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Management of Patients With Gastric and Duodenal Disorders Part 3

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Gastric secretory studies are of value in diagnosing achlorhydria and ZES. ... the stomach, pernicious anemia, achlorhydria, gastric ulcers, H. pylori infection, ... – PowerPoint PPT presentation

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Title: Management of Patients With Gastric and Duodenal Disorders Part 3


1
Management of PatientsWith Gastric andDuodenal
DisordersPart 3
  • Miss Iman Shaweesh
  • January 2008

2
  • An individuals nutritional status depends not
    only on the type and amount of intake but also on
    the functioning of the gastric and intestinal
    portions of the gastrointestinal (GI) system.

3
Gastritis
  • (inflammation of the gastric or stomach
    mucosa) is a common GI problem. Gastritis may be
    acute, lasting several hours to a few days, or
    chronic, resulting from repeated exposure to
    irritating agents or recurring episodes of acute
    gastritis.
  • Acute gastritis is often caused by dietary
    indiscretionthe person eats food that is
    contaminated with disease-causing microorganisms
    or that is irritating or too highly seasoned

4
Gastritis
  • Other causes of acute gastritis include overuse
    of aspirin and other nonsteroidal
    anti-inflammatory drugs (NSAIDs),
  • excessive alcohol intake, bile reflux, and
    radiation therapy.
  • Severe form of acute gastritis is caused by the
    ingestion of strong acid or alkali, which may
    cause the mucosa to become gangrenous or to
    perforate.

5
Gastritis
  • Chronic gastritis and prolonged inflammation of
    the stomach may be caused by either benign or
    malignant ulcers of the stomach or by the
    bacteria Helicobacter pylori.
  • Chronic gastritis is sometimes associated with
    autoimmune diseases such as pernicious anemia
    dietary factors such as caffeine the use of
    medications, especially NSAIDs alcohol smoking
    or reflux of intestinal contents into the
    stomach.

6
Pathophysiology
  • In gastritis, the gastric mucous membrane becomes
    edematous and hyperemic (congested with fluid and
    blood) and undergoes superficial erosion (Fig.
    37-1).
  • It secretes a scanty amount of gastric juice,
    containing very little acid but much mucus.
    Superficial ulceration may occur and can lead to
    hemorrhage.

7
Pathophysiology
8
Clinical Manifestations
  • The patient with acute gastritis may have
    abdominal discomfort, headache, lassitude,
    nausea, anorexia, vomiting, and hiccupping.
  • Some have no symptoms.
  • The patient with chronic gastritis may complain
    of anorexia, heartburn after eating, belching, a
    sour taste in the mouth, or nausea and vomiting.
    Patients with chronic gastritis from vitamin
    deficiency usually have evidence of malabsorption
    of vitamin B12 caused by antibodies against
    intrinsic factor.

9
Assessment and Diagnostic Findings
  • Gastritis is sometimes associated with
    hypochlorhydria (absence or low levels of
    hydrochloric acid HCl) or with hyperchlorhydria
    (high levels of HCl).
  • Diagnosis can be determined by endoscopy, upper
    GI radiographic studies, and histologic
    examination of a tissue specimen- biopsy.
  • diagnostic measures for detecting H. pylori
    include
  • serologic testing for antibodies against the
    H. pylori antigen, and a breath test.

10
Medical Management
  • The gastric mucosa is capable of repairing itself
    after a bout of gastritis. As a rule, the patient
    recovers in about 1 day.
  • nonirritating diet is recommended.
  • If bleeding is present, management is similar to
    the procedures used for upper GI tract hemorrhage
  • If itcaused by ingestion of strong acids or
    alkalis, treatment consists of diluting and
    neutralizing the offending agent. To neutralize
    acids, common antacids (eg, aluminum hydroxide)

11
Medical Management
  • to neutralize an alkali, diluted lemon juice or
    diluted vinegar is used.
  • If corrosion is extensive or severe, emetics and
    lavage are avoided because of the danger of
    perforation and damage to the esophagus. Therapy
    is supportive and may include nasogastric (NG)
    intubation.analgesic agents and sedatives,
    antacids, and intravenous (IV) fluids.
  • Fiberoptic endoscopy may be necessary. In
    extreme cases, emergency surgery may be required
    to remove gangrenous or perforated tissue.

