Pathologic anatomy of the liver

Malformations. The absence of the liver (agenesia) is observed only on amorphous freaks. Hypoplasia of the liver is very rare, more often the underdevelopment of the one of the left lobe. Congenital hepatomegaly (significant increase in the weight of the body), and also double the liver that is a complete division into two shares are rare. Deformation P. with the protrusion of larger or smaller parts of the observed with congenital diaphragmatic hernia.
Metabolic disorders and degenerative changes. Violation of protein and water exchange in the form of reactions of hepatocytes to moderately damaging factors taken to signify the term "cloudy swelling" (synonym grainy, parenchymatous dystrophy). The reaction this is characterized by the increasing size of hepatocytes, the appearance of rough protein grain in the cytoplasm, reducing its basophilia, increase of water content. The kernel is not changed. Functional cell damage is minor.

Fig. 9. Hydropic degeneration of the liver. Sharply swollen hepatocytes with light cytoplasm and centrally located kernel - balloon cells.

Hydropic dystrophy - the growth processes inherent cloudy swelling, with a sharp increase of water in the cytoplasm. Water is stored first in endoplazmaticheskogo reticulum, then in the rest of the cytoplasm. Microscopically in hepatocytes sparse cytoplasm, nucleus is the Central, well-defined contours of cells. Part of hepatocytes, mainly in Central slices, turns into a balloon cells (Fig. 9). There pikes and Coriolis cores and necrosis balloon cells. Hydropic degeneration, the presence balloon cells characteristic of the epidemic of hepatitis.
Acidophilus dystrophy - loss cytoplasm normal basophilia due to decrease in the content of ribonucleoproteins; observed in viral infections and other conditions.

Fig. 10. Eosinophilic body of Councilmen (arrow), ousted from the liver of the plate in the sinusoids (h).

Acidophilus coagulation cytoplasm (hyalinosis its) further development of acidophilus dystrophy: the cytoplasm is sealed, it becomes homogeneous, intensively turns sour paints. The kernel, first picketine, later disappears and the cell is ejected from hepatic plate (Fig. 10) in tissue cracks and sine waves (eosinophilic of the bullock and bull of Councilmen). At partial acidophilus coagulation in rarefied cytoplasm marked homogeneous pink glybki (bullock, Mallory).
Disorders of fat metabolism obesity liver cells is fine, atomized and globular, replacing almost all of cytoplasm and a pushing the core to the periphery. Kuperovskaya cells also often contain oil droplets. Obesity centers slices observed anemia and hypoxia, with nutritional deficiency.
Obesity periphery slices - toxemia, various infectious diseases, metabolic disorders, cachexia, poisonings, and also with nutritional fat P. In the diffuse fatty liver significantly increased, yellow, in the context of figure slices completely erased.

Fig. 11. Globular obesity hepatocytes (oil extracted) (x 180).

Fig. 12. Fatty cysts in the liver, alcoholic (h).

The surface of the section of shale. Microscopically: almost each liver cell filled with fat, sine wave crushed; in some cases there is a globular obesity (Fig. 11), in others - atomized. Of lipid droplets merge adjacent cells formation of fatty cysts (Fig. 12).
Lipids (primary) - lipid abnormalities and urine of currency, expressed in the accumulation of lipids mainly in coppersky cells and histiocytes portal tract, transforming into a kind of foam cells (Gaucher disease, Niemann - pick disease, gargoylism, Hand - shyullera - Christian disease).
Disorders of carbohydrate metabolism in the liver are expressed excessive accumulation or depletion of hepatic cells with glycogen. Especially intensive deposition of glycogen in the liver cells observed in glycogenic disease. The decrease in the amount of glycogen in P. seen poisoning, severe infectious diseases, starvation, enhanced muscle. Congenital disorder of carbohydrate metabolism - see Galactosemia. Disorders of mineral metabolism iron is deposited in liver and coppersky cells in the form of granular pigment hemosiderin, generated by increased disintegration of the blood (hemolytic disease, pernicious anemia). P. gets rusty-brown. Hemosiderin is detected in the peripheral parts of the lobules or at considerable content in the entire slice. Increased accumulation of iron in P. and other bodies - see Hemochromatosis. Increased amount of copper in P. observed in newborns and infants, pregnant women, and in some diseases: hemochromatosis, the gepatolentikuliarnaya degeneration.
The lime deposits of salts in the liver are rare or in the form of small lime metastases (bone lesions, chronic kidney disease), or in the form of focal dystrophic calcification of gum, tuberculo, parasites, necrosis. There are also lime deposits in blood vessels and periportal the histiocytes with universal calcification.
Deposits of pigments in P. observed very often. Some of them hemoglobinemia pigments (a breakdown product of red blood cells) - hemosiderin, enomelanin, bile pigments, others not associated with hemoglobin: lipofuscin, melanin.

