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Starvation Ketoacidosis Medscape

Blog - Clen Fat Burner

Blog - Clen Fat Burner

Clenbuterol abuse as a diet drug gained popularity a few years ago. Its side effects caused it to become a banned substance. In this interview with Medscape and Drs. McKeever and Hoffman, they break down the dangers of using Clenbuterol to gain muscle and lose weight. The original article can be found at MedScape.com To Dope or Not to Dope: Abuse of Clenbuterol as a Diet Drug: An Expert Interview With Drs. Ken McKeever and Hoffman Use and abuse. Misuse and overuse. These are topics that we have explored before in our To Dope or Not to Dope columns. Previously, we discussed the role of the team physician and why elite athletes may choose to use performance-enhancing drugs. In this column, we talk about the use of performance-enhancing drugs by the everyday weekend warrior. Clenbuterol has received substantial attention by the lay media as a miracle diet drug with only perfunctory regard to the dangers of its unsupervised use. When used appropriately under the supervision of a physician or veterinarian, clenbuterol can alleviate respiratory distress in horses and may have potential therapeutic benefits in human heart failure. However, off-label unsupervised overuse of the drug can be fraught with dangers and side effects. These interviews deal with the potential abuse of clenbuterol as an unlicensed diet drug, not its legitimate physician-supervised usages. Medscape: Clenbuterol is getting a lot of press these days for misuse by weight lifters and dieters. Could you tell Medscape readers about its legitimate uses in the United States? Dr. McKeever: Clenbuterol was approved 6 or 7 years ago for use in treating respiratory disease in horses. Its very similar to the bronchodilator albuterol, and is the only beta-2 agonist that has been licensed for use in treating respirato Continue reading >>

Euglycaemic Ketoacidosis In A Non-diabetic Primigravida Following An Appendicectomy

Euglycaemic Ketoacidosis In A Non-diabetic Primigravida Following An Appendicectomy

Pregnancy creates significant alterations in energy metabolism which itself is a physiological adaptation to provide continuous flow of energy metabolites to the foetus. The state of insulin resistance created by hormonal changes in pregnancy enables free flow of glucose to the foetus and allows its absorption through facilitated diffusion. As glucose is preferentially available for the foetus, maternal fasting glucose level would be less than that of a non-pregnant state and in contrast plasma ketones and free fatty acids levels are elevated, resulting in a state of accelerated starvation. These metabolic alterations place a pregnant woman at a higher risk of developing euglycaemic ketoacidosis when allowed to fast for prolonged periods due to medical, surgical and psychological reasons. We report a rare case of euglycaemic ketoacidosis causing severe increased anion gap metabolic acidosis in a non-diabetic mother following surgery for appendicitis at a gestation of 27 weeks. Euglycaemic ketoacidosis is a condition characterized by accelerated ketogenesis in cellular level in spite of adequate supply of glucose for energy metabolism, in contrast to diabetic ketoacidosis where there is intracellular glucose depletion resulting in accelerated ketogenesis providing keto acids as an alternative energy metabolite. The hormonal changes that occur in pregnancy create a state of insulin resistance allowing free flow of glucose to the foetus. Thus, prolonged starvation in a pregnant woman will place her at high risk of starvation ketosis. We describe a 27-year-old non-diabetic primigravida woman who presented with increased anion gap metabolic acidosis secondary to starvation ketoacidosis following prolonged fasting and vomiting due to appendicitis. A 27-year-old primigravida w Continue reading >>

