DEDICATION

We heartily dedicate this case study to:

Our parents and families, who fully supported us in

making this case study, encouraging us in order for us to make
this case study a possibility.
To our class adviser for her powerful urge in
motivating us to complete this study.
To our classmates and friends for giving us
inspiration and encourage them with this case study.
And most of all to our Almighty Heavenly Father and
to His son Jesus Christ for never ending guidance and support.
And we the son and daughters of Christ, return the entire honour
in His name.

1
 ACKNOWLEDGMENT

We acknowledge these following persons that aid our compilation:

- To God almighty that bestowed wisdom upon us

- To our loving family
- To our most respected dean of nursing department
- To our clinical instructors that patiently thought us to
learn
- Our dear classmates whom became our closest friends

2
 INTRODUCTION

Leptospirosis is an infection caused by corkscrew-

shaped bacteria called Leptospira. Signs and symptoms can range from
none to mild such as headaches, muscle pains, and fevers; to severe
with bleeding from the lungs or meningitis. If the infection causes
the person to turn yellow, have kidney failure and bleeding, it is
then known as Weil's disease. If it also causes bleeding into the
lungs then it is known as severe pulmonary hemorrhage syndrome.
The bacteria that cause leptospirosis are spread through the urine
of infected animals, which can get into water or soil and can survive
there for weeks to months. Many different kinds of wild and domestic
animals carry the bacterium (cattle, pigs, horses, dogs, rodents and
wild animals). When these animals are infected, they may have no
symptoms of the disease. Infected animals may continue to excrete the
bacteria into the environment continuously or every once in a while
for a few months up to several years. Humans can become infected
through:

 Contact with urine (or other body fluids, except saliva) from
infected animals.
 Contact with water, soil, or food contaminated with the urine of
infected animals

The bacteria can enter the body through skin or mucous membranes
(eyes, nose, or mouth), especially if the skin is broken from a cut or
scratch. Drinking contaminated water can also cause infection.
Outbreaks of leptospirosis are usually caused by exposure to
contaminated water, such as floodwaters. Person to person transmission
is rare. Without treatment, Leptospirosis can lead to kidney damage,
meningitis (inflammation of the membrane around the brain and spinal
cord), liver failure, respiratory distress, and even death. In
relation, acute kidney (renal) failure happens when your kidneys

3
suddenly lose the ability to eliminate excess salts, fluids, and waste
materials from the blood. This elimination is the core of your
kidneys’ main function. Body fluids can rise to dangerous levels when
kidneys lose their filtering ability. The condition will also cause
electrolytes and waste material to accumulate in your body, which can
also be life-threatening.

Mr. A is a rare case of Acute Renal Failure secondary to

Leptospirosis, as diagnosed by his attending physician, admitted last
February 22, 2018 at Surigao Medical Hospital. He is 19 years old,
single and a student, residing at Brgy. Hayanggabon, Claver Surigao
Del Norte. Within our duty to Medical Hospital, we received Mr. A
lying on his bed with oxygen tank attached to his nostrils to aid
resuscitation with abnormal yellow skin complexion and constantly
coughing while obtaining his vital signs. Within weeks of our duty in
Surigao Medical Hospital patient is progressing in recovery to his
health condition. Day by day patient can mobilize and can perform some
activity like eating and going to comfort room by himself.

4
 REVIEW OF RELATED LITERATURE

Acute kidney failure is also called acute kidney injury or acute

renal failure. Acute kidney failure happens when your kidneys suddenly
lose the ability to eliminate excess salts, fluids, and waste
materials from the blood. This elimination is the core of your
kidneys’ main function. Body fluids can rise to dangerous levels when
kidneys lose their filtering ability. The condition will also cause
electrolytes and waste material to accumulate in your body, which can
also be life-threatening.
More recently also called acute kidney injury. Many times this
is reversible but depending on the cause and severity, it may be
irreversible and lead to chronic renal failure or chronic kidney
disease. Normally, the kidneys filter the blood and remove waste and
excess salt and water. Acute kidney failure is when the kidneys
suddenly stop working. Acute renal failure can be due to many
different causes. Generally these causes can be divided into three
categories. Pre-renal means the cause is before the kidney or
glomerulus. Generally, this is caused by a decrease in the amount of
blood that gets to the kidney. Examples include heart failure, liver
failure, shock. Another class of acute renal failure is post-renal. In
this type, there is an obstruction to the flow of urine from the
kidney.
The most common example is prostate problems in men, urinary
tract cancers, which directly obstruct the urine flow, or cancers in
the abdomen or pelvis that push on the ureters that carry the urine
from the kidney to the bladder. The last category is termed renal and
is due to damage to the kidney itself, especially the filtering units
(glomeruli) or the tubules leading from the glomeruli. Examples of
renal injury include infections, cancer, some medications and other
nephrotoxins, and auto-immune diseases. As well, primary kidney
diseases (glomerulonephritis and nephrotic diseases, such as
membranous nephropathy) can damage the kidneys and cause acute renal
failure as well as chronic renal failure.
Treatment generally is directed at support of blood pressure and
flow of the blood to the kidneys. As well, any offending agents should
be discontinued and any nephrotoxic agents should be avoided. Some
cases will be severe enough to require dialysis to remove toxins from
the body until the kidneys can recover. Sometimes, the damage is
severe enough that it is irreversible and the patient will require
long-term dialysis or renal transplant.

Causes

There are many possible causes of kidney damage. They include:

 Acute tubular necrosis (ATN)

 Autoimmune kidney disease

5
  Blood clot from cholesterol (cholesterol emboli)

 Decreased blood flow due to very low blood pressure, which

can result from burns, dehydration, hemorrhage, injury,
septic shock, serious illness, or surgery

 Disorders that cause clotting within the kidney blood

vessels

 Infections that directly injure the kidney, such as acute

pyelonephritis or septicemia

 Pregnancy complications, including placenta abruption or

placenta previa

 Urinary tract blockage

 Illicit drugs such as cocaine and heroine

 Medicines including non-steroidal anti-inflammatory drugs

(NSAIDs), certain antibiotics and blood pressure medicines,
intravenous contrast (dye), some cancer and HIV drugs

Symptoms

Symptoms of acute kidney failure may include any of the

following:

 Bloody stools

 Breath odor and metallic taste in the mouth

 Bruising easily

 Changes in mental status or mood

 Decreased appetite

 Decreased sensation, especially in the hands or feet

 Fatigue or slow sluggish movements

 Flank pain (between the ribs and hips)

 Hand tremor

 Heart murmur

6
  High blood pressure

 Nausea or vomiting, may last for days

 Nosebleeds

 Persistent hiccups

 Prolonged bleeding

 Seizures

 Shortness of breath

 Swelling due to the body keeping in fluid (may be seen in

the legs, ankles, and feet)

 Urination changes, such as little or no urine, excessive

urination at night, or urination that stops completely

Exams and Tests

The health care provider will examine you.

Tests to check how well your kidneys are working include:

 BUN

 Creatinine clearance

 Serum creatinine

 Serum potassium

 Urinalysis

Other blood tests may be done to find the underlying cause of

kidney failure.

A kidney or abdominal ultrasound is the preferred test for

diagnosing a blockage in the urinary tract. X-ray, CT scan, or
MRI of the abdomen can also tell if there is a blockage.

7
Treatment

Once the cause is found, the goal of treatment is to help your

kidneys work again and prevent fluid and waste from building up
in your body while they heal. Usually, you will have to stay
overnight in the hospital for treatment.

The amount of liquid you drink will be limited to the amount of

urine you can produce. You will be told what you may and may not
eat to reduce the buildup of toxins that the kidneys would
normally remove. Your diet may need to be high in carbohydrates
and low in protein, salt, and potassium.

You may need antibiotics to treat or prevent infection. Water

pills (diuretics) may be used to help remove fluid from your
body.

Medicines will be given through a vein to help control your

blood potassium level.

You may need dialysis. This is a treatment that does what

healthy kidneys normally do -- rid the body of harmful wastes,
extra salt, and water. Dialysis can save your life if your
potassium levels are dangerously high. Dialysis will also be
used if:

 Your mental status changes

 You develop pericarditis

 You retain too much fluid

 You cannot remove nitrogen waste products from your body

Dialysis will most often be short term. In some cases, the

kidney damage is so great that dialysis is needed permanently.

When to Contact a Medical Professional

8
Call your provider if your urine output slows or stops or you
have other symptoms of acute kidney failure.

Prevention

To prevent acute kidney failure:

 Health problems such as high blood pressure or diabetes

should be well controlled.

 Avoid drugs and medicines that can cause kidney injury.

9
 NURSING HEALTH HISTORY

Biographic Data:

Hospital : Surigao Medical Center

Case No. : 112102
Room : SP21
Name of Patient : Patient A
Age : 19
Sex : Male
Civil Status : Single
Address : P-4 Brgy. Hayanggabon Claver,SDN
Occupation : Student
Date of Birth : August 28, 1998
Religion : Roman Catholic
Height : 5”5
Weight : 60 kg

Admission Data:

Mode of Transmission : Wheelchair

Date and Time of Admission : February 22, 2017
8:45 Am
Vital Signs upon admission
 Heart Rate : 94
 Respiratory Rate : 24
 Blood Pressure : 80/50
 Body Temperature : 36

Admitting Physician :Carina B. Benitez,MD

Attending Physician :Manolito C.Go ,MD
Chief Compliant : JAUNDICE AND FEVER
Final Diagnosis :ACUTE RENAL FAILURE SECONDARY TO
LEPTOSPIROSIS

10
 HISTORY OF PRESENT ILLNESS

Present condition started about 2 weeks prior to

admission. Patient claimed that he had calf pain, nausea and
vomiting. Patient was conscious and afebrile.

PAST HEALTH HISTORY

I- Childhood Illness

Patient verbalized at the age of 14 he experienced Mumps, and

chicken pox. Fever with colds and cough during his preschool years.
No history of serious complication until hospitalization.

II – Childhood Immunization

Patient verbalized of receiving childhood immunization such

as BCG, DPT, and OPV. Haven’t known of Hepa Vaccines and other
immunization aside from mentioned.

HISTORY OF HOSPITALIZATION
III- Medical History
No major problem experience regarding diseases, haven’t been
admitted to hospitals ever since the recent admission as verbalized
by Mr. A

IV – Surgical History

Haven’t undergone surgery ever since as verbalized by him.

V- Accidents and Injuries

Patient experienced minor cuts and bruises while playing

basketball. Patient experienced minor cut in his fingers while
cutting and pealing fruits or vegetables in their house. Never
experience dangerous and serious problems that injures and harm
him. Never experience motor or car accidents.

