ANGELES UNIVERSITY FOUNDATION

Angeles City

COLLEGE OF NURSING

AY 2016-2017

NCM 103 RLE

A Clinical Case Study:

Anemia secondary to Chronic Kidney Disease

secondary to Diabetes Nephropathy

Submitted by:
BSNIIIB – Group 8
David, Vincent Carl
Gonzales, Chelsea Johann
Manaloto, Fhay Aika
Songco, Neil Patrick
Tapnio, Crizzel Ann

Submitted to:
Mrs. Jasleen Yumang RN, MN
(Clinical Instructor- JBL Medicine Ward)
 I. INTRODUCTION

“Wherever the art of Medicine is loved, there is also a love of Humanity.”

- Hippocrates

The best doctors were those who followed the advice of Hippocrates to pay attention
to the patient, not just the disease, and to render treatments that would first do no harm.
They formed healing relationships with patients, understood their needs and psychology,
and helped them mobilize natural resiliency to face and fight illness. But what exactly is
the art of medicine? We believe that quality of care is based on creating the right
structures, implementing the right processes and identifying the right outcomes. Quality
care is a blend of technical and interpersonal skills that together create the art of
medicine.

The relationship between medical art and science is changing rapidly, with the science
now overwhelming the art. Doctors more and more function like technicians, not healers.
As doctors gained in science they have lost in art; often they treat the lab tests, not the
patient. The precious and powerful doctor/patient relationship is lost in the excessive
application of unnecessary, even quite harmful, medical technology. It is the ethical
dimension of individuals that is essential to a system’s success. Ultimately, the secret of
quality is love and passion. If you have these qualities, you can then work backward to
monitor and improve your care that you implement on the patient.

Anemia is a condition that develops when your blood lacks enough healthy red blood
cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If
you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low, the
cells in your body will not get enough oxygen. Symptoms of anemia -- like fatigue -- occur
because organs aren't getting what they need to function properly. Other symptoms of
anemia are easy fatigue and loss of energy, unusually rapid heartbeat, shortness of
breath and headache, particularly with exercise., difficulty concentrating, dizziness, pale
skin, leg cramps, and insomnia. In our case, it is secondary to Chronic Kidney Disease. In
CKD, the kidneys are damaged thus they do not make enough erythropoietin (EPO).
EPO are produced by healthy kidneys and prompts the bone marrow to make red blood
cells, which then carry oxygen throughout the body. As a result, the bone marrow makes
fewer red blood cells, causing anemia. The cause of CKD in our patient is Diabetes
Nephropathy. Nephropathy means kidney disease or damage. Diabetic nephropathy is
the damage to your kidneys caused by diabetes. In severe cases it can lead to kidney
failure. The kidneys have many tiny blood vessels that filter waste from your blood. High
blood sugar from diabetes can destroy these blood vessels. Over time, the kidney isn't
able to do its job as well. Later it may stop working completely. This is called kidney
failure.

Anemia, CKD, and Diabetes Nephropathy are one of the conditions which student-
nurses encounter during their exposure at the clinical setting. These diseases comprises
of complexities of the anatomical concepts that surveys a thorough description to
understand its manifestations and formulate interventions. It is interesting on our part to
learn their definition, causes, and proper management. The group chose this case
because we wanted to show the readers the process on how this case occurs and for
them to fully understand and be reminded on one of the complications associated with
their patients. We also want to have a further insight about the condition.

Globally, anemia affects 1.62 billion people (95% CI: 1.50–1.74 billion), which
corresponds to 24.8% of the population (95% CI: 22.9–26.7%). The highest prevalence is
in preschool-age children (47.4%, 95% CI: 45.7–49.1), and the lowest prevalence is in
men (12.7%, 95% CI: 8.6–16.9%). However, the population group with the greatest
number of individuals affected is non-pregnant women (468.4 million, 95% CI: 446.2–
490.6). (Source: http://www.who.int/)

General Objectives

After completion of the clinical case study, the student nurse shall have:

Student Nurse centered:

 Establish therapeutic relationship with the client

 Gained information on the client’s reason for admission
 Defined Anemia secondary to CKD secondary to Diabetic Nephropathy.
 Determined the possible risk factor that have contributed to the disease of the
patient.
 Reviewed the anatomy and physiology of organs that can be affected by Anemia
secondary to CKD secondary to Diabetic Nephropathy.
 Identified the clinical manifestations of the disease condition.
 Developed Nursing care plans for the manifestations of the disease condition.

Client Centered

 Established therapeutic relationship with the student nurse

 Understood his/her condition and its process
 Modified behaviors to improve health conditions
 Showed willingness to participate in all necessary management for his/her
condition
 Stated his/her concerns regarding her disease condition.
II. NURSING PROCESS

A. ASSESMENT
1. Personal History
a. Demographic Data
Mrs. Anemia (not her real name) is 49 years old female, born on March 12, 1967.
She is a Filipino citizen and was raised as Roman Catholic. Mrs. Anemia is married to Mr.
Anemia and they have four (4) children. They currently live in Mexico, Pampanga. Mrs.
Anemia was admitted at a tertiary hospital in City of San Fernando, Pampanga last
August 15, 2016 at 10:30 am with a chief complaint of difficulty of breathing (DOB). The
admitting diagnosis of Mrs. Anemia was Anemia Secondary to Chronic Kidney Disease V
Secondary to Diabetes Nephropathy, On Maintenance Hemodialysis; Diabetes Mellitus
Type 2; Hypertension 2.

b. Socio-Economic and Cultural Factors

B.1. Income and Expenses

Mr. Anemia is currently working as a carpenter while Mrs. Anemia is only a

housewife. Their oldest child and 2nd child are working in a company. According to Mrs.
Anemia, their family income is 12,500 php. The family’s expenses includes their food,
electricity, school and for transportation.

The family’s income is Php 12,500.00 per month; Php 2,083.33 is allotted per
family member. According to National Economic Development Authority, each family
member should have Php 2, 873.33 per month in order to meet the basic needs. The
family is considered poor, since each family member receives Php 2, 083.33 per month
which is less than the required amount of NEDA per month which is Php 2, 873.33

B.2. Educational Attainment

According to Mrs. Anemia, she took her primary education and finished only Grade
4 and unfortunately, she was not able to pursue a college degree due to financial
constraints.
B.3. Religious Affiliation

Mrs. Anemia and her family are Roman Catholic. According to her, they attend the
mass regularly every Sunday.

B.4. Cultural factors affecting health of the family

According to Mrs. Anemia, she verbalized that they do believe in herbolaryos and
hilots that is why whenever they have simple sickness like cough, colds, and fever, they
would usually seek help from them. But when major sickness occurs they would decide to
seek medical checkup and go to a tertiary hospital in City of San Fernando, Pampanga.

c. Environmental Factors
According to Mrs. Anemia, they own a nipa hut (Bahay Kubo) or native filipino style
house which is made of light materials such as wood, bamboo rods, and bamboo mats
called “sawali” and this nipa hut contains their bedroom, living room, kitchen and comfort
room. It has 2 windows and 1 door. As she described their house the ground is not
cemented. In their kitchen they use only a “Lutuan De Uling” for cooking. The family’s
source of water is from their pitcher-pump. This is utilized for laundry, coking, daily
hygiene and boiled it as they used it for their source of drinking water. The source of
electricity is supplied by ANAW that supplied their fluorescent bulb and electric fan. They
use bottles, cups and pitcher for their drinking water. They have one toilet facility without
water carriage. They put their accumulated garbage in a 1 sack and they put it on a one
place (dumping) and burn it. Their means of transportation is by using their private
motorcycle. Mrs. Anemia usually eat fish and she said that everytime she eats, she
always have seasonings with it. Mrs. Anemia doesn’t smoke and drink alcoholic
beverages.

The place where the patient resides is just near from commercial establishments
such as hospitals, public market, grocery stores and pharmacy. Mrs. Anemia mainly buy
their necessities from nearby grocery stores that have almost everything they need.
Generally speaking, they are contented from where they are situated, according to the
Mrs. Anemia commentary.
 2. Family Health-Illness History

Grandmother Grandmother
Grandfather Grandfather
HYPERTENSION OLD AGE

HYPERTENSION
+ OLD AGE
+
+ +
Father
Mother
ASTHMA
OLD AGE

+ +

Sister MRS. Sister Sister

ANEMIA
(1st) (3rd) (4th)
(2nd)

ANEMIA
DM DM HPN

Sister Sister Sister

(5th) (6th) (7th)

NO KNOWN NO KNOWN NO KNOWN

SICKNESS SICKNESS SICKNESS

According to Mrs. Anemia, her grandparents from the side of her father died
because of hypertension while her grandparents from the side of her mother died
because of old age. The father of Mrs. Anemia died because of asthma while her mother
died because of old age. According to Mrs. Anemia, her 1st and 3rd sisters have Diabetes
Mellitus while her 4th sister has hypertension. There were no known illnesses for the last
three sisters of Mrs. Anemia.

3. History of Past Illness

According to Mrs. Anemia, she never experience chickenpox, mumps, measles,

streptococcal infection, scarlet fever, and rheumatoid fever during her childhood. There is
no known allergy to any food and drugs. As common illness, she suffers from colds,
coughs and fever. In times when he feels any aforementioned illness: she will just
increase her oral fluid intake and she would usually take over the counter drugs such as
paracetamol for fever and Ambroxol for severe coughs until her condition minimizes. In
the year 2001, Mrs. Anemia manifested increase appetite, urination, and excessive thirst.
According to her, these manifestations happened when she was pregnant with her last
child. She was not able to consult from a physician because of financial constraints. For
the 14 years, she had no history of hospitalization. According to her, last year 2015 she
was hospitalized because of hypokalemia, hyponatremia, and feelings of bloatedness.
Last May 29, 2016 she undergone surgical procedure which is Subclavian Hemodialysis
Catheter which is contiuous dialysis and according to her, the catheter which was used is
the same all through out until the student nurses assessed her.

OBSTETRIC HISTORY

Mrs. Anemia is still in reproductive age which is 49 years old but she already had
menopausal period. She has an obstetrical history of G4P4T4P0L4M0. She had four
pregnancies and all passed the age of viability. The first child was born accidentally at a
Public utility jeepney (PUJ) while the second child was born at home assisted by a
midwife. The third child was born at a secondary hospital and her fourth child was born at
a tertiary hospital. All children were delivered via normal spontaneous delivery. All of
them reached their full term of 38 weeks and are all living. Mrs. Anemia has received
complete doses of Tetanus Toxoid immunization from their barangay health center in
Mexico, Pampanga.
Mrs. Anemia had her 1st menstruation at age of 11. She has a menstrual cycle of
28 days and menstrual period of 3-4 days and it is regular since she was 11 years old.
She experiences mild to moderate menstrual flow and uses 4-5 sanitary pads per day.
She added that she experience slight pain or dysmenorrhea during her menstrual period.

1st, 2nd, 3rd Child

During Mrs. Anemia first three pregnancies, she had experienced nausea and
vomiting. She did crave of apple during her 1st pregnancy. During her 2nd pregnancy, she
did crave of banana. She did crave of mango during her 3 rd pregnancy. For her
succeeding pregnancies, she did not disregard her responsibility towards proper diet and
nutrition needed by a pregnant woman. Mrs. Anemia had complete prenatal check-ups at
the barangay health center in Mexico, Pampanga for the first three pregnancies. All three
babies were born via normal spontaneous delivery, all at full term without any
complications.
4th Child
The last pregnancy of Mrs. Anemia was born at a tertiary hospital. According to
Mrs. Anemia, in the year 2001 she experienced a lot of complications during her last
pregnancy such as massive bleeding and developed gestational hypertension. According
to Mrs. Anemia, she manifested increased appetite, urination and excessice thirst. She
also experienced nausea and vomiting.

4. History of Present Illness

According to Mrs. Anemia, she is already experiencing difficulty of breathing last

August 14, 2016 (Sunday) which led her to experienced difficulty of sleeping at night.
Four days prior to the admission, a diagnostic procedure was done by Mrs. Anemia which
was Complete blood count (CBC) and she was advised to undergo blood transfusion but
she refused for admission because of financial constraints and she don’t like that
hospital. Last August 15, 2016, few hours before the admission, she suddenly
experienced DOB, SOB and easy fatigability and her family decided to bring her to
Mexico Community for consultation. Laboratory procedures were done at Mexico
Community then the family immediately transferred Mrs. Anemia at a tertiary hospital in
City of San Fernando, Pampanga. Mrs. Anemia was admitted with a Chief complaint of
DOB. According to her, DOB happened even if she is at rest and that is the only time
when she experienced DOB based on their assessment of the patient’s condition. Upon
admission, the physician ordered PNSS 1L X 10 gtts/min KVO, repeat for Complete
Blood Count (CBC) with Prothrombin time, ABO RH typing, Blood Urea Nitrogen (BUN),
Na (Sodium), K (Potassium), Ca (Calcium), Phosporus, Chest Radiography and the
patient was prepared and transfused 2 units of pack red blood cells (PRBC) properly
typed and cross matched. The following are the pre-blood transfusion medications order
for Mrs. Anemia: Paracetamol 300 mg/IV, Diphenhydramine 50 mg/IV, and FeSO4 + FA
tab/TID.

