Transcript Digestive and Gastrointestinal(GI) Function

Digestive and
Gastrointestinal(GI) Function
Miss Fatima Hirzallah
Objectives
• On completion of this chapter, the learner
will be able to:
• Describe the structure and function of the
organs of the gastrointestinal (GI) tract..
• Use assessment parameters appropriate for
determining the status of GI function.
• Describe the appropriate preparation, teaching,
and follow-up care for patients who are
undergoing diagnostic testing of the GI tract.
Anatomy of the GI Tract
• The gastrointestinal (GI) tract is a 23- to 26foot-long pathway that extends from the mouth
to the esophagus, stomach, small and large
intestines, and rectum, to the terminal structure,
the anus .
Management of Patients
With Gastric and
Duodenal Disorders
5
• An individual’s nutritional status depends not
only on the type and amount of intake but also
on the functioning of the gastric and intestinal
portions of the gastrointestinal (GI) system.
6
Gastritis .1
(inflammation of the gastric or stomach mucosa) is
a common GI problem. Gastritis may be acute,
lasting several hours to a few days, or chronic,
resulting from repeated exposure to irritating agents
or recurring episodes of acute gastritis.
 Acute gastritis is often caused by dietary
indiscretion—the person eats food that is
contaminated with disease-causing microorganisms
or that is irritating or too highly seasoned
7
Gastritis
Other causes of acute gastritis include overuse of
aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs),
 excessive alcohol intake, bile reflux, and
radiation therapy.
 Severe form of acute gastritis is caused by the
ingestion of strong acid or alkali, which may
cause the mucosa to become gangrenous or to
perforate.
• Scarring can occur, resulting in pyloric stenosis
or obstruction.
• Acute gastritis also may develop in acute
illnesses, especially when the patient has had
major traumatic injuries; burns; severe
infection; hepatic, renal, or respiratory failure;
or major surgery. Gastritis may be the first sign
of an acute systemic infection.
9
Gastritis
Chronic gastritis and prolonged inflammation of
the stomach may be caused by either benign or
malignant ulcers of the stomach or by the
bacteria Helicobacter pylori.
Chronic gastritis is sometimes associated with
autoimmune diseases such as pernicious
anemia; dietary factors such as caffeine; the use
of medications, especially NSAIDs; alcohol;
smoking; or reflux of intestinal contents into the
stomach.
10
Pathophysiology
In gastritis, the gastric mucous membrane
becomes edematous and hyperemic (congested
with fluid and blood) and undergoes superficial
erosion.
It secretes a scanty amount of gastric juice,
containing very little acid but much mucus.
Superficial ulceration may occur and can lead to
hemorrhage.
11
Pathophysiology
12
Clinical Manifestations
The patient with acute gastritis may have
abdominal discomfort, headache, lassitude,
nausea, anorexia, vomiting, and hiccupping.
Some have no symptoms.
• The patient with chronic gastritis may
complain of anorexia, heartburn after eating,, a
sour taste in the mouth, or nausea and vomiting.
• Patients with chronic gastritis from vitamin
deficiency usually have evidence of
malabsorption of vitamin B12 caused by
antibodies against intrinsic factor.
14
Assessment and Diagnostic Findings
 Gastritis is sometimes associated with
hypochlorhydria (absence or low levels of
hydrochloric acid [HCl]) or with
hyperchlorhydria (high levels of HCl).
 Diagnosis can be determined by endoscopy,
upper GI radiographic studies, and
histological examination of a tissue specimenbiopsy.
 diagnostic measures for detecting H. pylori
include
serologic testing for antibodies against the
H. pylori antigen, and a breath test
16
Medical Management
 The gastric mucosa is capable of repairing itself after
a bout of gastritis. As a rule, the patient recovers in
about 1 day.
 nonirritating diet is recommended.
 If bleeding is present, management is similar to the
procedures used for upper GI tract hemorrhage
 If it caused by ingestion of strong acids or alkalis,
treatment consists of diluting and neutralizing the
offending agent. To neutralize acids, common
antacids (eg, aluminum hydroxide)
17
Medical Management
to neutralize an alkali, diluted lemon juice .
If corrosion is extensive or severe, emetics and
lavage are avoided because of the danger of
perforation and damage to the esophagus.
 Therapy is supportive and may include
nasogastric (NG) intubation .analgesic agents
and sedatives, antacids, and intravenous (IV)
fluids.

• Fiberoptic endoscopy may be necessary. In
extreme cases, emergency surgery may be
required to remove gangrenous or perforated
tissue.
