ENGLISH IN NURSING II

NURSING CARE PLAN OF ENDOCRINE SYSTEM

(DIABETES MELLITUS)

Created by
Group 6 / A1 2015

Bunga Nur Rahmawati 131511133031

Fina Ainur Rohmah 131511133032
Talia Puspita Adianti 131511133118
Rian Priambodo 131511133119
Najla Khairunnisa 131511133120
Lili Putri Roesanti 131511133122
Adilla Kusuma Dewi 131511133124

NURSING FACULTY
AIRLANGGA UNIVERSITY
SURABAYA
2016

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 PROLOGUE

Praise be to Allah, The Cherisher and Sustainer of the worlds, God who has been giving
His blessing and mercy to the writers to complete the paper entitled ”Nursing Care Plan
Patient of Endocrine System (Diabetes Mellitus)". This paper is submitted to fulfill one of the
task of English In Nursing II subject in Faculty of Nursing. In finishing this paper, the writer
really gives their regards and thanks for people who has given guidance and help, they are:

1. Ira Suarilah, S.Kp., M.Sc as the English lecture, who have teached us and given detail
information.

2. Our Parents who has always pray for us.

3. And all of my friends who has given support to us and help us.

Finally, the writers realizes there are unintended errors in writing this paper. We are
really allows all readers to give their suggestion to improve the content of its paper in order to be
made as one of the good examples for the next paper. Thank you very much for the attention.

Surabaya, 8th of December 2016

Writers

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 TABLE OF CONTENTS

COVER ............................................................................................................................ i

PROLOGUE ..................................................................................................................... ii

TABLE OF CONTENTS ................................................................................................. iii

BAB I INTRODUCTION................................................................................................. 1

1.1. Background ......................................................................................................... 1

1.2. Formulation Problem .......................................................................................... 2

1.3. Purpose ................................................................................................................ 2

BAB II LITERATURE REVIEW..................................................................................... 3

2.1. Definition of Diabetes Mellitus ........................................................................... 3

2.2. Classification of Diabetes Mellitus ..................................................................... 3

2.3. Etiology and Risk Factor of Diabetes Mellitus………………………………… 5

2.4. Pathophysiology Diabetes Mellitus ……………………………………………. 9

2.5. Clinical Manifestations of Diabetes Mellitus …………………………………. 12

2.6. Complication of Diabetes Mellitus ……………………………………………. 12

2.7. Physical Examination of Diabetes Mellitus …………………………………… 14

2.8. First Aids of Diabetes Mellitus ………………………………………………… 19

2.9. Nursing Care Plan Patient with Diabetes Mellitus …………………………….. 20

BAB III CONCLUSION ..................................................................................................

3.1. Conclusion...........................................................................................................

BIBLIOGRAPHY ………………………………………………………………………

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 CHAPTER I

INTRODUCTION

1.1 Background

Diabetes mellitus is a combination of heterogeneous disorders commonly presenting with

episodes of hyperglycaemia and glucose intolerance, as a result of lack of insulin , defective
insulin action, or both (Sicree et al., 2006). Such complications arise due to derangements in
the regulatory systems for storage and mobilization of metabolic fuels, including the
catabolism and anabolism of carbohydrates, lipids and proteins emanating from defective
insulin secretion, insulin action, or both (Shillitoe, 1988; Votey and Peters, 2004).
85 to 95% of all diabetes in high-income countries are of type 2 accounting for an even
higher dominance in developing countries. It is intimately associated with improper
utilization of insulin by target cells and tissues. It is currently a common and serious health
concern globally. According to WHO, (1994), this problem has been aggravated by rapid
cultural and social dynamics, ageing populations, increasing urbanization, dietary changes,
reduced physical activity and other unhealthy lifestyle and behavioural patterns.
Diabetes mellitus and lesser forms of glucose intolerance, particularly impaired glucose
tolerance, can now be found in almost every population in the world and epidemiological
evidence suggests that, without effective prevention and control programmes, diabetes will
likely continue to increase globally (WHO, 1994).
In 2010, about 285 million people in the age group 20-79 were envisaged to have
diabetes worldwide, about 70% of whom live in developing nations. This estimate is
expected to increase to about 438 million, by 2030. Further, by 2030, the number of people
with IGT is projected to increase to 472 million, or 8.4% of the adult population (Sicree et
al., 2006).
The debilitating effects of diabetes mellitus include various organ failures, progressive
metabolic complications such as retinopathy, nephropathy, and/or neuropathy (Piero, 2006).
Diabetics are accompanied by risk of cardiovascular, peripheral vascular and cerebrovascular
diseases. Several pathogenetic processes are involved in the development of diabetes,

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including destruction of pancreatic β-cells that lead to lowered sensitivity of insulin action
(WHO, 1999; Votey and Peters, 2004).

1.2 Formulation Problem

1.2.1 What is definition of diabetes mellitus?
1.2.2 What is classification of diabetes mellitus?
1.2.3 What is the etiology and risk factor of diabetes mellitus?
1.2.4 How is the pathophysiology and WOC of diabetes mellitus?
1.2.5 What is the clinical manifestations of diabetes mellitus?
1.2.6 What is the complication of diabetes mellitus?
1.2.7 How is the physical examination of diabetes mellitus?
1.2.8 How is the first aids of diabetes mellitus?
1.2.9 How is the nursing care plan of diabetes mellitus?

