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CHAPTER I

INTRODUCTION

Brief Introduction:
Asthma (from the Greek ,sthma, "panting") is a common chronic inflammatory
disease of the airways characterized by variable and recurring symptoms, reversible airflow
obstruction

and

bronchospasm.Common

symptoms

include

wheezing,coughing,

chest

tightness, and shortness of breath.

It is clinically classified according to the frequency of symptoms, forced expiratory


volume in one second (FEV1), and peak expiratory flow rate. Asthma may also be classified as
atopic (extrinsic) or non-atopic (intrinsic) where atopy refers to a predisposition toward
developing type 1 hypersensitivity reactions.

Treatment of acute symptoms is usually with an inhaled short-acting beta-2 agonist


(such as salbutamol) and oral corticosteroids. In very severe cases, intravenous corticosteroids,
magnesium sulfate, and hospitalization may be required. Symptoms can be prevented by
avoiding triggers, such as allergens and irritants, and by the use of inhaled corticosteroids.
Long-acting beta agonists (LABA) or leukotriene antagonists may be used in addition to inhaled
corticosteroids if asthma symptoms remain uncontrolled.

Causes:
Asthma is caused by inflammation (swelling) in the airways. When an asthma attack
occurs, the lining of the air passages swells and the muscles surrounding the airways become
tight. This reduces the amount of air that can pass through the airway.

In persons who have sensitive airways, asthma symptoms can be triggered by breathing
in substances called allergens or triggers.

Common asthma triggers include:

Animals (pet hair or dander)

Dust mites

Certain medicines (aspirin and other NSAIDS)

Changes in weather (most often cold weather)

Chemicals in the air or in food

Exercise

Mold

Pollen

Respiratory infections, such as the common cold

Strong emotions (stress)

Tobacco smoke

Signs and Symptoms:


Most people with asthma have attacks separated by symptom-free periods. Some
people have long-term shortness of breath with episodes of increased shortness of breath.
Either wheezing or a cough may be the main symptom.
Asthma attacks can last for minutes to days, and can become dangerous if the airflow is
severely blocked.

Symptoms include:

Cough with or without sputum (phlegm) production

Pulling in of the skin between the ribs when breathing (intercostal retractions)
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Shortness of breath that gets worse with exercise or activity

Wheezing

Emergency symptoms that need prompt medical help:

Bluish color to the lips and face

Decreased level of alertness, such as severe drowsiness or confusion, during an asthma


attack

Extreme difficulty breathing

Rapid pulse

Severe anxiety due to shortness of breath

Sweating

Other symptoms that may occur:

Abnormal breathing pattern breathing out takes more than twice as long as breathing

Breathing temporarily stops

Chest pain

Tightness in the chest

Epidemiology:
As of 2011, 235330 million people worldwide are affected by asthma, and
approximately 250,000-345,000 people die per year from the disease. Rates vary between
countries with prevalences between 1 and 18%. It is more common in developed than
developing countries. One thus sees lower rates in Asia, Eastern Europe and Africa. Within
developed countries it is more common in those who are economically disadvantaged while in
contrast in developing countries it is more common in the affluent. The reason for these

differences is not well known. Low and middle income countries make up more than 80% of the
mortality.

While asthma is twice as common in boys as girls, severe asthma occurs at equal rates.
In contrast adult women have a higher rate of asthma than men and it is more common in the
young than the old. In children, asthma was the most common reason for admission to the
hospital following an emergency department visit in the US in 2011.

Global rates of asthma have increased significantly between the 1960s and 2008 with it
being recognized as a major public health problem since the 1970s. Rates of asthma have
plateaued in the developed world since the mid-1990s with recent increases primarily in the
developing world. Asthma affects approximately 7% of the population of the United States and
5% of people in the United Kingdom. Canada, Australia and New Zealand have rates of about
1415%. The latest recorded mortality rate of the Philippines is of 2004. ... The infant mortality
rate in the Philippines was 24 per 1,000 livebirths in 2006. In Davao City, in every 85, 000
livebirths, there are 19.8% prevalence rate

A. Objectives

General Objectives
At the end of two day hospital exposure, the researchers will be able to learn,
understand, form interventions, and the disease process and management of patients having
bronchial asthma.

Specific Objectives
In order for the group to meet the general objective the following specific objectives were
formulated to serve as a guide in case study.
1. To select case for the researchers case presentation related to biological crisis.
2. To present health history assessment of a patient having a bronchial asthma
3. To discuss anatomy and physiology of the affected organ or system related to the
illness.
4. To make a schematic diagram of pathophysiology of the illness.
5. To present the different drugs to be given to the patient.
6. To formulate nursing care plans that will address to the possible problems.
7. To provide health teachings concerning the illness
8. To provide recommendations to the client concerning the disease
9. Understand how and why certain diagnostic tests are done for the condition

B. Glossary of Terms

Atopic- denoting a form of allergy in which a hypersensitivity reaction such as dermatitis


or asthma may occur in a part of the body not in contact with the allergen.

Expiratory- of or relating to the exhalation of air from the lungs.

Extrinsic- not part of the essential nature of someone or something; coming or


operating from outside.

Inspiratory- relating to the act of breathing in

Intrinsic- contained wholly within the organ on which it acts

NSAIDS- Non Steroidal Anti-inflammatory Drugs

Phlegm- the thick viscous substance secreted by the mucous membranes of the
respiratory passages, especially when produced in excessive or abnormal quantities,
e.g., when someone is suffering from a cold.

Pollen- a fine powdery substance, typically yellow, consisting of microscopic grains


discharged from the male part of a flower or from a male cone. Each grain contains a
male gamete that can fertilize the female ovule, to which pollen is transported by the
wind, insects, or other animals.

Wheezing- breathe with a whistling or rattling sound in the chest, as a result of


obstruction in the air passages.

C. Significance of the Study

To the client and family


The study helps the client and the family to give full awareness of the disease and
proper health maintenance to ensure the safety and promotion of health of the patient having
bronchial asthma

To the students
This study helps us to understand of how this kind of disease exists to our client. As the
researchers conduct this study we are promoting cooperation just to come up with our
knowledge as a group. This will help the students to know their responsibility how to take care of
the patient with proper technique and procedure.

To the future nurses:


This study will help future nurses to know more about the disease and its management
and how to prevent them. It is essential to come up with this knowledge because of the
probability that they may encounter patients with such disease.

Chapter II
PATIENTS PROFILE

Name

Mr. A

Address

Purok 26, Riverside, Maa Davao City

Age

21 years old

Birthday

August 19, 1993

Sex

Male

Nationality

Filipino

Religion

Roman Catholic

Occupation

Self-employed

Admission Details
How Admitted :

Regular Admission

Date of Admission

August 18, 2014

Time

02:17 PM

Admitted by

Dr. C. Pepito

Physician

Dr. Chua & Dr. Racho

Admission Diagnosis: Bronchial Asthma secondary to Acute Sinusitis

A. Present Medical History


Four days prior to admission fever associated with colds and unproductive cough. No
other signs and symptoms, no meds and no consult done. One day prior to admission patient
experienced onset of body pain accompanied with the same signs and symptoms.

B. Past Medical History


The patient was diagnosed ease of hyperthyroidism last 2011 with maintenance
medication of methemazole once daily. He was diagnosed Pre- Hypertension during his college
days.

C. Family History
The patient lived at Purok 26, Riverside, Maa, Davao City together with his parents. The
patient is self-employed and her wife was in abroad. One of the factors of diseases was
hereditary, his mother had history of Bronchial Asthma and hypertension that passed away few
years ago, his father had also hypertension.