• A gastric resection or a gastrojejunostomy
(anastomosis of jejunum to stomach to detour
around the pylorus) may be necessary to treat
pyloric obstruction, a narrowing of the pyloric
orifice that cannot be relieved by medical
management.
20
Medical Management
Chronic gastritis is managed by modifying the
patient’s diet, promoting rest, reducing stress,
and initiating pharmacotherapy.
 H. pylori may be treated with antibiotics (eg,
tetracycline or amoxicillin, combined with
clarithromycin) and a proton pump inhibitor
(eg, lansoprazole [Prevacid]), and possibly
bismuth salts (Pepto-Bismol).
Research is being conducted to develop a
vaccine against H. pylori
21
22
Proton (Gastric Acid) Pump Inhibitor
23
Histamine 2 (H2) Receptor Antagonists
24
25
Gastric and Duodenal Ulcers .2
A peptic ulcer is an excavation (hollowed-out
area) that forms in the mucosal wall of the
stomach, in the pylorus (opening between
stomach and duodenum), in the duodenum
(first part of small intestine), or in the
esophagus.
A peptic ulcer is frequently referred to as a
gastric, duodenal, or esophageal ulcer,
depending on its location, or as peptic ulcer
disease.
26
Peptic ulcers are more likely to be in the duodenum than
in the stomach. As a rule they occur alone, but they may
occur in multiples. Chronic gastric ulcers tend to occur in
the lesser curvature of the stomach, near the pylorus.
In the past, stress and anxiety were thought to
be causes of ulcers. Research has identified that
peptic ulcers result from infection with the
gram-negative bacteria H. pylori
27
Familial tendency may be a significant
predisposing factor. A further genetic link is
noted in the finding that people with blood type
O are more susceptible to peptic ulcers than are
those with blood type A, B, or AB. There also is
an association between duodenal ulcers and
chronic pulmonary disease or chronic renal
disease.
28
Stress ulcers, which are clinically different from
peptic ulcers, are ulcerations in the mucosa that
can occur in the gastroduodenal area. Stress
ulcers may occur in patients who are exposed to
stressful conditions.
29
Pathophysiology
Peptic ulcers occur mainly in the gastroduodenal
mucosa because this tissue cannot withstand the
digestive action of gastric acid (HCl) and pepsin.
The erosion is caused by the increased
concentration or activity of acid-pepsin, or by
decreased resistance of the mucosa.
 A damaged mucosa cannot secrete enough
mucus to act as a barrier against HCl.
The use of NSAIDs inhibits the secretion of
mucus that protects the mucosa. Patients with
duodenal ulcer disease secrete more acid than
normal, whereas patients with gastric ulcer tend
to secrete normal or decreased levels of acid.
30
Pathophysiology
Stress ulcer is the term given to the acute
mucosal ulceration of the duodenal or gastric
area that occurs after physiologically stressful
events, such as burns, shock, severe sepsis, and
multiple organ traumas.
Differences of opinion exist as to the actual
cause of mucosal ulceration in stress ulcers.
Usually, it is preceded by shock; this leads to
decreased gastric mucosal blood flow and to
reflux of duodenal contents into the stomach. In
addition, large quantities of pepsin are released.
The combination of ischemia, acid, and pepsin
creates an ideal climate for ulceration.
31
Pathophysiology
Stress ulcers should be distinguished from
Cushing’s ulcers and Curling’s ulcers, two other
types of gastric ulcers.
 Cushing’s ulcers are common in patients with
trauma to the brain.
 Curling’s ulcer is frequently observed about 72
hours after extensive burns
32
Comparing Duodenal and Gastric Ulcers
• DUODENAL ULCER
Incidence
• Age 30–60
• Male: female 2–3:1
• 80% of peptic ulcers are
duodenal
GASTRIC ULCER
• Usually 50 and over
• Male: female 1:1
• 15% of peptic ulcers are gastric
33
Signs, Symptoms, and Clinical Findings
• DUODENAL ULCER
• Hypersecretion of
stomach acid (HCl)
• May have weight gain
• Pain occurs 2–3 hours
after a meal; often
awakened between 1–2
AM;
• ingestion of food relieves
pain
• Vomiting uncommon
• GASTRIC ULCER
• Normal—hyposecretion
of stomach acid (HCl)
• Weight loss may occur
• Pain occurs 1⁄2 to 1 hour
after a meal; rarely
occurs at night; may be
relieved by vomiting;
• ingestion of food does not
help, sometimes
increases
pain
• Vomiting common
34
Comparing Duodenal and Gastric Ulcers
• DUODENAL ULCER
• Hemorrhage less likely than
with gastric ulcer, but if
present melena more common
than Hematemesis More likely
to perforate than
gastric ulcers
• GASTRIC ULCER
• Hemorrhage more likely to
occur than with duodenal
ulcer; hematemesis more
common than melena
35
Comparing
Duodenal and Gastric Ulcers
DUODENAL ULCER •
•
•
•
•
Malignancy Possibility
Rare
Risk Factors
H. pylori, alcohol, smoking,
cirrhosis, stress
GASTRIC ULCER •
• Occasionally
• H. pylori, gastritis, alcohol,
smoking, use of NSAIDs,
stress
Clinical manifestation
• Symptoms of an ulcer may last for a few days,
weeks, or months and may disappear only to
reappear, often without an identifiable cause.
