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PEPTIC ULCER AND GASTRITIS
DR.RISHIKESAN K.V
SPECIALIST PHYSICIAN
VENNIYIL MEDICAL CENTRE
SHARJAH
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
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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)
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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
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GASTRIC MUCOSAL DEFENCE MECHANISMS
SEVERAL MUCOSAL DEFENCE MECHANISM PROTECT THE GASTRIC MUCOSA AGAINST ACID
AND NOXIOUS AGENTS
MAINLY A THREE-TIER SYSTEM OPERATES :
1. 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
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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
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MoI….
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
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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:
o SYSTEMIC MASTOCYTOSIS,
o BASOPHILIC LEUKAEMIAS,
o HYPERPARATHYROIDISM,
o CYSTIC FIBROSIS,
o SHORT BOWEL SYNDROME
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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
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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
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ALARM SYMPTOMS
o WEIGHT LOSS OF MORE THAN 10% IN 3 MONTHS
o ANEMIA
o HEME POSITIVE STOOL OR HAEMATEMESIS
o EARLY SATIETY
o ODYNOPHAGIA OR DYSPHAGIA
oOLDER THAN AGE 45 YEARS
o ABNORMAL PHYSICAL EXAMINATIONS
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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
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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.
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GASTRIC OUTLET
OBSTRUCTION
GASTRIC OUTLET OBSTRUCTION : RARE
COMPLICATION
SYMPTOMS
EARLY SATIETY
WEIGHT LOSS
VOMITING
DIAGNOSIS BY SCOPY
TREATMENT : SURGICAL
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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.
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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
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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
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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
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NSAID ASSOCIATED PEPTIC ULCER DISEASE
GUs ARE VISIBLE IN 30% OF PATIENTS ACTIVELY TAKING NSAIDS
THERE ARE TWO OPPOSING TRENDS:
1. H.PYLORI RECOGNITION AND TREATMENT: PUD REDUCED
2. 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
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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
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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
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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
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HELICOBACTER PYLORI INFECTION
oHELICOBACTER PYLORI INFECTION IS ASSOCIATED WITH BOTH TYPES OF PUD.
o 90% OF THE PEOPLE AFFECTED WITH PUD APPEAR TO BE POSITIVE FOR H.PYLORI
INFECTION.
o GRAM NEGATIVE SPIRAL SHAPED,FLAGELLATED BACILLUS
oFECO-ORAL TRANSMISSION
o PREVALENCE INCREASES WITH AGE: > 50% INFECTION AMONG THE GENERAL
POPULATION >60 YEARS
o HIGH PREVALENCE IN DEVELOPING COUNTRIES
oRISK FACTORS INCLUDE LOW SOCIOECONOMIC STATUS, DOMESTIC
CROWDING , INSTITUTIONALISATON
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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
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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:
1. CHRONIC GASTRITIS
2. ATROPHIC GASTRITIS
3. METAPLASIA OF THE INTESTINE, WHICH MAY EVOLVE INTO
DYSPLASIA
4. ADENOCARCINOMA OF THE STOMACH
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GASTRIC ULCERATION BY H.PYLORI
1. ADHERENCE AND
PENETRATION
2. AMMONIA PRODUCTION
3. PROLIFERATION, MIGRATION
and FORMATION OF
INFECTIOUS FOCUS
4. ULCERATION by
DESTRUCTION OF MUCOSA,
INFLAMMATION AND
MUCOSAL CELL DEATH
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TEST FOR H.PYLORI
THREE COMMONLY USED WAYS
1. SEROLOGY : MOST SENSITIVE IgG ANTIBODY ,ALWYS REMAIN POSITIVE AFTER
ERADICATION
2. GASTRIC BIOPSY: UREASE TEST - INSTANT RESULT,LOW COST MOST SPECIFIC, BUT
REQUIRES ENDOSCOPY
3. 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
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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
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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
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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.
