Peptic Ulcer Disease

cdunbar4's version from 2016-10-20 01:16


Question Answer
Definitionerosion of GI mucosa resulting from HCl acid and pepsin digestive actions. Any part of GI mucosa that contacts with gastric secretions can develop an ulcer.
Acute or Chronic depending ondegree and duration of mucosal involvement and gastric or duodenal (location dependent)
Acute characteristics superficial erosion, minimal inflammation
Chronic characteristicsmuscular wall erosion with formation of fibrous tissue; present continuously for many months or intermittently
Do you have to be producing excess gastric acid for development of an ulcer?No, the damage to the mucosal cells ↓'s function → release of histamine and pepsinogen to peptin → vasodilation = ↑ acid secretion
pH of gastric acid before and after mixing with gastric contents?0.8 before and 2-3 after
How often is the surface mucosa renewed?About every 3 days-mucosa repairs itself except in extreme instances


Question Answer
5 ulccerogenic drug classesASA, NSAIDS, corticosteroids, anticoagulants and some SSRIs (Prozac)
Aspirin & NSAIDs effects on mucosa?inhibit synthesis of prostaglandins = ↑ gastric acid secretion & ↓ integrity of mucosal barrier
Corticosteroids effects↓ rate of mucosal cell renewal thereby ↓ protective effects
H. Pyloribacterium colonizes epithelial cells in the mucosal layer → produces urease which activates immune response with antibodies and the release of cytokines
Lifestyle factorsETOH causes acute lesions as well as ↑'s acid secretions; coffee is a strong stimulant of gastric acid secretion; psychologic distress (stress & depression) negatively influences healing of ulcers once they've developed; smoking OF COURSE!
Gastric ulcer mostly found in antrum
Gastric ulcer etiologyH. Pylori, medications, smoking and bile reflux are RF
Duodenal ulcers most common cause?H. pylori (90-95% of all cases)
Zollinger-Ellison syndromesevere peptic ulceration, gastric acid hypersecretion elevated serum gastrin levels and gastrinoma of pancreas or duodenum


Question Answer
gastric ulcers, location of pain and how long after food?epigastric pain, 1-2 hours after food; "burning" or "gassy"
duodenal ulcers how long after food?4-5 hours after food - when HCl comes in contact
Location of pain - duodenal?below xyphoid, maybe some back pain; "burning" "crampy"
Characteristic of duodenal ulcertends to occur continuously for a few weeks or months & then disappear for a time, then recurs months later
Common to have no pain or other symptoms, why?gastric & duodenal ulcers are not rich in sensory pain fibers


Question Answer
3 major complications1. Hemorrhage 2. perforation 3. gastric outlet obstruction
Most common complicationhemorrhage; usually duodenal
most lethal complication; manis?perforation; sudden, dramatic onset - pain radiates to back, not releived by food or antacids; abdomen rigid and board like, respirations shallow & rapid
Perforation spillage of gastric or duodenal contents into peritoneal cavity
Size perforation is directly proportional long patient has had ulcer
Location of duodenal ulcer perforationslarge penetrating ones that haven't healed are located on posterior mucosal wall
perforation can result in what further complications?hypovolemia d/t third spacing; if untreated, bacterial peritonitis in 6-12 hours
perforated gastric ulcer locationoften located on lesser curvature of stomach
gastric outlet obstruction areasantrum, prepyloric & pyloric areas of stomach
Hypertrophy of stomach wall caused by...↑ contractile force needed to empty stomach
Over time, stomach enters decompensated phase = dilation and atony (loss of muscle tone)
Obstruction in the distal stomach & duodenum is the result of...edema, inflammation & pylorospasm
short duration or absence of pain is indicative of a malignant obstruction
Common manisvomiting (particles from hours or days, usually fowl odor), constipation (dehydration d/t ↓ roughage in diet); sometimes swelling in upper abdomen


Question Answer
Most accurate diagnostic procedureendoscopy- direct view & biopsy to rule out h.pylori & stomach cancer
H. pyloriurease test *gold standard for confirmation
barium contrast study reserved for which patients?who cannot undergo endoscopy
xraysineffective in differentiating ulcers from a malignant tumor
Test used to determine obstruction?barium contrast
gastric analysis
laboratory analysisCBC (anemia), urnalysis , liver enzyme studies (liver problems), serum amylase (pancretic function) & stool examination (blood)

