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Dka Pathophysiology Diagram

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) should be suspected in ill patients with diabetes. If either DKA or HHS is diagnosed, precipitating factors must be sought and treated. DKA and HHS are medical emergencies that require treatment and monitoring for multiple metabolic abnormalities and vigilance for complications. A normal blood glucose does not rule out DKA in pregnancy. Ketoacidosis requires insulin administration (0.1 U/kg/h) for resolution; bicarbonate therapy should be considered only for extreme acidosis (pH7.0). Note to readers: Although the diagnosis and treatment of diabetic ketoacidosis (DKA) in adults and in children share general principles, there are significant differences in their application, largely related to the increased risk of life-threatening cerebral edema with DKA in children and adolescents. The specific issues related to treatment of DKA in children and adolescents are addressed in the Type 1 Diabetes in Children and Adolescents chapter, p. S153. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are diabetes emergencies with overlapping features. With insulin deficiency, hyperglycemia causes urinary losses of water and electrolytes (sodium, potassium, chloride) and the resultant extracellular fluid volume (ECFV) depletion. Potassium is shifted out of cells, and ketoacidosis occurs as a result of elevated glucagon levels and absolute insulin deficiency (in the case of type 1 diabetes) or high catecholamine levels suppressing insulin release (in the case of type 2 diabetes). In DKA, ketoacidosis is prominent, while in HHS, the main features are ECFV depletion and hyperosmolarity. Risk factors for DKA include new diagnosis of diabetes mellitus, insulin omission, infection, myocardial infarc Continue reading >>

Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus

Classification, Pathophysiology, Diagnosis And Management Of Diabetes Mellitus

University of Gondar, Ethopia *Corresponding Author: Habtamu Wondifraw Baynes Lecturer Clinical Chemistry University of Gondar, Gondar Amhara 196, Ethiopia Tel: +251910818289 E-mail: [email protected] Citation: Baynes HW (2015) Classification, Pathophysiology, Diagnosis and Management of Diabetes Mellitus. J Diabetes Metab 6:541. doi:10.4172/2155-6156.1000541 Copyright: © 2015 Baynes HW. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Abstract Diabetes Mellitus (DM) is a metabolic disorder characterized by the presence of chronic hyperglycemia either immune-mediated (Type 1 diabetes), insulin resistance (Type 2), gestational or others (environment, genetic defects, infections, and certain drugs). According to International Diabetes Federation Report of 2011 an estimated 366 million people had DM, by 2030 this number is estimated to almost around 552 million. There are different approaches to diagnose diabetes among individuals, The 1997 ADA recommendations for diagnosis of DM focus on fasting Plasma Glucose (FPG), while WHO focuses on Oral Glucose Tolerance Test (OGTT). This is importance for regular follow-up of diabetic patients with the health care provider is of great significance in averting any long term complications. Keywords Diabetes mellitus; Epidemiology; Diagnosis; Glycemic management Abbreviations DM: Diabetes Mellitus; FPG: Fasting Plasma Glucose; GAD: Glutamic Acid Decarboxylase; GDM: Gestational Diabetes Mellitus; HDL-cholesterol: High Density Lipoprotein cholesterol; HLA: Human Leucoid Antigen; IDD Continue reading >>

The Pathophysiology Of Diabetic Ketoacidosis

The Pathophysiology Of Diabetic Ketoacidosis

People still die from diabetic ketoacidosis. Poor patient education is probably the mostimportant determinant of the incidence of the catastrophe that constitutes "DKA".In several series, only about a fifth of patients with DKA are first-time presenterswith recently acquired Type I diabetes mellitus. The remainder are recognised diabeticswho are either noncompliant with insulin therapy, or have serious underlying illess thatprecipitates DKA. Most such patients have type I ("insulin dependent", "juvenile onset") diabetes mellitus, but it has recently been increasingly recognised that patients with type II diabetes mellitusmay present with ketoacidosis, and that some such patients present with "typical hyperosmolar nonketotic coma", but on closer inspection have varying degrees of ketoacidosis. DKA is best seen as a disorder that follows on an imbalance between insulin levels andlevels of counterregulatory hormones. Put simply: "Diabetic ketoacidosis is due to a marked deficiency of insulin in the face of high levels of hormones thatoppose the effects of insulin, particularly glucagon. Even small amounts of insulin can turn off ketoacid formation". Many hormones antagonise the effects of insulin. These include: In addition, several cytokines such as IL1, IL6 and TNF alpha antagonise the effects ofinsulin. [J Biol Chem 2001 Jul 13;276(28):25889-93]It is thus not surprising that many causes of stress and/or the systemic inflammatory response syndrome,appear to precipitate DKA in patients lacking insulin. Mechanisms by which these hormones and cytokinesantagonise insulin are complex, including inhibition of insulin release (catecholamines), antagonistic metaboliceffects (decreased glycogen production, inhibition of glycolysis), and promotion of peripheral resistance tothe e Continue reading >>

