Peptic ulcer and gastritis

PUD PATIENTS WITHOUT ALARM SYMPTOMS OR REDFLAGS SHOULD BE TESTED FOR H.PYLORI WITH SEROLOGY BUT THOSE WITH ALARM SYMPTOMS SHOULD RECEIVE ENDOSCOPY.

1. PEPTIC ULCER AND GASTRITIS DR.RISHIKESAN K.V SPECIALIST PHYSICIAN VENNIYIL MEDICAL CENTRE SHARJAH

2. PEPTIC ULCER DISEASE # 2 MOST COMMONLY DIAGNOSED CAUSE OF EPIGASTRIC PAIN OPEN SORES ARE CALLED ULCERS AND THE WORD PEPTIC MEANS THAT ACID IS THE CAUSE OF ULCERS PEPTIC ULCER DISEASE IS THE DISEASE OR EROSION OF THE STOMACH OR DUODENAL TISSUE PAIN TENDS TO OCCUR AFTER EATING. WITH GASTRIC ULCERS IT USUALLY OCCURS BRIEFLY AFTER EATING. WITH DUODENAL ULCERS IT TENDS TO OCCUR A FEW HOURS AFTER EATING YOU CANNOT DIFFFERENTIATE BETWEEN GU AND DU BY SYMPTOMS ALONE. YOU HAVE TO SCOPE TO KNOW DEFINITELY 2/13/2018 2

3. CAUSES OF EPIGASTRIC PAIN IDIOPATHIC (#1) GERD PEPTIC ULCER DISEASE(#2) GASTRITIS (#3) PANCREATITIS OTHERS CANCER (GASTRIC; ESOPHAGEAL; PANCREATIC) REFERRED OR MISAPPROPRIATED PAIN (PELVIC PAIN ETC) 2/13/2018 3

4. PUD :GASTRIC AS WELL AS DUODENAL BY FAR THE MOST COMMON FORM OF PEPTIC ULCER DISEASE IS THE DUODENAL ULCER. HOWEVER FOR THE LEARNING PURPOSES WE WILL COVER BOTH THE DOUDENAL AS WELL AS GASTRIC ULCER DISEASES THERE IS A PHYSIOLOGIC BALANCE IN NORMAL CONDITIONS BETWEEN GASTRODUODENAL MUCOSAL DEFENSE AND GASTRIC ACID SECRETION WHEN THE BALANCE BETWEEN THE DEFENSIVE MECHANISM AND AGGRESSIVE FACTORS IS DISRUPTED MUCOSAL INJURY AND PEPTIC ULCERATION DEVELOPS 2/13/2018 4

5. GASTRIC MUCOSAL DEFENCE MECHANISMS SEVERAL MUCOSAL DEFENCE MECHANISM PROTECT THE GASTRIC MUCOSA AGAINST ACID AND NOXIOUS AGENTS MAINLY A THREE-TIER SYSTEM OPERATES : PRE EPITHELIAL PROTECTION IS PROVIDED BY THE MUCUS-BICARBONATE BARRIER . MUCUS AND BICARBONATE , SECRETED BY MUCUS CELLS IS AN ACTIVE PROCESS UNDER VAGAL INFLUENCE IT MAINTAINS A NEUTRAL pH AT THE EPITHELIAL SURFACE 2. AT THE EPITHELIAL LEVEL THE SURFACTANTS, NON PROTEIN –SH, RAPID CELL TURN OVER AND THE PROCESS OF RESTITUTION PLAY THE ROLE IN KEEPING THE INTEGRITY OF INTACT EPITHELIUM 3. IN SUB EPITHELIAL LEVEL PROSTAGLANDINS AND MUCOSAL BLOOD FLOW KEEPS THE MUCOSA HEALTHY AND HELPS IN DISPOSAL OF HYDROGEN IONS AND NOXIOUS AGENTS 2/13/2018 5

