Study Guide for N196 Gastrointestinal Regulation Disorders

If your patient has hematemesis, what type of ulcer are they likely to have? If your patients pain occurs within one
hour of their meal, why type of ulcer is likely?
Hematemesis (bright red, brown, or black vomitus) and is most common in peptic ulcer disease (duodenal?).
Gastric ulcer pain occur 1 to 2 hours after meal; duodenal ulcers occur 2 to 4 hours after meal (944)

What are the etiologies of peptic ulcer disease?

Peptic ulcers develop only in acid environment (excess HCl acid may not develop ulcer). Pepsinogen converts to
pepsin by presence of HCl acid and pH of 2 to 3. Stomach acid level is neutralized by food or antacids or acid
secretion blocked by drugs, pH is to 3.5 or more and deactivate pepsin activity. Breakdown of gastric mucosal
barrier cause acid back diffusion into mucosa resulting in cellular destruction and inflammation. Histamine released
from damaged mucosa, resulting in vasodilation and increased capillary permeability and further secretion of acid
and pepsin causing further erosion (943)

What is Famotidine (Pepcid) prescribed for?

Is a Histamine (H2)-Receptor Blockers blocks the action of histamine on H2 receptors to HCl acid secretion.
conversion of pepsinogen to pepsin, irritation of the esophageal and gastric mucosa

1. What complications are associated with peptic ulcers? What symptoms are associated with the complications?
Hemorrhage most common of PUD, Duodenal ulcers accounts for a greater percentage of upper GI bleeding than
gastric ulcers
Perforation Most lethal complication PUD, duodenal are more prevalent and perforate more often. Perforated
ulcer penetrates serosal surface with spillage of either gastric or duodenal contents into peritoneal cavity. Patient

experiences sudden, severe upper abdominal pain that spread throughout abdomen. Abdomen appears rigid and
boardlike to protect from further injury. RR shallow and rapid. HR tachy, pulse weak, bowel sounds absent.
Gastric outlet obstruction only occur with gastric ulcers, obstruction in distal stomach and duodenum is result of
edema, inflammation, or pylorospasm and fibrous scar tissue formation. PTs reports discomfort or pain worse toward
end of day as stomach fills and dilates, relief by belching or self-induced vomiting. Vomit often projectile, contain
food particles. Constipation occurs because of dehydration and diet intake secondary to anorexia. (945)
2. What are the nursing responsibilities associated with a/an EGD, ERCP or Colonoscopy?
Sign consent, preprep education, IV fluid, assess and monitor, discharged educaiton
3.

What color stools will a patient have if they are bleeding from an UGI site? If they are bleeding from a lower GI
site?
UGI Melena (black, tarry stools) indicates slow bleeding from an upper GI, the longer the passage of blood through
the intestines, the darker the stool color because of the breakdown of hemoglobin and release of iron (954)
LGI bright red, and maroon color

4.

What is the action of antacids? What are the nursing considerations associated with administering antacids? Which
antacids are associated with constipation? With diarrhea? (934)
Antacids use as adjunct therapy for PUD, gastric pH by neutralized the HCl acid and acid content of chyme
reaching duodenum. (e.g., aluminum hydroxide bind to bile salt that damaging affects on the mucosa).
Assess, location, duration, precipitating factors of gastric pain. Lab: monitor serum phosphate and calcium level,
may cause serum gastrin and serum phosphate , monitor pH of gastric secretion

5.

What is the action of Histamine-2 receptor antagonists? What are the two GI related side effects associated with this
class of drugs? What are two non-GI related side-effects? What are the nursing considerations associated with
administering H2- receptor antagonists?
Histamine (H2)-receptor antagonists Blocks action of histamine on H2-receptors to HCl acid secretion,
conversion of pepsinogen to pepsin, irritation of esophageal and gastric mucosa
Constipation, diarrhea
Headache, confusion, arrhythmias
Assess, epigastria/abdominal pain, occult blood in stool, Assess geriatric for confusion. Lab test: CBC, may serum
transaminases and creatinine

6.

Discuss proton pump inhibitors.

HCl acid secretion by inhibiting proton pump (H+, K+, ATPase) responsible for secretion of H+, irritation of
esophageal and gastric mucosa. More effective than H2-receptor blockers in reducing gastric acid secretion and

promoting ulcer healing. Also used in combination with antibiotics to treat ulcers caused by H. pylori. Long term use
has been associated with bone density, chronic hypochlorhydria, risk of C. difficile, pneumonia
7.

To what classification does sucralfate belong? How does it work?

Sucralfate (Carafate) belongs to antiulcer, Protectants. It acts to form a protective layer and serves as a barrier
against acid, bile salts, and enzymes in the stomach. Side effect is constipation

8. If a patient is receiving antacids, H2-receptor antagonists, and sucralfate; when should they take each of the drugs?
9.

