This document discusses interventions for stomach disorders including gastritis, peptic ulcer disease, Zollinger-Ellison syndrome, and gastric cancer. It begins with an introduction to the anatomy and physiology of the stomach. Gastritis is then defined and the types, risk factors, pathogenesis, clinical features, diagnostic evaluation, and management are outlined. Peptic ulcer disease is similarly defined and the classifications, risk factors, etiological factors, pathogenesis, signs and symptoms, complications, diagnosis, and medical and non-medical management are described.

2. PRESENTED BY,
UMADEVI.K
MSC NURSING
MEDICAL SURGICAL NURSING DPT
KERALA
BANGALORE

3. INTERVENTIONS FOR THE
CLIENTS WITH DISORDERS
OF STOMACH

4. SUBTOPICS
 GASTRITIS
 PEPTIC ULCERATIVE DISEASE
 ZOLLIGER ELLISON SYMDROME
 GASTRIC CANCER

5. ALERT MIND AND THINK CRITICALLY
BEFORE DOING

6. GASTROINTESTINAL SYSTEM

7. STRUCTURE OF STOMACH AND
ADJACENT ORGANS

8. REGIONS OF ABDOMEN

9. INTRODUCTION
 The stomach is an organ between the esophagus and the
small intestine. It is where digestion of protein begins.
The stomach has three tasks. It stores swallowed food. It
mixes the food with stomach acids. Then it sends the
mixture on to the small intestine.
 There are many types of chronic disorders which affect
the stomach. However since the symptoms are localized
to this organ, the typical symptoms of stomach problems
include nausea, vomiting, bloating, cramps, diarrhea
and pain. Disorders of the stomach are very common
and induce a significant amount of morbidity and
suffering in the population. Data from hospitals indicate
that more than 25% of the population suffers from some
type of chronic stomach disorder including abdominal
pain and indigestion. These symptoms occur for long
periods and cause prolonged suffering, time off work and
a poor quality of life.

10. GASTRITIS

11. DEFINITION
 Gastritis occurs when the lining of the stomach
becomes inflamed or swollen.
OR
Gastritis, an inflammation or irritation of the lining of
the stomach

12. TYPES

 GASTRITIS


 ACUTE
CHRONIC
 TYPE A ( FUNDAL) TYPE B (ANTRAL)
SUPERFICIAL


HYPERATROPIC

ATROPIC

13. OTHER TYPES
 ACUTE STRESS GASTRITIS
 PHEGMONOUS GASTRITIS
 EROSIVE AND HEMORRHAGIC GASTRITIS
 CHEMICAL
 ENVIRONMENTAL

14. INCIDENCE
Mortality rate of 65% (PHLEGMONOUS)
No sexual predilection
More common in adults, than in children
Second most common cancer-related death.
Korea, Japan, China, Taiwan high rates.
22,000 diagnosed annually in US.
14th most common cancer.
Difficult to cure, as advanced disease.

15. RISK FACTORS
Helicobactor pylori infection
Age
Gastric irritants
Chemotherapy and radiation therapy

16. ETIOLOGY
Medications
Medical and surgical conditions
Infections
Intake of spicy foods
Alcohol
Chemotherapy and radiationtherapy
Swallowed foreign bodies (paper clips or
pins)
Trauma

17. Chronic vomiting
Smoking
Extreme stress
Eating corrosive substances
Pernicious anemia
Bile reflux

18. PATHOPHYSIOLOGY
A MUCOSAL BARRIER COMPOSED OF
PROSTAGLANDINS NORMALLY PROTECTS
STOMACH TISSUE FROM AUTODIGESTION
OF ACID
WHEN THE BARRIERS IS BROKEN
BECAUSE OF ETIOLOGICAL
FACTOR,ACID CAN DIFFUSE INTO THE
MUCOSA

19.  ALLOWS HCL TO ENTER THERE BY
INCREASES THE SECRETION OF
PEPSINOGEN AND RELEASE OF
HISTAMINE FROM MAST CELLS
 INJURY TO SMALL VESSELS
 EDEMA,HEMORRHAGE AND ULCER
FORMATION

20. CLINICAL FEATURES
 ASYMPTOMATIC
 Upper central abdominal pain
 Nausea and Vomiting
 Belching (if present, usually does not relieve the
pain much)
 Bloating
 Feeling full after only a few bites of food
 Loss of appetite
 Unexplained weight loss

21.  In more severe gastritis,
 Bleeding may occur inside the stomach.
 Pallor, sweating, and rapid heart beat.
 Feeling faint or short of breath
 Chest pain or severe stomach pain
 Vomiting large amounts of blood
 Bloody bowel movements or dark, sticky,
very foul-smelling bowel movements

