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GENERAL OBJECTIVES:
After 1 hour and 30 minutes of lecture-discussion, the BSN III-B students will be able to gain knowledge, skills and positive attitude towards the principles of the
patient’s diagnoses such as Community Acquired Pneumonia-Moderate Risk, Hypertensive Cardiovascular Disease in Failure, Cardiovascular Disease secondary to
Nephropathy, Dyslipidemia, Hyperuricemia, Bronchial Asthma not in Exacerbation.
OBJECTIVE CONTENT TIME METHODOLOGY RESOURCES EVALUATION

ALLOTMENT
Opening Prayer Our Father, Who art in heaven 1 minute Prayer
Hallowed be Thy Name;
Thy kingdom come,
Thy will be done,
on earth as it is in heaven.
Give us this day our daily bread,
and forgive us our trespasses,
as we forgive those who trespass against us;
and lead us not into temptation,
but deliver us from evil. Amen.
Reading of
Objectives
Specifically,
After 1 hour and 30
minutes of lecture-
discussion, the BSN
III-B students will be
able to:
Define and 5 minutes Lecture-Discussion
understand the
following terms:
A. Community -an inflammatory condition of

Acquired the lung affecting primarily the microscopic air
Pneumonia- sacs known as alveoli. Typical signs and
Moderate Risk symptoms include a varying severity and
(CAP-MR) combination of productive or dry cough, chest
pain, fever, and trouble breathing, depending
on the underlying cause. Pneumonia is usually
caused by infection
. with viruses or bacteria and less commonly by
other microorganisms, certain medications and
conditions such as autoimmune diseases. Risk
factors include other lung diseases such
as cystic fibrosis, COPD,
and asthma, diabetes, heart failure, a history
of smoking, a poor ability to cough such as
following a stroke, or a weak immune system.
Diagnosis is often based on the symptoms
and physical examination. Chest X-ray, blood
tests, and culture of the sputum may help
confirm the diagnosis. The disease may be
classified by where it was acquired with
community, hospital, or health care associated
pneumonia.
-Refers to conditions that involve narrowed or

B. Hypertensive blocked blood vessels that can lead to a heart
Cardiovascular attack, chest pain (angina) or stroke. Other
Disease heart conditions, such as those that affect your
heart's muscle, valves or rhythm, also are
considered forms of heart disease, a class of
diseases that involve the heart or blood vessels.
Cardiovascular disease includes coronary
artery diseases (CAD) such
as angina and myocardial
infarction (commonly known as a heart attack).
Other CVDs are stroke, hypertensive heart
disease, rheumatic heart
disease, cardiomyopathy, heart
arrhythmia, congenital heart disease, valvular
heart disease, carditis, aortic
aneurysms, peripheral artery disease,
and venous thrombosis. The underlying
mechanisms vary depending on the disease in
question. Coronary artery disease, stroke, and
peripheral artery disease
involve atherosclerosis. This may be caused
by high blood pressure, smoking, diabetes,
lack of exercise, obesity, high blood
cholesterol, poor diet, and
excessive alcohol consumption, among others.
C. Nephropathy
-Is damage to or disease of
a kidney. Nephritis is inflammatory kidney
disease. Nephrosis is non-inflammatory
nephropathy. Kidney disease usually causes
kidney failure (renal failure) to more or less
degree, with the amount depending on the type
of disease. In
precise usage, disease denotes the structural an
d etiologic disease entity
whereas failure denotes the dysfunction (lack
of working well, that is, impaired renal
function); but in common usage these
meanings overlap; for example, the
terms chronic kidney disease and chronic renal
failure are usually considered synonymous.
Acute kidney disease has often been called
acute renal failure, although nephrologists now
D. Dyslipidemia often tend to call it acute kidney injury. About
1 in 8 Americans suffer from chronic kidney
disease.
-Is an abnormal amount of lipids

(e.g.,triglycerides, cholesterol and/or fat
phospholipids) in the blood. In developed
countries, most dyslipidemias
E. Hyperuricemia are hyperlipidemias; that is, an elevation of
lipids in the blood. This is often due to diet and
lifestyle. Prolonged elevation of insulin levels
can also lead to dyslipidemia.
-An abnormally high level of uric acid in

the blood. In the pH conditions of body fluid,
uric acid exists largely as urate, the ion form.
The amount of urate in the body depends on
the balance between the amount
F. Brochial Asthma of purines eaten in food, the amount of urate
synthesized within the body (e.g., through cell
turnover), and the amount of urate that is
excreted in urine or through the
gastrointestinal tract.
-A common long term inflammatory disease of

the airways of the lungs. It is characterized by
variable and recurring symptoms,
reversible airflow obstruction,
and bronchospasm. Symptoms include
episodes of wheezing, coughing, chest
tightness, and shortness of breath. These
episodes may occur a few times a day or a few
times per week. Depending on the person they
may become worse at night or with exercise.
2. To know the Name: A.L.T 2 minutes
patient’s General Age: 54
Data Address: Sto.Niño Compound, Panganiban
St.Cebu City
Sex: Female
Date of Birth: 10/18/1962
Place of Birth: Cebu City
Height: 5 ft. 4 inch.
Weight: 85 kls.
Marital Status: Married
Occupation: House Wife
Religon: Roman Catholic
Nationality: Filipino
Educational Attainment: College Level (3rd
Year)
Med.Case No.: 14968
Case No.: 7327
Date of Admission: 09/09/2016
Time of Admission: 8:40 am
Attending Physician: Dr. Norman.Santos, M.D
Chief Complaint: Edema on both feet, dry
cough
Diagnosis/Impression: Community Acquired
Pneumonia-Moderate Risk, Hypertensive
Cardiovascular Disease in Failure,
Cardiovascular Disease secondary to
Nephropathy, Dyslipidemia, Hyperuricemia,
Bronchial Asthma not in Exacerbation.
3. Patients past She has been vaccinated with complete 1 minute

health history immunization required during childhood. She
was admitted before, November 2015 due to
CAP-MR, CVD. She was (+) in hypertension,
(+) in Diabetes Mellitus, (+) in Brochial
Asthma. She usually sleeps 7-8 hours. Her
family had a history of Hypertension and
Diabetes Mellitus both paternal and maternal
side. She usually eats fruit and herbal coffee.
4. History of present Four days prior to admission, patient had onset 1 minute
illess of cough associated with fever, positive of
bypedal edema with shortness of breath with
difficulty breathing.
5. Physical A case of A.L.T 54 years old, Female, Roman 1 minute
Assessment: Catholic, Filipino, Residing in Sto.Niño
St.Panganiban Compound, Cebu City, was
admitted at Saint Vincent General Hospital due
to: Community Acquired Pneumonia-Moderate
Risk, Hypertensive Cardiovascular Disease in
Failure, Cardiovascular Disease secondary to
Nephropathy, Dyslipidemia, Hyperuricemia,
Bronchial Asthma not in Exacerbation. Patient
seen lying in bed conscious, responsive, using
sign language. Vital signs taken during first
contact with the patient:
Temperature: 37.1
Pulse rate: 92 bpm
Respiratory rate: 17 cpm
BP: 140/90
6. General state of A. Skin: Light Brown, Warm, Smooth, 2 minutes

health: Good Turgor
B. Hair: Evenly distributed, negative for
lice and fine
C. Scalp: shiny, dandruff noted, intact and
no lesion as observed
D. Head: Symmetrical, round, erect and in
midline. Proportion to the body with
smooth contour and without masses, no
injury noted
E. Face: Symmetrical facial features
F. Eyes: Eyelids appear symmetrical with
no dropping and infection, lacrimal
apparatus has no enlargement and
swelling, pupils are light brown, round
and of equal diameter ranging from 2-6
cm
G. Ears: Symmetrical, bilateral, fair in
color, smooth, no redness, postioned
centrally in proportion to the head.
H. Nose and Sinuses: Located
symmetrically in the midline of the
face
I. Mouth: Teeth is incomplete, gums are
pinkish with no bleeding, tongue is in
the middle of the mouth less
movement, smooth and without lesions
J. Neck: Symmetrical, Supine, patient is
unable to move her neck
K. Respiratory: cough is present,
presence of adventitious sounds upon
auscultation
L. Cardiovascular and peripheral
vasculator: palpitation noted and
abnormal heart soud auscultated.
M. Breast and Axilla: No redness, no
dimpling and swelling noted.
N. Musculoskeletal: the extremities are
proportional to the overall body size
and shape, positive bypedal edema
O. Neurologic: displays different facial
expression according to mood and
situation
P. Reproductive: No lesion and swelling
noted.
7. Gordon’s
functional pattern A. Health Perception
When one of the family member gets sick
they first treats the condition with herbal or
over-the-counter medication. If symptoms
persist, they seeks medical consults
immediately.
B. Nutritional Metabolic Pattern

The husband of the patient admits that his
wife was not fond of eating vegetables during
her younger years. And when they got married,
the patient prepare vegetables every weekdays
and meat every weekends. But now the patient
got hospitalized , her eating altered due to
nasogastric tube attached.
C. Elimination Pattern
The patient defecate one times a day and
urinate four to six times a day everyday with
soft stools. But now that she is hospitalized,
her elimination pattern altered. She have Foley
Bag catheter attached.
D. Activity/Exercise Pattern
The patient is a full time mother, her exercise
was doing household chores and gardening.
But she never stressed her self because she was
diagnosed to have Diabetes Millitus. Now that
she is hospitalized, she is on bedrest.
E. Cognitive or Perceptual Pattern

The patient was studied up to elementary
level.
F. Sleep Rest Pattern

The patient sleeps eight to nine hours a day.
She sleeps at 8pm and usually wakes up at
5am. Now that the patient got hospitalized, she
sleeps most of the time.
G. Self Perception Pattern

The husband of the patient admits that his
wife is kind, caring and loving wife and a
mother. Patient is aware that she have diabetes
and asthma.
H. Role Relationship Model

The patient is a happy married wife with
three sons and three daughters. They have a
nuclear type of family.
I. Sexual Reproductive Pattern

The patient’s husband admits that they are
sexually active during their adulthood days.
They are not fond of using any contraceptives.
But now, they are not sexually active.
J. Coping Stress Tolerance Pattern

Whenever the patient is stressed she just sleep
and sometimes do some household chores.
K. Value Belief System

Patient is a Roman Catholic. They go to
church every Sunday together with her
husband. They have strong faith in God. Her
source of hope through prayer to God and to
her family.
8. Normal Anatomy
and Physiology of A. RESPIRATORY SYSTEM 20 minutes
the affected area. An organ system that is responsible for
gaseous exchange between the circulatory
system and the outside world.
Nose and Nasal Cavity
The nose and nasal cavity constitute the main

external opening of the respiratory system. They
represent the entryway to the respiratory tract – a
passage through the body which air uses for travel in
order to reach the lungs. The nose is made out of
bone, muscle, cartilage and skin, while the nasal
cavity is, more or less, hollow space. Although the
nose is typically credited as being the main external
breathing apparatus, its role is actually to provide
support and protection to the nasal cavity. The cavity
is lined with mucus membranes and little hairs that
can filter the air before it goes into the respiratory
tract. They can trap all harmful particles such as dust,
mold and pollen and prevent them from reaching
any of the internal components. At the same time,
the cold outside air is warmed up and moisturized
before going through the respiratory tract. During
exhalation, the warm air that is eliminated returns the
heat and moisture back to the nasal cavity, so this
forms a continuous process.
Oral cavity
The oral cavity, more commonly referred to as the

mouth, is the only other external component that is
part of the respiratory system. In truth, it does not
perform any additional functions compared to the
nasal cavity, but it can supplement the air inhaled
through the nose or act as an alternative when
breathing through the nasal cavity is not possible or
exceedingly difficult. Normally, breathing through
nose is preferable to breathing through the mouth.
Not only does the mouth not possess the ability to
warm and moisturize the air coming in, but it also
lacks the hairs and mucus membranes to filter out
unwanted contaminants. On the plus side, the
pathway leading from the mouth is shorter and the
diameter is wider, which means that more air can
enter the body at the same speed.
Pharynx
The pharynx is the next component of the respiratory

tract, even though most people refer to it simply as
the throat. It resembles a funnel made out of muscles
that acts as an intermediary between the nasal cavity
and the larynx and esophagus. It is divided into three
separate sections: nasopharynx, oropharynx and
laryngopharynx. The nasopharynx is the upper
region of the structure, which begins at the posterior
of the nasal cavity and simply allows air to travel
through it and reach the lower sections. The
oropharynx does something similar, except it is
located at the posterior of the oral cavity. Once the air
reaches the laryngopharynx, something called the
epiglottis will divert it to the larynx. The epiglottis is
a flap that performs a vital task, by switching access
between the esophagus and trachea. This ensures that
air will travel through the trachea, but that food
which is swallowed and travels through the pharynx
is diverted to the esophagus.
Larynx
The larynx is the next component, but represents
only a small section of the respiratory tract that
connects the laryngopharynx to the trachea. It is
commonly referred to as the voice box, and it is
located near the anterior section of the neck, just
below the hyoid bone. The aforementioned epiglottis
is part of the larynx, as are the thyroid cartilage, the
cricoid cartilage and the vocal folds. Both cartilages
offer support and protection to other components,
such as the vocal folds and the larynx itself. The
thyroid cartilage also goes by a more common name
– the Adam’s apple – although, contrary to popular
belief, it is present in both men and women. It is
typically more pronounced in adult males. The vocal
folds are mucous membranes that tense up and
vibrate in order to create sound, hence the term voice
box. The pitch and volume of these sounds can be
controlled by modifying the tension and speed of the
vocal folds.
Trachea
The trachea is a longer section of the respiratory
tract, shaped like a tube and approximately 5 inches
in length. It has several C-shaped hyaline cartilage
rings which are lined with pseudostratified ciliated
columnar epithelium. (2) Those rings keep the
trachea open for air all the time. They are C-shaped
in order to allow the open end to face the esophagus.
This allows the esophagus to expand into the area
normally occupied by the trachea in order to permit
larger chunks of food to pass through. The trachea,
more commonly referred to as the windpipe,
connects the larynx to the bronchi and also has the
role of filtering the air prior to it entering the lungs.
The epithelium which lines the cartilage rings
produces mucus which traps harmful particles. The
cilia then move the mucus upward towards the
pharynx, where it is redirected towards the
gastrointestinal tract in order for it to be digested.
Bronchi & Bronchiole

