Transcript Gastrointestinal Digestive Disorders

Part I
“Air-Fluid Levels” seen in small bowel obstruction


Supplemental
Learning Objects:
Flash Cards (Terminology)

See the email I sent you yesterday

G-I System Games

Meds for the Gastro Intestinal System
http://www.quia.com/rr/612817.html

G-I System Part I
http://www.quia.com/rr/612592.html

GI System Part 2
http://www.quia.com/rr/612897.html

G-I System Part 3
http://www.quia.com/rr/612899.html
LEARNING OUTCOMES
At the conclusion of this learning
activity, the nurse will be able to:
 1. Describe the mechanism of action, signs and
symptoms, complications, treatments and nursing
interventions for gastrointestinal disorders
 2. Compare and describe the pathophysiology for
Crohn’s Disease and ulcerative colitis
 3. Explain pathophysiology, types, risk factors, and
treatment for gastritis
LEARNING OUTCOMES
At the conclusion of this learning
activity, the nurse will be able to:
 4. Explain the use of radiography in diagnosis of GI
health problems
 5. Discuss the physical assessment findings in a client
with digestion, nutrition, and elimination health
problems
 6. Describe procedures, risk factors, potential
complications, nursing monitoring, and interventions
for scope procedures
LEARNING OUTCOMES
At the conclusion of this learning activity,
the nurse will be able to:
 7. Describe preparation, post-op interventions, and
teaching needs for a patient with a new colostomy
 8. Analyze medications, usage, precautions, side
effects, and mechanism of action
 9. Apply the nursing process to medication
administration and usage
LEARNING OUTCOMES
At the conclusion of this learning activity,
the nurse will be able to:
 10. Explain causes, sign/ symptoms, nursing
interventions, treatments, and complications of a bowel
obstruction
 11. Explain pathophysiology, risk factors, and
medical management of gastrointestinal disorders
 12. Explain causes of bowel obstruction
 Terminology
 G-I
Pharmacology
 A&P
 GI
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Disorders
GERD
Hiatal Hernias
PUD
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Antacids
Prokinetic Agents
H 2 Receptor Antagonists
Proton Pump Inhibitors
Mucosal Barriers
 G-I
Diagnostic
Testing
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-algia
-dynia
volvulus
dyspepsia
regurgitation
hypersalivation
pyrosis
eructation
dysphagia
odynophagia
-enter/o
-col/o
-gastr/o
-esophag/o
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ulceration
aspiration
ischemia
diverticula
diverticulitis
colostomy
illeostomy
tenesmus
steatorrhea
diarrhea
fistula
defecation
--rrhea
steato-
Length =
27-30 feet
(9-10 meters)
 Secretion
 Digestion
 Absorption
 Motility
 Elimination
 Involves: esophagus, stomach, small
intestines, gallbladder, and large
intestines
 Parasympathetic:
stimulates motor and
secretory activity, relaxes sphincters
 Teeth: chewing
 Mucin
and amylase: breaks down food
 Tongue
 Pharynx
 Esophagus: 2 sphincters
 Ingestion
of food
 Food reservoir
 Digestive process:
-movement
-gastrin secretion: hydrochloric acid
and pepsin
-chyme
Anti-Acids (Antacids)
Physical Assessment
Inspection
Palpation
Percussion
Auscultation
KEY ASSESSMENTS
Lab Monitoring
Prototype: aluminum hydroxide
gel (Amphojel)
Prokinetic Agents:
Prototype: metoclopramide
(Reglan)
Histamine 2 Receptor Agonists
Prototype: ranitidine
hydrochloride (Zantac)
***Diagnostic Testing
Proton Pump Inhibitors)
Prototype: omeprazole (Prilosec)
Mucosal Barriers
Prototype: sucralfate (Carafate)
Disease Specific
Medications:
Care Planning
Plan for client adl’s,
Monitoring, med admin.,
Patient education, more…based
On Nursing Process:
A_D_O_P_I_E
***Preparing for Diagnostic Tests
Nursing Skills:
NG Tube Insertion
Enteral Feedings
Nursing Interventions &
Evaluation
Execute the care plan, evaluate for
Efficacy, revise as necessary
INFLAMMATORY
Upper GI
 Gastroesphageal Reflux
Disease
 Ulcers
 Gastritis
NON-INFLAMMATORY
Upper GI
 Gastroesphageal Reflux
Disease
 Hiatus Hernia/hernias
INFLAMMATORY
Lower GI
 Acute Appendicitis
 Peritonitis
 Ulcerative colitis
 Crohn’s Disease
 Diverticulitis
NON-INFLAMMATORY
Lower GI
 Constipation & Diarrhea
 Irritable bowel syndrome
 Dumping syndrome
 Intestinal Obstruction
 Hemorrhoids and polyps
 Malabsorption syndrome
 Acute
local inflammation:
-edema, pain, heat, and redness
-exudates may or may not be present
 Acute
systemic inflammation:
-fever
-leukocytosis (increased WBC)
-plasma protein synthesis
 Chronic
Inflammation:
-increased duration>2 weeks
-proceeds after unsuccessful acute
inflammatory response
-may occur without distinct inflammation
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GERD : common condition
(affects 14% of Americans)
characterized by gastric
content and enzyme
leakage into the
esophagus.
These corrosive fluids
