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2022DIABETES MELLITUS.pptx

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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.

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DIABETES MELLITUS Eric Mbindo Njunju Bsc; Msc
Body unable to control blood glucose levels adequately Symptoms: Frequent urination Thirst Weight loss
Long term complications: Cardiovascular disease (atherosclerosis and stroke) Damage to nerves, kidneys and eyes (blindness) Approx. 425 million people worldwide Rise in numbers associated with an increase in obesity
Metabolic diseases: Hyperglycemia Defects in insulin secretion Defects in Insulin action Both
Pathogenic processes: Auto immune destruction of the 硫- cells of the pancreas Resistance to insulin
Abnormalities in carbohydrate, fat and protein metabolism due to deficient action of insulin on target tissues
Atherosclerosis?- Hypertension and abnormalities of lipoprotein metabolism
Type 1 diabetes (5-10% of diabetics)- Absolute deficiency of insulin secretion Cells of body immune system cause destruction of insulin secreting 硫-cells in the pancreas. Antibodies against key pancreatic proteins involved in insulin storage and secretion- deficiency in Insulin production Usually diagnosed in childhood Not associated with weight gain
Type 2 diabetes More common form (90-95% of diabetics) Loss of ability to respond to insulin Over 30 years of age, overweight, high blood pressure unhealthy lipid profile Hypersecretion of insulin May progress towards insulin deficiency Overweight a strong risk factor for developing type 2 diabetes
Normal glucose levels 3.5 to 5.5 mmol/l before meals Maintained by insulin and glucagon mainly (adrenaline, cortisol and growth hormone)
Recall the following pathways: Gluconeogenesis Glycolysis Glycogenesis Lipogenesis
Figure 1. Insulin signalling in an adipocyte Abbreviation: P, phosphorylation on tyrosine.
Long term complications: Macrovascular and Microvascular Modifications of proteins and lipids. Glycation products Oxidative stress and damage to vascular endothelium lining blood vessels
Diabetic acidosis Alternative energy source Triglycerides from adipose tissue broken down to free fatty acids and taken up by the liver- converted to acetyl CoA (precursor for ketone bodies Lower blood pH (Coma and death if not untreated)
Fasting state Oral glucose load HbA1c
Adequate glycemic control achieved with weight reduction, exercise, oral glucose lowering agents
Metabolic abnormality can progress, regress or stay the same
Other Specific types of diabetes Genetic defects of the 硫-cell Associated with monogenic defects in 硫-cell function- onset of hyperglycemia at an early age Impaired insulin secretion Autosomal dominant pattern of inheritance Six genetic loci on different chromosomes identified
Most common form is associated with mutations on chromosome 12 in the hepatic transcription factor
Mutations in the glucokinase gene on chromosome 7p Glucokinase- glucose sensor for 硫-cell Defect in glucokinase gene implies only increased plasma levels of glucose are necessary to elicit normal levels of insulin secretion
Inability to convert proinsulin to insulin- autosomal dominant pattern of inheritance
END

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2022DIABETES MELLITUS.pptx

  • 2. Body unable to control blood glucose levels adequately Symptoms: Frequent urination Thirst Weight loss
  • 3. Long term complications: Cardiovascular disease (atherosclerosis and stroke) Damage to nerves, kidneys and eyes (blindness) Approx. 425 million people worldwide Rise in numbers associated with an increase in obesity
  • 4. Metabolic diseases: Hyperglycemia Defects in insulin secretion Defects in Insulin action Both
  • 5. Pathogenic processes: Auto immune destruction of the 硫- cells of the pancreas Resistance to insulin
  • 6. Abnormalities in carbohydrate, fat and protein metabolism due to deficient action of insulin on target tissues
  • 7. Atherosclerosis?- Hypertension and abnormalities of lipoprotein metabolism
  • 8. Type 1 diabetes (5-10% of diabetics)- Absolute deficiency of insulin secretion Cells of body immune system cause destruction of insulin secreting 硫-cells in the pancreas. Antibodies against key pancreatic proteins involved in insulin storage and secretion- deficiency in Insulin production Usually diagnosed in childhood Not associated with weight gain
  • 9. Type 2 diabetes More common form (90-95% of diabetics) Loss of ability to respond to insulin Over 30 years of age, overweight, high blood pressure unhealthy lipid profile Hypersecretion of insulin May progress towards insulin deficiency Overweight a strong risk factor for developing type 2 diabetes
  • 10. Normal glucose levels 3.5 to 5.5 mmol/l before meals Maintained by insulin and glucagon mainly (adrenaline, cortisol and growth hormone)
  • 11. Recall the following pathways: Gluconeogenesis Glycolysis Glycogenesis Lipogenesis
  • 12. Figure 1. Insulin signalling in an adipocyte Abbreviation: P, phosphorylation on tyrosine.
  • 13. Long term complications: Macrovascular and Microvascular Modifications of proteins and lipids. Glycation products Oxidative stress and damage to vascular endothelium lining blood vessels
  • 14. Diabetic acidosis Alternative energy source Triglycerides from adipose tissue broken down to free fatty acids and taken up by the liver- converted to acetyl CoA (precursor for ketone bodies Lower blood pH (Coma and death if not untreated)
  • 15. Fasting state Oral glucose load HbA1c
  • 16. Adequate glycemic control achieved with weight reduction, exercise, oral glucose lowering agents
  • 17. Metabolic abnormality can progress, regress or stay the same
  • 18. Other Specific types of diabetes Genetic defects of the 硫-cell Associated with monogenic defects in 硫-cell function- onset of hyperglycemia at an early age Impaired insulin secretion Autosomal dominant pattern of inheritance Six genetic loci on different chromosomes identified
  • 19. Most common form is associated with mutations on chromosome 12 in the hepatic transcription factor
  • 20. Mutations in the glucokinase gene on chromosome 7p Glucokinase- glucose sensor for 硫-cell Defect in glucokinase gene implies only increased plasma levels of glucose are necessary to elicit normal levels of insulin secretion
  • 21. Inability to convert proinsulin to insulin- autosomal dominant pattern of inheritance