INTERNAL MEDICINE

1.5A COPD
NORMAN MAGHUYOP, MD, FPCP, FPCCP || AUGUST 24, 2021

→ These are more of pathological terms but COPD is the

OUTLINE general/unified term now especially in clinics because it turns out
I. Case VII. Diagnosis that it has the same management
II. Definition VIII. Magnitude of Symptoms
III. Epidemiology IX. Management/Treatment III. EPIDEMIOLOGY
IV. Pathophysiology X. COPD and COVID-19 ● 251 million (2016), 3.17M deaths
A. Pathogenesis of COPD XI. Sample Case ● Low to middle income countries
B. Risk Factors → Why? Large percentage of cigarette smokers occurs in these
V. Assessment areas which mirrors its epidemiology; have something to do with
VI. Differential Diagnosis education level, economy, stress
● 7th leading cause of death in the Philippines Expected to be 5th in
LEGEND few years
Remember Lecturer Book Previous Presentation ● Male and Female almost equally affected
Trans
     IV. PATHOPHYSIOLOGY
A. Pathogenesis of COPD
LECTURE OBJECTIVES
At the end of the lecture, the student should be able to:
● Discuss pathophysiology and clinical presentation of COPD
● Formulate a diagnostic plan for a patient who probably has COPD
● Formulate a management plan for a patient with COPD

I. CASE
● M.C., 64/M, Filipino, Retired Seaman
● 41 pack year smoker
● CC: Chronic cough
→ Cough that has been going on for more than 3 weeks
● Previous intake of Azithromycin with temporary relief but still with
occasional sputum production
● No history of emergency consults or admissions
● No other symptoms reported
● Physical examination was essentially normal

Figure 2. COPD pathogenesis

● The triggers are again cigarette smoke and in people who have
genetic susceptibility to the toxins in the smoke which stimulates
macrophages, neutrophils which produce protease and oxidant
stress to the airways resulting to chronic inflammation
● It also affects cell death and there’s also impaired lung repair.
Pathobiological results is chronic airway inflammation in which end
result is tissue damage or scarring hence abnormalities
● Upon long-term exposure to cigarette smoke in genetically
susceptible individuals, lung epithelial cells and T and B
lymphocytes recruit inflammatory cells to the lung. Biological
pathways of protease-antiprotease imbalance, oxidant/antioxidant
imbalance, apoptosis, and lung repair lead to extracellular matrix
destruction, cell death, chronic inflammation, and ineffective repair.
Although most of these biological pathways influence multiple
pathobiological results, only a single relationship between pathways
Figure 1. Chest X-ray of the patient and results is shown. A subset of key molecules related to these
● Does the patient have COPD? biological pathways is listed.
● How should we go about working up and managing the patient?

II. COPD DEFINITION

● Persistent respiratory symptoms and airflow limitation that is NOT
fully reversible 
→ Important distinction from Bronchial asthma, which is often
times reversible
→ COPD is permanent in other words
● Due to airway and/or alveolar abnormalities
→ Not just a disease of airways, later on in the course when it’s
already severe, it also affects the lung parenchyma as opposed
again to Asthma in which most of the pathology is in the airways
→ Asthma = Airways ONLY
→ COPD = Airways + Parenchyma
● Caused by significant exposure to noxious gases or particles and
influenced by host factors
→ As well as the reactions of the host to noxious gases in which
the most important source is cigarette smoking
● Emphysema, Chronic Bronchitis, Small Airway Disease

