Pud Gastritis Lecture[1]

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Pud Gastritis Lecture[1]

  1. 1. 55 yo male c/ epigastric pain on/off x 1 mo
  2. 2. History <ul><li>Awoke him from sleep </li></ul><ul><li>Relieved by food, but pain worsened 1-3 hrs later </li></ul><ul><li>Fatigue </li></ul><ul><li>Dyspepsia/ bloating/ belching/ burning </li></ul><ul><li>Wt loss </li></ul><ul><li>No SOB/ pain radiation/N/V/D/F </li></ul><ul><li>Wife states that his diet is “poor” </li></ul>
  3. 3. History <ul><li>PMH </li></ul><ul><ul><li>No DM </li></ul></ul><ul><ul><li>No CAD </li></ul></ul><ul><ul><li>Etc. </li></ul></ul><ul><li>Family History </li></ul><ul><ul><li>Mother died 75 MI </li></ul></ul><ul><ul><li>Father died 70 stroke </li></ul></ul><ul><li>Surgical Hx </li></ul><ul><ul><li>None </li></ul></ul><ul><li>Social History </li></ul><ul><ul><li>+ Smoker 1ppd </li></ul></ul><ul><li>Medications </li></ul><ul><ul><li>“ some arthritis med” </li></ul></ul><ul><ul><li>“ some HTN med” </li></ul></ul><ul><li>NKDA </li></ul>
  4. 4. Physical Exam <ul><li>+ Epigastric tenderness </li></ul><ul><li>Guiaic + </li></ul>
  5. 5. Differential Diagnosis? <ul><li>Cardiac </li></ul><ul><ul><li>MI </li></ul></ul><ul><li>Aortic Dissection </li></ul><ul><li>Pulmonary </li></ul><ul><li>GI </li></ul><ul><ul><li>PUD </li></ul></ul><ul><ul><li>Pancreatitis </li></ul></ul><ul><ul><li>Gallstones </li></ul></ul><ul><ul><li>Inflammatory bowel ds. (crohn’s/UC) </li></ul></ul><ul><ul><li>Colon Ca </li></ul></ul>
  6. 6. Dx tests <ul><li>CBC (blood loss) </li></ul><ul><li>Chem c/ BUN/creat </li></ul><ul><li>Type & cross </li></ul><ul><li>H. pylori </li></ul><ul><li>EKG </li></ul><ul><li>CXR (free air) </li></ul><ul><li>Barium study </li></ul>
  7. 7. Procedures <ul><li>NG tube (if upper GI bleed) </li></ul><ul><li>IVF </li></ul><ul><li>Endoscopy </li></ul><ul><li>? Sig vs. colonoscopy? </li></ul>
  8. 8. Tx <ul><li>Antacids </li></ul><ul><li>GI cocktail </li></ul><ul><li>H2 blockers </li></ul><ul><li>PPI’s </li></ul><ul><li>Abx </li></ul>
  9. 9. Reflux Esophagitis Peptic Ulcer Disease, Gastritis, & GI Bleeding Pascale Gèhy-Andrè, PA-C
  10. 10. Anatomy & Physiology of the stomach <ul><li>The blood supply is from the Celiac artery </li></ul><ul><li>The vagus nerve stimulates the stomach </li></ul><ul><li>The epithelium is columnar cells pieced by numerous glands </li></ul><ul><li>The cardia and antrum have mostly mucous cells </li></ul>
  11. 11. Normal Gastric Function <ul><li>1. Primary function of the stomach </li></ul><ul><ul><li>A. secretion of substances important to digestion & absorption </li></ul></ul><ul><ul><li>B. movement of gastric contents downstream to small bowel </li></ul></ul><ul><li>2. Classes of secretory cells </li></ul><ul><ul><li>A. Mucous secreting cells of the cardia : </li></ul></ul><ul><ul><ul><li>1. Protect underlying cells from mechanical forces of digestion </li></ul></ul></ul><ul><ul><ul><li>2. Lubrication of mucosa to move food over surface </li></ul></ul></ul><ul><ul><ul><li>3. Retain water within the mucous gel providing aqueous environment for underlying cells. </li></ul></ul></ul><ul><ul><ul><li>4. Forming an unstirred layer above the mucosa impending but not blocking diffusion of hydrogen ions from the lumen to the superficial epithelial cells. </li></ul></ul></ul>
  12. 12. Normal Gastric Function <ul><li>2. Classes of secretory cells (cont.): </li></ul><ul><ul><li>B. HCL -Secreting parietal cells of the body which also secrete intrinsic factor. </li></ul></ul><ul><ul><li>C. Pepsinogen -Secreting chief cells of the body. </li></ul></ul><ul><ul><li>D. Gastrin -Secreting G cells of the Antrum (body has 2 sources of Gastrin stomach and pancreas). </li></ul></ul>
  13. 13. Gastric Function (cont.) <ul><li>3. Neural & Hormonal influence on gastric function: </li></ul><ul><ul><li>A. Cephalic phase : (smell/thinking) initiates cholinergic impulse via the vagus nerve stimulating parietal secretion of acid & G cell secretion of Gastrin which also stimulates acid. </li></ul></ul><ul><ul><li>B. Gastric phase : causes distention of the stomach by food which causes further secretion of acid and gastrin. Protein will also stimulate G cells to produce Gastrin and acid. </li></ul></ul><ul><ul><li>C. Intestinal phase : will cause gastric acids to stimulate secretion of secretin & cholecystokinin which will also inhibit the action of gastrin on the parietal cells. </li></ul></ul>
  14. 14. Reflux Esophagitis <ul><li>Definition: Recurrent reflux of gastric contents in the distal esophagus </li></ul><ul><li>Commonly called heartburn </li></ul><ul><li>20% of normal population at least one week </li></ul><ul><li>May cause erosions that leads to Barrett’s esophagitis which can predispose to malignancy </li></ul>
