Dm presentation

Standards of Medical
Care in Diabetes
Dr. Ahmed Al Montasir
Resident Physician
Department of Medicine
Rafatullah Community Hospital

1991
World Diabetes
Day begins
5
The International
Diabetes Federation
and the World
Health Organization
created World
Diabetes Day in
response to
diabetes epidemic

Every year on November 14,
World Diabetes Day brings diabetes
to the attention of the world.

November 14 is
the birthday of
Frederick Banting,
one of the
discoverers of
insulin.
(c) Banting House National Historic Site of Canada

The theme is set by
the International
Diabetes Federation
and the World Health
Organization.

In 2006,
the United Nations
passed resolution
61/225. It asks the world
to observe November 14
as World Diabetes Day
and to take action to
address the diabetes
threat.

The campaign evolved from one day in the
year to a multi-year campaign

The campaign has
grown in strength
from humble
beginnings. . .

. . .to become a truly
global event.

2009-2013
Diabetes Education and Prevention
The campaign slogan is:
Let's Take Control of Diabetes.
Now.

2009-2013
Understand diabetes and take control

2009-2013
Let’s Take Control of Diabetes. Now.
15

The global symbol for diabetes was developed
during the Unite for Diabetes campaign.
Why a circle?
A positive symbol across cultures, the circle
symbolizes life and health.
Why blue?
The colour blue reflects the sky that unites all
nations. The blue border of the circle reflects the
colour of the sky and the flag of the United
Nations. The blue circle signifies the unity of the
global diabetes community in response to the
diabetes epidemic.

Follow World Diabetes Day
English, French and Spanish campaign
website
http://www.worlddiabetesday.org
News & Events RSS feeds
“days to go” countdown newsletter
Facebook Group (English, French, Spanish)
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Become a fan of World Diabetes Day
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http://twitter.com/wdd
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World Diabetes Day Channel
International Diabetes Federation Channel
Flickr
World Diabetes Day group - http://www.flickr.com/groups/wdd

An ancient problemAn ancient problem

• Diabetes mellitus had been known since
ancient times. Egyptian writings from as
early as 1500BC described a wasting
disease in which the sufferer produced
sweet-tasting urine. Egyptian physician
Hesy Ra makes the first mention about it
from Egypt on the Ebers Papyrus.

• Greeks & RomansGreeks & Romans
• History of Diabetes reveals the contributions of
Greeks and Romans. The famous Greek
physician Aretaeus coined the Greek word
Diabetes which means siphon. It acts like a
siphon, melting down flesh and limbs in urine.
• He lived in the first Century AD. His work on
Diabetes is a relic of antiquity. Diabetes was
researched by the Egyptians as well.
From the Ancient Greek διαβαίνω (diabainō, “to pass through”), via the
participle διαβήτης (diabētēs, “passing through”). This refers to the excessive
amounts of urine produced by sufferers.

• Indian FindingsIndian Findings
• History of diabetes is 2500 years old. Diabetes
mentioned in the old Indian medical texts.
• Ayurvedic authorities Sushruta and Charaka had
described it as Madhu Meha. It meant Honey Urine.
• They found that its victims passed large amounts of
sugar laden urine which attracted ants.
• Hence they called it Madhu Meha before 2500 years, a
term which is even now commonly used.

• The medical identification of the disease:
• Paracelsus for the first time identified the gravity of the
disease.
• The word diabetes mellitus was first used by the English
physician Thomas Willis in the year 1675. In nineteenth
century chemical tests were conducted in laboratory to
diagnose the type of this disease.
• The French researcher Claude Bernard examined the
working of pancreas and rate of metabolism in the liver
area.
• The breakthrough occurred in 1869 by the German
medical student, Paul Langerhans, who discovered the
two systems of cells in pancreas. The one system is
responsible for normal production of juice, while the
function of the other system still remained a mystery.

• From the 1850's onwards, autopsies of
people who had died from diabetes
suggested that the problem was caused
when the pancreas did not function
properly.
• Many physicians speculated that
specialised cells, called the islets of
Langerhans, produced a chemical that
allowed the body to regulate its blood
sugar level. Diabetes was caused when
this chemical was not produced.

• 346 million people worldwide have diabetes.
• In 2004, an estimated 3.4 million people died
from consequences of high blood sugar.
• More than 80% of diabetes deaths occur in
low- and middle-income countries.
• WHO projects that diabetes deaths will
double between 2005 and 2030.
• Healthy diet, regular physical activity,
maintaining a normal body weight and
avoiding tobacco use can prevent or delay
the onset of type 2 diabetes.

• RESULTS— The prevalence of diabetes for all age-
groups worldwide was estimated to be 2.8% in 2000 and
4.4% in 2030. The total number of people with diabetes
is projected to rise from 171 million in 2000 to 366 million
in 2030.
• The prevalence of diabetes is higher in men than
women, but there are more women with diabetes than
men. The urban population in developing countries is
projected to double between 2000 and 2030.
• The most important demographic change to diabetes
prevalence across the world appears to be the increase
in the proportion of people 65 years of age.
• DIABETES CARE, VOLUME 27, NUMBER 5, MAY 2004

• The Worst Affected
• If the same trend continues in India, this
country will have 184 million diabetics in
2030 whereas WHO estimated it as 79
million. The true facts about diabetes are
staggering indeed!

