Medical Lung Flashcards
Summary of the revised guidelines for grading lung transplant rejection
A1
Minimal acute cellular rejection
A sparse perivascular mononuclear infiltrate is present, less than 3 cells thick.
A2
Mild acute cellular rejection
The perivascular mononuclear infiltrate is >3 cells thick, but remains associated with the perivascular interstitium without involvement or expansion of adjacent alveolar septae. Rare eos may be seen.
A3
Moderate acute cellular rejection
The perivascular mononuclear infiltrate (with plasmacytoid lymphocytes and occasional eosinophils) expands the perivascular interstitium and extends into the alveolar septa. This may result in a perivascular “interstitial pneumonitis.” PMNs may be present.
A4
Severe acute cellular rejection
Mononuclear and eosinophilic infiltrate extends into well into the interstitial space, and organization/active fibrosis may be identified. PMNs may be present.
B1R
Low grade lymphocytic bronchiolitis
Mononuclear cells within the bronchiolar sub-mucosa, but not invading the mucosa
B2R
High grade lymphocytic bronchiolitis
Mononuclear cells invading the mucosa
Bronchiolitis obliterans (C1)
Our role in chronic airway rejection is simply to say whether or not the finding of bronchiolitis obliterans is present or not (1 or 0). The grading of chronic rejection is best done clinically by measuring FEV1.
Accelerated graft atherosclerosis (D1)
This is considered a manifestation of chronic humoral rejection – effectively increased predisposition to atherosclerosis in transplanted pulmonary vasculature. It is reported as simply present (D1) or absent (D0).
Stages of humoral rejection
Organizing pneumonia
Squamous metaplasia of the alveolar lining following acute lung injury
Medical definition of acute lung injury and acute respiratory distress syndrome
- Physiologic evidence of impaired diffusion barrier
* ALI: PaO2 / FiO2 =/< 300
* ARDS: PaO2 / FiO2 =/< 200 - Lung infiltrate on CXR
- PCWP < 18 (ie, not due to heart failure)
Proliferative phase of diffuse alveolar damage with fibroblastic plugs
It can be hard to tell where the alveolar space is – look for the reactive pneumocytes to guide you.
Amiodarone lung toxicity
The hallmark feature is foamy macrophages AND foamy type II pneumocytes with very fine cytoplasmic vacuoles
Bronchiolitis obliterans
Aka constrictive bronchitis
Note the inflammation and the thickening of the fibrous tissue immediately underneath the basement membrane.
A “Masson body” in organizing pneumonia.
One fibroblastic plug has infiltrated through one of the pores of Kohn to an adjacent alveolus.
Pulmonary smooth muscle hyperplasia in chronic lung injury.
Sometimes called “pulmonary cirrhosis”
Chronic eosinophilic pneumonia
Occurs mostly in middle-aged women, often accompanied by asthma or allergic rhinitis.
The radiographic appearance has been likened to the “radiographic negative of pulmonary edema,” with bilateral subpleural infiltrates with poorly defined margins. Lesions may be “migratory.”
Histologically, very similar to acute eosinophilic pneumonia – the difference is often made based on clinical features. Dense infiltrate of eosinophils and macrophages in alveolar lumens, sometimes with eosinophilic microbascesses. Mild interstitial pneumonia with accumulation of fibrin in alveolar spaces accompany this, often with striking type II pneumocyte atypia.
Major ddx are acute eosinophilic pneumonia and eosinophilic granulomatosis with polyangiitis.
Acute eosinophilic pneumonia
Note the eosinophils within the alveolar spaces.
Hyaline membranes and intra-alveolar fibrin deposition may also be seen.
This is an especially important diagnosis to recognize because these patients respond very well to corticosteroids.
Granulomatosis and polyangiitis
Characterized by necrotizing granulomas and multinucleated giant cells involving the adventitia and media of small and middle-sized vessels
Associated with anti-PR3 ANCA (c-ANCA).
Microscopic polyangiitis
A vasculitis restricted to arterioles, venules, and capillaries.
The principal histologic manifestation of MP is alveolar hemorrhage with capillaritis. This may sometimes spill into the alveoli, simulating an acute bronchopneumonia. The intra-alveolar hemorrhage is often admixed with fibrin and hemosiderin-laden macrophages.
In the healing phase, a BOOP pattern may be present.
Associated with anti-MPO ANCA (p-ANCA).
Eosinophilic granulomatosis with polyangiitis
Distinctive syndrome of vasculitis, eosinophilic pneumonia, and granulomas.
Associated with anti-MPO ANCA (p-ANCA), but peripheral blood eosinophilia is really the most common lab association.
Behcet-associated pulmonary vasculitis
Lesions are characterized by a necrotizing vasculitis that involves arteries, veins, and capillaries. The inflammatory infiltrate is predominantly lymphocytic.
Resolving lesions may show recanalized thrombi and perivascular adventitial fibrosis. Hemorrhage with severe hemoptysis may result as a complication.
The diagnosis is made by fulfilling the clinical requirements, including oral aphtous ulcers occuring at a certain frequency. In addition, there should be absence of inflammatory bowel disease or other collagen-vascular disorder.
Classically Behcet is an ANCA-negative vasculitis, however occasional cases of p-ANCA-associated Behcet have been identified.
In a child with arthritic pain, Cr elevation, and purpura.
Henoch-Schonlein Purpura (IgA Vasculitis)
The pathologic findings in the lung are characterized by intra-alveolar hemorrhage and neutrophilic capillaritis, very similar to those of MPA. The capillaritis may be subtle and masked by the capillary congestion.
The findings are nonspecific and really require clinical history and laboratory studies to make the diagnosis – this is not a primary diagnosis for pathology, but may be brought up on a differential.
Giant cell arteritis
This disease is associated with upper respiratory tract symptoms and lower respiratory tract involvement only in a minority of cases.
Pulmonary involvement is usually bilateral resulting in interstitial opacities or small nodules. The disease involves principally the large and medium pulmonary arteries. The damage is centered principally in the elastic lamina of the vessel, which is destroyed by chronic inflammation admixed with multinucleated giant cells.
Unlike other pulmonary vasculidites, giant cell arteritis is distinguished by the lesions being confined to the vessel wall without involvement of the surrounding lung parenchyma.
