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Ketoacidosis Turbid Definition

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Pseudohyponatremia

Measurement of plasma/serum sodium concentration is one of the most frequently requested blood tests in clinical practice. Although usually performed in the laboratory, the test is also available at the point of care using technology incorporated into blood gas and other point-of-care analyzers. In health, sodium concentration is maintained between 135 and 145 mmol/L, so that hyponatremia (reduction in plasma sodium) is diagnosed if the concentration falls below 135 mmol/L. Effective, safe correction of plasma sodium depends on establishing the cause. Initial assessment of the hyponatremic patient should include due consideration of the rare possibility that the result is spuriously low: that this is not true hyponatremia but so-called "pseudo"hyponatremia. The main purpose of this article is to outline how some laboratory methods can, in certain well-defined clinical situations, give rise to a falsely low plasma sodium concentration, and thereby a diagnosis of pseudohyponatremia. Indicators that help establish a diagnosis of pseudohyponatremia will be discussed, and with the help of two published case histories, the danger of failing to recognize pseudohyponatremia will be highlig Continue reading >>

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Popular Questions

  1. Christian

    I read conflicting views about whether or not the human body can create glucose out of fat. Can it?

  2. David

    Only about 5–6% of triglyceride (fat) can be converted to glucose in humans.
    This is because triglyceride is made up of one 3-carbon glycerol molecule and three 16- or 18-carbon fatty acids. The glycerol (3/51-to-57 = 5.2–5.9%) can be converted to glucose in the liver by gluconeogenesis (after conversion to dihydroxyacetone phosphate).
    The fatty acid chains, however, are oxidized to acetyl-CoA, which cannot be converted to glucose in humans. Acetyl-CoA is a source of ATP when oxidized in the tricarboxylic acid cycle, but the carbon goes to carbon dioxide. (The molecule of oxaloacetate produced in the cycle only balances the one acetyl-CoA condenses with to enter the cycle, and so cannot be tapped off to gluconeogenesis.)
    So triglyceride is a poor source of glucose in starvation, and that is not its primary function. Some Acetyl-CoA is converted to ketone bodies (acetoacetate and β-hydroxybutyrate) in starvation, which can replace part — but not all — of the brain’s requirement for glucose.
    Plants and some bacteria can convert fatty acids to glucose because they possess the glyoxylate shunt enzymes that allow two molecules of Acetyl-CoA to be converted into malate and then oxaloacetate. This is generally lacking in mammals, although it has been reported in hibernating animals (thanks to @Roland for the last piece of info).

  3. blu potatos

    To be more detailed it is the irreversibly of the reaction carried by Pyruvate dehydrogenase that makes the conversion of the fatty acid chains to glucose impossible. The fatty acids chains are converted to acetyl-CoA.
    Acetyl-CoA to be converted into pyruvate need an enzyme that can do the Pyruvate Dehydrogenase's inverse reaction (in humans there is no such enzyme). Than the pyruvete inside the mitochondria is converted into glucose(gluconeogenesis).

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