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1、Disorders of Digestive System Basic structure of digestive system w Gastrointestinal tract w Histologic organization anatomy and physiology of STOMACH zonation of stomach • cardia • fundus • body • antrum w Receptor of parietal cell Acetylcholine w Recepto
2、rs of hypersecretion Gastrin Histamine Prostaglandins w Receptors of hyposecretion Somatostatin w Histologic organization of the GI tract epithelium mucosa lamina propria muscularis mucosae wall of the
3、GI submucosa muscularis inner circular layer outer longitudinal layer serosa w Digestive glands • liver : complex function • pancreas : endocrine:insulin two functions trypsin exocrine: amylopsin
4、 steapsin • biliary systeme LIVER Double blood supply Portal vein 75% Hepatic artery 25% lobules of liver fundamental unit of the liver Other associated organs • peritoneum • mesentery • omentum Function of the Digestive System w Digestion w Absorption w
5、 Metabolism w Excretion w Endocrine w Digestion: digestion refers to the conversion of ingested food molecules into smaller capable of being absorbed into the blood and lymph. w Absorption: Absorption refers to the process of absorbable molecules entering the blood or lymph.
6、 active transportation absorptive mechanisms simple diffusion facilitated diffusion endocytosis long-chain fatty acid →lymph monoglycerides other nutrients ───→blood w Metabolism of liver biochemical process
7、es absorbed nutrients are primarily managed toxins are detoxicated hormones are inactiveted w Excretion: bilirubin, cholesterine and some drugs are excreted by the liver. w Endocrin: endocrine cells in the stomach, intestine, and pancreas. They can secret a lot of hormones. • Til
8、l now, morn than twenty hormones have been found in the digestive system. • The number of hormone produced by the digestive system is increasing. • The hormones produced by GI tract not only modulate the activity of digestive system but also play an important role in the regulation of a lot of o
9、ther physiological functions. • In recent years, it is found that GI tract can produce a number of peptide hormones. • This peptide hormones previously found to be produced by the brain. • These peptides are named as`brain-gut peptides ` Diagnostic measures w History and symptoms w Physical
10、 examination(sign) w Laboratory symptoms and common diseases w History: History taking can provide very important information. For some digestive diseases only by these means can be established accurate diagnoses . Acute gastritis Acute appendicitis 1、esophagus History and sympt
11、oms chest pain dysphagia heart burn acid reflux Common disease esophagitis 、GERD、esophageal carcinoma、achalasia of cardia 2、stomach and duodenum History and symptoms epigastric pain anorexia nausea 、vomiting
12、belch、acid regurgitation Common disease acute and chronic gastritis 、peptic ulcer、gastric carcinoma、functional dyspepsia 3、intestine History and symptoms abdominal pain diarrhea malnutrition Common disease chordapsus 、intestinal tuberculo
13、sis 、Crohn disease 4、colon and rectum History and symptoms abdominal pain diarrhea、constipation rectal tenesmus Common disease Dysentery 、ulcerative colitis 、irritable bowel syndrome、carcinoma of large intestine 5、liver History and symptoms complaint or pain of hepatic r
14、egion hepatauxe tenderness of hepatic region portal hypertension jaundice hepatic encephalopathy nutrition dysmetabolism Common disease viral hepatitis、cirrhosis、primary hepatic carcinoma。 6、bill duct History and symptoms abdominal pain jau
15、ndice murphy’s sign Common disease cholelithiasis、cholecystitis、biliary tractroundworm、 biliary tract tumor 7、pancreas History and symptoms epigastric pain secretion disorder of pancreas external secretion：Intestinal malabsorption internal secretion： metabolic disorder Comm
16、on disease acute、chronic pancreatitis pancreatic carcinoma 8、peritoneum、mesentery History and symptoms abdominal pain abdominal tenderness、rebound tenderness、abdominal guarding （triad） ascites Common disease peritonitis, mesenteric lymphadenitis, tubercul
17、osis, metastatic carcinoma of abdominal membrane Common symptoms • anorexia • nausea • vomiting • acid regurgitation • belching • heart-burn • dysphagia • Abdominal distention • diarrhea • abdominal pain • constipation • hematemesis • melena • hematochezia Physical examination w co
18、mmon signs • abdominal shape • peristaltic rushes • abdominal varices and the direction of blood flow • abdominal tenderness and the location • rebound tenderness • abdominal guarding • shifting dullness • Bowel sounds • abdominal mass • jaundice • hepatomegaly • splenomegaly Laboratory
