PHYSICAL EVALUATION I (Dent 5121) Endocrine System: Diabetes Mellitus

Transcription

1 PHYSICAL EVALUATION I (Dent 5121) Endocrine System: Diabetes Mellitus

2 Lecture Objectives After today s lecture, the student will be able to: 1. Identify patients currently suffering from or having a history of diabetes mellitus through the past medical history, review of systems, and physical examination 2. Obtain information from the interview process and physical examination of the patient to determine the severity of the disease and the patient s current physical status 3. Identify potential medical complications of diabetes mellitus that may require modification of the dental management of the patient 4. Identify potential oral manifestations of diabetes mellitus or its treatment

3 Diabetes Mellitus Beta islet cells in the pancreas produce insulin Insulin regulates the level of glucose in the blood Insulin moves glucose from the blood into storage tissues. Glucose diffuses into most cells including neural, hepatic, and connective tissues. Adipose and muscle require insulin for entry of glucose.

4 Diabetes Mellitus Insulin is secreted in response to glucose absorption by the intestine and elevated blood glucose levels. Insulin performs 3 major functions: Lowers blood glucose concentration Enhances glucose uptake into muscle and adipose tissue by facilitating glucose transfer across cell membranes Stimulates glycogen formation in the liver.

5 Diabetes Mellitus Diabetes mellitus - a chronic metabolic disorder A lack of insulin and/or unresponsiveness of tissues to insulin Results in elevated blood glucose levels Metabolic and vascular components

6 Diabetes Mellitus Diabetes mellitus affects approximately 18 million people (7% of population) in the U.S. 14 million people diagnosed 6 million people undiagnosed Incidence is rising

7 Diabetes Mellitus Diabetes is a multifactorial disorder Genetic predisposition Primary destruction of islets of Langerhans in the pancreas Iatrogenic factors Infectious agents

8 Type 1 Diabetes Mellitus Previously called Insulin-dependent DM, IDDM, Type I Immunologically mediated destruction of pancreatic beta cells Leads to absolute insulin deficiency Accounts for 10% of patients with diabetes Onset before age 20 (juvenile onset) 20% of patients with type 1 diabetes have a positive family history for diabetes

9 Type 1 Diabetes Mellitus Thin body build Pancreas produces little or no insulin Daily injections of insulin are required More severe, greater fluctuations in blood glucose concentrations, more complications, and results in a shorter life span than diabetes mellitus type 2

10 Type 2 Diabetes Mellitus Previously called Noninsulin-dependent DM, NIDDM, Type II Altered sensitivity of peripheral tissues (especially muscle and fat cells) to insulin Relative insulin deficiency Accounts for 90% of patients with diabetes mellitus Develops gradually after age 40 Stronger genetic basis than type 1 diabetes mellitus

11 Type 2 Diabetes Mellitus Usually associated with obesity Normal or elevated levels of insulin and excess glucagon release by the pancreas Usually treated with diet and/or oral hypoglycemic drugs but ~25% require insulin Less severe complications, associated with 30% decrease in life span

12 Risk Factors For type 1 DM Scandinavian ethnic background For type 2 DM Over 45 yrs old Overweight (BMI > 25) Parent or sibling with DM Hypertension Hyperlipidemia Gestational diabetes Physically inactive

13 Other Categories of Diabetes Impaired glucose tolerance impaired response to glucose challenge but no signs or symptoms of diabetes Gestational diabetes

14 Other Categories of Diabetes Secondary diabetes mellitus other conditions that disturb insulin production or utilization such as: Hyperpituitarism (acromegaly) Cushing s syndrome Chronic pancreatitis Carcinoma of the pancreas

15 Clinical Findings Type 1 diabetes Hyperglycemia - elevation of blood glucose levels Glucosuria - glucose in urine Polyuria - increased urinary output Nocturia - urination at night Polydipsia - increased thirst Polyphagia - increased hunger Weakness Weight loss

16 Clinical Findings Type 1 diabetes Ketoacidosis Acetone breath Kussmaul respirations (deep and rapid) Nausea and vomiting Depressed cognitive function Cardiovascular insufficiency Coma Death

17 Clinical Findings Microangiopathy Small vessels Vascular proliferation, weakening of the vessel wall, and microaneurysms Focal bleeding leads to fibrosis and scarring

18 Retinopathy Clinical Findings New vessels grow on the surface of the hypoxic retina, gradually decreasing visual acuity and leading to blindness. Renal failure Microangiopathy Affects capillaries of the renal glomerulus Renal hypertension Decreased excretory function Proteinuria, uremia, and death.

