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SCHEMATIC DIAGRAM

Predisposing Factors Precipitating Factors

Genetics
Age (50-69 years old) – 58 years old

mutation in exon 11 of the c-KIT (tyrosine kinase)

Overexpression and autophospholyzation of c-KIT

increased proliferation of insterstitial cells of Cajal


(tumorigenesis)

GIST – Gastrointestinal Stromal Tumor

abdominal
satiety / feeling of discomfort
fullness continued growth of GIST generates increasing pressure to surrounding tissue nausea
dyspepsia vomiting
perforation loss of appetite

weakening of the surrounding tissues’ blood vessels

rupture / damage of blood vessels

black tarry stool


decreased Hct, Hgb
bloody vomiting UPPER GI BLEEDING
DOB
syncope

Stomach
The stomach is a J-shaped enlargement of the GI tract directly inferior to the diaphragm in the epigastric,
umbilical, and left hypochondriac regions of the abdomen. The stomach connects the esophagus to the
duodenum, the first part of the small intestine. Because a meal can be eaten much more quickly than the
intestines can digest and absorb it, one of the functions of the stomach is to serve as a mixing chamber and
holding reservoir. At appropriate intervals after food is ingested, the stomach forces a small quantity of material
into the first portion of the small intestine. The position and size of the stomach vary continually; the diaphragm
pushes it inferiorly with each inhalation and pulls it superiorly with each exhalation. Empty, it is about the size of a
large sausage, but it is the most distensible part of the GI tract and can accommodate a large quantity of food. In
the stomach, the digestion of starch continues, digestion of proteins and triglycerides begins, the semisolid bolus
is converted into a liquid, and certain substances are absorbed.
Anatomy
The stomach has four main regions: the cardia, fundus, body and pylorus. The
cardia surrounds the superior opening of the stomach. The rounded portion
superior to and to the left of the cardia is the fundus.

Inferior to the fundus is the large central portion of the stomach called the body.
The region of the stomach that connects to the duodenum is the pylorus; it has
two parts, the pyloric antrum, which connects to the body of the stomach, and the
pyloric canal which leads into the duodenum.

When the stomach is empty, the mucosa lies in large folds called ruggae that can
be seen with the unaided eye. The pylorus communicates with the duodenum of
the small intestine via a sphincter called the pyloric sphincter. The concave medial
border of the stomach is called the lesser curvature, and the convex lateral border
is called the greater curvature.

Histology
The stomach wall is composed of the same four basic layers as the rest
of the GI tract, with certain modifications. The surface of the mucosa is
a layer of simple columnar epithelial cells called surface mucous cells.
The mucosa contains a lamina propria (areolar connective tissue) and a
muscularis mucosae (smooth muscle).

Epithelial cells extend down into the lamina propria, where they form
columns of secretory cells called gastric glands that line many narrow
channels called gastric pits. Secretions from several gastric glands flow
into each gastric pit and then into the lumen of the stomach. The gastric
glands
contain three types of exocrine gland cells that
secrete their products into the stomach lumen:
mucous neck cells, chief cells and parietal cells. Both
surface mucous cells and mucous neck cells secrete
mucus. Parietal cells produce intrinsic factor (needed
for absorption of Vitamin B12) and hydrochloric acid.
The chief cells secrete pepsinogen and gastric lipase,

The secretion of the mucous parietal, and chief cells


from gastric juice, which totals 2000-3000ml (roughly
2-3qt.) per day. In addiction gastric glands include a
type of enteroendocrine cell, the G cell, which is
located mainly in the pyloric antrum and secretes
hormone gastrin into the bloodstream.

