Transcript UNIT TWO The GI Tract September 27, 2001

UNIT TWO
The GI Tract
Gastro-Intestinal Tract & Disorders
Objectives
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Review the A&P of the GI system
Discuss the significance of vitamins and our ability
to absorb them
Describe oral infections/inflammations and the
nursing care.
Discuss the pathophysiology of esophageal
disorders and the treatment /nursing care (i.e.
GERD, hiatal hernia)
Discuss the pathophysiology of disorders of the
stomach and upper small intestine (i.e. gastritis,
upper GI bleed, peptic ulcer disease).
Selected Readings
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In Your text chapters chapters 34, 35, 36, 37
Readings from your syllabus
Can you imagine:
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Not to be able to eat anything with wheat in
it? What condition?
What it is like to live with an esophageal
sphincter not closing? What condition?
Living with part of your stomach in your
esophagus?
Being incontinent of stool or continuous
diarrhea?
Open Sores over your lips on most important
occasions...
The main functions of
GI system:
• Ingestion & propulsion:
(movement )food done by
mouth, pharynx , esophagus
• Digestion (mouth, stomach,
small intestine)
• Absorption (mouth,
stomach, small intestine)
• Elimination (large intestine)
GI organs: liver, biliary tract &
pancreas.
Mouth &
Ulcerative Colitis /Crohn’s &Celiac
Food & GI System:
Food generally takes about four hours to make it
from the mouth to the end of the small intestine. The
non-digested residue normally spends one to three
days in the large intestine but can be there for seven
days.
Foods high in insoluble fiber (whole grains, wheat
and corn brans, some vegetables) speedup
intestinal transit. This is desirable because it prevents
constipation, hemorrhoids, and diverticular disease.
Vitamins
Fat Soluble (stored & need fat for absorption):
• A: vision (fish, fruit, veg)
• D: bone (dairy products esp calcium)
• E: Antitoxins (dairy)
• K: Blood clotting (milk, gr leafy veg)
Water Soluble (not stored):
• C: Connective tissue ascorbic acid, citrus, gr veg,
tomatoes, broccoli
• B1, B2,B6, B12: energy, lips, GI, RBC, heart, skin, gait,
eyes synthesis DNA/RNA (meat veg, dairy products)
NB: Vitamin B12 needs intrinsic factor
Vitamin B12
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Acts as antitoxidant
Essential to formation of the protein collagen
facilitates iron absorption
facilitates cholesterol conversion to bile acids
essential to serotonin synthesis
Vitamin B12
Intrinsic factor
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Parietal cells in the stomach
secrete the the intrinsic factor
necessary for the absorption of
vitamin B12 in the small
intestine.
A lack in Vitamin B12 results in
pernicious anemia.
Loss of intrinsic factor also
leads to degeneration of nerves
& spinal column
Pernicious Anemia:
Common Herbal Supplements
Herb
Side effects
Allium sativum (Garlic)
Anticlotting
Heartburn, flatulence, caution if client
is on ASA or anticoagulants
Echinacea
Immunostimulator
Some allergies; contraindicated in
several diseases
Ginkgo
Vasodilator, ↑ cerebral blood flow
Headache, GI upset, dizziness, N/V
decreased clotting time
St. John’s Wort
Antianxiety, antidepressant
Allergies, photosensitivity, avoid
concurrent use with MAO inhibitors,
opioids
Ginseng
Living fossil, ↑ vitality, ↓stress
Nervousness, excitation, skin eruptions,
avoid with hypertension
GI Tract:
Oral
Problems
Oral Inflammations & Infections:
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The person who is ill, on medication, or receiving
radiation is subject to alterations in ecology of the
mouth & subsequently to decay, periodontal disease,
and injury to the oral mucosa.
Identify oral stressors: mechanical, chemical,
infectious, or due to local or systemic disorder
Infections & Inflammation of the Mouth
Gingivitis
inflamed gingivae & interdental papillae, pus development,
bleeding during brushing, formation of abscess with loosening
of teeth.
