GO! Diabetes Program

1
GO! DiabetesProgram
2
Goals For Today

• Review evidence based guidelines and equip you to
  deliver state of the art care to your diabetic
  patients
• Understand tools that support practice
  performance and improvement
• Review oral and injectable medicines
  hypoglycemics
• Review multifaceted approach to cardiovascular
  disease protection

3
Effect of Tighter Glycemic Control on Progression
of Retinopathy DCCT
4
Effect of Intense Glycemic Control on Nephropathy
from DCCT
5
United Kingdom Prospective Diabetes Study

• Study summary 10 years
• Type 2 diabetics convention vs. intense control
• Glycemic control 7.0 vs. 7.9
• Hypertension control 144/82 vs. 154/87
• Glycemic control
• metformin, sulfonylureas, and insulin
• Hypertension
• captopril, atenolol

6
UKPDS Blood Pressure StudyTight vs. Less Tight
Control

• 1148 type 2 patients
• BP lowered to avg. 144/82 (controls-154/87) 9 yr
  follow-up
• Endpoint Risk Reduction() P Value______
• Any diabetes related endpoint 24 0.0046
• Diabetes related deaths 32 0.019
• Heart failure 56 0.0043
• Stroke 44 0.013
• Myocardial infarction 21 NS
• Microvascular disease 37 0.0092

UKPDS. BMJ. 317 703-713. 1998.
7
Glycemic Control Reduces Complications
DCCT UKPDS
HbA1C 9 7.2 8 7
Retinopathy 63 17 to 21
Nephropathy 54 24 to 33
Neuropathy 60 -
Cardiovascular Disease 41 16
Diabetes Control and Complications Trial (DCCT)
Research Group. N Engl J Med 1893329977-988 UK
Prospective Diabetes Study (UKPDS) Group. Lancet
1993 352837-853.
8
ABCs Of Diabetes Management
Glycemic control
A1C lt7.0
Preprandial plasma glucose 90-130 mg/dL
Postprandial plasma glucose lt180 mg/dL
Blood pressure lt130/80 mmHg
Lipids
LDL-cholesterol lt100 mm/dL
Triglycerides lt150 mm/dL
HDL gt40 mm/dL
Antiplatelet therapy Everyone over 40
Smoking cessation Universal
Diabetes Care 200932S6-12
9
Control of CV Risk Factors in Diabetic
Hypertensive Patients in Academic Medical Centers

• 27

• A1C lt7

• 36

• LDL lt100

• 27

• BP lt130/85 mmHg

• 46

• Daily Aspirin (ASA) Use

• 3

• BP, Lipids and A1C

• 2

• BP, Lipids, A1C ASA

McFarlane SI. Diabetes Care 200225718
10
Type 1 Vs Type 2How To Tell Them Apart
Type 1 Type 2
Treatment Always insulin 4 shots Pills ? Insulin
Age at Onset 10 of adults w/ new dx 50 of children w/ new dx
Weight 20 obese 10 thin
Family History 10 w/ a close relative gt50 w/ a close relative
DKA Can happen Can happen
Blood Glucose More variable big hypos More stable milder hypos
Thyroid Disease Often Sometimes
Antibodies Usually (Anti-GAD) Not usually
C-peptide Early low nl Late 0 Early high nl Late low nl
11
Diabetes Early Detection and Lifestyle Monitoring
12
Metabolic Syndrome

• Requires 3 or more
• Triglycerides gt 150
• HDL lt 40
• Waist size gt40 men, gt35 women
• BP gt 130/85
• Fasting glucose gt 100
• Caveat Treatment counts for requirements

(Grundy, Circulation, 2005)
13
Pre-Diabetes Definition
If FBG gt100 there is a 10-15 risk of DM within 7
years
or
Fasting
GTT
14
Who and When to Screen?

