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Question 1Question 1
What is our Global Ranking for DM ? What is our current estimated burden? Why is T2DM so important ?
Question 1Question 1
What is our Global Ranking for DM ? What is our current estimated burden? Why is T2DM so important ?
Numero Uno – RANK ONE Globally About 36 million (in 2003) DM = CAD + Its major complications !! Shortens longevity by 10-15 years
Question 2Question 2
What are the TWO major defects in Type 2 Diabetes ?
Question 2Question 2
What are the TWO major defects in Type 2 Diabetes ?
Insulin Resistance (IR) Insulin Deficiency (ID)
Question 3Question 3
What is cell apoptosis ? cell apoptosis occurs in how many
years ?
Question 3Question 3
What is cell apoptosis ? cell apoptosis occurs in how many
years ?
Progressive programmed cell death 10 to 15 years after the onset of DM Today’s approach is save the cell
Question 4Question 4
What are the core defects of Insulin Secretion in T2DM ?
Question 4Question 4
What are the core defects of Insulin Secretion in T2DM ?
Loss or delay of first phase of Insulin secretion
Blunting or flattening of second phase
Question 5Question 5
What is Gold Standard Test to Diagnose DM ?
Should we use Plasma Sugar or Whole blood Sugar for Diagnosis ?
Question 5Question 5
What is Gold Standard Test to Diagnose DM ?
Should we use Plasma Sugar or Whole blood Sugar for Diagnosis ?
O-GTT – Fasting sample and 2 hours Post Glucose (75g) sample
Obviously Plasma (venous sample)
Question 6Question 6
What is Normal FBG & What is IFG ? What is Normal PPBG & What is IGT ? Is it essential two have TWO readings ?
Question 6Question 6
What is Normal FBG & What is IFG ? What is Normal PPBG & What is IGT ? Is it essential two have TWO readings ?
N =100 mg FBG; 101-125 is IFG N =140 mg PPBG; 141-199 is IGT YES – Two readings are a must for Dx. FBG 126 or PPBG 200 is DM
Question 7Question 7
Can we use urine sugar for Dx. or F/u ? Can we use HbA1c for Diagnosis ? What is important in urine exam in DM ?
Question 7Question 7
Can we use urine sugar for Dx. or F/u ? Can we use HbA1c for Diagnosis ? What is important in urine exam in DM ?
No. Urine sugar is not all useful No. HbA1c is not for Diagnosis; only F/u Albumin, MAU, Ketones are very imp.
Question 8Question 8
What is the cause of Fasting Hyperglycemia ?
What is the defect that causes it ?
Question 8Question 8
What is the cause of Fasting Hyperglycemia ?
What is the defect that causes it ?
Increase in Hepatic Glucose Output – Called HGO
Decrease in Basal Insulin secretion
Question 9Question 9
What is the cause of Postprandial Hyperglycemia ?
What is the defect that causes it ?
Question 9Question 9
What is the cause of Postprandial Hyperglycemia ?
What is the defect that causes it ?
Decrease in peripheral utilization – removal of glucose by muscle & adipose tissue
Excess CHO meal load Delay or absence of 1st Phase Insulin
Question 10Question 10
What are the four mechanisms which contribute to ↑ plasma glucose ?
Question 10Question 10
What are the four mechanisms which contribute to ↑ plasma glucose ?
1. Hepatic Glucose Output (HGO) Basal In2. Lack of peripheral utilization (IR)3. Decrease in insulin secretion (ID)4. Increase in absorption from GIT
Question 11Question 11
What is HbA1c ? What is its normal value ? What does it reflect ?
Question 11Question 11
What is HbA1c ? What is its normal value ? What does it reflect ?
It is a Glycated hemoglobin Normal HbA1c is around 6% It represents the mean plasma glucose
over the previous 120 days
Question 12Question 12
What is the best measure to monitor glycemic control for follow up ?
What is its target value ?
Question 12Question 12
What is the best measure to monitor glycemic control for follow up ?
What is its target value ?
HbA1c is the measure for monitoring It must be kept below 7, preferably 6
Question 13Question 13
What is IDRS ? What are its components ?
Question 13Question 13
What is IDRS ? What are its components ?
Indian Diabetic Risk Score is used to assess ones risk for DM
Age, WC, family h/o, physical activity
Question 14Question 14
Can we prevent Diabetes ? If so, How ?
Question 14Question 14
Can we prevent Diabetes ? If so, How ?
Yes. 3 international studied confirmed it1. Identifying people in stage 1- IR2. Total Lifestyle Change – MNT, PA3. If necessary Metformin, Acarbose
Question 15Question 15
Where can we find all info on TLC ?
Question 15Question 15
Where can we find all info on TLC ?
www.mypyramid.gov
Question 16Question 16
What is the ‘Old Paradigm’ of Diabetes management ?
Question 16Question 16
What is the ‘Old Paradigm’ of Diabetes management ?
It is called the ‘Step Care’ approach It envisages Diet OAD Insulin
Question 17Question 17
What is the ‘New Paradigm’ of Diabetes management ?
Question 17Question 17
What is the ‘New Paradigm’ of Diabetes management ?
It is the ‘Stage Management’ approach Stage 1 – Insulin Resistance (IR) Stage 2 – IR + Insulin Deficiency (ID) Stage 3 – Insulin Deficiency (ID)
Question 18Question 18
What is total metabolic control ?
