Alcohol Lactic Acidosis Mechanism

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Metabolic Abnormalities In Alcoholic Patients: Focus On Acid Base Andelectrolyte Disorders

E-mail: [emailprotected] , [emailprotected] Received Date: December 20, 2014; Accepted Date: January 24, 2015; Published Date: January 27, 2015 Citation: Moses Elisaf MD, Rigas Kalaitzidis MD (2015) Metabolic Abnormalities in Alcoholic Patients: Focus on Acid Base and Electrolyte Disorders. J Alcohol Drug Depend 3:185. doi:10.4172/2329-6488.1000185 Copyright: 2015 Moses Elisaf MD, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Alcoholic patients commonly develop a variety of acid-base and electrolyte disturbances. The aim of this review is to describe the most commonly encountered abnormalities and their significant role in the patients morbidity and mortality. Physicians should be aware of these clinically important disturbances caused by alcohol abuse and their underlying pathophysiological mechanisms involved for their appropriate management. Alcoholic Keto Acidosis (AKA) is a medical emergency is more common than previously thought and is characterized by an increased anion gap metabo Continue reading >>

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  1. amsmith

    I understand that the guidelines state "uncontrolled" should be coded as hyperglycemia. What about the DKA type 2 portion? We have 2 opinions in our office and I am just looking for the correct way to code it.
    I suspect for my scenario E11.65, E11.69 and E87.2. Please help.
    There really should be an E11.1X...LOL!!
    Thank you,

  2. mitchellde

    Ketoacidosis is actually rare in a type 2 diabetic so that may be the reason for no specific code for it. So use the E11.69 with the E87.2

  3. amsmith

    Oddly, our physician's document it frequently. I will check with one of them to find out why we tend to have a higher volume.

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Alcoholism And Lactic Acidosis

Learn more about the SDN Exhibition Forums for exclusive discounts and contests. So the way I understood this is that both alcohol metabolism and latcate to pyrvuate conversion require NAD, and with too much alcohol consumption the body uses up all the NAD for alcohol metabolism right? The part that I'm a bit troubled with this mechanism is that unless we are doing extreme exercise, we don't really generate lactic acid. In most cases, the body uses oxidative phosphorylation, right? So lactic acidosis will most likely occur when you drink alcohol and then do extreme exercise, correct? SDN Members don't see this ad. About the ads. My understanding is that high NADH levels from EtOH metab drives the pyruvate -> lactate conversion. So you don't need to be exercising +drinking, either will do it on their own. I actually enjoy your questions, though some things are really easily looked up. The several different causes of lactic acidosis: I actually enjoy your questions, though some things are really easily looked up. The several different causes of lactic acidosis: But the reasons behind why lactic acidosis occurs for these is significantly different.... For example, in exercise- lactic Continue reading >>

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  1. anglgrl

    I've been following Aradasky's thread about her ketometer readings and thought I'd post my results as well.
    I haven't cheated since Feb. but I try to keep my carbs between 45-50g. (There's a long story behind this, but the short version is I started having anxiety attacks every time I left the house (while eating VLC) but when I went up to 50g a day they stopped. And I started losing weight a tiny bit faster. I know I'm a weirdo. :) )
    I have to be careful because I know I'm right on the edge of my limit. I've gone up to about 56g and it must have pushed me out of ketosis because I started getting hungry too much.
    I take vitamins that screw up using ketosticks so I've never even tried to use them. When I read about using blood for a reading I was excitied to finally have some feed back on what was going on in my body.
    Just a note: Right before I got my meter I got some readings I didn't like when I took my postprandial glucose readings. So I lowered my carbs for a few days to get it under control. (And added more fat) And BTW I count total carbs (not net).
    And I always try to eat between 55-88 g protein.
    I'll tell you what I ate the day before, then the reading the next day.
    Cal 1595
    Fat 122.92 69%
    Pro 83.03 21%
    Carb 37.56 10%
    Next day reading: 1.5 (For fun I took a reading 2 hours after eating just to see what it was and I got .9)
    Cal 1460
    Fat 117.48 72%
    Pro 63.73 19%
    Carb 31.97 9%
    Next day: 1.2
    Cal 1616
    Fat 126.26 70%
    Pro 73.83 19%
    Carb 41.90 11%
    Next day: 4.0
    Cal 1698
    Fat 141.92 75%
    Pro 59.40 15%
    Carb 41.70 10%
    Next day: 2.1
    Cal 2084
    Fat 167.19 72%
    Pro 95.05 19%
    Carb 45.82 9%
    Next day: 2
    Cal 1779
    Fat 130.12 70%
    Pro 84.05 19%
    Carb 48.96 11%
    Next day: 2.1
    Cal 1660
    Fat 130.95 71%
    Pro 66.03 17%
    Carb 49.67 12%
    Next day: 2.2
    Cal 1682
    Fat 133.01 71%
    Pro 67.25 17%
    Carb 49.62 12%
    Next day: ? (We were showing our house and I forgot to take it :mad: )
    Cal 1782
    Fat 141.15 71%
    Pro 77.08 18%
    Carb 49.35 11%
    Next day: 1.4
    I'll probably keep taking readings for the next 5 days, then I'll just take it once a week (maybe). I've lost 1.5 pounds since that first reading.
    Another note: I didn't take my fat back down when I added the carbs back in so I'm eating a lot more calories than I was before. I used to eat around 1500 cals a day, now I seem to be eating around 1700 (more or less). The extra calories do not seem to be slowing down my weight loss. I don't know if it's the extra fat or the extra veggies I've been eating.