The lower end of the trachea splits the respiratory
tract into two branches that are named the primary
bronchi. These first run into each of the lungs before
further branching off into smaller bronchi. These
secondary bronchi continue carrying the air to the
lobes of the lungs, then further split into tertiary
bronchi. The tertiary bronchi then split into even
smaller sections that are spread out throughout the
lungs called bronchioles. Each one of these
bronchioles continues to split into even smaller parts
called terminal bronchioles. At this stage, these tiny
bronchioles number in the millions, are less than a
millimeter in length, and work to conduct the air to
the lungs’ alveoli. The larger bronchi contain C-
shaped cartilage rings similar to the ones used in the
trachea to keep the airway open. As the bronchi get
smaller, so do the rings that become progressively
more widely spaced. The tiny bronchioles do not
have any kind of cartilage and instead rely on
muscles and elastin.
This system creates a tree-like pattern, with smaller
branches growing from the bigger ones. At the same
time, it also ensures that air from the trachea reaches
all the regions of the lungs. Besides simply carrying
the air, the bronchi and bronchioles also possess
mucus and cilia that further refine the air and get rid
of any leftover environmental contaminants. The
walls of the bronchi and bronchioles are also lined
with muscle tissue, which can control the flow of air
going into the lungs. In certain instances, such as
during physical activity, the muscles relax and allow
more air to go into the lungs.
Lungs
The lungs are two organs located inside the thorax
on the left and right sides. They are surrounded by a
membrane that provides them with enough space to
expand when they fill up with air. Because the left
lung is located lateral to the heart, the organs are not
identical: the left lung is smaller and has only 2 lobes
while the right lung has 3. Inside, the lungs resemble
a sponge made of millions and millions of small sacs
that are named alveoli. These alveoli are found at the
ends of terminal bronchioles and are surrounded by
capillaries through which blood passes. Thanks to an
epithelium layer covering the alveoli, the air that
goes inside them is free to exchange gasses with the
blood that goes through the capillaries.
Muscles of Respiration
The last component of the respiratory system is a
muscle structure known as the muscles of
respiration. These muscles surround the lungs and
allow the inhalation and exhalation of air. The main
muscle in this system is known as the diaphragm, a
thin sheet of muscle that constitutes the bottom of the
thorax. It pulls in air into the lungs by contracting
several inches with each breath. In addition to the
diaphragm, multiple intercostal muscles are located
between the ribs and they also help compress and
expand the lungs.
B. DIGESTIVE SYSTEM
The alimentary canal, which is also called

the gastrointestinal (GI) tract or gut, is the
entire length of tube that winds through the
body from the mouth to the anus. It digests,
breaks down and absorbs food through its
lining into the blood.
Oral Cavity
The oral cavity, or mouth, is the first part of
the digestive tract. It is bounded by the lips and
cheeks and contains the teeth and tongue. The
lips are muscular structures, formed mostly by
the orbicularis oris muscle. The outer surfaces
of the lips are covered by skin. The keratinized
stratified epithelium of the skin becomes thin
at the margin of the lips. The color from the
underlying blood vessels can be seen through
the thin, transparent epithelium, giving the lips
a reddish-pink appearance. At the internal
margin of the lips, the epithelium is continuous
with the moist stratified squamous epithelium
of the mucosa in the oral cavity. The cheeks
form the lateral walls of the oral cavity.
The buccinators muscles are located within the

cheeks and flatten the cheeks against teeth.
The lips and cheeks are important in the
process of mastication, or chewing. They help
manipulate the food within the mouth and hold
the food in place while the teeth crush or tear
it. Mastication begins the process of
mechanical digestion, in which large food
particles are broken down into smaller ones.
The cheeks also help form words during the
speech process.
Tongue
The tongue is a large, muscular organ that

occupies most of the oral cavity. The major
attachment of the tongue is in the posterior part
of the oral cavity. The anterior part of the
tongue is relatively free. There is an anterior
attachment to the floor of the mouth by a thin
fold of tissue called the frenulum.
The tongue moves food in the mouth and, in
cooperation with the lips and cheeks, holds the
food in place during mastication. It also plays a
major role in the process of swallowing. The
tongue is a major sensory organ for taste, as
well as being one of the major organs of
speech.
Teeth
There are 32 teeth in the normal adult mouth,

located in the mandible and maxillae. The
teeth can be divided into quadrants right upper,
left upper, right lower, and left lower. In
adults, each quadrant contains one central and
one lateral incisor; one canine; first and second
premolars; and first, second, and third molars.
The third molars are called wisdom teeth
because they usually appear in a person’s late
teens or early twenties, when the person is old
enough to have acquired some degree of
wisdom.
The teeth of adults are permanent, or
secondary, teeth. Most of them are
replacements of the 2 primary, or deciduous,
teeth.
Each tooth consists of a crown with one or
more cusps, a neck and a root. The center of
the tooth is a pulp cavity, which is filled with
blood vessels, nerves and connective tissue,
called pulp. The pulp cavity is surrounded by a
living, cellular, bonelike tissue called dentin.
The dentin of the tooth crown is covered by an
extremely hard, acellular substance called
enamel, which protects the tooth against
abrasion and acids produced by bacteria in the
mouth. The surface of the dentin in the root is
covered with cementum, which helps anchor
the tooth in the jaw.
The teeth are rooted within alveoli along the
alveolar processes of the mandible and
maxillae. The alveolar processes are covered
by dense fibrous connective tissue and moist
stratified squamous epithelium, referred to as
the gingival, or gums. The teeth are held in
place by periodontal ligaments, which are
connective tissue fibers that extend from the
alveolar walls and are embedded into the
cementum.
Palate and Tonsils
The palate, or roof of the oral cavity, consists

of two parts. The anterior part contains bone
and is called the hard palate, whereas the
posterior portion consists of skeletal muscle
and connective tissue and is called the soft
palate. The uvula is a posterior extension of the
soft palate. The palate separates the oral cavity
from the nasal cavity and prevents food from
passing into the nasal cavity during chewing
and swallowing.
The tonsils are located in the lateral posterior
walls of the oral cavity, in the nasopharynx,
and in the posterior surface of the tongue.
There are three pairs of salivary glands the
parotid, submandibular, and sublingual glands.
They produce saliva, which is a mixture of
serous and mucous fluids. Saliva helps keep
the oral cavity moist and contains enzymes that
begin the process of chemical digestion. The
salivary glands are compound alveolar glands.
They have branching ducts with clusters of
alveoli, resembling grapes, at the ends of the
ducts.
The largest of the salivary glands, the parotid
glands, are serous glands located just anterior
to each ear. Parotid ducts enter the oral cavity
adjacent to the second upper molars.
The submandibular glands produce more
serous than mucous secretions. Each gland can
be felt as a soft lump along the inferior border
of the mandible. The submandibular ducts
open into the oral cavity on each side of the
frenulum of the tongue. In certain people, if
the mouth is opened and the tip of the tongue
is elevated, saliva can squirt out of the mouth
from the ducts of these glands.
The sublingual glands, the smallest of the three
paired salivary glands, produce primarily
mucous secretions. They lie immediately
below the mucous membrane in the floor of
the oral cavity. Each sublingual gland has 10-
12 small ducts opening onto the floor of the
oral cavity.
Pharynx
The pharynx, or throat, which connects the

mouth with the esophagus, consists of three
parts the nasopharynx, oropharynx, and
laryngopharynx. Normally only the
oropharynx and laryngopharynx transmit food.
The posterior walls of the oropharynx and
laryngopharynx are formed by the superior,
middle, and inferior pharyngeal constrictor
muscles.
Esophagus
The esophagus is a muscular tube, lined with

moist stratified squamous epithelium that
extends from the pharynx to the stomach. It is
about 25 centimeters (cm) long and lies
anterior to the vertebrae and posterior to the
trachea within the mediastenum. It passes
through the diaphragm and ends at the
stomach. Upper and lower esophageal
sphincters, located at the upper and lower ends
of the esophagus, respectively, regulate the
movement of food into and out of the
esophagus. The lower esophageal sphincter is
sometimes called the cardiac sphincter.
Numerous mucous glands produce thick,
lubricating mucus that coats the inner surface
of the esophagus.
Stomach
The stomach is an enlarged segment of the

digestive tract in the left superior part of the
abdomen. The opening from the esophagus
into the stomach is called the cardiac opening
because it is near the heart. The region of the
stomach around the cardiac opening is called
the cardiac region. The most superior part of
the stomach is the fundus. The largest part of
the stomach is the body, which turns to the
right, forming a greater curvature on the left,
and a lesser curvature on the right. The
opening from the stomach into the small
intestine is the pyloric opening, which is
surrounded by a relatively thick ring of smooth
muscle called the pyloric sphincter. The region
of the stomach near the pyloric opening is the
pyloric region.
The muscular layer of the stomach is different

from other regions of the digestive tract in that
it consists of three layers an outer longitudinal
layer, a middle circular layer, and an inner
oblique layer. These muscular layers produce a
churning action in the stomach, important in
the digestive process. The sub mucosa and
mucosa of the stomach are thrown into large
folds called rugae when the stomach is empty.
These folds allow the mucosa and sub mucosa
to stretch, and the folds disappear as the
stomach is filled.
The stomach is lined with simple columnar
epithelium. The mucosal surface forms
numerous, tube-like gastric pits, which are the
openings for the gastric glands. The epithelial
cells of the stomach can be divided into five
groups. The first group consists of surface
mucous cells on the inner surface of the
stomach and lining the gastric pits. Those cells
produce mucus which coats and protect the
stomach lining. They are mucous neck cells,
which produce mucous; parietal cells, which
produce hydrochloric acids and intrinsic
factors; endocrine cells, which produce
regulatory hormones; and chief cells, which
produce pepsinogen, a precursor of the protein-
digesting enzyme pepsin.
Small Intestines
The small intestine is about 6 meters long and

consists of three partsthe duodenum, jejunum,
and ileum. The duodenum is about 25
centimeter (the term duodenum means 12,
suggesting that it is 12 inches long). The
jejunum is about 2.5 meter long and makes up
two-fifths of the total length of the small
intestine. The ileum is about 3.5 meter long
and makes up three-fifths of the small
intestine.
The duodenum nearly completes a nearly an
18degree arc as it curves within the abdominal
cavity. Part of the pancreas lies within this arc.
The common bile duct from the liver and the
pancreatic duct from the pancreas join each
other and empty into the duodenum.
The small intestine is the major site of
digestion and absorption of food, which are
accomplished by the presence of a large
surface area. The surface of the small intestine
has three modifications that increase surface
area about 600-foldcircular folds, villi, and
microvilli. The mucosa and sub mucosa form a
series of circular folds that run perpendicular
to the long axis of the digestive tract. Tiny
finger like projections of the mucosa forms
numerous villi, which are 0.5-1.5 mm long.
Most of the cells composing the surface of the
villi have numerous cytoplasmic extensions,
called microvilli. Each villus is covered by
simple columnar epithelium. Within the loose
connective tissue core of each villus is a blood
capillary called lacteal. The blood capillary
network and the lacteal are very important in
transporting absorbed nutrients.
The mucosa of the small intestine is simple
columnar epithelium with four major cell
types: Absorptive cells, which have microvilli,
produce digestive enzymes, and absorb
digested food Goblet cells, which produce a
protective mucus Granular cells, (Paneths
cells), which may help protect the intestinal
epithelium from bacteria; Endocrine cells,
which produce regulatory hormones. The
epithelial cells are produce within tubular
glands of the mucosa, called intestinal glands,
at the base of the villi. Granular and endocrine
cells are located in the bottom of the glands.
The sub mucosa of the duodenum contains
mucous glands, called duodenal glands, which
open into the base of the intestinal glands.
The duodenum, jejunum, and ileum are similar
in structure except that there is a granular
decrease in the diameter of the small intestine,
in the thickness of the intestinal wall, in the
number of circular folds, and in the number of
villi as one progress through the small
intestine. Lymph nodules are common along
the entire length of the digestive tract. Clusters
of lymph nodules, called Peyers patches, are
numerous in the ileum. These lymphatic
tissues in the intestine help protect the
intestinal tract from harmful microorganisms.
The junction between the ileum and the large
intestine is the ileocecal junction. It has a ring
of smooth muscle, the ileocecal sphincter, and
an ileocecal valve, which allows material
contained in the intestine to move from the
ileum to the large intestine, but not in the
opposite direction.
Liver
The liver weighs about 1.36 kilograms and is

