Gastroesophageal

Refluc Disease (GERD)

Syndrome
Secondary to reflux of gastric contents into lower esophagus
Most common UGI problem in adults

Happens when: Causes:
-Defenses of lower esophagus are overwhelmed by -Incompetent LES
reflux of gastric contents into esophagus - Primary factor in GERD
- Results in pressure in distal portion
Predisposing factors: of esophagus
-Hiatal hernia - Gastric contents move from stomach to
-Incompetent lower esophageal sphincter (LES) esophagus
- Antireflux barrier o d/t certain foods (caffeine,
- esophageal clearance chocolate, & drugs-
- gastric emptying anticholinergics)
-Acidic gastric secretions reflux= irritation & -Obesity risk
inflammation -Pregnancy risk
-Pepsin, intestinal enzymes & bile salts= corrosive -Cigarette & cigar smoking risk
(gradually destructing) esophageal mucosa

Complications: DERB
Clinical Manifestations: -Esophagitis- inflammation of esophagus
-Heartburn (pyrosis) - May result in dysphagia
-most common & felt intermittently -Barretts Esophagus- precancerous
-Dyspepsia -Respiratory- cough & bronchospasm
- pain or discomfort centered in - Potential for aspiration pneumonia
upper abdomen -Dental erosion
-Hypersalivation - d/t acid reflux into mouth
-Noncardiac chest pain - esp posterior teeth (duh)
- more common in older adults
-Regurgitation

Upper GI Disorders

 Collaborative Care
Lifestyle modifications:
-Avoid triggers
-Avoid smoking
-Elevate HOB 30 degrees (4-6 blocks)
-Do not lie down for 2-3 hours after eating
Nutritional Therapy:
-High fat foods
-Small frequent meals
-Fluids between meals rather than with meals
-Avoid ETOH
-Avoid milk products at night
-Avoid late-night snacking or meals
-Avoid chocolate, peppermint, caffeine, tomato products, OJ, coffee, tea
- Weight reduction therapy
Drug Therapy:
2 approaches=
- Step up Start with antacids & OTC H2R blockersprogress to prescription H2R finally PPIs
- Step Down Start with PPI titrate down to prescription H2R blockers finally OTC H2R
blockers & antacids







Classification Action Nursing
(drug) Considerations/Implementation
- Neutralizes refluxed material Take 1 hr before or 2 hrs after other oral
Antacids - discomfort meds
Assess for diarrhea/constipation
Aluminum salts Sodium preparations: Not be used in
Calcium salts(TUMS) elderly, pts with HTN, heart failure, liver
Mg salts (MOM) cirrhosis, or renal disease
Mg preperations: Not be used in patients
with renal failure
Histamine H2 Selectively block H2 receptors, Administer oral drug with or before meals
Receptor Antagonists which decreases gastric acid and at HS
ranitidine production (HCL) Decrease dosage with renal or hepatic
cimetidine dysfunction
famotidine IV: continually monitor for cardiac
arrhythmias
Proton Pump Suppresses gastric acid production Administer before meals
Inhibitors and secretion Do not crush, chew or open medication
ianso-prazole Swallow whole
ome-prazole
esome-prazole

Upper GI Disorders

 Surgical Intervention (if others fail): Gerontologic Considerations:
Nissen Fundoplication Incidence with age
- Reduce reflux of gastric contents by Medications commonly taken by older patients can LES
enhancing integrity of LES pressure
- Mostly laparoscopic LES may become less competent with aging
- Fundus of stomach is wrapped around First indications may be esophageal bleeding or
lower portion of esophagus respiratory complications
- Reinforce & repair defective barrier

Gastritis
Inflammation of gastric mucosa
Acute & Chronic

Result of breakdown in gastric mucosal barrier

Stomach tissue unprotected from autodigestion by HCL acid & pepsin
Tissue edema results
Disruption of capillary walls w/ loss of plasma into gastric lumen (possible hemorrhage)

Risk Factors:
DRUGS: direct irritating effect on gastric mucosa DIET: Alcohol & spicy food
- asprin, NSAIDS, & corticosteroids ENVIRONMENTAL: Radiation & smoking
MICROORGANSIMS: helicobacter pylori PATHOPHYSIOLOGIC CONDITIONS:
-important cause of chronic gastritis Burns, renal failure, sepsis
- promotes breakdown of gastric mucosal barrier OTHER: Psychologic stress, NG tube
- Staphylococcus organisms

