ANATOMY

Stomach
Hollow muscular organ

Function of stomach

Bluk storage of food

...

Parts

Cardia

Nearest region

Body

Midportion

Antrum

Most frequent site of ulcers

Pylorus

HISTOLOGY OF THE STOMACH

Gastric glands
Parietal cells (oxyntic cells)
Intrinsic factor and HCl

Chief cells (zymogen)

Pepsinogen
Enteroendocrine (APUD)
Serotonin
Pyloric glnds
Mucus
HCl and enzymes are corrosive - can damage the mucosa

DEFENSES
Preepithelial
Mucus
Bicarbonate

Surface active phospholipids

Epithelial

Cellular resistance

Restitution

Prostaglandins and growth factors

Cell proli

Subepithelial

Blood flow

Leukocytes

PHASES OF GASTRIC ACID SECRETION

Cephalic Phase
Stimulated by sight smell taste and thought of food

Center: CNS

Predominantly neural

Function: Prepare stomach for arrival

Duration: short (minutes)

 Mechanism: via preganglionic fibers in vagus nerve

Stimulation of mucus and enzyme production

Gastric phase
Enhance the secretions started in cephalic phase
Homogenizes and acidifies chyme

Initiate protein digestion by protein

Neural and hormonal mechanism

Increase acid and pepsinogen production

Intestinal phase
Control in the rate of entey of chyme into the duodenum
Longest phase (hours)

Neural and hormonal mechanisms

Feedback inhibition of gastric and pepsinogen secretion

Reduction in gastric motility - to set the stage for absorption

Hormones secreted
CCK

Somatostatin

ULCERS

Characteristics

Disruption of the mucosal integrity of the stomach leading to local defect or excavatiob due to
active inflammation

Greater than 5 mm depth to the submucosa

Erosions - superficial mucosal defects

Ulcers - extending through muscluaris mucosa

Gastritis - inflammatory response to mucosal injury; no disruption of mucosa

PEPTIC ULCER DISEASE

An endoscopic diagnosis
APD - no endoscopy diagnosis
Epidemiology
10% population is expected to develop PUD

10% of ER consulations are patients with PUD

Decreasing prevalence over the last 30 years

Due to treatments, medications

Discovery of the etiologic agent

Male predominance

Gastritis - similar for both sexes

Pathophysiology
Occurs because of an imbalance between aggressive factors and mechanisms that maintain
mucosal integrity

Risk factors for Gastric mucosal Disruption

H. Pylori
Almost all duodenal ulcers

NSAIDs/ASA (even at low doses)

Coee/Caeine

 Ethanol

Tobacco

Severe physiologic stress

Burns - Curlings

CNS trauma - Cushings

Surgery

Severe medical illness

Steroids

Helicobacter pylori
Gram negative rod

Fecal-oral MOT

Secretes urease
Convert urea to ammonia

Produces alkaline environment

Mechanisms:
Direct mucosal damage

Alterations in the host inflammatory response

Common in elderly individuals

Higher prevalence in LES

Asymptomatic in 70% of those who are H. Pylori (+)

Class 1 carcinogen - gastric ca

NSAIDs
15% of patients on prolonged therapy

Decrease prostaglandins by inhibition of the cyclooxygenase pathway

Cyclooxygenase- protective mechanism (epithelial)

H. Pylori Ulcer

More often dudenum

Often superficial

Less severe gi bleeding

Higher rate of recurrence - 60-85%

If without : 5-10%

NSAID ulcers

Stomach

Deep

More sever gi bleeding

Sometimes asymptomatic

Duodenal ulcer
Younger age group

Rarely malignant

Usually less than 1cm in diameter

Abdominal pain : 90 minutes to 3 hours after a meal

Awaken from sleep

Relieved by antacids or food intake

Pain-food-relief pattern
Gastric ulcer
Older age group

Greater propensity for Malignancy

Greater than 1cm

Abdominal pain: precipitated by food

Relieved by vomiting

Nausea and weight loss more common

Dierential Diagnosis
Neoplasms of the stomach

Pancreatitis

Pancreatic ca

Diverticulitis

Nonulcer dyspepsia

Cholecystitis

GERD

Acute MI - do an ecg

Physical Exam Findings

Epigastric tenderness - usually mild

Normal bowel sounds

Rectal exam - may show positive melena/guiac stool

Diagnostic Examination
H. pylori test
Biopsy-based

Rapid urease test

Simple

Histology

Culture

Nonivasive

Urea breath test

Serology

Upper GI series
Filling defect

Test can miss put ulcer if less than 2 cm

80% sensitivity

90% in double contrast

Decreased sensitivity when ulcers are small

Endoscopy
Considered as Gold Standard
Most sensitive and specific
Aords direct visualization of the mucosa

Biopsy - rule out malognancy and rule in presence of h. Pylori

Can identify lesions too small to detect through barium exam

Detect location of bleeding

Goals of Treatment for PUD without HP : Antisecretory agents

Goals of Treatment for PUD with HP

ERADICATION of HP for all confirmed DU and GU whether on inital presentation or
recurrence

 Anti-ulcer + 2 Antibiotics
Antiulcer
PPI
H2RA
Bismuth Compounds
Antibiotics
Clarithromycin - mainstay

Amoxicillin
Metronidazole
Goals of Treatment for PUD with NSAID and HP
Eradicate HP
Withdraw NSAIDS

If NSAIDS are needed - give with PPIs or give COX2 inhibitors

Complications
GI Bleeding
Most common cause of gi bleeding

Perforation
Gastric Outlet Obsteuction
Gastric Ca

GASTRITIS
Acute Gastritis
Lasts for several hours to days

Food alcohol bile reflux radiation

Chronic Gastritis
Repeated exposure to irritating agents

Type a: autoimmune

Type b: HP related; mc in antrum

Pathology
Gastric mucosa becomes edematpus and hyperemic and undergoes superficial erosion

Secretes scanty amounts of gastric juice

Signs and Symptoms

Acute gastritis
Abdomnial pain
Chronic gastritis
Pallor anemia - d/t decreased intrinsic factor

Assessment and Diagnostic Findings

Hypo or hyperchlorydia
H pylori detection

Medical Management
Acute gastritis
Gastric mucosa is capable of repairing itself
The patients recovers in abput 1 day

Symptomatic

 Bland diet
If bleeding:

If caused by ingestion of strong acids or alkali: treatment consists of diluting the agent

Chronic gastritis

Modifying patients diet

Promoting rest

Reducing stress

Initiating pharmacotherapy

H. Pylori

Antibiotics

PPI

Bismuth