Gastric disorder

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Gastric Disorder

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Gastric disorder

  1. 1. SMS 2044
  2. 2. Mucous: Mucus, Pepsinogen Ii Chief: Pepsinogen I Parietal: Acid Enteroendocrine: Histamine, Somatostatin, Endothelin
  3. 3. Condition Comment Pyloric stenosis 1 in 300 to 900 live births Male to female ratio 3:1 Pathology: muscular hypertrophy of pyloric smooth muscle wall Symptoms: persistent, nonbilious projectile vomiting in young infant Diaphragmatic hernia Rare Pathology: herniation of stomach and other abdominal contents into thorax through a diaphragmatic defect Symptoms: acute respiratory embarrassment in newborn Gastric heterotopia Uncommon Pathology: a nidus of gastric mucosa in the esophagus or small intestine ("ectopic rest") (The Latin word for "nest“) Symptoms: asymptomatic, or an anomalous peptic ulcer in adult Stomach
  4. 4. 6 Gastric heterotopia
  5. 5.  In keeping with the limited sensory apparatus of the alimentary tract, gastric disorders give rise to symptoms similar to esophageal disorders, primarily heartburn and vague epigastric pain.  Gastric mucosa and bleeding, hematemesis or melena may ensue.  Unlike esophageal bleeding,  blood quickly congeals and turns brown in the acid environment of the stomach lumen.  Vomited blood hence has the appearance of coffee grounds.
  6. 6. Gastritis: is simply defined as inflammation of the gastric mucosa. By far the majority of cases are chronic gastritis, but occasionally, distinct forms of acute gastritis are encountered. 1. Erosive gastritis caused by a noxious irritant 2. Reflux gastritis from exposure to bile and pancreatic fluids 3. Hemorrhagic gastritis 4. Infectious gastritis 5. Gastric mucosal atrophy
  7. 7. Acute Gastritis Acute gastritis is an acute mucosal inflammatory process, usually of a transient nature. The inflammation may be accompanied by hemorrhage into the mucosa and, in more severe circumstances, by sloughing of the superficial mucosal epithelium (erosion). Pathogenesis: The pathogenesis is poorly understood, in part because normal mechanisms for gastric mucosal protection are not totally clear.
  8. 8.  H pylori (most common cause of ulceration)  NSAIDs, aspirin  Gastrinoma (Zollinger-Ellison syndrome)  Severe stress (eg, trauma, burns), Curling ulcers  Alcohol  Bile reflux  Pancreatic enzyme reflux  Radiation  Staphylococcus aureus exotoxin  Bacterial or viral infection
  9. 9. 11
  10. 10. 12
  11. 11.  All variants are marked by :  Mucosal edema  Inflammatory infiltrate of neutrophils and possibly by chronic inflammatory cells.  Regenerative replication of epithelial cells in the gastric pits is usually prominent.  Erosion and hemorrhage is readily visible by endoscopy and is termed acute erosive gastritis. MORPHOLOGY
  12. 12. Free powerpoint template: www.brainybetty.com 14
  13. 13. 15 Histopathology usually demonstrates increased numbers of eosinophils
  14. 14.  Depending on the severity of the anatomic changes, acute gastritis may be entirely asymptomatic,  Epigastric to left upper quadrant  Frequently described as burning  May radiate to the back  Usually occurs 1-5 hours after meals  May be relieved by food, antacids (duodenal), or vomiting (gastric)  Typically follows a daily pattern specific to patient  vomiting, or may present as overt hematemesis, melena, and potentially fatal blood loss.
  15. 15.  Often, a diagnosis can be made based on the patient's description of his or her symptoms, but other methods may be used to verify:  Blood tests:  Blood cell count  Presence of H. pylori  Pregnancy  Liver, kidney, gallbladder, or pancreas functions  Urinalysis  Stool sample, to look for blood in the stool  X-rays  Endoscopy, to check for stomach lining inflammation and mucous erosion  Stomach biopsy, to test for gastritis and other conditions 17
  16. 16. Chronic Gastritis is defined as the presence of chronic mucosal inflammatory changes leading eventually to mucosal atrophy and epithelial metaplasia. In the western world, the prevalence of histologic changes indicative of chronic gastritis exceeds 50% in the later decades of adult life.
  17. 17.  A – autoimmune  B – bacterial (helicobacter)  C - chemical Autoimmune chronic gastritis Autoantibodies to gastric parietal cells Hypochlorhydria/achlorhydria Loss of gastric intrinsic factor leads to malabsorption of vitamin B12 with macrocytic, megaloblastic anaemia
  18. 18. Commonly seen with bile reflux (toxic to cells) Prominent hyperplastic response (inflammatory cells scanty)
  19. 19.  Common infection  10% of men, 4% women develop PUD *  1st Part of duodenum > antrum > G-E junction.  H.pylori related disorders:  Chronic gastritis – 90%  Peptic ulcer disease – 95-100%  Gastric carcinoma – 70%  Gastric lymphoma  Reflux Oesophagitis.  Non ulcer dyspepsia
  20. 20. The most important etiologic association is chronic infection by the bacillus Helicobacter pylori . This organism is a worldwide pathogen. Prevalence of infection among adults maybe reached to 80% it seems to be acquired in childhood and persists for decades. Most individuals with the infection also have the associated gastritis but are asymptomatic.
