Acute and Chronic I: Gastrointestinal Disorders

Obstructive Disorders: Intussusception

. A proximal segment of the bowel telescopes into a distal segment leads to results in lymphatic and venous obstruction. . As edema from obstruction increases, pressure within the area of intussusception increases, leading to obstruction of arterial blood flow. . When arterial blood flow stops, ischemia occurs and mucus pours into the intestine. Venous obstruction leads to leaking of blood into the intestinal lumen. Blood and mucus mix forming the classic currant jelly-like stools.

Appendicitis: Clinical Manifestations

. Acute abdominal pain— Typically begins with periumbilical pain; Vague at first, ↑s in intensity over 3 - 4 hours, subsides then recurs with a shift to RLQ. RLQ pain is due to extension of inflammation to surrounding tissues. . +Rovsing's sign—palpate LLQ, pain is felt in RLQ. . Pain at McBurney's point—most common point of tenderness, located half to two-thirds the distance between umbilicus and R iliac crest. . Rebound tenderness—pain on deep palpation with sudden release.

Obstructive Disorders: Hirschprung's Disease

. Also called congenital megacolon or aganglionic megacolon—an abnormality in which certain nerve fibers (called parasympathetic ganglion cells) are absent in segments of the large intestine. This results in loss of motility with dilation of the bowel proximal to the region of involvement and severe bowel obstruction.

Appendicitis: Other Manifestations

. Anorexia, nausea, vomiting . Diarrhea or constipation. . Fever—low grade; may be high (102° -103° F) with perforation. . ↑d WBCs, elevated bands (shift to the left) indicates inflammatory proces Signs of rupture....may lead to peritonitis -sudden pain relief or sudden increase in pain -rigid abdomen -progressive abdominal distention -rapid shallow respirations, tachycardia -pallor, chills, ↑ in temperature ***Abrupt change in the character of pain preoperatively could indicate perforation. Ruptured appendix can cause peritonitis.

GERD and Peptic Ulcer Disease: Pharmacology Management

. Antacids: prompt, but temporary relief of heartburn— neutralizes HCL acid. . Histamine receptor antagonists (H2 receptor blockers)— block histamine stimulated gastric secretions and inhibits gastrin release. . Proton pump inhibitors— potent inhibitor of acid secretion (better than H2 blockers, but more expensive), binds with enzymes to prevent acid formation and heals erosions. . Prostaglandin analogs have a protective and some antisecretory effects on gastric mucosa - misprostol. ***Using antacids and acid-controllers such as H2 blockers and proton pump inhibitors represents another risk factor for iron deficiency in people with acid reflux. Acid helps your body absorb iron in the foods you eat. Decreased absorption -- especially if you consume a diet that is already low in iron -- sets the stage for deficiency. Histamine blockers and PPIs--both drugs allow healing of ulcers. Histamine blockers block the action of histamine on the H2 receptors thus ↓ing HCL acid secretion; They also, ↓ the conversion of pepsinogen to pepsin and helps with ulcer healing. PPIs have a different mode of action...they block the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ATPase, or, more commonly, the gastric proton pump). These drugs actually prevent acid formation and H2 blockers inhibit secretion. Both drugs work by controlling the high acid environment which allows ulcers to heal naturally. PPIs have a longer action than H2 blockers which make them more effective. They also work better because of where they act....on the gastric proton pump which seems to be more of a problem in causing ulcers than histamine. Many times these drugs are used together for people who have major problems with excess acid....since they work on two different sites.

GERD: Risk Factors

. Any condition that ↑s intra-abdominal pressure— (frequent lifting or bending, frequent cough) *Obesity and weight gain *Pregnancy . Smoking, smokeless tobacco . High fat foods . Caffeine and chocolate weaken the LES . Alcohol . Long term NG intubation . Hiatal hernia (diaphragmatic hernia—protrusion of upper stomach into diaphragm) . Aspirin and NSAIDs ***Hiatal hernia increases GERD due to mechanical and motility factors. It raises the sphincter above the diaphragm, reducing pressure on the valve. This causes the sphincter muscle to open at the wrong time. Approximately 80% of patients with GERD have a hiatal hernia.

