This document discusses dysglycemia and chronic kidney disease (CKD). It begins with an agenda that covers background, pathophysiology, glycemic control, and insulin therapy and conclusions. It then discusses how diabetes is the most common cause of end-stage renal disease. It explains how dysglycemia includes sustained hyperglycemia and acute glucose fluctuations. The kidney plays an important role in glucose homeostasis by filtering, reabsorbing, and producing glucose. Both hyperglycemia and glucose variability can drive diabetic kidney disease through various pathways like protein kinase C activation and oxidative stress. Maintaining good glycemic control through lowering HbA1c can significantly reduce microvascular and cardiovascular complications in patients with CKD.
The Role of SGLT 2 Inhibitors and GLP 1 Receptor Agonists and DPP 4 InhibitorsPHAM HUU THAI
This document discusses the role of SGLT-2 inhibitors, GLP-1 receptor agonists, and DPP-4 inhibitors in managing type 2 diabetes. It provides background on the pathophysiology and progression of type 2 diabetes and limitations of older drug classes. It then describes the mechanisms and roles of the newer drug classes like SGLT-2 inhibitors in promoting urinary glucose excretion and GLP-1 agonists and DPP-4 inhibitors in augmenting the body's own incretin response. It also discusses ongoing cardiovascular outcome trials and FDA approvals of these newer agents.
This document summarizes recent developments in anti-diabetic therapies that target incretin hormones like GLP-1. DPP-4 inhibitors and GLP-1 agonists help address multiple defects in type 2 diabetes pathophysiology by increasing insulin secretion, reducing glucagon levels, and promoting satiety. While some DPP-4 inhibitors were found to increase heart failure risk, the GLP-1 agonists liraglutide and lixisenatide showed neutral cardiovascular outcomes. GLP-1 therapies may also help preserve pancreatic beta cell function and reduce weight. However, they have been linked to rare cases of thyroid cancer in rodents and should not be used in patients with personal or family history of medull
This document provides an overview of the pathophysiology of diabetes mellitus. It defines diabetes as a group of metabolic disorders resulting in hyperglycemia and dyslipidemia due to defects in insulin secretion or action. The document discusses the classification, symptoms, diagnosis and complications of both type 1 and type 2 diabetes. It also covers the physiology of insulin synthesis, secretion and action, as well as the risk factors and pathophysiology underlying different types of diabetes.
Fasting and Caloric Restriction Show Promise for Reducing Type 2 Diabetes Bio...Premier Publishers
The global epidemic of type 2 diabetes (T2D) and its co-morbidities threatens to overwhelm public health services and urgent patient intervention is necessary. A review of mainly randomised controlled trials investigating the reduction of biochemical T2D risk markers through fasting or caloric restriction (CR) found that in T2D or where baseline fasting glucose or HbA1c were elevated, there were significant improvements in fasting glucose and HbA1c, while fasting insulin and insulin resistance may show improvement regardless of condition or baseline levels. There may, however, be ethnic differences, with a clear positive correlation found only in Caucasians. Intermittent CR (i.e. non-continuous periods of fasting) is at least as effective as isocaloric continuous CR, while CR of 400-800 kcal/day is possibly more effective than higher levels for reducing fasting glucose and HbA1c. Time restricted feeding also shows promise but there are few human studies. The findings suggest that the optimum regimen to reduce biochemical risk markers for T2D is an intermittent fasting programme employing a very low-calorie diet with the longest possible number of consecutive days of fasting. The addition of liquid meal replacements, low carbohydrate CR and supplementation of vitamin D, ω-3 PUFAs and L-carnitine may also be of benefit.
This document discusses dysglycemia and chronic kidney disease (CKD). It begins with an agenda that covers background, pathophysiology, glycemic control, and insulin therapy and conclusions. It then discusses how diabetes is the most common cause of end-stage renal disease. It explains how dysglycemia includes sustained hyperglycemia and acute glucose fluctuations. The kidney plays an important role in glucose homeostasis by filtering, reabsorbing, and producing glucose. Both hyperglycemia and glucose variability can drive diabetic kidney disease through various pathways like protein kinase C activation and oxidative stress. Maintaining good glycemic control through lowering HbA1c can significantly reduce microvascular and cardiovascular complications in patients with CKD.
The Role of SGLT 2 Inhibitors and GLP 1 Receptor Agonists and DPP 4 InhibitorsPHAM HUU THAI
This document discusses the role of SGLT-2 inhibitors, GLP-1 receptor agonists, and DPP-4 inhibitors in managing type 2 diabetes. It provides background on the pathophysiology and progression of type 2 diabetes and limitations of older drug classes. It then describes the mechanisms and roles of the newer drug classes like SGLT-2 inhibitors in promoting urinary glucose excretion and GLP-1 agonists and DPP-4 inhibitors in augmenting the body's own incretin response. It also discusses ongoing cardiovascular outcome trials and FDA approvals of these newer agents.
This document summarizes recent developments in anti-diabetic therapies that target incretin hormones like GLP-1. DPP-4 inhibitors and GLP-1 agonists help address multiple defects in type 2 diabetes pathophysiology by increasing insulin secretion, reducing glucagon levels, and promoting satiety. While some DPP-4 inhibitors were found to increase heart failure risk, the GLP-1 agonists liraglutide and lixisenatide showed neutral cardiovascular outcomes. GLP-1 therapies may also help preserve pancreatic beta cell function and reduce weight. However, they have been linked to rare cases of thyroid cancer in rodents and should not be used in patients with personal or family history of medull
This document provides an overview of the pathophysiology of diabetes mellitus. It defines diabetes as a group of metabolic disorders resulting in hyperglycemia and dyslipidemia due to defects in insulin secretion or action. The document discusses the classification, symptoms, diagnosis and complications of both type 1 and type 2 diabetes. It also covers the physiology of insulin synthesis, secretion and action, as well as the risk factors and pathophysiology underlying different types of diabetes.
