Transcript Diabetes Update

Gutman Diabetes Institute
Einstein Medical Center, Philadelphia
Patricia C. Adams, RN, CDE
Gutman Diabetes Institute
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Distinguish the different types of diabetes
Discuss appropriate administration of insulin
Discuss prevention and treatment of
hypoglycemia
Review of ADA recommendations for antipsychotic drugs and obesity
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Diabetes - Epidemic Proportions
Glucose Toxicity
◦ 25.8 million Americans (8.3% of
population)
◦ 18.8 million have been diagnosed
◦ 7.0 million are unaware they have the
disease
Lipid Toxicity
http://www.cdc.gov/diabetes/pubsaccessed 3/8/2011
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‣ Areas Requiring Control
‣ Glycemic Control
‣ A1C < 7% (ADA Standards)
‣
< 6.5% (AACE Standards)
‣ Blood Pressure Control
‣ Goal is 130/80
‣ ACE vs ARB; Diuretics
‣ Lipid Management
‣ Statins
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Lipids
◦ Total Cholesterol < 200
◦ HDL > 45 (Men) > 55 (Women)
◦ LDL < 100; <70 (Hx of cardiac disease)
◦ Triglycerides (Tg) < 150
Aspirin (81 – 325) mg daily >21 yrs)
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Treatment recommendations and goals
 Statin therapy should be added to lifestyle
therapy, regardless of baseline lipid levels,
for diabetic patients:
◦ with overt CVD (A) / LDL < 70
◦ without CVD who are >40 years of age and have
one or more other CVD risk factors (A) / LDL < 100
ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S29.
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Type 1
◦ Approximately 5%
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Type 2
◦ Approximately 95%
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Gestational
◦ 7 – 14% of all pregnancies
◦ 5 – 10% have type 2 following delivery
◦ 20 – 50% chance of developing diabetes in the next
5 – 10 years
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Diabetes
Normal
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A1C > 6.5%
FPG> 126 mg/dl
OGTT > 200 mg/dl
(75g glucose load)
RPG > 200 mg/dl
with symptoms of
hyperglycemia
PreDiabetes

> 126
mg/dl
< 126
mg/dl
Diabetes
> 100 mg/dl
< 100 mg/dl
70 mg/dl
Diabetes Care, Clinical Practice Recommendations, 2011
Criteria for Testing for Diabetes in
Asymptomatic Adult Individuals
1.
Testing should be considered in all adults who are overweight (BMI
≥25 kg/m2*) and have additional risk factors:
• 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.
ADA. Testing in Asymptomatic Patients. Diabetes Care 2011;34(suppl 1):S14. Table 4.
•
2 – 3 fold increased mortality rate associated
with physical illness
• Most common cause of death – CVD
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More likely to be overweight, smoke, inactive
More likely to have family hx diabetes,
Limited access to primary care, cardiovascular
risk screening
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Baseline monitoring at initiation of
antipsychotic medications
◦ Personal/family hx diabetes, obesity, dislipidemia,
hypertension, CVD
◦ Calculate BMI
◦ Waist circumference
◦ BP, Fasting blood glucose, Fasting Lipid profile
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Interval monitoring
◦ 4, 8, & 12 weeks after initiation of therapy
◦ Weight gain > 5% consider change in therapy
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Consideration of metabolic risks when
starting SGAs
Patient, family, and care giver education
Baseline screening
Regular monitoring
Refer to specialized services, when needed
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Pancreas
Muscle
Insulin
Secretion
Release of
GIP &
GLP - 1
Intestine:
Glucose
Absorption
+
BLOOD GLUCOSE
+
Brain &
Nervous System
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+
Fat
Peripheral
Glucose
Uptake
Type 1 Diabetes
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Initially little insulin
production
Evolves into no
insulin production
Exogenous insulin
required daily
Auto-immune
response
Genetic component
5 - 10% prevalence
Type 2 Diabetes
◦ Slow, Insidious
◦ 6.5 years to manifest
as elevated FBG
◦ Elevated postprandial
blood glucose levels
◦ Damage vessel
endothelium
◦ Insulin Resistance
◦ Beta Cell
Deterioration
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Type 1
Type 2
Age of Onset
Usually <30
Usually >40
Onset
Rapid
Slowly - years
Insulin
Availability
Little to None
Some
•Progressive
Usually present
Insulin Resistance Develops w/Time
Treatment
Complications
Exogenous insulin
always needed
•Daily injections
Develop w/Time
MNT, Activity,
Oral Agents,
Insulin
Present at Dx
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Genes
Genes
Impaired insulin
secretion
Insulin
resistance
± Environment
IGT
IGT
Type 2 diabetes
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Genes
Vs.
