Diabetic Ketoacidosis
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Diabetic ketoacidosis (DKA) is typically associated with type 1 diabetes but can also occur in type 2 diabetes under extreme stress. DKA results from a lack of insulin and excess glucagon and catecholamines, leading to fat breakdown, ketone production, and high blood sugar. Symptoms include nausea, vomiting, fruity breath, and signs of dehydration. DKA is diagnosed based on hyperglycemia, ketonemia, and metabolic acidosis.
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This document discusses diabetes mellitus type 1 (DMT1), including its pathophysiology as an autoimmune destruction of pancreatic beta cells leading to insulin deficiency, epidemiology as accounting for less than 10% of diabetes cases, and temporal development with a gradual loss of beta cell mass over years. It also summarizes DMT1 complications such as diabetic ketoacidosis, hyperglycemic hyperosmolar state, and microvascular and macrovascular issues, as well as treatments including fluid replacement and insulin administration.
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Anaesth. consideration endocrine 2
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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
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Diabetes mellitus is a metabolic disease characterized by hyperglycemia caused by either defects in insulin secretion, insulin action, or both. If left untreated, diabetes can cause long-term damage to organs like the eyes, kidneys, nerves, heart, and blood vessels. The three main types of diabetes are type 1, type 2, and gestational diabetes. Type 1 is caused by autoimmune destruction of beta cells resulting in insulin deficiency. Type 2 results from insulin resistance and inadequate insulin secretion. Gestational diabetes occurs during pregnancy without a prior history of diabetes. Complications of diabetes include both microvascular issues like retinopathy, nephropathy, and neuropathy as well as macrovascular problems such as heart disease and stroke
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This document summarizes the etiopathogenesis of diabetes mellitus. It discusses the pathogenesis of type 1 and type 2 diabetes. For type 1 diabetes, the main mechanism is destruction of beta cells leading to insulin deficiency. This is explained by genetic susceptibility, autoimmune factors, and environmental triggers. For type 2 diabetes, factors include genetic susceptibility increased by obesity, insulin resistance causing impaired glucose utilization and increased hepatic glucose production, and eventually impaired insulin secretion as beta cells fail to compensate for insulin resistance.
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This document discusses diabetes mellitus and hypoglycemia. It defines diabetes as a clinical syndrome of hyperglycemia caused by insulin deficiency. There are two main types of diabetes - type 1 caused by autoimmune destruction of beta cells resulting in absolute insulin deficiency, and type 2 which is genetic and associated with obesity and insulin resistance. Without treatment, complications from hyperglycemia can include glycosuria, impaired immune function, hyperosmolarity, and glycosylation of proteins leading to long term damage. The pathophysiology revolves around metabolic alterations from insulin deficiency like hyperglycemia, ketoacidosis, and lipid abnormalities.
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This document discusses complications of diabetes, including acute and chronic complications that affect both large blood vessels (macrovascular) and small blood vessels (microvascular). It describes the two main types of diabetes (types 1 and 2) and gestational diabetes. It also explains two key mechanisms that contribute to diabetic complications - accumulation of sorbitol due to activation of the polyol pathway under hyperglycemic conditions, and glycation of proteins from nonenzymatic bonding of sugars. Finally, it outlines specific microvascular complications like retinopathy, nephropathy, and neuropathy.
Diabetes mellitus pathophysiology
Diabetes mellitus is a metabolic condition characterized by hyperglycemia due to ineffective insulin function or insulin resistance. It is classified into four main types: type 1, type 2, gestational diabetes, and other specific types. The pathophysiology of type 1 diabetes involves autoimmune destruction of pancreatic beta cells, while type 2 diabetes results from both impaired insulin secretion and insulin resistance. Both types can lead to serious complications affecting multiple organ systems if not properly treated through methods such as insulin therapy, oral hypoglycemic drugs, lifestyle changes, and managing comorbidities and risk factors.
Acute and chronic complications of DM
This document discusses the pathophysiology of acute and chronic complications of diabetes mellitus. It begins by outlining the objectives of understanding ketoacidosis, hyperosmolar state, and mechanisms of glucose-induced vascular damage. It then provides background on the prevalence and types of diabetes. The main pathophysiological mechanisms discussed are the polyol pathway, formation of advanced glycation end products, activation of protein kinase C, increased flux through the hexosamine pathway, and mitochondrial superoxide production. These lead to microvascular complications like nephropathy, retinopathy and neuropathy as well as macrovascular complications. The document concludes by summarizing diagnostic criteria for diabetic ketoacidosis and hyperosmolar hyperglyce
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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.
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This document provides an overview of diabetes mellitus (DM), including its pathogenesis, signs and symptoms, diagnostic criteria, complications, and management. It discusses the two main types of DM (type 1 and type 2), their distinguishing characteristics, and the role of insulin in the body. The document outlines microvascular and macrovascular complications of long-term hyperglycemia, such as retinopathy, nephropathy, neuropathy, and cardiovascular disease. It also covers diabetic ketoacidosis, risk factors for type 2 DM, and the increased risk of coronary heart disease in diabetic patients.
