Download Diabetes slides

All About Diabetes
By: Shirley
(My Notes)
What Causes Diabetes?
• Type I-The pancreas is unable to produce insulin. Childhood
and genetic tendency are two possibilities. There’s a change in
the pancreatic function and the cells that normally produce
insulin are destroyed. The body’s own immune system may
think the pancreas is a foreign body! This form often appears at
a time of physical stress or during illness when the body
produces more glucose. Unable to metabolize carbohydrates.
• Type II-The pancreas can still produce insulin but the amount
is inadequate and/or the insulin can’t be used to its full extent
by the tissues. Most people who have this type are overweight.
This type is the most prevalent.
*Glucose-70-110 mg/dl*
Signs & Symptoms
• Type I
-Polyuria (Frequent Urination)
-Polydipsia (Excessive thirst)
-Polyphagia (Excessive hunger)
-Fatigue/Weakness
-Weight loss
-Ketoacidosis (keton=form of
acetone. Acidosis=accumulation of
ketones in the body resulting from
extensive breakdown of fats because of
bad carbohydrate metobolism.)
• Type II
-Often nonspecific but may
have some of the same classic
symptoms as Type I.
-Fatigue
-Recurring infections
-Delayed wound healing.
-Visual disturbances.
Type I & Type II:
What’s the difference?
• Type I
(5-10%)
-More common in young people but
can happen at any age.
-Signs and symptoms have abrupt
onset.
-Minimal or ABSENT endogenous
insulin.
-Patient usually thin.
-Need insulin to live!
-Islet cell antibodies are often present
at onset.
-Virus & Toxins are environmental
factors.
-Prone to ketosis at onset or during
insulin insufficiency.
-Frequent neurologic and vascular
complications.
• Type II
(90%)
-Patient’s are usually 35+ but it can
occur at any age.
-Signs & symptoms occur gradually.
-Excessive endogenous insulin; may be
adequate but inadequate secretion and
use.
-Patient usually obese; May be normal
weight.
-Islet cells are absent.
-Insulin required for some. Diet, exercise
my be only necessary treatment for
others.
-Obesity & sedentary lifestyle are
environmental factors.
-Resistant to ketosis except during
infection or stress.
-Frequent neurologic and vascular
complications.
• Diabetes is more often seen in
Hispanics, Native Americans, and
African Americans. However,
anyone can get it.
Diagnosing Diabetes
Diagnosis must be confirmed on a
subsequent day by any of the
diagnostic methods used.
• FPG (Fasting Plasma Glucose)Preferred method of diagnosis.
Exceeding 200 mg/dl
• Random plasma glucose
measurement exceeding 200
mg/dl. Must have other signs
and symptoms too.
• 2-hour OGTT (Oral-glucose
tolerance test) exceeding 200
mg/dl using glucose load of
75g.
Treatment-Insulin
• Regular
(Humulin R, Novolin R, Regular
Iletin)
Short-acting
Onset: ½ -1 hour
Peak: 2-3 hours
Duration: 4-6 hours
• NPH or Lente
(Humulin N, Novolin N,
Humulin L, Novolin L)
Intermediate-acting
Onset: 2 hours
Peak: 6-8 hours
Duration: 12-16 hours
• Ultralente
(Humulin U)
Long-acting
Onset: 2 hours
Peak: 16-20 hours
Duration: 24+ hours
• Lispro (Humalog)
Rapid-Acting
Onset: 15 minutes
Peak: 60-90 minutes
Duration: 3-4 hours
• Insulin glargine (Lantus)
Long-acting
Onset: 1-2 hours
Peak: No pronounced peak
Duration: 24+ hours
In the past, pork and beef insulin was used. Now mostly
human insulin which is derived from common bacteria or
yeast cells using recombinant DNA. It is not harvested
from humans.
Insulin Regimens
Regimen
Type
of insulin
Time
interval
7 AM to a little
after 6 PM
Positives
Negatives
One injection
should cover lunch
and dinner.
No coverage of
fasting, breakfast, or
nighttime coverage
of hyperglycemia is
available.
Single Dose
Intermediate
Split-Mixed
70/30
Intermediate &
Regular or
Humalog
2 injections cover
24 hours.
2 injections are
required. Patient has
to have set meal
pattern.
Split-Mixed
Intermediate &
Regular or
Humalog
3 injections cover 24
hours, especially
during early AM
hours. Reduced
potential for 2-3 AM
hypoglycemia.
