DIABETES MELLITUS

Evelin Malinti, MSN

Objectives
• By the end of this lecture students should be
able to:
• Differentiate between type 1 and type 2
diabetes mellitus
– Identify the diagnostic and clinical
significance of blood glucose test results
– Describe the major complications of DM
–Differentiate between DKA and HHNS
Diabetes Mellitus

•A chronic multi-system disease

related to abnormal insulin
production or impaired insulin
utilization.
Risk Factors
• Family Hx. Of diabetes
• Obesity esp. abdominal and viseral adiposity.
• BMI> 27%
• Race/Ethnicity
• GDM or babies > 9 lbs.
• Mother is more at risk of developing DM if
she has big babies
• HTN > 140/90 mm Hg
• Triglycerides > 200mg/dL
• Prev. impaired glucose tolerance
Causes
•Genetics
•Autoimmune
•Viral
•Environmental
Metabolic Processes
• Three Metabolic processes are important in
ensuring a supply of glucose for body fuel.

• 1) Glycolysis-the process through which

glucose is broken down into water and carbon
dioxide with the release of energy
Metabolic Processes
• 2) Glycogenolysis- the breakdown of stored
glycogen ( from the liver or skeletal muscles).
This action is controlled by 2 hormones:
epinephrine-breaks down glycogen in the
muscle
glucagon-breaks down glycogen in the liver.
Glucose from here can be directly released into
the blood stream and used by the nervous
system
Metabolic Processes
• 3) Gluconeogenesis-building of glucose from
new sources.
• Hormones that stimulate gluconeogensis
• Glucagon
• Glucocorticoid hormones
• Thyroid hormones
• Process usually occurs in the liver
 Normal Insulin Metabolism
•Counterregulatory hormones. They
work to oppose the effects of insulin.
These hormones work to increase blood
glucose levels by stimulating glucose
production and output by the liver and
decreasing the movt of glucose into the
cells.
•Glucagons
•Epinephrine
•Growth hormone
•Cortisol
Hormonal Control of Metabolism
• Insulin
• A hormone secreted by the beta cells in the islet of Langerhans,
• Normally released in small increments when food is ingested.
• Controls blood glucose levels by regulating glucose production and storage
• Insulin is regulated by serum glucose levels.
• Consists of 2 polypeptide chains
• The amt of insulin a person is secreting can be tested by checking the levels of
C peptide
• Rise in plasma insulin after a meal stimulates storage of glucose as glycogen in
the liver and muscle. It also inhibits gluconeogenisis and enhances fat
deposition (enhances fat to be placed/stored in the adipose tissue) in the
adipose tissue and increase protein synthesis
• The fall in insulin levels during the night when you’re not eating facilitates the
release of the stored glucose from the liver, protein from the muscles and fat,
and that’s how it kind of compensates for your hypoglycemia
 Insulin
• Insulin and glucagon
are hormones secreted
by islet cells within the
pancreas

• Insulin is normally
secreted by the beta
cells (a type of islet cells)
of the pancreas

• Stimulus for insulin is

high blood glucose levels
Hormonal Control of Metabolism
• Amylin
• 2nd beta cell hormone
• Effects of Amylin
• Amylin and insulin together suppress the
secretion of glucagon by the liver
• Amylin slows the transfer of nutrients to
the intestine
Continued….
• Glucagon
• Produced in the alpha cells of the islets of
Langerhans in the pancreas
• Transported via the portal vein to the liver
• Glucagon acts in opposition to insulin
• Stimulates the break-down of glycogen
and fats to glucose and promotes
gluconeogensis from fats and proteins
 Continued….
• Catecholamines
• Epinephrine and norepinephrine
• Help maintain glucose levels during stressful
situations by
• 1. inhibiting insulin release and decreasing
movement of glucose into cells
• 2. promoting glycogenolysis by converting muscle
and liver glycogen to glucose
• 3 Increasing lipid activity, conserving energy.
Causes mobilization of fatty acids and conserves
glucose. The conservation of blood glucose
mediated by these actions is important in the
homeostatic effect which occurs with hypoglycemia
to increase the blood glucose levels
Continued….
• Somatostatin
• Produced in the pancreas by the delta cells in the
islets of Langerhans
• Somatostatin inhibits the secretion of insulin,
glucagon and growth hormone.
Diabetes Classifications
• Type 1
• Type 2
• Decreased sensitivity to insulin and impaired
beta cell functioning which results in
decreased insulin production
• Gestational diabetes mellitus
• Pre-diabetes
• Secondary
Type 1 Diabetes Mellitus
• Formerly Known as insulin-dependent