Collaborative Care

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Medical regimen consists ofadequate rest; dietary mods; drug therapy; elimination of smoking; long-term follow-up care
Aim of treatment program (3)↓ degree of gastric acidity; enhance mucosal defense mechanisms; minimize harmful effects on mucosa
Healing can take how long?3-9 weeks-pain disappears in 3-6 days
Patients are generally treated where?Ambulatory care clinics
Drug classes used **NTKantisecretry (H2 blockers, PPIs); Cytoprotective; neutralizing; antibiotics; and tricyclics
Nutritional Therapyavoid/eliminate irritating foods
Food source that is considered the best neutralizing food: protein
Foods high in __________ may irritate an inflamed mucosaroughage
_____ can neutralize gastric acidity & contains _________________ and growth factors-protects mucosaMilk; prostaglandins

Acute Complications

Question Answer
The big 3 complicationshemorrhage, perforation, obstruction
hemorrhagemost common complication; can be just leaky too
management for hemorrhageblood or blood products can be administered; careful monitoring of VS; I/O; lab studies, signs of impending shock
Endoscopic evaluation of hemorrhage revealsdegree of inflammation and ulcer location
perforation-what needs to happen immediately?ER! Focus on stopping spillage of gastric contents into peritoneal cavity; NG tube ASAP
In general with acute complications: NG tube with intermittent suction for 1-2 days; fluids/electrolytes via IV infusion until patient can tolerate eating
where should NG placement be located?as near to perforation as possible to facilitate decompression
Circulating blood volume must be replaced with ________ __________ and albumin solutions to prevent ____________.Lactated Ringers; hypovolemia
What should be inserted and monitored hourly?CVP line and indwelling catheter
Gastric outlet obstruction requiresdecompression of stomach with NG tube inserted in stomach, attached to continuous suction
How does NG tube and suction help with obstruction?stomach regains normal muscle tone; ulcer can heal; inflammation and edema subside
Obstructions cause vomiting, what would you expect for your patient to be placed on?IV fluids/electrolytes to correct dehydration
NG tube aspirate falls below 200mL, what can patient begin?oral intake of clear liquids


Question Answer
Goals and plans of PUDtherapeutic regimen; ↓ discomfort r/t PUD; No signs of big 3; complete healing; lifestyle changes
Implementation: generally ↑ n/v, bleeding; NPO for a few days with NG tube and fluids IV; physical/emot'l rest are necessary
Hemorrhage implementation: watch VS changes; more blood in gastric contents = less pain (blood neutralizes acid)
Implementation: how to keep clots from block NG tubeflush NG tube
Perforation causes abdomen to look likeboard-like and rigid; sudden severe abd pain unrelated to intensity and location to pain that brought patient to hospital
Referred pain from perforation can travel toshoulders
Respirations are shallow and grunting, why?pressure from diaphragm
Ensure allergies are reported on chart, what is usually started if a perforation?Antibiotics
Gastric outlet obstruction implemenationcan occur at any time; gradual onset; constant NG aspiration of stomach contents to relieve symptoms; regular irrigation of NG tube

Surgeries and surgery complications

Question Answer
Gastroduodenostomy (Bilroth 1)partial gastrectomy (upper 2/3) with re-connection to duodenum
Gastrojejunostomy (Bilroth 2)partial gastrectomy (upper 2/3 with re-connection to jejunum
Vagotomy"de-nerve" all or part of stomach: combo of vagotomy with Bilroth I or II will remove ulcer and stimulus for additional secretions
Pyloroplastyrepair (expand) pyloric opening
Dumping syndrome is direct result of surgical removal of a large portion of stomach and pyloric sphincter and ↓reservoir capacity of stomach
dumping syndrome: chyme is thicker (doesn't break down as much) so...will pull water and move it out of bowel faster!
absorption is a problem, what will be happening to patient's stools?liquid (less calories in, weight loss, B12 deficiency bc intrinsic factor is required)
Dumping syndrome nursing interventionsseperate fluids from food (smaller and more frequent meals; avoid bulk (fiber) avoid fluid with meals (expands foods); avoid high carb diet
Dumping syndrome manispain in perianal area (could get TPN if bad enough)
Postprandial hypoglycemia variant of dumping syndrome d/t less absorption: bolus of fluid high in carbs goes into SI →pancreas doesn't realize you aren't going to absorb it all and releases excessive amount of insulin into circulation
PUD gerontological considerations↑ use of NSAIDs; 1st sign can be flank pain or ↓ Hct

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