← Master Index· Section 15 · Respiratory Disorders · Chapter 79

Asthma

AsthmaGINA 2025AIR/MARTStep therapy

30-Second Snapshot

What it is:A heterogeneous, chronic inflammatory airway disease. Symptoms (wheeze, shortness of breath, chest tightness, cough) and expiratory airflow limitation vary over time and intensity, and both can basically disappear between attacks. That's why a normal exam or normal spirometry on a good day never rules asthma out.

The core problem:Chronic airway inflammation makes the airway twitchy (bronchial hyperresponsiveness) and structurally narrowed (remodeling, mucus plugging). Every trigger, allergen, exercise, cold air, viral infection, sits on top of that inflamed foundation and can tip it into bronchospasm or a full exacerbation.

What you do about it:Treat the inflammation, not just the bronchospasm. Every persistent asthma patient gets an inhaled corticosteroid. The reliever question (SABA alone vs a rapid-onset ICS-containing reliever) is now the single biggest paradigm shift in the field, and it's the thing most likely to be tested and most likely to be wrong in an old textbook.

Worth knowing

GINA's organizing idea for 2025 is simple: stop treating asthma with a bronchodilator-only rescue.SABA-alone treats the symptom (bronchospasm) and ignores the disease (inflammation). Every current GINA track now pairs the reliever with an anti-inflammatory, either by using ICS-formoterol as the reliever itself(Track 1, preferred) or by taking a dose of ICS alongside SABA every time it's used (Track 2). If you remember nothing else, remember that SABA monotherapy is no longer how GINA wants you to treat any step of persistent asthma.

Control & Severity - Two Different Questions

Students mix these up constantly. Controlasks "how is the patient doing right now, on their current regimen?" Severityasks "how much treatment does it take to keep them there?" You can only answer severity retrospectively, after months of optimized therapy.

GINA symptom control (last 4 weeks)

Ask about the last 4 weeksCounts as 1 point if yes
Daytime symptomsMore than twice a week
Night waking due to asthmaAny
Reliever needed for symptomsMore than twice a week (not counting pre-exercise dosing)
Any activity limitation due to asthmaAny
Scoring

0 = well controlled. 1–2 = partly controlled. 3–4 = uncontrolled.This is the tool you actually use at every visit, not a severity label. A patient using their reliever most days of the week with activity limitation, even with no nighttime symptoms, is uncontrolled (score 3) and needs a change in therapy, full stop.

Severity, defined the modern way

GINA deliberately moved away from grading severity by symptom frequency at diagnosis, because patients with "mild" symptoms can still have fatal attacks. Severity is now assessed afterthe patient has been on optimized treatment for a few months, based on the step of therapy required to achieve control.

SeverityDefined as
MildWell controlled with Step 1–2 treatment (PRN ICS-formoterol, or low-dose ICS + PRN SABA)
ModerateWell controlled with Step 3–4 treatment (low-to-medium dose ICS-LABA)
SevereRemains uncontrolled despite optimized Step 4–5 treatment, or requires high-dose ICS-LABA just to stay controlled
The trap

Uncontrolled asthma is not the same thing as severe asthma.Before you label someone severe, rule out the boring stuff first: poor inhaler technique, poor adherence, wrong diagnosis, ongoing allergen or smoke exposure, and comorbidities like GERD, obstructive sleep apnea, or rhinosinusitis. Most "severe asthma" is actually one of those.

Risk factors worth screening for at every visit

Pathophysiology - Why Each Drug Class Exists

The airway smooth muscle narrows through three mechanisms working together: smooth muscle contraction(the fast, reversible part), remodeling(structural, slow, less reversible), and mucus pluggingfrom goblet cell hypersecretion. Map the inflammatory cascade to the drug list and the whole chapter stops being memorization.

The allergic cascade

In allergic asthma, inhaled allergen binds IgE sitting on mast cells and macrophages. Within minutes (the early-phase reaction), those cells degranulate and dump histamine, leukotrienes C4/D4/E4, prostaglandins, and platelet-activating factor. The result is smooth muscle contraction, mucus secretion, and vascular leakage that thickens and narrows the airway wall.

