Our Lady of Fatima University College of Nursing Valenzuela
Campus
ACUTE GLUMERULONEPHRITISIn Partial Fulfillment of requirements
of NCM 106 RLE leading to the degree of Science in Nursing
EMERGENCY ROOM
TABLE OF CONTENTS
I. Introduction II. ObjectivesIII. Patients Profile IV. Anatomy
and Physiology V. Pathophysiology VI. Laboratory Examination
Results VII. Drug StudyVIII. Nursing Care Plans IX. Health
Teachings
I. INTRODUCTIONTheres 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,
progressivechronic renal failure(CRF); or simply a urinary
abnormality such ashematuria(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 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 a 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. OBJECTIVESNurse-centeredAfter 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 PROFILEName: Bah TuhAge: 7 years oldBirthday: July
28, 2007Adress: Metro ManilaNationality: FilipinoReligion: Roman
CatholicCivil Status: SingleDate Admission: March 1, 2015Time of
Admission: 3:00 PMChief Complaint's: Facial edema and Left lower
quadrant painInitial Diagnosis: Acute glomerulonephritisFinal
Diagnosis: Acute glomerulonephritisHistory 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 IllnessTwo 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 SIDEMOTHER SIDE
Lolo 1, 75y/o52 y/oLolo 2, 60 y/oLola 1, 72 y/oLola 2 ,60
y/o
36 y/o47 y/o39 y/o46 y/o30 y/o40 y/o30 y/o45 y/o49 y/.o42
y/o35y/oy/oy/o49 y/o50 y/o54 y/o
L neeKBONMJIHGFE neeDCA
SisterBrotherGrandmotherGrandfatherMOTHER
SIDEBrotherSisterFATHER SIDEGrandfather
Bah Tuh 7 y/o
DISEASESCHILDREN
Hypertension
DaughterMyocardial infarctionMellitus
GrandmotherSon
deceasedDiabetes 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 Interactiona. General
AppearancePatient 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 SignsTemp: 37
C/axillaPR: 82 bpmRR: 20 cpmc. Height and WeightHeight: 124
cmWeight: 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 colorg. Examination of
the Eyes Eyebrows and lashes are evenly distributed Eyelids are
symmetrical With approximately 15-20 involuntary blinks per minute
Pink palpebral conjuctivah. 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 earsi. 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 difficultyk. 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 palpationl. Examination of the Lymph Nodes Lymph
nodes not palpable, slightly movable No enlargement notedm.
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 Without
abdominal distention upon inspection and palpation Absence of
wounds and lacerations upon inspectiono. Examination of the Heart
With normal, regular, rate and rhythm of the heart upon
auscultationp. Examination of Extremities Extremities are
symmetrical and no deformations and tenderness There is no presence
of edema Radial pulse is regular and not boundingq. Examination of
Lower Extremities No presence of lesions present Extremities
symmetrical with no deformations and tenderness There is no
presence of edema
CRANIAL NERVE ASSESSMENTCRANIAL NERVETYPEFUNCTIONMETHOD
OFASSESSMENTFINDINGS
Cranial nerve I(Olfactory)SensorySmellThe Student Nurse asked
the patient to close her both eyes. He was asked to smell and to
identify aromas such as Vinegar and alcohol, which was prepared by
the student nurse (SN).Actual findings:Bah Tuh is able to smell and
identify different scents such as alcohol and vinegar.
CRANIAL NERVE II(Optic)
Sensory
Vision and Visual fields
The SN asked Bah Tuh to read a newspaper first with the 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 the newspaper by using his left eye.
CRANIAL NERVE III(Oculomotor)
Motor
Extraocular movement, movement of sphincter of pupil and ciliary
muscles of the lensThe SN asked patient to close first his one eye
as a penlight was introduced on the uncovered eye. Upon the
application of light, pupil size and changes were noticed. The same
thing was done on the other eye. Also, the blinking of the eyelids
of the patient was assessed during the whole period of the
interview. In addition, the student nurse who was holding a
penlight asked the patient to concentrate looking on the penlight
then observe for constriction of the pupil and then after that the
student nurse told the patient to look at the wall without moving
the head then observe for dilation of pupil.Actual Findings:Upon
the introduction of light on each pupil of the patient,
constriction of the pupil was noticed. It also constricts upon
focusing on the penlight holding by the student nurse and dilates
when looking at the wall without moving the head.
