-Gastroesophageal Reflux Disease (GERD)-
-patients with GERD do not necessarily have inflammation
-GERD is a condition that develops when the reflux of stomach contents that causes symptoms
-most common symptoms are pyrosis, regurgitation, and dysphagia
-GERD can cause bronchospasm laryngitis and chronic cough
-most patients experience the pyrosis post prandial
-other symptoms of dysphagia include chest pain, water brash, globus sensation, odynophagia, and nausea
-diagnosis of GERD can be made from clinical symptoms alone
-differential diagnosis includes: infectious esophagitis, pill esophagitis, eosinophilic esophagitis, peptic ulcer disease, non ulcer dyspepsia, biliary tract disease, coronary artery disease, and esophageal motility disorders
-ambulatory pH monitoring is useful for those with persistent symptoms who do not have evidence for mucosal damage on endoscopy
-Antacids are use to relief of mild GERD symptoms that occur less than once a week. Do not prevent GERD
-Surface agents and alginates (Sucralfate) adheres to mucosal surface, promotes healing, and protects injury
-Histamine 2 Receptors Blockers (H2 Blockers) decrease the secretion of acid by inhibiting the histamine 2 receptor of the parietal cells
-Proton Pump Inhibitors (PPI's) should be used in patients ho fail twice a day H2 Blocker therapy and patients with erosive esophagitis or two or more episodes per week of symptoms
-PPI's irreversibly bind to and inhibit hydrogen potassium ATPase pump
-Gastritis-
-Gastric inflammatory disease is classified into gastritides and gastropathies
-Gastritis is a inflammatory process, unlike gastropathy that has minimal or no inflammation
-a mucosal biopsy distinguishes between acute gastritis, chronic gastritis, and gastropathy.
-H. Pylori can be tested non invasively for gastritis
-low serum pepsinogen I levels strongly are associated with extensive intestinal metaplasia
-accuracy of biopsy is dependent of optimizing the site and number of specimens
-Causes of gastropathy include NSAIDS, alcohol, bile, circulatory failure, and chronic congestion
-Causes of gastritis include infectious agents such as H. Pylori, autoimmune and hypersensitivity reactions
-Granulomatous gastritis is a subtype of chronic gastritis that can be infectious, noninfectious, or idiopathic
-Noninfectious causes include Crohns Disease, Sarcoidosis, Adenocarcinoma, and MALT lymphoma
-Infectious causes include H. Pylori
-Up to 25 percent of the causes of granulomatous gastritis are idiopathic
-Treatment is directed at determining the etiology
-Metastatic Atrophic Gastritis is chronic gastritis, in addition to inflammation, has mucosal thinning, gland loss, and changes in epithelial cell types
-Gastritis is treated at finding cause and using antacids, surface agents, histamine blockers, and proton pump inhibitors
-Gastric Neoplasms-
-Over 90 percent of the gastric cancers are adenocarcinoma
-About 5 percent of the gastric cancers are lymphomas
-MALT (Mucosa Associated Lymph Tissue) lymphomas are associated with H.Pylori infections
-H.Pylori infections can progress to chronic active gastritis that can progress intestinal metaplasia that can progress to dysplasia which progresses to adenocarcinoma
-Signs and symptoms of gastric neoplasm include: abdominal discomfort, early satiety, nausea, vomiting, gastrointestinal bleeding, iron deficiency anemia, or frank GI bleeding. Anorexia or weight loss may accompany other symptoms
-Signs of metastatic disease can be found sometimes on physical exam Virchow (left subclavicular) node, a Blummer shelf (mass in the perirectal pouch, found on digital rectal exam), and a Krukenberg tumor (metastasis to the ovaries)
-Many paraneoplastic syndromes have been associated with gastric adenocarcinoma: Trousseau's syndrome (thrombosis), acanthosis nigricans (pigmented dermal lesions), membranous neuropathy, microangiopathic hemolytic anemia, Leser Trelat sign (seborrheic keratosis), and dermatomyositis
-Diagnosis usually made with endoscopy with biopsy
-Gastric carcinomas may appear ulcers, masses, or enlarged gastric folds
-CT scan may detect metastasis in the lung and liver but is otherwise poor for staging
-Laparoscopy is sometimes used for staging
-Surgical resection of the gastric cancer and removal of all gross and microscopic disease
-Chemotherapy and radiation therapy have proven not to be beneficial in treatment or palliation
-Peptic Ulcer Disease-
-Peptic Ulcer Disease (gastric and duodenal ulcers) is a loss of the lining of the stomach or duodenum
-the risk factors for peptic ulcer disease are H. Pylori infection, NSAIDS, and unopposed hypergastrinemia with Zollinger Ellison syndrome.