Three additional layers lie deep to the mucosa. The


submucosa of the
stomach is
composed of areolar
connective tissue. The muscalaris has three layers of smooth muscle (rather than
the two found in the small and large intestines): an outer longitudinal later, a
middle circular layer and an inner oblique layer. The oblique layer is limited
primarily to the body of the stomach. The serosa is composed of simple
squamous epithelium (mesothelium) and areolar connective tissue; the portion of
the serosa covering the stomach is part of the visceral peritoneum. At the lesser
curvature if the stomach the visceral peritoneum extends upward to the liver as the lesser omentum. At the
greater curvature of the stomach, the visceral peritoneum continues downward as the greater omentum drapes
over the intestines.

Gastrointestinal Stromal Tumor


Mesenchymal tumors of the gastrointestinal (GI) tract comprise a widely diverse group of neoplasms, completely
separate from carcinomas or neuroendocrine tumors. This diverse grouping of tumors includes histopathological
subtypes (e.g leiomyosarcoma, leiomyoma, neurofibroma, schwannoma, desmoid fibromatosis, benign and
malignant vascular tumors, glomus tumor and other rare subtypes of sarcoma) that can also occur outside the GI
tract; importantly thought the most common subtype of mesenchymal tumor of this origin system is the subtype
known as gastrointestinal stromal tumor (GIST) that occurs exclusively within the abdomen, retropretineum and
pelvis.
GISTs can occur at any age, although they are more common in adults with a peak incidence in the fifth and sixth
decades of life. Although numbers vary from study to study it appears that males and females are affected
equally. Although it is not possible to know the exact incidence of GISTs in the population these tumors are not
common.

GISTs occur along the entire length of the GI tract but with different frequencies at different anatomical locations.
Importantly GISTs from different GI sites of origin also exhibit different incidences of the underlying type of
molecular mechanism: In other words the specific activating pathway (usually through a specific activating
mutation in a signaling kinase such as the KIT pronco-oncogene) appears to correlate with the site of origin of the
primary GIST.

Most small GIST lesions are asymptomatic. When large lesions are present, or if
the tumor is highly infiltrative into vascular and neural structure initial symptoms
may include abdominal fullness, pain nausea, dyspepsia, acute abdominal crisis
with perforation, or evidence of GI bleeding. such as melena, hematemesis and
anemia. (Kelsen, 2002)

Gastrointestinal Stromal Tumors, or GISTs, are a relatively uncommon type of


cancer that occurs in the gastrointestinal (GI) tract. GISTs are believed to start in
special cells found in the wall of the GI tract, called the interstitial cells of Cajal
(ICCs), or in very early cells that can develop into ICCs. ICCs are part of the
autonomic nervous system, which sends signals to the GI tract. Some have called these cells the "pacemakers"
of the gastrointestinal tract. The nerve signals they send cause muscles of the digestive organs to contract, which
helps to move food and liquid through the GI tract. (Novartis Oncology,2009)
Common Causes of GI Bleeding
Upper GI tract Although these tumors can start anywhere in the GI tract, they occur
most often in the stomach (50% to 70%) or the small intestine (20% to
Duodenal ulcer (20–30%) 30%). The rest are found in the esophagus, large intestine (colon and
rectum), and anus.
Gastric or duodenal erosions (20–30%)
Interstitial Cells of Cajal
Varices (15–20%)
ICC serve a pacemaker cells to control autonomic function of the GI
Gastric ulcer (10–20%) tract muscles. (Kelsen, 2002)
Mallory-Weiss tear (5–10%) The Interstitial cell of Cajal (ICC) is a type of cell found in the
gastrointestinal tract. It serves as a pacemaker that triggers gut
Erosive esophagitis (5–10%)
contraction. Many types of smooth muscle tissues have now been
shown to contain ICC, but with few exceptions the function of these
Angioma (5–10%)
cells is not known and is currently an area of active research.
(Wikipedia, 2009)
Arteriovenous malformation (< 5%)

Upper Gastrointestinal Bleeding


Gastrointestinal stromal tumors
Lower GI tract (percentages vary with the
age group sampled) GI bleeding can originate anywhere from the mouth to the anus and
can be overt or occult. The manifestations depend on the location and
Anal fissures rate of bleeding.

