Upper Gi disorders 6
|PUD: Etiology|| NSAIDS use|
Bacterial infection with H. Pylori
Other causes: theophylline (Theo-Dur), caffeine, corticosteriod use, risk factors for gastritis same for PUD
|PUD: History: Assessment|| Ask pt about factors that promotes development of PUD:|
Certain irritating foods: spicy, acid content
Ask about meds
Ask about GI surgeries
Ask about pain in relation to eating and sleeping
|PUD: Clinical Manifestations|| Epigastric tenderness usually located at the midline between the umbilicus and the xiphoid process|
Dyspepsia: typically described as sharp, burning, or gnawing pain
Sensation of abdominal pressure or of fullness or hunger
|PUD Diagnostic Assessment|| Hemoglobin & Hematocrit (H & H)|
Stool specimen for occult blood
Blood test to detect H. pyloric (see Gastritis)
EGD (see GERD)
|PUD: Nursing Diagnoses|| Acute Pain related to physical (gastric and/or duodenal mucosal) injury.|
Chronic Pain related to physical (gastric and/or duodenal mucosal) injury.
Risk for GI bleeding
| PUD Four primary goals for drug therapy:|
Provide pain relief
| Eradicate Helicobacter pylori infection|
|PUD Drug Therapy|| Antacids|
H₂ Receptor Antagonists
Proton Pump Inhibitors
Mucosal Barrier Fortifiers
|Helicobacter pylori: Treatment|| Proton Pump Inhibitor plus 2 antibiotics|
lansoprazole (Prevacid) plus metronidazole (Flagyl)and tetracycline or clarithromycin (Biaxin) and amoxicillin for 7-14 days.
|Prostaglandin Analogues: Misoprostol (Cytotec)||Reduce gastric acid secretion and enhance gastric mucosal resistance to tissue injury when pt is taking NSAIDS|
|Prostaglandin Analogues: Misoprostol (Cytotec) Nursing Implications:|| Take with food--Protects against NSAID-induced ulcers. Avoid magnesium-containing antacids---Both Cytotec and magnesium-containing antacids can cause diarrhea.|
Uterine contraction is a significant adverse effect of misoprostol.
|PUD Nutrition Therapy|| Nutrition therapy may be directed toward neutralizing acid and reducing hypermotility. |
A bland, nonirritating diet is recommended during the acute symptomatic phase.
Avoid bedtime snacks.
Avoid alcohol and tobacco.
Avoid coffee, tea, cola
|Potential for GI Bleeding|| Interventions include:|
Monitoring and early recognition of complications (critical to the successful management of PUD)
Preventing and/or managing bleeding, perforation, and gastric outlet obstruction
Possible surgical treatment
|Upper GI Bleeding: Hypovolemia Management|| Monitor vital signs & O₂ Sat|
Observe for fluid loss from bleeding and vomiting.
Monitor serum electrolytes.
Monitor Hemoglobin & Hematocrit
Insert two large-bore peripheral IV catheters to replace both fluids and blood lost.
|Hypovolemia Management (Cont'd)|| Volume replacement should be started immediately.|
Blood products may be ordered to expand volume and correct abnormalities in the CBC.
Orthostatic hypotension is common in patients with decreased fluid volume.
|UGI Bleeding: Bleeding Reduction|| Monitor for s/s of bleeding. Hematest all secretions.|
Insert NGT to suction.
Perform gastric lavage, as appropriate
|UGI Bleeding: Bleeding Reduction cont.|| Endoscopic therapy can assist in achieving hemostasis.|
Acid-suppressive agents are used to stabilize the clot by raising the pH level of gastric contents.
|Nonsurgical Management of Other Complications of PUD|| Perforation is managed by immediately replacing fluid, blood, and electrolytes:|
Keeping the patient NPO
NGT to suction
Monitor I & O; Check VS
|Nonsurgical Management of Other Complications of PUD cont.|| Pyloric obstruction treatment is directed at restoring fluid and electrolyte balance and decompressing the dilated stomach. |
NGT to suction; Clamp after 72 hrs.
Treat metabolic alkalosis and dehydration
|Surgical Management of PUD Two surgical approaches are available:|| Minimally invasive surgery (MIS) via laparoscopy to remove a chronic gastric ulcer or treat hemorrhage from perforation|
Vagotomy (vagus nerve cutting) to control acid secretion
Pyloroplasty (open the pylorus) facilitates emptying of stomach contents.
|Gastric Cancer: Etiology|| Strong link between H. pylori and gastric cancer |
Pernicious anemia, gastric polyps, chronic atrophic gastritis, achlorhydria, Barrett's esophagus, gastric surgery—increases chances
|Gastric Cancer: Etiology cont|| Positive correlation between ingestion of pickled foods, salted meat, processed foods, high consumption of salt|
5 yr survival rate is low
|Gastric Cancer: Health Promotion|| Teach pts with gastritis and/or H. pyloric to follow treatment regimen to ensure that gastritis heal and H. pyloric infection is eliminated.|
Teach about eating well-balanced diet and limit pickled foods, salted food, and processed foods.
Teach about avoiding alcohol and tobacco.
|Gastric Cancer: Clinical Manifestations|| Early gastric cancer may be asymptomatic, but indigestion and abdominal discomfort are the most common symptoms.|
Advanced stage: N/V, obstructive symptoms, iron deficiency anemia, palpable epigastric mass, enlarged lymph nodes, weakness and fatigue, progressive weight loss
|Gastric Cancer: Other Pertinent Findings|| Low Hemoglobin & Hematocrit|
Stool positive for occult blood
Carcinoembryonic antigen (CEA) elevated
EGD for definitive diagnosis
Endoscopic Ultrasound to evaluate depth of tumor & lymph node involvement to determine staging of disease.
|Gastric cancer Nonsurgical Management|| Drug therapy:|
The use of this treatment is limited because the disease is often widely disseminated upon diagnosis.