• RESULTS—The prevalence of type 2 diabetes
was 4.3% and IFG was 12.4%.
• The subjects with higher family income had
significantly higher prevalence of type 2 diabetes
(5.9 vs. 3.5%), and IFG (15.6 vs. 10.8%), than
those with lower income.
• Wealthy class, family history of diabetes,
reduced physical exercise, and increased age,
BMI, and WHR were the important predictors of
diabetes.
• Diabetes and Impaired Fasting Glycemia in a Rural Population of Bangladesh
• M. Abu Sayeed, MD, PHD

Increasing mortality from diabetesIncreasing mortality from diabetes
mellitusmellitus
J. Olefsky, JAMA 2010:285:628-
632

Type 2 DM - global epidemic -
why ?
Prevalence depends on:
• Age
• Residence(urban/rural)
• Obesity
• Physical activity
• Ethnicity

0
20
40
60
80
15 20 25 30 35
BMI(kg/m
2
)
PrevalenceofDM(%)
Europe
Malta
India
China
Japan
Prevalence of DM in 60 years old Men
Decoda:Nakagami; Diabetologia 2010

• Diabetes AssociationsDiabetes Associations
• American Association of Clinical Endocrinologists
245 Riverside Ave. Suite 200
Jacksonville, FL 32202
(904) 353-7878
• American Dietetic Association
120 South Riverside Plaza, Suite
2000
Chicago, Illinois 60606-6995
(800) 877-1600
• American Association of Diabetes Educators
200 W. Madison Suite 800
Chicago, IL 60606
(800)338-3633
• American Diabetes Association
1701 North Beauregard Street
Alexandria, VA 22311
(800)342-2383
• President's Council on Physical Fitness and Sports
Department W - 200 Independence
Ave., SW Room 738-H
Washington, D.C. 20201-0004
(202) 690-9000
• Diabetes AssociationsDiabetes Associations
British Diabetes AssociationBritish Diabetes Association
Diabetes UK Central Office
10 Parkway, London NW1 7AA
020 7424 1000
Canadian Diabetes Association
1400-522 University Ave
Toronto ON M5G 2R5
(800) 226-8464
Centers for Disease Control and Prevention's Diab
4770 Buford Highway NE, Mailstop K-10,
Atlanta, GA 30341-3717
(770) 488-5000
International Diabetic Federation
Avenue Emile De Mot 19 - B-1000
Brussels, Belgium
+32-2-5385511 l
Diabetes Exercise and Sports Association
Formerly International Diabetic Athletes
Association
8001 Montcastle Dr.
Nashville, TN 37221
(800) 898-4322
• Juvenile Diabetes Research Foundation
International
120 Wall Street
New York, NY 10005-4001
(800) 533-2873

Classification of diabetes
• The classification of diabetes includes four clinicalThe classification of diabetes includes four clinical
classes:classes:
• Type 1 diabetes (results from β-cell destruction, usually
leading to absolute insulin deficiency)
• Type 2 diabetes (results from a progressive insulin
secretory defect on the background of insulin resistance)
• Other specific types of diabetes due to other causes,
e.g., genetic defects in β-cell function, genetic defects in
insulin action, diseases of the exocrine pancreas (such
as cystic fibrosis), and drug- or chemical-induced (such
as in the treatment of HIV/AIDS or after organ
transplantation)
• Gestational diabetes mellitus (GDM) (diabetes
diagnosed during pregnancy that is not clearly overt
diabetes)

Criteria for Testing for Diabetes inCriteria for Testing for Diabetes in
Asymptomatic Adult IndividualsAsymptomatic Adult Individuals
•Physical inactivity
•First-degree relative with
diabetes
•High-risk race/ethnicity (e.g.,
African American, Latino, Native
American, Asian American, Pacific
Islander)
•Women who delivered a baby
weighing >9 lb or were diagnosed
with GDM
•Hypertension (≥140/90 mmHg or
on therapy for hypertension)
• HDL cholesterol level
<35 mg/dl (0.90 mmol/l)
and/or a triglyceride level
>250 mg/dl (2.82 mmol/l)
• Women with polycystic ovarian
syndrome (PCOS)
• A1C ≥5.7%, IGT, or IFG on
previous testing
• Other clinical conditions
associated with insulin
resistance (e.g., severe
obesity, acanthosis nigricans)
• History of CVD
*At-risk BMI may be lower in some ethnic groups.
1. Testing should be considered in all adults who are overweight
(BMI ≥25 kg/m2
*) and have additional risk factors:
ADA. Testing in Asymptomatic Patients. Diabetes Care 2011;34(suppl 1):S14. Table 4.

2. In the absence of criteria (risk factors on previous slide),
testing for diabetes should begin at age 45 years
3. If results are normal, testing should be repeated at least
at 3-year intervals, with consideration of more frequent
testing depending on initial results and risk status
ADA. Testing in Asymptomatic Patients. Diabetes Care 2011;34(suppl 1):S14. Table 4.
Criteria for Testing for Diabetes inCriteria for Testing for Diabetes in
Asymptomatic Adult IndividualsAsymptomatic Adult Individuals

Criteria for the Diagnosis of DiabetesCriteria for the Diagnosis of Diabetes
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.

A1C ≥6.5%
The test should be performed in a laboratory using an
NGSP-certified method standardized to the DCCT assay*
*In the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing.
“National Glycohemoglobin Standardization Program”.
American Association for Clinical Chemistry (AACC)

Both Fasting and Postprandial Hyperglycemia
Contribute to A1C
Plasma Glucose
(mg/dL)
Adapted from Riddle MC. Diabetes Care. 1990;13:676-686
300
200
100
0
Time of Day
6 AM 12 PM 6 PM 12 AM 6 AM
Normal glycemic exposure
A1C ~5%
Uncontrolled Diabetes
With A1C ~8%
Postprandial
Hyperglycemia
Fasting
Hyperglycemia

Correlation of A1C with EstimatedCorrelation of A1C with Estimated
Average Glucose (eAG)Average Glucose (eAG)
Mean plasma glucose
A1C (%) mg/dl mmol/l
6 126 7.0
7 154 8.6
8 183 10.2
9 212 11.8
10 240 13.4
11 269 14.9
12 298 16.5
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S18. Table 9.
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.

Two-hour plasma glucose ≥200 mg/dl (11.1
mmol/l) during an OGTT
The test should be performed as described by the
World Health Organization, using a glucose load
containing the equivalent of 75 g anhydrous glucose
dissolved in water*
*n the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing.

In a patient with classic symptoms of hyperglycemia
or hyperglycemic crisis,
a random plasma glucose ≥200 mg/dl (11.1 mmol/l)

• The Expert Committee . . . recognized an
intermediate group of individuals whose
glucose levels do not meet criteria for
diabetes, yet are “higher than those
considered normal."

