I.

Introduction

Diabetic nephropathy (nephropatia diabetica)also known as kimmelstol. Wilson syndrome

and intercapillary glomerulonephritis, is a progressive kidney disease caused by angiopathy of
capillaries in the kidney glomeruli. It is characterized by nephritic syndrome and nodular
glomerulsclerosis. It is due to longstanding diabetes mellitus, and is a prime cause for dialysis in
many countries.

The exact cause of diabetic nephropathy is unknown, but it is believe that uncontrolled
high blood sugar leads to the development of kidney damage. In some cases, your genes or
family history may also play a role not all persons with diabetes develop this condition.
Each kidney is made of hundred of thousands of filtering units called nephrons. Each
nephron has a cluster of tiny blood vessels used a glomerulus. Together these structure help
remove waste from the body. Too much blood sugar can damage these structure, causing them to
thicken and became scarred. Slowly, over time more and more blood vessels are destroyed. The
kidney structure begins to lead and protein (albumin) begins to pass into the urine.
Persons with diabetes who have the following risk factors are more likely to develop this
condition: Family history of kidney disease of high blood pressure, Poor control of blood
pressure, Poor control of blood sugars

Diabetes nephropathy generally goes along with other diabetes complications including
high blood pressure, retinopathy, and blood vessels changes.

The endocrine system is a group of glands that work together and secrete many types of different
hormones that regulate the body. The field of study that deals with disorders of endocrine glands
is endocrinology, a branch of the wider field of internal medicine. The endocrine system is an
information signal system much like the nervous system. Hormones regulate many functions of
an organism, including mood, growth and development, tissue function, and metabolism.
The endocrine system is made up of a series of ductless glands that produce chemical messages
called hormones
A number of glands that signal each other in sequence is usually referred to as an axis, for
example, the hypothalamic-pituitary-adrenal axis. Typical endocrine glands are the pituitary,
thyroid, and adrenal glands. Features of endocrine glands are, in general, their ductless nature,
their vascularity, and usually the presence of intracellular vacuoles or granules storing their
hormones. In contrast, exocrine glands, such as salivary glands, sweat glands, and glands within
the gastrointestinal tract, tend to be much less vascular and have ducts or a hollow lumen. Also
controls metabolism in our body system.
Diseases of the endocrine system are common,[2] including conditions such as diabetes mellitus,
thyroid disease, and obesity. Endocrine disease is characterized by dysregulated hormone release
(a productive pituitary adenoma), inappropriate response to signaling (hypothyroidism), lack of a
gland (diabetes mellitus type 1, diminished erythropoiesis in chronic renal failure), or structural
enlargement in a critical site such as the testis (toxic multinodular goitre). Hypofunction of
endocrine glands can occur as a result of loss of reserve, hyposecretion, agenesis, atrophy, or
active destruction. Hyperfunction can occur as a result of hypersecretion, loss of suppression,
hyperplastic or neoplastic change, or hyperstimulation.
Endocrinopathies are classified as primary, secondary, or tertiary. Primary endocrine disease
inhibits the action of downstream glands. Secondary endocrine disease is indicative of a problem
with the pituitary gland. Tertiary endocrine disease is associated with dysfunction of the
hypothalamus and its releasing hormones.
As the thyroid, and hormones have been implicated in signaling distant tissues to proliferate, for
example, the estrogen receptor has been shown to be involved in certain breast cancers.
Endocrine, paracrine, and autocrine signaling have all been implicated in proliferation, one of the
required steps of oncogenesis.
II. Goal and Objectives

At the end of the 1st rotation the researchers will be able to apply necessary knowledge

and skills to render quality care and service to the patient.

