This document provides information about a case study presentation on chronic obstructive pulmonary disease (COPD). It includes sections on the symptoms of emphysema and chronic bronchitis, an overview of the patient's history and exam findings, and assessments from a nutrition consult. COPD is characterized by inflammation and narrowing of the airways and destruction of lung tissue, making it difficult to breathe over time. Smoking is the leading cause of COPD.

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CASE STUDY PRESENTATION
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Chronic Bronchitis
Bronchi are red and swollen, and congested with mucous secretions Healthy Bronchy Alveoli
are enlarged and destroyed Emphysema Healthy Alveoli
SYMPTOMS
EMPHYSEMA
Dyspnea (shortness of breath)
Most noticeable during physical activity
As emphysema progresses, dyspnea occurs at rest
CHRONIC BRONCHITIS
Chronic cough and sputum production
The sputum is usually clear and thick
As bronchitis progress infections occur more frequently
Periodic infections can cause fever, dyspnea, coughing,

2. production of purulent sputum and wheezing
OVERVIEW OF THE CASE
Patient history:
• Medical Dx: stage 1 COPD (emphysema) 5 years ago
• Meds: Combivent (ipratropium bromide and albuterol sulfate)
• PMH: Bronchitis and upper respiratory infections during winter
• Smoker: 1 ppd for 46 years – has quit 1 year ago
• Family hx: CA – mother, 2 aunts died from lung cancer
OVERVIEW OF THE CASE
Physical exam:
• General appearance: 62-years-old female in no acute distress
• Vitals: Temp. 98.8ºF HR 92 bpm RR 22bpm BP 130/88
• Heart: Regular rate and rhythm; mild jugular distension noted
• Extremities: 1+ bilateral pitting edema. No cyanosis or clubbing
OVERVIEW OF THE CASE
• Neurologic: Alert, oriented; cranial nerves intact
• Skin: Warm, dry
• Chest/lungs: Decreased breath sounds, percussion hyperresonant; prolonged expiration
with wheezing; ronchi throughout; using accessory muscles at rest
• Abdomen: Liver, spleen palpable; nondistended, nontender, normal bowel sounds Hospital
course:
• Admitting dx: Acute exacerbation of COPD, increasing dyspnea, hypercapnia, r/o pneumonia
• Tx plan: O2 1L/min via nasal cannula, O2 saturation 90-91% IVF D5 ½ NS with 20mEq KCL @
75 cc/hr
Corticosteroid -Methylprednisone: Solumedrol
Antibiotic -Chephalosporin: Ancef
Bronchodilator: Ipratropium bromide, Albuterol sulfate
ABGs q 6 hours, CXR, sputum cultures and Gram stain

3. OVERVIEW OF THE CASE
The Physician ordered a nutrition consult
Nutrition history:
• Appetite is poor, fast satiety
• Meal preparations are difficult
• In the previous 2 days, she has eaten very little
• Coughing has made eating difficult
• Food doesn’t taste good, it has a bitter taste
• 5 years ago she weighted 145-150lb, now she is 119lb, 5’3”
• She didn’t weight herself for a while, but clothes are bigger, dentures fit
loosely her family tells her how thin she has gotten
• Avoids milk: “People say it will increase mucus production”
• No previous MNT
• No vit/min supplementation
ASSESSMENT
Physical Examination Data
Head and neck
Teeth: Poorly fitting dentures
Skin
Skin: dry
Edema, peripheral: 1+ bilateral
Vital Signs
↑ Temperature: 98.8ºF
↑ Respiratory Rate: 22 bpm
Shortness of breath
ASSESSMENT
Client History Data