located in the right upper quadrant of the
abdomen, tucked against the inferior surface of
the diaphragm. The posterior surface of the
liver is in contact with the right ribs 5-12. it is
divided into two major lobes, the right and left
lobes, separated by a connective tissue septum,
the falciform ligament. Two smaller lobes, the
caudate and quadrate, can be seen from an
inferior view. Also seen from the inferior view
is the porta, which is the gate through which
blood vessels, ducts and nerves enter or exit
the liver.
Pancreas
Pancreas is a fish-shaped spongy grayish-pink

organ about 6 inches (15 cm) long that
stretches across the back of the abdomen,
behind the stomach. The head of the pancreas
is on the right side of the abdomen and is
connected to the duodenum (the first section of
the small intestine). The narrow end of the
pancreas, called the tail, extends to the left side
of the body.
The pancreas makes pancreatic juices and
hormones, including insulin. The pancreatic
juices are enzymes that help digest food in the
small intestine. Insulin controls the amount of
sugar in the blood.
Large Intestines
The colon is made up of 6 parts all working

collectively for a single purpose. Their purpose
is ridding the body of toxins that have entered
the body from food sources, environmental
poisons, or toxins produced within the body.
The colons role is to transfer nutrients into the
bloodstream through the absorbent walls of the
large intestine while pushing waste out of the
body. In this process, digestive enzymes are
released, water is absorbed by the stool, and a
host of muscle groups and beneficial
microorganisms work to maintain the digestive
system.
The colon is approximately 4.5 feet long, 2.5
inches wide, and is a muscular tube composed
of lymphatic tissue, blood vessels, connective
tissue, and specialized muscles for carrying out
the tasks of water absorption and waste
removal. The tough outer covering of the colon
protects the inner layer of the colon with
circular muscles for propelling waste out of the
body in an action called peristalsis. Under the
outer muscular layer is a sub-mucous coat
containing the lymphatic tissue, blood vessels,
and connective tissue. The innermost lining is
highly moist and sensitive, and contains the
villi- or tiny structures providing blood to the
colon.
Rectum and Anus
The rectum is about eight inches long and

serves, basically, as a warehouse for poop. It
hooks up with the sigmoid colon to the north
and with the anal canal to the south.
The rectum has little shelves in it called
transverse folds. These folds help keep stool in
place until you’re ready to go to the bathroom.
When you’re ready, stool enters the lower
rectum, moves into the anal canal, and then
passes through the anus on its way out.
The rectum intestinum acts as a temporary
storage facility for feces. As the rectal walls
expand due to the materials filling it from
within, stretch receptors from the nervous
system located in the rectal walls stimulate the
desire to defecate. If the urge is not acted upon,
the material in the rectum is often returned to
the colon where more water is absorbed. If
defecation is delayed for a prolonged period of
time constipation and hardened feces results.
When the rectum becomes full, the increase in
intrarectal pressure forces the walls of the anal
canal apart, allowing the fecal matter to enter
the canal. The rectum shortens as material is
forced into the anal canal and peristaltic waves
propel the feces out of the rectum. The internal
and external sphincter allows the feces to be
passed by muscles pulling the anus up over the
exiting feces.
C. CARDIOVASCULAR SYSTEM
The circulatory system consists of four major

components:
The Heart: About the size of two adult hands

held together, the heart rests near the center of
the chest. Thanks to consistent pumping, the
heart keeps the circulatory system working at
all times.
Arteries: Arteries carry oxygen-rich blood
away from the heart and where it needs to go.
Veins: Veins carry deoxygenated blood to the

lungs where they receive oxygen.
Blood: Blood is the transport media of nearly

everything within the body. It transports
hormones, nutrients, oxygen, antibodies, and
other important things needed to keep the body
healthy.
Oxygen enters the bloodstream through tiny
membranes in the lungs that absorb oxygen as
it is inhaled. As the body uses the oxygen and
processes nutrients, it creates carbon dioxide,
which your lungs expel as you exhale. A
similar process occurs with the digestive
system to transport nutrients, as well as
hormones in the endocrine system. These
hormones are taken from where they are
produced to the organs they affect.
The circulatory system works thanks to

constant pressure from the heart and valves
throughout the body. This pressure ensures that
veins carry blood to the heart and arteries
transport it away from the heart. (Hint: to
remember which one does which, remember
that that “artery” and “away” both begin with
the letter A.)
There are three different types of circulation
that occur regularly in the body:
Pulmonary circulation: This part of the cycle
carries oxygen-depleted blood away from the
heart, to the lungs, and back to the heart.
 Systemic circulation: This is the part that

carries oxygenated blood away from the heart
and to other parts of the body.
 Coronary circulation: This type of circulation
provides the heart with oxygenated blood so it
can function properly.
9. Pathohysiology A. COMMUNITY ACQUIRED 20 minutes
PNEUMONIA
Constant exposure to contaminated air and
frequent aspiration of nasopharyngeal flora
make lung parenchyma susceptible to virulent
micro-organisms. Most microorganisms reach
lower respiratory tract as inhaled and
contaminated micro droplets. Complex
interactions between virulence and quantum of
aspirated or inhaled microorganisms, that
arrive at lower respiratory tract, integrity of
defense barriers and host immunity status,
decide occurrence of pneumonia.1,2 Particles
with diameter more than 100 µm precipitate
easily and are not inhaled. Particles larger than
10 µm get trapped in nasal secretions. Most
particles increase in size due to humidification
in trachea and are trapped in major bronchi.3
Particles with diameter less than 5 µm reach
the alveoli. Such particles can transport a
bacterial inoculum of up to 100
microorganisms depending on bacterial size.
Although diameter of most bacteria is 1 µm or
more, Mycoplasma, Chlamydophila, and
Coxiella are 5 to 100 times smaller. Most
Community Acquired Pneumonia (CAP) are
bacterial in origin and often follow brief viral
upper respiratory tract infection. In upright
position lower lobes are best ventilated
therefore deposition of inhaled micro
organisms is higher in these lobes. Inhalation
pneumonia is most often due to
microorganisms (a) that can remain suspended
in air so as to be transported far away, (b)
survive long enough while in transit, (c) have a
size less than 5 µm (d) carry a high inoculum,
and (e) evade local host defence mechanisms.
Infection by intracellular bacteria such as
Mycoplasma pneumoniae, Chlamydophila and
Coxiella burnetii occurs through contaminated
aerosol inhalation route. CAP due to
Streptococcus pneumoniae, Haemophilus and
gram-negative bacilli occurs through micro
aspiration,
Some of these important respiratory tract
defence mechanisms are summarized in Table
2. Failure of these defences mechanisms and
presence of certain predisposing factors render
the person susceptible to infection causing
CAP. Some of these conditions are described
in brief as under: 1. Alteration of normal
oropharyngeal flora. Presence of local
immunoglobulins, specially immunoglobulin
A, complement, and normal flora also prevents
colonization of the oropharynx by virulent
micro organisms.4 Diabetes, malnutrition,
alcoholism and other chronic systemic
disorders reduce levels of salivary fibronectin
and increase colonization by gram-negative
bacilli.5 Antibiotics associated suppression of
normal oral flora also facilitate colonization by
resistant gram-negative bacilli. 2. Depressed
Cough and glottis reflexes. This may allow
gastric content aspiration specially in old age,
in patients with COPD, thoracoabdominal
surgery or neuromuscular disease 3. Altered
consciousness. Healthy adults have 10 to 100
million bacteria per milliliter of oropharyngeal
secretions and upto 50% of healthy adults
aspirate small volumes of pharyngeal
secretions during deep sleep.6 Oropharyngeal
contents may be aspirated more often in
situations like coma, seizures, cerebrovascular
accidents, alcoholism and CNS depressant
drugs overdose. 4. Impaired mucociliary
apparatus mechanism. Effective mucociliary
clearance is dependent on effective ciliary
motion and on physical properties of mucus.
Submucosal glands and surface epithelial
goblet cells produce airway surface fluid. This
fluid consists of an upper layer of gel like
mucin and a lower non gel liquid. The cilia
beat in this special medium and propel the gel
towards mouth. Protection offered by the
mucus covered ciliated epithelium from larynx
to the terminal bronchioles is impaired in many
situations like chronic cigarette smoking, viral
respiratory infections, exposure to hot/cold air
or other harmful gases
In the pre antibiotic era S pneumoniae causing
lobar pneumonia was traditionally seen to
evolve through four sequential but distinct
following stages:
A. Stage of congestion: This stage represents
early acute inflammatory response. Affected
lobe becomes red and heavy due to vascular
congestion. Copious proteinaceous fluid,
abundant neutrophils and many bacteria can be
seen in the alveoli. This stage lasts for 1 to 2
days
B. Stage of red hepatisation: Affected lobe
becomes red, firm and acquires liver like
consistency. Proteinaceous fluid transforms
into fibrin strands with marked cellular
exudates of neutrophils. Extravasation of red
cells which give red color to consolidated lung.
This stage lasts for 2 to 4 days.
C. Stage of gray hepatisation: Affected lobe
becomes dry, firm and gray due to lysed red
cells. Neutrophilic cellular exudates decreases
due to breakdown of inflammatory cells and
macrophages are now seen. Microorganism
load also reduces. This stage lasts for 4 to 7
days.
D. Stage of resolution: Due to enzymatic
action, fibrinous matter is liquefied and the
lung aeration is re-establish gradually.
Macrophages are the major cells in the alveoli.
There is progressive reduction of fluid and
cellular exudates from the alveoli by way of
expectoration and lymphatic drainage leading
to normal lung parenchyma in over 3 weeks.
SIGNS AND SYMPTOMS

he most common symptoms of pneumonia are:
 Cough (with some pneumonias you may cough

up greenish or yellow mucus, or even bloody
mucus)
 Fever, which may be mild or high
 Shaking chills
 Shortness of breath (may only occur when you
climb stairs or exert yourself)

Other symptoms include:
 Confusion, especially in older people

 Excess sweating and clammy skin
 Headache
 Loss of appetite, low energy, and fatigue
 Malaise (not feeling well)
 Sharp or stabbing chest pain that gets worse
when you breathe deeply or cough
 White nail syndrome, or leukonychia

 DIAGNOSTIC TESTS
-Blood tests. Blood tests are used to confirm
an infection and to try to identify the type of
organism causing the infection. However,
precise identification isn't always possible.
-Chest X-ray. This helps your doctor diagnose
pneumonia and determine the extent and
location of the infection. However, it can't tell
your doctor what kind of germ is causing the
pneumonia.
-Pulse oximetry. This measures the oxygen
level in your blood. Pneumonia can prevent
your lungs from moving enough oxygen into
your bloodstream.
-Sputum test. A sample of fluid from your
lungs (sputum) is taken after a deep cough and
analyzed to help pinpoint the cause of the
infection.
Your doctor might order additional tests if
you're older than age 65, are in the hospital, or
have serious symptoms or health conditions.
These may include:
-CT scan. If your pneumonia isn't clearing as
quickly as expected, your doctor may
recommend a chest CT scan to obtain a more
detailed image of your lungs.
-Pleural fluid culture. A fluid sample is taken
by putting a needle between your ribs from the
pleural area and analyzed to help determine the
type of infection.
 TREATMENT
Doctors use antibiotics to treat pneumonia
caused by bacteria, the most common cause of
the condition. Antibiotics have a high cure rate
for pneumonia.5
Your doctor will choose your antibioticbased
on a number of things, including your age,
your symptoms and how severe they are, and
whether you need to go to the hospital. The
number of days you take antibiotics depends
on your general health, how serious your
pneumonia is, and the type of antibiotic you
are taking.
Most people see some improvement in
symptoms in 2 to 3 days. Unless you get worse
during this time, your doctor usually will not
change your treatment for at least 3 days.
Other treatments include:
Oxygen therapy, chest tapping therapy and
suctioning (worst case scenario)
PREVENTION
Get Vaccinated
-Get a flu shot every year to prevent

seasonal influenza. The flu is a common cause
of pneumonia, so preventing the flu is a good
way to prevent pneumonia.
-Children younger than 5 and adults 65 and
older should get vaccinated against
pneumococcal pneumonia, a common form of
bacterial pneumonia. The pneumococcal
vaccine is also recommended for all children
and adults who are at increased risk of
pneumococcal disease due to other health
conditions. There are 2 types of pneumococcal
vaccine. Talk to your healthcare provider to
find out if one of them is right for you.
-There are several other vaccines that can
prevent infections by bacteria and viruses that
may lead to pneumonia, including pertussis,
chicken pox and measles. Please talk to your
doctor about whether you and your children
are up to date on your vaccines and to
determine if any of these vaccines are
appropriate for you.
Wash Your Hands
Wash your hands frequently, especially after

blowing your nose, going to the bathroom,
diapering, and before eating or preparing
foods.
Don't Smoke
Tobacco damages your lung's ability to fight

off infection, and smokers have been found to
be at higher risk of getting pneumonia.
Smokers are considered one of the high risk
groups that are encouraged to get the
pneumococcal vaccine.
Be Aware of Your General Health
-Since pneumonia often follows respiratory

