A 55-year-old male presented with epigastric pain for one month that was relieved by food but worsened 1-3 hours later. He also reported fatigue, dyspepsia, bloating, and weight loss. Differential diagnoses included peptic ulcer disease, pancreatitis, and gallstones. Recommended tests included a CBC, chemistries, H. pylori testing, EKG, CXR, and possible endoscopy or barium study. Treatment options included antacids, H2 blockers, PPIs, and antibiotics.

1. 55 yo male c/ epigastric pain on/off x 1 mo

2. History Awoke him from sleep Relieved by food, but pain worsened 1-3 hrs later Fatigue Dyspepsia/ bloating/ belching/ burning Wt loss No SOB/ pain radiation/N/V/D/F Wife states that his diet is “poor”

3. History PMH No DM No CAD Etc. Family History Mother died 75 MI Father died 70 stroke Surgical Hx None Social History + Smoker 1ppd Medications “ some arthritis med” “ some HTN med” NKDA

4. Physical Exam + Epigastric tenderness Guiaic +

5. Differential Diagnosis? Cardiac MI Aortic Dissection Pulmonary GI PUD Pancreatitis Gallstones Inflammatory bowel ds. (crohn’s/UC) Colon Ca

6. Dx tests CBC (blood loss) Chem c/ BUN/creat Type & cross H. pylori EKG CXR (free air) Barium study

7. Procedures NG tube (if upper GI bleed) IVF Endoscopy ? Sig vs. colonoscopy?

8. Tx Antacids GI cocktail H2 blockers PPI’s Abx

9. Reflux Esophagitis Peptic Ulcer Disease, Gastritis, & GI Bleeding Pascale Gèhy-Andrè, PA-C

10. Anatomy & Physiology of the stomach The blood supply is from the Celiac artery The vagus nerve stimulates the stomach The epithelium is columnar cells pieced by numerous glands The cardia and antrum have mostly mucous cells

11. Normal Gastric Function 1. Primary function of the stomach A. secretion of substances important to digestion & absorption B. movement of gastric contents downstream to small bowel 2. Classes of secretory cells A. Mucous secreting cells of the cardia : 1. Protect underlying cells from mechanical forces of digestion 2. Lubrication of mucosa to move food over surface 3. Retain water within the mucous gel providing aqueous environment for underlying cells. 4. Forming an unstirred layer above the mucosa impending but not blocking diffusion of hydrogen ions from the lumen to the superficial epithelial cells.

12. Normal Gastric Function 2. Classes of secretory cells (cont.): B. HCL -Secreting parietal cells of the body which also secrete intrinsic factor. C. Pepsinogen -Secreting chief cells of the body. D. Gastrin -Secreting G cells of the Antrum (body has 2 sources of Gastrin stomach and pancreas).

13. Gastric Function (cont.) 3. Neural & Hormonal influence on gastric function: 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. 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. 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.

14. Reflux Esophagitis Definition: Recurrent reflux of gastric contents in the distal esophagus Commonly called heartburn 20% of normal population at least one week May cause erosions that leads to Barrett’s esophagitis which can predispose to malignancy

15. Reflux Esophagitis Contributing Factors: Hiatal hernia Delayed gastric emptying (gastroparesis/obstruction) Incompetent Lower esophageal sphincter Irritant effects of gastric juices (refluxate) Clinical features: Heartburn most common presenting feature Hoarseness, cough, hiccup, atypical chest pain, sore throat

16. Reflux Esophagitis Laboratory studies Barium swallow may indicate a large hiatal hernia ENDOSCOPY with BIOPSY standard procedure describes the presence and extent of mucosal damage Endoscopy when symptoms do not respond to medical therapy pH monitoring can be done

17. Reflux Esophagitis Treatment: Life style modification ( DC smoking) Pharmacotherapy Antacids or alginic acid(gaviscon) Histamine (H2 blockers) Prokinetic drugs ( e.g. metoclopramide, cisapride, bethanechol) increase gastric emptying and can be combined with H2 blockers Acid-suppressant proton-pump inhibitor (e.g. omeprazole, lansoprazole) may be tried as last resort Anticholinergic, B - adrenergic, and calcium channel-blocking agents decrease lower esophageal sphincter pressure and should be avoided Complication: Barrett’s Esophagagus

