Transcript Chronic Complications of Diabetes

The Endocrine System
Endocrine System
• The endocrine system includes all the
endocrine cells and the tissues of the
body that produce hormones or
paracrine factors with effects beyond
their tissue origin.
• Endocrine cells are glandular secretory
cells that release their secretions into
the extracellular fluid.
• The organs that produce endocrine
secretions main function is to secrete
hormones while some organs have
other functions.
Organs of the Endocrine System are:
• Hypothalamus, pituitary gland, thyroid
gland, thymus, adrenal glands, pineal
gland, parathyroid glands, heart,
kidney, adipose tissue, pancreatic
islets, digestive tract, and gonads
On a busy day in the North Bay General Hospital’s
Emergency room department:
John Smith, a 18-year-old man presented to the emergency department with
nausea and headache for one day at 1020. He has recently moved to Burk’s
Fall and does not have a physician. He was in town visiting friends for a few
days. John was assigned a triage level of 4 based on his baseline vitals of
(37.1°C, 80bpm, 20rr, 90/50mmHg, 95% O2 sats) and sent back out into the
waiting room.
A COMPLEX HEALTH CHALLENGE
The Endocrine System: Pancreas
• Functions as an endocrine organ, where the islets of Langerhans
secrete various types of hormones, primarily:
• Glucagon: secreted by A cells
• Insulin: secreted by B cells
• The pancreas controls serum glucose
by regulating the rate at which glucose
is synthesized, stored and moved to
and from the bloodstream through the
actions of glucagon and insulin
Hormones:
Insulin:
- Controlled by chemical, hormonal and neural mechanisms
- Acts as a storage hormone to lower blood glucose by permitting
glucose to enter the cells of the liver, muscles and tissues
- Glucose within the cells is then stored as glycogen or used for energy
- Insulin signals the liver to stop
the release of glucose into
the blood
- In the absence of insulin,
glucose cannot enter the body
resulting in higher serum
osmolarity, hyperglycemia and
glucosuria
Hormones:
Glucagon:
- Hormone produced by the pancreas
- Is the antagonist to insulin: Increases blood glucose levels by:
- Breaking down glycogen (glucogenolysis)
- Breaking down amino acids and lipids to form glucose
(gluconeogenesis)
- Glucagon is released by the pancreas
in response to decreased levels of
blood glucose
- Epinephrine, adrenocorticosteroids,
growth hormone and thyroid hormones
have the same hypoglycemic effects
Euglycemia:
- Homeostasis between insulin and glucagon secretions
- As glucose in the blood rises, insulin is released, which allows glucose to be
transported across the cell membranes, and to be used or stored as energy
- Insulin signals the liver to cease breaking down glycogen or amino acid
reserves, and instead utilizes glucose,
provided by insulin secretion.
- Blood glucose levels decrease, reaching
euglycemia levels
-Capillary blood glucose reading falls
between 4-8mmol/L
Diabetes Insipidus:
- The body is unable to produce a therapeutic amount
of antidiruetic hormone (ADH)
- Decreased ADH concentrations lead to vast
water loss through the kidneys
Clinical Manifestations:
- Polyruia (>12L/d)
- secondary hypotension
- enlarged bladder
- glucosuria
- Insatiable polydipsia
- Dehydration
- Unexplainable weight loss
- Electrolyte imbalances: lethargy, headache, irritability and muscle pains
Treatment:
- Fluid replacement therapy with electrolyte supplements
- Pharmacological intervention (vasopressin)
Type I Diabetes Mellitus:
- Rare: accounts for 10% of diabetes mellitus
- Two types:
- Immune
- autoantibodies attack B cells causing destruction
- Non-Immune
- pancreatic destruction due to infection, medications and
viruses
- Causes insulin deficiency
Type I Diabetes Mellitus:
Manifestations:
1.Clinical
The stomach
changes food into glucose
2. -Glucose
enters the bloodstream
Glucosuria
Hyperglycemia
3. -The
pancreas makes little or no insulin
- Ketoacidosis if untreated- ketones (acids) buildup in the blood due to the
4. Little or no insulin enters the bloodstream
breakdown of lipids that are needed to
provide energy for the body. Metabolic
5. Glucose builds up in the bloodstream
acidosis results, leading to DKA.