Endocrine Emergencies

Endocrine Emergencies

This activity is intended for clinicians in primary care, notably emergency medicine, internal medicine, family medicine, diabetes and endocrinology, nurses, and medical students. The goal of this activity is to provide background and essential, practical information for healthcare providers to aid in the recognition and management of endocrine emergencies. Upon completion of this activity, participants will be able to: List common precipitating and risk factors of thyroid storm Describe diagnosis, including presentation, symptoms, and laboratory findings of thyroid storm Discuss treatment and the mortality rate of both treated and untreated thyroid storm Describe clinical presentation and findings of myxedema coma Recognize symptoms and interpret laboratory data of someone in DKA Discuss how to treat electrolyte abnormalities seen with DKA Describe how to recognize and treat adrenal crisis As an organization accredited by the ACCME, Medscape, LLC requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest. Medscape, LLC encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content. Assistant Professor of Medicine, Uniformed Services University of Health Science, Bethesda, Maryland; Internal Medicine Resident, Walter Reed Army Medical Center, Washington, DC Disclosure: Anita A. Shah, DO, has disclosed no rel Continue reading >>

Boosting Brain Ketone Metabolism: A New Approach To Alzheimers

Boosting Brain Ketone Metabolism: A New Approach To Alzheimers

Receive email when new articles are published onAlzheimer Disease Strategies that increase the brains uptake of ketones as an approach to the treatment of Alzheimers disease or mild cognitive impairment are gaining momentum, according to experts in the field. A whole session dedicated to the topic of brain ketone metabolism and ketogenic interventions was held during the recent Alzheimers Association International Conference (AAIC) 2017, with new clinical data showing some exciting preliminary observations. We know that in Alzheimers disease, the brain loses its ability to use glucose to produce energy, Stephen Cunnane, PhD, University of Sherbrooke, Quebec, Canada, explained. Some areas of the brain are down by 40% in terms of glucose metabolism. We believe that this energy gap increases the risk of neuronal dysfunction and cognitive decline. Preliminary studies presented here have suggested that the brain can use ketones instead of glucose to reduce the energy gap, Dr Cunnane said. These strategies warrant further research to see if they can delay cognitive decline in older people, he added. The new data included a pilot trial of a ketogenic diet, which was associated with improved cognitive function in patients with Alzheimers disease, and preliminary results from an ongoing study suggesting that giving a ketogenic supplement in the form of medium-chain triglycerides can partially restore the brain energy supply in patients who have mild cognitive impairment, with hints of associated improved cognitive function. Another study, presented as a poster, reported that exercise increased the uptake of ketones into the brain. Whether this is the mechanism responsible for the well-documented beneficial effects of exercise on cognitive function we dont know, but perhaps keto Continue reading >>

Concerning The Causes Of Alcoholism Quizlet. Alcoholic Ketoacidosis: Background, Pathophysiology, Etiology Alcoholism

Concerning The Causes Of Alcoholism Quizlet. Alcoholic Ketoacidosis: Background, Pathophysiology, Etiology Alcoholism

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. The cause of alcoholism. 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. A concomitant metabolic alkalosis is common, secondary to vomiting and volume depletion (see Workup). Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are: This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). Although the general physiological factors and mechanisms leading to AKA are understood, the precise factors have not been fully elucidated. The following are the 3 main predisposing events: During starvation there is decrease in insulin secretion and increases in production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone. Hormone-sensitive lipase is normally inhibited by insulin, and, when insulin levels fall, lipolysis is up-regulated, causing release of free fatty acids from peripheral adipose tissue. Free fatty acids are either oxidized to CO or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid. Carnitine acyltransferase (CAT) transports free fatty acids into the mitochondria and therefore regulates their entry into the oxidative pathway. The decreased insulin-to-glucagon ratio that occurs in starvation indirectly reduces the inhibition on C Continue reading >>