• Destruction of their pancreatic cells, genetic,

immunologic, and possibly environment

• Persons do not inherit Type 1 itself but rather

have a genetic predisposition
 DCCT Study
• Diabetes Control and Complications Trial (DCCT)
conducted in
• Results showed that you can prevent the
complications of diabetes.
• Retinopathy
• Nephropathy
• Neuropathy
“Maintaining blood glucose as close to normal as
possible prevents or slows the progression of long-
term diabetic complications”
Type 2 Diabetes Mellitus
• Most Prevalent
• Two main problems
• Insulin resistance
• Impaired insulin secretion
• Inappropriate glucose production by liver
• Alteration in the production of hormones and
cytokines by adipose tissue.
Gestational Diabetes

• Higher risk of C-section

• Perinatal death
• Neonatal complications
• Risk of developing type 2 DM in 5 to 10 years is
increased.
 Gestational Diabetes
• Any degree of glucose intolerance that causes during
pregnancy.

• Hyperglycemia develops during pregnancy- secretion

of placental hormones (which causes insulin
resistance)
Gestational Diabetes
• High risk women should be screened at 24-28
weeks of gestation

• Need oral glucose tolerance test or glucose

challenge

• A 2 hr. fasting level after 100ml glucose load of

155 would indicate GDM
Secondary Diabetes
• Causes
• Damage/injury/interference or destruction of
pancreas
• Conditions
• Cushing's
• Hyperthyroidism
• Recurrent pancreatitis
• Use of parenteral nutrition
Secondary Diabetes
• Medications
• Corticosteroids
• Thiazides
• Dilantin
• Atypical antipsychotics

• Resolves when treatment of underlying

condition is treated
Clinical Manifestations of Type 1
DM

• Frequent urination (Poliuria)

• Increase in thirst (Polidipsia)
• Weight loss
• Increase hunger (Poliphagia)
• Weakness
Clinical Manifestation of Type 2
Diabetes
• Type 2 –Non-specific –Gradual Onset Include
classic signs of Type 1
• Most common signs of Type 2
• Fatigue
• Recurrent infections
• Recurrent vaginal yeast infections
• Prolonged wound healing
• Visual changes- Blurred vision
Diagnostic Studies
• Three Methods
Fasting plasma glucose level->
126 mg-dl- no caloric intake for 8hr
Random or casual plasma glucose >
200mg/dl plus S/S
Two-hour OGTT level- > 200mg/dl using a
75g glucose load
Assessment
• History
• Signs related to Dx. Of DM
• hyperglycemia
• hypoglycemia
• Monitor frequency, timing, severity and
resolution
• BS monitoring
• Status of symptoms
• Adherence to Tx. Regimen
• Lifestyle. culture, psychosocial and economic
factors
• Effects of complications
Assessment
• Physical Exam

• B/P sitting and lying-(orthostatic chg.)

• BMI
• Dilated eye exam
• Foot exam
• Skin exam
• Neuro. exam
• Oral exam
 Continued…
• Labs
• Hgb A1C
• A long-term measure of glucose control that is a
result of glucose attaching to hemoglobin for the
life of the rbc (120 days).
• Fasting lipid profile
• Microalbuminuria
• Serum Creatine
• UA
• EKG
• Referrals-Opthal., Podiatry, Dietician
Goal
• Be an active participant
• To experience few or no episodes of acute
hyper/hypoglycemia emergencies
• Maintain BS levels as close to normal
• Prevent, minimize or delay complications
• Adjust lifestyle to decrease stress
Diabetes Prevention Program

•Obesity # 1 predictor of type 2 DM

•Modest wt. loss of 5-10% of body wt. with
regular exercise-30 min 5X/wk
•Dropped the risk of developing type 2 DM
up to 58%
Type 2 Diabetes Mellitus
• Metabolic Syndrome is increased with Type 2
DM
• Characterized by:
• Insulin resistance
• Elevated insulin levels
• High triglycerides
• Decreased HDL levels
• Increased LDL levels
• HTN
Type 2 Diabetes Mellitus