6. MECHANISM OF INJURY DIRECT MUCOSAL DAMAGE DUE TO TOXINS ,ETHANOL, NSAIDS, BILE, AND H.PYLORI WHEN WE CONSIDER THE PEPTIC ULCER DISEASE OF STOMCH IT IS ACTUALLY NOT DUE TO EXCESS ACID PRODUCTION . STOMACH LINING IS EFFECTIVELY PROTECTED NATURALLY FROM THE ACID ATTACK BY THE BICARBONATES AND PROSTAGLANDINS . HOWEVER THIS NATURAL PROTECTION OFFERED BY THE PROSTAGLANDINS IS OFTEN COMPROMISED WHEN NSAIDS INHIBIT THE PRODUCTION OF PGs THROUGH COX PATHWAY. STEROIDS KNOCK OUT THE PHOSPHOLIPASE A2 THEREBY BLOCK THE PGs PRODUCTION WHEN THE BILE REGURGITATES BACK INTO THE STOMACH IT MAY CAUSE DAMAGE TO THE STOMACH LINING 2/13/2018 6

7. M o I…. H.PYLORI RESIDING AT THE ANTRUM OF THE STOMACH IS CAPABLE OF SPLITTING UREA INTO AMMONIA WITH THE HELP OF THE ENZYME UREASE AT SOME POINT OF TIME THE BACTERIA CAN BURROW INTO THE LINING OF STOMACH AND WEAKEN THE LINING WHERE THE ACID CAN PRODUCE FURTHER DAMAGE RESULTING PEPTIC ULCER DISEASE . INCREASED ACID PRODUCTION IS THE MAJOR CAUSE OF PEPTIC ULCERATION IN THE DUODENAL MUCOSA MUCOSAL ISCHAEMIA IS ALWAYS A POSSIBILITY WHICH CAN COMPROMISE THE INTEGRITY OF MUCOSAL LINING OF STOMACH AND DUODENUM THEREBY LEADING TO EROSIONS AND ULCERATIONS 2/13/2018 7

8. CAUSES NSAIDS AND H.PYLORI INFECTION MAKE UP THE MAJORITY OF CASES HEAD TRAUMA (CUSHING’S ULCER), BURNS (CURLING’S ULCER), MECHANICAL VENTILATION , CROHN’S DISEASE , ZES HYPERSECRETORY STATES : SYSTEMIC MASTOCYTOSIS, BASOPHILIC LEUKAEMIAS, HYPERPARATHYROIDISM, CYSTIC FIBROSIS, SHORT BOWEL SYNDROME 2/13/2018 8

9. PEPTIC ULCER DISEASE EPIGASTRIC PAIN,NAUSEA AND EMESIS GI BLEEDING: MELENA,HAEMATEMESIS,HEMATOCHEZIA, IRON DEFICIENCY ANEMIA PERFORATION POSTERIORLY INTO THE PANCREAS (ONLY GASTRIC ULCERS) GASTRIC OUTLET OBSTRUCTION DUE TO PERIPYLORIC SCAR FORMATION GASTRIC ULCERS MAY BE MALIGNANT WHILE DUODENAL ULCERS ARE NOT CLINICAL PRESENTATIONS 2/13/2018 9

10. SYMPTOMS POST PRANDIAL EPIGASTRIC PAIN, EPIGASTRIC PAIN THAT AWAKENS THE PATIENT AT NIGHT, “HEART BURN” THAT DOESN’T RESPOND TO ANTACIDS, ALARM SYMPTOMS HISTORY: FREQUENT NSAID USE. ROUGHLY EQUAL BETWEEN MEN AND WOMEN 2/13/2018 10

11. ALARM SYMPTOMS WEIGHT LOSS OF MORE THAN 10% IN 3 MONTHS ANEMIA HEME POSITIVE STOOL OR HAEMATEMESIS EARLY SATIETY ODYNOPHAGIA OR DYSPHAGIA OLDER THAN AGE 45 YEARS ABNORMAL PHYSICAL EXAMINATIONS 2/13/2018 11

