WK2 - GERD, Gastritis, PUD, Dumping.pdf_20240822_205823_0000.pdf

NCM112 LECTURE: Gastrointestinal Prelim Week Disorders (Part 1) Bachelor of Science in Nursing Instructor:Mohamad M. Salipla, RN...

NCM112 LECTURE: Gastrointestinal Prelim Week Disorders (Part 1) Bachelor of Science in Nursing Instructor:Mohamad M. Salipla, RN 02 GERD, GASTRITIS, PUD, DUMPING SYNDROME - mo r e r e sistant to acid as a result of healing process Gastroesophageal Reflux Disease (GERD) brought about by the inflammation - Backward flow (reflux) of stomach contents into the - considered pre-malignant (  risk of CANCER) in esophagus resulting to inflammatory changes of the clients with prolonged GERD esophageal mucosa Hallmark of GERD: reflux esophagitis Other manifestations: - (acute symptoms of inflammation) Chronic cough especially at night (due to position), asthma Eructation (belching) Flatulence (gas) Bloating after eating Nausea & Vomiting Diagnostic test: - Most accurate method: 24-hour ambulatory pH monitoring - small catheter is placed through the nose into the distal esophagus, pH is continuously monitored & recorded) Endoscopy (esophagogastroduodenoscopy) Esophageal manometry “motility testing” - water-filled catheters are inserted via the client’s nose or Causes mouth & slowly withdrawn while measurements of LES pressure & peristalsis are recorded); not specific enough to inappropriate relaxation of the LES/  tone of LES establish a diagnosis fou GERD. gastric volume or intra-abdominal pressure is elevated delayed gastric emptying Nursing interventions: Diet therapy - limit or eliminate foods that decrease LES pressure (chocolate, fatty foods, caffeinated beverages such as coffee, tea, & cola, peppermints, alcohol) - restrict spicy & acidic foods (orange juice, tomatoes) - carbonated beverages ’s pressure in the stomach Lifestyle changes - sleep in the left lateral (side-lying) position to minimize the nighttime episodes of reflux Assessment Findings Heartburn - substernal or retro- sternal burning sensation - pain radiate to the neck, jaw, back (mimic ANGINA or MI) Regurgitation - warm fluid traveling up the throat (sour or bitter taste) - danger for aspiration (note for crackles in the lungs) Hypersalivation “water brash” Dysphagia (Difficulty of swallowing) Odynophagia (Painful swallowing) Barrett’s epithelium - change of the normal squamous cell epithelium to columnar epithelium J.A.K.E 1 of 5  GERD, GASTRITIS, PUD, DUMPING SYNDROME gastritis. Foods with a rough texture or those eaten at an extremely high temperature can also damage the stomach mucosa. Acute gastritis is usually of short - duration unless the gastric mucosa has suffered extensive damage. Pathophysiology - The mucosal lining of the stomach normally protects it from the action of gastric acid. This mucosal barrier is composed of prostaglandins. Due to any cause ↓ This barrier is penetrated ↓ Hydrochloric acid comes into contact with the mucosa ↓ Injury to small vessels Drug therapy ↓ Antacids Edema, hemorrhage, and possible ulcer formation - neutralizes HCL & deactivating pepsin Clinical Manifestation - Aluminum Hydroxide, Magnesium Hydroxide, Maalox, Mylanta Epigastric discomfort Histamine2 (H2) Receptor Antagonist Feeling of fullness, early satiety - ’s acid production of parietal cells Cramping - Famotidine, Ranitidine (Zantac), Cimetidine (Tagamet), Belching Nizatidine Flatulence Proton pump inhibitors (PPI’s): main treatment for GERD Severe nausea and vomiting Hematemesis - inhibition of proton pump of the parietal cell thereby  acid secretion Sometimes GI bleeding is the only manifestation - Omeprazole, Lansoprazole, Rabeprazole, Pantoprazole, When contaminated food is the cause of gastritis, diarrhea Esomeprazole; usually develops within 5 hours of ingestion Metoclopramide (Reglan) Diagnostic Findings -  gastric emptying - Diagnosis is based on a detailed history of food intake, Endoscopic Therapy medications taken, and any disorder related to gastritis. - Stretta procedure – the physician applies - The physician may also perform a gastroscopy. radiofrequency energy through needles placed near Medical Management gastroesophageal junction inhibiting the vagus nerve thus reducing the discomfort of the client. It will - Anti – emetic drugs like Inj. Perinorm or Tab, Domperidone reshape the ring of muscles in the lower esophagus. are frequently effective in vomiting. - Antacids, H2 Blockers like cimetidine, Ranitidine, or Surgical management: Laparoscopic Nissen Famotidine are effective to reduce the pain. Fundoplication - GOLD STANDARD - If ingestion of