Specific Objectives

At the end of the 1st rotation, the researchers will be able to:

1. Understand the patient’s condition.

2. Gain sufficient knowledge about patient’s medical regimen.

3. Assess the patient’s needs and know how to be of assistance.

4. Identify appropriate nursing diagnosis for patient care.

5. Implement nursing care.

6. Monitor patient’s condition and refer any unusualities promptly.

7. Maintain and observe precautionary measures.

8. Prevent development of any complications.

9. Enhance and maintain the health of the patient.

10. Impart health teachings to the patient’s family.

11. Provide emotional support to the patient’s family.

III. CLIENTS PROFILE

A. Socio demographic profile

Patient X, 49 years old, female, Roman Catholic, Filipino and married. Has
reached a height of 152.4 cm and weighs 60kgs.

B. Vital Signs

Patient X blood pressure was 130/90mmHg, pulse rate at 88 bpm, respiratory

rate at 20 and temperature was 37.3 Celsius.

C. Physical Exam

Head was normocephalic, facial movements were symmetrical, hair was fine,
and fontanels were closed. Eyelids were symmetrical, sclera was anicteric, and
both pupils were equal in size at 3mm and eyes were sensitive to light. Ears were
normal and symmetrical and no discharges. Hearing was quiet difficult. Nose was
normal with septum at midline, both nostrils are patent, mucosa was pale.
Mucoid discharges were not noted. Lips were pale and cracked. Also mucosa
and gums were pale. Tongue at the midline. Some teeth were missing. Uvula,
pharynx was at the midline. Tonsils were not inflamed, thyroids are non palpable.
For the cardiovascular status: pericardial area was the apex, midclavicular fifth
intercostals space. Peripheral pulses were regular. Capillary refill was 3 seconds
and has white nails noted. Respiratory status: breathing pattern was regular..
Lung expansion was symmetrical, and with cough noted. Abdomen was normal.
Bowel sounds was hypoactive. Urinary pattern was less about twice a day with
the characteristic of yellow, scanty urine as evidenced by I&O measurement.
Skin was pallor, rough in texture, firm and warm. With intra jugular catheter in
placed.

D. Health Pattern Assessment

1. Health perception and management

History of present illness: Patient has been diagnosed with chronic kidney
disease secondary to diabetes mellitus. About 5 days PTA: patient was admitted
at COMC due to unusual urinary pattern. She was then transferred at NMMC for
the continuation of her hospitalization. She was found to be positive in
hypertension and has Diabetes Mellitus.
2. Nutrition and metabolic pattern

Patient has been on kidney care medications. Patient was given low salt, low fat
diet. Appetite was fair and with episodes of vomiting.

3. Elimination pattern

Patient X’s elimination often has this bowel pattern of 3 days in a week. She
defecate a yellowish collared stool and has no discomforts reported. Urinates five
times a day.

4. Activity and Exercise pattern

Patient X does not perform any forms of exercise due to leg discomfort when
being moved.

5. Cognitive-perpetual pattern

Patient X was drowsy, oriented and restless.

6. Sleep- rest pattern

Regular sleeping pattern was 8-10 hrs. During admission his sleep pattern was
irregular due to discomfort and annoyance.

7. Values and belief pattern

Patient is a Roman Catholic, she is a church goer and does not forget to pray.
She merely believed in God that this illness was already planned by him and she
never fails to have faith on Him.

E. Significant findings of the assessment

From the assessment above the researchers had prioritized three problems. In
degree of importance, these are: Imbalanced nutrition less-than body
requirement related to abdominal pain and distention, Chronic pain related to
large abdomen (ascites), and Fluid volume excess related to ascites and edema
formation. This shall be discussed in detail in the Nursing Care Plan Section of
this report (Part VI).
IV. ANATOMY OF PACREAS