22. DIAGNOSTIC EVALUATION
 complete history and physical exiamination
 H. pylori tests
 Breath test
 Tissue test
 Barium x rays
 Stool test
 Blood tests:
 Blood cell count
 Presence of H. pylori
 Urinalysis
 X-rays
 ECGs An electrocardiogram(ECG, EKG) might be ordered if the
patient's heartbeat is rapid or they are having chest pain.
 Stomach biopsy, to test for gastritis and other conditions

23. COMPLICATIONS
Blood loss
gastric cancer
GI bleeding
Reflux esophagitis
PUD
Chronic gastritis

24. MANAGEMENT
 MEDICAL MANAGEMENT
During acute phase bed rest ,NPO,IV fluids
Fluid and electrolyte balance (I/O Chart)
For severe case NG tube intubation
substances that trigger gastritis symptoms
ANTIEMETICS FOR VOMITING
 ANTACIDS

25. ANTIBIOTICS
Amoxicillin
Clarithromycin (Biaxin)
Metronidazole (Flagyl)
Tetracycline
CYTO PROTECTIVE AGENTS
Coating agents: These medications protect the
stomach's lining.
Sucralfate (Carafate) - Coats and protects the
stomach lining
Misoprostol(Cytotec) -

26. Magnesium-containing antacids
Aluminum-containing antacids
Calcium-containing antacids
H2 antagonist (ranitidine ,emetidine )
Proton pump inhibitors (PPIs) -
omeprazole (Prilosec)
For patient with pernicious
anemia;regular vit B12 Injection
blood transfusion and fluid replacement
Stop taking aspirin, ibuprofen

27. 

28. VAGOTOMY Vagotomy is the surgical
cutting of the vagus nerve

29. PYLOROPLASTY (Pyloroplasty is an
elective surgical procedure in which the
lower portion of the stomach, the pylorus, is
cut and resutured

30. Dietary management
smaller, more frequent meals
Avoid any foods which is irritating
Limiting excessive use of alcohol
Foods containing flavonoids,
Mulltivitamins

31.  6-8 glasses of water
 Omega 3 fatty acids to redude inflammation
 Probiotics

32. NURSING DIAGNOSIS AND
MANGAMENT
PAIN related to irritation of gasric mucosa
Nausea and vomiting related to multiple
etiologies as manifested by episodes of
nausea and vomiting
Fluid volumedeficit related to prolonged
vomiting and inability to ingest digest and
absorb food and fluid as manifested by
decreased urinary output,increased urine
concentration,increased pulse
rate,hypotension

33. Anxiety related to lack of knowledge of
cause of the problegem,treatment plan and
follow up care as manifested by
verbalization of lack of knowledge
Risk for altered nutrition less than body
requirement related to nausea and
vomiting as manifested by lack of interest
in food,weight loss.

34. PAIN INTERVENTIONS
 ASSESS INTENSITY DURATION AND LOCATION OF PAIN
 COMFORT POSITION AND MEASURES
 MEDICATIONS
 REVIEW FACTORS AGRAVETING PAIN
 DIETARY MODIFICATIONS
NAUSEA AND VOMITING
Observe for potential complications
Position the patient: To prevent aspiration
 Conscious: semi fowler’s
 Unconscious: lateral
 Provide good oral care measures
 Suction mouth

35. FLUID VOLUME DEFICIT
 Moniter vital signs,capillary refill,status
 Daily fluidintake and output are monitored to detect early signs of dehydration
 (minimum 1.5 lit/day)
 Iv fluids 3L/day is administered usually
 Identify actions to regain optimal fluid balance
 Eg: Specific Fluid intake schedule
 ANXIETY
 Offer Supportive therapy to the patient
 Explain all the procedures before doing
 Provide calm and restful environment
 Help the patient to identify and initiate positive coping behaviors in the
past

36. Nurses role
Assessment
GOALS
implementing interventions

37. PREVENTION
Avoid those things that irritate or inflame the
stomach's lining.
Aspirin
NSAIDs
Smoking
Caffeine and other caffeine-like substances
Alcohol

38. GASTRITIS FOLLOW UP
Avoid those things that irritate the
stomach or cause symptoms to flare up.
Take all medications as prescribed by the
health care provider.
Return for medical attention if symptoms
worsen or persist.
Report any new symptoms to a health care
provider.

