The document discusses the management of diabetic ketoacidosis (DKA). It begins by describing the pathophysiology of DKA, noting that ketone body breakdown produces hydrogen ions leading to metabolic acidosis. It then outlines the diagnostic criteria for DKA and grades of severity. The initial goals of therapy are to replace fluid and electrolyte deficits, slowly correct hyperglycemia, and treat any precipitating illnesses. The document provides detailed guidance on evaluation, monitoring, fluid resuscitation, insulin therapy, and electrolyte replacement to safely manage a patient in DKA. It emphasizes close monitoring and individualization of treatment based on the patient's clinical status and laboratory values.
This is the fifth lecture. it is based on guidelines by NHS UK. the guidelines based are freely available in internet. the source and the used literature are trusted and accurate. i hope this level of a knowledge about the management side of the DKA touches the all areas of patient survival. patho-physiology not discussed here but will be discussed in another lecture in details. to a intern and final year MBBS students or ERPM students must process a level of knowledge described by the lecture. definitely more you read more knowledge you get. get the idea in the lecture and principles of management. so you will be much accurate in a ward. always take superior advice while managing emergencies.
The document discusses diabetic ketoacidosis (DKA), providing definitions, pathophysiology, precipitating events, symptoms, diagnosis, and treatment. DKA is defined as hyperglycemia, ketosis, and acidemia. It results from insulin deficiency leading to lipolysis, ketogenesis, and hyperglycemia. Common causes include infection, inadequate insulin, drugs like cocaine, and pregnancy. Treatment involves fluid resuscitation, insulin therapy to lower glucose levels to 140-180 mg/dL, electrolyte replacement, and treating the underlying precipitant once the patient is stabilized. Potassium levels require close monitoring during treatment.
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are acute complications of diabetes that result from insufficient insulin levels. DKA is characterized by high blood glucose, low pH and bicarbonate levels, and ketones in the blood or urine. HHS involves extremely high blood glucose without significant ketosis or acidosis. Treatment for DKA involves rehydration, insulin administration, and correcting electrolyte imbalances. Complications can include hypokalemia, hypoglycemia, and in rare cases cerebral edema in children. Proper patient education aims to prevent DKA episodes.
This document discusses diabetic ketoacidosis (DKA). It defines DKA as a condition characterized by hyperglycemia, ketosis, and acidosis. The pathogenesis of DKA involves insulin deficiency leading to increased glucose production and lipolysis. Diagnostic criteria for DKA include blood glucose over 250 mg/dL, pH below 7.3, and bicarbonate below 15 mEq/L. Management of DKA involves fluid resuscitation, insulin therapy to lower blood glucose levels, electrolyte replacement, and treating any precipitating causes. Transition to subcutaneous insulin therapy occurs once ketosis and acidosis are resolved.
A 40-year-old female presented to the emergency room with weakness, difficulty breathing, weight loss, and slight confusion. On physical exam, she was tachycardic and mildly confused. Initial labs showed elevated glucose, ketones, and an anion gap metabolic acidosis. She was diagnosed with diabetic ketoacidosis (DKA), a life-threatening complication of diabetes mellitus where the body produces high levels of blood acids called ketones. DKA is treated with intravenous fluids, electrolyte replacement, and insulin to lower blood glucose and resolve the acidosis. Hyperosmolar hyperglycemic state is a similar condition seen more often in type 2 diabetics that develops over days to weeks with severe de
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes resulting from severe insulin deficiency and manifested by dehydration, hyperglycemia, ketonemia, and metabolic acidosis. Treatment involves fluid replacement, insulin therapy, electrolyte replacement, and treating any precipitating infections. Patients must be closely monitored for changes in vital signs, glucose and electrolyte levels, pH, and ketones until stabilized.
This document provides an overview of the management of diabetic emergencies, specifically diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). It describes the clinical presentation, diagnostic criteria, and treatment approach for each condition. The treatment involves aggressive fluid resuscitation and insulin therapy to lower blood glucose levels, along with potassium supplementation and monitoring of electrolytes and fluid balance. Close monitoring of vital signs and laboratory values is required. Management may involve transfer to a higher level of care such as the ICU if certain instability criteria are met.
This is the fifth lecture. it is based on guidelines by NHS UK. the guidelines based are freely available in internet. the source and the used literature are trusted and accurate. i hope this level of a knowledge about the management side of the DKA touches the all areas of patient survival. patho-physiology not discussed here but will be discussed in another lecture in details. to a intern and final year MBBS students or ERPM students must process a level of knowledge described by the lecture. definitely more you read more knowledge you get. get the idea in the lecture and principles of management. so you will be much accurate in a ward. always take superior advice while managing emergencies.
The document discusses diabetic ketoacidosis (DKA), providing definitions, pathophysiology, precipitating events, symptoms, diagnosis, and treatment. DKA is defined as hyperglycemia, ketosis, and acidemia. It results from insulin deficiency leading to lipolysis, ketogenesis, and hyperglycemia. Common causes include infection, inadequate insulin, drugs like cocaine, and pregnancy. Treatment involves fluid resuscitation, insulin therapy to lower glucose levels to 140-180 mg/dL, electrolyte replacement, and treating the underlying precipitant once the patient is stabilized. Potassium levels require close monitoring during treatment.
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are acute complications of diabetes that result from insufficient insulin levels. DKA is characterized by high blood glucose, low pH and bicarbonate levels, and ketones in the blood or urine. HHS involves extremely high blood glucose without significant ketosis or acidosis. Treatment for DKA involves rehydration, insulin administration, and correcting electrolyte imbalances. Complications can include hypokalemia, hypoglycemia, and in rare cases cerebral edema in children. Proper patient education aims to prevent DKA episodes.
This document discusses diabetic ketoacidosis (DKA). It defines DKA as a condition characterized by hyperglycemia, ketosis, and acidosis. The pathogenesis of DKA involves insulin deficiency leading to increased glucose production and lipolysis. Diagnostic criteria for DKA include blood glucose over 250 mg/dL, pH below 7.3, and bicarbonate below 15 mEq/L. Management of DKA involves fluid resuscitation, insulin therapy to lower blood glucose levels, electrolyte replacement, and treating any precipitating causes. Transition to subcutaneous insulin therapy occurs once ketosis and acidosis are resolved.