Prediabetes: IFG, IGT, Increased A1CPrediabetes: IFG, IGT, Increased A1C
Categories of increased risk for diabetes
(Prediabetes)*
FPG 100-125 mg/dl (5.6-6.9 mmol/l): IFG
or
2-h plasma glucose in the 75-g OGTT
140-199 mg/dl (7.8-11.0 mmol/l): IGT
or
A1C 5.7-6.4%
*For all three tests, risk is continuous, extending below the lower limit of a range and becoming
disproportionately greater at higher ends of the range.

• Progression to diabetes among those with
prediabetes is not inevitable. Studies suggest
that weight loss and increased physical activity
among people with prediabetes prevent or delay
diabetes and may return blood glucose levels to
normal.
• People with prediabetes are already at
increased risk for other adverse health
outcomes such as heart disease and stroke.

ADA and AACE/ACE Guidelines:
Treatment Goals for A1C, FPG, and PPG
Parameter
Normal1,2
Level
ADA3
Goal
AACE/ACE2
Goal
FPG, mg/dL <100 90–130 <110
PPG, mg/dL <140 <180 <140
A1C, % 4–6 <7 ≤6.5
FPG=fasting plasma glucose; PPG=postprandial glucose; ADA=American Diabetes Association; AACE=American Association of Clinical Endocrinologists;
ACE=American College of Endocrinology.
1. Adapted from Buse J et al. In: Williams Textbook of Endocrinology. 10th ed. 2003. Permission requested.
2. AACE Diabetes Mellitus Clinical Practice Guidelines Task Force. Endocr Pract. 2007;13:(suppl 1)3–68.
3. ADA. Diabetes Care. 2007;30:S4–S41.
a
The goal for an individual patient is to achieve an A1C as close
to normal (<6%) as possible without significant hypoglycemia.

TESTING FOR DIABETES INTESTING FOR DIABETES IN
ASYMPTOMATIC PATIENTSASYMPTOMATIC PATIENTS

Recommendations: Testing for Diabetes inRecommendations: Testing for Diabetes in
Asymptomatic PatientsAsymptomatic Patients
• Consider testing overweight/obese adults with
one or more additional risk factors
– In those without risk factors, begin testing at age 45
years (B)
• If tests are normal
– Repeat testing at least at 3-year intervals (E)
• Use A1C, FPG, or 2-h 75-g OGTT (B)
• In those with increased risk for future diabetes
– Identify and, if appropriate, treat other CVD risk
factors (B)
ADA. II. Testing in Asymptomatic Patients. Diabetes Care 2011;34(suppl 1):S13-S14.

DETECTION AND DIAGNOSIS OFDETECTION AND DIAGNOSIS OF
GESTATIONAL DIABETES MELLITUSGESTATIONAL DIABETES MELLITUS

Gestational Diabetes Mellitus
• DefinitionDefinition
• Gestational diabetes mellitus (GDM) is defined
as any degree of glucose intolerance with onset
or first recognition during pregnancy.
• Approximately 7% of all pregnancies are
complicated by GDM, resulting in more than
200,000 cases annually. The prevalence may
range from 1 to 14% of all pregnancies,
depending on the population studied and the
diagnostic tests employed.

• The American Diabetes Association released new
guidelines for diagnosing gestational diabetes.
• Women without diabetes will still be tested for
gestational diabetes between weeks 24 and 28.
• But the criteria for gestational diabetes have been
broadened, and more diagnoses of the condition are
expected. Blood glucose cutoff points have been
lowered, and only one test showing high levels is
needed, not two as in the past.
• The new guidelines aim to catch more cases of
gestational diabetes, which can lead to a large baby,
posing risks for both newborn and mother. Gestational
diabetes can also lead to type 2 diabetes.
• Source: Diabetes Care, January 2011

Recommendations:Recommendations:
Detection and Diagnosis of GDMDetection and Diagnosis of GDM
• Screen for undiagnosed type 2 diabetes at the
first prenatal visit in those with risk factors, using
standard diagnostic criteria (B)
• In pregnant women not previously known to
have diabetes, screen for GDM at 24-28 weeks
gestation, using a 75-g OGTT and the diagnostic
cut points.(B)
ADA. III. Detection and Diagnosis of GDM. Diabetes Care 2011;34(suppl 1):S15.

• Low-risk status requires no glucose testing, but
this category is limited to those women meeting
all of the following characteristics:
• Age <25 years
• Weight normal before pregnancy
• Member of an ethnic group with a low
prevalence of GDM
• No known diabetes in first-degree relatives
• No history of abnormal glucose tolerance
• No history of poor obstetric outcome

Screening for and Diagnosis of GDMScreening for and Diagnosis of GDM
• Perform a 75-g OGTT, with plasma glucose
measurement fasting and at 1 and 2 h, at 24-28
weeks of gestation in women not previously
diagnosed with overt diabetes
• Perform OGTT in the morning after an overnight
fast of at least 8 h
• GDM diagnosis: when any of the following
plasma glucose values are exceeded
– Fasting ≥92 mg/dl (5.1 mmol/l)
– 1 h ≥180 mg/dl (10.0 mmol/l)
– 2 h ≥153 mg/dl (8.5 mmol/l)
ADA. III. Detection and Diagnosis of GDM. Diabetes Care 2011;34(suppl 1):S15. Table 6.

• With either approach, the diagnosis of
GDM is based on an OGTT. Diagnostic
criteria for the 100-g OGTT are derived
from the original work of O’Sullivan and
Mahan, modified by Carpenter and
Coustan.
• Alternatively, the diagnosis can be made
using a 75-g glucose load and the glucose
threshold values listed for fasting, 1 h, and
2 h ; however, this test is not as well
validated for detection of at-risk infants or
mothers as the 100-g OGTT.

Detection and Diagnosis of GDMDetection and Diagnosis of GDM
• Screen women with GDM for persistent diabetes
6-12 weeks postpartum (E)
• Women with a history of GDM should have
lifelong screening for the development of
diabetes or prediabetes at least every three
years (E)
ADA. III. Detection and Diagnosis of GDM. Diabetes Care 2011;34(suppl 1):S15.