E. Developmental History
Patient A was born on August 19, 1993 in Tubod, Carmen, Davao del Norte. He is the
youngest among the four children.

F. Nutritional History
The patient when assessed weighs 65 kg. He is in low fat low salt diet since he has
hypertension. Able to consume all foods being served to him and loves fruits such as papaya,
apple, banana and mango. He didn't have any food allergies but have allergy in PU drug. He is
not a smoker and not an alcohol beverages drinker.

GUIDELINES

NORMAL ASSESSMENT

DAY 1

DAY2

Alert, conscious, and

The patient was conscious, coherent

The patient was conscious, coherent

coherent

and responsive and was able to answer

and was able to answer questions.

I. MENTAL STATUS
a. State of mental
conscious

questions.
b. Orientation

Oriented to event, time,

The patient was able to determine his

The patient was able to determine his

person, and place

name, birthday, time as evidenced by

name, birthday, birthplace and time as

the patient is aware that it is already

evidenced by the patient is aware that

night, he knows that he is in DDH & was

it is already night, he knows that he is

able to identify his physician, nurse, and

in DDH & was able to identify his

student nurse.

physician, nurse, and student nurse.

c. Intellectual

Able to understand,

The patient is attentive and can

capacity

comprehend and read

comprehend to questions and had long

words

attention span for about 10 minutes


since she can recall his past and
present illnesses.

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The patient is attentive and can


comprehend to questions and had
long attention span for about 10
minutes since she can recall his past
and present illnesses

d. Vocabulary level

e. Attention span

f.

Ability to

Able to use simple & non-

Patient was able to respond in verbal

Patient was able to respond in verbal

technical words

questions

questions

Attention span an average

Good attention span, able to narrate his

Good attention span, able to narrate

of 15 minutes

hospital experiences

his hospital experiences

Can understand ideas

The patient is able and understands

. The patient is able and understands

instructions and can relate to current

instructions and can relate to current

understand

situations and his language can be


understood.

situations and his language can be


understood.

II.STATUS OF SPECIAL
SENSES
a. Auditory
perception
b. Visual perception

c. Speech perception

Sensitive to high, low, and

Able to hear and respond to questions

Able to hear and respond to questions

moderate pitched

during the interview

during the interview

Able to see objects clearly

Able to identify the color of his linens

Able to identify the color of his linens

without use of aids

and curtains color in his room.

and curtains color in her room.

Able to speak with slow,

Patient was able to utter words clearly

Patient was able to utter words clearly

clear & soft voice

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d. Tactile perception

Able to feel light and deep

Patient was able to determine cold

Patient was able to determine cold

touch as well as cold, hot, &

atmosphere because of air-conditioned

atmosphere because of air-condition

pain

room and can feel the BP cuffed

and can feel the BP cuffed attached.

attached.
e. Olfactory
perception

Can distinguish different

Patient is able to smell the aroma of the

. Patient is able to smell the aroma of

smells such as (alcohol,

viands served to him as the patient

perfume and other scents.)

stated Humuta sa sud.an oy

patient stated Humuta sa sud.an oy

Ambulatory, ableto sit and

Complete bed rest with bathroom

AAT (Activity as Tolerated)

stand without aids or

privileges.

the viands served to him as the

III. MOTOR ABILITY


a. Current mobility

support
b. Posture

Errect body posture of

The patient has good body posture.

The patient has good body posture.

Patient has wide range of motion on

Patient has wide range of motion on

both upper and lower extremities

both upper and lower extremities

standing, setting and


walking
c. Range of motion

Active ROM

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d. Muscle and
nervous status
e. Loss of extremities

Full range of motion of

Patient was able to flex & extend

Patient was able to flex & extend

joints on all factors

muscle well

muscle well

No loss of extremities

None

None

36.5-37.5 C

35.9-36.5C

36.5

Clear breath sounds

Upon auscultation, positive for wheezes

Upon auscultation, positive for

at the right lung during inspiration and

wheezes at the left lung during

IV. BODY
TEMPERATURE
a. Ranges
V. RESPIRATION
STATUS
a. Character

expiration
b. Use of respiratory

inspiration and expiration

None

None

None

Strong palpable pulse; 60-

Strong palpable pulse; @ 80 beats per

Strong palpable pulse; @ 85 beats

aids
VI. CIRCULATORY
STATUS
a. Characteristics of

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arterial pulse

100 bpm

b. Radial pulse

minute
80 beats per minute and are strong and
palpable

per minute
80 beats per minute and are strong
and palpable

c. Blood pressure

90/60 mmHg

110/80 mmHg

110/80 mmHg

d. Mean Arterial

MAP= ( Systole + Diastole )

95 mmHg

95 mmHg

Pressure
e. Intravenous fluids

/2
w/o IVF

#5 PNSS 1L @ 100 cc/hr

#5 PNSS 1L @ 100 cc/hr

VII. NUTRITIONAL
STATUS
a. Condition of buccal
activity
b. Digestion of food

Smooth and moist and free

Smooth and moist and free from lesions

Smooth and moist and free from

from lesions

and no dentures noted

lesions and no dentures noted

Able to chew and swallow

Able to chew and swallow foods on full

Able to chew and swallow foods on

foods

diet and can consume of foods being

full diet and can consume of foods

served to him

being served to him.

VIII. ELIMINATION

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STATUS
a. Bowel

Patient has not defecated during our 8

Patient has defecated once during our

hrs shift.

8 hrs shift.

Voiding freely

Voiding freely

Voiding freely

No abnormalities

No abnormalities

No abnormalities

13-15 y/o

N/A

N/A

b. Patterns of

Regular; 28 days cycle; 3-4

N/A

N/A

menses

days

Skin should be relatively dry

Skin is relatively dry w/ a minimal

Skin is relatively dry w/ a minimal

w/ a minimal amount of

amount of perspiration

amount of perspiration

b. Bladder
c. Abnormalities

Bowel movement 3x a day

IX. FEMALE
REPRODUCTIVE
STATUS
a. Age of Menarche

X. STATUS OF SKIN
AND APPENDAGES
a. Skin

perspiration

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b. Hair

Evenly distributed; smooth

Evenly distributed; smooth in texture

Evenly distributed; smooth in texture

Nails should be slightly

Nails are slightly curved on the surface

Nails are slightly curved on the

curved on the surface or flat

or flat on the edges

surface or flat on the edges

Able to sleep 8-10 hrs/day

Sleeps 8 hrs/day

Sleeps 8 hrs/day

None

None

None

None

None

None

Emotionally stable

Emotionally stable

Emotionally stable.

in texture
c. Nails

on the edges
XI. STATE OF PHYSICAL
REST AND COMFORT
a. Sleep/Rest pattern
b. Presence of
discomfort
c. Use of supportive
aids
XII. EMOTIONAL
STATUS
a. Emotional
Reaction

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b. Body Image

Normal body alignment and

Normal body alignment and confident

Normal body alignment and confident

confident with ones

with ones appearance

with ones appearance

Able to interact w/ others;

Patient was able to interact w/ others;

Patient was able to interact w/ others;

friendly and easily

friendly and easily approachable.

friendly and easily approachable.

appearance
c. Ability to relate to
others

approachable

NURSING DIAGNOSIS:
Impaired gas exchange RT ventilation perfusion imbalance AEB dyspnea, tachypnea, and tachycardia
Ineffective breathing pattern r/t presence of secretions AEB productive cough and dyspnea

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CHAPTER III
THE PATHOPHYSIOLOGY

A. Review of the Anatomy and Physiology

The Respiratory System is crucial to every human being. Without it, we would cease to
live outside of the womb. Let us begin by taking a look at the structure of the respiratory system
and how vital it is to life. During inhalation or exhalation air is pulled towards or away from the
lungs, by several cavities, tubes, and openings.
The organs of the respiratory system make sure that oxygen enters our bodies and
carbon dioxide leaves our bodies.

