REPUBLIC OF THE PHILIPPINES

NUEVA ECIJA UNIVERSITY OF SCIENCE AND TECHNOLOGY

CABANATUAN CITY 3100

TYPE II

DIABETES

MELLITUS
SUBMITTED BY: bsn iv- G

MARK ANTHONY S. CASTILLO

CHONAMARIE R. BUTARDO

SUBMITTED TO:

MS. HEIDEE FAJARDO, RN

 MRS LORY CRISANTO, RN

INTRODUCTION

The case study that is to be presented features a patient

who has a type 2 Diabetes Mellitus.

We as nurses are involved in learning what type of nursing

interventions we are to apply to this type of patient. Beyond

understanding the relevant health issue, this case study will also

explore other factors that can enhance our knowledge in the field

of our nursing practice. This is also the primary reason why we

choose this case study because we know that it is highly

beneficial aside from it is being considered distinctive or unique.

Included with the case study are the discussions of the

anatomical parts, through physical assessment of the patient,

laboratory results and their corresponding findings. Added to this

we also have a discussion of the patient’s daily activities and

nursing care plans.

 OBJECTIVES

General Objectives

 To be able to apply what we have learned theoretically

at the community and clinical setting and after that

study, we can be able to understand this disease more

deeper together with the help of our Clinical Instructors

and community health provider and able to provide

optimum or standard quality care to the patient

through making of the nursing intervention and health

education regimen.

Specific Objectives

Student-Nurse Centered:

 To gain knowledge about the disease process,

predisposing factors, clinical manifestation and the

disease management.
 To gain skills and appropriate attitudes needed to

function as a student-nurse in the community.

 Identify problems: Develop a teaching plan and

strategies appropriate for the goal attainment.

 To be able to use the nursing process as framework for

care of the patient.

 To develop and establish interpersonal relationship

while the case is ongoing.

Client Centered:

 To manage his disease.

 To know the importance of his compliance to his

disease.

 To prevent and manage the potential complication that

might occur.
  Perform emphasized health teaching and follow dietary

instruction and restriction as well as performing

appropriate exercise.

CLIENT’S PROFILE

Name: R.C.

Address: Purok 4, Singalat, Palayan City

Age: 36 years old

Sex: Male

Birthdate: November 28, 1972

Civil Status: Married

Educational Attainment: Vocational

Religion: Roman Catholic

Height: 5’1”

Weight: 63kg (140lbs)

Nationality: Filipino

No. of Children: 3

Occupation: Vendor
Physician: Dr. Narag
ASSESSMENT

Family History of Illness

According to patient, his father and grandmother had been

diagnosed of Type 2 Diabetes Mellitus.

Past History of Illness

According to the patient he never had any serious illnesses

during his childhood days.

Present History of Illness

Last 2008, the patient accompanied his father in the clinic of

Dr. Narag at General Tinio Street, Cabanatuan City for this follow

up check-up due to Type 2 Diabetes Mellitus. Because of

consciousness he then tried to obtain a blood glucose test and

they found out that the blood glucose level is high and diagnosed
to have Type 2 Diabetes Mellitus. Because of his diagnosis, he

became aware of the signs and symptoms of the disease and

found out frequency in urination and excessive thirst. The client

also stated that he is drinking alcoholic beverages, a smoker and

overweight. He was prescribed by his doctor a maintenance drug

(DIABETON) and is now avoiding to smoke and taking alcohol. He

is also controlling his food intake by avoiding sugar rich and

cholesterol rich food.

NUTRITION AND METABOLIC PATTERN

Usual Food Intake

 Breakfast – coffee, bread

 Lunch – rice, vegetable and 1-2 glasses of water

 Dinner – rice, vegetable and 1-2 glasses of water

Food Restriction

 Sugar rich and cholesterol rich food

Usual Fluid Intake

 6-8 glasses of water

 Problem with ability to Eat

 None

Supplement

 Multivitamins

ELIMINATION PATTERN

 Bladder : 3-4 times a day

 Bowel: Time – Morning and Afternoon

Frequency – 2 times a day

ACTIVITY AND EXERCISE PATTERN

Usual Daily Activity Exercise

 Walking and fetching water

Any Limitations of Physical Activities

 None

SLEEP PATTERN

Usual Sleep Pattern on Bed time

 9:00 PM

Usual Awaken Pattern on Morning

  5:00 AM

Hours Slept

 8 hours

Sleep Routine

 2 pillows: 1 in head, 1 in leg

PHYSICAL EXAMINATION

VITAL SIGNS

DATE TEMPERATUR PULS RESPIRATOR BLOOD

E E Y RATE PRESSURE

RATE
Novembe 36.8 70bp 18 bpm 110/70mmHg

r 20, m

2009

Weight – 63 kg (140lbs)

Height – 5’1”