3 injections are
required.
Multiple Dose
Intermediate &
Regular or
Humalog
More flexibility
allowed at
mealtimes and for
how much eaten.
4 injections are
required. Need
premeal glucose
checks. Pts. W/Type
I will need basal
insulin.
Multiple Dose
(Split-Dose longacting) Ultralente
Regular or
Humalog and
long-acting insulin
Insulin delivery
more like normal
insulin delivery.
Requires 3 or 4
injections, premeal
glucose checks;
retiring too.
Mixing Insulins
•
•
•
•
•
•
•
•
•
Wash Hands.
After inspection, carefully rotate
NPH insulin bottle to mix insulin.
Wipe off tops of insulin vials with
alcohol swab.
Draw back air into the syringe that
will equal the total dose. Ex: 36 U
of air/36 U of NPH insulin.
Inject that equal amount of air into
NPH vial.
Inject same amount of air equal to
regular dose of regular insulin. Ex.
12 U of air/12 U of Regular insulin.
Invert regular insulin bottle and
withdraw regular insulin dose.
Don’t add more air to NPH vial but
follow Regular by withdrawing
NPH.
36 + 12=48 U (Total Dose)
Injection Sites
• Most commonly by
subcutaneous (SQ). Given by
intravenous (IV) when
immediate action needed.
• Fastest absorption in the
abdomen, then the arm, then
the thigh, and lastly the buttock.
• Do not inject into a site that is
going to be exercised.
• Prevent lipodystrophy (lumps
& dents in the skin-Human
insulin reduces risk) by rotating
sites. Rotate injection within one
particular site. Think of the
abdomen as a checkerboard.
•
•
•
•
•
Insulin syringes
Most are U100 which equal 1 ml.
0.5 ml used for 50 U or less.
0.3 ml used for 30 U or less.
Smaller syringes=More advantages
No need to use alcohol swab on site before
injection when self-injecting.
• Insulin pens are good too. Usually preloaded with
insulin and look less medical. “InDuo” combines
an insulin syringe with a blood glucose monitor! 
• Insulin pumps-Continuous SQ insulin infusion.
Looks like a pager. Catheter inserted into SQ tissue
in the abdominal wall.
• Intensive insulin therapy-An alternative to the
insulin pump. Consists of multiple daily insulin
injections with frequent self-monitoring of blood
glucose.
Insulin, Insulin, Insulin
• After you open the insulin,
write the date on the vial.
• Insulin can be stored at room
temperature for 30 days.
After that, throw it away
even if there is some still left.
• Do not store insulin in very
cold places or very warm
places.
• Don’t store it in direct light.
• Take your insulin before you
eat. If you take Lantus, take
it at bedtime. Also, never
mix Lantus with another
insulin.
• Take Humalog or Novolog
15 minutes before eating.
• Take your insulin and eat at
the same time every single
day.
• Side Effects? Hypoglycemia,
weight gain.
Medicine
• Sulfonylureas-Primary use is to increase insulin production from the
pancreas. Examples: tolbutamide (Orinase), acetohexamide (Dymelor),
tolazamide (Tolinase), and chlorpropamide (Diabinese).
• Meglitinides-Also increases insulin production. Offers reduced potential for
hypoglycemia because of fast absorption. Examples: repaglinide (Prandin),
and nateglinide (Starlix).
• Biguanides-Primary action is to reduce glucose production from the liver.
Also enhances insulin sensitivity at tissue level and improves the transport of
glucose to the cells. Example: metformin (Glucophage). Combinations include
metformin with glyburide (Glucovance), rosiglitazone (Avandia), and
glipizide (Metaglip).
• a-Glucosidase inhibitors-Starch blockers.Works by slowing down the absorption of
carbohydrates in the small intestine. Most effective in lowering post-prandial blood
glucose when taken with the first bite of each main meal. Not effective against
fasting hyperglycemia. Examples: acarbose (Precose), and miglitol (Glyset).
• Thiazolidinediones-Insulin sensitizers. Most effective with people who have insulin
resistance. Improve insulin sensitivity, transport, and utilization of target tissues.
Will not cause hypoglycemia when used alone but still risky if used with a
sulfonylurea or insulin. This med may even improve lipid profiles and blood
pressure levels! Examples: pioglitazone (Actos), and rosiglitazone (Avandia).