Pancreas
Secreted hormone From cells Effect
Intake of glucose, glycogenesis and glycolysis
in liver and muscle from blood
Insulin (Primarily) β Islet cells
intake of lipids and synthesis of triglycerides in
adipocytes Other anabolic effects
Glucagon (Also glycogenolysis and gluconeogenesis in liver
α Islet cells
Primarily) increases blood glucose level
Inhibit release of insulin[8]
Somatostatin δ Islet cells Inhibit release of glucagon[8] Suppress the
exocrine secretory action of pancreas.
Pancreatic
PP cells Unknown
polypeptide
The pancreas is a long, irregularly shaped gland that is found in vertebrates (organisms
with a backbone). It is made of protein and is located behind the stomach. Some
describe the shape of the pancreas as a fishlike with a long tail and large head. Others
describe it as being shaped like the letter "J" with the top portion connecting to the
duodenum (the beginning part of the small intestine). The human pancreas is yellowish
in color and about 7 inches (17.8 cm) long and 1.5 inches (3.8 cm) wide. The pancreas
secretes both hormones and enzymes. Parts of the pancreas

There are five main parts of the human pancreas:

Head - the right side of the pancreas is located in the curve of the duodenum and is
called the head. It is the widest part of the organ.
Neck - the thin part of the pancreas located between the head and body.
Tail - the thin tip of the pancreas, located in the left part of the abdomen, and ends near
the spleen.
Body - the tapered, left side of the pancreas. The body is the middle portion of the
gland, between the head and the tail.
Uncinate - This is the part of the pancreas that bends backwards and underneath the
body of the pancreas. There are two very important blood vessels that cross in front of
the ucinate process called the superior mesenteric artery and vein.

The pancreas also contains the following:

Stalk - Inside the pancreas is a long duct called the "stalk." This duct runs down the
center of the pancreas.
Grapes - The inside of the pancreas contains a stalk (see above) with clusters attached.
These clusters resemble a stalk of grapes. The grapes are actually clusters of cells
which flow into the stalk-like duct and then later into the duodenum.
This system of stalk and grapes helps facilitate the digestion of protein, fats, and
carbohydrates.
Islet of langerhan’s- which includes Alpha, Beta, and Delta cells.
The Pancreas is made up of two types of tissues; exocrine and endocrine
Exocrine tissue of the pancreas
The chemicals produced by the exocrine cells in the pancreas are called
enzymes. These are proteins secreted into the duodenum (the beginning part of
the small intestine) where they help with the digestion of food.
Pancreatic exocrine tissue is comprised of Acinar cells and the pancreatic
ducts.These exocrine cells of the pancreas produce and transport enzymes
that help with digestion and will eventually exit the body through the digestive
tract.The exocrine tissue of the pancreas secretes digestive enzymes, or
pancreatic "juice," into the duodenum. Small numbers of these
exocrine cells in the tail of the pancreas, called PP cells, secrete pancreatic
polypeptide, which slows down nutrient absorption. This enzyme is also
responsible for coordinating exocrine and islet enzyme release.
Endocrine tissue of the pancreas
Pancreatic endocrine tissue consists of cell clusters known as islets of Langerhans.
These cells produce and secrete hormones into the bloodstream. Two of the main
pancreatic hormones are insulin and glucagon. These hormones work together to
maintain the proper level of sugar in the blood. Insulin works to lower blood sugar and
glucagon works to increase blood sugar.
When the insulin-secreting cells fail to function properly diabetes occurs. The two
major (but not all of the types of) diabetes are type 1 diabetes (juvenile diabetes) and
type 2 diabetes (adult onset ).The endocrine tissue includes the islets of Langerhans.

Islets of Langerhans (also called islands or isles of Langerhans)

The endocrine tissue of the pancreas includes the islets of Langerhans. This area is
responsible for the production and release of certain hormones into the bloodstream.
The main three types of cells that produce hormones in the islets of Langerhans are:

Alpha cells - release the hormone glucagon, which triggers the release of
glycogen form liver stores and helps to raise the level of glucose (sugar) in the
bloodstream
Beta cells - release the hormone insulin, which help regulate carbohydrate
metabolism into the bloodstream, and
Delta cells - release the hormone somatostatin into the bloodstream that acts as
an inhibitor to the pituitary hormone called somatotropin and helps tell the body
when to make other hormones like insulin, glucagon, gastrin, renin, and secretin.