Angiodysplasia (vascular ectasia) Hematemesis is vomiting of red


blood and indicates upper GI
Colitis: radiation, ischemic, infectious bleeding, usually from an arterial
source or varix. Coffee-ground
Colonic carcinoma emesis is vomiting of dark brown,
granular material that resembles
Colonic polyps coffee grounds. It results from upper
GI bleeding that has slowed or
Diverticular disease stopped, with conversion of red Hb
to brown hematin by gastric acid.
Inflammatory bowel disease: ulcerative
proctitis/colitis, Crohn's disease
Hematochezia is the passage of
gross blood from the rectum and
Internal hemorrhoids
Small-bowel lesions (rare)
usually indicates lower GI bleeding but may result from vigorous upper
GI bleeding with rapid transit of blood through the intestines.
Angiomas Melena is black, tarry stool and typically indicates upper GI bleeding,
but bleeding from a source in the small bowel or right colon may also
Arteriovenous malformations be the cause. About 100 to 200 mL of blood in the upper GI tract is
required to cause melena, which may persist for several days after
Meckel's diverticulum

Tumors
bleeding has ceased. Black stool that does not contain occult blood may result from ingestion of iron, bismuth, or
various foods and should not be mistaken for melena.

Chronic occult bleeding can occur from anywhere in the GI tract and is detectable by chemical testing of a stool
specimen. Acute, severe bleeding also can occur from anywhere in the GI tract. Patients may present with signs
of shock. Those with underlying ischemic heart disease may develop angina or MI because of hypoperfusion.

GI bleeding may precipitate hepatic encephalopathy (see Approach to the Patient With Liver Disease: Portal-
Systemic Encephalopathy) or hepatorenal syndrome (kidney failure secondary to liver failure—see Approach to
the Patient With Liver Disease: Renal and Electrolyte Abnormalities).
Review of symptoms should include presence of abdominal discomfort, weight loss, easy bleeding or bruising,
previous colonoscopy results, and symptoms of anemia (eg, weakness, easy fatigability, dizziness).

Physical examination: General examination focuses on vital signs and other indicators of shock or hypovolemia
(eg, tachycardia, tachypnea, pallor, diaphoresis, oliguria, confusion) and anemia (eg, pallor, diaphoresis). Patients
with lesser degrees of bleeding may simply have mild tachycardia (heart rate > 100). Orthostatic changes in pulse
(a change of > 10 beats/min) or BP (a drop of ≥ 10 mm Hg) often develop after acute loss of ≥ 2 units of blood.
However, orthostatic measurements are unwise in patients with severe bleeding (possibly causing syncope) and
generally lack sensitivity and specificity as a measure of intravascular volume, especially in elderly patients.

External stigmata of bleeding disorders (eg, petechiae, ecchymoses) are sought, as are signs of chronic liver
disease (eg, spider angiomas, ascites, palmar erythema) and portal hypertension (eg, splenomegaly, dilated
abdominal wall veins).

A digital rectal examination is necessary to search for stool color, masses, and fissures. Anoscopy is done to
diagnose hemorrhoids. Chemical testing of a stool specimen for occult blood completes the examination if gross
blood is not present.

Red flags:
Several findings suggest hypovolemia or hemorrhagic shock.

 Syncope

 Hypotension

 Pallor

 Diaphoresis

 Tachycardia

Medical Management

Airway: A major cause of morbidity and mortality in patients with active


upper GI bleeding is aspiration of blood with subsequent respiratory
compromise. To prevent these problems, endotracheal intubation should
be considered in patients who have inadequate gag reflexes or are
obtunded or unconscious—particularly if they will be undergoing upper
endoscopy.

