Module 2.3 Upper Gastrointestinal Disorders NS2P2

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  1. **Oral Cancer
    • Estimated 42K cases and 8200 deaths in 2014
    • Overall 5 year survival rate 62%
    • More common in males (average age 65 years)
    • Majority seen in lower lip, favorable prognosis because more noticeable so people will seek treatment earlier

    • => Risk factors
    • Tobacco (smoking and chewing)
    • HPV- rising fast in younger people
    • Excessive alcohol intake
    • Occupational sun exposure
    • Diet low in fruit and vegetables: low antioxidants
    • Chronic irritation-poor dentition
    • -bad tooth rubbing cheeks. pipe smokers...

    • =>Clinical Manifestations
    • Indurated(swollen hard), painless ulcer
    • Sore that bleeds easily and does not heal
    • Rough area felt by tongue
    • Leukoplakia-Lesion type
    • Erythroplakia-Lesion type
    • Early Nonspecific symptoms such as sore throat, voice changes, asymptomatic with neck mass = red flag for cancer!
    • Advanced signs of oral cancer: Pain, dysphagia, difficulty moving jaw
  2. **Leukoplakia vs. Erythroplakia:
    Leukoplakia: white rough patch on tongue, often mistaken for thrush. H&P diagnosis. Biopsy. Then CT/MRI to stage the cancer & metastasis.

    • Erythroplakia: different type of precancerious lesion
    • Premalignant squamous lesions of the oral cavity are areas of altered epithelium that are at an increased risk for progression to squamous cell carcinoma (SCC) The most common of these lesions is squamous dysplasia, which is the primary focus of this article.

    • Most often, these premalignant conditions manifest clinically as leukoplakia and erythroplakia. Leukoplakia is defined by the World Health Organization as a white lesion of the oral mucosa that cannot be scraped off and cannot be attributed to another definable lesion (see the first image below).[1, 2] Erythroplakia is a red patch on the oral mucosa that cannot be accounted for by any specific disease entity (see the second image below); it exists on a continuum both in appearance and behavior with leukoplakia and mixed erythroleukoplakia (a lesion that is both white and red; see the third image below).
    • -no screening or oral exam that's proven to decrease risk from dying from oral cancer
  3. **Oral Cancer: Collaborative Care
    • => Surgical
    • Most effective treatment esp if localized: Radical neck dissection-Most severe; performed for lymph node involvement; Take out larynx and lymphnode and patient would be on trach for life (prophylactic)
    • -Partial mandibulectomy: take out part of jaw if metastasized to boned
    • -Hemiglossectomy: partial tongue removal-normally a cure but problems talking and swallowing
    • -Glossectomy-problem with coughing and swallowing and eating
    • -Airway management: Prophylactic tracheostomy

    • =>Nonsurgical
    • Chemotherapy
    • Radiation-damages salivary glands and predispose to cavity
    • Combination of both
  4. **Nursing Management for Oral Cancer
    • Airway management
    • Pain relief
    • Providing nutritional support
    • Promoting communication
    • Emotional support: disfigguring, can't talk or communicate needs. You must be nonjudgemental atmosphere.
  5. **Gastroesophageal Reflux Disease (GERD)
    A syndrome; Chronic symptoms or mucosal damage secondary to reflux of gastric contents into the lower esophagus (Sphincter is iincompetent)

    Most common upper GI disorder

    Incidence increases with age

    Primary etiological factor is an incompetent LES

    Decreased esophageal clearance (swallowing) and delayed gastric emptying also predispose patient to GERD

    Hiatal Hernia is a common cause
  6. **GERD: Pathogenesis
    Impaired esophageal motility, Defective mucosal defense, LES dysfunction, Reflux of gastric contents, and delyaed gastric emptying.

    Incompetent lower esophageal sphincter allowing stomach contents into lower esophagus

    An incompetent LES results in decreased pressure in the distal portion of the esophagus.

