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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 >>

Pathophysiology Final Exam - Diabetes/dka

Pathophysiology Final Exam - Diabetes/dka

Sort Type I DM aka IDDM Onset within weeks or months of increased glucose levels Affects males:females 3:2 Age of onset <25 y/o Autoimmune disease -Body makes antibodies against insulin Low bodyweight Absent/low insulin levels Rare insulin resistance 50-60% genetics Very high ketosis Irreversible Risk factor -Insulin antibodies Type II DM Onset within months or years of increased glucose levels Affects females:males 3:2 Age of onset late teens - early 20s Lifestyle disease -Genetics, diet, physical activity Elevated bodyweight High insulin levels Very positive insulin resistance 90% genetics Positive ketosis Reversible Risk factors -Family history (concordance rate) -Age -Obesity -Pregnancy -Steroids -Diuretics -Ethnic background -ETOH -Pancreatic cancer Carbohydrate Metabolism Absorption of carbohydrate -Starts in the mouth Regulation -Blood sugar is kept down by insulin -4 counterregulatory hormones that keep blood sugar up --Glucagon --Adrenaline --Steroids --Growth hormone Storage -Glycogenesis --Formation of glycogen from glucose -Lipogenesis --Transformation of excess glucagon into fat Out of Storage -Glycolysis --Breakdown of glucagon into CO3, and H2O -Lipolysis --Breakdown of fat into ketones -Gluconeogenesis --Conversion of protein into calories -> NH3 Pathophysiology of DKA Lack of insulin -> Breakdown of fat for energy use -> Fats broken down into fatty acids -> Fatty acids converted to glucose in liver -> CNS breaks down fatty acids into ketones (increase acid in body) Excess glucose in circulation causes fluid to be pulled out of cells -> Intracellular dehydration -Kidneys try to compensate by excreting more glucose, but end up excreting valuable electrolytes Clinical Manifestations of DKA Polyuria Hypotension Tachycardia Weight loss Dry mucous membranes F 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 (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Cerebral Edema In Children With Diabetic Ketoacidosis

Cerebral Edema In Children With Diabetic Ketoacidosis

INTRODUCTION Cerebral edema (or cerebral injury) is an uncommon but potentially devastating consequence of diabetic ketoacidosis (DKA). It is far more common among children with DKA than among adults. Young children and those with newly diagnosed diabetes are at highest risk. Symptoms typically emerge during treatment for DKA, but may be present prior to initiation of therapy. The pathophysiology, diagnosis, and treatment of cerebral edema in children with DKA will be discussed here. The diagnosis and treatment of DKA in children is discussed separately. (See "Clinical features and diagnosis of diabetic ketoacidosis in children and adolescents" and "Treatment and complications of diabetic ketoacidosis in children and adolescents".) INCIDENCE Clinically significant cerebral edema occurs in approximately 1 percent of episodes of DKA in children and has a mortality rate of 20 to 90 percent [1-3]. Overall mortality rates for diabetic ketoacidosis (DKA) in children and adolescents range from 0.15 to 0.51 percent in national population studies in Canada, the United Kingdom, and the United States [4-9]; 50 to 80 percent of diabetes-related deaths are caused by cerebral edema [1,2,10]. Other causes of death from DKA include aspiration pneumonia, multiple organ failure, gastric perforation, and traumatic hydrothorax [5]. Subclinical brain swelling, as detected by ventricular narrowing on a computed tomography (CT) scan, has been reported in the majority of children with DKA in some studies [11,12], while others reported much smaller proportions [13]. All of these studies were limited by small numbers and lack of appropriate control groups. In a study of 41 children with DKA, the intercaudate width of the frontal horns of the lateral ventricles was measured by magnetic resonance 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 >>