• Starting at age 45, a fasting blood glucose every
  three years
• More frequent screening if

• Family history
• Overweight (BMI 25)
• Dyslipidemia
• HTN

• High risk ethnicity
• Vascular disease
• Prior glucose elevation
• Hx or exam findings

15
Role of Obesity in Diabetes

• Obesity (specifically abdominal) has one of the
  highest associations with insulin resistance and
  glucose intolerance
• Numerous studies have tied weight loss to
  diabetes prevention
• A 5-10 weight loss yields a 58 reduction in the
  incidence of diabetes!
• At the end of four years
• Diet and exercise regimens average a 4kg loss
  after two years
• Advice alone results in a 1kg gain

(Franz, Journal Amer. Diabetes Assoc, 2007)
16
Quantifying Obesity

• Easiest is by waist circumferences.
• 40 males, 35 females
• Some variation by ethnicity (35 and 31 for
  Asians)
• Measured across iliac crest in the back and the
  umbilicus in the front

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Healthcare Maintenance

• Latest ADA guidelines (2009)
• Lab surveillance
• Diabetic education
• Vaccinations/routine healthcare
• Smoking cessation
• Foot exams
• Eye exams

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Reasons to Look at Feet

• Up to 70 of diabetics eventually develop a
  neuropathy
• Up to 25 develop foot ulcers
• Diabetes doubles your risk of LE disease
  (vascular, neuro, skin)
• More than half of the foot ulcers become infected
  at some point

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Foot Surveillance

• Examine the feet at every visit
• Annual comprehensive evaluation
• Sensation
• Pulses
• Skin condition (ulcers, hair, nails)
• Anatomic deformities
• Shoe evaluation

20
Sensory Exam

• 10-gram monofilament
• Patient should not watch
• Five sites per foot
• Apply filament perpendicular to skin
• Allow slight buckle of filament in one motion
• Each site should take 1-2 sec
• Do not apply to ulcers or calluses

21
Eye Care

• Diabetic retinopathy is the leading preventable
  cause of blindness
• Prevalence of DR increases with duration of
  diabetes (100 Type 1, 60 Type 2 after 20 years)
• Of all recommendations, eye screening is the
  least likely to get done

22
Pathogenesis

• Increased circulating glucose leads to weakness
  of capillary walls
• Microaneurysms and leakage occurs causing
  eventual infarction of the nerve fiber layers
  (cotton wool spots)
• The localized hypoxia then leads to
  vasoproliferation
• Extension into the vitrea (/- hemorrhage) leads
  to fibrosis and vision loss

23
Diabetic Retinopathy
Normal Retina (left) contrasted with
Proliferative Diabetic Retinopathy (right) Refer
patients for ophthalmologist evaluation
24
Glycemic Control Oral Agents
25
General RulesHypoglycemic Therapy

• Normalize fasting glucose levels first (90-130
  mg/dl)
• Many patients will achieve A1C lt 7
• When to target postprandial glucose levels?
• Fasting and preprandial values are at goal
• A1C levels are not met
• Measure 1-2 hours after beginning of the meal
• Glucose are generally at their peak

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Glycemic Goals of Therapy
Verbal Target 100 ltlt200 As low as possible
w/o unacceptable adverse effects
Goal Premeal plasma glucose (mg/dL) 2-h
postprandial plasma glucose A1C
ADA 90-130 lt180 lt7

Evaluation and treatment of postprandial
glucose may be useful in the setting of suspected
postprandial hyperglycemia, with the use of
agents targeting postprandial hyperglycemia and
for suspected hypoglycemia More stringent
glycemic goals (i.e. a normal A1C, lt6) may
further reduce complications at the cost of
increased risk of hypoglycemia
Diabetes Care 200932S6-12
27
Biguanides Metformin

• Mechanism of action
• Reduces hepatic glucose production
• Depends upon presence of insulin
• Safety and efficacy
• Decreases A1C 1-2
• Adverse effects diarrhea and nausea main risk
  lactic acidosis
• Discontinuation rate 5
• Contraindications renal, cardiac, hepatic
  insufficiency IV contrast
• No direct effect on kidney
• Dosing
• Initial dose 500 mg once a day dosing usually
  BID
• Maximum effective dose 2,000 mg per day
• Titration frequency week(s) to months
• Alternate formulations XR and combinations