VII-Sexual History

Patient verbalized that he had never been engaged into sex

and never experienced sexual intercourse.

11
VIII-Allergies

Patient had no allergies to food and drugs. Never experience

skin allergy or internal allergies.

XI- Family Health History

Patient stated that his father is diabetic and relatives to

father’s side. His mother has no hereditary disease and terminal
illness that can pass through generation.

X- Personal Habits

Patient loved playing basketball and going out with friends.

Occasionally mingles and go out with friends to party. He likes to
take a long walk within their barangay. Inside their house he loves
to watch TV and listen to music.

XI – Diet

Patient stated that he occasionally drinks liquor such as

tanduay and emperador. He always drinks soft drinks instead of
water, minimal water intake daily as verbalized by the mother and
him. No special diet or specific food intake as stated by him, he
likes to eat anything serve but minimal in vegetables.

XII- Sleep/Rest pattern

Patient usually sleeps 8 hours a day sometimes takes an

afternoon nap after playing basketball. No difficulty in sleeping,
uses music in his pone as remedy to relax and sometimes watching
TV makes him fall asleep at their couch as stated by him and his
mother.

XIII-Elimination Pattern

Patient usually defecates every other day and urinates twice

in a day. He had no difficulty urinating and defecating. Patient
has poor skin moisture and dry skin.

12
SOCIAL DATA

XIV-Family Relationship/Friendship

His family, consist of five siblings and his mother, his

father died with diabetes mellitus at the age of 57 and his
youngest sister followed for unknown illness at the age of 6 months
two years before hospitalization and. His mother is a member of
4p’s and his siblings work to finance their living.

XV- Educational History

Patient is a grade 11 student, studying in their

municipality, active in school activities such as basketball. Can
speak and understand simple English and can calculate some
mathematical problems.

XVI- Occupational History

Patient is still a student and excused in classes due to

hospitalization.

XVII- Economic Status

Patient is supported by his mother and sibling, his mother is

a member in Phil health and utilizes membership for medical
purposes. Their family belong to low economic status.

XVIII-Patterns of Health Care

Patient is seen and monitored by his physician and

adequate care is being provided by health care team members of
the hospital institution.

13
 REVIEW OF SYSTEM

INTEGUMENTARY SYSTEM
 No history of skin infection as claimed by the patient
 With history of dandruff
 Brown skin complexion
 Patient has intact skin with good skin turgor
 Slightly swelling on her lower extremities and part of her
faces
 Skin is warm to touch
 Patient has no lesion and bruises.

RESPIRATORY SYSTEM
 No complaints of weaknesses and being exhaust on simple
activity.
 No appearance of difficulty in breathing
 Has no history of pneumonia, asthma or emphysema.
 No abnormality sounds upon auscultation

CARDIOVASCULAR SYSTEM

 No complaints of weaknesses and being exhaust on simple

activity.
 No complaints of palpitations.
 No history of chest pain.
 Has no history of hypertension, as claimed
 Patient’s blood pressure is
 Patient’s pulse rate is beat per minute

GENITOURINARY SYSTEM
 Urinates 2 times a day as claimed by the patient.
 No pain upon voiding.
 Color of the urine yellow
 No history of UTI.

GASTROINTESTINAL SYSTEM
 With no complaints of constipation as stated by the patient.
 Patient has no abnormality in defecating
 No abnormal bowel sounds, as claimed
 Patient With no history of hemorrhoids and rectal bleeding.

14
REPRODUCTIVE SYSTEM
 No erectile dysfunction
 Penis has no any lesion or any wound
 Scrotum is symmetrical
 Never engaged with sex.
MUSCULOSKELETAL SYSTEM
 With complaints of weakness
 With complaints of fatigue
 With complaints of lower back pain
 With complaints of pain in the lower extremities
 No history of fracture or any injury

ENDOCRINE SYSTEM
 Patient has no history of thyroid problem

CIRCULATORY SYSTEM
 With no history of painful tonsils
 With no history of having nodules on the neck
 No history of bleeding problems
 No history of hypertension
 With low blood pressure

NEUROLOGIC SYSTEM
 Patient is conscious to time, place and people
 Has no history of seizure
 Coherent and responsive

15
 PHYSICAL EXAMINATION

Skin

Inspection
 skin is yellow in color or Jaundice
 Has closed intact skin
 No lesions
 Slightly swelling in the lower extremities and past of her
face
Palpation
 Skin is warm to touch
 Has a good skin turgor

Hair
Inspection
 Color of hair is black
 No infestation of parasites
 With dandruff
 Has a short and straight hair

Nails
Inspection
 Pink nail bed
 Nails are completely distributed in her fingers
 Patient has no cracked or nail injuries

Skull and face

Inspection
 Facial skin uniform in color
 Normal facial movement
 No lesions
 Skull shape is round and symmetric

Eyes
Inspection
 Both eyes are symmetrical
 Eyelashes equally distributed, curled slightly outward
 Pupils are equally rounded
 The pupil was brown in color with yellow conjunctiva
 Blinking reflex was normal and functional
 Peripheral reflexes are normal and functional

16
  Vision acuity is in normal range and can read the Snellen
chart
 Patient is not using any glasses and contact lenses as
visional aid

Ears
Inspection
 Auricles yellow in color as facial skin, symmetrical and are
aligned with outer canthus of eye
 Pinna recoils after it is folded
 No cerumen
 Able to hear spoken words clearly
 No discharges

Nose
Inspection
 Has the same color as facial skin
 Not tender, no lesion
 No discharges
 Straight and symmetrical
 Able to identify odors like alcohol, cologne and coffee

Mouth and throat

Inspection
 Lips are dry and pale
 Lips are symmetrical
 Tongue moves freely
 Gums is dark in color

17
 CLINICAL LABORATORY

Patient Name: Patient M Date: Jan. 9, 2017

Room No. : MW-G3 Age : 17 y/o

Hematology

EXAM NAME RESULT UNIT NORMAL VALUE SIGNIFICANCE

HEMOGLOBIN 8.8 g/dL 12.0-17.0 Anemia

HEMATOCRIT 24.0 % 37-54 Anemia
RBC 3.0 x10^12/L 4.0-6.0 Anemia
MCV 85.4 fL 87+-5 Normal
MCH 31.3 Pg 29+-2 Normal
MCHC 36.7 g/dL 34+-2 Normal
RDW 13.2 11.6-14.6 Normal
PLATELET COUNT 198 x10^9/L 150-450 Normal
WBC 15.0 x10^9/L 4.5-10.0 Infection

DIFFERENTIAL COUNT
BANDS % 0-5
SEGMENTERS 79.8 % 50-70 neutrophilia
LYMPHOCYTES 11.7 % 20-40 lymphocytopenia
MID CELLS 8.5 % -------
MONOCYTES % 0-7
EOSINPHILS % 0-5
BASOPHILS % 0-1

BLOOD TYPE
CLOTTING TIME 3-6 MINUTES
BLEEDING TIME 1-3 MINUTES
ESR mm/hr MALE<10 FEMALE<20
RETICULOCYTE % 0.5-1.5 ADULT
COUNT
1.5-2.5 NEWBORN
REMARKS: DONE @6AM 1/09/17

18
 Patient Name: Date: Jan. 10, 2017
Room No. : MW-G3 Age : 17 y/o

Hematology

EXAM NAME RESULT UNIT NORMAL VALUE SIGNIFICANCE

HEMOGLOBIN 8.3 g/dL 12.0-17.0 Anemia

HEMATOCRIT 23.1 % 37-54 Anemia
RBC 2.67 x10^12/L 4.0-6.0 Anemia
MCV 86.7 fL 87+-5 Normal
MCH 31.1 pg 29+-2 Normal
MCHC 35.9 g/dL 34+-2 Normal
RDW 13.8 11.6-14.6 Normal
PLATELET COUNT 263 x10^9/L 150-450 Normal
WBC 16.2 x10^9/L 4.5-10.0 Infection

DIFFERENTIAL
COUNT
BANDS % 0-5
SEGMENTERS 83.9 % 50-70 neutrophilia
LYMPHOCYTES 9.0 % 20-40 lymphocytopenia
MID CELLS 7.1 %
MONOCYTES % 0-7
EOSINPHILS % 0-5
BASOPHILS % 0-1

BLOOD TYPE
CLOTTING TIME 3-6 MINUTES
BLEEDING TIME 1-3 MINUTES
ESR mm/hr MALE<10 FEMALE<20
RETICULOCYTE % 0.5-1.5 ADULT
COUNT
1.5-2.5 NEWBORN
REMARKS: DONE @ 7:50 AM

19
Patient Name: PATIENT M. Date : Jan.9,2017
Room No. : MW-G3 Age : 17 y/o
Gender: M
BLOOD CHEMISTRY

TEST RESULT REFERENCE / UNIT SIGNIFICANCE

CREATININE 1.73 0.73 – 1.36 Increased
mg/dl(H)
BLOODUREA 7.48 1.70-8.30 mmol/L Normal
NITROGEN
SODIUM 137 135.00-148.00 Normal
mmol/L
POTASSIUM 3.4 3.50- Hypokalemia
5.30mmol/L(L)
IONIZED CALCIUM 1.11 1.13-1.35 Decreased
mmol/L(L)

LUCKYLU SASTINE CABANAS #0073801

Medical Technologist

Patient Name: PATIENT M. Date : Jan.10,2017

Room No. : MW-G3 Age : 17 y/o
Gender: M
BLOOD CHEMISTRY
TEST RESULT REFERENCE / UNIT SIGNIFICANCE
CREATININE 2.03 0.73 – 1.36 Increased
mg/dl(H)
BLOODUREA 9.32 1.70-8.30 mmol/L Increased
NITROGEN
SODIUM 144 135.00-148.00 Normal
mmol/L
POTASSIUM 4.2 3.50- Normal
5.30mmol/L(L)
IONIZED CALCIUM 1.10 1.13-1.35 Decreased s
mmol/L(L)

LUCKYLU SASTINE CABANAS #0073801

Medical Technologist.

