1. Chronic atrophic gastritis and peptic ulcer

2. Trilogy: Viral hepatitis, liver cirrhosis and liver cancer

3. Digestive tract cancer: esophageal cancer, gastric cancer and colorectal cancer.

4. Appendicitis

Content:

chronic atrophic gastritis

1. Its occurrence is related to HP infection.

2. Pathological features:

1) The atrophy and thinning of mucosa and the decrease of glands are the most characteristic pathological changes of this disease.

2) Different degrees of lymphocyte and plasma cell infiltration can be seen in the lamina propria of mucosa.

3) Epithelial metaplasia: a) Pseudopyloric metaplasia: Gastric fundus cells and main cells are replaced by mucus-secreting cells similar to pyloric glands. B) Intestinal metaplasia: Gastric mucosa epithelium was replaced by intestinal gland epithelium, and goblet cells, absorptive epithelial cells and Paneth cells appeared.

Peptic ulcer disease

First, the cause of ulcer disease: indigestion of gastric juice, decreased anti-digestion ability of mucosa (HP)

Second, the pathological changes:

1. Location: the anterior or posterior wall of duodenal bulb, with small diameter.

2. The ulcer bottom four layers (from shallow to deep):

1) inflammatory exudate: a small amount of white blood cells, cellulose, etc.

2) necrotic tissue

3) Fresh inner bud tissue

4) Old scar tissue: proliferative endarteritis, nerve fiber injury and spherical hyperplasia.

Third, the outcome and complications:

1. Bleeding (10% ~ 35%)

2. Perforation (5%) is common in duodenal bulb.

3. Pyloric stenosis (3%)

4. Malignant change (≤ 1%, gastric ulcer is more common)

Benign ulcer (gastric ulcer) Malignant ulcer (ulcerative stomachache)

Round or oval, not plastic, dish or crater.

The diameter of large and small ulcers is generally 2cm.

There are deep and shallow.

The edges are neat, not bulging, irregular and not bulging.

The bottom is flat, with necrosis and bleeding.

The mucosal folds of the surrounding mucosa were interrupted to the ulcer, showing nodular hypertrophy.

appendicitis

Etiology and pathogenesis: bacterial infection and obstruction

Second, the pathological changes of acute appendicitis

* * * Same features: neutrophil infiltration can be seen in the appendix wall.

1. Acute simple appendicitis: neutrophils are confined to mucosa and submucosa.

2. Acute celluloid (suppurative) appendicitis: There are neutrophils in all layers of the appendix wall.

3. Acute gangrenous appendicitis: neutrophils infiltrate the entire appendix wall with necrosis.

Third, the outcome and complications

1. Most of them are surgical treatments.

Some of them will become chronic diseases.

3. Bacteria enter the liver along the portal vein, forming a liver abscess.

Viral hepatitis

1. Summary: It refers to a group of common infectious diseases caused by hepatitis virus, mainly liver parenchymal cell degeneration and necrosis.

Second, the characteristics of various hepatitis viruses and their corresponding hepatitis

Viral severe hepatitis turns into a chronic route of transmission.

HAV single-stranded RNA 0.1%-0.4%-0.4%, no intestine.

HBV DNA & lt； 1% has 5%- 10% close contact, blood transfusion and injection.

Few HCV single-stranded RNA >: 70% Same as above.

3%-4% HDV defective RNA

HEV single-stranded RNA 20% unknown, no intestine.

HGV single-stranded RNA unknown unknown no blood transfusion, no injection

Three. Etiology and pathogenesis:

1. Hepatitis virus propagates in the liver, causing liver cell damage. (HAV, hepatitis c virus)

2. Cytotoxic immune response: Virus-specific antigen is expressed on the surface of hepatocytes with virus replication. After the virus enters the blood, the antibodies produced by sensitized lymphocytes and B lymphocytes combine with liver cells, causing degeneration and necrosis of liver cells infected by the virus. The immune response of human body is different because of the number and virulence of infected viruses, which leads to liver cell damage and different pathological types, leading to the emergence of various hepatitis types.

