Benigne Diseases Of Stomach...
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Benigne Diseases Of Stomach...

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Benigne diseases of stomach are one of the serious conditions of our world.... so here u get littlebit information about these diseases...hope it will help you for your future study about these ...

Benigne diseases of stomach are one of the serious conditions of our world.... so here u get littlebit information about these diseases...hope it will help you for your future study about these diseases... thank you.

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Benigne Diseases Of Stomach... Benigne Diseases Of Stomach... Presentation Transcript

  • Presented By :- Biswanath Das. Student of AGMC.
  • Types BDS  Gastritis  PUD  Gastric polyp  Gastric lymphoma  Acute Gastric dilatation  Gastric volvulus  Menetrier’s disease
  • Gastritis
  • Definition  The term gastritis is used to denote inflammation associated with mucosal injury  Gastritis is mostly a histological term that needs biopsy to be confirmed  Gastritis is usually due to infectious agents (such as Helicobacter pylori) and autoimmune and hypersensitivity reactions.
  • Continue.. It also occurs after cholecystectomy, gastric surgery & also for prolonged use of NSAIDS……………………
  • Acute Gastritis
  • Types of gastritis  Type A gastritis  Type B gastritis  Reflux gastritis  Erosive gastritis  Stress gastritis  Lymphocytic gastritis  Menetrier’s gastritis
  • PEPTIC ULCER DISEASE (PUD)
  • An ulcer is defined as disruption of the mucosal integrity .So ‘peptic ulcer’ refers to an ulcer in the lower oesophagus, stomach or duodenum, in jejunum after surgical anastomosis to stomach or rarely in the ileum adjacent to meckel’s diverticulum leading to local defect or excavation due to active inflammation. DEFINITION
  • Although the prevalence of peptic ulcer is decreasing in many western countries it still affects approximately 10% of all adults at some time in their lives. The male to female ratio for duodenal ulcers varies from 5:1 to 2:1 whilist for gastric ulcers is 2:1 or less. INCIDENCE
  • Classification A . Depending on the site— -Chronic duodenal ulcer -Chronic gastric ulcer -Combind ulcer -Anastomotic ulcer B . Depending on the duration- -Acute peptic ulcer -Chronic peptic ulcer
  • Despite the constant attack on gastroduodeual mucosa by a host of noxious agents (acid, pepsin, bile, pancreatic enzymes, drugs & bacteria) integrity is maintained by an intricate system that provides mucosal defense & repair. GASTRIC PHYSIOLOGY
  • Gastroduodenal defense mechanisms  Mucus layer on surface  Bicarbonate section in mucosa  Adequate mucosal blood flow  Epithelial regenerative capacity  Postaglandin secretion  Intracellular tight junction  Apical surface membrane transport.
  • Causes of PUD
  • Acute peptic ulcer Drugs such as aspirin,steroids By stress (Stress ulcer):- May be following endotoxic shock :  Hypotension,  Haemorrhage or  Cardiac infarction.
  • Sepsis. After trauma or neurosurgical operations (Curling’s ulcers). After burns (curling’s ulcers). Patient on steroids (Steroids ulcers).The size of peptic ulcer Acute peptic ulcer
  • CHRONIC PEPTIC ULCERS GASTRIC ULCERS 1. NSAIDs. 2. H.pylori infection 3. Deficient mucous barriers. 4. Mucosal trauma. 5. Local Ischaemia. 6. Antral stasis. 7. Decrease mucosal resistance 8. Pyloroduodenal reflex
  • DUODENAL ULCER 1. Acid hyper secretion. 2. Genetics factor. 3. Endocrine organ dysfunction. 4. Liver abscess. 5. Emotional factors. 6. Diet & smoking. 7. Helicobacter pylori. 8. Decrease in bicarbonate production. CHRONIC PEPTIC ULCERS
  • Pathogenesis NSAIDs migrate across lipid membrane of epithelial cells. Trapped in an ionized form. Related with NSAIDs Cell injury. Topical NSAIDs. Alter surface mucous layer. back diffusion of H+ & Pepsin. Further cell damage.
