ادامه گوارش ۲
GERD علت اکثر موارد Chest Pain در بیماریهای مری می باشدو پس از آن اسپاسم مری قرار دارد.
کلستاز دارویی: فنوتیازین ها، OCP ، متیل تستسترون
یرقان بعد از عمل جراحی: 1تا 10 روز بعد از عمل جراحی بوجود می آید- متعاقب جراحی قلب 15% و متعاقب جراحی الکتیو شکم 1% -اتیولوژی مولتی فاکتوریال
دربیماری هپاتوسلولار: هر سه مرحله تولید بیلیروبین مختل ولی مرحله Excretion بیشتر از بقیه مختل- اغلب نوع کنژوگه
در هپاتیت حاد--› یرقان نشانه پیش آگهی بد نیست!!!
ولی در بیماریهای کبدی مزمن --› یرقان دائمی حاکی از پیش آگهی بد است.
Endoscopy is not a sensitive means of diagnosing GERD because only 15% of patients with GERD will have endoscopic evidence of esophagitis;
endoscopy is useful, however, in identifying complications of GERD, including esophageal ulcers, strictures, and Barrett's esophagus
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Table 34-1. Treatment of Gastroesophageal Reflux Disease |
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Table 34-2. Esophageal Motor Disorders |
Barrett's esophagus:
The risk of cancer in Barrett's esophagus is estimated to be 40 to 100 times that of the general population, with a 0.5% risk of developing cancer per patient-year.
Neither acid suppression therapy nor fundoplication leads to regression of Barrett's metaplasia.
At present, endoscopic surveillance is recommended for all patients with Barrett's esophagus.
Endoscopy is performed every 2 years, and biopsies are taken from the area of abnormal mucosa.
If the biopsies reveal:
low-grade dysplasia,à then the frequency of endoscopies is increased.
If high-grade dysplastic changes are seen,à and confirmed by a second pathologist,à then the risk of subsequent adenocarcinoma is greater than 25%, and surgical resection should be considered.
بیماریهای معده و دئودنوم:
STRESS-RELATED MUCOSAL INJURYآسیب مخاطی مرتبط با استرس:
Patients suffering from shock, sepsis, massive burns, severe trauma, or head injury can develop acute erosive gastric mucosal changes or frank ulceration with bleeding.
most commonly observed à in the acid-producing (fundus and body) portions of the stomach.
The most common presentation àGI bleeding
Risk factors for bleedingàRespiratory failure requiring mechanical ventilation and underlying coagulopathy are which tends to occur 48 to 72 h after the acute injury or insult.
Histologically, stress injury does not contain inflammation or H. pylori; thus “gastritis” is a misnomer.
Although elevated gastric acid secretion may be noted in patients with stress ulceration after head trauma (Cushing's ulcer) and severe burns (Curling's ulcer), mucosal ischemia and breakdown of the normal protective barriers of the stomach also play an important role in the pathogenesis.
use of preventive measuresà in high-risk patients:
mechanically ventilated,
coagulopathy,
multiorgan failure, or
severe burns.
Maintenance of gastric pH > 3.5 withà
1-continuous infusion of H2 blockers or liquid antacids administered every 2 to 3 h are viable options.
2-Sucralfate slurry (1 g every 4 to 6 h) has also been successful.
امپرازول(PPI) در پیشگیری از استرس اولسر تاثیری ندارد زیرا این بیماران ناشتا هستند!!!
If bleeding occurs despite these measures, endoscopy, intraarterial vasopressin, or embolization are options. If all else fails, then surgery should be considered.
Although vagotomy and antrectomy may be used, the better approach would be a total gastrectomy, which has an exceedingly high mortality rate in this setting.
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TABLE 274-4 Recommendations for Treatment of NSAID-Related Mucosal Injury | |||||||||||||||||||||
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TABLE 274-1 Tests for Detection of H. pylori | |||||||||||||||||||||||||||
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GASTRITISگاستریت:
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TABLE 274-7 Classification of Gastritis | ||||||||||||||||||||||
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The term gastritis à histologically documented inflammation of the gastric mucosa.
Gastritis is not the mucosal erythema seen during endoscopy and is not interchangeable with “dyspepsia.”
Therefore, there is no typical clinical manifestation of gastritis.
Acute Gastritis گاستریت حاد:
The most common causes of acute gastritis are infectious.
Acute infection with H. pylori induces gastritis.
Reported as presenting with sudden onset of epigastric pain, nausea, and vomiting, limited mucosal histologic studies demonstrate a marked infiltrate of neutrophils with edema and hyperemia. If not treated, this picture will evolve into one of chronic gastritis.
Hypochlorhydria lasting for up to 1 year may follow acute H. pylori infection.
Bacterial infection of the stomach or phlegmonous gastritisà is a rare potentially life-threatening disorder, characterized by marked and diffuse acute inflammatory infiltrates of the entire gastric wall, at times accompanied by necrosis. Elderly individuals, alcoholics, and AIDS patients may be affected. Potential iatrogenic causes include polypectomy and mucosal injection with India ink. Organisms associated with this entity include streptococci, staphylococci, Escherichia coli, Proteus, and Haemophilus sp. Failure of supportive measures and antibiotics may result in gastrectomy.
