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 TEMPERATURE PULSE RESPIRATORY BLOOD

RATE RATE PRESSURE

November 36.8 70bpm 18 bpm 110/70mmHg

20, 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 and No discharge

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

Intracellular Extracellular blood  Retinopathy

hypoglycemia hyperglycemia viscosity  Neuropathy
 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
 decreased Polydipsia
gamma
Diabetic Vasoconstriction
globulins
ketoacidosis  susceptibility
to infections
 iimpaired
wound healing  Myocardial
infarction
 Cerebrovascular
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/m 2 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 5%

data gathered. more of total body weight

indicate moderate to severe

fluid volume deficit or excess.

3. Monitor vital signs: 3a. A decreased body

a.Body temperature 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 fatigue.

 d. Blood Pressure 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 dressings

if needed using proper 3. Proper application and

techniques of changing changing of wound

and disposing dressing can facilitate

contaminated materials. the prevention of

progress or transfer of

infection.
4. Encourage patient to eat

foods rich in vitamin c

4. Fruits rich in vitamin c
 like citrus, oranges, can boost the immunity

pineapple etc. of an individual which

helps him fight infection.

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. If patient’s food
2.Identify food preferences can be

preferences, including incorporated into the

ethnic/cultural needs. meal plan,

cooperation with

dietary requirements

may be facilitated.

3. Proper intake and

3.Discuss proper distribution of meals

distribution of meals can help an individual

that the client prefers to maintain, reduce,

but may contribute in or gain the ideal

maintaining normal weight that he should

body weight. 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 complication

b. Blurred vision
of diabetes, therefore the

importance of careful

management is emphasized

to show the progression of

visual changes.

 Lungs remove carbonic acid

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

respiratory rate and pattern

d. Temperature, skin color
to approach normal. In
and moisture
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.

 Hypovolemia may be

manifested by hypotension

and tachycardia. Estimates

e. Note orthostatic BP
of severity of hypovolemia
changes
may be made when

patient’s systolic BP drops

more than 10 mmHg from a

recumbent to a
 sitting/standing position.

 Provides on going estimate

of volume replacement

needs, kidney functions

2. Monitor intake and output
and effective of therapy.

 For client to be aware of the

disease.

3. Client education about the

disease
 HYPEROSMOLAR HYPERGLYCEMIA NON-KETOTIC

SYNDROME

INTERVENTION RATIONALE
1. Monitor for signs and  Hyperosmolar

symptoms of Hyperosmolar Hyperglycemia Non-ketotic

Hyperglycemia Non-ketotic Syndrome or coma is a

Syndrome state of marked

dehydration and excessive

hyperglycemia with blood

a. Blood glucose of 600- glucose of 600 to 2,000

2000/dL mg/dL. Because of severe

hyperglycemia, it leads to
Severe dehydration
hyperosmolarity and
Serum osmolarity 350
osmotic dieresis which
mOsm/kg
cause severe dehydration.

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.

2. encourage patient to eat  Eating full meals at a

full meals and snacks as certain time can help

prescribed in the meal plan. prevent the occurrence of

hypoglycemia. Juice, milk

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.
a. 1 non proliferative
within the retina develop
a. 2 preproliferative
a. 3 proliferative
microaneutysms that leak

fluid, causing swelling and

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 are small shadows

c. Floaters 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. When floaters become more

 plenty full in the vitreous,

and microneurysm cause

blood and other fluid to leak

into the retina, vision

d. Spotty, blurry, or
become increasingly, and
hazy vision.
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. When the retina is

damaged, if often distorts

like ice and ability to focus

on thing close up leading,

sewing, writing and other

activities, requiring

adequate focusing power

e. Difficulty of become more and difficult.

breathing
 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. & d. If blood glucose

c. Protenuria levels are elevated,

d. Elevated WBC 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

it indicates ischemia.

 Administer medications

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.

 A decreased sensation of

bladder fullness and

 Manifestation of autonomic
urinary symptoms of
neuropathies related to
neurogenic.
a. Gl
 Bladder, result from
b. Renal system
autonomic neuropathy.
 Urinary retention
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.