This document provides information on diabetes mellitus, including:
1. It defines diabetes as a condition of glucose intolerance and describes the methods used to diagnose diabetes.
2. It outlines the two main types of diabetes - type 1 caused by autoimmune destruction of beta cells and type 2 caused by insulin resistance - and describes their pathogenesis.
3. It discusses the chronic complications of diabetes like retinopathy, nephropathy, and cardiovascular disease as well as acute complications like hypoglycemia and diabetic ketoacidosis. Diagnostic tests and the treatment of diabetes are also summarized.
This document discusses disorders of glucose homeostasis, including diabetes mellitus and hypoglycemia. It covers the key fuels in the body, glucose and fat metabolism, hormones that regulate glucose levels, symptoms and types of diabetes, pathogenesis of diabetic ketoacidosis and hyperosmolar hyperglycemic state, diagnosis of diabetes and hypoglycemia, and potential causes of hypoglycemia.
This document discusses carbohydrate metabolism disorders like diabetes mellitus. It defines diabetes as a group of chronic disorders characterized by hyperglycemia due to either insulin deficiency or insulin resistance. There are two main types of diabetes - type 1 caused by autoimmune destruction of beta cells leading to absolute insulin deficiency, and type 2 caused by insulin resistance and relative insulin deficiency often associated with obesity. Fasting hyperglycemia is caused by increased hepatic gluconeogenesis and glycogenolysis due to lack of insulin, while postprandial hyperglycemia results from inadequate insulin response after meals.
Update on DIABETES MELLITUS (2020) By Dr Rahul Jain , Dr Sharda JainLifecare Centre
DEFINITION
CLASSIFICATION AND ETIOLOGY
PATIENT PROFILE
METABOLIC SYNDROME
CLINICAL FEATURES
DIAGNOSIS AND INVESTIGATIONS
DAWN AND SOMOGYI PHENOMENON
MANAGEMENT
COMPLICATIONS AND METABOLIC MEMORY
This document discusses glycation and advanced glycation end products (AGEs) which are formed through non-enzymatic reactions between sugars and proteins over time. It describes how AGEs accumulate in tissues and contribute to diabetic complications by cross-linking proteins and altering their structure and function. The body has defense mechanisms like AGE receptors on macrophages to help break down and eliminate AGEs, but levels still rise with increased hyperglycemia and age, leading to tissue damage over the long term.
Glycogen storage diseases are caused by defects in glycogen synthesis or breakdown. There are several types affecting the liver or muscle. Type I is caused by glucose-6-phosphatase deficiency leading to liver enlargement and low blood sugar during fasting. Type III involves a debranching enzyme defect causing swollen abdomen and muscle weakness. Type VI deficiency of liver phosphorylase causes hepatomegaly, hypoglycemia, and growth issues. Symptoms, diagnosis, and treatments vary depending on the specific enzyme deficiency and tissues involved.
1) Glycogen storage diseases are inherited disorders caused by defects in glycogen metabolism enzymes, resulting in abnormal glycogen storage in tissues like the liver and muscle.
2) Symptoms vary depending on the type of enzyme defect and affected tissues, and can include hypoglycemia, hepatomegaly, muscle weakness, fatigue, and developmental delays.
3) The most common types are Von Gierke disease (type I) affecting glucose production in the liver, Pompe disease (type II) affecting heart and liver, and McArdle disease (type V) causing exercise intolerance due to a muscle enzyme defect.
This document discusses glycogen storage diseases, which are inherited disorders caused by deficiencies in enzymes involved in glycogen metabolism. It summarizes several types of glycogen storage diseases, categorized based on the organ(s) affected and the specific enzyme deficiency. Type I (von Gierke's disease) is the most common and is caused by glucose-6-phosphatase deficiency, affecting the liver, kidneys, and intestines. Type II (Pompe's disease) is caused by acid alpha-glucosidase deficiency and can range from an infantile to adult form. Type III (Cori or Forbes disease) involves glycogen debranching enzyme deficiency in the liver and/or muscle. The document provides details on
Current concept in the development of diabetes and its classificationSaptaparni Hazra
Diabetes is classified based on the underlying pathogenic process causing hyperglycemia. The two major types are type 1 (caused by autoimmune destruction of beta cells) and type 2 (caused by insulin resistance and impaired insulin secretion). Insulin regulates glucose homeostasis through its effects on glucose transport and metabolism in tissues. Insulin resistance is a key driver of type 2 diabetes pathogenesis, impairing glucose uptake and increasing hepatic glucose production. Over time, the pancreatic beta cells fail to compensate for insulin resistance, leading to relative insulin deficiency.
This document discusses disorders of glucose homeostasis, including diabetes mellitus and hypoglycemia. It covers the key fuels in the body, glucose and fat metabolism, hormones that regulate glucose levels, symptoms and types of diabetes, pathogenesis of diabetic ketoacidosis and hyperosmolar hyperglycemic state, diagnosis of diabetes and hypoglycemia, and potential causes of hypoglycemia.
This document discusses carbohydrate metabolism disorders like diabetes mellitus. It defines diabetes as a group of chronic disorders characterized by hyperglycemia due to either insulin deficiency or insulin resistance. There are two main types of diabetes - type 1 caused by autoimmune destruction of beta cells leading to absolute insulin deficiency, and type 2 caused by insulin resistance and relative insulin deficiency often associated with obesity. Fasting hyperglycemia is caused by increased hepatic gluconeogenesis and glycogenolysis due to lack of insulin, while postprandial hyperglycemia results from inadequate insulin response after meals.
