Holy Angel University

Angeles City
College of Nursing
AY 2008-2009

CHRONIC KIDNEY DISEASE

secondary to
TYPE 2 DIABETES MELLITUS

Presented by:
Group No. 4
N-402

Presented to:
Mr. Christian G. Garcia RN

June 28, 2010

 I.

INTRODUCTION

Chronic Kidney Disease (CKD) or Chronic Renal Disease is a progressive loss of

renal function over a period of months or years. It is diagnosed by screening people that are at

risk of the disease such as those with hypertension, Diabetes Mellitus and one who has a

history of renal disease in their family. The loss of protein and red blood cells through the

urine may indicate an early stage of the disease. The progression of it is characterized and

identified with increased creatinine levels from blood test which indicates falling of the

glomerular filtration rate as a result of the kidneys’ decreased ability to excrete waste

products. Some diagnostics to fully investigate the disease and its progression includes blood

tests, renal biopsy and medical imaging.

CKD is classified according to its severity in five stages. Stage 1 being the mildest

and causing no signs and symptoms while stage 5 which is a severe illness and with poor life

expectancy, it is also known as the established chronic kidney disease and synonymous to

End-Stage Renal Disease (ESRD), Chronic Kidney Failure (CKF), or Chronic Renal Failure

(CRF). There are no specific treatments that can hamper the progression of the disease. If

there is an underlying cause, such as in vasculitis, this may be treated directly and slow the

damage. Dialysis and kidney transplant are forms of renal replacement therapy that are

required treatments for more advanced stage of the disease.

According to data collected from 120 countries with dialysis programs, at the end of

2005 about 1,900,000 people were receiving renal replacement therapy (RRT). Among these

individuals, 1,297,000 (68%) received hemodialysis and 158,000 (8%) received peritoneal

dialysis; although an additional 445,000 (23%) were living with a kidney transplant. Precise

estimates of ESRD incidence and prevalence remain elusive.

(http://clinicalevidence.bmj.com/ceweb/)
 Worldwide, the highest incidence and prevalence rates are reported from the USA,

Taiwan, and Japan. In America, 34% of cases of ESRD each year are caused by diabetes,

25% by hypertension, 16% by glomerulonephritis, and 4% by kidney cysts. (Renal Data

Report, ANS, 1999)

In the Philippines, as of 2005, there is 2.6% of the total population of ages 20 years

and above that suffers from stage 3-5 of the disease. 2.2% comes from stage 3, 0.2% from

stage 4 and the other 0.2% from the stage 5 or the end stage.

End Stage Renal Disease (its progressed state) is already the 7th leading cause of

death among Filipinos. The population of ESRD patients requiring dialysis therapy in Asia is

expanding at a faster rate than in the rest of the world. In Philippines, the dialysis population

is growing at a rate of 10% or more annually. It is said that a Filipino is having the disease

hourly or 120 Filipinos per million populations per year. This shows that about 10, 000

Filipinos need to replace their kidney function. Unfortunately though only 73% or about 7,

267 patients received treatment. An estimate of about a quarter of the whole population

probably just died without receiving any treatment

Sugar mommy, a patient at Angeles Medical Center in the female ward bed 1, was

diagnosed with Chronic Kidney Disease (CKD) secondary to Diabetes Mellitus type 2. Her

current condition (as to what made her rush to the hospital), which is CKD, may be brought

about by the poor management of her progressive DM type2.

Diabetes Mellitus (DM) is a chronic disease characterized by relative or absolute

deficiency of insulin, resulting to glucose intolerance. This lack of insulin results to failure to

transfer glucose from the plasma to the cells. Insulin is a hormone that is needed to convert

sugar, starches and other food into energy needed for daily life. The body responds by the

stimulation of glucogenolysis, gluconeogenesis, and lipolysis producing ketone bodies as if it

is in the fasting state. Generally there are two types of Diabetes Mellitus namely type 1
(Insulin-dependent diabetes mellitus, IDDM) and type 2 (non-insulin-dependent diabetes

mellitus, NIDDM). It is the accumulation of the glucose absorbed from the meal in the blood

(hyperglycemia) to be excreted in the urine (glycosuria).

Diabetes Mellitus type 2 (non-insulin-dependent diabetes mellitus, NIDDM) has three

factors. First is the impaired insulin release resulting to failure of normal handling of the

glucose absorbed from the food. Second is the defect in tissue response to insulin which is

caused by the defective insulin receptors on the target cells. And third is inflammation.

Genetics, obesity and lack of exercise are believed to be the cause of the disease.

Per record, there are more than 24 million people in the United States and 190 million

people worldwide with diabetes (95% Type 2). Diabetes continues to grow at epidemic levels

as it affects more children and kills more people each year than AIDS and breast cancer

combined. “Diabetes is the fifth-deadliest disease in the United States, and it has no cure. But

let us bring the picture to the Philippines; it has 95% comprising the Type 2 diabetes (adult

onset). If we are going to plot diabetes, Type 2 form is much higher in percentage compared

to Type 1 diabetes, mostly obese individuals are affected and in the Philippines it is the Type

2 form of diabetes that dominates the disease spectrum.

A. OBJECTIVES

General Objective:

The main goal of the group is to be able to present the case study of our chosen client

that would provide a comprehensive discussion of the pathological mechanism of the disease

to yield significant information for the case study.

Specific Objectives:

In order to meet the general objective, the group aims to:

 establish rapport to the patient and the patient’s significant others;

 interpret the pertinent data gathered from the patient and her significant others;

 state past and present health history of the patient;

 trace the family genogram;

 present the cephalocaudal assessment obtained from the patient;

 discuss the anatomy and physiology of the organ involved in the patient’s

disease;

 trace the pathophysiology of the patient’s disease;

 interpret the laboratory test results of the patient;

 discuss the nature of the drugs given to the patient;

 present a specific, measurable, attainable, realistic and time-bounded nursing

care plans for the client; and

 provide the patient and family with proper discharge planning;

 II.

NURSING HISTORY

1. Personal History
A. Demographic Data

Sugar mommy, a 50 year old female married to Sugar Daddy living in Angeles City.
Sugar mommy was born on February12, 1960. She was blessed with 4 children, one of them
is married, the two are working in Manila and the other one stays at home to take care of her.
She was admitted last June 19, 2010 at Angeles Medical Center.

B. Socio Economic and Cultural Factors

B.1 Occupation and mode of expenditure

Sugar mommy never got a chance to work since she got married at an early age. Her
husband already stopped working, in the construction, site to take care of her. Currently, her
2 children in Manila are providing for them. Medical bills as well as expenditures at home
are being shouldered by these two daughters. According to sugar mommy, she also has a
monthly allowance of 2,000 pesos. With this money, she buys a bottle of soft drinks every
day and she eats a lot of rice too though she knows that these should not be part of her diet.

B.2 Educational Attainment

Sugar mommy finished high school at Holy Angel University. She failed to attend
college due to financial constriction. She also got married at a young age.

B.3 Religious affiliation

Sugar mommy is a Roman Catholic. She used to be a regular church goer but the
worsening of her condition January of 2009 led to her non-attendance of mass every Sunday.
She watch televised mass instead.

B.4 Cultural Factors Affecting health of the Family

Mrs. Sugar Mommy goes to “mananawas” for minor illnesses such as cough and
colds and tend to self medicate. Only when the illness is severe that she and her family go to
the hospital to seek medical treatment.

2. Family- Health Illness History

 a. Hereditary disease in family

Sugar mommy’s father died of diabetes. While on her mother’s side, they are known
to have hypertension and a lot died of stroke.

b. Existing disease in the family.

Sugar mommy was diagnosed 12 years ago of Diabetes mellitus type 2. She also has
hypertension as with her siblings. She’s the only diabetic though.
Family – Health Illness History

Grandfather Grandmother Grandfather Grandmother

Father Mother

Sugar
Mommy
- Diabetes Mellitus type 2

- Hypertension

Sibling - Stroke

- Goiter

- Dead

Sibling
History of past illness

Sugar mommy had already chicken pox, measles, mumps and rubella. When she was

17 years old, she had goiter and undergone thyroidectomy. She was hospitalized 12 years ago

and was diagnosed with type 2 diabetes. After a year, she was hospitalized again due to a

recurring goiter. Last January, 2009 she became very ill and her diabetes affected her kidney.

She was comatose at the Intensive Care Unit of Angeles Medical Center and had undergone

11 sessions of hemodialysis. Being unable to pay the bills right away, she stayed in the

hospital for a month.

History of present illness

Mrs. Sugar Mommy came to the hospital with a chief complaint of right upper

quadrant pain and body weakness night of June 19, 2010. A few days prior to admission,

Sugar Mommy experienced nausea and vomiting, loss of appetite, body weakness, frequent

urination with dark yellow urine. Two days before admission she began experiencing pain

in the right upper quadrant. She also had edema on both feet.

III.

PHYSICAL ASSESSMENT

(IPPA- Cephalocaudal Approach)

June 19, 2010

Initial assessment upon admission (lifted from the chart)

 Conscious, coherent, afebrile, BP= 140/70

 Pale palpebrae, white sclerae, dry lips

 NIDDM

 Symmetrical lung expansion, clear breath sounds

 Abdomen soft, (+) tenderness, right upper quadrant pain

  (+) bipedal edema stage 1

June 21, 2010 ( Monday) Initial nurse- patient interaction

 General Description

Sugarmommy is 50 years old, about five feet and 1 inch tall, petit and frail-looking. She

has a typical Filipina feature. She was sitting on bed when we first visited her, wearing a

light green blouse and chequered shorts and looking generally neat and presentable despite

her medical condition. She was accommodating, actively engages in conversation despite

experiencing abdominal pain that afternoon. Her husband was present during the interview

and from time to time, joins the conversation to confirm some of the information being

shared by his wife.

