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Can Metabolic Acidosis Be Caused By Seizures?

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

Topiramate In Monotherapy Or In Combination As A Cause Of Metabolic Acidosis In Adults With Epilepsy

159www.neurologia.com Rev Neurol 2015; 60 (4): 159-163 Topiramate has been widely used for the treatment of focal and generalized epilepsy since it received FDA approval in 1993. Its broad anticonvulsant properties rely on multiple inhibitory mechanisms, which include voltage-activated sodium channels, L-type high-voltage-activated calcium channels and kainate-evoked currents. In addition to aecting membrane currents, TPM also inhibits isoenzymes I-VI of carbonic anhydrase (CA), which are present in neurons and nephrons [1]. is results in a pre- disposition to metabolic acidosis that has been widely described in children due to its deleterious eect on the acid-base balance and its associated symptoms such as nausea, headache, diarrhea, hy- perventilation, and hypercalciuria, which may lead Because metabolic acidosis may have adverse clinical consequences, even in its milder forms, we performed this prospective cross-sectional study to assess the severity and prevalence of metabolic aci- dosis in adults taking topiramate and to attempt to dene some factors that determine its presence, specically if acidosis is signicantly associated with drug dose, concomitant drug regimen or with Continue reading >>

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  1. manohman

    Why can't fat be converted into Glucose?

    So the reason cited is that beta oxidation/metabolism of fats leads to formation of acetyl coa, a 2 carbon molecule, and that because of that it cannot be converted back into glucose.
    Why exactly is that the case?
    If Glucogenic amino acids can be converted into citric acid cycle intermediates and then turn back into glucose via gluconeogensis, then why cant Fatty Acids which yield Acetyl Coa. Can't you just have Acetyl Coa enter the citric acid cycle and produce the same intermediates that the glucogenic amino acids creat?

  2. Czarcasm

    manohman said: ↑
    So the reason cited is that beta oxidation/metabolism of fats leads to formation of acetyl coa, a 2 carbon molecule, and that because of that it cannot be converted back into glucose.
    Why exactly is that the case?
    If Glucogenic amino acids can be converted into citric acid cycle intermediates and then turn back into glucose via gluconeogensis, then why cant Fatty Acids which yield Acetyl Coa. Can't you just have Acetyl Coa enter the citric acid cycle and produce the same intermediates that the glucogenic amino acids creat?
    Click to expand... Both glucose and fatty acids can be stored in the body as either glycogen for glucose (stored mainly in the liver or skeletal cells) or for FA's, as triacylglycerides (stored in adipose cells). We cannot store excess protein. It's either used to make other proteins, or flushed out of the body if in excess; that's generally the case but we try to make use of some of that energy instead of throwing it all away.
    When a person is deprived of nutrition for a period of time and glycogen stores are depleted, the body will immediately seek out alternative energy sources. Fats (stored for use) are the first priority over protein (which requires the breakdown of tissues such as muscle). We can mobilize these FA's to the liver and convert them to Acetyl-CoA to be used in the TCA cycle and generate much needed energy. On the contrary, when a person eats in excess (a fatty meal high in protein), it's more efficient to store fatty acids as TAG's over glycogen simply because glycogen is extremely hydrophilic and attracts excess water weight; fatty acids are largely stored anhydrously and so you essentially get more bang for your buck. This is evolutionary significant and why birds are able to stay light weight but fly for periods at a time, or why bears are able to hibernate for months at a time. Proteins on the other hand may be used anabolically to build up active tissues (such as when your working out those muscles), unless you live a sedentary lifestyle (less anabolism and therefore, less use of the proteins). As part of the excretion process, protein must be broken down to urea to avoid toxic ammonia and in doing so, the Liver can extract some of that usable energy for storage as glycogen.
    Also, it is worth noting that it is indeed possible to convert FA's to glucose but the pathway can be a little complex and so in terms of energy storage, is not very efficient. The process involves converting Acetyl-CoA to Acetone (transported out of mitochondria to cytosol) where it's converted to Pyruvate which can then be used in the Gluconeogenesis pathway to make Glucose and eventually stored as Glycogen. Have a look for yourself if your interested: http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1002116.g003/originalimage (and this excludes the whole glycogenesis pathway, which hasn't even begun yet).
    TLDR: it's because proteins have no ability to be stored in the body, but we can convert them to glycogen for storage during the breakdown process for excretion. Also, in terms of energy, it's a more efficient process than converting FA's to glycogen for storage.

