Download Diabetes Essentials 2011 - Iowa Dental Association

This lecture is sponsored by a grant from the
Delta Dental of Iowa Foundation IDA Annual
Conference Guest Lecture Series.
Diabetes Essentials 2011
Richard LeBlond, MD, MACP
Chief Quality Officer
Professor, Internal Medicine
University of Iowa Health Care
Learning Objectives
• Appreciate the challenge of diabetes from the
patient’s perspective
• Differentiate type 1 from type 2
• Understand insulin action
• Understand complications of diabetes
• Know the major classes of medications
• Know the side effects of each class
• Recognize hypoglycemia as a serious
complication arising during dental care
Diabetes Incidence in Childhood
What is Diabetes?
Insufficient insulin activity
• Defined by the blood glucose level
• The definition is arbitrary
– Fasting glucose >125 mg/dL
– 2 hour post meal glucose > 200 mg/dL
– Any glucose > 200 mg/dL
– Glycohemoglobin > 6.5%
• Two predominant causes
– Decreased insulin levels: type 1
– Resistance to insulin action: type 2
Insulin
• Insulin is produced by the beta cells in the islets
of the pancreas
• Small amounts of insulin are necessary to
sustain life
• Insulin is necessary for the metabolism of
carbohydrates
• Insulin acts predominantly on three tissues
– Fat cells: take up glucose, convert to fatty acids, and
store energy as triglycerides
– Muscle cells: take up glucose and store as glycogen
– Liver: take up glucose and store as glycogen; stop
gluconeogenesis (making glucose from amino acids)
Causes of Diabetes
• Type 1: destruction of pancreatic islet cells
– Autoimmune, usually childhood onset; genetic
predisposition; probable viral trigger
– Non-immune destruction: acute and chronic
pancreatitis; hemochromatosis
• Type 2: resistance to insulin action
– Genetic factors
– Obesity: decreased adipocyte responsiveness to
insulin
– Maturity Onset Diabetes of the Young (MODY):
abnormal insulin signaling
– Corticosteroids & stress hormones: cortisol (Cushing
syndrome), growth hormone (acromegaly),
epinephrine
Type 1 Diabetes
Absolute Insulin Deficiency
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Incompatible with life
Ketoacidosis without insulin
Exogenous insulin is the only treatment
Usually young and thin
No family history of diabetes
Common causes of death:
– Ketoacidosis
– Hypoglycemia
– Kidney failure
– Heart attack
Type 2 Diabetes
Resistance to Insulin Action
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Gradual onset and progression over years
Strong family history
Usually overweight or obese
Diagnosis in middle age (this is changing
rapidly)
• Many treatment options
• Long survival even without treatment
• Common causes of death:
– Heart attack
– Kidney failure
Hypoglycemia
• Blood sugar <50 mg/dL associated with brain
dysfunction and can lead to death
• Type 1 diabetics more susceptible
• Medication overdose: insulin or sulfonylureas
• Taking medication but not eating, or unable to
eat
• Taking medication and exercising strenuously
• Symptoms
– Autonomic response: shaky, sweating, hunger,
agitation
– Neuroglycopenic symptoms: confusion, lethargy,
coma
• Treatment: oral glucose, glucagon, iv glucose
Hypoglycemia Unawareness
• Occurs in type1 diabetics with frequent episodes
of mild-moderate hypoglycemia
• Blunted autonomic reflex responses to
hypoglycemia
• Only neuroglycopenic symptoms occur
• Inability to think clearly (judgment is the first to
go) leads to inappropriate, ineffective or no
response
• Greatly increased risk of death
• Absolute avoidance of hypoglycemia for several
months restores responsiveness
Long Term Complications of Diabetes
Microvascular
• Damage to the small arterioles becomes manifest in
specific organs
• Retinopathy: leading cause of blindness in US
• Neuropathy:
– loss of protective sensation in the feet and legs
– Autonomic neuropathy: loss of cardiovascular and
gastrointestinal autoregulation
• Nephropathy: loss of functional nephron mass leading to
kidney failure. Leading cause for ESRD and dialysis in
the US
• Microvascular complications are slowed or prevented by
tight glucose control (Hb A1c < 6.5%)
Long Term Complications of Diabetes
Macrovascular
• Accelerated atherosclerosis of the major arteries
• Myocardial infarction: heart attack risk is the same as
someone who has had an MI
• Stroke: strong cofactor with hypertension
• Peripheral vascular disease: strong cofactors are
smoking and male gender
• Tight glucose control (Hb A1c < 6.5%) does not have an
advantage over good control (Hb A1c 7.5%)
• Prevention strategy is to manage all risk factors:
smoking, blood pressure (< 130/80), LDL-C (<70 mg/dL),
exercise, weight loss
Other Complications of Diabetes
• Increase with blood sugars > 200 mg/dL
• Mucocutaneous fungal infections:
– Oral candidiasis
– Vulvovaginal candidiasis
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Periodontal disease
Poor wound healing
Wound infections
Urinary tract infections
Skin and soft tissue infections
MANAGEMENT:
Goals, Objectives &Tools