12. COMPLICATIONS PERFORATED ULCER: PAIN IS SIGNIFICANTLY WORSE PROGRESSIVE PERITONEAL PAIN (GENERALISED,VERY SENSITIVE TO TOUCH, MOVEMENT, REBOUND TENDERNESS), ABDOMINAL DISTENSION, FEVER, SHOCK. THIS IS A SURGICAL EMERGENCY IF PATIENT HAS A HISTORY OF PUD AND PRESENTS WITH SUDDEN PERITONEAL PAIN AND BLOATING , THE BEST DIAGNOSTIC STEP IS TO GET AN ABDOMINAL FILM 2/13/2018 12

13. ENDOSCOPY:BEST TEST FOR DIAGNOSIS Duodenal ulcer in a 65-year-old man with osteoarthritis who presented with hematemesis and melena stools. The patient took naproxen on a daily basis Gastric ulcer with punched-out ulcer base with whitish fibrinoid exudates . 2/13/2018 13

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15. GASTRIC OUTLET OBSTRUCTION GASTRIC OUTLET OBSTRUCTION : RARE COMPLICATION SYMPTOMS EARLY SATIETY WEIGHT LOSS VOMITING DIAGNOSIS BY SCOPY TREATMENT : SURGICAL 2/13/2018 15

16. GASTRIC OUTLET OBSTRUCTION PATIENTS WHO DEVELOP GASTRIC OUTLET OBSTRUCTION AS A RESULT OF A CHRONIC, UNTREATED DUODENAL ULCER USUALLY REPORT A HISTORY OF FULLNESS AND BLOATING ASSOCIATED WITH NAUSEA AND EMESIS THAT OCCURS SEVERAL HOURS AFTER FOOD INTAKE. A COMMON MISCONCEPTION IS THAT ADULTS WITH GASTRIC OUTLET OBSTRUCTION PRESENT WITH NAUSEA AND EMESIS IMMEDIATELY AFTER A MEAL. ONLY 20%-25% OF PATIENTS WITH SYMPTOMS SUGGESTIVE OF PEPTIC ULCERATION ARE FOUND ON INVESTIGATION TO HAVE A PEPTIC ULCER. 2/13/2018 16

17. PEPTIC ULCER DISEASE: TREATMENT ANTACIDS MAGNESIUM AND ALUMINIUM CAUSE LONG TERM TOXICITY BE CAREFUL WITH ANTACIDS MILK ALKALI SYNDROME DUE TO PROLONGED USE OF CALCIUM H2 BLOCKERS BLOCK H2 RECEPTORS ON PARIETAL CELLS INHIBIT CYTOCHROME P450 DRUG METABOLISM DRUG – DRUG INTERACTION IS AN IMPORTNT SIDE EFFECT 2/13/2018 17

18. PUD : TREATMENT PPI IRREVERSIBLE BLOCKAGE OF H+/K+ ATPASE PUMP CAN INTERFERE WITH ABSORPTION OF OTHER DRUGS SUCRALFATE STIMULATES ENDOGENOUS PROSTAGLANDIN PRODUCTION FOR MUCOSAL HEALING AVOID IN RENAL INSUFFICIENCY 2/13/2018 18

19. PEPTIC ULCER DISEASE DURATION OF THERAPY DUODENAL ULCER : 4-6 WEEKS GASTRIC ULCER : 6-8 WEEKS WITH REPEAT EGD TO DOCUMENT HEALING TREATMENT OF H.PYLORI INFECTION H.PYLORI INFECTION BEING ASSOCIATED WITH BOTH OF THESE PATHOLOGY TREATMENT AND ERADICATION OF H.PYLORI INFECTION IS OF UTMOST IMPORTANCE 2/13/2018 19

20. NSAID ASSOCIATED PEPTIC ULCER DISEASE GUs ARE VISIBLE IN 30% OF PATIENTS ACTIVELY TAKING NSAIDS THERE ARE TWO OPPOSING TRENDS: H.PYLORI RECOGNITION AND TREATMENT: PUD REDUCED NUMBER OF ADMISSIONS FOR NSAID-RELATED ULCERS INCREASED OVERALL PUD ACCOUNTS FOR .5 - 2.5% OF ALL ADMISSIONS. 1.3% RISK OF GI BLEED WITH LONG TERM USE INCREASED RISK OF BLEEDING WITH LOW DOSE AND HIGH DOSE ASPIRIN ALTHOUGH THE INCREASED RISK IS DOSE DEPENDENT ENTERIC COATING DOESN’T REDUCE THE RISK OF BLEEDING HIGH RATE OF MORTALITY FOR NSAID ASSOCIATED GI BLEEDING 2/13/2018 20