28
Metformin Outperformed Other Meds in Obese
Patients (UKPDS)
Lancet 1998 Sep 12352(9131)854-65.
29
Insulin Secretagogues Sulfonylureas (SFU) and
Glinides

• Mechanism of action
• Stimulate basal and postprandial insulin
  secretion
• Require functioning beta cells (no effect on beta
  cell dysfunction)
• Work quickly
• Safety and efficacy
• Decrease A1C approximately 1-2
• Lower fasting glucose 20
• Adverse events weight gain, allergy (rare)
  main risk, hypoglycemia
• Dosing
• Initial dose 1/8 to 1/4 maximum dose dosing
  1-2 times/day (SFU), 3 times/day (glinides)
• Maximum effective dose 1/2 maximum(full dose
  with nateglinide)
• Titration frequency day(s) to weeks

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Preferred Sulfonylureas

• All available as generic agents
• Glipizide ER 5-20 mg once per day
• Once daily, flat profile, low plasma levels
  resulting in a low risk of weight gain and
  hypoglycemia
• Glipizide 2.5 to 20 mg twice a day
• Twice daily. Half-life 2-4 hours, peaks in 2-3
  hours. By taking it once a day at low dose it
  stimulates insulin secretion for 6-12 hours
• Glimepiride 1-8 mg per day
• Once daily. Half-life 9 hours, peak action for 4
  hours. Special utility like with glipizide but
  with longer half-life

Buse J. Personal Opinion Melander A. Diabetes
200453 Suppl 3S151
31
Thiazolidinediones (TZDs or Glitazones)
Pioglitazone and Rosiglitazone

• Mechanism of action
• Enhance insulin sensitivity in muscle, adipose
  tissue
• Inhibit hepatic gluconeogenesis
• Reduced rate of beta cell dysfunction
• Safety and efficacy
• Decrease A1C 1-2
• Adverse events edema, weight gain, anemia rare
  serious risk liver failure
• Dosing
• Initial dose (monotherapy) 1/2 to 2/3 maximum
  dosing,1-2 x/day
• Maximum effective dose maximum dose
• Titration frequency weeks to month(s)

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Oral Hypoglycemics TZD Lipid Effects

• Rosiglitazone (Avandia)
• LDL
• HDL
• Triglycerides

• Pioglitazone (Actos)
• LDL
• HDL
• -Triglycerides

• Rosiglitazone Black box warning for CHF and
  ischemic heart disease warnings about increased
  fracture risk in women
• Pioglitzaone Black box warning for CHF and
  warning about increase fracture risk. No
  evidence to suggest increased ischemic heart
  disease.

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AHA/ADA Consensus Statement for TZDs

• Not recommended for patients with NY Heart
  Association class III or IV heart failure
• TZDs alone, or particularly in combination with
  insulin, may cause fluid retention which can lead
  to heart failure
• Incidence of CHF lt1 with TZD monotherapy
• Increased to 2-3 in combination with insulin
• Patients should be observed for signs and
  symptoms of heart failure
• TZDs should be discontinued if any deterioration
  in cardiac status occurs

Nesto RW et al. Diabetes Care 200427256
34
Alpha-Glucosidase Inhibitors Acarbose And
Miglitol

• Mechanism of action
• Delay absorption of carbohydrates
• Depend upon postprandial hyperglycemia
• Safety and efficacy
• Decrease A1C 0.5-1
• Adverse events flatulence main risk rare
  liver enzyme elevation
• Dosing
• Initial dose 1/4 maximum once daily dosing 3
  times daily
• Maximum effective dose 1/2 maximum dose
• Titration frequency week(s) to months
• Used infrequently by most clinicians

