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Exam 5 Nursing 3

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An excess amount of gastric or duodenal contents into the esophagus
May occur due to an
incompetent lower esophageal sphincter
Pyloric stenosis ( narrowing)
Hiatel hernia
Motility disorder
Barrett’s esophagus (altered lining of the esophageal mucosa)

Gastroesophageal Reflux Disease (GERD)

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Pyrosis (burning sensation in the esophagus)
Dyspepsia (indigestion)
Regurgitation
Dysphagia or Odynophagia (pain on swallowing)
Hypersalivation
Esophagitis

Clinical Manifestations of GERD

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Endoscopy
Barium Swallow
12-36 hour esophageal ph monitoring to evaluate the extent of acid reflux (with the use of wireless capsule ph monitoring the procedure is easier to perform and is accurate).

ASSESSMENT AND DIAGNOSIS OF GERD

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Patient education about avoiding situations that decrease lower esophageal sphincter pressure or cause esophageal irritation’
Low fat diet
Avoid caffeinated products, tobacco, beer, milk, foods containing peppermint/spearmint, and carbonated beverages

Do not eat or drink 2 hours before bedtime
Maintain a normal body weight
Avoid wearing tight-fitting clothing
Elevate the head of bed 6 to 8 inches on blocks
Elevate head and chest area on pillows

Management of GERD

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Antacids

Histamine-2 (H2) receptor antagonists
famotidine and rantidine

Proton pump inhibitors
lansoprazole and omeprazole

Prokinetic agents
bethanechol and metoclopramide
Erythromycin (low doses)

Pharmacological Management GERD

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Pharmacological Management

SURGICAL PRODECURES GERD

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Pathophysiology
PUD occurs primarily in the gastroduodenal mucosa
Erosion is caused by increased concentration or activity of acid-pepsin or by decreased resistance of the mucosa
Damaged mucosa is unable to secrete enough mucus to protect from HCL

PEPTIC ULCER DISEASE

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Dietary factors
Smoking
Alcohol use
Familial tendency
Use of NSAID’s ( interferes with the secretion of mucus that provides protection for the mucosa)
H.pylori: a spiral-shaped gram-negative bacterium that colonizes the gastric mucosa

Risk Factors deep peptic ulcer

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Some individuals have no symptoms, perforation or hemorrhage may occur in 20 to 30 % of these individuals
Dull, gnawing pain or a burning sensation in the midepigastrium or the back
most commonly occurs 2-3 hours after a meal
Individuals express relief of pain after eating or taking an antacid
Vomiting
Hematemesis (vomiting blood)

Clinical Manifestations PUD

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Histamine-2 (H2) receptor antagonists
famotidine and rantidine
Proton pump inhibitors
lansoprazole and omeprazole
H. pylori therapy (first line/second line)
Retreatment for H. pylori therapy failure
Prophylactic therapy for NSAID ulcers

Pharmacological Management PUD

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Dietary Modification
Avoid extremes of temperature in foods and beverages
Avoid alcohol, coffee and other caffeinated beverages
Eating three regular meals a day
Smoking cessation:
smoking decreases the secretion of bicarbonate from the pancreas into the duodenum, which results in increased acidity in the duodenum.
Smoking inhibits ulcer repair.
Reoccurrence of PUD within 1 year may be prevented with prophylactic H2 blockers at a lower dose

Lifestyle Changes with PUD

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Vagotomy, with or without pyloroplasty (transecting nerves that stimulate acid secretion and opening the pylorus)

Antrectomy ( removal of the pyloric portion of the stomach with anastomosis (surgical connection) to either the duodenum (Billroth I) or jejunum (Billroth II)

Surgical Management PUD

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Pathophysiology
Chronic, functional bowel disorder that affects the frequency and consistency
Cause unknown
Either constipation, diarrhea or alternating

Irritable Bowel Syndrome (IBS)

