BETTY GRABLE:FREQUENT PEE’R OR DIABETIC UNDERCOVER?

By: N. Mattila, B. McKinley, C. Metcalf, D. Moening, B. Moore, M. Morrell, J. Nguyen, X. Nguyen

“You may remember diabetes from such famous movies as. . .”

“You may remember diabetes from such famous people as…”

Patient Presentation: Meet Betty

20 y.o. female No positive

responses on MHx/DHx

BP: 120/80 HR: Regular

70bpm

Betty Grable

Recent weight loss

Betty Grable

. . . Unintentionally

Betty Grable

Dry mouth “Cotton Mouth”

Betty Grable

Frequent thirst

Betty Grable

Frequent Urination

Betty Grable

Chronic Skin Infections

Betty Grable

Unusual periodontal disease and alveolar bone loss

Lateral periodontal abscesses on premolars and generalized vertical bone loss

Diabetes Background

Basic pathophysiologic dysfunction: lack of insulin or its function Type 1 – destruction of islet cells which produce insulin Type 2 – receptor decrease/insensitivity or insulin malsecretion

 Diabetes may be due to:

Destruction of pancreatic islet cells Endocrine condition (hyperpituitarism or hyperthyroidism) Iatrogenic disease after administration of steroids Genetic factor

 Primary physiological consequences that may occur:

Hyperglycemia – underutilized and overproduced Ketoacidosis – acidic drop in blood pH Vascular wall disease – microangiopathy and atherosclerosis

Neuropathy – motor and sensory complications

Questions to Ask

When was the last time she visited her primary physician? Results/findings Treatment Any Rx

Does she have symptoms of nephropathy? Renal failure

Questions to Ask

Does she have symptoms of microangiopathy or retinopathy Has she noticed any change in vision? Nonproliferative:

Microaneurysms Retinal hemorrhages Retinal edema Retinal exudates

Proliferative Neovascularization Glial proliferation Vitreoretinal traction Metabolic cataract

Frequent Urination

Questions to Ask

Does she have symptoms of macrovascular disease? Has she been diagnosed or suspect of

cholesterol or lipid problems or heart problems? LDL high, HDL low Atherosclerosis MI CHD

Questions to Ask

Symptoms of neuropathy Does she have any of the following

symptoms? Muscle weakness Muscle cramps Deep burning pain Tingling or numbness Loss of tendon reflex, two-point discrimination

and position sense Oral paresthesia Burning tongue Others: esophageal dysfunction, nocturnal

diarrhea, sexual impotence, bladder dysfunction

Questions to Ask

Does she have “other” complications typically associated with diabetes-decubitus ulcerations Gangrenous extremities Cataracts Skin rash Cutaneous fat deposits (xanthoma diabeticornum)

Does she have typical DDS findings? Xerostomia Poor wound healing Rampant caries Periapical abscess Gingivitis and periodontal disease (Type 1, <30 yo.) Oral/neurologic manifestations

Questions to Ask

Questions relating to diabetic origin. Does she have any… Type 1:

Family history/genetic component (parent, grandparent, aunt, uncle) Cardinal symptoms: polydispsia, polyuria, polyphagia, weight loss, loss

of strength Other symptoms: dry mouth, recurrent bed wetting, repeated skin infections,

marked irritability, headache, drowsiness, malaise. Type 2

Strong family history/ genetic component (parent, grandparent, aunt, uncle)

Cardinal symptoms: polydispsia, polyuria, polyphagia, weight loss, loss of strength Other Symptoms: Slight weight loss or gain, GI upset, nausea, urination at

night, vulvar pruritus, blurred vision, decreased vision, paresthesias, dry flushed skin, loss of sensation, impotence, postural hypotension

Gestational Reason to believe that she may be pregnant? Children born >9lbs at birth.

Has she been referred or screened for diabetes? Findings?

Other info required of known diabetics When was the last time she has been to her

primary care provider? How is her condition controlled (insulin or

diet/exercise)? Has she had breakfast/lunch today? How often does she monitor her glucose levels? What was her last reading (70-200 mg/dL)? Do she have any other medical conditions (HTN,

Renal failure, MI, Blindness, Stroke, ect.)? Change in Rx (drug interaction leading to

change in insulin effectiveness)?

Frequent Urination

Lab tests to request

Consult physician Fasting blood glucose Glucose tolerance test Glycohemoglobin Urinary Glucose and Acetone

Physical Evaluation of a Diabetic dehydration/thirst

(xerostomia) increase urination

(freq. & vol.) muscle weakness GI upset/nausea blurred vision/

blindness

increase hunger/ food intake

sudden weight fluctuation

susceptibility to infections

nocturnal urination/bedwetting

drowsiness/ malaise/ irritability

“italicized” signs/symptoms indicate cardinal symptoms often seen in most Type 1 patients but less common in Type 2 patients.

Pathophysiology

Normal: Glucose intake causes insulin release from β-islet cells which signals body to bring glucose into the cells from the blood.

Diabetes: Glucose intake causes:

No insulin release and thus no glucose uptake by body

OR insulin release but body does not recognize it and again does not take up glucose

Pathophysiology

No glucose uptake is problematic As the body tries to maintain homeostasis it

will increase internal glucose production by metabolism of glycogen, fat and protein.

But this production does not matter because insulin is still not released in response to this internal glucose production.

