Peptic Ulcer Disease

gastroesophageal reflux disease (GERD)

backflow of gastric or duodenum contents (gastric acid) into the esophagus causing burning pain or heart burn as a result of - an incompetent lower esophageal sphincter - pyloric stenosis - motility disorder Risks - ↑aging - obesity/pregnancy (BMI ↑30) - NG tubes - medications (Nitrates, CCBs, Benzodiazepines, NSAIDs, diet/intake "FACS") Sx - pyrosis (burning sensation in the esophagus) - dyspepsia (indigestion) - regurgitation - dysphagia (pain with swallowing) - hypersalivation (waterbrash) - esophagitis. *symptoms mimic heart attack (MI) Complications - adenocarcinoma of esophagus (secretory cell cancer) - esophageal bleed Diagnosis - rule out myocardial infarction via EKG and cardiac enzymes - assess esophageal deterioration to distinguish amount of perforation or hemorrhage via EGD (esophagogastroduodenoscopy) or Barium Swallow Test - monitor ambulatory esophageal reflux, administer proton-pump inhibitor (PPI), and perform Endoscopy if symptoms are severe - Barium studies and biopsy are not recommended Nursing Management 1. avoid situations that cause esophageal irritation or decrease LES pressure (dilate) including FACS & do not eat/drink 2 hrs before bedtime F - fried and fatty foods (milk) A - alcohol C - caffeine/carbonated, candy (chocolate, mint) S - smoking 2. diet should be low fat, high fiber in order to maintain or lose body weight to relieve pressure of LES and allow tightening 3. avoid tight clothes and elevate HOB 4. Medications such as - Antacids - H2 Receptor Antagonists (-tidine) such as Famotidine (Pepcid), Nizatidine (Axid), and Ranitidine (Zantac) - PPIs (-prazole) *caution as PPIs may reduce gastric acid, but increase intragastric bacterial growth = infection including Lansoprazole [Prevacid], Rabeprazole [AcipHex], and Esomeprazole [Nexium] - Prokinetic Agents to accelerate gastric emptying including Bethanechol (Urecholine), Domperidone (Motilium), and Metoclopramide (Reglan) *caution as this may cause extrapyramidal effects in PTs with neuromuscular disorder 6. Surgical Interventions - Fundoplication (reconstruction of the valve at the gastroesophageal junction via endoscopy in which portion of fundus or body of stomach is wrapped around LES like a turtleneck to tighten it)

Ulcer healing

H2 receptor antagonists (TAKEN AT BEDTIME) -Ranitidine -Cimetidine -Famotidine -Nizatidine Proton pump inhibitors (PPIs) -Omeprazole -Lansoprazole -Rabeprazole -Pantoprazole -Esomeprazole *use 4-6 wks for duodenal ulcer *use 6-8 weeks for gastric ulcer *stress compliance with regimen

Diagnosis of Peptic Ulcer

To establish the diagnosis of peptic ulcer, the following assessment and laboratory studies should be performed: Esophagogastroduodenoscopy. Confirms the presence of an ulcer and allows cytologic studies and biopsy to rule out H. pylori or cancer. Physical examination. A physical examination may reveal pain, epigastric tenderness, or abdominal distention. Barium study. A barium study of the upper GI tract may show an ulcer. Endoscopy. Endoscopy is the preferred diagnostic procedure because it allows direct visualization of inflammatory changes, ulcers, and lesions. Occult blood. Stools may be tested periodically until they are negative for occult blood. Carbon 13 (13C) urea breath test. Reflects activity of H. pylori.

