Care of Patient with Stomach Disorders Flashcards
Inflammation of gastric mucosa or submucosa after exposure to local irritants or other causes
Complete regeneration and healing occur within a few days
If the stomach muscle is not involved, complete recovery usually occurs with no residual gastric inflammation
If the stomach muscle is affected, hemorrhage could occur
Etiology/risk factors:
Gastritis acute
Helicobacter pylori (gram-negative bacterium) - HUGE RISK FACTOR
Long-term NSAID use
Diet: alcohol; coffee; caffeine
Corticosteroids
Radiation therapy
Accidental or intentional ingestion of corrosive substances
Etiology/risk factors: - Gastritis acute
Chronic inflammation of the mucosal lining of the stomach
Walls and lining of the stomach thin and atrophy
Intrinsic factor (critical for absorption of vitamin B12) is lost
Vitamin B12 stores are depleted, pernicious anemia results - decrease RBC because not absorb B12
Amount and concentration of acid in stomach secretions gradually decrease
Associated with increased risk for gastric cancer
Types
Gastritis chronic
Type A - autoimmune cause
Type B – H. pylori infection most common cause; Also associated with alcohol ingestion, radiation therapy, and smoking
Atrophic – caused by exposure to toxic substances in the workplace, H. pylori infection, or autoimmune factors
Types - Gastritis chronic
Eat a well-balanced diet
Avoid drinking excessive amounts of alcohol
Avoid taking large doses of aspirin, NSAIDs (e.g., ibuprofen), and corticosteroids
Avoid excessive intake of coffee/caffeine
Avoid contaminated water or food
Manage stress levels
Stop smoking
Avoid exposure to toxic substances in the workplace
Treat symptoms of esophageal reflux
Gastritis prevention
Limit foods with high acid contact or heavily seasoned with spices
Eat a well-balanced diet
Rapid onset of epigastric pain or discomfort
Nausea/vomiting
Hematemesis (vomiting blood)
Gastric hemorrhage – life-threatening emergency
Dyspepsia (indigestion)
Anorexia - not want to eat
Gastritis CM: Acute
Vague report of epigastric pain that is relieved by food
Anorexia
Nausea or vomiting
Intolerance of fatty and spicy foods and anything not bland
Pernicious anemia - not absorbing B12
Gastritis CM: Chronic
Biopsy via EGD is the gold standard for diagnosing gastritis
Tissue samples can confirm or rule out gastric cancer and detect H. pylori
Gastritis diagnostic testing: Esophagogastroduodenoscopy (EGD)
Treated symptomatically and supportively because the healing process is spontaneous
Drug therapy
Blood transfusion if bleeding
Fluid replacement for dehydration
Surgery with major bleeding
Gastritis interventions: Acute:
Varies with cause
Drug therapy
Elimination of causative agent: Ex. H pylori treated with antimicrobials
Treatment of any underlying disease
Avoidance of toxic substances
Gastritis interventions: Chronic:
H2-receptor antagonists (famotidine - Pepcid, nizatidine - Axid)
Mucosal barrier (Sucralfate - Carafate, Sulcrate): coat lining of stomach
Antacids (Maalox, Mylanta)
Proton pump inhibitors (omeprazole - Prilosec, pantoprazole - Protonix)
Vitamin B12
Gastritis interventions: Drug therapy - chronic and acute
Blocks gastric secretions
H2-receptor antagonists (famotidine - Pepcid, nizatidine - Axid)
Buffering agent
Antacids (Maalox, Mylanta)
Suppress gastric acid secretion
Proton pump inhibitors (omeprazole - Prilosec, pantoprazole - Protonix)
prevention or treatment of pernicious anemia (with chronic gastritis)
Vitamin B12
Open Mucosal lesion of the stomach or duodenum
Occurs when mucosal defenses become impaired and no longer protect the epithelium from the effects of acid and pepsin
3 types of ulcers - depends on location
Most gastric and duodenal ulcers are caused by H. pylori infection
Peptic ulcer disease
Gastric
Duodenal
Stress
3 types of ulcers - depends on location - Peptic ulcer disease
Develop in the antrum of the stomach near acid-secreting mucosa
Gastric ulcer
Develop in the upper portion of the duodenum
Duodenal ulcer
Occur after an acute medical crisis or trauma
Stress ulcer
Can be undiagnosed in older adults because of vague symptoms associated with physiologic changes of aging and comorbidities that mask dyspepsia
Most gastric and duodenal ulcers are caused by H. pylori infection - Peptic ulcer disease
Hemorrhage
Perforation