5. Physical Examination (Cephalocaudal Approach)

August 15, 2016 (FIRST DAY ADMISSION)

Ms. ANEMIA
LIFTED FROM THE CHART
This section provides the information necessary to determine the health status of the
patient. It includes the vital signs every Nurse-Patient interaction and it includes the
physical assessment and neurological assessment.

GENEREAL APPEARANCE:

(+) conscious HEART

(+) coherent Rate: tachycardia

SKIN:
LUNGS
(+) pale
(+) Tachypnea
(+) dry skin (+) Crackles located at left lung upper
warm field upon auscultation

HEENT Normal lung expansion

Pale palpebral conjunctiva Normal lung rhythm

 (+) left lower quadrant pain
ABDOMEN

VITAL SIGNS OBTAINED:

BP= 150/70 mmHg, HR=78 bpm , RR=19cpm , T=36.2C

1st day of NPI (August 18, 2016)

1th day of Hospitalization

General Survey

Patient IBS has a chief complaint difficulty of breathing. She was conscious and
coherent, oriented to time, place, and person. She was lying on bed on a semi fowler’s
position. Mrs. Anemia has an intact heplock on her right arm; patient appears to be weak
and pale in color

Integumentary System

Skin: The skin has uniform color, with fair complexion, with absence of lesions and
jaundice. Absence of nodules upon palpation, no signs of inflammation such as swelling
or edema, skin is warm to touch, and appears dry and pale.

Nails: The fingernails are short and clean same as the toenails. No clubbing observed.
Nails are intact on the epidermis, purplish and smooth.

Head

Scalp: Hair is black and evenly distributed, absence of lice and flakes. With intact skin.
No masses noted upon palpation

Skull: Normocephalic. No masses, nodules or tenderness upon palpation.

Face: Facial expressions is symmetrical with intact skin absence of lesions. No masses
noted upon palpation

Eyes

Eyes: Normal position and alignment in relation to the tip of the pinna.

Visual field: she can see and read clearly.

Eyebrows: With black, thin hair evenly distributed. Alignment is symmetrical with intact
skin and equal movement

Eyelids: Symmetrical with intact skin. Absence of lesions and with present blink reflex.

Eyelashes: Equally distributed black hair.

Cornea: Transparent, smooth and shiny; blink reflex is observed upon introduction of the
cotton ball to the cornea.

Iris: Black in color

Lacrimal apparatus: No tenderness and edema noted

Conjunctiva: Bulbar conjunctiva is transparent, smooth and the palpebral conjunctiva is

smooth, shiny and pink in color.

Pupils: Pupils are equal in size with consensual and direct response upon introduction of
light. Pupils dilate when staring at distant objects and constricting when staring at near
objects.

Ears

Auricle: The color is uniform with the facial skin, absence of redness or swelling and with
intact skin. Aligned with the outer canthus of the eye. It recoils after folding with no pain
felt upon application of pressure behind the ear.

External ear canal: Absence of discharge, moisten with earwax.

Hearing acuity: Able to hear normal voice tone

Nose and Sinuses

Nose: The external part has intact skin, the nasal septum is intact and in midline position.
No masses noted upon palpation.

Sinuses: No pain noted upon palpation of facial sinuses. No redness and swelling
observed.

Mouth and Throat

Lips: Dry, pale and symmetrical with intact skin.

Oral Mucosa: with intact skin, moist with uniform in color. No lesions or redness noted.

Gums: No tenderness
Teeth: The upper and lower sets of teeth are complete, strong, and whitish.

Palate and uvula: Moist, smooth, light pink. The anterior palate is hard whereas the
posterior palate is soft. Uvula is positioned in midline of the soft palate.

Tongue: Is centrally positioned, moves freely with no tenderness or swelling or lesions

observed.

Floor of the mouth: No lesions observed.

Pharynx: Absence of redness and swelling and with non-inflamed, pink tonsils.

Neck

Neck: No masses observed upon inspection. Absence of palpable lymph nodes. The
neck muscles are equal in size and smooth movement without discomfort is observed.
The head is centrally positioned.

Trachea: Centrally located, can be displace and returns to its normal position.

Thyroid Gland: Not visible during inspection and ascends during swallowing. With
absence of nodules or tenderness upon palpation.

Thorax and Lungs

Respirations: Presence of crackles located at left upper lung field upon

auscultation and presence of difficulty of breathingWith no inspiratory retraction of
the supraclavicular areas or no chest retractions were noted during inspiration.

Posterior chest: The spinal column is centrally aligned, without any deviations. With no
retractions of the intercostal muscles upon respiration. Upon palpation there were no
tenderness observed. With symmetrical expansion and even tactile fremitus palpated. No
dullness observed upon the percussion of the chest.

Anterior chest: Symmetrical chest expansion and with no intercostal retractions

observed during inspirations with intact skin. Upon palpation there is no tenderness seen.
Even tactile fremitus observed.

Cardiovascular system
Jugular vein: Not distended.

Carotid artery: no bounding pulse observed, fast full pulsation. Carotid pulse: adequate
pulsation, no bruit observed.

Heart: with normal heart rate.

Abdomen

There is no lesion and the skin is intact and unblemished. Has symmetric contour
and with symmetrical movements during inspiration. No pulsations seen. No evidence of
enlargement of liver and spleens. Upon auscultation bowel sounds are audible with
absence of arterial bruits. Tympanic over the stomach is observed and dullness on the
right upper quadrant. No masses or tenderness noted upon palpation.

Peripheral Vascular system

Upper extremities: symmetric, absence of swelling with palpable pulsation. Hair is

evenly distributed, muscles are equal in size, no contractures, no tremors, no bone
deformities, no tenderness palpated. With palpable pulse.

Lower extremities: symmetric, absence of swelling with palpable pulsation. Hair is

evenly distributed, muscles are equal in size, no contractures, no tremors, no bone
deformities, no tenderness palpated. With palpable pulse.

Muscles:

Muscle weakness noted.

Tendons: No contractures observed.

Motor Function

Fine motor test: Can repeatedly and symmetrically touch the nose. Can rapidly touch
each finger by the thumb of the same hand in finger to thumb test.

Bones and joints

 No deformities noted. No tenderness or swelling noted.

Mental status:

Orientation: oriented to person, time and place.

NERVOUS SYSTEM
CRANIAL NERVES:
Cranial Nerve I (Olfactory) The patient has good sense of smell
For sensory specifically for smell.
Cranial Nerve II (Optic) The patient was not able to read the text 14
For sensory specifically for vision. inches a way when asked to read module.
Cranial Nerve III (Oculomotor) and Cranial The patient showed positive (+) EOMS on
Nerve IV (Trochlear) both eyes
Motor to 4 of 6 eyes extrinsic muscle and
upper eyelid, parasympathetic constrict
pupils, thicken lens. Motor to one extrinsic
eye muscle.
Cranial Nerve V (Trigeminal) The patient had positive (+) Corneal reflex
Sensory to face and teeth and can clench jaw
Cranial Nerve VII (Facial) The patient can easily raise eyebrows

Cranial Nerve VIII (Vestibulocochlear) The patient can hear the tick of the watch
For hearing and balance. clearly with 1.5 inches away from him.

Cranial Nerve IX (Glossopharyngeal) and When patient speaks, her uvula and soft
Cranial Nerve X (Vagus) palate move straight up and the patient
Sensory to taste and touch to back of gags.
tongue.
Cranial Nerve XI (Accessory) Normal Range of motion of the patient’s of
Motor to neck and upper back muscle. patients neck and shoulders.

Cranial Nerve XII (Hypoglossal) Tongue is motionless and centered on

Motor to tongue muscle. mouth floor

Diagnostic and Laboratory Procedures:

Diagnostic/Lab Date Indication or Purpose Resu Normal Analysis an
oratory Ordered lts Values Interpretation
Procedure (Units of Results
Date Result- used in (Patient-
In the Centered)
hospital
)

Complete CBC provides valuable

Blood Count information about the blood
(CBC) and blood-forming tissues
(especially the bone
marrow), as well as other
body systems. Abnormal
results can indicate the
presence of a variety of
conditions-including
infections

(120-
160 g/L)

58
Measures the total amount
of hemoglobin in the blood to
determine the oxygen
carrying capacity of the
blood.
Hemoglobin
The patient
hemoglobin
D.O.: 8/16/16 count is
moderately
D.R.: low. This
means that the
8/16/16
patient has
problems with
tissue
perfusion that
could have
risen from the
kidney’s
inability to
produce
erythropoietin
which is
primarily
hormone for
red blood
 production.

106

The
hemoglobin
count on
the fourth
day slightly
increased
but still
below
normal
range
because the
patient
responded
well on the
given PRBC
(2units).

D.O.: 8/18/16

D.R.:

8/18/16

Hematocrit D.O.: 8/16/16 The hematocrit is a measure 0.21 (0.37- Hematocrit

of the volume of RBCs in 0.47) level is below
D.R.: whole blood expressed as a normal range,
percentage. meaning the
8/16/16 percentage of
RBC’s in a
sample of
D.O.: 8/18/16 whole blood is
below lower
D.R.: limits. Low
hematocrit is
8/18/16 related to
anemia.
 An RBC count is a blood test 4.10-
that measures how many 5.10
red blood cells (RBCs) you 0.32 x10^12/
have. L

A low RBC
count may
indicate
anemia.
2.86

D.O.: 8/16/16

D.R.:

Red Blood Cell 8/16/16

Count

D.O.: 8/16/16 Used for many years to help 4.0

detect inflammation associat
Erythrocytes D.R.: ed with conditions such (4.0-5.4 The result is
as infections, cancers, x109/L) within the
8/16/16 and autoimmune diseases. normal values.

4.5
D.O.: 8/18/16

D.R.:

8/18/16
WBC (White D.O.: 8/16/16 Determine the number of 13.0 (4.0- The first result
Blood Cell) circulating WBCs in the 10.0 of patient’s
D.R.: blood. An elevated WBC x10^9/L) WBC is
count occurs in infection, elevated due to
8/16/16 inflammation, tissue injury, the presence
and leukemia. A low WBC 7.3 of infection.
count may occur in some
D.O.: 8/18/16 viral infections,
immunodeficiency states,
D.R.: and bone marrow failure.

8/18/16

A neutrophil is a granulocyte
(a type of white blood cell)
that is designed to fight off
infections and diseases that
enter the body.

D.O.:
8/16/16 The second
result of
D.R.:
patient’s WBC
(55.0-
Neutrophils 8/16/16 90.0 is within
65.0%)
normal function
which indicates
absence of
D.O.: 8/18/16 infection and
patient
D.R.: responded well
on the given
8/18/16
antibiotic.
 65.6

Produces antibodies The result is

responsible for allergic elevated
reactions. the lymphocytes which is can be
produce antibodies to fight attributed to
the microorganisms. the presence
of inflammatory
process
brought about
by the kidney
injury.

The second
result is within
D.O.: the normal
8/16/16 7.8 values.
(25.0-
D.R.: 35.0%)

8/16/16 22.4
Lymphocytes

D.O.: 8/18/16 Lymphocytes

are below
D.R.: normal levels
even though
8/18/16 the patient has
signs of
infection. This
may indicate
that his body is
unable to
produce
enough
lymphocytes to
fight against
bacterial
infection
Monocytes D.O.: 8/16/16 Monocytes help the other 1.8 (3.0-6.0) Monocytes are
cells in the blood remove below normal
D.R.: damaged tissue. levels which
indicates an
8/16/16 increased risk
for infections.

D.O.: 8/18/16 6.7

D.R.: An increase in
Monocytes
8/18/16 count may be
due to
infection.

Eosinophils D.O.: 8/16/16 Eosinophils are a

component of the innate
D.R.: immune system. They have 3.0 (2.0- Result is within
a variety of functions but are 4.0%) normal range
8/16/16 especially important in 4.0 which indicate
defense against parasitic absence of
infections infection.
D.O.: 8/18/16

D.R.:

8/18/16

Basophils D.O.: Basophils are 0.2 (0.0-1.0%) Result is within

8/16/16 produced in bone normal range
marrow, circulate which indicate
D.R.: in the blood and absence of
are the least infection.
8/16/16 abundant of all
leukocytes.
0.4
D.O.:
8/18/16

D.R.:

8/18/16
Platelet count D.O.: Platelets (thrombocytes) 264 (150- The platelet
8/16/16 are the smallest type of 450x109/L) count is still
blood cell. They are 228 within the
D.R.: important in blood normal
clotting. When bleeding range, which
8/16/16 occurs. If there are too could
many platelets, there is indicate that
a chance of a blood clot the blood
D.O.: forming in a blood component
8/18/16 vessel. Also it may also was not
evaluate the risk of affected by
D.R.: having bleeding the disease
tendency both internally condition.
8/18/16 and externally.

MCV is a part of RBC

indices (erythrocyte
indices), which are
measurements and/or
calculations for
determining the size, (80-100
96.3 g/L
content, and
hemoglobin
concentration.

The result is
90.7 within the
normal
values
indicates
normocytic
(normal
average RBC
size).

