Bacterial 1. lobar pneumonia (lobarpneumonia) Congestive edema phase Gross: enlarged lobes, increased weight, dark red, wet and soft. Microscopically: alveolar septal capillaries dilated and congested, plasma exudate in the alveolar cavity, small amount of RBC, neutrophils, macrophages, and detectable bacteria. Coughing white foamy sputum, X-ray shows a large faint uniform shadow, auscultation is wet rhotic sound. Red hepatomegaly stage gross: enlarged lung lobes, increased weight, dark red, solid texture like liver, rough granular cut surface. Microscopically: the alveolar interstitial capillaries are dilated and congested, and the alveolar cavity is filled with fibrin and a large number of RBCs, a few neutrophils, and macrophages. The fibrin could be connected to the adjacent alveolar fibrin network through the alveolar interstitial pores. Bacteria can be detected in large amounts in the exudate. Coughing up rust-colored sputum, X-ray shows large dense shadows. Dyspnea and cyanosis are most obvious at this stage. It may spread to the pleura and cause fibrinous pleurisy. Gray hepatomegaly stage gross: enlarged lung lobes, grayish white, solid as liver, rough granular in cut surface. Microscopically: capillary compression, decongestion, increased fibrin in the alveolar cavity, more inter-alveolar pore connections are seen, a large number of neutrophils are seen, RBCs are rare. ab is produced, bacteria are not easily detected. Cough mucopurulent sputum, X-ray shows large dense shadow, dyspnea, cyanosis, hypoxia symptoms relief. The solid lesions disappear and become soft in texture during the dissolution and dissipation phase. Neutrophils in the alveolar cavity become necrotic and release protein hydrolase to dissolve fibrin. The alveoli regain their normal structure. X-rays show gradual dissipation of the shadow. Complications Pulmonary sarcoidosis: also known as mechanized pneumonia. Due to less exudation of neutrophils, insufficient protein hydrolase is released and fibrin is incompletely lysed and replaced by granulation tissue for mechanization. It appears as brown flesh-like. (1) Pleural hypertrophy and adhesions: caused by incomplete fibrin absorption after the occurrence of fibrinous pleurisy. (2) Lung abscess and abscess chest (3) Sepsis and sepsis (4) Infectious shock 2. lobar pneumonia Acute purulent inflammation, with the lung lobules as the unit, scattered in the center of the fine bronchi. Also known as bronchopneumonia. Pathological changes Gross: scattered distribution of solid grayish-yellow or dark red lesions, varying in size, about 0.5-1 cm, with fine bronchial cross-sections visible in the center of the lesions. The lesions may fuse and generally do not invade the pleura. Microscopically: the mucosa of the fine bronchus is congested, edematous, with mucus exudate on the surface, and the lumen and surrounding alveolar lumen are filled with neutrophils, a few RBCs, and detached alveolar epithelium. The surrounding lung tissue is congested and may have plasma exudate, and some alveoli appear to be compensated for emphysema. Mucopurulent or purulent sputum is coughed, and X-ray shows patchy shadows with high density. It can be complicated by respiratory insufficiency, heart failure, sepsis, lung abscess, and abscess chest. The risk is greater than that of lobar pneumonia. 3, viral pneumonia is often caused by the downward spread of upper respiratory virus. Pathological changes are mainly inflammation of the interstitial lung. Interstitial congestion and edema, lymphocyte and monocyte infiltration, and marked widening of the lobular septa and alveolar walls. The lumen is inflated or contains a small amount of plasma and exfoliated epithelium. There was hyaline membrane formation on the inner surface. Viral inclusion bodies are seen in epithelial cells and multinucleated giant cells.