Vital Signs

T=37.8 ◦ C

P=81bpm

R=20 bpm

BP= 110/90 mmHg

HEAD

Hair and Scalp

 Hair thick and evenly distributed

 Black in color with a few gray showing, shoulder length

 Scalp is slightly paler than body complexion and is free of redness and inflammation

 (-) infestations

 (-) flakes / dandruff

 Hair is slightly dry and brittle

Skull

 Skull is rounded with smooth skull contour

 (-) nodules or masses

Face

 Facial skin is light brown in color, with wrinkles

 Facial features are symmetrical ( eyebrows, nasolabial folds, and sides of the mouth)

 Symmetric facial movements

Eyes

 Eyebrows black in color and evenly distributed

 Eyelashes are equally distributed and slightly curled outwards

 Eyelids close symmetrically

 Bulbar conjunctiva is transparent and sclera appears white

 Pale palpebral conjunctiva

 Pupils are equally rounded and respond to light and accommodation

 (-) redness or discharge

Ears

 Ears are symmetrical, color same as facial skin

 Aligned with the outer canthus of the eye

 Presence of dry yellowish cerumen on both ears

 Pinna recoils after being folded

 No pain or discomfort upon manipulation of the pinna

 Able to hear finger snaps on both ears

 (-) tinnitus

Nose

 Nose is symmetric and uniform in color

 No discharge and flaring

 Nasal septum intact and in midline

 External nose is not tender, no lesions, masses, and nodules noted upon palpation

 Air moves freely as the client breathes through the nares

Mouth

 Lips are pale and slightly dry

 Has remaining 5 upper and 8 lower teeth

 Teeth yellowish in color

 Presence of dental caries on some teeth

 Moist and pale gums

 an Tongue is pink in color, moist, and with presence of whitish coating and papillae,

symmetrical in appearance and moves in a smooth and coordinated motion

 Hard and soft palate are light pink in color

 Uvula is positioned in midline of soft palate

 Taste not altered

NECK

 Skin is light brown in color

 Smooth coordinated movements with no discomforts

 Horizontal, linear scars on the center and the right side of the neck from previous

thyroidectomy

 No palpable lymph nodes

UPPER EXTREMITIES

 Skin is light brown in color

 Nails are convex shaped, untrimmed, and smooth in texture

 Nail bed pale in color

 With smooth coordinated movements on both extremities

 Radial pulse rate of 81 beats per minute

 With a capillary refill time of more than 3 seconds

 Skin pinch goes back after 2 seconds

 With body malaise

CHEST

 Skin is light brown in color

 Respiratory rate of 20 breaths per minute

 Chest is symmetrical in size and shape

 No visible impairment on respiratory movement

 With symmetrical lung expansion

 With clear lub-dub sounds upon auscultation

 Clear breath sounds heard upon auscultation

ABDOMEN

 Abdomen is rounded and light brown in color

 Audible bowel sounds

 With right upper quadrant pain

URINARY SYSTEM

 With a fluid intake of 680cc and urine output of 250cc

 Infrequent urination

 No difficulty upon urination

 No distention of the bladder noted upon palpation

LOWER EXTREMITIES

 Skin is light brown in thigh area, scaly on the lower legs with both feet almost

mahogany in color

 Presence of scars, dark brown in color, round shaped about 2 cm in size on the left

anterior thigh

 With bipedal edema, stage 1

 Presence of sore just below the right big toe with signs of delayed healing.

 Toenails are dirty, untrimmed ,brittle and easily gets damaged

 With numbness and tingling sensation on both feet

June 22, 2010 (Tuesday)

 General Description

During the next nurse-patient interaction, Sugarmommy was wearing a blue “duster”

and looking generally neat and presentable despite her medical condition. She was
accommodating as the other day and actively engages in conversation despite experiencing a

mild headache that afternoon. Her husband was present during the interview and from time

to time, joins the conversation to confirm some of the information being shared by his wife.

Vital Signs

T=36.7◦ C

P=79bpm

R=20 bpm

BP= 120/90 mmHg

HEAD

Hair and Scalp

 Hair thick and evenly distributed

 Black in color with a few gray showing, shoulder length

 Scalp is slightly paler than body complexion and is free of redness and inflammation

 (-) infestations

 (-) flakes/ dandruff

 Hair is slightly dry and brittle

Skull

 Skull is rounded with smooth skull contour

 (-) nodules or masses

 With complaints of dizziness and mild headache

Face

 Facial skin is light brown in color, with wrinkles

 Facial features are symmetrical ( eyebrows, nasolabial folds, and sides of the mouth)

 Symmetric facial movements

Eyes

 Eyebrows black in color and evenly distributed

 Eyelashes are equally distributed and slightly curled outwards

 Eyelids close symmetrically

 Bulbar conjunctiva is transparent and sclera appears white

 Pale palpebral conjunctiva

 Pupils are equally rounded and respond to light and accommodation

 (-) redness or discharge

Ears

 Ears are symmetrical, color same as facial skin

 Aligned with the outer canthus of the eye

 Presence of dry yellowish cerumen on both ears

 Pinna recoils after being folded

 No pain or discomfort upon manipulation of the pinna

 Able to hear finger snaps on both ears

 (-) tinnitus

Nose

 Nose is symmetric and uniform in color

 No discharge and flaring

 External nose is not tender, no lesions, masses, and nodules noted upon palpation

 Air moves freely as the client breathes through the nares

Mouth

 Lips are pale and slightly dry

 Has remaining 5 upper and 8 lower teeth

 Teeth yellowish in color

 Presence of dental caries on some teeth

 Moist and pale gums

 Tongue is pink in color, moist, and with presence of whitish coating and papillae,

symmetrical in appearance and moves in a smooth and coordinated motion

 Hard and soft palate are light pink in color

 Uvula is positioned in midline of soft palate

NECK

 Skin is light brown in color

 Smooth coordinated movements with no discomforts

 Horizontal, linear scars on the center and the right side of the neck from previous

thyroidectomy

 No palpable lymph nodes

UPPER EXTREMITIES

 Skin is light brown in color

 Nails are convex shaped, untrimmed, and smooth in texture

 Nail bed pale in color

 With smooth coordinated movements on both extremities

 Radial pulse rate of 79 beats per minute

 With a capillary refill of more than 3 seconds

 Skin pinch goes back after 2 seconds

 With body malaise

CHEST

 Skin is light brown in color

 Respiratory rate of 20 breaths per minute

 Chest is symmetrical in size and shape

 No visible impairment on respiratory movement

 With symmetrical lung expansion

 With clear lub-dub sounds upon auscultation

 Clear breath sounds heard upon auscultation

ABDOMEN

 Abdomen is rounded and light brown in color

 Audible bowel sounds

 No tenderness and pain

URINARY SYSTEM

 With a fluid intake of 450cc and urine output of 190cc

 Infrequent urination
 No difficulty upon urination

 No distention of the bladder noted

LOWER EXTREMITIES

 Skin is light brown in thigh area, scaly on the lower legs with both feet almost

mahogany in color

 Presence of edema on both feet, 2 to 4 mm deep, with the right foot looking fuller and

more swollen.

 Presence of scars, dark brown in color, round shaped about 2 cm in size on the left

anterior thigh

 Toenails are dirty, untrimmed ,brittle and easily gets damaged

 Presence of sore just below the right big toe with signs of delayed healing.

 With numbness and tingling sensation on both feet

June 23, 2010 (Wednesday)

 General Description

During the nurse-patient interaction, Sugarmommy was wearing a white shirt and

with blue shorts with her hair unneatly tied up. She was accommodating as the previous days

and actively engages in conversation. Her husband was present during the interview and from

time to time, joins the conversation to confirm some of the information being shared by his

wife.

Vital Signs

T=36.1◦ C

P=84bpm

R=18 bpm
BP= 130/80 mmHg

HEAD

Hair and Scalp

 Hair thick and evenly distributed

 Black in color with a few gray showing, shoulder length

 Scalp is slightly paler than body complexion and is free of redness and inflammation

 (-) infestations

 (-) flakes/ dandruff

 Hair is slightly dry and brittle

Skull

 Skull is rounded with smooth skull contour

 (-) nodules or masses

 No dizziness and headache

Face

 Facial skin is light brown in color, with wrinkles

 Facial features are symmetrical ( eyebrows, nasolabial folds, and sides of the mouth)

 Symmetric facial movements

Eyes

 Eyebrows black in color and evenly distributed

 Eyelashes are equally distributed and slightly curled outwards

 Eyelids close symmetrically

 Bulbar conjunctiva is transparent and sclera appears white

 Pale palpebral conjunctiva

 Pupils are equally rounded and respond to light and accommodation

 (-) redness or discharge

Ears

 Ears are symmetrical, color same as facial skin

 Aligned with the outer canthus of the eye

 Presence of dry yellowish cerumen on both ears

 Pinna recoils after being folded

 No pain or discomfort upon manipulation of the pinna

 Able to hear finger snaps on both ears

 (-) tinnitus

Nose

 Nose is symmetric and uniform in color

 No discharge and flaring

 External nose is not tender, no lesions, masses, and nodules noted upon palpation

