Diabetes mellitus diabetic coma

Insulin is necessary for controlling type 1 diabetes mellitus that is caused by a marked decrease in the amount of insulin produced by die pancreas. Insulin is also used to control the more severe and complicated forms of type 2 diabetes mellitus. However, many patients can control type 2 diabetes with diet and exercise alone or with diet, exercise, and an oral antidiabetic drug (see section Oral Antidiabetic Dmgp ). Insulin may also be used in the treatment of severe diabetic ketoacidosis (DKA) or diabetic coma. Insulin is also used in combination with glucose to treat hypokalemia by producing a shift of potassium from die blood and into die cells. 

Contraindications Diabetic complications, such as ketosis, acidosis, and diabetic coma, severe liver or renal impairment, sole therapy fortype 1 diabetes mellitus, or hypersensitivity to sulfonylureas... 

Sole therapy for type I diabetes mellitus, diabetic complications (ketosis, acidosis, diabetic coma), stress situations (severe infection, trauma, surgery), severe renal or hepatic impairment. 

Conventional insulin treatment with its fixed insulin dosage and food intake has dominated therapy of insulin-dependent diabetes mellitus for nearly 70 years. It has sharply reduced the mortality of diabetic coma. Nevertheless diabetic coma is still the largest single cause of death in diabetic patients under the age of 20 years with an episode rate of 7%, and diabetic coma accounts for 15% of deaths in diabetics under the age of 50 years. 

Blood pyruvate concentration is not altered in most cases of diabetes mellitus (A5, D14, S28). Previous results, obtained by use of the colorimetric technique of Friedemann and Haugen (F12) and showing an apparent high pyruvate level during diabetic coma, are erroneous and are due to the interference of acetoacetic acid on pyruvic add determination with that technique (Lll, L12, L13). 

IVIore than one person, found unconscious on the streets of some metropolis, has been carted to jail only to die of complications arising from uncontrolled diabetes mellitus. Others are fortunate enough to arrive in hospital emergency rooms. A quick test for diabetes mellitus-induced coma is the odor of acetone on the breath of the afflicted person. Acetone is one of several metabolites produced by diabetics that are known collectively as ketone bodies. 

The peptide hormone insulin (see Box 13.1) is produced by the pancreas and plays a key role in the regulation of carbohydrate, fat, and protein metabolism, hi particular, it has a hypoglycaemic effect, lowering the levels of glucose in the blood. A malfunctioning pancreas may produce a deficiency in insulin synthesis or secretion, leading to the condition known as diabetes mellitus. This results in increased amounts of glucose in the blood and urine, diuresis, depletion of carbohydrate stores, and subsequent breakdown of fat and protein. Incomplete breakdown of fat leads to the accumulation of ketones in the blood, severe acidosis, coma, and death. 

If the production of ketone bodies exceeds the demand for them outside the liver, there is an increase in the concentration of ketone bodies in the plasma (ketonemia) and they are also eventually excreted in the urine (ketonu-ria). Both phenomena are observed after prolonged starvation and in inadequately treated diabetes mellitus. Severe ketonuria with ketoacidosis can cause electrolyte shifts and loss of consciousness, and is therefore life-threatening (ketoacidotic coma). 

Hypersensitivity to sulfonylureas diabetes complicated by ketoacidosis, with or without coma sole therapy of type 1 (insulin-dependent) diabetes mellitus diabetes when complicated by pregnancy. 

Hyperglycemia and diabetes mellitus Hyperglycemia, in some cases extreme and associated with ketoacidosis or hyperosmolar coma or death, has been reported in patients treated with atypical antipsychotics. 

Contraindications Diabetic ketoacidosis with or without coma, type 1 diabetes mellitus... 

When a 45-year-old man with severe lithium-induced diabetes insipidus developed hyperosmolar, nonketotic hyperglycemia, it was suggested that poorly controlled diabetes mellitus may have contributed to the polyuria (684). Prior contact with a female patient who had developed hyperosmolar coma secondary to lithium-induced diabetes insipidus (685) allowed physicians 4 years later to treat her safely after a drug overdose and a surgical procedure, by avoiding intravenous replacement fluids with a high dextrose content (despite stopping lithium several years earlier, the patient continued to put out 10 liters of urine daily) (686). 

Type 1 diabetes accounts for approximately 10% of all patients diagnosed with diabetes mellitus. It is a major chronic disease of children and is now being recognized with increasing frequency in adults. In the absence of insulin, the resulting metabolic derangements in acute diabetic ketoacidosis eventually lead to coma and death. 

Q7 Ketoacidosis is a serious complication of diabetes mellitus. Because of insulin deficiency and consequent increased availability of fatty acids to the liver, the liver overproduces alpha-hydroxybutyrate and acetoacetic acid, increasing ketone production. The ketones are released into the circulation. They are strongly acidic and, when not effectively buffered, cause metabolic acidosis. Coma may then occur because of severe depression of the nervous system. 

Diabetes mellitus, the most common serious metabolic disease, is due to metabolic derangements resulting in an insufficiency of insulin and an excess of glucagon relative to the needs of the individual. The result is an elevated blood-glucose level, the mobilization of triacylglycerols, and excessive ketone-body formation. Accelerated ketone-body formation can lead to acidosis, coma, and death in untreated insulin-dependent diabetics. 

The oxide-semiconductor-based ethanol sensor is being used to screen intoxicated drivers. In the test condition on the road, the ambient concentrations of CO and N02 can be up to 100 and lOppm due to the emissions from gasoline and diesel engines, respectively.61 The results shown in Fig. 12.6 suggest that the present sensors may be applied for selective detection of ethanol. Acetone is a very rare component in an ordinary ambient atmosphere. However, the expiration of a diabetes patient can contain acetone.62 Acetone concentration in breath air can reach up to 300 ppm in the case of an aceto-acidotic coma related to diabetes mellitus.63,64 This might interfere the ethanol sensor. A high selectivity to ethanol is required for such applications. The SZ sensor at 300°C and the ZW sensor at 400°C can satisfy these requirements. On the contrary, to examine the health condition of a diabetes patient, selective detection of acetone without the interference with alcohol is desirable. In this case, the W sensor at 400°C will be of advantageous. 

An increase in blood serum organic acids has been found especially during uremic acidosis (B7), diabetes mellitus with acidotic coma (Rl), and toxicosis in infants (K23). 

Di Abietes, a 27-year-old woman with type 1 diabetes mellitus, had been J admitted to the hospital in a ketoacidotic coma a year ago (see Chapter 4). 

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