Download Digestive system disease

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
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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.
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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;
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(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
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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
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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
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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
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(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
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
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
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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
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 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
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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.
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