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Transcript
Gastric Ulcer
Even though gastric ulcer is a common disease, a
diagnosis can be difficult because it has a wide spectrum of
clinical presentations, ranging from:
-asymptomatic to vague epigastric pain, nausea, and
iron-deficiency anemia to
-acute life-threatening hemorrhage.
The normal stomach maintains a balance between:
 protective factors - such as mucus and bicarbonate
secretion and
 aggressive factors - such as acid secretion and pepsin
Gastric ulcers develop when aggressive factors overcome
protective mechanisms.
Causes
The two major etiological factors for peptic
ulcer disease (PUD) are:
 Helicobacter pylori infection
 nonsteroidal anti-inflammatory drug (NSAID)
consumption
70% of all gastric ulcers occurring in the United
States can be attributed to H pylori infection.
Helicobacter pylori
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the bacterium's spiral shape and
flagella facilitate its penetration into
the mucous layer and its
attachment to the epithelial layer
it releases phospholipase and
proteases, which cause further
mucosal damage
a cytotoxin-associated gene (cag A)
has been isolated in approximately
65% of the bacteria
the products of this gene are
associated with more severe
gastritis, gastric ulcer, gastric
cancer, and lymphoma
NSAID

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26% of gastric ulcers
secondary to a decrease in prostaglandin
production resulting from the inhibition of
cyclooxygenase.1
the typical effects of NSAIDs are superficial
gastric erosions and petechial lesions
the greatest risk of developing an ulcer occurs
during the first 3 months of NSAID use
patients with H pylori infection may be twice as
likely to get a bleeding peptic ulcer.

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In the Celecoxib Long-term Arthritis Safety Study
(CLASS), they found a significantly lower incidence of
symptomatic ulcers in patients taking celecoxib for the
initial 6 months as compared to patients taking ibuprofen
or diclofenac
Other medications that predispose patients to
gastroduodenal ulcers include potassium chloride,
chemotherapeutic agents, and bisphosphonates
A rare cause of PUD is Zollinger-Ellison syndrome
(gastrinoma). The hallmark of Zollinger-Ellison syndrome
is :



profound hypersecretion of gastric acid
significant disruption of the mucosal integrity
Cigarette smoking - people who smoke tend to develop
more frequent and recurrent ulcers and their ulcers are
more resistant to therapy


Frequency
United States - it is estimated to affect
0.92% of the population or 1.6 million
persons.
Epidemiological studies 1970-1985, a
marked decrease in the rate of duodenal
ulcer occurred, while the rate of gastric
ulcer remained stable.


people with low socioeconomic status are
more likely to acquire H pylori infection
individuals who are infected are 3 times more
likely to develop gastric ulcer compared to
those unexposed to the bacteria.


simple gastric ulcer is in decline, the incidence
of complicated gastric ulcer and
hospitalization has remained stable, partly
due to the concomitant use of aspirin in an
aging population
International

Denmark, lifetime prevalence of gastric cancer
is 1.2% for men and 0.6% for women
The annual incidence of gastric ulcers


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Japan - 1 case per 1000 population
Norway - 1.5 cases per 1000 population
Scotland - 2.7 cases per 1000 population
Mortality/Morbidity


the mortality rate is higher in patients older than 75
years (attributable to a high rate of NSAID use in this
age group)
the other high-risk groups - chronic renal insufficiency
and diabetes
Sex

the male-to-female ratio is 1:1 in the United States and
18:1 in India
Age

the incidence of gastric ulcer increases with age
 increasing NSAID use
 a high prevalence of H pylori infection in persons
older than 50 years
History

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Clinical
classic gastric ulcer pain is described as pain
occurring shortly after meals, for which
antacids provide minimal relief
the pain from gastric ulcer is typically located
in the epigastrium; in the right upper quadrant
and elsewhere
duodenal ulcer pain often occurs hours after
meals and at night; relieved with food or
antacids
pain with radiation to the back is suggestive of
a posterior penetrating gastric ulcer
complicated by pancreatitis
patients with bleeding gastric ulcers may give
a history of hematemesis, melena, or episodes
of presyncope
melena can be intermittent over several days
or multiple episodes in a single day.
Physical
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epigastric tenderness may or may not be present
right upper quadrant tenderness may suggest a
biliary etiology or, less frequently, PUD
in the presence of gastric outlet obstruction,
abdominal distension and succussion splash may
be found
a palpable mass should raise the suggestion of a
gastric malignancy
involuntary guarding is indicative of peritonitis
secondary to gastric perforation
patients should be checked for melena, which is
indicative of bleeding from a gastroduodenal
ulcer
digital rectal examination can be easily performed
in the office to check for melena.
Differential Diagnoses

