Gastrointestinal Disorders

Disturbances in Ingestion

Prepared by:
Jan Paul Valeros Sicat, PHRN, USRN
 Inflammation of stomach lining from irritation of
Gastritis gastric mucosa (normally protected from
gastric acid and enzymes by mucosal barrier)

Acute Gastritis
Disruption of mucosal barrier allowing Gastric mucosa rapidly regenerates;
hydrochloric acid and pepsin to have Self limiting disorder
contact with gastric tissue:
leads to irritation,
inflammation, superficial erosions
Causes of acute gastritis
➢Irritants include aspirin and other NSAIDS, corticosteroids,
alcohol, caffeine
➢Ingestion of corrosive substances: alkali or acid
➢Effects from radiation therapy, certain chemotherapeutic
agents
Erosive Gastritis
form of acute which is
stress-induced, complication
of life-threatening condition
(Curling’s ulcer with burns);
gastric mucosa becomes
ischemic and tissue is then
injured by acid of stomach
 Gastritis Manifestations

➢Mild: anorexia, mild

epigastric discomfort,
belching
➢More severe: abdominal
pain, nausea, vomiting,
hematemesis, melena
➢Erosive: not associated with
pain; bleeding occurs 2 or
more days post stress event
➢If perforation occurs, signs
of peritonitis
Gastritis Treatment

➢NPO status to rest GI tract for 6 – 12 hours,

reintroduce clear liquids gradually and
progress; intravenous fluid and
electrolytes if indicated
➢Medications: proton-pump inhibitor or H2-
receptor blocker; sucralfate (carafate)
acts locally; coats and protects gastric
mucosa
➢If gastritis from corrosive substance:
immediate dilution and removal of
substance by gastric lavage (washing out
stomach contents via nasogastric tube),
no vomiting
 Progressive disorder beginning with
Chronic Gastritis superficial inflammation and leads
to atrophy of gastric tissues

Type A:
➢autoimmune component and affecting
persons of northern European descent; loss
of hydrochloric acid and pepsin secretion;
develops pernicious anemia
➢Parietal cells normally secrete intrinsic factor
needed for absorption of B12, when they
are destroyed by gastritis pts develop
pernicious anemia
Chronic Gastritis

Type B:
➢more common and occurs with aging; caused by
chronic infection of mucosa by Helicobacter pylori;
associated with risk of peptic ulcer disease and gastric
cancer
Chronic Gastritis Manifestations

➢Vague gastric ➢Fatigue associated ➢Lack of B12

distress, epigastric with anemia; affects nerve
heaviness not symptoms associated transmission
relieved by with pernicious
antacids anemia: paresthesias
Chronic Gastritis Treatment

Type B:
eradicate H. pylori infection with
combination therapy of two antibiotics
(metronidazole (Flagyl) and clarithromycin
or tetracycline) and proton–pump inhibitor
(Prevacid or Prilosec)
Chronic Gastritis Collaborative Care
➢Usually managed in community
➢Teach food safety measures to prevent acute gastritis
from food contaminated with bacteria
➢Management of acute gastritis with NPO state and
then gradual reintroduction of fluids with electrolytes
and glucose and advance to solid foods
➢Teaching regarding use of prescribed medications,
smoking cessation, treatment of alcohol abuse
Chronic Gastritis Diagnostic Tests
➢Gastric analysis: assess hydrochloric acid
secretion (less with chronic gastritis)

➢Hemoglobin, hematocrit, red blood cell

indices: anemia including pernicious or Upper Blood
iron deficiency endoscopy Tests

➢Serum vitamin B12 levels: determine

pernicious anemia

➢Upper endoscopy: visualize mucosa,

identify areas of bleeding, obtain biopsies;
may treat areas of bleeding with electro
or laser coagulation or sclerosing agent Fecal occult
blood test
(stool test)

Nursing Diagnoses:
➢ Deficient Fluid Volume
➢ Imbalanced Nutrition: Less than body requirements
Peptic Ulcer Disease Break in mucous lining of GI tract
comes into contact with gastric juice;
(PUD) affects 10% of US population