Fig. 13. Congestive plethora liver. Atrophy of the liver plates up to their complete disappearance. Central necrosis cloves (X150).

Necrosis P. distinguish depending on the localization of them in slices. Central necrosis can be caused by toxic factors, congestive plethora (Fig. 13), obstruction to blood flow in the portal vein and hepatic artery, allergic and other factors
Intermediaries necrosis occur when yellow fever, trauma. Peripheral, or periportal, necrosis usually combined and, possibly caused by an inflammation on the periphery of segments and in the portal tracts. Massive necrosis are characterized by the loss of almost all of liver cells in the slice with the involvement of large areas or all of the liver (see below).

Fig. 14. The front edge of the liver, with brown atrophy.

Atrophy of the liver cells may be the result of squeezing them (tumor, cyst), as well as General or local malnutrition. General atrophy P. accompanied by the accumulation in the cells of brown pigment lipofuscin (brown atrophy P.). P. reduced, consistency cushioned surface wrinkled; the front edge sharp, often leathery (Fig. 14), color - from light brown to dark brown. Liver cells are small, in the cytoplasm of them, especially in the Central parts of segments detected clusters of grain brown pigment - lipofuscin.
Circulatory disorders. Active hyperemia., in conditions of a pathology is observed mainly in acute infectious diseases (toxic paresis vascular).
Stagnant (passive) plethora liver is often a result of pressure rise in the system of the inferior Vena cava in connection with disorders of cardiac activity. P. increased, the capsule is tense, edge stupid, bed swollen gall bladder; on the cut - underlined figure slices. Microscopically: Central Vienna and the surrounding capillaries expanded filled with blood, liver plates apart, crushed, reticulana stroma saved. In subacute stagnant plethora P. reduced its sharp edge. On the cut - center slices of dark red, zapasy, peripherals - yellow-brown (Muscat liver). Microscopically: hepatic plate in the center of slices atrophied, sometimes to the complete disappearance (Fig. 13). Chronic congestive plethora P. accompanied by a stagnant induration (Muscat liver fibrosis). P. dense, capsule thickened, gallbladder bed sclerotic (fibrous). Microscopically: collagenase collaborating reticulin fibers in devastated (destruction of hepatocytes) centers slices; thickening and multiple sclerosis Central veins, portal fibrosis.

Fig. 15. Multiple ischemic heart attacks the liver, with nodular the nodosa (longitudinal section).

