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

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HistoryHistory

Awoke him from sleepAwoke him from sleepRelieved by food, but pain worsened 1-3 Relieved by food, but pain worsened 1-3 hrs laterhrs laterFatigueFatigueDyspepsia/ bloating/ belching/ burningDyspepsia/ bloating/ belching/ burningWt lossWt lossNo SOB/ pain radiation/N/V/D/FNo SOB/ pain radiation/N/V/D/FWife states that his diet is “poor”Wife states that his diet is “poor”

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HistoryHistory

PMHPMH– No DMNo DM– No CADNo CADEtc.Etc.

Family HistoryFamily History– Mother died 75 MIMother died 75 MI– Father died 70 strokeFather died 70 stroke

Surgical HxSurgical Hx– NoneNone

Social HistorySocial History– + Smoker 1ppd+ Smoker 1ppd

MedicationsMedications– ““some arthritis med”some arthritis med”– ““some HTN med”some HTN med”

NKDANKDA

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Physical ExamPhysical Exam

+ Epigastric tenderness+ Epigastric tenderness

Guiaic +Guiaic +

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Differential Diagnosis?Differential Diagnosis?

CardiacCardiac– MIMI

Aortic DissectionAortic DissectionPulmonaryPulmonaryGIGI– PUDPUD– PancreatitisPancreatitis– GallstonesGallstones– Inflammatory bowel ds. (crohn’s/UC)Inflammatory bowel ds. (crohn’s/UC)– Colon CaColon Ca

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Dx testsDx tests

CBC (blood loss)CBC (blood loss)

Chem c/ BUN/creatChem c/ BUN/creat

Type & crossType & cross

H. pyloriH. pylori

EKGEKG

CXR (free air)CXR (free air)

Barium studyBarium study

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ProceduresProcedures

NG tube (if upper GI bleed)NG tube (if upper GI bleed)

IVFIVF

EndoscopyEndoscopy

? Sig vs. colonoscopy?? Sig vs. colonoscopy?

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TxTx

AntacidsAntacids

GI cocktailGI cocktail

H2 blockersH2 blockers

PPI’sPPI’s

AbxAbx

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Reflux Esophagitis Peptic Reflux Esophagitis Peptic Ulcer Disease, Gastritis, & Ulcer Disease, Gastritis, &

GI BleedingGI Bleeding

Pascale Gèhy-Andrè, PA-CPascale Gèhy-Andrè, PA-C

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Anatomy & Physiology of the Anatomy & Physiology of the stomachstomach

The blood supply is The blood supply is from the Celiac arteryfrom the Celiac artery

The vagus nerve The vagus nerve stimulates the stomachstimulates the stomach

The epithelium is The epithelium is columnar cells pieced columnar cells pieced by numerous glandsby numerous glands

The cardia and antrum The cardia and antrum have mostly mucous have mostly mucous cellscells

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Normal Gastric FunctionNormal Gastric Function

1. Primary function of the stomach1. Primary function of the stomach– A. secretion of substances important to digestion & A. secretion of substances important to digestion &

absorptionabsorption– B. movement of gastric contents downstream to small B. movement of gastric contents downstream to small

bowelbowel

2. Classes of secretory cells2. Classes of secretory cells– A. A. Mucous secreting cells of the cardiaMucous secreting cells of the cardia: :

1. Protect underlying cells from mechanical forces of 1. Protect underlying cells from mechanical forces of digestiondigestion2. Lubrication of mucosa to move food over surface2. Lubrication of mucosa to move food over surface3. Retain water within the mucous gel providing aqueous 3. Retain water within the mucous gel providing aqueous environment for underlying cells.environment for underlying cells.4. Forming an unstirred layer above the mucosa impending 4. Forming an unstirred layer above the mucosa impending but not blocking diffusion of hydrogen ions from the lumen to but not blocking diffusion of hydrogen ions from the lumen to the superficial epithelial cells.the superficial epithelial cells.

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Normal Gastric FunctionNormal Gastric Function2. Classes of secretory 2. Classes of secretory cells (cont.):cells (cont.):– B. B. HCLHCL-Secreting -Secreting parietal parietal

cellscells of the body which of the body which also secrete also secrete intrinsic intrinsic factor.factor.

– C. C. PepsinogenPepsinogen-Secreting -Secreting chief cellschief cells of the body. of the body.