What role does H. pylori play in peptic ulcers?

In the stomach the bacteria can survive a long time by colonizing gastric epithelial cells w/in mucosal layer. Bacteria
produce urease, which metabolizes urea-producing ammonium chloride and other damaging chemicals. Urease
activates immune response with both antibody production and release of inflammatory cytokines. H. pylori alters
gastric secretion and produces tissue damage, leading to PUD and influenced by genetics, environment, and diet.
942
SECTION 8 Problems of Ingestion, Digestion, Absorption, and Elimination
10. What drugs are used to treat H. pylori? (942)
T A B L E 42-13

Erosion

DRUG THERAPY

Helicobacter pylori Infection

Treatment

Duration

Eradication Rate

Triple-Drug Therapy
proton pump inhibitor (PPI)*
amoxicillin
clarithromycin (Biaxin)
Quadruple Therapy
PPI*
bismuth
tetracycline
metronidazole (Flagyl)

7-14 days

70%-85%

Acute
ulcer

Chronic
ulcer

Mucosa
Submucosa

10-14 days

85%

*See Table 42-10.

Bismuth is part of a combination capsule (Pylera) containing bismuth, tetracycline,
and metronidazole that is used in combination with a PPI (e.g., omeprazole [Prilosec]).

Muscularis
Serosa
Scarring
FIG. 42-9 Peptic ulcers, including an erosion, an acute ulcer, and a chronic
ulcer. Both the acute ulcer and the chronic ulcer may penetrate the entire
wall of the stomach.

11. Describe the diet for a pt with peptic ulcer disease.

NU
RSING AND
COLLABOdietary
RATIVEmodification
MANAGEMENT
No
specific
recommended
for PUD. Pt taught to eat and drink foods and fluids that do not cause
GASTRITIS
any distressing symptoms. Caffeine-containing beverage and food can symptoms distress in some. Eliminate
ACUTE because
GASTRITIS
alcohol
it can delay healing. Foods commonly cause gastric irritation (hot, spicy foods, pepper, carbonated
Eliminatingthecauseand preventingor avoidingit in thefuture
beverage,
broth
(meat
extract).
are generally all that is needed to treat acute gastritis. T e plan
of care is supportive and similar to that described for nausea

12. and
What
are the Ifnursing
implications
for acute
a patient
post Gastric
Bypass procedure: diet, meds, care?
vomiting.
vomiting
accompanies
gastritis,
rest,

NPO status, and IV f uids may be prescribed. Dehydration can

Initialrapidly
postoperative
care focuses
on carefulAntiemetics
assessmentare
and immediate intervention
cardiopulmonary
occur
in acute gastritis
with vomiting.
FIG. 42-10 for
Peptic ulcer of the duodenum.
given
for nauseathrombus
and vomiting
(see Table
42-1).
complications,
formation,
anastomosis
leaks, and electrolyte imbalances. Maintain airway and manage
In severe
cases
acute
gastritis,
NG tube may
be usedor sequential compression stockings and manage with low
pain.
Manage
riskoffor
DVT,
applyan
antiembolic
stockings
(1)
to
monitor
for
bleeding,
(2)
to
lavage
the
precipitating
agent as part
PEPTIC
ULCER
dose heparin, Active and passive range of motion exercises
of daily
care.DISEASE
Wound infection, dehiscence, and
from the stomach, or (3) to keep the stomach empty and free
delayed
healing
are
potential
problems.
Assess
skin
for
complications
related
to
wound
healing.
Patients characterized
are
of noxious stimuli. Clear liquids are resumed when symptoms
Peptic ulcer disease (PUD)
is a condition
by
discouraged
from
eating
sugary
foods
after
surgery
to
avoid
dumping
syndrome.
Poor
absorption
of
iron
due to action of
have subsided, with gradual reintroduction of solids.
erosion of the GI mucosa resulting from the digestive
bypassing
small intestine
can cause
need
take multivitamin
iron
If hemorrhage
is considered
likely, iron-deficiency
frequently checkanemia.
vital Patients
HCl acid
andtopepsin.
Any portion with
of the
GI and
tractcalcium
that comes
signs
and test the
vomitus
for blood.
Allbyofcobalamin
the management
intoare
contact
with gastric
secretions isor
susceptible
to ulcer develsupplements.
Chronic
anemia
caused
deficiency but
managed
with parenteral
intranasal
strategies
discussed
opment, including the lower esophagus, stomach, duodenum,
cobalamin
(918) in the section on upper GI bleeding apply
to the patient with severe gastritis (see p. 955).
and margin of a gastrojejunal anastomosis af er surgical proceDrug
therapy
focuses
on
reducing
irritation
of
the
gastric
350,000 new
casescan
of ulcers
13. What is dumping syndrome? What are the early symptoms? dures.
What Approximately
are the late symptoms?
How
it be arediagnosed
mucosa and providing symptomatic relief. H2-receptor blockers
each year.
controlled?
(e.g., ranitidine, cimetidine) or PPIs (e.g., omeprazole, lansoTypes
prazole) reduce gastric HCl acid secretion (see Table 42-10).
Teach the patient about the therapeutic ef ects of PPIs and H2Peptic ulcers can beclassif ed as acuteor chronic, depending on
receptor blockers.
the degree and duration of mucosal involvement, and gastric or
duodenal, according to the location. T e acute ulcer (Fig. 42-9)
CHRONIC GASTRITIS
is associated with superf cial erosion and minimal inf ammaT e treatment of chronic gastritis focuses on evaluating and
tion. It is of short duration and resolves quickly when the cause

