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Diabetes mellitus
- 1. DIABETES MELLITUS S A RA N A D G I R I
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- 3. BRIEF INTRODUCTION A metabolicdisorder of Multiple aetiology characterized by chronic hyperglycemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in Insulin secretion, insulin action or both.
- 4. PREDISPOSING FACTORS 1.Heredity isthe most common predisposing factor. 2.Obesity, where adipose tissues are more resistant to actions of insulin as compared to normal (non- obese).
- 5. TYPES AND STAGESOF DIABETES MELLITUS PRIMARY DIABETES MELLITUS 2 TYPES SECONDARY DIABETES MELLITUS INSULIN DEPENDENT DIABETES MELLITUS NON INSULIN DEPENDENT DIABETES MELLITUS • PANCREATITIS • CYSTIC FIBROSIS • ACROMEGALY • CUSHING SYNDROME TYPE I TYPE II
- 7. TYPE I VSTYPE II DIABETES MELLITUS GENERAL FEATURES TYPE 1 TYPE II DEFECT • Autoimmune disorder • Antibody destroys the β- cells of Islets of Langerhans • Absolute deficiency of insulin • Genetic disorder • Decreased Insulin receptors • Resistance to extrahepatic/ peripheral targeted tissues PREVALENCE 10-20% of diabetic population 80-90% of diabetic population AGE OF ONSET < 40 years > 40 years BODY WEIGHT Low (lean and thin) High ( obese or normal) GENE LOCUS Chromosome 6 Chromosome 1 • Why does Type 1 DM associated with low body weight as compared to type II DM? Renal Glycosuria, Lipolysis
- 8. CONTD.. (CLINICAL COMPARISON) CLINICALFEATURES TYPE 1 TYPE II DURATION OF SYMPTOMS WEEKS (rapid) MONTHS TO YEARS (slow) PRESENTING SYMPTOMS DIFFERENT COMPLICATIONS • Achanthosis nigricans – patches on skin • slow healing of wounds COMPLICATIONS AT THE TIME OF DIAGNOSIS ABSENT PRESENT (in 10-20% cases) ACUTE COMPLICATIONS KETOACIDOSIS HYPEROSMOLAR COMA POLUDYPSI A Achanthosis nigricans
- 9. BIOCHEMICAL FEATURES AND TREATMENT BIOCHEMICALFEATURES AND TREATMENT TYPE 1 TYPE 11 PLASMA INSULIN DECREASED OR ABSENT NORMAL OR INCREASED AUTOANTIBODIES PRESENT RARE KETONURIA PRESENT ABSENT TREATMENT INSULIN (oral hypoglycemics not required) ORAL HYPOGLYCEMICS not required)
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- 13. SYMPTOMS AND SIGNS POLYURIA POLYDYPSIA POLYPHAGIA WEIGHTLOSS IN SPITE OF POLYPHAGIA HYPERGLYCEMIA GLYCOSURIA KETOSIS ACIDOSIS DIABETIC COMA
- 14. PATHOPHYISOLOGY OF DIABETESMELLITUS
- 15. COMPLICATIONS OF DIABETESMELLITUS INFECTIONS NON- KETOTIC COMAACUTE KETOTIC COMA ATHEROSCLEROSISCHRONIC PRE- DISPOSING Prolonged DYSLIPIDEMIA & HYPERCHOLESTEROLEMIA Deposition of lipid underneath the tunica intima of blood vessels ( coronary, peripheral and cerebral arteries) Microangiopathy Capillary basement membrane becomes thicker • Diabetic Retinopathy • Diabetic Neuropathy • Diabetic Nephropathy
- 16. HYPERGLYCEMIA AND ITSCONSEQUENCES • Increased blood glucose level • Absence of Insulin • Characteristic feature of Uncontrolled Diabetes Mellitus • Decreased peripheral utilization of glucose • Increased hepatic output of glucose to carry out glycogenolysis and gluconeogenesis.
- 17. 1. GLYCOSURIA OSMOTI C DIURESIS POLYURIA POLYDYPSIA LOSS OFELECTROLYTE Na+, K+, PO4 3- LOSS OF BODY WEIGHT POLYPHAGIA CELLULAR DEHYDRATION
- 18. 2. IMPAIRED PHAGOCYTOSIS Hyperglycaemiaimpairs all aspects of leucocytic phagocytic function, i.e. adherence, diapedesis, phagocytosis and intracellular killing. Because of impaired phagocytic function, the diabetics are more prone to infections as compared to the non-diabetics.
- 19. 3. GLYCOSYLATION OFPROTEINS Glycosylation of tissue proteins Occurs when the blood glucose levels remain elevated for a prolonged duration (years). Glycosylation leads to irreversible changes in the chemical structure of tissue proteins. These chemical changes have been implicated in producing long-term complications of diabetes mellitus, such as: • Diabetic nephropathy, • Diabetic retinopathy, • Diabetic neuropathy and so on. Glycosylation of haemoglobin. Glycosylated haemoglobin refers to the glucose-derived products of normal hemoglobin(HbA). • Among the glycosylated hemoglobins, the most abundant form is HbA1C, which is produced by condensation of glucose with N- terminal valine of each β chain of hemoglobin A (HbA). • Normally, HbA1C concentration is about 3– 5% of the total haemoglobin. • During sustained hyperglycemia, as in diabetes mellitus, the concentration of HbA1C may be elevated to 10–20% of the total hemoglobin. • Determination of HbA1C has become an
- 20. 4. HYPERTRYGLYCERIDAEMIA INSULIN DEFICIENCY INCREASEDACTIVITY OF HORMONE SENSITIVE TG LIPASE INC. FFA PRODUCTION INCREASED LIPOLYSIS INC. TG SYNTHESIS INC. CHOLESTEROL SYNTHESIS
- 21. 5. KETOSIS INCREASED PLASMA KETONEBODIES LEVEL CELLULAR DEHYDRATION Rapid Deep Respiration (Dyspnea, KUSSMAUL breathing) Electrolyte loss Acidic urine due to ketonuria Acetone smell in patient’s breathe Coma and death Hypovolemia and Hypotension
- 22. EFFECT ON PROTEINCATABOLISM INSULIN PROMOTES PROTEIN SYNTHESIS INHIBITS PROTEOLYSIS (-) PROTEIN ANABOLISM IS SUPPRESSED (-) CATABOLISM INCREASED Protein depletion in the body Muscle Wasting Negative Nitrogen balance
- 23. HYPOGLYCAEMIA IN DIABETICS Hypoglycaemiain diabetics is more common in diabetics than in non- diabetics. About 4% deaths of IDDM are said to be due to hypoglycaemia. OVERDOSE OF ANTIDIABETIC DRUGS ( INSULIN) MISMATCH B/W INSULIN ADMINISTRATION AND FOOD HABITS HEAVY EXERCISE ALCOHOL INTAKE INTAKE OF TOO LITTLE OR NO FOOD
- 24. HYPOGLYCAEMIA NEUROGLYCOPENIC DERMATOLOGICAL GIT CVS • Palpitation • Tachycardia •Sinus Arrhythmia SIGNS • Nausea • Vomiting • Sweating • Hypothermia CNS becomes excitable • Hallucination • Extreme nervousness • Tremors • Confusions • Drowsiness • Convulsions SYMPTOMS