19、 tests • stool tests • acid secretion test • hepatic function tests Imaging procedures • plain film • barium meal and barium enema • ultrasonagraphy • computed tomography, CT • endoscopic retrograde cholangiopancreatogyaphy, ERCP • magnetic resonance imaging, MRI w Endoscopy • gastroscop
20、y • colonoscopy • laparoscopy others Ø biopsy Ø motion function Ø laparotomy Prevention and Treatment of digestive diseases w Prophylaxis w systemic treatment w psychological treatment w comprehensive measure medication surgery traditional chinese medicine general treatment ⒈
21、resting ⒉ noruishment(drink and food) ⒊ Supportive treatment pharmacotherapy ⒈treatment for causes and pathogenesis ⒉symptomatic treatment surgical or interventional treatment indications w points for attention contraindications side effects Advances and Forecast 1. medi
22、cation of peptic ulcer 2. diagnose and treatment of digestive malignancy 3. management of portal hypertension 4. diagnose and treatment of alimentary tract hemorrhage 5. clinical application of digestive endoscopy 6. interventional treatment Gastritis Definition w Defect of gastric mucosa
23、 :damage, inflammation, regeneration w Gastritis refers to the inflammation of gastric mucosa. w gastropathy w Is a common disease. classification According to the clinical process and pathology, gastritis is classified into : w 1.acute(erosive/hemorrhagic ) gastritis w 2. Chronic gast
24、ritis w 3.special gastrtis (corrosive gastritis, suppurative gastritis) ACUTE GASTRITIS Definition : • acute gastritis mainly refers to acute erosive/hemorrhagic of gastric mucosa • Other name: acute erosive and hemorrhagic gastritis , acute gastric mucosal lesion • Endoscopy: hyperemia,
25、 edema, hemorrhage, erosive, superficial ulcer • pathology: diffuse or localized superficial erosive that do not extent deeper than muscularis mucosae • the erosive may cause bleeding that range from occult blood loss to massive bleeding. Classification: • acute erosive and hemorrhagic gastrit
26、is • acute corrosive gastritis • acute suppurative gastritis Etiology and pathophysiology infectious factors External factors chemical factors（NSAID） physic factors stress （more common） Internal factors bile
27、reflux vascular factors 1 .chemical damage • Drugs : non-steroid anti-inflammatory drugs, NSAIDs – Aspirin, Paracetmol, Indometacin, Dicloeenac, Sodium ect • Ethanol • Strong tea • coffee 2. Stress: • seve
28、re surgical trauma – multi-fracture, severe trauma, burning trauma (curhing ulcer), brain trauma (cushing ulcer) • medical conditions – respiratory failure, renal failure, cardiac function failure 3. acute bacteria inflammation: • toxin • bacteria 4. Bile and pancreatic juice reflux • p
29、rincipally following surgery (pylorus is taken away) • pyloric dysfunction 5. other factors • ischemia • radiation • ingestion of alkali (NaHCO3) / acid (sulphuric acid, hydrochloric acid) Mechanism • The mechanisms of mucosal injury are not very clear • The damage of mucus /mucosal barrie
30、r is consider to be the key procedure resulting in acid back diffusion and mucosal injury caused by gastric mucosal ischemia . • NSAIDs and ethanol can inhibit cyclooxyenase (COX) and reduce endogenous prostaglandins (PGs) in gastric mucosa . PGs: increase gastric mucosal blood flow; enhance the
31、renewal of gastric mucosa ; increase the secretion of gastric mucus. • Since endogenous PGs play an important role in the maintenance of the mucosal integrity, decrease of endogenous PGs can cause mucosal damage. • Stress may cause reduction of mucosal blood supply or damage of other defensive m
32、echanisms. Some stress factors may also cause gastric acid oversecretion. • Bile salts and pancreatic enzymes decompose mucus and break biological membrane. These mechanism can all result in mucosal injury and erosion. Pathology ⒈diseased region：gastric antrum、gastric body or to fill with who
33、le stomach. ⒉pathological changes：hyperemia、oedema、erosio、hemorrhage、superficial ulceration with gastric mucosa . Characteristics of histology ⒈Inflammatory cell infiltrate of lamina propria mucosae； ⒉Deprivation and hemorrhage of epithelial cells； ⒊ Distort and effusion of gland in mucosa. Cl
34、inical feature w Bleeding • many cases of acute gastritis are insidious (asymptomatic or be covered up by other medical conditions ), so lead to escape diagnosis • in some cases, massive bleeding occurs and some times the bleeding may be vital • generally,the bleeding is self-limited w Other s