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Symptoms can vary in frequency and severity
Alteration in bowel patterns: constipation/diarrhea/ combination
Pain (begins after eating)
Bloating
Abdominal distention

Clinical Manifestations IBS

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Criteria for diagnosis to include
Recurrent abdominal pain or discomfort at least 3 days a month for the past 3 months with 2 or more of the following

Improvement with defecation
Onset associated with change in frequency of stool
Onset associated with change in appearance of stool

Testing to confirm the absence of structural or other disorders

Stool studies

Contrast x-ray studies

Proctoscopy

Assessment/ Diagnostic IBS

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To relieve abdominal pain

Control the diarrhea or constipation
Reduce stress

Food restriction with reintroduction of foods that are the irritants

High fiber diet

Exercise

Stress reduction or behavioral modification programs

Smoking cessation

No alcohol use

Medical Management IBS

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Hydrophilic colloids (ex: bulk)
Antidiarrheal agents
loperamide
Antidepressants (anxiety, depression, serotonin levels)
Anticholinergic or antispasmodic agents (ex: propantheline: Pro Banthine) decrease smooth muscle spasms.

Pharmacological Management IBS

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Pathophysiology
Appendix is inflamed and edematous due to becoming kinked or occluded by a fecalith (hardened mass of stool), tumor, lymphoid hyperplasia or foreign body

Appendicitis

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Vague epigastric or periumbillical pain (dull) that will progress to the right lower quadrant (sharp, well localized)
Febrile
Nausea/Vomiting
Decreased appetite
Local tenderness at Mc Burney’s point
Rebound tenderness
Ruptured appendix: diffuse pain, abdominal distention

Clinical Manifestations APPENDICITIS

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2/3RDS OF THE WAY FROM IMBILICUS ASIS

Mc BURNEYS POINT

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Physical exam
CBC: elevated WBC and neutrophils
Abdominal x-rays, US and CT: right lower quadrant density or localized distention of the bowel

What to look for

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Surgical removal if appendicitis diagnosed

Laparotomy (abdominal incision)

Laparoscopic

IV fluids and antibiotics are administered until surgery

Medical Management APPENDICITIS

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Inflammation of the gallbladder (acute or chronic)
Clinical Manifestations
Pain
Tenderness
Rigidity of the upper right abdomen that may radiate
Nausea/vomiting

Cholecystitis

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Pathophysiology
Two major types of stones, those composed of predominantly pigment and those composed of cholesterol.
Pigment stones form when unconjugated pigments in the bile precipitate to form stones 10-25 %

Cholelithiasis

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Gallstones can be silent, creating no pain
Mild GI symptoms
Symptoms can be due to gallbladder disease or due to obstruction of the bile passage by the gallstone
Acute or chronic symptoms
Epigastric distress: fullness, distention, vague pain in the RUQ
Distress may be after a meal high in fat or fried foods

Clinical Manifestations CHOLELITHIASIS

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Pain management
Dietary management
Remove the cause of cholecystitis by pharmacological therapy, endoscopic procedures, or surgical intervention
Provide patients with acute gallbladder inflammation with rest, IV fluids, nasogastric suction, analgesia, and antibiotic agents until the symptoms subside

Management CHOLETHIASIS

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Intracorporeal Lithotripsy: Mechanical shock waves to cause the stones to fragment. Repeated treatments can occur to break up stones.
Extracorporeal Shock Wave Lithotripsy: Shock waves are delivered to fragment the stones. The waves are delivered through a fluid filled bag or the patient is immersed in a water bath.

Nonsurgical Removal of Gallstones

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Cholecystectomy: the gallbladder is removed through an abdominal incision.
Laparoscopic Cholecystectomy: small incision or puncture made through the abdominal wall at the umbilicus.
CO2 is introduced into the abdominal cavity to help with visualizing the abdominal structures.
A camera attached to the laparoscope allows the surgeon to visualize the abdominal cavity on the monitor.

Surgical Management GALLSTONES

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