40. DEFINITION
 A peptic ulcer, also known as PUD or peptic
ulcer disease is the most common ulcer of an
area of the gastrointestinal tract that is
usually acidic and thus extremely painful. It is
defined as mucosal erosions equal to or greater
than 0.5 cm.
OR
 Peptic ulcer is the erosion of GI mucosa
resulting from the action of HCL and pepsin
that forms in the pylorus of stomach ,in the
duodenum or in the esophagus

41. CLASSIFICATION
 By Region/Location
Duodenum (called duodenal ulcer)
Oesophagus (called esophageal ulcer)
Stomach (called gastric ulcer)
Meckel's diverticulum (called Meckel's
diverticulum ulcer; is very tender with
palpation)

42. Modified Johnson Classification of
peptic ulcers:
Type I: Ulcer along the body of the stomach,
most often along the lesser curve at incisura
angularis along the locus minoris resistantiae.
Type II: Ulcer in the body in combination with
duodenal ulcers. Associated with acid
oversecretion.
Type III: In the pyloric channel within 3 cm of
pylorus. Associated with acid oversecretion.
Type IV: Proximal gastroesophageal ulcer
Type V: Can occur throughout the stomach.
Associated with chronic NSAID use (such as
aspirin).

43. INCIDENCE
 The incidence of duodenal ulcers has
dropped significantly during the last 30
years, while the incidence of gastric ulcers
has shown a small increase, mainly caused
by the widespread use of NSAIDs
 Nowadays peptic ulcer disease is about just
as common among women than among men
 Duodenal ulcers are most frequent among
individuals 30 to 55 years of age, while
gastric ulcers are more common among
individuals 55 to 70 years of age

44. RISK FACTORS
 An increased risk of peptic ulcers if:
 Smoking may increase the risk of
peptic ulcers in people who are
infected with H. pylori.
 Alcoholism
 Have uncontrolled stress

45.  Factors associated with an increased risk of duodenal
ulcers in the setting of NSAID use include
 history of previous peptic ulcer disease,
 advanced age,
 female sex,
 high doses or combinations of NSAIDs,
 long-term NSAID use,
 concomitant use of anticoagulants, and
 severe comorbid illnesses.
 Little evidence suggests that caffeine intake is
associated with an increased risk of duodenal ulcers.

46. ETIOLOGICAL FACTORS
INFECTION
DRUGS
HYPERSECRETORY
Gastrinoma
Basophilic leukemias
Cystic fibrosis
Short bowel syndrome
Lifestyle factors
Severe physiologic stress
Genetic factors

47. Additional etiologic factors
 Any of the following may be associated with PUD:
 Hepatic cirrhosis
 Chronic obstructive pulmonary disease
 Allergic gastritis and eosinophilic gastritis
 Cytomegalovirus infection
 Graft versus host disease
 Corrosive gastropathy
 Celiac disease
 Autoimmune disease

48. PATHOPHYSIOLOGY
Peptic ulcers are defects in the gastric or
duodenal mucosa that extend through the
muscularis mucosa.
Irritation of gastric or duodenal mucosa
due to various etiological factors
Epithelial cells of the stomach and
duodenum secrete mucus in response to
irritation of the epithelial lining and as a
result of cholinergic stimulation

49. The superficial portion of the gastric and
duodenal mucosa exists in the form of a gel layer,
which is impermeable to acid and pepsin
Other gastric and duodenal cells secrete
bicarbonate, which aids in buffering acid that
lies near the mucosa.
Prostaglandins of the E type (PGE) increases
the production of both bicarbonate and the
mucous layer.
In the event of acid and pepsin entering the
epithelial cells, additional mechanisms are in
place to reduce injury

50. Within the epithelial cells, ion pumps in the
basolateral cell membrane help to regulate
intracellular pH by removing excess hydrogen
ions.
 Through the process of restitution, healthy
cells migrate to the site of injury
 Mucosal blood flow removes acid that
diffuses through the injured mucosa and
provides bicarbonate to the surface
epithelial cells.

51. SIGNS AND SYMPTOMS
Bloating and abdominal fullness;
Nausea, and copious vomiting;
Loss of appetite and weight loss;
Pain
Hematemesis
Melena (Nausea or vomiting
Unexplained weight loss
Appetite changes(loss of appetite)
Bloating
Heartburn
Waterbrash

52. COMPLICATIONS
Gastrointestinal bleeding
Perforation
Penetration
Gastric outlet obstruction.
Cancer
Exacerbation
Gastric outlet obstruction
Peritonitis

53. DIAGNOSIS
History collection and physical examination
Testing for Bacterial Infection
Blood TesT
Blood tests such as
The enzyme-linked immunosorbent assay
(ELISA)
CBC
Breath Tests
Tissue Tests
Barium X-rays

54. MANAGEMENT
GOALS OF TREATMENT
The main goal for peptic ulcer treatment is
the immediate relief of pain in the patient.
to eliminate the conditions that aggravate
it and to prevent recurrence.
Relief of discomfort and protection of
gastric mucosa from complications.