Update on DIABETES MELLITUS (2020) By Dr Rahul Jain , Dr Sharda JainLifecare Centre
DEFINITION
CLASSIFICATION AND ETIOLOGY
PATIENT PROFILE
METABOLIC SYNDROME
CLINICAL FEATURES
DIAGNOSIS AND INVESTIGATIONS
DAWN AND SOMOGYI PHENOMENON
MANAGEMENT
COMPLICATIONS AND METABOLIC MEMORY
This document discusses glycation and advanced glycation end products (AGEs) which are formed through non-enzymatic reactions between sugars and proteins over time. It describes how AGEs accumulate in tissues and contribute to diabetic complications by cross-linking proteins and altering their structure and function. The body has defense mechanisms like AGE receptors on macrophages to help break down and eliminate AGEs, but levels still rise with increased hyperglycemia and age, leading to tissue damage over the long term.
Glycogen storage diseases are caused by defects in glycogen synthesis or breakdown. There are several types affecting the liver or muscle. Type I is caused by glucose-6-phosphatase deficiency leading to liver enlargement and low blood sugar during fasting. Type III involves a debranching enzyme defect causing swollen abdomen and muscle weakness. Type VI deficiency of liver phosphorylase causes hepatomegaly, hypoglycemia, and growth issues. Symptoms, diagnosis, and treatments vary depending on the specific enzyme deficiency and tissues involved.
1) Glycogen storage diseases are inherited disorders caused by defects in glycogen metabolism enzymes, resulting in abnormal glycogen storage in tissues like the liver and muscle.
2) Symptoms vary depending on the type of enzyme defect and affected tissues, and can include hypoglycemia, hepatomegaly, muscle weakness, fatigue, and developmental delays.
3) The most common types are Von Gierke disease (type I) affecting glucose production in the liver, Pompe disease (type II) affecting heart and liver, and McArdle disease (type V) causing exercise intolerance due to a muscle enzyme defect.
This document discusses glycogen storage diseases, which are inherited disorders caused by deficiencies in enzymes involved in glycogen metabolism. It summarizes several types of glycogen storage diseases, categorized based on the organ(s) affected and the specific enzyme deficiency. Type I (von Gierke's disease) is the most common and is caused by glucose-6-phosphatase deficiency, affecting the liver, kidneys, and intestines. Type II (Pompe's disease) is caused by acid alpha-glucosidase deficiency and can range from an infantile to adult form. Type III (Cori or Forbes disease) involves glycogen debranching enzyme deficiency in the liver and/or muscle. The document provides details on
Current concept in the development of diabetes and its classificationSaptaparni Hazra
Diabetes is classified based on the underlying pathogenic process causing hyperglycemia. The two major types are type 1 (caused by autoimmune destruction of beta cells) and type 2 (caused by insulin resistance and impaired insulin secretion). Insulin regulates glucose homeostasis through its effects on glucose transport and metabolism in tissues. Insulin resistance is a key driver of type 2 diabetes pathogenesis, impairing glucose uptake and increasing hepatic glucose production. Over time, the pancreatic beta cells fail to compensate for insulin resistance, leading to relative insulin deficiency.
This document summarizes several glycogen storage diseases and lysosomal storage diseases. For glycogen storage diseases, it lists the enzyme deficiency, symptoms such as hypoglycemia and hepatomegaly, and mnemonics to remember each disease. For lysosomal storage diseases, it provides the deficient enzyme, accumulated substrate, inheritance pattern, and key findings for each condition. It concludes by highlighting some distinguishing features between similar diseases, such as neurological symptoms in Niemann-Pick versus Gaucher's, and differences between Hunter's and Hurler's syndromes.
This document discusses liver glycogen storage diseases (GSDs). It begins with an overview of GSDs, noting they result from genetic deficiencies that cause abnormal glycogen storage. It then focuses on liver GSDs, including GSD Type Ia, Ib, III, IV, VI, and IX. For each type, it provides the deficient enzyme, affected tissues, clinical findings, diagnosis, and treatment approaches. Liver GSDs can cause hypoglycemia, hepatomegaly, hyperlipidemia, and other issues. Molecular testing and liver biopsy are important for diagnosis. Treatment focuses on preventing hypoglycemia through dietary adjustments and supplementation.
This document summarizes several glycogen storage diseases caused by deficiencies in enzymes involved in glycogen synthesis and breakdown. Key points include: glycogen storage diseases are inherited disorders characterized by abnormal glycogen deposition; deficiencies in enzymes like glucose-6-phosphatase and acid maltase can cause hypoglycemia, lactic acidosis, hyperlipidemia, and other issues; the organs and severity of symptoms vary depending on the specific enzyme deficiency.
This document summarizes the pathobiology of complications from diabetes mellitus. It introduces the three main types of diabetes and describes some of the major complications like retinopathy, cardiomyopathy, nephropathy, and neuropathy. It then discusses the pathogenesis of diabetes complications, outlining several key pathways involved like the polyol pathway, advanced glycation end product formation, protein kinase C activation, and the hexosamine pathway. References are provided to support the information presented.