Six to nine hours later, a late-phase reactionrecruits eosinophils, T lymphocytes, basophils, neutrophils, and more macrophages. TH2 lymphocytes release IL-4, IL-5, and IL-13, the cytokines that drive allergic inflammation and that most of the newer biologics are named after. Eosinophils then release granule proteins and leukotrienes that injure the airway epithelium directly, which is what heightens hyperresponsiveness further.

Map the pathway to the pharmacy

PathwayMediatorDrug class it explains
Airway smooth muscle β2 receptorsEndogenous catecholaminesSABA / LABA - direct bronchodilation
Vagal / parasympathetic toneAcetylcholineAnticholinergics (ipratropium, tiotropium)
IgE-mediated mast cell activationIgEOmalizumab (anti-IgE)
TH2 cytokine signalingIL-4, IL-13Dupilumab (blocks IL-4Rα, the shared receptor)
Eosinophilic inflammationIL-5Mepolizumab, reslizumab (anti-IL-5), benralizumab (anti-IL-5 receptor)
Leukotriene-driven bronchoconstriction and edemaLTC4/D4/E4Montelukast, zafirlukast (receptor blockers), zileuton (synthesis blocker)
Broad multi-cell inflammationEverything above at onceICS - the only reliably disease-modifying option for most patients
The unlock

Nothing on the asthma drug list makes the airway smooth muscle contract harder or "strengthens" anything. Bronchodilators relax existing constriction (fast, symptomatic), and ICS/biologics/LTRAs interrupt the inflammatory cells that caused the constriction in the first place (slower, disease-modifying). That's why SABA alone never controls asthma. It never touches the actual disease.

Clinical Presentation

Chronic asthma

Episodic shortness of breath, chest tightness, cough (often worse at night or early morning), and wheeze, frequently triggered by exercise, cold air, allergens, or infection. On exam you may hear expiratory wheeze and a dry cough, but physical exam findings are frequently completely normal between attacks, this is one of the most tested facts in the chapter. Don't let a normal lung exam talk you out of the diagnosis.

Acute severe asthma

Uncontrolled inflammation, mucus, and bronchospasm progress to airway narrowing that stops responding well to bronchodilators. Patients are anxious, dyspneic, and may only manage a few words per breath. Look for tachypnea, tachycardia, pallor or cyanosis, and a hyperinflated chest using accessory and supraclavicular muscles. Wheeze can be both inspiratory and expiratory, and breath sounds may be diminished with severe obstruction.

Silent chest

A quiet chest with no wheeze in a severely dyspneic patient is not reassuring, it's a crash-cart sign.Little air is moving at all. Combined with drowsiness or confusion, this means impending respiratory failure. Escalate immediately, this patient needs the ICU, not another nebulizer treatment on the floor.

Risk factors for asthma-related death

Prior near-fatal attack requiring intubation, hospitalization or ED visit in the past year, recent oral corticosteroid use, no current ICS use, SABA overuse (>1 canister/month), psychiatric disease or psychosocial problems, poor adherence, no written asthma action plan, and food allergy. Screen for these at every visit, not just during an exacerbation.

Diagnosis

Diagnosis needs two things: a historyconsistent with asthma (recurrent wheeze, cough, chest tightness, dyspnea that vary in intensity, often with known triggers or a personal/family history of atopy) and objective confirmationof variable expiratory airflow limitation.

Confirming variable airflow limitation (need at least one)

Baseline obstruction looks like FEV1/FVC <80%(or below the lower limit of normal) with a positive bronchodilator response as above. If the workup is unclear after all of this, refer to a specialist rather than guessing.

Don't confuse asthma and COPD spirometry

Asthma's hallmark is reversibility. COPD is defined by a post-bronchodilator FEV1/FVC <0.7that stays fixed. A patient whose obstruction fully normalizes with a bronchodilator points you toward asthma; one who doesn't fully reverse points toward COPD or asthma-COPD overlap.