 Air moves freely as the client breathes through the nares

Mouth

 Lips are pale and slightly dry

 Has remaining 5 upper and 8 lower teeth

 Teeth yellowish in color

 Presence of dental caries on some teeth

 Moist and pale gums

 Tongue is pink in color, moist, and with presence of whitish coating and papillae,

symmetrical in appearance and moves in a smooth and coordinated motion

 Hard and soft palate are light pink in color

 Uvula is positioned in midline of soft palate

NECK

 Skin is light brown in color

 Smooth coordinated movements with no discomforts

 Horizontal, linear scars on the center and the right side of the neck from previous

thyroidectomy

 No palpable lymph nodes

UPPER EXTREMITIES

 Skin is light brown in color

 Nails are convex shaped, untrimmed, and smooth in texture

 Nail bed pale in color

 With smooth coordinated movements on both extremities

 Radial pulse rate of 84 beats per minute

 With a capillary refill of more than 3 seconds

 Skin pinch goes back after 2 seconds

 With body malaise

CHEST

 Skin is light brown in color

 Respiratory rate of 18 breaths per minute

 Chest is symmetrical in size and shape

 No visible impairment on respiratory movement

 With symmetrical lung expansion

 With clear lub-dub sounds upon auscultation

 Clear breath sounds heard upon auscultation

ABDOMEN

 Abdomen is rounded and light brown in color

 Audible bowel sounds

 No tenderness and pain

URINARY SYSTEM

 With a fluid intake of 520cc and urine output of 260cc

 Infrequent urination

 No difficulty upon urination

 No distention of the bladder noted

LOWER EXTREMITIES

 Skin is light brown in thigh area, scaly on the lower legs with both feet almost

mahogany in color
 Presence of edema on both feet, 2 to 4 mm deep, with the right foot looking fuller and

more swollen.

 Presence of scars, dark brown in color, round shaped about 2 cm in size on the left

anterior thigh

 Toenails are dirty, untrimmed ,brittle and easily gets damaged

 Presence of sore just below the right big toe with signs of delayed healing.

 With numbness and tingling sensation on both feet

 IV.

DIAGNOSTIC AND LABORATORY PROCEDURES

DIAGNOSTIC/LA NORMAL
DATE ORDERED
BORATORY
INDICATIONS/PURPOS VALUES ANALYSIS AND
DATE RESULTS RESULTS
PROCEDURES E (UNITS INTERPRETATION
WERE
USED IN
RELEASED
HOSPITAL)

Hemoglobin To determine the oxygen June 19, 2010 9.0 11.6-15.5 It is below normal.
carrying capacity of the
blood. It evaluates the June 21,2010 8.8 It indicates that the level of
hemoglobin content of oxygen in the blood of the
erythrocytes. patient and factor that gives
blood red color is low. It is an
indication of possible pallor and
even anemia of the patient.
Also, it may lead to decrease
oxygen transfer and delivery to
cells.

Hematocrit To determine the percentage June 21, 2010 25.9 36.0-37.0 It is below normal.
of total blood volume
composed of RBC. 26.3 Decreased Hematocrit
percentage indicates that the
solid part or formed elements of
the blood like the hemoglobin
are in less concentration than the
 liquid part which is the plasma.

RBC To determine the number of June 19, 2010 2.75 4.20-5.40 It is below normal.
RBC per cubic millimeter of
blood. It indicates anemia.

WBC Determine presence of June 19, 2010 22.91 4.8-10.8 It is above normal.
infection and inflammation
This indicates that infection is
present.

Neutrophils To check if there is acute June 19, 2010 90.8 40-74 It is above normal.
bacterial infection
It indicates that there is acute
inflammation.

Lymphocytes To determine the number of June 19, 2010 2.5 19-48 It is below normal.
antibodies responsible for
allergic reactions. There are insufficient antibodies
that can affect the immunity.

Eosinophils To determine parasitic June 19, 2010 1.0 0-1 Normal

infections
No infections caused by
parasites.

Monocytes They circulate in the June 19, 2010 5.7 3-9 Normal
peripheral blood prior to
emigration into the tissues. No infection present.

Basophils To determine June 19, 2010 0 0-2 Normal

 hypersensitivity reactions No allergic reactions present.

Platelets They are vital to June 19, 2010 290 150-400 Normal
coagulation of the blood to
prevent bleeding. Immunologic functions with
regard to platelets is still
functional leading to resistance
to bleeding.

Nursing Responsibilities in getting CBC:

Before:

 Verify doctor’s order.

 Explain test procedure. Explain that slight discomfort maybe felt when skin is punctured.

 Avoid stress if possible because altered physiologic status influence and changes normal hemoglobin values.

During:

 Provides assistance if necessary.

 Provides privacy.
  Collect a venous sample according to the protocol of the laboratory

 Transport time for culture specimen must be minimized

 Handle specimen carefully.

After:

 Apply manual pressure and dressings to the puncture site on removal of the needle.

 Monitor the puncture site for oozing or hematoma formation.

 Bruising at the puncture site is not uncommon signs of inflammation are unusual and should be reported if the inflamed

area appear larger.

BLOOD CHEMISTRY

DIAGNOSTIC/LA NORMAL
DATE ORDERED
BORATORY INDICATIONS VALUES ANALYSIS AND
DATE RESULTS RESULTS
PROCEDURES (UNITS USED INTERPRETATION
PURPOSE WERE
IN
RELEASED
HOSPITAL)

Creatinine It is used to diagnose June 19, 2010 7.02 mg/dl 0.5-1.69 mg/dl It is above normal.
impaired kidney function
It indicates kidney damage.
 BUN To measure of the amount June 20, 2010 58.79 mg/dl 7.21mg/dl It is above normal.
of nitrogen in the blood in
the form of urea, and a It indicates a moderate-to-
measurement of renal severe degree of renal failure.
function.

Nursing Responsibilities in getting Blood Chemistry:

Before:

 Verify the doctor’s order.

 Explain the test procedure and blood drawing procedure. Obtain history of s/sx of the hypoglycemia.

 Ensure that the patient fasts, except for water, for 8 to 12 hours before blood is drawn.

During:

 Provides necessary assistance.

 Provide privacy.

After:

 Resume normal activities.

 Interpret test results and monitor as appropriate.

ARTERIAL BLOOD GAS

DATE ORDERED NORMAL

DIAGNOSTIC/LA
BORATORY INDICATIONS/P DATE RESULTS VALUES (UNITS ANALYSIS AND
RESULTS
URPOSE WERE USED IN INTERPRETATION
PROCEDURES
RELEASED HOSPITAL)

Ph The pH is a June 19, 2010 7.38 7.35-7.45 Within the normal range.
measurement of the
acidity or alkalinity Normal because of the
of the blood. compensatory mechanism of the
body making it able to have a
In order for normal normal metabolism.
metabolism to take
place, the

body must maintain

narrow range at all
times.

PCO2 The by-product of June 19, 2010 23.5 35-45 Lower than the normal range.
the cells that when
combined to water Metabolic acidosis brought by
in the body the failure of the kidneys, the
produces carbonic body compensates as it lowers
acid, thus, lowering the CO2 levels by altering the
the Ph of the blood. respiration. Low levels may
indicate respiratory alkalosis.

PO2 The partial pressure June 19, 2010 68.7 80-100 Lower than the normal range.
 of oxygen that is Inadequate supply of oxygen
dissolved in arterial present in the blood, indicates
blood. hypoxemia

HCO3 Through the help of June 19, 2010 12.4 22-26 Lower than the normal range.
the kidneys,
bicarbonate when With the kidney failure, there is
retained will deficit base in the blood or
increase the Ph and excess acid other than CO2.
when excreted will Low levels indicate Metabolic
then lower the Ph acidosis.
of the blood.

B.E. The base excess June 19, 2010 -11.3 meq/L 1-2 meq/L Lower than the normal range.
indicates the
amount of excess or Negative values indicates deficit
insufficient level of of base in the blood brought by
bicarbonate in the the kidney failure.

system.

O2 Saturation Indicates how June 19, 2010 93.2% 97% Lower than the normal range.
saturated the
circulating blood in Less percentage of oxygen the
the arteries with blood carries as it circulates in
oxygen. the body.
CAPILLARY BLOOD GLUCOSE

DIAGNOSTIC/LA INDICATIONS/P DATE ORDERED RESULTS NORMAL ANALYSIS AND

BORATORY URPOSE INTERPRETATION
DATE RESULTS VALUES (UNITS
PROCEDURES WERE USED IN
RELEASED HOSPITAL)

CBG To estimate the June 21, 2010

amount of glucose
present in our blood 6am 249 mg/dl 70-100 mg/dl It is above normal.
and the amount of 11am 305 mg/dl It indicates
insulin. hyperglycemia.
5pm 155 mg/dl

June 22, 2010

6am 227 mg/dl 70-100 mg/dl It is above normal.

11am 224 mg/dl It indicates

hyperglycemia.

URINALYSIS

DIAGNOSTIC/LA INDICATIONS/P DATE ORDERED RESULTS NORMAL ANALYSIS AND

BORATORY URPOSE INTERPRETATION
DATE RESULTS VALUES (UNITS
PROCEDURES WERE USED IN
 RELEASED HOSPITAL)

URINALYSIS To monitor the June 19, 2010 2.5 mg/dl Ketones: negative
kidney function of (quantitative 0.5–3.0
persons with mg/dL). It is normal.
diabetes mellitus. In
diabetics, the
excretion of greater It indicates that there is no any
than 200 μg/mL presence of acidosis.
albumin is
predictive of
impending kidney
disease.

Nursing Responsibilities in getting Urinalysis:

Before:

 Withhold diuretics for 3 days before the test. Check with clinician.