20
 ANATOMY AND PHYSIOLOGY OF THE LIVER AND KIDNEY

The liver is a vital

organ of vertebrates and
some other animals.In
the human, it is located
in the upper
right quadrant of
the abdomen, below
the diaphragm. The liver
has a wide range of
functions, including detoxification of
various metabolites, protein synthesis, and the production
of biochemicals necessary for digestion.
The liver is a gland and plays a major role in metabolism with
numerous functions in the human body, including regulation
of glycogen storage, decomposition of red blood cells, plasma
protein synthesis, hormone production, and detoxification.It is
an accessory digestive gland and produces bile,
an alkaline compound which aids in digestion via
the emulsification of lipids. The gallbladder, a small pouch
that sits just under the liver, stores bile produced by the
liver.[4] The liver's highly specialized tissue consisting of
mostly hepatocytes regulates a wide variety of high-volume
biochemical reactions, including the synthesis and breakdown of
small and complex molecules, many of which are necessary for
normal vital functions.[5] Estimates regarding the organ's total
number of functions vary, but textbooks generally cite it being
around 500.
Terminology related to the liver often starts in hepat- from
ἡπατο-, the Greek word for liver.
There is currently no way to compensate for the absence of liver
function in the long term, although liver dialysis techniques
can be used in the short term. Artificial livers are yet to be
developed to promote long term replacement in the absence of the
liver. As of now,liver transplantation is the only option for
complete liver failure.
Gross Anatomy
The liver is a roughly triangular organ that extends across the
entire abdominal cavity just inferior to the diaphragm. Most of
the liver’s mass is located on the right side of the body where
it descends inferiorly toward the right kidney. The liver is
made of very soft, pinkish-brown tissues encapsulated by a
connective tissue capsule. This capsule is further covered and

21
 reinforced by the peritoneum of the abdominal cavity, which
protects the liver and holds it in place within the abdomen.
The peritoneum connects the liver in 4 locations: the coronary
ligament, the left and right triangular ligaments, and the
falciform ligament. These connections are not true ligaments in
the anatomical sense; rather, they are condensed regions of
peritoneal membrane that support the liver.

 The wide coronary ligament connects the central superior portion

of the liver to the diaphragm.
 Located on the lateral borders of the left and right lobes,
respectively, the left and right triangular ligaments connect
the superior ends of the liver to the diaphragm.
 The falciform ligament runs inferiorly from the diaphragm across
the anterior edge of the liver to its inferior border. At the
inferior end of the liver, the falciform ligament forms the
round ligament (ligamentum teres) of the liver and connects the
liver to the umbilicus. The round ligament is a remnant of the
umbilical vein that carries blood into the body during fetal
development.
The liver consists of 4 distinct lobes – the left, right,
caudate, and quadrate lobes.

 The left and right lobes are the largest lobes and are separated
by the falciform ligament. The right lobe is about 5 to 6 times
larger than the tapered left lobe.
 The small caudate lobe extends from the posterior side of the
right lobe and wraps around the inferior vena cava.
 The small quadrate lobe is inferior to the caudate lobe and
extends from the posterior side of the right lobe and wraps
around the gallbladder.
Bile Ducts
The tubes that carry bile through the liver and gallbladder are
known as bile ducts and form a branched structure known as the
biliary tree. Bile produced by liver cells drains into
microscopic canals known as bile canaliculi. The countless bile
canaliculi join together into many larger bile ducts found
throughout the liver.
These bile ducts next join to form the larger left and
right hepatic ducts, which carry bile from the left and right
lobes of the liver. Those two hepatic ducts join to form the
common hepatic duct that drains all bile away from the liver.
The common hepatic duct finally joins with the cystic duct from
the gallbladder to form the common bile duct, carrying bile to
the duodenum of the small intestine. Most of the bile produced
by the liver is pushed back up the cystic duct by peristalsis to

22
 arrive in the gallbladder for storage, until it is needed for
digestion.
Blood Vessels
The blood supply of the liver is unique among all organs of the
body due to the hepatic portal vein system. Blood traveling to
the spleen, stomach, pancreas, gallbladder,
and intestines passes through capillaries in these organs and is
collected into the hepatic portal vein. The hepatic portal vein
then delivers this blood to the tissues of the liver where the
contents of the blood are divided up into smaller vessels and
processed before being passed on to the rest of the body. Blood
leaving the tissues of the liver collects into the hepatic
veins that lead to the vena cava and return to the heart. The
liver also has its own system of arteries and arterioles that
provide oxygenated blood to its tissues just like any other
organ.
Lobules
The internal structure of the liver is made of around 100,000
small hexagonal functional units known as lobules. Each lobule
consists of a central vein surrounded by 6 hepatic portal veins
and 6 hepatic arteries. These blood vessels are connected by
many capillary-like tubes called sinusoids, which extend from
the portal veins and arteries to meet the central vein like
spokes on a wheel.
Each sinusoid passes through liver tissue containing 2 main cell
types: Kupffer cells and hepatocytes.

 Kupffer cells are a type of macrophage that capture and break

down old, worn out red blood cells passing through the
sinusoids.
 Hepatocytes are cuboidal epithelial cells that line the
sinusoids and make up the majority of cells in the liver.
Hepatocytes perform most of the liver’s functions – metabolism,
storage, digestion, and bile production. Tiny bile collection
vessels known as bile canaliculi run parallel to the sinusoids
on the other side of the hepatocytes and drain into the bile
ducts of the liver.
Digestion
The liver plays an active role in the process of digestion
through the production of bile. Bile is a mixture of water, bile
salts, cholesterol, and the pigment bilirubin. Hepatocytes in
the liver produce bile, which then passes through the bile ducts
to be stored in the gallbladder. When food containing fats
reaches the duodenum, the cells of the duodenum release the
hormone cholecystokinin to stimulate the gallbladder to release
bile. Bile travels through the bile ducts and is released into
the duodenum where it emulsifies large masses of fat. The

23
emulsification of fats by bile turns the large clumps of fat
into smaller pieces that have more surface area and are
therefore easier for the body to digest.
Bilirubin present in bile is a product of the liver’s digestion
of worn out red blood cells. Kupffer cells in the liver catch
and destroy old, worn out red blood cells and pass their
components on to hepatocytes. Hepatocytes metabolize hemoglobin,
the red oxygen-carrying pigment of red blood cells, into the
components heme and globin. Globin protein is further brokendown
and used as an energy source for the body. The iron-containing
heme group cannot be recycled by the body and is converted into
the pigment bilirubin and added to bile to be excreted from the
body. Bilirubin gives bile its distinctive greenish color.
Intestinal bacteria further convert bilirubin into the brown
pigment stercobilin, which gives feces their brown color.
Metabolism
The hepatocytes of the liver are tasked with many of the
important metabolic jobs that support the cells of the body.
Because all of the blood leaving the digestive system passes
through the hepatic portal vein, the liver is responsible for
metabolizing carbohydrate, lipids, and proteins into
biologically useful materials.
Our digestive system breaks down carbohydrates into the
monosaccharide glucose, which cells use as a primary energy
source. Blood entering the liver through the hepatic portal vein
is extremely rich in glucose from digested food. Hepatocytes
absorb much of this glucose and store it as the macromolecule
glycogen, a branched polysaccharide that allows the hepatocytes
to pack away large amounts of glucose and quickly release
glucose between meals. The absorption and release of glucose by
the hepatocytes helps to maintain homeostasis and protects the
rest of the body from dangerous spikes and drops in the blood
glucose level. (See more about glucose in the body.)
Fatty acids in the blood passing through the liver are absorbed
by hepatocytes and metabolized to produce energy in the form of
ATP. Glycerol, another lipid component, is converted into
glucose by hepatocytes through the process of gluconeogenesis.
Hepatocytes can also produce lipids like cholesterol,
phospholipids, and lipoproteins that are used by other cells
throughout the body. Much of the cholesterol produced by
hepatocytes gets excreted from the body as a component of bile.

Dietary proteins are broken down into their component amino

acids by the digestive system before being passed on to the
hepatic portal vein. Amino acids entering the liver require
metabolic processing before they can be used as an energy
source. Hepatocytes first remove the amine groups of the amino

24
acids and convert them into ammonia and eventually urea. Urea is
less toxic than ammonia and can be excreted in urine as a waste
product of digestion. The remaining parts of the amino acids can
be broken down into ATP or converted into new glucose molecules
through the process of gluconeogenesis.

Detoxification
As blood from the digestive organs passes through the hepatic
portal circulation, the hepatocytes of the liver monitor the
contents of the blood and remove many potentially toxic
substances before they can reach the rest of the body. Enzymes
in hepatocytes metabolize many of these toxins such as alcohol
and drugs into their inactive metabolites. And in order to keep
hormone levels within homeostatic limits, the liver also
metabolizes and removes from circulation hormones produced by
the body’s own glands.
Storage
The liver provides storage of many essential nutrients,
vitamins, and minerals obtained from blood passing through the
hepatic portal system. Glucose is transported into hepatocytes
under the influence of the hormone insulin and stored as the
polysaccharide glycogen. Hepatocytes also absorb and store fatty
acids from digested triglycerides. The storage of these
nutrients allows the liver to maintain the homeostasis of blood
glucose. Our liver also stores vitamins and minerals - such as
vitamins A, D, E, K, and B12, and the minerals iron and copper -
in order to provide a constant supply of these essential
substances to the tissues of the body.
Production
The liver is responsible for the production of several vital
protein components of blood plasma: prothrombin, fibrinogen, and
albumins. Prothrombin and fibrinogen proteins are coagulation
factors involved in the formation of blood clots. Albumins are
proteins that maintain the isotonic environment of the blood so
that cells of the body do not gain or lose water in the presence
of body fluids.
Immunity
The liver functions as an organ of the immune system through the
function of the Kupffer cells that line the sinusoids. Kupffer
cells are a type of fixed macrophage that form part of the
mononuclear phagocyte system along with macrophages in the
spleen and lymph nodes. Kupffer cells play an important role by
capturing and digesting bacteria, fungi, parasites, worn-out
blood cells, and cellular debris. The large volume of blood
passing through the hepatic portal system and the liver allows
Kupffer cells to clean large volumes of blood very quickly.

25
 ANATOMY OF KIDNEY

The kidneys are a pair of organs found

along the posterior muscular wall of the
abdominal cavity. The left kidney is
located slightly more superior than the
right kidney due to the larger size of
the liver on the right side of the body.
Unlike the other abdominal organs, the
kidneys lie behind the peritoneum that
lines the abdominal cavity and are thus
considered to be retroperitoneal organs.
The ribs and muscles of the back protect the kidneys from
external damage. Adipose tissue known as perirenal fat surrounds
the kidneys and acts as protective padding.

Structure

The kidneys are bean-shaped with the convex side of each organ
located laterally and the concave side medial. The indentation
on the concave side of the kidney, known as the renal hilus,
provides a space for the renal artery, renal vein, and ureter to
enter the kidney.
A thin layer of fibrous connective tissue forms the renal
capsule surrounding each kidney. The renal capsule provides a
stiff outer shell to maintain the shape of the soft inner
tissues.

Deep to the renal capsule is the soft, dense, vascular renal

cortex. Seven cone-shaped renal pyramids form the renal medulla
deep to the renal cortex. The renal pyramids are aligned with
their bases facing outward toward the renal cortex and their
apexes point inward toward the center of the kidney.
Each apex connects to a minor calyx, a small hollow tube that
collects urine. The minor calyces merge to form 3 larger major
calyces, which further merge to form the hollow renal pelvis at
the center of the kidney. The renal pelvis exits the kidney at
the renal hilus, where urine drains into the ureter.