– D. D. GastrinGastrin-Secreting -Secreting G G cellscells of the Antrum (body of the Antrum (body has 2 sources of Gastrin has 2 sources of Gastrin stomach and pancreas).stomach and pancreas).

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Gastric Function (cont.)Gastric Function (cont.)3. Neural & Hormonal influence on gastric 3. Neural & Hormonal influence on gastric function:function:– A. A. Cephalic phaseCephalic phase: (smell/thinking) initiates : (smell/thinking) initiates

cholinergic impulse via the vagus nerve stimulating cholinergic impulse via the vagus nerve stimulating parietal secretion of acid & G cell secretion of Gastrin parietal secretion of acid & G cell secretion of Gastrin which also stimulates acid.which also stimulates acid.

– B. B. Gastric phaseGastric phase: causes distention of the stomach by : causes distention of the stomach by food which causes further secretion of acid and food which causes further secretion of acid and gastrin. Protein will also stimulate G cells to produce gastrin. Protein will also stimulate G cells to produce Gastrin and acid.Gastrin and acid.

– C. C. Intestinal phaseIntestinal phase: will cause gastric acids to : will cause gastric acids to stimulate secretion of secretin & cholecystokinin stimulate secretion of secretin & cholecystokinin which will also inhibit the action of gastrin on the which will also inhibit the action of gastrin on the parietal cells.parietal cells.

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Reflux EsophagitisReflux Esophagitis

Definition: Recurrent reflux of gastric Definition: Recurrent reflux of gastric contents in the distal esophaguscontents in the distal esophagus

Commonly called heartburnCommonly called heartburn

20% of normal population at least one 20% of normal population at least one weekweek

May cause erosions that leads to Barrett’s May cause erosions that leads to Barrett’s esophagitis which can predispose to esophagitis which can predispose to malignancymalignancy

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Reflux EsophagitisReflux Esophagitis

Contributing Factors:Contributing Factors:– Hiatal herniaHiatal hernia– Delayed gastric emptying (gastroparesis/obstruction)Delayed gastric emptying (gastroparesis/obstruction)– Incompetent Lower esophageal sphincterIncompetent Lower esophageal sphincter– Irritant effects of gastric juices (refluxate) Irritant effects of gastric juices (refluxate)

Clinical features: Clinical features: – Heartburn most common presenting featureHeartburn most common presenting feature– Hoarseness, cough, hiccup, atypical chest pain, sore Hoarseness, cough, hiccup, atypical chest pain, sore

throatthroat

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Reflux EsophagitisReflux Esophagitis

Laboratory studiesLaboratory studies– Barium swallow may indicate a large hiatal Barium swallow may indicate a large hiatal

herniahernia– ENDOSCOPY with BIOPSY ENDOSCOPY with BIOPSY standard standard

procedure procedure describes the presence and extentdescribes the presence and extent of mucosal damageof mucosal damage

– Endoscopy when symptoms do not respond to Endoscopy when symptoms do not respond to medical therapy medical therapy

– pH monitoring can be done pH monitoring can be done

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Reflux EsophagitisReflux Esophagitis

Treatment: Treatment: Life style modificationLife style modification ( (DC smoking)DC smoking)– PharmacotherapyPharmacotherapy

Antacids or alginic acid(gaviscon)Antacids or alginic acid(gaviscon)

Histamine (H2 blockers) Histamine (H2 blockers)

Prokinetic drugs ( e.g. metoclopramide, cisapride, bethanechol) Prokinetic drugs ( e.g. metoclopramide, cisapride, bethanechol) increase gastric emptying and can be combined with H2 blockersincrease gastric emptying and can be combined with H2 blockers

Acid-suppressant proton-pump inhibitor (e.g. omeprazole, Acid-suppressant proton-pump inhibitor (e.g. omeprazole, lansoprazole) may be tried as last resortlansoprazole) may be tried as last resort

Anticholinergic, Anticholinergic, BB--adrenergic, and calcium channel-blocking agents adrenergic, and calcium channel-blocking agents decrease lower esophageal sphincter pressure and decrease lower esophageal sphincter pressure and should be should be avoidedavoided

Complication: Complication: Barrett’s Esophagagus

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GastritisGastritisAcute GastritisAcute Gastritis is an inflammation of the is an inflammation of the gastric mucosa. gastric mucosa.