Appendicitis

. Appendix becomes obstructed with stool, tumor, or bacteria. . Intraluminal pressure ↑s. . Obstruction and ↑d pressure lead to ↓d venous drainage, thrombosis, edema and bacterial invasion of the bowel wall. . With continued obstruction, gangrene can develop, followed by perforation.

Pyloric Stenosis Management

. Assess for manifestations of pyloric stenosis. . Daily weights. . Monitor for and prevent dehydration and electrolyte imbalances. . Upper GI showing passage of contrast through narrow pylorus .Pyloric ultrasound showing thickened pyloric muscle in a 4 week old infant with pyloric stenosis

Gastroesophageal Reflux (GERD)

. Backward flow of acidic gastric contents in to the alkaline esophagus—gradually breaks down the esophageal mucosa. . Gastric enzyme (pepsin), intestinal enzyme (trypsin), and bile salts are corrosive to esophageal mucosa. . Due to lower esophageal sphincter not functioning properly (gastroesophageal sphincter). ***GERD arises from contact of esophageal epithelium with acidic gastric contents. Under normal circumstances, reflux is prevented by multiple barriers. GERD occurs when these barriers are impaired. Mechanisms causing GERD: Transient relaxation of the LES—relaxes in the absence of swallowing; occurs when lying down after eating a large or fatty meal. Weakened LES—caused by certain foods (coffee, chocolate), certain medications (calcium channel blockers, etc.), and tobacco and alcohol. Hiatal hernia—increases intraabdominal pressure and pressure on the LES; obesity, pregnancy, ascites, intense physical exertion, heavy lifting are all contributing factors to developing a hiatal hernia. Impaired esophageal defenses—esophageal peristalsis is dysfunctional resulting in impaired acid clearance; Saliva, mucus, and bicarbonate (produced in the esophagus) play important roles in neutralizing refluxed acids, and promoting healing and restoration of the esophageal lining. Insufficient acid clearance and an increased incidence of GERD are seen in patients with chronic xerostomia (dry mouth from reduced or absent saliva flow) secondary to medications or an autoimmune disease

Diverticulitis: Diagnostics

. CBC . Urinalysis . Abdominal x-ray . U/S and CT of abdomen . Barium enema . Colonoscopy

Peptic Ulcer Disease (PUD): Causes Helicobacter Pylori (H. pylori) II

. Causes death of mucosal epithelial cells and ↑d levels of gastrin and pepsinogen. High serum gastrin levels remain high longer than normal after eating and continue to stimulate secretion of acid and pepsin (failure of the feedback mechanism leads to normally, acid in the gastric antrum inhibits gastrin release). . Releases toxins and enzymes that promote inflammation and ulceration. Ulcers lead to rapid gastric emptying which overwhelms the buffering capacity of the bicarbonate-rich pancreatic enzymes. Duodenal ulcers can cause ↓d mucosal bicarbonate secretion. ***Gastrin is a hormone that stimulates parietal cells of the stomach to secrete hydrochloric acid (HCl)/gastric acid. Pepsin is a gastric or digestive enzyme that breaks down protein. Other factors that contribute to ulcer formation: Chronic alcohol abuse Drug induced—NSAIDs, aspirin, corticosteroids Chronic gastritis Tobacco use stimulates acid production Physiological stress Psychological stress Family history Zollinger-Ellison syndrome—a condition in which tumors form in the pancreas, duodenum or the lymph nodes adjacent to the pancreas. These tumors, called gastrinomas, secrete large amounts of the hormone gastrin, which causes the stomach to produce too much acid. The excess acid, in turn, leads to peptic ulcers.

