jr pud presentation

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The digestive

system

includes the

organs that

ingest food,

transport food,

digest the food into smaller

usable

components,

absorb the

nutr ients, and

expel the waste

products from

the body.



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Stomach



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Gastric

ruga

e allowstretching of

the stomach

Note greater and

lesser curvatures



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GastritisGastritis Acute Gastritis Acute Gastritis is an inflammation of theis an inflammation of thegastric mucosa.gastric mucosa.

GastropathyGastropathy: epithelial or endothelial: epithelial or endothelialdamage without inflammationdamage without inflammation

Gastritis has 3 basic types:Gastritis has 3 basic types: ± ± Acute (erosive/ hemorrhagic) Acute (erosive/ hemorrhagic)

± ± NonNon--erosive, Nonerosive, Non--specific/Chronicspecific/Chronic

± ± Special FormsSpecial Forms



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Acute Gastritis Acute Gastritis

(Erosive/Hemorrhagic)(Erosive/Hemorrhagic)

Most common causes:Most common causes: ± ± NSAIDS gastric injury by diminishingNSAIDS gastric injury by diminishing

prostaglandin production in stomach andprostaglandin production in stomach and

duodenumduodenum ± ± Alcohol use is the Alcohol use is the leading cause of gastritisleading cause of gastritis

± ± Stress from CNS injury burns, sepsis, surgeryStress from CNS injury burns, sepsis, surgery

± ± Portal hypertension (portal gastropathy)Portal hypertension (portal gastropathy)

Other causes:Other causes:

± ± ingestioningestion

± ± radiationradiation



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Chronic GastritisChronic Gastritis

Nonerosive/nonspecificNonerosive/nonspecificInfectious gastritis Type B:Infectious gastritis Type B: H Pylori H Pylori ± ± Involves antrum and body of stomachInvolves antrum and body of stomach

majority of patients asymptomaticmajority of patients asymptomatic

± ± Strong association with PUDStrong association with PUD ± ± 2 to 6 fold risks of gastric adenocarcinoma and also2 to 6 fold risks of gastric adenocarcinoma and alsogastric lymphomagastric lymphoma

Autoimmune gastritis Type A: Pernicious anemia Autoimmune gastritis Type A: Pernicious anemia ± ± Body and fundus, It usually spares the antrum & affectsBody and fundus, It usually spares the antrum & affects

the parietal cells.the parietal cells. ± ± Pernicious anemia caused by impaired absorption of Pernicious anemia caused by impaired absorption of

vitamin Bvitamin B--1212 occurs due to lack of intrinsic factor fromoccurs due to lack of intrinsic factor fromparietal cells and decrease in acid productionparietal cells and decrease in acid production

± ± Increased risk of adenocarcinomaIncreased risk of adenocarcinoma



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Special forms of GastritisSpecial forms of Gastritis

Infectious (Phlegmonous or necrotizing gastritis)Infectious (Phlegmonous or necrotizing gastritis) ± ± Emergency gastric resection, and Abx therapyEmergency gastric resection, and Abx therapy

± ± CMV, candidal (fungal) in immunocompromised pt¶sCMV, candidal (fungal) in immunocompromised pt¶s

± ± Larvae ingestion requires endoscopic removalLarvae ingestion requires endoscopic removal

Eosinophilic GastritisEosinophilic Gastritis

Giant Cell (Menetrier¶s disease) (HypertrophicGiant Cell (Menetrier¶s disease) (HypertrophicGastropathy)Gastropathy) ± ± only found on biopsyonly found on biopsy

Lymphocytic GastritisLymphocytic Gastritis

Granulomatous GastritisGranulomatous Gastritis ± ± TuberculosisTuberculosis

± ± SyphilisSyphilis

± ± FungalFungal

± ± SarcoidSarcoid

± ± Crohn¶sCrohn¶s



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GastritisGastritisLab:Lab: ± ± Endoscopy c/ biopsy is the gold standardEndoscopy c/ biopsy is the gold standard

± ± A urea breath test A urea breath test

± ± Specific test for underlying conditions (e.g) B12 and CBC for Specific test for underlying conditions (e.g) B12 and CBC for pernicious anemiapernicious anemia

Differential Diagnosis:Differential Diagnosis: ± ± 1. Peptic ulcer 1. Peptic ulcer 2. Gastroparesis2. Gastroparesis

± ± 3. Gastric carcinoma3. Gastric carcinoma 4. GERD4. GERD

± ± 5. Pancreatitis5. Pancreatitis 6. Lymphoma6. Lymphoma

Treatment:Treatment: (same as duodenal ulcers)(same as duodenal ulcers)

± ± Remove irritantRemove irritant

± ± Treat for H pyloriTreat for H pylori

± ± Antacids & H2 blockers Antacids & H2 blockers

± ± Avoid smoking & alcohol Avoid smoking & alcohol



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Peptic Ulcer DiseasePeptic Ulcer Disease

DefinitionDefinition: PUD is describes: PUD is describesany ulcer of the upperany ulcer of the upperdigestive tract.digestive tract. (duodenal #(duodenal #1)1)

and stomachand stomach (gastric #2)(gastric #2)Break in the duodenal orBreak in the duodenal or

gastric mucosa extendinggastric mucosa extendingthrough the muscularisthrough the muscularis

mucosae, and are usuallymucosae, and are usually5mm5mm--1cm.1cm.



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R ead about peptic ulcers

in the clinical view in the

text



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Zollinger Zollinger--Ellison SyndromeEllison Syndrome

UlcersUlcers--associatedassociated

with thewith the Zollinger Zollinger--

Ellison (ZE)Ellison (ZE)Syndrome (#3Syndrome (#3) are) are

caused by gastrincaused by gastrin--

releasing islet cellreleasing islet cell

tumors (gastrinomas),tumors (gastrinomas),

& are also considered& are also considered

a form of peptic ulcer.a form of peptic ulcer.



