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Starvation Ketoacidosis Symptoms

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Is Keto Healthy? Ketosis Vs Ketoacidosis

Is Keto Healthy? Ketosis Vs Ketoacidosis

Is Keto Healthy? Ketosis vs Ketoacidosis When looking at a ketogenic diet and ketosis, it’s common for some people to confuse the process with a harmful, more extreme version of this state known as diabetic ketoacidosis. But there are a lot of misconceptions out there about ketosis vs ketoacidosis, and it’s time to shed some light on the subject by looking at the (very big) differences between the two. An Overview of Ketosis A ketogenic, or keto, diet is centered around the process of ketosis, so it’s important to understand exactly what ketosis is first before we get into whether or not it’s safe (spoiler: it is): Ketosis is a metabolic state where the body is primarily using fat for energy instead of carbohydrates. Burning carbohydrates (glucose) for energy is the default function of the body, so if glucose is available, the body will use that first. But during ketosis, the body is using ketones instead of glucose. This is an amazing survival adaptation by the body for handling periods of famine or fasting, extreme exercise, or anything else that leaves the body without enough glucose for fuel. Those eating a ketogenic diet purposely limit their carb intake (usually between 20 and 50 grams per day) to facilitate this response. That’s why the keto diet focuses on very low carb intake, moderate to low protein intake, and high intakes of dietary fats. Lower protein is important because it prevents the body from pulling your lean muscle mass for energy and instead turns to fat. Ketone bodies are released during ketosis and are created by the liver from fatty acids. These ketones are then used by the body to power all of its biggest organs, including the brain, and they have many benefits for the body we’ll get into later. But first, let’s address a common mi Continue reading >>

What Is Ketosis, And How Long Does It Take To Get Into Ketosis?

What Is Ketosis, And How Long Does It Take To Get Into Ketosis?

Ketosis is a natural state of the body in which it is fueled almost solely by fat. This happens when a person fasts or adheres to a very low carbohydrate diet. The exciting thing about ketosis and ketogenic diets is that you can lose a lot of weight while eating a normal quantity of food. You don’t have to suffer through skimpy portions. There are other benefits of keeping a ketogenic diet as well. These will be explained in the following article. An Explanation of Ketosis The root “keto” in the word ketosis comes from the type of fuel that the body produces when blood sugar is in low supply. The small molecules that are used as fuel are called “ketones.” If you consume very few carbohydrates and only a moderate amount of protein, then the body begins to produce ketones. Ketones are made by the liver from fat. Both the body and the brain can use them as fuel. The brain cannot directly function from fat. It must convert the fat into ketones. Legionella Testing Lab - High Quality Lab Results CDC ELITE & NYSDOH ELAP Certified - Fast Results North America Lab Locations legionellatesting.com When you go on a ketogenic diet, your body almost solely runs on fat. Your insulin levels become rather low as well. Since you are burning so much fat, this is a great way to lose weight. Studies show that ketogenic diets result in greater weight loss. The fastest way to get into ketosis is by fasting. However, you cannot fast for very long, so you need to start a low carb diet. The Brain and Ketones Many people think that the brain needs carbohydrates to function. This is not really true. The brain can work well simply by burning ketones. The reality is that many people feel like they have even more energy and focus when they are fueled by ketones. Benefits of Ketosis There ar Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis Damian Baalmann, 2nd year EM resident A 45-year-old male presents to your emergency department with abdominal pain. He is conscious, lucid and as the nurses are hooking up the monitors, he explains to you that he began experiencing abdominal pain, nausea, vomiting about 2 days ago. Exam reveals a poorly groomed male with dry mucous membranes, diffusely tender abdomen with voluntary guarding. He is tachycardic, tachypneic but normotensive. A quick review of the chart reveals a prolonged history of alcohol abuse and after some questioning, the patient admits to a recent binge. Pertinent labs reveal slightly elevated anion-gap metabolic acidosis, normal glucose, ethanol level of 0, normal lipase and no ketones in the urine. What are your next steps in management? Alcoholic Ketoacidosis (AKA): What is it? Ketones are a form of energy made by the liver by free fatty acids released by adipose tissues. Normally, ketones are in small quantity (<0.1 mmol/L), but sometimes the body is forced to increase its production of these ketones. Ketones are strong acids and when they accumulate in large numbers, their presence leads to an acidosis. In alcoholics, a combination or reduced nutrient intake, hepatic oxidation of ethanol, and dehydration can lead to ketoacidosis. Alcoholics tend to rely on ethanol for their nutrient intake and when the liver metabolizes ethanol it generates NADH. This NADH further promotes ketone formation in the liver. Furthermore, ethanol promotes diuresis which leads to dehydration and subsequently impairs ketone excretion in the urine. Alcoholic Ketoacidosis: How do I recognize it? Typical history involves a chronic alcohol abuser who went on a recent binge that was terminated by severe nausea, vomiting, and abdominal pain. These folk Continue reading >>

