Stomach Disorders
Introduction to Stomach Disorders
Discussion led by Mrs. Paige focusing on disorders affecting the stomach.
The stomach plays a crucial role in the digestive process.
Stomach problems can impair or alter digestion and nutrition.
Anatomy of the Stomach
Key anatomical landmarks:
- Esophagus
- Gastroesophageal junction
- Duodenum
- PylorusDisorders discussed will be related to these specific parts.
Nausea and Vomiting
Definitions:
Nausea: A vague, unpleasant sensation of sickness or queasiness.
Vomiting: A forceful expulsion of contents from the upper gastrointestinal tract.
Medications for Nausea/Vomiting:
Serotonin receptor antagonists:
- Example: Ondansetron (Zofran)Dopamine antagonists:
- Examples: Promethazine (Phenergan), Prochlorperazine (Compazine), DroperidolAntihistamines:
- Examples: Meclizine (Antivert), DramamineCannabinoids:
- Example: Dronabinol (Marinol)
Interventions for Nausea/Vomiting:
Encourage deep breathing to suppress the vomiting reflex.
Instruct patient to consume small amounts of clear liquids.
Foods should be consumed at separate times from fluids.
Monitor for signs of dehydration.
Eliminate offensive odors.
Perform oral care.
Position the patient upright while vomiting.
Monitor for complications:
- Dehydration
- Hypokalemia
- Metabolic alkalosis
- Aspiration pneumonia
- Esophageal ruptures or tears
Gastritis
Definition:
Gastritis: Inflammation of the gastric mucosa.
Classification:
Classified according to
- Cause
- Cellular change
- Distribution of lesionsErosive gastritis: Causes ulcers.
Non-erosive gastritis: Auto-digestion due to a protective mucosal barrier failure.
Types of Gastritis:
Acute Gastritis:
Inflammation of the mucosa or submucosa.
Causes:
- Infections (e.g., H. pylori, Staphylococcus, Streptococcus, E. coli, Salmonella)
- Long-term NSAID use, alcohol, caffeine, corticosteroids, radiation therapy
- Accidental ingestion of corrosive substances (acids, alkalines)Manifestations:
- Thickened red mucous membranes with prominent rugae
- Mucosal necrosis and inflammatory reactionSigns and Symptoms:
- Acute epigastric pain or discomfort
- Abdominal tenderness
- Abdominal bloating
- Nausea and vomiting
- Hematemesis
- Melena
- Gastric hemorrhage
- Dyspepsia
- Anorexia
Chronic Gastritis:
Diffuse, asynchronous inflammation of the gastric lining.
Results in mucosal thinning and atrophy of parietal cells, leading to lack of intrinsic factor and possible pernicious anemia.
Two types:
Type A Chronic Gastritis:
Characterized as non-erosive; causes inflammation in the body and fundus of the stomach.
Often due to autoimmune factors.
Type B Chronic Gastritis:
Affects the antrum and can encompass the whole stomach, typically caused by H. pylori infection.
Associated with:
- Alcohol ingestion
- Smoking
- Radiation therapy
- Crohn's disease
- Graft versus host disease
- UremiaAtrophic gastritis: Common in older adults from toxic work substance exposure, potential gastric cancer risk.
Signs and Symptoms of Chronic Gastritis:
Epigastric pain relieved by food.
Anorexia.
Nausea and vomiting.
Intolerance to fatty and spicy foods.
Pernicious anemia.
Diagnostic Tests:
EGD: Gold standard for diagnosis.
Biopsies: For cellular assessment.
Gastric analysis: To check for intrinsic factor deficiency.
H. pylori testing: Rapid urease testing recommended without antacids for a week.
Prevention of Gastritis:
Well-balanced diet avoiding distress-causing foods (caffeine, chocolate, spicy foods).
Regular exercise to maintain peristalsis.
Limiting alcohol and quitting smoking.
Caution with NSAIDs, aspirin, and coffee intake.
Stress management techniques (yoga, meditation, reading).
Protect against workplace toxicity.
Treatment:
Acute gastritis typically heals spontaneously within days; symptomatic treatment is sufficient.
Severe cases may require blood transfusions or surgery for ulceration.
For chronic gastritis, eliminate causative agents (e.g., antibiotics for H. pylori, avoid toxic substances).