irritate the esophageal
tissue and limit its ability to
clear the esophagus.
Causes are related to the
weakness or transient
relaxation of the lower
esophageal sphincter (LES)
at the base of the
esophagus, or delayed
gastric emptying.
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The chief symptom of GERD is
frequent and prolonged
retrosternal heartburn
(dyspepsia) and regurgitation
(acid reflux) in relationship to
eating or activities.
Other symptoms can include
chronic cough, dysphagia,
belching (eructation),
flatulence (gas), atypical chest
pain, and asthma
exacerbations.
 Backward
flow of gastrointestinal
contents into esophagus
 Inappropriate
relaxation of lower
esophageal sphincter (food, medication,
etc)
 ETIOLOGY:
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Any factor that relaxes the
LES, such as smoking, caffeine,
alcohol, or drugs.
Any factor that increases the
abdominal pressure, such as
obesity, tight clothing at the
waist, ascites, or pregnancy.
Older age and/or a
debilitating condition that
weakens the LES tone.
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CONTIBUTING FACTORS:
Excessive ingestion of foods that relax LES,
e.g., fatty / fried foods, chocolate, tomatoes,
alcohol
Distended abdomen from overeating or
delayed emptying
Increased abdominal pressure resulting
from obesity, pregnancy, bending at the
waist, ascites or tight clothing at the waist
Drugs that relax the LES, such as
theophylline, nitrates, calcium channel
blockers, anticholinergics, and diazepam
(Valium)
Drugs, such as NSAIDs, or events (stress)
that increase gastric acid
Debilitation or age-related conditions
resulting in weakened LES tone
Hiatal hernia (LES displacement into the
thorax with delayed esophageal clearance)
Lying flat
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Classic symptoms:
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Dyspepsia, especially
after eating an offending
food / fluid, and
regurgitation.
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Other symptoms:
Symptoms from throat
irritation (chronic
cough, laryngitis),
hypersalivation,
eructation, flatulence,
or atypical chest pain
from esophageal
spasm.
Chronic GERD can
lead to dysphagia
(difficulty swallowing).
 Irritation
to esophagus and mucosal
injury
 Aspiration
 Barrett’s esophagus
 Esophageal erosions, ulcerations, or tears
 Chronic bronchitis
 Asthma (adult onset)
Barrett’s Esophagus
 History
and Physical
 Dietary monitoring
 24 hour ambulatory pH monitoring
 Esophageal manometry
 Endoscopy
 Barium
Upper GI:
 Prepare
the client for
the procedure.
procedure:
Assess
for bowel sounds and
potential
constipation.
 Endoscopy
:
 Conscious
sedation
to observe for tissue
damage
 Post
 Post
procedure:
Verify gag response
prior to providing
oral fluids or food.
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Goals: relief of symptoms and prevent
complications
Life style changes:
-Diet: smaller meals more frequent, limit or avoid
carbonated beverages, coffee, chocolate, fats,
mints, spicy or acidic food
 Life
Style Changes:
-Elevate HOB, sleep on LEFT side
-AVOID smoking and ETOH
-Avoid tight or restrictive clothing
-Lose weight
 Antacids,
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E.g., aluminum hydroxide (Mylanta),
neutralize excess acid. -- should be
administered when the acid secretion is
highest (1 to 3 hr after eating and at
bedtime). --Antacids should be
separated from other medications by at
least 1 hr.
2 (H2)
receptor antagonists
 Proton
Pump
inhibitors (PPI)
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 Histamine
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E.g., ranitidine (Zantac), famotidine
(Pepcid), nizatidine (Axid), and
cimetidine (Tagamet), reduce the
secretion of acid.
The onset is longer than antacids, but the
effect has a longer duration.
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E.g., pantoprazole
(Protonix),omeprazole (Prilosec),
esomeprazole (Nexium), and
lansoprazole (Prevacid) reduce
gastric acid by inhibiting the
cellular pump necessary to
secrete it.
Studies show that PPI are more
effective than H2 antagonists.
 Other
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Medications
E.g., metoclopramide
hydrochloride (Reglan), increase
the motility of the esophagus and
stomach.
 Endosopic
therapy: BESS (Bard
EndoCinch Suturing System), Stretta, and
Enteryx procedures
 Surgery: Laparoscopic Nissen
Fundoplication (The”Gold Standard”)
 Post
operative or procedure management:
- Monitor vital signs
-Monitor swallow/gag reflex
-Assess for abdominal pain
-Monitor for bleeding
-Assess incision sites
-Assess and monitor NG
tube
 Altered
Nutrition
 Acute or Chronic pain
 Risk for aspiration
 Alteration in sleep patterns
 Knowledge Deficit
 Impaired Swallowing
