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SEMINAR
ON
DIABETES
MELLITUS
Submitted To: Submitted By
Mr.Mohammed Nasim Jasmin T V
Lecturer Msc Nursing 1st
year
Al- Shifa College of nursing Al- Shifa College of nursing
Submitted On:
18-7-2013

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CENTRAL OBJECTIVE:
At the end of session, the group will be able to acquire knowledge regarding
diabetes mellitus and develop positive attitude towards care of patients with
diabetes mellitus and will apply this knowledge in their daily practical
situations.
SPECIFIC OBJECTIVES:
At the end of session, the group will be able to
define diabetes mellitus
understand types of diabetes mellitus
describe classification of diabetes mellitus
explain various signs and symptoms of diabetes mellitus
explain various diagnostic studies used in diabetes mellitus
discuss management of diabetes mellitus
explain complications of diabetes mellitus

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INTRODUCTION
Diabetes mellitus, a chronic disease characterized by elevated blood sugar
levels, is a significant contributor to morbidity and mortality and throughout the
world. Diabetes can cause debilitating and costly complications such as
blindness, renal failure, lower extremity amputations, and cardiovascular
disease. Much of the health and economic burden of diabetes can be averted
through known prevention measures. Diabetes mellitus is known colloquially as
"Sugar diabetes" as it results in excessively high levels of blood sugar and the
presence of glucose in the urine. Symptoms of diabetes include a grossly
exaggerated thirst, loss of weight, a sweet smell on the breath, a worsening
appetite, and later on, cataracts can develop in the eyes. It certainly occurs in
both dogs and cats, but is more common in the former.
TERMINOLOGIES
 Ketoacidosis: Ketoacidosis with an accumulation of ketone bodies,
occurs primarily in diabetes mellitus
 Gastroparesis: is a medical condition consisting of a paresis (partial
paralysis) of the stomach also called delayed gastric emptying
 Diabetes mellitus: It is a chronic multisystem disease related to abnormal
insulin production, impaired insulin utilization, or both (American
Diabetes Association)
INCIDENCE
According to recent estimates of epidemiology of Diabetes in India,
approximately 285 million people worldwide (6.6%) in the 20–79 year age
group will have diabetes in 2010 and by 2030, 438 million people (7.8%) of
the adult population, is expected to have diabetes. Hospitalization rates for
people with diabetes are 2.4 times greater for adults and 5.3 times greater for
children than for the general population. The economic cost of diabetes
continues to rise because of increasing health care costs and an aging
population. Half of all people who have diabetes and who are older than 65 are

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hospitalized each year, and severe and life-threatening complications often
contribute to the increased rates of hospitalization.
ETIOLOGY AND PATHOPHYSIOLOGY
Current theories link the causes of diabetes singly or in combination to genetic,
autoimmune, viral and environmental factors. Regardless of its cause
diabetes is a disorder of glucose metabolism related to absent or insufficient
insulin supplies and or poor utilization of insulin that is available.
NORMAL INSULIN METABOLISM
Insulin is a hormone 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. When a person eats a meal, insulin secretion increases and moves
glucose from the blood into muscle, liver, and fat cells.
In those cells, insulin:
Transports and metabolizes glucose for energy
Stimulates storage of glucose in the liver and muscle (in the
Form of glycogen)
Signals the liver to stop the release of glucose
Enhances storage of dietary fat in adipose tissue
Accelerates transport of amino acids (derived from dietary protein) into
cells
Insulin inhibits the breakdown of stored glucose, protein,
and fat. During fasting periods (between meals and overnight)
Pancreas continuously releases a small amount of insulin (basal insulin)
another pancreatic hormone called glucagon (secreted by the alpha cells
of the islets of Langerhans) is released when blood glucose levels
decrease and stimulate the liver to release stored glucose.
The insulin and the glucagon together maintain a constant level of
glucose in the blood by stimulating the release of glucose from the liver.
Initially, the liver produces glucose through the breakdown of glycogen
(glycogenolysis). After 8 to 12 hours without food, the liver forms
glucose from the breakdown of noncarbohydrate substances, including
amino acids (gluconeogenesis).

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CLASSIFICATION
TYPE 1 DIABETES MELLITUS
Type 1 diabetes is characterized by destruction of the pancreatic beta cells
which leads to alteration in the production of insulin. It is combined genetic,
immunologic, and possibly environmental (eg, viral) factors contribute to beta
cell destruction.
 Genetic susceptibility is a common underlying factor in the development
of type 1 diabetes. People do not inherit type 1 diabetes itself; rather, they
inherit a genetic predisposition, or tendency, toward developing type 1
diabetes. genetic mutation causes killer (CD8) T-cell lymphocytes to
attack and destroy the insulin-producing islet cells.
 Autoantibodies against islet cells and against endogenous insulin have
been detected in people at the time of diagnosis and even several years
before the development of clinical signs of type 1 diabetes
 Environmental factors, such as viruses or toxins, that may initiate
destruction of the beta cells.
Regardless of the specific etiology, the destruction of the beta cells results in
decreased insulin production, unchecked glucose production by the liver, and
fasting hyperglycemia. In addition, glucose derived from food cannot be stored
in the liver but instead remains in the bloodstream and contributes to
postprandial Hyperglycemia
Onset of disease: it is associated with a long pre clinical period. The islet cell
autoantibodies present for months to years before the onset of symptoms
PRE-DIABETES MELLITUS
People with pre-diabetes, which can lead to type 2 diabetes, heart disease, and
stroke. People with pre-diabetes may have either impaired fasting glucose (IFG)
or impaired glucose tolerance (IGT), or both. A person with IFG has a fasting
blood glucose level of 100 to 125 mg/dL after an overnight fasting. In IGT, a
person has a blood glucose level of 140 to 199 mg/dL after a glucose tolerance
test lasting 2 hours. A significant number of those with pre-diabetes will
develop the disease; however, many can delay or avoid type 2 diabetes with
weight loss and increased physical activity.

