My Study Guide!
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PEPTIC ULCER DISEASE
(PUD)
What is it?
PUD is a condition characterized by erosion of the GI mucosa resulting from the
digestive action of HCl acid and pepsin. It involves ulceration, circumscribed breaks in
the mucosa, occurring in the duodenum (duodenal ulcers), the stomach (gastric ulcers),
and less commonly, the distal esophagus and the jejunum. PUD develops only in an acid
environment. Patients with pernicious anemia and achlorhydria rarely have gastric
ulcers. People with gastric ulcers have normal to less than normal gastric acidity
compared to people with duodenal ulcers. Still, some intraluminal acid would seen to be
necessary for a gastric ulcer to occur.
Risk Factors-Smoking, aspirin, spicy foods, stress, Emphysema, rheumatoid arthritis,
cirrhosis, etc.
Often asymptomatic!
Duodenal Ulcers-When pain does occur, it is described as “burning” or “cramplike”.
Most often located in the midepigastric region beneath the xyphoid process.
Gastric Ulcers-Pain described as “burning” or “gaseous”. Located high in the
epigastrium.
Physiologic Stress Ulcers-Acute ulcers. Develop during a major physiological
insult such as trauma or surgery.
Peak incidence for duodenal ulcers is between the ages of 25-30 and for gastric ulcers,
those older than 50 years.
EtiologyThought to result from Helicobacter pylori (H pylori) infection. Other factors are related
to gastric acid secretion like:
 Altered gastric acid and serum gastrin levels
 Tobacco smoking and alcohol use
 Use of aspirin, other nonsteroidal anti-inflammatory drugs, and corticosteroids
 Genetic predisposition
 Psychosomatic or psychological factors (chronic anxiety, Type A personality)
Comparison:
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Gastric Ulcers-Less Common
Lesion
Location
Gastric Secretion
Incidence
Superficial, smooth margins:
Round, oval, cone-shaped
Usually antrum. Also in body and
fundus of stomach.
Normal to ↓ secretion
Greater in women
Peak age 50-60
More common in lower
socioeconomic status & unskilled
laborers.
↑ with smoking, drug and alcohol
use.
↑ with incompetent pyloric
sphincter and bile reflux.
↑ with stress ulcers after severe
burns, head trauma, major
surgery.
Clinical manisfestations
Burning, gaseous pressure in high
left epigastrium and back and
upper abdomen.
Pain 1-2 hours after meals. If
penetrating ulcer, aggravating
of discomfort with food.
Occasional nausea and vomiting,
weight loss.
Recurrence rate
Complications
High
Hemorrhage, perforation, outlet
obstruction, intractability.
Aspirin, corticosteroids,
NSAIDS(ibuprofen, Serpasil)
Possible/probable culprits?
Duodenal Ulcers-More
Common
Penetrating 
First 1-2 cm of the duodenum.
↑ secretion
Greater in men-Increasing in
women (postmenopausal)
Peak age 35-45
Associated with psychological
stress.
↑ with smoking, drug and alcohol
use.
Assoc. with other diseases
(COPD, Pancreatic disease,
hyperparathyroidism, ZollingerEllison syndrome, chronic renal
failure.
More often in Type O blood!
Burning, cramping, pressure-like
pain across mid-epigastrium and
upper abdomen. Back pain with
posterior ulcers.
Pain 2-4 hours after meals and
midmorning. Sometimes in the
midafternoon, middle of the
night, periodic or episodic.
Pain relief with antacids and
food. Occasion nausea and
vomiting.
High
Hemorrhage, perforation,
obstruction.
H pylori, genetics, People with
Type O have ↑ incidence.
Complications!! 
Hemorrhage-Most common. Develops from erosion of the granulation tissue found at the
base of the ulcer during healing or from erosion of the ulcer through a major blood
vessel. Duodenal ulcers account for most of these.
 Take VS every 15-30 minutes. Maintain IV infusion.
 Monitor HCT and HGB.
 Record I & O.
 Prepare patient for possible endoscopy or surgery.
Perforation-The most lethal complication. Most commonly seen in large penetrating
duodenal ulcers that have not healed and are located on the posterior mucosal wall. Most
often located on the lesser curvature of the stomach. The size of the perforation depends
on how long the patient has had the ulcer. Sometimes spontaneous sealing occurs. This is
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from large amounts of fibrin being produced and leads to fibrinous fusion of the
duodenum or gastric curvature to adjacent tissue, most often the liver. OUCH!!