Diabetic Gi Problems Type Smoothies 2

Diabetic Gi Problems Type Smoothies 2

When it comes to health benefits many cultures eat bitter melon or take it in supplement form as a traditional medicine to treat diabetes. 22nd December 2011- The charity Diabetes UK had been concerned that people with diabetes could have their driving licences taken away unfairly because of a new Explains tooth discoloration Mouth rinses and washes containing chlorhexidine and cetylpyridinium chloride can also stain your teeth. Diabetic Gi Problems Type Smoothies 2 i have a pancreatic lesion 3. Cellular Aspects of ER-Stress and Metabolic Diseases. If you feel nauseous and dizzy after the glucose test does that likely mean you have gestational diabetes? Find helpful customer reviews and review ratings for LFI Balance Glucose Your Cardiologist Recommended 100% Trusted Natural Blood Sugar Management Supplement For Diabetes mellitus type 2: Ik heb een verhoogde kans op diabetes mellitus type 2. insulin bottle and inject the air. Boosts energy burns fat and supports a healthy metabolism. Role in Diabetes Pancreas is closely related to diabetes. it is composed of several interacting systems of which hormone regulation is the. Warshaw is owner of Hope Warshaw Associates Alexandria VA and is a diabetes educator; A. Traumatic Brain Injury: A Guide For Patients Traumatic ain injury (TBI) occurs when a sudden trauma such as a blow or jolt to the head causes damage to the ain. Screening and Monitoring of Prediabetes. Nutritional changes Extremely high fat content diets (60% fat) can cause acute pancreatitis in some dogs if they are kept on it for 14-38 weeks. 4 November 2006 diabetic coma vs hypoglycemic shock london shoes Volume 51 Special Issue For people with diabetes like Ashish a young man from a rural village in India managing their diabetes involves travelling Quick Guide Continue reading >>

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Go to: A 34-year-old man with a 19-year history of type 1 diabetes presented as an emergency with a 4-day history of nausea, vomiting, and flu-like symptoms. He was on a basal bolus insulin regime comprising 8 units of bolus insulin lispro injected at mealtimes and 12 units of basal isophane insulin at bedtime, but did not monitor capillary blood glucose levels. He did however empirically increase his insulin doses during times of illness and had increased his isophane insulin to 15 units during the 3 days prior to presentation. He had only one prior hospital admission, which occurred 6 years previously and was due to an episode of DKA precipitated by gastroenteritis. He was single, unemployed, did not drink alcohol, had no previous psychiatric history, no family history of diabetes or other medical conditions, and lived in a hostel. He had a record of poor clinic attendances and a history of long-term cannabis use. He denied any salicylate consumption, but admitted to some weight loss; however, he was unable to quantify this. His body mass index (BMI) was 19 kg/m2, and he looked unkempt. Physical examination revealed a temperature of 36.4°C (97.5°F), heart rate of 106 beats per minute, supine blood pressure of 131/85 mmHg, and sitting blood pressure of 122/80 mmHg. He had a respiratory rate of 30 breaths per minute, and his oxygen saturation using a pulsoximeter was 99% on room air. He appeared clinically dehydrated with dry oral mucosa, but cardiovascular, respiratory, abdominal, and neurological examinations were otherwise normal. Diabetic ketoacidosis (DKA) was suspected; metabolic acidosis was confirmed with a pH of 7.3, bicarbonate concentration of 10 mEq/l, and an elevated anion gap of 29 mEq/l [sodium = 134 mEq/l, potassium = 5.7 mEq/l, chloride = 101 mEq/l, b Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Background 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: This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

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 been fully elucidated. The following are the 3 main predisposing events: Delay and decrease in insulin secretion and excess glucagon secretion, induced by starvation and counter-regulatory hormones Elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+) secondary to alcohol metabolism Volume depletion resulting from vomiting and poor oral intake of fluids During starvation there is decrease in insulin secretion and increases in production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone. Hormone-sensitive lipase is normally inhibited by insulin, and, when insulin levels fall, l Continue reading >>

