1. Case 1 History: Mr Raju, 49 yrs, banker by profession, presents with c/o fatigue, gradually increasing over last few months. He has also increase frequency of urine, He lives sedentary life. Past History: No major illness in past. Family History: Father was Diabetic of over 25 years, died at age of 72.

2. Personal History: Not significant, O/E: Weight : 80 kg Height: 148 cm Pulse: 80/min Regular BP : 150/80 mm of hg. Obesity CVS/RS/AS/CNS : Normal Peri Pulse: Normal felt Feet / Nails / Sensation : clinically Normal

3. Laboratory Ix: 1. Hb : 14 %, CBC: 10,500 TC 2. FBS: 156 mg/dL, F urine: Nil 3. PP2BS: 225 mg /dL, PP2 urine: ++ 4. Urine R/M : proteins, Ketones absent 5. Hba1c: 8.5 % 6. Urea: 26 mg/dL, S. Creat: 0.8 mg/dL 7. Lipids: TC: 263, TG : 320, HDL : 24

4. Q: 1. Based on Above History what is Provisional Diagnosis? 1. Type 1 DM 2. Type 2 DM 3. Type 2 DM with Dyslipidemia 4. Type 1 DM with Dyslipidemia

5. Why Type 2 : 1. Adult Onset 2. Positive Family History 3. Sedentary life style 4. Obesity

6. Why Dyslipidemia? Lipids: TC: 263, TG : 320, HDL : 24 What about Renal function: 1. Urine R/M, 2. S. creatinine. 3. Urea All are normal.... Any Ix remaining for renal function?

7. 2 – 3 abnormal readings in 3 – 6 months must to confirm diagnosis > 300 > 200 > 300 Clinical Albuminuria 30 – 299 20 – 199 30 – 299 Micro Albuminuria (Stage III Nephropathy) < 30 < 20 < 30 Normal Spot collection µgm/mg creatinine Timed collection ( µgm/min) 24 Hr Collection (mg/24 Hr) ABNORMALITIES IN URINE ALBUMINE EXCREATION

8. Q : 2 In Type 2 DM: 1. Relative Insulin deficiency occurs due to resistance of action of Insulin in muscle, fats, and Liver, and an inadequate response by B cells of Pancreas. 2. IR occurs 3. Pancreatic B cell function declines gradually over time. 4. All of the above.

9. Analysis: 1. Type 2 DM have IR, and have relative Insulin deficiency 2. Autoimmune destruction of Pancreatic B cell does not occur. 3. Mostly Type 2 DM are Obese ( cause of IR), those who are not by BMI, have increase percentage of body fat distributed predominantly in the abdomen. 4. Hyperglycemic stat develops gradually, so goes undetected in early stages, they have defective insulin secretion which is not sufficient to compensate for IR.

10. Q. 3: Causes for IR: 1. Obesity 2. Physical Inactivity 3. Genetic factors 4. All of the above.

11. Analysis: 1.Type 2 DM is complex disease, Multigenic / Polygenic, resulting due to interaction of Environment and Genes. 2. Relative Insulin deficiency, occurs because of resistance of action of Insulin in muscles, fat and liver, so there is inadequate response of B cell of Pancreas. 3. IR is due to Increase FFA level in plasma, so there is Decrease transport of glucose in muscle, Increase hepatic glucose production Increase breakdown of fat

12. Type 2 DM occurs when diabetogenic lifestyle (environmental factors), like excessive caloric intake, decrease caloric expenditure, leading to Obesity is superimposed on susceptible genotype (genetic factor)

13. Q: 4 Lab test useful in Diagnosis of DM are: 1. FBG 2. 2 Hr PPBG 3. RBG 4. Hba1c. 5. All of the above.

14. Conversion: 1. m mol/ L = mg/dL X 18 None > 200 mg/dL Symptoms of Hyperglycemia and RBG 2 > 6.5 % 5.7 – 6.4 % < 5.7 % Hba1c 2 > 200 mg/dL 140 – 199 mg/dL < 140 mg/dL PPBG 2 Hr (75 gm oral glucose) 2 > 126 mg/dL 101 - 125 mg/dL < 100 mg/dL FBG ( 8-10 Hr of zero caloric intake) Confirmation test required DM Risk of DM (Pre Diabetes) Normal Venous sample ADA criteria for diagnosis of DM

15. Q. 4 Categories with increased risk of DM and CV risk includes: 1. IFG 2. IGT 3. Hba1c : b/n 5.7 % to 6.4 % 4. all of above.

16. What are the targets level in DM?