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TYPE 2 DIABETES MELLITUS
Four main abnormalities related to type 2 diabetes are there
 Insulin resistance
Insulin resistance refers to decreased tissue sensitivity to insulin. Normally,
insulin binds to special receptors on cell surfaces and initiates a series of
reactions involved in glucose metabolism. In type 2 diabetes, these intracellular
reactions are diminished, thus rendering insulin less effective at stimulating
glucose uptake by the tissues and at regulating glucose release by the liver.
 Marked decrease in the ability of pancreas to produce insulin
Beta cell become fatigued from compensatory over production of insulin
or when beta cell mass is lost
 Inappropriate glucose production by the liver
Instead of properly regulating the release of glucose in response to blood
level glucose, liver does so in a haphazard manner that does not
correspond to the body’s needs at the correct time
 Alteration in the production of hormones and cytokines by adipose tissue
Onset of disease: it is usually gradual. The person may go for many years
with undetected hyperglycemia. If patient has marked hyperglycemia
(eg: 500-1000mg/dL) a sufficient endogenous insulin supply may
prevent DKA
GESTATIONAL DIABETES
Gestational diabetes is any degree of glucose intolerance with its onset during
pregnancy. Hyperglycemia develops during pregnancy because of the secretion
of placental hormones, which causes insulin resistance.
For women who meet one or more of the following criteria,
 selective screening for diabetes during pregnancy is now being
recommended between the 24th and 28th weeks of gestation
 age 25 years or older; age 25 years or younger and obese
 family history of diabetes in first-degree relatives
 member of an ethnic/racial group with a high prevalence of diabetes

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(eg, Hispanic American, Native American, Asian American, African
American, or Pacific Islander)
SECONDARY DIABETES
Diabetes occurs because of another medical condition or due to treatment of a
medical condition.
These include cushing syndrome, hyperthyroidism, cystic fibrosis, recurrent
pancreatitis etc. medications include corticosteroids, thiazides, phenytoin and
atypical antipsychotics. This usually resolves when underlying condition
resolved.
CLINICAL MANIFESTATOINS
Type 1 Diabetes mellitus
 Classic symptoms are polyuria, polydipsia, polyphagia.
 Osmotic effect of glucose produces manifestations of polydipisa and
ployuria
 Polyphagia is a consequence of cellular malnourishment when insulin
deficiency prevents utilization of glucose for energy
 Weight loss may occur as the body cannot get glucose and turns to other
energy sources such as fat and protein
 Weakness and fatigue may also be experienced, as body cells lack needed
energy from glucose
Type 2 Diabetes mellitus
Clinical manifestations are non specific
 Fatigue
 Recurrent infections
 Recurrent vaginal yeast infection
 Prolonged wound healing
 Visual changes
DIAGNOSTIC STUDIES

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 Random blood glucose Blood specimen is drawn without preplanning.
Greater than or equal to 200 mg/dL in the presence of symptoms is
suggestive of diabetes mellitus.
 Fasting blood glucose Blood specimen is obtained after 8 hours of
fasting. In the nondiabetic client the glucose level will be between 70 and
110 mg/dL. In the diabetic client glucose is _ 110 mg/dL but <126
mg/dL.
 Postprandial glucose Blood sample is taken 2 hours after a
highcarbohydrate meal. In the nondiabetic client, the glucose level will be
between 70 and 110 mg/dL. In the client with diabetes mellitus, the result
is greater than or equal to 140 mg/dL but <200 mg/dL.
 Oral glucose tolerance test Diet high in carbohydrates is eaten for 3
days. Client then fasts for 8 hours. A baseline blood sample is drawn and
a urine specimen is collected. An oral glucose solution is given and time
of ingestion recorded. Blood is drawn at 30 minutes and 1, 2, and 3 hours
after the ingestion of glucose solution. Urine is collected simultaneously.
Drinking water is encouraged to promote urine excretion. In the

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nondiabetic client, the glucose returns to normal in 2 to 3 hours and urine
is negative for glucose. In the diabetic client, blood glucose level returns
to normal slowly; urine is positive for glucose.
 Glycosylated hemoglobin or hemoglobin A1c Single sample of venous
blood is withdrawn. The amount of glucose stored by the hemoglobin is
elevated above 7.0% in the newly diagnosed client with diabetes mellitus,
in one who is noncompliant, or in one who is inadequately treated.
COMPLICATIONS OF DIABETES MELLITUS
 Acute complications
 Diabetic ketoacidosis (DKA)
DKA is caused by an absence or markedly inadequate amount of insulin.
This deficit in available insulin results in disorders in the metabolism of
carbohydrate, protein, and fat. The three main clinical features of DKA are:
• Hyperglycemia
• Dehydration and electrolyte loss
• Acidosis
Pathophysiology
DKA can develop despite the client’s compliance with the prescribed treatment
regimen When the amount of glucose transported across cell membranes
decreases, the liver increases its production of glucose. The blood glucose level
becomes extremely elevated. The kidneys attempt to excrete the glucose, which
is well beyond the renal threshold. In the process, excessive amounts of water,
sodium, and potassium are excreted as well. The client becomes dehydrated; the
skin is warm, dry, and flushed. Stored fat is broken down, causing ketones to
accumulate in the blood and urine. As ketones mount, the pH of the blood
becomes acidotic. The client begins breathing rapidly and deeply in an attempt
to eliminate carbon dioxide and prevent it from forming carbonic acid, which
would contribute even more to the acidotic state. If the condition is severe and
prolonged, the client becomes comatose. Death results with untreated or
ineffective treatment of DKA

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Assessment Findings
Early symptoms are vague and become more definite and serious as increasing
ketones accumulate in the bloodstream.
 Weakness, thirst, anorexia, vomiting, drowsiness, and abdominal pain
 The cheeks are flushed, and the skin and mouth are dry
 The breath has an odor of acetone. Kussmaul respirations often are
evident
 The pulse is rapid and weak.
 Hypotension
 The client may become unresponsive but restless
 Blood glucose levels are elevated to 300 to 1000 mg/dL or more. Urine
contains glucose and ketones.
 blood pH ranges from 6.8 to 7.3
 serum bicarbonate level is decreased to levels from 0 to 15 mEq/L
 lower partial pressure of carbon dioxide in arterial blood (PaCO2) to
levels of 10 to 30 mm Hg.

