Gastritis

Upper Gastrointestinal problems

Gastritis
An inflammation of the gastric mucosa, is one of the most common problems affecting the stomach.
May be acute or chronic
There is two types (A fundal and B antral)
Etiology and pathophysiology
Gastritis occurs as the result of a breakdown in the normal gastric mucosal barrier.
This mucosal barrier normally protects the stomach tissue from autodigestion by acid and the enzyme
pepsin.
When the barrier is broken, acid can diffuse back into the muscosa.
This allows hydrochloric (HCL) acid to enter.
The HCL acid stimulates the conversion of pepsinogen to pepsin and stimulates the release from Mast
cells.
Etiology and Patho Continue
The combined result of these occurrence is tissue edema, disruption of capillary walls with loss of
plasma into the gastric lumen and possible hemorrhage.
Causes of gastritis
Aspirin
Nonsteriodal anti-inflammatory drugs
Alcohol
radiation
H. Plyori
Salmonella
Smoking
sepsis

 burns
renal failure
Chronic Gastritis Type A and B
Type A= Likely to be an autoimmune disorder.
Type B= is related to H. Pylori
Clinical Manifestation Acute gastritis
Anorexia
Nausea and vomiting
epigastric tenderness
felling of fullness
Hemorrhage is commonly associated with alcohol abuse
Is self-limiting, lasting from a few hours to a few days, with complete healing of the mucosa
expected.
Clinical Manifestation of Chronic gastritis
Similar to to those described for acute gastritis.
Anemia (due to acid-secreting cells that are lost or do not function as a result of atrophy, the source
of intrinsic factor is lost.
Intrinsic factor combines with B12. When b !2 is unavailable it cannot absorb in the ileum.
The storage of B12 is depleted from the liver and the lack of this is essential for growth and
maturation of RBCs, resulting in anemia.
Diagnostic Studies
Endoscopic exam
Biopsy
Breath
Urine
Serum

 CBC (to check for anemia)

Stools are tested for occult blood
Collaborative Care
Elimination of the cause and preventing or avoiding it in the future are generally all that is needed to
treat acute gastritis.
Bed rest
NPO status
IV fluids
Vomiting
Diarrhea
Severe case an NG tube may be placed to either keep stomach empty or for a lavage.
Continue Collaborative Care
Antiemetics (n/v)
Antacids
H2 antagonist (Zantac, Tagment, Prilosec, Prevcaid) This reduces gastric HCL acid secretion.
Chronic Gastritis-antibodies
Patient with pernicious anemia= regular injections of B12
bland diet
antacids
Nursing Management
Nursing Assessment
Dehydration can occur rapidly if patient is vomiting
Keep patient quiet
Maintain NPO
Monitoring IVF

 Frequent V/S and testing vomit for blood

Nursing Diagnosis
Vomiting
Fluid Volume Deficit
Anxiety
Altered nutrition less than body requirements
Goals
Experience minimal or no symptoms of gastritis
Have no recurrent episodes of acute gastritis
achieve am optimal pattern of gastric function relative to the state of the disease.
Peptic Ulcers
Upper Gi Problem
Peptic Ulcer
Is an erosion of the GI mucosa resulting from the digestive action of HCL acid and pepsin.
Any portion of the GI tract that comes in contact with gastric secretions is susceptible to ulcer
development.
It is estimated that 10% of men and 4% OF WOMEN IN THE us WILL HAVE DUODENAL ULCERS DURING
THEIR LIFE TIME.
Types
Peptic ulcer can be classified as acute or chronic and to the location.
ACUTE= is associated with superficial erosion and minimal inflammation.
It is short duration and resolves quickly when the cause is identified and removed.
CHRONIC=is one of long duration, eroding through the muscular wall with the formation of fibrous
tissue.
It is present continuously for many months or intermittently throughout a persons lifetime.
Gastric Ulcers

 More prevalent in women than in men.

