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Lactic Acidosis Cirrhosis

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Click The Link Below For Instant Access: http://x.vu/hearingcorrectreview Sensorineural Hearing Loss - sensorineural hearing loss - improve your hearing naturally Hearing correct system talks in detail about a product, how it can help treat cases of hearing loss, and the benefits of using it. Do you have problem with your ears? Do you encounter problems engaging in a normal conversation with your friends and family members or you have to rely on hearing aids or sign languages for you to be able to communicate effectively? Good quality hearing aids and the use of sign language work well but they are tedious. Hearing correct system is what you need to have a very sound conversation unlike the use of hearing aid and sign languages which are hard to use and do not cure hearing loss totally, whether it presents in youth or in adulthood. However, this does not mean all is lost. Hearing correct system is a revolutionary wellness system which has helped millions to treat hearing loss in a chemical free way. Hearing correct system is effective and can help you to reverse hearing loss if it is used as directed. One major problem that people who are trying to back ward the effects of age, inf

Coxpd9 An Evolving Multisystem Disease; Congenital Lactic Acidosis, Sensorineural Hearing Loss, Hypertrophic Cardiomyopathy, Cirrhosis And Interstitial Nephritis

COXPD9 an Evolving Multisystem Disease; Congenital Lactic Acidosis, Sensorineural Hearing Loss, Hypertrophic Cardiomyopathy, Cirrhosis and Interstitial Nephritis Part of the JIMD Reports book series (JIMD, volume 34) We present the second report of combined oxidative phosphorylation deficiency-9. The infant presented in the neonatal period with poor feeding, lactic acidosis and sensorineural hearing loss. He subsequently developed a lethal hypertrophic cardiomyopathy during infancy. Cirrhosis and interstitial nephritis were identified at autopsy. Exome sequencing has detected compound heterozygous mutations in the MRPL3 gene which encodes a large mitochondrial ribosome subunit protein. We identified a known heterozygous variant NM_007208 c.950>G (Pro317Arg) in the MRPL3 gene and a novel heterozygous mutation NM_007208 c.49delC p.(Arg17Aspfs*57). Mutations in MRPL3 have previously been shown to alter ribosome assembly and cause abnormal function of multiple respiratory chain complexes. Our case adds to the evolving knowledge of disorders of mitochondrial translation. This is a preview of subscription content, log in to check access. David Coman, Carolyn Bursle, Anna Narendra, Raymo Continue reading >>

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  1. Laurie R Zawiskie, RHIT

    Has anyone tried to code DKA in a patient with DM 2? The 3M encoder takes you to the code for secondary/other diabetes and then when you try to code other diabetic manifestations you get an excludes 1 notes saying they can't be coded with other diabetes. My code book is a 2014 draft, so I don't know if this has been corrected in the 2015 version, but there is not an entry for DM 2 with DKA. I think the 3M encoder is wrong to code it as secondary/other diabetes, but I can't find another way to code it.

  2. Lynn M Farnung

    Laurie,
    There is a Coding Clinic that addresses the type of DM with DKA. I have pasted it below.
    Diabetes mellitus with diabetic ketoacidosis
    Coding Clinic, First Quarter 2013 Page: 26-27 Effective with discharges: March 27, 2013
    Related Information
    Question:
    What is the correct code assignment for type 2 diabetes mellitus with diabetic ketoacidosis?
    Answer:
    Assign code E13.10, Other specified diabetes mellitus with ketoacidosis without coma, for a patient with type 2 diabetes with ketoacidosis. Given the less than perfect limited choices, it was felt that it would be clinically important to identify the fact that the patient has ketoacidosis. The National Center for Health Statistics (NCHS), who has oversight for volumes I and II of ICD-10-CM, has agreed to consider a future ICD-10-CM Coordination and Maintenance Committee meeting proposal.
    © Copyright 1984-2015, American Hospital Association ("AHA"), Chicago, Illinois. Reproduced with permission. No portion of this publication may be copied without the express, written consent of AHA. ------------------------------
    Lynn Farnung
    Inpatient/Outpatient coder, AHIMA Approved ICD-10 Trainer
    Original Message

  3. Laurie R Zawiskie, RHIT

    Thanks, Lynn. If a patient also has DM 2 w/nephropathy (E11.21), I guess we will have to ignore the Excludes 1 note that says E13.10 can't be coded with Type 2 DM (E11.-).
    ------------------------------
    Laurie Zawiskie
    Coder III
    Original Message

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Bala Venkatesh (University of Queensland, Australia) busting lactate myths at #SGANZICS on 22 April 2017. Mark your calendar for SGANZICS 17-21 May 2018!