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 Serum sodium and potassium levels reflect the degree of dehydration
(i.e., they may be elevated because they are concentrated in a low volume
of body fluid
Management
Treatment depends on the severity of DKA. The main goals of treatment are to
(1) reduce the elevated blood glucose,
(2) correct fluid and electrolyte imbalances
(3) Clear the urine and blood from ketones
 Insulin is given intravenously - Insulin reduces the production of ketones
by making glucose available for oxidation by the tissues and by restoring
the liver’s supply of glycogen. Regular insulin is added to an IV solution
and infused continuously. The amount of insulin and the rate of infusion
depend on the blood glucose levels, but the rate may be in the range of 5
Units per hour. Isotonic fluid is instilled at a high volume, As insulin
begins to lower the blood glucose level, the IV solution is changed to
include one with glucose. This helps to avoid the potential for
hypoglycemia.
 Potassium replacements are given despite elevated serum levels to raise
intracellular stores. Periodic monitoring of serum electrolytes and blood
glucose levels is necessary. The urine is tested for glucose and ketones
 Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
HHNKS, an acute complication of diabetes, is characterized by hyperglycemia
without ketosis. It is not unusual to find the blood glucose level well over 500
mg/dL, but the pH of the blood remains within the normal range of 7.35 to 7.45.
Fluid and electrolyte imbalances accompany HHNKS.
Pathophysiology
Extreme hyperglycemia
Severe osmotic dieresis

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Fluid volume deficit
Decreased sodium Decreased potassium Decreased phosphorus
Electrolyte imbalance
Profound dehydration
Hyperosmolality
Hypovolemia
Decreased renal perfusion hypotension hemoconcentation
Oliguria tissue anoxia hyperviscosity
Anuria increased lactic acid thrombosis
Seizures
Shock
Coma
Death
Assessment Findings
 Hypotension, mental changes, extreme thirst, dehydration,
 tachycardia, and fever
 Neurologic signs include paralysis, lethargy, coma, and seizures

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 Symptoms of hypokalemia and hyponatremia usually are present.
 Physical examination reveals dry mucous membranes and poor skin
turgor
 Blood glucose levels are exceedingly high and serum potassium and
sodium levels are low.
 The serum osmolarity is increased
Medical Management
 Treatment includes the administration of insulin
 Correction of fluid and electrolyte imbalances.
 A central catheter may be used to monitor the client’s hemodynamic
response to fluid replacement.
 Hypoglycemia
Hypoglycemia, a low blood glucose level, is always a potential adverse reaction
when administering medications for diabetes
Pathophysiology and Etiology
 When too much insulin (hyperinsulinism) is in the bloodstream relative to
the amount of available glucose, hypoglycemia occurs.
 The blood glucose level falls below 70 mg/dL. Because glucose is the
primary source of cellular energy, especially for the brain
 hypoglycemia tends to manifest in neurologic changes such as confusion,
difficulty processing information, anxious feelings, emotional irritability,
and headache.
 The client feels hungry, a homeostatic mechanism to stimulate eating
 If the condition is untreated, seizures, permanent brain damage, or death
can occur.
 Hypoglycemia occurs when a client with diabetes is
(1) Not eating at all and continues to take insulin or oral
antidiabetic medications
(2) not eating sufficient calories to compensate for glucose-
lowering medications

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(3) Exercising more than usual, this lowers available blood
glucose.
 Alcohol consumption also interferes with the liver’s ability to synthesize
glucose from noncarbohydrates,
 placing clients with diabetes who drink at higher risk for
hypoglycemia.
Assessment Findings
 Initial symptoms include weakness, headache, nausea, drowsiness,
nervousness, hunger, tremors, malaise, and excessive perspiration.
 Some clients have characteristic personality or behavioral changes.
Confusion and dizziness can occur.
 If hypoglycemia is not corrected, symptoms can progress to difficulty
with coordination.
 The client may complain of double vision.
 Although symptoms vary, each client tends to have a
 uniquely repetitious pattern when hypoglycemia develops.
Medical Management
 The medical treatment for a hypoglycemic reaction is administration of
15 g of simple carbohydrate as soon as possible.
 If the client is unconscious, glucose gel can be applied in the buccal
cavity.
 If the client does not respond after two administrations of rapidly
absorbed carbohydrate the physician may order glucagon, a hormone that
stimulates the liver to release glycogen, or 20 to 50 mL of 50% glucose is
prescribed for IV administration.
 Once the hypoglycemic symptoms are relieved, the client with diabetes
is given complex carbohydrates such as graham crackers and milk to
sustain and prolong an adequate level of blood glucose.
CHRONIC COMPLICATIONS
Although clients with diabetes can develop many complications, extremely
common ones include peripheral neuropathy, nephropathy, retinopathy, and