35
INCRETINSRole of Glucagon Like Peptide (GLP-1)
in Glucose Homeostasis
Deficiency Type 2 DM//-type 1
Site of synthesis Small intestine
Glucose dependent stimulation of insulin secretion Yes
Slow gastric emptying Yes
Reduce inappropriate glucagon secretion Yes
Weight loss Yes (exenatide)
Beta cell proliferation/regeneration Yes
Therapies Exenatide (Byetta) Sitagliptin (Januvia)
Target population Type 2 on oral agents
36
Incretin Drugs

• Exenatide (Byetta) GLP-1 analog
• Injection twice daily
• 5mcg bid AC x 1 month, then 10mcg bid AC
• Beneficial effects described previously
• Expensive
• Weight loss
• Reduction in HgBA1C
• Sitagliptin (Januvia) DPP4 inhibitor
• Technically not an incretin but similar effects
• Oral administration
• 100mg daily
• Weight neutral

37
Key Points to Consider for Therapy
Maximal benefits of metformin are observed at
the recommended daily dose of 2000 mg (1 g
BID)1 Thiazolidinediones should be started at low
doses and slowly increased to minimize side
effects2 Glucose-lowering effects of a
sulfonylurea plateau at half the maximum
recommended dose3

1. Garber AJ et al. Am J Med 1997103491
2. Nesto RW et al. Diabetes Care 200427256
3. Stenman S et al. Ann Intern Med 1993118169

38
Glycemic Control - Injected Therapies
39
63 Of Patients with DiabetesAre Not at ADA A1C
Goal lt7
Adults aged 20-74 years with previously diagnosed
diabetes who participated in the interview and
examination components of the National Health And
Nutrition Examination Survey (NHANES), 1999-2000
A1C
of Subjects n404
Saydah SH et al. JAMA 2004291335
40
Difficulties In AchievingTarget A1C Values

• Challenges
• Late diagnosis and initiation of therapy
• Therapeutic inertia
• Lack of effective lifestyle intervention
• Secondary failure
• Adverse events associated with antihyperglycemic
  therapies
• Complexity of care
• Role of postprandial glucose in failure

41
Common Concerns When Transitioning To Insulin

• Fear of needles or pain from injections
• Fear of hypoglycemia
• Weight gain

Funnel M. Self-management Support for Insulin
Therapy in Type 2 Diabetes. The Diabetes Educator
200430274
42
Common Concerns When Transitioning To Insulin

• Adverse impact on lifestyle inconvenient loss
  of personal freedom and independence
• Belief that insulin means diabetes is worse or
  more serious disease
• Insulin as a personal failure
• Insulin causes complications
• Treated differently by family members

Funnel M. Self-management support for insulin
therapy in type 2 diabetes. The Diabetes
Educator 200430274
43
Potential Insulin Regimens

• Insulin pump Physiologic/COMPLEX
  /Flexible
• Multiple daily injections
• Free mixing - twice daily
• Pre-mixed - twice daily
• Basal only SIMPLE/Inflexible

How do we balance simplicity and flexibility
to achieve glycemic control?
44
Indications for Insulin

• Not contraindicated at anytime
• Consider as initial therapy
• HgbA1C gt 10
• Fasting glucose gt 250mg/dl
• Random glucose gt 300
• Recommended as initial therapy
• Polyuria, polydipsia, weight loss, ketones

45
Insulin InitiationAnswers to Provider Concerns

• Normalize the fasting glucose
• Fasting FSBS 70-130
• Once Daily Options
• Start 10 units or 0.2 u/kg
• Basal Insulin (glargine or detemir)
• NPH (bedtime)
• Premixed before dinner
• Increase 2-3 units every 3 days prn to reach
  target of 70-130 fasting
• Decrease 3 units for fasting lt 70