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1.5 COPD LONG EXAM 1

● Respiratory infections
● Occupational exposures With regards also to interstitial lung
diseases
● Ambient air pollution (outdoor)
● Passive, or Second-hand, smoking exposure
● Genetic considerations – A1 Antitrypsin Deficiency
→ Alpha 1 Anti-Trypsin Deficiency
▪ Hyperinflation
▪ Hyperlucency
▪ Low set flat diaphragm
▪ Vertical heart
▪ Pre and infra cardiac lungs
▪ Barrel shape
● Indoor pollution*
● Age, Sex*
● Lung growth and development*
Figure 3. Airway changes in COPD patients
● Socioeconomic status*
● Just a review! With persistent inflammation, the wall of airways is ● Chronic Bronchitis*
TN: Additional risk factors from GOLD but it’s also included in the mid part of ppt,
swollen and there’s exudate. Airway lumen will become narrowed pinag-isa lang RF
and there’s many secretions
V. ASSESTMENT
A. Chest X-ray
● Obvious bullae, hyperlucency (Emphysema)
● Increased lung volumes and flattening of the diaphragm
suggest hyperinflation (airflow limitation)

Figure 4. Obstructive diseases. Chronic Bronchitis VS Emphysema

● Emphysema – an anatomically defined condition characterized

Figure 5. Chest X-ray of COPD
by destruction of the lung alveoli with air space enlargement
● When you do your X-ray, what you’ll see actually are signs of
→ Avascular zones
hyperinflation of the airways (caused by blockages in the air
→ Cephalization of upper lung fields is not evident passages which interferes with the expulsion of air); results to
→ Predominant basal involvement (not evident) flattening of the diaphragm (push downward), di ba dapat dome
● Chronic Bronchitis – a condition with productive cough lasting shaped ‘yan. while the heart appears vertically/tubular and intercostal
more than 3 months occurring within a span of 2 years spaces are widened
● Small airway disease – a condition in which small bronchioles 
are narrowed and reduced in number B. Computed Tomography (CT) Scan
● Definitive test for emphysema (pattern of emphysema, and the
Main Pathophsyiologic Effects are: presence of significant disease involving medium and large airways)
● Airflow Obstruction ● Enables the discovery of coexisting interstitial lung disease and
▪ Because of the narrowed airways bronchiectasis
▪ Airflow limitation which is typically determined for clinical ● Smokers with COPD are at high risk for development of lung
purpose by spirometry cancer, which can be identified on a chest CT scan
● Hyperinflation ● In advanced COPD, CT scans can help determine the possible
▪  There is air trapping; you can inhale air but it is hard and value of surgical therapy
slow to exhale (naiipon)
▪ In COPD there is often “air trapping” (increased residual
volume and increased ratio of residual volume to total lung
capacity) and progressive hyperinflation (increased total lung
capacity) late in the disease
▪ Hyperinflation of the thorax during tidal breathing preserves
maximum expiratory airflow, because as lung volume
increases, elastic recoil pressure increases, and airways
enlarge so that airway resistance decreases
● Gas Exchange
▪ Involvement of lung parenchyma at the alveolar level, there
will be impairment in gas exchange which is the worst-case
scenario

B. Risk Factors
● Cigarette smoking Most important, elicited in history taking
● Airway hyperresponsiveness History of asthma
Figure 6. CT scan (left) and Chest X-ray (right) in COPD

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● When you do your CT scan, we can see here the alveolar

damage; signs of emphysema – dilated alveoli
C. Spirometry
● Diagnosis;  confirmatory testing
● Assessment of severity of airflow obstruction (for prognosis)
 Going back with the case, let’s look at the post-bronchodilator
(maneuver is done after administering Salbutamol, which is a
bronchodilator) values. Ang mangyayari is hihinga nang malalim at
ibo-blow niya nang malakas na malakas. Pansinin niyo sa unang part
ng expiratory maneuver, ang bilis ng flow (red dot, first from 0 then it
went up to 4)