CRANIAL NERVE IV(Trochlear)
MotorExtraocular movements specifically movements of eyeball in
downward lateral directions.The SN made use of a penlight and moved
it in different directions: upward lateral, right side, downward
lateral, and left side. The SN instructed the patient to follow the
movements of the penlight through his eyes only without moving his
head.
Actual Findings:He has good, coordinated eye movements (both
eyes) and is able to follow the direction of the penlight with his
eyes without moving his head.
CRANIAL NERVE V(Trigeminal)Sensory andMotorSensation of cornea,
skin of face and nasal mucosa, muscle of mastication, sensation of
skin surface.The SN made use of the corneal reflex test by gently
touching the cornea with sterile cotton and gently stroking the
eyelashes. And uses a pin to test for skin sensation.The group also
observed the patent when eating and speaking.Actual Findings:The
patient elicited blinking reflex.He can also differentiate the
dullness or sharpness of the pin.He is able to make chewing
movements, open the mouth against resistance, and move his jaw from
side to side
CRANIAL NERVE VI(Abducens)Motor
Extraocular movement, lateral movement of the eyeballThe student
nurse asked patient to move the eyeballs in lateral sides.
Actual Findings:The patient was able to move both eyeballs
laterally.
Cranial Nerve VII(Facial)Sensory and Motor
Facial expressions, sense of taste on the anterior two thirds of
the tongue and movement of muscles in the face.The student nurse
asked patient to smile, raise his eyebrows and puff out his cheeks,
and frown.The student nurse also asks the patient to taste salt and
sugar.
Actual Findings: Bah Tuh was able to smile, puff out his cheeks
and raise his eyebrows and frown his face. The patient was able to
identify the difference of salt, and sugar.
Cranial Nerve VIII(Acoustic)
SensoryHearing and Balance
The student nurse whispered a word to his and instructed his to
repeat the word whispered.
Performed the Rombergs Test. Instructed patient to close his
eyes and stand straight with hands on side.Actual findings:The
patient was able to hear and repeat the exact word whispered to
him.
Actual findings:The patient was able to balance his self without
any excessive swaying movements.
Cranial Nerve IXGlossopharyngealSensoryandMotorSense of taste on
the posterior one-third of the tongue, pharyngeal movement and
swallowing.The student nurse instructed the patient to drink water
and swallow it. And asked the patient to moves his tongue in
different sides.Actual findings:The patient demonstrated a good
swallowing behavior without any difficulty and move tongue from
side to side and up and down.
CRANIAL NERVE X(Vagus)SensoryandMotorTaste, Salivary glands,
pharyngeal muscles, larynxFor taste, the student nurse introduced a
sugar and salt on the posterior part of the tongue. For motor, the
SN introduced a tongue depressor on the anterior part of the
tongue.Actual findings:The patient was able to identify the
different taste of the substances and was able to elicit gag reflex
upon introducing a tongue depressor at the back of the tongue,
normal swallowing noted.
CRANIAL NERVE XI(Accessory)MotorMotor to neck and upper back
musclesApplied a force on the head and shoulders, instructed
patient to resist the forceActual findings:Bah Tuh was able to
exert force on the head and shoulders upon the student nurse
applied force.
CRANIAL NERVE XII(Hypoglossal)MotorTongue musclesAsked the
patient to protrude tongue and move it from side to side.Actual
findings:The patient was able to protrude the tongue without any
deviation and move it from side to side.
71
IV. ANATOMY AND PHYSIOLOGY
Figure 1.1 The male urinary systemThe 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.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 Urinary Bladder
Urethra
KidneysThe 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 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.
UretersEach 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.
Figure 1.4 The UreterThe 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 BladderThe 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 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 BladderThere 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
Urethra
Figure 1.6 The UrethraThe 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.
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 mechanismThe 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 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.ActivationThe 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.EffectsIt is believed that angiotensin I may
have some minor activity, but angiotensin II is the major
bio-active product. Angiotensin II has a variety of effects on the
body: 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 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 illnessb. Synthesis of the Disease (Booked Based)b.1.