bulk laxative

given to increase fiber during DIVERTICULOSIS 1. Metamucil

Peptic Ulcer Disease

the presence of a peptic ulcer (an excavation of hollowed out area of mucosa due to erosion of hydrochloric acid and pepsin) found in the stomach as Gastric Ulcers, found in the duodenum as Duodenal Ulcers, or found in the esophagus as Esophageal Ulcers pylorus (opening btw stomach and duodenum) duodenum (1st part of small intestine)**most common esophagus and it can extend deeper into the muscle layer or the peritoneum that surrounds the organs - may occur alone or in multiples Chronic Gastric Ulcers occur in the lesser curvature of the stomach near the pylorus. Table 23-2 compares the features of gastric and duodenal ulcers. Esophageal ulcers occur as a result of the backward flow of HCl from the stomach into the esophagus (gastroesophageal reflux disease [GERD]). Peptic ulcers occur mainly in the gastroduodenal mucosa because this tissue cannot withstand the digestive action of gastric acid (HCl) and pepsin. The erosion is caused by the increased concentration or activity of acid-pepsin or by decreased resistance of the mucosa. A damaged mucosa cannot secrete enough mucus to act as a barrier against HCl. The use of NSAIDs inhibits the secretion of mucus that protects the mucosa. Patients with duodenal ulcer disease secrete more acid than normal, whereas patients with gastric ulcer tend to secrete normal or decreased levels of acid. Damage to the gastroduodenal mucosa allows for decreased resistance to bacteria, and, thus, infection from H. pylori bacteria may occur. Zollinger-Ellison syndrome (ZES) is suspected when a patient has several peptic ulcers or an ulcer that is resistant to standard medical therapy (Kim, 2015). ZES is identified by the hypersecretion of gastric juice, duodenal ulcers, and gastrinomas (islet cell tumors) in the pancreas. Ninety percent of tumors are found in the "gastric triangle," which encompasses the cystic and common bile ducts, the second and third portions of the duodenum, and the junction of the head and body of the pancreas. Approximately one third of gastrinomas are malignant. Diarrhea and steatorrhea (unabsorbed fat in the stool) may be evident. The patient may have coexisting parathyroid adenomas (benign tumor of glandular origin) or hyperplasia and, therefore, may exhibit signs of hypercalcemia. The most common symptom is epigastric pain. H. pylori is not a risk factor for ZES (Kim, 2015). Stress-related mucosal disease (SRMD) is a term used to describe the phenomenon of injury to the lining of the stomach and the duodenum during conditions of physiologic stress. Other terms commonly used include stress erosion, stress ulcer, stress gastritis, erosive gastritis, and hemorrhagic gastritis. These terms also have been given to the acute mucosal ulceration of the duodenal or gastric area that occurs after physiologically stressful events, such as burns, shock, severe sepsis, and multiple organ traumas (Bardou, Quenot, & Barkun, 2015). These ulcers, which are clinically different from peptic ulcers, are most common in ventilator-dependent patients after trauma or surgery. Fiberoptic endoscopy within 24 hours of trauma or surgery reveals shallow erosions of the stomach wall; by 72 hours, multiple gastric erosions are observed. The prevalence of SRMD has been reported to be as high as 74% to 100% in critically ill patients (Bardou, Quenot, & Barkun, 2015). As the stressful condition continues, the ulcers spread. When the patient recovers, the lesions are reversed. This pattern is typical of stress ulceration. Differences of opinion exist as to the actual cause of mucosal ulceration in stress ulcers, but the etiology is thought to be multifactorial. Usually, the ulceration is preceded by a shock state; often involving hypovolemia and hypoperfusion; leading to decreased gastric mucosal blood flow and gastric ischemia. This hypoperfusion triggers the body's protective mechanisms of activation of the sympathetic nervous system, increased catecholamine release causing further vasoconstriction, and reduced gastric blood flow. Gastric hypoperfusion leads to decreased gastric motility, decreased capacity to neutralize hydrogen ions, and the reflux of duodenal contents into the stomach. In addition, large quantities of pepsin are released. The combination of ischemia, acid, and pepsin creates an ideal climate for ulceration (Kim, 2015). Stress ulcers should be distinguished from Cushing ulcers and Curling ulcers, two other types of gastric ulcers. Cushing ulcers are common in patients with head injury and brain trauma. They may occur in the esophagus, stomach, or duodenum and usually are deeper and more penetrating than stress ulcers. Curling ulcer is frequently observed about 72 hours after extensive burns and involves the antrum of the stomach or the duodenum.