1.3 Purpose
1.3.1 Knowing definition of diabetes mellitus
1.3.2 Knowing classification of diabetes mellitus
1.3.3 Knowing etiology and risk factor of diabetes mellitus
1.3.4 Knowing the pathophysiology and WOC of diabetes mellitus
1.3.5 Knowing clinical manifestations of diabetes mellitus
1.3.6 Knowing complication of diabetes mellitus
1.3.7 Knowing the physical examination of diabetes mellitus
1.3.8 Knowing the first aids of diabetes mellitus
1.3.9 Knowing the nursing care plan of diabetes mellitus

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 CHAPTER II
LITERATURE REVIEW

2.1 Definition of Diabetes Mellitus

Diabetes mellitus is a chronic, progressive disease characterized by the body’s inability to
metabolize carbohydrates, fats, and protein, leading to hyperglycemia (high blood glucose level).
Diabetes mellitus is sometimes referred to as “High Sugars” by both clients and health care
providers. The nation of associating sugar with diabetes mellitus is appropriate because the
passage of large amounts of sugar-laden urine of characteristic of poorly controlled diabetes
mellitus. While hyperglycemia plays an important role the development of diabetes- related
complication, high levels of blood glucose are only one component of the pathologic process and
clinical manifestations associated with diabetes mellitus. Other pathologic process and risk
factors are just as important, and sometimes independent factors. Diabetes mellitus can be
associated with serious complications, but people with diabetes mellitus can take preventive
measures to reduce the likelihood of such occurrences.

Diabetes mellitus has become an epidemic in the United States with 21 million people (e.g.
70% of the U.S population) having this disease. Approximately 15 million people are diagnosed
with diabetes mellitus, with nearly an additional 6 million estimated to have disease but who are
undiagnosed. As a significant public health problem, diabetes mellitus is the 6 leading cause of
death in the United States. In addition, total estimated diabetes mellitus coast in the United States
2002 were $132 billion (direct and indirect cost) with direct medical cost (e.g., disability, work
loss, and premature morality). While the increasing burden of diabetes mellitus is alarming,
much of the burden of this major public health problem can be prevented by early detection,
improved delivery of care, and better education for diabetes self-management.

2.2 Classification of Diabetes Mellitus

Diabetes mellitus is a classified as one of four different clinical states including type 1, type
2, gestational, or other specific types of diabetes mellitus. Type 1 diabetes mellitus is the result
of autoimmune beta-cell destruction, leading to absolute insulin deficiency. Type 2 diabetes
mellitus is the result of a progressive insulin secretory defect along with insulin resistance,
usually associated with obesity. Gestational diabetes mellitus is type diabetes mellitus diagnosis

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during pregnancy. Other types of diabetes may occur as a result of genetic defect in beta-cell
function, disease of the pancreas (e.g., cystic fibrosis), or disease induced by drugs.

In 1979 the National Diabetes Data Group (NDDG) developed criteria for the classification
and diagnosis of diabetes mellitus. By 1977 and again in 2003, the Expert Committee on the
Diagnosis and Classification.

Types of Diabetes Mellitus and Abnormal Glucose Metabolism:

Diabetes Mellitus:

1. Type 1
2. Type 2
3. Causes of secondary diabetes mellitus
a. Genetic defect
b. Diseases of the pancreas (such as pancreatitis, neoplasia, trauma/
pancreatectomy)
c. Endocrinopathies (such as acromegaly, cushing’s syndrome,
pheochromocytoma, hyperthyroidism)
d. Drug/ chemical-induced (as from glucocorticoid, thyroid
hormone, diazoxide, thiazides, phenytoin sodium {Dilantin},
nicotinic acid
4. Gestational diabetes mellitus

Pre Diabetes Mellitus

1. Impaired glucose tolerance (IGT) (2 hours post-glucose load 140 to

199 mg/dl)
2. Impaired fasting glucose (IFG) (fasting blood glucose 100 to
125mg/dl)

of diabetes mellitus proposed changes to the original NDDG classification. Such changes were
supported by the American Diabetes Association (ADA) and The International Institute of
Diabetes Mellitus and Kidney Disease (NIDKK). Previously, diabetes mellitus was classified as

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either insulin-dependent diabetes mellitus (IDDM) or non-insulin-dependent diabetes mellitus
(NIDDM). With the use of insulin therapy commonplace with both types of diabetes mellitus,
IDDM is now referred to as type 1 diabetes mellitus and NIDDM is referred to as type 2 diabetes
mellitus. The ADA also recommended using Arabic numerals, type 1 and type 2, rather than
Roman numerals in referring in referring to the two types of diabetes mellitus.

Client who do not have type 1 or type 2 diabetes mellitus. May be classified as having an
impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) an IFG is a glucose
concentration between 100 and 125 mg/dl while an IGT while an IGT is defined as a 2-hour oral
glucose tolerance test (>75-g glucose load) with a glucose concentration between 140 and 199
mg/dl. Both IFG and IGT refer to a metabolic state between normal and diabetes mellitus,
referred to as prediabetes.

Diabetes mellitus may also result from other disorders or treatments. Genetic defect in the
beta cells can lead to the development of diabetes mellitus. Several hormone, such as growth
hormone, cortisol, glucagon, and epinephrine can antagonize counteract insulin. Excess amount
of these hormones (as in acromegaly, Cushing’s syndrome, glucagonoma, and
pheochromocytoma) cause diabetes mellitus. Such types of secondary diabetes mellitus. In
addition, certain drugs (e.g., glucocorticoid and thiazides) may cause diabetes mellitus. Such
type of secondary diabetes mellitus account for 1% to 2% of all diagnosed cases of diabetes
mellitus.

Gestational diabetes mellitus is a diagnosis of diabetes mellitus that applies to women in

whom glucose intolerance develops or is first discovered during pregnancy. Gestational diabetes
mellitus develop in 2% to 5% of all pregnant women but usually disappears when the pregnancy
is over. It occurs more frequently in African American, Hispanic Americans, Native Americans,
and women with family history of diabetes mellitus or bebies over 9 pounds at birth; obesity is
also a risk factor.