Mortality rate from gastric ulcers is greater than that form duodenal ulcers because the peak
incidence of gastric ulcers occurs in person over 50 years of age.
More prevalent in those with executives or managerial positions.
Persons with socioeconomic class and manual or unskilled workers are more prone to gastric ulcers.
H. Pylori
Provides a new understanding of ulcer formation (please read)
It survives in the human upper GI tract for long periods of time as a result of its ability to move in
mucus and attach to mucosal cells.
It secretes a substance called urease, which buffers the area around the bacterium and protects it
from destruction in an acidic environment.
H. Pylori is more common in low socioeconomic area.
Route of transmission is unknown it is thought that infection occurs during childhood via transmission
form family members tot he child, possible through oral-oral route.
Ulcers can develop from medication
Stress
Duodenal Ulcers
Accounts for about 80% of patients.
Steady increase in women.
May be because of overuse of ASA and NSAIDS and increase consumption of alcohol abuse.
H.Pylori has been identified as being a key role.
Manifestations
No pain or other symptoms can occur.
When pain does occur it is described as burring or cramplike.
Located in the mid-epigastrium region beneath the xiphoid process.
Pain can occur when the stomach is empty or when food has been digested.

 Gastric ulcer=located high in the epigastrium and occurs spontaneously 1-2 hours after meals.
Complications
Hemorrhage (most common)
Perforation
Gastric outlet obstruction
Diagnostic Studies
CBC
Urinalysis
Liver enzymes
Serum electrolytes
Endoscopy
Upper GI barium contrast study
gastric analysis
H.pylori testing of breath, urine, blood and stool
Collaborative Therapy
Adequate rest
bland diet
cessation of smoking
antacids
H2 receptor blocking agents
Anticholinergics
Stress reduction
Collaborative care acute exacerbation without complications
NPO
NG suction

 Bed rest to moderate light activity

Cessation of smoking
IVF
Antacids
H2 receptor antagonist
Sedatives
Anticholinergic
Acute exacerbation with complications (hemorrhage, perforation or obstruction
NPO
NG suction Bed rest
IVF
Blood transfusions
Stomach lavage
Surgical Therapy
Perforation
Gastric outlet obstruction
Bilroth I and II (please read)
Nursing Management
Nursing Assessment
read p. 1119 table 39-23
Nursing Diagnosis
Pain
Ineffective management of therapeutic regimen
Vomiting
Planning

 Experience reduction or absence of discomfort related to Peptic Ulcer disease

Exhibit no signs of GI complications related to the ulcerative process
Have complete healing of the peptic ulcer
comply with the prescribed therapeutic regimen.
Nursing Implementation
Read p. 1119-1123
Health Promotion
Acute intervention
Surgical Therapy for Peptic Ulcers
Approximately 20% of patients with ulcers need surgical intervention
Bilroth I= Partial gastrectomy with removal of the distal two thirds of the stomach and anastomosis of
the gastric stump to the duodenum.
Billroth II= Partial gastrectomy with removal of the distal two thirds of the stomach and anastomosis
of the gastric stump to the jejunum.
Continue with surgical therapy
Vagotomy=Severing the vagus nerve, either totally or selectively at some point in its innervation to
the stomach.
Pyloroplasty=surgical enlargement of the pyloric sphincter to facilitate the easy passage of contents
from the stomach.
Postoperative Complications
Dumping syndrome
Postprandial hypoglycemia
bile reflux gastritis
Postpranidal hypoglycemia
A variant of dumping syndrome
result of uncontrolled gastric emptying of a bolus of fluid high in carbohydrate in tot he small
intestine.