Definition of the DiseaseThe 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 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 urineb.2 NON MODIFIABLE AND MODIFIABLE
FACTORSNon-Modifiable 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).ModifiableInfectionsPost-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 DiseasesLupus. 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)VasculitisPolyarteritis. 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 scarHigh 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. b. Synthesis of the
disease (Patient Centered)b.1. Definition of the diseaseThe 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 antigen- antibody
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 FactorsNon 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: 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.
V. PathophysiologyBook basedOliguria and increase waste product
in the bloodHematuriaIrritation on the tissueProteinuria and
albuminuriaExcretion of protein and albuminDecrease protein and
albumin in the bodyIncrease capillary permeabilityOliguria and
increase waste product in the bloodDecrease GFRScarring
occursDamage GlomeruliBffnffnCffnffnFeverImpedes function of
kidneyGlomerular proliferationStimulation of hypothalamus (hear
regulating system)Attack glomerular basement membraneActivities
complement pathwaysActivation of RAASDecrease GFRDecrease blood
flowNarrowing of capillary lumenProduce swelling of cellsTraps in
glomerulusGoes in the circulationAntigen-antibody
reactionInflammation process occursEtiology Post infection
(GABHS)
Risk Factor Children Male
AffnffnCffnffnCffnffnRAAS activationDecrease fluid in the
circulationFluid shiftingDecrease oncotic
pressureHyperlipidemiaMuscle weakness, fatigue and poor
appetiteASynthesis of lipoproteinDecrease protein and albumin in
the body
Oliguria and increase waste product in the
bloodSeizureAccumulates in the brainIncrease creatinine and
potassiumUnable to excrete wastesRAAS activationDecrease
GFRConstipationStomachHypoxemia to different tissueIncrease amount
of acidAnaerobic metabolismKidneyDiminished blood flowDecrease
erythropoiesisHyperventilateAcidosisDecrease specific gravity and
pHDecrease concentration of urineRAAS activationB
HypertensionIncrease blood volume
Generalized edema (ANASARCA)Periorbital edemaFacial
edemaAscitesEdema on both upper and lower
extremitiesHemoptysisRupture of microvascular aneurysmIncrease
pulmonary arterial pressurePulmonary hypertensionAccumulation of
fluid in the lung capillariesDifficulty of breathingCompression of
diaphragmascitesFluid shiftingSodium and Water RetentionRAAS
activationC
Patient based Permeability of base membraneSwelling capillary
membrane and infiltration with leukocytesProliferation of
epithelial cells lining glomerulus and cells between endothelium
and epithelium of capillary membraneInflammatory responseImmune
complex reaction in the glomerular capillaryFormation of
antibodyRelease of material from the organism, into the circulation
(antigen)Post-streptococcal infection (group-A, beta hemolytic)
ACUTE GLOMERULONEPHRITISEdemaHypertensionurinary outputUrine
dark in colorAnorexiaIrritability lethargyRetention of H2O and Na;
hypovolemia; circulatory congestion Ability to form filtrate from
glomeruli plasma flow Glomerular filtration rateOcclusions of the
capillaries of the glomeruli vasospasm of afferent ventrioles
VI. LABORATORY EXAMINATION REPORTS DIAGNOSTIC/LABORATORY
PROCEDURESDATE ORDERED, DATE RESULTS ININDICATIONSRESULTSNORMAL
VALUESANALYSIS AND INTERPRETATION
BLOOD CHEMISTRY
CREATININE
DO: 03/01/15
DR: 03/01/15This is to reveal if there is alteration with the
excretory function of the patients kidney and it suggests its
chronicity since it tends to rise in the later part of the disease
condition.
70.7
63.6-110.5 umol/LCreatinine is within normal level. Which
indicates that urination is normal.
DIAGNOSTIC/LABORATORY PROCEDURESDATE ORDERED, DATE RESULTS
ININDICATIONSRESULTSNORMAL VALUESANALYSIS AND INTERPRETATION
BLOOD CHEMISTRY
SODIUM
DO: 03/01/15
DR: 03/01/15This is to reveal water and electrolyte imbalance in
the body, and to find cause of symptoms from or high levels of
sodium.
131.4 mmol/L
135-148 mmol/LSodium in low levels are called hyponatremia,
which can cause damage to cells, it makes them swell up with too
much water. This may be particularly dangerous in areas like the
brain.