  21. 21.  H. pylori is a noninvasive, non-spore-forming,S-shaped gram-negative rod measuring approximately 3.5 × 0.5 μm.  Causes cell damage and inflammatory cell infiltration  In most countries the majority of adults are infected
  22. 22. Peptic ulcer disease (Helicobacter) Adenocarcinoma (all types)
  23. 23. 1. Lymphocytic and plasma cell infiltrate in the lamina propria, occasionally accompanied by neutrophilic inflammation of the neck region of the mucosal pits. 2. Gland loss and mucosal atrophy. 3. Intestinal metaplasia refers to the replacement of gastric epithelium with columnar and goblet cells of intestinal variety. 4. lymphoid tissue within the gastric mucosa has been implicated as a precursor of gastric lymphoma Histological F. A Steiner silver stain demonstrates the numerous darkly stained H. pylori organisms along the luminal surface of the gastric epithelial cells. Note that there is no tissue invasion by bacteria.
  24. 24. 26 Chronic gastritis with lymphoid follicle formation in the gastric mucosa (arrow) Some gastric glands are still found (arrowhead).
  25. 25. 27 Chronic gastritis with chronic inflammatory cell infiltration and lymphoid follicle formation (arrowhead) in the gastric mucosa. Atrophy of the gastric glands is seen.(arrow). (M: mucosa, and SM: submucosa)
  26. 26. Clinical Features  Chronic gastritis usually causes few or no symptoms;  upper abdominal discomfort, nausea and vomiting.  Hypochlorhydria or achlorhydria (referring to levels of gastric luminal hydrochloric acid)  Hypergastrinemia are characteristically present.  Most important is the relationship of chronic gastritis to the development of peptic ulcer and gastric carcinoma.
  27. 27. Normal Acute gastritis Chronic gastritis Atrophic gastritis Intestinal metaplasia Dysplasia Cancer
  28. 28.  Ulcers are defined as a breach in the mucosa of the alimentary tract that extends through the muscularis mucosa 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. GASTRIC ULCERATION
  29. 29.  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  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
  30. 30. Neurogenic or catecholamine-induced vasoconstriction Mucosal ischemia Damage the mucosal barrier Directly injure mucosal cells by oxygen or metabolic deprivation
  31. 31. Fig. 40-14
  32. 32. Free powerpoint template: www.brainybetty.com 35
  33. 33.  Acute stress ulcers are usually circular and small (less than 1 cm in diameter).  The ulcer base is frequently stained a dark brown by the acid digestion of extruded blood.  They may occur singly, but more often they are multiple, located throughout the stomach and duodenum  Microscopically, acute stress ulcers are abrupt lesions, with essentially unremarkable adjacent mucosa. Multiple stress ulcers of the stomach, highlighted by the dark digested blood in their bases. MORPHOLOGY
  34. 34.  An ulcer is distinguished from an erosion by its penetration through the muscularis mucosa or the muscular coating of the gastric or duodenal wall occurring as a result of acid and pepsin attack  The lesion of peptic ulcer disease (PUD) is a disruption in the mucosal layer of Sites:  Duodenum (DU)  Stomach (GU)  Oesophagus  Gastro-enterostomy stoma  Related to ectopic gastric mucosa (e.g. in Meckel’s diverticulum)
  35. 35.  Peptic ulcers are remitting, relapsing lesions that are most often diagnosed in middle-aged to older adults, but they may first become evident in young adult life.  Genetic or racial influences appear to play little or no role in the causation of peptic ulcers.  Duodenal ulcers are more frequent in patients with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure, and hyperparathyroidism.  Even with healing, however, the propensity to develop peptic ulcers remains.
  36. 36. Etiology of PUD Normal Increased Attack Hyperacidity,Zollinger Ellison syndrome. Weak defense Stress, drugs, smoking Helicobacterpylori*
  37. 37. Schematic presentation of the presumed action of H. pylori in the development of chronic gastritis and peptic ulceration. The histologic features of the two disease conditions are depicted
  38. 38. There are two key facts.  First, the fundamental requisite for peptic ulceration is mucosal exposure to gastric acid and pepsin. • At pH level 3.5 or more, stomach acid is neutralized  Second, there is a very strong causal association with H. pylori infection.  Mucosa can continually repair itself except in extreme instances Despite the clarity of these two statements, the actual pathogenesis of mucosal ulceration remains murky. Pathogenesis
  39. 39.  The array of host mechanisms that prevent the gastric mucosa from being digested like a piece of meat include the following: 1. Secretion of mucus by surface epithelial cells include the water-insoluble mucous gel layer. 2. Secretion of bicarbonate into the surface mucus, to create a buffered surface microenvironment. 3. 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
  40. 40. 43
  41. 41. 4. 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 5. Mucosal elaboration of prostaglandins (Vasodilation ), which help maintain mucosal blood flow. The possible mechanisms are as follows: Although H. pylori don’t invade the tissues, it induces an intense inflammatory and immune response.