Feline Diabetic Ketoacidosis

Feline Diabetic Ketoacidosis

Fall 2008 Ketoacidosis is a metabolic imbalance that is most commonly seen as a sequel to unmanaged or poorly regulated diabetes mellitus. It is caused by the breakdown of fat and protein in a compensatory effort for the need of more metabolic energy. The excessive breakdown of these stored reserves creates a toxic by-product in the form of ketones. As ketones build up in the blood stream, pH and electrolyte imbalances proceed. This condition is a potentially life-threatening emergency that requires immediate medical attention. Diabetes mellitus is a common endocrine disease in geriatric felines. It is caused by a dysfunction in the beta cells of the exocrine pancreas resulting in an absolute or relative deficiency of insulin. Insulin has been called the cells' gatekeeper. It attaches to the surface of cells and permits glucose, the cells' primary energy source, to enter from the blood. A lack of insulin results in a build up of glucose in the blood, physiologically causing a state of cellular starvation. In response to this condition the body begins to increase the mobilization of protein and fat storage. Fatty acids are released from adipose tissue, which are then oxidized by the liver. Normally, these fatty acids are formed into triglycerides. However, without insulin, these fatty acids are converted into ketone bodies, which cannot be utilized by the body. Together with the increased production and decreased utilization an abnormally high concentration of ketone bodies develop. These fixed acids are buffered by bicarbonate; however, the excessive amounts overwhelm and deplete the bicarbonate leading to an increase in arterial hydrogen ion concentration and a decrease in serum bicarbonate. This increase in hydrogen ions lowers the body's pH, leading to a metabolic ac Continue reading >>

Metabolism And Ketosis

Metabolism And Ketosis

Dr. Eades, If the body tends to resort to gluconeogenesis for glucose during a short-term carbohydrate deficit, are those who inconsistently reduce carb intake only messing things up by not effecting full blown ketosis? If the body will still prefer glucose as main energy source unless forced otherwise for at least a few days, is it absolutely necessary to completely transform metabolism for minimal muscle loss? Also, if alcohol is broken down into ketones and acetaldehyde, technically couldn’t you continue to drink during your diet or would the resulting gluconeogenesis inhibition from alcohol lead to blood glucose problems on top of the ketotic metabolism? Would your liver ever just be overwhelmed by all that action? I’m still in high school so hypothetical, of course haha… Sorry, lots of questions but I’m always so curious. Thank you so much for taking the time to inform the public. You’re my hero! P.S. Random question…what’s the difference between beta and gamma hydroxybutyric acids? It’s crazy how simple orientation can be the difference between a ketone and date rape drug…biochem is so cool! P.P.S. You should definitely post the details of that inner mitochondrial membrane transport. I’m curious how much energy expenditure we’re talkin there.. Keep doin your thing! Your Fan, Trey No, I don’t think people are messing up if they don’t get into full-blown ketosis. For short term low-carb dieting, the body turns to glycogen. Gluconeogenesis kicks in fairly quickly, though, and uses dietary protein – assuming there is plenty – before turning to muscle tissue for glucose substrate. And you have the Cori cycle kicking in and all sorts of things to spare muscle, so I wouldn’t worry about it. And you can continue to drink while low-carbing. Continue reading >>

