Peptic Ulcer Disease Flashcards
Peptic Ulcer Disease
Erosion of GI mucosa resulting from digestive action of HCl acid and pepsin
Acute Peptic Ulcer Disease
Superficial, minimal inflammation and short duration
Chronic Peptic Ulcer Disease
Muscular wall involved, scar tissue, and longer duration
Gastric vs Duodenal
Based on location
Patho
Defects in gastric or duodenal mucosa that extends through muscularis mucosa
Develop only in presence of gastric acid
Excess gastric acid may not be necessary
Etiology: Helicobacter pylori
Produces enzyme urase
-mediates inflammation making mucosa more vulnerable
Etiology: Aspirin and NSAIDs
Inhibit syntheses of prostaglandins
-Cause abnormal permeability
Etiology: Corticosteroids
Decrease rate of mucosal cell renewal
-Decrease protective effects
Etiology: Lifestyle factors
Alcohol
Smoking
Coffee
Etiology: stress (physiological and psychological)
Burns, Surgery, Sever medical illness, sepsis, traumatic injuries
Cushing ulcers
Gastric Ulcers
Occurs in any portion of stomach Less common than duodenal ulcers Prevalent in women, older adults Peaking incidence >50 years of age Risk factors: H. pylori, medications, smoking, bile reflux
Duodenal Ulcers
Occur at any age and in anyone
-Increase between ages 35-45
Account for 80% 0f all peptic ulcers
Familial tendency
-Blood group O increased risk
Associated with increased HCl acid secretion
-Alcohol, cigarette smoking
H. pylori is found in 90% - 95% of patients
Increased risk:
-COPD, cirrhosis of liver, chronic pancreatitis, hyperparathyroidism, chronic kidney disease
Zollinger-Ellison syndrome
Gastric ulcer pain
Pain high in epigastrium
- 1-2 hrs after meals
- Burning or gaseous
- Food aggravates pain as ulcer has eroded through gastric mucosa
Duodenal Ulcer pain
Midepigastric region beneath xiphoid process
Back pain: if ulcer is located in posterior aspect
2-5 hrs after meals
Burning of cramplike
intermittent
3 major complications
Hemorrhage (most common)
Perforation
Gastric outlet obstruction (treatment)
*All considered emergency situations!
Gastric Outlet Obstruction
Both acute and chronic can result in this
Predisposition: ulcers located in antrum and pre-pyloric and pyloric areas of stomach/duodenum
Occurs due to:
-edema, inflammation, pyloro-spasm, fibrous scar tissue formation
Diagnostic studies
Endoscopy w/ biopsy
Tests for H. pylori:
-Urea breath test & stool antigen test
-biopsy and testing for urease (GOLD STANDARD)
Barium contrast study
Radioloy
Gastric analysis
Lab analysis
CBC
Liver enzymes
Guaiac stool test
Serum amylase
Medical regimen consists of:
Adequate rest Drug therapy Elimination of smoking and alcohol Dietary modification Long-term follow-up care Stress management
Collaborative care
Complete healing may take 3-9 weeks
-Should be assessed by means of x-rays or endoscopic examination
Aspirin and nonselective NSAIDs may be stopped for 4-6 weeks
Smoking cessation
Drug Therapy
H2R blockers PPI Antibiotics Antacids Anticholinergics Cytoprotective therapy Tricyclic antidepressants
Nutritional Therapy
Dietary modifications
-Food and beverages irritating to patient are avoided or eliminated
Bland diet may be recommended
Six small meals a day during symptomatic phase
Nursing assessment
Past Heatlh hx Medication usage Heartburn Weight loss Black, tarry stools Epigastric tenderness N/V Abnormal lab values
Overall goals
Comply w/ prescribed therapeutic regimen
Experience a reduction in or absence of discomfort
Exhibit no signs of GI complications
Have complete healing
Make lifestyle changes to prevent recurrence