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Outline Digestive system disease Gastritis Purpose and Request Knowing that acute and chronic gastritis are general diseases. Knowing their clinical presentation and the important points of diagnosis. Being Familiar with principles of prevention and treatment. [Acute gastritis] 1, Etiology and pathogenesis Causes are variety. Intrinsic motivation include stress reaction and ischemia. Extrinsic motivation include drugs, bile regurgitation,and Helicobacter pylori (Hp). 2, Clinical presentation and diagnosis The clinical manifestation is acute hemorrhage of upper digestive tract. Final diagnosis depends on gastroscopy. 3, Prevention and treatment Treating the primary diseases Controlling causes Haemostasis actively H-2 receptor antagonist Gastric mucosal protective agent [Chronic gastritis] Pathology Superficial and atrophic gastritis would develop pathological metaplasia and dysplasia. Clinical classification and etiology B type - Chronic antral gastritis is the most familiar, mainly be caused by Hp( H. pylori) infection. A type - Chronic corpus gastritis is seldom seen, mainly be caused by autoimmune reaction. Clinical presentation Having no special and typical symptoms and signs. The manifestation of B type 1 is dyspepsia. A type presents anorexia, loss of weight and anemia. laboratory and other findings Gastric juice analysis-A type: absent gastric acidity. B type: normal or low. Serodiagnosis: the level of serum gastrin and related antibody are different in the two types. Gastroscopy and biopsy. Diagnosis The final diagnosis depends on gastroscopy and biopsy. Treatment B type: Sterilization when HP is positive and active. Once HP is negative, analyse the causes, then treat. A type: Gastric mucosal protective agent. Regular following-up severe dysplasia and metaplasia Teaching method Instruction and demonstration Upper Gastrointestinal Bleeding 1.Purpose and Request (1) Knowing the concept of upper gastrointestinal bleeding and common causes. (2) Being familiar with the clinical presentation and estimation the volume of losed blood. (3) Knowing principles of treatment and the progress of therapeutic endoscopy. 2.Teaching Contents Etiology:The major causes are pepticulcer, esophagus-gastric variceal hemorrhage caused by portal hypertension, carcinoma (esophagus or stomach). Others are seldom . Clinical presentation:Hematemesis and melena, peripheral circulatory failure, anemia,fever,and azotemia. Diagnosis: ① Identifying upper gastrointestinal hemorrhage early. Differentiate hematemesis and hemoptysis, eliminate the bleeding of no-alimentary tract. ② Estimating the volume of losed blood: According the volume of hematemesis and melena, signs and symptoms after blood loss, the mean corpuscular volume. ③ Etiologic diagnosis: History, signs and symptoms, laboratory finding and emergency gastroscopy have important value. 2 Treatment General first-aid measure. Compensate Blood volume actively , include liquor, blood necessarily Haemostasis ① Drug ② Balloon tamponade (Sengstaken-Blakemore tube) ③ Endoscopy and control of hemorrhage ④ Surgical intervention 3.Teaching method Instruction and demonstration Peptic ulcer 1.Purpose and Request (1) Knowing the clinical presentation and diagnosis. (2) Being familiar with differential diagnosis, principles of prevention and treatment. (3) Knowing the etiology and pathogenesis. 2.Teaching Contents (1) Etiology and pathogenesis: Etiology:① HP;② Hypersecretion of Gastric acid;③ NSAID;④ Others etiological factors, include hereditary predisposition; astrointestinal motility disorder, stress, psychological factor and smoking. Pathogenesis: Ulcer is the end result of an imbalance between aggressive and defensive factors in the gastroduodenal mucosa. The major aggressive factor is gastric acid. Duodenal ulcer: aggressive factors, gastric acid and pepsin hypersecretion are the main role, gastric mucosal defensive factors are subcardinal. Gastric ulcer: the main cause is the decrease of gastric mucosal defensive and plerosis capacity. (2) Pathology: The morphologic change (3) Clinical presentation: Symptoms: Character and regularity of epigastric pain Signs: gently Idiopathic ulcer ① Asymptomatic ulcer ② Senile peptic ulcer ③ Compound ulcer ④ Pyloric channel ulcer ⑤ Postbulbar duodenal ulcer (4) laboratory check: ① Test of Hp; ② stomach liquid analysis; ③ Test of gastrin; 3 (5) Diagnosis: significance of analysis history; radiography; gastroscopy and biopsy (6) Differential diagnosis ①functional dyspepsia;②gastrinoma; ③ Carcinomatous ulcer; ④disease of gallbladder (7) Complications:①bleeding; ② perforation;③pyloric obstruction;④ carcinomatous change (8) Treatment: Purpose and principle general treatment drug treatment ① Radical Hp ② anti-excretion of gastric acid: H2-receptor antagonist, PPI and other antacid agents.