Davao Doctors College

General Malvar St., Davao City

BACHELOR OF SCIENCE IN NURSING

Nursing Management of a patient with

A Case Study Presented to the Nursing Clinical Instructors

Of Davao Doctors College

In Partial Fulfillment of the Requirements in

Nursing Care Management 107

Laquindanum, Pamela; Lumapas, Nicole; Mancia, Sweetcelle;

Manligas,Gladys; Mendez, Carolina; Navarro, Monic;
Pahamutang, Leah; Parmiasano, Arisa;
Pascual, Grace; Pesical, Rossil

February 2019
 TABLE OF CONTENTS

A. Objectives 2
B. Introduction 3
C. Definition of Diagnosis 5
D. Patient’s Profile 8
i. Biographic Data 8
ii. Past Health History 8
iii. Present Health History 8
iv. Family History 9
v. Developmental History 9
vi. Nutritional History 10
vii. Immunization 10
E. Review of Anatomy and Physiology 11
F. Comprehensive Health Assessment 19
G. Pathophysiology 30
i.Etiology
ii.Symptomatology
iii.Schematic Diagram
iv.Narrative
H. Course in the ward/Treatment/Interventions 46
i. Medical Management
1. Doctor’s Progress Notes 46
2. Laboratory/Diagnostic Examinations 50
3. Pharmacology 70
ii. Nursing Management 77
I. Discharge Plan 86
J. Bibliography 88

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 A. Objectives

i. General

The group aims to formulate and present this case in a systemic, analytical way
and be guided by the formulated specific objectives for the enhancement of our knowledge that
would help us apply the lessons learned, and develop our skills toward nursing care.

ii. Specific

At the end of our case study, the group would be able to:

• To find an appropriate case.

• To organize patient’s data to establish good background information;

• Obtain initial data about the client through his records along with a personal interview;

• Gather, trace and collate the predisposing and precipitating factors that could have
contributed to the client’s illness;

• Gather and review the results of the diagnostic exams done to the client;

• Make a drug study on the discontinued and current prescribed medicines;

• Identify nursing problems and come up with an appropriate and effective nursing care
plan;

• Formulate prognosis based on the gathered information; and

• Provide appropriate health teachings and recommendation for the client, family and
community.

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 B. Introduction

The corona radiata is a bundle of nerve fibers located in the brain. Specifically, the
nerves of the corona radiata carry information between the brain cells of the cerebral cortex
and the brain cells in the brain stem. The corona radiata had a nerve cells that is composed of
both afferent and efferent fibers that connect the cerebral cortex and the brain stem, which is
an important group of nerves because of its role in sending and receiving messages between
regions in the brain. A corona radiata stroke is described as a “lacunar stroke” or a “small
vessels stroke” because the corona radiata receives blood supply from small branches of the
arteries in the brain. People who suffer from multiple small strokes in the corona radiata or
elsewhere in the brain are often described as having cerebrovascular disease, which is a
condition characterized by narrow, blood clot prone blood vessels in the brain and small
strokes. Strokes involving the corona radiata might be relatively small, and may not cause
symptoms. Such strokes are often called silent strokes.

It is estimated that lacunar infarcts account for 25% of all ischemic strokes, with an annual
incidence of approximately 15 per 100,000 people. They may be more frequent in men and in
people of African, Mexican, and Hong Kong Chinese descent

The Republic of the Philippines is an archipelagic Southeast Asian country with Manila
as its capital. The population comprises 34·8% and 4·2% belonging to 65 years and above.
Stroke epidemiology as seen in other developing countries, while the upswing of
noncommunicable diseases is evident, Deaths in Southeast Asian nations are mainly due to
noncommunicable diseases, the leading causes being diseases of the heart, stroke, cancer,
chronic obstructive pulmonary disease, diabetes mellitus, kidney disease, and accidents. Stroke
is 2nd to diseases of the cardiovascular system as leading cause of mortality. In a 2013
community-based survey of stroke, prevalence was twice as high among men compared with
women for both below and above the 40-year-old population groups.

In Davao City, Ischemic stroke is now the top cause of morbidity in the city, with 1,800
people dying from the disease in 2010, a member of a Multisectoral Task Force who did a
research on National Nutrition Health Survey for 2014, said cardiovascular disease is
responsible for at least 76 of every 100,000 deaths yearly.

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 The group’s patient is 52 years old, male, who was admitted at the Davao Doctors
Hospital at 2:17 am on December 18, 2018, under the service of Dr. Orlino Pacioles A M.D. .
Complaining about his slurred speech with experiencing of dizziness, and known had a Diabetes
and Hypertensive for more than 10 years, with maintenance of Tozam and Glacalize, but then
further assessment and laboratories he was diagnosed with Acute Ischemic infract at Corona
Radiata Pulmonary Congestion secondary to Chronic Kidney Disease secondary to
Hypertension Diabetes Mellitus poorly controlled. As a nursing students, who were assigned in
2C ward department we chose Acute Ischemic Infract at Corona Radiata as our case to present,
to gather, trace and collate the predisposing and precipitating factors that could have contributed
to the client’s illness and to provide appropriate health teachings and recommendation for the
client, family and community.

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 C. Definition of Diagnosis

Ischemic strokes occur when blood supply is cut off to part of the brain. This type of stroke
accounts for the majority of all strokes. The blocked blood flow in an ischemic stroke may be
caused by a blood clot or by atherosclerosis, a disease which causes narrowing of the arteries
over time. Ischemic strokes can be caused by a blockage anywhere along the arteries feeding
the brain. Immediate emergency treatment is critical to surviving a stroke with the least amount
of damage to the brain and ability to function.

Most ischemic stroke occur rapidly, over minutes to hours, and immediate medical care
is vital. The signs of a stroke are:

• Sudden numbness or weakness of the • Sudden trouble walking

face, arm or leg, especially on one side of • Sudden dizziness, loss of balance or
the body coordination
• Sudden confusion • Sudden, severe headache with no known
• Sudden trouble speaking cause
• Sudden trouble seeing in one or both
eyes

The corona radiata refer to a pair of white matter tracts seen at the level of the lateral
ventricles. Superiorly they are continuous with the centrum semiovale. Inferiorly these tracts
converge as the internal capsule.

Pulmonary edema is a condition in which the lungs fill with fluid. It’s also known as lung
congestion, lung water, and pulmonary congestion. When pulmonary edema occurs, the body
struggles to get enough oxygen and you start to have shortness of breath. Pulmonary edema is
often caused by congestive heart failure. When the heart is not able to pump efficiently, blood
can back up into the veins that take blood through the lungs. As the pressure in these blood
vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs. This fluid reduces
normal oxygen movement through the lungs. These two factors combine to cause shortness of
breath.

Symptoms may continue to worsen until you get treatment. Symptoms depend on the type of
pulmonary edema. The symptoms for pulmonary edema include:

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• shortness of breath when being physically • waking up at night with a breathless
active feeling that goes away when you sit up

• difficulty breathing when lying down • rapid weight gain, especially in the legs

• wheezing • swelling in the lower part of the body

• fatigue

Chronic kidney disease, also called chronic kidney failure, describes the gradual loss of
kidney function. Your kidneys filter wastes and excess fluids from your blood, which are then
excreted in your urine. When chronic kidney disease reaches an advanced stage, dangerous
levels of fluid, electrolytes and wastes can build up in your body. In the early stages of chronic
kidney disease, you may have few signs or symptoms. Chronic kidney disease may not become
apparent until your kidney function is significantly impaired.

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) or a kidney transplant.

Signs and symptoms of chronic kidney disease develop over time if kidney damage progresses
slowly. Signs and symptoms of kidney disease may include:

• Nausea • Swelling of feet and ankles

• Vomiting • Persistent itching

• Loss of appetite • Chest pain, if fluid builds up around the

lining of the heart
• Fatigue and weakness
• Shortness of breath, if fluid builds up in
• Sleep problems
the lungs
• Changes in how much you urinate
• High blood pressure (hypertension)
• Decreased mental sharpness that's difficult to control

• Muscle twitches and cramps

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 High blood pressure is a common condition in which the long-term force of the blood
against your artery walls is high enough that it may eventually cause health problems, such as
heart disease. Blood pressure is determined both by the amount of blood your heart pumps and
the amount of resistance to blood flow in your arteries. The more blood your heart pumps and
the narrower your arteries, the higher your blood

Most people with high blood pressure have no signs or symptoms, even if blood pressure
readings reach dangerously high levels. A few people with high blood pressure may have
headaches, shortness of breath or nosebleeds, but these signs and symptoms aren't specific
and usually don't occur until high blood pressure has reached a severe or life-threatening stage.

Diabetes prevents your body from properly absorbing energy from the food you eat.
Diabetes mellitus is a disease that prevents your body from properly using the energy from the
food you eat. Diabetes occurs in one of the following situations:

• The pancreas (an organ behind your stomach) produces little insulin or no insulin at all.
Insulin is a naturally occurring hormone, produced by the beta cells of the pancreas, which
helps the body use sugar for energy.

-Or-

• The pancreas makes insulin, but the insulin made does not work as it should. This
condition is called insulin resistance.

Your body is made up of millions of cells. To make energy, the cells need food in a very simple
form. When you eat or drink, much of your food is broken down into a simple sugar called
glucose. Glucose provides the energy your body needs for daily activities. The blood vessels
and blood are the highways that transport sugar from where it is either taken in (the stomach) or
manufactured (in the liver) to the cells where it is used (muscles) or where it is stored (fat). Sugar
cannot go into the cells by itself. The pancreas releases insulin into the blood, which serves as
the helper, or the "key," that lets sugar into the cells for use as energy. When sugar leaves the
bloodstream and enters the cells, the blood sugar level is lowered. Without insulin, or the "key,"
sugar cannot get into the body's cells for use as energy. This causes sugar to rise. Too much
sugar in the blood is called "hyperglycemia" (high blood sugar)

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 D. Patient’s Profile

i. Biographic Data

Name: Patient X

Age: 52 years old

Sex: Male

Civil status: Married

Birthday: November 19, 1936

Religion: Catholic

Nationality: Filipino

Admitting Physician: Dr. Pacioles, Orlino A.M.D.

Date of admission: 12/18/2018

Time of admission: 2:17 AM

Room #: 2102

ii. Past Health History

The patient is a known diabetic and hypertensive for more than 10 years with
maintenance medications of Gliclazide (Diamicron) for DM and Losartan (Amodipine) for
hypertension. Way back on year 2013, the patient was diagnosed with Pulmonary Tuberculosis
(PTB) and treated for 1 year. Other than that, there no other previous surgeries and
hospitalization.

iii.Present Health History

2 days prior to admission, patient noted uncoordinated movements while walking so

patient took a rest. Hours later patient noticed slurring of speech so they sought consult on a
traditional & oriental medicine center with temporary relief. 1 day PTA, patient noted dizziness

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and right sided weakness while standing. No medicines taken. Sought consult on a nearby
hospital and was referred to this instituition for admission.

iv.Family History (with Genogram)

Patient’s family history was traced with hypertension on both maternal and paternal sides. His
maternal side was also traced with Diabetes Mellitus while on the paternal side, liver cancer was
traced. The patient has 3 siblings, 2 are male while 2 are female.

v. Developmental History

The patient is in normal stage of growth. Base on Erick Erickson’s theory which is the
stages of psychosocial development, our patient belongs to the 7 th stage which is Generativity
vs. Stagnation ages 40-65 years of age. In this stage, adult stage of generativity has broad
application to family, relationships, work, and society. Generativity then is primarily the concern
establishing and guiding the next generation the concept is meant to incude productivity and
creativity. The patient is in success regarding to this stage since he shows feelings of usefulness
and accomplishment.

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 vi. Nutritional History

The patient doesn’t practice any diet in regards to his condition. He prefers to eat salty
and fatty foods all the time. He is also a heavy smoker since he was 30 years old. He verbalized
that he can finish a pack of cigarettes in a day. He is also a heavy drinker of alcoholic beverages
and he started drinking he’s on his 20s.

vii. Immunization

Patient’s mother stated that he was fully immunized with BCG, DPT1, DPT2, DPT3,
Measles, OPV1, OPV2, OPV3, MMR1, Hepa B1, Hepa B2, Hepa B3, Chickenpox, Hib 1, Hib 2
and Hib 3 according to their age and intervals.