2.3 Etiology and Risk Factor of Diabetes Mellitus

2.3.1 Type 1 diabetes mellitus

Type 1 diabetes mellitus,previously called IDMM or juevenile-onset diabtese

mellitus, is characterized by destruction of pancreatic beta cells,leading to absolute

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insulin deficiency. Type 1 diabetes mellitus affects 10% of all people in the united states
who have diabetes mellitus and is usually diagnosed before the age of 30. The incidence
of type 1 diabetes mellitus is 12 to 14 cases per 100,000 people younger than 20
years,with an incidence of 1 case per 500 people younger than 16 years. Type 1 diabetes
mellitus is one of the mostcommon childhood disease,being three to four times more
common than such chronic childhood disease as cystic fibrosis,juvenile rheumatoid
arthritis,and leukemia. The incidence of type 1 diabetes mellitus in males is similar to that
in females with the condition more commonly seen among african americans,hispanic
americans,asian americans,and native americans that in whites. Risk factors are less well-
defined for type 1 diabetes mellitus than for type 2 diabetes mellitus.

Type 1 diabetes mellitus is inherited as a heterogeneous,multigenic trait.identical

twins have a risk of 25% to 50% of inheriting the disease,whereas siblings have a 6% risk
and offspring a 5% risk. Despite this strong familial influence, 90% of people in whom
type 1 diabetes mellitus develops do not have a first-degree relative with diabetes
mellitus. An association also exists between type 1 diabetes mellitus and several human
leukocyte antigens (HLAs). Environmental factors such as viruses appear to trigger an
autoimmune process that destroys beta cells. Islet cell antibodies (ICAs) then appear,
increasing in ammount over months to year as beta cells are destroyed. Fasting
hyperglycemia (elevated blood glucose level) occurs when 80% to 90% of beta-cell mass
has been destroyed.

Identification of ICAs has made it possible to detect type 1 diabetes mellitus in its
preclinical stage. Autoantibodies directed against insulin are found in 20% to 60% of
clients with type 1 diabetes mellitus before initiation of exogenous insulin therapy. The
combination of large amounts of ICAs, presence of insulin autoantibodies, and decreased
first-phase insulin secretion (representing insulin stored in beta cells) can predict the
onset of type 1 diabetes mellitus within 5 years.

There are no known health promotion activities to prevent type 1 diabetes

mellitus; however, physical activity and adherence to a prescribed meal plan may limit
the development of diabetes-related complications.

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 In some instances, high-risk individuals (i.e., firstdegree relatives of people with
type 1 diabetes mellitus) are screened and appropriate counseling and follow-up
instituted.

Health maintenance activities involve the following :

 Maintaining blood glucose at levels as normal as possible

 Preventing hypoglycemia and hyperglycemia with stress, ilness, or exercise by closely
monitoring blood glucose levels and taking early action
 Performing daily foot care
 Preventing complications of diabetes mellitus by removing or treating coexisting risk
factors sush as smoking,hypertension,hyperlipidemia, and used of nephtoroxic drugs

Health restoration actions include the following :

 Prompt treatment of foot abrasions or infections

 Follow-up visits to assess for complications of diabetes mellitus and to reinforce
learning needs
 Yearly funduscopic examinatios by an ophthalmologist with treatment as needed
 Treatment of coexisting risk factors as described previously

2.3.2 Type 2 diabetes mellitus

Type 2 diabetes mellitus, previously called NIDDM or adult-onset diabetes

mellitus, is a disorder involving both genetic and environmental factors. Type 2 diabetes
mellitus is the most common type of diabetes mellitus, affecting 90% of all people who
have the disease. Type 2 diabetes mellitus is usually diagnosed after the age of 40 and is
more common among older adults,obese adults, and certain ethnic and racial populations.
However,the diagnosis of type 2 diabetes mellitus in children and adoloscents is on the
increase, particularly in african americans and hispanic/latino americans. On
average,people diagnosed with type 2 diabetes mellitus have had the diagnosis for about
6.5 years before clinical identification and treatment.

The prevalence of type 2 diabetes mellitus is markedly higher in native americans,

africans americans and hispanic americans, as well as in order and obese people. Diabetes

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 mellitus is the leading cause of new blindness in adults 20 to 74 years of age and is the
leading cause of chronic renal failure,accounting for about 40% of new cases. Likewise,
diabetes mellitus is responsible for more than half the number of nontraumatic
amputations in the united states.

Type 2 diabetes mellitus is not associated with HLA tissue types,and circulating
ICAs are rarely present. Heredity plays a major role in the expression of type 2 diabetes
mellitus. It is more common in identical twins (58% to 75% incidence) than in the
general population.

Obesity is a major risk factor,with 85% of all people with type 2 diabetes mellitus
being obese. It is unclear wheather impaired tissue (liver and muscle) sensitivity to
insulin or impaired insulin secretion is the primary defect in this type of diabetes mellitus.
In addition, the prevalence of coronary artery disease in people with type 2 diabetes
mellitus is twice that in the non-diabetic population,and cardiovascular and total mortality
rates are two-fold to trhee-fold greater than in non-diabetic people. These issues are
explored in the translating evidence into practice feature on p.1065. Also see the
community-based practice feature on p.1066 for a discussion of diabetes mellitus health
promotion and maintenance activities.