Chapter 344. Diabetes Mellitus

Chapter 344. Diabetes Mellitus

Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia. Several distinct types of DM are caused by a complex interaction of genetics and environmental factors. Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production. The metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual with diabetes and on the health care system. In the United States, DM is the leading cause of end-stage renal disease (ESRD), nontraumatic lower extremity amputations, and adult blindness. It also predisposes to cardiovascular diseases. With an increasing incidence worldwide, DM will be a leading cause of morbidity and mortality for the foreseeable future. DM is classified on the basis of the pathogenic process that leads to hyperglycemia, as opposed to earlier criteria such as age of onset or type of therapy (Fig. 344-1). The two broad categories of DM are designated type 1 and type 2 (Table 344-1). Both types of diabetes are preceded by a phase of abnormal glucose homeostasis as the pathogenic processes progress. Type 1 DM is the result of complete or near-total insulin deficiency. Type 2 DM is a heterogeneous group of disorders characterized by variable degrees of insulin resistance, impaired insulin secretion, and increased glucose production. Distinct genetic and metabolic defects in insulin action and/or secretion give rise to the common phenotype of hyperglycemia in type 2 DM and have important potential therapeutic implications now that pharmacologic agents are available to target specific metabolic derangements. T Continue reading >>

Living With Diabetes

Living With Diabetes

Managing diabetes is a daily challenge. There are so many variables to keep in mind -- food, exercise, stress, general health, etc. -- that keeping blood sugar levels in the desired range is a constant balancing act. We want to make managing diabetes easier. So, the DRI's Education Team hasdeveloped short brochures about the topics listed below -- offering useful tips on many of the day-to-day issues facing people living with diabetes. And, most of the materials are offered in English and Spanish. If you can benefit by learning about one or more of these subjects, just click on the title to expand. Do you know what foods have the greatest impact on your blood sugars? If you answered CARBOHYDRATE FOODS...youre right! Carbohydrates -- "carbs" -- are broken down into glucose. So if you eat too much of them, your blood sugar level may rise. For this reason, people with diabetes find it helpful to keep track of the carbs they eat in order to manage their blood sugars. Carb counting is easy. It just takes some practice at first. Caring for older people with diabetes requires special thought and consideration. The older individual is more likely to have other health problems and may be taking a variety of different medications. Many people are frightened to check their blood sugar -- or "blood glucose" -- levels because they do not want to see levels that are higher or lower than their target range. But, checking blood sugar at home, in school, and in the workplace is key to managing diabetes. It puts you in control of your diabetes. Remember, your blood sugar levels remain the same whether you know about them or not. Checking blood sugar levels is the most accurate way to see if your lifestyle changes and medications are helping you to better manage your diabetes. If levels Continue reading >>

Diabetes Mellitus

Diabetes Mellitus

4 Treatment The clinical syndrome described by the term diabetes mellitus results from intolerance to glucose. It is a chronic disease caused by an absolute or relative deficiency of insulin and, although all body systems are ultimately affected, it is primarily a disorder of carbohydrate metabolism. The approximate incidence of the disease is 13 cases/10,000 dogs years at risk[1]. Insulin is produced in the beta cells of the pancreatic islets of Langerhans and is released into the circulation to act on specific cell-surface receptors. Its release is stimulated by rising blood glucose concentration and it is principally insulin which is responsible for the post-prandial cellular glucose uptake and storage observed in humans and dogs. Several hormones (including corticosteroids, progesterone, oestrogen, growth hormone, glucagon and catecholamines) have an antagonistic effect to insulin and cause the blood glucose concentration to increase. Interruptions at any stage in this pathway may produce the clinical syndrome of diabetes mellitus, including: Failure to produce insulin resulting in an absolute deficiency - This may be due to degenerative changes in the beta cells or it may occur with severe exocrine pancreatic disease that disrupts the islets of Langerhans. The major example of the latter disease process is pancreatitis and, in cases of this diesase, diabetes mellitus is often found concurrently with exocrine pancreatic insufficiency. Degeneration of the beta cells, whether it involves the immune system or not, results in type 1 diabetes mellitus and miniature Poodles, Dachshunds and terriers appear to be predisposed to this condition. In humans, it is speculated that immune responses directed at certain pathogens (notably coxsackie virus B1) may cross-react with an Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. They are part of the spectrum of hyperglycemia, and each represents an extreme in the spectrum. The treatment of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) Continue reading >>

