Pulmonology
Showing 37 of 37 topics
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Worsening dyspnea, cough, and sputum production beyond daily variation. Treat with short‑acting bronchodilators, systemic steroids, and antibiotics when increased sputum purulence/volume or ventilatory support is needed; use noninvasive ventilation for hypercapnic respiratory failure.
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An adult asthma exacerbation is an acute worsening of dyspnea, cough, wheeze, or chest tightness with increased expiratory airflow limitation. Severe attacks can progress rapidly and may present with a quiet chest or exhaustion rather than prominent wheeze. Treatment requires repeated inhaled bronchodilator therapy, early systemic corticosteroid, oxygen when hypoxemic, and escalation for impending respiratory failure.
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Give inhaled short acting beta agonist with anticholinergic for moderate to severe attacks, early systemic corticosteroids, oxygen as needed, and consider magnesium for severe cases.
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Evaluate anatomic and functional causes of aspiration; use instrumental swallow studies; implement dietary/positional strategies, optimize reflux control, and consider surgical interventions.
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Chronic productive cough for ≥3 months per year for two consecutive years, caused by airway inflammation from chronic irritant exposure (most commonly tobacco). Evaluate with spirometry to assess for obstructive physiology consistent with COPD. Manage with smoking cessation, vaccinations, bronchodilators, inhaled corticosteroids in selected cases, pulmonary rehab, and treatment of exacerbations.
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Cough >8 weeks: evaluate common causes (UACS, asthma, GERD), meds (ACEi), and red flags; CXR and spirometry guide workup; sequential empiric therapy is typical.
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COPD maintenance therapy should be anchored to confirmed persistent airflow obstruction, current symptoms, exacerbation history, inhaler technique, comorbidities, and the GOLD 2026 ABE framework. Long-acting bronchodilators are the foundation; inhaled corticosteroid benefit is greatest in patients with an exacerbation-prone phenotype and higher blood eosinophils, while smoking cessation, vaccination, exercise, and pulmonary rehabilitation remain core disease-modifying interventions.
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Short acting bronchodilators, systemic corticosteroids, and antibiotics when bacterial features present; consider noninvasive ventilation for hypercapnic respiratory failure.
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A COPD exacerbation is an acute worsening of dyspnea, cough, and/or sputum over days that requires additional therapy. Management centers on controlled oxygen for hypoxemia, short-acting bronchodilators, a short systemic corticosteroid course, antibiotics when bacterial features or ventilatory support indicate benefit, and early noninvasive ventilation for acute hypercapnic respiratory failure when appropriate.
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Treat acute COPD exacerbations with short‑acting bronchodilators (SABA/SAMA), systemic corticosteroids (e.g., prednisone 40 mg daily ×5 days), and antibiotics when increased sputum purulence/volume and dyspnea are present. Use controlled O2 (SpO2 88–92%) and early NIV for hypercapnic respiratory failure.
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A COPD exacerbation is an acute worsening of dyspnea and/or cough and sputum over less than about two weeks, often triggered by viral or bacterial infection, air pollution, or another cardiopulmonary stressor. Treatment includes short-acting bronchodilators, a short course of systemic corticosteroid, controlled oxygen, selective antibiotics, and noninvasive ventilation for acute hypercapnic respiratory failure when appropriate.
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Exacerbation management: SABA/SAMA, systemic steroids, antibiotics when indicated, and NIV for hypercapnic respiratory failure; arrange follow‑up and optimize maintenance therapy.
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Worsening dyspnea, cough, and sputum with respiratory acidosis benefits from noninvasive ventilation, short‑course systemic steroids, bronchodilators, controlled oxygen (SpO2 88–92%), and antibiotics when purulence/volume increase or mechanical ventilation is required.
D
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Hemoptysis (often absent), hypoxemia, and new diffuse alveolar infiltrates with falling hemoglobin; bronchoscopy with sequentially bloodier BAL confirms hemorrhage. Pulse‑dose IV steroids are first‑line; add cyclophosphamide or rituximab for ANCA vasculitis, and add plasma exchange for anti‑GBM disease or severe overlap; manage respiratory failure with lung‑protective ventilation.
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Hemoptysis ranges from blood-streaked sputum to life-threatening airway hemorrhage. Severity is defined by physiologic effect and airway risk rather than volume alone. Stabilize oxygenation and ventilation, position the suspected bleeding lung dependent when feasible, correct coagulopathy, localize the source with CT angiography when stable, and use bronchoscopy and bronchial artery embolization for significant or persistent bleeding.
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Noncardiogenic pulmonary edema occurring 2–5 days after rapid ascent above ~2500–3000 m with dyspnea at rest, cough, and hypoxemia. Immediate descent and supplemental oxygen are primary; add nifedipine and consider portable hyperbaric therapy when descent is delayed; avoid exertion and cold exposure.
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Immune-mediated ILD from inhaled antigens. Identify antigen and remove exposure; use steroids for inflammatory phases; consider antifibrotics for progressive fibrotic disease.
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Progressive fibrosing ILD with UIP pattern. Confirm diagnosis in multidisciplinary discussion; treat with antifibrotics; manage comorbidities; refer early for transplant and pulmonary rehab.
