CONTENT

NO TITLE PAGE

1 Acknowledgement 2

2 Overview of COPD 3-7

3 Aetiology of COPD 8-10

Pathophysiology 11-14

5 Case

1) Real case 15-23

2) Reference A 24-30

3) Reference B 31-35

6 Discussion 36-39

7 Conclusion 40

8 Reference 41

1
 ACKNOWLEGEMENT

The internship opportunity I had at Emergency department, Hospital slim river was a great
chance for learning and professional development. Therefore, I consider myself as a very lucky
individual as I was provided with an opportunity to be part of it. I am also grateful for having
a chance to meet so many wonderful people who led me though this internship period.

Bearing in mind previous I am using this opportunity to express my deepest gratitude and
special thanks to our coordinator instructor Encik Mahidzir Bin Hassan, Madam Maimunah
Ahmad and our lecturer who in spite of being extraordinary busy with their duties, took time
out to hear, guide and keep me on the correct path and allowing me to carry out my project at
their esteemed organization, extending during the training and giving necessary advices and
guidance and arranged all facilities to make life easier.

It is my radiant sentiment to place on record my best regards, deepest sense of gratitude to

Hospital Slim River and all the Medical staff at emergency department for their careful and
precious guidance which were extremely valuable for my study both theoretically and
practically.

I express my deepest thanks to Mr Mohamed Noor Bin Uda and his family to giving me correct
information about the patient and help me to carry out my project.

Last but not least, I would like to thank my batch mates who guide me on the correct path and
giving advices during carry out my project.

I perceive as this opportunity as a big milestone in my career development. I will strive to use
gained skills and knowledge in the best possible way, and I will continue to work on their
improvement, in order to attain desired career objectives. Hope to continue cooperation with
all of you in the future.

2
 OVERVIEW OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

Chronic obstructive pulmonary disease (COPD) is estimated to affect 32 million persons in the
United States and is the third leading cause of death in this country. Patients typically have
symptoms of chronic bronchitis and emphysema, but the classic triad also includes asthma or
a combination of the above (see the image below).

Venn diagram of chronic obstructive pulmonary disease (COPD). Chronic obstructive lung
disease is a disorder in which subsets of patients may have dominant features of chronic
bronchitis, emphysema, or asthma. The result is airflow obstruction that is not fully
reversible.
Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3
months during each of 2 consecutive years (other causes of cough being excluded).
Emphysema is defined pathologically as an abnormal, permanent enlargement of the air
spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without
obvious fibrosis.

Signs and symptoms

Patients typically present with a combination of signs and symptoms of chronic bronchitis,
emphysema, and reactive airway disease. Symptoms include the following:
 Cough, usually worse in the mornings and productive of a small amount of colorless
sputum
 Breathlessness: The most significant symptom, but usually does not occur until the sixth
decade of life
 Wheezing: May occur in some patients, particularly during exertion and exacerbations
While the sensitivity of physical examination in detecting mild-to-moderate COPD is relatively
poor, the physical signs are quite specific and sensitive for severe disease. Findings in severe
disease include the following:
 Tachypnea and respiratory distress with simple activities

3
  Use of accessory respiratory muscles and paradoxical indrawing of lower intercostal
spaces (Hoover sign)
 Cyanosis
 Elevated jugular venous pulse (JVP)
 Peripheral edema
Thoracic examination reveals the following:
 Hyperinflation (barrel chest)
 Wheezing – Frequently heard on forced and unforced expiration
 Diffusely decreased breath sounds
 Hyperresonance on percussion
 Prolonged expiration
 Coarse crackles beginning with inspiration in some cases
Certain characteristics allow differentiation between disease that is predominantly chronic
bronchitis and that which is predominantly emphysema. Chronic bronchitis characteristics
include the following:
 Patients may be obese
 Frequent cough and expectoration are typical
 Use of accessory muscles of respiration is common
 Coarse rhonchi and wheezing may be heard on auscultation
 Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and
cyanosis
Emphysema characteristics include the following:
 Patients may be very thin with a barrel chest
 Patients typically have little or no cough or expectoration
 Breathing may be assisted by pursed lips and use of accessory respiratory muscles;
patients may adopt the tripod sitting position
 The chest may be hyperresonant, and wheezing may be heard
 Heart sounds are very distant

Diagnosis

The formal diagnosis of COPD is made with spirometry; when the ratio of forced expiratory
volume in 1 second over forced vital capacity (FEV1/FVC) is less than 70% of that predicted
for a matched control, it is diagnostic for a significant obstructive defect. Criteria for assessing

4
the severity of airflow obstruction (based on the percent predicted post bronchodilator FEV1)
are as follows:
 Stage I (mild): FEV1 80% or greater of predicted
 Stage II (moderate): FEV1 50-79% of predicted
 Stage III (severe): FEV1 30-49% of predicted
 Stage IV (very severe): FEV1 less than 30% of predicted or FEV1 less than 50% and
chronic respiratory failure
Arterial blood gas (ABG) findings are as follows:
 ABGs provide the best clues as to acuteness and severity of disease exacerbation
 Patients with mild COPD have mild to moderate hypoxemia without hypercapnia
 As the disease progresses, hypoxemia worsens and hypercapnia may develop, with the
latter commonly being observed as the FEV1 falls below 1 L/s or 30% of the predicted
value
 pH usually is near normal; a pH below 7.3 generally indicates acute respiratory
compromise
 Chronic respiratory acidosis leads to compensatory metabolic alkalosis
In patients with emphysema, frontal and lateral chest radiographs reveal the following:
 Flattening of the diaphragm
 Increased retrosternal air space
 A long, narrow heart shadow
 Rapidly tapering vascular shadows accompanied by hyperlucency of the lungs
 Radiographs in patients with chronic bronchitis show increased broncho vascular
markings and cardiomegaly
Advantages of high-resolution CT include the following:
 Greater sensitivity than standard chest radiography
 High specificity for diagnosing emphysema (outlined bullae are not always visible on a
radiograph)
 May provide an adjunctive means of diagnosing various forms of COPD (example, lower
lobe disease may suggest alpha1-antitrypsin (AAT) deficiency
 May help the clinician determine whether surgical intervention would benefit the patient
Other tests are as follows:
 Hematocrit – Patients with polycythemia (hematocrit greater than 52% in men or 47% in
women) should be evaluated for hypoxemia at rest, with exertion, or during sleep

5
  Serum potassium – Diuretics, beta-adrenergic agonists, and theophylline act to lower
potassium levels
 Measure AAT in all patients younger than 40 years, in those with a family history of
emphysema at an early age, or with emphysematous changes in a nonsmoker
 Sputum evaluation will show a transformation from mucoid in stable chronic bronchitis
to purulent in acute exacerbations
 Pulse oximetry, combined with clinical observation, provides instant feedback on a
patient's status
 Electrocardiography can help establish that hypoxia is not resulting in cardiac ischemia
and that the underlying cause of respiratory difficulty is not cardiac in nature
 Two-dimensional echocardiography can screen for pulmonary hypertension
 Right-sided heart catheterization can confirm pulmonary artery hypertension and gauge
the response to vasodilators

