Care of Patient with Stomach Disorders Flashcards by Kelsey Klipfel

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

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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

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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

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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

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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

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Limit foods with high acid contact or heavily seasoned with spices

Eat a well-balanced diet

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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

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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

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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)

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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:

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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:

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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

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Blocks gastric secretions

H2-receptor antagonists (famotidine - Pepcid, nizatidine - Axid)

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Buffering agent

Antacids (Maalox, Mylanta)

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Suppress gastric acid secretion

Proton pump inhibitors (omeprazole - Prilosec, pantoprazole - Protonix)

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prevention or treatment of pernicious anemia (with chronic gastritis)

Vitamin B12

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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

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Gastric
Duodenal
Stress

3 types of ulcers - depends on location - Peptic ulcer disease

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Develop in the antrum of the stomach near acid-secreting mucosa

Gastric ulcer

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Develop in the upper portion of the duodenum

Duodenal ulcer

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Occur after an acute medical crisis or trauma

Stress ulcer

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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

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Hemorrhage
Perforation
Pyloric obstruction
Intractable disease

Peptic ulcer disease comps

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Emergency and life threatening
Occurs more often in patients with gastric ulcers and in older adults

Hemorrhage - Peptic ulcer disease comps

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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