A 40-year-old female presented to the emergency room with weakness, difficulty breathing, weight loss, and slight confusion. On physical exam, she was tachycardic and mildly confused. Initial labs showed elevated glucose, ketones, and an anion gap metabolic acidosis. She was diagnosed with diabetic ketoacidosis (DKA), a life-threatening complication of diabetes mellitus where the body produces high levels of blood acids called ketones. DKA is treated with intravenous fluids, electrolyte replacement, and insulin to lower blood glucose and resolve the acidosis. Hyperosmolar hyperglycemic state is a similar condition seen more often in type 2 diabetics that develops over days to weeks with severe de
Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes resulting from severe insulin deficiency and manifested by dehydration, hyperglycemia, ketonemia, and metabolic acidosis. Treatment involves fluid replacement, insulin therapy, electrolyte replacement, and treating any precipitating infections. Patients must be closely monitored for changes in vital signs, glucose and electrolyte levels, pH, and ketones until stabilized.
This document provides an overview of the management of diabetic emergencies, specifically diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). It describes the clinical presentation, diagnostic criteria, and treatment approach for each condition. The treatment involves aggressive fluid resuscitation and insulin therapy to lower blood glucose levels, along with potassium supplementation and monitoring of electrolytes and fluid balance. Close monitoring of vital signs and laboratory values is required. Management may involve transfer to a higher level of care such as the ICU if certain instability criteria are met.
This document provides guidance on the diagnosis, treatment, and management of type 1 diabetes mellitus. It discusses diagnostic criteria including A1C levels and oral glucose tolerance tests. The goals of treatment are outlined as maintaining tight glucose control while avoiding hypoglycemia. Insulin therapy is described as the primary treatment involving multiple daily injections or continuous infusion. Target blood glucose ranges and total daily insulin doses are provided for different age groups. Guidance is also given on managing diabetic ketoacidosis, including precipitating factors, treatment approach involving fluid resuscitation and insulin therapy, and electrolyte monitoring and replacement.
This document provides guidelines for the management of diabetic ketoacidosis (DKA) in adults. DKA is characterized by high blood glucose, ketone levels, and metabolic acidosis. The main goals of treatment are to correct dehydration, lower blood glucose and ketone levels, and treat any underlying causes. Treatment involves intravenous fluid replacement, insulin therapy via continuous intravenous infusion, electrolyte replacement, and monitoring until resolution of DKA. Guidelines are provided for fluid administration, insulin dosing, treatment targets, and conversion to subcutaneous insulin when stable. Special considerations are discussed for certain patient groups.
A 23-year-old female with a 15-year history of type 1 diabetes presents with disturbed consciousness after a normal vaginal delivery without anesthesia. Her vitals show signs of dehydration and metabolic acidosis. Labs reveal high blood glucose, ketones in blood and urine, and a high anion gap metabolic acidosis. The patient is diagnosed with diabetic ketoacidosis (DKA), which requires careful rehydration, insulin therapy, and electrolyte replacement to correct dehydration, hyperglycemia, and acidosis while avoiding complications like cerebral edema.
This document provides guidelines for the management of diabetic ketoacidosis (DKA). It defines DKA and classifies its severity. The main goals of treatment are rehydration, electrolyte replacement, and insulin administration to lower blood glucose levels slowly. Treatment involves initial fluid resuscitation followed by intravenous fluids and insulin. Potassium levels must be closely monitored and replaced as needed. Fluids are given over 48 hours and patients transition to subcutaneous insulin before discharge. Complications like cerebral edema are risks that require careful monitoring of fluid, electrolyte and glucose levels during treatment.
Uncontrolled blood sugar levels can lead to metabolic emergencies like diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), and hypoglycemia in diabetics. DKA and HHS are caused by high blood sugar and result from insulin deficiency, while hypoglycemia is caused by low blood sugar levels. Treatment for these conditions aims to restore fluid and electrolyte balance, lower blood sugar levels, and treat any underlying precipitating causes. Insulin therapy and intravenous fluids are used to treat DKA and HHS, while oral carbohydrates or intravenous dextrose are given for hypoglycemia. Close monitoring of blood sugar, electrolytes, and acid-base status is
Management of diabetic ketoacidosis dkasahar Hamdy
This document discusses the management of diabetic ketoacidosis (DKA). It begins by explaining the pathophysiology of DKA involving hyperglycemia, ketonemia, and acidosis due to counterregulatory hormones and insulin deficiency. The diagnostic criteria for DKA are then provided. The document then outlines the initial evaluation and laboratory tests that should be performed. Finally, it details the five parts of treatment: 1) fluid replacement, 2) insulin administration, 3) potassium supplementation, 4) bicarbonate infusion if needed, and 5) phosphate/magnesium/calcium supplementation. Complications to watch out for during treatment are also listed.
Academic discussion/ Lecture class for 5th year MBBS students on Diabetic Emergencies, types, their sign-symptoms and managements. Most of the Data was taken from Davidson's Principles and Practice of Medicine.
A 55-year-old male presented with pain and swelling in his left foot and lower leg along with abdominal pain and drowsiness. Examination revealed tachycardia, hypotension, tachypnea, and abdominal tenderness. Laboratory findings were consistent with diabetic ketoacidosis (DKA): hyperglycemia, ketonemia, and metabolic acidosis. The patient was diagnosed with DKA likely precipitated by infection and treated with insulin, intravenous fluids, potassium supplementation, and monitoring of electrolytes and glucose levels.
Hyperglycemic crises like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are medical emergencies caused by low insulin levels and high counterregulatory hormones. DKA is diagnosed when blood glucose is over 250 mg/dl, pH is below 7.3, and bicarbonate is under 18; HHS when glucose is over 600 mg/dl and pH is above 7.3. Treatment involves fluid resuscitation, insulin therapy to lower blood glucose, electrolyte replacement, and identifying/treating precipitating causes. Careful monitoring of glucose, electrolytes, pH and clinical status is required for resolution. Complications can include hypogly
DKA clinical presentation of diabetic keto acidosisnanikhelma
DKA is a life-threatening complication of diabetes caused by lack of insulin and high blood glucose levels. It is characterized by hyperglycemia over 250 mg/dL, metabolic acidosis with blood pH below 7.3 and bicarbonate below 15 mEq/L, and ketones in the blood. Treatment involves rapid fluid resuscitation, insulin therapy to lower blood glucose levels, electrolyte replacement, and treating any underlying infections. The goals are to correct dehydration, lower blood glucose, reverse acidosis, and replenish electrolytes like potassium. Management involves IV fluids, IV or subcutaneous insulin, monitoring labs closely and watching for complications.