Every cell in the human body needs energy in order to function. The body’s
primary energy source is glucose, a simple sugar resulting from the digestion of foods
containing carbohydrates (sugars and starches). Glucose from the digested food
circulates in the blood as a ready energy source for any cells that need it. Insulin is a
hormone or chemical produced by cells in the pancreas, an organ located behind the
stomach. Insulin bonds to a receptor site on the outside of cell and acts like a key to
open a doorway into the cell through which glucose can enter. Some of the glucose can
be converted to concentrated energy sources like glycogen or fatty acids and saved for
later use. When there is not enough insulin produced or when the doorway no longer
recognizes the insulin key, glucose stays in the blood rather entering the cells.

Kidney
Secreted hormone From cells Effect
Activates the renin-angiotensin system by
Renin (Primarily) Juxtaglomerular cells
producing angiotensin I of angiotensinogen
 Extraglomerular
Erythropoietin (EPO) Stimulate erythrocyte production
mesangial cells
Active form of vitamin D3
Calcitriol (1,25- Increase absorption of calcium and phosphate
dihydroxyvitamin D3) from gastrointestinal tract and kidneys inhibit
release of PTH
stimulates megakaryocytes to produce
Thrombopoietin
platelets[4]

The kidneys are paired organs, which have the production of urine as their primary function.
Kidneys are seen in many types of animals, including vertebrates and some invertebrates. They
are an essential part of the urinary system, but have several secondary functions concerned with
homeostatic functions. These include the regulation of electrolytes, acid-base balance, and blood
pressure. In producing urine, the kidneys excrete wastes such as urea and ammonium; the
kidneys also are responsible for the reabsorption of glucose and amino acids. Finally, the kidneys
are important in the production of hormones including vitamin D, renin and erythropoietin.

Located behind the abdominal cavity in the retroperitoneum, the kidneys receive blood from the
paired renal arteries, and drain into the paired renal veins. Each kidney excretes urine into a
ureter, itself a paired structure that empties into the urinary bladder.

Renal physiology is the study of kidney function, while nephrology is the medical specialty
concerned with diseases of the nephron, which is the functional unit of the kidney. Diseases of
the kidney are diverse, but individuals with kidney disease frequently display characteristic
clinical features. Common clinical presentations include the nephritic and nephrotic syndromes,
acute kidney failure, chronic kidney disease, urinary tract infection, nephrolithiasis, and urinary
tract obstruction.

Location

In humans, the kidneys are located behind the abdominal cavity, in a space called the
retroperitoneum. There are two, one on each side of the spine; they are approximately at the
vertebral level T12 to L3.[2] The right kidney sits just below the diaphragm and posterior to the
liver, the left below the diaphragm and posterior to the spleen. Resting on top of each kidney is
an adrenal gland (also called the suprarenal gland). The asymmetry within the abdominal cavity
caused by the liver typically results in the right kidney being slightly lower than the left, and left
kidney being located slightly more medial than the right.[3][4] The upper (cranial) parts of the
kidneys are partially protected by the eleventh and twelfth ribs, and each whole kidney and
adrenal gland are surrounded by two layers of fat (the perirenal and pararenal fat) and the renal
fascia. Each adult kidney weighs between 125 and 170 g in males and between 115 and 155 g in
females. The left kidney is typically slightly larger than the right.

Structure

Renal pyramid, Interlobar artery, Renal artery, Renal vein, Renal hilum, Renal pelvis, Ureter,
Minor calyx, Renal capsule, Inferior renal capsule, Superior renal capsule, Interlobar vein,
Nephron, Minor calyx, Major calyx, Renal papilla, Renal column.

The kidney has a bean-shaped structure, each kidney has concave and convex surfaces. The
concave surface, the renal hilum, is the point at which the renal artery enters the organ, and the
renal vein and ureter leave. The kidney is surrounded by tough fibrous tissue, the renal capsule,
which is itself surrounded by perinephric fat, renal fascia (of Gerota) and paranephric fat. The
anterior (front) border of these tissues is the peritoneum, while the posterior (rear) border is the
transversalis fascia.

