Our Lady of Fatima University

College of Nursing
Valenzuela Campus

ACUTE GLUMERULONEPHRITIS
In Partial Fulfillment of requirements of NCM 106 RLE leading to the degree of Science in Nursing

EMERGENCY ROOM

TABLE OF CONTENTS

I. Introduction
II. Objectives
III. Patients Profile
IV. Anatomy and Physiology
V. Pathophysiology
VI. Laboratory Examination Results
VII. Drug Study
VIII. Nursing Care Plans
IX. Health Teachings

I.

INTRODUCTION

Theres a saying that goes like this An ounce of prevention is worth a pound of cure means
that the most effective interventions in promoting health is the early prevention of the disease
and to have a balanced well-being.
Acute glomerulonephritis (AGN) is an active inflammation of the kidneys filtering
mechanisms, called the glomeruli. Each kidney is composed of about 1 million microscopic
filtering "screens" known as glomeruli that selectively remove uremic waste products. The
inflammatory process usually begins with an infection or injury (e.g., burn, trauma), then the
protective immune system fights off the infection, scar tissue forms, and the process is
complete. (Accessed at: http://www.nephrology/channel.com/agn/index.shtml on August 20,
2010)
There are many diseases that cause an active inflammation within the glomeruli. Some
of these diseases are systemic (i.e., other parts of the body are involved at the same time) and
some occur solely in the glomeruli. When there is active inflammation within the kidney, scar
tissue may replace normal, functional kidney tissue and cause irreversible renal impairment.
(Accessed at: http://www.nephrology/channel.com/agn/index.shtml on August 20, 2010)
The severity and extent of glomerular damagefocal (confined) or diffuse (widespread)
determines how the disease is manifested. Glomerular damage can appear as subacute renal
failure, progressive chronic renal failure (CRF); or simply a urinary abnormality such
as hematuria (blood in the urine) or proteinuria (excess protein in the urine). (Pais, Kump, &
Greenbaum, 2008)
Acute glomerulonephritis is more common in children between the ages of 2 and 12,
particularly boys. Children with frequent streptococcal infections are at a higher risk of
developing acute glomerulonephritis. Acute glomerulonephritis often occurs after a streptococcal
infection, such as strep throat. When this is the cause, the condition is called acute
poststreptococcal glomerulonephritis (APSGN), or postinfectious glomerulonephritis. It can also
occur when certain toxins, such as paints or glues, are inhaled and then excreted through the
urine. (Lippincott-Raven, 2001:899929.Kaplan B, Meyers K, Bell L. Eds. Pediatric Nephrology
and Urology: The Requisites in Pediatrics. Philadelphia: Mosby Inc; 2004.)
Many people with acute glomerulonephritis have no symptoms. When symptoms occur,
they are often flu-like, such as general fatigue, nausea, vomiting, loss of appetite, fever, and
abdominal and joint pain. These types of general symptoms can continue for up to one month
2

before symptoms of kidney failure appear. Patients whose kidneys are failing will produce only
small amounts of urine and have swelling (edema) from fluid build-up. Symptoms of acute
glomerulonephritis usually occur around two to three weeks after a streptococcal infection and
begin with swelling. They can progress to high blood pressure, visual disturbances, shortness of
breath,

blood

in

the

urine,

and

reduction

in

urine

production.

(Accessed

at:

http://emedicine.medscape.com/article/777272-diagnosis on August 21, 2010)

AGN comprises 25-30% of all cases of end-stage renal disease (ESRD). About one
fourth of affected patients present with acute nephritis syndrome. Most cases that progress do
so relatively quickly, and end-stage renal failure may occur within weeks or months of acute
nephritic syndrome onset. (Papanagnou, 2008; & Fuiano, et. al, 2001)
The goal of treatment is to stop the ongoing inflammation and lessen the degree of
scarring that ensues. Depending on the diagnosis, there are different treatment strategies. Often
the treatment warrants a regimen of immunosuppressive drugs to limit the immune systems
activity. This decreases the degree of inflammation and subsequent irreversible scarring.
The reason for choosing this case study is to aid in opening up bright innovations about
the disease condition and to contribute in the goal of eliminating these terrifying diseases, and in
line with that, the student nurse is eager to exhaust their hard work to study the disease
condition as their means of helping their clients through formulating nursing care plans based on
the prioritized health needs of the client and discussing management and treatment and to
provide better nursing care and health teachings through the utilization of the nursing process.
This case study will enlighten the student nurse about the currently occurring trend of illnesses
and will increase competency as the student nurse finishes research.
Through this case study, the student nurse was given an opportunity to know more about
this condition so that the student nurse could apply the knowledge they learn in the nursing
practice. To widen the understanding of the student nurse about the disease process and
familiarize themselves about the pathophysiology of the disease, the signs and symptoms, the
treatment and other aspects regarding acute glomerulonephritis.

II. OBJECTIVES
Nurse-centered
3

After the completion of this case study, the student nurse should have:
Discusses management and treatment and provide better nursing care and health teachings
through the utilization of the nursing process.
Analyze and interpret the different diagnostic and laboratory procedures, its purpose and its
essential relationship to clients disease condition, identified treatment modalities and its
importance like drugs, diet and exercise.
Interpreted the current trends and statistics regarding the disease condition and relate the
state of the client with her personal and pertinent family history.
Formulate nursing care plans based on the prioritized health needs of the client and
maintained sound communication by making use of self as a therapeutic agent.

Specific objectives:
After the completion of this case study, the student nurse shall have:
Define what AGN is and identified the causative agent and its manifestations.
Determine the different factors that have contributed to the occurrence of AGN, both modifiable
and non-modifiable.
Identified the diagnostic tests, laboratory results, and pathophysiology, medical and nursing
management applicable to manage AGN.
Identified and enumerate measures in the prevention of AGN.

Patient-centered
General objectives:
During the course of the study, the patient and the family shall have:
Acquired knowledge on the risk factors that have contributed to the development of AGN
Gained understanding and demonstrated compliance on the treatment management
rendered by the health care team to prevent reoccurrence of the disease.

Specific objectives:

During the course of the study, the patient and the family shall have:
Built a trusting relationship with the researchers as well as the other members of the health
care team.
Gained knowledge on the definition of AGN, its causative agents, risk factors, possible
complications and prevention.
Received the best possible medical and nursing care, leading to a feeling of security,
comfort, and good prognosis of the disease condition.

III. PATIENTS PROFILE

Name: Bah Tuh
Age: 7 years old
Birthday: July 28, 2007
Adress: Metro Manila
Nationality: Filipino
Religion: Roman Catholic
Civil Status: Single
Date Admission: March 1, 2015
Time of Admission: 3:00 PM
Chief Complaint's: Facial edema and Left lower quadrant pain
Initial Diagnosis: Acute glomerulonephritis
Final Diagnosis: Acute glomerulonephritis
History of Past Illness

Bah Tuh usually had conditions such as coughs and colds as well as fever, which they
treated, as stated by his father, by giving him BIOGESIC or other over the counter drugs. Father
stated that he already experienced serious infections such as chickenpox and measles. The last
time he was admitted to the hospital is when he was 5 years old due to UTI. Bah Tuh has no
family history of kidney-related diseases. Bah Tuh was not taking any medication. He has no
known food and drug allergies. Bah Tuh is fond of eating salty foods such as chips and
preservative foods. He rarely eats vegetables and drinks water, most of time he drinks soda.