avoid late night meals

GERD

Nursing Interventions

Relieving Pain and Improving Nutrition Administer prescribed medications. Avoid aspirin, which is an anticoagulant, and foods and beverages that contain acid-enhancing caffeine (colas, tea, coffee, chocolate), along with decaffeinated coffee. Encourage patient to eat regularly spaced meals in a relaxed atmosphere; obtain regular weights and encourage dietary modifications. Encourage relaxation techniques. Reducing Anxiety Assess what patient wants to know about the disease, and evaluate level of anxiety; encourage patient to express fears openly and without criticism. Explain diagnostic tests and administering medications on schedule. Interact in a relaxing manner, help in identifying stressors, and explain effective coping techniques and relaxation methods. Encourage family to participate in care, and give emotional support. Monitoring and Managing Complications If hemorrhage is a concern (hematemesis or melena) Assess for faintness or dizziness and nausea, before or with bleeding; test stool for occult or gross blood; monitor vital signs frequently (tachycardia, hypotension, and tachypnea). Insert an indwelling urinary catheter and monitor intake and output; insert and maintain an IV line for infusing fluid and blood. Monitor laboratory values (hemoglobin and hematocrit). Insert and maintain a nasogastric tube and monitor drainage; provide lavage as ordered. Monitor oxygen saturation and administering oxygen therapy. Place the patient in the recumbent position with the legs elevated to prevent hypotension, or place the patient on the left side to prevent aspiration from vomiting. Treat hypovolemic shock as indicated. If perforation and penetration are concerns: Note and report symptoms of penetration (back and epigastric pain not relieved by medications that were effective in the past). Note and report symptoms of perforation (sudden abdominal pain, referred pain to shoulders, vomiting and collapse, extremely tender and rigid abdomen, hypotension and tachycardia, or other signs of shock). Home Management and Teaching Self Care Assist the patient in understanding the condition and factors that help or aggravate it. Teach patient about prescribed medications, including name, dosage, frequency, and possible side effects. Also identify medications such as aspirin that patient should avoid. Instruct patient about particular foods that will upset the gastric mucosa, such as coffee, tea, colas, and alcohol, which have acid-producing potential. Encourage patient to eat regular meals in a relaxed setting and to avoid overeating. Explain that smoking may interfere with ulcer healing; refer patient to programs to assist with smoking cessation. Alert patient to signs and symptoms of complications to be reported. These complications include hemorrhage (cool skin, confusion, increased heart rate, labored breathing, and blood in the stool), penetration and perforation (severe abdominal pain, rigid and tender abdomen, vomiting, elevated temperature, and increased heart rate), and pyloric obstruction (nausea, vomiting, distended abdomen, and abdominal pain). To identify obstruction, insert and monitor nasogastric tube; more than 400 mL residual suggests obstruction.

H. pylori therapy (Initial Infection)

"triple therapy" = PPI + Antibiotic + Antibiotic Metronidazole + Clarithromycin + Amoxicillin for 10-14 days if this doesnt work, try "quadruple therapy" PPI + Antibiotic + 2 Bismuth Salts Metronidazole + Tetracycline + 2 BIsmuth Salts for 14 day if H. pylori returns, "Triple Therapy" for 14 days then add the second line therapy (no more than 2 rounds)

H2 Receptor Antagonists

(-tidine) - suppresses gastric acid secretion by blocking histamine release from parietal cells - TREATS GERD (heartburn) and PREVENTS PUD COMPLICATIONS - prevents stress ulcers and recurring ulcer formation - oral, IV, IM and IV may cause hypotension or dysrhythmias Cimetidine (Tagamet) -TAKE ON EMPTY STOMACH (food ↓ absorption) - taken 1 hr apart from antacids - lower the dose for PTs with kidney impairment as elderly or kidney/liver impairment may cause confusion, agitated, psychosis, depressed, anxiety, or disorient Ranitidine (Zantac) - TAKEN WITH OR WITHOUT FOOD - no side effects Famotidine (Pepcid) - safe for immunosupressed PTs - used for short term relief of GERD Nizatidine (Axid) - used to treat GERD or PUD Roxatidine (Roxane) - taken at BEDTIME with 1 PPI to reduce noctural acid reflux (GERD)

Triple Therapy

1 PPI + 2 ANTIBIOTICS - Esomeprazole (Nexium), Amoxicillin, Clarithromycin (Biaxin) - Lansoprazole (Prevacid), Amoxicillin, Clarithromycin (Biaxin) - Lansoprazole (Prevacid), Amoxicillin, Levofloxacin

Quadruple Therapy

1 PPI + 2 ANTIBIOTICS + 1 ANTIDIARRHEA - Esomeprazole (Nexium), Metronidazole (Flagyl), Tetracycline, Busmuth Subsalicylate (Pepto Bismol) or SUBSTITUTE PPI for H2 RECEPTOR ANTAGONIST - Ranitidine (Zantac), Metronidazole (Flagyl), Tetracycline, Busmuth Subsalicylate (Pepto Bismol)