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The respiratory tract is the path of air from the nose to the lungs. It is divided into two
sections: Upper Respiratory Tract and the Lower Respiratory Tract. Included in the upper
respiratory tract are the Nostrils, Nasal Cavities, Pharynx, Epiglottis, and the Larynx. The
lower respiratory tract consists of the Trachea,Bronchi, Bronchioles, and the Lungs.
As air moves along the respiratory tract it is warmed, moistened and filtered.

Function
Four processes of respiration are:
1. Breathing or ventilation
2. External respiration, which is the exchange of gases (oxygen and carbon dioxide)
between inhaled air and the blood.
3. Internal respiration, which is the exchange of gases between the blood and tissue
fluids.
4. Cellular respiration
In addition to these main processes, the respiratory system serves for:

Regulation of blood ph, which occurs in coordination with the kidneys, and as a

'Defense against microbes

Control of body temperature due to loss of evaporate during expiration

Breathing and Lung Mechanics


Ventilation is the exchange of air between the external environment and the alveoli. Air
moves by bulk flow from an area of high pressure to low pressure. All pressures in the
respiratory system are relative to atmospheric pressure (760mmHg at sea level). Air will move in
or out of the lungs depending on the pressure in the alveoli. The body changes the pressure in
the alveoli by changing the volume of the lungs. As volume increases pressure decreases and
as volume decreases pressure increases. There are two phases of ventilation; inspiration and
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expiration. During each phase the body changes the lung dimensions to produce a flow of air
either in or out of the lungs.
The body is able to stay at the dimensions of the lungs because of the relationship of the
lungs to the thoracic wall. Each lung is completely enclosed in a sac called the pleural sac. Two
structures contribute to the formation of this sac. The parietal pleura is attached to the thoracic
wall where as the visceral pleura is attached to the lung itself. In-between these two membranes
is a thin layer of intrapleural fluid. The intrapleural fluid completely surrounds the lungs and
lubricates the two surfaces so that they can slide across each other. Changing the pressure of
this fluid also allows the lungs and the thoracic wall to move together during normal breathing.
Much the way two glass slides with water in-between them are difficult to pull apart, such is the
relationship of the lungs to the thoracic wall.
The rhythm of ventilation is also controlled by the "Respiratory Center" which is located
largely in the medulla oblongata of the brain stem. This is part of the autonomic system and as
such is not controlled voluntarily (one can increase or decrease breathing rate voluntarily, but
that involves a different part of the brain). While resting, the respiratory center sends out action
potentials that travel along the phrenic nerves into the diaphragm and the external intercostal
muscles of the rib cage, causing inhalation. Relaxed exhalation occurs between impulses when
the muscles relax. Normal adults have a breathing rate of 12-20 respirations per minute.

The Pathway of Air


When one breathes air in at sea level, the inhalation is composed of different gases.
These gases and their quantities are Oxygen which makes up 21%, Nitrogen which is 78%,
Carbon Dioxide with 0.04% and others with significantly smaller portions.
In the process of breathing, air enters into the nasal cavity through the nostrils and is
filtered by coarse hairs (vibrissae) and mucous that are found there. The vibrissae filter
macroparticles, which are particles of large size. Dust, pollen, smoke, and fine particles are
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trapped in the mucous that lines the nasal cavities (hollow spaces within the bones of the skull
that warm, moisten, and filter the air). There are three bony projections inside the nasal cavity.
The superior, middle, and inferior nasal conchae. Air passes between these conchae via the
nasal meatuses.
Air then travels past the nasopharynx, oropharynx, and laryngopharynx, which are the
three portions that make up the pharynx. The pharynx is a funnel-shaped tube that connects
our nasal and oral cavities to the larynx. The tonsils which are part of the lymphatic system,
form a ring at the connection of the oral cavity and the pharynx. Here, they protect against
foreign invasion of antigens. Therefore the respiratory tract aids the immune system through this
protection. Then the air travels through the larynx. The larynx closes at the epiglottis to prevent
the passage of food or drink as a protection to our trachea and lungs. The larynx is also our
voicebox; it contains vocal cords, in which it produces sound. Sound is produced from the
vibration of the vocal cords when air passes through them.
The trachea, which is also known as our windpipe, has ciliated cells and mucous
secreting cells lining it, and is held open by C-shaped cartilage rings. One of its functions is
similar to the larynx and nasal cavity, by way of protection from dust and other particles. The
dust will adhere to the sticky mucous and the cilia helps propel it back up the trachea, to where
it is either swallowed or coughed up. The mucociliary escalator extends from the top of the
trachea all the way down to the bronchioles, which we will discuss later. Through the trachea,
the air is now able to pass into the bronchi.

Inspiration
Inspiration is initiated by contraction of the diaphragm and in some cases the
intercostals muscles when they receive nervous impulses. During normal quiet breathing, the
phrenic nerves stimulate the diaphragm to contract and move downward into the
abdomen. This downward movement of the diaphragm enlarges the thorax. When necessary,
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the intercostal muscles also increase the thorax by contacting and drawing the ribs upward and
outward.
As the diaphragm contracts inferiorly and thoracic muscles pull the chest wall outwardly,
the volume of the thoracic cavity increases. The lungs are held to the thoracic wall by negative
pressure in the pleural cavity, a very thin space filled with a few milliliters of lubricating pleural
fluid. The negative pressure in the pleural cavity is enough to hold the lungs open in spite of the
inherent elasticity of the tissue. Hence, as the thoracic cavity increases in volume the lungs are
pulled from all sides to expand, causing a drop in the pressure (a partial vacuum) within the lung
itself (but note that this negative pressure is still not as great as the negative pressure within the
pleural cavity--otherwise the lungs would pull away from the chest wall). Assuming the airway is
open, air from the external environment then follows its pressure gradient down and expands
the alveoli of the lungs, where gas exchange with the blood takes place. As long as pressure
within the alveoli is lower than atmospheric pressure air will continue to move inwardly, but as
soon as the pressure is stabilized air movement stops.

Expiration
During quiet breathing, expiration is normally a passive process and does not require
muscles to work (rather it is the result of the muscles relaxing). When the lungs are stretched
and expanded, stretch receptors within the alveoli send inhibitory nerve impulses to the medulla
oblongata, causing it to stop sending signals to the rib cage and diaphragm to contract. The
muscles of respiration and the lungs themselves are elastic, so when the diaphragm and
intercostal muscles relax there is an elastic recoil, which creates a positive pressure (pressure
in the lungs becomes greater than atmospheric pressure), and air moves out of the lungs by
flowing down its pressure gradient.

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Although the respiratory system is primarily under involuntary control, and regulated by
the medulla oblongata, we have some voluntary control over it also. This is due to the higher
brain function of the cerebral cortex.
When under physical or emotional stress, more frequent and deep breathing is needed,
and both inspiration and expiration will work as active processes. Additional muscles in the rib
cage forcefully contract and push air quickly out of the lungs. In addition to deeper breathing,
when coughing or sneezing we exhale forcibly. Our abdominal muscles will contract suddenly
(when there is an urge to cough or sneeze), raising the abdominal pressure. The rapid increase
in pressure pushes the relaxed diaphragm up against the pleural cavity. This causes air to be
forced out of the lungs.
Another function of the respiratory system is to sing and to speak. By exerting conscious
control over our breathing and regulating flow of air across the vocal cords we are able to create
and modify sounds.

