Download Type 2 Diabetes Mellitus

Drug Therapy for Diabetes Mellitus
Drug Therapy in Diabetes Mellitus: Learning objectives
1
Overview:
prevalence, types,
pathology, S/S, patient &
disease characteristics
Diabetes: a global problem for the 21st century
overview
• Diabetes mellitus
– Greek word “fountain”
– Latin word “honey”
• Primarily a disorder of carbohydrate metabolism
– Deficiency of insulin
– Resistance to action of insulin
– Both of which lead to hyperglycemia and glucosuria
• But protein and lipid metabolism are also affected
• Demographics:
– Global epidemic: 10% of the world’s adult population
has T2DM
– Risk factors are not consistent around the world
– very expensive in real terms and in human costs
– 21st century challenge
Diabetes: a global problem for the 21st century
prevalence of diabetes increasing world -wide
Types of Diabetes Mellitus
•
•
•
•
•
Type 1 diabetes
Type 2 diabetes
Gestational diabetes
Other
Basic similarities
– All types of diabetes mellitus are primarily a disorder of
carbohydrate metabolism (regulation of blood glucose levels) but
protein and lipid metabolism are also affected
– T1DM and T2DM have same long-term complications
– For T1DM and T2DM, insulins are increasingly used to manage
both
• Different etiologies
– Can manifest differently at time of diagnosis
– Early in the course of the disease, T1DM and T2DM are managed
somewhat differently
Type 1 Diabetes Mellitus
• 5% to 10% of all cases
• Rate is consistent world-wide
• Autoimmune disease
—Primary defect is destruction of pancreatic beta cells
oInitially, inadequate levels of insulin are produced
oEventually, insulin release from pancreas ceases entirely
—Symptom onset is relatively abrupt
—Most commonly develops before age 30 years, but may
develop at any age
—Trigger for this immune response is not entirely known, but
genetic, environmental, and infectious factors likely play a role
• Risk of DKA, diabetic ketoacidosis, if sustained hyperglycemia
• Now referred to as “Type 1 Diabetes (Mellitus)”, T1DM
—Historically: T1DM developed in childhood/ adolescence,
“juvenile-onset diabetes mellitus”, fatal before insulin
—Later referred to as “insulin-dependent diabetes mellitus” (IDDM)
Type 1 Diabetes Mellitus
• Characterized by Impaired or absent ß cell
function:
–  insulin secretion
• However, there is normal insulin responsiveness
and effect on cells:
–  insulin sensitivity
• Results in unacceptable blood glucose control,
which requires insulin replacement for survival
www.diabetesclinic.ca
8
Type 2 Diabetes Mellitus
• 90% to 95% of all cases
— Affects approximately 22 million Americans; 8.3% US popl’n
— Most commonly develops in adulthood, but may develop in
childhood, especially in obese pre-teens and adolescents
— Progressive disease
• T2DM characterized by:
— “insulin resistance”
i. Reduced binding of insulin to its receptors on target cells
ii. Fewer insulin receptors
iii.Cell response is reduced when insulin binds to receptor
As a result of insulin resistance, target tissues (liver, muscle,
adipose) are less able to bring glucose into cells and utilise
the glucose to produce energy
— Early in the disease, hyperinsulinemia is common (but insulinreceptor binding doesn’t induce the normal response)
— Later, as pancreatic beta cells “wear out”, impaired insulin
production and secretion develops. The patient then begins a
pattern much like T1DM.
Type 2 Diabetes Mellitus
• Risk factors which increase risk of developing T2DM:
o
o
o
o
o
o
o
o
o
Overweight/obesity
Fat distribution primarily in abdomen (“apple” shape)
Inactivity/ sedentary lifestyle
Family history
Strong ethnic associations (Blacks, Hispanics, Asian Americans,
Native Americans, Alaska Natives, Pacific Islanders)
Age over 45 years (but T2DM is also increasing dramatically
among children, adolescents and younger adults)
Prediabetes
History of gestational diabetes (or a baby born > 9 pounds)
Polycystic ovary syndrome, PCOS
(List from http://www.mayoclinic.org/
• Now referred to as “Type 2 Diabetes Mellitus”, T2DM
— Historically: T2DM developed in adulthood, “adult-onset diabetes
mellitus” and then later referred to as “non-insulin-dependent
diabetes mellitus “ (NIDDM)
Type 2 Diabetes Mellitus:
Double Impairment
• Characterized by Impaired ß cell function:
–  insulin secretion
• AND Impaired insulin action:
–  insulin resistance
• Results in unacceptable blood glucose control
www.diabetesclinic.ca
12
Gestational Diabetes
Develops in pregnant woman during the pregnancy (4% )
Diabetic state usually resolves almost immediately after
delivery
If diabetic state persists beyond delivery, it is no longer
considered gestational, and should be rediagnosed and
treated accordingly
Managed in much the same manner as a diabetic woman who
becomes pregnant Except all newly diagnosed diabetics need
tremendous support, education, guidance, mentorship
 Blood glucose should be monitored closely (checking BG 6-7
times daily), and BG managed using insulin
 Proper glucose levels are needed in the pregnant patient and
in the fetus
 Hyperglycemia and hyperinsulinism are unhealthy and
teratogenic to the fetus
 Fetal death frequently occurs near term
 Earlier delivery is desirable
14
2Complications
T1DM and T2DM have the same complications
• Short-term
– Hyperglycemia
– Hypoglycemia
• Long-term
– Macrovascular
– Hypertension
– Microvascular
S/S of Hyperglycemia: BG greater than 180 mg/dL.
http://www. http://www.mayoclinic.org/diseases-conditions/hyperglycemia/basics/symptoms/con-20034795
Hyperglycemia doesn't cause symptoms until glucose values are
significantly elevated — above 200 mg/dL
Symptoms of hyperglycemia develop slowly over several days or weeks.
The longer blood sugar levels stay high, the more serious the symptoms
become. However, some people who've had type 2 diabetes for a long
time may not show any symptoms despite elevated blood sugars.