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QUADRUPLE THERAPY
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HELICOBACTER PYLORI INFECTION : ASSOCIATED
DISEASES
1. DUODENAL ULCER
2. GASTRIC ULCER
3. CHRONIC ATROPHIC GASTRITIS (TYPE B)
4. GASTRIC ADENOCARCINOMA
5. MALT ( MUCOSA ASSOCIATED LYMPHOID TISSUE ) LYMPHOMA
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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 BURNS WE CALL IT CURLING’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
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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
1. MEN -1 A FAMILIAL AUTOSOMAL DOMINANT SYNDROME.
2. ZOLLINGER-ELLISON SYNDROME MAY STILL OCCUR SPORADICALLY
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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.
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Z-E SYNDROME
oHIGH DOSE PROTON PUMP INHIBITORS ARE THE MAIN
MEDICATIONS USED IN THE CONTROL OF GASTRIC ACID
HYPERSECRETION
o PARIETAL CELL VAGOTOMY FOR GASTRIC HYPERSECRETION
oSURGICAL TREATMENT OF THE TUMOR IS THE MAIN THERAPY
o SURGERY RARELY CURES THE CONDITION IN MEN TYPE 1
o INTERFERON, OCTREOTIDE AND
CHEMOTHERAPY MAY BE USED IN THE MANAGEMENT OF PATIENTS WITH
METASTATIC DISEASE.
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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
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GASTRITIS Vs. 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
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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
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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.
1. IT CAN BE CAUSED BY PERSISTENT
INFECTION WITH H.PYLORI (TYPE B) OR
2. CAN BE AUTOIMMUNE IN ORIGIN (TYPE
A)
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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
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CHRONIC ATROPHIC AUTOIMMUNE 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
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CHRONIC GASTRITIS
TYPE A TYPE B
INVOLVES ANTRUM AND FUNDUS INVOLVES ANTRUM
USUALLY AUTOIMMUNE ASSOCIATED WITH HELICOBACTER PYLORI
NORMAL SERUM GASTRIN
INCREASED INCIDENCE OF GASTRIC AND DUODENAL
ADENOCARCINOMA , MALTOMA
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GASTRITIS DUE TO B12 DEFICIENCY
GASTRITIS CAUSED BY LOW B12 LEVELS
HISTORY: MALNUTRITION ,
ALCOHOLISM
SYMPTOMS:
EPIGASTRIC PAIN
FATIGUE
PALLOR
REDUCED PERIPHERAL VIBRATION
DIAGNOSIS
oB12 LEVELS WILL BE LOW
oMMA LEVELS WILL BE HIGH
oTHERE WILL BE A MACROCYTIC
ANEMIA WITH MCV >100
oANTI PARIETAL CELL ABS. NEGATIVE
oSO ALSO NEGATIVE ANTI INTRINSIC
FACTOR ANTIBODIES
oTREATMENT: B12 REPLACEMENT
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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
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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.
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CONCLUSIONS
o FIRST STEP FOR PATIENTS WITH NO ALARM Sx. IS TO TEST FOR H.PYLORI SEROLOGY
o POSITIVE H.PYLORI : START TRIPLE THERAPY
o NEGATIVE H.PYLORI: PPI
o ERADICATION OF HP INFECTION ALTERS THE NATURAL HISTORY OF PEPTIC ULCER
DISEASE.
o SUCCESSFUL ERADICATION REDUCES PUD RECURRENCE UNLESS NSAID USE IS
PRESENT.
o PERSISTENT SYMPTOMS AFTER 2 WEEKS OF THERAPY SUGGEST AN ALTERNATIVE
DIAGNOSIS.
o PATIENTS SHOULD ALSO HAVE CBC,CMP,B12 AND MMA
o LOW B12 AND OR HIGH MMA: B12 REPLACEMENT
o ANTI PARIETAL CELL ANTIBODIES : B12 REPLACEMENT
4/20/2018
52
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.