 Potential for complications
 EDUCATION:
-Medication Compliance
-Dietary changes
-Lifestyle changes
 Post
operative or procedure management
 Involve
protrusion of the stomach wall
through the esophageal hiatus of the
diaphragm
 Sliding: (Most
Common) esophagogastric
junction and portion of the fundus slide
upward through the esophageal hiatas
 Rolling: the
fundus and portions of the
stomach rolls through the esophageal
hiatas
 Muscle
weakness
 Anatomic defects
 Congenital weakness
 Prolonged increased abdominal pressure
 Surgery
 Trauma
 Obesity
SLIDING
 Adult
onset asthma
 Symptoms worse
after meals
 Symptoms worse in
recumbent position
ROLLING
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Feeling full after
eating
Breathlessness or
feeling of not be able
to breath
Chest pain like
angina
feeling of suffocation
Symptoms worse in
recumbent position
 Barium
Swallow Study
 Diet
 Medications
 Weight
(GERD)
Loss
 Avoid late night food
 Avoid straining/vigorous exercise
 No restrictive or binding clothes
 Surgical repair:
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Laparoscopic Nissen Fundoplication
 Education:
-Medication compliance
-Dietary changes and monitoring
-Lifestyle changes and monitoring
 Post-op management
 Assess coping mechanisms
A
mucosal lesion of the stomach or
duodenum
 Results
when gastric mucosal defenses
become impaired and no longer protect
the epithelium from the effects of acid
and pepsin
 Gastric
Ulcers:
-a break in mucosal barrier, hydrochloric acid
injures epithelium
-back diffusion of acid or dysfunction of the
pyloric sphincter
-Mucosal Inflammation
 Duodenal
Ulcers:
-increase acid content dumped into duodenum
 “Stress
Ulcers:”
-Unknown etiology, presence of
increased levels of hydrochloric acid,
ischemia, and erosive gastritis seen
-Trauma, head injuries,
respiratory failure, shock
sepsis
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Intermittent sharp, burning, or gnawing
pain
Gastric pain occurs to the left and may be
relieved by food
A change in appetite with or weight loss
(gastric)
Nausea or vomiting
Bloody stools
 Frequent
burping or bloating
 Duodenal
pain is usually to the right of
the epigastruim and pain occurs 90 min-3
hours after eating.
 Pain often awakes patient’s up at night
 A change in appetite with weight gain
(duodenal)
 History
and Physical (family history)
 Endoscopy (EGD)
 Stool for occult blood
 H-pylori test (carbon ureas breath test)
 Gastric secretion studies
 Biopsy
 Drug
Therapy
 Diet Therapy
 Lifestyle Changes
 Surgical Intervention
 Actual
pain
 Anxiety/Fear
 Ineffective individual coping
 Potential fluid volume deficit
 Knowledge deficit
 Disturbed sleep pattern
 Nutrition deficit
 Assessment
of symptoms and family
history
 Assess for complications
 Medication and diet education
 Monitor pain management
 Monitor nutritional status
 Encourage smoking and alcohol
cessation
 Gastrointestinal
bleeding
 Gastric Perforation
 Pyloric obstruction
 GI
bleed
 Perforation
 Pyloric obstruction
 Vagotomy
& Pyloroplasty
 Gastroenterostomy
 Assess
patient
 Assess vital signs
 Monitor gastric decompression and
output
 Monitor labs
 Monitor continued ileus
 Monitor for gastric delay emptying and
recurrent ulcerations
End
of Part I
Gastrointestinal System
The
Appendix follows
on this Power Point
(Medication Information, etc…)
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Pharmacological Action
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Neutralize gastric acid and inactivate pepsin.
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Evaluation of Medication
Effectiveness
Mucosal protection may occur by the antacid’s
ability to stimulate the production of
prostaglandins.
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Depending on therapeutic intent, effectiveness
may be evidenced by:
Therapeutic Uses
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Healing of gastric and duodenal ulcers.
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Reduced frequency or absence of GERD
symptoms.
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No signs or symptoms of GI bleeding.
Treat peptic ulcer disease (PUD) by promoting
healing and relieving pain.
Symptomatic relief for clients with GERD.
Nursing Interventions and Client
Education
Clients taking tablets should be instructed to chew the
tablets thoroughly and then drink at least 8 oz of water
or milk.
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Teach the client to shake liquid formulations to ensure
even dispersion of the medication.
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Compliance is difficult for clients because of the
frequency of administration.
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Administered seven times a day: 1 hr before and 3 hr after
meals, and again at bedtime.
