dm2
DESCRIPTION
DM2. Outpatient Glycemic Control. DM. Inpatient Glycemic control. Criteria for the Diagnosis of Diabetes. ADA. I. Classification and Diagnosis. Diabetes Care 2011;34(suppl 1):S13. Table 2. Components of the Comprehensive Diabetes Evaluation:. - PowerPoint PPT PresentationTRANSCRIPT
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DM2
Outpatient Glycemic Control
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DMInpatient Glycemic control
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Criteria for the Diagnosis of Criteria for the Diagnosis of DiabetesDiabetes
A1C ≥6.5%OR
Fasting plasma glucose (FPG)≥126 mg/dl (7.0 mmol/l)
OR
Two-hour plasma glucose ≥200 mg/dl (11.1 mmol/l) during an OGTT
OR
A random plasma glucose ≥200 mg/dl (11.1 mmol/l)ADA. I. Classification and Diagnosis. Diabetes Care 2011;34(suppl 1):S13. Table 2.
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Components of the Comprehensive Components of the Comprehensive Diabetes EvaluationDiabetes Evaluation::
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
Physical examination (1)•Height, weight, BMI
• Blood pressure determination, including orthostatic measurements when indicated•Fundoscopic examination*•Thyroid palpation
• Skin examination (for acanthosis nigricans and insulin injection sites)
*See appropriate referrals for these categories.
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Components of the Comprehensive Diabetes Components of the Comprehensive Diabetes EvaluationEvaluation::
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
*See appropriate referrals for these categories.
Physical examination :
• Comprehensive foot examination
–Inspection
– Palpation of dorsalis pedis and posterior tibial pulses
– Presence/absence of patellar and Achilles reflexes
– Determination of proprioception, vibration, and monofilament sensation
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Initial Metabolic Evaluation
Referrales
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Laboratory evaluation:
• A1C, if results not available within past 2–3 months
• If not performed/available within past year– Fasting lipid profile, including total, LDL- and HDL-
cholesterol and triglycerides– Liver function tests– Test for urine albumin excretion with spot urine
albumin/creatinine ratio– Serum creatinine and calculated GFR– TSH in type 1 diabetes, dyslipidemia, or women
>50 years of age
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
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Referrals:
•Annual dilated eye exam
•Family planning for women of reproductive age
•Registered dietitian for MNT
•Diabetes self-management education
• Dental examination
• Mental health professional, if neededADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17. Table 8.
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Target HbA1C
A -B -C –D- E
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Correlation of A1C with Estimated Average Glucose Correlation of A1C with Estimated Average Glucose
(eAG)(eAG)
Mean plasma glucose
A1C (%)mg/dlmmol/l
61267.0
71548.6
818310.2
921211.8
1024013.4
1126914.9
1229816.5
These estimates are based on ADAG data of ~2,700 glucose measurements over 3 months per A1C measurement in 507 adults with type 1, type 2, and no diabetes. The correlation between A1C and average glucose was 0.92. A calculator for converting A1C results into estimated average glucose (eAG), in either mg/dl or mmol/l, is available at http://professional.diabetes.org/GlucoseCalculator.aspx.
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Considering:
Age Body weight
GFR
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Outpatient Management:
Bp controlLipid managementCigar discontinuous
Glycemic control
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Early and aggressive insulin therapy:
Reduces long-term vascular risk and potentially may prolong B-cell lifespan andFunction.
.
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initiating combination therapy or insulin immediately for all patients
with A1C ≥9% at diagnosis. ;
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Recent clinical treatment guidelines, suggest that these agents may be less effective as add-on therapy for patients with an A1C ≥ 9.5% and therefore recommend the initiation of insulin in all patients with an A1C > 10%.
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Indication for insulin therapy:
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ketosis-prone type 2 diabetes:
At presentation, they have markedly impaired insulin secretion and insulin action, but aggressive management with insulin improves insulin secretion and action to levels similar to those of patients with type 2 diabetes without DKA.
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Recently, it has been reported that the nearnormoglycemic remission is associated with a greater recovery of basal and stimulated insulin secretion and that 10 years after diabetes onset, 40% of patients are still non-insulin dependent.
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Fasting C-peptide levels of >1.0 ng/dl (0.33 nmol/1) and stimulated C-peptide levels >1.5 ng/dl (0.5 nmol/1) are predictive of long-term normoglycemic remission in
patients with a history of DKA .
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Barriers to insulin initiation and intensification:
The steps involved in insulin therapy:
InitiationOptimisation
Intensification
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Patient barriers:
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Physician barriers:
Low motivationEducation barriers
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Insulin initiation strategies: In general, patients are initiated on
relatively less intensive insulin regimens to ease them into an appropriate routine. The insulin regimen can then be intensified as needed to meet glycemic
goals . .
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Basal insulins:
NPHGlarginDetemir
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Treat-to-Target trial: Glargine or NPH?
A1c reduction of:1.6%Nocturnal hypoglycemia?
Variablity in duration?
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Long-acting analogs may also possess added benefit when compared to NPH insulin in regard to rates of hypoglycemia and, in the case of insulin detemir, decreased weight
gain . .
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Titration:
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Starting with a basal insulin analogue:
The OADs,including metformin and a
secretagogue, are usually retained.
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For patients who experience dose waning toward the end of the dosing interval, twice-daily dosing may be considered or the administration time for single-dose regimens can be moved to earlier in the day during the period the patient will be using prandial coverage or periods of greater physical activity .
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Premixed insulin: initiating a once-daily regimen in
patients for whom hyperglycemia is not severe and a twice-daily regimen in patients with an AlC > 8.5% .
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Rapid-acting products:
Ideally, these agents should be administered with a lag time before eating that is proportional to the preprandial glucose level. The higher the glucose level, the greater amount of time before the meal the insulin should be administered to allow for onset of effect and a downward trend of premeal
hyperglycemia before eating. .
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Rapid-acting products:rapid-acting insulin should be
administered earlier (e.g., 10-15 minutes before the meal) for meals that contain primarily rapidly absorbed carbohydrates to ensure onset during carbohydrate absorption. Conversely, this insulin could be administered later (e.g., at the first bite or 15 minutes after the meal) for meals with high fat content, which may slow carbohydrate
absorption. .
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Most patients start a once-dailyregimen before dinner, while
maintaining sensitisersand discontinuing evening
secretagogues, andshould use 12 U initially.
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A recent study shows 41% of patients with type 2 diabetes
attained an A1C less than 7% on a once-daily
regimen of BIAsp 30 and OADs.
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the addition of oncedaily biphasic insulin aspart 70/30 before the evening meal in patients failing to meet glycemic goals on metformin resulted in A1C reductions of 1.1-1.3%.
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it is important to note that whenA1C levels are 8.5% or above, initiating insulin therapywith a twice-daily premixed insulin analogue is more effective at achieving glycaemic control thanbasal insulin.
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Lingvay et al, recently demonstrated a 100% success rate in achieving a goal AlC of < 7.0% in patients with newly diagnosed type 2 diabetes by initiating twice-daily biphasic insulin aspart 70/30 insulin in combination
with metformin. .
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Patients usually remain on sensitisers
whereas secretagogues are generally discontinued if using two or more injections.
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Basal–bolus insulin regimens:
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Use of insulin glargine and cancer incidence in Scotland:a study from the Scottish Diabetes Research NetworkEpidemiology Group-Diabetologia(2009)
Overall, insulin glargine usewas not associated with an increased risk
of all cancers over a 4 year time frame.
In the subgroup of insulin glargine only users
to more likely reflect allocation bias rather
than an effect of insulin glargine itself .
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