STOMACH AND INTESTINAL DISEASES

• Peptic Ulcer Disease

• Gastritis
• Cancer of the stomach
 PEPTIC ULCER DISEASE (PUD)
• A peptic ulcer is a break in the gastric/stomach
or duodenal mucosa that penetrates down to
the muscularis mucosae.
• The presence of such an ulcer constitutes the
diagnosis of PUD.
• Peptic ulcers become more common with
↑ing age.
• More common in men than in women.
• Persons infected with Helicobacter pylori have
nearly a tenfold ↑se in incidence at 1% per yr.
 Pathophysiology of PUD
• The acidic stomach and the ingestion of
noxious agents create a fertile ground for the
development of ulcers.
• Peptic ulcers are the result of an imbalance
between mucosal insults and mucosal defense
mechanisms.
• Several protective mechanisms keep peptic
ulcers from developing in the healthy state:
e.g.,,,.
 The surface mucus and bicarbonate layer
The epithelial barrier
Tight intercellular junctions
Mucosal blood flow-mediates removal of
back-diffused acid
Cell restitution and epithelial renewal
• When these mechanisms are interrupted or
are nonfunctioning, the mucosa is vulnerable
to various insults.
• Most ulcers occur when the normal mechanisms
are disrupted by superimposed mucosal insults
that overwhelm the protective mechanisms.
• The most common insults are the result of –
H. pylori infection
Use of NSAIDs.
Virus
Smoking
Alcohol
• Uncommon causes include –
Gastric acid hypersecretion (Zollinger-Ellison
syndrome)
 H. pylori Infection
• Major cause of PUD worldwide.
• Infection is acquired typically in childhood.
• Specific mode of transmission not been
defined fully.
• Evidence exists that the organism is
transmitted from person to person.
• Likely is transmitted by oral-oral or fecal-oral
routes.
• In the developing world, the majority of
children are infected with H. pylori b4 the age
of 10 yrs and more than 80% of adults are
infected by the age of 50 yrs.
• H. pylori is a gram-negative helical-shaped
bacterium that has 4 to 6 flagella.
• The bacteria colonize only gastric epithelium.
• To survive the hostile environment of the
stomach, H. pylori produce urease that
generates ammonia, which, in turn,
neutralizes acid.
• The bacteria also produce a protease that
allows it to move thro’ the mucous layer.
• Unfortunately, this protease thins the mucous
layer and is responsible for damaging this first
barrier of mucosal defense.
• H. pylori infection causes a chronic active
gastritis that involves predominantly the
gastric antrum.
• The presence of these bacteria in the antrum
leads to a loss of somatostatin releasing cells,
and this allows the uninhibited release of
gastrin by antral G cells.
• This leads to ↑sed gastric acid secretion that
promotes and sustains ulcer formation.
• H. pylori infection also incites the
development of duodenitis which may
contribute to the development of duodenal
ulceration.
• The critical role of H. pylori in the devlopment
of PUD is clear.
• What is not clear is why so few pts with H.
pylori infection develop clinical ulcerations.
 Nonsteroidal Antiinflammatory Drugs
• PUD that is not due to H. pylori infection
usually is due to the use of NSAIDs.
• Many pts do not report using these drugs.
• For any pt with PUD, clinicians must maintain
a high degree of suspicion.
• Research indicates that up to 3% of all NSAID
users will develop serious GI complications
(symptomatic PUD, bleeding, or perforation),
and 20% will develop asymptomatic PUD
within the 1st yr of use.
• NSAIDs disrupt the GIT mucosal defense
mechanisms via –
– Topical effects
– Systemic effects
• Topical damage occurs within the stomach by
direct injury to the gastric epithelium.
• Systemically, the inhibition of prostaglandins –
– Disrupts mucosal blood flow
– Alters mucus secretion
– Inhibits bicarbonate (HCO3-)secretion
• All of the above NSAIDs effects may lead to ↑sed
H+ back diffusion and mucosal injury.
 Gastric Acid
• The presence of gastric acid is the reason the
upper GIT is esp prone to the development of
ulceration.
• Whenever there is a mucosal break, (failure of
the inherent protective mechanisms or
overwhelming mucosal injury), the break is
maintained and propagated by the presence of
gastric acid.
• Gastric acid is produced by parietal cells.
• Parietal cells have receptors for three
stimulants: histamine, acetylcholine, and
gastrin.
• Histamine - produced by enterochromaffin-
like cells and mast cells.
• Acetylcholine - released by the vagus nerve.