infections, be aware of any symptoms that
linger more than a few days.
-Good health habits—a healthy diet, rest,
regular exercise, etc.—help you from getting
sick from viruses and respiratory illnesses.
They also help promote fast recovery when
you do get a cold, the flu or other respiratory
illness
B. HYPERTENSIVE CARDIOVASCULAR
DISEASE
The cause of hypertensive heart disease is
chronically elevated blood pressure (BP);
however, the causes of elevated BP are
diverse. Essential hypertension accounts for
90% of cases of hypertension in adults.
Secondary causes of hypertension account for
the remaining 10% of cases of chronically
elevated BP.
According to the Framingham Study,
hypertension accounts for about one quarter
of heart failure cases. In the elderly population,
as many as 68% of heart failure cases are
attributed to hypertension. Community-based
studies have demonstrated that hypertension
may contribute to the development of heart
failure in as many as 50-60% of patients. In
patients with hypertension, the risk of heart
failure is increased by 2-fold in men and by 3-
fold in women.
Cardiovascular effects of hypertension
Uncontrolled and prolonged elevation of BP
can lead to a variety of changes in the
myocardial structure, coronary vasculature,
and conduction system of the heart. These
changes in turn can lead to the development of
left ventricular hypertrophy (LVH), coronary
artery disease (CAD), various conduction
system diseases, and systolic and diastolic
dysfunction of the myocardium, complications
that manifest clinically as angina or
myocardial infarction, cardiac arrhythmias
(especially atrial fibrillation), and congestive
heart failure (CHF).
Thus, hypertensive heart disease is a term
applied generally to heart diseases, such as
LVH (seen in the images below), coronary
artery disease, cardiac arrhythmias, and CHF,
that are caused by the direct or indirect effects
of elevated BP. Although these diseases
generally develop in response to chronically
elevated BP, marked and acute elevation of BP
can lead to accentuation of an underlying
predisposition to any of the symptoms
traditionally associated with chronic
hypertension.
The following conditions should also be
considered when evaluating hypertensive heart
disease:
Patient education
It is important to educate patients about the
nature of their disease and the risks associated
with untreated hypertension. In addition,
dietary modifications and the importance of
regular exercise, taking medications regularly,
weight loss, and avoiding medications and
foods that can potentially elevate blood
pressure should be emphasized.
C. DIABETES MELLITUS TYPE 2
Type 2 diabetes mellitus is a heterogeneous

disorder with varying prevalence among
different ethnic groups. In the United States
the populations most affected are native
Americans, particularly in the desert
Southwest, Hispanic-Americans, and Asian-
Americans. The pathophysiology of type 2
diabetes mellitus is characterized by peripheral
insulin resistance, impaired regulation of
hepatic glucose production, and declining β-
cell function, eventually leading toβ -cell
failure.
The primary events are believed to be an initial
deficit in insulin secretion and, in many
patients, relative insulin deficiency in
association with peripheral insulin resistance.
The β-cell
β-Cell dysfunction is initially characterized by

an impairment in the first phase of insulin
secretion during glucose stimulation and may
antedate the onset of glucose intolerance in
type 2 diabetes.
Initiation of the insulin response depends upon
the transmembranous transport of glucose and
coupling of glucose to the glucose sensor. The
glucose/glucose sensor complex then induces
an increase in glucokinase by stabilizing the
protein and impairing its degradation. The
induction of glucokinase serves as the first step
in linking intermediary metabolism with the
insulin secretory apparatus. Glucose transport
inβ -cells of type 2 diabetes patients appears to
be greatly reduced, thus shifting the control
point for insulin secretion from glucokinase to
the glucose transport system. This defect is
improved by the sulfonylureas.
Later in the course of the disease, the second
phase release of newly synthesized insulin is
impaired, an effect that can be reversed, in part
at least in some patients, by restoring strict
control of glycemia. This secondary
phenomenon, termed desensitization or β-cell
glucotoxicity, is the result of a paradoxical
inhibitory effect of glucose upon insulin
release and may be attributable to the
accumulation of glycogen within the β-cell as a
result of sustained hyperglycemia. Other
candidates that have been proposed are sorbital
accumulation in the β-cell or the noN-
nenzymatic glycation of β -cell proteins.
Other defects in β-cell function in type 2
diabetes mellitus include defective glucose
potentiation in response to non-glucose insulin
secret a gogues, asynchronous insulin release,
and a decreased conversion of proinsulin to
insulin.
An impairment in first phase insulin secretion
may serve as a marker of risk for type 2
diabetes mellitus in family members of
individuals with type 2 diabetes mellitus and
may be seen in patients with prior gestational
diabetes. However, impaired first phase insulin
secretion alone will not cause impaired glucose
tolerance.
Autoimmune destruction of pancreatic β-cells
may be a factor in a small subset of type 2
diabetic patients and has been termed the
syndrome of latent autoimmune diabetes in
adults. This group may represent as many as
10% of Scandinavian patients with type 2
diabetes and has been identified in the recent
United Kingdom study, but has not been well
characterized in other populations.
Glucokinase is absent within the β-cell in some
families with maturity-onset diabetes of young.
However, deficiencies of glucokinase have not
been found in other forms of type 2 diabetes.
In summary, the delay in the first phase of
insulin secretion, although of some diagnostic
import, does not appear to act independently in
the pathogenesis of type 2 diabetes. In some
early-onset patients with type 2 diabetes
(perhaps as many as 20%), there may be a
deficiency in insulin secretion that may or may
not be due to autoimmune destruction of the β-
cell and is not due to a deficiency in the
glucokinase gene. In the great majority of
patients with type 2 diabetes (±80%), the delay
in immediate insulin response is accompanied
by a secondary hypersecretory phase of insulin
release as a result of either an inherited or
acquired defect within the β-cell or a
compensatory response to peripheral insulin
resistance. Over a prolonged period of time,
perhaps years, insulin secretion gradually
declines, possibly as a result of intraislet
accumulation of glucose intermediary
metabolites. In view of the decline in β-cell
mass, sulfonylureas appear to serve a
diminishing role in the long term management
of type 2 diabetes (Unanswered is whether
amelioration of insulin resistance with earlier
detection or newer insulin-sensitizing drugs
will retard the progression of β-cell failure,
obviating or delaying the need for insulin
therapy.
THERAPY
Diet. Diet therapy, although important for the

prevention as well as the treatment of all stages
of type 2 diabetes, continues to remain poorly
understood and high controversial. When
obesity coexists with hyperglycemia, as seen in
the majority of individuals with type 2
diabetes, weight reduction is the major goal of
dietary therapy. Traditional recommendations
emphasize reduction of both the total and
saturated fat content and replacement with
complex carbohydrates to 50–55% of the
dietary calories. In type 2 diabetic patients,
such diets may cause marked postprandial
hyperglycemia. As there is considerable
patient variability in the rate of glucose
absorption, arduous attention to postprandial
glucose monitoring and the addition of high
fiber contents to the diet become critically
important. Moreover, as the glycemic response
of the diet is also dependent upon the texture
and content of other food stuffs in the diet as
well as the rate of intestinal motility, the diet
as well as the stage and duration of type 2
diabetes have to be considered on an individual
basis.
EXERCISE
Exercise has been shown to be beneficial in the

prevention of the onset of type 2 diabetes
mellitus as well as in the improvement of
glucose control as a result of enhanced insulin
sensitivity. Decreased intraabdominal fat, an
increase in insulin-sensitive glucose
transporters (GLUT-4) in muscle, enhanced
blood flow to insulin-sensitive tissues, and
reduced free fatty acid levels appear to be the
mechanisms by which exercise restores insulin
sensitivity. In addition, exercise provides the
added benefits of lowering blood pressure,
improving myocardial performance, and
lowering serum triglycerides while raising high
density lipoprotein cholesterol levels.
D. DIABETIC NEPHROPATHY
The key pathophysiologic event in diabetic

nephropathy is basement membrane
damage.29 With renal damage, there is
progressive thickening of the basement
membrane, pathologic change in mesangial
and vascular cells, formation of AGEs,
accumulation of polyols via the aldose
reductase pathway, and activation of protein
kinase C. Passage of macromolecules through
the basement membrane may also activate
inflammatory pathways that contribute to the
damage secondarily.
The renal hemodynamic abnormality is similar
in type 1 and type 2 diabetes. An early
physiologic abnormality is glomerular
hyperfiltration associated with intraglomerular
hypertension. This is accompanied by the onset
of microalbuminuria, the first practical
evidence of renal involvement in diabetes. This
is a critical time in the evolution of diabetic
renal disease, since the greatest impact of
treatment is to intercept this point in the
otherwise inexorable downward path of renal
function.
A clinically asymptomatic period of decline
follows, with progression of microalbuminuria
(30300 mg albumin per day) to
macroalbuminuria (>300 mg albumin per day).
Once overt nephropathy (macroalbuminuria)
has developed, renal function falls at a
significant but variable rate (decline in GFR of
220 ml/min/year). The rate of decline depends
on type of diabetes, genetic predisposition,
glycemic control, and, very importantly, blood
pressure. Hypertension is the single most
important cause of progression and point of
successful intervention in diabetic
nephropathy. Later stages may also be
accompanied by clinically significant
albuminuria, edema, and nephrotic syndrome.
Eventually, the characteristic clinical picture of
renal failure develops
E. BRONCHIAL ASTHMA
Inflammation has a central role in the
pathophysiology of asthma. As noted in the
definition of asthma, airway inflammation
involves an interaction of many cell types and
multiple mediators with the airways that
eventually results in the characteristic
pathophysiological features of the disease:
bronchial inflammation and airflow limitation
that result in recurrent episodes of cough,
wheeze, and shortness of breath. The processes
by which these interactive events occur and
lead to clinical asthma are still under
investigation. Moreover, although distinct
phenotypes of asthma exist (e.g., intermittent,
persistent, exercise-associated, aspirin-
sensitive, or severe asthma), airway
inflammation remains a consistent pattern. The
pattern of airway inflammation in asthma,
however, does not necessarily vary depending
upon disease severity, persistence, and duration
of disease. The cellular profile and the
response of the structural cells in asthma are
quite consistent.
Inflammatory Cells
Lymphocytes
An increased understanding of the
development and regulation of airway
inflammation in asthma followed the discovery
and description of subpopulations of
lymphocytes, T helper 1 cells and T helper 2
cells (Th1 and Th2), with distinct
inflammatory mediator profiles and effects on
airway function. After the discovery of these
distinct lymphocyte subpopulations in animal
models of allergic inflammation, evidence
emerged that, in human asthma, a shift, or
predilection, toward the Th2-cytokine profile
resulted in the eosinophilic inflammation
characteristic of asthma. In addition,
generation of Th2 cytokines (e.g., interleukin-4
(IL-4), IL-5, and IL-13) could also explain the
overproduction of IgE, presence of
eosinophils, and development of airway
hyperresponsiveness. There also may be a
reduction in a subgroup of lymphocytes,
regulatory T cells, which normally inhibit Th2
cells, as well as an increase in natural killer
(NK) cells that release large amounts of Th1
and Th2 cytokines. T lymphocytes, along with
other airway resident cells, also can determine
the development and degree of airway
remodeling. Although it is an
oversimplification of a complex process to
describe asthma as a Th2 disease, recognizing
the importance of n families of cytokines and
chemokines has advanced our understanding of
the development of airway inflammation
Mast cells
Activation of mucosal mast cells releases
bronchoconstrictor mediators (histamine,
cysteinyl-leukotrienes, prostaglandin D2).
Although allergen activation occurs through
high-affinity IgE receptors and is likely the
most relevant reaction, sensitized mast cells
also may be activated by osmotic stimuli to
account for exercise-induced bronchospasm
(EIB). Increased numbers of mast cells in
airway smooth muscle may be linked to airway
hyperresponsiveness. Mast cells also can
release a large number of cytokines to change
the airway environment and promote
inflammation even though exposure to
allergens is limited.
Eosinophils
Increased numbers of eosinophils exist in the
airways of most, but not all, persons who have
asthma. These cells contain inflammatory
enzymes, generate leukotrienes, and express a
wide variety of pro-inflammatory cytokines.
Increases in eosinophils often correlate with
greater asthma severity. In addition, numerous
studies show that treating asthma with
corticosteroids reduces circulating and airway
eosinophils in parallel with clinical
improvement. However, the role and
contribution of eosinophils to asthma is
undergoing a reevaluation based on studies
with an anti-IL-5 treatment that has
significantly reduced eosinophils but did not
affect asthma control. Therefore, although the
eosinophil may not be the only primary
effector cell in asthma, it likely has a distinct
role in different phases of the disease.
Neutrophils
Neutrophils are increased in the airways and
sputum of persons who have severe asthma,
during acute exacerbations, and in the presence
of smoking. Their pathophysiological role
remains uncertain; they may be a determinant
of a lack of response to corticosteroid
treatment. The regulation of neutrophil
recruitment, activation, and alteration in lung
function is still under study, but leukotriene
B4 may contribute to these processes
Dendritic cells
These cells function as key antigen-presenting
cells that interact with allergens from the
airway surface and then migrate to regional
lymph nodes to interact with regulatory cells
and ultimately to stimulate Th2 cell production
from naïve T cells.
Macrophages
Macrophages are the most numerous cells in

the airways and also can be activated by
allergens through low-affinity IgE receptors to
release inflammatory mediators and cytokines
that amplify the inflammatory response.
Resident cells of the airway

Airway smooth muscle is not only a target of
the asthma response (by undergoing
contraction to produce airflow obstruction) but
also contributes to it (via the production of its
own family of pro-inflammatory mediators).
As a consequence of airway inflammation and
the generation of growth factors, the airway
smooth muscle cell can undergo proliferation,
activation, contraction, and hypertrophy—
events that can influence airway dysfunction of
asthma.
Epithelial cells
Airway epithelium is another airway lining cell

critically involved in asthma. The generation
of inflammatory mediators, recruitment and
activation of inflammatory cells, and infection
by respiratory viruses can cause epithelial cells
to produce more inflammatory mediators or to
injure the epithelium itself. The repair
process,may be abnormal in asthma, thus
furthering the obstructive lesions that
occurasthma.
MEDICAL MANAGEMENT
 DIAGNOSTIC EXAMINATION/LABRATORIES
CLINICAL CHEMISTRY 9/24/16