 Avoid excessive water (liquid) intake and excessive salt intake.

 Determine the patient’s usual liquid intake and request that intake not to be increase beyond this daily amount during

testing.

During:
  Provide privacy.

 Provide assistance if necessary

After:

 Patient can resume normal fluid and dietary intake and medication unless specifically ordered otherwise.

 Interpret test outcomes and counsel appropriately.

 V.

THE PATIENT AND HER ILLNESS

1. Anatomy and Physiology

ENDOCRINE SYSTEM

In general, the endocrine system is in charge of body processes that happen slowly,

such as cell growth. Faster processes like breathing and body movement are monitored by the

nervous system. But even though the nervous system and endocrine system are separate

systems, they often work together to help the body function properly.

The Pancreas

Pancreas is a glandular organ that secretes

digestive enzymes and hormones. Pancreas is

a yellowish organ about 7 in. (17.8 cm) long

and 1.5 in. (3.8 cm) wide. It lies beneath the

stomach and is connected to the small intestine

at the duodenum. Most of the pancreatic tissue

consists of grapelike clusters of cells that

produce a clear fluid (pancreatic juice) that flows into the duodenum through a common duct

along with bile from the liver. Pancreatic juice contains three digestive enzymes: tryptase,

amylase, and lipase along with intestinal enzymes, complete the digestion of proteins,

carbohydrates, and fats, respectively. Scattered among the enzyme-producing cells of the

pancreas are small groups of endocrine cells, called the islets of Langerhans that secrete two

hormones, insulin and glucagon.

The pancreatic islets contain several types of cells: alpha-2 cells, which produce the

hormone glucagon; beta cells, which manufacture the hormone insulin; and alpha-1 cells,
which produce the regulatory agent somatostatin. These hormones are secreted directly into

the bloodstream, and together, they regulate the level of glucose in the blood. Insulin lowers

the blood sugar level and increases the amount of glycogen (stored carbohydrate) in the liver;

glucagon has the opposite action. Failure of the insulin-secreting cells to function properly

results in diabetes.

Function

Exocrine functions of pancreas are carried out by the Acinar, within the tubular and

acinar units of the gland. These cells secrete digestive enzyme that catalyze the digestion of

protein, carbohydrates and fats.

Endocrine functions of pancreas are carried out by the islet of langerhans. The islet,

containing Alpha, beta, and delta cells are scattered throughout the pancreatic tissue. The islet

cells are arranged in cords and are separated by a rich blood supply of capillaries. Insulin and

glycogen are two hormones secreted by the islets, play a vital role in the control of

carbohydrate metabolism.

Insulin synthesized by the beta cells, also helps control fat and protein metabolism.

Insulin is a powerful hypoglycemic agent it lowers blood sugar levels by promoting passage

of glucose in the cell. Insulin helps stimulate the active transport of glucose into muscle and

adipose tissue cells and protein synthesis within the tissues and inhibits the breakdown of

protein into amino acids. It also regulate the rate at which carbohydrate are used by cells for

energy.

Glucose is a hyperglycemic agent, synthesized by the alpha cells. Somatostatin and

gastrin are synthesized by the duct cells. Gastrin is used in the metabolism of foods and

somatostatin decreased the secretion of insulin, glycogen, growth hormone, gastrin and

secretion. And the secretion of pancreatic polypeptides is carried out by the F-cells. Any
alterations in the exocrine and endocrine functions of the pancreas would mean alterations in

the insulin and blood glucose level that may bring several abnormalities.

Actions of Insulin

The major function of insulin is to counter the concerted action of a number of

hyperglycemia-generating hormones and to maintain low blood glucose levels. Because there

are numerous hyperglycemic hormones, untreated disorders associated with insulin generally

lead to severe hyperglycemia and shortened life span.

Insulin is synthesized as a preprohormone in the islets of Langerhans. Its signal

peptide is removed in the cisternae of the endoplasmic reticulum and it is packaged into

secretory vesicles in the Golgi, folded to its native structure, and locked in this conformation

by the formation of 2 disulfide bonds. Specific protease activity cleaves the center third of the

molecule, which dissociates as C peptide, leaving the amino terminal B peptide disulfide

bonded to the carboxy terminal A peptide.

Insulin secretion from cells is principally regulated by plasma glucose levels.

Increased uptake of glucose by pancreatic cells leads to a concomitant increase in

metabolism. The increase in metabolism leads to an elevation in the ATP/ADP ratio. This in

turn leads to an inhibition of an ATP-sensitive K + channel. The net result is a depolarization

of the cell leading to Ca2+ influx and insulin secretion. In fact, the role of K+ channels in

insulin secretion presents a viable therapeutic target for treating hyperglycemia due to insulin

insufficiency.

Glucose Metabolism

Uncontrolled IDDM leads to increased hepatic glucose output. First, liver glycogen

stores are mobilized then hepatitis gluconeogenesis used to produce glucose. Insulin
deficiency also impairs non-hepatic tissue utilization of glucose. In particular in adipose

tissue and skeletal muscle, insulin stimulates glucose uptake. This is accomplished by insulin-

mediated movement of glucose transporter proteins to the plasma membrane of these tissues.

Reduced glucose uptake by peripheral tissues in turn leads to a reduced rate of glucose

metabolism. In addition, the level of hepatic glucokinase is regulated by insulin. Therefore, a

reduced rate of glucose phosphorylation in hepatocytes leads to increased delivery to the

blood. Other enzymes involved in anabolic metabolism of glucose are affected by insulin

(primarily through covalent modifications). The combination of increased hepatic glucose

production and reduced peripheral tissues metabolism leads to elevated plasma glucose

levels. When the capacity of the kidneys to absorb glucose is surpassed, glucosuria ensues.

Glucose is an osmotic diuretic and an increase in renal loss of glucose is accompanied by loss

of water and electrolytes, termed polyuria. The result of the loss of water (and overall

volume) leads to the activation of the thirst mechanism (polydipsia). The negative caloric

balance which results from the glucosuria and tissue catabolism leads to an increase in

appetite and food intake (polyphagia).

URINARY SYSTEM

Kidneys are bean-shaped organs about the size

of a human fist. They are near the middle of the spine,

just below the ribcage. A kidney consists of about 1

million filtering units termed nephrons A nephron is

the basic structural and functional unit of the kidney. It

is a tiny tubule consisting of a cluster of capillaries called the glomerulus, surrounded by a

hollow bulb known as Bowman's capsule. Bowman's capsule leads into a long, convoluted

tubule consisting of four sections: the proximal tubule, loop of Henle, distal tubule, and

collecting duct. The collecting ducts empty into the central cavity of the kidney, the renal

pelvis, which connects to the ureter. Each human kidney has about a million nephrons.

Glomerulus refers to two unrelated structures in the body, both named for their globular

form.

 For the kidney structure which filters blood

 For the olfactory bulb structure of converging axons from the olfactory epithelium

Capillaries are the smallest of a body's blood vessels, measuring 5-10 μm. They

connect arteries. Blood is filtered by the glomerulus, and the resultant "prourine" passes

through the tubular system where water, electrolytes and nutrients are reabsorbed. The

kidney plays a crucial role in regulating electrolytes An electrolyte is a substance which

dissociates free ions when dissolved (or molten), to produce an electrically conductive

medium. Because they generally consist of ions in solution, electrolytes are also known as

ionic solutes.

Potassium is a chemical element in the periodic table that has the symbol K (L.

kalium) and atomic number 19. The name potassium comes from potash the source it was

first isolated from. This is a soft, silvery-white metallic alkali metal that occurs naturally

bound to other elements in seawater and many minerals. It oxidizes rapidly in air, is very

reactive, especially in water, and resembles sodium chemically.

Urine Formation
 The primary functions of the nephrons include removing waste substances from the

blood and regulating water and electrolyte concentrations within the body fluids. The end

product of these functions is urine, which is excreted to the outside of the body, containing

wastes, excess water, and excess electrolytes. Urine formation involves glomerular filtration,

tubular reabsorption, and tubular secretion.

Glomerular Filtration

Urine formation begins when water and

various dissolved substances are filtered out

of the glomerular capillaries and into the

glomerular capsules. The filtration of

these materials through the capillary walls is

much like the filtration that occurs at the arteriole ends of other capillaries throughout the

body.

The glomerular capillaries, however, are many times more permeable than the capillaries in

other tissues due to the presence of numerous tiny openings (fenestrae) in their walls.

Filtration Pressure

As in case of other capillaries, the main force responsible for moving substances

through the glomerular capillary wall is the pressure of the blood inside (glomerular

hydrostatic pressure). This movement is also influenced by the osmotic pressure of the

plasma in the glomerulus and by the hydrostatic pressure inside the glomerular capsule. An

increase in either of these pressures will oppose movement out of the capillary and, thus,

reduce filtration. The net pressure acting to force substances out of the glomerulus is called

the filtration pressure.

The glomerular filtrate consists of substances that enter the space within the glomerular

capsule, and it has about the same composition as the filtrate that becomes tissue fluid

elsewhere in the body. That is, glomerular filtrate is largely water and contains essentially the

same substances as the blood plasma, except for the larger protein molecules, which the

filtrate lacks.

Filtration Rate

The rate of glomerular filtration is directly proportional to the filtration pressure.

Consequently, the factors that affect the glomerular hydrostatic pressure, glomerular plasma

osmotic pressure, or hydrostatic pressure in the glomerular capsule will also affect the rate of

filtration.

