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Hyperchloremic Metabolic Acidosis Pathophysiology

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The Pathophysiology Of Hyperchloremic Metabolic Acidosis After Urinary Diversion Through Intestinal Segments.

The pathophysiology of hyperchloremic metabolic acidosis after urinary diversion through intestinal segments. The pathophysiology of hyperchloremic metabolic acidosis after urinary diversion through intestinal segments has not been defined. This study employs a caninemodel in which an ileal segment is interposed between one kidney and the urinary bladder. Comparison of urinary solute excretion rates between the normal andinterposed renal units allows quantitation of solute reabsorption and secretionby the ileal segment. Ileal segments reabsorb urinary chloride, potassium, andammonium. Ammonium is reabsorbed in part as its conjugate free base, ammonia,with the liberated hydrogen ion reabsorbed with chloride or excreted astitratable acid. Inability to excrete acid as ammonium results in depletion ofbody buffers and a diminished capacity to compensate an additional acidchallenge. Bicarbonate is secreted by the ileal segments but not in amounts that are physiologically significant. Impaired renal function predisposes to thedevelopment of this syndrome but is not a primary pathophysiologic mechanism. Continue reading >>

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  1. datums

    Unfortunately, biochemistry is not the kind of topic that can be easily researched online without formal training. There are a number of points you make that are incorrect. I keto myself, so don't think I am trying to attack your general position here.
    Starvation and the keto diet are actually nearly identical from a biochemical perspective. The key pathway is fat mobilization, where fatty acid chains are broken down two carbons at a time to produce energy. When this process starts to happen faster than your body can manage it, some of the chemical constituents of the process actually break down to become the ketones that can be detected in the urine and breath. In other words, ketones are a side effect, rather than a major player.
    The idea that a calorie deficit, ie starvation, is somehow bad, is incorrect. Anybody who is using diet and exercise to become more lean is doing the same thing. There is no magic method to lose weight without some form of starvation. The reason why the keto diet does not cause significant lean tissue loss is that the starvation involved is not sufficiently severe.
    An important point that you bring up is the idea that the keto diet stabilizes insulin levels. This is basically correct. Insulin signals cells to take up glucose from the blood, and also tells the liver to begin glycogenesis - the process of packing glucose into glycogen. High blood sugar triggers this. These effects are basically reversed by adrenaline, which tells the liver to start breaking glycogen down to make glucose.
    Part of the difficulty with this is that with a normal diet, blood sugar spikes after meals. This leads to cyclic variance in levels of glucose, insulin and adrenaline. As the cycle progresses toward the adrenaline end, you start to get cravings for foods that will once again spike your blood glucose.
    However, when you are relying on fat mobilization to make glucose, these spikes are greatly reduced. Fat mobilization is not efficient, and is not able to provide sudden bursts of glucose. It is more constant. This makes athletic activity much more difficult aswell.
    But this is the real reason why the keto diet works - it mitigates the cycle of spiking and lowering blood sugar, providing a more level and constant supply. This reduces the propensity for craving food.
    In essence, the keto diet is not unique in terms of the basic biochemistry of metabolism. It simply makes 'starvation' more tolerable, and easier to manage. For many of us, that is exactly what we need.
    Edit - swapped 'gluconeogenesis' with 'glycogenesis'.

  2. gogge

    Insulin signals cells to take up glucose from the blood, and also tells the liver to begin gluconeogenesis - the process of packing glucose into glycogen. High blood sugar triggers this. These effects are basically reversed by adrenaline, which tells the liver to start breaking glycogen down to make glucose.
    Insulin inhibits gluconeogenesis (creation of new glucose), you probably meant glycogenesis (conversion of glucose to glycogen)?

  3. datums

    You are right on that one. The word I was looking for was glycogenesis. It can be a little tricky to remember that between glycolysis, glucogenesis, and gluconeogenesis, one means glycogen synthesis, and the other two mean glycogen breakdown.

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Hyperchloremia Why And How - Sciencedirect

Volume 36, Issue 4 , JulyAugust 2016, Pages 347-353 Hyperchloremia Why and howHipercloremia: por qu y cmo Author links open overlay panel Glenn T.Nagami Open Access funded by Sociedad Espaola de Nefrologa Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance. La hipercloremia es una alteracin electroltica frecuente que se asocia a una serie de distintos trastornos clnicos. El rin desempea una funcin importante en la regulacin de la concentracin de cloruro a travs de diversos transportadores que se encuentran a lo largo de la nefrona. Sin Continue reading >>

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  1. DustinX

    Fasting to get into ketosis... faster?

    The other day I remembered that when I was young I had to get a physical. Well to keep the story short, I hadn't eaten much the day before and didn't eat breakfast before I went. After he looked at the urine results I remember him asking if I ate breakfast, he said he asked because I had alot of ketones in my urine.
    I was thinking, would it be possible to do a 24 hour fast to enter ketosis and then the next day continue a keto diet (I'm saying for when you're first starting a keto diet). Maybe 12 hours of fasting would get you into ketosis? I'm not sure, but I figured this could be a quick way to get into ketosis without having to wait 3 or even 4 days when you first begin.

