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Difference Between Lactic Acidosis And Ketoacidosis

To Initiate Synjardy Or Synjardy Xr, Determine Appropriate Combination Of The Active Ingredient Of Jardiance And Metformin*

To Initiate Synjardy Or Synjardy Xr, Determine Appropriate Combination Of The Active Ingredient Of Jardiance And Metformin*

Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Symptoms included malaise, myalgias, respiratory distress, somnolence, and abdominal pain. Laboratory abnormalities included elevated blood lactate levels, anion gap acidosis, increased lactate/pyruvate ratio, and metformin plasma levels generally >5 mcg/mL. Risk factors include renal impairment, concomitant use of certain drugs, age ≥65 years old, radiological studies with contrast, surgery and other procedures, hypoxic states, excessive alcohol intake, and hepatic impairment. Steps to reduce the risk of and manage metformin-associated lactic acidosis in these high risk groups are provided in the Full Prescribing Information. If lactic acidosis is suspected, discontinue SYNJARDY or SYNJARDY XR and institute general supportive measures in a hospital setting. Prompt hemodialysis is recommended. JARDIANCE is indicated to reduce the risk of cardiovascular (CV) death in adults with type 2 diabetes mellitus and established CV disease. JARDIANCE, SYNJARDY, AND SYNJARDY XR are indicated as adjuncts to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. SYNJARDY and SYNJARDY XR are indicated when both empagliflozin and metformin hydrochloride are appropriate. Empagliflozin, a component of SYNJARDY AND SYNJARDY XR, is indicated to reduce the risk of CV death in adults with type 2 diabetes mellitus and established CV disease. However, the effectiveness of SYNJARDY AND SYNJARDY XR on reducing the risk of CV death in adults with type 2 diabetes mellitus and CV disease has not been established. JARDIANCE, SYNJARDY, AND SYNJARDY XR are not recommended for patients with type 1 diabetes or for the treatment of Continue reading >>

Lab Test

Lab Test

Initial evaluation and monitoring of diabetic ketoacidosis (DKA): Anion gap is > 10 mEQ/L in mild DKA and > 12 mEq/L in moderate to severe cases. After initial evaluation, calculate the anion gap every 2 to 4 hours to monitor resolution of acidosis. Initial evaluation of suspected hyperglycemic hyperosmolar state (HHS): About 50% of patients have an increased anion gap metabolic acidosis due to concomitant ketoacidosis and/or an increases in serum lactate levels. Suspected alcoholic ketoacidosis Suspected hypermagnesemia Suspected lactic acidosis Suspected metabolic acidosis Other conditions other than metabolic acidosis that could cause an elevated anion gap are: Dehydration, treatment with sodium salts of strong acids, treatment with sodium salts of antibiotics (e.g., penicillin, carbenicillin), alkalosis, decreased unmeasured cation (e.g., hypokalemia, hypocalcemia, hypomagnesemia), hyperalbuminemia, increased inorganic anion (e.g., phosphate, sulfate), laboratory error (e.g., falsely increased serum sodium falsely decreased serum chloride or bicarbonate). The anion gap may be lowered by one of three mechanisms: Increased unmeasured cation (e.g., hyperkalemia, hypercalcemia, hypermagnesemia, multiple myeloma, lithium intoxication, polymyxin B) By decreased unmeasured anion (e.g., hypoalbuminemia or bromide (Br-) intoxication) By laboratory error (e.g., falsely decreased serum sodium, falsely increased serum chloride or bicarbonate hyperviscosity, hyperlipidemia, dilutional studies). Calculation of the anion gap should be adjusted for albumin. The anion gap falls by approximately 2.5 mgEq/L for every 1 g/dL reduction in serum albumin concentrations. The anion gap is the measurement in the difference between the cations and the anions in the extra-cellular space. Altho Continue reading >>

