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Starvation Ketoacidosis Medscape

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 >>

Reference Range

Reference Range

Acetoacetate, beta-hydroxybutyrate, and acetone are ketone bodies. In carbohydrate-deficient states, fatty-acid metabolism spurs acetoacetate accumulation. The reduction of acetoacetate in the mitochondria results in beta-hydroxybutyrate production. Beta-hydroxybutyrate and acetoacetate, the predominant ketone bodies, are rich in energy. Beta-hydroxybutyrate and acetoacetate transport energy from the liver to other tissues. Acetone forms from the spontaneous decarboxylation of acetoacetate. Acetone is the cause of the sweet odor on the breath in persons with ketoacidosis. [1, 2] Ketone bodies fuel the brain with an alternative source of energy (close to two thirds of its needs) during periods of prolonged fasting or starvation, when the brain cannot use fatty acids for energy. The reference range for ketone is a negative value, at less than 1 mg/dL (< 0.1 mmol/L). [3] Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. 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 >>

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 >>

Ketotic Hypoglycemia

Ketotic Hypoglycemia

Ketotic hypoglycemia is a medical term used in two ways: (1) broadly, to refer to any circumstance in which low blood glucose is accompanied by ketosis, and (2) in a much more restrictive way to refer to recurrent episodes of hypoglycemic symptoms with ketosis and, often, vomiting, in young children. The first usage refers to a pair of metabolic states (hypoglycemia plus ketosis) that can have many causes, while the second usage refers to a specific "disease" called ketotic hypoglycemia. Hypoglycemia with ketosis: the broad sense[edit] There are hundreds of causes of hypoglycemia. Normally, the defensive, physiological response to a falling blood glucose is reduction of insulin secretion to undetectable levels, and release of glucagon, adrenaline, and other counterregulatory hormones. This shift of hormones initiates glycogenolysis and gluconeogenesis in the liver, and lipolysis in adipose tissue. Lipids are metabolized to triglycerides, in turn to fatty acids, which are transformed in the mitochondria of liver and kidney cells to the ketone bodies— acetoacetate, beta-hydroxybutyrate, and acetone. Ketones can be used by the brain as an alternate fuel when glucose is scarce. A high level of ketones in the blood, ketosis, is thus a normal response to hypoglycemia in healthy people of all ages. The presence or absence of ketosis is therefore an important clue to the cause of hypoglycemia in an individual patient. Absence of ketosis ("nonketotic hypoglycemia") most often indicates excessive insulin as the cause of the hypoglycemia. Less commonly, it may indicate a fatty acid oxidation disorder. Ketotic hypoglycemia in Glycogen storage disease[edit] Some of the subtypes of Glycogen storage disease show ketotic hypoglycemia after fasting periods. Especially Glycogen storage Continue reading >>

Invokana Lawsuit

Invokana Lawsuit

The Food and Drug Administration has recently issued a Black Box warning about Invokana and the risk of amputation. Other safety concerns have been raised over serious side effects such as severe urinary tract infection, kidney failure and heart attack. If you or a loved one have been harmed after taking Invokana, you may be eligible to file an Invokana lawsuit. Should I talk to a lawyer about the experience I had with the drug Invokana? If you or a loved one used the type 2 diabetes medication Invokana, you might be eligible for financial compensation. Some Invokana users have required amputation of the leg, foot or toe after using the drug. Others have developed diabetic ketoacidosis or suffered other side effects such as severe kidney infection, heart attack or stroke after taking Invokana. Invokana (canagliflozin) is an SGLT2 inhibitor, which is a type of medication that works by lowering blood glucose levels. It does this by encouraging higher amounts of sugar to be released through urine. Though the medication does help control blood sugar levels, it triggers a number of other side effects, many of which are severe. Some Invokana users experienced cardiovascular issues including heart attacks and strokes, as well as diabetic ketoacidosis and kidney health issues. Final results from two clinical studies, CANVAS and CANVAS-R have shown that use of Invokana may double the risk for limb amputation and have prompted the FDA to release a black box warning about the risk. For some, the use of Invokana triggered side effects so severe they needed hospitalization. Others suffered permanent disability. In response to these devastating medical emergencies, many Invokana users have opted to take legal action against the makers of the drug. Both Janssen Pharmaceuticals and its Continue reading >>

What Is Ketosis?

What Is Ketosis?

