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Acetazolamide Induced Metabolic Acidosis

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Anion gap usmle - anion gap metabolic acidosis normal anion gap metabolic acidosis

Drug-induced Metabolic Acidosis

Go to: Introduction Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis 1. Humans possess homeostatic mechanisms that maintain acid-base balance ( Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO 2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis ( Figure 1). Drug-induced metabolic acidosis is often mild, but in rare cases it can be severe or even fatal. Not only should physicians be keenly aware of this potential iatrogenic complication but they should Continue reading >>

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  1. Johanna

    I have found various sources saying that ketones are acidic (pKa=20), and then relate it to the formation of the enolate ion. However, isn't an enolate ion of a ketone basic due to the oxygen's negative charge and all the pairs of electrons surrounding it?

  2. bon

    I think you need to recall the definition of an acid (in the Bronsted-Lowry scheme). An acid is a proton donor. A base is a proton acceptor. When a acid dissociates, it forms a hydrogen ion and the conjugate base of the acid. Remember, acid and base are only relative terms. The species which loses a proton in the reaction is acting as an acid and that which gains a proton is a base.
    In the example above, the ketone is acting as an acid because it donates a proton. The hydride anion is acting a base because it accepts a proton. The resulting enolate anion is stabilised by delocalisation of the negative charge onto the oxygen. In the reverse reaction, the enolate would act as a base, accepting a proton from hydrogen (this is unlikely to happen though because the hydrogen will be liberated as a gas).

  3. DraggyWolf

    It will shift the places of the double bond and one of the hydrogen atoms, which will end up in a compound with a double bond between two of the carbon atoms.
    That makes an enol which isn't as stable as a Ketone. The enol and Ketone are in a equilibrium which causes the enol to lose an hydrogen ion which then - the enol will become an enolate.

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Acetazolamide, Metabolic Acidosis, And Intraocular Pressure

In order to investigate whether or not there is a causal relationship between the metabolic acidosis and the ocular hypotension induced by acetazolamide, we undertook to correlate over a period of time the blood-acidifying and ocular-hypotonizing effects of administering the lowest intravenous effective dose of acetazolamide; to treat the metabolic acidosis induced by acetazolamide by means of the intravenous introduction of bases, and pulmonary hyperventilation (respiratory alkalosis); to evaluate the effects on the intraocular pressure (IOP) by neutralizing the acetazolamide-induced metabolic acidosis by means of a continuous infusion of sodium bicarbonate; to determine the relationship between the metabolic acidosis induced by blood-acidifying agents, which do not inhibit carbonic anhydrase, and the IOP; and to determine the changes in the acid-base status of the aqueous humor induced by acetazolamide and other blood-acidifying drugs. We found that the hypertonic buffering solution of sodium bicarbonate could reduce the IOP by itself through an osmotic mechanism. On the basis of our results, we believe that a causal relationship exists between the metabolic acidosis induced by Continue reading >>

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  1. Polly_ana85

    Is keto worth the effort or would I lose just as much restricting 800 calories? Keto would be 1000.
    What's better?

  2. Procaffeinating

    I've wondered the same thing. There seem to be a lot of people who swear by keto, so I'm thinking of giving it a try. Following this thread

  3. Polly_ana85

    Yeah I'm wanting to lose weight! I'm over eating at the moment and hover at 1200 cals but a weekend away I was averaging 3000 over three days...alchol and food
    So I need a change!! I'm thinking keto because restricting makes me bingy

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A lecture on the differential diagnosis of a normal anion gap metabolic acidosis, focusing on renal tubular acidosis, but also covering diarrhea, saline infusion, hyperkalemia, kidney failure, and ureteral diversion

Normal Anion Gap Metabolic Acidosis

Home | Critical Care Compendium | Normal Anion Gap Metabolic Acidosis Normal Anion Gap Metabolic Acidosis (NAGMA) HCO3 loss and replaced with Cl- -> anion gap normal if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis -> this could be considered a ‘relative hyperchloraemia’. Extras – RTA, ingestion of oral acidifying salts, recovery phase of DKA loss of bicarbonate with chloride replacement -> hyperchloraemic acidosis secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. some typical at risk clinical situations are: external drainage of pancreatic or biliary secretions (eg fistulas) this should be easily established by history normally 85% of filtered bicarbonate is reabsorbed in the proximal tubule and the remaining 15% is reabsorbed in the rest of the tubule in patients receiving acetazolamide (or other carbonic anhydrase inhibitors), proximal reabsorption of bicarbonate is decreased resulting in increased distal delivery and HCO3- appears in urine this results in a hyperchloraemic metabolic acidosis and is essentially a form of proximal renal tubular aci Continue reading >>

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  1. JoeBroganII

    I eat a decent amount of cheese daily. I try to stop myself after 3 sticks or slices for breakfast and dinner but I'm wondering if I just made this limit up in my brain at some point. Found this on an atkins forum: http://www.lowcarbsite.com/f10/967-why-limit-cheese.html saying limit to 4oz, and that dairy will be burned before body fat. Anyone confirm/deny/add thoughts?

  2. Junkbot

    If you can handle dairy, and you eat only when hungry and stop when you are full, you cannot have too much cheese.

  3. damnzel

    I have heard a lot of people being able to break through plateaus by dropping dairy, but maybe they just incidentally lowered their total calories in doing so.

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