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 E. Review of Anatomy and Physiology

Brain

The brain is an amazing three-pound organ that controls all functions of the body,
interprets information from the outside world, and embodies the essence of the mind and soul.
Intelligence, creativity, emotion, and memory are a few of the many things governed by the brain.
Protected within the skull, the brain is composed of the cerebrum, cerebellum, and brainstem.
The brain receives information through our five senses: sight, smell, touch, taste, and hearing -
often many at one time. It assembles the messages in a way that has meaning for us, and can
store that information in our memory. The brain controls our thoughts, memory and speech,
movement of the arms and legs, and the function of many organs within our body.

Cerebrum: is the largest part of the brain and is composed of right and left hemispheres. It
performs higher functions like interpreting touch, vision and hearing, as well as speech,
reasoning, emotions, learning, and fine control of movement.

Cerebellum: is located under the cerebrum. Its function is to coordinate muscle movements,
maintain posture, and balance.

Brainstem: acts as a relay center connecting the cerebrum and cerebellum to the spinal cord.
It performs many automatic functions such as breathing, heart rate, body temperature, wake and
sleep cycles, digestion, sneezing, coughing, vomiting, and swallowing.

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Right brain – left brain

The cerebrum is divided into two halves: the right and left hemispheres. They are joined
by a bundle of fibers called the corpus callosum that transmits messages from one side to the
other. Each hemisphere controls the opposite side of the body. If a stroke occurs on the right
side of the brain, your left arm or leg may be weak or paralyzed.

Lobes of the brain

The cerebral hemispheres have distinct fissures, which divide the brain into lobes. Each
hemisphere has 4 lobes: frontal, temporal, parietal, and occipital. Each lobe may be divided,
once again, into areas that serve very specific functions. It’s important to understand that each
lobe of the brain does not function alone. There are very complex relationships between the
lobes of the brain and between the right and left hemispheres.

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Deep structures

Pathways called white matter tracts connect areas of the cortex to each other. Messages can
travel from one gyrus to another, from one lobe to another, from one side of the brain to the
other, and to structures deep in the brain.

The Respiratory System

The human respiratory system is a series of organs responsible for taking in oxygen and
expelling carbon dioxide. The primary organs of the respiratory system are lungs, which carry
out this exchange of gases as we breathe.

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Upper Respiratory Tract

The major passages and structures of the upper respiratory tract include the nostrils, the
nasal cavity, the pharynx, the epiglottis, and the larynx. The upper respiratory tract is lined a
mucous membrane. Mucus helps to trap smoke, dust and other small particles. The membrane
is lined with cilia (hair-like structures that move the mucous upwards only the upper respiratory
tract). The lining of the tract and the close laying blood vessels (especially in the nose) help to
warm and moisten air as it passes.

The pharynx, commonly called the throat, is a passageway that extends from the base of
the skull to the level of the sixth cervical vertebra. It serves both the respiratory and digestive
systems by receiving air from the nasal cavity and air, food, and water from the oral cavity.
Inferiorly, it opens into the larynx and oesophagus.

The larynx, commonly called the voice box or glottis, is the passageway for air between
the pharynx above and the trachea below. It extends from the fourth to the sixth vertebral levels.
The larynx plays an essential role in human speech. During sound production, the vocal cords
close together and vibrate as air expelled from the lungs passes between them.

Lower Respiratory Tract

The major passages and structures of the lower respiratory tract include the trachea, the
right & left bronchus, the bronchioles, and the lungs containing the alveoli. Deep in the lungs,
each bronchus divides into secondary and tertiary bronchi, which continue to branch to smaller
airways called the bronchioles. The bronchioles end in air sacs called the alveoli. Alveoli are
bunched together into clusters to form alveolar sacs. Gas exchange occurs on the surface of
each alveolus by a network of capillaries carrying blood that has come through veins from other
parts of the body.

The trachea, commonly called the windpipe, is the main airway to the lungs. It divides into
the right and left bronchi at the level of the fifth thoracic vertebra, channeling air to the right or
left lung. The cartilage in the tracheal wall provides support and keeps the trachea from
collapsing. The mucous membrane that lines the trachea is similar to that in the nasal cavity.
Mucus traps airborne particles and microorganisms, and the cilia propel the mucus upward,
where it is either swallowed or expelled.

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 The alveoli are grouped together like a lot of interlinked caves, rather than existing as
separate individual sacs. The alveoli have a structure specialised for efficient gaseous
exchange: the alveoli walls are extremely thin; they have a large surface area in relation to
volume, they are fluid lined enabling gases to dissolve; and they are surrounded by numerous
capillaries.

Cardiovascular System

The cardiovascular system can be thought of as the transport system of the body. This
system has three main components: the heart, the blood vessel and the blood itself. The heart
is the system’s pump and the blood vessels are like the delivery routes. Blood can be thought of
as a fluid which contains the oxygen and nutrients the body needs and carries the wastes which
need to be removed. The following information describes the structure and function of the heart
and the cardiovascular system as a whole.

Function and Location of the Heart

The heart’s job is to pump blood around the body. The heart is located in between the
two lungs. It lies left of the middle of the chest.

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Structure of the Heart

The heart is a muscle about the size of a fist, and is roughly cone-shaped. It is about
12cm long, 9cm across the broadest point and about 6cm thick. The pericardium is a fibrous
covering which wraps around the whole heart. It holds the heart in place but allows it to move
as it beats. The wall of the heart itself is made up of a special type of muscle called cardiac
muscle.

Chambers of the Heart

The heart has two sides, the right side and the left side. The heart has four chambers.
The left and right side each have two chambers, a top chamber and a bottom chamber. The two
top chambers are known as the left and right atria (singular: atrium). The atria receive blood from
different sources. The left atrium receives blood from the lungs and the right atrium receives
blood from the rest of the body. The bottom two chambers are known as the left and right
ventricles. The ventricles pump blood out to different parts of the body. The right ventricle pumps
blood to the lungs while the left ventricle pumps out blood to the rest of the body. The ventricles
have much thicker walls than the atria which allows them to perform more work by pumping out
blood to the whole body.

Blood Vessels

Blood Vessel are tubes which carry blood. Veins are blood vessels which carry blood from
the body back to the heart. Arteries are blood vessels which carry blood from the heart to the
body. There are also microscopic blood vessels which connect arteries and veins together called
capillaries. There are a few main blood vessels which connect to different chambers of the heart.
The aorta is the largest artery in our body. The left ventricle pumps blood into the aorta which
then carries it to the rest of the body through smaller arteries. The pulmonary trunk is the large
artery which the right ventricle pumps into. It splits into pulmonary arteries which take the blood
to the lungs. The pulmonary veins take blood from the lungs to the left atrium. All the other veins
in our body drain into the inferior vena cava (IVC) or the superior vena cava (SVC). These two
large veins then take the blood from the rest of the body into the right atrium.

Valves

Valves are fibrous flaps of tissue found between the heart chambers and in the blood
vessels. They are rather like gates which prevent blood from flowing in the wrong direction. They

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are found in a number of places. Valves between the atria and ventricles are known as the right
and left atrioventricular valves, otherwise known as the tricuspid and mitral valves respectively.
Valves between the ventricles and the great arteries are known as the semilunar valves. The
aortic valve is found at the base of the aorta, while the pulmonary valve is found the base of the
pulmonary trunk.

THE KIDNEYS

The kidneys are part of the urinary system. There are 2 kidneys in the body, one on either
side of the spine under the lower ribs, deep inside the upper part of the abdomen. The ureters
are thin tubes that connect each kidney to the bladder. They are about 25–30 cm (10–12 in)
long. The urethra is a small tube that connects the bladder to the outside of the body. There is
an adrenal gland just above each kidney.

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Functions

The blood from the body enters the kidneys through the renal arteries. Once in the kidney,
the blood passes through the nephrons, where waste products and extra water are removed.
The clean blood is returned to the body through the renal veins.

The waste products filtered from the blood are then concentrated into urine. The urine is
collected in the renal pelvis. The ureters move the urine to the bladder, where it is stored. Urine
is passed out of the bladder and the body through the urethra.

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 F.Comprehensive Health Assessment

Integument

● Skin: The client’s skin is light brown and uniform in color, unblemished and no
presence of any foul odor. He has a good skin turgor and skin’s temperature is within
normal limit.
● Hair: The hair of the client is thick, silky hair is evenly distributed and has a variable
amount of body hair. There are also no signs of infection and infestation observed.
● Nails: The client has a light brown nails and has the shape of convex curve. It is
smooth and is intact with the epidermis. When nails pressed between the fingers
(Blanch Test), the nails return to usual color in less than 2-3 seconds.

Head

● Head: The head of the client is rounded; normocephalic and symmetrical.

● Skull: There are no nodules or masses and depressions when palpated.
● Face: The face of the client appeared smooth and has uniform consistency and with
no presence of nodules or masses.

Eyes and Vision

● Eyebrows: Hair is evenly distributed. The client’s eyebrows are symmetrically aligned
and showed equal movement when asked to raise and lower eyebrows.
● Eyelashes: Eyelashes appeared to be equally distributed and curled slightly outward.
● Eyelids: There were no presence of discharges, no discoloration and lids close
symmetrically with involuntary blinks approximately 15-20 times per minute.
● Eyes
○ The Bulbar conjunctiva appeared transparent with few capillaries evident.
○ The sclera appeared white.
○ The palpebral conjunctiva appeared shiny, smooth and pink.
○ There is no edema or tearing of the lacrimal gland.
○ Cornea is transparent, smooth and shiny and the details of the iris are visible.
The client blinks when the cornea was touched.

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 ○ The pupils of the eyes are black and equal in size which is 2mm diameter.
The iris is flat and round. PERRLA (pupils equally round respond to light
accommodation), illuminated and non-illuminated pupils constricts. Pupils
constrict when looking at near object and dilate at far object. Pupils converge
when object is moved towards the nose.
○ When assessing the peripheral visual field, the client can see objects in the
periphery when looking straight ahead.
○ When testing for the Extraocular Muscle, both eyes of the client coordinately
moved in unison with parallel alignment.

Ears and Hearing

• Ears: The Auricles are symmetrical and has the same color with his facial skin. The
auricles are aligned with the outer canthus of eye. When palpating for the texture, the
auricles are mobile, firm and not tender. The pinna recoils when folded. During the
assessment of Watch tick test, the client was able to hear ticking in both ears.

Nose and Sinus

● Nose: The nose appeared symmetric, straight and uniform in color. There was no
presence of discharge or flaring. When lightly palpated, there were no tenderness and
lesions
● Mouth:
○ The lips of the client are uniformly pink; moist, symmetric and have a smooth
texture. The client was able to purse his lips when asked to whistle.
○ Teeth and Gums: There are no discoloration of the enamels, no retraction
of gums, pinkish in color of gums
○ The buccal mucosa of the client appeared as uniformly pink; moist, soft,
glistening and with elastic texture.
○ The tongue of the client is centrally positioned. It is pink in color, moist and
slightly rough. There is a presence of thin whitish coating.

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 ○ The smooth palates are light pink and smooth while the hard palate has a
more irregular texture.
○ The uvula of the client is positioned in the midline of the soft palate.
● Neck:
○ The neck muscles are equal in size. The client showed coordinated, smooth
head movement with no discomfort.
○ The lymph nodes of the client are not palpable.
○ The trachea is placed in the midline of the neck.
○ The thyroid gland is not visible on inspection and the glands ascend during
swallowing but are not visible.

