Diabetes Claire Nowlan Nov 28, 2003

Comparison of type 1 and 2 diabetes Type 1 10% of diabetics Age of onset – young Severe Requires insulin Normal build Little genetic component Type 2 90% of diabetics Age of onset – 40+ Mild May require insulin, usually hypoglycemics Obese Strong genetic component

Pathophysiology 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 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 Polydipsia (increased drinking) Polyuria (increased urination) Weight loss Weakness Increased infections Blurred vision

Complications Macrovascular Stroke MI Ulcers Amputation Microvascular Retinopathy - blindness Nephropathy – renal failure Neuropathy – numbness, tingling, pain, sensory deficits, and autonomic involvement Infections

Lab tests - diagnosis Random glucose – >11.0 mmol/L + symptoms Fasting glucose – >6.9 mmol/L Hb A1c – A long term measure of diabetic control – > 8%

Emergencies Ketoacidosis – 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 Hypoglycemia – 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 The tighter the control, the fewer complications– BUT – the more risk of getting hypoglycemic IDEAL management – 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 Assess control/severity – 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: 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 Xerostomia Infections – especially candidiasis Increases caries “Burning mouth syndrome” So – test for diabetes in suspicious patients