Blood Supply

1. The renal arteries branch directly from the abdominal aorta and
enter the kidneys through the renal hilus.
2. Inside our kidneys, the renal arteries diverge into the smaller
afferent arterioles of the kidneys.
3. Each afferent arteriole carries blood into the renal cortex,
where it separates into a bundle of capillaries known as a
glomerulus.
26
4. From the glomerulus, the blood recollects into smaller efferent
arterioles that descend into the renal medulla.
5. The efferent arterioles separate into the peritubular
capillaries that surround the renal tubules.
6. Next, the peritubular capillaries merge to form veins that merge
again to form the large renal vein.
7. Finally, the renal vein exits the kidney and joins with
the inferior vena cava, which carries blood back to the heart.

The Nephron

Each kidney contains around 1 million individual nephrons, the

kidneys’ microscopic functional units that filter blood to
produce urine. The nephron is made of 2 main parts: the renal
corpuscle and the renal tubule.
Responsible for filtering the blood, our renal corpuscle is
formed by the capillaries of the glomerulus and the glomerular
capsule (also known as Bowman’s capsule). The glomerulus is a
bundled network of capillaries that increases the surface area
of blood in contact the blood vessel walls. Surrounding the
glomerulus is the glomerular capsule, a cup-shaped double layer
of simple squamous epithelium with a hollow space between the
layers. Special epithelial cells known as podocytes form the
layer of the glomerular capsule surrounding the capillaries of
the glomerulus. Podocytes work with the endothelium of the
capillaries to form a thin filter to separate urine from blood
passing through the glomerulus. The outer layer of the
glomerular capsule holds the urine separated from the blood
within the capsule. At the far end of the glomerular capsule,
opposite the glomerulus, is the mouth of the renal tubule.
A series of tubes called the renal tubule concentrate urine and
recover non-waste solutes from the urine. The renal tubule
carries urine from the glomerular capsule to the renal pelvis.

1. The curvy first section of the renal tubule is known as the

proximal convoluted tubule. The tubule cells that line the
proximal convoluted tubule reabsorb much of the water and
nutrients initially filtered into the urine.
2. Urine next passes through the loop of Henle, a long straight
tubule that carries urine into the renal medulla before making a
hairpin turn and returning to the renal cortex.
3. Following the loop of Henle is the distal convoluted tubule.
4. Finally, urine from the distal convoluted tubules of several
nephrons enters the collecting duct, which carries the
concentrated urine through the renal medulla and into the renal
pelvis.

27
5. From the renal pelvis urine from many collecting ducts combines
and flows out of the kidneys and into the ureters.

PHYSIOLOGY OF THE KIDNEY

Excretion of Wastes

The primary function of the kidneys is the excretion of waste

products resulting from protein metabolism and muscle
contraction. The liver metabolizes dietary proteins to produce
energy and produces toxic ammonia as a waste product. The liver
is able to convert most of this ammonia into uric acid and urea,
which are less toxic to the body. Meanwhile, the muscles of our
body use creatine as an energy source and, in the process,
produce the waste product creatinine. Ammonia, uric acid, urea,
and creatinine all accumulate in the body over time and need to
be removed from circulation to maintain homeostasis.
The glomerulus in the kidneys filter all four of these waste
products out of the bloodstream, allowing us to excrete them out
of our bodies in urine. Around 50% of the urea found in the
blood is reabsorbed by the tubule cells of the nephron and
returned to the blood supply. Urea in the blood helps to
concentrate other more toxic waste products in urine by
maintaining the osmotic balance between urine and blood in the
renal medulla.

Filtration, Reabsorption, and Secretion

1. The kidneys filter blood as it passes through the capillaries

that form the glomerulus. Blood pressure forces most of the
blood plasma through the lining of the capillaries and into the
glomerular capsule. Blood cells are too large to pass through
the capillary lining and so remain within the capillaries along
with some residual plasma. The filtered plasma, now known as
tubular fluid, begins to flow out of the glomerular capsule and
into the proximal convoluted tubule.
2. At the same time, the concentrated blood that remains inside the
capillaries of the glomerulus moves into the efferent arterioles
and on to the peritubular capillaries surrounding the proximal
convoluted tubule. Epithelial cells lining the tubule actively
reabsorb valuable molecules of glucose, amino acids, and ions
from the filtrate and deposit them back into the blood. These
cells also absorb any waste products remaining in the blood
(such as ammonia and creatinine) and secrete these chemicals
into the filtrate. While these solutes are being exchanged,

28
 osmotic pressure pushes water from the dilute, hypotonic
filtrate back into the concentrated, hypertonic blood.
3. From the proximal convoluted tubule, the tubular fluid next
enters the loop of Henle, where water and ions are reabsorbed.
The descending limb of the loop of Henle is permeable to water
and carries the filtrate deep into the medulla of the kidney.
Tissues in the medulla surrounding the tubule contain a high
concentration of ions and very little water compared to the
filtrate. Osmotic pressure between the hypotonic filtrate and
hypertonic medullary cells pushes water out of the filtrate and
into the cells. The cells of the medulla return this water to
the blood flowing through nearby capillaries.
4. Filtrate next passes through the ascending limb of the loop of
Henle as it exits the medulla. The tissues surrounding the
ascending limb are not permeable to water but are permeable to
ions. The filtrate is very concentrated after passing through
the descending limb, so ions easily diffuse out of the filtrate
and into the cells lining the ascending limb. These ions are
returned to the blood flowing through nearby capillaries.
5. Tubular fluid exiting the loop of Henle next passes through the
distal convoluted tubule and the collecting duct of the nephron.
These tubules continue to reabsorb small amounts of water and
ions that are still left in the filtrate. The tissues
surrounding the collecting duct actively absorb excess potassium
and hydrogen ions from the nearby capillaries and secrete these
excess ions as waste into the filtrate.
6. When filtrate reaches the end of the collecting duct, almost all
of the valuable nutrients, ions, and water have been returned to
the blood supply while waste products and a small amount of
water are left to form urine. The urine exits the collecting
duct and joins with urine from other collecting ducts in the
renal pelvis.

Water Homeostasis

The kidneys are able to control the volume of water in the

body by changing the reabsorption of water by the tubules of the
nephron. Under normal conditions, the tubule cells of the
nephron tubules reabsorb (via osmosis) nearly all of the water
that is filtered into urine by the glomerulus.
Water reabsorption leads to very concentrated urine and the
conservation of water in the body. The hormones antidiuretic
hormone (ADH) and aldosterone both increase the reabsorption of
water until almost 100% of the water filtered by the nephron is
returned to the blood. ADH stimulates the formation of water
channel proteins in the collecting ducts of the nephrons that
permit water to pass from urine into the tubule cells and on to

29
 the blood. Aldosterone functions by increasing the reabsorption
of Na+ and Cl- ions, causing more water to move into the blood
via osmosis.

In situations where there is too much water present in the

blood, our heart secretes the hormone atrial natriuretic peptide
(ANP) in order to increase the excretion of Na+ and Cl- ions.
Increased concentration of Na+ and Cl- in urine draws water into
the urine via osmosis, increasing the volume of urine produced.

Acid/Base Homeostasis

The kidneys regulate the pH level of the blood by controlling

the excretion of hydrogen ions (H+) and bicarbonate ions (HCO3-
). Hydrogen ions accumulate when proteins are metabolized in the
liver and when carbon dioxide in the blood reacts with water to
form carbonic acid (H2CO3). Carbonic acid is a weak acid that
partially dissociates in water to form hydrogen ions and
bicarbonate ions. Both ions are filtered out of the blood in the
glomerulus of the kidney, but the tubule cells lining the
nephron selectively reabsorb bicarbonate ions while leaving
hydrogen ions as a waste product in urine. The tubule cells may
also actively secrete additional hydrogen ions into the urine
when the blood becomes extremely acidic.
The reabsorbed bicarbonate ions enter the bloodstream where they
can neutralize hydrogen ions by forming new molecules of
carbonic acid. Carbonic acid passing through the capillaries of
the lungs dissociates into carbon dioxide and water, allowing us
to exhale the carbon dioxide.

Electrolyte Homeostasis

The kidneys maintain the homeostasis of important electrolytes

by controlling their excretion into urine.
 Sodium (Na+): Sodium is a vital electrolyte for muscle function,
neuron function, blood pressure regulation, and blood volume
regulation. Over 99% of the sodium ions passing through the
kidneys are reabsorbed into the blood from tubular filtrate.
Most of the reabsorption of sodium takes place in the proximal
convoluted tubule and ascending loop of Henle.
 Potassium (K+): Just like sodium, potassium is a vital
electrolyte for muscle function, neuron function, and blood
volume regulation. Unlike sodium, however, only about 60 to 80%
of the potassium ions passing through the kidneys are
reabsorbed. Most of the reabsorption of potassium occurs in the
proximal convoluted tubule and ascending loop of Henle.

30
 Chloride (Cl-): Chloride is the most important anion (negatively
charged ion) in the body. Chloride is vital to the regulation of
factors such as pH and cellular fluid balance and helps to
establish the electrical potential of neurons and muscle cells.
The proximal convoluted tubule and ascending loop of Henle
reabsorb about 90% of the chloride ions filtered by the kidneys.
 Calcium (Ca2+): Calcium is not only one of the most important
minerals in the body that composes the bones and teeth, but is
also a vital electrolyte. Functioning as an electrolyte, calcium
is essential for the contraction of muscle tissue, the release
of neurotransmitters by neurons, and the stimulation of cardiac
muscle tissue in the heart. The proximal convoluted tubule and
the ascending loop of Henle reabsorb most of the calcium in
tubular filtrate into the blood. Parathyroid hormone increases
the reabsorption of calcium in the kidneys when blood calcium
levels become too low.
 Magnesium (Mg2+): Magnesium ion is an essential electrolyte for
the proper function of enzymes that work with phosphate
compounds like ATP, DNA, and RNA. The proximal convoluted tubule
and loop of Henle reabsorb most of the magnesium that passes
through the kidney.