  15. 15. Reflux Esophagitis <ul><li>Contributing Factors: </li></ul><ul><ul><li>Hiatal hernia </li></ul></ul><ul><ul><li>Delayed gastric emptying (gastroparesis/obstruction) </li></ul></ul><ul><ul><li>Incompetent Lower esophageal sphincter </li></ul></ul><ul><ul><li>Irritant effects of gastric juices (refluxate) </li></ul></ul><ul><li>Clinical features: </li></ul><ul><ul><li>Heartburn most common presenting feature </li></ul></ul><ul><ul><li>Hoarseness, cough, hiccup, atypical chest pain, sore throat </li></ul></ul>
  16. 16. Reflux Esophagitis <ul><li>Laboratory studies </li></ul><ul><ul><li>Barium swallow may indicate a large hiatal hernia </li></ul></ul><ul><ul><li>ENDOSCOPY with BIOPSY standard procedure describes the presence and extent of mucosal damage </li></ul></ul><ul><ul><li>Endoscopy when symptoms do not respond to medical therapy </li></ul></ul><ul><ul><li>pH monitoring can be done </li></ul></ul>
  17. 17. Reflux Esophagitis <ul><li>Treatment: Life style modification ( DC smoking) </li></ul><ul><ul><li>Pharmacotherapy </li></ul></ul><ul><ul><ul><li>Antacids or alginic acid(gaviscon) </li></ul></ul></ul><ul><ul><ul><li>Histamine (H2 blockers) </li></ul></ul></ul><ul><ul><ul><li>Prokinetic drugs ( e.g. metoclopramide, cisapride, bethanechol) increase gastric emptying and can be combined with H2 blockers </li></ul></ul></ul><ul><ul><ul><li>Acid-suppressant proton-pump inhibitor (e.g. omeprazole, lansoprazole) may be tried as last resort </li></ul></ul></ul><ul><ul><ul><li>Anticholinergic, B - adrenergic, and calcium channel-blocking agents decrease lower esophageal sphincter pressure and should be avoided </li></ul></ul></ul><ul><li>Complication: Barrett’s Esophagagus </li></ul>
  18. 18. Gastritis <ul><li>Acute Gastritis is an inflammation of the gastric mucosa. </li></ul><ul><li>Gastropathy : epithelial or endothelial damage without inflammation </li></ul><ul><li>Gastritis has 3 basic types: </li></ul><ul><ul><li>Acute (erosive/ hemorrhagic) </li></ul></ul><ul><ul><li>Non-erosive, Non-specific/Chronic </li></ul></ul><ul><ul><li>Special Forms </li></ul></ul>
  19. 19. Acute Gastritis (Erosive/Hemorrhagic) <ul><li>Most common causes: </li></ul><ul><ul><li>NSAIDS gastric injury by diminishing prostaglandin production in stomach and duodenum </li></ul></ul><ul><ul><li>Alcohol use is the leading cause of gastritis </li></ul></ul><ul><ul><li>Stress from CNS injury burns, sepsis, surgery </li></ul></ul><ul><ul><li>Portal hypertension (portal gastropathy) </li></ul></ul><ul><li>Other causes: </li></ul><ul><ul><li>Caustic ingestion </li></ul></ul><ul><ul><li>radiation </li></ul></ul>
  20. 20. Chronic Gastritis Nonerosive/nonspecific <ul><li>Infectious gastritis Type B: H Pylory </li></ul><ul><ul><li>Involves antrum and body of stomach </li></ul></ul><ul><li>majority of patients asymptomatic </li></ul><ul><ul><li>Strong association with PUD </li></ul></ul><ul><ul><li>2 to 6 fold risks of gastric adenocarcinoma and also gastric lymphoma </li></ul></ul><ul><li>Autoimmune gastritis Type A: Pernicious anemia </li></ul><ul><ul><li>Body and fundus, It usually spares the antrum & affects the parietal cells. </li></ul></ul><ul><ul><li>Pernicious anemia caused by impaired absorption of vitamin B-12 occurs due to lack of intrinsic factor from parietal cells and decrease in acid production </li></ul></ul><ul><ul><li>Increased risk of adenocarcinoma </li></ul></ul>
  21. 21. Special forms of Gastritis <ul><li>Infectious (Phlegmonous or necrotizing gastritis) </li></ul><ul><ul><li>Emergency gastric resection, and Abx therapy </li></ul></ul><ul><ul><li>CMV, candidal (fungal) in immunocompromised pt’s </li></ul></ul><ul><ul><li>Larvae ingestion requires endoscopic removal </li></ul></ul><ul><li>Eosinophilic Gastritis </li></ul><ul><li>Giant Cell (Menetrier’s disease) (Hypertrophic Gastropathy) </li></ul><ul><ul><li>only found on biopsy </li></ul></ul><ul><li>Lymphocytic Gastritis </li></ul><ul><li>Granulomatous Gastritis </li></ul><ul><ul><li>Tuberculosis </li></ul></ul><ul><ul><li>Syphilis </li></ul></ul><ul><ul><li>Fungal </li></ul></ul><ul><ul><li>Sarcoid </li></ul></ul><ul><ul><li>Crohn’s </li></ul></ul>
  22. 22. Gastritis Symptoms <ul><li>Clinical features of gastritis generally reflects the underlying syndrome rather than the gastric injury itself </li></ul><ul><li>Acute: </li></ul><ul><ul><li>Dyspepsia and abdominal pain are common indicators of gastritis </li></ul></ul><ul><ul><li>Mild epigastric discomfort </li></ul></ul><ul><ul><li>Occasional N/V </li></ul></ul><ul><ul><li>Headache, excessive salivation, flatus </li></ul></ul><ul><li>Chronic: </li></ul><ul><ul><li>Non specific symptoms c/ chronic abdominal discomfort </li></ul></ul><ul><li>Key signs: (usually none) </li></ul><ul><ul><li>Hematemesis, bloody nasogastric aspirate </li></ul></ul><ul><ul><li>Abdominal tenderness </li></ul></ul><ul><ul><li>Bloating </li></ul></ul><ul><ul><li>Emesis </li></ul></ul>