Lung Compliance
Lung Compliance is the magnitude of the change in lung volume produced by a change
in pulmonary pressure. Compliance can be considered the opposite of stiffness. A low lung
compliance would mean that the lungs would need a greater than average change in
intrapleural pressure to change the volume of the lungs. A high lung compliance would indicate
that little pressure difference in intrapleural pressure is needed to change the volume of the
lungs. More energy is required to breathe normally in a person with low lung compliance.
Persons with low lung compliance due to disease therefore tend to take shallow breaths and
breathe more frequently.
Determination of Lung Compliance Two major things determine lung compliance. The
first is the elasticity of the lung tissue. Any thickening of lung tissues due to disease will
decrease lung compliance. The second is surface tensions at air water interfaces in the alveoli.
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The surface of the alveoli cells is moist. The attractive force, between the water cells on the
alveoli, is called surface tension. Thus, energy is required not only to expand the tissues of the
lung but also to overcome the surface tension of the water that lines the alveoli.
To overcome the forces of surface tension, certain alveoli cells (Type II pneumocytes)
secrete a protein and lipid complex called ""Surfactant, which acts like a detergent by
disrupting the hydrogen bonding of water that lines the alveoli, hence decreasing surface
tension.

Upper Respiratory Tract


The upper respiratory tract consists of the nose and the pharynx. Its primary function is
to receive the air from the external environment and filter, warm, and humidify it before it
reaches the delicate lungs where gas exchange will occur.
Air enters through the nostrils of the nose and is partially filtered by the nose hairs, then
flows into the nasal cavity. The nasal cavity is lined with epithelial tissue, containing blood
vessels, which help warm the air; and secrete mucous, which further filters the air. The
endothelial lining of the nasal cavity also contains tiny hairlike projections, called cilia.
The cilia serve to transport dust and other foreign particles, trapped in mucous, to the back of
the nasal cavity and to the pharynx. There the mucus is either coughed out, or swallowed and
digested by powerful stomach acids. After passing through the nasal cavity, the air flows down
the pharynx to the larynx.

Lower Respiratory Tract


The lower respiratory tract starts with the larynx, and includes the trachea, the two bronchi
that branch from the trachea, and the lungs themselves. This is where gas exchange actually
takes place.
1. Larynx
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The larynx (plural larynges), colloquially known as the voice box, is an organ in our neck
involved in protection of the trachea and sound production. The larynx houses the vocal cords,
and is situated just below where the tract of the pharynx splits into the trachea and the
esophagus. The larynx contains two important structures: the epiglottis and the vocal cords.
The epiglottis is a flap of cartilage located at the opening to the larynx. During
swallowing, the larynx (at the epiglottis and at the glottis) closes to prevent swallowed material
from entering the lungs; the larynx is also pulled upwards to assist this process. Stimulation of
the larynx by ingested matter produces a strong cough reflex to protect the lungs. Note: choking
occurs when the epiglottis fails to cover the trachea, and food becomes lodged in our windpipe.
The vocal cords consist of two folds of connective tissue that stretch and vibrate when
air passes through them, causing vocalization. The length the vocal cords are stretched
determines what pitch the sound will have. The strength of expiration from the lungs also
contributes to the loudness of the sound. Our ability to have some voluntary control over the
respiratory system enables us to sing and to speak. In order for the larynx to function and
produce sound, we need air. That is why we can't talk when we're swallowing.
1. Trachea
2. Bronchi
3. Lungs

Homeostasis and Gas Exchange


Homeostasis is maintained by the respiratory system in two ways: gas exchange and
regulation of blood pH. Gas exchange is performed by the lungs by eliminating carbon dioxide,
a waste product given off by cellular respiration. As carbon dioxide exits the body, oxygen
needed for cellular respiration enters the body through the lungs. ATP, produced by cellular
respiration, provides the energy for the body to perform many functions, including nerve

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conduction and muscle contraction. Lack of oxygen affects brain function, sense of judgment,
and a host of other problems.

Gas Exchange
Gas exchange in the lungs and in the alveoli is between the alveolar air and the blood in
the pulmonary capillaries. This exchange is a result of increased concentration of oxygen, and a
decrease of C02. This process of exchange is done through diffusion.

External Respiration
External respiration is the exchange of gas between the air in the alveoli and the blood
within the pulmonary capillaries. A normal rate of respiration is 12-25 breaths per minute. In
external respiration, gases diffuse in either direction across the walls of the alveoli. Oxygen
diffuses from the air into the blood and carbon dioxide diffuses out of the blood into the air. Most
of the carbon dioxide is carried to the lungs in plasma as bicarbonate ions (HCO3-). When
blood enters the pulmonary capillaries, the bicarbonate ions and hydrogen ions are converted to
carbonic acid (H2CO3) and then back into carbon dioxide (CO2) and water. This chemical
reaction also uses up hydrogen ions. The removal of these ions gives the blood a more neutral
pH, allowing hemoglobin to bind up more oxygen. De-oxygenated blood "blue blood" coming
from the pulmonary arteries, generally has an oxygen partial pressure (pp) of 40 mmHg and
CO2 pp of 45 mmHg. Oxygenated blood leaving the lungs via the pulmonary veins has a O2 pp
of 100 mmHg and CO2 pp of 40 mmHg. It should be noted that alveolar O2 pp is 105 mmHg,
and not 100 mmHg. The reason why pulmonary venous return blood has a lower than expected
O2 pp can be explained by "Ventilation Perfusion Mismatch".

Internal Respiration
Internal respiration is the exchanging of gases at the cellular level.
26

The Passage Way From the Trachea to the Bronchioles


There is a point at the inferior portion of the trachea where it branches into two directions
that form the right and left primary bronchus. This point is called the Carina which is the keellike cartilage plate at the division point. We are now at the Bronchial Tree. It is named so
because it has a series of respiratory tubes that branch off into smaller and smaller tubes as
they run throughout the lungs.
The Left Primary Bronchus has the same setup as the right with the lobar, segmental
bronchi and the bronchioles.
The lungs are attached to the heart and trachea through structures that are called
the roots of the lungs. The roots of the lungs are the bronchi, pulmonary vessels, bronchial
vessels, lymphatic vessels, and nerves. These structures enter and leave at the hilus of the
lung which is "the depression in the medial surface of a lung that forms the opening through
which the bronchus, blood vessels, and nerves pass" (medlineplus.gov).
There

are

number

of terminal

bronchioles connected

to respiratory

bronchioles which then advance into the alveolar ducts that then become alveolar sacs.
Each

bronchiole

terminates

in

an

elongated

space

enclosed

by

many

air

sacs

called alveoli which are surrounded by blood capillaries. Present there as well, are Alveolar
Macrophages,

they

ingest

any

microbes

that

reach

the

alveoli.

The Pulmonary

Alveoli are microscopic, which means they can only be seen through a microscope,
membranous air sacs within the lungs. They are units of respiration and the site of gas
exchange between the respiratory and circulatory systems.

Lung Capacity
The normal volume moved in or out of the lungs during quiet breathing is called tidal
volume. When we are in a relaxed state, only a small amount of air is brought in and out, about
500 mL. You can increase both the amount you inhale, and the amount you exhale, by
27

breathing deeply. Breathing in very deeply isInspiratory Reserve Volume and can increase
lung volume by 2900 mL, which is quite a bit more than the tidal volume of 500 mL. We can also
increase

expiration

by

contracting

our

thoracic

and

abdominal

muscles.

