Pulmonology
Showing 34 of 34 topics
A
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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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Bronchodilators (SABA ± ipratropium), systemic corticosteroids early, oxygen to SpO₂ 93–95%; consider IV magnesium for severe; assess peak flow and disposition.
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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.
C
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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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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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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.
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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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Short-acting bronchodilators, systemic steroids, and antibiotics when indicated; use controlled oxygen targeting SpO2 88–92%; consider noninvasive ventilation for hypercapnic respiratory failure.
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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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Short-acting bronchodilators, systemic steroids (e.g., prednisone 40 mg × 5 days), antibiotics if increased sputum purulence/volume or ventilation; target O₂ 88–92%; use NIV for hypercapnic respiratory failure.
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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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Use GOLD ABE assessment to guide inhaled therapy; emphasize smoking cessation, vaccinations, and pulmonary rehab; ICS use guided by exacerbation history and eosinophils.
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.
H
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Stabilize airway and position bleeding lung down; obtain CT angiography to localize source; bronchoscopy and bronchial artery embolization for significant 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.
I
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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.
M
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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.
P
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Tension pneumothorax is a clinical diagnosis requiring immediate decompression; management of stable pneumothorax depends on size and underlying lung disease.
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Progressive dyspnea with 'crazy‑paving' on HRCT suggests pulmonary alveolar proteinosis (PAP).
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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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Risk stratify with Wells and PERC; D-dimer for low/intermediate risk; confirm with CT pulmonary angiography; anticoagulate most patients; consider thrombolysis for massive PE with shock.
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Use clinical pretest tools (Wells/Geneva, PERC), D-dimer when appropriate, and CTPA to confirm; start anticoagulation when suspicion is high and bleeding risk acceptable; consider lysis for massive PE.
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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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Pulmonary rehab improves dyspnea, exercise tolerance, and quality of life in COPD and other chronic lung diseases; refer after hospitalization and for symptomatic outpatients.
S
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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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Primary small events may be observed with oxygen; large or symptomatic events need aspiration or chest tube; secondary pneumothorax favors admission and tube with oxygen.
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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.
T
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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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