Fasting and Caloric Restriction Show Promise for Reducing Type 2 Diabetes Bio...Premier Publishers
The global epidemic of type 2 diabetes (T2D) and its co-morbidities threatens to overwhelm public health services and urgent patient intervention is necessary. A review of mainly randomised controlled trials investigating the reduction of biochemical T2D risk markers through fasting or caloric restriction (CR) found that in T2D or where baseline fasting glucose or HbA1c were elevated, there were significant improvements in fasting glucose and HbA1c, while fasting insulin and insulin resistance may show improvement regardless of condition or baseline levels. There may, however, be ethnic differences, with a clear positive correlation found only in Caucasians. Intermittent CR (i.e. non-continuous periods of fasting) is at least as effective as isocaloric continuous CR, while CR of 400-800 kcal/day is possibly more effective than higher levels for reducing fasting glucose and HbA1c. Time restricted feeding also shows promise but there are few human studies. The findings suggest that the optimum regimen to reduce biochemical risk markers for T2D is an intermittent fasting programme employing a very low-calorie diet with the longest possible number of consecutive days of fasting. The addition of liquid meal replacements, low carbohydrate CR and supplementation of vitamin D, ω-3 PUFAs and L-carnitine may also be of benefit.
1) Prediabetes is a condition where blood sugar levels are higher than normal but not high enough for a diagnosis of diabetes. It affects an estimated 14% of people in India and 9.9-25% of people in other countries.
2) Lifestyle changes like diet modification, increased physical activity, weight loss and smoking cessation can help prevent or delay progression from prediabetes to diabetes. Medications like metformin have also shown effectiveness.
3) People with prediabetes have an increased risk of cardiovascular diseases like heart attack and stroke, even at blood sugar levels below the prediabetes threshold. Intensive lifestyle interventions or metformin treatment can significantly reduce risk of developing diabetes.
This document discusses diabetes and new antidiabetic drugs. It notes that diabetes cases are rising significantly worldwide and that diabetes increases the risk of serious health complications. It describes the different types of diabetes and their presentations. It recommends screening guidelines for prediabetes and notes the importance of lifestyle changes to prevent progression to diabetes. It discusses treatment targets and factors like hypoglycemia. It also provides an overview of various drug classes used to treat diabetes, including their mechanisms and effects.
Type 2 Diabetes Mellitus: The Concerned Complications and Target OrgansApollo Hospitals
Diabetes has been considered as the most dreaded non-communicable disease consuming the mankind rapidly. WHO has predicted the number of diabetics to be approximately 366 millions by 2030. The disease is characterized by hyperglycemia and the basic symptoms are polyphagia, polydipsia and polyuria. The autoimmune type 1 diabetes represent almost 1% of the total diabetic population, the rest being that of type 2 diabetes (T2D). Type 2 diabetes has been linked to a variety of factors such as heredity, environmental factors, unhealthy eating habits, sedentary lifestyle, stress etc. The uncontrolled hyperglycemia has profound deleterious effects on almost all the organs and results in various cardiovascular disorders, retinopathy, neuropathy, and nephropathy. Recent studies have revealed an array of pulmonary dysfunctions related with T2D ranging from respiratory defects to tuberculosis. Diabetes also predisposes the person to hepatic dysfunctions like NAFLD and HCC and a range of infections at various sites which are difficult to manage. Post-surgical infections are of special interest for subjects with uncontrolled hyperglycemia prior to surgery. Scientists all over the world are revealing different pathways and associated therapies for type 2 diabetes in order to control the pathological effects covering almost whole body physiology.
This document discusses the challenges of managing diabetes in patients with chronic kidney disease (CKD). It notes that diabetes is a leading cause of CKD progression and that CKD increases mortality risk in diabetes patients. Managing glucose levels in CKD patients is difficult due to risks of hypoglycemia from insulin clearance issues and need to adjust oral medications for kidney function. The CARMELINA trial demonstrated the renal safety of the DPP-4 inhibitor linagliptin in high cardio-renal risk patients, showing no increase in sustained decrease in eGFR or other renal outcomes compared to placebo over 2 years.
Modern therapy in diabetics with cad scintic dayOsama Almaraghi
This document provides information on modern therapy for diabetics with coronary artery disease. It discusses the following key points in 3 sentences:
Diabetes is a global epidemic that is increasing worldwide. Cardiovascular disease is the leading cause of death for diabetics, as they face comparable heart attack risks to those with a previous heart attack. The document reviews guidelines for glycemic, blood pressure, and lipid control to reduce cardiovascular risks and discusses various drug therapy options for treating diabetes in patients with cardiovascular disease.
This document provides an overview of diabetes pharmacology and anesthesia management. It begins by describing glucose regulation and the pathophysiology of diabetes. It then discusses the various medications used to treat diabetes, including insulin formulations and non-insulin agents. The document explains how these medications impact anesthesia care and strategies for maintaining glycemic control in surgical patients with diabetes. The objectives are to describe glucose physiology, identify diabetes medications and their effects, and discuss perioperative glycemic management strategies.
This document discusses the underlying pathophysiology of type 2 diabetes, specifically insulin resistance and beta-cell dysfunction. It provides evidence that these defects are core features of type 2 diabetes and addressing them through treatments targeting insulin resistance can help improve diabetes care and outcomes. The document recommends understanding and treating the underlying pathophysiology, including insulin resistance, in order to better manage type 2 diabetes and reduce complications.