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Zollinger Zollinger--Ellison SyndromeEllison Syndrome A tumor of the pancreas that secretes gastrin A tumor of the pancreas that secretes gastrin

((Gastrinoma)Gastrinoma)

Usually found in head of pancreas but can alsoUsually found in head of pancreas but can alsobe found in duodenum, liver & lungbe found in duodenum, liver & lung

7575--80% of ulcers produced develop in the80% of ulcers produced develop in theduodenal bulbduodenal bulb

Suspect in any patient with:Suspect in any patient with: ± ± Multiple or recurring duodenal ulcersMultiple or recurring duodenal ulcers

± ± Post bulbar or jejunal ulcersPost bulbar or jejunal ulcers

± ± Ulcers associated with diarrheaUlcers associated with diarrhea

± ± Elevated serum gastrin levelsElevated serum gastrin levels

Usually only tested when suspect ZE syndromeUsually only tested when suspect ZE syndrome



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Peptic Ulcer Disease (PUD)Peptic Ulcer Disease (PUD)

Men 3 : 1 WomenMen 3 : 1 Women

Most commonly occur inMost commonly occur in::

± ± #1 Duodenum (Duodenal)#1 Duodenum (Duodenal)

± ± #2 Stomach (Gastric)#2 Stomach (Gastric)

± ± EsophagusEsophagus

± ± GastroentericGastroentericanastomosesanastomoses

± ± Meckel¶s DiverticulumMeckel¶s Diverticulum



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PUDPUDThe spectrum of the disease is broad from mild mucosalThe spectrum of the disease is broad from mild mucosalinjury to frank ulcerations.injury to frank ulcerations.

Symptoms vary and are not related to the severity of Symptoms vary and are not related to the severity of tissue damage.tissue damage.

11--2% of population have an ulcer at the present time2% of population have an ulcer at the present time

10% of population will have ulcer in their lifetime10% of population will have ulcer in their lifetime

Gastric and Duodenal ulcers tend to recur in the sameGastric and Duodenal ulcers tend to recur in the same

location.location.

Recurrent hemorrhage occurs in 50% of patients whoRecurrent hemorrhage occurs in 50% of patients whohave had a prior bleed.have had a prior bleed.



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Duodenal Ulcer vs. Gastric Ulcer Duodenal Ulcer vs. Gastric Ulcer

DuodenalDuodenal ± ± Increased acidIncreased acid

productionproduction

± ± H. pyloriH. pylori

± ± relieved by foodrelieved by food &&

typically awakenstypically awakens

patient around 1:00ampatient around 1:00am

GastricGastric ± ± Normal or decreasedNormal or decreased

acid productionacid production

± ± Decreased mucosalDecreased mucosal

resistanceresistance

± ± H. pyloriH. pylori

± ± NSAIDSNSAIDS

± ± worsened by foodworsened by food



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Duodenal Vs. Gastric (cont)Duodenal Vs. Gastric (cont)DuodenalDuodenal

± ± Onset more common age 25Onset more common age 25to 55to 55

± ± never malignantnever malignant

± ± mostly located in the duodenalmostly located in the duodenal

bulb or immediately post bulbar.bulb or immediately post bulbar. ± ± Ulcers distal to the duodenalUlcers distal to the duodenalbulb should raise suspicion for bulb should raise suspicion for Zollinger Zollinger--Ellison SyndromeEllison Syndrome(also c/ multiple frequently(also c/ multiple frequentlyoccurring duodenal ulcers.)occurring duodenal ulcers.)

± ± Men 3:1 WomenMen 3:1 Women

± ± Duodenal 5 times moreDuodenal 5 times morecommon than gastriccommon than gastric

± ± 6060--80% have recurrence within80% have recurrence withinone year.one year.

GastricGastric ± ± Onset more common ageOnset more common age

40 to 7040 to 70

± ± BenignBenign more likely @more likely @lesser curvature/lesser curvature/ antrumantrum

± ± Gastric ulcers are moreGastric ulcers are morecommon @ lesser common @ lesser curvaturecurvature

± ± Malignancies more likelyMalignancies more likely

@ greater curvature@ greater curvature

± ± 11--3% occur in carcinomas3% occur in carcinomas



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PUD EtiologiesPUD Etiologies

1.1. Helicobacter pylori (H. pylori) infection: (#1 cause)Helicobacter pylori (H. pylori) infection: (#1 cause)

± ± A. Associated c/ 70 A. Associated c/ 70--95% of Peptic ulcers.95% of Peptic ulcers.

± ± B. Treatment of H. pylori improves healing rate & markedlyB. Treatment of H. pylori improves healing rate & markedly

decreases the recurrence rate.decreases the recurrence rate.

2.2. NSAIDS: (#2 cause)NSAIDS: (#2 cause) (inhibit prostaglandins which normally(inhibit prostaglandins which normally

stimulate production of mucous secretions & bicarb.)stimulate production of mucous secretions & bicarb.)

± ± A. may cause gastric or duodenal ulcers (steroids also) A. may cause gastric or duodenal ulcers (steroids also)

± ± B. accounts for the majority of non H. pylori ulcersB. accounts for the majority of non H. pylori ulcers



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PUD Etiologies (cont)PUD Etiologies (cont)

3.3.H

ypersecretion states: (#3 althoughH

ypersecretion states: (#3 althoughuncommon)uncommon) ± ± Gastrinomas (Zollinger Gastrinomas (Zollinger--Ellison Syndrome)Ellison Syndrome)

± ± Multiple endocrine neoplasia (MENMultiple endocrine neoplasia (MEN--1)1)

4. Stress:4. Stress: physiologic stressphysiologic stress (eg. Burns,(eg. Burns,surgery, & severe medical conditions)surgery, & severe medical conditions)

5. Rare causes: viral, radiation, vascular insuff.5. Rare causes: viral, radiation, vascular insuff.

Diseases assoc. c/ peptic ulcers:Diseases assoc. c/ peptic ulcers: ± ± Cirrhosis, renal failure, pulmonary ds.Cirrhosis, renal failure, pulmonary ds.

