Diabetes Step Care Approach

Diabetes:Step care approach to management

Diabetes:Step care approach to management

Dr. B. K. IyerDr. B. K. Iyer

Diabetes:classification, diagnosis, management

Diabetes:classification, diagnosis, management

Classification Diagnosis Treatment


Diabetes classification – a relookDiabetes classification – a relook



ClassificationClassification

Type 1 diabetes Type 2 diabetes Other

1. Genetic defects of beta cell function2. Genetic defects in insulin action3. Diseases of the exocrine pancreas4. Endocrinopathies5. Drug/ chemical - induced 6. Infections7. Uncommon forms of immune-mediated diabetes8. Genetic syndromes sometimes associated with diabetes

Gestational diabetes mellitus

Type 1 diabetes Type 2 diabetes Other

1. Genetic defects of beta cell function2. Genetic defects in insulin action3. Diseases of the exocrine pancreas4. Endocrinopathies5. Drug/ chemical - induced 6. Infections7. Uncommon forms of immune-mediated diabetes8. Genetic syndromes sometimes associated with diabetes

Gestational diabetes mellitus

Type 1 diabetesType 1 diabetes

Type 1 diabetes is characterized by β-cell destruction, usually leading to absolute insulin deficiency.

A. Immune-mediated

B. Idiopathic

Type 1 diabetes is characterized by β-cell destruction, usually leading to absolute insulin deficiency.

A. Immune-mediated

B. Idiopathic

* Diagnosis and Classification of Diabetes Mellitus. ADA 2009.

* Atkinson MA and Eisenbarth GS. Lancet 2001;358:221-229.

Type 1 diabetes - progressionType 1 diabetes - progression

Type 1 diabetes – immune mediated Type 1 diabetes – immune mediated

Absolute insulin deficiency Usually due to autoimmune destruction of the

pancreatic beta cells Islet-cell antibodies (ICA) or other autoantibodies

antibodies to glutamic acid decarboxylase [anti-GAD] and anti-insulin)

Absolute insulin deficiency Usually due to autoimmune destruction of the

pancreatic beta cells Islet-cell antibodies (ICA) or other autoantibodies

antibodies to glutamic acid decarboxylase [anti-GAD] and anti-insulin)

Type 2 diabetesType 2 diabetes

Hyperglycemia Insulin resistance Relative insulin secretion/ response impairment

Hyperglycemia Insulin resistance Relative insulin secretion/ response impairment

Type 2 diabetes - causesType 2 diabetes - causes

Hyperglycemia in type 2 diabetes can be due to 2 causes:Hyperglycemia in type 2 diabetes can be due to 2 causes:

Pancreas

Insulin Resistance

Liver

HyperglycemiaHyperglycemia

Islet Cell Degranulation;Reduced Insulin Content

Muscle Adipose Tissue

Decreased Glucose Transport & Activity

(expression) of GLUT4

Increased Lipolysis

↑GlucoseProduction

↓GlucoseUptake

ReducedPlasma Insulin

Increased Glucose Output

Cell Dysfunction

Elevated Plasma FFA

Elevated Plasma FFA

Type 2 diabetes & declining β–cell function : UKPDS

Type 2 diabetes & declining β–cell function : UKPDS

Dashed line = extrapolation from UKPDS data

Lebovitz HE, Diabetes reviews, 1999;7: 139-153

Maturity–onset diabetes of the young (MODY) 6 subtypes:

MODY 1 - Mutation in HNF-4-alpha (transcription factor), chromosome 20

MODY 2 - Mutation in glucokinase gene, chromosome 7 MODY 3 - Mutation in HNF-1-alpha (transcription factor),

chromosome 12 (most common form) MODY 4 - Mutation in insulin promoter factor-1 (IPF-1),

chromosome 13 MODY 5 - Mutation in HNF-1-beta, chromosome 17 MODY 6 - Mutation in Neurogenic Differentiation Factor-

1 (NEUROD1) , chromosome 2

Maturity–onset diabetes of the young (MODY) 6 subtypes:

MODY 1 - Mutation in HNF-4-alpha (transcription factor), chromosome 20

MODY 2 - Mutation in glucokinase gene, chromosome 7 MODY 3 - Mutation in HNF-1-alpha (transcription factor),

chromosome 12 (most common form) MODY 4 - Mutation in insulin promoter factor-1 (IPF-1),

chromosome 13 MODY 5 - Mutation in HNF-1-beta, chromosome 17 MODY 6 - Mutation in Neurogenic Differentiation Factor-

