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How To Induce Ketoacidosis

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 >>

Ketosis Vs. Ketoacidosis: What You Should Know

Ketosis Vs. Ketoacidosis: What You Should Know

Despite the similarity in name, ketosis and ketoacidosis are two different things. Ketoacidosis refers to diabetic ketoacidosis (DKA) and is a complication of type 1 diabetes mellitus. It’s a life-threatening condition resulting from dangerously high levels of ketones and blood sugar. This combination makes your blood too acidic, which can change the normal functioning of internal organs like your liver and kidneys. It’s critical that you get prompt treatment. DKA can occur very quickly. It may develop in less than 24 hours. It mostly occurs in people with type 1 diabetes whose bodies do not produce any insulin. Several things can lead to DKA, including illness, improper diet, or not taking an adequate dose of insulin. DKA can also occur in individuals with type 2 diabetes who have little or no insulin production. Ketosis is the presence of ketones. It’s not harmful. You can be in ketosis if you’re on a low-carbohydrate diet or fasting, or if you’ve consumed too much alcohol. If you have ketosis, you have a higher than usual level of ketones in your blood or urine, but not high enough to cause acidosis. Ketones are a chemical your body produces when it burns stored fat. Some people choose a low-carb diet to help with weight loss. While there is some controversy over their safety, low-carb diets are generally fine. Talk to your doctor before beginning any extreme diet plan. DKA is the leading cause of death in people under 24 years old who have diabetes. The overall death rate for ketoacidosis is 2 to 5 percent. People under the age of 30 make up 36 percent of DKA cases. Twenty-seven percent of people with DKA are between the ages of 30 and 50, 23 percent are between the ages of 51 and 70, and 14 percent are over the age of 70. Ketosis may cause bad breath. Ket Continue reading >>

Original Communication Postmortem Biochemistry In Suspected Starvation-induced Ketoacidosis

Original Communication Postmortem Biochemistry In Suspected Starvation-induced Ketoacidosis

Highlights • Starvation ketoacidosis is a rare cause of metabolic acidosis. • The levels of ketonemia in starvation ketoacidosis is usually mild. • Starvation-ketoacidosis has been rarely described in the forensic setting. • The role that hyperketonemia may play in the death process should be evaluated. Significantly increased blood ketone body levels can be occasionally observed in the forensic setting in situations other than exposure to cold, diabetic or alcoholic ketoacidosis. Though infrequent, these cases do occur and deserve thorough evaluation in order to establish appropriate differential diagnoses and quantify the role that hyperketonemia may play in the death process. Starvation ketoacidosis is a rare cause of metabolic acidosis and is a phenomenon that occurs normally during fasting, as the body switches from carbohydrate to lipid energy sources. The levels of ketonemia in starvation ketoacidosis is usually mild in comparison to those seen in diabetic or alcoholic ketoacidosis. In the clinical setting, several cases of starvation-induced ketoacidosis mainly associated with gastric banding, pregnancy, malnutrition and low-carbohydrate diets have been reported. However, starvation ketosis causing severe metabolic acidosis has been rarely described in the medical literature. In the realm of forensic pathology, starvation-induced hyperketonemia has been rarely described. In this paper we present the postmortem biochemical results observed in situations of suspected starvation-induced hyperketonemia that underwent medico-legal examination. In all these cases, the diagnosis of starvation induced-hyperketonemia and the subsequent ketoacidosis was established per exclusionem based on all postmortem investigation findings. A review of the literature pertainin Continue reading >>

Can You Die Of Starvation With Large Amounts Of Adipose Tissue?

Can You Die Of Starvation With Large Amounts Of Adipose Tissue?

This paper gives an numbers based answer, and by extrapolation, it would seem the more adipose tissue you have, the longer you can without food: “Anaverage human of 165 pounds has roughly 33 pounds of fat…and 26 pounds of protein suspended in 132 pounds of lean body mass, mostly muscle. Practicallyall of the body fat is expendable without serious adverse effects. In contrast, only one-half of the body’s protein can be mobilized and used as fuel before death occurs. Theconversion of 6 kg of protein to glucose results in the formation of only 3.4 kg of glucose. If the brain oxidizes 100–145 g of glucose daily, the average human could starve for only 23–34 days. The fact that the brain can derive two-thirds of its energy from ketone bodies, synthesized mostly from fat, allows humans to survive total starvation for 60–90 days.”1 1. Owen OE. Ketone Bodies as a Fuel for the Brain during Starvation. Biochemistry And Molecular Biology Education. 2005. Vol. 33, No. 4, pp. 246–251, 2005. Continue reading >>

Pancreatic Ketoacidosis (kabadi Syndrome): Ketoacidosis Induced By High Circulating Lipase In Acute Pancreatitis