For example, since the glomerular

capillary is located between two arterioles - the

afferent and efferent arterioles- any change in

the diameters of these vessels is likely to cause

a change in the glomerular hydrostatic pressure

and will be accompanied by a change in the

glomerular filtration rate. The afferent

arteriole, though which the blood enters the

glomerulus, may constrict as a result of mild

stimulation by sympathetic nerve impulses. If

this occurs, the blood flow diminishes, the

glomerular hydrostatic pressure decreases,

and the filtration rate drops. If, on the other

hand, the efferent arteriole (through which the

 blood leaves the glomerulus) constricts, the

blood backs
up into the glomerulus, the glomerulus, the glomerular hydrostatic pressure increases, and

the filtration rate rises. Converse effects are produced by vasodilation of these vessels. In

the capillaries, the blood pressure, acting to force water and dissolved substances outward, is

opposed by the effect of the plasma osmotic pressure that attracts water inward. As

filtration occurs through the capillary wall, the proteins remaining in the plasma cause the

osmotic pressure within the glomerular capillary to rise. When this pressure reaches a

certain high level, filtration ceases. Conversely, conditions that tend to decrease plasma

osmotic pressure, such as a decrease in plasma protein concentration, cause an increase in

the filtration rate. The hydrostatic pressure in the glomerular capsule sometimes changes as

a result of an obstruction, such as may be caused by a stone in a ureter or an enlarged prostate

gland pressing on the urethra. If this occurs, fluids tend to back up into the renal tubules and

cause the hydrostatic pressure in the glomerular capsules to rise. Since any increase in

capsular pressure opposes glomerular filtration, the rate of filtration may decrease

significantly.

In an average adult, the glomerular filtration rate for the nephrons of both kidneys is about

125 milliliters per minute, or 180,000 milliliters (180 liters) in 24 hours. Since this 24-hour

volume is nearly 45 gallons, it is obvious that not all of it is excreted as urine. Instead, most

of the fluid that passes through the renal tubules is re absorbed and reenters the plasma.

Regulation of filtration rate

The regulation of glomerular filtration rate involves the juxtaglomerular apparatus,

which was described previously, and two negative feedback mechanisms. These mechanisms

are triggered whenever the filtration rate is decreasing. For example, as the rate decreases,

the concentration of chloride ions reaching the macula densa in the distal convoluted
tubule also decreases. In response, the macula densa signals the smooth muscles in the wall

of the afferent arteriole to relax, and the vessel becomes dilated. This action allows more

blood to flow into the glomerulus, increasing the glomerular pressure, and as a consequence,

the filtration rate rises toward its previous level. At the same time that the macula densa

signals the afferent arteriole to dilate, it stimulates the juxtaglomerular cells to release renin.

This enzyme causes a plasma globulin (angiotensinogen) to form a substance called

angiotensin I, which is converted quickly to angiotensin II by an enzyme (converting

enzyme) present in the lungs and plasma.

Angiotensin II is a vasoconstrictor, and it stimulates the smooth muscle cells in the wall for

the efferent arteriole to contract, constricting the vessel. As a result of this action, blood

tends to back up into the glomerulus, and as the glomerular hydrostatic pressure increases, the

filtration rate also increases. These two mechanisms operate together to ensure a constant

blood flow through the glomerulus and a relatively stable glomerular filtration rate, in spite of

marked changes occurring in the arterial blood pressure.

Tubular Reabsorption

If the composition of the glomerular filtrate entering the renal tubule is compared with

that of the urine leaving the tubule, it is clear that changes occur as the fluid passes through

the tubule. For example, glucose is present in the filtrate, but absent in the urine. Also, urea

and uric acid are considerably more concentrated in the urine than they are in the glomerular

filtrate. Such changes in fluid composition are largely the result of tubular reabsorption, a

process by which substances are transported out of the glomerular filtrate, through the

epithelium of the renal tubule, and into the blood of the peritubular capillary.

Since the efferent arteriole is narrower than the peritubular capillary, the blood flowing from

the former into the latter is under relatively slow pressure. Also, the wall of this capillary is
more permeable than that of other capillaries. Both of these factors enhance the rate of fluid

reabsorption from the renal tubule.

Although tubular reabsorption occurs throughout the renal

tubule, most of it occurs in the proximal convoluted

portion. The epithelial cells in this portion have

numerous microscopic projections, called microvilli, that

form a "brush border" on their free surfaces. These tiny

extensions greatly increase the surface area exposed to the

glomerular filtrate and enhance the reabsorption process.

Various segments of the renal tubular are adapted to

reabsorb specific substances, using particular modes of

transport. Glucose reabsorption, for example, occurs

primarily through the wall of the proximal tubule by

active transport.
Water also is reabsorbed rapidly though the epithelium of the proximal tubule by osmosis;

however, portions of the distal tubule and collecting duct are almost impermeable to

water. This characteristic of the distal tubule and collecting duct is important in the regulation

of urine concentration and volume.

Active transport depends on the presence of carrier molecules in a cell membrane.

These carriers transport passenger molecules through the membrane, release them, and return

to the other side to transport more passenger molecules. Such a mechanism has a limited

transport capacity; that is, it can only transport a certain number of molecules in a given

amount of time, because the number of carriers is limited. Usually all of the glucose in the

glomerular filtrate is reabsorbed, because there are enough carrier molecules to transport it.

Sometimes, however, the plasma glucose concentration increases, and if it reaches a critical

level, called the renal plasma threshold, there will be more glucose molecules in the filtrate
than the active transport mechanism can handle. As a result, some glucose will remain in the

filtrate and be excreted in the urine.

Amino acids also enter the glomerular filtrate and are reabsorbed in the proximal

convoluted tubule, apparently by three different active transport mechanisms. Each

mechanism is though to reabsorb a different group of amino acids, whose members have

molecular similarities. As a result of their actions, only a trace of amino acids usually remains

in the urine. Although the glomerular filtrate is nearly free of protein, some albumin may be

present. These proteins have relatively small molecules, and they are reabsorbed by

pinocytosis through the brush border of the epithelial cells lining the proximal convoluted

tubule. Once they are inside an epithelial cell, the proteins are converted to amino acids and

moved into the blood of the peritubular capillary. Other substances reabsorbed by the

epithelium of the proximal convoluted tubule include creatine, lactic acid, citric acid, uric

acid, ascorbic acid (vitamin C), phosphate ions, sulfate ions, calcium ions, potassium ions,

and sodium ions. As a group, these substances are reabsorbed by active transport mechanisms

with limited transport capacities. Such a substance usually does not appear in the urine until it

concentration in the glomerular filtrate exceeds its particular threshold.

Sodium and Water Reabsorption

Substances that remain in the renal tubule tend to become more and more

concentrated as water is reabsorbed from the filtrate. Most water reabsorption occurs

passively by osmosis in the proximal convoluted tubule and is closely associated with the

active reabsorption of sodium ions. In fact, if sodium reabsorption increase, water

reabsorption increase; is sodium reabsorption decreases, water reabsorption decreases also.

 About 70 percent of sodium ion reabsorption occurs

in the proximal segment of the renal tubule by active

transport (the sodium pump mechanism). As these

positively charged ions (Na+) are moved though the

tubular wall, negatively charged ions including

chloride ions (Cl-), phosphate ions (PO4-3), and

bicarbonate ions (HCO3-) accompany them. This

movement of negatively charged ions is due to the

electrochemical attraction between particles of

opposite charge. It is termed passive transport

because it does no require a direct expenditure of

cellular energy. As more and more sodium ions are

actively transported into the peritubular capillary,

along with various negatively charged ions,

the concentration of solutes within the peritubular blood is increased. Furthermore, since

water moves through cell membranes from regions of lesser solute concentration (hypotonic)

toward regions of greater solute concentration (hypertonic), water is transported by osmosis

from the renal tubule into the peritubular capillary. Because of the movement of solutes and

water into the peritubular capillary, the volume of fluid within the renal tubule is greatly

reduced.

Tubular Secretion

This is a process by which certain substances are transported from the plasma of the

peritubular capillary into the fluid of the renal tubule. As a result, the amount of
particular substance excreted into the urine may be greater than the amount filtered from the

plasma in the glomerulus.

Some substances are secreted by active transport

mechanisms similar to those that function in reabsorption.

Secretory mechanisms, however, transport substances in

the opposite direction. For example, certain organic

compounds, including penicillin, creatinine, and

histamine, are actively secreted into the tubular fluid by

the epithelium of the proximal convoluted segment.

