DIABETES

DIABETES

 is a group of metabolic diseases

characterized by elevated of glucose
in the blood (hypergltcemia) resulting
from defects in insulin and insulin
action. Major sources of this glucose
are absorption of ingested food in
gastrointestinal tract and formation of
glucose by the liver from food
substance.
 Insulin a hormone produced by the
pancreas, controls the level of
glucose in the blood by regulating the
production and storage of glucose
 In diabetic state, the cells may stop
responding to insulin or the pancreas
may stop producing insulin intirely.
 Leads to hyperglycemia, which may
result in acute metabolic
complication sush as:
a. diabetic ketoacidosis (DKA)
b. hyperglycemic hyperosmolar
nonketotic syndrome (HHNS)
 Long-term effects of hyperglycemic
contribute to:
1. macro vascular complication
(coronary artery disease,
cerebrovascular disease and
peripheral vascular disease)
2. chronic macrivascular complication
(kidney and eye disease)
3. neuropathic complication (disease of
the nerve)
 Primary Goal of treatment for patients
with diabetes
 controlling blood glucose level
 preventing acute
 long term complication
  CLASSIFICATION OF
DIABETES
 Several different types of DM
a. cause
b. clinical course
c. treatment
 Major classifications of diabetes are
a. type 1 diabetes (previously
referred to as insulin-independent
diabetes mellitus) IDDM
b. type 2 diabetes (previously
referred to as non-insulin-
independent diabetes mellitus)
NIDDM
c. gestational diabetes mellitus
d. DM with others conditions or
syndrome
 OVERVIEW

 terms “insulin-dependent diabetes”

and “non-insulin-dependent diabetes”
are no longer used because they have
resulted in classification of patients on
the basis of the treatment of their
diabetes rather than the underlying
etiology.
 Approximately 5% to 10% of people
with diabetes have type 1 diabetes,
which the insulin- producing
pancreatic beta cells are destroyed by
an autoimmune process.
 type 1 diabetes is characterized by
an acute onset, usually before age
30
 approximately 90% to 95% of people
with diabetes have type 2 diabetes,
which result from decreased
sensitivity to insulin (called insulin
resistance) and impaired beta cell
functioning resulting in decreased
insulin production.
 type 2 diabetes occurs more among
people who are older than 3o years
and obese
 type 2 diabetes is first treated with
diet and exersice
 borderline diabetes is classified as
impaired glucose tolerance (IGT) or
impaired fasting glucose (IFG) and
refers to a condition in which blood
glucose level fall between normal
levels and levels considered
diagnostic for diabetes.
 Risk Factors for Diabetes Mellitus

1. Family history of diabetes

2. Obesity
3. Race/Ethnicity
4. Age
5. Previously independent impaired
fasting glucose or impaired glucose
tolerance
6. Hypertension
7. HDL cholesterol level or triglyceride
level
8. History of gestational diabetes or
delivery of babies over 9 lbs.
 PHYSIOLOGY AND
PATHOPHYSIOLOGY OF DIABETES
 
 insulin is secreted by beta cells, which are
one of four types of cells in the islets of
Langerhans in the pancreas.
 Insulin is an anabolic, or storage,
hormone.
 Insulin secretion increases and moves
glucose from the blood into muscle, liver,
and fat cells, when the person eats a
meal.
 In those cells, insulin:
1. transports and metabolize glucose
for energy
2. stimulates storage of glucose in the
liver and muscle
3. signals the liver to stop the release
of glucose
4. enhances storage of dietary fat in
adipose tissue
5. accelerates transport of animo acids
into cells

insulin also inhibits the breakdown of

stored glucose, protein, and fat.
 Classification of Diabetes Mellitus and
Related Glucose Intolerances

Current Classification Previous Classification Characteristics and

Implication

Type 1 Juvenile diabetes Onset any age, but

usually young (<30yrs).
Juvenile-onset diabetes
Usually thin at diagnostic;
Ketosis-prone diabetes with recent weight loss.
Brittle diabetes Etiology includes genetics,
Insulin-dependent immunologic, or
environmental factors.
Diabetes mellitus(IDDM)
Often have islet cell
antibiotics.
Little or no endogenous
insulin.
Need insulin to reserve life
Ketosis-prone when insulin
absent.