Pancreatic Ketoacidosis (kabadi Syndrome): Ketoacidosis Induced By High Circulating Lipase In Acute Pancreatitis

Broadlawns Medical Center, Des Moines University, Des Moines, Iowa and University of Iowa, Iowa City, Iowa, USA. *Corresponding Author: 17185, Berkshire Parkway Clive, Iowa, 50325, USA Phone +5152823041 E-mail [email protected] Visit for more related articles at JOP. Journal of the Pancreas Abstract Introduction Ketoacidosis is well established as a metabolic complication of both type 1 and type 2 diabetes Mellitus (Diabetic Ketoacidosis). It is often an initial presentation of type 1 diabetes in children and adolescents and occasionally in adults. Alternatively, it is induced of an onset of an acute disorder, e. g, sepsis, myocardial infarction, stroke, pregnancy etc. in subjects with type 1 and 2 diabetes. Ketoacidosis is also known to occur following an ethanol binge (Alcoholic Ketoacidosis). Finally, ketonemia with a rare progression to Ketoacidosis is documented to ensue following prolonged starvation. Methods The review of English literature for over 35 years from 01/1980 till 12/2015 for terms, 'ketonemia, ketonuria and ketoacidosis' 'pancreatic lipase' and 'acute pancreatitis'. Results 1) Description of individual patients presented as case reports, 2) Documentation of a series of consecutive subjects hospitalized for management of acute pancreatitis with special attention to establishing the prevalence of the disorder as well as examining the relationship between the severity of the disorder and occurrence of Ketoacidosis, 3) Studies demonstrating the relationship between progressively rising circulating pancreatic lipase concentrations with ketonuria, ketonemia and Ketoacidosis in subjects presenting with acute pancreatitis irrespective of the etiology and documenting resolution of ketonuria, ketonemia and ketoacidosis following the declining serum lipase leve Continue reading >>

Ketoacidosis

Ketoacidosis

Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate. Ketoacidosis is a pathological metabolic state marked by extreme and uncontrolled ketosis. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased. In extreme cases ketoacidosis can be fatal.[1] Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct by-product of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover.[2] Ketosis may also give off an odor, but the odor is usually more subtle due to lower concentrations of acetone. Treatment consists most simply of correcting blood sugar and insulin levels, which will halt ketone production. If the severity of the case warrants more aggressive measures, intravenous sodium bicarbonate infusion can be given to raise blood pH back to an acceptable range. However, serious caution must be exercised with IV sodium bicarbonate to avoid the risk of equally life-threatening hypernatremia. Cause[edit] Three common causes of ketoacidosis are alcohol, starvation, and diabetes, resulting in alcoholic ketoacidosis, starvation ketoacidosis, and diabetic ketoacidosis respectively.[3] In diabetic ketoacidosis, a high concentration of ketone bodies is usually accomp Continue reading >>

What Are The Main Differences Between Nutritional Ketosis, And Ketosis?

What Are The Main Differences Between Nutritional Ketosis, And Ketosis?

I believe these can be used interchangeably. Ketosis is ketosis - this term describes a metabolic state characterized by elevated level of ketone bodies in your blood and low blood glucose levels, induced either by consumption of exogenous ketones or medium-chain triglycerides that are quickly metabolized into ketones, or by starvation (or, at least, restriction of carbohydrates), which switches your body’s metabolic machinery to utilizing fat oxidation as the main source of energy (byproducts of fat oxidation in the absence of glucose are then metabolized further into ketone bodies that can be used as energy substrate by most tissues). “Nutritional ketosis” is more often used to describe a voluntary exercise of inducing ketosis through certain dietary practices (in other words, this is ketosis as a result of a specific nutrition). But, given that nutrition (or lack thereof) still remains a primary method of inducing ketosis (barring direct consumptino of ketone esters, etc.) - most of the time, any ketosis is nutritional ketosis. Continue reading >>