W3l Para204 Dka, Hhs, Aka

W3l Para204 Dka, Hhs, Aka

Poorly managed/undiagnosed diabetes (Type I Diabetes is first presentation of SKA fast or slow how can a DKA patient technically be hypoglycaemic A decrease in the circulating insulin level forces the body to source glucose from the break down of fat/protein at an how does a DKA patient become dehydrated and hypovolaemic (A decrease in the circulating insulin level forces the body to source glucose from the break down of fat/protein at an increased rate to fuel the body > Lysis (break down) of protein and lipids produces ketones as a by product ) The increased ketone production and hyperglycaemia produces osmotic diuresis and as a result a concentration gradient occurs. Fluid moves out of cells into the blood resulting in cellular how does a DKA patient become hyperkalaemic Metabolic acidosis occurs due to the increase in acid The hyperosmolality and acidic state cause potassium to what does hyperkalaemic patient present as on ECG what is the risk of moving a DKA patient which has been lying down for an extended period of time and how should this be managed If a Pt has been lying down for an extended period, K will have been accumulating in blood stream. Once you stand them up the heart will be flooded with K and has high risk of arrhythmias or even arrest. before you move a DKA pt you should have a large bore IVC in situ and a bag of fluid ready to go. This will dilute K in blood stream and will increase vascular resistance and force fluid back into cells Respiratory compensation for metabolic acidosis Pts presenting with this have been shown to present with: Low partial pressure of CO2 (+low bicarbonate) Pt feels urge to breathe (appears involuntary) High BGL increases blood osmolarity drawing water out of cells resulting in cellular dehydration, polydipsia and fatig Continue reading >>

Sickly Sweet: Understanding Diabetic Ketoacidosis

Sickly Sweet: Understanding Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life threatening condition that can occur to people with diabetes. It is observed primarily in people with type 1 diabetes (insulin dependent), but it can occur in type 2 diabetes (non-insulin dependent) under certain circumstances. The reason for why it is not often seen in people with type 2 diabetes is because their body is still able to produce insulin, so the pathophysiology explained in the flowchart below is not as dramatic as compared to people with type 1 diabetes who do not make any insulin at all. There are various symptoms associated with DKA including: Hyperglycaemia Polyphagia (increased appetite and hunger) Polydipsia (increased thirst) Polyuria (increased urination) Glycosuria (glucose in the urine) Ketonuria (ketones in urine) Ketones in blood Sweet, fruity breath Tachypnoea leading to Kussmaul breathing (deep and laboured breathing pattern) The body tries to compensate for the ketone bodies (acid) by eliminating carbon dioxide (also an acid) thereby attempting to make the body more alkalotic to normalise the pH The compensation between the metabolic and respiratory system can be read about in this article Decreased bicarbonate The body tries to use the available bicarbonate (base) to buffer the ketone bodies (acid) in order to improve the metabolic ketoacidosis This actually worsens the situation the lower the bicarbonate becomes with a continual production of ketones Increased drowsiness/decreased level of consciousness As the pH decreases and becomes more acidotic, it has a direct effect on decreasing the level of consciousness in a person Increased urea Electrolyte disturbances Tachycardia and other cardiac arrhythmias Tachycardia is often a compensatory mechanism for the hypotension Cardiac arrhythmias a Continue reading >>

Nurse Pediatric Hyperglycemia And Diabetic Ketoacidosis (dka)

Nurse Pediatric Hyperglycemia And Diabetic Ketoacidosis (dka)