Pyloric obstruction
Intractable disease
Peptic ulcer disease comps
Emergency and life threatening
Occurs more often in patients with gastric ulcers and in older adults
Hemorrhage - Peptic ulcer disease comps
Surgical emergency and can be life threatening
Symptoms include sharp, sudden pain beginning in the mid-epigastric region and spreads over the entire abdomen
Septic quickly; abdomen rigid quickly
Abdomen is tender, rigid, and boardlike
Perforation - Peptic ulcer disease comps
Symptoms include abdominal bloating and N/V
Pyloric obstruction - Peptic ulcer disease comps
Characterized by a lack of response to conservative management and with symptoms that interfere with ADLs
Intractable disease - Peptic ulcer disease comps
Primarily associate with H. pylori and NSAIDS
Certain substances may contribute by altering gastric secretion
Peptic ulcer disease etiology
Corticosteroids (prednisone)
Theophylline (Theo-Dur)
Caffeine
Radiation therapy
Certain substances may contribute by altering gastric secretion - Peptic ulcer disease etiology
History
Physical assessment/clinical manifestations:
Laboratory assessment:
Diagnostic testing:
Peptic ulcer disease assessment
Dyspepsia (indigestion)
Epigastric tenderness - pain
N/V
Physical assessment/clinical manifestations: - Peptic ulcer disease assessment
Most common symptom
Described as sharp, burning, or gnawing pain
Dyspepsia (indigestion)
Serologic testing for H. pylori antibodies
Decreased hemoglobin and hematocrit, if bleeding
Stool may be positive for occult blood, if bleeding
Laboratory assessment: - Peptic ulcer disease assessment
Esophogastroduodenoscopy (EGD)
Nuclear medicine scan to test for bleeding
Diagnostic testing: - Peptic ulcer disease assessment
no special preparation
patient injected with a radioactive contrast medium and the GI system is scanned for the presence of bleeding after a waiting period; see if bleeding through GI tract
Nuclear medicine scan to test for bleeding
Acute or chronic pain
Upper GI bleeding
Peptic ulcer planning - Priority problems:
Bland diet may assist in relieving symptoms
Teach the patient to exclude foods that cause discomfort
Avoid bedtime snacks, alcohol, tobacco, caffeine-containing beverages, and both caffeinated and decaffeinated coffees and foods highly acidic
Peptic ulcer disease interventions - Diet
Hypnosis
Imagery
Yoga
Mediation techniques
Peptic ulcer disease interventions - Complementary and alternative therapies - stress sig risk factor for peptic ulcer disease so these can help
Antacids
H2 antagonists
Mucosal barrier fortifier
Proton pump inhibitors (PPI)
Prostaglandin analogs
Purpose of Medications:
Peptic ulcer disease meds
increases pH of gastric contents by deactivating pepsin
Buffer
Antacids - Peptic ulcer disease meds
decreases gastric acid secretions by blocking histamine receptors in parietal cells
H2 antagonists - Peptic ulcer disease meds
binds with bile acids and pepsin to protect stomach mucosa
stimulates mucosal protection
may cause the stools to be discolored black
Coat lining
Mucosal barrier fortifier - Peptic ulcer disease meds
suppresses H, K-ATPase enzyme system of gastric acid secretion
Proton pump inhibitors (PPI) - Peptic ulcer disease meds
stimulates mucosal protection and decreases gastric acid secretions, helps resist mucosal injury in patients taking NSAIDs and/or high-dose corticosteroids
Build up mucosal lining
Prostaglandin analogs - Peptic ulcer disease meds
Eliminate H. pylori infection
Heal ulcerations
Prevent recurrence
Provide pain relief
Purpose of Medications: - Peptic ulcer disease meds
PPI triple therapy
PPI quadruple therapy
Eliminate H. pylori infection
PPI: decrease gastric acid secretions
Two antibiotics such as metronidazole (Flagyl) and tetracycline or clarithromycin (Biaxin) and amoxicillin (Amoxil) for 10-14 days
PPI triple therapy
PPI: decrease gastric acid secretions
Any two antibiotics as above
Bismuth (Pepto-Bismol)
PPI quadruple therapy
Teach the patient who has peptic ulcer disease to seek immediate medical attention if experiencing any of these symptoms:
Sharp, sudden, persistent, and severe epigastric or abdominal pain
Bloody or black stools
Bloody vomit or vomit that looks like coffee grounds
Upper GI bleeding
Maintain airway, breathing, circulation
Provide oxygen and other ventilatory support as needed