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Vascular changes, stroke, dermopathy, atherosclerosis, CAD, gangrene, erectile
dysfunction, infections
 Macrovascular complications
It is the disease of large and medium sized blood vessels that occur with greater
frequency. These complications include cerebrovascular, cardiovascular and
peripheral vascular diseases,
 Microvascular complications
It results from thickening of vessel membranes in capillaries and arterioles in
response to conditions of chronic hyperglycemia
 peripheral neuropathy
Neuropathy is a general term that refers to pathologic changes in nerves.
Neuropathies in clients with diabetes can affect motor, sensory, and autonomic
nerves. Neuropathies develop 10 or more years after the onset of diabetes, but
the incidence increases with the duration. Because their onset is gradual, the
client usually is oblivious to the development in early stages.
Pathophysiology and Etiology
Neuropathy results from poor glucose control and decreased blood circulation to
nerve tissue. Manifestations of peripheral neuropathies are more common
among clients with diabetes who smoke and whose blood glucose level is
poorly controlled. Because nitric acid dilates blood vessels, some believe that
consistently elevated blood glucose levels lower nitric acid levels, impair
circulation, and subsequently damage peripheral nerves.
 Motor Neuropathy
When motor nerves are affected, the muscles weaken and atrophy. Joint support
is diminished. The feet widen. Eventually bone structure is affected, resulting in
skeletal deformities, usually in the feet and ankles, with subsequent changes in
gait. Areas of skin and soft tissue that are subjected to friction and pressure are

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prone to ulcerate If there is infection or impaired healing, portions of the
affected extremity may require amputation.
 Sensory Neuropathy
Neuropathy involving sensory nerves leads to paresthesias, abnormal sensations
such as prickling, tingling, burning, orneedle-like pain in the feet, legs, and
sometimes hands. In severe cases, feeling is totally lost. This lack of sensitivity
increases the potential for soft tissue injury without the client’s awareness.
 Autonomic Neuropathy
Neuropathy of autonomic nerves that affect organ functioning has several
consequences. Gastroparesis, atony of the stomach, retards the movement of
food from the stomach. If nerves that innervate the bladder are affected, the
client does not sense the urge to void, and retained urine supports bacterial
growth, causing frequent urinary tract infections. Incontinence also may occur
when the bladder is overfilled. When autonomic nerves that affect
cardiovascular function fail to function effectively, episodes of orthostatic
hypotension occur.
Signs and Symptoms
 Pain is one of the leading symptoms
 Skeletal muscles in the extremities become smaller.
 The feet swell and become insensitive to temperature or other tactile
stimuli
 digestive, urinary, and sexual dysfunction
 Dizziness when rising
Management
o Diet, exercise, and medication to control blood glucose levels.
o Several medications can reduce pain, such as non-narcotic analgesics or a
tricyclic antidepressant such as imipramine (Tofranil).
o Nonpharmacologic pain relief can be facilitated with transcutaneous
electrical nerve stimulation.
o Elastic compression stockings

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o antihypotensive agent such as midodrine (ProAmatine), help reduce
orthostatic hypotension.
o Small, frequent meals and administration of metoclopramide (Reglan) are
recommended for the relief of symptoms associated with gastroparesis.
o Antibiotic therapy, increased oral fluid intake, and urinating every 3
hours helps eliminate urinary tract infections
 Diabetic nephropathy
Diabetic nephropathy refers to the progressive decrease in renal function that
occurs with diabetes mellitus. Clients with type 1 diabetes are more likely to
develop diabetic nephropathy, but clients with type 2 diabetes also are affected.
Pathophysiology and Etiology
Nephropathy is a consequence of glomerular deterioration resulting in impaired
filtration of blood during urine formation. There are five stages of nephropathy,
each characterized by a successive progression of renal dysfunction Essentially,
the glomeruli excrete serum proteins, especially albumin, and lose their ability
to excrete nitrogen waste products. Poor glucose control contributes to the onset
of nephropathy. Although hypertension is an eventual consequence of diabetic
nephropathy
Assessment Findings
In the early stages, the client does not manifest any obvious signs and
symptoms.
 Swelling of the feet and hands, most likely from the loss of albumin
 BP increases gradually.
 The client feels tired and weak.
 Albumin in the urine.
 Blood urea nitrogen and serum creatinine become elevated.
 renal creatinine clearance is decreased
Management

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Controlling both blood glucose levels and hypertension canprevent or
delay the development of diabetic nephropathy
clients with diabetes maintain their BP at or below 130/85mmHg. The
target BP of clients with diabetes who already have developed proteinuria
is at or lower than 125/75 mm Hg.
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II
receptor antagonist slow the progressive nature of nephropathy
A moderate reduction in dietary protein is beneficial.
Smoking cessation is strongly recommended.
Nursing Management
 The nurse monitors the client’s blood glucose and hemoglobin A1c
results.
 check urine with a test strip to detect evidence of albuminuria.
 The nurse provides additional teaching if the client’s blood glucose level
is not controlled.
 refers the client to programs that assist with smoking cessation or
discusses the possibility of nicotine patches or gum to control further
habituation.
 The nurse explains the therapeutic regimen associated with prescribed
antihypertensive drugs and dietary measures for lowering BP and
complications from vascular disease
 Diabetic retinopathy
Diabetic retinopathy refers to pathologic changes in the retina that are
experienced by persons with diabetes. On average, it develops 10 or more years
after the onset of diabetes. The earlier retinopathy develops, the more likely it is
that vision will rapidly deteriorate.
Pathophysiology and Etiology
Diabetic retinopathy is a consequence of inadequately controlled blood glucose
levels, which cause vascular changes in the retina .

