Gastrointestinal System 2 PDF

Gastrointestinal System 2 Karen Gil MD, MHSN Stomach J-shape Lies inferior to the diaphragm Connects the esophagus to the duodenum Four regions: Cardia Fundus Body Pylorus Between the pylorus and the duodenum is the pyloric sphincter Stomach Mayor functions Storage of ingested food for digestion 0.8...

Gastrointestinal System 2 Karen Gil MD, MHSN Stomach J-shape Lies inferior to the diaphragm Connects the esophagus to the duodenum Four regions: Cardia Fundus Body Pylorus Between the pylorus and the duodenum is the pyloric sphincter Stomach Mayor functions Storage of ingested food for digestion 0.8 – 1.5 lts. Vagus nerve in charge of involuntary contractions for the movement of the food Mixing Semi fluid or paste (chyme) food water juices degree of digestion Stomach Absorbs water, ions and drugs Mechanically breaks down the bolus and mixes the bolus with gastric secretions Histology Mucosa Submucosa Muscularis Serosa Stomach posses an additional layer of skeletal muscle – oblique layer Stomach Mucosa Simple columnar epithelial cells - surface mucous cells Lamina propria form columns of secretory cells – gastric glands Gastric pits – channels where gastric cells are aligned Gastric Secretion – Gastric Glands Entire surface composed mucus secreting glands: produce mucus Body or fundus Mucous Neck glands: produce mucus Oxyntic of parietal cells: produce hydrochloric acid (HCL) and intrinsic factor Chief or peptic cells: produce pepsinogen and gastric lipase G cells: produce gastrin into the blood (hormone) 2000-3000 ml of gastric juice is produced daily Mechanical and Chemical digestion in the Stomach Mixing waves of peristalsis mix food with gastric juice – producing the chyme Gastric emptying allows 3ml of chyme into the duodenum on each wave Salivary amylase is inactivated by gastric juice, only continue acting at the fundus HCL production CO2 diffuses into the parietal cells it combines with H2O in an enzymatic reaction that is catalyzed by CA (carbonic anhydrase) to form H2CO3 (Carbonic acid) H2CO3 dissociate into HCO3- and supply H+ (hydrogen) Bicarbonate ions are transported back to the bloodstream and Clenters to the cell H+/K+ ATPase: actively transport H+ into the lumen, bringing K+ into the parietal cell HCL- is produced in the parietal cells and enter the stomach lumen Secretion HCL Sensory stimuli (sight, smell, thought) Stimulate parasympathetic release of acetylocline to secrete more HCl- Direct contact with food – Activation of enteric nervous system Tactile Chemical irritation Distention Autonomic nervous system – Glossopharyngeal N. (CN IX) – Vagus N. (CN X) Local neurohormonal secretion http://highered.mcgrawhill.com/sites/0072507470/student_view0/c hapter24/animation__hydrochloric_acid_pr oduction____of_the_stomach.html HCL regulation Enterochromaffin like cell Release histamine (in response to Gastrin) Vagal stimulation (acetylcholine) Enteric nervous system Intrinsic factor Glycoprotein produced by Parietal cell Stimulates gastric secretion Necessary for Vit. B12 absorption in terminal ileum Pepsin secretion Secreted by chief cells Breaks down proteins in aminoacids When release is a pro-protein (pepsinogen) In contact with HCL it is activated (biologic activity in pH range: 1.8 – 3.5) In pH value higher than 5.0 it loses the proteolytic activity (protein digestion) activated by acid pH Regulatuion Stimulation by acetylcholine Stimulation by HCL (indirectly) Gastrin Produced by G cells in the antral and pyloric regions of the stomach Large form (34 a.a.) Small form ( 17 a.a.) (more abundant form) Secreted in presence of meat or protein containing food peptide hormone that stimulates secretion of gastric acid by the parietal cells of the stomach and aids in gastric motility Stimulate vigorous mixing of juices Increase stomach motility and relaxes the pyloric sphincter Stomach Absorption Limited to Water Ions Short chain fatty acids Certain drugs Aspirin Alcohol Pyloric Sphincter Opens to permit passage of chyme into duodenum Regulates the passage from the stomach to the duodenum Prevents backflow of chyme Phases of gastric secretion Cephalic Gastric Intestinal http://highered.mcgrawhill.com/sites/0072507470/student_view0/chapter24/animation__three_phases_of_ gastric_secretion.html Stomach emptying Neuro – hormonal Peristaltic waves Pyloric pump Gastrin Duodenal “signals” Degree of distention Degree of acidity Degree of osmolality Break down products proteins lipids Stomach emptying delay or inhibition Hormonal – CCK (cholecystokinin) – Secretin – GIP (gastric inhibitory peptide) Nervous – Enteric nervous system – Inhibitory sympathetic nerve fibers – Vagus nerve (inhibit normal excitatory signals) Inhibit gastrin secretion Gastric Disorders A. Congenital anomalies Pyloric stenosis 1:300-900 live born More common in males 3:1 due to hypertrophy of smooth muscle of the pyloric sphincter