Management

Smoking cessation continues to be the most important therapeutic intervention for COPD. Risk
factor reduction (example, influenza vaccine) is appropriate for all stages of COPD.
Approaches to management by stage include the following:
 Stage I (mild obstruction): Short-acting bronchodilator as needed
 Stage II (moderate obstruction): Short-acting bronchodilator as needed; long-acting
bronchodilator(s); cardiopulmonary rehabilitation
 Stage III (severe obstruction): Short-acting bronchodilator as needed; long-acting
bronchodilator(s); cardiopulmonary rehabilitation; inhaled glucocorticoids if repeated
exacerbations
 Stage IV (very severe obstruction or moderate obstruction with evidence of chronic
respiratory failure): Short-acting bronchodilator as needed; long-acting
bronchodilator(s); cardiopulmonary rehabilitation; inhaled glucocorticoids if repeated
exacerbation; long-term oxygen therapy (if criteria met); consider surgical options such
as lung volume reduction surgery (LVRS) and lung transplantation
Agents used include the following:
 Short-acting beta2 -agonist bronchodilators (example, albuterol, metaproterenol,
levalbuterol, pirbuterol)
 Long-acting beta2 -agonist bronchodilators (example, salmeterol, formoterol,
arformoterol, indacaterol, vilanterol)

6
  Respiratory anticholinergics (example, ipratropium, tiotropium, aclidinium, revefenacin)
 Xanthine derivatives (example, theophylline)
 Phosphodiesterase-4 Inhibitors (example, roflumilast)
 Inhaled corticosteroids (example, fluticasone, budesonide): Peripheral blood eosinophil
counts may help stratify the likelihood of efficacy.
 Oral corticosteroids (example, prednisone)
 Beta2 -agonist and anticholinergic combinations (example, ipratropium and albuterol,
umeclidinium bromide/vilanterol inhaled)
 Beta2 -agonist and corticosteroid combinations (example, budesonide/formoterol,
fluticasone and salmeterol, vilanterol/fluticasone inhaled)
Pulmonary rehabilitation programs are typically multidisciplinary approaches that emphasize
the following:
 Patient and family education, smoking cessation
 Medical management (including oxygen and immunization), respiratory and chest
physiotherapy
 Physical therapy with broncho pulmonary hygiene, exercise, and vocational rehabilitation
 Psychosocial support
Indications for admission for acute exacerbations include the following:
 Failure of outpatient treatment, marked increase in dyspnea
 Altered mental status, increase in hypoxemia or hypercapnia
 Inability to tolerate oral medications such as antibiotics or steroids

7
 ETIOLOGY OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

Cigarette smoking
The primary cause of COPD is exposure to tobacco smoke. Overall, tobacco smoking accounts
for as much as 90% of COPD risk.
Cigarette smoking induces macrophages to release neutrophil chemotactic factors and
elastases, which lead to tissue destruction. Clinically significant COPD develops in 15% of
cigarette smokers, although this number is believed to be an underestimate. Age of initiation
of smoking, total pack-years, and current smoking status predict COPD mortality.
People who smoke have an increased annual decline in FEV1: the physiologic normal decline
in FEV1 is estimated to be 20-30 ml/y, but the rate of decline in COPD patients is generally 60
ml/y or greater.
Second-hand smoke, or environmental tobacco smoke, increases the risk of respiratory
infections, augments asthma symptoms, and causes a measurable reduction in pulmonary
function.

Environmental factors

COPD does occur in individuals who have never smoked. Although the role of air pollution in
the aetiology of COPD is unclear, the effect is small when compared with that of cigarette
smoking. In developing countries, the use of biomass fuels with indoor cooking and heating is
likely to be a major contributor to the worldwide prevalence of COPD. Long-term exposure to
traffic-related air pollution may be a factor in COPD in patients with diabetes and asthma. [20]

Airway hyper responsiveness

Airway hyper responsiveness stipulates that patients who have nonspecific airway
hyperactivity and who smoke are at increased risk of developing COPD with an accelerated

8
decline in lung function. Nonspecific airway hyperactivity is inversely related to FEV1 and
may predict a decline in lung function.
The data regarding the possible role of airway hyper responsiveness as a risk factor for the
development of COPD in people who smoke are unclear. It is important to note, however, that
60% demonstrate bronchial hyper responsiveness. Moreover, bronchial hyperactivity may
result from airway inflammation observed with the development of smoking-related chronic
bronchitis. This may contribute to airway remodelling, leading to a more fixed obstruction, as
is seen in persons with COPD.

Alpha1-antitrypsin deficiency

Alpha1-antitrypsin (AAT) is a glycoprotein member of the serine protease inhibitor family that
is synthesized in the liver and is secreted into the bloodstream. The main purpose of this 394-
amino-acid, single-chain protein is to neutralize neutrophil elastase in the lung interstitium and
to protect the lung parenchyma from elastolytic breakdown. Severe AAT deficiency
predisposes to unopposed elastolysis with the clinical sequela of an early onset of panacinar
emphysema.
AAT deficiency is the only known genetic risk factor for developing COPD and accounts for
less than 1% of all cases in the world. Severe AAT deficiency leads to premature emphysema
at an average age of 53 years for nonsmokers and 40 years for smokers.

Intravenous drug use

Emphysema occurs in approximately 2% of persons who use intravenous (IV) drugs. This is
attributed to pulmonary vascular damage that results from the insoluble filler (example, corn-
starch, cotton fibers, and cellulose) contained in methadone or methylphenidate.
The bullous cysts found in association with IV use of cocaine or heroin occur predominantly
in the upper lobes. In contrast, methadone and methylphenidate injections are associated with
basilar and panacinar emphysema.

Immunodeficiency syndromes

Human immunodeficiency virus (HIV) infection has been found to be an independent risk
factor for COPD, even after controlling for confounding variables such as smoking, IV drug
use, race, and age.

9
Apical and cortical bullous lung damage occurs in patients who have autoimmune deficiency
syndrome and Pneumocystis carinii infection. Reversible pneumatoceles are observed in 10-
20% of patients with this infection.

Vasculitis syndrome

Hypocomplementemic vasculitis urticaria syndrome (HVUS) may be associated with

obstructive lung disease. Other manifestations include angioedema, non-deforming arthritis,
sinusitis, conjunctivitis, and pericarditis.