• Goals:
– the long term outcomes desired by the patient
and the physician
• Objectives:
– the objective easily measurable way points
marking progress towards the goals
• Tools:
– techniques, medications and other
interventions used to achieve the objectives
Long-term Goals
1. Life Goals
– Family
– Employment
– Avocations
2. Medical Goals
-Prevent microvascular disease
-Decrease risk for macrovascular disease
-Prevent hypoglycemic complications
-Prevent the 5 D’s: death, disability, depression,
dependency, destitution
Long-term Objectives
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Meaningful clinically
Meaningful to the patient
Objective
Measurable
Easily assessed by the patient
Transparent: easily interpreted
Long-term Objectives
1. Normal function
2. No severe hypoglycemia
3. Hemoglobin A1c ≤ 7%
4. Maximum glucose <180 mg/dL checked
1 ½ to 2 hours after meals
Long-term Objectives
Prioritized
1. Normal function
2. No severe hypoglycemia
3. Hemoglobin A1c ≤ 7%
4. Maximum glucose <180 mg/dL checked
1 ½ to 2 hours after meals
Tools
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Education
Diet
Glucose monitoring
Exercise
Medications
Devices
Doctors: exams, other labs
Tools
Priority
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7.
Education
Diet
Glucose monitoring
Exercise
Medications
Devices
Doctors: exams, other labs
Non Blood Sugar Objectives
Gaede P, et al. Effect of a multifactorial intervention on mortality in type 2 diabetes. N
Engl J Med 2008;358:580-91
1.
2.
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BP < 130/80, lower is better: whatever it takes
Lipid control, TC, LDL-C, TG: statin
Diet:
-total calories
-low carbohydrate diet
4.
Obesity
-diet, drugs, surgery
-progressive weight loss, weight target
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Exercise: rehab, PT, 10,000 steps daily
Preventive Care: foot exam, immunizations, etc
Manage albuminuria & CKD: ACE-I, BP control
Mood, depression impairs management: ? SSRI
Modern Insulin Management:
All Type 1 and some Type 2 patients
• Optimal insulins are synthetic & humanized
• Basal insulin: very long acting
– Given daily, often in the evening
– Humanized long acting: glargine (Lantus®), detemir
• Prandial insulin: very short acting insulins
– Given with meals
– Humanized very short acting: lispro (Humalog®), aspart,
glulisine
• Correction dose insulin
– Lower glucose elevated above premeal target level
– Given 30-60 minutes before meals
– Humanized very short acting insulins
Other Drugs for Type 1 and Type 2
• Glucagon:
– antagonizes insulin effect for rapid reversal of
hypoglycemia
• Older Insulins: suboptimal treatment
choices, but less expensive
– Animal derived intermediate acting: NPH,
Lente
– Animal derived short acting: Regular
– Fixed dose mixtures: 70/30 (70% NPH, 30%
Regular)
Drugs To Treat Type 2 Diabetes
• Injectable:
– Insulin
– Incretin (GLP-1) agonists
• Oral
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Metformin
Sulfoylureas
TZDs: thiazolidinediones
DPP4 inhibitors
Gut absorption blockers
Meglitinides
Metformin
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Drug of first choice for type 2 diabetes
Generic and low cost
Twice daily dosing
Increases insulin effect
Decrease liver glucose production
Increases peripheral glucose uptake
Does not cause hypoglycemia
Does not cause weight gain
Side effects:
– Diarrhea
– Lactic acidosis, rare
Sulfonylureas
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Older agents
Inexpensive
Long acting
Stimulate insulin release by beta cells
Side effects
– Weight gain
– hypoglycemia
Meglitinides
• Repaglinide, neglitinide
• Increase insulin release by a different
mechanism than sulfonylureas
• Fast and short acting
• Taken before meals to lower post prandial
glucose rise
• Side effects
– hypoglycemia
Incretin (GLP-1) mimetics
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Two available: exenatide (Byetta®)
Injectable
Once daily
Expensive
Used alone rarely causes hypoglycemia
Does not cause weight gain
Side effects
– Nausea is very common (> 40%)
– Slowed gastric emptying
DPP4 Inhibitors
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Oral once or twice a day
Two drugs available: sitagliptin, saxagliptin
Newer, expensive, second line
Inhibit breakdown of incretins
Do not cause weight gain
Do not cause hypoglycemia
Side effects: few
Thiazolidinediones
• Oral, intermediate duration, once or twice a day
• Increase sensitivity to insulin action
• Two drugs in class: pioglitazone (Actos®),
rosiglitasone (Avandia®)
• Do not cause hypoglycemia
• Cause weight gain
• Side effects
– Fluid retention and heart failure
– Possible increased risk of MI
Second Line Drugs
• Alphaglucosidase inhibitors (acarbose and
others)
– Blocks carbohydrate digestion
– Slows glucose absorption
– Used in combination with metformin
– Flatulence and diarrhea
• Lipase inhibitors: orlistat (Xenical®)
– Block fat digestion
– Diarrhea
Hypoglycemia:
Which patient should concern you?