Question 18Question 18
What is total metabolic control ?
Glycemic control is essential but we also need to control all components
We must maintain the B.P <130/80 The lipids under target values See that pt. avoids smoking Reduce his weight and waist This is total METABOLIC CONTROL
Question 19Question 19
List the microvascular complications
Question 19Question 19
List the microvascular complications
1. Diabetic Retinopathy (DR)2. Diabetic Kidney Disease (DKD) –
Nephropathy3. Diabetic Neuropathy – DPN, DAN
These start right at the onset of ↑ BGWe must screen for and prevent them
Question 20Question 20
List the macrovascular complications
Question 20Question 20
List the macrovascular complications
1. Coronary Artery Disease - CAD2. Cerebro Vascular Disease, TIA3. Peripheral Vascular Disease PVD
These start right at the onset of IRWe must screen for and prevent them
Question 21Question 21
How do we identify persons with IR ?
Question 21Question 21
How do we identify persons with IR ?
1. IGT or IFG2. WC > 36 (32) BMI > 233. B.P > 140/904. Dyslipidemia –TG>150, HDL<40(50)5. Acanthosis Nigricans6. Fasting C-Peptide levels increased
Question 22Question 22
What is C-Peptide ?
Question 22Question 22
What is C-Peptide ?
1. When proinsulin is cleaved into active Insulin, C-peptide is formed
2. It is measured in the fasting serum3. It reflects the endogenous insulin
secretion by cells4. It is used in HOMA IR model
Question 23Question 23
What are the ABC of Diabetes ?
Question 23Question 23
What are the ABC of Diabetes ?
1. A1c target of < 7%2. B.P 130/803. Cholesterols
TG <150, HDL> 40(50), Lp(a) <25
Question 24Question 24
What are the 4 major classes of OAD ?
Question 24Question 24
What are the 4 major classes of OAD ?
Those That decrease HGO - Metformin Improve insulin Resistance - Met, TZD Stimulate cell – SU, Repaglinide Slow absorption of CHO - Acarbose
Question 25Question 25
Which OAD is the sheet anchor of Diabetes treatment ?
Question 25Question 25
Which OAD is the sheet anchor of Diabetes treatment ?
Metformin in all 3 stages Not SU – it is only in stage 2 (IR+ID) Not Glitazone – It is not 1st line drug
Question 26Question 26
What is the relative efficacy of OAD in terms of the glucose lowering potency ?
Question 26Question 26
What is the relative efficacy of OAD in terms of the glucose lowering potency ?
1. Metformin and SU –HbA1c ↓ 1.5% 2. Pio and Rosi – HbA1c ↓ 1.0% 3. Acarbose – HbA1c ↓ 0.5%
Question 27Question 27
What are the cut-off levels of HbA1c to make treatment decisions ?
Question 27Question 27
What are the cut-off levels of HbA1c to make treatment decisions ?
1. HbA1c of 9 or above straight away consider Insulin
2. HbA1c of < 9 to 7 consider OAD3. HbA1c of < 7 – TLC only + Follow up
Question 28Question 28
What are the key contraindications of OAD ?
Question 28Question 28
What are the key contraindications of OAD ?
1. ALD – Met, SU, TZD2. Renal Insufficiency – Met, SU3. CHF, edema – TZD, Metformin4. IBD, ALD – Acarbose5. Pregnancy – All OADs6. Age > 80 – Metformin, Glibenclamide
Question 29Question 29
What are the key side effects of Rx. ?
Question 29Question 29
What are the key side effects of Rx. ?
1. Metformin – GI side effects, Lactic Acidosis2. SU – Hypoglycemia, allergy, weight gain3. TZD – Weight gain, edema, abn. LFT4. Acarbose – Flatulence, GI side effects5. Insulin – Weight gain, Hypoglycemia
Question 30Question 30
Which are the best SU ?
Question 30Question 30
Which are the best SU ?
In the order of superiority Glimepiride Gliclazide Glipizide Not Glibenclamide
Question 31Question 31
Which Glitazone is preferable ? Why ?
Question 31Question 31
Which Glitazone is preferable ? Why ?
Both Rosi and Pio are equally good Slight differences in their lipid effects Choice is individualized
Question 32Question 32
What is the difference between Analog insulins and conventional insulins ?
Question 32Question 32
What is the difference between Analog insulins and conventional insulins ?
1. Precise onset of action2. No need to give 30’ before a meal3. Highly predictable duration4. Predictable absorption kinetics5. Smaller dose sufficient (70%)6. But costly 2 to 3 times
Question 33Question 33
What medicines are must for all Diabetics to prevent CAD ?
Question 33Question 33
What medicines are must for all Diabetics to prevent CAD ?
1. Aspirin daily 100 mg o.d.2. Atorvastatin – min of 10 mg or equivalent3. ACEi or ARB to protect kidney and heart4. Adequate control of B.P and Lipids
Question 34Question 34
What is the take home message ?
Question 34Question 34
What is the take home message ?
1. Diabetes is mainly asymptomatic (80%)2. Not screening for DM is a Deadly SIN 3. Only 70 % of diabetics are detected4. Less than 20% are under < 7% HbA1c5. The A, B, C, D, E must be kept in mind
always and targets must be achieved6. Early use of insulin is essential for this
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