Respiratory
Asthma: outpatient stepwise management per GINA guidelines
— Affects ~8% of US adults and ~7% of children; disproportionately impacts non-Hispanic Black and Puerto Rican patients.
— Leading cause of pediatric ED visits and missed school/work days; ~3,500 US deaths/year, most preventable with proper controller therapy.
— Episodic symptoms worse at night or early morning, triggered by exercise, cold air, allergens, viral URIs, NSAIDs, or beta-blockers.
— History of atopy (allergic rhinitis, eczema), family history of asthma.
— Recurrent "bronchitis," chronic cough >8 weeks, or exercise intolerance disproportionate to fitness.
— Diagnosis requires (1) history of variable respiratory symptoms AND (2) documented variable expiratory airflow limitation.
— Treatment is built on a stepwise track (Track 1 preferred: ICS-formoterol as both controller and reliever; Track 2 alternative: ICS + SABA reliever).
— SABA-only treatment is no longer recommended for any adult/adolescent with asthma due to mortality risk.
— Severity = retrospective, based on the step of treatment required to maintain control.
— Control = prospective, assessed every visit using symptom frequency, night waking, reliever use, activity limitation.
Board pearl: A young adult with seasonal "recurrent bronchitis," nocturnal cough, and a normal exam in clinic still has asthma until proven otherwise — order spirometry with bronchodilator reversibility, not empiric antibiotics. The Step 3 trap is ordering a chest CT or starting azithromycin instead of confirming reversible obstruction.

— Allergic asthma: childhood onset, atopy, eosinophilia, responds well to ICS.
— Late-onset eosinophilic asthma: adult onset, often less allergic, frequently nasal polyps, may need biologics.
— Exercise-induced bronchoconstriction (EIB): symptoms 5–10 min after exertion, resolves in 30–60 min; consider in athletes.
— Aspirin-exacerbated respiratory disease (AERD): asthma + nasal polyps + NSAID sensitivity (Samter triad).
— Occupational asthma: symptoms improve on weekends/vacations; isocyanates, flour, latex, animal proteins.
— Cough-variant asthma: chronic dry cough as sole symptom; diagnosed by methacholine challenge.
— Allergens (dust mites, cockroach, pet dander, pollen, mold)
— Irritants (tobacco/vaping, wood smoke, cleaning chemicals, ozone)
— Infections (rhinovirus, RSV, influenza)
— Drugs (NSAIDs, nonselective beta-blockers, ACE inhibitor cough is a mimic)
— Comorbid: GERD, obesity, OSA, chronic rhinosinusitis, vocal cord dysfunction — all worsen control.
— ≥1 severe exacerbation in past year
— ICU admission or intubation ever
— High SABA use (>1 canister/month) — strongest modifiable mortality predictor
— Poor adherence or incorrect inhaler technique
— Low FEV1 (<60% predicted), high blood eosinophils/FeNO
— Psychosocial: depression, food allergy, low socioeconomic support.
Step 3 management: At every outpatient visit, score control with the Asthma Control Test (ACT) (≥20 = well-controlled) or GINA 4-question assessment over the prior 4 weeks. Document SABA refill frequency from the pharmacy — this is the single most predictive number for future exacerbation and the most commonly tested ambulatory data point.

— Expiratory wheeze, prolonged expiratory phase (I:E ratio <1:2).
— Use of accessory muscles, tachypnea, tachycardia.
— Hyperresonance to percussion, diminished breath sounds if severe air trapping.
— Silent chest (no wheeze due to inadequate airflow)
— Inability to speak in full sentences, single-word dyspnea
— Paradoxical thoracoabdominal motion
— Pulsus paradoxus >12 mmHg
— Altered mental status, cyanosis, bradycardia, diaphoresis
— SpO2 <90% on room air despite supplemental O2.
— Nasal mucosa pale/boggy with clear discharge (allergic rhinitis)
— Nasal polyps (think AERD)
— Eczematous skin changes in antecubital/popliteal fossae
— Allergic shiners, Dennie-Morgan lines, transverse nasal crease in children.
— Mild: RR <25, HR <110, SpO2 >95%, PEF >50% personal best
— Moderate: PEF 50–80%
— Severe: PEF <50%, SpO2 <90%, unable to complete sentences.
Key distinction: Wheeze on inspiration that is loudest over the neck = vocal cord dysfunction (VCD), not asthma. VCD does not respond to bronchodilators, has normal SpO2 even when distressed, and is diagnosed by laryngoscopy showing paradoxical vocal cord adduction. Treatment is speech therapy, not steroid escalation — a classic Step 3 misdiagnosis trap in young women and athletes.