Figure 8.1. Spirometry result of the patient in the case

Tapos habang nauubos ang air, umuunti na yung flow. Kapag

mayroong mabagal na pag-flow dito sa terminal part (red dot) – that
Figure 7. Diagram for the diagnosis of COPD is characteristic of COPD called, SCOOPING. Flattened yung part ng
curve sa dulo kasi nga hirap yung air end ng maneuver.
●  When you assess patients in the clinics for COPD, consider 3
important clinical factors:
→  Exposure to risk factors (most important is cigarette smoke
then the duration of exposure)
→  Age (generally among patients who are older than 40 y/o
except those with genetic abnormality like A1 antitrypsin
deficiency which occur commonly in children)
→  Cardinal manifestations: cough, dyspnea, sputum
production (unfortunately there are others diseases that presents
with these symptoms)
▪  The distinguishing factor is the duration in which in COPD,
it should be chronic (not just 1 day only)
▪  But sometimes, there is confusion like there’s chronic
symptoms but with acute worsening – acute on top of chronic
which is also consistent with COPD
−  COPD may be punctuated by period of acute worsening Figure 8.2. Spirometry result of the patient in the case
of respiratory symptoms called exacerbations
●  When these factors are present, it is worthwhile to suspect COPD ● The FEV1/FVC is only 62.5 (encircled) which is less than 70% hence
then you will now do the confirmatory testing which is Spirometry – a the diagnosis of COPD in this case is confirmed with spirometry
pulmonary function test which will determine if there’s airway results
obstruction or not ● Notice also the FEV1 in pre-bronchodilator with a result of 1.07 L
→ Airway obstruction: Post-bronchodilator FEV1/FVC <70% while comparing it with the post-bronchodilator result of 1.04 L in
▪ Kung meron ‘non ang patient -- COPD na ‘yon. which it did not increased and implies no bronchodilator response,
▪  Review! Forced Vital Capacity (FVC) is the air that you also it became negative which is again a characteristic of COPD (di
can expire/exhale after full inspiration/inhalation (but you can’t masyadong responsive sa administration ng bronchodilator)
expire all the air because there’s Residual Volume; basta
lahat ng nakalabas ay FVC) while FEV1 is the air that exhaled D. Modified MRC Dyspnea Scale
on the first second of the FVC maneuver
−  If there’s no airflow obstruction, most of the FVC will be
expired in 1 sec
−  If there’s obstruction, the route is narrowed, the
airflow will be slow, the expiratory time will be
prolonged which is again characteristic of COPD patients

Figure 9. Modified MRC Dyspnea Scale

● The next aspect that we want to determine in a patient with COPD

is how does it affect the patient’s way of life specifically in
Figure 8. Spirometry result of the patient in the case symptomatology

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→ One example of tool to measure it is the Modified MRC

Dyspnea Scale (mMRC). The patient will just answer what
applies to him/her then it will have a corresponding grade (it also Scan me for GOLD
has a tagalog/fil version); ano lang to, simple question lang 2021 Report
TN: Pls check the description of each grading above, binasa lang din ni doc and
yung may yung applicable sa px dun sa case bale COPD mMRC grade 2 sya
VI. DIFFERENTIAL DIAGNOSIS
E. Global initiative for chronic Obstructive Lung Disease
(GOLD)
● In order to guide us in the management of COPD patients, I recommend utilizing
GOLD guidelines which is updated annually and used as standard
● GOLD was launched in 1997 in collaboration with the National Heart,
Lung, and Blood Institute, National Institutes of Health, USA, and the
World Health Organization
● GOLD’s program is determined and its guidelines for COPD care are
shaped by committees made up of leading experts from around the
world
● 2021 GOLD Reports – Global Initiative for Chronic Obstructive Lung
Disease – GOLD (goldcopd.org)
●  But before utilizing any guidelines, you have to see first if it’s valid:

Table 1. Questions for Validating Guidelines

Is the GOLD 2021 Global Strategy for Prevention, Diagnosis and
Management of COPD valid?
1. Were all important NO (patients, primary care
stakeholders represented in physicians)
consensus panel?  The consensus panel is more on
specialists
2. Were conflicts of interest Not stated
managed adequately? Figure 11. Differential Diagnosis of COPD (lifted from GOLD)
3. Were systematic reviews of YES
evidence done? The GOLD guidelines present some differential diagnosis well as
4. Were all important treatment YES clinical information that suggest kung ito ba yung differential na yun. So,
options considered? sa COPD, onset is midlife or late in life, slowly progressive chronic
5. Were all important outcomes YES symptom and cigarette smoking. Asthma is a disease of childhood, or
considered? earlier in life yung presentation the symptoms vary widely from day to
6. Was a formal consensus YES day, ibig sabihin today – asymptomatic, bukas – hingal na hingal.
making process used? Symptoms worst at night or early morning as supposed sa COPD na
7. Were costs considered? YES throughout the day. Very important ang history ng Atopy, allergy, allergic
8. Were patient preferences YES rhinitis, eczema and family history of asthma and there’s coexistence of
considered? obesity. Minsan ang ddx ay hindi man lang sa respiratory system, they
can be mistaken from congestive heart failure and vice versa. So, when
you look at the patient, do not limit yourself to the respiratory system,
COPD GOLD 2021 (Definition)
kasi baka mamaya heart failure pala yung pasyente and if it is indeed
● COPD is a heterogenous disease/syndrome that is characterized by heart failure, then CXR would show heart enlargement, pulmonary
persistent respiratory symptoms and airflow limitation that is due to edema, and if you do perform pulmonary function and lalabas ay volume
airway and/or alveolar abnormalities usually caused by significant restriction rather than airflow limitation, so restrictive lung disease yung
exposure to noxious particles or gases and influenced by host factors pattern.
● Significant co-morbidities have an impact on mortality/morbidity
→  Remember that the causative agent is cigarette smoke and
this factor doesn’t only cause COPD so you have to screen the COMPLETE ASSESSMENT AND DIAGNOSIS OF COPD:
patient for other co-morbidities in relation to smoking as well as in ● Spirometric Abnormality
older age ● Patient’s Symptoms
● History of exacerbations gaano kadalas, at gaano kalala
● Presence of Comorbidities

VII. DIAGNOSIS
A. Key Indicators for COPD

Figure 12. Key indicator for Considering COPD (lifted from GOLD)

Key indicators in considering a diagnosis of COPD in terms of

Figure 10. Etiology, Pathobiology and Pathology of COPD leading to Airflow Symptomatology: Dyspnea, Chronic cough, Chronic Sputum
Limitation and Clinical Manifestations (lifted from GOLD) Production

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Kung meron nga siyang Dyspnea, dapat progressive yun overtime,

palala ng palala, persistent, hindi katulad ng asthma na mayroon days
na wala siyang dyspnea and it characteristically worsens with exercise
or exertion. Chronic cough, it doesn't need to be productive and there
may even be wheezing, which again is confusing kasi ang asthma may
wheeze din. Chronic sputum production, kahit ano pang sputum yan
be it purulent or clear basta may production

B. Classification of Airflow Limitation Severity in COPD

In patients with FEV1/FVC <0.70:
GOLD 1 Mild FEV1 ≥ 80% predicted
GOLD 2 Moderate 50% ≤ FEV1 < 80% predicted
GOLD 3 Severe 30% ≤ FEV1 < 50% predicted
GOLD 4 Very Severe FEV1 < 30% predicted
Table 2. Classification of Airflow Limitation Severity in COPD; Based on Post-
bronchodilator FEV1 (lifted from GOLD)

In simplifying the severity of COPD in terms of Spirometic figures, Figure 16. COPD Assessment Tool (lifted from GOLD)
this will be based on the comparison of the patient’s FEV1 with a person
na walang COPD na same with age and size ang tawag dun ay – C. COPD Control Questionnaire
Percent Predicted ng FEV1. So kapag ang FEV1 ng patient ≥ 80% of D. 6 Minute Walk Test
predicted, (Predicted = ano ang FEV1 ng isang normal na patient) pag ● Papalakarin mo yung patient for 6 minutes, tapos titignan
80% of normal, MILD lang yun or GOLD 1. Kapag between 50 and < kung gaano kalayo ang kaya niyang lakarin na comfortable
80%, MODERATE and kanyang COPD, classified as GOLD 2. Between phase
30 < 50%, then SEVERE, GOLD 3. Kapag 1/3 lang ang FEV1 ng patient,
compared to a normal person that is VERY SEVERE, GOLD 4. These
classifications, pertains to the severity of the airflow limitations, so kapag
very severe, halos 1/3 na lang ang performance ng patient, less than
30% FEV1.