This document discusses SIADH (Syndrome of Inappropriate Antidiuretic Hormone) and Diabetes Insipidus. It begins by explaining the physiology of vasopressin/antidiuretic hormone and its role in water regulation. It then defines and describes the diagnostic criteria and clinical manifestations of DI and SIADH. The types and causes of DI, including central DI, nephrogenic DI, and secondary/dipsogenic DI are outlined. Tests for evaluating DI like the Miller-Moses test are explained. Management strategies for central DI, nephrogenic DI, and SIADH are provided, including fluid replacement protocols, use of desmopressin, and v
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) and diabetic ketoacidosis (DKA) are complications of diabetes that can occur when insulin levels are inadequate. HHNS typically occurs in non-insulin dependent diabetics and is characterized by severe hyperglycemia and hyperosmolality without acidosis. DKA usually occurs in insulin-dependent diabetics and results in hyperglycemia, dehydration, and metabolic acidosis. Treatment of DKA involves fluid resuscitation, electrolyte replacement, and administration of insulin to resolve the acidosis.
This case report describes a 25-year-old man with a history of type 2 diabetes who presented with diabetic ketoacidosis (DKA). He reported symptoms of nausea, vomiting, polyuria, polydipsia and weight loss. Laboratory results showed metabolic acidosis, hyperglycemia and ketones consistent with DKA. While being treated for DKA, he developed worsening back pain and new neurological symptoms. Imaging revealed an epidural abscess, which was surgically treated. He required intensive rehabilitation for residual lower extremity weakness following treatment and resolution of the abscess.
This document provides information on diabetic ketoacidosis (DKA), including its pathophysiology, clinical manifestations, diagnosis, and management. DKA most commonly presents as the first symptom of type 1 diabetes. The main goals of DKA treatment are to correct acidosis, dehydration, and hyperglycemia. Treatment involves intravenous fluid resuscitation and insulin therapy to rehydrate and lower blood glucose levels. Electrolyte imbalances are also addressed. Complications of DKA include cerebral edema, which requires careful monitoring during treatment. Strict protocols are followed to resolve DKA and transition patients to subcutaneous insulin regimens.
This document discusses diabetic ketoacidosis (DKA), providing definitions, symptoms, pathophysiology, diagnosis, treatment, and complications. DKA results from a lack of insulin and causes the body to burn fat and produce acidic ketones. It is defined by hyperglycemia, ketosis, and acidemia. Treatment involves fluid replacement, insulin therapy to lower blood glucose levels, and monitoring for complications like shock, thrombosis, pulmonary edema, and cerebral edema. The goal is to resolve the DKA and transition the patient to their usual insulin regimen and diet to prevent future occurrences.
diabetesketoacidosis about education pdfAkash782029
This document discusses diabetic ketoacidosis (DKA), providing definitions, symptoms, pathophysiology, diagnosis, treatment and complications. DKA results from a lack of insulin causing the body to burn fat and produce acidic ketones. It is defined by hyperglycemia, ketosis and acidemia. Treatment involves fluid replacement, insulin therapy to lower blood glucose while replenishing electrolytes and monitoring for complications like shock, thrombosis and cerebral edema.
This document provides an overview of metabolic emergencies that can occur in people with diabetes mellitus, focusing on diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), and hypoglycemia. It discusses the diagnostic criteria and pathophysiology of DKA and HHS, as well as their precipitating factors, symptoms, treatment goals, and management including fluid replacement, insulin therapy, electrolyte monitoring and supplementation, and criteria for resolution. Complications of DKA are also reviewed. The document concludes with sections on prevention of DKA and hypoglycemia.
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)MuskanShingari
Skin is the largest organ of the human body, serving crucial functions that include protection, sensation, regulation, and synthesis. Structurally, it consists of three main layers: the epidermis, dermis, and hypodermis (subcutaneous layer).
1. **Epidermis**: The outermost layer primarily composed of epithelial cells called keratinocytes. It provides a protective barrier against environmental factors, pathogens, and UV radiation.
2. **Dermis**: Located beneath the epidermis, the dermis contains connective tissue, blood vessels, hair follicles, and sweat glands. It plays a vital role in supporting and nourishing the epidermis, regulating body temperature, and housing sensory receptors for touch, pressure, temperature, and pain.
3. **Hypodermis**: Also known as the subcutaneous layer, it consists of fat and connective tissue that anchors the skin to underlying structures like muscles and bones. It provides insulation, cushioning, and energy storage.
Skin performs essential functions such as regulating body temperature through sweat production and blood flow control, synthesizing vitamin D when exposed to sunlight, and serving as a sensory interface with the external environment.
Maintaining skin health is crucial for overall well-being, involving proper hygiene, hydration, protection from sun exposure, and avoiding harmful substances. Skin conditions and diseases range from minor irritations to chronic disorders, emphasizing the importance of regular care and medical attention when needed.
Nano-gold for Cancer Therapy chemistry investigatory projectSIVAVINAYAKPK
chemistry investigatory project
The development of nanogold-based cancer therapy could revolutionize oncology by providing a more targeted, less invasive treatment option. This project contributes to the growing body of research aimed at harnessing nanotechnology for medical applications, paving the way for future clinical trials and potential commercial applications.
Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
This document provides guidance on the diagnosis, treatment, and management of type 1 diabetes mellitus. It discusses diagnostic criteria including A1C levels and oral glucose tolerance tests. The goals of treatment are outlined as maintaining tight glucose control while avoiding hypoglycemia. Insulin therapy is described as the primary treatment involving multiple daily injections or continuous infusion. Target blood glucose ranges and total daily insulin doses are provided for different age groups. Guidance is also given on managing diabetic ketoacidosis, including precipitating factors, treatment approach involving fluid resuscitation and insulin therapy, and electrolyte monitoring and replacement.