-Ulcers aère an end result of imbalance of aggressive and defense factors in the gastroduodenal mucosa
-H. Pylori, NSAIDS, and acid secretory abnormalities are major factors that disrupt the equilibrium
-Duodenal and gastric ulcers develop in the minority of patients with H. Pylori
-Duodenal ulcers involves enhanced gastric secretion caused by dysregulation of somatostatin and gastrin. Gastrin release is increase. HCO3 secretion is inhibited by H. Pylori infection
-Dyspepsia is the cardinal symptom of peptic ulcer disease
-Other symptoms of PUD includes upper abdominal pain, fullness, bloating, distention and nausea
-Four diagnostic approaches for dyspepsia include: a trial of antacids, immediate endoscopy, non invasive testing for H. Pylori followed by antibiotic treatment for positive patients, and empirical antibiotic therapy for H. Pylori with no testing
-Invasive tests for H. Pylori include rapid urease test, histology and culture. The CLO test on biopsy
-Non invasive tests for H. Pylori include: serology and urea breath test
-Treatment options for PUD include H2 Blockers, Proton Pump Inhibitors, Antacids, and Sucralfate
-Treatment of H. Pylori involves 2 antibiotics plus proton pump inhibitors or ranitidine plus bismuth
-Antibiotic combinations can include clarithromycin and metronidazole, metronidazole plus tetracycline, or amoxicillin plus clarithromycin
-consider stopping NSAIDS
-surgery really does not have a role in management of PUD
-PUD is the most common cause of upper GI bleeding and occurs in 15-20 percent of the patients with PUD
-Bleeding resolves itself about 80 percent of the time, can lead to death 6-7 percent of the time
-Gastric outlet obstruction can occur by a pyloric channel or duodenal ulceration in the setting of acute ulceration. Edema, spasm or inflammation causes the obstruction
-Perforation occurs when there is ulcer penetration through the full thickness of the stomach and duodenum
-Zollinger Ellison Syndrome is characterized by hypersecretion of acid caused by elevated levels of gastrin from a gastrin secreting tumor.
-ZE syndrome should be suspected with recurrent PUD in the absence of H. Pylori infection or NSAID consumption
-the diagnosis of ZE syndrome is made with high levels of gastrin fasting in the setting of gastrin acid hypersecretion
-Surgical resection of the gastrin secreting tumor in the standard in ZE syndrome
-Pyloric Stenosis-
-pyloric stenosis is characterized by hypertrophy of the pylorus with elongation and thickening progressing to a near complete gastric outlet obstruction
-more common in males and females
-Thirty percent of the cases are in the first born children
-Maternal smoking during pregnancy increases the risk
-classic presenting symptoms are 3-6 week old baby who has immediate postprandial, non villous projectile vomiting and demands to be refer after the vomiting episode
-patients are described as being emaciated and dehydrated with a palpable "olive like" mass at the lateral edge of the rectus abdominus muscle in the RUQ
-labs usually reveal a low chloride and a metabolic acidosis
-diagnosis can be confirmed with a ultrasound or upper GI
-Surgical treatment is a pyloromyotomy
-surgery should be delayed until metabolic derangement and dehydration is corrected if present
No comments:
Post a Comment