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Sheet 96/3/2014??? ???? ?????? ??????Gastrointestinal tract (2):Today we will discuss diseases of the stomachThey are classified into inflammatory disorders of the stomach most of them are gastritis and gastric ulcers wither acute or chronic and the tumors of the stomach.1-acute gastritis:Acute: develop suddenly (at short period of time) also it last for a short period of time.In acute gastritis there is transient mucosal inflammation and the inflammation of acute gastritis is mainly congestion of blood vessels.it is not that inflammation with neutrophils ,not as we see in acute nephritis, it is not associated with fever.mucosal inflammatory process transient may be asymptomatic and may be associated with variant degree of symptoms.It's just associated with epigastric pain, nausea and vomiting.Severe acute gastritis: the inflammation is more severe, the patient suffers from vomiting of blood and hematemesis so it depends on the degree.Also mild cases may be not associated with erosion and ulceration of the surface of the stomach, erosion means there is no loss of whole epithelial layer but in ulceration the whole epithelial layer and even below is lost, so erosion is superficial but ulceration is deeper.Severe cases of acute gastritis may cause ulceration, and if there is ulceration there will be blood may be with vomiting in the form of hematemesis, and may be with stool in the form of melena.acute gastritis can occur after disruption of any protective mechanism in the stomach, now stomach is an acidic media, have very low PH but this acidic media may destruct the gastric mucosa, however in certain protective mechanism the stomach produce mucus material cover the whole surface of the stomach so the acidity will not cause much destruction on the epithelium, anything decrease the mucus secretion will decrease the protection.The second protective mechanism: bicarbonate also produced by surface epithelium to produce alkaline media between epithelium and mucus and this for protection from the acidity.Also vascular perfusion of the stomach carry the protons and ions that produce acidity so the acidity remains at certain range and the blood flow will replenish the damage cells to replace it with new cells.any one may have shock state with very severe reduction in blood pressure so blood flow in stomach will reduce because of that they may have gastric ulcer, in this case prostaglandin (production of cyclooxygenase pathway)cause dilation of blood vessels of the stomach so increase blood flow to it.So all of these are productive mechanisms(mucus, bicarbonate, vascular perfusion and prostaglandins) any imbalance of them will lead to predisposition of acute gastritis or acute ulcer, e.g.: the drugs which inhibit prostaglandins such as non-steroidal anti-inflammatory drugs (NSAIDs) and aspirin are very much associated with gastritis and gastric ulcers.Other causes: alcohol, smoking some times, radiation , certain chemicals, the alkaline and acids that affect the esophagus and cause esophagitis also have same effect on the stomach, chemotherapy and radiotherapy for cancer patients all of these are injurious.Morphology:Mild forms may be just hyperemia, vascular congestion in mucosa and mild erosion, however in severe cases may cause more ulceration and hemorrhage, the severe form of acute gastritis which cause severe erosion with hemorrhage we call it (acute erosive hemorregic gastritis) its descriptive term because it include hemorrhage and erosion, so its subtype of gastritis which is very severe and in this case the patient will have hematemesis, melena and sometime massive blood lose.2-Acute Peptic Ulceration: Any acute gastritis may turn to acute ulcer in the severe form and we call it(acute peptic ulceration) when we say peptic we mean any surface exposed to acid and pepsin(products of stomach) .It's mainly occur in the stomach but it can occur in duodenum and esophagus such as when we have gastric heterotopia and we have ulcer there. When we say acute we mean that it is suddenly occur, we don't see changes of the chronic peptic ulcer which we will talk about later on.They are focal.Acute ulcer it’s a combination of either drugs such as NSAIDs or physiological stress.physiological stress: any stress condition in the body such as trauma, surgery , blood lose,…physiological stress includes three forms:a-Stress ulcers: when the patient has a shock state this will decrease blood flow to stomach so there is reduction in the protection so probability of acute gastritis and acute ulcer increase, or when patient has severe trauma.in the most of the time these are small and multiple and the result will be hematemesis or melena.b- Curling ulcers: occurring in the proximal duodenum as we said peptic not only occur in stomach.They are usually associated with severe burns, why severe pain cause ulcer? Because burns is a physiological stress condition, if the burns is severe the patient will have hypovolemia and dehydration so the end