Rule out the mimics

Chronic upper airway cough syndrome, GERD, heart failure or arrhythmia, COPD, obstructive sleep apnea, pulmonary embolism, bronchiectasis, cystic fibrosis, tuberculosis, and anxiety can all present with asthma-like symptoms. If the history, exam, and spirometry don't line up, work through this list before treating empirically.

Treatment - GINA Tracks and Stepwise Therapy

Goals:good symptom control with normal activity levels, and minimizing future risk, exacerbations, fixed airflow limitation, and treatment side effects. Every persistent asthma patient starts on ICS-containing therapy; there is no step that's ICS-free once symptoms are more than occasional.

TRACK 1 - PREFERRED

AIR / MART with ICS-formoterol

Formoterol is the only LABA with an onset fast enough (5 minutes) to double as a reliever. One inhaler does both jobs.

Steps 1–2: PRN low-dose ICS-formoterol only(AIR). Steps 3–5: scheduled ICS-formoterol plusPRN doses of the same inhaler (MART).
TRACK 2 - ALTERNATIVE

ICS maintenance + SABA (or ICS-SABA) reliever

The traditional approach. Still valid, and sometimes forced by cost, insurance, or patient preference.

Scheduled ICS (dose escalates by step) with SABA PRN, or as-needed combination ICS-SABA where available.
Why GINA moved away from SABA-only

SABA-only treats bronchospasm and ignores inflammation. Trials repeatedly show higher SABA use tracks with more exacerbations and higher mortality, regular SABA use can actually increasehyperresponsiveness and blunt future bronchodilator response, and patients started on a SABA alone tend to believe it istheir asthma treatment, which predicts poor adherence to any controller added later. AIR/MART strategies cut severe exacerbation risk compared with SABA-reliever strategies in head-to-head trials (SYGMA 1, SYGMA 2). Exceptions exist for patient preference or cost, but plain SABA monotherapy is no longer a GINA-endorsed strategy at any step.

Stepwise therapy, ages 12+ (Track 1, preferred column)

StepMaintenanceReliever
1None scheduledPRN low-dose ICS-formoterol (AIR)
2None scheduled, ordaily low-dose ICSPRN low-dose ICS-formoterol (AIR)
3Low-dose ICS-formoterol scheduledSame inhaler PRN (MART)
4Medium-dose ICS-formoterol scheduledSame inhaler PRN (MART)
5Medium–high dose ICS-LABA + LAMAPRN SABA or ICS-formoterol MART
6High-dose ICS-LABA + oral corticosteroidPRN SABA

Assess control 2–6 weeks after any change. Step up if uncontrolled (after checking technique, adherence, and triggers first). Step down only after ≥3 consecutive months of good control, typically by reducing ICS dose 25–50% at a time. Consult an asthma specialist at Step 4 and above; consider it at Step 3.

What an actual prescription looks like

Steps 1–2:budesonide/formoterol 160/4.5 mcg, 1 inhalation PRN for symptoms. Step 3:mometasone/formoterol 100/5 mcg, 1 inhalation BID scheduled plus 1 PRN. Steps 4–5:budesonide/formoterol 160/4.5 mcg, 2 inhalations BID scheduled plus 1 PRN. Salmeterol/fluticasone (Advair) BID plus a separate PRN dose is a classic wrong answer: salmeterol's onset is too slow to serve as a reliever, so it can never be used for MART.

MART dosing limits

Maximum formoterol exposure with budesonide (Symbicort) or beclomethasone (Dulera) MART is 12 inhalations in 24 hoursfor age 12+ (8 for ages 4–11). The reliever dose is always the low-doseICS-formoterol strength, even if the patient's maintenance inhaler is a higher-dose formulation, so double-check they have the correct strength device to make that math work.

