GASTROINTESTINAL DISORDERS
Authors: Linda Anne Silvestri
Sandra M. Nettina
ANATOMY AND PHYSIOLOGY
Functions of the gastrointestinal system
Process food substances
Absorb the products of digestion into the blood
Excrete unabsorbed materials
Provide an environment for microorganisms to
Synthesize nutrients, such as vitamin K
For risk factors associated with the gastrointestinal system
Risk Factors Associated with the Gastrointestinal System
allergic reactions to food or medicationsCardiac, respiratory, and endocrine disorders that
may lead to slowed gastrointestinal (GI) movement or constipation
Chronic alcohol use
Chronic high stress levels
Chronic laxative use
Chronic use of aspirin or nonsteroidal anti-inflammatory drugs Diabetes mellitus, which
may predispose to oral candidal infections or other GI disorders
Family history of GI disorders
Long-term GI conditions, such as ulcerative colitis, that may predispose to colorectal
cancer
Neurological disorders that can impair movement, particularly with chewing and
swallowing
Previous abdominal surgery or trauma, which may lead to adhesions
Tobacco use
Mouth
Contains the lips, cheeks, palate, tongue, teeth, salivary glands, muscles, and maxillary bones
Saliva contains the enzyme amylase (ptyalin), which aids in digestion.
Esophagus
Collapsible muscular tube about 10 inches long
Carries food from the pharynx to the stomach
The Stomach
Contains the cardia, fundus, the body, and the pylorus
Mucous glands are located in the mucosa and prevent autodigestion by providing an alkaline
protective covering.
The lower esophageal (cardiac) sphincter prevents reflux of gastric contents into the esophagus.
The pyloric sphincter regulates the rate of stomach emptying into the small intestine.
Hydrochloric acid kills microorganisms, breaks food into small particles, and provides a chemical
environment that facilitates gastric enzyme activation.
Pepsin is the chief coenzyme of gastric juice, which converts proteins into proteases and
peptones.
Intrinsic factor is necessary for the absorption of vitamin B12.
Gastrin controls gastric acidity.
Small intestine
The duodenum contains the openings of the bile and pancreatic ducts.
The jejunum is about 8 feet long.
The ileum is about 12 feet long.
The small intestine terminates in the cecum.
Pancreatic intestinal juice enzymes
Amylase digests starch to maltose.
Maltase reduces maltose to monosaccharide glucose.
Lactase splits lactose into galactose and glucose.
Sucrase reduces sucrose to fructose and glucose.
Nucleases split nucleic acids to nucleotides.
Enterokinase activates trypsinogen to trypsin.
Large intestine
About 5 feet long
Absorbs water and eliminates wastes
Intestinal bacteria play a vital role in the synthesis of some B vitamins and vitamin K.
Colon: Includes the ascending, transverse, descending, and sigmoid colons and rectum
The ileocecal valve prevents contents of the large intestine from entering the ileum.
The anal sphincters control the anal canal.
Peritoneum
Lines the abdominal cavity and forms the mesentery that supports the intestines and blood
supply
Liver
The largest gland in the body, weighing 3 to 4 pounds
Contains Kupffer’s cells, which remove bacteria in the portal venous blood
Removes excess glucose and amino acids from the portal blood
Synthesizes glucose, amino acids, and fats
Aids in the digestion of fats, carbohydrates, and proteins
Stores and filters blood (200 to 400 mL of blood stored)
Stores vitamins A, D, and B and iron
The liver secretes bile to emulsify fats (500 to 1000 mL of bile/day).
Hepatic ducts
Deliver bile to the gallbladder via the cystic duct and to the duodenum via the common bile
duct.
The common bile duct opens into the duodenum, with the pancreatic duct at the ampulla of
Vater.
The sphincter prevents the reflux of intestinal contents into the common bile duct and
pancreatic duct.
Gallbladder
Stores and concentrates bile and contracts to force bile into the duodenum during the digestion
of fats
The cystic duct joins the hepatic duct to form the common bile duct.
The sphincter of Oddi is located at the entrance to the duodenum.
The presence of fatty materials in the duodenum stimulates the liberation of cholecystokinin,
which causes contraction of the gallbladder and relaxation of the sphincter of Oddi.