Figure 17. 6 Minute Walk Test (lifted from PowerPoint)

E. Shuffling Walking Test

Figure 13. Patient’s Result (lifted from PowerPoint)

Sa patient natin kanina, if we compare yung kanyang performance Figure 18. Shuffle Walk Test (lifted from PowerPoint)
sa isang normal person, 1.04, and percent predicted niya ay 44% so
compared to a normal person, actually less than half na lang and So why is this important? Again, confirmation of the diagnosis,
kanyang FEV1 at kapag 44% SEVERE and kanyang COPD. assessment of the severity, and symptomatology and exacerbation
history. Importante ito, because it will come altogether when we give our
final diagnosis. This will matter in the management of the patient.
VIII. MAGNITUDE OF SYMPTOMS
A. Modified MRC Dyspnea Scale (MMRC)
Only dyspnea ang pinag-uusapan

Figure 15. MMRC Scale lifted from Batch 2023 Trans

Figure 19. Refined ABCD Assessment Tool (lifted from GOLD)
B. COPD ASSESSTMENT TEST (CAT)
 So, this is what GOLD recommends:
● Advantage: many domains, comprehensive
→ Confirm the diagnosis using the spirometry
● Disadvantage: complicated
→ Assessing the airflow limitation and
→ Assess the risk of exacerbations.

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To confirm the diagnosis: FEV1/FVC <0.7 (critical number), the

severity of the airflow limitation uses the GOLD Grade Classification. To
assess for risk of exacerbation, tanungin niyo in the past year
“nagexacerbate kaba?” pag more than 2 or more OR 1 or more pero na-
ospital siya then malala yun (High Risk). Malaki ang chance na mag
exacerbate siya ulit . Kapag 0 to 1 tapos hindi naman na-ospital, bababa
ang risk na hindi mag exacerbate. This is the way to evaluate the risk for
exacerbation, tatanungin niyo lang sa history. The last domain that you
will ask is the severity of the symptoms.
→ MMRC 0 to 1 or CAT <10 = ASYMPTOMATIC
→ MMRC ≥ 2 or CAT ≥10 = SYMPTOMATIC
Mas mataas ang score mas malala ang symptoms. Now if you
combine risk for exacerbation and symptoms, pwede kang gumawa ng Figure 22. Asthma Treatment Strategy for adults and adolescence (lifted from GINA)
4 categories ng COPD:
→ A = Low Risk + hindi malala symptoms niya  Comparing it with the step wise approach for ASTHMA, ibang
→ B = Symptomatic + hindi masyado naoospital/exacerbate ibang ang treatment kahit sabihin nating parehong disease of the
→ C = Hindi symptomatic + madalas naoospital airways yun, parehong may obstruction of the airway. Kaya importante
→ D = Symptomatic + Madalas naoospital na ma-diagnose ng mabuti.
You could classify the patient into A, B,C & D, na COPD by
combining yung Risk for Exacerbations and the Symptoms

