Management of the Diabetic Patient

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Management of the Diabetic Patient

• Dr. Griffin

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Diabetes

• Diabetes has two components Metabolic and
  Vascular.
• The metabolic component consists of elevation of
  blood glucose associated with alterations in
  lipid protein metabolism, resulting from a
  relative or absolute lack of insulin.
• The vascular component includes the microvascular
  disease of the kidney and the eye as well as with
  premature macrovascular pathology and serious
  microangiopathy pathology.

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Diabetes in the US

• 15-20 million persons with diabetes
• Half of these people are unaware that they are
  diabetic
• 1.4 million have Type I, 14.5 million have Type
  II, the remainder have other specific types
• Prevalence rates have increased six fold over the
  last 40 years
• 3rd leading cause of death

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Diabetes Etiology

• Diabetes may result from any of the following
• Autoimmune disorder
• Primary destruction of islet cells by
  inflammation, cancer, or surgery
• Endocrine condition such as hyperpituitarism or
  hyperthyroidism
• Iatrogenic disease following the administration
  of steroids

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Pathophysiology of Diabetes

• Glucose is the major fuel for the body and the
  most important stimulus for insulin secretion.
• When levels exceed 180mg/100ml, glucose is
  excreted into the urine which results in
  increased urinary volume
• This increase leads to dehydration, and loss of
  electrolytes

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Pathophysiology of Diabetes

• Insulin is needed for muscle, fat, and liver to
  utilize glucose from the blood. The CNS and
  renal cortex, however, can utilize glucose from
  blood without insulin.
• Insulin is released from islet cells of Langerhan
  in the pancreas to have 4 actions

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Pathophysiology of Diabetes

• Transfer glucose from blood to insulin-dependent
  tissues
• Stimulate transfer of amino acids from blood to
  cells
• Stimulate triglyceride synthesis from fatty acids
• Inhibit breakdown of triglycerides for
  mobilization of fatty acids

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Pathophysiology of Diabetes

• Without insulin, cells are impermeable to glucose
  and they begin to breakdown triglycerides into
  fatty acids, the byproducts of this gives rise to
  Ketoacidosis.

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Type I Diabetes

• Insulin is virtually absent
• Plasma glucagon is elevated
• Pancreatic Beta cells fail to respond to all
  insulingoenic stimuli

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Type I Diabetes

• Onset usually before 40, most likely children and
  teenagers
• Polyuria, polydipsia, increased fat metabolism,
• Prone to ketoacidosis
• Caused by Genetic predispositionHLA, Extrinsic
  factors viral (mumps, Coxsackie's, CMV,
  hepatitis)
• Require exogenous insulin replacement

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Type II Diabetes

• Tissue insensitivity to insulin
• Deficiency in the response of pancreatic B cells
  to glucose
• Etiology Obesity, Genetics
• Accounts for more than 90 of all Diabetics

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Type II Diabetes

• Onset is usually adulthood
• Tendency to be obese
• Polyuria, polydipsia, but usually not prone to
  ketoacidosis
• Treatment is usually weight loss, diet
  restrictions, and oral hypoglycemics

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Other Specific Types

• Genetic Defects of pancreatic B cell function
• Diseases of the exocrine pancreas
• Endocrinopathies i.e.) Acromegaly, Cushing's

• Genetic Defect in insulin action
• Drug or chemical induced
• Other genetic syndromes i.e.) Downs, Turners

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Signs and Symptoms

• Polyuria and polydipsia-due to osmotic diuresis
  secondary to sustained hyperglycemia
• Results in loss of glucose, water, and
  electrolytes

• Polyphagia- initially due to depletion of water,
  glycogen, and triglycerides
• Then due to reduced muscle mass as amino acids
  are diverted to form glucose, and ketone bodies

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Signs and Symptoms

• Weakness and Postural Hypotension-due to lowered
  plasma volumes, total body potassium loss, and
  general catabolism of muscle protein

• Recurrent blurred vision- lenses and retinas are
  exposed to hypermolar state
• Paresthesias

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Signs and Symptoms

• Macrovascular Disease (atherosclerosis)-found in
  individuals with uncontrolled diabetes
• Increased levels of LDL
• Increased risk of ulceration and gangrene of the
  feet, HTN, renal failure, coronary insufficiency,
  MI, and CVA
• MI is the leading cause of death in Type II
  patients