BMI – 26.22
MENTAL STATUS

 Attitude: Cooperative

 Mood: Appropriate to situation

 Quantity/Quality and Organization of Speech:

understandable and with coherence of thought

BODY PARTS ASSESSMENT NORMAL

FINDINGS
> Round Palpation

SKULL >Normocephalic Round,

>Symmetrical normocephalic and

symmetrical
>Hair is evenly Inspection

HAIR distributed Evenly distributed

>Black in color
Inspection

FACE >Symmetrical Symmetrical, facial

> No voluntary expression is

movement dependent on
 feeling and mood

and no involuntary

muscle movement

Inspection

EYES >Parallel and evenly Placed evenly,

placed symmetrical, non

>Non-protruding protruding in both

>Reactive to light eyes, pink

conjunctiva, white

sclera, pupils are

reactive to light
Inspection

VISUAL FIELDS >Can see objects, When looking

place in side and straight ahead

periphery clients is still able to

distinguish objects

displayed in his

periphery
>Color is same in Inspection

EARS face Color is the same

 >Symmetrical with face,

>Flexible symmetrically

aligned auricle with

the outer cantus of

the eye
>Symmetrical Inspection

NOSE >No discharges Symmetrical and

straight

No discharge or

flaring
Inspection

LIPS >Slightly reddish- Pink and

brown symmetrical,

moisture
>Pink Inspection

GUMS >Moist Pink mucous

membrane
Inspection

TEETH >Complete teeth Align 32 sets of

teeth
>No lesion Inspection

TONGUE >Moist Moist and no lesion

 NECK >Uniform in color Inspection

>No mass No palpable masses

and no tenderness
Inspection

BREAST >Uniform in color Uniform in color

> No mass palpated No palpable masses

and no tenderness
Inspection

THORAX(ANTERIOR >Symmetrical Symmetrical

)
>No black spot on Inspection

ABDOMEN the upper umbilical Unblemished skin

>Umbilical is

centrally located
>Symmetrical Inspection

>Equal in length Equal in length

>No lesion No lesion

UPPER >No deformities No deformities on

EXTREMITIES >with complete extremities

number of digits With complete digits

>Uniform Palpation
 temperature Uniform

temperature

>Symmetrical Inspection

>Equal in length Equal in length

>No lesion No lesion

LOWER >No deformities No deformities on

EXTREMITIES >with complete extremities

number of digits With complete digits

>Uniform Palpation

temperature Uniform

temperature

Inspection

NAILS >flattened angle No discharge

and nail beds are

pink in color
 CASE DISCUSSION

ANATOMY & PHYSIOLOGY

THE DIGESTIVE SYSTEM
 The human digestive system is a complex series of organs

and glands that processes food. In order to use the food we eat,
our body has to break the food down into smaller molecules, and

it also has to excrete waste.

Most of the digestive organs (like the stomach and the

intestines) are tube-like and contain the food as it makes its way

through the body. The digestive system is essentially a long,

twisting tube that runs from the mouth to the anus, plus few other

organs (like the liver and pancreas) that produce or store

digestive enzymes.

THE DIGESTIVE PROCESS

The digestive process begins in the mouth. Food is partly

broken down by the process of chewing and by chemical action of

salivary enzymes (these enzymes are produced by the salivary

glands and break down starches into smaller molecules).

After being chewed and swallowed, the food enters the

esophagus. The esophagus is a long tube that runs from the

mouth to the stomach. It uses rhythmic, wave-like muscle

movements.
 Then, food enters the stomach which is a large, sac-like

organ that churns the food and bathes it in a very strong acid

(gastric acid). Food in the stomach that is partly digested and

mixed with stomach acids is called chyme.

After being in the stomach, food enters the jejunum, the

duodenum and then the ileum of the small intestine. In the small

intestine, bile (produced in the liver and stored in the bladder),

pancreatic enzymes and other digestive enzymes produced by

the inner wall of the small intestine help in the break down

of food.

After passing through the small intestine, food passes into

the large intestines. Here, some of the water and electrolytes are

removed from the food. Many microbes (like Bacteroides,

Lactobacillus acidophilus, Escherichia coli and Klebsiella) in the

large intestines help in the digestion process. The first part of the

large intestine is called cecum in which the appendix is

connected, food then travels upward in the ascending colon, then

travels across the abdomen in the transverse colon to the

descending colon then to the sigmoid colon.

 Solid waste is then stored in the rectum until excreted via

the anus.

The illustration above shows two cycles occurring separately to

maintain homeostasis in the body. When glucose levels are too

high the pancreas secretes insulin to convert excess glucose to

gycogen for storage. When glucose levels are too low the

pancreas produces glucagon to convert stored glycogen to

glucose, resulting in an increase in glucose levels.

DIABETES MELLITUS
DESCRIPTION

Diabetes Mellitus is a group of metabolic disorders

characterized by elevated levels of blood glucose (hyperglycemia)

resulting from defects in insulin production or secretion,

decreased cellular response to insulin or both. Because cells

cannot use glucose, fats and even proteins are broken down and

used to meet the energy requirements of the body. As a result,

body weight begins to decline. Loss of body proteins leads to a

decreased ability to fight infections, so diabetics must be careful

with their hygiene and in caring for even small cuts and bruises.

TYPES OF DIABETES MELLITUS

TYPE I DIABETES MELLITUS

TYPE 1 Diabetes Mellitus also called Insulin Dependent

Diabetes Mellitus starts in childhood or adolescence is usually

more severe than that beginning in middle or old age. Patients

have little or no ability to produce the hormone and are entirely

dependent on insulin injections for survival.

