INTERNAL MEDICINE- GASTROINTESTINAL SYSTEM

CHAPTER-1 GASTRITIS
I.ANATOMY AND PHYSIOLOGY OF
STOMACH
✓ The digestive or gastrointestinal (GI) tract
includes the esophagus, stomach, small
intestine, large intestine or colon, rectum,
and anus.
1.Structure of human stomach
✓ The stomach is divided into four regions—
the cardia, fundus, body, and antrum.
✓ The stomach has three layers of muscle: an
outer longitudinal layer, a middle circular
layer, and an inner oblique layer
✓ The inner lining consists of four layers: the
serosa, the muscularis, the submucosa, and
the mucosa.
✓ The mucosa is densely packed with gastric
glands, which contain cells that produce
digestive enzymes, hydrochloric acid, and
mucus.
✓ Erosion is a breakdown of the outer layers of the skin,
while an ulcer penetrates the muscularis mucosa,with
depth to the sub-mucosa
✓ The gastric epithelium is coated by a protective layer of
mucus seceted by specialized epithelial cells.
2.Various types of cells in the Stomch:Gastric pits contain
several cell types, including mucus secreting cells and
enteroendocrine cells. The array of cell types found in
individual gastric pits varies in different regions of the stomach.
H. pylori colonization is largely confined to the antrum, which
lacks acid-secreting parietal cells.
i.Glands within the gastric cardia comprise <5% of the gastric
gland area and contain mucous and endocrine cells.
ii.The majority of gastric glands (75%) are found within the
oxyntic mucosa and contain mucous neck, parietal, chief,
endocrine, and enterochromaffin cells
iii.Pyloric glands contain mucous and endocrine cells (including
gastrin cells) and are found in the antrum.
iv.The parietal cell, also known as the oxyntic cell, is usually found in the neck, or isthmus, or the oxyntic
gland.
3.Transformation of gastric parietal cell
✓ The resting, or unstimulated, parietal cell has prominent cytoplasmic tubulovesicles and
intracellular canaliculi containing short microvilli along its apical surface .

 ✓ H+, K+-ATPase(Hydrogen potassium ATPase) is expressed in the tubulovesicle membrane; upon

cell stimulation, this membrane, along with apical membranes, transforms into a dense network of
apical intracellular canaliculi containing long microvilli.
✓ Acid secretion, a process requiring high energy, occurs at the apical canalicular surface.
✓ Numerous mitochondria (30 to 40% of total cell volume) generate the energy required for
secretion.
4.Gastroduodenal Mucosal Defense
The mucosal defense system can be envisioned as a three-level barrier, composed of preepithelial,
epithelial, and subepithelial elements
i.Mucus forms a hydrophobic surface with fatty acids that extend into the lumen from the cell membrane.
✓ The mucous gel functions as a nonstirred water layer impeding diffusion of ions and molecules
such as pepsin.
✓ Bicarbonate, secreted by surface epithelial cells of the gastroduodenal mucosa into the mucous
gel, forms a pH gradient ranging from 1 to 2 at the gastric luminal surface and reaching 6 to 7
along the epithelial cell surface.
ii.Surface epithelial cells provide the next line of defense through several factors, including mucus
production, epithelial cell ionic transporters that maintain intracellular pH and bicarbonate production,
and intracellular tight junctions.
iii.An elaborate microvascular system within the gastric submucosal layer is the key component of the
subepithelial defense/repair system. A rich submucosal circulatory bed provides HCO3-, which
neutralizes the acid generated by parietal cell secretion of HCl. Moreover, this microcirculatory bed
provides an adequate supply of micronutrients and oxygen while removing toxic metabolic by-products.
iv.Prostaglandins play a central role in gastric epithelial defense/repair
5.Physiology of Gastric Secretion
Acid secretion induced by excitation of parietal cell receptors (H2-R, M3-R and CCK2-R) by specific
agonists (histamine, acetylcholine and gastrin) and activation by protein-kinases of the resting proton
pumps with their fusion with membrane covering intracellular canaliculi and secreting H+ into theses
canaliculi.
Three phases of Gastric secretion
1. Cephalic phase: 30% of the total gastric acid to be produced is stimulated by anticipation of
eating and the smell or taste of food.—— stimulates gastric secretion via the vagus nerve.
2. Gastric phase: 60% of the acid secreted is stimulated by the distention of the stomach with food.
Plus, digestion produces proteins, which stimulate the G cell to release gastrin, which in turn
activates the parietal cell .
3. Intestinal phase: the remaining 10% of acid is secreted when chyme enters the small intestine,
and is stimulated by small intestine distention.Gastritis