Early signs and symptoms
• Frequent urination
• Increased thirst
• Blurred vision
• Fatigue
• Headache
Later signs and symptoms
If hyperglycemia goes untreated, it can cause
toxic acids (ketones) to build up in blood and
urine (ketoacidosis). Signs and symptoms
include:







Fruity-smelling breath
Nausea / vomiting
Shortness of breath
Dry mouth
Weakness, Confusion
Coma
Abdominal pain
S/S of Hypoglycemia: BG less than 70 mg/dL
http://www.diabetesforecast.org/2013/aug/signs-of-hypoglycemia.html
Milder symptoms
• Shakiness, tremor
• Nervousness or anxiety
• Sweating, chills, and clamminess
• Irritability or impatience
• Confusion
• Rapid/fast heartbeat, palpitations
• Light-headedness or dizziness
• Hunger and nausea
• Color draining from the skin (pallor)
• Sleepiness
• Blurred/impaired vision
• Tingling or numbness in lips/ tongue
• Headaches
• Weakness or fatigue
• Anger, sadness, or stubbornness
• Lack of coordination, clumsiness
• Nightmares or crying out during sleep
• Bizarre behavior
• Seizures, convulsions
• Unconsciousness
death
Most severe
Treat Hypoglycemia: usually BG less than 70 mg/dL
Source: American Diabetes Association
 Glucose tablets (15–20 g) is the preferred
treatment for the conscious individual,
although any form of simple carbohydrate
may be used (juice, table sugar).
 If swallowing reflex or gag reflex is
suppressed: nothing should be given by mouth
 Fifteen minutes after treatment,
if SMBG shows continued hypoglycemia,
the treatment should be repeated.
 Once SMBG returns to normal, the
individual should consume a meal or snack
to prevent recurrence of hypoglycemia.
4g/ tablet
Severe Hypoglycemia is very serious:
loss of consciousness may occur.
• Hypoglycemic emergency: “Diabetic shock” (sometimes called
“insulin shock”). Symptoms include fatigue, light-headedness or
fainting, weakness, convulsions, potentially coma, and often
reddening of the skin if the patient is Caucasian.
• If unconscious or unable to swallow: IV glucose or parenteral
glucagon is preferred treatment, but subcut glucagon may be
more readily available
Glucagon
emergency kit
Hypoglycemia: Fear
• As a group, people with diabetes fear hypoglycemia more
than they fear the long-term complications of diabetes.
• The rational fear of hypoglycemia can lead to worsening of
metabolic control as well as tension with, and a restriction of,
personal freedoms and responsibilities by anxious and overprotective loved ones, colleagues, or employers.
• The psychological reactions can be quite frightening and can
extend beyond the patient to include family, friends, and
coworkers.
• If neuroglycopenia occurs while the individual is performing
a critical task, such as driving, the individual and others are
placed at risk of injury and death.
Hypoglycemia: Unawareness
• Hypoglycemia unawareness (by reducing the
sympathoadrenal and the resulting symptomatic
responses) can initiate a vicious cycle of recurrent
hypoglycemia.
• …concept has been extended recently to include
exercise- and sleep-related hypoglycemia-associated
autonomic failure.
• Hypoglycemia unawareness is reversible in most
affected patients, and the reduced epinephrine
component of defective glucose counter-regulation is
variably improved, by as little as 2–3 weeks of scrupulous
avoidance of iatrogenic hypoglycemia. Importantly,
antecedent plasma glucose levels as high as 70 mg/dl
cause reduced sympathoadrenal responses to
subsequent hypoglycemia.
http://care.diabetesjournals.org/content/28/5/1245.full
Short-term Complications of Diabetes: Recap
• Short-term complications: glycemic control is imperfect
– Hyperglycemia
• Def:
• Symptoms:
• Tx:
• Hyperglycemic emergencies: DKA and HHS/HHNS result
from sustained insulin deficiency… ending in confusion,
coma, death
– Hypoglycemia
• Def:
• Symptoms:
• Tx:
• Hypoglycemic emergency: Diabetic shock (“insulin shock”)
usually result from administering too much insulin, or (drug)
interactions. … ending in fainting, weakness, fatigue, bizarre/
confused behavior, potentially convulsions, coma, and death.
Long-term
complications
Long-term complications of Diabetes: Macrovascular
• MACROvascular complications of diabetes:
− Due to hyperglycemia, altered lipid metabolism
− Atherosclerosis develops earlier and progresses faster in diabetics
• Ischemic heart disease:
—Cardiovascular disease is #1 cause of death in diabetics
− MI, angina, cardiac failure
− Risk of CVD 2 – 4 times higher for those with diabetes
− Higher case fatality as compared to non diabetic individuals.
− Reduced survival post-MI, post-CABG, and esp post-PTCA
• Cerebrovascular disease: Cerebrovascular Accident (CVA)
− Diabetics have a 2-4 times higher risk for stroke
• Peripheral arterial disease
− 60% of nontraumatic lower-extremity amputations; claudication
• Hypertension; very common comorbidity; accelerates disease
• Treatment: Lifestyle + glycemic control
CV exercise. Healthy diet. No smoking.
Control of blood pressure, blood lipids, blood glucose.
Long-term complications of Diabetes: Macrovascular
Macrovascular disease affects Cardiovascular,
Neurovascular, Peripheral vascular…
Long-term complications of Diabetes: Microvascular
Long-term complications are the same for T1DM and T2DM
MICROvascular disease:
• Destruction of small blood vessels, leads to ischemia,
dysfunction, and cell death.
• Directly related to degree & duration of hyperglycemic
episodes.
• Microvascular injury likely reducible by optimal glycemic
control over the long-term.
− Retinopathy (Blindness)
− Nephropathy (Renal disease)
− Neuropathy (Sensory and motor neurons. Lower extremity
injuries and poor wound healing.)
− Amputations (secondary to infection, poor wound healing)
− Gastroparesis (Autonomic neuropathy to GI causes
dysfunction such as delayed gastric emptying)
− Erectile dysfunction (Autonomic neuropathy to GU causes
dysfunction such as ED; sildenafil)
NORMAL RETINA
Normal healthy retina as it appears on
funduscopic examination.
DIABETIC RETINOPATHY
Diabetic retinopathy as it may be seen on
funduscopic examination. DM is the major
cause of blindness among adults in US.
Cataracts of the crystalline lens with
opacification, as shown here, are more
frequent in persons with diabetes mellitus.
• DN begins as a
glomerular disease:
results in proteinuria,
reduced GFR, and
increased blood pressure.
 Screen for
microalbuminuria.
• Nephropathy is the
primary cause of
morbidity and mortality in
T1DM
 T1DM rate of DN is
12x higher than T2DM
• DN = #1 cause of End
Stage Renal Disease.
Angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB)
can slow progression of diabetic nephropathy, but are not effective in primary prevention.
Gangrenous necrosis and ulceration involving the lower extremity is shown here.
Diabetics have accelerated atherosclerosis that can be extensive to involve peripheral
vasculature and predispose to this complication.