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Progressive dyspnea from accumulation of malignant exudative pleural fluid; establish the diagnosis with ultrasound-guided thoracentesis and cytology or pleural biopsy, recognize that it indicates advanced cancer, and relieve symptoms using repeated drainage, pleurodesis, or indwelling pleural catheter based on lung expandability, prognosis, and patient preferences, alongside systemic oncologic therapy.
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Life-threatening bleed from the lower respiratory tract. Prioritize airway protection and isolate bleeding lung (lateral decubitus with bleeding side down). Use bronchoscopy for localization and temporary control; definitive management often with bronchial artery embolization.
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Life‑threatening bleeding (>100–200 mL/h or any bleed causing instability/respiratory failure). Prioritize airway and bleeding‑lung isolation, position bleeding side down, localize with bronchoscopy/CTA, and arrange bronchial artery embolization; treat the underlying cause.
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Localize by mediastinal compartment to narrow the differential; use CT/MRI and targeted labs; involve multidisciplinary team for biopsy vs resection strategy.
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Pneumothorax is air in the pleural space causing partial or complete lung collapse. Primary spontaneous pneumothorax occurs without known underlying lung disease, while secondary spontaneous pneumothorax occurs in structurally abnormal lungs and is generally less well tolerated. Tension pneumothorax is a clinical emergency in which rising intrapleural pressure causes obstructive shock and must be decompressed immediately without waiting for imaging. Management of stable spontaneous pneumothorax depends on s
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Primary ciliary dyskinesia is an inherited disorder of motile cilia that causes impaired mucociliary clearance, chronic upper and lower respiratory disease, bronchiectasis, neonatal respiratory distress, laterality abnormalities, hearing problems, and infertility. Diagnosis uses a combination of phenotype, nasal nitric oxide, genetic testing, and ciliary structural or functional studies rather than a single screening test.
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Progressive dyspnea with 'crazy‑paving' on HRCT suggests pulmonary alveolar proteinosis (PAP).
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Pulmonary embolism ranges from incidental low-risk thromboembolism to obstructive shock. Diagnosis should combine pretest probability, D-dimer when appropriate, and definitive imaging. Treatment centers on anticoagulation, with urgent reperfusion or advanced intervention for hemodynamic collapse and carefully selected intermediate-risk deterioration.
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Acute pulmonary embolism requires simultaneous confirmation of diagnosis, hemodynamic risk assessment, and prompt anticoagulation when bleeding risk permits. The 2026 multisociety PE guideline favors low-molecular-weight heparin over unfractionated heparin when initial parenteral therapy is required and favors direct oral anticoagulants over vitamin K antagonists for eligible patients. Hemodynamic instability, right-ventricular failure, or clinical deterioration requires rapid evaluation for reperfusion the
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Use PESI/sPESI and Hestia criteria to identify low‑risk PE for outpatient therapy; ensure reliable anticoagulation access and follow‑up.
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Suspect PE with unexplained dyspnea, pleuritic pain, or syncope. Use Wells/Geneva and D-dimer to select imaging. Start anticoagulation when probability is high and bleeding risk acceptable. Thrombolysis or catheter therapy is reserved for massive PE (shock) and selected submassive cases with RV dysfunction and clinical deterioration.
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Classify PE as massive (hypotension/shock), submassive (RV dysfunction/biomarkers, normotensive), or low risk. Start anticoagulation promptly. Consider systemic thrombolysis for massive PE; catheter-directed thrombolysis/thrombectomy for selected submassive with clinical deterioration; assess bleeding risk.
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Use clinical scores, cardiac biomarkers, and echocardiography/CT to identify intermediate-high risk PE with right ventricular dysfunction; consider systemic thrombolysis or catheter-directed therapy in select deteriorating patients; anticoagulate all unless contraindicated.
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Pulmonary rehab improves dyspnea, exercise tolerance, and quality of life in COPD and other chronic lung diseases; refer after hospitalization and for symptomatic outpatients.
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Use 2019 ATS/IDSA severe criteria (major/minor) and consider MRSA/Pseudomonas risk factors. Start guideline‑concordant empiric antibiotics, add anti‑MRSA only with risk factors, and support with oxygenation and early mobilization; de‑escalate by cultures and viral testing.
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Spontaneous pneumothorax management depends on physiologic stability, symptoms, pneumothorax size, whether disease is primary or secondary, and the patient's ability to follow up. Stable minimally symptomatic primary events may be observed or managed conservatively, while symptomatic, enlarging, secondary, or unstable cases require pleural intervention and specialist input.
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Confirm with chest imaging; choose observation, needle aspiration, or chest drain based on size and symptoms; provide oxygen and counsel on recurrence and air travel.
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Severe, refractory asthma with impending respiratory failure. Use aggressive bronchodilation, systemic steroids, and controlled ventilation with permissive hypercapnia when intubated; consider ketamine, epinephrine, and MgSO₄ as adjuncts.
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Dynamic collapse of central airways due to weakness of cartilaginous support; diagnose with dynamic CT/bronchoscopy; manage with airway clearance, CPAP, stents, or tracheobronchoplasty.
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