18. Gastritis Acute Gastritis is an inflammation of the gastric mucosa. Gastropathy : epithelial or endothelial damage without inflammation Gastritis has 3 basic types: Acute (erosive/ hemorrhagic) Non-erosive, Non-specific/Chronic Special Forms

19. Acute Gastritis (Erosive/Hemorrhagic) Most common causes: NSAIDS gastric injury by diminishing prostaglandin production in stomach and duodenum Alcohol use is the leading cause of gastritis Stress from CNS injury burns, sepsis, surgery Portal hypertension (portal gastropathy) Other causes: Caustic ingestion radiation

20. Chronic Gastritis Nonerosive/nonspecific Infectious gastritis Type B: H Pylory Involves antrum and body of stomach majority of patients asymptomatic Strong association with PUD 2 to 6 fold risks of gastric adenocarcinoma and also gastric lymphoma Autoimmune gastritis Type A: Pernicious anemia Body and fundus, It usually spares the antrum & affects the parietal cells. 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 Increased risk of adenocarcinoma

21. Special forms of Gastritis Infectious (Phlegmonous or necrotizing gastritis) Emergency gastric resection, and Abx therapy CMV, candidal (fungal) in immunocompromised pt’s Larvae ingestion requires endoscopic removal Eosinophilic Gastritis Giant Cell (Menetrier’s disease) (Hypertrophic Gastropathy) only found on biopsy Lymphocytic Gastritis Granulomatous Gastritis Tuberculosis Syphilis Fungal Sarcoid Crohn’s

22. Gastritis Symptoms Clinical features of gastritis generally reflects the underlying syndrome rather than the gastric injury itself Acute: Dyspepsia and abdominal pain are common indicators of gastritis Mild epigastric discomfort Occasional N/V Headache, excessive salivation, flatus Chronic: Non specific symptoms c/ chronic abdominal discomfort Key signs: (usually none) Hematemesis, bloody nasogastric aspirate Abdominal tenderness Bloating Emesis

23. Gastritis Lab: Endoscopy c/ biopsy is the gold standard A urea breath test can be used to detect HP Specific test for underlying conditions (e.g) B12 and CBC for pernicious anemia Differential Diagnosis: 1. Peptic ulcer 2. Gastroparesis 3. Gastric carcinoma 4. GERD 5. Pancreatitis 6. Lymphoma Treatment: (same as duodenal ulcers) Remove irritant Treat for H pylori Antacids & H2 blockers Avoid smoking & alcohol

24. Peptic Ulcer Disease Definition : PUD is describes any ulcer of the upper digestive tract. (duodenal # 1) and stomach (gastric #2) Break in the duodenal or gastric mucosa extending through the musularis mucosae, and are usually 5mm-1cm.

25. Zollinger-Ellison Syndrome 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.

26. Zollinger-Ellison Syndrome A tumor of the pancreas that secretes gastrin ( Gastrinoma) Usually found in head of pancreas but can also be found in duodenum, liver & lung 75-80% of ulcers produced develop in the duodenal bulb Suspect in any patient with: Multiple or recurring duodenal ulcers Post bulbar or jejunal ulcers Ulcers associated with diarrhea Elevated serum gastrin levels Usually only tested when suspect ZE syndrome

27. Peptic Ulcer Disease (PUD) Men 1.3 : 1 Women Most commonly occur in : #1 Duodenum (Duodenal) #2 Stomach (Gastric) Esophagus Gastroenteric anastomoses Meckel’s Diverticulum

28. PUD The spectrum of the disease is broad from mild mucosal injury to frank ulcerations. Symptoms vary and are not related to the severity of tissue damage. 1-2% of population have an ulcer at the present time 10% of population will have ulcer in their lifetime Gastric and Duodenal ulcers tend to recur in the same location. Recurrent hemorrhage occurs in 50% of patients who have had a prior bleed.