Gastric heterotopia Nests of gastric cell in esophagus or bowel Congenital Diaphragmatic Hernia Herniation of stomach or other intra-abdominal structures Uncommon Diaphragmatic Hernia Diagnosis Respiratory distress Cyanosis Feeding intolerance Tachycardia Scaphoid abdomen Breath sounds diminish Bowel sounds at chest Treatment Surgery to repair diaphragm opening Gastritis A. Acute Acute mucosal inflammation with superficial erosion (usually transient) Symptoms Burning esophagic distress Nausea and/or vomiting Pathogenesis Associated with: NSAID use Heavy smoking ETOH Uremia Sepsis Ischemia and shock Suicide attempts Gastritis B. Chronic 1. Inflammatory Chronic mucosal inflammatory changes leading to atrophy and mucosal metaplasia Symptoms: abdominal discomfort nausea and vomits Associated with (H. Pylori) which increases risk for developing ulcer or malignancies 2. Autoimmune higher risk for cancer (2-4%) Gastritis Diagnosis Endoscopy Treatment Diet Avoid acid or spicy food Avoid High carbohydrate diet Avoid fat diet Decrease acid secretion PPI Omeprazole Pantoprazole Lansoprazole H2 Antagonists Famotidine Acute Gastric Ulcers Severe trauma major surgical procedures sepsis Excessive burns Curling’s ulcer Trauma or surgery to CNS Cushing’s ulcer (elevated intracranial pressure) Gastric irritant drugs chronic exposure Peptic Ulcer Disease Erosion Loss of superficial epithelium Ulcer Mucosal breach extending up to or deeper than the submucosa Pathogenesis of Peptic Ulcer Peptic Ulcers Genetic Zollinger Ellison Syndrome multiple ulcerations secondary to Gastrin secreting tumor Solitary 98% are found in 1st portion of Duodenum or stomach (4:1) Remitting relapsing lesion Duodenal more common ETOH Peptic Ulcers Upper GI endoscopy is the preferred diagnostic test in the evaluation of patients with suspected PUD Provides an opportunity to visualize the ulcer, to determine the presence and degree of active bleeding, and to attempt hemostasis by direct measures, if required Perform endoscopy early in patients older than 45-50 years and in patients with associated symptoms Peptic Ulcer Complications Bleeding Occurs in 15-20% of patients Most frequent complication May be life-threatening Accounts for 25% of ulcer deaths May be first indication of an ulcer perforation Perforation Occurs in about 5 % of patients Accounts for 2/3 of ulcer deaths Rarely is first indication of an ulcer Peptic Ulcer Complications Obstruction from edema or scarring Occurs in about 2% of patients Most often due to pyloric channel ulcers May also occur with duodenal ulcers Causes incapacitating, crampy abdominal pain Rarely may lead to total obstruction with intractable vomiting Intractable pain Peptic Ulcer Treat H pylori infection and/or avoidance of nonsteroidal antiinflammatory drugs (NSAIDs) and anti-secretory therapy In the United States, the recommended primary therapy for H pylori infection is PPI-based triple therapies 14-day regimen as shown below: Omeprazole (Prilosec): 20 mg PO bid or Lansoprazole (Prevacid): 30 mg PO bid or Rabeprazole (Aciphex): 20 mg PO bid or Esomeprazole (Nexium): 40 mg PO qd Plus Clarithromycin (Biaxin): 500 mg PO bid and Amoxicillin (Amoxil): 1 g PO bid or Metronidazole (Flagyl): 500 mg PO bid cure of infection and ulcer healing in approximately 85-90% of cases Peptic Ulcer In patients with NSAID-associated peptic ulcers discontinuation of NSAIDs For patients who must continue with their NSAIDs, proton pump inhibitor (PPI) maintenance is recommended to prevent recurrences Maintenance therapy with anti-secretory medications (eg, H2 blockers, PPIs) for 1 year is indicated in high-risk patients The indications for urgent surgery include failure to achieve hemostasis endoscopically Hypertrophic Gastropathy Group of conditions characterized by giant “cerebriform” rugal folds Types 1. Menétrier disease 2. 3. profound hyperplasia of surface mucosal cells and glandular atrophy Hypertrophic-hypersecretory gastropathy Gastric glands hyperplasia due to excessive Gastrin secretion.- Zollinger-Ellison syndrome (tumor) Clinical importance: mimics gastric carcinoma hypersecretion of gastrin and hypersecretion H+ - stimulates growth of gastric mucosa Gastric tumors A. Benign Polyps nodule or mass which projects above the level of surrounding mucosa Hyperplastic (80-85%) Fundic glands (10%) Adenomatous (5%) Gastric Tumors B. Malignant 3% of all cancer deaths Adenocarcinoma (90-95%) Lymphomas (4%) Carcinoid (3%) Gross appearance exophytic depressed excavated Microscopic intestinal type diffuse type Gastric Malignant tumors Signs and symptoms of gastric cancer include the following: Indigestion Nausea or vomiting Dysphagia Postprandial fullness Loss of appetite Melena pallor from anemia Hematemesis Weight loss Palpable enlarged stomach Enlarged lymph nodes such as Virchow nodes (left supraclavicular) and Irish node (anterior axillary) Irish nodule