Fourth, the basic pathological changes

3-2-2-4

The basic pathological change of inflammation is accompanied by degeneration and necrosis of liver cells. Main pathological changes

2) Different degrees of inflammatory cell infiltration.

3) Hepatocyte regeneration and fibrous tissue proliferation.

2 2 kinds of hepatocyte degeneration 1) cell edema

2) Eosinophilic changes

2 2 kinds of hepatocyte necrosis 1) lysis necrosis.

2) Eosinophilic necrosis

4 4 kinds of necrosis range 1) punctate necrosis: refers to the necrosis of single or multiple hepatocytes, which is found in acute common hepatitis.

2) Fragmentary necrosis: refers to the focal necrosis and disintegration of liver cells in the boundary plate around hepatic lobule, which is seen in chronic hepatitis.

3) Bridging necrosis: refers to the necrotic zone between central vein and portal area, between two portal areas or between two central veins, which is common in moderate and severe chronic hepatitis.

4) Large-scale necrosis: Large-scale hepatocyte necrosis involving almost the entire hepatic lobule is common in severe hepatitis.

Verb (abbreviation of verb) Clinicopathological types:

Acute hepatocyte degeneration and focal necrosis in common hepatitis.

Chronic mild: focal necrosis, occasionally with slight fragmented necrosis.

Moderate: moderate fragmented necrosis with characteristic bridging necrosis.

Severe: severe fragmentation and necrosis, extensive bridging necrosis.

Severe hepatitis with acute massive hepatocyte necrosis, no obvious hepatocyte regeneration and yellow/red atrophy of liver.

Subacute massive hepatocyte necrosis and nodular hepatocyte regeneration.

Chronic hepatitis used to be divided into chronic persistent hepatitis and chronic active hepatitis, and now it is divided into mild, moderate and severe chronic hepatitis.

Six, ground glass hepatocytes:

There is HBsAg in the cytoplasm of hepatocytes, and HBsAg reaction is positive in immunoadsorption test. Histologically, the cytoplasm is full of eosinophilic fine particles, opaque and ground glass-like. Under electron microscope, HBsAg particles accumulated in smooth endoplasmic reticulum of cytoplasm.

cirrhosis

I. Overview:

Due to diffuse degeneration, necrosis, fibrous tissue hyperplasia and nodular regeneration of liver cells, these three diseases are repeatedly interlaced, leading to liver deformation and sclerosis, which is a common chronic liver disease. In the late stage, portal vein pressure is often increased and liver function is abnormal to varying degrees.

Portal cirrhosis, necrotizing cirrhosis, secondary biliary cirrhosis

Etiology The main cause of China: viral hepatitis.

European and American countries: Chronic alcoholism is mostly caused by subacute severe hepatitis, long-term biliary obstruction and cholestasis.

With naked eyes, 1) small nodules spread all over the liver, with similar size, 0. 15 ~ 0.5 cm.

2) There are gray-white fibers around, and the fiber spacing thickness is relatively consistent. 1) Nodules vary greatly in size, and the largest can reach 5 ~ 6 cm.

2) Wide fiber spacing and uneven thickness; 1) Small nodules or no obvious nodules.

2) Dark green

Microscopically, the normal hepatic lobule structure was destroyed, forming a false lobule. Pseudolobular features:

1) The arrangement of hepatocytes is disordered, and there may be degeneration, necrosis and regenerative hepatocytes.

1) Regenerated hepatocytes have large volume, large and deeply stained nuclei, or binuclear cells.

2) The central vein is missing, offset or has more than two.

3) A small amount of chronic inflammatory cells infiltrated.

4) Small bile duct hyperplasia can be seen.

Macronodular cirrhosis with mixed size nodules or

Micronodular cirrhosis, incomplete division type.

Characteristic liver dysfunction is more obvious than cirrhosis, which appears earlier, portal hypertension is lighter and appears later. The canceration rate is higher than that of portal cirrhosis.

primary carcinoma of liver

1. Etiology: unknown, related factors are as follows:

1. Viral hepatitis B (the most common) and hepatitis C (the second most common).

2. Cirrhosis 85% of liver cancer is complicated with cirrhosis. Necrotic cirrhosis is the most common, followed by posthepatitic cirrhosis.

