Benign Peptic Stricture or Gastro-Esophageal Reflux Disease (GERD )
Week 2-1 - GERD, Hiatus Hernia, Peptic Ulcer
Transcript of Week 2-1 - GERD, Hiatus Hernia, Peptic Ulcer
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GERD HIATUS HERNIA
PEPTIC ULCER DISEASE
MAY 2011
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Upper GI Stucture
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GERD
• Presence of gastric secretions into the lower esophagus
• Affects 7% of adults; common in children
• Not a disease but a syndrome
• Frequency and severity of S/S determines the outcome
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Etiology and Pathophysio• No single cause, several contributing factors
• Lower esophageal sphincter (LES) damaged /weakened allows gastric content to enter into esophagus esophagitis
• Pepsin and bile salts corrode esophageal lining
• Severity depends on weakness of LES, and amount and duration of acid refluxed into the esophagus
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GERD Risk Factors• Predisposing conditions: incompetent LES,
impaired esoph motility, hiatal hernia, defective mucosal defense, decreased gastric emptying
• Diet: Citrus, pineapple, tomato, coffee and tea, caffeinated drinks, hot/cold foods, spices
• Smoking, alcohol
• Age
Exacerbating foods:
• Acid producing foods, fatty foods (increase the time food remains in the stomach), chocolate, mint, coffee, alcohol
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Clinical Manifestation• Pyrosis (heartburn): Burning tight sensation
that spreads to jaw and throat.Mild S/S for 5+ years, linked w/ difficulty swallowing, or more severe/often (>once/week)
• Sudden awaken at night with dyspnea
• Respiratory problems: wheezing, coughing
• Autolaryngologic S/S: hoarseness, sore throat, choking, ‘lump’ in the throat, regurgitation
• Early satiety, PC bloating, N&V
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Clinical manifestations in PEDS• Spitting up (in infants)• Projectile vomiting• Weight loss, failure to thrive• Gagging or choking at the end of feeding• Respiratory problems• Hematemesis: vomiting of blood• Melena: black, tarry stool• Anemia• Heartburn/irritability• Apnea
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GERD Complications• Esophagitis, esophageal ulcerations• Esophageal stricture• Dysphagia• Barrett’s Syndrome: serious change in the
cells lining the esophagusMay lead to esophageal cancer
• Respiratory: bronchospasm, laryngeospasm, aspiration pneumonia
• Dental erosions• Anemia
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Diagnostic Tests• Upper GI endoscopy**• Biopsy• Barium Swallow• Manometry Studies• Radionucleid tests• Spinctigraphy(detects radioactive substance
in the esophagus after feeding of a compound, it also assesses gastric emptying
• Medical History
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Treatment
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Collaborative Care AdultGOALS: to reduce reflux damage to esophageal
lining and lifestyle changes in the adult.
Elevate head of the bed with block 4-6” high.• PPI• H2 receptor blockers• Cholinergic drugsOther meds such as Reglan tighten the LESuseful at night when reflux often occurs.Avoid lying down immediately after eating. Avoid late
evening snacks. • Avoid tight clothing and bending over after eating.
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Therapeutic Mgmt – Peds
• Depends on the severity
• None if infant is thriving
• Diet changes
• High Fowler’s when eating
• Small frequent meals with frequent burping for infants
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Sx Intervention: Nissen Fundoplication
• Fundus of stomach wrapped and sutured around distal portion of the esophagus
• Restores normal pressure to LES and prevents acid from refluxing into the esophagus.
• The patient is usually started on clear liquids the first day after surgery and discharged later that day
• The patient is given a general anesthesia. Then the abdomen is inflated with carbon dioxide
• The laparoscope, a thin tube carrying the video camera, is inserted.
• Four pinpoint incisions are then made in the upper abdomen through which needle-like instruments are inserted
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Post OP Nsg Care – Adult • Resp assessment
• Fluid/electrolyte balance
• Chest tubes (if done via open approach)
• Clear fluids
• I/O, N/G tube
• Pain management
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Post OP Nsg Care – Peds• Ongoing assessment of infants • Educating parents re: positioning, feeding &
meds• Appropriate care post op• Coping strategies• Fluid & electrolyte imbalance• Prevention of infection• N/G tube patency
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Nissen Complications• Internal bleeding or infection
• Gas-bloat: Since the LES muscle has been tightened, the patient may be unable to belch, resulting in a feeling of bloating and discomfort.
