1. Management Type 2 DM
Adam Ibrahim
MBBS.

2. Remember the Big Picture
 Manage DM in the context of reducing MI
and CVA
 Don’t forget other comorbidities
 HTN -- goal BP 130/80 or less
 Dyslipidemia – goal LDL 70-100

Obesity – Goal wt. loss 2 kg/month
 Remember blood glucose as one risk factor
among many contributing to microvascular
and macrovascular disease
 Goal HgA1c < 7.0

3. Management Impaired
Glucose Tolerance
 Diabetes Prevention Trial
 NIH sponsored 5 year study completed
2003
 Designed to test strategies for reducing
progression of IGT to DM

Oral agent – metformin
 Lifestyle modification
 Placebo

4. Diabetes Prevention Trial
 Lifestyle Intervention group
 Achieve and maintain 7% wt. loss
 150 minutes exercise per week
 Diet and exercise education
 16 one on one sessions
 Monthly group sessions

5. Metformin Group
 Metformin 850 mg QD X 1 month, then
BID
 Lifestyle recommendations
 20-30 session with handouts
 Food Pyramid
 Encourage “more exercise”

6. Placebo
 Placebo QD X1 month, then BID
 Lifestyle recommendations

7. Results
 Metformin reduced progression by 31%
 Intensive Lifestyle Modification reduced
progression by 58%
 Weight loss
 Placebo 0.1 kg
 Metformin 2.1 kg
 Lifestyle 5.6 kg

8. Management IGT
 Educate patient as much as possible of the
benefits of intensive lifestyle modification
 Exercise 150 min/wk
 Low calorie, low fat diet
 Goal weight loss at leas 7%
 May consider metformin if high clinical
suspicion that pt will develop DM
 Monitor glucose tolerance at least yearly to
catch DM early

9. Therapy For DM Type 2
Treatment 1999-2000
Diet Only 20.2
Insulin Only 16.4
Oral Agents Only 52.5
Orals and Insulin 11.0

10. Oral Medications
 Biguinides (metformin, glucophage)
 Primarily reduce hepatic glucose production
 Also sensitize tissues to insulin
 Average change in FBS 60-70, HgA1c 1.0 -2.0
 Causes modest weight loss
 Best evidence at preventing macrovascular
complications
 No hypoglycemia
 FIRST CHOICE if renal function ok
 GI side effects
 Hold if creatinine >1.5

11.  Sulfonylureas (glibenclimide, glyburide,
chlorpropramide)
 Primarily function to stimulate the pancreas
to produce more insulin
 Change in FBS 60-70, HgA1c 1.0-2.0
 Readily available
 Inexpensive
 Can cause hypoglycemia, mild weight gain
 Choose short-acting over long-acting

12.  Thiazolidinediones (rosiglitazone,
pioglitazone)
 Primarily sensitize tissues to insulin
 Reduce hepatic glucose production
 Reduce FBS 35-40, HgbA1c 0.5-1
 6 weeks to see maximum effects
 Caution in CHF – contraindicated class III or IV
 May cause edema
 Can potentiate hypoglycemia if taken with insulin
or sulfonylureas
 Expensive

13.  Meglitinides (repaglinide, nateglinide)
 Stimulate insulin release in the presence of
glucose
 Reduces post-prandial glucose
 Alpha-glucosidase inhibitors (acarbose)
 Block enzymes that dissolve starches in
the small intestine

14. New Medicines
 Sitagliptin (Januvia)
 Causes more insulin to be secreted in
response to eating
 Less hypoglycemia
 Byetta (exanatide)
 Incretin mimetic – increased insulin
production related to glucose load
 Twice a day injection
 More for weight loss

16. Insulin Therapy
 Most Type 2 diabetics will eventually
have reduced insulin production
 If patient is not well controlled on 2 or
more oral agents, should consider
starting insulin
 Nearly all Type 2 diabetics will
eventually require insulin

17. Insulin Therapy
 If available, consider long acting
(glargine) insulin at bedtime or at AM
 Consider NPH if glargine not available
 Start with low dose (10 units glargine, 5
units NPH) and slowly increase as
tolerated
 May need to reduce or discontinue
some orals (sulfonylureas, TZD)

18. Summary Treatment Goals
 Reduce microvascular and
macrovascular complications
 Glucose goal HgbA1c <7.0
 Fasting glucose 90-130
 Post-prandial glucose 140-180
 BP <130/80
 LDL < 100 (close to 70)
 TG < 250
 HDL >40 men, >50 women

19.  Look for a reason to add an ACE
inhibitor
 Reduces diabetic nephropathy
 Look for a reason to add a statin
 Lowers cardiovascular and all cause
mortality

20. Summary of Treatment
Diagnosis
Lifestyle Modification
Oral Monotherapy
Oral Combination Therapy
Combination Oral and Insulin

21. Case
 Ahmed is a 54 yr old Somali male who comes
to see you complaining of fatigue and
increased thirst. What other history would
you like to ask?
 Past medical hx – HTN, CVD, dyslipidemia, AAA
 Family history – CAD, CVD, DM
 Smoking history
 Activity history
 Symptoms – polyuria, wt loss, wt gain, blurry
vision

22.  Ahmed also has HTN and is taking a-
methylopa. BP is 140/90. Lipids unkown.
He complains of blurry vision. His father died
of MI at age 55. What physical exam would
you like to focus on?
 Dilated retinal exam – microaneurysms, blot
hemorrhages, hard-exudates, cotton-wool spots
(retinal infarcts), A-V knicking
 Monofilament exam
 Heart and lungs

23.  Exam reveals decreased sensation with
monofilament exam, A-V knicking, and one
cotton wool spot. What lab would you like to
order next?
 RBS
 OGTT
 Creatinine
 Lipids (if available)
 Glycosylated hemoglobin

24.  RBS is 190.
 OGTT reveals fasting glucose 132, 2 hour
glucose 210 – HgbA1c 8.7
 Creatinine 1.3
 LDL 158
 How would you like to manage the patient
next?
 Metformin
 Enalapril
 Lovastatin

25.  When would you like to see the patient
back?
 What would you like the patient to bring
with him if possible?
 Diet log
 Glucose log
 BP log
 What labs would you like to check?
 RBS
 Creatinine

26.  RBS is 155, creatinine is 1.3, BP is 130/80
 When would you like to see him back?
 What labs would you like to order?
 RBS
 Creatinine
 SGOT
 Lipids
 Glycosylated hemoglobin