Acute Pain

: Unpleasant sensory and emotional experience arising from actual or potential tissue damage or described in terms of such damage; sudden or slow onset of any intensity from mild to severe with anticipated or predictable end and a duration of <6 months. Abdominal distention Abdominal muscle spasm Recent nonsteroidal anti-inflammatory drug (NSAID) or acetylsalicylic acid (ASA) use Possibly evidenced by Early satiety Nausea and vomiting Pain relieved by food or antacid Weight loss Assess the client's pain, including the location, characteristics, precipitating factors, onset, duration, frequency, quality, intensity, and severity. Clients with gastric ulcer typically demonstrate pain 1 to 2 hours after eating. The client with duodenal ulcers demonstrate pain 2 to 4 hours after eating or in the middle of the night. With both gastric and duodenal ulcers, the pain is located in the upper abdomen and is intermittent. Client may report relief after eating or taking an antacid. Encourage the use of nonpharmacological pain relief measures: Acupressure Biofeedback Distraction Guided imagery Massage Music therapy Nonpharmacological relaxation techniques will decrease the production of gastric acid, which in turn will reduce pain. Instruct the client to avoid NSAIDs such as aspirin. These medications may cause irritation of the gastric mucosa. Instruct the client that meals should be eaten ar regularly paced intervals in a relaxed setting. An irregular schedule of meals may interfere with the regular administration of medications. Encourage the importance of smoking cessation. Smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, resulting in increased acidity of the duodenum. Administer the prescribed drug therapy: Antacids Antibiotics such as amoxicillin, clarithromycin, metronidazole, tetracycline Histamine receptor antagonists Prostaglandin analogues Proton pump inhibitor Sucralfate Antacids buffer gastric acid and prevent the formation of peptin. This mechanism of action promotes of healing of the ulcer. Antibiotics treat the Helicobacter pylori infection and promote healing of the ulcer. As the ulcer heals, the client experience less pain. H2 receptor antagonists block the secretion of gastric acid. Prostaglandin analogue reduces acid secretion and enhance the integrity of the gastric mucosa to resist injury. Proton pump inhibitors block the production and secretion of gastric acid and thereby reduce gastric pain. Sucralfate forms a barrier at the base of the ulcer crater to protect the healing ulcer from gastric acid.

Anxiety

: Vague uneasy feeling of discomfort or dread accompanied by an autonomic response. May be related to Fear of the unknown Nature of the disease. Situational crisis Stress Possibly evidenced by Abdominal pain Apprehensive Expressed concerns about changes in life events Fatigue Irritability Assess client's level of anxiety. Clients with peptic ulcers are anxious, but their anxiety level is not visible. Acknowledge awareness of the client's anxiety. Acknowledgement of the client's feelings validates the feelings and communicates the acceptance of those feelings. Encourage to express fears openly Open communication enable the client to develop a trusting relationship that aids in reducing anxiety and stress. Use simple language and brief statements when giving instructions to the client. When experiencing moderate to severe anxiety, clients may be unable to comprehend anything more than simple, clear, and brief instructions. Decrease sensory stimuli by maintaining a quiet environment. Anxiety may escalate to a panic state with excessive conversation, noise, and equipment around the client. Provide emotional support to client. Providing emotional support will give a client calming and relaxing mood that will lower anxiety, and stress related to the condition. Assist the client in developing anxiety-reducing measures such as biofeedback, positive imagery, and behavior modification. Learning these methods provides the client with a variety of ways to manage anxiety.

NPO during hospitalization, NG tube placement, bed rest

Diverticulitis

Compare Duodenal v. Gastric Ulcers

Duodenal Ulcer Gastric Ulcer ages 30-60 age 50 ↑ ↑ risk for males males = females 80% of peptic ulcers 15% of peptic ulcers ↑ HCL normal to ↓ HCL weight gain weight loss **food relieves pain **vomiting relieves pain pain 2-3 hr after eating or pain ½-1 hr after eating as at night (empty stomach) food increases the pain NO VOMITING HEMATESIS melena (dark blood in stool; tarry) (bright red blood in vomit) ↑ risk of perforation ↑ risk of hemorrhage ↓ malignancy ↑ malignancy caused by H. pylori, caused by H. pylori, alcohol, smoking, stress, alcohol, smoking, stress, cirrhosis of liver gastritis, use of NSAIDs

Gastric Ulcers vs. Duodenal Ulcers

Feature Duodenal Ulcer Gastric Ulcer Incidence ages 30-60 age 50 & up men at higher risk men = women 80% of all peptic ulcers 15% of all peptic ulcers Sx Hypersecretion of stomach acid (HCl) weight gain Pain 2-3 hrs after a meal wake up at 1 or 2 AM at night eating food relieves the pain(neutralizes) Vomiting uncommon Hemorrhage less likely than with gastric ulcer, but if present, melena more common than hematemesis More likely to perforate than gastric ulcers Normal to hyposecretion of stomach acid (HCl) Weight loss may occur Pain occurs ½ to 1 hour after a meal; rarely occurs at night; may be relieved by vomiting; ingestion of food does not help, sometimes increases pain Vomiting common Hemorrhage more likely to occur than with duodenal ulcer; hematemesis more common than melena Malignancy Possibility Rare Occasionally Risk Factors H. pylori, alcohol, smoking, cirrhosis, stress H. pylori, gastritis, alcohol, smoking, use of nonsteroidal anti-inflammatory drugs (NSAIDs), stress