History of Present Illness

Two days prior to admission, Bah Tuh manifested intermittent fever ranging from 38-39
degrees Celsius. He also manifested epigastric pain and oliguria. With no medications and
consultation given.
One days prior to admission, Bah Tuh manifested facial edema, left quadrant abdominal
pain and oliguria. Then few hours prior to admission, facial edema and left quadrant pain has
worsened.

Familys Genogram (up to 3rd degree relationship, including dates)

FATHER SIDE

Lola 1, 72
y/o

Lolo 1, 75y/o

54
y/o

52
y/o

50
y/o

MOTHER SIDE

49
y/o

35y
/o

Lolo 2, 60
y/o

46
y/
o

42
y/o

39
y/o

49
y/.o

47
y/o

45
y/o

Lola 2 ,60

30
y/o

40
y/o

L nee

30
y/o

36
y/o

Bah Tuh 7
y/o

CHILDREN
FATHER SIDE

MOTHER SIDE
Daughter

Grandfather
Grandmother

DISEASES

Grandfather

Son

Hypertension

Myocardial
infarction

Grandmother
Brother

Brother

Sister

Sister

deceased

Diabetes
mellitus

patient

The patient comes from a nuclear family. His grandfather from the fathers side had a
history of Diabetes Mellitus while his grandmother has Hypertension. Uncle A suffers from
hypertension, while his father and his other siblings have no known disease. On his mothers
side, the grandfather is already dead; he suffered from hypertension and its complications. His
grandmother had a history of myocardial infarction. Auntie I is hypertensive and Uncle M has
Diabetes Mellitus. The remaining siblings including his mother are not suffering from any
diseases. The patients siblings do not have any conditions that are detrimental to their health.
The mother also stated that there are no known relatives that have suffered from any kidney or
renal diseases connected what Bah Tuh is suffering.
PERSONAL HISTORY
He is currently going to school. Bah Tuh spends most of his time playing outside with his
friends; he doesnt like wearing slippers and likes to go outside the house just after going to
school. He and his friends play patintero, hide and seek or they just dig the ground for fun. Bah
Tuh spends time with his grandmother most of time while his father works as a vegetable
vendor everyday. After playing outside, he eats junk foods and carbonated drink. He usually
consumes 3 bottles of 355ml-carbonated drinks daily. He prefers salty foods with high
cholesterol because its delicious and tastier than vegetables or fruits. His grandmother believes
in hilot and takes him when he has minor illnesses. Bah Tuh is fully immunized by the time he
reached school age.
1. PHYSICAL EXAMINATION (IPPA Cephalocaudal Approach)
March 2 (Monday) First Nurse-Patient Interaction
a. General Appearance
Patient is 7-year-old male, conscious and coherent with coordinated movements.
Upon observation he was wearing a gray pajama and a white shirt. His nails were dirty.
He is cooperative when the student nurses approach him.
b. Vital Signs
Temp: 37 C/axilla
PR: 82 bpm
RR: 20 cpm

c. Height and Weight

Height: 124 cm
Weight: 25 kgs.
d. Examination of the Skin

Brown in complexion uniformed in skin color

Skin is warm to touch

Good skin turgor

Pallor

Dry skin
e. Examination of Hair and Nails

Hair is equally distributed

No infestations and dandruff

No depressions noted upon palpation

With dirty finger and toenails

With normal capillary refill of 2 seconds

With nail beds, smooth in texture, convex curvature of finger plate; angle of 160
degrees.
f.

Examination of the Skull and Face

Skull rounded with no presence of lesions or deformations

Presence of facial edema on the left side of the face

With symmetric facial movements

Uniformed color
g. Examination of the Eyes
Eyebrows and lashes are evenly distributed

Eyelids are symmetrical

With approximately 15-20 involuntary blinks per minute

Pink palpebral conjuctiva

h. Examination of the Ears

Auricles are in symmetrical size, aligned with outer cantus

Pinna coils after being folded

Client responds to normal voice tones

minimal presence of cerumen on both ears

i.

Examination of the Nose

External nose is properly aligned in between eyes and straight

With nasal flaring, no discoloration noted, no tenderness and no lesions

Nasal septum is in middle and intact

Presence of clear nasal secretions

j.

Examination of the Mouth

Outer upper and lower lips are pink in color with soft and smooth texture and have the
ability to purse lips

Inner lips and buccal mucosa is uniform and pink in color, smooth texture and
glistening

With incomplete set of teeth

The tongue is in central position, pink in color, slightly rough, with raised taste buds
and can be able to move side to side and up and down

Uvula is positioned in midline of soft palate

Can open and clench jaw without difficulty

k. Examination of the Neck

Neck is symmetrical

No masses noted

Coordinated head movement with slight difficulty

Trachea in midline at the suprasternal notch upon inspection and palpation

l.

Examination of the Lymph Nodes

Lymph nodes not palpable, slightly movable

No enlargement noted

m. Examination of the Chest (Lungs)

Normal respiratory rate (20 cpm)

Symmetrical chest expansion

Presence of any adventitious breath sounds upon auscultation

n. Examination of Abdomen

10

Without abdominal distention upon inspection and palpation

Absence of wounds and lacerations upon inspection

o. Examination of the Heart

With normal, regular, rate and rhythm of the heart upon auscultation
p. Examination of Extremities

Extremities are symmetrical and no deformations and tenderness

There is no presence of edema

Radial pulse is regular and not bounding

q. Examination of Lower Extremities
No presence of lesions present
Extremities symmetrical with no deformations and tenderness
There is no presence of edema

CRANIAL NERVE ASSESSMENT

11

CRANIAL
NERVE

CRANIAL

METHOD OF
TYPE

FUNCTION

FINDINGS
ASSESSMENT

Sensory

Smell

The

NERVE I

Student

Nurse Actual findings:

asked the patient to

close her both eyes.

(Olfactory)

He was asked to smell

and to identify aromas
such as Vinegar and
alcohol,

which

was

Bah Tuh is able to

smell and identify
different

scents

such

alcohol

as

and vinegar.

prepared by the student

nurse (SN).

CRANIAL

Sensory

NERVE II

Vision

and The SN asked

Visual fields

Tuh

to

read

Bah
a

newspaper first with the

(Optic)

right eye and then with

the left and finally both
eyes with a distance of
12 inches.

Actual Findings:
The patient cannot
see anything when
his left eye was
covered,

while

when covering the

right eye the left
can read the words
written

in

the

newspaper. When
using both eyes he
can

read

newspaper

the
by

using his left eye.

CRANIAL
NERVE III
(Oculomotor)

Motor

Extraocular

The SN asked patient

movement,

to close first his one

movement

of eye as a penlight was

sphincter

of introduced

pupil

on

the

and uncovered eye. Upon

ciliary muscles the application of light,

of the lens

pupil size and changes

were

noticed.

The

same thing was done

on the other eye. Also,

Actual Findings:
Upon

the

introduction of light
on each pupil of
the

patient,

constriction of the
pupil was noticed.
It

also

constricts
12
upon focusing on
the penlight holding

IV. ANATOMY AND PHYSIOLOGY

Figure 1.1 The male urinary system

The principal function of the urinary system is to maintain the volume and composition of
body fluids within normal limits. One aspect of this function is to rid the body of waste products
that accumulate as a result of cellular metabolism, and because of this, it is sometimes referred
to as the excretory system. Although the urinary system has a major role in excretion, other
organs contribute to the excretory function. The lungs in the respiratory system excrete some
waste products, such as carbon dioxide and water. The skin is another excretory organ that rids
the body of wastes through the sweat glands. The liver and intestines excrete bile pigments that
result from the destruction of hemoglobin. The major task of excretion still belongs to the urinary
system. If it fails the other organs cannot take over and compensate adequately.