DIAGNOSTIC/LABORATORY PROCEDURESDATE ORDERED, DATE RESULTS
ININDICATIONSRESULTSNORMAL VALUESANALYSIS AND INTERPRETATION
BLOOD CHEMISTRY
POTASSIUM
DO: 03/01/15
DR: 03/01/15This is to detect concentrations that are too high
(hyperkalemia) or too low (hypokalemia), and also for monitoring of
an electrolyte imbalance, metabolic acidosis and or diagnosing
alkalosis.
3.96 mmol/L
3.6-5.2 mmol/LPotassium is within normal range which indicates
that patient is having enough amount of potassium in his diet which
helps the nerves and muscles to communicate. It also helps moves
nutrients into cells and waste products out of cells.
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
diagnostic or laboratory proceduresdate oredered, date results
inindications or purposesresultsnormal valuesanalysis and
interpretation
complete blood count (CBC) or hematology
> Consists of several tests that allow for the evaluation of
different cellular components of the blood on a broad range of
clients. The items commonly evaluated include hgb, hct, RBC, RBC
indices, WBC, WBC differential, platelets and microscopic
examination of stained blood smears.
WBC DIFFERENTIAL COUNT determines the percentage of each kinds
of white blood cells in the white blood cell count
D.O: 03/01/15D.R: 03/01/15Hemoglobin (HGB)-to monitor Hgb value
in the RBC-to suggest the presence of body fluid deficit due to
elevated Hgb level.108 g/dLMale: 140-170 Female: 120-140The
patients Hgb is in the below the normal range which means that the
patient does not have a sufficient volume of the red blood
cell.
RBC COUNT-it measures the number of RBC to detect the oxygen
carrying cells.-it used to assess further if the patient had
episodes of bleeding
4.36
Male: 4.5-5.9 Female: 4.5-5.1
The patients RBC count is within normal range.
Hematocrit (HCT)- to aid diagnosis of abnormal states of
hydration, polycythemia and anemia.It measures the concentration of
RBC within the blood volume and is expressed as a
percentage.0.345
Male: 0.40-0.50Female: 0.38-0.48
The hematocrit level of the patient is below the normal limit.
It indicates that there is a low concentration of red blood cells
within the blood volume and due to retention of fluid thus, causing
dilutional anemia.
WBC COUNT-to detect infection or inflammation-this blood test
evaluates the number of condition and differentiates causes of
alteration in the total WBC count including inflammation, infection
and tissue necrosis.11.65-10The WBC count Is at the above the
normal range. Which causes patients facial edema. WBCs are cells of
the immune system involved in defending the body against both
infectious disease and foreign materials.
LYMPHOCYTES-to determine viral infection-produces antibodies and
other chemicals responsible for destroying microorganisms;
contributes to allergic reactions, graft rejection, tumor control,
and regulation of the immune system.
0.16
0.25-0.50
The value is below normal range, which means that there is
presence of viral infections. The body has the ability produce
antibodies and other chemicals responsible for destroying
microorganisms.
SEGMENTERS-are erythrocytes ratio indicative of
inflammation.0.33%0.40-0.60% Segmenters are below the normal range
indicating that there is presence of inflammation.
PLATELETS-are special cell fragments that play an important role
in blood clotting. If a patient does not have enough platelets, he
will be at an increased risk of excessive bleeding and bruising. -
The CBC measures the number and size of platelets present.
368150-450The platelet count of the patient is within the normal
limit. It indicates that the patient has enough platelet production
and is lesser risk for bleeding.
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 / LABORATORY PROCEDURESDATE ORDEREDDATE
RESULTSINDICATION OR PURPOSERESULTSNORMAL VALUESANALYSIS AND
INTERPRETATION OF RESULTS
URINALYSISAurinalysisis a group of manual and/or automated
qualitative and semi-quantitative tests performed on a urine
sample. A routineurinalysisusually includes the following tests:
color, transparency,specific gravity, pH, protein, glucose,
ketones, blood, bilirubin, nitrite, urobilinogen, and leukocyte
esterase.DO: 03/01/15DR: 03/01/15Evaluates physical characteristics
of urine; determines specific gravity and pH; defects and measures
protein, glucose and ketone bodies; examines for sediment for blood
cells, casts and crystals.
To screen the patients urine for renal or urinary tract
disease.