MCV D.O.:
(Mean Corpuscular
Volume) 8/16/16

D.R.:

8/16/16

D.O.:
8/18/16

D.R.:

8/18/16

MCH (Mean D.O.: Parts of red cell indices 31.5 (27.0- The result is
Corpuscular 8/16/16 (parameters reflecting 34.0) within the
Hemoglobin) size and hemoglobin normal
D.R.: content of red cells) that values.
have traditionally been
8/16/16 used to aid in the
differential diagnosis of 30.0
anemia.
D.O.:
8/18/16

D.R.:

8/18/16

D.O.: Measures the

8/16/16 concentration 327
of The result is
MCHC D.R.: hemoglobin in an within the
average red blood cell. (310-370 normal
(Mean corpuscular 8/16/16 These numbers help in g/L values.
hemoglobin the diagnosis of
concentration) D.O.: different types of 331
8/18/16 anemia.

D.R.:

8/18/16
 D.O.:
8/16/16
RDW-CV (Red Blood Measures 0.014 (0.110- The result is
Cell Distribution Width D.R.: variation in red 0.160%) below normal
Corpuscular Volume ) blood cell size or indicates. any
8/16/16 red blood cell number of
volume. things,
including low
D.O.: vitamin B12
8/18/16 and liver
0. 015 problems.
D.R.:

8/18/16 49.5

The result is
D.O.: The RDW-SD is within the
RDW-SD (Red Cell
8/16/16 an actual (35.0- normal values.
Distribution Width - 51.1
measure of size. It 56.0fL)
Standard Deviation)
D.R.: is derived by
finding the width
8/16/16 in fluid Liters at
the 20% height of
the distribution
histogram.
D.O.:
8/18/16

D.R.:

8/18/16

BUN (Blood Urea

Nitrogen) D.O.: This fast, simple 28.20 (2.78- High BUN
8/16/16 blood test is most 8.07mmol/L levels can
commonly used to indicate high
D.R.: evaluate kidney protein levels
function. and patient
8/16/16 kidneys are
not working
well.

Creatinine D.O.: A serum creatinine test 811.0 (44-80 Increased patient’s

8/16/16 — which measures the umol/L) creatinine may
level of creatinine in your indicate impaired
D.R.: kidney functioning
blood — can indicate
to eliminate
8/16/16 whether your kidneys are excess waste
working properly. products of the
body.

140.0
Sodium is a mineral (136-145
essential to your body. It The result is within
mmol/L)
is also referred to as normal rang
Na+ or natrium. Sodium
is particularly important
6.70
for nerve and muscle
D.O.:
Sodium function.
8/16/16 (3.5-5.1
The result shows
Potassium (K+) helps mmol/L)
D.R.: that potassium
nerves and muscles level is elevated.
8/16/16 communicate. It also Elevation is
helps move nutrients into caused by the
cells and waste products chronic kidney
out of disease since it is
cells. Potassium levels in the primary route
the body are mainly for potassium
controlled by the excretion.
hormone aldosterone.

D.O.:
8/16/16
Potassium D.R.: Phosphorus is greatly 2.02 (0.81-1.45
eliminated through urine. mmol/L)
8/16/16 Since the patient
manifests congestion
and decrease urination,
phosphorus is evaluated The result shows
to determine that phosphorus is
abnormalities in slightly elevated
phosphorus level. from normal level.
Since principle
with potassium,
phosphorus is
excreted by the
kidney. Since
patient’s kidney
are unable to form
urine, phosphorus
is not excreted
Ionized calcium levels resulting retention.
give more information
about active, ionized (1. 12-1.32
calcium. It may be 1.22 mmol/L)
important to know
D.O.: ionized calcium levels if
8/16/16 patient have abnormal
levels of proteins, such The result is within
D.R.: as albumin, or the normal values.
Phosphorus
immunoglobins in blood.
8/16/16
 D.O.:
8/16/16

D.R.:

8/16/16
Ionized
Calcium

Urinalysis D.O.: Urinalysis was ordered Color: Straw The patient has
8/16/16 to determine whether the normal color urine.
urine contains Light yellow
D.R.: substances indicate or
normally absent from
8/16/16 urine and detected by
Trans: Clear
urinalysis are proteins, The patient urine
acetone, blood, pus and Turbid is turbid in color
casts. because of the
presence of pus ,
albumin and RBC
in the urine.

Rxn:

Acidic Slightly
acidic

Patient has acidic

urine. This is
None caused by
Albumin compromised
kidney function of
++++ minting acid-base
homeostasis.
 The result shows
the there is the
presence of
albumin in patients
urine caused by
failure of the
kidneys to filter
macromolecules
secondary from
Specific (1.010- the increased
gravity: 1030) permeability of the
glomerular
1.020 membrane.

RESULTS

A microscopic Microscopic The result shows

examination may or may Examination is within normal
not be performed as part range.
of a routine urinalysis. It
will typically be done Pus cells,
Pus Cells 1-2/HPF
when there are abnormal epithelial cells,
findings on the physical mucus threads,
or chemical examination bacteria, and
and the results from all crystals are all
will be taken into account normal findings.
for interpretation Epithelial Cells Red blood cells in
Rare the urine are found
as abnormal and
as seen in the
results, the
patient’s RBC’s in
the urine are way
Mucus below normal
Threads N/A levels. RBC’s in
the urine may also
coincide with
proteinuria/albumi
nuria, which is
expected from a
patient with
Diabetes.
Bacteria Few

Crystals N/
ANATOMY AND PHYSIOLOGY
(Source: SEELEY’S ESSENTIALS OF ANATOMY & PHYSIOLOGY, 8TH EDITION,
International Edition 2013)

ENDOCRINE SYSTEM

The endocrine system performs their regulatory functionsby means of chemical

messenger sent to specific cells. The endocrinesystem, secreting cells send hormones by
way of the bloodstream tosignal specific target cells throughout the body. Hormones
diffuse intothe blood to be carried to nearly every point in the body. Theendocrine glands
secrete their products, hormones, directly into theblood. There are two classifications of
hormones: steroid hormones andnon-steroid hormones. The steroid hormones which are
manufacturedby the endocrine cells from cholesterol, is an important lipid in thehuman
body. Non-steroid hormones are synthesized primarily fromamino acids rather from
the cholesterol. Non-steroid hormones arefurther subdivided into two: protein hormones
and glycoproteinhormones.

Aldosterone
- Its primary function is the maintenance of the sodiumhomeostasis in the blood
byincreasing the sodium reabsorption in thekidneys. It is secreted from the adrenal
cortex; it triggers the release of ADH which results to the conservation of water by
the kidney.Aldosterone secretion is controlled by the rennin-
angiotensinmechanism.
Estrogen
It is secreted by the cells of the ovarian cells that promoteand maintain the female sexual
characteristics.

Progesterone
- It is secreted by the corpus luteum. It is also known as apregnancy- promoting
steroid and it prevents the expulsion of thefetus in the uterus.

Anti-diuretic hormone (ADH)

- It is secreted in the neurohypophysis (posterior pituitary);it literally opposes the
formation and production of a large urinevolume. It helps the body to retain and
conserve water from thetubules of the kidney and returned to the blood.

EXOCRINE SYSTEM

The exocrine system’s main function is to regulate the volume and composition of
body fluids and excrete unwanted materials, but it is not the only system in the body
that is able to excrete unnecessary substances.

Kidneys

The kidneys resemble the lima beans in shape. The average-sized kidneymeasures
around 11cm by7cm by 3cm. The left kidney is often larger than the right. The kidneys
are highly vascular organs.Approximately, one-fifth of the blood pumped fromthe heart
goes to the kidneys. The kidneysprocess blood plasma and form urine fromwaste to be
excreted and emoved from the body. These functions arevital because theymaintain the
homeostatic balance of the body. The kidneys maintainthe fluid-electrolyte and acid-base
balance. In addition, they alsoinfluence the rate of secretion of thehormones ADH and
aldosterone.Microscopic functional units called nephrons make up the bulk of the kidney.
The nephron is uniquely suited to its function of blood plasma processing and urine
function. A nephron containscertain structures in which fluid flows through them and they
are asfollows: renal corpuscle, Bowman’s capsule, proximal convulted tubule,Loop of
Henle, distal convoluted tubule and the collecting tube. TheBowman’s capsule is a cup-
shaped mouth of a nephron. It is usuallyformed by two layers of epithelial cells. Fluids,
electrolytes and waste products that pass through the porous glomerular capillaries and
enterthe space that constitute the glomerular filtrate, which will beprocessed in the
nephron to form urine.The Glomerulus is the body’s well-known capillary networkand is
surely one of the most important ones for survival. Glomerulusand Bowman’s capsule
together are called renal corpuscle. The permeability of the glomerular endothelium
increases sufficiently toallow plasma proteins to filter out into the capsule.

Blood has always fascinated humans, and throughout history they have speculated
about its function. Some societies consider blood the “essence of life” because the
uncontrolled loss of it can result in death. Many cultures around the world, both ancient
and modern, believed blood has magical qualities. Blood has also been thought to define
our characters and emotions. Blood performs many functions essential to life and can
reveal much about our health. The heart pumps blood through blood vessels and extend
throughout the body.

Composition and Function of Blood

Components

Blood is a type of connective tissue that consists of a liquid matrix containing cells and
cell fragments. The liquid matrix is the plasma, and the cells and cell fragments are the
formed elements. The plasma accounts for slightly more than half of the total blood
volume, and the formed elements account for slightly less than half. The total blood
volume in the average adult is about 4-5 liters (L) in females and 5-6 L in males. Blood
makes up about 8%of total body weight.

Physical Characteristics and Volume

Blood is a sticky opaque fluid with a characteristics metallic taste. As children, we

discover its saltiness the first time we stick a cut finger into the mouth. Depending on the
amount of oxygen it is carrying, the color of blood varies from scarlet (oxygen rich) to a
dull red (oxygen poor). Blood is heavier than water and about five times thicker, or more
viscous, largely because of its formed elements. Blood is slightly alkaline with a pH
between 7.35 and 7.45. Its temperature (38 C or 100.4 F) is always slightly higher than
the body temperature.

Plasma

Plasma is a pale yellow fluid that consists of about 91% water, 7% proteins and 2% other
components, such as ions, nutrients, gases, waste products, and regulatory substances.
Plasma maintains osmotic pressure, is involved in immunity, prevents blood loss, and
transports molecules. Unlike the fibrous proteins found in other connective tissues,
plasma contains dissolved proteins. Plasma proteins include albumin, globulins, and
fibrinogen. Albumin makes up 58% of the plasma proteins. Globulins account for 38% of
the plasma proteins. Other globulins and albumins function as transport molecules
because they bind to molecules, such as hormones, and carry them in the blood
throughout the body. Fibrinogen is a clotting factor that constitutes 4% of plasma
proteins. Activation of clotting factor results in the conversion of fibrinogen to fibrin, a
threadlike protein that forms blood clots.

Formed Elements

About 95% of the volume of the formed elements consists of red blood cells (RBCs), or
erythrocytes. The remaining 5% of the volume of formed elements consists of white blood
cells (WBCs), or leukocytes, and cell fragments called platelets, or thrombocytes. Red
blood cells are 700 times more numerous than white blood cells and 17 times more
numerous than platelets.

Red Blood Cells

Red blood cells are disk-shaped cells containing hemoglobin, which transports oxygen
and carbon dioxide. Red blood cells also contain carbonic anhydrase, which is involved
with carbon dioxide transport. In response to low blood oxygen levels, the kidneys
produce erythropoietin, which stimulates red blood cell production in red bone marrow.
Worn-out red blood cells are phagocytized by macrophages in the spleen or liver.
Hemoglobin is broken down, iron and amino acids are reused, and heme becomes
bilirubin that is secreted in bile.

White Blood Cells

White blood cells protect the body against microorganisms and remove dead cells and
debris. Granulocytes contain cytoplasmic granules. The three types of granulocytes are
neutrophils, small phagocytic cells; basophils, which promote inflammation; and
eosinophils, which influence inflammation. Agranulocytes have very small granules and
are of two types: Lymphocytes are involved in antibody production and other immune
system responses; monocytes become macrophages that ingest microorganisms and
cellular debris.

Types of white blood cells

Among your white blood cells are:

Monocytes. They have a longer lifespan than many white blood cells and help to break
down bacteria.

Lymphocytes. They create antibodies to defend against bacteria, viruses, and other
potentially harmful invaders.

Neutrophils. They kill and digest bacteria and fungi. They are the most numerous type of
white blood cell and your first line of defense when infection strikes.
Basophils. These small cells appear to sound an alarm when infectious agents invade
your blood. They secrete chemicals such as histamine, a marker of allergic disease, that
help control the body's immune response.

Eosinophils. They attack and kill parasites, destroy cancer cells, and help with allergic
responses.

Platelets

Platelets are cell fragments involved with preventing blood loss.

Platelets are the smallest of the three major types of blood cells.

Platelets are only about 20% of the diameter of red blood cells. The normal platelet count
is 150,000-350,000 per microliter of blood, but since platelets are so small, they make up
just a tiny fraction of the blood volume.

Red blood cells are the most numerous blood cell, about 5,000,000 per microliter. Red
blood cells make up about 40% of our total blood volume, a measure called the
hematocrit. Their color is caused by hemoglobin, which accounts for nearly all of the red
cell volume. Hemoglobin is the critical protein that transports oxygen from our lungs to
the tissues. Red cells are normally shaped as round, biconcave discs. With microscopic
examination, they look like a red or orange tire with a thin, almost transparent center.