This document provides guidelines for the management of diabetic ketoacidosis (DKA) in adults. DKA is characterized by high blood glucose, ketone levels, and metabolic acidosis. The main goals of treatment are to correct dehydration, lower blood glucose and ketone levels, and treat any underlying causes. Treatment involves intravenous fluid replacement, insulin therapy via continuous intravenous infusion, electrolyte replacement, and monitoring until resolution of DKA. Guidelines are provided for fluid administration, insulin dosing, treatment targets, and conversion to subcutaneous insulin when stable. Special considerations are discussed for certain patient groups.
A 23-year-old female with a 15-year history of type 1 diabetes presents with disturbed consciousness after a normal vaginal delivery without anesthesia. Her vitals show signs of dehydration and metabolic acidosis. Labs reveal high blood glucose, ketones in blood and urine, and a high anion gap metabolic acidosis. The patient is diagnosed with diabetic ketoacidosis (DKA), which requires careful rehydration, insulin therapy, and electrolyte replacement to correct dehydration, hyperglycemia, and acidosis while avoiding complications like cerebral edema.
This document provides guidelines for the management of diabetic ketoacidosis (DKA). It defines DKA and classifies its severity. The main goals of treatment are rehydration, electrolyte replacement, and insulin administration to lower blood glucose levels slowly. Treatment involves initial fluid resuscitation followed by intravenous fluids and insulin. Potassium levels must be closely monitored and replaced as needed. Fluids are given over 48 hours and patients transition to subcutaneous insulin before discharge. Complications like cerebral edema are risks that require careful monitoring of fluid, electrolyte and glucose levels during treatment.
Uncontrolled blood sugar levels can lead to metabolic emergencies like diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), and hypoglycemia in diabetics. DKA and HHS are caused by high blood sugar and result from insulin deficiency, while hypoglycemia is caused by low blood sugar levels. Treatment for these conditions aims to restore fluid and electrolyte balance, lower blood sugar levels, and treat any underlying precipitating causes. Insulin therapy and intravenous fluids are used to treat DKA and HHS, while oral carbohydrates or intravenous dextrose are given for hypoglycemia. Close monitoring of blood sugar, electrolytes, and acid-base status is
Management of diabetic ketoacidosis dkasahar Hamdy
This document discusses the management of diabetic ketoacidosis (DKA). It begins by explaining the pathophysiology of DKA involving hyperglycemia, ketonemia, and acidosis due to counterregulatory hormones and insulin deficiency. The diagnostic criteria for DKA are then provided. The document then outlines the initial evaluation and laboratory tests that should be performed. Finally, it details the five parts of treatment: 1) fluid replacement, 2) insulin administration, 3) potassium supplementation, 4) bicarbonate infusion if needed, and 5) phosphate/magnesium/calcium supplementation. Complications to watch out for during treatment are also listed.
Academic discussion/ Lecture class for 5th year MBBS students on Diabetic Emergencies, types, their sign-symptoms and managements. Most of the Data was taken from Davidson's Principles and Practice of Medicine.
A 55-year-old male presented with pain and swelling in his left foot and lower leg along with abdominal pain and drowsiness. Examination revealed tachycardia, hypotension, tachypnea, and abdominal tenderness. Laboratory findings were consistent with diabetic ketoacidosis (DKA): hyperglycemia, ketonemia, and metabolic acidosis. The patient was diagnosed with DKA likely precipitated by infection and treated with insulin, intravenous fluids, potassium supplementation, and monitoring of electrolytes and glucose levels.
Hyperglycemic crises like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are medical emergencies caused by low insulin levels and high counterregulatory hormones. DKA is diagnosed when blood glucose is over 250 mg/dl, pH is below 7.3, and bicarbonate is under 18; HHS when glucose is over 600 mg/dl and pH is above 7.3. Treatment involves fluid resuscitation, insulin therapy to lower blood glucose, electrolyte replacement, and identifying/treating precipitating causes. Careful monitoring of glucose, electrolytes, pH and clinical status is required for resolution. Complications can include hypogly
DKA clinical presentation of diabetic keto acidosisnanikhelma
DKA is a life-threatening complication of diabetes caused by lack of insulin and high blood glucose levels. It is characterized by hyperglycemia over 250 mg/dL, metabolic acidosis with blood pH below 7.3 and bicarbonate below 15 mEq/L, and ketones in the blood. Treatment involves rapid fluid resuscitation, insulin therapy to lower blood glucose levels, electrolyte replacement, and treating any underlying infections. The goals are to correct dehydration, lower blood glucose, reverse acidosis, and replenish electrolytes like potassium. Management involves IV fluids, IV or subcutaneous insulin, monitoring labs closely and watching for complications.
This document discusses SIADH (Syndrome of Inappropriate Antidiuretic Hormone) and Diabetes Insipidus. It begins by explaining the physiology of vasopressin/antidiuretic hormone and its role in water regulation. It then defines and describes the diagnostic criteria and clinical manifestations of DI and SIADH. The types and causes of DI, including central DI, nephrogenic DI, and secondary/dipsogenic DI are outlined. Tests for evaluating DI like the Miller-Moses test are explained. Management strategies for central DI, nephrogenic DI, and SIADH are provided, including fluid replacement protocols, use of desmopressin, and v
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) and diabetic ketoacidosis (DKA) are complications of diabetes that can occur when insulin levels are inadequate. HHNS typically occurs in non-insulin dependent diabetics and is characterized by severe hyperglycemia and hyperosmolality without acidosis. DKA usually occurs in insulin-dependent diabetics and results in hyperglycemia, dehydration, and metabolic acidosis. Treatment of DKA involves fluid resuscitation, electrolyte replacement, and administration of insulin to resolve the acidosis.
This case report describes a 25-year-old man with a history of type 2 diabetes who presented with diabetic ketoacidosis (DKA). He reported symptoms of nausea, vomiting, polyuria, polydipsia and weight loss. Laboratory results showed metabolic acidosis, hyperglycemia and ketones consistent with DKA. While being treated for DKA, he developed worsening back pain and new neurological symptoms. Imaging revealed an epidural abscess, which was surgically treated. He required intensive rehabilitation for residual lower extremity weakness following treatment and resolution of the abscess.