Pancreas
Exocrine gland
a. Secretes sodium bicarbonate to neutralize the acidity of the stomach contents that enter the
duodenum.
b. Pancreatic juices contain enzymes for digesting carbohydrates, fats, and proteins.
Endocrine gland
a. Secretes glucagon to raise blood glucose levels and secretes somatostatin to exert a
hypoglycemic effect.
b. The islets of Langerhans secrete insulin.
c. Insulin is secreted into the bloodstream and is important for carbohydrate metabolism.
DIAGNOSTIC PROCEDURES
Upper gastrointestinal tract study (barium swallow)
Examination of the upper gastrointestinal tract under fluoroscopy after the client.
Pre procedure:
NPO after midnight the day of the test
Post procedure
A laxative may be prescribed.
Instruct the client to increase oral fluid intake to help pass the barium.
Instruct the patient to increased oral fluid intake
Monitor stools for the passage of barium (stools will appear chalky white) because barium can
cause a bowel obstruction.
Lower gastrointestinal tract study (barium enema)
A fluoroscopic and radiographic examination of the large intestine is performed after rectal
instillation of barium sulfate.
The study may be done with or without air.
Pre procedure
A low-fiber diet is given for 1 to 2 days before the test.
A clear liquid diet and laxative are given the evening before the test.
NPO after midnight the day of the test cleansing enemas may be prescribed on the morning of
the test.
Post procedure
Instruct the client to increase oral fluid intake to help pass the barium.
Administer a mild laxative as prescribed to facilitate emptying of the barium.
Monitor stools for the passage of barium.
Notify the physician if a bowel movement does not occur within 2 days.
Gastric Analysis
Requires the passage of the NGT into the stomach to aspirate gastric contents for the analysis of
acidity (pH), appearance, and volume; the entire gastric contents are aspirated, and then
specimens are collected every 15 minutes for 1 hour.
Histamine or pentagastrin may be administered subcutaneously to stimulate gastric secretions;
these medications may produce a flushed feeling.
Esophageal reflux of gastric acid may be diagnosed by ambulatory pH monitoring; a probe is
placed just above the lower esophageal sphincter and connected to an external recording
device. It provides a computer analysis and graphic display of results.
Pre procedure
Fasting for 8 to 12 hours is required before the test.
Use of tobacco and chewing gum are avoided for 6 hours before the test.
Medications that stimulate gastric secretions are withheld for 24 to 48 hours.
Post procedure
Client may resume normal activities.
Refrigerate gastric samples if not tested within 4 hours.
Upper gastrointestinal Fiberoscopy
Also known as esophagogastroduodenoscopy b. Following sedation, an endoscope is passed
down the esophagus to view the gastric wall, sphincters, and duodenum; tissue specimens can
be obtained.
Pre procedure
The client must be NPO for 6 to 12 hours before the test.
A local anesthetic (spray or gargle) is administered along with medication that provides
conscious sedation and relieves anxiety, such as intravenous (IV) midazolam (Versed), just
before the scope is inserted.
Atropine sulfate may be administered to reduce secretions, and glucagon may be
administered to relax smooth muscle.
Client is positioned on the left side to facilitate saliva drainage and to provide easy access of
the endoscope.
Airway patency is monitored during the test and pulse oximetry is used to monitor oxy- gen
saturation; emergency equipment should be readily available.
Post procedure
Client must be NPO until the gag reflex returns (1 to 2 hours).
Monitor for signs of perforation (pain, bleeding, unusual difficulty swallowing, elevated
temperature).
Maintain bed rest for these dated client until alert.
Lozenges, saline gargles, or oral analgesics can relieve a minor sore throat (not given to the client
until the gag reflex returns).
Anoscopy, proctoscopy, and sigmoidoscopy
Anoscopy requires the use of a rigid scope to examine the anal canal; the client is placed in the
knee-chest or left lateral position.
Proctoscopy and sigmoidoscopy require the use of a flexible scope to examine the rectum and
sigmoid colon; the client is placed on the left side with the right leg bent and placed anteriorly.
Biopsies and polypectomies can be performed.
Pre procedure
Enemas are administered to cleanse the bowel.