Management of
Diabetes Mellitus

Nutrition Recommendations
• Carbohydrate
– 60-70% calories from carbohydrates and
monounsaturated fats
• Protein
– 10-20% total calories

Nutrition Recommendations
• Fat
– <10% calories from saturated fat
– 10% calories from PUFA
– <300 mg cholesterol
• Fiber
– 20-35 grams/day
• Alcohol
– Type I – limit to 2 drinks/day, with meals
– Type II – substitute for fat calories

Physical activity
Recommendations
• People with diabetes should be advised to perform at
least 150 min/week of moderate-intensity aerobic
physical activity (50–70% of maximum heart rate). (A)
• In the absence of contraindications, people with type 2
diabetes should be encouraged to perform resistance
training three times per week. (A)

• Exercise is an important part of the diabetes
management plan. Regular exercise has been
shown to improve blood glucose control, reduce
cardiovascular risk factors, contribute to weight
loss, and improve well-being.
• Furthermore, regular exercise may prevent type
2 diabetes in high-risk individuals.
• Structured exercise interventions of at least 8
weeks' duration have been shown to lower A1C
by an average of 0.66% in people with type 2
diabetes, even with no significant change in BMI.

Old and new drugs…
• Combination therapy
• Favorites: metformin, sulfonylureas,
thiazolidinediones
• New classes…
• -DPP4 inhibitors: Sitagliptin and Vildagliptin
(Galvus)
• -GLP-1 agonists: Exenatide and Liraglutide
• -Glitazars: Muraglitazar

Which oral drug to start with?
• Although there are numerous options in oral medications
for type 2 diabetes, an older drug -- metformin -- may be
the best first-line option, according to a new analysis of
research on diabetes medications.
• The analysis included six classes of oral diabetes
medications, and found that all of them lower blood
sugar levels by a similar amount. The authors suggest
that metformin is probably the best first-line choice
because it has fewer side effects than other drugs and,
because it's an older medication and available in a
generic form, it also costs less.

• Metformin………Welcome back?
• Metformin is usually the first oral
medication chosen to treat elevated
blood sugars in Type 2 diabetics. Its
main action is to decrease glucose
production in the liver. It may cause
gastrointestinal upset, such as nausea
and diarrhea, but these effects can be
minimized by starting with a low dose
and increasing gradually. Often,
metformin leads to weight loss which is
usually a beneficial side effect.
• References
• American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Manage
2011
• Medical Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and
• "American Family Physician"; Management of Blood Glucose in Type 2 Diabetes Mellitus; Cynthia
Ripsin
, M.D., Helen Kang, M.D. and Randall Urban, M.D.; January 2009
• Centers for Disease Control and Prevention: National Diabetes Fact Sheet 2007

Why the Interest in Incretins ?

GLP-1 secreted upon
the ingestion of food

78
The Incretin Defect in Type 2
Diabetes
Insulin
Resistance
Incretin
“Defect”
Relative Insulin
Deficiency
Hyperglycemia
Type 2 Diabetes
Incretin effect accounts for up to 70% of the insulin response to oral glucose intake1
1. Holst JJ, Gromada J. Role of incretin hormones in the regulation of insulin secretion in diabetic and nondiabetic humans. Am J
Physiol Endocrinol Metab. 2004;287(2):E199-E206.

DPP4 inhibitors
• Sitagliptin and Vildagliptin
• Incretins are hormones released by the GI tract in response to
nutrient ingestion that stimulate beta cells to secrete insulin—these
effects are diminished in T2DM
• DPP4 is a protease that breaks down the endogenous incretin
glucagon-like peptide (GLP)-1
• This class prevents the degradation of GLP-1 by competitively and
reversibly inhibiting the protease DPP4, and leads to longer
presence and actions of GLP-1
• Side Effects: No weight gain! rare hypoglycemia.
• Both to be used as a combination, both oral. Sitagliptin approved in
2006, Vildagliptin awaiting approval.

GLP-1 agonists
• Exenatide and Liraglutide
• Exogenous GLP-1 products that are resistant to DPP4
degradation, same actions as the endogenous incretin.
• Also known as incretin mimetics.
• Exenatide a 2xd inj. approved 2005 for use with
metformin and/or a sulfonylurea.
• Side effects: hypoglycemia (esp with sulfonylureas),
weight loss.
• Contra: GI dz, renal Cr <30mL/min. Current trials for
once weekly injection.
• Liraglutide is awaiting approval. Has longer half life than
exenatide thus only requiring once daily injections. Same
side effects, no contraindications identified yet.

Glitazars
• Muraglitazar
• Approved by FDA, then withdrawn in Spring 2006. Other trials in this
category are in progress.
• Glitazars activate two subtypes of receptors called peroxisome
proliferator–activated receptors (PPARs).
• PPARgamma activation reduces insulin resistance and improves
glycemic control, while activation of PPARalpha reduces
triglycerides and increases HDL concentration by increasing fatty
acid oxidation.
• Oral dose. Side effects: w. gain, edema, low incidence of coronary
and cerebral vascular events, possible congestive heart failure-FDA
decided it was of enough significance.
• Goodbye Glitazars?Goodbye Glitazars?

Why Insulin in Type 2 Diabetes?

• Studies show that insulin may slow the
progression of diabetes mellitus Type 2
and delay its devastating consequences,
because taking insulin eliminates the
stress that the beta cells of the pancreas
go through to make and release the
hormone.

Insulin Analogs
• Analogs are more predictable and more reliable and
consistent in action. Less chance of hypoglycemia.
• Rapid Acting:
-Humalog (Lispro)
-Novolog (Aspart)
-Apidra (Glulisine)
• Long Acting (Basal):
- Lantus (Glargine)
- Levemir (Detemir)
Mixes: Novolog 70/30 and Humalog 75/25 & 50/50

Insulin
analogs
Regular
insulin
Peak Time = 80 – 120 min
Peak Time = 40 – 50 min
Capillary
membrane
Subcutaneoustissue
Dissociation and Absorption of
Analogs

Glycemic Recommendations for Non-PregnantGlycemic Recommendations for Non-Pregnant
Adults with DiabetesAdults with Diabetes
A1C <7.0%*
Preprandial capillary plasma
glucose
70–130 mg/dl*
(3.9–7.2 mol/l)
Peak postprandial capillary
plasma glucose†
<180 mg/dl*
(<10.0 mmol/l)
*Postprandial glucose measurements should be made 1–2 h after the beginning of the meal,
generally peak levels in patients with diabetes.

