Streptococcus pneumoniae

Reduced respiratory defenses

young adults

Fibrinitis

No destruction of lung tissue structure

Typical stage IV lesions are rarely seen clinically due to antibiotic intervention

Bacteria invade the alveoli and multiply → Type I allergic reaction → telangiectasia and increased permeability → serous exudation → fibrinogen exudation → spread through the inter-alveolar pores → involve the large lobes of the lungs

Congestion and edema period (days 1 to 2)

Red hepatoid degeneration stage (3rd to 4th day)

Gray liver-like transformation stage (days 5 to 6)

Dissolution period (after 1 week)

Lung fleshy change/organizing pneumonia

Pleural hypertrophy and adhesions

Lung abscess and empyema

Sepsis and Sepsis

septic shock

Acute suppurative inflammation of pulmonary lobules

children, elderly

It is often a complication of certain diseases, such as post-measles pneumonia, post-operative pneumonia, aspiration pneumonia, accumulation pneumonia, etc.

under the mirror

naked eye

clinical

respiratory failure

heart failure

Lung abscess and empyema

bronchiectasis

There is exudate in the alveolar cavity

Hyaline membrane formation (influenza, measles, and adenovirus)

Bronchial epithelium and alveolar epithelium fuse into multinucleated giant cells

Viral inclusion bodies—the first diagnostic basis

Often segmentally distributed, with interstitial edema and large amounts of lymphocytes, monocytes and plasma cells infiltrating

More common in lower leaves

Mucosal damage

Smoke stimulates bronchospasm

spoil

ooze

hyperplasia

Mucous exudate is visible on the mucosal surface

The lumen of the tube is narrowed and the tube wall becomes hard

Bronchopneumonia

bronchiectasis

Central alveolar type (most common)—respiratory bronchioles

Periacinar type - alveolar duct alveolar sac

Holoacinar type—all

Broken ribs, severe coughing

Paracicatricial emphysema, compensated emphysema, senile emphysema

Alveoli expand, the alveolar septa break, and the expanded alveoli fuse into larger cysts

Decreased pulmonary capillary atrophy

Fibrous intimal thickening of pulmonary arterioles

The lungs are enlarged in size, gray in color, lack elasticity, and have a spongy cut surface.

Cellular silicon nodules—macrophages proliferate and aggregate, and the essence is granuloma

Fibrous silica nodules—composed of a large number of fibroblasts and collagen fibers

Hyalinized silica nodules—hyalinous degeneration of collagen fibers

Hilar lymph node enlargement and less silicon nodules

There is no significant change in lung weight, volume, and hardness.

Silicon nodules may form in the pleura, but the thickening is not obvious

The lesions do not exceed 1/3 of the whole lung, mainly in the middle and lower lobes near the hilus. The number of silicon nodules increases and the lungs are significantly fibrotic.

Increased lung weight, volume, and stiffness

pleural thickening

Silicon nodules are densely fused into lumps, hilar lymph nodes are swollen, eggshell-like calcification can be seen, and the lung tissue around the lesion is emphysema or atelectasis.

The weight and hardness of the lungs increase significantly, and the whole lung sinks when it enters the water.

Brachybranchs in COPD (most common)

Pneumoconiosis, chronic fibrocavitary tuberculosis, diffuse interstitial pulmonary fibrosis

Pulmonary hypertension → increased right ventricular load → right ventricular hypertrophy and dilation

Reduced number of capillaries in the alveolar walls

Muscular arteriole media hyperplasia and hyperplasia

Amuscular arteriole muscularization

Pulmonary arteritis and arteriolar thrombosis

Malignant transformation of bronchial mucosal epithelium through squamous metaplasia

Older man, history of smoking

bronchial glands

Women, mostly with a history of passive smoking

The alveolar tissue is not damaged, but the inside is covered with cancer cells

Neuroendocrine function of bronchial epithelial cells

Cancer cells are small and form a false rosette-like structure around small blood vessels.