peptic ulcer disease
acute ulcer
associated w/ superficial erosion and minimal inflammation. Is of short duration; resolves quickly when cause is identified and removed.
Gastric outlet obstruction - symptoms?
- N/V - relief by belching or vomiting - epigastric fullness -constipation - swelling in stomach and upper abdomen - anorexia and weight loss
Histamine 2 receptor blockers
-suppresses the secretion of gastric acid by blocking H2 receptors in parietal cells in the stomach lining. -usually take at bedtime once a day, oral or IV -↓ HCl acid secretion ↓ Conversion of pepsinogen to pepsin ↑ Ulcer healing
esophageal ulcers
caused by reflux of HCL into esophagus
Cushings ulcers
common in pts w/ head injury and brain trauma. May occur in the esophagus, stomach, or duodenum. Usually deeper and more penetrating than typical stress ulcers.
Biliroth 1: gastroduodenostomy
removal of the lower portion of the antrum of the stomach.
Biliroth II gastrojejunostomy
removal of the lower portion of the stomach and then sutured to the jejunum.
Misoprostol (Cytotec)
synthetic prostaglandins specifically prescribed for prevention of gastric ulcers caused by NSAIDS and ASA. - cant be given to pregnant women because it induces labor
duodenal ulcer
ulcer in the duodenum
gastric ulcer
ulcer in the stomach
other therapy
- H2 blockers and PPIs used alone are used for ulcers not associated w/ H pylori
gastric outlet obstruction tx
- NG tube placement for continuous suctioning -assess residual from NG, >400 ml indicates obstruction - after several days NG is clamped and residuals are checked - when residual is <200 ml then oral intake of clears can begin - as residual obstruction goes down then solid foods are slowly re introduced nursing care: IV fluids and electrolytes endoscopy or upper GI study to dx I&Os surgery may be required to remove scar tissue
Cytoprotective drug therapy
- Sucralfate (carafate) - Misoprostol (Cylotec) -short term tx - accelerates healing and protects GI tract from stomach acid and prevents reduction of mucus, also an acid buffer - lowers the PH, give 30 min before or after antacids
pyloroplasty
- Surgical enlargement of pyloric sphincter -Commonly done after vagotomy -↓ Gastric motility and gastric emptying -If accompanying vagotomy, ↑ gastric emptying
Antacids
- adjunct therapy for PUD - increases gastric PH by neutralizing HCL acid
dietary modifications for PUD
- avoid extremes of temperature in food and beverages--> alcohol, coffee, caffeinated beverages - neutralize acid by eating 3 regular meals a day
more PUD diagnostic studies
- barium contrast studies--> 1) not accurate for shallow superficial ulcers 2) for patient who can't go endoscopy 3) for gastric outlet obstruction gastric analysis - ng tube is inserted and gastric contents aspirated to analyze for HCL acid
gastric outlet obstruction
- caused by ulcers located in antrum and prepyloric and pyloric areas of stomach, also in duodenum - obstruction due to: --> edema inflammation pylorospasm fibrous scar tissue formation - these all contribute to narrowing of pylorus
Diagnostic Studies PUD
- endoscopy with biopsy most commonly used--> EGD(Esophogastroduodenoscopy) - tissue specimens from endoscopy can rule out gastric cancer -
Antibiotic therapy
- eradicates H pylori infection - most important in treatment of H pylori - usually tx lasts 10-14 days - used in combo w/ ppi's and bismuth salts
Tx for hemorrhage
- immediate correction of blood loss to prevent hemorrhagic shock via IV fluid resuscitation - assess vital signs -labs: CBC stool for blood - hourly I&O's -NG tube placement to remove blood clots and acid -saline lavage--> cleaning the contents out of stomach via tube where small amounts of saline are infused and remove - blood transfusion for blood loss -endoscopic eval- may include injecting bleeding site with epinepherine or alcohol, cauterizing site, or clipping ulcer - selective embolization--> interventional radiological procedure, inject emboli of patients own blood clots with gelfoam through catheter in artery above the bleeding lesion
hemorrhage
- most common in PUD - develops b/c 1) erosion of granulation tissue found at base of ulcer during healing 2) ulcer through major blood vessel
Helicobacter pylori(gram negative bacteria)
