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