TYPE II DIABETES MELLITUS

Type 2 Diabetes Mellitus also called adult-onset diabetes

or Noninsulin Dependent Diabetes Mellitus. This form of diabetes

occurs most often in people who are overweight and who do not

exercise. Type II is considered a milder form of diabetes mellitus

because of its slow onset and can usually be controlled with diet

and oral medication. In Type II diabetes, the pancreas may

produce enough insulin, however, cells have become resistant to

the insulin produced and it may not work as effectively.

Symptoms can begin so gradually that a person may not know

that he has it.

GESTATIONAL DIABETES MELLITUS

Gestational Diabetes Mellitus 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. After delivery, blood

glucose levels in women with Gestational diabetes mellitus

usually return to normal. However, many women who have had

Gestational diabetes mellitus develop type 2 diabetes later in life.

Therefore, a woman who has Gestational diabetes mellitus should

be counseled to maintain her ideal body weight and to exercise

regularly to reduce her risk for type 2 diabetes.

 Insufficient insulin / insulin
resistance

Reduced tissue uptake of

glucose

Extracellular blood  Retinopathy

Intracellular
hyperglycemia viscosity  Neuropathy
hypoglycemia
 nephropathy

glycogenolysis Hyperosmotic Renal Decreased blood

plasma threshold of flow to O2 kidney
blood glucose supply

gluconeogenesis
Dehydration of glucosuria Stimulate rennin
cells release

Breakdown of Decreased protein Converted

fats synthesis Osmotic diaresis angiotensin I
Hyperglycemic
coma (polyuria)

High level of  cachexa Converted

ketones  lethargy angiotensin II
 poyphagia
Polydipsia
 decreased
Diabetic gamma
Vasoconstriction
ketoacidosis globulins
 susceptibility
to infections
 iimpaired  Myocardial
wound healing infarction
 Cerebrovascul
ar disease
 Peripheral
vascular disease
MANAGEMENT OF DIABETES

 TYPE I Diabetes Mellitus – Insulin

 TYPE II Diabetes Mellitus – Diet, Exercise, OHA (Oral

Hypoglycemic Agent)

 Gestational Diabetes Mellitus – Insulin, Diet, Exercise

DIET

DIABETIC DIET

 PURPOSE

Maintain blood glucose as near as normal as

possible, delay or prevent onset of diabetic

complications.

 FOODS ALLOWED

 Choose foods with low glucose index compose of:

a. 45-55% carbohydrates

b. 30-35% fats
 c. 10-25% protein

 Coffee, tea, broth, spices and flavorings can be

used as desired

 Exchange groups include milk, vegetables, fruits,

bread/starch, meat (divided in lean, medium fat,

and high fat), and fat exchanges.

 The number of exchanges allowed from each

group is dependent on the total number of calories

allowed

 Non-nutritive sweeteners (sorbitol) in moderation

with controlled, normal weight diabetics.

 FOODS TO BE AVOIDED

 Concentrated sweets or regular soft drinks

EXERCISE

 PURPOSE

 Helps burn fats which in excess may lead to

obesity that can cause serious complications.

  Not allowed during period of stress (illness or

surgery).

INSULIN

Insulin increases glucose transport into cells and promotes

conversion of glucose to glycogen, decreasing serum glucose

levels. Primarily acts in the liver, muscle, adipose tissue by

attaching to receptors on cellular membranes and facilitating

transport of glucose, potassium and magnesium. Hormone

secreted by the alpha cells of the islets of langerhans in the

pancreas. Increase blood glucose by stimulating glycogenolysis in

the liver.

 Given subcutaneously, intramuscularly or

intravenously.

TYPES OF INSULIN ONSET PEAK DURATION

1. SHORT – ACTING

o REGULAR 30 minutes 3 hours 7 hours

o SEMI LENTE to 1 hour

o HUMULIN R
2. INTERMEDIATE –
 ACTING

o LENTE 3 hours 7 hours 21 hours

o HUMULIN N

o NPH (NEUTRAL

PROTAMINE

HAGEDON)
3. LONG – ACTING

o ULTRA LENTE

o HUMULIN U 7 hours 21 hours 28 hours

o PZI (PROTAMINE

ZINC INSULIN)

CHARACTERISTICS

o CLEAR – REGULAR, HUMULIN R

o CLOUDY – REST OF INSULINS

DO’S AND DON’T’S IN ADMINISTERING INSULIN

 Check the expiration date.

 Never aspirate.

 Never massage the injection site.

 Never inject a cold insulin.

 Rotate the injection site.

ORAL HYPOGLYCEMIC AGENT

If normal blood glucose levels are not achieved after 2-3

months of lifestyle modifications, treatment with an oral

antihyperglycemic drug is often prescribed. However, the patient

should be clearly advised that the ability of any drug therapy to

improve the health of any diabetic patient is aided by appropriate

changes in diet and activity level.

 SULFONYLUREAS

The sulfonylureas are group of oral antidiabetic

drugs that are able to stimulate insulin secretion from

the beta cells of the pancreas. This increased insulin

then helps to transport the glucose out of the blood and

into the tissues, cells and organs in which it is needed.