13

The urinary system maintains an appropriate fluid volume by regulating the amount of
water that is excreted in the urine. Other aspects of its function include regulating the
concentrations of various electrolytes in the body fluids and maintaining normal pH of the blood.
In addition to maintaining fluid homeostasis in the body, the urinary system controls red
blood cell production by secreting the hormone erythropoietin. The urinary system also plays a
role in maintaining normal blood pressure by secreting the enzyme renin.

The urinary system consists of the kidneys, ureters, urinary bladder, and urethra. The
kidneys form the urine and account for the other functions attributed to the urinary system. The
ureters carry the urine away from kidneys to the urinary bladder, which is a temporary reservoir
for the urine. The urethra is a tubular structure that carries the urine from the urinary bladder to
the outside. To learn more

about the components of the urinary system, select a topic listed

below.

Kidneys

Ureters

14

Urinary Bladder

Urethra

Kidneys
The kidneys are the primary organs of the urinary system. The kidneys are the organs
that filter the blood, remove the wastes, and excrete the wastes in the urine. They are the
organs that perform the functions of the urinary system. The other components are
accessory structures to eliminate the urine from the body.
The paired kidneys are located between the twelfth thoracic and third lumbar vertebrae,
one on each side of the vertebral column. The right kidney usually is slightly lower than the
left because the liver displaces it downward. The kidneys protected by the lower ribs, lie in
shallow depressions against the posterior abdominal wall and behind the parietal
peritoneum. This means they are retroperitoneal. Each kidney is held in place by connective
tissue, called renal fascia, and is surrounded by a thick layer of adipose tissue, called
perirenal fat, which helps to protect it. A tough, fibrous, connective tissue renal capsule
closely envelopes each kidney and provides support for the soft tissue that is inside.
In the adult, each kidney is approximately 3 cm thick, 6 cm wide, and 12 cm long. It is
roughly bean-shaped with an indentation, called the hilum, on the medial side. The hilum

15

leads to a large cavity, called the renal sinus, within the kidney. The ureter and renal vein
leave the kidney, and the renal artery enters the kidney at the hilum.
The outer, reddish region, next to the capsule, is the renal cortex. This surrounds a
darker reddish-brown region called the renal medulla. The renal medulla consists of a series
of renal pyramids, which appear striated because they contain straight tubular structures
and blood vessels. The wide bases of the pyramids are adjacent to the cortex and the
pointed ends, called renal papillae, are directed toward the center of the kidney. Portions of
the renal cortex extend into the spaces between adjacent pyramids to form renal columns.
The cortex and medulla make up the parenchyma, or functional tissue, of the kidney.
The central region of the kidney contains the renal pelvis, which is located in the renal
sinus and is continuous with the ureter. The renal pelvis is a large cavity that collects the
urine as it is produced. The periphery of the renal pelvis is interrupted by cuplike projections
called calyces. A minor calyx surrounds the renal papillae of each pyramid and collects urine
from that pyramid. Several minor calyces converge to form a major calyx. From the major
calyces the urine flows into the renal pelvis and from there into the ureter.
Each kidney contains over a million functional units, called nephrons, in the parenchyma
(cortex and medulla). A nephron has two parts: a renal corpuscle and a renal tubule. The
renal corpuscle consists of a cluster of capillaries, called the glomerulus, surrounded by a
double-layered epithelial cup, called the glomerular capsule. An afferent arteriole leads into
the renal corpuscle and an efferent arteriole leaves the renal corpuscle. Urine passes from
the nephrons into collecting ducts then into the minor calyces.
The juxtaglomerular apparatus, which monitors blood pressure and secretes renin, is
formed from modified cells in the afferent arteriole and the ascending limb of the nephron
loop.

Ureters
Each ureter is a small tube, about 25 cm long, that carries urine from the renal pelvis to
the urinary bladder. It descends from the renal pelvis, along the posterior abdominal wall, behind
the parietal peritoneum, and enters the urinary bladder on the posterior inferior surface.

16

Figure 1.4 The Ureter

The wall of the ureter consists of three layers. The outer layer, the fibrous coat, is a
supporting layer of fibrous connective tissue. The middle layer, the muscular coat, consists of
inner circular and outer longitudinal smooth muscle. The main function of this layer is peristalsis
to propel the urine. The inner layer, the mucosa, is transitional epithelium that is continuous with
the lining of the renal pelvis and the urinary bladder. This layer secretes mucus, which coats and
protects the surface of the cells.

Urinary Bladder
The urinary bladder is a temporary storage reservoir for urine. It is located in the pelvic cavity,
posterior to the symphysis pubis, and below the parietal peritoneum. The size and shape of the
urinary bladder varies with the amount of urine it contains and with pressure it receives from
surrounding organs.
The inner lining of the urinary bladder is a mucous membrane of transitional epithelium that is
continuous with that in the ureters. When the bladder is empty, the mucosa has numerous
folds called rugae. The rugae and transitional epithelium allow the bladder to expand as it fills.
The second layer in the walls is the submucosa that supports the mucous membrane. It is

17

composed of connective tissue with elastic fibers.

The next layer is the muscularis, which is composed of smooth muscle. The smooth muscle
fibers are interwoven in all directions and collectively these are called the detrusor muscle.
Contraction of this muscle expels urine from the bladder. On the superior surface, the outer
layer of the bladder wall is parietal peritoneum. In all other regions, the outer layer is fibrous
connective tissue.

Figure 1.5 The Urinary Bladder

There is a triangular area, called the trigone, formed by three openings in the floor of the
urinary bladder. Two of the openings are from the ureters and form the base of the trigone.
Small flaps of mucosa cover these openings and act as valves that allow urine to enter the
bladder but prevent it from backing up from the bladder into the ureters. The third opening, at
the apex of the trigone, is the opening into the urethra. A band of the detrusor muscle encircles
this opening to form the internal urethral sphincter

18

Urethra

Figure 1.6 The Urethra

The final passageway for the flow of urine is the urethra, a thin-walled tube that conveys
urine from the floor of the urinary bladder to the outside. The opening to the outside is the
external urethral orifice. The mucosal lining of the urethra is transitional epithelium. The wall
also contains smooth muscle fibers and is supported by connective tissue.
The internal urethral sphincter surrounds the beginning of the urethra, where it leaves
the urinary bladder. This sphincter is smooth (involuntary) muscle. Another sphincter, the
external urethral sphincter, is skeletal (voluntary) muscle and encircles the urethra where it goes
through the pelvic floor. These two sphincters control the flow of urine through the urethra.
In females, the urethra is short, only 3 to 4 cm (about 1.5 inches) long. The external urethral
orifice opens to the outside just anterior to the opening for the vagina.

19

In males, the urethra is much longer, about 20 cm (7 to 8 inches) in length, and transports both
urine and semen. The first part, next to the urinary bladder, passes through the prostate gland
and is called the prostatic urethra. The second part, a short region that penetrates the pelvic
floor and enters the penis, is called the membranous urethra. The third part, the spongy urethra,
is the longest region. This portion of the urethra extends the entire length of the penis, and the
external urethral orifice opens to the outside at the tip of the penis.