The substance, or parenchyma, of the kidney is divided into two major structures: superficial is
the renal cortex and deep is the renal medulla. Grossly, these structures take the shape of 8 to 18
cone-shaped renal lobes, each containing renal cortex surrounding a portion of medulla called a
renal pyramid (of Malphigi). Between the renal pyramids are projections of cortex called renal
columns (of Bertin). Nephrons, the urine-producing functional structures of the kidney, span the
cortex and medulla. The initial filtering portion of a nephron is the renal corpuscle, located in the
cortex, which is followed by a renal tubule that passes from the cortex deep into the medullary
pyramids. Part of the renal cortex, a medullary ray is a collection of renal tubules that drain into a
single collecting duct.The tip, or papilla, of each pyramid empties urine into a minor calyx,
minor calyces empty into major calyces, and major calyces empty into the renal pelvis, which
becomes the ureter.

Blood supply

The kidneys receive blood from the renal arteries, left and right, which branch directly from the
abdominal aorta. Despite their relatively small size, the kidneys receive approximately 20% of
the cardiac output.

Each renal artery branches into segmental arteries, dividing further into interlobar arteries which
penetrate the renal capsule and extend through the renal columns between the renal pyramids.
The interlobar arteries then supply blood to the arcuate arteries that run through the boundary of
the cortex and the medulla. Each arcuate artery supplies several interlobular arteries that feed
into the afferent arterioles that supply the glomeruli.
After filtration occurs the blood moves through a small network of venules that converge into
interlobular veins. As with the arteriole distribution the veins follow the same pattern, the
interlobular provide blood to the arcuate veins then back to the interlobar veins which come to
form the renal vein exiting the kidney for transfusion for blood.

V. PATHOPHYSIOLOGY
Predisposing Factor:
Precipitating factor:
Long Standing DM -------------Early Glomerular hemodynamic-------- 49
yrs old
Old Age changes
Hypertension
Hyperglycemia

Hyperfiltration & Hyperperfusion

Microalbuminuria Dysfunction of auroregulatory response

 Increased arterial dilation
Increased itraglomerular pressure
Increased Increased extracellular
messangial cell
matrix production Matrix deposition & messangial
hypertrophy
Decreased glomerular filtration Expansion of Messangial
area for filtration hghgffjhgjfiltrationfiltrationfiltrationfiltration
Marks the beginning of Rena
Incease Sodium creatinine
Increased BUN Decreased glomerular

Hypertrophy of remaining nephrons Inability to concentrate urine

Further loss of nephron function

Loss of excretory renal function

Loss of nonexcretory renal function

Immune disturbance

Failure to produce erythropoietin

Anemia, pallor, weakness, fatigue

Infection Decreased sodium
Reabsorption in tubule Water Retention
retention
Water

EDEMA
Edema

PATHOPHYSIOLOGY: DIABETES MELLITUS TYPE II

Non-modifiable Factors
- Age - Older than 40 years
- Family history of type 2 diabetes
- Hispanic, Native American, African American, Asian
American, or Pacific Islander descent, Asian
Modifiable Factors
- History of previous impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)
- Obesity - Weight >20% of desirable body weight (true for approximately 90% of patients with type
2 diabetes)
- Hypertension (>140/90 mm Hg) or dyslipidemia (high-density lipoprotein [HDL] cholesterol level
<40 mg/dL or triglyceride level >150 mg/dL)
- History of GDM or of delivering a baby with a birth weight of > 9 lbs
- Polycystic ovarian syndrome (which results in insulin resistance)
- Viruses: certain viruses may destroy beta cells
- Faulty Immune System: multiple factors may cause the immune system to destroy beta cells,
such as infection
- Physical Trauma: injury or trauma may destroy the ability of the pancreas to produce insulin
- Drugs: drugs used for other conditions could cause the development of diabetes
- Stress: hormones at times of stress may block the effectiveness of insulin
- Pregnancy: hormones produced during pregnancy can block the effectiveness of insulin
 HYPERGLYCEMIA