They may also enhance the actions of insulin in muscle,

liver and adipose tissue, which allows these tissues to

take up and store glucose more easily as a later source

of energy. They may also increase the availability of

 insulin by preventing the liver from breaking insulin

down as fast as it ordinarily would. In summary, the

overall effect of the sylfonylureas is that they improve

both insulin secretion and the sensitivity to insulin in

tissues.

 CHLORPROPAMIDE (DIABINASE)

 TOLBUTAMIDE (ORINASE)

 GLIMEPIMIDE (SOLOSA)

 ACETOHEXAMIDE (DYMELOR)

 MEGLITINIDES

These are structurally different from the

sulfonylureas but have similar mechanism of action in

that they also increase insulin secretion form the

pancreas.

 REPAGLINIDE (NOVONORM)

 ROSIGLITAZONE (AVANDIA)
 BIGUANIDES

Have complex peripheral actions in the presence

of residual insulin, increasing glucose uptake in striated

muscle and inhibiting hepatic glucose output and

intestinal glucose absorption. It does not stimulate

insulin release.

 METFORMIN

 THIAZOLIDINEDIONES

Increase insulin sensitivity and lower blood

glucose in type 2 diabetes. Work to decrease insulin

resistance by enhancing the insulin sensitivity of insulin

receptors in such areas as the liver, skeletal muscle and

adipose tissue. These results in enhanced glucose

 uptake and storage have no known effect on insulin

secretion.

 ROSIGLITAZONE

 DIOGLITAZONE

 ALPHA-GLUCOSIDASE INHIBITORS

These drugs reduce carbohydrate digestion and

delay rate of glucose absorption. Take with first bite of

the meal or 15 minutes after. Less commonly used than

the oral drug classes.

 ACARBOSE

 MIGLITOL

 VOGLIBOSE
CLINICAL MANIFESTATIONS:

Manifested by client: Signs and Symptoms (from

the book)

 Polyuria  polyuria

 Weight loss  polydipsia

 polyphagia
 Poly dipsia

 fatigue

 weakness

 sudden vision changes

 tingling or numbness in

hands or
  feet

 weight loss

 sores that heal slowly

 dry skin

RISK FACTORS OF TYPE II DM

OBESITY

Obesity is a medical condition in which excess body part

has occumulated to the extent that it may have an adverse effect

on health, leading to reduce life expectancy. Body mass index,

which compares weight and height, is used to define a person as

overweight when their BMI is between 25 kg/m2 and 30kg/m2 and

obese when it is greater than 30 kg/m2 .

The primary treatment for obesity is dieting and physical

exercise. If this fails, antiobesity drugs may be taken to reduce

appetite or inhibit fat absorption.

IMPAIRED GLUCOSE TOLERANCE

 Several factors have contributed to induce the impairment

of glucose tolerance in the elderly. Especially, changes of body

composition with aging, the loss of skeletal muscle mass and

relatively increased fat tissues, could occur the insulin resistance

state. Such state would be well known to accompany with

diabetes mellitus and hypertension. Therefore, the treatment of

hypertension with diabetes in the elderly would be very important

to prevent not only microangiopathy but also macroangiopathy.

The optimal blood pressure levels to reduce hypertension –

related morbidity and mortality in diabetic elderly have been

proposed 130/85. The first step therapy in this case would be

recommended calcium channel blocker, angiotensin converting

enzyme inhibitor, and angiotensin receptor blocker. In addition,

comprehensive geriatric assessment must be important to

maintain drug compliance for well controlled blood pressure

levels.

GENETICS/HEREDITARY
 In a study of 200 adults with type 2 diabetes, about 2/3

reported atleast one close relative with diabetes and nearly 50 %

had atleast two relatives with the disease. In particular, people

whos mother had diabetes where twice as likely to get the

disease as those whos father had diabetes.

RACE

Diabetes occurs more often in Hispanic/Latino Americans,

African-Americans, Native Americans, Asian Americans, Pacific

Islanders, and Alaska Natives.

HYPERTENSION

Hypertension, or high blood pressure, is a major risk factor

of diabetes. High blood pressure is generally defined as 140/90

mmHg or higher. Low levels of HDL ( good cholesterol) and high

triglyceride levels also put you at risk.

SEDENTARY LIFESTYLE
 Being inactive – exercising fewer than 3 times a week

makes you more likely to develop diabetes.

AGE

Some doctors advise anyone over 45 to be screened for

diabetes. That’s because increasing age puts you at higher risk of

developing type 2 dibetes. It’s important to remember, though,

that people at any age can develop diabetes.

PREVENTION
 Maintain body weight and prevent obesity through proper

nutrition and physical activity/exercise.

 Encourage proper nutrition – eat more dietary fiber, reduce

salt and fat intake, avoid simple sugars like cakes and

pastries; avoid junk foods.

 Promote regular physical activity and exercise to prevent

obesity,hypercholesterolimia, and enhance insulin action in

the body.

 Advise smoking cessation for active smokers and prevent

exposure to second hand smoke. Smoking among diabetes

increases risk for heart attack and stroke.

 DIABETIC KETOACIDOSIS (DKA)

Ketoacidosis is a serious condition that can lead to diabetic

coma or even death. When the cells don’t get the glucose they

need for energy, your body begins to burn fat for energy, which

produces ketones. Ketones are acids that build up in the blood

and appear in the urine when your body doesn’t have enough

insulin. Ketoacidosis may happen to anyone with diabetes, though

it is rare in people with Type 2.