Jci -effect Of Starvation On The Turnover And Metabolic Response To Leucine

Jci -effect Of Starvation On The Turnover And Metabolic Response To Leucine

Effect of Starvation on the Turnover and Metabolic Response to Leucine Find articles by Sherwin, R. in: JCI | PubMed | Google Scholar Published in Volume 61, Issue 6 (June 1, 1978) J Clin Invest.1978;61(6):14711481.doi:10.1172/JCI109067. Copyright 1978, The American Society for Clinical Investigation. l-Leucine was administered as a primed continuous 3-4-h infusion in nonobese and obese subjects in the postabsorptive state and for 12 h in obese subjects after a 3-day and 4-wk fast. In nonobese and obese subjects studied in the post-absorptive state, the leucine infusion resulted in a 150-200% rise in plasma leucine above preinfusion levels, a small decrease in plasma glucose, and unchanged levels of plasma insulin and glucagon and blood ketones. Plasma isoleucine (60-70%) and valine (35-40%) declined to a greater extent than other amino acids (P < 0.001). After 3 days and 4 wk of fasting, equimolar infusions of leucine resulted in two- to threefold greater increments in plasma leucine as compared to post-absorptive subjects, a 30-40% decline in other plasma amino acids, and a 25-30% decrease in negative nitrogen balance. Urinary excretion of 3-methylhistidine was however, unchanged. Plasma glucose which declined in 3-day fasted subjects after leucine administration, surprisingly rose by 20 mg/100 ml after 4 wk of fasting. The rise in blood glucose occurred in the absence of changes in plasma glucagon and insulin and in the face of a 15% decline in endogenous glucose production (as measured by infusion of [3-3H]glucose). On the other hand, fractional glucose utilization fell by 30% (P < 0.001), thereby accounting for hyperglycemia. The estimated metabolic clearance rate of leucine fell by 48% after 3 days of fasting whereas the plasma delivery rate of leucine was unchan Continue reading >>

Shock: Symptoms, Causes & Treatment Of Trauma

Shock: Symptoms, Causes & Treatment Of Trauma

The word shock is used differently by the medical community and the general public. The connotation by the public is an intense emotional reaction to a stressful situation or bad news. The medical definition of shock is much different. Medically, shock is defined as a condition where the tissues in the body don't receive enough oxygen and nutrients to allow the cells to function. This ultimately leads to cellular death, progressing to organ failure, and finally, if untreated, whole body failure and death. Cells need two things to function: oxygen and glucose. This allows the cells to generate energy and do their specific jobs. Oxygen in the air enters the body through the lungs . Oxygen molecules cross from the air sacs of the lungs into the smallest blood vessels, the capillaries, and are picked up by red blood cells and attached to hemoglobin molecules. The red blood cells are pushed through the body by the actions of the pumping heart and deliver the oxygen to cells in all the tissues of the body. The hemoglobin then picks up carbon dioxide, the waste product of metabolism , which it is then taken back to the lungs and breathed out into the air. The whole cycle begins again. Glucose is generated in the body from the foods we eat. Glucose travels in the blood stream and uses an insulin molecule to "open the door," where it then enters the cell to provide energy for cellular metabolism . If cells are deprived of oxygen, instead of using aerobic (with oxygen) metabolism to function, the cells use the anaerobic (without oxygen) pathway to produce energy. Unfortunately, lactic acid is formed as a by-product of anaerobic metabolism. This acid changes the acid-base balance in the blood, making it more acidic, and can lead to a situation in which cells begin to leak toxic c Continue reading >>

Breastfeeding On A Low-carb Diet – Is It Dangerous?

Breastfeeding On A Low-carb Diet – Is It Dangerous?

Is it dangerous to breastfeed while on a low-carb, high-fat diet? Recently, the journal of the Swedish Medical Association published a case report (summary in English) of a woman who, six weeks after giving birth, had to be hospitalized for severe ketoacidosis. Luckily, she recovered quickly and her numbers were back to normal the next day. Ketoacidosis is a dangerous condition, most often seen in type 1 diabetics with acute insulin deficiency. In rare cases, ketoacidosis may occur in non-diabetics after prolonged periods of starvation or inadequate food intake, in which case it typically occurs in combination with stress or other medical conditions. The woman in this case had been eating low-carb, high fat for a long time before the incident. After giving birth however, she had suffered flu-like symptoms of fever, nausea and a complete loss of appetite. Despite this, she was still able to breastfeed her baby, which of course ramped up her nutritional requirements. The case study report brings up the woman’s low-carbohydrate diet as one possible contributing factor to the situation. However, as soon as the media found out, they immediately exaggerated this possible contributing factor to the guaranteed sole cause of the condition (which, as we shall see, is unikely): Metro: Woman Falls Seriously Ill of LCHF Diet During Lactation (Google translated from Swedish) In the woman’s own words The woman described in the case report in the journal contacted me of her own accord through common acquaintances. She tells a different story from the one perpetuated by the media: What isn’t made clear is that I, the breastfeeding woman, had been eating LCHF for approximately six years before this incident, but, because of stress during my second pregnancy and after childbirth I s Continue reading >>