Blood Sugar Level

↑Blood exceeds renal threshold Glucose uptake
Osmolarity Normal = 180mg/dl by the cells

Excretion of excess glucose ↓Energ

↓Energy
Fluid shifting from Cellular starvation y
intracellular to in the urine Level
Level
extracellular
Hunger due to the
Intracellular Glucosuria stimulation of Satiety Center Body
dehydration / volume of Hypothalamus malaise
depletion
Glucose attracts water
Body
Thirst sensation due to the malaise
stimulation of Thirst Center
of hypothalamus ↑Urine Output:
Polyuria Polyphagia

Polydipsia

Sluggish blood flow

Delayed biochemical
Decreased organ perfusion mediation

Slow-healing cuts or
Nephropat Neuropath Confusio sores
hy y n
Dry,
itchy Blurred
Numbness vision,
skin and retinopath
tingling y
sensation

VI. LABORATORY RESULTS

NURSING CARE PLAN

ASSESSMENT NURSINGDIAGNOSIS GOALS & NURSING
DATA (Subjective (Problem & Etiology) OBJECTIVES INTERVENTIONS EVALUATION
& Ojective Cues) & RATIONALE
• After
Excess fluid volume After 16 hours of • Determine 16
Subjective: related to compromised nursing patient’s hours
“Na- admit siya regulatory mechanisms intervention, the specific of
kay grabe na iyang from renal patient will be able renal cause nursing
kidney tungod sa insufficiency. to: of fluid interve
excess ntion,
iyang Diabetes” as • Have
allow the
verbalized by the equivalen
identificatio patient
husband. tintake &
n of source was
output
to provide portally
for achiev
Ojective: • With no
appropriate e to
• Drowsy edema,
treatment have
and will
• Restless period. equival
be able to
• Blury • Measure ent
maintain
vission intake & I&O,
her
output , this with no
specific
provides edema
dry
accurate and will
weight.
comparison be able
of patient’s maintai
fluid status. n her
• Weigh specific
reaction dry
everyday at weight
the same .
time, same
scale, this
helps to
provide
data to
correlate
with I & O.
• Maintain
patient’s
dietary
restriction
including
fluid
• Administer
diuretics as
ordered,to
excrete
sodium.
• Prepare
patient for
and assist
with
hemodialysi
s procedure
as
warranted
to remove
toxins
fromsystem
ic
circulation
by osmosis,
diffussion,
and
convection
or
ultrafiltratio
n.
 NURSING CARE PLAN

ASSESSTMENT NURSING GOALS & NURSING EVALUATION

DATA DIANOSIS OBJECTIVES INTERVENTIONS
(Subjective & (Prolem & AND
Objective Cues) Etiology) RATIONALE

Subjective: Risk for injury After 16 hours • Assess After 16 hours of

“Na-admit siya R/T Renal of nursing patient for nursing
kay grabe na insufficiency & intervention, the weakness, intervention the
iyang kidney failure. patient will flaudity of patient partially
tungod sa iyang have electrolyte muscles, balances the
diabetes” as imbalances abdominal electrolyte with
cramping
verbalized by the corrected & no respiratory
& irregular
husband. maintained with dysfunction,
pulse
the absense of because urinary infection
Objective: respiratory this & bleeding
• Drowsy dysfunction, indicates tendency.
• Restless urinary hyperkale-
• Blury infection or mia
vision bleeding
tendency. • Assess
patient for
lethargy,
weakness,
restlessne
ss or
increased
tendon
reflexes,
because
this
indicates
hypernatr
emia as
nephrons
lose
ability to
filter
sodium.