resulting in hyperglycemia and the
buildup of ketones in the blood
Treatment:
- When serum glucose levels increase past
- Resolve underlying factors
9.9mmol/L the renal threshold is surpassed
causing
glucosuria
- Pharmacological
intervention
- Pancreatic transplant
- Ketone bodies are produced due to
the uninhibited breakdown of fats and amino
acids
Type I Diabetes
Back to John, who is waiting anxiously in the busy ER waiting room:
At 1120 in the waiting room others noticed he had become increasingly lethargic,
confused, and hyperventilating with breath smelling like Juicy Fruit and dry-heave
vomiting.
On secondary assessment he was drowsy and dehydrated with tachypnea (24rr),
tachycardia (100), and a temperature of 37.1°C. On admission the athletically built
young man weighed 100 kg. There were no localizing clinical signs of infection.
A urine dipstick test detected ketones, and bedside capillary testing with a glucometer
showed "high" glucose concentrations at 28.
Blood samples were sent to the laboratory.
More thorough history includes that he is a diabetic and over the last 24 hours he
had felt increasingly tired, lethargic, polyuric, and thirsty. As he was unable to keep
any food down, but continued to drink alcohol with his friends the previous night.
He also had omitted two insulin injections, including one on the morning of admission
because he had left his insulin back in Burk’s Fall. He has no history of chest pain.
He has been recently diagnosed with type-1 diabetes and was injecting Humulin U
once a day, and Humulin R sliding scale insulin three times a day with meals.
He has not been in contact with any hospital clinic and has no known complications
of diabetes.
The arterial blood gas analysis indicated metabolic acidosis (pH 7.16,
carbon dioxide partial pressure 1.8 kPa, oxygen partial pressure 15.9 kPa,
bicarbonate concentration 12 mmol/l). His other indicative lab values include plasma
glucose level 28 mmol/L, positive for serum ketones, effective serum osmolarity of 315,
anion gap of 15 mmol/L, BUN of 30 mg/dl, and electrolytes have increase
potassium 6 mEq/L, and decreased sodium of 125 mEq/L.
HbA1c
• Glucose sticks to the haemoglobin to make a
‘glycosylated haemoglobin’ molecule, called
haemoglobin A1c or HbA1c.
• The more glucose in the blood, the more haemoglobin
A1c or HbA1c will be present in the blood.
• Red cells live 120 days before they are replaced. By
measuring the HbA1C it can tell you how high your blood
glucose has been on average over the last 8-12 weeks.
A normal non-diabetic HbA1C is 3.5-5.5%. In diabetes
about 6.5% is good.
• The HbA1C test is currently one of the best ways to
check diabetes is under control; the HbA1C is not the
same as the glucose level.
Type I Diabetes Mellitus:
Diabetic Ketoacidosis
Causes:
-Inadequate insulin production as seen
in type I diabetes
-Infection
-Trauma
-Myocardial infarction
-Insulin interruption for type I diabetics
Pathophysiology:
-Due to the decrease of insulin supply,
and as a result of circulating antagonistic
hormones such as epinephrine, glucagon
catecholamines, growth hormone and
cortisol, hyperglycemia develops
-Lipids and amino acids are catabolized
to provide energy for the body, and
produce ketone acids within the body
-Body is sent into metabolic acidosis, with
bicarbonate reserves being quickly depleted- fruity-smelling breath
Type I Diabetes Mellitus:
Diabetic Ketoacidosis
-If not treated, hyperglycemia leads to diabetic ketoacidosis (DKA) due to the
accumulation of ketones produced by lipids
Clinical Manifestations:
- Hyperglycemia Signs & Symptoms
-Polydipsia
-Polyphagia
-Polyuria
-Dehydration
-Nausea & vomiting
-Weakness
-Fatigue
-Altered mental status
-Tachycardia
-Hypotension
- Unique DKA Signs & Symptoms
-Tachypnea
-Kussmaul’s breathing
-Electrolyte imbalances
-Hypokalemia
-Hyopnatremia
-Seizures
-Ketonuria
-Acetone breath
-Coma
Laboratory Tests:
SO:
TABLE 2
Diagnostic Criteria for Diabetic Ketoacidosis
John is now diagnosed
diabetic ketoacidosis
(DKA is a triad of hyperglycemia,
ketonemia and acidemia)
which criteria for conclusion are
included in table 2.