21. NSAID ASSOCIATED PUD :RISK FACTORS AGE > 70 HIGHER DOSE OF NSAID OFTEN ASSOCIATED WITH H.PYLORI INFECTION CONCOMITANT CORTICOSTEROID. COMBINATION OF NSAIDS AND CORTICOSTEROID IS DEFINITELY GOING TO COMPROMISE THE PRODUCTION OF PROSTGLANDINS SO THAT MUCOSAL PROTECTION IS AT JEOPARDY LEADING TO THE DEVELOPMENT OF EROSIONS AND ULCERATIONS CONCOMITANT ANTICOAGULANTS PRIOR HISTORY OF PUD H/O CVD 2/13/2018 21

22. NSAIDS PUD : THE TREATMENT NSAIDS DEFINITELY GOING TO COMPROMISE AND INHIBIT THE PRODUCTION OF PROSTGLANDINS SO THAT NATURAL MUCOSAL PROTECTION CONFERRED BY THE PG IS AT JEOPARDY LEADING TO THE DISRUPTION OF MUCOSAL INTEGRITY RESULTING IN EROSIONS AND ULCERATIONS . TREATMENT IS PPI AND WITHDRAWAL OF NSAIDS TREAT H.PYLORI 2/13/2018 22

23. NSAIDS PUD :PROPHYLAXIS PROPHYLAXIS : MISOPROSTOL PG-E DERIVATIVE INHIBITS NSAID INDUCED MUCOSAL DAMAGE DIARRHOEA IS A DOSE LIMITING SIDE EFFECT IT IS CONTRAINDICATED IN PREGNANCY PPI SUPERIOR TO H2 BLOCKERS IN STUDIES OF CHRONIC NSAID USE COX 2 SELECTIVE INHIBITORS LACK CARDIOVASCULAR PROTECTIVE EFFECT GI PROTECTIVE EFFECT LOST WITH CONCOMITANT BABY ASA USE 2/13/2018 23

24. HELICOBACTER PYLORI INFECTION HELICOBACTER PYLORI INFECTION IS ASSOCIATED WITH BOTH TYPES OF PUD. 90% OF THE PEOPLE AFFECTED WITH PUD APPEAR TO BE POSITIVE FOR H.PYLORI INFECTION. GRAM NEGATIVE SPIRAL SHAPED,FLAGELLATED BACILLUS FECO-ORAL TRANSMISSION PREVALENCE INCREASES WITH AGE: > 50% INFECTION AMONG THE GENERAL POPULATION >60 YEARS HIGH PREVALENCE IN DEVELOPING COUNTRIES RISK FACTORS INCLUDE LOW SOCIOECONOMIC STATUS, DOMESTIC CROWDING , INSTITUTIONALISATON 2/13/2018 24

25. H.PYLORI INFECTIONS H. PYLORI IS INVOLVED IN MANY DISEASES OTHER THAN PUD SUCH AS CORONARY ARTERY INFLAMMATION, GERD SKIN DISEASE, IRON DEFICIENCY ANEMIA, RHEUMATOLOGIC ISSUES, MALTOMA THERE IS A STRONG ASSOCIATION BETWEEN GASTRIC ADENOCARCINOMA AND LYMPHOMA ELECTRON MICROGRAPH OF H.PYLORI WITH MULTIPLE FLAGELLA 2/13/2018 25

26. STAGING OF H.PYLORI INFECTION H. PYLORI INFECTIONS DO NOT HAVE A STAGING SYSTEM. HOWEVER, THE PROCESS OF THE DISEASE MAY BE DESCRIBED IN THE FOLLOWING STEPS: CHRONIC GASTRITIS ATROPHIC GASTRITIS METAPLASIA OF THE INTESTINE, WHICH MAY EVOLVE INTO DYSPLASIA ADENOCARCINOMA OF THE STOMACH 2/13/2018 26