Health promotion actions for type 2 diabetes mellitus include the following :

 Following eating habits based on “MyPyramid” (as noted later)

 Avoiding foods high in refined sugars and saturated fats
 Maintaining ideal body weight,starting in childhood
 Exercising regularly
 Returning to pre-pregnancy weight or ideal body weight postpartum

Health maintenance activities involve the following :

 Screening high-risk individuals (i.e., people with family history of diabetes mellitus in
first or second generation; members of certain racial or ethnic backgrounds [african
american, native american, mexican american,asians/pacific islander]; people older than
age 45 with any other risk factor; people with hypertension or hyperlipidemia; clients
with previous impaired glucose tolerance;women with previous gestational diabetes

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 mellitus or those who have had a baby weighing more than 9 pounds; and people with a
history of recurrent infevtion,habitual physical inactivity,or polycystic ovary syndrome)
by measuring a fasting blood glucose level
 Performing periodic assessments to determine the client’s learning needs and to assess
glycemic control
 Using strategies shown to reduce complications of diabetes mellitus by removing or
treating coexisting risk factors such as smoking, hypertension, hyperlipidemia, and use of
nephrotoxic drugs
 Performing daily foot care
 Preventing hypoglycemia or hyperglycemia by closely monitoring blood glucose levels
and taking early action

Health restoration actions include the following:

 Teach meal planning and physical activity programs to reduce obesity

 Prompt treatment of foot abrasions or infections
 Follow-up visits to assess for complications of diabetes mellitus and reinforce learning
needs
 Yearly funduscopic examinations by an ophthalmologist with treatment as needed
 Treatment of previously described risk factors
 Control of angina and peripheral vascular disease

2.4 Pathophysiology Diabetes Mellitus

2.4.1 Type 1 Diabetes Mellitus
Type 1 diabetes mellitus does not develop in all people who have a genetic
predisposition. Of those in whom gene markers (DR3 or DR4 HLA) indicate risk,
diabetes mellitus ultimately develops in less than 1%. Environmental triggers have long
been suspected in type 1 diabetes mellitus. Incidence is increased in both spring and fall,
and onset is often coincidental with epidemics of various viral diseases. Active
autoimmunity is directed against the beta cells of the pancreas and their products. ICAs
and insulin antibodies progressively decrease the effective circulating insulin level.

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 This slow, progressive insult to the beta cells and endogenous insulin molecules can
result in an abrupt onset of diabetes mellitus. Hyperglycemia can result from acute illness
or stress, which increases insulin demand beyond the reserves of the damaged beta-cell
mass. When the acute illness or stress resolves, the client may revert to a compensated
state of variable duration in which the pancreas once again manages to produce adequate
amounts of insulin. This compensated state, referred to as the honeymoon period,
typically lasts for 3 to 12 months. The process ends when the diminishing beta-cell mass
cannot produce enough insulin to sustain life. The client then becomes dependent on
exogenous insulin (produced outside the body) administration to survive.

2.4.2 Type 2 Diabetes Mellitus

The pathgenesis of type 2 diabetes mellitus differs significantly from that of type
1. A limited beta-cell response to hyperglycemia appears to be a major factor in its
development. Beta cells chronically exposed to high blood levels of glucose become
progressively less efficient when responding to further glucose elevations. This
phenomenon, termed desensitization, is reversible by normalizing glucose levels. The
ratio of proinsulin (a precursor to insulin) to insulin secreted also increases.

A second pathophysiology process in type 2 diabetes mellitus is resistance to the

biologic activity of insulin in both the liver and peripheral tissues. This state is known as
insulin resistance. People with type 2 diabetes mellitus have a decreased sensitivity to
glucose levels, which results in continued hepatic glucose production, even with high
blood glucose levels. This is coupled with an inability of muscle and fat tissues to
increase glucose uptake. The mechanism causing peripheral insulin resistance is not
clear; however, it appears to occur after insulin binds to a receptor on the cell surface.

Insulin is a building (anabolic) hormone. Without insulin, three major metabolic

problems occur: (1) decreased glucose utilization, (2) increased fat mobilization, and (3)
increased protein utilization.

2.4.3 Decreased Glucose Utilization

Cells that require insulin as a carrier for glucose can take in only about 25% of the
glucose they require for fuel. Nerve tissues, erythrocytes, and the cells of the intestines,

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liver, and kidney tubules do not require insulin for glucose transport. However, adipose
tissue, along with skeletal and cardiac muscle, requires insulin for glucose transport.
Without adequate amounts of insulin, much of the ingested glucose cannot be used.

With inadequate amounts of insulin, blood glucose levels rise. This elevation
continues because the liver cannot store glucose as glycogen without sufficient insulin
levels. In an attempt to restore balance and return blood glucose levels to normal, the
kidney excretes the excess glucose. Glucose appears in the urine (glucosuria). Glucose
excreted in the urine acts as an osmotic diuretic and causes excretion of increased
amounts of water, resulting in fluid volume deficit.

2.4.4 Increased Fat Mobilization

In type 1 diabete mellitus and occasionally with severe stress in type 2 diabete mellitus,
the body turns to fat stores for energy production when glucose is unavailable. Fat
metabolism causes breakdown products called ketones to form. Ketones accumulate in
the blood and are excreted through the kidneys and lungs. Ketone levels can be measured
in the blood and urine; high levels can indicate uncontrolled diabetes mellitus.

Ketones interfere with the body’s acid-base balance by producing hydrogen ions.
The pH can decrease, and metabolic acidosis can develop. In addition, when ketones are
excreted, sodium is also eliminated, resulting in sodium depletion and further acidosis.
The excretion of ketones also increases osmotic pressure, leading to increased fluid loss.
Also, when fats are the primary source of energy, body lipid levels can increase to five
times normal, leading to increased atherosclerosis.

