Stomach disorders

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WELCOME

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STOMACH DISORDERS

Transcript of Stomach disorders

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WELCOME

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PRESENTED BY,

UMADEVI.KMSC NURSING

MEDICAL SURGICAL NURSING DPTKERALA

BANGALORE

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SEMINAR ON INTERVENTIONS FOR THE CLIENTS WITH DISORDERS OF STOMACH

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SUBTOPICSGASTRITIS

PEPTIC ULCERATIVE DISEASE

ZOLLIGER ELLISON SYMDROME

GASTRIC CANCER

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ALERT MIND AND THINK CRITICALLY BEFORE DOING

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GASTROINTESTINAL SYSTEM

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STRUCTURE OF STOMACH AND ADJACENT ORGANS

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REGIONS OF ABDOMEN

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INTRODUCTIONThe 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.

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GASTRITIS

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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

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TYPES GASTRITIS    ACUTE

CHRONIC

TYPE A ( FUNDAL) TYPE B (ANTRAL) SUPERFICIAL

HYPERATROPIC

ATROPIC

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OTHER TYPES

ACUTE STRESS GASTRITISPHEGMONOUS GASTRITISEROSIVE AND HEMORRHAGIC GASTRITISCHEMICALENVIRONMENTAL

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INCIDENCE Mortality rate of 65% (PHLEGMONOUS)

No sexual predilection More common in adults, than in childrenSecond 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.

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RISK FACTORS

Helicobactor pylori infectionAgeGastric irritants Chemotherapy and radiation therapy

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ETIOLOGYMedicationsMedical and surgical conditionsInfectionsIntake of spicy foodsAlcoholChemotherapy and radiationtherapySwallowed foreign bodies (paper clips or pins) Trauma

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Chronic vomitingSmokingExtreme stressEating corrosive substancesPernicious anemiaBile reflux

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PATHOPHYSIOLOGYA 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

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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

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CLINICAL FEATURES ASYMPTOMATICUpper central abdominal painNausea and VomitingBelching (if present, usually does not relieve the

pain much)BloatingFeeling full after only a few bites of foodLoss of appetiteUnexplained weight loss 

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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

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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

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COMPLICATIONSBlood loss gastric cancerGI bleedingReflux esophagitisPUDChronic gastritis

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MANAGEMENTMEDICAL MANAGEMENTDuring acute phase bed rest ,NPO,IV fluidsFluid and electrolyte balance (I/O Chart)For severe case NG tube intubationsubstances that trigger gastritis symptomsANTIEMETICS FOR VOMITING ANTACIDS

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ANTIBIOTICS

AmoxicillinClarithromycin (Biaxin)Metronidazole (Flagyl)TetracyclineCYTO PROTECTIVE AGENTS

Coating agents: These medications protect the stomach's lining. Sucralfate (Carafate) - Coats and protects the stomach lining Misoprostol(Cytotec) -

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Magnesium-containing antacidsAluminum-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 replacementStop taking aspirin, ibuprofen

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PARTIAL GATRECTOMY( partial surgical removal of the stomach.)

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VAGOTOMY Vagotomy is the surgical cutting of the vagus nerve

 

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

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Dietary management

smaller, more frequent meals

Avoid any foods which is irritating

Limiting excessive use of alcohol

Foods containing flavonoids,

Mulltivitamins

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6-8 glasses of waterOmega 3 fatty acids to redude

inflammationProbiotics

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NURSING DIAGNOSIS AND MANGAMENT

PAIN related to irritation of gasric mucosaNausea and vomiting related to multiple etiologies as manifested by episodes of nausea and vomitingFluid 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

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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.

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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’sUnconscious: lateralProvide good oral care measures Suction mouth

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FLUID VOLUME DEFICITMoniter 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 balanceEg: Specific Fluid intake schedule

ANXIETYOffer Supportive therapy to the patientExplain all the procedures before doingProvide calm and restful environmentHelp the patient to identify and initiate positive

coping behaviors in the past

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Nurses role

Assessment

GOALS

implementing interventions

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PREVENTIONAvoid those things that irritate or inflame the stomach's lining.

AspirinNSAIDsSmokingCaffeine and other caffeine-like substances Alcohol

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GASTRITIS FOLLOW UPAvoid 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.

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PEPTIC ULCERATIVE DISEASE

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DEFINITIONA 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

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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)

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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 ulcerType V: Can occur throughout the stomach. Associated with chronic NSAID use (such as aspirin).

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INCIDENCEThe 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

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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.

AlcoholismHave uncontrolled stress

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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.

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ETIOLOGICAL FACTORSINFECTIONDRUGSHYPERSECRETORYGastrinomaBasophilic leukemiasCystic fibrosisShort bowel syndromeLifestyle factorsSevere physiologic stressGenetic factors

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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

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PATHOPHYSIOLOGYPeptic 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

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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

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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.

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S

SIGNS AND SYMPTOMS

Bloating and abdominal fullness;Nausea, and copious vomiting;Loss of appetite and weight loss;PainHematemesis Melena (Nausea or vomitingUnexplained weight lossAppetite changes(loss of appetite)Bloating Heartburn Waterbrash

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COMPLICATIONSGastrointestinal bleedingPerforation Penetration Gastric outlet obstruction. CancerExacerbationGastric outlet obstructionPeritonitis

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DIAGNOSIS

History collection and physical examinationTesting for Bacterial InfectionBlood TesT Blood tests such as The enzyme-linked immunosorbent assay (ELISA)

CBCBreath TestsTissue Tests

Barium X-rays

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MANAGEMENT

GOALS OF TREATMENTThe 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.