•Metabolic Syndrome
•Risk Factors
•Central obesity
•Sedentary lifestyle
Five Components of Diabetes
Management
• Nutritional management
• Exercise
• Monitoring
• Pharmacologic management
• Education
Types of Insulin
• Only human insulin is used
• Insulin's differ in onset, peak, and duration
• Matched to client’s activity
Rapid-Acting Insulin
• Humalog or Novolog (LISPRO) (Aspart) (Glulisine)
• Onset 10 – 30 min. Peak 1-2 hours. Effects last 2 hrs – 6 hrs
• Used to
• Rapidly reduce glucose level
• Treat postprandial hyperglycemia
• Prevent nocturnal hypoglycemia
• Usually one shot a day before each meal for a total of 3 shots a day
Short-Acting Insulin
• Humilin R, Novolin R, ReliOn R
• Onset 30 min. – 1 hr, Peak 2 – 4 hr
• Effects last 4 – 6 hrs
• Administer 20-30 mins. before eating
• If mixing with NPH Regular is always drawn up
first.
Intermediate –Acting Insulin
• NPH, Novolin N, Humulin N, ReliOn N
• Cloudy
• Onset 2 – 4 hrs, Peak 4 – 14 hrs
• Effects last 16 – 24 hrs
• 30 mins before meal
 Long-Acting Insulin
• Glargine (Lantus) clear
• Onset 1-2 hours
• Duration 12 - 24 hours
• No peak
• Cannot mix with other insulins
• Cannot Prefill
• Normally given once a day
• Detemir (levemir) clear
• (onset 3-4, peaks in 3-9, duration is 6-23 hours)
• Both are for basil gylcemic control, doesn’t control
post prandial levels (levels after you eat)
Storing Insulin
• Insulin can be stored at room temp. for 30 days
• In the refrigerator until expiration date
• Pre-filled pens 30 days in refrigerator
• Pre-filled pens with insulin mixture are usually
good for 30 days
Do’s and Don’ts of Insulin
• Keep spare insulin
• Inspect for flocculation (frosted whitish coating)
before use
• Avoid extreme temperatures , do not freeze
• Keep out of direct sunlight or in a hot car
Selecting Sites
• Recommendations
• Do not use same site more than once in 2-3
weeks
• Do not inject insulin to limb which will be used
to exercise.
• Use same anatomic area at the same time of
day
Selecting Sites
• Abdomen- more stable and rapid absorption
• Arms- posterior surface
• Thighs anterior surface
• Hips
Insulin Syringes
• Syringes selected should match insulin
concentration
• 3 types of syringes available
• 1 ml-holds 100 units
• 0.5ml-holds 50u
• 0.3 ml-holds 30u
Complications of insulin Therapy
• Local allergic reaction( itching, erythema, and
burning around inject. Site
• Systemic allergic reactions (urticaria and
antiphylactic shock)
• Insulin lipodystrophy( atrophy of tissue)
Complications of Insulin Therapy
• Dawn Phenomenon-hyperglycemia that is
present when awakening from release of
counterregulatory hormones in the predawn
hours.
• More severe when growth hormone is peaking
(Adolescence and young adulthood)
• Treatment- adjustment in timing of insulin or an
increase in insulin
Complications of Insulin Therapy
• Somogyi effect
• Rebound effect –overdose of insulin produces
hypoglycemia
• During the hours of sleep
• Counterregulatory hormones released ,
stimulate lipolysis, gluconeogensis, and
glycogenolysis and in turn produce rebound
hyperglycemia and ketosis.
Major Classes of Medications
• Thiazolidnedones & Biguanides Drugs that
sensitize the body to insulin and/or hepatic
glucose production
Sulfonylures & Meglitnides
Drugs that stimulate the pancreas to make
more insulin
Major Classes of Medications
Alpha-glucosidase Inhibitors
Drugs that slow the absorption of starches
Incretin Mimetic
Stimulate release of insulin, decrease glucagon
secretion, increase satiety and decrease gastric
emptying
Amylin Analog
Decrease gastric emptying , decrease glucagon
secretion, decrease endogenous glucose output from
liver, increase satiety
Incretin Mimetic
• Byetta –Exenatide
• Synthetic peptide stimulates release of insulin
from pancreatic B cells.
• Suppression of glucagon, decrease glucose
from liver
• Slowing of gastric emptying
• Not indicated with insulin use
• Administer SubQ
Nutrition
• Nutrition –meal planning and weight control are the foundation of
diabetes self-management