55.  3 stages in medical treatment.
 These are ;
 the preventive,( by providing information and
educating the population on how to identify
symptoms and avoiding the causes of the
disease)
 curative and (where patients suffering the
disease undergo treatment)
 rehabilitation phases of treatment.( patient
recovery and prevention of disease
recurrence).

56. MEDICAL MANAGMENT
 Antibiotic medications
 Pain Relief through Medications
 Medications that block acid production and
promote healing(PPI)
 Medications to reduce acid production. (H2
BLOCKERS)
 Antacids that neutralize stomach acid.

57. Medications that protect the lining of
your stomach and small intestine
NON MEDICAL MANAGEMENT
.Lifestyle changes
Eating meals at regular intervals.
avoid or manage stressful conditions
Avoid smoking
Maintain proper diet and avoid food or
beverages which upset the gastric mucosa
like coffee, tea, colas and alcohol.

58. Ulcers that fail to heal
Peptic ulcers that don't heal with
treatment are called refractory ulcers.
These reasons may include:
Not taking medications according to directions.
The fact that some types of H. pylori are resistant to
antibiotics.
Regular use of tobacco.
Regular use of pain relievers that increase the risk of ulcers
Extreme overproduction of stomach acid, such as occurs in
Zollinger-Ellison syndrome
An infection other than H. pylori
Stomach cancer
Other diseases that may cause ulcer-like sores in the stomach
and small intestine, such as Crohn's disease
Treatment for refractory ulcers generally involves eliminating
factors that may interfere with healing, along with using
different antibiotics

59. SURGICAL INTERVENTIONS
 vagotomy
Vagotomy is the surgical cutting of the
vagus nerve

60. Truncal or total abdominal
vagotomy

61. SELECTED TOTAL GASTRIC
VAGOTOMY

62. Highly selective vagotomy (HSV)


63. Thoracoscopic vagotomy

64. PYLOROPLASTY (Widening the
opening of the bottom of the stomach
 ANTRECTOMY
 surgical removal, of a part of the stomach
known as the antrum

65. GASTRODUEODENOSTO
MY(BILLROTH 1)
 Removal of lower portion of antrum of
stomach(which contains cells that secrete
gastrin)as well as small portion of
dueodenum and pylorus.the remaining
segment is anostomised with dueodenum

66. GASTROJEJUNOSTOMY(BILLROTH 2)
Gastrojejunostomy (GJ) is a surgical procedure in which an
anastomosis is created between the stomach and the proximal
loop of the jejunum.
.

67. SUBTOTAL GASTRECTOMY WITH
BILLROTH 1 AND 2 ANASTOMOSIS)
Removal of distal part of stomach and
anastomised with dueodenum and jejunum
 LOW HIGH

68. DIETARY MANAGEMENT
 IT INCLUDES;
 Avoiding spicy foods, coffee, and alcohol
 increasing consumption of bland foods and
milk.
Avoiding High–fiber diets
 INTAKE Diets high in vitamin A
 Avoid Green tea
 Probiotics

69. NURSING DIAGNOSIS AND
MANAGEMENT
 Nursing diagnosis
 Increased risk of GI bleeding and perforation of stomach,
related to gastric or intestinal wall erosion.

Increased risk of pyloric obstruction as complication of the
peptic ulcer.

increased risk of anemia due to acute or chronic GI bleeding,
related to ulcer.

Pain and heartburn, related to diagnosis of peptic ulcer..
Appetite changes and weight changes due to symptoms of the
ulcer.increased risk of aspiration due to vomiting, related to
ulcer.

Anxiety related to the symptoms of disease and fear of the
unknown.

70. Goals

1. Reduce or completely eliminate
contributing factors.
2. Assist with stress management.
3. Promote adequate nutrition.
4. Prevent avoidable injury.
5. Then surgical intervention prescribed,
prevent postoperative complications.
6. Relief or diminish symptoms.