Pathophysiology Of Diabetic Ketoacidosis

Pathophysiology Of Diabetic Ketoacidosis

Diabetic ketoacidosis is one of the potentially life-threatening acute complications of diabetes mellitus. In the past, diabetic ketoacidosis was considered as the hallmark of Type I diabetes, but current data show that it can be also diagnosed in patients with type II diabetes mellitus. It is often seen among patients who are poorly compliant to insulin administration during an acute illness. It is commonly precipitated by an acute stressful event such as the development of infection leading to overt sepsis, organ infarction such as stroke and heart attack, burns, pregnancy or intake of drugs that affect carbohydrate metabolism such as corticosteroids, anti-hypertensives, loop diuretics, alcohol, cocaine, and ecstasy. The presence of these stressful conditions incite the release of counter-regulatory hormones such as glucagon, catecholamines and growth hormone. These hormones induce the mobilization of energy stores of fat, glycogen and protein. The net effect of which is the production of glucose. As a result of absent or deficient insulin release, diabetic ketoacidosis present with the following metabolic derangements: profound hyperglycemia, hyperketonemiaand metabolic acidosis. The production of ketones outweighs its excretion by the kidneys. This results in further reduction of systemic insulin, elevated concentrations of glucagon, cortisol, growth hormone and catecholamine. In peripheral tissues, such as the liver, lipolysis occurs to free fatty acids, resulting in further production of excess ketones. Thereby, causing ketosis and metabolic acidosis. Symptoms of diabetic ketoacidosis usually develop within 24 hours. Gastrointestinal symptoms such as nausea and vomiting are very prominent. If these symptoms are present in diabetics, investigation for diabetic keto Continue reading >>

How To Survive 40 Days Starvation

How To Survive 40 Days Starvation

The obesity epidemic and how to beat it This special mini-series tells you the latest on how metabolic interventions can make genes work to slim you down. This series was first published in Science and Society 21 Some conventional health fears need to be questioned, as, like fasting, they may contain health-restoring opportunities. Dr. Mae-Wan Ho explains Fear of ketosis Ketosis is the dreaded condition of having too much of certain metabolic products called ketones circulating in the blood. Generations of physicians have been taught to be very afraid of it, because of the potentially fatal episodes of ‘ketoacidosis’ in people with diabetes. In these individuals, severe insulin deficiency causes fatty acids to pour out of fat tissues and undergo metabolic conversion in the liver to the ketones, D-b-hydroxybutyrate and acetoacetate. The concentration of ketones circulating in the blood can reach 25mM, upsetting the delicate acid-base balance in the blood, so it turns severely acid. The body excretes ketones in the urine, losing a lot of sodium and potassium ions in the process. At the same time, the high blood glucose is also passed out of the body in the urine together with a lot of water, leading to a drop in blood volume. All these processes contribute to death, if untreated. However, the fear of ketosis may be exaggerated, as milder forms of it occur under other circumstances, and may have therapeutic potential. Such is the claim of senior biochemist Richard Veech in the Unit of Metabolic Control, in one of the National Institutes of Health in the United States. He has a number of prominent veteran biochemists supporting his ideas, and, together, they have written a fascinating review on the potential therapeutic uses of ketosis. How David Blaine could survive 40 Continue reading >>

Ketoacidosis

Ketoacidosis

GENERAL ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. a relative or absolute insulin deficiency is present in all cases. CAUSES The three major types of ketosis are: (i) Starvation ketosis (ii) Alcoholic ketoacidosis (iii) Diabetic ketoacidosis STARVATION KETOSIS when hepatic glycogen stores are exhausted (eg after 12-24 hours of total fasting), the liver produces ketones to provide an energy substrate for peripheral tissues. ketoacidosis can appear after an overnight fast but it typically requires 3 to 14 days of starvation to reach maximal severity. typical keto-anion levels are only 1 to 2 mmol/l and this will usually not alter the anion gap. the acidosis even with quite prolonged fasting is only ever of mild to moderate severity with keto-anion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. ketone bodies also stimulate some insulin release from the islets. patients are usually not diabetic. ALCOHOLIC KETOSIS Presentation a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake for a few days (ethanol and fasting) volume depletion is common and this can result in increased levels of counter regulatory hormones (eg glucagon) levels of free fatty acids (FFA) can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions GI symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena) acidaemia may be severe (eg pH down to 7.0) plasma glucose may be depressed or normal or Continue reading >>