Post procedure
Monitor for rectal bleeding and
Signs of perforation and peritonitis
a. Guarding of the abdomen
b. Increased fever and chills
c. Pallor
d. Progressive abdominal distention and abdominal pain Restlessness
e. Tachycardia and tachypnea
Some specimens require that a certain diet be followed or that certain medications be with-
held; check agency guidelines regarding specific procedures.
Urea breath test
The urea breath test detects the presence of Helicobacter pylori, the bacteria that cause peptic
Ulcer disease.
The client consumes a capsule of carbon-labeled urea and provides a breath sample 10 to 20
minutes later.
Certain medications may need to be avoided before testing; these may include antibiotics or
bismuth subsalicylate (Pepto-Bismol) for 1 month before the test; sucralfate (Carafate) and
omeprazole (Prilosec) for 1 week before the test; and cimetidine (Tagamet), famotidine (Pepcid),
ranitidine (Zantac), or nizatidine (Axid) for 24 hours before breath testing.
H. pylori can also be detected by assessing serum antibody levels.
Liver biopsy
A needle is inserted through the abdominal wall to the liver to obtain a tissue sample for biopsy
and microscopic examination.
Pre procedure
Assess results of coagulation tests (prothrombin time, partial thromboplastin time, plate- let
count).
Administer a sedative as prescribed.
Note that the client is placed in the supine or left lateral position during the procedure to expose
the right side of the upper abdomen.
Post procedure
Assess vital signs.
Assess biopsy site for bleeding. Position: Right -side lying position to place pressure on the area
of biopsy, preventing bleeding.
GASTROINTESTINAL DISORDERS
INFLAMMATORY BOWEL DISEASE
Is an idiopathic disease caused by a dysregulated immune response to host intestinal microflora.
It results from a complex interplay between genetic and environmental factors. Similarities
involve (1) chronic inflammation of the alimentary tract and (2) periods of remission
interspersed with episodes of acute inflammation. There is a genetic predisposition for IBD, and
patients with this condition are more prone to the development of malignancy.
The two major types of inflammatory bowel disease are ulcerative colitis (UC) and Crohn disease (CD).
ULCERATIVE COLITIS (UC): A chronic condition of unknown cause usually starting in the rectum
and distal portions of the colon and possibly spreading upward to involve the sigmoid and
descending colon or the entire colon. It is usually intermittent (acute exacerbation with long
remissions), but some individuals (30%–40%) have continuous symptoms. Cure is affected only
by total removal of colon and rectum/rectal mucosa.
It Is also an inflammatory disease of bowel that results in poor absorption of nutrients.
This condition causes long-lasting inflammation and sores (ulcers) in the innermost lining of your
large intestine (colon) and rectum.
Both ulcerative colitis and Crohn’s disease usually involve severe diarrhea, abdominal pain,
fatigue and weight loss.
Figure 28: Colon and Rectum
PATHOPHYSIOLOGY AND ETIOLOGY OF ULCERATIVE COLITIS
The exact cause of ulcerative colitis is UNKNOWN. Possible theories include:
Genetic predisposition.
Environmental factors may trigger disease (viral or bacterial pathogens, dietary).
Immunologic imbalance or disturbances
Detect intestinal barrier causing hypersensitive mucosa and increased permeability.
Defect repair of mucosal injury, which may develop into a chronic condition.
Multiple crypt abscesses develop in intestinal mucosa that may become necrotic and lead to
ulceration.
Most common in young adulthood and middle life, peak incidence at 20 – 40 years of age.
Incidence greatest in Caucasians of Jewish descent.
Risk factors
Age. Most people who develop IBD are diagnosed before they’re 30 years old. But some people
don’t develop the disease until their 50s or 60s.
Race or ethnicity. Although whites have the highest risk of the disease, it can occur in any race. If
you’re of Ashkenazi Jewish descent, your risk is even higher.
Family history. You’re at higher risk if you have a close relative — such as a parent, sibling or child
— with the disease.
Cigarette smoking. Cigarette smoking is the most important controllable risk factor for
developing Crohn’s disease. Although smoking may provide some protection against ulcerative
colitis, the overall health benefits of not smoking make it important to try to quit.
Nonsteroidal anti-inflammatory medications. These include ibuprofen (Advil, Motrin IB, others),
naproxen sodium (Aleve), diclofenac sodium (Voltaren) and others. These medications may
increase the risk of developing IBD or worsen disease in people who have IBD.