Complications of Diabetes
• Hypoglycemia
• Diabetic Ketoacidosis (DKA)
• Hyperosmolar Hyperglycemic
Nonketotic Syndrome (HHNS)
• If the patient is sick, make sure they
know to stay on their insulin or meds
for diabetes and to continue their
nutritional therapy.
Acute Complications
• Diabetic Ketoacidosis (DKA)
-Also known as diabetic acidosis and diabetic coma.
-Caused by a major deficiency of insulin.
-Is characterized by hyperglycemia, ketosis, acidosis, and dehydration.
-Most often seen in Type I but can occur in Type II also.
-Factors that cause it include illness, infection, inadequate insulin dose,
undiagnosed Type I diabetes, poor self-care and management.
-Renal failure may occur from hypovolemic shock.
-Patient may become comatose from dehydration, electrolyte
imbalance, and acidosis. If untreated, the patient would die.
-Signs and Symptoms of DKA include poor skin turgor from
dehydration, dry mucous membranes, tachycardia, and orthostatic
hypotension. Early symptoms may show lethargy and weakness. Skin
may become dry and loose and the eyeballs may become soft and
sunken in. Abdominal pains is another symptom. There may be
anorexia and vomiting. Breath may have a fruity, acetone odor.
-Kussmaul respirations (rapid, deep breathing) will be another
ultimate sign.
Lab:Blood Glucose >250 mg/dl, pH <7.35, serum bicarbonate <15 mEq/L,
ketones in blood and urine.
Emergency Treatment for
DKA
• Initial Interventions
-Ensure patent airway.
-Administer O2 via nasal
cannula or non-rebreather
mask.
-Establish IV access with largebore catheter.
-Begin fluids with 0.9% NaCl
solution 1L/hr until blood
pressure is stable and urine
output is 30-60 ml/hr.
Begin continuous regular
insulin drip. 0.1 U/kg/hr.
-Identify history of diabetes,
time patient last ate, and
time/amount of last insulin
injection.
• Monitoring
-Monitor VS, level of
consciousness (LOC), cardiac
rhythm, O2 Sat., and urine
output.
-Assess breath sounds for fluid
overload.
-Monitor serum glucose and
serum potassium.
-Give potassium to correct
hypokalemia.
-Give sodium bicarbonate if
acidosis is severe. (pH <7.0)
Another Complication
• Hyperosmolar hyperglycemic
nonketotic syndrome (HHNS)
-Life-threatening!
-May occur in the diabetic who can produce enough insulin to prevent
DKA but not enough to avoid severe hyperglycemia, osmotic diuresis,
and extracellular fluid depletion.
-Unlike the patient with DKA, the patient with HHNS usually has
enough insulin so that ketoacidosis does not occur.
-In the early stages of HHNS, there are few symptoms which means
that blood glucose levels can get really high before the problem is
noticed.
-Often occurs in the older Type II diabetes patient.
-Signs & Symptoms of HHNS include extreme hyperglycemia, severe
osmotic diuresis, decreased sodium, potassium, and phosphorous,
dehydration, decreased renal perfusion, hypotension,
hemoconcentration, oliguria, thrombosis, increased lactic acid.
-Ultimately seizures, shock, coma, and death.
Lab: Blood glucose >400 mg/dl, marked increase in serum
osmolality. Ketone bodies are absent or minimal in blood or
urine.
Emergency Treatment for
HHNS
• High mortality rate. Needs greater fluid replacement than DKA.
• Therapy is similar to that of DKA and includes immediate IV
administration of 0.9% or 0.45% NaCl at a rate dependent on the
patient’s cardiac status and the degree of fluid volume deficit.
• Regular insulin given by IV bolus. Afterwards it’s given as an infusion
after fluid replacement therapy is begun to help in reducing the
hyperglycemia.
• After the blood glucose levels fall to about 250 mg/dl the IV fluids that
contain glucose are given to prevent hypoglycemia.
• Electrolytes are monitored and will be replaced if necessary.
• Hypokalemia (low potassium) is not as significant in HHNS as in DKA
although there may still be potassium deficits that need replacement.
• VS, I&O, skin turgor, lab values, and cardiac monitoring are constantly
assessed to keep a check on the fluid and electrolyte replacement.
• Patients with renal or cardiac problems need special monitoring to
avoid fluid overload.
Hypoglycemia
• Low blood glucose. This occurs when there is too much insulin
in proportion to available glucose in the blood, causing the
blood glucose level to fall to <70mg/dl.
• As the brain needs a constant supply of glucose, mental
functioning can be compromised.