12
Medical Management
  • Chronic gastritis is managed by modifying the
    patients diet, promoting rest, reducing stress,
    and initiating pharmacotherapy.
  • H. pylori may be treated with antibiotics (eg,
    tetracycline or amoxicillin, combined with
    clarithromycin) and a proton pump inhibitor (eg,
    lansoprazole Prevacid), and possibly bismuth
    salts (Pepto-Bismol) (Table 37-1).
  • Research is being conducted to develop a vaccine
    against H. pylori

13
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14
Histamine 2 (H2) Receptor Antagonists
15
Proton (Gastric Acid) Pump Inhibitor
16
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17
Gastric and Duodenal Ulcers
  • A peptic ulcer is an excavation (hollowed-out
    area) that forms in the mucosal wall of the
    stomach, in the pylorus (opening between stomach
    and duodenum), in the duodenum (first part of
    small intestine), or in the esophagus. A peptic
    ulcer is frequently referred to as a gastric,
    duodenal, or esophageal ulcer, depending on its
    location, or as peptic ulcer disease.

18
  • Peptic ulcers are more likely to be in the
    duodenum than in the stomach. As a rule they
    occur alone, but they may occur in multiples.
    Chronic gastric ulcers tend to occur in the
    lesser curvature of the stomach, near the
    pylorus.
  • In the past, stress and anxiety were thought to
    be causes of ulcers. Research has identified that
    peptic ulcers result from infection with the
    gram-negative bacteria H. pylori

19
  • Familial tendency may be a significant
    predisposing factor. A further genetic link is
    noted in the finding that people with blood type
    O are more susceptible to peptic ulcers than are
    those with blood type A, B, or AB. There also is
    an association between duodenal ulcers and
    chronic pulmonary disease or chronic renal
    disease.

20
  • Stress ulcers, which are clinically different
    from peptic ulcers, are ulcerations in the mucosa
    that can occur in the gastroduodenal area. Stress
    ulcers may occur in patients who are exposed to
    stressful conditions.

21
Comparing Duodenal and Gastric Ulcers
  • DUODENAL ULCER Incidence
  • Age 3060
  • Male female 231
  • 80 of peptic ulcers are duodenal
  • GASTRIC ULCER
  • Usually 50 and over
  • Male female 11
  • 15 of peptic ulcers are gastric

22
Signs, Symptoms, and Clinical Findings
  • DUODENAL ULCER
  • Hypersecretion of stomach acid (HCl)
  • May have weight gain
  • Pain occurs 23 hours after a meal often
    awakened between 12 AM
  • ingestion of food relieves pain
  • Vomiting uncommon
  • GASTRIC ULCER
  • Normalhyposecretion of stomach acid (HCl)
  • Weight loss may occur
  • Pain occurs 1/2 to 1 hour after a meal rarely
    occurs at night may be relieved by vomiting
  • ingestion of food does not
  • help, sometimes increases
  • pain
  • Vomiting common

23
Comparing Duodenal and Gastric Ulcers
  • DUODENAL ULCER
  • Hemorrhage less likely than with gastric ulcer,
    but if present melena more common than
    Hematemesis More likely to perforate than
  • gastric ulcers
  • GASTRIC ULCER
  • Hemorrhage more likely to occur than with
    duodenal
  • ulcer hematemesis more common than melena

24
Comparing Duodenal and Gastric Ulcers
  • DUODENAL ULCER
  • Malignancy Possibility
  • Rare
  • Risk Factors
  • H. pylori, alcohol, smoking,
  • cirrhosis, stress
  • GASTRIC ULCER
  • Occasionally
  • H. pylori, gastritis, alcohol, smoking, use of
    NSAIDs, stress

25
Pathophysiology
  • Peptic ulcers occur mainly in the gastroduodenal
    mucosa because this tissue cannot withstand the
    digestive action of gastric acid (HCl) and
    pepsin. The erosion is caused by the increased
    concentration or activity of acid-pepsin, or by
    decreased resistance of the mucosa.
  • A damaged mucosa cannot secrete enough mucus to
    act as a barrier against HCl.
  • The use of NSAIDs inhibits the secretion of mucus
    that protects the mucosa. Patients with duodenal
    ulcer disease secrete more acid than normal,
    whereas patients with gastric ulcer tend to
    secrete normal or decreased levels of acid.