Acute complication of
Type 2 Adult-onset diabetes hyperglycemia:diabetics
ketoacidosis.
Maturity-onset diabetes
Onset any age, usually
Ketosis-resistant over 30 years.
diabetes Usually obese at
diagnose
Stable diabetes
Causes include obesity,
Non-insulin-independent heredity, or
diabetes (NIDDM) environmental factors.
No islet cell antibodies
Decrease in
endogenous insulin, or
increased with insulin
resistance.
Moat patients can
control  blood glucose
through weight loss if
obese.
Oral antidiabetes
agents may improve
blood glucose levels
if dietary
modification and
exercise are
unsuccessful.
May need insulin on
a short- or long-term
basis to prevent
hyperglycemia.
Ketosis rare, except
in stress or infection.
Acute complication
Diabetes mellitus Secondary diabetes hyperglycemic
associated with other Hyperosmolar
conditions or nonketonic syndrome.
syndrome Accompanied by
condition known or
suspected to cause the
disease: pancreatic
diseases, hormonal
abnormalities,
medications such as
corticosteroids and
estrogen-containing
preparation.
Depending on the
ability of the pancreas

to
 produces insulin, the patient
Gestational diabetes Gestational diabetes may require treatment with
oral antidiabetes agents or
  insulin.
Onset during pregnancy,
usually in the second or third
trimester
Due to hormones secreted by
the placenta, which inhibit
the action of insulin.
Above-normal risk for
perinatal complication,
especially macrosomia.
Treatment with diet and if
needed insulin to strictly
maintain normal blood
glucose level.
Occurs in about 2%-5% of all
pregnancies.
Glucose intolerance transitory
but may recur:
 in subsequent pregnancies
30%-40% will develop
overt diabetes within 10
years
Impaired glucose Borderline diabetes Risk factors include
Intolerance Latent diabetes obesity, age older than
30years, family history of
Chemical diabetes diabetes, previous large
Subclinical diabetes babies.
Asymptomatic diabetes Screening tests should be
performed on all pregnant
women between 24 and 28
wks gestation.
Oral glucose tolerated test
value between 140 mg/dL
and 200 mg/dL.

Impaired fasting glucose

 is defined as a fasting
plasma glucose between
110 mg/dL and 126
mg/dL.
Prediabetes Previous
29% eventually develop
abnormality of glucose diabetes
tolerated Above-normal
  susceptibility to
atherosclerosis disease.
Renal and retinal
complication usually not
significant.
May be obese or
nonobese; obese should
reduce weight.
Should be screened for
diabetes periodically.
Current normal glucose
metabolism.
Previous history of
hyperglycemia
Periodic blood glucose
screening after age 40 if
there is a family history of
diabetes or if symptomatic.
Encourage ideal body weight,
because loss of 10-15 lbs
may improve glycemic
control.
No history of glucose
intolerance.
Increased risk of diabetes if:
positive family history
obesity mother of babies over
9lbs at birth
Screening and weight advice

as in PrevAG
 CLINICAL MANIFESTATION

1. 3P’s – polyuria, polydipsia and

polyphagia
2. Fatigue
3. Weakness
4. Sudden vision changes
5. Tingling or numbness in hands or
feet
6. Dry skin
7. Skin lesions or wounds slowly to
heal
8. Recurrent infections
9. Onset of type 1 diabetes – sudden
weight loss, nausea, vomiting.
10. Abdominal pain – if DKA developed.
 ASSESSMENT AND
DIAGNOSTIC FINDING
 
Criteria for the Diagnostic of Diabetes Mellitus

1. Symptoms of diabetes plus casual plasma glucose

concentration
equal to or greater than 200 mg/dL. Casual is defined as
any time of day without regard to time since last meal. The
classic symptoms of diabetes include polyuria, polydipsia
and unexplained weight loss.
2. Fasting plasma glucose greater than or equal to 126
mg/dL. Fasting is defined as no caloric intake for at least 8
hours.
3. 2-hours postload glucose equal to or greater than 200
mg/Dl during an oral glucose tolerated test.
 ASSESSMENT

1. history
2. physical examination
3. laboratory examination
4. need for referral 
 MANAGEMENT