TEST RESULT UNITS REFERENCE RANGE
Sodium Low 130.10 mmol/L 135-148
Potassium High 9.43 mmol/L 3.5-5.3
HEMATOLOGY COMPLETE BLOOD COUNT 9/24/16

BLEEDING TIME 4’6” min 2-6
CLOTTING TIME 2’32” min 1-3
Leukocyte H 26.50 x10^9/L 4-10
Neutrophil H 90.70 % 45-65
Lymphocytes L 3.40 % 20-40
Monocytes 4.10 % 2-11
Eosinophil 1.30 % 0-5
Basophil 0.5 % 0-2
RBC L 3.09 X10^12/L 4.2-5.4
Hemoglobin L 8.40 g/dL 12.0-16.0
Hematocrit L 25.30 % 37-47
MCV 82.00 fL 80-100
MCH 27.20 Pg 27.0-32.0
MCHC 33.30 % 32.0-36.0
RDW 12.50 % 11-16
Platelet Count 247.00 x10^9/L 140-440
IMMUNOLOGY
(Prothrombin Time)
Control 13.30 secs
Test 13.20 secs
% Activity 101.30 %
INR 0.99
OPTI CCA-TS2
Patient Report
27-Sep-16 15:14
PATIENT INFORMATION
Temperature: 37.2˚C
Patient ID: TANAJURA
Patient First Name: ANGELINA
Patient Last Name: TANAJURA
Sample No.: 977
ACID/BASE HEMOGLOBIN/OXYGEN STATUS

pH 7.450 tHb ↓ 9.5 g/dL
PCO2 35.9 mmHg SO2 97.2 %
PO2 91.8 mmHg Hct(c) ↓ 28.6 %
BE 0.6 mmol/L SO2(c) 97.5 %
tCO2 25.5 mmol/L AaDO2 ↑ 150.4 mmHg
HCO3 ↑ 24.4 mmol/L O2Ct ↓ 13.1 %vol
stHCO3 ↑ 24.8 mmol/L P50(c) 26.3 mmHg
TEMPERATURE CORRECTED ENTERED PARAMETERS

pH 7.447 FIO2: 0.40 REFERENCE RANGES
PCO2 36.2 mmHg tHb: 7.7 g/dL pH 7.200 – 7.600
PO2 92.9 mmHg PCO2 30.0 – 50.0 mmHg
AaDO2 ↑ 148.9 mmHg PO2 70.0 – 700.0 mmHg
tHb 12.0 – 17.0 g/dL
SO2 90.0 – 100.0 %
pH 7.200 – 7.600 Barometer: 753.0 mmHg
PCO2 30.0 – 50.0 mmHg User ID:
PO2 70.0 – 700.0 mmHg Lot: 606100
tHb 12.0 – 17.0 g/Dl S/N: 1207
SO2 90.0 – 100.0 % Version: 1.00.0050
Patient Name:
Attending Physician: SANTOS, NORMAN BAJARIAS Age: 53Y11M9D Room No.: 304
Examination: CHEST AP Plate No.: 15-17355
RADIOLOGIC FINDINGS
Findings:
Follow-up to CXR taken on 09/16/2016 shows persistent opacity at the right upper lung. The rest of the lung fields is now clear. There is complete resorption of the
right pleural effusion. The heart is enlarged. The pulmonary vessels are not engorged. There is calcification in the aortic knob. The trachea is in the midline. The
right hemidiaphragm is now distinct. The osseous thoracic cage has no bony abnormality. There is an ETT in place. An IJ shunt on the right in satisfactory position.
IMPRESSION:
>> INTERVAL RESOLUTION OF THE PNEUMONIC PROCESS AND MINIMAL PLEURAL EFFUSION IN THE RIGHT
LUNG.
>> PTB, RIGHT UPPER LOBE, STATUS QUO
>> CARDIOMEGALY
>> ATHEROMATOUS THORACIC AORTA
>> ETT, IJ SHUNT, IN PLACE
First name = ANGELINA Age = 53
Middle name = LIM Sex = f
Identification number = 20151101-14 Room = 304-A
Specimen type = Tracheal aspirate Site =
Collection date = 20-Sep-2016 Physician = SANTOS, NORMAN MD
Report date 23-Sep-2016

Organism = Klebsiella pneumoniae ss. Ozaenae
Amikacin S Amoxicillin/Clavulanic Acid R

Ampicillin R Ampicillin/Sulbactam R
Aztreonam R Cefazolin R
Cefepime R Cefotaxime R
Cefoxitin S Ceftazidime R
Ceftriaxone R Cefuroxime R
Chloramphenicol R Ertapenem S
Gentamicin R Imipenem S
Levofloxacin S Meropenem S
Piperacillin R Piperacillin/Tazobactam I
Tetracycline R Tobramycin R
Trimethoprim/Sulfamethoxale R
Medical technologist RICAMEL C. CANALES, RMT

Microbiologist VIRGINIA P. MESOLA, MD
Name: TAÑAJURA, ANGELINA LIM
Hospital No.: 201511010000014 Age: 53 Gender: FEMALE
Specimen: TRACHEAL ASPIRATE Date Received: 09-20-2016
Request: CULTURE & SENSITIVITY Physician: DR. NORMAN
DIAGNOSTIC MICROBIOLOGY
REPORT:
DATE FINDINGS
____09-21-2016____ GRAM STAIN: Pus Cells: Moderate /OIF

Gram (+) yeast cells: Rare /OIF
P.R.
Colony Count: Less than 10,000 CFU/ml
Smear of Culture: Gram negative bacilli
____09-23-2016____ F.R.
Culture: Klebsiella pneumoniae ss. Ozaenae
Remarks: Sensitivity testing of culture was performed.
Please refer to attached form.
DRUG STUDY
GENERIC/BRAND DOSE, INDICATION/ ADVERSE/SIDE NURSING RATIONALE CLIENT
NAME AND STRENGTH & MECHANISM OF EFFECT AND RESPONSIBILITIES TEACHING
CLASSIFICATION FORMULATION ACTION DRUG
INTERACTION
GENERIC NAME: ORDERED: INDICATION:  fever; >Monitor therapeutic >To prevent >Inform the patient to
 cold symptoms such effectiveness and patients from any report any changes in
Omeprazole 1 tab 40 mg Belongs to group of as stuffy nose, adverse reactions at complications. urinary elimination
drugs called proton sneezing, sore beginning of therapy such as pain or
pump inhibitors. It throat; and periodically discomfort associated
BRAND NAME: TIMING: decreases the amount  throughout therapy. with urination, or
stomach pain, gas;
of acid produced in the blood in urine.
Prilosec 6 A.M stomach. Omeprazole  nausea, vomiting, >Assess GI system: >Help's the
is used to treat mild diarrhea; or. bowel sounds every physician to >Inform the patient to
symptoms  headache. 8hours, abdomen for prevent early the report severe diarrhea;
CLASSIFICATION: DURATION: of gastroesophageal pain and swelling, said signs and drug may need to be
reflux appetite loss. symptoms. discontinued.
Proton pump 1-2 hours disease (GERD) and
inhibitors other conditions caused >Monitor hepatic >Let the patient take
by excess stomach enzymes: AST, ALT, >Help's the the drug before eating.
OTHER acid. increased alkaline physician to
FORMS: phosphatase during prevent early the
MECHANISM OF treatment. said effects.
Tablet, syrup ACTION:
belongs to a class of >Assess

antisecretory knowledge/teach
compounds, the appropriate use of this >To educate the
substituted medication, patient on what is
benzimidazoles, that interventions to reduce the best thing to do
suppress gastric acid side effects, and in the taking the
secretion by specific adverse symptoms to said drug.
inhibition of the report.
H+/K+ ATPase enzyme
system at the secretory >Report severe
surface of the gastric headache, unresolved
parietal cell. severe diarrhea, or >To prevent
changes in respiratory severeness of said
status. pains.
DRUG STUDY
INTERACTION
GENERIC NAME: ORDERED: INDICATION: -hypoglycemia - Injecting insulin at -to prevent any - Tell patient to learn
 -sweating room temperature. complication injection technique
Insulin 12 u -Insulin is always  -dizziness
used for the  -palpitation - Making sure no air - to prevent - Tell patient Inject
treatment of insulin- -tremor bubbles remain in the inconsistencies insulin into the
BRAND NAME: TIMING: dependent diabetes  -hunger syringe before with dosing abdomen rather than a
mellitus (type I  -restlessness injection. near muscle that will
Humulin R 6pm diabetes) and  -tingling in the -the drug will not be heavily taxed, if
occasionally also for hands, feet, lips, or - Waiting until topical effect engaged in active
the treatment of tongue alcohol (if used) has sports.
therapy  -inability to evaporated completely
CLASSIFICATION: DURATION: refractorynon- concentrate before injection. -Tell patient notify
insulin-dependent  headache -the drug will not physician of local
Antidiabetic agent diabetes  -drowsiness - Keeping muscles in effect reactions at injection
2-4 hr mellitus (type II). the injection area site
 -sleep disturbances
This therapy is relaxed, not tense,
 -anxiety
obligatory for when injecting. -Tell patient to check
 -blurred vision
OTHER individuals with -to notify blood glucose
 -slurred speech
FORMS: ketoacidosis and it -Monitor patient after physician any regularly
can be taken into  -depressed mood injecting insulin signs and
none consideration for all  -irritability symptoms may -Tell patient to notify
subjects who remain -abnormal behavior occur physician of S&S
symptomatic, lose  -unsteady movement diabetic ketoacidosis
weight, or have  -personality changes
continuously high
blood glucose
concentrations (in
fasting state more
than 7-8 mmol/l,
postprandial more
than 10-12 mmol/l)
despite another
treatment. Insulin can
also become
temporarily
necessary during
surgical interventions
or acute diseases.
MECHANISM OF
ACTION:
-Insulin is a peptide
hormone, produced
by beta cells of the
pancreas, and is
central to regulating
carbohydrate and fat
metabolism in the
body. Insulin causes
cells in the liver,
skeletal muscles, and
fat tissue to absorb
glucose from the
blood.
DRUG STUDY
INTERACTION
GENERIC NAME: ORDERED: INDICATION: -Stuffy or runny -Before taking -to prevent from any -Tell patient if signs
Linagliptin nose linagliptin, assess if the complication and symptoms occur,
1 tab 5mg OD Treating type client have allergy in stop med.
2 diabetes in >Sore throat medication.
BRAND NAME: TIMING: patients who cannot -Tell patient or SO that
control blood sugar >Allergic reactions -tell physician if signs -to prevent any Linagliptin is used
Tradjenta 6:00 am levels by diet and and symptoms occur complication together with diet and
exercise alone. It is >Muscle pain exercise to treat type 2
used along with diet -Do not give this -not appropriate diabetes.
CLASSIFICATION: DURATION: and exercise. It may >Diarrhea medication to anyone
Antidiabetic be used alone or under 18 years old - Tell patient and SO if
2-4 hr with other >Increased uric without medical signs and sypmtoms
antidiabetic acid levels advice. occur, notify physician
medicines.
OTHER Linagliptin is a >Cough -take medication once -to prevent oversose -Tell SO/patient to
FORMS: dipeptidyl peptidase- a day only Follow the directions
4 (DPP-4) inhibito on your prescription
tablet -follow doctors order -to prevent errors label.
MECHANISM OF -Tell patient or SO that