Renin Angiotensin System

Figure 1.7 The RAAS mechanism

The renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS)
is a hormone system that regulates blood pressure and water (fluid) balance.
When blood volume is low, the kidneys secrete renin. Renin stimulates the production of
angiotensin. Angiotensin causes blood vessels to constrict, resulting in increased blood
pressure. Angiotensin also stimulates the secretion of the hormone aldosterone from the
adrenal cortex. Aldosterone causes the tubules of the kidneys to increase the reabsorption of

20

sodium and water into the blood. This increases the volume of fluid in the body, which also
increases blood pressure.
If the renin-angiotensin-aldosterone system is too active, blood pressure will be too high. There
are many drugs that interrupt different steps in this system to lower blood pressure. These drugs
are one of the main ways to control high blood pressure (hypertension), heart failure, kidney
failure, and harmful effects of diabetes.
Activation
The system can be activated when there is a loss of blood volume or a drop in blood pressure
(such as in hemorrhage). Alternatively, a decrease in plasma NaCl concentration will stimulate
the macula densa to release renin.
1. If the perfusion of the juxtaglomerular apparatus in the kidney's macula densa
decreases, then the juxtaglomerular cells release the enzyme renin.
2. Renin cleaves a zymogen, an inactive peptide, called angiotensinogen, converting it into
angiotensin I.
3. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme
(ACE) which is found mainly in lung capillaries.
4. Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to
receptors on intraglomerular mesangial cells, causing these cells to contract along with
the blood vessels surrounding them and causing the release of aldosterone from the
zona glomerulosa in the adrenal cortex. Angiotensin II acts as an endocrine,
autocrine/paracrine, and intracrine hormone.
Effects
It is believed that angiotensin I may have some minor activity, but angiotensin II is the major bioactive product. Angiotensin II has a variety of effects on the body:

21

Throughout the body, it is a

potent

vasoconstrictor

of

arterioles.

In

the

kidneys,

it

constricts

glomerular arterioles, having a

greater

effect

on

efferent

arterioles than afferent. As with

most other capillary beds in the
body, the constriction of afferent
arterioles
Figure 1.7 RAAS

increases the arteriolar resistance, raising systemic arterial blood pressure and
decreasing the blood flow. However, the kidneys must continue to filter enough blood
despite this drop in blood flow, necessitating mechanisms to keep glomerular blood
pressure up. To do this, angiotensin II constricts efferent arterioles, which forces blood to
build up in the glomerulus, increasing glomerular pressure. The glomerular filtration rate
(GFR) is thus maintained, and blood filtration can continue despite lowered overall
kidney blood flow. Because the filtration fraction has increased, there is less plasma fluid
in the downstream peritubular capillaries. This in turn leads to a decreased hydrostatic
pressure and increased osmotic pressure (due to unfiltered plasma proteins) in the
peritubular capillaries. The effect of decreased hydrostatic pressure and increased
osmotic pressure in the peritubular capillaries will facilitate increased reabsorption of
tubular fluid.

Angiotensin II decreases medullary blood flow through the vasa recta. This decreases
the washout of NaCl and urea in the kidney medullary space. Thus, higher
concentrations of NaCl and urea in the medulla facilitate increased absorption of tubular
fluid. Furthermore, increased reabsorption of fluid into the medulla will increase passive
reabsorption of sodium along the thick ascending limb of the loop of Henle.

Angiotensin II stimulates Na+/H+ exchangers located on the apical membranes (faces the
tubular lumen) of cells in the proximal tubule and thick ascending limb of the loop of

22

Henle in addition to Na+ channels in the collecting ducts. This will ultimately lead to
increased sodium reabsorption

Angiotensin II stimulates the hypertrophy of renal tubule cells, leading to further sodium
reabsorption.

In the adrenal cortex, it acts to cause the release of aldosterone. Aldosterone acts on the
tubules (e.g., the distal convoluted tubules and the cortical collecting ducts) in the
kidneys, causing them to reabsorb more sodium and water from the urine. This
increases blood volume and, therefore, increases blood pressure. In exchange for the
reabsorbing of sodium to blood, potassium is secreted into the tubules, becomes part of
urine and is excreted.

Release of anti-diuretic hormone (ADH), also called vasopressin -- ADH is made in the
hypothalamus and released from the posterior pituitary gland. As its name suggests, it
also exhibits vaso-constrictive properties, but its main course of action is to stimulate
reabsorption of water in the kidneys. ADH also acts on the central nervous system to
increase an individual's appetite for salt, and to stimulate the sensation of thirst.
These effects directly act in concert to increase blood pressure.

V. The patient and His illness

b. Synthesis of the Disease (Booked Based)
b.1. Definition of the Disease
The kidneys are complex organs whose primary task is to eliminate wastes, excess fluid
and unneeded electrolytes from the body. Any condition that interferes with the kidney function
can lead to a potentially dangerous build up of waste products in the blood stream.
According to Joyce Black et al, acute glomerulonephritis is a kidney disease that results
from inflammation of the glomerulus, a small condensed group of blood vessels, which serves to
filter the blood. It is an immunologic disorder that causes inflammation and increased cells in the
glomerulus. Because the primary function of the glomerulus is to filter the, most cases result
when antigen-antibody complexes produced by an infection elsewhere in the body become

23

trapped in the glomerulus. This entrapment causes inflammatory damage and impedes
glomerular function, reducing the glomerular membranes capacity of selective permeability. The
source of the antigens may be either exogenous (e.g. after streptococcal infection) or
endogenous (as in SLE). Evidence also indicates that some antigen-antibody complexes mat
form in the kidney itself.
The primary presenting features of AGN are hematuria, edema, azotemia (concentration
of urea and nitrogenous wastes in the blood) and proteinuria (< 3.0 g proteinuria/day).
The initial event of acute glomerulonephritis in most cases is antigen-antibody reaction
at the glomerulus. The glomerulus become inflamed leading to glomerular damage,which can
be a result of increased glomerular membrane permeability, proteinuria, and hypoalbuminemia.
Hypoalbuminimia, by decreasing colloid osmotic pressure, favors the transduction of fluid out of
the vascular compartment into the interstitium. This mechanism is fairly direct for the production
of edema. In addition, hypovolemia results in a decrease of renal plasma flow and glomerular
filtration rate, activating the rennin-angiotensin mechanism. The retained salt and water, further
aggravating the edema. By repetition of these chain events, massive edema (anascara) may
occur. The amount of protein lost, however, does correlate precisely with the severity of the
edema, because people vary in the rate of protein synthesis to replace that which is lost. The
cause of hyperlipidemia that often accompanies AGN is obscure. Most patients increased blood
cholesterol levels, triglyceride, very low density of lipoprotein, low lipoprotein, lipoprotein and
apoprotein, and there is also a decreased high density lipoprotein concentration in some
patients. These defects seem to be due in part to increased synthesis of lipoprotein in the liver,
abnormal transport of circulating lipid particles, and decreased catabolism. Lipiduria follows the
hyperlipidemia because not only albumin molecules but also lipoproteins leak across the
glomerular capillary wall. Other complications of AGN includes hypertension because off the
kidneyss reflex fluid retention response in the phase of declining filtration. The result is a rise in
fluid volume that boosts blood pressure. There is also an increased susceptibility to infection,
which may causes by loss of immunoglobulin in the urine
b.2 NON MODIFIABLE AND MODIFIABLE FACTORS
Non-Modifiable

24

Family History- an underlying or hereditary cause of renal disease may be initially

suspected based on a positive familial history of kidney disease such as polycystic
kidney and hereditary nephritis.

Age-is an non-modifiable factor which the occurrence of acute glomerulonephritis

prevalent among school age, with slightly higher incidence in boys.

Sex-is a non-modifiable factor in which the occurrence of the said disease is prevalent in
males more it is in females (James, et.,al. 2002).

