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Diabetic Ketoacidosis Pathophysiology

Pathophysiology Of Diabetic Ketoacidosis : Animation

Pathophysiology Of Diabetic Ketoacidosis : Animation

When the rate of synthesis of ketone bodies exceeds the rate of utilization, their concentration in blood increases, this is known as ketonemia. This is followed by ketonuria – excretion of ketone bodies in urine. The overall picture of ketonemia and ketonuria is commonly referred to as ketosis. Mechanism: Hyperglycaemia occurs due to decreased glucose uptake in fat and muscle cells due to insulin deficiency Lipolysis in fat cells now occurs promoted by the insulin deficiency releasing Free fatty acids (FFA) into the blood which provide substrate to the liver A switch in hepatic lipid metabolism occurs due to the insulin deficiency and the glucagon excess, so the excess FFA is metabolised resulting in excess production of acetyl CoA The excess hepatic acetyl CoA (remaining after saturation of TCA cycle) is converted to ketone bodies which are released into the blood Ketoacidosis and hyperglycaemia both occur due to the lack of insulin and the increase in glucagon and most of the clinical effects follow from these two factors 1. ↓ Insulin, ↑Glucogon (glycogen à glucose) - Glucose 500-700 mg/dl 2. Glucose-derived osmotic diuresis 3. ↑ Glucagon - ↑ FFA esterfied à ketone bodies à acidosis Diagnostic tests: Blood glucose greater than 250 mg/dL Blood pH less than 7.3 Blood bicarbonate less than 15 mEq/L Ketones present in blood (exceeds 90 mg/dl) Ketones excreted in urine exceeds 5000 mg/24 hrs Signs and Symptoms: Kussmal's respiration Fruity odor of breath Nausea and abdominal pain Dehydration Lethargy Coma Polydipsia, polyuria, polyphagia Read more Ketone bodies, Ketosis and Ketoacidosis | Medchrome Continue reading >>

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Laboratory tests, including blood and urine tests, are used to confirm a diagnosis of diabetic ketoacidosis. Tests for ketones are available for home use. Keep some test strips nearby in case your blood sugar level becomes high. When ketoacidosis is severe, it must be treated in the hospital, often in an intensive care unit. Treatment involves giving insulin and fluids through your vein and closely watching certain chemicals in your blood (electrolyt Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

Diabetic Ketoacidosis: Pathophysiology, Management And Complications

Diabetic Ketoacidosis: Pathophysiology, Management And Complications

Diabetic ketoacidosis (DKA) is a common and potentially life-threatening complication of diabetes mellitus, the second most common chronic childhood disease [1]. Prior to the introduction of insulin to clinical medicine by Banting and Best in 1922, DKA had a mortality rate greater than 60% [2]. As insulin was introduced into clinical practice, there was a gradual decrease in mortality associated with DKA over the subsequent 30 years. Recent epidemiological data reveal current mortality varies from 0 to 19% [3,4]. DKA continues to be the most common cause of death in patients younger than 24 years of age; it accounts for as many as 50% of deaths of young diabetic patients [5–7]. In elderly diabetics who have coexisting diseases, DKA carries a high mortality [8]. Despite many advances in the care of diabetic patients, the prevalence of DKA is not declining; it accounts for 14% of all diabetes-related hospital admissions [3, 4, 9]. The incidence of insulin-dependent diabetes mellitus continues to increase worldwide and has roughly doubled in each recent decade [10–13]. Because insulin-dependent diabetes mellitus is increasing, and preventative measures to avoid DKA in diabetic patients have not been successful, the incidence of DKA can also be expected to increase in coming years. Prevention of DKA is the ultimate goal (80% of hospital admissions for DKA occur in treated diabetics) [3,8]. It is necessary for clinicians to understand the pathophysiology and treatment of DKA to care for this increasing diabetic population. We discuss the pathophysiology of diabetic ketoacidosis, its management, and its complications. 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 >>

What Are Symptoms Of Diabetes Complications?

What Are Symptoms Of Diabetes Complications?