Thorax, Lungs, and Abdomen

● Lungs / Chest: The chest wall is intact with no tenderness and masses. There’s a full
and symmetric expansion and the thumbs separate 2-3 cm during deep inspiration
when assessing for the respiratory excursion. The client manifested quiet, rhythmic
and effortless respirations.
● The patient has Chronic Inflammatory Lung Disease compatible with PTB. Patient
diagnosed of PTB since 2013 with 1 year treatment.
● Heart: There were no visible pulsations on the aortic and pulmonic areas. There is no
presence of heaves or lifts.
● Abdomen: The abdomen of the client has an unblemished skin and is uniform in color.
The abdomen has a symmetric contour. There were symmetric movements caused
associated with client’s respiration.
○ The jugular veins are not visible.
○ When nails pressed between the fingers (Blanch Test), the nails return to
usual color in less than 2-3 seconds.

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Extremities

● Patient has pitting edema on his lower extremities grade 2

● Muscles: The muscles are not palpable with the absence of tremors. Patient was
noted with uncoordinated movement while standing. Patient is right hemiplegia.
● Bones: There were no presence of bone deformities, tenderness and swelling.
● Joints: There were no swelling, and tenderness. Only at the right side of the body that
has no joint movements.

Nursing Assessment in Tabular Form

Assessment Findings

Integumentary

● Skin When skin is pinched it goes to previous

state immediately (2 seconds).

With light brown complexion.

With dry skin

● Hair Evenly distributed hair.

With short, black and shiny hair.

● Nails Smooth and has intact epidermis

With short and clean fingernails and

toenails.

Convex and with good capillary refill time

of 2-3 seconds.

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Skull Rounded, normocephalic and
symmetrical, smooth and has uniform
consistency. Absence of nodules or
masses.

Face Symmetrical facial movement, palpebral

fissures equal in size, symmetric
nasolabial folds.

Eyes and Vision

● Eyebrows Hair evenly distributed with skin intact.

Eyebrows are symmetrically aligned and

have equal movement.

● Eyelashes Equally distributed and curled slightly

outward.

● Eyelids Skin intact with no discharges and no

discoloration.

Lids close symmetrically and blinks

involuntary.

● Bulbar conjunctiva Transparent with capillaries slightly

visible

● Palpebral Conjunctiva Shiny, smooth, pink

● Sclera Appears white.

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 ● Lacrimal gland, Lacrimal sac, No edema or tenderness over the
Nasolacrimal duct lacrimal gland and no tearing.

Cornea

● Clarity and texture Transparent, smooth and shiny upon

inspection by the use of a penlight which
is held in an oblique angle of the eye and
moving the light slowly across the eye.

Has [brown] eyes.

● Corneal sensitivity Blinks when the cornea is touched

through a cotton wisp from the back of
the client.

Pupils Black, equal in size with consensual and

direct reaction, pupils equally rounded
and reactive to light and
accommodation, pupils constrict when
looking at near objects, dilates at far
objects, converge when object is moved
toward the nose at four inches distance
and by using penlight.

Visual Fields When looking straight ahead, the client

can see objects at the periphery which is
done by having the client sit directly
facing the nurse at a distance of 2-3 feet.

The right eye is covered with a card and

asked to look directly at the student
nurse’s nose. Hold penlight in the

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 periphery and ask the client when the
moving object is spotted.

Visual Acuity Able to identify letter/read in the

newsprints at a distance of fourteen
inches.

Patient was able to read the newsprint at

a distance of 8 inches.

Ear and Hearing

● Auricles Color of the auricles is same as facial

skin, symmetrical, auricle is aligned with
the outer canthus of the eye, mobile,
firm, non-tender, and pinna recoils after
it is being folded.

● External Ear Canal Without impacted cerumen.

● Hearing Acuity Test Voice sound audible.

● Watch Tick Test Able to hear ticking on right ear at a

distance of one inch and was able to
hear the ticking on the left ear at the
same distance

Nose and sinuses

25
 ● External Nose Symmetric and straight, no flaring,
uniform in color, air moves freely as the
clients breathes through the nares.

● Nasal Cavity Mucosa is pink, no lesions and nasal

septum intact and in middle with no
tenderness.

Mouth and Oropharynx Symmetrical, pale lips, brown gums and

able to purse lips.

● Teeth With dental caries and decayed lower

molars

● Tongue and floor of the mouth Central position, pink but with whitish
coating which is normal, with veins
prominent in the floor of the mouth.

● Tongue movement Moves when asked to move without

difficulty and without tenderness upon
palpation.

Uvula Positioned midline of soft palate.

Gag Reflex Present which is elicited through the use

of a tongue depressor.

Neck Positioned at the midline without

tenderness and flexes easily. No
masses palpated.

26
Head movement Coordinated, smooth movement with no
discomfort, head laterally flexes, head
laterally rotates and hyperextends.

Muscle strength With unequal strength. Patient is Right

Hemiplagia.

Lymph Nodes Non-palpable, non tender

● Thyroid Gland Not visible on inspection, glands ascend

but not visible in female during
swallowing and visible in males.

Thorax and lungs

Posterior thorax Chest symmetrical

● Spinal alignment Spine vertically aligned, spinal column is

straight, left and right shoulders and hips
are at the same height.

Breath Sounds With wheezing sounds upon

auscultation without dyspnea.

● Anterior Thorax Quiet, rhythmic and effortless respiration

Abdomen Unblemished skin, uniform in color,

symmetric contour, not distended.

Abdominal movements Symmetrical movements cause by

respirations.

27
 ● Auscultation of bowel sounds With audible sounds of 23 bowel
sounds/minute.

Upper Extremities Right arm cannot move.

Lower Extremities Has pitting edema grade 2.

Muscles Equal in size both sides of the body, with

uncoordinated movements.

Bones and Joints No deformities or swelling, joints move

smoothly.

Mental Status

Language Can express oneself by speech or sign.

Orientation Oriented to a person, place, date or time.

Attention span Able to concentrate as evidence by

answering the questions appropriately.

Level of Consciousness A total of 15 points indicative of complete

orientation and alertness.

Motor Function

Gross Motor and Balance

● Walking gait Uncoordinated movements, has activity

intolerance due to Right sided paralyzed.

28
Standing on one foot with eyes closed Unable to stand due to Right sided
paralyzed body.

Heel toe walking Unable to do heel toe walking.

Toe or heel walking Unable to do tor or heel walking.

Fine motor test for Upper Extremities

Finger to nose test Repeatedly and rhythmically touches the

nose on left side of the hand only.

Alternating supination and pronation of Can alternately supinate and pronate

hands on knees hand at rapid pace at left hand only.

Finger to nose and to the nurse’s finger Perform with coordinating and rapidity at
left fingers only.

Fingers to fingers Perform with accuracy and rapidity at left

fingers only.

Fingers to thumb Rapidly touches each finger to thumb

with left hand only.

Fine motor test for the Lower Extremities

Pain sensation Able to discriminate between sharp and

dull sensation when touched with needle
and cotton. But cannot feel pain in his
right side of the body.

29
 G. Pathophysiology

i. Etiology

viii. PRECIPITA PRESENT JUSTIFICATION

TING
FACTORS
Diabetes mellitus is the leading cause of
Diabetes Mellitus chronic kidney disease (CKD) and a major
public health issue worldwide.
Approximately 20–30% of patients with
type 2 diabetes mellitus (T2DM) have
renal impairment, classified as moderate-
to-severe CKD (glomerular filtration rate
(GFR) <60 mL/min/1.73 m2).
(Glucose lowering therapeutic strategies
for type 2 diabetic patients with chronic
kidney disease in primary care setting in
france: a cross-sectional study. Int J
Endocrinol. 2013)
Hypertension is one of the leading causes
Hypertension of CKD due to the deleterious effects that
increased BP has on kidney vasculature.
Long-term, uncontrolled, high BP leads to
high intraglomerular pressure, impairing
glomerular filtration.
(American Heart Association 2013)
Sedentary Lifestyle Chronic renal disease is accompanied by
(smoking, alcohol, diet characteristic abnormalities of lipid
and physical inactivity) metabolism, which appear as a
consequence of nephrotic syndrome or
renal insufficiency and are reflected in an
altered apolipoprotein profile as well as
elevated plasma lipid levels.
(Acta paul, enferm. São Paulo Mar/Apr.
2014)

30
 PREDISPOSING PRESENT JUSTIFICATION
FACTOR
Age (older 45 for men The most powerful independent predictor
and 55 for women) for the development of CKD, including
presentation with Hypetrension, is age.
(Keith A A Fox, 2014)

Gender Well documented that the incidence of ckd

is higher in men approximately in age up
to 45 years old than women
(Falcone and Chong, 2017
Family History Most cases of CKD are acquired rather
than inherited, although CKD in a child is
more likely to have a genetic or inherited
cause. Well-described genetic syndromes
associated with CKD include autosomal
dominant polycystic kidney
disease(ADPKD) and Alport syndrome.
Other examples of specific single-gene or
few-gene mutations associated with CKD
include Dent disease, nephronophthisis,
and atypical hemolytic uremic syndrome
(HUS).
(Hoseini K, et al. Monaldi Arch Chest Dis.
2013)

ii.Symptomatology

SYMPTOMS PRESENT JUSTIFICATION

Edema Kidney damage. Damage to the tiny,

filtering blood vessels in your kidneys can
result in nephrotic syndrome. In nephrotic
syndrome, declining levels of protein
(albumin) in your blood can lead to fluid
accumulation and edema.
(American Heart Association)
Shortness of Breath Fatigue or weakness — a build-
up of wastes or a shortage of red blood
cells (anemia) can cause these problems
when the kidneys begin to fail. Shortness
31
 of breath — kidney failure is sometimes
confused with asthma or heart failure,
because fluid can build up in the lungs.
(Porth 2017)
Increased glucose Insulin is a hormone that helps regulate
level sugar (glucose) in the blood. When blood
sugar levels get too high, the condition is
called hyperglycemia. If your diabetes is
not controlled, it can lead to increased loss
of kidney function, cardiovascular disease,
vision loss and other complications.
(Patrick Gallagher, 2013)
Slurred speech Dysarthria often is characterized
by slurred or slow speech that can be
difficult to understand. Common causes of
dysarthria include nervous system
(neurological) disorders such as stroke,
brain injury, brain tumors, and conditions
that cause facial paralysis or tongue or
throat muscle weakness.
(Porth 2017).
Metabolic Acidosis As a result, CKD leads to retention of
hydrogen ions. The retained acid is
buffered by bicarbonate in the extracellular
fluid, by tissue buffers, and by bone. With
worsening renal function, however,
progressive metabolic acidosis can
develop.
(Sethi SS, et al. Curr Diab Rep. 2013
Increased urine output Diuresis is determined not only by residual
GFR, but also by the rate of tubular
reabsorption . The equilibrium between
GFR and tubular reabsorption is lost in
advanced uremia, sometimes in earlier
stages, depending on the concomitant
complications as hypertension or/ and the
primary renal diseases.
(Association between extracellular water,
left ventricular mass and hypertension in
haemodialysis patients. Nephrol Dial
Transplant. 2003)

32
 iii. Schematic Diagram

Precipitating Factor: Predisposing Factor:

Hereditary Hypertension
Age Hyperlipidemia
Gender Diabetes Mellitus
race Smoking
Diet

Hypertension

Vasoconstriction

Increase afterload,
preload and pressure

Increase workload

Increase force on LV
Injury of the
endothelial vessel
layer Increase stress on Increase cardiac
the LV output

Scarring
LV Hypertrophy

Atherosclerosis
Ventricular LV hypoxia
remodelation
CAD

Decrease LV force

33
 Decrease cardiac
tissue Increase LA pressure
Decrease cardiac
output
Decrease cardiac Back flows
muscle
Decrease systemic
output
Increased residual
volume blood from LA
Activation of
baroreceptor in LV Decreased
perfusion tissue of
the body Blood returns to
pulmonary
Stimulation of
vasomotor regulator
Decreased
GFR
Increased pulmonary
Activation of capillary hydrostatic
Decreased renal
sympathetic nervous pressure
perfusion
system

Hydrostatic pressure
Increased exceeds osmotic
catecolamines Hyponatre Juxtoglomelular pressure
mia cells

Renin Fluids moves to

interstitial space

Angiotensinogen
RAAS
Amount of fluid
Arteriolar exceeds lymphatic
Angiotensin I
vasoconstric systems ability to
tion remove it
Angiotensin II
Increased
peripheral PULMONARY
resistance Adrenal cortex EDEMA