This document provides information on diabetic ketoacidosis (DKA), including its pathophysiology, clinical manifestations, diagnosis, and management. DKA most commonly presents as the first symptom of type 1 diabetes. The main goals of DKA treatment are to correct acidosis, dehydration, and hyperglycemia. Treatment involves intravenous fluid resuscitation and insulin therapy to rehydrate and lower blood glucose levels. Electrolyte imbalances are also addressed. Complications of DKA include cerebral edema, which requires careful monitoring during treatment. Strict protocols are followed to resolve DKA and transition patients to subcutaneous insulin regimens.
This document discusses diabetic ketoacidosis (DKA), providing definitions, symptoms, pathophysiology, diagnosis, treatment, and complications. DKA results from a lack of insulin and causes the body to burn fat and produce acidic ketones. It is defined by hyperglycemia, ketosis, and acidemia. Treatment involves fluid replacement, insulin therapy to lower blood glucose levels, and monitoring for complications like shock, thrombosis, pulmonary edema, and cerebral edema. The goal is to resolve the DKA and transition the patient to their usual insulin regimen and diet to prevent future occurrences.
diabetesketoacidosis about education pdfAkash782029
This document discusses diabetic ketoacidosis (DKA), providing definitions, symptoms, pathophysiology, diagnosis, treatment and complications. DKA results from a lack of insulin causing the body to burn fat and produce acidic ketones. It is defined by hyperglycemia, ketosis and acidemia. Treatment involves fluid replacement, insulin therapy to lower blood glucose while replenishing electrolytes and monitoring for complications like shock, thrombosis and cerebral edema.
This document provides an overview of metabolic emergencies that can occur in people with diabetes mellitus, focusing on diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), and hypoglycemia. It discusses the diagnostic criteria and pathophysiology of DKA and HHS, as well as their precipitating factors, symptoms, treatment goals, and management including fluid replacement, insulin therapy, electrolyte monitoring and supplementation, and criteria for resolution. Complications of DKA are also reviewed. The document concludes with sections on prevention of DKA and hypoglycemia.
Storyboard on Skin- Innovative Learning (M-pharm) 2nd sem. (Cosmetics)MuskanShingari
Skin is the largest organ of the human body, serving crucial functions that include protection, sensation, regulation, and synthesis. Structurally, it consists of three main layers: the epidermis, dermis, and hypodermis (subcutaneous layer).
1. **Epidermis**: The outermost layer primarily composed of epithelial cells called keratinocytes. It provides a protective barrier against environmental factors, pathogens, and UV radiation.
2. **Dermis**: Located beneath the epidermis, the dermis contains connective tissue, blood vessels, hair follicles, and sweat glands. It plays a vital role in supporting and nourishing the epidermis, regulating body temperature, and housing sensory receptors for touch, pressure, temperature, and pain.
3. **Hypodermis**: Also known as the subcutaneous layer, it consists of fat and connective tissue that anchors the skin to underlying structures like muscles and bones. It provides insulation, cushioning, and energy storage.
Skin performs essential functions such as regulating body temperature through sweat production and blood flow control, synthesizing vitamin D when exposed to sunlight, and serving as a sensory interface with the external environment.
Maintaining skin health is crucial for overall well-being, involving proper hygiene, hydration, protection from sun exposure, and avoiding harmful substances. Skin conditions and diseases range from minor irritations to chronic disorders, emphasizing the importance of regular care and medical attention when needed.
Nano-gold for Cancer Therapy chemistry investigatory projectSIVAVINAYAKPK
chemistry investigatory project
The development of nanogold-based cancer therapy could revolutionize oncology by providing a more targeted, less invasive treatment option. This project contributes to the growing body of research aimed at harnessing nanotechnology for medical applications, paving the way for future clinical trials and potential commercial applications.
Cancer remains one of the leading causes of death worldwide, prompting the need for innovative treatment methods. Nanotechnology offers promising new approaches, including the use of gold nanoparticles (nanogold) for targeted cancer therapy. Nanogold particles possess unique physical and chemical properties that make them suitable for drug delivery, imaging, and photothermal therapy.
Storyboard on Acne-Innovative Learning-M. pharm. (2nd sem.) CosmeticsMuskanShingari
Acne is a common skin condition that occurs when hair follicles become clogged with oil and dead skin cells. It typically manifests as pimples, blackheads, or whiteheads, often on the face, chest, shoulders, or back. Acne can range from mild to severe and may cause emotional distress and scarring in some cases.
**Causes:**
1. **Excess Oil Production:** Hormonal changes during adolescence or certain times in adulthood can increase sebum (oil) production, leading to clogged pores.
2. **Clogged Pores:** When dead skin cells and oil block hair follicles, bacteria (usually Propionibacterium acnes) can thrive, causing inflammation and acne lesions.
3. **Hormonal Factors:** Fluctuations in hormone levels, such as during puberty, menstrual cycles, pregnancy, or certain medical conditions, can contribute to acne.
4. **Genetics:** A family history of acne can increase the likelihood of developing the condition.
**Types of Acne:**
- **Whiteheads:** Closed plugged pores.
- **Blackheads:** Open plugged pores with a dark surface.
- **Papules:** Small red, tender bumps.
- **Pustules:** Pimples with pus at their tips.
- **Nodules:** Large, solid, painful lumps beneath the surface.
- **Cysts:** Painful, pus-filled lumps beneath the surface that can cause scarring.
**Treatment:**
Treatment depends on the severity and type of acne but may include:
- **Topical Treatments:** Such as benzoyl peroxide, salicylic acid, or retinoids to reduce bacteria and unclog pores.
- **Oral Medications:** Antibiotics or oral contraceptives for hormonal acne.
- **Procedures:** Such as chemical peels, extraction of comedones, or light therapy for more severe cases.
**Prevention and Management:**
- **Cleanse:** Regularly wash skin with a gentle cleanser.
- **Moisturize:** Use non-comedogenic moisturizers to keep skin hydrated without clogging pores.