Blood Pressure Homeostasis

The kidneys help to control blood pressure in the body by

regulating the excretion of sodium ions and water and by
producing the enzyme renin. Because blood is mostly made of
water, an increased volume of water in the body results in an
increase in the volume of blood in the blood vessels. Increased
blood volume means that the heart has to pump harder than usual
to push blood into vessels that are crowded with excess blood.
Thus, increased blood volume leads to increased blood pressure.
On the other hand, when the body is dehydrated, the volume of
blood and blood pressure decrease.
The kidneys are able to control blood pressure by either
reabsorbing water to maintain blood pressure or by allowing more
water than usual to be excreted into urine and thus reduce blood
volume and pressure. Sodium ions in the body help to manage the
body’s osmotic pressure by drawing water towards areas of high
sodium concentration. To lower blood pressure, the kidneys can
excrete extra sodium ions that draw water out of the body with
them. Conversely, the kidneys may reabsorb additional sodium
ions to help retain water in the body.

Finally, the kidneys produce the enzyme renin to prevent the

body’s blood pressure from becoming too low. The kidneys rely on
a certain amount of blood pressure to force blood plasma through

31
 the capillaries in the glomerulus. If blood pressure becomes too
low, cells of the kidneys release renin into the blood. Renin
starts a complex process that results in the release of the
hormone aldosterone by the adrenal glands. Aldosterone
stimulates the cells of the kidney to increase their
reabsorption of sodium and water to maintain blood volume and
pressure.

Hormones

The kidneys maintain a small but important endocrine function by

producing the hormones calcitriol and erythropoietin.
 Calcitriol is the active form of vitamin D in the body. Tubule
cells of the proximal convoluted tubule produce calcitriol from
inactive vitamin D molecules. At that point, calcitriol travels
from the kidneys through the bloodstream to the intestines,
where it increases the absorption of calcium from food in the
intestinal lumen.
 Erythropoietin (EPO) is a hormone produced by cells of the
peritubular capillaries in response to hypoxia (a low level of
oxygen in the blood). EPO stimulates the cells of red bone
marrow to increase their output of red blood cells. Oxygen
levels in the blood increase as more red blood cells mature and
enter the bloodstream. Once oxygen levels return to normal, the
cells of the peritubular capillaries stop producing EPO.
Several hormones produced elsewhere in the body help to control
the function of the kidneys.

 Antidiuretic hormone (ADH), also known as vasopressin, is a

hormone produced by neurosecretory cells in the brain’s
hypothalamus. These cells extend into the posterior pituitary,
which stores and releases ADH. ADH production is stimulated by a
decrease in blood volume and increased blood osmolarity. ADH
helps the body retain water by increasing the number of water
channels in the cells of the collecting ducts of the kidneys.
These water channels allow water remaining in urine to be
reabsorbed into the blood, resulting in extremely concentrated
urine.
 Angiotensin II is a hormone made in the liver and activated by
the enzymes renin and angiotensin-converting enzyme. Once
activated, angiotensin II increases the reabsorption of sodium
and chloride ions in the proximal convoluted tubule, leading to
an increased reabsorption of water as well.
 Aldosterone is a hormone produced in the adrenal cortex in
response to Angiotensin II. Aldosterone binds to target cells in
the walls of the nephron’s collecting ducts. These cells
reabsorb additional sodium and chloride ions that would have

32
 been excreted as urine. The target cells also remove potassium
ions from the blood and excrete it into urine.
 Atrial natriuretic peptide (ANP) is a hormone produced by
cardiac muscle cells in the atria of the heart. These cells
produce ANP in response to high levels of sodium in the blood or
increased blood pressure. In the kidneys, ANP increases the
glomerular filtration rate so that more blood plasma is forced
into the glomerular capsule and into the renal tubules. ANP also
removes some solutes from the cells of the renal medulla, making
the loop of Henle less efficient in reabsorbing water and ions
from the filtrate. The net result of ANP is that more sodium and
water end up being excreted into urine, blood volume decreases,
and blood pressure decreases as well.

33
 PATHOPHYSIOLOGY

Predisposing Factor:
Rainy Season Leptospire from
Home town is near to infected animals
rice field

Direct invasion of tissue on susceptible host

Leptospires appears in the blood and invades

All tissue and organs

Capillary vascularitis

In the kidney, interstitial nephritis tubular necrosis

and impaired capillary permeability resulting in renal
failure

Scanty and concentrated urine output

Initial creatinine 2.03 mg/dl

Blood Urea Nitrogenous 9.32 mmol/dl

Acute Renal Failure

Liver involvement is marked by

with hepatocellular dysfumction

Icteric Sclera and Jaundice

Pulmonary involvement is secondary to aveolar and

interstitial vascular damage resulting in hemorrhage

Shortness of breath SPO2 99%

34
Skeletal muscle involvement is secondary
to edema and vessels damage

Myalgia and Arthralgia

Hypovolemia, hypotension BP: 80/ 50

35
DRUG SUTDY #1

Brand Name : Biogesic

Generic Name : Paracetamol
Drug Classification : Antipyretic
Indications : Symptomatic relief of minor aches and pains
Mechanism of Action :
Produce analgesia by blocking pain impulses by inhibiting
prostaglandin synthesis in the CNS or of other substances that
sensitize pain receptors to stimulation. The drug may relief
fever through central action in the hypothalamic heat regulating
center.

Precaution : Pain of >5 days for children and 10 days for

adults. Fever of >3 days.
Adverse Reaction : Allergic skin reactions and GI disturbances
Contraindications :
-Anemia, cardiac and pulmonary disease. Hepatic or severe renal
disease.
- Contraindicated in patients hypersensitive to drug.
Side Effects:
- Skin Redness -Abnormal Blood Cell Count.
- Allergic reaction - Facial Swelling
- SOB - Blisters on skin
- Running Nose
- Nausea
- Liver
Nursing Intervention and Precautions
- Assess patient’s fever or pain.
- Assess allergic reactions : rash, urticarial; if these
occur, drug may have to be discontinued.
- Teach patient to recognize signs of chronic overdose.
(bleeding, bruising,malaise,fever,sore throat)

36
DRUG STUDY #2

Brand Name: Hydrocortisone

Generic Name: HYDROCORTISONE SODIUM SUCCINATE 100mg
Drug Classification: Adrenocortical steroid , Corticoid (short-
acting), Glucocorticoid, Hormone
Indications :
- Replacement therapy in adrenal cortical insufficiency
- Allergic states – severe or incapacitating allergic
conditions.
- Use cautiously with kidney disease ; liver disease,
inflammatory bowel disease.
Adverse Effects:
Systematic :
 CNS : Vertigo, headache, paresthesias, insomnia,
seizures, psychosis.
 CV: Hypotension, shock, hypertension and heart
failure secondary to fluid retention,
thromboembolism, thrombophlebitis, fat embolism,
cardiac arrhythmias secondary to electrolyte
disturbances.
 Dermatologic: Thin, fragile, skin, petechie;
ecchymoses; purpura, striae; subcutaneous fat
atrophy.
 EENT: Cataracts, glaucoma (long-term therapy),
increased IOP
 Endocrine: Amenorrhea, irregular menses; growth
retardation, decreased carbohydrate tolerance and
diabetes mellitus, cushing state (long-term
therapy), HPA suppression systematic with therapy
longer than 5 days, Cushing’s syndrome,
hyperglycemia.
 GI : Peptic or esophageal ulcer, pacreatitis,
abdominal distention, nausea, vomiting, increased
appetite and weight gain (long-term therapy).
 Others: Immunosuppression, aggravation ir masking of
infection impaired wound healing.
Intervention
- Space multiple doses evenly throughout the day.
- Do not give IM injections if patient has thrombocytopenic
purpura.
- Rotate sites if IM repository injections to avoid local
atrophy.
- Use minimal doses for minimal duration to minimize adverse
effects.

37
- Taper doses when discontinuing high-dose or long-term
therapy.
- Arrange for increased dosage when patient is subject to
unusual stress.
- Ensure that adequate amount of Ca2+ is taken if prolonged
administration of steroids.
- Use alternate-day maintenance therapy with short-acting
corticoids whenever possible.

38
DRUG STUDY #3

Brand Name: K-lyte

Generic Name: Potassium (as bicarbonate and citrate)
Drug Classification :
Indication :
- For use as an electrolyte replenisher and in the treatment
of hypokalemia.

Contraindications:
- Hyperkalemia
- Chronic renal Disease
- Acute dehydration
- Heat cramps.
- Severe tissue destruction
- Adrenal insufficiency
- Familial periodic paralysis
- Acidosis (potassium chloride products)
- Alkalosis (potassium bicarbonate products)
- Tablets: Esophageal compression due to enlarged left
atrium. Decreased GI motility.
Adverse Effects :
 Dermatologiv: Rash (rare)
 GI: Nausea, vomiting, diarrhea, abdominal discomfort, GI
obstruction, GI bleeding, GI ulceration or perforation.
 Hematologic: Hyperkalemia – increased serum potassium,
ECG changes (peaking of T waves, loss of P waves,
depression of ST segment, prolongation of QTc interval)
Interactions:
- Increased risk of hyperkalemia with potassium-sparing
diuretics, salt substitutes using potassium.
Nursing Considerations
Assessment
- Assess for signs and symptoms of hypokalemia. (weakness,
fatigue, U wave on ECG, arrhythmias, polyuria, polydipsia)
and hyperkalemia.
- Treatment includes discontinuation of potassium,
administration of sodium bicarbonate to correct acidosis,
dextrose and insulin to facilitate passage of potassium
into cells, calcium salts to reverse ECG effects (in
patients who are not receiving digoxin), sodium polystyrene
used as an exchange resin, and/or dialysis for patient with
impaired renal function.
Interventions:
 Arrange for serial serum potassium levels before and
during therapy.

39
 Administer liquid form to any patient with delayed GI
emptying
 Administer oral drug after meals or with food a full glass
of water to decrease GI upset.
 Caution patient not to chew or crush tablets; have patient
swallow tablet whole.
 Arrange for further dilution or dose reduction if GI
effects are severe.

40
DRUG STUDY #4

Brand Name: Mepraz

Generic Name: Omeprazole
Drug Classifications: Anitsecretory drug , Proton pump inhibitor
Indications:
- Short-term treatment of active duodenal ulcer.
- Short-term treatment of active benign gastric ulcer
- GERD, severe erosive esophagitis, poorly responsive
symptomatic GERD
Contraindications and cautions:
- Contraindicated with hypersensitivity to omeprazole or its
components.
- Use cautiously because of possible increased risk of
Clostridium difficile infection.
Adverse Effects:
- CNS: Headache, dizziness, asthenia, vertigo, insomnia,
apathy, anxiety, paresthesias, dream abnormalities.
- Dermatologic : Rash, inflammation, urticarial, pruritus,
alopecia, dry skin
- GI : Diarrhea, abdominal pain, nausea, vomiting,
constipation, dry mouth, tongue atrophy.
- Respiratory: URI symptoms, cough, epistaxis
- Other: Cancer in preclinical studies, back pain, fever,
decreased bone density, bone fractures.
Interactions:
- Increased serum levels and potential increase in toxicity
of benzodiazepines, phenytoin, warfarin, if these
combinations are used, monitor patient closely.
- Administration with clopidalgrel; avoid this combination.
- Decreased absorption with sucralfate; give these drugs at
least 30 min apart.
Interventions:
 Administer before meals. Caution patient to swallow
capsules whole —- not to open, chew , or crush them.
 Be aware that patient may be at increased risk for hip,
wrist, and spine fracture; weigh benefits and risks before
use.