CLINICAL MANIFESTATIONS

EARLY SYMPTOMS INCLUDE:

  Thirst or a very dry mouth

 Frequent urination

 High blood glucose levels

 High levels of ketones in the urine

 Polyphagia

OTHER SYMPTOMS APPEAR

 Constantly feeling tired

 Dry or flushed skin

 Nausea, vomiting or abdominal pain

 Short, deep breaths

 Fruity odor or breath

 Confusion

HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC

SYNDROME (HHNS)
 Hyperglycemic Hyperosmolar Nonketotic Syndrome is a

serious condition most frequently seen in older persons. HHNS

can happen in either type 1 or type 2 diabetes, but it occurs more

often in people with type 2. In HHNS, blood sugar levels rise, and

your body tries to get rid of the excess sugar by passing it into

your urine. If HHNS continues, the severe dehydration will lead to

seizures, coma and eventually death.

CLINICAL MANIFESTATIONS

 Blood sugar level over 600 mg/dl

 Dry, parched mouth

 Extreme thirst

 Weakness

 Weak, rapid pulse

 Polyuria

 Polydipsia

 Polyphagia
 NEPHROPATHY

Kidneys are remarkable organs. Inside them are millions of

tiny blood vessels that act as filters. Their job is to remove waste

products form the blood. Diabetes can damage the kidneys and

cause them to fail. High levels of blood sugars make kidneys filter

too much blood. At this extra work is hard on the filters. After

many years, they start to leak and useful protein is lost in the

urine.

CLINICAL MANIFESTATIONS

The kidneys work hard to make up for the failing capillaries

so kidney disease produces no symptoms until most all functions

are gone. The first symptom of kidney disease is often fluid build

up. Other symptoms of kidney disease include:

 Loss of sleep

 Poor appetite

 Weakness
  Microalbuminuria

RETINOPATHY

Retinopathy is a damage to the retina caused by

complications of diabetes mellitus, which can eventually lead to

blindness. It is an ocular manifestation of systematic disease

which affects up to 80% of all patients who have had diabetes for

10 years or more.

CLINICAL MANIFESTATIONS

Diabetic retinopathy often has no warning signs.

 Blurring of vision

 Few specks of blood

 Floating spots
 HYPOGLYCEMIA

Hypoglycemia, sometimes called an insulin reaction, can

happen even during those times where you’re doing all you can to

manage your diabetes.

CLINICAL MANIFESTATIOS

 Shakiness

 Dizziness

 Sweating

 Hunger

 Pale skin color

 Clumsy or jerky movements

 Confusion

NEUROPATHY
 Neuropathy affects all peripheral nerves: pain fibers, motor

neurons, autonomic nerves. It therefore necessarily can affect all

organs and systems since all are innervated

CLINICAL MANIFESTATIONS

 Numbness and tingling of extremities

 Decreased or loss of sensation to a body part

 Muscle weakness

 Difficulty swallowing

 Speech impairment

 Vision changes

 Urinary incontinence

MACROVASCULAR DISEASES

Cerebrovascular disease is a group of brain dysfunctions

related to disease of the blood vessels supplying the brain.

Hypertension is the most important cause; it damages the blood

vessel lining, endothelium, exposing the underlying collagen

where platelets aggregate to initiate a repairing process which is

not always complete and perfect. Sustained hypertension

permanently changes the architecture of the blood vessels

making them narrow, stiff, deformed, uneven and more

vulnerable to fluctuations in blood pressure.

A fall in blood pressure during sleep can then lead to a

marked reduction in blood flow in the narrowed blood vessels

causing ischemic stroke in the morning. Conversely, a sudden rise

in blood pressure due to excitation during the daytime can cause

tearing of the blood vessels resulting in intracranial hemorrhage.

Cerebrovascular disease primarily affects people who are elderly

or have a history of diabetes, smoking, or ischemic heart disease.

Myocardial infarction (MI) or acute myocardial

infarction (AMI), commonly known as a heart attack, is the

interruption of blood supply to part of the heart, causing some

heart cells to die. This is most commonly due to occlusion

(blockage) of a coronary artery following the rupture of a

vulnerable atherosclerotic plaque, which is an unstable collection

of lipids (fatty acids) and white blood cells (especially

macrophages) in the wall of an artery. The resulting ischemia

(restriction in blood supply) and oxygen shortage, if left untreated

for a sufficient period of time, can cause damage or death

(infarction) of heart muscle tissue (myocardium).

PERIPHERAL VASCULAR DISEASE

In peripheral vascular disease, a diabetic client can develop

arterial occlusion and thrombosis that can lead to gangrene but

this can be developed years after you have been diagnosed of

diabetes mellitus and not properly treating it. Both the types of

diabetes mellitus have a risk to develop this type of disease.

CLINICAL MANIFESTATIONS

 Tingling sensation of affected area

 Numbness / loss of sensation

 Pale skin color

 DIAGNOSTIC EXAMS

 Random blood glucose test (RBS)

For a Random blood glucose test, blood can be drawn at

any time throughout the day, regardless of when the person

last ate. A random blood glucose level of 200mg/dl

(11.1mmol/L) or higher in persons who have symptoms of

high blood glucose suggest a diagnosis of diabetes.