Vincent’s Infection
painful, bleeding gingivae, bleeding ulcers, increased saliva with
metallic taste, odor, fever, malaise & anorexia.
Oral Candidiasis
pearly, milk-curd like lesions on mucosa of mouth & larynx,
sore, yeasty halitosis.
Herpes Simplex
lip & mouth lesions, vesicle formation, painful.
Canker Sore
ulcer mouth & lips, extreme pain, ulcer
surrounded erythematous base.
Parotitis
inflammation parotid gland. Pain gland & ear, absence of
salivation, purulent exudate from gland.
Stomatitis
inflammation of mouth with excessive salivation, halitosis, sore
mouth
St. Vincent’s
Stomatitis
Herpes Simplex I Cold Sore
Gingivitis
Oral Candidiasis
Parotitis
Oral Candidiasis
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Oral Candidiasis Care:
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Candidiasis: topical nystatin suspension (2 ml four
times a day) or miconazole gel (5-10 ml four times
daily, held in the mouth with dentures removed).
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Resistant candidacies: usually responds to systemic
oral fluconazole (50 mg capsule daily for 7-14 days).
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Very frequent mouth care is essential
Herpes Simplex
This close-up view of early herpes outbreak shows small, grouped
blisters (vesicles) and lots of inflammation (erythema).
Transmission HSV:
Herpes is most easily passed through inoculation
from active lesions. The virus may also spread
during times when there are no symptoms, and
from sites that are seemingly inactive.
There is a significant percentage of genital herpes
infections resulting from oral to genital sexual
contact. Most of these oral to genital
transmissions will be of the type 1 variety,
although type 2 incidence is not uncommon.
Transmission HSV:
Parotiditis- inflammation of parotid
gland
General Nursing Interventions for Oral
Pain Relief:
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Careful, regular, frequent mouth care
Oral agents such as Lidocaine 2% viscous, Benadryl elixir,
Antacid, & Kaopectate, Acetaminophen
Topical agents such as coating agents
Swishing agents providing topical & anti-inflammatory action
analgesia
Iced water or a dish of crushed ice (with spoon).
Mouth sprays - a small hand-held spray filled with iced fruit
juice is simple and effective. It can be easily used by client or
relative
Artificial saliva - frequent sips of `artificial saliva' may help some
patients. An artificial saliva aerosol spray such as An artificial
saliva spray such as Moistir is also available.
Oral Cancer
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Occur lips or anywhere within the mouth.
Smoking, excessive alcohol, chronic irritation from a jagged
tooth, poor dental care, constant exposure to sun are
predisposing factors
Usually appears painless ulcer on lip
Ca tongue ulcer or area of thickness, sore
Biopsy to diagnose
Treatment surgery, radiation, chemotherapy or combination.
Oral Cancer
Esophageal Disorders
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Mechanical : Tumor, Diverticulum, injury
CV: aneurysm, varices
Neurogenic: Neuro, CVA
Esophageal Disorders
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GERD (Gastroesophageal Reflux Disease)
Hiatal Hernia
Esophageal Cancer
Esophageal Diverticula
Esophageal Strictures
Achalasia
Esophageal Varices
Common Signs & Symptoms of
Esophageal Disorders
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Problem swallowing *
Pain *
Hoarseness *
Weight loss *
Bleeding *
Regurgitation (water brash)
Heart burn
Hiccups
GERD
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Syndrome
No one single cause
Factors causing GERD:
• Impaired esophageal mobility
• Delayed gastric emptying
• Defective mucosal defense
• Reflux of gastric contents
• Lower Esophageal Sphincter (LES) dysfunction –main
factor.
GERD
Normally, after a meal, the lower esophageal
sphincter (LES) usually remains closed.
Secondary peristalsis returns approx. 90% of
the acid and food to the stomach. Once
peristalsis ends, the LES closes again.
The remaining acid in the esophagus is
neutralized by successive swallows of saliva,
which is alkaline in nature - it is then cleared
into the stomach.