ACTION: Your doctor may
occasionally change
Linagliptin is an your dose to make
inhibitor of DPP-4, sure you get the best
an enzyme that results.
degrades the incretin
hormones glucagon-
like peptide-1 (GLP-
1) and glucose-
dependent
insulinotropic
(GIP).
DRUG STUDY
GENERIC/BRAND DOSE, INDICATION/ ADVERSE/SIDE NURSING RATIONALE CLIENT TEACHING
NAME AND STRENGTH & MECHANISM EFFECT AND RESPONSIBILITIES
CLASSIFICATION FORMULATION OF ACTION DRUG
INTERACTION
GENERIC NAME: ORDERED: INDICATION: >staining of -Check doctors order. -To prevent any - Use after breakfast
errors
the teeth and other and before bedtime
Chlorhexidine 15 ml 1tbsp Chlorhexidine -Stop chlorhexidine if
gluconate oral oral areas, allergic reactions occur -notify physician for unless otherwise
BRAND NAME: TIMING: rinse is indicated faster treatment instructed by your
for use between >dental tartar -If the patient is taking doctor.
Peridex q 4 8a,12a,4p dental visits as part (dental calculus), herbal meds or non-
of a professional prescribe meds, tell the - it can cause bad
-First brush your teeth.
DURATION: program for the physician interactions
CLASSIFICATION: treatment >altered sense of Measure the prescribed
2-4 hrs of gingivitis as taste, -Chlorhexidine amount in the cap,
antiseptic and characterized by gluconate should be which is marked for
antimicrobial oral OTHER redness and store at room medicine dosing. Rinse
>toothache, and
rinse FORMS: swelling of the temperature between 15 -so that the drug will
gingivae, including C to 30 C F (59 F to 86 effect normaly for 30 seconds, then
Oral solution gingival bleeding >oral mucosal F). spit out the medicine.
upon probing. irritation. Do not swallow
chlorhexidine solution.
MECHANISM
OF ACTION:
-Do not rinse with
Chlorhexidine is water or other
an antiseptic and mouthwashes, brush
antimicrobial oral
rinse. It provides teeth, or eat
protection against a immediately after using
wide range of chlorhexidine solution.
bacteria. It kills
bacteria by binding
-If you miss a dose of
to bacteria cell
chlorhexidine solution,
use it as soon as
possible. If it is almost
time for your next dose,
skip the missed dose
and go back to your
regular dosing schedul
DRUG STUDY
INTERACTION
GENERIC NAME: ORDERED: INDICATION:  -Unusually slow -Check first doctors -To prevent any -Advise to report
heart rate, order. errors. significant decreases
Ivabradine 5 mg To reduce the risk of headaches, in HR or symptoms
hospitalization for venticular -Monitor patient such as dizziness,
worsening heart extrasystoles, dizzine hourly if signs and -To prevent any fatigue, or
BRAND NAME: TIMING: failure in patients with ss and/or blurred symptoms occur. complication of the hypotension.
stable, symptomatic vision. patient.
Coralan 1 P.M - 6 P.M chronic heart failure -Follow doctors order -Advise to report
with LVEF ≤35%, when to take the drug. -To prevent the side symptoms of A-fib
CLASSIFICATION: DURATION: who are in sinus effects of the drug (eg, heart palpitations
rhythm with resting and any or racing, chest
Antianginal agent 2 - 4 hours heart rate ≥70 bpm complications to pressure, worsened
and either are on -Monitor for A-fib, the patient. SOB).
maximally tolerated bradycardia, sinus
OTHER doses of beta-blockers arrest, heart block, and -To monitor cardiac -Advise about the
FORMS: or have a other adverse rhythm regularly. possible occurrence
Tablet, syrup, contraindication to reactions. of luminous
injections. beta-blocker use phenomena
(phosphenes) and that
phosphenes may
MECHANISM OF subside
ACTION: spontaneously during
continued treatment.
acts by reducing the
heart rate via specific -Advise to use
inhibition of the funny caution if driving or
channel, using machines in
a mechanism different situations where
from that of beta sudden changes in
blockers and calcium light intensity may
channel blockers, two occur, especially
commonly prescribed when driving at
antianginal night.
drugs. Ivabradine is a
cardiotonic agent. -Advise to avoid
ingestion of
grapefruit juice.
DRUG STUDY
INTERACTION
GENERIC NAME: ORDERED: INDICATION: CNS:Anxiety, >check the patient >to notify the patient >tell patient to take
dizziness, fatigue, conditions. condition. missed dosed as soon
Amlodipine 10 mg >to control headache, lethargy, as remembered and
hypertension light headedness, >check the doctor’s >to check if the next dose in 24 hours.
BRAND NAME: paresthesia, order. doctor’s ordered the
TIMING: MECHANISM OF somnolence,, medication. >tell patient immediate
Norvasc ACTION: syncope,tremor >check the patient’s >to check the patient notify prescriber of
8:00 am EENT: dry mouth, bracelet name. dizziness, arm, or leg
CLASSIFICATION: Binds to pharyngitis swelling, difficulty in
DURATION: dihydropyridine and ENDO: hot flashes >ask the patient if >to clarify the breathing, hives or
Antianginal, nondihydropiridine GI: abdominal there is allergy in patient’s profile rash.
antihypertensive 24 hours cell membrane cramps, abdominal drugs
receptor sites on pain, constipation, >suggest taking
myocardial and diarrhea,esophagitis, >Administer the >as prescribed by the amlodipine with food
OTHER vascular smooth – Indigestion,nausea medication. doctor. to reduce GI upset.
FORMS: muscle cells and GU: decreased
Tablet, syrup, inhibits influx of libido, impotence, >record the time and >For documentation >advise patient to
injections. extracellular calcium urinary frequency date of data routinely have blood
ions acroos slow MS: myalgia pressure checked for
calcium channels. RESP: dyspnea >for possible possible hypotension
This decreases SKIN: >Monitor the patients hypotension
intracellular calcium dermatitis,flushing, blood pressure every 2
level , inbiting rash hours.
smooth muscle cell OTHER: weight loss
contractions and >advise the patient to >to notify
relaxing coronary report any sign of immediately to the
and vascular adverse reactions of doctor.
resistance , and drugs.
reducing systolic and
diastolic blood
pressure.decreased
peripheral vascular
resistance also
decrease myocardial
workload , oxygen
demand, possibly
angina. Also , by
inhibiting coronary
artery muscle cell
contractions and
restoring blood flow,
drug may relieve
prinzmetal angina.
DRUG STUDY
INTERACTION
GENERIC NAME: ORDER: INDICATIONS: CNS: amnesia, >check the patient >to notify the patient >Urge patient taking
asthenia, benign conditions. condition. oral capsules to
Budesonide 128 mcg >To manage intracranial swallow them whole
symptoms of hypertension, >check the doctor’s >to check if the and not to chew or
BRAND NAME: TIMING: seasonal or prernial. dizziness, fatigue, order. doctor’s ordered the break them.
fever, headache medication.
Entocort EC, 8:00 am-6:00 pm >to provide EENT: bad taste, >check the patient’s >instruct the patient
pulmicort flexhaler, BID maintenance therapy cataracts, dry bracelet >to check the patient who uses nasal spray to
turbuhaler. in chronic bronchial mouth,epistaxis, name. shake container before
Pulmicort respules, DURATION: asthma Glaucoma,, nasal >ask the patient if use.
Rhinocort, rhinocort irritation, oral or there is allergy in >to clarify the
Aqua, rhinocort 3 days-3 wks pharyngeal drugs. patient’s profile. >Instruct her to blow
turbuhaler MECHANISM OF candidiasis, her nose, tilt her head
OTHER ACTION: pharyngitis, >Administer the slightly forward, and
CLASSIFICATION: FORMS: rhinitis, medication. >to provide insert tube into a
Antiasthmatic, Inhibits Sinusitis maintenance therapy nostril, pointing toward
antiinflammatory Capsules inflammatory ENDO: growth in chronic bronchial inner corner of eye,
Cells mediators, suppression in astma. away from nasal
possibly by children >to provide septum. Tell her to
decreasing influx GI: abdominal pain >record the time and documentation of hold other nostril
into nasal passages Diarrhea, date when it data. closed and spray while
or bronchial walls. dyspepsia, administered the drugs. inhaling gently. Then
As a result, nasal or Flatulence, >notify the prescriber have her repeat in the
airway indigestion, nausea, >Assess the patient for immediately. other nostril.
inflammation vomiting effectiveness of
decreases. Oral GU: UTI budesonide therapy, >caution patient not to
inhalation form also MS: arthralgia, especially if being use oral inhaler with
inhibits mucous back pain weaned from a >to notify the the spacer device.
secretionin airways, RESP: systemic prescriber
decreasing the bronchospasm, corticosteroid. If the immediately, expect >advise patient to rinse
amount and increased cough, patient has increased to stop her mouth with warer
viscosity of sputum. respiratory tract asthma or an Budesonide therapy after dose and to spit
infection. immunologic condition and provide the water out. Tell
previously suppressed emergency supportive herto contact her
corticosteroid. care. prescriber if she
develop a mouth or
throat infection.
>instruct the patient

