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Partially Compensated Metabolic Acidosis

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Metabolic Acidosis - Endocrine And Metabolic Disorders - Msd Manual Professional Edition

By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Metabolic acidosis is primary reduction in bicarbonate (HCO3), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3 loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see Table: Causes of Metabolic Acidosis ). Lactic acidosis (due to exogenous toxins) Toluene (initially high gap; subseq Continue reading >>

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  1. visvavasu

    Observation: My Blood Glucose levels in nutritional ketosis are markedly higher than normal. Following a meal, glucose levels rise higher, and take longer to come back to their equilibrium levels (which are higher). I have observed this myself (I'm not a diabetic, and yet when in keto FBG ~100 mg/dl, post prandial ~130 mg/dl for 4-8 hours), and so have others [1]
    Theory: This is termed 'physiological insulin resistance' by some sources [1] [2] [3]. I'd be grateful here if the experts here can verify if my articulation below is accurate, and help me with my questions.
    The only sources of blood glucose are ingested carbs and in-vivo production by glycogenolysis or gluconeogenesis. In ketosis, there is a scarcity of carbs. The presence of insulin would cause blood glucose to be absorbed by the three insulin-dependent glucose sinks (muscle, fat and liver tissue) [Q1]. Therefore, in order to sustain blood glucose levels in ketosis [Q2], circulating insulin levels are forced to be lower [Q3] AND the three insulin-dependent glucose sinks become insulin resistant [Q4].
    By the net effect of lower insulin AND lower effectiveness of that insulin, catabolic events dominate. Glycogen is broken down in the liver and muscles, and glycogen synthesis is retarded. Muscle tissue switches to using fatty acids and ketones for energy. Lipids are broken down, causing lipid levels in the blood to rise (leading to higher HDL, LDL and triglyceride levels in keto blood tests). The usual blood-glucose level dependent signalling for appetite is disrupted, as likely are the leptin/ghrelin equilibria. All effects of ketosis (weight loss, different energy levels, etc.) follow.
    But what happens to blood glucose levels? With a diminished role of insulin, the only sink for glucose levels are neurons, which are the only cells that can use glucose without insulin. A new equilibrium is reached between the sources glucose production (only in-vivo glycogenolysis or gluconeogenesis) and glucose consumption by the neurons. This equilibrium is higher than the equilibrium levels enforced by insulin [FBG 100 mg/dl vs 80 mg/dl normally] [Q5]. However, since the body is itself the source of the glucose, there is no cause for worry [Q6]
    What happens if one eats a cheat meal with lots of carbs? The body is not immediately ready to handle the ingested carbs. The diminished role of insulin will cause glucose levels to spike and stay high. At some point [Q7], the body starts producing more insulin in response [Q8]. This takes much longer when keto-adapted than otherwise, which is why it may take 10-12 hours to bring blood glucose down after a cheat meal. As a direct consequence of higher insulin, much of the conditions in ketosis are reversed and one is 'kicked out of keto': glycogen synthesis instead of glycogenolysis, shut down ketone production and gluconeogenesis, etc.
    Corollary 1: When in ketosis, it makes little sense to test glucose response of foods. Cookies, quest bars, etc. must be tested only outside of ketosis
    Corollary 2: When fully adjusted to keto, a cheat meal will cause blood glucose levels to be elevated for a long duration. Muscles/fat don't want glucose in keto, and the brain which does now has a surplus. Therefore cheat meals cause a significant loss of appetite for 10-12 hours following. I have observed this in myself, anybody else?
    Questions for experts
    [Q1] Are these the only insulin-dependent glucose sinks?
    [Q2] Why should blood glucose levels be sustained if ketones are available for use? What mandates a minimum glucose level?
    [Q3] Is this true? Is post-prandial insulin release really lower in ketosis? Both first pass as well as pulsatory?
    [Q4] Is this true? If so, do all 3 become insulin resistant? By what mechanism?
    [Q5] Why is the new equilibrium higher?
    [Q6] Is this true?
    [Q7] At what point?
    [Q8] Are there also changes to the insulin resistance asked in Q4?
    Broader questions
    [BQ1] Diabetic ketoacidosis has the exact same mechanism of ketone production as ketosis. Cells cannot use glucose, and so the liver starts producing ketones. What makes the former uncontrolled and dangerous, and the latter controlled and benign?
    [BQ2] Insulin resistance must necessarily lead to weight loss, never weight gain. Diabetes cannot lead to obesity, in fact diabetes must necessarily lead to weight loss. Is this true?
    [BQ3] A person in ketosis loses fat by the same mechanism as a diabetic loses weight. Far from being the "opposite" of diabetes, ketosis employs the same mechanisms to produce the same results. What makes the former safe and the latter dangerous?
    References
    [1] http://high-fat-nutrition.blogspot.com/2007/10/physiological-insulin-resistance.html
    [2] Resources referred to in http://ketopia.com/physiological-insulin-resistance/
    [3] http://ketopia.com/high-blood-sugar-in-ketogenic-dieters-plus-a-special-surprise-hint-genotypes-and-metabolism/

