Week 1 (Exam 1): Chapter 55 Flashcards
(48 cards)
Gastritis
Inflammation of gastric mucosa (stomach lining).
Erosive
Causing ulcers
Acid autodigestion
A process where prostaglandins provide a protective mucosal barrier that prevents the stomach from digesting itself.
What protects the stomach mucosa from autodigestion?
Prostaglandins
Acute Gastritis
- Damage by local irritants
- Inflammation of the gastric mucosa or submucosa after exposure to local irritants or other causes.
Chronic Gastritis
- Appears as a patchy, diffuse (spread out) inflammation of the mucosal lining of the stomach.
- Associated with an increased risk for gastric cancer.
- May be categorized as type A, type B, or atrophic
- Chronic local irritation and toxic effects caused by alcohol ingestion, radiation therapy, and smoking have been linked.
Chronic Atrophic gastritis
- Old age- mostly work related (exposure to lead, nickel and all) or H. pylori infection, or related to autoimmune factors.
- Diffuse inflammation and destruction of deeply located glands accompany the condition
- Affects all layers of the stomach, thus decreasing number of cells
- Characterized by total loss of fundal glands, minimal inflammation, thinning of the gastric mucosa, and intestinal metaplasia (abnormal tissue development).
Type A (nonerosive) chronic gastritis
Refers to an inflammation of the glands and the fungus and body of the stomach.
Type B Chronic Gastritis
Usually affects the glands of the antrum but may involve the entire stomach.
Etiology of gastritis
- H. Pylori (gram-negative bacterium that penetrates the mucosal gel layer of the gastric epithelium).
- Long-term NSAID, high risk for acute gastritis. Inhibit prostaglandin production in mucosal barrier.
- Use of alcohol, coffee, caffeine, and corticosteroids.
- Local irritation from radiation therapy
- Accidental or intentional ingestion of corrosive materials (acids or alkalis ex: lye and drain cleaners).
- Autoimmune causes
What can atrophic gastritis lead to?
- Gastric cancer
- Gastric mucosa-associated lymphoid tissue (MALT) lymphoma
Health Promotion and Maintenance
- Balanced diet (limiting caffeine, chocolate, mustard, pepper, and other strong or hot spices)
- Regular exercise (helps prevent gastric contents from irritating the gastric mucosa)
- Stress-reduction techniques (aerobic exercise, meditation, reading, and/or yoga)
- Limit foods and spices that cause gastric distress
- Avoid tobacco (causes vasoconstriction), alcohol
- Avoid excessive use of aspiring, NSAIDs (ibuprofen), and corticosteroids.
- Protect yourself against exposure to toxic substances in the workplace (lead and nickel).
Assessment: Noticing
Acute Gastritis
- Rapid onset of epigastric pain or discomfort
- N/V
- Hematemesis (vomiting blood)
- Gastric hemorrhage
- Dyspepsia (heartburn)
- Anorexia
What are some diagnostic assessments for gastritis?
- EGD with biopsy
- Cytologic examination
- Rapid urease testing
What may the patient report with gastritis?
Epigastric alteration in comfort or pain, anorexia, cramping, and N/V.
What should you assess with gastritis?
Assess for abd. tenderness and bloating, hematemesis (vomiting blood), or melena (dark, sticky feces, as evidence of blood in the stool).
What may result from Aspirin/NSAID-related gastritis?
Dyspepsia (heartburn)
What can often occur with ingestion of contaminated food? Time?
Severe N/V often occur within 5 hours of ingestion of the contaminated food.
In some cases gastric hemorrhage is the presenting sx, which is a life-threatening emergency.
Assessment: Noticing
Chronic Gastritis
- Vague report of epigastric pain that is relieved by food
- Anorexia
- N/V
- Intolerance of fatty and spicy foods
- Pernicious anemia
- Periodic epigastric pain may occur after a meal
- Radiation therapy. Smoking and alcohol use are known to be associated with the development of chronic gastritis
Interventions: Responding
- Acute gastritis treated with supportive care
- Chronic gastritis treated based on causative agents
- Pharmacological Management: H2-receptor antagonists (famotidine (Pepcid)), sucralfate (Carafate, Sulcrate), antacids (maalox and mylanta), antisecretory agents/PPI (Prilosec), prostaglandin analogs, and animicrobials
Treatment for acute gastritis
- If bleeding severe, a blood transfusion may be necessary
- Fluid replacement is prescribed with severe fluid loss
- Surgery, such as partial gastrectomy, pyloroplasty, and/or vagotomy, may be needed for patients with major bleeding or ulceration.
- Primary health care provider prescribes drugs that block and buffer gastric acid secretions to relieve pain.
Treatment for chronic gastritis
- Includes the elimination of causative agents, treatment of any underlying disease (Uremia, Crohn’s disease), avoidance of toxic substances (alcohol, tobacco), and health teaching.
- Primary treatment is eliminating the causative factors, such as H. pylori infection if present.
- Drugs and nutritional therapy
H2 Antagonists (Blockers)
- Block gastric secretions
- Decrease gastric acid secretions
- Give single dose at bedtime for tx of GI ulcers, heartburn, and PUD
- Ex: famotidine (Pepcid), nizatidine (Axid), and ranitidine (Zantac)
Mucosal Barrier Fortifiers
- Protect stomach mucosa
- Ex: sucralfate (Carafate, Sulcrate)- Give 1 hr before and 2 hr after meals and at bedtime (food may interfere with drug’s adherence to mucosa). Do not give within 30 min of giving antacids or other drugs.
- Ex: Bismuth subsalicylate (Pepto-Bismol)- Remind pt to refrain from taking aspirin while on this drug (aspirin is a salicylic acid and can lead to OD).