Dyspnea, cough,
Increased crackles, orthopnea,
aldosterone frothy blood sputum

34
Increased Na
reabsorption
 Increased H2O
reabsorption

Increased plasma
volcano (ECF)

Increased BP

Decreased Decreased O2 supply

perfusion of tissue to tissue
in the body

Increased • Myocardium:
sympathetic activity increased cardiac
workload
• Brain: decreased
oxygen supply to
Decreased Increased peripheral
cerebral tissue
BP, HR vasoconstriction
• GI Tract: decreased
O2 supply to GI
• Liver: dysfunction
Renal
vasoconstriction

Lack of oxygen
Increased renin supply and hypoxia
nutrients to
supply
UA: Hematuria, Capillary endothelial
albumin damage Altered cerebral
metabolism

Aneurysm

Brain tissue necrosis

ACUTE ISCHEMIC
Paralysis 35
INFARCT
 Decreased GFR • Increased
Serum
creatinine
Hyperthropy of • Increased
Loss of
remaining nephrons NA BUN
Dilute urine

Hyponatremia
Inability to
Dehydration concentrate urine Oliguria

Further loss of
nephron function

Loss of Loss of excretory

nonexcretory renal renal function
function

Failure to Failure to Impaired Increased

convert forms of produce insulin Immune
productio
calcium erythropoietin function disturbance
n of lipids

Decreased calcium
Anemia Erratic Advance Delayed
absorption
Decreased blood artherosclero wound
hemoglobin glucose sis healing
Hypocalcemia

Infection

36
 Loss of excretory
renal function

Decreased Decreased
excretory of NA Decreased Decreased Decreased
nitrogenous reabsorption K excretion phosporus hydrogen
waste in tubule excretion

Hyperkalem hypophosp
Decreased Water ia athemia Metabolic
uremia retention acidosis

Hypertensi
• Increased on
BUN,Creatinin Heart
e, uric acid failure
• Protenuria Edema
• Peripheral
nerve changes
• CNS changes

CHRONIC KIDNEY
DISEASE

37
 iv. Narrative

The pathogenesis of essential hypertension is multifactorial and highly complex. The

kidney is both the contributing and the target organ of the hypertensive processes,and the
disease involves the interaction of multiple organ systems and numerous mechanisms of
independent or interdependent pathways. Factors that play an important role in the
pathogenesis of hypertension include genetics, activation of neurohormonal systems such as
the sympathetic nervous system and renin-angiotensin-aldosterone system, obesity, and
increased dietary salt intake.Arterial hypertension is the condition of persistent elevation of
systemic blood pressure (BP). BP is the product of cardiac output and total peripheral vascular
resistance.

Multiple factors are involved in short-term and long-term regulation of BP for adequate tissue
perfusion; these include the following:

• Cardiac output and circulatory blood • Humoral mediators

volume
• Neural stimulation
• Vascular caliber, elasticity, and
reactivity

Over the course of its natural history, essential hypertension progresses from
occasional to established hypertension. After a long, invariable, asymptomatic period,
persistent hypertension develops into complicated hypertension, in which target organ damage
to the aorta and small arteries, heart, kidneys, retina, and central nervous system is evident.

The progression of essential hypertension begins with prehypertension in persons aged

10-30 years (by increased cardiac output); then advances to early hypertension in persons
aged 20-40 years (in which increased peripheral resistance is prominent); then progresses to
established hypertension in persons aged 30-50 years; and finally advances to complicated
hypertension in persons aged 40-60 years.

Acute ischemic strokes result from vascular occlusion secondary to thromboembolic

disease . Ischemia causes cell hypoxia and depletion of cellular adenosine triphosphate (ATP).
Without ATP, there is no longer the energy to maintain ionic gradients across the cell
membrane and cell depolarization. Influx of sodium and calcium ions and passive inflow of
water into the cell lead to cytotoxic edema.

38
Ischemic core and penumbra

An acute vascular occlusion produces heterogeneous regions of ischemia in the affected

vascular territory. Local blood flow is limited to any residual flow in the major arterial source
plus the collateral supply, if any.

Affected regions with cerebral blood flow of lower than 10 mL/100 g of tissue/min are referred
to collectively as the core. These cells are presumed to die within minutes of stroke onset.

Zones of decreased or marginal perfusion (cerebral blood flow < 25 mL/100g of

tissue/min) are collectively called the ischemic penumbra. Tissue in the penumbra can remain
viable for several hours because of marginal tissue perfusion.

Ischemic cascade

On the cellular level, the ischemic neuron becomes depolarized as ATP is depleted and
membrane ion-transport systems fail. Disruption of cellular metabolism also impairs normal
sodium-potassium plasma membrane pumps, producing an intracellular increase in sodium,
which in turns increases intracellular water content. This cellular swelling is referred to as
cytotoxic edema and occurs very early in cerebral ischemia.

Cerebral ischemia impairs the normal sodium-calcium exchange protein also found on
cell plasma membranes. The resulting influx of calcium leads to the release of a number of
neurotransmitters, including large quantities of glutamate, which in turn activates N -methyl-D-
aspartate (NMDA) and other excitatory receptors on other neurons.

These neurons then become depolarized, causing further calcium influx, further
glutamate release, and local amplification of the initial ischemic insult. This massive calcium
influx also activates various degradative enzymes, leading to the destruction of the cell
membrane and other essential neuronal structures. Free radicals, arachidonic acid, and nitric
oxide are generated by this process, which leads to further neuronal damage.

Ischemia also directly results in dysfunction of the cerebral vasculature, with breakdown
of the blood-brain barrier occurring within 4-6 hours after infarction. Following the barrier’s
breakdown, proteins and water flood into the extracellular space, leading to vasogenic edema.
This produces greater levels of brain swelling and mass effect that peak at 3-5 days and
resolve over the next several weeks with resorption of water and proteins.

39
 Within hours to days after a stroke, specific genes are activated, leading to the
formation of cytokines and other factors that, in turn, cause further inflammation and
microcirculatory compromise. [ Ultimately, the ischemic penumbra is consumed by these
progressive insults, coalescing with the infarcted core, often within hours of the onset of the
stroke.

Infarction results in the death of astrocytes, as well as the supporting oligodendroglial

and microglial cells. The infarcted tissue eventually undergoes liquefaction necrosis and is
removed by macrophages, with the development of parenchymal volume loss. A well-
circumscribed region of cerebrospinal fluid–like low density, resulting from encephalomalacia
and cystic change, is eventually seen. The evolution of these chronic changes may be seen in
the weeks to months following the infarction.

A normal kidney contains approximately 1 million nephrons, each of which contributes

to the total glomerular filtration rate (GFR). In the face of renal injury (regardless of the
etiology), the kidney has an innate ability to maintain GFR, despite progressive destruction of
nephrons, as the remaining healthy nephrons manifest hyperfiltration and compensatory
hypertrophy. This nephron adaptability allows for continued normal clearance of plasma
solutes. Plasma levels of substances such as urea and creatinine start to show measurable
increases only after total GFR has decreased to 50%.

The plasma creatinine value will approximately double with a 50% reduction in GFR.
For example, a rise in plasma creatinine from a baseline value of 0.6 mg/dL to 1.2 mg/dL in a
patient, although still within the adult reference range, actually represents a loss of 50% of
functioning nephron mass.

The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the
reasons noted, has been hypothesized to represent a major cause of progressive renal
dysfunction. The increased glomerular capillary pressure may damage the capillaries, leading
initially to secondary focal and segmental glomerulosclerosis (FSGS) and eventually to global
glomerulosclerosis. This hypothesis is supported by studies of five-sixths nephrectomized rats,
which develop lesions identical to those observed in humans with chronic kidney disease
(CKD).

40
Factors other than the underlying disease process and glomerular hypertension that may
cause progressive renal injury include the following:

• Systemic hypertension • Proteinuria (in addition to being a

marker of CKD)
• Nephrotoxins (eg, nonsteroidal anti-
inflammatory drugs [NSAIDs], • Hyperlipidemia
intravenous contrast media)
• Hyperphosphatemia with calcium
• Decreased perfusion (eg, from phosphate deposition
severe dehydration or episodes of
• Smoking
shock)
• Uncontrolled diabetes

Another important note for childhood CKD is that physicians caring for children must be
aware of normal blood pressure levels by age, sex, and height. Prompt recognition of
hypertension at any age is important, because it may be caused by primary renal disease.

Fortunately, CKD during childhood is rare and is usually the result of congenital defects,
such as posterior urethral valves or dysplastic kidney malformations. Another common cause
is FSGS. Genetic kidney diseases are also frequently manifested in childhood CKD. Advances
in pediatric nephrology have enabled great leaps in survival for pediatric CKD and end-stage
renal disease (ESRD), including for children who need dialysis or transplantation.

Aging and renal function

The biologic process of aging initiates various structural and functional changes within
the kidney. Renal mass progressively declines with advancing age, and glomerulosclerosis
leads to a decrease in renal weight. Histologic examination is notable for a decrease in
glomerular number of as much as 30-50% by age 70 years.

The GFR peaks during the third decade of life at approximately 120 mL/min/1.73 m2; it
then undergoes an annual mean decline of approximately 1 mL/min/y/1.73 m2, reaching a
mean value of 70 mL/min/1.73 m2 at age 70 years.

41
Genetics

Most cases of CKD are acquired rather than inherited, although CKD in a child is more
likely to have a genetic or inherited cause. Well-described genetic syndromes associated with
CKD include autosomal dominant polycystic kidney disease(ADPKD) and Alport syndrome.
Other examples of specific single-gene or few-gene mutations associated with CKD include
Dent disease, nephronophthisis, and atypical hemolytic uremic syndrome (HUS).

Immune-system and RAS genes

A number of genes have been associated with the development of ESRD. Many of
these genes involve aspects of the immune system (eg, CCR3, IL1RN, IL4).

Unsurprisingly, polymorphisms in genes involving the renin-angiotensin system (RAS)

have also been implicated in predisposition to CKD. One study found that patients with CKD
were significantly more likely to have the A2350G polymorphism in the ACE gene, which
encodes the angiotensin-converting enzyme (ACE). They were also more likely to have the
C573T polymorphism in the AGTR1 gene, which encodes the angiotensin II type 1 receptor.

Hyperkalemia

The ability to maintain potassium excretion at near-normal levels is generally

maintained in CKD, as long as aldosterone secretion and distal flow are maintained.

Another defense against potassium retention in patients with CKD is increased

potassium excretion in the gastrointestinal tract, which also is under control of aldosterone.

Hyperkalemia usually does not develop until the GFR falls to less than 20-25
mL/min/1.73 m², at which point the kidneys have decreased ability to excrete potassium.
Hyperkalemia can be observed sooner in patients who ingest a potassium-rich diet or have low
serum aldosterone levels. Common sources of low aldosterone levels are diabetes mellitus
and the use of ACE inhibitors, NSAIDs, or beta-blockers.

Hyperkalemia in CKD can be aggravated by an extracellular shift of potassium, such as

occurs in the setting of acidemia or from lack of insulin.

Metabolic acidosis
42
 Metabolic acidosis often is a mixture of normal anion gap and increased anion gap; the
latter is observed generally with stage 5 CKD but with the anion gap generally not higher than
20 mEq/L. In CKD, the kidneys are unable to produce enough ammonia in the proximal tubules
to excrete the endogenous acid into the urine in the form of ammonium. In stage 5 CKD,
accumulation of phosphates, sulfates, and other organic anions are the cause of the increase
in anion gap.

Metabolic acidosis has been shown to have deleterious effects on protein balance, leading to
the following:

• Negative nitrogen balance • Reduced albumin synthesis

• Increased protein degradation • Lack of adaptation to a low-protein

diet
• Increased essential amino acid
oxidation

Hence, metabolic acidosis is associated with protein-energy malnutrition, loss of lean body
mass, and muscle weakness. The mechanism for reducing protein may include effects on
adenosine triphosphate (ATP)–dependent ubiquitin proteasomes and increased activity of
branched-chain keto acid dehydrogenases.