This document discusses the underlying pathophysiology of type 2 diabetes, specifically insulin resistance and beta-cell dysfunction. It notes that insulin resistance, where tissues do not respond properly to insulin, is a major defect in type 2 diabetes and closely associated with obesity. Beta-cell dysfunction refers to the reduced ability of pancreatic beta cells to secrete insulin in response to high blood glucose levels. Over time, the combination of insulin resistance and beta-cell dysfunction leads to chronically high blood glucose levels and a diagnosis of type 2 diabetes. The document recommends that treatment of type 2 diabetes should target these underlying defects by addressing insulin resistance through medications like thiazolidinediones in addition to other antidiabetic agents.
A 63-year-old man with a history of IHD, 1VD, HTN, hyperlipidemia, and an HbA1c of 8.2% is taking 26 units of insulin glargine daily. His LDL is 80 mg/dL and TG is 160 mg/dL. His BMI is 26. The document discusses treatment options with pioglitazone given his medical history and risk factors. Pioglitazone has been shown to improve insulin sensitivity and reduce cardiovascular events and microvascular complications in patients with type 2 diabetes when used as monotherapy or in combination with other antidiabetic agents. However, pioglitazone can cause side effects like edema,
This document provides an overview of diabetic ketoacidosis (DKA). It begins with definitions of diabetes mellitus and discusses the types, causes, epidemiology, physiology, pathophysiology, clinical presentation, diagnosis, complications, and treatment of DKA. Key points include that DKA is caused by absolute or relative insulin deficiency, which leads to metabolic derangements including dehydration, electrolyte imbalances, and ketosis. Presenting symptoms range from nausea and vomiting to altered mental status. Treatment involves fluid resuscitation and insulin administration to resolve the metabolic abnormalities.
1. Diabetes mellitus results from inadequate insulin supply or inadequate tissue response to insulin, leading to hyperglycemia. There are three main types: type 1 is autoimmune and causes complete insulin deficiency; type 2 is more common and involves relative insulin deficiency and insulin resistance; type 1b is a rare form not caused by autoimmunity.
2. Symptoms of diabetes include fatigue, weight loss, polyuria, polydipsia, and blurry vision. Diagnosis involves blood glucose criteria and HbA1c levels. Treatment involves lifestyle changes, oral medications like metformin and sulfonylureas, and insulin for more severe cases.
3. Complications include diabetic ketoacidosis, characterized by
This document summarizes key information about type 2 diabetes drug candidates in phase 3 clinical trials, including their mechanisms of action and endpoints. Five major drugs are discussed: BMS-512148, Victoza, D-Tagatose, JNJ-28431754, and Albiglutide. BMS-512148 and JNJ-28431754 are SGLT2 inhibitors, Victoza is a GLP-1 receptor agonist, D-Tagatose blocks glucose absorption, and Albiglutide is a GLP-1 agonist fused to human albumin for extended effects. The average trial duration is 2.5 years and endpoints include HbA1c, weight, and
Ponencia realizada por el Dr. Eduard Montanya Mias del Hospital Universitari de Bellvitge (Barcelona). Director Científico CIBERDEM en la sesión 'Diabetes 2021. Cardiólogos y endocrinólogos: ¿matrimonio o divorcio?' del 13 de mayo de 2021
This document summarizes a review article on type 2 diabetes mellitus. It discusses the pathophysiology, epidemiology, screening, diagnosis, and management of type 2 diabetes. Some key points include:
- Type 2 diabetes is characterized by insulin resistance and impaired insulin secretion, accounting for 90% of diabetes cases worldwide.
- Rates of type 2 diabetes have increased dramatically in recent decades due to obesity and decreased exercise.
- Screening for type 2 diabetes involves measuring fasting plasma glucose levels, and an oral glucose tolerance test may also be used for diagnosis.
- Management of type 2 diabetes focuses on lifestyle changes as well as medications to lower blood sugar and prevent complications.
1) The document discusses guidelines for initiating basal insulin therapy in patients with type 2 diabetes, including benefits such as lowering HbA1c and reducing cardiovascular risk.
2) It compares different basal insulin options like glargine, detemir, and NPH insulin, finding that the long-acting analogs glargine and detemir have advantages like lower rates of hypoglycemia and weight gain compared to NPH.
3) Studies show that early initiation of basal insulin can help preserve beta-cell function and provide better long-term glycemic control for patients with type 2 diabetes.
This document discusses the benefits of early initiation of basal insulin in managing type 2 diabetes. It recommends starting with low doses of long-acting basal insulin, which can help lower HbA1c and reduce complications by providing consistent insulin levels throughout the day. Basal insulin is preferred over premix insulins when first adding insulin. Clinical guidelines support initiating basal insulin when oral medications fail to control blood sugar levels. Studies show basal insulin improves beta-cell function and glycemic control long-term compared to late insulin initiation.
1) Exenatide once weekly (QW), also known as Bydureon, provides glycemic control through reductions in HbA1c of 1.3-1.9% over 24-30 weeks according to clinical trials.
2) Head-to-head trials show Exenatide QW results in similar or greater HbA1c reductions and more weight loss compared to other GLP-1 receptor agonists such as liraglutide.
3) Exenatide QW has been shown to maintain glycemic control over the long term with reductions in HbA1c of 1.5% maintained out to 6 years, along with significant and sustained weight loss from
This document discusses diabetes mellitus and its management. It provides information on:
1) The classification and prevalence of diabetes in Saudi Arabia, finding an overall prevalence of 23.7% with higher rates in males.
2) The diagnostic criteria and thresholds for diabetes based on HbA1c, fasting plasma glucose, and oral glucose tolerance tests. Screening is recommended for those over 45 or with risk factors.
3) Treatment involves lifestyle modifications, metformin as first line therapy, and additional oral medications or insulin as needed to achieve glycemic targets. Managing associated cardiovascular risk factors is also emphasized.
