T2DM management - Evidence based medicin


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T2DM Management-Evidence based medicine : 

T2DM Management-Evidence based medicine Dr. Girish Vaswani

T2DM -Clinical implementation of theory : 

T2DM -Clinical implementation of theory Mr. Milind Kulkarni, a 48 year old bank manager, residing in Mumbai attended my clinic with a history of feeling excessively hungry and thirsty and passing a lot of urine throughout the day. He also complained of tiredness and weight loss. His father was diagnosed as T2DM at an age of 55 years

Slide 3: 

On examination, Mr. Milind weighed 80 kgs and he was 5ft 6 in. tall. His waist circumference was 42 inches ( 106.6 cms). He was afebrile and his pulse was 80/min reg, good vol, equal on both sides, PP were well felt and there was no radio-femoral delay.There was no cyanosis, pallor or icterus. BP was 160/106 in Rt upper limb in the supine position and no postural drop was noted.JVP was not raised and there was no edema feet, lymphadenopathy or clubbing.

Slide 4: 

Systemic examination of the cardiovascular system was normal as were examinations of the other systems. Fundoscopy did not reveal any abnormality.

Clinical application of theory : 

Clinical application of theory Considering his symptoms, I did a random capillary test for sugar which revealed a level of 280 mg %. He was then advised a battery of investigations and asked to follow up with the reports the next day.

DM – ADA criteria for DM : 

DM – ADA criteria for DM An RBG (irrespective of caloric intake) level of 200 mg/dl or greater with the presence of symptoms suggestive of DM Or A FPG (no caloric intake for 8 hrs) level of 126 mg/dl or greater Or Two hour PG level of 200 mg/dl or greater during an oral GTT.

Pre-diabetes – ADA criteria : 

Pre-diabetes – ADA criteria IFG is defined as a fasting glucose level between 100 mg/dl to 125 mg/dl And IGT (after 75 gm oral glucose) is defined as 2 hr glucose level between 140 to 199 mg/dl during an oral GTT. Those having pre-diabetes are at 25-40% risk of developing T2DM within the next 5 yrs as also are at increased risk of CV disease.

Slide 8: 

So our patient was diagnosed as having DM. No further testing in this patient was required to differentiate between T1DM and T2DM as Age > 45 yrs Obese, sedentary life-style

Whether T2DM ? : 

Whether T2DM ? T1DM Non-obese young patient Generally auto-immune Ketosis prone Islet cell auto-antibodies Activated T lymphocytes in pancreas, peripancr nodes and circulation Cytokine induced damage Immunologic markers –GAD 65, IA-2/ICA-512 T2DM Generally obese with age 45 yrs Non autoimmune LA, HNKC prone Insulin resistance, impaired insulin secretion and increased HGO Adipose cells – insulin resistance, lipotoxicity and glucotoxicity Amyelin in pancreas Immunological markers are absent

Labs – T2DM : 

Labs – T2DM The following blood reports were done and their results were as follow: FBS – 155 PPBS – 268 HbA1c – 8.9 CBC, ESR, CXR – were normal ECG – Left ventricular hypertrophy Lipid profile – TG 180, TC 240, LDL 160, HDL 30

Slide 11: 

Creatinine, electrolytes and uric acid – normal Urine routine revealed micro-albuminuria Liver function tests were normal. Retinal examination – normal

Slide 12: 

How would you approach this patient?

Typical T2DM patient profile : 

Typical T2DM patient profile First of all, our patient has a BMI of 27.68 (i.e he is obese) and leads a sedentary life-style. His blood pressure level was 160/106 mmHg and HDL level of 30 mg/dl. It is not surprising that he was detected to have T2DM as he has a family history with multiple risk factors.

Risk factors of T2DM : 

Risk factors of T2DM F/H of diabetes (parent or sibling with T2DM) Obesity (BMI of 25kg/m2 or greater) Habitual physical inactivity Race/ethnicity Previously identified IFG or IGT History of GDM or delivery of baby > 4kg Hypetension of 140/80 mmHg or greater level HDL < 35 mg/dl TG > 250 mg/dl PCOD H/O vascular disease

Screening for T2DM - ADA : 

Screening for T2DM - ADA Screen earlier if obese (BMI > 25 kg/m2) plus one additional risk factor for T2DM. Otherwise 45 yrs of age or greater every 3 years

Diabetes: Complications : 

Macrovascular Microvascular Stroke Heart disease and hypertension 2-4 X increased risk Foot problems Diabetic eye disease (retinopathy and cataracts) Renal disease Peripheral Neuropathy Peripheral vascular disease Diabetes: Complications Meltzer et al. CMAJ 1998;20(Suppl 8):S1-S29. Complications Erectile Dysfunction

Slide 17: 

Of course our patient had no evidence of end-organ damage except for micro-albuminuria and had been detected to have LVH due to hypertension and hyperlipidemia.

