All About Diabetes

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All About Diabetes
By Shirley(My Notes)
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What Causes Diabetes?

• Type I-The pancreas is unable to produce insulin.
  Childhood and genetic tendency are two
  possibilities. Theres a change in the pancreatic
  function and the cells that normally produce
  insulin are destroyed. The bodys 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
  cant 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
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Signs Symptoms

• Type I-Polyuria (Frequent Urination)-Polydipsia
  (Excessive thirst)-Polyphagia (Excessive
  hunger)-Fatigue/Weakness-Weight
  loss-Ketoacidosis (ketonform of acetone.
  Acidosisaccumulation 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.

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Type I Type IIWhats the difference?

• Type II(90)-Patients 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.

• 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.

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• Diabetes is more often seen in Hispanics, Native
  Americans, and African Americans. However, anyone
  can get it.

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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.

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Treatment-Insulin

• Regular(Humulin R, Novolin R, Regular
  Iletin)Short-actingOnset ½ -1 hourPeak 2-3
  hoursDuration 4-6 hours
• NPH or Lente(Humulin N, Novolin N, Humulin L,
  Novolin L)Intermediate-actingOnset 2
  hoursPeak 6-8 hoursDuration 12-16 hours
• Ultralente(Humulin U)Long-actingOnset 2
  hoursPeak 16-20 hoursDuration 24 hours

• Lispro (Humalog)Rapid-ActingOnset 15
  minutesPeak 60-90 minutesDuration 3-4 hours
• Insulin glargine (Lantus)Long-actingOnset 1-2
  hoursPeak No pronounced peakDuration 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.
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Insulin Regimens
Regimen Type of insulin Time interval Positives Negatives
Single Dose Intermediate 7 AM to a little after 6 PM One injection should cover lunch and dinner. No coverage of fasting, breakfast, or nighttime coverage of hyperglycemia is available.
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 long-acting) 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.
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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.
• Dont add more air to NPH vial but follow Regular
  by withdrawing NPH.
• 36 1248 U (Total Dose)

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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.

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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 syringesMore 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.

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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.
• Dont 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.

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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).

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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.

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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.

LabBlood Glucose gt250 mg/dl, pH lt7.35, serum
bicarbonate lt15 mEq/L, ketones in blood and
urine.
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Emergency Treatment for DKA

• Initial Interventions-Ensure patent
  airway.-Administer O2 via nasal cannula or
  non-rebreather mask.-Establish IV access with
  large-bore 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
  lt7.0)

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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 gt400 mg/dl, marked increase in
serum osmolality. Ketone bodies are absent or
minimal in blood or urine.
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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 patients cardiac
  status and the degree of fluid volume deficit.
• Regular insulin given by IV bolus. Afterwards
  its 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, IO, 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.

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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 lt70mg/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 shouldnt aim for
  intense blood glucose control.

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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
  quick-acting 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 didnt 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 dont subside after 2 or
  3 administrations of quick-acting carbs.
• Worse symptoms or comatose patient-SQ or IM
  (quickest in deltoid) injection of 1 mg glucagon.
  Watch for rebound effect of hypoglycemia.-IV
  administration of 50 ml 50 glucose.

Once blood glucose is gt70 mg/dl the patient
should eat the regularly scheduled meal or snack
to keep hypoglycemia from happening again.
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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

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Angiopathy

• Macrovascular 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
  high-density lipoprotein (HDL).

• Microvascular Complications-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 dont appear
  until 10-20 years following the onset of
  diabetes.

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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 Proliferative
-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 -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 cant 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.
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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 theyre 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.

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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
  youre 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.

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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!

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Foot Care!

• 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 dont heal
  to HCP right away!
• Cut toenails straight across. Do not cut down
  corners.
• Overlapping toes? Use lambs wool to separate
  them.
• Dont 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 theyre colorfast.
• Dont wear clothing that leaves fabric
  impressions-Circulation!
• Dont use hot water bottles or heating pads to
  warm the feet.

• 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. Dont forget to look on the
  bottoms!
• Protect against frostbite.
• Exercise feet daily by walking or flexing. Dont
  sit or stand for long time or cross legs.

Dont go barefoot!
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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.

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Nutritional Therapy for Diabetes

• Type I-May need to increase calories to gain
  weightand 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 rapid-acting
  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 patients
  diabetes is controlled with sulfonylurea or
  insulin.

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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.
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Alcohol?

• Its 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 youre going to drink alcohol, eat carbs!
• Drink with food, use sugar-free mixes, and drink
  dry, light wines.

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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 dont overdo it.
• Dont exercise at the time of the day when
  insulin action is waning.

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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.
• Dont skip doses of insulin, even if sick.
• Dont run out of insulin!

• Dont get involved in fad diets.
• Dont rub area where injection was given.
• Follow diet, regular meals-regular times.
• Learn cholesterol level and dont eat fried
  foods.
• Dont 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.

Carry Identification that says you have Diabetes!
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Diabetes Links

• http//www.diabetes.org
• http//www.diabetes.com
• http//www.cdc.gov/diabetes/
• http//www.diabetes.ca/Section_Main/welcome.asp
• http//www.niddk.nih.gov/
• http//www.jdf.org/