    Gastric contents are able to move from area of high pressure (stomach) to area of lower pressure (esophagus)
  7. **Factors that Weaken the LES
    • Obesity
    • Pregnancy
    • Alcohol
    • Nicotine
    • Dietary substances: chocolate, mint, caffeine
    • Medications: Anticholinergics, beta blockers, calcium channel blockers, valium, morphine, and theophylline
  8. **GERD Clinical Manifestations
    =>Pyrosis (Heartburn)Burning, tight, intermittent pain behind lower sternum might mimic heart attack; May radiate to throat/jaw. Frequency of Heartburn >2x a week--> diagnosis of gerd

    • =>Dyspepsia (Indigestion): Pain centered in the upper abdomen
    • -episgastric pain relieved by tums, water and milk the rule out heart attack


    =>Regurgitation: Hot bitter or sour liquid in throat

    =>Dysphagia: Difficulty swallowing

    =>Globus sensation: Lump in the throat

    =>Can mimic heart attack: Burning, squeezing, pain that radiates to back, neck, jaw, arms; Relieved with antacids

    =>Respiratory symptoms: Sob when lying down and have to sit up

    Link between gerd and asthma because there might be micro aspiration of gastric content into lungs causing allergic rxn like asthma
  9. **GERD Complications
    • =>Esophagitis
    • Inflammation of esophagus
    • Repeated episodes can cause scar tissue (strictures)
    • Leads to disphagia and difficulty to swallow

    • =>Barrett’s esophagus
    • Esophageal cells change to pre-cancerous
    • 5-15% of people with GERD have Barrett’s esophagus
    • S/S include bleeding and perforation (late)
    • Endoscopic screening is recommended every 2-3 years
    • More common in white males with history of gerd
    • Surgical options remove cancerous cells
    • Recommended to have endoscopic screening every 2 years
    • Gerd can get so bad that stomach contents can be found aorund heart and lungs because the esophagus had been so irritated.
  10. **GERD Diagnosis and Management
    • =>Diagnosis
    • H&P followed by monitoring of therapeutic response to treatment

    Upper GI, endoscopy, motility studies (watching how they swallow), pH monitoring of stomach acid

    -EGB:Esophagogastroduodenoscopy (EGD) allows visualization of the esophagus revealing esophagitis or Barrett’s epithelium (premalignant cells). It is done usingmoderate sedation to observe for tissue damage (in 60% of clients with GERD)and possibly to dilate structures.

    • =>Management
    • Conservative( Lifestyle modifications, Drug therapy)
    • Surgical
  11. **GERD Lifestyle Modifications
    • Avoid triggers: Chocolate, peppermint, tomatoes, alcohol, caffeine
    • Stop smokingWeight reduction
    • Dietary therapy (Small, high protein, low fat meals, Avoid late night meals and nocturnal snacking (laying down right after eating).
    • Six small meals a day.
    • Elevate the head of the bed And don’t lay down for 2 to 3 after eating
  12. **GERD: Pharmacological Management
    • =>Goals
    • Decrease volume and acidity of reflux
    • Improve LES function-or strength
    • Increase esophageal clearance
    • Protect esophageal mucosa


    Step Down (strongest drug firrst-Proton Pump Inhibitors--> H2 Blockers (pepcid/zantac)

    Step Up (most mild drug). H2 first to PPI
  13. **Antacids
    • Neutralize stomach acid-only for mild or intermittent GERD
    • Aluminum, magnesium, or calcium based
    • Available OTC in multiple forms
    • Include Tums, Rolaids, Mylanta Take 1-3 hours after meals and at bedtime--not preventative, after you eat
    • GI side effects: calcium causes constipation, Magnesium diarrhea
    • Drug interactions: with drugs that need acidic environment--Iron.
    • Only for mild or intermittent gerd
    • Not preventative
  14. **H2 Receptor Blockers
    -step up from antacids

