Professional Documents
Culture Documents
Mithileswer Kadiyala
Contents
Diabetes-Introduction Normal blood glucose levels Classification Diagnosis Pathophysiology Symptoms & Complications Oral manifestations Management & Emergency Treatment
Diabetes mellitus
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 make glucose available to various cells in the body & thus decrease blood glucose levels.
HYPOGLYCEMIA.
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)
Type 1 (IDDM)
Autoimmune destruction of the insulin-producing beta cells of pancreas. 5-10% of DM cases. Mostly occurs in childhood and adolescence or any adolescence, age. Absolute insulin deficiency. High incidence of severe complications complications. Prone to autoimmune diseases (Graves, Addison, diseases. Hashimotos thyroiditis)
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 history and lack of physical activity..etc.
Comparison
Clinical
Type 1
-onset <20 years -normal weight -decreased blood insulin -anti-islet cell antibodies
Type 2
-onset >30 years -obesity -normal or increased blood insulin -no anti-islet cell antibodies ketoacidosis rare No HLA association insulin resistance
Genetics
Pathogenesis
relative insulin deficiency no insulitis focal atrophy and amyloid deposits mild beta-cell depletion
Islet Cells
Diagnosis
A Random plasma glucose(RBS) level of >=200 mg/dL with symptoms presented. Fasting plasma glucose level(FBS) of >=126. (Normal <110 mg/dL,) Oral glucose tolerance test (OGTT) value in blood of >=200 mg/dL. Glycosylated haemoglobin (HbA1c ) value >7%
Pathophysiology of Diabetes
In type1:- -insulin is not secreted by beta cells -as a result,glucose doesnot enter into cells. -so cells are starved of glucose inspiteof its presence in plenty. In type2:-cells are resistant to insulin -hence though insulin is present, glucose is not taken by cells.
Pathophysiology of Diabetes(cont.)
Lack of insulin or insulin resistance, result in inability of insulin-dependent cells to use glucose. As a result cells utilize fats for energy Triglycerides broken down to fatty acids blood ketones diabetic ketoacidosis(diabetic coma). The chances of occurrence of ketoacidosis is more common in type1 diabetes..
Symptoms of Diabetes
As blood glucose levels become elevated (hyperglycemia), Glucose is excreted in the urine and excessive urination (polyuria) occurs because of osmotic diuresis. Increased fluid loss leads to dehydration and excessive thirst (polydipsia). Since cells are starved of glucose, the patient experiences increased hunger (polyphagia). Paradoxically, the diabetic patient often loses weight, since the cells are unable to take up glucose. These are the classic signs and symptoms of DM.
Complications of Diabetes
Many complications of diabetes are attributed to Microangiopathy caused by the disease Microangiopathy results in occlusion of small peripheral blood vessels, resulting in ischemia, which inturn predisposes to infection, gangrene, decreased wound healing Another factor for complications is impaired neutrophil chemotaxis making the host susceptable to infections..
Complications of Diabetes
Major organs/systems showing changes Cardiovascular system
islet cell loss; insulitis (Type 1); amyloid (Type 2) nephrosclerosis; glomerulosclerosis; arteriosclerosis; pyelonephritis retinopathy; cataracts; glaucoma autonomic neuropathy; peripheral neuropathy peripheral vascular atherosclerosis; infections; gangrene
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 Xerostomia is common, but reason is unclear. Tenderness, pain and burning sensation of tongue. May secondary enlargement of parotid glands with sialosis.
Salivary glands
Medical management
Exercise and diet control Insulin : rapid, short, intermediate, long acting. Oral antidiabetic agents
Medical history : take history and assess glycemic control at initial appt.
Glucose levels Frequency of hypoglycemic episodes Medication, dosage and times. Consultation
Emergency management
Hypoglycemia(Insulin shock):Initial signs: weakness; dizziness pale ; moist skin headache ; altered consciousness management: . i.v. injection of 50% dextrose sol. . i.m. injection of glucagon. .administration of oral forms of sugars.
Emergency management
Hyperglycemia(Ketosis):
Initial signs:
dry, warm skin ; kussmauls breathing; acetone breath; rapid weak pulse; headache ; altered consciousness management: . i.v. injection of 50% dextrose sol. .careful administration of i.m. insulin by monitering blood glucose levels. .administration of oxygen..
After treatment..
Patients with poorly controlled DM are at greater risk of developing infections and may demonstrate delayed wound healing. Therefore, antibiotic coverage may be necessary for patients with overt oral infections or for those undergoing extensive surgical procedures.
Conclusion
It is important for dentists to be familiar with the medical management of patients with DM, and to recognize the signs and symptoms of undiagnosed or poorly controlled disease. By taking an active role in the diagnosis and treatment of oral conditions associated with DM, dentists also may contribute to the maintenance of optimum health in patients with this disease.