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Diabetes
Claire Nowlan
Nov 28, 2003
Comparison of type 1 and 2
diabetes
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Type 1
10% of diabetics
Age of onset – young
Severe
Requires insulin
Normal build
Little genetic component
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Type 2
90% of diabetics
Age of onset – 40+
Mild
May require insulin,
usually hypoglycemics
Obese
Strong genetic
component
Pathophysiology
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Type 1 diabetes – beta cells are destroyed,
eventually no insulin is produced
Type 2 diabetes – insulin secretion is reduced,
target cells become relatively insulin resistant
The Pancreas
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Main role is to excrete digestive enzymes
Islets of Langerhans contain alpha cells which excrete
glucagon, and beta cells which excrete insulin
Glucose stimulates insulin secretion from beta-cells
Insulin binds with cells surface receptors to allow
glucose transport into the cell
Glucagon mobilizes glucose to be released from the
liver
Symptoms of diabetes
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Polydipsia (increased drinking)
Polyuria (increased urination)
Weight loss
Weakness
Increased infections
Blurred vision
Complications
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Macrovascular
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Microvascular
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Stroke
MI
Ulcers
Amputation
Retinopathy - blindness
Nephropathy – renal failure
Neuropathy – numbness, tingling, pain , sensory
deficits, and autonomic involvement
Infections
Lab tests - diagnosis
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Random glucose
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Fasting glucose
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>11.0 mmol/L + symptoms
>6.9 mmol/L
Hb A1c
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A long term measure of diabetic control
> 8%
Emergencies
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Ketoacidosis
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In type 1 patients only
Marked hyperglycemia (high serum glucose) causes osmotic
diuresis
Patient loses excess water, Na, K, and ketones released from
the liver cause an acidosis
Precipitated by an infection, insulin error or omission, or occurs
in a previously undiagnosed patient
Treated with insulin, fluid replacement, K replacement
Type 2 diabetics can have a much less serious variant of this
called Hyperglycemic hyperosmolar nonketotic state
Emergencies
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Hypoglycemia
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May occur with an overdose of insulin/oral medication or a
missed meal
Only some medications cause hypoglycemia – Glyburide,
Glicazide, Chlorpropamide
Patient gets diaphoretic, weak, shaky, palpitations, difficulty
thinking, vision changes and may lose consciousness
Patient needs glucose – a glass of juice, a candy, or if
comatose, IV 50% glucose solution, IM glucagon, glucose gel
Some patients are totally unaware of their hypoglycemia until
they lose consciousness
Medical management
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The tighter the control, the fewer complications– BUT –
the more risk of getting hypoglycemic
IDEAL management
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Fasting glucose 4.0 – 7.0 mmol/L
1-2 hour postmeal 5.0 – 11.0 mmol/L
Type 1 diabetes – insulin tx– usual starting dose about
20 units/day (testing 2-5 x/day)
Type 2 diabetes – oral hypoglycemics +/- insulin
(testing 1-2x/day)
- diet only (testing 2x/month)
Infection, stress, pregnancy, surgery will all disturb
control
Dental management
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Assess control/severity
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What medications are you taking (or diet only)
Type 1 vs Type 2
When were they first diagnosed
How often do they measure their glucose
What are their usual measurements
Frequency of hypoglycemic reactions (can they feel them
coming on?)
How much insulin do they use
When did they last see their doctor
Your biggest worries:
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Hypoglycemia during a procedure
Oral surgeries that will prevent the patients from getting
their usual caloric requirements
Brittle diabetics (extreme fluctuations of
hypo/hyperglycemia) – usually occurs after years of
high dose insulin therapy
Acute oral infections that precipitate hyperglycemia
Be more aggressive with antibiotics in patients with
high sugars
Oral complications
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Xerostomia
Infections – especially candidiasis
Increases caries
“Burning mouth syndrome”
So – test for diabetes in suspicious patients