10
 PATHOPHYSIOLOGY OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Pathologic changes in chronic obstructive pulmonary disease (COPD) occur in the large
(central) airways, the small (peripheral) bronchioles, and the lung parenchyma. Most cases of
COPD are the result of exposure to noxious stimuli, most often cigarette smoke. The normal
inflammatory response is amplified in persons prone to COPD development. The pathogenic
mechanisms are not clear but are most likely diverse. Increased numbers of activated
polymorph nuclear leukocytes and macrophages release elastases in a manner that cannot be
counteracted effectively by anti-proteases, resulting in lung destruction.
The primary offender has been found to be human leukocyte elastase, with synergistic roles
suggested for proteinase-3 and macrophage-derived matrix metalloproteinase (MMPs),
cysteine proteinases, and a plasminogen activator. Additionally, increased oxidative stress
caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and
polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells.
Accelerated aging and autoimmune mechanisms have also been proposed as having roles in
the pathogenesis of COPD.
Cigarette smoke causes neutrophil influx, which is required for the secretion of MMPs; this
suggests, therefore, that neutrophils and macrophages are required for the development of
emphysema.
Studies have also shown that in addition to macrophages, T lymphocytes, particularly CD8+,
play an important role in the pathogenesis of smoking-induced airflow limitation.
To support the inflammation hypothesis further, a stepwise increase in alveolar inflammation
has been found in surgical specimens from patients without COPD versus patients with mild
or severe emphysema. Indeed, mounting evidence supports the concept that dysregulation of
apoptosis and defective clearance of apoptotic cells by macrophages play a prominent role in
11
airway inflammation, particularly in emphysema. Azithromycin (Zithromax) has been shown
to improve this macrophage clearance function, providing a possible future treatment modality.
In patients with stable COPD without known cardiovascular disease, there is a high prevalence
of microalbuminuria, which is associated with hypoxemia independent of other risk factors.

Chronic bronchitis

Mucous gland hyperplasia (as seen in the images below) is the histologic hallmark of chronic
bronchitis. Airway structural changes include atrophy, focal squamous metaplasia, ciliary
abnormalities, and variable amounts of airway smooth muscle hyperplasia, inflammation, and
bronchial wall thickening.

Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration

of the airway wall with inflammatory cells.

Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of

the airway wall with inflammatory cells (high-powered view).

Damage to the endothelium impairs the mucociliary response that clears bacteria and mucus.
Inflammation and secretions provide the obstructive component of chronic bronchitis.
Neutrophilia develops in the airway lumen, and neutrophilic infiltrates accumulate in the
submucosa. The respiratory bronchioles display a mononuclear inflammatory process, lumen
occlusion by mucus plugging, goblet cell metaplasia, smooth muscle hyperplasia, and
distortion due to fibrosis. These changes, combined with loss of supporting alveolar
attachments, cause airflow limitation by allowing airway walls to deform and narrow the
airway lumen.
In contrast to emphysema, chronic bronchitis is associated with a relatively undamaged
pulmonary capillary bed. The body responds by decreasing ventilation and increasing cardiac
output. This V/Q mismatch results in rapid circulation in a poorly ventilated lung, leading to

12
hypoxemia and polycythemia. Eventually, hypercapnia and respiratory acidosis develop,
leading to pulmonary artery vasoconstriction and cor pulmonale. With the ensuing hypoxemia,
polycythemia, and increased CO2 retention, these patients have signs of right heart failure and
are known as "blue bloaters."

Emphysema

Emphysema is a pathologic diagnosis defined by permanent enlargement of airspaces distal to

the terminal bronchioles. This leads to a dramatic decline in the alveolar surface area available
for gas exchange. Furthermore, loss of alveoli leads to airflow limitation by 2 mechanisms.
First, loss of the alveolar walls results in a decrease in elastic recoil, which leads to airflow
limitation. Second, loss of the alveolar supporting structure leads to airway narrowing, which
further limits airflow.
Emphysema has 3 morphologic patterns:
 Centriacinar
 Panacinar
 Distal acinar, or paraseptal
Centriacinar emphysema is characterized by focal destruction limited to the respiratory
bronchioles and the central portions of the acini. This form of emphysema is associated with
cigarette smoking and is typically most severe in the upper lobes.
Panacinar emphysema involves the entire alveolus distal to the terminal bronchiole. The
panacinar type is typically most severe in the lower lung zones and generally develops in
patients with homozygous alpha1-antitrypsin (AAT) deficiency.
Distal acinar emphysema, or paraseptal emphysema, is the least common form and involves
distal airway structures, alveolar ducts, and sacs. This form of emphysema is localized to
fibrous septa or to the pleura and leads to formation of bullae (as seen in the images below).
The apical bullae may cause pneumothorax. Paraseptal emphysema is not associated with
airflow obstruction.

Gross pathology of a patient with emphysema showing bullae on the surface.

The gradual destruction of alveolar septae (shown in the image below) and of the pulmonary
capillary bed in emphysema leads to a decreased ability to oxygenate blood. The body

13
compensates with lowered cardiac output and hyperventilation. This V/Q mismatch results in
relatively limited blood flow through a fairly well oxygenated lung with normal blood gases
and pressures in the lung, in contrast to the situation in chronic bronchitis. Because of low
cardiac output, the rest of the body also suffers from tissue hypoxia and pulmonary cachexia.
Eventually, these patients develop muscle wasting and weight loss and are identified as "pink
puffers."

At high magnification, loss of alveolar walls and dilatation of airspaces in emphysema can be
seen.
Emphysematous destruction and small airway inflammation

Emphysematous destruction and small airway inflammation often are found in combination in
individual patients, leading to the spectrum that is known as COPD. When emphysema is
moderate or severe, loss of elastic recoil, rather than bronchiolar disease, is the dominant
mechanism of airflow limitation. By contrast, when emphysema is mild, bronchiolar
abnormalities are most responsible for the majority of the deficit in lung function. Although
airflow obstruction in emphysema is often irreversible, bronchoconstriction due to
inflammation accounts for some reversibility. Airflow limitation is not the only
pathophysiologic mechanism by which symptoms occur.

Dynamic hyperinflation

Lung volumes, particularly dynamic hyperinflation, have also been shown to play a crucial role
in the development of dyspnoea perceived during exercise. In fact, the improvement in exercise
capacity brought about by several treatment modalities, including bronchodilators, oxygen
therapy, lung volume reduction surgery (LVRS), and maneuvers learned in pulmonary
rehabilitation, is more likely due to delaying dynamic hyperinflation rather than improving the
degree of airflow obstruction. Additionally, hyperinflation (defined as the ratio of inspiratory
capacity to total lung capacity [IC/TLC]) has been shown to predict survival better than forced
expiratory volume in 1 second (FEV1).

14
 CASES
REAL CASE

A) Patient History
Real case I studied is acute exacerbation chronic obstructive pulmonary disease. Patient name,
Mohamed Noor Bin Uda (RN 5135), aged 75 years old, came to emergency department of
Hospital Slim River from Klinik Kesihatan (Felda) Trolak Selatan via ambulance with the chief
complaint of fever for 4 days ago. The history of presenting complaint made by the patient is
minimal oral intake and cough for 4 days with whitish sputum, body weakness for 3 days, and
shortness of breath (on and off) since 2 days ago, loss of appetite since 3 days ago and
orthopnea. This patient has past medical history of diabetes mellitus and hypertension since 20
years ago, diagnosed on medications and regular follow up at Klinik Kesihatan (Felda) Trolak
Selatan, congestive cardiac (CCF) with restriction of fluid 1 liter per day, not compliant since
4 years ago, echo done 2 years ago and have history of cardio follow up at Hospital Raja
Permaisuri Bainun (HRPB) Ipoh 2 years ago and angiogram not done. Not only that, other past
medical history of this patient is asthma since 21 years ago, have history of admission in year
1999 and requiring nebulizer 1 times in year. This medical history diagnosed on medications
and regular follow up at Klinik Kesihatan (Felda) Trolak Selatan and this patient also do not
have any surgical history.