Fluid resuscitation: IV fluids are initiated as for any patient with


hypovolemia or hemorrhagic shock\: healthy adults are given normal
saline IV in 500- to 1000-mL aliquots until signs of hypovolemia remit—up
to a maximum of 2 L (for children, 20 mL/kg, that may be repeated once).
Patients requiring further resuscitation should receive transfusion with
packed RBCs. Transfusions continue until intravascular volume is restored
and then are given as needed to replace ongoing blood loss. Transfusions in older patients or those with coronary
artery disease may be stopped when Hct is stable at 30 unless the patient is symptomatic. Younger patients or
those with chronic bleeding are usually not transfused unless Hct is < 23 or they have symptoms such as dyspnea
or coronary ischemia.

Platelet count should be monitored closely; platelet transfusion may be required with severe bleeding. Patients
who are taking antiplatelet drugs (eg, clopidogrel) have platelet dysfunction, often resulting in increased bleeding.
Platelet transfusion should be considered when patients taking these drugs have severe ongoing bleeding,
although a residual circulating drug (particularly clopidogrel) may inactivate transfused platelets. Fresh frozen
plasma should be transfused after every 4 units of packed RBCs.

Nursing Management
Preoperative care and teachings which would include removing jewelry, nail polish, make-up, bowel preparation,
supportive care, vital signs monitoring and administration of preoperative medications.

Insert a nasogastric tube if ordered pre-operatively. Although it is often inserted in the surgical site just prior to
surgery, the nasogastric tube may be placed preoperatively to remove secretions and empty stomach contents.

Postoperative care that would include: assessment of gastric drainage (initial drainage is bright red, clear or
greenish yellow in 2-3 days), maintain intravenous fluid while nasogastric suction is in place, monitor bowel
sounds and abdominal distention (bowel sounds: indicating resumption of peristalsis, distention: third-spacing,
obstruction, infection), resume oral food and fluids as ordered, encourage ambulation (to stimulate peristalsis).

Client with Gastrostomy or Jejunostomy Tube


1. Assess tube placement by aspirating stomach contents
2. Inspect the skin surrounding the insertion site for healing, redness, swelling, and the presence of any drainage.
3. Assess the abdomen for distention, bowel sounds and tenderness.
4. Until stoma is well healed, use sterile technique for dressing changes and site care.
5. Cleansing surgical site with saline or soap and water, patting it dry with a 4X4 gauze and allow air to dry
6. Irrigate the tube with 30-50ml of water, and clean the tube inside and out.
7. Provide mouth care or remind client to do so.

Surgical Management
When gastric cancer is identified prior to the development of metastasis, surgical removal of part or all of the
stomach and regional lymph nodes is the treatment of choice. Partial gastrectomy involves removal of a portion of
the stomach usually the distal half to two-thirds. In partial gastrectomy the surgeon constructs an anastamosis
from the reaminder of the stomach directly to the duodenum or to the proximal jejunum. The
gastroduodenostomy, or Billroth I, and the gastrojejunostomy, or BillRoth II, are commonly usued partial
gastrectomy procedures. A total gastrectomy, removal of the entire stomach, may be done for diffuse cancer that
is spread throughout the gastric mucosa but limited to the stomach. In a total gastrectomy, the surgeon constructs
an anastamosis from the esophagus to to the duodenum or jejunum. Total gastrectomy with esophageal
jejunostomy.

Sources:
Kelsen, D., et.al. (2002) Principles and Practice of Gastrointestinal Oncology 2nd Edition pp.693-699
Porth, C. (2005) Pathophysiology Concepts of Altered Health Status 7th Edition pp. 886-887
Tortora, G., Derrickson, B. (2006) Principles of Anatomy and Physiology 11th Edition pp. 911-913
Lemone P., Burke, K. (2004) Medical Surgical Nursing Critical Thinking in Client Care 3 rd Edition Volume 1
pp.556-571
Porter, R. (2004-2008) Merck Manual Online Edition: http://www.merck.com/mmpe/sec02/ch010/ch010a.html

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