How can you tell this has occurred? Sudden and dramatic onset! The patient
experiences sudden, severe upper abdominal pain that quickly spreads throughout the
abdomen. The abdomen muscles contract, appearing rigid and boardlike. The patient’s
respirations become shallow and rapid. Bowel sounds are usually absent. Referred pain.
Drawing up of knees. Nausea and vomiting mayyyy occur, but not necessarily. Bacterial
peritonitis may occur in 6-12 hours!!
 Need to stop the spillage of gastric or duodenal contents into the peritoneal cavity
and restore blood volume. NG tube to provide continuous aspiration and
gastric decompression. Replace blood volume with lactated Ringer’s and
albumin solutions.
 If patient has history of cardiac disease, ECG monitoring or pulmonary artery
catheter. Broad-spectrum antibiotic therapy.
 Pain Meds.
Gastric Outlet Obstruction-If the ulcers are located in the antrum and the prepyloric and
pyloric areas of the stomach and duodenum, this can occur. In the early phase, gastric
emptying is normal or near normal. The patient usually has a long history of ulcer pain. If
the ulcer pain is of short duration or if there is complete absence of pain, this is more
indicative of malignant obstruction. Pain worse at end of day as the stomach fills and
dilates. Sometimes relief via belching or self-induced vomiting (with food particles from
even the meal the day before!). There is often an offensive odor (after all, the food is
old!) The patient who vomits a lot will be anorectic with evident weight loss. Will
probably complain of thirst and a bad taste in the mouth. Constipation is also a common
complaint. The patient may show a swelling in the upper abdomen. Loud peristalsis can
be heard with visible peristaltic waves.
 If patient is NPO, check patency of NG tube. Reposition patient from side to side.
 Decompress the stomach! Correct fluid and electrolyte imbalances. Measure
gastric residue periodically. Clamp the tube overnight for 8-12 hours; measure
gastric residue in the morning. If aspirate below 200 ml, normal. Patient can
resume oral intake. (Begin oral liquids at 30 ml/hour). Pain relief
 Pyloric obstruction treated nonsurgically by balloon dilations via an endoscope.
 H2R blockers, PPIs.
 A lot of vomiting = ALKALOSIS! Watch that!
How to Diagnose? (Besides H & PE)
Endoscopy! Most often used. Upper GI.
H.Pylori testing. (Breath, urine, blood, tissue)
Upper GI Barium Contrast-(Really kewl to check for gastric ulcer obstruction)
CBC-(Anemia?)
Urinalysis
Liver Enzymes-(Liver probs like cirrhosis?)
Serum Electrolytes
Maybe a serum amylase test to check pancreatic function.
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How to Treat?
Goal is to maintain mucosa, elevate pH, inactivate pepsin, and relieve pain!
Patient needs adequate rest, dietary modifications, drug therapy, elimination of smoking,
and long-term follow-up care. Aim is to decrease gastric acidity. Requires many weeks of
therapy in ambulatory setting. Pain may disappear quickly but ulcer healing is slower.
Find out if the ulcer is healed via x-ray or endoscopic exam. Eliminate stressors!
Food! Food! Food!
Bland diets are best-Six small meals a day. Eliminate alcohol and caffeine-containing
products. Foods known to upset: hot, spicy foods and pepper, alcohol, carbonated
beverages, tea, coffee, and even broth from meat extract. Foods high in roughage like
raw fruit, salads, and vegetables, may irritate! However, if well chewed, seldom a
problem.
Protein-Good neutralizing food. However, it stimulates gastric secretions. Carbs and fats
are the least stimulating to HCl acid but do not neutralize well.
Milk is okay for PUD.
Drug therapy-Meds remove excess hydrogen ions so less chance of tissue injury. HCO
secreted by mucosa helps neutralize acid. Think buffer here.
Acute exacerbation? If recurrent vomiting or gastric outlet obstruction, place NG tube in
stomach with intermittent suction for 24-48 hours.
Replace fluids and electrolytes via IV until oral feedings tolerated.
May need transfusion.
5-year follow-up program recommended after acute exacerbation.
SURGERY!!
Less than 20% patients need surgery.
Why need it?
 Intractability-when an ulcer fails to heal or comes back after therapy.