IX. MANAGEMENT/TREATMENT
A. Pharmacologic Treatment
Table 3. Initial Pharmacological Treatment for COPD (GOLD)
≥≥≥ 2 moderate GROUP C GROUP D
exacerbations or LAMA LAMA or
≥ 1 leading to
LAMA + LABA* or
hospitalization
ICS + LABA**
*Consider if highly
symptomatic (e.g., CAT >20)
**Consider if Eosinophil count
≥ 300
0 or 1 moderate GROUP A GROUP B
exacerbation LONG-ACTING
(not leading to
BRONCHODILATOR BRONCHODILATOR
hospital
admission) (LABA or LAMA) Figure 23. Patient’s Result (lifted from PowerPoint)
mMRC 0-1, CAT < 10 mMRC ≥ 2, CAT ≥ 10
LAMA: Long-Acting Muscarinic ANTAgonist
LABA: Long-Acting Beta AGOnist
Going back to our case, confirmed COPD siya kasi <70 ang
ICS: Inhaled Corticosteroid kanyang FEV1/FVC. GOLD 3, no history of hospitalization pero ang
score niya ay mataas sa mMrc = 2 so complete diagnosis is GOLD
3B. So, when you give your diagnosis of a COPD patient, hindi enough
na sabihin niyo lang na COPD, tell the GOLD classification as well as
the grouping.

Figure 20. Article (lifted from PowerPoint)

These recommendations are based on large randomized controlled

trials which showed improvement in outcomes among patients in
different categories

LAMA + LABA as effective as

LAMA + LABA + ICS except for patient with eosinophilia
LAMA + LABA had lower pneumonia rates

Figure 21. Article lifted from PowerPoint

LABA + LAMA + ICS vs LAMA + LABA vs LABA + ICS

Improvement in Lung Function (Improvement in FEV 1)
Prevention of Moderate to Severe Exacerbations

Figure 24. Follow Up Pharmacological Treatment (lifted from GOLD)

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If the response to the initial treatment is appropriate then you

maintain it. If not, you need to check several possible reasons why the
patient did not respond. First consider the predominant treatable trait to
target, either dyspnea or exacerbation kapag meron both, use the
exacerbation pathway. Dalawa ang pathways natin, dyspnea or
exacerbation, pag follow up ng patient, ask mo, “okay na po ba kayo,
wala na kayong dyspnea or exacerbation?” Pag sagot niya ay YES,
continue medication. Pag ang sagot niya ay NO, hinihingal parin ako,
use the DYSPNEA PATHWAY, pag sinabi niyang nao-ospital parin ako
then use EXACERBATION PATHWAY. If both, use EXACERBATION
PATHWAY. In DYSPNEA PATHWAY, hindi parin gumana ang LABA +
LAMA, consider switching inhaler device or molecules and work up for
other causes of dyspnea. Kapag ang intial treatment niya ay LABA +
ICS, then consider either giving triple therapy OR mag switching
treatment to LAMA + LABA if there is increase frequency of pneumonia,
that is the danger of giving ICS, the patient is at risk for pneumonia. Kung
exacerbation and predominant problem and giving LABA or LAMA
alone, you could give LABA + LAMA or give LABA + ICS particularly if
may frequent exacerbation yung patient. Now if the patient has high
eosinophil count the next step is TRIPLE THERAPY. If LOW eosinophil
count, you could add ROFLUMILAST or chronic antibiotic use particular
AZITHROMYCIN

Figure 26b. Pharmacologic options for the management of COPD. IIE

\AD
B. Non-pharmacologic Treatment
● Smoking cessation  very important kasi ito ung causative agent
ng COPD
● Pulmonary rehabilitation (Supervised exercised training)
● Vaccination very important to protect the patient from infection
particularly pneumonia and influenza
● Nutrition (Zinc, Selenium, Vitamins C and E,)
● Oxygen therapy
● Intervention Bronchoscopy and Lung Surgery  only for select
patients

Figure 25. Management Plan for COPD C. Oxygen at Home

● Who are patients that required oxygen at home based on the gold
 Review the symptoms. Assess the inhaler technique, and consider guidelines:
non-pharmacologic approaches including pulmonary rehabilitation and → If the paO2 is at 55 or oxygen saturation (SatO2) is 88% with or
education, Adjust, pwedeng mag-escalate, switch and pwedeng mag without hypercapnia confirmed twice over a three-week period
de-escalate. So di pwedeng yung biniday mo nung una is yun → If the paO2 55-60 or SatO2 88% with pulmonary hypertension,
na,kailangan continuous ang management cycle, remember that no peripheral edema (suggestive of CHF) or Polycythemia
cure has been develop for COPD (hematocrit >55)
● Prescription of supplemental oxygen to COPD patients:
Arterial Hypoxemia defined as:
PaO2 <55 mmHg (8 kPa) or SaO2 <88%
Or
PaO2 >55 but <60 mmHg (>7.3 kPa but <8 kPa) with right
heart failure or erythrocytosis

