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PHYSICAL EVALUATION I(Dent 5121)

Endocrine System:

Diabetes Mellitus

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Lecture Objectives

After todays lecture, the student will be able to:

1. Identify patients currently suffering from or having ahistory of diabetes mellitus through the pastmedical history, review of systems, and physicalexamination

2. Obtain information from the interview process andphysical examination of the patient to determinethe severity of the disease and the patientscurrent physical status

3. Identify potential medical complications of diabetesmellitus that may require modification of thedental management of the patient

4. Identify potential oral manifestations of diabetes

mellitus or its treatment

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Diabetes Mellitus

Beta islet cells in the pancreas produceinsulin

Insulin regulates the level of glucose in theblood

Insulin moves glucose from the blood intostorage tissues.

Glucose diffuses into most cells includingneural, hepatic, and connective tissues.

Adipose and muscle require insulin for entry

of glucose.

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Diabetes Mellitus Insulin is secreted in response to

glucose absorption by the intestine andelevated blood glucose levels.

Insulin performs 3 major functions: Lowers blood glucose concentration

Enhances glucose uptake into muscle and

adipose tissue by facilitating glucosetransfer across cell membranes

Stimulates glycogen formation in the liver.

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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

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Diabetes Mellitus Diabetes mellitus affects approximately

18 million people (7% of population) inthe U.S.

14 million people diagnosed

6 million people undiagnosed

Incidence is rising

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Diabetes Mellitus Diabetes is a multifactorial disorder

Genetic predisposition Primary destruction of islets of Langerhans

in the pancreas

Iatrogenic factors

Infectious agents

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Type 1 Diabetes Mellitus

Previously called Insulin-dependent DM,IDDM, Type I

Immunologically mediated destruction ofpancreatic 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

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Thin body build

Pancreas produces little or no insulin

Daily injections of insulin are required

More severe, greater fluctuations in bloodglucose concentrations, morecomplications, and results in a shorter life

span than diabetes mellitus type 2

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Previously called Noninsulin-dependentDM, 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

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Usually associated with obesity

Normal or elevated levels of insulin andexcess glucagon release by the pancreas

Usually treated with diet and/or oralhypoglycemic drugs but ~25% requireinsulin

Less severe complications, associated with30% decrease in life span

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Risk Factors

For type 1 DM Scandinavian ethnic

background

For type 2 DM Over 45 yrs old

Overweight (BMI > 25)

Parent or sibling withDM

Hypertension

Hyperlipidemia

Gestational diabetes

Physically inactive

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Other Categories of Diabetes

Impaired glucose tolerance impairedresponse to glucose challenge but no signs

or symptoms of diabetes

Gestational diabetes

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Other Categories of Diabetes

Secondary diabetes mellitus otherconditions that disturb insulin production or

utilization such as:

Hyperpituitarism (acromegaly)

Cushings syndrome

Chronic pancreatitis

Carcinoma of the pancreas

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Clinical Findings

Type 1 diabetes

Hyperglycemia - elevation of blood glucoselevels

Glucosuria - glucose in urine

Polyuria - increased urinary output Nocturia - urination at night

Polydipsia - increased thirst

Polyphagia - increased hunger

Weakness

Weight loss

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Clinical Findings

Type 1 diabetes

Ketoacidosis Acetone breath

Kussmaul respirations (deep and rapid)

Nausea and vomiting Depressed cognitive function

Cardiovascular insufficiency

Coma

Death

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Clinical Findings

Microangiopathy

Small vessels Vascular proliferation, weakening of the

vessel wall, and microaneurysms

Focal bleeding leads to fibrosis andscarring

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Clinical Findings

Retinopathy

New vessels grow on the surface of thehypoxic retina, gradually decreasing visualacuity and leading to blindness.

Renal failure

Affects capillaries of the renal glomerulus

Renal hypertension

Decreased excretory function

Proteinuria, uremia, and death.