27. GASTRIC ULCERATION BY H.PYLORI ADHERENCE AND PENETRATION AMMONIA PRODUCTION PROLIFERATION, MIGRATION and FORMATION OF INFECTIOUS FOCUS ULCERATION by DESTRUCTION OF MUCOSA, INFLAMMATION AND MUCOSAL CELL DEATH 2/13/2018 27

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29. TEST FOR H.PYLORI THREE COMMONLY USED WAYS SEROLOGY : MOST SENSITIVE IgG ANTIBODY ,ALWYS REMAIN POSITIVE AFTER ERADICATION GASTRIC BIOPSY: UREASE TEST - INSTANT RESULT,LOW COST MOST SPECIFIC, BUT REQUIRES ENDOSCOPY STOOL ANTIGEN: CHECKS FOR PRESENT INFECTION. (HIGH SENSITIVITY 94% AND SPECIFICITY 98%) THIS IS GOOD TO USE IF PATIENT DOESN’T RESPOND TO THERAPY. USEFUL TO DOCUMENT ERADICATION 2/13/2018 29

30. H.PYLORI TESTING THE BEST FIRST STEP IN THE MANAGEMENT OF A PATIENT WITH SUSPECTED PUD WITH NO ALARM SYMPTOMS IS H.PYLORI SEROLOGY (HIGH SENSITIVITY AND SPECIFICITY OF OVER 90%) THE MOST ACCURATE TEST FOR H.PYLORI INFECTION IS GASTRIC BIOPSY UREA BREATH TEST HIGH SENSITIVITY AND SPECIFICITY STOP PPI THERAPY BEFORE TESTING HISTOLOGY HIGHEST SENSITIVITY AND SPECIFICITY,REQUIRES ENDOSCOPY TISSUE CULTURE CUMBERSOME ,USED FOR ANTIBIOTIC RESISTANCE TESTING 2/13/2018 30

31. ACG GUIDELINES FOR TESTING FOR H.PYLORI The 2017 American College of Gastroenterology (ACG) guidelines for the treatment of  H pylori  infection (HPI) include the following recommendations for testing for  H pylori    : All patients with active or past history of PUD (unless previous cure of HPI has been documented), low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma, or a history of endoscopic resection of early gastric cancer Patients with dyspepsia who are undergoing upper endoscopy (gastric biopsy specimens) Patients on long-term, low-dose aspirin Patients initiating long-term therapy with NSAIDs Patients with unexplained iron deficiency anemia following standard workup Adults with idiopathic thrombocytopenic purpura 2/13/2018 31

32. H. PYLORI INFECTION: TREATMENT COMBINATION ANTIBIOTIC AND ANTISECRETORY AGENTS RESULT IN ERADICATION RATES FROM 80- 93% METRONIDAZOLE RESISTANCE IS HIGH UPTO 43% RE INFECTION CAN OCCUR NOT RECOMMENDED FOR ASYMPTOMATIC PATIENTS SEVERAL TRIPLE THERAPY REGIMENS . FDA APPROVED REGIMEN BISMUTH+METRONIDAZOLE+TETRACYCLINE+ PPI X10 D LANZOPRAZOLE+AMOXICILLIN+CLARITHROMYCIN X2W . 2/13/2018 32

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34. QUADRUPLE THERAPY 2/13/2018 34

35. HELICOBACTER PYLORI INFECTION : ASSOCIATED DISEASES DUODENAL ULCER GASTRIC ULCER CHRONIC ATROPHIC GASTRITIS (TYPE B) GASTRIC ADENOCARCINOMA MALT ( MUCOSA ASSOCIATED LYMPHOID TISSUE ) LYMPHOMA 2/13/2018 35