When LES relaxes at inappropriate time, it
allows acid and food particles to reflux into the
esophagus. (GERD)
LES & GERD
LES & GERD
Factors that Increase LES Pressure:
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Reglan
Urocholine
Motilium
Gastrin
Nonfat milk
Chewing gum
Some Common Agents that Decrease
LES Pressure:
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Alcohol, Nicotine, ASA
Anticholenergic drugs
Beta-adrenergetic blocking drugs
Calcium channel blockers
Chocolate, Coffee, Fatty foods, Peppermint
Demerol, Estrogen, Lidocaine, Morphine
Clinical Manifestations GERD
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Heartburn very common due to gastroesophageal
reflux
chest pain
Respiratory systems- wheezing, coughing, dyspnea
Otolaryngologic symptoms- hoarseness, sore throat,
feeling as though a lump in throat, choking
Regurgitation common
Gastric symptoms- early satiety, post meal bloating,
N&V.
Complications of GERD
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Esophagitis
Barrett’s esophagus
Respiratory complications: bronchospasms,
laryngospasms, pneumonia
Dental erosion
Barrett’s Esophagus:
Diagnosing GERD
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Barium swallow /X-ray if protrusion upper part of
stomach
Esophageal Endoscopy
Biopsies to determine ca stomach or Barrett’s
esophagus
Esophageal manometric studies- measure pressure
esophagus & LES
PH measuring devices to determine if acid in esophagus
High-dose proton pump inhibitor (PPI)
Barium Swallow X-ray
Esophageal Endoscopy
Esophageal Endoscopy
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NPO 6-10 hours pre examination.
Why?
Why is a local spray anesthetic
used?
Why suction & CPR equipment
ready?
Why withhold fluid & food post
exam?
How long?
What can you do for throat
discomfort?
What do you check for post
procedure?
Nursing Interventions for GERD
Assess cause
• Position-elevate head
no lying down 2-3 hrs.
post eating
• Nutrition
• Drugs as ordered
• Lifestyle- stop smoking,
Weight loss
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Drugs for GERD:
Drugs for GERD focus on:
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Improving LES function (urecholine)
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Increasing esophageal clearance
(metoclopramide)
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Decreasing volume & acidity of reflux (H2
receptor blockers, PPI, maalox, mylanta)
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Protecting esophageal mucosa (gaviscon,
carafate)
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If they do not work surgery maybe required
Nissen Fundoplication
Angelchick antireflux Surgery
B
Menu
F
Hiatal Hernia
Normally:
The stomach is below the diaphragm
Hiatal Hernia
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Is herniation of a portion of the stomach into the
esophagus through an opening, or hiatus, in the
diaphragm.
The weakest part of the diaphragm is the opening
through which the esophagus passes.
Most common abnormality found on x-ray examination
of upper GI tract
Common older adults
More common women than men
There are two types sliding or rolling hiatal hernias
Hiatal Hernia:
Sliding Hiatal
Hernia
A hiatus hernia occurs
when the upper part of the
stomach, which is joined to
the esophagus moves up
into the chest through an
enlargement (called a hiatus)
in the diaphragm.
Gastroesophageal junction
above the diaphgram
Black, 2001
B
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Sliding Hiatal Hernia/ Without Hernia
Rolling Hiatal Hernia
B
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Sliding
Rolling
B
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Hiatal Hernia Causes:
Structural causes such as weakening of muscles in diaphragm
around the esophagogastric opening
Factors that increase intrabd. pressure:
obesity
Pregnancy
Ascites
Tumors
Tight corsets
Intense physical exertion
Heavy lifting continual basis
Increased age
Trauma
Poor nutrition
Forced recumbent position
Clinical Manifestation Hiatal Hernia
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Maybe asymptomatic
Heartburn after a meal or after lying supine
Dysphagia
Reflux & discomfort associated with position lying
down
Bending over may cause severe burning pain, relieved
by standing
Pain with large meals, alcohol, & smoking
Heartburn at night common
Complications of Hiatal Hernia:
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GERD
Hemorrhage from erosion
Stenosis of esophagus
Ulcerations of herniated portion of stomach
Strangulation of the hernia
Regurgitation with tracheal aspiration
Increased risk for respiratory disease
Diagnosis of Hiatal Hernia
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Barium swallow: may show protrusion of gastric
mucosa through the esophagus
X-rays
Endoscopy: visualization of the lower esophagus
provides info on the degree of mucosal
inflammation or other abnormalities.