Start two large bore IV lines
Monitor VS and oxygen
Labs to monitor:
Monitor fluid replacement
NG tube placement and gastric lavage; might suction
Prepare for endoscopic therapy or interventional radiologic procedures
EGD to cauterize certain areas
Upper GI bleeding treatment: If actively bleeding/life-threatening emergency:
Replace fluids, blood and fresh frozen plasma (help blood clot)
Start two large bore IV lines
Hemoglobin/hematocrit and coagulation studies
Labs to monitor:
I/O
BIG
Monitor fluid replacement
Perforation
Obstruction
Upper GI bleeding complications
Replace fluids, blood, electrolytes
Most have NG tubes
Administer antibiotics
Keep patient NPO
NGT and suction
Monitor I/O and VS
Monitor for septic shock (fever, pain, tachycardia, lethargy, anxiety)
Surgery
Upper GI bleeding complications: Perforation
Replace fluids and electrolytes
NGT and suction to decompress dilated stomach
Surgery may be required
Upper GI bleeding complications: Obstruction
Teach risk factors for recurrence
Recognize new complications and what to do if they occur and s/s of GI bleeding
Help them plan ways to make needed lifestyle changes
Avoid OTC products containing aspirin or other NSAID - irritate stomach lining; acidic foods, alcohol, smoking, coffee, stress
Identify situations that cause stress and develop a plan for coping with stressors
Upper GI bleeding teaching
Severe Abdominal pain; N/V; black, tarry stools; weakness; dizziness
Recognize new complications and what to do if they occur and s/s of GI bleeding
Usually adenocarcinomas
Usually begins in the glands of the stomach mucosa
Symptoms
Etiology and genetic risk:
Diagnostic testing:
Gastric cancer
Early stages: heartburn and abdominal discomfort
Late stages: progressive weight loss and N/V
Symptoms - Gastric cancer
H. pylori largest risk factor
Medical history risk factors: pernicious anemia, gastric polyps, chronic atrophic gastritis, and achlorhydria (absence of secretion of hydrochloric acid); chronic peptic ulcer disease
Diet risks: eating pickled food, nitrates from processed foods, added salt and low intake of fruits and vegetables
Increased risk: gastric surgery, Barrett’s esophagus from prolonged or severe GERD
Etiology and genetic risk: - Gastric cancer
EGD for definitive diagnosis
Biopsies
CT, PET, and MRI are used in determining the extent of the disease and planning therapy
Diagnostic testing: - Gastric cancer
Drug therapy, radiation and/or chemotherapy
Gastric cancer interventions - Nonsurgical:
Resection of tumor
Total gastrectomy - attach esophagus to dejunum because no longer have stomach - issues with diet
Subtotal (partial) gastrectomy - issues with diet
Gastric cancer interventions - Surgical:
Surgical dressing changes
Review manifestations of incisional infection
Side effects of radiation therapy/chemotherapy (N/V, fatigue)
Instruct patient to eat small, frequent meals
Issues if stomach removed
Avoid drinking liquids with meals
Avoid foods that cause discomfort
Eliminate caffeine and alcohol consumption
Stop smoking
B12 injections
Lie flat after eating for a short time
Gastric cancer interventions - Patient/family teaching:
Prob if part/all stomach removed
Refers to a group of vasomotor symptoms that occur after eating
Rapid emptying of food contents into the small intestine
Early manifestations (occurs within 30 minutes of eating):
Late dumping (occurs 90 minutes to 3 hours after eating):
Managed by nutrition changes:
Dumping syndrome
Can occur after gastric surgery
Causes abdominal distension
Rapid emptying of food contents into the small intestine - Dumping syndrome
Vertigo, tachycardia, syncope, sweating, pallor, palpitations, desire to lie down
Early manifestations (occurs within 30 minutes of eating): - Dumping syndrome
Caused by a release of an excessive amount of insulin and BG dropping quickly
Dizziness, light-headedness, palpitations, diaphoresis, confusion
Late dumping (occurs 90 minutes to 3 hours after eating): - Dumping syndrome
Decrease the amount of food taken at one time
Eliminate liquids ingested with meals - not eat and drink at same time
Eat high protein, high fat, and low to moderate carbohydrate - best meal
In severe cases some medications are used that slows stomach and intestinal motility
Managed by nutrition changes: - Dumping syndrome
