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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?