- **Avoid Irritants:** Such as harsh cosmetics or excessive scrubbing.
- **Sun Protection:** Use sunscreen to prevent exacerbation of acne scars and inflammation.
Acne treatment can take time, and consistency in skincare routines and treatments is crucial. Consulting a dermatologist can help tailor a treatment plan that suits individual needs and reduces the risk of scarring or long-term skin damage.
CLASSIFICATION OF H1 ANTIHISTAMINICS-
FIRST GENERATION ANTIHISTAMINICS-
1)HIGHLY SEDATIVE-DIPHENHYDRAMINE,DIMENHYDRINATE,PROMETHAZINE,HYDROXYZINE 2)MODERATELY SEDATIVE- PHENARIMINE,CYPROHEPTADINE, MECLIZINE,CINNARIZINE
3)MILD SEDATIVE-CHLORPHENIRAMINE,DEXCHLORPHENIRAMINE
TRIPROLIDINE,CLEMASTINE
SECOND GENERATION ANTIHISTAMINICS-FEXOFENADINE,
LORATADINE,DESLORATADINE,CETIRIZINE,LEVOCETIRIZINE,
AZELASTINE,MIZOLASTINE,EBASTINE,RUPATADINE. Mechanism of action of 2nd generation antihistaminics-
These drugs competitively antagonize actions of
histamine at the H1 receptors.
Pharmacological actions-
Antagonism of histamine-The H1 antagonists effectively block histamine induced bronchoconstriction, contraction of intestinal and other smooth muscle and triple response especially wheal, flare and itch. Constriction of larger blood vessel by histamine is also antagonized.
2) Antiallergic actions-Many manifestations of immediate hypersensitivity (type I reactions)are suppressed. Urticaria, itching and angioedema are well controlled.3) CNS action-The older antihistamines produce variable degree of CNS depression.But in case of 2nd gen antihistaminics there is less CNS depressant property as these cross BBB to significantly lesser extent.
4) Anticholinergic action- many H1 blockers
in addition antagonize muscarinic actions of ACh. BUT IN 2ND gen histaminics there is Higher H1 selectivitiy : no anticholinergic side effects
Fexofenadine is sold under the brand name Allegra.
It is a selective peripheral H1 blocker. It is classified as a second-generation antihistamine because it is less able to pass the blood–brain barrier and causes lesser sedation, as compared to first-generation antihistamines.
It is on the World Health Organization's List of Essential Medicines. Fexofenadine has been manufactured in generic form since 2011.
The biomechanics of running involves the study of the mechanical principles underlying running movements. It includes the analysis of the running gait cycle, which consists of the stance phase (foot contact to push-off) and the swing phase (foot lift-off to next contact). Key aspects include kinematics (joint angles and movements, stride length and frequency) and kinetics (forces involved in running, including ground reaction and muscle forces). Understanding these factors helps in improving running performance, optimizing technique, and preventing injuries.
Allopurinol, a uric acid synthesis inhibitor acts by inhibiting Xanthine oxidase competitively as well as non- competitively, Whereas Oxypurinol is a non-competitive inhibitor of xanthine oxidase.
Nutritional deficiency Disorder are problems in india.
It is very important to learn about Indian child's nutritional parameters as well the Disease related to alteration in their Nutrition.
- Video recording of this lecture in English language: https://youtu.be/RvdYsTzgQq8
- Video recording of this lecture in Arabic language: https://youtu.be/ECILGWtgZko
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3. KETONES
1. Ketones –Acetone,3-β
hydroxybutyrate and
acetoacetate
2. Predominant ketone -
3-β hydroxybutyrate
3. Dissociation of
ketones produces
hydrogen ions that
cause metabolic
acidosis
DR JOHN OKIDI
4. DKA DIAGNOSTIC TRIAD
I. Ketonemia
≥3mmol/l or
significant ketonuria(≥ ++on urine
II. Blood glucose
>200mg/dl (11.0mmol/l or known diabetic
III. Bicarbonate
<15mmol/l,venous PH <7.3 or both
Other diagnostic creterion
Anion Gap:>12
DR JOHN OKIDI
5. GRADES OF DKA
1.Mild –pH 7.21-7.3,HCO3 10mmol to
15mmol/l
2.Moderate –pH 7.11-7.2,HCO3 5mmol to
10mmol/l
3.Severe-pH<7.1,HCO3 <5mmol/l
6. INITIAL GOALS OF
THERAPY
To replace fluid and electrolyte deficits
Slowly correct the hyperglycemia
Treat the precipitating illnesses
Treat the potential complications that may
arise during medical therapy:
•Hypoglycemia
•Hypokalemia
•Hypophosphatemia
•Fluid overload-cerebral edema
DR JOHN OKIDI
7. MANAGEMENT OF DKA
Action 1:Initial evaluation
Action 2:Full clinical assessment
Action 3:calculate
Anion Gap
correcting sodium for hyperglycemia
Osmolarity
Interpret ABGS
Action 4:decide whether icu patient or not
Action 5:intervene
Replace fluids
Insulin therapy
Serum potassium replacement
Bicarbonate therapy
Monitoring RX
DR JOHN OKIDI
8. MANAGEMENT OF DKA
Action 1:Initial evaluation
In the first minute assess the ABCs
Obtain venous access(large bore cannulae)
Obtain blood for:
•Serum Glucose levels
•serum electrolytes
•Blood ketone(superior to urine ketone)
•Creatinine.
•CBC
•Leukocytosis (common in DKA)
•BUN
•ABGs(venous or capillary)
Obtain urine for urinalysis and ketones
Obtain weight
DR JOHN OKIDI
9. ACTION 2:FULL CLINICAL
ASSESSMENT
a) Conscious level(GCS):NGT GCS <9
b) Airway: ensure patency & adequate ventilation
c) Breathing: Respiratory rate, supplemental oxygen till
shock if any is resolved
d) Circulation: check capillary refill time, peripheral
pulses, skin temperature, BP & urine output.