— Obstruction: FEV1/FVC below the lower limit of normal (commonly <0.70 in adults, <0.85 in children).
— Reversibility (adults): post-bronchodilator increase in FEV1 >12% AND >200 mL from baseline, 10–15 min after 200–400 mcg albuterol.
— In children: >12% increase from baseline is sufficient.
— Repeat during symptoms.
— Peak expiratory flow (PEF) diary for 2 weeks: average diurnal variability >10% (adults) or >13% (children) supports asthma.
— Refer for bronchoprovocation testing (see chunk 5).
— FeNO (fractional exhaled nitric oxide): >50 ppb supports type 2/eosinophilic inflammation and predicts ICS response; <25 ppb argues against eosinophilic asthma.
— Blood eosinophils ≥300/µL suggests T2-high phenotype and biologic candidacy.
— Total IgE + specific IgE/skin prick testing when allergic triggers suspected or for omalizumab eligibility.
Step 3 management: Do not start step-2+ controllers based on history alone in adults — document obstruction and reversibility first. A common stem: a smoker with chronic dyspnea has FEV1/FVC 0.62 with <8% reversibility — that is COPD, not asthma, and the management track diverges (LAMA-based vs. ICS-formoterol-based). Misclassification leads to inappropriate biologic referrals and missed smoking cessation counseling.

— Methacholine challenge (direct): PC20 ≤8 mg/mL indicates airway hyperresponsiveness; high negative predictive value — a negative test essentially rules out asthma.
— Mannitol or exercise challenge (indirect): more specific, useful for EIB; ≥10% fall in FEV1 with exercise is diagnostic of EIB.
— Eucapnic voluntary hyperventilation: preferred for elite athletes per IOC.
— Skin prick testing or serum specific IgE for perennial and seasonal allergens.
— Drives environmental control counseling and biologic selection.
— High-resolution CT chest: consider for suspected bronchiectasis, ABPA, eosinophilic granulomatosis with polyangiitis (EGPA), tracheomalacia, or if poor response to therapy.
— Blood eosinophils, total/specific IgE, FeNO
— Aspergillus-specific IgE and IgG to screen for ABPA (suspect if central bronchiectasis, very high IgE >1000, eosinophilia, brown mucus plugs).
— ANCA if suspecting EGPA (asthma + eosinophilia >10% + sinusitis + neuropathy/rash).
— Laryngoscopy for VCD
— Cardiac echo/BNP if cardiac asthma suspected
— Alpha-1 antitrypsin level in early-onset airflow obstruction without smoking
— Sweat chloride/CFTR testing in young patients with bronchiectasis.
Board pearl: In a patient with "refractory asthma" plus peripheral eosinophilia, sinusitis, and mononeuritis multiplex or purpuric rash, stop escalating ICS and order ANCA + tissue biopsy — this is EGPA (Churg-Strauss). Initiating LTRA (montelukast) can unmask EGPA when systemic steroids are tapered, a frequently tested association.

— Daytime symptoms >2x/week?
— Any night waking from asthma?
— Reliever needed >2x/week (excluding pre-exercise)?
— Any activity limitation?
— 0 yes = well controlled; 1–2 = partly controlled; 3–4 = uncontrolled.
— Step 1: as-needed low-dose ICS-formoterol
— Step 2: as-needed low-dose ICS-formoterol (same; eliminates need for daily controller in mild)
— Step 3: low-dose MART (maintenance and reliever therapy) — daily + as-needed ICS-formoterol
— Step 4: medium-dose MART
— Step 5: add-on LAMA (tiotropium), refer for phenotyping/biologic; consider high-dose ICS-formoterol MART
Step 3 management: Before stepping up, run the "4 A's" checklist: Adherence, Aerosol technique, Allergen/trigger exposure, Alternative diagnosis. ~50% of "refractory" asthma cases are explained by one of these — addressing them is higher-yield than escalating drug class on the exam.

