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Diabetes
Michele Ritter, M.D.
Argy Resident – February, 2007
Definition of Diabetes
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A chronic metabolic condition characterized by
elevated circulating glucose concentrations resulting
from the insufficient supply or action of the hormone
insulin.
Insulin
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Stimulates glucose uptake by peripheral tissues (mainly
skeletal muscles)
Suppresses endogenous glucose production (but hepatic
glycogenlysis and gluconeogenesis)
Suppreses lipolysis in adipocytes and proteolysis in
muscle.
Effects of Diabetes
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Toxic effects of hyperglycemia on blood
vessels results in chronic vascular
complications.
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Diabetic retinopathy
Diabetic neuropathy
Diabetic nephropathy
Poor wound healing
Cardiovascular disease
Symptoms of Diabetes
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Increased thirst (polydypsia)
Increased urination (polyuria)
Weight loss despite increased food intake
Fatigue
Poor wound healing
Blurred vision
Nausea/vomiting (if in Diabetic ketoacidosis)
Diagnosis of Diabetes
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American Diabetes Association and the World
Health Organization:
Diagnosis
Normal glucose
homeostasis
Fasting Plasma
Glucose
Random Plasma
Glucose
2-Hour Plasma Glucose
(after 75-g oral glucose load)
< 100 mg/dL
< 140 mg/dL
Impaired Glucose
homeostasis
(“pre-diabetes”)
100-125 mg/dL
140-199
Diabetes
≥ 126 mg/dL
≥ 200 mg/dL
(with symptoms)
≥ 200 mg/dL
Diagnosis of Diabetes (cont.)
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Fasting = no food/drink for 8 hours
These tests should be repeated on additional
visit to verify.
HgbA1C is NOT recommended for diagnosis!
Diabetes – Type 1
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Destruction of the pancreatic beta cells, leading to absolute
insulin deficiency
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Type 1A - due to autoimmune destruction of the pancreatic beta cells
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Can check for islet-cell antibodies, anti-insulin antibodies, antibodies to
glutamic acid dehydrogenase (anti-GAD)
Type 1B – idiopathic
Have an absolute requirement for insulin, and will develop
ketoacidosis if they don’t receive it.
Adult-onset Type I Diabetes
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Is actual cause of diabetes in ~7.5-10% of previously diagnosed Type II
diabetes in adults
Often found in non-obese adults
Diagnosed by positive auto-antibodies (especially anti-GAD)
Diabetes – Type 2
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The most common cause of Diabetes
Variable degrees of insulin resistance and
deficiency
Typically present with hyperglycemia, and not
ketoacidosis (though type II can go into
diabetic ketoacidosis!)
Diabetes – Other Causes
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Gestational Diabetes
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Drug-Induced
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Placenta produces anti-insulin antibodies – at times body’s own pancreatic
function is unable to keep up with them
Occurs in 2.1% of women, usually in 2nd or 3rd trimester
Steroids!
HIV meds: protease inhibitors, pentamadine
Atypical anti-psychotics (Clozapine)
Tacrolimus, Cyclosporine
Niacin
Hemochromatosis
Cushing’s Syndrome
Acromegaly
Chronic pancreatitis
Health Maintenance in Diabetic Patient
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Question tobacco use – Smoking cessation!
Diet and Exercise
Foot care
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Avoid going barefoot, even in the home.
Test water temperature before stepping into a bath.
Trim toe nails to shape of the toe; remove sharp edges with a nail file.
Do not cut cuticles.
Wash and check feet daily.
Shoes should be snug but not tight and customized if feet are
misshapen or have ulcers.
Socks should fit and be changed daily.
Home glucose log book
Health Maintenance in Diabetic Patient
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Blood Pressure Check
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Dilated eye exam (ophthalmologist)
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Goal is ≤ 130/80
Type 1: within 3-5 years of diagnosis.
Type 2: shortly after diagnosis (within months)
Both should have subsequent annual eye exams.
Foot exam
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Visual examination of feet at every visit
Comprehensive foot exam annually
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Includes monofilament testing
Check skin for integrity, signs of erythema, calluses, ulcers
Monofilament foot exam
Routine Labs in Diabetic Patient
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Chemistry
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Microscopic urinalysis
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Watch for protein (microalbuminuria)
Best way to catch early signs of nephropathy
Annually (or more frequently if abnormal)
TSH
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Annually
Watch for increase in creatinine
At least once after diagnosis
Fasting lipid panel
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Every five years, or more frequently if abnormal
Goal LDL is < 100! (or less than <70)
Routine labs in Diabetic Patients
(cont.)
