Asthma vs COPD

The reversible one vs the one that gave up trying

A 55-year-old with 30 pack-years presents with chronic dyspnea and wheezing. PFTs show FEV1/FVC < 0.7. After albuterol, FEV1 improves by 8%.

Asthma or COPD?

The Core Split

These two diseases both cause airflow obstruction and wheezing. That's where the similarity ends. Flip between tabs — notice how different the stories are.

⚑ ASTHMA
🫁 COPD

Who Gets It

Young. Often childhood onset. Atopic history — eczema, allergic rhinitis, food allergies. Family history of asthma. The kid who couldn't run the mile in gym class.

What's Happening

Eosinophilic inflammation → bronchial hyperreactivity → airway smooth muscle spasm → reversible obstruction. The airways are twitchy, not destroyed.

The Key Feature

REVERSIBLE. Give albuterol → FEV1 jumps β‰₯12% AND β‰₯200mL. The airways open back up because the walls are still intact. They're just spasming.

Triggers

Treatment Backbone

Inhaled corticosteroids (ICS) are the controller. SABA for rescue. Step up with LABA + ICS combo. The goal is no symptoms — and that's actually achievable.

Who Gets It

Older smoker. Usually 40+ with significant smoking history. The guy who smoked a pack a day for 30 years and now can't climb stairs.

What's Happening

Neutrophilic inflammation → protease-antiprotease imbalance → alveolar wall destruction (emphysema) + mucus gland hypertrophy (chronic bronchitis). The architecture is permanently damaged.

The Key Feature

IRREVERSIBLE. Give albuterol → FEV1 improves <12% or <200mL. The obstruction is structural. You can't relax a wall that's been demolished.

Subtypes

Treatment Backbone

LAMA (tiotropium) is the first-line controller. Add LABA. ICS only added for frequent exacerbations (β‰₯2/year). Smoking cessation is the ONLY thing proven to slow decline. O2 if PaO2 ≀55.

Feature-by-Feature

One screen. All the differences. Lead with what's DIFFERENT, not what's shared.

⚑ Asthma
🫁 COPD
Age
Young (childhood–20s)
>40, smoker
Reversibility
Yes (β‰₯12% + 200mL)
No (<12%)
Inflammation
Eosinophils
Neutrophils
FEV1/FVC
Normal between attacks
<0.7 always
Symptoms
Episodic, triggered
Persistent, progressive
CXR
Usually normal
Hyperinflation, flat diaphragms
1st-line controller
ICS
LAMA
Prognosis
Can achieve full control
Progressive decline
Key history
Atopy, allergies, eczema
Pack-years, occupational exposure
DLCO
Normal
↓↓ (destroyed alveoli)

Memory Hooks

πŸ”‘
Reversibility is the whole game. Tap for the hook →
Asthma is a rubber band — stretches and snaps back. COPD is a broken rubber band — once it snaps, you can't unsnap it. Albuterol tests which one you're holding.
πŸ”‘
First-line controllers are backwards. Tap →
Asthma = ICS (the Inflammation is the problem — calm it down). COPD = LAMA (the Lungs are structurally locked — force them open). ICS doesn't fix broken walls. LAMA doesn't fix twitchy muscles. Match the drug to the damage.
πŸ”‘
The cell tells you the disease. Tap →
Eosinophils = Early onset, Episodic → Asthma. Neutrophils = Never going back, Nicotine damage → COPD. The inflammatory cell IS the diagnosis.
πŸ”‘
Pink puffer vs blue bloater. Tap →
Pink puffer (emphysema): hyperventilates to compensate → stays pink but exhausted. Thin because all that breathing burns calories. Blue bloater (chronic bronchitis): stops trying to compensate → CO2 retention → cyanosis. Overweight because NOT burning extra calories breathing. The body's coping strategy determines the phenotype.

The Algorithm

Board vignette drops. Patient is wheezing. Walk through it.

Step 1: How old is the patient?
Child / young adult (<40)
Older adult (>40)

Elimination Rounds

Five patients walk in wheezing. Don't give them the wrong inhaler.

Board Questions

Random selection from the pool. Reload for different questions.