Other types of infectious gastritis may occur in immunocompromised individuals such as AIDS patients.--> herpetic (herpes simplex) or CMV gastritis (intranuclear inclusions in CMV )
Chronic Gastritisگاستریت مزمن:
Chronic gastritis is identified histologically by an inflammatory cell infiltrate consisting primarily of lymphocytes and plasma cells, with very scant neutrophil involvement.
Distribution of the inflammation may be patchy, initially involving superficial and glandular portions of the gastric mucosa. This picture may progress to more severe glandular destruction, with atrophy and metaplasia.
Chronic gastritis has been classified according to histologic characteristics.
These include superficial atrophic changes and gastric atrophy.
1-The early phase of chronic gastritis is superficial gastritis. The inflammatory changes are limited to the lamina propria of the surface mucosa, with edema and cellular infiltrates separating intact gastric glands. Additional findings may include decreased mucus in the mucous cells and decreased mitotic figures in the glandular cells.
2-The next stage is atrophic gastritis. The inflammatory infiltrate extends deeper into the mucosa, with progressive distortion and destruction of the glands.
3-The final stage of chronic gastritis is gastric atrophy. Glandular structures are lost; there is a paucity of inflammatory infiltrates. Endoscopically the mucosa may be substantially thin, permitting clear visualization of the underlying blood vessels.
Gastric glands may undergo morphologic transformation in chronic gastritis. Intestinal metaplasia is an important predisposing factor for gastric cancer.
Chronic gastritis à Type A refers to the body-predominant form (autoimmune) and
Type B is the antral-predominant form (H. pylori–related).
The term AB gastritis has been used to refer to a mixed antral/body picture.
TYPE A GASTRITIS à Auto immune!!!, Pernicious Anemia تیپ- الف گاستریت مزمن:
The less common of the two forms
involves primarily the fundus and body, with antral sparing.
associated with pernicious anemia in the presence of circulating antibodies against parietal cells and IF; thus it is also called autoimmune gastritis.
H. pylori infection can lead to a similar distribution of gastritis. The characteristics of an autoimmune picture are not always present.
Antibodies to parietal cells have been detected in >90% of patients with pernicious anemia and in up to 50% of patients with type A gastritis.
The parietal cell antibody is directed against H+,K+-ATPase.
T cells are also implicated in the injury pattern of this form of gastritis.
Parietal cell antibodies and atrophic gastritis are observed in family members of patients with pernicious anemia.
These antibodies are observed in up to 20% of individuals over age 60 and in ~20% of patients with vitiligo and Addison's disease.
About half of patients with pernicious anemia have antibodies to thyroid antigens, and about 30% of patients with thyroid disease have circulating anti-parietal cell antibodies.
Anti-IF antibodies are more specific than parietal cell antibodies for type A gastritis, being present in ~40% of patients with pernicious anemia.
Another parameter consistent with this form of gastritis being autoimmune in origin is the higher incidence of specific familial histocompatibility haplotypes such as HLA-B8 and -DR3.
The parietal cell–containing gastric gland is preferentially targeted in this form of gastritis, and achlorhydria results.
Parietal cells are the source of IF, lack of which will lead to vitamin B12 deficiency and its sequelae (megaloblastic anemia, neurologic dysfunction).
Gastric acid plays an important role in feedback inhibition of gastrin release from G cells. Achlorhydria, coupled with relative sparing of the antral mucosa (site of G cells), leads to hypergastrinemia.
Gastrin levels can be markedly elevated (>500 pg/mL) in patients with pernicious anemia. ECL cell hyperplasia with frank development of gastric carcinoid tumors may result from gastrin trophic effects.
The role of gastrin in carcinoid development is confirmed by the observation that antrectomy leads to regression of these lesions.
TYPE B GASTRITIS تیپ- ب گاستریت مزمن:
Type B, or antral-predominant, gastritis
is the more common form of chronic gastritis.
H. pylori infection is the cause of this entity.
The conversion to a pan-gastritis is time-dependent—estimated to require 15 to 20 years. This form of gastritis increases with age,
being present in up to 100% of persons over age 70.
Histology improves after H. pylori eradication. The number of H. pylori organisms decreases dramatically with progression to gastric atrophy, and the degree of inflammation correlates with the level of these organisms. Early on, with antral-predominant findings, the quantity of H. pylori is highest and a dense chronic inflammatory infiltrate of the lamina propria is noted accompanied by epithelial cell infiltration with polymorphonuclear leukocytes.
Multifocal atrophic gastritis, gastric atrophy with subsequent metaplasia, has been observed in chronic H. pylori–induced gastritis. This may ultimately lead to development of gastric adenocarcinoma.
H. pylori infection is now considered an independent risk factor for gastric cancer. Seropositivity for H. pylori is associated with a three- to sixfold increased risk of gastric cancer.
However, eradication of H. pylori as a general preventative measure for gastric cancer is not recommended.
Infection with H. pylori is also associated with development of a low-grade B cell lymphoma, gastric MALT lymphoma.
The chronic T cell stimulation caused by the infection leads to production of cytokines that promote the B cell tumor. Tumor growth remains dependent upon the presence of H. pylori in that its eradication is often associated with complete regression of the tumor. The tumor may take more than a year to regress after treating the infection. Such patients should be followed by EUS every 2 to 3 months. If the tumor is stable or decreasing in size, no other therapy is necessary. If the tumor grows, it may have become a high-grade B cell lymphoma. When the tumor becomes a high-grade aggressive lymphoma histologically, it loses responsiveness to H. pylori eradication.
