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Patient name: A.B.R Age: 70 years old Sex: Male Civil Status: Married
“Difficulty of Breathing”
“Cyanotic”
Patient has been diagnosed with COPD and Diabetes Mellitus Type II just
this year 2011. He was then prescribed with Ansimar 40mg once a day and
Seretide 2 puffs per day. For his DM Type II, he has a maintenance of
Glucovance 500mg. Patient didn’t undergo any operation. Patient’s family has a
history of Hypertension and Diabetes Mellitus from his father side then was
acquired by his siblings. His brother also has COPD at present. Furthermore one
of his siblings has a Cancer at present but it was not specified by the relative.
Patient doesn’t have any allergies on medications, pollens, food and other
chemicals. Also, patient is a smoker which consumes 20 stick per day and an
alcoholic drinker three times a week but stopped ten years ago.
III. PATHOPHYSIOLOGY: CHRONIC OBSTRUCTIVE PULMONARY DISEASE
NON MODIFIABLE FACTORS: MODIFIABLE FACTORS:
• history of respiratory • smoking
function
• exposure to air
• heredity pollution and industrial
• decrease alpha1 pollutants
antitrypsin (AAT) • second hand smoke
stimulation of excess mucus destroys ciliary function loosening elastic ability of air sacs
production
cough infection
inflammation
CHRONIC BRONCHITIS
(cough of at least 3 mos. of the
year for 2 consecutive years)
Chronic obstructive pulmonary disease (COPD) is one of the most common lung
diseases. It makes it difficult to breathe. There are two main forms of COPD which is
Chronic bronchitis defined by a long-term cough with mucus and Emphysema defined
by destruction of the lungs over time. Most people with COPD have a combination of
both conditions. Smoking is the leading cause of COPD. The more a person smokes,
the more likely that person will develop COPD although some people smoke for years
and never get COPD. In rare cases, nonsmokers who lack a protein called alpha-1
antitrypsin can develop emphysema. Other risk factors for COPD are exposure to
smoke and pollution and frequent use of cooking gas without proper ventilation.
between alveoli. The destruction of the alveolar walls reduces the elasticity of the lung
overall. Loss of elasticity leads to the collapse of the bronchioles obstructing airflow out
of the alveoli. Air becomes "trapped" in the alveoli and reduces the ability of the lung to
shrink during exhalation. This trapped air takes up space and results in a reduced
amount of air that can be taken in during the next breath. As a result, less air gets to the
alveoli for the exchange of gasses. This trapped air also can compress adjacent less
damaged lung tissue, preventing it from functioning to its fullest capacity. The exchange
of carbon dioxide and oxygen between air and the blood in the capillaries takes place
across the thin walls of the alveoli. Destruction of the alveolar walls decreases the
number of capillaries available for gas exchange. This adds to the decrease in the
Usually, energy is only required for inhalation to inflate the lungs. The stretch of
the lungs and distension of the chest cavity springs back to rest during exhalation, a
passive process that does not require energy. However, in emphysema, inefficient
breathing occurs because extra effort and energy has to be expended to empty the
lungs of air due to the collapse of the airways. This essentially doubles the work of
breathing, since now energy is required for both inhalation and exhalation. In addition,
because of the reduced capacity to exchange gases with each breath (due to the
frequently.
In COPD, there is less air that comes in and out because the airways and air
sacs lose their elastic ability; the walls between the air sacs become destroyed; airways
produce mucus more than normal; and the airways and air sacs are thickened and
inflamed. Smoking is the primary risk factor for the occurrence of COPD. Other
modifiable factors included are exposure to air pollution, secondhand smoke as well as
to industrial pollutants. History of respiratory tract infections and heredity can also
potentiate an individual to develop such disorders. When exposed to the numerous
irritants and other risk factors, enlargement and hyperactivity of the mucus secreting
glands happened. An inflammatory response then would occur throughout the airways,
parenchyma and pulmonary vasculature. Chronic coughing, destroyed ciliary function
and eventual scarring of the bronchial lining results from the initial inflammation of the
bronchi. This can continue for at least 3 months of the year for 2 consecutive years and
is known as chronic bronchitis. Because of the inflammation and the body’s attempt to
repair it, narrowing of the small airways occur reducing the ciliary efficiency. Over time,
this injury and repair process scar tissue formation and may eventually lead to lung
tissue damage (emphysema).