This

is

called expiratory reserve volume and is about 1400 ml of air. Vital capacity is the total of
tidal, inspiratory reserve and expiratory reserve volumes; it is called vital capacity because it is
vital for life, and the more air you can move, the better off you are. There are a number of
illnesses that we will discuss later in the chapter that decrease vital capacity. Vital Capacity can
vary a little depending on how much we can increase inspiration by expanding our chest and
lungs. Some air that we breathe never even reaches the lungs! Instead it fills our nasal cavities,
trachea, bronchi, and bronchioles. These passages aren't used in gas exchange so they are
considered to be dead air space. To make sure that the inhaled air gets to the lungs, we need
to breathe slowly and deeply. Even when we exhale deeply some air is still in the lungs,(about
1000 ml) and is called residual volume. This air isn't useful for gas exchange. There are certain
types of diseases of the lung where residual volume builds up because the person cannot fully
empty the lungs. This means that the vital capacity is also reduced because their lungs are filled
with useless air.
Stimulation of Breathing
There are two pathways of motor neuron stimulation of the respiratory muscles. The first
is the control of voluntary breathing by the cerebral cortex. The second is involuntary breathing
controlled by the medulla oblongata.
There are chemoreceptors in the aorta, the carotid body of carotid arteries, and in the
medulla oblongata of the brainstem that are sensitive to pH. As carbon dioxide levels increase
there is a buildup of carbonic acid, which releases hydrogen ions and lowers pH. Thus, the
chemoreceptors do not respond to changes in oxygen levels (which actually change much more
slowly), but to pH, which is dependent upon plasma carbon dioxide levels. In other words, CO2
is the driving force for breathing. The receptors in the aorta and the carotid sinus initiate a
28

reflex that immediately stimulates breathing rate and the receptors in the medulla stimulate a
sustained increase in breathing until blood pH returns to normal.
This response can be experienced by running a 100 meter dash. During this exertion (or
any other sustained exercise) your muscle cells must metabolize ATP at a much faster rate than
usual, and thus will produce much higher quantities of CO2. The blood pH drops as CO2 levels
increase, and you will involuntarily increase breathing rate very soon after beginning the sprint.
You will continue to breathe heavily after the race, thus expelling more carbon dioxide, until pH
has returned to normal. Metabolic acidosis therefore is acutely corrected by respiratory
compensation (hyperventilation).

Source: Marieb, Elaine. 2012. Human Anatomy and Physiology, 9th Ed.

29

B. The Diagram
Predisposing Factors:
Family History

Precipitating Factors:
URTI (Acute sinusitis)
Air pollution
Environmental
allergens and irritants

Exposure to different allergens (stimulus)

Nasal mucosa responds to the virus by increased production of mucus

Stagnation of secretions

Ostial obstruction including mucosal congestion

Blockage to normal ventilation and drainage of the sinus

Decreases in the pH and changes in the mucosal metabolism

Subsequent damage to the epithelium and cilia, generating


favorable conditions for bacterial growth

Acute sinusitis

S/sy: Nasal congestion,


Fever, Purulent nasal
discharge, maxillary pain,
impairments of smell

Stimuli enters from the nasopharynx, the trachea then to


the bronchial tree

30

Differentiation into plasma cells

Release of Immunoglobulin E (IgE)

Mast cell degranulation

Release of different chemical mediators

Mediator release results in opening of the mucosal intercellular junctions

Inflammatory mediator release from mast cells, macrophages, & epithelial cells

Leukotriene

Histamine

Inflammatory cell
infiltration in the airway

Increased mucosal
production

Increased mucosal
secretions
Reduced airflow in
the alveoli

Bradykinin

Prostaglandin

Increased vascular
permeability

Bronchial smooth muscle contraction

Constriction of
vascular smooth
Acts on thermoregulatory
center of hypothalamus

Bronchoconstriction

Epithelial injury and edema (due to vascular permeability)


Decreased mucociliary function & reduced clearance of respiratory tract secretions
Increased airway responsiveness
Asthma attack

31

Diagnostic test:
Spirometry
Peak Expiratory Flow
Chest X-ray

Medical Management:
Oxygen therapy
Medications:
- Inhaled steroid
- Beta2 adrenergic
agent
- Bronchodilator
Deep breathing,
coughing exercise
Adequate rest

Asthma attack

Sign & Symptoms: Fever,


Wheezing, Tachypnea (with
prolonged expiration),
Tachycardia, Difficulty of
breathing, coughing (sputum is
yellow and sticky), Accessory
muscle breathing, supraterbal
retraction, restlessness, anxiety

If not treated:
Hyperventilation

Compensatory mechanism failed

Altered CO2 & O2 exchange

Carbon dioxide retention

Increased airway resistance

Hypercapnia, Hypoxemia

Respiratory alkalosis
alkalosis

S/s: Cyanosis, Decreased level of


consciousness

Impaired gas exchange

Good Prognosis

Decreased tissue perfusion


Cellular ischemia
Tissue Necrosis
Hypoxia
Vital organ failure/Death
Death

32

C. Narrative

The National Heart, Lung, and Blood Institutes Second Expert Panel on the
Management of Asthma defined bronchial asthma as a chronic inflammatory disorder of the
airways in which many cells and cellular elements play a role, in particular, mast cells,
eosinophils, T lymphocytes, and epithelial cells. This inflammatory process produces recurrent
episodes of airway obstruction, characterized by wheezing, breathlessness, chest tightness,
and a cough that often is worse at night and in the early morning. These episodes, which
usually are reversible either spontaneously or with treatment, also cause an associated increase
in bronchial responsiveness to a variety of stimuli.

The pathophysiology of involves a genetic (atopy) predisposition coupled with


environmental factors (viruses, allergens, and occupational exposure). Based on their
mechanism of response, these triggers can be divided into two categoriesbronchospastic or
inflammatory. Bronchospastic triggers depend on the existing level of airway responsiveness.
They do not normally increase airway responsiveness but produce symptoms in persons who
already are predisposed to bronchospasm. Bronchospastic triggers include cold air, exercise,
emotional upset, and exposure to bronchial irritants such as cigarette smoke. Inflammatory
triggers exert their effects through the inflammatory response. They cause inflammation and
prime the airways so they are hyperresponsive to allergic and nonallergic stimuli.

The pathophysiology of the disease was most likely triggered by the untreated cute
rhinosinusitis. Acute rhinosinusitis is most likely to be caused by the interaction of a
predisposing condition (such as environmental triggers), a viral infection, and a consequent
inflammatory response within the sinonasal mucosa. With increased oedema and mucus
production, the sinus ostium is obstructed, blocking normal ventilation and drainage of the sinus.
33

With decreased mucociliary clearance, stasis of secretions occurs and a secondary bacterial
infection can take place. From an inflammatory standpoint, high levels of tumour necrosis factorbeta and interferon-gamma are associated with release of various pro-inflammatory cytokines.

The mechanisms whereby asthma attack takes place is when the stimulus, or the
allergen from the nasopharynx is then pulled into the trache down to the bronchioles causing
now exposure to an asthmatic trigger. The late-phase response involves inflammation and
increased airway responsiveness that prolong the asthma attack and set into motion a vicious
cycle of exacerbations. Typically, the response reaches a maximum within a few hours and may
last for days or even weeks. An initial trigger causes the release of inflammatory mediators from
mast cells, macrophages, and epithelial cells. These substances induce the migration and
activation of other inflammatory cells, which then produce epithelial injury and edema, changes
in mucociliary function and reduced clearance of respiratory tract secretions, and increased
airway responsiveness. Responsiveness to cholinergic mediators often is heightened,
suggesting changes in parasympathetic control of airway function. Chronic inflammation can
lead to airway remodeling, in which case airflow limitations may be only partially reversible.