NURSE Pediatric Hyperglycemia and Diabetic Ketoacidosis (DKA) Published by Jack West Modified over 4 years ago Presentation on theme: "NURSE Pediatric Hyperglycemia and Diabetic Ketoacidosis (DKA)" Presentation transcript: 1 NURSE Pediatric Hyperglycemia and Diabetic Ketoacidosis (DKA) Welcome to the Pediatric Hyperglycemia and Diabetic Ketoacidosis educational module. Illinois EMSC is a collaborative program between the Illinois Department of Public Health and Loyola University Health System. Development of this presentation was supported in part by: Grant 5 H34 MC from the Department of Health and Human Services Administration, Maternal and Child Health Bureau 2 Today, almost a century after the discovery of insulin, the most common cause of death in a child with diabetes, from a global perspective, is lack of access to insulin or improper use of insulin. Many children die even before their diabetes is diagnosed. Around the world, forces have united to make it come true that no child should die from diabetes or its complications. Childhood diabetes is becoming a world wide health issue. Statistics available at the time of this publication indicate that type 1 diabetes is growing globally at 3 percent per year in children and adolescents, and at an alarming 5 percent per year among children five years of age and younger. In addition, type 2 diabetes, once known as an adult disease, is growing rapidly among children worldwide. Almost a century after the discovery of insulin, the most common cause of death in a child with diabetes from a global perspective is lack of access to insulin or improper use of insulin. Many of these children die even before their diabetes is diagnosed. Around the world, forces have united to ensure that no child should die from diabetes or its Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis.[4] Symptoms include signs of dehydration, weakness, legs cramps, trouble seeing, and an altered level of consciousness.[2] Onset is typically over days to weeks.[3] Complications may include seizures, disseminated intravascular coagulopathy, mesenteric artery occlusion, or rhabdomyolysis.[2] The main risk factor is a history of diabetes mellitus type 2.[4] Occasionally it may occur in those without a prior history of diabetes or those with diabetes mellitus type 1.[3][4] Triggers include infections, stroke, trauma, certain medications, and heart attacks.[4] Diagnosis is based on blood tests finding a blood sugar greater than 30 mmol/L (600 mg/dL), osmolarity greater than 320 mOsm/kg, and a pH above 7.3.[2][3] Initial treatment generally consists of intravenous fluids to manage dehydration, intravenous insulin in those with significant ketones, low molecular weight heparin to decrease the risk of blood clotting, and antibiotics among those in whom there is concerns of infection.[3] The goal is a slow decline in blood sugar levels.[3] Potassium replacement is often required as the metabolic problems are corrected.[3] Efforts to prevent diabetic foot ulcers are also important.[3] It typically takes a few days for the person to return to baseline.[3] While the exact frequency of the condition is unknown, it is relatively common.[2][4] Older people are most commonly affected.[4] The risk of death among those affected is about 15%.[4] It was first described in the 1880s.[4] Signs and symptoms[edit] Symptoms of high blood sugar including increased thirst (polydipsia), increased volume of urination (polyurea), and i 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 >>

Hypovolemic Shock Pathophysiology, Symptoms, Signs, Treatment | Ehealthstar

Hypovolemic Shock Pathophysiology, Symptoms, Signs, Treatment | Ehealthstar

By Jan Modric ,August 6th 2013. Last reviewed 20th March 2018. Hypovolemic shock is an urgent medical condition, which occurs when a rapid decrease of the volume of the intravascular fluidusually due to severe bleedingresults in inadequate perfusion of the peripheral tissues and, eventually, in multiple organ failure 1,43. Hemorrhagic shock is hypovolemic shock caused by bleeding. Typical symptoms and signs: a person does not look right, is anxious, has pale, cool and sweaty skin and weak pulse, is lethargic and may lose consciousness. Treatment includes stopping bleeding, intravenous fluid infusion, oxygen and drugs. The most common cause of hypovolemic shock in adults is severe bleeding, and in children diarrhea 1. Sickle cell anemia with splenic sequestration, mostly in young children 28 NOTE: Many authors use the term third spacing for both second as third spacing. There are other types of shock and other conditions that may resemble hypovolemic shock: Distributive shock due to massive vasodilation with an increase in the volume of the intravascular space with insufficient volume of the existing blood to fill this space and therefore a drop of blood pressure Toxic shock syndrome, mainly in women in which a tampon-associated infection with staphylococci or streptococci results in vasodilation, high fever and rash) 7 Neurogenic shock due to spinal cord injury above Th4 or Th6 5 (low blood pressure, no tachycardia, warm skin, paraplegia or tetraplegia, numbness2 Toxic shock (poisoning with nitroprusside, bretylium) Cardiogenic shock due to heart failure (myocardial infarction, arrhythmia, cardiomyopathy, heart valve disease) 7,27 The term relative hypovolemic shock can be used when the volume of the circulatory system increases due to vasodilation, for example in neur Continue reading >>