Whether he has syndrome X ? : 

Whether he has syndrome X ? Weight 80 kgs Waist circumference 42 inches (106.6 cms) TG 180 mg/dl HDL 30 mg/dl BP 160/106 mmHg with FPG 155 mg/dl

Yes -ATP III: The Metabolic Syndrome* : 

Yes -ATP III: The Metabolic Syndrome* *Diagnosis is established when 3 of these risk factors are present. †Abdominal obesity is more highly correlated with metabolic risk factors than is BMI. ‡Some men develop metabolic risk factors when circumference is only marginally increased. Expert Panel on Detection, Evaluation, and Treatment ofHigh Blood Cholesterol in Adults. JAMA. 2001;285:2486-2497. © 2001, Professional Postgraduate Services® www.lipidhealth.org

But would it change the approach? : 

But would it change the approach? NO

What can we offer him ? : 

What can we offer him ?

Treatment of type 2 DM -Overview : 

Treatment of type 2 DM -Overview Exercise MNT Obesity management Counseling for T2DM and Medicinal intervention: Oral agents and insulin Risk factor management Patient Education SMBG S.Lipids Renal Cardiovascular Neurological Foot examination

What we can do : 

What we can do Our patient was obese, lead a sedentary life-style and was hypertensive. He had high blood sugar levels and evidence of target organ damage in the form of micro-albuminuria and LVH. His serum lipids were abnormal and all the criteria for the metabolic syndrome were satisfied. He was thus at increased risk of developing the various complications of T2DM

Life-style modification : 

Life-style modification These include medical nutrition therapy, exercise, weight loss and obesity management. Smoking de-addiction and education about diabetes, vascular episodes and cardiac disease would make the patient an eager partner in the management of his disease.

Medical nutrition therapy : 

Medical nutrition therapy There is nothing like a Diabetic diet. Eating right is the only way to not only prevent ill health but also manage other medical conditions and diabetes. All chronic medical conditions require a modification in the foods you eat and the calories consumed. These modifications are similar to those suggested as a healthy, balanced diet according to the nutritionists. Hence eat right and eat healthy from childhood to live longer.

Slide 26: 

Glycemic Load to the Extreme

Slide 27: 

Low Glycemic Load Pyramid

Slide 28: 

1/2 is non-starchy vegetables such as salad or cooked vegetables. 1/4 is starchy foods such as breads, grains or starchy vegetables. 1/4 is meat, fish or poultry or meat substitute. Milk and fruit complete the meal. Fill Your Plate for Healthy Eating

Hints for Weight Loss Success : 

Hints for Weight Loss Success Follow a reduced calorie, low-fat diet Exercise at least 30 minutes most days Keep a record of what and how much is eaten Eat breakfast every day Check weight weekly Food and exercise habits of successful weight losers:

Medicinal Therapy : 

Medicinal Therapy Various available options Oral hypoglycemic agents Insulin and its analogues GLP analogues

2008 ADA Recommendations for glycemic control in T2DM : 

2008 ADA Recommendations for glycemic control in T2DM HbA1C <6.5-7 % Preprandial blood glucose 70 –100 mg/dl Postprandial blood glucose <140 mg/dl

2008 Recommendations for BP Targets in T2DM : 

2008 Recommendations for BP Targets in T2DM Without nephropathy <130/85 mmHg With nephropathy <120/80 mmHg As low as 115/75 mmHg is associated with Decreased cardiovascular mortality

2008 ADA Lipid targets in T2DM : 

2008 ADA Lipid targets in T2DM LDL Cholesterol <100 <70 (in pts with CAD) HDL Cholesterol >40 (women) >50 (men) Triglycerides <150

Target Practice : 

Target Practice Our patient FBG 155 PPBG 268 HbA1c 8.9 BP 160/106 LDL 160 HDL 30 TG 180 ADA goals FBG 70-100 mg/dl PPBG < 140 mg/dl HbA1c < 6.5 – 7 % BP < 120/80 mmHg LDL < 100 HDL > 50 TG < 150

Treatment of CVRFs : 

Treatment of CVRFs Being a diabetic with micro-albuminuria and HT with LVH and hyperlipidemia the 2 drugs that I would want to start would include an ACE inhibitor and a hypo-lipidemic agent. He would require additional testing such as 2DECHO and a stress test. The ACE inhibitor is the drug of choice in diabetic micro-albuminuria with or without HT and LVH. Besides their other benefits include reduction of cardio and cerebro vascular risk and a neutral metabolic profile

Slide 40: 

Do we offer our patient insulin or its analogues ?