Obstructive Disorders: Hypertrophic Pyloric Stenosis:

. Circumferential muscle of pyloric sphincter becomes thickened, resulting in severe narrowing of pyloric canal (between the stomach and duodenum)—produces obstruction, hypertrophy, hyperperistalsis of the stomach. . Affects babies between 2 and 8 weeks of age and causes forceful vomiting that can lead to dehydration. It's the second most common problem requiring surgery in newborns.

Intussusception: Management

. Condition is potentially life-threatening and reduction is emergent procedure; if not, bowel becomes hypoxic, ischemic, and can infarct or perforate leads to septic shock and death. . May reduce spontaneously. Passage of a normal brown stool usually indicates the intussusception has reduced itself. . Conservative treatment: *water-soluble contrast *air pressure (air enema) or saline enema often pushes the bowel back into its original position—may be given IV fluids, NG tube decompression, and antibiotics prior to procedure. . May require surgery if nonsurgical interventions are not successful. ***Non-operative reduction is successful in approximately 80% of cases. Pre-op and post-op care does not differ from any child undergoing abdominal surgery.

GERD and Peptic Ulcer Disease: Pharmacology Management

. Cytoprotective drugs— ulcer coating agents—relieve pain and promote healing—sucralfate . Cholinergic drugs— ↑ LES pressure, improve esophageal emptying in supine position, and ↑ gastric emptying—not used often because they stimulate the secretion of gastric acid—bethanechol - if used, they are given with antacids and a histamine receptor antagonist. . Prokinetic drugs— ↑ LES pressure by stimulating smooth muscle of the GI tract and ↓ing the time food and fluids are in the stomach (↑ rate of gastric emptying)—metoclopramide. . Antibiotics— Most patients are + for H.pylori—antibiotics for 7 to 14 days.

Peptic Ulcer Disease (PUD): Types

. Duodenal ulcers—Usually occur within 1.5 cm of the pylorus. Patients have hypersecretion of acid and pepsin, and rapid emptying of the stomach which reduce the buffering effect of food and result in a large acid load in the duodenum. Helicobacter pylori bacteria is found in up to 95% of patients. . Gastric ulcers—Usually form within 1 inch of the pylorus of the stomach. Acute gastric ulcers are caused by aspirin, steroids, ibuprofen (or other NSAIDs), smoking, hot spicy foods. Helicobacter pylori bacteria is found in 60% - 80% of patients. ***Duodenal ulcers account for 80% of all peptic ulcers.

Hirschsprung's Disease Diagnostics

. During a physical examination, may be able to feel loops of bowel in the swollen belly. A rectal examination may reveal a loss of muscle tone in the rectal muscles. Abdominal x-ray. . Anal manometry—a balloon is inflated in the rectum to measure pressure in the area. Barium enema. Rectal biopsy—shows absence of ganglion cells. . Colored barium X-ray of the abdomen of a child with Hirschsprung's disease

Peptic Ulcer Disease (PUD) Pathophysiology

. Gastric mucosal barrier prevents autodigestion by acid and pepsin. If barrier is disrupted, then back-diffusion of acid enters mucosa. . Damages mucosal cells, causing inflammation. . This ↑s histamine which causes vasodilation and ↑s acid secretion. . Further mucosa breakdown and ulceration result.

Peptic Ulcer Disease: Complications

. Hemorrhage—Most common complication of PUD—vomiting coffee ground type material or passing tarry stools (melena). . Perforation—Most lethal complication - usually a surgical emergency; gastroduodenal contents empty through the anterior wall of the stomach into the peritoneal cavity leads to chemical peritonitis, bacterial septicemia, hypovolemic shock; peristalsis diminishes and paralytic ileus develops. Manifestations— . Sudden, dramatic onset . Sudden severe upper abdominal pain that quickly spreads throughout the abdomen . Abdomen becomes rigid and "board-like" - bowel sounds are usually absent . Nausea/vomiting . Shoulder pain if leakage causes irritation to phrenic nerve. ***Peritonitis occurs with a perforation: an inflammation of the serosal membrane that lines the abdominal cavity and the organs contained therein. It is most often caused by introduction of an infection into the otherwise sterile peritoneal environment through organ perforation. Complications of peritonitis: ARDS Hypovolemic shock Septic shock Intra-abdominal abscess Paralytic ileus Organ failure