26
Pathophysiology
  • Stress ulcer is the term given to the acute
    mucosal ulceration of the duodenal or gastric
    area that occurs after physiologically stressful
    events, such as burns, shock, severe sepsis, and
    multiple organ traumas.
  • Differences of opinion exist as to the actual
    cause of mucosal ulceration in stress ulcers.
    Usually, it is preceded by shock this leads to
    decreased gastric mucosal blood flow and to
    reflux of duodenal contents into the stomach. In
    addition, large quantities of pepsin are
    released. The combination of ischemia, acid, and
    pepsin creates an ideal climate for ulceration.

27
Pathophysiology
  • Stress ulcers should be distinguished from
    Cushings ulcers and Curlings ulcers, two other
    types of gastric ulcers.
  • Cushings ulcers are common in patients with
    trauma to the brain.
  • Curlings ulcer is frequently observed about 72
    hours after extensive burns

28
Clinical Manifestations
  • As a rule, the patient with an ulcer complains of
    dull, gnawing pain or a burning sensation in the
    midepigastrium or in the back. It is believed
    that the pain occurs when the increased acid
    content of the stomach and duodenum erodes the
    lesion and stimulates the exposed nerve endings.
  • pyrosis (heartburn), vomiting, constipation or
    diarrhea, and bleeding. Pyrosis is a burning
    sensation in the esophagus and stomach that moves
    up to the mouth. Heartburn is often accompanied
    by sour eructation, or burping, which is common
    when the patients stomach is empty. Fifteen
    percent of patients with gastric ulcers
    experience bleeding.

29
Assessment and Diagnostic Findings
  • A physical examination may reveal pain,
    epigastric tenderness, or abdominal distention.
  • A barium study of the upper GI tract may show an
    ulcer however, endoscopy is the preferred
    diagnostic procedure because it allows direct
    visualization of inflammatory changes, ulcers,
    and lesions-biopsy.

30
  • Stools may be tested periodically until they are
    negative for occult blood. Gastric secretory
    studies are of value in diagnosing achlorhydria
    and ZES. H. pylori infection may be determined by
    biopsy and histology with culture.
  • There is also a breath test that detects H.
    pylori, as well as a serologic test for
    antibodies to the H. pylori antigen.

31
Medical Management
  • peptic ulcers treated with antibiotics to
    eradicate H. pylori have a lower recurrence rate
    than those not treated with antibiotics. The
    goals are to eradicate H. pylori and to manage
    gastric acidity. Methods used include
    medications, lifestyle changes, and surgical
    intervention.

32
PHARMACOLOGIC THERAPY
  • Currently, the most commonly used therapy in the
    treatment of ulcers is a combination of
    antibiotics, proton pump inhibitors, and bismuth
    salts that suppresses or eradicates H. pylori.
  • Rest, sedatives, and tranquilizers may add to the
    patients comfort and are prescribed as needed.
    Maintenance dosages of H2 receptor antagonists
    are usually recommended for 1 year.

33
STRESS REDUCTION AND REST
  • SMOKING CESSATION
  • DIETARY MODIFICATION
  • SURGICAL MANAGEMENT
  • surgery is usually recommended for patients with
    intractable ulcers (those that fail to heal
  • after 12 to 16 weeks of medical treatment),
    include vagotomy, with or without pyloroplasty,
    and the Billroth I and Billroth II procedures

34
  • Severing of the vagus nerve. Decreases gastric
    acid by diminishing cholinergic stimulation to
    the parietal cells, making
  • them less responsive to gastrin. May be done
    via open surgical approach,
  • laparoscopy, or thoracoscopy

35
  • A surgical procedure in which a longitudinal
  • incision is made into the pylorus and
    transversely sutured closed to enlarge the outlet
    and relax the muscle

36
  • Removal of the lower portion of the antrum of the
    stomach (which contains
  • the cells that secrete gastrin) as well as a
    small portion of the duodenum
  • and pylorus. The remaining segment is
    anastomosed to the duodenum (Billroth I) or to
    the jejunum (Billroth II)

37
  • Removal of distal third of stomach anastomosis
    with duodenum or jejunum.
  • Removes gastrin-producing cells in the
  • antrum and part of the parietal cells.

38
Morbid Obesity
  • obesity is the term applied to people who are
    more than two times their ideal body weight or
    whose body mass index (BMI) exceeds 30 kg/m2.
  • Another definition of morbid obesity is body
    weight that is more than 100 pounds greater than
    the ideal body weigh.
  • Patients with morbid obesity are at higher risk
    for health complications, such as cardiovascular
    disease, arthritis, asthma, bronchitis, and
    diabetes. They frequently suffer from low
    self-esteem, impaired body image, and depression.