II.GASTRITIS
Gastritis refers to the inflammation of gastric mucosa.Inflammation of the gastric mucosa is caused by
any causes.
1.Classification of Gastritis
✓ Acute gastritis
✓ Chronic Atrophic Gastritis
✓ Uncommon Forms of Gastritis

 A.ACUTE GASTRITIS:
a.Causes:It is mainly caused by Acute H. pylori infection
✓ Other acute infectious gastritis include: Bacterial (other than H. pylori) ;Helicobacter helmanni
Phlegmonous;Mycobacterial ;Syphilitic ;Viral ;Parasitic;Fungal
b.Clinical manifestation
i.Abdominal cramping and pain ii.Nausea iii.Vomiting iv.Diarrhea v.Fever vi.Loss of appetite
vii.Belching or gas viii.Weakness
✓ Mild :dyspepsia --pain ,anorexia,nausea and vomiting.
✓ Typical :
➢ acute erosive and hemorrhagic gastritis with bleeding (hematemesis and hematochezia) with
a little, intermissive, self-ceasing.
➢ emergency endoscopy is used within 24-48 hours for severe bleeding,
➢ the gastric mucosa appears petechia ,hemorrhage,diffuse erosion and superficial ulceration .
c.Treatment
i.Limit or avoid alcohol and caffeine ii.If possible avoid drugs that are irritating to stomach
iii.Avoid foods that you don't digest easily iv.Stop smoking
v.Eat regularly and moderately vi.Wipe out predisposing causes
vii.Antacid and H2RA or PPI. viii.Bacterial infections:antibiotics

B.CHRONIC GASTRITIS
a.Def: Chronic gastritis is identified histologically by an inflammatory cell infiltrate consisting primarily
of lymphocytes and plasma cells, with very scant neutrophil involvement.
b.Phases of gastritis:
✓ early phase -superficial gastritis.
✓ next stage- atrophic gastritis.
✓ final stage -gastric atrophy
c.Classification:
i.Whitehead(1972):
✓ Superficial gastritis
✓ Atrophic gastritis
ii.Strikland (1973) :According to the anatomic portion predominantly involved , atrophic gastritis is
classified
✓ type A( body gastritis)
✓ type B( antral gastritis)

iii.Sydney system(1996):
✓ Non-atrophic(superficial gastritis)
✓ Atrophic:multifocal atrophic,autoimmune
✓ Special forms
➢ Type A refers to the body-predominant form (autoimmune)
➢ Type B is the central-predominant form (H. pylori-related).
➢ The term AB gastritis has been used to refer to a mixed antral/body picture.
B.i.TYPE ‘A’ GASTRITIS
The less common type which involves primarily the fundus and body, with antral sparing.
✓ associated with pernicious anemia
✓ presence of circulating antibodies against parietal cells and intrinsic factor; thus it is also called
autoimmune gastritis.