71. Interventions
1. Assess, report , and record signs and symptoms and reactions to treatment.
2. Monitor fluids input and output closely.
3. Administer antacid agents, analgesics, H2-receptors antagonists,
anticholinergics, sedatives as prescribed, monitor for side effects.
4. Monitor client’s vital signs and signs of possible GI bleeding or perforation
closely.
5. Monitor laboratory tests results (CBC, electrolytes, Hb levels) for abnormal
values.
6. Undertake appropriate intervention in case of GI bleeding, vomiting, or
perforation.
7. Provide prescribed diet – avoid irritating foods, coffee, etc.
8. Prepare client and his family for surgical intervention if required for
recurrent ulcer, hemorrhage, or perforation.
9. For client after surgical intervention provide postoperative care and inform
about possible postoperative complications, such as dumping syndrome.
10. Provide emotional support to client, explain all procedures to decrease
anxiety and to obtain cooperation.
11. Instruct client regarding disease progress, diagnostic procedures, treatment
and its complications, home care, daily activities, diet, restrictions and follow-up.

72. Nursingmanagement
 1. Assess for chronic use of certain medications (such as aspirin, steroids).
2. Collect information of complaints that brought client to the hospital.
3. Obtain history of onset and progression of symptoms.
4. Obtain information of diet, use of alcohol and tobacco, ingestion of irritating
foods, previous diseases or infections of GI tract, emotional stress.
5. Assess connection of pain attacks to meals, certain drugs, ingestion of coffee,
alcohol.
6. Perform complete physical assessment including weight, vital signs, signs of GI
bleeding, and acute abdomen.
7. Assess diagnostic tests and procedures for abnormal values.
 Evaluation
1. Reports increased comfort, decreased anxiety.
2. Verbalizes absence of heartburn and pain.
3. No evidence of nausea, vomiting, GI bleeding, or acute abdomen.
4. Maintains stable vital signs, fluid balance, and body weight.
5. Laboratory tests results shows no abnormalities.
6. No postoperative complications.
7. Demonstration of understanding of disease progress, diagnostic and treatment
procedures, prevention, and need for follow-up.


73. ZOLLINGER ELLLISSON
SYNDROME

74.  Zollinger-Ellison syndrome is a condition in
which there is increased production of the
hormone gastrin, causing the stomach to
produce excess hydrochloric acid
Zollinger–Ellison syndrome is a triad of
gastric acid hypersecretion,
severe peptic ulceration, and
non-beta cell islet tumor of pancreas
(gastrinoma)

75. Incidence andRisk factors
 Incidence
 Annual incidence is estimated at 1-2 cases per
million.
 The condition is slightly more common in
females than males (sex ratio of 1.3:1).
 ZES is usually diagnosed in the fifth decade of
life
 Risk factors
 Multiple endocrine neoplasia type 1 syndrome,
characterised by other endocrine tumours.

76. Causes
 Zollinger-Ellison syndrome is caused by
 tumors, usually found in the head of the pancreas and
the upper small intestine. These tumors produce the
hormone gastrin and are called gastrinomas. High
levels of gastrin cause production of too much
stomach acid.

77.  Due to tumours(gastrinomas)
 Production of excess gastrin
 Gastrin works on stomach parietal cells
 Secrete more hydrogen ions into the
stomach lumen.

78.  In addition, gastrin acts as a trophic factor for
parietal cells
 parietal cell hyperplasia.
 Increase in the number of acid-secreting cells
 cells produces acid at a higher rate
 development of multiple peptic ulcers in the
stomach and duodenum (small bowel).

79. Signs and Symptoms
 Abdominal pain
 Diarrhea
 Vomiting blood (occasional)
 Signs include ulcers in the stomach and small
intestine.
 Gnawing, burning pain in the abdomen
 This pain is usually located in the area between the
breastbone and the navel.
 Sensation of pressure, bloating, or fullness
 This pain usually develops 30 to 90 minutes after a
meal, and is often relieved by antacids.
 Pain or burning sensation in the abdomen that
travels up toward the throat

80.  This is caused by heartburn, or gastroesophageal reflux
and occurs when stomach contents back up into the
esophagus
 Vomiting
 The vomit may contain blood or resemble coffee grounds.
 Diarrhea
 Stools may be foul smelling.
 Black, tarry stools
 Blood in the stools will turn them dark red or black, and
make them tarry or sticky.
 Nausea
 Fatigue
 Weakness
 Weight loss

81. Diagnostic tests
 Tests include:
 Abdominal CT scan
 Calcium infusion test
 Endoscopic ultrasound
 Exploratory surgery
 Gastrin blood level
 Octreotide scan
 Secretin stimulation test

82. Complications
 Bleeding
 Perforation
 Fluid and electrolyte imbalance Complications
 Failure to locate the tumor during surgery
 Intestinal bleeding or hole (perforation) from ulcers in
the stomach or duodenum
 Severe diarrhea and weight loss
 Spread of the tumor to other organs (most often liver
and lymph nodes)