White blood cells are the largest of the blood cells but also the fewest. There are only
5,000 to 10,000 white blood cells per microliter. There are several different types of white
cells but all are related to immunity and fighting infection.

Platelet Production

Platelets are produced in the bone marrow, the same as the red cells and most of the
white blood cells. Platelets are produced from very large bone marrow cells called
megakaryocytes. As megakaryocytes develop into giant cells, they undergo a process of
fragmentation that results in the release of over 1,000 platelets per megakaryocyte. The
dominant hormone controlling megakaryocyte development is thrombopoietin.
Platelet Structure

Platelets are actually not true cells but merely circulating fragments of cells. But even
though platelets are merely cell fragments, they contain many structures that are critical
to stop bleeding. They contain proteins on their surface that allow them to stick to breaks
in the blood vessel wall and also to stick to each other. They contain granules that can
secrete other proteins required for creating a firm plug to seal blood vessel breaks. Also
platelets contain proteins similar to muscle proteins that allow them to change shape
when they become sticky.

Platelet Function

In addition to being the smallest blood cell, platelets are also the lightest. Therefore
they are pushed out from the center of flowing blood to the wall of the blood
vessel. There they roll along the surface of the vessel wall, which is lined by cells called
endothelium. The endothelium is a very special surface, like Teflon, that prevents
anything from sticking to it. However when there is an injury or cut, and the endothelial
layer is broken, the tough fibers that surround a blood vessel are exposed to the liquid
flowing blood. It is the platelets that react first to injury. The tough fibers surrounding the
vessel wall, like an envelope, attract platelets like a magnet, stimulate the shape change
that is shown in the pictures above, and platelets then clump onto these fibers, providing
the initial seal to prevent bleeding, the leak of red blood cells and plasma through the
vessel injury.

Serum Proteins

Proteins make up 6-8% of the blood. They are about equally divided between serum
albumin and a great variety of serum globulins. After blood is withdrawn from a vein and
allowed to clot, the clot slowly shrinks. As it does so, a clear fluid called serum is
squeezed out. Thus, Serum is blood plasma without fibrinogen and other clotting factors.
The serum proteins can be separated by electrophoresis. A drop of serum is applied in a
band to a thin sheet of supporting material, like paper, that has been soaked in a slightly-
alkaline salt solution.

RESPIRATORY SYSTEM

The respiratory system (also referred to as the ventilator system) is a complex biological
system comprised of several organs that facilitate the inhalation and exhalation of oxygen
and carbon dioxide in living organisms (or, in other words, breathing).

For all air-breathing vertebrates, respiration is handled by the lungs, but these are far
from the only components of the respiratory system. In fact, the system is composed of
the following biological structures: nose and nasal cavity, mouth, pharynx, larynx,
trachea, bronchi and bronchioles, lungs and the muscles of respiration.

Nose and Nasal Cavity

The nose and nasal cavity constitute the main external opening of the respiratory system.
They represent the entryway to the respiratory tract – a passage through the body which
air uses for travel in order to reach the lungs. The nose is made out of bone, muscle,
cartilage and skin, while the nasal cavity is, more or less, hollow space. Although the
nose is typically credited as being the main external breathing apparatus, its role is
actually to provide support and protection to the nasal cavity. The cavity is lined with
mucus membranes and little hairs that can filter the air before it goes into the respiratory
tract. They can trap all harmful particles such as dust, mold and pollen and prevent them
from reaching any of the internal components. At the same time, the cold outside air is
warmed up and moisturized before going through the respiratory tract. During exhalation,
the warm air that is eliminated returns the heat and moisture back to the nasal cavity, so
this forms a continuous process.

Oral cavity

The oral cavity, more commonly referred to as the mouth, is the only other external
component that is part of the respiratory system. In truth, it does not perform any
additional functions compared to the nasal cavity, but it can supplement the air inhaled
through the nose or act as an alternative when breathing through the nasal cavity is not
possible or exceedingly difficult. Normally, breathing through nose is preferable to
breathing through the mouth. Not only does the mouth not possess the ability to warm
and moisturize the air coming in, but it also lacks the hairs and mucus membranes to filter
out unwanted contaminants. On the plus side, the pathway leading from the mouth is
shorter and the diameter is wider, which means that more air can enter the body at the
same speed.

Pharynx

The pharynx is the next component of the respiratory tract, even though most people
refer to it simply as the throat. It resembles a funnel made out of muscles that acts as an
intermediary between the nasal cavity and the larynx and esophagus. It is divided into
three separate sections: nasopharynx, oropharynx and laryngopharynx. The nasopharynx
is the upper region of the structure, which begins at the posterior of the nasal cavity and
simply allows air to travel through it and reach the lower sections. The oropharynx does
something similar, except it is located at the posterior of the oral cavity. Once the air
reaches the laryngopharynx, something called the epiglottis will divert it to the larynx. The
epiglottis is a flap that performs a vital task, by switching access between the esophagus
and trachea. This ensures that air will travel through the trachea, but that food which is
swallowed and travels through the pharynx is diverted to the esophagus.

Larynx
The larynx is the next component, but represents only a small section of the respiratory
tract that connects the laryngopharynx to the trachea. It is commonly referred to as the
voice box, and it is located near the anterior section of the neck, just below the hyoid
bone. The aforementioned epiglottis is part of the larynx, as are the thyroid cartilage, the
cricoid cartilage and the vocal folds. Both cartilages offer support and protection to other
components, such as the vocal folds and the larynx itself. The thyroid cartilage also goes
by a more common name – the Adam’s apple – although, contrary to popular belief, it is
present in both men and women. It is typically more pronounced in adult males. The
vocal folds are mucous membranes that tense up and vibrate in order to create sound,
hence the term voice box. The pitch and volume of these sounds can be controlled by
modifying the tension and speed of the vocal folds.

Trachea

The trachea is a longer section of the respiratory tract, shaped like a tube and
approximately 5 inches in length. It has several C-shaped hyaline cartilage rings which
are lined with pseudostratified ciliated columnar epithelium. (2) Those rings keep the
trachea open for air all the time. They are C-shaped in order to allow the open end to face
the esophagus. This allows the esophagus to expand into the area normally occupied by
the trachea in order to permit larger chunks of food to pass through. The trachea, more
commonly referred to as the windpipe, connects the larynx to the bronchi and also has
the role of filtering the air prior to it entering the lungs. The epithelium which lines the
cartilage rings produces mucus which traps harmful particles. The cilia then move the
mucus upward towards the pharynx, where it is redirected towards the gastrointestinal
tract in order for it to be digested.

Bronchi

The lower end of the trachea splits the respiratory tract into two branches that are named
the primary bronchi. These first run into each of the lungs before further branching off into
smaller bronchi. These secondary bronchi continue carrying the air to the lobes of the
lungs, then further split into tertiary bronchi. The tertiary bronchi then split into even
smaller sections that are spread out throughout the lungs called bronchioles. Each one of
these bronchioles continues to split into even smaller parts called terminal bronchioles. At
this stage, these tiny bronchioles number in the millions, are less than a millimeter in
length, and work to conduct the air to the lungs’ alveoli. The larger bronchi contain C-
shaped cartilage rings similar to the ones used in the trachea to keep the airway open. As
the bronchi get smaller, so do the rings that become progressively more widely spaced.
The tiny bronchioles do not have any kind of cartilage and instead rely on muscles and
elastin.
This system creates a tree-like pattern, with smaller branches growing from the bigger
ones. At the same time, it also ensures that air from the trachea reaches all the regions of
the lungs. Besides simply carrying the air, the bronchi and bronchioles also possess
mucus and cilia that further refine the air and get rid of any leftover environmental
contaminants. The walls of the bronchi and bronchioles are also lined with muscle tissue,
which can control the flow of air going into the lungs. In certain instances, such as during
physical activity, the muscles relax and allow more air to go into the lungs.

Lungs

The lungs are two organs located inside the thorax on the left and right sides. They are
surrounded by a membrane that provides them with enough space to expand when they
fill up with air. Because the left lung is located lateral to the heart, the organs are not
identical: the left lung is smaller and has only 2 lobes while the right lung has 3. Inside,
the lungs resemble a sponge made of millions and millions of small sacs that are named
alveoli. These alveoli are found at the ends of terminal bronchioles and are surrounded
by capillaries through which blood passes. Thanks to an epithelium layer covering the
alveoli, the air that goes inside them is free to exchange gasses with the blood that goes
through the capillaries.

Muscles of Respiration

The last component of the respiratory system is a muscle structure known as the muscles
of respiration. These muscles surround the lungs and allow the inhalation and exhalation
of air. The main muscle in this system is known as the diaphragm, a thin sheet of muscle
that constitutes the bottom of the thorax. It pulls in air into the lungs by contracting
several inches with each breath. In addition to the diaphragm, multiple intercostal
muscles are located between the ribs and they also help compress and expand the lungs.

PHYSIOLOGY

Pulmonary Ventilation
Pulmonary ventilation is the main process by which air flows in and out of the lungs. This is done
through the contraction of muscles, as well as through a negative pressure system that is
accomplished by the pleural membrane covering the lungs. When the lungs are completely sealed
in this membrane, they remain at a pressure that is slightly lower than the pressure of the lungs at
rest. As a result of this, the air passively fills the lungs until there is no more pressure difference. At
this point, if necessary, additional air can be inhaled by contracting the diaphragm as well as the
surrounding intercostal muscles. During exhalation, the muscles relax and this reverses the
pressure dynamic, increasing the pressure on the outside of the lungs and forcing air to escape
them until both pressures equalize again. Thanks to the elastic nature of the lungs, they revert
back to their state at rest and the entire process repeats itself.

External Respiration
External respiration is a process that allows an exchange of gases to take place between the air
located in the alveoli and the blood that is traveling through the capillaries. This is possible through
a difference in pressure between the oxygen and carbon dioxide located in the air, and the oxygen
and carbon dioxide in the blood. As a result of this, oxygen from the air is transferred to the blood
while carbon dioxide from the blood goes into the air. The useful oxygen is then carried out
throughout the body while the carbon dioxide is dispelled through exhalation.

Internal Respiration
Internal respiration is a similar process except it involves gas exchange between the blood in the
capillaries and body tissue. Again, a difference in pressure allows oxygen to leave the blood and
enter the tissue while carbon dioxide does the opposite.

Transportation of Gases
This function of the respiratory system enables oxygen and carbon dioxide to travel throughout the
body to wherever they are needed. Most of the gases are carried through blood attached to
transport molecules such as hemoglobin, although blood plasma will also have a minimal content
of gas. Almost 99% of the entire oxygen found in the human body is transported by hemoglobin.
Most of the carbon dioxide is transported from all areas of the body back to the lungs by plasma in
the form of bicarbonate ions. This is created from a catalytic reaction (caused by a carbonic
anhydrase enzyme) between water and carbon dioxide, which combine to form carbonic acid. The
carbonic acid then splits into hydrogen and bicarbonate ions, with the latter eventually being
transformed into carbon dioxide again, taken to the lungs and exhaled.

Homeostatic Control of Respiration

The last physiological role of the respiratory system is the homeostatic control of respiration or, in
other words, the body’s ability to maintain a steady breathing rate. This is termed eupnea. This
state should remain constant until the body has a demand for increased oxygen and carbon
dioxide levels due to increased exertion, most likely caused by physical activity. When this
happens, chemoreceptors will pick up on the increased partial pressure of the oxygen and carbon
dioxide and send triggers to the brain. The brain will then signal the respiratory center to make
adjustments to the breathing rate and depth in order to face the increased demands.
Synthesis of the disease (Diabetic nephropathy)

Diabetes is a metabolic disorder characterized by a relative or absolute lack of the hormone

insuin, or insulin resistance , or both, which results in impaired use of carbohydrates and altered
metabolism of fats and protein. The kidneys usually are affected in diabetes. About 20% of deaths
in diabetes under age 40 can be related to kidney failure.

A lot of different factors may have a contribution in the development of the disease. These
have been labeled as risk factors that cannot be altered (non-modifiable) and those that can be
changed by lifestyle changes (modifiable). Among the modifiable factors is diet, stress, sedentary
lifestyle and obesity. Also, in addition to that is the presence of non-modifiable factors such as
age, gender, pregnancy, genetic heritage and race.

Changes in the blood flow related to chronic increase in blood glucose that is poorly
controlled causes blood to become viscous thus increase in the arterial wall blood pressure. This
event will result in microvascular changes where there is thickening of the capillary membrane.
Aside from that, macrovascular changes would also occur due to the increased fat deposits and
increased in the arterial resistance. The occurrence of macrovascular changes would result to a
complication known as Coronary artery disease (CAD). Furthermore, narrowing of the small
arterioles and capillary will impair blood supply to the other parts of the body which eventually
result to tissue ischemia if prolonged.

In impaired renal blood supply, tubular ischemia and production of intestinal fibrosis may
occur and unfortunately later leads to the destruction of nephrons. A reduced number of
functioning nephrons causes decrease in glomerular filtration rate. As a compensatory
mechanism glomerular hypertrophy occurs. As a result, increased in arterial blood pressure
(hypertension) and functional vasodilation follows. Due to this event, kidneys will not be able to
concentrate the urine leading to increased urine production which the patient has manifested
during hospital stay. Aside from that tubules functions to reabsorb electrolytes has decreased.
Sodium loss occurred because sodium attracts water, polyuria occurred.