 Characteristics:
✓ Autoimmunity and heredity autoantibody in the blood : parietal cell antibody, PCA; & intrinsic
factor antibody, IFA
✓ autoimmune disease: accompaniment Hashimoto thyroiditis;vitiligo
Pathogenisis of Autoimmunization :
parietal cell damage (antigen) antibody to parietal cell parietal cell gastric acid and
antibody to intrinsic factor vitaminB12 pernicious anemia .
B.ii.TYPE ‘B’ GASTRITIS
✓ The most common form which has perdominat antral involvement
✓ Manily caused by H. pylori infection
✓ There is progression of the inflammatory process towards the body and fundus of infected
individuals
✓ The conversion to a pan-gastritis is time-dependent-estimated to require 15 to 20 years.
✓ It increases with age, being present in up to 100% of people over age 70.
✓ Histology improves after H. pylori eradication.
H. pylori and acid peptic disorders
a. Chronic gastritis
b. Peptic ulcer
c. gastric mucosal-associated lymphoid tissue (MALT) lymphoma
d. gastric adenocarcinoma.
Characteristics of H.Pylori
✓ a gram-negative microaerophilic rod
✓ the deeper portions of the mucous gel coating the gastric mucosa or between the mucous layer
and the gastric epithelium
✓ contains multiple sheathed flagella
✓ capable of transforming into a coccoid
Key bacterial factors
a. urease (converting urea to NH3 and water, thus alkalinizing the surrounding acidic environment),
b. Catalase,
c. lipase,
d. adhesins,
e. platelet-activating factor,
f. cytotoxin-associated gene protein (Cag A),
g. pic B (induces cytokines),
h. and vacuolating cytotoxin (Vac A).
Treatment :
✓ Treatment in chronic gastritis is aimed at the sequelae and not the underlying inflammation.
✓ Patients with pernicious anemia will require parenteral vitamin B12 supplementation on a long-
term basis.
✓ Eradication of H. pylori is not routinely recommended unless PUD or a low-grade MALT
lymphoma is present.
B.iii.MISCELLANEOUS FORMS OF GASTRITIS
✓ Lymphocytic
✓ Eosinophilic
✓ Crohn's disease
✓ Sarcoidosis
✓ Isolated granulomatous gastritis

 III.ZOLLINGER-ELLISON SYNDROME
i.Epidemiology
✓ 0.1 to 1% of individuals presenting with PUD.
✓ Males are more commonly affected than females
✓ ages 30 and 50.
✓ sporadic tumors (more common) and those associated with multiple
endocrine neoplasia (MEN) type I
ii.Pathophysiology
✓ Gastrin stimulates acid secretion through gastrin receptors on parietal cells and by inducing
histamine release from ECL cells.
✓ Gastrin also has a trophic action on gastric epithelial cells.
✓ Longstanding hypergastrinemia leads to markedly increased gastric acid secretion. The increased
gastric acid output leads to the peptic ulcer diathesis, erosive esophagitis, and diarrhea.
iii.Tumor Distribution
✓ within the pancreas and extrapancreatic sites
✓ Over 80% , within the hypothetical gastrinoma triangle
✓ most common nonpancreatic sites -- up to 50% duodenal tumors
✓ Less common -- stomach, bones, ovaries, heart, liver, and lymph nodes.
✓ >60% malignant, with up to 30 to 50% of patients having multiple lesions or metastatic disease at
presentation.
✓ Well differentiated, expressing markers (chromogranin, neuron-specific enolase).

HYPOTHETICAL GASTRINOMA TRIANGLE

The gastrinoma triangle is formed by a line joining the confluence of the cystic and common bile ducts
(A) superiorly, the junction of the second and third portion of the duodenum inferiorly (B), and the
junction of the neck and body of the pancreas medially (C).
iv.Clinical Manifestations--- Gastric acid hypersecretion
a.Peptic ulcer : most common>90%
1.Initial presentation and ulcer location (duodenal bulb)
✓ ulcers in unusual locations (second part of the duodenum and beyond),
✓ ulcers refractory to standard medical therapy,
✓ ulcer recurrence after acid-reducing surgery,
✓ or ulcers presenting with frank complications (bleeding, obstruction, and perforation).
2.Symptoms of esophageal origin : two-thirds mild esophagitis to frank ulceration with stricture and
Barrett's mucosa.
b.Diarrhea : up to 50%, Multifactorial
✓ marked volume overload to the small bowel,
✓ pancreatic enzyme inactivation by acid,
✓ damage of the intestinal epithelial surface by acid.
A mild degree of maldigestion and malabsorption of nutrients.
The diarrhea may also have a secretory component
✓ direct stimulatory effect of gastrin on enterocytes
✓ the cosecretion of additional hormones from the tumor, such as vasoactive intestinal peptide.
c.Presence of MEN I (Multiple Endocrine Neoplasia, Type 1)syndrome :25%.