 Goal
1. to normalize insulin activity
2. blood glucose levels to reduce the
development of vascular and
nauropathic complication
1. Nutritional Management
 Goals

a. Providing all the essential food

constituents necessary for optimal
nutrition.
b. Meeting energy
c. Achieving wide daily fluctuations in
blood glucose levels, with blood
glucose levels as close to normal as
is safe and practical to prevent or
reduce the risk for complication.
d. Decreasing serum lipid levels, if
elevated, to reduce the risk for
macrovascular disease.
 Meal planning and related teaching
 caloric requirements
 caloric distribution
 carbohydrates
 fats
 Fiber
 food classification systems
 exchanges lists
 food guide pyramid
 glycemic index
 Other Dietary concerns
 Alcohol consumption
 Sweetness
 Misleading food lebels
2. Exercise
 Benefits
 Exercise precaution
 General Precautions for Exercise
in Diabetes:
a. Use proper foor wear and, if
appropriate, other protective
equipment.
 b. Avoid exercise in extreme heat
or cold
c. Inspect feet daily after exercise
d. Avoid exercise during after
periods of poor metabolic
control
 Exercise recommendations
3. Monitoring Glucose levels and
Ketones
 blood glucose is monitoring is
cornerstone of diabetes
management and self-
monitoring of blood glucose
(SMBG) level by patients has
dramatically altered diabetes
care.
 Advantages and disadvantages of
SMBG system common sources of
error include:
1. Improper application of food
2. Improper meter cleaning and
maintenance
3. Damage to the reagent strips
 Candidates for SMBG
 Unstable diabetes
 A tendency for severe ketosis or
hypoglycemia
 Hypoglycemia without warning
symptoms
 Frequency of SMBG
 Responding to SMBG results
 Glycosylated hemoglobin
 Glycosylated hemoglobin = (referred
to as HgbA or A1C) is a blood test
that reflects average blood glucose
levels over a period of approximately
2 to 3 months.
 Urine testing for glucose
 Disadvantages of urine testing
include the following:
 Result does not accurately reflect
the blood glucose level at the time
of the rest.
 The renal threshold foe glucose is
180-200 mg/dL, for above target
blood glucose levels.
 Hypoglycemia cannot be detected
because a “negative” urine glucose
result may occur when the blood
glucose leel ranges from 0-180
mg/dl or higher.
 Patients may have a false of being
in good control when results are
always negative.
  Various medications may interfere
with the test result.
 In elderly patients and patients
with kidney disease, the renal
threshold is raised, thus the false
negative may occur at dangerously
elevated glucose levels

 Testing for ketones

4. Pharmacology therapy
 Insulin Therapy and Insulin
Preparations
 Time course of action
 Species (source)
 Manufacturer
 Insulin Regimens
 Conventional regimens
 Intensive regimens
 Complication of insulin therapy
 Local allergic reactions
 Systemic allergic reactions
 Insulin resistance
 Insulin lipodystrophy
 Morning hyperglycemia
 Alterative methods of insulin delivery
 Insulin pens
 Jet injections
 Insulin pumps
 Implantable and inhalant insulin
delivery
 Transplantation of pancreatic cells
 Oral Antidiabetes Agents
 First-Generation Sulfonylureas
 acetohexamide (Dymelor)
 chlorpropamide (Diabinese)
 tolazamide (Tolinase)
 talbutamide (Orinase)
 Second-Genaration Sulfonylureas
 glipizide (Glucatrol)
 glipizide (Glucatrol XL)
 glyburide (Micronase)
 glimepiride (Amaryl)
 Biguanides
 metformin
(Glucophage+GlucosephageXL)
 metformin with glyburine
(Glucovance)
 Alpha Glucosidase Inhibitors
 Acarbose (Precose)
 Thiazolidinediones
 Pioglitazone (actos)
 Rosiglitazone (Avandia)
 Meglitinides
 Repaglinide (Prandin)
 Nateglinide (Starix)
 General Considerations for Oral
Agents
 NURSING MANAGEMENT