  23. 23. Gastritis <ul><li>Lab: </li></ul><ul><ul><li>Endoscopy c/ biopsy is the gold standard </li></ul></ul><ul><ul><li>A urea breath test can be used to detect HP </li></ul></ul><ul><ul><li>Specific test for underlying conditions (e.g) B12 and CBC for pernicious anemia </li></ul></ul><ul><li>Differential Diagnosis: </li></ul><ul><ul><li>1. Peptic ulcer 2. Gastroparesis </li></ul></ul><ul><ul><li>3. Gastric carcinoma 4. GERD </li></ul></ul><ul><ul><li>5. Pancreatitis 6. Lymphoma </li></ul></ul><ul><li>Treatment: (same as duodenal ulcers) </li></ul><ul><ul><li>Remove irritant </li></ul></ul><ul><ul><li>Treat for H pylori </li></ul></ul><ul><ul><li>Antacids & H2 blockers </li></ul></ul><ul><ul><li>Avoid smoking & alcohol </li></ul></ul>
  24. 24. Peptic Ulcer Disease <ul><li>Definition : PUD is describes any ulcer of the upper digestive tract. (duodenal # 1) and stomach (gastric #2) </li></ul><ul><li>Break in the duodenal or gastric mucosa extending through the musularis mucosae, and are usually 5mm-1cm. </li></ul>
  25. 25. Zollinger-Ellison Syndrome <ul><li>Ulcers-associated with the Zollinger-Ellison (ZE) Syndrome (#3 ) are caused by gastrin-releasing islet cell tumors (gastrinomas), & are also considered a form of peptic ulcer. </li></ul>
  26. 26. Zollinger-Ellison Syndrome <ul><li>A tumor of the pancreas that secretes gastrin ( Gastrinoma) </li></ul><ul><li>Usually found in head of pancreas but can also be found in duodenum, liver & lung </li></ul><ul><li>75-80% of ulcers produced develop in the duodenal bulb </li></ul><ul><li>Suspect in any patient with: </li></ul><ul><ul><li>Multiple or recurring duodenal ulcers </li></ul></ul><ul><ul><li>Post bulbar or jejunal ulcers </li></ul></ul><ul><ul><li>Ulcers associated with diarrhea </li></ul></ul><ul><ul><li>Elevated serum gastrin levels </li></ul></ul><ul><ul><ul><li>Usually only tested when suspect ZE syndrome </li></ul></ul></ul>
  27. 27. Peptic Ulcer Disease (PUD) <ul><ul><li>Men 1.3 : 1 Women </li></ul></ul><ul><ul><li>Most commonly occur in : </li></ul></ul><ul><ul><li>#1 Duodenum (Duodenal) </li></ul></ul><ul><ul><li>#2 Stomach (Gastric) </li></ul></ul><ul><ul><li>Esophagus </li></ul></ul><ul><ul><li>Gastroenteric anastomoses </li></ul></ul><ul><ul><li>Meckel’s Diverticulum </li></ul></ul>
  28. 28. PUD <ul><li>The spectrum of the disease is broad from mild mucosal injury to frank ulcerations. </li></ul><ul><li>Symptoms vary and are not related to the severity of tissue damage. </li></ul><ul><li>1-2% of population have an ulcer at the present time </li></ul><ul><li>10% of population will have ulcer in their lifetime </li></ul><ul><li>Gastric and Duodenal ulcers tend to recur in the same location. </li></ul><ul><li>Recurrent hemorrhage occurs in 50% of patients who have had a prior bleed. </li></ul>
  29. 29. Duodenal Ulcer vs. Gastric Ulcer <ul><li>Duodenal </li></ul><ul><ul><li>Increased acid production </li></ul></ul><ul><ul><li>H. pylori </li></ul></ul><ul><ul><li>relieved by food & typically awakens patient around 1:00am </li></ul></ul><ul><li>Gastric </li></ul><ul><ul><li>Normal or decreased acid production </li></ul></ul><ul><ul><li>Decreased mucosal resistance </li></ul></ul><ul><ul><li>H. pylori </li></ul></ul><ul><ul><li>NSAIDS </li></ul></ul><ul><ul><li>worsened by food </li></ul></ul>
  30. 30. Duodenal Vs. Gastric (cont) <ul><li>Duodenal </li></ul><ul><ul><li>Onset more common age 25 to 55 </li></ul></ul><ul><ul><li>never malignant </li></ul></ul><ul><ul><li>mostly located in the duodenal bulb or immediately post bulbar. </li></ul></ul><ul><ul><li>Ulcers distal to the duodenal bulb should raise suspicion for Zollinger-Ellison Syndrome (also c/ multiple frequently occurring duodenal ulcers.) </li></ul></ul><ul><ul><li>Men 2:1 Women </li></ul></ul><ul><ul><li>Duodenal 5 times more common than gastric </li></ul></ul><ul><ul><li>60-80% have recurrence within one year. </li></ul></ul><ul><li>Gastric </li></ul><ul><ul><li>Onset more common age 40 to 70 </li></ul></ul><ul><ul><li>Benign more likely @ lesser curvature/ antrum </li></ul></ul><ul><ul><li>Gastric ulcers are more common @ lesser curvature </li></ul></ul><ul><ul><li>Malignancies more likely @ greater curvature </li></ul></ul><ul><ul><li>1-3% occur in carcinomas </li></ul></ul>
  31. 31. PUD Etiologies <ul><li>1. Helicobacter pylori (H. pylori) infection: (#1 cause) </li></ul><ul><ul><li>A. Associated c/ 70-95% of Peptic ulcers. </li></ul></ul><ul><ul><li>B. Treatment of H. pylori improves healing rate & markedly decreases the recurrence rate. </li></ul></ul><ul><li>2. NSAIDS: (#2 cause) (inhibit prostaglandins which normally stimulate production of mucous secretions & bicarb.) </li></ul><ul><ul><li>A. may cause gastric or duodenal ulcers (steroids also) </li></ul></ul><ul><ul><li>B. accounts for the majority of non H. pylori ulcers </li></ul></ul>
  32. 32. PUD Etiologies (cont) <ul><li>3. Hypersecretion states: (#3 although uncommon) </li></ul><ul><ul><li>Gastrinomas (Zollinger-Ellison Syndrome) </li></ul></ul><ul><ul><li>Multiple endocrine neoplasia (MEN-1) </li></ul></ul><ul><ul><li>Systemic mastocytosis (mast cells infiltrate intestinal wall, release histamine- stimulates acid. Symptoms are diarrhea, flushing, urticaria. Histamine in blood. Confirmed by biopsy.) </li></ul></ul><ul><li>4. Stress: physiologic stress (eg. Burns, surgery, & severe medical conditions) </li></ul><ul><li>5. Rare causes: viral, radiation, vascular insuff. </li></ul><ul><li>Diseases assoc. c/ peptic ulcers: </li></ul><ul><ul><li>Cirrhosis, renal failure, pulmonary ds. </li></ul></ul><ul><ul><ul><li>Any pt. c/ systemic ds. (COPD, renal failure, cirrhosis of liver) are prone to ulcers so should be started on H2 blockers. </li></ul></ul></ul>