result will also be an ulcer.c- Cushing ulcers:can seen in any part of GI tract, in stomach duodenum, or esophagus.It's particularly associated with any diseases in the CNS that increase the intracranial pressure.so stress ulcer occur in stressful condition, sepsis, shock state , trauma, surgery. Curling ulcer with pain. and crushing ulcer with high intracranial ulcer.Morphology:The morphology of ulcers is variable, some ulcers are small, shallow, superficial and some ulcers if they are severe they will be deep and may cause perforation. So its variable may be single or multiple, e.g.: stress ulcers are usually multiple small ulcers.the most important thing to now is the scarring and thickening of blood vessels that characterize chronic peptic ulcers which are result of inflammation and repair are absent in acute ulcer which is mainly associated with blood loss and hemorrhage.most of the time the acute ulcer are small , multiple, and shallow ulcer and in severe cases may cause perforation , when we have perforation the problem is not in the food leakage, the problem is in the blood leakage to peritoneum.Symptoms:Symptoms of gastric ulcers are variable may be just nausea and vomiting or may be severe ulceration and coffee-ground hematemesis, coffee-ground hematemesis means the blood altered to brownish blood because of the acidity of gastric juice not as malaria ulceration the vomiting with fresh blood(red color). Chronic Gastritis:The second type of gastritis is a chronic gastritis its means the symptoms appear for a long period of time and last for long period of time also. and the cause are different:in acute gastritis most of the time the alcohol ,smoking ,radiation and chemical injures are the causes, here in chronic gastritis the most common cause is infection by a bacteria called bacillus Helicobacter pylori which cause 90% of causes of chronic gastritis, autoimmune gastritis is another important cause of chronic gastritis but it represents less than 10% of cases, very rare or less common causes are the radiations and chronic bile reflux, the bile is normally go to duodenum then go to intestine in some cases we see incompetence in gastric sphincter as a result the bile will reflux. Also we can see incompetence in lower esophageal.In all form of chronic gastritis it's mainly associated with inflammatory infiltrate in the stomach, acute gastritis it's mainly hemorrhage in mucosa, congestion of blood vessels and the inflammation is not common. While in chronic gastritis it's mainly inflammation and the inflammatory cells are lymphocytes (its chronic inflammation), in some cases when the infection is active we will found lymphocytes and neutrophil especially with H.pylori.Helicobacter pylori Gastritis:H.pylori almost associated with duodenal ulcers and a majority of gastric ulcers or chronic gastritis, why it's associated with duodenal ulcers? the media in duodenum is alkaline media not acidic but the H.pylori cause hyperchlorhydria, its increase the HCl production and increase the acidity so the gastric juice which reach the duodenum will be very acidic, so all duodenum ulcers are caused by H.pylori and the majority of chronic gastritis and gastric ulcers are also caused by H.pylori .90% of chronic gastritis affecting the antrum( the majority of H.pylori are found in antrum so the best type of biopsy to find H.pylori is taken from antrum).Associated with H.pylori is the increase of acid secretion in peptic ulcer of the stomach and the duodenum.The acid secretion increase and the gastrin level decrease as a reflux mechanism,, The stomach has G cells they produce gastrin,so because the H.pylori stimulate the acid production in stomach it cause decrease in gastrin level so cause hypogastrinemia.Also confers increased risk of gastric cancer , so there is strong relation between H.pylori chronic gastritis and gastric cancer(adenocarcinoma) in the way that H.pylori cause chronic gastriris, chronic gastritis with time may cause intestinal metaplasia in the stomach , intestinal metaplasia with time will convert to dysplasia which convert to carcinoma.The infection with H.pylori is associated with developing countries and crowding areas may be all of you or 70% of you will have H.pylori without causing any symptoms.the H.pylori their infection is acquired in childhood and remains there for adulthood, but if the bacteria does not make increase in acid production or the productive mechanism of the stomach is strong it will not cause gastritis. 