• Gastrin - produced and released by the antral
G cells.
• G cells are inhibited by gastric acid, creating an
important negative feedback mechanism to
protect against the hypersecretion of gastric
acid.
• The 2 major inhibitors of acid production by
parietal cells are prostaglandins (PGs) and
somatostatin.
• PGs are released by both epithelial and
nonepithelial cells in the stomach.
• Somatostatin is released by D cells in the
stomach.
• Hypersecretion of Gastric Acid –
o The risk of developing PUD is augmented by
hypersecretion of gastric acid.
 Disease States associated with Gastric Acid
Hypersecretion
Zollinger-Ellison Syndrome –
– Xrized by PUD, gastric acid hypersecretion,
and a gastrin producing tumor (gastrinoma).
– Gastrinomas are rare and occur in fewer
than 1% of pts who have PUD.
• Treatment –
– Surgical resection of the gastrinoma
– Admin of a PPI – to suppress gastric acid secretion.
 Viral Causes of Upper GIT Ulceration
• Viruses can cause ulceration of the upper GIT
in any pt.
• However, it is more common in pts with
immunodeficiency.
• Viruses commonly associated with upper GIT
ulceration include herpes simplex virus and
cytomegalovirus (CMV).
• NB: Viral infection should be strongly
suspected in pts who are immunosuppressed
and develop PUD.
 Smoking and PUD
• Smoking has a facilitative role for PUD.
• Smokers are more likely to develop ulcers.
• Ulcers are more difficult to treat and more
likely to recur among smokers.
• Potential mechanisms by which smoking can
foster PUD –
– Compromised blood flow to the mucosa
– Nicotine stimulation of basal acid output
 Alcohol and PUD
• Alcohol can damage the gastric mucosal
barrier directly.
• It can cause acute gastric mucosal lesions
xrized by mucosal hemorrhages.
• Alcohol also stimulates acid secretion.
 Corticosteroids and PUD
• Current evidence supports a role of
corticosteroids in increasing the risk of PUD,
but only when co-administered with NSAIDs.
 Clinical Features of PUD
• Range from silent ulceration to
dyspepsia/indigestion and epigastric pain.
• The classic clinical feature of PUD –
– Pain that occurs 2 to 3 hrs after a meal,
improves with food or antacids, and
awakens the pt several hrs after the pt falls
asleep.
• Complicated PUD implies that the pt has
suffered systemically from PUD; e.g., with GIT
hemorrhage or perforation.
• History, P.E
• H Pylori testing
• The diagnosis of PUD usually is based on the
results of an upper GIT radiographic study or
esophagogastroduodenoscopy (EGD).
• EGD is the preferred method for evaluating
PUD bcoz –
– It allows for biopsy of the antrum for H.
pylori
– It allows taking of biopsy of gastric ulcers to
differentiate benign from malignant ones
 Complications of ulcers
• Hemorrhage in 15-25% of clients
• Perforation—severe pain will ensue. Abdomen
is tender, rigid, and boardlike and the client
will assume the knee-chest position to
decrease abdominal wall tension-----is a
surgical emergency
• Pyloric obstruction—caused by scarring,
edema, inflammation or a combination of
these
 Drug Therapy
• Antisecretory drugs such as Prilosec, Prevacid,
Aciphex, Nexium
• Proton pump inhibitors (PPI): Examples -
omeprazole, pantoprazole, lansoprazole, and
rabeprazole
• Histamine receptor antagonists such as Pepcid,
Zantac, Axid, Tagamet
• Prostaglandin analogs such as Cytotec. Actually
enhances the mucosal resistance
• Antacids: Mylanta and Maalox are examples
(aluminum and magnesium hydroxide).
• Avoidance of NSAIDs
• Mucosal barrier fortifiers such as carafate -
Creates a protective coat
• Cure of H pylori infection: The recommended
primary therapy for H pylori infection is proton
pump inhibitor (PPI)–based triple therapy.
• PPI-based triple therapy regimens for H. pylori
consist of a PPI, amoxicillin, and clarithromycin
for 7-14 days.
• In pts with complicated ulcers caused by H.
pylori, treatment with a PPI beyond the 14-
day course of antibiotics and until the
confirmation of the eradication of H pylori is
recommended.