41
DRUG STUDY #5

Brand Name: Fer -In-Sol, Slow Fe, Feosol, Feratab and many more.
Generic Name: Ferrous sulfate
Classification: Iron Preparation
MECHANISM OF ACTION:
•Elevates the serum iron concentration which then helps to
form High or trapped in the reticuloendothelial cells for
storage and eventual conversion to a usable form of iron.
INDICATIONS:
•Prevention and treatment of iron deficiency anemias.
Dietary supplement for iron.
CONTRAINDICATIONS:
•Hypersensitivity
•Severe hypotension.
ADVERSE EFFECT:
• Dizziness
• N & V
• Nasal Congestion
• Dyspnea
• Hypotension
• CHF
• MI
• Muscle cramps
• Flushing
NURSING CONSIDERATION
• Advise patient to take medicine as prescribed.
• Caution patient to make position changes slowly to
minimize orhtostatic hypotension.
• Instruct patient to avoid concurrent use of alcohol or OTC
medicine without consulting the physician
• Advise patient to consult physician if irregular
heartbeat, dyspnea, swelling of hands and feet and
hypotension occurs.
• Inform patient that angina attacks may occur 30 min. after
administration due reflex tachycardia.
• Encourage patient to comply with additional intervention
for hypertension like proper diet, regular exercise,
lifestyle changes and stress management.
Precautions:Before taking this medication, tell your doctor or
pharmacist if you are allergic to it; or if you have any
other allergies. This product may contain inactive ingredients,
which can cause allergic reactions or other problems. Talk to
your pharmacist for more details.

This medication should not be used if you have certain

medical conditions.

42
Drug Study #6

Generic Name: Vitamin K (Pytonadione)

Brand name: Aqua-Mephyton
Classification: fat-solublevitamins, Antifibrinolytic Agents
Action:
Phytonadione is used in prophylaxis and treatment of
hemorrhagic disease of the newborn. It promotes liver formation
of the clotting factors II, VII, IX and X. At birth, the newborn
does not have bacteria in the colon that necessary for
synthesizing fat-soluble vitamin K.Therefore,the newborn may
have deceased levels of prothrombin during the first 5 to 8 days
of life reflected by a prolongation of prothrombin time.
Side Effects
•Pain
•Swelling or soreness at the injection site may occur
•Temporary flushing
• Taste changes
•Dizziness
•Rapid heartbeat
•Sweating
•Shortness of breath
•Bluish lips/skin/nails may also rarely occur
If any of these effects persist or worsen, tell your doctor or
pharmacist promptly.

Overdose:
If someone has overdosed and has serious symptoms such as
passing out or trouble breathing, call 911. Otherwise, call a
poison control center right away. US residents can call their
local poison control center at 1-800-222-1222. Canada residents
can call a provincial poison control center.

Uses:
Vitamin K is used to treat and prevent low levels of
certain substances (blood clotting factors) that your body
naturally produces. These substances help your blood to thicken
and stop bleeding normally (e.g., after an accidental cut or
injury). Low levels of blood clotting factors increase the risk
for unusual bleeding. Low levels may be caused by
certain medications (e.g., warfarin) or medical conditions
(e.g., obstructive jaundice). Vitamin K helps to treat and
prevent unusual bleeding by increasing the body's production of
blood clotting factors.

43
Indications and Usage:
Vitamin K1 Injection (Phytonadione Injectable Emulsion,
USP) is indicated in the following coagulation disorders which
are due to faulty formation of factors II, VII, IX and X when
caused by vitamin K deficiency or interference with vitamin K
activity.
Vitamin K1 Injection is indicated in:
•anticoagulant-induced prothrombin deficiency caused by
coumarin or indanedione derivatives;
•prophylaxis and therapy of hemorrhagic disease of the
newborn;
•hypoprothrombinemia due to antibacterial therapy;
•hypoprothrombinemia secondary to factors limiting absorption
or synthesis of vitamin K, e.g., obstructive jaundice, biliary
fistula, sprue, ulcerative colitis, celiac disease, intestinal
resection, cystic fibrosis of the pancreas, and regional
enteritis;
•other drug-induced hypoprothrombinemia where it is definitely
shown that the result is due to interference with vitamin K
metabolism, e.g., salicylates.

Contraindications:
Vitamin K is an important nutrient that aids in blood
clotting and helps your body develop strong, healthy bones. Your
age and gender dictate how much vitamin K your body needs daily,
with recommended daily intakes ranging from 2 micrograms in
infants to 90 in pregnant or breast-feeding women. Despite the
importance of this vitamin, certain people shouldn't take
vitamin K supplements and should limit their dietary intake of
vitamin K-rich foods, such as green leafy vegetables.

44
Drug Study #7

Generic Name: Tranexamic acid

Brand Name: Hemostan
Side Effects:
•Diarrhoea
• Vomiting
•Nausea
•Giddiness
•Disturbances in color vision
•Thromboembolic events
•Hypotension
Consult a doctor in case any of these side effects become
persistent and problematic.

Precautions: Information Not Available

Storage: Intravenous store at room temperature above 15 degree

Celsius and below 30 degree celcisus. Keep away from direct
light, heat and moisture.
Oral: Store at room temperature above 15 degree Celsius and
below 30 degree celcisus. Keep away from direct light, heat and
moisture. Keep away from the reach of children.

Absorption: Riveted from the GI tract; peak plasma absorbtions

after three hrs (when administered orally). Bioavailability: 30-
50 percent, unaltered by food ingestion.

Distribution: It is broadly distributed all through the human

body. Protein-binding: Very low. Transports over the placenta
and disseminated into breast milk.

Excretion: Urine (discharged as unaltered drug); two hrs

(elimination half-life).

45
Drug Study #8

Brand Name: Godex DS

Generic Name: Godex
Indications:
Treatment of acute & chronic hepatitis, fatty liver, liver
cirrhosis, liver intoxication by drug or chemical substances,
mitochondrial dysfunctions.
Dosage:
Godex Adult 2 cap tid. Godex DS 1 cap tid for the 1st 4-12
mth.
Administration:
May be taken with or without food.
Precautions:
Prolongation of dose >10 mcg/day of vit B12 may produce
hematological response in patients w/ folate deficiency.
Storage:
conditions for details to ensure optimal shelf-life.
Description:
for details of the chemical structure and excipients
(inactive components).
Mechanism of Action:
for pharmacodynamics and pharmacokinetics details.
ATC Classification:
A05BA - Liver therapy ; Used in liver therapy.
Description:
Godex: Each capsule contains carnitineorotate 150 mg, 17
amino acids 12.5 mg, pyridoxine HCl (vit B6) 25 mg, adenine HCl
2.5 mg, cyanocobalamin (vit B12) 125 mcg and riboflavin (vit B2)
500 mcg.
Godex preparation has been developed by a Spanish
pharmaceutical company as ethical therapeutics for mitochondrial
dysfunctions.
Mechanism of Action:
Pharmacology: Godex: Carnitineorotate is a
pharmacologically activated ionic complex salt with carnitine
and orotic acid. When administered to the body, it is more
easily absorbed than administration of carnitine and orotic acid
individually. These 2 substances represent dramatic synergistic
effect when administered with a type of complex salt for
increasing solubility and biological absorption.
After absorption, the complex salt is divided into 2
separate components and represents pharmacologic actions
separately.
Pharmacokinetics: General: Godex DS peak plasma concentrations
are observed about 30 min after dosing.

46
Drug Study #9

GENERIC NAME: Atovaquone

Brand Name: Mepron
Side Effect:
•Nausea
•Vomiting
•Diarrhea
•Headache
•Dizziness
•Trouble Sleeping
•Runny Nose may occur.
If any of these effects last or get worse, tell your doctor or
pharmacist promptly.
Uses:
Atovaquone is used to prevent or treat a
serious lung infection called Pneumocystis pneumonia (PCP).
This medication helps to stop infection symptoms such as
fever, cough, tiredness, and shortness of breath.
How to use Mepron:
Shake the bottle gently but well before each dose.
Carefully measure the dose using a special measuring
device/spoon. Do not use a household spoon because you may not
get the correct dose.
Interactions:
may change how your medications work or increase your risk
for serious side effects. This document does not contain all
possible drug interactions. Keep a list of all the products you
use (including prescription/nonprescription drugs and herbal
products) and share it with your doctor and pharmacist. Do not
start, stop, or change the dosage of any medicines without your
doctor's approval.
Overdose:
If someone has overdosed and has serious symptoms such as
passing out or trouble breathing, call 911. Otherwise, call a
poison control center right away. US residents can call their
local poison control center at 1-800-222-1222. Canada residents
can call a provincial poison control center
Pharmacokinetics:
Absorption: Atovaquone is a highly lipophilic compound
with low aqueous solubility. The bioavailability of atovaquone
is highly dependent on formulation and diet. The suspension
formulation provides an approximately 2-fold increase in
atovaquone bioavailability in the fasting or fed state compared
to the previously marketed tablet formulation.

47
INDICATIONS AND USAGE:
MEPRON Suspension is indicated for the prevention of
Pneumocystis carinii pneumonia in patients who are intolerant to
trimethoprim-sulfamethoxazole (TMP-SMX). MEPRON Suspension is
also indicated for the acute oral treatment of mild-to-moderate
PCP in patients who are intolerant to TMP-SMX

CONTRAINDICATIONS:
MEPRON Suspension is contraindicated for patients who
develop or have a history of potentially life-threatening
allergic reactions to any of the components of the formulation.
PRECAUTIONS:
General: Absorption of orally administered MEPRON is
limited but can be significantly increased when the drug is
taken with food. Plasma atovaquone concentrations have been
shown to correlate with the likelihood of successful treatment
and survival. Therefore, parenteral therapy with other agents
should be considered for patients who have difficulty taking
MEPRON with food (see CLINICAL PHARMACOLOGY). Gastrointestinal
disorders may limit absorption of orally administered drugs.
Patients with these disorders also may not achieve plasma
concentrations of atovaquone associated with response to therapy
in controlled trials.
Drug Interactions:
Atovaquone is highly bound to plasma protein (>99.9%).
Therefore, caution should be used when administering MEPRON
concurrently with other highly plasma protein-bound drugs with
narrow therapeutic indices, as competition for binding sites may
occur. The extent of plasma protein binding of atovaquone in
human plasma is not affected by the presence of therapeutic
concentrations of phenytoin (15 mcg/mL), nor is the binding of
phenytoin affected by the presence of atovaquone.
Adverse reaction:
22% 31% 31% Infection
•Diarrhea
•Headache
•Cough increased
•Rhinitis
•Asthenia
•Abdominal Pain
•Dyspnea
•Vomiting
Patients discontinuing therapy due to an adverse experience
,Patients reporting at least 1 adverse experience.