Modifiable
Infections
Post-streptococal infection. Glomurulonephritis may develop after a step infection in the
throat or, rarely, on the skin (impetigo). Post-infectious glomerulonephritis becoming less
common, most likely because of rapid and complete antibiotic of most streptococcal
infenctions.
Bacterial endocarditis. Bacteria can occasionally spread through the blood stream lodge in
the heart, causing an infection on the valvular tissues inside the heart. Glomerulus in the
kidneys may be affected through the spread of infection through the bloodstream.
Viral infections. Among the viral infection that may trigger glomurulonephritis are the human
immune deficiency virus (HIV), which causes AIDS and hepatitis B and C viruses which
affect the liver and become chronic infections.
After bacteria or virus had directly or indirectly invaded the glomerulus the antigen-antibody
reaction of the body is stimulated to fight against these pathogens. The nephrons become
inflamed; leukocyte infiltrates in the glomerulus and epithelial cells. WBC is increased
leading to the release endogenous pyrogens, there is stimulation to the thalamus to secrete
prostaglandin. As a body reaction it causes hyperthermia.
Immune Diseases

25

Lupus. A chronic inflammatory disease, lupus can affect many parts of the body including
the skin, joints, kidneys, blood cells, heart and lungs.
Good pastures syndrome. A rare immune lung disorder that may mimic pneumonia, good
pastures syndrome causes bleeding into the lungs as well as glomerulonephritis.
IGA nephropathy. Characterized by recurrent episodes of blood in the urine, this condition
results from deposits of immunoglobulin A in the glomeruli. IGA nephropathy can progress
for years with no noticeable symptoms. The disorder seems to be more common in men
than in women. Immune complex disease results in the formation of antigen- antibody
complexes that activate a variety of serum factors, this results in precipitation of complexes
in vulnerable areas leading to inflammation as consequence of complement activation. The
end result is inflammatory reaction that leads to tissue destruction. (porth, 1998)
Vasculitis
Polyarteritis. This form of vasculitis affects small and medium blood vessels in many parts of
the body, such as your heart, kidneys and intestines.
Wegeners granulomatosis. This form of vasculitis affects small and medium blood vesses in
the lungs, upper airways and kidneys.
Henoch-schonlein purpura: it is a type of hypersensitivity vasculitis and inflammatory
response within a blood vessel. It is caused by an abnormal response of the immune
system.

Conditions that cause glomeruli to scar

High blood pressure. Damage to the kidneys and the vessels to alter their normal functions
can occur or result to high BP. Glomerulonephritis can also elevate Bp because it reduces
kidney function.
Diabetic Kidney Disease. DM patients can manifest polydipsia or frequent urination which
may cause several kidney dysfunctions.

26

b. Synthesis of the disease (Patient Centered)

b.1. Definition of the disease
The kidneys are complex organs whose primary task is to remove waste, excess fluids
and uneeded electrolytes form the body. Any condition that interferes with kidney function can
lead to potentially dangerous build up of waste products in the blood stream.
According to Joyce Black, Acute glomerulonephritis is a kidney disease that results from
inflammation of the glumeruli a small condensed group of blood vessels which strives to filter
the blood. It is an immunologic disorder that causes inflammation and increased in blood cells in
the glumerulos. Because the primary job of the glumerolus is to filter blood, most cases results
when antigen- antibody complexes produced by an infection anywhere in the body became
trapped in the glumerulos.These entrapment causes damage and empedes glumerula function
reducing the glumerular membrane capacity for selective permeability. The source of the
antigens may be either exogenous or endogenous. Evidence also indicatesthat some antigenantibody complexes may form in the kidney itself.
The primary presenting features of AGN are hematuria, edema, azotemia, and
proteinuria.
b.2 Non Modifiable and Modifiable Factors
Non Modifiable Factors

Age. Kid Nee is a 9 year old and he is in school age where in AGN is prevalent.
Gender: AGN is prevalent among males. According James, et al 2002, occurrence is
prevalent in males than females.

Modifiable Factors
High sodium and High Fat diet. The patient loves to eat high fats and sodium foods
which highly contribute in altering the kidneys normal function. Since Kid nees family
owns a sari sari store which houses a lot of opportunity for him to indulge in junk foods
and carbonated drinks. This could contribute in the development of hypertension. The

increase in peripheral vascular resistance could result to decrease renal perfusion.

Elevated WBC. Elevated WBC indicates presence of infection.

Signs and Symptoms:

27

Hematuria. May be caused by the inflammatory and further scarring of the glumeruli. In
addition to that, large molecules pass through the kidneys which may further introduce

trauma to the tissue.

Hyperthermia. One of the inflammatory response if increase in WBC count which
signals increase in activity of the immune system thus releases pyrogenes which may

alter the basal temperature of the body, which leads to increase in temperature.
Decreased Hematocrit. Because low concentration of RBC, due to excretion through
the urine. And there is also increase in interstitial fluid which might dilute the

concentration of body fluid, resulting to decreased hematocrit.

Albuminuria. The kidney losses its capability to selective permeability, in that way, large
molecules will pass through the glumerulus including albumin, which is responsible for
colloid oncotic pressure for pulling force in the vessel to hold the fluids inside the cell,

thus preventing edema.

Edema. Albuminuria allows excretion of albumin responsible for oncotic pressure, which

increases the fluid in interstitial spaces, thus forming edema.

Elevated RBC. Indicates excessive trauma and loss of RBC which forces the body to

produce more RBC to compensate for its loss.

Hypertension. Elevated BP can be caused by edema due to fluid retention, or in some
cases it can be the effect of excessive accumulation of fluid in the interstitial spaces that
elevates the blood pressure.

28

V. Pathophysiology

Book based
Risk Factor
Children

Etiology

Male

Post infection (GABHS)

Antigen-antibody reaction
Goes in the circulation
Traps in glomerulus
Produce swelling of cells

Oliguria and
increase
waste
product in
the blood
C

Narrowing of capillary lumen

Decrease blood flow
Decrease GFR
Activation of RAAS

Stimulation of hypothalamus
Inflammation process occurs
(hear regulating system)
Activities complement
pathways

Fever

Attack glomerular basement

membrane
Glomerular proliferation

Impedes function of kidneyB

Damage Glomeruli

Irritation on the tissue

Scarring occurs

Hematuria

Decrease GFR
Oliguria and increase waste
product in the blood

Increase capillary
permeability

Decrease
Excretionprotein
of protein
and
albumin
and albumin
in the body
Proteinuria and albuminuria
A

29

A
Decrease protein and
albumin in the body

Muscle weakness, fatigue

and poor appetite

Synthesis of lipoprotein

Decrease oncotic pressure

Hyperlipidemia

Fluid shifting

Decrease fluid in the

circulation

RAAS activation
C

30

RAAS activation

Decrease concentration of
urine

Decrease erythropoiesis

Diminished blood flow

Decrease specific gravity
and pH

Increase creatinine and

potassium
Unable to excrete wastes
Accumulates in the brain
Seizure

Decrease
GFR
Hypoxemia to different
tissue
Acidosis
Kidney
Hyperventilate

Anaerobic metabolism

Stomach
RAAS activation

Constipation

Increase amount of acid

Oliguria and increase waste
product in the blood

31

C
RAAS activation

Sodium and Water Retention

Fluid shifting

Increase blood volume

Hypertension
ascites

Accumulation of fluid in the

lung capillaries

Compression of diaphragm
Pulmonary hypertension
Difficulty of breathing
Increase pulmonary arterial
pressure