Surgery in diabetes patients Dr nesar Ahmad
This document discusses diabetes, its classification, signs and symptoms, and management in surgical patients. It notes that diabetes is a chronic condition characterized by high blood glucose resulting from insulin deficiency or resistance. It also discusses the increased risks that diabetic patients face during surgery due to hormonal and metabolic responses to trauma. The document provides guidelines for evaluating, monitoring, and controlling blood glucose levels in diabetic patients before, during, and after surgical procedures.
Determination of Blood Glucose Using Glusose Oxidase-Peroxidase Method
This document discusses blood glucose determination using the oxidase-peroxidase method. It begins by introducing diabetes and its prevalence worldwide. It then describes the materials and methodology used, which involves collecting a blood sample, separating the plasma, and adding an O-toluidine reagent before measuring absorbance. The results showed the patient's glucose level was within the normal range. It further discusses hyperglycemia and hypoglycemia, the different types of diabetes, diagnostic criteria, and gestational diabetes.
DIABETES MELLITUS by dr aftab ahmed
This document provides an overview of diabetes mellitus, including its classification, pathophysiology, clinical features, investigations, diagnostic criteria, and management. It discusses the different types of diabetes, risk factors, characteristics, and laboratory findings. Type 1 diabetes results from beta cell destruction leading to insulin deficiency, while type 2 involves insulin resistance with relative insulin deficiency. Gestational diabetes occurs during pregnancy.
Diabetes melitus by dr aftab ahmed
This document provides an overview of diabetes mellitus, including its classification, pathophysiology, clinical features, investigations, diagnostic criteria, and management. It discusses the different types of diabetes, focusing on type 1 and type 2. Key points include that diabetes results from defects in insulin secretion or action leading to hyperglycemia, its classification is now based on etiology rather than treatment, and management involves lifestyle modifications, oral medications, and possibly insulin therapy.
Diabetes mellitus - 2
This document summarizes the clinical manifestations and complications of diabetes mellitus. It discusses the symptoms of type 1 and type 2 diabetes, including polyuria, polydipsia, weight loss, and ketoacidosis in type 1 patients. Acute complications covered are diabetic ketoacidosis, hyperglycemic hyperosmolar state, lactic acidosis, and hypoglycemia. Chronic complications are also briefly mentioned. The pathophysiology, clinical features, diagnosis, and management of diabetic ketoacidosis are described in detail.
Diabetes & glycemic disorders
diabetes,different types, complications,major characteristics,diagnosis OGTT,PREDIABETES,IGT iFG,metasbolic syndrome,DKA, HHNS,HBA1c
Diabetes Mellitus
The document discusses perioperative management of diabetes mellitus. It covers types of diabetes, complications, preoperative assessment and glycemic control goals. Glycemic control is important to minimize complications from hyperglycemia and hypoglycemia. For major surgery, an intravenous insulin and glucose infusion provides optimal control and prevents fluctuations in blood sugar levels. Frequent monitoring of blood glucose levels is essential in the perioperative period.
Diabetes Mellitus patients in dental management
Diabetes mellitus is a metabolic disorder characterized by relative or absolute insulin deficiency that affects 6% of the US population. There are two main types of diabetes: type 1 is characterized by autoimmune destruction of insulin-producing cells and requires insulin treatment; type 2 is more common and results from impaired insulin function and insulin resistance. Without proper glucose control, diabetes can lead to serious long-term complications affecting many organ systems like the eyes, kidneys, heart, and nerves. Dental professionals need to consider a patient's medical history and glycemic control to minimize risks during treatment and manage emergencies like hypoglycemia or hyperglycemia.
nursingcareofptwithdiabetes1.ppt
This document defines diabetes mellitus and describes its two main types, type 1 and type 2. It discusses the impact of diabetes on health, including that it is a leading cause of death, end-stage renal failure, blindness, and amputations in the US. Complications of diabetes discussed include cardiovascular disease, retinopathy, nephropathy, and hypoglycemia or hyperglycemia. Treatment involves managing blood glucose levels and risks through medication, diet, exercise and screening to prevent or treat complications.
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This document defines diabetes mellitus and describes its two main types, type 1 and type 2. It discusses the impact of diabetes on health, including that it is a leading cause of death, end-stage renal failure, blindness, and amputations in the US. Complications of diabetes discussed include cardiovascular disease, retinopathy, nephropathy, and hypoglycemia or hyperglycemia. Treatment involves managing blood glucose levels and risks through medication, diet, exercise and screening to prevent or treat complications.
