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Dka Pathophysiology Diagram

Pathophysiology Of Diabetic Ketoacidosis

Pathophysiology Of Diabetic Ketoacidosis

Diabetic Ketoacidosis is a serious complication of Diabetes Mellitus Type 1. The problem in Diabetes Mellitus Type 1 is the absolute lack of insulin. Without insulin, glucose will not be transported to the cells. Consequently, a person feels hungry despite of eating adequately and the level of glucose in the body is increasing because cell transportation is impossible. Consequently, as a response to cell hunger, the body will begin to breakdown proteins. If not managed promptly, the break down will continue and this time, it’s the fats. These will give rise to a high level of ketones in the blood. Ketones are blood acids and will result to Diabetic Ketoacidosis. If left untreated, this is fatal. Causes Decreased or missed dose of insulin – deficient insulin supply Illness or infection – causes resistance to insulin Undiagnosed and untreated diabetes Error in drawing up or injecting insulin – common in patients with visual impairment Intentional skipping of insulin doses – common in adolescents and those who have difficulty coping with the disease Equipment problems – example is occlusion of insulin pump tubing Clinical Manifestations Hyperglycemia – leads to polyuria, polydipsia, blurred vision, weakness, and headache Orthostatic hypotension – a decrease of 20 mmHg or more in systolic blood pressure caused by marked intravascular volume depletion; weak, rapid pulse is noted Ketosis and acidosis – lead to gastrointestinal symptoms such as anorexia, nausea, vomiting, and abdominal pain, acetone (a fruity odor) breath Kussmaul respirations – hyperventilation with very deep, but not labored, respirations Mental status varies widely. Patient may be alert, lethargic, or comatose Assessment and Diagnostic Findings Blood glucose level is between 300-800 mg/d 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 >>

Incidence Of Diabetic Ketoacidosis Among Patients With Type 2 Diabetes Mellitus Treated With Sglt2 Inhibitors And Other Antihyperglycemic Agents

Incidence Of Diabetic Ketoacidosis Among Patients With Type 2 Diabetes Mellitus Treated With Sglt2 Inhibitors And Other Antihyperglycemic Agents

Jump to Section 1. Introduction Diabetic ketoacidosis (DKA) is a serious, acute metabolic complication of diabetes characterized by absolute or relative insulin deficiency [[1], [2]], with an overall mortality rate of up to 5% in experienced healthcare centers [3]. Insulin deficiency, increased insulin counter-regulatory hormones (cortisol, glucagon, growth hormone, and catecholamines) and peripheral insulin resistance lead to hyperglycemia, dehydration, ketosis, and electrolyte imbalance, which underlie the pathophysiology of DKA [2]. While DKA is a commonly recognized vulnerability in autoimmune diabetes, stressful conditions such as trauma, surgery, or infection also increase DKA risk in patients with type 2 diabetes mellitus [4]. In fact, studies have reported that patients with type 2 diabetes accounted for 12–56% of the DKA cases, had longer hospital stays, and higher mortality (which possibly was due to advanced age and comorbidities) than patients with type 1 diabetes [[3], [5]]. Sodium glucose co-transporter 2 inhibitors (SGLT2i’s) are a new class of oral antihyperglycemic agents (AHA) that lower blood glucose through an insulin-independent mechanism, by suppressing renal glucose reabsorption and increasing urinary glucose excretion [6]. Currently, 3 SGLT2i’s have been approved in the US and Europe for the treatment of type 2diabetes: canagliflozin, dapagliflozin, and empagliflozin (initial approval March 29, 2013, January 8, 2014, August 1, 2014 in the US, November 15, 2013, November 12, 2012, May 22, 2014 in Europe, respectively). By mid-2015, based on spontaneous adverse event reports, the US Food and Drug Administration and the European Medicines Agency [7] had both issued statements that medicines in the SGLT2i class of drugs may be associated with a Continue reading >>

