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Diabetes mellitus ketoacidosis

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. [Pg.490]

Higher than normal quantities of ketone bodies present in the blood or urine constitute ketonemia (hyperke-tonemia) or ketonuria, respectively. The overall condition is called ketosis. Acetoacetic and 3-hydroxybutyric acids are both moderately strong acids and are buffered when present in blood or other tissues. However, their continual excretion in quantity progressively depletes the alkah reserve, causing ketoacidosis. This may be fatal in uncontrolled diabetes mellitus. [Pg.188]

Mechanical obstruction Diabetes mellitus (diabetic ketoacidosis)... [Pg.308]

In patients with type 1 insulin-dependent diabetes mellitus not adequately treated with insulin, fatty add release from adipose tissue and ketone synthesis in the liver exceed the ability of other tissues to metabolize them, and a profound, life-threatening ketoaddosis may ocxnir. An infection or trauma (causing an increase in cortisol or epinephrine) may predpitate an episode of ketoaddosis. Patients with type 2 non-insulin-dependent diabetes meUitus (NIDDM) are much less likely to show ketoaddosis. The basis for this observation is not completely understood, although type 2 disease has a much slower, insidious onset, and insulin resistance in the periphery is usually not complete. Type 2 diabetics can develop ketoacidosis after an infection or trauma. In certain populations with NIDDM, ketoaddosis is much more common than previously appredated. [Pg.232]

During anaerobic glycolysis in the muscles and erythrocytes, glucose is converted into lactate, releasing protons in the process (see p. 338). The synthesis of the ketone bodies acetoacetic acid and 3-hydroxybutyric acid in the liver (see p. 312) also releases protons. Normally, the amounts formed are small and of little influence on the proton balance. If acids are formed in large amounts, however (e. g., during starvation or in diabetes mellitus see p. 160), they strain the buffer systems and can lead to a reduction in pH (metabolic acidoses lactacidosis or ketoacidosis). [Pg.288]

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). [Pg.312]

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. [Pg.314]

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. [Pg.1103]

Diabetes mellitus/Hyperglycemia New-onset diabetes mellitus, exacerbation of pre-existing diabetes mellitus, diabetic ketoacidosis, and hyperglycemia have been reported in HIV-infected patients receiving protease inhibitors. [Pg.1807]

Onset of type 1 diabetes mellitus usually occurs within the first two decades of life presenting symptoms Include hyperglycemia, polyuria, polydipsia, and polyphagia (excessive urination, thirst, and appetite, respectively), often with serious ketoacidosis in response to a stressor such as a viral infection. [Pg.65]

Contraindications Diabetic ketoacidosis with or without coma, type 1 diabetes mellitus... [Pg.564]

Treatment of insulin-dependent type 1 diabetes mellitus and non-insulin-dependent type 2 diabetes mellitus when diet or weight control has failed to maintain satisfactory blood glucose levels or in event of fever, infection, surgery, ortrauma, or severe endocrine, hepatic, or renal dysfunction emergency treatment of ketoacidosis (regular insulin) to... [Pg.629]

Contraindications Active hepatic disease diabetic ketoacidosis increased serum transaminase levels, including ALT greater than 2.5 times normal serum level type 1 diabetes mellitus... [Pg.995]

Lindenmayer JP, Patel R, et al. Olanzapine-induced ketoacidosis with diabetes mellitus. Am J Psychiatry 1999 156 836-837. [Pg.99]

Definition of ketoacidosis and example of a disease where it occurs Ketoacidosis occurs when the rate of formation of ketone bodies is greater than the rate of use, as seen in cases of uncontrolled, insulin-dependent diabetes mellitus... [Pg.486]

DKA diabetic ketoacidosis dL deciliter DM diabetes mellitus DMARD disease-modifying... [Pg.456]

The three compounds, acetoacetate, acetone, and 3-hydroxybutyrate, are known as ketone bodies.60b The inability of the animal body to form the glucose precursors, pyruvate or oxaloacetate, from acetyl units sometimes causes severe metabolic problems. The condition known as ketosis, in which excessive amounts of ketone bodies are present in the blood, develops when too much acetyl-CoA is produced and its combustion in the critic acid cycle is slow. Ketosis often develops in patients with Type I diabetes mellitus (Box 17-G), in anyone with high fevers, and during starvation. Ketosis is dangerous, if severe, because formation of ketone bodies produces hydrogen ions (Eq. 17-5) and acidifies the blood. Thousands of young persons with insulin-dependent diabetes die annually from ketoacidosis. [Pg.946]

NIDDM is a much more common disease than IDDM, accounting for about 85—90% of all cases of diabetes mellitus. 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 frequently 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. [Pg.338]

Takaike H, Uchigata Y, Iwasaki N, Iwamoto Y. Transient elevation of liver transaminase after starting insulin therapy for diabetic acidosis or ketoacidosis in newly diagnosed type 1 diabetes mellitus. Diabetes Res Clin Pract 2004 64 27-32. [Pg.416]

A 50-year-old man developed acute ketoacidosis with de novo diabetes mellitus after 8 months of adjunctive olanzapine (865). His dosage was then gradually titrated to 30 mg/day over 6 months, and after withdrawal of olanzapine his diabetes mellitus disappeared completely. [Pg.632]

There has been a report of diabetic ketoacidosis in a 42-year-old man, without a prior history of diabetes mellitus, who took risperidone (2 mg bd) (1039). The authors pointed out that in premarketing studies of risperidone, diabetes mellitus occurred in 0.01-1% of patients. [Pg.645]

Jin H, Meyer JM, Jeste DV. Phenomenology of and risk factors for new-onset diabetes mellitus and diabetes ketoacidosis associated with atypical antipsychotics an analysis of 45 cases. Ann Clin Psychiatry 2002 14 59-64. [Pg.680]

Physical therapists and occupational therapists may help reinforce the importance of patient compliance during pharmacologic management of diabetes mellitus. Therapists can question whether patients have been taking their medications on a routine basis. Regular administration of insulin is essential in preventing a metabolic shift toward ketone body production and subsequent ketoacidosis, especially in patients with type 1 diabetes. In addition, therapists can help explain that adequate control of blood glucose not only prevents acute metabolic problems but also seems to decrease the incidence of the neurovascular complications. [Pg.491]

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. [Pg.353]


See other pages where Diabetes mellitus ketoacidosis is mentioned: [Pg.233]    [Pg.233]    [Pg.1229]    [Pg.215]    [Pg.147]    [Pg.722]    [Pg.1819]    [Pg.1828]    [Pg.768]    [Pg.217]    [Pg.223]    [Pg.196]    [Pg.337]    [Pg.344]    [Pg.1003]    [Pg.625]    [Pg.482]    [Pg.283]    [Pg.151]   
See also in sourсe #XX -- [ Pg.840 ]

See also in sourсe #XX -- [ Pg.840 ]

See also in sourсe #XX -- [ Pg.241 ]




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