  33. 33. The pathogenesis of PUD is related to the imbalance between normal protective factors and injurious factors <ul><li>No Ulcer </li></ul><ul><ul><li>Normal </li></ul></ul><ul><li>Ulcer </li></ul><ul><li>Aggressive forces </li></ul><ul><ul><li>Gastric acid </li></ul></ul><ul><ul><li>Digestive enzymes </li></ul></ul><ul><li>Vs. </li></ul><ul><li>Defensive forces </li></ul><ul><ul><li>Mucus </li></ul></ul><ul><ul><li>Bicarb </li></ul></ul><ul><ul><li>Prostaglandins </li></ul></ul><ul><ul><li>Epithelial regeneration </li></ul></ul>
  34. 34. Ulcers result from: <ul><li>1. Increased aggression </li></ul><ul><ul><li>H. pylori infection </li></ul></ul><ul><ul><li>NSAIDS </li></ul></ul><ul><ul><li>Cigarettes </li></ul></ul><ul><ul><li>ETOH </li></ul></ul><ul><li>Or </li></ul><ul><li>2. Impaired Defense </li></ul><ul><ul><li>Ischemia </li></ul></ul><ul><ul><li>Prostaglandin Inhibition (NSAIDS) </li></ul></ul><ul><ul><li>Delayed gastric emptying </li></ul></ul>
  35. 35. PUD <ul><li>ADVERSE EFFECTS OF SMOKING </li></ul><ul><ul><li>1. Interferes c/ action of H2 antagonists </li></ul></ul><ul><ul><li>2. Increases rate of gastric emptying </li></ul></ul><ul><ul><li>3. Increases duodenogastric reflux </li></ul></ul><ul><ul><li>4. Decreases pancreatic bicarb secretion </li></ul></ul><ul><ul><li>5. Decreases mucosal blood flow </li></ul></ul><ul><ul><li>6. Depresses gastric mucosal prostaglandin synthesis </li></ul></ul>
  36. 37. Peptic Ulcer Disease Facts <ul><li>Most ulcers are caused by H. pylori infection, not spicy food, acid or stress. </li></ul><ul><li>You can test for H. pylori infection. </li></ul><ul><li>H. pylori / ulcers can be tx’d c/ antibiotics. </li></ul><ul><li>Complications: </li></ul><ul><ul><li>A Major complication is bleeding & perforation </li></ul></ul><ul><ul><li>Erosion of a small vessel at the base of the ulcer is the cause of the bleeding </li></ul></ul><ul><ul><li>Perforation is usually catastrophic causing peritonitis </li></ul></ul>
  37. 38. What is H. pylori <ul><li>Helicobacter pylori ( H. pylori ) is a gram negative spiral-shaped bacillus found in the gastric mucous layer or adherent to the epithelial lining of the stomach. </li></ul><ul><li>H. pylori causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers. </li></ul>
  38. 39. How do people get infected with H. pylori ? <ul><li>It is not known how H. pylori is transmitted or why some patients become symptomatic while others do not. </li></ul><ul><li>The bacteria are most likely spread from person to person through fecal-oral or oral-oral routes. </li></ul><ul><li>Possible environmental reservoirs include: </li></ul><ul><ul><li>contaminated water sources </li></ul></ul><ul><ul><li>Iatrogenic spread through contaminated endoscopes has been documented but can be prevented </li></ul></ul>
  39. 40. What can people do to prevent H. pylori infection? <ul><li>Since the source of H. pylori is not yet known, recommendations for avoiding infection have not been made. </li></ul><ul><li>In general, it is always wise for persons to wash hands thoroughly, to eat food that has been properly prepared, and to drink water from a safe, clean source. </li></ul>
  40. 41. H. pylori infection <ul><li>Before this bacterium was discovered, spicy food, acid, stress, and lifestyle were considered the major causes of ulcers. </li></ul><ul><li>The majority of patients were given long-term medications, such as H2 blockers, and more recently, proton pump inhibitors, without a chance for permanent cure. </li></ul><ul><li>These medications relieve ulcer-related symptoms, heal gastric mucosal inflammation, and may heal the ulcer, but they do NOT treat the infection. </li></ul>
  41. 42. H. Pylori infection <ul><li>When acid suppression is removed, the majority of ulcers, particularly those caused by H. pylori , recur. </li></ul><ul><li>Since we now know that most ulcers are caused by H. pylori , appropriate antibiotic regimens can successfully eradicate the infection in most patients, with complete resolution of mucosal inflammation and a minimal chance for recurrence of ulcers. </li></ul>
  42. 43. What illnesses does H. pylori cause? <ul><li>Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however, H. pylori causes chronic active, chronic persistent, and atrophic gastritis in adults and children. </li></ul><ul><li>Infection with H. pylori also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts. </li></ul><ul><li>The role of H. pylori in non-ulcer dyspepsia remains unclear. </li></ul>