Along with the inability of kidneys to concentrate urine, passage of large volume of dilutes
urine with large amount of sodium (salt-wasting). The formation of sclerotic lesions or
glomerulosclerosis developed in chronic increase in pressure and stretch of small arterioles and
glomeruli. Further loss of kidney function and ablation of renal mass will cause loss of regulatory
and excretory renal functions. Loss of renal regulatory functions leads to inability of the kidneys
dihydroxycolecalciferol, and to produce bicarbonate because of the inability of the kidney to
maintain homeostasis, insulin degradation will be impaired making the blood glucose unstable as
to either hypoglycemia or hyperglycemia. Erythropoietin has a role in production of red blood cells
therefore a decreased in number or RBC will lead to hypoxemia and symptoms include pallor and
weakness.

The loss of excretory renal functions leads to compromised excretion of ketones, hydrogen
ions, nitrogenous wastes and of Potassium. If excretion of hydrogen ions is compromised,
hydrogen ions will replace sodium in the extracellular fluid which eventually leads to the
development of metabolic acidosis. Compromised excretion of potassium will result to an
increase in potassium level in the blood known as hyperkalemia. Also, retention of nitrogenous
waste in the blood known to as uremia will cause drying of the skin and elevated serum
creatinine. There is also a decreased reabsorption of sodium in the kidneys which is parallel to
inability to remove excess water thereby causing water retention as being manifested by anuria.
Consequently, circulating blood volume will increase followed by increases blood pressure, fluid
shifting and alterations in the CNS, heart and lung function, Fluid shifting will greatly cause
bipedal edema or anasraca and pulmonary congestion, signs and symptoms of pulmonary
congestion include rales and dyspnea.

The alteration in the lung, heart, and CNS function will lead to respiratory distress. Metabolic
acidosis as a result of increase hydrogen ion and respiratory distress both could lead to death.

RISK FACTORS

A. NON-MODIFIABLE RISK FACTORS

1. Age

Increasing Age is related to a decline in glucose tolerance and on increase in insulin resistance
with an increase on insulin resistance with an increased prevalence of diabetes. The frequency
rises sharply after age 40, probably reflecting a general change in glucose tolerance. The blood
glucose is low in childhood and rises progressively after age 70, about 15% of the population may
show a mild abnormal glucose tolerance.

2. Gender
Diabetes is more frequent in women rather than in men. Between ages 40 and 60, women
diabetics outnumber men almost 2:1. The reason for increased occurrence in women may be
related to the late effects of high parity, which may not be manifested until after age 45.

3. Hereditary

For centuries, it has been noted that diabetes “runs in families” because about 40% of people
who develop the disease have a positive family history. A genetic component is accepted in the
etiology. The human insulin receptor gene is believed to have a role in insulin resistance and
glucose intolerance believed to contribute to the disorder.

4. Race

Because of Asians are more likely to eat foods rich in carbohydrates such as rice, they are said to
have high incidence of Diabetes Mellitus.

B. MODIFIABLE RIK FACTORS

1. Diet

Certain factors implicate diet as possible causative factor in the onset of diabetes. Modification of
dietary intake of carbohydrates minimizes hyperglycemia in this population and limitation of
saturated fat intake may delay the onset of atherosclerosis.

2. Stress

Any form of stress with the neuroendocrine response increases glucogenesis and glycogenolysis.
Infection, life changes and various environmental factors can be stressors that induce or women
to a diabetic state.

3. Body-weight

About 80% of persons with DM are obese, and the frequency of diabetes in obese people is
greater than in general population. The interrelations occurs because obesity is associated with
insulin insensitivity in larger tissue (muscles, liver, adipose cells). It is well known that blood levels
of insulin are higher in an obese person and take longer to return to the fasting state. Obesity acts
a diabetogenic factor because the accompanying insulin resistance increases the need for insulin.

4. Family History
Family history is a factor in the development of both diabetes and high blood

B. MODIFIABLE RISK FACTORS

1. High blood pressure

Elevated blood pressure gradually damages the tiny blood vessels in the kidneys

2. Diabetes

A persistently high blood sugar glevel can damage blood vessels in the kidneys. Over time,
kidney damage can progress and the kidneys may stop working together

3. Eating high protein and fats

Eating a diet low in protein and fat may reduce your risk of developing kidney disease

4. Certain medicines

Avoid long-term use of medicines that can damage the kidneys, such as pain relievers called
NSAIDs and certain antibiotics.

SIGNS AND SYMPTOMS

Hunger and fatigue. Your body converts the food you eat into glucose that your cells use for
energy. But your cells need insulin to bring the glucose in. If your body doesn't make enough or
any insulin, or if your cells resist the insulin your body makes, the glucose can't get into them and
you have no energy. This can make you more hungry and tired than usual.

Peeing more often and being thirstier. The average person usually has to pee between four
and seven times in 24 hours, but people with diabetes may go a lot more. Normally your body
reabsorbs glucose as it passes through your kidneys. But when diabetes pushes your blood
sugar up, your body may not be able to bring it all back in. It will try to get rid of the extra by
making more urine, and that takes fluids. You'll have to go more often. You might pee out more,
too. Because you're peeing so much, you can get very thirsty. When you drink more, you'll also
pee more.

Dry mouth and itchy skin. Because your body is using fluids to make pee, there's less moisture
for other things. You could get dehydrated, and your mouth may feel dry. Dry skin can make you
itchy.

Blurred vision. Changing fluid levels in your body could make the lenses in your eyes swell up.
They change shape and lose their ability to focus.

Hyperglycemia- is an abnormally high blood glucose (blood sugar) level. Hyperglycemia is a

hallmark sign of diabetes (both type 1 diabetes and type 2 diabetes) and prediabetes. Diabetes is
the most common cause of hyperglycemia.

Numbness of below ankle area- because of adequate blood supply toward the peripheral
tissues since the blood of the patient is highly viscous. Furthermore, cells of the body cannot
uptake glucose because of inadequate insulin production, which in turn alters normal functioning
of the cell.

Yeast infections- Both men and women with diabetes can get these. Yeast feeds on glucose, so
having plenty around makes it thrive. Infections can grow in any warm, moist fold of skin,
including in between fingers and toes, under breast, in or around sex organs

Slow-healing sores or cuts- Over time, high blood sugar can affect your blood flow and cause
nerve damage that makes it hard for your body to heal wounds.

Unplanned weight loss- If your body can't get energy from your food, it will start burning muscle
and fat for energy instead. You may lose weight even though you haven't changed how you eat.

Nausea and vomiting- When your body resorts to burning fat, it makes “ketones.” These can
build up in your blood to dangerous levels, a possibly life-threatening condition called diabetic
ketoacidosis. Ketones can make you feel sick to your stomach.
b. SYNTHESIS OF THE DISEASE

In the year 2001, Mrs. Anemia manifested increase in appetite, urination, and excessive
thirst. According to her, these manifestations happened when she was pregnant with her last
child. She said that she did not seek any consultation from a physician because of financial
constraint. In 2015, she was diagnosed to have Diabetes Mellitus and at the same year, her
consulting physician said that her kidneys were also affected.

The patient has DM type II. Her disorder started with inadequacy of insulin secretion by
her pancreas. This causes an increase in he blood glucose level since the glucose is not
transported well within her cells. At the same time, the beta cells will produce more insulin as a
form of compensation in order for the cell to utilize glucose. Since there is still inadequate amount
of insulin secreted, the blood glucose continuously increases until the beta cells can no longer
compensate from high blood glucose level. This causes decreases utilization of glucose and then
further elevated blood glucose and the brain interprets it as a decrease in blood glucose level
since the cells are not using the available glucose. With that, the liver is stimulated to produce
glucose from carbohydrate resources, which further elevates the glucose levels in the blood. But
the produced glucose cannot still be utilized by the cell because of inadequate insulin secretion.
In this situation, the brain would sense this as a decrease in available glucose in the blood which
would again stimulated the liver and by this time, non-carbohydrate sources such as fats and
proteins are utilized which would further elevated blood glucoses level resulting to cellular
starvation which led to weakness that was manifested by the patient 1 week prior to consultation
last 2015. As a compensatory mechanism, brain was stimulated to increase appetite, known as
polyphagia, which further elevated blood glucose levels. Since the situation has been prolonged,
the chronic elevation of blood glucoses increased the osmolality of the blood as well as it has
formed a glycol protein cell wall. The increase in blood osmolality has caused the blood to be very
viscous and has also attracted fluid from the interstitial and intracellular spaces toward the
intravascular spaces, which led to cellular dehydration. This condition has stimulated the brain
which in turn has stimulated thirst receptors to increase fluid intake, known as polydipsia. After
the fluids have shifted toward the intravascular spaces, the volume of blood going to the kidneys
has now increase but still has increase osmolality. With that, glucose, being an osmotic diuretic,
attracts water towards the glomerular membrane upon filtration. Upon chronic exposure of the
glomerular membrane to the increase volume of fluid and glucose, which is a macromolecule,
microvascular changes in the glomerular capillaries occur. With regards to the formed glycol
protein cell wall deposits, reduction in the assimilation of lipids toward peripheral tissues occur
since lipids are blocked by the glycol protein leading to increase in the lipid levels in the blood
which later on accumulates in the lumen of blood vessels. The accumulation of lipids then leads
to formation of atherosclerotic plaques narrowing the lumen of blood vessel and which would then
cause hardening of blood vessel. Hardening of blood vessels increased peripheral resistance,
which led to an increase in blood pressure of the patient that was manifested by the patient last
2015. The deposition of fats together with the decreased blood supply toward the kidney has also
influenced microvascular changes. Microvascular changes include diffused capillary membrane
thickening, which later on led to the narrowing of small arteries and capillaries that further
decreased the blood supply going to the nephrons. As a result, formation of tubular ischemia and
interstitial fibrosis occurred leading to the destruction of nephrons. The destruction of nephrons
has increased the glomerular spaces which allowed large molecules such as glucose to pass the
membrane. Together with the glucose is a large volume of fluid since glucose is an osmotic
diuretic. And lastly it has also reduced the renal reserve as well as the number of functioning
nephrons leading to a decrease in glomerular filtration rate. As a compensatory mechanism, the
workload of other functioning nephrons has increased in order to filter the blood properly that
have cause hypertrophy of nephrons. The increase in workload of healthy nephrons resulted to
vasodilation to accommodate the blood to be filtered and an increase in the patient’s blood
pressure further aggravate the patient’s hypertension. With the increased pressure, the nephrons
fail to reabsorbs water in the tubule causing increase urine output at the same time, because of
increased urine output, the tubules fail in reabsorbing electrolytes.

The decrease of kidney function has altered the regulatory and excretory function of the
kidney. The altered regulatory mechanism includes the following: first, the glomerulus has
increased in permeability allowing macromolecules to pass through including protein and RBS.
Since the protein is lost, there is also a decrease available protein for the formation of
immunoglobulin such as lymphocytes. Loss of RBC in the urine also contributes to the anemia
experienced by the patient. And because of decrease number of RBC circulating in the blood,
there is insufficient supply of oxygen to the different parts of the body causing weakness and
pallor.

Next is the inability of the kidneys to maintain homeostasis. The anemia experienced by
the patient is not only primarily caused by excretion of blood in urine, but due to inability of the
kidney to produce erythropoietin, which is needed for the production of RBCs, as evidence by the
decrease in Hgb and Hct concentration, resulting to decrease oxygen and glucose transported to
different parts of the body which led to the manifestations of muscle weakness and paleness of
membranes. As a compensatory mechanism, the patient increases her respiratory rate and uses
accessory muscles in order to supply the increase oxygen demand of the accessory muscled in
order to supply the increase oxygen demand of the patient. Phosphorus homeostasis is normally
maintained through several mechanisms. GI absorption must be matched by renal excretion, and
cellular release is balanced by uptake in other tissues. Lastly because the patient’s kidneys are
experiencing continuous inflammation from chronic injury, neutrophils are stimulated causing
them to elevate in number in response to the injury. These neutrophils then phagocytize the dead
fragments of tissue injury. The combination of neutrophils and cell debris forms pus that was
noted to be present in the patient’s urine upon urinalysis.

Last of excretory renal function also occurs because of decrease renal function. As a
result, phosphate and potassium accumulates leading to hyperphosphatemia and hyperkalemia
since these ions are greatly excreted through the urine. Hyperkalemia is also caused by tissue
injury since as tissue injury occurs; K is released from the cell to the blood. Furthermore,
phosphate and calcium are inversely related, this will allow excretion of calcium making the
calcium level on lowest normal value. Aside from that because of decreased sodium absorption in
the tubule with kidneys, there is a failure to excrete urine, which caused water retention. With
water retention, hypertension and decreased oncotic pressure, fluid shifting occurs as manifested
by pulmonary congestion as evidence by difficulty of breathing. :lastly, the patient kidneys failed
to excrete nitrogenous product due to impaired excretory function. This has caused to increase
BUN and creatinine level that lead to uremia. Uremia cuases drying of the skin.
MODIFIABLE FACTORS:

 Non-compliance to diabetic diet – non-compliance to diabetic surely can poorly control

diabetes. Because of the late diagnosis of Mrs. Anemia, she failed to comply with the diet
regimen. She also confessed to the student nurses that she loves eating foods high in
sodium and also loves drinking coffee, a potent vasoconstrictor
 Sedentary lifestyle - sedentary lifestyle also makes cells insensitive to insulin. During
health history taking, the patient reported to student nurses that she fails to perform
exercises. According to her, most of her time were spent sitting, watching and playing
cards and majong
 Pregnancy – according to research, diabetic nephropathy is probably the most common
CKD seen in pregnancy. Type 1 diabetes was the most common type of diabetes in
pregnancy; however, with increasing prevalence of type 2 diabetes in women of child-
bearing age, an increasing number of pregnant women with type 2 diabetes is seen. Mrs.
Anemia reported that she started experiencing manifestations of Diabetes on her last
pregnancy. Her last pregnancy may have triggered her risk for diabetes.
 Stress – any form of stress with the neuroendocrine response increase glucogenesis and
gluconeogenesis. According to Mrs. Anemia, she often experience stress that could
contribute to her condition.