DR JOHN OKIDI
10. ACTION 3:FULL EXAMINATION
Full examination(particular interest on evidence
of:
o cerebral edema
(headache,vomiting,hypertension,bradycar
dia,hypoventilation,papilloedema(late sign)
o ileus
o Identify any precipitating factor
o Infection
o Myocardial infection
o Stroke
o Pulmonary embolism
DR JOHN OKIDI
11. ACTION
4:CALCULAT
E
ANION GAP
Anion Gap = ((Na+) + (K+) )–((Cl
-
)+
(HCO3
-
) ]
Normal Range :10-18 mmol/l
Mainly used in diagnosing different
causes of metabolic acidosis
In metabolic acidosis, plasma HCO3
-
is ↓
Na+ unexchange→↑ Cl
-
so as to maintain
electro neutrality thus
hyperchloremic metabolic acidosis
Ref :oxford clinical handbook of
medicine 10ed pg 670
DR JOHN OKIDI
12. INTERPRETI
NG ABGS
Normal blood pH range is 7.35- to
7.45
Normal bicarbonate level is 22 to 28
mEq/L.
Look at the pH
is the primary problem
acidosis (low) or alkalosis
(high)
2. Check the CO2 (respiratory
indicator)
is it less than 35 (alkalosis)
or more than 45 (acidosis)
3. Check the HCO3 (metabolic
indicator)
is it less than 22 (acidosis) or
more than 26 (alkalosis)
4. Which is primary disorder (Resp. or
Metabolic)?
If the pH is low (acidosis),
then look to see if CO2 or
HCO3 is acidosis (which ever
is acidosis will be primary).
If the pH is high (alkalosis),
then look to see if CO2 or
HCO3 is alkalosis (which ever
is alkalosis is the primary).
The one that matches the pH
(acidosis or alkalosis), is the
primary disorder. DR JOHN OKIDI
13. CALCULATE
:PLASMA
OSMOLALITY
Calculation of plasma Osmolality
= 2 x (Na + K)+ Glucose/18 +
BUN/3
•One osmole=1mole(6.02×1023 of
solute particles)
•Osmolality =osmole/kilogram water
•Osmolarity=osmole/litre of solution.
•Isotonic solution ; water concentration
is equal for the two compartment thus
solute cannot enter or leave the cell.
•D5
•0.9% N/S
•Hypotonic solution: solution having
lower conc of impermeant solute thus
H20 will diffuse into the cell causing it
to swell
•N/S < 0.9% n/s
•Hypertonic solution: soln having a
higher conc of impermeant solutes,
water will flow out of the cell into the
extracellular fluid, concentrating the
intracellular fluid and diluting the
extracellular fluid
•e.g Nacl soln > 0.9%
DR JOHN OKIDI
14. CALCULATE:
CORRECTING SODIUM
FOR HYPERGLYCEMIA
Corrected Na+ = measured Na +
1.6 meq/L x (glucose-100)/100))
Example:
Measured laboratory Na+ = 123 mmol/l/L and
Glucose = 1,250 mg/dl
1,250 – 100 = 1,150 / 100 = 11.5 x 1.6 = 18
mmol/l/L
Corrected Na+ = 123 + 18 = 141 mmol/L
From the above example if one
didn’t correct that patient would have
been managed for hyponatraemia yet
with correction he is not
hyponaetraemic
Calculating plasma osmolarity and
corrected sodium helps in choice of
fluids
Na+ is depressed by 1.6 mEq/L per 100
mg/dl glucose
Normal [Na+]=133-146
mmol/l
Mild hyponatraemia:
plasma Na >120mEq/l
but<133.
Severe
hyponatremia:plasma Na
<109mEq/l
Main extracellular cation
Pathophysiology:
• Loss of sodium
• Water retention
DR JOHN OKIDI
Recall
15. ACTION 4:CRETERIA FOR
HDU/ICU ADMISSION
Patient WITH severe DKA or
has any of the following
1. Hypokalaemia on admission
(<3.5 mmol/L)
2. Bicarbonate <5 mmol/L
3. Anion gap >16
4. Blood ketones > 6 mmol/L
5. Venous/arterial pH below 7.1
Clinical assessment
1. GCS <12
2. SBP <90 mmHg
3. Pulse >100 or < 60 bpm
4. SPO2 < 92% on air
(assuming normal baseline
respiratory function)
DR JOHN OKIDI
16. MANAGEME
NT
Rehydration
Replace fluids: 1L of
0.9% saline over first
1hr (5–10 mL/kg per
hour); subsequently,
0.45% saline at 150–
300 mL/h;
change to 5%-10%
glucose and 0.45%
saline at 100–200
mL/h when plasma
glucose reaches 250
mg/dL (14 mmol/L).
Rule of thumb
0.9% saline is the replacement
fluid of choice
Typical fluid deficit is
100ml/kg so an average 70kg
man=7litres
DR JOHN OKIDI
17. GUIDE TO FLUID REPLACEMENT IN A
70KG MAN WITH DKA
FLUID RATE DURATION OF
INFUSION
1 Liter 0.9% Saline 1000ml/hr 1 HR
1 Liter 0.9% Saline 500ml/hr(May add KCL) 2HR
1 Liter 0.9% Saline 500ml/hr 2HR
1 Liter 0.9% Saline 250ml/hr 4HR
1 Liter 0.9% Saline 250ml/hr 4HR
1 Liter 0.9% Saline 150ml/hr >6HR-8hours
1 Liter 0.9% Saline
Clinical assessment
Depends on clinical
judgement
18. FLUID REPLACEMENT
DILEMMA
Choice :
If corrected Na
+
> 150 mmol/l or osmolarity>350mosm/kg use
0.45%.
When blood sugar <14mmol/l change to 5% -10% but should also
continue with N/S
Caution:
If patient is old or has a heart rate or renal failure or sign of cerebral
edema ,titrate I.V fluids with caution.
Rate :
Faster if SBP<90mmHg
Procedures:
Catheter if has not passed fluid by 1hour of fluid therapy
Consider NGT if vomiting or drowsy or GCS <9
DR JOHN OKIDI
19. INSULIN THERAPY
Administer regular insulin: IV (0.1
units/kg) or IM (0.4 units/kg), then 0.1
units/kg per hour by continuous IV
infusion;increase 2- to 10-fold if no
response by 2–4 h.