  43. 44. Peptic Ulcer Disease Symptoms <ul><li>#1. Epigastric Pain </li></ul><ul><ul><li>Burning </li></ul></ul><ul><ul><li>Occurs 1-3 hrs p/ meals </li></ul></ul><ul><ul><li>Relieved by food </li></ul></ul><ul><ul><li>May occur @ night </li></ul></ul><ul><ul><li>May radiate to back or shoulders if perforated </li></ul></ul><ul><li>Nausea </li></ul><ul><li>Vomiting </li></ul><ul><ul><li>May be related to partial or complete gastric outlet obstruction </li></ul></ul><ul><li>Dyspepsia </li></ul><ul><ul><li>Belching/ Bloating </li></ul></ul><ul><li>Heartburn </li></ul><ul><li>Chest Discomfort </li></ul><ul><li>Anorexia </li></ul><ul><li>Weight loss </li></ul><ul><ul><li>In gastric ulcers (also in pancreatic ds.) </li></ul></ul><ul><li>Weight gain </li></ul><ul><ul><li>In duodenal ulcers </li></ul></ul><ul><li>Hematemesis or melena </li></ul><ul><ul><li>Due to GI bleeding </li></ul></ul><ul><ul><li>If severe = hematochezia </li></ul></ul>
  44. 45. Chinese Proverbs <ul><li>Man with one chopstick go hungry. </li></ul><ul><li>Man who scratch ass should not bite fingernails. </li></ul><ul><li>  Man who eat many prunes get good run for money. </li></ul><ul><li>Baseball is wrong: man with four balls cannot walk. </li></ul><ul><li>Panties not best thing on earth! But next to best thing on earth. </li></ul><ul><li>Man who fight with wife all day get no piece at night. </li></ul><ul><li>It take many nails to build crib, but one screw to fill it. </li></ul><ul><li>Man who drive like hell, bound to get there. </li></ul>
  45. 46. Who should be tested and treated for H. pylori ? <ul><li>Persons with active gastric or duodenal ulcers or documented history of ulcers should be tested for H. pylori , and if found to be infected, they should be treated. </li></ul><ul><li>To date, there has been no conclusive evidence that treatment of H. pylori infection in patients with non-ulcer dyspepsia is warranted. </li></ul>
  46. 47. PUD Tests <ul><li>Laboratory Test: </li></ul><ul><ul><li>Routine tests are of little importance. Having a CBC is helpful. </li></ul></ul><ul><li>Upper GI endoscopy c/ biopsy* </li></ul><ul><li>Upper GI series (barium) (limited today) </li></ul><ul><li>Serum Test </li></ul><ul><ul><li>Amylase </li></ul></ul><ul><ul><li>Electrolytes </li></ul></ul><ul><ul><li>Serum Gastrin level if ZE syndrome is suspected </li></ul></ul><ul><ul><ul><li>Frequently occurring duodenal ulcers or multiple Duodenal Ulcers* </li></ul></ul></ul>
  47. 48. How is H. pylori infection diagnosed? <ul><li>Several methods may be used to diagnose H. pylori infection. </li></ul><ul><li>Serological tests that measure specific H. pylori IgG antibodies can determine if a person has been infected. </li></ul><ul><ul><li>The sensitivity and specificity of these assays around 80% </li></ul></ul><ul><li>Fecal Antigen Assay </li></ul><ul><li>Urea Breath test </li></ul><ul><ul><li>In this test, the patient is given either 13C- or 14C-labeled urea to drink. </li></ul></ul><ul><ul><li>H. pylori metabolizes the urea rapidly, and the labeled carbon is absorbed. </li></ul></ul><ul><ul><li>This labeled carbon can then be measured as CO2 in the patient's expired breath to determine whether H. pylori is present. </li></ul></ul><ul><ul><li>The sensitivity and specificity of the breath test ranges from 94% to 98%. </li></ul></ul><ul><ul><li>PPI’s can give false negative results </li></ul></ul>
  48. 49. How is H. pylori infection in PUD diagnosed? <ul><li>Upper endoscopy (esophagogastroduodenal) is considered the reference method of diagnosis. </li></ul>
  49. 50. Dx of H. pylori by Endoscopy <ul><li>During endoscopy, biopsy specimens of the stomach and duodenum are obtained and the diagnosis of H. pylori can be made by several methods: </li></ul><ul><ul><li>The biopsy urease test - a colorimetric test based on the ability of H. pylori to produce urease; it provides rapid testing at the time of biopsy. </li></ul></ul><ul><ul><li>Histologic identification of organisms - considered the gold standard of diagnostic tests. </li></ul></ul><ul><ul><li>Culture of biopsy specimens for H. pylori, which requires an experienced laboratory and is necessary when antimicrobial susceptibility testing is desired </li></ul></ul>
  50. 51. Peptic Ulcer Disease Therapy <ul><li>Non-Pharmacological </li></ul><ul><ul><li>Diet change is of no value </li></ul></ul><ul><ul><li>Smoking Cessation </li></ul></ul><ul><ul><ul><li>Smoking delays healing </li></ul></ul></ul><ul><ul><li>DC medications that enhance the progression </li></ul></ul><ul><ul><ul><li>NSAIDS </li></ul></ul></ul><ul><li>Pharmacological Therapy </li></ul><ul><ul><li>Inhibit secretion of acid </li></ul></ul><ul><ul><li>Neutralizing gastric acids </li></ul></ul><ul><ul><li>Augmentation of protection of mucosa </li></ul></ul><ul><ul><li>Antibiotics prn </li></ul></ul><ul><li>Maintenance Therapy </li></ul><ul><ul><li>Prevention c/ colloid bismuth </li></ul></ul><ul><ul><li>Bedtime dosage of H2 blockers </li></ul></ul>