Any pt. c/ systemic ds. (COPD, renal failure, cirrhosis of liver) Any pt. c/ systemic ds. (COPD, renal failure, cirrhosis of liver)are prone to ulcers so should be started on H2 blockers.are prone to ulcers so should be started on H2 blockers.



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The pathogenesis of PUD is related to theThe pathogenesis of PUD is related to the

imbalance between normal protective factors andimbalance between normal protective factors and

injurious factorsinjurious factorsNo Ulcer No Ulcer

± ± NormalNormal

Ulcer Ulcer

Aggressive forces Aggressive forces ± ± Gastric acidGastric acid

± ± Digestive enzymesDigestive enzymes

Vs.Vs.

Defensive forcesDefensive forces ± ± MucusMucus

± ± BicarbBicarb

± ± ProstaglandinsProstaglandins

± ± Epithelial regenerationEpithelial regeneration



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Ulcers result from:Ulcers result from:

1. Increased aggression1. Increased aggression

± ± H. pylori infectionH. pylori infection

± ± NSAIDSNSAIDS

± ± CigarettesCigarettes

Or Or

2. Impaired Defense2. Impaired Defense ± ± IschemiaIschemia

± ± Prostaglandin Inhibition (NSAIDS)Prostaglandin Inhibition (NSAIDS)

± ± Delayed gastric emptyingDelayed gastric emptying



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PUDPUD

ADVERSE EFFECTS OF SMOKING ADVERSE EFFECTS OF SMOKING

± ± 1. Interferes c/ action of H2 antagonists1. Interferes c/ action of H2 antagonists

± ± 2. Increases rate of gastric emptying2. Increases rate of gastric emptying ± ± 3. Increases duodenogastric reflux3. Increases duodenogastric reflux

± ± 4. Decreases pancreatic bicarb secretion4. Decreases pancreatic bicarb secretion

± ± 5. Decreases mucosal blood flow5. Decreases mucosal blood flow

± ± 6. Depresses gastric mucosal prostaglandin6. Depresses gastric mucosal prostaglandin

synthesissynthesis



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Peptic Ulcer Disease FactsPeptic Ulcer Disease FactsMost ulcers are caused by H. pyloriMost ulcers are caused by H. pylori

inf ection, not spicy food, acid or stress.infection, not spicy food, acid or stress.

You can test for You can test for H. pylori H. pylori infection.infection.

H. pylori H. pylori / ulcers can be tx¶d c/ antibiotics./ ulcers can be tx¶d c/ antibiotics.

Complications:Complications:

± ± A Major complication is bleeding & perforation A Major complication is bleeding & perforation

± ± Erosion of a small vessel at the base of theErosion of a small vessel at the base of theulcer is the cause of the bleedingulcer is the cause of the bleeding

± ± Perforation is usually catastrophic causingPerforation is usually catastrophic causingperitonitisperitonitis



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What is H. pyloriWhat is H. pylori

Helicobacter pylori Helicobacter pylori ((H. pylori H. pylori ) is a) is agram negative spiralgram negative spiral--shaped bacillusshaped bacillusfound in the gastric mucous layer or found in the gastric mucous layer or

adherent to the epithelial lining of theadherent to the epithelial lining of thestomach.stomach.

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



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How do people get infected withHow do people get infected with

H. pylori H. pylori ??

It is not known howIt is not known how H. pylori H. pylori is transmitted or is transmitted or why some patients become symptomatic whilewhy some patients become symptomatic whileothers do not.others do not.

The bacteria are most likely spread from personThe bacteria are most likely spread from personto person through fecalto person through fecal--oral or oraloral or oral--oral routes.oral routes.

Possible environmental reservoirs include:Possible environmental reservoirs include: ± ± contaminated water sourcescontaminated water sources

± ± Iatrogenic spread through contaminated endoscopesIatrogenic spread through contaminated endoscopeshas been documented but can be preventedhas been documented but can be prevented



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What can people do to preventWhat can people do to prevent H.H.

pylori pylori infection? infection?

Since the source of Since the source of H. pylori H. pylori is not yet known,is not yet known,

recommendations for avoiding infection haverecommendations for avoiding infection have

not been made.not been made.

In general, it is always wise for persons to washIn general, it is always wise for persons to wash

hands thoroughly, to eat food that has beenhands thoroughly, to eat food that has been

properly prepared, and to drink water from aproperly prepared, and to drink water from a

safe, clean source.safe, clean source.



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H. pylori H. pylori infectioninfectionBefore this bacterium was discovered, spicyBefore this bacterium was discovered, spicy

food, acid, stress, and lifestyle were consideredfood, acid, stress, and lifestyle were consideredthe major causes of ulcers.the major causes of ulcers.

The majority of patients were given longThe majority of patients were given long--termterm

medications, such as H2 blockers, and moremedications, such as H2 blockers, and morerecently, proton pump inhibitors, without arecently, proton pump inhibitors, without achance for permanent cure.chance for permanent cure.

These medications relieve ulcer These medications relieve ulcer--relatedrelatedsymptoms, heal gastric mucosal inflammation,symptoms, heal gastric mucosal inflammation,and may heal the ulcer, but they do NOT treatand may heal the ulcer, but they do NOT treatthe infection.the infection.



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H. Pylori H. Pylori infectioninfection

When acid suppression is removed, the majorityWhen acid suppression is removed, the majorityof ulcers, particularly those caused byof ulcers, particularly those caused by H. pylori H. pylori ,,recur.recur.