    Block action of histamine on the H2 receptors and thus reduce HCl acid secretion

    Decrease conversion of pepsinogen to pepsin and reduce irriation of esophageal mucosa

    Available OTC and Rx

    • =>Reduces symptoms and promotes healing in 50% of patients
    • Cimetidine (Tagamet)- IV or PO
    • Ranitidine (Zantac)- IV or PO
    • Famotidine (Pepcid)- IV or PO
    • Nizatidine (Axid)- PO only
  15. **Proton Pump Inhibitors
    Antacids--H2 blockers --> PPI (highest)

    Decrease gastric HCL acid secretion by inhibiting proton pump-responsible for secretion of hydrogen ions

    • More effective at healing erosions (80-90% of patients) more than H2 blockers
    • -increased fracture risk? changes in acidic environment intereferes with calcium absorption

    • =>Available OTC and RX
    • Omeprazole (Prilosec)- PO
    • Lansoprazole (Prevacid)- IV, PO
    • Pantoprazole (Protonix-) IV, PO
    • Esomeprazole (Nexium)- PO
  16. **Thoughts on PPI therapy
    Ulcer prophylaxis is well-established for selected patients in the ICU setting-stress from hospital, ulcers from stress.

    PPI use has become widespread on general medical/surgical floors

    =>Growing concern forUse in non-critical populations

    Possible links between c. difficle (decrease gastric acidity which prevent bacterial growth) and pneumonia (more bacteria to aspirate)

    • Failure to discontinue therapy
    • Economic considerations: expensive
  17. **Additional Medications 
    Sucralfate (Carafate)
    bismuth Subsalicylate (Pepto)
    Meoclopramide (Reglan)
    • =>Sucralfate (Carafate) PO
    • Cytoprotectant-coats stomach and decrease ulcer formation and decreases pepsin
    • Give 1 hour prior to meals
    • Drug interactions: Give 2hrs before thyroid medication, dilantin(seizures), floroquinolone(levequin)

    • =>Bismuth Subsalicylate(aspirin) (Pepto-Bismol) PO
    • Weak antacid
    • Use with caution: don't use with pregnant woman, dark stools
    • Because it can caue blood thining
    • Can turn stool black

    • =>Metoclopramide (Reglan) IV, PO
    • Prokinetic agent
    • Increases gastric emptying of stomach and treats nausea which moves acid quicker and it doesn’t just sit there to give you antacid
    • Dopamine agonist
    • increase
    • Limited to 12 weeks of therapy-not for long term use-because it interferes with neurotransmitter dopamine agonist
  18. **Surgical Intervention for GERD:
    Reserved for patients with complications or severe resistant symptoms

    Nissen fundoplication

    Stretta procedure
  19. **Nissen Fundoplication:  
    Client Education
    • take fundus around stomach and wrap it around the esophageal sphincter to strengthen it and prevents back up
    • can be done through abdomen or chest
    • done in conjunction with hiatal hernial repairs:can be open or laprascopic

    This surgical option may be indicated for clients who fail to respond to other treatments. The fundus of the stomach is wrapped around and behind the esophagus through a laparoscope to create a physical barrier.

    • =>Client Education
    • ■ Diet
    • Avoid offending foods.
    • Avoid large meals.
    • Remain upright after eating.
    • Avoid eating before bed.

    • ■ Lifestyle
    • Avoid tight-fitting clothing around the middle.
    • Lose weight, if applicable.
    • Elevate the head of the bed 15.2 to 20.3 cm (6 to 8 in) with blocks. The use of pillows is not recommended as this rounds the back bringing thestomach contents up closer to the chest.
    • Sleep on the right side.
  20. **Hiatal Hernia
    aka diapghramatic hernia; caused by stuctureal changes and increased intraabdominal pressure.