Where you live. If you live in an industrialized country, you’re more likely to develop IBD.
Therefore, it may be that environmental factors, including a diet high in fat or refined foods, play
a role. People living in northern climates also seem to be at greater risk.
Clinical manifestations
Diarrhea – maybe blood or contain pus and mucus.
Tenesmus (painful straining), sense of urgency, and frequency.
Increased bowel sounds; abdomen may appear flat, but, as condition continues, abdomen may
appear distended.
There more often is weight loss, fever, dehydration, hypokalemia, anorexia, nausea and
vomiting, iron deficiency anemia, and cachexia (general lack of nutrition and wasting with
chronic disease).
Crampy abdominal pain
The disease usually begins in the rectum and sigmoid and spreads proximally, at times, involving
the entire colon. Anal area maybe irritated and reddened; left lower abdomen may be tender on
palpation.
There is a tendency for the patient to experience remission and exacerbations.
Increased risk of developing colorectal cancer.
May inhibit extracolonic manifestation of eye, joint, and skin complaints.
DIAGNOSTIC EVALUATION
Diagnosis is based on a combination of laboratory, radiologic, endoscopic, and histologic findings.
Laboratory Tests
Stool examination – to rule out enteral pathogens; fecal analysis positive for blood during active
disease.
Complete blood count - hemoglobin and hematocrit may be low due to bleeding; WBC may
increase.
Increased prothrombin time possible.
Elevated ESR erythrocyte sedimentation rate.
Decrease serum level of potassium, magnesium, and albumin may be present.
Other diagnostic test
Barium enema – to assess extent of disease and detect psuedopolyps, carcinoma, and strictures,
may show haustral markings, narrow, lead – pipe appearance; superficial ulceration.
Flexible proctosigmoidoscopy/colonoscopy findings reveal mucosal erythema and edema, ulcers,
inflammation that begin distally in the rectum and spreads proximally for variable distances.
Psuedopolyps and friable tissue may be present.
Changes in crypt height, loss of crypts, crypt abscess with neutrophils infiltrates on biopsy.
MEDICAL MANAGEMENT
Drug therapy
1. 5 – aminosalicylic acid – sulfasalazine (Azulfidine) – main stay drug for acute and maintenance
therapy, dose related side effects include vomiting, anorexia, headache, skin discoloration,
dyspepsia, and lowered sperm count.
2. Oral salicylates, such as mesalamine (Pentasa), olsalazine (Dipentum) – appear to be as effective
as sulfasalazine and are used when patients are allergic to sulfa.
Nephrotoxicity can occur with mesalamine; diarrhea; with olsalazine.
3. Mesalamine enema available for proctosigmoiditis; suppository for proctitis.
4. Corticosteroids – primary agent used in the management of inflammatory disease. Should be
treated concomitantly with 5 – aminosalicylic acid preparations to benefit from their potential
steroid sparring effects. Corticosteroids must be prepared slowly over 6 – 8 weeks period;
Prednisolone (Delta – cortef) IV, to induce remission of acute severe disease.
Prednisone (Orsone) – orally, for moderate to severe disease.
Hydrocortisone (Corftef) – enema used for proctitis and left sided colitis.
5. Immunosuppressive drugs – purine analogues, 6 mercaptopurine, azathioprine may be indicated
when patient is refractory or dependent or corticosteroids.
6. Antidiarrheal medications may be prescribed to control diarrhea, rectal urgency and cramping,
abdominal pain; not routinely ordered – treat with caution.
SURGICAL INTERVENTIONS
1. Total Proctocolectomy with permanent ileostomy
a. The procedure is curative and involves the removal of the entire colon (colon, rectum,
and anus with anal closure).
b. The end of the terminal ilium forms the stoma, which is located in the right lower
quadrant.
2. Kock ileostomy (continent ileostomy)
a. The Kock ileostomy is an intraabdominal pouch that stores the feces and is constructed
from the terminal ilium.
b. The pouch Is connected to the stoma with a nipple like valve constructed from a portion
of the ileum. The stoma is flush with the skin.
c. A catheter Is used to empty the pouch, and a small dressing or adhesive bandage of
worn over the stoma between emptying’s.