1. Education
2. Developing a Diabetes Teaching
Plan
 Organizing Information
 Teaching Survival Skills
 Outline of survival information
include:
1. Simple pathophysiology
a. Basic definition of diabetes
b. Normal blood glucose ranges
and target blood glucose levels.
c. Effects of insulin and exercise
d. Effects of food and stress,
including illness and infections
e. Basic treatment approaches
2. Treatment modalities
a. Administration of insulin and
oral antidiabetes medications
b. Diet information
c. Monitoring of blood glucose and
ketones
3. Recognition, treatment, and
prevention of acutr complications
a. Hypoglycemia
b. Hyperglycemia
4. Recognition, treatment, and
prevention of acutr complications
a. Where to buy and store insulin,
syringes and glucose monitoring
supplies
b. When and how to reach the
physician
 Planning in Depth and Continuing
Education
 Preventive measures include:
 Foot care
 Eye care
 General hygiene
 Risk factor management
 Assessment Readiness to Learn
 Determining Teaching Methods
3. Implementing The Plan
 Teaching Experienced Diabetic
Patients
 Teaching Patients to Self-
Administer Insulin
 Storing insulin
 Selecting syringes
 Preparing the injection: Mixing
insulin
Withdrawing insulin
Selecting and Rotating the
injection site
Preparing the skin
Injecting the needle
Promoting home and community-
based care
Teaching patients self-care
 The following approaches by the
nurse are help for promoting self-care
management skills:
 Address any underlying factors that
may affect diabetic control.
 Simply the treatment regimen if it is
too difficult for the patient to follow
 Adjust the treatment regimen to
meet patient’s request.
 Establish a specific plan or contract
with the patients with simple,
measurable goals.
 Provide positive reinforcement of
self-care behaviors performed
instead of focusing on behaviors
that were neglected.
 Help the patients to identify
personal motivating factors rather
than focusing on wanting to please
the doctors or nurse.
 Encourage the patients to pursue
life goals and interest: discourage
an undue focus on diabetes.
 Continuing Care
  ACUTE COMPLICATION OF
DIABETES

1. Hypoglycemia (insulin reactions)

 hypoglycemia (abnormally low
blood glucose level) occurs when
the blood glucose falls to less than
50 to 60 mg/dL.
 It caused by too much insulin or
oral hypoglycemic agents, too little
food, or excessive physical activity.
 May occur at any time of the day or
night and often occurs before
meals; if meals are delayed or
snacks are omitted.
 Clinical Manifestations
 Mild hypoglycemia
 Blood glucose levels falls
 Sympathetic nervous stystem is
stimulated
 Resulting in a surge of epinephrine
and norepinephrine
 Causes symptoms sush as
sweating, tremor, tachycardia,
palpitation, nervouaness and
hunger
 Moderate hypoglycemia
 Fall in blood glucose level deprives
the brain cells of needed for
functioning.
 Signs of impaired function of the
CNS may include inability to
concentrate, headache,
lightheadedness, confusion, memory
lapses, numbness of the lips and
tongue, slurred speech impaired
coordination, emotional changes,
irrational or combative behavior,
double vision and drowsiness
 Severe hypoglycemia
 CNS function is so impaired that
the patient needs the assistance of
another person for treatment of
hypoglycemia.
 Symptoms may include disoriented
behavior, seizures, difficulty
arousing from sleep, or loss of
consciousness
 Assessment and Diagnostic Finding
 Symptoms can occur suddenly and
unexpectedly
 Patients who have usually a
blood glucose level in the
hyperglycemic range (eg. 200s or
greater) may feel hypoglycemic
symptoms when their blood glucose
quickly drops to 120mg/dL or less.
 Patients who frequently have a
glucose level in the low range of
normal be symptomatic when the
blood glucose slowly falls to less than
50mg/dL
 To altered hypoglycemic symptoms is
a decreased hormonal response to
hypoglycemia
 Severe CNS impairment patients
perform SMBG frequently.
 Management
 the usual recommended is for 15g
of a fast-acting concentrated
source of carbohydrate such as the
following, given orally,
 three or four commercially
prepared glucose tablets
 4 to 6oz of fruit or regular soda
 6 to 10 life savers or other hand
candies
 2 to 3 teaspoons of sugar or honey
 1. Teaching Patients
2. Initiating Emergency Measures
3. Promoting Home and Community-
Based Care