• A common but usually short-term problem
• Tx: Sit pt up, provide meds for gas allevation, assure pt that bloating is temporary
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Hiatus HerniaHiatus Hernia• Sliding of part of the stomach through the
diaphragm (muscular sheet that separates the lungs and chest from the abdomen)
• Also known as diaphragmatic/esophageal hernia • Often causes no symptoms, but can cause pain
and heartburn. • It is not usually a serious condition, often needs
no treatment.• Most S/S can usually be treated with drugs, or if
severe, a surgical intervention (Nissen).
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Hiatal Hernia
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Etiology and Patho
• Etiology unknown, • Weaken of the muscle in the diaphram and the
espgogastric opening. • Increased intra abdominal pressure • Wearing of Tight corset, • Pregnancy• Obesity• Ascites• Tumors• Lifting of heavy objects continuously
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Other Predisposing Factors
• Trauma• Old age • Poor nutrition• Prolonged illness, (that confines patient to
bed in a constant recombinant position)• Congenital• A rare form of hiatus hernia may be present at
birth due to incorrect development of the diaphragm or stomach
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Types of hiatus hernia
1) Sliding hiatus hernia: the lower esophageal sphincter slides up through the diaphragm•Most common type of hiatus hernia.
2) Paraesophageal or rolling hernia: esophagogastric junction remains in a normal position, but the fundus and greater curvature of the stomach rolls up into the diaphragm and causes a pocket to form beside the esophagus.
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Clinical Manifestations
Usually similar to GERD•Bleeding (from erosions)•Stenosis •Ulcerations•Strangulation: cuts off supply of blood flow tissue necrosis•Non-radiating pain and discomfort behind the breastbone (sternum). If severe, this can feel similar to a heart attack
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Diagnostic Test
• Barium swallow
• Endoscopic visualisation of lower esophagus
• Other tests the same as GERD
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Collaborative ManagmentSimilar to GERD•Lifestyle modification•Decrease intrabdominal pressures•Avoid lifting Heavy Object, straining•Avoid alcohol and smoking•Elevate head of the bed•Same medications as for GERD•Weight Loss
•Small frequent meals rather than fewer large meals•Avoid bending over or lying down after a meal
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DietAvoid (or use in moderation) foods and substances that increase reflux of acid into the esophagus: •nicotine (cigarettes) •caffeine •chocolate •fatty foods •peppermint •alcohol •spearmint
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Meds /Surgical Intervention
Rare, but if a hiatus hernia causes such severe symptoms or complications then surgery is recommended.
• Niessen Fundoplication
• Laporoscopic
• Traditional
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Peptic Ulcer Disease• Erosion on the lining of the stomach or
duodenum from the digestive action of HCL and pepsin.
• Common – 2000 Cdn die each year from PUD
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PUD Etiology• Hypersecretion NOT the primary mechanism by
which most ulceration occurs. • Certain factors disrupt the normal mucosal defense
and repair, making the mucosa more susceptible to the attack of acid.
• Cancerous tumors in the stomach or pancreas• Not caused by stress or eating spicy food, but are
contributing factors.• Usually develop in the presence of an acid env’t or
people with pernicious anemia
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PUD Risk factors• Overproduction of acids, bile salts
• Meds: ASA, NSAIDs
• Alcohol
• Ischemia• **Bacterial infection (H. pylori) – Responsible
for the majority of peptic ulcers• Common in the US, 20% of people <40 and
50% >60 are affected (by orofecal contamination)
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Types
• Peptic ulcers are classified as acute or chronic depending on the degree and or duration of mucosal involvement, and gastric or duodenal and according to the location.
• Gastric and Duodenal Ulcers
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Gastric vs. Duodenal Ulcers
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Gastric Ulcers
• Lesions are superficial with smooth margins round, oval or cone shaped.