• Need to control total caloric intake to attain or maintain a

reasonable body weight and have good glycemic control
Nutrition Management Goals
• Near normal blood glucose
• Meet energy needs
• Achieve lipid profile and B/P levels to reduce cardiovascular risks
• Improve health thru healthily food choices and exercise
• Cultural preferences of each individual
Nutrition Management
• Weight loss is the key to treatment
• BMI of 25 – 29 is considered overweight
• BMI ≥ 30 is considered obese
• Obesity is associated with increased resistance to insulin
• http://www.nhlbi.nih.gov/guidelines/
obesity/bmi_tbl.htm for a BMI table
 Meal Planning

• Meal plans needs to be adjusted to patient’s ethnic background and

culture.
• If patient is on insulin, timing and meal content can be adjusted if a
person is exercising.
• Advances of insulin allows for more flexibility.
Meal Planning
• Review patient’s diet history.
• Identify patient’s eating habits and lifestyle.
• Assess need for weight loss, weight gain, or weight maintenance.
Dietary Needs
• For most diabetics a healthy diet consists of
• 50% to 60% of calories from carbohydrates
• 10-20% of calories from protein
• 20-30% or less of calories from fat
Carbohydrates
• Recommended 50% to 60% of calories from carbohydrates
• Carbohydrates consist of sugars and starches
• Carb. counting is a useful tool for blood glucose management
• Low Carb. Diets are not recommended for persons with DM
Fats
• Recommended fat content <20-30% of total calories
• Saturated fats limited to 10% total calories
• Limit total dietary cholesterol to <300mg per day
• May help reduce cholesterol levels
Proteins
• Less than 10% of total energy consumed.
• Moderate to high protein not recommended- Too much saturated
fat and unnecessary stress on kidney to excrete excess nitrogen
Fiber
• Helps lower total cholesterol and low-density lipoprotein
cholesterol in the blood
• Soluble and Insoluble
• Addition/increase of fiber in the meal plan should be gradual
Alcohol
• High in calories
• No nutritive value
• Promotes triglycerdemia
• Promotes hypoglycemia
• Weight gain
Considerations
• Decrease caloric intake by 500-1000 calories if client needs to lose 1-
2 per week.
• Self-prescribed diets not good due to hormonal changes that can
occur from fasting. Include increased synthesis and release of
glucagons and stimulate liver glucogenalysis and could increase BS
Different Meal Plans
• Carbohydrate Counting
• Exchange List
• Food Pyramid Guide
• Glycemic Index
• Portion Control
• Plate Method
Sweeteners
•Nutritive
• Contain calories
• Fructose (fruit sugar)
• Sorbitol and Xylitol

• Non-nutritive
• Few or no calories
• NutraSweet (aspartame)-4 cal. Per packet
• Splenda (sucralose)
Benefits of Exercise

• Lowers blood glucose

• Decrease Cardiovascular risk factors.

• Psychological well being.

• Improvement in insulin secretions.

Exercise

• Lowers blood glucose

• Increases uptake of glucose by body muscles
• Improving insulin usage
• Improves circulation and muscle tone
Benefits of Exercise
• Lowers blood glucose
• Decreases cardiovascular risk factors
• Improved functioning of the cardiovascular system.
• Improved strength and physical activity capacity
• Reduced risk factors of coronary artery disease
Exercise
• Resistance strength training increases lean muscle mass thereby
increasing resting metabolic rate.
• Also helps to decrease weight, decrease stress, and maintains well
being.
Exercise and Cardiovascular
Diseases
• Alters blood lipid levels
• Increases levels of high density lipo-protein
(HDL)
• Decreases total cholesterol and triglyceride
levels
Important to patients with diabetes with an
increase risk of cardiovascular disease.
Precautions with Exercise
• Blood glucose levels > 250 mg/dl and ketones
urine should not exercise until urine test
negative for ketones and blood glucose levels
are near to normal ( ADA, 2009).
Precautions
• Exercising increases blood glucose
• Exercising increases the secretion of glucagon,
growth hormone and catecholamines
• Liver releases more glucose resulting in an
increase in blood glucose level.
Type 1 and Exercise
• Do not have same effect as Type 2