3
Healthy pancreas
and glycemic norms
Pancreas Function:
Normal function of the
pancreas is to secrete
endocrine hormones
insulin (from beta cells) and
glucagon (from alpha cells),
in response to blood
glucose levels.
DIABETES PATHOLOGY:
In all types of DM,
there is dysfunction with
insulin levels and/or
responsiveness to insulin
in target tissues.
Result: BG not maintained
within normal range.
Insulin Physiology: Secretion
Normal healthy beta cells in the pancreas secrete insulin
in response to blood glucose.
Insulin Physiology
Normally , plasma levels of insulin and glucose
are very tightly coupled.
Normal blood glucose levels
• In a person without diabetes, homeostatic mechanisms
normally maintain fasting blood sugar levels to a narrow
range of about 60 to 110 mg/dL most of the time .
• Overnight and between meals, the normal, non-diabetic
(fasting blood glucose) levels range 60-100 mg/dl.
• Shortly after meals or snacks, the BG may temporarily
rise to 140 mg/dl (or less.)
• Despite widely variable intervals between meals, or the
occasional consumption of meals with a substantial
carbohydrate load, human blood glucose levels tend to
remain within the normal range.
http://dtc.ucsf.edu/, www.diabetes.org
6 am
6 pm
6 am
• In a nondiabetic, the pancreas secretes a small
amount of insulin continuously (about 0.5 to 1 unit
per hour) to cover the body’s non-food related
insulin needs.
• This is the human body’s basal insulin release
• www.diabetesclinic.ca
www.diabetesclinic.ca
42
4Monitoring
• Self- monitoring of blood glucose (SMBG)
− to adjust/ evaluate insulin, diet, and exercise
• Urine testing for both glucose and ketones prn
• HbA1c = best index for evaluating long-term glycemic
control
Monitoring: SMBG
• All pts using insulin, and most pts with
T2DM should check SMBG.
Ideal Testing Frequency
• Stable T2DM: 1-2 readings/ day
• Unstable T2DM: 3-8 readings/ day
• Patients on multiple-dose insulin (MDI) or insulin pump therapy
should check SMBG at varying times: (maintain logbook)
– prior to meals and snacks; occasionally postprandially
– prn during day or night
– when they suspect low blood glucose; after treating low blood
glucose until they are normoglycemic;
– pre- and post-exercise
– Prior to critical tasks (eg driving and ideally 1 hour later)
– Perform two SMBG 30 minutes apart prior to bedtime (confirming
rising or falling BG)
– Identify individual’s glycemic profile
– Typically 6-8 times daily
Monitoring Treatment: SMBG p 673
Monitoring: Hemoglobin A1c

Provides an index of average glucose levels over the
prior 2 to 3 months


Blood draw every 3 – 6 months
How well is diabetes self-care/ treatment regimen working?
 A1c goal of below 7% is good for most patients
 Also called glycosylated hemoglobin
or glycated hemoglobin
45
Monitoring Treatment: Hemoglobin A1C p 674
Hemoglobin A1c goals (“BG targets”) are individualized
 Tight glycemic control (such as <6.5%) may be appropriate
for selected individual patients, if this can be achieved
without significant hypoglycemia or other adverse effects of
treatment
•
Appropriate patients might include those with short duration of
diabetes, long life expectancy, and no significant CVD
 Tight glycemic control may be inappropriate in some
populations.
Goal below 8% may be appropriate for patients with:
• History of long-standing diabetes in whom the general goal is
difficult to attain
• History of severe hypoglycemia
• Limited life expectancy/ advanced age
• Severe or advanced microvascular or macrovascular
complications
• Extensive comorbid conditions
• Hypoglycemia unawareness
• Other individual patient considerations
46
5
Diabetes:
Diagnostic criteria
& Targets
Criteria for Diagnosis of Diabetes: 4 options
 Hemoglobin A1C ≥6.5%*
Perform in lab using NGSP-certified method and standardized to
DCCT assay
 Fasting Plasma Glucose FPG ≥126 mg/dL (7.0 mmol/L)*
Fasting defined as no caloric intake for ≥8 hrs
 2-hr PG ≥200 mg/dL (11.1 mmol/L) during OGTT (75-g)*
Performed as described by the WHO, using glucose load
containing the equivalent of 75g anhydrous glucose dissolved in
water. Oral glucose tolerance test (OGTT)
 Random PG ≥200 mg/dL (11.1 mmol/L)
In persons with symptoms of hyperglycemia or hyperglycemic
crisis
*In the absence of unequivocal hyperglycemia results should be
confirmed using repeat testing.
Unless clinical diagnosis is clear, same test to be repeated using a
new blood sample for confirmation.
2015 American Diabetes Association (ADA) Diabetes Guidelines
49
Prediabetes
• Defined as: Impaired fasting plasma glucose between
100 mg/dL and 125 mg/dL
– Impaired glucose tolerance test
• Increased risk for developing type 2 diabetes
• Risk might decrease with dietary changes, CV exercise
and possibly with certain oral antidiabetic drugs
• Many people who meet criteria for “prediabetes” never
develop diabetes, even if they do not take precautions
against diabetes
50
“Classic” signs/ symptoms of diabetes
The following symptoms of diabetes are typical for people newly
diagnosed with T1DM, and for some pts newly dxd with T2DM.
However, many people with type 2 diabetes have symptoms so subtle
or mild that they often are not noticed by the patient.
• Polyuria = Urinating often
• Polydipsia = Feeling very thirsty, drinking a lot
• Polyphagia = Feeling very hungry - even though eating
• Extreme fatigue
• Blurry vision
• Cuts/bruises that are slow to heal
• Weight loss - even though you are eating more (type 1)
• Tingling, pain, or numbness in the hands/ feet (type 2)
• Early detection and treatment of diabetes can decrease the risk of
developing complications of diabetes.
http://www.diabetes.org/diabetes-basics/symptoms/
Glycemic targets: non-pregnant adults
Lehne, p 674
ABCs of diabetes care:
Reaching Goals
A1c
A
B
Less than 7%
(8% for some people)
(6.5 % may be appropriate for other people)
SMBG mg/dL
Common target values for SMBG blood glucose
80 - 130 before meals
180 or less = Peak postprandial target
100 – 140 at bedtime
Blood
Pressure
Less than 140/ 90 mmHg
LDL:
<100 mg/ dL
American Diabetes Association. Standards of medical care in diabetes – 2015. Diabetes Care.
2015; 38 (suppl 1): S1 – S93.