46
Once Daily Insulin OptionsBasals vs. NPH vs.
Premixed
INSULIN TYPE ADVANTAGES DISADVANTAGES
Glargine Peakless, less hypoglycemia, less wt gain simple Cost cant mix no meal time coverage
Detemir Less wt gain, less hypoglycemia simple Cost, shorter duration than glargine cant mix, basal only
Pre Mixed 70/30 or 75/25 Covers meal time and basal easy transition to bid More hypoglycemia and weight gain than basals
NPH Less expensive More hypoglycemia than basals
47
Insulin ActionEffect Of Various Formulations
140
120
100
Short (Regular)
Insulin Level (?U/ml)
80
Intermediate (NPH)
60
40
Detimir
20
0
0
2
4
8
10
12
14
16
6
Hours
48
Fasting Glucose at TargetHgbA1C Not at Goal

• Must Normalize Post Prandial Glucose
• Options
• Change HS NPH to BID NPH
• Change Pre-mixed Insulin from QD to BID
• Add Mealtime Insulin to Basal Insulins

49
Monomeric Insulin Analogs

• How to switch or start
• Insulin immediately before the meal (or after)
• Review signs, symptoms and management of
  hypoglycemia
• Safety
• Arguably, glulisine, aspart, lispro and are safer
  than regular human insulin
• Patient preference
• Significant patient preference for monomeric
  analog versus regular human insulin
• Duration of action
• Covers postprandial glucose surge well
• In type 1 diabetes, will need an additional
  injection of basal or NPH

50
Carbohydrate Counting

• Technique based on the concept that most
  meal-related glucose increase is due to the
  carbohydrate content
• Patients count either
• Carbohydrate choices (milk, fruit, breads,
  sweets, starchy vegetables)
• Grams of total carbohydrates on food label
• Providers prescribe insulin-to-carbohydrate ratio
• Start with 1 unit per choice or 1 unit per 15
  grams
• Typical dose is 2-4 units per choice in type 2
  diabetes
• Titrate based on postprandial glucose monitoring
• Generally, start with glulisine/lispro/aspart
  administered just after meals

51
Mixed-Analog Insulin BID

• Starting dose in most
• Pre-breakfast 10 units
• Pre-supper 10 units
• Titration, once or twice a week (self-adjusted or
  with supervision)
• Alternatively, could just increase at both
  breakfast and supper in parallel

If most values over the last 3 days fall in the range Adjust dose by
80 mg/dL -2 units
80-109 mg/dL no change
110-139 mg/dL 2 units
140-179 mg/dL 4 units
180 mg/dL 6 units
Buse JB et al. Clinical Diabetes 20052378
52
Pre-Mixed Insulin BID Compared to Basal Alone
INITIATE Study

• 
  Aspart 70/30 bid Glargine qhs
• Minor hypoglycemia 43 16
• Median rate per pt per mo 0.3
  0.2
• Severe hypoglycemia None 1 episode
• Weight gain (Kg) 5.4 ?4.8 3.5 ?4.5
• Total daily insulin (u/Kg) 0.82 ?0.40
  0.55 ?0.27

Raskin P et al. Diabetes Care 200528260
53
Oral Meds What to Do When Insulin Started
(General Rules)

• Metformin
• Continue unless contraindicated
• Sulfonylureas
• Continue with basals generally
• Stop if using large doses of insulin
• Stop if using premixed insulin
• TZDs
• Proceed with caution
• Exacerbates weight gain and edema

54
Non Insulin Injectables
55
General Prescribing ConsiderationsDosing
Stable Dose
10 mcg BID
Stable Dose
5 mcg BID
?1 Mo
Initiation
Indicated for use in patients failing metformin
or sulfonylurea Generally reduce SFU dose to
smallest tablet to minimize risk of
hypoglycemia No dosage adjustments based on meal
size or physical activity No additional glucose
monitoring required
Exenatide Prescribing Information. 2005
56
Glargine Vs Exenatidein Patients Failing Oral
Therapies
ITT patient sample Mean SE shown plt0.0001,
exenatide vs insulin glargine at same time point
Heine RJ et al. Ann Intern Med 2005143(8)559
57
Treatment Algorithm - Glucose
Diagnosis by screening or with symptoms
58
Causes of Hypoglycemia