not to use budesonide
as a resque inhaler.
DRUG STUDY

NAME AND STRENGTH & MECHANISM EFFECT AND RESPONSIBILITIES TEACHING
INTERACTION
GENERIC: ORDER: INDICATION: CNS:mental or >check the patient >to notify the patient >Advise patient not to
mood changes conditions. condition. take sodium
Sodium Bicarbonate 10 g >To treat CV: irregular bicarbonate with large
hyperacidity heartbeat, peripheral >check the doctor’s >to check if the amount of dairy
BRAND NAME: TIMING: edema(with large order. doctor’s ordered the products or for longer
>to provide urinary doses), weak pulse medication. than 2 weeks, unless
Arm and hammer PRN alkalization EENT: dry mouth >to check the patient directed by the
pure baking soda, GI: abdominal name. prescriber
Bell/ ans, DURATION: >to treat metabolic cramp, thirst >check the patient’s
citrocarbonate, soda acidosis during MS: muscle spasm, bracelet >to clarify the >caution patient not
mint 4:00-8:00 hrs cardiac arrest myalgia patient’s profile to take more drug
SKIN: extravasation >ask the patient if there than prescribed to
CLASSIFICATION: OTHER FORM: MECHANISM with necrosis, tissue is allergy in drugs >as prescribed by the avoid adverse
OF ACTION: sloughing, or physician reaction.
Antacid, electrolyte Tablet ulceration >Administer the
replenisher, systemic Increases plasma medication >to check if there is >direct patient not to
and urinaryalkalizer bicarbonate level, any obstruction of IV take drug within 2
buffersexcess >check the IV site site hours of other oral
hydrogen ions, and drugs.
rises blood PH, >for documentation of
there by reversing >record the time and data. >advise patient to
metabolic acidosis. date when it given. avoid taking other
Sodium >to determine drug’s prescribed or OTC
bicarbonate also >monitor I&O effectiveness as urine drugs without
increase excretion alkalizer. If the patient prescriber’s approval
of free long term in sodium because many drugs
bicarbonateions in bicarbonate therapy is interact with sodium
urine,risisng urine consuming calcium or bicarbonate.
PH; increased milk watch for renal
alkalinity of urine >Instruct the patient insufficiency.
may helpto To report evidence of
dissolve uric acid adverse effect of the >to notify the doctor’s
calculi. In addition, medication. immediately.
it relieves sumptom
of hyperacidityby > advise patient to
neutralizingor avoid taking other
buffering prescribed or OTC
existingstomach drugs without > because many drugs
acid, there by prescriber’s approval. interact with sodium
increasing thethe bicarbonate
PH of stomach
content.
DRUG STUDY
NAME AND STRENGTH & MECHANISM OF EFFECT AND DRUG RESPONSIBILITIES TEACHING
CLASSIFICATION FORMULATION ACTION INTERACTION
GENERIC: ORDER: INDICATION: CSN: dizziness, >check the patient >to notify the >inform patient
hemiparesis, lacunar conditions. patient condition. that a gout attack
Febuxostat 40mg >To treat chronic infarction,stroke, may occur when
hyperuricemia in trancient ischemic >check the doctor’s >to check if the febuxostat therapy
BRAND NAME: TIMING: patient with gout. attack,chest pain or order. doctor’s ordered start and that
discomport, ECG the medication. NSAID or
Uloric 8:00 am-6:00 pm MECHANISM OF abnormalities,MI colchicines may be
ACTIONS: CV:angina,chest pain or >check the patient’s >to check the prescribed,
CLASSIFICATION: DURATION: discomport,ECG bracelet patient name. usaually along with
Inhibits the action of abnormalities, MI febusxostat to
Antigout 1-5hours xanthine oxidase, the EENT: blurred vision, >ask the patient if >to clarify the prevent it.
key deafness,epistaxis,nasal there is allergy in patient’s profile
OTHER enzymersponsible for dryness, paranasal sinus drugs >instruct patient to
FORMS: purinebreakdown. hypersecretionpharngeal >to note the seek emergency
Xanthine edema,sneezing, taste >check the name & expiration care immediately
None oxidasecatalyzes disturbance,throat expiry date of the signs and
conversionof irritation, tinnitus drug’s. symptoms of heart
xanthine of uric acid, ENDO: breast pain, >as order by the attack or stroke.
thereby increasing gynecomastia, hot >administer the physician
uric acid levels. High flashes, hypoglycemia medication. >tell patient that
uris acid levels cuase GI: diarrhea, dyspepsia, >for periodic blood test
gout attack. GI discomfort, >record the time and documentation of will be needed to
Inhibiting xanthine hepatomegaly, liver date of medication data determine drug’s
oxidase cause uric function abnormalities, given effectiveness and to
acid level to drop , nausea, vomiting >for evidence of detect adverse
decreasing the risk of GU: drecreased libido, >Monitor the blood cardiovascular effect.
gout attack. erectile dysfunction, pressure. thrombosis, such
hematuria,nephrolithiasis, as acute MI,
pollakiuria,proteinuria, stroke, because
renal failure or drug may increase
insufficiency,urgency risk of developing
HEME: anemia, these disorder.
idiopathic
thrombocytopenic >To notify the
purpura, leukocytosis, >Advise the patient to doctor’s
leukopenia, , neutropenia, note the adverse effect immediately.
pancytopenia, of the medication.
splenomegaly,
thrombocytopenia
MS: arthralgia,joint
stiffness or swelling
RESP: upper respiratory
tractinfection
SKIN: dermatitis,
ecchymosis, eczema,
flushing, hair color or
hair changes,
hyperhidrosis, peeling
skin, petechiae,
photosensitivity, rash
OTHER: gout flares,
hypersensitivity
DRUG STUDY
GENERIC/BR DOSE, INDICATION/ ADVERSE/SIDE NURSING RATIONALE CLIENT
AND NAME STRENGTH MECHANISM OF EFFECT AND DRUG RESPONSIBILITIE TEACHING
AND & ACTION INTERACTION S
CLASSIFICAT FORMULAT
ION ION
GENERIC: ORDER: INDICATION: CVS: asthenia, >check the patient >to notify the >encourage patient to
depression, dizziness, conditions. patient condition. follow a low fat, low
Rosuvastatin 40mg/PO >to treat hyperlipidemia, headache,hypertonia, cholesterol diet
mixed dyslipidemia, insomnia, memory loss, >check the doctor’s >to check if the
BRAND TIMING: hypertriglyceridemia, and paresthesia order. doctor’s ordered the >tell patient to wait at
NAME: primarydysbetalipoprotein CV: chest pain, medication. least two hours after
PRN emia (type III hypertension, peripheral taking rosuvastatin
Crestor hyperlipoproteinemia);to edema >check the patient’s >to check the before taking antacids
DURATION: slow progression of EENT: pharyngitis, bracelet patient name.
CLASSIFICAT atherosclerosis rhinitis, sinusitis >instruct patient to
ION: 3-5 hrs ENDO: thyroid function >ask the patient if >to clarify the notify prescriber
Antihyperlipide MECHANISM OF abnormalities there is allergy in patient’s profile immediately about
mic OTHER ACTIONS: GI: abdominal pain, drugs. muscle pain ,
FORMS: constipation, diarrhea, tenderness, or
Cholesterol elevated liver function >Administer the >As prescribed by weakness, especially
none andtriglycerides circulate test results, midecation the doctor. if accompanied by
in the blood as part of gastroenteritis, hepatic malaise or fever.
lipoproteincomlexes. failure, hepatitis, >record the time and >for documentation
Rosuvastatin inhibits the jaundice, nausea, date when it given. of data.
enzymes 3 hydroxy- 3- pancreatitis
methyglutaryl- coenzyme GU: acute rnal failure, >Monitor the >to evaluate
(HMG CoA) reductase. proteinuria, UTI lipoprotein level, as response to therapy.
This inihbitionreduces MS: arthralgia, arthritis, ordered.
lipid levels by increasing back pain, myalgia, >to avoid
thenumber of hepatic low- myophaty, >encourage patient to complications of
density-lipoprotein(LDL) rhabdomyolysis, follow a low fat, low the disease
receptors on the RESP: bronchitis, cholesterol diet.
cellsurface to increase increase cough
uptake and catabolism of SKIN: rash, urticaria
LDL. It also inhibits OTHER: angioedema,
hepatic synthesis of very flulike symptoms,
low density lipoprotein generalized pain,
(VLDL), which decreases infection.
the total number of VLDL
AND LDL particles.
DRUG STUDY
GENERIC/BRAN DOSE, INDICATION/ ADVERSE/SIDE NURSING RATIONALE CLIENT
D NAME AND STRENGTH & MECHANISM OF EFFECT AND RESPONSIBILITIE TEACHING
CLASSIFICATIO FORMULATI ACTION DRUG S
N ON INTERACTION
GENERIC: ORDER: INDICATION: CNS:dizziness, fever, >check the patient >to notify the patient >instruct the patient
headache, paresthesia, conditions. condition. not to chew form of
Ferrous sulfate 1omg >to prevent iron syncope iron except for
deficiency based on CV: chest pain, >check the doctor’s >to check if the chewable tablet.
BRAND NAME: TIMING: US and Canadian tachycardia order. doctor’s ordered the
recommended daily EENT: metallic taste, medication. >inform patient that
Apo Ferrous 8:00 am, 1:00 allowance. tooth discoloration iron deficiency may
Sulfate (CAN), pm, 6:00 pm GI: abdominal >check the patient’s >to check the patient cause decreased
feosol, feratab, fer- MECHANISM OF cramps, constipation, bracelet name. stamina, learning
gen-sol, Fir-In-Sol DURATION: ACTIONS: epigastric pain, problems, shortness
capsules, iron, nausea, stool >ask the patient if >to clarify the of breath, and
ferralyn lanacaps, unknown Acts to normalize discoloration, there is allergy in patient’s profile tiredness.
Fer-Iron drops RBC production vomiting drugs.
OTHER bybinding with HEME: >taught patient for
CLASSIFICATIO FORMS: hemoglobinor by hemochromatosis, >Administer the >As prescribed by improve iron
N: being oxidized and hemolysis, midecation the doctor. absorption to eat lean
IVF stored as hemosiderosis red meat, chicken,
Antianemic, hemosiderinor RESP: dyspnea >record the time and >for documentation turkey, and fish as
nutritional aggregated ferritin in SKIN: diaphoresis, date when it given. of data. well as food rich in
supplement reticoendothetial flushing, rash vitamin C
cells of the liver, >Monitor the >to evaluate (such as citrus fruits
spleen and bone lipoprotein level, as response to therapy. and fresh vegetables.
marrow. Iron is ordered.
essential component >to avoid >urge patient to avoid
of hemoglobin, >encourage patient to complications of the foods that impair iorn
myoglobin, and follow a low fat, low disease absorbtion, incliding
several enzymes, cholesterol diet. dairy product,eggs,
includingcytochrome spinach, and high
s, catalase and fiber foods, such as
peroxidase,.iron is whole grain breads
needed and cereals and
forcatecholamine brand.
metabolism and >advise patient to
normal neutrophil avoid drinking coffee
function. and tea within 1 hour
of iron intake.
DRUG STUDY
INTERACTION
GENERIC: ORDER: INDICATION: CNS: Vertigo, -You should not use -To prevent further -Advise patient to
headache, this medication if you complications take oral medication
Hydrocortisone 100mg, q6 IVTT -Replacement therapy paresthesias, are allergic to with food to
in adrenal cortical insomnia, seizures, hydrocortisone, or if minimize GI upset.
BRAND NAME: TIMING: insufficiency psychosis you have a fungal
- Allergic states – CV: Hypotension, infection anywhere in - Warn patient not to
Hydrocortone 12am severe or shock, HPN and your body. stop taking drug
6am incapacitating heart failure - There are many abruptly.
CLASSIFICATION: 12pm allergic conditions secondary to fluid - tell your doctor about other diseases that
6pm - Hematologic retention, all of your medical can be affected by - Caution diabetic
Pharmacologic disorders thromboembolism, conditions, and about steroid use, and patients that insulin
Class DURATION: - Ulcerative colitis thrombophlebitis, all other medicines you many other or oral hypoglycemic
Adrenal cortical fat embolism, are using. medicines that can agent needs may
steroid unknown MECHANISM OF cardiac arrhythmias interact with steroids. increase.
Corticosteroid ACTIONS: Dermatologic:
Glucocorticoid OTHER Thin, fragile skin, - Vaccines may not - Instruct elderly
FORMS: Enters target cells petechiae, work as well while patient to have BP,
and binds to ecchymoses, - Do not give live you are taking a blood glucose, and
none cytoplasmic receptor; purpura, striae, vaccines with steroid. electrolytes
initiates many subcutaneous fat immunosuppressive monitored at least
complex reactions atrophy doses of every 6 mo.
that are responsible EENT: Cataracts, hydrocortisone. - To avoid - Advise patient that
for its anti- glaucoma, increased withdrawal sunglasses may
inflammatory, IOP - Do not give IM symptoms when reduce sensitivity to
immunosuppressive Endocrine: injections if patient has stopping the sunlight that occurs
(glucocorticoid), and Amenorrhea, thrombocytopenic medication. with optic
salt-retaining irregular mens, purpura. administration.
(mineralocorticoid) growth retardation, - Caution against eye
actions. Some actions decreased contact with topical
may be undesirable, carbohydrate - Taper doses when - To monitor any agents.
depending on drug tolerance and DM, discontinuing high- adverse effects and
use. cushingoid state, dose or long-term reactions to the - Instruct patient to
HPA suppression therapy. patient wash or soak areas
(Lippincott Williams systemic , for topical
& Wilkins. 2013) hyperglycemia - Monitor client for at administration prior
GI: Peptic or least 30 minutes. to administration to
esophageal ulcer, increase absorption.
pancreatitis, - In case of
abdominal emergency - Advise patient to
distention, nausea, apply topical agents
vomiting, increased sparingly, rubbing in
appetite and weight lightly.
gain
Hematologic: Na - Caution against
and fluid retention, covering topically
hypocalcemia, treated areas unless
increased blood specifically
sugar, increased prescribed by health
serum cholesterol, care provider.
decreased T3 and T4
levels
Hypersensitivity:
Anaphylactoid or
hypersensitivity
reactions
Musculoskeletal:
Muscle weakness,
steroid myopathy
and loss of muscle
mass, osteoporosis,
spontaneous
fractures
Other:
Immunosuppression,
aggravation or
masking of
infections, impaired
wound healing
DRUG STUDY
INTERACTION
GENERIC: ORDER: INDICATION: -Tachycardia -Assess vital signs -To have a baseline -Use drug exactly
-Nausea and throat before drug data as prescribed by
Salbutamol Salbutamol nebule - Asthma irritation administration your doctor.
every 4 hours - Chronic bronchitis -Dizziness, tremors, To prevent
BRAND NAME: - Any lung disease headache, vomiting -Instruct patient to complications -Tell your doctor
TIMING: - Bronchospasm -Lowers peripheral contact health care about all of the
Ventolin - Emphysema vascular resistance professional medicines you
2am - -Increase blood immediately if take.
CLASSIFICATION: 6am MECHANISM OF pressure shortness of breath is
10am ACTIONS: -Tends to increase not relieved by -Do not use other
Bronchodilators 2pm blood glucose levels medication or is inhaled medicines
Stimulates B2 accompanied by unless prescribed
DURATION: adrenergic receptors diaphoresis, dizziness by your doctor.
which are predominant ,palpitations, or chest
8 hours receptors in bronchial pain -To avoid sensitivity
smooth muscle of the
OTHER lung. -Use Cautiously to
FORMS: (Lippincott Williams patients with known
& Wilkins. 2013) sensitivity to atropine,
Aerosol: 90 mcg soybeans, soya
Tablet: 2 mg, 4 mg lecithin, and peanuts
Syrup: 2 mg/ 5 ml
Injection: 5-10 ml
DRUG STUDY
GENERIC/BRAND DOSE, INDICATION/ ADVERSE/SIDE NURSING RATIONALE CLIENT TEACHING
NAME AND STRENGTH & MECHANISM EFFECT AND RESPONSIBILITIES
INTERACTION
GENERIC: ORDER: INDICATION: CNS: Headache, >check the patient >to notify the patient - Advise patient it may
dizziness, conditions. condition. take longer than usual to
Clopidogrel 75mg/tab 1 tab - Treatment of weakness, stop bleeding. Tell him to
patients at risk for syncope, flushing >check the doctor’s >to check if the refrain from activities in
OD ischemic events— CV: order. doctor’s ordered the which trauma and
history of MI, Hypertension, medication. bleeding may occur, and
BRAND NAME:
ischemic stroke, edema encourage him to wear a
TIMING: peripheral artery Dermatologic: >check the patient’s >to check the patient seat belt when in a car.
Plavix
disease Rash, pruritus bracelet name.
8am GI: Nausea, GI - Instruct patient to notify
- Treatment of distress, >ask the patient if there >to clarify the patient’s prescriber if unusual
CLASSIFICATION:
patients with constipation, is allergy in drugs. profile bleeding or bruising
DURATION: acute coronary diarrhea, GI bleed occurs.
Therapuetic class:
syndrome Other: Increased >Administer the
Antiplatelet 5 days bleeding risk midecation >As prescribed by the - Tell patient to inform all
MECHANISM doctor. health care providers,
Pharmacologic class:
OF ACTIONS: >record the time and including dentists, before
Platelet aggregation OTHER date when it given. >for documentation of undergoing procedures or
FORMS: data. starting new drug
inhibitor Inhibits platelet
>Monitor the theraphy, that he is taking
aggregation by
Pregnancy risk capsule lipoprotein level, as >to evaluate response drug.
blocking ADP
ordered. to therapy.
category B receptors on
platelets,
>encourage patient to >to avoid
preventing
follow a low fat. complications of the
clumping of
disease
platelets
DRUG STUDY
GENERIC/BRAND DOSE, INDICATION/ MECHANISM ADVERSE/SIDE NURSING RATIONALE CLIENT

NAME AND STRENGTH & OF ACTION EFFECT AND RESPONSIBILITIES TEACHING
CLASSIFICATION FORMULATION DRUG
INTERACTION
GENERIC: ORDER: INDICATION: CNS: dizziness, >check the patient >to notify the - Tell patient
headache, vertigo, conditions. patient to take drug
Azithromycin 500mg, PO Bacteriostatic orbectericidal in somnolence, condition. as prescribed,
susceptible bacteria fatigue >check the doctor’s even after he
BRAND NAME: TIMING: GI: diarrhea, order. >to check if feels better.
treatment of – abdominal pain, the doctor’s
Zithromax 8am - lower respiratory infections such nausea, dyspepsia, ordered the - Advise
as community-acquired pneumonia flatulence, >check the patient’s medication. patient to
CLASSIFICATION: DURATION: - genital ulcer disease in men vomiting, melena, bracelet avoid
- uncomplicated skin infections pseudomembranous >to check the excessive
Pharmacologic: 24hours - nongonococcal urethritis and colitis >ask the patient if patient name. sunlight and
macrolide antibiotic cervicitis; Other: there is allergy in to wear
OTHER superinections, drugs. >to clarify the protective
Therapeutic: FORMS: treatment of PID angioedema, rash, patient’s clothing and
Bacteriostatic - otitis media photosensitivity, >Administer the profile use sunscreen
Tablets – 250, 500, - pharyngitis and tonsillitis vaginitis midecation when outside.
Pregnancy Category 600mg; (Lippincott
Risk: B MECHANISM OF ACTIONS: Williams & >record the time and >As prescribed - Tell patient
injection – 2.5g; Wilkins. 2013) date when it given. by the doctor. to
Azithromycinblockstranspeptidation reportadverse
powder for oral by binding to50s ribosomalsubunit >Monitor the >for reactions
suspension – of susceptibleorganisms lipoprotein level, as documentation promptly.
100mg/5ml, anddisrupting RNA- ordered. of data.
200mg/5ml, dependentproteinsynthesis at - Tell patient
1g/packet; thechainelongation step. >encourage patient to >to evaluate to take at least
(Lippincott Williams & Wilkins. follow a low fat. response to 1 hour before
2013) therapy. or 2 hours
after a meal.
- Teach
patient to
reconstitute
medication
and to shake
well before
use.
NURSING CARE PLAN