1 (NEUROD1) , chromosome 2

Other specific types of diabetes: Genetic defects in β-cell functionOther specific types of diabetes:

Genetic defects in β-cell function

Other specific types of diabetes: Genetic defects in insulin actionOther specific types of diabetes: Genetic defects in insulin action

Type A insulin resistance Leprechaunism Rabson- Mendenhall syndrome Lipoatrophic diabetes Others

Type A insulin resistance Leprechaunism Rabson- Mendenhall syndrome Lipoatrophic diabetes Others

*A clinical screening tool identifies autoimmune diabetes in adults. Fourlanos S; Perry C; Stein MS; Stankovich J; Harrison LC; Colman PG. Diabetes Care. 2006 May;29(5):970-5

Latent Autoimmune Diabetes in Adults (LADA)

Latent Autoimmune Diabetes in Adults (LADA)

Adult-onset diabetes with circulating islet antibodies but not requiring insulin therapy initially

Adults who should be considered for antibody testing*: age of onset <50 years acute symptoms BMI <25 kg/m2 personal or family history of autoimmune disease

Adult-onset diabetes with circulating islet antibodies but not requiring insulin therapy initially

Adults who should be considered for antibody testing*: age of onset <50 years acute symptoms BMI <25 kg/m2 personal or family history of autoimmune disease

Gestational DMGestational DM

Any degree of impaired glucose tolerance with onset or first recognition during pregnancy

Gestational diabetes (GDM) occurs when pancreatic function is not sufficient to overcome the insulin resistance created by changes in diabetogenic hormones during pregnancy.

Most have impaired glucose tolerance that begins in pregnancy

Some have previous undiagnosed type 2 diabetes. 10% have circulating islet cell antibodies

Any degree of impaired glucose tolerance with onset or first recognition during pregnancy

Gestational diabetes (GDM) occurs when pancreatic function is not sufficient to overcome the insulin resistance created by changes in diabetogenic hormones during pregnancy.

Most have impaired glucose tolerance that begins in pregnancy

Some have previous undiagnosed type 2 diabetes. 10% have circulating islet cell antibodies

Diabetes diagnosisDiabetes diagnosis



DiagnosisDiagnosis

Diabetes mellitus

Impaired fasting glucose (IFG)

Impaired glucose tolerance (IGT)

Gestational diabetes mellitus (GDM)

Diabetes mellitus

Impaired fasting glucose (IFG)

Impaired glucose tolerance (IGT)

Gestational diabetes mellitus (GDM)

Diagnosis: Diabetes mellitusDiagnosis: Diabetes mellitus Symptoms of diabetes (polydipsia, polyuria,

unexplained weight loss) PLUS a random plasma glucose >200 mg/dL (11.1 mmol/L)

or

Fasting plasma glucose > 126 mg/dL (7.0 mmol / L) after overnight (at least 8 hours) fast

or

Two-hour plasma glucose> 200mg/dL (11.1 mmol / L) during a standard 75g oral glucose tolerance test

Symptoms of diabetes (polydipsia, polyuria, unexplained weight loss) PLUS a random plasma glucose >200 mg/dL (11.1 mmol/L)

or

Fasting plasma glucose > 126 mg/dL (7.0 mmol / L) after overnight (at least 8 hours) fast

or

Two-hour plasma glucose> 200mg/dL (11.1 mmol / L) during a standard 75g oral glucose tolerance test

Any of these criteria establishes the diagnosis but needs to be confirmed on a later day

Diagnosis: Impaired fasting glucose (IFG)Diagnosis: Impaired fasting glucose (IFG)

Fasting plasma glucose (FPG) < 100 mg/dl (5.6 mmol/l) = normal

FPG 100-125 mg/dl (5.6-6.9 mmol/l) = impaired fasting glucose (IFG)

Fasting plasma glucose (FPG) < 100 mg/dl (5.6 mmol/l) = normal

FPG 100-125 mg/dl (5.6-6.9 mmol/l) = impaired fasting glucose (IFG)

Oral glucose tolerance test (OGTT) – glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water

2-h post-load glucose < 140 mg/dl (7.8 mmol/l) = normal

2-h post-load glucose 140 - 199 mg/dl (7.8 – 11.1 mmol/l) = impaired glucose tolerance (IGT)

Oral glucose tolerance test (OGTT) – glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water

2-h post-load glucose < 140 mg/dl (7.8 mmol/l) = normal

2-h post-load glucose 140 - 199 mg/dl (7.8 – 11.1 mmol/l) = impaired glucose tolerance (IGT)