35、ymptoms : apigastric pain nausea vomiting indigestion diarrhea w Signs: slight tenderness in epigastrium Diagnosis w History: w Symptoms: w definitive diagnosis: endoscopic exam . generally, the acute endoscopic examination should be performed within 24~
36、48 hours after the bleeding. w Endocopy: hyperemia petechia hemorrhage erosions superficial ulceration w These changes may be diffuse or limited to the antrum , fundus or body. w In the strictest sense, the diagnosis of acute gastritis should be ma
37、de by pathologists from the histopathologic findings of the biopsy specimen. • Inflammatory cells(usually neutrophils and mononuclear cells) infiltrate the lamina propria, where the glandular areas are distorted by edema and hemorrhage. Differential diagnosis w Peptic ulcer disease w hepatic c
38、irrhosis w gastric carcinoma Treatment 1. Removal of the causes • avoidance and discontinuance of the administration of NSAIDs and ethanol • effective treatment of severe diseases 2. prevention and treatment • reduce gastric acid . • Neutralizing gastric acid(antacids) – colloidal
39、 alumiun hydroxid, NaHCO3 • reducing gastric acid secretion H2RA PPI • Protect mucose : prostaglandin 3. management of gastric bleeding : ①general treatment：bed rest liquid diet overview and surveille ②blood volume supplement：f
40、luid infusion、blood transfusion—first elect ③stop bleeding：anti acid medicine endoscopic hemostasis surgery CHRONIC GASTRITIS Introduction • Chronic gastritis main refer to chronic inflammation of gastric mucosa caused by H.pylori and involves inflammatory change
41、s in the mucosa • Is a very common disease. • The inflammation cells in chronic gastritis are mainly lymphocytes and plasma cells,and there may be a few of neutrophils and eosinophils. • The inflammatory changes are usually patchily distributed . In late stage atrophy and metaplasia can be foun
42、d in the gastric mucosa . Epidemiology w Prevalence : >50% w H.pylori: in population ,the infection rate is 40%-70% in chronic gastritis, the infection rate is 87% Classification w There are many classifications: • Whitehead(1972): • superficial gastritis • atrophic gastritis •
43、 Strikland (1973) :According to the anatomic portion predominantly involved , atrophic gastritis is classified : • type A( body gastritis) • type B( antral gastritis) • Misiewicz and Tytgat (1990): Sydney System • 1996: Updated Sydney System • non-atrophic gastritis atrophic gastritis sp
44、ecial gastritis etiology and mechanism w H.pylori infection • A gram-negative bacterium • a quite strong infective ability • incidence is very high. • It is estimated that 50% of the population over the age of 50 years are infected with H.pylori in developed countries. • The H.pylori infe
45、ctive rate is 80%-95% in the chronic gastritis H. pylori • Stay in gastric antrum, lives in the gastric crypts, gastric metaplasia (duodenal bulb) w Mechanism • H. pylori have the ability to produce a wide variety of virulence factors. • Most H.pylori associated gastritis dose not develop to
46、erosions,but the inflammation can progress to depth of the mucosa and lead to atrophy. w Autoimmunity and heredity • autoantibody in the blood : parietal cell antibody, PCA; intrinsic factor antibody, IFA • autoimmune disease: accompaniment Hashimoto t
47、hyroiditis; vitiligo w Other factors : • duodenal juice(Bile and pancreatic juice) reflux • damage gastric mucosa factors: NSAID, alcohol abuse pathology w H.pylori infection w inflammation :The inflammation cells in chronic gastritis are mainly lymphocytes and plasma cells w a
48、ctivity: Classified phase • static phase: • the predominant inflammatory cells in chronic gastritis are lymphocytes and plasma cells ,and this kind of inflammatory conditions is called “static phase” • active phase: • there are predominant collections of neutrophils and eosinaphils free in the
49、 lamina propria and in the lining epithelium ,this condition is called “active phase” w atrophic gastritis • atrophic gastritis is characterized by a variable glands loss and encroachment of inflammatory cells into the gland zones. w Metaplasia • intestinal metaplasia : goblet cell • pseudop
50、yloric gland metaplasia w dysplasia • moderate and severe dysplasia is considered to be possible precancerous conditions atrophia inflammation metaplasia Clinical manifestation symptoms : dyspepsia signs : without; or lightly tenderness in epigastrium Others: anore
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