4. Social history
Physical activity, easy fatigue with increased activity; unable to
achieve desired levels
Medical/ Health history
Chronic Obstructive Pulmonary Disease
Upper respiratory infections or pneumonia
Signs and symptoms
Shortness of breath or dyspnea on exertion or at rest
Meds and supplements
Medications that cause anorexia: Albuterol sulfate
What Is COPD?
COPD, or chronic obstructive pulmonary (PULL-mun-ary) disease, is a progressive disease that
makes it hard to breathe. "Progressive" means the disease gets worse over time.
COPD can cause coughing that produces large amounts of mucus (a slimy substance), wheezing,
shortness of breath, chest tightness, and other symptoms.
Cigarette smoking is the leading cause of COPD. Most people who have COPD smoke or used to
smoke. Long-term exposure to other lung irritants—such as air pollution, chemical fumes, or
dust—also may contribute to COPD.
Overview
To understand COPD, it helps to understand how the lungs work. The air that you breathe goes
down your windpipe into tubes in your lungs called bronchial (BRONG-ke-al) tubes or airways.
Within the lungs, your bronchial tubes branch into thousands of smaller, thinner tubes called
bronchioles (BRONG-ke-ols). These tubes end in bunches of tiny round air sacs called alveoli (al-
VEE-uhl-eye).
Small blood vessels called capillaries (KAP-ih-lare-ees) run through the walls of the air sacs.
When air reaches the air sacs, oxygen passes through the air sac walls into the blood in the
capillaries. At the same time, carbon dioxide (a waste gas) moves from the capillaries into the
air sacs. This process is called gas exchange.
The airways and air sacs are elastic (stretchy). When you breathe in, each air sac fills up with air
like a small balloon. When you breathe out, the air sacs deflate and the air goes out.
In COPD, less air flows in and out of the airways because of one or more of the following:

5.  The airways and air sacs lose their elastic quality.
 The walls between many of the air sacs are destroyed.
 The walls of the airways become thick and inflamed.
 The airways make more mucus than usual, which can clog them.
Normal Lungs and Lungs With COPD
Figure A shows the location of the lungs and airways in the body. The inset image shows a
detailed cross-section of the bronchioles and alveoli. Figure B shows lungs damaged by COPD.
The inset image shows a detailed cross-section of the damaged bronchioles and alveolar
walls.
In the United States, the term "COPD" includes two main conditions—emphysema (em-fih-
SE-ma) and chronic bronchitis (bron-KI-tis). (Note: The Health Topics article about bronchitis
discusses both acute and chronic bronchitis.)
In emphysema, the walls between many of the air sacs are damaged. As a result, the air sacs
lose their shape and become floppy. This damage also can destroy the walls of the air sacs,

6. leading to fewer and larger air sacs instead of many tiny ones. If this happens, the amount of
gas exchange in the lungs is reduced.
In chronic bronchitis, the lining of the airways is constantly irritated and inflamed. This causes
the lining to thicken. Lots of thick mucus forms in the airways, making it hard to breathe.
Most people who have COPD have both emphysema and chronic bronchitis. Thus, the general
term "COPD" is more accurate.
Outlook
COPD is a major cause of disability, and it's the third leading cause of death in the United
States. Currently, millions of people are diagnosed with COPD. Many more people may have the
disease and not even know it.
COPD develops slowly. Symptoms often worsen over time and can limit your ability to do
routine activities. Severe COPD may prevent you from doing even basic activities like walking,
cooking, or taking care of yourself.
Most of the time, COPD is diagnosed in middle-aged or older adults. The disease isn't passed
from person to person—you can't catch it from someone else.
COPD has no cure yet, and doctors don't know how to reverse the damage to the airways and
lungs. However, treatments and lifestyle changes can help you feel better, stay more active,
and slow the progress of the disease.
Other Names for COPD
Chronic bronchitis - Chronic productive cough for 3 months in 2 successive years
• Emphysema – Defined as a pathological term referring to permanent changes in terminal
bronchioles & alveoli
• Asthma – Inflammatory disease of airways, with reversible changes
 Chronic bronchitis
 Chronic obstructive airway disease
 Chronic obstructive lung disease
 Emphysema
What Causes COPD?
• Exposure to pipe, cigar, tobacco smoke
• Exposure to second hand smoke
• Exposure to heavy air pollution
• Exposure to heavy dust

7. • Exposure to chemical/toxic fumes
• Genetic conditions
Risk Factors
• Major
• • Age
• • Male
• • Occupation
• • Smoking
• • Alpha – one – antitrypsin
• Deficiency
Risk Factors
• Minor
• • Air Pollution
• • Alcohol
• • Race
• • Nutritional Status
• • FH
• • Bronchial Reactivity
What Are the Signs and Symptoms of COPD?
• Wheezing
• Coughing
• Sputum production
• Shortness of breath
• Chest tightness
• ANATOMY AND PHYSIOLOGY:
• The respiratory system consists of all the organs involved in breathing. These include the
nose, pharynx, larynx, trachea, bronchi and lungs. The respiratory system does two very
important things: it brings oxygen into our bodies, which we need for our cells to live and