- most peptic ulcers come from H pylori - comes from ingestion of food and water, and person to person contact and exposure to emesis - person w/ H pylori can be asymptomatic - produce enzyme urease - mediates inflammation, making mucosa vulnerable
Tx for perforation
- ng tube placement--> aspiration constantly - circulating blood volume replaced with lactated ringers and albumin solutions - blood transfusion - will need central line - needs immediate surgery - monitor fluids and electrolytes - assess for infection or peritonitis --> temp abdomen pain absent bowel sounds abdominal distention - treat peritonitis with iv antibiotics -procedure to repair: open laparoscopic repair--> simple oversewing involves the lease risk, gastric contents suctioned from cavity, broad spectrum antibiotics, pain meds - nursing care: --> bowel sounds will be diminished check vitals q15min stop all oral, NG feed/drugs IV fluids for volume lost
Anticholinergic drugs
- occasionally used - ↓ Cholinergic stimulation of HCl acid -↓ Gastric motility: not used for gastric outlet obstruction
perforation and penetration
- perforation-->Erosion of ulcer through gastic serosa into peritoneal cavity -erosion of ulcer thru gastric serosa into adjacent structures such as pancreas, or biliary tract - 10-25% mortality rate - requires emergency surgery
Tests for H pylori
- urea breath tests--> urea is byproduct of metabolism of H pylori--> clients drinks carbon enriched urea solution and spits into collection container, if H pylori present CO2 will be released -serological testing--> identifies presence of H pylori based on antibody assays in blood - stool antigen tests for presence of H pylori antigen -biopsy of the antral mucosa and testing of urease is considered gold standard for H pylori
Aspirin and NSAIDS
- use of is major risk for peptic ulcers - infection w/ H pylori and use of these have synergistic risk - inhibits synthesis of prostoglandins - cause abnormal permeability
Standard drug treatment of PUD
-2 PUD antibiotics, proton pump inhibitors, and bismuth salts that suppress and eradicate H-pylori. - typically prescribed for 10-14 days
Stress ulcers
-Acute mucosal ulceration of the duodenal or gastric area that occurs after physiological stressful events (burns, shock, severe sepsis, Multiple organ traumas). -Most common on ventilator dependent patients after trauma or surgery. -The process is a combo of ischemia due to blood shunting to other areas of body (decreased blood flow), duodenal contents refluxing back into stomach. -also large amounts of pepsin are released in stress or SNS event -Shallow erosions occur w/n 24 hours of events. By 72 hrs multiple ulcers will have formed and spread through GI tract. Will resolve as pt recovers.
common Histamine 2 Receptor blockers
-Cimetidine (Tagament) -Ranitidine (Zantac) -Famotidine (Pepcid) -Nizatidine (Axid)
most common S&S of ulcers
-Dull, gnawing pain - burning sensation in midepigastrium or the back
causes of PUD
-Helicobactor pylori (H pylori) - medication induced injury - lifestyle - familial tendency - ZES - Stress Ulcers--> 1) Curlings Ulcers 2) Cushings ulcers
chronic ulcer
-Long duration -Erodes through the muscular wall w/ formation of fibrous tissue. -Present for months; may last intermittently throughout persons lifetime. -More common than acute erosions. - form usually in lesser curvature of stomach
Duodenal ulcer pain
-Mid-epigastric region beneath xiphoid process -Back pain—if ulcer is located in posterior aspect -Occurs 2-5 hours after meals -Feels like "Burning" or "cramplike" -Tendency to occur, then disappear, then occur again -50%-80% patients awake during the night with abdominal pain from duodenal ulcers. -More likely to express relief of pain after eating or after taking an antacid than any other patients with ulcers. Other s/s -Vomiting, pyrosis (heartburn), constipation, diarrhea, bleeding -Pyrosis is often accompanied by burping -Vomiting could be a sign of a complication from PUD, such as gastric outlet obstruction. Emesis may contain undigested food. 15% of patients experience a GI bleed from PUD.
Dumping syndrome
-Occurs at end of meal or 15-30 minutes after eating Symptoms: Include weakness, sweating, palpitations, dizziness, abdominal cramps, borborygmi (excessive noises in the stomach), urge to defecate -Last no longer than an hour -Encourage the patient to lie down after eating, slows movement of food through the intestines. -eliminate liquids with meals, avoid milks and sugars.