Changes P. and circulatory disorders in the system of the hepatic veins [the narrowing of the lumen, thrombosis, sclerosis, obliteration clearance one or more branches (see Chiari disease)] are expressed in stagnant plethora with atrophy and loss of liver cells (congestive heart attack P.). Changes P. at disorder of blood circulation in the system of portal vein depend on the state of the hepatic artery and heart. The closure of one of the branches of the portal vein with the weakening of the General circulation and pressure decrease in the hepatic artery causes a reverse flow of blood from the Central and hepatic veins, overflow extended capillaries, atrophy of hepatocytes and education sharply demarcated area P. wedge-shaped dark red colour, the tip of the wedge addressed to clogged branch of the portal vein (atrophic red heart attack, liver). Thrombosis extrahepatic branches of the portal vein changes in Petrograd can be completely absent with a good heart and if there are no changes in hepatic artery. Thrombosis intrahepatic branches of the portal vein and capillary observed at post-transfusion complications in eclampsia and accompanied by formation of hemorrhagic and symptoms of heart attacks. Disorders of blood circulation in the hepatic artery or its branches (embolism, thrombosis, periarteritis nodosa, cancer metastases etc) occurs ischemic necrosis of the liver tissue, which is called "blood anemic heart attack" P. (Fig. 15). Such attacks have the form of yellowish or yellowish-red-limited parts of irregular shape with bleeding on the periphery. In subsequent heart attack exposed fibrous transformation.
Subcapsular hemorrhage in the liver observed in infants during birth trauma, prematurity and asphyxia contribute to the formation of such haematomas; sometimes they reach large sizes, usually localized on the upper surface P. Gap hematomas with bleeding in the abdomen may cause death. Bleeding in P. arise if the injuries, strikes and other forms of trauma, accompanied by the loss of the liver tissue and localized sometimes in Central areas of Petrograd (Central hematoma) at preservation of the outer layers of the liver tissue. Haemorrhages from capillaries were observed in any disorders of blood circulation in Petrograd, infectious-toxic processes, with haemorrhagic diathesis.
Particularly acute disorders of blood circulation in the liver, with eclampsia, in which there is a combination of necrosis, thrombosis and hemorrhage, giving the surface of the cut P. very colorful view (printing. Fig. 1).

Fig. 1. Liver-eclampsia. Fig. 2. Solitary gum liver. Fig. 3. Pylephlebitis liver abscesses.
miliary gum liver
Fig. 4. Miliary gum liver.

Fig. 16. Swelling of the liver. Expansion perisinusoidal spaces.

When embolism P. emboli fall in Petrograd on the portal vein in the presence of blood clots in her roots by hepatic artery from the heart and aorta, hepatic veins retrograde from the right atrium. Swelling of the liver - vpotevanie in perisinusoidal space of a liquid with small protein (Fig. 16). Swelling caused by increased capillary permeability due to anoxia or increased venous pressure.
Inflammation of the liver may be agnouni and purulent. Nagnoenie inflammation is divided into diffuse and focal (see Hepatitis).
Purulent inflammation caused by P. arrival in Petrograd pyogenic infection, causing purulent fusion of the liver with the formation of abscesses (printing. Fig. 3), while diffuse soaking interstitial tissue P. with the emergence of a cellulitis. Ways of infection - hematogenous, through the extrahepatic bile duct or to contact (with neighboring organs). When hematogenous dissemination of the most frequent way - portal vein. Usually the source of abscesses P. serve ulcer processes in the gastrointestinal tract: dysenteric ulceration of the colon (bacillary dysentery and amebiasis ulcers), typhoid ulcers ileum, phlegmonously and gangrenous appendicitis, ulcerative proctitis, phlegmonously paraproctitis, stomach ulcer, duodenal ulcer (less)cellulitis of the stomach, chronic pancreatitis, chronic mesenteric lymphadenitis, purulent umbilici. Less frequent way of spreading pyogenic infection through the hepatic artery (in ulcerative endocarditis, septicopyemia of different origin). The most rare path - retrograde through the hepatic vein (septic processes in the brain, in the middle ear).
With the spread of infection through the extrahepatic bile ducts (of the gall bladder, intestines) develop intrahepatic purulent cholangitis and cholangitis abscesses P. (see Cholangitis, a pathological anatomy). When spread by touching the transition of a purulent process in P. happens with the neighbouring organs: from the pleura, the lung, pancreas, right kidney, stomach, duodenum. Purulent inflammation and liver abscesses occur when parasitic diseases P. (see below).

Fig. 17. Portal fibrosis cloves (silver impregnation method on Foot; h).

