Upper Gastrointestinal Diseases
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Transcript of Upper Gastrointestinal Diseases
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)
Achalasia
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
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
Theophylline Caffeine Coffee Chocolate High levels of
estrogen/progesterone
Gastroesophageal Reflux (GER)
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
Other tests– Barium swallow– Esophagoscopy– Esophagial biopsy
Gastroesophageal Reflux (GER)
Complications of GERD– 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
Ulcer:A lesion on an epithelial surface (skin or mucous membrane) caused by superficial loss of tissue.
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
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
Duodenum:– within duodenal bulb– can cause outlet obstruction – usually single– multiple/large/more distal ulcers (Zollinger-Ellison sdr.)
The defensive forces– Bicarbonate– Mucus layer– Mucosal blood flow– Prostaglandins– Growth factors
The aggressive forces– 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.
Gastric Mucosa & Secretions
Gastritis
Causes of Acute Gastritis
Alcohol NSAIDs Helicobacter Stress/ICU associated
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
Chronic Gastritis
A – autoimmune B – bacterial
(helicobacter) C - chemical
Chronic Gastritis
Type A - Autoimmune (associated with vitamin B12 malabsorption (pernicious anaemia)
Type B - Helicobacter pylori infection Type C - Chemical damage (bile reflux,
drugs)
Helicobacter Pylori
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)
Consequences of Gastritis
Peptic ulcer disease (Helicobacter) Adenocarcinoma (all types)
Definitions
Peptic UlcerAn 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.
The two most common causes of PUD are:
– Helicobacter pylori infection– Non-steroidal anti-inflammatory drugs (NSAIDS)
Other uncommon causes include:
– Gastrinoma (Gastrin secreting tumor)– Stress ulceration (trauma, burns, critical illness)– Viral infections– Vascular insufficiency
Etiology
Etiology – Helicobacter pylori
Helicobacter pylori
Symptoms of PUD
Pain– Epigastric pain– Hunger pain– Nocturnal pain
Other symptoms– Waterbrash– Heartburn– Vomiting
Asymptomatic – 1% - 3% adults endoscopy volunteers– 20% of complicated ulcers present without previous symptoms
PUD – Clinical Presentation
Peptic Ulcer Disease - Diagnosis
Diagnosis of ulcer 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
Diagnosis of H. pylori
Complications of PUD
Bleeding
Perforation
Gastric outlet or duodenal obstruction
Chronic anemia
PUD – Complications