Low Co2 In Dka

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Diabetic Ketoacidosis

I. Review of normal lipid metabolism Triglycerides in adipose ==lipolysis==> Long-chain FAs Long-chain FAs==hepatic beta-oxidation==>Acetyl CoA Acetyl CoA==hepatic ketogenesis==>ketone bodies Ketone bodies are Beta-hydroxybutyrate and Acetoacetate Beta-OHB is oxidized to AcAc-; their relative concentrations depend on redox state of cell; Beta-OHB predominates in situation favoring reductive metabolism (e.g. decreased tissue perfusion, met. acidosis, catabolic states--like DKA!) Typical ratio Beta-OHB:AcAc- is 3:1; us. increases in DKA II. Hormonal influences on glucose and lipid metabolism Insulin In liver, increases glu uptake from portal blood; stimulates glycogenesis, inhibits glycogenolysis and gluconeogenesis In skeletal muscle, increases glu uptake from blood, stimulates protein synth, inhibits proteolysis In adipose tissue, required for glu and lipoprotein uptake from blood; stimulates lipogenesis, inhibits lipolysis Tissues which don't require insulin to transport glucose into cells: brain, renal medulla, formed blood elements Counterregulatory hormones: glucagon (major player in DKA), epi/norepi, cortisol, growth hormone (no acute effects, only over days-weeks) Glucagon: i Continue reading >>

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Popular Questions

  1. TheCommuter

    You can post this question on this site's Nursing Student Assistance Forums and perhaps get an answer. One of our frequent users, Daytonite, loves to give detailed answers to these types of questions.

  2. ICRN2008

    Here is the formula for anion gap:
    Agap = Na + K - Cl -CO2
    I would think that the doctor would be monitoring the glucose level (not the agap) to determine when to stop the insulin drip. Anyone else have an idea?

  3. P_RN

    One of our wonderful members Mark Hammerschmidt has a great FREE MICU site:
    Check section 4.2
    It's all acidosis/alkalosis

  4. -> Continue reading
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