2.4.5 Increased Protein Utilization

Lack of insulin leads to protein wasting. In healthy people, proteins are constantly being
broken down and rebuilt. In people with type 1 diabetes mellitus, without insulin to
stimulate protein synthesis, the balance is altered, which leads to increased catabolism
(destruction). Amino acids are converted to glucose in the liver, further elevating glucose
levels. If this condition goes untreated, clients with type 1 diabetes mellitus appear
emaciated. The pathophysiology processes of diabetes mellitus continue, leading to many
acute and chronic complications, discussed later in the capter.

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 2.5 WOC of Diabetes Mellitus

2.6 Clinical Manifestations of Diabetes Mellitus

An elevated blood glucose level, called hyperglycemia, leads to commn clinical

manifestations associated with diabetes mellitus. In type 1 diabetes mellitus, the onset of clinical
manifestations may be subtle with the possibility of life-threatening situations likely to happen
(i.e., diabetic ketoacidosis). In type 2 diabetes mellitus, the onset of clinical manifestations may
develop so gradually that clients may noticed few or no clinical manifestations for a number of
years.

The clinical manifestations of diabetes mellitus are increased frequency of urination

(polyuria), increased thirst or fluid intake (polydipsia), and, as the disease progresses, weight
loss despite hunger and increased food intake (polyphagia).

2.7 Complication of Diabetes Mellitus

2.6.1 Acute Complication of Diabetes Mellitus

Variable Hypoglycemia Insulin Shock DKA HHNKS

Onset Rapid Slow Slowest
Symptoms Weak, anxious, confused, Nausea, vomiting, Similar to DKA,
tachycardia polyuria, stuporous, hypotension,
polyphagia, dehydration
polydipsia,
headache, irritable,
comatose
Skin Sweating Hot, flushed, dry Very dry

Mucous Normal Dry Extremely dry

membranes
Respirations Normal Hyperventilation, Normal
“fruity” or acetone
odor to breath

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Those at risk Type 1 and 2 diabetes
mellitus; fluctuating blood
glucose levels; insufficient
food intake; excessive
exercise; oral medication;
excessive insulin
Type 1 diabetes Elderly or young; type 2
mellitus; stressful diabetes mellitus; high
situations; omission carbohydrate diets;
of insulin dieresis; hyperosmolar
dialysis

Blood sugar/dl 35 mg or less in newborns, 300 to 750 mg 600 to 4800 mg

60 mg or less in adults

Treatmet Fast-acting carbohydrate; Low-dose insulin; Fluid replacement with

intravenous glucose; electrolyte and crystalloids and colloids
subcutaneous glucagon fluid replacement

2.6.2 Chronic Complication of Diabetes Mellitus

Chronic hyperglycemia involves

*Nonenzymatic glycosylation
*shunting of glucose to polyol pathway
*Activation of protein kinase C
Leading to:

Diabetic Neuropathies Microvascular Disease Macrovascular Disease Infection

Axonal and Schwann Retinopathy* Coronary heart disease* Sensory

Cell degenerations, Nephropathy* CVA * impairment,
altered motor nerve Capillary basement Peripheral vascular disease* atherosclerosis,
conduction, sensory membrance thickening Proliferation of fibrous ischemia,
alterations , decreased tissue plaques, atherosclerosis hypoxia,
perfusion or ischemia, because of high serum lipids, leukocytic
hypertension ischemia impairment

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2.8 Diabetes Mellitus Physical Examination
2.8.1 Type 1 Diabetes Mellitus Clinical
In new cases of diabetes, physical examination findings are usually normal.
Patients with DKA, however, will have Kussmaul respiration, signs of dehydration,
hypotension, and, in some cases, altered mental status.
In established cases, patients should be examined every 3 months for
macrovascular and microvascular complications. They should undergo funduscopic
examination for retinopathy and monofilament testing for peripheral neuropathy.

Diabetes-focused examination

A diabetes-focused physical examination includes assessment of vital signs,

funduscopic examination, limited vascular and neurologic examinations, and foot
examination. Other organ systems should be assessed as indicated by the patient’s
clinical situation. A comprehensive examination is not necessary at every visit.
Assessment of vital signs
Patients with established diabetes and autonomic neuropathy may have orthostatic
hypotension. Orthostatic vital signs may be useful in assessing volume status and in
suggesting the presence of an autonomic neuropathy. Measurement of the pulse is
important, in that relative tachycardia is a typical finding in autonomic neuropathy, often
preceding the development of orthostatic hypotension. If the respiratory rate and pattern
suggest Kussmaul respiration, DKA must be considered immediately, and appropriate
tests must be ordered.
Funduscopic examination
The funduscopic examination should include a careful view of the retina. Both the
optic disc and the macula should be visualized. If hemorrhages or exudates are seen, the
patient should be referred to an ophthalmologist as soon as possible. Examiners who are
not ophthalmologists tend to underestimate the severity of retinopathy, which cannot be
evaluated accurately unless the patients’ pupils are dilated.
Foot examination

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 The dorsalis pedis and posterior tibialis pulses should be palpated and their presence
or absence noted. This is particularly important in patients who have foot infections: poor
lower-extremity blood flow can delay healing and increase the risk of amputation.
Documenting lower-extremity sensory neuropathy is useful in patients who
present with foot ulcers because decreased sensation limits the patient’s ability to protect
the feet and ankles. If peripheral neuropathy is found, the patient should be made aware
that foot care (including daily foot examination) is very important for the prevention of
foot ulcers and lower-extremity amputation.
2.8.2 Type 2 Diabetes Mellitus Clinical
Early in the course of diabetes mellitus, the physical examination findings are
likely to be unrevealing. Ultimately, however, end-organ damage may be observed.
Potential findings are listed in the image below.

Possible physical examination findings in patients with type 2 diabetes mellitus.