The document discusses emerging therapy options for controlling protein glycation and its role in diabetes complications. It describes the biochemical pathways involved in advanced glycation end product (AGE) formation, including the polyol pathway, hexosamine pathway, and protein kinase C pathway. Inhibiting AGE formation through therapies like benfotiamine and L-carnosine may help reduce inflammation and complications in diabetics by preventing cross-linking of proteins in tissues like the retina, kidneys, and blood vessels. Controlling glucose levels and diet are also important to limit the formation of damaging AGE products.
Glycogen storage diseases are a group of inherited metabolic disorders caused by deficiencies of enzymes involved in glycogen breakdown or synthesis. This leads to abnormal glycogen buildup in tissues. The main types are GSD I, III and IV. In GSD I, glucose-6-phosphatase is deficient causing hypoglycemia and liver enlargement. GSD III results from a debranching enzyme defect causing abnormal glycogen structure. GSD IV involves branching enzyme deficiency and liver cirrhosis. Symptoms vary by type but may include low blood sugar, enlarged liver, muscle cramps and failure to thrive. Treatment focuses on a high-carbohydrate diet and cornstarch to manage blood sugar levels. Prognosis depends on
This document discusses six types of glycogen storage disorders caused by deficiencies in enzymes involved in glycogen metabolism. The six types are Von Gierke's disease, Pompe's disease, limit dextrinosis, amylopectinosis, McArdle's disease, and Her's disease. Each type is characterized by the deficient enzyme, inheritance pattern, glycogen structure, affected tissues, clinical features, and prognosis. The types vary in their symptoms and severity, from fatal in early infancy to survival into adulthood.
GLYCOGEN STORAGE DISEASE , GSD , Von Gierke DiseaseRAHUL KATARIA
Detailed presentation about glycogen storage disease.
description about all types of GSDs like .
1. GSD I
2.GSD III
3. GSD IV
4. GSD VI
5. GSD IX
6. GSD 0
This document summarizes information from a presentation on liver glycogen storage diseases (GSDs). It discusses several types of GSD including GSD Ia, Ib, III, IV, VI, and IX. Key points include:
- GSDs result from genetic deficiencies that cause abnormal glycogen storage in the liver and sometimes other tissues. Symptoms vary by type and can include hypoglycemia, hepatomegaly, lactic acidosis, and hyperlipidemia.
- Treatment goals are to prevent hypoglycemia and correct metabolic issues through frequent feedings, continuous glucose, and cornstarch intake. Medical management focuses on complications like gout, lipids, kidney issues. Liver transplantation may be used
1. The document discusses disorders of carbohydrate metabolism, focusing on diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).
2. DKA is characterized by high blood glucose, low pH, and ketones in the blood or urine. HHS involves extremely high blood glucose without acidosis or significant ketones.
3. Treatment for both involves fluid resuscitation, insulin administration, electrolyte replacement, and monitoring for complications. Careful attention must be paid to fluid balance, electrolyte levels, and glucose control during resuscitation.
Lipid storage disorders are inherited metabolic disorders where harmful amounts of lipids accumulate in cells and tissues due to deficiencies or issues with lipid metabolizing enzymes. Over time, excess lipid storage can damage the brain, nerves, liver, spleen, and bone marrow. These disorders can be inherited autosomally recessively or x-linked recessively. Specific disorders discussed include cholelithiasis, obesity, fatty liver, and atherosclerosis.
Advanced Glycation Endproducts and diabetes gowri shanker
This document discusses advanced glycation end products (AGEs), which are compounds formed when sugars bind to proteins or lipids. AGEs accumulate in tissues over time and can promote oxidative stress and inflammation. The document notes that AGEs can enter the body through diet, as many cooking methods promote AGE formation, and through smoking. It explores the mechanisms by which AGEs may contribute to diseases like diabetes through depletion of antioxidant defenses. The document also discusses evidence that a low-AGE diet can help reduce circulating AGE levels and markers of oxidative stress and inflammation.
Glycogen storage disease is a group of metabolic disorders caused by the body's inability to properly store glycogen. There are several types classified by the enzyme deficiency. Type I involves the liver and causes low blood sugar and high lactate levels. Type III is caused by a debranching enzyme deficiency and results in an enlarged liver and low blood sugar. Type IV is a branching enzyme deficiency leading to liver enlargement and cirrhosis. Treatment focuses on managing symptoms and in some cases enzyme replacement therapy.
This document discusses different types of biochemical disorders caused by enzyme deficiencies. It covers several key areas:
- Metabolic disorders are often inherited and can affect enzyme activity levels. Disorders like Parkinson's disease and schizophrenia may involve alterations in the enzyme tyrosine hydroxylase.
- Enzyme deficiencies can occur in various metabolic pathways like phenylalanine, urea cycle, carbohydrate, steroid, lipid, lysosomal, purine, copper, and peroxisome metabolism.
- Specific disorders touched on include homocystinuria, urea cycle disorders, glycogen storage diseases, congenital adrenal hyperplasia, familial hypercholesterolemia, Wilson's disease, Zellwe
This document discusses the regulation of blood glucose levels in the human body. It describes what happens when glucose levels decrease (hypoglycemia) or increase too much (hyperglycemia), including the symptoms. Key organs and hormones involved in regulating glucose include the liver, skeletal muscles, pancreas, adipose tissue, insulin, and glucagon. Insulin acts to lower blood glucose levels by stimulating glucose uptake and storage, while glucagon acts to raise blood glucose levels by stimulating glucose production and release from the liver. The document also discusses factors that can cause hyperglycemia or hypoglycemia.