Prescribe supplemental oxygen and titrate to keep SaO2

≥ 90%

Recheck in 60 to 90 days to assess:

• If supplemental oxygen is still needed
• If prescribed supplemental oxygen is effective
 Actually, long term oxygen therapy is one of the few treatments that
has been proven to increase the lifespan of patients

D. Assessment for Exacerbation

● COPD Exacerbation is defined as ana cute worsening of respiratory
symptoms that result in additional therapy
● Classified as:
Figure 26a. Pharmacologic options for the management of COPD
→ MILD: treated with SABAs only
→ MODERATE: treated with SABA + antibiotics and/or oral
corticosteroids

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→ SEVERE: Patient requires hospitalizations/ER; may also be  If there are symptoms of COPD also consider COVID-19 kasi similar
associated with acute respiratory failure. ung presentation. An important impact of Covid 19 pandemic is that we
● Can also be guided by biomarkers: CRP and procalcitonin cannot perform spirometry because of the generation of respiratory
● One important information that we need to elicit is the quality of droplets. Assure that the patient is following health precaution standards
sputum and that he has enough supply of medication.
 Green or Yellow sputum are more likely to yield bacteria than
purulent or rust color sputum XI. SAMPLE CASE
● Managed with SABA with or without anticholinergics
● Systemic corticosteroids (not more than 5-7 days) CASE 1: A 70yo retired army colonel is brought to the ER for
● Antibiotics DOB. He has been having gradually progressive dyspnea on
● Methylxanthine (Theophylline) not recommended in exertion since 8 months ago, associated with nonproductive
exacerbations cough. His son says this is his 2nd severe attack requiring
● Noninvasive ventilation should be the first option for ARF in hospitalization this year. He is a known hypertensive and smokes
COPD exacerbation. 1/2 pack per day since he was 25yo. PE: he is sitting in tripod
position, tachycardic and tachypneic, BP 130/80 and T=36.9C,
decreased breath sounds on both lung fields, (+) wheezing, both
E. Admission or Send Home
lung fields, (-) cyanosis, (-) clubbing of digits. His lab workup
● Criteria for Outpatient: shows ABG: pH 7.25, PaO2 70 mmHg, PaCO2 50mmHg, SpO2-
→ Non-life threatening ARF: 94% at room air and the following chest x-ray:
▪ > 30 CPM
▪ Use of accessory muscles
▪ No change in Mental Status
▪ Hypoxemia improved with supplemental oxygen
▪ Hypercarbia (PaCo2 increase from baseline)
● Criteria for Hospital Admission
→ Life threatening ARF
▪ Change in mental status
▪ Non improving hypoxemia on supplemental oxygen