39
Medical Management
  • There is a belief that depression may be a
    contributing factor to weight gain, and treatment
    of the depression with bupropion
  • hydrochloride
  • Several medications have recently been approved
    for obesity. They include sibutramine HCl
    (Meridia) and orlistat (Xenical). By inhibiting
    the reuptake of serotonin and norepinephrine,
    sibutramine decreases appetite.

40
  • Gastric bypass and vertical banded gastroplasty
    are the current operations of choice. These
    procedures may be performed laparoscopically or
    by an open surgical technique. In gastric bypass
    surgery, the proximal segment of the stomach is
    transected to form a small pouch with a small
    gastroenterostomy stoma. The Roux-en-Y gastric
    bypass is the recommended procedure for long-term
    weight loss. In this procedure, a horizontal row
    of staples creates a stomach pouch with a 1-cm
    stoma that is anastomosed with a portion of
    distal jejunum, creating a gastroenterostomy. The
    transected proximal portion of the jejunum is
    anastomosed to the distal jejunum.

41
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42
NSG Intervention
  • Complications that may occur in the immediate
    postoperative period include peritonitis, stomal
    obstruction, stomal ulcers, atelectasis and
    pneumonia, thromboembolism, and metabolic
    imbalances resulting from prolonged vomiting and
    diarrhea.
  • small feedings consisting of a total of 600 to
    800 calories per day and encourages fluid intake
    to prevent dehydration.

43
  • The nurse explains that noncompliance by eating
    too much or too fast or eating highcalorie liquid
    and soft foods results in vomiting and painful
    esophageal distention. The nurse discusses
    dietary instructions before discharge and
    schedules monthly outpatient visits.

44
Gastric Cancer
  • Most of these deaths occur in people older than
    40 years of age, but they occasionally occur in
    younger people. Men have a higher incidence of
    gastric cancers than women do.
  • Diet appears to be a significant factor. A diet
    high in smoked foods and low in fruits and
    vegetables may increase the risk of gastric
    cancer.
  • chronic inflammation of the stomach, pernicious
    anemia, achlorhydria, gastric ulcers, H. pylori
    infection, and genetics.

45
Pathophysiology
  • Most gastric cancers are adenocarcinomas and can
    occur in any portion of the stomach. The tumor
    infiltrates the surrounding mucosa, penetrating
    the wall of the stomach and adjacent organs and
    structures.
  • Metastasis through lymph to the peritoneal cavity
    occurs later in the disease.

46
Clinical Manifestations
  • Some studies show that early symptoms, such as
    pain relieved with antacids, resemble those of
    benign ulcers.
  • Symptoms of progressive disease may include
    anorexia, dyspepsia (indigestion), weight loss,
    abdominal pain, constipation, anemia,
  • and nausea and vomiting.

47
Assessment and Diagnostic Findings
  • physical examination is not helpful in detecting
    cancer because most gastric tumors are not
    palpable. Ascites may be apparent if the cancer
    cells have metastasized to the liver.
  • Endoscopy for biopsy and cytologic washings is
    the usual diagnostic study, and a barium x-ray
    examination of the upper GI tract may also be
    performed

48
  • Because metastasis often occurs before warning
    signs develop, a computed tomography (CT) scan,
    bone scan, and liver scan are valuable in
    determining the extent of metastasis.
  • A complete x-ray examination of the GI tract
    should be performed when any person older than 40
    years of age has had indigestion (dyspepsia) of
    more than 4 weeks duration.

49
Medical Management
  • no successful treatment for gastric carcinoma
    except removal of the tumor. If the tumor can be
    removed while it is still localized to the
    stomach, the patient can be cured.
  • If the tumor has spread beyond the area that can
    be excised, cure is impossible. Palliative rather
    than radical surgery is performed if there is
    metastasis to other vital organs.
  • If a radical subtotal gastrectomy is performed,
    the stump of the stomach is anastomosed to the
    jejunum, as in the gastrectomy for ulcer.

50
  • Chemotherapeutic medications include cisplatin,
    irinotecan, or a combination of 5-fluorouracil,
    doxorubicin (Adriamycin), and mitomycin-C. Some
    studies are being conducted on the use of
    chemotherapy before surgery. Radiation therapy
    also may be used for palliation. Assessment of
    tumor markers (blood analysis for antigens
    indicative of colon cancer) such as
    carcinoembryonic antigen, CA 19-9, and CA 50 may
    help determine the effectiveness of treatment.
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