Conservative Treatment Hiatal Hernia
• Keep to weight as ideal as possible
• Avoid stooping
• Avoid smoking
• Reduce alcohol and coffee
• Avoid tight clothing/under garments
• Adjust bed - elevate HOB
• Take antacid such as TUMS
• Have small meals especially at supper
• Avoid spicy food
• Avoid hot drinks
• Avoid gassy drinks
Other Esophageal Disorders
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Esophageal Diverticula- saclike outpouchings of one or more
layers of the esophagus
Esophageal Strictures – narrowing of esophagus caused by
acids or alkalis ingested and reflux of gastric juices
Esophageal cancer-rare
Achalasia- peristalsis of the lower two thirds of esophagus is
absent. LES increased pressure & incomplete relaxation LES.
Esophageal Varices- dilated veins occurring in lower portion
of the esophagus as a result of portal hypertension. Common
cirrhosis of liver.
DIGESTIVE SYSTEM
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The stomach, intestines, and digestive
glands produce acid and various
enzymes, including pepsin, that break
down and digest the starch, fat, and
protein in food.
The stomach itself is composed mostly
of protein and must be protected from
the same acid and enzymes, or it too can
be attacked and broken down
The main function of the stomach
is to process and transport food.
THE ANATOMY OF THE STOMACH
Anatomically, the stomach can be divided into three major
regions: fundus (the most proximal), corpus and antrum
Disorders of Stomach & Upper Small
Intestine
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Gastritis
Upper GI Bleeding
Peptic Ulcer Disease
Gastric Ulcers
Duodenal Ulcers
Gastric cancer
Food Poisoning
Gastritis
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Inflammation of gastric mucosa as a result of
breakdown in normal gastric mucosal barrier.
Most common problems affecting stomach
Gastritis have tissue edema, disruption of capillary
walls with loss of plasma into gastric lumen &
possible hemorrhage.
Broken mucosal barrier, autodigestion, HCL &
pepsin cause gastritis.
Can be acute or chronic (loss of intrinsic factor)
Causes of Gastritis
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Drugs- aspirin, corticosteroids, NSAIDS, digitalis
Diet-alcohol, spicy irritating foods
Microorganisms-Helicobacter (H-Pylori), Salmonella,
Staphylococcus organisms.
Environmental-smoking, radiation
Pathophysiologic Conditions- burns, lg. hiatal hernia,
stress, reflux bile & pancreatic secretions, renal failure,
sepsis, shock
Other factors- endoscopic procedures, NG suction,
psychologic stress
Clinical Manifestation Gastritis:
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Anoxeria
N&V
Epigastric tenderness
Feeling of fullness
Hemorrhage-common alcohol abuse
Acute gastritis- self-limiting, lasts few hrs to few
days, complete healing mucosa
Chronic gastritis-loss of intrinsic factor
Diagnosis Gastritis
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Acute – based on history drugs & alcohol
Chronic- non-specific symptoms:
endoscopic examination with BX
CBC-anemia/bld. Loss/lack intrinsic factor
Stools Occult blood
gastric analysis- HCL present
serum tests antibodies
tissue BX- R/O gastric cancer
Nursing Management Gastritis
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Acute Gastritis: eliminate cause
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Supportive care
Vomiting-bedrest, npo, IV, antiemetics
Severe V – NG
Hemorrhage-V/S freq. check v blood
Administer antacids (raise ph above 6),
H2R blockers & PPI.