FAMILY TREE

PATIENT Wife
75 years old 68 years old
Retired wooden company worker Diabetes mellitus,
hypertension
Hypertension, gout, diabetes mellitus,
asthma, congestive cardiac failure (CCF) Incision and drainage at
right second toe
No surgical history available

Son 1st Daughter 2nd daughter 3RD daughter

26 years old 25 years old 23 years old, 22 years old
Studying at KL married housewife
Hypertension, 15 Studying at Perlis, NIL
asthma Diabetes mellitus NIL
Based on patient’s family history, we know that this patient’s wife also has medical history of
diabetes mellitus and hypertension and have 4 children.

Drug history
This patient does not have any drug allergic. While he still have taken some medicines to
control his medical history. There are as shown below;

MDI Salbutamol 11/11 PRN

MDI Flixotide 1/1 BD

T.Cardiprin 100mg OD

T.Perindropil 8mg OD

T.Simvastatin 20mg ON

T. Lasix 20mg OD

Social history

While according to social history, we get to know this patient is a retired wooden company
worker, non-alcoholic and smoking person.

B) Physical examination

During general examinations, this patient was look alert, CRT< 2 seconds, have good pulse
volume, look mildly tachypnea, conscious which achieve 15/15 glasgow coma scale (GCS),
and have a good hydration. His vital signs are observed and recorded.

The vital sign of this patient is,

Vital Sign On arrival Current

Blood pressure (BP) 191/108 mmHg 141/80 mmHg
Pulse rate (PR) 115 bpm 103 bpm
Respiration rate (RR) 21/min 29/min
Body temperature (BT) 37.6 degree Celsius 36.6 degree Celsius
Spo2 91 % under room air 96 % under facemask
oxygen
DXT 6.5 mmol/L 5.9 mmol/L

16
Cardiovascular system is shows dual rhythm no murmur (DRNM). When auscultate the lungs,
crepitation can be listen at the base of the lungs. While during palpitation, stomach shows soft,
no mass, non-tender and found bowel sound active at stomach.

Other physical examination found in his body is bilateral knee pedal edema.

Pedal oedema at
both knees

C) Differential diagnosis

- Fluid overload secondary to non-compliance to restriction of fluid (ROF)

- Hypertension

- Congestive cardiac failure on restriction of fluid

- Gross haematuria secondary to traumatic catheter bladder drainage insertion

- Acute exacerbation chronic obstructive pulmonary disease (COPD) secondary to community-

acquired pneumonia (CAP)

D) Investigation

After undergoing the history of patient, physical examination and finding differential
diagnosis, next doctor carries out some laboratory and radiology investigations to make a
correct diagnosis. For laboratory test, full blood count (FBC) were taken. The result is as shown
below:

17
 Full blood count Result Normal range
White blood count (WBC) 11.81 x10^3/UL 4.0-10.0

Total red cells 5.07 x10^6/UL 4.5-5.5

Haemoglobin 15.7 g/dl 13-18
Platelet count 193 x 10^3/UL 150-450
HCT 45.8 % 40-50
Next, result for renal profile (RP) is as shown below:

Renal profile Result Normal range

Blood urea nitrogen 3.6 mmol/L 1.7-8.3
Sodium 136.3 mmol/L 135-154
Potassium 3.8 mmol/L 3.6-5.4
Chloride 105.4 mmol/L 93-108
Creatinine 33 umol/L 48-95

Next laboratory test used by doctor in my case is INR which shows the result 1.05.

Arterial blood gas (ABG) also shows the result as shown below:

Arterial blood gas Result Normal range

pH 7.4 7.380-7.440
pCO2 38.4 mmol/L 35.0-40.0
pO2 68.1 mmol/L 75.0-100.0
Haematocrit 4.8% 36-50

Beside this laboratory investigations, doctor carry out other radiology tests like
electrocardiogram (ECG) which shows sinus tachycardia and chest x-ray shows hyperinflated
lungs.

E) Diagnosis

Acute exacerbation chronic obstructive pulmonary disease (COPD) secondary to community-

acquired pneumonia (CAP)

18
F) Treatment and management

Initial Management

Patient came to emergency department from Klinik Kesihatan (Felda) Trolak Selatan via
ambulance due to fever since 4 days ago. Next, assistant medical officer was checking for the
patients’ vital sign. Next initial management done in secondary triage was triage this patient to
red zone. Before triage this patient, assistant medical officer in charged was took patient’s
family, drug history include allergic and social history.

Routine Management

- Doing bed making before patient arrive to red zone

- Checking for the patient’s vital sign every 15 minutes
- Insert branula and observe branula intact to avoid from occurring bleeding
- Administer oxygen via 3 litre/minute of nasal prong
- Take blood as doctor’s order
- Provide nursing care and patient rest in bed
- Give medication to patient based on doctor’s order
- Chest x-ray was taken
- Electrocardiogram is taken to see the rhythm of heart
- Strict input and output (I/O) chart

Specific Management

- Insert catheter bladder drainage (CBD) bag to patient after arriving to red zone
- Give 3 litre of nasal prong oxygen to maintain SPO2 above 97%
- Take blood glucose test (DXT) 4 hourly
- Patient refer to medical department for further management
- Doctor in medical department plan to admit this patient to ward 10
- Medical doctor who is in charged order to remove nasal prong oxygen and order to
administer 5 liter/minute of oxygen via face mask to keep SPO2 more than 90%
- Patient refer to surgical department due to gross haematuria post catheter bladder
drainage (CBD) insertion
- Bladder irrigation done to this patient due to gross haematuria post catheter bladder
drainage (CBD) insertion

19
 - ABG (arterial blood gas) test was took in red zone as doctor’s order
- Doctor asked the patient to bring old notes and old medicine to ward 10

Treatment

Pharmacological treatment

Drugs Generic name Trade name Dose Indication

IV Augmentin Amoxicillin 1g AUGMENTIN ADULT: Infection caused by
1.2g stat &TDS &Clavulanate 1.2 g injection 1.2g by IV or susceptible organisms.
200mg injection intermittent Respiratory tract, skin
infusion 6-8 soft tissue, GUT
hourly infection, septicaemia
IV Ranitidine Ranitidine ZANTAC 1.ADULT: 1.Benign gastric/
50 mg stat&BD 25mg/ml Injection Slow IV duodenal ulceration,
injection injection of reflux oesophagitis,
50 mg diluted Zollinger Ellison
to 20 ml and syndrome
given over at
least 2
minutes. May
be repeated
every 6-8
hours or IV
infusion at
rate of 25
mg/hour for 2
hours, may be
repeated at 6-
8 hours
intervals or
IM.