Insulin therapy - Indications : 

Insulin therapy - Indications Type 1 Diabetes Mellitus Diabetic ketoacidosis

Insulin therapy - Indications : 

Insulin therapy - Indications Lactic acidosis Hyperosmolar non ketotic coma

Insulin therapy – T2DM : 

Insulin therapy – T2DM Primary OHA failure Uncontrolled sugars inspite of use of multiple oral agents ( secondary OHA failure) Very high blood sugar at outset Willing patient

Insulin therapy – Indications in T2DM : 

Insulin therapy – Indications in T2DM Trauma, stress, surgery, burns, sepsis, infections , acute coronary syndrome, pancreatitis, etc Hepatic or renal disease Chronic infections like TB Use of steroids,immunosuppressants

What are the problems associated with insulin therapy? : 

What are the problems associated with insulin therapy? Weight gain is usual as glycosuria is reduced Hypoglycaemia will occur in some people – education is needed Failure of dose titration to get adequate glucose control Worsening of control as islet β-cell failure progresses These risks can be minimized by use of insulin analogues in those with problems using basal insulin only when starting at lower HbA1c appropriate education on eating and physical activity active and continuing support for dose titration intensification of insulin regimens over following years

Other problems with insulin therapy : 

Other problems with insulin therapy Insulin allergy Lipoatrophy Insulin edema ? malignancy

Barriers to Insulin Therapy : 

Barriers to Insulin Therapy 1. Psychological insulin resistance, both from patient & treating doctor. Patients. “Once on insulin I will get addicted to it” “Insulin is the last tool to use” “Insulin means frequent hypos” “No doctor… give me 1 more month, I will show you !!!” Doctors. “Insulin has many side-effects”… even bone thinning!!! “If you do not show good control, next time I will put you on Insulin”… A punishment to the patient & guilt

Barriers to Insulin therapy … con’td : 

Barriers to Insulin therapy … con’td 2. Cost 3. Pain and Needle phobia 4. Inconvenience 5. Non realization of the seriousness of the consequences of Diabetes 6. Fear of Weight gain 7. Need to monitor blood glucose more frequently

Slide 50: 

Do we offer him oral hypoglycemic agents ?

Ideal Oral hypoglycemic Agent : 

Ideal Oral hypoglycemic Agent Corrects hyperglycemia & prevents microvascular complications. Improves known CVRFs & prevents macrovascular complications.

Increasing Insulin SecretionSulfonylureas : 

Increasing Insulin SecretionSulfonylureas First generation- chlorpropamide, tolbutamide second generation- gliburide,gliclazide,glibenclamide,glipizide; Third generation-glimiperide. Generally long-acting and stimulate insulin secretion Reduce PPG greater than FPG & HbA1C reduction of 1.5 to 2 %. Side effects are hypoglycemia & wt gain

Insulin Sensitising Agents : 

Insulin Sensitising Agents Metformin Thiazolidinediones

Metformin prescribing considerations : 

Metformin prescribing considerations Contraindicated in Renal dysfunction –s.creat >1.5 or abnormal creat clearance Use of imaging contrast dyes CHF requiring medicines Metabolic acidosis Unstable acute medical conditions like shock, infective and non infective diseases. Hypersensitivity to metformin

TZDs:Effects on CVRFs : 

TZDs:Effects on CVRFs Lipids: decrease TGs increase HDL decrease small dense LDL reduce LDL oxidation Coagulation & fibrinolysis:dec PAI-1 dec fibrinogen Vasc endothelial dysfunc:dec intima media thickness vasodilation inflammation(CRP) Anti-inflammatory

Primary Endpoint : 

Primary Endpoint All cause mortality Non-fatal MI(including silent MI) Acute coronary syndrome Cardiac intervention(CABG/PTCA) Major leg amputation(above ankle) Leg revascularisation

Slide 85: 

In our patient both fasting and post prandial sugars are elevated. A good approach would be to reduce the fasting sugar with metformin which would reduce the HGO and improve the post prandial sugar too. Moreover, the use of metformin in this patient would improve the insulin sensitivity and also cause weight loss with no hypos.He would gain benefit of favourable alteration in lipid profile. On the other hand addition of Pioglit would result in unnecessary weight gain.