Histamine H2 Receptor Antagonists
Inhibits acid secretion
Proton Pump Inhibitors
Decreased acid secretion
Nursing Management Gastritis
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Chronic Gastritis: evaluation & eliminating cause
(cessation alcohol, abstance from drugs, H.pylori
eradication)
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(Flagyl) Antibiotics & antisecretory agents –rid Hpylori
Strict adherence drug regime
Non-irritating diet
Smoking cessation
Close medical follow-up as increase incidence Gastric
cancer
Upper GI
Bleeding
Upper Tract GI Bleeding
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Upper GI bleeding greater incidence older adults, esp. women
using NSAID
A sudden onset, insidious bleeding
Can be venous, capillary or arterial
Common sites esophagus, stomach & duodenum
Types upper GI Beeding:
• Hematemesis- bldy vomit bright red or coffee-grounds
• Melena-black, tarry stools (foul smelling)
• Occult Blding- sm. Amt bld in gastric secretions,
vomitus or stool not apparent by appearance.
Common Causes Upper GI Bleeding
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Drugs- Corticosteriods, NSAIDS, Salicylates
(stimulate acid production, suppress mucous
production and cause local damage)
Esophagus- Varices, esophagitis, Mallory-Weiss
tear (complication of Bulemia)
Stomach & duodenum- gastric Ca, hemorrhagic
gastritis, peptic ulcers, polyps, stress ulcer
Systemic diseases-leukemia, renal failure
(increase secretion gastric acid)
Upper GI Bleed: Emergency Assessment &
Management
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Immediate physical exam
VS Q 15-30 mins., capillary refill, check distension neck veins
Abdominal exam (BS) & Resp assessment
Labs- CBC, E+, PT, PTT, liver enzymes, ABG’s
Assess stool, vomit bld.
UA & specific gravity
Start 2 IV’s (Bld & fluid replacement R/L)
O2 & meds as ordred
Foley indwelling (accurate measures urine )
May have Central line inserted (measure venous pressures)
NG tube (mouth) removes bld from stomach & alleviates need to
vomit & gastric lavage H2O or saline
Some prefer endoscopy to NG
Diagnosis Upper GI Bleed
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Endoscopy- identifies specific source bleeding.
Angiography-when endoscopy not done.
Invasive procedure catheter placed into gastric
or superior mesenteric artery & advanced until
site discovered.
Barium Contrast- used after acute phase blding
to detect lesion can’t verify blding source.
Nursing Management: Upper GI
Bleeding
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Accurate & thorough assessment
VS
History drugs, ulcers, previous bleeds, varcies
Approach calm manner acute phase bleed
Start IV
I/O measurements
draw bloods
Administer meds as ordered
Nursing Diagnosis Upper GI Bleed
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Fluid volume deficit re: acute loss blood
Ineffective tissue perfussion re: loss circulatory
volume
Anxiety re: upper GI bleed, uncertain outcome
Risk of aspiration re: active blding & altered
LOC
Decreased cardiac output re: loss of blood
Peptic Ulcer
Disease
Peptic Ulcer Disease
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Condition characterized by erosion of GI mucosa
resulting from the digestive action of HCL acid &
pepsin.
Can occur in any portion of GI tract comes in contact
with gastric secretions
Lower esophagus, stomach, duodenum, or jejunum
after surgical procedure (gastroenterostomy)
10% males & 4% women will have ulcers during their
lifetime
Peptic Ulcers
Facts Relating To Peptic Ulcers
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Peptic ulcer Disease (PUD) is the most common
stomach disorder.
Peptic Ulcers are responsible for up to 50% of
all upper GI bleeding episodes
PUD is a chronic disorder
Types Peptic Ulcers:
Acute- superficial erosion & minimal inflammation of
mucosa. Short in duration & resolves quickly when cause
identified & removed.
• Chronic-long duration, eroding through muscular wall &
formation fibrous tissue.
• Gastric –occur any portion stomach, more common
lesser curvature close to the pylorus.
