Questions to control the knowledge
1. Etiology, pathogenesis, morphological characteristic and outcome of acute and chronic gastritis.
2. Etiology, pathogenesis, morphological changes, complications and outcomes of appendicitis, ulcerous disease of the stomach and duodenum.
3. Etiology and pathogenesis, morphological characteristic and outcomes of basic diseases of the intestine.
Angina, tonsillitis, esophagitis, gastrobiopsy, gastritis, peptic ulcer, anabrosis of the stomach, acute ulcer of the stomach, chronic ulcer of the stomach, arrosive bleeding, perforation, peritonitis, hidden perforation, penetration, chlorine-hydropenic uremia, malignancy, enteritis, colitis, jejunitis, ileitis, enteropathy, intestinal fermentopathy, syndrome of disturbed adsorption, nonspecific ulcerative colitis, Kron's disease, appendicitis, mucocele, myxoglobulosis of the process.
DISEASES OF THE LIVER
There are various diseases of the liver. According to the origin they are classified into inherited and acquired, primary or secondary (as a result other diseases).
According to the morphological changes there are several groups of these diseases: hepatosis (when degeneration and necrosis in the hepatocytes prevail), hepatitis (when inflammation in the liver prevail), cirrhosis (when disregeneration is observed) and hepatic tumors.
The term hepatosis is used to describe degeneration and necrosis in the liver caused by microbiologic, toxic, circulatory or traumatic agents.
Hepatosis may be inherited and acquired. Inherited hepatosis develops in accumulation diseases or enzymopathy. Acquired hepatosis may be acute and chronic.
The massive necrosis is the most common acute hepatosis. The steatosis (fat hepatosis) is the most common chronic one.
Massive necrosis (toxic degeneration of the liver) is acute (rarely chronic) diseases characterized by massive necrosis of the hepatocytes with development of the hepatic failure.
Etiology. It is most commonly caused by viral hepatitis, drug or mushroom toxicity.
Pathology. There are 2 stages in this hepatosis.
1. Stage of yellow degeneration, when liver becomes enlarged, dense and yellow. Then it size increases, it consistency becomes flabby, capsule is shrunken. The cut surface is grey. Microscopically fat degeneration, necrosis and autolysis of hepatocytes are observed.
2. Stage of red degeneration is characterized by progressive reduction of liver size and mass. Macro-scopically the liver is red due to necrosis and autolysis of hepatocytes with appearance of plethoric blood vessels. Jaundice, hyperplasia of lymph nodes and spleen, numerous hemorrhages in the skin and mucous, necrosis of the renal epithelium, degenerative and necrotic changes in pancreas, myocardial, CNS are observed in the patients with massive necrosis of the liver.
Steatosis is a chronic disease which characterized by increase of fat amount in the cytoplasm of the hepatocytes.
Etiology of steatosis is similar to massive necrosis of the liver. But in this case pathologic agent has less toxicity and as a rule human compensatory and adaptive processes are higher.
Macroscopically the liver is enlarged, flabby. Fat drops are seen on the incision. The colour is yellow. This is called «gooses's» liver.
Microscopically—dust-like, small and large drop in the liver cells are observed.
Viral hepatitis is infection of the liver caused by hepatotropic viruses. There are 6 varieties of these viruses. Four of them are main ones causing distinct types of viral hepatitis:
1. Hepatitis A virus (HAV), causing a fecally-spread self-limiting disease.
2. Hepatitis B virus (HBV), causing aparenterally transmitted disease that may become chronic.
3. Hepatitis C virus (HCV), also termed non-A, non-B (NANB) hepatitis virus involved chiefly in transfusion-related hepatitis.
4. Hepatitis delta virus (HDV), which is sometimes associated as superinfection with hepatitis B infection.
Hepatitis A is responsible for 20—25% of clinical hepatitis in the developing countries of the world. The disease occurs in epidemic form as well as sporadically. The spread is related to close personal contact such as in overcrowding, poor hygiene and sanitation. An incubation period carries on 15—45 days.
Hepatitis B has a longer incubation period (30— 180 days) and is transmitted parenterally such as in recipients of blood and blood products, intravenous drugs, etc.
Pathology. The typical pathologic changes of hepatitis A, B and C are similar. The various clinical patterns and pathologic consequences of different hepatotropic viruses can be considered under the following headings:
1. Carrier state.
2. Acute hepatitis.
3. Chronic hepatitis.
4. Fulminant hepatitis (Submassive to massive necrosis).
Acute hepatitis clinically is divided into 4 phases: incubation period, pre-icteric phase, icteric phase and post-icteric phase. Macroscopically the liver is slightly enlarged, soft and greenish. Microscopically the changes are follows:
1. Hepatocellular injury: a) ballooning degeneration, b) appearance of the necrotic acidophilic mass, d) bridging necrosis is characterized by bands of necrosis linking portal tracts to central hepatic veins, one central hepatic vein to another, or a portal tract to another tract.
2. Inflammatory infiltration by mononuclear cells in the portal tracts.
3. Kupffer cell hyperplasia.
4. Cholestasis — biliary stasis.
5. Regeneration — as a result of necrosis of hepatocytes, there is lobular disarray.
Chronic hepatitis is a chronic inflammatory hepatic disease continuing for more than six months. It is divided into 2 types: persistent hepatitis and active (aggressive) hepatitis.
Two important factors which determine the vulnerability of a patient of viral hepatitis to develop chronicity are: the impaired immunity, and the extremes of age at which the infection is contracted. Chronic persistent hepatitis is a benign, selflimiting condition in which recovery from an attack of acute viral hepatitis is delayed beyond six months.
Pathology. The diagnosis of chronic persistent hepatitis is confirmed by needle biopsy of the liver which is invaluable in distinguishing it from more serious form of chronic active hepatitis.
Microscopically: 1) there is portal triaditis characterized by expansion of the portal tract by mononuclear inflammatory cells, 2) the lobular architecture of hepatic parenchyma is usually preserved, 3) there is absence of piecemeal necrosis.
Chronic active (aggressive) hepatitis is defined as a progressive form of chronic necrotising and fibrosing disease involving portal tracts as well as hepatic parenchyma.
Microscopically: 1) there is abundant mononuclear inflammatory cell infiltrate that is not confined to portal tracts, but the infiltrate spills out into the periportal hepatic parenchyma after eroding the limiting plate. There may be formation of lymphoid follicles, 2) two types of necrosis develop. They are piecemeal and bridging, 3) the collapsed reticulin framework left at the areas of bridging necrosis undergoes fibrous scarring, eventually progressing to cirrhosis.
The major cases of death are liver failure with hepatic encephalopathy, cirrhosis with hematemesis, and hepatocellular carcinoma.
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