GERD: Diagnostics

. History from adults. . History/observation of vomiting episodes and feeding habits of children. . Esophageal pH probe. . Barium swallow—checks for problem in upper stomach. . Endoscopy allows visualization and confirmation of pathologic changes in the mucosa (any inflammation, scarring, strictures). . Give proton pump inhibitor for 2 weeks and monitor for ↓d symptoms. . Biopsy—r/o cancer

Hirschsprung's Disease Clinical Manifestations

. In a newborn period, there is failure to pass a meconium stool within 24-48 hours after birth, reluctance to eat, vomiting, and abdominal distention. . During infancy the child has difficulty gaining weight, constipation with ribbon-like/foul-smelling stools, abdominal distention, large fecal mass on abdominal palpation, episodes of watery diarrhea (may be explosive) and vomiting. . In older children, symptoms become chronic and include constipation, passage of ribbon-like, foul-smelling stools, abdominal distention and visible peristalsis. Usually there is evidence of poor nutrition and anemia. ***Complications: Complete intestinal obstruction with bilious vomiting Ischemia of the intestinal mucosa leading to infarction Sepsis Death

Complications of Surgery: Dumping Syndrome

. Ingested food passes directly and quickly into the small intestines. . Undigested food, enzymes, and glucose make the food bolus large and hypertonic. . Because the food mass has a high hyperosmolality, fluid is drawn into the small intestines from the vascular compartment in an attempt to dilute intestinal contents. .This process results in ↑d volume and ↑d peristalsis = cramping, abdominal pain, hypermotility and diarrhea. .Patient is at risk for hypovolemia. ***With removal of large portion of stomach and pyloric sphincter, dumping syndrome can occur.

Peptic Ulcer Disease (PUD): Causes Helicobacter Pylori (H. pylori)

. It plays a key role in the formation of duodenal ulcers. . Also linked to gastric cancer and non-Hodgkin's lymphoma. . This bacteria survives in the GI tract for a long time as a result of its ability to move in mucus and attach to mucosal cells. . It also secretes a substance that buffers the area around it, and protects it from destruction in the acidic environment. . Checked by blood specimen (to identify H.pylori antibodies) and/or tissue sample (biopsy) through endoscopy. ***Until recently, it was felt that most ulcers were caused by lifestyle factors such as poor diet, too much stress, heavy drinking, and smoking. But amazingly, it now seems in the majority of cases the real culprit may be this tiny bacteria..........H. pylori--first reported in the stomach of patients with ulcers in 1982. By age 20, over one-fourth of Americans are infected. The rate of infection increases with age, so it occurs more often in older people. But, no one has satisfactorily explained how anyone picks up this bacteria in the first place, though it probably reaches the stomach by way of the mouth through contaminated food, fluids, or utensils.

Complications of Surgery

. Marginal Ulcers—develop where gastric acids contact the operative site. Ulceration may cause scarring, obstruction, hemorrhage, and perforation. . Hemorrhage. . Alkaline reflux gastritis—caused by duodenal contents. . Acute gastric dilation—stomach distention in the immediate post-op period. . Gastrojejunocolic fistula. . Pyloric Obstruction. . Nutritional problems: pernicious anemia is a long-term complication of total gastrectomy. ***Nutritional problems: *Vitamin B12 deficiency (with gastrectomy, you lose the Intrinsic Factor - pernicious anemia)—can cause peripheral neuropathy and patients will require vitamin B12 injections. *Folic acid deficiency. *Ca++ metabolism disorders—↓d absorption of Ca++ & vit. D.