This document provides information on diabetes mellitus including its definition, classification, epidemiology, pathophysiology, complications, and clinical presentation. It defines diabetes as a group of metabolic disorders characterized by hyperglycemia resulting from defects in insulin secretion and/or action. The two main types of diabetes are type 1 resulting from beta cell destruction and type 2 associated with insulin resistance. Obesity and genetic factors contribute to the development of type 2 diabetes. Acute complications include diabetic ketoacidosis.
Etiology & pathogenesis of Diabetes MellitusEneutron
This document discusses the etiology, pathogenesis, classification, diagnosis and clinical presentation of diabetes mellitus. It begins with an overview of normal insulin physiology and the mechanisms of insulin secretion. It then covers the classification of diabetes into type 1, type 2 and gestational diabetes based on etiology. The document discusses the pathogenesis of type 1 and type 2 diabetes in detail. It provides criteria for the diagnosis of diabetes, including symptoms and results of fasting plasma glucose, oral glucose tolerance and HbA1c tests. The document concludes with a discussion of laboratory tests used to diagnose and monitor diabetes.
This document summarizes several glycogen storage diseases and lysosomal storage diseases. For glycogen storage diseases, it lists the enzyme deficiency, symptoms such as hypoglycemia and hepatomegaly, and mnemonics to remember each disease. For lysosomal storage diseases, it provides the deficient enzyme, accumulated substrate, inheritance pattern, and key findings for each condition. It concludes by highlighting some distinguishing features between similar diseases, such as neurological symptoms in Niemann-Pick versus Gaucher's, and differences between Hunter's and Hurler's syndromes.
This document discusses liver glycogen storage diseases (GSDs). It begins with an overview of GSDs, noting they result from genetic deficiencies that cause abnormal glycogen storage. It then focuses on liver GSDs, including GSD Type Ia, Ib, III, IV, VI, and IX. For each type, it provides the deficient enzyme, affected tissues, clinical findings, diagnosis, and treatment approaches. Liver GSDs can cause hypoglycemia, hepatomegaly, hyperlipidemia, and other issues. Molecular testing and liver biopsy are important for diagnosis. Treatment focuses on preventing hypoglycemia through dietary adjustments and supplementation.
This document summarizes several glycogen storage diseases caused by deficiencies in enzymes involved in glycogen synthesis and breakdown. Key points include: glycogen storage diseases are inherited disorders characterized by abnormal glycogen deposition; deficiencies in enzymes like glucose-6-phosphatase and acid maltase can cause hypoglycemia, lactic acidosis, hyperlipidemia, and other issues; the organs and severity of symptoms vary depending on the specific enzyme deficiency.
This document summarizes the pathobiology of complications from diabetes mellitus. It introduces the three main types of diabetes and describes some of the major complications like retinopathy, cardiomyopathy, nephropathy, and neuropathy. It then discusses the pathogenesis of diabetes complications, outlining several key pathways involved like the polyol pathway, advanced glycation end product formation, protein kinase C activation, and the hexosamine pathway. References are provided to support the information presented.
The document discusses emerging therapy options for controlling protein glycation and its role in diabetes complications. It describes the biochemical pathways involved in advanced glycation end product (AGE) formation, including the polyol pathway, hexosamine pathway, and protein kinase C pathway. Inhibiting AGE formation through therapies like benfotiamine and L-carnosine may help reduce inflammation and complications in diabetics by preventing cross-linking of proteins in tissues like the retina, kidneys, and blood vessels. Controlling glucose levels and diet are also important to limit the formation of damaging AGE products.
Glycogen storage diseases are a group of inherited metabolic disorders caused by deficiencies of enzymes involved in glycogen breakdown or synthesis. This leads to abnormal glycogen buildup in tissues. The main types are GSD I, III and IV. In GSD I, glucose-6-phosphatase is deficient causing hypoglycemia and liver enlargement. GSD III results from a debranching enzyme defect causing abnormal glycogen structure. GSD IV involves branching enzyme deficiency and liver cirrhosis. Symptoms vary by type but may include low blood sugar, enlarged liver, muscle cramps and failure to thrive. Treatment focuses on a high-carbohydrate diet and cornstarch to manage blood sugar levels. Prognosis depends on
This document discusses six types of glycogen storage disorders caused by deficiencies in enzymes involved in glycogen metabolism. The six types are Von Gierke's disease, Pompe's disease, limit dextrinosis, amylopectinosis, McArdle's disease, and Her's disease. Each type is characterized by the deficient enzyme, inheritance pattern, glycogen structure, affected tissues, clinical features, and prognosis. The types vary in their symptoms and severity, from fatal in early infancy to survival into adulthood.
GLYCOGEN STORAGE DISEASE , GSD , Von Gierke DiseaseRAHUL KATARIA
Detailed presentation about glycogen storage disease.
description about all types of GSDs like .
1. GSD I
2.GSD III
3. GSD IV
4. GSD VI
5. GSD IX
6. GSD 0
This document summarizes information from a presentation on liver glycogen storage diseases (GSDs). It discusses several types of GSD including GSD Ia, Ib, III, IV, VI, and IX. Key points include:
- GSDs result from genetic deficiencies that cause abnormal glycogen storage in the liver and sometimes other tissues. Symptoms vary by type and can include hypoglycemia, hepatomegaly, lactic acidosis, and hyperlipidemia.