Many people with ulcers have no symptoms, and
perforation or hemorrhage may occur in 20% to
30% of patients who had no preceding
manifestations.
37
Clinical Manifestations
As a rule, the patient with an ulcer complains of
dull, pain or a burning sensation in the
midepigastrium or in the back. It is believed that
the pain occurs when the increased acid content
of the stomach and duodenum erodes the lesion
and stimulates the exposed nerve endings.
• pyrosis (heartburn), vomiting, constipation or
diarrhea, and bleeding. Pyrosis is a burning
sensation in the esophagus and stomach that
moves up to the mouth. Heartburn is often
accompanied by sour taste , or burping, which is
common when the patient’s stomach is empty.
• Fifteen percent of patients with gastric ulcers
experience bleeding.
39
Assessment and Diagnostic Findings
A physical examination may reveal pain,
epigastric tenderness, or abdominal distention.
 A barium study of the upper GI tract may show
an ulcer; however, endoscopy is the preferred
diagnostic procedure because it allows direct
visualization of inflammatory changes, ulcers,
and lesions-biopsy.
40
Stools may be tested periodically until they are
negative for occult blood. Gastric secretory
studies are of value in diagnosing achlorhydria
pylori infection may be determined by biopsy
and histology with culture.
There is also a breath test that detects H. pylori,
as well as a serologic test for antibodies to the H.
pylori antigen.
41
Medical Management
peptic ulcers treated with antibiotics to eradicate
H. pylori have a lower recurrence rate than
those not treated with antibiotics. The goals are
to eradicate H. pylori and to manage gastric
acidity. Methods used include medications,
lifestyle changes, and surgical intervention.
Pharmacologic Therapy
• Currently, the most commonly used therapy for
peptic ulcers is a combination of antibiotics,
proton pump inhibitors, and bismuth salts that
suppress or eradicate H. pylori.
• Histamine-2 (H2) receptor antagonists and
proton pump inhibitors are used to treat NSAIDinduced ulcers and other ulcers not associated
with H. pylori infection.
Nursing Diagnoses
• Acute pain related to irritated stomach mucosa
• Imbalanced nutrition, less than body
requirements, related to inadequate intake of
nutrients
• Risk for imbalanced fluid volume related to
insufficient fluid intake and excessive fluid loss
subsequent to vomiting
• Anxiety related to treatment
Surgical Management
• The introduction of antibiotics to eradicate H.
pylori and of H2 receptor antagonists as
treatment for ulcers has greatly reduced the
need for surgical intervention. However, surgery
is usually recommended for patients with
intractable ulcers (those that fail to heal after 12
to 16 weeks of medical treatment), lifethreatening hemorrhage, perforation.
• obstruction and for those with hypersecreation
of acid not responding to medications .
• Surgical procedures include vagotomy ,
Antrectomy (Gastrojejunostomy),
Gastroduodenostomy)
vagotomy
Decreases gastric acid by 
diminishing cholinergic
stimulation to the parietal
cells, making them less
responsive to gastrin. May be
performed via open surgical
approach, laparoscopy, or
thoracoscopy
(Gastroduodenosto
my
• Removal of the lower portion
of the antrum of the stomach
(which contains the cells that
secrete gastrin)as well as a
small portion of the duodenum
• (Gastrojejunostomy) : Removal of lower portion
(antrum) of stomach with anastomosis to
jejunum
• Complication :Dumping syndrome, anemia,
mal-absorption, weight loss. Recurrence rate of
ulcer is 10%–15%
Nursing Diagnoses
• Acute pain related to the effect of gastric acid
secretion on damaged tissue
• Anxiety related to an acute illness
• Imbalanced nutrition related to changes in diet
• Deficient knowledge about prevention of
symptoms and management of the condition
Thanks
•