20
IV Maxolon Metoclopramide MAXOLON ADULT over 1)Dyspepsia,
10mg stat HCL 5mg/ml injection 20 years: flatulence, peptic
injection 10mg 3 times ulceration, reflux
daily. esophagitis, gastritis,
Maximum nausea, vomiting
daily dose is
30mg or
0.5mg/kg
T.Paracetamol Paracetamol PANADOL ADULT: Mild to moderate pain
1g STAT 500mg stat Tablet 500-1000mg pyrexia
every 4-6
hours,
maximum of
4g daily
T.Azithromycin Azithromycin ZITHROMAX 1g as a single 1)Adult treatment of
500mg Stat 250mg Tablet 250MG Tablet dose, 500mg uncomplicated genital
&OD daily for 3 infection due to
days, 1g Chlamydia trichomatis
weekly or susceptible
Neisseria gonorrhoea
IV Lasix 40mg Frusemide LASIX Initially 20- Pulmonary disease
Stat/IV 10mg/ml injection 40 mg IM or
injection slow IV (rate
not exceeding
4mg/min).
CHILD: 0.5-
1.5 mg/kg.
Max: 20mg
daily.
MDI Salbutamol VENTOLIN 2ml may be Asthma and other
Salbutamol 0.5% Inhalation inhalation inhaled up to conditions associated
11/11 PRN solution solution 4 times daily with reversible airway
over a period obstruction

21
 of 3 minutes
per
inhalation(0.5
ml diluted in
2.5 ml of
normal saline
by inhalation
over 5 to 15
minutes)
MDI Flixolide Fluticasone FLIXOTIDE Adult and Prophylactic treatment
1/1 Bd Propionate Child more for asthma
125mcg/dose than 16 years
inhaler 1)Mild
asthma:100-
250mcg twice
daily
2)Moderate
asthma:250-
500mcg twice
daily
3)Severe
asthma:500-
1000mcg
twice daily
T.Cardiprin Acetylsalicylic CARDIPRIN, 1 tablet daily Prevention of
100mg OD acid 100mg, GLYPRIN myocardial infract,
Glycline 45mg smoke and deep vein
Tablet thrombosis
T.Perindopril Perindopril 8mg COVERSYL 4mg as single 1)Hypertension
8mg OD tablet 8mg dose, may be 2)Congestive heart
increased to a failure
single 8mg 3)Stable coronary
dose artery disease

22
T.Simvastatin Simvastatin ZOCOR 20mg 10-20mg Hypercholesterolemia,
20mg ON 20mg tablet once daily. and coronary heart
Maximum: disease intolerant or
80mg daily not responsive to other
forms of therapy

G) Advice
 Ask patient to have follow up at Klinik Kesihatan (Felda) Trolak Selatan
 Eat medications followed by the dosage that had been prescribed by doctor
 Take plenty of rest
 Drink water according to doctors’ order, which is 1 litre per day
 Avoid stress
 Eat diabetic and vitamin rich diet
 Do simple exercise
 Avoid harmful environment factor such as smoke or dust and chemical
 Take care personal hygiene to avoid from infection
 Stop smoking

23
 REFERENCE A

DEFINITION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

According to Sarah Edward from the article Mayoclinic (11 August 2017) said chronic
obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease that causes
obstructed airflow from the lungs. Emphysema and chronic bronchitis are the two most
common conditions that contribute to COPD. Chronic bronchitis is inflammation of the lining
of the bronchial tubes, which carry air to and from the air sacs (alveoli) of the lungs. It's
characterized by daily cough and mucus (sputum) production.

Emphysema is a condition in which the alveoli at the end of the smallest air passages
(bronchioles) of the lungs are destroyed as a result of damaging exposure to cigarette smoke
and other irritating gases and particulate matter.

COPD is treatable. With proper management, most people with COPD can achieve good
symptom control and quality of life, as well as reduced risk of other associated conditions.

SIGN AND SYMPTOMS OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

(COPD)

COPD symptoms often don't appear until significant lung damage has occurred, and they
usually worsen over time, particularly if smoking exposure continues. For chronic bronchitis,
the main symptom is a daily cough and mucus (sputum) production at least three months a year
for two consecutive years.

24
Other signs and symptoms of COPD may include:

 Shortness of breath, especially during physical activities

 Wheezing

 Chest tightness

 Having to clear your throat first thing in the morning, due to excess mucus in lungs

 A chronic cough that may produce mucus (sputum) that may be clear, white, yellow or
greenish

 Blueness of the lips or fingernail beds (cyanosis)

 Frequent respiratory infections

 Lack of energy

 Unintended weight loss (in later stages)

 Swelling in ankles, feet or legs

People with COPD are also likely to experience episodes called exacerbations, during which
their symptoms become worse than usual day-to-day variation and persist for at least several
days.

INVESTIGATION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

Spirometer

COPD is commonly misdiagnosed former smokers may sometimes be told they have COPD,
when in reality they may have simple deconditioning or another less common lung condition.

25
Likewise, many people who have COPD may not be diagnosed until the disease is advanced
and interventions are less effective.

To diagnose the condition, doctor will review signs and symptoms, discuss with family, carry
out physical exam and medical history, and discuss any exposure we've had to lung irritants,
especially cigarette smoke. Doctor may order several tests to diagnose this condition.

Tests may include:

 Lung (pulmonary) function tests. Pulmonary function tests measure the amount of air
you can inhale and exhale, and if the lungs are delivering enough oxygen to blood.

Spirometry is the most common lung function test. During this test, patient be asked to
blow into a large tube connected to a small machine called a spirometer. This machine
measures how much air lungs can hold and how fast we can blow the air out of lungs.

Spirometry can detect COPD even before we have symptoms of the disease. It can also
be used to track the progression of disease and to monitor how well treatment is working.
Spirometry often includes measurement of the effect of bronchodilator administration.
Other lung function tests include measurement of lung volumes, diffusing capacity and
pulse oximetry.

 Chest X-ray. A chest X-ray can show emphysema, one of the main causes of COPD. An
X-ray can also rule out other lung problems or heart failure.

 CT scan. A CT scan of the lungs can help detect emphysema and help determine if might
benefit from surgery for COPD. CT scans can also be used to screen for lung cancer.

 Arterial blood gas analysis. This blood test measures how well lungs are bringing
oxygen into blood and removing carbon dioxide.

Laboratory tests. Laboratory tests aren't used to diagnose COPD, but they may be used to
determine the cause of symptoms or rule out other conditions. For example, laboratory tests
may be used to determine if we have the genetic disorder alpha-1-antitrypsin (AAt) deficiency,
which may be the cause of some cases of COPD. This test may be done if have a family history
of COPD and develop COPD at a young age, such as under age 45.

26
TREATMENT OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)

A diagnosis of COPD is not the end of the world. Most people have mild forms of the disease
for which little therapy is needed other than smoking cessation. Even for more advanced stages
of disease, effective therapy is available that can control symptoms, reduce your risk of
complications and exacerbations, and improve your ability to lead an active life.