Pathophysiology And Treatment

Pathophysiology And Treatment

The Kabod Volume 2 Issue 1 Fall 2015 Article 3 Diabetic Ketoacidosis: Pathophysiology and Treatment Laura E. Mumme Liberty University, [email protected] Follow this and additional works at: Part of the Medical Biochemistry Commons, and the Medical Physiology Commons Recommended Citations MLA: Mumme, Laura E. "Diabetic Ketoacidosis: Pathophysiology and Treatment," The Kabod 2. 1 (2015) Article 3. Liberty University Digital Commons. Web. [xx Month xxxx]. APA: Mumme, Laura E. (2015) "Diabetic Ketoacidosis: Pathophysiology and Treatment" The Kabod 2( 1 (2015)), Article 3. Retrieved from Turabian: Mumme, Laura E. "Diabetic Ketoacidosis: Pathophysiology and Treatment" The Kabod 2 , no. 1 2015 (2015) Accessed [Month x, xxxx]. Liberty University Digital Commons. Running head: DIABETIC KETOACIDOSIS 1 Diabetic Ketoacidosis Pathophysiology and Treatment Liberty University 1 Mumme: Diabetic Ketoacidosis Published by [email protected] University, 2015 DIABETIC KETOACIDOSIS 2 Diabetic Ketoacidosis: Pathophysiology and Treatment Diabetic ketoacidosis (DKA), also known as diabetic acidosis or diabetic coma, is a severe complication of diabetes mellitus (DM; Michel, 2011). More commonly seen in patients with type 1 diabetes (T1D), DKA results when lipid breakdown generates a surplus of acidic ketone bodies (Guven, Matfin, & Kuenzi, 2009). According to Dods (2013), DKA can be defined as a condition with “blood glucose greater than 250 mg/dL, blood bicarbonate less than 15 mEq/L, pH less than 7.35, ketonemia, and increased anion gap†(p. 266). The pathophysiology of DKA in patients with T1D will first be addressed, followed by a discussion of proper emergency treatment for this life-threatening condition. The three main abnormalities of DKA patients include hyperglycemia, 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 >>

Endocrine Pathophysiology Diabetes, Dka, Hhs

Endocrine Pathophysiology Diabetes, Dka, Hhs

Sort Life-threatening problem that affects people w/diabetes, occurs when body cannot use sugar for fuel because there is no insulin or not enough insulin. Fat is used for fuel instead. Waste products called ketones build up in blood/urine, levels are poisonous. Diabetic Ketoacidosis Continue reading >>

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

Diabetic Ketoacidosis

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr Continue reading >>

Understanding The Presentation Of Diabetic Ketoacidosis

Understanding The Presentation Of Diabetic Ketoacidosis

Hypoglycemia, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) must be considered while forming a differential diagnosis when assessing and managing a patient with an altered mental status. This is especially true if the patient has a history of diabetes mellitus (DM). However, be aware that the onset of DKA or HHNS may be the first sign of DM in a patient with no known history. Thus, it is imperative to obtain a blood glucose reading on any patient with an altered mental status, especially if the patient appears to be dehydrated, regardless of a positive or negative history of DM. In addition to the blood glucose reading, the history — particularly onset — and physical assessment findings will contribute to the formulation of a differential diagnosis and the appropriate emergency management of the patient. Pathophysiology of DKA The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA. Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are rece Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>

Diabetic Ketoacidosis: A Current Appraisal Of Pathophysiology And Management

Diabetic Ketoacidosis: A Current Appraisal Of Pathophysiology And Management

This is a current appraisal of new insights into the pathophysiology and management of diabetic ketoacidosis (DKA), including laboratory work-up, monitoring of insulin, and fluid management. This article also discussed the complications of DKA and its treatment, focusing on cerebral edema (CE). The author recommends that fluid deficits be replaced at an even rate over 48 h, not to exceed 4/L/m2/24 h. Regular insulin should be started at 0.1 units/kg/h (no bolus). In general, it is recommended that bicarbonate not be administered unless correction of a pH < 6.9 is necessary. To access this article, please choose from the options below 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 >>

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