Patho sheet # 7 - Yasmi Nofal

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Patho sheet # 7 - Yasmi Nofal

Post by Shadi Jarrar on 25/2/2011, 2:38 am

بسم الله الرحمن الرحيم

patho 8.docx

In this lecture we will talk about the stomach…
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. .
Chronic Gastritis :
Chronic gastritis is defined as the presence of chronic inflammatory changes in the mucosa leading eventually to mucosal atrophy and epithelial metaplasia. In the Western world, the prevalence of histological changes indicative of chronic gastritis is higher than 50% in the later decades of life.
by far the most important etiologic association is chronic infection by the bacillus H. pylori. This organism is a worldwide pathogen that has the highest infection rates in developing countries. American adults older than age 50 show prevalence rates approaching 50%. In areas where the infection is endemic, it seems to be acquired in childhood and persists for decades. Most individuals with the infection also have the associated gastritis but are asymptomatic. H. pylori is a noninvasive, non-spore-forming, S-shaped gram-negative rod measuring approximately 3.5 μm × 0.5 μm. The mechanisms by which H. pylori causes tissue injury develops as a result of the combined influence of bacterial enzymes and toxins and release of noxious chemicals by the recruited neutrophils. After initial exposure to H. pylori, gastritis may develop in two patterns: (1) an antral-type with high acid production and higher risk for the development of duodenal ulcer, and (2) a pangastritis with multifocal mucosal atrophy, with low acid secretion and increased risk for adenocarcinoma. Persons with chronic gastritis and H. pylori usually improve symptomatically when treated with antibiotics and proton pump inhibitors(ex..omeprazole)...
Improvement in the underlying chronic gastritis may take much longer. Relapses are associated with reappearance of this organism.
Other forms of chronic gastritis are much less common in the United States. Autoimmune gastritis, which represents no more than 10% of cases of chronic gastritis, results from the production of autoantibodies to the gastric gland parietal cells, in particular to the acid-producing enzyme H+,K+-ATPase. The autoimmune injury leads to gland destruction and mucosal atrophy, with concomitant loss of acid and intrinsic factor production. The resultant deficiency of intrinsic factor leads to pernicious anemia (intrinsic factor is responsible for the absorption vitamin B12 in the terminal ileum so pernicious anemia leads to B 12 deficiency which causes autoantibody against the parietal cells or the intrinsic factor..the autoimmune disease is associated with another autoimmune disorders).
Clinically,, chronic gastritis usually causes few or no symptoms; upper abdominal discomfort and nausea and vomiting can occur. When severe parietal cell loss occurs in the setting of autoimmune gastritis, hypochlorhydria or achlorhydria and hypergastrinemia (gastrin leads to increase acid secretions)… Most important is the relationship of chronic gastritis to the development of peptic ulcer and gastric carcinoma. Most individuals with a peptic ulcer, whether duodenal or gastric, have H. pylori infection. The long-term risk of gastric carcinoma for persons with H. pylori-associated chronic gastritis is increased about fivefold relative to the normal population. For autoimmune gastritis, the risk for cancer is in the range of 2% to 4% of affected individuals, which is well above that of the normal population.(in chronic gastritis we can goblet cells in the stomach as a result of metablasia..and we can see atrophy in the stomach, we use special stain which is stinal stain it’s a silver stain which stains the H.pylori in a black color) (H .pylori invades the mucus of the gland &doesn’t invade the tissue)

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). This severe erosive form of the disease is an important cause of acute gastrointestinal bleeding. (the difference between erosion and ulcer is that the erosion is a mucosal inflammation and defect in it while the ulcer involves the submucosa layer so it goes through the submucosa).
Acute gastritis is frequently associated with:
Heavy use of nonsteroidal anti-inflammatory drugs (NSAIDs), particularly aspirin, Excessive alcohol consumption, Heavy smoking, Treatment with cancer chemotherapeutic drugs, Uremia (uremia happens in patients with chronic renal failure, the urea and creatinine is increased in the blood), Systemic infections (e.g., salmonellosis),Severe stress (e.g., trauma, burns, surgery),Ischemia and shock, Mechanical trauma (e.g., nasogastric intubation)Reflux of bilious material after distal gastrectomy.

Histological, All variants are marked by mucosal edema and an inflammatory infiltrate of neutrophils and possibly by chronic inflammatory cells.
Clinically, Depending on the severity of the anatomic changes, acute gastritis may be entirely asymptomatic, may cause variable epigastric pain with nausea and vomiting, or may present as overt hematemesis( vomiting of black blood as a result of acid action named coffee ground !!!), melena, and potentially fatal blood loss. Overall, it is one of the major causes of hematemesis, particularly in alcoholics. The risk of gastric bleeding from NSAID-induced gastritis is dose related, thus increasing the likelihood of this complication in persons requiring long-term use of such drugs ( like rheumatoid arthritis patients that take aspirin,profen,naproxin for long periods).