— Budesonide, fluticasone propionate/furoate, beclomethasone, mometasone, ciclesonide.
— Low/medium/high dose categories defined per GINA (e.g., budesonide low 200–400 mcg/day, medium >400–800, high >800).
— AEs: oral candidiasis, dysphonia (mitigated by spacer + rinse mouth after use), rare adrenal suppression at high doses, slight growth velocity reduction in children (~1 cm, non-cumulative).
— Budesonide-formoterol and mometasone-formoterol are approved for MART; formoterol's rapid onset (1–3 min) allows both maintenance and rescue dosing.
— Fluticasone-salmeterol is NOT a reliever — salmeterol has slow onset.
— Montelukast: useful adjunct in EIB, AERD, and concurrent allergic rhinitis.
— FDA boxed warning (2020): neuropsychiatric effects (depression, suicidal ideation, agitation, sleep disturbance) — counsel patients and avoid as first-line in mild asthma.
CCS pearl: When advancing therapy on CCS, always order "inhaler technique training" and "asthma action plan" as separate items. The grader credits these as distinct management actions, and they reflect real outpatient care priorities.

— Omalizumab (anti-IgE): allergic asthma, perennial allergen sensitization, IgE 30–1500 IU/mL. Dosed SC q2–4 weeks by weight/IgE. Watch for anaphylaxis (rare).
— Mepolizumab, reslizumab, benralizumab (anti-IL-5/IL-5R): eosinophilic asthma with blood eos ≥300/µL (≥150 for mepolizumab in some criteria). Reduce exacerbations by ~50%.
— Dupilumab (anti-IL-4Rα): eosinophilic OR oral-steroid-dependent asthma; also treats atopic dermatitis, nasal polyps, EoE. Watch for transient hypereosinophilia and conjunctivitis.
— Tezepelumab (anti-TSLP): broadest indication — works in both T2-high and T2-low severe asthma; no eosinophil threshold required.
Board pearl: Before starting any biologic, document (1) phenotype biomarkers (eos, IgE, FeNO), (2) adherence verified by pharmacy refill, (3) inhaler technique observed, (4) comorbidity optimization (rhinitis, GERD, obesity, OSA), (5) exclusion of mimics (VCD, EGPA, ABPA). Skipping this workup is the most common reason a Step 3 stem labels a case as "inappropriate biologic initiation."

— Often less reversibility, more fixed obstruction → distinguish from COPD and from asthma-COPD overlap (ACO).
— Higher risk of misdiagnosis as CHF — check BNP, echo when ambiguous.
— Comorbid CAD limits use of high-dose SABA (tachyarrhythmia risk).
— Beta-blockers: nonselective (propranolol, timolol eye drops) can precipitate bronchospasm — use cardioselective (metoprolol, bisoprolol) if a beta-blocker is required for CAD/HFrEF.
— NSAIDs: caution given AERD prevalence; ask before recommending.
— Anticholinergic burden: tiotropium generally safe but watch urinary retention in BPH, narrow-angle glaucoma.
— ICS: higher risk of pneumonia, cataracts, osteoporosis, skin bruising, diabetes — use lowest effective dose, ensure DEXA screening and vaccinations.
— Montelukast: use cautiously in severe hepatic disease.
— Theophylline (rarely used): narrow therapeutic index, hepatically cleared, multiple CYP1A2 interactions (ciprofloxacin, cimetidine) — avoid in elderly when possible.
— Ciclesonide is a prodrug activated in lung — lower systemic exposure, attractive option in hepatic concerns.
Step 3 management: In an older patient with new wheeze, always rule out CHF, vocal cord dysfunction, and lung cancer with post-obstructive wheeze before labeling as new-onset asthma. Obtain CXR, BNP, and consider CT chest if smoker — a missed lung cancer presenting as "asthma" is a high-stakes Step 3 vignette.