CUES NURSING SCIENTIFIC GOAL AND NURSING ACTION RATIONALE OF EVALUATION
DIAGNOSIS BASIS OUTCOME AND ORDERS NURSING ORDER
CRITERIA
SUBJECTIVE: Ineffective The inflammatory After 8 hours of >Assess airway for > Maintaining patent After 8 hours of Nursing
airway clearance response to Nursing Interventions patency. airway is always the Interventions the patient
“Nahihirapan na related to infection causes the patient will be able first priority, especially will be able to:
siya huminga ineffective cough tissue edema and to: in cases like trauma or
dahil sa plema and retained exudates cardiac arrest. >Identify and avoid
niya hindi niya secretions. formation in the >Maintain clear, open specific factors that
mailabas, grabe lungs, the airways as evidence by >Perform > Suctioning is needed inhibit effective airway
nakasi ang ubo inflammatory normal breath sounds, nasotracheal when patients are clearance.
niya eh.” As response can normal rate and depth suctioning as unable to cough out
verbalized by the narrow and of respirations, and necessary, especially secretions properly due >Shall have
S.O. potentially ability to effectively if cough is to weakness, mucus expectorated retained
obstruct bronchial cough up secretions ineffective. production. secretions and
OBJECTIVES: passages and after treatments and maintained normal
alveoli. deep breaths. > Patient will breathing pattern.
-Inability to > Educate patient on understand the
remove airway >Demonstrate coughing, deep underlying principle > Airway patency will
secretions. increased air breathing, and and proper techniques be maintained and signs
-Difficulty of exchange. splinting techniques. to keep the airway clear of dyspnea will
breathing. of secretions. disappear.
-Abnormal >Classify methods to
respiratory rate, enhance secretion
rhythm, and removal.
depth.
NURSING CARE PLAN
CRITERIA
SUBJECTIVE: Risk for Pneumonia is an After 8 hours of >Monitor v/s >To know potential After 8 hours of Nursing
infection r/t infection in one Nursing Interventions closely,especially fatal complication that Interventions the patient
“nag pneumonia presence of or both lung. It the patient will be during initiation of may occur. will be able to:
mani siya existing can be caused by able to: therapy.
ma’am” as infection. fungi, bacteria, or >Tachypnea, is >The patient’s S.O have
verbalized by viruses. >Free from possible >Assess depth/rate frequently presented verbalized his
patient’s husband. Pneumonia spread of infection. of respiration and because of discomfort understanding of
causes chest movement. of the moving chest individual causative/risk
OBJECTIVES: inflammation in >Achieve timely wall and/or fluid in the factors and demonstrate
your lung’s air resolution of current lungs. lifestyle changes to
>Skin is pale in sacs, or alveoli. infection without > Administer prevent further infection.
color The alveoli fill complications. antimicrobials as > To combat microbial
>Restlessness with fluid or pus, ordered. pneumonias. > Demonstrate complete
>Activity making it difficult >Identify recovery from infection.
intolerance to breathe. interventions to >Encourage the > To prevent entry of
Receiving gastric (Normandin,2015 prevent and reduce mother to keep an microbes. >Goal partially met.
feedings ) risk and spread of a eye to the patient
secondary infection. and observe
anything.
NURSING CARE PLAN

CUES NURSING SCIENTIFIC BASIS GOAL AND NURSING ACTION RATIONALE OF EVALUATION
DIAGNOSIS OUTCOME AND ORDERS NURSING ORDER
CRITERIA
SUBJECTIVE: Risk for Hemodialysis is a fast After 8 hours of > Measure all sources >Aids in evaluating After 8 hours of Nursing
deficient fluid and efficient method Nursing of intake and output. fluid status. Interventions the patient
“Naa gyud times volume r/t for removing urea and Interventions the Have client’s S.O. will be able to:
na weak siya ultrafiltration, other toxic products patient will be keep diary.
ma’am” as fluid restriction, and correcting fluid able to: >Hypotension, >Demonstrate behaviors
verbalized by the and actual blood and electrolyte >Monitor BP, pulse tachycardia, and to monitor fluid status
patient’s husband. loss secondary to imbalances but > Good Skin and hemodynamic falling hemodynamic and reduce recurrence of
disconnection of requires permanent turgor pressures, if available. pressures suggest fluid excess
shunt. arteriovenous access. volume depletion.
Procedure is usually >Moist mucous >Patient will manifest
OBJECTIVES: performed three times membranes >Maximizes venous stabilize fluid volume
per week for 4 hr. HD >Place patient in a return if hypotension AEB balance I & O,
>Restlessness may be done in the >Absence of supine or occurs. normal VS, stable
>Weakness hospital, outpatient bleeding Trendelenburg weight, and free from
>Fluid dialysis center, or at position, as necessary. signs of edema.
restrictions home. >Appropriate >May reduced
> Edema (Doenges,2010) weight >Monitor laboratory because of anemia, > Goal partially met.
Vital sign as studies, as indicated hemodilution or
follows: >Maintain patent such as actual blood loss.
BP: vascular access Hemoglobin/hematocr
Temp: it, Serum electrolytes,
PR: clotting time and
RR: platelet count.
NURSING CARE PLAN

CRITERIA
SUBJECTIVE: Fatigue r/t Beta cell After 8 hours of >Assess skin turgor > Dry skin and After 8 hours of Nursing
mascular functioning Nursing and mucous mucous membranes Interventions the patient
“Dapat gyud nga strength. resulting in Interventions the membrane. is a sign of will be able to:
mag assist ug mo decreased insulin patient will be able dehydration.
lihok siya” as production. Glucose to: >Patient verbalized
verbalized by the derived from food >Provide comfort and >To be free from feelings of increased
patient’s husband. cannot be stored in >Verbalize increase safety measures. injury during energy and improved well
the liver thereby energy level. activity. being.
OBJECTIVES: remaining into the >Assess muscle
bloodstream. The >Display improved strength of patient and > Patient is able to
>Generalized beta cells of the ability to participate functional level of > To determine the identify factors that
weakness islets of Langerhans in desired activities. activity. level of activity. aggravate and relieved
>Fatigue release glucagon her fatigue.
>Limited range of which stimulates >The client will >Promote energy
motion the liver to release report improved conservation >Patient demonstrates a
>Inability to the stored glucose. sense of energy. techniques by >Symptoms of more positive and
perform activities The liverforms discussing ways of fatigue are alleviated happier attitude
of daily living glucose from the conserving energy with rest. Also, than before the
breakdown of while bathing, patient will be able interventions were
noncarbohydrate transferring and to accomplish more applied.
substances, performing ADLs. with a decreased
including amino expenditure of
acids resulting to energy.
muscle wasting
which results to
weakness.
(Wiley,2014)
NURSING CARE PLAN

CRITERIA
SUBJECTIVE: Deficient There is this After 8 hours of -Review importance of -Knowledge of the After 8 hours of nursing
Knowledge presence of nursing interventions weight control, cessation significance of risk interventions , the patient
“Pwede ba related to knowledge deficit , the patient was able of smoking, dietary factors provides patient was able to :
mausab gihapon condition, due to some to : changes, and exercise. with opportunity to -Participate in learning
ni akong sakit” prognosis, unfamiliar -Participate in -Encourage patient to make needed changes. process.
as verbalized by treatment, self- information that learning process. follow prescribed -Fear of triggering
the patient. care, and cause some reconditioning program; attacks may cause -Verbalize understanding
discharge needs. confusion to the -Assume caution to avoid patient to avoid o the disease and
client that needs responsibility for own exhaustion. participation in activity potential complication.
OBJECTIVE: to be discussed. learning, looking for that has been prescribed
information and to enhance recovery. -Initiation of lifestyle
-Frequently asking questions. -Provides knowledge changes and participate
asking question -Review disease base from which patient in treatment regimen.
about her -Verbalize process/ prognosis, can make informed
condition, understanding of Discuss hospitalization choices effective
treatment and condition/disease and prospective communicating and
diet. process and potential treatment as indicated. support at this time can
-Expresses complications. diminish anxiety and
confusion on the promote healing
nature of -Initiate necessary
condition. lifestyle changes.
DISCHARGE PLAN
PATIENT’S OUTCOME CRITERIA NURSING ORDERS
As soon as patient will be discharged from the hospital, the patient

significant others will be able to:
ASSESSMENT
1. Assess clients and significant others the importance of proper  Demonstrate to patient and family how to take down patient vital
monitoring of the vital signs. signs properly and record.
2. Assess patients knowledge regarding the present health  Encourage client to do proper hygiene to prevent from contamination to
condition. microorganism that will cause infection
3. Assess proper diet and nutrition.  Encourage patient to eat fruits and vegetables that help to promote better
health.
PLANNING
 Instruct patient and SO to create a schedule and activities

1. Plan activities to facilitate rest periods. providing time for accomplishing of recreation ample rest.
 Emphasized the importance of including patients preferred food.
2. Plan a menu within the limits of prescribed diets.  Encourage patient to return visit for monitoring its health and any
unpleasant circumstances.
3. Plan for retime visit.
IMPLIMENTATION
M-Medication  Tell the patient or S.O to continuance of medication at home is

 Patient will continue the medication as ordered by the doctor. very important.
 Provide medication schedule.
E-Environment and Exercise
 Provide a comfortable and a quite environment for the  Tell the patient and the S.O to minimize stressors that can trigger
patient. patient’s situation.
 Keep environment clean.  Instruct the patient and the S.O to maintain cleanliness of her environment
to promote fast recovery.
T- treatment
 The patient will take the prescribe medication as indicated at the  Instruct the patient to take the medication as prescribed and do not stop
right time, right route and right dose. even if feel better.
 Encourage patient to eat nutritious food.  Instruct patient and S.O the importance of maintaining proper
nutrition.
H- Health Teaching
 Taught the patient to do personal hygiene.

 Instruct the patient provide clean environment to prevent loading
microorganism. Encourage patient to avoid stressful matter to avoid
depression.
O- Out Patient Follow Up
 Emphasize the importance of follow up check up. Even  Advice patient and significant others to have a follow up check up
though patient feels better. for his additional assistance.
D- diet
 Tell the patient to eat hypoallergic diet.  Instruct patient to eat healthy foods such as fresh fruits, vegetables
and foods that lot of vitamins and nutrients.
S-Spiritual
 Advice patient to continue her spiritual activities to promote
 Pray always and and have faith in God. spiritual being.
EVALUATION  Encourage patient to verbalize understanding or the things taught

to her for this will help in her recovery.
- Verbalizes understanding on instruction given.  Ask the significant others to test if they listens and gain
- Evaluate progress of the patient’s condition. knowledge.
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GENERAL OBJECTIVES:

OBJECTIVE CONTENT TIME METHODOLOGY RESOURCES EVALUATION

A. Community -an inflammatory condition of

-Refers to conditions that involve narrowed or

-Is an abnormal amount of lipids

-An abnormally high level of uric acid in

-A common long term inflammatory disease of

3. Patients past She has been vaccinated with complete 1 minute

6. General state of A. Skin: Light Brown, Warm, Smooth, 2 minutes

B. Nutritional Metabolic Pattern

E. Cognitive or Perceptual Pattern

F. Sleep Rest Pattern

G. Self Perception Pattern

H. Role Relationship Model

I. Sexual Reproductive Pattern

J. Coping Stress Tolerance Pattern

K. Value Belief System

Nose and Nasal Cavity

The nose and nasal cavity constitute the main

The oral cavity, more commonly referred to as the

The pharynx is the next component of the respiratory

Bronchi & Bronchiole

The alimentary canal, which is also called

The buccinators muscles are located within the

The tongue is a large, muscular organ that

There are 32 teeth in the normal adult mouth,

Palate and Tonsils

The palate, or roof of the oral cavity, consists

The pharynx, or throat, which connects the

The esophagus is a muscular tube, lined with

The stomach is an enlarged segment of the

The muscular layer of the stomach is different

The small intestine is about 6 meters long and

The liver weighs about 1.36 kilograms and is

Pancreas is a fish-shaped spongy grayish-pink

The colon is made up of 6 parts all working

Rectum and Anus

The rectum is about eight inches long and

The circulatory system consists of four major

The Heart: About the size of two adult hands

Veins: Veins carry deoxygenated blood to the

Blood: Blood is the transport media of nearly

The circulatory system works thanks to

 Systemic circulation: This is the part that

SIGNS AND SYMPTOMS

 Cough (with some pneumonias you may cough

 Confusion, especially in older people

-Get a flu shot every year to prevent

Wash Your Hands

Wash your hands frequently, especially after

Tobacco damages your lung's ability to fight

Be Aware of Your General Health

-Since pneumonia often follows respiratory

C. DIABETES MELLITUS TYPE 2

Type 2 diabetes mellitus is a heterogeneous

β-Cell dysfunction is initially characterized by

Diet. Diet therapy, although important for the

Exercise has been shown to be beneficial in the

The key pathophysiologic event in diabetic

Macrophages are the most numerous cells in

Resident cells of the airway

Airway epithelium is another airway lining cell

CLINICAL CHEMISTRY 9/24/16

09-21-2016 GRAM STAIN: Pus Cells: Moderate /OIF