 1.Autosomal dominant disorder involves primarily three organ sites:

✓ Parathyroid glands (80 to 90%),
✓ Pancreas (40 to 80%),
✓ Pituitary gland (30 to 60%).
2.Feature:
✓ parathyroidectomy reduces gastrin and gastric acid output in gastrinoma patients.
✓ higher incidence of gastric carcinoid tumor development
- Gastrinomas tend to be smaller, multiple, and located in the duodenal wall
- Establishing the diagnosis of MEN I is critical not only from the standpoint of providing genetic
counseling to the patient and his or her family but also from the surgical approach.
3.Diagnosis:Fasting gastrin levels: usually <150 pg/mL.
✓ All gastrinoma patients >150 to 200 pg/mL. Even >500 pg/mL.
✓ Measurement of fasting gastrin should be repeated to confirm the clinical suspicion.
4.Differential Diagnosis -Multiple processes can lead to an elevated fasting gastrin level
✓ Hypochlorhydria or achlorhydria with or without pernicious anemia
✓ Retained gastric antrum
✓ G cell hyperplasia
✓ Gastric outlet obstruction
✓ Renal insufficiency
✓ Massive small-bowel obstruction
✓ Others: rheumatoid arthritis, vitiligo, diabetes, pheochromocytoma
ACID SECRETION
✓ A nasogastric tube , drawing samples at 15-min intervals for 1 h during unstimulated or basal
state (BAO), followed by continued sampling after administration of intravenous pentagastrin
(MAO).
✓ BAO > 15 meq/h (normal <4 meq/h). Up to 90% of gastrinoma
✓ A BAO/MAO ratio >0.6 is highly suggestive of ZES, but a ratio <0.6 does not exclude the
diagnosis.
GASTRIN PROVOCATIVE TESTS: secretin stimulation test,calcium infusion study,standard meal test.
v.Treatment
✓ To ameliorate the signs and symptoms related to hormone overproduction,
✓ To do curative resection of the neoplasm,
✓ To control tumor growth in metastatic disease.
✓ PPIs
✓ Surgery to provide a definitive cure.
✓ Therapy of metastatic endocrine tumors in general remains suboptimal: chemotherapy , hepatic
artery embolization , Surgical approaches(debulking surgery and liver transplantation for hepatic
metastasis)
PROTON PUMP INHIBITORS(PPI’s)
✓ Initial doses of omeprazole 60 mg/d.
✓ Adjusted to achieve a BAO <10 meq/h (at the drug trough) in surgery-naive patients and to <5
meq/h in individuals who have previously undergone an acid-reducing operation.

CHAPTER-2 PEPTIC ULCER

1.DEFINITION



 An ulcer is disruption of the mucosal integrity of the gastrointestinal mucosa.Breaks in the

✗
mucosal surface equal to or greater than 0.5 cm in size , with depth to the sub-mucosa.
✗ Peptic ulcers usually occur in the stomach,pylorus or duodenal bulb, also can develop in the
esophagus and the past bulbar duodenum.
✗ All ulcers in the upper gastrointestinal tract are believed to be caused by the aggressive action of
hydrochloric acid and pepsin on the mucosa, thus they became knows as peptic ulcer.
2.EPIDEMIOLOGY
✗ PU is a common disorder in the world. 10%of all individuals develop symptomatic peptic ulcer in
their lifetime.
✗ Ulcer incidence varies site, sex and age. DU is more than GU in both man and women. DU:
GU=1.5-5.6:1.