Prognosis Of Alcohol-associated Lactic Acidosis In Critically Ill Patients: An 8-year Study

Prognosis of alcohol-associated lactic acidosis in critically ill patients: an 8-year study Scientific Reports volume 6, Articlenumber:35368 (2016) Lactic acidosis is common in critical care; by contrast, a subtype called alcohol-associated lactic acidosis (AALA) is rarely encountered. The primary purpose of this study was to determine the prognosis of AALA in critically ill patients and the second aim was to determine whether the survival was associated to the peak blood lactate concentration. An 8-year retrospective analysis of adult patients admitted to the intensive care unit (ICU) with AALA between January 2007 and December 2014 was considered in a tertiary care hospital. In total, 23 patients were analyzed and the median peak blood lactate level was 15.9 mmol/L. Only 2 patients (8.7%) presented peak blood lactate levels <10 mmol/L. In this study, 21 patients survived from ICU and hospital, the mortality rate was 8.7%. The result indicted the survival of AALA was not associated with peak blood lactate concentration although survivors still had a better lactate clearance rate per hour than non-survivors. Moreover, AALA patients with coexisting sepsis presenting higher lactate Continue reading >>

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  1. Man2kx

    Read: Achieve Ketosis in under 24 hours.

    Purpose
    I've been seeing an abundance of posts about people concerned in getting into Ketosis as quick as they possibly can. While some individuals prefer not to spend their glycogen stores early and to gradually roll through the week, other's want the snippy snappy get into Keto to start burning fat. People talk about adjusting ratios, eatings loads of fat, or just being plain lucky. Well thats not the case!
    What will get you into Keto is eating normally what you would eat in Keto phase, and plain EXCERCISE! Not a suprise, excercise will burn up your glycogen, depleted glycogen stores = Ketosis time! In order to successfully get into Ketosis in under 24 hours, you need to do a good deal of excercise! It's not extremely difficult to do, and the following has always worked for me:
    1. Resistance Training
    About 35-45min resistance training (weights), (my recommendation is) with 8-10 reps, minimum of 20 sets total and 6 different excercises (4 sets per excercise). This resistance training should not be a walk in the park, nor should it be something extremely difficult, just leave it intense, I usually aim for 8 reps, but if you can do more than 10 then you should up the weight. Or of course, you can do your own regiment of weight lifting. This should be performed before cardio.
    2. Cardio
    You want a good 25min+ cardio session after your resistance training to burn up some more glycogen. Jogging/running is fine, eliptical is fine, but I'd personally recommend the stationary bike as you'd get a minor leg workout and you'd burn up some glycogen there. Choose med-high intensity, but the workout shouldn't be to the point where you barely could do it and you're struggling, just intense enough to feel your legs a little bit .
    Note: I choose high intensity on stationary bike because I work out my legs on the last day of Keto, rather than doing a full body workout. It's practically a full-body workout in it's sense, it's a great deal of your body, so I usually find excellent results with doing legs rather than a full body.
    If it didn't work out for you...
    You need to re-evaluate your diet as something is messed up and you need to look closely at possible culprits: too many carbs, perhaps the artifical sweetners or that diet soda. If it is nothing in your diet, re-evaluate the intensity of your workout.
    I will put this in my article along with other information in a few weeks. I felt it was an important topic to cover as it was a frequently asked question.
    Here's my article, it will most likely cover any of your lingering questions!
    http://forum.bodybuilding.com/showthread.php?t=639169
    Good luck with your diet and keep on Keto-ing .

  2. stinglikebee

    well ive been having between 4-5 diet sodas a day ,do you think thats why im not in ketosis,should i drink a lot of water??also when using the ketostix...do i just pass it through my stream of urine or do i pee on it till my bladder is empty?

  3. Man2kx

    Originally Posted by stinglikebee
    well ive been having between 4-5 diet sodas a day ,do you think thats why im not in ketosis,should i drink a lot of water??also when using the ketostix...do i just pass it through my stream of urine or do i pee on it till my bladder is empty?

    Try ditching the diet sodas until you get into Keto. As far as the Ketosix go, you only need to pass it through the stream of urine, and you are looking for any tint of pink, it's not necessary to have dark purple.
    Check #2 out in my sig, I'm sure it would answer your questions.

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VISIT: http://livercirrhosis.vital101.com How To Cure Liver Cirrhosis Naturally - Liver Cirrhosis Natural Treatment - Liver Cirrhosis Diet What is cirrhosis of the liver? Cirrhosis is a condition that results from permanent damage or scarring of the liver. This leads to a blockage of blood flow through the liver and prevents normal metabolic and regulatory processes. What are the major causes of cirrhosis? The major causes of cirrhosis are as follows: - Chronic alcoholism. - Viral infections caused by chronic viral hepatitis (types B, C and D). - Metabolic diseases such as alpha-1-antitrypsin deficiency, galactosemia and glycogen storage disorders. - inherited diseases such as Wilson disease and hemochromatosis. - Biliary cirrhosis resulting from diseases such as primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). - Toxic hepatitis caused by severe reactions to prescribed drugs or prolonged exposure to environmental toxins. - repeated bouts of heart failure with liver congestion. What are some early symptoms of cirrhosis? People in the early stages of cirrhosis have few symptoms. Some symptoms an individual may notice include: - Loss Of Appetite. - Nausea. -

