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Transcript of GO! Diabetes Program. Goals For Today Review evidence based guidelines and equip you to deliver...
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GO! DiabetesProgram
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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
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Effect of Tighter Glycemic Control on Progression of Retinopathy DCCT
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Effect of Intense Glycemic Control on Nephropathy from DCCT
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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
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UKPDS Blood Pressure Study:Tight 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 0.0046Diabetes related deaths 32 0.019Heart failure 56 0.0043Stroke 44 0.013Myocardial infarction 21 NSMicrovascular disease 37 0.0092
UKPDS. BMJ. 317: 703-713. 1998.
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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 1893:329:977-988
UK Prospective Diabetes Study (UKPDS) Group. Lancet 1993; 352:837-853.
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ABCs Of Diabetes Management
Glycemic control
A1C <7.0%
Preprandial plasma glucose
90-130 mg/dL
Postprandial plasma glucose
<180 mg/dL
Blood pressure <130/80 mmHg
Lipids
LDL-cholesterol <100 mm/dL
Triglycerides <150 mm/dL
HDL >40 mm/dL
Antiplatelet therapy Everyone over 40
Smoking cessation UniversalDiabetes Care 2009;32:S6-12
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Control of CV Risk Factors in Diabetic Hypertensive Patients in Academic
Medical Centers
McFarlane SI. Diabetes Care 2002;25:718
•2%•BP, Lipids, A1C + ASA
•3%•BP, Lipids and A1C
•46%•Daily Aspirin (ASA) Use
•27%•BP <130/85 mmHg
•36%•LDL <100
•27%•A1C <7%
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Type 1 Vs Type 2:How 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 >50% w/ a close relative
DKA Can happen Can happen
Blood Glucose More variable; big hypo’s More stable; milder hypo’s
Thyroid Disease Often Sometimes
Antibodies Usually (Anti-GAD) Not usually
C-peptide Early: low nl; Late: ~0 Early: high nl; Late: low nl
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Diabetes: Early Detection and Lifestyle Monitoring
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Metabolic Syndrome
• Requires 3 or more:– Triglycerides > 150– HDL < 40– Waist size >40” men, >35” women– BP > 130/85– Fasting glucose > 100
• Caveat: Treatment counts for requirements…
(Grundy, Circulation, 2005)
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Pre-Diabetes Definition
Fasting GTT
or
If FBG >100 there is a 10-15% risk of DM within 7 years…
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Who and When to Screen?
• Family history• Overweight (BMI 25)• Dyslipidemia• HTN
• High risk ethnicity• Vascular disease• Prior glucose
elevation• Hx or exam findings
• Starting at age 45, a fasting blood glucose every three years
• More frequent screening if:
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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)
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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
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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
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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
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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
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Diabetic Retinopathy
Normal Retina (left) contrasted with Proliferative Diabetic Retinopathy (right)
Refer patients for ophthalmologist evaluation
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Glycemic Control – Oral Agents
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General RulesHypoglycemic Therapy
• Normalize fasting glucose levels first (90-130 mg/dl)
– Many patients will achieve A1C < 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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Diabetes Care 2009;32:S6-12
GoalPremeal plasma glucose (mg/dL)
2-h postprandial plasma glucose
A1C
ADA
90-130
<180*
<7%**
Glycemic Goals of Therapy
* 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, <6%) may further reduce complications at the cost of increased risk of hypoglycemia
Verbal Target~100
<<200
As low as
possible w/o unacceptable
adverse effects
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Biguanides: MetforminMechanism 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
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Metformin Outperformed Other Meds in Obese Patients (UKPDS)
Lancet 1998 Sep 12;352(9131):854-65.
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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 OpinionMelander A. Diabetes 2004;53 Suppl 3:S151
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Thiazolidinediones (TZD’s 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
• 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.
• Pioglitazone (Actos)
– +LDL
– +HDL
– -Triglycerides
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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 <1% 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 2004;27:256
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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
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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
TherapiesExenatide (Byetta)Sitagliptin (Januvia)
Target population Type 2 on oral agents
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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
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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 1997;103:4912. Nesto RW et al. Diabetes Care 2004;27:256 3. Stenman S et al. Ann Intern Med 1993;118:169
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Glycemic Control - Injected Therapies
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63% Of Patients with DiabetesAre Not at ADA A1C Goal <7%
0
20
40
60
80
100
>10%
>9%
>8%
7-8%
<7%
37.2%>8%63%
7%
7.8%
25.8%
37.0%
17.0%
12.4%
% of Subjects
n=404
A1C
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
Saydah SH et al. JAMA 2004;291:335
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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
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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 2004;30:274
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• 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 2004;30:274
Common Concerns When Transitioning To Insulin
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Potential Insulin Regimens
Insulin pump Physiologic/COMPLEX/Flexible
Multiple daily injections
Free mixing - twice daily
Pre-mixed - twice daily
Basal only SIMPLE/InflexibleHow do we balance simplicity and flexibility to achieve glycemic control?