“Overproduction and Underuse”

Pathophysiology: Overproduction Unintentional weight loss Metabolic acidosis from failure of

buffering, respiratory and renal regulatory systems

Decreased ability to fight infection Skin Infections Perio Abscesses

Accelerated atherosclerosis Ulcers, gangrenous feet, HTN, renal failure,

coronary insufficiency, myocardial infarction, stroke

Frequent Urination

Pathophysiology: Underuse

Hyperglycemic State Increased urination w/ glucose (not

normally present) Urination causes dehydration

Thirst Xerostomia

Diabetes Flow Chart

ASA Physical Status

ASA PS III: Presents with uncontrolled and undiagnosed

diabetes mellitus. Clinical presentation guides a diagnosis to

type 1. Currently no signs of renal failure, organ

damage, or other complications that would elevate her to a ASA PS IV level.

If physical exam or physician diagnostics yields any signs of end organ damage ASA PS level will increase.

How do you treat today?

Consult primary physician of status Survey functional capacity

< 4 METs increased risk of complications Monitor vital signs closely

BP, pulse, respiratory rate, temperature Antibiotic treatment Watch for symptoms of

hypoglycemia/hyperglycemia Keep glucose source available in operatory

Others: adequate fluids and moisture (thirst and dry mouth)

Diabetes Management

Diabetes Mellitus is NOT a curable disease!

Treatment consist of lifetime therapy with prevention and treatment of complications

Frequent Urination

Diabetes Management

Therapeutic goals: Good hyperglycemic control

Keeping blood glucose level as close to normal as possible without repeated episodes of hypoglycemia

Maintain normal body weight Control hypertension and hyperlipidemia Develop a flexible treatment plan that allows

the most normal lifestyle possible Continual re-eval and monitoring is

ESSENTIAL

Diabetes Management

Diet and physical activity Rigid control of caloric

intake; must be balanced with physical activity and body weight

Intensive Insulin Conventional, Multiple

daily injections, Continuous infusion, pancreatic transplantation (IDEAL)

Diet and physical activity

Oral Antidiabetic Hypoglycemic Drugs

Insulin therapy

TYPE 1 TYPE 2

Insulin

Parameters for selection: Speed of onset, peak affect, duration of action

Types available: Human insulin and analogues, bovine and

porcine pancreatic extracts; rapid/short/intermediate/long-acting preparations available

Delivery: Into subcutaneous fat tissue

(needle or Siastic infuser, pen-and-cartridge devices, pumps)

Others considerations: nasal, pulmonary, oral, transdermal, peritoneal

Four classes of Hypoglycemic Drugs(Divided by mechanism of action)

Larg

est

Sm

alle

st

“A” for Betty

Anesthetics: Routine use of local anesthetic with 1:100,000 epinephrine should be tolerated well by patients with diabetes; however, the epinephrine may cause blood glucose levels to rise in these patients. Caution is also indicated in diabetics with hypertension, post myocardial infarction, and cardiac arrhythmias. 

Analgesics: Large doses of NSAIDs may interact with insulin to increase hypoglycemic effects in diabetic patients.

Antibiotics: Antibiotic prophylaxis can be considered for patients with extreme hyperglycemia and hypoglycemia and those taking high doses of insulin who also have chronic states of oral infection.

“B” for Betty

Bacteremia: Diabetic patients are at increased risk of developing infections due to their fluctuating blood glucose levels.

Blood pressure: Vital signs serve as a guide to the control and management of disease in the diabetic patient. Patients with abnormal pulse rate, rhythm or elevated blood pressure should be treated with caution.

Frequent Urination

“C” for Betty

Systemic complications: Unintentional weight loss Decreased ability to fight infection Delayed wound healing Atherosclerosis occurs earlier and can lead to:

Retinopathy and blindness Diabetic nephropathy and renal failure Increased risk of hypertension, MI, and stroke

Risk of ulceration, gangrene of the feet, and amputation

Diabetic neuropathy Early death

“C” for Betty

Oral complications: Xerostomia Increased prevalence and severity of

caries Infections are more common Poor wound healing Gingivitis and periodontitis Periapical abscesses Burning mouth Parotid hypertrophy

“D” for Betty

Insulin drug interactions or the hypoglycemic effect hypoglycemic effect:

Salicyclates, NSAIDS (if large dose/chronic use), alcohol, ketoconazole, non-selective beta-blockers

hypoglycemic effect Corticosteroids, epinephrine

More D for Betty…(for TYPE 2)

Incretin mimetics – increased insulin response (Exenatide)

Amylinomimetics – modulates gastric emptying, preventing rise in serum glucagon and decreases satiety (Pramlintide – cannot be mixed with insulin)

Frequent Urination

“D” for Betty

Dental Management Considerations: Monitor insulin and blood glucose levels Adjust insulin if necessary (consult physician) Monitor vitals Prevent insulin shock:

Have patient eat normal Take normal insulin Early, short, non-stressful appointments Have patient inform you if symptoms arise

Have glucose source available Prevent and treat infection aggressively Be cautious of drug interactions

What to do. . .

“E” for Betty

Emergency: 3 stages of hypoglycemic shock:

Mild: Hunger, weakness, tachycardia, pallor, diaphoresis,

paresthesias Moderate:

Incoherence, uncooperativeness, belligerence, lack of judgment, poor orientation

Severe: Unconciousness, tonic or clonic movements,

hypotension, hypothermia, rapid thready pulse Treatment: glucose (orange juice, Glucola etc)

Advisable to keep a source of sugar in your office NPO if unconscious Activate EMS

“E” for Betty

Dental emergency Make sure patient has taken insulin and

eaten normally Monitor blood glucose levels Monitor vitals Watch for signs and symptoms of

hypoglycemic shock Refer to physician Consider antibiotic therapy

Dr. Rhodus?