In emphysema, when the alveolar walls are further destroyed along with the
distal airways, this leads to permanent over distention of the air space. Air passages
then are obstructed. This disorder may also result from a breakdown in the lung’s
normal defense mechanisms (alpha1-antitrypsin) against enzymes protease and
elastase that can attack and destroy the tissues of the lungs. When there is destruction
of the entire alveolus of the lower portion of the lungs, because of AAT it is known as
panacinar/panlobular emphysema. If damage occurs in the bronchioles or upper lung
regions, it is termed as centriacinar/centrilobular emphysema and lastly, destruction of
the distal airway structures such as alveolar ducts and alveolar sacs is coined as
paraseptal/distal acinar emphysema.
Destruction of the walls between the alveoli, partial airway collapse and loss of
elastic recoil result to difficult expiration in emphysema. Increased ventilatory dead
space from the areas that do not participate in gas or blood exchange occurs as the
alveoli and septa collapse. The work of breathing is increased because there is less
functional lung tissue for exchange of gases. Pulmonary capillaries are also destructed
further decreasing oxygen perfusion and ventilation.
Measure
how many
platelets in
the blood. It
helps the
blood clot.
Identify
bleeding
disorders.
Procedure Indication Normal Actual Nursing Responsibility
Findings Findings
5-16-11 05-16-11
Blood Urea • To confirm PRE
Nitrogen bactericemia • Tell the patient that the BUN test
• To identify 2.10 - 7.10 4.90 is used to evaluate kidney
causative mmol/L function.
NORMAL • Inform the patient that he need
organism in
bactericemia not to restrict food and fluids, but
should avoid diet high in meat.
and
• Tell the patient that the test
septicemia.
requires a blood sample. Explain
who will perform the
venipuncture and when.
• Explain to the patient that he may
experience slight discomfort from
the tourniquet and needle
puncture.
• Notify the laboratory and
physician of medications the
patient is taking that may affect
test results; they may need to be
restricted.
INTRA
• Clean the venipuncture site first
with an alcohol swab and then
with a providone-iodine swab,
starting at the site and working
outward in a circular motion.
• Wait at least 1 minute for the skin
to dry.
• Perform a venipuncture and draw
10 to 20 ml of blood for an adult,
or 2 to 6 ml for a child.
• Clean the diaphragm tops of the
culture bottles with alcohol or
iodine and change the needle on
the syringe.
• If using broth, add blood to each
bottle until achieving a 1:5 or
1:10 dilution. For example, add
10 ml of blood to a 100-ml bottle.
Note that the size of the bottle
may vary depending on hospital
protocol.
• If using a special resin, add blood
to the resin in the bottles
according to facility protocol, and
invert gently to mix it.
• Draw the blood directly into
special collection processing
tube if using lysis-centrifugation
technique (Isolator).
• Document the tentative diagnosis
and current or recent
antimicrobial therapy on the
laboratory request.
• Send each sample to the
laboratory immediately.
• Collect blood cultures before
V. Medications and Treatment
POST:
• Advise patient to
report these side
effects of the
drug such as
headache, pain,
influenza, chest
pain; nausea.
Bronchitis,
dyspnea,
coughing,
pneumonia,
bronchospasm,
VI. Nursing Priorities
Content Strategy
1.Compliance • infection control in COPD health teaching/
a. hand hygiene education
b. flu vaccination
c. cleaning and maintenance
of respiratory equipment
• assessment of clinical
manifestations of
pulmonary infection
- change in color/volume of
sputum
- fever
- chills
- malaise
- productive cough
- confusion
- dyspnea
(Chronic Obstructive
Pulmonary Disease:
Emphysema in Acute
Exacerbation)