DR JOHN OKIDI
20. INSULIN THERAPY
•Daily total body insulin requirement 0.5-0.7 u/kg
•Use only regular insulin
•Critical to resolve acidosis, not hyperglycemia
•Decreases blood glucose by 50-100 mg/dl/hr (2.7-
5.5mmol/l)/hr
•Must continue insulin therapy to correct acidosis
•How to constitute insulin: 250 units regular insulin in
250 cc of 0.9%NS or 50 units in 50mls of NS OR 100
units in 100mls of NS = (1.0 units/ml) =0.1 u/ 0.1 ml
21. MANAGEMENT-INSULIN THERAPY
How to Dose insulin :
initial load dose 0.1u/kg insulin regular ,then maintain on 0.1 unit/kg/hr continuous
drip (regular insulin ) e.g a 70kg man will require ; 70x0.1units=7 units/hr=7mls of
constituted insulin drip above and this can be easily given with the syringe or
volumetric pumps in HDU/ICU . This is called Fixed Rate I.V insulin
Infusion(FRIII) .Aim for a target fall in blood ketones of 0.5mmol/l/hr, or a rise in
venous bicarbonate of 3mmol/l/hr with a fall of 3mmol/l/hr. if not achieving this
,increase insulin infusion by 1unit/hr until target is achieved
Continue FRIII until serum ketones <6mmo/l, venous PH >7.3,venous bicarbonate
>15mmol/l.
If NOT IN HDU give :
I.V soluble insulin 6-10units /hour till blood sugar is < 14 mmo/l.
If no improvement in blood glucose or ketosis double insulin dose every 2 hours
If blood sugar is in range of :
>14 to < 16 mmol/l start subcutaneous insulin
Start to run 5% -10% Dextrose or dextrose saline run at rate of 100-200ml/hr
alongside saline.
Insulin infusion may be decreased to 0.05–0.1 units/kg per hour.
Administer intermediate or long-acting insulin as soon as patient is eating. Allow for
overlap in insulin infusion and subcutaneous insulin injection
DR JOHN OKIDI
22. INSULIN THERAPY…
If patient is a wake and can eat start on Basal-Prandial regimen.
If patient is still drowsy and can’t eat give 500mls of 5-10% dextrose
on one arm as you continue with normal saline and put on modified
sliding scale
Modified sliding scale should include insulitard insulin or any other
long acting insulin and soluble insulin.
This should be done for a short time i.e 24-48 hours and then patient
changed to Basal –Prandial insulin if he/she can feed
DR JOHN OKIDI
24. SERUM POTASSIUM
REPLACEMENT
If initial serum potassium is 3.3
mmol/L(3.3 mEq/L), do not administer
insulin until the potassium is corrected
to 3.3 mmol/L (3.3.mEq/L).
K+ level kcl per litre of
fluid(mmol/l)
>5.5 nil
3.5-5.5 30-40mmol/l
<2.2 60-
80mmol/l(ICU,HDU)
DR JOHN OKIDI
25. MANAGEMENT
Replace K: using KCl or Kphos
•10 mEq/hr when
•plasma K <5.5 meq/L
• ECG normal
•Adequate urine flow
• normal creatinine document
•NB:
•Administer 40–80 mEq/h when plasma K< 3.5 mEq/L
or if bicarbonate is given.
•If K >5.5 mEq/l , withhold the potassium therapy and
treat the hyperkalemia if ECG changes are present
DR JOHN OKIDI
26. BICARBONATE THERAPY
Bicarbonate therapy not always indicated as adequate
hydration and insulin correct it.
It may be indicated if ph< 7.1, bicarbonates are <
10mmol/l( profound acidosis)
Do not give in case of life threatening hyperkalemia
± Mannitol(↑ risk of cerebral edema)
DR JOHN OKIDI
27. MANAGEMENT: CONTINUOUS RE-
EVALUATION
1.Reassess patient for precipitating factors
noncompliance, infection, trauma, infarction, cocaine
Initiate appropriate workup for precipitating event (cultures, CXR, ECG).
2.Measure
• capillary glucose every 1–2 hours
• Electrolytes (especially K, bicarbonate, phosphate) every 4 hour for first 24
hour.
• Review patient’s response to Fixed Rate IV Insulin Infusion hourly by calculating rate of
change of ketone level fall (or rise in bicarbonate or fall in glucose).
• Assess for reduction in Ketones of 0.5mmol/hr and Blood sugar of 3mmol/hr or if
bicarbonates are not rising by 3mmol/hr
• Anion gap every 4 h for first 24 hour.
o 10-18mmol/l=anion gap=(Na++k+)-(Cl-+Hco3
-)
3. Monitor every 1–4 h.
Blood pressure
pulse
Respirations
mental status
fluid intake and output
DR JOHN OKIDI
28. KETOSIS MGT
Moderate DKA-KETOSIS resolves spontaneously with
standard Rx
Ph<6.9 requires bicarbonate therapy
Ph 6.9-7.0 50 mEq/l over 1hr 0f NaHCO3
PH <6.9 100 mEq/l of NaHCO3
Monitor arterial ph.
DR JOHN OKIDI
29. RESOLUTION OF DIABETES
KETOACIDOSIS
DKA is resolved when:
1. Serum ketones<0.3mmol/l
2. Venous PH>7.3
3. Venous Bicarbonates >18mmol/l
NB Do not rely on urinary ketone clearance to indicate
resolution of DKA
After resolution of DKA establish why it occurred.
Review patient’s regimen with glycosylated
haemoglobin. Adjust or change regimen accordingly
30. COMPLICATIONS OF DKA
Death
Hypokalemia
Acute Lung Injury
Infection
Venous Thromboembolism
Myocardial infarction
Cerebral edema (reperfusion of previously ischemic brain
tissue)
31. SUMMARY OF DKA
MANAGEMENT
1.Confirm diagnosis (plasma glucose, positive
serum ketones, metabolic acidosis).
2. Admit to hospital; intensive-care setting may
be necessary for frequent monitoring or if pH
<7.00 or unconscious.
3. Assess:
Serum electrolytes (K, Na, Mg, Cl ,bicarbonate,
phosphate)
Acid-base status(pH, HCO3, PCO ,
hydroxybutyrate)
Renal function (creatinine, urine output)
DR JOHN OKIDI