4/20/2018
53
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
4/20/2018
54

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Peptic ulcer and gastritis

  • 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 4/20/2018 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) 4/20/2018 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 4/20/2018 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 : 1. 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 4/20/2018 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 4/20/2018 6
  • 7. MoI…. 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 4/20/2018 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: o SYSTEMIC MASTOCYTOSIS, o BASOPHILIC LEUKAEMIAS, o HYPERPARATHYROIDISM, o CYSTIC FIBROSIS, o SHORT BOWEL SYNDROME 4/20/2018 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 4/20/2018 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 4/20/2018 10
  • 11. ALARM SYMPTOMS o WEIGHT LOSS OF MORE THAN 10% IN 3 MONTHS o ANEMIA o HEME POSITIVE STOOL OR HAEMATEMESIS o EARLY SATIETY o ODYNOPHAGIA OR DYSPHAGIA oOLDER THAN AGE 45 YEARS o ABNORMAL PHYSICAL EXAMINATIONS 4/20/2018 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 4/20/2018 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. 4/20/2018 13
  • 15. GASTRIC OUTLET OBSTRUCTION GASTRIC OUTLET OBSTRUCTION : RARE COMPLICATION SYMPTOMS EARLY SATIETY WEIGHT LOSS VOMITING DIAGNOSIS BY SCOPY TREATMENT : SURGICAL 4/20/2018 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. 4/20/2018 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 4/20/2018 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 4/20/2018 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 4/20/2018 19
  • 20. NSAID ASSOCIATED PEPTIC ULCER DISEASE GUs ARE VISIBLE IN 30% OF PATIENTS ACTIVELY TAKING NSAIDS THERE ARE TWO OPPOSING TRENDS: 1. H.PYLORI RECOGNITION AND TREATMENT: PUD REDUCED 2. 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 4/20/2018 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 4/20/2018 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 4/20/2018 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 4/20/2018 23
  • 24. HELICOBACTER PYLORI INFECTION oHELICOBACTER PYLORI INFECTION IS ASSOCIATED WITH BOTH TYPES OF PUD. o 90% OF THE PEOPLE AFFECTED WITH PUD APPEAR TO BE POSITIVE FOR H.PYLORI INFECTION. o GRAM NEGATIVE SPIRAL SHAPED,FLAGELLATED BACILLUS oFECO-ORAL TRANSMISSION o PREVALENCE INCREASES WITH AGE: > 50% INFECTION AMONG THE GENERAL POPULATION >60 YEARS o HIGH PREVALENCE IN DEVELOPING COUNTRIES oRISK FACTORS INCLUDE LOW SOCIOECONOMIC STATUS, DOMESTIC CROWDING , INSTITUTIONALISATON 4/20/2018 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 4/20/2018 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: 1. CHRONIC GASTRITIS 2. ATROPHIC GASTRITIS 3. METAPLASIA OF THE INTESTINE, WHICH MAY EVOLVE INTO DYSPLASIA 4. ADENOCARCINOMA OF THE STOMACH 4/20/2018 26
  • 27. GASTRIC ULCERATION BY H.PYLORI 1. ADHERENCE AND PENETRATION 2. AMMONIA PRODUCTION 3. PROLIFERATION, MIGRATION and FORMATION OF INFECTIOUS FOCUS 4. ULCERATION by DESTRUCTION OF MUCOSA, INFLAMMATION AND MUCOSAL CELL DEATH 4/20/2018 27