- Treatment goals are to prevent hypoglycemia and correct metabolic issues through frequent feedings, continuous glucose, and cornstarch intake. Medical management focuses on complications like gout, lipids, kidney issues. Liver transplantation may be used
1. The document discusses disorders of carbohydrate metabolism, focusing on diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).
2. DKA is characterized by high blood glucose, low pH, and ketones in the blood or urine. HHS involves extremely high blood glucose without acidosis or significant ketones.
3. Treatment for both involves fluid resuscitation, insulin administration, electrolyte replacement, and monitoring for complications. Careful attention must be paid to fluid balance, electrolyte levels, and glucose control during resuscitation.
Lipid storage disorders are inherited metabolic disorders where harmful amounts of lipids accumulate in cells and tissues due to deficiencies or issues with lipid metabolizing enzymes. Over time, excess lipid storage can damage the brain, nerves, liver, spleen, and bone marrow. These disorders can be inherited autosomally recessively or x-linked recessively. Specific disorders discussed include cholelithiasis, obesity, fatty liver, and atherosclerosis.
Advanced Glycation Endproducts and diabetes gowri shanker
This document discusses advanced glycation end products (AGEs), which are compounds formed when sugars bind to proteins or lipids. AGEs accumulate in tissues over time and can promote oxidative stress and inflammation. The document notes that AGEs can enter the body through diet, as many cooking methods promote AGE formation, and through smoking. It explores the mechanisms by which AGEs may contribute to diseases like diabetes through depletion of antioxidant defenses. The document also discusses evidence that a low-AGE diet can help reduce circulating AGE levels and markers of oxidative stress and inflammation.
Glycogen storage disease is a group of metabolic disorders caused by the body's inability to properly store glycogen. There are several types classified by the enzyme deficiency. Type I involves the liver and causes low blood sugar and high lactate levels. Type III is caused by a debranching enzyme deficiency and results in an enlarged liver and low blood sugar. Type IV is a branching enzyme deficiency leading to liver enlargement and cirrhosis. Treatment focuses on managing symptoms and in some cases enzyme replacement therapy.
This document discusses different types of biochemical disorders caused by enzyme deficiencies. It covers several key areas:
- Metabolic disorders are often inherited and can affect enzyme activity levels. Disorders like Parkinson's disease and schizophrenia may involve alterations in the enzyme tyrosine hydroxylase.
- Enzyme deficiencies can occur in various metabolic pathways like phenylalanine, urea cycle, carbohydrate, steroid, lipid, lysosomal, purine, copper, and peroxisome metabolism.
- Specific disorders touched on include homocystinuria, urea cycle disorders, glycogen storage diseases, congenital adrenal hyperplasia, familial hypercholesterolemia, Wilson's disease, Zellwe
This document discusses the regulation of blood glucose levels in the human body. It describes what happens when glucose levels decrease (hypoglycemia) or increase too much (hyperglycemia), including the symptoms. Key organs and hormones involved in regulating glucose include the liver, skeletal muscles, pancreas, adipose tissue, insulin, and glucagon. Insulin acts to lower blood glucose levels by stimulating glucose uptake and storage, while glucagon acts to raise blood glucose levels by stimulating glucose production and release from the liver. The document also discusses factors that can cause hyperglycemia or hypoglycemia.
This document provides information on diabetes mellitus including its definition, classification, epidemiology, pathophysiology, complications, and clinical presentation. It defines diabetes as a group of metabolic disorders characterized by hyperglycemia resulting from defects in insulin secretion and/or action. The two main types of diabetes are type 1 resulting from beta cell destruction and type 2 associated with insulin resistance. Obesity and genetic factors contribute to the development of type 2 diabetes. Acute complications include diabetic ketoacidosis.
Etiology & pathogenesis of Diabetes MellitusEneutron
This document discusses the etiology, pathogenesis, classification, diagnosis and clinical presentation of diabetes mellitus. It begins with an overview of normal insulin physiology and the mechanisms of insulin secretion. It then covers the classification of diabetes into type 1, type 2 and gestational diabetes based on etiology. The document discusses the pathogenesis of type 1 and type 2 diabetes in detail. It provides criteria for the diagnosis of diabetes, including symptoms and results of fasting plasma glucose, oral glucose tolerance and HbA1c tests. The document concludes with a discussion of laboratory tests used to diagnose and monitor diabetes.
This document discusses the pathogenesis and etiology of metabolic disorders, including disorders of carbohydrate and lipid metabolism. It covers several key points:
1. Metabolic disorders can be caused by genetic factors like enzymopathies, damage to membranes/receptors, endocrine dysfunction, and neural impairment.
2. Dietary and digestive issues as well as other organ dysfunction can also contribute to metabolic disorders.
3. Glucose regulation is maintained through a balance of insulin and counter-regulatory hormones like glucagon, with disorders resulting in hyperglycemia or hypoglycemia.
4. The two primary types of diabetes mellitus - type 1 and type 2 - differ in etiology and pathogenesis
1. Diabetes mellitus is a metabolic disorder characterized by high blood glucose due to insulin deficiency or resistance. It affects carbohydrate, fat, and protein metabolism and can cause serious complications if left untreated.
2. There are four main types of diabetes: type 1 caused by lack of insulin; type 2 caused by insulin resistance; gestational diabetes during pregnancy; and other rare forms.
3. Management involves lifestyle changes like diet, exercise and weight control as well as pharmacological therapy with insulin or oral drugs depending on the type of diabetes.