F. Intubation
● Indications for noninvasive ventilation (NIV)
→ Respiratory acidosis (ph < 7.35, PaCo2 > 45) 1. What is the most likely diagnosis for this patient’s clinical picture?
→ Severe dyspnea (clinical) 2. What is the cause of the patient’s elevated pCO2 on ABG?
→ Persistent hypoxemia despite supplemental oxygen 3. Which of the ff is the most probable cause of his lung PE findings?
● Indications for invasive ventilation A. Inflammatory response to noxious stimuli
→ Unable to tolerate NIV B. Rupture of blebs into the pleural space
→ Post arrest C. Mast cell degranulation with subsequent CMI response
→ Decreased sensorium D. Vascular occlusion due to a hypercoagulable state
→ Risk of Aspiration or with vomiting E. Airway cell dysplasia because of exposure to carcinogens
4. Which of the ff diagnostic tools will confirm your diagnosis
→ Hemodynamic instability
A. ABG
→ Cardiac arrhythmias B. Spirometry
→ Life threatening hypoxemia despite NIV C. Chest CT scan
D. MRI chest
G. Patient discharge and Follow-Up Checkup E. Bronchoscopy
● Full review of all clinical and laboratory data 5. Which of the ff statements is an accurate interpretation of his lab test
findings?
● Re assess inhaler technique
A. Has respiratory alkalosis
● Ensure follow up less than 4 weeks (1-4 weeks, 12 weeks classified B. Patient is in ARDS
as follow up) C. CXR findings show evidence of hyperinflation
● Spirometry yearly D. A and B only
E. AOTA
X. COPD and COVID-19
Reference: Pugad Agila (The ASMPH Board Operations)
CASE 2: A 55-year-old male, farmer from Pampanga came
to ER because of difficulty of breathing. Present condition
started 2 weeks prior to consult as cough productive of
opious grayish yellow sputum accompanied by moderate
grade fever, body malaise, and loss of appetite. Condition
progressed despite over-the-counter anti-tussive medication,
until 1 day PTC he started to have difficulty of breathing.
Personal History: Smoker, 1 pack of cigarette/day since age
of 25; No other illness in the past. Pertinent PE findings: RR-
28/min; Chest Exam: Symmetrical expansion, resonance of
percussion includes crackles on the left midlung to base
posteriorly with bilateral forced on expiration.

1. What disease conditions would you consider/entertain?

A. COPD
B. Mycosis
C. Pneumonia
D. AOTA
2. What diagnostic laboratory examination would you request for?
A. CXR
B. Sputum GS, CS
Figure 27. Key points from Gold’s guidelines on COPD and Covid- 19
C. CBC
D. AOTA

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3. How would you start your management?

A. O2 Inhalation
B. IV Antibiotic
C. Nebulization
D. AOTA
4. If arterial blood gas examination showed a pH of 7.33, pCO2 of 50 mmHg,
pO2 of 75 mmHg and HCO3 of 28 mEq/L. What would be your
interpretation?
A. Respiratory Acidosis with Hypoxemia
B. Respiratory Alkalosis with Hypoxemia
C. Respiratory and Metaolic Acidosis
D. Adequate Oxygenation
5. What further laboratory examination would you add aside from above
examinations?
A. Pulmonary Function Test
B. Sputum for fungus
C. A & B
D. A only
6. What is most likely the diagnosis?
A. PTB
B. Asthma
C. COPD
D. Pneumonia
7. What laboratory examination will you request to confirm the diagnosis?
A. CXR
B. Sputum Exam
C. Chest CT
D. Spirometry
8. The mainstay treatment of this patient?
A. Inhaled bronchodilator
B. Inhaled corticosteroid
C. Methylxanthines
D. Antibiotics

Case 1 Answers: COPD, Due to expiratory airflow limitation, A, B, C

Case 2 Answers: D, D, D, A, C, C, D, A,
REFERENCES
● Doc Maghuyop’s PPT and zoom recording
● HPIM 20th Ed.
● Batch 2022 trans
● GOLD 2021 Report

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NORMAN MAGHUYOP, MD, FPCP, FPCCP || AUGUST 24, 2021

APPENDIX

Figure 10. Etiology, Pathobiology and Pathology of COPD leading to Airflow Limitation and Clinical Manifestations (lifted from GOLD)

Figure 11. Differential Diagnosis of COPD (lifted from GOLD)

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1.5 COPD LONG EXAM 1

Figure 12. Key indicator for Considering COPD (lifted from GOLD)

Figure 15. MMRC Scale lifted from Batch 2023 Trans

Figure 19. Refined ABCD Assessment Tool (lifted from GOLD)

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Figure 16. COPD Assessment Tool (lifted from GOLD)

Figure 22. Asthma Treatment Strategy for adults and adolescence (lifted from GINA)

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