Fibrosis - increase in the amount of connective tissue in Petrograd - is due to collagenase preexisting damaged and collaborating argyrophilic fibers, and also due to tumor tissue structures of fibroblasts. Unlike cirrhosis (see), fibrosis causes no nodular regeneration P., no deep and diffuse restructuring P. and its vessels. Distribution fibrosis may be a focal or diffuse, localization or Central portal (Fig. 17). Liver fibrosis is the process of reparative that develops place infiltrates and granulomas of different origin, the site of the abscess, necrosis, gum etc.

Fig. 18. Giant multi-core simplasta for persistent hepatitis (X 300).

Fig. 19. Education pseudotubuli (1) of the liver cells (x 550).

Regeneration P. Nature of regenerative processes in paragraph (depends on the degree of damage. When scattered necrosis separate liver cells recovery is due to the multiplication by cardioceratinae and direct division. Vnutriportovaya regeneration, with significant damage to liver cells, while preserving the structure of the segments is also due cardioceratinae and direct cell division, however, differs from physiological regeneration of the fact that these develop hepatic plate thickness not one cell in health, in two cells and more (back to embryonic structure slices). Significantly increase the kernel liver cells, they become hyperchromic, increases the number of nucleoli; conventional dual-core cells; often observed the formation of simpleton (Fig. 18) as a result of the rapidly flowing regeneration of liver cells with incomplete direct division. If changes parenchyma are localized near the portal tract, causing destruction edge of the plate and breaking the link between gall precapillaries and bile ducts, on the periphery of the segments are formed epithelial bands and tubes, known as pseudotubuli. Some data evidence about their origin from liver cells (Fig. 19).
In the conditions of the death of the liver parenchyma group of liver cells, separated from the rest of the parenchyma or escaped from death, can regenerate gathering capillaries, reticular the stroma, forming the nodes of alignment. Sites regenerates arise when massive and submissive necrosis P. from the remaining parts of segments by tumors of the liver cells, reticular stroma, sinusoidal and even the portal tract, as well as from parts of the liver segments separated growing into a slice of walls connecting Central and portal vein. Numerous observations of fast recovery of the initial mass and function P. a person even when you remove the greater part of it. Regeneration occurs in the remaining part P. due to hyperplasia and hypertrophy of hepatocytes.
Hypertrophy of hepatocytes accompanied intracellular hyperplastic processes, improved energy opportunities cells. This includes a number of observations of other researchers have reason D. S. Sarkisov the highlight of regenerative processes in ultra structures of cells, in particular hepatocytes (1964), an independent kind of reparative process, which he called "intracellular" form of regeneration.
Food rich in protein, nucleic acids, and vitamin B12 are favorable for the regeneration processes. Of great importance is also the amount of blood circulating in the portal vein, and its pressure. Young age and some hormonal influences (extract of the thyroid gland, corticosteroids) stimulate the processes of regeneration. Factor, braking regenerative processes, is a stagnation of bile in the liver. The regulatory role both in physiological and reparative regeneration belongs CNS Experiments with parapente identify the regulatory role of humoral factors of growth factors liver tissue contained in the P.
Blood in the liver. When postgemorragicakih anemiah, common osteosclerosa, malignant anemia, under certain infectious diseases (for example, with scarlet fever, tuberculosis, poisoning) in Petrograd there are pockets of extramedullary hematopoiesis.
When leukemia observed in the liver leukemic infiltration of different intensity.
With chlamydia liver increased: it defines white-grey and nodular or stripped expansion.
Postmortem changes. Mapping histologic P. biopsies with the one in the autopsy reveals a number of changes related to the agonal period and with posthumous autolysis: hypoxia in the agonal period promotes protein accumulation of fluid in the spaces of the thesis; in the long agony of the glycogen stores quickly lost (detection of glycogen shows a fast death); in the post-mortem period due to the beginning of proteolysis may come cloudy swelling of the liver cells, disconnecktie hepatic plates, bad crashevenmore nucleus and cytoplasm, kariorexis. Post-mortem penetration in Petrograd microorganisms on the portal vein and gall ways comes cadaveric decomposition. P. flabby, the edge and the bottom surface of it, adjacent to the hinges thick guts, greenish-brown color because of the formation of iron sulfide.