— Uncontrolled asthma is more dangerous than asthma medications — risks include preeclampsia, IUGR, preterm birth, perinatal mortality.
— Continue ICS (budesonide has the most safety data — Category B historically); continue LABA, montelukast, omalizumab if needed for control.
— Manage exacerbations the same as non-pregnant: SABA, systemic steroids, oxygen to SpO2 ≥95% (higher target to protect fetus).
— Avoid live vaccines (e.g., LAIV); give inactivated influenza and Tdap as standard.
— Track 1 (children 6–11): daily low-dose ICS with as-needed SABA OR daily ICS + as-needed ICS-SABA combination; MART is an option at Steps 3–4.
— Monitor growth velocity annually on ICS.
— Spacer with mask for <4 years; spacer with mouthpiece for 4–6 years.
— Diagnosis is clinical (spirometry unreliable); use Asthma Predictive Index (frequent wheeze + 1 major criterion: parental asthma, eczema, aeroallergen sensitization; or 2 minor: food allergy, eosinophilia ≥4%, wheezing apart from colds).
— Trial of low-dose ICS for 3 months → if improved and relapses off, supports diagnosis.
— Pre-exercise SABA or ICS-formoterol 15 min before activity; warm-up routines; daily ICS if frequent.
— Optimize control 1 week pre-op; continue all inhalers through morning of surgery; stress-dose steroids if on chronic oral prednisone >5 mg/day for >3 weeks within past 6 months.
Key distinction: In pregnancy, the priority order is (1) keep mother oxygenated and controlled, (2) use established medications, (3) avoid the temptation to "minimize drug exposure" — undertreatment causes more fetal harm than ICS, LABA, or even systemic steroids during exacerbation.

— Status asthmaticus → respiratory failure, hypercapnia, intubation.
— Pneumothorax, pneumomediastinum from high intrathoracic pressures.
— Mucus plugging with atelectasis; secondary bacterial pneumonia.
— Lactic acidosis from high-dose beta-agonist therapy (usually benign, self-resolves).
— Hypokalemia from beta-agonists; tachyarrhythmias.
— Airway remodeling: subepithelial fibrosis, smooth muscle hypertrophy, fixed obstruction over years if poorly controlled.
— Reduced lung function trajectory; possible adult COPD overlap.
— Recurrent exacerbations → cumulative oral steroid exposure → osteoporosis, DM, cataracts, glaucoma, adrenal suppression, weight gain, mood disorders.
— ICS: dysphonia, oral candidiasis, easy bruising, cataracts (high dose), pneumonia risk modest.
— LABA monotherapy: increased asthma death — never alone.
— Montelukast: neuropsychiatric symptoms, rare EGPA unmasking.
— Theophylline: nausea, seizures, arrhythmias at toxic levels (>20 mcg/mL).
— Biologics: injection-site reactions, rare anaphylaxis (omalizumab — observe 2 hours after first 3 doses, 30 min thereafter), conjunctivitis (dupilumab).
— Anxiety and depression are 2–3× more common; screen with PHQ-9.
— School/work absenteeism, exercise avoidance, sleep disruption.
Board pearl: A patient using ≥3 SABA canisters per year has elevated exacerbation risk; ≥12 per year is associated with increased asthma mortality. This pharmacy-refill data point is one of the most testable single numbers in ambulatory asthma management.

— PEF <50% personal best after initial bronchodilator
— SpO2 <92% on room air
— Unable to speak in full sentences, accessory muscle use
— Drowsiness, confusion, silent chest
— No improvement or worsening after 1 hour of SABA + oral steroid
— Inability to return promptly for re-evaluation; lives alone with limited support.
— Supplemental O2 to SpO2 93–95% (88–92% if at risk of hypercapnia)
— Albuterol nebulized 2.5–5 mg q20 min × 3 or continuous; add ipratropium 500 mcg q20 min × 3 in moderate-severe.
— Systemic steroids within 1 hour: prednisone 50 mg PO or methylprednisolone 40–60 mg IV — equivalent if able to swallow.
— IV magnesium sulfate 2 g over 20 min for severe exacerbation not responding to initial therapy.
— Consider heliox, ketamine, BiPAP as bridge.
— Persistent hypoxia despite high-flow O2
— Rising PaCO2 (>42 mmHg in asthma exacerbation = ominous — patient tiring)
— Altered mental status
— Hemodynamic instability or arrhythmia
— Need for intubation (use ketamine for induction; lung-protective ventilation with permissive hypercapnia, low RR, long expiratory time).
— Diagnosis uncertain or atypical features
— Step 4–5 therapy required
— ≥2 exacerbations/year requiring oral steroids
— ≥1 hospitalization or ICU admission
— Suspected occupational asthma, ABPA, EGPA, AERD
— Biologic candidate evaluation.
CCS pearl: On CCS, after stabilizing an acute exacerbation, the discharge bundle must include: (1) 5–7 day prednisone course, (2) start/resume ICS-containing controller, (3) asthma action plan, (4) PCP follow-up within 1–2 weeks, (5) inhaler technique check, (6) trigger counseling. Missing any of these costs points.