 This results in hyperglycemia and the release of excessive amounts on insulin in to the circulation.
Secondary hypoglycemia then occurs, with symptoms appearing about 2 hours after meals.
Symptoms: Sweating, weakness, mental confusion, palpitations, tachycardia and anxiety.
Bile Reflux gastritis
Prolonged contact with bile, especially bile salts, causes damage to the gastric mucosa.
Paradoxically, peptic ulcer can reoccur after surgical treatment that was intended as a cure.
Symptoms are continuos epigastric distress that increases after meals. Vomiting relives the distress
but only temporarily.
Questran either before or after meals has met with considerable success.
Nutritional therapy related to surgical therapy
DC planning and instruction should be started as soon as the immediate postoperative period is
successfully passed.
Dietary instructions
Eliminate drinking fluids with meals
Dry foods with low carbs and moderate protein and fats. This can reduces the likelihood of dumping
syndrome.
Patient and family teaching
Read p.1122, table 39-24
Inflammatory bowel disease
Lower Gastrointestinal problem
Inflammatory bowel Disease
Ulcerative Colitis and Chrons disease are immunologically related disorders to as IBD
Their has been extensive research on the etiology of IBD, the cause is still unknown.
Possible causes can be: and infection agent Lupus, food allergies and heredity.
Ulcerative Colitis
Characterized by inflammation and ulceration of the colon and rectum.It may occur at any age but
peaks between the ages of 15-25 years.

 There is a second, smaller peak onset between 50-80 years of age.

Can occur in both sexes but has a higher incidence in women.
More common in Jewish and upper-middle class urban populations.
Clinical Manifestations
Bloody diarrhea
Abdominal pain
Pain may vary from mild-severe
With mild disease=diarrhea may consist of one or tow semi-formed stools containing amounts of blood
per day.
In moderate= increased stool output (4 to 5 a day), increased bleeding and systemic symptoms (fever,
malaise, anorexia)
Severe=10 -20 stools a day. With fever, weight loss and dehydration are present.
Complications
Hemorrhage
strictures
perforation
toxic megacolon (dilation and paralysis of the colon
colon dilation
Diagnostic studies
Fiberoptic colonoscopy
Sigmoidoscopy
Barium enema
CBC
Stool for blood, culture and sensitivity
Collaborative Care
Mild-moderate

 Low roughage diet and not milk or milk products

Antimicrobal therapy
Corticosteriods
Anticholinergic therapy
Anti-diarrheal agents
Continue collaborative care
Severe
IVF with electrolytes
Blood transfusions
NPO status
NG tube to low suction
Anti-microbial therapy
Corticosteriods
TPN
Surgery if no improvement
Surgical Therapy
Total protocolectomy with permanent ileostomy
Total proctocolectomy with continent ileostomy
Total colectomy and ileal reservoir
Please read p.1156
Nursing Diagnosis
Diarrhea
Aniexty
Altered nutrition: less than body requirements
Impaired skin integrity

 Ineffective individual coping

Ineffective management of therapeutic regimen
Goals
Experience decrease in number and severity of acute exacerbations
Maintain normal fluid and electrolyte balance
be free from pain and discomfort
comply with medical regimens
maintain nutritional balance
Chrons Disease
Lower Gastrointestinal Problems
Chrons Disease
A chronic, nonspecific inflammatory bowel disorder of unknown origin that can affect any part of the
GI tract.
May occur most often between the ages of 15-30 years.
When it occurs in older adults the mortality and morbidity is higher.
Incidence of Chrons is lower than Ulcerative Colitis.
Manifestations
The onset is usually insidious with nonspecific complaints such as diarrhea, fatigue, abdominal pain,
weigh loss and fever.
Diarrhea is usually non-bloody and is the result of the inflammation process of malabsorption.
Pain may be severe and intermittent ro constant.
Abdominal cramping, tenderness, abd. Distension, fever and fatigue.
Weight loss, dehydration, electrolyte imbalance, anemia and increased peristalsis.
Diagnostic Studies
CBC
Serum Chemistries

