This presentation is all about the well-known disease "Diabetes". I have tried to focus on the molecular level of the disease, and I've discussed in detail the proteins and genes related in the process. I definitely looked through many references, watched many videos and read many articles about it. I was pretty much confused, but thanks to God, I was finally able to put together all I had learned into a nice, neat PowerPoint presentation. Wether you are a college student seeking a presentation about diabetes, or maybe just a normal person wanting to get some info, maybe a patient with diabetes, then you should be in the right place. My presentation should help you get through!
I have first begun with an introduction to the disease, including some data from International Diabetes Federation to show the huge number of people worldwide having diabetes.
I have then talked about how our body functions normally without diabetes. This will help you understand what goes wrong during the disease.
After that, I have discussed both type 1 and type 2 diabetes and what causes each type at a molecular level as well as talking about some differences.
Then I've come to talk about symptoms and complications of diabetes. The signs that could indicate someone has diabetes, and if someone has it for a long time, it's going to have impact on the various body systems and cause other diseases - known as complications. So I have also made clear what the complications of diabetes are in very easy to understand diagrams.
Finally, I have talked about how diabetes may be diagnosed and what the possible treatments are for each type. I've used many graphics in my presentation, so I'm sure you're going to enjoy studying it!
Diabetes and various types have been discussed in detail as regard for Pg entrance and with various images, tables .....
Topics discussed: 1) introduction
2) types of diabetes
3) comp0lication of diabetes
4) DKA
5) NKHOC
6) Diabetic nephropathy
7) skin diseases in diabetes
This presentation is all about the well-known disease "Diabetes". I have tried to focus on the molecular level of the disease, and I've discussed in detail the proteins and genes related in the process. I definitely looked through many references, watched many videos and read many articles about it. I was pretty much confused, but thanks to God, I was finally able to put together all I had learned into a nice, neat PowerPoint presentation. Wether you are a college student seeking a presentation about diabetes, or maybe just a normal person wanting to get some info, maybe a patient with diabetes, then you should be in the right place. My presentation should help you get through!
I have first begun with an introduction to the disease, including some data from International Diabetes Federation to show the huge number of people worldwide having diabetes.
I have then talked about how our body functions normally without diabetes. This will help you understand what goes wrong during the disease.
After that, I have discussed both type 1 and type 2 diabetes and what causes each type at a molecular level as well as talking about some differences.
Then I've come to talk about symptoms and complications of diabetes. The signs that could indicate someone has diabetes, and if someone has it for a long time, it's going to have impact on the various body systems and cause other diseases - known as complications. So I have also made clear what the complications of diabetes are in very easy to understand diagrams.
Finally, I have talked about how diabetes may be diagnosed and what the possible treatments are for each type. I've used many graphics in my presentation, so I'm sure you're going to enjoy studying it!
Diabetes and various types have been discussed in detail as regard for Pg entrance and with various images, tables .....
Topics discussed: 1) introduction
2) types of diabetes
3) comp0lication of diabetes
4) DKA
5) NKHOC
6) Diabetic nephropathy
7) skin diseases in diabetes
CME Sohag | internal medicine | Diabetes mellitusEmad Qasem
CME Sohag | internal medicine | Diabetes mellitus training session 22 may 2016 By Dr. Ahmed othman Abodooh, assistant lecturer of internal medicine, Sohag university
Diabetes mellitus (DM)
Introduction Sign and symptoms
complications
Types Etiology
Risk factors
Comparison between type 1 & type 2 DM
Causes of gestational DM
Q. Is there any impact of gestational DM on children?
Insulin Mechanism of action
Clinical features
List of oral hypoglycemic drugs available in BD
Diabetes Mellitus type 1 major comorbidity now days.
Insulin injection being the major treatment Diabetes Mellitus.
Some other drugs used to treat the Diabetes Mellitus are Tablet Metformin 500 mg and other hypoglycemic drugs.
Diabetes Mellitus and Hypertension how they are interlinked.
lecture about diabetes mellitus for undergraduated student, master student
its include definition of diabetes, type 1 diabetes, type2, gestational, diagnosis criteria, complication, world day
Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action.