3.PATHOLOGY
-Ulcer may be single or multiple. The shape is round or ovoid. The base of ulcer may be relatively clean
and covered with a layer of pale fibrous exudates.
➢ DU: usually be found in anterior wall of duodenal bulbar. The diameter< 10mm.
➢ GU: usually be found in gastric angle and small curvature of gastric antrum. The diameter of GU
is slightly larger than that of DU.
➢ Giant ulcer: the diameter of ulcer >2cm. even 3 to 6 cm
4.ETIOLOGY AND PATHOGENESIS
✓ Increased acid-pepsin secretion, decreased mucosal resistance, or these two factors in
combination are ulcerogenic.
✓ Imbalance between the invasive activity of acid-pepsin and mucosal resistance
1.Invasive(Aggressive) Factors :Acid-Pepsin, HPBile salt,Alcohol, Drugs,( aspirin, steroids) Smoking
Stress. ……
2.Defensive Factors : Mucus/Bicarbonate Barrier,Mucosal Blood flow, Prostaglandin, Epidermal growth
factor
I.H. pylori and UGI disorders
• Chronic gastritis
• Peptic ulcer
• gastric mucosal-associated lymphoid tissue (MALT) lymphoma
• gastric adenocarcinoma.
A.HP AND PEPTIC ULCER
i.HP Infection: as the major cause in PU (no Hp,no ulcer) .
ii.The key bacterial factors
✗ urease (converting urea to NH3 and water, thus alkalinizing the surrounding acidic environment),
✗ adhesins,
✗ cytotoxin-associated gene protein (Cag A),
✗ vacuolating cytotoxin (Vac A).
iii.Mechanisms of Helicobacter pylori (Hp) infection :Hp may go through mucus layer and adhere to
mucosa surface with flagellum motility .
(1)Hp release urease urea ammonia + water damage the epithelium and maintain neutral
environment.
(2) Hp induced epithelium to release IL-8 inflammatory reaction .
(3)Hp secrete VacA protein the epithelium injury.
Hp secrete CagA protein inflammatory reaction .

 (4)Hp wall antigen immunoreaction.(antigen-antibody reaction)

(5)H .pylori damage D cells in antral mucusa somatostatin gastrin gastric acid
(6)H .pylori release urease urea ammonia PH gastrin gastric acid
B. NSAIDs
Long-term taking non-steroid anti-inflammatory drugs (NSAIDs) may induce PU, delay the healing of
PU, increase therecurrence rate and complications occurrence rate of PU. NSAIDs relate to GU more
closely..
Pathogenic Mechanisms of NSAIDs
①Suppress endogenous Prostaglandin synthesis
②Cause decreased mucus and bicarbonate secretion
③Diminished mucosal blood flow
④Reduced epithelial cell renewal
The gastric mucosa protects itself from gastric acid with a layer of prostaglandins. NSAIDs block the
function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins.
Newer NSAIDs (celecoxib) only inhibit cox-2, which is less essential in the gastric mucosa, and roughly
halve the risk of NSAID-related gastric ulceration.
Prostaglandins play a critical role in maintaining gastroduodenal mucosal integrity and repair. It
therefore follows that interruption of prostaglandin synthesis can impair mucosal defense and repair.
C. ACID-PEPSIN : Acid-pepsin,no acid no ulcer
The existence of gastric acid is the decisive factor for occurrence of ulcers. it plays an key role in the
development of PU.
D.CIGARETTE SMOKING :smokers have ulcers more frequently than do nonsmokers,
smoking appears to decrease healing rates, impair response to therapy, and increase ulcer-related
complications such as perforation.
E.HEREDITY(GENETIC FACTOR) :Familial aggregation(clustering) of PU.Individuals with blood
group O have an increased risk of PU
5.CLINICAL MANIFESTATIONS
The clinical course of PU is characterized by chronicity (from several years to more than ten years),
periodicity (periods of exacerbation and remission) rhythmical pain.
A Symptoms
1. epigastric pain.
2. epigastric discomfort
3. epigastric distention, anorexia, nausea, vomiting, sour regurgitation and eructation
B SignTenderness may appear in the area of pain.
C Special types of PU
1. Complex ulcers(5%,first DU then GU)
2. Pyloric channel ulcer(similar DU)
3. Post-bulbar ulcer(3%,easy bleeding)
4. Refractory ulcer
5. Senile ulcer (GU >DU,corpus>antrum)
6. Silence ulcer(15%-35%)
DIFFERENTIAL DIAGNOSIS OF PEPTIC ULCER AND DUODENAL ULCER
DUODENAL ULCER GASTRIC ULCER
Age 20-30 30-40