 Fasting blood glucose test (FBS)

Fasting blood glucose testing involves measuring blood

glucose after not eating or drinking for 8 to 12 hours (usually

overnight). A normal fasting blood glucose level is <100 mg/dL. A

fasting blood glucose of 126 mg/dL (7.0 mmol/L) or higher

indicates diabetes. The test is done by taking a small sample of

blood from a vein or fingertip. It must be repeated on another day

to confirm that it remains abnormally high.

 Hemoglobin A1C test (HbA1c)

The A1C blood test measures the average blood glucose

level during the past 2 to 3 months. It is used to monitor blood

glucose control in people with known diabetes, but is not normally

used to diagnose diabetes. Normal values for A1C are 4 to 6

percent. The test is done by taking a small sample of blood from a

vein or fingertip.

 Oral glucose tolerance test (OGTT)

Oral glucose tolerance testing is the most sensitive test for

diagnosing diabetes and pre-diabetes. However, the OGTT is not

routinely recommended because it is inconvenient compared to a

fasting blood glucose test.

The standard OGTT includes a fasting blood glucose test.

The person then drinks a 75 gram liquid glucose solution (which

taste very sweet, & is usually cola or orange flavored). Two hours

later, a second blood glucose level is measured.

INDICATORS

NORMAL VALUES
Random Blood Sugar 90 to 140 mg/dL
Fasting Blood Sugar 70 to 110 mg/dL
Post Prandial Blood Sugar < 200 mg/dL
Glycosylated Hemoglobin 4.5 to 6.5%

(HbA1c)
Blood Pressure 120/80 mmHg
Pulse Rate 60-100 bpm
Respiratory Rate 16-20 bpm
Temperature 36.8-37 oC
 NURSING DIAGNOSIS

 Risk for fluid volume deficit related to frequent

urination.

Goal: Provision of fluid balance. Demonstrate adequate

hydration as evidenced by stable vital signs palpable peripheral

pulses, good skin turgor and capillary refill, individually

appropriate urinary output.

 Risk for infection related to insufficient knowledge on

Proper wound care.

Goal: Have knowledge on proper wound care. Identify

interventions to prevent or reduce risk of infection. Demonstrate

techniques, lifestyle changes to prevent development of infection.

  Imbalanced Nutrition: less than body requirements

related to inability to utilize nutrients.

Goal: Maintain normal nutritional status. Demonstrate stabilized

weight or gain toward usually or desired range.

NURSING CARE PLAN

NURSING DIAGNOSIS: Risk for fluid volume deficit related to

frequent urination.

Goal: Provision of fluid balance. Demonstrate adequate hydration

as evidenced by stable vital signs, palpable peripheral pulses,

good skin turgor and capillary refill, individuality appropriate

urinary output.

INTERVENTIONS RATIONALE

1. Obtain history from 1. Assists in estimation of

 patient related to total volume depletion.

duration of intensity of

symptoms like excessive

urination.

2. Weight daily and record 2. Rapid losses or gains of

data gathered. 5%

more of total body weight

indicate moderate to severe

fluid volume deficit or excess.

3. Monitor vital signs:

a.Body temperature 3a. A decreased body

temperature may result from

hypovolemia. Although fever,

chills, diaphoresis are

common with infection

process, fever with flushed,

dry skin may reflect

dehydration.

b. Pulse rate
 3b. An increased pulse

rate and a weak, thread

pulse may occur with fluid

volume deficit.

c. Respiratory rate

3c. Correction of

hyperglycemia will cause the

rate and pattern to approach

normal. In contrast,

increased work of breathing,

shallow, rapid respirations;

and presence of cyanosis

may indicate respiratory

d. Blood Pressure fatigue.

3d. Hypovolemia may

be manifested by

hypotension and tachycardia.

Estimates the severity of

hypovolemia may be made

 when patient’s systolic blood

pressure drops more than

10mmhg from a Recumbent

to a sitting or standing

position.

4. Maintain fluid intake of 4. Adequate and increase in

at least 2500 ml/day fluid intake can maintain

within cardiac tolerance hydration or circulating

when oral intake is volume.

resumed.
NURSING DIAGNOSIS: Risk for infection related to

insufficient knowledge on proper wound care.

Goal: Have knowledge on proper wound care. Identify

interventions to prevent or reduce risk of infection.

Demonstrate techniques, lifestyle changes to prevent

development of infection.

INTERVENTIONS RATIONALE

1. Observe for signs of 1. Proper assessment for

infection and signs of infection can

inflammation, like fever, prevent any other

flushed appearance, complication and can

wound drainage. provide essential care.

2. Educate the patient on 2. Prevention of infection is

how to care properly the best achieved through

wounds on step by step following the guidelines

process. of wound care obtained

during educating

process.

3. Change wound 3. Proper application and

dressings if needed changing of wound

using proper techniques dressing can facilitate

of changing and the prevention of

disposing contaminated progress or transfer of

materials. infection.

4. Fruits rich in vitamin c

4. Encourage patient to eat can boost the immunity

foods rich in vitamin c of an individual which

like citrus, oranges, helps him fight infection.

pineapple etc.
NURSING DIAGNOSIS: Imbalanced Nutrition: less than body

requirements related to inability to utilize nutrients.