• Antrum, body and fundus of the stomach affected.
• Gastric secretions are usually normal of decreased.
• Greater in women fifty to sixty years old
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Gastric Ulcers• Low socioeconomic status• Unskilled labourers• Smokers• Alcoholics• Weak or incompetent pyloric sphincter• Individuals with bile reflux• Head trauma (affects CNS control of cortisol
levels)• Major surgery• H. pyloria
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Clinical Manisfestation
• Burning or gaseous pressure in the left epigastris region abdomen and back.
• Pain 1 to 2 hours after meals
• Nausea/vomiting and weight loss.
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Clinical Manisfestation
• Symptoms of gastric ulcer often do not follow a consistent pattern (eg, eating sometimes exacerbates rather than relieves pain).
• This is especially true for pyloric channel ulcers, (Chronic) which are often associated with symptoms of obstruction (eg, bloating, nausea, vomiting) caused by edema and scarring.
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Complications
• Hemorrhage
• Perforation
• Outlet obstructions
• Intractability
• Secondary duodenal ulcers
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Duodenal Ulcers
• Devlopment is associated with high HCL• Scretions, • patient with COPD, • Age group 35 years to 45.• Greater in Men• Research shows it is increasing in
females, mainly post menopausal, • Associated with psycological stress
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Duodenal Ulcers
• Smoking• Alcohol• Drugs• Chronic Renal Failure• Hyper parthryoidism• Zollinger-Ellison syndrome (is a condition in
which there is increased production of the hormone gastrin. Usually, a small tumor (gastrinoma) in the pancreas or small intestine produces the high levels of gastrin in the blood.
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Gastric ulcers• Smooth, superficial
lesions
• Stomach affected
• Normal-low gastric secretions
• More among women
• Burning, gaseous pain 1-2h PC
Duodenal ulcers• **Penetrating lesions• Increased secretions• **Greater among men• Peak 30-45 years• Burning, cramping,
pressure-like pain 2-4h PC and mid-AM, mid-PM, **mid-HS
• **Relieved by antacids and food
Clinical manifestations
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SEVERE S/S o duedonal Ulcers• Sharp, sudden, persistent stomach pain
• Bloody or black stools
• Bloody vomitus
• Vomit that resembles coffee grounds
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Diagnostic Tests of PUD
• Endoscopy
• Contrast studies
• Tissue specimen, to r/o H-pylori virus
• Urea Breath test – H-pylori detection**
• Stomach Biopsy
• Chest x-rays
• CBC, SMA-14 (to determine coagulation, liver Fx, absorption of nutrients)
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Collaborative Care
• Objective is to decrease the production of gastric acidiy
• Enhance mucual defense mechanisms
• And to decrease harmfull effects of on the mucosa
• Rest, physical and emotional support
• Job modifications
• NSAIDS, and COX 2 inhibitors
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Collaborative Care Con’t
• PPI and H2 receptor blockers
• Antibiotics
• Antacids
• Anticholinergic (decrease vagal stimulation of HCl and to decrease gastric motility
• Cyto-protective drug therapy (Cytotec)
• Nutritional Therapy
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COX-2 inhibitors
Class of drugs which selectively inhibit COX-2, an enzyme involved in the inflammation pathway, while sparing COX-1, thereby reducing gastrointestinal toxicity (Celecoxib)
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Cytotec (misoprostol)
• Prostaglandin analog gastric acid secretion– Enhances mucosal resistance to injury
• Uses: prevention and treatment of NSAID related ulcers– NSAIDs inhibit prostaglandins
• Side effects: Nausea, vomiting, abdominal pain• Contraindication: pregnancy miscarriage
– Used therapeutically to induce labor
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PUD Complications• Hemorrhage: Most common complication of
PUD.
S/S:
• hematemesis (vomiting of fresh blood or "coffee ground" material); passage of bloody or black tarry stools ( melena), weakness, syncope.