Nonpharmacologic therapy

Dosing Reference

Relievers and maintenance inhalers

DrugCommon product / strengthTypical dosing
SABA
Albuterol MDIProAir/Ventolin/Proventil HFA 90 mcg/act1–2 inh q4–6h PRN
Albuterol nebulizer0.083% (2.5 mg/3 mL)1 vial q4–6h PRN
LevalbuterolXopenex HFA 45 mcg/act1–2 inh q4–6h PRN; less tachycardia/tremor at equivalent effect
ICS-formoterol (AIR / MART)
Budesonide/formoterolSymbicort 80/4.5 or 160/4.5 mcg/actStep 1–2: 1 inh PRN. Step 3–4: 1–2 inh BID scheduled + PRN (max 12 inh/24h)
Mometasone/formoterolDulera 100/5 or 200/5 mcg/act1–2 inh BID scheduled + PRN
Albuterol-ICS combination reliever (AIR, asthma only)
Albuterol/budesonideAirsupra 90/80 mcg/act2 inh PRN, not to exceed 12 inh/day
ICS-LABA (Track 2 maintenance)
Fluticasone/salmeterolAdvair Diskus 100–500/50 mcg1 inh BID + separate SABA reliever
Fluticasone/vilanterolBreo Ellipta 100–200/25 mcg1 inh once daily + separate reliever
LTRA / 5-LO inhibitor
MontelukastSingulair 10 mg (5 mg chewable age 6–14)Once daily in the evening
ZafirlukastAccolate 20 mgBID, 1h before or 2h after meals (food ↓ bioavailability 40%)
ZileutonZyflo IR 600 mg / ER 1200 mgIR: QID with meals + QHS. ER: BID within 1h of meals (total 2400 mg/day)

Comparative ICS daily dosing, ages 12+ (mcg/day)

AgentLow doseMedium doseHigh dose
Beclomethasone DPI80–240>240–480>480
Budesonide DPI180–540>540–1080>1080
Ciclesonide HFA MDI160–320320–640>640
Fluticasone propionate HFA MDI88–264264–440>440
Fluticasone propionate DPI100–300300–500>500
Fluticasone furoate DPI100200-
Mometasone DPI110–220>220–440>440

Acute severe exacerbation drug doses (≥12 years old)

DrugDoseComment
Albuterol nebulizer2.5–5 mg q20min ×3, then 2.5–10 mg q1–4h PRN, or 10–15 mg/h continuousDilute to at least 4 mL, gas flow 6–8 L/min
Albuterol MDI4–8 puffs q30min up to 4h, then q1–4h PRNNebulizer preferred if patient is in severe distress
Ipratropium nebulizer500 mcg q30min ×3, then q2–4h PRNAdd-on only, can mix in the same nebulizer as albuterol
Ipratropium MDI8 puffs q20min PRN up to 3hStop once hospitalized
Prednisone / methylprednisolone / prednisolone40–50 mg/day (max 50 mg), 1–2 divided doses, 5–7 daysNo advantage of IV over oral unless the patient can't take PO; no taper needed if course <2 weeks and ICS is started
Magnesium sulfate2 g IV single infusionReserve for FEV1 <25–30% predicted or persistent hypoxemia after standard treatment

Class-by-Class Detail

β2-agonists - SABA, LABA, and why formoterol is special

SABAs(albuterol, levalbuterol) are the fastest and most effective bronchodilators available and remain first-line for acute bronchospasm and exercise-induced symptoms. Levalbuterol is the single active R-isomer, roughly twice as potent per milligram, with a possible edge on side effects, though real-world benefit over albuterol is modest.

LABAs(formoterol, salmeterol) bronchodilate for 12+ hours and are dosed BID. LABA monotherapy is discouraged in asthma(unlike COPD) because it's linked to increased exacerbations and death when not paired with ICS. Only formoterolhas an onset fast enough (about 5 minutes, similar to albuterol) to double as a reliever, which is the entire premise behind AIR and MART. Salmeterol's onset is too slow, roughly 30 minutes, so it can never be used that way.

Ultra-LABAs(indacaterol, olodaterol, vilanterol) bronchodilate for 24 hours. Only vilanterol, combined with fluticasone furoate, is approved once daily for asthma in the US; indacaterol and olodaterol are COPD-only products.

