Medicine — Respiratory Medicine, NMC MBBS licence examination syllabus (Nepal Medical Council).
Asthma and COPD: the same complaint, two different diseases
One airway closes and opens again. The other closes and stays shut.
A breathless, wheezing patient could have either. The symptoms overlap, the examination overlaps, and both respond at least partly to a bronchodilator — so the distinction cannot be made from the bedside alone with any confidence.
It rests on one property: reversibility. Asthma is variable, inflammatory airway narrowing that opens up again — between attacks the patient can be entirely well. COPD is largely fixed obstruction from destroyed lung, and no drug restores what has been destroyed. Every difference in treatment, prognosis and emergency management follows from that single distinction.
🩺 Where this lives: In Nepal and much of South Asia, a substantial share of COPD occurs in people who have never smoked a cigarette — the exposure is biomass smoke from cooking on open fires in poorly ventilated indoor spaces, and it falls disproportionately on women. A history that stops at "non-smoker" and rules out COPD is taking the wrong history. Ask what they cook on, and for how many years.
The distinction that decides everything
The reason the label matters is not classification for its own sake — it is that inhaled corticosteroids transform asthma and do far less in COPD. Asthma is driven by airway inflammation that steroids suppress; COPD is driven by structural destruction that they cannot reverse. Mislabel a patient and you either withhold the drug that would control them, or expose them to one that mostly brings side effects.
SPIROMETRY — the numbers to know
OBSTRUCTION FEV₁/FVC ratio < 0.70
FEV₁ falls more than FVC, because the problem is
getting air OUT.
RESTRICTION ratio PRESERVED or high, both volumes low
A different problem entirely — fibrosis, chest wall,
neuromuscular disease.
REVERSIBILITY TESTING
Repeat spirometry after a bronchodilator.
Substantial improvement in FEV₁ → asthma.
Obstruction persisting → COPD.
PEAK FLOW
Cheap, repeatable, and it captures asthma's VARIABILITY
— diurnal variation and the response to treatment —
which a single spirometry snapshot misses.
Asthma: mechanism and presentation
🔍 What is happening in the airway
InflammationChronic eosinophilic inflammation of the airway wall, often with an atopic background — eczema, allergic rhinitis, family history.
HyperresponsivenessThe airway overreacts to stimuli that would not trouble a normal lung: cold air, exercise, allergens, smoke, infection.
ObstructionSmooth muscle contraction, mucosal oedema and mucus plugging — all three narrow the lumen, and all three are potentially reversible.
Clinical patternEpisodic wheeze, cough and chest tightness, characteristically worse at night and in the early morning, with identifiable triggers and symptom-free intervals. That variability is the diagnosis.
💡 Exam angle: aspirin and NSAIDs can precipitate severe bronchospasm in a subset of asthmatics, classically with nasal polyps and chronic rhinosinusitis. The mechanism is inhibition of cyclo-oxygenase shunting arachidonic acid down the leukotriene pathway. Beta-blockers are the other classic precipitant — connecting directly to the beta-blockers chapter, where blocking bronchial beta-2 receptors permits bronchoconstriction.
Acute asthma: assessing severity
💡 Exam angle: the two findings that sound reassuring and are not. A silent chest means too little air is moving to generate a wheeze — the patient has deteriorated, not improved. And a normal or rising pCO₂ in an acutely distressed asthmatic means they can no longer sustain the hyperventilation that should be blowing it off. Both indicate exhaustion and demand escalation. This is the same trap the acid–base chapter sets from the other direction.
Treating the acute attack
Note that steroids do not act quickly — they take hours. That is precisely why they are given early: a steroid given late in an attack contributes little to the attack you are currently treating.
Long-term asthma control
THE PRINCIPLE — treat the INFLAMMATION, not just the wheeze
A patient using a reliever inhaler frequently is a patient
whose underlying inflammation is NOT controlled. Rising
reliever use is a warning sign, not a solution.
STEPWISE APPROACH
Inhaled corticosteroid is the foundation of control.
Add a long-acting bronchodilator if control is
inadequate — and always in combination with a steroid,
never as a lone long-acting reliever.
Further add-on therapy and specialist referral for
difficult asthma.
AT EVERY STEP, CHECK THESE BEFORE ESCALATING
Inhaler TECHNIQUE — frequently poor, and it makes an
effective drug useless
ADHERENCE
Ongoing TRIGGER exposure, including smoking
The diagnosis itself
Step DOWN when control has been sustained. Treatment
should follow the disease in both directions.
