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首页 > 期刊问答网 > 期刊问答 > 关于胃溃疡的论文

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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 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 Presentations of gastritis and PUD usually are indistinguishable in the ED, and thus the ED management is generally the Emergent complications include hemorrhagic shock and peritonitis secondary to a perforated The clinician should be concerned about other life-threatening conditions (eg, acute coronary syndromes and aortic aneurysms), which can mimic the presentation of For more information, see Medscape's Peptic Ulcer Disease Resource CPathophysiologyThe 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 Erosive gastritis usually is associated with serious illness or with various Stress, ethanol, bile, and nonsteroidal anti-inflammatory drugs (NSAIDs) disrupt the gastric mucosal barrier, making it vulnerable to normal gastric 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 NSAID H pylori colonize the deep layers of the mucosal gel that coats the gastric mucosa and presumably disrupts its protective H pylori is thought to infect virtually all patients with chronic active Eradication of H pylori was thought to be the pathway to curing ulcer disease, but that has proven increasingly NSAIDs and aspirin also interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity, reducing levels of mucosal 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 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 InternationalFrequency of PUD is decreasing in the developed world but increasing in developing Mortality/MorbidityComplications of gastritis include PUD and, rarely, extensive PUD accounts for more than 50% of all causes of upper gastrointestinal bleeds in the United SComplications of peptic ulcer disease include bleeding, occasionally massive, and perforation leading to peritonitis and sepsis (rare)The mortality rate is 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 Duodenal ulcers usually occur in those aged 25-75 Gastric ulcer prevalence peaks in those aged 55-65 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 Sudden onset of symptoms may indicate Gastritis may present as bleeding, which is more likely in elderly Symptoms consistent with anemia (eg, fatigue, dyspnea) may PhysicalEpigastric tenderness is present and usually Bowel sounds are Signs of peritonitis or GI bleeding may be Perform a rectal examination and Hemoccult 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

关于胃溃疡的论文

224 评论(9)

小跳的树

恩,我印象中就是胃酸腐蚀了血管吧。论文?去CNKI吧。
102 评论(10)

醋栗Mason

注意不能吃辣、酸,最好吃一点消炎的药
295 评论(10)

当冬夜渐暖呀

胃溃疡诊断依据  (1)慢性病程,周期性发作,常与季节变化、精神因素、饮食不当有关;或长期服用能致溃疡的药物如阿司匹林等。  (2)上腹隐痛、灼痛或钝痛,服用碱性药物后缓解。典型胃溃疡常于剑突下偏左,好发于餐后半小时到1~2小时,痛常伴反酸嗳气。  (3)基础泌酸量及最大泌酸量测定有助诊断。胃溃疡的基础泌酸量正常或稍低,但不应为游离酸缺乏。  (4)溃疡活动期大便隐血阳性。  (5)X线钡餐检查可见龛影及粘膜皱襞集中等直接征象。单纯局部压痛,激惹变形等间接征象仅作参考。  (6)胃镜检查,可于胃部见圆或椭圆、底部平整、边缘整齐的溃疡。根据溃疡面所见,可分为:①活动期:溃疡面为灰白或褐色苔膜覆盖,边缘肿胀,色泽红润、光滑而柔软。②愈合期:苔膜变薄,溃疡缩小,其周围可见粘膜上皮再生的红晕;或溃疡面几乎消失,其上有极少的薄苔。③瘢痕期:溃疡面白苔已消失,变成红色充血的瘢痕;可见皱襞集中。  具备以上(1)(2)(5)或(2)(6)项者可作胃溃疡诊断,对诊断为胃溃疡者须与恶性溃疡鉴别,凡能进行胃镜检查者应做胃粘膜活检予以确诊。如果确认请及时去医院就诊。 胃癌诊断方法    胃癌须与胃溃疡、胃内单纯性息肉、良性肿瘤、肉瘤、胃内慢性炎症相鉴别。有时尚需与胃皱襞肥厚、巨大皱襞症、胃粘膜脱垂症、幽门肌肥厚和严重胃底静脉曲张等相鉴别。鉴别诊断主要依靠X线钡餐造影、胃镜和活组织病理检查。  (一)实验室检查 早期可疑胃癌,游离胃酸低度或缺,如红血球压积、血红蛋白、红细 胞下降,大便潜血(+)。血红蛋白总数低,白/球倒置等。水电解质紊乱,酸碱平衡失调等化验异常。   (二)X线表现气钡双重造影可清楚显示胃轮廓、蠕动情况、粘膜形态、排空时间,有无充盈缺损、龛影等。检查准确率近80%。   (三)纤维内窥镜检查 是诊断胃癌最直接准确有效的诊断方法。   (四)脱落细胞学检查 有的学者主张临床和x线检查可疑胃癌时行此检查。   (五)B超 可了解周围实质性脏器有无转移。   (六)CT检查 了解胃肿瘤侵犯情况,与周围脏器关系,有无切除可能
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