• 14-day PPI-based therapy –
o Omeprazole: 20 mg PO bid or Lansoprazole:
30 mg PO bid or Rabeprazole: 20 mg PO bid
or Esomeprazole: 40 mg PO qd +
Clarithromycin: 500 mg PO bid +
Amoxicillin: 1 g PO bid
• Quadruple therapy
o Generally reserved for pts in whom the
standard course of treatment has failed.
o Quadruple treatment includes the following
drugs, administered for 14 days:
1) PPI, standard dose, or ranitidine 150
mg, PO bid
2) Bismuth 525 mg PO qid
3) Metronidazole 500 mg PO qid
4) Tetracycline 500 mg PO qid
 Diet Therapy
• Bland diet(soft foods that are not spicy) may be
helpful
• Food itself acts as an antacid
• Avoid caffeine
• Avoid both decaffeinated and caffeinated coffee
because coffee causes stimulation of gastrin
• Avoid bedtime snacks which increase secretion of
acid
• Eat small regular meals
• Avoid acidic foods
 Surgical Management
• Used to:
Reduce the acid-secreting ability of the stomach
Treat patients who do not respond to medical
therapy
Treat a surgical emergency that develops as a
complication of PUD
 Surgical procedures
• Gastroenterostomy—permits neutralization of
gastric acid by regurgitation of alkaline
duodenal contents into the stomach. Also will
perform vagotomy to decrease vagal
influences
• Vagotomy—eliminates the acid-secreting
stimulus to gastric cells and decreases the
responsiveness of parietal cells.
• Pyloroplasty—widens the exit of the lower
stomach so that contents can empty to the
intestines
 GASTRITIS
• Gastritis - inflammation of the gastric or stomach
mucosa.
• Common GI problem.
• May be acute or chronic.
• Causes of gastritis –
– Dietary indiscretion – eating irritating foods, highly
seasoned, or contaminated with disease-causing
microorganisms.
• Caffeine
• Onset of infection with H.pylori can result in gastritis
• Other pathogens implicated are CMV (in HIV patients),
staph, strep, E.coli or salmonella
– NSAIDs
– Excess alcohol
– Bile reflux.
– Radiation therapy.
– Ingestion of strong acid or alkali –
o Severe form; may cause the mucosa to become
gangrenous or to perforate.
o Scarring can occur, resulting in pyloric stenosis
or obstruction.
– Smoking
– Autoimmune diseases; e.g., pernicious
anemia.
 Chronic Gastritis
• Type A has autoimmune pathogenesis,
genetically linked
• Type B is caused by H. pylori. Direct
correlation between number of organisms and
degree of cellular abnormality.
• Can also be caused by alcohol ingestion,
radiation therapy and smoking.
 Physical Manifestations
• Abdominal tenderness
• Bloating
• Hematemesis- vomiting blood
• Melena –traces of blood in stool
• Can progress to shock
• Etc
 Interventions
• Treat symptomatically
• Remove causative agents
• Treat H. pylori
• Treat with H2 receptor antagonists to block gastric
secretions
• Antacids as buffers
• May need B12 due to malabsorption- a cause of
pernicious anemia
• Instruct patient about medications that exacerbate the
problem such as steroids, NSAIDS, ASA and
chemotherapeutic agents
 Diet Therapy
• Avoid known foods that cause S/S
• Tea, coffee, cola, chocolate, mustard, paprika,
cloves, pepper and hot spices may cause
discomfort
• Avoid stress
 CANCER OF THE STOMACH
• Leading cause of cancer deaths annually.
• Early diagnosis (as with most other cancers),
improves survival including possible cure.
• The typical pt with gastric cancer is between
40 and 70 yrs but can affect younger pts.
• Men have a higher incidence of gastric cancer
than women.
• Globally, Japan and Korea have the highest
incidence of stomach cancer.
 Risk Factors for Stomach Cancer
• Helicobacter pylori infection (strongest risk
factor).
• Diet - rich in salt, high intake of smoked foods,
salted meat or fish and pickled vegetables, low
in fruits and vegetables.
• Smoking.
• Hereditary factors.
 Prevention, Screening, and Early Detection
• The prevention of stomach cancer is divided
into 2 main areas:
– Moderating environmental factors.
– Eradicating H. pylori infection.
• Moderating environmental factors –
– Consumption of fresh fruits and vegetables
– may have nutrients – vit C and E, selenium
and carotenoids (e.g., beta-carotene).
• Eradicating H. pylori infection.
• The early detection and diagnosis of stomach
cancer is vital to obtain a positive outcome.
• Early stomach cancer is a potentially curable
disease, 5-yr survival rate approaching 90%.
• In high-risk pops (Japan), nationwide mass
screening programs have been in place for the
past 50 yrs.
