Save
Busy. Please wait.
Log in with Clever
or

show password
Forgot Password?

Don't have an account?  Sign up 
Sign up using Clever
or

Username is available taken
show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
Your email address is only used to allow you to reset your password. See our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
focusNode
Didn't know it?
click below
 
Knew it?
click below
Don't Know
Remaining cards (0)
Know
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

Nursing 3 Test 3

Peptic Ulcer Disease

QuestionAnswer
The term peptic ulcer is used to describe... both gastric and duodenal ulcers
peptic ulcer disease an erosion of the gastrointestinal mucosa resulting from the digestive action of hydrocholoric acid and pepsin, can be acute or chronic
HCL Hydrochloric acids.
HCL secretes... 1-3 liters each day. helps breakdown food, activates pepsinogen & kills microbes
parietal cells secrete HCL and Intrinsic factor
Intrinsic Factor is essential for the absorption of B-12
Pathophysiology of Gastric ulcers commonly found in the greater curvature of stomach,more superficial;leasions are round,oval or cone shaped,peak age 50-60, normal to low gastric secretion,normal or delayed emptying rate of stomach,increased w/an incompetent pyloric sphincter(bile reflux)
pathophysiology of duodenal ulcers penetrating;usually occurs in the first 1-2 cm of duodenum, peak age:35-45 yrs old, increased gastric acid secretion-if not buffered w/food can cause irritation, increased rate of gastric emptying
pathophysiology of duodenal ulcers increased acide and decreased buffering by food results in a large acid load in the duodenum
incidence of peptic ulcer disease approximately 60-70 million americans are affected by a digestive disease, PUD:10% of americans
gastric ulcers are more commen in which sex? females
duodenal ulcers are 2-3 times more likely to occur in which sex? males
risk factors for PUD H.pylori
Helicobacter pylori culprit is urease produced by H.pylori which increases ammonia>H2 ions>damage to mucosa
H.pylori is found in what percentage of gastric ulcer pt's 60-80%
H.pylori is found in what percentage of duodenal ulcer pt's 95%
H.pylori is transmitted via oral-fecal route
over half the population have H.pylori but this doesn't guarantee they will develop... PUD
Social class for duodenal ulcer high stress job, community leaders, lack of sleep & relaxation
social class for gastric ulcer low socioeconomic class, manual or unskilled labor
stressful situations decrease mucous production
stress situations cause blood vessels to constrict
stressful situations increase gastric secretion, which increases curling's ulcer(burns, mult trauma esp r/t prolonged stress)
cigarette smoking increases bile reflux from the duodenum into the stomach by decreasing the secretion of bicarbonate ions from the pancreas
HCO3 bicarbonate ions, neutralizes acid and is secreted from the pancreas
which blood group has more duodenal ulcers O, and at an increase of 35%
why does blood group O have more duodenal ulcers have stomach cells w/receptors that attract H.pylori(explains why it runs in families)
prevention of PUD methods to increase relaxation & sleep, improve nutrition, decrease smoking, decrease alcohol intake, enteric coated ASA, take meds w/milk or food
nursing assessment of pt w/PUD pain:may have little or no pain, earliest symptoms may be a serious complication
nursing assessment of pt with gastric ulcer burning, left epigastric pain usually after food(w/in 1 hr), made worse by or unrelated to food, anorexia, wt loss(about 40%), great indivial variation
nursing assessment of pt with duodenal ulcer pain may be described as "burning,cramping or pressure-like"(back pain), midepigastric area(below xyphoid process), pain occurs 2-4 hrs after eating, often associated w/other diseases(COPD,pancreatic dx,chronic renal failure),pain relief w/antacids & food
medications for PUD adrenocorticosteroids, indomethacin
adrenocorticosteroids increase susecptibility of mucosa
indomethicin decreases mucosal resistance(both drugs inhibit prostaglandin synthesis)
caffeine and alcohol increase acid production
ASA and NSAID suppress mucous secretion
syptoms of PUD vomiting(not typical in PUD), partially undigested and digested food, bile coffee ground emesis(old blood), bright red blood, bleeding-from erosion of blood vessels
Melena black,tarry stools, dark colored caused by enzymes in the GI tract that oxidizes the blood passed in stools