• Type 1 on insulin
• Not obese
• History of hypoglycemia (high risk for
hypoglycemia unawareness)
• Acute oral issues impairing chewing or
swallowing
• Sedation
• Longer procedures
What signs should concern you?
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Anxiety
Sweating
Uncooperativeness
Confusion
Sedation
Decreased pain response
What Should You Do?
• Immediately stop the procedure
• If aware and cooperative, give something
to eat
• If possible have the patient check their
glucose
• For unresponsive patient:
– Call 911
– Give glucagon if available
– 50% dextrose intravenously
– Do not put food in the mouth
Learning Objectives
• Appreciate the challenge of diabetes from the
patient’s perspective
• Differentiate type 1 from type 2
• Understand insulin action
• Understand complications of diabetes
• Recognize major classes of medications
• Recognize side effects of each class
• Recognize potential complications affecting
dental care
Diabetes Essentials 2011
QUESTIONS?
Richard LeBlond, MD, MACP
Chief Quality Officer
Professor, Internal Medicine
University of Iowa Health Care
Complications of Diabetes: Ketoacidosis
• Insufficient insulin
• Glucose cannot enter muscle so glucose levels
rise
• Absent insulin signal to liver and fat
• Fat releases triglycerides which are metabolized
in muscle to ketoacids
• Liver starts making glucose further increasing
glucose
• Osmotic diuresis leads to volume depletion
• Ketoacids produces metabolic acidosis
aggravated by volume depletion
• Death from severe acidosis and hypotension
Treatment of Ketoacidosis
1. Replace volume deficits with normal
saline, usually several liters
2. Intravenous insulin drip
3. Replace electrolytes, particularly KCl
4. Continue insulin drip even when glucose
becomes normal
5. Transition to subcutaneous insulin after
all metabolic abnormalities are corrected
Care at Home
Locus of Care
Personal Organism
Social Person
Shared Responsibility: Who is
responsible and accountable for what
• Ask the patient “whose problem is this?”
– Repeat and wait until the patient (not the spouse,
family member, etc.) acknowledges their responsibility
– The outcome is most dependent upon the patient’s
not the doctor’s activities
– The patient will receive the benefits or consequences
of the decisions and actions
What should we conclude?
• Benefit is achieved in reducing A1c from > 9.0 to
<7.0%
• No clear benefit with lowering A1c to ≤ 6.5%
• A1c is a continuous not dichotomous variable
– One studies “intensive” is the next study’s control
• Recent studies show increased harm, including
death, with more intensive therapy
• Severe hypoglycemia increased with intensive
therapy
• Achieving tight control is resource intensive
(time, drugs, supplies, emotional)
In the absence of clearly-defined goals we
become strangely loyal to performing daily
trivia until ultimately we become enslaved
by it.
-Robert Heinlein
Symptoms of Diabetes
• Weight Loss
• Increased Appetite
• Increased Urination
– Large urine volumes
– Frequent voiding at night
• Visual Changes: blurring
• Fatigue, decreased energy
Diabetes Management
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The patient not the doctor manages diabetes
Doctor, docere L. teacher
Diet: count carbohydrates and total calories
Exercise: regular aerobic exercise 30+ minutes >
3 days per week
• Home glucose monitoring: a learning tool
• Glucose lowering medications
• Manage other risk factors: BP, cholesterol,
tobacco use
The main problem with communication is
the assumption that it has occurred.
-George Bernard Shaw