"Ketosis" is a word you'll probably see when you're looking for information on diabetes or weight loss. Is it a good thing or a bad thing? That depends. Ketosis is a normal metabolic process, something your body does to keep working. When it doesn't have enough carbohydrates from food for your cells to burn for energy, it burns fat instead. As part of this process, it makes ketones. If you're healthy and eating a balanced diet, your body controls how much fat it burns, and you don't normally make or use ketones. But when you cut way back on your calories or carbs, your body will switch to ketosis for energy. It can also happen after exercising for a long time and during pregnancy. For people with uncontrolled diabetes, ketosis is a sign of not using enough insulin. Ketosis can become dangerous when ketones build up. High levels lead to dehydration and change the chemical balance of your blood. Ketosis is a popular weight loss strategy. Low-carb eating plans include the first part of the Atkins diet and the Paleo diet, which stress proteins for fueling your body. In addition to helping you burn fat, ketosis can make you feel less hungry. It also helps you maintain muscle. For healthy people who don't have diabetes and aren't pregnant, ketosis usually kicks in after 3 or 4 days of eating less than 50 grams of carbohydrates per day. That's about 3 slices of bread, a cup of low-fat fruit yogurt, or two small bananas. You can start ketosis by fasting, too. Doctors may put children who have epilepsy on a ketogenic diet, a special high-fat, very low-carb and protein plan, because it might help prevent seizures. Adults with epilepsy sometimes eat modified Atkins diets. Some research suggests that ketogenic diets might help lower your risk of heart disease. Other studies show sp Continue reading >>

Mcq Masterset Krom Flashcards | Quizlet

Mcq Masterset Krom Flashcards | Quizlet

- Renal effects - mild proteinuuria & HTN - Widespread - RA, cancer, B cell lymphoma, Crohn's, anti-platelet, MS, psoriasis, severe allergic asthma, osteoporosis,organ transplant, ank spond, nocturnal haematuria, pain (bony) 8 hrs after 1 dose, 14 after multiple- doubles in severe renal impairment; steady state reached at 3 days. Dose dep in crease in aPTT & PT, thrombin time but wide variation. Normal thrombin clotting time exclude clinical effect. Fentanyl Patch - What is time to reach peak concentration? Transdermal drug delivery system, duration 72 hrs. Rectangular patch, rounded corners with backing layer and fentanyl containing silicone layer. Strengths dep on area. 12.5mcg/25/50/75/100 per hour. After initial patch application serum levels increase until 12-24hrs then remain stable until 72 hrs. (Model suggests adding a new patch after 24 hrs will increase levels still) Mean half life after 72hr patch is 24 hrs (IV doses 3-12 hrs; slower transdermally due to ongoing slow absorption from skin)) Most common cause of epidural catheter related infection Staph aureus - as per Oxford Handbook & google search A patient known to have porphyria is inadvertently administered thiopentone on induction of anaesthesia. In recovery the patient complains of abdominal pain prior to having a seizur and losing consciousness. Which drug should NOT be given Porphyria = group of disease with enzyme defect in harm synthesis leading to accumulation of porphyrins. Porphyrins (purple) are organic substances with particular sturcuture; porphyrins with iron called harm. There are hepatic & erythoropoietic types of porphyria. Only the heaptic types affect anaesthesia - Acute intermittent porphyrins - common & variaegate & heridatory coroporphyria. Issue - Anaesthetic drugs + peri-op stress Continue reading >>

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment Of Alcoholic Ketoacidosis

Exenatide extended-release causes an increased incidence in thyroid C-cell tumors at clinically relevant exposures in rats compared to controls. It is unknown whether BYDUREON BCise causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of exenatide extended-release-induced rodent thyroid C-cell tumors has not been determined BYDUREON BCise is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with the use of BYDUREON BCise and inform them of symptoms of thyroid tumors (eg, mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for detection of MTC in patients treated with BYDUREON BCise Acute Pancreatitis including fatal and non-fatal hemorrhagic or necrotizing pancreatitis has been reported. After initiation, observe patients carefully for symptoms of pancreatitis. If suspected, discontinue promptly and do not restart if confirmed. Consider other antidiabetic therapies in patients with a history of pancreatitis Acute Kidney Injury and Impairment of Renal Function Altered renal function, including increased serum creatinine, renal impairment, worsened chronic renal failure, and acute renal failure, sometimes requiring hemodialysis and kidney transplantation have been reported. Not recommended in patients with severe renal impairment or end-stage renal disease. Use caution in patients with renal transplantation or moderate renal impairment Gastrointestinal Disease Because exenatide is commonly associated with gastrointestinal adverse reactions, not recommended in patients with sev Continue reading >>