NON-MODIFIABLE FACTORS:

 Age – Mrs. Anemia is at risk because she is 49 years old. According to literature,
acquiring DM increases as you get older, especially after age 45 because most often than
not, people tend to exercise less, lose muscle mass and gain weight as they age.
 Race – blacks, Hispanics, American Indians and Asians, are more likely to develop type 2
diabetes. During history taking, the patient stated that she is naturan born citizen o fht
ephilippines, whichis a part of the Asian continent.
 Gender – Diabetes is more freuqnt in women that in men. Between ages 40 and 60,
women diabetics outnumber men alsmot 2:1. The reason for increased occurrence in
women may be relt=ated to the late effects of high parity, which may not be manifested
until after age 45.The patient was 46 years old when diagnosed to have DM.
 Hereditary – For centuries, it has been noted that diabetes “runs in families” because
about 40% of people who develop the disease have a positive family history. Upon history
taking, the patient was noted to have an aunt who had Diabetes Mellitus.
MANIFESTATIONS:

Diabetes Mellitus Manifestations:

 Polydipsia - The increase in blood osmolality has caused the blood to be very viscous
and has also attracted fluid from the interstitial and intracellular spaces toward the
intravascular spaces, which led to cellular dehydration. This condition has stimulated the
brain, which in turn has stimulated thirst receptors to increase fluid intake, known as
polydipsia.
 Polyuria - or increased frequency of urination is due to excess fluid intake and glucose-
induced urination.
 Polyphagia - or increased hunger due to loss or excess glucose in urine that leads the
body to crave for more glucose.
 Hyperglycemia - because of inadequacy of insulin secretion of pancreas, this caused an
increase in he blood glucose level since the glucose is not transported well within the
cells. At the same time, the beta cells will produce more insulin as a form of compensation
in order for the cell to utilize glucose. Since there is still inadequate amount of insulin
secreted, the blood glucose continuously increases until the beta cells can no longer
compensate from high blood glucose level. This causes decreases utilization of glucose
and then further elevated blood glucose and the brain interprets it as a decrease in blood
glucose level since the cells are not using the available glucose. With that, the liver is
stimulated to produce glucose from carbohydrate resources, which further elevates the
glucose levels in the blood. Upon consultation last 2015, the patient had elevated blood
glucose upon having diagnostic exam.

Electrolyte Imbalance:

 Water Retention – water retention was caused by the inability of the kidneys to reabsorb
Sodium. Furthermore, loss of protein through the urine decreases oncotic pressure, which
is responsible for the pulling force of the blood toward the intravascular spaces. With such
loss, fluid found intravascular shifts towards interstitial spaces.
  Hyponatremia – hyponatremia occurs because of the salt wasting properties of the failing
kidneys. Furthermore, this is also due to hemodilution effect of water retention.
Hyponatremia was noted last August 16, 2016 with Na level of 10 mmol/L respectively.
(lifted from the chart)
 Hyperkalemia – most of the potassium ions are excreted through urine. Since the kidneys
are incapable of producing normal amount of urine, potassium accumulates in the blood.
This was noted last May 2015 and August 2016 with K level of 7.70mmol/L upon
diagnostic examination. (Lifted from the chart)
 Hyperphosphatemia – a same principle with potassium, phosphorus is greatly excreted
through the urine. Cine the kidneys are unable to form sufficient urine, phosphorus
accumulates in the blood. This was noted last August 1016 (with phosphate level of 2.02
mmol/L) on the patient’s laboratory findings. (lifted from the chart)

Metabolic changes:

 Elevated BUN and Serum Creatinine – urea is the by-product of protein metabolism
while creatinine is the by product of muscle metabolism. Both are nitrogenous waste that
should be excreted by the body through urination. Elevation of BUN and Serum Creatinine
is primarily caused by the failure of kidneys to eliminate nitrogenous waste. This was
noted last August 2016; BUN level of 28.20mmol/L and Serum creatinine of 811.0 mmol/L.
(lifted from the chart)

Hematologic Changes:

 Anemia – this is caused by the impairment in the production of the erythropoietin, a

hormone responsible for the production of RBC, by the kidneys. Furthermore, hematuria
also adds to the anemia experiencing by the patient. This was noted last August 16, 2016
with hemoglobin of 68g/L, hematocrit level of 0.21 g/L, erythrocytes level of 2.2x10^9/L.
(lifted from the chart)
Immunologic Changes:

 Elevated Neutrophil count – presence of chronic tissue injure continuously stimulates

inflammatory process. Presence of inflammatory process stimulates Neutrophils to
elevate. This was noted last August 16, 2016 with a value of 90%.
 Decreased lymphocyte count – this secondary from the decreased available proteins
used to form immunoglobulins. This was noted last August 16, 2016, with lymphocytes
level of 7.8%

Cardiovascular changes:

 Hypertension – hypertension comes form many causes. First, it is influenced by water

retention since increase in blood volume increases blood pressure. Next reason is the
accumulation of fatty streaks in the vessels caused by the formation o glycol protein cell
wall deposits secondary from chronic elevated blood glucose. In addition, hypertrophy of
nephrons caused as a compensation for decreased filtrated rate resulting to hypertension
with BP readings of 150/70 mmHg, noted last August 18, 2016.

Respiratory Changes:

 Tachypnea – since the lung I accumulated with fluid, it is unable to stretch completely. In
order to suffice oxygen demand, the patient increased the rate of breathing. In addition,
this is another form of compensation since there is decreased Hgb concentration in the
blood.
 Crackles – because of the loss of excretory renal function, it lead to the decreased
sodium reabsorption in the tubule kidneys. Due to the inability of kidneys to remove
excess water, the patient manifested water retention thus increasing blood volume.
Increase in blood volume lead to fluid shifting resulting to pulmonary congestion.
Pulmonary congestion manifested by crackles located at her left upper lung field upon
auscultation is noted last August 15, 2016.
 Dyspnea - loss of excretory renal function lead to the decreased sodium reabsorption in
the tubule kidneys. Due to the inability of kidneys to remove excess water, the patient
manifested water retention thus increasing blood volume. Increase in blood volume lead to
fluid shifting resulting to pulmonary congestion. Pulmonary congestion manifested by
difficulty of breathing is noted last August 15, 2016, which is the patient’s chief complaint.
MEDICAL MANAGEMENT:

Integumentary Changes

 Dry Skin – the skin of the patient was noted to be dry all throughout the physical
examination. This arose from the atrophy of sweat glands that is due to the presence of
uremia

Other Manifestations:

 Weakness – because of decreased RBC production, there is an insufficient supply of

oxygen going to different parts of the body. Low oxygen can be felt in the brain and
muscles as dizziness, fatigue and weakness. The body senses the need for oxygen, and
sends a message to the heart to work harder, work faster, and pump more blood.
 Proteinuria and Hematuria – this has occurred secondary from the increased in the
permeability of the glomerular membrane secondary from the chronic elevation of blood
glucose.
 Name of Drugs; Date Ordered Route of General Indication(s) Client's
Generic Name Date Admin. Indication or Purposes Response
Brand Name Performed Dosage & to the
Date Changed frequency treatment
of admin

Generic Paracetamol Date Ordered: IV Decreases fever by This drug was Mrs.
Name: (PRN) 8/15/16 300mg inhibiting the indicated to Anemia
Brand Name: Biogesic Date effects of pyrogens Mrs. Anemia responded
Performed: on the in order to well to the
8/16/16 hypothalamus heat manage her medication
regulating centers fever and is as
Date Changed: & by a given as a evidenced
--- hypothalamic pre-BT by a
action leading to medication decreased
sweating in body
&vasodilatation. temperature
to the
PRN normal
range value
and she did
not
experience
any local
allergic
reactions
during and
after BT.
Before administering the medication:
 Check that the patient is not taking any other medication containing paracetamol.
During administering the medication:
 Alcohol increases the risk of liver damage that can occur if an overdose of paracetamol is taken. The hazards of
paracetamol overdose are greater in persistent heavy drinkers and in people with alcoholic liver disease.
 Small amounts may pass into breast milk. However, there are no known harmful effects when used by
breastfeeding mothers.
After administering the medication:
Evaluate therapeutic response
Drugs (generic, Date ordered, Route or admin, General action Indication Clients
brand name) date dosage and (functional response
taken/given, frequency classification)
date changed/
D/C

Diphenhydramine Date Ordered: 50mg IV An antihistamine Diphenhydramine There were no

8/15/16 that reduces the is used to treat side effects or
Date Performed: effects of natural sneezing, runny allergic reactions
8/16/16 chemical histamine nose, watery eyes, noted upon
in the body. hives, skin rash, administration of
Date Changed: itching, and other medication
--- cold or allergy
symptoms and is
given as a pre-BT
medication

Nursing Considerations (Diphenhydramine)

Before:
1. Assess for any allergy to antihistamines.
2. Obtain vital sign
3. Inform patient about the drug and what it is for.
*Administer with food if GI upset occurs
After
1. Document the procedure done.
2. Inform patient about the sedative effect of the drug. Instruct patient to avoid activities requiring mental alertness
and avoid alcohol consumption while taking the drug.

Name of Drugs; Date Ordered Route of General Indication Indication(s) Client's

Generic Name Date Admin. or Purposes Response
Brand Name Performed Dosage & to the
Date Changed frequency treatment
of admin
Generic FeSO4 + Folic Date Ordered: Oral Ferrous sulfate is a This drug was Mrs.
Name: Acid 8/15/16 Tab type of iron. You indicated to Anemia
Brand Name: Date normally get iron Mrs. Anemia responded
Iron Sulfate, Performed: from the foods you in order to well to the
Folvite 8/16/16 eat. In your body, help produce medication
8/17/16 iron becomes a healthy blood as
8/18/16 part of your cells. evidenced
Date Changed: hemoglobin and by an
--- myoglobin increase
Hemoglobin carries hemoglobin
oxygen through from 58 to
your blood to 106
TID tissues and organs.
Myoglobin helps
your muscle cells
store oxygen.
Folic acid helps
your body produce
and maintain new
cells, and also
helps prevent
changes to DNA
 that may lead to
cancer.

Before administering the medication:

 Identify the client name.
 Explain the procedure and important of the drug.
 Assess for allergies before initiation of treatment
 Ensure that patient is well hydrated.
 Transient staining of mucousmembranes and teeth willoccur with liquid iron preparation. To avoid, placeliquid on
the back of thetongue with dropper or usestraw
After administering the medication:
 Reorient patient as needed.
 Monitor vital signs.
 Assess for clinicalimprovement, record of relief of symptoms (fatigue,irritability, pallor, paresthesia,and headache).
 Note the pt.’s reaction to the drug.
 Document the procedure done

Name of Drugs; Date Ordered Route of General Indication Indication(s) Client's

Generic Name Date Admin. or Purposes Response
Brand Name Performed Dosage & to the
Date Changed frequency treatment
of admin
Generic NaHCO3 Date Ordered: Oral Sodium This drug was Mrs.
Name: 8/15/16 Tab bicarbonate is an indicated to Anemia
Brand Name: Neut Date electrolyte. It works Mrs. Anemia responded
Performed: TID by neutralizing in order to well to the
 8/16/16 excess acid in the treat her medication
8/17/16 blood. It may also hyponatremia as
8/18/16 replace evidenced
Date Changed: bicarbonate when by a
--- there are excess normal
losses from the sodium
body. value
140mmol/L

Before administering the medication:

 Identify the client name.
 Explain the procedure and important of the drug.
 Assess for allergies before initiation of treatment
 Ensure that patient is well hydrated.
During:
 Have patientchew oraltabletsthoroughlybefore swallowing, andfollow them witha full glass of water.

After administering the medication:

 Reorient patient as needed.
 Monitor vital signs.
 Note the pt.’s reaction to the drug.

Name of Drugs; Date Ordered Route of General Indication Indication(s) Client's

Generic Name Date Admin. or Purposes Response
Brand Name Performed Dosage & to the
Date frequency treatment
of admin
 Generic Calcium Date Ordered: Oral It controls of This drug was Mrs.
Name: Carbonate 8/15/16 Tab hyperphosphatemia indicated to Anemia
Brand Name: Caltrate Date in end-stage renal Mrs. Anemia responded
Performed: disease without in order to well to the
8/16/16 promoting use in medication
8/17/16 aluminum preventing as
8/18/16 absorption. phosphorus evidenced
TID absorption by a
Date Changed: decrease in
--- phosphorus
level
2.02mmol/L

Before administering the medication:

 Identify the client name.
 Explain the procedure and important of the drug.
 Assess for allergies before initiation of treatment
 Ensure that patient is well hydrated.
 Give calcium carbonate antacid 1 and 3hr after meals and at bed time
 Asses for heartburn, indigestion, abdominal pain.
 Monitor serum calcium before treatment.