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There are two types: nonproliferative retinopathy is the milder manifestation,
and proliferative retinopathy, the more severe form, can lead to blindness.
 In nonproliferative retinopathy, microaneurysms, outpouchings in retinal
capillaries, develop from high vascular pressure and compromised
circulation.
 The stasis of blood flow interferes with transferring substances between
the retina and blood vessels.
 The deprived retinal cells swell
 In the more advanced, proliferative form, damaged blood vessels are
replaced with new ones that grow along the surface of the retina.
 The newer blood vessels are more fragile
 They tend to rupture and leak blood into the vitreous, the gel-like fluid
that fills the posterior portion of the eye.
 Inelastic scar tissue forms, which alters the shape of the retina, causes
distorted vision, and pulls at the retina, increasing the potential for retinal
detachment.
Assessment Findings
Clients with nonproliferative and proliferative retinopathy may not experience
any visual changes for some time.
 blurred vision
 Visual acuity is diminished.
 Ophthalmic examination reveals swelling near the macula of the eye, an
area lateral to the optic nerve that provides acute central vision.
Management
 The client with diabetes is referred for an ophthalmic evaluation within 3
to 5 years after diagnosis
 If there is evidence of retinal vessel changes, an ACE inhibitor such as
lisinopril is prescribed to dilate the retinal blood vessels and improve
blood flow
 If vitreous hemorrhage already has occurred, some physicians prefer to
let the condition resolve on its own, which may take up to 18 months.
 Seal leaking or newly forming blood vessels with laser photocoagulation.

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 A vitrectomy, removal of bloodied vitreous, also improves the clarity of
vision.
 In 2004, the FDA approved ovine hyaluronidase (Vitrase), a genetically
engineered form of angiopoietin, a vascular growth factor that stimulates the
repair of leaky retinal blood vessels.
 Vascular disturbances
Vascular disturbances affect many tissues and organs, in clients with diabetes,
all the arteries and arterioles are more susceptible to accelerated atherosclerotic
and arteriosclerotic changes than in clients without diabetes.
Pathophysiology and Etiology
A consistent finding in clients with diabetes is thickening of the arterial walls.
The incidence of coronary artery disease also is increased. One possible
explanation for obesity in clients with diabetes is that the brain may be
insensitive to leptin, a chemical that signals satiation. A lack of response to
leptin promotes overeating, which contributes to hyperlipidemia.
Assessment Findings
Peripheral vascular changes are one of the most common complications
associated with diabetes
 extremities are pale and cool due to decreased blood supply
 Leg cramps
 Gangrene develops if blood supply to the extremities is markedly
diminished.
 Uncontrolled infection leads to skin ulcers.
 Myocardial infarctions occur at a much earlier age than among the
nondiabetic population.
.
Medical and Surgical Management
Atherosclerosis is managed with lipid-lowering measures such as a low-
fat diet, exercise, and medications
Vasodilators are prescribed to combat the effects of arteriosclerosis

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Drugs that reduce platelet aggregation (e.g., aspirin) are prescribed
prophylactically
Smoking cessation is advised
Uncontrolled gangrene of the extremities can result in amputation
 Infections
Infection is very common due to defect in the mobilization of inflammatory
cells and an impairment of phagocytosis by neutrophils and monocytes. Loss of
sensation may delay the detection of an infection
MANAGEMENT
NUTRITIONAL THERAPY
Diet is a major component of treatment for every person withdiabetes.
Formulation of a diabetic diet depends on the client’s sex, age, height and
weight, activity level, occupation, state of health, former dietary habits, and
cultural background.
Specific goals include the following
 Maintain blood glucose level to as near normal as safely possible to
prevent or reduce the risk for complications
 Achieve lipid profiles and BP level that reduce the risk of cardiovascular
complications
 Modify lifestyle as appropriate for prevention and treatment of obesity ,
dyslipidemia, nephropathy
 Address individual nutritional needs
Food composition
 Carbohydrates
Carbohydrates and monodaturated fats should provide 45%-65% of total energy
intake each day. It includes sugar, starches, fiber, low fat milk, fruits, and
vegetables
 Fats
Fat should compose no more than 25-30% of meal plan
 Protein
It should less than 10% of total energy consumed

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 Alcohol
It is high in calories but no nutritive value and promotes hypertriglyceridemia. It
has detrimental effects on the liver
EXERCISE
Exercise helps metabolize carbohydrates and control blood glucose levels
because glucose-transporting receptors within skeletal muscles allow the
muscles to take in glucose from the blood independent of insulin. This provides
energy during exercise and lowers blood sugar. Exercise, therefore, reduces the
need for insulin because blood sugar can be lowered without it, an advantage for
those with diabetes. Exercise also improves circulation of blood, which is
compromised in the client with diabetes. Exercise also lowers cholesterol and
triglyceride levels and improves muscle tone. An exercise program for the client
with diabetes specifies the type of exercise and the length of time to perform it.
The program is tailored according to the client’s needs and life-style. Most
importantly, the client needs to exercise consistently each day. Sporadic periods
of exercise are discouraged because wide fluctuations in blood glucose levels
can occur. It is necessary to regulate food and insulin requirements during times
of increased activities
PHARMACOLOGICAL MANAGEMENT
Insulin
Insulin is needed when a patient has inadequate insulin to meet specific
metabolic needs. People with type 1 DM require exogenous insulin to survive
and people with type 2 DM usually controlled by diet, exercise. May require
exogenous insulin during periods of severe stress like illness and surgery
Insulin has been available since 1925. It was initially extracted from beef and
pork pancreases. In the early 1980’s, technology became available to produce
human insulin synthetically. Synthetic human insulin has replaced beef and
pork insulin. Now, insulin analogs are replacing human insulin.
There are many forms of insulin to treat diabetes. They are classified by how
fast they start to work and how long their effects last.