Jeans
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Normal
Impaired
glucose
tolerance
Type 2
diabetes
Late type 2
diabetes
complications
Insulin
sensitive
Hyperglycaemia
Normal insulin
secretion
Insulin
resistance
Normoglycaemia
β-cell
exhaustion
Insulin resistance
Fasting plasma glucose
Insulin sensitivity
Insulin secretion
Adapted from Bailey CJ et al. Int J Clin Pract 2004;58:867–876.
Groop LC. Diabetes Obes Metab 1999;1 (Suppl. 1):S1–S7.
How Do Oral Diabetes Medicines Work?
Secretagogues
Increase insulin
secretion
Glyburide Glipizide
Glimepiride
Repaglinide
Nateglinide
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Biguanides
Glucosidase
Inhibitors
TZD’S
DPP IV
Inhibitors
Increase insulin
action
Decrease hepatic
glucose
Decrease breakdown
of GLP-1- increase
insulin secretion
Slow glucose
absorption
Metformin
Metformin XR
Metformin/Glyburide
Pioglitazone
Rosiglitazone
Acarbose
Miglitol
Sitaglipton
Saxaglipton
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Basal
 Amount needed to prevent excess
gluconeogenesis and ketogenesis
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Prandial
 Amount needed to cover discrete meals and/or
nutritional supplements
 Tube Feedings, IV dextrose, TPN
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 Regular
 NPH
 70/30
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Humalog (Lispro)
Humalog Mix 75/25
NovoLog (Aspart)
NovoLog Mix 70/30
Apidra (Glulisine)
Lantus (Glargine)
Levemir (Detemir)
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Novolog u100: _____
units with 1st meal
______units with 2nd meal
______units with 3rd meal
@_____
@_____
@_____
Lantus u100 :
_____ units in the morning @_____
0
1
2
3
1
4
5
6
2
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
3
_____
Hours of sleep:
_____
_____
23
24
1
Sleeping
Meal times:
22
______________
Premix (cloudy)
Short acting insulin
0
1
2
3
4
5
6
7
8
Intermediate acting insulin
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
Insulin type: Human u100 Premix R & NPH
Onset (Begins to work)
½ - 1 hour
following injection
Peak action (Works the strongest)
Dual
following injection
Effective duration
following injection
Actual maximum duration
10-16 hrs
24
Type
Starts
Peaks
Ends
Lispro
(Humalog)
5 min.
60 min.
3 – 4 hr.
Aspart
(Novolog)
5 min.
60 min.
3 – 5 hr.
Glulisine
(Apidra)
5 min.
60 min.
3 – 4 hr.
Regular
30 – 60 min.
2 – 4 hr.
6 – 8 hr.
NPH
1.5 hours
4 – 12 hr.
10 – 16 hr.
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Type
Starts
Peaks
Ends
Glargine
(Lantus)
4 – 6 hr.
None
24 hr.
Levemir
(Detemir)
< 2 hr.
3 – 14 hr
16 – 24 hr.
70/30
0.5 – 1.0 hr.
Dual (NPH/R)
12 – 20 hr.
Mix 75/25
10 min.
Dual (Lispro/Lispro
12 – 20 hr.
Protamine)
Mix 70/30
10 min.
Dual
(Aspart/Aspart
Protamine)
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12 – 20 hr.
70/30 – 30 minutes prior to meal
 Regular – 20 to 30 minutes prior to
meal
 NPH – 20 to 30 minutes prior to meal
 Aspart- 5 – 10 minutes prior to meal
 Lispro- 5 – 10 minutes prior to meal
 Apidra - 5 – 10 minutes prior to meal
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Glucose Level
Insulin Peak action
0
1
3
2
Time in Hours
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4
Glucose Level
Hypoglycemia
Hyperglycemia
Insulin Peak Action
0
1
3
2
Time in Hours
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4
Basal insulin
You wouldn’t hold
the pancreas, so
don’t hold the
lantus
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Without insulin, in
an insulin deficient
individual, blood
glucose will
increase passively
by as much as 45
mg/dl per hour
even in the
absence of food.