6
management
Foundations
of
Care:
Diabetes
Treatment
The responsibility for managing diabetes rests with the patient
2015 Recommendations:
start drug therapy at
time of diagnosis
Healthy eating
Increasing
And/ Or
Frequent
Extensive
Smoking Cessation
Psychosocial Care- depression extremely common
Weight control
Immunization
Regular appointments with primary
care/ internal medicine providers and
specialists: ophthalmologist,
cardiologist, endocrinologist, etc
Type 1 Diabetes: comprehensive plan
• Health alterations at time of dx and medical priorities often result in
admissions to hospital:
– Screen for certain other autoimmune disorders.
• Integrated treatment plan
– dietary measures, insulin replacement, SMBG, physical activity/
exercise, ongoing education, and regularly scheduled care
– Smoking cessation, alcohol in control, psychosocial care
• Management of hypertension
 An ACE inhibitor (for example, lisinopril) or an ARB (for example,
losartan) can reduce the risk of diabetic nephropathy


ADA: keep BP at or below 140/90
Some people will benefit from a lower systolic bp
• Dyslipidemia
– Statins (for example, atorvastatin)
– colesevelam
• Patient/provider should have a plan for:
– travel; illness at home “sick days”; admission to hospital; power
outage; and other non-routine circumstances.
57
Type 1—Goal
 Goal of insulin replacement strategies is to
− duplicate how the pancreas secretes insulin in a
non-diabetic pt
− maintain glucose levels within an acceptable range
 Manage other comorbidities aggressively
 prevent long-term complications
Type 2 Diabetes: comprehensive plan
• Priorities of care at time of dx vary.
• All require integrated treatment plan
– dietary measures, physical activity, ongoing education , regularly
scheduled care, oral and/or injectables if needed
– Smoking cessation, alcohol in control, psychosocial care, weight
management
• Patient should be screened and treated for:
– Hypertension, dyslipidemias (HDL, LDL, triglycerides)
– nephropathy, retinopathy, neuropathy
• Manage other comorbidities aggressively
• Patient/ provider should have a plan for travel; illness at home
“sick days”; admission to hospital; power outage; and other
non-routine circumstances.
 Goal is to maintain glucose levels within an acceptable range
using diet, blood glucose monitoring, exercise, and step-wise
increases in oral antidiabetic agents or injectables including
insulin if needed
 prevent long-term complications
59
Type 2—Strategy and Goal
Step-wise advances in therapy until glycemic control is attained: p. 672
Step 1: Treatment is started with lifestyle measures (modified diet,
physical activity) PLUS drug therapy. Metformin, if not contraindicated
and if tolerated, is the preferred initial pharmacological agent for type 2
diabetes. In patients with newly diagnosed type 2 diabetes and
markedly symptomatic and/or elevated blood glucose levels or A1C,
consider initiating insulin therapy (with or without additional agents).
Adding agents is more effective than switching agents.
Step 2. Continue lifestyle changes plus metformin, and add a second
drug: either an antidiabetic agent or basal insulin.
Step 3. Continue lifestyle changes plus metformin, and progress to a
three drug regimen. switch from basal insulin or a sulfonylurea to
intensive insulin therapy.
Step 4. If three-drug combination therapy (that includes basal insulin)
fails to achieve treatment goals after 3 – months, proceed to a more
complex insulin regimen usually in combination with one or more noninsulin medications.
•prevent long-term complications
7
Drug Therapy:
insulin replacement
– must always be paired with monitoring
– T1DM and some T2DM
Insulin: Therapeutic Uses
Indications for insulin:
• Principal – diabetes mellitus as insulin replacement therapy
• Required by all type 1 and some type 2 patients
• Some faster-acting insulins can be administered IV in emergency or
intensive care settings (eg DKA)
• Regular is usually the only insulin administered IV
• NEVER EVER give highly concentrated insulin intravenously
• Hyperkalemia – can promote uptake of potassium.
• Glucose and potassium enter the cell in response to insulin
Potassium must be co-administered or carefully monitored
• Gestational diabetes
• Aids in the diagnosis of growth hormone (GH) deficiency
Insulin Physiology: Biosynthesis
• Biosynthesis
– Connecting peptide,
aka “C peptide”,
is marker for native
insulin production
• Insulin is a protein,
therefore cannot be
taken orally
Conversion of proinsulin to insulin.
63
Insulin Physiology: Metabolic Actions
• Metabolic actions of insulin are primarily anabolic
– What does this mean?
• Insulin stimulates cellular transport (uptake) of glucose,
amino acids, nucleotides, and potassium
• Insulin promotes synthesis of complex organic molecules
– Glucose is converted into glycogen
– Amino acids are assembled into proteins
– Fatty acids are incorporated into triglycerides
Insulin Physiology: Deficiency
Metabolic consequences of insulin deficiency
T1DM – in the absence,
(or relative absence)
of insulin…
glucose can’t enter cells.
T2DM – in the state of insulin resistance, with or without a
relative deficiency of insulin, glucose can’t enter cells.
Therefore a catabolic mode predominates. Instead of
“building up stores of glycogen, proteins and triglycerides”,
macromolecule stores are harvested for energy…
 Increased glycogenolysis
 Increased gluconeogenesis
 Reduced glucose utilization
Insulin: Types of Insulin:
Rate of onset, peak & duration
• Short duration: Rapid acting
– Insulin lispro [Humalog]
– Insulin aspart [NovoLog]
– Insulin glulisine [Apidra]
• Short duration: Slower acting
– Regular insulin [Humulin R, Novolin R]
Human insulin has less allergy or lipoatrophy.
• Intermediate duration
– Neutral protamine Hagedorn (NPH) insulin
– Insulin detemir [Levemir]
• DURATION of detemir is DOSE-DEPENDENT.
• Duration of detemir can range from 12-24 hours
• Long duration
– Insulin glargine
66
Types of Insulin:
rate of onset, peak & duration
Type of Insulin
(prototype)
Onset
Peak
Duration
Bolus insulins
Short duration: Rapid acting (Lispro)
15-30 min
0.5 -3h
3 – 6h
Short duration: Slower acting (Regular)
30-60 min
1- 5h
5 - 10h
60-120 min
4– 14h
12 – 24h
60+ min
None
24+h
* Regular insulin is often just referred to as “short acting.”
Basal Insulins
Intermediate duration (NPH)
Long duration (Glargine)
**Regular and NPH insulin do not require a prescription for purchase, per Lehne.
“BASAL”
Continuous
infusion
“BOLUS”
Types of Insulin:
rate of onset, peak & duration
Goal of insulin replacement strategies is to administer
exogenous insulin in such a way that it duplicates
the normal patterns of insulin secretion
by the pancreas of a person who is nondiabetic.