 History of hemorrhage or increased risk of bleeding during treatment.
 Prepyloric or pyloric ulcers because of their high recurrence rates.
 Concurrent conditions (burns, trauma, sepsis)
 Multiple ulcer sites.
 Drug-induced ulcers.
 Possibility of malignant ulcer.
 Obstruction.
What kinds?
Partial gastrectomy, vagotomy, pyloroplasty?
Great picture of these on Page 1041!
Vagotomy-The severing of the vagus nerve. Can be total (truncal) or selective. In a
truncal Vagotomy both the anterior and posterior trunks are severed. In a selective
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Vagotomy, a nerve is cut at a particular branch of the vagus nerve, resulting in
denervation of only a portion of the stomach, such as the antrum or the parietal cell mass.
This decreases gastric motility and gastric emptying.
Pyloroplasty-This consists of surgical enlargement of the pyloric sphincter to facilitate
the easy passage of contents from the stomach. Most commonly done after Vagotomy or
to enlarge an opening that is constricted from scar tissue. If done with a Vagotomy, it
increases gastric emptying.
Billroth I-AKA Gastroduodenostomy-Partial gastrectomy with removal of the
distal 2/3 of the stomach and anastomosis of the gastric stump to the duodenum.
Billroth II-AKA Gastrojejunostomy-Partial gastrectomy with removal of the
distal 2/3 of the stomach and anastomosis of the gastric stump to the jejunum. The
preferred surgical procedure because the duodenum is bypassed.
The antrum and pylorus are removed in both procedures.
NOTE: With partial removal of the stomach, you lose intrinsic factor! This means
pernicious anemia! Will probably require life-long B12 (cobalamin) injections.
Post-Op complications: 
Dumping Syndrome-It is the direct result of surgical removal of a large portion of the
stomach and the pyloric sphincter. Reduced reservoir capacity of the stomach. More
common after Billroth II procedure.
Associated with meals having a hyper-osmolar composition. Stomach can’t control the
amount of gastric chyme entering the small intestine. Because of this, a large bolus of
hypertonic fluid enters the intestine and causes fluid to be drawn into the bowel lumen,
creating a decrease in plasma volume.
Symptoms usually occur 15-30 minutes after a meal. Patient usually feels weak, sweaty,
may have palpitations and dizziness. This is because of the sudden decrease in plasma
volume. The patient may complain of abdominal cramps, borborygimi (loud abdominal
sounds like we’re often annoyed with while in a quiet classroom!), and the urge to
defecate. Symptoms usually last an hour after a meal; no longer.
Postprandial hypoglycemia-A variant of the dumping syndrome. The result of
uncontrolled gastric emptying of a bolus of fluid high in carbs into the small intestine.
Hypoglycemic-like symptoms.
Bile reflux gastritis-Prolonged exposure to bile=Damage to gastric mucosa. Can
actually CAUSE peptic ulcer! May result in back diffusion of hydrogen ions through
the gastric mucosa. Give cholestyramine (Questran) either before or with meals.
Sometimes aluminum hydroxide antacids too!
Post-Op foods?
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No fluids with meals!
Dry foods with low-carb content.
Moderate protein and fats.
If hypoglycemic, fluids or candy.
Limit the amount of sugar in meals.
Eat small, frequent meals.
Post-Op Care?
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NG tube for decompression. Check patency!!
Observe gastric aspirate-May be bright red at first with gradual darkening within
first 24 hours after surgery.
Color changes to yellow-green in about 36-48 hours.
Observe for decreased peristalsis. Absent bowel sounds?
Lower abdominal discomfort? Obstruction?
Monitor I & O, VS.
Ambulation encouraged.
Notes on the Elderly
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Increased use of NSAIDS that may cause PUD.
Pain may not be the first symptom!
May be frank gastric bleeding or a decrease in hematocrit! [Norm:Male-41.5%
to 50.4%. Female-35.9% to 44.6%]
Morbidity and mortality rates higher-Decreased ability to withstand hypovolemiaChronic illnesses (CV, Pulmonary)
Treatment and management about the same as in the younger folks.
Other Problems-
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Gastritis
Esophagitis
Bezoars-Hard mass of tangled stuff. Ewwwwww
GU Quickees!