Medical Definition Of Ketonuria

Medical Definition Of Ketonuria

Ketonuria: A condition in which abnormally high amounts of ketones and keytone bodies (a byproduct of the breakdown of cells) are present in the urine. Ketonuria is a sign seen in diabetes mellitus that is out of control. Diabetics prone to ketonuria need to monitor their urine for signs of ketone buildup that could lead to life-threatening symptoms unless promptly treated. Ketonuria can also develop as a result of fasting, dieting, starvation and eating disorders. Alternate names for ketonuria include ketoaciduria and acetonuria. Digestion and the Role of Insulin When food is digested, the body turns fats, proteins and carbohydrates into components that sustain and nurture the body. Fats are converted into fatty acids, proteins into amino acids and carbohydrates into glucose (a sugar) that enters the bloodstream. The body needs glucose as fuel to perform activities. However, glucose has to be delivered. It does not automatically route itself to body sites requiring fuel. Insulin, a hormone secreted by the pancreas, carries out this task, delivering glucose to cells throughout the body. Muscles and tissues then have the energy to do their jobs. Ketones and Ketone Bodies: What They Are, How They Accumulate In some people with diabetes mellitus, the pancreas releases insufficient amounts of insulin or no insulin at all. Consequently, glucose goes largely undelivered. In a desperate attempt to provide fuel, the body begins feeding on itself -- that is, it breaks down muscle and fat to burn as fuel. Ketone bodies are a byproduct of this process. Ketone bodies consist chemically of three substances (beta-hydroxybutyric acid, acetoacetic acid, and acetone). When ketone bodies are released, they enter the bloodstream, acidify the blood, and are eventually excreted mostly in ur Continue reading >>

Why Ditch The Infant Cereals?

Why Ditch The Infant Cereals?

nutritional philosophy, tradition has weight. After all, weve survived anywhere from 7,000 to 77,000 generations on this planet (depending on whose science you believe). If we didnt know how to adequately nourish our children all that time, how did we even get here? And guess what? Traditional cultures didnt (and dont) feed their young babies infant cereal. Among the few cultures who fed their babies a gruel of grains, their practice radically differed from what we do today. First, they only introduced the gruel after the baby was more than a year old. And second, they ensured that the gruel was mildly fermented by soaking the grains for 24 hours or more. In order to digest grains, your body needs to make use of an enzyme called amylase. Amylase is the enzyme responsible for splitting starches. And, guess what? Babies dont make amylase in large enough quantities to digest grains until after they are a year old at the earliest. Sometimes it can take up to two years. You see, newborns dont produce amylase at all. Salivary amylase makes a small appearance at about 6 months old, but pancreatic amylase (what you need to actually digest grains) is not produced until molar teeth are fully developed! First molars usually dont show up until 13-19 months old, on average. Undigested grains wreak havoc on your babys intestinal lining. It can throw off the balance of bacteria in their gut and lead to lots of complications as they age including: food allergies, behavioral problems, mood issues, and more. What does this mean? Dont feed your baby grains (or even highly starchy foods), until all of their first molars have emerged. This means no rice cereals, no Cheerios, no Goldfish, no oatmeal, no infant crackers. It means that when you sit down with them at a restaurant, you shouldnt Continue reading >>

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