GERD: Clinical Manifestations

. May be sudden or gradual onset . Slowed wt. gain in babies, wt. loss in adults . Excessive vomiting . Dysphagia . Pain in swallowing food . Acid regurgitation . Heartburn—(occurs in the chest) pain is described as an intermittent, burning/tight sensation—if severe, pain radiates to back, neck, or jaw; usually occurs after meals and is relieved with antacids or milk; discomfort may be relieved by standing and walking. . Dyspepsia—epigastric pain (indigestion) . Respiratory symptoms—wheezing, coughing ***GERD: Clinical Manifestations in Children: Excessive vomiting Respiratory—recurrent pneumonia, stridor, chronic cough Slowed weight gain in babies Unusual irritability Iron deficiency anemia can occur from loss of blood Dysphagia

Appendicitis: Management

. No medical treatment—surgery must be performed: IV fluids and electrolytes, and IV antibiotics are administered preoperatively. . If non-perforated—laparoscopic surgery Open appendectomy (incision in the RLQ) if ruptured— pre-op: -IV fluids and electrolytes -IV antibiotics -NG tube to decompress stomach -On antibiotics for 7 - 10 days if the child has developed peritonitis.

Hirschsprung's Disease: Management

. Observe the passage of meconium and bowel patterns in the neonatal period. . Prepare parents for medical-surgical intervention. Foster parent-infant bonding. Pre-op care: . Low-fiber, high calorie, high protein diet.....If child is severely malnourished (FTT)—TPN. . Saline enemas for older children—to empty bowel and ↓ bacterial flora. Newborn's bowel is sterile—no preparation is necessary. . Antibiotics. . Maintain fluid and electrolyte balance and monitor for signs of shock. ***Offer small frequent feedings. Several days prior to surgery—low fiber diet which will aid in keeping the stool soft. It also slows down bowel movements and decreases the amount of stool in the intestines. It can also reduce blockage.

Intussusception: Clinical Manifestations

. Occurs between 3 months and 3 years of age . Infant suddenly develops crampy, colicky, abd. pain . Inconsolable, draws knees up to chest with colicky pain episode when pain episode subsides, child appears normal . Palpable sausage-shaped abdominal mass . Currant jelly-like stools (diarrhea) . Vomiting . Anorexia and weight loss . Rectal bleeding . Signs of sepsis

Appendicitis: Management III

. Post-op care continued: Unruptured appendix—recovery time is relatively quick. The morning after surgery, clear liquids are offered. Once those are tolerated, the diet progresses to solid food. Once the patient is eating and drinking, the intravenous line is removed. . Monitor the patient for signs of infection and check that the incision is healing. Teach patient/parents to monitor for infection. . Heavy lifting and strenuous activity should be avoided during recovery....full recovery may take 4 to 6 weeks. . Diet high in protein, high calories, and high in vitamin C. ***Important discharge teaching: Diet high in protein, high calories, and high in vitamin C. Supplemental vitamin C, iron, and multivitamins aid in wound healing and formation of RBCs.

Hirschsprung's Disease: Management III

. Post-op: child will be NPO, have an NG tube to low intermittent suction, will be on IV fluids. . May have a Foley cath to prevent abdominal wound contamination. . Monitor intake and output; monitor for return of bowel sounds and passage of stool; diet will be advanced slowly with the return of bowel sounds (starting with clear liquids). . Monitor fluid and electrolyte balance. . Ostomy care and teaching. . If available use the enterostomal therapist for expert assistance in planning home care; colostomy is temporary. ***Post-op: child will be NPO, have an NG tube to low intermittent suction, will be on IV fluids. May have a Foley cath to prevent abdominal wound contamination. Monitor intake and output; monitor for return of bowel sounds and passage of stool; diet will be advanced slowly with the return of bowel sounds (starting with clear liquids). Monitor fluid and electrolyte balance. Ostomy care and teaching. If available use the enterostomal therapist for expert assistance in planning home care; colostomy is temporary.