Mild DKA
Moderate DKA
Severe DKA
Plasma glucose
(mg per dL [mmol
per L])
> 250 (13.9)
> 250
> 250
Arterial pH
7.25 to 7.30
7.00 to 7.24
< 7.00
Serum
bicarbonate (mEq
per L)
15 to 18
10 to < 15
< 10
Urine ketones
Positive
Positive
Positive
Serum ketones
Positive
Positive
Positive
Betahydroxybutyrate
High
High
High
Effective serum
osmolality (mOsm
per kg)*
Variable
Variable
Variable
Anion gap†
> 10
> 12
> 12
Alteration in
sensoria or
mental
obtundation
Alert
Alert/drowsy
Stupor/coma
DKA = diabetic ketoacidosis
*-Effective serum osmolality = 2 3 measured Na (mEq per L) + (glucose [mg per dL]
÷ 18).
†-Anion gap = Na+ - (Cl- + HCO3- [mEq per L]).
Adapted with permission from Kitabchi AE, Umpierrez GE, Murphy MB, Barrett EJ, Kreisberg
RA, Malone JI, et al. Hyperglycemic crises in diabetes. Diabetes Care 2004;27(suppl 1):S95,
with additional information from
John was placed, as per physician’s orders, on the NBGH Pre-printed orders for
Treatment protocol: Adult Diabetic Ketoacidosis
He was started on fluid replacement with 0.9% saline at 150 ml/hr and a
secondary line of intravenous soluble insulin at 10 units/hour. The patient was
transferred to the Critical Care Unit.
At 1220 Secondary CBG is 20 mmol/L.
The nurse’s main concern was his electrolyte balance and dehydration.
Nurses there also watched for other complications that could occur, which include:
myocardial infarction(MI), acute gastric dilation, erosive gastritis, late hypoglycemia,
respiratory distress, infection, hypophosphatemia, mucormycosis (inhaled fungal
infection).
Type I Diabetes Mellitus:
Diabetic Ketoacidosis
Nursing Interventions:
- Prevention of hyperglycemia
- Insulin administration: bolus dose calculated 0.1-0.15U/kg
- Vital signs q1h, I&O, mental status and neurological impairment
- Administration 1L isotonic solution within the first hour
- Monitor lab values, and replace lost electrolytes: Na, K, Ph, bicarbonate etc.