SABA overuse

≥3 canisters/year signals rising exacerbation risk; >1 canister/month signals rising mortalityrisk. Overuse doesn't mean the patient needs more albuterol, it means their maintenance regimen is failing and needs to step up.

Inhaled corticosteroids - the backbone of every persistent asthma regimen

ICS are preferred long-term control therapy because they're the only class shown to reduce the risk of dying from asthma. Response is delayed: most patients improve within 1–2 weeks, with maximum symptom improvement by 4–8 weeks and maximum FEV1/PEF improvement possibly taking 3–6 weeks. Set that expectation up front or patients quit early thinking it "isn't working."

Local adverse effects(oropharyngeal candidiasis, dysphonia) are dose-dependent and reduced by spacer use and mouth rinsing. Systemic effects(growth suppression in children, osteoporosis, cataracts, dermal thinning, easy bruising, adrenal insufficiency) are minimal at low-to-moderate doses but climb with high, chronic dosing.

Anticholinergics - ipratropium vs tiotropium

Anticholinergics reverse cholinergic-mediated bronchoconstriction. Ipratropiumis adjunctive therapy in acute severe asthma not fully responsive to SABA alone, and a rescue option for patients intolerant of SABAs. It's slower to reach maximum bronchodilation than SABA (30–60 min vs 5–10 min), though some effect starts within 30 seconds. Duration is 4–8 hours.

Tiotropium(Spiriva) is a 24-hour LAMA that can be added on when asthma isn't controlled on medium-to-high dose ICS-LABA (this is Step 5 territory). Umeclidinium is available combined with fluticasone/vilanterol (Anoro) but is not FDA-approved for asthmaor for acute bronchospasm relief, that's a COPD-only product, a classic distractor.

Leukotriene modifiers and zileuton - why they've fallen out of favor

Montelukast(10 mg daily, evening, 5 mg chewable ages 6–14) and zafirlukast(20 mg BID, empty stomach) block the leukotriene D4 receptor. Both are less effective than low-dose ICS and less effective than adding a LABA to ICS. They're not for acute exacerbations and must be taken continuously, even when symptom-free.

Boxed warning

Montelukast carries an FDA boxed warning (since March 2020) for neuropsychiatric events, irritability, aggression, sleep disturbance, and rare suicidality, especially within the first few weeks. Warn patients and families to watch for mood or behavior changes. Zafirlukast carries a hepatotoxicity risk, including rare fatal hepatic failure, and both drugs have been linked to a rare Churg-Strauss-like eosinophilic vasculitis syndrome.

Zileuton(Zyflo) blocks 5-lipoxygenase upstream of all the leukotrienes. Its use is limited by hepatic enzyme elevation risk (watch closely in the first 3 months) and by CYP3A4 inhibition, which raises levels of theophylline and warfarin. Reach for an LTRA before zileuton in most cases; reach for something else before either if there are psychiatric comorbidities or if allergic rhinitis is the only real complaint LTRAs would help with.

Biologics - matching the antibody to the phenotype

Biologics target IgE or the Th2/eosinophilic pathway (IL-4, IL-5, IL-13, TSLP) and are reserved for moderate-to-severe persistent asthma with poor control on high-dose ICS-LABA, or patients needing chronic oral corticosteroids. All require in-clinic administration with anaphylaxis monitoring after each dose.

DrugTargetAgeRoute / frequencyPredictive biomarker
Omalizumab (Xolair)Anti-IgE≥6ySC q2–4wk, dose by weight + IgEFeNO ≥24 ppb + eos >260/mcL on high-dose ICS
Mepolizumab (Nucala)Anti-IL-5≥6ySC q4wkPeripheral eosinophil count
Reslizumab (Cinqair)Anti-IL-5≥18yIV q4wkPeripheral eosinophil count
Benralizumab (Fasenra)Anti-IL-5 receptor≥12ySC q4wk ×3, then q8wkPeripheral eosinophil count
Dupilumab (Dupixent)Anti-IL-4Rα (blocks IL-4 and IL-13)≥12ySC q2wkFeNO >25 ppb + eos ≥150/mcL
TezepelumabAnti-TSLP≥12ySCBroadest eligibility, not eosinophil-restricted

Omalizumab carries a boxed warning for anaphylaxis(~0.1% of patients), which is why in-office observation after dosing is mandatory. For exam purposes, know which target goes with which drug name more than the exact eligibility cutoffs.