Source: Porth, CM. Pathophysiology: Concepts of Altered Health States. 7th Edition. 2004, Pp
695 - 699

34

CHAPTER IV
RESULTS, ANALYSIS, AND JUSTIFICATION

A. Course in the Ward


DOCTORS ORDER

Aug. 18, 2014 3pm


-

Please admit under the service of Dr. Pepito

V/S Q4

Venoclysis PNSS 1L @ 100cc/hr

Labs: CBC PLT, UA, XRAY PARANASAL

Meds: Paracetamol 500mg/tab Q4 for fever 1 dose now

Will inform AP with thos admission. NOD will follow up without fail.

Please inform MROD/BRIC floor of this admission

Refer accordingly

Thank you

To continue maintenance

Add meds: Omeprazole 40mg 1tab OD, Norgesic Forte 1tab TID PRN for headache.

Aug. 18, 2014 MROD


-

Plan to start Co amoxiclav 1.2g Q8 IVTT after (-) skin test

Fluticasone nasal spray 2spray/nostrils OD

Refer

35

Aug. 19, 2014 10am


-

Rounds with Dr. Pepito

Start Co-amoxiclav 1.2g Q8 IVTT

Decrease Norgesic Forte q8 to PRN

Attach initial result CBC, XRAY

Last dose of co-amoxiclav IVTT tomorrow 2pm then shift to co-amoxiclav 1g BID

B. Laboratory Findings

Procedure: Chest X-ray

Date Performed: Aug. 18, 2014

INTERPRETATION:
Heart size is within normal limits. Its configuration unremarkable. Pulmonary vascularity
is normal. A 1.2 x 0.7 ovoid in density is seen in right upper lobe overlying the 4th intercostals
space. Rests of the lungs are clear. The lateral costophrenic sinuses are sharp. Hili are not
enlarged. Visualized osseous structures are normal.

IMPRESSION:
-

Solitary pulmonary nodule, consider pulmonary granuloma right.

Procedure: Paranasal Xray

Date Performed: Aug. 18, 2014

INTERPRETATION:
Both anterior and posterior group of sinuses are well aerated. Bony walls are intact.
Nasal septum is in the midline

36

IMPRESSION:
-

Normal Study

37

C. Nursing Care Plan


Problem

Scientific Basis

Objective:
- wheezing
upon

Nursing Intervention

Systemic

foreign

clearance

keeps

microorganism

absence

the

AEB
of

signs

lymphocyte

and -

to Patient will verbalize


encourage the use

produce

understanding

that
of diaphragmatic

antibodies that are allergens

like

dust
breathing

- coughing,

specific

sputum

is
and

sticky

to

that ,fumes,

animal

These dander,

pollen,

antibodies

then extremes

attach

mast of temperature

to

and

and

cells in the lungs. humidity are irritants

prolonged

The mast cell with or factors that can

- tachycardia

the
attaches

antibody contribute
to

the ineffective

hydration Short Term


secretion

help

to

to
airway

such as cigarette
smoke,

aerosols,

mobilize

secretions

without

causing

signs

Long Term
and

:The

patient

shall

have

Bronchial irritants
demonstrated
cause

broncho
behaviors and

constriction

and
understood

extremes

increased mucus

of temperature, and

production, which

38

free from

and distress.

ventilation

3. Instruct pt to avoid
irritants

be

improve of respiratory

breathlessness

bronchial

: The pt shall

techniques any

These

fatigue.

- tachypnea,

expiration

and

coughing exercises.
antigen.

Evaluation

easier to expectorate.

B of respiratory distress

- dyspnea

yellow

the pt.

2. Teach

and expiration

Rationale

The presence of a Patient will maintain/ 1. Adequately hydrate -

triggers

inspiration

Objectives

causative

antigen

- chest

and clearance and should

begins

tightness

to be

degranulate. This will

avoided.

fumes.

then interfere with factors

Patient

airway clearance.

prevent

demonstrate

recurrence

behaviors that would

of problem.

- supra sternal
degranulation
retraction
causes the release prevent the recurrence
- restlessness

of certain chemical of the problem.

- anxiety

mediators,

- cyanosis

namely, histamine,
bradykinin,

- loss
prostaglandin, and
of consciousn
leukotriene. These

4. Teach

early

ess
signs

chemical
mediators
Analysis:

clearance

infection

cause

are

bronchospasm

ineffective airway leading

n,

constriction,

vascular

that

to

be

reported to the

to

clinician

RT bronchoconstrictio

broncho

of

immediately.

increased

Minor respiratory
infections that are
of

no

consequence

to

the person with


normal lungs can
produce
disturbances

39

Increases

fatal
in

to

increased mucus permeability


production,
respiratory
infection

and leading

to

fluid

leakage from the


AEB lung

vasculature

wheezing,

and

increased

dyspnea, and

mucus

cough

sputum

the lungs of an

production

asthmatic person.

Change in color

is crucial.

of sputum
-

Increased

thickness

Reduction. These
lead

to

of the

swelling

of sputum

bronchi,

mucus buildup that


plugs the airway
and

decreased

diameter.
causes

of chest,
This

fatigue

an
-

increased

Increased SOB
,tightness

bronchial

Increased

airway
coughing

resistance and a
constricted

40

Fever or chills.

Early recognition

or

pathway for air. Air


cannot

pass

effectively and this


manifests

as

whistling sound.

Coughing is a way
to

expel

the

obstruction
-

Uses gravity to

(mucus plug) while


help
dyspnea

is

raise

a
secretions

manifestation

so

5. If indicated,

of

they can be more


the

perform

increased

easily
postural

airway resistance.

expectorated.
drainage

with

percussion and
vibration in the
morning and at
41

night

as

prescribed.
6.

Assist

in

ensures

adequate delivery

administering
nebulizer,

This

of medications to
as

the airways.

indicated.

Antibiotics maybe
prescribed

7.Administer
ATX
prescribed

42

to

treat the infection


as

Problem
Objective:
-

Scientific Basis
Presences

Objectives
Patient

Nursing Intervention
will

wheezing

of secretions in the demonstrate

upon

bronchi

inspiration

resulting

to

and

blockage

of

expiration

that will enter the manifest

signs

dyspnea

body

respiratory

coughing,

producing

will lip

and

yellow and needed

by

and

rapport

monitor

air breathing. Patient will

thus decreased

To gain pt.s

Patient

and

obtain of

To

Serve

of

to

track effort

important

absence

changes

of dyspnea

AEB absence

air of dyspnea Patient will

3. Auscultate

breath

sounds

presence

understanding

and

assess

of adventitious

of causative

breath sounds.

factors

tachypnea

to maintain clear of causative

airway.

prolonged

obstruction

expiration

further heightened improve

of the bed and

difficulty

tachycardi

by bronchospasm breathingpattern1.

change position

breathing.

due

of the pt. every

factors

will

To check for the verbalize

body. And inability understanding

airway pattern

demonstrate

is behaviors that would

AEB

Patient

the verbalize

This and

decreased

data, respiratory

baseline

record

will

manifest signs

sticky

to

Evaluation

Trust.

