Histology and Explanation of Bronchopneumonia (Lobular pneumonia)

Bronchopneumonia (Lobular pneumonia) is an acute exudative inflammation of the lungs characterised by foci of consolidation surrounded by normal parenchyma. Usually, bronchopneumonia affects one or more lobes and is bilateral.


Bronchopneumonia : focus of inflammatory condensation centred by a bronchiole with acute bronchiolitis (suppurative exudate in the lumen and parietal inflammation). Alveolar lumens surrounding the bronchia are filled with neutrophils ("leukocytic alveolitis"). Inflammatory foci are separated by normal, aerated parenchyma.

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Histology and Explanation of Lobar pneumonia (leukocytic alveolitis)

Lobar pneumonia is an acute exudative inflammation of an entire pulmonary lobe, produced in 95 % of cases by Streptococcus pneumoniae (pneumococci).

If not treated, lobar pneumonia evolves in four stages :

* Congestion (first 2 days)
* Red hepatisation (fibrinous alveolitis) (2nd to 4th day)
* Grey hepatisation (leukocytic alveolitis) (4th to 8th day)
* Resolution (after 8th day)


Leukocytic alveolitis is the 3rd phase of the lobar pneumonia. Alveolar lumens are filled with leukocytic (suppurative) exudate (neutrophils and macrophages, in order to remove the fibrin). Alveolar walls are thickened due to capillary congestion and edema.

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Histology and Explanation of Ischemic fibrosis of myocardium (diffuse ventricular myocardial fibrosis)

Ischemic Heart Disease is the result of an imbalance between adequate oxygen supply to the myocardium and its' necessities, due to total or partial obstruction of the coronary arteries. Depending on the degree of coronary artery insufficiency and the rapidity of onset, ischemic heart disease might be acute or chronic. These include four anatomical and clinical entities :

* Chronic ischemic heart disease
o stabile angina pectoralis
* Acute ischemic heart disease
o unstabile angina pectoralis
o myocardium infarct
o sudden death

Etiology : coronary artery atherosclerosis (90 %), inflammation of coronary arteries (systemic lupus erythematosus, polyarteritis nodosa), tromboembolism (bacterial endocarditis), spasm, arrhythmia (e.g. : tachycardia in hyperthyroidism, anemia, intoxication, infections), syphilis.


Ischemic fibrosis of the myocardium (diffuse ventricular myocardial fibrosis) represents the morphological change in chronic ischemic heart disease. Clinically, may be silent or producing stabile angina pectoralis leading to congestive heart failure.

Pathology : during a diffuse coronary atherosclerosis, in which the stenosis is less than 70 % of the artery cross-section (this means, it is not enough to produce an infarct), some myocardial cells or small groups of cells, are inadequately supplied with blood (oxygen). These myocardial cells will become atrophic and necrotic. With time, the small areas of necrosis will be replaced by fibrosis.

At gross examination, the heart varies in size : normal, small (atrophic) or large (compensatory hypertrophy), dilated (in patients with congestive heart failure). Endocardium and pericardium are normal or with white plaques, corresponding to fibrosis. On section surface, the myocardium has a "tiger-spotted" aspect, due to intermingled normal myocardium (red) and fibrosis (ivory, white). Large areas of scarring might be visible if the patient had a previous infarct.

Microscopically, one can see small fibrous scars (with collagen fibers) surrounding viable myocardial cells (fibers), normal, with atrophy or with hypertrophy ("tiger-spotted" aspect). Also, might be present focal myocytolisis : isolated "empty" myocardial cells (no nuclei, no striations, eosinophilic cytoplasm) - ischemic necrosis.



Diffuse myocardial fibrosis (Ischemic fibrosis of the myocardium) (Simionescu trichromic staining, ob. x4) : myocardial cells (red) intermingled with collagen-rich fibrosis (blue) which completely replaced the necrotic myocardial cells. Capillaries (with yellow-orange red blood cells) within fibrosis remained from repair by connective tissue process.

Diffuse myocardial fibrosis (Ischemic fibrosis of the myocardium) (Simionescu trichromic staining, ob. x10) : viable myocardial cells (red) with nuclei (brown) surrounded by collagen-rich fibrosis (blue). Fibrosis completely replaced the necrotic myocardial cells. Capillaries (with yellow-orange red blood cells) within fibrosis remained from repair by connective tissue process.

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Histology and Explanation of Acute viral myocarditis

Myocarditis is an inflammation of the myocardium. Acute viral myocarditis is produced most often by Coxsackie B virus and echovisuses. Myocardial interstitium presents an abundant edema and inflammatory infiltrate, mainly with lymphocytes and macrophages. Focal destruction of myocytes may be present, generating loss of contractile function of the myocardium.

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Histology and explanation of Recent coronary thrombosis

Thrombosis : recent thrombus in a coronary artery (branch in the epicardium) : The arterial lumen is completely obstructed by a recent thrombus - fibrin network (pink) containing red blood cells and platelets. The thrombus is developed on an ulcerated atherosclerotic (fibrous) plaque and is adherent to the arterial wall.