Canagliflozin-induced Diabetic Ketoacidosis

Canagliflozin-induced Diabetic Ketoacidosis

Go to: Case Report A 62-year-old woman with type 2 diabetes mellitus, hypertension, gastroesophageal reflux disease, and depression presented with 4 days of nausea, vomiting, and generalized weakness. Her symptoms became progressively worse such that by the day of admission she had decreased appetite, polydipsia, polyuria, and could not walk. The patient denied fever, chills, abdominal pain, diarrhea, or sick contacts. Home medications were atorvastatin, metformin, sucralfate, pioglitazone, canagliflozin, exenatide, omeprazole, fluoxetine, ranitidine, lisinopril, and alprazolam. On physical examination, the patient’s vital signs included a temperature of 38.3°C, blood pressure 134/61, heart rate 107, respiratory rate 24, and oxygen saturation of 100% on 2 liters nasal cannula oxygen. The patient appeared ill and distressed. She had dry mucous membranes, clear lung sounds bilaterally, and her heart was regular without murmurs, gallops, or rubs. Her abdomen was soft and nontender with present bowel sounds. Extremities showed no edema, and she had no focal neurological findings. Laboratory revealed a metabolic acidosis with a pH of 7.08 and anion gap >17. Chemistry panel indicated sodium 134 mEq/L, potassium 5.2 mEq/L, chloride 112 mEq/L, CO2 <5 mEq/L, blood urea nitrogen 22 mg/dL, and creatinine 1.3 mg/dL. Blood glucose was 213 mg/dL, and urinalysis revealed glucose 2+ and ketones 3+. Serum ketones were present at 1:8 dilution, with a lactic acid of 0.8 mmol/L. The patient’s hemoglobin A1C (HbA1c) was 11.1. The patient was admitted to the intensive care unit for severe metabolic acidosis secondary to DKA. Aggressive fluid resuscitation was undertaken and an insulin drip initiated. Within 6 hours, the anion gap metabolic acidosis improved. On further review of her med Continue reading >>

Ketosis: Fear, Uncertainty And Doubt

Ketosis: Fear, Uncertainty And Doubt

Perhaps nothing is more damaging to the new low-carber than the intentional spread of fear, uncertainty and doubt regarding the state of ketosis compared to the dangerous state of ketoacidosis. The former is a natural and healthy state of existence, the latter is a condition that threatens the life of type 1 diabetics and type 2 diabetics whose disease has progressed to the point where their pancreatic beta cells can no longer produce insulin (ketoacidosis is also a risk for alcoholics). So if you’re not an alcoholic, a type 1 diabetic or a late-stage type 2 diabetic, fear of ketosis is misdirected. You should regard with suspicion anyone who confuses the two and warns you against a low-carb diet because they cannot tell the difference. The confusion between ketosis and ketoacidosis is a sign of a grave misunderstanding of basic biology (if not a complete lack of critical faculty). So too is the assumption that ketosis is the “early stage” of ketoacidosis or that “ketosis leads to ketoacidosis” in a person whose pancreas is still able to produce insulin. If you don’t trust me (and why should you), you should consider listening to some people who know a lot more about this than either you or I ever will: Nutritional ketosis is by definition a benign metabolic state… by contrast, ‘diabetic ketoacidosis’ is an unstable and dangerous condition that occurs when there is inadequate pancreatic insulin response to regulate serum B-OHB. This occurs only in type-1 diabetics or in late stage type-2 diabetics with advanced pancreatic burnout. (Dr. Phinney & Dr. Volek, The Art and Science of Low Carbohydrate Living, p.4) Later in the book (p.80), Phinney and Volek explain further: [Type-1 diabetics] need insulin injections not just to control blood glucose levels, Continue reading >>

How Does Diabetic Ketoacidosis Cause Vomiting?

How Does Diabetic Ketoacidosis Cause Vomiting?

DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body’s cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can’t get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn’t available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body’s metabolic processes aren’t able to function as well. A higher level of ketones also affects levels of sugar and electrolytes in the body. As ketones accumulate in the blood, more ketones will be passed in the urine, taking sodium and potassium salts out with them. Over time, levels of sodium and potassium salts in the body become depleted, which can cause nausea and vomiting. The result is a vicious cycle. The most important prevention strategies are to monitor blood glucose levels routinely, keep blood glucose levels controlled (e.g., Continue reading >>

Steroid-induced Diabetic Ketoacidosis.

Steroid-induced Diabetic Ketoacidosis.

This content is PDF only. Please click on the PDF icon to access. Abstract Although diabetes mellitus is not uncommon in patients on highdose steroid treatment, ketoacidosis is distinctly rare. Indeed only a few patients have been reported, and the ketoacidosis was so mild that none required insulin. We have studied four patients with systemic lupus erythematosus (SLE) who developed diabetic ketoacidosis after treatment with large doses of steroids. All received at least 60 mg of prednisone for 2 to 8 months. In addition, two had been maintained on small doses for 1 and 10 years. Family history of diabetes mellitus was present in two. One patient was on chlorothiazide diuretic for several months, Continue reading >>

Would You Recommend The Ketogenic Diet To An 18 Year Old Girl For Weight Loss?

Would You Recommend The Ketogenic Diet To An 18 Year Old Girl For Weight Loss?