• Signs & Symptoms: confusion, irritability, diaphoresis, tremors,
hunger, weakness, and visual disturbances.
• Can look a lot like drunkenness.
• If untreated, it can progress to loss of consciousness, seizures,
coma, and death.
•
Hypoglycemic Unawareness-Patient may not have any warning
signs or symptoms. Autonomic diabetic neuropathy interferes with the
secretion of the hormones that cause the symptoms. Also at risk are
elderly patients who are on B-adrenergic blockers.
-If patient has a risk factor for hypoglycemic unawareness they
shouldn’t aim for intense blood glucose control.
Hypoglycemia Care
•
•
•
•
•
•
•
Get a blood glucose immediately.
Get patients history if possible and physical
examination.
Try and find out what caused the hypoglycemia
after you correct the problem.
To the conscious patient, give 15-20g of a quickacting carb (Ex: 6-8 oz Coke, 8-10 Life Savers, a
tablespoon of syrup or honey, or frosting in a
tube.) Avoid sweet foods that also contain fat.
Monitor blood glucose.
Repeat the treatment in 15 minutes if first
treatment didn’t work.
Give more food of longer-acting carbs (Ex: slice of
bread, crackers) after symptoms calm down. Be
careful not to overtreat! (Hyperglycemia!)
If patient outside hospital, notify HCP
immediately if symptoms don’t subside after 2 or
3 administrations of quick-acting carbs.
• Worse symptoms or comatose patient:
Once blood glucose is >70 mg/dl the patient should
eat the regularly scheduled meal or snack to keep
hypoglycemia from happening again.
-SQ or IM (quickest in deltoid) injection of 1 mg
glucagon. Watch for rebound effect of
hypoglycemia.
-IV administration of 50 ml 50% glucose.
Chronic Complications
• End-organ disease from chronic hyperglycemia.
Possible causes include:
-The accumulation of damaging by-products of glucose metabolism,
like sorbitol, which is associated with nerve cell damage.
-Abnormal glucose molecules forming in the basement membrane of
small blood vessels like those that circulate to the eye and kidney.
-Derangement of red blood cell function that leads to a decrease in
oxygen to tissues.
• Angiopathy-Blood vessel disease.
-Estimated to account for the majority of deaths from
diabetes.This chronic blood vessel dysfunction is
divided into two categories:
-Macrovascular Complications
-Microvascular Complications
Angiopathy
• Macrovascular Complications: • Microvascular Complications:
-Diseases of the large and medium-sized
blood vessels that happen more often and
earlier in people with diabetes.
-Even though the formation of
atherosclerotic plaque is believed to have a
genetic origin, its development appears
related to the altered lipid metabolism
common in diabetes.
-Tight glucose control may help.
-These diseases include cerebrovascular,
cardiovascular, and peripheral vascular
diseases.
-Risk factors are smoking, obesity, HTN,
high fat intake, and sedentary lifestyle.
-Insulin resistance plays an important role
in the development of CV disease and is
implicated in the pathogenesis of essential
HTN and dyslipidemia.
-The term insulin resistance syndrome is
clinically associated with insulin resistance,
HTN, increased very-low-density
lipoprotein (VLDL) and decreased highdensity lipoprotein (HDL).
-Results from thickening of the vessel
membranes in the capillaries and arterioles
in response to conditions of chronic
hyperglycemia.
-Differs from macrovascular in that it is
specific to diabetes.
-Areas most affected are the eyes
(retinopathy), the kidneys (nephropathy),
and the skin (dermopathy).
-Thickening of cap basement membrane has
been found in some people.
-Clinical manifestations usually don’t
appear until 10-20 years following the onset
of diabetes.
Diabetic Retinopathy
• This refers to the process of microvascular damage to the retina
because of chronic hyperglycemia in patients with diabetes. Very
common in people who have had diabetes for a long time, more-so in
those with Type I.
Nonproliferative
-Most common form.
-Partial occlusion of the small blood
vessels in the retina causes
microaneurysms in the capillary walls.
-Capillary fluid may leak out causing
retinal edema, hard exudates, and
intraretinal hemorrhaging. If the macula
is involved, vision may be affected.
Treatment
-Early photocoagulation of the retina.
-Cryotherapy
-Vitrectomy
Proliferative
-Most severe form.
-Involves the retina and the vitreous.
-Neovascularization-When the body tries
to compensate by forming new blood
vessels to supply the retina the blood.