Free Physiology Flashcards About Kidney Lect 13

Free Physiology Flashcards About Kidney Lect 13

Acedemia cannot exist without acidosis, but acidosis can exist at any blood pH if more than one disturbance is present; same thing for alkalosis/alkalemia An acidosis or alkalosis resulting from a primary change in the serum bicarbonate concentration What is the difference between acidosis and acidemia? Acidosis: pathophysiological process that tends to decrease blood pH; acidemia: arterial blood pH <7.36 What is the difference between alkalosis and alkalemia? Alkalosis: pathophysiological process that tends to decrease blood pH; alkalemia: arterial blood pH <7.36 An acidosis or alkalosis resulting from a primary change in the P CO2 The physiologic metabolic (renal) and respiratory changes to return the pH toward normal in response to a primary acidosis or alkalosis. Not completely; time course varies: buffering (minutes to 6 hours), respiratory (minutes to 12 hours), metabolic (24-72 hours) A single acid-base process (acidosis or alkalosis) and its expected compensation are present two or more primary acid base disturbances are present. The arterial blood pH will depend on the direction and magnitude of the disturbances What is the primary process and compensation in metabolic acidosis? Primary process: decreased HCO3-; Compensation: decrease PCO2 What is the primary process and compensation in metabolic alkalosis? Primary process: increased HCO3-; Compensation: increase PCO2 What is the primary process and compensation in respiratory acidosis? Primary process: increased PCO2; Compensation: increase [HCO3-] What is the primary process and compensation in respiratory alkalosis? Primary process: decreased PCO2; Compensation: decreased [HCO3-] Metabolic acidoses are categorized on the basis of ... the anion that accumulates replacing the bicarbonate ioninto hyperchloremi Continue reading >>

Hyperchloremic Acidosis During The Recovery Phase Of Diabetic Ketosis

Hyperchloremic Acidosis During The Recovery Phase Of Diabetic Ketosis

Hyperchloremic Acidosis During the Recovery Phase of Diabetic Ketosis MAN S. OH, M.D.; HUGH J. CARROLL, M.D.; DAVID A. GOLDSTEIN, M.D.; I. ALAN FEIN, M.D. Author, Article, and Disclosure Information Requests for reprints should be addressed to Man S. Oh, M.D.; Box 21, Downstate Medical Center, 450 Clarkson Ave.; Brooklyn, NY 11203. We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis is a state of insulin deficiency, characterised by rapid onset, extreme metabolic acidosis, a generally intact sensorium, and only mild hyperglycaemia. DKA comes up frequently in the CICM SAQs, but usually as an ABG interpretation exercise. This chapter focuses on the medical side of DKA, including its causes, manifestations, complications, and management strategies. Questions which have required such thinking have included the following: Question 1 from the second paper of 2016 (differences between HONK and DKA) Question 17 from the first paper of 2014 (differences between HONK and DKA) Question 2 from the second paper of 2009 (general approach to management) Question 15 from the second paper of 2000 (whether or not saline is appropriate) Definition of diabetic ketoacidosis How does one discriminate between DKA and HONK even when in about 30% of instances the two disorders coexist? Arbitrary definitions exist, proposed by the American Diabetes Association. In summary: DKA presents with acidosis as the major feature HONK presents with hyperglycaemia as the major feature Discriminating Between HONK and DKA Domain Features suggestive of DKA Features suggestive of HONK Demographic Young Known Type 1 diabetic Elderly Known Type 2 diabetic History Rapid clinical course History of noncompliance with insulin Abdominal pain Shortness of breath Prolonged course History of noncompliance with oral antihyperglycaemic agents and insulin Polydipsia, polyuria, weight loss Neurological symptoms Examination Tachypnoea Normal level of consciousness, or only slightly decreased Coma Seizures Biochemistry Severe acidosis Severe ketosis Mild hyperglycaemia Renal function normalises rapidly Mild acidosis Little ketosis; mainly lactate is raised Severe hyperglycaemia Esta Continue reading >>