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Hemoglobin A1c
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Goal is HgbA1c <7 (or in some cases < 6.1)
Should be checked twice yearly in patients with
good glycemic control, and quarterly in poorly
controlled patients, or those changing therapies.
Treatment of Diabetes
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Aspirin (75-325 mg)
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Given to everyone ≥ 40 years, or to those with
high risk for cardiovascular disease
Do not give to patients ≤ 21 because of risk of
Reye’s syndrome
Oral Therapies
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Usually lower HgbA1c 1-2 %
Insulin
ACE inhibitor!
Oral Agents for Type 2 Diabetes
Medication
Mechanism of Action
Benefits
Risks
Sulfonylureas:
glyburide,
glipizide
Binds to sulfonylurea
receptor, stimulates
insulin reslease
Improved microvascular
outcomes; low cost; daily dosing
Hypoglycemia; weight gain
Meglitinides:
repaglinide,
nateglinide
Binds to sulfonylurea
receptor, stimulating
insulin release
Target postprandial glucose;
mimics physiological insulin
secretion
Hypoglycemia; weight gain; no
long-term experience;
expensive frequent dosing
(compliance)
Biguanides:
Metformin
Decreases hepatic
glucose production; also
might improve insulin
sensitivity
Weight loss or weight-neutrality;
improved macrovascular
outcomes; daily dosing available;
Good in pre-diabetes
Diarrhea; lactic acidosis; many
contraindications (Don’t give
in CHF!)
Alpha-glucosidase
inhibitors:
acarbose, miglitol
Retards gut carbohydrate
absorption
Targets postprandial glucose;
weight-neutral; nonsystemic
Intestinal gas; expensive;
frequent dosing (compliance)
Thiazolidinediones:
Rosiglitazone,
Pioglitazone
Activates PPAR-g,
increasing peripheral
insulin sensitivity
No hypoglycemia; lipid and
vascular benefits; potential for
beta-cell preservationi; daily
dosing
Liver monitoring advised;
edema, weight gain; no longterm experience, expensive.
Insulin Therapy
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Required for all Type I Diabetics, and many Type II
Diabetics
Type I: Require between 0.5 and 1.0 units of insulin
per kilogram of bodyweight per day.
Types:
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Subcutaneous
Pump – primarily in Type I diabetics
Inhaled (Exubera®)
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Approved by FDA in last year
Short-Acting (given before meals)
Need PFTs prior to starting
Insulin
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Rapid-Acting
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Lispro
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Aspart
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Onset: 10-15 min.
Peak: 1-2 hours
Duration: 3 – 5 hours
Onset: 10-15 min.
Peak: 1-2 hours
Duration: 3-5 hours
Short-acting: Regular
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Onset: 0.5 – 1 hour
Peak: 2-4 hours
Duration: 4-8 hours
Insulin (cont.)
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Intermediate-Acting
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Neutral Protamine Hagedorn (NPH)
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Onset: 1-3 hours
Peak: 4-10 hours
Duration: 10-18 hours
Lente
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Onset: 2-4 hours
Peak: 4-12 hours
Duration: 12-20 hours
Insulin (cont.)
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Long-acting
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Insulin detemir
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Onset: 2-3 hours
Peak: none
Duration: up to 24 hours
Insulin glargine (lantus)
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Onset: 2-3 hours
Peak: none
Duration: 24 + hours
Insulin
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Pre-mixed
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NPH/Regular 70/30
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NPH/Regular 50/50
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Onset: 0.5 – 1 hour
Peak: 2 – 10 hours
Duration: 10 -18 hours
Onset: 0.5 – 1 hour
Peak: 2 -10 hours
Duration: 10-18 hours
NPH/Aspart 70/30
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Onset: 10 -15 min.
Peak: 1-3 hours
Duration: 10-16 hours
Insulin – the nitty-gritty
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Good option:
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Long-acting insulin daily (Lantus!)