Medications:
H2 receptor antagonists: Block gastric secretions.
Antacids: Buffer agents enhancing gastric pH.
Mucosal barriers: Such as sucralfate, to protect mucosa.
Proton pump inhibitors (PPIs): Suppresses gastric acid secretion.
Peptic Ulcer Disease
Definition:
Peptic Ulcer: A mucosal lesion within the stomach or duodenum, arising when mucosal defenses are impaired.
Etiology:
Primarily caused by H. pylori infections.
H. pylori transmission via contaminated food/water.
Urease produced by H. pylori neutralizes stomach acid, aiding bacterial survival.
Types of Peptic Ulcers:
Gastric Ulcers:
Develop in the stomach's antrum near acid-secreting mucosa.
Causes:
- Break in the mucosal barrier due to infection
- Dysfunctional pyloric sphincter leading to bile refluxManifestations:
- Delayed gastric emptying with regurgitation
- Decreased blood flow to gastric mucosa, increasing ulcer risk.
Duodenal Ulcers:
Occur in the upper duodenum, deep and sharply demarcated.
Causes:
- Protein-rich meals, calcium intake, vagal nerve stimulation, rapid gastric emptying.
- High gastric acid secretion with low pH.
Stress Ulcers:
Develop after medical crisis or trauma (e.g., sepsis, increased intracranial pressure).
Complications: Gastric erosion leading to bleeding.
Complications of Peptic Ulcer Disease:
Hemorrhage: Most severe complication.
- Signs: Hematemesis, melena.Perforation: Full thickness erosion, leading to peritonitis.
- Symptoms: Sudden mid-epigastric pain, rigid abdomen, abdominal tenderness.Pyloric Obstruction: Resulting from scarring/inflammation causing blockage.
- Signs: Abdominal bloating, nausea, vomiting, potential metabolic alkalosis.
Assessment:
History taking focusing on risk factors (alcohol, tobacco, diet, stress).
Physical assessment for tenderness, bowel sounds, ulcers' relationship to eating/sleeping patterns.
Diagnostic Tests:
Various types of H. pylori tests (serum, urea breath, stool antigen).
Imaging studies (X-rays, EGD).
Interventions:
Drug Therapy:
Antibiotics for H. pylori with a proton pump inhibitor.
Antacids, H2 receptor antagonists, and mucosal protectants (e.g., sucralfate).
Nutrition Therapy:
Bland diet, avoidance of bedtime snacking, and alcohol.
Complementary Therapy:
Stress reduction techniques (e.g., yoga).
Herbs (consult healthcare provider before use).
Non-surgical Interventions:
IV fluids, NG tube for bleeding assessment, EGD with cautery.
Surgical Options:
Minimally invasive and conventional surgeries, gastrectomy, pyloroplasty, vagotomy.
Gastric Cancer
Definition:
Most gastric cancers are adenocarcinomas.
Often asymptomatic in early stages, usually diagnosed at advanced stages.
Risk Factors:
H. pylori infection, pernicious anemia, gastric polyps, chronic atrophic gastritis, toxic substance exposure, dietary factors (processed foods, low fruit and vegetable intake).
Assessment:
History focusing on risk factors, physical symptoms (indigestion, fullness, retrosternal pain, anemia).
Diagnostic Tests:
Laboratory tests (hemoglobin, occult blood).
- Possible elevated carcinoembryonic antigen (CEA) levels.EGD confirmation with biopsy, CT, PET, or MRI.
Interventions:
Non-surgical:
Chemotherapy and radiation.
Surgical:
Tumor removal (total or subtotal gastrectomy).
Postoperative Care:
Focus on preventing complications (atelectasis, infection, ileus).
Monitor lung sounds, bowel sounds, and surgical site regularly.
Complications of Gastric Cancer:
Dumping Syndrome:
Rapid gastric content emptying leading to symptoms post-eating (e.g., tachycardia, vertigo).
Management includes diet modification (high protein, high fat, limited carbohydrates) and meal timing.
Alkaline Reflux Gastropathy:
Bile reflux into the stomach, leading to abnormal fullness and distension.
Delayed Gastric Emptying:
Causes and management similar to gastric surgery complications.
Nutritional Deficiencies:
Vitamin B12, folate, iron deficiencies post-cancer treatment; dietary adaptations recommended.