• Hypoglycemia can occur many hours after

exercise. (Up to 48 hours) due to depletion of
glycogen stores is a contributing factor of
hypoglycemia

• Food amount required varies from person to

person.
Exercise and Insulin
• The physiologic decrease in circulating insulin
that normally occurs cannot occur in persons
being treated with insulin.
• Need to monitor BS before, during and after
exercise to determine alterations in food or
insulin
• Food amount varies from person to person.
Carbohydrate Replacement During
Exercise
Intensity Duration in CHO Replacement Frequency
Minutes

Mild to < 30 May Not Need

Moderate

Moderate 30-60 15gm Every hour

High 60+ 30 to 50gm Every hour

Type 1 and Exercise
• If you are participating in long periods of
exercise
• Check blood sugar before, during and after
exercise period and snack on carbohydrate
snacks as needed to maintain blood glucose
level.
Type 2 and Exercise
• Obese people with Type 2
• Exercise and dietary management improves
glucose metabolism and enhances loss of body
fat
• Improves insulin sensitivity and may decrease
the need for insulin or oral agents.
 Recommendations
• Exercise at the same time each day.
• Exercise the same amount of time each day.
• If patient has diabetic complications, alter the
exercise type and amount as necessary. Increased B/P
assoc. with exercise may aggravate diabetic
retinopathy
Recommendations
• Start slow and gradually increase exercise

• Always discuss with physician before starting

any exercise program for a medical evaluation
with appropriate diagnostic studies before
beginning.
Monitoring
• Blood glucose monitoring is a cornerstone in
diabetes management.
• Self-monitoring of blood glucose (SMBG) is
recommended by the ADA.
• Many types of glucometers-Pick the one that
best suits the patient. Consider ease of use, skill
level,cost of strips, visual numbers etc….
Monitoring
• Potential hazards of SMBG- patients may report
erroneous blood glucose values as a result of
using incorrect technique.
• Improper application of blood
• Improper meter cleaning
• Damage to reagent strips
• Coding of meter
Candidates for SMBG
• Uncontrolled diabetes
• A tendency for hypoglycemia
• Hypoglycemia unawareness
• Patients on insulin
• During illness
Monitoring
• According to the ADA patients on insulin should
test at least four times a day, usually before
meals and at bedtime.
• Persons not receiving insulin and on orals should
test two-three times a day, including a 2hpp
• Important to keep a logbook and take to all
doctor’s appointments.
• Persons will tend not to monitor if not taught
how to use results.
Continuous Glucose Monitoring
• Available
• Senor attached to an infusion set inserted
subcutaneously in the abdomen and connected
to a device worn on a belt.
• Worn for 72 hours and downloaded for review.
• Glucowatch- worn on wrist
Glycated Hemoglobin

• Referred to as HgbA1c or A1C

• Reflects average blood glucose levels over a
period of approximately 2 to 3 months, (ADA,
2004)
Acute Complications

•Hypoglycemia-Abnormally low blood

glucose level (<70mg/dL)
• Causes
• Too much insulin or oral hypoglycemic agents
• Too little food or excessive exercise
• Delayed or skipped meals
Hypoglycemia
• Two categories
• Adrenergic
• Mild hypoglycemia- sympathetic nervous
system is stimulated- surge of epinephrine
and norepinephrine
• S/S- sweating, tremor, tachycardia,
palpitations, nervousness, and hunger.
Hypoglycemia
• Central nervous symptoms
• Moderate hypoglycemia- deprives the brain
cells of needed fuel for functioning
• S/S- inability to concentrate, headache,
lightheadness, confusion, memory lapse,
numbness of the lips and tongue, slurred
speech, impaired coordination, emotional
changes, irrational or combative behavior,
double vision and drowsiness
Management/Teaching
• Treat hypoglycemia using Rule of 15