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Histology and Explanation of Coronary atherosclerosis - the fibrous plaque with calcification

Coronary artery with atherosclerosis (fibrous plaque). The atheromatous fibrous plaque is localized in the intima of the artery, beneath the endothelium, producing the thickening of the wall and, secondary, the narrowing of the lumen and the atrophy of the muscular layer by compression. The fibrous plaque contains collagen fibres (eosinophilic), precipitates of calcium (hematoxylinophilic) and rare lipid-laden cells.

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Histology and Explanation of Acute myocardial infarct

Myocardial infarct - circumscribed area of ischemic necrosis - coagulative necrosis. In the first 12 - 24 hours, myocardial fibers are still well delineated, with intense eosinophilic (pink) cytoplasm, but lost their transversal striations and the nucleus (left side of the picture). Notice a few myocardial fibers showing hypertrophy (increased size of the fiber, irregular shape of the nuclei).


Recent myocardial infarct (in the first 12 - 24 hours): myocardial fibers are still well delineated, with intense eosinophilic (pink) cytoplasm, but lost their transversal striations and the nucleus. The interstitial space may be infiltrated with red blood cells. Make the distinction between interstitial leucocytes (small, outside the myocardial fibers) and the myocardial nucleus (should be central and unique, but is absent here).



Recent myocardial infarct (first 24 hours) (detail).

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Histology and Explanation of Hemorrhagic infarct lung

Pulmonary infarct (hemorrhagic infarct of the lung) is an area of ischemic necrosis produced by venous thrombosis on a background of passive congestion of lung. In infarct area, alveolar walls, vascular walls and bronchioles are necrotic. They appear eosinophilic (pink), homogenous, lacking the nuclei, but keep their shapes - "structured necrosis". Alveolar lumens from infarcted area are invaded by red blood cells - hemorrhagic infarct (red).



Pulmonary infarct in an area of passive congestion. The hemosiderin-laden macrophages present inside the alveolar lumen are witnesses of pre-existent passive congestion.




Pulmonary (hemorrhagic) infarct produced by venous thrombosis.

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Histology and Explanation of Recent coronary thrombosis

Thrombosis : recent thrombus in a coronary artery (branch in the epicardium) : The arterial lumen is completely obstructed by a recent thrombus - fibrin network (pink) containing red blood cells and platelets. The thrombus is developed on an ulcerated atherosclerotic (fibrous) plaque and is adherent to the arterial wall.

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Histology and Explanation of Passive congestion of the liver

Hyperemia (congestion) represents the increase of blood in a territory, due to dilatation of small vessels. According to the mechanism, it may be active or passive.

Active hyperemia (congestion) is a result of arteriolar distension (e.g., skeletal muscle activity, inflammation, local neuro-vegetative reaction).
Passive hyperemia (congestion), also termed stasis, is a consequence of an impaired venous drainage (heart failure, compression or obstruction of veins), followed by dilatation of venules and capillaries.

Passive congestion (Passive hyperemia) (liver)



Hyperemia (congestion) represents the increase of blood in a territory, due to dilatation of small vessels. According to the mechanism, it may be active or passive.

Active hyperemia (congestion) is a result of arteriolar distension (e.g., skeletal muscle activity, inflammation, local neuro-vegetative reaction).
Passive hyperemia (congestion), also termed stasis, is a consequence of an impaired venous drainage (heart failure, compression or obstruction of veins), followed by dilatation of venules and capillaries.
Passive congestion (Passive hyperemia) (liver)

Passive congestion of the liver. Central veins, spaces of Disse and central vascular sinusoids are dilated, compressing the hepatocytes which are atrophied and, with progression, will necrotize - central hemorrhagic necrosis (compression and/or ischemic mechanism). Mediolobular hepatocytes may present fatty change (hypoxic mechanism); periportal hepatocytes are normal.

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Histology and Explanation of Coronary atherosclerosis - fibro fatty plaque

Coronary artery with atherosclerosis (fibro-lipid or fibro-fatty plaque). The atheromatous fibro-fatty plaque is characterized by the accumulation of lipids in the intima of the arteries, narrowing the lumen and compressing the muscular layer. Beneath the endothelium it has a "fibrous cap" covering the atheromatous "core" of the plaque, which consists in cholesterol, cholesterol esters, fibrin, lipid-laden cells (macrophages and smooth muscle cells), proteoglycans, collagen, elastin and cellular debris. The cholesterol crystals form empty, needle-like clefts. At the periphery of the plaque are "foamy" cells and capillaries.

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Histology and explanation of Passive congestion (Passive hyperemia) (lung)

Hyperemia (congestion) represents the increase of blood in a territory, due to dilatation of small vessels. According to the mechanism, it may be active or passive.