Complications of Peptic Ulcer

Hemorrhage. Hemorrhage, the most common complication, occurs in 10% to 20% of patients with peptic ulcers in the form of hematemesis or melena. Perforation and penetration. Perforation is the erosion of the ulcer through the gastric serosa into the peritoneal cavity without warning, while penetration is the erosion of the ulcer through the gastric serosa into adjacent structures. Pyloric obstruction. Pyloric obstruction occurs when the area distal to the pyloric sphincter becomes scarred and stenosed from spasm or edema or from scar tissue that forms when an ulcer alternately heals and breaks down.

Malnutrition

Imbalanced Nutrition: Less Than Body Requirements: Intake of nutrients insufficient to meet metabolic needs. May be related to Abdominal pain Alcohol intake Anorexia Diarrhea Gastrointestinal bleeding Nausea, vomiting Possibly evidenced by Inadequate dietary intake Malabsorption of irons, minerals, and vitamins Weight loss btain a nutritional history. Clients may often overestimate the amount of food eaten. The client may not eat sufficient calories or essential nutrients as a way to reduce pain episodes with peptic ulcer disease. Because of this, clients are at high risk for malnutrition. Assess for body weight changes. Weight loss is an indication of inadequate nutritional intake. Gastric ulcers are more likely to be associated with vomiting, loss of appetite and weight loss than duodenal ulcers. Assist the client with identifying foods hat cause gastric irritation. Clients need to learn what foods they can tolerate without gastric pain. Soft, bland, non acidic foods cause less gastric irritation. The client is more likely to increase food intake if the foods are not associated with pain. Foods that may contribute to mucosal irritation include spicy foods, pepper, aNd raw fruits and vegetables. Monitor laboratory values for serum albumin. This test indicates the degree of protein depletion (2.5 g/dL indicates severe depletion; 3.8 to 4.5 g/dL is normal). Instruct in the importance of abstaining from excessive alcohol. Alcohol causes gastric irritation and increases gastric pain. Encourage the client to limit the intake of caffeinated beverages such as tea and coffee. Caffeine stimulates the secretion of gastric acid. Coffee, even if decaffeinated, contains a peptide that stimulates the release of gastrin and increases acid production. Teach about the importance of eating a balanced diet with meals at regular intervals. Specific dietary restrictions are no longer part of the treatment for PUD. During the symptomatic phase of an ulcer the client may find benefit from eating small meals at more frequent intervals.

Medications for PUD

Indications Drug Regimen Comments Ulcer healing -H2 receptor antagonists - Proton Pump Inhibitors (PPI) Ranitidine 150 mg b.i.d. or 300 mg at bedtime Cimetidine 400 mg b.i.d. or 800 mg at bedtime Famotidine 20 mg b.i.d. or 40 mg at bedtime Nizatidine 150 mg b.i.d. or 300 mg at bedtime Proton pump inhibitors (PPIs) Omeprazole—20-40 mg daily Lansoprazole—15-30 mg daily Rabeprazole—20 mg daily Pantoprazole—40-80 mg daily Esomeprazole—20-40 mg daily Should be used for 6 weeks for duodenal ulcer; 8 weeks for gastric ulcer Should be used for 4 weeks for duodenal ulcer and 6 weeks for gastric ulcer Healing occurs in 90% of patients who are compliant with therapy Initial Helicobacter pylori therapy First-line therapy, also referred to as "triple therapy" PPI b.i.d. plus clarithromycin 500 mg b.i.d. plus amoxicillin 1,000 mg b.i.d. or metronidazole 500 mg b.i.d. for 10 to 14 days Second-line therapy, also referred to as "Quadruple therapy" Bismuth Salt compound 2 tabs q.i.d. plus tetracycline 250 mg q.i.d. plus metronidazole 250 mg q.i.d. PPI b.i.d. daily for 14 days Efficacy of therapy is approximately 85% QID dosing may decrease compliance Therapy for retreatment of H. pylori therapy failure Repeat first-line therapy, substitute metronidazole for amoxicillin (or vice versa) for 14 days; may add Bismuth salt compound q.i.d. Add second-line H. pylori therapy. Efficacy of retreatment not known; success of more than two courses of treatment is very low Prophylactic therapy for NSAID ulcers Peptic ulcer healing doses of PPIs (above) Misoprostol 200 μg q.i.d. Prevents recurrent ulceration in approximately 80%-90% of patients