Magnesium and methylxanthines - why they're niche

Magnesium sulfaterelaxes smooth muscle by blocking calcium influx and may have anti-inflammatory effects. A single 2 g IV dose can reduce hospital admissions in severe exacerbations (FEV1 <25–30% predicted, persistent hypoxemia despite standard treatment). Watch for hypotension, flushing, sweating, depressed reflexes, and CNS/respiratory depression.

Theophyllineis a moderately potent bronchodilator with mild anti-inflammatory activity, but it's rarely used now given the narrow therapeutic index, seizure and death risk with toxicity, and heavy CYP1A2/CYP3A4 drug interaction burden. It's not recommended by GINA for either acute exacerbations or maintenance persistent asthma.

Acute Severe Asthma - ED Management

Goal number one in an acute exacerbation is preventing death by recognizing deterioration early and treating fast. Give the first three bronchodilator treatments together and reassess at 1 hour.

Triage by clinical status

Mild-moderateSevere
SpeechTalks in phrases, prefers sittingTalks in words, sits hunched forward, agitated
Respiratory rateIncreased>30/min
Pulse100–120 bpm>120 bpm
O2 saturation (room air)90–95%<90%
PEF>50% predicted/best≤50% predicted/best
TreatmentSABA ± ipratropium, controlled O2 to 93–95% (children 94–98%), oral corticosteroidAdd IV/oral corticosteroid, consider IV magnesium and high-dose ICS

Any of drowsiness, confusion, or a silent chestmeans skip the algorithm: consult ICU, start SABA and oxygen, and prepare for possible intubation.

Reassess at 1 hour

Obtain history and exam whiletreatment is already running, don't delay bronchodilators to finish the interview. Screen for anaphylaxis, complicating infection, and risk factors for asthma-related death in parallel. Arterial blood gases are reserved for patients doing poorly or deteriorating; get a CBC only if there are signs of infection (fever, purulent sputum).

Self-management for early worsening (before it becomes an ED visit)

On MART, the written action plan for early/mild worsening is to increase the reliever(ICS-formoterol as needed, up to a total formoterol dose of 72 mcg/day) and continue maintenance therapy. For late/severe worsening, at least double the maintenance ICS (consider escalating to high dose, max 2000 mcg/day BDP-equivalent), and add oral corticosteroids while contacting the prescriber. For Track 2 patients, the action plan instead centers on increasing SABA frequency and starting oral corticosteroids at the same trigger points.

Exercise-Induced Bronchospasm & Asthma-COPD Overlap

EIB

Asthma-COPD overlap

Persistent airflow limitation with features of both diseases. Diagnostic criteria are debated and these patients tend to be more symptomatic and are often excluded from major trials, so the evidence base is thin. Practically: still avoid LABA or LAMA monotherapy (the asthma rule), still be cautious with ICS/maintenance oral steroid dosing given pneumonia risk (the COPD rule), and still require FEV1/FVC <70% for diagnosis. Management generally follows the asthma pathway: start around Step 3–4 and keep the ICS dose low-to-moderate.

Monitoring

ParameterWhenWatching for
Symptom control (4-question tool)Every visitWell controlled vs partly controlled vs uncontrolled
SpirometryAt diagnosis, then yearly during ongoing careFixed airflow limitation developing over time
PEFShort-term (~2wk) after a therapy change; long-term only in severe/poor-perceiving patientsVariability, response to treatment
Reliever (SABA or ICS-formoterol PRN) useEvery visitOveruse as an early warning of loss of control and mortality risk
Inhaler techniqueMonthly initially, then every 3–6 monthsPoor technique masquerading as "treatment failure"
Growth (children), bone density, ocular examPeriodically on chronic high-dose ICSSystemic corticosteroid effects
Eosinophils, FeNOBefore starting a biologic, then periodicallyConfirming phenotype and tracking response
Validated questionnaires(Asthma Control Test, ACQ, ATAQ)RegularlyObjective trend the patient can't easily fudge from memory