8. function properly; and it helps us get rid of carbon dioxide, which is a waste product of
cellular function. The nose, pharynx, larynx, trachea and bronchi all work like a system
of pipes through which the air is funneled down into our lungs. There, in very small air
sacs called alveoli, oxygen is brought into the bloodstream and carbon dioxide is pushed
from the blood out into the air. When something goes wrong with part of the respiratory
system, such as an infection like pneumonia, chronic obstructive pulmonary diseases, it
makes it harder for us to get the oxygen we need and to get rid of the waste product
carbon dioxide. Common respiratory symptoms include breathlessness, cough, and
chest pain
• The Upper Airway and Trachea
• When you breathe in, air enters your body through your nose or mouth. From there, it
travels down your throat through the larynx (or voice box) and into the trachea (or
windpipe) before entering your lungs. All these structures act to funnel fresh air down
from the outside world into your body. The upper airway is important because it must
always stay open for you to be able to breathe. It also helps to moisten and warm the air
before it reaches your lungs.
• The Lungs
• Structure
• The lungs are paired, cone-shaped organs which take up most of the space in our chests,
along with the heart. Their role is to take oxygen into the body, which we need for our
cells to live and function properly, and to help us get rid of carbon dioxide, which is a
waste product. We each have two lungs, a left lung and a right lung. These are divided up
into µlobes¶, or big sections of tissue separated by µfissures¶ or dividers. The right lung
has three lobes but the left lung has only two, because the heart takes up some of the
space in the left side of our chest. The lungs can also be divided up into even smaller
portions, called broncho pulmonary segments .These are pyramidal-shaped areas which
are also separated from each other by membranes.There are about 10 of them in each
lung. Each segment receives its own blood supply and air supply.
• Blood supply The lungs are very vascular organs, meaning they receive a very large
blood supply. This is because the pulmonary arteries, which supply the lungs, come
directly from the right side of your heart. They carry blood which is low in oxygen and
high in carbon dioxide into your lungs so that the carbon dioxide can be blown off, and
more oxygen can be absorbed into the bloodstream. The newly oxygen-rich blood then
travels back through the paired pulmonary veins into the left side of your heart. From
there, it is pumped all around your body to supply oxygen to cells and organs.
• The Work ofBreathing The Pleurae
• The lungs are covered by smooth membranes that we call pleurae. The pleurae have two
layers, a visceral layer which sticks closely to the outside surface of your lungs, and a
µparietal layer which lines the inside of your chest wall (ribcage). The pleurae
are important because they help you breathe in and out smoothly, without any friction.
They also make sure that when your ribcage expands on breathing in, your lungs expand
as well to fill the extra space.
• The Diaphragm and Intercostal Muscles
• When you breathe in (inspiration), your muscles need to work to fill your lungs with air.
Thediaphragm, a large, sheet-like muscle which stretches across your chest under the
ribcage, doesmuch of this work. At rest, it is shaped like a dome curving up into your
chest. When you breathein, the diaphragm contracts and flattens out, expanding the