Generalized edema
(ANASARCA)
Periorbital edema
Facial edema
Ascites
Edema on both upper and
lower extremities

Rupture of microvascular
aneurysm

Hemoptysis

32

Patient based
Post-streptococcal infection
(group-A, beta hemolytic)

Release of material from the organism,

into the circulation (antigen)

Formation of antibody

Immune complex reaction in the

glomerular capillary

Inflammatory response

Proliferation of epithelial cells lining

glomerulus and cells between
endothelium and epithelium of capillary
membrane

Swelling capillary membrane and

infiltration with leukocytes

Permeability of base membrane

Occlusions of the capillaries of the

glomeruli vasospasm of afferent
ventrioles

Glomerular filtration rate

Ability to form filtrate from glomeruli

plasma flow

Retention of H2O and Na; hypovolemia;

circulatory congestion

Edema
Hypertension
urinary output
Urine dark in color
Anorexia
Irritability lethargy

ACUTE
GLOMERULONEPHRITIS

VI. LABORATORY EXAMINATION REPORTS

DIAGNOSTIC/

DATE
ORDERED,

LABORATORY

DATE

PROCEDURES

RESULTS IN

BLOOD CHEMISTRY

DO: 03/01/15

CREATININE

DR: 03/01/15

INDICATIONS

RESULTS

NORMAL

ANALYSIS

AND

VALUES

INTERPRETATION

This is to reveal if

Creatinine

there is alteration

normal

with the excretory

indicates that urination

function

is normal.

patients

of

the

kidney

and it suggests its

70.7

is

within

level.

Which

63.6-110.5
umol/L

chronicity since it
tends to rise in the
later part of the
disease condition.
DIAGNOSTIC/

DATE
ORDERED,

LABORATORY

DATE

PROCEDURES

RESULTS IN

INDICATIONS

RESULTS

NORMAL

ANALYSIS

AND

VALUES

INTERPRETATION

BLOOD CHEMISTRY

DO: 03/01/15

This is to reveal

Sodium in low levels

water

are

called

hyponatremia,

which

and

electrolyte
SODIUM

DR: 03/01/15

imbalance in the

131.4 mmol/L

body, and to find

cause

135-148

can cause damage to

mmol/L

cells, it makes them

of

swell up with too much

symptoms from or

water. This

high

particularly

levels

of

sodium.

DIAGNOSTIC/

may

be

dangerous

in areas like the brain.

DATE
ORDERED,

LABORATORY

DATE

PROCEDURES

RESULTS IN

INDICATIONS

RESULTS

NORMAL

ANALYSIS

AND

VALUES

INTERPRETATION

BLOOD CHEMISTRY

POTASSIUM

DO: 03/01/15

DR: 03/01/15

This is to detect

Potassium

concentrations that

normal

are

high

indicates that patient is

or

having enough amount

too

(hyperkalemia)
too

low

(hypokalemia), and

3.96 mmol/L

3.6-5.2 mmol/L

is

within

range

which

of potassium in his diet

which helps the nerves

also for monitoring

and

of

communicate. It also

an

electrolyte

muscles

to

imbalance,

helps moves nutrients

metabolic acidosis

into cells and waste

and or diagnosing

products out of cells.

alkalosis.

NURSING RESPONSIBILITIES
Before :
Explain to the patient what you are going to do, why it is necessary and how she can
cooperate.
Tell the patient that a blood sample will be taken. Explain who will perform the
venipuncture and when.
Explain to the patient that he may feel slight discomfort from the needle puncture and the
tourniquet.
Assemble the equipment and supplies needed in the procedure.
During:
Observe appropriate infection control procedures.
Select and prepare the vascular puncture site. Clean the site with the antiseptic swab
allows it to dry completely before obtaining the blood specimen.
Ensure that the subdermal bleeding has stopped before removing pressure.
After:
Send the sample to the laboratory promptly.
Report abnormal laboratory findings to the health care provider in a timely manner
consistent with the severity of the abnormal results

DATE
DIAGNOSTIC OR

OREDERED

LABORATORY

, DATE

PROCEDURES

RESULTS

INDICATIONS OR

RESULTS

PURPOSES

NORMAL

ANALYSIS AND

VALUES

INTERPRETATION

IN

COMPLETE
COUNT

BLOOD D.O:

(CBC)

OR 03/01/15

HEMATOLOGY
>

Consists

The patients Hgb is in the

-to monitor Hgb value

D.R:

in the RBC

03/01/15

-to

suggest

the

several

presence of body fluid

tests that allow for the

deficit due to elevated

evaluation

Hgb level.

cellular

of

Hemoglobin (HGB)

of

different

components
of

clients.

items

The

commonly

evaluated

include

hgb,

hct, RBC, RBC indices,

WBC, WBC differential,
platelets and microscopic
examination

of

stained

DIFFERENTIAL

COUNT
determines

the

percentage of each kinds

of white blood cells in the
white blood cell count

170

which

means

that

the

Female:

patient does not have a

120-140

sufficient volume of the red

blood cell.

RBC COUNT
-it

measures

number

of

detect

the

the

RBC

4.36

to

used

to

4.5- The patients RBC count is

5.9

oxygen

within normal range.

Female:

carrying cells.
-it

Male:

4.5-5.1
assess

further if the patient

had

episodes

of

bleeding

blood smears.

WBC

108 g/dL

of

the blood on a broad

range

Male: 140- below the normal range

Hematocrit (HCT)

The hematocrit level of the

- to aid diagnosis of

patient is below the normal

abnormal

limit. It indicates that there

states

of

hydration,
polycythemia

Male: 0.40- is a low concentration of

and

anemia.
It

measures

the

concentration of RBC

0.345

0.50

red blood cells within the

Female:

blood volume and due to

0.38-0.48

retention

of

fluid

thus,

causing dilutional anemia.

NURSING RESPONSIBILITIES:
Before:
Explain the procedure to the patients significant other.
Explain to the patient that this test will help in the patients response to treatment.
Tell the patients significant other that no fasting is required.
Explain to the patient that the test requires blood sample and venipuncture will be
performed.
Inform the patient that the patient will experience discomfort from the needle puncture
and pressure of the tourniquet.
Inform that she will be experiencing mild pain on site where the needle was pricked.
Assure that collecting the blood sample take less than 3 minutes.
During:
Maintain sterile technique.
Collect 5-7 ml of venous blood in a vacuum.
After:
Apply pressure or pressure dressing to the venipuncture site.
Check the venipuncture site for bleeding.
Fill-up the laboratory form properly and send it to the laboratory technician during the
collection of the sample of the specimen.

DIAGNOSTIC

ORDERED
DATE

LABORATORY
PROCEDURES

manual

automated
and

and/or
qualitative

semi-quantitative

tests performed on a
urine

sample.

routine urinalysis usuall

y includes the following
tests:

color,

transparency, specific
gravity,

pH,

glucose,

INDICATION

OR

PURPOSE

RESULTS

NORMAL
VALUES

RESULTS

URINALYSIS
A urinalysis is a group
of

DATE

DO: 03/01/15
DR: 03/01/15

Evaluates

physical Color: Dark Yellow

characteristics
urine;

of

determines

specific gravity and

pH;

defects

measures

and

for
blood

blood, bilirubin, nitrite,

urobilinogen,
leukocyte esterase.

and

INTERPRETATION OF
RESULTS

Yellow colored urine is

colored to amber

an

colored.

hydration.

indication

of

Transparency:
Cloudy

protein,

Clear to slightly
hazy

Cloudy urine indicates

renal infection or
kidney stones.

examines

sediment
cells,

for

pH: 6.0

casts

5.5 6.5

and crystals.

protein,
ketones,

AND

Pale yellow, straw

glucose and ketone

bodies;

ANALYSIS

To

screen

patients

urine

the
for

renal or urinary tract

disease.

