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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 ?
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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 ?
Numero Uno – RANK ONE Globally About 36 million (in 2003) DM = CAD + Its major complications !! Shortens longevity by 10-15 years
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Question 2Question 2
What are the TWO major defects in Type 2 Diabetes ?
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Question 2Question 2
What are the TWO major defects in Type 2 Diabetes ?
Insulin Resistance (IR) Insulin Deficiency (ID)
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Question 3Question 3
What is cell apoptosis ? cell apoptosis occurs in how many
years ?
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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
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Question 4Question 4
What are the core defects of Insulin Secretion in T2DM ?
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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
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Question 5Question 5
What is Gold Standard Test to Diagnose DM ?
Should we use Plasma Sugar or Whole blood Sugar for Diagnosis ?
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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)
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Question 6Question 6
What is Normal FBG & What is IFG ? What is Normal PPBG & What is IGT ? Is it essential two have TWO readings ?
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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
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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 ?
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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.
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Question 8Question 8
What is the cause of Fasting Hyperglycemia ?
What is the defect that causes it ?
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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
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Question 9Question 9
What is the cause of Postprandial Hyperglycemia ?
What is the defect that causes it ?
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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
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Question 10Question 10
What are the four mechanisms which contribute to ↑ plasma glucose ?
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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
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Question 11Question 11
What is HbA1c ? What is its normal value ? What does it reflect ?
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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
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Question 12Question 12
What is the best measure to monitor glycemic control for follow up ?
What is its target value ?
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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
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Question 13Question 13
What is IDRS ? What are its components ?
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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
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Question 14Question 14
Can we prevent Diabetes ? If so, How ?
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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
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Question 15Question 15
Where can we find all info on TLC ?
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Question 15Question 15
Where can we find all info on TLC ?
www.mypyramid.gov
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Question 16Question 16
What is the ‘Old Paradigm’ of Diabetes management ?
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Question 16Question 16
What is the ‘Old Paradigm’ of Diabetes management ?
It is called the ‘Step Care’ approach It envisages Diet OAD Insulin
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Question 17Question 17
What is the ‘New Paradigm’ of Diabetes management ?
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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)
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Question 18Question 18
What is total metabolic control ?
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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
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Question 19Question 19
List the microvascular complications
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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
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Question 20Question 20
List the macrovascular complications
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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
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Question 21Question 21
How do we identify persons with IR ?
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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
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Question 22Question 22
What is C-Peptide ?
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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
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Question 23Question 23
What are the ABC of Diabetes ?
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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
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Question 24Question 24
What are the 4 major classes of OAD ?
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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
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Question 25Question 25
Which OAD is the sheet anchor of Diabetes treatment ?
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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
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Question 26Question 26
What is the relative efficacy of OAD in terms of the glucose lowering potency ?
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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%
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Question 27Question 27
What are the cut-off levels of HbA1c to make treatment decisions ?
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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
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Question 28Question 28
What are the key contraindications of OAD ?
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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
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Question 29Question 29
What are the key side effects of Rx. ?
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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
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Question 30Question 30
Which are the best SU ?
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Question 30Question 30
Which are the best SU ?
In the order of superiority Glimepiride Gliclazide Glipizide Not Glibenclamide
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Question 31Question 31
Which Glitazone is preferable ? Why ?
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Question 31Question 31
Which Glitazone is preferable ? Why ?
Both Rosi and Pio are equally good Slight differences in their lipid effects Choice is individualized
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Question 32Question 32
What is the difference between Analog insulins and conventional insulins ?
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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
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Question 33Question 33
What medicines are must for all Diabetics to prevent CAD ?
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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
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Question 34Question 34
What is the take home message ?
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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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