— Older, smoking history, less reversibility (post-BD FEV1 increase <12% or <200 mL), persistent FEV1/FVC <0.70.
— Treatment centers on LAMA ± LABA, with ICS added only if eosinophils ≥300 or frequent exacerbations.
— Asthma-COPD overlap: features of both → use ICS-containing therapy first (never LABA/LAMA alone).
— Chronic productive cough, large mucopurulent sputum, recurrent infections, hemoptysis.
— HRCT shows dilated bronchi, "signet ring" sign.
— Treat with airway clearance, inhaled antibiotics for chronic Pseudomonas, immunization.
Key distinction: Wheeze + normal spirometry + normal methacholine challenge = NOT asthma. Methacholine has high negative predictive value. Pivot the workup to VCD, eosinophilic bronchitis, GERD-related cough, ACE inhibitor cough, or postnasal drip syndrome rather than empirically stepping up controller therapy.

— Older, orthopnea, PND, peripheral edema, elevated JVP, S3, bibasilar crackles, elevated BNP.
— CXR: cardiomegaly, Kerley B lines, pulmonary edema.
— Wheeze from peribronchial edema; treatment is diuresis, not bronchodilators (though may be co-administered acutely).
— Sudden dyspnea, pleuritic chest pain, tachycardia, hypoxia disproportionate to exam; risk factors (immobilization, malignancy, OCP, recent surgery).
— Wells score → D-dimer or CTPA.
— Postprandial, supine cough; heartburn; responds to PPI trial 8 weeks.
— Often coexists with and worsens asthma.
— Dyspnea at rest, paresthesias, carpopedal spasm, normal SpO2, respiratory alkalosis.
— Coexists with asthma — manage both.
Board pearl: The acute wheeze + urticaria + hypotension stem is anaphylaxis — give IM epinephrine first, before any IV access, antihistamine, or steroid. Delays in epinephrine administration are the leading cause of anaphylaxis death and a recurring Step 3 patient-safety theme.

— Green zone (PEF ≥80% personal best, no symptoms): continue daily controller.
— Yellow zone (PEF 50–79% OR symptoms): increase ICS-formoterol dosing or quadruple ICS dose for 7–14 days; start oral steroid if no improvement in 48 hours.
— Red zone (PEF <50% OR severe symptoms): start prednisone, call provider, seek ED care.
— Smoking cessation and elimination of secondhand/vaping exposure — single highest-impact intervention.
— Allergen avoidance: mattress/pillow encasings for dust mites, HEPA filtration, pet exclusion from bedroom, cockroach extermination, mold remediation.
— Avoid wood smoke, strong fragrances, occupational triggers.
— Allergic rhinitis → intranasal steroid ± antihistamine
— GERD → PPI trial if symptomatic
— Obesity → 5–10% weight loss improves control significantly
— OSA → CPAP if AHI ≥15 or symptomatic AHI ≥5
— Depression/anxiety → screen and treat.
— Annual inactivated influenza
— PCV15/PCV20 then PPSV23 per ACIP for adults with asthma on chronic high-dose ICS or oral steroids
— COVID-19 per current ACIP schedule
— RSV in adults ≥60 with chronic lung disease per shared decision-making
— Tdap, zoster per age standards.
Step 3 management: Every asthma visit should generate a documented AAP, technique check, adherence assessment, trigger review, vaccination update, and step-up/step-down decision — this 6-item bundle is the ambulatory care template Step 3 expects.

