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.

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 β- 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 β-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

• 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 β-cell
• Associated with monogenic defects in β-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 β-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

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.

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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

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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.

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Diabetes is a chronic disorder caused by insufficient insulin or insulin resistance. It can be asymptomatic and lead to complications if not properly managed. There are two main types - Type 1 is an autoimmune disorder destroying pancreatic beta cells, while Type 2 is caused by insulin resistance and often related to obesity. Chronic hyperglycemia can cause complications through non-enzymatic glycation and sorbitol accumulation, leading to damage in small and large blood vessels causing issues like heart disease, stroke, neuropathy, kidney disease and retinopathy. Proper management through lifestyle changes, medication and monitoring can prevent complications of diabetes.

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2022DIABETES MELLITUS.pptx

1. DIABETES MELLITUS Eric Mbindo Njunju Bsc; Msc

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 β- 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 β-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 β-cell • Associated with monogenic defects in β-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 β-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

22. • END

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2022DIABETES MELLITUS.pptx

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