    Risk factors: weakned musc, obesity, preg, ascites and heavy lifting

    Herniation of a portion of the stomach into the esophagus through an opening in the diaphragm

    More common in older adults and in women

    Structural changes and increased intraabdominal pressure predispose to hernia development

    Clinical presentation similar to GERDDiagnosed with endoscope
  21. **2 Types of Hiatal Hernia
    • =>Sliding hernia: most common
    • Upper stomach and gastro-esophageal junction are displaced upward and slide in and out of thorax and diaphram
    • 90% cases are sliding hernia

    • =>Rolling hernia:
    • 10%; All or part of stomach pushes through the diaphragm beside the esophagus
  22. **Hiatal Hernia Diagnosis and Management
    =>Diagnosed by XR, endoscopy

    • =>Conservative management
    • Recommendations for GERD
    • Reduction of intraabdominal pressure: normal weight. No heavy lifting

    • =>Surgical therapy
    • Hernia repair Antireflux treatment
  23. **Upper GI bleeding
    • Frequent cause of hospitalization
    • More common in older adults
    • Types of GI bleeding include: Hematemesis, Melena, Occult Significant cause of anemia
    • Numerous potential causes
  24. **Gastritis
    • Inflammation of the gastric mucosa
    • Can be acute or chronic
    • Results as a breakdown of gastric mucosal barrier
    • -stomach linking secrets a lot of mucosa to protect body from the low pH from our stomachs
    • -HCL and pepsin can then diffuse into mucosa, if there is breakdown of mucosal barrier caussing inflammation and irritation
    • -Causes inflammation and edema, capillary destruction, possible hemorrhage

    Nsaids and cortocosteroids cause this!!
  25. **Causes of Gastritis
    Medications-nsaids and corticosteroid: Inhibits prostaglandin synthesis which is a potent inflamatory mediator--making mucosa more susceptible to injury

    Infection w/ H. pylori-casues stomach cancer

    Radiation-causes acute inflamation

    Smoking-causes gatric lining to be inflamed and Increases production of acid

    Alcohol: either binge or chronic

    Cocaine-erosive gastritis

    Pathophysiological conditions-hospital stress, burns , shock , trauma and sepsis
  26. **Gastritis: Manifestations & Diag & Collaborative Care
    • =>Clinical Manifestations
    • May be asymptomatic
    • Nonspecific epigastric discomfort-cramping burning

    Anorexia, N/V, belching, bloating, epigastric tenderness, fullness

    s/s pernicious anemia-b12 deficiency lack of intrinsic factor b/c parietal stomachs being distroyed in stomach. Numness, tingling, paresthesias...glossitis,because parietal cell of stomach are being damaged so not producing intrinsic factor so can’t absorb b12

    • =>Diagnosis
    • H&P
    • H. pylori testing
    • Endoscopy to visulaize the stomach lining

    • **Collaborative Care
    • Eliminate cause(s) Avoid smoking and other irritants
    • Eradication of H. pylori
    • Frequent, bland meals*-not proven to cure anything
    • Drug therapyAntacids, PPIs, H2 blockers
    • Management of complications such as acute hemorrhage
  27. **Helicobacter pylori infection
    Bacterial infection present in half the world’s population; usually acquired in childhood.

    -spread in food water, fecal matter in water in developing country

    -predispose to ulcers and gastritis.

    Infected person usually asymptomatic

    Bacterium colonizes epithelial cells in gastric mucosa; Can contribute to gastritis, ulcers, stomach cancer

    Treatable with antibiotics

    Secrets enzyme that allows it to live in harse environments
  28. **H. pylori: Pharmaceutical Treatment
    • PPI
    • Bismuth (Pepto-Bismol)

    • =>Antibiotics
    • Triple therapy: clarithromycin, PPI, amoxicillin or metronidazole (Flagyl)
    • 10-14 day regimen (higher cure rate with 14 days)