Since we now know that most ulcers are causedSince we now know that most ulcers are causedbyby H. pylori H. pylori , appropriate antibiotic regimens can, appropriate antibiotic regimens cansuccessfully eradicate the infection in mostsuccessfully eradicate the infection in most

patients, with complete resolution of mucosalpatients, with complete resolution of mucosalinflammation and a minimal chance for inflammation and a minimal chance for recurrence of ulcers.recurrence of ulcers.



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What illnesses doesWhat illnesses does H. pylori H. pylori

cause?cause?Most persons who are infected with H. pylori never suffer Most persons who are infected with H. pylori never suffer any symptoms related to the infection; however,any symptoms related to the infection; however, H. pylori H. pylori causes chronic active, chronic persistent, and atrophiccauses chronic active, chronic persistent, and atrophicgastritis in adults and children.gastritis in adults and children.

Infection withInfection with H. pylori H. pylori also causes duodenal and gastricalso causes duodenal and gastriculcers. Infected persons have a 2ulcers. Infected persons have a 2-- to 6to 6--fold increasedfold increasedrisk of developing gastric cancer and mucosalrisk of developing gastric cancer and mucosal--associatedassociated--lymphoidlymphoid--type (MALT) lymphoma comparedtype (MALT) lymphoma compared

with their uninfected counterparts.with their uninfected counterparts.

The role of The role of H. pylori H. pylori in nonin non--ulcer dyspepsia remainsulcer dyspepsia remainsunclear.unclear.



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Peptic Ulcer Disease SymptomsPeptic Ulcer Disease Symptoms

#1. Epigastric Pain#1. Epigastric Pain

± ± BurningBurning

± ± Occurs 1Occurs 1--3 hrs p/ meals3 hrs p/ meals

± ± Relieved by foodRelieved by food

± ± May occur @ nightMay occur @ night ± ± May radiate to back or May radiate to back or

shoulders if perforatedshoulders if perforated

NauseaNausea

VomitingVomiting

± ± May be related to partial or May be related to partial or

complete gastric outletcomplete gastric outlet

obstructionobstruction

DyspepsiaDyspepsia

± ± Belching/ BloatingBelching/ Bloating

HeartburnHeartburnChest DiscomfortChest Discomfort

Anorexia Anorexia

Weight lossWeight loss ± ± In gastric ulcers (also inIn gastric ulcers (also in

pancreatic ds.)pancreatic ds.)Weight gainWeight gain ± ± In duodenal ulcersIn duodenal ulcers

Hematemesis or melenaHematemesis or melena ± ± Due to GI bleedingDue to GI bleeding

± ± If severe = hematocheziaIf severe = hematochezia



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Who should be tested andWho should be tested and

treated for treated for H. pylori H. pylori ??

Persons with active gastric or duodenalPersons with active gastric or duodenalulcers or documented history of ulcersulcers or documented history of ulcers

should be tested for should be tested for H. pylori H. pylori , and if found, and if foundto be infected, they should be treated.to be infected, they should be treated.

To date, there has been no conclusiveTo date, there has been no conclusiveevidence that treatment of evidence that treatment of H. pylori H. pylori infection in patients with noninfection in patients with non--ulcer ulcer dyspepsia is warranted.dyspepsia is warranted.



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PUD TestsPUD Tests

Laboratory Test:Laboratory Test: ± ± Routine tests are of little importance. Having a CBC isRoutine tests are of little importance. Having a CBC is

helpful.helpful.

Upper GI endoscopy c/ biopsy*Upper GI endoscopy c/ biopsy*

Upper GI series (barium) (limited today)Upper GI series (barium) (limited today)Serum TestSerum Test ± ± Amylase Amylase

± ± ElectrolytesElectrolytes

± ± Serum Gastrin level if ZE syndrome is suspectedSerum Gastrin level if ZE syndrome is suspectedFrequently occurring duodenal ulcers or multipleFrequently occurring duodenal ulcers or multipleDuodenal Ulcers*Duodenal Ulcers*



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How isHow is H. pylori H. pylori infection diagnosed?infection diagnosed?Several methods may be used to diagnoseSeveral methods may be used to diagnose H. pylori H. pylori

infection.infection.Serological testsSerological tests that measure specificthat measure specific H. pylori H. pylori IgGIgGantibodies can determine if a person has been infected.antibodies can determine if a person has been infected. ± ± The sensitivity and specificity of these assays around 80%The sensitivity and specificity of these assays around 80%

Fecal Antigen AssayFecal Antigen Assay

Urea Breath testUrea Breath test ± ± In this test, the patient is given either 13CIn this test, the patient is given either 13C-- or 14Cor 14C--labeled urea tolabeled urea to

drink.drink.

± ± H. pylori H. pylori metabolizes the urea rapidly, and the labeled carbon ismetabolizes the urea rapidly, and the labeled carbon is

absorbed.absorbed. ± ± This labeled carbon can then be measured as CO2 in the patient'sThis labeled carbon can then be measured as CO2 in the patient's

expired breath to determine whether expired breath to determine whether H. pylori H. pylori is present.is present.

± ± The sensitivity and specificity of the breath test ranges from 94%The sensitivity and specificity of the breath test ranges from 94%to 98%.to 98%.



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How isHow is H. pylori H. pylori infection in PUDinfection in PUD

diagnosed? diagnosed?

Upper Upper endoscopyendoscopy(esophagogastroduodenal) is(esophagogastroduodenal) is

considered the reference method of considered the reference method of

diagnosis.diagnosis.



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Dx of Dx of H. pylori H. pylori by Endoscopyby Endoscopy

During endoscopy, biopsy specimens of theDuring endoscopy, biopsy specimens of thestomach and duodenum are obtained and thestomach and duodenum are obtained and thediagnosis of diagnosis of H. pylori H. pylori can be made by severalcan be made by severalmethods:methods:

± ± The biopsy urease testThe biopsy urease test -- a colorimetric test based ona colorimetric test based onthe ability of the ability of H. pylori H. pylori to produce urease; it providesto produce urease; it providesrapid testing at the time of biopsy.rapid testing at the time of biopsy.