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The types of insulin include:
Rapid-acting
Short-acting
Intermediate-acting
Long-acting
Pre-mixed
Fast-acting insulin
These types of insulin are designed to take care of the sugar a person eats. They
include:
 Aspart — Starts to act in 5 to 15 minutes, peaks in 90 minutes, lasts 3
hours
 Lispro — Starts to act in 5 to 15 minutes, peaks in 90 minutes, lasts 3
hours
 Regular — Starts to act in 30 to 60 minutes, peaks in 2 hours, lasts 4 to 6
hours
Intermediate and long-acting insulin
These types of insulin, also called basal or background insulin, work
continuously, similar to the way a normal pancreas produces insulin. They are
absorbed slowly and last from 10 to 24 hours, . Basal insulin types include:
 NPH — Starts to act about 2 hours after taking, peaks at 6 to 8 hours,
lasts 10 to 16 hours
 Glargine — Starts to act about 2 hours after taking, and can last 20 to 24
hours
 Detemir – Starts to act about 2 hours after taking, and lasts between 14
and 24 hours
Combination insulin
Combination insulin mixtures have a later action with an earlier and stronger
peak. The mixtures are tailored to a person’s individual needs. Combination
insulin includes human and analog mixtures:
Human mixtures combine NPH and regular insulin.
classification Examples
Rapid acting insulin Lispro clear

24. 24
Aspart clear
Glulisine clear
Short acting insulin Regular clear
Intermediate acting insulin NPH cloudy
Long acting insulin Glargine clear
Detemir clear
Combination therapy NPH cloudy
Lispro cloudy
Apart cloudy
Insulin regimens
The timing of insulin administration in relation to meal is very important
Regimen Type of insulin Comments
Once a day single
dose
Intermediate
Or
Long acting
At bed time
 One
injection
should cover
noon meal
 1 injection
will last
24hrs with
no peaks
and less
chance for
hypoglycem
ia
 Does not
cover
postprandial
blood sugars
Twice a day
Split mix dose
NPH regular
Or NPH rapid
Before breakfast,
2 injections
provide coverage
for 24hrs

25. 25
and at dinner
Three times a day
Combination of
mixed and single
dose
NPH regular
Or NPH rapid
Before breakfast
and dinner as well
as at bed time
Three injections
provide coverage
or 24hrs
Particularly during
early hours
Four times a day
Multiple dose
Regular or rapid
injection
Before breakfast,
lunch and dinner
AND
NPH at bed time
More flexibility is
allowed at meal
times and for
amount of food
intake
Good postprandial
control
Basal bolus Before breakfast,
lunch and dinner
Long acting once a
day, usually at
bedtime
Four injection
srequired per day
Storage of insulin
As a protein insulin requires special storage considerations
 Heat and freeze alters insulin molecules
 Insulin vials that patient currently using may be left at room temperature
for upto 4 weeks unless the room temperature is higher than 86o
F or
below freezing lessthan 37o
F
 Prolonged exposure to direct sunlight should be avoided
 Prefilled syringes are stable upto 30 dayswhen stored in the refrigerator
Administration of insulin
Insulin is prescribed in units. 1 mL contains 100 units of insulin. The physician
specifies both the dosage and the type of insulin to be used. When combining

26. 26
two types of insulin in the same syringe, the short-acting regular insulin is
withdrawn into the syringe first and the intermediate- acting insulin is added
next, a practice referred to as ‘‘clear to cloudy.’’ The mixture is administered
within 15 minutes to ensure that the onset, peak, and duration of each separate
insulin remains intact. Glargine (Lantus) insulin cannot be mixed with other
types of insulin in the same syringe. Combination mixtures of insulin, such as
Humulin 70/ 30, Novolin 70/30, and Humulin 50/50, eliminate the need for
mixing insulins from two separate vials. Regular insulin can be administered
intravenously and subcutaneously.
 The intravenous route is used to treat severe hyperglycemia or prevent or
control elevated blood sugar by adding it to a total parenteral nutrition
solution that contains a high concentration of glucose.
 The subcutaneous route is used most commonly for administering insulin
insulin is absorbed more rapidly when injected in the abdomen than in the
arms or thighs.
 Clients with diabetes are taught to use the abdomen as the preferred site
for self-administration. Subcutaneous injection sites require rotation to
avoid lipoatrophy, breakdown of subcutaneous fat at the site of repeated
injections, and lipohypertrophy, buildup of subcutaneous fat at the site of
repeated injections, either of which eventually interferes with insulin
absorption in the tissue.
 Insulin is an anabolic hormone, it also causes weight gain.
 Other techniques for injecting insulin subcutaneously include an insulin
pen, jet injector, or insulin pump.
Insulin Pen
An insulin pen is a device in which a cartridge containing 150 to 300 units of
insulin is loaded into an injecting pen with a disposable needle attached. Each
time the insulin is injected, a new needle is attached. Once the device is loaded,
the client
 Selects the number of units for injection by dialing in the dose in 1- to 2-
unit increments
 cleans and pierces the skin,
 injects the programmed amount

27. 27
Jet Injector
A jet injector uses high pressure and rapid speed, rather than a needle, to instill
insulin through the skin. The pressure transforms the liquid into a fine mist that
is distributed over a wide area of tissue, resulting in faster absorption Although
a jet injector offers several advantages, such as reducing pain at the site and
eliminating the use of needles and their appropriate disposal, the cost tends to
make this form of administration less practical.
Insulin Pump
An insulin pump provides a means for delivering insulin by continuous
infusion. The device has three components: pump, tubing, and needle .The
pump itself contains a reservoir for rapid-acting or short-acting insulin, a
battery-operated infuser, and a computer chip that enables a person to regulate
basal (continuous) and pre meal bolus doses in 0.05- to 0.1-unit increments. The
pump, which is worn in a pouch or belt holder, is attached to tubing with a
needle. The needle is inserted in the subcutaneous tissue of the abdomen and
can remain in the same site for up to 3 days. Clients who are interested in
controlling their diabetes with an insulin pump need to consider both its
advantages and disadvantages
Advantages
• Resembles the normal pancreatic release of insulin
• Decreases the necessity for multiple daily injections in different sites
• Helps maintain consistent blood sugar levels; reduces the potential for
episodes of hyperglycemia and ketoacidosis
• Provides more flexibility for eating food at varying times during the day
• Facilitates the instillation of smaller doses than those of insulin syringes

