166. Precancer and colon cancer: predisposing factors, pathological anatomy. Forms of growth, features of colon cancer metastasis, complications, outcomes, clinical significance.

Precancerous diseases of the colon are: polyps (especially adenomatous), diffuse polyposis, ulcerative colitis, Crohn's disease, previously transferred tumors of the colon, breast, genitals.

Predisposing factors: nutrition, benign tumors, chronic colon diseases, a history of malignant tumors. (The predominance of protein and fatty foods, low fiber content contributes to the formation of polycyclic hydrocarbons, the development of microflora, and the formation of secondary bile acids. This increases the time of contact of carcinogens with the intestinal epithelium. The predominance of food with a high fiber content in the diet contributes to the timely emptying of the intestine, reduces the concentration of carcinogenic agents in it, prevents the development of bacteria and the accumulation of toxic metabolic products involved in the mechanism of malignant cell transformation).

Pathological anatomy:

The intestine at the site of the tumor is expanded, the folds are smoothed, the mucosa is thinned, and there is atrophy below the tumor. The tumor itself rises above the mucous membrane, its surface is lumpy, flabby, has no boundaries, which indicates the malignancy of the tumor.

Forms of growth:

exophytic tumors growing into the lumen of the intestine — plaque-like, polypous and large-lobed;

endophytic tumors, often ulcerating ulcerative and diffuse infiltrative cancer, usually narrowing the lumen of the intestine;

a combination of exo- and endophytic growth (transitional) and ulceration, most often - saucer-shaped cancer.

Metastasizes: Lymphogenously: pararectal lymph nodes and lymph nodes of the pelvis, then mesenteric lymph nodes. Hematogenic-liver, lungs

A complication:

1.Intestinal bleeding

2. Germination into neighboring organs

3. Intestinal obstruction

4. Cancerous cachexia

5. Perforation of the intestine with the development of peritonitis

Outcomes:

Surgical treatment in combination with chemotherapy, death from complications related to metastases and the tumor itself (For example, death from poisoning by toxins of nerve centers and the heart with intestinal obstruction caused by the tumor; anemia; cachexia).

Clinic:

Symptoms of intestinal discomfort, pain, signs of impaired patency, the appearance of blood in the stool, anemia, signs of intoxication, the detection of a tumor is possible with a palpatory examination of the intestine

167. Massive liver necrosis: causes, macro- and microscopic characteristics, complications, outcomes.

Massive liver necrosis is an acute, rarely chronic disease characterized by progressive massive liver necrosis and liver failure.

Causes: Massive liver necrosis often occurs with intoxication:

– exogenous — poisoning with substandard food products, mushrooms, heliotrope, phosphorus, arsenic, etc.;

– endogenous — pregnancy toxicosis, thyrotoxicosis.

It develops in viral hepatitis as an expression of its malignant (lightning-fast) form. In pathogenesis, the main importance is attached to the hepatotoxic effect of the venom (virus). Allergic and autoallergic factors play a role.

Macro- and microscopic characteristics:

Liver changes vary in different periods of the disease, which usually takes about 3 weeks.:

In the early days, the liver is slightly enlarged, dense or flabby and acquires a bright yellow color on the surface and on the incision. Then it progressively decreases (melts before our eyes), becomes flabby, and the capsule becomes wrinkled; on the incision, the liver tissue is gray, clay-like. Microscopically, in the early days, fatty degeneration of hepatocytes in the center of the lobules is noted, quickly followed by their necrosis and autolytic decay with the formation of fatty protein detritus, in which crystals of leucine and tyrosine are found. By the end of the 2nd week of the disease, necrosis engulfs all parts of the lobules, only a thin layer of hepatocytes in a state of fatty degeneration remains on their periphery. These liver changes are characteristic of the stage of yellow dystrophy. At the 3rd week of the disease, the liver continues to shrink and turns red. These changes are associated with phagocytosis and resorption of fatty protein detritus of the hepatic lobules; as a result, the reticular stroma with sharply expanded, overflowing sinusoids is exposed; cells are preserved only on the periphery of the lobules. Liver changes at the 3rd week of the disease are characteristic of the stage of red dystrophy.

Complications:

Jaundice, hyperplasia of the peri-portal lymph nodes and spleen (sometimes it resembles septic), multiple hemorrhages on the skin, mucous membranes and serous membranes, in the lungs, necrosis of the epithelium of the renal tubules, dystrophy and necrobiosis in the pancreas, myocardium, central nervous system

Outcomes:

The mortality rate is close to 100% - hepatic coma, hepatorenal insufficiency. Postnecrotic cirrhosis of the liver is possible.