The Nobel Prize in Physiology or Medicine 2005

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The Nobel Prize in Physiology or Medicine 2005

• discovery of the bacterium Helicobacter pylori
  and its role in gastritis and peptic ulcer disease

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Syllabus

• Helicobacter pylori
• Gastritis
• Peptic ulcer disease (PUD)

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Helicobacter pylori

• Kingdom Bacteria
• Phylum Proteobacteria
• Class Epsilon Proteobacteria
• Order Campylobacterales
• Family Heliobacteraceae
• Genus Helicobacter
• Species H.pylori

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Helicobacter pylori
Microaerophilic bacteria microorganism that
requires oxygen to survive but oxygen levels must
be lower than atmosphere level

• Helical shaped about 3 um long 0.5 um in
  diameter
• Use flagella for motility
• Circular chromosome with 1,667,867 base pairs
• Gram-negative microaerophilic
• Infects stomach and duodenum

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Helicobacter pylori

• Flagella move through stomach lumens mucus
  layer
• Lives inside the mucus layer above or inside
  epithelial cells
• Dependent of the enzyme urease
• Combat the acidic environment by forming a
  neutralized protective cloud
• Ammonia, protease, catalase and phospholipase
  cause damage

Urease metabolizes urea into carbon dioxide and
ammonia
Molecular model of H.pylori urease enzyme
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Helicobacter pylori

• H. Pylori colonized on the surface of
  regenerative epithelium

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Helicobacter pylori

• Contagious gastro-oral /fecal-oral transmission
• Colonizes within the stomach of about 50 of all
  humans
• Transmitted via mother to child during early
  childhood and the bacteria may remain in the
  stomach for the whole life

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Helicobacter pylori

• Diagnosed by antibody tests, biopsies taken
  during endoscopy or by non-invasive breath tests
• Antibody treatment has backfired due to gene
  mutations
• Eating broccoli sprouts or drinking green tea can
  inhibit its growth
• Yogurt can also reduce infection rate

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Summary in Chinese

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C13??????

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??(GASTRITIS)
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Peptic Ulcer Disease
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Introduction
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Introduction
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Introduction

• PUD(Peptic Ulcer Disease)
• Sores or eroded areas that form in the lining of
  the digestive tract
• Usually occurs in two places
• Duodenum(duodenal ulcer)
• Stomach(gastric ulcer)
• Can also incur esophageal ulcer

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Causes
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Causes

• Helicobacter pylori disrupts the mucous layer and
  causes the release of certain enzymes/toxins
• Long-term use of nonsteroidal anti-inflammatory
  agents (NSAIDs), such as aspirin, naproxen, and
  ibuprofen
• Another
• Preventive mechanisms do not function properly
• Lifestyle factors ex smoking, drinking

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Preventive mechanism

• Digestive mechanism HCl and enzymes(expepsin)
• Preventive mechanism mucous layer and
  prostaglandins(????)

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Infection of H. pylori

• Asymptomatic, cronic, life-long infection
• Usually by transmission from mother to child

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Inflammation

• an infiltration of inflammatory cells
• an inflammation of the underlying gastric mucosa

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Decreasing Protection

• Decrease the protection of gastric mucosa
• Inflammation and perforation become easier

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Ulcer

• Bleeding, perforation of the stamoch and
  duo-denum

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NSAIDs Intro. I

• non-selective inhibitors of cyclooxygenase(COX),
  an enzyme catalyzes prostaglandins and
  thromboxane from arachidonic acid (itself derived
  from the cellular phospholipid bilayer by
  phospholipase A2).
• Prostaglandins act as messenger molecules in the
  process of inflammation.

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NSAIDs Intro. II

• The main adverse drug reactions associated with
  NSAIDs relate to irritation of the
  gastrointestinal tract .
• NSAIDs cause a dual insult on the
  gastrointestinal tract
• the acidic molecules directly irritate the
  gastric mucosa
• inhibition of COX-1 reduces the levels of
  prostaglandins

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Symptoms

• Abdominal pain
• Bloating
• Rush of saliva
• Heartburn
• Nausea or vomiting
• Dark or black stool (due to bleeding)
• Vomiting blood ("coffee-grounds" appearance)
• Loss of appetite and weight loss
• gastric or duodenal perforation

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Treatments

• Antibiotic medication
• Acid blocker
• Antacid
• Proton pump inhibitor(PPI)
• Cyto-protective agent
• Quit using NSAIDs (if it is the cause of PUD)
• Surgery
• Lifestyle change