Fibrous exudate contains a large amount of fibrin as the characteristic exudate. The large amount of fibrin exudate indicates that the capillaries and small veins are heavily damaged, the permeability is significantly increased, and a large amount of fibrinogen leaks out into the extravasation and is converted into fibrin by the action of tissue factors released from necrotic tissue. What can cause fibrinous exudate? Fibrinitis is mostly caused by certain bacterial toxins (e.g., toxins from Bacillus diphtheriae, Bacillus dysenteriae, and S. pneumoniae) or a variety of endogenous and exogenous toxins (e.g., urea and ascending mercury toxicity in uremic syndrome). It often occurs in the mucous membranes (pharynx, larynx, trachea, and intestines), plasma membranes (pleura, peritoneum, and pericardium), and lungs. When fibrinitis occurs in the plasma membrane and lungs, a small amount of fibrin exudates and can be dissolved and absorbed; a large amount of fibrin exudation is prone to mechanization and even occlusion of the plasma membrane cavity, causing organ dysfunction. For example, in fibrinous pericarditis, the two layers of the dirty wall of the pericardium rub against each other due to the heart’s movement, so that the fibrin exuded in the pericardial cavity is in the shape of villi on the surface of the pericardium, which is called “villi heart”. If the neutrophils exude less and the released protein hydrolase is relatively insufficient to completely dissolve and absorb the fibrin, it can be mechanized through the growth of granulation tissue and finally lead to fibrosis. If the disease occurs in the pleura, it causes thickening and adhesion of the pleura, and even occlusion of the pleural cavity. If it occurs in the lung, such as the gray liver-like stage of lobar pneumonia, a large amount of fibrin exudes from the alveolar cavity, causing solid lung changes.