  2. mfish

    Love this!!
    I've been following all the recent threads RE: blood ketones... This is great info thanks for posting your readings. It's good to see that NK can be maintained with some carbohydrate in the diet, my T3 dipped low after a while on VLC. Which meter are you using? I ordered the free Nova Max last night. Just recently I've been testing my BG and seeing some very interesting things, now I want to test for serum ketones too.
    ETA: nevermind the "which meter" question... I just read your post in the other thread that you are using the Nova Max!

  3. LaZigeuner

    anglgrl, have you noticed a difference in how you feel, between when your blood ketones are 1.x versus 2.x versus that 4?
    I'm so curious about this, and considering doing my own testing as well.
    Thanks for posting your data! :)

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Metabolic Acidosis In The Alcoholic: A Pathophysiologic Approach.

Metabolic acidosis in the alcoholic: a pathophysiologic approach. Halperin ML , Hammeke M , Josse RG , Jungas RL . The purpose of this paper is to review the acid-base abnormalities in patients presenting with metabolic acidosis due to acute ethanol ingestion and to review the theoretical constraints on ethanol metabolism in the liver. Alcohol-induced acidosis is a mixed acid-base disturbance. Metabolic acidosis is due to lactic acidosis, ketoacidosis and acetic acidosis but the degree of each varies from patient to patient. Metabolic alkalosis is frequently present due to ethanol-induced vomiting. However, it could be overlooked because of an indirect loss of sodium bicarbonate (as sodium B-hydroxybutyrate in the urine). Nevertheless, the accompanying reduction in ECF volume may play an important role in the pathogenesis of alcoholic acidosis because it could lead to a relative insulin deficiency. Treatment of alcohol acidosis should include sodium, chloride, potassium, phosphorus, magnesium and thiamine replacements along with attention to concomitant clinical problems. Unless hypoglycemia is present, glucose need not be given immediately. We feel that insulin should be withheld Continue reading >>

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  1. Andalyne

    Chapter 24 reading quiz question 3 part a which

    Chapter 24 Reading Quiz Question 3
    Part A
    Which nutrient molecule CANNOT be used in the oxidative pathways?
    No cell uses cholesterol as a fuel that it oxidizes to create energy for itself. Oxidative pathways involve energy
    production. glycolysis
    both glycolysis and the citric acid cycle
    the citric acid cycle
    neither glycolysis nor the citric acid cycle
    fatty acids
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    Chapter 24 Reading Quiz Question 5
    Part A
    __________ is the conversion of acetyl CoA into ketone bodies.
    Ketogenesis is the conversion of acetyl CoA (fatty acid fragments, not whole fat) into ketone bodies whenever acetyl
    CoA cannot be oxidized. But a fat molecule must first be broken into fatty acids by another process.
    Chapter 24 Chapter Test Question 7
    Part A
    The citric acid cycle occurs in the __________ of cells and is an __________ process.
    The citric acid cycle occurs in the mitochondria of cells. While the citric acid cycle does not directly use oxygen, it is
    part of the aerobic pathways for metabolism.
    Chapter 24 Chapter Test Question 8
    Part A
    Most ATP in cellular respiration is regenerated in substrate level phosphorylation.
    ANSWER: Ketogenesis
    Beta oxidation
    cytosol; aerobic
    mitochondria; aerobic
    mitochondria; anaerobic
    cytosol; anaerobic
    Most of the ATP in cellular respiration is regenerated in oxidative phosphorylation.
    Chapter 24 Chapter Test Question 9
    Part A
    Which of the following is NOT an end product of the citric acid cycle?
    Citric acid is the initial reactant required for the citric acid cycle.
    Chapter 24 Chapter Test Question 12
    Part A
    Ammonia, which is a byproduct of protein metabolism, is converted to __________ primarily in the __________.
    Ammonia produced during protein metabolism is converted into urea in the liver.
    Chapter 24 Chapter Test Question 13 True
    FADH 2
    citric acid
    CO 2
    ketones; liver
    ketones; kidney
    urea; kidney
    urea; liver
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    Part A
    __________ is the key hormone regulator of the postabsorptive state.
    Glucagon raises the blood glucose level and is the key hormone used to handle the postabsorptive state.
    Chapter 24 Chapter Test Question 14
    Part A
    Which of these happens during the postabsorptive state?
    After glucose levels stabilize after a meal, the body tries to maintain the blood sugar until the next meal.
    Chapter 24 Reading Quiz Question 8
    Part A
    Which of the following is NOT an essential role of the liver?
    ANSWER: Glucagon
    Parathyroid hormone
    Glycogen is formed.
    Blood glucose levels are maintained within an adequate range.
    Glucose is broken down in the liver.
    Fat reserves are built.
    Though the liver is involved in creating urea from ammonia and carbon dioxide, it is up to the kidney to eliminate the
    urea thus formed.
    Chapter 24 Chapter Test Question 15
    Part A
    __________ are considered "bad" cholesterol; high blood levels are believed to increase the risk of cardiovascular disease.

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