 Pathophysiology
• Most gastric cancers are adenocarcinomas.
• They can occur anywhere in the stomach.
• The tumor infiltrates the surrounding mucosa,
penetrating the wall of the stomach and
adjacent organs and structures.
• The liver, pancreas, esophagus, and
duodenum are often already affected at the
time of diagnosis.
• Metastasis thro’ lymph to the peritoneal cavity
occurs later in the disease.
 Clinical Manifestations
• Stomach cancer is frequently diagnosed at an
advanced stage, as symptoms are often vague
or nonexistent in the early stages.
• Symptoms of early disease (e.g., pain)
resemble those of benign ulcers.
• Symptoms such as dyspepsia are nonspecific
and may initially be treated as a peptic ulcer
or dismissed altogether.
• Symptoms of progressive disease –
– Dyspepsia/indigestion.
– Early satiety.
– Weight loss.
– Abdominal pain just above the umbilicus.
– Loss or decrease in appetite.
– Bloating after meals.
– Nausea and vomiting.
– Symptoms similar to those of PUD.
 Assessment and Diagnostic Findings
• Most early gastric tumors are not palpable; PE
not very helpful.
• Advanced gastric cancer may be palpable as a
mass.
• Ascites and hepatomegaly may be apparent if
the cancer cells have metastasized to the liver.
• Palpable nodules around the umbilicus, called
Sister Mary Joseph’s nodules, are a sign of a GI
malignancy, usually a gastric cancer.
• Diagnostic studies –
– Esophagogastroduodenoscopy for biopsy
and cytologic washings (preferred).
– Barium x-ray exam of the upper GIT.
– CT scan of the chest, abdomen, and pelvis is
valuable in staging gastric cancer.
 Therapeutic Approaches and Nursing Care
• Surgical resection remains the treatment of
choice for pts with locoregional stomach
cancer.
• Location and stage of the stomach tumor
determine the type of surgical procedure.
• Pts with metastasized tumors do not require
surgery.
 Surgical Management
• There is no successful treatment for gastric
carcinoma except removal of the tumor.
• If the tumor can be removed while it is still
localized to the stomach, the pt may be cured.
• If the tumor has spread beyond the area that
can be excised, cure is less likely.
• In many pts, effective palliation to prevent
discomfort caused by obstruction or dysphagia
may be obtained by resection of the tumor.
• Chemotherapy & radiation therapy may also be
indicated
• The pt with a tumor that is deemed resectable
undergoes an open surgical procedure to
resect the tumor.
• The pt with an unresectable tumor and
advanced disease undergoes chemotherapy &
radiation therapy.
• For a resectable cancer, total gastrectomy may
be performed.
• Entire stomach plus duodenum, the lower
portion of the esophagus, supporting
mesentery, and lymph nodes are removed.
• Reconstruction of the GI tract is performed by
anastomosing the end of the jejunum to the
end of the esophagus, a procedure called an
esophagojejunostomy.
 Complications associated with partial
or total gastrectomy
• Deficiency of
– Vitamin B12- Pernicious anemia
– Folic acid- Folate deficiency anemia
– Iron- Iron deficiency anemia
• Reduced absorption of vitamin D-activated Vit D is necessary
for calcium absorption
• Impaired calcium absorption
• Result of shortage of intrinsic factor and the now rapid entry of
food into the bowel which decreases absorption
• Nurse should monitor CBC, assessment of tongue for atrophic
glossitis, s/s of anemia
• Dumping syndrome
• Dumping syndrome –
– Shock-like state that occurs when
undigested food “dumps” into the small
intestine often results from gastrectomy.
– Has 2 components, GI and vasomotor
symptoms.
– The GI symptoms- abdominal cramping,
early satiety, nausea and vomiting, and
severe diarrhea.
– Vasomotor symptoms - dizziness,
palpitations, flushing, and diaphoresis.
 Management of the Dumping
Syndrome
• Decrease the amount of food taken at one time
• Eliminate liquids ingested with meals
• Consume high protein, high fat, low
carbohydrate diet
• Pectin may help reduce severity of s/s(purified
carbohydrate obtained from peel of citrus fruits
or from apple pulp)
• Somatostatin may be used in severe cases
(inhibits the secretion of insulin and gastrin)
 Indications for Gastric Surgery –
– PUD pts with –
oLife-threatening hemorrhage.
oObstruction.
oPerforation.
oPenetration.
oPUD does not respond to medication.
– Pts with gastric cancer or trauma.
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