Transcript Peptic Ulcer Disease

Upper Gastrointestinal
Diseases
Upper GI Diseases
Esophagus
 Stomach
 Duodenum

Esophageal Diseases
Esophageal Diseases
Esophageal Symptoms
 Esophageal Motility Disorders
 Gastroesophageal Reflux

Esophageal Swallowing Disorders
Esophageal Symptoms

Dysphagia = difficulty swallowing
– oropharyngeal dysphagia = difficulty initiating
swallow or transferring food from mouth into
esophagus. Can also experience nasopharyngeal
regurgitation (comes out nose) or pulmonary
aspiration.
– esophageal dysphagia = food gets stuck in
esophagus after swallowing
Esophageal Motility Disorders
Achalasia (failure to relax)
 Diffuse Esophageal Spasm (DES)
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Achalasia
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Most often results from post-ganglionic
denervation of smooth muscle of esophagus
absence of inhibitory neural input to LES ↑
LES pressure
 Functional esophageal obstruction  can
lead to esophageal dilatation
 Similar disorder in Chagas disease
(Trypanosoma cruzi causes injury to
myenteric plexuses of esophagus)
Diffuse Esophageal Spasm (DES)

periodic chest pain & dysphagia high
amplitude, simultaneous, repetitive SM
contractions
– can be spontaneous or initiated by swallow
barium swallow  “corkscrew” appearance to
esophagus
 pathogenesis unknown
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Gastroesophageal Reflux (GER)

A little bit of GER is normal in all of us
– Normally, thoraxic cavity has negative pressure
during inspiration
– GER would occur continuously without antireflux
mechanisms
– a portion of esophagus is below the diaphragm 
intra-abdominal pressure (+5 mm Hg) can
reinforce LES pressure (antireflux effect)
– Loss of subdiaphragmatic LES  correlation
between esophageal hernia and GERD
Gastroesophageal Reflux (GER)
Mechanisms
Incompetent anti-reflux mechanisms
 Ineffective esophageal clearance
 Decreased gastric emptying

Gastroesophageal Reflux (GER)
Risk factors

Obesity
 Pregnancy
 Smoking
 High-fat foods
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Theophylline
Caffeine
Coffee
Chocolate
High levels of
estrogen/progesterone
Gastroesophageal Reflux (GER)
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Pyrosis
 Dyspepsia
 Regurgitation
 Dysphagia
Gastroesophageal Reflux (GER)
Diagnosis of GER
 Best test: pH probe
– checks for existence of acid reflux and association
between esophageal acid and chest pain
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Other tests
– Barium swallow
– Esophagoscopy
– Esophagial biopsy
Gastroesophageal Reflux (GER)
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Complications of GERD
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Erosive esophagitis
Esophageal ulcer
Bleeding
Esophageal stricture
Intestinal metaplasia (Barrett’s)
Adencarcinoma from Barrett’s
Lung diseases
Gastritis and Ulcer Disease
Peptic Ulcer Disease – Range of injury
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Ulcer:
A lesion on an epithelial surface (skin or mucous
membrane) caused by superficial loss of tissue.
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Erosion:
A lesion on an epithelial surface (skin or mucous
membrane) caused by superficial loss of tissue
which is limited to the mucosa.
Peptic Ulcer Disease – Location
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Stomach:
– typically in antrum (distal stomach
– normally lined by columnar
epithelium that does not secrete
acid - more susceptible to peptic
ulceration)
– parietal cells located in
body/fundus (proximal stomach ulcers not found as often here)
Peptic Ulcer Disease – Location
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Duodenum:
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within duodenal bulb
can cause outlet obstruction
usually single
multiple/large/more distal ulcers (Zollinger-Ellison sdr.)
Gastric Mucosa & Secretions
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The defensive forces
– Bicarbonate
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The aggressive forces
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Mucus layer
Mucosal blood flow
Prostaglandins
Growth factors
Helicobacter pylori
HCl acid
Pepsins
NSAIDs
Bile acids
Ischemia and hypoxia
Smoking and alcohol
When the aggressive factors increase or the defensive
factors decrease, mucosal damage will result, leading to
erosions and ulcerations.
Gastritis
Causes of Acute Gastritis
Alcohol
 NSAIDs
 Helicobacter
 Stress/ICU associated
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Mechanisms of Acute Gastritis
Drugs (non-steroidal anti-inflammatory
drugs NSAID), alcohol cause acute
erosion (loss of mucosa superficial to
muscularis mucosae).Can result in
severe haemorrhage
 Acute Helicobacter infection has a
prominent neutrophil infiltrate
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Chronic Gastritis
A – autoimmune
 B – bacterial
(helicobacter)
 C - chemical
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Chronic Gastritis
Type A - Autoimmune (associated with
vitamin B12 malabsorption (pernicious
anaemia)
 Type B - Helicobacter pylori infection
 Type C - Chemical damage (bile reflux,
drugs)
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Helicobacter Pylori
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Adapted to live in
association with surface
epithelium beneath mucus
barrier
 Causes cell damage and
inflammatory cell infiltration
 In most countries the
majority of adults are
infected
Helicobacter Gastritis
Acute inflammation mediated by
complement and cytokines
 Polymorphisms infiltrate epithelium and
may be partly responsible for its
destruction
 An immune response is also initiated
(antibodies may be detected in serum)
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Consequences of Gastritis
Peptic ulcer disease (Helicobacter)
 Adenocarcinoma (all types)
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Definitions
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Peptic Ulcer
An ulcer of the alimentary tract
mucosa, usually in the stomach
or duodenum, and rarely in the
lower esophagus, where the
mucosa is exposed to the acid
gastric secretion.
It has to be deep enough to
penetrate the muscularis
mucosa.
Etiology
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The two most common causes of PUD are:
– Helicobacter pylori infection
– Non-steroidal anti-inflammatory drugs (NSAIDS)
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Other uncommon causes include:
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Gastrinoma (Gastrin secreting tumor)
Stress ulceration (trauma, burns, critical illness)
Viral infections
Vascular insufficiency
Etiology – Helicobacter pylori
Helicobacter pylori
PUD – Clinical Presentation
Symptoms of PUD
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Pain
– Epigastric pain
– Hunger pain
– Nocturnal pain
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Other symptoms
– Waterbrash
– Heartburn
– Vomiting
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Asymptomatic
– 1% - 3% adults endoscopy volunteers
– 20% of complicated ulcers present without previous
symptoms
Peptic Ulcer Disease - Diagnosis
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Diagnosis of ulcer
Diagnosis of H. pylori
Diagnosis of H. pylori
Tests for Helicobacter pylori
Non-invasive
 C13 or C14 Urea Breath Test
 Stool antigen test
 H. pylori IgG titer (serology)
Invasive
 Gastric mucosal biopsy
 Rapid Urease test
PUD – Complications
Complications of PUD
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Bleeding
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Perforation
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Gastric outlet or duodenal obstruction
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Chronic anemia