GOAL: Maintain normal nutritional status. Demonstrate stabilized

weight or gain toward usual/desired range.

INTERVENTIONS RATIONALE

1. Weight daily or as 1. Assesses adequate of

indicated. nutritional intake

By absorption and

utilization of

nutrients.

2. Identify food 2. If patient’s food

preferences, including preferences can be

ethnic/cultural needs. incorporated into the

meal plan,
 cooperation with

dietary requirements

may be facilitated.

3. Discuss proper 3. Proper intake and

distribution of meals distribution of meals

that the client prefers can help an individual

but may contribute in to maintain, reduce,

maintaining normal or gain the ideal

body weight. weight that he should

achieve.
 NURSING CARE PLAN FOR

COLLABORATIVE PROBLEMS

DIABETIC KETOACIDOSIS

INTERVENTION RATIONALE
1. Monitor for signs and

symptoms of diabetic

ketoacidosis

 When large amounts of

a. Polyuria, dehydration
glucose build up in its

blood stream the glucose

is removed from the body

in urine. Additional water

excreted to dilute the

glucose, as a result patient

begin to urinate more

 frequently. Frequency in

urination can cause

dehydration.

 Diabetic retinopathy is one

of the possible
b. Blurred vision
complication of diabetes,

therefore the importance

of careful management is

emphasized to show the

progression of visual

changes.

 Lungs remove carbonic

c. Respiratory pattern,
acid through respirations,
e.g., Kuss maul’s
producing a compensatory
respirations
alkalosis for ketoacidosis.

Acetone breath is due to

breakdown of acetoacetic

acid and should diminish

as ketosis is corrected

 Correction of
 hyperglycemia and

acidosis will cause the

d. Temperature, skin color respiratory rate and

and moisture pattern to approach

normal. In contrast,

increased work of

breathing; shallow, rapid

respirations; and presence

of syanosis may indicate

respiratory fatigue and/or

that patient is losing ability

to compensate for

acidosis.

e. Note orthostatic BP  Hypovolemia may be

changes manifested by hypotension

and tachycardia. Estimates

of severity of hypovolemia

may be made when

patient’s systolic BP drops

more than 10 mmHg from

 a recumbent to a

sitting/standing position.

2. Monitor intake and output  Provides on going estimate

of volume replacement

needs, kidney functions

and effective of therapy.

 For client to be aware of

3. Client education about the
the disease.
disease
 HYPEROSMOLAR HYPERGLYCEMIA NON-KETOTIC

SYNDROME

INTERVENTION RATIONALE
1. Monitor for signs and  Hyperosmolar

symptoms of Hyperglycemia Non-ketotic

Hyperosmolar Syndrome or coma is a

Hyperglycemia Non-ketotic state of marked

Syndrome dehydration and excessive

hyperglycemia with blood

glucose of 600 to 2,000

a. Blood glucose of 600- mg/dL. Because of severe
2000/dL hyperglycemia, it leads to

hyperosmolarity and
Severe dehydration
osmotic dieresis which
Serum osmolarity 350
cause severe dehydration.
mOsm/kg
There is body weakness,

increased thirst, nausea,

lethargy and coma.

 Hypotension in
 b. Hypotension Hyperosmolar

hyperglycemia non-ketotic

syndrome is due to severe

dehydration that needs for

immediate fluid

replacement.

HYPOGLYCEMIA

INTERVENTION RATIONALE
1. Monitor for signs and

symptoms of

hypoglycemia such as:

a. Hunger  hypoglycemia may occur

b. Sweating because of omission of

c. Tremor meals. Because of lack of

d. Tachycardia glucose, cells in the body

e. palpitations cannot produce enough

energy that will later on be

 used on daily activity. This

can result to tremors and

palpitations. Profuse

sweating indicates

hypoglycemia so

administration of insulin

should be avoided.

 Eating full meals at a

2. encourage patient to eat certain time can help

full meals and snacks as prevent the occurrence of

prescribed in the meal hypoglycemia. Juice, milk

plan. or glucose tablets are used

for treatment of

hypoglycemia.

DIABETIC RETINOPATHY

INTERVENTIONS RATIONALE
1. Monitor for sign and 1. Diabetic Retinopathy is

symptoms of diabetic caused by changes in the

retinopathy small blood vessels in the

retina, the area of the eye

that receives images and

sends information about

the image of the brain.

a. 1-a.3. Asymptomatic
a. Stages of
retinopathy blood vessels
retinopathy.
within the retina develop
a. 1 non proliferative
microaneutysms that leak
a. 2 preproliferative
fluid, causing swelling and
a. 3 proliferative
forming deposits or

exudates. In some cases

macular edema causes

distorted vision. In

proliferative retinopathy

there are more widespread

 vascular changes and loss

of nerve fivers. It

represents increase

destruction of retinal

vessel while in proliferative

neuropathy there is an

abnormal growth of blood

vessel in the retina. New

vessels rupture, bleeding

into vitreous and blocking

light. Raptured blood

vessels in the vitreous

forms scar tissue, which

can full on and detached

the retina.
b. Retinal changes

b. Even though a patient may

have no vision

impairment, retinal
 changes notice during a

vision exam can be

symptoms of diabetic

retinopathy. These

changes include retinal

swelling, blood vessels

leaking fluids, and any scar

tissue or abnormal

deposits on the retina.

c. Floaters

c. Floaters are small shadows

cast on the retina by tiny

floating cells of vitreous

pulls away from the back

of the eye. Blood cells that

have leaked in the vitreous

can also lead to floaters. It

is manifested as small

spots that are suspended

 or moved around within

the line of vision.

d. Spotty, blurry, or
d. When floaters become
hazy vision.
more plenty full in the

vitreous, and

microneurysm cause blood

and other fluid to leak into

the retina, vision become

increasingly, and impaired.