  51. 52. Peptic Ulcer Disease Therapy <ul><li>Pharmacological Therapy </li></ul><ul><ul><li>Inhibition of acid </li></ul></ul><ul><ul><ul><li>H2 blockers </li></ul></ul></ul><ul><ul><ul><li>Antacids </li></ul></ul></ul><ul><ul><ul><li>Proton pump inhibitors </li></ul></ul></ul><ul><ul><ul><li>Anticholinergics </li></ul></ul></ul><ul><ul><ul><li>Prostaglandins </li></ul></ul></ul><ul><ul><ul><li>Augmentation protection </li></ul></ul></ul>
  52. 53. Peptic Ulcer Disease Therapy <ul><li>Antacids (magnesium, aluminum, & calcium based) </li></ul><ul><ul><li>cause diarrhea </li></ul></ul><ul><li>Moderate to high doses of H2 blockers result in improved healing rates </li></ul><ul><ul><li>Used 1 hr PC & HS for 6-8 wks </li></ul></ul><ul><ul><li>Side effects: </li></ul></ul><ul><ul><ul><li>Hypermagnesemia (careful in renal patients) </li></ul></ul></ul><ul><ul><ul><li>Aluminum causes phosphate depletion & osteoporosis </li></ul></ul></ul><ul><ul><ul><li>Sodium overload in CHF </li></ul></ul></ul><ul><ul><ul><li>Hypercalcium causing Milk alkali syndrome </li></ul></ul></ul><ul><ul><ul><li>Inhibits absorption of antibiotics, digoxin, warfarin </li></ul></ul></ul>
  53. 54. PUD Therapy (cont) <ul><li>Proton Pump Inhibitors: </li></ul><ul><ul><li>Inhibit the H,K-ATPase pump </li></ul></ul><ul><ul><li>Healing rate 80-100% </li></ul></ul><ul><ul><li>Prilosec (Omeprazole) </li></ul></ul><ul><li>Anticholinergics: reduce acid by 50% and cause blurred vision </li></ul><ul><ul><li>pupil dilation, consider pt’s occupation or driving restriction </li></ul></ul>
  54. 55. PUD Therapies (cont) <ul><li>Prostaglandins (Do not use in pregnancy) </li></ul><ul><ul><li>Inhibit the parietal cell cyclic AMP function in response to histamine </li></ul></ul><ul><ul><li>Healing rate are equal to H2 blockers </li></ul></ul><ul><ul><li>Primary role is to be used as a prophylactic agent to prevent NSAID induced ulcers. Not used as a primary therapy </li></ul></ul><ul><ul><li>Mosoprostol (Cytotec) </li></ul></ul><ul><li>Sucralfate (Carafate) its action is unknown </li></ul><ul><ul><li>It forms a viscous shield over the mucosa </li></ul></ul><ul><ul><li>Absorbs bile & pepsin </li></ul></ul>
  55. 56. Screw the environment carpooling is bad
  56. 57. What are the treatment regimens used for H. pylori eradication? <ul><li>Current therapy for H. pylori infection consists of 10 days to 2 weeks of one or two effective antibiotics, </li></ul><ul><ul><li>amoxicillin, </li></ul></ul><ul><ul><li>tetracycline </li></ul></ul><ul><ul><ul><li>not to be used for children <12 yrs </li></ul></ul></ul><ul><ul><li>metronidazole, or </li></ul></ul><ul><ul><li>clarithromycin, </li></ul></ul><ul><li>Plus either </li></ul><ul><ul><li>ranitidine bismuth citrate (H2 blocker), </li></ul></ul><ul><ul><li>bismuth subsalicylate (pepto-bismol), </li></ul></ul><ul><ul><li>or proton pump inhibitor. </li></ul></ul>
  57. 58. PUD Therapies (cont) <ul><li>Acid suppression by the H2 blocker or proton pump inhibitor in conjunction with the antibiotics helps </li></ul><ul><ul><li>alleviate ulcer-related symptoms (i.e., abdominal pain, nausea), </li></ul></ul><ul><ul><li>helps heal gastric mucosal inflammation, </li></ul></ul><ul><ul><li>and may enhance efficacy of the antibiotics against H. pylori at the gastric mucosal surface. </li></ul></ul>
  58. 59. H. Pylori Tx <ul><li>Currently, eight H. pylori treatment regimens are approved by the Food and Drug Administration (FDA); however, several other combinations have been used successfully. </li></ul><ul><li>Antibiotic resistance and patient noncompliance are the two major reasons for treatment failure. </li></ul><ul><li>Overall, triple therapy regimens have shown better eradication rates than dual therapy. Longer length of treatment (14 days versus 10 days) results in better eradication rates. </li></ul>
  59. 60. FDA-approved treatment options <ul><li>1. Omeprazole 40 mg QD + clarithromycin 500 mg TID x 2 wks, then omeprazole 20 mg QD x 2 wks </li></ul><ul><li>-OR- </li></ul><ul><li>2. (Zantac) Ranitidine bismuth citrate (RBC) 400 mg BID + clarithromycin 500 mg TID x 2 wks, then RBC 400 mg BID x 2 wks </li></ul><ul><li>-OR- </li></ul><ul><li>3. Bismuth subsalicylate (Pepto Bismol®) 525 mg QID + metronidazole 250 mg QID + tetracycline 500 mg QID* x 2 wks + H2 receptor antagonist therapy as directed x 4 wks </li></ul><ul><li>-OR- </li></ul><ul><li>4. Lansoprazole 30 mg BID + amoxicillin 1 g BID + clarithromycin 500 mg TID x 10 days </li></ul>
  60. 61. FDA-approved treatment options (cont.) <ul><li>5. -OR- Lansoprazole 30 mg TID + amoxicillin 1 g TID x 2 wks** </li></ul><ul><li>6. -OR- Rantidine bismuth citrate 400 mg BID + clarithromycin 500 mg BID x 2 wks, then RBC 400 mg BID x 2 wks </li></ul><ul><li>7. -OR- Omeprazole 20 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days </li></ul><ul><li>8. -OR- Lansoprazole 30 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days </li></ul>
  61. 62. Long-term consequences of H. pylori infection? <ul><li>Recent studies have shown an association between long-term infection with H. pylori and the development of gastric cancer . </li></ul><ul><li>Gastric cancer is the second most common cancer worldwide ; it is most common in countries such as Colombia and China, where H. pylori infects over half the population in early childhood. </li></ul><ul><li>In the United States, where H. pylori is less common in young people, gastric cancer rates have decreased. </li></ul>