Color: Dark Yellow
Transparency: Cloudy
pH: 6.0
Sugar: negative
Specific gravity: 1.015
Pus cells:35 40
RBC: MANY
Epithelial Cells: Occasional
Bacteria: ModeratePale yellow, straw colored to amber
colored.
Clear to slightly hazy
5.5 6.5
negative
1.003 1.035
(-) Negative
OO>Patient manifested: >periorbital edema >positive
albumin in urinalysis result pt may manifest:-edema/
anasarca-weight gain over a short period of time- decreased urine
output, urinating less frequent than usual-changes in mental
status/ restlessness-abnormal breath sounds(rales and crackles)
Excess fluid volume r/t failure of regulatory
mechanism(inflammation of glomerular membrane inhibiting
filtration)
Glomerulonephritis is an inflammation of the filtration membrane
within the renal corpuscle. The permeability of the filtration
membrane increases, and plasma proteins enter the filtrate.The
plasma proteins cause the urine volume to increase because they
increase the osmotic pressure of the filtrate.Short term:After 3-4
hours of NI, pt will be able to demonstrate behaviors to monitor
fluid status and reduce recurrence of fluid excess
Long-term:After 3 days of NI, pt will be able to stabilize fluid
volume AEB balanced I/O, VS within clients normal limits, stable
weight, and free of signs and symptoms of edema.> Assess
patients condition. Monitor and record VS.>Assess fluid status
(daily weight, I/O balance, skin turgor and presence of edema, BP,
PR, and rhythm, RR and effort).>Identify potential sources of
fluids(medications, oral and IV fluids, foods)>Limit sodium and
fluid intake to prescribed volume.
>Evaluate edematous extremities. Change position frequently
>Place in semi-fowlers position as appropriate
>Explain to pt and family rationale for fluid restriction
>administer medications(diuretics, plasma/albumin volume
expanders)>to gather baseline data
>assessment provides baseline and ongoing database for
monitoring changes and evaluating interventions>unrecognized
sources of excess fluids may be identified
>fluid restriction will be determined on basis of weight,
urine output and responses to therapy>to reduce tissue pressure
and risk for skin Breakdown
> to facilitate movement of diaphragm improving
respiration>understanding promotes pt and family cooperation
with fluid restriction>to reduce edema and fluid volume
excessShort term:Pt shall have demonstrated behaviors to monitor
fluid status and reduce recurrence of fluid excess.
Long-term:Pt shall have stabilized fluid volume AEB balanced
I/O, VS within clients normal limits, stable weight, and free of
signs and symptoms of edema.
Problem # 2: Altered nutrition less than body requirements
Assessment Nursing diagnosis Scientific explanation Objectives
Interventions Rationale Expected outcome
S: wala akong ganang kumain walang las yung pagkain, nakakasuka
O: the patient manifests:>nausea >body malaise >thinness
with poor muscle tone >22 kg
The patient may manifest: >weakness or inability to swallow
or masticate food, abdominal cramping >vomiting Altered
nutrition less than body requirements related to decrease appetite
2 decrease ability to absorb nutrients Patient had altered
nutrition less than body requirements because of decreased
nutritional intake and poor eating habits Short term:
After 2 days of nursing interventions, the patient will have an
increase in appetite
Long term: After 2 weeks of nursing interventions, patient will
maintain normal weight
>determine weight before patient was diagnosed
>ascertain understanding of individual nutrition needs
>encourage diet low in protein
>determine ability to chew, swallow and taste >discuss
eating habits including food preferences >encourage use of
flavoring agents such as herbs and lemons if salt is restricted
>encouraged SO to give soft foods for the patient such as soup
and oat meal
>to have preference for the following results >to
determine what information to provide client
>to avoid intoxication of the kidneys
>these factors can affect ingestion of nutrient >to appeal
to patients likes and dislikes
>to enhance food satisfaction and stimulate appetite
>to meet the desired nutrients
Short term:The patient shall have an increase in appetite
Long term: The patient shall have maintained normal weight
IX. HEALTH TEACHINGMETHODM: instructed the patient to take the
following Co amoxiclav Furosemide E: Instructed the client to have
adequate bed restT: 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 therapyO:
Instructed patient to come back after 7 daysD: instructed client on
low fat low salt diet
DIARYDoing 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.