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Teach clients to take all medications at least 1 hr before or
after taking an antacid.
Back to Concept Map
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Pharmacological Action
Block dopamine and serotonin receptors in
the chemoreceptor trigger zone (CTZ), and
thereby suppress emesis.
Prokinetic agents augment action of
acetylcholine which causes an ↑ in upper
GI motility.
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Therapeutic Uses
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Control postoperative and chemotherapyinduced nausea and vomiting.
Prokinetic agents are used to treat GERD.
Prokinetic agents are used to treat diabetic
gastroparesis.
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Side Effects / Adverse Effects
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Extra Pyramidal Symptoms (EPS)
Sedation
Diarrhea
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Contraindications / Precautions
Contraindicated in clients with GI perforation, GI
bleeding, bowel obstruction, and hemorrhage
Contraindicated in clients with a seizure disorder
due to ↑ risk of seizures
Use cautiously in children and older adults due to
the ↑ risk for EPS.
Nursing Interventions and Client
Education
Monitor clients for CNS depression and EPS.
Can be given orally or intravenously. If dose is < 10
mg, it may be administered undiluted over 2 min.
If the dose is > 10 mg, it should be diluted and infused
over 15 min. Dilute medication in at least 50 mL of D5W or
lactated Ringer’s solution.
Evaluation of Medication
Effectiveness
Control of nausea and vomiting
Back to Concept Map
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Pharmacological Action
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Suppress the secretion of gastric acid by
selectively blocking H2 receptors in
parietal cells lining the stomach.
Treatment of peptic ulcer disease is usually started
as an oral dose twice a day until he ulcer is healed,
followed by a maintenance dose, which is usually
taken once a day at bedtime.
Evaluation of Medication
Effectiveness
Therapeutic Uses
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Gastric and peptic ulcers,
gastroesophageal reflux disease (GERD),
and hypersecretory conditions, such as
Zollinger-Ellison syndrome.
Used in conjunction with antibiotics to treat
ulcers caused by H. pylori.
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No signs or symptoms of GI bleeding.
Therapeutic Nursing Interventions
and Client Education
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Healing of gastric and duodenal ulcers.
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Depending on therapeutic intent, effectiveness
may be evidenced by:
Reduced frequency or absence of GERD
symptoms (e.g., heartburn, bloating, belching).
Encourage client to avoid aspirin and other
nonsteroidal anti-inflammatory drugs (NSAIDs).
Ranitidine can be taken with or without food.
Back to Concept Map
Pharmacological Action
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Reduce gastric acid secretion by irreversibly
inhibiting the enzyme that produces gastric
acid.
Reduce basal and stimulated acid production.
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Therapeutic Uses
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Prescribed for gastric and peptic ulcers,
GERD, and hypersecretory conditions (e.g.,
Zollinger-Ellison syndrome).
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Precaution:
Increases the risk for pneumonia. Omeprazole ↓ gastric
acid pH, which promotes bacterial colonization of the
stomach and the respiratory tract.
Use cautiously in clients at high risk for pneumonia
(e.g., clients with COPD).
Nursing Interventions and Client Education
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Do not crush, chew, or break sustained-release
capsules.
The client may sprinkle the contents of the
capsule over food to facilitate swallowing.
The client should take omeprazole once a day
prior to eating.
Encourage the client to avoid irritating
medications (e.g., ibuprofen and alcohol).
Active ulcers should be treated for 4 to 6
weeks.
Pantoprazole (Protonix) can be administered to
the client intravenously.
Monitor the client’s IV site for signs of
inflammation (e.g., redness, swelling, local
pain) and change the IV site if indicated.
Teach clients to notify the primary care
provider for any sign of obvious or occult GI
bleeding (e.g., coffee ground emesis).
Evaluation of Medication Effectiveness
Depending on therapeutic intent, effectiveness
may be evidenced by:
Healing of gastric and duodenal ulcers.
Reduced frequency or absence of GERD
symptoms (e.g., heartburn, sour stomach).
No signs or symptoms of GI bleeding.
Back to Concept Map