This document discusses key aspects of medical nutrition therapy (MNT) for diabetes and related disorders. It covers goals of MNT including healthful eating patterns and glycemic control. It provides recommendations for carbohydrate, protein, fat, fiber and other macronutrient intake. Micronutrient supplementation and herbal supplements marketed for diabetes are also addressed. Guidelines are provided for MNT in type 1 and type 2 diabetes, including for pediatric patients. Estimates for energy requirements in different populations are also summarized.
This document discusses cell and tissue damage from various causes and their effects. It begins by explaining prefixes, suffixes, and roots used in medical terminology. It then defines pathology and discusses basic terminology like disease, etiology, pathogenesis, diagnosis, and prognosis. Various types of cellular adaptation and degeneration are described, including atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia. Necrosis, or lethal cell injury, is defined and the stages are outlined. Various causes of cell injury are provided like oxygen deprivation, chemicals, infections, immunological reactions, genetics, nutrition, physical agents, and aging.
1) Prediabetes is a condition where blood sugar levels are higher than normal but not high enough for a diagnosis of diabetes. It affects an estimated 14% of people in India and 9.9-25% of people in other countries.
2) Lifestyle changes like diet modification, increased physical activity, weight loss and smoking cessation can help prevent or delay progression from prediabetes to diabetes. Medications like metformin have also shown effectiveness.
3) People with prediabetes have an increased risk of cardiovascular diseases like heart attack and stroke, even at blood sugar levels below the prediabetes threshold. Intensive lifestyle interventions or metformin treatment can significantly reduce risk of developing diabetes.
This document discusses diabetes and new antidiabetic drugs. It notes that diabetes cases are rising significantly worldwide and that diabetes increases the risk of serious health complications. It describes the different types of diabetes and their presentations. It recommends screening guidelines for prediabetes and notes the importance of lifestyle changes to prevent progression to diabetes. It discusses treatment targets and factors like hypoglycemia. It also provides an overview of various drug classes used to treat diabetes, including their mechanisms and effects.
Type 2 Diabetes Mellitus: The Concerned Complications and Target OrgansApollo Hospitals
Diabetes has been considered as the most dreaded non-communicable disease consuming the mankind rapidly. WHO has predicted the number of diabetics to be approximately 366 millions by 2030. The disease is characterized by hyperglycemia and the basic symptoms are polyphagia, polydipsia and polyuria. The autoimmune type 1 diabetes represent almost 1% of the total diabetic population, the rest being that of type 2 diabetes (T2D). Type 2 diabetes has been linked to a variety of factors such as heredity, environmental factors, unhealthy eating habits, sedentary lifestyle, stress etc. The uncontrolled hyperglycemia has profound deleterious effects on almost all the organs and results in various cardiovascular disorders, retinopathy, neuropathy, and nephropathy. Recent studies have revealed an array of pulmonary dysfunctions related with T2D ranging from respiratory defects to tuberculosis. Diabetes also predisposes the person to hepatic dysfunctions like NAFLD and HCC and a range of infections at various sites which are difficult to manage. Post-surgical infections are of special interest for subjects with uncontrolled hyperglycemia prior to surgery. Scientists all over the world are revealing different pathways and associated therapies for type 2 diabetes in order to control the pathological effects covering almost whole body physiology.
This document discusses the challenges of managing diabetes in patients with chronic kidney disease (CKD). It notes that diabetes is a leading cause of CKD progression and that CKD increases mortality risk in diabetes patients. Managing glucose levels in CKD patients is difficult due to risks of hypoglycemia from insulin clearance issues and need to adjust oral medications for kidney function. The CARMELINA trial demonstrated the renal safety of the DPP-4 inhibitor linagliptin in high cardio-renal risk patients, showing no increase in sustained decrease in eGFR or other renal outcomes compared to placebo over 2 years.
Modern therapy in diabetics with cad scintic dayOsama Almaraghi
This document provides information on modern therapy for diabetics with coronary artery disease. It discusses the following key points in 3 sentences:
Diabetes is a global epidemic that is increasing worldwide. Cardiovascular disease is the leading cause of death for diabetics, as they face comparable heart attack risks to those with a previous heart attack. The document reviews guidelines for glycemic, blood pressure, and lipid control to reduce cardiovascular risks and discusses various drug therapy options for treating diabetes in patients with cardiovascular disease.
This document provides an overview of diabetes pharmacology and anesthesia management. It begins by describing glucose regulation and the pathophysiology of diabetes. It then discusses the various medications used to treat diabetes, including insulin formulations and non-insulin agents. The document explains how these medications impact anesthesia care and strategies for maintaining glycemic control in surgical patients with diabetes. The objectives are to describe glucose physiology, identify diabetes medications and their effects, and discuss perioperative glycemic management strategies.
This document discusses the underlying pathophysiology of type 2 diabetes, specifically insulin resistance and beta-cell dysfunction. It provides evidence that these defects are core features of type 2 diabetes and addressing them through treatments targeting insulin resistance can help improve diabetes care and outcomes. The document recommends understanding and treating the underlying pathophysiology, including insulin resistance, in order to better manage type 2 diabetes and reduce complications.
This document discusses the underlying pathophysiology of type 2 diabetes, specifically insulin resistance and beta-cell dysfunction. It notes that insulin resistance, where tissues do not respond properly to insulin, is a major defect in type 2 diabetes and closely associated with obesity. Beta-cell dysfunction refers to the reduced ability of pancreatic beta cells to secrete insulin in response to high blood glucose levels. Over time, the combination of insulin resistance and beta-cell dysfunction leads to chronically high blood glucose levels and a diagnosis of type 2 diabetes. The document recommends that treatment of type 2 diabetes should target these underlying defects by addressing insulin resistance through medications like thiazolidinediones in addition to other antidiabetic agents.