A diabetes-focused examination includes vital signs, funduscopic examination,

limited vascular and neurologic examinations, and a foot assessment. Other organ
systems should be examined as indicated by the patient's clinical situation.

15
 Assessment of vital signs

Baseline and continuing measurement of vital signs is an important part of

diabetes management. In addition to vital signs, measure height, weight, and waist and
hip circumferences.
In many cases, blood pressure measurement will disclose hypertension, which is
particularly common in patients with diabetes. Patients with established diabetes and
autonomic neuropathy may have orthostatic hypotension. Orthostatic vital signs may be
useful in assessing volume status and in suggesting the presence of an autonomic
neuropathy.
If the respiratory rate and pattern suggest Kussmaul respiration, diabetic
ketoacidosis (DKA) must be considered immediately, and appropriate tests ordered. DKA
is more typical of type 1 diabetes, but it can occur in type 2.

Funduscopic examination

The funduscopic examination should include a careful view of the retina. The
optic disc and the macula should be visualized. If hemorrhages or exudates are seen, the
patient should be referred to an ophthalmologist as soon as possible. Examiners who are
not ophthalmologists tend to underestimate the severity of retinopathy, especially if the
patients' pupils are not dilated.
Whether patients develop diabetic retinopathy depends on the duration of their
diabetes and on the level of glycemic control maintained.  [97, 98]Because the diagnosis of
type 2 diabetes often is delayed, 20% of these patients have some degree of retinopathy at
diagnosis. The following are the 5 stages in the progression of diabetic retinopathy:
 Dilation of the retinal venules and formation of retinal capillary
microaneurysms
 Increased vascular permeability
 Vascular occlusion and retinal ischemia
 Proliferation of new blood vessels on the surface of the retina
 Hemorrhage and contraction of the fibrovascular proliferation and the vitreous
The first 2 stages of diabetic retinopathy are known as background or
nonproliferative retinopathy. Initially, the retinal venules dilate, then microaneurysms

16
(tiny red dots on the retina that cause no visual impairment) appear. As the
microaneurysms or retinal capillaries become more permeable, hard exudates appear,
reflecting the leakage of plasma.
Larger retinal arteriolar and venular calibres have been associated with lower
scores on memory tests but not with lower scores on other cognitive tests.  [99] This
association was strong in men. Impaired arteriolar autoregulation may be an underlying
mechanism of memory decrements.
Rupture of intraretinal capillaries results in hemorrhage. If a superficial capillary
ruptures, a flame-shaped hemorrhage appears. Hard exudates are often found in partial or
complete rings (circinate pattern), which usually include multiple microaneurysms. These
rings usually mark an area of edematous retina. The patient may not notice a change in
visual acuity unless the center of the macula is involved.
Macular edema can cause visual loss; therefore, all patients with suspected
macular edema must be referred to an ophthalmologist for evaluation and possible laser
therapy. Laser therapy is effective in decreasing macular edema and preserving vision but
is less effective in restoring lost vision. (For more information, see Macular Edema in
Diabetes.)
Preproliferative and proliferative diabetic retinopathy are the next stages in the
progression of the disease. Cotton-wool spots can be seen in preproliferative retinopathy.
These represent retinal microinfarcts caused by capillary occlusion; they appear as
patches that range from off-white to gray, and they have poorly defined margins.
Proliferative retinopathy is characterized by neovascularization, or the
development of networks of fragile new vessels that often are seen on the optic disc or
along the main vascular arcades. The vessels undergo cycles of proliferation and
regression. During proliferation, fibrous adhesions develop between the vessels and the
vitreous. Subsequent contraction of the adhesions can result in traction on the retina and
retinal detachment. Contraction also tears the new vessels, which hemorrhage into the
vitreous.
Patients with preproliferative or proliferative retinopathy must immediately be
referred for ophthalmologic evaluation because laser therapy is effective in this condition,
especially before actual hemorrhage occurs.

17
 Often, the first hemorrhage is small and is noted by the patient as a fleeting, dark
area, or "floater," in the field of vision. Because subsequent hemorrhages can be larger
and more serious, the patient should be referred immediately to an ophthalmologist for
possible laser therapy. Patients with retinal hemorrhage should be advised to limit their
activity and keep their head upright (even while sleeping), so that the blood settles to the
inferior portion of the retina, thus obscuring less central vision.
Patients with active proliferative diabetic retinopathy are at increased risk of
retinal hemorrhage if they receive thrombolytic therapy; therefore, this condition is a
relative contraindication to the use of thrombolytic agents.
One study has shown that individuals with gingival hemorrhaging have a high
prevalence of retinal hemorrhage. [100] Much of this association is driven by
hyperglycemia, making it possible to use gingival tissue to study the natural course of
microvascular disease in patients with diabetes.

Foot examination

The dorsalis pedis and posterior tibialis pulses should be palpated and their
presence or absence noted. This is particularly important in patients who have foot
infections, because poor lower-extremity blood flow can slow healing and increase the
risk of amputation.
Documenting lower-extremity sensory neuropathy is useful in patients who
present with foot ulcers because decreased sensation limits the patient's ability to protect
the feet and ankles. This can be assessed with the Semmes Weinstein monofilament or by
assessment of reflexes, position, and/or vibration sensation.
If peripheral neuropathy is found, the patient should be made aware that foot care
(including daily foot examination) is very important for preventing foot ulcers and
avoiding lower-extremity amputation. (For more information, see Diabetic Foot and
Diabetic Foot Infections.)