Pyloric Stenosis: Management II

. Post-op: some vomiting may occur up to 48 hours; continue IV fluids until retaining adequate amounts by mouth. . Feedings are usually started 4 to 6 hours post-operatively—clear liquids containing glucose and electrolytes, advancing as tolerated. . Position on right side pre- and post-op to prevent aspiration of vomitus. Pain management.

Surgical Management for GERD/PUD

. Pre-op teaching should include an explanation of what the surgery generally involves....may be done laparoscopic (most common) or open surgery technique. . Demonstrate and discuss the importance of frequent coughing and deep breathing exercises. Patient must use an incentive spirometer. With open surgery: warn patients that the high abdominal incision makes deep breathing and coughing very uncomfortable. The high incision greatly ↑s the risk of respiratory complications. Respiratory complications are less with a laparoscopic procedure. . Post-op care: ABCs—monitor and maintain fluid and electrolytes; NG tube to decrease pressure on suture line; pain management; monitor for and manage complications.

Pyloric Stenosis: Management

. Pre-op: correct metabolic alkalosis and dehydration first (surgery may be delayed up to 48 hours until child's fluid and electrolyte status is stabilized). Usually started on IV fluids with dextrose and electrolytes. . NPO with NG tube to decompress stomach. . Monitor strict I & O. . Frequent vital signs. . Protect from infection—at risk due to nutritional status . Encourage parent(s) to stay with child. . Must have surgical relief of pyloric obstruction: Pyloromyotomy

Hypertrophic Pyloric Stenosis: Clinical Manifestations

. Projectile vomiting—usually begins at 3 weeks of age (can start as early as 1 week). . Infant is irritable and cries a lot—very hungry and will suck hard on the nipple, however, vomiting during or shortly after feeding; Child then resumes eating right after vomiting. . Decreases # of stools and abdominal distention. . Weight loss. . Dehydration. . Failure to Thrive. . visible gastric peristalsis, dehydration, loss of subcutaneous fat

Diverticulitis: Management Surgery

. Reserved for patients with complications such as abscess or obstruction that cannot be managed medically; 20% to 30% require surgical treatment: *Bowel resection with anastomosis. *If surgery is required during acute phase - temporary colostomy may be necessary until inflammation has subsided; colostomy is usually closed within 3 months.

Diverticulitis

. Results from the occurrence of abnormal saclike protrusions or pouches in the intestinal wall. These abnormal sacs are called diverticula. . Diverticula can occur anywhere in the GI tract except the rectum—usually occur in the distal large intestine (sigmoid colon). . Diverticulitis occurs when bacteria and stool become trapped in the diverticula, causing inflammation and infection. ***What causes the development of diverticula? Low-fiber diet that's high in processed foods leads to constipation. Straining to have a bowel movement ↑s pressure inside the colon. This pressure results in the development of the pouches, or diverticula, in the large intestine. Aging (when combined with a low fiber diet) can also lead to the development of diverticula—there is a loss of muscle mass and collagen, leading to weak points in the intestinal wall.

GERD/PUD Dietary and Other Management

. Small frequent meals . Drink lots of fluids .Avoid eating and drinking 3 hours before bedtime . Avoid extremely hot or cold foods . Avoid fatty foods—fatty foods ↓ rate of gastric emptying, ↓ LES pressure . Avoid chocolate and excess coffee/tea (5 - 6 cups/day)— ↓ LES pressure . Avoid milk products at bedtime—milk ↑s gastric acid secretion . Avoid spicy foods and citrus juices—irritate esophagus . Avoid tobacco and alcohol—↓ LES pressure . Avoid aspirin and NSAIDs . Elevate head of bed . Lose weight ***Small frequent meals - 4 to 6 per day, avoid eating and drinking 3 hours before bedtime; Eat slowly and chew thoroughly.