Lactic Acidosis In Patients With Hepatitis C Virus Related Cirrhosis And Combined Ribavirin/sofosbuvir Treatment

Background/aims: Sofosbuvir (SOF) based interferon-alfa free antiviral therapy has become the treatment of choice for patients with chronic hepatitis C virus (HCV) infection. Little is known about safety of drug combinations using two nucleos(t)ide polymerase inhibitors in patients with HCV associated advanced cirrhosis. Here, we report frequent occurrence of lactic acidosis associated with acute-on-chronic hepatic decompensation during ribavirin (RBV) plus SOF based antiviral therapy.Methods: 35 patients with chronic hepatitis C and advanced fibrosis, compensated cirrhosis, and decompensated cirrhosis before and after liver transplantation were treated with SOF based antiviral therapy with and without RBV. Adverse events including lactic acidosis (pH < 7.35, lactate > 20 mg/dL) were recorded 24 weeks before and during (meanSD, 1811 weeks) antiviral therapy. Efficacy was determined by assessment of serum HCV RNA.Results: We observed severe adverse events in 15/35 (43%) patients before (24 weeks) and in 12/35 (34%) patients during antiviral therapy, the majority in association with acute-on-chronic hepatic decompensation. Lactic acidosis occurred in 5/35 (14%) patients during thera Continue reading >>

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  1. parkscs

    Just my opinion, but worrying about "optimal ketosis" and pricking your finger all the time is just wasting your time and money. Ketostix are even more of a waste of your resources. In terms of body composition and performance, I'm not sure what you stand to gain from having a particular blood ketone level. Ketogenic diets are useful to create a caloric deficit because they're particularly satiating and there are some adaptations where your body learns to more easily rely on fat to fuel certain forms of exercise... but beyond that, I'm not aware of anything you stand to gain in terms of body composition and performance from being in "optimal ketosis." And for that matter, you can influence ketone levels by things like by simply consuming a very fatty meal, which may well put you further away from your goals rather than closer to them.
    I'd nix the blood tester and focus your time and resources on your calories, training and overall body composition. But like I said, just my $0.02.

  2. NLPz

    Well, I think that although I'm a newbie in keto I have the biochemistry and physiology background that allow me to understand some concepts that I think you may be dismissing: Nutritional Ketosis and Optimal Ketosis.
    When your body is fully keto adapted, you can use lipids with high efficiency. There are numerous pubmed papers on that, and it's not just for the "fat loosing" before Mr. Olympia: not just "relax, just keto on for the burn". The main benefit is the actual performance and also the carb-freedom - wit the satiety and all the stuff you refer. Not to mention the long term health benefits: there are also a lot of scientific papers on that.
    That being said, I recommend to dwell into the blog of Dr. Andreas Eenfeldt, dietdoctor.com, and let me suggest his article about some measurements he made himself: Experiment: Optimal Ketosis for Weight Loss and Improved Performance
    In another post, he explains the ketosis levels:
    Below 0.5 mmol/L is not considered “ketosis”. At this level, you’re far away from maximum fat-burning. Between 0.5-1.5 mmol/L is light nutritional ketosis. You’ll be getting a good effect on your weight, but not optimal. Around 1.5 – 3 mmol/L is what’s called optimal ketosis and is recommended for maximum weight loss. Values of over 3 mmol/L aren’t neccessary. That is, they will achieve neither better nor worse results than being at the 1.5-3 level. Higher values can also sometimes mean that you’re not getting enough food. For type 1 diabetics, it can be caused by a severe lack of insulin, see below.
    By those definitions and the graph he posted, you can see its not "easy and clean" to be in optimal ketosis.
    Since I'm starting, I prickI test my levels to understand my variations, and because you don't always understand what happens to you, and if I feel tachycardia during the day, one possible explanation may be I was keto-offed by some meal (it's impossible to control everything and to always eat at home) and re-starting the adaptation.
    I found, also, that as the time goes by I can re-enter ketosis with few side effects, meaning my body is becoming more and more adapted.

  3. parkscs

    You're citing a blog that talks about "maximum fat burning" and "maximum weight loss", yet the studies show there is no metabolic advantage to ketogenic diets or low carb diets in general. In short, the science doesn't support any extra fat loss from a ketogenic diet beyond the calorie deficit you're creating. Thinking you're going to lose more fat because of your "optimal ketone level" is just deluding yourself. All we're talking from a high "ketone level" is burning lots of fat that includes both dietary fat and stored fat, but there's no increase in body fat burned from being in "optimal ketosis." It's the same way you can get a high "ketone level" measurement after you eat a very fatty meal - yes, you'll have a higher concentration of ketones on your little test strip, but that doesn't mean you're any closer towards your goals. To the extent the calories in that very fatty meal push you into a surplus, you're further away from your goals even though your ketone level is "great."
    As for performance, keto is pretty much worse in terms of optimal performance in nearly every way. There are ways you can mitigate the impact on performance, but doing keto for "actual performance" reasons doesn't make a lot of sense.

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