— Newly diagnosed or recently stepped-up: 2–6 weeks to reassess.
— Stable, well-controlled: every 3–6 months.
— Post-exacerbation: within 1–2 weeks of ED discharge — single most impactful follow-up touchpoint.
— Pregnancy: every 4–6 weeks throughout gestation.
— Symptom control (ACT or GINA 4 questions, prior 4 weeks)
— SABA refill count from pharmacy
— Inhaler technique observed
— Adherence (ask non-judgmentally: "How many days a week do you actually use it?")
— Side effects: thrush, dysphonia, easy bruising, growth (peds)
— Trigger exposure changes
— Comorbidity status.
— Spirometry at diagnosis, after 3–6 months of controller therapy, then every 1–2 years (more often if severe).
— PEF home monitoring useful in poor perceivers of dyspnea and severe disease.
— FeNO and eosinophils trended in severe asthma on biologics.
— After ≥3 months of well-controlled asthma, reduce ICS dose by ~25–50%.
— Document baseline FEV1 before step-down; recheck at 3 months.
— Never discontinue ICS entirely in adults — strong recurrence risk; minimum maintenance is low-dose ICS-formoterol as-needed.
— Difference between controller and reliever
— Spacer use with every pMDI
— Rinse mouth after ICS
— When to use the AAP zones
— Recognize early warning signs (nocturnal cough, increased reliever use).
CCS pearl: Schedule "return to clinic in 2 weeks" after every exacerbation discharge on CCS. This single order reduces 30-day re-presentation by ~30% in trial data and is consistently rewarded by the case grader.

— Asthma mortality is 2–3× higher in non-Hispanic Black patients and Puerto Ricans; driven by environmental exposures (housing quality, pollution), under-prescription of controllers, and access barriers.
— Address medication affordability — generic ICS-formoterol availability, manufacturer assistance, 90-day fills, $4 pharmacy programs. Non-adherence is often economic, not behavioral.
— Adolescents should be primary historians and demonstrate inhaler technique themselves.
— Confidentiality around vaping and substance use — vaping triggers asthma; counsel privately, document carefully under state minor-confidentiality laws.
— School-based AAP sharing requires guardian consent in most states.
— ED-to-PCP handoff: ensure prescriptions filled, AAP written, follow-up booked. Discharge without an ICS after asthma admission is a national patient-safety quality metric failure.
— Pediatric-to-adult transition: structured handoff between age 18–21 to prevent loss to follow-up and treatment regression.
— If suspected, document exposure history and refer for workplace evaluation; patients may qualify for workers' compensation. Reportable to OSHA in some jurisdictions.
— Biologics: discuss anaphylaxis risk (omalizumab) and need for observation; document.
— Bronchial thermoplasty: discuss limited durability data and risk of transient worsening.
— Prescribing LABA monotherapy — sentinel safety event.
— Prescribing nonselective beta-blockers in asthmatics.
— Failing to discontinue ACE inhibitor when cough mimics asthma.
— Over-reliance on SABA — pharmacy refill alert systems should be set up.
Board pearl: A patient discharged from the ED after an asthma exacerbation without ICS-containing therapy is a documentable patient-safety failure. On the exam, "what is the most important next step at discharge?" is almost always start or resume an ICS-containing controller, not "schedule pulmonology."

Key distinction: Differentiate "controller" (daily anti-inflammatory) from "reliever" (rescue) — and remember that with MART, ICS-formoterol fills both roles simultaneously. Mixing these up in patient counseling is a common safety event and exam trap.

Step 3 management: When asked "what is the most appropriate next step?" in a poorly controlled asthmatic, the answer is almost never another medication first — it is assess adherence and inhaler technique, then reconsider diagnosis, then step up.

Bottom line: Outpatient asthma management per GINA centers on confirming variable airflow obstruction with spirometry, then treating every patient — even mild — with an ICS-containing regimen (preferably as-needed or maintenance low-dose ICS-formoterol), titrated stepwise based on prospective symptom control while continuously addressing adherence, inhaler technique, triggers, and comorbidities.
Board pearl: If you remember only three numbers — >12% and >200 mL (reversibility), >1 SABA canister/month (overuse mortality flag), and 2 g IV magnesium (severe exacerbation rescue) — you will correctly handle the majority of Step 3 asthma vignettes.