Diabetes mellitus
Hyperglycemia
metabolism
health
Health
CME Sohag | internal medicine | Diabetes mellitusEmad Qasem
CME Sohag | internal medicine | Diabetes mellitus training session 22 may 2016 By Dr. Ahmed othman Abodooh, assistant lecturer of internal medicine, Sohag university
Diabetes mellitus (DM)
Introduction Sign and symptoms
complications
Types Etiology
Risk factors
Comparison between type 1 & type 2 DM
Causes of gestational DM
Q. Is there any impact of gestational DM on children?
Insulin Mechanism of action
Clinical features
List of oral hypoglycemic drugs available in BD
Diabetes Mellitus type 1 major comorbidity now days.
Insulin injection being the major treatment Diabetes Mellitus.
Some other drugs used to treat the Diabetes Mellitus are Tablet Metformin 500 mg and other hypoglycemic drugs.
Diabetes Mellitus and Hypertension how they are interlinked.
lecture about diabetes mellitus for undergraduated student, master student
its include definition of diabetes, type 1 diabetes, type2, gestational, diagnosis criteria, complication, world day
Diabetes mellitus is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action.
Diabetes mellitus
Hyperglycemia
metabolism
health
Health
The Presentation gives a detailed idea of Medicinal Chemistry and Pharmacology of Hypoglycemic agents useful for undergraduate and postgraduate students in Pharmacy, Medicine, Nursing, Pharmacology and Medicinal Chemistry
Environmental Transmission of Antimicrobial ResistancePranab Chatterjee
This is the second lecture I took for the MPH students at the Indian Institute of Public Health, Delhi, as a part of the Environmental Health module. In this lecture I introduce the students to the basics of AMR and some common modes and routes of transmission of the same through the environment.
What role does urbanization have to play in the changing epidemiology and emergence of infectious diseases? These slides accompanied my interactive lecture taken as a part of the Environmental Health module of the MPH course for the students at the Indian Institute of Public Health, Delhi.
This was the first training session I did for using Mendeley as a Reference Management software after being inducted into the Mendeley Advisors' Group. The target group for this presentation was Master's students with no prior experience of doing research or using reference management software. These students had applied for competitive grants to the Research Capacity Building Program being run by the India Research Initiative on Peri-Urban Human-Animal-Environment Health (which employs me at the time of uploading this presentation). In addition to providing them with seed funding to support their Master's theses, the Capacity Building Program also provided multiple opportunities for learning, networking and skill building, including a workshop on the Basics of EcoHealth Research Methods, in course of which this presentation was made.
Diabetes Mellitus: Presentation and CLinical ExaminationPranab Chatterjee
The presentation which won the Best Paper award at the Students' Paper Presentation in Rhapsody 2010. This paper was presented by Dr. Rimesh Pal Medical College Kolkata, 3rd Professional MBBS Student.