- Maintenance dose of insulin, typically 5-7u SC (sliding scale) to maintain
euglycemia
- Close monitoring is crucial to assess for rebound hypoglycemia, fluid overload,
pulmonary edema, cerebrovascular changes, and renal complications
- Check urine for glucose and ketones periodically with a urine dip test
Type II Diabetes Mellitus:
- Characterized by insulin resistance of peripheral cells
- Insulin cannot adequately bind to cell receptor sites, thereby rendering insulin less
effective at stimulating glucose uptake
Predisposing Factors
Sedentary Lifestyle
Poor Diet
Overweight
Advancing Age
Heredity
Type II Diabetes Mellitus:
- Characterized by insulin resistance of peripheral cells
- Insulin cannot adequately bind to cell receptor sites, thereby rendering insulin less
effective at stimulating glucose uptake
Predisposing Factors
Sedentary Lifestyle
Poor Diet
Overweight
Advancing Age
Heredity
Clinical Manifestations:
- Signs and symptoms of hyperglycemia
Type II Diabetes Mellitus:
Clinical Manifestations:
Hyperglycemic Symptoms
- Lab values may indicate dyslipidemia and hyperinsulinemia
- History of recurrent infections
- Controlled type-II diabetics usually will not progress to ketoacidosis because there
is enough insulin within circulation to control the breakdown of fat and amino acids
- Uncontrolled type II diabetics will lead to another acute complication:
Hyperglycemic Hyperosmolar Nonketotic Syndrome
Type II Diabetes Mellitus:
Treatment:
- Attempt to restore euglycemia
- Pharmacological interventions
- Dietary measures
- Exercise
Type II Diabetes Mellitus:
Hyperglycemic Hyperosmolar Nonketotic Syndrome
Causes:
-Occurs during periods of stress and more
commonly in the elderly
Pathophysiology:
- Severe condition of hyperglycemia and
hyperosmolarity due to insulin resistance
but with no ketone production
- Endogenous insulin is able to regulate catabolism
of amino acids, however this leads to heightened
hyperglycemia
- Hyperglycemia surpasses the renal threshold,
allowing for glucose and electrolytes to be lost in
polyuria. Severe dehydration, cerebro-vascular
edema and seizures can occur, and finally
hypovolemic shock
-Individuals with HHNS do not exhibit abdominal S/S that are associated with DKA:
therefore there is a greater degree of dehydration and a higher mortality rate of 15%
Type II Diabetes Mellitus:
Hyperglycemic Hyperosmolar Nonketotic Syndrome
Clinical Manifestations:
- CBG level can reach >33.3mmol/L
- Extreme glucosuria and proteinuria
- Hypotension related to profound dehydration
- Altered neurological state combined with edema and seizure activity
Diagnostic Tests:
- Lab tests
- Blood glucose: 600-1200mg/d
- Electrolytes- osmotic diureses causes severe dehydration
- BUN
- CBC
- Serum osmolarity: exceeds 350mOsm/kg
- Arterial blood gas analysis
Treatment
- Fluid replacement with electrolyte replacement
- Insulin administration and close monitoring related to rebound effects
Acute Complications of Diabetes:
Hypoglycemia:
- Referred to as insulin reactions, or insulin shock
- Defined as CBG of 2.7-3.3mmol/L
- Caused by:
- over-administration of insulin
- too little food intake or excessive exercise
Acute Complications of Diabetes:
Hypoglycemia:
Clinical Manifestations:
Hypoglycemic Symptoms
Acute Complications of Diabetes:
Hypoglycemia:
Treatment:
- Must give some form of glucose, otherwise death will ensue
- Follow with a snack containing
protein and starch
- Patient teaching
Chronic Complications of Diabetes:
- Long-term complications of diabetes affects nearly every organ system
- Three categories:
Macrovascular Complications
Microvascular Complications
Neuropathy
Chronic Complications of Diabetes:
Macrovascular Complications:
- Hyperglycemia causes atherosclerosis which causes other
cardiovascular complications
- Coronary Artery Disease: 60% of diabetics die related to CAD
- Peripheral Vascular Disease: Diabetics are 2-3 times more likely to develop thrombi
- In the lower extremities, arterial occlusion is responsible for gangrene
- CVAs are common due to atherosclerotic changes
Cerebral Vascular Disease:
•MI is more 2 times more likely to occur in
diabetic men, three times in woman
•Silent ‘ischemic attacks’- due to neuropathies
Chronic Complications of Diabetes:
Microvascular Complications:
- hyperglycemia and hypertension causes capillary membrane thickening throughout the body
Diabetic Retinopathy