COPD: mechanism and presentation
🔍 Two overlapping processes
Chronic bronchitisDefined clinically: productive cough on most days for three months in two consecutive years. Mucus gland hypertrophy and small airway inflammation.
EmphysemaDefined structurally: destruction of alveolar walls, so gas-exchange surface is lost and the airways lose the tethering that holds them open. This is why they collapse on expiration and air becomes trapped.
PresentationProgressive exertional breathlessness, chronic cough with sputum, recurrent chest infections. Unlike asthma, symptoms are persistent rather than episodic, and there is no genuinely well interval.
Alpha-1 antitrypsin deficiencyConsider it in emphysema that is early-onset, in a non-smoker, or predominantly basal — it is the inherited cause, and it may come with liver disease.
MANAGING STABLE COPD — what changes outcome
STOP SMOKING the ONLY intervention that alters
the rate of decline in lung function
VACCINATION influenza and pneumococcal
PULMONARY REHABILITATION large, evidence-based benefit on
symptoms and exercise capacity;
consistently under-prescribed
INHALED BRONCHODILATORS long-acting; inhaled steroids for
selected patients, particularly
those with frequent exacerbations
LONG-TERM OXYGEN THERAPY improves survival in chronic
hypoxaemia — but only if used for
enough hours per day, and not for
breathlessness alone
Note what is FIRST on that list. Smoking cessation and
rehabilitation outperform every inhaler in this disease.
Oxygen in COPD
💡 Exam angle: this is asked often and answered badly in both directions. Uncontrolled high-flow oxygen in a patient at risk of retention can cause rising CO₂, acidosis and drowsiness — but the opposite error, withholding oxygen from a hypoxic patient for fear of CO₂, kills faster. The correct answer is neither: give controlled oxygen targeting 88–92%, and check a blood gas to guide you. Note also that the mechanism is not purely "loss of hypoxic drive" — ventilation–perfusion mismatching and the Haldane effect contribute substantially.
Clinical reasoning: four presentations
🔍 Case 1 — the reassuring emergency
PresentationA 24-year-old with acute asthma. On arrival she was wheezing loudly; forty minutes later the chest is quiet and she is drowsy. SpO₂ 89%. A gas shows pCO₂ 5.6 kPa, having been 3.2.
TrapLess wheeze plus a "normal" CO₂ reads as improvement.
ReasoningA silent chest means insufficient airflow to generate a wheeze. A pCO₂ that has climbed into the normal range means she can no longer sustain hyperventilation. Both are exhaustion.
AnswerLife-threatening, indeed near-fatal, asthma. Maximal therapy, immediate senior and critical care involvement, and prepare for ventilatory support. Observing her would be a fatal error.
🔍 Case 2 — the wrong history
PresentationA 58-year-old woman from a rural village with four years of progressive breathlessness and daily productive cough. She has never smoked. Spirometry shows FEV₁/FVC 0.58 with minimal bronchodilator response.
The distractor"Never smoked" is taken to exclude COPD.
ReasoningFixed obstruction with poor reversibility is COPD physiologically, whatever the exposure. Decades of cooking over biomass indoors is a well-recognised cause, and it predominantly affects women.
AnswerCOPD from biomass smoke exposure. Manage as COPD, and address the exposure — improved ventilation or a cleaner stove is a therapeutic intervention here, not lifestyle advice.
🔍 Case 3 — the escalation question
PresentationA 19-year-old with asthma uses her salbutamol inhaler most days and wakes twice a week coughing. She takes a preventer inhaler "when the chest feels tight". She asks for a stronger reliever.
Key clueThe preventer is being used as though it were a reliever — that is, not being used at all.
ReasoningFrequent reliever use and night waking indicate uncontrolled inflammation. Escalating the reliever treats the symptom and leaves the disease untouched.
AnswerBefore adding any drug: check inhaler technique, explain that the preventer is taken daily regardless of symptoms, confirm adherence and review triggers. Most "uncontrolled asthma" is untaken or badly taken medication.
🔍 Case 4 — the oxygen decision
PresentationA 70-year-old with known COPD arrives with an infective exacerbation. SpO₂ 79% on air. A colleague hesitates to give oxygen for fear of CO₂ retention.