  3. soccerman93

    This is where biochem comes in handy. Czarcasm gives a really good in depth answer, but a simpler approach is to count carbons. The first step of gluconeogenesis(formation of glucose) requires pyruvate, a 3 carbon molecule. Acetyl Co-A is a 2 carbon molecule, and most animals lack the enzymes (malate synthase and isocitrate lyase) required to convert acetyl co-A into a 3 carbon molecule suitable for the gluconeogenesis pathway. The ketogenic pathway is not efficient, as czarcasm pointed out. While acetyl co-A can indeed be used to form citric acid intermediates, these intermediates will be used in forming ATP, not glucose. Fatty acid oxidation does not yield suitable amounts of pyruvate, which is required for gluconeogenesis. This is part of why losing weight is fairly difficult for those that are overweight, we can't efficiently directly convert fat to glucose, which we need a fairly constant supply of. Sorry, that got a little long-winded

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What is BASAL METABOLIC RATE? What does BASAL METABOLIC RATE mean? BASAL METABOLIC RATE meaning - BASAL METABOLIC RATE definition - BASAL METABOLIC RATE explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. Basal metabolic rate (BMR) is the minimal rate of energy expenditure per unit time by endothermic animals at rest. It is reported in energy units per unit time ranging from watt (joule/second) to ml O2/min or joule per hour per kg body mass J/(hkg)). Proper measurement requires a strict set of criteria be met. These criteria include being in a physically and psychologically undisturbed state, in a thermally neutral environment, while in the post-absorptive state (i.e., not actively digesting food). In bradymetabolic animals, such as fish and reptiles, the equivalent term standard metabolic rate (SMR) is used. It follows the same criteria as BMR, but requires the documentation of the temperature at which the metabolic rate was measured. This makes BMR a variant of standard metabolic rate measurement that excludes the temperature data, a practice that has led to problems in defining "standard" rates of metabolism for many mammals. Metabolism comprises the processes that the body needs to function. Basal metabolic rate is the amount of energy expressed in calories that a person needs to keep the body functioning at rest. Some of those processes are breathing, blood circulation, controlling body temperature, cell growth, brain and nerve function, and contraction of muscles. Basal metabolic rate (BMR) affects the rate that a person burns calories and ultimately whether that individual maintains, gains, or loses weight. The basal metabolic rate accounts for about 60 to 75% of the daily calorie expenditure by individuals. It is influenced by several factors. BMR typically declines by 12% per decade after age 20, mostly due to loss of fat-free mass, although the variability between individuals is high. The body's generation of heat is known as thermogenesis and it can be measured to determine the amount of energy expended. BMR generally decreases with age and with the decrease in lean body mass (as may happen with aging). Increasing muscle mass has the effect of increasing BMR. Aerobic (resistance) fitness level, a product of cardiovascular exercise, while previously thought to have effect on BMR, has been shown in the 1990s not to correlate with BMR when adjusted for fat-free body mass. But anaerobic exercise does increase resting energy consumption (see "aerobic vs. anaerobic exercise"). Illness, previously consumed food and beverages, environmental temperature, and stress levels can affect one's overall energy expenditure as well as one's BMR. BMR is measured under very restrictive circumstances when a person is awake. An accurate BMR measurement requires that the person's sympathetic nervous system not be stimulated, a condition which requires complete rest. A more common measurement, which uses less strict criteria, is resting metabolic rate (RMR).

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as sev Continue reading >>

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  1. Vita oldie

    I have been puzzling over this for some time.
    I read or understood after reading, that it is better to test at night (diabetics are a different case as they need to check for medical reasons but may be interested.)
    Most people seem to test in the morning and also people have suggested cutting the sticks in half as they are a little pricy! This being the case then when to use them is important.
    To me testing in the morning after no food overnight seems strange as the ketosis reading will be different to that at the end of the day-when food has been eaten!
    The evening reading will be a warning that you've over done it or "joy of joys" you are on plan!
    THE DAWN INSULIN SURGE is something every has as it the bodies way of preparing us for waking and rising.
    Insulin makes the cells use energy but what we want is to have the body use an alternative-our body fat and not our muscle mass!
    This MUST have an effect on Ketosis and for those only just in Ketosis the reading could be disappointing because the insulin has caused a shift in the readings.
    This is a second reason why evening is perhaps the answer.
    I don't know if this is correct but perhaps someone with an understanding of chemistry could tell me if my reasoning is correct or if not, then why not!
    I have too much time on my hands and I want the correct answer!

  2. Vita oldie

    Showing my age!
    Could't find this on the site so assumed I hadn't posted it properly now it is down twice!!!

  3. svenskamae

    Are you talking about the pricey strips that use blood to test for nutritional ketosis, rather than the urine ketostix? The Phinney and Volek book says that readings for ketosis level are lowest in the morning, so if you were "in ketosis" (reading 0.5 or higher) then, you would presumably be so throughout the day, unless you ate enough carbs to throw you out of ketosis. (Presumably your early morning ketosis reading is reflecting more or less how your body processed what you ate the preceding day). But I think you could pick any time that was convenient for you, so long as you always tested at that time of day. Hope this helps.