③protect gastric Mucosa Theraputic strategy and surgical intervention 3.Teaching method Instruction and demonstration Hepatic cirrhosis 1.Purpose and Request Knowing the clinical presentation and diagnosis of cirrhosis . Being familiar with differential diagnosis and complication. Knowing the etiology, pathogenesis and principles of treatment. 2.Teaching Contents Etiology and classification: Etiologic classification: viral hepatitis ; alcohol intoxication; cholestasis; circulatory disorder; industrial poison or drug; metabolism disorder; dystrophy; immunity disorder. Pathologic classification: Micronodular; Macronodular; mixed nodule; untransparent regenerated nodule. Pathology:Cell degeneration and necrosis comprehensively. Formation of regenerated nodule. Fiber connective tissue hyperplasia. Portal hypertension (1)Morphologic change (2)Histologic change Clinical presentation: (1)Liver hypofunction, (2)Portal hypertension (3)liver palpation 4 Complications Upper gastrointestinal hemorrhage Hepatic encephalopathy Infection Functional renal failure Primary liver carcinoma Disturbance of acid-base balance and electrolur Laboratory check and others Test of blood Urine function Liver function Immunological function Endoscopy Radiograph Diagnosis and Difference Diagnose in phase of compensation is difficult Differentiate hepatomegaly and ascites and other complications Treatment: (1) General treatment (2) Drug (3) Ascites (4) Portal hypertension (5) Other complications (6) Liver transplant Teaching method Instruction and demonstration Primary liver carcinoma 1.Purpose and Request Knowing the etiology, differential diagnosis and treatment Knowing the clinical presentation and diagnosis Being familiar with auxiliary examination and differential diagnosis 2.Teaching Contents Etiology and classification Causes-multifactor effect Viral hepatitis Hepatic cirrhosis Some carcinogen 5 Aflatoxin; Environment pollution Pathology Morphologic Typing Histologic Typing Pathway of metastasis Clinical presentation Major manifestation Hepatomegaly progressively Jaundice Manifestation of transfer Typing and Staging Three types and three stages Complications Upper gastrointestinal hemorrhage Hepatic encephalopathy Infection Hepatocarcinoma nod disruption Auxiliary examination (1) Test of tumor marker: AFP; other serological tests (2) Ultrasonic examination. (3) Computer tomography (CT) (4) Angiography (5) Nuclear magnetic resonance (MRI) (6) Puncture biopsy Diagnosis Strive for earlier period diagnosis Think highly of high-risk group survey Differential diagnosis Secondary Hepatocarcinoma Hepatic cirrhosis Hepatic abscess Active hepatopathy; Treatment: Surgical operation Local radiation theraphy Regions interventional therapy Biological and immunosuppressive therapy Synthetic therapy Prevention Actively prevente hepatitis 6 Notice the food hygiene Defending mildew Protecting drinking-water 3.Teaching method Instruction and demonstration Hepatic encephalopathy 1.Purpose and Request Knowing the clinical presentation and diagnosis. Knowing the etiology and pathogenesis. Being familiar with evoking factor and treatment. 2.Teaching Contents Etiology and pathogenesis: Ammonia intoxication theory; Pseudo-neurotransmitter theory; Amino acid metabolism imbalance theory; Pathology Clinical presentation : According to the degree of conscious disturbance, nervous system manifestation and eletroencepalograph (EEG). Hepatic encephalopathy are divided into four stage. Auxiliary examination: Blood Ammonia Test EEG Psychometry Diagnosis and Differential diagnosis Diagnosis evidence Severe Hepatopathy and/or collateral circulation Aabalienation; lethargy and coma Evoking factor Liver hypofunction;thrill EEG Differentiate from other coma Treatment (1) Treat causes (2) Reduce intestinal tract poison’s production and absorption (3) Promote noxious substance excretion, rectify acid metabolism imbalance 7 (4) Redress disturbance of acid-base balance and electrolur. (5) Bendopa; hemoperfusion; liver transplantation,etc. Prevention: Prevente liver disease Prevente evoking factor Early detection and early treatment 3.Teaching method Instruction and demonstration Acute pancreatitis 1.Purpose and Request Knowing the etiology, prevention and treatment. Being familiar with clinical presentation and diagnosis, pathology. Knowing the develop regularity. 