Blood Glucose (mmols)
scale used in Canada
1086420
8am
noon
6pm
2am
4am
8am
Time
Red brown = glucose levels
www.diabetesclinic.ca
69
examples of insulin replacement
strategies
– must always be paired with SMBG
– T1DM and some T2DM
I. “Twice Daily Premixed Regimen”
Two injections per day; provides some basal and
some prandial coverage. Has weaknesses.
II. “Intensive Basal/ Bolus Strategy”
Four injections per day;
often used by pts with T1DM
Intensive Basal/ Bolus Strategy
effect on blood glucose levels
III. “Continuous Subcutaneous Insulin Infusion” (CSII)
CSII portable pump connected to an indwelling subcutaneous cannula
Drug Therapy: types of insulin
Short-Duration, Rapid-Acting Insulin
• Insulin aspart [NovoLog]
• Insulin lispro [Humalog]
– Rapid-acting analog of regular (human) insulin
– Onset: 15-30 minutes after subcutaneous (subQ) injection
– Duration: 3-6 hours
– Usual route is subQ via injection or use of an insulin pump
– Acts faster than regular insulin but has a shorter duration of action
– Should be injected 5-10 minutes before meals
• Insulin glulisine [Apidra]
– Synthetic analog of natural human insulin
– Rapid onset (10-15 minutes)
– Short duration (3-5 hours)
– Should be administered close to the time of eating
77
Short-Duration, Slower-Acting Insulin
• Regular insulin [Humulin R, Novolin R]
– Unmodified human insulin
– Four approved routes:
• SubQ injection, subQ infusion,
• intramuscular (IM) injection (used rarely)
• and oral inhalation (approved but not currently used)
– Effects begin in 30 to 60 minutes
– Peak in 1 to 5 hours
– Duration up to 10 hours
– Clear solution
*Special Considerations/ things to know:
– Two strengths: Regular insulin [Humulin R, Novolin R]
• U-100 (100 units/mL)
• Humulin-R is the only insulin available in U-500 (500 units/mL)
78
Intermediate-Duration Insulin
• NPH insulin [Humulin N, Novolin N]
– Drug is injected twice or three times daily to provide
glycemic control between meals and during the night
– NPH insulin is the only one suitable for mixing with shortacting insulins
– Allergic reactions are possible
– NPH insulins are cloudy suspensions that must be gently
agitated before administration
– NPH insulins are administered by subQ injection only
– NPH, Neutral protamine Hagedorn.
79
Long-Duration Insulin
• Insulin glargine [Lantus]
– Modified human insulin
– Prolonged duration of action (up to 24 hours)
– Once-daily subQ dosing to treat adults and children
with type 1 diabetes and adults with type 2 diabetes
– Clear solution
80
Long-Duration Insulin
• Insulin detemir [Levemir]
– Human insulin analog
– Slow onset
– dose-dependent duration of action
• At 0.2 units/kg, effects persist about 12 hours
• At 0.4 units/kf, effects persist about 24 hours
• Used only for basal glycemic control
– Clear, colorless solution
– Dosing: Once or twice daily by subQ injection
– Do not mix with other insulins
– Must not be given IV
81
Additional clinical considerations
- adverse effects
- complications of insulin drug
therapy
 problem-solve case-by-case
Adverse Effects of Insulin: Hyperglycemia
doses too low
fear of hypoglycemia too great
insulin lost its potency
Hyperglycemia = Blood Glucose 180 mg/dl or higher
–
–
–
–
–
–
Polyphagia
Polyuria
Polydipsia
Dry mouth
Fatique
Weight loss
If persists . . .
Poor wound healing
Dry or itchy skin
Recurrent infectionsBlurred vision
Adverse Effects of Insulin: Hypoglycemia
doses too high
goals too stringent
delayed meals
interactions
Hypoglycemia = Blood Glucose 70mg/dl or less (ADA)
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–
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–
–
Tachycardia
Palpations
Sweating
Nausea
Headache
Confusion
Drowsiness
Convulsions
Coma
Death
Complications of Insulin Treatment
• Hypoglycemia
– Beware drug interactions
• Hypokalemia
• Allergic reactions
• Lipodystrophies
• Hyperglycemia
– Beware drug interactions
More on insulin
Insulin: Just the Facts, please
•
•
•
•
•
•
Sources of insulin
Appearance
Concentration
Mixing insulins in the same syringe
Delivery Methods & Administration
Storage
Sources of Insulin
• Sources of insulin
– Recombinant DNA technology
– Derived from common bacteria (e-coli) or
yeast cells
– Previously derived from beef and pork
pancreas, but high level of allergic reactions
• Appearance-
Insulin
– ALL insulins (made in the United States) are formulated as
clear, colorless solutions (except NPH)
– NPH is a cloudy suspension that should be gently agitated before use:
• equally distribute all components
• don’t make frothy bubbles
– Patients should inspect their insulin before using it and discard the vial if
the insulin looks abnormal. See table 57-8
• Concentration
– 100 units/mL (U-100) ; standard concentration
– 500 units/mL (U-500)- only for select pts with needs for high doses of
insulin; high concentration vial should never be stored where it can get
mixed up with any other insulin; only the Humulin- R brand of regular
insulin; NEVER EVER IV
• Mixing insulins in the same syringe
– ONLY NPH can be mixed with a shorter-acting insulin
– Short-acting insulin drawn first
Insulin Delivery Methods
& Administration
• Subcutaneous injection
– Syringe and needle
– Pen injectors
– Jet injectors
• Inhalation
– Exubera – now off market
• Subcutaneous infusion (continuous delivery)
– Portable insulin pumps
– Implantable insulin pumps
– Insulin pod
• Intravenous
infusion- ONLY PER HOSPITAL PROTOCOL
90
Where to Give Insulin:
On Target!
• Inject into fat layer under skin
• Rotate sites
• Leave at least 1 inch of space
91
between
• Common sites: abdomen,
thigh, buttocks, upper arms
Storing Insulin
•
Always review product storage instructions; check
expiration date
–
Unopened vials or pens should be stored under refrigeration
until needed. Properly stored insulin should retain potency
through expiration date on the vial. Do NOT freeze.
–
Read package insert for safe temperature range;
place thermometer in fridge near insulin.
•
After opening, the vial in current use can be kept at room
temperature (less than 86 degrees) for up to one month without
significant loss of activity. Keep out of direct sunlight and away
from extreme heat. Date the vial when opened.