29. Duodenal Ulcer vs. Gastric Ulcer Duodenal Increased acid production H. pylori relieved by food & typically awakens patient around 1:00am Gastric Normal or decreased acid production Decreased mucosal resistance H. pylori NSAIDS worsened by food

30. Duodenal Vs. Gastric (cont) Duodenal Onset more common age 25 to 55 never malignant mostly located in the duodenal bulb or immediately post bulbar. Ulcers distal to the duodenal bulb should raise suspicion for Zollinger-Ellison Syndrome (also c/ multiple frequently occurring duodenal ulcers.) Men 2:1 Women Duodenal 5 times more common than gastric 60-80% have recurrence within one year. Gastric Onset more common age 40 to 70 Benign more likely @ lesser curvature/ antrum Gastric ulcers are more common @ lesser curvature Malignancies more likely @ greater curvature 1-3% occur in carcinomas

31. PUD Etiologies 1. Helicobacter pylori (H. pylori) infection: (#1 cause) A. Associated c/ 70-95% of Peptic ulcers. B. Treatment of H. pylori improves healing rate & markedly decreases the recurrence rate. 2. NSAIDS: (#2 cause) (inhibit prostaglandins which normally stimulate production of mucous secretions & bicarb.) A. may cause gastric or duodenal ulcers (steroids also) B. accounts for the majority of non H. pylori ulcers

32. PUD Etiologies (cont) 3. Hypersecretion states: (#3 although uncommon) Gastrinomas (Zollinger-Ellison Syndrome) Multiple endocrine neoplasia (MEN-1) Systemic mastocytosis (mast cells infiltrate intestinal wall, release histamine- stimulates acid. Symptoms are diarrhea, flushing, urticaria. Histamine in blood. Confirmed by biopsy.) 4. Stress: physiologic stress (eg. Burns, surgery, & severe medical conditions) 5. Rare causes: viral, radiation, vascular insuff. Diseases assoc. c/ peptic ulcers: Cirrhosis, renal failure, pulmonary ds. Any pt. c/ systemic ds. (COPD, renal failure, cirrhosis of liver) are prone to ulcers so should be started on H2 blockers.

33. The pathogenesis of PUD is related to the imbalance between normal protective factors and injurious factors No Ulcer Normal Ulcer Aggressive forces Gastric acid Digestive enzymes Vs. Defensive forces Mucus Bicarb Prostaglandins Epithelial regeneration

34. Ulcers result from: 1. Increased aggression H. pylori infection NSAIDS Cigarettes ETOH Or 2. Impaired Defense Ischemia Prostaglandin Inhibition (NSAIDS) Delayed gastric emptying

35. PUD ADVERSE EFFECTS OF SMOKING 1. Interferes c/ action of H2 antagonists 2. Increases rate of gastric emptying 3. Increases duodenogastric reflux 4. Decreases pancreatic bicarb secretion 5. Decreases mucosal blood flow 6. Depresses gastric mucosal prostaglandin synthesis

37. Peptic Ulcer Disease Facts Most ulcers are caused by H. pylori infection, not spicy food, acid or stress. You can test for H. pylori infection. H. pylori / ulcers can be tx’d c/ antibiotics. Complications: A Major complication is bleeding & perforation Erosion of a small vessel at the base of the ulcer is the cause of the bleeding Perforation is usually catastrophic causing peritonitis

38. What is H. pylori 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. H. pylori causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers.

39. How do people get infected with H. pylori ? It is not known how H. pylori is transmitted or why some patients become symptomatic while others do not. The bacteria are most likely spread from person to person through fecal-oral or oral-oral routes. Possible environmental reservoirs include: contaminated water sources Iatrogenic spread through contaminated endoscopes has been documented but can be prevented

40. What can people do to prevent H. pylori infection? Since the source of H. pylori is not yet known, recommendations for avoiding infection have not been made. 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.

41. H. pylori infection Before this bacterium was discovered, spicy food, acid, stress, and lifestyle were considered the major causes of ulcers. 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. These medications relieve ulcer-related symptoms, heal gastric mucosal inflammation, and may heal the ulcer, but they do NOT treat the infection.

42. H. Pylori infection When acid suppression is removed, the majority of ulcers, particularly those caused by H. pylori , recur. 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.

43. What illnesses does H. pylori cause? 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. 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. The role of H. pylori in non-ulcer dyspepsia remains unclear.