36. Stress ulcers GASTRIC MUCOSAL ISCHAEMIA WITH SUPERFICIAL ULCERATIONS DUE TO UNDERLYING ILLNESS SUCH AS: TRAUMA,SEPSIS AND BURNS THESE ARE EXTREME STRESSFUL SITUATIONS HAEMORRHAGE OCCURS 3-7 DAYS AFTER INJURY IN B UR NS WE CALL IT C UR LING’S ULCER , SECONDARY TO LOSS OF PLASMA VOLUME CUSHING’S ULCER , SEEN IN HEAD INJURY,CAN BE DEEP AND CAN PERFORATE CUSHING’S TRIAD: HTN, WIDENED PULSE PRESSURE,BRADYCARDIA PROPHYLAXIS : MAINTAIN GASTRIC LUMINAL pH >4 ENDOSCOPIC OR SURGICAL THERAPY IS RARELY NECESSARY 2/13/2018 36

37. ZOLLINGER-ELLISON SYNDROME ZES IS A RARE DISORDER THAT CAN CAUSE GASTRODUODENAL ULCERS (USUALLY MULTIPLE) FROM EXCESSIVE ACID SECRETION. HYPERSECRETION OF GASTRIN FROM TUMORS IN THE PANCREAS, DUODENAL WALL ,OR PERIPANCREATIC TISSUE(GASTRINOMA TRIANGLE) MULTIPLE ULCERS IN THE STOMACH,DUODENUM AND JEJUNUM,MAY BE REFRACTORY TO TREATMENT DIARRHOEA DUE TO HIGH VOLUME OF GASTRIC ACID 2/3 OF GASTRINOMAS ARE MALIGNANT TWO TYPES MEN -1 A FAMILIAL AUTOSOMAL DOMINANT SYNDROME. ZOLLINGER-ELLISON SYNDROME MAY STILL OCCUR SPORADICALLY 2/13/2018 37

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39. ZE SYNDROME CONSIDER ZES IF A PATIENT HAS SEVERE PEPTIC ULCERATION, KIDNEY STONES, WATERY DIARRHEA, OR MALABSORPTION. ZES : FASTING S. GASTRIN LEVELS > 1000 PG/ML; GASTRIC pH <2 AND BASAL GASTRIC ACID HYPERSECRETION > 10 MEQ/H. SECRETIN STIMULATION TEST FAILS TO SUPPRESS GASTRIN SECRETION PPI SHOULD BE DISCONTINUED AT LEAST 2 WEEKS BEFORE THE GASTRIN LEVEL IS MEASURED. LOCALISATION OF TUMOR: EUS, CT SCAN, ANGIOGRAPHY,SURGICAL EXPLORATION SOMATOSTATIN RECEPTOR SCINTIGRAPHY : IT IS THE IMAGING STUDY OF CHOICE : IS THE MOST SENSITIVE IMAGING MODALITY FOR THE DETECTION OF BOTH PRIMARY AND METASTATIC TUMORS. 2/13/2018 39

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41. Z-E SYNDROME HIGH DOSE PROTON PUMP INHIBITORS ARE THE MAIN MEDICATIONS USED IN THE CONTROL OF GASTRIC ACID HYPERSECRETION PARIETAL CELL VAGOTOMY FOR GASTRIC HYPERSECRETION SURGICAL TREATMENT OF THE TUMOR IS THE MAIN THERAPY SURGERY RARELY CURES THE CONDITION IN MEN TYPE 1 INTERFERON, OCTREOTIDE  AND CHEMOTHERAPY MAY BE USED IN THE MANAGEMENT OF PATIENTS WITH METASTATIC DISEASE. 2/13/2018 41

42. GASTRITIS VS.PUD #3 MOST COMMONLY DIAGNOSED CAUSE OF EPIGASTRIC PAIN MORE GENERALISED INFLAMMATION OF THE STOMACH TISSUE GASTRITIS CAN BE ACUTE OR CHRONIC CLINICALLY VERY DIFFICULT TO DIFFERENTIATE FROM PUD LIKE PUD: OFTEN PRESENTS WITH EPIGASTRIC PAIN, CAN BE CAUSED BY ALL THE SAME THINGS esp. NSAIDs AND H.PYLORI PATIENT MAY HAVE HEMATEMESIS OR MELENA 2/13/2018 42