PH of 6.0 is within the

Sugar: negative
negative

normal

range

and

indicates slightly acid

urine.
Negative
sugar

result
denies

for
the

presence of glycosuria.
Urine
Specific

not

concentrated

gravity:
1.003 1.035

1.015

is

which

indicates the absence

of dehydration.
Presence of pus cells
suggests the presence

Pus cells:
35 40

(-) Negative

of infection.

The result

is

within

normal range.

RBC: MANY

<2

An

increase

in

the

epithelial cells which

shows tubule cell injury
brought about by the
Epithelial
Occasional

Cells:

Few

large
passing

molecules
through

glomerular
membranes.

the

The result shows the

presence
Few

which

bacteria

indicates

that

pathogens are present

into the sterile system
of the tubules and its
Bacteria: Moderate

presence in the urine

also indicates that the
glomerular membrane
allows the passage of
this

large

molecules

out of the body.

NURSING RESPONSIBILITIES
Before:
Confirm the patients identity using two patient identifiers according to facility
policy.
Explain that this analysis helps to diagnose renal or urinary track disease and to
evaluate overall body function.
Inform the patient that there are no dietary restrictions required.
Notify the laboratory and practitioner of drugs the patient is taking that may affect
the results.
During:
Collect a random urine specimen of at least 15 ml. Obtain a first voided morning
specimen if possible
Keep the specimen container clean. Make sure that the container wont come in
contact with any article, this may contaminate the specimen.
After:
Inform the patient that he may resume his usual diet and medications.
Notify the physician for abnormal findings.

IX. DRUG STUDY AND MANAGEMENT

a. IVFs, heplock
MEDICAL
MANAGEMENT/
TREATMENT

Heplock

DATE ORDERED
DATE PERFORMED

GENERAL

INDICATION(S)

OR

CLIENTS RESPONSE

DESCRIPTION

PURPOSES(S)

TO THE TREATMENT

Heparin Locks, or Hep

To keep open a vein for

Pain

Locks, are small tubes

easy access in order to

insertion.

CHANGED/ D/C

DO: 03/01/15
DP: 03/01/15

is

felt
The

upon
patient

attached to a catheter, administer drugs, saline,

experienced discomfort

inserted into the arm

antibiotics

while

and held in place with

without

tape

or

blood
causing

in

order

to

unnecessary stress on

administer

drugs

and

the patient, while saving

fluids without injecting

time.

patients multiple times

advantages of using this

unnecessarily.

method

Emergency
require

an

situations

One

medication

of
is
may

many
that
be

accessible

given without disturbing

vein fast; the Hep Lock

the patient while asleep.

provides
accessibility.

that
Medicine

the

inserted.

heplock

is

may be injected easily,

making life simple for
nursing staff and less
painful for patients.

NURSING RESPONSIBILITIES IN HEPLOCK INSERTION

Before insertion:
Inform the patient about the purpose of the heplock.
Sterilize the area where the heplock is to be inserted.
During insertion/administration of drug through the heplock:

Sterilize the heplock before administration of drugs.

Flush normal saline solution before administration.
Do not continue if there is resistance, this could indicate that the heplock is not
intact anymore.

After administration:
Maintain the cleanliness of the area.
Make sure it is in the vein.

Date Ordered/ Date Dosage,

Name of Drugs

Performed/

Route,

Date Frequency

of General Action

Given

Administration

GN: Furosemide

DO: 03/01/15

Furosemide

BN: Lasix

DP: 03/01/15

25

mg Furosemide

Indication

inhibits Indicated

TIV every 6 hours, absorption of sodium patient

refer if BP IS less

and chloride from the elevated

than 97/57 mmHg.

proximal

and

distal pressure a

tubules

and

ascending limb of the

loop of henle. Leading
to

sodium

rich

diuresis,

thus

reducing

edema

associated

to

renal

disease resulting to
decrease BP.
b. Drugs

NURSING RESPONSIBILITIES:
Prior to:

Monitor BP if less than 90/60. Do not give and refer.

Ensure the patency of the IVF if present.
Give early in the morning so that increase urination will not disturb sleep.

During:

Administer with food or milk to prevent GI upset.

Administer trough slow IV push

After:

Monitor BP.
Monitor intake and output.
Encourage increase oral fluid intake.
Arrange for potassium rich diet/ supplemental potassium as needed.
Refrigerate oral solution.

GN: Pebicillin G Na

DO: 03/01/15
DP: 03/01/15

Pen G Na 621,000
u IV q 6

Penicillins,
other

It is indicated fo
like infection specificall
-lactam involving
rena

antibiotics,

block system.
not only the division
of

bacteria,

including
cyanobacteria, but
also the division of
cyanelles,

the

photosynthetic
organelles of

the

glaucophytes,

and

the

division

of

chloroplasts

of

bryophytes.

In

contrast, they have

no effect on the
plastids
highly

of

the

developed

vascular

plants.

This supports the

endosymbiotic
theory

of

the

evolution of plastid
division
plants.

in

land

NURSING RESPONSIBILITIES:
Before:
Assess for allergic reactions. Perform skin test first.
Note for previous hypersensitivity to penicillin.
During:
This medication may be taken without regards to meal.
Note for any allergic reactions, such as changes in skin color or temperature.
After:
The reconstituted suspensions should be kept refrigerated and discarded after 10 days.
Instruct patient to comply with the regimen.
Note for any late allergic reaction.

Type of exercise

Date ordered
Date Given
Date Changed

General Description

Indications/ Purposes

Specific
Activity taken

Complete bed
rest

DO: 03/01/15

03/01/15

c. Diet

The
patient
is
restricted to continue
any activity and is
advice to rest.

It was ordered
patient
to
discomfort and
energy. Also to
metabolic and
demand
for
conservation.

to the Sleep, rest

relieve
regain
reduce
oxygen
energy

NURSING RESPONSIBILITIES:
Before:

Check the doctors order

Explain the procedure and importance to the client
Offer and assist the client with hand washing and oral hygiene before meal

During:

After:

Assist patient to a comfortable position

Check the correct food were to be taken by the patient
Assist the patient while eating if necessary
Observe the amount of food the client consumed
Give health teachings on food requirements and diet
Instruct patient to strictly comply to the treatment given
Monitor intake and output.
Monitor patients vital signs.

Type of exercise

Date ordered
Date Given
Date Changed

General Description

Indications/ Purposes

Specific
Activity taken

Low salt diet

DO: 03/01/15
DP: 03/01/15

Foods

containing To prevent aggravation Rice, Banana

of the patient condition Fish Vegetables
minimal amount of salt
since eating such food
and fat. Preserved may
increase
the
workload of the heart
food such as canned
goods

should

prevented
their
content

d. Exercise

high

owing

be
to

sodium

NURSING RESPONSIBILITIES:
Before:

Check the doctors order

Explain the procedure and importance of the diet to the client

Offer and assist the client with hand washing and oral hygiene before meal

During:

Assist patient to a comfortable position

Check the correct food were to be taken by the patient

Assist the patient while eating if necessary

Observe the amount of food the client consumed

After:

Give health teachings on food requirements and diet

Instruct patient to strictly comply to the treatment given

Monitor intake and output.

Check hydration status.