Death From Dehydration Is Usually Serene

Death From Dehydration Is Usually Serene

Though the legal wrangling in the Terri Schiavo case has been loud and contentious, the brain-damaged woman's physical response to having her feeding tube removed is likely to be very serene. "The process of starving to death seems very barbaric but in actuality is very peaceful," said Dr. Fred Mirarchi, assistant clinical professor of emergency medicine at Drexel University College of Medicine in Philadelphia. "The patient's experience is really pretty benign," said Dr. Joanne Lynn, a hospice physician associated with Americans for Better Care of the Dying, a group working for improved end-of-life care. "Overwhelmingly, what will happen is nothing." Lynn, who has worked with numerous families facing end-of-life situations, said most patients who are removed from life support will die within a matter of a few days or weeks. "Some people can last four or five days -- some people can last 20 days," she said. Schiavo's feeding tube was removed March 18 following a contentious battle between her husband, who said his wife would not want to live in a vegetative state, and her parents, who wanted her kept on life support. Schiavo's feeding tube was removed twice before, in 2001 and 2003. The second time, the tube was replaced after six days when Florida Gov. Jeb Bush signed a hastily passed law allowing him to intervene in the case. "Terri's Law" was later ruled unconstitutional. The Body Begins Shutting Down The physical process of dying after life support is removed follows a pattern familiar to hospice workers. And the fact that Schiavo is in a vegetative state will likely make her death faster and less painful, Lynn said. "It depends on whether she has the ability to swallow anything -- and if that anything is offered," she said. "If she's unable to swallow anything, the Continue reading >>

Case Of Nondiabetic Ketoacidosis In Third Term Twin Pregnancy | The Journal Of Clinical Endocrinology & Metabolism | Oxford Academic

Case Of Nondiabetic Ketoacidosis In Third Term Twin Pregnancy | The Journal Of Clinical Endocrinology & Metabolism | Oxford Academic

We provided appropriate management with fluid infusion after cesarean delivery. The patient and her two daughters survived, and no disabilities were foreseen. Alcohol, methanol, and lactic acid levels were normal. No signs of renal disease or diabetes were present. Pathological examination revealed no abnormalities of the placentae. Toxicological tests revealed a salicylate level of less than 5 mg/liter, an acetaminophen level of less than 1 mg/liter, and an acetone level of 300 mg/liter (reference, 520 mg/liter). We present a case of third term twin pregnancy with high anion gap metabolic acidosis due to (mild) starvation. Starvation, obesity, third term twin pregnancy, and perhaps a gastroenteritis were the ultimate provoking factors. In the light of the erroneous suspicion of sepsis and initial fluid therapy lacking glucose, one wonders whether, under a different fluid regime, cesarean section could have been avoided. Severe ketoacidosis in the pregnant woman is associated with impaired neurodevelopment. It therefore demands early recognition and immediate intervention. A 26-yr-old patient was admitted to our hospital complaining of rapid progressive dyspnea and abdominal discomfort. She was pregnant with dichorial, diamniotic twins for 35 wk and 4 d. Medical history showed that she was heterozygous for hemochromatosis. Two years before, she had given birth to a healthy girl of 3925 g by cesarean section, and 1 yr before, she had had a spontaneous abortion. Her preadmission outpatient surveillance revealed slightly elevated blood pressure varying from 132158 mm Hg systolic and 7995 mm Hg diastolic. Glucose and glycosylated hemoglobin were tested at 24 wk and were normal at 4.6 mmol/liter and 5.4% (36 mmol/mol), respectively. Urine analysis at the outpatient obstetri Continue reading >>