28. 28
Disadvantages
• Requires high motivation to control diabetes by frequently checking blood
glucose levels and adjusting the infusion
• Creates a potential for hyperglycemia if the pump fails, the tubing becomes
kinked or obstructed, or the needle is displaced
• Interferes or creates a nuisance factor when participating in active sports,
sexual intercourse, or bathing; the pump can be temporarily disconnected
without removing the needle, but doing so stops the delivery of insulin until it is
reconnected
Injection site selection for insulin
The most common injection site is the abdomen (or stomach). The back of the
upper arms, the upper buttocks or hips, and the outer side of the thighs are also
used. These sites are the best to inject into for two reasons:
They have a layer of fat just below the skin to absorb the insulin, but not
many nerves - which means that injecting there will be more comfortable
than injecting in other parts of your body.
They make it easier to inject into the subcutaneous tissue, where insulin
injection is recommended.
Problems with insulin therapy
 Allergic reactions: local inflammatory reactions may occur such as
erythema, itching, burning around injection site. These may be self
limiting within 1 – 3 months or may improve with a low dose if
antihistamine drugs

29. 29
 Lipodystrophy: atrophy of subcutaneous tissue may occur if same
injection site used frequently
 Somogyi effect: Somogyi effect is a rebound effect in which an overdose
of insulin induces hypoglycemia. Usually ocuurs during night times.
Counterregulatory mechanisms are released, stimulating lipolysis,
gluconeogenesis, glycogenolysis which inproduces rebound
hyperglycemia and ketosis
 Dawn phenomenon: hyperglycemia that is present on awakening ikn the
morning due to the release of counter regulatory hormones in the
predawn hours
Patient education on self administration of insulin
 With one hand, stabilize the skin by spreading it or pinching up a large
area
 Pick up syringe with the other hand and hold it as a pencil
 Insert needle straight into the skin
 To inject the insulin, push the plunger all the way in
 Pull needle straight out of skin
 Press cotton ball over injection site for several seconds
 Use disposable syringe only once and discard
ORAL ANTIDIABETIC AGENTS
Drug category &
examples
Mechanism
Of action
Side effects
Second-Generation
Sulfonylureas
glimepiride (Amaryl),
glipizide
(Glucotrol), glyburide
(DiaBeta, Glynase
PresTab, Micronase)
Stimulates insulin
release; more
potent than
firstgeneration
sulfonylureas
Increased risk of
cardiovascular
mortality, anorexia,
nausea,
vomiting, heartburn,
diarrhea,
hypoglycemia, allergic
skin reactions, insulin
‘‘burn
out’’
Alpha-Glucosidase Delays digestion of

30. 30
Inhibitors
acarbose (Precose),
miglitol (Glyset)
carbohydrates Abdominal pain,
flatulence, diarrhea,
hypoglycemia
Give three times a day
15 min before
each meal.
Biguanide Compound
metformin (Glucophage)
Augments glucose
uptake by tissues,
especially muscles,
decrease hepatic glucose
production
Anorexia, nausea,
heartburn, diarrhea,
lactic acidosis,
hypoglycemia,
allergic skin
reactions, flatulence
Thiazolidinediones
(TZDs)
rosiglitazone (Avandia),
pioglitazone (Actos)
Increases effects of
circulating insulin,
decrese endogenous
glucose production
Headache, pain, liver
injury,
hypoglycemia,
hyperglycemia,
infections, fatigue, risk
for heart attack and heart
failure
Meglitinides
repaglinide (Prandin) Stimulates insulin
release
Upper respiratory
infections,
hypoglycemia,
hyperglycemia,
headache
Dipeptidyl peptidase IV
(DPP-4) Inhibitor
sitagliptin (Januvia
Increases effects of
incretin; prolongs
the release of insulin
and reduces production
of glucose
by the liver
Upper respiratory tract
infection;
nasopharyngitis and
headache.
Adjuvant Drugs
exenatide (Byetta
Stimulate release of
insulin
Heartburn, headache,
nausea,

31. 31
vomiting, diarrhea,
weight
loss, dizziness,
pancreatitis
Combination Drugs
metformin and sitagliptin
Combination product
for use as adjunct to
diet and exercise to
improve glycemic
control in adults
with type 2 diabetes
when mono-therapy
is not controlling
; upper respiratory
infection; headache.
Amylin analog
pramlintide
Decrease gastric
empying, glucagose
secretion, endogenous
glucose output from liver
Hypoglycemia, nausea,
vomiting, headache
SURGICAL MANAGEMENT

32. 32
Pancreas Transplantation
 Replacing the pancreas involves a whole or partial organ transplant.
 The usual candidate is a client with type 1 diabetes who has renal failure
and will benefit from a combined kidney and pancreas transplant.
 Clients with type 2 diabetes are not offered the option of a pancreas
transplant because usually their problem is insulin resistance, which does
not improve with a transplant.
 pancreas is both an exocrine and endocrine gland, transplanting it
requires a means for exocrine enzymatic drainage and venous absorption
of insulin.
 Exocrine drainage is accomplished by establishing a duodenal or urinary
bladder connection with the transplanted pancreas. Insulin is released into
the portal vein, which carries blood to the liver.
 As with any transplant, lifelong immunosuppressive drug therapy is
required because without it, the new organ is destroyed.
Islet Cell Transplantation
 Some clients with type 1 diabetes are recipients of islet cell transplants,
the insulin-producing components of the pancreas, rather than a transplant
of the entire organ or part of the organ.
 Two human pancreases are necessary to obtain sufficient numbers of islet
cells for transplantation. The fragile islet cells must be transplanted
within 12 hours of harvesting
 After the pancreas is harvested, the islet cells are separated from the
tissue and injected through the abdominal wall into the client’s portal
vein, where they migrate to the liver and begin to release insulin
NURSING MANAGEMENT
 Imbalanced Nutrition: More than Body Requirements related to decreased
activity, and habituation of pre illness eating habits
 Provide three meals and snacks within prescribed caloric limits
 Suggest free foods such as up to 1 cup of raw