A 63-year-old man with a history of IHD, 1VD, HTN, hyperlipidemia, and an HbA1c of 8.2% is taking 26 units of insulin glargine daily. His LDL is 80 mg/dL and TG is 160 mg/dL. His BMI is 26. The document discusses treatment options with pioglitazone given his medical history and risk factors. Pioglitazone has been shown to improve insulin sensitivity and reduce cardiovascular events and microvascular complications in patients with type 2 diabetes when used as monotherapy or in combination with other antidiabetic agents. However, pioglitazone can cause side effects like edema,
This document provides an overview of diabetic ketoacidosis (DKA). It begins with definitions of diabetes mellitus and discusses the types, causes, epidemiology, physiology, pathophysiology, clinical presentation, diagnosis, complications, and treatment of DKA. Key points include that DKA is caused by absolute or relative insulin deficiency, which leads to metabolic derangements including dehydration, electrolyte imbalances, and ketosis. Presenting symptoms range from nausea and vomiting to altered mental status. Treatment involves fluid resuscitation and insulin administration to resolve the metabolic abnormalities.
1. Diabetes mellitus results from inadequate insulin supply or inadequate tissue response to insulin, leading to hyperglycemia. There are three main types: type 1 is autoimmune and causes complete insulin deficiency; type 2 is more common and involves relative insulin deficiency and insulin resistance; type 1b is a rare form not caused by autoimmunity.
2. Symptoms of diabetes include fatigue, weight loss, polyuria, polydipsia, and blurry vision. Diagnosis involves blood glucose criteria and HbA1c levels. Treatment involves lifestyle changes, oral medications like metformin and sulfonylureas, and insulin for more severe cases.
3. Complications include diabetic ketoacidosis, characterized by
This document summarizes key information about type 2 diabetes drug candidates in phase 3 clinical trials, including their mechanisms of action and endpoints. Five major drugs are discussed: BMS-512148, Victoza, D-Tagatose, JNJ-28431754, and Albiglutide. BMS-512148 and JNJ-28431754 are SGLT2 inhibitors, Victoza is a GLP-1 receptor agonist, D-Tagatose blocks glucose absorption, and Albiglutide is a GLP-1 agonist fused to human albumin for extended effects. The average trial duration is 2.5 years and endpoints include HbA1c, weight, and
Ponencia realizada por el Dr. Eduard Montanya Mias del Hospital Universitari de Bellvitge (Barcelona). Director Científico CIBERDEM en la sesión 'Diabetes 2021. Cardiólogos y endocrinólogos: ¿matrimonio o divorcio?' del 13 de mayo de 2021
This document summarizes a review article on type 2 diabetes mellitus. It discusses the pathophysiology, epidemiology, screening, diagnosis, and management of type 2 diabetes. Some key points include:
- Type 2 diabetes is characterized by insulin resistance and impaired insulin secretion, accounting for 90% of diabetes cases worldwide.
- Rates of type 2 diabetes have increased dramatically in recent decades due to obesity and decreased exercise.
- Screening for type 2 diabetes involves measuring fasting plasma glucose levels, and an oral glucose tolerance test may also be used for diagnosis.
- Management of type 2 diabetes focuses on lifestyle changes as well as medications to lower blood sugar and prevent complications.
1) The document discusses guidelines for initiating basal insulin therapy in patients with type 2 diabetes, including benefits such as lowering HbA1c and reducing cardiovascular risk.
2) It compares different basal insulin options like glargine, detemir, and NPH insulin, finding that the long-acting analogs glargine and detemir have advantages like lower rates of hypoglycemia and weight gain compared to NPH.
3) Studies show that early initiation of basal insulin can help preserve beta-cell function and provide better long-term glycemic control for patients with type 2 diabetes.
This document discusses the benefits of early initiation of basal insulin in managing type 2 diabetes. It recommends starting with low doses of long-acting basal insulin, which can help lower HbA1c and reduce complications by providing consistent insulin levels throughout the day. Basal insulin is preferred over premix insulins when first adding insulin. Clinical guidelines support initiating basal insulin when oral medications fail to control blood sugar levels. Studies show basal insulin improves beta-cell function and glycemic control long-term compared to late insulin initiation.
1) Exenatide once weekly (QW), also known as Bydureon, provides glycemic control through reductions in HbA1c of 1.3-1.9% over 24-30 weeks according to clinical trials.
2) Head-to-head trials show Exenatide QW results in similar or greater HbA1c reductions and more weight loss compared to other GLP-1 receptor agonists such as liraglutide.
3) Exenatide QW has been shown to maintain glycemic control over the long term with reductions in HbA1c of 1.5% maintained out to 6 years, along with significant and sustained weight loss from
This document discusses diabetes mellitus and its management. It provides information on:
1) The classification and prevalence of diabetes in Saudi Arabia, finding an overall prevalence of 23.7% with higher rates in males.
2) The diagnostic criteria and thresholds for diabetes based on HbA1c, fasting plasma glucose, and oral glucose tolerance tests. Screening is recommended for those over 45 or with risk factors.
3) Treatment involves lifestyle modifications, metformin as first line therapy, and additional oral medications or insulin as needed to achieve glycemic targets. Managing associated cardiovascular risk factors is also emphasized.
This document discusses key aspects of medical nutrition therapy (MNT) for diabetes and related disorders. It covers goals of MNT including healthful eating patterns and glycemic control. It provides recommendations for carbohydrate, protein, fat, fiber and other macronutrient intake. Micronutrient supplementation and herbal supplements marketed for diabetes are also addressed. Guidelines are provided for MNT in type 1 and type 2 diabetes, including for pediatric patients. Estimates for energy requirements in different populations are also summarized.
This document discusses cell and tissue damage from various causes and their effects. It begins by explaining prefixes, suffixes, and roots used in medical terminology. It then defines pathology and discusses basic terminology like disease, etiology, pathogenesis, diagnosis, and prognosis. Various types of cellular adaptation and degeneration are described, including atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia. Necrosis, or lethal cell injury, is defined and the stages are outlined. Various causes of cell injury are provided like oxygen deprivation, chemicals, infections, immunological reactions, genetics, nutrition, physical agents, and aging.