The document discusses diabetes mellitus (DM), specifically:
1) DM occurs when the body does not properly regulate blood glucose levels due to insufficient insulin production or impaired insulin function, leading to hyperglycemia.
2) There are several types of DM including type 1 caused by autoimmune destruction of beta cells, type 2 related to lifestyle and genetics, and gestational DM occurring during pregnancy.
3) Insulin resistance and impaired beta cell function contribute to the development and progression of type 2 DM.
The document discusses the endocrine pancreas. It begins by introducing the pancreas and its endocrine and exocrine functions. It then describes the anatomy of the pancreas and the different cell types in the islets of Langerhans. It discusses the hormones produced by each cell type and their actions. The document also covers the regulation of insulin release and the pathophysiology of diabetes mellitus, including the mechanisms, classification, and complications of both type 1 and type 2 diabetes.
Diabetes mellitus is a metabolic disease where the body is unable to properly control blood glucose levels, leading to high blood sugar (hyperglycemia). There are two main types: type 1 diabetes results from an autoimmune destruction of insulin-producing beta cells in the pancreas causing absolute insulin deficiency, while type 2 diabetes involves insulin resistance and sometimes relative insulin deficiency, associated with obesity. Long-term complications of high blood sugar include damage to nerves, kidneys, eyes and cardiovascular disease. Diabetes affects over 425 million people worldwide and is on the rise due to increasing obesity rates.
Diabetes mellitus is a group of metabolic diseases characterized by high blood glucose levels due to defects in insulin secretion or insulin action. The two main types are type 1 diabetes, caused by destruction of beta cells resulting in insulin deficiency, and type 2 diabetes, caused by insulin resistance and relative insulin deficiency. Chronic hyperglycemia can lead to damage of various organs, especially the eyes, kidneys, nerves, heart and blood vessels. Treatment involves lifestyle management, oral medications or insulin to maintain blood glucose levels as close to normal as possible.
This document discusses various aspects of diabetes and its treatment with insulin and other drugs. It provides details on:
1) The two main types of diabetes - Type 1 characterized by a lack of insulin production and Type 2 characterized by insulin resistance.
2) How insulin controls blood glucose levels via its effects on various tissues like liver, muscle and fat.
3) The different types of insulin preparations used in treatment ranging from short-acting to prolonged-acting insulins.
4) Other oral hypoglycemic drugs used to treat Type 2 diabetes like sulfonylureas and meglitinide analogs which work by stimulating insulin secretion.
This document discusses glucose homeostasis and diabetes. It covers:
- The roles of insulin, glucagon, and other hormones in regulating blood glucose levels. Insulin lowers glucose while glucagon raises it.
- The differences between type 1 and type 2 diabetes, including causes and treatments. Type 1 is an autoimmune disease treated with insulin, while type 2 is due to insulin resistance and may be treated with diet, exercise, or oral medication.
- How insulin works by binding receptors on cells and increasing glucose uptake, utilization, and storage. This lowers blood glucose levels.
This document provides information on the pathophysiology of diabetes mellitus. It discusses the basic anatomy and function of the pancreas and islets of Langerhans. It then describes the different cell types within the islets and their roles in regulating blood sugar levels. The mechanisms of insulin secretion and action are explained in detail. The document also covers the natural history and development of type 2 diabetes, noting that it arises from a combination of insulin resistance and progressive beta cell dysfunction over time.
Lecture 7. diabetic mellitus & pancreatic tumourAyub Abdi
1. Diabetes mellitus is a metabolic disorder characterized by hyperglycemia that affects over 29 million people in the US and 422 million worldwide.
2. There are several types of diabetes including type 1 caused by autoimmune destruction of beta cells, type 2 caused by insulin resistance and relative insulin deficiency, and gestational diabetes during pregnancy.
3. Chronic complications of diabetes include damage to blood vessels leading to heart disease, stroke, and kidney failure as well as nerve damage causing neuropathy. Rare forms include monogenic diabetes and pancreatic tumors such as insulinomas.
DIABETES MELLITUS Definition :It is a clinical syndrome characterized by hyperglycemia due to absolute or relative deficiency of insulin.
Type 1 Diabetes :
Charactarized by an absolute deficiency of insulin secretion caused by pancreatic beta cell destruction usually resulting from auto immune attack
Type 2 Diabetes :
Caused by relative insulin deficiency due to combination of peripheral resistance to insulin action and an inadequate compensatory response to insulin secretion by pancreatic beta cells.
Introduction
pancreas
Pathology of insulin
Pathogenesis of DM
What is diabetes mellitus
Types of diabetes mellitus
Evaluation of plasma glucose levels
Clinical features of DM
Complications of DM
Treatment
PATHOGENESIS OF TYPE 1 DIABETES MELLITUS.pptxRadhaJoshi14
Insulin increases glucose utilization and glycogen synthesis while reducing gluconeogenesis and glycogenolysis. It also promotes lipogenesis and amino acid uptake. Type 1 diabetes is an autoimmune disease involving genetic and environmental factors like viral infections. It results from destruction of pancreatic beta cells. Type 2 diabetes is multifactorial involving factors like age, obesity, ethnicity, and family history. It results from insulin resistance and relative insulin deficiency due to beta cell dysfunction over time. Characteristics include insulin resistance, abnormal insulin secretion and action, increased hepatic glucose production, and abnormal fat metabolism.