    • =>Quadruple therapy includes Bismuth
    • Kills pylori by self but need antibiotics to kill bacteria-one thing you knock out and then you're done.
  29. **Peptic Ulcer Disease (PUD)
    • Erosion of the gastric mucosa in a localized area
    • Classified as Acute vs. chronic(deeper in mucosa , so more severe) AND Gastric vs. duodenal
    • Occurs in greatest frequency in ages 40-60

    • =>Causes include
    • H. pylori
    • Physiological stress increase suspetibility and healing process
    • NSAIDs and other drugs-are more common for non h pylori ulcers
    • High alcohol intake
    • Smoking
  30. **Pathophysiology: PUD
    Breakdown of gastric mucosal barrier-goes through mucosa, submucoa and muscle..

    Due increased acid or decrease resistance of the barrier itself

    Acid back-diffusion acid goes to lining and cause damage

    Cellular destruction and inflammation

    Increased permeability and further acid/pepsin secretion

    Further mucosal erosion, bleeding from destruction of blood vessels, and ulceration

    long use of NSAIDS involved, used to think physiological stress caused ulcer, but it increases susceptibility to develop ulcers and decreases healing time

    high alcohol intake is risk facttor
  31. **Gastric Ulcers & Manifestations
    • -chronic ulcers causes scaring--decreases ability for it to heal .
    • Worse case: Ulcer fully erodes and causes peritonitis: meaning GI content are now out in the abdominal cavity (VERY DANGEROUS!)

    Commonly found in the lesser curvature of the stomach close to the antral junction

    Less common than duodenal ulcers but higher mortality rate-associated more with malignancy

    More prevalent in women, older adults, lower socioeconomic status

    • =>Risk factors
    • NSAID use
    • H. pylori
    • Smoking/alcohol

    • **Gastric Ulcers Clinical Manifestations
    • Epigastric pain 1-2 hours postprandial(after eating)
    • Burning, gassy pain
    • Occasional N/V, anorexia
    • Food aggravates w/ penetrating ulcer
    • Earliest symptom may be w/out complication
  32. **Duodenal Ulcers
    • 80% of all peptic ulcers
    • Can occur at any age
    • Peak age 35-45
    • Associated with smoking, drugs, alcohol use, chronic conditions
    • Most common cause is H. pylori not nsaids; Found in 90-95% of cases

    • =>Clinical Manifestations
    • Burning, crampy pain
    • Mid-epigastric and back
    • 2-4 hours after eating
    • Can occur at night, early morning
    • Pain relief w/ antacids and food
    • Occasional N/V
  33. **Zollinger-Ellison Syndrome
    • =>Rare condition characterized by:Severe peptic ulcers
    • Gastric acid hypersecretion
    • Elevated serum gastrin (hormone in blood that increases secretion of gastric acid)
    • Associated with gastrinoma (gastric tumors) of the pancreas or duodenum-many little tiny ulcers, all over stomach--pin point mucosal erosions
    • not result of increased acid secretios BUT result of decreased resistance of mucosal barrier!PPI used
  34. **Complications: PUD
    • =>Hemorrhage
    • Most common complication
    • More common w/ duodenal ulcers

    • =>Perforation-most sever complication can lead to peritonitis (GI contents in abdom cavity)
    • Most lethal complication
    • Sudden, severe pain and s/s peritonitis
    • Hypovolemia and bacterial peritonitis

    • =>Gastric Outlet Obstruction
    • Increasing discomfort and projectile vomiting
    • Less common w/ better PUD management
  35. **PUD Diagnosis

    • =>H. pylori testing
    • Biopsy
    • Stool testing
    • Breath testing-swallow substance has urea and then converted to co2 which is exhaled and measure amount of c02 (C 13 Urea breath testing is when the client exhales into a collection container (baseline), drinks carbon-enriched urea solution, and is asked to exhale into a collection container. The client should take nothing by mouth(NPO) prior to the test. If H. pylori is present, the solution will break downand carbon dioxide will be released. The two collections are compared toconfirm the presence of H. pylori)