  2. anbeav

    For the most part, yes

    Other tissues use glucose like red blood cells, glucose acts in the bloo as an important molecule to regulate osmotic pressure

    It depends, everyone is different with varying insulin sensitivity

    Not everyone shows elevated fasting glucose

    Glucose is spared for tissues that need it
    BQ1. Without insulin you can't control the process. Ketones themselves feedback to reduce ketone produciton (high ketones stimulate insulin secretion as well as lipolysis. Insulin facilitates glucose uptake in to cells, without that you become hyperglycemic which has an osmotic effect and causes other issues in addition to acidosis. Without insulin, and without cellular utilization of glucose, counterregulatory hormones are activated like glucagon which increases lipolysis as well as gluconeogenesis both of which further increase ketones as well as blood glucose.
    BQ2. Why? That's completely untrue. Have you seen diabetic people recently most are overweight
    BQ3. Ketoacidosis is unregulated ketone production, so much so that you become acidotic, there's a huge difference between that and regulated nutritional ketosis

  3. visvavasu

    Thanks for the prompt reply.
    BQ1 ... Ketones themselves feedback to reduce ketone produciton (high ketones stimulate insulin secretion as well as lipolysis. Insulin facilitates glucose uptake in to cells, without that you become hyperglycemic which has an osmotic effect and causes other issues in addition to acidosis. ...
    Do ketones reduce ketone production via insulin?
    In essence, the concern in ketoacidosis is not the ketones but the hyperglycemia? i.e. the hyperglycemia causes dehydration, increasing the acidity of the blood. But this does not answer why the liver continues runaway production of ketones in ketoacidosis, and not in ketosis. Please help.
    BQ2: Yes, this is the contradiction I'm trying to resolve. Per the theory, a diabetic person's muscles/fat cannot utilize blood glucose due to insulin resistance. How can lipogenesis occur when insulin is ineffective?
    Of course, the reverse is easily understood: obesity can cause diabetes by the increased adipose tissue becoming resistant to insulin. Once they're resistant though, I can't understand how they can continue to grow.
    BQ3: Agree, but by what mechanism is nutritional ketosis regulated?

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Respiratory Acidosis

Respiratory acidosis is an abnormal clinical process that causes the arterial Pco2 to increase to greater than 40 mm Hg. Increased CO2 concentration in the blood may be secondary to increased CO2 production or decreased ventilation. Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Respiratory acidosis can arise from a break in any one of these links. For example, it can be caused from depression of the respiratory center through drugs or metabolic disease, or from limitations in chest wall expansion due to neuromuscular disorders or trauma (Table 90-1). It can also arise from pulmonary disease, card iog en ic pu lmon a ryedema, a spira tion of a foreign body or vomitus, pneumothorax and pleural space disease, or through mechanical hypoventilation. Unless there is a superimposed or secondary metabolic acidosis, the plasma anion gap will usually be normal in respiratory acidosis. Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition) , 2017 Respiratory acidosis is characterized by an increased arterial blood PCO2 and H+ ion concentration. The major cause of respiratory acido Continue reading >>