 Teaching patients self care

2. Diabetic Ketoacidosis
 caused by an absence or
markedly inadequate amount of
insulin
 disorder in the metabolism of
carbohydrate, protein and fat
 3 main clinical features
 Hyperglycemia(300-800mg/dL)
 Dehydration (6.5 L water loss) and
electrolyte loss (400-500meq of 
Na+,K+ and C1-24 hr period)
 Acidosis (low serum HCO3=0-
15meq/L; low pH=6.8-7.3)
 3 main causes:
 Decreased or missed dose of insulin
 Illness or infection
 Undiagnosed and untreated
diabetes
 Clinical Manifestation
 hyperglycemia leads to polyuria,
polydipsia, blurred vision,
weakness, and headache
 intravascular volume depletion-
orthostatic hypotension
 volume depletion leads to trank
hypotension with a weak rapid
pulse
 ketosis and acidosis of DKA lead to
GI symptoms such as anorexia,
nausea, vomiting and abdominal
pain.
 Acute breath- elevated ketone
levels
 Hyperventilation
 Assessment and Diagnostic Findings
 blood glucose levels may vary
from 300-800 mg/dl
 severity of DKA is not necessarily
related to the blood glucose level
 patient mat have severe acidosis
with modestly elevated blood
glucose levels
 blood glucose levels of 400-
500mg/dl have no evidence of DKA
 Evidence of ketoacidosis is
reflecting in low serum bicarbonate
and low pH values.
 Low PCO2 level reflect to
respiratory compensation for the
metabolic acidosis
 Sodium and potassium levels may
be low, normal or high depending
on the amount of water loss
 Elevated levels of creatinine,
blood urea nitrogen (BUN),
hemoglobin and hematocrit
 Prevention
 patients must be taught “sick day”
rules
GUIDELINE TO FOLLOW DURING PERIODS OF ILLNESS (“sick day rules”)
take insulin or oral antidiabetes agents as usual
test blood report glucose and test urine ketones every 3-4 hours
report elevated glucose levels or urine ketones to the physician insulin-
requiring patients may need supplemental doses of regular insulin q3 -4

hrs
if usual meal plan cannot be fallowed, substitute soft foods(eg. 1/3 cup
regular cola or orange juice, ½ cup broth, 1 cup Gatorade)q ½ - 1 hr to

prevent dehydration and to provide calories

report nausea, vomiting and diarrhea to the physician, because extreme

fluid loss may be dangerous.