• 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
–Hypoglycemia unawareness
–Individual patient considerations
Glycemic Recommendations for Non-Glycemic Recommendations for Non-
Pregnant Adults with DiabetesPregnant Adults with Diabetes

• Postprandial glucose may be targeted if A1C
goals are not met despite reaching preprandial
glucose goals
• More or less stringent glycemic goals may be
appropriate for individual patients

• Metformin for gestational diabetes in routine clinical practice
• J. E. L. Goh1, L. Sadler2, J. Rowan2
• Article first published online: 15 AUG 2011
• © 2011 The Authors. Diabetic Medicine © 2011 Diabetes UK
• Diabetic Medicine
• Volume 28, Issue 9, pages 1082–1087, September 2011
• Keywords:
• gestational diabetes;metformin;pregnancy
• Diabet. Med. 28, 1082–1087 (2011)
• Abstract
• Aims To compare maternal and neonatal outcomes in women with gestational diabetes treated with diet,
metformin and/or insulin in routine clinical practice in a single centre.
• Methods We analysed prospectively collected data from the National Women’s Health database for all
women with gestational diabetes who delivered between January 2007 and December 2009. Since June
2007, women requiring medication have been given a choice of either metformin or insulin treatment, except
women with a fetal abdominal circumference less than the 10th percentile, who were not offered metformin.
• Results There were 1269 women with gestational diabetes; treatment was diet in 371, insulin in 399 and
metformin in 465 (249 metformin alone, 216 metformin and insulin). Women treated with metformin and/or
insulin had significantly higher BMIs compared with those in the diet group (P < 0.001) and had a higher
fasting glucose at diagnosis (p < 0.001). Women treated with insulin had higher rates of Caesarean delivery
(45.6% insulin, 37% metformin, 34% diet, P = 0.02) than women treated with metformin or diet. They also
had higher rates of preterm births (19.2% insulin, 12.5% metformin, 12.1% diet, P = 0.005), customized
large-for-gestational-age infants (18.5% insulin, 12.5% metformin, 12.4% diet, P = 0.02), neonatal
admissions (18.7% insulin, 12.7% metformin, 14.0% diet, P = 0.04) and neonatal intravenous dextrose use
(11.1% insulin, 5.1% metformin, 7.4% diet, P = 0.004). Neonatal outcomes were similar between diet- and
metformin-treated women.
• Conclusions In routine practice, use of metformin in gestational diabetes was
associated with fewer adverse outcomes compared with insulin.

Recommendations: Glucose MonitoringRecommendations: Glucose Monitoring
• Self-monitoring of blood glucose should be
carried out 3+ times daily for patients using
multiple insulin injections or insulin pump
therapy (A)
• For patients using less frequent insulin
injections, noninsulin therapy, or medical
nutrition therapy alone
– SMBG may be useful as a guide to success of
therapy (E)
– However, several recent trials have called into
question clinical utility, cost-effectiveness, of routine
SMBG in non–insulin-treated patients
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S17.

Recommendations: A1CRecommendations: A1C
• Perform A1C test at least twice yearly in patients
meeting treatment goals (and have stable
glycemic control) (E)
• Perform A1C test quarterly in patients whose
therapy has changed or who are not meeting
glycemic goals (E)
• Use of point-of-care testing for A1C allows for
timely decisions on therapy changes, when
needed (E)

A1C <7.0%*
Preprandial capillary plasma
glucose
70–130 mg/dl*
(3.9–7.2 mol/l)
Peak postprandial capillary
plasma glucose†
<180 mg/dl*
(<10.0 mmol/l)
*Postprandial glucose measurements should be made 1–2 h after the beginning of the meal,
generally peak levels in patients with diabetes.

Medical Nutrition Therapy (MNT)Medical Nutrition Therapy (MNT)
• Individuals who have prediabetes or diabetes
should receive individualized MNT as needed to
achieve treatment goals (A)
– For people with diabetes, it is unlikely one optimal mix
of macronutrients for meal plans exists
– The best mix of carbohydrate, protein, and fat
appears to vary depending on individual
circumstances

Look AHEAD (Action for Health in Diabetes):Look AHEAD (Action for Health in Diabetes):
One-Year ResultsOne-Year Results
1. Look AHEAD Research Group. Diabetes Care. 2007;30:1374-1383;
2. Look AHEAD Research Group. Arch Intern Med. 2010;170:1566–1575.
• Intensive lifestyle intervention resulted in1
– Average 8.6% weight loss
– Significant reduction of A1C
– Reduction in several CVD risk factors
• Benefits sustained at 4 years2
• Final results of Look AHEAD to provide insight
into effects of long-term weight loss on important
clinical outcomes

Recommendations: Physical ActivityRecommendations: Physical Activity
• Advise people with diabetes to perform at least
150 min/week of moderate-intensity aerobic
physical activity (50-70% of maximum heart rate)
(A)
• In absence of contraindications, people with type
2 diabetes should be encouraged to perform
resistance training three times per week (A)

Psychosocial Assessment and CarePsychosocial Assessment and Care
• Ongoing part of medical management of
diabetes (E)
• Psychosocial screening/follow-up: attitudes
about diabetes, medical management/outcomes
expectations, affect/mood, quality of life,
resources, psychiatric history (E)
• When self-management is poor, screen for
psychosocial problems: depression, diabetes-
related anxiety, eating disorders, cognitive
impairment (C)

Recommendations: HypoglycemiaRecommendations: Hypoglycemia
• Glucose (15-20 g) is preferred treatment for
conscious individual with hypoglycemia (E)
• Glucagon should be prescribed for all individuals
at significant risk of severe hypoglycemia, and
caregivers/family members instructed in
administration (E)
• Those with hypoglycemia unawareness or one
or more episodes of severe hypoglycemia
should raise glycemic targets to reduce risk of
future episodes (B)