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Signs and Symptoms

• Microvascular disease
• Thickening of intima
• Endothelial proliferation
• Lipid depositions
• Mostly effects the retinas and small vessels of
  the kidneys

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Signs and Symptoms

• Diabetic Retinopathy
• Reflects the rate of absorption, uptake by tissue
  and excretion in urine
• Nonproliferative changes i.e.) microaneruysms,
  retinal changes
• Proliferative changes i.e.) neovascularization

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Signs and Symptoms

• Diabetic Nephropathy
• Sustained hyperglycemia leads to increased
  albumin levels. This decreases GFR and leads to
  ESRD.
• Leading cause of death in Type I Diabetes

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Signs and Symptoms

• Diabetic Neuropathy
• Muscle Weakness, Muscle cramps, deep burning
  pain, tingling sensation, numbness
• Loss of intestinal mobility, gastric distention,
  sexual impotence, bladder dysfunction, esophageal
  dysfunction

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Diabetic Ketoacidosis

• Leads to decrease in the bloods pH or metabolic
  acidosis. As the blood levels of ketoacids
  rises, the blood pH drops below 7.3, and induces
  hyperventilation
• Signs anorexia, nasuea/vomitting, polyuria,
  tachypnea, dehydration, and coma
• Patients may have sweet or fruity breath due to
  the byproduct acetone

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Oral signs and symptoms

• Xerostomia, increased caries
• Dry atrophic cracked oral mucosa, angular
  chellitis
• Mucositis, ulcers, and desquamative gingivitis,
  burning mouth syndrome
• Difficulty swallowing
• Opportunistic bacteria, fungal, viral infection

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Oral Signs and Symptoms

• Poor Wound Healing
• Periodontal Disease-usually in poorly controlled
  or undiagnosed diabetics
• Incidence of Perio Disease increases among
  patients with diabetes as they age
• Diabetics with advanced systemic conditions have
  periodontal disease more frequently and severe.

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Diagnosing the Diabetic

• Symptoms of Diabetes and non-fasting plasma
  glucose concentration is 200mg/ml or greater
• Fasting glucose is 126mg/dl
• Lowered oral glucose tolerance test (after 75g
  glucose load) blood glucose is 200mg/dl or greater

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Diagnosing the Diabetic

• Glycosylated Hemoglobin Hb1Ac
• Glycohemoglobin increases in presence of
  hyperglycemia
• Levels help monitor progress of disease and level
  of patient control
• Reflects glucose levels in blood over 6-8 weeks
  preceding the test

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Dental Management

• Important to get a complete health history
• Ask the undiagnosed diabetic about signs and
  symptoms, family history, and determine if they
  are at risk
• Ask the known diabetic about their glucose
  levels, how they control their glucose, their
  last doctors visit, and if they are displaying
  any symptoms of diabetes now

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Treatment Modifications

• Short morning appointments
• Instruct patient to eat normal AM meal
• Frequent hygiene recalls
• Stress reduction protocol
• Antibiotic management for acute infections

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Elective treatment

• If fasting glucose levels are less than 70 mg/dl,
  defer elective treatment and give patient
  carbohydrates
• Err on the side of hyperglycemia

• If fasting glucose is above 200 mg/dl, defer
  elective treatment and give patient hypoglycemic
  agent
• Refer to physician

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Managing the Hypoglycemic Emergency

• Hypoglycemia presents with
• Nervousness
• Sweating
• Tremor
• Headache
• Confusion
• LOC with decreased respiration

• Treatment of the conscious patient includes
  giving oral carbs, and continue assessing vitals
• Unresponsive patient-activate ABCs, and
  administer parenteral carbohydrates

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Managing the Hyperglycemic Diabetic

• Blood glucose levels greater than 250 mg/dl
• Dry, warm skin
• Hyperventilation
• Fruity, sweet breath
• Rapid weak pulse, and normal to low BP

• Conscious patient-supportive care
• Unconscious patient- ABCs, Call 911
• Do not administer insulin
• Start IV of 5 Dextrose and normal saline before
  EMT arrive