9. space in your chest and drawing air into your lungs. Other muscles, including the muscles
between your ribs (the intercostal muscles)also help by moving your ribcage in and out.
Breathing out (expiration) does not normallyrequire your muscles to work. This is
because your lungs are very elastic, and when your
• muscles relax at the end of inspiration your lungs simply recoil back into their resting
position, pushing the air out as they go.
• The Respiratory Systemand Ageing
• The normal process of ageing is associated with a number of changes in both the
structure andfunction of the respiratory system. These include:
• Enlargement of the alveoli. The air spaces get bigger and lose their elasticity,
meaningthat there is less area for gases to be exchanged across. This change is sometimes
referredto as ¶senile emphysema¶.
• The compliance (or springiness) of the chest wall decreases, so that it takes more effort
to breathe in and out.
• The strength of the respiratory muscles (the diaphragm and intercostal muscles)decreases.
This change is closely connected to the general health of the person.All of these changes
mean that an older person might have more difficulty coping with increasedstress on their
respiratory system, such as with an infection like pneumonia, than a younger person
would.
• DIAGNOSTIC EVALUATION
• PFTs demonstrative airflow obstruction ± reduced forced vital capacity
(FVC), FEV1,FEV1 to FVC ration; increased residual volume to total lung capacity
(TLC) ratio, possibly increased TLC.2.
• ABG levels- decreased PaO2, pH, and increased CO2.3.
• Chest X-ray ± in late stages, hyperinflation, flattened diaphragm, increased
rettrosternalspace, decreased vascular markings, possible bullae.4.
• Alpa1-antitrypsin assay useful in identifying genetically determined deficiency
inemphysema
• ABG’s
•Mild decrease pO2 early, gradual
decrease
•Gradual increase pCO2
•May change during sleepErythrocytosis with Hct > 55 as pO2 levels fall; non
specific
CT Scan
•High resolution 1-2 mm slices
•More sensitive than CXR
•Does not alter basic therapyCXR Not useful for diagnosing early COPD
Findings
•Over distended lungs
•Flattened diaphragms
•Long narrow cardiac silhouette
•Increased retro sternal airspace
•Bullae

10. PATHOPHYSIOLOGY In COPD
, the airflow limitation isboth progressive and associatedwith anabnormal inflammatory response of
the lungs to noxious particles or gases.The inflammatory response occurs throughout the airways,
parenchyma, and pulmonary vasculature. Because of the chronic inflammation and the body
attempts to repairit, narrowing occurs inthe small peripheral airways. Over time, this injury-and-repair
processcauses scartissue formation and narrowing ofthe airway lumen. Airflow obstruction mayalso
becaused by parenchymal destruction, asisseenwith emphysema, a diseaseof the alveoli orgas
exchange units. In additionto inflammation, processes related to imbalances of proteinases and anti
proteinases inthe lung mayberesponsible for airflow limitation. When activated by chronic
inflammation, proteiness and other substances may bereleased, damagingthe parenchymal of the
lung. The parenchymal changes may occur asaconsequence of inflammation or environmental or
genetic factors (eg. Alpha1-antitrypsin deficiency)
Early in the course of COPD , the inflammatory response causes pulmonary vasculature changes
that are characterized by thickening of the vessel wall. These changes may result from exposure to
cigarette smoke, use of tobaccoproducts, and the release ofinflammatory medicators.
CHRONIC BRONCHITIS
Lung damageand inflammation inthe large airways results inchronic bronchitis. Chronic bronchitis is
defined inclinical terms asa cough withsputum production onmost days for 3months of a year, for
2 consecutive years. In the airways ofthe lung, the hallmark of chronic bronchitis isanincreased
number (hyperplasia)and increased size (hypertrophy) of the goblet cells and mucous glands of the
airway. Asa result, there ismore mucus than usual inthe airways, contributing to narrowing of the
airways and causing a cough with sputum. Microscopically there isinfiltration of the airwaywalls with
inflammatory cells. Inflammation isfollowed by scarring and remodeling that thickens the walls and
also results innarrowing of the airways. Aschronic bronchitis progresses, there issquamous
metaplasia (anabnormal change inthe tissue lining the insideof the airway) and fibrosis(further
thickening and scarring of the airwaywall). The consequence of these changes isalimitation of
airflow. Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema
were commonly referred to as³blue bloaters´ because of the bluish color of the skin and lips
(cyanosis) seen in them. The hypoxia and fluid retention leads to them beingcalled ³Blue
Bloaters.´
ACUTE BRONCHITIS
PHYSICAL MANIFESTATIONS
One of the most common symptoms of COPD
isshortness of breath(dyspnea). Peoplewith COPD
commonly describe this as: ³My breathing requires effort´, ³I feel out of breath´, or ³I can
not getenough airin´. Peoplewith COPD typically first notice dyspnea during vigorous exercise when