This document summarizes diabetic retinopathy (DR), including its causes, risk factors, classifications, complications, treatments, and prevention strategies. DR is caused by damage to the small blood vessels in the retina from poorly controlled diabetes. It can be classified as non-proliferative DR or proliferative DR depending on whether abnormal blood vessel growth is present. Risk factors include the duration and control of diabetes, hypertension, and nephropathy. Treatments include intensive glycemic control, laser therapy, and medications that may inhibit damaging pathways like sorbitol. Regular eye exams are important for monitoring and preventing vision loss from DR.
This document provides an overview of biochemistry concepts related to the nervous system. It discusses topics like transport through the blood-brain barrier, metabolism of neurotransmitters, energy metabolism in the central nervous system, and biochemical aspects of CNS diseases. It describes the structure and functions of neurons and glial cells. It also summarizes the synthesis, release, and metabolism of important neurotransmitters like acetylcholine, catecholamines, serotonin, GABA, glutamate, histamine, and their roles in the nervous system. The document discusses energy metabolism in the brain and metabolic dysfunction in Alzheimer's disease.
A species is a group of creatures that share similar features and interbreed to generate viable offspring. 1. A genus is the highest level of taxonomic categorisation, ranking below family and above species. 2. They are the most basic level of biological categorisation.
1. Pathophysiology is the study of the underlying mechanisms by which diseases occur and develop, and the study of the changes within the body caused by diseases. It provides a theoretical basis for prevention, diagnosis, and treatment of diseases.
2. Pathophysiology focuses on the alterations in structure, function, and metabolism that occur in the body and the mechanisms underlying the development of diseases. It emphasizes the developmental process of diseases.
3. Pathophysiology plays an important role in bridging basic medical sciences and clinical medicine. It examines both the normal and abnormal functioning of the body.
This document provides an overview of pathology, cell and tissue damage. It defines pathology as the study of diseases and discusses basic terminology like etiology, pathogenesis, diagnosis and clinical manifestation. It also describes different types of cellular adaptation like atrophy, hypertrophy and hyperplasia in response to injury. The document outlines the stages and types of necrosis, or cell death, as well as various causes of cell injury such as oxygen deprivation, chemicals, infections, immune reactions and physical trauma.
This document provides an overview of human metabolism. It discusses key topics such as:
- Metabolism involves chemical reactions that create or breakdown energy for physical and physiological activity and maintaining body temperature.
- Energy balance depends on the difference between energy intake (calories consumed) and energy expenditure (calories burned), which occurs through basal metabolic rate, thermogenesis, and physical activity.
- Basal metabolic rate is the minimum calories burned at rest and can be estimated using the Harris Benedict Equation.
- Metabolic pathways like glycolysis, the Krebs cycle, and the electron transport chain occur in cell respiration to ultimately produce ATP through oxidative phosphorylation.
1) Enzymes can act as diagnostic markers of underlying diseases and as reagents for biochemical estimations and detections. Certain enzymes are present in normal plasma and perform physiological functions, while others arise from cell destruction.
2) Increased levels of enzymes like creatine phosphokinase, lactate dehydrogenase, and aspartate transaminase can help diagnose acute myocardial infarction by indicating heart muscle damage. Measuring the different isoenzymes of creatine phosphokinase and lactate dehydrogenase can determine the source of elevated levels.
3) Elevated levels of aminotransferases like alanine aminotransferase and aspartate aminotransferase indicate liver cell injury and are useful for recognizing acute
This document summarizes lipid metabolism in the body. It discusses how fatty acids are taken up by cells and used as precursors, fuels, or substrates for ketone body synthesis. Ketone bodies can then be exported to other tissues for energy production. The document also outlines the multi-step digestive process that triglycerides must undergo to be broken down and absorbed, including hydrolysis by pancreatic lipase and transport via micelles and chylomicrons. Triglycerides are stored in adipose tissue and mobilized through lipolysis triggered by hormones like epinephrine and glucocorticoids. Glycerol and fatty acids are released from triglycerides and can be used for energy production.
The document discusses vitamins, minerals, and water. It explains that vitamins are nutrients required in small amounts that assist chemical reactions in the body, while minerals are required in larger amounts and regulate reactions. There are two classes of vitamins - fat-soluble vitamins like A, D, E, K that can be stored, and water-soluble vitamins like C and B vitamins that cannot be stored. Key minerals include calcium, sodium, potassium, magnesium, phosphorus, chloride, sulfur, iron and zinc. Water makes up about 65% of the body and is essential for chemical reactions and homeostasis. A balanced diet typically provides sufficient vitamins and minerals so supplements are usually unnecessary.
Protein digestion begins in the stomach where pepsin and hydrochloric acid break proteins into smaller polypeptides. In the small intestine, proteases like trypsin further break polypeptides into amino acids. Amino acids are absorbed into the bloodstream and transported to cells. Excess amino acids or those from protein breakdown are converted into urea to be excreted, using glutamate as an intermediate. Urea is produced through a cyclic urea cycle that involves several steps and uses multiple substrates including ammonia, carbon dioxide, and aspartate. Hemoglobin breakdown produces bile pigments like bilirubin that are conjugated and excreted in bile or form the pigments seen in bruises and stools.
This chapter introduces metabolism and its significance in medicine. Metabolism consists of catabolic reactions that break down molecules, and anabolic reactions that build them up. Glycolysis is the first pathway of glucose degradation, converting it into pyruvate while generating ATP. Glycolysis occurs in ten enzyme-catalyzed steps located in the cytosol of cells.
This document discusses lipid and lipoprotein metabolism. Key points include:
1) Cholesterol is synthesized in tissues and absorbed from the diet, while triglycerides are absorbed after dietary fat is broken down.