The Lowly Urinalysis: How To Avoid Common Pitfalls

The Lowly Urinalysis: How To Avoid Common Pitfalls

You are at: Home More Departments Clinical Focus The Lowly Urinalysis: How to Avoid Common Pitfalls The Lowly Urinalysis: How to Avoid Common Pitfalls You may think you know everything about the humble pee test, but there are subtleties you might be missing. A 53-year-old female presents with malodorous urine. She denies dysuria, urgency, incontinence, and frequency, but she is concerned for UTI. She had one UTI several years ago, but at that time had dysuria and urgency. A urinalysis sent from triage demonstrates 3 WBCs, trace LE, and 2 squamous cells, but nitrites are negative. A diagnosis of UTI is made. Is this the right call? URINALYSIS/URINE DIPSTICK AND ITS COMPONENTS Urinalysis and urine dipstick are commonly ordered tests in the ED and can be useful in many clinical conditions, including urolithiasis and urinary tract infection (UTI). [1-5] Where can we go wrong? You may think you know how to interpret these tests, but there are several subtleties. In this article well evaluate several components, including bedside analysis, dipstick, and pitfalls in analysis (especially in UTI). The most common collection method is midstream cleancatch into a clean dry container, while others include urethral catheterization or suprapubic aspiration. [2,3,6,7] Though external cleaning is usually recommended for midstream collection, it really does not have proven benefit in decreasing contamination. [1,3] One study found contamination rates were similar between those with and without cleansing. [6] Even with external cleansing, close to 30% of samples are contaminated. [6] Once urine is collected, it should be rapidly analyzed, as bacteria can proliferate in warm urine. If the sample cannot be analyzed quickly, refrigeration is recommended. A delay of two hours or more can pr 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 >>

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 >>

Blood Ketones

Blood Ketones

On This Site Tests: Urine Ketones (see Urinalysis - The Chemical Exam); Blood Gases; Glucose Tests Elsewhere On The Web Ask a Laboratory Scientist Your questions will be answered by a laboratory scientist as part of a voluntary service provided by one of our partners, the American Society for Clinical Laboratory Science (ASCLS). Click on the Contact a Scientist button below to be re-directed to the ASCLS site to complete a request form. If your question relates to this web site and not to a specific lab test, please submit it via our Contact Us page instead. Thank you. Continue reading >>

Phosphate Salts Effectiveness, Safety, And Drug Interactions On Rxlist

Phosphate Salts Effectiveness, Safety, And Drug Interactions On Rxlist

Dosing considerations for Phosphate Salts. What other names is Phosphate Salts known by? Aluminum phosphate, Bone Phosphate, Calcium phosphate, Calcium Orthophosphate, Calcium Phosphate Dibasic Anhydrous, Calcium Phosphate-Bone Ash, Calcium Phosphate Dibasic Dihydrate, Calcium Phosphate Dibasique Anhydre, Calcium Phosphate Dibasique Dihydrate, Calcium Phosphate Tribasic, Calcium Phosphate Tribasique, Dibasic Calcium Phosphate Dihydrate, Di-Calcium Phosphate, Dicalcium Phosphate, Dicalcium Phosphates, Neutral Calcium Phosphate, Orthophosphate de Calcium, Phosphate d'Aluminium, Phosphate de Calcium, Phosphate de Magnsium, Phosphate Neutre de Calcium, Phosphate d'Os, Phosphate Tricalcium, Precipitated Calcium Phosphate, Prcipitation du Phosphate de Calcium, Prcipit de Phosphate de Calcium, Tertiary Calcium Phosphate, Tricalcium Phosphate, Whitlockite, Magnesium Phosphate, Merisier, Potassium phosphate, Dibasic Potassium Phosphate, Dipotassium Hydrogen Orthophosphate, Dipotassium Monophosphate, Dipotassium Phosphate, Monobasic Potassium Phosphate, Potassium Acid Phosphate, Potassium Biphosphate, Potassium Dihydrogen Orthophosphate, Potassium Hydrogen Phosphate, Phosphate de Dipotassium, Phosphate d'Hydrogne de Potassium, Phosphate de Potassium, Phosphate de Potassium Dibasique, Phosphate de Potassium Monobasique, Sodium phosphate, Anhydrous Sodium Phosphate, Dibasic Sodium Phosphate, Disodium Hydrogen Orthophosphate, Disodium Hydrogen Orthophosphate Dodecahydrate, Disodium Hydrogen Phosphate, Disodium Phosphate, Phosphate of Soda, Sales de Fosfato, Sels de Phosphate, Sodium Orthophosphate, Orthophosphate Disodique d'Hydrogne, Phosphate Disodique d'Hydrogne, Orthophosphate de Sodium, Phosphate de Sodium Anhydre, Phosphate de Sodium Dibasique, Phosphorus. Phosphate salts ref Continue reading >>

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