Nature: fibrotic inflammation, exudative inflammation, mainly in the alveoli

Cause: Streptococcus pneumoniae infection Diffusion route: Diffusion to adjacent lung tissue through interalveolar pores or respiratory bronchioles

Pathological changes

complication

Nature: Purulent inflammation centered on bronchioles

Cause: It is related to the flora with weak resistance. It is easy to get sick when the body's resistance is reduced. (Often as a complication of certain diseases, such as post-measles pneumonia, post-operative pneumonia, aspiration pneumonia, and accumulation pneumonia)

Pathological changes

complication

Manifested as inflammation of the lung interstitium

The alveolar septa are significantly widened, the blood vessels within them are dilated and congested, the interstitium is edema, and lymphocytes and monocytes are infiltrated

Hyaline membrane formation: Serous exudate is concentrated into a thin layer of red-stained membrane attached to the inner surface of the alveoli.

Viral inclusion bodies can be seen in proliferating epithelial cells and multinucleated giant cells. (Diagnose based on)

The mucus and ciliary drainage system of the respiratory tract is damaged, the ciliated columnar epithelium is degenerated, necrotic and shed, and squamous epithelial metaplasia

Hyperplasia and hypertrophy of submucus glands and mucinous gland metaplasia of serous epithelium, leading to increased secretion of mucus

Infiltration of lymphocytes and plasma cells in the vessel wall

Smooth muscle rupture in the wall, atrophy of the cartilage, variable atrophy or ossification

Bronchiolitis and peribronchiolitis are the underlying causes of chronic obstructive emphysema

Charcot-Leyden crystals, the disintegration products of eosinophils, can be seen.

Mostly secondary to chronic bronchitis, bronchopneumonia and tuberculosis after measles and whooping cough

Destruction of supporting structures such as smooth muscle elastic fibers and cartilage in the wall

Formation of fibrous scarring, tissue traction and increase in intrabronchial pressure during coughing

The lower lobe of the left lung is most common

Mucosal epithelial hyperplasia accompanied by squamous metaplasia, which may lead to erosion and small ulcer formation

The glands, smooth muscles, elastic fibers and cartilage of the tube wall are destroyed to varying degrees, atrophy or disappear, and are replaced by granulation tissue or fibrous tissue

alveolar emphysema

barrel chest

chronic pulmonary heart disease

SiO2 is phagocytosed by macrophages

Lung disease continues to develop even after patients are removed from the silica dust working environment

Silicon nodules (characteristic lesions of the lungs)

diffuse fibrosis of lung tissue

tuberculosis

chronic pulmonary heart disease

Lung infections and obstructive emphysema

Asbestos has obvious carcinogenic effects

smoking

air pollution

molecular genetic changes

General type

Histological type

Direct spread: often directly invades the mediastinum, pericardium and surrounding tissues, and can directly invade the pleura

transfer

Alveolar capillary damage

Damage to pulmonary vascular endothelium and alveolar epithelium is the central link in the pathogenesis

Pulmonary interstitial capillaries are dilated and congested, and there is a large amount of protein-containing serous fluid in the alveolar space and pulmonary interstitium (pulmonary edema)

The components of the hyaline membrane are plasma proteins and necrotic alveolar epithelial debris.

Hyaline thrombi and leukocyte embolism are common in microvessels

All diseases that increase pulmonary circulatory resistance, the most common of which is chronic obstructive pulmonary disease (chronic bronchitis complicated by obstructive emphysema)

Bronchial asthma, bronchiectasis, pneumoconiosis, chronic fibrocavitary tuberculosis and interstitial pulmonary fibrosis, etc.

Amuscular arteriole muscularization

Muscular arteriole media hyperplasia and hyperplasia

Decreased number of capillaries in the alveolar septa

Mainly right ventricular disease

increased heart weight

Significant dilation of the pulmonary artery cone in the anterior wall of the right ventricle

The papillary muscles and meat columns in the right ventricle were significantly thickened.

Supraventricular ridge thickening

The thickness of the anterior right ventricular wall muscle layer 2cm below the pulmonary valve exceeds 5mm as the pathomorphological criterion for the diagnosis of cor pulmonale.