Dumping Syndrome direct result of surgical removal of large portion of stomach and pyloric sphincter. Normally
gastric chyme enters small intestine in small amounts. However, after surgery the stomach no longer has control over
amount of gastric chyme entering small intestine. A large bolus of hypertonic fluid enters intestine and results in fluid
being drawn into bowel lumen. This creates in plasma volume along with distention of bowel lumen and rapid
intestinal transit.
Early symptoms occurs w/in 15-30minutes after eating: feelings of generalized weakness, sweating, palpitations, and
dizziness due to sudden in plasma volume.
Abdominal cramps, borborygmi (audible abdominal sounds produced by hyperactive intestinal peristalsis), and urge
to defecate usually less than 1 hour after eating
Controlled by nutritional therapy. Divide meals into six small feedings to avoid overloading stomach and intestine at
mealtimes. Do not take fluids with meals but at least 30-45 minutes before or after meals to help prevent distention or
feeling of fullness. Avoid concentrated sweets (honey, sugar, jelly, jam, candies, sweet pastries, sweetened fruits)
because they sometimes cause dizziness, diarrhea, and sense of fullness. protein and fats to promote rebuilding of
body tissues and to meet energy needs. Meet, cheese, and eggs are specific foods to in diet. (949-950)
14. What medication (injection) might a patient need to be on for the rest of their life following a gastrectomy or gastric
bypass?
Pt requires cobalamin supplementation because intrinsic factor (normally made in stomach) is not available to bind
with cobalamin so that this vitamin can be absorbed in the ileum.
15. What are the risk factors associated with cholecystitis?
Cholecystitis inflammation of the gallbladder. Associated with obstruction caused by gallstones or biliary sludge.
Absence of obstruction occurs most frequently in older adults and in patients who are critically ill. Acalculous
cholecystitis is also associated with prolonged immobility and fasting, prolonged parenteral nutrition, and DM.
Bacteria reaching the gallbladder via the vascular or lymphatic route, or chemical irritants in the bile, can produce
cholecystitis.
Complications of choletlithiasis ad cholecystitis: gangrenous cholecystitis, subphrenic abscess, pancreatitis,
cholangitis (inflammation of biliary ducts), biliary cirrhosis, fistulas, and rupture of gallbladder which an produce
peritonitis
16. What symptoms are associated with biliary tract obstruction?
Pain usually located in left upper quadrant, but may be in midepigastrium. Commonly radiates to back because of
retroperitoneal location of pancreas. Sudden onset (severe, deep, piercing, and continuous or steady). Pain
aggravated by eating and frequent
17. Describe the tests commonly used to make a diagnosis of cholelithiasis.
Cholelithiasis stones in the gallbladder. Develops when balance that keeps cholesterol, bile salts, and calcium in
solution is altered so that substances precipitate caused by infection and disturbances in metabolism of cholesterol.
Ustrosonography is commonly used to diagnose gallstones. Lab tests reveal an increased WBC result of
inflammation. Direct and indirect bilirumbin levels are elevated, urinary bilirubin level elevated if obstructive process
present. If common bile duct obstructed, no bilirubin will reach small intestine to be converted to urobilinogen.
Alkaline phosphate, ALT, AST may elevated. Amylase if pancreatic involved (1038)
18. What foods stimulate the gallbladder to release bile?
Fat, bile salt will surround the fat particles and emulsify the fat
19. What complications are likely to occur in the patient with incision cholecystectomy?