2) Lipoproteins like LDL and HDL transport lipids in the blood and are composed of a lipid core surrounded by proteins and phospholipids.
3) The liver plays a central role in lipid homeostasis, regulating cholesterol synthesis and bile acid production.
4) Derangements in lipid metabolism can occur in conditions like metabolic syndrome and increase disease risk. Reverse cholesterol transport via HDL is an important protective process.
9- biochemical aspect of bile acid and salt.pdfDrirFaisalHasan
Bile acids and salts are synthesized in the liver from cholesterol. The primary bile acids, cholic acid and chenodeoxycholic acid, are conjugated with glycine or taurine to form bile salts like glycocholic acid and taurochenodeoxycholic acid. Bile salts emulsify lipids in the small intestine to aid in digestion and absorption. They undergo enterohepatic circulation where they are reabsorbed in the ileum and returned to the liver and gallbladder. Diseases that disrupt bile salt production or circulation can impair lipid digestion leading to conditions like gallstones or malabsorption.
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Hypotension, or low blood pressure, is when the pressure of blood circulating in the body is lower than normal or expected. It's only a problem if it negatively impacts the body and causes symptoms. Normal blood pressure is usually between 90/60 mmHg and 120/80 mmHg, but pressures below 90/60 are generally considered hypotensive.
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This particular slides consist of- what is Pneumothorax,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is a summary of Pneumothorax:
Pneumothorax, also known as a collapsed lung, is a condition that occurs when air leaks into the space between the lung and chest wall. This air buildup puts pressure on the lung, preventing it from expanding fully when you breathe. A pneumothorax can cause a complete or partial collapse of the lung.
1. www.excemed.org
IMPROVING THE PATIENT’S LIFE
THROUGH
MEDICAL EDUCATION
Pathophysiology of type 2 diabetes
Bruno Almeida
M.D., M.Sc. Clinical Nutrition,
PhD Student
October 2015
2. DISCLOSURES
• I have no actual or potential conflict of interest in relation to
this program/presentation;
• Speaker: Merck Serono, Lilly, Novonordisk, Novartis;
11. Definition
• Diabetes is a group of metabolic diseases characterized by
hyperglycaemia resulting from defects in insulin secretion,
insulin action or both.
• The chronic hyperglycaemia of diabetes is associated with
long-term damage, dysfunction and failure of various organs,
especially the eyes, kidneys, nerves, heart and blood vessels.
ADA position statement. Diabetes Care 2009; 31(S1): S55-S60
12. Old view: predominantly insulin resistance and relative (rather
than absolute) insulin deficiency.
Current view: progressive insulin secretory defect on the
background of insulin resistance.
Type 2 Diabetes
• The most prevalent form of diabetes (accounts up to 90-95% of
all the forms of diabetes)
ADA Position Statement. Diabetes Care 2009; 31(S1): S55-S60
ADA Position Statement. Diabetes Care 2014; 37(S1): S14-S78
13. Glucose influx and outflow
• Any rise in glycaemia is the net result of glucose influx
exceeding glucose outflow from the plasma compartment.
• In the fasting state, hyperglycemia is directly related to
increased hepatic glucose production.
• In the postprandial state, further glucose excursions result
from the combination of insufficient suppression of this
glucose output and defective insulin stimulation of glucose
disposal in target tissues.
Inzucchi E, et al. Diabetes Care 2012; 35:1364-79
15. 15
Effects of insulin on glucose influx/outflow
Increases glycogen synthesis
Decreases glycogenolysis
Inhibits gluconeogenesis
Increases the uptake of glucose
by stimulating the exposure of
GLUT4 in cell membrane
Stimulates glycolysis
Kahn R, et al. Joslin’s Diabetes Mellitus, 2005.
Dimitriadis G, et al. Diabetes Res Clin Pract 2011; 93 (S1):S52-S59
16. • Interaction between genes and environment can lead
to obesity and insulin resistance.
• Genetically susceptible β- cells are unable to
compensate the increased secretory demand, resulting
in type 2 diabetes.
Adapted from Kahn, Hull, et al 2006
Etiology of type 2 diabetes
17. 17
The β-cell in type 2 diabetes: function
HOMA: homeostasis model assessment
0
20
40
100
–4 6
–10 –8 –6 –2 0 2 4
80
60
–12 8
Diabetes diagnosis
Years to diagnosis
-cell
function
(%,
HOMA)
Adapted from: Lebovitz, Diabetes Reviews 1999;7:139–53
(data are from the UKPDS population: UKPDS 16. Diabetes 1995;44:1249–58)
At the time of diagnosis patients with T2D already show an
impaired β-cell function, that progressively decreases during the
disease
18. 18
The β-cell in type 2 diabetes: mass
0
0,5
1
1,5
2
2,5
3
NGT IFG T2D NGT T2D LADA
Lean
Obese
-50%
-63%
-cell
volume
(%)
Butler AE et al. Diabetes 2003; Leslie RD e Pozzilli P, J Clin Endocrinol Metab 2006; Deng S et al. Diabetes 2004
19. 19
The loss of β-cell mass and function results in the
progressive insulin secretory defect…
Hours
0
200
400
600
800
6.00 10.00 14.00 18.00 22.00 2.00 6.00
Breakfast Lunch DInner
normal
type 2 diabetes
Insulin
secretion
(pmol/min)
Polonsky KS et al. N Engl J Med, 1988
20. …on the background of insulin resistance
IR: Insulin Resistance
PG: Plasma glucose
IS: Insulin Secretion
• Increased insulin resistance in muscle, liver and adipose tissue
causes hepatic glucose overproduction, impaired glucose uptake
from muscles and increased plasma levels of FFA
Taylor R Diabetologia 2008; 51: 1781-89
21. 21
The twin vicious cycle of insulin resistance leading to
T2D
Plasma
glucose
Taylor R Diabetologia 2008; 51: 1781-89
24. OMINOUS OCTET
DeFronzo RA. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus.