Diagnosis: Impaired glucose tolerance (IGT)Diagnosis: Impaired glucose tolerance (IGT)

Diagnosis: Gestational Diabetes Mellitus (GDM)

Diagnosis: Gestational Diabetes Mellitus (GDM)

1. Unequivocal hyperglycemia(confirmed on a subsequent day)

Fasting plasma glucose > 126 mg/dL > 126 mg/dL (7.0 mmol/L)(7.0 mmol/L)

Random plasma glucose >200 mg/dL Random plasma glucose >200 mg/dL (11.1 mmol/L)(11.1 mmol/L)

OR

2. Diagnostic OGTT

100-g glucose load

7.81403-h

8.61552-h

10.01801-h

5.395Fasting

mmol/lmg/dl

Diabetes:management

Diabetes:management

Classification Diagnosis Treatment – drugs in brief

Classification Diagnosis Treatment – drugs in brief

TreatmentTreatmentTreatment

Lifestyle intervention Hypoglycaemic drugsHypoglycaemic drugs

•Weight loss•Increased exercise

Oral hypoglycemic

drugs

Insulin & insulin analogs

Others [incretins,

pramlintide]

1. Biguanides2. Sulfonylureas3. Meglitinide analogs4. Thiazolidinediones5. α-Glucosidase Inhibitors6. DPP-4 Inhibitors

Treatment:Oral Antihyperglycemic Drugs

Treatment:Oral Antihyperglycemic Drugs

Oral antihyperglycemic drugs: Biguanides

Oral antihyperglycemic drugs: Biguanides

Metformin & Extended-release metformin now available decrease hepatic glucose

output lower fasting glycemia reduce HbA1c by 1.5%

adverse effects: lactic acidosis, gastro-intestinal disturbances

Metformin & Extended-release metformin now available decrease hepatic glucose

output lower fasting glycemia reduce HbA1c by 1.5%

adverse effects: lactic acidosis, gastro-intestinal disturbances

AMPK - adenosine monophosphate-activated protein kinase, ACC - acteyl-CoA carboxylase, SREPB-1 - sterol-regulatory-element-binding-protein-1

Diagram adapted from Alice Y.Y. Cheng, I. George Fantus, 'Oral antihyperglycemic therapy for type 2 diabetes mellitus' Canadian Medical Association Journal 172(2),2005 pp213-226

Oral antihyperglycemic drugs: Metformin titration

Oral antihyperglycemic drugs: Metformin titration

1. Begin with low-dose metformin (500 mg) taken once or twice per day with meals (breakfast and/or dinner).

2. After 5–7 days, if GI side effects have not occurred, advance dose to 850 or 1,000 mg before breakfast and dinner.

3. If GI side effects appear as doses advanced, can decrease to previous lower dose and try to advance dose at a later time.

4. The maximum effective dose is usually 850 mg twice per day, with modestly greater effectiveness with doses up to 3 g per day. GI side effects may limit the dose that can be used.

5. Based on cost considerations, generic metformin is the first choice of therapy. A longer-acting formulation is available in some countries and can be given once per day.

Oral antihyperglycemic drugs: Sulfonylureas

Oral antihyperglycemic drugs: Sulfonylureas

1st generation no longer used: Chlorpropamide Tolbutamide 2nd generation : Glyburide, Glipizide, Glimepiride

enhance insulin secretion lower HbA1c by 1.5 % side effects: hypoglycemia, weight gain

1st generation no longer used: Chlorpropamide Tolbutamide 2nd generation : Glyburide, Glipizide, Glimepiride

enhance insulin secretion lower HbA1c by 1.5 % side effects: hypoglycemia, weight gain

Black C, Donnelly P, McIntyre L et al. Meglitinide analogues for type 2 diabetes mellitus. Cochrane Database Syst Rev. 2007 Apr 18;(2):CD004654.