2. assess pt.s VS

a diaphragmatic

effort

sputum is insufficient

breathing

1. Establish

pursed-

Rationale

and

demonstrate
4. Elevate

the

43

head

To

minimize behaviors that


in would improve
breathing
pattern.

chest

contraction

tightness

smooth muscles in

supra

the bronchi. This is

deep breathing

sternal

caused

and

retraction

parasympathetic

restlessne

stimulation of the

ss

muscarinic

anxiety

receptors as well

and

cyanosis

as

breathing.

loss

mediators

of conscio

released

usness

response

by

presence
allergen.

Ineffective

of the

2hours.
5. Encourage

by

coughing

for

expectoration.

diaphragmatic

chemical

pursed-lip

7. Encourage
in

efficient

increase in fluid

the

To decrease air
trapping and for

intake.

breathing.
-

of

To

prevent

fatigue.
8. Encourage
opportunities for

r/t

rest

secretions

maximize

6. Demonstrate

to

To
effort

exercises.

breathing pattern
presence

of

AEB

productive cough

44

and

limit

To

prevent

physical

situations that will

activities.

aggravate

the

and dyspnea

9. Reinforce low1.

condition10.

To

mobilize

Patient

will

demonstrate
pursed-lip
breathing
diaphragmatic
breathing

45

and

Problem

Scientific Basis

Objective:
-

Objectives

Nursing Intervention

Bronchial asthma Patient will improve gas

wheezing

is

upon

wherein

absence of respiratory

inspiration

the airways diameter

distress

and

Is highly reduced. demonstrate improved

expiration

This

dyspnea

severe

adequate oxygenation

coughing,

bronchospasm,

of

sputum

condition exchange

is

is mucosal

due

AEB

Patient

to ventilation

2. assess pt.s

Auscultatebreath

edema tissues by ABGs within sounds

and

assess

airway pattern.

formation. There is Limits and absence

tachypnea,

arise

prolonged

resistance

expiration

leads

tachycardia

decreased amount understand

chest

of air that enters of causative

tightness

upon inspiration as and

airway of symptoms

5.

Elevate

To gain pt.s

Pt. will improve


gas exchange

head

which of respiratory distress. of the bed and change

Serve

appropriate breathing and coughing

46

absence

of respiratory

track distress Patient

important

will

changes.

demonstrate

To check for the improved


presence

ventilation and

of adventitious

adequate

breath sounds.

oxygenation of

minimize tissues by ABGs

To

in within

breathing

2hours.
6. Encourage deep

to

difficulty

to Patient will verbalize position of the pt. every

factors

obtain AEB

To

baseline data

3. VS monitor and

4.

Evaluation

Trust.

and record.

sticky

in

rapport.

will Condition.

yellow and and mucus plug clients normal

1. Establish

Rationale

normal
Limits

To
effort

clients

and

maximize absence
for of symptoms

supra

well as expiration. interventions

(deep exercises.

sternal

Thus, ventilation is breathing,

cough

retraction

impaired.

restlessnes

bronchial asthma,

perfusion

anxiety

directly

cyanosis

However,

Alteredered

balance

loc

ventilation

In exercises, etc

is

7.

expectoration
Demonstrate

diaphragmatic

and

pursed-lip breathing.

the
between
and

perfusion

8.

Encourage

increase in fluid intake.


9.

To decrease air distress.


trapping and for Patient

not

affected.

efficient

verbalize

breathing.

understand

To

factors

fatigue.

To

prevent interventions

and

situations that will (deep

gas (V/Q ratio) is lost

limitphysicalactivities.1

aggravate

breathing,

exchange

RT because

0.Reinforce low salt, low

thecondition10.

cough

ventilation

the

perfusion

perfusion (capillary

adequate

imbalance

AEB circulation),

dyspnea,

much

gas

fat diet1.

is

tachypnea,

and available to diffuse

tachycardia

from the alveoli to

To mobilize Patient exercises, etc)


secretions

not

47

and

appropriate

Impaired

despite

will

prevent of causative

Encourage

opportunities for rest

of respiratory

the capillaries.
Conversely,
the gases in the
capillaries
diffuse

do
to

the

alveoli but since


expiration

is

impaired,

such

gases fail to be
ventilated

out.

Thus,

gas

exchange

is

impaired.

48

D. Drug Study
Generic/Bra

Mechanism of Action

Indication

Contraind

nd Name

Adverse Effect

Dosage

Nursing

ication
Omeprazole

is

in

a omeprazole is used Contraindi

GENERIC

class of drugs called for

NAME:

proton pump inhibitors induced

omeprazole,

(PPI)

omeprazole/s

production of acid by ulcers

odium

the

stomach

bicarbonate

stomach. Omeprazole,

duodenum; gastro

BRAND

like other proton-pump esophageal

NAME:

inhibitors,

Prilosec,
Zegerid

that

block

treating

acid- cated

and itivity

of

the the

The
common

hypersens

the inflammation

Responsibilities
most Capsules:
side 10, 20 and

effects

to are diarrhea, na
drug, usea, vomiting,

and pregnant
and

Tablets:

give

before

food

mg.

preferably

20

breakfast;

mg (Prilosec

capsules

OTC).

must

h and dizziness. Powder

for

be

swallowed

Nervousness,

oral

whole (do not

abnormal

suspension:

chew

enzyme in the wall of erosive esophagitis

heartbeat, musc

20

crush)

the

le

mg

blocks

stomach

produces
blocking

acid.
the

reflux lactating

headaches, ras

40

Oral

the disease (GERD);

that ,

mothers

heartburn;

By prevention of upper

pain, weakness,

enzyme, gastrointestinal

leg cramps, and

49

and

40

or

the production of acid is bleeding in critically

water retention

decreased,

occur

and

this ill

patients;

and

allows the stomach and Zollinger-Ellison


esophagus to heal.

infrequently.

Syndrome.

50

Generic/Brand

Mechanism of

Name

Action

Indication

Contraindication

Adverse Effect

Dosage

Nursing
Responsibilities

Brand Name:

Amoxicillin is

Co-amoxiclav is

Hypersensitivity

GI: Abdominal

Co-amoxiclav

If parenteral

Amoclav

semisynthetic

indicated for the

to the active

discomfort,

may be

administration of high

penicillin (beta-

treatment of the

substances, to

anorexia, and

administered

Co-amoxiclav doses

lactam antibiotic)

following in adults

any of the

flatulence,

either by IV

is necessary, the

that inhibits one or

and children

penicillins or to

dyspepsia,

injection or by

sodium content

more enzymes

Severe infections

any of the

diarrhea/loose

intermittent

should be taken into

(often referred to

of the ear, nose

excipients.

stools, nausea,

infusion. It

consideration in

as penicillin-

and throat (such

vomiting,

isNOT suitabl

patients for whom

binding proteins,

as mastoiditis,

indigestion,

e for IM

sodium intake is of

PBPs) in the

peritonsillar

administration.

medical concern.

biosynthetic

infections,

Co-amoxiclav

During administration

pathway of

epiglottitis and

should be

of high doses of

given by slow

amoxicillin, it is

IV

recommended to

injection over

maintain adequate

Generic Name:
Amoxicillin +
Clavulanic acid
Co-amoxiclav
500mg/100mg
Powder for
Solution for
Injection or
Infusion
Therapeutic
Category
Anti-infectives

bacterial
peptidoglycan,
which is an

sinusitis when
accompanied by
severe systemic

History of a
severe immediate
hypersensitivity

CNS: Dizziness

reaction (e.g.