Incisional (open) cholecystectomy removal of gallbladder through right subcostal incision. Postoperative care
focuses on adequate ventilation and prevention of respiratory complications (1040).
20. Describe the care of a patient with a T-tube. Why does a pt have a T-tube? How long will they have the T-tube?
If patient has T tube, maintain bile drainage and observe for T-tube functioning and drainage (1040). A T tube may be
inserted into common bile duct during surgery when common bile duct exploration is part of surgical procedure. This
ensures patency of duct until edema produced by trauma of exploring and probing duct subsided. It also allows excess
bile to drain while the small intestine is adjusting to receiving continuous flow of bile (1039).
21. Describe the pre-op and post-op care of the patient receiving a cholecystectomy? What tubes might they have postoperatively? Describe the function of a Penrose drain?
22. What diet instructions should be given to the patient with a cholecystectomy?
Instruct patient to have liquids for the rest of the day and eat light meals for a few days for laparoscopic procedure.
For Incisional, the patient will progress from liquids to regular diet once bowel sounds have returned. The amount of
fat in postoperative diet depends on patients tolerance of fat. A low-fat diet may be helpful if the flow of bile is
reduced (usually only in early postoperative period) or if patient is overweight. Sometimes the patient is instructed to
restrict fats for 4 to 6 weeks. Otherwise no special dietary instructions are needed other than to eat nutritious meals
and avoid excessive fat intake (1039)
23. What discharge instructions will you give to a patient following a laparoscopic cholecystectomy? (I.e. wound care,
showering, activity, when to call the physician)
24. Which type of nutritional supplement is preferred for a patient who has Altered Nutrition: Less than Required?
(Enteral or Parenteral?) Why?
Enteral nutrition (EN): EN may be ordered for patient who has functioning GI tract but unable to take any or enough
oral nourishment, or when it is unsafe to do so. EN is easily administered, safer, more physiologically efficient, and
typically less expensive than parenteral (PN). This question required more information as it stands, the best route
would be Enteral (EN) because it is less invasive. If more information were to state that pt is altered nutrition: less
than required r/t malabsorption of GI tract, than PN may be used. PN is usually indicated when GI tract cannot be
used for ingestion, digestion, and absorption of essential nutrients. PT sustain severe injury, surgery, or burns and
those who are malnourished due to medical treatment or disease processes have greatly increased nutritional needs
(903)
25. List two reasons a patient receiving only tube feedings (with no supplemental water) may develop dehydration.
26. What principles should be applied to safely administer a tube feeding?
27. What is the ultimate purpose of TPN?
28. What is the difference between PPN and TPN?
29. What complications are associated with TPN? What actions are used to avoid them?
30. What standards of care are indicated for the patient receiving TPN? What should be considered when controlling
glucose levels?
31. Considering osmotic and hydrostatic pressure, explain the pathophysiology of ascites.
32. Identify five important things to assess and include in your charting for the patient with cirrhosis.
33. What laboratory changes in liver enzymes, prothrombin time/INR, cholesterol, bilirubin and albumin are seen in
liver failure?

34. Describe the normal circulation of blood in the liver.

36. What is the relationship between portal hypertension and bleeding esophageal varies?
37. What measures are used to treat bleeding esophageal varices?
38. What are the nursing responsibilities associated with the use of balloon tamponade?
39. Why do coagulation defects occur in the patient with cirrhosis?
40. What is the pathophysiology associated with hepatic encephalopathy?
41. Why is rest so important for a patient with hepatitis?
42. What are the nursing responsibilities associated with an abdominal paracentesis?
43. What diet therapy is used to treat the Fluid Volume Excess associated with cirrhosis? What drug therapy is used to
treat the Fluid Volume Excess?
44. How would you monitor Fluid Volume status in cirrhosis?
45. Which diuretic, Lasix or Aldactone, would you hold if a patient has a low serum potassium? Which would you hold
for an increased serum potassium?
46. What interventions would you implement for the patient with Risk for Impaired Skin Integrity related to edema?
47. What measures are used to reduce the ammonia level of a patient with hepatic encephalopathy?
48. What is the pathophysiology associated with acute pancreatitis? What is the pathophysiology associated with chronic
pancreatitis?
49. What are the risk factors for developing pancreatitis?
50. Compare and contrast the signs and symptoms of acute pancreatitis and chronic pancreatitis.
51. What laboratory abnormalities are associated with pancreatitis?
52. Identify at least three items you would include in a focused assessment of the patient with pancreatitis. What is the
rationale for each of these items?
53. Why is enzyme replacement used in treating chronic pancreatitis? How do you know if the treatment is being
effective?
54. Why are antacids and or H2 receptor antagonists used to treat acute pancreatitis?
55. Why are patients with acute pancreatitis NPO initially and likely to have an NG tube to low suction?
56. What is the drug of choice in treating the pain associated with pancreatitis?
57. Which will the patient with pancreatitis be a candidate for tube feedings or TPN?
58. Other than the GI system, what other system is often negatively affected in the patient with pancreatitis? (i.e., what
system needs careful monitoring)
59. What type of diet is typical for the patient with pancreatitis when they resume oral feedings?
60. What can a patient do to decrease their risk of developing pancreatitis again?

61. How does the nurse calculate NGT output when normal saline irrigation is used?