19 Clinical Findings Macroangiopathy Large blood vessels Thickened vascular endothelium Platelet aggregation and release of growth factors Stimulation of smooth muscle proliferation Thickening of the internal layer of the endothelium Vascular narrowing Atherosclerotic plaques form at damaged endothelial sites Altered coagulation promotes thrombosis

20 Clinical Findings Macroangiopathy Atherosclerosis Ischemic heart disease Myocardial infarction Cerebrovascular accidents Peripheral vascular disease

21 Clinical Findings Peripheral neuropathy Numbness, paresthesia, anesthesia, pruritis, and burning pain Decubitus ulcers and amputations Muscle weakness and cramps

22 Clinical Findings Autonomic insufficiency Orthostatic hypotension Impotence Urinary incontinence Alternating bouts of diarrhea and constipation

23 Clinical Findings Susceptibility to infection Gangrene of the soft tissues and osteomyelitis of bone Abnormal collagen production, altered chemotaxis, and poor response to infections

24 Clinical Findings Type 2 diabetes Symptoms and signs are often innocuous and longstanding before the diagnosis is made Symptoms (less common than in DM 1) Polyuria Polyphagia Polydipsia Weight loss

25 Clinical Findings Type 2 diabetes Retinopathy and neuropathy may be present but usually not until later in the course of the disease Ketoacidosis and renal disease occur less frequently in type 2 diabetes mellitus than in type 1

26 Diagnosis Clinical signs and symptoms Hyperglycemia Fasting blood glucose level greater than 126 mg/dl on more than one occasion defines diabetes mellitus. 2 hour postprandal glucose level greater than 200 mg/dl after administration of 75 to100 grams of glucose

27 Medical Treatment Type 1 diabetes Diet and physical activity Insulin therapy Short-acting (regular or semilente) Intermediate-acting (NPH or lente) Long-acting (ultralente) Quantity and type of insulin is a gauge of the degree of hyperglycemia Pancreatic transplant

28 Medical Treatment Type 2 diabetes Caloric restriction, weight reduction, and mild to moderate exercise Oral hypoglycemic agents require functioning beta islet cells in pancreas Insulin in 25-30% of patients

29 Medical Treatment Monitoring the effectiveness of therapy Fasting and preprandial glucose levels between mg/dl Glycosylated hemoglobin (hemoglobin A 1C ) less than 7% of total hemoglobin

30 Medical Treatment Level of Control of Diabetes Well-controlled Moderately wellcontrolled Poorly controlled Fasting and preprandial glucose levels <120 mg/dl mg/dl >160 mg/dl Hemoglobin A 1C levels <7% 7-10% >10%

31 Medical Treatment Self-monitoring blood glucose levels Handheld glucometers

32 Review of Systems Do you have diabetes or high blood sugar? Does any one in your family have diabetes or high blood sugar? Do you urinate frequently, drink a lot, and feel hungry a lot?

33 Review of Systems When were you first diagnosed as diabetic? What has your physician told you about your high blood sugar? What was your last blood glucose level? What does it normally run? What was your last hemoglobin A 1C level? What medications are you taking for your high blood sugar?

34 Review of Systems Do you have high blood pressure or problems with your kidneys? Have you had any chest pain, heart attacks, or strokes? Do you have any areas of numbness, tingling, or pain, especially in your legs and feet? Do you have any bedsores or areas that are not healing very quickly? Have you ever had any body parts amputated because of your diabetes?

35 Review of Systems How often do you have infections? Have you had any changes in your vision? Have you ever had to go to the emergency room because of your diabetes? How often do have dizziness, weakness, sweating anxiety and confusion or other symptoms of low blood sugar?

36 Level of Control Complications Assessment ASA Physical Status Renal failure Retinopathy Atherosclerosis/ischemic heart disease/cva Peripheral neuropathy Autonomic insufficiency Susceptibility to infection/gangrene/amputations

37 Assessment ASA Physical Status ASA PS II Well-controlled with dietary modifications, oral hypoglycemic agents or insulin and without complications

38 ASA PS III Assessment Well-controlled or moderately well-controlled with insulin with mild to moderate complications Poorly controlled without complications ASA PS IV ASA Physical Status Moderate or poorly controlled with severe complications Moderate or poorly controlled with renal failure

39 Oral manifestations and dental considerations Xerostomia Burning tongue

40 Oral manifestations and dental considerations Gingivitis and periodontitis Caries

41 Oral manifestations and dental considerations Candidiasis

42 Oral manifestations and dental considerations Delayed wound healing Acetone breath Parotid gland swelling Lichenoid drug reactions (oral hypoglycemics)

43 Lecture Objectives After today s lecture, the student will be able to: 1. Identify patients currently suffering from or having a history of diabetes mellitus through the past medical history, review of systems, and physical examination 2. Obtain information from the interview process and physical examination of the patient to determine the severity of the disease and the patient s current physical status 3. Identify potential medical complications of diabetes mellitus that may require modification of the dental management of the patient 4. Identify potential oral manifestations of diabetes mellitus or its treatment

44 Preparation for Class Exercise on 4/17/08 Anderson to Lund Cerebrovascular Accidents (strokes) Maier to Yeboah Diabetes mellitus

45 Clinical Seminar Session Group 7/8 Tomorrow 1:30 3:30 pm 7 th Floor North Clinic Bring your name tag, safety glases and a pen! Dress appropriately for patients!

46 Review Session Tuesday, April 22 nd 8 am Moos

47 Clinical Seminar Examination Friday, April 25 th Time change: New time: 9:40-12 pm Room change: New room: Moos 2-620