Oral antihyperglycemic drugs: Meglitinide analogs

Oral antihyperglycemic drugs: Meglitinide analogs

Repaglinide Nateglinide

enhance insulin secretion (early-phase insulin release) lower HbA1c by 0.1- 2.1 % (repaglinide) and by 0.2- 0.6%

(nateglinide) side effects: weight gain, hypoglycemia

Repaglinide Nateglinide

enhance insulin secretion (early-phase insulin release) lower HbA1c by 0.1- 2.1 % (repaglinide) and by 0.2- 0.6%

(nateglinide) side effects: weight gain, hypoglycemia

Oral antihyperglycemic drugs: Thiazolidinediones (TZDs)

Oral antihyperglycemic drugs: Thiazolidinediones (TZDs)

Rosiglitazone & Pioglitazone peroxisome proliferator-activated receptor γ

modulators (PPAR γ) insulin sensitizers (increase the sensitivity of muscle,

fat and liver to endogenous and exogenous insulin) lower HbA1c by 0.5 - 1.4 %

adverse effects: weight gain, fluid retention

Rosiglitazone & Pioglitazone peroxisome proliferator-activated receptor γ

modulators (PPAR γ) insulin sensitizers (increase the sensitivity of muscle,

fat and liver to endogenous and exogenous insulin) lower HbA1c by 0.5 - 1.4 %

adverse effects: weight gain, fluid retention

Oral antihyperglycemic drugs:-Glucosidase Inhibitors

Oral antihyperglycemic drugs:-Glucosidase Inhibitors

Acarbose Miglitol

reduce the rate of digestion of polysaccharides in the proximal small intestine, primarily lowering post-prandial glucose levels

lower HbA1c by 0.5 – 0.8 % side effects: increased gas production and

gastro-intestinal symptoms

Acarbose Miglitol

reduce the rate of digestion of polysaccharides in the proximal small intestine, primarily lowering post-prandial glucose levels

lower HbA1c by 0.5 – 0.8 % side effects: increased gas production and

gastro-intestinal symptoms

Oral antihyperglycemic drugs: DPP-IV inibitors

Oral antihyperglycemic drugs: DPP-IV inibitors

Sitagliptin : DPP-IV inhibitor Dipeptidyl peptidase IV (DPP-

IV) is a ubiquitous enzyme that deactivates a variety of bioactive peptides, including GIP and GLP-1

Used alone or in combination with metformin or TZDs

Reduces HbA1c by 0.5 – 0.7 % Side effects: increased rate of

respiratory infections, headaches

Sitagliptin : DPP-IV inhibitor Dipeptidyl peptidase IV (DPP-

IV) is a ubiquitous enzyme that deactivates a variety of bioactive peptides, including GIP and GLP-1

Used alone or in combination with metformin or TZDs

Reduces HbA1c by 0.5 – 0.7 % Side effects: increased rate of

respiratory infections, headaches

Other antihyperglycemic drugs: Incretins

Other antihyperglycemic drugs: Incretins

Glucagon-like peptide 1 (GLP-1) agonist Exenatide - active ingredient in Exenatide

(Byetta) is a synthetic version of a protein present in the saliva of the Gila monster

Glucagon-like peptide 1 (GLP-1) agonist Exenatide - active ingredient in Exenatide

(Byetta) is a synthetic version of a protein present in the saliva of the Gila monster

Glucagon-like Peptide - 1Glucagon-like Peptide - 1 The majority of GLP-1 producing cells are in the

terminal ileum and proximal colon. GLP-1 levels in the blood increase rapidly after a meal. Half-life is very short, approximately one minute. GLP-1 binding to its G-protein coupled receptor on ß-

cells increases glucose stimulated insulin secretion GLP-1 infused into healthy subjects decreases gastric

emptying, causes a sensation of satiety, and decreases appetite.

Effects: enhances insulin secretion limits postprandial hyperglycemia.

The majority of GLP-1 producing cells are in the terminal ileum and proximal colon.

GLP-1 levels in the blood increase rapidly after a meal. Half-life is very short, approximately one minute. GLP-1 binding to its G-protein coupled receptor on ß-

cells increases glucose stimulated insulin secretion GLP-1 infused into healthy subjects decreases gastric

emptying, causes a sensation of satiety, and decreases appetite.

Effects: enhances insulin secretion limits postprandial hyperglycemia.

Other antihyperglycemic drugs: Incretins [Exenatide]

Other antihyperglycemic drugs: Incretins [Exenatide]

Added to metformin or sulfonylureas will reduce HbA1c by 0.4-0.6 %

Side effects: nausea (dose-

depended, declines with time)

acute pancreatitis (some necrotizing or hemorrhagic pancreatitis cases

reported as well)

Added to metformin or sulfonylureas will reduce HbA1c by 0.4-0.6 %

Side effects: nausea (dose-

depended, declines with time)

acute pancreatitis (some necrotizing or hemorrhagic pancreatitis cases

reported as well)

Figure 1. Insulin levels following oral vs IV glucose administration in healthy individuals. Despite identical glucose concentrations, plasma insulin levels peaked much earlier and were greater in response to an oral vs IV dose of glucose.