Patient Counseling

  • "Carry your reliever inhaler with you at all times."Whether that's albuterol or ICS-formoterol depends on their track, but every patient needs one on hand.
  • If they're on MART:"This inhaler is both your everyday medicine and your rescue medicine. Take your scheduled doses every day, and take an extra puff of the same inhalerif you get symptoms, don't reach for a different rescue inhaler."
  • Rinse and spit after every ICS-containing inhaler,whether it's a controller or a MART reliever dose. "This keeps you from getting thrush or a hoarse voice."
  • "If you're using your rescue inhaler more than twice a week, that's not normal, it means your asthma isn't controlled and we need to adjust your treatment."Reframe overuse as a signal to call, not a personal failure.
  • Set expectations on ICS:"This won't work like your rescue inhaler. You might not feel a difference for a week or two, and it can take up to two months for your lung function to fully catch up. Keep taking it even when you feel fine."
  • Review the written asthma action planat every visit: what their baseline meds are, what to do for early worsening, and exactly when to seek emergency care (word difficulty, blue lips, no relief from reliever).
  • Avoid triggers:smoke (including vaping), strong scents, known allergens, and very cold air if it's a personal trigger. Encourage smoking cessation directly, it's one of the highest-yield things you can say in the visit.
  • For montelukast specifically:"Call us right away if you or your family notice new mood changes, irritability, trouble sleeping, or anything that feels off mentally. This isn't common, but it's serious when it happens."
  • Vaccinations:annual influenza (especially with moderate-severe asthma), plus pneumococcal, pertussis, RSV, and COVID-19 per current guidance.

High-Yield Recall Sheet

  • SABA-only is no longer a GINA-endorsed strategyat any step. Every reliever now pairs with an anti-inflammatory.
  • Formoterol is the only LABA fast enough to be a reliever.Salmeterol can never be used for MART.
  • MART max formoterol dose is 72 mcg/day; max 12 inhalations/24h for Symbicort/Dulera in adults (8 for ages 4–11).
  • Physical exam is often completely normalbetween asthma attacks. Don't let that rule out the diagnosis.
  • Bronchodilator reversibility = FEV1 (or FVC) increase ≥12% and ≥200 mLafter SABA.
  • PEF variability >10%over 2 weeks of twice-daily monitoring also confirms variable airflow limitation.
  • Silent chest = ominous, not reassuring. Little air is moving. Same for drowsiness/confusion.
  • SABA overuse cutoffs:≥3 canisters/year → exacerbation risk. >1 canister/month → mortality risk.
  • Control (4-question tool, last 4 weeks) ≠ severity(assessed retrospectively by step of therapy needed).
  • Uncontrolled asthma ≠ severe asthma.Check technique, adherence, and comorbidities first.
  • LABA or LAMA monotherapy is avoided in asthma(opposite of COPD, where LABA/LAMA monotherapy is fine).
  • Montelukast carries a boxed warningfor neuropsychiatric events; zafirlukast carries hepatotoxicity risk.
  • Zileuton needs LFT monitoring, especially in the first 3 months, and inhibits CYP3A4.
  • Biologic selection follows the biomarker:IgE → omalizumab; eosinophils → mepolizumab/reslizumab/benralizumab; eosinophils + FeNO → dupilumab; broadest eligibility → tezepelumab.
  • Omalizumab carries a boxed warning for anaphylaxis(~0.1%); dose in a clinical setting with post-dose observation.
  • Systemic corticosteroid burst: 40–50 mg/day, 5–7 days, no taper neededif the patient starts or continues an ICS.
  • IV magnesium reservedfor FEV1 <25–30% predicted or persistent hypoxemia despite standard treatment.
  • Asthma-COPD overlap is managed on the asthma pathway: no LABA/LAMA monotherapy, start Step 3–4, keep ICS low-moderate.