Pneumonia Flashcards
Risk Factors for Aspiration
Branching tubular opacities may be seen, usually predominantly or exclusively involving upper lobes.
Allergic bronchopulmonary Aspergillosis
Nonspecific bilateral consolidations and reticular opacities.
Acute eosinophilic lung disease
Diffuse micronodular interstitial infiltrates. May see ground-glass densities in the lower or mid-lung fields. Bases spared.
Hypersensitivity pneumonitis (extrinsic allergic alveolitis)
Patchy multifocal alveolar infiltrates without effusion.
Organizing pneumonia (bronchiolitis obliterans organizing pneumonia [BOOP])
Bilateral peripheral, patchy, alveolar infiltrates and nodules.
Antinuclear cytoplasmic antibody (ANCA)–associated vasculitides: granulomatosis with polyangiitis (Wegener’s granulomatosis), Churg- Strauss syndrome
Normal for first 12–24 h. Bilateral
opacities with sparing of costophrenic angles. Minimal or no pleural effusion. “White lung” due to extensive consolidation.
Acute interstitial pneumonia
4 stages: bilateral hilar adenopathy; bilateral hilar adenopathy with reticulo- nodular pulmonary opacities; pulmonary opacities only; pulmonary fibrosis.
Sarcoidosis
Diffuse, bilateral, predominantly alveolar densities with sparing of the apices and costophrenic angles.
Anti–glomerular basement membrane antibody disease (Goodpasture’s syndrome)
Typically, bilateral interstitial infiltrates.
Drug-induced pneumonitis
Diffuse alveolar and interstitial infiltrates.
Chemical pneumonitis
Subtle hazy ground-glass densities to marked patchy infiltrates or homogenous consolidation. Air bronchograms are commonly present.
Radiation pneumonitis
Peripheral alveolar infiltrates. May see peripheral nodule or mass.
Alveolar cell carcinoma,
often called bronchiolar or bronchioloalveolar carcinoma
Interstitial or alveolar infiltrates. Diffuse infiltrates associated with hypoxia and need for intubation; focal infiltrates associated with coexistent pneumonia.
Leukemic infiltrates
Interstitial prominence, suggesting interstitial edema. Radiographic findings may be delayed by hours after trauma
Fat emboli
Focal or diffuse alveolar infiltrates.
Alveolar hemorrhage
Classically, patchy peripheral infiltrates that extend to the lateral lung margins suggest the diagnosis.
Acute respiratory distress syndrome
Autoimmune disease affecting the lungs and kidney due to autoantibodies to type IV collagen. Causes hemorrhagic interstitial pneumonitis.
Anti–glomerular basement membrane antibody disease (Goodpasture’s syndrome)
Systemic granulomatous disease of unknown etiology. Noncaseating pulmonary granulomas.
Sarcoidosis
Idiopathic or secondary (chemical agents). Three stages: interstitial edema spreads to alveoli with hemorrhage and hyaline membrane formation (exudative), organization of fibrinous exudate (proliferative), scarring and cyst formation and honey comb fibrosis (fibrotic).
Acute interstitial pneumonia
Both systemic vasculitides of small and medium-sized vessels of unknown origin. Wegener’s characterized by necrotizing granulomatous vasculitis with involvement of upper respiratory tract, lung parenchyma, and kidneys. Churg-Strauss disease is an allergic eosinophilic condition. Most are asthmatic.
Antinuclear cytoplasmic antibody (ANCA)–associated vasculitides: granulomatosis with polyangiitis (Wegener’s granulomatosis), Churg- Strauss syndrome
Inflammation of the bronchioles and surrounding tissues, leading to loss of the integrity of the bronchioles and organizing pneumonia without infection. Cryptogenic organizing pneumonia if immunocompromised or con- nective tissue diseases (e.g., SLE, rheumatoid arthritis, dermatomyositis).
Organizing pneumonia (bron- chiolitis obliterans organizing pneumonia [BOOP])
Cause unknown. Association with new or binge smoking. Eosinophils accumulate in distal airways and alveolar and interstitial spaces.
Acute eosinophilic lung disease
Symptoms occur 1–6 months after treat- ment: low-grade fever, cough, fullness in the chest.
Radiation pneumonitis