43. GASTRITIS V s . pud UNLIKE PUD GASTRITIS MAY ALSO BE CAUSED BY Et OH, TOBACCO, VIT B12 DEFICIENCY, AND A SPECIAL CONDITION ATROPHIC GASTRITIS MUST BE WARY OF ALL THE SAME ALARM SYMPTOMS; IF PRESENT PROCEED TO ENDOSCOPY 2/13/2018 43

44. gastritis DIAGNOSIS : FIRST STEP FOR PATIENTS WITH NO ALARM Sx. IS TO TEST FOR H.PYLORI SEROLOGY PATIENTS SHOULD ALSO HAVE CBC,CMP,B12 AND MMA REDUCE RISK FACTORS: TOBACCO CESSATION,ETOH AVOIDANCE POSITIVE H.PYLORI : START TRIPLE THERAPY NEGATIVE H.PYLORI: PPI LOW B12 AND OR HIGH MMA: B12 REPLACEMENT ANTI PARIETAL CELL ANTIBODIES : B12 REPLACEMENT 2/13/2018 44

45. ATROPHIC GASTRITIS ATROPHIC GASTRITIS  IS A PROCESS OF CHRONIC INFLAMMATION  LEADS TO LOSS OF GASTRIC GLANDULAR CELLS AND THEIR EVENTUAL REPLACEMENT BY INTESTINAL AND FIBROUS TISSUES. IT CAN BE CAUSED BY PERSISTENT INFECTION WITH H.PYLORI (TYPE B) OR CAN BE A UTOIMMUNE IN ORIGIN (TYPE A ) 2/13/2018 45

46. ATROPHIC GASTRITIS: EMAG / AMAG THE END STAGE OF CHRONIC GASTRITIS REQUIRES ENDOSCOPY AND BIOPSY FOR DIAGNOSIS (DECREASED RUGAL FOLDS) CHRONIC INFLAMMATION DAMAGES THE PARIETAL CELLS AND THEREFORE EVERYTHING THAT THE PARIETAL CELLS SECRETE WILL BE REDUCED ACHLORHYDRIA/HYPOCHLORHYDRIA LOW B12 LEVELS DUE TO DECREASED INTRINSIC FACTOR SECRETION INCREASED RISK OF GASTRIC CARCINOMA 2/13/2018 46

47. CHRONIC ATROPHIC A UTOIMMUNE GASTRITIS TYPE A GASTRITIS WITH ATROPHIC MUCOSA INVOLVING THE BODY AND FUNDUS AUTO ANTIBODIES KNOCKING OUT THE PARIETAL CELLS PERNICIOUS ANEMIA WITH ACHLORHYDRIA MAY RESULT ANTI PARIETAL CELL ANTIBODIES FOUND IN 90% OTHER AUTOIMMUNE DISEASES OFTEN PRESENT ASSOCIATED WITH CARCINOID SYNDROME, GASTRIC METAPLASIA, AND GASTRIC ADENOCARCINOMA 2/13/2018 47

48. CHRONIC GASTRITIS TYPE A TYPE B INVOLVES ANTRUM AND FUNDUS INVOLVES ANTRUM USUALLY AUTOIMMUNE ASSOCIATED WITH HELICO B ACTER PYLORI NORMAL SERUM GASTRIN INCREASED INCIDENCE OF GASTRIC AND DUODENAL ADENOCARCINOMA , MALTOMA 2/13/2018 48

49. GASTRITIS DUE TO B12 DEFICIENCY GASTRITIS CAUSED BY LOW B12 LEVELS HISTORY: MALNUTRITION , ALCOHOLISM SYMPTOMS: EPIGASTRIC PAIN FATIGUE PALLOR REDUCED PERIPHERAL VIBRATION DIAGNOSIS B12 LEVELS WILL BE LOW MMA LEVELS WILL BE HIGH THERE WILL BE A MACROCYTIC ANEMIA WITH MCV >100 ANTI PARIETAL CELL ABS. NEGATIVE SO ALSO NEGATIVE ANTI INTRINSIC FACTOR ANTIBODIES TREATMENT: B12 REPLACEMENT 2/13/2018 49