3. Ileoanal reservoir
a. Creation of an ileoanal reservoir is a two stage procedure that involves the excision of
the rectal mucosa, an abdominal colectomy, construction of a reservoir to the anal canal,
and a temporary loop ileostomy.
b. The ileostomy is closed 3 – 4 month after the capacity of the reservoir is increase and
has had time to heal.
4. Ileoanal anastomosis
a. Does not require and ileostomy
b. A 12 – to 15 cm rectal stump is left after the colon is removed, and the small intestine is
inserted into this rectal sleeve anastomosed.
c. Ileorectostomy requires a large, compliant rectum.
5. Preoperative colostomy and ileostomy interventions.
a. Consult with enterostomal therapist to assist in identifying optimal placement of the
ostomy.
b. Reinforce instructions to eat a low – fiber diet for 1 – 2 days before surgery as
prescribed.
c. Administer intestinal antiseptic and antibiotics of prescribed to cleanse the bowel and to
decrease the bacterial content of the colon.
d. Administer laxative and enemas as prescribe.
6. Postoperative colostomy interventions.
a. Place petrolatum gauze over the stoma as prescribe to keep moist, followed by a dry,
sterile dressing if a pouch (external) system is not in place.
b. Place a pouch system on the stoma as soon as possible.
c. Monitor the stoma for size, unusual bleeding, or necrotic tissue.
d. Monitor for color changes in the stoma.
e. Note that the normal stoma color is PINK to BRIGHT RED and SHINY, indicating highly
vascularity.
f. Note the a pale pink stoma indicates low hemoglobin and hematocrit levels, and a
purple – black stoma indicates compromised circulation, requiring health care
practitioner notifications.
g. Monitor the functioning of the colostomy and check for bowel sounds
h. Expect that the stool is liquid in the immediate postoperative period but becomes more
solid, depending on the area of the colostomy; ascending colon – liquid; transverse colon
– loose to semiformed; and descending colon – close to normal.
i. Monitor the pouch system for proper fit and signs of leakage.
j. Empty the pouch when it is one third full.
k. Fecal matter should not be allowed on the skin.
l. Administer analgesics and antibiotics as prescribed.
m. Assist to irrigate the perineal wound (if present) as prescribed, and monitor for signs of
infection.
n. Reinforce instructions about the stoma care and irrigations.
Colostomy Irrigation
Purpose: an enema is given through the stoma to stimulate bowel emptying.
Description: irrigation is performed by instilling 500 – 1000 ml of Luke warm tap water through
the stoma and allowing the water and stool drain into a collection of bag.
Procedure:
o If ambulatory, position the client sitting on the toilet
o If on bed rest, position the client on his or her side
o Hang the irrigation bag so that the bottom of the bag is level of the client shoulder or
slightly higher.
o Insert the irrigation tube carefully without force.
o Clamp the tubing if cramping occurs; release the tubing as cramping subside.
o Avoid frequent irrigations, which can lead to loss of fluid and electrolytes.
o Perform irrigation at about the same time each day.
o Perform irrigation preferably 1 hour after a meal.
o To enhance effectiveness of the irrigation, massage the abdomen gently.
o. Reinforce instruction that normal activities may be resumed when approved by the
health care provider.
7. Post-operative ileostomy interventions.
Note that normal stool is liquid.
Monitor for dehydration and electrolyte imbalance.
NURSING INTERVENTIONS
1. Acute phase: Maintain NPO status and assist to administer fluids and electrolytes intravenously
or via parenteral nutrition as prescribed.
2. Restrict the client activity to reduce intestinal activity.
3. Monitor bowel sounds and for abdominal tenderness and cramping.
4. Monitor stool, noting color, consistency, and the presence or absence of blood.
5. Monitor for bowel preparation, peritonitis, and hemorrhage.
6. Following the acute phase, the diet progresses from clear liquid to low – fiber diet; usually a low
fiber is tolerated.
7. Reinforce instruction about diet; usually a low fiber, high – protein diet with vitamins and iron
supplements is prescribe.
8. Reinforce instruction to avoid gas – forming foods, milk products, and food such as whole- wheat
grains, nuts, raw fruits and vegetable, pepper, alcohol, and caffeine containing products.
9. Reinforce instruction to avoid smoking.
10. Administer medication as prescribed, which may include a combination of medications such as
salicylate compounds, corticosteroids, immunosuppressants and antidiarrheal.
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