• Duodenal-80% of ulcers, associated with high HCL acid
secretion, mostly occur duodenum
• Stress – Most occur in the proximal portion of the
stomach. Often a result of medical crisis or trauma such
as head injury, burn, respiratory failure, shock, or septic
state.
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Pathophysiology Peptic Ulcer
disease
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Caused by breakdown gastric muscosal barrier
Acid back up resulting in diffusion into mucosa
Destruction of mucosal cells
Increase acid & pepsin release
Further mucosal erosion, destruction blood
vessels, bleeding, ulcerations
Pathophysiology con’t
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Drugs, aspirin, NSAIDs,
Ischemia
Gastinoma (Zollinger-Ellison Syndrome)
Severe Stress
Alcohol
Radiation/chemo
Bacterial or Viral Infection (H-pylori)
Helicobacter Pylori
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Most common cause of Peptic Ulcers
A short, spiral-shaped, microaerophillic gram-negative
bacillus
Live in the mucus layer of the stomach
Secrete proteins that interact with the stomachs
epithelial cells and attract macrophages and neutrophils
cells that cause inflammation
Secrete toxins that contribute to the formation of
Peptic Ulcers
H-Pylori
Zollinger-Ellison Syndrome
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The third leading cause
of peptic ulcers
A tumor in the pancreas
produce excessive
amounts of gastrin, a
hormone that stimulates
gastric acid formation
Signs & Symptoms: Peptic Ulcers
Disease
• Anemia (Fatique, dyspnea)
• GI bleeding
• Dyspepsia – encompasses a wide variety of problems in
the upper abdomen/epigastric dysfunction after meals.
Pain
Discomfort
Bloating
Nausea
Heartburn
Regurgitation
Belching
Gastric Ulcers
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Commonly located lesser curvature close to pylorus
Normal to low secretion gastric acids but back
diffusion of acid is greater (than with duodenal ulcers)
Can be acute or chronic
H-pylori 50-70% of patients
NSAIDS, aspirin & corticosteroids cause acute gastric
ulcers
Chronic alcohol abuse, smoking
Duodenal Ulcers
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Most common of all peptic ulcers
Associated with high acid secretion
Increased risk with COPD, cirrhosis, chronic
pancreatitis, CRF, Zollinger-Ellison Syndrome,
alcohol & heavy smoking.
H-pylori identified 90-95%
Persons with blood type O have an increased
incidence (genetic etiology)
Stress Ulcers
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Acute ulcers
Develop following major physiologic insult trauma or
surgery
Form of erosive gastritis
Gastric muscosa undergoes a period of transient
ischemia in association of hypotension, severe injury,
extensive burns & complicated surgery
multiple superficial erosions may bleed
Risk factors for developing stress ulcers bleeding, resp
failure & coagulopathy
Medications
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Antacids ( Maalox, Mylanta) -Neutralizes gastric acidity
H2 Receptor Antagonists (Pepcid, Zantac) – Inhibits
acid secretion
Proton Pump Inhibitors (Prevacid) – Inhibits the
mechanism that pumps acid into stomach
Gastrointestinal Agents (Carafate) – Prevent relapse
Prostaglandins (Cytotec) – Prevention in Pt’s taking
NSAIDS and may be used with NSAIDS in Pt’s at a
high risk of complications
QUESTION
What factors do you
think the nurse
should consider when
conducting a nursing
assessment of a client
suspected of a peptic
ulcer?
Patient Assessment
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Age & Sex
Occupation/daily stressors
Diet- including caffeine and alcohol intake
Use of Tobacco
Medical and family History
Medications
History of when GI upset and pain occur
Three major Complications Peptic Ulcer
Disease
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Hemorrhage- most common complication.
