Upper Gastrointestinal
Upper Gastrointestinal Overview
University of Kentucky
College of Nursing
HCl Secretion in the Stomach
Cells responsible for HCl secretion:
G-cells
Parietal cells
Chief cells
Epithelial cells
Esophageal Disorders
Common Disorders
GERD (Gastroesophageal Reflux Disease)
Upper GI Problems
Inflammatory Disorders of the Stomach
Gastritis
Hiatal Hernia
Acute Gastroenteritis
Peptic Ulcer Disease (PUD)
Dysphagia
Definition: Difficulty swallowing
Characteristics:
Begins with solids and progresses to liquids
Causes of Dysphagia:
Mechanical obstruction:
Stenosis or stricture
Diverticula
Tumors
Neuromuscular dysfunction:
Cerebrovascular accident (CVA)
Achalasia (Lower Esophageal Sphincter (LES) cannot open properly)
GERD
Definition
Gastroesophageal Reflux Disease:
Backflow of highly acidic material from the stomach into the esophagus via the lower esophageal sphincter (LES)
Potential results:
Inflammation
Pain
Complications: ulceration, scarring, strictures, Barrett esophagus
Etiology
Factors that alter closure strength of LES or increase abdominal pressure:
Fatty foods
Caffeine
Large amounts of alcohol
Cigarette smoking
Sleep position
Obesity
Pregnancy
Pharmacologic agents
Clinical Manifestations
Heartburn (pyrosis)
Dyspepsia
Regurgitation
Chest pain
Dysphagia
Pulmonary symptoms (Asthma related to GERD)
Esophagitis
Causes
Other causes of esophagitis include:
Infection
Chemical ingestion
Drugs
Frequent emesis (bulimia)
Hiatal Hernia
Definition
Hiatal Hernia: Defect in the diaphragm allowing part of the stomach to pass into the thorax
Types of Hiatal Hernia:
Sliding hernia
Paraesophageal hernia
Pathophysiology
Risk Factors for Hiatal Hernia:
Age
Conditions that loosen the muscular band around the gastroesophageal junction
Clinical Manifestations:
Asymptomatic
Symptoms similar to those of GERD
Contributing Factors to Gastroesophageal Reflux
Factors contributing to reflux:
Decreased LES strength
Increased abdominal pressure
Excessive gastric motility
Overproduction of HCl
Mucosal injury and inflammation
Barrett’s esophagus and esophageal cancer
Gastritis
Acute Gastritis
Definition: Temporary inflammation of the stomach lining
Etiology:
Irritating substances (e.g., alcohol)
Drugs (NSAIDs)
Infection
Chronic Gastritis
Definition: Progressive disorder featuring chronic inflammation in the stomach
Main Etiologies:
Autoimmune causing attack on parietal cells
H. pylori infection
H. pylori
Overview
What is H. pylori?
Helicobacter pylori
Thrives in acidic environment, causing persistent inflammation
Implications: Chronic gastritis, PUD, stomach cancer
Transmission: Not specified in transcript
Acute and Chronic Gastritis: Clinical Manifestations
Common symptoms:
Sometimes none present
Anorexia
Nausea and Vomiting (N/V)
Postprandial discomfort
Hematemesis
Anemia
Vomiting blood
Stomach burning
Loss of appetite
Black stool
Acute Gastroenteritis
Definition: Inflammation of the stomach and small intestine
Etiology:
Clinical Manifestations:
Diarrhea
Abdominal pain
N/V
Fever, malaise
Complication: Fluid volume depletion
Peptic Ulcer Disease (PUD)
Overview
Definition: Ulcerative disorders affecting the upper GI tract including esophagus, stomach, duodenum
Cause of Development: Exposure of GI tract to acid and pepsin
Balancing Act in Upper GI Health
Aggressive Factors
H. pylori
NSAIDs
Acid
Pepsin
Smoking
Defensive Factors
Mucus
Bicarbonate
Blood flow
Prostaglandins
PUD Etiology
Primary causes include:
H. pylori
Injury-causing substances (NSAIDs, ASA, alcohol)
Excessive secretion of acid
Stress
Smoking
Family history
Mechanism of H. pylori in PUD
Process:
Secretes an endotoxin destroying the mucus layer
Secretes protease destroying gastric epithelium
Secretes urease, irritating mucosal cells
Triggers inflammatory response in colonization area