44. Peptic Ulcer Disease Symptoms #1. Epigastric Pain Burning Occurs 1-3 hrs p/ meals Relieved by food May occur @ night May radiate to back or shoulders if perforated Nausea Vomiting May be related to partial or complete gastric outlet obstruction Dyspepsia Belching/ Bloating Heartburn Chest Discomfort Anorexia Weight loss In gastric ulcers (also in pancreatic ds.) Weight gain In duodenal ulcers Hematemesis or melena Due to GI bleeding If severe = hematochezia

45. Chinese Proverbs Man with one chopstick go hungry. Man who scratch ass should not bite fingernails. Man who eat many prunes get good run for money. Baseball is wrong: man with four balls cannot walk. Panties not best thing on earth! But next to best thing on earth. Man who fight with wife all day get no piece at night. It take many nails to build crib, but one screw to fill it. Man who drive like hell, bound to get there.

46. Who should be tested and treated for H. pylori ? 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. To date, there has been no conclusive evidence that treatment of H. pylori infection in patients with non-ulcer dyspepsia is warranted.

47. PUD Tests Laboratory Test: Routine tests are of little importance. Having a CBC is helpful. Upper GI endoscopy c/ biopsy* Upper GI series (barium) (limited today) Serum Test Amylase Electrolytes Serum Gastrin level if ZE syndrome is suspected Frequently occurring duodenal ulcers or multiple Duodenal Ulcers*

48. How is H. pylori infection diagnosed? Several methods may be used to diagnose H. pylori infection. Serological tests that measure specific H. pylori IgG antibodies can determine if a person has been infected. The sensitivity and specificity of these assays around 80% Fecal Antigen Assay Urea Breath test In this test, the patient is given either 13C- or 14C-labeled urea to drink. H. pylori metabolizes the urea rapidly, and the labeled carbon is absorbed. This labeled carbon can then be measured as CO2 in the patient's expired breath to determine whether H. pylori is present. The sensitivity and specificity of the breath test ranges from 94% to 98%. PPI’s can give false negative results

49. How is H. pylori infection in PUD diagnosed? Upper endoscopy (esophagogastroduodenal) is considered the reference method of diagnosis.

50. Dx of H. pylori by Endoscopy During endoscopy, biopsy specimens of the stomach and duodenum are obtained and the diagnosis of H. pylori can be made by several methods: 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. Histologic identification of organisms - considered the gold standard of diagnostic tests. Culture of biopsy specimens for H. pylori, which requires an experienced laboratory and is necessary when antimicrobial susceptibility testing is desired

51. Peptic Ulcer Disease Therapy Non-Pharmacological Diet change is of no value Smoking Cessation Smoking delays healing DC medications that enhance the progression NSAIDS Pharmacological Therapy Inhibit secretion of acid Neutralizing gastric acids Augmentation of protection of mucosa Antibiotics prn Maintenance Therapy Prevention c/ colloid bismuth Bedtime dosage of H2 blockers

52. Peptic Ulcer Disease Therapy Pharmacological Therapy Inhibition of acid H2 blockers Antacids Proton pump inhibitors Anticholinergics Prostaglandins Augmentation protection

53. Peptic Ulcer Disease Therapy Antacids (magnesium, aluminum, & calcium based) cause diarrhea Moderate to high doses of H2 blockers result in improved healing rates Used 1 hr PC & HS for 6-8 wks Side effects: Hypermagnesemia (careful in renal patients) Aluminum causes phosphate depletion & osteoporosis Sodium overload in CHF Hypercalcium causing Milk alkali syndrome Inhibits absorption of antibiotics, digoxin, warfarin

54. PUD Therapy (cont) Proton Pump Inhibitors: Inhibit the H,K-ATPase pump Healing rate 80-100% Prilosec (Omeprazole) Anticholinergics: reduce acid by 50% and cause blurred vision pupil dilation, consider pt’s occupation or driving restriction

55. PUD Therapies (cont) Prostaglandins (Do not use in pregnancy) Inhibit the parietal cell cyclic AMP function in response to histamine Healing rate are equal to H2 blockers Primary role is to be used as a prophylactic agent to prevent NSAID induced ulcers. Not used as a primary therapy Mosoprostol (Cytotec) Sucralfate (Carafate) its action is unknown It forms a viscous shield over the mucosa Absorbs bile & pepsin

56. Screw the environment carpooling is bad

57. What are the treatment regimens used for H. pylori eradication? Current therapy for H. pylori infection consists of 10 days to 2 weeks of one or two effective antibiotics, amoxicillin, tetracycline not to be used for children <12 yrs metronidazole, or clarithromycin, Plus either ranitidine bismuth citrate (H2 blocker), bismuth subsalicylate (pepto-bismol), or proton pump inhibitor.