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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).

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MEDICAL MANAGMENT

Antibiotic medicationsPain Relief through Medications

Medications that block acid production and promote healing(PPI)

Medications to reduce acid production. (H2 BLOCKERS)

Antacids that neutralize stomach acid.

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Medications that protect the lining of your stomach and small intestine

NON MEDICAL MANAGEMENT.Lifestyle changesEating meals at regular intervals.avoid or manage stressful conditionsAvoid smoking Maintain proper diet and avoid food or

beverages which upset the gastric mucosa like coffee, tea, colas and alcohol.

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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 ulcersExtreme overproduction of stomach acid, such as occurs in Zollinger-Ellison syndromeAn infection other than H. pyloriStomach cancerOther diseases that may cause ulcer-like sores in the stomach and small intestine, such as Crohn's diseaseTreatment for refractory ulcers generally involves eliminating factors that may interfere with healing, along with using different antibiotics

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SURGICAL INTERVENTIONS

 vagotomyVagotomy is the surgical cutting of the vagus

nerve

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Truncal or total abdominal vagotomy

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SELECTED TOTAL GASTRIC VAGOTOMY

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Highly selective vagotomy (HSV)

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Thoracoscopic vagotomy

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PYLOROPLASTY (Widening the opening of the bottom of the stomach

ANTRECTOMY surgical removal, of a part of the stomach

known as the antrum

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GASTRODUEODENOSTOMY(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

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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.

.

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SUBTOTAL GASTRECTOMY WITH BILLROTH 1 AND 2 ANASTOMOSIS)Removal of distal part of stomach and anastomised with dueodenum and jejunumLOW HIGH

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DIETARY MANAGEMENT

IT INCLUDES;Avoiding spicy foods, coffee, and alcohol increasing consumption of bland foods

and milk. Avoiding High–fiber dietsINTAKE Diets high in vitamin AAvoid Green teaProbiotics

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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.

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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.

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Interventions1. 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.

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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.

 

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ZOLLINGER ELLLISSON SYNDROME

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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)

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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 factorsMultiple endocrine neoplasia type 1 syndrome,

characterised by other endocrine tumours.

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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.

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Due to tumours(gastrinomas)

Production of excess gastrin

Gastrin works on stomach parietal cells

Secrete more hydrogen ions into the stomach lumen.

 

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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). 

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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

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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

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Diagnostic tests 

Tests include:Abdominal CT scanCalcium infusion testEndoscopic ultrasoundExploratory surgeryGastrin blood levelOctreotide scanSecretin stimulation test

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ComplicationsBleeding PerforationFluid and electrolyte imbalance

ComplicationsFailure to locate the tumor during surgeryIntestinal bleeding or hole (perforation) from

ulcers in the stomach or duodenumSevere diarrhea and weight lossSpread of the tumor to other organs (most

often liver and lymph nodes)

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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 

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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.

 

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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.

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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.

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GASTRIC CANCER

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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.

ORA gastric carcinoma is a malignant

tumour arising from the epithelium of the stomach

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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.

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  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.

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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

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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. .

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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

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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

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DIFFERENTIAL DIAGNOSIS

EsophagitisGastric UlcersGastritis, AcuteGastritis, AtrophicGastritis, ChronicGastroenteritis, BacterialGastroenteritis, ViralLymphoma, Non-HodgkinMalignant Neoplasms of the Small Intestine

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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

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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

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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).

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DIAGNOSTIC TESTS

The following tests can help diagnose gastric cancer:History collection and physical examinationComplete blood count (CBC) to check for anemiaEsophagogastroduodenoscopy (EGD) with biopsy to

examine the stomach tissueStool test to check for blood in the stools  Endoscopy:Upper Gastrointestinal Series/Barium RadiographyEndoscopic UltrasoundComputed Tomography (CT) ScanPositron Emission Tomography (PETMagnetic Resonance Imaging (MRI)Chest X-Ray

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COMPLICATIONSMortality 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.

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MANAGEMENT

Surgery

Chemotherapy Radiation therapy

Biological therapy

Radical surgery

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Surgery

Endoscopic mucosal resection(EMR)

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Endoscopic submucosal dissection (ESD)

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Gatrectomy

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RADICAL SURGERY

CRS(CYTO REDUCTIVE SURGERY)

+HIPEC (HYPERTHERMIC INTRAPERITONEAL CHEMOTHERAPY)

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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 taxotereClinical 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.

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RadiationRadiation 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.

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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

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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

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“D” NomenclatureDescribes 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.

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NURSING DIAGNOSIS AND INTERVENTIONS

Pain related to underlying disease process and sideffects of surgery,chemotherapy and radiation therapy

 

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

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

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

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Anticipatory grieving related to percoieved unfavourable diagnosis and impending death.

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PREVENTION

Avoiding risk factors and increasing protective factors may help to prevent stomach cancer and includes avoiding;

Certain medications like NSAIDSCertain diet like spicy foodsSmokingAlcoholismStressHelicobacter infection

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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.

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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.

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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

 

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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.

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WE WANT MORE NURSES……

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THANK UUU….

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THANK UUUUUUUUU

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