  62. 64. GI Bleeding
  63. 65. Gastrointestinal Bleeding <ul><li>May present as: </li></ul><ul><ul><li>Occult blood (not visualized) </li></ul></ul><ul><ul><li>Melena (black stool) </li></ul></ul><ul><ul><li>Hematemesis (vomiting blood) </li></ul></ul><ul><ul><li>Hematochezia (passage of BRBPR in stool) </li></ul></ul>
  64. 66. Kinds of GI Bleeding <ul><li>Hematemesis </li></ul><ul><ul><li>Rapid bleed: vomiting bright red blood </li></ul></ul><ul><ul><li>Slow bleed: “coffee-grounds” </li></ul></ul><ul><li>Melena </li></ul><ul><ul><li>Black tarry stool </li></ul></ul><ul><ul><li>Source: </li></ul></ul><ul><ul><ul><li>Upper GI </li></ul></ul></ul><ul><ul><ul><li>Or lower GI to right colon </li></ul></ul></ul><ul><li>Hematochezia </li></ul><ul><ul><li>Bright red blood in stool </li></ul></ul><ul><ul><li>Source: </li></ul></ul><ul><ul><ul><li>Lower GI </li></ul></ul></ul><ul><ul><ul><li>Or Upper GI if massive </li></ul></ul></ul>
  65. 67. Occult blood <ul><li>Hemacult/Guiaic is the most commonly used test </li></ul><ul><li>False positives <2% </li></ul><ul><li>Obtain 2 different samples from 2 stools over a 3 day period </li></ul><ul><li>Laxatives alter results causing both false-positive and false-negative results </li></ul><ul><li>False positive results from food rich in peroxidase </li></ul><ul><ul><li>Bloody meats </li></ul></ul><ul><ul><li>Broccoli </li></ul></ul><ul><ul><li>Turnips </li></ul></ul><ul><ul><li>Cauliflower </li></ul></ul><ul><li>False negatives from taking Vit. C or food containing vitamin C </li></ul><ul><li>Neoplasms is #1 cause of occult blood loss </li></ul>
  66. 68. Guiaic/ Hemoccult
  67. 69. Causes of GI bleeding by location <ul><li>Upper GI </li></ul><ul><ul><li>#1 PUD </li></ul></ul><ul><ul><ul><li>Duodenal </li></ul></ul></ul><ul><ul><ul><li>Gastric </li></ul></ul></ul><ul><ul><li>Esophageal varices </li></ul></ul><ul><ul><ul><li>(Secondary to portal HTN) </li></ul></ul></ul><ul><ul><li>Mallory-Weiss tear </li></ul></ul><ul><ul><ul><li>(Mucosal laceration @ EG junction) </li></ul></ul></ul><ul><ul><li>Gastritis </li></ul></ul><ul><li>Lower GI </li></ul><ul><ul><li>#1 Hemorrhoids </li></ul></ul><ul><ul><li>#2 Anal Fissure </li></ul></ul><ul><ul><li>Diverticulosis </li></ul></ul><ul><ul><li>IBD </li></ul></ul><ul><ul><li>Intussusception </li></ul></ul><ul><li>Upper & Lower GI </li></ul><ul><ul><li>Neoplasms </li></ul></ul><ul><ul><li>Angiodysplasias </li></ul></ul><ul><ul><ul><li>(Osler’s disease) </li></ul></ul></ul>
  68. 71. GI Bleed <ul><li>GI bleeding is a powerful laxative </li></ul><ul><li>GI bleeding may be life threatening </li></ul><ul><li>GI bleeding may be acute or chronic </li></ul><ul><li>Adult anemia is secondary to GI bleeding until proven otherwise </li></ul><ul><li>GI bleeding is secondary to cancer until proven otherwise </li></ul>
  69. 72. GI Bleed <ul><li>Nature & duration helps with evaluation </li></ul><ul><li>Presence of pain is important </li></ul><ul><li>Watch for associated symptoms: fever, weight loss </li></ul><ul><li>Medication and past surgery history </li></ul><ul><li>The initial step is assessment of hemodynamic status. A systolic BP <100mm Hg is high risk c/ acute bleeding. </li></ul><ul><li>CAN BE MASSIVE AND DEADLY </li></ul><ul><li>MUST BE TREATED RAPIDILY AND AGGRESSIVELY </li></ul><ul><li>ALWAYS R/O CANCER </li></ul>
  70. 73. Upper GI bleed <ul><li>4x more common than lower GI bleed </li></ul><ul><li>R/O upper GI source by NG tube aspirate </li></ul>
  71. 74. Upper GI Differential Dx aids <ul><li>Signs of chronic liver disease implicates bleeding due to portal HTN. </li></ul><ul><li>A hx of dyspepsia, NSAID use, or PUD, suggests Peptic Ulcer. </li></ul><ul><li>Acute bleeding after heavy alcohol ingestion or retching suggests a Mallory-Weiss tear. </li></ul>
  72. 75. Lower GI bleeds <ul><li>Hematochezia </li></ul><ul><ul><li>(however, 10% is from upper GI source) </li></ul></ul><ul><li>Defined as below ligament of Treitz </li></ul><ul><ul><li>(divides duodenum/ jejunum) </li></ul></ul><ul><li>95% from Colon </li></ul><ul><li>Less likely than Upper GI bleed to present in shock, or require transfusion </li></ul><ul><li>85% spontaneous cessation </li></ul>
  73. 76. Complications of GI bleed <ul><li>DIC from both massive blood loss & coagulation </li></ul><ul><li>Multi-organ failure </li></ul><ul><li>Hemodynamic collapse </li></ul><ul><li>Hyper-ammonia toxicity </li></ul><ul><li>Hepatorenal failure </li></ul><ul><li>Encephalopathy </li></ul>