Hematochezia bright red blood from the rectum
guiac test positive stool tested for occult blood
serum test for H.pylori looks for immunoglobulin G antibodies to H.pylori antigen
breath test for urease activity is when... drink carbon enriched urea & exhale into a bag(if H.pylori is present, it breaks down the compound and releases CO2
finding CO2 in a breath test indicates H.pylori diagnosis
breath test is also useful to see if rx is working for H.pylori
Upper Gi series barrium contrast studies(inject radiopaque batrium and visualized under fluoroscopy)
gastric analysis aspiration of gastric contents to assess gastric acidity
lab values in a pt with GI bleeding decreased Hct & Hgb, increased PT or PTT occur with prolonged bleeding, electrolyte imbalances r/t fluid loss,vomiting
complications of GI bleeding hemorrhage, perforation, gastric outlet obstruction
hemorrhage most common:results from penetration of the ulcer into an artery or vein
clinical manifestations of hemorrhage occult blood, tarry stools, coffee ground emesis, hematemesis, shock symptoms(pallor,diaphoresis,hypotension,weak thready pulse,palpitations)
treatment for hemorrhage replace lost fluids, hourly urine output, monitor central venous pressure(CVP line), iced saline lavage or tap water(constricts blood vessels)
perforation most serious erosion of the ulcer through muscular walls providing an opening from GI tract into peritoneal cavity-peritonitis
clinical manifestations of perforation pain(sudden,severe,upper abd,shoulder pain), rigid abdomen, absent bowel sounds, rapid shallow respirations, leukocytosis, x-ray air under diaphragm
treatment for perforation gastric decompression, fluids, antibiotics, surgery
complication:pyloric obstruction results from edema, inflammation and pylorospasm or by scar tissue from a healed ulcer, causes complete or partial obstruction
clinical manifestations of pyloric obstruction long history of ulcer pain, projectile vomiting, wt loss, constipation, swelling in upper abdomen, borborygmus(rumbling in bowels)
borborygmus rumbling in bowels
treatment for pyloric obstruction gastric decompression,fluids,antacids & liquids after 72 hrs if obstruction decreased, surgery if obstruction persists
surgery for PUD rare, subtotal gastrectomy
subtotal gastrectomy removes acid secreting portion of stomach
types of subtotal gastrectomy biliroth I and biliroth II
biliroth I suture to duodenum
biliroth II suture to proximal jejunum
more surgery for PUD vagotomy and pyloroplasty
vagotomy severing the vagus nerve, totally(truncal) or selectively to eliminate the acid secreting stimulus to gastric cells
pyloroplasty enlargement of the pyloric sphincter
post op nusing care nasogastric tube(assess drainage,assess patency,montitor for abdominal distention,never irrigate), assess dressings, bowel sounds, resumption of previous diet(may take up to a yr before resuming 3 meals/day)
goals of drug therapy reduction of secretions, neutralization or buffering of acid, protection of the mucous barrier by decreasing the activity of pepsin and hydrochloric acid
5 major durg classes for PUD antibiotics, alkaline antacids,H-2 receptor antagonists(hydrogen ions-very acidic), proton pump inhibitors, cytoprotective, misc drugs
antibiotics combination therapy with several antibiotics to destroy H.pylori(gram negative bacterium), the primary cause of PUD
examples of antibiotics used amoxicillin, clarithromycin(biaxin), metronidazole(flagyl)
antacids previously considered "mainstay" therapy, better results with H2 receptors
examples of antacids aluminum antacids(amphogel),magnesium antacids(milk of magnesia),calcium carbonate(TUMS),sodium carbonate(alka seltzer),aluminum magnesium combinations(maalox)
action of antacids neutralizes acidity, inhibits proteolytic action of pepsin, increase pH to >5
side effects of antacids diarrhea(magnesium preparations),constipation(aluminum preparations)
nursing implications for antacids monitor stools, low sodium preparations, after meals & hs, may interfere w/absorption of other drugs
nursing actions for antacids take 1-3 hrs after meals & hs, rationale:neutralizing effects of antacids taken on an empty stomach last 20-30 mins(quickly evacuated). taken after meals, its effects last as long as 3-4 hrs
histamine H2 receptor antagonists action blocks histamine on H2 receptors
examples of histamine H2 receptor antagonists cimetidine(tagament), ranitidine(zantac), famotidine(pepcid)
side effects of histamine H2 receptor antagonists dizziness,h/a, diarrhea, constipation, somnolence, confusion, disorientation, hallucinations, gynecomastia