33. 33
 unlimited sugar free drinks if the client becomes hungry between meals
or snacks.
 Encourage client to drink 8 ounces of water before eating a meal
 Advise client to eat slowly and wait 15 seconds between chewing
thoroughly, swallowing, and taking the next bite
 Risk for Imbalanced Fluid Volume related to hyperglycemia and polyuria
 Monitor intake and output a deficit in fluid intake or excess urine output
suggests a deficit in fluid volume.
 Provide at least 1500 to 3000 mL of fluid per day
 Risk for Injury related to orthostatic hypotension and impaired vision
secondary to neuropathy and retinopathy
 Assist client when rising from a sitting or lying position. Autonomic
neuropathy causes orthostatic hypotension and the potential for fainting
and falling
 Have client dangle on the side of the bed before ambulating. Dangling
allows a period during which blood flow is restored to the brain.
 Keep the floor dry and the environment free of clutter
 Risk for Impaired Skin Integrity related to loss of sensation in feet and
impaired blood circulation
 Examine skin and feet daily. Client may be insensitive to injuries and
slow to heal because of peripheral neuropathy and vascular disturbances.
 Assess skin for signs of breakdown, poor healing, change in color or
temperature, or infection
 Impaired blood supply compromises the integrity of the integument
 Dry client’s skin well after bathing, especially in areas of the body that
are dark and moist
 Fungal infections are common increases and folds of skin
 Inspect inside the client’s shoes for foreign objects or
disrepair.
 Risk for Ineffective Management of Therapeutic Regimen related to
insufficient knowledge regarding diabetes self-management
 Assess client’s ability and willingness to learn about diabetes and self-
management
 Teaching is more effective when the learner is capable and motivated to
acquire information.
 Teach client about insulin and how to self-administer using proper
technique
 Clients learn in various ways: verbal explanations, reading information,
seeing a demonstration, or using a hands-on application

34. 34
HEALTH EDUCATION
Blood glucose
 Monitor blood glucose and record it in a diary
 Take medication on time
 Obtain a HbA1c blood test every 3 – 6 months
 Carry some forms of glucose at all times
Exercise
 Begin a medically supervised exercise program
 Learn how exercise affect blood glucose level
Diet
 Follow diet created by a dietitian
 Eat slowly and chew food thoroughly
 Choose food low in saturated fats
 Limit amount of alcohol
Other guidelines
 Perform an annual eye examination and urine testing for protein
 Examine feet at home
 Know symptoms of hyper and hypoglycemia
 Quit smoking
REVIEW OF LITERATURE
Alginate dressings for healing diabetic foot ulcers.
Source
Department of Nursing, Midwifery and Social Work, University of Manchester,
Manchester, UK, M13 9PL.
Abstract
BACKGROUND:
Foot ulcers in people with diabetes mellitus are a common and serious global
health issue. Dressings form a key part of ulcer treatment, with clinicians and
patients having many different types to choose from including alginate
dressings. A clear and current overview of current evidence is required to
facilitate decision-making regarding dressing use.

35. 35
OBJECTIVES:
To compare the effects of alginate wound dressings with no wound dressing or
alternative dressings on the healing of foot ulcers in people with diabetes
mellitus.
SELECTION CRITERIA:
Published or unpublished randomized controlled trials (RCTs) that have
compared the effects on ulcer healing of alginate dressings with alternative
wound dressings or no dressing in the treatment of foot ulcers in people
with diabetes.
DATA COLLECTION AND ANALYSIS:
Two review authors independently performed study selection, risk of bias
assessment and data extraction.
MAIN RESULTS:
Included six studies (375 participants) in this review; these compared alginate
dressings with basic wound contact dressings, foam dressings and a silver-
containing, fibrous-hydrocolloid dressing. Meta analysis of two studies found
statistically significant difference between alginate dressings and basic wound
contact dressings. Pooled data from two studies comparing alginate dressings
with foam dressings found statistically significant difference in ulcer healing .
There was statistically significant difference in the number of
diabetic foot ulcers healed when an anti-microbial (silver) hydrocolloid dressing
was compared with a standard alginate dressing
SUMMARY
Lifestyle modification is the most cost-effective intervention for prevention of
diabetes in high-risk groups in India. However, control of diabetes with diet,
weight control and physical activity has been difficult and will not be sufficient
for most of the patients. Moreover, the steady increase in the incidence of type
2 diabetes has significant socioeconomic
Implications
BIBLIOGRAPHY
1. Brunner and Suddarth’s, Text Book of Medical Surgical Nursing, 9th
edition, 2005, Lippincott
2. John Luckmann, Medical Surgical Nursing, 3rd edition, 1987, Saunders
Company, Philadelphia London

36. 36
3. Joyce M. Black, Jane Hokanson Hawks, Medical Surgical Nursing-
Clinical Mangement for positive outcomes, 7th edition, 2005, Elsevier,
India.
4. Lewis, Heitkemper & Dirksen Medical Surgical Nursing Assessment and
Management of Clinical Problem (6th ed) (2000) Mosby
5. Haslett C., Chilvers E. R., Hunder J.A.A. & Boon, N. A. Davidson’s
Principles and Practice of Medicine, 18th ed, (1999) Churchill living
stone.
6. Nettina, Sandra, Lippincott Williams & Wilkins, The Lippincott Manuel
of Nursing practice, 7th ed, 2001, Philadelphia
7. library.med.utah.edu/WebPath/TUTORIAL/DIABETES/DIABETES.htm
8. en.wikipedia.org/wiki/Diabetes_mellitus
9. diabetes.webmd.com/types-of-diabetes-mellitus
10.www.nlm.nih.gov/medlineplus/diabetesmellitus.htm