Lactic Acidosis: What You Need To Know

Lactic Acidosis: What You Need To Know

Lactic acidosis is a form of metabolic acidosis that begins in the kidneys. People with lactic acidosis have kidneys that are unable to remove excess acid from their body. If lactic acid builds up in the body more quickly than it can be removed, acidity levels in bodily fluids — such as blood — spike. This buildup of acid causes an imbalance in the body’s pH level, which should always be slightly alkaline instead of acidic. There are a few different types of acidosis. Lactic acid buildup occurs when there’s not enough oxygen in the muscles to break down glucose and glycogen. This is called anaerobic metabolism. There are two types of lactic acid: L-lactate and D-lactate. Most forms of lactic acidosis are caused by too much L-lactate. Lactic acidosis has many causes and can often be treated. But if left untreated, it may be life-threatening. The symptoms of lactic acidosis are typical of many health issues. If you experience any of these symptoms, you should contact your doctor immediately. Your doctor can help determine the root cause. Several symptoms of lactic acidosis represent a medical emergency: fruity-smelling breath (a possible indication of a serious complication of diabetes, called ketoacidosis) confusion jaundice (yellowing of the skin or the whites of the eyes) trouble breathing or shallow, rapid breathing If you know or suspect that you have lactic acidosis and have any of these symptoms, call 911 or go to an emergency room right away. Other lactic acidosis symptoms include: exhaustion or extreme fatigue muscle cramps or pain body weakness overall feelings of physical discomfort abdominal pain or discomfort diarrhea decrease in appetite headache rapid heart rate Lactic acidosis has a wide range of underlying causes, including carbon monoxide poisoni Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Continue reading >>

Acid/base Disorders: Metabolic Acidosis

Acid/base Disorders: Metabolic Acidosis

Are there clinical practice guidelines to inform decision-making? Does this patient have metabolic acidosis? Metabolic acidosis is generally defined by the presence of a low serum bicarbonate concentration (normal range 22-28 mEq/L), although occasionally states can exist where the serum bicarbonate is normal with an elevated anion gap (e.g., patients with a lactic acidosis who have received a bicarbonate infusion or patients on hemodialysis). In general, a metabolic acidosis is associated with a low urine pH but depending on the presence or absence of a respiratory alkalosis, this may also be normal or elevated. Thus, a patient can have an acidosis but not be acidemic. Metabolic acidoses occur when there is excess acid in the plasma. In the basal state, the body generates about 12,000 to 13,000 mmol of carbon dioxide (CO2), and 1-1.5 mmol per kilogram body weight of nonvolatile acid. The body has a large buffering capacity, with CO2-HCO3 as the major buffer system. The two major routes of acid excretion are the lungs (for CO2) and the kidneys (for nonvolatile acids) A metabolic acidosis can be caused by three major mechanisms: 1) increased acid production; 2) bicarbonate loss; and 3) decreased renal acid excretion Increased acid production leads to anion-gap (AG) metabolic acidosis, and involves a variety of different clinical processes, see An anion gap acidosis may also result for ingestion of an acid load. Both bicarbonate loss and decreased renal acid excretion lead to normal-anion gap (NG) metabolic acidosis. When there is HCO3 loss, chloride is retained to maintain electrical neutrality. The different clinical processes are summarized in Toxic ingestions are common causes of AG metabolic acidosis. The commonest causes are methanol and ethylene glycol intoxicatio Continue reading >>

Dka In Hypoglycemia

Dka In Hypoglycemia

#2 0 They are two different entities. While they will both cause acidosis the mechanism of acidosis is different. DKA is from ketosis and acidosis from Hypoglycamia is lactic acid. Is this what you are asking? 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. 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. Diabetic Ketoacidosis Causes, Symptoms, and Treatment by eMedicineHealth.com An insulin reaction occurs when a person with diabetes becomes confused or even unconscious because of hypoglycemia (hypo=low + glycol = sug Continue reading >>