Appendicitis-Inflammation of the appendix, a narrow blind tube that extends from the
inferior part of the cecum. More common in males than females. Most common cause is
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obstruction of the lumen by a fecalith (a piece of poop, for goodness sake!). Can also be
obstructed by foreign bodies, tumor of the cecum or appendix, or intramural thickening
caused by hypergrowth of lymphoid tissue. Thus, distention, venous engorgement,
accumulation of mucus and bacteria…..Gangrene and perforation! Pain!!!
 Periumbilical pain followed by nausea, vomiting. Anorexia.
 Pain persistent and continuous, localized at McBurney’s point.
 Localized tenderness, rebound tenderness, muscle guarding.
 Rovsing’s sign from palpation of the LLQ causing pain to be felt in the RLQ.
 Complications are perforation, peritonitis, abscesses.
Need complete history and PE, differential WBC count, urinalysis to rule out GU probs.
Need immediate surgical removal! Appendectomy time!
Peritonitis-Results from localized or generalized inflammatory process in the
peritoneum. Primary causes are blood-borne organisms, genital tract organisms,
cirrhosis with ascites. Secondary causes are appendicitis with rupture, blunt or
penetrating trauma, diverticulitis with rupture, Ischemic bowel disorders, obstruction in
the GI tract, pancreatitis, perforated peptic ulcer, peritoneal dialysis, post-op (breakage of
anastomosis).
S & S/Tests:
 Severe localized or diffuse abdominal pain.
 Paralytic ileus. Bowel sounds decreased or absent.
 Fever, tachycardia, chills (sepsis?)
 Shallow, guarded respirations.
 Dehydration and ACIDOSIS, late manisfestations.
 WBC count (leukocytosis, leukopenia)
 Radiograph, Peritoneoscopy(endoscope via a stab wound in the abdomen)
 Treat with antibiotics, NG suction, analgesics, IV fluids, Surgery. May need TPN.
Life-threatening complications include bowel obstruction, renal failure, respiratory
insufficiency, shock, and in some cases, liver failure.
Gastroenteritis-Inflammation of the mucosa of the stomach and small intestine. Nausea,
vomiting, diarrhea, abdominal cramping, distention. May see fever, ↑ WBC, blood or
mucus in the stool. Patient will need to be NPO until vomiting stops. Will need IV
replacement. Afterwards, foods with glucose and electrolytes (Pedialyte?).
Inflammatory Bowel Disease-Crohn’s disease and ulcerative colitis. These disorders are
characterized by chronic, recurrent inflammation of the intestinal tract. Cause remains
unknown.
Gastroesophageal Reflux Disease (GERD)-Excessive reflux of HCl acid into the
esophagus. Incidence increases with age. Usually results from an incompetent LES,
pyloric stenosis, or motility disorder. Associated with Hiatal Hernia.
S & S-
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Pyrosis
Regurgitation of sour-tasting secretions (BLECHHH!)
Dysphagia (difficulty swallowing) and odynophagia (pain on swallowing).
Symptoms sometimes mimic a heart attack!
Treatment Meds (antacids, H2-receptor antagonists, PPIs)
 Low-fat, high-fiber diet.
 Avoid spicy or acidic foods. No alcohol, caffeine, tobacco.
 Avoid food and drink 2 hours before bedtime. No lying down right after eating.
 Elevate the head of the bed on 6- to 8- inch blocks.
 Lose weight if obese.
 If symptoms persist, surgical repair! (fundoplication)
Portal Hypertension-Characterized by increased venous pressure in the portal
circulation, as well as splenomegaly, large collateral veins, ascites, systemic
hypertension, and esophageal varices. Elevated pressure in the portal vein associated with
increased resistance to blood flow through the portal venous system. Incidence is similar
to that for cirrhosis.
 Ascites
 Shifting dullness or fluid wave on abdominal percussion.
 Dilated abdominal vessels radiating from the umbilicus.
 Enlarged, palpable spleen.
 Bruits detected over the upper abdominal area.
Treatment Meds (may include diuretics)
 Measure and record abdominal girth (ascites!)
 Elevate lower extremities, wear support hose
 Give salt-poor albumin to raise serum albumin level. This increases serum
osmotic pressure, helping to reduce edema by causing ascitic fluid to go back to
the bloodstream so it can be eliminated by the kidneys.
 May need paracentesis (removal of fluid)
 May need peritoneojugular (LaVeen) shunting. Not used often.