• Incorrect amount of insulin/oral agents
• Skipped or delayed meal/snack
• Carbohydrate intake less than normal
• Alcohol intake without food
• Exercise without insulin/food adjustment
• Not re-testing 1 to 2 hours after hypoglycemia
  treatment if meal or snack is not eaten

59
Treatment of Hypoglycemia

• Definition of hypoglycemia Plasma glucose lt70
  mg/dL
• Symptoms may or may not be present
• Sweaty, cold, unable to concentrate, dizzy
• Treatment
• Treat with 15 g carbohydrate wait 15 minutes
  test BG, if BG not gt70 mg/dL, treat again
• All carbohydrates raise blood glucose
• On average, 15 g of glucose can increase BG from
  60 to 110 mg/dL (50mg/dL) over 40 minutes
• BG starts to fall at 60 minutes and reaches
  previous treatment level at 2 hours

Cryer et al. Diabetes Care 2003261902
60
Treatment of Severe Hypoglycemia

• Definition Requires assistance to treat
• Inject glucagon with loss of consciousness or
  seizure
• Administered by another person
• May be given intramuscular or subcutaneous
• Standard dose
• 1.0 mg for adults 0.5 mg for children under 5
  yrs
• Prescription is required
• Precautions
• May cause nausea/vomiting/headache
• Call 911

61
Cardiovascular Disease PreventionBlood
Pressure, Dyslipidemia, Antiplatelet Therapy
62
Diabetes and Hypertension Key Questions

• Why should we pay so much attention?
• What parameters?
• Non Drug Recommendations
• Which drugs and how many?
• What do others besides the ADA say?
• What about resistant cases?

63
Diabetes and HypertensionWhy?

• Volume Expansion
• Increased insulin levels
• Higher sympathetic activity
• Increased glucose level
• Increased sodium resorption with hyperglycemia
• Decreased arterial compliance
• Obesity

64
UKPDS Blood Pressure StudyTight vs. Less Tight
Control

• 1148 type 2 patients
• BP lowered to avg. 144/82 (controls-154/87) 9 yr
  follow-up
• Endpoint Risk Reduction() P Value
• Any diabetes related endpoint 24
  0.0046
• Diabetes related deaths 32 0.019
• Heart failure 56 0.0043
• Stroke 44 0.013
• Myocardial infarction 21 NS
• Microvascular disease 37 0.0092

UKPDS. BMJ. 317 703-713. 1998.
65
Diabetes Treatment Goalsfor Blood Pressure

• Control blood pressure
• 130/80 mmHg for most patients
• 125/75 mmHg for patients who have proteinuriagt1
  g/day and renal insufficiency
• Reduce the risk of end-organ failure
• Reduce the risk of cardiovascular events
• Myocardial infarction
• Cardiovascular death
• Delay or prevent the progression to heart failure

JNC 7 Report. JAMA 20032892560 Bakris GL et
al. Am J Kidney Dis 200036646 ADA. Diabetes
Care 200730(suppl 1)S15
66
Number of Medications to Achieve Goal BP In 5
Trials of DM and/or Renal Disease
UKPDS (lt150/85 mmHg)
2.7
ABCD (lt75 mmHg DBP)
2.8
MDRD (lt92 mmHg MAP)
3.6
HOT (lt80 mmHg DBP)
3.3
AASK (lt92 mmHg MAP)
3.8
0
1
2
3
4
Number Of BP Meds
Bakris. J Clin Hypertens 19991141
67
NKF Recommendations On TreatmentOf Hypertension
And Diabetes

• Blood pressure goal 130/80 mmHg
• BP-lowering medications should reduce both BP
  proteinuria
• Lower goal has been recommended to reduce renal
  disease progression and incidence of ischemic
  heart disease
• Antihypertensive drug classes shown to reduce
  proteinuria and cardiovascular events
• ACE inhibitors
• ?-?-blocker (carvedilol)
• ?-blockers
• CCBs
• Diuretics