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

Gastritis has 3 basic types:Gastritis has 3 basic types:– Acute (erosive/ hemorrhagic)Acute (erosive/ hemorrhagic)– Non-erosive, Non-specific/ChronicNon-erosive, Non-specific/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 diminishing NSAIDS gastric injury by diminishing

prostaglandin production in stomach and prostaglandin 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:– Caustic ingestion Caustic ingestion – radiation radiation

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Chronic Gastritis Chronic Gastritis Nonerosive/nonspecificNonerosive/nonspecific

Infectious gastritis Type B: Infectious gastritis Type B: H Pylory H Pylory – Involves antrum and body of stomachInvolves antrum and body of stomach

majority of patients asymptomaticmajority of patients asymptomatic– Strong association with PUD Strong association with PUD – 2 to 6 fold risks of gastric adenocarcinoma and also 2 to 6 fold risks of gastric adenocarcinoma and also

gastric lymphomagastric lymphoma

Autoimmune gastritis Type A: Pernicious anemia Autoimmune gastritis Type A: Pernicious anemia – Body and fundus, It usually spares the antrum & affects Body 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 B-12vitamin B-12 occurs due to lack of intrinsic factor from occurs due to lack of intrinsic factor from parietal 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 GastritisGiant Cell (Menetrier’s disease) (Hypertrophic Giant Cell (Menetrier’s disease) (Hypertrophic Gastropathy) Gastropathy) – only found on biopsyonly found on biopsy

Lymphocytic GastritisLymphocytic GastritisGranulomatous GastritisGranulomatous Gastritis– TuberculosisTuberculosis– SyphilisSyphilis– FungalFungal– SarcoidSarcoid– Crohn’sCrohn’s

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Gastritis SymptomsGastritis SymptomsClinical features of gastritis generally reflects the underlying Clinical features of gastritis generally reflects the underlying syndrome rather than the gastric injury itselfsyndrome rather than the gastric injury itselfAcute:Acute:– Dyspepsia and abdominal pain are common indicators of gastritisDyspepsia and abdominal pain are common indicators of gastritis– Mild epigastric discomfortMild epigastric discomfort– Occasional N/VOccasional N/V– Headache, excessive salivation, flatusHeadache, excessive salivation, flatus

Chronic:Chronic:– Non specific symptoms c/ chronic abdominal discomfortNon specific symptoms c/ chronic abdominal discomfort

Key signs: (usually none)Key signs: (usually none)– Hematemesis, bloody nasogastric aspirateHematemesis, bloody nasogastric aspirate– Abdominal tendernessAbdominal tenderness– BloatingBloating– EmesisEmesis

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GastritisGastritisLab:Lab:– Endoscopy c/ biopsy is the gold standardEndoscopy c/ biopsy is the gold standard– A urea breath test can be used to detect HPA urea breath test can be used to detect HP– 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 ulcer1. 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 blockersAntacids & H2 blockers– Avoid smoking & alcoholAvoid smoking & alcohol

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Peptic Ulcer DiseasePeptic Ulcer Disease

DefinitionDefinition: PUD is describes : PUD is describes any ulcer of the upper any ulcer of the upper digestive tract. digestive tract. (duodenal #(duodenal #1) 1) and stomach and stomach (gastric #2)(gastric #2)

Break in the duodenal or Break in the duodenal or gastric mucosa extending gastric mucosa extending through the musularis through the musularis mucosae, and are usually mucosae, and are usually 5mm-1cm.5mm-1cm.

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Zollinger-Ellison SyndromeZollinger-Ellison Syndrome

Ulcers-associated Ulcers-associated with the with the Zollinger-Zollinger-Ellison (ZE) Ellison (ZE) Syndrome (#3Syndrome (#3) are ) are caused by gastrin-caused by gastrin-releasing islet cell releasing 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-Ellison SyndromeZollinger-Ellison SyndromeA 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 also Usually found in head of pancreas but can also be found in duodenum, liver & lungbe found in duodenum, liver & lung

75-80% of ulcers produced develop in the 75-80% of ulcers produced develop in the duodenal 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 1.3 : 1 WomenMen 1.3 : 1 Women

Most commonly occur inMost commonly occur in::– #1 Duodenum (Duodenal) #1 Duodenum (Duodenal)

– #2 Stomach (Gastric)#2 Stomach (Gastric) – EsophagusEsophagus– Gastroenteric Gastroenteric

anastomosesanastomoses– Meckel’s DiverticulumMeckel’s Diverticulum

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PUDPUDThe spectrum of the disease is broad from mild mucosal The spectrum of the disease is broad from mild mucosal injury 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.