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Indications for Insulin
• Not contraindicated at anytime• Consider as initial therapy
– HgbA1C > 10%– Fasting glucose > 250mg/dl– Random glucose > 300
• Recommended as initial therapy– Polyuria, polydipsia, weight loss,
ketones
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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 < 70
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Once Daily Insulin OptionsBasals vs. NPH vs. Premixed
INSULIN TYPE ADVANTAGES DISADVANTAGES
Glargine Peakless, less hypoglycemia, less wt gain; simple
Cost; can’t mix; no meal time coverage
Detemir Less wt gain, less hypoglycemia; simple
Cost, shorter duration than glargine; can’t 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
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Insulin ActionEffect Of Various Formulations
0
20
40
60
80
100
120
140
0 2 4 6 8 10 12 14 16
Short (Regular)
Rapid (Glulisine, Lispro, Aspart,)
InsulinLevel
(U/ml)
Hours
Intermediate (NPH)
Long (Glargine)
Detimir
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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
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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
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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
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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
rangeAdjust 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 2005;23:78
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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 2005;28:260
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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
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Non Insulin Injectables
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Initiation 1 Mo
5 mcg BIDStable Dose
10 mcg BIDStable Dose
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
General Prescribing ConsiderationsDosing
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Glargine Vs Exenatidein Patients Failing Oral Therapies
ITT patient sampleMean ± SE shown* p<0.0001, exenatide vs insulin glargine at same time point
Body Weight (lbs)
* ** *
* *
A1C (%)
Heine RJ et al. Ann Intern Med 2005;143(8):559
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Diagnosisby screening or with symptoms
Treatment Algorithm - Glucose
Yes
Quarterly to semi-annual
follow-up
Lifestyle interventionMNT, physical activity, education
Are A1C/FPG targets achieved?Monthly to quarterly follow-up
Target PPGTarget Insulin Deficiency
FPG >200 mg/dL FPG <130 mg/dL
Metformin, glitazone
Exenatide, nateglinide, α-glucosidase inhibitors, rapid-acting insulin, pramlintide
SFUs/glinide, insulin, exenatide
*
* Keep adding agents until target reached. Self-titration at home when possible
Target Insulin Resistance
No
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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
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Treatment of Hypoglycemia • Definition of hypoglycemia: Plasma glucose <70 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 >70 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 2003;26:1902
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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
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Cardiovascular Disease Prevention
Blood Pressure, Dyslipidemia, Antiplatelet Therapy
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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?
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Diabetes and HypertensionWhy?
• Volume Expansion– Increased insulin levels
• Higher sympathetic activity
– Increased glucose level• Increased sodium resorption with
hyperglycemia
• Decreased arterial compliance• Obesity
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UKPDS Blood Pressure Study:Tight 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 0.0046Diabetes related deaths 32 0.019Heart failure 56 0.0043Stroke 44 0.013Myocardial infarction 21 NSMicrovascular disease 37 0.0092
UKPDS. BMJ. 317: 703-713. 1998.
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Diabetes Treatment Goalsfor Blood Pressure
•Control blood pressure– 130/80 mmHg for most patients – 125/75 mmHg for patients who have proteinuria
>1 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 2003;289:2560; Bakris GL et al. Am J Kidney Dis 2000;36:646ADA. Diabetes Care 2007;30(suppl 1):S15
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Number of Medications to Achieve Goal BP In 5 Trials of DM and/or Renal Disease
3.8
3.3
3.6
2.8
2.7
0 1 2 3 4
AASK (<92 mmHg MAP)
HOT (<80 mmHg DBP)
MDRD (<92 mmHg MAP)
ABCD (<75 mmHg DBP)
UKPDS (<150/85 mmHg)
Number Of BP Meds
Bakris. J Clin Hypertens 1999;1:141
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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 2000;36:646
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UKPDS: ACE Inhibitor Vs -Blocker Aggregate Clinical Endpoints
0.5 1 2
Relative Risk & 95% CI
Any diabetes-related endpoint 1.10 0.43
PRR
UKPDS Group. BMJ 1998;317:713
FavorsACE Inhibitor
Favors-Blocker
Diabetes-related deaths
All-cause mortality
Myocardial infarction
Stroke
Microvascular disease
1.27
1.14
1.20
1.12
1.29
0.28
0.44
0.74
0.35
0.30
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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
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Additional BP Recommendations• Lower blood pressure gradually in the elderly
• If unable to achieve goal, don’t 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 2007;30(Suppl1):16
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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
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Statins:Primary And Secondary Prevention
Adapted from Illingworth. Med Clin North Am 2000;84:23 and LaRosa. N Engl J Med 2005;352 (e-pub) and Colhoun. Lancet 2004;364:685
50 21070 190170150130110900
5
10
15
20
25
% WithCVD
Event
LDL-C (mg/dL)
WOSCOPS
AFCAPSHPS
(estimated)
CARDS
CARE
4S
LIPIDHPS
(estimated)
TNTTNT
PROVE-IT
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ADA Standards 2009Dyslipidemia
• Fasting lipid profile annually• Without overt CVD
– LDL<100– At age 40 start on statin regardless of LDL to
reduce LDL 30-40%
• With overt CVD– Start statin to reduce LDL 30-40%– LDL<70 is an option– Normalizing triglycerides and raising HDL with
fibrates reduces CV events
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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
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Anti-platelet TherapyADA Standards
• Recommendations for Aspirin– ASA 75-162 mg/day for 2o prevention– ASA 75-162 mg/day for 1o prevention
• Age > 40• Any age with CV risk factors (htn, hyperlipidemia,
renal disease, family history, smoking)
– Not recommended ages < 21 (Reye’s syndrome)
• Clopidogrel– Very high risk diabetics; intolerance to ASA
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Practice Performance and Improvement
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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
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Questions?