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
a. type 2 diabetes (previously
referred to as non-insulin-
independent diabetes
mellitus) NIDDM
b. gestational diabetes mellitus
c. 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
1. Previously independent
impaired fasting glucose or
impaired glucose tolerance
2. Hypertension
3. HDL cholesterol level or
triglyceride level
4. 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
1. enhances storage of dietary fat
in adipose tissue
2. 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 Previous Characteristics

Classification Classification and Implication
Onset any age, but

Type 1 Juvenile diabetes usually young (<30yrs).

Usually thin at
Juvenile-onset diagnostic;
diabetes with recent weight loss.
Ketosis-prone Etiology includes
diabetes genetics,
immunologic, or
Brittle diabetes
environmental factors.
Insulin-dependent Often have islet cell
Diabetes antibiotics.
mellitus(IDDM) Little or no endogenous
insulin.
Need insulin to reserve
life
Ketosis-prone when
insulin
Type 2 Adult-onset diabetes hyperglycemia:diabetic
s
Maturity-onset ketoacidosis.
diabetes Onset any age, usually
Ketosis-resistant over 30 years.
Usually obese at
diabetes
diagnose
Stable diabetes Causes include obesity,
Non-insulin- heredity, or
independent environmental factors.
No islet cell antibodies
diabetes (NIDDM)
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,
Diabetes mellitus Secondary hyperglycemic
associated with diabetes Hyperosmolar
other 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
Gestational produces insulin, the
Gestational diabetes patient
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
 in subsequent
pregnancies
30%-40% will develop
overt diabetes within 10
Impaired glucose Borderline diabetes years
Risk factors include
Intolerance Latent diabetes obesity, age older than
Chemical diabetes 30years, family history
of
Subclinical diabetes
diabetes, previous large
Asymptomatic babies.
diabetes Screening tests should
be
performed on all
pregnant
women between 24 and
28
wks gestation.
Oral glucose tolerated
test
value between 140
 is defined as a fasting
plasma glucose
between
110 mg/dL and 126
Prediabetes Previous mg/dL.
abnormality of glucose 29% eventually
tolerated develop
diabetes
 
Above-normal
susceptibility to
atherosclerosis
disease.
Renal and retinal
complication usually
not
significant.
May be obese or
nonobese; obese
should
reduce weight.
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
 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
1. Dry skin
2. Skin lesions or wounds slowly to
heal
3. Recurrent infections
4. Onset of type 1 diabetes –
sudden weight loss, nausea,
vomiting.
5. Abdominal pain – if DKA
developed.
 ASSESSMENT AND
DIAGNOSTIC FINDING
 
Criteria for the Diagnostic of Diabetes Mellitus

3. 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.
5. Fasting plasma glucose greater than or equal to
126
mg/dL. Fasting is defined as no caloric intake for at
least 8
hours.
 ASSESSMENT

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

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

b. Providing all the essential

food constituents necessary
for optimal nutrition.
c. Meeting energy
a. 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.
b. 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
 Exercise
 Benefits
 Exercise precaution
 General Precautions for
Exercise in Diabetes:
b. Use proper foor wear and, if
appropriate, other
protective equipment.
  Avoid exercise in extreme
heat or cold
 Inspect feet daily after
exercise
 Avoid exercise during after
periods of poor metabolic
control
 Exercise recommendations
 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

1. 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
 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.
a. Effects of insulin and
exercise
b. Effects of food and stress,
including illness and
infections
c. Basic treatment approaches
1. Treatment modalities
a. Administration of insulin
and oral antidiabetes
medications
b. Diet information
c. Monitoring of blood glucose
and ketones
1. Recognition, treatment, and
prevention of acutr
complications
a. Hypoglycemia
b. Hyperglycemia
1. 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
1. 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.
 Itcaused 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
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

1. 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
 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
 Acute breath- elevated ketone
levels
 Hyperventilation
 Assessment and Diagnostic
Findings
 blood
 blood glucose levels may vary
from 300-800 mg/dl
 severity
 severity of DKA is not
necessarily related to the blood
glucose level
 patient
 patient mat have severe
acidosis with modestly
elevated blood glucose levels
 blood glucose levels of 400-
500mg/dl have no evidence of
DKA
 Evidence
Evidence of ketoacidosis is
reflecting in low serum
bicarbonate and low pH values.
 Low
 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
Elevated levels of creatinine,
blood urea nitrogen (BUN),
hemoglobin and hematocrit
 Prevention
 patients
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
 Medical Management
1. Rehydration
 important
important for maintaining
tissue perfusion
 fluid
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
1. 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
1. Reserving Acidosis
 ketones bodies accumulate as
result of fat breakdown,
 hourly blood glucose values
must be measured
 administered IV solution with
concentration
1. 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
a. Encourage oral fluid intake
b. Monitor laboratory values of
serum electrolytes(sodium
& potassium)
c. Monitor VS
d. For sign of dehydration
1. 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
1. 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
1. Improving Self-Care
a. Patients teaching
2. 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
 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
 a. Hypokalemia
 Low serum levels may result
rehydration,
 Prevention include cautions
replacement of potassium
a. Hyperglycemia and Ketoacidosis
b. Hypoglycemia
c. Cerebral Edema
1. 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
 CAD typical ischemic
symptoms
 CVA
 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
a. Basement membrane surrounds
the endothelial cells of the
capillary
b. Increase blood glucose level
reacts through a series of
biochemical response to thicken
the basement membrane to
several times it’s normal thickness
c. 2 areas are affected
 Retina
 Kidney
a. 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
a. richly supplied with blood vessels
of all kinds
 small arteries
 veins
 arterioles
 venules capillaries
a. 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.
1. NORMAL vitreous are clear
allowing light to be
transmitted to the retina
2. If hemorrhage occur the
vitreous becomes clouded
and cannot transmit light
resulting in loss of vision
1. Another consequence is that
vitreous hemorrhage
resorption of blood in the
vitreous leads to the
formation of fibrous scar
tissue
2. scar tissue place traction in
the retina resulating in retinal
detachment and subsequent
visual loss
1. 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
1. 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
1. 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
1. 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
 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
1. decreased sensation to pain and
temperature place patient with
neuropathy at high risk for foot
injury
2. Chariot joint – neuropathy
related to joint. Abnormal
distribution on joint due to lack
of propioception
3. 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
 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
1. Sudomotor neuropathy refers to
a decrease or absence of
sweating (adhidrosis) of the
extremities
2. 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
 Peripheral vascular dse. Poor
circulation of the lower ext,.
contributing to poor wound
healing and development of
gangrene
 immunocompromise
hyperglycemia impairs the
ability of specialized
leukocytes to destroy
bacteria.
 typical sequence 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