Metabolic acidosis also leads to an increase in fibrosis and rapid progression of kidney
disease, by causing an increase in ammoniagenesis to enhance hydrogen excretion.

In addition, metabolic acidosis is a factor in the development of renal osteodystrophy,

because bone acts as a buffer for excess acid, with resultant loss of mineral. Acidosis may
interfere with vitamin D metabolism, and patients who are persistently more acidotic are more
likely to have osteomalacia or low-turnover bone disease.

Salt- and water-handling abnormalities

Salt and water handling by the kidney is altered in CKD. Extracellular volume expansion
and total-body volume overload results from failure of sodium and free-water excretion. This
generally becomes clinically manifested when the GFR falls to less than 10-15 mL/min/1.73
m², when compensatory mechanisms have become exhausted.

43
 As kidney function declines further, sodium retention and extracellular volume
expansion lead to peripheral edema and, not uncommonly, pulmonary edema and
hypertension. At a higher GFR, excess sodium and water intake could result in a similar
picture if the ingested amounts of sodium and water exceed the available potential for
compensatory excretion.

Tubulointerstitial renal diseases represent the minority of cases of CKD. However, it is

important to note that such diseases often cause fluid loss rather than overload. Thus, despite
moderate or severe reductions in GFR, tubulointerstitial renal diseases may manifest first as
polyuria and volume depletion, with inability to concentrate the urine. These symptoms may be
subtle and require close attention to be recognized. Volume overload occurs only when GFR
reduction becomes very severe.

Anemia

Normochromic normocytic anemia principally develops from decreased renal synthesis

of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell
(RBC) production. The anemia starts early in the course of the disease and becomes more
severe as, with the shrinking availability of viable renal mass, the GFR progressively
decreases.

Using data from the National Health and Nutrition Examination Survey (NHANES),
Stauffer and Fan found that anemia was twice as prevalent in people with CKD (15.4%) as in
the general population (7.6%). The prevalence of anemia increased with stage of CKD, from
8.4% at stage 1 to 53.4% at stage 5.

No reticulocyte response occurs. RBC survival is decreased, and bleeding tendency is

increased from the uremia-induced platelet dysfunction. Other causes of anemia in CKD
include the following:

Bone disease

Renal bone disease is a common complication of CKD. It results in skeletal

complications (eg, abnormality of bone turnover, mineralization, linear growth) and
extraskeletal complications (eg, vascular or soft-tissue calcification).
44
 Bone disease in children is similar but occurs during growth. Therefore, children with
CKD are at risk for short stature, bone curvature, and poor mineralization (“renal rickets” is the
equivalent term for adult osteomalacia).

CKD–mineral and bone disorder (CKD-MBD) involves biochemical abnormalities related

to bone metabolism. CKD-MBD may result from alteration in levels of serum phosphorus, PTH,
vitamin D, and alkaline phosphatase.

Calcium and calcitriol are primary feedback inhibitors; hyperphosphatemia is a stimulus

to PTH synthesis and secretion.

Hyperphosphatemia and hypocalcemia

Phosphate retention begins in early CKD; when the GFR falls, less phosphate is filtered
and excreted, but because of increased PTH secretion, which increases renal excretion, serum
levels do not rise initially. As the GFR falls toward CKD stages 4-5, hyperphosphatemia
develops from the inability of the kidneys to excrete the excess dietary intake.

Hyperphosphatemia suppresses the renal hydroxylation of inactive 25-hydroxyvitamin D

to calcitriol, so serum calcitriol levels are low when the GFR is less than 30 mL/min/1.73 m².
Increased phosphate concentration also effects PTH concentration by its direct effect on the
parathyroid glands (posttranscriptional effect).

Hypocalcemia develops primarily from decreased intestinal calcium absorption because

of low plasma calcitriol levels. It also possibly results from increased calcium-phosphate
binding, caused by elevated serum phosphate levels.

Increased PTH secretion

Low serum calcitriol levels, hypocalcemia, and hyperphosphatemia have all been
demonstrated to independently trigger PTH synthesis and secretion. As these stimuli persist in
CKD, particularly in the more advanced stages, PTH secretion becomes maladaptive, and the
parathyroid glands, which initially hypertrophy, become hyperplastic. The persistently elevated
PTH levels exacerbate hyperphosphatemia from bone resorption of phosphate.

45
 H. Course in the ward/Treatment/Interventions

i. Medical Management
1. Doctor’s Progress Notes

12/18/18
➢ Please admit under the service of Dr. Pacioles
➢ Secure consent for management
➢ VS q4
➢ I & O qShift
➢ IVF: PNSS 1L @ 120ml/hr
➢ May have LS,LF DM diet
➢ Labs: CBC, ECG 12L, ABG, S. Na, k, Ca, S. Crea, CXR AP Ultrasound
cranial CT scan plain
➢ Meds
1. Citicoline 1g q6 IVTT
2. Cilostazol 100 mg (pletaal SR) 2 tabs PO OD
➢ Meds Recon:
1. Diamicron 60 mg 1tab PO OD
2. Amlodipine+ Losartan 5/50 mg 1tab PO Daily
➢ Will inform Dr.Pacioles of this admission
➢ Inform MRCI/ MROD

12/18/18 5:30 am MROD

➢ Pt. seen and examined
➢ History examined
➢ For MRI Stat- Hold
➢ Will update AP
➢ Facilitate labs. Please relay once with result
➢ Refer

46
12/18/18 08:50 am Confirmed with Dr. Pacioles
➢ CT Scan cranial plain

12/18/18 03:20 pm Rounds : Dr. Pacioles

➢ CBG TID before meals
➢ Use Citilin for Citicoline
➢ Cilostazol 100 mg/tab (Pletaal SR) 2 Tabs OD PO
➢ Increase Citicoline to every 6 hrs.
➢ Follow up ECG result
➢ Monitor BP q4

12/19/18 11:20 am Rounds: Dr. Pacioles

➢ Refer to HC endo and nephro for co-mgt.
➢ Hydroxyzine (Atarax) 25 mg/tab PO now then OD PO
➢ Trop I HS STAT
➢ For – lipid profile
- HbAIC
- SGPT
- Urinalysis
- S. Uric Acid
➢ CBG TID HS
➢ CBG now

12/19/18 MRIC
➢ Cilostazol 100 mg/tab (Pletaal SR) 2 Tabs OD PO
➢ Citicoline 1g q6 IVTT
➢ Atorvastatin 80 mg/tab , 1tab OD
➢ Gliclazide (Diamicron) 60 mg 1tab OD
➢ Amlodipine + Losartan 5/50 mg 1tab OD

47
12/19/18 3:40 pm Rounds: Dr. Racho
➢ Paracetamol 500 mg/tab, 1 tab PO now
(Xanax) alprazolam 250 mg ½ tab now then OD at HS
➢ May given Insulin Apidra, CBG >180: 12 units
➢ Insulin Lantus 16 units at HS;
➢ Insulin Apidra 8 units TID pre meals

12/19/18 4:50 pm Rounds: Dr. Villanueva

➢ For UTZ- Kidney
➢ Follow up ECG result
➢ Decrease IVF rate to KVO
➢ STAT Furosemide 40mg IVTT now then record output after 1hr; refer urine
Output 1hr after Furosemide
➢ Follow up pending labs

12/19/18 11:00 pm MROD

➢ Confirmed with Dr. Villanueva,
STAT Furosemide 40 mg IVTT given
➢ For strict I&O monitoring
➢ Refer for any unusual ties

12/20/18 11 am MRIC
➢ 1. Insulin Lantus 16 units OD HS
➢ 2. Furosemide 40mg IVTT q6
➢ 3. Insulin Apidra 8 units TID pre meals
➢ 4. Cilostazol 100 mg/tab (Pletaal SR) 2 Tabs OD PO
➢ 5. Atorvastatin 80 mg/tab , 1tab OD
➢ 6. Citicoline 1g q6 IVTT
➢ 7. Diamicron 60 mg 1tab PO OD
➢ 8. Alprazolam 250 mg/tab (Xanax) 1 tab OD HS
➢ Will update AP

48
 ➢ Refer

12/20/18 9:30 am MRIC

➢ Facilitate ultrasound
➢ Follow up ECG official – done-
➢ Continue mgt.
➢ Follow up lipid profile

12/20/18 11:30 am Rounds: Dr. Pacioles

➢ Follow up ultrasound
➢ Continue meds.

49
 2. Laboratory/Diagnostic Examinations

TYPE OF TEST INDICA NORMAL ACTUAL IMPRESSIONS IMPLICATIONS NURSING

TION VALUES RESULT RESPONSIBILI
TIES
-Chest AP Chest x-rays are The lungs look The heart size * Suggestive of Experiencing Keep the record
(Adult) performed for normal in size cannot be a chronic symptoms such of the procedure
December 18, screening and shape, and assessed due to inflammatory as shortness of and inform the
2018 purposes, such the lung tissue position. lung disease breath, client regarding
as pre-operative looks normal. Pulmonary compatible with coughing, the procedure.
clearance, No growths or vascularity is PTB. wheezing, Nurse may need
many chest x- other masses normal. chronic mucus to reduce
rays are can be seen Infiltrates are production, etc. anxiety in some
performed in within the lungs. seen in the right then your patients,particul
response to The pleural upper lobe. The physician may arly in those
patient spaces (the rest of the lungs order a chest x- who are
symptoms like spaces are clear. The ray. Conditions confused or
cough, fever, or surrounding the lateral such as heart anxious. And
pain. Chest x- lungs) also look costophrenic failure, also during the
ray is an normal. sinusesare pneumonia, procedure,
excellent first sharp. Hili are lung cancer, ensure that the
imaging test to not enlarged. tuberculosis, client is wearing
assess for Visualized sarcoidosis,
50
 pneumonia, osseous pleural loose fitting
pulmonary structures are effusion, gown.
edema, or normal. embolisms,
pleural effusion. emphysema,
Reference: and lung
Brunner and scarring would
Suddarth’s all show up on
Medical Surgical chest scans in
Nursing 13th various ways.
edition by:
Janice Hinkle
pg.485

-CHEST AP Chest x-rays are A comparison

SITTING performed for The lungs look with the Experiencing
screening normal in size radiograph symptoms such Keep the record
December purposes, such and shape, and dated December as shortness of of the procedure
19,2018 as pre-operative the lung tissue 18,2018 shows breath, and inform the
clearance, looks normal. no significant coughing, client regarding
many chest x- No growths or change of the wheezing, the procedure.

