Patient will present as → a 22-year-old female presents with intermittent wheezing and dyspnea triggered by exercise and cold air, occurring about twice monthly. She denies nighttime symptoms or prior exacerbations. Physical exam and spirometry are normal; bronchodilator testing confirms reversible obstruction. She is diagnosed with asthma (GINA Step 1) and started on as-needed low-dose ICS–formoterol. She receives education on trigger avoidance and inhaler technique and is given an asthma action plan. Follow-up is planned in 6–8 weeks.
You are called to see a 10 y/o with a cough and difficulty breathing
Patient
Gender: Male
Age: 10 years
Weight: 50.7 lb/23 kg
Vitals
Temperature: 98.7 F/37.1 C
Blood Pressure: 117/74
Heart Rate: 114
Respiratory Rate: 40
Pulse Oximetry: 94% RA
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Asthma is a chronic, reversible inflammatory airway disease characterized by episodic bronchoconstriction, airway hyperresponsiveness, and mucus production
Common triggers include allergens, exercise, cold air, respiratory infections, and irritants like smoke or pollution
Presents with episodic wheezing, cough (especially at night), chest tightness, and dyspnea
Physical exam may show prolonged expiration, wheezing, and accessory muscle use during exacerbations
Diagnosis and Monitoring
Monitor with peak flow
PFTs: Greater than 12% increase in FEV1 after bronchodilator therapy
FEV1 to FVC ratio <80% (reflects obstruction due to inflammation)
In asthma, since there is an obstruction (inflammation), you will have a decreased FEV1 and, therefore, a reduced FEV1 to FVC ratio
In a patient with asthma, a chest X-ray may show hyperinflation (a flattened diaphragm and increased lung volume), peribronchial thickening, or atelectasis due to mucus plugging during an exacerbation.
Treatment Guidelines
Previously, asthma was labeled 'mild intermittent' or 'severe persistent,' but GINA now recommends a treatment-based approach (Step 1–5) based on both symptom control and exacerbation risk.
Track 1: The preferred treatment option is an as-needed combination of low-dose ICS-formoterol
Track 2: An alternative option that uses SABA as the reliever, along with a separate preventer inhaler. This track may be used if ICS-formoterol is not available or if patients have no risk factors for exacerbations
Table 1: GINA Track 1
Preferred initial treatment for most patients
Suitable for patients who respond well to ICS and have a low risk of side effects
Table 2: GINA Track 2
Alternative for patients concerned about ICS side effects, or if ICS + LABA isn't preferred
Can also be used for quick relief of symptoms, streamlining treatment
Acute Treatment
Oxygen, nebulized SABA, ipratropium bromide, and oral corticosteroids
GINA treatment steps — adults and adolescents (12 years and older)
Track 1 (preferred) — ICS-formoterol is the reliever at every step
Steps 1–2: as-needed low-dose ICS-formoterol only (e.g., budesonide-formoterol 160/4.5 mcg, 1 inhalation as needed) — no daily inhaler needed
Step 3: low-dose ICS-formoterol maintenance and reliever therapy (MART) — 1 inhalation twice daily plus 1 inhalation as needed
Step 4: medium-dose MART — 2 inhalations twice daily plus 1 inhalation as needed (maximum 12 inhalations/day)
Step 5: add a long-acting muscarinic antagonist (LAMA, e.g., tiotropium), check the asthma phenotype, and refer for biologic therapy (anti-IgE, anti-IL-5/5R, anti-IL-4R, anti-TSLP)
Track 2 (alternative) — SABA is the reliever
Step 1: take low-dose ICS whenever the SABA is used
Step 2: daily low-dose ICS + as-needed SABA
Step 3: daily low-dose ICS-LABA + as-needed SABA
Step 4: daily medium- or high-dose ICS-LABA + as-needed SABA
Step 5: add a LAMA and refer for biologic therapy
SABA-only treatment is no longer recommended at any step — it raises the risk of severe exacerbations and asthma death
Step up when asthma is uncontrolled (after checking inhaler technique and adherence); step down after about 3 months of good control
Making Sense of Forced Vital Capacity
Forced expiratory volume (FEV) measures how much air a person can exhale during a forced breath. The amount of air exhaled may be measured during the first (FEV1), second (FEV2), and/or third seconds (FEV3) of the forced breath. Forced vital capacity (FVC) is the total amount of air exhaled during the FEV test
You would expect the amount of air exhaled during the first second to be the greatest amount. In asthma, since there is an obstruction (inflammation), you will have a decreased FEV1 and, therefore, a reduced FEV1 to FVC ratio.
