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Alcoholic Ketoacidosis Post Mortem

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What is DIABETIC KETOACIDOSIS? What does DIABETIC KETOACIDOSIS mean? DIABETIC KETOACIDOSIS meaning - DIABETIC KETOACIDOSIS definition - DIABETIC KETOACIDOSIS explanation. Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/... license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6Uu... Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases people may not realize they previously had diabetes. DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids. DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine. The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually potassium is also needed to prevent the development of low blood potassium. Throughout treatment blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. About 4% of people with type 1 diabetes in United Kingdom develop DKA a year, while in Malaysia the condition affects about 25% a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost universally fatal. The risk of death with adequate and timely treatment is currently around 1–4%. Up to 1% of children with DKA develop a complication known as cerebral edema. The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. Those who measure their glucose levels themselves may notice hyperglycemia (high blood sugar levels). In severe DKA, breathing becomes labored and of a deep, gasping character (a state referred to as "Kussmaul respiration"). The abdomen may be tender to the point that an acute abdomen may be suspected, such as acute pancreatitis, appendicitis or gastrointestinal perforation. Coffee ground vomiting (vomiting of altered blood) occurs in a minority of people; this tends to originate from erosion of the esophagus. In severe DKA, there may be confusion, lethargy, stupor or even coma (a marked decrease in the level of consciousness). On physical examination there is usually clinical evidence of dehydration, such as a dry mouth and decreased skin turgor. If the dehydration is profound enough to cause a decrease in the circulating blood volume, tachycardia (a fast heart rate) and low blood pressure may be observed. Often, a "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. If Kussmaul respiration is present, this is reflected in an increased respiratory rate.....

Alcoholic Ketoacidosis

Author: George Ansstas, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... In 1940, Dillon and colleagues first described alcoholic ketoacidosis (AKA) as a distinct syndrome. AKA is characterized by metabolic acidosis with an elevated anion gap, elevated serum ketone levels, and a normal or low glucose concentration. [ 1 , 2 ] Although AKA most commonly occurs in adults with alcoholism, it has been reported in less-experienced drinkers of all ages. Patients typically have a recent history of binge drinking, little or no food intake, and persistent vomiting. [ 3 , 4 , 5 ] A concomitant metabolic alkalosis is common, secondary to vomiting and volume depletion (see Workup). [ 6 ] Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are: An elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+) This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). The pathogenesis of AKA is complex. [ 7 ] Although the general physiological factors and mechanisms leading to AKA are understood, the precise factors have not Continue reading >>

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  1. 2high

    I've had ketones (anywhere between moderate and large) for the last two weeks, and have no idea how I can get rid of them. The drs have called them "starvation" ketones because they are due to not being able to eat properly, and have nothing to do with my bgls, but I'm still finding it extremely difficult to eat, so I cant get rid of them that way.
    I was wondering if anybody had any ideas on how to flush ketones from the system? Theyre a bit of a worry because I've had a couple of hypos, and am not feeling them at all while I have the ketones...
    Thanks lovelies,
    Kit

  2. JediSkipdogg

    If you aren't eating what your body needs to stabilize your weight, then you will always produce ketones. As your body breaks down fat for energy it creates a ketone as a byproduct. Therefore you CANNOT eliminate them without eating normal again.

  3. 2high

    JediSkipdogg said:

    If you aren't eating what your body needs to stabilize your weight, then you will always produce ketones. As your body breaks down fat for energy it creates a ketone as a byproduct. Therefore you CANNOT eliminate them without eating normal again.
    Boooo... thanks though.

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how to quit alcohol addiction in hindi alcoholic alcoholism withdrawal alcohol abuse stop drinking treatment :-In this video there are 6 tips which can help you in stop drinking alcohol. This video is in Hindi language. Quieting Alcohol addiction is not a simple task. But you can leave this habit using given home remedies.

Postmortem Diagnosis Of Alcoholic Ketoacidosis | Alcohol And Alcoholism | Oxford Academic

Aims: The aim of this article is to review the forensic literature covering the postmortem investigations that are associated with alcoholic ketoacidosis fatalities and report the results of our own analyses. Methods: Eight cases of suspected alcoholic ketoacidosis that had undergone medico-legal investigations in our facility from 2011 to 2013 were retrospectively selected. A series of laboratory parameters were measured in whole femoral blood, postmortem serum from femoral blood, urine and vitreous humor in order to obtain a more general overview on the biochemical and metabolic changes that occur during alcoholic ketoacidosis. Most of the tested parameters were chosen among those that had been described in clinical and forensic literature associated with alcoholic ketoacidosis and its complications. Results: Ketone bodies and carbohydrate-deficient transferrin levels were increased in all cases. Biochemical markers of generalized inflammation, volume depletion and undernourishment showed higher levels. Adaptive endocrine reactions involving insulin, glucagon, cortisol and triiodothyronine were also observed. Conclusions: Metabolic and biochemical disturbances characterizing alc Continue reading >>

