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Diabetes Mellitus patients in dental management

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Title: Diabetes Mellitus patients in dental management


1
Diabetes Mellitus patients in dental management
  • shabeel pn

2
Introduction
  • Diabetes mellitus is a metabolic disorder
    characterized by relative or absolute
    insufficiency of insulin, and resultant
    disturbances of carbohydrate metabolism.
  • The major function of insulin is to counter the
    concerted action of a number of
    hyperglycemia-generating hormones and to maintain
    low blood glucose levels.

3
Epidemiology
  • 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
4
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5
Etiologic classification of DM
  • 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
6
Type 1 (IDDM)
  • 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. (Graves, Addison,
    Hashimotos thyroiditis)

7
Type 2 (NIDDM)
  • 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.

8
Comparison Type 1 Type 2
Clinical onset lt20 years onset gt30 years
  normal weight obesity
  decreased blood insulin normal or increased blood insulin
  anti-islet cell antibodies no anti-islet cell antibodies
Genetics ketoacidosis common ketoacidosis rare
  human leukocyte antigen (HLA)-D linked No HLA association
Pathogenesis autoimmunity, immunopathologic mechanisms insulin resistance
  severe insulin deficiency relative insulin deficiency
Islet Cells insulitis early no insulitis
  marked atrophy and fibrosis focal atrophy and amyloid deposits
  severe beta-cell depletion mild beta-cell depletion
9
Other specific types
  • Genetic defects of beta-cell functions
  • Decrease of exocrine pancreas
  • Endocrinepathothies
  • Drug or chemical usage
  • Infections
  • .

10
Gestational diabetes mellitus (GDM)
  • Defined as any degree of glucose intolerance with
    onset or first recognition during pregnancy.
  • 4 of pregnancy in US.

11
Pathophysiology
  • 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.

12
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.

13
Pathophysiology
  • As blood sugar levels became elevated
    (hyperglycemia), glucose is excreted in the urine
    and excessive of urination occurs due to osmotic
    diuresis (polyuria).
  • Increased fluid loss leads to dehydration and
    excess thirst (polydipsia).
  • Since cells are starved of glucose, the patient
    experiences increased hunger (polyphagia).
  • Paradoxically, the diabetic patient often loss
    weight, since the cells are unable to take up
    glucose.

14
Complications
  • 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
15
Diagnosis
  • A casual plasma glucose level of 200 mg/dL or
    greater with symptoms presented.
  • Fasting plasma glucose level of 126 or
    greater.(Normal lt110 mg/dL,IGT,IFG)
  • Oral glucose tolerance test (OGTT) value in blood
    of 200 mg or greater.
  • ADA recommend gt45 y/o screened every 3 years.

Diabetes Care, 2000 National Institutes of
Health, Aug 2001
16
Medical management
  • Objective maintain blood glucose levels as
    close to normal as possible.
  • Good glycemic control inhibits the onset and
    delay of type 1 DM, similar in type 2 DM.

17
Medical management
  • Glycated hemoglobin assay (HbA1c ) reflects mean
    glycemia levels over the proceding 23 months.
    (normal lt 7)
  • HbA1c also a predictor for development of chronic
    complications.

18
Medical management
  • Exercise and diet control
  • Insulin rapid, short, intermediate, long
    acting.
  • Oral antidiabetic agents

19
Oral manifestations and complications
  • No specific oral lesions associated with
    diabetes. However, there are a number of problems
    by present of hyperglycemia.
  • Periodontal disease
  • 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.

20
Oral manifestations and complications
  • Salivary glands
  • Xerostomia is common, but reason is unclear.
  • Tenderness, pain and burning sensation of tongue.
  • May secondary enlargement of parotid glands with
    sialosis.
  • Dental caries
  • Increase caries prevalence in adult with
    diabetes. (xerostomia, increase saliva glucose)
  • Hyperglycemia state shown a positive association
    with dental caries.

21
Oral manifestations and complications
  • Increased risk of infection
  • 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

22
Oral manifestations and complications
  • Delayed healing of wounds
  • Due to microangiopathy and ultilisation of
    protein for energy, may retard the repair of
    tissues.
  • Increase prevalence of dry socket.
  • Miscellaneous conditions
  • 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
23
Dental management considerations
  • 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.
  • Glucose levels
  • Frequency of hypoglycemic episodes
  • Medication, dosage and times.
  • Consultation

24
Dental management considerations
  • Scheduling of visits
  • Morning appt. (endogeneous cortisol)
  • Do not coincide with peak activity.
  • Diet
  • Ensure that the patient has eaten normally and
    taken medications as usual.
  • Blood glucose monitoring
  • Measured before beginning. (lt70 mg/dL)
  • Prophylactic antibiotics
  • Established infection
  • Pre-operation contamination wound
  • Major surgery

25
Dental management considerations
  • During treatment
  • The most complication of DM occur is hypoglycemia
    episode.
  • Hyperglycemia
  • After treatment
  • Infection control
  • Dietary intake
  • Medications salicylates increase insulin
    secretion and sensitivity? avoid aspirin.

26
Emergency management
  • Hypoglycemia
  • Initial signs mood changes, decreased
    spontaneity, hunger and weakness.
  • Followed by sweating, incoherence, tachycardia.
  • Consequenced in unconsiousness, hypotention,
    hypothermia, seidures, coma, even death.

27
Emergency management
  • 15 grams of fast-acting oral carbonhydrate.
  • Measured blood suguar.
  • Loss of conscious, 25-30ml 50 dextrose solution
    iv. over 3 min period.
  • Glucagon 1mg.
  • 911, 119

28
Emergency management
  • Severe hyperglycemia
  • A prolonged onset
  • Ketoacidosis may develop with nausea, vomiting,
    abdominal pain and acetone odor.
  • Difficult to different hypo- or hyper-.

29
Emergency management
  • Hyperglycemia need medication intervention and
    insulin administration.
  • While emergency, give glucose first !
  • Small amount is unlikely to cause significant
    harm.

JADA, Oct 2001
30
Conclusion
31
Thanks for ur attention !!
32
(No Transcript)
33
1.Liver
glucose
glucose TG glycerol-po4 glyce
rol FA glycerol FAALB
2.Adipose
  • ketone body
  • ATPco2
  • acetyl coA
  • TG
  • FA
  • Glycerol-po4
  • glucose
  • glucose

3.Muscle
glucose
glucose
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