51
rays are other masses infiltrates in the chronic mucus Nurse may need
performed in can be seen right upper lobe. production, etc. to reduce
response to within the lungs. The rest of the then your anxiety in some
patient The pleural lungs are physician may patients,particul
symptoms like spaces (the clear,heart size order a chest x- arly in those
cough, fever, or spaces cannot be ray. Conditions who are
pain. Chest x- surrounding the assessed due to such as heart confused or
ray is an lungs) also look Position. failure, anxious. And
excellent first normal. Pulmonary pneumonia, also during the
imaging test to vascularity is lung cancer, procedure,
assess for normal. The tuberculosis, ensure that the
pneumonia, lateral sarcoidosis, client is wearing
pulmonary costophrenic pleural loose fitting
edema, or sinuses are effusion, gown.
pleural effusion. sharp. Hili are embolisms,
Reference: not enlarged. emphysema,
Brunner and Visualized and lung
Suddarth’s osseous scarring would
Medical Surgical structures are all show up on
Nursing 13th normal. chest scans in
edition by: various ways.
Janice Hinkle
pg.485

52
TYPE OF TEST INDICATION NORMAL ACTUAL IMPRESSIONS IMPLICATIONS NURSING
VALUES RESULT RESPONSIBILI
TIES
ULTRASOUND A Kidney Specifically,the Right kidney ( * minimal Experiencing Keep the record
-KIDNEYS ultrasound may current literature 9.6 x 3.8 x 5.1 x hydronephrosis, symptoms such of the procedure
be used to reference 1.4 cm, left as weight loss and inform the
assess the values,principall CCxAPxTxPT) *normal and poor client regarding
size,location,and y from and left kidney ultrasound study appetite,swollen the procedure.
the shape of the ultrasonography (10.0 x 4.9 x 5.0 of the right ankles,feet or Nurse may need
kidneys and measurements x 1.8 kidney. hands,shortness to reduce
related suggest that a cm,CCxAPxTxP of breath,an anxiety in some
structures such normal adult T) show normal increased need patients,particul
as ureters and kidney is corticomedullary to urinate etc. arly in those
bladder. approximately parenchymal then your who are
Ultrasound can 11+- 1.0 cm echotexture with physician may confused or
detect long( 7 to 12) good order a kidney anxious. And
cysts,tumors,ab with a normal differentiation of ultrasound. also during the
scesses,obstruct volume of 110 to the cortex and Conditions procedure,
ions,fluid 190 ml in men medulla. The such as chronic ensure that the
collection,and and 90 to 150 ml right central kidney disease client is wearing
infection within in women. echocomplex is that often loose fitting
or around the The kidneys normal. accompanies gown.
kidneys. look normal in Proximal ureters with
size and shape, are not dilated. cardiovascular

53
Reference: and the lung There is minimal disease are
Brunner and tissue looks separation of the mostly
Suddarth’s normal. No left central recommended
Medical Surgical growths or other echocomplex by for kidney
Nursing 13th masses can be echolucent ultrasound.
edition by: seen within the areas.
Janice Hinkle structures such
pg.1476 as ureters and
bladder.

54
TYPE OF TEST INDICATION NORMAL ACTUAL IMPRESSIONS IMPLICATIONS NURSING
VALUES RESULT RESPONSIBILI
TIES
CT SCAN OF Ct scanning of The head Low attenuation * acute ischemic Doctors Nurse may need
THE HEAD the head is specially changes is seen infact,left corona recommend a ct to reduce
typically used to skull,brain look in the left corona radiata scan to help anxiety in some
detect: bleeding, normal in size radiata. There is * atherosclerosis diagnose patients,particul
brain injury and and shape, and normal gray * bilateral muscle and arly in those
skull fractures in the brain tissue white matter maxillary bone disorders who are
patients with looks normal. interface. There sinusitis such as bone confused or
head injuries. It No growths or is no focal zone tumors and anxious. And
is a special x-ray other masses of hemorrhage fractures. Helps also during the
used to take can be seen nor mass lesion assess head procedure,
picture of within the head appreciated. injuries,severe ensure that the
patients and the brain. Peripheral headaches, client is wearing
skull,brain,and cortical sulci are dizziness and loose fitting
sinuses as well normal. other symptoms gown.
as blood Lentiform of
vessels. nucleus,thalami, aneurysm,bleedi
midbrain and ng,stroke and
pons reveal brain tumors.
normal tissue
density.
Ventricles are

55
normal size and
configuration.
Midline cerebral
structures are
not shifted.
Posterior fossa
structures,petro
mastoids and
bony calvarium
are
unremarkable.
Calcified
plaques are
seen in the
vertebrobasilar
arteries.
Mucosal
thickening is
noted in both
maxillary
sinuses.

56
TYPE OF INDICATION NORMAL ACTUAL IMPLICATIONS NURSING
TEST VALUES RESULT RESPONSIBILITIES
CREATININ A creatinine blood te Adult male: 220.00 ^umol/L Creatinine is one of the > Instruct patient about any
E st measures the 0.6 to 1.2 (2.49 mg/dL) substances that your prescription or over-the-counter
December level ofcreatinine in mg/dL > HIGH kidneys normally (OTC) medications you’re
18,2018 the (60-110 eliminate from the body. currently taking. Some drugs
blood. Creatinine is ^umol/L) Doctors measure the may increase your creatinine
a waste product that level of creatinine in the levels without causing kidney
forms Adult blood to check kidney damage and interfere with your
when creatine, female: function. High levels of test results. Let your doctor
which is found in 0.5 to 1.1 creatinine may indicate know if you take:
your muscle, breaks mg/dL that your kidney is • cimetidine (Tagamet,
down. Creatinine lev (45-90 damaged and not Tagamet HB)
els in the blood can ^umol/L) working properly. • nonsteroidal anti-
provide your doctor inflammatory drugs
with information (NSAIDs), such as
about how well your aspirin (Bayer) or
kidneys are working. ibuprofen (Advil, Midol)
• chemotherapy drugs
• cephalosporin
antibiotics, such
as cephalexin (Keflex)
and cefuroxime (Ceftin)

57
TYPE OF INDICATION NORMAL ACTUAL IMPLICATIONS NURSING
TEST VALUES RESULT RESPONSIBILITIES
TROPONIN I A troponin Reference 32.90 pg/ml Very high levels of >Monitor patients ECG result
test measures the range: 28.9- troponin are a sign that and assess patient for possible
levels of troponin T 39.2 pg/ml a heart attack has recurrent signs and symptoms
or troponin I proteins occurred. of heart attack.
in the blood. These Most patients who have
proteins are had a heart attack have
released when the increased troponin
heart muscle has levels within 6 hours.
been damaged, After 12 hours, almost
such as occurs with everyone who has had
a heart attack. The a heart attack will have
more damage there raised levels.
is to the heart, the Troponin levels may
greater the amount remain high for 1 to 2
of troponin T and I weeks after a heart
there will be in the attack.
blood.

58
TYPE OF INDICATION NORMAL ACTUAL IMPLICATIONS NURSING
TEST VALUES RESULT RESPONSIBILITIES
MAGNESIU A magnesium test is used to 0.7-1 0.85 Magnesium can be Follow your healthcare
M measure the level ^mmol/L ^mmol/L excreted by your provider's instructions for
December of magnesium in the blood NORMAL kidneys. Any damage to increasing your blood
18, 2018 (or sometimes urine). ... your kidneys, when they magnesium level. If your blood
The test for magnesium may are not working levels are severely lowered, he
be ordered, along with properly, may cause a or she may prescribe
calcium and decrease in magnesium medications to increase the
phosphorus testing, to levels. levels to a safe range.
monitor calcium •Take all of your
supplementation. Magnesiu medications as directed.
m testingmay be ordered as •Drink 2 to 3 liters of
a follow up to chronically low fluid every 24 hours,
blood levels of calcium and unless you were told to
potassium. restrict your fluid intake.
•Follow all of your
healthcare provider's
recommendations for
follow up blood work and
laboratory tests if blood
test results indicate
hypomagnesemia.

59
CALCIUM A blood calcium test is 2.2-2.6 2.25 If your calcium test > Instruct patient to stop taking
DECEMBER ordered to screen for, ^mmol/L ^mmol/L results are not in the certain medications or
18,2018 diagnose, and monitor a NORMAL normal range, it doesn't supplements before the test.
range of conditions relating necessarily mean that These medications can include:
to the bones, heart, nerves, you have a medical • lithium
kidneys, and teeth. condition needing • thiazide diuretics
Thetest may also be ordered treatment. Other • antacids containing
if a person has symptoms of factors, such as diet calcium
a parathyroid disorder, and certain medicines, • vitamin D supplements
malabsorption, or an can affect your calcium • calcium supplements
overactive thyroid. levels. prior to the test.
Your doctor may also order
a calcium blood test if they
suspect that you have
kidney disease, parathyroid
disease, cancer,
or malnutrition.

60
TYPE OF INDICATION NORMAL ACTUAL IMPLICATIONS NURSING
TEST VALUES RESULT RESPONSIBILITIES
POTASSIUM Potassium test 3.6-5.1 4.25 These messages are delivered in the form Monitor intake and
may be used to mmol/L mmol/L of nerve impulses and help regulate your output
help diagnose muscle contractions, heartbeat, reflexes And watch out for
and monitor and many other body functions (12). dehydration.
kidney Interestingly, nerve impulses are
disease,the most generated by sodium ions moving into
common cause of cells and potassium ions moving out of
high potassium. It cells.
is also important A potassium test is performed for basic
in muscle function metabolic panel,which is the group of
helping transmit chemical test run on the blood serum,the
messages doctor may order potassium test for:
between nerves * checking for or monitoring an electrolyte
and muscles and imbalance
is important to * monitoring certain medication that
heart function. affects potassium levels particularly
diuretics,heart medication,high blood
pressure medications
* diagnosing heart problems
*diagnosing or monitoring kidney disease
* checking for metabolic acidosis

61
TYPE OF INDICATION NORMA ACTUAL IMPLICATIONS NURSING
TEST L RESULT RESPONSIBILITIES
VALUE
S
SODIUM Sodium test is 1.36- 1.35 mmol/L Hyponatremia refers to a low level of Due to the possibility of
used to detect 1.44 LOW sodium in the blood. Hyponatremia or low mental changes,initiates
abnormal mmol/L sodium blood levels may result from and maintain appropriate
concentration excess fluid in the body relative to a safety measures,monitor
s of normal amount of sodium, or it may be due serum sodium
sodium,includ to a loss of sodium and body fluid caused levels,hematocrit and
ing low by chronic conditions like kidney or hemoglobin. And monitor
sodium( congestive heart failure. intake and output.
hyponatremia (Hinkle & Cheever, 2014)
) and high Hyponatremia is the most common
sodium electrolyte disorder encountered in
hypernatremi clinical practice and clinical
a. consequences of hyponatremia include
neurologic dysfunction, decreased mental
function.cerebral edema and fractures.
Hyponatremia occurs when the
concentration of sodium on the blood is
abnormally low. Sodium is an electrolyte
that helps regulate the amount of water
that’s in around the cells

62
Laboratory Test/ Values/ Normal Date: Interpretation
Studies Result Value: 12/18/18
Complete Blood Count Hemoglobin- 140-170 104.0 A low hemoglobin count can also be due to blood loss, which
(CBC) LOW can occur because of:
Bleeding from a wound
(Mayoclinic, 2017)
Hematocrit 0.40-0.50 0.41 Hematocrit measures the percentage of the red blood cells in
the body. Low hematocrit indicate overhydrated or anemic.
(Hinkle & Cheever, 2014)

Erythrocytes 4.5-5.0 5.19 High RBC occurs or maybe a symptoms of a disease or

HIGH disorder although it doesnt always indicates a health problem.
(Hinkle & Cheever, 2014)
Leukocytes 5.0-10.0 8.90 An increase in WBC indicates that the body is fighting against
NORMAL an infection.
(Hinkle & Cheever, 2014)

Thrombocyte 140-440 244.00 Low platelet is due to the destruction caused by bacterial
s NORMAL infection they paly essential role in the control of bleeding.
(Hinkle & Cheever, 2014)

63
*Neutrophil 0.55-0.65 0.81 High count of neutrophil indicates infection a second line of
HIGH defense for the body against inflammation and infection
(Hinkle & Cheever, 2014)

*Lymphocyte 0.35-0.45 0.20 High lymphocyte count, is an increase in white blood cells
s LOW called lymphocytes. Lymphocytes are an important part of the
immune system. They help fight off diseases, so it's normal to
see a temporary rise in the number of lymphocytes after
an infection.
(Mayoclinic, 2017)

*Monocytes 0.06-0.12 0.07 A low number of monocytes in the blood (monocytopenia)

NORMAL can be caused by anything that decreases the overall white
blood cell count (such as a bloodstream infection.
www.msdmanuals.com/home/blood-disorders/white-blood-
cell.../monocyte-disorders

*Eosinophil 0.2-0.4 0.06 Eosinophils are important in the phagocytosis of parasites and
HIGH during allergic reactions, eosinopenia is part of the normal
response to stress. Eosinopenia is due to acute infection that
is a secondary response to stress caused by the infection.
https://ccforum.biomedcentral.com/articles/10.1186/cc6883

64
*Basophils 0-0.02 0.00
NORMAL

Any infection or acute stress increases your number of white

Absolute 1.8-7.8 5.1 blood cells. ... It is important to realize that an abnormal
Neutrophil NORMAL increase in one type of white blood cell cancause a decrease
*actual in the percentage of other types of white blood cells. An
number increased percentage of neutrophils may be due to: Acute
infection.
(Hinkle & Cheever, 2014)
Absolute 1.0-4.8 1.5
*Lymphocyte NORMAL
s

Absolute 0.0-0.60 0.62

*Monocytes NORMAL

The MCV will be lower than normal when red blood cells are
MCV 80-97 79 too small. This condition is called microcytic anemia.
LOW Microcytic anemia may be caused by: iron deficiency, which
can be caused by poor dietary intake of iron, menstrual
bleeding, or gastrointestinal bleeding.