• Teaching Component
• Teach patients to carry some form of simple sugar with
them at all times.
• Avoid over treating hypoglycemia
• Consistent pattern of eating and administering of
insulin.
Hypoglycemia
• Emergency Measures
• For patients who are unconscious or cannot
swallow.
• Glucagon 1mg injection can be given SubQ
Hypoglycemia Unawareness
• No warning signs and symptoms of
hypoglycemia
• Increase risk of dangerously low BS
• Related to autonomic neuropathy
Diabetic Ketoacidosis (DKA)
• DKA caused by an absence or markedly
inadequate amounts of insulin.
• Caused by disorders in the metabolism of fats,
CHO, and proteins.
Ketoacidosis
• Signs and Symptoms
• Nausea and vomiting
• Rapid breathing
• Extreme tiredness and drowsiness
• Weakness
DKA
• Three main clinical features:
• Hyperglycemia
• Dehydration and electrolyte loss
• Acidosis
• Insulin defeciency leads to breakdown of fat (
lipolysis) into free fatty acids and glycerol.
• Free fatty acids are converted into ketone
bodies by the liver.
DKA
•Three main causes of DKA
•Decreased or missed dose of insulin
•Illness or infection
•Undiagnosed or untreated diabetes
•Treatment
•IV fluid and electrolyte replacement
DKA Treatment
• Correct fluid and electrolytes
• Correct acidosis
• Provide adequate insulin
• Establish cause of DKA
• Can be mild to severe
DKA
• Signs and Symptoms
• Due to Na and K+ loss in urine clients
experience
• Muscle weakness
• Extreme fatigue
• Malaise
• Cardiac arrhythmias can lead to cardiac
arrest
• Acidosis-fruity breath, tachycardia and
hypotension
Monitoring and Managing
Potential Complications
• Fluid Overload- Administering fluids rapidly to
treat DKA or HHNS

• Hypokalemia-due to treatment of DKA-loss of

potassium

• Cerebral Edema-cause unknown, may be by

rapid correction of hyperglycemia- resulting in
fluid shift
 Hyperglycemia Hyperosmolar
Nonketotic Syndrome (HHNS)
• Serious condition – Blood glucose 800-1000 mg/dl
• Ketosis usually minimal or absent
• Defect is usually lack of effective insulin (insulin resistance)
• Presistent hyperglycemia causes osmotic diuresis which results
in losses of water and electrolytes. To maintain osmotic
equilibrium, water shifts from the intracellular fluid space to the
extracellular fluid space. With glycosuria and dehydration,
hypernatremia and increased osmolarity occurs.
• Usually occurs in older adults
Causes of HHNS
• Acute illness
• Medications that exacerbate hyperglycemia
• Dialysis treatment
HHNS

• Hypotension
• Profound dehydration
• Tachycardia
• Variable neurological signs
• Morality rate- 10% to 40%
• Treatment-fluid replacement and correct
electrolytes
 Comparison of DKA and HHNS
DKA HHNS
• While can occur in both, usually occurs in Type 1 • While can occur in both, usually occurs in Type 2
(esp. elderly)
• Precipitated by:
• omission of insulin, physiologic stress (infection, • Precipitated by:
surgery, etc.) • Physiologic stress (infection, surgery, etc.)
• Onset • Onset
• Rapid (<24 hours) • Slower (over several days)
• Blood Glucose Levels • Blood Glucose Levels
• Usually >250 • Usually > 600
• Arterial pH levels • Arterial pH levels
• < 7.3 • Normal
• Serum and urine ketones • Serum and urine ketones
• Present • Absent
• Serum Osmolality • Serum Osmolality
• 300-350 • >350
• BUN and Creatinine levels • BUN and Creatinine levels
• Elevated • Elevated
• Mortality Rate • Mortality Rate
• < 5% • 10-40%
Macrovascular Complications
• Diseases of large and medium-size vessels
• Atherosclerosis- From altered lipid metabolism
• Cerebral Vascular
• Peripheral Vascular Disease
• Adults with DM – 2-4 times increased risk of
heart and cerebral vascular
 Microvascular Diseases
• Microvascular diseases are unique to diabetes
• Capillary basement membrane thickening
• The basement membrane surrounds the endothelial
cells of the capillary. Researchers believe that
increased blood glucose levels react thru a series of
biochemical responses to thicken the basement
membrane to several times its normal thickness
• 2 areas affected
• Retina
• kidneys
Diabetic Retinopathy
• Results from chronic hyperglycemia
• Most common cause of new cases of blindness
in persons ages 20-74
• Non-proliferative-most common form
• Proliferative- most severe form
Retinopathy
• Non-Proliferative- Partial occlusion of small
blood vessels in the retina-develop
microanueryms. Vision can be affected if
Macula is involved.
• Proliferative-Retinal capillaries become
occluded, hemorrhage. If blood vessels pull
retina can cause a tear or partial or complete
detachment of retina.
Legal Blindness
• A visual acuity that is <20/200 in the better eye
with corrective lenses and or a visual acuity field
of < 20 degrees.
Nursing Management
• Prevention is key