, headache

anaphylaxis) to
another -lactam
agent (e.g. a
cephalosporin,

(Systemic

51

Other Adverse
Effects: Phlebiti
s at the
injection site,

integral structural

signs and

carbapenem or

superficial tooth

a period of 3

fluid intake and

component of the

symptoms)

monobactam).

discoloration

to 4 mins and

urinary output in order

bacterial cell wall.

Acute

History of

(brown, yellow,

within 20 mins

to reduce the

exacerbations of

jaundice/hepatic

or gray

of

possibility of

chronic bronchitis

impairment due to

staining)

reconstitution.

crystalluria associated

(adequately

amoxicillin/clavula

It may be

with amoxicillin

diagnosed)

nic acid (see

injected

therapy.

Community

section 4.8).

Inhibition of
peptidoglycan
synthesis leads to
weakening of the
cell wall, which is
usually followed by

directly into
the vein or via

acquired
cell lysis and

a drip tube.
pneumonia

death.
Cystitis
Amoxicillin is
susceptible to

Pyelonephritis

Appropriate
monitoring should be
undertaken when

1000 mg/ 200

anticoagulants are

mg every 8

prescribed

hours

concomitantly with

degradation by

Skin and soft

beta-lactamases

tissue infections

produced by

in particular

resistant bacteria

cellulitis, animal

been reported rarely

and therefore the

bites, severe

in patients receiving

Actual
Dosage; 1.2g
Q8 IVTT

52

Co-amoxiclav since
prolongation of
prothrombin time has

spectrum of

dental abscess

activity of

with spreading

amoxicillin alone

cellulitis.

does not include

Bone and joint

organisms which
produce these
enzymes.
Clavulanic acid is
a beta-lactam
structurally related

Co-amoxiclav.

infections, in
particular
osteomyelitis
Intra-abdominal
infections
Femal genital

to penicillins. It
infections
inactivates some
beta-lactamase
enzymes thereby
preventing
inactivation of
amoxicillin.
Clavulanic acid

Prophylaxis
against infections
associated with
major surgical
procedures in
adults, such as

53

alone does not

those involving

exert a clinically

the:

useful antibacterial

Gastrointestinal

effect.

tract
Pelvic cavity
Head and neck

54

Generic/Brand

Mechanism of

Name

Action

Indication

Contraindication

Adverse Effect

Dosage

Nursing
Responsibilities

Brand Name:

Fluticasone is a

Fluticasone

FLONASE

Nasal

Fluticasone

Shake the medicine

Nasoflo

steroid. It

nasal is used to

(fluticasone

dryness/irritatio

nasal spray

bottle well just before

Generic Name:

prevents the

treat nasal

propionate) Nasal

n, nausea, or

2spray/nostrils

each use.

fluticasone

release of

symptoms such

Spray is

vomiting may

OD

propionate

substances in

as congestion,

contraindicated in

occur.

the body that

sneezing, and

patients with a

cause

runny nose

hypersensitivity to

inflammation.

caused by

any of its

seasonal or

ingredients.

Nasal Spray, 50
mcg
Fluticasone
propionate is a
synthetic,
trifluorinatedcorti
costeroid with
antiinflammatory.

year-round

Store this medication in


an upright position at

GI

room temperature,

Effects: Nausea

away from moisture

, vomiting,

and heat. Throw the

abdominal pain,

medication away after

diarrhea

you have used 120

allergies

sprays, even if there is

FLONASE

still medicine left in the


Ocular

(fluticasone

bottle.
Effects: Drynes

propionate)

s and irritation,

Nasal Spray is

conjunctivitis,

55

Fluticasone nasal can


lower the blood cells

Fluticasone

indicated for the

blurred vision,

that help your body

propionate is a

management of

glaucoma,

fight infections. Avoid

topically active,

the nasal

increased

being near people who

synthetic,

symptoms of

intraocular

are sick or have

trifluorinated

seasonal and

pressure, and

infections. Call your

corticosteroid. It

perennial allergic

cataract

doctor for preventive

has a high

and non

affinity for

allergic rhinitis in

treatment if you are


exposed to chicken pox
Miscellaneous:

glucocorticoid

adults and

or measles
Headache,

receptor with

pediatric patients

negligible activity

4 years of age

dizziness,
drowsiness,
at androsterone,

and older
lethargy, .

progesterone,
fatigue or

estrogen, or

arthralgia,

mineralocorticoid

fever, flu-like

receptors.

symptoms,
menstrual

56

cramps, aches

It has anti-

and pains, and

inflammatory

cases of growth

and

suppression

immunosuppres

have been

sant activities

reported.

after topical
application to the
nasal mucosa.

57

CHAPTER V

Summary:

Asthma is a common chronic inflammatory disease of the airways characterized by variable and
recurring symptoms, reversible airflow obstruction and bronchospasm.Common symptoms
include wheezing,coughing, chest tightness, and shortness of breath.

Our patient, Patient D resides at Ma-a, Davao City, 21 years old male has a chief complaint of
fever. Four days prior to admission, patient was already positive for fever associated with colds.
Two days prior to admission, there is already onset of body pain and a day before admission the
patient has headache. During admission , the patient was diagnosed to have bronchial asthma
not on acute exacerbation associated with acute sinusitis. Patient is also positive of
hypertension.

Conclusion:

Upon the making of this case study, the researchers have finally had an outcome on how to
prevent, treat, diagnose and provide the appropriate nursing care of patients with bronchial
asthma. And by means of proper education rendered during the period of assessment and care,
the researchers were able to fully understand and recognize the disease condition. The client
learned the importance of healthy lifestyle and identified the factors that aggravated his
condition.

58

Recommendation:

Medication

Instruct family to continue taking drug as ordered to prevent further complication

Take Paracetamol 500mg q4 for fever. Decreased dose of Norgesic Forte q8 to PRN
and a dose of co-amoxiclav 1g BID as ordered.

Instruct the client and his watcher to take/give the medications on time and if a dosage
was missed, instruct them not to take double-up doses

Exercise

Exercise triggers bronchial narrowing in asthma by bringing large volumes of air deep
into the chest. When breathing quietly, about one gallon of air enters the lungs during
each minute.

Instruct family to avoid strenuous exercises

Instruct the clients watcher to perform passive range of motion exercises to the client.

Encourage adequate rest and sleep to provide comfort

Instruct the patient that when exercising, make it remain at slow phase as possible.

Treatment

Encourage patient to participate in the treatment prescribed by the physician to improve


health and condition though there is still no treatment for asthma, it is just controlled.

Encourage the client to have adequate time for rest.

Direct the clients watcher to comply the therapeutic regimen of the client

Instruct the client to comply follow-up check-up of physician as prescribe to ensure full
recovery and rehabilitation

59

Hygiene

Encourage Patient to promote good personal hygiene.

Encourage self care by hand washing everytime even if an untidy event has been done
or not to simply deter the spread of microbes causing diseases and may contribute to
such disease like asthma.

Outpatient order

Instruct family to follow the therapeutic regimens prescribed by the physician such as
medication. Diet and exercise to promote health and wellness

Follow up schedule of check up to monitor health status

Discuss with the clients watcher on the administration, side effects and indications of
home medications as ordered

Diet

Teach the clients watcher to give meals to the client regularly and eat healthy Foods to
facilitate healthy metabolic activity.

Encourage the client to balance food intake and physical activity. Though there is so
specific or special diet for asthma, still encourage the patient to take on healthy foods
and take unhealthy dies at a minimum as possible.

Spiritual

Encourage to have time in praying together with family members to enhance self
concept and develop a sense of hope that aids in the wellness of clients health
condition.

60

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