Transcript Diabetes Mellitus patients in dental management

Diabetes Mellitus
patients
in dental management
Reporter : 吳和泰
Modulator: Dr. 雷文天
Introduction
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Diabetes mellitus is a metabolic disorder
characterized by relative or absolute
insufficiency of insulin, and resultant
disturbances of carbonhydrate metabolism.
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The major function of insulin is to counter the
concerted action of a number of hyperglycemiagenerating hormones and to maintain low blood
glucose levels.
Epidemiology
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6% (16 million persons) of the general population
in the US have diabetes mellitus.
Almost 20% of adult older than 65 y/o have DM.
A dental practice serving an adult population of
2,000 can expect to encounter 40-80 persons with
diabetes, about half of whom will be unaware of
their condition.
National Institutes of Health, Aug 2001
國人之糖尿病盛行率
Etiologic classification of DM
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There are two types of Diabetes Mellitus:
 Type
1, insulin-dependent or, juvenile-onset diabetes
(IDDM)
 Type
2, non-insulin-dependent, adult-onset diabetes
(NIDDM)
 Other
specific types
JADA, Oct 2001
Type 1 (IDDM)
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Autoimmune destruction of the insulin-producing
beta cells of pancreas.
5-10% of DM cases.
Common occurs in childhood and adolescence,
or any age.
Absolute insulin deficiency.
High incidence of severe complications.
Prone to autoimmune diseases. (Grave’s,
Addison, Hashimoto’s thyroiditis)
Type 2 (NIDDM)
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Result from impaired insulin function. (insulin
resistance)
Constitutes 90-95% of DM
Specific causes of this form are unknown.
Risk factors : age, obesity, alcohol, diet, family
Hx and lack of physical activity..etc.
Comparison
Type 1
Type 2
Clinical
onset <20 years
onset >30 years
normal weight
obesity
decreased blood insulin
normal or increased blood
insulin
anti-islet cell antibodies
no anti-islet cell
antibodies
ketoacidosis common
ketoacidosis rare
human leukocyte antigen
(HLA)-D linked
No HLA association
autoimmunity,
immunopathologic
mechanisms
insulin resistance
severe insulin deficiency
relative insulin deficiency
insulitis early
no insulitis
marked atrophy and
fibrosis
focal atrophy and amyloid
deposits
severe beta-cell depletion
mild beta-cell depletion
Genetics
Pathogenesis
Islet Cells
Other specific types
Genetic defects of beta-cell functions
 Decrease of exocrine pancreas
 Endocrinepathothies
 Drug or chemical usage
 Infections
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Gestational diabetes mellitus (GDM)
Defined as any degree of glucose
intolerance with onset or first recognition
during pregnancy.
 4% of pregnancy in US.
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Pathophysiology
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Healthy people blood glucose level maintained
within 60 to 150 mg/dL.
Insulin synthesized in beta cells of pancreas and
secreted rapidly into blood in response to
elevations in blood sugar.
Promoting uptake of glucose from blood into
cells and its storage as glycogen
Fatty acid and amino acids converted to
triglyceride and protein stores.
Pathophysiology
Lack of insulin or insulin resistance, result
in inability of insulin-dependent cells to use
glucose.
 Triglycerides broken down to fatty acids
blood ketones↑  diabelic ketoacidosis.
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Pathophysiology
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As blood sugar levels became elevated (hyperglycemia),
glucose is excreted in the urine and excessive of
urination occurs due to osmotic diuresis (polyuria).
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Increased fluid loss leads to dehydration and excess
thirst (polydipsia).
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Since cells are starved of glucose, the patient
experiences increased hunger (polyphagia).
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Paradoxically, the diabetic patient often loss weight, since
the cells are unable to take up glucose.
Complications
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People with DM have an increased incidence of both
microvascular and macrovascular complications.
Major organs/systems showing changes
Long term complications
Cardiovascular system: heart,
brain, blood vessels
myocardial infarct; atherosclerosis;
hypertension; microangiopathy;
cerebral vascular infarcts; cerebral
hemorrhage
Pancreas
islet cell loss; insulitis (Type 1); amyloid
(Type 2)
Kidneys
nephrosclerosis; glomerulosclerosis;
arteriosclerosis; pyelonephritis
Eyes
retinopathy; cataracts; glaucoma
Nervous system
autonomic neuropathy; peripheral
neuropathy
Peripherals
peripheral vascular atherosclerosis;
infections; gangrene
Diagnosis
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A casual plasma glucose level of 200 mg/dL or
greater with symptoms presented.