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  1. milk

    Hello everyone,
    I am on week 2 day 5 of the ketogenic diet. I have been consuming high fat, moderate protein, and low carb. On average, my carbs have been 10-40g (the first few days around 30-40, and lately 10-20)
    I am 17 yo (about to be 18) female, and 5'5.5" with a start weight of 132lbs.
    Today I am about 129.5lbs, though my weight has been fluctuating.
    I thought I would have dropped water weight because of my low carbs, but I did not. I have been consuming 2-4L water a day on average.
    My average calories have been 1400-2300 calories, being closer to 2300 at the beginning and lessening towards this week when I was not seeing loss.
    I have not been doing any exercise, save walking up/down stairs in my house to do various things or walking around in the store for an hour or two.
    My problem now is that I checked my menstrual cycle calendar and saw that today is the day that I was supposed to end my period! I was very surprised. I am 6 days late. My last period was April 7-12. I usually have a 6-7 day period every 19 days.
    *EDIT
    (I forgot to mention I couldn't be pregnant because I am a virgin.)
    I was supposed to start May 1. A few days ago I began to have the feeling that it was coming, so hopefully it will be here within a few days.
    My question is, could my lack of weight loss be due to my period? And could my period's lateness be due to ketosis? I saw that when fat is metabolized, estrogen is lost, and low-estrogen can result in missed or late periods. If I am losing estrogen, does that mean it is coming from body fat, or could it also be from metabolized dietary fat (does dietary fat contain estrogen?i have no idea)? If it is from body fat, does that mean I have lost weight, even though it is not showing?
    When I get my period, should I expect weight loss soon (the week) after? I suspect that I may experience a "whoosh" because this is my first time doing low-carb intentionally, though it may not be my first time in ketosis, as I have fasted before because of my Christian Faith, though it has never affected my period. My period has been regular for the last 5-6 years. Once I had two periods in a month because of stress, but that has been the only irregularity.
    Sorry for the overload of questions haha. I'm just confused about what's going on right now.
    Thanks for your help and may GOD Bless you with His Lovingkindness and mercy, and with the Love of His Son Jesus Christ forever!

  2. kaylakala

    I actally at first had the very heavy period problem. My Doctor who is a 10 year lc dieter himself said it was normal with a diet change for it to mess up your period.
    I missed mine this month and I've never missed while on the pill. So, I'm assuming it can go both ways. I of course since I'm married. LOL a newlywed at that. Took a pregnancy test and It was negative.
    Good luck!!

  3. milk

    Thanks.
    I started my period later on the day I posted the OP. I can't tell yet if it's different than normal yet; usually it's heavy with cramping on the first day and slight cramps day 2. Yesterday I had cramps which was normal and today I didn't. I have a feeling it will be shorter than normal, but my TOM calendar calculator app says it will be longer than a week (whew) hope I'm right. sorry for slight grossness

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Seaghan Kearney collapses during a football match just like Muamba from Bolton Collapsing. His club had a defibrillator which saved his life. A C T is an awareness campaign being run by The Mater Heart Foundation. http://www.galvinfilms.com

Sudden Unexplained Death In Alcohol Misuse (sudam) Patients Have Different Characteristics To Those Who Died From Sudden Arrhythmic Death Syndrome (sads)

, Volume 13, Issue3 , pp 278283 | Cite as Sudden unexplained death in alcohol misuse (SUDAM) patients have different characteristics to those who died from sudden arrhythmic death syndrome (SADS) There is growing awareness of sudden unexplained death in alcohol misuse (SUDAM) in which there is no obvious cause of death, no evidence of acute alcohol toxicity or alcoholic ketoacidosis, and the heart is morphologically normal. This study describes the characteristics of a cohort with SUDAM from a tertiary cardiovascular referral center and compares the findings with those of individuals who died from sudden arrhythmic death syndrome (SADS). Cases in this retrospective cross-sectional study were identified from a database of referrals to our center spanning approximately 40 years. Cases with recorded heavy use of alcohol and non-alcohol users were selected, then limited to those with SUDAM or SADS aged 16 to 64 years. 62 cases of SUDAM and 41 cases of SADS were identified. The SUDAM group were older than the SADS group; mean age 35.8 years and 27.7 years respectively (P=0.0002). There was also a higher incidence of significant psychiatric illness in SUDAM (19.7%) than SADS (2.4%) case 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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