58. PUD Therapies (cont) Acid suppression by the H2 blocker or proton pump inhibitor in conjunction with the antibiotics helps alleviate ulcer-related symptoms (i.e., abdominal pain, nausea), helps heal gastric mucosal inflammation, and may enhance efficacy of the antibiotics against H. pylori at the gastric mucosal surface.

59. H. Pylori Tx Currently, eight H. pylori treatment regimens are approved by the Food and Drug Administration (FDA); however, several other combinations have been used successfully. Antibiotic resistance and patient noncompliance are the two major reasons for treatment failure. 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.

60. FDA-approved treatment options 1. Omeprazole 40 mg QD + clarithromycin 500 mg TID x 2 wks, then omeprazole 20 mg QD x 2 wks -OR- 2. (Zantac) Ranitidine bismuth citrate (RBC) 400 mg BID + clarithromycin 500 mg TID x 2 wks, then RBC 400 mg BID x 2 wks -OR- 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 -OR- 4. Lansoprazole 30 mg BID + amoxicillin 1 g BID + clarithromycin 500 mg TID x 10 days

61. FDA-approved treatment options (cont.) 5. -OR- Lansoprazole 30 mg TID + amoxicillin 1 g TID x 2 wks** 6. -OR- Rantidine bismuth citrate 400 mg BID + clarithromycin 500 mg BID x 2 wks, then RBC 400 mg BID x 2 wks 7. -OR- Omeprazole 20 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days 8. -OR- Lansoprazole 30 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days

62. Long-term consequences of H. pylori infection? Recent studies have shown an association between long-term infection with H. pylori and the development of gastric cancer . 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. In the United States, where H. pylori is less common in young people, gastric cancer rates have decreased.

64. GI Bleeding

65. Gastrointestinal Bleeding May present as: Occult blood (not visualized) Melena (black stool) Hematemesis (vomiting blood) Hematochezia (passage of BRBPR in stool)

66. Kinds of GI Bleeding Hematemesis Rapid bleed: vomiting bright red blood Slow bleed: “coffee-grounds” Melena Black tarry stool Source: Upper GI Or lower GI to right colon Hematochezia Bright red blood in stool Source: Lower GI Or Upper GI if massive

67. Occult blood Hemacult/Guiaic is the most commonly used test False positives <2% Obtain 2 different samples from 2 stools over a 3 day period Laxatives alter results causing both false-positive and false-negative results False positive results from food rich in peroxidase Bloody meats Broccoli Turnips Cauliflower False negatives from taking Vit. C or food containing vitamin C Neoplasms is #1 cause of occult blood loss

68. Guiaic/ Hemoccult

69. Causes of GI bleeding by location Upper GI #1 PUD Duodenal Gastric Esophageal varices (Secondary to portal HTN) Mallory-Weiss tear (Mucosal laceration @ EG junction) Gastritis Lower GI #1 Hemorrhoids #2 Anal Fissure Diverticulosis IBD Intussusception Upper & Lower GI Neoplasms Angiodysplasias (Osler’s disease)

71. GI Bleed GI bleeding is a powerful laxative GI bleeding may be life threatening GI bleeding may be acute or chronic Adult anemia is secondary to GI bleeding until proven otherwise GI bleeding is secondary to cancer until proven otherwise

72. GI Bleed Nature & duration helps with evaluation Presence of pain is important Watch for associated symptoms: fever, weight loss Medication and past surgery history The initial step is assessment of hemodynamic status. A systolic BP <100mm Hg is high risk c/ acute bleeding. CAN BE MASSIVE AND DEADLY MUST BE TREATED RAPIDILY AND AGGRESSIVELY ALWAYS R/O CANCER

73. Upper GI bleed 4x more common than lower GI bleed R/O upper GI source by NG tube aspirate

74. Upper GI Differential Dx aids Signs of chronic liver disease implicates bleeding due to portal HTN. A hx of dyspepsia, NSAID use, or PUD, suggests Peptic Ulcer. Acute bleeding after heavy alcohol ingestion or retching suggests a Mallory-Weiss tear.