Improving Care For Pediatric Diabetic Ketoacidosis

Improving Care For Pediatric Diabetic Ketoacidosis

Abstract OBJECTIVE: We sought to create and implement recommendations from an evidence-based pathway for hospital management of pediatric diabetic ketoacidosis (DKA) and to sustain improvement. We hypothesized that development and utilization of standard work for inpatient care of DKA would lead to reduction in hypokalemia and improvement in outcome measures. METHODS: Development involved systematic review of published literature by a multidisciplinary team. Implementation included multidisciplinary feedback, hospital-wide education, daily team huddles, and development of computer decision support and electronic order sets. RESULTS: Pathway-based order sets forced clinical pathway adherence; yet, variations in care persisted, requiring ongoing iterative review and pathway tool adjustment. Quality improvement measures have identified barriers and informed subsequent adjustments to interventions. We compared 281 patients treated postimplementation with 172 treated preimplementation. Our most notable findings included the following: (1) monitoring of serum potassium concentrations identified unanticipated hypokalemia episodes, not recognized before standard work implementation, and earlier addition of potassium to fluids resulted in a notable reduction in hypokalemia; (2) improvements in insulin infusion management were associated with reduced duration of ICU stay; and (3) with overall improved DKA management and education, cerebral edema occurrence and bicarbonate use were reduced. We continue to convene quarterly meetings, review cases, and process ongoing issues with system-based elements of implementing the recommendations. CONCLUSIONS: Our multidisciplinary development and implementation of an evidence-based pathway for DKA have led to overall improvements in care. We Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

1. PRESENTED BY:SHINY MATHEWHEAD NURSE MMW 2. DIABETES MELLITES Diabetes mellitus is a group of metabolic disease results from the production of insufficient amount of insulin by the pancreas. Without insulin the body cannot utilize glucose. So creating high level of glucose in the blood and a low level of glucose absorption by the tissue. Type 1 diabetes -- insulin dependant diabetes Type2 diabetes-- Non insulin dependant diabetes 3. DIABETIC KETOACIDOSISDiabetic keto acidosis is an acute state of severeuncontrolled diabetic that requires emergencytreatment with insulin and intravenous fluids.biochemically DKA is defined as an increase in theserum concentration of ketons greater than 5meq/l a blood glucose level of greater than 250mg/l,blood PH less than 7.2 and HCO3 is 18meq/lor less. 4. PRECIPITATING FACTORS Infections Acute stroke Pancreatitis Myocardial infarction Interruption of insulin Pregnancy Dietery indiscretion Trauma and stress 5. INFECTION MISSED INSULIN DOSE STRESS NEW-ONSET DIABETES EXCESS SECRETION OF INADEQUATEGLYCOGEN AND OTHER INSULINCOUNTER REGULATORY HORMONES DCREASEINCREASED LIPOLYSIS GLYCOGENENOLYSIS GLUCOSE UPTAKE OF ADIPOSE TISSUE AND GLUCONEOGENESIS BY THE LIVER HYPERGLYCEMIA KETOGENESIS OSMOTIC KETOSIS DIURESIS VOMITING ACIDOSIS POTASSIUM LOSS DEHYDRATION 6. LACK OF INSULINDECREASED UTILIZATION INCREASEDOF GLUCOSE BY MUSCLE, BREAKDOWNFAT AND LIVER OF FATINCREASED PRODUCTION •ACETONEOF GLUCOSE BY LIVER BREATH INCREASED •POOR APPETITE FATTY ACIDS •NAUSEA HYPERGLYCEMIA INCREASED KETONE •NAUSEA BODIESBLURRED POLYURIA •VOMITING VISION •ABDOMINAL PAIN ACIDOSISWEAKNESS DEHYDRATIONHEADACHE INCREASINGLY INCREASED THIRST RAPID (POLYDIPSIA) RESPIRATIONS 7. COMMON CLINICAL FEATURES Poly urea ,poly dipsia,po Continue reading >>

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