• If vision loss occurs, nursing education must

address the patient’s adjustment to vision
impairment
Medical Management

•Control of blood glucose

•Tight control of blood glucose
reduced risk of developing
retinopathy by 76% compared to
that of conventional therapy
•Control of hypertension
•Cessation of smoking
Nephropathy
• Microvascular complication
• Damage to small blood vessels that supply
glomeruli of the kidney
• Leading cause of end-stage renal disease
• About 50% of all new ESRD cases a year are
diabetics
 Risk factors
• HTN
• Genetic predisposition
• Native Americans, Hispanics, and African Americans
with Type 2 DM are at greater risk of developing
ESRD than Whites
• Smoking
• Chronic hyperglycemia
• Studies DCCT and UKPDS showed significant
reduction when near-normal blood glucose control
was achieved and maintained
Treatment
• Aggressive B/P management with Ace inhibitor
• Yearly screening for microalbuminuria in the
urine
 Treatment of Diabetic Nephropathy
• Hypertension Control - Goal: lower blood pressure to
<120/80 mmHg
• Antihypertensive agents
• Angiotensin-converting enzyme (ACE) inhibitors
• captopril, enalapril, lisinopril, benazepril,
fosinopril, ramipril, quinapril, perindopril,
trandolapril, moexipril
• Angiotensin receptor blocker (ARB) therapy
• candesartan cilexetil, irbesartan, losartan
potassium, telmisartan, valsartan, esprosartan
• Beta-blockers
 Treatment of Diabetic Nephropathy
(cont.)
• Glycemic Control
• Pre-prandial plasma glucose 90-130 mg/dl
• A1C <7.0%
• Peak postprandial plasma glucose <180 mg/dl
• Self-monitoring of blood glucose (SMBG)
• Medical Nutrition Therapy

• Restrict dietary protein to RDA of 0.8 g/kg body weight per day
 Diabetic Neuropathy
 About 60-70% of people with diabetes
have mild to severe forms of nervous
system damage, including:
 Impaired sensation or pain in the feet or hands
 Slowed digestion of food in the stomach
 Carpal tunnel syndrome
 Other nerve problems

 More than 60% of nontraumatic lower-

limb amputations in the United States
occur among people with diabetes.
Risk Factors
• Glucose control
• Duration of diabetes
• Damage to blood vessels
• Mechanical injury to nerves
• Autoimmune factors
• Genetic susceptibility
• Lifestyle factors
• Smoking
• Diet
Pathogenesis of Diabetic Neuropathy

• Metabolic factors
• High blood glucose
• Advanced glycation end products
• Abnormal blood fat levels

• Ischemia
• Nerve fiber repair mechanisms
 Autonomic neuropathy
• Affects the autonomic nerves controlling internal organs
• Peripheral
• Genitourinary
• Gastrointestinal

• Cardiovascular
• Is classified as clinical or sub-clinical based on the presence or absence of
symptoms
Continued….
• Hypoglycemic unawareness

• Sudomotor neuropathy- absence of sweating of the extremities

with a compensatory increase in upper body sweating.