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Watch more Epilepsy & Seizure Disorders videos: http://www.howcast.com/videos/502007-... Patty McGoldrick NP, MPA: So absence or petit mal seizures as they used to be called are a form of generalized seizures. So again, the whole brain lights up with electricity all at once. They often present in childhood, usually around six to eight years old, maybe a little older, but we've had kids as young as three or four presenting with it. So they look like a sort of eye roll or an eye deviation and a staring spell. Steve Wolf MD: I'll act it for you. So they could be talking to you, and suddenly they'll. . . [pause]. . .What did you say? Patty: Right. And it's more than just your child not paying attention to you. And this goes on repeatedly, and then you realize after a while that they're sort of missing things. And they occur in all situations. They occur watching TV, watching movies. They occur during a conversation. So you have to really weed out and say to the parents when they come in, "Does this only happen when they're watching TV? Or does it only happen in school when the lesson is something they don't understand?" Steve: And there short. They're like three to five seconds sometimes. It can be very easy to miss them. Sometimes the teachers pick them up. But you know, it's hard to differentiate from daydreaming. How do you do that? Patty: Well that's when you bring them in and you do an EEG, because it has a very distinct pattern on the EEG. Steve: But the most important part on the EEG is if you don't capture the episode of the staring spells, then you haven't made the diagnosis. Patty: So on the EEG, there is a pattern that's called 3-hertz spike and wave, and if you look at the EEG you see this big burst of electricity that lasts for a few seconds, and it's across the whole EEG. The problem is that if you do a short EEG for 30 or 40 minutes, you may not get one of these events, and you may not see the abnormality. Because the EEG otherwise is perfectly normal. Steve: But we tell families that this is like one of the better epilepsies, because it has the highest chance of outgrowing it. But if you don't treat it, it really can affect things academically. You worry about kids walking down the block, not you know walking into the street because they'll zone out, falling down the stairs if they zone out. So it's important to treat. Patty: It is important to treat, and it's very important to treat as the kids get older and they're taking subways or buses alone, or they're driving cars, because you don't want them to have an absence seizure or a staring spell in the middle of that. So again, absence seizures are a form of generalized seizures. The electricity lights up in the whole brain all at once. They're short. They can happen many times a day. They may not happen every hour, so they may not be captured on a short EEG. They're very treatable, and it's very important to treat them so a, the child doesn't get hurt, and b, that the child is not missing information in school and doing poorly academically.

Severe Diabetic Ketoacidosis Complicated By Hypocapnic Seizure

Summary In clinical practice, seizures independent of hypoglycemia are observed in patients with type 1 diabetes mellitus (T1DM) more frequently than expected by chance, suggesting a link. However, seizures during management of diabetic ketoacidosis (DKA) have generally been considered a bad prognostic factor, and usually associated with well-known biochemical or neurological complications. We present the case of a 17-year-old girl with known T1DM managed for severe DKA complicated by hypocapnic seizure. We review the literature on this rare occurrence as well as outline other possible differentials to consider when faced with the alarming combination of DKA and seizure. Learning points: Seizures during DKA treatment require immediate management as well as evaluation to determine their underlying cause. Their etiology is varied, but a lowered seizure threshold, electrolyte disturbances and serious neurological complications of DKA such as cerebral edema must all be considered. Sudden severe hypocapnia may represent a rare contributor to seizure during the treatment of DKA. Background Diabetic ketoacidosis (DKA) is an endocrine emergency occurring in patients with both new-onset and Continue reading >>

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  1. gear2d

    Could anyone explain how this occurs? From my understanding high glucose levels draws K+ out of cells (HypERkalemia), low insulin promotes less shift of K+ in to cells (HypERkalemia), and acidosis causes K+ to shift out of cells (hypERkalemia)....so how does DKA cause hyPOkalemia? From my understanding DK:
    High glucose (hypertonicity which cause the shift of K+ to ECF),
    Low insulin
    Low pH

  2. blade

    USMLE Forums Guru

    Quote:

    Originally Posted by gear2d
    Could anyone explain how this occurs? From my understanding high glucose levels draws K+ out of cells (HypERkalemia), low insulin promotes less shift of K+ in to cells (HypERkalemia), and acidosis causes K+ to shift out of cells (hypERkalemia)....so how does DKA cause hyPOkalemia? From my understanding DK:
    High glucose (hypertonicity which cause the shift of K+ to ECF),
    Low insulin
    Low pH Hypokalemia in DKA???which book is that pls?your analysis above is correct but
    In DKA=hyperkalemia but with low intracellular K+ hence in treatment of DKA,you treat as if hypokalemia to restore the intracellular loss

  3. gear2d

    Quote:

    Originally Posted by blade
    Hypokalemia in DKA???which book is that pls?your analysis above is correct but
    In DKA=hyperkalemia but with low intracellular K+ hence in treatment of DKA,you treat as if hypokalemia to restore the intracellular loss This is from Step to Med 3rd ed on page312 in the flow diagram.

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