2.Teaching Contents Etiology and pathogenesis: Mostly pancreatemphraxis completely or partly active pancreatin, then causes pancreas self-digestion. Interpret the mechanism of shock. Common causes: Obstruction of biliary tract: Stone; Ascarid Pancreatemphraxis: Stone; Ascarid; pancreatic duct constriction, Neoplasm; Diet: Binge overeating, alcoholism; Others: operation and trauma, drug. Pathology Interstitial pancreatitis; Necrotizing pancreatitis; The two types can inter-converse. Clinical presentation : Signs: abdominal pain; Nausea; vomit; abdominal distention; Fever; tenderness; Abdominal wall tension;shock. Paralysis of intestine; Abdominal wall ecchymosis; jaundice. Complication: local Complication Remote Complications Multiple organ failure Chronic pancreatitis and diabetes mellitus Auxiliary examination: Blood and urine amylase 8 Numeration of leukocyt; lipase Radiograph Abdomen ultrasound and CT; Diagnosis and Differential diagnosis According to clinical finding and laboratory examinaton. Differential diagnosis: peptic ulcer perforation; cholelithiasis; acute ileus; Intestinal obstruction Treatment Medical treatment Custodial; treat shock and redress disturbance of acid-base balance and electrolur. Inhibite and decrease pancreatic juice excretion; fasting; gastrointestinal decompression; somatostatin; Anti-Cholinergic agent; H2-receptor antagonist Antispasticity and analgesia: Atropine Antibiotic Endoscopy Sphincterotomy; The traditional Chinese medicine; Prevention Cure disease of biliary tract; Temperance; Avoid binge overeating 3.Teaching method Instruction and demonstration Intestinal tuberculosis; Tuberculous peritonitis 1.Purpose and Request Knowing the clinical presentation and diagnosis. Bing familiar with pathogenesis, pathology and differential diagnosis Knowing the laboratory examination and complication. 2.Teaching Contents Intestinal tuberculosis Etiology and pathogenesis: (1)Tubercle bacillus invade Pathway (2)Sites and pathogenesis Pathology Ulcerative intestinal tuberculosis 9 Proliferative intestinal tuberculosis Clinical presentation Abdominal pain Diarrhoea; constipation Abdominal mass Parenteral tuberculosis Complication: Tuberculous peritonitis; Pulmonary tuberculosis; Hemorrhage; Acute bowel disturbance Auxiliary examination: Blood and urine test; Erythrocyte sedimentation; Tuberculin test Radiograph Colonoscopy Diagnosis and Differential diagnosis Diagnose according to clinical presentation, Parenteral tuberculosis, auxiliary examination, radiograph and colonoscopy. Differential diagnosis: Crohn disease Colon carcinoma Amebiasis Treatment: General treatment. Anti-tuberculosis medicine treatment. Control signs. Surgical operation. Tuberculous peritonitis Etiology and pathogenesis: Primary lesion Tubercle bacillus invade Pathway and pathogenesis Pathology Exudativeness; Adhesiveness; Caseous tubercle; Clinical presentation--diversity Toxemia and dystrophy The pathology type determinate the clinical finding Complication 10 Intestinal obstruction; Acute intestinal perforation; Abdominal abscess; Intestinal fistula Auxiliary examination: Blood and urine test;erythrocyte sedimentation; Tuberculin test; Ascites test Radiograph Laparoscopy Diagnosis and Differential diagnosis Diagnose according to clinical presentation, Parenteral tuberculosis, auxiliary examination, radiograph and colonoscopy. Diagnostic treatment necessarily Differential diagnose from fever, ascites, abdominal mass, abdominal pain, etc. Treatment: General treatment. Anti-tuberculosis medicine treatment. Adrenal cortical hormone. Surgical operation. 3.Teaching method Instruction and demonstration Ulcerative colitis 1.Purpose and Request Knowing the clinical presentation and diagnosis. Being familiar with differential diagnosis Knowing etiology, pathogenesis and treatment. 2.Teaching Contents Etiology and pathogenesis: Infestation; Immunity; Heredity; Mentality Pathology Morphology and histology 11 Clinical presentation Digestive system: Diarrhoea; bloody pus in stool; abdominalgia; Total body manifestion Out-bowel manifestion Type and phase Complication: Toxic megacolon; Carcinomatous change; Others Auxiliary examination: Blood and stool test; Stool cultivation colonoscopy Radiograph Diagnosis and Differential diagnosis Diagnose according to clinical presentation, colonoscopy, biopsy,radiograph. Differential diagnosis: Chronic bacillary dysentery; Chronic amebic dysentery; Cancer of colon; Treatment: General treatment. Drug: Salicylic Acid; adrenal cortical hormone; local medical treatment; Surgical operation. 3.Teaching method Instruction and demonstration, discussion. 12