Figure 2. Insulin levels following oral vs IV glucose administration in patients with type 2 diabetes. The markedly reduced early peak of insulin after oral glucose, along with the smaller differences in insulin levels in response to oral and IV glucose doses, illustrate the diminished incretin effect.

Data extrapolated from Perley, et al. @ http://www.byettahcp.com/hcp/hcp_incretin_effect.jsp

Incretin EffectIncretin Effect

Antihyperglycemic drugs: OthersAntihyperglycemic drugs: Others

Pramlintide (Symlin) synthetic analog of amylin Delays gastric emptying,

suppresses glucagon secretion, decreases appetite

Associated with weight loss (1 - 1.5 kg over 6 months)

Used only in conjunction with insulin treatment

↓ HbA1c by 0.5- 0.7 % Side effects: nausea, gastro-

intestinal symptoms

Pramlintide (Symlin) synthetic analog of amylin Delays gastric emptying,

suppresses glucagon secretion, decreases appetite

Associated with weight loss (1 - 1.5 kg over 6 months)

Used only in conjunction with insulin treatment

↓ HbA1c by 0.5- 0.7 % Side effects: nausea, gastro-

intestinal symptoms

AmylinAmylin

Stored in insulin secretory granules in the ß-cells

Co-secreted with insulin Decreases glucagon Satiety signal? Decreases GI motility

Stored in insulin secretory granules in the ß-cells

Co-secreted with insulin Decreases glucagon Satiety signal? Decreases GI motility

* Onset and duration are rough estimates. They can vary greatly within the range listed and from person to person

** Human insulin is made by recombinant DNA technology

Available insulin preparationsAvailable insulin preparations

Summary of antidiabetic interventions as monotherapy

Summary of antidiabetic interventions as monotherapy

InterventionsExpected

decrease in A1C (%)

Advantages Disadvantages

Step 1: initial

Lifestyle to decrease weight and increase activity

1–2 Low cost, many benefits Fails for most in 1st year

Metformin 1.5Weight neutral, inexpensive

GI side effects, rare lactic acidosis

Step 2: additional therapy

Insulin 1.5–2.5No dose limit, inexpensive, improved lipid profile

Injections, monitoring, hypoglycemia, weight gain

Sulfonylureas 1.5 Inexpensive Weight gain, hypoglycemia

TZDs 0.5–1.4 Improved lipid profile Fluid retention, weight gain, expensive

Other drugs

α-Glucosidase inhibitors 0.5–0.8 Weight neutralFrequent GI side effects, three times/day dosing, expensive

Exenatide 0.5–1.0 Weight lossInjections, frequent GI side effects, expensive, little experience

Glinides 1–1.5† Short duration Three times/day dosing, expensive

Pramlintide 0.5–1.0 Weight lossInjections, three times/day dosing, frequent GI side effects, expensive, little experience

Diabetes:management

Diabetes:management

Classification Diagnosis Treatment – goals

Classification Diagnosis Treatment – goals

* Postprandial measurements should be made 1-2 h after the beginning of the meal, generally peak levels in patients with diabetes.

Standards of Medical Care in Diabetes–2009. ADA Position Statement. Diabetes Care;32:S13-S61.

Glycemic goals: non-pregnant adults with diabetes


Key concepts in setting glycemic goals HbA1c is the primary target for glycemic

control HbA1c < 7.0% Preprandial capillary plasma glucose 70-130

mg/dl (3.9-7.2 mmol/l) Peak postprandial capillary plasma glucose <

180 mg/dl (< 10.0 mmol/l)*

Key concepts in setting glycemic goals HbA1c is the primary target for glycemic

control HbA1c < 7.0% Preprandial capillary plasma glucose 70-130

mg/dl (3.9-7.2 mmol/l) Peak postprandial capillary plasma glucose <

180 mg/dl (< 10.0 mmol/l)*

* Postprandial measurements should be made 1-2 h after the beginning of the meal, generally peak levels in patients with diabetes.

Standards of Medical Care in Diabetes–2009. ADA Position Statement. Diabetes Care;32:S13-S61.