Diabetes. 2009;58:773-795
25. 25
-60 0 60 120 180 240
Insulin
Glucagon
Glucose
meal
T2D
Controls
Impaired insulin secretion
Increases in glucagon levels
t
De Fronzo’s octet: increased glucagon
Muller WA et al. N EnglJ Med. 1970
26. The role of the adipose tissue
• Glucose derived from diet or endogenous sources stimulates
insulin secretion.
Evans R, et al. Nat Rev Endocrinol 2004; 10: 1-10
27. • Insulin promotes glucose uptake by skeletal muscle and fat,
opposes hepatic glycogenolysis and gluconeogenesis, and
inhibits fat lipolysis.
• Free fatty acids liberated from adipose tissue contribute to
insulin resistance in skeletal muscle and liver.
• Additional fat-derived signals, including TNF-α, resistin and
visfatin, modulate insulin sensitivity and fatty acid metabolism in
muscle and liver.
Evans R, et al. Nat Rev Endocrinol 2004; 10: 1-10
The role of the adipose tissue
28. Incretins
• Insulin response in humans is greater after the oral ingestion
of glucose than after the intravenous infusion of glucose. This
phenomena is known as “incretin effect”.
• GIP and GLP1 are two hormones, namely the incretins,
secreted by the gut (GIP in the jejunum and GLP-1 in distal
ileum) that are responsible for the incretin effect.
• Incretins have a short half-life in-vivo because they are rapidly
metabolized by an enzyme called DPP4.
Meier JJ. Nat Rev Endocrinol 2012; 8: 728-742
29. 29
Total GLP-1, controls
Total GLP-1, T2D
Intact GLP-1, controls
Intact GLP-1, T2D
0
10
20
30
0 50 100 150
Tempo (min)
GLP-1
(pmol/l)
*
*
*
P <0,05
Vilsbøll T, et al. Diabetes. 2001
In T2D the secretion of GLP-1 after a meal is impaired
30. The role of the kidney
• The kidney filters 162 g ([glomerular filtration rate 180 l/day]
[fasting plasma glucose 900 mg/l]) of glucose every day.
• The sodium-glucose co-transporter 2 (SGLT2) is expressed in the
proximal tubule and mediates reabsorption of approximately 90
percent of the filtered glucose load.
• SGLT2 inhibitors promote the renal excretion of glucose and
thereby lower elevated blood glucose levels in patients with type
2 diabetes.
• The glucose-lowering effect is independent of insulin (beta cell
function and insulin sensitivity).
David K McCulloch. UpToDate 2014.
31. SGLT2
Sodium-glucose transporters
SGLT1
1. Chao EC, Henry RR. Nat Rev Drug Discov 2010;9:551–9; 2. Mather A, Pollock C. Kidney Int Suppl 2011;120:S1–S6; 3. Wright EM, et al. J Intern Med
2007;261:32–43.
Main uptake mechanism for
glucose and galactose in the
intestine
S2 and S3 segments of the proximal
renal tubule are responsible for the
remaining 10% of the renal glucose
High-affinity (Km=~0.5 mM),
low-capacity transporter, which
transfers glucose and sodium with
a Na+:glucose coupling ratio of 2:1
Almost completely expressed in the
brush-border membrane of
proximal renal tubular cells in the
S1 and S2 segment
Responsible for 90% of the total
renal glucose reabsorption
Low-affinity (Km=~2 mM),
high-capacity transporter, which
transfers glucose and sodium with a
Na+:glucose coupling ratio of 1:1
Intestine Kidney
32. Neurotrasmitter dysfunction
Murray, S. et al. Nat. Rev. Endocrinol. 2014,
Abbreviations: ARC, arcuate nucleus of the hypothalamus; DAT, dopamine active transporter; DRD1, dopamine D1 receptor;
DRD2, dopamine D2 receptor; LHA, lateral hypothalamic area; MOR, μ-opioid receptor; NAc, nucleus accumbens; TH,
tyrosine hydroxylase; VTA, ventral tegmental area
33. Major complications of diabetes
Diabetic
retinopathy
Leading cause of
blindness in adults1,2
Diabetic
nepropathy
Principal causa de
doença renal
terminal3,4
Cardiovascular
disease
Stroke
Aumento de 2 a 4
vezes da
mortalidade CV e de
AVC5
Diabetic
neuropathy
Principal causa
não traumática de
amputações das
extremidades
inferiores7,8
Oito em cada dez
indivíduos com
diabetes morrem por
eventos CV6
1. UKPDS Group. Diabetes Res 1990;13(1):1–11;2. Fong DS, e colab. Diabetes Care 2003;26(Suppl 1):S99–S102; 3. Hypertension in Diabetes Study. J Hypertens 1993;11(3):309–317;4. Molitch ME, e colab. Diabetes Care
2003;26(Suppl 1):S94–S98;5. Kannel WB, e colab. Am Heart J 1990;120(3):672–676; 6. Gray RP, e colab. In Textbook of Diabetes 2nd Edição, 1997; 7. King’s Fund. London: British Diabetic Association, 1996; 8. Mayfield
JA, e colab. Diabetes Care 2003;26(Suppl 1):S78–S79
34. Conclusions
• The pathophysiology of type 2 diabetes is complex and
involves multiple molecular pathways in various organs.
• The decreased insulin secretion by the pancreas, on the
background of insulin resistance in the liver and muscles, have
historically played a key role in the determination of
hyperglycaemia in type 2 diabetes.
• In the last few years increasing evidences showed that also
other organs like the gut, the kidney and the brain are involved
in the pathogenesis of type 2 diabetes and are currently
targeted by available and developing therapies for subjects
affected by type 2 diabetes.