Peptic Ulcer Disease (PUD): Types II

. Stress ulcers—Acute gastric erosion - usually multiple sites of ulceration throughout stomach or duodenum; develop because of: . Severe trauma or major illness . Severe burns (Curling's ulcers) . Severe head injury or intracranial disease (Cushing's ulcers)—due to decrease mucosal blood flow and hypersecretion of acid caused by overstimulation of vagal branches that supply acid-secreting (parietal) cells. . Drug ingestion— (aspirin, NSAIDs, and alcohol) . Shock, sepsis . Severe emotional stress

Surgical Management for PUD II:

. Subtotal Gastrectomy- partial removal of the stomach . Billroth I procedure—the pylorus is removed and the distal stomach is anastomosed directly to the duodenum; performed in cases of stomach cancer, a malfunctioning pyloric valve, gastric obstruction, and peptic ulcers. . Billroth II procedure—the lower part of the stomach (antrum) is removed and a loop of small bowel (jejunum) is brought up and joined to it in a side-to-side manner for drainage (gastrojejunostomy).

Pyloric Stenosis: Clinical Manifestations continued

. Tetany—due to low calcium levels . Gastric peristalsis visible on examination—reverse peristaltic waves (going left to right) . Olive-shaped mass can be palpated in the epigastrium, just to the right of the umbilicus Complications: Metabolic alkalosis Hypovolemic shock

Peptic Ulcer Disease: Diagnostics

. Upper GI endoscopy .Gastroscopy—EGD (esophageal gastroduodenoscopy) CBC . Liver enzymes—to determine liver problems that may complicate PUD . Breath, urine, serum, stool, and gastric tissue biopsy tests for H.pylori . Stool for occult blood (guaiac stool) . Gastric analysis—to assess for gastric acid hypersecretion

Diverticulitis: Clinical Manifestations

. Usually asymptomatic. . LLQ abdominal pain (if diverticulitis is in the sigmoid colon—most common site); pain may start off as intermittent, then become steady as inflammation progresses; described as mild to severe in quality. . Change in bowel habits (constipation or diarrhea). Fever. . Abdominal distention and flatulence. . Upon palpation—tender in LLQ. . Elderly may have generalized abdominal pain and/or symptoms of bowel obstruction.

Surgical Management for PUD:

. Vagotomy—severing of the vagus nerve; performed to eliminate the acid-secreting stimulus to gastric cells. . Gastroenterostomy—permits regurgitation of alkaline duodenal contents, therefore neutralizing gastric acid. . Antrectomy—performed to reduce acid-secreting portions of the stomach; the entire antrum of the stomach is removed thus the cells that secrete gastrin are excised (AKA subtotal gastrectomy). . Total Gastrectomy—intervention for extensive gastric cancer ***About 30% of total acid secretion occurs BEFORE food enters the stomach. These sensory and mental inputs converge on the hypothalamus, which relays signals to the medulla oblongata. Vagus nerve fibers from the medulla stimulate the enteric nervous system of the stomach which, in turn, stimulates gastric secretion.

Peptic Ulcer Disease (PUD)

A break in the continuity of esophageal, gastric, or duodenal mucosa (ulceration). It can occur in any part of the GI tract that comes in contact with gastric juices.

Diverticulitis: Management II

Acute Disease Process..... Bowel rest—NPO and may require an NGT. IV fluids to maintain fluid and electrolyte balance. Bed rest—avoid any activity that ↑s intra- abdominal pressure, thereby ↑ing the risk of perforation. Monitor for manifestations of peritonitis. . Broad spectrum antibiotics - metronidazole, ciprofloxacin. . Opioids may be necessary for severe pain - meperidine or morphine. . Stool softeners. Avoid laxatives or enemas - both↑ intra-colonic pressure. . Once acute attack subsides, clear liquid diet, advancing to semisolids.

Diverticulitis II

Complications: . Peritonitis from perforation—inflamed pouches rupture spilling intestinal waste into the abdomen. . Abscess and fistula formation—most fistulas form between the large intestine and bladder - intestinal contents, including normal bacteria, enter the bladder and cause urinary tract infections. . Bowel obstruction. . Ureteral obstruction. . Bleeding.