Ketosis & Acidosis

Ketosis & Acidosis

Ketosis occurs when the fat in your body does not break down completely, producing ketones. It's a condition that can occur when you go on a low-carb diet and glycogen stores in your liver are depleted. When you have too much acid in your system, you can develop acidosis. The acid build-up can take place in your kidneys or lungs for a variety of reasons. The build-up of ketones can cause an imbalance that leads to excessive acid production. Video of the Day Diabetics may be prone to ketosis or acidosis when insulin levels drop below healthy levels or when ketones build up in the body due to uncontrolled insulin levels. Ketones are the byproduct produced when the body relies primarily on fat stores for energy. While short-term ketosis can help you lose weight, ketones that continue to build up in your blood and urine are poisonous and lead to diabetic ketoacidosis, also referred to as diabetic acidosis. The condition is a more common complication of Type 1 diabetes. In addition to low insulin levels, trauma, severe infection, a heart attack or surgery can lead to diabetic ketoacidosis. Diabetic acidosis requires immediate medical attention. As insulin levels drop, your body produces blood sugar by uncontrollably burning fat. Your body turns acidic as glucose begins to appear in your urine. As your body tries to find a balance, your breathing becomes deeper and quicker, leading to a temporary balance as you blow off excess carbon dioxide. Symptoms may start with confusion, thirst, fatigue and increased urination. You may become unconscious. As acidosis progresses, you can smell acetone on your breath. Symptoms usually appear quickly, so you should seek emergency treatment. A high fat and high protein diet that's low in carbohydrates can lead to ketosis. At the same time, Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea 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 >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Clinical Aspects Of The Anion Gap

Clinical Aspects Of The Anion Gap

The anion gap (AG) is a calculated parameter derived from measured serum/plasma electrolyte concentrations. The clinical value of this calculated parameter is the main focus of this article. Both increased and reduced anion gap have clinical significance, but the deviation from normal that has most clinical significance is increased anion gap associated with metabolic acidosis. This reflects the main clinical utility of the anion gap, which is to help in elucidating disturbances of acid-base balance. The article begins with a discussion of the concept of the anion gap, how it is calculated and issues surrounding the anion gap reference interval. CONCEPT OF THE ANION GAP - ITS DEFINITION AND CALCULATION Blood plasma is an aqueous (water) solution containing a plethora of chemical species including some that have a net electrical charge, the result of dissociation of salts and acids in the aqueous medium. Those that have a net positive charge are called cations and those with a net negative charge are called anions; collectively these electrically charged species are called ions. The law of electrochemical neutrality demands that, in common with all solutions, blood serum/plasma is electrochemically neutral so that the sum of the concentration of cations always equals the sum of the concentration of anions [1]. This immutable law is reflected in FIGURE 1, a graphic display of the concentration of the major ions normally present in plasma/serum. It is clear from this that quantitatively the most significant cation in plasma is sodium (Na+), and the most significant anions are chloride (Cl-) and bicarbonate HCO3-. The concentration of these three plasma constituents (sodium, chloride and bicarbonate) along with the cation potassium (K+) are routinely measured in the clinica Continue reading >>

Methamphetamine Overdose And Metabolic Acidosis

Methamphetamine Overdose And Metabolic Acidosis

Begin your recovery from addiction today. Change starts with one call. (855) 837-1334 Brought to you by Elements Behavioral Health Methamphetamine Overdose and Metabolic Acidosis Posted in Stimulants by Arny Escobar Metabolic acidosis is a term used to describe the buildup of excessive amounts of acid in the bodys various fluids. In some cases, this buildup stems from excessive acid production inside the body; in other cases, it stems from the kidneys inability to eliminate sufficient amounts of acid from the bloodstream. Whatever the underlying cause, unchecked metabolic acidosis can kill an affected individual. People who use/abuse the illegal street drug methamphetamine can develop metabolic acidosis during the course of a drug overdose. The condition arises as an end result of an unsustainable methamphetamine-related increase in body temperature. Doctors refer to the relative acidity of the human body as the bodys pH level. If this level falls too low, the internal environment becomes too acidic to support good health; if the pH level rises too high, the internal environment becomes too alkaline to support good health. Relative pH is measured on a scale of 0 to 14. A pH level between 0 and 7 falls within the acidic range of this scale, while a pH level between 7 and 14 falls within the alkaline range of the scale. Under normal circumstances, the pH level of human blood falls somewhere between 7.35 and 7.45, which means it has a slightly alkaline quality. Levels that fall below 6.8 or rise above 7.8 can kill a human being. Metabolic acidosis is actually a general term that groups together several specific types of acidosis, including conditions called lactic acidosis, diabetic acidosis and hyperchloremic acidosis. Lactic acidosis occurs when the body contains too mu Continue reading >>

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