  • 29. TEST FOR H.PYLORI THREE COMMONLY USED WAYS 1. SEROLOGY : MOST SENSITIVE IgG ANTIBODY ,ALWYS REMAIN POSITIVE AFTER ERADICATION 2. GASTRIC BIOPSY: UREASE TEST - INSTANT RESULT,LOW COST MOST SPECIFIC, BUT REQUIRES ENDOSCOPY 3. 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 4/20/2018 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 4/20/2018 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 4/20/2018 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. 4/20/2018 32
  • 35. HELICOBACTER PYLORI INFECTION : ASSOCIATED DISEASES 1. DUODENAL ULCER 2. GASTRIC ULCER 3. CHRONIC ATROPHIC GASTRITIS (TYPE B) 4. GASTRIC ADENOCARCINOMA 5. MALT ( MUCOSA ASSOCIATED LYMPHOID TISSUE ) LYMPHOMA 4/20/2018 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 BURNS WE CALL IT CURLING’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 4/20/2018 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 1. MEN -1 A FAMILIAL AUTOSOMAL DOMINANT SYNDROME. 2. ZOLLINGER-ELLISON SYNDROME MAY STILL OCCUR SPORADICALLY 4/20/2018 37
  • 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. 4/20/2018 39
  • 41. Z-E SYNDROME oHIGH DOSE PROTON PUMP INHIBITORS ARE THE MAIN MEDICATIONS USED IN THE CONTROL OF GASTRIC ACID HYPERSECRETION o PARIETAL CELL VAGOTOMY FOR GASTRIC HYPERSECRETION oSURGICAL TREATMENT OF THE TUMOR IS THE MAIN THERAPY o SURGERY RARELY CURES THE CONDITION IN MEN TYPE 1 o INTERFERON, OCTREOTIDE AND CHEMOTHERAPY MAY BE USED IN THE MANAGEMENT OF PATIENTS WITH METASTATIC DISEASE. 4/20/2018 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 4/20/2018 42
  • 43. GASTRITIS Vs. 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 4/20/2018 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 4/20/2018 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. 1. IT CAN BE CAUSED BY PERSISTENT INFECTION WITH H.PYLORI (TYPE B) OR 2. CAN BE AUTOIMMUNE IN ORIGIN (TYPE A) 4/20/2018 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 4/20/2018 46
  • 47. CHRONIC ATROPHIC AUTOIMMUNE 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 4/20/2018 47
  • 48. CHRONIC GASTRITIS TYPE A TYPE B INVOLVES ANTRUM AND FUNDUS INVOLVES ANTRUM USUALLY AUTOIMMUNE ASSOCIATED WITH HELICOBACTER PYLORI NORMAL SERUM GASTRIN INCREASED INCIDENCE OF GASTRIC AND DUODENAL ADENOCARCINOMA , MALTOMA 4/20/2018 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 oB12 LEVELS WILL BE LOW oMMA LEVELS WILL BE HIGH oTHERE WILL BE A MACROCYTIC ANEMIA WITH MCV >100 oANTI PARIETAL CELL ABS. NEGATIVE oSO ALSO NEGATIVE ANTI INTRINSIC FACTOR ANTIBODIES oTREATMENT: B12 REPLACEMENT 4/20/2018 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 4/20/2018 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. 4/20/2018 51
  • 52. CONCLUSIONS o FIRST STEP FOR PATIENTS WITH NO ALARM Sx. IS TO TEST FOR H.PYLORI SEROLOGY o POSITIVE H.PYLORI : START TRIPLE THERAPY o NEGATIVE H.PYLORI: PPI o ERADICATION OF HP INFECTION ALTERS THE NATURAL HISTORY OF PEPTIC ULCER DISEASE. o SUCCESSFUL ERADICATION REDUCES PUD RECURRENCE UNLESS NSAID USE IS PRESENT. o PERSISTENT SYMPTOMS AFTER 2 WEEKS OF THERAPY SUGGEST AN ALTERNATIVE DIAGNOSIS. o PATIENTS SHOULD ALSO HAVE CBC,CMP,B12 AND MMA o LOW B12 AND OR HIGH MMA: B12 REPLACEMENT o ANTI PARIETAL CELL ANTIBODIES : B12 REPLACEMENT 4/20/2018 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. 4/20/2018 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 4/20/2018 54