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首页 > 学术期刊 > 关于胃呕吐论文的文献

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阿满思密达

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IntroductionBackgroundGastritis includes a myriad of disorders that involve inflammatory changes in the gastric mucosa, including erosive gastritis caused by Helicobacter pylori bacterial infections, other infectious gastritises, nonsteroidal anti-inflammatory drugs (NSAIDs), noxious irritants, reflux gastritis from exposure to bile and pancreatic fluids, infectious gastritis, and gastric mucosal atrophy.Peptic ulcer disease (PUD) refers to a discrete mucosal defect in the portions of the gastrointestinal tract (gastric or duodenal) exposed to acid and pepsin secretion. Presentations of gastritis and PUD usually are indistinguishable in the ED, and thus the ED management is generally the same. Emergent complications include hemorrhagic shock and peritonitis secondary to a perforated ulcer. The clinician should be concerned about other life-threatening conditions (eg, acute coronary syndromes and aortic aneurysms), which can mimic the presentation of gastritis.For more information, see Medscape's Peptic Ulcer Disease Resource Center.PathophysiologyThe mechanisms of mucosal injury in gastritis and PUD are thought to be mainly caused by H pylori infections, coupled an imbalance of aggressive factors, such as acid production or pepsin, and defensive factors, such as mucus production, bicarbonate, and blood flow.Erosive gastritis usually is associated with serious illness or with various drugs. Stress, ethanol, bile, and nonsteroidal anti-inflammatory drugs (NSAIDs) disrupt the gastric mucosal barrier, making it vulnerable to normal gastric secretions.Infection with H pylori, a short, spiral-shaped, microaerophilic gram-negative bacillus, is the leading cause of PUD and is associated with virtually all ulcers not induced by NSAIDs. H pylori colonize the deep layers of the mucosal gel that coats the gastric mucosa and presumably disrupts its protective properties. H pylori is thought to infect virtually all patients with chronic active gastritis. Eradication of H pylori was thought to be the pathway to curing ulcer disease, but that has proven increasingly challenging.NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal prostaglandins. Many people with known H pylori colonization or who are taking NSAIDs do not suffer from gastritis or PUD, which indicates other important causative factors must be involved.FrequencyUnited StatesApproximately 10% of Americans eventually develop PUD, and about 10% of patients presenting to the ED with abdominal pain are diagnosed with PUD. Prevalence has decreased in the United States over the last 30 years.InternationalFrequency of PUD is decreasing in the developed world but increasing in developing countries.Mortality/MorbidityComplications of gastritis include PUD and, rarely, extensive bleeding. PUD accounts for more than 50% of all causes of upper gastrointestinal bleeds in the United States.Complications of peptic ulcer disease include bleeding, occasionally massive, and perforation leading to peritonitis and sepsis (rare).The mortality rate is low.SexMale-to-female ratio of gastritis is approximately 1:1Male-to-female ratio of PUD is approximately 2:1AgeAn estimated 60% of Americans older than 60 years harbor H pylori.Duodenal ulcers usually occur in those aged 25-75 years.Gastric ulcer prevalence peaks in those aged 55-65 years.ClinicalHistoryPatients typically present with abdominal pain that has the following characteristics:Epigastric to left upper quadrantFrequently described as burningMay radiate to the backUsually occurs 1-5 hours after mealsMay be relieved by food, antacids (duodenal), or vomiting (gastric)Typically follows a daily pattern specific to patientNSAID-induced gastritis or ulcers are usually silent.Sudden onset of symptoms may indicate perforation.Gastritis may present as bleeding, which is more likely in elderly patients.Symptoms consistent with anemia (eg, fatigue, dyspnea) may manifest.PhysicalEpigastric tenderness is present and usually mild.Bowel sounds are normal.Signs of peritonitis or GI bleeding may be manifest. Perform a rectal examination and Hemoccult testing.CausesH pylori (most common cause of ulceration)NSAIDs, aspirinGastrinoma (Zollinger-Ellison syndrome)Severe stress (eg, trauma, burns), Curling ulcersAlcoholBile refluxPancreatic enzyme refluxRadiationStaphylococcus aureus exotoxinBacterial or viral infection

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DoughnutTOP

1、《灵枢·邪气脏腑病形》:“胃病者,腹胀,胃脘当心而痛,上支两胁,膈咽不通,食饮不下,取之三里也。”2、《三因极一病证方论·九痛叙论》:“夫心痛者,……以其痛在中脘,故总而言之曰心痛,其实非心痛也,……若十二经络外感六淫,则其气闭塞,郁于中焦,气与邪争,发为疼痛,属外所因;若五脏内动,汨以七情,则其气痞结,聚于中脘,气与血搏,发为疼痛,属内所因;饮食劳逸,触忤非类,使脏气不平,痞隔于中,食饮遁疰,变乱肠胃,发为疼痛,属不内外因。”3、《景岳全书·心腹痛》:“胃脘痛证,多有因食,因寒,因气不顺者,然因食因寒,亦无不皆关于气。盖食停则气滞,寒留则气凝。所以治痛之要,但察其果属实邪,皆当以理气为主。” 4、《临证指南医案·胃脘痛》:“初病在经,久痛人络,以经主气,络主血,则可知其治血之当然也,凡气既久阻,血也因病,循行之脉络自痹,而辛香理气,辛柔和血之法,实为对待必然之理。” 5、《顾氏医镜·胃脘痛》:“须知拒按者为实,可按者为虚;痛而胀闭者多实,不胀不闭者多虚;喜寒者多实,爱热者多虚;饱则甚者多实,饥则甚者多虚;脉实气粗者多实,脉少气虚者多虚;新病年壮者多实,久病年老者多虚;补而不效者多实,攻而愈剧者多虚。必以望、闻、问、切四者详辨,则虚实自明。”

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