•
Mixtures of insulin, and pre-filled syringes containing mixtures of
insulin- read package insert, or Lehne p 681
92
Examples of
Storage Information
• Mixtures of insulin in vials are stable for 1
month at room temperature and 3 months
under refrigeration
• Mixtures in prefilled syringes should be stored
in refrigerator for up to 1 week and should be
stored vertically – needle pointing up
Let’s talk labels . . . .
Let’s talk syringes . . . .
2nd: check increments
1st: Quantity?
Units or ml?
Dual scale identifies odd and even units
Let’s talk concentrations . . . .
U-500
What is it?
When is it used?
What special considerations must be followed?
What syringe is used for U-500 concentration insulin?
“Medication administration rights” of Insulin Therapy:
you won’t find this in a textbook
•
•
•
•
Right overall strategy for that specific individual patient
Right baseline assessment (SMBG)
Right timing of insulin and carbohydrate ingestion
Right insulin, right dose, right purpose
−Read label, verify strength, use INSULIN syringe!
−Right independent verification/ double-check by peer
• Right monitoring
• Individual pt’s insulin requirements (dosing) varies from
person-to-person and changes over time
• Right insulin storage, correctly dated and initialed when
opened. Right glucometer test strips (stored properly, not
damaged or expired), and right calibration of the glucometer
8
Drug Therapy
Oral antidiabetic agents
and non-insulin injectables
American Association of Clinical Endocrinologists Algorithm
107
American association of clinical endocrinologists’ comprehensive diabetes management algorithm 2013. Endocrine Practice. 2013; 19 (2).
Antihyperglycemic Therapy inType 2 Diabetes
ADA. 7. Approaches to Glycemic Treatment. Diabetes Care 2015;38(suppl 1):S43. Figure 7.1;
adapted with permission from Inzucchi SE, et al. Diabetes Care, 2015;38:140-149
Classes of non-insulin antidiabetic agents
-naming convention in italics, if there is one
drug prototype
Oral Hypoglycemics
• ***Biguanides (metformin)
• Sulfonylureas (glyburide)
• Meglitinides (-glinides; repaglinide)
• Thiazolidinediones (-glitazones; pioglitazone)
• Alpha-glucosidase inhibitors (acarbose)
• DPP-IV Inhibitors (-gliptins; sitagliptin)
DPP-4 = Dipeptidyl peptidase-4 = enzyme that inactivates
incretin hormones
• *SGLT-2 inhibitors =
• Dopamine Agonist
• Combination products
Non-Insulin Injectables
• Incretin mimetics (exenatide)
• Amylin mimetics (pramlintide)
Diabetes medication
Oral medicines can  A1c from 0.5% to up to 2%.
Combinations improve A1c lowering but insulin  A1c the most.
Endotext.org
Table 57-10
Biguanide: Metformin
Trade names: Glucophage, Glucophage XR, Fortamet (ER), Riomet
2015 “Drug of choice” for initial therapy in most pts with T2DM
Average 1.8% reduction in HbA1c (60-80 mg/dL glucose reduction). Weight neutral.
MOA:
• Inhibits glucose production in liver (↓ gluconeogenesis, ↓ glycogenolysis)
• Increases insulin-stimulated glucose uptake in skeletal muscle and
adipocytes
• Reduces glucose absorption (slightly)in gut
Therapeutic uses: T2DM. Being trialed in prevention of type 2 diabetes. PCOS.
Adverse Effects
• Diarrhea (53%); Nausea (26%); Gas/bloating (12%); anorexia/ decreased
appetite
• Lactic acidosis, a potentially fatal complication, is rare
• Can lead to deficiencies of Vitamin B12 and folic acid
Special Considerations/ things to know:
• Used alone, usually does not cause hypoglycemia. Good for people who skip meals.
• ↓SE if starting dose 250 or 500 mg daily, slowly titrated up. Typical doses 500 – 1000
mg BID; Max dose: 2550mg daily (850 mg TID). Allow 1-2 weeks between dose
adjustments. Better taken with food, SLOW dose adjustments, and divided doses.
~3-5% pts can’t tolerate SE.
• Absorption- Oral bioavailability = 50-60%. Distribution- steady state in about
24-48 hours, non-protein bound. Metabolism- no liver metabolism
• Excreted unchanged by kidneys. Monitor renal function at least yearly.
Toxic accumulation if renal impairment.
Biguanide: Metformin
Metformin Contraindications:
 Renal disease or renal dysfunction
 SCr = 1.4 mg/dL for women, 1.5 for men (Cut-offs to discontinue
metformin)
 Increased risk of lactic acidosis (50% fatality rate) if liver disease; severe
infection, hx lactic acidosis, acute or chronic metabolic acidosis, including
diabetic ketoacidosis (DKA); excess alcohol use; shock; hypoxemia; renal
insufficiency; CHF requiring Rx intervention, cimetidine, iodinated contrast.
 Hypersensitivity to metformin
 Stop before all surgeries/contrast dye
 Resume 48 hours after CT if SCr is OK
 Resume after surgery if pt is PO and SCr is OK
 Metformin is dialyzable for lactic acidosis/OD
Metformin Precautions:
• Hypoxic states; Hepatic disease; Alcohol intake should be “non-excessive”
(NMT 1 drink daily for women, 2 drinks daily for men)
OTHER
• FDA approved: monotherapy/combo. Immediate release + XR .
• Data suggestive that metformin is cardioprotective
• Pregnancy category B. Historically, only insulin has been used for gestational
diabetes, but recent studies suggest metformin may be acceptable
alternative.
Sulfonylureas (SFU’s)
• (First-generation: First oral antidiabetics available. Cardiovascular
Warning.)
Second-generation agents: significant drug-drug intx are much less
common
– Glipizide (Glucotrol or Glucotrol XL)
– Glyburide ( Diabeta, Micronase)- Pregnancy Category B
– Glimepiride (Amaryl)- has dft MOA, may not impair CV ischemic
preconditioning post MI (like glipizide and glyburide)
MOA:
– Stimulate insulin release from pancreas
– With prolonged use, SFU may enhance target cell sensitivity to insulin
Therapeutic uses: only useful for T2DM
Adverse effects: Weight gain.
Hypoglycemia (esp with alcohol or other predisposing factors.)
Hypoglycemia incidence: glimepiride<glipizide<glyburide
Sulfonylureas (SFU’s)
Second-generation agents, continued:
PK: Absorption: 100%
 Glipizide: 30 minutes onset, peak 2-3 hours
 Glipizide XL: 2-3 hours onset, peak 6-12 hours
 Glyburide: 1 hour onset, peak 4 hours
 Glimepiride: 2-3 hours peak, 24 hour duration
 Distribution: 97-99% protein bound
 Metabolism: extensively liver
 Excretion: renal and feces as metabolites, less than 10%
unchanged (parent) drug. Extensive metabolism in the liver
(avoided post-transplant). If renal dysfunction, then no glyburide.