± ± Histologic identification of organismsHistologic identification of organisms -- considered theconsidered the

gold standard of diagnostic tests.gold standard of diagnostic tests. ± ± Culture of biopsy specimens for Culture of biopsy specimens for H. pylori,H. pylori, whichwhich

requires an experienced laboratory and is necessaryrequires an experienced laboratory and is necessarywhen antimicrobial susceptibility testing is desiredwhen antimicrobial susceptibility testing is desired



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Peptic Ulcer Disease TherapyPeptic Ulcer Disease TherapyNonNon--PharmacologicalPharmacological

± ± Diet change is of no valueDiet change is of no value

± ± Smoking CessationSmoking CessationSmoking delays healingSmoking delays healing

± ± DC medications that enhance the progressionDC medications that enhance the progression

NSAIDSNSAIDSPharmacological TherapyPharmacological Therapy ± ± Inhibit secretion of acidInhibit secretion of acid

± ± Neutralizing gastric acidsNeutralizing gastric acids

± ± Augmentation of protection of mucosa Augmentation of protection of mucosa ± ± Antibiotics prn Antibiotics prn

Maintenance TherapyMaintenance Therapy ± ± Prevention c/ colloid bismuthPrevention c/ colloid bismuth

± ± Bedtime dosage of H2 blockersBedtime dosage of H2 blockers



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Peptic Ulcer Disease TherapyPeptic Ulcer Disease Therapy

Pharmacological TherapyPharmacological Therapy

± ± Inhibition of acidInhibition of acid

H2 blockersH2 blockers

Antacids Antacids

Proton pump inhibitorsProton pump inhibitors

Anticholinergics Anticholinergics

ProstaglandinsProstaglandins

Augmentation protection Augmentation protection



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Peptic Ulcer Disease TherapyPeptic Ulcer Disease Therapy

Antacids Antacids (magnesium, aluminum, & calcium based)(magnesium, aluminum, & calcium based)

± ± cause diarrheacause diarrhea

Moderate to high doses of H2 blockers result inModerate to high doses of H2 blockers result inimproved healing ratesimproved healing rates

± ± Used 1 hr PC & HS for 6Used 1 hr PC & HS for 6--8 wks8 wks

± ± Side effects:Side effects:Hypermagnesemia (careful in renal patients)Hypermagnesemia (careful in renal patients)

Aluminum causes phosphate depletion & osteoporosis Aluminum causes phosphate depletion & osteoporosis

Sodium overload in CHFSodium overload in CHF

Hypercalcium causing Milk alkali syndromeHypercalcium causing Milk alkali syndrome

Inhibits absorption of antibiotics, digoxin, warfarinInhibits absorption of antibiotics, digoxin, warfarin



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PUD Therapy (cont)PUD Therapy (cont)

Proton Pump Inhibitors:Proton Pump Inhibitors:

± ± Inhibit the H,KInhibit the H,K--ATPase pump ATPase pump

± ± Healing rate 80Healing rate 80--100%100%

± ± Prilosec (Omeprazole)Prilosec (Omeprazole)

Anticholinergics: reduce acid by 50% and Anticholinergics: reduce acid by 50% and

cause blurred visioncause blurred vision ± ± pupil dilation, consider pt¶s occupation or driving restrictionpupil dilation, consider pt¶s occupation or driving restriction



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PUD Therapies (cont)PUD Therapies (cont)

Prostaglandins (Do not use in pregnancy)Prostaglandins (Do not use in pregnancy) ± ± Inhibit the parietal cell cyclic AMP function inInhibit the parietal cell cyclic AMP function in

response to histamineresponse to histamine

± ± Healing rate are equal to H2 blockersHealing rate are equal to H2 blockers

± ± Primary role is to be used as a prophylactic agent toPrimary role is to be used as a prophylactic agent toprevent NSAID induced ulcers. Not used as aprevent NSAID induced ulcers. Not used as aprimary therapyprimary therapy

± ± Mosoprostol (Cytotec)Mosoprostol (Cytotec)

Sucralfate (Carafate) its action is unknownSucralfate (Carafate) its action is unknown ± ± It forms a viscous shield over the mucosaIt forms a viscous shield over the mucosa

± ± Absorbs bile & pepsin Absorbs bile & pepsin



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What ar the tr eat ent r egi ens sed f r What ar e the tr eat ent r egi ens sed f r

H . l ri H . l ri er adi ati n?er adi ati n?

Curr ent ther apy f r Curr ent ther apy f r H

. l ri H

. l ri inf ecti n consists of inf ection consists of 10 days to 2 weeks of one or two eff ective 10 days to 2 weeks of one or two eff ective antibiotics,antibiotics, ± ± amoxicillin,amoxicillin,

± ± tetracyclinetetracycline

not to be used for children <12 yrsnot to be used for children <12 yrs ± ± metronidazole, or metronidazole, or

± ± clarithromycin,clarithromycin,

Plus either Plus either ± ± ranitidine bismuth citrate (H2 blocker),ranitidine bismuth citrate (H2 blocker),

± ± bismuth subsalicylate (peptobismuth subsalicylate (pepto--bismol),bismol),

± ± or proton pump inhibitor . or proton pump inhibitor .