TrapFear of hypercapnia leading to withheld oxygen.
ReasoningSevere hypoxia causes organ injury and death within minutes; CO₂ retention develops more slowly and is manageable. The answer is controlled oxygen, not absent oxygen.
AnswerGive oxygen targeting 88–92%, take an arterial gas, and adjust from it. Treat the exacerbation with bronchodilators, steroids and antibiotics if infection is suggested. If the gas shows respiratory acidosis despite treatment, non-invasive ventilation is the next step.
Commonly confused
Confusion
The distinction
Why it matters
Asthma vs COPD
Reversibility on spirometry after a bronchodilator
Inhaled steroids transform asthma and do much less in COPD.
Obstructive vs restrictive
Obstruction lowers the FEV₁/FVC ratio; restriction preserves it
Entirely different differential diagnoses.
Silent chest vs improvement
No wheeze because no air is moving
It is a life-threatening sign, not a good one.
Normal pCO₂ vs stability
An acute asthmatic should be hypocapnic
A normalising pCO₂ signals exhaustion.
Reliever vs preventer
The preventer is taken daily regardless of symptoms
Misuse is the commonest cause of "uncontrolled" asthma.
Never smoked vs no COPD
Biomass smoke is a major cause in South Asia
A smoking-only history misses these patients entirely.
Controlled oxygen vs no oxygen
Target 88–92% in retention risk — but never withhold it
Hypoxia kills faster than hypercapnia.
Rapid revision
MUST-KNOW FACTS
1. Asthma is REVERSIBLE, variable airway inflammation; COPD is largely FIXED.
2. Obstruction = FEV₁/FVC < 0.70.
3. Restriction preserves the ratio with reduced volumes.
4. Reversibility testing after a bronchodilator separates the two.
5. Peak flow captures asthma's variability; spirometry is a snapshot.
6. Asthma: episodic, nocturnal, trigger-related, symptom-free intervals.
7. Asthma triggers include NSAIDs, beta-blockers, cold air, exercise, infection.
8. Beta-blockers cause bronchospasm through beta-2 blockade.
9. Acute severe asthma: PEF 33–50%, RR ≥ 25, HR ≥ 110, cannot complete sentences.
10. Life-threatening: PEF < 33%, SpO₂ < 92%, SILENT CHEST, cyanosis, exhaustion.
11. A silent chest means no air movement — escalate.
12. A normal or rising pCO₂ in acute asthma is NEAR-FATAL, not reassuring.
13. Acute treatment: oxygen, salbutamol, steroids early, ipratropium, magnesium.
14. Steroids take hours — which is exactly why they are given early.
15. Long-term asthma: treat the inflammation; ICS is the foundation.
16. Never a long-acting bronchodilator without an inhaled steroid.
17. Check technique, adherence and triggers BEFORE escalating treatment.
18. COPD = chronic bronchitis (clinical) plus emphysema (structural).
19. Biomass smoke is a major COPD cause in South Asia, especially in women.
20. Consider alpha-1 antitrypsin deficiency in young or non-smoking emphysema.
21. Smoking cessation is the only intervention that alters decline in lung function.
22. Pulmonary rehabilitation has large benefit and is under-used.
23. COPD oxygen target 88–92% if at risk of retention; otherwise 94–98%.
24. NEVER withhold oxygen from a hypoxic patient — hypoxia kills faster.
25. Persisting respiratory acidosis in an exacerbation → non-invasive ventilation.
💡 Exam angle: the reliable threads are (a) reversibility separating the two diseases, (b) the silent chest and the normalising pCO₂ as deterioration, (c) checking inhaler technique before escalating, (d) biomass exposure causing COPD in non-smokers, and (e) controlled rather than withheld oxygen. Three of those five are situations where an apparently improving or normal finding is the emergency — the same pattern running through the acid–base and shock chapters.
Syllabus points
Reversibility: the distinction that decides treatment
Spirometry, obstruction versus restriction, and peak flow
Asthma: inflammation, hyperresponsiveness and triggers
Drugs that precipitate asthma: NSAIDs and beta-blockers
Acute asthma severity assessment
The silent chest and the normalising pCO₂
Treating the acute attack
Stepwise long-term asthma control
COPD: chronic bronchitis and emphysema
Biomass smoke and non-smoking COPD
Managing stable COPD
Controlled oxygen therapy and its rationale
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