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Understanding Diabetes Mellitus Complications and Management

Explore how diabetes mellitus affects the body, its complications, diagnostic tests, treatment options, and relevant patient case studies. Learn about glycated hemoglobin, metabolic acidosis, and advanced glycation end products.

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Understanding Diabetes Mellitus Complications and Management

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  1. DIABETES MELLITUS • Group no..29 • Stuti, Fenil, Ravi, Neha, Dharti. • Group mentor:-DR. Alok Parekh

  2. History of patient • Patient is 61yr old, residing at pandesara, come to New Civil Hospital, • Chief complain of.. • Breathlessness since 7 days • Cough since 3 weeks • No complain of fever & Hemoptysis • H/O Diabetes Mellitus since 10 years • H/O Coronary Angioplasty in 2008

  3. First time diagnosed with accidental Hairfall & weight loss, • No H/O Polyuria, Polydipsia, Polyphagia • Due to Controllled Diabetes Mellitus • No H/O Palpitation • No any Edema (Diabetic Nephropathy) • Operated for cataract in both eyes • No fatigue, weakness ( Cells are starving)

  4. Investigation Haemoglobin = 9.9 gm % Total RBC = 3.88 millions/ cu.mm Total WBC = 16,200 / cu.mm Random Blood Sugar= 469 mg/dl Serum Creatinine = 1.4 mg% (0.4 – 1.2 )

  5. Advanced Glycated Endproducts (AGEs) Free Amino groups of Proteins + Carbonyl groups of Reducing sugar (Non-enzymetic reaction) (Increase Rate of AGE with Hyperglycemia)

  6. RAGE = Receptor for AGE AGEs bind to RAGEs RAGEs is present on Inflammatory cells Endothelium Vascular smooth muscle. So More Chances of Microvascular disease Macrovascular disease Renal cell disease Atherosclerosis due to endothelial damage

  7. Pathogenesis of AGE • Crosslinking of Collagen (In large vessels) Decrease in elasticity Endothelial injury AGE is resistant to proteolytic digestion Reversal of AGEs difficult Day by Day increase AGE

  8. Atherosclerosis Due to AGE AGEs damage Endothelial Componant of Vessels Turbulant Blood Flow Trap Nonglycated Plasma proteins Trapping of LDL in large vessels Increase deposition of LDL- cholesterol in intima of the vessels Atherogenesis

  9. Nephropathy due to AGE AGE in capillaries of Renal glomeruli Thickening & Damage to Basement membrane & Decrease Negative charge of Basement membrane Decrease repulsion of Protein during filteration Proteinuria Diabetic Microangiopathy + Diabetic Nephropathy

  10. HbA1c = Glycated haemoglobin Glucose + Haemoglobin (Protein) Life of Haemoglobin = 120 days Glycation remain for 120 days Idea about Glysemic control of last 120 days Idea about Glycation of all Other protein Idea about Probabilty of Other Complication

  11. ABG Report Referenc Range pH = 7.4 (7.35 – 7.45) pO2 = 110 mm Hg ( 90 – 100 ) pCO2 = 22 mm Hg (32 – 40 ) HCO3- = 15.4 mmol/l ( 22 – 28 ) SpO2 = 99% ( 90 – 100 ) Fully Compansated Metabolic Acidosis

  12. Fully compensated metabolic Acidosis Here HCO3 conc. is low = Metabolic Acidosis. But with that CO2 = Low = Washed out So pH level = Maintained at Normal So , it is fully copensated metabolic acidosis.

  13. Chest X – Ray • Left side Hazziness in Lower & Middle zone • Right side Mild Hazziness lower zone • Obliterated Costro-Phrenic angle Conclusion : • Left side huge pleural effusion • Right side mild pleural effusion • Left middle & lower zone pneumonitis

  14. Infections in diabetes • AGE affect Immunoglobulin • Decrease Immunity • AGE afect Microvessels • Decrease Blood Supply to Distal tissue • Decrease chemotaxis at injured site • Delay healing of injured site • AGE affect Nerves • Neuropathy • Sensory loss in the limbs • Repeated Injury • Cell has more glucose • Nutrition for Bacteria = Bacteria “Like It” More Chance of “Diabetec Foot”

  15. What to be needed in this patient? • Serum Ketone Body Level • Serum Insulin Level • Serum C-peptide level • Serum Protein level • Urinary Micro-protein level ( 30 – 300 mg/day) • Pleural Fluid Examination • Sputum Culture

  16. Treatment • Aspirin • Antiplatelet Action • Cyclo-oxygenase inhibitor • Suicide inhibition • Oral Hypoglycemic drugs • Glipizide (Sulfonylurea group) • Block K+ of Beta cell of pancrease • Increase Calcium Influx of in the Cell • Increase Insulin Release from The Beta Cell • Metformin (Biguanide group) • Inhibit Gluconeogenesis in Liver • Decrease activation of Following Enzyme • Phophoenolpyruvate Carboxykinase (PEPCK) • Glucose 6 Phosphatase

  17. Mechanism of Sulfonylurea (Glipizide)

  18. Treatment 3. Nikoran & Sorbotrate Nitrate Like Action Dilate the Coronary Artery 4. Pantoprazole Proton Pump Inhibitor Decrease H+ Secreation in GIT. Prevent Peptic Ulcer & Drug induce Gastritis 5. Thyroxine = For Correction of Hypothyroidism 6. Antibiotic

  19. Question to be learn from this case. Why cataract is common in patient of uncontrolled DM? What is Advance Glycate End Products? What is nephropathy & why it is common with patient of uncontrolled DM? What chances of infection and repeated injury to foot is common with uncontrolled DM? Why hypercholesteremia occurs in patient of uncontrolled DM? What is significant of micro-proteinuria? Why metabolic acid can more commonly with type – 1 DM? What is difference between uncomponsated ,partially componsated & fully componsated metabolic acidosis? What advantage of during C-Peptide level & Glycated haemoglobin, after diagnosis of diabetes mellitus?

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