 Stool for occult blood

Barium enema of small and large int.
Sigmoidoscopy and colonoscopy with biopsy
Collaborative Care
High Calorie, high vitamin, high protein , low residue milk free diet.
Anti-microbial agents
Corticosteriods drugs
Supplemental parental nutrition
Elemental diet
Physical and emotional rest
surgery
Nursing Management
Similar to that of ulcerative colitis
as the patient improves the nurse should allow for more self-care, provide frequent rest period and
advise the patient of the importance of rest and avoidance or control of emotional stress.
Intestinal Obstruction
Lower GI Problems
Intestinal Obstruction
Occurs when intestinal contents cannot pass through the GI tract, and it requires prompt treatment.
Obstruction may be partial or complete
May be classified as mechanical or nonmechanical
Mechanical
May be caused by an occlusion of the lumen of the intestinal tract.
Most occur in the small intestine, most often in the ileum.
Adhesions accounts for 50% hernias and neoplasms for 15% of obstructions of the small intestine.

 Adhesions can develop after abdominal surgery.

Pain that comes and goes in waves. This id due to intestinal peristalsis trying to move bowel contents
past the obstructed area.
Nonmechanical
May result form a neuromuscular or vascular disorder.
Paralytic ileus is the most common form of nonmechanical obstruction.
It occurs to some degree after abd. Surgery.
Pseudoobstruction=mechanical obstruction o the intestine without demonstration of obstruction by
radiographic methods.
Etiology and Patho
Normally 6-8Lof fluid enters the small bowel daily.
Most of the fluid is absorbed before it reaches the colon.
Approm. 75% of intestinal gas is swallowed air.
This combination causes distention, distal bowel may collapse.
Read p.1164-1165
Manifestations
Manifestations depends on the location of the obstruction, it includes
Nausea and vomiting
abdominal pain
distention
inability to pass flatus
Abdominal distention
Continue Manifestations
The vomitus may be orange brown and foul smelling because of bacterial overgrowth.
Vomiting may be entirely absent in large bowel obstruction if the ileocecal valve is competent,
otherwise the patient may eventually vomit fecal material.

 Vomiting usually relives abdominal pain high intestinal obstructions.

Persistent colicky abdominal pain is seen with lower intestinal obstruction.
Paralytic ileus produces a more constant generalized discomfort.
Strangulation causes sever, constant pain that is rapid on onset.
Diagnostic Studies
History and physical
abdominal x-ray
Barium enemas (not used if perforation is suspected)
CBC
BUN
WBC
H/H
Serum electrolytes
Collaborative Care
NG tube (should be inserted before surgery to empty out the stomach)
Intestinal tube (controversial).Difficult and time consuming.
Sigmoidoscopy
Colon decompression
IVF
Nursing Diagnosis
Pain
Fluid volume deficit
Altered nutrition: less than body requirements
Planning
Relief of the obstruction and return to normal bowel obstruction

 Minimal to no discomfort
Normal fluid and electrolytes
Diverticulosis and Diverticulitis
Lower GI tract
Manifestations
Crampy abdominal pain located in the lower left quadrant that is usually relieved by passage flatus or
bowel movement.
Acute diverticulosis progress to acute diverticulitis
Patients with diverticulitis experience abdominal pain that localized over the involved area of the
colon.
Tender left quadrant mass may be felt on palpation of the abd.
Fever
Chills
nausea
anorexia
leukocytosis
Complications
Perforations with peritonitis
Abscess and fistula formation
Bowel obstruction
ureteral obstruction
Bleeding
Diagnostic
Stool for occult blood
BE
Sigmoidoscopy

 Colonscopy
CBC
Urinalysis
Blood culture
Collaborative Care
Ambulatory and Home Care
High-residue diet
Fiber supplement
Stool softeners
Anticholonergic Mineral oil
Clear liquid diet
Oral antibodics
Bulk Laxatives
Acute Care: Diverticulitis
Antibodics
NPO status
IVF
Possible colon resection for obstruction or hemorrhage
Bed rest
NG suction