Duodenal ulcers: Gastric ulcers:

most common; affect mostly affect older persons (ages 55 – 70);
males ages 30 – 55; ulcers found on lesser curvature and
found near pylorus associated with increased incidence of
gastric cancer
Risk factors
Smokers, users of NSAIDS; familial pattern, ASA,
alcohol, cigarettes
Peptic Ulcer Disease (PUD) Pathophysiology

1. Ulcers or breaks in mucosa of GI tract

occur with:
➢H. pylori infection (spread by oral to oral,
fecal-oral routes) damages gastric
epithelial cells reducing effectiveness of
gastric mucus
➢Use of NSAIDS: interrupts prostaglandin
synthesis which maintains mucous barrier
of gastric mucosa

2. Chronic with spontaneous remissions

and exacerbations associated with
trauma, infection, physical or
psychological stress
Peptic Ulcer Disease Diagnosis
➢EGD-
➢Endoscopy esophagogastroduodenoscopy
with cultures

➢Looking for
H. Pylori
➢Serum and stool studies

➢Upper GI barium contrast

studies
Peptic Ulcer Disease (PUD) Manifestations
➢Pain is classic symptom: gnawing, ➢Symptoms less clear in older adult;
burning, aching hunger-like in may have poorly localized discomfort,
epigastric region possibly radiating dysphagia, weight loss; presenting
to back; occurs when stomach is symptom may be complication: GI
empty and relieved by food (pain:
food: relief pattern) hemorrhage or perforation of stomach
or duodenum
 Peptic Ulcer Disease Treatment

➢Rest and stress ➢Nutritional ➢ NG suction

reduction management
Peptic Ulcer Disease Treatment

➢Pharmacological management

1. Antacids (Mylanta) – Neutralizes acids

2. Proton pump inhibitors (Prilosec, Prevacid) – Block gastric acid secretion

3. Histamine blockers (Tagamet, Zantac, Axid) - Blocks gastric acid secretion

4. Carafate - Forms protective layer over the site

5. Mucosal barrier enhancers (colloidal bismuth, prostoglandins) - Protect mucosa

from injury

6. Antibiotics (PCN, Amoxicillin, Ampicillin) - Treat H. Pylori infection

Peptic Ulcer Disease Treatment
➢ Surgical intervention

Billroth I Billroth II
1. Minimally invasive gastrectomy - 2. Billroth I and II –
Partial gastric removal with Removal of portions of the stomach
laproscopic surgery

3. Vagotomy – 4. Pyloroplasty –
Cutting of the vagus nerve to Widens the pyloric sphincter
decrease acid secretion
 Peptic Ulcer Disease Complications

➢ Hemorrhage: frequent in older adult: hematemesis,

melena, hematochezia (blood in stool); weakness,
fatigue, dizziness, orthostatic hypotension and
anemia; with significant bleed loss may develop
hypovolemic shock

➢Obstruction: gastric outlet (pyloric sphincter)

obstruction: edema surrounding ulcer blocks GI tract
from muscle spasm or scar tissue
1.Gradual process
2.Symptoms: feelings of epigastric fullness, nausea,
worsened ulcer symptoms
 Peptic Ulcer Disease Complications

➢Perforation: ulcer erodes through mucosal wall and gastric

or duodenal contents enter peritoneum leading to
peritonitis; chemical at first (inflammatory) and then
bacterial in 6 to 12 hours
1.Time of ulceration: severe upper abdominal pain
radiating throughout abdomen and possibly to shoulder
2.Abdomen becomes rigid, boardlike with absent bowel
sounds; symptoms of shock
3.Older adults may present with mental confusion and non-
specific symptoms
Complications associated with
gastric surgery
➢1. Dumping Syndrome
a.Occurs with partial gastrectomy;
hypertonic, undigested chyme bolus
rapidly enters small intestine and pulls
fluid into intestine causing decrease in
circulating blood volume and increased
intestinal peristalsis and motility
b.Manifestations 5 – 30 minutes after
meal: nausea with possible vomiting,
epigastric pain and cramping,
borborygmi, and diarrhea; client
becomes tachycardic, hypotensive,
dizzy, flushed, diaphoretic
c.Manifestations 2 – 3 hours after meal:
symptoms of hypoglycemia in response
to excessive release of insulin that
occurred from rise in blood glucose
when chyme entered intestine
 Mortality approx 10%
Predisposing factors include: drugs,
Upper GI Bleed esophageal varicies, esophagitis, PUD, gastritis
and carcinoma