83. Treatment
 Medications
 Histamine H2-receptor antagonists
 (such as famotidine and ranitidine) are used to slow
down acid secretion

 proton pump inhibitors ::These drugs reduce acid
production by the stomach, and promote healing of
ulcers in the stomach and small intestine. They also
relieve abdominal pain and diarrhea.
 omeprazole, lansoprazole, etc

84. Surgery
 Cure is only possible if the tumors are surgically
removed, or treated with chemotherapy
 to remove a single gastrinoma is done if there is no
evidence that it has spread to other organs (such as
lymph nodes or the liver).
 Surgery on the stomach (gastrectomy) to control acid
production is done rarely.


85. Prognosis
 Even with early diagnosis and surgery to remove the
tumor, the cure rate is relatively low. However,
gastrinomas grow slowly, and patients may live for
many years after the tumor is discovered. Acid-
suppressing medications are very effective at
controlling the symptoms of too much acid
production.

86. NURSING DIAGNOSIS
AND MANAGEMENT
 Nursing diagnosis
1. Increased risk of GI bleeding and perforation of
stomach, related to gastric or intestinal wall erosion.
2. Increased risk of pyloric obstruction as complication of
the peptic ulcer.
3. Increased risk of anemia due to acute or chronic GI
bleeding, related to ulcer.
4. Pain and heartburn, related to diagnosis of peptic
ulcer.
5. Appetite changes and weight changes due to symptoms
of the ulcer.
6. Increased risk of aspiration due to vomiting, related to
ulcer.
7. Anxiety related to the symptoms of disease and fear of
the unknown.

88.  Stomach cancer, or gastric cancer, refers to
cancer arising from any part of the
stomach. Stomach cancer causes about
800,000 deaths worldwide per year. Gastric
cancer was once the second most common
cancer in the world.
OR
 A gastric carcinoma is a malignant tumour
arising from the epithelium of the stomach

89. INCIDENCE
 Stomach cancer is the fourth most common cancer worldwide
 It is more common in men and in developing countries.
 Frequency
 United States
 The American Cancer Society estimates that 21,130 cases of gastric cancer was
diagnosed in the year 2009 (12,820 in men, 8,310 in women) and that 10,620
persons diedof the disease. Gastric cancer is the seventh leading cause of cancer
deaths.
 International
 Once the second most common cancer worldwide, stomach cancer has dropped to
fourth place, after cancers of the lung, breast, and colon and rectum.
 However, stomach cancer remains the second most common cause of death from
cancer
 Ratesof the disease are highest in Asia and parts of South America and lowest in
North America. The highest death rates are recorded in Chile, Japan, South
America, and the former Soviet Union.
 Metastasis occurs in 80-90% of individuals with stomach cancer, with a six month
survival rate of 65% in those diagnosed in early stages and less than 15% of those
diagnosed in late stages.

90.  Mortality/Morbidity
 survival rate for curative surgical resection ranges from 30-50%
for patients with stage II disease and from 10-25% for patients with
stage III disease.
 The operative mortality rate less than 3%.
 high death rate (Approximately 800,000 per year) making it the
second most common cause of cancer death worldwide after lung
cancer
 Race
 The rates of gastric cancer are higher in Asian and South
American countries than in the United States.
 Japan, Chile, and Venezuela have developed a very rigorous early
screening program that detects patients with early stage disease
(ie, low tumor burden). These patients appear to do quite well.

91.  In fact, in many Asian studies, patients with resected stage II
and III disease tend to have better outcomes than similarly
staged patients treated in Western countries.
 In the United States, Asian and Pacific Islander males and
females have the highest incidence of stomach cancer, followed
by black, Hispanic, white, American Indian, and Inuit
populations.
 Sex
 In the United States, gastric cancer affects slightly more men
than women
 Worldwide, however, gastric cancer rates are about twice as
high in men as in women.
 Age
 Most patients are elderly at diagnosis.
 common in 50 – 70 yrs

92. STAGES
 The clinical stages of stomach cancer are:
 Stage 0. Limited to the inner lining of the
stomach..
 (Stage I)
 (Stage 1A. Penetration to the second or
third layers of the stomach.
 (Stage 1B).. the second layer and nearby
lymph nodes.

.