Recommendations: ImmunizationRecommendations: Immunization
• Provide an influenza vaccine annually to all
diabetic patients ≥6 months of age (C)
• Administer pneumococcal polysaccharide
vaccine to all diabetic patients ≥2 years
• One-time revaccination recommended for those
>64 years previously immunized at <65 years if
administered >5 years ago
• Other indications for repeat vaccination:
nephrotic syndrome, chronic renal disease,
immunocompromised states (C)

PREVENTION/DELAY OF TYPE 2 DIABETESPREVENTION/DELAY OF TYPE 2 DIABETES

Prevention/Delay of Type 2 DiabetesPrevention/Delay of Type 2 Diabetes
• Refer patients with IGT (A), IFG (E), or A1C 5.7-
6.4% (E) to support program
– Weight loss 7% of body weight
– At least 150 min/week moderate activity
• Follow-up counseling important (B);
third-party payors should cover (E)
• Consider metformin if multiple risk factors,
especially if hyperglycemia (e.g., A1C>6%)
progresses despite lifestyle interventions (B)
• In those with prediabetes, monitor for development
of diabetes annually (E)
ADA. IV. Prevention/Delay of Type 2 Diabetes. Diabetes Care 2011;34(suppl 1):S16.

PREVENTION AND MANAGEMENT OF
DIABETES COMPLICATIONS

Recommendations: Hypertension/BloodRecommendations: Hypertension/Blood
Pressure ControlPressure Control
Screening and diagnosis
• Measure blood pressure at every routine
diabetes visit
• If patients have systolic blood pressure
≥130 mmHg or diastolic blood pressure ≥80
mmHg
– Confirm blood pressure on a separate day
– Repeat systolic blood pressure ≥130 mmHg or
diastolic blood pressure ≥80 confirms a diagnosis of
hypertension (C)
ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S27.

Goals
• A goal systolic blood pressure <130 mmHg is
appropriate for most patients with diabetes (C)
• Based on patient characteristics and response
to therapy, higher or lower systolic blood
pressure targets may be appropriate (B)
• Patients with diabetes should be treated to a
diastolic blood pressure <80 mmHg (B)

Treatment
Lifestyle therapy for hypertension
– Weight loss if overweight
– DASH-style dietary pattern including reducing sodium,
increasing potassium intake
– Moderation of alcohol intake
– Increased physical activity (B)

Treatment
Pharmacologic therapy for patients with diabetes and
hypertension
– Pair with a regimen that includes either an ACE inhibitor
or angiotensin II receptor blocker
– If one class is not tolerated, the other should be
substituted
• If needed to achieve blood pressure targets
– Thiazide diuretic should be added to those with
estimated GFR ≥30 ml x min/1.73 m2
– Loop diuretic for those with an estimated GFR <30 ml x
min/1.73 m2
(C)

Treatment
Multiple drug therapy (two or more agents at
maximal doses)
– Generally required to achieve blood pressure targets
(B)
• If ACE inhibitors, ARBs, or diuretics are used
– Kidney function, serum potassium levels should be
monitored (E)

Dyslipidemia/Lipid ManagementDyslipidemia/Lipid Management
Screening
• In most adult patients
– Measure fasting lipid profile at least annually
• In adults with low-risk lipid values (LDL
cholesterol <100 mg/dl, HDL cholesterol >50
mg/dl, and triglycerides <150 mg/dl)
– Lipid assessments may be repeated every 2 years (E)

Treatment recommendations and goals
• To improve lipid profile in patients with diabetes,
recommend lifestyle modification (A), focusing
on
– Reduction of saturated fat, trans fat, cholesterol
intake
– Increased n-3 fatty acids, viscous fiber,
plant stanols/sterols
– Weight loss (if indicated)
– Increased physical activity

• Statin therapy should be added to lifestyle
therapy, regardless of baseline lipid levels, for
diabetic patients:
– with overt CVD (A)
– without CVD who are >40 years of age and have one
or more other CVD risk factors (A)

• For patients at lower risk (e.g., without overt
CVD and <40 years of age) (E)
– Statin therapy should be considered in addition to
lifestyle therapy if LDL cholesterol remains >100
mg/dl
– In those with multiple CVD risk factors

• In individuals without overt CVD
– Primary goal is an LDL cholesterol
<100 mg/dl (2.6 mmol/l) (A)
• In individuals with overt CVD
– Lower LDL cholesterol goal of <70 mg/dl
(1.8 mmol/l), using a high dose of a statin, is an
option (B)

• If targets not reached on maximal tolerated statin
therapy
– Alternative therapeutic goal: reduce LDL cholesterol
~30–40% from baseline (A)
• Triglyceride levels <150 mg/dl (1.7 mmol/l), HDL
cholesterol >40 mg/dl (1.0 mmol/l) in men and >50
mg/dl (1.3 mmol/l) in women, are desirable
– However, LDL cholesterol–targeted statin therapy
remains the preferred strategy (C)

• If targets are not reached on maximally tolerated
doses of statins
– Combination therapy using statins and other lipid
lowering agents may be considered to achieve lipid
targets
– Has not been evaluated in outcome studies for either
CVD outcomes or safety (E)
• Statin therapy is contraindicated in pregnancy

Antiplatelet AgentsAntiplatelet Agents
• Consider aspirin therapy (75–162 mg/day) (C)
– As a primary prevention strategy in those with type 1
or type 2 diabetes at increased cardiovascular risk
(10-year risk >10%)
– Includes most men >50 years of age or women >60
years of age who have at least one additional major
risk factor
• Family history of CVD
• Hypertension
• Smoking
• Dyslipidemia
• Albuminuria

• Aspirin should not be recommended for CVD
prevention for adults with diabetes at low CVD
risk, since potential adverse effects from
bleeding likely offset potential benefits (C)
• 10-year CVD risk <5%: men <50 and women <60
years of age with no major additional CVD risk factors
• In patients in these age groups with multiple
other risk factors (e.g., 10-year risk 5%-10%)
clinical judgment is required (E)

• Use aspirin therapy (75–162 mg/day)
– Secondary prevention strategy in those with diabetes
with a history of CVD (A)
• For patients with CVD, documented aspirin
allergy
– Clopidogrel (75 mg/day) should be used (B)
• Combination therapy with ASA (75–162 mg/day)
and clopidogrel (75 mg/day)
– Reasonable for up to a year after an acute coronary
syndrome (B)

Coronary Heart Disease TreatmentCoronary Heart Disease Treatment
• To reduce risk of cardiovascular events in
patients with known CVD, use
– ACE inhibitor(C)
– Aspirin (A)
– Statin therapy (A)
• In patients with a prior MI
– Beta-blockers should be continued for at least 2 years
after the event (B)
*If not contraindicated.