    • =>Secondary diagnostics
    • Gastrin levels in blood
    • CBCStool guaic for blood
  36. **PUD: Conservative Therapy
    • Adequate rest
    • Smoking cessation
    • Dietary modifications

    • =>Discontinuation/reduction of NSAIDs
    • Can switch to cox 2 inhibitor like celebrex if have arthritis
    • Cytotec-protects gastric mucosa, doesn't interfere with nsaids

    • =>Drug therapy
    • Antisecretory- PPIs, H2 blockers
    • Neutralizing- antacids
    • Cytoprotective- Carafate, Pepto-Bismal
    • Antibiotics for H. Pylori

    -complete ulcer healing takes 3-9w eeks. Recurrence is comment, so keep up with therapy. THe H2 blockers and PPI can be stoped after ulcer heals
  37. **Peptic Ulcer Disease: Surgical Treatment

    • =>Vagotomy
    • Severing of the vagus nerve, Decreases gastric acid by diminishing parietal cell stimulation to prevent ulcer formation

    • =>Pyloroplasty
    • Surgical enlargement of the pylorus (part that connects to duodenum) to allow for easy passage of contents from the stomach to intestine Done together with vagotomy to increase gastric

    Gastrectomy (partial) sever cases-

    • =>Billroth I (gastroduodenostomy)
    • -Partial gastrectomy, with the remaining segment anastomosed to the jejunum
    • Removal of lower 2/3 of stomach
    • Anastomosis(connect straight) to duodenum

    • =>Billroth II (gastrojejunostomy)
    • Patial gastretomy with the remaining segment anastomosed to the jejunum
    • Removal of lower 2/3 of stomach
    • Anastomosis (connect) to jejunum

    • =>Total Gastrectomy
    • Removal of total stomach
    • Esophagus anastomosed to jejunum
  38. **Peptic Ulcer Disease: Surgical Treatment- Complications
    Dumping syndrome

    Postprandial hypoglycemia


    Malabsorption: especially if you bypass duodenumWeight loss
  39. **Dumping Syndrome
    =>Dumping syndrome is a complication of gastric surgery that consists of vasomotor symptoms occurring in response to food ingestion. Symptoms result from the rapid emptying of gastric contents into the small intestine. In response to the sudden influx of a hypertonic fluid, the small intestine pulls fluid from the extracellular space to convert the hypertonic fluid to an isotonic fluid. This fluid shift causes a decrease in circulating volume, resulting in vasomotor symptoms (syncope, pallor, palpitations, dizziness, headache). Gastric surgery, especially gastrojejunostomy (Billroth II), poses the greatest risk for dumping syndrome. Following gastric surgery, the reduced stomach has less ability to control the amount and rate of chyme that enters the small intestine after a meal.

    Direct result of surgical removal of a large portion of stomach and pyloric sphincter

    Gastric “chyme” is no longer regulated and literally dumps in small intestine; doesn't come out in little controlled small amounts like it normally does

    Hypertonic food brings water into bowel lumen-causes symptoms of hypovolemic shock -->Results in decreased intravascular volume, rapid intestinal transit (diarrhea)-dizziness and diaphoriesis and increased peristalsis

    Patient experiences palpitations, dizziness, weakness, sweating-because decrease of plasma volume, complain of abdominal cramps and hyperactivity inintestines

    Symptoms occur at the end of meal or within 15 to 30 minutes after eating

    Lasts no longer than 1 hour after meal

    Symptoms self-limited (1-3 wks postop)

    More frequent after Billroth II-because bipass duodnem
  40. **Dumping Syndrome: Treatment & Education
    Six small meals a day – dry foods (goal: slow rapid amount of food into intestines)

    Diet low in carbohydrates- moderate fat and protein, and restricted in refined sugars

    Fluids between meals (30-45 min. before or after)-because don’t want to full stomach because to much will dump to much into intestines