Microangiopathy

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Clinical Findings

Macroangiopathy Large blood vessels

Thickened vascular endothelium

Platelet aggregation and release of growthfactors

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

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Clinical Findings

Atherosclerosis

Ischemic heart disease

Myocardial infarction Cerebrovascular accidents

Peripheral vascular disease

Macroangiopathy

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Clinical Findings

Peripheral neuropathy Numbness,

paresthesia,anesthesia, pruritis,

and burning pain

Decubitus ulcers andamputations

Muscle weakness andcramps

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Clinical Findings

Autonomic insufficiency

Orthostatic hypotension

Impotence

Urinary incontinence

Alternating bouts of diarrhea andconstipation

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Clinical Findings

Susceptibility to infection Gangrene of the soft tissues andosteomyelitis of bone

Abnormal collagen production, alteredchemotaxis, and poor response toinfections

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Clinical Findings

Type 2 diabetes

Symptoms and signs are often innocuousand longstanding before the diagnosis ismade

Symptoms (less common than in DM 1)

Polyuria

Polyphagia Polydipsia

Weight loss

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Clinical Findings

Type 2 diabetes

Retinopathy and neuropathy may bepresent but usually not until later in thecourse of the disease

Ketoacidosis and renal disease occur lessfrequently in type 2 diabetes mellitus than

in type 1

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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 ofthe degree of hyperglycemia

Pancreatic transplant

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Medical Treatment

Type 2 diabetes

Caloric restriction, weight reduction, andmild to moderate exercise

Oral hypoglycemic agents requirefunctioning beta islet cells in pancreas

Insulin in 25-30% of patients

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Medical Treatment

Monitoring the effectiveness of therapy

Fasting and preprandial glucose levelsbetween 70-120 mg/dl

Glycosylated hemoglobin (hemoglobin A1C)less than 7% of total hemoglobin

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Medical Treatment

Level of Control of Diabetes

>10%>160 mg/dlPoorly controlled

7-10%121-160 mg/dl

Moderately well-

controlled

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Medical Treatment

Self-monitoringblood glucose levels

Handheldglucometers

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Review of Systems

Do you have diabetes or high bloodsugar?

Does any one in your family havediabetes or high blood sugar?

Do you urinate frequently, drink a lot, andfeel hungry a lot?

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Review of Systems

When were you first diagnosed as diabetic?

What has your physician told you about yourhigh blood sugar?

What was your last blood glucose level? Whatdoes it normally run?

What was your last hemoglobin A1C level?

What medications are you taking for your highblood sugar?

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Review of Systems

Do you have high blood pressure or problems

with your kidneys?

Have you had any chest pain, heart attacks, orstrokes?

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 nothealing very quickly?

Have you ever had any body parts amputated

because of your diabetes?

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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 othersymptoms of low blood sugar?

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Assessment

Level of Control

Complications

Renal failure

Retinopathy

Atherosclerosis/ischemic heart disease/CVA

Peripheral neuropathy

Autonomic insufficiency

Susceptibility to

infection/gangrene/amputations

ASA Physical Status

A

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Assessment

ASA PS II

Well-controlled with dietary modifications, oralhypoglycemic agents or insulin and withoutcomplications

ASA Physical Status

A

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Assessment

ASA PS III

Well-controlled or moderately well-controlledwith insulin with mild to moderate complications

Poorly controlled without complications

ASA PS IV

Moderate or poorly controlled with severecomplications

Moderate or poorly controlled with renal failure

ASA Physical Status

Oral manifestations and dental

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Oral manifestations and dentalconsiderations

Xerostomia

Burning tongue

O l if t ti d d t l

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considerations

Gingivitis andperiodontitis

Caries

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considerations

Candidiasis

O l if i d d l

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considerations

Delayed wound healing

Acetone breath

Parotid gland swelling

Lichenoid drug reactions

(oral hypoglycemics)

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Lecture Objectives

After todays lecture, the student will be able to:1. Identify patients currently suffering from or having a

history of diabetes mellitus through the pastmedical history, review of systems, and physicalexamination

2. Obtain information from the interview process andphysical examination of the patient to determine

the severity of the disease and the patientscurrent physical status

3. Identify potential medical complications of diabetesmellitus that may require modification of thedental management of the patient

4. Identify potential oral manifestations of diabetesmellitus or its treatment

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Preparation for Class Exercise on4/17/08

Anderson to Lund

Maier to Yeboah

CerebrovascularAccidents (strokes)

Diabetes mellitus

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Clinical Seminar SessionGroup 7/8

Tomorrow1:30 3:30 pm

7

th

Floor North Clinic

Bring your name tag, safety glases

and a pen!Dress appropriately for patients!

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Review Session

Tuesday, April 22nd

8 am

1-451 Moos

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Clinical Seminar Examination

Friday, April 25th

Time change:

New time: 9:40-12 pm

Room change:

New room: Moos 2-620

27 diabetes 2008

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