Non-Invasive Procedures

LABS - CBC (Hematocrit, Hgb) - serum amylase (used to rule out pancreatitis) - stool specimen (detect occult blood) - EGD (upper endoscopy to detect inflammation in esophagus, stomach, ulcer, lesions, gastric outlet obstruction) - histologic exam (detect cancer) - culture (detect H. pylori) - biopsy - rapid urea test & biospy (gold standard for diagnosis of H. pylori) Non-Invasive Labs h. pylori antigen stool antigen testing rapid urea test (breath test) barium studies Upper GI (gastric outlet obstruction used for COPD PTs who cannot undergo anesthesia with EGD) liver enzymes Medications 1. Proton Pump Inhibitors (-prazole) - more effective in healing esophagitis than H2 receptors inhibitors however monitor bone density loss - hypochlorhydria (low HCL) increases risk of C Diff and other invading microbes 2. H2 Receptor Inhibitors 3. if H. pylori diagnosed, use Triple Therapy (1 PPI + 2 Antibiotics) PPI + Amoxicillin + Clarithromycin or Mtetronizol for 10-14 days Quadruple Therapy Bismuth + PPI + Tetracycline (causes for anal itch) + Metronidizol

Risk For Deficient Fluid Volume

May be related to Gastrointestinal (GI) bleeding Nausea, vomiting Assess for the signs of hematemesis or melena. The client with a bleeding ulcer may vomit bright red blood or coffee grounds emesis. Melena occurs when there is bleeding in the upper GI tract. Monitor the client's fluid intake and urine output. The kidney will reabsorb water into circulation to support a decrease in blood volume. This compensatory mechanism results in decreased urine output. A decrease in circulatory blood volume leads to decreased renal perfusion and decreased urine output Monitor the client's vital signs, and observes BP and HR for signs of orthostatic changes. The erosion of an ulcer through the gastric or duodenal mucosal layer may cause GI bleeding. The client may develop anemia. If bleeding is brisk, changes in vital signs and physical symptoms of hypovolemia may develop rapidly. A decrease in BP and an increase in HR with changes in position is an early indicator of decreased circulatory volume. Instruct the client to immediately report symptoms of nausea, vomiting, dizziness, shortness of breath, or dark tarry stools. These assessment findings are signs of GI bleeding and should be reported immediately. Monitor hemoglobin and hematocrit levels. Erosion of the gastric mucosa by an ulcer results in GI bleeding. A decrease in hemoglobin and hematocrit occurs with bleeding. Administer IV fluids, volume expanders, and blood products as ordered. Isotonic fluids, volume expanders, and blood products can restore or expand intravascular volume.

Prokinetic Agents

Metoclopramide - stimulates motility of upper GI tract and increases rate of gastric emptying without stimulating gastric acid - used to treat GERD - may cause restlessness, drowsiness, extrapyramidal reactions, dizziness, or insomnia and headache - GIVEN 30 MIN BEFORE MEALS and AT BEDTIME - do not use if obstruction, perforation or GI hemorrhage present - may precipitate hypertension crisis - may cause neurological reactions - do not use with anticholinergics (Atropine) or Opioid Analgesics (Morphine) -

Proton Pump Inhibitors

PPIs (-prazole) - suppresses gastric acid secretion by slowing down H+/K+ pump on the surface of parietal cells - used to treat active ulcer disease, erosive esophagitis, and hypersecretion conditions - side effects include headache, diarrhea, abdominal pain and nausea - MUST BE TAKEN BEFORE MEALS Esomeprazole (Nexium) - TREATS DUODENAL ULCERS & H. PYLORI INFECTION - ↑ warfarin effects = blood thinning Lansoprazole (Prevacid) - ↓ theophylline levels Omeprazole (Prilosec) Pantoprazole (Protonix) - may cause hyperglycemia and abnormal LFTs Rabeprazole (AcipHex) - interferes with digoxin, iron and warfarin

Prophylactic Therapy for ulcers caused by NSAIDs

PPIs used to heal the peptic ulcer -Misoprostol prevents recurrent ulceration** -Omeprazole -Lansoprazole -Rabeprazole -Pantoprazole -Esomeprazole

avoid alcohol and caffine

PUD

encourage weight loss, regular exercise, sitting upright and elevating HOB 2-3 hrs after eating

