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Ulcers

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A BRIEF DISCUSSION ON ULCERS …

A BRIEF DISCUSSION ON ULCERS

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  • The array of host mechanisms that prevent the gastric mucosa from being digested like a piece of meat include the following: Secretion of mucus by surface epithelial cells Secretion of bicarbonate into the surface mucus, to create a buffered surface microenvironment Secretion of acid- and pepsin-containing fluid from the gastric pits as "jets" through the surface mucus layer, entering the lumen directly without contacting surface epithelial cells Rapid gastric epithelial regeneration Robust mucosal blood flow, to sweep away hydrogen ions that have back-diffused into the mucosa from the lumen and to sustain the high cellular metabolic and regenerative activity Mucosal elaboration of prostaglandins, which help maintain mucosal blood flow
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    • 1. ANKIT GILANIDEPT. OF PHARMACOLOGY & TOXICOLOGY SEMISTER 01 NIPERD AHMEDABAD
    • 2. CONTENTS : INTRODUCTION PATHOGENESIS SIGNS & SYMPTOMS LABORATORY FINDINGS COMPLICATIONS
    • 3. INTRODUCTION Ulcers are defined as a breach in the mucosa of the alimentary tract that extends through the muscularis mucosae into the submucosa or deeper. This is to be contrasted to erosions, in which there is a breach in the epithelium of the mucosa only. Erosions may heal within days, whereas healing of ulcers takes much longer. Although ulcers may occur anywhere in the alimentary tract, none are as prevalent as the peptic ulcers that occur in the duodenum and stomach.
    • 4. GROSS FEATURES : Peptic ulcers are usually single well delineated lesion. Shape: Round, oval or linear. Size: Usually less than 2cm in diameter.Lesions less than 0.3 cm are likely to be shallow erosions.Giant ulcers are usually greater than 3cm in diameter.May also reach upto 10cm (particularly on lesser curvature ).Mortality rate is higher in these patients.Size does not differentiate benign from malignant ulcer.Some carcinomatous ulcers are less than 4cm and 10%of benign ulcers are more than 4cm .
    • 5. PATHOGENESIS AGGRESSIVE FORCES DEFENSIVE FORCESpeptic ulcers are induced by an imbalance between thegastroduodenal mucosal defenses and the countervailingaggressive forces that overcome such defenses
    • 6. AGGRESSIVE FORCES GASTRIC ACIDITY PEPTIC ACTIVITY
    • 7. DEFENSIVE FORCES Secretion of mucus by surface epithelial cells Secretion of bicarbonate into the surface mucus, to create a buffered surface microenvironment Secretion of acid- and pepsin-containing fluid from the gastric pits as "jets" through the surface mucus layer, entering the lumen directly without contacting surface epithelial cells Rapid gastric epithelial regeneration Robust mucosal blood flow, to sweep away hydrogen ions that have back-diffused into the mucosa from the lumen and to sustain the high cellular metabolic and regenerative activity Mucosal elaboration of prostaglandins, which help maintain mucosal blood flow
    • 8. CAUSES INCREASED IMPAIRED AGGRESSION DEFENCE H.Pylori INFECTION, ISCHAEMIA, NSAIDs (ASPIRIN), SHOCK, SMOKING,DELAYED GASRIC ALCOHOL, EMPTYING, IMPAIRED REGULATION GASRO- OF ACID-PEPSIN OESOPHAGEAL SECRETION, REFLUX BILE ACIDS, GENETIC FACTORS
    • 9. H.pylori infection : Helicobacter pylori previously named Campylobacter pyloridis, Gramnegative,microaerophilic bacterium found in the stomach Among the "aggressive forces," H. pylori is very important, because this infection is present in 70% to 90% of patients with duodenal ulcers and in about 70% of those with gastric ulcers
    • 10. POSSIBLEMECHANISMS OFH.pylori INFECTION : Although H. pylori does not invade the tissues, it induces an intense inflammatory and immune response. There is increased production of proinflammatory cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor (TNF), and, most notably, IL-8 H. pylori secretes a urease that breaks down urea to form toxic compounds such as ammonium chloride and monochloramine. elaborate phospholipases that damage surface epithelial cells. Toxin encoding genes : vacuolating toxin (VacA), cytotoxin- associated gene A (CagA) metaplastic foci (colonization) Immunogenic proteins of H.pylori.
    • 11.  . The possible mechanisms are as follows: Although H. pylori does not invade the tissues, it induces an intense inflammatory and immune response. There is increased production of proinflammatory cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor (TNF), and, most notably, IL-8. This cytokine is produced by the mucosal epithelial cells, and it recruits and activates neutrophils. Several bacterial gene products are involved in causing epithelial cell injury and induction of inflammation. H. pylori secretes a urease that breaks down urea to form toxic compounds such as ammonium chloride and monochloramine. The organisms also elaborate phospholipases that damage surface epithelial cells. Bacterial proteases and phospholipases break down the glycoprotein-lipid complexes in the gastric mucus, thus weakening the first line of mucosal defense. Epithelial injury is also caused by a vacuolating toxin (VacA). Another toxin, encoded by the cytotoxin-associated gene A (CagA), is a powerful stimulus for the production of IL-8 by the epithelial cells. H. pylori enhances gastric acid secretion and impairs duodenal bicarbonate production, thus reducing luminal pH in the duodenum. This altered milieu seems to favor gastric metaplasia (the presence of gastric epithelium) in the first part of the duodenum. Such metaplastic foci provide areas for H. pylori colonization. Several H. pylori proteins are immunogenic, and they evoke a robust immune response in the mucosa. Both activated T cells and B cells can be seen in chronic gastritis caused by H. pylori. The B lymphocytes aggregate to form follicles. The role of T and B cells in causing epithelial injury is not established, but T-cell-driven activation of B cells may be involved in the pathogenesis of gastric lymphomas.