Smoking cessation

The most essential step in any treatment plan for COPD is to stop all smoking. It's the only way
to keep COPD from getting worse, which can eventually reduce ability to breathe. But quitting
smoking isn't easy. And this task may seem particularly daunting if we tried to quit and have
been unsuccessful.

Talk to doctor about nicotine replacement products and medications that might help, as well as
how to handle relapses. Doctor may also recommend a support group for people who want to
quit smoking. It's also a good idea to avoid second-hand smoke exposure whenever possible.

Medications

Doctors use several kinds of medications to treat the symptoms and complications of COPD.
Patinet may take some medications on a regular basis and others as needed.

Bronchodilators

These medications which usually come in an inhaler relax the muscles around airways. This
can help relieve coughing and shortness of breath and make breathing easier. Depending on
the severity of disease, you may need a short-acting bronchodilator before activities, a long-
acting bronchodilator that you use every day or both.

Short-acting bronchodilators include albuterol (ProAir HFA, Ventolin HFA, others),

levalbuterol (Xopenex HFA), and ipratropium (Atrovent). The long-acting bronchodilators
include tiotropium (Spiriva), salmeterol (Serevent), formoterol (Foradil, Perforomist),
arformoterol (Brovana), indacaterol (Arcapta) and aclidinium (Tudorza).

27
Inhaled steroids

Inhaled corticosteroid medications can reduce airway inflammation and help prevent
exacerbations. Side effects may include bruising, oral infections and hoarseness. These
medications are useful for people with frequent exacerbations of COPD. Fluticasone
(Flovent HFA, Flonase, others) and budesonide (Pulmicort Flexhaler, Uceris, others) are
examples of inhaled steroids.

Combination inhalers

Some medications combine bronchodilators and inhaled steroids. Salmeterol and fluticasone
(Advair) and formoterol and budesonide (Symbicort) are examples of combination inhalers.

Oral steroids

For people who have a moderate or severe acute exacerbation, short courses (for example, five
days) of oral corticosteroids prevent further worsening of COPD. However, long-term use of
these medications can have serious side effects, such as weight gain, diabetes, osteoporosis,
cataracts and an increased risk of infection.

Phosphodiesterase-4 inhibitors

A new type of medication approved for people with severe COPD and symptoms of chronic
bronchitis is roflumilast (Daliresp), a phosphodiesterase-4 inhibitor. This drug decreases
airway inflammation and relaxes the airways. Common side effects include diarrhea and weight
loss.

Theophylline

This very inexpensive medication may help improve breathing and prevent exacerbations. Side
effects may include nausea, headache, fast heartbeat and tremor. Side effects are dose related,
and low doses are recommended.

28
Antibiotics

Respiratory infections, such as acute bronchitis, pneumonia and influenza, can

aggravate COPD symptoms. Antibiotics help treat acute exacerbations, but they aren't
generally recommended for prevention. However, a recent study shows that the antibiotic
azithromycin prevents exacerbations, but it isn't clear whether this is due to its antibiotic effect
or its anti-inflammatory properties.

Lung therapies

Doctors often use these additional therapies for people with moderate or severe COPD:

 Oxygen therapy. If there isn't enough oxygen in blood, patient may need supplemental
oxygen. There are several devices to deliver oxygen to lungs, including lightweight,
portable units that you can take with us to run errands and get around town.

Some people with COPD use oxygen only during activities or while sleeping. Others use
oxygen all the time. Oxygen therapy can improve quality of life and is the
only COPD therapy proven to extend life. Talk to doctor about needs and options.

 Pulmonary rehabilitation program. These programs generally combine education,

exercise training, nutrition advice and counselling. We work with a variety of specialists,
who can tailor your rehabilitation program to meet needs.

Pulmonary rehabilitation may shorten hospitalizations, increase ability to participate in

everyday activities and improve quality of life. Talk to doctor about referral to a program.

Managing exacerbations

Even with ongoing treatment, we may experience times when symptoms become worse for
days or weeks. This is called an acute exacerbation, and it may lead to lung failure if we don't
receive prompt treatment.

Exacerbations may be caused by a respiratory infection, air pollution or other triggers of

inflammation. Whatever the cause, it's important to seek prompt medical help if notice a
sustained increase in coughing, a change in your mucus or if we have a harder time breathing.

29
When exacerbations occur, we may need additional medications (such as antibiotics, steroids
or both), supplemental oxygen or treatment in the hospital. Once symptoms improve, doctor
will talk with patient about measures to prevent future exacerbations, such as quitting smoking,
taking inhaled steroids, long-acting bronchodilators or other medications, getting annual flu
vaccine, and avoiding air pollution whenever possible.

Surgery

Surgery is an option for some people with some forms of severe emphysema who aren't helped
sufficiently by medications alone. Surgical options include:

 Lung volume reduction surgery. In this surgery, your surgeon removes small wedges
of damaged lung tissue from the upper lungs. This creates extra space in your chest cavity
so that the remaining healthier lung tissue can expand and the diaphragm can work more
efficiently. In some people, this surgery can improve quality of life and prolong survival.

 Lung transplant. Lung transplantation may be an option for certain people who meet
specific criteria. Transplantation can improve your ability to breathe and to be active.
However, it's a major operation that has significant risks, such as organ rejection, and it's
necessary to take lifelong immune-suppressing medications.

 Bullectomy. Large air spaces (bullae) form in the lungs when the walls of the air sacs are
destroyed. These bullae can become very large and cause breathing problems. In a
bullectomy, doctors remove bullae from the lungs to help improve air flow.

30
 REFERENCE B

DEFINITION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

According to author named Linda Hepler from the article Heathline (7 November 2018) said
chronic obstructive pulmonary disease, commonly referred to as COPD, is a group of
progressive lung diseases. The most common are emphysema and chronic bronchitis. Many
people with COPD have both of these conditions.

Emphysema slowly destroys air sacs in lungs, which interferes with outward air flow.
Bronchitis causes inflammation and narrowing of the bronchial tubes, which allows mucus to
build up. The top cause of COPD is tobacco smoking. Long-term exposure to chemical irritants
can also lead to COPD. It’s a disease that usually takes a long time to develop.

SIGN AND SYMPTOMS OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Many people don't recognize the symptoms of COPD until later stages of the disease.
Sometimes people think they are short of breath or less able to go about their normal activities
because they are "just getting older." Shortness of breath can be an important symptom of
lung disease. If we experience any of these symptoms, or think you might be at risk for COPD,
it is important to discuss this with doctor.

31
  Chronic cough
 Shortness of breath while doing everyday activities (dyspnea)
 Frequent respiratory infections

 Blueness of the lips or fingernail beds (cyanosis)

 Fatigue

 Producing a lot of mucus (also called phlegm or sputum)

 Wheezing

INVESTIGATION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

To diagnose chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis
and emphysema, your doctor will evaluate symptoms, ask for the complete health history,
conduct a health exam and examine test results.