Coronary Heart Disease TreatmentCoronary Heart Disease Treatment
• Longer-term use of beta-blockers in the absence
of hypertension
– Reasonable if well tolerated, but data are lacking (E)
• Avoid TZD treatment
– In patients with symptomatic heart failure (C)
• Metformin use in patients with stable CHF
– Indicated if renal function is normal
– Should be avoided in unstable or hospitalized patients
with CHF (C)

Recommendations: NephropathyRecommendations: Nephropathy
• To reduce risk or slow the progression of
nephropathy
– Optimize glucose control (A)
– Optimize blood pressure control (A)

Nephropathy ScreeningNephropathy Screening
• Assess urine albumin excretion annually (E)
– In type 1 diabetic patients with diabetes duration of 5
years
– In all type 2 diabetic patients at diagnosis
• Measure serum creatinine at least annually (E)
– In all adults with diabetes regardless of degree of
urine albumin excretion
– Serum creatinine should be used to estimate GFR
and stage level of chronic kidney disease, if present

Nephropathy TreatmentNephropathy Treatment
• Nonpregnant patient with micro- or macroalbuminuria
– Either ACE inhibitors or ARBs should be used (A)

• In patients with type 1 diabetes, hypertension,
and any degree of albuminuria
– ACE inhibitors have been shown to delay progression
of nephropathy (A)
and microalbuminuria
– Both ACE inhibitors and ARBs have been shown to
delay progression to macroalbuminuria (A)
ADA. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S33.

macroalbuminuria, and renal insufficiency
(serum creatinine >1.5 mg/dl)
– ARBs have been shown to delay progression of
nephropathy (A)
• If one class is not tolerated, the other should be
substituted (E)

Definitions of Abnormalities in Albumin ExcretionDefinitions of Abnormalities in Albumin Excretion
Category
Spot collection
(µg/mg creatinine)
Normal <30
Microalbuminuria 30-299
Macroalbuminuria (clinical) ≥300
ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S34. Table 13.

Recommendations: RetinopathyRecommendations: Retinopathy
• To reduce risk or slow progression of retinopathy
– Optimize glycemic control (A)
– Optimize blood pressure control (A)

• FACTS
• Diabetic retinopathy is the leading cause of vision loss in
adults of working age (20 to 65 years) in industrialised
countries. It is estimated that more than 2.5 million
people worldwide are affected by it.
• 74 percent of people who have diabetes for 10 years or
more will develop some form of diabetic retinopathy.
• Approximately 14 per cent of people with diabetes have
diabetic macular oedema and prevalence increases to
29 per cent for people with diabetes who use insulin for
more than 20 years.
• Left untreated, 25 per cent of people with diabetic
macular oedema will develop moderate vision loss within
three years.
• Estimates of the rate of annual eye exams vary greatly
by country and study, but the rate of screening is
generally fairly low (from 40 to 65 percent).

Retinopathy ScreeningRetinopathy Screening
• Initial dilated and comprehensive eye
examination by an ophthalmologist or
optometrist
– Adults and children aged 10 years or older with type 1
diabetes
• Within 5 years after diabetes onset (B)
– Patients with type 2 diabetes
• Shortly after the diagnosis of diabetes (B)

• Subsequent examinations for type 1 and type 2
diabetic patients
– Should be repeated annually by an ophthalmologist or
optometrist
• Less frequent exams (every 2–3 years)
– May be considered following one or more normal eye
exams
• More frequent examinations required if
retinopathy is progressing (B)

• High-quality fundus photographs
– Can detect most clinically significant diabetic
retinopathy
• Interpretation of the images
– Performed by a trained eye care provider
• While retinal photography may serve as a
screening tool for retinopathy, it is not a
substitute for a comprehensive eye exam
– Perform comprehensive eye exam at least initially
and at intervals thereafter as recommended by an
eye care professional (E)

Neuropathy Screening, TreatmentNeuropathy Screening, Treatment
• All patients should be screened for distal
symmetric polyneuropathy (DPN)
– At diagnosis
– At least annually thereafter using simple clinical tests
(B)
• Electrophysiological testing rarely needed
– Except in situations where clinical features are
atypical (E)

DIABETES CARE IN SPECIFIC POPULATIONS

PediatricPediatric
Glycemic ControlGlycemic Control
• Consider age when setting glycemic goals in
children and adolescents with diabetes (E)
ADA. VII. Diabetes Care in Specific Populations. Diabetes Care. 2011;34(suppl 1):S38.

Recommendations: Older AdultsRecommendations: Older Adults
• Functional, cognitively intact older adults with
significant life expectancies should receive
diabetes care using goals developed for younger
adults (E)
• Glycemic goals for those not meeting the above
criteria may be relaxed using individual criteria,
but hyperglycemia leading to symptoms or risk
of acute hyperglycemic complications should be
avoided in all patients (E)
ADA. VII. Diabetes Care in Specific Populations. Diabetes Care. 2011;34(suppl 1):S42.

DIABETES CARE IN SPECIFIC SETTINGS

Diabetes Care in the HospitalDiabetes Care in the Hospital
• All patients with diabetes admitted to the hospital
should have
– Their diabetes clearly identified in the medical record
(E)
– An order for blood glucose monitoring, with results
available to the health care team (E)
ADA. VIII. Diabetes Care in Specific Settings. Diabetes Care. 2011;34(suppl 1):S43.