Diabetic Ketoacidosis Explained

Diabetic Ketoacidosis Explained

Twitter Summary: DKA - a major complication of #diabetes – we describe what it is, symptoms, who’s at risk, prevention + treatment! One of the most notorious complications of diabetes is diabetic ketoacidosis, or DKA. First described in the late 19th century, DKA represented something close to the ultimate diabetes emergency: In just 24 hours, people can experience an onset of severe symptoms, all leading to coma or death. But DKA also represents one of the great triumphs of the revolution in diabetes care over the last century. Before the discovery of insulin in 1920, DKA was almost invariably fatal, but the mortality rate for DKA dropped to below 30 percent within 10 years, and now fewer than 1 percent of those who develop DKA die from it, provided they get adequate care in time. Don’t skip over that last phrase, because it’s crucial: DKA is very treatable, but only as long as it’s diagnosed promptly and patients understand the risk. Table of Contents: What are the symptoms of DKA? Does DKA occur in both type 1 and type 2 diabetes? What Can Patients do to Prevent DKA? What is DKA? Insulin plays a critical role in the body’s functioning: it tells cells to absorb the glucose in the blood so that the body can use it for energy. When there’s no insulin to take that glucose out of the blood, high blood sugar (hyperglycemia) results. The body will also start burning fatty acids for energy, since it can’t get that energy from glucose. To make fatty acids usable for energy, the liver has to convert them into compounds known as ketones, and these ketones make the blood more acidic. DKA results when acid levels get too high in the blood. There are other issues too, as DKA also often leads to the overproduction and release of hormones like glucagon and adrenaline 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 >>

Diabetes Pathophysiology

Diabetes Pathophysiology

Diabetes occurs when there is a dis-balance between the demand and production of the hormone insulin. Control of blood sugar When food is taken, it is broken down into smaller components. Sugars and carbohydrates are thus broken down into glucose for the body to utilize them as an energy source. The liver is also able to manufacture glucose. In normal persons the hormone insulin, which is made by the beta cells of the pancreas, regulates how much glucose is in the blood. When there is excess of glucose in blood, insulin stimulates cells to absorb enough glucose from the blood for the energy that they need. Insulin also stimulates the liver to absorb and store any excess glucose that is in the blood. Insulin release is triggered after a meal when there is a rise in blood glucose. When blood glucose levels fall, during exercise for example, insulin levels fall too. High insulin will promote glucose uptake, glycolysis (break down of glucose), and glycogenesis (formation of storage form of glucose called glycogen), as well as uptake and synthesis of amino acids, proteins, and fat. Low insulin will promote gluconeogenesis (breakdown of various substrates to release glucose), glycogenolysis (breakdown of glycogen to release gluose), lipolysis (breakdown of lipids to release glucose), and proteolysis (breakdown of proteins to release glucose). Insulin acts via insulin receptors. Liver Adipose or fat Tissue Muscle High insulin Glycolysis Glycogenesis Triglyceride synthesis Amino acid uptake Protein synthesis Low insulin Gluconeogenesis Glycogenolysis Lipolysis Proteolysis Normal Responses to Eating and Fasting In a fed state: there is increased insulin secretion, causing glycolysis, glycogen storage, fatty acid synthesis/storage, and protein synthesis. After an overnight fast: 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 >>

Management Of A Dka Patient With Severe Metabolic And Ketoacidosis With Chronic Renal Insufficiency Brian Albany Otterbein University, Boomer.albany@otterbein.edu

Management Of A Dka Patient With Severe Metabolic And Ketoacidosis With Chronic Renal Insufficiency Brian Albany Otterbein University, [email protected]