50. NON ULCER DYSPEPSIA FUNCTIONAL DYSPEPSIA IS A DIAGNOSIS OF EXCLUSION . PATIENTS WILL HAVE CHRONIC PERSISTENT EPIGASTRIC PAIN A THOROUGH EVALUATION SHOWS NO ORGANIC DISEASE. PATIENTS MAY PRIMARILY HAVE EPIGASTRIC PAIN, AS ULCER LIKE DYSPEPSIA , OR THEY MAY HAVE SYMPTOMS OF POSTPRANDIAL BLOATING, WHICH IS REFERRED TO AS MOTILITY-LIKE DYSPEPSIA . DO ALCOHOL AND TOBACCO CAUSE ULCERS? NO . THEY DELAY HEALING 2/13/2018 50

51. CROHN’S CROHN’S ULCERATION CAN INVOLVE ANY PART OF THE GI TRACT FROM THE BUCCAL MUCOSA TO THE RECTUM. ISOLATED CROHN ULCERATION OF THE STOMACH IS RARE, ALTHOUGH IT MAY CAUSE DUODENAL OR ILEAL ULCERATIONS. 2/13/2018 51

52. CONCLU SIONS FIRST STEP FOR PATIENTS WITH NO ALARM Sx. IS TO TEST FOR H.PYLORI SEROLOGY POSITIVE H.PYLORI : START TRIPLE THERAPY NEGATIVE H.PYLORI: PPI ERADICATION OF HP INFECTION ALTERS THE NATURAL HISTORY OF PEPTIC ULCER DISEASE. SUCCESSFUL ERADICATION REDUCES PUD RECURRENCE UNLESS NSAID USE IS PRESENT. PERSISTENT SYMPTOMS AFTER 2 WEEKS OF THERAPY SUGGEST AN ALTERNATIVE DIAGNOSIS. PATIENTS SHOULD ALSO HAVE CBC,CMP,B12 AND MMA LOW B12 AND OR HIGH MMA: B12 REPLACEMENT ANTI PARIETAL CELL ANTIBODIES : B12 REPLACEMENT 2/13/2018 52

53. TAKE HOME MESSAGE PUD PATIENTS WITHOUT ALARM SYMPTOMS SHOULD BE TESTED FOR H.PYLORI WITH SEROLOGY . PATIENTS WITH ALARM SYMPTOMS SHOULD RECEIVE ENDOSCOPY. ACTIVE BLEEDING SHOULD GET SCOPED RIGHT AWAY REFERRAL TO THE GE SHOULD OCCUR FOR ALL PATIENTS WITH SIGNS AND SYMPTOMS OF COMPLICATED ULCER DISEASE AND FOR PATIENTS WHO FAIL INITIAL THERAPY BASED ON A NONINVASIVE HP TEST. 2/13/2018 53

54. REFERENCES PEPTIC ULCER DISEASE:MEDSCAPE Author: BS Anand, MD; Chief Editor: Julian Katz, MD, [Guideline] Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG clinical guideline: treatment of Helicobacter pylori infection.  Am J Gastroenterol . 2017 Jan 10. Ramakrishnan K, Salinas RC. Peptic ulcer disease.  Am Fam Physician . 2007 Oct 1. 76 (7):1005-12.  [Medline] . Yang M, He M, Zhao M, et al. Proton pump inhibitors for preventing non-steroidal anti-inflammatory drug induced gastrointestinal toxicity: a systematic review.  Curr Med Res Opin . 2017 Jan 25. 1-8.  Kajihara Y, Shimoyama T, Mizuki I. Analysis of the cost-effectiveness of using vonoprazan-amoxicillin-clarithromycin triple therapy for first-line Helicobacter pylori eradication.  Scand J Gastroenterol . 2017 Feb. 52 (2):238-41.  [Medline] . Peptic Ulcer Disease and Gastritis - CRASH! Medical Review Series Paul W. Bolin Lecturio e- learning 2/13/2018 54