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Perforation• Most lethal complication when ulcer
penetrates through the stomach wall, allowing digestive juices and food to leak into the abdominal cavity
S/S:• Sudden severe upper abd pain• Shoulder pain (irritation of phrenic nerve)• Rigid abd muscles• Shallow resp• N/V• Absent bowel sounds• Bacterial peritonitis 6-12hrs
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Peptic Ulcer Sx: Indications• Intractability: failure of ulcer to heal or
recurrence
• Hx or increased risk of hemorrhage during Tx
• Prepyloric/pyloric ulcers
• Multiple ulcer sites
• Drug-induced ulcers, potentially malignant ulcer
• Concurrent conditions: severe burns, trauma, sepsis
• Obstruction
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Peptic Ulcer Sx: Types1) Partial gastrectomy – distal 2/3 of stomach and
anastomosis to:
– Duodenum – gastroduodenostomy (Billroth I)
– Jejunum – gastrojejunstomy (Billroth II)
2) Vagotomy: severing the vagus nerve to stomach
3) Pyloroplasty: surgical enlargement of pyloric sphincter
Commonly done after vagotomy or dev’t of scar tissue
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Gastroduodenostomy / Billroth I Billroth ISx reconstruction procedure that reconnects
the remaining 1/3 of the stomach to the first portion of the small intestine (duodenum) is created.
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Gastroduodenostomy / Billroth I Billroth I
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Bill Roth II
• The surgical resection of the pylorus to the The surgical resection of the pylorus to the stomach, followed by closure of the cut stomach, followed by closure of the cut
ends of the duodenum and ends of the duodenum and gastrojejunostomy..gastrojejunostomy..
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Billroth II anastomosis
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Vagotomy
• A vagotomy is the removal of all or some A vagotomy is the removal of all or some of the branches of the vagus nerve.of the branches of the vagus nerve.
• Vagotomy may be used to treat peptic Vagotomy may be used to treat peptic ulceration; it has gradually superseded ulceration; it has gradually superseded partial gastrectomy as the surgical partial gastrectomy as the surgical treatment of choice for chronic duodenal treatment of choice for chronic duodenal ulceration.ulceration.
• Vagotomy can be performed using closed Vagotomy can be performed using closed approach (laparoscopic)approach (laparoscopic)
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Vagotomy
• Performed under general anesthesia. The surgeon makes an incision in the abdomen and locates the vagus nerve.
• Either the trunk or the branches leading to the stomach are cut. The abdominal muscles are sewn back together, and the skin is closed with sutures.
• Often, other gastrointestinal surgery is performed (e.g., part of the stomach may be removed) at the same time.
• Vagotomy causes a decrease in peristalsis, and a change in the emptying patterns of the stomach. To ease this, a pyloroplasty is often performed to widen the outlet from the stomach to the small intestine
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Post-OP• Patients who have a traditional vagotomy
stay in the hospital for about seven days.• NG suctioning is required for the first three
or four days. • Approximately 6 weeks to fully recover • Sutures can be removed in 7-10 days**• Early ambulation • Pain medication• Stool softeners• Prophylactic antibiotics may be prescribed
following the operation.
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Vagotomy Complications
• Gastric or esophageal perforation. May occur from an electrocautery injury or by clipping the branch of the nerve .
• Delayed gastric emptying. Most common after truncal and selective vagotomy, particularly if a drainage procedure is not perform.
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Pyloroplasty• The pylorus valve at the lower portion of the
stomach is cut and anastomosed, relaxing and widening the pyloric sphincter into the duodenum
• Surgical enlargement of the pyloric sphincter assist in the flow of the stomach contents.
• Treats patients at high risk for gastric or peptic ulcer disease (PUD).
• Commonly done after vagotomy or to enlarge an opening narrowed as a result of scar tissue
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Pyloroplasty
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Partial Gastrectomy• Removal of part of the stomach.
• After the operation the stomach is smaller but the cardiac sphincter between esophagus and stomach remain intact.