NSAIDs is a problem, a prostaglandin E1 (PGE1) analog may be prescribed to protect the stomach Gastritis mucosa and inhibit gastric acid secretion. - Gastritis is an inflammation of the gastric mucosa, is classified as either acute or chronic. Diet Therapy - Incidence: The incidence of gastritis is highest in the fifth -- Initially foods and fluids are withheld until nausea and - vomiting subside. and sixth decades of life; men are more frequently affected than women. The incidence is greater in clients who are Once the client tolerates food, the diet includes heavy drinkers and smokers. decaffeinated tea, gelatin, toast, and simple bland foods. Acute Gastritis The client should avoid spicy foods, caffeine and large, Etiology and Risk Factors: heavy meals. - It usually stems from ingestion of a corrosive, erosive, - In the continued absence of nausea, vomiting and bloating, or infectious substance. the client can slowly return to a normal diet. - Aspirin and other non-steroidal anti-inflammatory drugs Chronic Gastritis (NSAIDs), chemotherapeutic drugs, steroids, acute - 3 forms alcoholism and food poisoning (typically caused by - Superficial gastritis, which causes a reddened, edematous Staphylococcus organisms) are common causes. mucosa with small erosions and hemorrhages. - Food substances including excessive amounts of tea, - Atrophic gastritis, which occurs in all layers of the carbonated drinks and pepper can precipitate acute stomach, develops frequently in association with gastric 2 of 5  GERD, GASTRITIS, PUD, DUMPING SYNDROME ulcer and gastric cancer, and is invariably present in - If pernicious anemia develops, intramuscular injections of pernicious anemia; it is characterized by a decreased vitamin B12 may be administered monthly for the remainder of number of parietal and chief cells. the client’s life. - Hypertrophic gastritis, which produces a dull and nodular Nursing Management rugae; mucosa with irregular, thickened, or nodular Nursing Diagnosis: hemorrhages occur frequently. 1) Acute pain related to irritated stomach mucosa. Etiological Factors 2) Imbalanced nutrition, less than body requirement, - Infection with surgery Helicobacter may leadpylori to bacteria chronic gastritis. or gastric After related to inadequate intake of nutrition. gastric resection with a gastro- jejunostomy, bile and bile 3) Risk for imbalanced fluid volume related to insufficient - acids may reflux into the remaining stomach, causing fluid intake and excessive fluid loss subsequent to gastritis. H.Pylori infection can lead to chronic atrophic vomiting. 4) Anxiety related to treatment. 5) Deficient gastritis. Age is also a risk factor; chronic gastritis is more knowledge about dietary management and - common in older adults. - disease process. Peptic Ulcer Disease Pathophysiology The stomach lining first becomes thickened and erythematous and then becomes thin and atrophic. ↓ Continued deterioration and atrophy ↓ Loss of function of the parietal cells ↓ Acid secretion decreases ↓ Inability to absorb vitamin B12 ↓ Development of pernicious anemia Clinical Manifestation - Causes Manifestations are vague and may be absent because the - Break in the mucosal barrier problem does not cause an increase in hydrochloric acid. o mucus & bicarbonate secretion (1st line of defense in Assessment may reveal pH maintenance) o Anorexia o Gastromucosal PG (’s barrier resistance to o Feeling of fullness ulceration) o Dyspepsia o adequate blood supply o Belching o pyloric sphincter dysfunction (bile may enter stomach & o Vague epigastric pain cause damage to lipid plasma membrane of gastric o Nausea mucosa) o Vomiting o delayed gastric emptying o Intolerance of spicy and fatty foods o H. pylori infection Complications Note: There is normal gastric acid secretion!!! - Bleeding - Pernicious anemia - Gastric cancer Medical Management - Discomfort may lessen with a bland diet, small frequent meals, antacids, H2 receptor antagonists, proton pump inhibitors, and avoidance of food that cause manifestations. - If H.pylori bacteria are present, anti-biotics and other medications are administered to eliminate the bacteria. - If 1 week of this regimen does not succeed in eliminating the bacteria, the regimen may be repeated for an additional week. 3 of 5  GERD, GASTRITIS, PUD, DUMPING SYNDROME Duodenal ulcer: causes Laboratory assessment - rapid emptying of food in the stomach  Hgb/Hct (indicates bleeding) (+) occult blood in stool - acid-bolus delivery, reduce buffering effect of food specimen Endoscopy (EGD) reveals ulceration; BIOPSY is to duodenum