2.8.3 Differentiation of type 2 from type 1 diabetes

Type 2 diabetes mellitus can usually be differentiated from type 1 diabetes
mellitus on the basis of history and physical examination findings and simple laboratory

18
 tests (see Workup: Tests to Differentiate Type 2 and Type 1 Diabetes). Patients with type
2 diabetes are generally obese, and may have acanthosis nigricans and/or hirsutism in
conjunction with thick necks and chubby cheeks.

2.9 First Aids of Diabetes Mellitus

2.9.1 Hyperglycaemia
High blood sugar (hyperglycaemia) develops slowly over a period of days. Those
who suffer from hyperglycaemia may wear warning bracelets, cards or medallions
alerting a first aider to the condition. If it is not treated, hyperglycaemia will result in
unconsciousness (diabetic coma) and so requires urgent treatment in hospital.
1. Call 999/112 for emergency help; tell ambulance control that you suspect
hyperglycaemia.
2. Monitor and record vital signs – level of response, breathing and pulse while waiting
for help to arrive.
2.9.2 Hypoglycaemia
Low blood sugar (hypoglycaemia) is characterised by a rapidly deteriorating level
of response. It develops if the insulin-sugar balance is incorrect; for example, when a
person with diabetes misses a meal or takes too much exercise. It is more common in a
person with newly diagnosed diabetes while they are becoming used to balancing sugar
levels. More rarely, hypoglycaemia may develop following an epileptic seizure or after
an episode of binge drinking. It can also occur with heat exhaustion or
hypothermia. People with diabetes may carry their own blood-testing kits to check their
blood sugar levels, as well as their insulin medication, so are well prepared for
emergencies; for example many carry sugar lumps or a tube of glucose gel. If the
hypoglycaemic attack is at an advanced stage, consciousness may be impaired and you
must seek emergency help.

1. Help the casualty to sit down.  Give him a sugary drink, sugar lumps or sweet food. If
he has his own glucose gel, help him to take it.

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 2.  If the casualty responds quickly, give him more food or drink and let him rest until
he feels better. Help him find his glucose testing kit so that he can check his glucose
level. Monitor him until he is completely recovered.
3. If his condition does not improve, look for other possible causes. Call 999/112 for
emergency help and monitor and record vital signs – level of response, breathing and
pulse – while waiting for help to arrive.

2.10 Nursing Care Plan Patient with Diabetes Mellitus

2.9.1 Assessment
Anamnesa

1. Client identity
Includes the name, age, sex, religion, education, occupation, address, marital
status, ethnicity, registration number, date of admission and medical
diagnostics.
2. Main Complaint
Their tingling in the foot / lower leg, decreased sense of touch, the wounds
do not heal - heal and smell, pain in the wound.
3. Medical history
a) Present health history
Contains about when the occurrence of injuries, the cause of the injury as
well as the efforts made by people to cope.
b) Past medical history
A history of diabetes disease or diseases - diseases that are related to
insulin deficiency diseases such as pancreas. A history of heart disease,
obesity, and atherosclerosis, the medical action ever in the can and
medicines used by the patient.
c) Family health history
From the family genogram usually are one of the family members who
also suffer from diabetes or hereditary disease that can cause insulin
deficiency such as hypertension, heart.
d) Psychosocial History

20
 Includes information about behavior, feelings and emotions experienced
by patients in connection with illness and family responses to disease
sufferers.

Physical Examination

1) The general health status

Covers the state of the patient, consciousness, speech sounds, height, weight
and signs- vital signs.
2) Head and neck
Assess the shape of the head, the state of the hair, is there any enlargement of
the neck, ears sometimes ringing, is there any hearing loss, the tongue is often
thick, saliva becomes more viscous, dental volatile, easy gum swelling and
bleeding, whether blurred vision / double, diplopia, cloudy eye lens.
3) Integumentary system
Decreased skin turgor, their wounds or scars blackish color, moisture and shu
skin in the area around the ulcer and gangrene, redness of the skin around the
wound, the texture of the hair and nails.
4) Respiratory system
5) Is there shortness of breath, cough, sputum, chest pain. In patients with
DM easy infection.
6) The cardiovascular system
Decreased tissue perfusion, weak or diminished peripheral pulses,
tachycardia/ bradycardia, hypertension / hypotension, arrhythmia,
kardiomegalis.
7) Gastrointestinal system
There polifagi, polidipsi, nausea, vomiting, diarrhea, constipation, dehidrase,
weight changes, increased abdominal girth, obesity.
8) Urinary system
Polyuria, urinary retention, urinary incontinence, burning sensation or pain
during urination.
9) Musculoskeletal system

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 Fat distribution, muscle mass deployment, perubahn height, fatigue, weakness
and pain, presence of gangrene in the extremities.
10) The neurological system
There was a decrease sensory, parasthesia, anesthetics, lethargy, drowsiness,
slow reflexes, chaotic mental disorientation.

Laboratory Tests

Laboratory tests were conducted:

1. Blood tests
Blood tests include: GDS> 200 mg / dl, fasting blood glucose> 120 mg / dl
and a two-hour post-prandial> 200 mg / dl.
2. Urine
Examination found the presence of glucose in the urine. Inspection is done by
Benedict (reduction). Results can be seen through changes in urine color:
green (+), yellow (++), red (+++), and red brick (++++).
3. Kultur pussy
Knowing the type of bacteria in wounds and administering antibiotics
appropriate to the type of germs.
4. Data Analysis
Data have been collected and analyzed further grouped and synthesis of data.
In classifying the data distinguished on subjective data and objective data and
be based on Abraham Maslow's theory consisting of:
 Basic needs or physiological
 The need for a sense of security
 The need for love and affection
 The need for self-esteem
 The need for self-actualization