 Medical Management
1. Rehydration
 important for maintaining
tissue perfusion
 fluid replacement
 Patients may need 6-10 liters of IVF
initially
 After the first few hours: 0.45% NS
200-500ml/hr
 monitor V/S, I&O, electrolyte
2. Restoring Electrolytes
 Potassium is a major electrolyte
concern during treatment.
 Factors related to treating DKA
that reduce the serum potassium
concentration include:
 Rehydration, which leads to increased
plasma volume and subsequent
decreased in the concentration of
serum potassium. Rehydration also
leads to increased urinary excreation
of potassium.
 Insulin administration, which
enhances the movement of potassium
from the extracellular fluid into cells.
3. Reserving Acidosis
 ketones bodies accumulate as
result of fat breakdown,
 hourly blood glucose values must
be measured
 administered IV solution with
concentration
4. Hyperglycemic Hyperosmolar
Nonketotic Syndrome
 Serious condition in which
hyperosmolarity and
hyperglycemia predominate, with
alteration of the sensorium.
 Clinical Manifestation
 hypotension
 dehydration ( dry mucous
membrane, poor skin turgor)
 tachycardia
 variable neurologic signs (eg.
Alteration of sensorium, seizures,
hemiparesis)
 Assessment and Diagnostic Findings
 laboratory Test
 blood glucose
 electrolytes
 BUN
 Complete blood count
 Serum osmolality
 And arterial blood gas analysis
 mental status changes,
 Medical Management
 fluid replacement
 correction of electrolyte imbalance
 insulin administration 
 Nursing Management
 monitor vital sign, fluid status, and
laboratory values
 maintain safety
 prevent injury
 I&O monitor
 Nursing Intervention
1. Maintaining Fluid and Electrolyte
Balance
a. Measured I&O
b. Administered IV fluids and
electrolyte as prescribed
c. Encourage oral fluid intake
d. Monitor laboratory values of
serum electrolytes(sodium &
potassium)
e. Monitor VS
f. For sign of dehydration
2. Improving Nutritional Intake
a. Diet is planned with control of
glucose as the primary goal.
b. Appropriate caloric intake allows
the patient to achieve and
maintain the desired body weight
c. Encourage the patient to eat full
meals and snacks as prescribed
3. Reducing Anxiety
a. Provide emotional support
b. Assisted to focus on learning self-
care behaviors
c. Encourage to perform the skills
that are feared most.
d. Positive reinforcement
4. Improving Self-Care
a. Patients teaching
5. Monitoring and Managing Potential
Complication
a. Fluid Overload
Occur because of the administration of
a large volume of fluid at a rapid rate is
often required to treat the patient with
DKA or HHNS
 Risk is increased in elderly patients
and in those with preexsisting cardiac
disease.
 Nurse monitor fluid intake and keeps
careful records of IV and other fluid
intake, with urine output
measurement
 b. Hypokalemia
 Low serum levels may result
rehydration,
 Prevention include cautions
replacement of potassium
c. Hyperglycemia and Ketoacidosis
d. Hypoglycemia
e. Cerebral Edema
6. Monitoring Home and Community-
based Care
a. Teaching Patients self-care
b. Continuing care
 Long term complications
 Are seen in both type 1 and type 2
diabetes but usually do not occur
with in 1st 5-10 yrs. Of diagnosis
 Renal disease is more prevalent
among patient with type 1 diabetes
 Cardiovascular complication is more
prevalent among older patient with
type 2 diabetes
 MACROVASCULAR COMPLICATION
 Result from changes in the medium
to large blood vessels
 Blood vessel wall thicken, sclerose
and become occluded by plaque
that adheres to the vessel wall
 Three main types of macrovascular
complication
a. CAD typical ischemic symptoms
b. CVA
c. Peripheral vascular disease.
 Cerebral blood vessels are similarly
affected by accelerated
atherosclerosis, occlusive changes or
the formation of an embolus.
 vascular that lodges in a cerebral
blood vessel can lead to transient
ischemic attacks and stroke
 Cerebrovascular disease is common
among diabetic patient. Recovery
from a stroke may be impaired in
patient who have elevated blood
glucose level at the time of or
immediately after stroke
 It is important to assess the blood
glucose level
 atherosclerosis changes increasing of
occlusive peripheral arterial disease in
patient with diabetes
 Severe form of arterial occlusive
disease due to lower ext. is largely
responsible for the increased
incidence of gangrene and
subsequent amputation in diabetic
patient.
 Neuropathy and impairment in
wound healing also play a role in
diabetic
 signs and symptoms of peripheral
vascular dse.
a. diminished peripheral pulse
b. intermittent claudication – pain in
the buttocks, thigh, calf during
walking
 ROLE OF DIABETES IN
MACROVASCULAR DISEASE
 one of the main feature of
diabetes in elevated blood glucose
 Risk factor for macrovascular
disease
a. obesity
b. inc. triglyceride level
c. hypertension
 Diabetes itself is seen as an
independent risk factor for the
development of accelerated
atherosclerosis
 Other potential factor that may play
a role in diabetes related
atherosclerosis include
a. platelet
b. clotting factor abnormalities
c. dec. flexibility of RBC
d. changes in the arterial wall related
to hyperglycemia
e. hyperinsulinemia
 MANAGEMENT
 Diet and exercise- for managing
obesity, hypertension,
hyperlipidemia
 Use of medication- to control
hypertension and hyperlipidemia
 Smoking cessation
 Control blood glucose- to reduce
triglyceride\
 Patient may require increase ed
the amount of insulin
 May need to switch from oral
antidiabetic agents to insulin
 MICROVASCULAR COMPLICATIONS
AND DIABETIC RETINOPATHY
1. Diabetic microvascular dse.
a. AKA microangiopathy
b. Characterized by capillary
basement membrane thickening
c. Basement membrane surrounds the
endothelial cells of the capillary
d. Increase blood glucose level reacts
through a series of biochemical
response to thicken the basement
membrane to several times it’s normal
thickness
e. 2 areas are affected
 Retina
 Kidney
f. changes in microvasculature
 microaneurysm
 intraretinal hemorrhage
 hard exudates
 focal capillary closure
1. Diabetic retinopathy- leading cause
of blindness
a. is caused by changes in small
blood vessel in the retina the area
of the eye that receive images
and sends information to the
brain
b. richly supplied with blood vessels of all
kinds
 small arteries
 veins
 arterioles
 venules capillaries
c. 3 main stages of retinopathy
 Non proliferative
 Preproliferative
 Proliferative
 type 1 and type 2 diabetes- lead to
visual distortion and loss of central
vision
 preproliferative retinopathy- is
considered a precursor to the more
serious proliferative retinopathy
 proliferative retinopathy widespread
vascular changes and loss of nerve
fibers
 if visual changes occur during
preproliferative stage caused by
macular edema
 PROLIFERATIVE RETINOPATHY
1. characterized by proliferation of
new blood vessel growing from
the retina into the vitreous
2. Blood vessel are prone to bleeding
3. Vitreous hemorrhage caused
visual losses associated with
proliferative retinopathy.
4. NORMAL vitreous are clear
allowing light to be transmitted to
the retina
5. If hemorrhage occur the vitreous
becomes clouded and cannot
transmit light resulting in loss of
vision
6. Another consequence is that
vitreous hemorrhage resorption of
blood in the vitreous leads to the
formation of fibrous scar tissue
7. scar tissue place traction in the
retina resulating in retinal
detachment and subsequent
visual loss
8. SIGNS AND SYMPTOMS
 Blurry vision secondary to macular
edema
 Indicative of hemorrhaging

