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Gastric Ulcer Duodenal Ulcer Pancreatitis Ileus

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Gastric Ulcer Duodenal Ulcer Pancreatitis Ileus Gastric ulcer Duodenal ulcer Pancreatitis Ileus Barbora Konečná [email protected] Peptic ulcers of stomach and duodenum (PUD) • Ulcers are chronic, often solitary lesions, that occur in any part of GIT that is exposed to aggresive factors of the gastric fluids • Ulceration – disruption of mucosa at least to the muscularis mucosae layer due to secretion of HCl and activation of pepsinogen • Erosion – superficial damage (mucosa) • 10% of population have or will develop an ulcer Peptic ulcers of stomach and duodenum (PUD) • Occur due to dysbalance of gastro-duodenal protective mechanisms and aggressive factors, while the effects are further enhanced by external or immunological factors Peptic ulcers of stomach and duodenum (PUD) Protective factors Agressive factors • normal • Helicobacter pylori composition and • drugs with production of ulcerogenous effects mucin (NSAIDs) • Alk. secretion of • deleterious effects of HCO3- duodenal fluids • intact • smoking, alcohol microcirculation • disruptions of • regeneration of microcirculation in the gastric mucosa mucosa and • secretion of submucosa endogenous prostaglandins PUD – H. pylori infection • colonization of gastric mucosa • Does not enter cells, only mucosa (extracellular pathogens) • Urease → ammonium → acid neutralization → reflexive production of acid • Proteases → disruption of mucous layer • Weak resistance of the mucosa • Digestion of the mucosa by acid and pepsin • Chronic ulcerations PUD – Other factors • Zollinger – Elisson syndrome (gastrinoma) • Meckel´s diverticulum and ectopic gastric mucous membrane PUD – symptomes • Epigastric pain (heatburn) • Pain worse at night and 1-3 hours after meal • Nauseas, vomiting, loss of weight • Complications: anemia, bleeding, perforation • Cancer development is rare and connected to gastritis PUD – animal models • NSAIDs • Acetic acid / acetic acid + H.pylori • Ethanol • Histamine Gastric ulcer • More in men, 5th-6th decade • Similar to duodenal ulcer but surrounded by gastritis • More acid, more probability – usually at the border of corpus and antrum • Production of acid – Normal or decreased – Sometimes achlorhydria (absence of HCl) • 10-20% have duodenal ulcer • Damage of mucus barrier dominates • Epigastric pain – the most often symptom • Heals but appears again on the same spot Duodenal ulcer • 4x more often than gastric • Chronic, recurrent • Oval, 1 cm, • Into submucosis and muscularis propria • Bottom – blood or exsudate with erythrocytes and cell infiltration, inflammation • Acid secretion – normal to increased, sometimes increased secretion of pepsin – 50% have increased pepsinogen in serum • Often hereditary • Increased incidence – HLA-B5 antigens • Connected to smoking ß decreased microcirculation – Bicarbonates secretion inhibition – Quick emptying of gaster to duodenum • Incidence – Chronic kidney disease – Alcoholic cirrhosis – COPD • 80-100% - H. pylori à bad healing • Epigastric pain 90min-3 hours after food • Penetration sometimes Pancreatitis • Inflammation of the pancreas connected with edema, different degree of autodigestion, necrosis and haemorrhagia • 5th decade • Acute (reversible) vs chronic (irreversible damage) Acute - etiology • Gallstones Other causes: • Alcohol • Drugs and toxic • Idiopathic substances • Diseases of duodenum • hypercalciemia • Endocrine or metabolic • Renal failure disease • Viral infections • Immunological facotors • Cystic fibrosis • Hereditary factors • Trauma, operations • Drugs • ERCP • Infections • hyperlipidemia Alcohol • Direct toxic effect on pancreatic cells • Alcohol is metabolized by pancreas and causes oxidative stress • Promotes synthesis of digestive enzymes • Destabilizes intracellular membranes • Predisposes to autodigestion Pancreatitis Autodigestion • Proteolytic enzymes are activated in pancreas instead of duodenum • Endotoxines, viruses, ischemia... etc. • Activated proteolytic enzymes may activate other • Proteolysis, edema, interstitial bleeding, vascular damage, necrosis Acute - pathophysiology • Abnormal activation of digestive enzymes within the pancreas (trypsinogen – trypsin) • Cell death – apoptosis and necrosis 2 types based on predominant response to cell injury 1. Mild – Inflammation and edema 2. Severe – Necrosis - No capsule over pancreas – spreading of inflammation and necrosis Acute - symptoms • Severe upper abdominal pain • Nausea and vomiting • Loss of appetite • Fever and chills • Shock • Tachycardia • Respiratory distress • Peritonitis • Hiccup Acute – less common signs • Grey-Turner's sign (hemorrhagic discoloration of the flanks) • Cullen's sign (hemorrhagic discoloration of the umbilicus) • Körte's sign (pain or resistance in the zone where the head of pancreas is located) • Kamenchik's sign (pain with pressure under the xiphoid process) Differential diagnosis • Perforated peptic ulcer • Ciliary colic • Acute cholecystitis • Pneumonia • Peuritic pain • Myocardial infarction Balthazar score Balthazar grade Appearance on CT CT grade points Grade A Normal CT 0 points Focal or diffuse enlargement of the Grade B 1 point pancreas Pancreatic gland abnormalities and Grade C 2 points peripancreatic inflammation Grade D Fluid collection in a single location 3 points Two or more fluid collections and / or gas Grade E 4 points bubbles in or adjacent to pancreas Necrosis percentage Points No necrosis 0 points 0 to 30% necrosis 2 points 30 to 50% necrosis 4 points Over 50% necrosis 6 points Acute - treatment • Fluid replacement • Pain control • Bowel rest • Nutritional support • Antibiotics • ERCP • Surgery Chronic - causes • Alcohol • Autoimmune disorders • Intraductal obstruction • Tumors • Ischemia • Calcific stones • Idiopathic Chronic – risk factors • Smoking • Genetic predisposition • Cystic fibrosis Chronic - symptoms • Upper abdominal pain – increases after drinking and eating • Nausea and vomiting • Steatorrhea • Weight loss even when eating habits and amounts are normal • Type 1 diabetes Animal models of Pancreatitis • Caerulein (↑proteolytic enzymes secretion) • Lipopolysacharide + ethanol Ileus • intestinal distension and slower or no movement of stool in the intestinal lumen – failure of peristalsis • Laparotomy, metabolic/electrolytic hypokaliemia • Hyponatremia, hypomagnesemia, uremia, diabetic coma, abdominal infection, retroperitoneal bleeding, intestinal ischemia, sepsa, spinal cord injuries • Drugs – opiates, psychotropics, anticholinergics Ileus • Mechanical – obstruction (volvulus, gallstone, adhesion) • Paralytic – bowel paralysis (surgery, medications, muscle and nerve disorders, cancer, Crohn disease) • Signs and symptoms: – Abdominal pain that comes and goes – Loss of appetite – Constipation – Vomiting – Swelling of abdomen Ileus • Complications: – Necrosis – Peritonitis • Treatment – Obstruction – diet, surgery – Paralysis – identifying the cause, surgery Thank you J .
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