Urine ketones

Fasting blood glucose Hemoglobin A Hemoglobin A, Urine ketones Urine glucose... 

Willis (W12, W14) reported the determination of lead in urine. Lead was chelated with ammonium pyrrolidine dithiocarbamate and extracted into methyl-n-amyl ketone. Urine samples of 50 ml had to be extracted into 1.5 ml of the solvent to obtain sufficient concentration of the metal. Differences in the efficiency of extraction from water and urine at various pH values were noted. The availability of a reliable and simple method such as the one described will be welcomed by medical laboratories, but unfortunately the limited sensitivity requiring large original samples makes the method less applicable for the determination of lead in blood. 

Methyl-2-pentanone 100.2 Methyl isobutyl ketone Urine... 

MEK in urine METHYL ISOBUTYL KETONE (MIBK) End of shift 2 mg/l ... 

Fhtients with diabetes Levodopa may interfere witii urine tests for glucose or ketones. Report any abnormal result to the primary care provider before adjusting the dosage of die antidiabetic medication. 

Urine testing can play a role in identifying ketone excretion in patients prone to ketoacidosis. If urine testing is done, it is usually recommended tiiat the nurse use the second voided specimen (ie, fresh urine collected 30 minutes after the initial voiding) to check glucose or acetone levels, ratiier than die first specimen obtained. 

Although elderly patients taking the oral antidiabetic drugs are particularly susceptible to hypoglycemic reactions these reactions may be difficult to detect in the elderly. The nurse notifies the health care provider if blood sugar tevetsare elevated (consistently > 200 mg/dL) or if ketones are present in the urine. 

Test blood for glucose and urine for ketones as directed by the health care provider. Keep a record of test results and bring this record to each visit to the health care provider or clinic. 

The patient is able to use die glucometer correcdy to monitor blood sugar or test urine for glucose and ketones. 

In moderate ketonemia, the loss of ketone bodies via the urine is only a few percent of the total ketone body production and utilization. Since there are renal threshold-like effects (there is not a true threshold) that vary between species and individuals, measurement of the... 

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. 

The assessment of clearance is complicated by the numerous mechanisms by which compounds may be cleared from the body. These mechanisms include oxidative metabolism, most commonly by CYP enzymes, but also in some cases by other enzymes including but not limited to monoamine oxidases (MAO), flavin-containing monooxygenases (FMO), and aldehyde oxidase [45, 46], Non-oxidative metabolism such as conjugation or hydrolysis may be effected by enzymes such as glucuronyl transferases (UGT), glutathione transferases (GST), amidases, esterases, or ketone reductases, as well as other enzymes [47, 48], In addition to metabolic pathways, parent compound may be excreted directly via passive or active transport processes, most commonly into the urine or bile. 

Because ketones are passed out of the body in the urine, a doctor can detect the onset of diabetic acidosis by doing a urine test. If ketones are present in the urine, it is a signal to the doctor that the patients diabetes is out of control. Without treatment, the patient could get very sick. On rare occasions, even Type I or Type II diabetics who take their medication can develop acidosis, usually as a result of some other serious health issue such as an infection or a heart attack. 

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. 

In addition to these interconversions, the metabolism of fat and the metabolism of carbohydrate are inseparably related. This fact is most clearly demonstrated by the appearance of such abnormal products of fat oxidation as the so-called ketone bodies in the blood and urine whenever the supply of carbohydrate is deficient or in cases where the organism is unable to metabolize this foodstuff. Whether ketonuria results because the metabolism of fat must occur concomitantly with that of D-glucose (ketolysis), or whether the presence of D-glucose prevents any fat breakdown because it is preferentially oxidized (antiketogenesis) is still a moot question. 

Fructose-1,6-bisphosphatase deficiency, first describ ed by Baker and Winegrad in 1970, has now been reported in approximately 30 cases. It is more common in women and is inherited as an autosomal recessive disorder. Initial manifestations are not strikingly dissimilar from those of glucose-6-phosphatase deficiency. Neonatal hypoglycemia is a common presenting feature, associated with profound metabolic acidosis, irritability or coma, apneic spells, dyspnea, tachycardia, hypotonia and moderate hepatomegaly. Lactate, alanine, uric acid and ketone bodies are elevated in the blood and urine [11]. The enzyme is deficient in liver, kidney, jejunum and leukocytes. Muscle fructose-1,6-bisphosphatase activity is normal. 

A number of workers have described methods for the determination of mercury in which the mercury is first reduced to the element or collected as the sulfide on a cadmium sulfide pad. It is then volatilized into a chamber for measurement. These techniques are extremely sensitive. Thillez108) recently described a procedure for urinary mercury in which the mercury is collected on platinum and then volatilized into an air stream. Rathje109) treated 2 ml of urine with 5 ml of nitric acid for 3 min, diluted to 50 ml, and added stannuous chloride to reduce the mercury to the element. A drop of Antifoam 60 was added and nitrogen was blown through the solution to carry the mercury vapor into a quartz end cell where it is measured. Six nanograms of mercury can be detected. Willis 93) employed more conventional methods to determine 0.04 ppm of mercury in urine by extracting it with APDC into methyl-n-amyl ketone. Berman n°) extracted mercury with APDC into MIBK to determine 0.01 ppm. 

Willis 93) extracted lead directly from 200 ml of urine with APDC into 1.5 ml of methyl-n-amyl ketone. He was able to determine as little as 0.02 ppm of lead. Kopito and Shwachman 141>, on the other hand, co-precipitate the lead from urine with bismuth nitrate by adding ammonia. The precipitated bismuth hydroxide is dissolved in acid and this solution is aspirated. Coprecipitation of the lead is not quantitative, and so standards should be prepared in the same manner. It should be possible to employ this procedure with protein free filtrates of blood without the necessity of close pH control. 

Zhao WY, Misumi J, Yasui T, et al. 1998. Effects of methyl ethyl ketone, acetone, or toluene coadministration on 2,5-hexanedione concentration in the sciatic nerve, serum, and urine of rats. Int Arch Occup Environ Health 71 236-244. 

Endrin and endrin aldehyde can enter your body when you eat foods or drink beverages or breathe air that contain this substance, or when it comes in contact with your skin. When endrin enters your body in any of these ways, it is rapidly changed into other substances. Endrin and its metabolic breakdown products are rapidly removed from the body, usually within a few days, through the urine and feces. There is some evidence that small amounts of endrin may remain in the fatty tissue of your body when you are exposed to high levels. No information is known about how endrin aldehyde or endrin ketone leaves the body. 

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