65
MCH 27.0-31.2 26.2 Different types of anemia can cause low MCH levels. For
LOW example, microcytic anemia occurs when the blood cells are
too small and cannot take in as much hemoglobin as they
should. ... Low amounts of iron in the blood can also
cause low MCH levels. The body uses iron to make
hemoglobin.

MCHC 318-354 343.9 A high MCHC value is often present in conditions where
NORMAL hemoglobin is more concentrated within your red blood cells.
It can also occur in conditions where red blood cells are fragile
or destroyed, leading to hemoglobin being present outside of
the red blood cells.
(Hinkle & Cheever, 2014)

RDW 11.5-14.5 13.40 Elevated RDW helps provide a clue for a diagnosis of early
NORMAL nutritional deficiency such as iron, folate, or vitamin B12
deficency as it becomes elevated earlier than other red blood
cell parameters.
https://emedicine.medscape.com/article/2098635-
overview#a2

66
MPV 2-20 8.20 MPV stands for mean platelet volume. Platelets are small
NORMAL blood cells that are essential for blood clotting, the process
that helps you stop bleeding after an injury.
An MPV blood test measures the average size of
your platelets. The test can help diagnose bleeding
disorders and diseases of the bone marrow.

67
LABORATORY TEST 12/18/18 UNIT REFERENCE VALUE
(ARTERIAL BLOOD GAS TEST)

RR 18 ^b/min -
FiO2 28 ^% -
pH 7.341 7.350-7.450

40.5 35.0-45.0
pCO2 216 ^mmHg
pO2 -4 -
Base Excess ^mmol/L

Bicarbonates 21.9 -
O2 Sat ^mmol/L
100 80.0-100
^%

Metabolic Acidosis happens when the chemical balance of acids and bases in the blood gets thrown off,the body is making too
much acid,isn’t getting rid of enough acid and doesn’t have enough base to offset a normal amount of acid. Also occur when the
kidneys are not removing enough acid from the body.
The acidity of the blood is measured by determining pH,a lower pH means that the blood is more acidic,acidosis is characterized
by a pH of 7.35.

68
URINALYSIS December 19, 2018

Physical examination:

Color Straw

Character clear

Reaction 6.5

Specific gravity 1.008

CHEMICAL EXAMINATION

Albumin Negative

Sugar +++

URINE FLOW CYTOMETRY

TEST NAME RESULT UNITS REFERENCE RANGE

WBC 3 /uL 0-17

RBC 3 /uL 0-11

BACTERIA 1 /uL 0-278

JUSTIFICATION:

Urinalysis can reveal diseases that have gone unnoticed because they do not produce striking signs or symptoms. Examples
include diabetes mellitus, various forms of glomerulonephritis, and chronic urinary tract infections.

69
 3. Pharmacology

BRAND MECHANISM OF INDICATION CONTRAINDICATION SIDE EFFECTS DOSAGE NURSING MANAGEMENT

NAME ACTION
Lasix Inhibits reabsorption of • Edema due • Anuria • low blood 40mg 1. Assess patient underlying
sodium and water in to heart pressure IVTT Q8 condition before starting
• Hepatic coma and
the ascending limb of failure, therapy.
precoma • dehydration and
the loop of Henle by hepatic
electrolyte 2.Monitor for renal, cardiac,
interfering with the impairment, • Severe hypokalemia
depletion neurologic, GI manifestations
chloride binding site of or renal • Svere hyponatremia of hypokalemia.
the 1Na+, 1K+, 2C1 disease. • Jaundice
• Hypovolemia with or 3. Assess fluid status. Monitor
contransport system. • Ringing in the
• without hypotension
Generic daily weight, intake and output
Loop diuretics. ears (tinnitus)
Hypertension.
Name: • Hypersensitivity to ratios, amount and location of
Increase the rate of
• Photophobia edema, lung sounds, skin
Furosemide delivery of tubular fluid sulfonamides.
and electrolytes to the • Rash turgor, and mucous

distal sites of hydrogen membranes. Notify health

• Pancreatitis
Classification: and potassium ion care professional if thirst, dry
Diuretics • Nausea mouth, lethargy, weakness,
secretion, while plasma
hypotension, or oliguria
volume contraction • Diarrhea
increase aldosterone occurs.
• Abdominal pain
production. The 4. Assess patient for tinnitus
and dizzines
increased delivery and and hearing loss. Audiometry
high aldosterone levels is recommended for patients

70
promote sodium receiving prolonged high-dose
reabsorption at the IV therapy. Hearing loss is
distal tubules, thus most common after rapid or
increasing the loss of high-dose IV administration in
potassium and patients with decreased renal
hydrogen ions. function or those taking other
ototoxic drugs.

5. Instruct pt to avoid getting

up too fast from a sitting or
lying position, or he/she may
feel dizzy. Get up slowly and
steady yourself to prevent a
fall.

71
 BRAND MECHANISM INDICATION CONTRAINDICATION SIDE DOSAGE NURSING MANAGEMENT
NAME OF ACTION EFFECTS
Diamicron increases the This medication is an Contraindicated in GI 60mg 1 1.Observe for signs and
amount of insulin oral hypoglycemic patients with diabetic- disturbances, Tab daily symptoms of hypoglycemia
(hunger, weakness, sweating,
released by the (anti-diabetic drug), ketoacidosis, severe skin reaction, dizziness, tachycardia and
pancreas and prescribed for type 2 liver and kidney decrease in anxiety)

helps the body diabetes. It impairment, and blood cell 2. Monitor serum glucose and
use insulin more stimulates the hypersensitivity. counts, glycosylated hemoglobin
efficiently. pancreas, which jaundice,
helps in more insulin vomiting,
Generic
secretion. diarrhea and
Name:
stomach
Glicalize inflammation.

Classification:
AntiDiabetics

72
 BRAND MECHANISM INDICATION CONTRAINDICATION SIDE EFFECTS DOSAGE NURSING MANAGEMENT
NAME OF ACTION
Lipitor This drug works Reduction of risk Hypersensitivity, active • Cold 80mg 1 1.Stress that atorvastatin is an
adjunct to not a substitute for low-
by lowering your of stroke and liver disease or symptoms such tab PO
cholesterol diet
low-density heart attack in unexplained persistent as runny nose, Daily Hs
2. Tell patient to take drug at the
lipoprotein (LDL) type 2 diabetes elevations of serum sneezing, and same time each day to maintain its
Generic or “bad” patients without transaminase, coughing. effects

name: cholesterol and evidence of porphyria, pregnancy, 3. Instruct patient to take a missed
• Diarrhea
dose as soon as possible. If it’s
Atorvastatin raising your high- heart disease lactation.
almost time for his next dose, he
density but with other • Hearrtburn
should skip the missed dose.
lipoprotein (HDL) CV risk factors, •Joiint pain 4. Advise pt. to notifify prescriber
or “good” and immediately if he develops
•Forgetfulness
cholesterol. revascularization unexplained muscle pain,
Classification:
Atorvastatin procedures in •Confusio
tenderness, or weakness,
Antilipidaemic
improves your patients without especially if accompanied by
body’s ability to evidence of fatigue or fever.
get rid of LDL coronary heart
cholesterol disease (CHD)
through your but with multiple
liver. risk factors other
than diabetes
(eg, smoking,
HTN, low HDL-
C, family history

73
of early CHD)
Patients with
CHD, to reduce
risks of MI,
revascularization
procedures,
hospitalization
for CHF, and
angina

74
 BRAND MECHANISM OF INDICATION CONTRAINDICATIO SIDE EFFECTS DOSAGE NURSING
NAME ACTION N MANAGEMENT
Citicoline is derivative Treatment of stupor Patients with •Shock 1g Q6 hrs 1. Monitor
Citicoline of choline and cytidine caused by head parasympathetic IVTT bloodpressure, pulse
•Hypersensitivity
involved in the trauma, cerebral hypertonia and heart rate.
•Hypotension
biosynthesis of surgery, acute stage of
2. Assess
lecithin. It is claimed to cerebral infarction and •Insomnia
Generic allergicreaction like GI
increase blood flow hemiplegia after •Excitement
Name: disturbances.
and oxygen cerebral apoplexy.
Citilin consumption in the Treatment of 3. Instruct relative to

brain Parkinson's disease in give only prescribed

combination with dose.

Classification:
anticholinergics. 4. Advise relative to
Neurotrophic
Concomitant therapy consult the physician if

with antiproteolytic any problems occur to

agents for pancreatitis. the patient during

medication.

75
BRAND NAME MECHANIS INDICATION CONTRAI SIDE EFFECTS DOSAGE NURSING MANAGEMENT
M OF NDICATIO
ACTION N
Tozam works by • High blood pressure Hypersensi Heart - First-dose 5/50mg 1 1. Monitor BP for therapeutic
effectiveness.
inhibiting the tivity. Avoid hypotension. tab PO
•Hypertension
influx of concomitan Daily 2. Monitor for S&S of dose-related
Central nervous peripheral or facial edema that
calcium ions • Kidney disease in type t potassium may not be accompanied by
System - Headache,
into vascular 2 diabetes mellitus supplement weight gain; rarely, severe edema
dizziness, weakness, may cause discontinuation of
smooth patients s
fatigue. drug.
muscle and • Coronary artery
3. Monitor BP with postural
cardiac Musculoskeletal -
disease changes. Report postural
Generic Name: Back pain, muscle hypotension. Monitor more
muscles;
• Chronic stable angina pain. frequently when additional
Amlodipine + blocking the
antihypertensives or diuretics are
Losartan action of • Vasospastic angina Gastrointestinal - GI added.
natural disturbances, 4. Monitor heart rate; dose-related
• Kidney disease in high
substances palpitations (more common in
blood pressure patients transient elevation of
women) may occur.
Classification: that tighten liver enzymes; taste
Antihypertensive the blood • Chronic heart failure
disturbances.
vessels • Stroke in heart disorder
Miscellaneous -
patients
Respiratory tract
• Stroke in high blood disorders, cough,
pressure patients rash, allergic
reactions.

76
ii. Nursing Management

Assessment Diagnosis Scientific Goals and Nursing Rationale Evaluation

Basis Objectives Intervention
S>”Maam, Impaired Deprivation of Within 8 hours • Establishing • To offer Goal met as
tabange ko physical oxygen supply span of nursing rapport. one’s self. evidenced by
paadto’g CR mobility related of the brain care, the To gain patient’s
ky malipong to tissue may patient will be cooperation. verbalization and
ko.”as neuromuscular result to nerve able to understanding of the
verbalized by involvement as damage which verbalized situation and utilized
the patient. manifested by may affect the understanding • Evaluated • To assess safety measures
slowed individual’ of situation and degree of causative or such as side rails
O> Postural movement, sensorimotor appropriate impairement contributing and call button.
instability difficulty in ability that may safety using 0- 4 factors.
during turning and result to measures. functional
performance of when trying to limitation of the level
routine ADL’s move on side independent, classification.
to side. purposeful
>Requires movement of • Instructed to • Prevent
help from the body, use side further
another person confused, tired, rails. injury.
for assistance. clumsy, off
balance when
performing
routine ADL’s, • Encourage to • Feelings of
or any verbalize frustration
combination of feelings may impede
these. The about his attainment
patient may situation. of goals.
perceive a
sensation of
movement, • Assisted • To help
spinning or when perform
whirling of transferring
77
themselves or from bed to activities of
the room. Thus toilet. daily living.
this perception
can alter a • Encouraged • To prevent
patient’s adequate and replace
mobility. intake of electrolyte
fluids/ imbalance.
nutritious
foods.