#25: Master Hyperglycemia And Dka

#25: Master Hyperglycemia And Dka

Master the management of hyperglycemia, DKA, and learn to avoid common pitfalls. This episode is packed with clinical pearls from repeat guest, Endocrinologist, Dr. Jeffrey Colburn. Recommend a guest or topic and give feedback at [email protected] Rate us on iTunes. Clinical Pearls: Type 1 diabetes (DM1) occurs by autoimmune destruction of beta cells occurs at any age Typically lean body type and normal lipid profiles Type 2 diabetes (DM2) Typically obese and insulin resistant Eventually fat deposition in pancreas destroys insulin production 15-20 years after onset of DM2 leading to absolute insulin deficiency Triad of DKA = hyperglycemia, ketonemia, acidemia DKA occurs w/total lack of insulin leads to inability to utilize glucose (hyperglycemia) Simulated starvation occurs Counter regulatory hormones kick in Free fatty acids are broken down for fuel Keto acids are made as a by product (ketonemia) Acidemia occurs DKA can occur in DM2 if overwhelming infection, or infarction (MI or CVA) Even just a little bit of insulin can keep patient out of DKA! Dehydration is a cardinal issue in DKA from osmotic diuresis Often 6-8 liters depleted! Sick day rules for Type 1 diabetes Early contact with healthcare team Reduce, but do not discontinue insulin during the illness (see #8) Check frequent fingersticks Use antipyretics to manage fever Push the fluids Educate family members about signs/symptoms of DKA If sick, then drop basal insulin by 20% whether SQ or basal rate on insulin pump Keep mealtime insulin dose the same, but skip if not eating Ketones Beta hydroxybutyrate is the predominant ketone in DKA Urine ketones measure acetoacetate (strongly) and acetone (weakly) NOT beta hydroxybutyrate Serum ketones measure acetoacetate and acetone NOT beta hydroxybutyrate Thus, che Continue reading >>

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 Continue reading >>

Ketosis Vs Ketoacidosis

Ketosis Vs Ketoacidosis

Ever since the discovery of the Atkins diet, low carb diets have been hugely popular amongst people of all ages, genders, shapes, and sizes. It wasn’t until the media decided to focus on them so much however, largely because many Hollywood celebrities were using them to drop body fat, increase lean muscle mass and build physiques to be proud of, that the general public began experimenting with them and trying them for themselves. In order for any low carb to be deemed as effective however, the body has to fall into a metabolic state known as ketosis. Ketosis is considered largely beneficial, but is also often confused for ketoacidiosis, which couldn’t be more different. Here we’ll be taking a look at what ketosis and ketoacidosis is, and exactly how and why they’re so different from one another. So, without any further hesitation, let’s get started. What is ketosis? – Ketosis naturally occurs when blood circulating throughout the body contains naturally high concentrations of ketones, or ketoacids. Ketosis occurs because of a change in the body’s natural pathways of energy creation. Normally, the body’s preferred energy source is glucose, which is a form of sugar. Glucose can naturally be absorbed via the diet, and it can also be synthesised from other forms of sugar. When we take away glucose, sugars, and food sources that the body can use to convert into glucose however, the body then falls into starvation mode because it literally has no energy. The body will begin to panic as it will fear it is starving and it will therefore begin looking elsewhere for other sources of energy. It will begin using stored body fat for energy once it falls into a state of ketosis. Ketosis is able to occur as a result of our livers actually burning body fat and using it Continue reading >>

Diabetic, Alcoholic And Starvation Ketoacidosis

Diabetic, Alcoholic And Starvation Ketoacidosis

Copious amounts of ketones which are generated in insulin-deficient or insulin-unresponsive patients will give rise to a high anion gap metabolic acidosis. Ketones are anions, and they form the high anion gap. Management of DKA and HONK is discussed elsewhere. Meet the ketones Chemically speaking, a ketone is anything with a carbonyl group between a bunch of other carbon atoms. The above are your three typical ketoacidosis-associated ketone bodies. The biochemistry nerds among us will hasten to add that the beta-hydroxybutyrate is in fact not a ketone but a carboxylic acid, but - because it is associated with ketoacidosis, we will continue to refer to it as a ketone for the remainder of this chapter, in the spirit of convention. In the same spirit, we can suspend our objections to acetone being included in a discussion of ketoacidosis, which (though a true ketone) is in fact not acidic or basic, as it does not ionise at physiological pH (its pKa is 20 or so). So really, the only serious ketone acid is acetoacetate, which has a pKa of 3.77. However, beta-hydroxybutyrate is the prevalent ketone in ketoacidosis; the normal ratio of beta-hydroxybutyrate and acetoacetate is 3:1, and it can rise to 10:1 in diabetic ketoacidosis. Acetone is the least abundant. The metabolic origin of ketones The generation of ketones is a normal response to fasting, which follows the depletion of hepatic glycogen stores. Let us discuss normal physiology for a change. You, a healthy adult without serious alcohol problems, are fasting from midnight for a routine elective hernia repair. You will go to be after dinner with a few nice lumps of undigested food in your intestine, as well as about 75g of hepatic glycogen. As you sleep, you gradually digest the food and dip into the glycogen store. At Continue reading >>

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