Erosion of granulation tissue at base of ulcer during healing or
erosion through a major blood vessel- mostly duodenal
Perforation- most lethal peptic ulcer. Large penetrating
duodenal ulcers have not healed & posterior mucosal wall
Gastric outlet obstruction- ulcers antrum & pyloric areas
stomach & duodenum cause predisposition
Narrowing pylorus due to edema, inflammation & spasms
Long hx ulcer pain
Relief from belching or self-induced vomiting (projectile)
Interventions Hemorrhage
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Npo, IV
Note changes in V/S
NG maintain patency
Assess abd distension infers
blocked NG
CBC- hgb & hct
Administer meds as ordered IV
Interventions Perforation
Assessment sudden severe, severe abd pain
Rigid, boardlike abd, severe generalized abd & shoulder
pain, drawing up knees
• BS may diminish & become absent
• Q 15 min V/S
• Npo, IV
• Patient allergies know
• Initiate A/B
• Prep for surgery
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Interventions for Outlet gastric
Obstruction
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Insert NG tube and prepare for iced saline
lavage
Prepare for surgery protocol
Monitor vitals
Arrange Hemoglobin and Hematocrit evaluation
– determines blood loss status
Withhold all oral foods and fluids –prepares
bowel for surgery, decreases stimulus to the area
Diagnostic Tests
• Endoscopy-view entire gastric & duodenal mucosa,
determine degree healing after Rx, tissue specimens
(H.pyloir, ca)
• Cytology (H-pylori, CBC, liver enzymes, serum
amylase)
• U/A & stool specimens (blood)
• Urea breath test
• Upper GI Series ( Barium swallow)- beneficial Dx
gastric outlet obstruction
• Gastric analysis
QUESTION
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What are the main
nursing diagnosis related
to a client diagnosed with
a peptic ulcer?
NURSING DIAGNOSIS
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Pain
Potential for
• hemorrhage
• perforation
• obstruction
Constipation/ Diarrhea
Potential altered health
maintenance
Diagnosis
cont’d
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Constipation/Diarrhea r/t effects of medication
on bowel function
Potential altered health maintenance r/t lack of
knowledge of disease process, contraindications,
S&S of complications, and treatment regimen
PAIN R/T GASTRIC & MUCOSAL
INJURY
• As manifested by :
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Epigastric to left upper quadrant
Frequently described as burning
May radiate to the back
Usually occurs 1-5 hr after meals
May be related by food, antacids (Duodenal), or
vomiting (Gastric)
Intervention for Pain
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Administer antacids, anticholinergics, H2
blockers as directed by physician
Encourage lifestyle changes such as diet,
exercise, stress, smoking, alcohol, caffeine, etc.
Teach rationale avoiding OTC drugs (aspirin)
Antibiotics for H-Pylori
Nutrition PUD
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•
•
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Have small and more frequent meals
Avoid drinking liquids with meals
Refrain from skipping meals
Eliminate caffeine and alcohol
Abstain from hot ,spicy foods
If a smoker, QUIT
Surgery
•
•
Ulcer surgery is a
procedure used to cure
PUD when medications
and other interventions
have failed
Used to relieve a present
PUD and to prevent
recurrence
Types of Surgery PUD
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•
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Vagotomy: Cutting of vagus nerve (decreases gastric
motility & gastric emptying)
Pyloroplasty: To widen the exit of the pylorus and
facilitates emptying of stomach contents, done post
vagotomy.
Billroth I: (Gastroduodenostomy) – The distal portion
of the stomach is removed and the remainder is
anastomosed to the duodenum.
Billroth II (Gastrojejunostomy) – The lower portion
of the stomach is removed and the remainder is
anastomosed to the jejunum
Surgery
Cont’d
• Total Gastrectomy
•
•
remove the stomach from the level of the lower
esophagus to the jejunum
Gastric cancer
Total Gastrectomy
Post-op Complications
Effects of surgery:
1. Dumping syndrome
2. Reoccurrence
3. Reflux gastritis: prolonged contact with bile
causes damage to gastric mucosa.
4.
Delayed gastric emptying
Dumping Syndrome
Read on Gastric cancers:
Clinical manifestations
Nursing care
Food Poisoning
Next Class: Lower GI