Complications of Diabetes can be many and while the pathophysiology is deeply satisfying to learn because it incorporates so many different aspects of pathology & physiology. I will simply just line a simple overview of some of the most common complications of Diabetes. In acute / short term complications, these two are the most prominent: In Type I DM - Ketoacidosis is a terrible complication that results from the production of ketone bodies that acidify the blood when the brain is going hungry and needs ketones to fuel it. In Type II DM, we tend to see complications of Hyperosmolar Hyperglycemic Coma. In the long term or chronic long standing uncontrolled Diabetes, we can see complications such as: Blindness Kidney Diseases Nerve Damage Amputations Heart Attack / Stroke Hope that helps! Continue reading >>

How Does Diabetic Ketoacidosis Develop?

How Does Diabetic Ketoacidosis Develop?

Diabetic ketoacidosis, DKA, is a serious, life-threatening condition that can cause a diabetic coma and possibly death. It develops when the body does not get enough sugar in order to produce energy because of a lack of insulin. This causes the body to start using stored fat for energy. According to WebMD, when the body cannot convert the sugar into energy, it stays inside of the bloodstream (WebMD, 2017). This causes the kidneys to filter some of the sugar from the blood into the urine. This causes ketones to be released from the breakdown of fat, making the blood’s pH level to become acidic. DKA is a condition that should not be taken lightly. It can cause several different problems inside of the body. It is very important that you take care of your body in order to prevent the development of DKA. How does DKA start? WebMD said, “Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things” (WebMD, 2017). There are things that you can control. Frequent communication with your doctor will assist you in determining how much insulin you should take and when. If you keep taking it consistently and on time, it will help immensely. It is difficult to control if you get a severe infection or illness. However, you do have control on how you will react. Do not be afraid to go to the doctor. Get the medical treatment that you need so it does not become much worse. DKA can also be caused by dehydration. Drinking water is a great way to prevent dehydration. Also, cutting out beverages like soda can also help a ton! Focusing more on water will also help you to cut out unnecessary sodium, trans fats, and sugars that you do not need. By drinking healthier, it will make yo Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, And Preventable Safety Concern With Sglt2 Inhibitors

Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, And Preventable Safety Concern With Sglt2 Inhibitors

The Case At Hand Recently, the U.S. Food and Drug Administration (FDA) issued a Drug Safety Communication that warns of an increased risk of diabetic ketoacidosis (DKA) with uncharacteristically mild to moderate glucose elevations (euglycemic DKA [euDKA]) associated with the use of all the approved sodium–glucose cotransporter 2 (SGLT2) inhibitors (1). This Communication was based on 20 clinical cases requiring hospitalization captured between March 2013 and June 2014 in the FDA Adverse Event Reporting System database. The scarce clinical data provided suggested that most of the DKA cases were reported in patients with type 2 diabetes (T2D), for whom this class of agents is indicated; most likely, however, they were insulin-treated patients, some with type 1 diabetes (T1D). The FDA also identified potential triggering factors such as intercurrent illness, reduced food and fluid intake, reduced insulin doses, and history of alcohol intake. The following month, at the request of the European Commission, the European Medicines Agency (EMA) announced on 12 June 2015 that the Pharmacovigilance Risk Assessment Committee has started a review of all of the three approved SGLT2 inhibitors (canagliflozin, dapagliflozin, and empagliflozin) to evaluate the risk of DKA in T2D (2). The EMA announcement claimed that as of May 2015 a total of 101 cases of DKA have been reported worldwide in EudraVigilance in T2D patients treated with SGLT2 inhibitors, with an estimated exposure over 0.5 million patient-years. No clinical details were provided except for the mention that “all cases were serious and some required hospitalisation. Although [DKA] is usually accompanied by high blood sugar levels, in a number of these reports blood sugar levels were only moderately increased” (2). Wit Continue reading >>