The document discusses the gastrointestinal system and its organs including the mouth, stomach, pancreas, small intestine, and liver. It then describes the liver's functions of producing proteins and bile, storing vitamins and minerals, converting and utilizing fats and carbohydrates, and removing waste. The document notes that carbohydrates provide 60% of the body's energy, with proteins and fats each contributing around 10-12% and 30%, respectively. It outlines the journey of glucose from food to different body parts and its utilization and storage. Key steps in glucose utilization are its entry into cells, phosphorylation, and energy release.
The document discusses endocrine disorders and focuses on diabetes mellitus. It defines the endocrine system and describes how hormones are secreted and transported. It then discusses the different types of diabetes (type 1, type 2, gestational), their causes and pathophysiology. Type 1 diabetes results from an autoimmune destruction of insulin-producing pancreatic beta cells, leading to little or no insulin production. This causes unchecked glucose production and fasting/postprandial hyperglycemia.
This document discusses diabetes pharmacotherapy. It provides an overview of the different types of diabetes, including type 1, type 2, gestational diabetes, and maturity onset diabetes of youth. It describes the pathogenesis and clinical presentation of type 1 and type 2 diabetes. The major components of diabetes treatment are diet, exercise, oral hypoglycemic medications, and insulin therapy. The document discusses the different types of insulin preparations, including their sources, structures, mechanisms of action, and uses. It provides guidance on calculating insulin doses and adjusting doses based on blood sugar levels.
The document discusses the pancreas and its role in producing insulin and other hormones that regulate blood glucose levels. It specifically focuses on the types of cells within the pancreas that produce these hormones, including beta cells that produce insulin, alpha cells that produce glucagon, and delta cells that produce somatostatin. It then provides details on insulin, its functions in facilitating glucose transport and maintaining normal blood glucose levels, as well as the role of glucagon and somatostatin in regulating insulin and glucose levels.
3. Normal Glucose Homeostasis
REGULATED BY:
1. Glucose production in the liver
2. Glucose uptake and utilization by peripheral tissues
(skeletal muscle)
3. Actions of hormones
Normal glucose levels: 70-120mg/dl
• FXN of Insulin: to increase the rate of glucose transport
into certain cells of the body
4. Glucose Metabolism: Words you need to know!
• Gluconeogenesis: formation of glucose from excess amino acids,
fat, and other noncarbohydrate sources.
• Glycogenesis: formation of glycogen.
• Lipogenesis: formation of fats
• Glycogenolysis: process that coverts glycogen to glucose.
• Glycolysis: hydrolysis of glucose to pyruvate.
• Lipolysis: catabolic degradation of triacylglycerol.
5. Glucose Metabolism
Synthesis of glycogen Breaking down stored glycogen
Production of glucose
from a.a. & other
substances
Cellular
Respiration
6. PANCREAS
Exocrine
Endocrine
Islets
Alpha Cells glucagon
Beta Cells proinsulin
Delta Cells somatostatin
(suppress insulin and glucagon)
F cells Pancreatic Polypeptide
(PP) cells
Epsilon Cells make gherlin, which
causes hunger
8. Regulation of Glucose Metabolism
• HORMONAL REGULATION
• Glucose–dependent insulinotropic
polypeptide (GIP)
• Glucagon-like peptide 1 (GLP-1)
– from cells in the gut
– stimulate the production of insulin and inhibit
glucagon
12. Metabolic
Action of
Insulin
Liver Adipose Muscle
Inhibits Glycogenolysis Lipolysis Protein break down
Gluconeogenesis Amino acid release
Ketogeneis
Simulates Glycogen fatty acid Glycerol and fatty acid Glucose uptake and
synthesis synthesis metabolism
Amino acid uptake
Synthesis of protein
Glycogenesis
13. Fed State Fasting State
Glucose provides primary energy source Glucose is produced by
Amylin acts on area postrema (AP) glycogenolysis and gluconeogenesis
INSULIN dominated GLUCAGON dominates
14. Regulation of Glucose Metabolism
• EXERCISE
– Initially insulin levels
drop and glucagon and
catecholamine levels rise
• STRESS
– Production of stress
hormones
(corticosteroids and
catecholamines) increase
production of glucose
– Increase production of
FFAs
– Lead to hyperglycemia
16. Who has Diabetes Mellitus
• 16 Million in the USA
• 1 Million/yr
• 50K people die of it per year in the USA
17. What is diabetes mellitus?
• GLUCOSE INTOLERANCE
• How do you diagnose DM?
• More than one fasting plasma glucose level
(>126)
• Elevated plasma glucose in response to an oral
glucose tolerance test (>200)
• Polydipsia, polyphagia, polyuria
18.
19. * MODY might be regarded
as the third type
TWO* Types of DM
Type 1 Type 2
• Genetic • Genetic, but diff. from Type
• Autoimmune 1
• Childhood (juvenile) • NOT autoimmune
onset • Adult, or maturity onset,
• Antibodies to beta cells, e.g., 40’s, 50’s
insulitis • Insulin may be low, BUT,
peripheral resistance to
• Beta cell depletion
insulin is the main factor
• NON-OBESE patients
• OBESE patients
22. Pathogenesis of Diabetes Mellitus
• HLAs: expression of certain HLAs is associated with increased
susceptibility to type I diabetes.
• Viruses: are considered initiating factors in autoimmune
cause of type I diabetes.