Special Considerations/ things to know:
Hemoglobin A1c lowering 1-2%. Numerous precautions. drug intx.
Possible risk of sudden cardiac death (controversial. ).
Pregnancy: Avoid. Teratogenic in animals; risk of severe ↓BG nearterm/birth. Do not use in lactation: excretion in breastmilk poses risk of
↓BG to infant. (Glyburide Pregnancy Category B).
Contraindications: hypersensitivity
Meglitinides (Glinides)
• Repaglinide (Prandin)
MOA:
– Stimulate insulin release from pancreas
– same MOA as SFU’S, but dft PK: glinides are more short-acting and pt must eat
within 30 minutes of taking a dose
Therapeutic uses: only useful for TT2DM
Adverse effect: hypoglycemia; liver dysfunction increases risk of ↓BG
PK: ADME blood levels peak within 1 hour; return to baseline ~4 hours later. T½ = 1
hour. Highly protein bound. Hepatic metabolism followed by biliary excretion.
Special Considerations/ things to know:
• Generally well tolerated
• Drug interactions: gemfibrozil [Lopid] incresses hypoglycemia.
• Pts who do not respond to SFU’S will not trespond to glinides either
Thiazolidinediones TZD’s (Glitazones)
• Rosiglitazone [Avandia]: Restricted use (Are restrictions lifted?)
Stigma r/t 2010 data re ↑MI; REMS = prescriber training; 2013 data =
no increased risk
• Pioglitazone (Actos): Generally well tolerated
MOA:
• reduces insulin resistance in skeletal muscle by activating increased
glucose and lipid metabolism
• decreases endogenous glucose production
Therapeutic uses: T2DM; Also as add-on to metformin.
Note: any med in T2DM is ALWAYS an adjunct to diet and exercise.
Adverse Effects: hypoglycemia, upper respiratory tract infection, URI,
headache, sinusitis, and myalgia; Heart Failure r/t renal retention of
fluid, bladder cancer.
Precautions: Concurrent use of insulin (possible increased risk of
cardiovascular events). Concurrent use of other hypoglycemic agents
PK: Hepatic metabolism by CYP2C8
Special Considerations/ things to know:
Drug intx with other drugs metab’d by CYP2C8; and drugs that induce or
inhibit CYP2C8. *Black box warning*. “Troubled past, uncertain future.”
Alpha-Glucosidase Inhibitors
Acarbose (Precose)
*
MOA:
– delay the intestinal absorption of carbohydrates through
inhibition of the brush-border enzymes that breakdown
polysaccharides to glucose
– ↓ rise in blood glucose after meals
– Does not depend on the presence of insulin
Therapeutic Use: T2DM
Adverse Effects
− Frequently causes flatulence, cramps, abdominal distention,
borborygmus, and diarrhea. Decreased iron absorption.
PK: minimal absorption;
Special Considerations/ things to know:
– Monotherapy or combination. Increased risk of ↓BG if combined
with SFU or insulin. Longterm high dose tx may cause liver
dysfunction; therefore LFT’S Q 3 mos x 1 year, then prn.
Not used much in US per Lehne.
DPP-4 Inhibitors (Gliptins)
•
•
•
•
Sitagliptin (Januvia)
Linagliptin (Tradjendta)
Saxagliptine (Onglyza)
Alogliptine (Nesina)
*DPP-4 = Dipeptidyl peptidase-4= enzyme that inactivates incretin hormones
Therefore, DPP-4 Inhibitors prevent the breakdown of incretins
MOA
- Inhibits the breakdown of incretin hormones, therefore enhancing the
following effects induced by incretins:
- Stimulate glucose-dependent release of insulin from pancreas
- Decreases hepatic glucose production
Therapeutic Use: T2DM
Adverse effects: URI, headache. Rare pancreatitis. Serious hypersensitivity
similar to Stevens-Johnson
PK: rapid, nearly complete absorption; Peak 1-4 hours after dosing;
excreted unchanged in urine. T1/2 = 12 hours.
Special Considerations/ things to know:
When added on to metformin tx, A1c deceases ~0.5%. No known drug
intx or contraindications, including pregnancy. Take with or without food.
Reduce dose if decreased renal clearance.
SGLT 2 Inhibitors
• Sodium-glucose co-transporter 2 (SGLT-2) inhibitors
• Canagliflozin (Invokana)
• MOA: blocks reabsorption of filtered glucose by the renal tubules,
thereby increasing the amount of glucose excreted in the urine
(glucosuria)
• Adverse effects: Genital fungal infections in female patients,
urinary tract infections, increased urination, dehydration
• Special Considerations/ things to know:
Non-Insulin Injectable Drugs
“GLP-1 receptor agonists”
(aka
incretin
mimetics)
(non-insulin
injectable)
Glucagon-like peptide-1 receptor agonists (GLP-1 receptor agonists)
Exenatide (Byetta = twice daily) (Budureon ER = once weekly, inj site rx)
MOA: structurally similar to incretin hormones (thereby activating incretin
receptors) but are resistant to metabolism by DPP-4. Incretin effects:
– slow gastric emptying, thereby causing ↑satiety
– stimulates glucose-dependent insulin release
– Inhibit post-prandial release of glucagon
– Suppress appetite and can induce weight loss
–and increases insulin biosynthesis? Suppresses hepatic production of
glucose? true?
Therapeutic uses: T2DM
Adverse effects
– Nausea is common; vomiting, diarrhea. Hypoglycemia, esp if given with SFU
– Risk of acute pancreatitis. Risk of renal failure, esp if dehydrated.
– Risk of serious hypersensitivity rxs, angioedema, anaphylaxis.
PK: Byetta levels peak 2 hrs after subcut. T1/2 = 2.4 hrs. Excreted unchanged in
the urine. Do not use with severe renal impairment.
Special Considerations/ things to know: four GLP-1 on market, more in dev’t
Must take 0 – 60 minutes BEFORE a meal, morning and evening.
Pregnancy Category C.
