内科学DisordersofDigestiveSys.docx

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 Receptors 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 GI submucosa
muscularis inner circular layer
outer longitudinal layer
serosa
w Digestive glands
• liver : complex function
• pancreas : endocrine:insulin
two functions trypsin
exocrine: amylopsin
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 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.
active transportation
absorptive mechanisms simple diffusion
facilitated diffusion
endocytosis
long-chain fatty acid
→lymph
monoglycerides
other nutrients ───→blood
w Metabolism of liver
biochemical processes
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.
• Till 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 other 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 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 symptoms
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
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 tuberculosis 、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 region
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
jaundice
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
Common 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,
tuberculosis, 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 common 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 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
• gastroscopy
• 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 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. medication 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 :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 gastritis
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, 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 gastritis
• acute corrosive gastritis
• acute suppurative gastritis
Etiology and pathophysiology
infectious factors
External factors chemical factors（NSAID）
physic factors
stress （more common）
Internal factors bile 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:
• severe 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
• principally 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 barrier 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 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 mechanisms. 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 whole 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.
Clinical 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 symptoms :
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 24~48 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 made 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 cirrhosis
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 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：fluid 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 changes 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 found 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
• 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
special 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 infective 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 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 thyroiditis;
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 activity: 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 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
• pseudopyloric 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