nursing implications for histamine H2 receptor antagonists watch drug interactions, take w/food, >60 yrs old reduce dose of tagament
proton pump inhibitors(PPI) action blocks the enzyme responsible for secreting of hydrochloric acid from parietal cells
PPI examples esomeprazole, lansoprazole, omeprazole, pantaprazole,rabeprazole
side effects of PPI's diarrhea, h/a, muscle pain, fatigue. if rash develops,stop tx.
esomeprazole nexium
lansoprazole prevacid
omeprazole prilosec
pantoprazole protonix
PPI's are more effective than H2R blockers in reducing gastric acid and promoting healing
cytoprotective drug actions decreases acid secretion & increases production of protective mucus
examples of cytoprotective drug actions sucralfate(carafate)
side effects of cytoprotective drugs constipation
nrusing implications for cytoprotective drugs give 1 hr ac & hs
pepto bismol(bismuth subsalicylate) antidiarrheal drug, decreases synthesis of intestinal prostaglandins, contains salicylate so contraindicated in children & those w/hypersensitivity reactions to ASA
anticholinergic action blocks action of acetylcholine on smooth muscles(thus decrease gastric motility and inhibits gastric secretions)
examples of anticholinergics dicyclomine hydrochloride(bentyl), propantheline bromide(probanthine)
side effects of anticholinergics blurred vision, tachycardia, constipation, urinary retention,(can't see pee, can't spit, can't shit)
nursing implications for anticholinergics monitor output and pulse, impaired sweating
reglan action increases gastric contractions & peristalsis but relaxes pyloric sphincter thus accelerating gastric emptying
side effects of reglan drowsiness, fatigue, restlessness
nursing implications for reglan safety precautions, caution in diabetes & pregnant & nrusing mothers
Nursing diagnosis: pain take meds at prescribed times, have antacids available, avoid ulcerogenic drugs(asa & nsaids), eat at regular intervals, avoid snacking, avoid alcohol, caffeine, and cigarette smoking
nursing diagnosis: anxiety avoid stressful situations, psychological counseling, recognize stress, develop coping mechanisms, relaxation techniques
nursing diagnosis: altered tissue perfusion vital signs, nasogastric tube, IV, I&O, blood transfusion
nursing diagnosis: altered nutrition, less than drugs have replaced the role of diet in tx of PUD, regularity of melatimes & individualization of diet impt, avoid food & drugs that cause indigestion(caffeine,coffee,chocolate,pepper,alcohol), empasis on high quality protein, ascorbic acid & iron
diet following gastrectomy loss of reservoir for food, absence of pepsin & hydrochloric acid, proteins digested by enzymes of small intestines,m may be increased intestinal motility, iron less readily absorbed
dumping syndrome rapid entry of ingested food into jejunum
s/s of dumping syndrome vertigo, tachycardia, sweating r/t rapid fluid shift, syncope
dietary interventions for pt with dumping syndrome meals divided into 5 or 6 feedings, emphasis on foods high in protein, moderate in fat, carbs are kept low, limit fluids taken with meals
medications for dumping syndrome antacids
magnesium hydroxide milk of magnesia; s/e: diarrhea
aluminum hydroxide amphogel; contains significant amt of sodium;therefore use with caution in pateints with CHF, kidney dx or HTN
Created by: jbittner
Popular Nursing sets

 

 



Voices

Use these flashcards to help memorize information. Look at the large card and try to recall what is on the other side. Then click the card to flip it. If you knew the answer, click the green Know box. Otherwise, click the red Don't know box.

When you've placed seven or more cards in the Don't know box, click "retry" to try those cards again.

If you've accidentally put the card in the wrong box, just click on the card to take it out of the box.

You can also use your keyboard to move the cards as follows:

If you are logged in to your account, this website will remember which cards you know and don't know so that they are in the same box the next time you log in.

When you need a break, try one of the other activities listed below the flashcards like Matching, Snowman, or Hungry Bug. Although it may feel like you're playing a game, your brain is still making more connections with the information to help you out.

To see how well you know the information, try the Quiz or Test activity.

Pass complete!
"Know" box contains:
Time elapsed:
Retries:
restart all cards