Short-acting insulin (Novolog) before each meal (pre-prandial) or
with sliding scale insulin before each meal
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Pre-meal insulin should be given ~ 30 min. before eating
Use the am glucose to determine best dose of lantus (If running
high, increase lantus; if running low, decrease lantus)
Use sugars throughout the day to determine pre-meal/Sliding
scale insulin
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If sugars are increasing throughout day, and are really high by
dinner time, increase pre-meal insulin doses.
If sugars keep getting low throughout day, could try
decreasing pre-meal insulin.
What happens when patient admitted
to hospital???
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If only on oral hypoglycemics…
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If patient is insulin…
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Best to hold hypoglycemics (especially metformin!)
Place on Sliding scale insulin
Continue current insulin dose
Sliding scale insulin
If patient is NPO…
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Hold all oral hypoglycemics
Give ½ to ⅔ of usual long-acting insulin.
Sliding scale insulin (with short-acting insulin)
ACE Inhibitors
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Have been shown to be very beneficial in
preventing nephropathy in patients with
Diabetes.
Every diabetic patient with hypertension
should be on ACE Inhibitor.
More extreme treatments for diabetes
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Pancreas transplant
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Usually always in conjunction with kidney
transplant, or in patient who has already
undergone kidney transplant.
Islet cell transplant
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Showing a great deal of promise in clinical trials.
Case # 1
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A 52-year old female with a history of alcohol abuse presents
to your clinic for a first time appointment for unexplained
weight loss. The patient states that she has noticed about a 30
pound weight loss over the last year, approximately 20
pounds of which were lost over the last 2 months, along with
worsening fatigue. She states that 2 months ago she had an
episode of “bronchitis” and went to an urgent care clinic
where she was given a prednisone taper. She states that she
eats “a ton” including an Ensure shake three times a day. She
states that she also drinks water and ice tea all day long –
frequently has two glasses on her desk at any given time.
Case # 1
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PMH:
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h/o Alcohol abuse – quit 9 months ago
h/o pancreatitis – recurrent episodes over last several years; has
not had any problems for last year
PSH: None
Allergies: NKDA
Meds: None
Social History:
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married; history of alcohol abuse, as above; 2 packs/day
tobacco for 40 years; no IV drug use; Currently unemployed
Case # 1 (cont.)
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Physical Exam:
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136/72, 92
Ht: 5’7” Wt: 102 lb.
Gen: Emaciated female; alert and oriented, in NAD;
during the exam she asks if she can sneak out to use the
bathroom
HEENT: very dry mucous membranes
CV: RRR
Resp: LCTA bilaterally
Abd: soft, nontender, NABS
Ext.: no LE edema
Accucheck: >500!
Case # 1
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What would you do with this patient?
What labs would you check?
What consults might you make?
What medications would you start?
Case # 2
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A 45 year-old male with a history of
hypertension and GERD presents to your
office. He states that he is worried that he
may be diabetic, since both his parents and his
brother have diabetes. He’s not been to a
doctor in a couple of years, but had previously
been prescribed Hydrochlorothiazide for
hypertension, and was taking OTC prilosec
for his GERD.
Case # 2
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PMH: Hypertension, GERD
PSH: none
Allergies: Sulfa (rash)
Outpatient meds: OTC prilosec
Social History: divorced, works as manager
of bank; no tobacco, 1-2 beers per week
ROS: no fevers, no polyuria, no polydypsia,
no N/V, no diarrhea/constipation
Case # 2
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Physical Exam
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168/92, 78, Ht: 5’11” Wt: 238
Gen: Alert, oriented; in NAD
CV: RRR
Resp: LCTA bilaterally
Abd: soft, nontender, NABS
Ext.: no LE edema
Case # 2 - Labs
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Sodium: 140
Potassium: 3.8
Chloride: 102
CO2: 26
BUN: 17
Cr.: 1.1
Glucose (fasting): 154
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Total Cholesterol: 208
HDL: 43
LDL: 148
Case # 3
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What additional testing would you like this
patient to undergo?
What medications would you start at this
time?
Would your management change if his fasting
glucose was 124?
Final thoughts
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Control of sugars is crucial in protecting
diabetic patients from vascular damage.
Diabetes is now considered a coronary heart
disease equivalent!
Smoking cessation!
Use ACE inhibitors in all diabetic patients
with hypertension.