    Rest periods in recumbent position at least 30min after meals (HOB up); only for 1 to 3 weeks forbody adjust

    • => Client Education
    • ■■Instruct the client that lying down after a meal will slow the movement of food within the intestines.
    • ■■ Limit the amount of fluid ingested at one time.
    • ■■ Eliminate liquids with meals for 1 hr prior to and following a meal.
    • ■■ Consume a high-protein, high-fat, low-fiber, and a low to moderate carbohydrate diet.
    • ■■ Avoid milk, sweets, or sugars (fruit juice, sweetened fruit, milk shakes, honey, syrup, jelly).
    • ■■ Small, frequent meals rather than large meals.
  41. **Postprandial Hypoglycemia
    Considered a variant of dumping syndrome-if high carb content

    Uncontrolled gastric emptying of fluid high in carbohydrates into small intestine

    Bolus of carbs stimulate HYPERglycemia; stimulate pancrease to release Insulin in large amounts

    Excessive insulin results in rebound HYPOglycemia 2 to 3 hours after meals

    Symptoms occur about 2-3 hours after eating

    Sweating, weakness, mental confusion, palpitation, tachycardia, and anxiety

    Treatment:Immediate ingestion of sugary fluids or candy

    Frequent meals low in refined sugar
  42. **Stomach Cancer & Manifestations
    Adenocarcinoma of stomach wall

    Incidence declining in the US but second most common cancer worldwide

    More prevalent in men of low socioeconomic class in urban areas: Majority of cases are people over 65 years old

    At time of diagnosis, 50% have metastasis

    Overall 5 year survival rate is 28%

    • => Risk Factors
    • H. pylori infection
    • Smoking
    • High intake of smoked/pickled foods
    • Previous history of stomach surgery
    • Family history of stomach CA
    • Type A blood
    • Certain infections/occupational exposure

    • =>Clinical Manifestations
    • Anemia Pernicius anemia
    • Indigestion
    • Unexplained weight loss (late)
    • Anorexia
    • Occult blood (from ulcer)
    • Palpable epigastric mass very late sign
    • Enlarged lymph nodes very late sign
    • Ascites
  43. **Stomach Cancer Diagnosis and Treatment
    • =>Diagnosis
    • Endoscopy w/ biopsy
    • Imaging studies to stage

    • =>Treatment
    • Total or partial gastrectomy same as previous (biliroth)
    • Chemotherapy and radiation; dependent on staging
  44. Stomach Cancer Postoperative Nursing Management  & ND's
    • Pain relief
    • Incision care
    • Emotional support
    • =>Post gastrectomy diet
    • NGT to suction initially, then clear liquids and advance as tolerated
    • Supplementation as needed: Vitamin b injectction, And vitamin b12 and vitamin d and calcium supplements
    • =>Patient Education

    • **Nursing Diagnoses
    • Imbalanced Nutrition
    • Less Than Body Requirements related to nausea, vomiting and no appetite
    • Acute pain related to the growth of cancer cells
    • Acute pain related to interruption of the body secondary to invasive procedures or surgical intervention
    • Risk for infection related to an increased susceptibility secondary to the procedure.
Card Set:
Module 2.3 Upper Gastrointestinal Disorders NS2P2
2015-05-09 06:15:33
Upper Gastrointestinal Problems Cancer oral cavity Gastroesophageal Reflux Disease GERD Hiatal Hernia GI bleeding Gastritis Peptic ulcer disease stomach NS2 NSP2 Michelle Ulcer
**Upper Gastrointestinal Problems Cancer of the oral cavity Gastroesophageal Reflux Disease (GERD) Hiatal Hernia Upper GI bleeding: Gastritis,Peptic ulcer disease Cancer of the stomach
**Upper Gastrointestinal Problems Cancer of the oral cavity Gastroesophageal Reflux Disease (GERD) Hiatal Hernia Upper GI bleeding: Gastritis, Peptic ulcer disease Cancer of the stomach
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