Health History

Doctor will want to know if patient:

 Smoke or have a history of smoking

 Are exposed to second-hand smoke, air pollution, chemicals or dust

 Have symptoms such as shortness of breath, chronic cough or lots of mucus

 Have family members who have had COPD

During the physical exam, doctor will use a stethoscope to listen to the lungs as breathe. Based
on all this information, doctor may order some of these tests to get a more complete picture:

 Spirometry is a non-invasive test to assess lung function. During the test, we’ll take a deep
breath and then blow into a tube connected to the spirometer.

32
 Imaging tests include a chest X-ray or CT scan. These images can provide a detailed look
at your lungs, blood vessels, and heart.

 An arterial blood gas test involves taking a blood sample from an artery to measure blood
oxygen, carbon dioxide, and other important levels. These tests can help determine if have
COPD or a different condition, such as asthma, a restrictive lung disease, or heart failure.

TREATMENT OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Treatment can ease symptoms, prevent complications, and generally slow disease
progression. Your healthcare team may include a lung specialist (pulmonologist) and physical
and respiratory therapists.

Medication

Bronchodilators are medications that help relax the muscles of the airways, widening the
airways so we can breathe easier. They’re usually taken through an inhaler or a nebulizer.
Glucocorticosteroids can be added to reduce inflammation in the airways.

To lower risk of other respiratory infections, ask doctor if patient should get a yearly flu shot,
pneumococcal vaccine, and a tetanus booster that includes protection from pertussis (whooping
cough).

Oxygen therapy

If blood oxygen level is too low, we can receive supplemental oxygen through a mask or nasal
cannula to help breathe better. A portable unit can make it easier to get around.

33
Pulmonary Rehabilitation

If we or someone love suffers from a chronic lung disease like COPD, there is hope for
rebuilding strength and enjoying a fuller, more active life. Pulmonary rehabilitation programs
typically combine education, exercise training, nutrition advice and counselling.

Surgery

Surgery is reserved for severe COPD or when other treatments have failed, which is more likely
when you have a form of severe emphysema.

One type of surgery is called bullectomy. During this procedure, surgeons remove large,
abnormal air spaces (bullae) from the lungs.

Another is lung volume reduction surgery, which removes damaged upper lung tissue. Lung
transplantation is an option in some cases.

Medications for COPD

Medications can reduce symptoms and cut down on flare-ups. It may take some trial and error
to find the medication and dosage that works best for you. These are some of the options:

Inhaled bronchodilators

Medicines called bronchodilators help loosen tight muscles of your airways. They’re typically
taken through an inhaler or nebulizer.

Short-acting bronchodilators last from four to six hours. Patient only use them when you need
them. For ongoing symptoms, there are long-acting versions you can use every day. They last
about 12 hours.

Some bronchodilators are selective beta-2-agonists, and others are anticholinergic. These
bronchodilators work by relaxing tightened muscles of the airways, which widens airways for

34
better air passage. They also help your body clear mucus from the lungs. These two types of
bronchodilators can be taken separately or in combination by inhaler or with a nebulizer.

Corticosteroids

Long-acting bronchodilators are commonly combined with inhaled glucocorticosteroids. A

glucocorticosteroid can reduce inflammation in the airways and lower mucus production. The
long-acting bronchodilator can relax the airway muscle to help the airways stay wider.
Corticosteroids are also available in pill form.

Phosphodiesterase-4 inhibitors

This type of medication can be taken in pill form to help reduce inflammation and relax the
airways. It’s generally prescribed for severe COPD with chronic bronchitis.

Theophylline

This medication eases chest tightness and shortness of breath. It may also help prevent flare-
ups. It’s available in pill form. Theophylline is an older medication that relaxes the muscle of
the airways, and it may cause side effects. It’s generally not a first-line treatment for COPD
therapy.

Antibiotics and antivirals

Antibiotics or antivirals may be prescribed when develop certain respiratory infections.

Vaccines

COPD increases risk of other respiratory problems. For that reason, your doctor might
recommend that you get a yearly flu shot, the pneumococcal vaccine, or the whooping cough
vaccine.

35
 DISCUSSION

SIMLARITIES
Real case, Reference A and Reference B

Based on my case study, there have a few similarity I found in real case, Reference A and B.
First similarity want to discuss is the definition of chronic obstructive pulmonary disease.
These three vases said that chronic obstructive pulmonary disease is the chronic inflammatory
lung disease that causes airflow to be blocked from the lungs. Emphysema and chronic
bronchitis is the two common conditions contribute to chronic obstructive pulmonary disease
(COPD). Next similarity from these cases is the sign and symptoms of chronic obstructive
pulmonary disease (COPD). This three cases said chronic obstructive pulmonary disease starts
with cough with produce of sputum and shortness of breath.

Next similarity from these cases is the investigation of chronic obstructive pulmonary disease
(COPD). Real case, reference A and B used patient’s medical history for their investigation.
The doctor will ask about patient’s personal and family medical history as well as recent and
current symptoms which may help them to relate recent diagnosis with the medical history.
Next same investigation used by these three cases is the physical exam. The physical
examination is the process by which a medical professional investigates the body of a patient
for signs of disease. It generally follows the taking of the medical history which an account of
the symptoms as experienced by the patient. During physical examination, doctor will use
stethoscope to listen to the lungs as breathe. This can help to listen sounds like wheezing,
crepitation and rhonchi.

Not only that, according to the laboratory test, these three cases used arterial blood gases (ABG)
which is a blood test that measures the acidity, or pH, and the levels of oxygen (O2) and carbon
dioxide (CO2) from an artery. The test is used to check the function of the patient's lungs and
how well they are able to move oxygen and remove carbon dioxide. This test also help to
determine if the patient have chronic obstructive pulmonary disease or a different condition
such as asthma or heart failure.

Other same investigation used by real case and the references is taking chest x-ray. This exam
help support the diagnosis of COPD by producing images of the lungs to evaluate symptom of
chronic cough and shortness of breath. While chest x-rays may not show chronic obstructive
pulmonary disease (COPD) until it severe, the images may show enlarged lungs, irregular air

36
pockets or a flattened diaphragm.

Oxygen therapy is one of the best treatment and management used in this three cases. For
example, this three cases used oxygen therapy such a administer oxygen via mask and nasal
cannula to maintain the SPO2.

In conclusion, we can understand that the real case, reference A and B are used few same sign
and symptoms, medical history, physical examination, arterial blood gases, chest x-ray and
giving oxygen therapy for chronic obstructive pulmonary disease (COPD).

37
DIFFERENCES
Real case, Reference A and Reference B

Based on my case study, there also have a few differences found in real case, reference A and
B. First difference I found from these cases is the sign and symptoms of chronic obstructive
pulmonary disease. Even few sign and symptoms mentioned in similarity but there also have
some symptoms that seems different in these cases. Real case said chronic obstructive
pulmonary disease starts with fever, body weakness, loss of appetite, orthopnea and have
minimal oral intake that not mentioned in both references. While both references said sign and
symptoms of chronic obstructive pulmonary disease is the wheezing, cyanosis and frequent
respiratory infections that are not mentioned in real case. Not only that, only reference A said
this disease starts with chest tightness, lack of energy, weight loss and swelling in ankles, feet
and legs that not mentioned in real case and in reference B.

