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)

7. 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 )

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

9. 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

10. Pathogenesis of AGE Day by Day increase 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

11. 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

12. Diabetic Microangiopathy + Diabetic Nephropathy
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

13. 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

15. 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

17. 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.

19. 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

20. Infections in diabetes More Chance of “Diabetec Foot”
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”

21. 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

23. 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

24. Mechanism of Sulfonylurea (Glipizide)

25. Treatment Nitrate Like Action Dilate the Coronary Artery
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

26. 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?