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PUD Therapies (cont)PUD Therapies (cont)

Acid suppression by the H2 blocker or Acid suppression by the H2 blocker or

proton pump inhibitor in conjunction withproton pump inhibitor in conjunction with

the antibiotics helpsthe antibiotics helps

± ± alleviate ulcer alleviate ulcer--related symptoms (i.e.,related symptoms (i.e.,

abdominal pain, nausea),abdominal pain, nausea),

± ± helps heal gastric mucosal inflammation,helps heal gastric mucosal inflammation,

± ± and may enhance efficacy of the antibioticsand may enhance efficacy of the antibioticsagainstagainst H. pylori H. pylori at the gastric mucosalat the gastric mucosal

surface.surface.



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H. Pylori TxH. Pylori Tx

Currently, eightCurrently, eight H. pylori H. pylori treatment regimens aretreatment regimens areapproved by the Food and Drug Administrationapproved by the Food and Drug Administration(FDA); however, several other combinations(FDA); however, several other combinationshave been used successfully.have been used successfully.

Antibiotic resistance and patient noncompliance Antibiotic resistance and patient noncomplianceare the two major reasons for treatment failure.are the two major reasons for treatment failure.

Overall, triple therapy regimens have shownOverall, triple therapy regimens have shownbetter eradication rates than dual therapy. better eradication rates than dual therapy. Longer length of treatment (14 days versus 10Longer length of treatment (14 days versus 10days) results in better eradication rates.days) results in better eradication rates.



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FDAFDA--approved treatment optionsapproved treatment options

1. Omeprazole 40 mg QD + clarithromycin 500 mg TID x1. Omeprazole 40 mg QD + clarithromycin 500 mg TID x

2 wks, then omeprazole 20 mg QD x 2 wks2 wks, then omeprazole 20 mg QD x 2 wks--OROR--

2. (Zantac) Ranitidine bismuth citrate (RBC) 400 mg BID2. (Zantac) Ranitidine bismuth citrate (RBC) 400 mg BID

+ clarithromycin 500 mg TID x 2 wks, then RBC 400 mg+ clarithromycin 500 mg TID x 2 wks, then RBC 400 mg

BID x 2 wksBID x 2 wks--OROR--

3. Bismuth subsalicylate (Pepto Bismol®) 525 mg QID +3. Bismuth subsalicylate (Pepto Bismol®) 525 mg QID +

metronidazole 250 mg QID + tetracycline 500 mg QID* xmetronidazole 250 mg QID + tetracycline 500 mg QID* x

2 wks + H2 receptor antagonist therapy as directed x 42 wks + H2 receptor antagonist therapy as directed x 4

wkswks

--OROR--

4. Lansoprazole 30 mg BID + amoxicillin 1 g BID +4. Lansoprazole 30 mg BID + amoxicillin 1 g BID +

clarithromycin 500 mg TID x 10 daysclarithromycin 500 mg TID x 10 days



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FDAFDA--approved treatment optionsapproved treatment options

(cont.)(cont.)

5.5. --OROR-- Lansoprazole 30 mg TID + amoxicillin 1 g TID xLansoprazole 30 mg TID + amoxicillin 1 g TID x2 wks**2 wks**

6.6. --OROR-- Rantidine bismuth citrate 400 mg BID +Rantidine bismuth citrate 400 mg BID +clarithromycin 500 mg BID x 2 wks, then RBC 400 mgclarithromycin 500 mg BID x 2 wks, then RBC 400 mgBID x 2 wksBID x 2 wks

7.7. --OROR-- Omeprazole 20 mg BID + clarithromycin 500 mgOmeprazole 20 mg BID + clarithromycin 500 mg

BID + amoxicillin 1 g BID x 10 daysBID + amoxicillin 1 g BID x 10 days

8.8. --OROR-- Lansoprazole 30 mg BID + clarithromycin 500Lansoprazole 30 mg BID + clarithromycin 500mg BID + amoxicillin 1 g BID x 10 daysmg BID + amoxicillin 1 g BID x 10 days

LongLong term consequences ofterm consequences of HH



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LongLong--term consequences of term consequences of H.H.

pylori pylori infection? infection?

Recent studies have shown an associationRecent studies have shown an associationbetween longbetween long--term infection withterm infection with H. pylori H. pylori andandthe development of the development of gastric cancer gastric cancer..

Gastric cancer is the second most commonGastric cancer is the second most commoncancer cancer worldwideworldwide; it is most common in; it is most common incountries such as Colombia and China, wherecountries such as Colombia and China, whereH. pylori H. pylori infects over half the population in earlyinfects over half the population in early

childhood.childhood.

In the United States, whereIn the United States, where H. pylori H. pylori is lessis lesscommon in young people, gastric cancer ratescommon in young people, gastric cancer rates

have decreased.have decreased.



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GI BleedingGI Bleeding



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Gastrointestinal BleedingGastrointestinal Bleeding

May present as:May present as:

± ± Occult blood (not visualized)Occult blood (not visualized)

± ± Melena (black stool)Melena (black stool)

± ± Hematemesis (vomiting blood)Hematemesis (vomiting blood)

± ± Hematochezia (passage in stool)Hematochezia (passage in stool)



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Kinds of GI BleedingKinds of GI Bleeding

HematemesisHematemesis ± ± Rapid bleed: vomiting bright red bloodRapid bleed: vomiting bright red blood

± ± Slow bleed: ³coffeeSlow bleed: ³coffee--grounds´grounds´

MelenaMelena ± ± Black tarry stoolBlack tarry stool

± ± Source:Source:Upper GIUpper GI

Or lower GI to right colonOr lower GI to right colon

HematocheziaHematochezia ± ± Bright red blood in stoolBright red blood in stool

± ± Source:Source:Lower GILower GI

Or Upper GI if massiveOr Upper GI if massive



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Occult bloodOccult blood

Hemacult/Guiaic is the most commonly used testHemacult/Guiaic is the most commonly used testFalse positives <2%False positives <2%

Obtain 2 different samples from 2 stools over a 3 dayObtain 2 different samples from 2 stools over a 3 dayperiodperiod