Hydrogen ions are also actively secreted. In this case, the

proximal segment of the renal tubule is specialized to

secrete large quantities of hydrogen ions between the

plasma and the tubular fluid, where the hydrogen ions

play an important role in the regulation of the pH of the

body fluids.
Although most of the potassium ions in the glomerular filtrate are actively reabsorbed in the

proximal convoluted tubule, some may be secreted passively in the distal segment and

collecting duct. During this process, the active reabsorption of sodium ions out of the fluid

produces a negative electrical charge within the tube. Because the positively charged

potassium ions (K+) and hydrogen ions (H+) are attracted to regions that are negatively

charged, these ions move through the tubular epithelium and enter the tubular fluid.
 2. Pathophysiology Precipitating factors
 Stress
PATEINT-CENTERED (SCHEMATIC DIAGRAM)  Sedentary lifestyle
Predisposing factors  Unhealthy eating habits
 Age ( 50 years old)  Hypertension
 Race (Asian)  Alcoholism
 Hereditary ( father side)  smoking

Production of excess glucagon

Decrease Elevated blood

CBG of 249 mg/dl
glucose glucose Production of glucose from protein and fat stores
utilization
Chronic elevations
in blood glucose
Osmolarity due to glucose Wasting of lean Weight loss
Fatigue
body mass (25 lbs)

Water not absorbed Glycoprotein cell

from the renal wall deposits
tubules Osmotic pressure in
the blood Impaired Infection (wbc
immune fxn -22.91)
Diabetic neuropathy
Triggers
thirst Attracts ICF
Fluid shifting from
Numbness and tingling in Delayed
intracellular to the extremities Small vessel healing
general circulation Cellular dehydration disease
polydipsia
Dry lips, dry mucous membranes, poor skin
turgor of > 2 sec, capillary refill > 3 sec Nephropathy
Retinopathy
 Damage to the
Blood volume Progressive capillaries that supplies Hypertension
Fever Nephrosclerosis the glumeruli (june 23-130/80)
(June 21
Perfusion in the kidneys -37.8 C)

Pyelonephritis Fluid filtration Fluid Volume

Glucose acts as an deficit overload
Renal papillary
osmotic diuretic necrosis
Increased Gross albuminuria,
WBC (wbc Scarring of renal
Creatinine(7.02
-22.91) parenchyma Edema
Urination mg/dl) and
BUN(58.79 mg/dl)

polyuria Increased WBC Schemia/ Chronic Accumulation of sulfates, Metabolic

(wbc -22.91) Disease phosphates, uric acid etc. Acidosis (HCO3-
12.4)

Decreased Erythropoietin Uremia

synthesis

Death
Anemia (RBC2.75)

Fatigue
b. Synthesis of the Disease

Diabetes mellitus is a group of metabolic disorders characterized by elevated levels of

blood glucose (hyperglycemia) resulting from defects in insulin production and secretion,

decreased cellular response to insulin or both. Hyperglycemia may lead to acute metabolic

complications, such as diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar

nonketitic syndrome (HHNS). Long-term hyperglycemia may contribute to chronic

microvascular complications (kidney and eye disease) and neuropathic complications.

Diabetes is also associated with an increased occurrence of macrovascular diseases, including

coronary artery disease (myocardial infarction), cerebrovascular disease (stroke) and

peripheral vascular disease.

Type 2 diabetes accounts to about 90% to 95% of diabetic. It results from a decreased

sensitivity to insulin (insulin resistance) or from a decreased amount of insulin production.

Type 2 is first treated with diet and exercise, then oral hypoglycemic agents as needed. And

type 2 most frequently occurs in patients older than 30 years of age and in obese patients.

b.1. Predisposing / Precipitating Factors of DM

PREDISPOSING FACTORS (NON-MODIFIABLE)

a. Age (50 years old) – Type 2 DM usually occurs at the age 45 years old and above

(Braunwald,ed.., 2001). Type 2 DM occurs most commonly in people older than 30 years

who are obese.

b. Race (Asian) – Type 2 DM is more prevalent among colored races although Type 1 DM is

more common in whites than in non-white.

c. Hereditary - A genetic predisposition, lowered beta-cell mass either through genetic and/or

beta-cell cytotoxic factors predisposes for glucose intolerance.

PRECIPITATING FACTORS (MODIFIABLE)

a. Stress – An increase in stress hormone triggers the release of epinephrine and

norepinephrine which will promote the secretion of glucose leading to hyperglycemia.

(Black, et, .al, 2001)

b. Diet – Foods rich in carbohydrates can easily promote the increasing level of glucose along

the bloodstream.

c. Sedentary lifestyle - a sedentary lifestyle is damaging to health and bears responsibility for

the growing obesity problems." Inactivity and being overweight go hand in hand towards a

diagnosis of type 2.

d. Unhealthy eating habits – 90% of people who have been diagnosed with type 2 diabetes

are overweight. Unhealthy eating contributes largely to obesity. Too much fat, not enough

fiber and too many simple carbohydrates all contribute to a diagnosis of diabetes.

e. Excessive drinking of alcohol - Alcohol is processed in the body very similarly to the way

fat is processed, and alcohol provides almost as many calories. Therefore, drinking alcohol in

people with diabetes can cause your blood sugar to rise.

f. Smoking (15 sticks a day) - Smoking raises your blood glucose (sugar) and reduces your

body's ability to use insulin, making it more difficult to control your diabetes.

g. Hypertension – Blood flows slowly due to its difficulty passing through the narrow blood

vessels.

b.2. Signs and Symptoms with rationale

1. Hyperglycemia

Due to increased hepatic glucose production secondary to decreased insulin production

associated with impaired Beta cell functions.

2. Polyuria (excessive urination)

This is due to the excessive blood volume secondary to increase volume of water in the

blood and due to the osmotic diuretic effect of glucose.

3. Polydipsia (excessive drinking)

Due to dehydration brought by frequent urination, in return, thirst center of the brain will be

triggered making the patient to urge for thirst and also ude to the activation of the thirst center

as a result of dehydration.

4. Hypertension

Due to increase blood flow secondary to increased blood viscosity, in return due a decrease

blood flow will activate the renin-agiotensin system.

5. Fatigue (malaise)

This is caused by decreased plasma volume in the systemic circulation.

6. Nephropathy

Occurs when there is too much inflammation and glucose in the bloodstream, clogging the

small capillaries that feed into the kidneys

Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss

ofrenal function over a period of months or years. The symptoms of worsening kidney

function are unspecific, and might include feeling generally unwell and experiencing

a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of

people known to be at risk of kidney problems, such as those with high blood

pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic

kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate

a falling glomerular filtration rate and as a result a decreased capability of the kidneys to

excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the
condition is discovered if urinalysis (testing of a urine sample) shows that the kidney is

allowing the loss of protein or red blood cells into the urine. To fully investigate the

underlying cause of kidney damage, various forms of medical imaging, blood tests and often

renal biopsy (removing a small sample of kidney tissue) are employed to find out if there is a

reversible cause for the kidney malfunction.  Recent professional guidelines classify the

severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually

causing few symptoms and stage 5 being a severe illness with poor life expectancy if

untreated. Stage 5 CKD is also called established chronic kidney disease and is

synonymous with the now outdated terms end-stage renal disease (ESRD), chronic kidney

failure (CKF) or chronic renal failure (CRF).

Stage 1
Slightly diminished function; Kidney damage with normal or relatively high GFR (>90
mL/min/1.73 m2). Kidney damage is defined as pathologic abnormalities or markers of
damage, including abnormalities in blood or urine test or imaging studies.[1]
Stage 2
Mild reduction in GFR (60-89 mL/min/1.73 m2) with kidney damage. Kidney damage is
defined as pathologic abnormalities or markers of damage, including abnormalities in blood
or urine test or imaging studies.[1]
Stage 3
Moderate reduction in GFR (30-59 mL/min/1.73 m2).[1] British guidelines distinguish
between stage 3A (GFR 45-59) and stage 3B (GFR 30-44) for purposes of screening and
referral.[4]
Stage 4
Severe reduction in GFR (15-29 mL/min/1.73 m2)[1] Preparation for renal replacement
therapy
Stage 5
Established kidney failure (GFR <15 mL/min/1.73 m2, or permanent renal replacement
therapy (RRT
b.2. Signs and Symptoms with rationale

1. blood pressure is increased due to fluid overload and production of vasoactive hormones,
increasing one's risk of developing hypertensionand/or suffering from congestive heart
failure
2. Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from
lethargy to pericarditis and encephalopathy). Urea is excreted by sweating and crystallizes
on skin ("uremic frost").
3. Erythropoietin synthesis is decreased (potentially leading to anemia, which
causes fatigue)
4. Fluid volume overload - symptoms may range from mild edema to life-
threatening pulmonary edema
5. Metabolic acidosis, due to accumulation of sulfates, phosphates, uric acid etc. This may
cause altered enzyme activity by excess acid acting on enzymes and also increased
excitability of cardiac and neuronal membranes by the promotion of hyperkalemia due to
excess acid (acidemia)
6. Higher levels of creatinine, BUN indicate a falling glomerular filtration rate and as a
result a decreased capability of the kidneys to excrete waste products.
 VI.

THE PATIENT AND HER CARE

A. Medical Management

A.1. Intravenous Fluid

Date Ordered, Date

Medical Indication/
General Description Started And Date Client’s Response to Treatment
Management Purposes
Changed

Plain NSS Normal Saline Solution To increase both Date Ordered: June 19, Patient’s blood volume increases
1000ml x 40 is an isotonic crystalloid blood volume and 2010 and cells are rehydrated.
ugtts/min that contains 0.9 % to rehydrate the
(KVO) sodium chloride (salt) in cells. Date Started: June 19, 2010
sterile water.

NURSING RESPONSIBILITIES:

Prior:

 Verify doctor’s order.

 Know the type, amount, and indication of IV therapy.
 Practice strict asepsis.
  Inform the client and explain the purpose of IV therapy.
 Prime/ ready/ set-up IV tubing to expel air. This will prevent air embolism.
 Clean the insertion site of IV needle from center to the periphery with alcoholized cotton swab.
During:

 (Ideally) Change IV tubing every 72 hours, to prevent contamination.

 (Ideally) Change/alter IV needle insertion site every 72 hours to prevent thrombophlebitis.
After:

 Regulate IV every 20 minutes to ensure administration of proper volume of IV fluid as ordered.