  • Figure shows machanisms by which NSAIDs may induce nucosal injury :
  • Risk factors for NSAIDs – induced Gastroduodenal ulcers Established Advanced age. History of ulcer. Concomitant use of glucocorticoids. High dose of NSAIDs. Multiple NSAIDs. Concomitant use of anticoagulants serious or multi system disease. Possible Concomitant infection with H. pylori. Cigarette smoking. Alcohol consumption.
  • Related to H. Pylori Factors predisposing to higher colonization rate includes :- Poor socio – economic status. Less education. Transmission :-  Oral-oral.  Fecal-oral route.
  • Role of H.pylori  It secretes urease,portease & phospholipase.  Urease generates ammonia that binds with H+ & decreases acidity ,thus colonization & survival of the organism is favoured.  Protease damages the glycoprotein of gastric mucus  Phospholipases damages the surface epithelium & release leukotrines & eicosanoids.
  • Continue..  Increase production of proinflammatory cytokines e.g-IL-1,IL- 6,TNF & IL-8  May cause thrombotic occlusion leading to ischemia.  Epithelial injury is induced by VacA regulated by CagA …..
  • Clinical feature Acute peptic ulcers Dyspepsia due to minor bleeding. Haematemesis- fresh blood can cause hypotension & shock . Present of abdominal pain due to erosions/perforation Sometimes melaena is also present & drop in BP Chronic Peptic ulcers
  • C/F along with comparison Chronic gastric ulcers Incidence –less common Periodicity Less marked Attack lasts for several weeks followed by interval of freedom from symmetrical for 2 – 6 months. Chronic Duodenal ulcers Common ….. Well marked Attack lasts for several wks with interval of freedom from 2 – 6 months usually appears in spring & autumn. Continued….
  • Chronic gastric ulcers Pain Strictly epigastric. Pricking natures pain. On ulcer penetration pain radiate to back. Site Mid – epigastrium / slightly to its left. Chronic Duodenal ulcers Pain more severe & spasmodic in nature. Pain on right hypocondrium.. Continued…..
  • Chronic gastric ulcers Relation with food  Almost immediately or any time up to 1½ hr. after meal as food irritates ulcer.  Pain not felt empty stomach.  Pain not felt at night.  Food aggravates pain. Chronic Duodenal ulcers  Starts usually 2½ - 3 hr. after food.When stomach pushes chyme into duodenum & irritate ulcer.  Felt empty stomach ‘Hunger – Pain’.  Pain at night, is characteristic.  Food relieves pain. Continued…
  • Chronic gastric ulcers Vomiting Noticeable in half cases. Occur after food. Relieves pain. May be self induces. Appetite Good. Patient afraid to take food. Diet Patient avoids fried & spicy food. Chronic Duodenal ulcers Rare. Quite good. Eat frequently to around pain. No particular food initiates pain. Continued…
  • Chronic gastric ulcers Weight Patient Losses weight. Hemorrhage Less common. Haematemesis is more – than melaena. On Examination Tenderness in midepigastric / slightly to left of it. Chronic Duodenal ulcers  Patient gains the weight  More common.  Melaena more common than haematemesis.  Tenderness at right hypocondrium..
  • SPECIAL INVESTIGETIONS -OGD -Barium meal study -Test for H.pylori. -USG -Examination of blood. -Examination of stool. -Gastric function test
  • Endoscopy and radiology examination of PUD :
  • Treatment Basic Treatment  Rest.  Diet (avoid spicy food, use balance diet, no alcohol and smoking).
  • Medical Treatment Antacids. H2 receptor antagonistic. Proton pump inhibitors. Cytoprotective agents. Bismuth – containing preparations. Prostaglandin analogues.
  • Drugs used in Treatment of PUD Drug Eg. Dose Acid suppressing drug ‘Antacids’. Mylanta 100 – 140 mg /d Maalox, Tums, 120mg/d H2 receptor antagonists. Roxatidine 75mg bd/6wks Ranitidine 150mg bd/6wks Famotidine 2o mg bd/6wks
  • Drugs used in Treatment of PUD Drug Eg. Dose Proton pump inhibitors. Omeprazol 20 mg /d Lansoprazol 30 mg /d Rabeprazol 20 mg /d Pantoprazol 40 mg/d Mucosal protective agents. Sucralfate. Sucralfatet 1g qid. Prostaglandis analogus. Misoprostol 200 mcg. qid. Bismuth – containing compounds. Bismuth subsalicylate (BSS) 2 tablet qid.