usually -  secretion of acid is triggered also by CHON rich done to detect H. pylori infection & to rule out - food, Ca++, vagal excitation MALIGNANCY!!! H. pylori produces urease Gastric analysis: normal gastric acidity in gastric - Urease hydrolyzes urea to ammonia ulcer ( - H+ ions are released in response to the presence of in duodenal ulcer Medical/ Nursing Management ammonia  further gastric mucosal damage - Supportive (rest, bland diet, stress management) Drug therapy: o Antacids o H2-receptor antagonists o Proton pump inhibitors o Anticholinergics (gastric juice secretion) o Probanthine, Pirenzepine Antibiotic for H. pylori infection (Metronidazole (Flagyl), Tetracycline & Pepto-bismol) Surgery: various combinations of gastric resections and anastomosis - Performed when PUD does not respond to medical management Gastroduodenostomy (Billroth I): - distal end of the stomach is removed, and the remainder is anastomosed to the duodenum Gastrojejunostomy (Billroth II): Other factors that contributes PUD: - removal of the antrum and distal portion of the drugs (aspirin, ibuprofen) stomach and duodenum with anastomosis of the cigarette smoking remaining portion of the stomach to the jejunum chronic anxiety Vagotomy: Type A personality - Transection of vagus nerve that eliminates the acid- secreting stimulus to gastric cells & causing a decrease gastric acid secretion Pyloroplasty: performed in conjunction with vagotomy to widen the exit of pylorus to facilitate emptying of stomach contents Subtotal Gastrectomy: removal of 75% - 85% of the stomach Antrectomy: removal of the antrum of the stomach to eliminate the gastric phase of digestion Gastroenterostomy: - creating a passage between the body of the stomach & the jejunum to permit neutralization of gastric acid by regurgitation of alkaline duodenal contents into the stomach Esophagojejunostomy (total gastrectomy) - removal of the entire stomach with a loop of jejunum Complications of PUD anastomosed to the esophagus Hemorrhage – most serious complications; hematemesis Routine preoperative nursing care: (coffee-ground blood) usually indicates upper GI bleeding - informed consent, NPO, Medications Perforation – surgical EMERGENCY!!! Postoperative nursing care: Gastroduodenal contents leaks into the surrounding - Provide routine post-op care abdomen - Ensure adequate function of NG tube Sharp pain, client becomes apprehensive assuming knee- - Measure drainage accurately to determine necessity for chest position, chemical peritonitis occurs, bacterial fluid and electrolyte replacement; notify physician if septicemia & hypovolemic shock follows. there is no drainage. Anticipate frank, red bleeding for Peristalsis diminishes & paralytic ileus develops. 12-24°; Do not manipulate the tube and ensure its patency 4 of 5  GERD, GASTRITIS, PUD, DUMPING SYNDROME - Promote adequate pulmonary ventilation - Place client in mid- or high-Fowler’s position to promote chest expansion; Teach client to splint high upper abdominal incision before turning, coughing, and deep breathing Promote adequate nutrition. - After removal of NG tube, provide clear liquids with gradual introduction of small amounts of bland food at frequent intervals; Monitor weight daily. Assess for regurgitation; if present, instruct client to eat smaller amounts of food at a slower pace Provide client teaching and discharge planning concerning Dietary Management: - Gradually increasing food intake until able to tolerate 3- meals/day - Decrease the amount of food taken at one time & - Daily monitoring of weight eliminating liquids ingested with meals - Instruct client to consume a high-CHON ( colloidal - Stress-reduction measures - Need to report signs of complications to physician osmotic pressure), high-fat, low- to moderate-CHO diet immediately (hematemesis, vomiting, diarrhea, pain, abdominal melena, weakness, feeling of fullness/distension) - Methods of controlling symptoms associated with Dumping syndrome Dumping Syndrome - Constellation of vasomotor symptoms after eating, especially following after billroth II procedure - There is rapid gastric emptying into the small intestine causing abdominal distention (shifting of fluids to the GUT) Early manifestation: - occur w/in 30mins - Symptoms: vertigo, tachycardia, syncope, sweating, pallor, palpitations & desire to lie down Late dumping syndrome: - occurs 1½ - 3hrs p.c. - due to rapid entry of high-CHO food into the jejunum  Hyperglycemia   insulin release  Rebound hypoglycemia - Symptoms: dizziness, light-headedness, palpitations, diaphoresis & confusion 5 of 5