-Glaucoma may result from this.
-These new vessels are extremely fragile
and hemorrhage easily which produces
vitreous contraction.
-Light can’t reach the retina.
-Patient sees black or red spots or lines.
-Complete retinal detachment can occur.
-If the macula is involved, vision is lost.
-Without treatment, more than half the
patients will go blind.
Nephropathy
• A microvascular complication that is associated with damage to the
small blood vessels that supply glomeruli of the kidney.
• Leading cause of end-stage renal disease in the U.S.A!
• Risk about the same in either Type I or Type II.
• Risk factors for diabetic nephropathy are HTN, genetic
predisposition, smoking, and chronic hyperglycemia.
• Kidney disease can be reduced a lot with maintenance of near-normal
blood glucose.
• HTN can speed up nephropathy. Patient may be put on ACE
inhibitors (ex.lisinopril). Patient may be put on ACE inhibitors even if
they’re not hypertensive.
• This is because ACE inhibitors have a protective effect on the kidney.
• Angiotensin II receptor agonists (losartan) may also be used to protect
the kidney.
• Need yearly screening for presence of microalbuminuria (MAU) in the
urine.
Neuropathy
• This is nerve damage that is associated with diabetes. About 60%-70% of
diabetics have some degree of neuropathy.
• Most common is sensory neuropathy which can lead to the loss of sensation in
the lower extremities. The other major classification is autonomic neuropathy.
• Coupled with other factors, this increases the risk of complications that can
result in a lower limb amputation.
• May be caused by an accumulation of sorbitol and fructose in the nerves from
persistant hyperglycemia.
• Sensory Characteristics besides loss of feeling (numbness) are abnormal
sensations (feeling like you’re walking on pillows), pain, and paresthesias.
• Pain usually described as burning, crushing, cramping, or tearing.
• Control of blood glucose is the only treatment.
• Drug therapy: Topical creams (capsaicin), antiseizure meds (gabapentin),
Tricyclic antidepressants (to control the symptoms).
• Autonomic: Bowel incontinence and diarrhea, urinary retention; complication
is delayed gastric emptying. Can trigger hyperglycemia by delaying food
absorption!
• Sexual dysfunction in men and women. Is the problem organic or physiologic?
• Patient may need to learn self-catheterization.
Complications of the feet and
lower extremities
• The most common cause of hospitalization in the person with
diabetes.
• Results from a combination of macrovascular and microvascular
diseases.
• Sensory neuropathy (remember, loss of feeling) and peripheral
vascular disease are risk factors, along with clotting problems,
impaired immunity, and autonomic neuropathy.
• Smoking and PVD increase the risk for amputation.
• Reduce and manage risk factors, especially smoking, high
cholesterol, and HTN.
• LOPS-Loss of Protective Sensation. Person may not know they hurt
their foot! Need to check daily!
• Neuropathic arthropathy (Charcot foot): Ankle and foot changes;
abnormal distribution of weight over the foot. Increases chance of
foot ulcers from new pressure points. Neuropathic ulcers look like a
BB shot or punched out.
• Danger of infection!
Foot Care!
• Wash feet daily with mild soap and
warm water.
• Test water temp with hands first!
• Pat them dry gently, especially
between the toes.
• Examine daily for cuts, blisters,
swelling, and tender areas. Don’t
forget to look on the bottoms!
• Protect against frostbite.
• Exercise feet daily by walking or
flexing. Don’t sit or stand for long
time or cross legs.
•
•
•
•
•
•
•
•
•
•
Don’t go
barefoot!
•
Use lanolin on feet to keep from drying
but not between toes.
Use mild foot powder for sweaty feet.
Do not use OTC remedies to get rid of
calluses or corns.
Do not use iodine, rubbing alcohol, or
strong adhesives on cuts.
Report skin infections or sores that
don’t heal to HCP right away!
Cut toenails straight across. Do not cut
down corners.
Overlapping toes? Use lamb’s wool to
separate them.
Don’t wear open-toe, open-heel, or
high-heel shoes. Leather shoes are
preferred over plastic.
Wear cotton or wool socks. If you wear
colored, make sure they’re colorfast.
Don’t wear clothing that leaves fabric
impressions-Circulation!
Don’t use hot water bottles or heating
pads to warm the feet.
Skin Complications
• Diabetic dermopathy
• Necrobiosis lipoidica diabeticorum
-believed to be a result of the breakdown of collagen in the skin.