Fasting plasma glucose level of 126 or
greater.(Normal <110 mg/dL,IGT,IFG)
Oral glucose tolerance test (OGTT) value in
blood of 200 mg or greater.
ADA recommend >45 y/o screened every 3 years.
Diabetes Care, 2000
National Institutes of Health, Aug 2001
Medical management
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Objective : maintain blood glucose levels
as close to normal as possible.
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Good glycemic control inhibits the onset
and delay of type 1 DM, similar in type 2
DM.
Medical management
Glycated hemoglobin assay (HbA1c )
reflects mean glycemia levels over the
proceding 2~3 months. (normal < 7%)
 HbA1c also a predictor for development of
chronic complications.
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Medical management
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Exercise and diet control
Insulin : rapid, short, intermediate, long acting.
Oral antidiabetic agents
Oral manifestations and
complications
No specific oral lesions associated with diabetes. However,
there are a number of problems by present of hyperglycemia.
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Periodontal disease
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Microangiopathy altering antigenic challenge.
Altered cell-mediated immune response and impaired of
neutrophil chemotaxis.
Increased Ca+ and glucose lead to plaque formation.
Increased collagen breakdown.
Oral manifestations and
complications
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Salivary glands
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Xerostomia is common, but reason is unclear.
Tenderness, pain and burning sensation of tongue.
May secondary enlargement of parotid glands with sialosis.
Dental caries
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Increase caries prevalence in adult with diabetes. (xerostomia,
increase saliva glucose)
Hyperglycemia state shown a positive association with dental
caries.
Oral manifestations and
complications
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Increased risk of infection
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Reasons unknown, but macrophage metabolism altered with
inhibition of phagocytosis.
Peripheral neuropathy and poor peripheral circulation
Immunological deficiency
High sugar medium
Decrease production of Ab
Candical infection are more common and adding effects with
xerostomia
Oral manifestations and
complications
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Delayed healing of wounds
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Due to microangiopathy and ultilisation of protein for energy, may
retard the repair of tissues.
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Increase prevalence of dry socket.
Miscellaneous conditions
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Pulpitis : degeneration of vascular.
Neuropathies : may affect cranial nerves. (facial)
Drug side-effects : lichenoid reaction may be associated with
sulphonylurea. (chlopropamide)
Ulcers
New Zealand Journal, Jan 1985
Dental management
considerations
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To minimize the risk of an intraoperative emergency,
clinicians need to consider some issues before initiating
dental tx.
Medical history : take hx and assess glycemic control at
initial appt.
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Glucose levels
Frequency of hypoglycemic episodes
Medication, dosage and times.
Consultation
Dental management
considerations
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Scheduling of visits
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Morning appt. (endogeneous cortisol)
 Do not coincide with peak activity.
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Diet
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Blood glucose monitoring
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Ensure that the patient has eaten normally and taken medications as
usual.
Measured before beginning. (<70 mg/dL)
Prophylactic antibiotics
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Established infection
Pre-operation contamination wound
Major surgery
Dental management
considerations
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During treatment
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The most complication of DM occur is hypoglycemia episode.
Hyperglycemia
After treatment
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Infection control
Dietary intake
Medications : salicylates increase insulin secretion and
sensitivity avoid aspirin.
Emergency management
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Hypoglycemia
 Initial
signs : mood changes, decreased
spontaneity, hunger and weakness.
 Followed by sweating, incoherence,
tachycardia.
 Consequenced in unconsiousness,
hypotention, hypothermia, seidures, coma,
even death.
Emergency management
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15 grams of fast-acting oral carbonhydrate.
Measured blood sugua.
Loss of conscious, 25-30ml 50% dextrose
solution iv. over 3 min period.
Glucagon 1mg.
911, 119
Emergency management
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Severe hyperglycemia
 A prolonged
onset
 Ketoacidosis may develop with nausea,
vomiting, abdominal pain and acetone odor.
 Difficult to different hypo- or hyper-.
Emergency management
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Hyperglycemia need medication intervention
and insulin administration.
While emergency, give glucose first !
Small amount is unlikely to cause significant
harm.
JADA, Oct 2001
Conclusion
Thanks for ur attention !!
1.Liver
glucose
2.Adipose
glucose
ketone body
TG
ATP+co2
glycerol-po4
acetyl coA
glycerol +FA
TG
FA
Glycerol-po4
glycerol
FA+ALB
glucose
3.Muscle
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glucose
glucose
glucose