Clinical Medicine Exam II | Pulmonology | Complete Exam Prep | Practice Questions & Answers
Chronic Obstructive Pulmonary Disease (COPD) Heterogeneous lung condition with chronic respiratory symptoms (dyspnea,
cough, sputum, exacerbations) due to airway (bronchitis/bronchiolitis) + alveolar
(emphysema) damage → persistent, progressive airflow obstruction.
Chronic bronchitis = productive cough ≥3 mo for ≥2 yrs.
Emphysema = alveolar wall destruction, enlarged spaces, ↓ elastic recoil.
COPD Etiology & Risk Factors å Smoking = #1 cause (~85-90%)
Environmental/occupational exposures (asbestos, silica, dust, pollution)
Alpha-1 antitrypsin deficiency (AATD) → suspect if <45yo or minimal smoking hx
Risk ↑ with: recurrent infections, asthma, HIV/TB, prematurity, FHx
what happens to the airways in COPD chronic inflammation → goblet cell hyperplasia (↑ mucus), ciliary dysfunction,
fibrosis → airflow obstruction
what happens to the alveoli protease-antiprotease imbalance, oxidative stress → alveolar wall destruction → air
trapping + hyperinflation
what happens to the Pulmonary vessels: chronic hypoxia → pulmonary HTN → cor pulmonale (right heart failure)
“You can have Chronic bronchitis and not have COPD, reduced FEV1/FVC ratio
which would be if the spirometry results did not show a
_________ BUT if you do have the _____, it becomes
COPD” - Mully
COPD Sx Triad: Dyspnea + chronic cough + sputum production
Other: wheeze, fatigue, chest tightness, morning symptoms, weight loss
(emphysema)
stuvia 2026-2027
, Clinical Medicine Exam II | Pulmonology | Complete Exam Prep | Practice Questions & Answers
COPD PE Hyperinflation → ↓ breath sounds, hyperresonant chest
Barrel chest (↑ AP diameter)
Accessory muscle use, prolonged expiration, pursed-lip breathing
Crackles at bases, wheezing
Cyanosis, possible clubbing, dependent edema, tripoding
COPD Labs PTFs/Spirometry = gold standard → FEV₁/FVC < 0.70 confirms dx
Test ALL COPD patients for AATD
Imaging: CXR → flat diaphragm, long narrow heart, bullae, tram track lines
GOLD number + letter classification → guides therapy
Group A meds key traits and goal Few symptoms + 0–1 exacerbations (no hospitalizations)
Start simple: bronchodilator PRN
Group B meds key traits and goal More symptoms (think daily dyspnea) but 0–1 exacerbations
Add maintenance bronchodilators
Group E meds key traits and goal ≥2 exacerbations or ≥1 hospitalization
Go big: dual or triple therapy
c Group A: Preferred LAMA + PRN SABA
LAMA : Tiotropium (Spiriva)
PRN SABA: Albuterol (ProAir)
→ Example combo: Spiriva daily + Albuterol as needed.
Group A: Alternative LABA + PRN SAMA-SABA or SABA
LABA: Salmeterol (Serevent)
SAMA: Ipratropium (Atrovent)
SABA: Albuterol (ProAir)
→ Example combo: Serevent daily + Combivent (Ipratropium/Albuterol) PRN.
stuvia 2026-2027
, Clinical Medicine Exam II | Pulmonology | Complete Exam Prep | Practice Questions & Answers
Õ Group B:
s
You’ve got symptoms every day → step up to two long-acting bronchodilators.
LAMA-LABA + PRN SABA
Example: Tiotropium + Olodaterol (Stiolto)
Rescue inhaler: Albuterol (ProAir)
→ Regimen: Stiolto daily + Albuterol PRN
á Group E: "Exacerbations = Escalate!"
r
This group gets frequent flare-ups or hospitalizations.
Start the same as Group B
→ Stiolto + ProAir
BUT if eosinophils ≥300 or hospitalized → Add ICS
(Triple therapy: ICS + LAMA + LABA)
Example: Fluticasone + Umeclidinium + Vilanterol (Trelegy Ellipta)
Rescue inhaler: Albuterol (ProAir)
NEVER use ______ in COPD (risk of pneumonia). ICS monotherapy
If frequent exacerbations: check eosinophil count → if ≥300 → add ICS.
SABA and SAMA should not be used together → overlap = more side effects.
LABA + LAMA is more effective than either alone for daily control.