- Increased wall thickness causes decrease
perfusion across the membrane
- Edema and scarification occurs due to cellular necrosis
- New blood vessels attempt to perfuse the retina, which
lead to clouding of the vitreus, and block light from reaching
the retina
- New blood vessels dislodge the retina, leading to blindness
Chronic Complications of Diabetes:
Microvascular Complications:
Diabetic Retinopathy
Clinical Manifestations:
- Painless process
- Blurry Vision
Cobweb’s
Assessment:
- Direct assessment with an opthalmascope
Treatment:
- Maintenance of euglycemia
- Photocoagulation and surgery
Complete loss of vision
Chronic Complications of Diabetes:
Microvascular Complications:
Diabetic Nephropathy:
- Renal disease due to microvascular changes
in the kidneys
- Changed capillary basement membrane
thickness affects the kidney’s ability to filter
blood
- Results in albuminurea with simultaneous
necrosis of renal tissue
- When the kidney’s have lost 85% of their
function = end stage renal failure
Chronic Complications of Diabetes:
Microvascular Complications:
Diabetic Nephropathy:
Clinical Manifestations of End-Stage Renal Failure:
- Uremia
- Aggravated hypertension, heart failure, and pulmonary edema due to
fluid overload
- Gastrointestinal symptoms
-Neurological changes
- altered mental status
- change in consciousness
- muscle twitching
- seizures
- Electrolyte and fluid imbalances due to acidosis
End-Stage Renal Failure ultimately results in multiple-system organ failure
Chronic Complications of Diabetes:
Microvascular Complications:
Diabetic Nephropathy:
Assessment:
- Lab values to highlight albumin leakage in urine
- BUN/creatinine assessment
Treatment:
- Control of hyperglycemia from ACE-inhibitors
- Low sodium/low protein diet
- Dialysis
Chronic Complications of Diabetes:
Diabetic Neuropathies:
- Group of diseases that affect peripheral, autonomic and spinal nerve innervations
- Prevalence increases with age and length of disease
- Results in clinically diverse disorders
- Caused by hyperglycemia due to its vascular and metabolic
effects on the cell, and due to its demylenization of nerve
fibers
Two Types:
1. Peripheral Neuropathy
2. Autonomic Neuropathy
Chronic Complications of Diabetes:
Diabetic Neuropathies:
Peripheral Neuropathy
- Parenthesis and burning sensation of the lower extremities
Decreased proprioception
Decreased sensation of pain and temperature
Clinical Manifestations & Complications:
- Unsteady and altered gait
- Charcot joints
- Increased risk for tissue damage
Chronic Complications of Diabetes:
Diabetic Neuropathies:
Autonomic Neuropathy
Results in a broad range of dysfunctions that affect almost every
organ system
Cardiovascular complications:
-tachycardia, orthostatic hypotension, silent symptoms for MI
Gastrointestinal complications:
-delayed gastric emptying, nausea, vomiting,
constipation, and early satiety
Renal complications:
-urinary retention due to decreased sensation leads to
bladder distention and increased risk for UTIs
Hypoglycemia Unawareness:
-Autonomic neuropathy masks adrenergic symptoms of diaphoresis
shaking, tachycardia and palpitations
-Can lead to DKA
Chronic Complications of Diabetes:
Foot and Leg Complications
- 50-70% of lower extremity amputations are performed on diabetics
- Complications that increase the risk for foot and leg complications include:
Peripheral Neuropathy Complications:
- Loss of pain and pressure sensation and Charcot joints
increases the risk for the development of wounds
Autonomic Neuropathy Complications:
- Dryness and fissuring of the skin due to decreased
sweating increases the risk for infection and skin breakdown
Macrovascular Complications:
- Altered blood flow impairs the ability for disease-fighting cells
to reach wound sites
Immunocompromised :
- Hyperglycemia decreases the potency of WBCs, thus there
is a lowered resistance to infection
Chronic Complications of Diabetes:
Foot and Leg Complications
Prevention
1. Never go barefoot, even indoors.
2. Wear shoes that fit properly and are supportive.
3. Wash, dry and moisturize your feet daily. Wipe off excess lotion.
4. Wear fresh clean socks every day. Do not wear tight socks, garters or elastics.
5. Inspect your feet daily: Check for blisters, scrapes, cuts, sores or cracks.
6. Clean cuts and scrapes with mild soap and water.
7. Do not attempt to treat foot complications yourself. Do not have manicures by
non-professionals.