Laxatives alter results causing both falseLaxatives alter results causing both false--positive andpositive andfalsefalse--negative resultsnegative results

False positive results from food rich in peroxidaseFalse positive results from food rich in peroxidase ± ± Bloody meatsBloody meats

± ± BroccoliBroccoli

± ± TurnipsTurnips ± ± Cauliflower Cauliflower

False negatives from taking Vit. C or food containingFalse negatives from taking Vit. C or food containingvitamin Cvitamin C

Neoplasms is #1 cause of occult blood lossNeoplasms is #1 cause of occult blood loss



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Guiaic/ HemoccultGuiaic/ Hemoccult



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Causes of GI bleeding by locationCauses of GI bleeding by location

Upper GIUpper GI ± ± #1 PUD#1 PUD

DuodenalDuodenal

GastricGastric

± ± Esophageal varicesEsophageal varices(Secondary to portal HTN)(Secondary to portal HTN)

± ± MalloryMallory--Weiss tear Weiss tear (Mucosal laceration @ EG(Mucosal laceration @ EG

junction) junction)

± ± GastritisGastritis

Lower GILower GI ± ± #1 Hemorrhoids#1 Hemorrhoids

± ± #2 Anal Fissure#2 Anal Fissure

± ± DiverticulosisDiverticulosis ± ± IntussusceptionIntussusception

Upper & Lower GIUpper & Lower GI

± ± NeoplasmsNeoplasms ± ± Angiodysplasias Angiodysplasias(Osler¶s disease)(Osler¶s disease)



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GI BleedGI Bleed

GI bleeding is a powerful laxativeGI bleeding is a powerful laxativeGI bleeding may be life threateningGI bleeding may be life threatening

GI bleeding may be acute or chronicGI bleeding may be acute or chronic

Adult anemia is secondary to GI bleeding Adult anemia is secondary to GI bleedinguntil proven otherwiseuntil proven otherwise

GI bleeding is secondary to GI bleeding is secondary to

cancer until proven otherwise cancer until proven otherwise



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GI BleedGI Bleed

Nature & duration helps with evaluationNature & duration helps with evaluationPresence of pain is importantPresence of pain is important

Watch for associated symptoms: fever, weight lossWatch for associated symptoms: fever, weight loss

Medication and past surgery historyMedication and past surgery history

The initial step is assessment of hemodynamic status.The initial step is assessment of hemodynamic status.

A systolic BP <100mm Hg is high risk c/ acute A systolic BP <100mm Hg is high risk c/ acute

bleeding.bleeding.

CAN BE MASSIVE AND DEADLYCAN BE MASSIVE AND DEADLY

MUST BE TREATED RAPIDILY AND AGGRESSIVELYMUST BE TREATED RAPIDILY AND AGGRESSIVELY

ALWAYS R/O CANCER ALWAYS R/O CANCER



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Upper GI bleedUpper GI bleed

4x more common than lower GI4x more common than lower GI

bleedbleed

R/O upper GI source by NG tubeR/O upper GI source by NG tube

aspirateaspirate



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Upper GI Differential Dx aidsUpper GI Differential Dx aids

Signs of chronic liver diseaseSigns of chronic liver disease

implicates bleeding due to portal HTN.implicates bleeding due to portal HTN.

A hx of dyspepsia, NSAID use, or PUD,A hx of dyspepsia, NSAID use, or PUD,

suggests Peptic Ulcer .suggests Peptic Ulcer .

Acute bleeding after heavy alcoholAcute bleeding after heavy alcohol

ingestion or retching suggests aingestion or retching suggests a

MalloryMallory--Weiss tear .Weiss tear .



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Lower GI bleedsLower GI bleeds

HematocheziaHematochezia

± ± (however, 10% is from upper GI source)(however, 10% is from upper GI source)

Defined as below ligament of TreitzDefined as below ligament of Treitz ± ± (divides duodenum/ jejunum)(divides duodenum/ jejunum)

95% from Colon95% from Colon

Less likely than Upper GI bleed to presentLess likely than Upper GI bleed to presentin shock, or require transfusionin shock, or require transfusion

85% spontaneous cessation85% spontaneous cessation



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Complications of GI bleedComplications of GI bleed

DIC from both massive blood loss &DIC from both massive blood loss &

coagulationcoagulation

MultiMulti--organ failureorgan failure

Hemodynamic collapseHemodynamic collapse

Hyper Hyper--ammonia toxicityammonia toxicity

Hepatorenal failureHepatorenal failureEncephalopathyEncephalopathy



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2/5/20112/5/2011 6161



2/5/20112/5/2011 6262



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MCC of GI BleedingMCC of GI Bleeding

2006 Current2006 Current

Upper GIUpper GI

± ± PUDPUD

± ± Portal HTNPortal HTN

± ± Mallory WeissMallory Weiss ± ± Vascular abnVascular abn

± ± Gastric NeoplasmsGastric Neoplasms

± ± Erosive gastritisErosive gastritis

± ± othersothers

Lower GILower GI

± ± Under 50 y/oUnder 50 y/o

Infectious colitisInfectious colitis

Anorectal ds Anorectal dsInflammatory bowel dsInflammatory bowel ds

± ± Over 50 y/o c Major BleedOver 50 y/o c Major Bleed

DiverticulosisDiverticulosis

Vascular ectasiasVascular ectasias

MalignancyMalignancy

ischemiaischemia



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GI BLEED



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LABS

1.CBC

1.PT/PTT/Thrombin time- DIC panel (FSPfibrin split products, fibrinogen, FDPfibrin degradation products, clottingtime, D dimer assay)

2.Electrolytes/BUN/creatinine

3.Blood Type and Cross match

4.CXR/ AXR rarely helpful only if perforated

GI BLEED



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Anoscopy/ Sigmoidoscopy VS. Anoscopy/ Sigmoidoscopy VS.