Current Concepts In The Pathophysiology And Management Of Diabetic Ketoacidosis

Current Concepts In The Pathophysiology And Management Of Diabetic Ketoacidosis

Abstract Recent studies indicate that for the development of diabetic ketoacidosis glucagon excess is essential in addition to a deficiency of insulin. Glucagon activates the carnitine acyl transferase I leading to ketonemia. Low dose continuous infusion of insulin appears to be the ideal mode of therapy for the correction of hyperglycemia. The use of sodium bicarbonate and phosphate as adjuvants in management is discussed in the light of recent observations. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious complication of diabetes mellitus. Before the availability of insulin in the 1920s, DKA was a uniformly fatal disorder. Even after the discovery of insulin, DKA continued to carry a grave prognosis with a reported mortality rate in humans ranging from 10% to 30%. However, with the expanding knowledge regarding the pathophysiology of DKA and the application of new treatment techniques for the complications of DKA, the mortality rate for this disorder has decreased to less than 5% in experienced human medical centers (Kitabchi et al, 2008). We have experienced a similar decrease in the mortality rate for DKA in our hospital over the past two decades. DKA remains a challenging disorder to treat, in part because of the deleterious impact of DKA on multiple organ systems and the frequent occurrence of concurrent often serious disorders that are responsible for the high mortality rate of DKA. In humans, the incidence of DKA has not decreased, appropriate therapy remains controversial, and patients continue to succumb to this complication of diabetes mellitus. This chapter summarizes current concepts regarding the pathophysiology and management of DKA in dogs and cats. • Diabetic ketoacidosis (DKA) is a severe form of complicated diabetes mellitus that requires emergency care. • Acidosis and electrolyte abnormalities can be life threatening. • Fluid therapy and correction of electrolyte abnormalities are the two most important components of therapy. • Concurrent disease increases the risk for DKA and must be addressed as part of the diagnostic and therapeutic plan. • Bicarbonate therapy usually is not needed and its use is controversial. • About 70% of treated dogs and cats are discharged from the hospital after 5 to 6 days Continue reading >>

How Does A Diabetic Ketoacidosis State Differ From A Hyperosmolar Hyperglycemic State?

How Does A Diabetic Ketoacidosis State Differ From A Hyperosmolar Hyperglycemic State?

A difficult question to answer, but try to put it in a simple way. Both are same but slightly differ. The root cause of DKA and HHS is lack of insulin effect, so the first key aim of treatment is insulin. While subcutaneous insulin may suffice in less severe cases, intravenous administration is to be preferred in more severe cases because severe dehydration and hypovolemia may interfere with the absorption of subcutaneous insulin. Use of insulin pumps must be carefully monitored by trained staff. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. 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. Electrolyte disturbances result from loss of water usually in excess of salt loss; hypovolaemia and severe intravascular dehydration will be accompanied by tachycardia and may give rise to thromboembolic complications (such as stroke or myocardial infarction), whereas cellular dehydration may ultimately cause the hyperosmolar coma. My Mother died on July 13th -2017 7.56 PM because of the same. Diabetic ketoacidosis is the characteristic metabolic emergency of t 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 >>

Acute Complications Of Diabetes - Diabetic Ketoacidosis

Acute Complications Of Diabetes - Diabetic Ketoacidosis

- [Voiceover] Oftentimes we think of diabetes mellitus as a chronic disease that causes serious complications over a long period of time if it's not treated properly. However, the acute complications of diabetes mellitus are often the most serious, and can be potentially even life threatening. Let's discuss one of the acute complications of diabetes, known as diabetic ketoacidosis, or DKA for short, which can occur in individuals with type 1 diabetes. Now recall that type 1 diabetes is an autoimmune disorder. And as such, there's an autoimmune destruction of the beta cells in the pancreas, which prevents the pancreas from producing and secreting insulin. Therefore, there is an absolute insulin deficiency in type 1 diabetes. But what exactly does this mean for the body? To get a better understanding, let's think about insulin requirements as a balancing act with energy needs. Now the goal here is to keep the balance in balance. As the energy requirements of the body go up, insulin is needed to take the glucose out of the blood and store it throughout the body. Normally in individuals without type 1 diabetes, the pancreas is able to produce enough insulin to keep up with any amount of energy requirement. But how does this change is someone has type 1 diabetes? Well since their pancreas cannot produces as much insulin, they have an absolute insulin deficiency. Now for day-to-day activities, this may not actually cause any problems, because the small amount of insulin that is produced is able to compensate and keep the balance in balance. However, over time, as type 1 diabetes worsens, and less insulin is able to be produced, then the balance becomes slightly unequal. And this results in the sub-acute or mild symptoms of type 1 diabetes such as fatigue, because the body isn Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

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 >>

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