Next difference found from these cases is the investigation of chronic obstructive pulmonary
disease. For example, according to laboratory radiology test, real case used electrocardiogram
(ECG) which help for heart’s electrical activity and will identify the heart rate and rhythm, and
display existing arrhythmias, hypertrophy, and ischemia that not mentioned in both references.
While next laboratory test used by real case is full blood count that used to evaluate overall
health and detect a wide range of disorders, including anaemia, infection and leukaemia, renal
profile is a group of tests that may be performed together to evaluate kidney function and INR.

But other different investigation used by authors in both references is the lung function test and
computed tomography (CT scan). Lung function test is measure the amount of air which can
inhale and exhale, and if the lungs are delivering enough oxygen to the blood. Spirometry is
the common lung function test. Spirometry can detect chronic obstructive pulmonary disease
before experience symptoms of the disease. Other test is computed tomography (CT scan) used
to detect bone and joint problems, help locate tumour and show internal injuries and bleeding.
This two investigations are not mentioned in real case.

Next difference found from real case and the references is the treatment of chronic obstructive
pulmonary disease (COPD). Real case used medications such as IV Augmentin 1.2g stat&TDS,
IV Ranitidine 50mg stat& BD, IV Maxolon 10mg Stat, T.Paracetamol 1g stat, T.Azithromycin
500mg stat& OD, IV Lasix 40mg stat/IV, MDI Salbutamol 11/11 Prn, MDI Flixolide 1/1 BD
used for his past medical history of asthma since 20 years ago, T.Cardiprin 100mg OD,

38
T.Perindopril 8mg OD and T.Simvastatin 20mg ON for the treatment. This medications are not
used in both references.

While next treatment and management used by authors from both references is the pulmonary
rehabilitation program that provide education, exercise training, nutrition advice and
counselling. Next according to medication, this three cases used medications such as
bronchodilator which help to relax the muscle around airway, theophylline, antibiotic and
antiviral, corticosteroid, inhaled steroids, oral steroid, combination inhaler and
phosphodiesterase-4 inhibitors that not mentioned in real case. According to surgery, authors
from both references used bullectomy. During this procedure, surgeons remove large, abnormal
air spaces (bullae) from the lungs. Next surgery recommended by authors from reference A
and B is lung transplant which is a surgical procedure to replace a diseased or failing lung with
a healthy lung, usually from a deceased donor. A lung transplant is reserved for people who
have tried other medications or treatment, but their conditions have not fully improved.

Other than that, next surgery is lung volume reduction surgery. This surgery is a surgical
procedure to removed diseased, emphysematous lung disease. This procedure reduces the size
of an over-inflated lung and allows the expansion of the remaining, often more functional lung.

Beside this treatment, only author in reference A used smoking cessation. This smoking
cessation is most essential step in treatment plan for chronic obstructive pulmonary disease is
to stop all smoking and keep this disease from getting worse. This smoking cessation is not
mentioned in real case and reference B.

In conclusion, we can understand that these three cases are used different sign and symptoms,
investigations like electrocardiogram (ECG), full blood count, renal profile, INR and lung
function test, treatments and pharmacology drugs.

39
 CONCLUSION

As a conclusion we get know that COPD (chronic obstructive pulmonary disease) makes it
hard for you to breathe. The two main types are chronic bronchitis and emphysema. The main
cause of chronic obstructive pulmonary disease (COPD) is long-term exposure to substances
that irritate and damage the lungs. This is usually cigarette smoke. Air pollution, chemical
fumes, or dust can also cause it.
At first, chronic obstructive pulmonary disease (COPD) may cause no symptoms or only mild
symptoms. As the disease gets worse, symptoms usually become more severe. They include
cough that produces a lot of mucus, shortness of breath, especially with physical activity,
wheezing and chest tightness.

Doctors use lung function tests, imaging tests, and blood tests to diagnose chronic obstructive
pulmonary disease (COPD). There is no cure. Treatments may relieve symptoms. They include
medicines, oxygen therapy, surgery, or a lung transplant. Quitting smoking is the most
important step you can take to treat chronic obstructive pulmonary disease (COPD).

According to Healthline, chronic obstructive pulmonary disease (COPD is the third leading
cause of death in the world. In terms of chronic obstructive pulmonary disease (COPD as the
underlying cause of death, absolute mortality rates for patients aged 25 years or older (2005)
were 77.3 deaths per 100,000 males and 56.0 deaths per 100,000 females, or 64.3 persons per
100,000 overall.

Not only that, beside learned about chronic obstructive pulmonary disease (COPD), during
posting in emergency department, I got chance to do case study about this disease. I gained
knowledge in depth by comparing the care with patient, I collected information from internet,
doctors, ward sisters, nurses, lab, radiology and record section and compared it with patient in
real situation. During my duty period in emergency department, I provided her a holistic care,

40
diversional therapy in very aspects like physical, emotional, economical and socio-cultural
view.

I also gained the knowledge about the Medical Assistant theory and application in real
situation. So, this case, not only gives the cognitive domain but also provides us the opportunity
to develop psychomotor domain, which is very important in Medical Assistant course, so the
patient is the main source of conveying knowledge in practical.

REFERENCE

https://www.copdfoundation.org/What-is-COPD/Understanding-COPD/How-is-COPD-
Diagnosed.aspx
https://www.copdfoundation.org/What-is-COPD/Understanding-COPD/Statistics.aspx
https://www.mayoclinic.org/diseases-conditions/copd/symptoms-causes/syc-20353679
https://www.lung.org/lung-health-and-diseases/lung-disease-lookup/copd/

https://www.lung.org/lung-health-and-diseases/lung-disease-lookup/copd/symptoms-causes-
risk-factors/symptoms.html

https://www.lung.org/lung-health-and-diseases/lung-disease-lookup/copd/diagnosing-and-
treating/how-is-copd-diagnosed.html

https://www.pharmacytimes.com/publications/health-system-edition/2017/may2017/chronic-
obstructive-pulmonary-disease-in-hospitalized-patients-managing-exacerbations
https://www.atsjournals.org/doi/full/10.1164/rccm.201309-1651ED
https://emedicine.medscape.com/article/297664-overview#a6
https://slideplayer.com/slide/3468860/

https://www.copdfoundation.org/What-is-COPD/Understanding-COPD/What-is-COPD.aspx

https://www.nhlbi.nih.gov/health-topics/education-and-awareness/copd-learn-more-breathe-
better

Sarawak Handbook of Medical Emergencies 2nd edition by Hua Huat Soo (August 2014)

https://rbpaonline.com/pathophysiology-of-copd-flow-chart/pathophysiology-copd-think-
copdifferently/

https://www.immunology.org/public-information/bitesized-immunology/pathogens-and-
disease/chronic-obstructive-pulmonary-disease

41