Diabetes coma and

A second principle used widely for glucose analysis, is that of the oxidation of glucose enzymatically, mediated by the action of glucose oxidase with the formation of gluconic acid and hydrogen peroxide (22). In this procedure it is the hydrogen peroxide which is usually assayed for determination of glucose. This method suffers from the action of inhibitors which occur, particularly with patients in a diabetic coma and these need to be removed. 

Patients generally seek medical help because they want relief from disease. They have little interest in diagnosis—except in so far as it helps the doctor treat them more efficiently—and still less in the mechanism of their illness. Nevertheless, clinical chemistry traditionally has been more concerned with diagnosis and the elucidation of the mechanism of disease than with treatment. In only a few circumscribed areas, such as management of water and electrolyte imbalance, diabetic coma, and renal dialysis, has clinical biochemistry proved indispensable for treatment, the overall raison d etre of the health industry. 

Emergency Treatments. There are two life-threatening crises which may occur in diabetes diabetic coma, and hypoglycemia. The meeisures to be taken depend upon the correct identification of the critical condition, since the wrong treatment may do more harm than good. The characteristics of each condition are presented in Table D. ... 

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. 

The energy substrates are contraindicated in patients with hypersensitivity to any component of the solution. Dextrose solutions are contraindicated in patients with diabetic coma with excessively high blood sugar. Concentrated dextrose solutions are contraindicated in patients with increased intracranial pressure, delirium tremens (if patient is dehydrated), hepatic coma, or glucose-galactose malabsorption syndrome Alcohol dextrose solutions are contraindicated in patients with epilepsy, urinary tract infections, alcoholism, and diabetic coma... 

Diabetic acidosis can develop in a matter of hours. Therefore, under certain circumstances, doctors may ask a diabetic patient to test for ketones at home using special test strips that can detect ketones in urine. For example, doctors recommend that diabetic patients test their urine every 4 to 6 hours if their blood sugar levels are very high. Patients should also test for ketones if they are sick with a cold or the flu, or if they experience any of the symptoms of acidosis. These symptoms include a very dry mouth, frequent urination, shortness of breath, and fruity smelling breath. Diabetic acidosis can be life-threatening, leading to a diabetic coma or death. It needs immediate medical care. Diabetic acidosis is also called ketoacidosis. 

Diabetes is a medical condition that develops when a person s body is unable to metabolize glucose ("blood sugar") properly. The glucose accumulates in the body and may damage the heart, kidneys, eyes, and nervous system. Left untreated, diabetes can lead to very serious health problems, including coma and death. Diabetes is currently the sixth most common cause of death in the United States. 

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. 

The increased degradation of fat that occurs in insulin deficiency also has serious effects. Some of the fatty acids that accumulate in large quantities are taken up by the liver and used for lipoprotein synthesis (hyperlipidemia), and the rest are broken down into acetyl CoA. As the tricarboxylic acid cycle is not capable of taking up such large quantities of acetyl CoA, the excess is used to form ketone bodies (acetoacetate and p-hydroxy-butyrate see p. 312). As H"" ions are released in this process, diabetics not receiving adequate treatment can suffer severe metabolic acidosis (diabetic coma). The acetone that is also formed gives these patients breath a characteristic odor. In addition, large amounts of ketone body anions appear in the urine (ketonuria). 

Type II diabetics are less prone to develop ketone bodies or diabetic ketoacidosis but may develop hyperosmolar coma, a condition characterized by severe hyperglycemia and dehydration. Both diabetic ketoacidosis and hyperosmolar coma are medical emergencies that require prompt insulin administration and intravenous fluids. 

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... 

A specific complication of the use of large amounts of insulin during hyperosmolar diabetic coma is rhabdomyo-lysis (123). Low intramuscular phosphate and potassium concentrations, often masked by relatively high blood glucose concentrations, may be important contributory factors. 

Insulin, a large polypeptide, is not suitable for oral administration. Even if the insulin molecule survived digestion by proteases in the stomach and small intestine, this compound is much too large to be absorbed through the gastrointestinal wall. Consequently, insulin is usually administered through subcutaneous injection. Insulin may also be administered by the intravenous route in emergency situations (e.g., diabetic coma). 

Lithium Carbonate Common symptoms of lithium toxicity are nausea, vomiting, and diarrhea followed by tremor, increased muscle tone, and rigidity. Acute kidney problems and nephrogenic diabetes insipidus may be possible hazards. In serious cases, coma and convulsions can be observed along with toxicity. 

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. 

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. 

Hyperosmolar diabetic coma occms chiefly in noninsulin-dependent diabetics who fail to compensate for their continuing, osmotic glucose diuresis. It is characterised by severe dehydration, a very high blood sugar (> 33 mmol/1 600 mg/100 ml) and lack of ketosis and acidosis. Treatment is with isotonic (0.9%) saline, at half the rate recommended for ketoacidotic coma, and with less potassium than in severe ketoacidosis. Insulin requirements are less than in ketoacidosis, where the acidosis causes resistance to the actions of insuhn, and should generally be half those shown in Table 35.2. Patients are more liable to thrombosis and prophylactic heparin is used. 

If an insulin-dependent diabetic who has failed to take insulin, is suffering from an illness, or is subjected to stress, blood glucose may rise markedly. Elevated glucagon levels cause adipose tissue to release increased amounts of fatty acids, which are converted to ketone bodies by the liver. Ketone body levels may become extremely high, causing a metabolic acidosis that, if not treated rapidly and effectively, may lead to coma and death. 

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