PUD and GERD

Urea Breath Test

Patient ingests Urea with radio labeled Carbon capsule and provides a breath sample 10-20 min later to detect if H. pylori of PUD is present 1. avoid antibotics, bismuth subsalicylates 1 month before test, sucralfate and omeprazole for 1 week before cimetidine, famotidine, ranitidine, and nixatidine for 24 hrs before test - h pylori detected by assessing serium antibody levels

Risk Factors

Peptic ulcer disease occurs with the greatest frequency in people between 40 and 60 years of age. It is relatively uncommon in women of childbearing age, but it has been observed in children and even in infants. After menopause, the incidence of peptic ulcers in women is almost equal to that in men. Peptic ulcers in the body of the stomach can occur without excessive acid secretion. In the past, stress and anxiety were thought to be causes of ulcers, but research has documented that peptic ulcers result from infection with the gram-negative bacteria H. pylori, which may be acquired through ingestion of food and water. Person-to-person transmission of the bacteria also occurs through close contact and exposure to emesis. Although H. pylori infection is common in the United States, most infected people do not develop ulcers. It is not known why H. pylori infection does not cause ulcers in all people, but most likely the predisposition to ulcer formation depends on certain factors, such as the type of H. pylori and other as yet unknown factors (Kim 2015; Franceschi et al., 2014; Watari et al., 2014). In addition, excessive secretion of HCl in the stomach may contribute to the formation of peptic ulcers, and stress may be associated with its increased secretion. The ingestion of milk and caffeinated beverages, smoking, and alcohol also may increase HCl secretion. Stress and eating spicy foods may make peptic ulcers worse. Familial tendency also may be a significant predisposing factor. People with blood type O are more susceptible to peptic ulcers than are those with blood type A, B, or AB; this is another genetic link. There also is an association between peptic ulcers and chronic pulmonary disease or chronic kidney disease. Other predisposing factors associated with peptic ulcer include chronic use of NSAIDs, alcohol ingestion, and excessive smoking. Peptic ulcers are found in rare cases in patients with tumors that cause secretion of excessive amounts of the hormone gastrin. ZES consists of severe peptic ulcers, extreme gastric hyperacidity, and gastrin-secreting benign or malignant tumors of the pancreas.

emergency symptoms; painful abdomen, rebound tenderness, and increasing fever indicate

Peritonitis (emergency notify PCP)

Sx of Ulcer

Symptoms of ulcer may last for a few days, weeks, months, and may disappear only to reappear, often without an identifiable cause. Pain. As a rule, the patient with an ulcer complains of dull, gnawing pain or a burning sensation in the midepigastrium or the back that is relieved by eating. Pyrosis. Pyrosis (heartburn) is a burning sensation in the stomach and esophagus that moves up to the mouth. Vomiting. Vomiting results from obstruction of the pyloric orifice, caused by either muscular spasm of the pylorus or mechanical obstruction from scarring. Constipation and diarrhea. Constipation or diarrhea may occur, probably as a result of diet and medications. Bleeding. 15% of patients may present with GI bleeding as evidenced by the passage of melena (tarry stools).

Antiulcers

also known as Prostaglandins which protect the gastric mucosa barrier - MUST BE GIVEN 30 MIN-1 HR BEFORE EATING 1. Misoprostol (Cytotec) - supresses gastric acid by ↑mucus and ↑HCO3 (bicarb) production and maintains blood flow to submucosa by vasodilation - PREVENTS GASTRIC ULCER FORMATION BY NSAIDs - may cause diarrhea or abdominal cramping - do not use during pregnancy 2. Sucralfate (Carafate) - creates protective barrier around the ulcer to prevent further digestion and erosion - used to treat DUODENAL ULCERS - may cause constipation or nausea - wait 2 hrs to take other medications as Sucralfate may interfere with the absorption of Warfarin, Phenytoin, Theophylline, Digoxine, and antibiotics

BARRETT ESOPHAGUS

condition in which the lining of the esophageal mucosa is altered. The tissue at the gastroesophageal junction changes from squamous epithelium (flat) to columnar epithelium (elongated). Barrett esophagus is sometimes found in patients being evaluated with a history of chronic regurgitation or heartburn. The disease may lead to esophageal cancer in some patients.