2. ETIOLOGIC CLASSIFICATION OF DIABETES MELLITUS Type I Diabetes (β-cell destruction, usually leading to absolute insulin deficiency) A. Immune mediated B. Idiopathic Type II Diabetes ( may range from predominantly insulin resistance with relative insulin deficiency to a predominantly insulin secretory defect with insulin resistance) Other specific types of Diabetes A. Genetic defects of β-cell function characterized by mutations in: i) Hepatocyte Nuclear Transcription Factor (HNF) 4α (MODY 1) ii) Glucokinase (MODY 2) iii) HNF 1α (MODY 3)
3. iv) Insulin Promoter Factor(IPF) 1 (MODY 4) v) HNF 1β (MODY 5) vi) Neuro D1 (MODY 6) vii) Mt DNA viii) Subunits of ATP sensitive Potassium Channel ix) Proinsulin or insulin conversion B. Genetic defects in insulin action: i) Type A insulin resistance ii) Leprechaunism iii) Rabson-Mendenhall syndrome iv) Lipodystrophy syndrome C. Diseases of exocrine pancreas –pancreatitis, pancreatectomy, neoplasia, cystic fibrosis, hemochromatosis, fibrocalculous pancreatopathy, mutations in carboxyl ester lipase D. Endocrinopathies-acromegaly, Cushing’s syndrome, glucagonoma, pheochromocytoma, hyperthyroidism, somatostatinoma, aldosteronoma E. Infections-congenital rubella, cytomegalovirus, cox sackie
4. F. Drug or chemical induced-Vacor, pentamidine, nicotinic acid, glucocorticoids, thyroid hormone, diazoxide, β-adrenergic agonists, thiazides, phenytoin, α-interferon, protease inhibitors, clozapine G. Uncommon forms of immune mediated diseases-stiff person syndrome, anti- insulin receptor antibodies H. Other genetic diseases sometimes associated with diabetes-Down’s syndrome, Kleinfelter’s syndrome, Turner’s syndrome, Wolfram’s syndrome, Freiderich’s ataxia, Huntington’s chorea, Lawrence-Moon-Biedl syndrome, myotonic dystrophy, porphyria, Prader-Willi syndrome 4. Gestational diabetes mellitus
5. TYPE -I DIABETES Genetic Factor: Genetic factor accounts for about one-third of the susceptibility to Type-I diabetes mellitus. Over 20 diferent regions of human genome show linkage with the disease, but the main focus remains on the HLA region within the major histocompatibility complex on the short arm of chromosome 6; the locus being designated as the IDDM 1. The region of the insulin gene on chromosome 11p is also linked with the disease, the locus being designated as IDDM 2. Other loci lying on chromosomes 15q, 11q and 6q are IDDM 3, IDDM 4 and IDDM 5 respectively.
6. RISK OF DEVELOPING TYPE-I DIABETES IN AN INDIVIDUAL WHO HAS A FIRST DEGREE RELATIVE WITH THE DISEASE
8. (2) ENVIRONMENTAL FACTOR:Although genetic susceptibility appears to be a prerequisite for the development of Type-I diabetes, the concordance rate between monozygotic twins is less than 40%, and environmental factors have an important role in promoting clinical expression of the disease. (3) VIRUS: Several viruses like mumps virus, Coxsackie B4, retrovirus, rubella (in utero), cytomegalovirus and Epstein-Barr virus have been found to be associated with the etiogenesis of the disease. DIET : Dietary factors like Bovine Serum Albumin (BSA) of cow’s milk, nitrosamines (in smoked and cured meats) and coffee have been proposed as potentially diabetogenic.
9. (5) STRESS:Stress may progress development of Type-I diabetes by stimulating secretion of counter-regulatory hormones and possibly by modulating immune activity. (6) IMMUNOLOGICAL FACTORS: Type-I diabetes is a slow T-cell mediated autoimmune disorder. Family studies have produced evidence that destruction of the insulin secreting cells in the pancreatic islets takes place over many years. Hyperglycemia accompanied by the classical symptoms of diabetes occurs only when 70-90% of beta cells have been destroyed. In humans and animals with spontaneous type-I diabetes the immune system retains the capacity to recognize and destroy transplanted pancreatic beta cells indefinitely.
10. (7) PANCREATIC PATHOLOGY: Proposed pathogenesis of Type-I Diabetes Viral infection in pancreatic beta cells Secretion of interferon-α by islet cells Normal islet Hyper expression of MHC class-I antigen within islets Insulinitis Selective Destruction of Beta cells Insulin deficient islet
11. TYPE-II DIABETES GENETIC FACTORS: Type-II diabetes has a strong genetic component. The concordance of the disease in identical twins is between 70 and 90%. Individuals with a parent having the disease have an increased risk of diabetes. If both the parents have type-II diabetes, then the risk is about 40%. Of the genes that predispose to type-II diabetes, the most prominent is a variant of the transcription factor-7 like gene and the genes encoding PPARγ, IRS, calpain 10,etc.