ColonoscopyColonoscopy

Anoscopy/Anoscopy/

SigmoidoscopySigmoidoscopy

± ± Acceptable in <45 yo Acceptable in <45 yo

otherwise healthy tootherwise healthy toevaluate for:evaluate for:

Anorectal ds. Anorectal ds.

Inflammatory bowel ds.Inflammatory bowel ds.

Infectious colitisInfectious colitis

± ± If lesion found, noIf lesion found, no

further eval neededfurther eval needed

ColonscopyColonscopy

± ± Used DiagnosticallyUsed Diagnostically

and Therapeuticallyand Therapeutically

± ± All >40 All >40--45 yo c/ +45 yo c/ +guiaic or Fe+guiaic or Fe+

deficiency anemiadeficiency anemia



2/5/20112/5/2011 6767

Flex SigFlex Sig



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Anoscopy/ Rigid Sigmoidoscopy Anoscopy/ Rigid Sigmoidoscopy



2/5/20112/5/2011 6969

Super Duper Pooper Scooper Super Duper Pooper Scooper



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ColonoscopyColonoscopy



2/5/20112/5/2011 7171



2/5/20112/5/2011 7272



2/5/20112/5/2011 7373



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U t t f U GIU t t f U GI



2/5/20112/5/2011 7575

Urgent management of Upper GIUrgent management of Upper GI

bleedsbleeds2 Large bore IV lines need started c/ colloid solution2 Large bore IV lines need started c/ colloid solutionstarted until PRBC can be infused, if needed.started until PRBC can be infused, if needed.

OctreotideOctreotide-- Decreases portal HTN (it is administeredDecreases portal HTN (it is administeredpromptly to all patients with active upper GI bleeds,promptly to all patients with active upper GI bleeds,and liver ds, or known portal HTN, until source can beand liver ds, or known portal HTN, until source can be

ID¶d by endoscopy.ID¶d by endoscopy.PPI¶s reduce risk of rebleed in PUDPPI¶s reduce risk of rebleed in PUD

EndoscopyEndoscopy ± ± To ID sourceTo ID source

± ± Determine risk of rebleedDetermine risk of rebleed ± ± HemostasisHemostasis

Other Tx modalities (used only if endoscopy fails)Other Tx modalities (used only if endoscopy fails) ± ± Angiographic embolization Angiographic embolization

± ± Transvenous shunts (for portal HTN, and variceal bleeds)Transvenous shunts (for portal HTN, and variceal bleeds)



2/5/20112/5/2011 7676

ReviewReviewAcute Erosive GastritisAcute Erosive Gastritis ± ± D/C NSAIDS or add misoprostolD/C NSAIDS or add misoprostol

± ± If bleeding caused by ASA; consider plateletIf bleeding caused by ASA; consider plateletadministrationadministration

± ± Sucralfate/ H2 antagonistsSucralfate/ H2 antagonists

Chronic Gastritis (Nonerosive)Chronic Gastritis (Nonerosive) ± ± Type AType A

Eradicate H. pylori: amox + tetracycline + PPIEradicate H. pylori: amox + tetracycline + PPI

± ± Type BType BTreat pernicious anemia: monthly lifelong IM B12Treat pernicious anemia: monthly lifelong IM B12

Specific Types of GastritisSpecific Types of Gastritis



2/5/20112/5/2011 7777

ReviewReviewPeptic Ulcer DiseasePeptic Ulcer Disease

± ± Almost all need Pepsin, Acid, & Almost all need Pepsin, Acid, & H. pylori H. pylori to form ulcer to form ulcer

± ± Eradicate H. pyloriEradicate H. pylori

± ± Endoscopic bx to exclude adenocarcinomaEndoscopic bx to exclude adenocarcinomarecommended for all patientsrecommended for all patients

± ± If refractory: obtain fasting serum gastrin levels toIf refractory: obtain fasting serum gastrin levels to

exclude Zollinger exclude Zollinger--EllisonEllison

± ± Consider parietal cell vagotomy.Consider parietal cell vagotomy.Partial gastrectomy c/ gastroPartial gastrectomy c/ gastro--duodenostomy (Billroth I) or duodenostomy (Billroth I) or

gastrojejunostomy (Billroth II) are rarely used now.gastrojejunostomy (Billroth II) are rarely used now.



2/5/20112/5/2011 7878

ReviewReviewUpper GI BleedUpper GI Bleed ± ± Evaluate hemodynamic status, stabilizeEvaluate hemodynamic status, stabilize

± ± Nasogastric tubeNasogastric tube

± ± OctreotideOctreotide

± ± Endoscopy if bleeding is severe enough toEndoscopy if bleeding is severe enough torequire blood transfusionsrequire blood transfusions

± ± Bleeding from esophageal varices: endoscopicBleeding from esophageal varices: endoscopicsclerotherapy preferredsclerotherapy preferred



ReviewReviewLower GI BleedLower GI Bleed

± ± T he most common cause of significant bleeding isT he most common cause of significant bleeding is

diverticular bleeding; that of intermittent minor diverticular bleeding; that of intermittent minor

hematochezia is hemorrhoidal bleeding hematochezia is hemorrhoidal bleeding

± ± Evaluate hemodynamic status, stabilizeEvaluate hemodynamic status, stabilize

± ± Colonoscopy if bleeding is severe or patient >50 yrsColonoscopy if bleeding is severe or patient >50 yrs

(neoplasms)(neoplasms)

± ± If bleeding continues consider nuclear bleeding scan or If bleeding continues consider nuclear bleeding scan or

mesenteric angiography (often of limited use if mesenteric angiography (often of limited use if

bleeding is slow or intermittent), or Intrableeding is slow or intermittent), or Intra--arterialarterial

vasopressin or embolization.vasopressin or embolization.

±± Surgery as last resortSurgery as last resort

jr pud presentation

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