93.  Stage II. Penetration to the second layer and
more distant lymph nodes, or the third layer
and only nearby lymph nodes, or all four layers
but not the lymph nodes
 Stage III. Penetration to the third layer and
more distant lymph nodes, or penetration to
the fourth layer and either nearby tissues or
nearby or more distant lymph nodes.
 Stage IV. Cancer has spread to nearby tissues
and more distant lymph nodes, or has
metastatized to other organs

94. ETIOLOGICAL FACTORS
 Diet
 Smoking
 . Helicobacter pylori infection
 Previous gastric surgery
 Genetic factors
 Li-Fraumeni syndrome
 familial adenomatous polyposis and
 Peutz-Jeghers syndrome
 Epstein-Barr virus
 Pernicious anemia
 Obesity
 Radiation exposure
 Bisphosphonates

95. DIFFERENTIAL DIAGNOSIS
 Esophagitis
 Gastric Ulcers
 Gastritis, Acute
 Gastritis, Atrophic
 Gastritis, Chronic
 Gastroenteritis, Bacterial
 Gastroenteritis, Viral
 Lymphoma, Non-Hodgkin
 Malignant Neoplasms of the Small Intestine

96. PATHOPHYSIOLOGY
 Initiation,prioliferation and progression
 The tumour growth is insiduos and follows
a pattern of continuos
infiltration.
 Cancer of stomach may spread by direct
extension along the mucosal surface and
infiltration through the gastric wall

97.  Once the stomach wall has been penetrated
by tumour growth adjascent organs and
structures that may become involed are the
esophagus ,dueodenum , omentum,liver and
pancreas
 Distant maetastasis is falicitated by rich
lymphatic plexuses in the stomach wall.
 Seeding of tumour cells into the peritoneal
cavity occurs late in the course of disease

98. CLINICAL FEATURES
 SYMPTOMS
 Abdominal fullness or pain which may occur after eat a small meal
 Dark stools
 Difficulty swallowing, which becomes worse over time
 Excessive belching
 General decline in health
 Loss of appetite
 Nausea
 Vomiting, which may contain blood
 Weakness or fatigue
 Weight loss
 SIGNS
 Diagnosis is often delayed because symptoms may not occur in the
early stages of the disease.patients may self-treat symptoms that
gastric cancer has in common with other, less serious gastrointestinal
disorders (bloating, gas, heartburn, and a sense of fullness).

99. DIAGNOSTIC TESTS
 The following tests can help diagnose gastric cancer:
 History collection and physical examination
 Complete blood count (CBC) to check for anemia
 Esophagogastroduodenoscopy (EGD) with biopsy to
examine the stomach tissue
 Stool test to check for blood in the stools

 Endoscopy:
 Upper Gastrointestinal Series/Barium Radiography
 Endoscopic Ultrasound
 Computed Tomography (CT) Scan
 Positron Emission Tomography (PET
 Magnetic Resonance Imaging (MRI)
 Chest X-Ray

100. COMPLICATIONS
 Mortality 1-2%
 Anastamotic leak, bleeding, ileus, transit
failure, cholecystitis, pancreatitis,
pulmonary infections, and
thromboembolism.
 Late complications include dumping
syndrome, vitamin B-12 deficiency, reflux
esophagitis, osteoporosis.

101. MANAGEMENT
Surgery
 Chemotherapy

 Radiation therapy
Biological therapy
Radical surgery

102. Surgery
Endoscopic mucosal resection(EMR)

103.  Endoscopic submucosal dissection
 (ESD)

104. Gatrectomy

105. RADICAL SURGERY
 CRS(CYTO REDUCTIVE SURGERY)
+
HIPEC (HYPERTHERMIC
INTRAPERITONEAL
CHEMOTHERAPY)

106. Chemotherapy
Some drugs used in stomach cancer treatment have
included:
 5-FU (fluorouracil)
 capecitabine,
 BCNU (carmustine),
 methyl-CCNU (Semustine), and
 doxorubicin(Adriamycin),
 Mitomycin C, and
 cisplatin and taxotere
 Clinical researchers have explored the benefits of
giving chemotherapy before surgery to shrink the
tumor, or as adjuvant therapy after surgery to
destroy remaining cancer cells.

107. Radiation
 Radiation therapy (also called
radiotherapy) is the use of high-energy rays
to damage cancer cells and stop them from
growing.
 When used, it is generally in combination
with surgery and chemotherapy, or used
only with chemotherapy in cases where the
individual is unable to undergo surgery.
 Radiation therapy may be used to relieve
pain or blockage by shrinking the tumor for
palliation of incurable disease.