11. the demands onthe lungs aregreatest. Over the years, dyspnea tends to getgradually worse sothat
itcan occur during milder, everyday activities such as housework. In the advanced stages of COPD ,
dyspnea can becomesobad that itoccurs during rest and isconstantly present. Other symptoms of
COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and
tiredness. Peoplewith advanced (very severe) COPD sometimes develop respiratory failure. When
this happens, cyanosis, abluish discoloration of the lips caused byalack of oxygen inthe blood, can
occur. Anexcess of carbon dioxideinthe blood cancause headaches, drowsiness or twitching
(asterixis). Acomplicationof advanced COPD is corpulmonal, astrain onthe heart due tothe extra
work required by the heart to pump bloodthrough the affected lungs.
Symptoms of cor pulmonale areperipheral edema, seenasswelling of the ankles, and dyspnea.
There are afew signsof COPD that ahealthcare worker may detect although they can beseenin
other diseases.Somepeople have COPD and have none of these signs. Commonsigns are:
tachypnea, arapidbreathing rate wheezing sounds orcrackles in the lungs heard through a
stethoscope breathing out taking a longer timethan breathing in enlargement of the chest, particularly
the front-to-back distance (hyperinflation) active use of muscles inthe neck to help with breathing
breathing through pursed lips increased antero posterior tolateral ratio of the chest(i.e. barrel chest).
Emphysema
isachronic obstructive pulmonary isease (COPD,asit isotherwise known, formerly termed achronic
obstructive lung disease).It isoften caused by exposure to toxic chemicals ,including long-term
exposure to tobacco smoke. Emphysema ischaracterized byloss of elasticity(increased pulmonary
compliance) of the lung tissue caused by destruction of structures feeding the alveoli, owing to the
actionof alpha 1antitrypsin deficiency. This causes the small airways to collapse during forced
exhalation, asalveolar collapsibility has decreased.As aresult, airflow is impededand airbecomes
trapped inthe lungs, inthe same way asother obstructive lung diseases. Symptoms include
shortness of breathon exertion, and anexpanded chest. However, the constriction of airpassages
isnt always immediately deadly, and treatment isavailable.
• NURSINGINTERVENTIONS
• Monitoring
1.Monitor for adverse effects of bronchodilators ± tremulousness, tachycardia, cardiac
arrhythmias, central nervous system stimulation, hypertension.2.
• Monitor condition after administration of aerosol bronchodilators to assess for improved
aeration, reduced adventitious sounds, reduced dyspnea.3.
• Monitor serum theophylline level, as ordered, to ensure therapeutic level and
preventtoxicity.4.
• Monitor oxygen saturation at rest and with activity.
•
• Supportive Care
• Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation usually
reduces pulmonary irritation, sputum production, and cough. Keep the patients room
asdust-free as possible.
• 2.

12. • Use postural drainage positions to help clear secretions responsible
for airwayobstructions.3.
• Teach controlled coughing.4.
• Encourage high level of fluid intake ( 8 to 10 glasses; 2 to 2.5 liters daily) within level
of cardiac reserve.5.
• Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum. Add
moisture (humidifier, vaporizer) to indoor air.6.
• Avoid dairy products if these increases sputum production.7.
• Encourage the patient to assume comfortable position to decrease dyspnea.8.
• Instruct and supervise patient breathing retraining exercises.9.
• Use pursed lip breathing at intervals and during periods of dyspnea to control rate and
depth of respiration and improve respiratory muscle coordination.10.
• Discuss and demonstrate relaxation exercises to reduce stress, tension, and anxiety.11.
• Maintain the patient nutritional status.12.
• Reemphasize the importance of graded exercise and physical conditioning programs.13.
• Encourage use of portable oxygen system for ambulation for patients with hypoxemia
and marked disability.14.
• Train the patient in energy conservation technique.15.
• Assess the patient for reactive-behaviors such as anger, depression and acceptance.
Education and heaLthmaintenance
• Review with the patient the objectives of treatment and nursing management.2.
• Advise the patient to avoid respiratory irritants. Suggest that high efficiency particular the
air filter may have some benefit.3.
• Warn patient to stay out of extremely hot or cold weather and to avoid
aggravating bronchial obstruction and sputum obstruction.4.
• Warn patient to avoid persons with respiratory infections, and to avoid crowds and areas
with poor ventilation.5.
• Teach the patient how to recognize and report evidence of respiratory infection promptly
such as chest pain, changes in character of sputum (amount, color and
consistency),increasing difficulty in raising sputum, increasing coughing and wheezing,
increasing of shortness of breath.
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