Chronic obstructive pulmonary disease
Chronic Obstructive Pulmonary Disease (COPD) is a progressive, irreversible airway disease characterized by airflow limitation due to chronic bronchitis, emphysema, or both
Chronic bronchitis is defined by clinical features (chronic cough) vs. emphysema, which is characterized by structural changes (enlarged air spaces secondary to alveolar destruction)
A type of COPD marked by a chronic, mucus-producing cough lasting at least 3 months per year for 2 or more years, not due to another apparent cause.
A form of COPD characterized by enlargement of air spaces and destruction of alveolar septae, often resulting in a barrel-chested appearance.
Chronic cough: Persistent cough for 3+ months/year for 2 years
Sputum production: Lots of mucus, often daily
Smokers: Mostly caused by smoking
"Blue Bloaters": Cyanosis (blue) and edema (bloating) from low oxygen
Stocky build: Often stocky, not always overweight
Pneumonia: Frequent lung infections
↓ FEV1/FVC (<0.7): Obstructive pattern on spirometry
Bronchial markings: Thickened airway walls on imaging
↑ Hemoglobin/Hematocrit: Higher due to low oxygen
Crackles and wheezes: Lung sounds from mucus and narrowing
Minimal cough/sputum, lots of shortness of breath: Less mucus, more lung damage
"Pink Puffers": Pink skin, heavy breathing: Hyperventilation keeps oxygen up
Smokers: Mostly caused by smoking: Smoking destroys alveoli
Thin and underweight: Breathing burns calories
Loss of lung markings on imaging: Fewer vessels from alveolar loss
Hyperinflation and flattened diaphragm: Trapped air expands lungs
Barrel chest: Chest widens from air trapping
Small, thin-looking heart on X-ray: Lungs compress heart
↓ FEV1/FVC (<0.7): Airways collapse
Bullae in lung tissue: Air pockets from damage
Quiet breath sounds and long exhales: Less tissue, slow airflow
Faint heart sounds: Lungs muffle heart
Chronic hyperventilation, usually no CO2 buildup: Fast breathing clears CO2
Normal HCT and Hb (unless end-stage with low oxygen): Oxygen stays normal
Picmonic
Obstructive lung disease
Obstructive lung disease is characterized by airway obstruction and associated with inflammation of the airways. Air trapping as a result of airway obstruction causes an increase in the residual volume of the lungs, which means the volume of air left in the lungs after fully exhaling is increased. Forced vital capacity, the volume of air that can be forcibly blown out after one full inspiration, is decreased. FEV1, the forced expiratory volume in 1 second or the volume of air that can be forcibly blown out in 1 second, is also decreased. More importantly, the ratio of FEV1/FVC is decreased because even though FVC is decreased, the FEV1 decreases even greater resulting in an overall decrease in the FEV1/FVC ratio. This can be clearly distinguished from restrictive lung disease which has a ratio greater than 80%. Common obstructive lung diseases include chronic bronchitis, emphysema, asthma, and bronchiectasis.
Patient will present as → a 56-year-old female with shortness of breath and a productive cough that has occurred over the past two years for at least three months each year. She is a heavy smoker. Physical exam reveals a respiratory rate of 32, slightly labored breathing, and a temperature of 98.9°F. Her SpO2 is 90% while receiving oxygen via nasal cannula at 2 LPM.
Chronic bronchitis is defined as a chronic cough that is productive of phlegm occurring on most days for 3 months of the year for two or more consecutive years without an otherwise defined acute cause
Chronic Bronchitis = Blue Bloaters (2º to chronic hypoxia)
Common in smokers (80% of COPD patients)
Frequent cough and expectoration are typical (compared to emphysema)
Stocky, overweight
Increased HCT and Hb due to chronic hypoxemia
"The common organisms causing pneumonia in patients with COPD are Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Patients who smoke are often colonized with Haemophilus influenzae."
DX:
Board bottom line: spirometry makes the diagnosis — a post-bronchodilator FEV1/FVC <0.70 — and GOLD 1–4 grades how severe.
Diagnosis (spirometry):post-bronchodilator FEV1/FVC <0.70 = persistent airflow limitation that is not fully reversible (the key contrast with asthma)
Severity — GOLD 1–4 by FEV1 % predicted (the “80–50–30” cutoffs): 1 mild ≥80 · 2 moderate 50–79 · 3 severe 30–49 · 4 very severe <30
↓ DLCO in emphysema (normal in chronic bronchitis); exam: prolonged expiration, wheezes/crackles, hyperresonant percussion in emphysema
TX:
Board pearl: only smoking cessation and long-term oxygen reduce mortality — everything else treats symptoms and exacerbations.