  74. 80. MCC of GI Bleeding 2006 Current <ul><li>Upper GI </li></ul><ul><ul><li>PUD </li></ul></ul><ul><ul><li>Portal HTN </li></ul></ul><ul><ul><li>Mallory Weiss </li></ul></ul><ul><ul><li>Vascular abn </li></ul></ul><ul><ul><li>Gastric Neoplasms </li></ul></ul><ul><ul><li>Erosive gastritis </li></ul></ul><ul><ul><li>others </li></ul></ul><ul><li>Lower GI </li></ul><ul><ul><li>Under 50 y/o </li></ul></ul><ul><ul><ul><li>Infectious colitis </li></ul></ul></ul><ul><ul><ul><li>Anorectal ds </li></ul></ul></ul><ul><ul><ul><li>Inflammatory bowel ds </li></ul></ul></ul><ul><ul><li>Over 50 y/o c Major Bleed </li></ul></ul><ul><ul><ul><li>Diverticulosis </li></ul></ul></ul><ul><ul><ul><li>Vascular ectasias </li></ul></ul></ul><ul><ul><ul><li>Malignancy </li></ul></ul></ul><ul><ul><ul><li>ischemia </li></ul></ul></ul>
  75. 82. <ul><li>LABS </li></ul><ul><li>CBC </li></ul><ul><li>PT/PTT/Thrombin time- DIC panel (FSP fibrin split products, fibrinogen, FDP fibrin degradation products, clotting time, D dimer assay) </li></ul><ul><li>Electrolytes/BUN/creatinine </li></ul><ul><li>Blood Type and Cross match </li></ul><ul><li>CXR/ AXR rarely helpful only if perforated </li></ul>GI BLEED
  76. 83. CXR Pneumoperitoneum
  77. 84. Anoscopy/ Sigmoidoscopy VS. Colonoscopy <ul><li>Anoscopy/ Sigmoidoscopy </li></ul><ul><ul><li>Acceptable in <45 yo otherwise healthy to evaluate for: </li></ul></ul><ul><ul><ul><li>Anorectal ds. </li></ul></ul></ul><ul><ul><ul><li>Inflammatory bowel ds. </li></ul></ul></ul><ul><ul><ul><li>Infectious colitis </li></ul></ul></ul><ul><ul><li>If lesion found, no further eval needed </li></ul></ul><ul><li>Colonscopy </li></ul><ul><ul><li>Used Diagnostically and Therapeutically </li></ul></ul><ul><ul><li>All >40-45 yo c/ + guiaic or Fe+ deficiency anemia </li></ul></ul>
  78. 85. Flex Sig
  79. 86. Anoscopy/ Rigid Sigmoidoscopy
  80. 87. Super Duper Pooper Scooper
  81. 88. Colonoscopy
  82. 93. Urgent management of Upper GI bleeds <ul><li>2 Large bore IV lines need started c/ colloid solution started until PRBC can be infused, if needed. </li></ul><ul><li>Octreotide - Decreases portal HTN (it is administered promptly to all patients with active upper GI bleeds, and liver ds, or known portal HTN, until source can be ID’d by endoscopy. </li></ul><ul><li>PPI’s reduce risk of rebleed in PUD </li></ul><ul><li>Endoscopy </li></ul><ul><ul><li>To ID source </li></ul></ul><ul><ul><li>Determine risk of rebleed </li></ul></ul><ul><ul><li>Hemostasis </li></ul></ul><ul><li>Other Tx modalities (used only if endoscopy fails) </li></ul><ul><ul><li>Angiographic embolization </li></ul></ul><ul><ul><li>Transvenous shunts (for portal HTN, and variceal bleeds) </li></ul></ul>
  83. 94. Chinese Proverbs <ul><li>Man who stand on toilet is high on pot. </li></ul><ul><li>Man who live in glass house should change clothes in basement. </li></ul><ul><li>Man who fish in other man's well often catch crabs. </li></ul><ul><li>Man who fart in church sit in own pew. </li></ul><ul><li>Crowded elevator smell different to midget. </li></ul>
  84. 95. Review <ul><li>Acute Erosive Gastritis </li></ul><ul><ul><li>D/C NSAIDS or add misoprostol </li></ul></ul><ul><ul><li>If bleeding caused by ASA; consider platelet administration </li></ul></ul><ul><ul><li>Sucralfate/ H2 antagonists </li></ul></ul><ul><li>Chronic Gastritis (Nonerosive) </li></ul><ul><ul><li>Type A </li></ul></ul><ul><ul><ul><li>Eradicate H. pylori: amox + tetracycline + PPI </li></ul></ul></ul><ul><ul><li>Type B </li></ul></ul><ul><ul><ul><li>Treat pernicious anemia: monthly lifelong IM B12 </li></ul></ul></ul><ul><li>Specific Types of Gastritis </li></ul>
  85. 96. Review <ul><li>Peptic Ulcer Disease </li></ul><ul><ul><li>Almost all need Pepsin, Acid, & H. pylori to form ulcer </li></ul></ul><ul><ul><li>Eradicate H. pylori </li></ul></ul><ul><ul><li>Endoscopic bx to exclude adenocarcinoma recommended for all patients </li></ul></ul><ul><ul><li>If refractory: obtain fasting serum gastrin levels to exclude Zollinger-Ellison </li></ul></ul><ul><ul><li>Consider parietal cell vagotomy. </li></ul></ul><ul><ul><ul><li>Partial gastrectomy c/ gastro-duodenostomy (Billroth I) or gastrojejunostomy (Billroth II) are rarely used now. </li></ul></ul></ul>
  86. 97. Review <ul><li>Upper GI Bleed </li></ul><ul><ul><li>Evaluate hemodynamic status, stabilize </li></ul></ul><ul><ul><li>Nasogastric tube </li></ul></ul><ul><ul><li>Octreotide </li></ul></ul><ul><ul><li>Endoscopy if bleeding is severe enough to require blood transfusions </li></ul></ul><ul><ul><li>Bleeding from esophageal varices: endoscopic sclerotherapy preferred </li></ul></ul>
  87. 98. Review <ul><li>Lower GI Bleed </li></ul><ul><ul><li>The most common cause of significant bleeding is diverticular bleeding; that of intermittent minor hematochezia is hemorrhoidal bleeding </li></ul></ul><ul><ul><li>Evaluate hemodynamic status, stabilize </li></ul></ul><ul><ul><li>Colonoscopy if bleeding is severe or patient >50 yrs (neoplasms) </li></ul></ul><ul><ul><li>If bleeding continues consider nuclear bleeding scan or mesenteric angiography (often of limited use if bleeding is slow or intermittent), or Intra-arterial vasopressin or embolization. </li></ul></ul><ul><ul><li>Surgery as last resort </li></ul></ul>

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