Amylin Mimetics
(non-insulin injectable)
• Pramlintide (Symlin) – first drug in this new class
• * amylin is a peptide hormone produced in the pancreas and coreleased with insulin
• MOA:
– slows gastric emptying, thereby causing ↑satiety;
– Increases release of insulin,
– Decrease glucagon secretion,
– Increase satiety
• Therapeutic uses: supplement to mealtime insulin in T1DM or T2DM
• Adverse effects
− Severe hypoglycemia is a concern, and nausea is common, early
satiety, injection site reactions
• PK:
• Special Considerations/ things to know:
9
Diabetic
emergencies
Diabetic Emergencies
• Hyperglycemic emergencies
– DKA = Diabetic Ketoacidosis
– HHS or HHNS = Hyperglycemic Hyperosmolar (Nonketotic) State
– Advanced state = coma
• Hypoglycemic emergency
Insulin overdose or “diabetic shock” can quickly lead to
brain injury or death
− Advanced state = coma
Diabetic Emergency: hyperglycemia
•
•
•
•
•
•
•
•
•
•
Severe manifestation of insulin deficiency
Symptoms evolve quickly – period of hours or days
Most common complication in pediatric patients and leading cause of death
Diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state
(HHS) are the two most serious acute metabolic complications of
diabetes.
DKA is characterized by the triad of uncontrolled hyperglycemia, metabolic
acidosis, and increased total body ketone concentration.
HHS/HHNS is characterized by severe hyperglycemia, hyperosmolality, and
dehydration in the absence of significant ketoacidosis.
These metabolic derangements result from the combination of absolute or
relative insulin deficiency and an increase in counter-regulatory hormones
(glucagon, catecholamines, cortisol, and growth hormone).
Most patients with DKA have autoimmune type 1 diabetes; however,
patients with type 2 diabetes are also at risk during the catabolic stress of
acute illness such as trauma, surgery, or infections.
Kitabchi, et al (2009). Hyperglycemic Crises in Adult Patients With Diabetes.
American Diabetes Association. USA.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699725/pdf/zdc1335.pdf
Diabetic Ketoacidosis
• Treatment
• Characteristics
– Insulin replacement
– Hyperglycemia
– Bicarbonate for acidosis
– Ketoacids
(controversial)
– Hemoconcentration
– Fluid and sodium
– Acidosis
replacement
– Coma
– Potassium replacement
• Altered glucose metabolism
– Normalization of glucose
– Hyperglycemia
levels
– Water loss
– Hemoconcentration
• Altered fat metabolism
– Production of ketoacids
• Can lead to:
→ acidosis
→ coma
→ death
Diabetic Ketoacidosis
Stress, infection, = increased counterregulatory hormones
or insulin deficiency
Diabetic Emergency: Severe hypoglycemia
• Insulin overdose may rapidly lead to unconscious
patient. Take immediate efforts to raise blood glucose
levels.
• Preferred treatment is IV glucose
– Immediately raises blood glucose level
• Glucagon can be used if IV glucose is not available
– Delayed elevation of blood glucose
10
Resources and
appendix
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Abbreviations and Synonyms
DM = diabetes mellitus = diabetes (and not diabetes insipidus)
T1DM = type 1 DM
T2DM = type 2 DM
BG = blood glucose
FPG = fasting plasma glucose (venous)
PPG = post-prandial plasma glucose (venous, 2 hours after meal)
FBS = fasting blood sugar (venous)
PPBS = post prandial blood sugar (venous, 2 hours after meal)
Pre-prandial = before meal
Post-prandial = after meal (usually 2 hour)
Fasting = no calorie intake for 8 hours
Random = anytime other than fasting (test taken from a non-fasting
subject)
Glycated Hemoglobin = Hemoglobin A1c = HbA1c = Hb1c = HbA1c = A1c
A1C
SMBG = self monitoring (measurement) of blood glucose = capillary
whole blood/plasma glucose
SMUG = self monitoring (measurement) of urine glucose
CGM = continuous glucose monitoring
Hyperglycemia = high blood glucose
Hypoglycemia = low blood glucose
When you ask FBS/PPBS from lab, they usually do FPG/PPG.
ADA = American Diabetes Association
IDF = International Diabetes Federation
Clinical Practice Recommendations – CURRENT YEAR
ADA Clinical Practice Recommendations are based on a
complete review of the relevant literature by a diverse group
of highly trained clinicians and researchers. After weighing
the quality of evidence, from rigorous double-blind clinical
trials to expert opinion, recommendations are drafted,
reviewed, and submitted for approval to the ADA Executive
Committee; they are then revised
on a regular basis, and subsequently
published in Diabetes Care.
• Standards of care
• Frequency of exams
• Treatment Guidelines
• And so much more
Published annually in January.
www.diabetes.org
UWCNE Conference 2016 | Diabetes Update Tuesday - February 23, 2016
Learning Objectives
• Review the advantages and limitations of hemoglobin A1c.
• Discuss the harmful effects of prolonged hyperglycemia on the systems that support human
movement.
• Identify educational resources available to use during discussions with patients about
carbohydrates and blood glucose that reflect common dietary practices and foods commonly
consumed in particular ethnic populations.
• Identify new diabetes agents that have been approved recently and the evidence behind
them.
• Discuss what can be done to reduce the burden of insulin cost for patients with type 2
diabetes.
• Explain the bi-directional impact of periodontal disease and diabetes on oral and overall
health.
• Discuss/understand/practice engaging patients in their own self-management and goalsetting.
• Describe strategies for nutrition and lifestyle treatment for women with diabetes.
Topics
• A1C Is Not the “Be-All and End-All”
• Exercise for Glycemic Control, an Evidence-Based Approach
• Culturally-Tailored Nutrition Education for Patients with Diabetes
• Reconciling Higher Drug Costs with Optimal Diabetes Agent Selection (Rx)
• The Cost of Insulin in 2016: How Did We Get Here and What Can We Do?
• Diabetes and Oral Health: A Two-Way Street
• Goal-Setting: Developing Relevant, Practical, Effective & Meaningful Plans with Your Patients
• Nutrition Challenges for Women with Diabetes
• Videos from Kahn Academy developed in collaboration
with the American Association of Colleges of Nursing:
(AACN)
• Many helpful vignettes on diabetes- pathophysiology,
diagnosis, pharmacological management and more
•
•
•
•
Pathophysiology of Type 1 Diabetes
Treating Type 1 Diabetes
Pathophysiology of Type 2 Diabetes
Treating Type 2 Diabetes
Terminology & Targets
> 180 mg/ dL
=
hyperglycemia
• Common target values for SMBG blood glucose
• 80 - 130 mg/dL before meals
• Peak postprandial target 180 mg/ dL or less
• 100 - 140 mg/dL at bedtime
• Important to stress the need to vary testing times
– AC, PC, h.s. and prn during the night
– Identify individual’s glycemic profile