Colonoscopy

fiberoptic endoscopy study in which lining of large intestine is visually examined and biopsys are taken - monitor HR and RR continuously - position PT on left side iwth knees up to chest Pre-Op 1. adequate cleansing of colon with enemas (increases risk of fluid and electrolyte imbalance) 2. clear liquid diet 1 day before 3. withhold certain medications 4. NPO 4-6 hrs before test 5. administer sedation and medications to relax smooth muscle Post-Op 1. monitor vitals and signs of bowel perforation and peritonitis 2. remain on bed rest until alert 3. expected findings include flatus, abdominal fullness, and mild cramping 4. abnormal finding - bleeding

Surgical Intervention of Peptic Ulcer

introduction of antibiotics to eradicate H. pylori and of H2 receptor antagonists as treatment for ulcers has greatly reduced the need for surgical interventions. Pyloroplasty. Pyloroplasty involves transecting nerves that stimulate acid secretion and opening the pylorus. Antrectomy. Antrectomy is the removal of the pyloric portion of the stomach with anastomosis to either the duodenum or jejunum.

Antacids

neutralize acid by increasing pH above 5 to protect the mucosa layer - may affect absorption of other medications - GIVEN 1 HR BEFORE MEALS OR 3 HRS AFTER - TREAT GERD AND PUD 1. TUMS

increasingly severe shoulder pain, abdominal pain, or anterior chest pain 2 hrs after an EDG indicates

perforation (emergency notify PCP)

Lack of Knowledge

sess the client's knowledge and misconceptions regarding peptic ulcer disease, lifestyle behaviors, and the treatment regimen. Clients may have inaccurate information about how lifestyle behaviors contribute to peptic ulcer disease. The client needs accurate knowledge to make informed decisions about taking prescribed medications and modifying behaviors that contribute to peptic ulcer disease or GI bleeding. Explain the pathophysiology of disease and how it relates to the functioning of the body. An understanding of the disease process helps to foster the willingness to follow the recommended treatment plan and modify behaviors to prevent recurrent episodes or related complications. Instruct the client in what signs and symptoms to report to the health care provider. Recognizing the signs and symptoms can help ensure the early initiation of treatment. Discuss the therapy options and the rationales for using these options. The correct use of antibiotics and acid suppression medications can promote rapid healing of an ulcer. Discuss the lifestyle changes required to prevent further complications or episodes of peptic ulcer disease. The modifications of lifestyle behaviors such as alcohol use, coffee, and other caffeinated beverages, and the overuse of aspirin or other nonsteroidal anti-inflammatory drugs is necessary to prevent recurrent ulcer development and prevent complications during the healing phase.

Antidiarrhea medications

supress H. pylori in gastric mucosa and help heal ulcers - usually given with antibiotics - TAKEN ON EMPTY STOMACH 1. Bismuth Subsalicylate (Pepto Bismol)

Medical Management of Peptic Ulcer

the condition can be controlled. Pharmacologic therapy. Currently, the most commonly used therapy for peptic ulcers is a combination of antibiotics, proton pump inhibitors, and bismuth salts that suppress or eradicate the infection. Stress reduction and rest. Reducing environmental stress requires physical and psychological modifications on the patient's part as well as the aid and cooperation of family members and significant others. Smoking cessation. Studies have shown that smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, resulting in increased acidity of the duodenum. Dietary modification. Avoiding extremes of temperature of food and beverages and overstimulation from consumption of meat extracts, alcohol, coffee, and other caffeinated beverages, and diets rich in cream and milk should be implemented.

Antibiotics

used in combination with PPIs to treat of H. pylori infection (bactericidal/bacteriostatic) via TRIPLE THERAPY (2 antibitoics + 1 PPI) or QUADRUPLE THERAPY (3 antibiotics + 1 PPI) - may cause GI upset, headache, metallic taste, diarrhea, anorexia, photosensitivity - do not use if allergic to Penicillin, impaired kidney/liver function, or with dairy products (↓ effectiveness) - TAKE WITH FOOD to prevent upset stomach 1. Amoxicillin (Amoxil) 2. Clarithromycin (Biaxin) 3. Metronidazole (Flagyl) 4. Tetracycline

stool softeners

used to prevent constipation from DIVERTICULOSIS

Upper Endoscopy (EGD)

used to visualize the gastric wall, sphincters, duodenum, and obtain tissue specimens (cancer, h. pylori) - used to diagnose inflammation, ulcers, lesions, gastric outlet obstruction Pre-op 1. NPO 6-8 hrs 2. local anesthetic and medications to relax smooth muscle and reduce secretions before scope is inserted 3. position PT on left side to facilitate saliva drainage and easy access 4. monitor airway patency and SpO2 Post-Op 1. monitor vitals and signs of perforation (pain, bleeding, difficulty swallowing, fever) 2. maintain bed rest and NPO until gag reflex returns in 1-2 hrs 3. administer lozenges, saline gargle, oral analgesics for sore throat after gag reflex returns