Ð Rapid Recall Mnemonics for this SABA, SAMA, LABA,
LAMA craziness
“A = As needed” (simple bronchodilator)
“B = Both bronchodilators” (LAMA + LABA)
“E = Escalate” (Add ICS for eosinophils or exacerbations)
Acute COPD acute ↑ dyspnea, cough, sputum in <14 days
acute COPD causes viral (rhinovirus, flu, RSV), bacterial (H. flu, S. pneumo, M. catarrhalis), pollution,
CHF, PE, med non-adherence
stuvia 2026-2027
, Clinical Medicine Exam II | Pulmonology | Complete Exam Prep | Practice Questions & Answers
Hospital management of acute COPD confusion? ur going to ER babe = hypoxemia
O₂ to keep sats 88–92%
DuoNebs (albuterol/ipratropium)
IV steroids (methylpred 60–125mg)
Antibiotics:
No pseudomonas risk → Ceftriaxone, Levofloxacin
Pseudomonas risk → Pip-tazo, Cefepime
Outpt management of acute COPD SABA ± SAMA, continue long-acting inhalers
Prednisone 40mg x 5d
Abx if ≥2 of: ↑ dyspnea, ↑ sputum vol/viscosity, ↑ sputum purulence
Choices: Augmentin, Levofloxacin, Azithro
BODE index predicts 4-yr survival
Chronic Bronchitis (the “Blue Bloater”) Productive cough ≥3 months/year for ≥2 consecutive years.
A type of COPD characterized by airway disease (not alveoli like emphysema).
yoooo whats the chronic bronch patho Goblet cell hyperplasia → excessive mucus (“mucus plugger”)
Ciliary dysfunction → impaired clearance
Airway wall thickening + fibrosis → narrowed lumen
Chronic neutrophilic inflammation
Leads to: airflow obstruction, air trapping, hypoxemia, hypercapnia
End game: pulmonary HTN → cor pulmonale (right HF)
Chronic Bronchitis CM Chronic cough + sputum production (esp. morning)
Dyspnea (progressive)
“Blue bloater”:
Cyanosis (hypoxemia)
Edema (RHF/cor pulmonale)
Overweight body habitus
Chronic Bronchitis PE prolonged expiration, crackles, use of accessory muscles
Chronic Bronchitis Labs Spirometry: ↓ FEV₁, ↓ FEV₁/FVC <0.70, not fully reversible (but also class question
has 0.78 so who tf knows)
CXR: bronchial wall thickening, ↑ bronchovascular markings
ABG: chronic respiratory acidosis (↑ CO₂, ↓ O₂)
CBC: ↑ Hct (secondary polycythemia from
Chronic Bronchitis Tx æ Smoking cessation = most effective intervention
Vaccinations (influenza, pneumococcal, COVID)
Bronchodilators: SABA, LABA, SAMA, LAMA
ICS if frequent exacerbations/eosinophilia
Pulmonary rehab, exercise, nutrition
stuvia 2026-2027
Chronic Obstructive Pulmonary Disease (COPD) Heterogeneous lung condition with chronic respiratory symptoms (dyspnea,
cough, sputum, exacerbations) due to airway (bronchitis/bronchiolitis) + alveolar
(emphysema) damage → persistent, progressive airflow obstruction.
Chronic bronchitis = productive cough ≥3 mo for ≥2 yrs.
Emphysema = alveolar wall destruction, enlarged spaces, ↓ elastic recoil.
COPD Etiology & Risk Factors å Smoking = #1 cause (~85-90%)
Environmental/occupational exposures (asbestos, silica, dust, pollution)
Alpha-1 antitrypsin deficiency (AATD) → suspect if <45yo or minimal smoking hx
Risk ↑ with: recurrent infections, asthma, HIV/TB, prematurity, FHx
what happens to the airways in COPD chronic inflammation → goblet cell hyperplasia (↑ mucus), ciliary dysfunction,
fibrosis → airflow obstruction
what happens to the alveoli protease-antiprotease imbalance, oxidative stress → alveolar wall destruction → air
trapping + hyperinflation
what happens to the Pulmonary vessels: chronic hypoxia → pulmonary HTN → cor pulmonale (right heart failure)
“You can have Chronic bronchitis and not have COPD, reduced FEV1/FVC ratio
which would be if the spirometry results did not show a
_________ BUT if you do have the _____, it becomes
COPD” - Mully
COPD Sx Triad: Dyspnea + chronic cough + sputum production
Other: wheeze, fatigue, chest tightness, morning symptoms, weight loss
(emphysema)
stuvia 2026-2027
, Clinical Medicine Exam II | Pulmonology | Complete Exam Prep | Practice Questions & Answers
COPD PE Hyperinflation → ↓ breath sounds, hyperresonant chest
Barrel chest (↑ AP diameter)
Accessory muscle use, prolonged expiration, pursed-lip breathing
Crackles at bases, wheezing
Cyanosis, possible clubbing, dependent edema, tripoding
COPD Labs PTFs/Spirometry = gold standard → FEV₁/FVC < 0.70 confirms dx
Test ALL COPD patients for AATD
Imaging: CXR → flat diaphragm, long narrow heart, bullae, tram track lines
GOLD number + letter classification → guides therapy
Group A meds key traits and goal Few symptoms + 0–1 exacerbations (no hospitalizations)
Start simple: bronchodilator PRN
Group B meds key traits and goal More symptoms (think daily dyspnea) but 0–1 exacerbations
Add maintenance bronchodilators
Group E meds key traits and goal ≥2 exacerbations or ≥1 hospitalization
Go big: dual or triple therapy
c Group A: Preferred LAMA + PRN SABA
LAMA : Tiotropium (Spiriva)
PRN SABA: Albuterol (ProAir)
→ Example combo: Spiriva daily + Albuterol as needed.