1. floaters
2. cobwebs in visual field
3. sudden visual changes – spotty
hazy vision complete loss of
vision
 DIAGNOSTIC PROCEDURE
1. Flourescein angiography – where
dye is injected into an arm vein is
carried to various parts of the
body SIDE EFFECTS of this
procedure
Nausea during dye injection
Yellowish fluorescent
discoloration of the skin and
urine
  This side effects last for 12- 24
hours
 Allergic reaction Hives and
itching
2. Opthalmoscope
 MEDICAL MANAGEMENT
1. intensive insulin therapy-
decreases development of
retinopathy
2. Argon laser Photocoagulation-
main treatment of diabetic
retinopathy.
a. This is a laser treatment that
destroys blood vessel and areas
of neovascularization
3. panretinal photocoagulation- patient
increase risk for hemorrhaging
 reduces the rate of progression
to blindness
 this stops the widespread of
new vessel and hemorrhaging
of damaged blood vessel
4. Vitrectomy- removal of fluid with a
special drill like instrument and
replaced with saline
 NURSING MANAGEMENT
regular opthalmoligoc
examination
Blood glucose control
Self management of eye care
regimen
 NEPHROPATHY

Patient with type 1 diabetes

frequently show initial signs of
renal disease after 10-15 yrs
Type 2 diabetesw develop renal
disease within 10 yrs of the
diagnosis
Soon after the onset of diabetes
and especially if the glucose
levels are elevated, the kidney’s
filtration mechanism is stressed,
allowing blood protein to leak
into the urine. Pressure in the
blood vessels of the kidney
increases
 ASSESSMENT

 Albumin is the most important blood

proteins that leaks into the urine
1. urine should be checked annually
for microalbuminuria
2. Urine dipstick test for albumin,
creatinine and BUN level are
obtained
 MANAGEMENT

Control of hypertension – use of

ACE inhibitors
Prevention or treatment of UTI
Avoidance of nephroroxic
substances
Adjustment of medication as renal
Ffunction changes
Low Sodium diet
Low protein diet
 if the patient has already developed
microalbuminuria and level exceeds
30mg/24hours in 2 consecutive test.
An ACE inhibitor should be prescribed
 IN chronic endstage of renal failure
1. Hemodialysis
2. Peritoneal dialysis has major risk
factor --- infection and peritonitis

 Laser or surgery may be performed

 DIABETIC NEUROPATHIES
Include the peripheral
sensorimotor, autonomic and
spinal nerve
Elevated blood glucose level over
a period of years have been
implicated in the etiology of
neuropathy
Capillary basement membrane
thickening and demyelinization of
the nerves related to
hyperglycemia
Nerve conduction is disrupted
when there are aberration of the
myelin sheaths
 Most common type of diabetic
neuropathy are
1. sensorimotos polyneuropathy
commonly affects the distal
portions of the nerves
2. Autonomic neuropathy
3. Cranial nerve also occurs in
diabetes common among
elderly
 Peripheral Neuropathy
 Signs and symptoms

1. paresthesia
2. burning sensation
3. feet become numb
4. decreased sensation of light
touch which can lead to an
unsteady gait
5. decreased sensation to pain and
temperature place patient with
neuropathy at high risk for foot
injury
6. Chariot joint – neuropathy related to
joint. Abnormal distribution on joint
due to lack of propioception
7. On physical examination the there is
a decreased in deep tendon reflex
 MANAGEMENT
 intensive insulin therapy and control
of blood glucose level that delays the
progression of neuropathy
 for some patients neuropathic pain
spontaneously resolve within 6 mos.
 Nonopiod analgesic
 Triclylic antidepressant
 Transcutaneous electric nerve
stimulation
AUTONOMIC NEUROPATHY