Ulcers of the alimentary tract are defined histologicaly as a breach in the mucosa that extends through the muscularis mucosae into the submucosa or deeper. Although ulcers may occur anywhere in the alimentary tract, by far, the most common are the peptic ulcers that occur in the duodenum and stomach.
Peptic Ulcers

Peptic ulcers are chronic, most often solitary, lesions that occur in any portion of the gastrointestinal tract exposed to the aggressive action of acidic peptic juices( as a result of the acids and enzymes produced by the stomach). At least 98% of peptic ulcers are either in the first portion of the duodenum or in the stomach, in a ratio of about 4:1.
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. They often appear without obvious precipitating influences and may then heal after a period of weeks to months of active disease. Even with healing, however, the propensity to develop peptic ulcers remains, in part because of recurrent infection with H. pylori. The male/female ratio for duodenal ulcers is about 3:1. For both men and women in the United States, the lifetime risk of developing peptic ulcer disease is about 10%.Duodenal ulcers are more frequent in persons with alcoholic cirrhosis, chronic obstructive pulmonary disease, chronic renal failure, and hyperparathyroidism. With respect to the last two conditions, hypercalcemia, whatever its cause, stimulates gastrin production and therefore acid secretion. Two conditions are key for the development of peptic ulcers: (1) H. pylori infection, which has a strong causal relationship with peptic ulcer development, and (2) mucosal exposure to gastric acid and pepsin. H. pylori infection is the most important condition in the pathogenesis of peptic ulcer. The infection is present in 70% to 90% of persons with duodenal ulcers and in about 70% of those with gastric ulcers. Furthermore, antibiotic treatment of H. pylori infection promotes healing of ulcers and tends to prevent their recurrence. Although H. pylori does not invade the tissues, it induces an intense inflammatory and immune response. There is increased production of pro inflammatory cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor, and, most notably, IL-8. IL-8 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. Epithelial injury is mostly caused by a vacuolating toxin called VacA, which is regulated by the cytotoxin-associated gene A (CagA). 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. H. pylori enhances gastric acid secretion and impairs duodenal bicarbonate production, thus reducing luminal pH in the duodenum. 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 the mucosa and in chronic gastritis caused by H. pylori. T-cell-driven activation of B cells may be involved in the pathogenesis of MALT lymphomas.(sometimes when we cure H.pylori infection this MALT lymphoma fade away).

Only 10% to 20% of individuals worldwide who are infected with H. pylori actually develop peptic ulcer. strains producing VacA and CagA cause more intense tissue inflammation, more severe epithelial damage, and higher cytokine production( this explains why some people who have H.pylori predispose ulcer and gastritis while other people who have it are asymptomatic and don’t have a disease). NSAIDs are the major cause of peptic ulcer disease in persons 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. Risk factors for NSAID-induced gastroduodenal toxicity are increasing age, higher dose, and prolonged usage. Suppression of mucosal prostaglandin synthesis, which increases secretion of hydrochloric acid and reduces bicarbonate and mucin production( NSAIDS inhibit prostaglandin synthesis ,,decrease in the mucin production in the stomach which protect the surface from acid secretion and decrease the bicarbonate secretion in the duodenum, make injury in the mucosa)
. Other events may act alone or in concert with H. pylori and NSAIDs to promote peptic ulceration. Gastric hyperacidity may be strongly ulcerogenic. Excess production of gastric acid from a tumor in individuals with the Zollinger-Ellison syndrome causes multiple peptic ulcerations in the stomach, duodenum, and even in the jejunum (we can differentiate zolinger syndrome by the presence of multiple peptic ulcers in abnormal sites like if we have peptic ulcer in the jejunum). 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.(corticosteroids inhibit prostaglandin synthesis and all eicosanoids that why we use them as an anti-inflammatory). Personality(type A) and psychological stress are important contributing variables. Most peptic ulcers cause epigastric pain, often described as gnawing, burning, or boring, but a significant minority first come to light with complications such as hemorrhage or perforation. Bleeding is the chief complication, occurring in as many as one-third of patients, and may be life-threatening. Perforation occurs in about 5% of patients but accounts for two-thirds of deaths from this disease in the United States. Obstruction of the pyloric channel is rare. Malignant transformation occurs in about 2% of patients, generally from ulcers in the pyloric channel.
The End 
Pathology lec. #7
Yasmine Nofal
Shadi Jarrar
مشرف عام

عدد المساهمات : 997
النشاط : 12
تاريخ التسجيل : 2009-08-28
العمر : 27
الموقع : Amman-Jordan

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