70% of population they have this bacteria and they are immune against it, they have certain immunoglobulin's in the serum such as the viruses when the person has immune against hepatitis viruses same is here with H.pylori so it's may be present in the stomach without causing any inflammation, if I take biopsy from the patient and we found the H.pylori without causing any infection ,here non need to treat it.H.pylori usually does not go inside the cells it's found within the superficial mucus layer overlying antral epithelial cells.as we said its start in the antrum but over time, if it became very severe it may progress to pangastritis( whole the stomach become affected so it will end with atrophy in the stomach and this atrophy is the end result of inflammation after a long period of time, also in the beginning the acid secretion is high but with severe pangastritis and damage of acid producing cells which are found in the body (parietal cells of the stomach)as we now in the body we have parietal cells and chief cell secrete pepsin so if the parietal cells destructed, the acid will reduce ,so early in H.pylori infection when it's still in the antrum when it's still in the antrum there is hyperacidity, later on when it progress to pangastritis and atrophy of mucosa, the acid production will reduce.As we said intestinal metaplasia, dysplasia and adenocarcinoma are also associated with infection, also patient with H.pylori itself increase risk for gastric lymphoma.Note: H.pylori associated with: 1-chronic gastritis.2-gastric adenocarcinoma.3-gastric lymphoma.Generally H.pylori just seen in the antrum thus an antral biopsy is preferred for evaluation of H.pylori gastritis.H.pylori is not seen over intestinal metaplasia, it is not live in duodenal epithelium nor gastric body except if there is pangastritis. so typically it is present in the antrum.Refer to Slide 10 to see the Morphology of Helicobacter pylori Gastritis:there is a mucus layer overlying surface epithelia , we can see a mark inflammation, all are lymphocytes and associated neutrophils attacking the surface epithelia( this mean that there is inflammation).and these are microorganisms , they are bacilli rod shaped and concaved, and there is a goblet cells. Diagnosis:1- Serologic test for anti–H. pylori antibodies:Endoscopy, biopsy (we diagnose bacteria by histology)or by serum(they do measurement for immunoglobulin level we conceder the IgM not the IgG because IgM indicate acute process while IgG indicate old immunity for bacteria.2- Fecal bacterial detection:it can detected in stool, it’s a fecal oral way of transitions!3- Urea breath test based on the generation of ammonia by bacterial urease, not much used; usually we use endoscopy, biopsy and serum antibodies. Treatment:Combinations of antibiotics and proton pump inhibitors:Proton pump inhibitors: to decrease acid production.Antibiotics: to get rid of the bacteria (eradication therapy).The second form of chronic gastritis is:Autoimmune Gastritis:Note: the different between the H.plyori gastritis and autoimmune gastritis is very important.Typically spares the antrum, the disease affecting the parietal cells (acid producing cells and induces hyper gastrenemia.the patient with autoimmune gastritis characterized by having:1-antibodies to parietal cells and antibodies to intrinsic factor which is needed for vitamin B.12 absorption, so these antibodies cause destruction of parietal cells, so this type of gastritis is associated with hypochlorhydria or achlorhydria so there is no acid production while H.plyori in early stage there is increase in acid production and this one of the important difference.2-antral endocrine cell (G cell) hyperplasia while in H.pylori the G cells suppressed but here the G cells increase in number to increase production of gastrin for hope to stimulate acid production, remember we have hypochlorhydria(hypoacidity)in autoimmune gastritis.3-vitamin B.12 deficiency because the patient has antibodies against intrinsic factors so decrease in vitamin B.12 absorption which cause megaloblastic anemia (pernicious anemia)so autoimmune gastritis well associated with megaloblastic anemia(vitamin B.12 deficiency).4-Defective gastric acid secretion (achlorhydria) because of damage of parietal cells.5- Diffuse damage of the oxyntic (acid-producing) mucosa (parietal cells).6- Damage to the antrum and cardia typically is absent or mild .7- Chief cell loss also can occur in association with parietal cells loss because they are in the same area.8- Intestinal metaplasia may develop.9- Diffuse atrophy with time, sometimes autoimmune gastritis called (atrophic gastritis) because the wall of the stomach become very thin with time and atrophic.Clinical features:Antibodies to parietal cells and intrinsic factor are present early in disease.Pernicious anemia develops in only a minority of patients.The median age at diagnosis is 60 years.Slight female predominance.Often is associated with other autoimmune diseases.Refer to the table in slide 15 which is repetition of all what we said as a differentiation between H.pylori gastritis and autoimmune gastritis.Some notes related to the table:*sequelae: both of them may cause atrophy at the end but the association of adenocarcinoma, lymphoma and peptic ulcer are high with H.pylori but the association of atrophy, pernicious anemia, adenocarcinoma also can occur and carcinoid tumor are high with autoimmune gastritis. * carcinoid tumor: it’s a tumor of endocrine cells of the stomach , the patients have very active G cells which cause G cell hyperplasia in the autoimmune gastritis.