Active hyperemia (congestion) is a result of arteriolar distension (e.g., skeletal muscle activity, inflammation, local neuro-vegetative reaction).
Passive hyperemia (congestion), also termed stasis, is a consequence of an impaired venous drainage (heart failure, compression or obstruction of veins), followed by dilatation of venules and capillaries.



Etiology of passive congestion of the lung : chronic left heart (ventricular) failure.
Alveolar walls are thickened due to dilated capillaries. Alveolar lumens are filled with transudate (amorphous, eosinophilic and homogenous) which replaced the air, red blood cells (microhemorrhages) and hemosiderin-laden macrophages (also called "heart failure cells").

With progression, interstitial fibrosis may appear and, together with hemosiderin pigmentation, generates the aspect of "brown induration". Extensive fibrosis leads to intrapulmonary hypertension.

Passive congestion of the lung. Hemosiderin-laden macrophages contain in cytoplasm hemosiderin pigment (brown, granular), resulted from destruction of red blood cells in alveolar lumen.

Perls reaction is useful in distinguishing hemosiderin pigment from anthracotic (carbon) pigment : trivalent iron from hemosiderin stains in green-blue, while anthracotic pigment remains dark-brown and is mainly located perivascular.

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Histology and Explanation of Pulmonary Edema

Edema represents the accumulation of excess liquid in the interstitial (extracellular) spaces of a tissue or in pre-existing cavities. It may affect any organ, but most often it appears in : subcutaneous tissues, lung and brain.
According to the etiology, edema may be localized (in inflammation or in impaired venous drainage) or systemic (in right heart failure or in nephrotic syndrome). A generalized and severe edema is called anasarca.
Accumulation of transudate or non-inflammatory fluid (effusions) in body cavities :

* Peritoneal cavity - ascites
* Pleural cavity - hydrothorax
* Pericardial cavity - hydropericardium

Pulmonary edema

Etiology of pulmonary edema : acute left heart (ventricular) failure, pulmonary failure in syndrome of adult respiratory distress, pulmonary infections and hypersensitivity reactions.

Pulmonary edema. Alveolar walls are thickened due to acute distention of capillaries and interstitial edema. Alveolar lumen is filled with transudate (pale-eosinophilic, finely granular), a liquid which replaces the air.

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Histology and Explanation of Benign microcystic teratoma of the ovary

Teratoma is a tumor which arises from tutipotent germinal cells. Frequently, it is localized in gonads (testis, ovary). It contains a variety of tissues (derived from one, two or three embryonic cell layers - mesoderm, endoderm or ectoderm), tissues which normally are foreign to the site of growth.

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Histology and Explanation of leiomyoma Uterus

Uterine leiomyoma is a benign connective tissue tumor of the smooth muscle cells of the myometrium. Tumor cells resemble normal cells (uniform, elongated, spindle-shaped, with a cigar-shaped nucleus) and form bundles with different directions (whirled). The tumor may present areas of fibrosis, calcification and/or hemorrhage. The tumor is well circumscribed, but not encapsulated.

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Histology and explanation of Cavernous hemangioma liver

Cavernous hemangioma is a benign connective tissue tumor resulted from endothelial cells proliferation. It is a non-encapsulated tumor, with an infiltrative, lobular growing. The tumor consists in large (cavernous) spaces, lined by tumor endothelial cells (which appear very similar to normal cells). These interconnected spaces are filled with blood and separated by a fibrous tissue.

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Histology and Explanation of chondroma

Chondroma is a benign cartilaginous tumor, encapsulated, with a lobular growing pattern. Tumor cells (chondrocytes, cartilaginous cells) resemble normal cells and produce the cartilaginous matrix (amorphous, basophilic material). Characteristic are the vascular axes within the tumor, which make the distinction with normal hyaline cartilage.

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Histology and explanation of Carcinoma metastasis (lymph node)

Lymph node with carcinoma metastasis : clusters of tumor cells, atypical, with carcinomatous character.

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Histology and explanation of Renal cell carcinoma (Grawitz tumor)

Renal clear cell carcinoma (Grawitz tumor) is a malignant epithelial tumor resulted from proliferation of tubule cells. Tumor cells form cords, papillae, tubules or nests, and are atypical, polygonal and large. Because these cells accumulate glycogen and lipids, their cytoplasm appears "clear", lipid-laden, the nuclei remain in the middle of the cells, and the cellular membrane is evident. Some cells may be smaller, with eosinophilic cytoplasm, resembling normal tubular cells. The stroma is reduced, but well vascularized. The tumor grows in large front, compressing the surrounding parenchyma, producing a pseudocapsule.

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Histology and explanation of Poorly differentiated hepatocellular carcinoma

Hepatocellular carcinoma, poorly differentiated (photo - upper right), developed on liver cirrhosis. This malignant epithelial tumor consists in tumor cells, discohesive, pleomorphic, anaplastic, giant. The tumor has a scant stroma and central necrosis because of the poor vascularization. In well differentiated forms, tumor cells resemble hepatocytes, form cords and nests, and may contain bile pigment in cytoplasm.

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