Acute Gastritis Chronis Gastritis
Self-limiting:
Lasts few hours to a few days Loss of intrinsic factor can occur when acid-secreting
Complete healing of mucous is expected cells are lost or nonfunctioning
Clinical Manifestations: - essential for absorption of cobalamin (B12)
Anorexia - results in pernicious anemia & neuro comps
N/V
Epigastric tenderness
Feeling full Clinical Manifestations: SX similar to acute
Hemorrhage
- common with alcohol abuse
- may be the only symptom
Collaborative Care:
Collaborative Care: Focuses on evaluating & eliminating cause:
If vomiting; NPO - helicobacter pylori : antibiotics
- Fluids (dehydration can occur) - Pernicious anemia: lifelong cobalamin
- Rest supplements*
- Antiemetics
NG tube- if sx are severe Lifestyle Changes:
If hemorrhage is likely - diet, alcohol, smoking
- Frequent V/S & testing vom for blood -
- Close medical follow-up
Drug Therapy:
Focus on reducing irritation of mucosa
Providing symptomatic relief
- Antacids, H2R blockers, PPIs, & combinations
GI Disorders
Upper

 Peptic Ulcer Disease (PUD)
Erosion of GI mucosa resulting from digestive action of HCL acid & pepsin
Gastric VS. Duodenal (location)
Acute VS. Chronic (degree/duration)

Acute VS. Cronic
Acute:
- Superficial erosion
Ulcers can develop in:
- Minimal inflammation
-Lower esophagus
- Short duration resolves quickly when cause is
-Stomach
identified & removed
-Duodenum
Chronic:
-Margin of gastrojejunal anastomosis
- Muscular wall erosion with formation of fibrous
after surgical procedures
tissue
- Long duration- present continuously for many
months or intermittently
- 4 X as common as acute erosions

Etiology & Pathophysiology:
-Develop ONLY in presence of acid environment (dont need excess gastric acid to develop)
-Stomach normally protected from autodigestion by gastric mucosal barrier
-Surface mucosa of stomach is renewed about every 2 days
-Mucosa can continually repair itself except in extreme instances
-Water, electrolytes, & water-soluble substances can pass through barrier
-Mucosal barrier prevents back-diffusion of acid & pepsin from gastric lumen through mucosal layers to
underlying tissue
mucosal barrier can be impaired & back-diffusion can occur
- Destroyers of mucosal barrier= Helicobacter pylori, Asprin & NSAIDS, & Corticosteroids

Gastric Ulcers: Duodenal Ulcers:

normal to low secretion of gastric acid HCL acid secretion


Occur in any portion of the stomach (most Occur at any age and in anyone
common- lesser curvature in close to antral - between ages 35-45
junction) 80% of all peptic ulcers
Prevalent in women & older adults Familial tendency
Peak incidence= 50 y.o. 90-95% pts found with Helicobacter pylori
- not all patients with H. pylori develop ulcers


Causes:

Drugs (Asprin, NSAIDS, Corticosteroids)

Chronic alcohol abuse

Chronic Gastritis

Bile reflux

Nicotine

60-80% present with Helicobacter pylori

H. pylori more destructive when drugs or

smoking are involved

Upper GI Disorders

 CLINICAL MANIFESTATIONS
Common no pain or other symptoms

Gastric Ulcers: Duodenal Ulcers:



High in epigastrium Midepigastric region beneath xiphoid process
Back pain- if located posterior aspect

1-2 hours after meals 2-4 hours after meals

Burning or gaseous Burning , cramping, & pressure

Tendency to occur, then disappear, then occur
again

Pain may be exacerbated by eating Pain relieved by eating

COMPLICATIONS:
ALL EMERGENCY SITUATIONS
Hemorrhage ulcer through a major blood vessel (most common complication of PUD)
Perforation most lethal complication of PU
Gastric outlet obstruction

Perforation:

Clinical Manifestations:

-Sudden dramatic onset

-Severe upper abd pain spreads throughout abd

-Possible shoulder pain

-Rigid, board-like abd muscles

-Shallow, rapid respirations

-Bowel sounds ABSENT

-N/V

- HX reporting symptoms of indigestion or previous ulcer



*Bacterial peritonitis can occur within 6-12 hours

*Difficult to determine from symptoms alone if gastric or duodenal ulcer has perforated

Upper GI Disorders

 PUD Diagnostic Studies:
Endoscopy with Biopsy:
- Most often used- allows for direct viewing of mucosa
- Determines degree of ulcer healing after TX
- During procedure- tissue specimens can be obtained to identify H. pylori & rule out gastric cancer

PUD Collaborative Care:

Medical regimen consists of:
- Adequate rest Aim of TX program:
- Dietary modification -Reduce degree of gastric acidity
- Drug therapy -Enhance mucosal defense mechanisms
- Elimination of smoking & alcohol -Minimize harmful effects of mucosa
- Long-term follow-up care
- Stress MGMT