Intestinal tubes used for decompression!
Harris Tube-aspirating holes, black silk tie
Miller-Abbott Tube-Double lumen
Cantor tube-aspirating holes
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Define
Pyrosis-Heartburn
Eructation-Belching :-\
Steatorrhea-Bulky, foul-smelling, yellow-gray, greasy stools with putty-like
consistency; float in water. Ewwwww 
Diverticulosis/Diverticulitis
A diverticulum is a saccular dilation our outpouching of the mucosa through the circular
smooth muscle of the intestinal wall. Occurs in two forms: diverticulosis and
diverticulitis.
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Diverticulosis-develops in about 50% of persons over age 60. Occurs when there is
multiple diverticula without inflammation or symptoms. Patient usually asymptomatic.
Diverticulitis-Condition involving inflammation of the diverticula. Occurs when food or
bacteria becomes trapped in the diverticula. Change in bowel habits, dull pain in the
abdominal LLQ or the epigastrium, rectal bleeding, anorexia, low-grade fever,
constipation, flatulence.
The sigmoid colon is the most common site for diverticulitis. Stools may be narrow
(remember, those sacs can distort!).
From increased intraluminal pressure (decreased bulk of the stool, more narrowed lumen)
from factors such as a low-fiber diet, chronic constipation, and obesity.
Complications of diverticular diseaseAcute-hemorrhage, perforation, periodic abscess, general peritonitis, local suppuration,
fistula.
Chronic-pericolic abscess, stricture, fistula, local suppuration, intestinal obstruction,
perforation, etc.
BLEEDING-A common complication. Manifested by hematochezia (maroon stools).
Usually stops spontaneously.
Tests
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CBC (↑ WBC level and elevated sed rate)
Colonoscopy
Barium enema
A tender, LLQ mass may be palpated.
Treatment High-fiber diet and bulk laxatives (Metamucil?)
 Anticholinergic drugs (Bentyl, Donnatal).
 Increased fluids
 Reduction in weight, if obese.
 No tight clothing, straining during BM, bending, lifting, vomiting
 ALLOW THE COLON TO REST so inflammation can subside.
 NPO, bed rest, parenteral fluids; maybe NG tube.
 If acute, broad-spectrum antibiotics.
 May need temporary diversional colostomy.
 No foods with little seeds (popcorn, strawberries, etc)
Hiatal Hernia
It is a herniation of a portion of the stomach into the esophagus through an opening, or
hiatus, in the diaphragm. Also referred to as diaphragmatic hernia and esophageal
hernia.
Occur more often in women than in men! Exact cause unknown.
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Types
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Sliding-The junction of the stomach and esophagus is above the hiatus of the
diaphragm, and a part of the stomach slides through the hiatal opening in the
diaphragm. The stomach “slides” into the thoracic cavity when the patient is
supine and usually goes back into the abdominal cavity when the patient is
standing up. This is the most common type.
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Paraesophageal or Rolling-The esophagogastric junction remains in the normal
position, but the fundas and the greater curvature of the stomach roll up through
the diaphragm, forming a pocket alongside the esophagus.
What causes it? Signs of it?
Exact cause is unknown.
 Structural changes may contribute: Weakening of the muscles in the diaphragm
around the esophagogastric opening.
 Obesity, pregnancy, ascites, tumors, tight corsets, intense physical exertion, heavy
lifting on a continual basis. (Weightlifters, Beware!)
 Also, increasing age, trauma, poor nutrition, forced recumbent position (when
prolonged illness keeps a person in bed)
 Persons may be asymptomatic. Symptoms may be a lot like GERD. Heartburn
is a classic symptom.
 Symptoms may also mimic gallbladder disease, PUD, and angina.
 Reflux often associated with position, occurring soon or several hours after laying
down.
 Bending over may cause a severe burning pain.
Complications:
 GERD
 Hemorrhage from erosion.
 Stenosis (narrowing of the esophagus)
 Ulcerations of the herniated portion of the stomach.
 Strangulation of the hernia
 Regurgitation with tracheal aspiration.
 Patients with hiatal hernias are more at risk for hospitalization for
respiratory disease!
Diagnosis Barium swallow
 Endoscopic visualization
 Monitoring of pH.
 Motility studies
 Fluoroscopy, X-rays
Treatment-
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Conservative therapy similar to that of GERD.