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  1. Natalia & Enana

    Hi.
    I just put my cat in a veterinary emergency clinic with high ketoacidosis. They gave her an IV and insulin and other things I could afford. They told me to keep her there for 48 hours but I'm picking her up tomorrow and taking her to her vet. I dont know if my beautiful cat will survive. What are her chances? What are your suggestions.
    Thanks,
    Nat

  2. Sue and Oliver (GA)

    I am so sorry your kitty has DKA, Nat. It is possible to turn it around and she is in the best place to have that happen. We do have many cats who have survived and come home and lived long lives.
    What you can do - learn how to keep her safe at home. The best way to do that is to home test for blood glucose and for ketones. We test our cat's blood glucose levels just like we would our diabetic children. Here is a good site for beginning info: Newbie hometesting site and a video: Video for hometesting We have taught hundreds of people how to test over the internet. We would love to teach you. Testing for ketones will help you determine before DKA that he is heading into dangerous territory: ketones
    You can get the supplies for both these kinds of testing at any drug store. We use human glucometers and ketostix.
    Read about the best diet for your cat here: http://www.catinfo.org We feed wet lo carb food. BUT don't change the diet until you are hometesting. Oliver went down 100 points overnight when we switched from dry to wet. If we hadn't been hometesting, he would have overdosed.
    I am giving you a lot of info at once. The board is going down in 25 minutes and will be off for 2 hours for maintenance. Come back on later tonight or in the morning and post specifically for DKA. People who have dealt with it can give you lots of tips on how to care for your kitty when she gets home.

  3. Robert and Echo

    Nat, sending best wishes for your cat. Please keep us updated on her condition. Many cats do recover from DKA but, as you already know, it can be expensive treatment.
    _Rebecca

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Metabolic Alkalosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

(Video) Overview of Buffering and the Henderson-Hasselbalch Equation By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Metabolic alkalosis is primary increase in bicarbonate (HCO3) with or without compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO3 excretion must be present to sustain alkalosis. Symptoms and signs in severe cases include headache, lethargy, and tetany. Diagnosis is clinical and with arterial blood gas and serum electrolyte measurement. The underlying condition is treated; oral or IV acetazolamide or hydrochloric acid is sometimes indicated. Metabolic alkalosis is bicarbonate (HCO3) accumulation due to Intracellular shift of hydrogen ion (H+as occurs in hypokalemia ) Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3 reabsorption, because HCO3 is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increa Continue reading >>

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  1. Ellie_Baum

    I've been debating about putting this up for a while. I don't want to create fear or confusion. I've been very grateful for the keto way of eating. The story below does not make me want to change back to a SAD diet. I can't believe the benefits I get from eating Keto.
    But at the same time, if it can happen to one person it can happen to more than one. And I love this community and want to protect it.
    On the Keto reddit (an internet forum like this) recently, there was a story about a guy on Keto who was supplementing with lite salt. A LOT of lite salt. Like 2 tsp in a 32oz of keto-friendly lemonade everyday. And then had another major dose of it in broth when he wasn't feeling well. Long story short, he ended up in the hospital with Hyperkalemia - dangerously high levels of potassium in the blood. He should have died, the levels he had.
    I know a lot of Newbies on here will be feeling bad and we in the community will recommend taking more electrolytes. While that is usually true, please be careful about recommending that as a miracle cure for any and every aliment. If someone has a weird symptom, if you're not a doctor, be careful about chiming in. I also think that everyone should be aware that there is an upper limit of appropriate amounts of potassium.
    Here is the reddit link:
    reddit.com
    86
    Morton Lite Salt and Potassium Supplementation: A Cautionary Tale • r/keto
    Edit: So this got pretty big, and I'm glad I've been able to make a positive impact for some people. But I want to make a brief clarification...

    KCKO, eat an avocado not 2 tsp of lite salt.

  2. Mare

    I didn't end up so badly, but a couple of weeks ago, I felt the 'need' for more potassium, so I used that LiteSalt regularly for a couple of days.

    I was due for labs soon after, and my endo mentioned my high potassium (it's usually right in range) and suggested I avoid 'potassium rich' foods for a while. I didn't mention the LiteSalt but quickly put it away in the cupboard when I got home.

  3. Ellie_Baum

    So glad you're ok!!

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