After administering the medication:

 Reorient patient as needed.
 Monitor vital signs.
 Note the pt.’s reaction to the drug.
 Assess for nausea and vomiting, anorexia, thirst, severe constipation.02
 Name of Drugs; Date Ordered Route of General Indication(s) Client's
Generic Name Date Admin. Indication or Purposes Response to
Brand Name Performed Dosage & the
Date Changed frequency treatment
of admin
Generic Amlodipine Date Ordered: Oral Amlodipine is a Treatmentof Mrs. Anemia
Name: 8/15/16 10mg calcium channel Hypertension responded
Brand Name: Norvasc Date blocking agent that well to the
Performed: selectively blocks medication
8/16/16 calcium ion reflux as evidenced
8/17/16 across cell by a
8/18/16 membranes of decreased in
cardiac and BP from
Date Changed: vascular smooth 130/90mmHg
--- muscle without to 110/80
changing serum
OD calcium
concentrations. It
predominantly acts
on the peripheral
circulation,
decreasing
peripheral vascular
resistance, and
increases cardiac
output.

Before administering the medication:

 Identify the client name.
 Explain the procedure and important of the drug.
  Assess for allergies before initiation of treatment
 Ensure that patient is well hydrated.
 Administer drugwithout regards tomeal
 Ensure patient is not pregnant
After administering the medication:
 Reorient patient as needed.
 Monitor vital signs.
 Note the pt.’s reaction to the drug.
 Monitor patientclosely in anysituation thatmay lead to adecrease in BPsecondary toreduction in fluidvolume-
excessiveperspiration,dehydration,vomiting,diarrhea-excessivehypotension canoccur.
 Document the procedure done
Name of Drugs; Date Ordered Route of General Indication(s) Client's
Generic Name Date Admin. Indication or Purposes Response to
Brand Name Performed Dosage & the treatment
Date Changed frequency
of admin

Generic Rosuvastatin Date Ordered: Oral Lowering high Anti- Mrs. Anemia
Name: 8/15/16 20mg cholesterol and hyperlipidemic responded well
Brand Name: Crestor Date triglycerides in HMG-CoA to the
Performed: certain patients. It reductase medication as
8/16/16 also increases inhibitor evidenced by
8/17/16 ODHS high-density an increase in
8/18/16 lipoprotein (HDL) HDL cholesterol
Date Changed: ("good") levels
--- cholesterol levels.
Before administering the medication:
 Identify the client name.
 Explain the procedure and important of the drug.
 Assess for allergies before initiation of treatment
 Before beginningrosuvastatin therapy, tryto controlhypercholesterolemiawith appropriate diet andexercise, wt.
reduction inobese clients andtreatment of underlyingmedical problems.
 Arrange for proper consultation about need for diet and exercise changes
 Administer drug at bed time
 Ensure that patient is well hydrated.

After administering the medication:

 Reorient patient as needed.
 Monitor vital signs.
 Note the pt.’s reaction to the drug.
 Monitor patient closely for signs of muscle injury, especially higher doses
 Provide comfort measures to deal with headache, muscle cramps, or nausea
 Offer support and encouragement to deal with disease, diet, drug therapy, and follow-up care.
 Document the procedure done.
PROBLEM #1: FLUID VOLUME EXCESS RELATED TO IMPAIREDURINARY EXCRETION AND DECREASED
ONCOTIC PRESSURE

Assessment Nursing Scientific Objectives Intervention

Diagnosis Explanation
S> Ø Fluid volume Because there was Short term: 1. Establish rapport
excess r/t impaired a decrease After 6 to 8 hours of  To gain the trust and
urinary excretion perfusion in the nursing intervention, compliance of the patient
O> the patient and decreased kidneys, the 2. Monitor vital signs
manifested the the patient will
oncotic pressure patient’s nephrons demonstrate  To obtain baseline data of the
following signs were damaged patient’s current condition
and symtpms behaviors to monitor
reducing the fluid status and 3. Auscultate breath sounds
 Crackles glomerular filtration reduce recurrence of  To assess degree of fluid
upon rate leading to fluid excess congestion
auscultatio functional 4. Record intake and output
n on left vasodilation and  To monitor hydration status
upper lung increased arterial Long term: and degree of compromised
field BP. An increased urinary excretion
After 2-3 days of
 Pale nail urine output was
nursing interventions, 5. Weigh daily on regular
beds with caused by inability schedule
the patient will
capillary of the kidneys to  Provides a comparative data
manifest stabilize fluid
refill of 4 concentrate urine. and hydration status and
volume as evidenced
sec Since there was a water retention
by balance intake and
 Dyspnea decrease in 6. Evaluate edematous
output, normal vital
 Fatigue reabsorption of extremities, change position
signs, stable weight,
electrolytes,  To reduce tissue pressure
and free from signs of
sodium was and risk of skin breakdown
edema
The patient may excreted from the 7. Encourage position changes
manifest: body resulting to every 1-2 hours, dangle legs
decreased cardiac  To reduce risk of orthostatic
 Rales
output.
 Bipedal hypotension
enema 8. Elevate edematous
 Increase extremities
urine  To promote venous return
production 9. Ensure proper IVF regulation
 Fainting  To ensure that there is
 anxiety adequate hydration
10. administer anti-hypertensive
drug and diuretics as ordered
 to directly decrease arterial
resistance, thus, an increase
in cardiac output
PROBLEM #2: INEFFECTIVE BREATHING PATTERN RELATED TO FATIGUE
Assessment Nursing Scientific Objectives Intervention
Diagnosis Explanation
S> Ø Ineffective Ineffective STO: 1. Establish a therapeutic
breathing Breathing Pattern After 2-3 hours of nursing relationship to patient and
pattern related is defined as interventions, the patient significant other
O> the patient to fatigue inspiration and/or  To build trust and cooperation
manifested: will demonstrate
expiration that do appropriate coping 2. Assess patient’s general
-nasal flaring not provide behaviors such as deep condition
-tachypnea
adequate breathing and coughing  To determine general health
ventilation. A exercises AEB absence of status of the patient and
-shallow breathing dyspneic person provide appropriate nursing
nasal flaring and stable
-use of accessory often appears vital signs within patient’s interventions
muscles anxious and may normal range. 3. Monitor and Record vital signs
-pale palpebral
experience  To obtain baseline data and for
shortness of future comparison
conjunctiva
breath, a feeling LTO: 4. Provide rest periods
-body malaise of being unable  To conserve energy
After 4-6 hours of nursing
to get enough air. 5. Assess respiratory rate and
interventions, the patient
Dyspnea have depth. Note use of accessory
> the patient may will establish a normal,
many causes, muscles, pursed-lip breathing,
manifest: effective respiratory
most of which and inability to speak /
pattern AEB absence of
-increased anterior- stem from converse.
tachypnea and stable vital
posterior diameter cardiac and  Useful in evaluating the degree
signs within patient’s
respiratory of respiratory distress and/ or
normal range.
disorders. It is a chronicity of the disease
subjective feeling process
as it cannot be 6. Assess/ routinely monitor the
directly observed skin and mucous membrane
but is reported by color
the patient.  Cyanosis may be peripheral
(noted in nail beds) or central
 (noted around lips/ earlobes).
Duskiness and central
cyanosis indicate advanced
hypoxemia
7. Elevate head of bed and
change position every 2 hours
 To take advantage of gravity
decreasing pressure on the
diaphragm and enhancing
drainage of/ ventilation of
different lungs segments.
8. Demonstrate deep breathing
and coughing exercises
 To maximize breathing effort
and chest expansion
9. Auscultate breath sounds and
assess air movement
 To ascertain status and
progress
10. Evaluate changes in sleep
pattern
 To perform/ note for
contributing factors
11. Encourage to avoid cold
liquids
 To prevent constriction of the
bronchioles and alveoli which
could directly narrow spaces
for gas exchange
12. Provide quiet and restful
environment
 To promote comfort
13. Position head midline with
 flexion appropriate for age/
condition
 To open or maintain airway at
rest
14. Monitor for dyspnea and
respiratory effort on exertion,
length of inspiratory effort and
expiratory phase
 Evaluating the degree of
respiratory distress
15. Monitor level of
consciousness/ mental status
 Restlessness and anxiety are
common manifestations of
hypoxia. Worsening ABG’s
accompanied by confusion/
somnolence are indicative of
cerebral dysfunction due to
hypoxemia.
16. Administer medications as
ordered
 To help in managing the
patient’s condition
17. Identify and refer to specific
suppliers for supplemental
oxygen/ necessary respiratory
devices, as well as other
individually appropriate
resources, such as home care
agencies
 To facilitate independence
PROBLEM #3: INEFFECTIVE TISSUE PERFUSION RELATED TO DECREASED HEMOGLOBIN CONCENTRATION
IN THE BLOOD
Assessment Nursing Scientific Objectives Intervention
Diagnosis Explanation
S> Ø Ineffective As the glucose After 6 hours of nursing 1. Monitor vital signs
tissue continue to interventions, the • To obtain a baseline data
perfusion increase, it patient will show signs of the patients condition
O> the patient related to makes the blood of increase tissue
manifested: decreased concentrated perfusion as evidence
 Pale palpebral hemoglobin thus causing it to by normal capillary refill 2. Determine duration of
conjunctiva concentration become viscous of less than 3 seconds problem, frequency of occurrence
 Pale nail beds in the blood which causes a and demonstrate and aggravating factors.
with capillary delay or behaviors and lifestyle
• To assess causative or
refill of 4 improper changes
contributing factors
seconds transportation of
 Weakness substances
 Fatigue needed by the 3. Elevate HOB and maintain
 Activity cells such as After 2 days of nursing head/neck midline or neutral
Intolerance oxygen. This interventions, the position
delay decreases patient will not manifest
 Difficulty of • To promote circulation
O2 supply in the signs of ineffective
Breathing
cells causing tissue perfusion AEB
 Hgb of (106g/L)
ineffective tissue having stable vital 4. Encourage quiet, restful
> the patient may perfusion signs and increase atmosphere
manifest: another factor is level of Hgb and Hct
 Restlessness the presence of and no pallor.
 Dysrhythmias decreased • To conserve energy and
 Skin hemoglobin lowers O2 demands
discolorations which results to
decreased
 Skin 5. Caution patient to avoid
oxygen carrying
temperature activities that increases workload
capacity of the
changes of the heart
cells leading to
decreased • To maximize tissue
oxygen supplied perfusion
to different
tissues.
6. Discourage sitting/standing for
long periods, wearing constrictive
clothing and crossing legs
• To facilitate venous return
to the heart

7. Encourage use of relaxation

techniques or exercise
• To decrease tension level

8.Give due medications such as

antiplatelet agents, thrombolytics,
antibiotics as ordered
• To facilitate faster recovery
and improve tissue perfusion

9.Administer supplemental
erythropoietin as ordered

• To stimulate RBC
production

10.Administer blood transfusions

(PRBC) as ordered.
• Provides a direct increase
in the blood content of the patient
in terms of RBC which could
increase hemoglobin level

12. Encourage early ambulation

 To promote peripheral
circulation and limit
complications associated
with poor perfusion
PROBLEM #4: ACTIVITY INTOLERANCE

Assessment Nursing Scientific Objectives Interventions & rationale

diagnosis explanation
S: ““Nanghihina Activity Decreased STO:
ako,kadalasan hindi ko Intolerance oxygen carrying  After 30 minutes of 1. Take VS and record.
matapos ang mga related to capacity of Hgb nursing  To promote well student
gawain ko.” anemia as leading to interventions, the nurse-patient interaction.
evidenced decreased client will be able to 2. Note client’s reports of
O: by nutrition in cells demonstrate and use weakness and difficulty
 Pale, dry lips decreased leading to energy conservation accomplishing tasks.
 Decreased skin RBC and decreased techniques given as  To have baseline data of
turgor hemoglobin ATP production evidenceed by the patient’s current
 Decreased count. since oxygen is gradual increase in situation.
RBC and needed for activities.
platelet count. oxidation 3. Increase activity levels
 Hemoglobin of CHO/glucose gradually
count of 106 & which leads to LTO:  Symptoms may be result
Hematocrit decreased energy After 4 hours of nursing of or contribute to
count of 0.32 or muscle interventions, the client will intolerance of activity.
 Exertional weakness be able to perform basic
discomfort/dysp resulting activity activities without excessive 4. Teach client to rest for 3
nea intolerance. exhaustion or loss of mins during a 10 min walk.
energy.  To conserve energy
The pt may manifest:
 ECG changes 5. Assist with patient’s
reflecting activities.
arrhythmias or  To protect client from
ischemia. injury.
 Abnormal heart
rate or blood 6. Promote comfort
pressure measures.
response to  To enhance ability to
activities.
 participate in activities
.
7. Provide positive
atmosphere, while
acknowledging the
difficulty of the situation for
the client.
 Helps in minimizing
frustration and rechannel
energy.