48
Drug Study #10

Generic Name: KRIMEL S

Indications and usages, anatomical therapeutic chemical and
diseases classification codes:
•A02AF02 - Ordinary salt combinations and antiflatulents
Pharmaceutical companies, researchers, developers,
manufacturers, distributors and suppliers:
•Great Eastern Drug
•Therapharma
•United Laboratories
Indication: For relief of heartburn and acid indigestion.
Contraindications:
•Allergic reactions
•Do not use before onset of bleeding during periods
•Extreme loss of body water
•High amount of calcium in the blood
•Incomplete or infrequent bowel movements
•Increased activity of the parathyroid gland
•Kidney stone
•Possibility to gastric malignancy
Indications:
•Heartburn
•Indigestion
•Acidity
•Gastric Ulcers
•Dietary Supplement
•Bones Weakening
•Better Absorption
•Stomach Ulcer
•Increases Water In The Intestines
Side effects:
•Fatigue
•Unexplained Bleeding Or Bruising
•Muscle Discomfort
•Vomiting Or Stomach Pain
•Severe Dizziness Or Nausea
•Yellowing Of Eye Or Skin
•Swelling Of Face
•Discolouration Of Urine
•Loss Of Appetite
•Muscle Weakness
Precautions & How to Use:
Before using this drug, inform your doctor about your current
list of medications, over the counter products (e.g. vitamins,
herbal supplements, etc.), allergies, pre-existing diseases, and
current health conditions (e.g. pregnancy, upcoming surgery,

49
etc.). Some health conditions may make you more susceptible to
the side-effects of the drug. Take as directed by your doctor or
follow the direction printed on the product insert.
Drug Interactions:
If you take other drugs or over the counter products at the
same time, the effects of Kremil-S Advance Tablet may change.
This may increase your risk for side-effects or cause your drug
not to work properly. Tell your doctor about all the drugs,
vitamins, and herbal supplements you are using, so that you
doctor can help you prevent or manage drug interactions. Kremil-
S Advance Tablet may interact with the following drugs and
products:
•Alcohol
•Alendronate
•Calcium acetate
•Ciprofloxacin
•Digoxin

50
Drug Study # 11

Generic Name: Hyoscine-N-butylbromide

Brand Name: Buscopan
Classification: Antispasmodic
Action:
Inhibits acetylcholine at receptor sites
in autonomicnervous system, which controls secretions,
free acids to stomach; blocks central muscarinic receptors,
which decreases involuntary movements.
Indication:
 Acute GI
 Biliary and Genitourinary Spasm,
 Biliary and RenalColic,
 Dysmenorrhea.
Parenterally also as an aid in diagnostic and therapeutic
procedures, e.g. gastroduodenal endoscopy, radiology.
Adverse Reactions:
 Xerostomia
 Tachycardia
 Urinary retention.
When administered IV, visual accomodation disturbances,
dizziness, agranulocytosis, pancytopenia and bronchospasm.
Side effects:
 difficulty urinating
 shortness of breath
 skin rash and itching
 vision changes
Dosage / Direction for Use:
Tab Adult &childn>6 yr 1-2 tab 3-5 times daily. Inj Acute
attacks of colicky pain Adult & adolescent >12 yr 1-2 amp IV, IM
or SC several times daily. Max: 100 mg daily. Infant & young
childnSevere cases: 0.3-0.6 mg/kg body wt by slow IV, IM or SC
several times daily. Max: 1.5 mg/kg body wt/day.
Overdosage: View Buscopanoverdosage for action to be taken in
the event of an overdose
.Administration: May be taken with or without food.
Contraindications:
•Tab: Myasthenia gravis &megacolon. Should not be used in
patients who have prior sensitivity to hyoscine-N-butylbromide
or any component of Buscopan
• Inj: Untreated narrow-angle glaucoma
•Prostate hypertrophy w/ urinary retention
•Mechanical stenosis in the GIT

51
 •Tachycardia
•megacolon
•myasthenia gravis
•IM inj in patients on anticoagulants.
Precautions: Avoid driving & operating machinery after
parenteral administration.

Adverse Reactions
•Xerostomia
•Tachycardia
•Urinary retention
•Allergic & skin reactions
•Rarely dyspnea (in patients w/ history of bronchial asthma
or allergy).
•Inj: Visual accommodation disturbance
•Infrequently inj site pain (after IM inj)
•Rarely anaphylactoid reactions & anaphylactic shock.
Interactions:
Intensifies anticholinergic effects of TCAs, antihistamines,
quinidine, amantadine, disopyramide& other anticholinergics
(egtiotropium, ipratropium). Enhanced tachycardiac effects of β-
adrenergic agents. Dopamine antagonists reduce effects of both
drugs on GIT.
Mechanism of Action: View Buscopan mechanism of action for
pharmacodynamics and pharmacokinetics details.

52
 NURSING CARE PLAN # 1

Assessment

Subjective : “maam di na ako ganahan mu gawas kay masipog na ako

sa ako pang lawas” as verbalized by the patient.

Objetive:

 Jaundice in the whole body

 Edema +2 in the lower extremities
 Generalized weakness
 Decreased hemoglobin
 No hygiene: no bathe for 3days

Diagnosis:

Disturbed body image r/t acute illness with changes in usual

roles or body image.

Planning:

After 3 hours of nursing intervention patient will be able

demonstrate adaptation to changes that have occurred, as
evidence by accepting changes that need occurred and realize it
is temporary.

Intervention:

INTERVENTION
Assess level of client’s
knowledge about condition and
treatment and anxiety related
to current situation.
RATIONALE
Identifies extent of problem/
concern and necessary
interventions.

Support active information Concern / belief that sharing

seeking by client/ SO
Acknowledge normalcy of
feeling
of information may be
“controlled “ by healthcare
providers perpetuates sense of
a “ power differential,”
potentiating dependence/
mistrust.
Recognition that feelings are
to be expected helps client

53

Determine clients role in
family constellation and
clients perception of
expectation of self and others
Recommend SO treat client
normally and not as an
invalid.
Identify strengths, past
success, previous methods
client has used to deal with
life stressors.
Assist and encourage the
client and the SO to provide
and practice proper hygiene.
accept and deal with them more
effectively.
Long-tem /permanent illness
and disability alters clients
ability to fulfill usual roles
in family/ school setting.
Unrealistic expectations can
undermine self-esteem and
affect outcomes of illness.
Conveys expectation that
client is able to manage
situation and helps maintain
sense of self-worth and
purpose in life
Focusing on these reminders of
own ability to deal with
problems can help client deal
with current situation
Proper hygiene can enhance
client’s physical appearance
and can help gain self-esteem.

Evaluation:

After 3 hours of nursing intervention patient was able to

demonstrate adaptation to changes that have occurred, as
evidence by setting realistic goals and active participation in
self-care and he gain self-confidence.

54
 NURSING CARE PLAN #2

Assessment:

Subjective: “Sakit ako hawak” as verbalized by the patient.

Objective:

 Facial grimace during movements

 Guarding behavior over flank area
 Irritable and restless behavior
 Pain scaled 7 to 10
 Sleep pattern disturbance(eye bags present)
 Restlessness
 Increased WBC of 15.0x10^9/L

Diagnosis:

Acute pain r/t infection process.

Planning:

After 2 hours of nursing intervention the patient will be

able to verbalized the reduction of pain scaled from 7 to 2 as
tolerated.

Nursing Intervention:

INTERVENTION RATIONALE
introduce self, ask patient Established rapport
name check name tag to determine
the right patient to perform
correct procedure and to gain
cooperation
Vital signs checked and For monitoring purposes and to
recorded be able to know if there is any
unusual happened to the patient
and can provide care.
Provided comfort and bed To be able to promote comfort
rest by stretching and and rest to the patient through
avoiding linens folds or proper positioning.
patient bed.

55
 Encouraged patient to To be able to provide care
verbalized any concerns immediately if there will be any
unusual happen and needs.
Divert attention Like let Diverting attention of the
the patient watch TV or patient to other things can
listen to music lessen the pain because his
attention will not be focus to
his feeling of pain.

Dependent

 Administered IV fluid D5LR This is to maintain patient

1000ml @ 15 gtts @ right fluid and for medication
arm as ordered by AP. administration purposes.

 Administered medication Produce analgesia by blocking

BIOGESIC 500mg as ordered. pain impulses by inhibiting
prostaglandin synthesis in the
CNS or of other substances that
sensitize pain receptor to
stimulation.

Evaluation:

Goal partially met. After 2 hours of nursing intervention the

patient pain was reduced to 2 from pain of 7 out of 10.

56
 NURSING CARE PLAN # 3

Assessment:

Subjective: “Ma’am waya man gud anay namo tambaya ang ako samad,
amo pa kami ni lihok pag adto nag yellow nako, nan ya ako mag
tuo na masakit baja ako” as verbalized by the patient.

Objective:

 Asking many question

 Irritability
 Confuse about his disease
 Request for information
 Statement of misconception
 Patients is a Grade 11 student
 Patient’s age is 19 years old
Diagnosis:

Knowledge deficit r/t lack of information and interest in

learning health condition.

Planning:

Within 1 hour of doing nursing intervention the patient will be

able to verbalize understanding of condition or disease process and
initiate necessary lifestyle changes and participate in treatment
regimen.

Nursing Intervention:

INTERVENTION
Review disease process and
precipitating factors if known.
Explain level of renal function
after acute episode is over.
Review dietary plan/
restrictions. Include fact sheet
listing food restrictions.
RATIONALE
Provides knowledge base from
which client can make informed
choices.
Client may experience residual
defects in kidney function which
may/ may not be permanent.
Adequate nutrition is necessary
to promote healing/tissue
regeneration; adherence to

57

Discuss reality of continued
presence of fatigue.
Determine/prioritize ADLs and
personal responsibilities.
Identify available resources/
support systems.
Recommend scheduling activities
with adequate rest periods.
Identify symptoms requiring
medical intervention; e.g.,
decreased urinary output, sudden
weight gain, presence of edema,
lethargy, bleeding, signs of
infection, altered mentation.
Convey acceptance and listen to
client’s statements and problems.
restrictions may prevent
complication.
Decreased metabolic energy
production, presence of anemia
and state of discomfort commonly
results in fatigue.
Helps client manage lifestyle
change and meet personal/family
needs.
Prevents excessive fatigue and
conserves energy for healing,
tissue generation.
Prompt evaluation and
intervention may prevent serious
complications/ progression to
CRF.
Proving interest to the patient
allows him to share and interact
to the activity.