Otterbein University Digital Commons @ Otterbein MSN Student Scholarship Student Research & Creative Work Fall 2014 Follow this and additional works at: Part of the Endocrine System Diseases Commons, Medical Pathology Commons, and the Nursing Commons This Project is brought to you for free and open access by the Student Research & Creative Work at Digital Commons @ Otterbein. It has been accepted for inclusion in MSN Student Scholarship by an authorized administrator of Digital Commons @ Otterbein. For more information, please contact [email protected] Recommended Citation Albany, Brian, "Management of a DKA patient with severe metabolic and ketoacidosis with chronic renal insufficiency" (2014). MSN Student Scholarship. Paper 6. Implications for nursing care Management of a DKA patient with severe metabolic and ketoacidosis with chronic renal insufficiency Brian Albany BSN, CCRN Introduction Case Study References Underlying Pathophysiology Diabetic ketoacidosis (DKA) serves as one the leading causes of mortality in diabetic patients [14]. The mortality has decreased over the past several decades due to the rapid recognition of the disease state and the improvement of management of DKA [14]. Despite a decline in mortality rates over the past twenty years from 7.96% to 0.67%, errors in management of the disease state are associated with significant morbidity and mortality [2]. Utilization of DKA protocols in the acute care setting have allowed congruency in care and delivery of effective lifesaving treatment. Despite advances in standardized DKA protocols, there still remains a gap in how to manage specific patient populations with end stage renal disease. Understanding the pathophysiology behind these patient populations will yield better outcomes with the ultimate 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 >>

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 >>

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 >>

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 >>

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Figure 3. Timeline in DKA management. GCS:Glascow Coma Scale, CBC:Complete Blood Counting, ECG:Electrocardiogram, HR:Heart Rate, BP:Blood Pressure, BUN:Blood Urea Nitrogen, Cr: Creatinine, WBC:White Blood Cell, CRP:C-reactive protein, CE:Cerebral edema (adapted from reference 165) Figure 4. A 15 years old male patient firstly diagnosed T1DM with DKA infected by rhino-orbita-cerebral mucormycozis (Picture from the reference [218]) 1. Introduction A chronic autoimmune destruction of the pancreatic beta cells results in decreasing endogenous insulin secretion and the clinical manifestation of type 1 diabetes mellitus (T1DM). The clinical onset of the disease is often acute in children and adolescents and diabetic ketoacidosis (DKA) is present in 20-74% of the patients [1-7]. DKA is a serious condition that requiring immediate intervention. Even with appropriate intervention, DKA is associated with significant morbidity and possible mortality in diabetic patients in the pediatric age group [8]. Young age and female sex have been associated with an increased frequency of DKA [3,9]. The triad of uncontrolled hyperglycemia, metabolic acidosis and increased total body ketone concentration characterizes DKA [10]. In addition to possible acute complications, it may also influence the later outcome of diabetes [11]. 2. Epidemiology Worldwide, an estimated 65 000 children under 15 years old develop T1DM each year, and the global incidence in children continues to increase at a rate of 3% a year [12,13]. The current incidence in the UK is around 26/100 000 per year [14]. Patterson et al. were aimed to establish 15-year incidence trends for childhood T1DM in European centres with EURODIAB study. 29 311 new cases of T1DM were diagnosed in children before their 15th birthday during a 1 Continue reading >>

Diabetes Mellitus

Diabetes Mellitus

Melvin, a 32-year- old,always complains of his increasing need for water. He also feels an increasing need to urinate almost every now and then,and always feels hungry. There is tingling on his extremities and numbness. His once clear vision is now experiencing cloudiness. He already feels tired just a few hours after waking up even though he does not have any job and only stays at home. The wound on his right knee has been there weeks but no improvement is seen. 11 Nursing Management The major sources of the glucose that circulates in the blood are through the absorption of ingested food in the gastrointestinal tract and formation of glucose by the liver from food substances. Diabetes mellitus is a group of metabolic diseases that occurs with increased levels of glucose in the blood. Diabetes mellitus most often results in defects in insulin secretion, insulin action, or even both. The classification system of diabetes mellitus is unique because research findings suggest many differences among individuals within each category, and patients can even move from one category to another, except for patients with type 1 diabetes. Diabetes has major classifications that include type 1 diabetes, type 2 diabetes, gestational diabetes, and diabetes mellitus associated with other conditions. The two types of diabetes mellitus are differentiated based on their causative factors, clinical course, and management. Diabetes Mellitus has different courses of pathophysiology because of it has several types. Insulin is secreted by beta cells in the pancreas and it is an anabolic hormone. When we consume food, insulin moves glucose from blood to muscle, liver, and fat cells as insulin level increases. The functions of insulin include the transport and metabolism of glucose for energy, sti Continue reading >>

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