Patient lose the ability

tosee objects with great

detail and often have

difficulty driving at night or

experience blind spots in

part of their visual fields.

e. Difficulty of
e. When the retina is
breathing
 damaged, if often distorts

like ice and ability to focus

on thing close up leading,

sewing, writing and other

activities, requiring

adequate focusing power

become more and difficult.

DIABETIC NEPROPATHY

INTERVENTIONS RATIONALE
1. Monitor for signs and

symptoms of diabetic
nephropathy

a. Uncontrolled diabetes a. Nephropathy or renal

disease secondary to

diabetic microvascular in

the kidney is a common

complication of diabetic.

About 20 to 30% of people

with type 1 and type 2

diabetes develops

nephropathy but fewer of

those with type 2 diabetes

progress to end stage

renal disease.

b. Patients with type 1

b. Hypertension diabetes mellitus

frequently show initial

changes of renal disease

after 10 to 15 years,
 whereas patients with type

2 diabetes within 10 years

after diagnosis. Many

patient with type 2

diabetes develop renal

disease within 10 years

after the diagnosis of

diabetes. Many patients

with type 2 diabetes had

diabetes for many years

before the diabetes is

diagnosed and treated.

Therefore, they may have

evidence of nephropathy

at the time of diagnosis

c. Protenuria c. & d. If blood glucose

d. Elevated WBC levels are elevated,

consistently for significant

 period of time,the kidneys

filtration mechanism is

stressed, allowing blood

proteins to leak into urine.

It is thought that this

elevated pressure serves

as a stimulus for the

development of

nephropathy.

MACROVASCULAR DISEASE

INTERVENTION RATIONALE
 Assess Characteristics of  Assisting the client in pain

chest pain including may differentiate existing

a. Location & current pain patterns as

b. Duration well as identify

 c. Intensity complications

 Obtain history of previous  This provides information

cardiac pain and familial that may help to

history of cardiac problem differentiate current pain

from previous problems &

complications

 Respiratory rate may be

 Assess respiratory rate,
increased as a result of
blood pressure and heart
pain & associate anxiety.
rate each episode of chest

pain.

 Decrease oxygen

consumption & demand to

 Maintain bed rest, during
reduce competing stimuli
pain position of comfort,
and reduce anxiety.
maintain relaxing

environment to promote

calmness.
 Pain control is a priority as
 Administer medications it indicates ischemia.

and monitor response to

drug therapy notify

physician if rain does not

abate.

NEUROPATHY

INTERVENTION RATIONALE
 Initial symptoms of

peripheral Neuropathy

includes:
a. Paresthesia (prickling,  As the neuropathy

tingling or lightened progress, the feet become

sensation) numb. In addition, a

decrease in

propriconception and a

decreased sensation of

light touch may lead to an

unsteady gait. Decreased

sensation of pain and

temp. place patient with

neuropathy at increased

risk for injury and

undetected foot infections

b. Burning sensation  Delayed gastric emptying

may occur with the typical

symptoms of early saliety,

bloating nausea and

vomiting. In addition there

 may be unexplained wide

swings in blood glucose

levels related to

inconsistent absorption of

glucose from ingested

foods secondary to

inconsistent gastric

emptying.

 Manifestation of autonomic  A decreased sensation of

neuropathies related to bladder fullness and

a. Gl urinary symptoms of

b. Renal system neurogenic.

 Urinary retention  Bladder, result from

autonomic neuropathy.

Patient with neurogenic

bladder are pre disposed

to developing urinary
 EVALUATION

After an exposure to the community, the client:

 Participated in planning the activities and started showing

operation in every task he makes.

 The client will be able to gain knowledge about possible

complications of the disease.

 Demonstrated compliance with dietary restrictions and to

take his medication as scheduled and how to manage any

side effects of therapy.

 Experienced increase comfort.

After an exposure to the community, the students:

 We, the students realize the value of teamwork and

cooperation as an integral part and the smooth flow of our

work in the area fostering unity thereby leading us to

effective nursing care provider and satisfaction as well.

 We are able to identify the problem as well as discussing its

causes, manifestation, treatment and prevention of the

possible complications.

 To know the common disease found in the community.

 Assist the client in developing ways to incorporate the

therapeutic plan into their lives rather than merely giving

client list of instruction.

 Recommendation

 Have a regular check-up and follow therapeutic regimen.

 Provide an extra effort in managing his disease.

 Advise to avoid stressors that trigger to his disease.

 Instruct the client on how to promote and maintain

nutritional status.

 Advise the client to avoid alcoholic beverages or to limit his

intake because alcohol interference with the utilization of

essential nutrients.