75. Lower GI bleeds Hematochezia (however, 10% is from upper GI source) Defined as below ligament of Treitz (divides duodenum/ jejunum) 95% from Colon Less likely than Upper GI bleed to present in shock, or require transfusion 85% spontaneous cessation

76. Complications of GI bleed DIC from both massive blood loss & coagulation Multi-organ failure Hemodynamic collapse Hyper-ammonia toxicity Hepatorenal failure Encephalopathy

80. MCC of GI Bleeding 2006 Current Upper GI PUD Portal HTN Mallory Weiss Vascular abn Gastric Neoplasms Erosive gastritis others Lower GI Under 50 y/o Infectious colitis Anorectal ds Inflammatory bowel ds Over 50 y/o c Major Bleed Diverticulosis Vascular ectasias Malignancy ischemia

82. LABS CBC PT/PTT/Thrombin time- DIC panel (FSP fibrin split products, fibrinogen, FDP fibrin degradation products, clotting time, D dimer assay) Electrolytes/BUN/creatinine Blood Type and Cross match CXR/ AXR rarely helpful only if perforated GI BLEED

83. CXR Pneumoperitoneum

84. Anoscopy/ Sigmoidoscopy VS. Colonoscopy Anoscopy/ Sigmoidoscopy Acceptable in <45 yo otherwise healthy to evaluate for: Anorectal ds. Inflammatory bowel ds. Infectious colitis If lesion found, no further eval needed Colonscopy Used Diagnostically and Therapeutically All >40-45 yo c/ + guiaic or Fe+ deficiency anemia

85. Flex Sig

86. Anoscopy/ Rigid Sigmoidoscopy

87. Super Duper Pooper Scooper

88. Colonoscopy

93. Urgent management of Upper GI bleeds 2 Large bore IV lines need started c/ colloid solution started until PRBC can be infused, if needed. 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. PPI’s reduce risk of rebleed in PUD Endoscopy To ID source Determine risk of rebleed Hemostasis Other Tx modalities (used only if endoscopy fails) Angiographic embolization Transvenous shunts (for portal HTN, and variceal bleeds)

94. Chinese Proverbs Man who stand on toilet is high on pot. Man who live in glass house should change clothes in basement. Man who fish in other man's well often catch crabs. Man who fart in church sit in own pew. Crowded elevator smell different to midget.

95. Review Acute Erosive Gastritis D/C NSAIDS or add misoprostol If bleeding caused by ASA; consider platelet administration Sucralfate/ H2 antagonists Chronic Gastritis (Nonerosive) Type A Eradicate H. pylori: amox + tetracycline + PPI Type B Treat pernicious anemia: monthly lifelong IM B12 Specific Types of Gastritis

96. Review Peptic Ulcer Disease Almost all need Pepsin, Acid, & H. pylori to form ulcer Eradicate H. pylori Endoscopic bx to exclude adenocarcinoma recommended for all patients If refractory: obtain fasting serum gastrin levels to exclude Zollinger-Ellison Consider parietal cell vagotomy. Partial gastrectomy c/ gastro-duodenostomy (Billroth I) or gastrojejunostomy (Billroth II) are rarely used now.

97. Review Upper GI Bleed Evaluate hemodynamic status, stabilize Nasogastric tube Octreotide Endoscopy if bleeding is severe enough to require blood transfusions Bleeding from esophageal varices: endoscopic sclerotherapy preferred

98. Review Lower GI Bleed The most common cause of significant bleeding is diverticular bleeding; that of intermittent minor hematochezia is hemorrhoidal bleeding Evaluate hemodynamic status, stabilize Colonoscopy if bleeding is severe or patient >50 yrs (neoplasms) 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. Surgery as last resort