2.9.2 Nursing Diagnosis

1. Risk for unstable blood glucose level

2. Ineffective peripheral tissue perfusion r/t diabetes mellitus

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 3. Defiisit fluid volume r/t active fluid volume loss
4. Imbalanced nutrition: less than body requirements r/t Insufficient dietary intake

Nursing Diagnosis NOC NIC

1. Risk for unstable After treatment for 2x24 1. Diet Staging
blood glucose level expected results:  Collaborate with
Risk factors : 1. Knowledge: Healthy other health care team
Inadequate blood glucose Diet members to progress
monitoring outcomes: diet as rapidly as
(code 00179; domain 2; class  Relationship among possible without
4) diet, exercise and complications
weight  Find ways to include
 Fluid intake patient preferences in
appropriate for the prescribed diet
metabolic needs 1. Nutritional
 Caloric intake Counseling
appropriate for  Use accepted
metabolic needs nutritional standards
 Nutrient intake to assist client in
appropriate for evaluating adequacy
individual needs of dietary intake
 Recommended  Provide information,
nutritional guidelines as necessary, about
 Foods consistent with the health need for
nutritional guidelines diet modification:
 Dietary weight loss, weight
recommendations for gain, sodium
healthy fats, proteins, restriction, cholesterol
and carbohydrates reduction, fluid

 Interpretation of restriction, and so on

nutritional  Discuss nutritional

23
 information on food requirements and
labels patient’s perceptions
of
prescribed/recommen
ded diet
 Review with patient
measurements of fluid
intake and output,
hemoglobin values,
blood pressure
readings, or weight
gains
 and losses, as
appropriate

2. Nutritional
Monitoring
 Identify recent
changes in body
weight
 Determine energy
recommendation
(e.g., Recommended
Dietary Allowance)
based on patient
factors (e.g., age,
weight, height,
gender, and physical
activity level)
2. Ineffective peripheral After treatment for 2x24 1. fluid management
tissue perfusion r/t expected results:  Weigh daily and

24
 diabetes mellitus 1. Self-Management: monitor trends
(code 00204; domain 4; Diabetes  Monitor vital signs, as
class 4) outcomes appropriate
 Distribute the fluid
 Accepts diagnosis intake over 24 hours,
 Seeks information as appropriate
about methods to  Monitor nutrition
prevent complications status
 Performs treatment 2. Vital Signs
regimen as prescribed Monitoring
 Performs correct  Monitor blood
procedure for blood pressure, pulse,
glucose testing temperature, and
 Monitors blood respiratory status, as
glucose appropriate
 Treats symptoms of
hyperglycemia
 Treats symptoms of
hypoglycemia
 Reports symptoms of
complications
 Uses diary to
monitor blood
glucose level over
time
 Uses preventive
measures to reduce
risk
for complications
 Obtains health care if
blood glucose levels

25
 fluctuate outside of
recommendations
3. Defiisit fluid volume After treatment for 2x24 3. fluid management
r/t active fluid volume expected results:  Weigh daily and
loss 1. blood glucose levels monitor trends
(code 00027; domain 2;  Monitor vital signs, as
class 5) outcomes appropriate
 blood glucose  Distribute the fluid
intake over 24 hours,
as appropriate
 Monitor nutrition
status
4. Vital Signs
Monitoring Monitor
blood pressure, pulse,
temperature, and
respiratory status, as
appropriate
4. Imbalanced nutrition: After treatment for 2x24 5. Nutrition
less than body expected results: Management
requirements r/t 1. submissive behavior:  Identify patient’s food
Insufficient dietary the recommended diet allergies or
intake intolerances
(code 00002 domain 2; outcomes  Administer
class 1)  Participate in setting medications prior to
diet can be achieved eating (e.g., pain
by health relief, antiemetics), if
professionals needed
 Using the nutritional 6. Vital Signs
information on labels Monitoring
to make choices  Monitor blood

26
  Choose foods and pressure, pulse,
fluids in accordance temperature, and
with the prescribed respiratory status, as
diet appropriate
 Following the 7. Diet Staging
recommendation  Collaborate with
between interludes of other health care team
food and fluids members to progress
 The meal plan in diet as rapidly as
accordance with the possible without
prescribed diet complications
 Plan strategies to  Find ways to include
situations that affect patient preferences in
the intake of food and the prescribed diet
fluids
 Changing the diet
within certain limits
when changes occur
activity
 Following a
recommendation in
the diet phase
 Avoid foods and
liquids interacting
with medication

2.9.3 Evaluation
1. The imbalance in blood sugar levels can be resolved
2. Ineffective peripheral tissue perfusion is resolved
3. Fluid volume deficit is resolved
4. Nutrition less than body requirements are met
27
CHAPTER III

28
 CONCLUSION

A stroke can occurs when the blood supply to part of the brain is suddenly interrupted or
when a blood vessel in the brain bursts, spilling blood into the spaces between brain cells.
There are two major kinds of stroke. The first, called an ischemic stroke, is caused by a
blood clot that blocks a blood vessel or artery in the brain, cutting off the supply of blood
to an area of the brain. The second type, called hemorrhagic stroke, is caused by a blood
vessel in the brain that breaks and bleeds into the brain.
Prevention is the best course when it comes to stroke. Have your blood pressure
checked regularly. If you alreadyhave high blood pressure, follow your doctor’s
instruction for bringing it down into the normal range. If you have heart disease, diabetes,
or unfavorable cholesterol levels, get them under control―and keep them under
control―and you will greatly reduce your chances of having a stroke. If you smoke, quit
now. Prompt treatment for a stroke can be lifesaving and can significantly reduce the
paralysis and loss of function that often result from a stroke and improve the chances of
recovery. The earlier that treatment is given, the better the outcome.

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BIBLIOGRAPHY

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