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Pharmacological Action
Changes into a viscous substance that
adheres to an ulcer; protects ulcer from
further injury by acid and pepsin.
Viscous substance adheres to the ulcer for
up to 6 hr.
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Sucralfate has no systemic effects.
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Therapeutic Uses
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Acute duodenal ulcers and
maintenance therapy.
Investigational use in gastric ulcers
and gastroesophageal reflux disease.
(GERD)
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Nursing Interventions and Client
Education
Assist the client with the medication regimen.
Instruct the client that the medication should be
taken on an empty stomach.
Instruct the client that sucralfate should be taken
four times a day, 1 hr before meals, and again at
bedtime.
The client can break or dissolve the medication in
water, but should not crush or chew the tablet.
Encourage the client to complete the course of
treatment.
Evaluation of Medication
Effectiveness
Depending on therapeutic intent, effectiveness
may be evidenced by:
Healing of gastric and duodenal ulcers.
No signs or symptoms of GI bleeding.
Back to Concept Map
 Blood Tests
 Complete Blood Count (CBC c Diff)
 Radiology:
 Stool Tests:
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Upper GI Series (UGI)
Upper GI Series with Small Bowel
Follow-Through (UGI-SBFT)
Barium Enema
Endoscopy
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Stool for occult blood; (Guiac)
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Stool for ova & parasites (O&P);
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Stool for Clostridium difficile (C-Diff)
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Stool Culture & Sensitivity (C&S)
 Endoscopy:
Clostridium difficile
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Return to
Concept Map