 Ratio 2-4 1
Gastric acid Higher levels Lower levels
HP 90%-100% 70%-80%
Complication More few
Canceration No 1-7%
Pain location Under the sword,near the middle Under the sword, centerlly or
line or right of it slightly to the left
Rhythm of pain Occurs at 3-4hr after the Occurs at 0.5-1 after the meal
meal(empty pain) until next meal
Relieved by eating and anti-acid Can be Can’t
Night pain 50% Rare
6.DIAGNOSIS: Confirmed diagnosis relay on endoscopy and x-ray barium examination .
Endoscopy and biopsy -better than the other examination
Active Stage, A1 , A2
Healing Stage, H1, H2
Scar Stage ,S1,S2
Endoscopy is more reliable than barium contrast x-rays for detecting ulcers
Endoscopy of PU
a. Location:
DU:Anterior wall of duodenal bulb
GU:Lesser curvature of gastric antrum, gastric angle
b.Number:Single or multiple
c.Size & Shape:Round or oval in shape,
X-ray barium examination- particularly gas-barium double contrast technique.
An ulcer crater is demonstrable by X-ray in 50-70% of duodenal ulcer, but may be obscured by deformity
of duodenal bulb. When no ulcer is demonstrated, the following are suggestive of ulceration.
(1).Deformity of the bulb.
(2) irritability of the bulb.
(3).point tenderness over the bulb.
(4).pylorospasm. Spastic notch
(5).gastric hyperperistalsis.
Typical radiographic features of duodenal ulcer-It is associated with marked edema, resulting in the
appearance of radiating folds to the ulcer crater.
7.LABORATORY EXAMINATION
1.Detection of H.Pylori:routine examination of peptic ulcer.
✗ Rapid urease tests are considered the endoscopic diagnostic test of choice.
✗ The presence of H pylori in gastric mucosal biopsy specimens is detected by testing for the
bacterial product urease. If H pylori are present, bacterial urease converts urea to ammonia, which
changes pH and produces a color change.
✗ Antibodies (immunoglobulin G [IgG]) to H pylori can be measured in serum, plasma, or whole
blood. saliva



 ✗Urea breath tests detect H pylori infection by testing for the enzymatic activity of bacterial urease.
In the presence of urease produced by H pylori, labeled carbon dioxide (carbon-13 or 14) is
produced in the stomach, absorbed into the bloodstream, diffused into the lungs, and exhaled.
2. The analysis of gastric juice: mainly is the accessory diagnosis of gastrinoma. BAO>15mmol/h,
MAO>60mmol/h, BAO/MAO>60% suggest gastrinoma.
3. The assay of serum gastrin:>500pg/ml, Gastrinoma(Zollinger-Elison syndrome)
8.DIFFERENTIAL DIAGNOSIS
1.Functional dyspepsia
2.Cholecystitis and cholecystolithiasis
3.Gastric carcinoma
4.Gastrinoma(Zollinger-Elison syndrome)

GASTRIC ULCER GASTRIC CARCINOMA

Age (40y↓) (40y↑)
Courses Longer,Episodicity Shorter, progress
Characters Rhythmicity pain No rhythmicity
Condition well poor
Treatment Effective treatment Difficult treatment
Occult blood Temporary + Continued +
Acid test N or↓ ↓↓↓
X-ray Crater outside gastric wall Within
Endoscopy Small, Smooth,Clear,Flat Opposite

9.COMPLICATIONS
1.Hemorrhage:PU is the commonest cause of upper GI-tract hemorrhage occupying 50%of all causes.
Bleeding occurs in about 10%-20% of ulcer patients.
The manifestations of hemorrhage are hematemesis and/or melena.
50-100ml→ melena
＞ 1000ml→ circulatory dysfunction (vertigo, sweating, BP↓and tachycardia)
＞ 1500ml →can cause shock
Bleeding is easily induced by NSAIDs. The endoscopic examination within 24-48hrs of bleeding is
necessary for a established diagnosis.