 Observe for potential complications
 Check the site of the hand where the needle is inserted if bulging is not visible. If so, reinsertion is to be undertaken.
 Advice patient to avoid scratching the site and less movement of the hand were the needle was inserted to let the needles inserted
be on its right place.
 Instruct patient and SO to inform Nurse-on-duty, if bulging of the site is visible, if there is backflow of blood, or if IVF is not
infusing well.
 Always check the Doctor’s Order for new orders regarding the IVF supplement of the patient.
 Always check if the IVF is infusing well and intact.
 Monitor the patient’s skin integrity

B. Drugs
 Generic and General
Indication D/O, D/S, D/C Client’s Response
Brand name Description

MOTILIUM is indicated for:

Domperidone ANTI- D/O: June 19, 2010 Patient’s nausea and vomiting was
Motillium EMETIC/ *Delayed gastric emptying of D/S: June 19, 2010 controlled or relieved.
ANTI- functional origin with gastro- D/C: June 22, 2010
VERTIGO oesophageal reflux and/or
dyspepsia.
*Control of nausea and vomiting of
central or local origin.

BEFORE:

 Check the doctor’s order.

 Explain the procedure to the patient the importance of the drug, its uses, and effects.

 Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

 Give with food to decrease GI distress

 should be used with caution in patients with renal impairment or in those at risk of fluid retention
DURING:

 Adhere to standard precautions.

 Administer at the right route

AFTER:

 Monitor for rash, urticaria and abdominal cramps.

Generic and General

Indication D/O, D/S, D/C Client’s Response
Brand name Description

Pantoprazole ANTI-ULCER/ To treat gastrophageal reflux D/O: June 19, 2010 Patient’s risk for stomach ulcers
Sodium Gastric Acid disease. D/S: June 19, 2010 due to medications was prevented.
Pantoloc Proton Pump To treat or reduce the risk of D/C: June 21, 2010
Inhibitor stomach ulcers due to
medications.

BEFORE:

 Check the doctor’s order.

  Explain the procedure to the patient the importance of the drug, its uses, and effects.

 Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

 Give with food to decrease GI distress

 Store this medication at room temperature

 Do not chew or crush the tablets, and take them with a glass of water in the morning before, during, or after breakfast.

DURING:

 Adhere to standard precautions.

 Administer at the right route

AFTER:

 Monitor for dizziness, headache and flu-like symptoms

Generic and General

Indication D/O, D/S, D/C Client’s Response
Brand name Description
Gaviscon ANTACID Help reduce the number of reflux D/O: June 19, 2010 Patient’s reflux episodes were
episodes and may provide longer D/S: June 19, 2010 reduced.
lasting action against heartburn. D/C: June 21, 2010

BEFORE:

 Check the doctor’s order.

 Explain the procedure to the patient the importance of the drug, its uses, and effects.

 Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

 Shake the oral liquid well before each use to mix the medicine evenly

DURING:

 Adhere to standard precautions.

 Administer at the right route

 Drink a full glass of water after taking the tablets

AFTER:
  Monitor for upset stomach, vomiting and belching

Generic and General

Indication D/O, D/S, D/C Client’s Response
Brand name Description

Paracetamol/ ANTI- Commonly used for relief of fever, D/O: June 19, 2010 Patient’s headache and minor
Acetaminophe PYRETIC headaches, and other minor pains D/S: June 19, 2010 pains are relieved.
n ANALGESIC and aches. D/C: June 23, 2010
Tylenol

BEFORE:

 Check the doctor’s order.

 Explain the procedure to the patient the importance of the drug, its uses, and effects.

 Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

 Do not mix either paracetamol or NSAIDs with alcoholic drinks.

 Assess for clinical improvement and relief of pain, fever

DURING:

 Adhere to standard precautions.

 Administer at the right route

AFTER:

 Monitor for hypersensitivity and adverse reactions

Generic and General

Indication D/O, D/S, D/C Client’s Response
Brand name Description

Kremizin Oral absortive Can delay the progression of D/O: June 22, 2010 The progression of chronic kidney
chronic renal failure in undialyzed D/S: June 22, 2010 disease of the patient was can be
patients with uremic syndrome delayed.

BEFORE:

 Check the doctor’s order.

 Explain the procedure to the patient the importance of the drug, its uses, and effects.
  Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

DURING:

 Adhere to standard precautions.

 Administer at the right route

AFTER:

 Monitor for hypersensitivity and adverse reactions

 Serum creatinine and blood pressure levels were measured every month for 6 months

Generic and General

Indication D/O, D/S, D/C Client’s Response
Brand name Description

Ferrous Anti-anemic/ To preven iron defeincy and to D/O: June 22, 2010 Patient was provided with iron
Sulfate nutritional provide iron supplementation. D/S: June 22, 2010 supplements.
supplement
Fergon
BEFORE:

 Check the doctor’s order.

 Explain the procedure to the patient the importance of the drug, its uses, and effects.

 Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

 Protect liquid for freezing

DURING:

 Adhere to standard precautions.

 Administer at the right route

 Give with full glass of water

 Don’t crush enteric tablets and open capsules

 Dilute and administer with straw because it can cause staining of teeth

 Milk, eggs, or caffeine beverages when taken with the iron preparation may inhibit absorption.

 Give on an empty stomach if possible because oral preparations are best absorbed then. Minimize gastric distress if needed by giving

with or immediately after meals with adequate liquid.

  Ascorbic acid increases the absorption of iron

AFTER:

 Monitor for hypersensitivity and adverse reactions

 Monitor patient for iron overdose which may include abdominal pain, diarrhea, nausea and sharp abdominal cramping

 Be aware that iron preparations cause dark green or black stools.

Generic and General

Indication D/O, D/S, D/C Client’s Response
Brand name Description

Dolacet ANALGESIC To treat moderate to severe back D/O: June 23, 2010 The patient reported decreased
Dolacet pain and pain from arthralgia, D/S: June 23, 2010 pain.
cancer, dental procedures,
headache and myalgia

BEFORE:

 Check the doctor’s order.

  Explain the procedure to the patient the importance of the drug, its uses, and effects.

 Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

DURING:

 Adhere to standard precautions.

 Administer at the right route

AFTER:

 Monitor for hypersensitivity and adverse reaction

 Monitor signs of overdose such as blurred vision, cold, clammy skin, confusion and dizziness

 Avoid using of alcohol

 If patient is dry mouth, suggest that he use sugarless candy or gum.

Generic and General

Indication D/O, D/S, D/C Client’s Response
Brand name Description

Epoetin Alfa ANTI- Anti – anemic D/O: June 21, 2010 Well tolerated and no
Renogen ANEMIC *To treat infection like D/S: June 21, 2010 further aggravation of
septicemia and skin D/C: June 21, 2010 infection resulted. No
infection due to necrosis adverse effects noted. Side
effects include experience
of soft stools.

BEFORE:

 Check the doctor’s order.

 Explain the procedure to the patient the importance of the drug, its uses, and effects.

 Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

DURING:

 Adhere to standard precautions.

 Administer at the right route

AFTER:

 Monitor for hypersensitivity and adverse reaction

  Encourage patient to eat iron rich food

 Take seizure precaution

 Stress the importance of complying with the dosage regimen

Generic and
General Description Indication D/O, D/S, D/C Client’s Response
Brand name

Cefuroxime 2ND GENERATION Treatment of infections D/O: June 22, 2010 Well tolerated and no
Zinnat CEPHALOSPORIN specifically in the upper further aggravation in
ANTIBIOTIC respiratory tract. D/S: June 22, 2010 infection resulted. Side
effects experienced include
nausea and presence of soft
stools during defecation.
No adverse effects noted.

BEFORE:

 Check the doctor’s order.

 Explain the procedure to the patient the importance of the drug, its uses, and effects.
  Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

DURING:

 Adhere to standard precautions.

 Administer at the right route

AFTER:

 Monitor for hypersensitivity and adverse reaction

 Used cefuroxime cautiously in patients hypersensitive to penicillin

 Monitor IV site for extravasation and phlebitis

 Instruct patient to immediately report for severe diarrhea or blood dyscrasia

Generic and
General Description Indication D/O, D/S, D/C Client’s Response
Brand name
Cephalexin 1ST To treat infection like D/O: June 21, 2010 Well tolerated and no
HCL GENERATION septicemia and skin further aggravation of
Kefox CEPHALOSPORIN infection due to necrosis D/S: June 21, 2010 infection resulted. No
ANTIBIOTIC D/C: June 21, 2010 adverse effects noted. Side
effect includes experience
of soft stools.

BEFORE:

 Check the doctor’s order.

 Explain the procedure to the patient the importance of the drug, its uses, and effects.

 Determine hypersensitivity to the drug.

 Prepare the right medication at the right time and with the right dosage.

DURING:

 Adhere to standard precautions.

 Administer at the right route

AFTER:
  Monitor for hypersensitivity and adverse reaction

 Use cephalexin cautiously in patients hypersensitive to penicillin

 Monitor fluid intake and output

 Monitor for allergic reactions a few days after therapy starts

 Advise patient to complete prescribed course of therapy

Generic and
General Description Indication D/O, D/S, D/C Client’s Response
Brand name

Calcium ANTACID / To alleviate heart burn D/O: June 22, 2010 Well tolerated and
Carbonate ANTIHYPER- due to hyperacidity and to D/S: June 22, 2010 hyperacidity decreased.
Calsan, Tums PHOSPHATEMIC treat hyperphosphatemia D/C: June 22, 2010 Side effects experienced
due to renal disorder include nausea and
sensation of warmth in the
skin. No adverse effects
noted.
BEFORE:

 Check the doctor’s order.

 Explain the procedure to the patient the importance of the drug, its uses, and effects.

 Determine hypersensitivity to the drug.

  Prepare the right medication at the right time and with the right dosage.

 Instruct patient to take it 1 – 2 hours after meals

DURING:

 Adhere to standard precautions.