*inflammatory infiltrate: both of them are gastritis so in both of them you will find the lymphocytes, neutrophils are more common in .pylori gastritis because it’s a bacterial infection.Peptic Ulcer Disease (PUD):may occur in any portion of the GI tract exposed to acid and pepsin it can occur in the stomach , duodenum and esophagus but its most common in the gastric antrum (it’s the site of chronic gastritis) and the duodenum(it’s the site of H.pylori).Most often is associated with H.pylori infection or NSAIDs use.It's usually imbalance, as we said in acute ulcers, imbalance between protective mechanism (mucosa, prostaglandins and bicarbonate) and destructive mechanism (acid and pepsin), that is why even NSAIDs at long term cause chronic peptic ulcer.Gastric hyperacidity is fundamental to the pathogenesis of PUD.In the past they used to say if no acid no ulcer, so in the duodenum if there is no hyperacidity caused by H. pylori there is will not be any ulcers.(All ulcers in the duodenum are caused by H.pylori).Cofactors in peptic ulcerogenesis include:1-Chronic NSAID use, is the main cause.2-Cigarette smoking.3-High-dose corticosteroids, its decrease the protective mechanism in stomach(decrease bicarbonate and mucus secretion).4-Alcoholic cirrhosis.5-Any chronic disease such as chronic obstructive pulmonary disease, chronic renal failure, and hyperparathyroidism.6-Psychologic stress may increase gastric acid production and exacerbate PUD.Zollinger-Ellison syndrome:Characterized by multiple peptic ulcerations in the stomach, duodenum, and even jejunum, is caused by uncontrolled release of gastrin by a tumor and the resulting massive acid production.Neoplastic disease of the stomach:They are benign or malignant:Gastric Polyps: the most common1-Inflammatory and Hyperplastic Polyps (75%), it's just hyperplasia of laying epithelia of the stomach, and they are completely benign.2-Fundic Gland Polyps (with PPI and FAP), also benign and they are present in fundus area, usually found in patients with familial adenomatous polyposis coli syndrome we will say about it in the intestine lecture, characterized by multiple polyps all over GI tract especially in the colon with fundic gland polyp.and its associated with proton pump inhibitors, people with chronic gastritis and they use proton pump inhibitor for a long period of time as a treatment may develop this polyps.3-Gastric Adenoma (10%), they are polyps with dysplasia and atypia ,so they increase risk of carcinoma.Gastric Adenocarcinoma:more than 90% of all gastric cancers(Benign are most common overall but adenocarcinoma is most common in gastric cancers).It can be intestinal type (they tend to form glands) or diffuse type:1-intestinal type: tend to be bulky mass and are composed of glandular structures.Exophytic mass (protruded above the level of the surface as a polypoid lesion) or an ulcerated tumor.Cells often contain apical mucin vacuoles, and abundant mucin may be present in gland lumina.Arise on a background of H.pylori chronic gastritis and dysplasia.2-Diffuse gastric cancers: called diffuse because it does not produce mass its infiltrate through the wall, its infiltrative growth pattern of discohesive cells with large cytoplasmic mucin vacuoles creating a signet ring cell morphology, on the surface of the stomach not protruded to the lumen of the stomach.A mass may be difficult to appreciate.Often evoke a desmoplastic reaction in the wall giving appearance of linitis plastica (it’s a fibrous thickening on the wall of stomach ),) linitis plastic. ????? ??? ??? ?????? )Morphology: refer to slide 21:Picture on the left: single cell have mucus inside it or mucin and the nucleus is pushed to one side such as fat cells.Picture on the right: this is the linitis plastic a not cause mass but cause thickening on the wall.So the intestinal type forms glands while the diffuse type its infiltrating of single cells.Intestinal type arises on background of dysplasia, adenoma and chronic gastritis but diffuse type not arises from these backgrounds.Pathogenesis:Mutations: it's associated with both types.Majority of gastric cancers are not hereditary. They are sporadic.TP53 mutations are present in a majority of sporadic gastric cancers of both histologic types.H. pylori:Increased risk of chronic gastritis associated intestinal-type gastric cancer.Symptoms:It depend on the stage of the cancer, may be as the symptoms of gastritis: - dyspepsia (its impairment of the power or function of digestion; usually applied to epigastric discomfort following meals) also dysphagia, and nausea ,also all of these are symptoms of chronic gastritis and chronic peptic ulcers.- The depth of invasion and the extent of nodal and distant metastasis at the time of diagnosis remain the most powerful prognostic indicators for gastric cancer, if its severe condition especially if they have exophytic or ulceration, they may cause blood loss.Done by: AREEJ HAMMADGOOD LUCK ^_^ ................
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