12. RISK OF DEVELOPING TYPE-II DIABETES UPTO AGE OF 80 YEARS FOR SIBLINGS OF PROBANDS WITH THE DISEASE
13. SINGLE GENE DEFECTS OF PANCREATIC BETA CELL FUNCTION CAUSING MATURITY ONSET DIABETES OF THE YOUNG (MODY)
14. (2) LIFESTYLE: Epidemiological studies of Type-II diabetes provide evidence that overeating, especially when combined with obesity and underactivity, is associated with the development of this type of diabetes. MALNUTRITION IN UTERO: Retrospective analysis of the birth weight of males born in England in 1930s has demonstrated an inverse relationship between weight at birth and at 1 year, and the development of type-II diabetes in late adulthood. AGE: Type-II diabetes is principally a disease of the middle age and elderly, affecting 10% population over the age of 65. PREGNANCY: During normal pregnancy, insulin sensitivity is reduced through the action of placental hormone and this affects glucose tolerance. The insulin secreting cells of pancreatic islets are unable to meet this increased demand in women genetically predisposed to the disease.
15. (6) IMPAIRED INSULIN SECRETION: In type-II diabetes, insulin secretion initially increases in response to insulin resistance to maintain normal glucose tolerance. Eventually, the insulin secretory defect progresses to a state of grossly inadequate insulin secretion. Though the reason for the decline in the insulin secretory capacity is unclear, it is assumed that a second genetic defect-superimposed upon insulin resistance leads to beta cell failure. Islet amyloid polypeptides secreted from beta cells is deposited on the islets in long standing cases of the disease.
17. (7) INSULIN RESISTANCE SYNDROMES: Insulin resistance syndrome or Metabolic syndrome or Syndrome X are terms used to describe a constellation of metabolic derangements that includes hyperinsulinemia, impaired glucose tolerance, hypertension, low HDL cholesterol, elevated triglycerides, central obesity, microalbuminuria, increased fibrinogen, increased plasminogen activator inhibitor-1 and elevated plasma uric acid. A number of relatively rare forms of severe insulin resistance include features of type-II diabetes. Two distinct syndromes of severe insulin resistance have been described in adults-Type A affecting young women and Type B affecting middle aged women. Insulin resistance is seen in a significant subset of women with Polycystic Ovarian Syndrome.
18. (8) INCREASED HEPATIC GLUCOSE AND LIPID PRODUCTION: Increased hepatic glucose production occurs early in the course of diabetes , though likely after the onset of insulin secretory abnormalities and insulin resistance in skeletal muscle. As a result of insulin resistance in adipose tissue and obesity, free fatty acid flux from adipocytes is increased, leading to increased lipid synthesis in hepatocytes. This lipid storage or steatosis in the liver may lead to Non Alcoholic Fatty Liver Disease and abnormal liver function tests.
19. (9) ABNORMAL MUSCLE AND FAT METABOLISM:Insulin resistance impairs glucose utilization by insulin-sensitive tissues and increases hepatic glucose output, both contributing to hyperglycemia. In skeletal muscle, there is greater impairment in the non-oxidative glucose usage (Glycogen formation) than in oxidative glucose metabolism through glycolysis. Though the precise molecular mechanism of insulin resistance is not known, it is believed that insulin receptor levels and tyrosine kinase activity in skeletal muscle are reduced, but these alterations are most likely secondary to the hyperinsulinemia and not primary defect. Therefore, ‘post-receptor’ defects in insulin mediated phosphorylation/dephosphorylation may play the predominant role in insulin resistance. For example, a PI3 kinase signalling defect may reduce translocation of GLUT4 to the plasma membrane. The obesity accompanying type-II diabetes, particularly in a central or visceral location is thought to be a part of the pathogenic process. The increased adipocyte mass leads to increased levels of circulating free fatty acids and other fat cell products like non-esterified free fatty acids, retinol binding protein 4, leptin, TNFα, resistin and adiponectin that modulate insulin sensitivity. This increased production of free fatty acids and some adipokines may cause insulin resistance in skeletal muscle and liver.