  42. 42. Bacteria over epithelial cells
  43. 43.  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.
  44. 44.  Gram negative, Spirochete.  Does not invade cells  Colonize Gastric mucosa only *  Common cause of Duodenal ulcer * ?  Urease  Breakdown urea  ammonia  high pH  reflex acid prod…  Protease  Break down mucosa  expose epithelium for digestion.  Chronic infl.  Gastric Metaplasia Ulceration.  Complications: Bleeding, perforation, stenosis, Carcinoma.
  45. 45. Diagram of aggravating causes of, and defense mechanisms against, peptic ulceration.
  46. 46. NSAIDs are the major cause of peptic ulcer disease in patients who do not have H. pylori infection. The gastroduodenal effects of NSAIDs range from acute erosive gastritis and acute gastric ulceration to peptic ulceration in 1% to 3% of users. Thus, those who take these drugs for chronic rheumatic conditions are at particularly high risk.
  47. 47.  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.  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.
  48. 48. 1. defects in the mucosa that penetrate at least into the submucosa, and often into the muscularis propria or deeper. 2. Most are round, sharply punched-out craters 2 to 4 cm in diameter. 3. Those in the duodenum tend to be smaller, and occasional gastric lesions are significantly larger. 4. Favored sites are the anterior and posterior walls of the first portion of the duodenum and the lesser curvature of the stomach. Morphology
  49. 49. 5. The base of the crater appears remarkably clean, owing to peptic digestion of the inflammatory exudate and necrotic tissue. 6. Infrequently, an eroded artery is visible in the ulcer (usually associated with a history of significant bleeding). 7. If the ulcer crater penetrates through the duodenal or gastric wall, a localized or generalized peritonitis may develop and adjacent structure such as adherent omentum, liver, or pancreas could be affect.
  50. 50. o In open ulcer, four zones can be distinguished: o (1) The base and margins have a thin layer of necrotic fibrinoid debris. o (2) Fibrous, collagenous scar that fans out widely from the margins of the ulcer. o (3) Granulation tissue o (4) a zone of active nonspecific inflammatory infiltration with neutrophils predominating Histologic Appearance
  51. 51. (FIgure 2).  Four zones of active peptic ulcer.  The necrotic fibrinoid debris and nonspecific inflammatory infiltrate are labeled by arrowhead.  Beneath the necrotic and inflammatory zones, there is granulation tissue (arrow).  Below the granulation tissue, fibrotic tissue is seen (F). Figure 3). Necrotic fibrinoid debris and inflammatory infiltrate in the ulcer base.
  52. 52. Figure 4). Granulation tissue in the ulcer base. New blood vessels lined by plump endothelial cells (arrow). Edema and inflammatory infiltrate are also seen. (Figure 5). Fibrotic tissue beneath the ulcer base
  53. 53. (Figure 8) Intestinal metaplasia in chronic gastritis. The gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow). The intestinal epithelium has goblet cells. Chronic inflammatory cell infiltration is also (Figure 7) Chronic gastritis with intestinal metaplasia (arrow) seen in the mucosa around the peptic ulcer. The mucinous gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium
  54. 54.  Most peptic ulcers cause epigastric gnawing, burning, or boring pain  but a significant minority first come to light with complications such as hemorrhage or perforation.  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.  Nausea, vomiting, bloating, belching, and significant weight loss (raising the specter of some hidden malignancy) are additional manifestations.  Bleeding is the chief complication, occurring in up to one third of patients, and may be life-threatening.
  55. 55.  Pain or discomfort  A feeling of fullness -- people with severe dyspepsia are unable to drink as much fluid as people with mild or no dyspepsia  Hunger and an empty feeling in the stomach, often 1 - 3 hours after a meal  Mild nausea (vomiting may relieve symptoms)  Regurgitation (sensation of acid backing up into the throat)  Occasionally, symptoms of GERD are present  Obstruction of the pyloric channel is rare. 63
  56. 56. Sharp edges, converging folds of mucosa in the upper half. The ulcer bed is covered by fibrinopurulent exudate.
  57. 57. Free powerpoint template: www.brainybetty.com 65
  58. 58. (Figure 1) Peptic ulcer of stomach (arrow). The whole mucosa and part of submucosa are denuded.(M: mucosa, SM: submucosa, MP: muscularis propria)
  59. 59.  Neutralize stomach acid  Calcium  Tums, Rolaids  Aluminum + Magnesium  Maalox, Riopan, Mylanta, Gelusil  Sodium  Alka-Seltzer  Magnesium  Milk of Magnesia
  60. 60.  Standard Therapy  14-16 days  Bismuth subsalicylate (Pepto Bismol)  Metronidazole  Tetracycline  Newest Treatment  Helidac (three antibiotic regimen)
  61. 61. Free powerpoint template: www.brainybetty.com 71 I don’t want qzzzzzzzzzzzzzzzz

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