Gastric Ulcers S/S
-Pain is high in epigastrium -Occurs 1-2 hours after meals -Feels like "Burning" or "gaseous" -Food aggravates pain if ulcer has eroded through gastric mucosa -More likely to result in obstruction.
background of stomach
-Stomach is normally protected from autodigestion by gastric mucosal barrier -Surface mucosa of stomach is renewed about every 3 days -Mucosa can continually repair itself, except in extreme instances -Water, electrolytes, and water-soluble substances can pass through barrier -Destroyers of mucosal barrier: Increased concentration of or activity of acid-pepsin or gastric acid (HCL)
S/S of perforation
-Sudden, dramatic onset -->: 1)Severe upper abdominal pain spreads throughout abdomen 2)Tachycardia, weak pulse 3)Rigid, board like abdominal muscles -shallow rapid respirations - no bowel sounds - N/V - Hx of symptoms of indigestion or previous ulcers -bacterial peritonitis can occur within 6-12 hrs
lifestyle factors
-alcohol--> stimulate acid secretion -coffee -smoking-->stimulate acid secretion -psychological stress
three major complications of PUD
-hemorrhage, -perforation -gastric outlet obstruction all considered emergency situations
Zollinger-Ellison Syndrome (ZES)
-rare condition characterized by severe peptic ulceration and HCL acid hypersecretion. This condition is suspected when a pt has several peptic ulcers or ulcers that do not respond to standard treatment. -Can also develop gastrinomas (islet cell tumors) in the pancreas. - 60-90% of gastrinomas are malignant - most common symptom is epigastric pain - diarrhea -steatorrhea--> fat in stool - genetic 25% of time
quadruple therapy
2 antibiotics (metronidazole and tetracycline + proton pump inhibitor +Pepto Bismol.
peptic ulcer
A peptic Ulcer is a hollowed out area that forms in the mucosal wall of the stomach in the pylorus (opening between the stomach and duodenum) or esophagus. - more likely in duodenum - occurs in areas of less curvature - can extend into peritoneum and cause peritonitis
Labs For PUD
CBC--> anemia due to bleeding ulcers UA---> check for blood in urine liver enzyme--> detect liver problems that may complicate tx check stool for blood serum amylase--> determines pancreatic function when post duodenal ulcer penetration of the pancreas is suspected
most common postop complications
Dumping syndrome Postprandial hypoglycemia Bile reflux gastritis
common PPIs
Esomeprazole (Nexium), Omeprazole(Prilosec)
triple therapy
Metronidazole (Flagyl) or Amoxicillin + Clarithromycin (Biaxin) + and a PPI {omeprazole (Prilosec) or lansoprazole (Prevacid
nutritional therapy post op
Small, dry feedings daily Low carbohydrates Restricted sugar with meals Moderate amounts of protein and fat Rest for 30 minutes after each meal
Bile reflux gastritis
Surgery can result in reflux alkaline gastritis -prolonged contact of bile causes damage to gastric mucosa, PUD may reoccur -Continuous epigastric distress that ↑ after meals -Administration of cholestyramine (Questran) relieves irritation
Trycyclic antidepressants
Usually used in those with chronic ulcers, and those with persistent pain and recurring ulcers. Have to use maximum doses of medication which causes side effects. - has Anticholinergic properties: decreases acid secretion; interrupts afferent pain fiber transmissions
postprandial hypoglycemia
Variant of dumping syndrome Result of uncontrolled gastric emptying of a bolus of fluid high in carbohydrate into small intestine -↑ Blood glucose; Release of excessive amounts of insulin into circulation -Secondary hypoglycemia occurs with symptoms approximately 2 hours after meals Symptoms include sweating, weakness, mental confusion, palpitations, tachycardia, and anxiety
Curling's ulcer
frequently observed @72 hours after extensive burns and involves antrum of the stomach or the duodenum
Proton Pump inhibitors
inhibit the enzyme that produces gastric acid and inhibits basal and stimulated acid production. - block ATPase enzyme that is important for secretion of HCL acid -more effective than H2 receptor blockers -take prior to meals
Gerontologic Considerations
patients older than 60 years old are connected with more NSAID use which causes PUD
vagotomy
vagus nerve is cut to decrease gastric acid production in the stomach. selective vagotomy results in denervation of only portion of the stomach, highly selective