  2. Eileen

    If you are young and active, then you'll get into ketosis quickly. Someone who is older or less active will take longer the first time.
    Fasting will get out into ketosis, but so will eating high fat meals. Don't know about you, but I get very crabby if I miss my breakfast.

  3. jg_girl088

    yeah it sure will. I remember reading in Good Calories Bad Calories that the original recommendation for the ketogenic diet was to start with a 48 hour fast, however, atkins was the one who changed it to a 2 week induction period of minimal carbs.

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Whether due to bicarbonate loss or volume repletion with normal saline, the primary problems is in hyperchloremic metabolic acidosis hcl ammonium chloride loading, reabsorption proximal tubule reduced, part, because of hyperchloraemic acidosis, anion gap (in most cases). Administration of ns will decrease the plasma sid causing an acidosis this patient also had a normal anion gap hyperchloremic metabolic (hcma). Googleusercontent search. Normal anion gap (hyperchloremic) acidosis semantic scholar. Hyperchloremic metabolic acidosis is it clinically relevant? (pdf hyperchloremic in diabetes mellitus. Hyperchloremic acidosis wikipedia. Treatment of acute non anion gap metabolic acidosis ncbi nih. Aug 4, 2016 a normal ag acidosis is characterized by lowered bicarbonate concentration, which counterbalanced an equivalent increase in plasma chloride concentration. Acid base physiology 8. Hyperchloraemic metabolic acidosisdepartment of medicine. Mechanism of hyperchloremic metabolic acidosis. Hyperchloremic acidosis background, etiology, patient education emedicine. Respiratory acidosis alkalosis as with the hyperchloremic may result from chloride replacing lost bicarbonate. Although it ca

Hyperchloremic Acidosis

Normal human physiological pH is 7.35 to 7.45. A decrease in pH below this range is acidosis, an increase in this range is alkalosis. Hyperchloremic acidosis is a metabolic disease state disease state where acidosis (pH less than 7.35) with an ionic chloride increase develops.Understanding the physiological pH buffering process is important. The primary pH buffer system in the human body is the HCO3 (Bicarbonate)/CO2 (carbon dioxide) chemical equilibrium system. Where: HCO3 functions as an alkalotic substance.CO2 functions as an acidic substance. Therefore, increases in HCO3 or decreases in CO2 will make blood more alkalotic. The opposite is also true where decreases in HCO3 or an increase in CO2 will make blood more acidic. CO2 levels are physiologically regulated by the pulmonary system through respiration, whereas the HCO3 levels are regulated through the renal system with reabsorption rates. Therefore, hyperchloremic metabolic acidosis is a decrease in HCO3 levels in the blood. Anytime a metabolic acidosis is suspected, it is extremely useful to calculate the anion gap. This is defined as: Where Nais plasma sodium concentration, HCO3 is plasma bicarbonate concentration, and Cl Continue reading >>

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  1. INDYENNE

    Hi,
    I got these quotes for you:
    Robert C. Atkins :
    "Here's the problem with all alcoholic beverages, and the reason I recommend refraining from alcohol consumption on the diet. Alcohol, whenever taken in, is the first fuel to burn. While that's going on, your body will not burn fat. This does not stop the weight loss, it simply postpones it, since the alcohol does not store as glycogen, you immediately go back into ketosis/lipolysis after the alcohol is used up.
    If you must drink alcohol, wine is an acceptable addition to levels beyond the Induction diet. If wine does not suit your taste, straight liquor such as scotch, rye, vodka, and gin would be appropriate, as long as the mixer is sugarless; this means no juice, tonic water; or non-diet soda. Seltzer and diet soda are appropriate."
    Drs. Michael R. and Mary Dan Eades (Protein Power)
    "Can I drink alcohol on the Protein Power Plan?"
    "Yes, you can! But, like with everything else, you are limited by your Carbohydrate Maximum. Dry white or red wine (3 oz.) or Miller Lite beer (12 oz.) will cost you 3 or 4 effective carb grams, but are still reasonable choices as long as you count them in your daily totals. Hard liquor will cost you a lot of empty calories. Take it easy and count those carbs! Wine-in moderation-can even help improve insulin sensitivity."
    Ray Audette –– Author of "NeanderThin":
    "Don't Drink Alcohol"
    "It is best not to consume alcohol in any amount from any source. Alcohol is a by-product of yeast digestion (the yeast equivalent of urine) and is known to damage the stomach, kidneys, and liver. Alcohol adds fat principally by producing cravings for both itself and other carbohydrates (see snack trays at any bar) and even other addictive substances (ask any former smoker.) It is almost impossible to drink alcohol and follow the hunter-gatherer lifestyle. If you must drink, do so only on special occasions (once or twice a year) and stick to alcohols derived from fruit (wine and champagne.) Be aware, however, that once you have been on the NeanderThin program for any length of time, drinking any form of alcohol could make you queasy. It is best to avoid alcohol altogether."
    You're worth so much more

    Pounds lost: 25.0



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  2. LAA06C

    I was wondering if a small glass of red wine would stop ketosis. Red wine generally only has 1 or 2 carbs and no fat or sugar. I guess its too late cuz i am already sipping on one. :( I gave in i'm weak. Has anyone else slipped up and done this? and did it stop or ruin the ketosis?

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