• Restrict
sodium,
potassium
& protein
intake diet
to as
ordered
amount to
avoid
sodium &
potassium
retention.
 NURSING CARE PLAN

ASSESSMENT NURSING GOALS & NURSING EVALUATION

DATA DIAGNOSIS OBJECTIVES INTERVENTIONS
(Subjective & (Problem & AND RATIONALE
Objective) Etiology )
Subjective: Activity After 8 hours of • Encourage After 8 hours of
“Dili na kaayo Intolerance nursing patient not nursing
siya kabuhat sa R/T Renal intervention, the to be intervention,
iyang gusto, dili Failure patient will be able depressed the patient was
pareha sauna” as Associateed to: to able to alleviate
verbalized by the with • Alleviate improved the depression
the her
husband. depression. felt & was able
depressio condition.
to have positive
n felt. outlook about
• Transfer
Objective: her her condition &
• Restless • Positive did not lose
outlook attention &
• Drowsy not to hope.
about her
• Blurry follow on
condition
Vision negative
& never
lose hope. ones.

• Provide
health
teachings
about her
condition
to achieve
cooperatio
n.

IX. HEALTH TEACHINGS AND DISCHARGE PLAN

The patient and so with the watcher was taught about the importance of medications

prescribed by the physician such as cefuroxime to bend his bacterial cell wall

membrane causing cell death (anti-infectives) , omeprazole to suppress his gastric acid

secretion by specific inhibition of the hydrogen potassium enzyme system at the

secretory surface of the gastric parietal cells that blocks the final step of acid production

(anti-secretory agent), Benadryl and diphenhydramine to competitively blocks the

effects of histamine at H1-receptro site, for anti-pruritic and sedative effects

(antihistamine) compliance of these medication was being emphasize thoroughly to the

watcher.

The watcher was instructed to keep the patient free from any stressful things and

maintaining the environment quiet. Upon the admission, series of laboratories test that

the patient had undergone accompanied with the close monitoring of vital signs.

Medications to treat underlying condition were given at ordered schedules.

The researchers educated the watcher regarding the condition of the patient. Since the

patient has liver cirrhosis, the researchers informed the watcher that the patient will

experience some unusualities in regards with his conditions. For home management,

the researchers instructed the watcher to provide patient complete bed rest to avoid

stressful activities. To comply with medication regimen, to provide good ventilation and

peaceful environment in and order for the patient to have adequate rest. Then report

any unusualities for immediate treatment. If the patient is to be discharge, the

researchers instructed the watcher to keep on visiting their physician to monitor

patient’s health and condition.

X. Related Learning Experience

The experiences we have gained were awfully out of depiction for the reason that the

accurate or the proper assimilation of different field of theoretical knowledge must have

to be seen through application in the clinical scenery. As usually felt by the first timer

students in the NMMC area, the first 2 days of our duty was terribly an exhausting part

of our duty, it is so far different in other hospitals that we are assigned to.
But at the same time we are also aiming for our progressive change. In fact we have

been reprimanded by our clinical instructor which has stimulated our mind to refrain

from doing mistakes, in some way we are still thankful for being reprimanded for the fact

of reaching our aim to have the progressive change.

A task of making a case study triggered us to know further as regards to managing our

time to finish our requirements as well as giving time for the other subjects. By means of

making our case study we also have much fun, brain storming activity, new knowledge

imparted and discovered. Aside from that we also learn to be more responsible in

organizing our work and in focusing by the task that was given to us. Furthermore, the

manner of research, reading and surfing in the internet are main reason for us to finally

be able to come up with this heartily made output.

Through this, we can now be able to provide quality care to the patient in relation to this

case study. Patients are the audience of our field they sometimes display an attitude of

being pleased by the nursing student’s performance or more often were discontented

however we still have the spirit of professionalism and having the positive attitude

towards certain situation. A nurse must be the one to adjust or adapt not the patient.

Last but not least, this study wouldn’t be possible without the help of our Clinical

Instructor and Practicing Clinical Instructors who were there to support us. To our

families for their understanding when we were away from our homes while doing this

study and sometimes go home late at night just to come up with this output. And most

especially, to our Almighty God who has been there to give us the never ending

enlightenment and the inestimable wisdom that were showered upon us.