• Sexual Dysfunction
 Essentials of Foot Care
•Examination
• Annually for all patients
• Patients with neuropathy - visual inspection of feet at every
visit with a health care professional
•Advise patients to:
• Use lotion to prevent dryness and cracking
• File calluses with a pumice stone
• Cut toenails weekly or as needed
• Always wear socks and well-fitting shoes
• Notify their health care provider immediately if any foot
problems occur
Foot Care
• Complications of DM contribute to an increased risk of foot
infections.
• A foot infection is a preventable infection.
• Foot care measures should be practiced on a daily basis.
• Foot care tips-chart pg. 1287
Complications
• Diabetic foot ulcers
• Begins with soft tissue injury of foot.
• Formation of fissure between toes or in area of
dry skin.
• Formation of callus.
• Ingrown toenails
• Cracks in skin
• Venous insufficiency is a contributing cause of
foot ulcers
Type of Injuries
• Chemical
• Traumatic
• Thermal
Foot Infections
• Signs and Symptoms
• Drainage
• Swelling
• Redness (cellulites of leg)
• Gangrene

Usually first signs of foot problem

Treatment of Foot Ulcers
• Bed rest
• Antibiotics
• Debridement

• Good control of blood glucose (usually increases

with infection).
Treatment of Foot Ulcers
• If patient has PVD, ulcers may not heal due to
the decreased ability of oxygen, nutrients, and
antibiotics to reach the injured tissue.
• Amputation may be necessary to prevent
spread of infection
Other Complications
• Skin- Acanthosis nigricans- dark , coarse,
thicken skin on the neck.
• Diabetic dermatopathy-red-brown flat-topped
papules
• Granuloma annulare- type 1- autoimmune-
partial rings of papules, often in dorsal surface
of hands and feet
Infections
• More susceptible to infections
• Defect in the mobilization of inflammatory cells
and an impairment of phagocytosis.
• Recurrent yeast infections
• Treatment must be prompt and aggressive.
Special Issues
• Patient undergoing surgery
• During stress such as surgery, blood glucose
levels rise as a result of an increase level of
stress hormones.
• If hyperglycemia is not controlled- osmotic
diuresis may lead to excessive loss of fluids and
electrolytes.
• Hypoglycemia- withhold SQ insulin morning of
surgery
Hospitalization
• Factors affecting hyperglycemia
• Changes in treatment regimen
• Medications (eg. Glucocorticoids
• IV Dextrose
• Overly vigorous treatment of hypoglycemia.
Continued…

• Factors affecting hypoglycemia

• Overuse of sliding scale
• Lack of dosage changes when dietary intake is changed.
• Overly vigorous treatment of hyperglycemia
• Delayed meal after lispro or aspart insulin

• The chart she wants us to look at shows a stick with a wire

on the end of it (a mono-filiament) being poked at 5
pressure points on the bottom of the foot (big toe, 4th toe,
and 3 spots along the ball of the foot). You poke them to
see if they can feel it. This is what you do when assessing
the sensory threshold in pt’s with DM. They can also do it
themselves
Alterations in Meal Plan
• If client is NPO- insulin dose may need to be
changed for type 2
• Type 1 may need to administer insulin
• Frequent blood glucose monitoring.
• Clear liquids need to be caloric
• Tube feeding-important to administer insulin at
regular intervals.
Promoting Self-Care
• Address any underlying factors affecting
diabetes control.
• Simplify the treatment regimen
• Adjust regimen to meet patient’s request.
• Provide positive reinforcement and
encouragement.
Education
• Flexibility is important.
• Teach what client wants to learn not what you think they need to
learn!!
• The major goal of education is an educated client.
• Do not try to teach everything in one session.
Nursing Diagnoses
• Deficient knowledge r/t diabetes self care
skills/information.
• Potential self care deficit r/t physical
impairments or social factors.
• Anxiety r/t loss of control, fear of inability to
manage diabetes, misinformation r/t diabetes,
fear of diabetes complications.
• Risk for infection r/t potential sensory loss in
feet.
Nursing Diagnoses
• Imbalanced Nutrition Related to increase in
stress hormones
• Risk for impaired skin integrity related to
immobility and lack of sensation.
Goals
• Improved nutritional status
• Maintenance of skin integrity
• Ability to perform basic diabetes self-
management.
• Prevent short and long term diabetes
complications
Reference
• Brunner & Suddarth’s Text Book of Medical Surgical Nursing, 12 ed
Vol. 2, Lippincott William Wilkins