Ketoacidosis, diabetic, treatment

Treatment of metabolic acidosis is focused on correcting the underlying problem. For example, in lactic acidosis, the correction will center on oxygenation to prevent anaerobic metabolism or fixing other causes of the condition. Similarly, in diabetic ketoacidosis, treatment focuses on correcting the insulin deficit to decrease the burning of fats and production of ketones. 

Fig. 16.6 Prosthetic gene networks. (A) Selfsufficient synthetic circuit to control blood-urate homeostasis. (B) Obesity treatment. (C) Diabetic ketoacidosis treatment (D) Artificial insemination. cAMP, cyclic adenosine monophosphate CREBl, cAMP-responsive element binding protein 1 KRAB, Kriippel associated box LHR, luteinizing hormone receptor TtgR-specific operator promoter activated by CREBl human cytomegalovirus promoter hEFia elongation factor 1 alpha promoter, P, simian virus 40 promoter PPARa, human...

NIDDM is a much more common disease than IDDM, accounting for about 85—90% of all cases of diabetes meUitus. Whereas NIDDM may be present at any age, the incidence increases dramatically with advanced age over 10% of the population reaching 70 years of age has NIDDM. Patients with NIDDM do not require insulin treatment to maintain life or prevent the spontaneous occurrence of diabetic ketoacidosis. Therefore, NIDDM is frequendy asymptomatic and unrecognized, and diagnosis requires screening for elevations in blood or urinary sugar. Most forms of NIDDM are associated with a family history of the disease, and NIDDM is commonly associated with and exacerbated by obesity. The causes of NIDDM are not well understood and there may be many molecular defects which lead to NIDDM. 

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. 

Insulin Exenatide is not a substitute for insulin in insulin-requiring patients. Do not use exenatide in patients with type 1 diabetes or for the treatment of diabetic ketoacidosis. The concurrent use of exenatide with insulin, thiazolidinediones, D-phenylalanine derivatives, meglitinides, or alpha-glucosidase inhibitors has not been studied. 

Renal disease or renal dysfunction (eg, as suggested by serum creatinine levels greater than or equal to 1.5 mg/dL [males], greater than or equal to 1.4 mg/dL [females], or abnormal Ccr) that may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction (Ml), and septicemia CHF requiring pharmacologic treatment hypersensitivity to metformin acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. Treat diabetic ketoacidosis with insulin. 

Colli A, Cocciolo M, Francobandiera R, et al. Diabetic ketoacidosis associated with clozapine treatment. Diabetes Care 1999 22 176-177. 

When giving insulin for diabetic ketoacidosis an increase in liver enzymes can occur. These patients have often higher concentrations of HbAic, glucose, and triglycerides, need more insulin, and have more fat disposition in the liver during treatment of the acute phase (117). 

In 40 patients aged 4-25 years with type 1 diabetes who were given continuous subcutaneous insulin infusion for 6 months the number of episodes of hypoglycemia was reduced by a half (192). There were two episodes of diabetic ketoacidosis. In 10 patients lipohypertrophy developed at the insertion site and three patients had signs of skin redness, which improved with local antibiotic treatment. 

In a meta-analysis of the metabolic and psychosocial impact of pumps, 52 studies were found 22 were published before 1987 and 13 after 1993, the year in which the results of the DCCT were published (225). The authors stated that therefore conclusions about efficacy are not definitive. All pump malfunctions were reported before 1988. All types of changes were reported when the frequency and severity of hypoglycemia were compared with prepump times. Infection and skin irritation were expressed in different ways in the various studies. The risk of diabetic ketoacidosis fell after 1993. Most users preferred to continue pump treatment, mainly because of more flexibility, greater freedom, and improved glycemic control. 

Gatta B, Rigalleau V, Gin H. Diabetic ketoacidosis with olanzapine treatment. Diabetes Care 1999 22(6) 1002-3. 

A 13-year-old boy with Prader-Willi syndrome and steatohepatitis was given growth hormone 0.23 mg/kg/ week (63). His HbAic concentration before treatment was 5.6%. Four weeks later he developed diabetic ketoacidosis. He was given insulin and the growth hormone was withdrawn. Insulin was then gradually withdrawn and blood glucose concentrations remained normal for the next 6 months. 

Yigit S, Estrada E, Bucci K, Hyams J, Rosengren S. Diabetic ketoacidosis secondary to growth hormone treatment in a boy with Prader-Willi syndrome and steatohe-patitis. J Ped Endocrinol Metab 2004 17 361 —4. 

Croarkin PE, Jacobs KM, Bain BK. Diabetic ketoacidosis associated with risperidone treatment Psychosomatics 2000 41(4) 369-70. 

Diabetic ketoacidosis may either result from or be aggravated by infection, surgery, trauma, shock, emotional stress, or failure to take sufficient amounts of insulin. Treatment is focused on reversing the hypokalemia by administering potassium chloride and on offsetting the acidosis by providing bicarbonate. The dehydration and electrolyte imbalance are treated with appropriate measures and crystalline zinc insulin is administered to counter the hyperglycemia. 

Insulin is an endogenous hormone produced by fi-cells of islets of Langerhans of the pancreas, which consist of two chains of amino acids. It is required to be administered by a parenteral routes as it is destroyed when given orally. Insulin is used for the control of IDDM and in the emergency management of diabetic ketoacidosis.30 Insulin promotes the intracellular uptake of potassium and is used in hyperkalemia. Baker et al.31 have used insulin and glucagon in the treatment of liver disorders. Recent evidence indicates that the effects of insulin with glucose and potassium in ischemic heart disease have proved beneficial.32 It also is used in acute myocardial infarction.32... 

Correct answer = C. Protamine complexes with insulin to form an insoluble complex that is slowly absorbed. Insulin is not administered orally because it is destroyed by proteases in the Gl tract. Diet therapy and/or sulfonylureas are often effective without additional insulin In the therapy of Type II diabetics. Ketoacidosis is the most life-threatening consequence of Type I diabetics and requires adequate treatment with insuiin, not sulfonylureas. Insulin acts by binding to specific receptors in the cell membrane, not in the nucleus. 

What is the main reason for administering insulin in the treatment of diabetic ketoacidosis (DKA) ... 

Foster DW, McGarry JD The metabolic derangements and treatment of diabetic ketoacidosis. N Engl J Med 309 159-169,1983. 

CM is a 27-year-old white woman with type 1 diabetes diagnosed at age 14 when she presented with diabetic ketoacidosis. Her initial insulin treatment was complicated by poor glycaemic control, frequent hypoglycaemia and weight gain. 

CM was started on intravenous insulin, fluids, and electrolyte replenishment. Her nausea and vomiting resolved and, although initially, she required 60-70 units of insulin intravenously per day to attain glycaemic control, her blood glucose dropped to 7.4 mmol/L after 4 days of intensive care. However, despite treatment of her diabetic ketoacidosis, including significant rehydration therapy, CM was still found to have an elevated but stable serum creatinine of 246 micromol/L, and so she was transferred from the intensive care unit to the renal unit for further management. 

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