 Administer at the right route

 Urge patient to chew them thoroughly before swallowing and to drink a glass of water afterwards

AFTER:

 Monitor for hypersensitivity and adverse reaction

 Tell patient to avoid the use of alcohol and tobacco use

C. DIET

Type of Diet General Description Indication/Purpose Date Client’s Response

and/or Reaction to the
Diet

Low salt, Low fat diet The low fat and salt diet Indicated for bed patient Date Ordered: June 19, >The client complied
is design to limit the whose condition
 total amount of fat, salt required modified diet in 2010 with the prescribed diet.
and cholesterol in the order to prevent further
diet to reduce serum aggravation, like not
lipid levels and avoid increase fat levels in the Date Started: June 19, >Well tolerated and no
excessive sodium blood and to prevent 2010 complaints.
retention further damage to
kidneys

BEFORE:

 Check the doctor’s order for the type of diet prescribed.

 Explain the importance of the diet given.

 Explain the importance of compliance to the diet given.

 Inform dietary department on the patient’s diet.

 Inform dietary department on the patient’s diet.

DURING:

 Give appropriate food to the pa tient.

 Enumerate the foods that the patient may or may not take.

 Emphasize strict compliance to the diet.

  Reiterate diet frequently

AFTER:

 Document the patient’s tolerance to the diet given.

 VII.

NURSING CARE PLAN

Problem # 1: Imbalanced Nutrition; Less than body requirements

Cues Nursing Scientific Objectives Interventions Rationale Expected outcome

Diagnosis explanation
S> “Mangalam- Altered Type 2 diabetes Short term: > Establish > To gain Patient is expected to
but ku” nutrition; less is characterized After 2 hrs. of rapport. patient’s trust identify measures to
O> patient than body primarily by nursing and cooperation. prevent the occurrences
manifested: requirements r/t insulin interventions, of alteration in nutrition
insulin deficiency. > Monitor and > For baseline
patient will less than body
 Weight deficiency 2º Hence, without record v/s. measurement.
loss of 25 diabetes mellitus enough insulin identify requirements.
lbs. (from that serves as a measures to > Ascertain > To determine As well as
66 kg to vehicle for prevent the understanding of informational demonstration of
55 kg) for glucose to enter occurrences of individual needs of client behaviors or lifestyle
the span of the cells, it could alteration in nutritional needs changes to regain
6 years. lead to protein nutrition less appropriate weight.
 Pale nail and fat
than body
beds and metabolism > Discuss eating > To appeal to
mucous (muscle wasting) requirements. habits, including client’s likes and
membrane eventually food preferences, dislikes
s leading to intolerances or
 CBG of insufficient Long term: aversions
224mg/dl metabolic needs. After 5 days of
nursing > Emphasize > To promote
> Patient may interventions, importance of wellness
manifest: patient will well balanced
 Fatigue nutritious intake
 Poor demonstrate
muscle behaviors or > Advise patient > To prevent
tone lifestyle changes to comply to the nutrition
to regain dietary regimen imbalance.
appropriate but with
weight. adequate
nutrition.

> Promote > To enhance

pleasant, food intake
relaxing
environment

> Provide > To reduce

adequate rest metabolic
periods demands and
prevent fatigue

> Weigh the pt. > To monitor wt.

daily. losses and gains.
Problem #2: Fatigue

Cues Nursing Scientific Objectives Nursing Rationale Expected Outcome

Diagnosis Explanation Interventions
S> “Mangalambut Fatigue r/t Type 2 diabetes Short Term: > Establish > To gain Patient is expected to
ku” decreased is caused by After 2 hrs. of rapport. patient’s trust identify the basis of
O> patient metabolic rate 2 insufficient nursing and cooperation. fatigue and individual
manifested: diabetes mellitus number of interventions, areas of control as
 Weakness insulin receptors the patient will > Monitor and > For baseline well as report
 Lethargy on target cells be able to record v/s. measurement. improved sense of
that do not identify the basis energy.
> Patient may respond of fatigue and > Instruct to > To reduce
manifest: normally to individual areas combine and fatigue.
 Decreased insulin. Without of control. simplify
work enough insulin, activities.
perfor- glucose cannot Long Term:
mance enter the cells After 5 days of > Review > Certain drugs
which results to nursing medication are known to
decreased interventions, regimen/ use. exacerbate
metabolic rate the patient will fatigue.
and lack of be able to report
energy therefore improved sense > Suggest use of > Participating
causing fatigue. of energy. diversional in pleasurable
activities like activities can
listening to help refocus
music. energy.

> Encourage > To promote

nutritionally energy.
dense foods and
avoid caffeine
and high sugar
foods/ drinks.

> Provide > To reduce

adequate rest fatigability.
periods.

> Discuss > To understand

therapy regimen relationship of
relating to fatigue to illness
individual
causative factors
Problem #3: Ineffective Peripheral Tissue Perfusion

Cues Nursing Scientific Objectives Interventions Rationale Expected outcome

Diagnosis explanation
S> “ Mangalambut ku Ineffective Since the blood Short term: > Establish > To gain Patient is expected
tapus pane lang pata Peripheral glucose level is After 3 hrs. of rapport. patient’s trust to demonstrate
ding bitis ku”. Tissue perfusion increased with nursing and cooperation. participation on
r/t increased Diabetes interventions, therapeutic
O> patient manifested: blood viscosity Mellitus (DM), patient will > Monitor and > For baseline measures given to
2° to alteration in demonstrate record v/s . measurement prevent
 BP of 130/80
Hyperglycemia blood flow participation on complications.
 (+) bipedal occurs. Hence, therapeutic >Assess lower > To monitor for
edema less oxygen is measures given extremities; impairment of
being distributed to prevent noting skin blood flow in the
 delayed healing all over the body occurrence of texture, presence lower
of a sore on the complications. of ulcerations. extremities.
right big toe
Long term: > Explain the
 capillary refill After 3 days of client’s > To inform the
of > 3 seconds nursing condition. pt.of her
patient may manifest: interventions, individual
patient will condition
 Temperature demonstrate > Discourage
changes tissue perfusion sitting and > To enhance
as evidenced by standing for long venous return
 Diminished decreased HGT periods, wearing and maximize
pulses results, normal constrictive tissue perfusion
v/s. clothing and
crossing legs
> Instruct the
patient to have
enough rest. > To conserve
energy and to
increase O2
supply to the
> Turn patient body
from side to side
every 2 hours > To prevent
and provide complications
foam or padding such as
on bony formation of
prominences. ulcers.
Problem #4: Fluid Volume Excess

Cues Nursing Scientific Objectives Interventions Rationale Expected outcome

Diagnosis explanation
S>ø Fluid volume Due to increase Short term >Assess skin > To check if
O> patient deficit r/t blood glucose After 3 hours of turgor/ oral the patient is Patient is expected to
manifested; excessive fluid level leading to nursing mucous dehydrated. demonstrate
 Bipedal loss increased blood interventions, membranes. participation on
edema osmolarity, patient will individual therapeutic
 Infrequent there is fluid demonstrate >Encourage >To maximize interventions and
urination shift from the participation on increase fluid intake. medication regimen as
 Wt loss 25 intracellular to individual intake. well as maintain fluid
lbs. the general therapeutic volume as evidenced by
 Delayed circulation. interventions > Weigh daily. > To monitor good skin turgor
capillary Glucose acts as and medication fluid gain or
refill (3-4 an osmotic regimen. losses.
seconds) diuretic, hence
polyuria occurs. Long term > Assess > Indicators of
After 3 days of peripheral pulses level of
nursing and capillary hydration,
interventions, refill. adequacy of
patient will be circulating
able to maintain volume.
fluid volume as
evidenced by > Promote > Overheating
good skin comfortable of patient could
turgor. environment. promote further
Cover patient fluid loss.
with light sheets.

> Investigate
changes in > Changes in
mentation/ mentation can
sensorium. be due to
abnormally high
or low glucose,
electrolyte
abnormalities,
and decreased
cerebral
perfusion.
 VIII.

DISCHARGE PLAN

Topic: Diet

Time Allotment: 2hrs

Objective Content Time Teaching Strategies

allotment

To determine whether This includes 2hrs Teach either a

teaching free-living artificial conventional meal plan
subjects with type 2 sweeteners that (no concentrated sweets)
diabetes how to contain lower sugar or one permitting as much
incorporate added content than the as 10% of total energy as
sugars or sweets into natural sugar. added sugars or sweets.
their daily meal plan
results in a greater
consumption of
calories (fat or sugar)
and deteriorates their
glycemic or lipid Avoid refined
profiles but improves This includes food carbohydrates and sugars,
their perceived quality preferences that replacing them with
of life. contain complex carbohydrates
carbohydrates from (such as wholemeal
grains, fruits and bread);
vegetables.

Emphasize the 2hrs

importance of These are foods Encourage patient to
including food that contain high lessen the intake of high
containing protein like meats protein foods especially
carbohydrate from that may also meat. Also, inform patient
whole grains, fruits, contain high fats that weight loss may
vegetables, and low-fat that triggers manifest.
milk in the diet. cholesterol.

To urge the patient to

avoid foods high in Compose of Strictly advise the patient
protein such as meats. alcoholic drinks to avoid drinking too
To encourage the such as beer or much alcohol especially
patient to refrain from brandy and other those high in alcohol
vices like alcoholic vices that may volume. Also advise them
beverages and contain toxic to stop smoking (if the
cigarettes that can substances. patient is a smoker).
aggravate the disease
and may lessen the
chances of
healing/recovery.