• Goals for blood glucose levels
– Critically ill patients: 140-180 mg/dl
(10 mmol/l) (A)
– More stringent goals, such as 110-140 mg/dl (6.1-7.8
mmol/l) may be appropriate for selected patients, if
achievable without significant hypoglycemia (C)
– Non-critically ill patients: base goals on glycemic control,
severe comorbidities (E)

• Initiate glucose monitoring in any patients not
known to be diabetic who receives therapy
associated with high risk for hyperglycemia (B)

• A hypoglycemia management protocol should
be adopted and implemented by each hospital
or hospital system
– Establish a plan for treating hypoglycemia for each
patient; document episodes of hypoglycemia in
medical record and track (E)
• Obtain A1C for all patients if results within
previous 2-3 months unavailable (E)
• Patients with hyperglycemia who do not have a
diagnosis of diabetes should have appropriate
plans for follow-up testing and care documented
at discharge (E)ADA. VIII. Diabetes Care in Specific Settings. Diabetes Care. 2011;34(suppl 1):S43.

Goals of Inpatient DM Management
• “Avoid hypoglycemia and marked hyperglycemia”
• Target Blood sugar: 7.0 - 11.0 mmol/l
• Avoid Hypoglycemia
• Precipitating arrhythmia or other cardiac events
• Inducing seizure, focal or cognitive defects periop
• Avoid Marked Hyperglycemia (BS > 11.1 mM)
• Treat (and avoid) DKA, HONC

DM Inpatient Management
1. Eating
2. NPO: temporary (for a test or surgery)
3. NPO: prolonged

1. Eating
Diet (T2DM)
OHA (T2DM)
Insulin (T2DM and T1DM)
2. NPO: temporary (for a test or surgery)
3. NPO: prolonged

Guideline for Insulin Adjustments
1. Adjust the insulin that accounts for the high or low
reading.
2. Always compare an abnormal BS reading with the one
previous.
3. If insulin dose is:
• Less than 8U, adjust by 1U
• 8-20U, adjust by 2U
• > 20 U, adjust by 10% (increase), 20% (decrease)

1. Eating
2. NPO: temporary (for a test)
3. NPO: prolonged

NPO for a test:
T2DM on Diet or OHA
• Schedule test for the AM
• Hold OHAs on AM of test
• CBG @ 7AM:
< 3.0 Consider postpone test
3.1-4.0 IV 5%DA @ 75-100 ml/h
4.1-11.0 Proceed with test, no Rx necessary
> 11.1 Insulin R or analogue SC supplemental
or
IV insulin & IV 5%DA @ 75-100 cc/h
> 20.0 Check urine ketones, consider postpone test

Insulin IV drip
• Add 50 U of regular insulin to 500 ml 5%DA
(1U/10cc).
• Start insulin @ 0.9 U/h (9ml/h) or start at a
rate dependent on patient’s insulin dose:
IV insulin gtt rate = ( ½ TDD ) / 24

1. Eating
2. NPO: temporary (for a test)
3. NPO: prolonged
• Patient put on D5W if not on feeds or TPN
• IV insulin drip
• SC NPH or UL q12h (+/- supplemental scale)
» Starting dose 0.2 U/Kg q12h

Newer Directions
• The role of Dopamine in type 2 Diabetes
• The use of constant glucose monitors
(CGMS).

Proposed mechanism of action of Bromocriptine
in relation to type 2 DM
• Diabetes patients may have low morning levels of hypothalamic dopamine,
which is thought to lead to hyperglycemia and dyslipidemia
• CYCLOSET (special form of bromocriptine) is thought to reset aberrant low
morning hypothalamic dopaminergic activity, which may reset
neuroendocrine metabolic control
Meier, Diabetes Reviews 2010: 476-487
Decreased
lipolysis in
adipose tissue
Decreased
postprandial
hepatic glucose
output
Decreased insulin
resistance

Glucose Fluctuations Are Not Adequately
Measured by A1C
Type 1 diabetes, N = 9
24-h CGMS glucose sensor data
Data on file, Amylin Pharmaceuticals, Inc.
100
200
300
400
12 AM 4 AM 8 AM 12 PM 4 PM 8 PM 12 AM
Glucose
Concentration
(mg/dL)
0
Mean A1C = 6.7%

Constant Glucose Monitoring Devices
(CGMS)

Match the Insulin to the Site
• Fast acting insulin can be injected into any
approved site.
• If injecting regular insulin, the abdomen
should be used.
• NPH should be injected into the thigh or
buttock.

A Straight Shot is Best
• On an angle or straight-in – patients have
been told to inject both ways.
So which won?
• Straight-in, in almost all cases. No skin
fold (pinch), use 90 degree—but if you
use a skin fold, you should angle your
injection.

A summary of the
Clinical Practice Recommendations as stated by the
American Diabetes Association and WHO in 2011
• “Transitions in care for youth with diabetes” was added.
• A section titled “Monogenic forms of diabetes” was
added.
• The use of the 75-g oral glucose tolerance test and new
diagnostic criteria was revised in the section titled
“Detection and diagnosis of gestational diabetes
mellitus”.
• “Prevention/Delay of Type 2 Diabetes”, the
hypertension/BP control text was revised to incorporate
new evidence reinforcing the importance of
individualization of BP goals.
• “Children and Adolescents”, the text was revised to
remove lower limits on A1C targets and to include
discussion on appropriate individualization and safety.

ADA Evidence Grading System for ClinicalADA Evidence Grading System for Clinical
RecommendationsRecommendations
Level ofLevel of
EvidenceEvidence DescriptionDescription
A Clear or supportive evidence from adequately powered
well-conducted, generalizable, randomized controlled
trials Compelling nonexperimental evidence
B Supportive evidence from well-conducted cohort studies
or case-control study
C Supportive evidence from poorly controlled or
uncontrolled studies
Conflicting evidence with the weight of evidence
supporting the recommendation
E Expert consensus or clinical experience
ADA. Diabetes Care 2011;34(suppl 1):S12. Table 1.

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