Signs and Symptoms

➢ Coffee ground ➢ Black, tarry stools/ ➢ Decreased B/P ➢ syncope

vomitus Melena

➢ Vertigo ➢ Drop in Hct, Hgb ➢ Confusion

Upper GI Bleed Diagnosis

➢History
➢Blood, stool, vomitus studies
➢Endoscopy
Upper GI Bleed Treatments

➢ Volume replacement ➢ NG lavage

1. Crystalloids- normal saline
2. Blood transfusions

➢EGD
1. Endoscopic treatment of bleeding ulcer
2. Sclerotheraphy-injecting bleeding ulcer with necrotizing agent to
stop bleeding
Upper GI Bleed Treatments
➢Sengstaken-Blakemore tube - ➢Surgical intervention –
Used with bleeding esophageal Removal of part of the stomach
varacies
Cancer of Stomach

1. Incidence
➢Worldwide common cancer, but less
common in US
➢Incidence highest among Hispanics,
African Americans, Asian Americans, males
twice as often as females
➢Older adults of lower socioeconomic
groups higher risk
2. Pathophysiology
➢Adenocarcinoma most common form
involving mucus-producing cells of stomach
in distal portion
➢Begins as localized lesion (in situ) progresses
to mucosa; spreads to lymph nodes and
metastasizes early in disease to liver, lungs,
ovaries, peritoneum
Cancer of Stomach Risk Factors

➢ Genetic predisposition ➢ Chronic gastritis,

➢ H. pylori infection pernicious anemia,
gastric polyps

➢ Achlorhydria ➢ Diet high in smoked foods and

(lack of hydrochloric acid) nitrates
Cancer of Stomach Manifestations

➢Disease often advanced with metastasis when diagnosed

➢Early symptoms are vague: early satiety, anorexia, indigestion,
vomiting, pain after meals not responding to antacids
➢Later symptoms weight loss, cachexia (wasted away
appearance), abdominal mass, stool positive for occult blood
Cancer of Stomach Collaborative Care

➢ Support client through testing

➢ Assist client to maintain adequate nutrition

Diagnostic Tests
➢CBC indicates anemia
➢Upper GI series, ultrasound identifies
a mass
➢Upper endoscopy: visualization and
tissue biopsy of lesion
Cancer of Stomach Treatment

➢Surgery, if diagnosis made prior

to metastasis
1.Partial gastrectomy with
anastomosis to duodenum:
Bilroth I or gastroduodenostomy
2.Partial gastrectomy with
anastomosis to jejunum: Bilroth II
or gastrojejunostomy
3.Total gastrectomy (if cancer
diffuse but limited to stomach)
with esophagojejunostomy
Cancer of Stomach Treatment
➢dietary pattern to delay gastric emptying and allow smaller amounts of chyme
to enter intestine
1. Liquids and solids taken separately
2. Increased amounts of fat and protein
3. Carbohydrates, especially simple sugars, reduced
4. Client to rest recumbent or semi-recumbent 30 – 60 minutes after eating
5. Anticholinergics, sedatives, antispasmodic medications may be added
6. Limit amount of food taken at one time
Cancer of Stomach Treatment

➢ Radiation and/or chemotherapy to

control metastasic spread ➢ Palliative treatment including
surgery, chemotherapy; client may
have gastrostomy or jejunostomy
tube inserted

Nursing Diagnoses
➢Imbalanced Nutrition: Less than body requirement,
consult dietician since client at risk for protein-calorie
malnutrition
➢Anticipatory Grieving
Cancer of Stomach
Common Post-Op Complications

➢Pneumonia ➢Anastomotic leak ➢Hemorrhage ➢Reflux aspiration

➢Sepsis ➢Reflux gastritis

➢Paralytic ileus ➢Bowel obstruction

➢Wound infection ➢Dumping syndrome

Cancer of Stomach
➢Nutritional problems related to rapid entry of food into
the bowel and the shortage of intrinsic factor
Anemia: iron deficiency and/or pernicious
Folic acid deficiency
Poor absorption of calcium, vitamin D
END