• Shin spots
• Mechanisms for susceptibility to infection include
defective mobilization of inflammatory cells and
impaired phagocytosis by neutrophils or monocytes.
• May see recurring or persistent infections, boils, and
furuncles.
• LOS (loss of sensation) may delay detection of
infection.
• Need prompt, vigorous, antibiotic therapy.
Nutritional Therapy for
Diabetes
• Type I
-May need to increase
calories to gain weight
and restore body tissues.
-Glucose control is via diet and
insulin.
-Equal distribution of carbs via
meals or adjusting the amount
of carbs for insulin activity.
-Consistency needed for glucose
control.
-Timing of meals very
important for NPH/lente
insulin programs. Need
flexibility with multidose rapidacting insulin.
-Snacks throughout day and at
bedtime are frequently needed.
-Need 20 g/hr of carbs for
regular physical activity.
• Type II
-Need to reduce caloric intake;
lose weight.
-Control of diet may be only
thing necessary for glucose
control.
-Need equal distribution. Best to
have low-fat diet. Need
consistency of carbs during
meals.
-Consistency necessary for
weight loss and controlling blood
glucose levels.
-Timing of meals would be good
but not absolutely essential.
-Snacks throughout the day and
at bedtime not recommended.
-May need nutritional
supplements of patient’s diabetes
is controlled with sulfonylurea or
insulin.
Food Groups
• Protein-15% to 20%. If the patient has
nephropathy(disorder of the kidney).
• Fat-Less than 10% from saturated fat. Cholesterol
needs to be lower than 300 mg/day.
• Carbohydrates-Should make up the remaining
necessary calories after meeting protein and fat
needs. Should be whole grains, and fresh vegetables
and fruit. Simple sugar is acceptable in small
amounts when counted as part of the carb intake.
• Sodium-Should be lower than 2400 mg/day.
• Fiber-25 to 30 g/day needed from a variety of food
sources.
Meal planning: Learn the “plate method”, the amount of
necessary food that will fill a 9-inch plate.
Alcohol?
•It’s high in calories and has no nutritional
value. It also promotes hypertriglyceridemia
(an excess of glycerides, especially
triglycerides, in the blood.)
•Had really bad effects on the liver. Alcohol
can inhibit glucose production and cause
severe hypoglycemia in patients who are on
insulin or oral hypoglycemic agents that
increase insuline secretion.
•It can increase the risk of lactic acidosis.
•If glucose is well-controlled then alcohol
could possibly be safe if glucose under control
and if the patient is not on meds that can cause
reactions.
•If you’re going to drink alcohol, eat carbs!
•Drink with food, use sugar-free mixes, and
drink dry, light wines.
Exercise
• Increases insulin sensitivity and
can help lower blood glucose
levels.
• May also help lower
triglyceride and LDL
cholesterol levels, lower blood
pressure, and improve
circulation.
• Schedule exercises about 1 hour
after a meal if on meds that
cause hypoglycemia or have a
10-15g carbohydrate snack
before exercising.
• If on meds that place the patient
at risk or if already
hypoglycemic, advise to carry
glucose tablets, hard candy like
Life Savers, or frosting in a tube,
when exercising.
•Strenuous exercise can be
perceived by the body as stress so
don’t overdo it.
•Don’t exercise at the time of the
day when insulin action is waning.
Patient Teaching
• Monitor blood glucose at home and
record in log.
• Take insulin and oral meds as
prescribed.
• Get a HgB1c blood test every 3-6
months.
• Carry some form of glucose at all
times to treat hypoglycemia.
• Instruct family members in giving
glucagon in case of emergencies.
• Don’t skip doses of insulin, even if
sick.
• Don’t run out of insulin!
Carry
Identification
that says you
have Diabetes!
• Don’t get involved in fad diets.
• Don’t rub area where injection
was given.
• Follow diet, regular mealsregular times.
• Learn cholesterol level and don’t
eat fried foods.
• Don’t exercise if blood glucose
levels very high.
• Get annual eye exam.
• Get annual urine protein exam.
• Treat other medical problems,
especially high blood pressure.
• Know the symptoms of
hyperglycemia and
hypoglycemia.
• Quit smoking.
Diabetes Links
•
•
•
•
http://www.diabetes.org
http://www.diabetes.com
http://www.cdc.gov/diabetes/
http://www.diabetes.ca/Section_Main/welc
ome.asp
• http://www.niddk.nih.gov/
• http://www.jdf.org/