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A1C
<7.0%*
Preprandial capillary plasma 70–130 mg/dl*
glucose
(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.
ADA. V. Diabetes Care. Diabetes Care 2011;34(suppl 1):S21. Table 10.
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Hyperglycemia needs to be controlled.
◦ Any glucose excursion causes endothelial damage
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Don’t relax with one good glucose reading
Need to look at trends over 24 – 48 hours
Need basal and prandial insulin coverage
Rare to withhold basal insulin
Insulin sliding scales do not work alone!
◦ Reactive vs proactive
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DM medication given
too early
DM medication dosage
too high
Meals delayed or not
eaten
Problems
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Give DM medication at
right time
Advocate for
adjustment of
medication
Offer food when
appropriate
Nursing solutions
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“Test don’t Guess”
Anything under 70 mg/dl is hypoglycemia
Treat
◦ 16 grams of carbohydrate – “fast acting”
 Glucose gel – 15 grams
 Glucose Tabs –4
 ½ cup juice or regular soda
◦ Wait 15 minutes, - retest
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500
450
400
350
300
250
200
150
100
50
0
Patient
Carbs
1:00 3:00 5:00 7:00 11:00 3:00 5:00 9:00 11:00
AM AM AM AM AM PM PM PM PM
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No longer a diabetic diet (ADA)
◦ Currently Carb Controlled
Requires Individualization
Need for Consistent Carbohydrates
◦ Some sweets OK
Meals – 4.5to 5 Hours Apart
Divide Protein and Fats
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Consume Fewer Animal Fats
Emphasize Low Fat Dairy Products
Emphasize Monounsaturated Fats
Emphasis upon Fiber
Decrease Use of Sweets
Decrease Use of Alcohol
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The Plate Method
The Plate Method is an easy to remember technique for meal planning.
This method recommends a healthy distribution of carbohydrates, a lower fat intake, and a greater amount of fruits and
vegetables. It can be used to eat healthfully, lose weight, and/or manage your diabetes.
Fill a quarter of
your plate with
starch or bread
Fill half
your plate
up with
non
starchy
vegetables
Fill a
quarter of
your plate
with
protein
(choose
lean cuts)
To learn more about how meal planning can help prevent or manage your diabetes,
contact the Gutman Diabetes Institute, 215-456-6839 or [email protected]
Source: National
Diabetes Education
Program
Even Light Juice
Cocktail Contains
˜ 8 gm CHO
No Sugar Free Juices
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Non-nutritive sweeteners are OK
Sugar contains 4 kcal/gm
Sugar alcohols contain  2-3 kcal/gm
◦ End in “ol”
◦ May contain more carbohydrate than
regular item
◦ Need to read the label
◦ Can cause diarrhea
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Role of Physical Activity
◦ 150 mins / week; most days of the week
Cells More Receptive to Insulin
◦ Decreases Insulin Resistance
◦ Lowers Blood Glucose
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Integral Part of Diabetes Management
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Precipitating Factors
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Infection
Insulin Omission
Inadequate Amount of Insulin
Newly Diagnosed Diabetes
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Clinical Features
◦ Hyperglycemia - >250 mg/dL
◦ Ketonuria or ketonemia
◦ Acidosis
 pH <7.3
 and/or serum bicarb <15 mEq/L
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 Absence
or reduced effect of
insulin
 Excess of counter regulatory
hormones
◦
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◦
Glucagon
Cortisol
Growth hormone
Catecholemines
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Clinical Presentation
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Presence of Acidosis
Abdominal Pain
◦ Nausea
◦ Vomiting
◦ Anorexia
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Clinical Presentation
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Hyperglycemia 3 – 4 Days
Metabolic Alterations < 24 Hours
Respiratory Symptoms
◦ Kussmaul Respirations
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Lab Values
 Glucose > 600 mg/dl
 No Ketones or Only Small Amounts
 Plasma Osmolality > 320 mOsm/kg
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DKA
HHS
Mild
Moderate
Severe
250
>250
.250
>600
7.25-7.30
7.00-7.24
<7.00
>7.30
15-18
10-15
<10
>15
Urine
Ketones
+
+
+
small
Serum
Ketones
+
+
+
small
Anion Gap
>10
>12
>12
<12
Mentation
Alert
Alert/Drowsy
Stupor/Coma
Glucose
pH
BiCarb
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