NSAID Induced Gastric Injury
Mechanisms:
NSAIDs block secretion of protective prostaglandins via COX-1 inhibition
Direct irritation to gastric wall
Increased pepsin production via COX-2 inhibition
Clinical Manifestations of PUD
Some patients may be asymptomatic
Common symptoms include:
N/V
Anorexia
Weight loss
Bleeding
Pain based on ulcer type:
Gastric ulcer:
Burning, cramping, gas-like
Timing: 1-2 hours post meals
Duodenal ulcer:
Same symptoms as gastric
Timing: 2-4 hours post meals
Complications of PUD
HOP:
H: Hemorrhage
O: Obstruction
P: Perforation and Peritonitis
Mechanism: Spurting artery from erosion into an artery
Drug Treatments for Upper GI Problems
Classes of Drugs
Antacids
Sucralfate
Antibiotics
H2 receptor antagonists
Proton pump inhibitors
Metoclopramide
Antacids
Mechanism of Action
Large doses: Neutralizes acid
Example Reaction:
Small doses: Increases secretion of mucus, PG, and HCO3
Indications
PUD (healing)
GERD (symptom relief)
Stress ulcers (prophylaxis)
Major Forms of Antacids
Aluminum (Al): Basajel; Side Effect: Constipation
Calcium (Ca): Tums; Side Effect: Constipation
Magnesium (Mg): Milk of Magnesia; Side Effect: Diarrhea
Al + Mg: Maalox, Mylanta; Balanced approach
Adverse Effects
Diarrhea or constipation
Acid rebound
Drug interactions: chelation & altered gastric absorption
Sucralfate (Carafate)
Composition
Unique drug composed of:
Sucrose-base
Aluminum hydroxide
Mechanism of Action
Alters when exposed to gastric acid, forming a sticky gel providing a protective barrier
Indication
Uses:
Duodenal ulcers (FDA-approved)
Gastric ulcers (evidence supporting use)
Mode of Delivery
Oral (tablet or suspension)
Adverse Effects
No major adverse effects
Interactions: decreased drug absorption (require 2-hour separation)
Treating H. pylori
Treatment Plan
Approach: Several antibiotics + gastric acid inhibitor (e.g., Metronidazole, tetracycline, bismuth, different PPI or H2RA)
Rationale for Combination Therapy: Minimize resistance (H. pylori thrives in acidic environments)
Length of Treatment: 10-14 days
Cost: Approximately $200, can involve up to 12 pills
Drug Targets in Gastric Acid Production
Compounds involved include:
Histamine
H2 Receptor
Proton Pump
Other receptors in parietal cells
Histamine Type 2 Receptor Antagonists (H2RA)
Prototypes
Cimetidine (Tagamet)
Famotidine (Pepcid)
Mechanism of Action
Blocks H2 receptor, reducing gastric acid secretion
Indication
GERD (relieves symptoms)
PUD (promotes healing, prophylaxis)
Adverse Effects
Generally well-tolerated
Possible CNS effects in elderly
Slightly increased risk for pneumonia in elderly patients
Proton Pump Inhibitors (PPI)
Prototypes
Omeprazole (Prilosec)
Pantoprazole (Protonix)
Mechanism of Action
Binds to proton pump, irreversibly inhibiting the secretion of HCl
Indications
Short-term treatment of PUD and GERD
Adverse Effects
Short-term effects: Not specified
Long-term effects: May include pneumonia, hip fractures, stomach cancer
Interactions: Limited
Nursing Implications: Short-term use recommended; some PPIs given IV in specific cases
Prokinetic Agent
Metoclopramide (Reglan)
Classification
Prokinetic, antiemetic
Mechanism of Action
Increases upper GI motility
Suppresses emesis
Indications
GERD
Chemotherapy induced N/V or post-operative N/V
Adverse Effects
Multiple side effects noted
Neuro effects include: sedation or restlessness
Extrapyramidal reactions possible
Extrapyramidal Reactions
Definition: Network of neurons in the brain responsible for movement coordination
Symptoms can include:
Akinesia (difficulty in initiating movement)
Akathesia (inability to remain still)
Tardive dyskinesias (involuntary movements of the face and extremities)
Tardive Dyskinesias
Description: Movement disorder caused by certain medications; symptoms often involve abnormal, involuntary muscle movements.