of St Vincent was the result of international efforts to improve the care accorded to diabetics. Diabetes is enormously expensive for healthcare systems and governments. In North America, it is the largest single non-traumatic cause of amputation, blindness, and dialysis (from kidney failure).
Work in the Puget Sound area of N. America (by the heath organization Group Health) shows that, for its large and varied patient population, retaining minimum dataset for diabetic patients, keeping it up to date, and basing their continuing care on that data reduced total healthcare costs for those patients by US$1000 per year per patient for the rest of their life. Recognition of this reality drove the Hawkes Bay initiative which established such a system, and resulted in various activities throughout the world including the Black Sea Telediab project which produced elements of a distributed diabetic record and management system as an open source computer program.
Until 1922, when insulin was discovered and made available (in an early and rapidly improved form), clinical diagnosis of diabetes was an invariable death sentence. Non-progressing Type IIs almost certainly often went undiagnosed then; they still do. The endocrine role of the pancreas (and of insulin) in metabolism was not fully clarified until 1921, when Frederick Grant Banting[?] and Charles Herbert Best[?] managed to isolate a preparation of the hormone insulin at McGill University in Canada. This led to an effective treatment (insulin injection) in 1922, and Banting received the Nobel Prize in Medicine in 1923. The two researchers did not patent their discovery and the therapy rapidly spread around the world.
- "Conditions in Occupational Therapy: effect on occupational performance." ed. Ruth A. Hansen and Ben Atchison (Baltimore: Lippincott Williams & Williams, 2000), 298-309. ISBN 0-683-30417-8
See also: endocrinology, diabetes insipidus, diabetes dictionary, diabetic coma, List of Celebrities With Diabetes.
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