Check for presence of edema.

Limit
intake

oral

fluid DO: 03/01/15

DP: 03/01/15

It

is

prevent

diet

to It is indicated for 1000

further prevention

excess in body fluid

ml

of

of intake per day

fluid Patient

responded

to the diet regimen

excessive

as

recurrence of body

decrease edema.

fluid

in

the

interstitial space. It
is use for reduction
of edema, and for
patient
excrete
water.

unable

to

excess

evidence

by

NURSING RESPONSIBILITIES:
Prior:

Check for the doctors order regarding activity and position.

Explain to the patient and SO the type of activity that was ordered

During:

Assist the patient in position changes.

Provide for safety measures such as placing pillows, raising the side rails.

After:

Assess for patient condition; how he responds to the activity.

Instruct the patient to follow the activity.

Explain the importance of the said activity

VIII: NURSING CARE PLAN

Problem # 1: Excess fluid volume r/t failure of regulatory mechanism (inflammation of glomerular membrane inhibiting
filtration)
CUES

NSG

SCIENTIFIC

OBJECTIVES

DIAGNOSI

EXPLANATION

NSG

RATIONALE

EXPECTED

INTERVENTIONS

OUTCOME

S
S>O

Excess fluid

O>

Glomerulonephriti

volume

r/t s

failure

of

is

an

inflammation

of

Patient

regulatory

the

manifested:

mechanism

membrane within

>periorbital edema
>positive

albumin

in urinalysis result
pt may manifest:
-edema/ anasarca

(inflammatio
n

of

glomerular
membrane
inhibiting
filtration)

filtration

the

renal

corpuscle.

The

permeability
the

of

filtration

membrane
increases,
plasma

and

proteins

Short term:
After

>

3-4

hours of NI, pt

time

of

The
proteins

plasma
cause

the urine volume

Monitor

(daily

weight,

I/O

to balance, skin turgor

monitor

fluid

status

and edema, BP, PR, and

and

presence

reduce

rhythm,

recurrence of

effort).

fluid excess

>Identify

RR

of
and

After 3 days

Pt shall have

potential
of

fluids(medications,
oral and IV fluids,
foods)

>assessment
provides

baseline

and

ongoing

database

for

monitoring changes
and

evaluating

behaviors

to

monitor

fluid

status

and

reduce

recurrence of
fluid excess.

interventions

sources
Long-term:

data

Short term:

demonstrate

demonstrate
behaviors

>to gather baseline

and record VS.

>Assess fluid status

-weight gain over a

period

condition.

patients

will be able to

enter the filtrate.

short

Assess

>unrecognized

Long-term:

sources of excess
fluids
identified

may

be

Pt shall have
stabilized
fluid volume

- decreased urine

to

output,

urinating

because

they

less frequent than

increase

the

usual

osmotic pressure

volume

of the filtrate.

balanced I/O,

-changes in mental
status/

>Limit

sodium

and

be

fluid

intake

to

able

to

stabilize fluid

VS

prescribed volume.

breath
and

AEB
within

free

signs

of
and

symptoms of
edema.

>fluid restriction will

basis

of

weight,

urine

output

responses

and
to

therapy

stable weight,
and

AEB

be determined on

normal limits,

sounds(rales
crackles)

of NI, pt will

clients

restlessness
-abnormal

increase

>Evaluate
edematous
extremities.

Change

in

semi-

fowlers position as
appropriate

fluid restriction

for

normal limits,
stable
weight,

and

pressure and risk

symptoms of

for skin

edema.

Breakdown

>

to

facilitate

movement

of

respiration

rationale

clients

and

improving

family

within

>to reduce tissue

diaphragm

>Explain to pt and

VS

free of signs

position frequently
>Place

balanced I/O,

>understanding
promotes

pt

and

family cooperation
with fluid restriction

>to reduce edema

and

fluid

excess
>administer
medications(diuretics
,

plasma/albumin

volume expanders)

Problem # 2: Altered nutrition less than body requirements

volume

Assessment

Nursing

Scientific

diagnosis

explanation

S: wala akong

Altered nutrition

Patient

ganang kumain

less than body

walang las yung

requirements

pagkain,

related

nakakasuka

decrease

O: the patient
manifests:

appetite

poor

had

>to

altered nutrition

weight

before

preference

less than body

patient

was

requirements

Short term:

After 2 days of
of

decreased

tone

and poor eating

have

habits

increase

an
in

nursing
patient

The

patient

The patient shall

have

an

increase
determine

in

appetite

>ascertain

Long term: The

understanding of

patient

individual

>to

nutrition needs

intoxication

avoid
of

the kidneys
>encourage diet
>these
can

will

maintain normal
weight

may manifest:

following

to provide client

low in protein

interventions,

for

Short term:

what information

term:

After 2 weeks of

>22 kg

the

>to

to

Long

have

results

interventions,

with
muscle

diagnosed

nursing

appetite

>thinness

Expected
outcome

the patient will

absorb

Rationale

>determine

because
2

Interventions

decrease ability nutritional intake

>nausea >body nutrients

malaise

to

Objectives

factors
affect

ingestion
nutrient

>determine
ability to chew,

>weakness

or

swallow

inability

to

taste

swallow

or

of

and

>to

appeal

patients
and dislikes

to

likes

shall

have maintained
normal weight

masticate

food,

>discuss eating

abdominal

habits including

cramping

food preferences

>vomiting

>encourage use and

of

flavoring

>to

enhance

food satisfaction
stimulate

appetite

agents such as
herbs

and

lemons if salt is

>to

restricted

desired nutrients

>encouraged
SO to give soft
foods

for

the

patient such as
soup
meal

and

oat

meet

the

IX. HEALTH TEACHING

METHOD
M: instructed the patient to take the following
Co amoxiclav
Furosemide
E: Instructed the client to have adequate bed rest
T: Instructed t he client on strict compliance to medication and therapy
H: Instructed patient to always have adequate rest periods in a

comfortable position
Instructed patient to avoid high fat and high sodium content food
instructed patient to schedule regular follow-up check-up appointments

with physician to monitor progress

nstructed client to continue therapy
O: Instructed patient to come back after 7 days
D: instructed client on low fat low salt diet

DIARY

Doing an internship in the Emergency Room is a very challenging job. It

entails a lot of work. It takes a lot of courage to perform a skin test, insertion of

catheter, computation of medications and most especially taking vital signs within
minutes. Because every second in the ER is important to save a life of a patient
who is in need of emergent care.
In addition, doing a case study it entails a lot of work and knowledge. The
beginning process, objectives were set that had served as guidelines with
regards to proper nursing assessment and also in implementing optimum nursing
care. Through its utilization, I was able to acquire knowledge that can help me
gain a deeper understanding of the diagnosis. With the cooperation of the patient
and the family members I was able to attain holistic care and Therapeutic
measurement was implemented.
Before I only knew basic about acute glomerulonephritis. But through the
case study I was able to acquire a deeper knowledge. Learned how people
acquire this disease, what are the predisposing and precipitating factors, the
signs and symptoms and the management. And become aware of the different
signs and symptoms, current trends that significantly play a role in the
occurrence of acute glomerulonephritis throughout the world.
Through the case study, my nursing skill has improved especially in the
nursing process: assessment, planning, implementation, and evaluation. I
learned on how to do comprehensive assessment of with the patient through
interview, observation, and physical assessment.
In making this case this case study and completing the ER RLE there
were many problems that came in the way. I was able to learn to beat the
problems because I knew that all is just a stepping-stone of a greater challenge.