• Assisted with • Promotes

treatment of well being.
underlying
condition
causing
dysfunction
as ordered.

78
 Assessment Diagnosis Scientific Goals and Nursing Rationale Evaluation
Basis Objectives Intervention
S>” Maglisod Ineffective A dyspneic After 30 ➢ Monitor vital ➢ These signs After 30
kog ginhawa breathing person often minutes of signs. which should minutes of
maam.”as pattern related appears nursing looked at in nursing
verbalized by to respiratory anxious and intervention, total, are intervention,
the patient. muscle fatigue may the client will checked to goal are
as manifested experience be able to monitor partially met,
O> O2 at by irregular shortness of reestablished functions of with RR of
3L/min breathing. breath, a and maintain the body. 22cpm and
>nasal flaring feeling of being effective The signs of with no signs of
>rapid unable to get respiratory reflect nasal flaring,
shallow enough air. pattern via changes in rapid shallow
breathing Dyspnea have oxygen function that breathing; still
>tachypnea, many causes, administration otherwise with O2
RR of 28cpm most of which thru nasal might not support.
>labored stem from cannula observe.
breathing cardiac and without the use ➢ Assess ➢ Respiratory
>use of respiratory of accessory respiratory rate and
accessory disorders. It is muscle and rate , rhythm
muscles. a subject as it other signs of rhythm and changes are
cannot be hypoxia. depth early
directly warning
observed but is signs of
reported by the impending
client. respiratory
difficulties.
(Kozier, Vol. 2,
7th ed.,) ➢ Encouraged ➢ Promotes
to deep chest
breathing expansion
exercises.

➢ Position ➢ Positioning
patient to helps
semi- maximize

79
 fowler’s lung
position. expansion.

➢ Administer ➢ For
O2 via management
nasal of underlying
cannula as pulmonary
ordered. condition
and
respiratory
distress.

80
 Assessment Diagnosis Scientific Goals and Nursing Rationale Evaluation
Basis Objectives Intervention
O: > speaks with Impaired A CVD, which After 2 days ➢ Monitored ➢ Establishes Goal partially
difficulty verbal may caused of nursing vital signs baseline data met after 2
➢ Slurring communicatio by, intervention, with for review of days of
➢ Difficulty in n related to hemorrhage, the patient will emphasis to existing nursing
forming words alteration of thrombus, establish BP. condition. intervention
or sentence motor speech embolism or method of the patient
➢ Difficulty in area of the vasospasm, communicatio ➢ Provide an ➢ Impaired needs further
comprehendin brain. can result in n in which atmosphere ability to intervention for
g or local area of needs can be of acceptance communicate communicatio
maintaining cell death, expressed. and privacy spontaneousl n.
usual called infarct. through y is
communicatio It is caused by speaking frustrating
n pattern. a lack of slowly and in and
blood supply a normal embarrassin
which is then tone, not g. Nursing
surrounded by forcing the actions
an area of client to should focus
cells that are communicate. on
secondarily decreasing
affected. the tension
Since and
symptoms conveying an
depend on the understandin
location of the g of how
stroke and difficult the
size of the situation
infarct, it must be for
could involve the client.
the brain’s
broccas’s ➢ Taught ➢ Deliberate
area, which is techniques to action can be
primary improve taken to
responsible speech by improve
for initially asking speech. As
communicatio questions that the client’s
81
n through client can speech
facial answer with a improves, his
expressions “yes” or “no”. confidence
and speech. will increase
By causing and he
damage to makes more
this area, the attempts at
patient’s speaking.
communicatin
g skills are ➢ Involved the ➢ Enhances
greatly altered significant participation
and affected. others in the and
plan of care. commitment
to plan.
(Medical
Surgical ➢ Educated ➢ Imparts
Nursing, vol.2, relatives to thought and
9th edition, establish a answers the
Brunner and method of needs of the
Suddarths.) communicatio client with
n through lessened
sign difficulty.
language.

82
ASSESSMENT DIAGNOSIS SCIENTIFIC PLANNING INTERVENTION RATIONALE EVALUATION
BASIS
Subjective: Risk for CVA patient Short Tearm: Goal Met:
“Mulihok rmn is at risk for 1.) Established >To promote
injury related After 4 hrs of After 4 hours of
na siya iyaha injury, since rapport. cooperation
maam ba,bsag to it may affect proper nursing proper nursing
kbalo mi the anterior 2.) Monitor vital >To have a baseline
hemiplegia Intervention, the intervention, the
malisodan or middle signs data
siya.” As secondary to cerebral patient will be patient was able to
verbalized by artery 3.) Keep the >To protect patient
CVA infarct. able to: verbalized
the watcher. leading to an side rails of from falling out of bed.
infarction in a.) Verbalize the raised. understanding of
Objective: the motor
Reference: understanding of individual factors
strip of the 4.) Encourage
>Right sided Nurses frontal cortex individual factors client to >It is use to lessen that contribute to
paralysis and this may walk slowly, further injury that
Pocket that contributes any possibility of
(Hemiparesis) cause rest patient may encounter.
Guide 14th hemiparalesi to possibility of adequately injury and
>Body s or between
edition injury. demonstrated
weakness hemiplegia intervals of
pp.479-485 with the walking use behaviors, lifestyle
>Decreased in manifestatio b.)Demonstrate effective >It is somehow
changes to reduce
Range of ns it may lighting. alleviate the patient’s
behaviors ,
Motion predisposed suffering and helps self from injury.
an individual lifestyle changes 5.) Facilitate him on her
for any injury patients rehabilitation.
to reduce risk
since part of rehabilitatio
their body is factors and n
not
protect self from
functioning
well. injury.

83
 Assessment Diagnosis Scientific Basis Goals and Nursing Rationale Evaluation
Objectives Intervention
Ineffective History of lack of Short Term: Independent: Short Term:
Subjective: self-health health seeking After 8 hours >Establish rapport. >to gain patient’s
management behavior; reported of effective trust and have a After 8 hours
“Kung maayo nako
related to or observed lack of nursing good nurse patient of effective
unsaon nalng man knowledge equipment, financial, interventions, relationship nursing
deficit and/or other patient will interventions,
nako pag alaga
concerning resources; reported be able to: a. >.Evaluate >determine patient shows
sakong sarili.” as the or observed understands desire/readiness s amount or level of participation,
diagnosis, impairment of disease of patient to learn. information to understanding
verbalized by the
and self-care personal support state, provide at any of his disease
patient after systems; expressed recognizes given moment. and
discharge interest in improving need for motivation to
health behaviors; medications, > Provide an >important when learn.
Objective: demonstrated lack and atmosphere of providing
of knowledge understands respect, openness, education to GOAL
>Demonstrated
regarding basic treatments. trust, and patients with PARTIALLY
lack of knowledge health practices; b. shows collaboration. different values MET.
demonstrated lack motivation to and beliefs about
>Expressed
of adaptive learn. c. lists health and illness.
interest in behaviors to internal resources > Assess
and external that can be motivation and >some patient are
improving
environmental used for willingness of ready to learn as
behaviors > Right changes; reported or more patient and soon after they are
observed inability to information caregivers to learn diagnosed; others
sided Hemiparesis
take responsibility or support cope better by
for meeting basic after denying or
health practices in discharge. delaying the need
any or all functional for instruction
pattern areas
> Obtain or design > Verbal
educational reinforcement of
material that is personalized
Reference: Brunner appropriate for the written instructions
& Suddarth’s client; use pictures appears to be the
Medical - Surgical if possible. best intervention.
84
Nursing 13th
Edition. >The client brings
to the learning
>Ensure that follow situation a unique
-up appointments personality,
are scheduled established social
before the client is interaction
discharged; discuss patterns, cultural
a way to ensure norms and values,
that appointments and environmental
are kept. influences.

85
 I. Discharge Plan

M- Medication
• Review of Medications. To ensure that the patient has taken the right dosage, right route
and right timing of each prescribed medication as well as the expected side effects.
• Explain to the patient or significant others the reasons or purpose of why he is taking the
prescribed medicine.
• Instruct the patient or the significant others not to alter doses of medication and
immediately notify a healthcare provider for any signs of unusualities regarding to the
medication prescribed such as allergic reactions.

E- Exercise
• Encourage to have a physical therapy for improving strength and ambulation.
• Advice patient to take adequate rest and sleep.

T-Teaching
• Explain to the patient or significant others the importance of following the advice and
orders of doctors, nurses and other health care professionals.
• Explain the importance of taking the medication according to its given prescription.
• Encourage family member to provide patient emotional support.
• Instruct the family member to provide a safe environment.

H-Hygiene
• Encourage taking a bath daily to promote good personal hygiene.
• Encourage the patient to do oral hygiene.

• Instruct the patient or significant others to do hand washing to prevent possible infections
and to minimize contamination that causes further complication to the health of patient.

86
 • Encourage the patient or significant others to the importance of cleanliness, proper
hygiene, and sanitation.

O-Outpatient
• Advice patient and the significant others to prompt report for any unusualties.
• Advice the patient to have regular follow up check up to monitor patient condition.
• Instruct the patient to continue what the doctors and other health care professional’s
advice.
• Encourage patient to have adequate rest and sleep to promote healing.

D-Diet
• Educate patient about the importance of taking proper diet.
• Instruct patient to take variety of nutritious food such as fruits and vegetable.
• Encourage the patient to follow the instructions of healthcare providers about his specific
diet recommendations based on his condition and response to the treatment. And may
apply what the dietician or nutritionist orders about the meal planning guidance based on
his specific needs.

S-Spiritual
• Encourage the patient to draw self-closure to God to impart the importance of spirituality.
• Encourage the patient to keep more praying to our Almighty God to gain more strength.

• Encourage the patient having a bond together with the family members like simply eating
or praying together to improve or enhance self-concept as well as a sense of hope that
will help in improving the wellness of the patient.

87
 J. Bibliography

Book
• Hinkle, J. L., PhD RN CNRN, & Cheever, K. H., PhD RN. (n.d.). Brunner & Suddarth's
Textbook of Medical-Surgical Nursing (Textbook of Medical-Surgical Nursing (Brunner &
Sudarth's)(13th ed., Vol. 1&2, Ser. 2014).
• Hinkle, J. L., PhD RN CNRN, & Cheever, K. H., PhD RN. (n.d.). Brunner & Suddarth's
Textbook of Medical-Surgical Nursing (Textbook of Medical-Surgical Nursing (Brunner &
Sudarth's)(12th ed., Vol. 1&2, Ser. 2013).
• Hinkle, J. L., PhD RN CNRN, & Cheever, K. H., PhD RN. (n.d.). Brunner & Suddarth's
Handbook of Laboratory and Diagnostic Tests(2nd ed., Vol. 1).
• Doenges, M. E., APRN, Moorhouse, M., RN, MSN, CRRN, LNC, & Murr, A. C., BSN, RN.
(n.d.). Nurse's Pocket Guide Diagnosis, Prioritized, Intervention and Rationale(14th ed.).
• Williams, L., & Wilkins. (n.d.). Nursing Drug Handbook(Ser. 2013).
• Kozier, B. (n.d.). Fundamentals Of Nursing(7th ed.).
• Jarvis, C., PhD APN CNP. (n.d.). Physical Examination and Health Assessment / Edition
7 by ... Retrieved January 27, 2019, from https://barnesandnoble.com/w/physical-
examination-and-health-assessment-carolyn-jarvis/1123480209

Journal
•

Site
• Ischemic Stroke. (2019, January). Retrieved January 27, 2019, from
https://www.cedars-sinai.edu/Patients/Health-Conditions/Ischemic-Stroke.aspx
• Vega, J., MD, PhD. (2018, December 17). The Corona Radiata and Stroke. Retrieved
January 27, 2019, from https://www.verywellhealth.com/what-is-the-corona-radiata-
3146130
• Soler, E., & Ruiz, V. (2010, August). Epidemiology and Risk Factors of Cerebral Ischemia
and Ischemic Heart Diseases: Similarities and Differences. Retrieved January 27, 2019,
from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994106/

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