    • 12. NSAIDs(aspirin, ibuprofen, naproxen): Suppression of mucosal prostaglandin synthesis is the key to NSAID-induced peptic ulceration. Inhibition of prostaglandin synthesis increases secretion of hydrochloric acid and reduces bicarbonate and mucin production. Loss of mucin degrades the mucosal barrier that normally prevents acid from reaching the epithelium. Synthesis of glutathione, a free radical scavenger, is also reduced. Some NSAIDs can penetrate the gut mucosal cells as well. By mechanisms not clear, some NSAIDs also impair angiogenesis, thus impeding the healing of ulcers.
    • 13. SOME OTHER CAUSES OFULCERS : Cigarette smoking impairs mucosal blood flow and healing. Alcohol has not been proved to directly cause peptic ulceration, but alcoholic cirrhosis is associated with an increased incidence of peptic ulcers. Corticosteroids in high dose and with repeated use promote ulcer formation.
    • 14. ACUTE GASTRICULCERATION Focal, acutely developing gastric mucosal defects may appear after severe stress and are designated stress ulcers. Generally, there are multiple lesions located mainly in the stomach and occasionally in the duodenum. Stress ulcers are most commonly encountered in the following conditions: Severe trauma, including major surgical procedures, sepsis, or grave illness of any type Extensive burns (the ulcers are then referred to as Curling ulcers ) Traumatic or surgical injury to the central nervous system or an intracerebral hemorrhage (the ulcers are then called Cushing ulcers) Chronic exposure to gastric irritant drugs, particularly NSAIDs and corticosteroids
    • 15. SIGNS AND SYMPTOMS Epigastric pain : The pain tends to be worse at night and occurs usually 1 to 3 hours after meals during the day. Classically, the pain is relieved by alkalis or food, but there are many exceptions. (duodenal ulcers are relieved by food, while gastric ulcers are exacerbated by it) waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in oesophagus - although this is more associated with GERD) nausea, and copious vomiting loss of appetite and weight loss hematemesis (vomiting of blood) this can occur due to bleeding directly from a gastric ulcer, or from damage to the oesophagus from severe/continued vomiting.
    • 16. SIGNS AND SYMPTOMS(cont.) melena (tarry, foul-smelling feces due to oxidized iron from hemoglobin) rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis. This is extremely painful and requires immediate surgery. Bloating and abdominal fullness Bleeding is the chief complication, occurring in up to one third of patients, and may be life-threatening. When untreated, the average individual requires 15 years for healing of a peptic ulcer.
    • 17. LABORATORY FINDINGS : Endoscopy is a highly sensitive diagnostic method because it allows accurate assessment of the ulcer, by recognizing the lesion, by demonstrating it’s activity and by demonstrating the presence of a hemorrhage. Moreover, endoscopy allows biopsies in peptic ulcers which can highlight the benign or malignant character of the lesion. Evaluation of a healed peptic ulcer is also done by endoscopy which can demonstrate the existence of the scar. Radiography of peptic ulcer, may be a complementary method of diagnostic, especially when is suspected a gastric emptying disorder (pyloric stenosis).
    • 18.  Determination Helicobacter pylori, the causative agent of most peptic ulcers, is a compulsory element in the diagnosis of peptic ulcer. Determination of Helicobacter pylori is made by direct methods and indirect methods. Direct methods require endoscopy with biopsy. The presence oh Helicobacter pylori is determined by histological examination. Indirect methods do not require endoscopy and are represented by the determination of Helicobacter pylori antibodies from the plasma and respiratory tests. Helicobacter pylori antibodies, also can be detereminated in saliva and eradication of Helicobacter pylori infection can be demonstrated by determination of bacteria in the stool (fecal test antigen against Helicobacter pylori). The most sensitive indirect methods of diagnosis of infection with Helicobacter pylori are respiratory tests and fecal antigen anti Helicobater pylori
    • 19. COMPLICATIONS The possible complications of peptic ulcer are: Upper gastrointestinal bleeding, is the most common complication, approximately 15% Perforation leading to peritonitis penetration Pyloric stenosis Malignancy of the ulcer, the risk of developing this complication is low.
    • 20.  Complications Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life-threatening.[5] It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery. Perforation (a hole in the wall) often leads to catastrophic consequences. Erosion of the gastro-intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity. Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain. Posterior wall perforation leads to bleeding due to involvement of gastroduodenal artery that lies posterior to the 1st part of duodenum. Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas.[6] Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction. Patient often presents with severe vomiting. Cancer is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.[7]
    • 21. Data from Death and DALY estimates for 2004by cause for WHO Member States(Persons, all ages)

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