8. Trim toenails straight across.
9. Ask your physician to check your feet every visit, and to check for neuropathy
at least once a year.
10. Seek medical attention if you notice redness, swelling or warmth in your legs
and feet, or if you notice signs of infection concurrent with abrasions.
MEDICATIONS FOR DIABETES:
ORAL MEDICATIONS
Five types of oral medications for diabetes to control insulin:
1. Sulfonylureas (e.g. Diabeta)
- Stimulates insulin secretion by attaching to the sulfonylurea
receptor on the beta cells of the pancreas
Meglitinides
2. Meglitinides (e.g. Prandin)
- stimulate insulin secretion by attaching to a different receptor
on the beta cells of the pancreas.
[Alpha]-Glucosidase 3. [Alpha]-Glucosidase Inhibitors (e.g. Precose)
Inhibitors
-inhibits enzymes in the intestines to retard the entry of glucose
into systemic circulation.
Sulfonylureas
Thiazolidinediones 4. Thiazolidinediones (e.g. Avandia
-improved insulin responsiveness in skeletal muscle, facilitate
glucose uptake and utilization
Biguanides
5. Biguanides (e.g. Metformin)
-multiple effects that are not completely understood. Reduces
liver glucose output, boost glucose uptake by insulin sensitive
cells, and decrease glucose absorption by the small intestine
MEDICATIONS FOR DIABETES:
INSULIN
Type
Trade names
Rapid acting
(Clear)
Humalog
(insulin lispro)
NovoRapid (insulin aspart)
Fast acting
(clear)
Humulin-R
Novolin ge
Toronto
Intermediate
acting
(cloudy)
Novolin ge NPH
Humulin- L
Humulin- N
Long acting
(cloudy)
Humulin -U
Extended
long acting
analogue
Lantus (insulin glargine)
approved, but not yet
available in Canada
Premixed
(cloudy)
Humalog mix 25 TM
Humulin (20/80, 30/70)
Novolin ge (10/90, 20/80,
30/70, 40/60, 50/50)
Onset of
Action
Peak Action
Duration of
Action
10-15min
60-90 min
4-5 hours
30-60 min
2-4 hours
5-8 hours
1-3 hours
5-8 hours
up to 18 hours
3-4 hours
8-15 hours
22-26 hours
90 min
-
24 hours
MEDICATIONS FOR DIABETES:
INSULIN
Five methods to deliver insulin:
1. Intravenous
2. Syringes
3. Pens
4. Jet Injectors
5. Insulin Pumps
MEDICATIONS FOR DIABETES:
SODIUM BICARBONATE
- Alkalizing agent used for the treatment and reversal
of metabolic acidosis
- At NBGH it is given IV as per the diabetic protocol:
- if pH is less than 7.0 add 50mmol NaHCO3 to
200ml of 4.5% saline, infuse at 200ml/h
- if pH is less than 6.9 add 100mmol NaHCO3 to
400ml of 4.5% saline, infuse at 200ml/h
- if pH is greater than 7.0- do not give NaHCO3
Nurse’s Role for Clients with Diabetes
Education
One of the biggest challenges in recent years regarding diabetic management is taking
responsibility for your own care. It’s not just the doctor, or the nurse that takes care of
your diabetes. Now it is a collaborative approach with the client. (Canadian Diabetes Association, 2006)
Nursing Role:
-To slow progression of diabetes, and to minimize the complications of the
disease, the nurse works with the client to enhance wellness and health.
