<prompt> Sections of the lung from a patient with Wegeners granulomatosis who presents clinically with hemoptysis are most likely to showLarge, serpiginous necrosis with peripheral, palisading macrophagesAtypical lymphocytes invading blood vesselsGranulomatous inflammation of blood vessels with numerous eosinophilsGranulomatous inflammation of bronchi with Aspergillus  <response>: The pulmonary hemorrhagic syndromes are characterized by hemorrhage within the alveoli, which may be severe enough to produce hemoptysis. Several of these diseases are associated with blood vessel abnormalities, namely inflammation of the vessels angiitis. Necrotizing granulomatous aeritis affecting the upper and lower respiratory tracts and the kidneys is seen in patients with Wegeners granulomatosis. These areas of necrosis are characteristically large and serpiginous, and exhibit peripheral palisading of macrophages. In patients with Wegeners granulomatosis, the nose, sinus, antrum, and trachea often exhibit ulcerations. Originally the disease was lethal, but the prognosis is now much improved by immunosuppressive drugs. Eosinophilic granulomatous aeritis occurs in some patients with asthma who have eosinophilic pulmonary infiltrates; this abnormality is called Churg-Strauss syndrome. The areas of necrosis are not large and serpiginous as in Wegeners. Granulomatous inflammation centered around bronchi bronchocentric granulomatosis is often related to allergic pulmonary aspergillosis. Lymphomatoid granulomatosis is a disease of middleaged people that is characterized by an angiocentric and angioinvasive infiltrate of atypical lymphoid cells. Goodpastures syndrome is characterized by the development of a necrotizing hemorrhagic interstitial pneumonitis and rapidly progressing glomerulonephritis because of antibodies directed against the capillary basement membrane in alveolar septa and glomeruli. A linear IgG immunofluorescence pattern is present, which is characteristic of a type II hypersensitivity reaction. The prognosis for Goodpastures syndrome has been markedly improved by intensive plasma exchange to remove circulating anti-basement membrane antibodies and by immunosuppressive therapy to inhibit fuher antibody production Reference: Robbins Cotran Pathologic Basis of Disease, 9edition. 