  • Two wks Regimens recommended for eradication of H. pylori : Drug Dose 1. Lansoprazole 30+ Amoxicillin1000+ clarithromycin 500 all BD 2. Lansoprazole 30 +Tinidazole 500 + Clarithromycin 250 all BD 3. Lansoprazole 30 + Tinidazole 500 + amoxicillin 750 all BD
  • RECOMMENDED TREATMENT FOR NSAID – RELATED MUCOSAL INJURY : Active ulcer --NSAID discontinued. --Prophylactic therapy. --H. Pylori infection. H2 receptor antagonist or PPI. Misoprostol. Selective Cox – 2 inhibitor. Eradication if active ulcer present or there is a past history of PUD.
  • Surgical therapy Indications When ulcer fails to heal with medical management (2 months for gastric ulcer & 6 month for duodenal ulcers). Patient in need of quick relief. Long-standing non – healing ulcer. Ulcer producing obstruction. Haemorrhagic ulcers. Perforation of ulcers. Suspicion of malignancy. Continued…
  • Surgical therapy Surgical procedures A. For Duodenal Ulcer--- • Billroth II gastrectomy • Gastrojejunostomy • Truncal vagotomy & drainage • HSV • Tv & antrectomy B.For Gastric Ulcer---- • Billroth I gastrectomy. Continued…
  • Billroth II gastrectomy  The lower 2/3 rd of the stomach is removed and the remainder is anastomosed to the jejunum
  • Gastroenterostomy  Jejunum is anastomosed to the post. Dependent wall of stomach  Gastroenterostomy allows regurgitation of alkaline duodenal contents into the stomach  Creates a passage between the body of stomach to small intestines  Keeps acid away from ulcerated area
  • Vagotomy  Two types— A . Total truncal vagotomy with gastrojejunostomy— mayo or pyloroplasty B . Highly selective vagotomy
  • Pyloroplasty  Pyloroplasty  Widens the pylorus to guarantee stomach emptying even without vagus nerve stimulation  Two types- A.Heinecke-Mickulicz Pyloroplasty B. Finney pyloroplasty
  • Vagotomy & antrectomy  Vagotomy is done followed by  Antrectomy/ Subtotal Gastrectomy  Lower half of stomach (antrum) makes most of the acid  Removing this portion (antrectomy) decreases acid production
  • Billroth I Gastrectomy  The lower half of the stomach is removed  The remainder is anastomosed to the first part of duodenum.
  • Postoperative Care  NG tube – care and management  Monitor for post-operative complications
  • Postoperative complication  Bleeding  Occurs at the anastomosed site  First 24 hours and post-op days 4-7  Duodenal stump leak  Billroth II  Severe abdominal pain  Bile stained drainage on dressing  Gastric retention  WILL NEED TO PUT NG TUBE BACK IN
  • Post-op Complications  Recurrent ulceration  Small stomach syndrome  Bile vomiting  Post vagotomy diarrhoea  Malignant transformation  Nutrional consequences  Early & late dumping
  • Dumping Syndrome  Rapid emptying of food and fluids from the stomach into the jejunum  Symptoms  Weakness  Faintness  Palpitations  Fullness  Discomfort  Nausea  diarrhoea
  • Minimize Dumping Syndrome  Decrease high carbohydrate intake  Eat slowly  Avoid fluids during meals  Increase fat  Eat small, frequent meals
  • Management of PU
  • Complications A. Acute complication -Perforation - Haematemesis & melaena B. Sub acute complication-Residual abscess C. Chronic complication -Gastric outlet obstruction -Teapot deformity -Hourglass contracture of stomach -penetration into surrounding structure -Ca stomach
  • Perforated peptic ulcer  Common in man . Ratio 8:1  Anterior duodenal ulcer perforate & posterior duodenal ulcer bleed . Posterior stomach wall also perforate to the lesser sac  Chronic use of NSAIDS & H.pylori infection are the common cause.  Mortality rate 5-10%  Golden time to operate within 6hrs.