 THERE ARE THREE

MANIFESTATIONS
1. cardia
2. GI
3. renal system
Cardiovascular symptoms range
from fixed, slightly tachycardic
heart rate, orthostatic
hypertension, silent or painless
myocardial ischemia and
infarction
Delayed gastric emptying
bloating, nausea and vomiting
In addition there is unexplained
absorption of glucose from
ingested food secondary to the
inconsistent gastric emptying
Urinary retention a decreased
sensation of bladder, fullness and
other urinary symptoms of
neurologic bladder result form
autonomic neuropathy
 HYPOGLYCEMIC
UNAWARENESS
1. autonomic neuropathy of the
adrenal medulla is responsible
for diminished or absent
adrenergic symptoms of
hypoglycemia.
a. Patient may report that they no
longer feel the shakiness,
sweating, nervousness and
palpitations associated to
hypoglycemia
2. Sudomotor neuropathy refers to a
decrease or absence of sweating
(adhidrosis) of the extremities
3. Sexual dysfunction
 impotence in men and
 decreased libido, reduced vaginal
secretions in women
 if there is vaginal infection there is
vaginal itching, decreased lubrication
and tenderness
MANAGEMENT
Avoid strenuous activities
High sodium diet in orthostatic
hypotension
The discontinuation of medication
that impede autonomic response
and use of sympathomometics
and other agents
That stimulate an autonomic
response and the use of lower
body elastic garments that
minimize venous return and
prevent pooling of blob in the
extremities
Treatment delayed gastric
emptying includes low fat diet,
small frequent meals, close blood
glucose control and the use of
other agents that increases
gastric motility
Treatment of diarrhea bulk
forming laxative or antidiarrheal
agents
Treatment for constipation use
laxative and enemas
 FOOT AND LEG PROBLEMS

 Complications of diabetes that

contribute to the increased risk of
foot infection
1. Neuropath: sensory neuropathy
leads to loss of pain and pressure
sensation and autonomic
neuropathy leads to dryness and
fissuring of the skin(secondary to
sweating decrease
2. Peripheral vascular dse. Poor
circulation of the lower ext,.
contributing to poor wound
healing and development of
gangrene
3. immunocompromise
hyperglycemia impairs the ability
of specialized leukocytes to
destroy bacteria.
 typicalsequence of events in the
development of diabertic foot ulcer
begins with a soft tissue injury of
the foot. Formation of a fissure
between the toes or in an area pf
dry skin or formation of callus.
In patient with peripheral
vascular dse. Ulcers of the foot
may not heal because there is
decrease oxygen
Amputation may be necessary to
prevent infection
Drainage, swelling redness from
cellulitis of the leg or gangrene
may be the 1st sign of foot
problems
Treatment of foot ulcer involves
bedrest, antibiotics and
debridement
HIGH RISK PERSONS ARE

1. Duration of diabetes more than

10n years
2. age older than 40 yrs.
3. history of smoking
4. decreased peripheral pulse
5. decreased sensation
6. anatomic deformities
7. history of foot ulcer or amputation
 MANAGEMENT

 the feet must be inspected daily for

redness, blisters, fissures, calluses,
ulceration, changes in skin
temperature and development of
deformities
 Aspect of preventive foot care
 proper bathing, drying, and lubricating
the feet
 wearing closed toe shoe that fit well

 trimming of toenails
 reducing risk factors such as smoking,
elevated lipids
 avoiding home remedies to treat foot
problems
 HYPERGLYCEMIA DURING
HOSPITALIZATION
 Factors that may contribute to
hyperglycemia
1. changes in the usual treatment
regimen
2. medications
3. IV dextrose
4. mismatched timing of meals and
insulin
short acting insulin is usually
needed to avoid postprandial
hyperglycemia
IV antibiotics should be mixed in
normal saline to avoid excess
infusion of dextrose
 HYPOGLYCEMIA DURING
HOSPITALIZATION
 Factors that may contribute to
hypoglycemia
1. Overuse of regular insulin
2. lack of dosage change when
dietary intake is changed
3. overuse medications for
hyperglycemia
successive does of subcutaneous
regular insulin should be
administered no more frequently
that every 3-4 hours
Should have snacks
 Common alteration in Diets
1. NPO- if the patient has procedure
usual insulin dosage should be
changed
2. Clear fluid Diet- patient may take
juice and gelatin desserts
3. Enteral tube feeding
4. Parenteral nutrition
5. hygiene- foot should be clean and
dried, use lubricating lotion to