Transcript 13. Endocrine: diabetes

Diabetes
Normal Anatomy
and
Physiology
Pancreas: abdominal organ
responsible for exocrine secretion
of digestive enzymes into the gut
And
Endocrine secretion of
hormones of glucose control:
insulin and glucagon
Pancreas:
Exocrine
And
Endocrine:
Islets of
Langerhans
Glucose: 6 carbon sugar
that is the principle
source of energy for
cellular metabolism
Glucose circulates in the
blood and is transported
into cells for use as an energy
source
Glucose concentration in the
blood is normally controlled
between 3.6 and 11 mmol/L by
various hormonal influences
including:
Insulin
and
Glucagon
Insulin: peptide hormone
released by beta cells of the
Islets of Langerhans
in response to rising
levels of blood glucose
Acts by increasing cellular
transport of glucose and
increased storage of glucose
Glucagon: peptide hormone
released by alpha cells of the
Islets of Langerhans
in response to falling
levels of blood glucose
Acts by increasing release of
glucose from the liver by
breakdown of glycogen
Alpha cells:
Glucagon
Beta cells:
Insulin
Diabetes mellitus :
A metabolic disease caused by
an absolute or relative lack of
insulin resulting in abnormalities
in carbohydrate, protein and lipid
metabolism.
Diabetes mellitus:
Prevalence: 6% of the population
(estimate 30,000 in London area)
(120 diabetics in a 2,000 patient practice)
Diabetes mellitus:
Classfication:
Type 1 10% of diabetics
(estimate 3,000 in London area)
Type 2 90% of diabetics
(estimate 27,000 in London area)
Pathophysiology
 Type 1 diabetes – beta cells are
immunologically destroyed, eventually no
insulin is produced
 Type 2 diabetes – insulin secretion is
reduced, target cells become relatively
insulin resistant ( receptors and postreceptor activity
Comparison of type 1 and 2
Type 1
Type 2










10% of diabetics
Age of onset – young
Severe
Requires insulin
Normal build
Little genetic
component
 Autoimmune
90% of diabetics
Age of onset – 40+
Mild
May require insulin,
usually diet or oral
hypoglycemics
 Obese
 Strong genetic
component
Diabetes is characterized by:
Hyperglycemia
Loss of glucose (and water) in the
urine
Paradoxical cellular starvation
Symptoms of diabetes
 Polyuria (increased urination)
 Polydipsia (increased drinking)
 Weight loss
 Weakness
 Increased infections and
impaired healing
 Blurred vision
Lab tests - diagnosis
 Normal range of fasting blood glucose:
3.9 to 6.1 mmol/L
Diagnosis of DIABETES is based on
 Random glucose
 >11.0 mmol/L + symptoms
or
 Fasting glucose
 >6.9 mmol/L on 2 occasions
Medical management
 The tighter the glycemic control, the fewer
complications– BUT – the more risk of getting
hypoglycemic
 IDEAL management
 Fasting glucose 4.0 – 7.0 mmol/L
 Infection, stress, pregnancy, surgery will all
disturb control
Treatment: Type 1
 Diet and physical acitivity plus
 Insulin: usual starting dose about 20 units/day
(OD, BID, multiple, continuous infusion pump)
 Testing 2-5 x/day
 ACE inhibitors (captopril / ramipril) to control
nephropathy
 Cholesterol lowering drugs
Treatment: Type 2
 Diet and physical activity only (testing
2x/month)
 +/- Oral hypoglycemics (increase insulin
secretion, receptors or post-receptor activity)
 Sulphonylureas (glyburide = Diabeta)
(can induce hypoglycemia)
 Biguanides (metformin = Glucophage)
 Gamma-glucosidase inhibitor (acarbose =
Prandase
 +/- Insulin
Lab tests - monitoring
 Daily (or more) finger pick and
glucometer readings
 Hb A1c (Normal = 4.0 to 6.0)
 A long term (3 month) measure of
diabetic control (glycosylated Hb)
 Good
<7.0
 Fair
7.0 to 8.9
 Poor
>9.0
Diabetic complications
•Related to the strictness of
glycemic control and are
characterized as:
•Macrovascular complications
atherosclerosis
•Microvascular complications
eye and kidney
Complications
 Macrovascular
 Stroke
(2-5 X increased risk)
 MI
(2-5 X increased risk)
 Cutaneous ulcers (PVD)
 Amputation (40 X increased risk)
Complications
 Microvascular
 Retinopathy – blindness
(20 X increased risk)
 Cataracts (5 X risk)
 Nephropathy – renal failure
(25 X increased risk)
Complications
 Neuropathy – numbness, tingling, pain,
glove and stocking sensory deficits
 Autonomic involvement
 Infections secondary to impaired
vascularity and PMN defects
 Decreased duration and quality of life
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 a
metabolic acidosis
 Precipitated by an infection, insulin error or
omission, or occurs in a previously
undiagnosed patient
Emergencies: ketoacidosis
 Treated with insulin, fluid replacement, K
replacement
 Type 2 diabetics can have a much less
serious variant of this called:
Hyperglycemic hyperosmolar nonketotic
state secondary to dehydration
Emergencies: hypoglycemia
May occur with an overdose of insulin / oral
medication or a missed meal
 Only some oral medications cause
hypoglycemia – (Sulfonylureas) Glyburide,
Glicazide, Chlorpropamide
 Patient gets diaphoretic, weak, shaky,
palpitations, difficulty thinking, aggressive,
vision changes and may lose consciousness
Emergencies: hypoglycemia
 Patient needs glucose – a glass of juice, a
candy, or if comatose, IV 50% glucose
solution or IM glucagon (1 mg)
 Some patients are totally unaware of their
hypoglycemia until they lose consciousness
Dental management
 Assess control / severity / compliance (CSC)
 Treatment plan modification (based on CSC)








Possibly … None
AM appointments
Normal meds and diet pre-op
Limit treatment duration
Antibiotic coverage???
Post-op diet instructions
Hospitalization / GA and NPO status
Consultation with the MD
Dental management
 Assess control / severity /compliance
 When were they first diagnosed
 Type 1 vs Type 2
 What medications are they taking (or diet only)
 How much insulin do they use / how frequently
 How often do they measure their glucose and
what are their usual measurements
Dental management
 Assess control / severity / compliance
 Frequency of hypoglycemic reactions (can
they feel them coming on?)
 Complications: brain, eye, heart, kidney, toes
 How often and when last did they see their MD
 Did they take meds and have meals today
 Be alert to changes in “control”
Dental management
 Assess control / severity / compliance
 BRITTLENESS: poor control of diabetes
as a function of the nature of the disease
or other complicating factors such as
infection (?dental abscess?)
 COMPLIANCE: an indication of the patient’s
willingness or ability to manage his/her
medications or diet for optimal control
Dental conerns:
 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
Dental conerns:
 Acute oral infections that precipitate
hyperglycemia
 Be more aggressive with antibiotics in
patients with high sugars
Oral complications
 Xerostomia secondary to
dehydration
 Mucosal fungal infection:
candidiasis
 Increased caries and periodontal
disease
Oral complications
 Poor post surgical wound healing
 “Burning mouth syndrome”
…diabetic neuropathy
 Consult MD in suspicious patients
Questions?