Reduction of intraabdominal pressure by eliminating constricting garments,
avoiding lifting and straining, eliminating alcohol and smoking, elevating the
head of the bed.
The use of antacids and antisecretory agents (PPIs and H2R blockers)
Don’t want to use anticholinergics because they relax the esophageal
sphincter.
Elevate the head of the bed on 4- to 6- inch blocks to assist gravity (prevent
reflux and tracheal aspiration.)
Eliminate caffeine-containing beverages and chocolate.
Surgical Therapy Nissen fundoplication
 Toupet fundoplication
 Hill gastropexy
 Belsey fundoplication.
 These procedures are all variations of fundiplication which involves wrapping
the fundus of the stomach around the lower portion of the esophagus in
varying positions. These procedures reduce the hernia, provide and acceptable
LES pressure, and prevent movement of the gastroesophageal junction.
 Usually laparoscopic. May also be done thoracic or open abdominal.
Cholecystitis and Cholelithiasis
Cholecystitis-Acute or chronic inflammation of the gallbladder. Acute may be
calculous (with gallstones) or acalculous (without gallstones). Most common in middle-
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aged people. Greater in women than men. Chronic may follow acute. Usually associated
with gallstone formation. The chronic form usually affects the elderly. Still greater in
women.
Can occur from trauma, extensive burns, or recent surgery. Can also occur from
prolonged immobility and fasting. Bacteria can also cause it (Esherichia coli). Also,
adhesions, neoplasms, anesthesia, and narcotics.
Cholelithiasis-Refers to formation of calculi (gallstones) in the gallbladder. Associated
with about 90% of gallbladder disease in the U.S. Incidence greater in women than men
before age 50. After that, about equal.
Occurs when the balance that keeps cholesterol, bile salts, and calcium in solution is
altered so that precipitation of these substances occur. The bile is usually
supersaturated with cholesterol (lithogenic bile). The same thing happens to the bile in
the gallbladder. Other components of bile that precipitate into stones are bile salts,
bilirubin, calcium, and protein.
Clinical Manisfestations
Obstructive jaundice
Dark amber urine that foams when shaken.
No urobilinogen in urine.
Clay-colored stools
Pruritis (itch, itch, itch)
Intolerance for fatty foods
(Nausea, feeling full, anorexia)
Bleeding tendencies
Steatorrhea
Etiology
No bile flow into duodenum.
Soluble bilirubin in urine
No bilirubin reaching the small intestine to be
converted to urobilinogen.
Same as above!
Deposition of bile salts in skin tissues.
No bile in small intestine for fat digestion.
Lack of or ↓ absorption of vitamin K, resulting
in ↓ production of prothrombin.
No bile salts in duodenum, preventing fat
emulsion and digestion.
Pain is usually in RUQ but can radiate to mid-upper back.
Jaundice indicates that stone(s) is in common bile duct.
Bilirubin and alkaline phosphatase may increase.
Pain must be differentiated from the pain caused by other disorders like pancreatitis, MI,
or kidney.
Diagnosis Cholangiography or radioactive scan.
 Oral cholecystogram (may outline stones)
 Endoscopic or percutaneous cholangiography.
 Must be NPO
Treatment Laparoscopic cholecystectomy preferred treatment. Also, Incisional
Cholecystectomy.
 Drugs that dissolve the stones.
 Bile acid chemodeoxycholic acid (CDCA) can completely or partially dissolve.
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Patient may need vitamin K if Prothrombin levels are low or if patient is
jaundiced.
T-Tube to drain bile while duct is edematous. Record amount, color, consistency;
report any sudden change in drainage (may mean edema or spasm), skin integrity.
Empty bag as needed.
IV fluid
NPO with NG tube, later progressing to low-fat diet
Antiemetics
Analgesics
Fat-soluble vitamins (A, D, E, and K)
Anticholinergics (Antispasmodics)
Antibiotics (for secondary infection)
ERCP with sphincterotomy (papillotomy)
Extracorporeal shock-wave lithotripsy
Dissolution therapy-Ursodeoxycholic acid (UDCA), Ursodiol (Actigall),
Chenodeoxycholic acid (CDCA)
COLON Cancer
Third most common kind of cancer in the U.S. Most prevalent over the age of 50. In both
sexes, the incidence of right colon cancers has increased and cancers in the rectum have
decreased. Most often seen in the rectum, ascending colon, and sigmoid colon.