Slide 86: 

As the patient is young and obese and is a recently detected diabetic, it would be preferable to avoid SU considering their property to accelerate beta cell failure (5 % experience 2o failure) no cardiovascular benefit, weight gain and repeated hypos. Another good choice would be the addition of an alpha glucosidase inhibitor especially if the post prandial sugar remains elevated inspite of therapy with metformin.

Role of AGIs : 

Role of AGIs These drugs are a good choice for post prandial sugar control. They act by competitive inhibition of the disaccharidases and pancreatic amylase and hence delay intestinal absorption of carbohydrates. They would then best work if the patient is on a high CHO diet.

Slide 88: 

Alpha- Glucosidase Inhibitors ! Efficacy ! decreases PPG by 40-60 mg/dl ! decreases FBG by 10-20 mg/dl ! decreases HbA1c by 0.5-1.0% in patients treated with diet, sulfonylureas or metformin ! Adverse Effects ! Most common within first 8 weeks of treatment ! flatulence ! diarrhea ! Abdominal cramping or discomfort

Benefits of AGIs : 

Benefits of AGIs Are not dependant on the presence of beta cell function for their glucose lowering effect and hence may be used even late in the course of the disease. They have been shown not only to reduce the PPG but also reduce the flux of post-prandial lipid surge which has been co-related to an increase in the risk of CV events.

AGI – Conditions apply : 

AGI – Conditions apply Monitoring of liver functions is advisable as AGIs are associated with hepatic side effects and hence are not to be used in those with liver disease and cirrhosis. They should be discontinued in renal failure when the creatinine is 2 mg/dl or more. A watch for LV function deterioration in patients with congestive heart failure is warranted.

Slide 92: 

FBS, PPBS and HbA1c responses to OHAs in T2DM AACE Diabetes Guidelines FBS PP HBA1c Metformin 53 - 1.4% AGIs 20-30 20-74 0.5-1 Pioglitazone 20-55 - 0.3-0.9% Rosiglitazone 25-55 - 0.1-0.7% Glinides 30.3 56.5 1.1% Sulfonylureas 40-60 - 1.0-2.0%

OHAs and renal failure : 

OHAs and renal failure The Safe OHAs include Gliclazide, glipizide, rosi, pio, repaglinide and exanetide. Do not use other SUs. Metformin may be continued upto creat 1.5, after which it should not be used. Acarbose, miglitol, nateglinide upto creat 2 – use The doses of Gliptins, pramlinitide, glimiperide should be adjusted when eGFR is <25-50ml/min

Which drug to use and when ? : 

Which drug to use and when ? Elderly Obese FBS reduction PPBS reduction Cardiac failure IHD Hepatic failure Metformin Metformin, gliptins, AGI Metformin, gliptin,TZD SU, TZD, AGIs, gliptin Avoid TZD,SU,metformin Avoid TZD, SU, metformin Avoid SU, TZD, metformin, gliptin, AGI

Slide 102: 

Clinical assessment and initiation of nutrition and physical activity Mild to moderate hyperglycemia (A1C <9.0%) Overweight (BMI 25 kg/m2) Non-overweight (BMI 25 kg/m2) Biguanide alone or in combination with 1 of: insulin sensitizer* insulin secretagogue insulin alpha-glucosidase inhibitor 1 or 2† antihyperglycemic agents from different classes biguanide insulin sensitizer* insulin secretagogue insulin alpha-glucosidase inhibitor Add a drug from a different class or Use insulin alone or in combination with: biguanide insulin secretagogue insulin sensitizer* alpha-glucosidase inhibitor Marked hyperglycemia (A1C 9.0%) 2 antihyperglycemic agents from different classes † biguanide insulin sensitizer* insulin secretagogue insulin alpha-glucosidase inhibitor Basal and/or preprandial insulin Add an oral antihyperglycemic agent from a different class of insulin* Intensify insulin regimen or add biguanide insulin secretagogue** insulin sensitizer* alpha-glucosidase inhibitor L I F E S T Y L E Timely adjustments to and/or additions of oral antihyperglycemic agents and/or insulin should be made to attain target A1C within 6 to 12 months

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