Goals should be individualized based on: duration of diabetes age/life expectancy comorbid conditions known CVD or advanced microvascular complications hypoglycemia unawareness individual patient considerations

More or less stringent glycemic goals may be appropriate for individual patients

Postprandial glucose may be targeted if HbA1c goals are not met despite reaching preprandial glucose goals

Goals should be individualized based on: duration of diabetes age/life expectancy comorbid conditions known CVD or advanced microvascular complications hypoglycemia unawareness individual patient considerations

More or less stringent glycemic goals may be appropriate for individual patients

Postprandial glucose may be targeted if HbA1c goals are not met despite reaching preprandial glucose goals

Glycemic goals - pregnant adults with diabetes

Glycemic goals - pregnant adults with diabetes

Women with GDM

Maternal capillary glucose concentrations: preprandial:≤95 mg/dl

(5.3 mmol/l) and either 1-h postmeal: ≤140

mg/dl (7.8 mmol/l)

Women with GDM

Maternal capillary glucose concentrations: preprandial:≤95 mg/dl

(5.3 mmol/l) and either 1-h postmeal: ≤140

mg/dl (7.8 mmol/l)

Women with preexisting diabetes who become pregnant

Maternal capillary glucose concentrations: premeal, bedtime, and

overnight: 60-99mg/dl Peak postprandial: 100-

129 mg/dl HbA1c <6.0%

Women with preexisting diabetes who become pregnant

Maternal capillary glucose concentrations: premeal, bedtime, and

overnight: 60-99mg/dl Peak postprandial: 100-

129 mg/dl HbA1c <6.0%

Road map to achieve glycaemic goals:Naive to type 2 therapy

Road map to achieve glycaemic goals:Naive to type 2 therapy

Diabetes:management

Diabetes:management

Classification Diagnosis Treatment – step care approach

Classification Diagnosis Treatment – step care approach

Algorithm for the metabolic management of type 2 diabetes; Reinforce lifestyle interventions at every visit and check A1C every 3 months until A1C is <7% and then at least every 6 months. The interventions should be changed if A1C is ≥7%. a)Sulfonylureas other than glybenclamide (glyburide) or chlorpropamide. b)Insufficient clinical use to be confident regarding safety.

ADA Treatment AlgorithmADA Treatment Algorithm

Algorithm for the metabolic management of type 2 diabetes. Reinforce lifestyle intervention at every visit. *Check A1C every 3 months until <7% and then at least every 6 months. +Although three oral agents can be used, initiation and intensification of insulin therapy is preferred based on effectiveness and expense.


Initiation and adjustment of insulin regimens. Insulin regimens should be designed taking lifestyle and meal schedule into account. The algorithm can only provide basic guidelines for initiation and adjustment of insulin. See reference 90 for more detailed instructions. aPremixed insulins not recommended during adjustment of doses; however, they can be used conveniently, usually before breakfast and/or dinner, if proportion of rapid- and intermediate-acting insulins is similar to the fixed proportions available. bg, blood glucose.


Initiation and adjustment of insulin regimens. Insulin regimens should be designed taking lifestyle and meal schedule into account. The algorithm can only provide basic guidelines for initiation and adjustment of insulin. See ref. 71 for more detailed instructions. +Premixed insulins are not recommended during adjustment of doses; however, they can be used conveniently, usually before breakfast and/or dinner if proportion of rapid- and intermediate-acting insulins is similar to the fixed proportions available. bg, blood glucose.


Initiation and adjustment of insulin regimens. Insulin regimens should be designed taking lifestyle and meal schedule into account. The algorithm can only provide basic guidelines for initiation and adjustment of insulin. See ref. 71 for more detailed instructions. +Premixed insulins are not recommended during adjustment of doses; however, they can be used conveniently, usually before breakfast and/or dinner if proportion of rapid- and intermediate-acting insulins is similar to the fixed proportions available. bg, blood glucose.


Clarifications on the watch listClarifications on the watch list

Insulin therapy in outpatient and inpatient settings

Glycemic control and inpatient outcomes Does a perfect eating plan exist? Medical Nutrition Therapy for Diabetes Review goals and outcomes of Medical Nutrition

Therapy [MNT] Discuss basic recommendations for MNT Review specific recommendations for patient

population groups

Insulin therapy in outpatient and inpatient settings

Glycemic control and inpatient outcomes Does a perfect eating plan exist? Medical Nutrition Therapy for Diabetes Review goals and outcomes of Medical Nutrition

Therapy [MNT] Discuss basic recommendations for MNT Review specific recommendations for patient

population groups

Road Maps to Achieve Glycemic Control in Type 2

Diabetes Mellitus

Road Maps to Achieve Glycemic Control in Type 2

Diabetes MellitusACE/AACE Diabetes Road Map

Task ForceACE/AACE Diabetes Road Map

Task Force

Health & Medicine

Diabetes Step Care Approach