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Rapid sequence intubation (RSI) is an emergency method used to safely and rapidly intubate a patient's airway while minimizing the risks of regurgitation and aspiration. The steps of RSI include preoxygenation, positioning the patient, administering premedication, applying cricoid pressure, rapidly inducing unconsciousness with drugs like propofol or ketamine, paralyzing the patient with succinylcholine or rocuronium, intubating the trachea, and providing post-intubation care and ventilation. RSI aims to protect patients from complications of aspiration that can occur if the airway is not properly protected during emergency intubation.
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Title: Sense of Taste
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Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
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Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
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Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
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Structure and Function of Taste Buds:
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Location of Taste Buds:
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Influence of receptors and neural pathways
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Abnormalities of Taste Detection:
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2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Diabetic Ketoacidosis
- 1. Diabetic Ketoacidosis (DKA) Epidemiology Diabetic ketoacidosis (DKA) is typically associated with type 1 diabetes. It also occurs in type 2 diabetes under conditions of extreme stress such as serious infection, trauma, cardiovascular or other emergencies, and, less often, as a manifestation of type 2 diabetes, a disorder called ketosis-prone diabetes mellitus. DKA is more common in young (<65 years) patients. The National Diabetes Surveillance Program of the Centers for Disease Control (CDC) estimated that there were 140,000 hospital discharges for DKA in 2009 in the United States, compared to 80,000 in 1988. The mortality rate for hyperglycemic crisis declined from 54% to 18% between 1980 and 2009. Mortality in hyperglycemic crisis is primarily due to the underlying precipitating illness and only rarely to the metabolic complications of hyperglycemia or ketoacidosis. The prognosis of hyperglycemic crisis is substantially worse at the extremes of age and in the presence of coma and hypotension. Pathogenesis a) Metabolic Abnormalities · Insulin deficiency and/or resistance à impairs glucose utilization in peripheral tissues & skeletal muscle, increases the delivery of gluconeogenic precursors to the liver (such as glycerol from fat and alanine from muscle), activates multiple enzymes in the gluconeogenic metabolic pathway, and increases glucagon secretion by removing its (insulin) inhibitory effect, elevates potassium levels because insulin normally promotes potassium cellular uptake · Glucagon hormone excess à Increased hepatic/renal gluconeogenesis and glycogenolysis · Increased secretion of catecholamines, cortisol, and growth hormone à opposes the actions of insulin, and contributes to the increases in glucose and ketones production b) Sources of Energy · Decreased Glucose Utilization à Decreased cell entry of blood glucose as the body’s normal source of energy · Enhanced Lipolysis à As an alternative source, the body begins to use and transfer fatty acids from peripheral fat stores to hepatocytes to produce ketones as a water soluble energy source Etiology · Infection (pneumonia, UTIs) · Discontinuation or inadequate insulin therapy · Severe dehydration (compromised water intake due to comorbid diseases requiring volume restriction) · Acute major illness (myocardial infarction, cerebrovascular accident, sepsis, pancreatitis) · New onset type 1 diabetes · Drugs that decrease carbohydrate metabolism (glucocorticoids, high-dose thiazide diuretics (HCTZ, chlorthalidone), sympathomimetics (dobutamine, terbutaline), and 2nd generation “atypical” antipsychotics (aripiprazole, clozapine, lurasidone, olanzapine, paliperidone, quetiapine, risperidone, ziprasidone) · SGLT2 inhibitors (empaglifozin, canaglifozin, dapaglifozin) · Cocaine use
- 2. · Psychological issues (eating disorders, intentional insulin nonadherence particularly in young patients with type 1 diabetes due to fear of weight gain, hypoglycemia, rebellion from authority, and the stress from chronic disease Clinical Presentation · Nausea, vomiting, abdominal pain frequent urination, hyperglycemia, lethargy, dyspnea with hyperventilation (Kussmaul respirations), fruity odor on breath (due to exhaled acetone, similar to scent of nail polish remover), · Signs of dehydration: decreased skin turgor or dry skin, dry mouth or thirst, hypotension, tachycardia Diagnostic Evaluation https://www.aafp.org/afp/2013/0301/p337.html http://care.diabetesjournals.org/content/32/7/1335 http://www.diabetes.org/living-with-diabetes/complications/ketoacidosis-dka.html https://www-uptodate-com.jerome.stjohns.edu/contents/diabetic-ketoacidosis-and-hyperosmolar- hyperglycemic-state-in-adults-clinical-features-evaluation-and- diagnosis?search=diabetic%20ketoacidosis&source=search_result&selectedTitle=2~150&usage_ty pe=default&display_rank=2 https://www-uptodate-com.jerome.stjohns.edu/contents/diabetic-ketoacidosis-and-hyperosmolar- hyperglycemic-state-in-adults- treatment?search=diabetic%20ketoacidosis&source=search_result&selectedTitle=1~150&usage_typ e=default&display_rank=1#H1 http://spectrum.diabetesjournals.org/content/15/1/28#T1