Group A: Alternative LABA + PRN SAMA-SABA or SABA
LABA: Salmeterol (Serevent)
SAMA: Ipratropium (Atrovent)
SABA: Albuterol (ProAir)
→ Example combo: Serevent daily + Combivent (Ipratropium/Albuterol) PRN.
stuvia 2026-2027
, Clinical Medicine Exam II | Pulmonology | Complete Exam Prep | Practice Questions & Answers
Õ Group B:
s
You’ve got symptoms every day → step up to two long-acting bronchodilators.
LAMA-LABA + PRN SABA
Example: Tiotropium + Olodaterol (Stiolto)
Rescue inhaler: Albuterol (ProAir)
→ Regimen: Stiolto daily + Albuterol PRN
á Group E: "Exacerbations = Escalate!"
r
This group gets frequent flare-ups or hospitalizations.
Start the same as Group B
→ Stiolto + ProAir
BUT if eosinophils ≥300 or hospitalized → Add ICS
(Triple therapy: ICS + LAMA + LABA)
Example: Fluticasone + Umeclidinium + Vilanterol (Trelegy Ellipta)
Rescue inhaler: Albuterol (ProAir)
NEVER use ______ in COPD (risk of pneumonia). ICS monotherapy
If frequent exacerbations: check eosinophil count → if ≥300 → add ICS.
SABA and SAMA should not be used together → overlap = more side effects.
LABA + LAMA is more effective than either alone for daily control.
Ð Rapid Recall Mnemonics for this SABA, SAMA, LABA,
LAMA craziness
“A = As needed” (simple bronchodilator)
“B = Both bronchodilators” (LAMA + LABA)
“E = Escalate” (Add ICS for eosinophils or exacerbations)
Acute COPD acute ↑ dyspnea, cough, sputum in <14 days
acute COPD causes viral (rhinovirus, flu, RSV), bacterial (H. flu, S. pneumo, M. catarrhalis), pollution,
CHF, PE, med non-adherence
stuvia 2026-2027
, Clinical Medicine Exam II | Pulmonology | Complete Exam Prep | Practice Questions & Answers
Hospital management of acute COPD confusion? ur going to ER babe = hypoxemia
O₂ to keep sats 88–92%
DuoNebs (albuterol/ipratropium)
IV steroids (methylpred 60–125mg)
Antibiotics:
No pseudomonas risk → Ceftriaxone, Levofloxacin
Pseudomonas risk → Pip-tazo, Cefepime
Outpt management of acute COPD SABA ± SAMA, continue long-acting inhalers
Prednisone 40mg x 5d
Abx if ≥2 of: ↑ dyspnea, ↑ sputum vol/viscosity, ↑ sputum purulence
Choices: Augmentin, Levofloxacin, Azithro
BODE index predicts 4-yr survival
Chronic Bronchitis (the “Blue Bloater”) Productive cough ≥3 months/year for ≥2 consecutive years.
A type of COPD characterized by airway disease (not alveoli like emphysema).
yoooo whats the chronic bronch patho Goblet cell hyperplasia → excessive mucus (“mucus plugger”)
Ciliary dysfunction → impaired clearance
Airway wall thickening + fibrosis → narrowed lumen
Chronic neutrophilic inflammation
Leads to: airflow obstruction, air trapping, hypoxemia, hypercapnia
End game: pulmonary HTN → cor pulmonale (right HF)
Chronic Bronchitis CM Chronic cough + sputum production (esp. morning)
Dyspnea (progressive)
“Blue bloater”:
Cyanosis (hypoxemia)
Edema (RHF/cor pulmonale)
Overweight body habitus
Chronic Bronchitis PE prolonged expiration, crackles, use of accessory muscles
Chronic Bronchitis Labs Spirometry: ↓ FEV₁, ↓ FEV₁/FVC <0.70, not fully reversible (but also class question
has 0.78 so who tf knows)
CXR: bronchial wall thickening, ↑ bronchovascular markings
ABG: chronic respiratory acidosis (↑ CO₂, ↓ O₂)
CBC: ↑ Hct (secondary polycythemia from
Chronic Bronchitis Tx æ Smoking cessation = most effective intervention
Vaccinations (influenza, pneumococcal, COVID)
Bronchodilators: SABA, LABA, SAMA, LAMA
ICS if frequent exacerbations/eosinophilia
Pulmonary rehab, exercise, nutrition
stuvia 2026-2027