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Cholecystitis
Crohn Disease
Duodenal Ulcers
Gastric Cancer
Pancreatitis, Chronic
Zollinger-Ellison Syndrome
Other Problems to Be Considered


Nonulcer dyspepsia (NUD) or functional dyspepsia (a
diagnosis of exclusion in the absence of any organic
disease after thorough evaluation are thought to have
functional dyspepsia
Crohn disease: Crohn ulceration can involve any part
of the GI tract from the buccal mucosa to the rectum.
Isolated Crohn ulceration of the stomach is rare,
although it may cause duodenal or ileal ulcerations.
Laboratory Studies
Routine laboratory tests:
 complete blood cell count
 iron studies, can help detect anemia.
Anemia and weight loss are alarm signals
and mandate early endoscopy to rule out
other sources of chronic GI blood loss.
Imaging Studies
Upper GI radiography

a double-contrast barium study -benign gastric
ulcers
Malignant gastric ulcers
Other Tests

H pylori testing

Invasive tests
Biopsy
 Culture
 Rapid urease test

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Noninvasive tests
Antibody testing
 Urea breath testing
 Stool antigen

Procedures

Esophagogastroduodenoscopy (EGD)

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endoscopy is a relatively safe procedure in
experienced hands
direct visualization to obtain biopsy specimens and
also to perform endoscopic therapy for bleeding
ulcers
the preferred modality for the diagnosis of gastric
ulcer and gastric cancer
a repeat endoscopy after 6 weeks of therapy is
recommended to confirm healing of a gastric ulcer
and to help definitively rule out gastric malignancy
upper endoscopy with biopsy is the most sensitive
and specific method for diagnosing gastric and
esophageal cancer
7 biopsy samples obtained from the base and ulcer
margins increase the sensitivity to 99%
Benign ulcers
Malignant ulcers
Treatment

H pylori eradication



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Bismuth, metronidazole, and tetracycline qid
with H2 blockers bid
Bismuth, metronidazole, and tetracycline bid
with a PPI (Helidac)
Prevacid, amoxicillin, and clarithromycin bid
(PrevPac)
Prilosec, metronidazole, and clarithromycin bid
Ranitidine, bismuth, and clarithromycin with
amoxicillin, metronidazole, or tetracycline bid

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Endoscopic therapy
Surgical Care
Consultations
Diet
Medication

Proton pump inhibitors

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Omeprazole (Prilosec) - 40 mg PO
Lansoprazole (Prevacid) - 15-30 mg PO
Rabeprazole (Aciphex) - 20 mg tab PO
Pantoprazole (Protonix) - 40 mg PO
Esomeprazole (Nexium) - 40 mg PO
Histamine H2 antagonists


Nizatidine (Axid) - 75 mg PO
Ranitidine (Zantac) - 150 mg PO

Helicobacter pylori eradication agents
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Clarithromycin (Biaxin) - 250-500 mg PO
Metronidazole (Flagyl) - 250 mg PO
Bismuth subsalicylate (Pepto-Bismol) - 2 tab or
30 mL PO
Tetracycline (Sumycin) - 250 mg PO
Amoxicillin (Trimox) - 500 mg PO
Gastrointestinal agents

Sucralfate (Carafate) - 1 g PO
Complications

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hemorrhage
perforation
gastric outlet obstruction
gastric malignancy

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the risk is approximately 2% in the initial 3 years
H pylori infection is associated with gastric lymphoma
or mucosa-associated lymphoid tissue (MALT)
lymphoma
malignancy should be strongly considered in the case
of a persistent nonhealing gastric ulcer
Patient Education


Instruct patients to avoid NSAIDs.
Discourage alcohol consumption and
cigarette smoking because these activities
impair gastric mucosal protection.