  • Stages Stages of duodenal peritonitis Stages of reaction Stage of bacterial peritonitis
  • Investications  Complete blood picture & electrolyte study  Plain x-ray chest or abdomen in erect position  CT of abdomen
  • Perforated PU
  • Treatment A. Aspiration of stomach content. B. Blood grouping & cross matching. C. Chrats-tp/bp/pulse/uo. D. Drugs-antibiotics . E. Exploratory laparotomy . F. Fluids .
  • Haemorrhage from PU  Haemorrhage from pu in acute case causes anaemia bt in chronic case causes haematemesis & melaena.  Commonest site- post. Duodenal wall & in case of stomach lesser curvature.  Precipiting factor-Chronicity -Irritants -Atherosclerosis
  • Risk factors  Increased age  Male  CVD  DM & RD  Increased nmb of medication  Oral anticoagulant use
  • Clinical Feature  Previous h/o PU+ abdominal pain  H/o haematemesis / melaena one/more attack.  Features of haemorrhagic shock. Feeble , thready pulse , hypotension , syncope , oliguria , brainstem hypoxia , mild abdominal distension.
  • Managment  Emergency upper OGD  Resuscitation  Endoscopy A. Conservative management- -emergency replacement of blood. -ryle’s tube is passed & cold saline stomach wash . -cold antacids , every 3hrly,about 10-20ml -IV Ranitidine 50mg,8 hrly /IV Pantoprazole 40mg is given to reduce the acidity.
  • Continue…. B. Non surgical treatment— -Laser coagulation -Sclerotherapy - Haemoclip application. C. Surgical control of bleeding—
  • Continue… INDICATION -Failure of endoscopic haemostasis. -Rebleeding in hospita - 6 units blood already given. - Elderly patient with rebleeding. -Massive haemorrhage leading to shock or cardiac instability. -Recurrent haemorrhage require hospitalization. .
  • Continue.. TYPES OF SURGERY 1. Surgery for bleeding duodenal ulcer--- - Laparotomy & anterior gastroduodenotomy - Visualise the bleeding site. - Under-running ulcer base by direct suture/4 quadrant ligation of gd artery. - followed by gastroduodenotomy incision in converted into a pyloroplasty followed by vagotomy .
  • Continue.. 2. Surgery for bleeding gastric ulcer .. -Laparotomy , gastrotomy & visualise the site. -Under-running of the ulcer base. -Partial gastrectomy is the best treatment. -Haemostatic method include thermotherapy. -When bleeding is controlled employed long term medical therapy-pph / H.pylory t/t…. -If H.pylori infection present then eradication therapy also should be performed.
  • D/D of Haematemesis  Stress ulceration.  Gastric erosions  Mallory-Weiss tear  Dieulafoy’s disease.  Tumours  Portal hypertension  portal gastropathy  Aortic enteric fistula
  • Gastric outlet obstruction -Earlier it was called as pyloroc stenosis. -Chronic cicatrisation of a duodenal ulcer or juxtapyloric ulcer narrowing of pyloric antrum pyloric stenosis -More common in South India -Metabolic changes such as paradoxical aciduria are usually seen…
  • Symptoms  Hunger pain of DU disappears.  It may be replaced by dull aching pain bec of gastric distention  Colicky pain is due to hyperperistalsis of stomach  Vomiting is profuse , projectile , foul smelling & nonbilious  May be distension of upper abdomen with epigastric fullness.
  • Signs  VGP  Succussion splash  Auscultopercussion test/auscultoscraping test.
  • Investigations A . Barium meal x-ray -hugely dilated stomach -mosaic appearance at the gastrodeodenal junction B. Gastroscopy C . Electrolyte study---- hypochloraemic alkalosis, hyponatraemai,hypokalaemia, paradoxical aciduria
  • Barium meal x-ray- Hugely dilated stomach
  • Treatment A. Aspiration of stomach content. B. Blood grouping & cross matching. C. Chrats-tp/bp/pulse/uo. D. Drugs-antibiotics E. Exploratory laparotomy . Vagotomy followed by GJ is done. Pyloplasty is contraindicated. F. Fluids .