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Gastrectomy: Post-op assessment• NG tube (3-4 days) – suction, patency• Drsg – bleeding, odor, drainage• Gastric aspirate:
– Colour – bright red, gradual darkening over 24h; yellow-green within 36-48h
– Amount– Odor
• Peristalsis, comfort in lower abdomen (to prevent bowel obstruction complications)
• VS q4h• Accurate I&O
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Post-op care• Drsg cleaning
• If NG tube clogged irrigate /c NS (order req’d)
• Breathing – As incision is high in epigastrium may interfere w/ deep breathing and coughing
Splint w/ pillow, encourage breathing exercises
• NPO, TPN – K+ and vitamin supplements added
Then CL diet PO aspirate stomach within 1-2h to assess qty digested, colour, consistency
Tube removed, increase CL 6 small SF meals QD
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Gastrectomy complications• Dumping syndrome: Results fm reduced capacity
of post-gastrectomy bolus of excess hypertonic fluid (chime) enters intestines fluids drawn into lumen plasma volume drops
S/S (onset 15-30 min PC, lasts for 1h): weakness, sweating, palpitations, abd cramps, hyperactive bowel (borborygmi), urge to defecate
• Postprandial hypoglycemia – Bolus w/ high carb levels into intestines excessive rls of insulin
S/S (2h PC): weakness, sweating , tachycardia, anxiety, confusion
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• Bile reflux gastritis – Pylorectomy allows bile access back up GI tract damage to gastric mucosaS/S (continuous, increase PC): upper abd pain, frequent heartburn, N&V, wt loss, hoarseness
• Pernicious anemia (total gastrectomy only)Removal/absence of parietal cells intrinsic factor loss Vit-B12 absorption loss anemiaS/S: Fatigue, dizziness, SOB, pallor, arrhythmia, chest pain, cold extremities
Gastrectomy complications
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Post-op nutrition• Small, frequent meals (6 per day)
• Avoid fluids within 30-45min before/after meals
• Short rest PC
• Start w/ low-carb, mod-protein and -fat dry diet
• Limit refined sweets: sugar, honey, jam, candy
• If exp. postprandial hypoglycemia sweet fluid
• Bile reflux Questran or alum. hydroxide antacids
• Anemia Vit-B12 supplements for rest of life
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Peptic Ulcer: Pt Teaching• Modify diet (to prevent epigastric distress)
• Avoid smoking and alcohol
• Avoid OTC meds unless first approved by MD
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Stress Ulcers• A GI mucosal injury related to illness.
• Ulceration may vary from diffuse superficial injuries to deep hemorrhaging ulcerations.
• The development of stress ulceration is not related to a history of PUD or H-pylori infection. The cause is multifactorial and related to hypoperfusion and loss of host defenses.
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Causes of stress ulcers• Overproduction of gastric acid, bile and
digestive enzymes. • Mucosal blood flow is diminished, and there is
an imbalance of demand for and supply of oxygen.
• Mucosa is compromised by ischemia and attacked (mostly) by acid.
• Injury and the presence of acid decrease the ability to repair itself (hostile environment)
Risk Factors: Sepsis, Liver failure, Hypotension, Renal failure
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Treatment of stress ulcers
• Prevention – focus on reducing the quantity of acid
• Use of H2 receptor antagonists or antacids
• Patients in shock, sepsis, respiratory distress, hepatic or renal failure, or coagulopathy, should all be given stress ulcer prophylaxis meds.
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Question
• Client with GERD is having discomfort further teaching is necessary when client states
1- Use antacids between meals and bedtime
• 2-Quit smoking ,but I chew a lot of gum• 3-Sleep with my bed elevated on blocks• 4-Keep my diet low in fat and eat small
meals throughout the day and at bed time
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Question
• When teaching client with GERD nurse should teach client to avoid foods that increase pressure in the LES
• 1-Acid and pickled foods
• 2- Coffee tea chocolate
• 3- dairy products (bloats GI)
• 4-Spicy and highly seasoned foods
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Question
Client with recurrent heart burn diagnosed with hiatal hernia. Nurse explains to client that this involves•1-Extension of the esophagus through the diaphragm•2-Displacement of the duodenum through the stomach to the esophagus•3-Twisting of the stomach around the esophagus, occluding the esophagus•4-Protrusion of the stomach into the esophagus through an opening the diaphragm