108. Multimodality therapy
 While previous studies of multimodality therapy
(combinations of surgery, chemotherapy and
radiation therapy) gave mixed results
 The combination of chemotherapy and radiation
therapy in patients with nonmetastatic, completely
resected gastric cancer is benefited.
 Patients were randomized after surgery to the
standard group of observation alone, or the study
arm of combination chemotherapy and radiation
therapy.
 Those in the study arm receiving chemotherapy
and radiation therapy survived on average 36
months; compared to 27 months with observation

109. Residual Disease R Status
 Tumor status following resection.
 Assigned based on pathology of margins.
 R0- no residual gross or microscopic disease.
 R1- microscopic disease only.
 R2- gross residual disease.
 Long term survival only in R0 resection

110. “D” Nomenclature
 Describes extent of resection and
lymphadenectomy.
 D1- removes all nodes within 3cm of tumor.
 D2- D1 plus hepatic, splenic, celiac, and left
gastric nodes.
 D3- D2 plus omentectomy, splenectomy, distal
pancreatectomy, clearance of porta hepatis
nodes.
 Current standards include a D1 dissection only.

111. NURSING DIAGNOSIS AND
INTERVENTIONS
 Pain related to underlying disease process and
sideffects of surgery,chemotherapy and radiation
therapy

112.  Imbalanced nutrition less than body requirements
related to inability to ingest,digest or absorb nutrients

113.  Activity intolerance related to generalized weakness
,abdominal discomfort and nutritional deficits

114.  Anxiety related to lack of knowledge of diagnostic
tests,unknown diagnostic outcomes,disease process

115.  Anticipatory grieving related to percoieved
unfavourable diagnosis and impending death.

116. PREVENTION
 Avoiding risk factors and increasing protective factors
may help to prevent stomach cancer and includes
avoiding;
 Certain medications like NSAIDS
 Certain diet like spicy foods
 Smoking
 Alcoholism
 Stress
 Helicobacter infection

117. RESEARCH STUDY
 RESEARCH IN STOMACH CANCER
 Current Areas of Stomach Cancer Research
 Stomach cancer research scientists are testing new approaches for treatment,
including:

 Anticancer drugs and drug combinations
 Different methods, doses, and schedules of radiation therapy
 Combination therapy (which includes chemotherapy, surgery, and radiation
therapy).

 Other research trials are studying the effectiveness of using biological therapy
to treat the disease. This therapy uses substances made by the body or in a
laboratory to boost, direct, or restore the body's natural defenses against
cancer. This type of treatment is also called biotherapy or immunotherapy.

118. RESEARCH STUDIES
RELATED TO GASTRITIS
 New study identifies potential vaccine to prevent gastritis,
ulcer disease, gastric cancer February 2, 2011 A new study led
by researchers at Rhode Island Hospital in collaboration with
the University of Rhode Island (URI) and EpiVax. Inc, a
privately owned vaccine development company in Providence,
RI, has identified a potential vaccine capable of reducing
colonization of Helicobacter pylori (H. pylori) -- known cause
of gastritis, ulcer disease and cancer.

119. RESCENT RESEARCH RELATED TO
GASTRIC CARCINOMA
 Risk of Cancer from Heartburn Pills

The group of medicines which can alleviate heartburn quickly and is the most widely prescribed class
of drugs in Britain can actually increase the risk of cancer, reveals a recent study.

 The group of medicines which can alleviate heartburn quickly and is the most widely prescribed class
of drugs in Britain can actually increase the risk of cancer, reveals a recent study.

Researchers said that the class of drugs commonly prescribed for heart burn known as proton pump
inhibitors (PPIs), can increase the risk of cancer, heart disease and infections.

Even though the drugs controlled symptoms of acid reflux, they actually increased the risk of cancer
rather then reducing it.

Peter Weissberg, medical director of the British Heart Foundation, said: "Doctors need to be sure they
are really necessary." - JULY 25 2012

120. CONCLUSION
 There is a plethora of literature
concerning gastritis and peptic ulcer disease caused by
the bacterium Helicobacter pylori. Nevertheless, there is
still much to be learned about this bacterium and its
effects on the human body. It may not be known exactly
how H. pylori is transmitted but at least we are able to
detect and eradicate the bacterium with relative ease
and efficiency. Many new ways to help prevent and
inhibit the activity of H. pylori are being discovered.
Now it is up to the scientists to discover even better
ways to treat the disease caused by this bacterium and to
find ways to prevent the disease. When H. pylori’s mode
of transmission is finally discovered, it may lead to more
efficient ways to prevent transmission and infection. As
a nurse its very important to give health education as
primary prevention and also secondary and tertiary
prevention once disease occurred.

121. WE WANT MORE NURSES……

122. 
 THANK UUU….