2. Perforation:The perforation causes 3 kinds of consequences:

1. free perforation( usually occurs on anterior wall of DU).
2. penetrate deep through serosa and adhesions into the adjacent solid organs (usually occurs on
posterior wall of DU or GU)
3.penetrate into hollow organs forming fistula (DU into common bile duct, GU into duodenum or
transverse colon)

 3. Pyloric obstruction Occupying 2%-4%Clinically, and the vomitus is large in amount with un-
digested foods taken the previous day. If vomiting becomes severe, symptoms of hypovolemia and
alkalosis may develop, and weight loss and malnutrition can be profound.
4. CancerationSmall number of gastric ulcers(1%-2%) may develop the carcinoma of stomach. Should
pay attention to a patient with GU, who has the age exceeds 45 and resistance to medical treatment.

10.TREATMENT
Drug therapy
1. eradicable therapy of HP - Tri-therapy of eradicable HP
PPI or Bi colloid antibiotics
Omeprazole 40mg/d clarithromycin 500-1000mg/d
Lansoprazole 60mg/d amoxicillin 1000-2000mg/d
Pantoprazole 40mg/d metronidazole 800mg/d
Rabeprazole 10mg/d
Colloidal bismuth 480mg/d
Chose 1 kind chose 2 kinds
The above dosage twice a day for 7 days

2. Acid-inhibitor drugs
(1). Antacids: such as aluminum hydroxide gel
(2). Anticholinergic drugs: atropine
(3).H2RA: include cimetidine, ranitidine, famotidine, nizatidine.
Side effects: gynecomastia, leukopenia, dermatitis.
(4). PPI: include Omeprazole, Lansoprazole,Pantoprazole, Rabeprazole.
Comparison of alternative H2RA
H2-RAs, 4-6weeks(healed rate 65%-85%)
PPI, 6-8weeks(healed rate 80%-100%)
3. Drugs protecting mucosa
kinds: sucralfate, colloidal bismuth, misoprostol
Enhancing Mucosal Defense Drugs :sucralfate
① Effect: Forming a viscous shield to cover the ulcer crater; Stimulating the synthesis of Prostaglandins;
Recruiting EGF to the ulcer crater.
②Used: 1g qid, after meal and before sleeping, 4--6 weeks.
③Side effects:Constipation
⑵ Colloidal Bismuth Subcitrate (CBS)
① Effect: Forming a viscous shield to cover the ulcer crater;Killing H. Pylori .Mainly used for GU.
② Used :120mg qid, after meal and before sleeping, 4--6 weeks.
③ Side effects :Constipation



 ⑶Prostaglandins: Misoprostal
① Effect: Inhibit acid secretion;Stimulating the secretion of HCO3- and mucus;Increase mucosal blood
flow.
② Used:200mg qid
③ Side effects: Abdominal pain, Diarrhea.
11.PREVENTION OF ULCER RECURRENCE
✓ Avoid risk factors for recurrence(Smoking, Acid hypersecretion, Complications, HP infection,
NSAIDs).
✓ Eradication of H. Pylori: Important
✓ Maintenance Therapy
✗ H2RA half dosage ,qn, or PPI
✗ 3 - 6 months or 1 - 2 years
Surgical Therapy Indications:
① Massive bleeding poorly responding to medical therapy
② Free perforation
③ Chronic obstruction
④ Intractable ulcer disease
⑤ Suspicious malignancy