-Informing the client regarding signs and symptoms of complications, adherence to
medication regimes, as well as diet, food choices and exercise
-Linking the client to multiple resources in the community that provide counseling,
information sessions, as well as a variety of other programs that will be beneficial
to the client
-Depression affects 15% of diabetics due to complications resulting from the
condition. The nurse should educate clients and family members about this
heightened risk factor, and acknowledge the steps clients can take to minimize this
complication.
Nurse’s Role for Clients with Diabetes
Teaching Regarding Nutrition
-What, when and how much you eat all play an important role in regulating blood
glucose levels.
-The amount of food you need to eat daily depends on:
-Age
-Body size
-Activity level
-Gender
-Pregnancy or breastfeeding
-Diabetics are urged to follow the Glycemic Index for foods
-Scale that ranks carbohydrate-rich food by how much they raise
blood glucose levels
-Adherence to the Glycemic Index can help control blood cholesterol levels
control appetite cravings, lower the risk for cardiovascular disease and
slow the progression of type II diabetes by controlling blood glucose levels
Nurse’s Role for Clients with Diabetes
Teaching Regarding Nutrition
Glycemic Index:
-Postprandial blood glucose rises in response to the type and amount of food that
is ingested
-The degree that food elevates blood glucose is called it’s glycemic response
-The glycemic response is influenced by what type of food it is, how the food is
processed, and how much is eaten:
-Canada’s Food Guide states that 55% of calories
consumed per day should originate from carbohydrates
- But, not all carbohydrates have the same glycemic response
- Many can drastically elevate blood glucose quickly, putting the client at risk for
complications of diabetes
Nurse’s Role for Clients with Diabetes
Glycemic Index:
Low Glycemic Response
Skim milk
Plain Yogurt
Soy beverage
Apple/plum/orange
Sweet potato
Oat bran bread
Oatmeal (slow cook oats)
All-Bran™
Converted or Parboiled rice
Pumpernickel bread
Al dente (firm) pasta
Lentils/kidney/baked beans
Chick peas
Medium Glycemic Response
Banana
Pineapple
Raisins
New potatoes
Popcorn
Split pea or green pea soup
Brown rice
Couscous
Basmati rice
Shredded wheat cereal
Whole wheat bread
Rye bread
High Glycemic Response
Watermelon
Dried dates
Instant mashed potatoes
Baked white potato
Parsnips
Rutabaga
Instant rice
Corn Flakes™
Rice Krispies™
Cheerios™
Bagel, white
Soda crackers
Jellybeans
French fries
Ice cream
Digestive cookies
Table sugar (sucrose)
Benefits of low glycemic index foods are not limited to the minimal effect on blood glucose
They tend to be healthier, lower in fat, and high in fiber, nutrients, and antioxidants.
Nurse’s Role for Clients with Diabetes
Teaching Regarding Exercise
- Regular physical activity helps your body lower blood glucose levels, promotes
weight loss, reduces stress and enhances overall fitness
-The benefits of exercise include:
Lower rates of illness and death
Higher rates of weight loss
Better heart and lung health
Better blood pressure control
Enhanced lipid control
Stronger bones and optimal balance
Reduced levels of stress and depression
Improved mental skills
Lower rates of heart disease, stroke, cancer and depression
More energy
Higher self-esteem
Nurse’s Role for Clients with Diabetes
Teaching Regarding Exercise
Type I Diabetics:
What do you think is important in educating type I diabetics about exercise?
-Blood glucose levels fluctuate due to the type, duration, and intensity of the exercise
and the timing of the last insulin administration and carbohydrate intake
-Low to moderate intensity exercise lowers blood glucose levels and can lead to
hypoglycemia
-High intensity exercise can lead to hyperglycemia due to increased stress placed upon
the muscles and cardiovascular system
Nursing Interventions:
-Educate clients to take CBG before exercising, along with a meal rich in low glycemic
carbohydrates to normalize blood glucose levels throughout exercising
-Keep a source of emergency glucose reserves on hand