Transcript Type DM Q and A by Dr Sarma

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Question 1
 What is our Global Ranking for DM ?
 What is our current estimated burden?
 Why is T2DM so important ?
Question 1
 What is our Global Ranking for DM ?
 What is our current estimated burden?
 Why is T2DM so important ?
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Numero Uno – RANK ONE Globally
About 36 million (in 2003)
DM = CAD + Its major complications !!
Shortens longevity by 10-15 years
Question 2
 What are the TWO major defects in
Type 2 Diabetes ?
Question 2
 What are the TWO major defects in
Type 2 Diabetes ?
 Insulin Resistance (IR)
 Insulin Deficiency (ID)
Question 3
 What is  cell apoptosis ?
  cell apoptosis occurs in how many
years ?
Question 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 4
 What are the core defects of Insulin
Secretion in T2DM ?
Question 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 5
 What is Gold Standard Test to
Diagnose DM ?
 Should we use Plasma Sugar or
Whole blood Sugar for Diagnosis ?
Question 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 6
 What is Normal FBG & What is IFG ?
 What is Normal PPBG & What is IGT ?
 Is it essential two have TWO readings ?
Question 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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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 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 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 8
 What is the cause of Fasting
Hyperglycemia ?
 What is the defect that causes it ?
Question 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 9
 What is the cause of Postprandial
Hyperglycemia ?
 What is the defect that causes it ?
Question 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 10

What are the four mechanisms which
contribute to ↑ plasma glucose ?
Question 10

What are the four mechanisms which
contribute to ↑ plasma glucose ?
1. Hepatic Glucose Output (HGO) Basal In
2. Lack of peripheral utilization (IR)
3. Decrease in insulin secretion (ID)
4. Increase in absorption from GIT
Question 11
 What is HbA1c ?
 What is its normal value ?
 What does it reflect ?
Question 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 12
 What is the best measure to monitor
glycemic control for follow up ?
 What is its target value ?
Question 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 13
 What is IDRS ?
 What are its components ?
Question 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 14
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Can we prevent Diabetes ?
If so, How ?
Question 14
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Can we prevent Diabetes ?
If so, How ?
Yes. 3 international studied confirmed it
1. Identifying people in stage 1- IR
2. Total Lifestyle Change – MNT, PA
3. If necessary Metformin, Acarbose
Question 15
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Where can we find all info on TLC ?
Question 15
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Where can we find all info on TLC ?
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www.mypyramid.gov
Question 16

What is the ‘Old Paradigm’ of
Diabetes management ?
Question 16
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What is the ‘Old Paradigm’ of
Diabetes management ?
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It is called the ‘Step Care’ approach
It envisages Diet  OAD  Insulin
Question 17

What is the ‘New Paradigm’ of
Diabetes management ?
Question 17
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What is the ‘New Paradigm’ of
Diabetes management ?
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It is the ‘Stage Management’ approach
Stage 1 – Insulin Resistance (IR)
Stage 2 – IR + Insulin Deficiency (ID)
Stage 3 – Insulin Deficiency (ID)
Question 18

What is total metabolic control ?
Question 18
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What is total metabolic control ?
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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 19
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List the microvascular complications
Question 19
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List the microvascular complications
1. Diabetic Retinopathy (DR)
2. Diabetic Kidney Disease (DKD) –
Nephropathy
3. Diabetic Neuropathy – DPN, DAN
These start right at the onset of ↑ BG
We must screen for and prevent them
Question 20
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List the macrovascular complications
Question 20
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List the macrovascular complications
1. Coronary Artery Disease - CAD
2. Cerebro Vascular Disease, TIA
3. Peripheral Vascular Disease PVD
These start right at the onset of IR
We must screen for and prevent them
Question 21
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How do we identify persons with IR ?
Question 21
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How do we identify persons with IR ?
1.
2.
3.
4.
5.
6.
IGT or IFG
WC > 36 (32) BMI > 23
B.P > 140/90
Dyslipidemia –TG>150, HDL<40(50)
Acanthosis Nigricans
Fasting C-Peptide levels increased
Question 22
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What is C-Peptide ?
Question 22
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What is C-Peptide ?
1. When proinsulin is cleaved into active
Insulin, C-peptide is formed
2. It is measured in the fasting serum
3. It reflects the endogenous insulin
secretion by  cells
4. It is used in HOMA IR model
Question 23
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What are the ABC of Diabetes ?
Question 23
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What are the ABC of Diabetes ?
1. A1c target of < 7%
2. B.P  130/80
3. Cholesterols
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TG <150, HDL> 40(50), Lp(a) <25
Question 24
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What are the 4 major classes of OAD ?
Question 24
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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 25
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Which OAD is the sheet anchor of
Diabetes treatment ?
Question 25
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Which OAD is the sheet anchor of
Diabetes treatment ?
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Metformin in all 3 stages
Not SU – it is only in stage 2 (IR+ID)
Not Glitazone – It is not 1st line drug
Question 26
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What is the relative efficacy of OAD in
terms of the glucose lowering potency ?
Question 26
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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 27
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What are the cut-off levels of HbA1c
to make treatment decisions ?
Question 27
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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 OAD
3. HbA1c of < 7 – TLC only + Follow up
Question 28
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What are the key contraindications of
OAD ?
Question 28
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What are the key contraindications of
OAD ?
1.
2.
3.
4.
5.
6.
ALD – Met, SU, TZD
Renal Insufficiency – Met, SU
CHF, edema – TZD, Metformin
IBD, ALD – Acarbose
Pregnancy – All OADs
Age > 80 – Metformin, Glibenclamide
Question 29
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What are the key side effects of Rx. ?
Question 29
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What are the key side effects of Rx. ?
1.
2.
3.
4.
5.
Metformin – GI side effects, Lactic Acidosis
SU – Hypoglycemia, allergy, weight gain
TZD – Weight gain, edema, abn. LFT
Acarbose – Flatulence, GI side effects
Insulin – Weight gain, Hypoglycemia
Question 30
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Which are the best SU ?
Question 30
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Which are the best SU ?
In the order of superiority
 Glimepiride
 Gliclazide
 Glipizide
 Not Glibenclamide
Question 31
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Which Glitazone is preferable ? Why ?
Question 31
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Which Glitazone is preferable ? Why ?
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Both Rosi and Pio are equally good
Slight differences in their lipid effects
Choice is individualized
Question 32

What is the difference between Analog
insulins and conventional insulins ?
Question 32

What is the difference between Analog
insulins and conventional insulins ?
1.
2.
3.
4.
5.
6.
Precise onset of action
No need to give 30’ before a meal
Highly predictable duration
Predictable absorption kinetics
Smaller dose sufficient (70%)
But costly 2 to 3 times
Question 33
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What medicines are must for all
Diabetics to prevent CAD ?
Question 33
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What medicines are must for all
Diabetics to prevent CAD ?
1.
2.
3.
4.
Aspirin daily 100 mg o.d.
Atorvastatin – min of 10 mg or equivalent
ACEi or ARB to protect kidney and heart
Adequate control of B.P and Lipids
Question 34
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What is the take home message ?
Question 34
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1.
2.
3.
4.
5.
What is the take home message ?
Diabetes is mainly asymptomatic (80%)
Not screening for DM is a Deadly SIN
Only 70 % of diabetics are detected
Less than 20% are under < 7% HbA1c
The A, B, C, D, E must be kept in mind
always and targets must be achieved
6. Early use of insulin is essential for this
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