Generally TXed in ambulatory clinics
- ulcer healing requires many weeks of therapy
- Pain disappears after 3-6 days

Complete healing may take 3-9 WEEKS
- should be assessed by means of x-rays or endoscopic exam
- Asprin & nonselective NSAIDS may be stopped

Drug Therapy:
- H2R blockers
- PPIs
- Antacids
- Cytoprotective therapy
- Antibiotics

Recurrence of peptic ulcer is frequent*
- interruption or discontinuation of therapy can have determined results

No other drugs should be taken (unless prescribed by HCP)
- Ulcerogenic effect


Nutritional Therapy:
-Dietary modifications food & beverages irritating to patients are avoided or eliminated
-Bland diet
-6 small meals a day during symptomatic phase
-Foods to avoid= hot, spicy foods & pepper, alcohol, carbonated drinks, tea, coffee, broth
-Foods in roughage may irritate mucosa

Upper GI Disorders

 Nursing Management:

ASSESSMENT: Hemorrhage
- Past heath HX - Monitor for changes in V/S, in amount &
- Med usage redness of aspirate (signal massive UGI
- Weight loss bleeding)
- Hematemesis - Monitor for amount of blood in gastric
- Black, tarry stools contents ( pain b/c blood neutralizes acidic
- Epigastric tenderness/pain/discomfort gastric contents)
- N/V - Maintain patency of NG tube
- Abnormal lab values - Prevent blood clot blockage
- Acute/chronic stress - Distention results if blocked

NURSING DX: Perforation
- Acute pain - Monitor for sudden, severe abd pain unrelated
- Nausea in intensity & location to pain that brought pt to
- Deficient fluid volume hospital
- Ineffective therapeutic regimen mgmt. -Possibility of perforation
- Indicated by rigid, board-like abd
IMPLEMENTATION: - Assess for severe generalized abd & shoulder
Health promotion pain
- Identify patients at risk - Assess respirations (shallow, grunting)
- Early detection & TX - Bowel sounds (diminished or absent)
- Encourage pts to take ulcerogenic drugs - VS q 15-30 minutes
with food or milk - Stop all oral NG feeds/drugs til HCP notified
- Teach to report symptoms related to - IV fluids may be to replace volume lost
gastric irritation to HCP - Ensure any known allergies are reported on
chart
- antibiotic therapy usually started
- Anticipate surgical or laparoscopic closure may
be necessary if perforation does not heal
spontaneously

Upper GI Disorders

 SURGICAL THERAPY:
-Uncommon b/c of use of antisecretory agents
-Indications for surgery:
- Unresponsive to med mgmt.
- Concern about gastric cancer
- PUD caused by drugs patient takes but pt cannot be withdrawn from
-Procedures:
Billroth I: Gastroduodenostomy
partial gastrectomy with removal of distal 2/3 stomach and anastomosis
of gastric stump to duodenum
Billroth II: Gastrojejunostomy
partial gastrectomy with removal of distal 2/3 stomach and anastomosis
of gastric stump to jejunum
MOST COMMON POST-OP COMPLICATIONS:
Dumping Syndrome:
-33-50% of patients after surgery
-Direct result of surgical removal of a large portion of stomach
and pyloric sphincter
- Ability of stomach to comtrol amount of gastric chyme entering sm intestine
- Large bolus of hypertonic fluid enters intestine
- Fluid drawn into bowel lumen
-Occurs at end of meal or 15-30 minutes after eating
-Symptoms=
- weakness, sweating, palpitations, dizziness, abd cramps, borborygmi, urge to defecate
- Lasts no longer than an hour

Postprandial Hypoglycemia:
-Variant of dumping syndrome
-Result of uncontrolled gastric emptying of a bolus of fluid high in CHO into small intestine
- Blood sugar
- Release of excessive amounts of insulin into circulation
-When symptoms occur, immediate ingestion of sugared fluids or candy relieves symptoms
-Secondary hypoglycemia occurs with symptoms- 2 hrs after meals
-Symptoms=
- sweating, weakness, mental confusion, palpitations, tachycardia, anxiety

Nutrition POST-OP:
Start as soon as immediate postop period is
successfully passed Gerontologic Considerations:
Advise not to drink fluids with meals & take Patients 60 yrs old
fluids 30-45 minutes before or after meals (use of NSAIDS)
Diet should consist of: 1ST manifestation may be frank gastric bleeding
- Small, dry meals daily or hematocrit
- Low in carbs TX similar to younger adults
- Restrict sugar with meals Emphasis placed on prevention of both gastritis
- Moderate amounts of protein & fat & peptic ulcers
- 30 min rest after each meal

Upper GI Disorders