I’ve been on the diet for about 6 months. I am now 18 years old. The thing about Keto is that it’s a difficult diet and requires dedication, but the results are admirable. I’ve lost about 40 pounds over the course of the first 4 months and am now at 132 pounds, exercising once a week for an hour at best. I’ll give you the info you actually need to know, and then the rest will be my response to Sally’s post :) Also, remember that most people who give advice about weight loss have never been obese or overweight to a significant degree. Weight loss is a struggle and a battle, and you cannot rely on people who only criticize from afar. Would a soldier take advice on how to shoot a rifle from a civilian who has played Call of Duty? No? Thought not. Pros: Most people on keto do not need to consciously restrict food intake, you should never feel hungry. Generally preserves muscle mass and maximizes fat loss. You can eat fat again! Do not be afraid of fat. The fattiest animals, ruminants, consume low fat, grain based diets high in fiber. In contrast, every carnivore preferentially eats the fattiest part of the animal, yet they are lean. Why in the world would we assume that humans would get fat off of fat, when we have hundreds of contradictory examples in nature? Lots of natural substitutes for carb based foods available now, Low Carb Tortillas, Ice Creams, you name it. Watch for artificial sweeteners though. Not wholly reliant on exercise for weight loss, but it’s good for personal sanity to do so. Frees you from sugar addiction Cons: No carbs. It’s for life, you don’t “leave it.” It is not a “fad diet” that you do for 2 months and stop, it’s a lifestyle change and an approach to appreciate food. Don’t think of it as a thing that you can have cheat Continue reading >>

Glucocorticoid-induced Diabetic Ketoacidosisin A Non-diabetic Patient Treated For Graves' Orbitopathy

Glucocorticoid-induced Diabetic Ketoacidosisin A Non-diabetic Patient Treated For Graves' Orbitopathy

Abstract: Introduction: Hyperglycemia is a common side effect in patients on high dose steroid treatment, but diabetic ketoacidosis is observed rarely and is usually so mild that most patients do not require insulin therapy. We report a case of severe diabetic ketoacidosis requiring insulin therapy in a patient treated with high dose glucocorticoid therapy for Graves’ orbitopathy. Clinical case: A 54 year old woman presented with hyperthyroidism and exophthalmos. She was diagnosed with Graves’ disease and orbitopathy and treated with methimazole, metoprolol and Artificial Tears. Over the next few months her hyperthyroidism improved greatly; however thyroid orbitopathy got worse. She complained of dryness, grittiness and double vision on upward gaze of both eyes. Physical examination showed severe periorbital edema, worsening bilateral proptosis and lid retraction. She was referred to an ophthalmologist who started oral prednisone at dose of 80 mg/day. On day 5 of prednisone therapy she presented to an emergency department with two day history of nausea, vomiting and diffuse abdominal pain. There was no family history of diabetes mellitus. Blood glucose and urine examinations had been normal 4 weeks prior. On physical examination she was mildly tachycardic and markedly dehydrated. Laboratory results revealed serum glucose of glucose of 400 mg/dl, BUN of 15 mg/dl, creatinine of 1.28 mg/dl, sodium of 136 mEq/l, chloride of 110 mEq/l, CO2 of 12 mmol/l, and potassium of 5.2 mEq/l; room air arterial blood gas showed a pH of 7.10, pCO2 of 18 mmHg, and bicarbonate of 6.0 mEq/l. Urinalysis revealed 4+ glucose and 3+ ketones. Hemoglobin A1C was found to be 5.6%. Urine and blood specimens were sterile. She was diagnosed with DKA and was managed with fluids, insulin and potassi Continue reading >>

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

An Unusual Cause For Ketoacidosis

An Unusual Cause For Ketoacidosis

Abstract Introduction In our continuing series on the application of principles of integrative physiology at the bedside, once again the central figure is an imaginary consultant, the renal and metabolic physiologist, Professor McCance, who deals with data from a real case. On this occasion his colleague Sir Hans Krebs, an expert in the field of glucose and energy metabolism, assists him in the analysis. Their emphasis is on concepts that depend on an understanding of physiology that crosses subspecialty boundaries. To avoid overwhelming the reader with details, key facts are provided, but only when necessary. The overall objective of this teaching exercise is to demonstrate how application of simple principles of integrative physiology at the bedside can be extremely helpful for clinical decision-making (Table 1). Principle Comment 1. A high H+ concentration per se is seldom life-threatening The threat to survival is usually due to the cause for the acidosis rather than the pH per se 2. Finding a new anion means a new acid was added Look in plasma (anion gap) and urine (net charge) to identify the new anions 3. Identify the acid by thinking of the properties of the anion Rate of production, rapidity of clearance from plasma, and unique toxic effects may all provide clues 4. Metabolic acidosis develops when the kidney fails to add new HCO3 to the body The kidney generates HCO3− by excreting NH4+, (usually with Cl−), in the urine 5. Ketoacids are brain fuels, produced when there is a prolonged lack of insulin The usual causes are diabetic ketoacidosis, alcoholic ketoacidosis, starvation or hypoglycemia-induced ketoacidosis, or that associated with salicylate overdose 6. Ketoacids are produced in the liver from acetyl-CoA, usually derived from fatty acids A low net in Continue reading >>

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