Tumors in small intestine are rare. Arises from epithelial lining.
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Adenocarcinoma is the most common type of colon cancer. All colorectal cancers
appear to arise from adenomatous polyps.
Spread through the walls of the intestine and into the lymphatic system. Spread to the
liver because the venous blood flow from the colorectal tumor is through the portal vein.
Clinical Manisfestations: Depends on Where the Lesion Is!
Cancer on the right side of the colon gives rise to clinical manisfestations that are
different from those on the left side of the colon. Rectal bleeding, the most common
symptom of colorectal cancer, is most often seen with left-sided lesions.
Also on the left side-Alternating constipation and diarrhea, change in stool caliber
(narrow, ribbonlike) and sensation of incomplete evacuation. Obstruction symptoms
appear earlier with left-sided lesions because of the smaller lumen size.
Cancers of the right side are usually asymptomatic. Vague abdominal discomfort or
crampy, colicky abdominal pain. Iron deficiency anemia and occult bleeding indicate
further investigation. See weakness and fatigue.
Risk Factors:
 Age >50 years
 Familial polyposis
 Colorectal polyps
 Chronic IBD
 Family Hx of colorectal cancer or adenomas
 Previous Hx of colorectal cancer
 History of ovarian or breast cancer
 High-fat and/or low-fiber diet (controversial)
S & S:
Transverse colon: Pain, obstruction, change in bowel habits, anemia.
Ascending colon: Pain, mass, change in bowel habits, anemia.
Descending colon: Pain, change in bowel habits, bright red blood in stool, obstruction.
Rectum: Blood in stool, change in bowel habits, rectal discomfort.
[Pain, abdominal or rectal. Tenesmus, anal spasms, Feeling bloated even after BM,
Unexplained weight loss! Sudden obstruction, heme in stools, anemia, fatigue,
narrowing with stools.]
Diagnose:
 Digital rectal exam
 Fecal occult blood testing
 Sigmoidoscopy
 Double-contrast barium enema
 Colonoscopy
 Endorectal ultrasonography
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CT scan (before surgery)
Elevated CEA and alpha fetoprotein (CEA does not exclude the possibility of a
malignant condition. Elevated or increasing CEA levels suggest residual tumor or
tumor spread.
DCC gene products expressed as tumor antigens
CO17-1A glycoprotein expressed by colorectal cancer.
TreatmentSurgical Therapy-The only curative treatment of colorectal cancer.
 Right hemicolectomy-Performed when the cancer is located in the cecum,
ascending colon, hepatic flexure, or transverse colon to the right of the middle
colic artery. A portion of the terminal ileum, the ileocecal valve, and the appendix
are removed and an ileotransverse anastomosis is performed.
 Left hemicolectomy-Resection of the left transverse colon, the splenic flexure,
the descending colon, the sigmoid colon, and the upper portion of the rectum.
 Abdominal-Perineal Resection-Performed when the cancer is located within 5
cm of the anus. Abdominal incision made; proximal sigmoid brought through the
abdominal wal lin a permanent colostomy. The distal sigmoid, rectum, and anus
are removed through a perineal incision.
 Low-Interior Resection-May be indicated for tumors of the rectosigmoid and the
mid-to-upper rectum. The use of EEA (end-to-end anastomosis) staplers has
allowed lower and more secure anastomoses.
Chemotherapy-When the patient has positive lymph nodes at the time of surgery or has
metastatic disease.
 Combination of 5-fluorouracil (5-FU) plus leucovorin and irinotecan
(Camptosar)-1st line chemo for patients with metastatic colorectal cancers.
 5-FU and levamisole (Ergamisol) with or without leucovorin (Wellcovorin)
 Also oxaliplatin (Eloxatin), raltitrexed (Tomudex), and monoclonal antiobodies.
Radiation-May be used postoperatively as an adjuvant to colon resection and chemo or as
a palliative measure. (Reduce tumor size and provide symptomatic relief.)
Care
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Some NSAIDS or long-term use of aspirin may reduce the risk of colorectal cancer.
Teach side-to-side positioning (Post-op)
Drainage for surgical wound-Usually serosanguineous.
Observe for signs of edema, erythema, drainage around suture line, fever, elevated WBCs.
Moist heat for vasodilation. Not too much though; May cause TOO much vasodilation.
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