• Insulin receptor defects:
Insulin resistant: can be due to malfunction in insulin receptor, but the
cause is not known. In type II diabetes.
Antibodies to insulin receptor: in type II diabetes.
• Glucose transport: low levels of glucose transporters in type I
and II diabetes.
23. Pathogenesis of Diabetes Mellitus
• Type I diabetes mellitus: caused by destruction of
islet cells as a result of autoimmune reaction to -
cells.
• Type II diabetes mellitus: caused by a defect in
glucose transport after insulin binds to its receptor.
24. Type 1 DM
Genetic susceptibility
Environmental factors
Immunologically mediated destruction of beta cells
Peak about 10-14 years of age
25. • A 12-year-old female is newly diagnosed with
type 1 diabetes mellitus (DM). Which of the
following is the most likely cause of her
disease?
A. A familial, autosomal dominant gene defect
B. Obesity and lack of exercise
C. Immune destruction of the pancreas
D. Hyperglycemia from eating too many sweets
28. Type 2 DM
• RESISTANT TO THE ACTION OF INSULIN
• Very common: many undiagnosed cases
• Interactions of metabolic, genetic, &
environment
• RISK FACTORS: high BMI (intra-abdominal
obesity), family history of DM2, ethnic
minority, female gender
29. • Insulin is less able to facilitate entry of
glucose into live, skeletal muscles, adipose
tissue
• Pancreas eventually “burns out”
31. MODY (Maturity Onset Diabetes of
the Young)
• Multiple types
• 2-5% of diabetics
• Primary beta cell defects
• Multiple genetic mechanisms, especially
GLUCOKINASE mutations
32. Hyperglycemia in type 2 diabetes mellitus is a
result of:
A. insulin deficiency.
B. hyperinsulinemia and insulin resistance.
C. glucagon deficiency.
D. liver dysfunction.
40. Acute Complications: Diabetic ketoacidosis
Insulinopenia (in type I diabetes)
Use of fatty acids from triglycerides as a major source of energy
Fatty acid degradation
Production of acetyl CoA
Production of keto acids (ketone bodies)
(acetoacetate, -hydroxybutyrate)
42. A 19-year-old female with type 1 diabetes mellitus was
admitted to the hospital with the following lab values: serum
glucose 500 mg/dl (high); urine glucose and ketones 4+
(high); arterial pH 7.20 (low). Her parents state that she has
been sick with the “flu” for a week. Which of the following
statements best explains her acidotic state?
A. Increased insulin levels promote protein breakdown and
ketone formation.
B. Her uncontrolled diabetes has led to renal failure.
C. Low serum insulin promotes lipid storage and a
corresponding release of ketones.
D. Insulin deficiency promotes lipid metabolism and ketone
formation.
43. Acute Complications Protein glycation
• Nonenzymatic binding of free amino groups of
proteins to glucose and other sugars.
• Protein glycation commonly occurs in RBCs,
glumeruli, nerve cells, and other tissues.
• Extent of protein glycation is proportional to
extracellular glucose concentration.
• Excessive glycation causes alterations in
protein’s physical and biochemical properties.
• New research suggest that many diabetes
complications are caused by glycation of
specific proteins.
44. Diagnostic Tests for Diabetes Mellitus
Function tests in diabetes
• Postprandial plasma glucose
• Oral glucose tolerance test
Other tests in diabetes
• Glucose
• Glycated hemoglobin
• Albumin (protein)
• Insulin
• Keto acids
• Hydrogen ion
• Electrolytes
• Osmolality
• Body fluid volume
• Anion gap
• BUN
• Lipids
45. Function tests in diabetes
Both tests measure clearance rate of glucose load from the
blood.
Postprandial plasma glucose:
• A high in carbohydrate meal is used (75 g glucose drink is preferred) as
carbohydrate load.
• Plasma glucose is measured 2 hours after carbohydrate ingestion.
• Two postprandial tests with glucose levels 200 mg/dl are suggestive of diabetes.
Oral glucose tolerance test (OGTT): under controlled conditions.
• Carbohydrate intake is controlled 3 days before the test.
• Glucose load is 40 g glucose/m2 body area.
• Blood glucose is measured 2 hours after glucose load.
• Glucose level 200 mg/dl is suggestive of diabetes.
46. Glucose
Fasting plasma glucose:
• Repeated levels 126 mg/dl…strongly suggest diabetes.
• Levels 100 – 126 mg/dl …impaired fasting glucose.
• Increase in fasting plasma glucose is directly proportional to
severity of diabetes mellitus.
Urinary glucose:
• Renal threshold for glucose is 180 g/dl, and in diabetics it is
increased to 300 mg/dl.
Urinary glucose is a poor marker for diabetes mellitus.
47. Insulin
• Type I diabetics: fasting plasma insulin is low.
• Type II diabetics: fasting plasma insulin is normal, it is
high if plasma glucose 250 mg/dl
48. Keto acids
• Measured in both blood and urine.
• Plasma keto acids may be normal even though urinary
keto acids are high, this is due to increase urinary
excretion of keto acids from renal compensation to low
pH.
• Controlled diabetics should have both normal plasma
and urinary keto acid levels.
49. Albumin
• Urinary protein (microalbuminuria) is one of the
earliest signs of glomerular nephropathy.
• Albumin / creatinine 20-30 mg/day suggests
microalbuminuria.
• Without intervention macroalbuminuria
(>300mg/day)
– Leading cause of end stage renal disease in US