Evaluation:
Goal met. After 1 hour of doing nursing intervention the
patient was able to verbalized understanding of condition or disease
process and initiate necessary lifestyle changes and participate in
treatment regimen.

58
 NURSING CARE PLAN #4

Assessment:

 general weakness
 Jaundice skin (entire body)
 Irritable
 Restless
 Disturbed sleep (presence of eye bags)
 BP:80/50
 PR:94
 RR:24
 TEMP:38 c
 Increased segmenters
 Decreased lymphocyte
 Decreased hemoglobin of 8.8g/dl
 Increased WBC of 15.0x10^9/L
 Increased creatinine of 2.03
 Increased blood Urea nitrogen of 9.32
 Leptospirosis

DIAGNOSIS:

Infection of r/t bacterial invasion in the body.

PLANNING:

Within 2 hours of nursing intervention patient will show

signs of recovery to health condition.

INTERVENTION:

INTERVENTION Rationale

59
Establish rapport to the client
Vital signs monitored and
recoded.
I and O monitored and recorded
Checked and individually
assesse medication prepared to
be administered according to
time and proper dose needed by
the patient.
Comfort provided
Assessed the patient visitation
of AP and check for new orders.
DEPENDENT
Administered IVF D5LR 1000mL at
15gtts/min in right metacarpal
as ordered.
Administered
medication of
 Atovaquone Mepron as
ordered
 Cefuroxime
EVALUATION:
Goal partially met. Patients showed signs of recovery to
health condition like Blood Pressure became normal and lessen
body weakness.
Introduce self to gain
cooperation and trust, asking
the name of the patient to
assure the right client and to
perform the given procedure.
For monitoring purposes and to
be able to know if there is
any unusual happened to the
patient and can provide care.
Helps estimate fluid
replacement needs. Fluid
intake should approximate
losses through urine,
nasogastric or wound drainage
and insensible losses.
To be able to administer
medication properly
To provide rest and comfort to
the patient and proper
position.
RATIONALE
This is to maintain patient
fluid and for medication
administration purposes.
This is administered to
eliminate or lessen the
bacterial infection in the
body.
60
 NURSING CARE PLAN #5

ASSESSMENT:

Subjective:” Maam kapaso sa ako kalawasan “as verbalized by

the patient.

Objective:

 Body weakness
 Skin is warm to touch
 Dry skin
 Flushed skin
 Restless
 WBC 15.0x10^9/L
 Temperature 38.9 c
 BP-80/50
 Leptospirosis

DIAGNOSIS
Hyperthermia related to infection process.

PLANNING:
Within 4 hours of nursing intervention patient
temperature will be decreased from 38.9 c to 37.0 c

INTERVENTION:
INTERVENTION Rationale
Establish rapport to the Introduce self to gain
client cooperation and trust,
asking the name of the
patient to assure the right
client and to perform the
given procedure.
Provided comfort and To be able to promote comfort
bed rest and rest to the patient
through proper positioning.

61
I and O monitored and Helps estimate fluid
recorded replacement needs. Fluid
intake should approximate
losses through urine,
nasogastric or wound
drainage and insensible
losses.
Provide tipid sponge bath This allows the temperature
to decrease because this
provides fresh feeling and
bath to the patient.
Ventilate environment This allows the environment
to be cool and not to be
compressed with high
temperature. This could
allow patient to feel fresh
and ventilated.
Encouraged patient to So that the patient will not
increased oral fluid intake be dehydrated.
Vital signs monitored and For monitoring purposes and
recoded. to be able to know if there
is any unusual happened to
the patient and can provide
care.
Checked and individually To be able to administer
assesse medication prepared medication properly
to be administered according
to time and proper dose
needed by the patient.
Administer Paracetamol To be able to decrease
BIOGESIC 500mg as ordered. patient temperature.

EVALUATION:
Goal met. Within 4 hours of doing nursing intervention
patient temperature was decreased from 38.9 c to 37.0 c.

62
 DISCHARGE PLAN
Upon discharge from the hospital, the patient and her
significant others will be given home care instructions
containing in the following:

MEDICATIONS  Continue taking the medicines

prescribed by the physician such as:
 FeSO4 + FA 1 TAB BID
 Godex 1 cap BID
 Butammate atrate 1 TAB BID
 Tergecef 400mg/tab 1 TAB OD

ENVIRONMENTAL  Advised patient or SO to have

CONSIDERATION psychological and by providing
quiet environment, and avoiding
stressful
Situation
TREATMENT  Instructed patient to follow proper
instructions medications prescribed
by the physician
 Drink at least 8-10 glasses a day
 Eat more fruits and vegetables to
facilitate easy bowel movement

HEALTH TEACHING  Encourage personal hygiene regularly

and make him understand of its
importance
 Encourage to take at least 8 glass
of water a day
 Encourage patient to eat healthy
food like vegetables
 Encourage patient to avoid contact
with canals and dirty water.
OUT-PATIENT CHECK-  Instructed patient to follow
UP scheduled check up
 Instructed patient to seek medical
attention when adverse reactions and
sign and symptom occur

63
 DIET  Advised the patient’s SO to let the
patient eat nutritious food like
fruits, vegetables and green leafy
 Instructed SO to control or limit the
food of the patient which contain
sodium
SPIRITUAL  Encourage patient to be more faithful
and have trust in God
 Encourage patient and SO to pray for
the patients early recovery

64
 IVF SHEET

SUMMARY OF INTRAVENOUS FLUIDS

BOTTLE DATE Solution Auditive Drop Rate

No. Volume (gtts/min)

1 1/2/17 1L PNSS FAST DRIP

2 1L PNSS FAST DRIP

3 1L PNSS 50 gtts/min

4 1L PNSS 50 gtts/min

5 1L PNSS 50 gtts/min

6 1/3/17 1L PNSS 50 gtts/min

7 1/4/17 1L PNSS 50 gtts/min

8 1/5/17 1L PNSS 20 gtss/min

9 1/5/17 1L PNSS 20gtts/min

10 1/6/17 1L PNSS 30gtts/min

11 1L PNSS 30 gtts/min

12 1/7/17 1L PNSS 20 gtts/min

13 1L PNSS 15 gtts/min

65
14 1/8/17 1L PNSS 30 gtts/min

15 1/9/17 1L PNSS 30 gtts/min

16 1/9/17 1L PNSS 30 gtts/min

66
 DEFINATION OF TERMS
Leptospirosis - is a bacterial disease that affects humans and
animals. It is caused by bacteria of the genus Leptospira.

Dialysis- the clinical purification of blood by dialysis, as a

substitute for the normal function of the kidney.

Nephron is the microscopic structural and functional unit of

the kidney.

Neutrophilia refers to a higher than normal number

of neutrophils or segmenters.

Lymphocytopenia - is the condition of having an abnormally low

level of lymphocytes in the blood.

Vasculitis- inflammation of a blood vessel or blood vessels.

Nephritis- inflammation of the kidneys

Necrosis- the death of most or all of the cells in an organ or

tissue due to disease, injury, or failure of the blood supply.

icteric sclera- the yellowing of the "white of the eye

alveoli- any of the many tiny air sacs of the lungs which allow
for rapid gaseous exchange.

Myalgia- pain in a muscle or group of muscles , without a

traumatic history is often due to viral infections.

Arthralgia- pain in a joint in the body, including the hands,

knees, and ankles or joint stiffness

Glomerulus- a cluster of capillaries around the end of a kidney

tubule, where waste products are filtered from the blood.

Glomerulonephritis- acute inflammation of the kidney, typically

caused by an immune response.

Nephropathy - kidney disease or damage.

Nephrotoxicity- occurs when your body is exposed to a drug or toxin

that causes damage to your kidneys. When kidney damage occurs, you are
unable to rid your body of excess urine, and wastes.

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 VITAL SIGNS

Date and B/P PR RR TEMP SPO

Time (%)
1-2-17
12nn 100/60 85 22 36
4pm 90/60 90 20 38.4
8pm 90/60 96 38 37.1
12MN 80/60 58 12 37.1 99%
2am 90/60 90 32 36.8 96%
4am 90/60 83 27 36.6 99%

Date and B/P PR RR TEMP SPO

Time (%)
1-3-17
8am 110/60 80 30 36 99%
10am 100/60 77 27 36 99%
12nn 100/60 80 33 36 C-095%
2pm 100/60 76 29 36 99%
4pm 120/80 90 24 36 96%
6pm 130/80 76 24 36 98%
8pm 150/80 74 26 36 99%
10pm 140/80 76 24 36 99%

BLOOD PULSE RESPIRATORY TEMPERATURE SPO

TIME PRESSURE RATE RATE (°C) (%)
(mm/hg) (bpm) (cpm)
1-4-17
8am 120/80 74 22 36.2
10am 110/60 80 22 36.4
12nn 110/80 68 20 36.2
2pm 100/60 76 20 36
4pm 120/80 67 24 36

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 6pm 110/60 86 22 36.2
8pm 120/80 82 22 36.8
10pm 110/80 75 20 36.2
12mn 120/80 78 20 36.6
2am 140/70 77 20 36.7
4am 130/80 70 20 36.3
6am 110/80 36 20 36.7
1-5-17
8am 120/80 83 26 36
10am 130/70 78 23 36.4
12nn 130/80 77 26 36.4
4pm 130/60 77 26 36.5
5pm 120/70 70 26 36.8
6pm 122/54 72 22 36
7pm 120/60 77 20 36
8pm 120/60 76 21 36
9pm 120/90 70 21 36
10pm 120/60 74 22 36
11pm 100/80 78 20 36
12mn 120/80 82 20 36.7
2am 120/70 80 20 36.7
4am 110/70 76 20 37
6am 100/60 80 20 37
1-9-17
11pm 120/60 80 20 37
12pm 100/60 84 20 27
4pm 110/70 78 20 36.6
8pm 120/70 82 20 37
12mn 110/60 76 20 37.3
2am 100/60 70 20 37
4am 110/60 69 20 37
1-10- 36.6
17
8am 110/70 71 20 36.7
10pm 110/70 82 20 36
12pm 110/80 84 20 36
4am 110/70 84 20 36
8am 120/80 26 20 36.5

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REFERENCES

(https://medlineplus.gov/ency/article/000501.htm)

(http://www.medicinenet.com/script/main/art.asp?articlekey=30776
)

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