Smoking cessation = the single most important step (slows lung-function decline; lowers mortality)
Bronchodilators = backbone: short-acting albuterol (SABA) / ipratropium (SAMA) = rescue; long-acting LAMA (tiotropium) ± LABA = maintenance (ipratropium is short-acting, not a maintenance inhaler)
Step up by GOLD group (A / B / E): A → one long-acting bronchodilator; B & E → LABA + LAMA; add ICS only if eosinophils ≥300 (avoid <100 — pneumonia risk)
GOLD A / B / E groups — initial maintenance therapy
Group
Past-year exacerbations + symptoms
Initial therapy
A
0–1 moderate (no hospitalization) + few symptoms (mMRC 0–1, CAT <10)
A single long-acting bronchodilator (LAMA or LABA)
B
0–1 moderate (no hospitalization) + more symptoms (mMRC ≥2, CAT ≥10)
LABA + LAMA
E
≥2 moderate OR ≥1 needing hospitalization (any symptom level)
LABA + LAMA; add ICS (triple) if blood eosinophils ≥300
Long-term oxygen if resting SpO2 ≤88% → improves survival
Patient with emphysema will present as → a 65-year-old male complaining of fatigue and shortness of breath with exertion. The patient reports minimal cough. On physical exam, you note a thin, barrel-chested man with decreased heart and breath sounds, pursed-lip breathing, end-expiratory wheezing, and scattered rhonchi. Chest X-ray reveals a flattened diaphragm, hyperinflation, and a small, thin-appearing heart. PFTs show a decreased FEV1/FVC ratio.
Emphysema is a condition in which air spaces are enlarged due to destruction of the alveolar septa
The body's natural response to ↓ lung function is chronic hyperventilation, also known as Pink Puffers. Usually NOT CO2 retainers — the body increases ventilation to blow off CO2 (CO2 retention appears only in end-stage disease)
Minimal cough (compared to chronic bronchitis), quiet lungs
Minimal sputum(compared to chronic bronchitis)
Thin, underweight, and barrel-chested
Normal HCT and Hb in most cases, unless end-stage disease leads to severe hypoxemia
DX:
PFTs: FEV1/FVC ratio of less than 0.7
Destruction of alveoli (air sacs) reduces lung elasticity. Without elastic recoil, airways collapse during exhalation, trapping air and blocking outflow. FEV1 decreases due to poor airflow, while FVC can be near normal or slightly reduced, yielding a ratio <0.7
Chest X-ray shows hyperinflation, flattened diaphragm, reduced lung markings, bullae, and a small, thin-appearing heart
Parenchymal bullae and subpleural blebs are pathognomonic:
Bullae are larger air spaces (>1 cm) in the lung parenchyma, common in emphysema from merged, broken alveoli
Subpleural blebs are smaller air pockets (<1 cm) under the pleura, also from alveolar damage, but more superficial
Chest X-ray of bullous emphysema showing large bullae (air pockets from alveolar destruction) (arrow), hyperinflation, reduced lung markings, a small, thin appearing heart, and a flattened diaphragm.
Patient will present as → a 7-year-old boy brought by his parents due to a persistent cough, wheezing, and recurrent lung infections since infancy. The parents also report the child having bulky, foul-smelling stools and difficulty gaining weight despite a good appetite. On exam, he appears underweight with digital clubbing. Sweat chloride test shows 88 mmol/L. The stool elastase test is low. Genetic testing confirms CFTR mutations. Management includes airway clearance, enzyme replacement, a high-calorie diet, and referral to a CF center.
Cystic fibrosis (CF) affects secretions — they become thick and sticky → block airways and ducts
CFTR modulators: elexacaftor/tezacaftor/ivacaftor (Trikafta) for eligible CFTR variants, including at least one F508del; ivacaftor alone for gating mutations
Acute exacerbations: oral or IV antibiotics for Pseudomonas & Staph
Chronic suppression: inhaled tobramycin or aztreonam
Lung transplant for advanced disease
Complications include respiratory failure, diabetes, cirrhosis, and pneumothorax
Meconium ileus in preterm twins revealing a novel cystic fibrosis mutation. Image by Department of Pediatrics, Albert-Ludwigs-University of Freiburg, Mathildenstrasse 1, D 79106 Freiburg, Germany. [email protected]. License: CC BY 2.0
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