Peptic Ulcer Disease: Clinical Manifestations

Gastric Ulcers: . Burning, gaseous pain in upper epigastrium, back, upper abdomen . Pain 1 to 2 hours after meals secondary to hypersecretion of acid . Occasional n/v, weight loss . Hematemesis if ulcer erodes through blood vessel (bright red or dark) . Usually patient is over 50 years old Duodenal Ulcers: . Burning, pressure, cramping pain across mid epigastrium, upper abdomen, or back . Pain 2 - 4 hours after meals secondary to hypersecretion of acid; may occur in the middle of the night . Pain periodic and episodic . Occasional nausea/vomiting . Pain relief with antacids and eating food that neutralize and dilute HCL acid. . Bloating, abdominal distention, intolerance to fatty foods . Melena: stool specimen = + guaiac (if large amt. blood loss—signs of shock) ***Duodenal ulcers can occur at any age, but peak incidence is between 35 and 40 years of age.

Manage Complications: Peptic Ulcer Disease

Hemorrhage: *Continuous cardiac/respiratory monitoring *NPO *Monitor for and treat hypovolemic shock; prevent dehydration and electrolyte imbalances (LR or NS) *I and O *Stop bleeding—cool or room temperature saline lavage, IV H2 receptor blocker or PPI *NGT if n/v or gastric outlet obstruction suspected—intermittent suction for about 24 - 48 hours *If bleeding continues beyond 48 hours, surgery may be required or endoscopic procedures *Monitor CBC—blood transfusions

Surgical Management: GERD

Nissen fundoplication - recreates a valve by wrapping the fundus of the stomach around the lower esophagus.

PUD: Complications

Obstruction—Most often occurs in the pylorus; Ulcers in the antrum and pyloric areas of the stomach and duodenum predisposes to gastric outlet obstruction; Edema, inflammation, pylorospasm, and scar tissue (from repeated ulcerations and healing) contribute to narrowing of the pylorus; Overtime, ↑d contractile force is needed to empty stomach leads to hypertrophy of stomach wall. Manifestations— . History of chronic ulcer pain . Projectile vomiting . Anorexia . Weight loss . Constipation due to dehydration and lack of fiber in diet . Loud peristalsis with visible peristaltic waves.

Manage Complications: Peptic Ulcer Disease II

Perforation and Obstruction— *ABCs—provide O2 as needed. *IV fluids and electrolyte replacement; may need blood transfusion if perforation. *Vital signs every 15 to 30 minutes with assessments. *NPO with NGT—gastric decompression to halt spillage with perforation. With obstruction—decompression helps with ulcer healing, and ↓s inflammation and edema. *I and O—insert a urinary catheter. *Prepare for surgery or laparoscopic procedure. *Antibiotics, antiemetics, analgesics (morphine); antacids and antisecretory drugs for obstruction.

Appendicitis: Management II

Post-op care: . IV fluids and IV antibiotics. . Low, intermittent suction (NG tube) to keep stomach decompressed....continue until bowel sounds are auscultated. . Dressing changes.....patient may have a drain in place if appendix was ruptured. . Pain management is essential—administer analgesia and provide a small pillow for abdominal splinting, position for comfort. . Physical activity, such as getting out of bed, begins on the same day as surgery or the next morning.

Hirschsprung's Disease Management II

Pre-op care: Monitor for signs of bowel perforation (fever, increasing abdominal pain and tenderness, increasing distention, vomiting, irritability, dyspnea, cyanosis); measure abdominal circumference at the level of the umbilicus and mark with a pen. Teach child and parents ostomy care by verbal explanations and demonstration using a doll. ***Colostomy is temporary. It is placed in the portion of normal innervated colon just proximal to the defect. This gives the bowel time to rest while the normal bowel regains its tone.

Diverticulitis: Management

Prevention..... *High fiber diet (fruits and vegetables) *Low fat *Reduced amount of red meat in diet *Exercise *Weight reduction *Avoid factors that increase intra-abdominal pressure—straining with BMs, heavy lifting, frequent bending, restrictive clothing