3. Fungi and toxin Aspergillus flavus are the most important.

Second, typing with the naked eye

1. Early liver cancer: diameter

2. Advanced liver cancer:

1) giant type: huge, such as the head of a baby, mostly located in the right lobe of the liver, with no or only mild cirrhosis.

2) Multinodular type: the most common type, often accompanied by obvious cirrhosis.

3) Diffuse type: the cancer tissue is diffuse in the liver without obvious nodules, and it is often complicated with cirrhosis, which is not easy to distinguish from cirrhosis.

Three. pattern of organization

1. Hepatocellular carcinoma: the most common.

2. Bile duct cell carcinoma.

3. Mixed cell hepatocellular carcinoma: Hepatocellular carcinoma and cholangiocarcinoma coexist.

Fourth, the transfer route

(1) direct intrahepatic transmission

(2) Intrahepatic metastasis. Intrahepatic metastasis usually spreads and metastasizes along portal vein branches.

(3) Extrahepatic metastasis: lymph, blood circulation and implantation metastasis.

esophageal cancer

pathological change

1. The most common sites: middle esophagus (most common), lower esophagus (second) and upper esophagus (rare).

2. Early esophageal cancer: no muscular invasion, no lymph node metastasis. Include carcinoma in situ, submucosal carcinoma and submucosal carcinoma.

3. Advanced (intermediate and advanced) cancer

1) General classification: medullary type, mushroom umbrella type, ulcer type and constrictive type.

2) Histological type: more than 90% were squamous cell carcinoma. Adenocarcinoma is rare, mainly related to Barrett's esophageal adenocarcinoma, and a few come from esophageal submucosal glands.

gastric cancer

First, the cause:

Nitrosamines, Helicobacter pylori, chronic atrophic gastritis, gastric ulcer with gastric dysplasia and colorectal metaplasia.

Second, the disease.

1. The most common position: the small curved side of the gastric antrum.

2. Early gastric cancer: gastric cancer that has not invaded the muscularis and may be accompanied by lymph node metastasis.

1) Special types of cancer:

Microcarcinoma: diameter

Small gastric cancer: the diameter is between 0.6 ~ 1.0 cm.

A little cancer: cancer was diagnosed by endoscopic biopsy, and no cancer was found by sectioning the surgical specimens.

2) Naked eye type: uplift type, superficial type and depression type (the most common).

3. Advanced cancer:

1) General classification: mushroom type or polyp type, ulcer type, infiltration type (bladder stomach) and colloid type.

2) Histological type: The main type is adenocarcinoma, and a few are squamous cell carcinoma.

Three. spread

1. Direct propagation

2. Lymphatic metastasis: Late transthoracic metastasis to left supraclavicular lymph node (Virchow signal lymph node).

3. Blood transfer; later stage

4. Implantation metastasis: bilateral ovarian metastatic mucinous carcinoma (Krukenberg tumor)

colorectal cancer

I. Etiology and pathogenesis

1. High-fat and low-fiber diet

2. Genetic factors: hereditary familial polyposis.

3. Chronic intestinal diseases: villous adenoma, chronic schistosomiasis and chronic ulcerative colitis.

Second, the disease.

1. The most common site is rectum (50%), followed by sigmoid colon, cecum and ascending colon, transverse colon and descending colon.

2. Macro types: uplift type, ulcer type, infiltration type and colloid type.

3. Histological types: adenocarcinoma, mucinous adenocarcinoma or signet ring cell carcinoma, followed by undifferentiated carcinoma, adenosquamous carcinoma and squamous cell carcinoma.

Dukes staging and prognosis of colorectal cancer

5-year survival rate of staging tumor growth range (%)

A limited to mucosa (severe intraepithelial neoplasia) 100

B 1 invades muscularis, does not penetrate, and has no lymph node metastasis.

B2 penetrated the muscularis without lymph node metastasis.

C 1 did not penetrate the muscular layer, but there was lymph node metastasis 43.

C2 penetrates the intestinal wall with lymph node metastasis.

The metastasis rate of distant organs is extremely low.