8. Plan care to carefully

balance rest periods with
activities.
 To reduce fatigue.
9. Encourage client to
maintain positive attitude.
 To enhance sense of well
being.

10. Provide health teachings

regarding foods rich in
iron.
 Helps in treating anemia.
PROBLEM #5: NUTRITION LESS THAN BODY REQUIREMENTS RELATED TO INSULIN DEFICIENCY

Assessment Nursing Scientific Objectives Intervention

Diagnosis Explanation
S> Ø Nutrition Less The patient has STO: 1. Establish a therapeutic relationship to
Than Body impairment in After 4 hours patient and significant other
Requirements insulin  To build trust and cooperation.
O> The patient related to secretion, which of nursing 2. Assess patient’s general condition.
manifested: insulin is a needed intervention,  To determine general health status of
deficiency hormone for the patient and provide appropriate
 Dry skin glucose uptake the patient nursing interventions.
of the cells will 3. Monitor and Record vital signs.
 Pale palpebral which alters  To obtain baseline data and for future
conjunctiva blood glucose demonstrate comparison.
levels leading to behaviors. 4. Provide quiet and restful
 Pale nail beds hyperglycemia. environment.
with capillary Because of this lifestyle  To promote comfort.
the patient cells changes to
refill of 4 sec tend to receive 5. Provide rest periods.
insufficient regain and/or  To conserve energy.
 Weakness
 Fatigue amount of maintain 6. Encourage client to increase fluid
glucose leading intake as tolerated.
to fats and appropriate
 To prevent dehydration.
protein weight. 7. Assess history of food intake.
metabolism as  Provides information needed to
The patient may a compensatory evaluate nutritional pattern, habits and
mechanism for adequacy.
manifest: the demand of LTO: 8. Assess height and weight, head
the cells for the
 Restlessness After 2-3 circumference skin fold thickness
glucose. and arm circumference and compare
days of
 Dysrhythmias nursing with previous values and standard
 Skin intervention charts.
discolorations the patient  Provides anthropometric information
 Syncope will about body’s fat and protein content
experience general nutritional status.
balanced 9. Assess difficulty in swallowing,
nutrition as chewing, gag reflex, teeth, oral
individually mucous membrane, lips, and palate
appropriate. for abnormalities, presence of oral
pain or infection.
 Provides information about ability to
ingest foods.
10. Assess presence of nausea,
vomiting and if splitting up projectile.
 Provides information about emesis
which affects nutrition and is
controlled by the vomiting center in
the medulla.
11. Place patient in position of comfort
for feeding/meals.
 Provides most appropriate position to
enhance movement of food by gravity
and peristalsis and to prevent
vomiting and or/ aspiration.
12. Demonstrate deep breathing and
coughing exercises

 To maximize breathing effort and

chest expansion.

13. Initiate and monitor IV administration

of nutrients as prescribed.
 For uptake of glucose.
 D. Evaluation

1. Clients Daily Progress Chart (From Admission to 5th day)

1st Day 2nd Day 3rd Day 4th Day SNPI

(08/15/ (08/16/ (08/17/ (08/18/ (08/19/16)
16) 16) 16) 16)
1. Nursing Problems
1. Fluid Volume Excess *
2. Ineffective Breathing Pattern *
3. Ineffective Tissue Perfusion *
4. Activity Intolerance *
5. Imbalance Nutritition : Less *
than the body requirements
Vital Signs
Temperature 36.9 C 36.2 C
Pulse Rate 103 bpm 78 bpm
Respiratory Rate 28 cpm 19 cpm
Blood Pressure 130/90 150/70
mmHg mmHg
2. Complete Blood Count
Hemoglobin (120-160 g/L) 58 106
Hematocrit (0.37-0.47 g/L) 0.21 0.32
Platelet Count (150-450x 109/L) 264 228
White Blood Cell (4.0-10.0x 13.0 7.3
109/L)
Neutrophils (55.0-65.0%) 90.0 65.6
Lymphocytes (25.0-35.0%) 7.8 22.4
Monocytes (3.0-6.0%) 1.8 6.7
Blood Chemistry
Sodium (136-145 mmol/L) 140.0
Potassium (3.5-5.1 mmol/L) 6.70
Phosphorus (0.81-1.45 mmol/L) 2.02
Ionized Calcium (1.12-1.32 1.22
mmol/L)
Creatinine (44-80 umol/L) 811.0
BUN (2.78-8.07mmol/L) 28.20
MCV (80-100 g/L) 96.3 90.7
MCH (27.0-34.0 pg) 31.5 30.0
MCHC (310-370 g/L) 327.0 331
RDW-CV (0.110-0.160%) 0.014 0.015
RDW-SD (35.0-56.0 fL) 49.5 51.1
3. Urinalysis
Color (Straw) Light
Yellow
Trans (Clear) Turbid
Rxn (Slightly acidic) Acidic
Specific Gravity (1.010-1.030) 1.020
Pus (None) 1-2
Medical Management
IVF
a. PNSS 1L * * * * *
BLOOD TRANSFUSION
a. PRBC 2 Units * *
DRUGS
1. Paracetamol *
2. FeSO4 + Fa * * *
3. Diphenhydramine * *
4. NaHCO3 * * *
5. Calcium Carbonate * * *
6. Amlodipine * * *
7. Rosuvastatin * * *
8. Isosorbide Dinitrate * * *
9. Albuterol Sulfate * * *
10. Furosemide * * *
11. Calcium Gluconate *
DIET
1. LOW SALT * * * * *
2. LOW FAT * * * * *
3. DM DIET * * * * *
 E. Evaluation

2. Clients Daily Progress Chart (From Admission to 5th day)

1st Day 2nd Day 3rd Day 4th Day SNPI

(08/15/ (08/16/ (08/17/ (08/18/ (08/19/16)
16) 16) 16) 16)
4. Nursing Problems
1. Fluid Volume Excess *
2. Ineffective Breathing Pattern *
3. Ineffective Tissue Perfusion *
4. Activity Intolerance *
5. Imbalance Nutritition : Less *
than the body requirements
Vital Signs
Temperature 36.9 C 36.2 C
Pulse Rate 103 bpm 78 bpm
Respiratory Rate 28 cpm 19 cpm
Blood Pressure 130/90 150/70
mmHg mmHg
5. Complete Blood Count
Hemoglobin (120-160 g/L) 58 106
Hematocrit (0.37-0.47 g/L) 0.21 0.32
Platelet Count (150-450x 109/L) 264 228
White Blood Cell (4.0-10.0x 13.0 7.3
109/L)
Neutrophils (55.0-65.0%) 90.0 65.6
Lymphocytes (25.0-35.0%) 7.8 22.4
Monocytes (3.0-6.0%) 1.8 6.7
Blood Chemistry
Sodium (136-145 mmol/L) 140.0
Potassium (3.5-5.1 mmol/L) 6.70
Phosphorus (0.81-1.45 mmol/L) 2.02
Ionized Calcium (1.12-1.32 1.22
mmol/L)
Creatinine (44-80 umol/L) 811.0
BUN (2.78-8.07mmol/L) 28.20
MCV (80-100 g/L) 96.3 90.7
MCH (27.0-34.0 pg) 31.5 30.0
MCHC (310-370 g/L) 327.0 331
RDW-CV (0.110-0.160%) 0.014 0.015
RDW-SD (35.0-56.0 fL) 49.5 51.1
6. Urinalysis
Color (Straw) Light
Yellow
Trans (Clear) Turbid
Rxn (Slightly acidic) Acidic
Specific Gravity (1.010-1.030) 1.020
Pus (None) 1-2
Medical Management
IVF
b. PNSS 1L * * * * *
BLOOD TRANSFUSION
b. PRBC 2 Units * *
DRUGS
12. Paracetamol *
13. FeSO4 + Fa * * *
14. Diphenhydramine * *
15. NaHCO3 * * *
16. Calcium Carbonate * * *
17. Amlodipine * * *
18. Rosuvastatin * * *
19. Isosorbide Dinitrate * * *
20. Albuterol Sulfate * * *
21. Furosemide * * *
22. Calcium Gluconate *
DIET
4. LOW SALT * * * * *
5. LOW FAT * * * * *
6. DM DIET * * * * *
SUMMARY OF FINDINGS:

 Anemia is pervasive in the diabetic patient with CKD.

 Anemia occurs earlier, and is more severe in chronic kidney disease related to
diabetes than in non-diabetic kidney disease.
 Reasons for anemia in CKD include EPO deficiency, iron deficiency, decreased
lifespan of red blood cells, chronic blood loss, secondary hyperparathyroidism,
chronic inflammation, oxidative stress, nutritional folate deficiency, uremia and
chronic suppression of erythropoesis.
 Glomerular filtration rate (GFR) is the best estimate of kidney function.
 Hypertension causes CKD and CKD causes hypertension.
 Treatment for chronic kidney disease focuses on slowing the progression of the
kidney damage, usually by controlling the underlying cause. Chronic kidney
disease can progress to end-stage kidney failure, which is fatal without artificial
filtering (dialysis)
 There are no symptoms in the early stages of diabetic nephropathy. If you have
kidney damage, you may have small amounts of protein leaking into your urine
(albuminuria).
 Important treatments for kidney disease are tight control of blood glucose and
blood pressure. Blood pressure has a dramatic effect on the rate at which the
disease progresses. Even a mild rise in blood pressure can quickly make kidney
disease worsen.

CONCLUSION:

In conclusion, Anemia commonly occurs in people with chronic kidney disease

(CKD)—the permanent, partial loss of kidney function. Anemia might begin to

develop in the early stages of CKD, when someone has 20 to 50 percent of
normal kidney function. Anemia tends to worsen as CKD progresses. Most
people who have total loss of kidney function, or kidney failure, have anemia.
 The student nurses have learned in this case study the characteristics of three
interrelated disease conditions, their risk factors that predisposed the client to such condition,
and the management for such condition. They were able to understand different mechanisms,
physiology, as well as the pathophysiology of the disease.

The student-nurse patient interaction plays a very crucial role because it serves as a way to
know more about the disease condition & its manifestation through thorough assessment of the
patient’s history.

V. RECOMMENDATIONS

To all health care providers, that they may have more knowledge and updated
information about the disease condition and aid in its early detection so that nursing care may
be rendered to be of quality to the patient.

To the nursing administration, that they may conduct seminars on the topic so that
clients may be more aware of the disorder process and thereby, prevent its occurrence.

To the public, that they may become more knowledgeable of the disease condition risk factors
and signs and symptoms. Also, the management involved in its course.

For the patients who are undergoing this kind of condition for them to be more familiar of
their diagnosis and to know certain alternatives to avoid the progress of the disease and
improve their health status.

This will help the patients and their significant others to have their activities and lifestyle
modified to prevent further complications. Proper maintenance and care for the patient is
essential. Stress the significance of regular check-up so that secondary complications may be
prevented. Advise the family to maintain healthy and harmonious relationships and provide
holistic support to the patient.
 VI. LEARNING DERIVED:

Learning is a continuous process which we gain not only through books and lectures
but also with the situations we encounter around us in our everyday life. Seeing a
person experience difficulty because of a disease condition is an eye opener. Life is
always at stake in this profession. Thus, making a mistake or assumption must never be
an option. One of the most important things we learned is to change our view about
doing a case study. We usually see this requirement as a burden since it requires too
much time and effort. However, we realized that this case study is not conducted for us
to complete our requirements but for us to learn a little about our profession compare to
the vast knowledge that lies ahead of us. It is a method of widening the horizon of
learning as it is an essential part of students especially nursing students who are
aspiring to handle life of their patients.

In this case study, we were able to learn more about Anemia, CKD and Diabetic
Nephropathy. We learned about its causes, complications, manifestations and reasons
why these manifestations appeared. We were able to connect and rationalize the
manifestations of our patient with the disease condition.

It made the nursing care we are rendering more appropriate for the patient. As future
nurses, perseverance is always a key to our profession. Not all patients and SOs are
cooperative enough to accommodate us with this case study. However, it must never be
a reason for us to stop from carrying out our duties as a nurse.

We learned that we can always find a good case if we persevere. In line with this
struggle, we also learned the value of building a trusting relationship with our patient. It
is true that every information they share is a part of them they entrust to us. Therefore,
we should appreciate their kindness of sharing themselves especially their time to us.

It’s not actually the paper output that is rewarding, but rather, it is the thought that we
were able to help a person once in our lives. Truly, a sense of fulfillment touched our
hearts which makes us a better person. A better student nurse.

VII. BIBLIOGRAPHY

 Fundamentals of Anatomy and Physiology Workbook (Ian Peate)

 Susan C. deWit, Candice K. Kumagai’s Medical-Surgical Nursing: Concepts & Practice,
2nd Edition
 Black and Hawk’s Medical-Surgical Nursing: Clinical Management for Positive
Outcomes, 8th edition
 Lemone’s Medical-Surgical Nursing: Critical Thinking in Patient Care, 5th edition
 Karch, Amy. Lippincott Nursing Drug Guide, 2015
 http://www.who.int/
 https://www.niddk.nih.gov/health-information/health-topics/kidney-disease/anemia-in-
kidney-disease-and-dialysis/Pages/facts.aspx
 http://www.karger.com/Article/Abstract/418267
 http://patient.info/doctor/chronic-kidney-disease-pro