Bakris GL et al. Am J Kidney Dis 200036646
68
UKPDS ACE Inhibitor Vs ?-Blocker Aggregate
Clinical Endpoints
Relative Risk 95 CI
0.5
1
2
P
RR
Any diabetes-related endpoint
1.10
0.43
Diabetes-related deaths
1.27
0.28
1.14
All-cause mortality
0.44
1.20
Myocardial infarction
0.35
1.29
Microvascular disease
0.30
1.12
Stroke
0.74
FavorsACE Inhibitor
Favors?-Blocker
UKPDS Group. BMJ 1998317713
69
Which Class Of Agents Should Be Added Second-Line?

• Thiazide diuretics
• Complementary mechanism to ACEs or ARBs
• ALLHAT showed benefit
• Particularly effective in African American
  patients
• BUT slightly higher deterioration of glucose
  metabolism
• Beta blockers
• Good evidence of benefit particularly for those
  with coronary heart disease or congestive heart
  failure
• BUT mechanism of action may not complement ACEs
  or ARBs

70
Additional BP Recommendations

• Lower blood pressure gradually in the elderly
• If unable to achieve goal, dont hesitate to
  discuss with peers
• Check for orthostasis in some patients when
  clinically indicated
• If angiotensin modifying drugs or diuretics are
  used, monitor renal function and potassium
• Use as many medicines as necessary to achieve
  blood pressure target
• 130/80 mmHg
• 125/75 mmHg if proteinuria is found
• Begin with an angiotensin modifying drug
• Add a thiazide in African American patients
• Add a Beta blocker in patients with heart disease

ADA. Diabetes Care 200730(Suppl1)16
71
Causes Of Resistant Hypertension

• Improper blood pressure measurement
• Excess sodium intake
• Inadequate diuretic therapy
• Medication
• Inadequate doses
• Drug actions and interactions (e.g. nonsteroidal
  anti-inflammatory drugs (NSAIDs), illicit drugs,
  sympathomimetics, oral contraceptives)
• Over-the-counter (OTC) drugs and herbal
  supplements
• Excess alcohol intake
• Identifiable causes of hypertension

72
StatinsPrimary And Secondary Prevention
25
20
With CVD Event
15
10
5
0
50
210
70
190
170
150
130
110
90
LDL-C (mg/dL)
Adapted from Illingworth. Med Clin North Am
20008423 and LaRosa. N Engl J Med 2005352
(e-pub) and Colhoun. Lancet 2004364685
73
ADA Standards 2009Dyslipidemia

• Fasting lipid profile annually
• Without overt CVD
• LDLlt100
• At age 40 start on statin regardless of LDL to
  reduce LDL 30-40
• With overt CVD
• Start statin to reduce LDL 30-40
• LDLlt70 is an option
• Normalizing triglycerides and raising HDL with
  fibrates reduces CV events

74
ADA Standards 2009Dyslipidemia

• High LDL, High triglycerides, Low HDL
• Consider statin fibric acid
• Remember the increased risk of rhabdomyolysis
• Consider statin niacin
• Remember niacin can increase glucose levels
• moderate doses mild changes in glycemia

75
Anti-platelet TherapyADA Standards

• Recommendations for Aspirin
• ASA 75-162 mg/day for 2o prevention
• ASA 75-162 mg/day for 1o prevention
• Age gt 40
• Any age with CV risk factors (htn,
  hyperlipidemia, renal disease, family history,
  smoking)
• Not recommended ages lt 21 (Reyes syndrome)
• Clopidogrel
• Very high risk diabetics intolerance to ASA

76
Practice Performance and Improvement
77
METRIC

• Metric stands for Measuring, Evaluating, and
  Translating Research Into Care.
• It is an innovative online practice improvement
  program where you will input records of 10
  diabetic patients prior to today and again within
  90 days.
• www.aafp.org/metric

78
Questions?