1-2% of population have an ulcer at the present time1-2% 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 lifetimeGastric and Duodenal ulcers tend to recur in the same Gastric and Duodenal ulcers tend to recur in the same location.location.

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

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Duodenal Ulcer vs. Gastric UlcerDuodenal Ulcer vs. Gastric UlcerDuodenalDuodenal– Increased acid Increased acid

productionproduction

– H. pyloriH. pylori

– relieved by foodrelieved by food & & typically awakens typically awakens patient around 1:00ampatient around 1:00am

GastricGastric– Normal or decreased Normal or decreased

acid productionacid production– Decreased mucosal Decreased 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 25 Onset more common age 25

to 55to 55– never malignantnever malignant

– mostly located in the duodenal mostly located in the duodenal bulb or immediately post bulbar. bulb or immediately post bulbar.

– Ulcers distal to the duodenal Ulcers distal to the duodenal bulb should raise suspicion for bulb should raise suspicion for Zollinger-Ellison Syndrome Zollinger-Ellison Syndrome (also c/ multiple frequently (also c/ multiple frequently occurring duodenal ulcers.)occurring duodenal ulcers.)

– Men 2:1 WomenMen 2:1 Women– Duodenal 5 times more Duodenal 5 times more

common than gastriccommon than gastric

– 60-80% have recurrence within 60-80% have recurrence within one year.one year.

GastricGastric– Onset more common age Onset more common age

40 to 7040 to 70

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

– Gastric ulcers are more Gastric ulcers are more common @ lesser common @ lesser curvaturecurvature

– Malignancies more likely Malignancies more likely @ greater curvature@ greater curvature

– 1-3% occur in carcinomas1-3% occur in carcinomas

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PUD EtiologiesPUD Etiologies1. 1. Helicobacter pylori (H. pylori) infection: (#1 cause)Helicobacter pylori (H. pylori) infection: (#1 cause)

– A. Associated c/ 70-95% of Peptic ulcers.A. Associated c/ 70-95% of Peptic ulcers.– B. Treatment of H. pylori improves healing rate & markedly B. 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. Hypersecretion states: (#3 although Hypersecretion states: (#3 although uncommon)uncommon)– Gastrinomas (Zollinger-Ellison Syndrome)Gastrinomas (Zollinger-Ellison Syndrome)– Multiple endocrine neoplasia (MEN-1)Multiple endocrine neoplasia (MEN-1)– Systemic mastocytosis Systemic mastocytosis (mast cells infiltrate intestinal wall, (mast cells infiltrate intestinal wall,

release histamine- stimulates acid. Symptoms are diarrhea, flushing, release histamine- stimulates acid. Symptoms are diarrhea, flushing, urticaria. Histamine in blood. Confirmed by biopsy.)urticaria. Histamine in blood. Confirmed by biopsy.)

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 the The pathogenesis of PUD is related to the imbalance between normal protective factors and imbalance between normal protective factors and

injurious factorsinjurious factors

No UlcerNo Ulcer– NormalNormal

UlcerUlcerAggressive forcesAggressive 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– ETOHETOH

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 SMOKINGADVERSE 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 prostaglandin 6. Depresses gastric mucosal prostaglandin

synthesissynthesis

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Peptic Ulcer Disease FactsPeptic Ulcer Disease FactsMost ulcers are caused by H. pylori Most ulcers are caused by H. pylori infection, not spicy food, acid or stress.infection, not spicy food, acid or stress.

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

H. pyloriH. pylori / ulcers can be tx’d c/ antibiotics. / ulcers can be tx’d c/ antibiotics.

Complications:Complications:– A Major complication is bleeding & perforationA Major complication is bleeding & perforation– Erosion of a small vessel at the base of the ulcer is Erosion of a small vessel at the base of the ulcer is

the cause of the bleedingthe cause of the bleeding– Perforation is usually catastrophic causing peritonitisPerforation is usually catastrophic causing peritonitis

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What is H. pyloriWhat is H. pylori

Helicobacter pyloriHelicobacter pylori ( (H. pyloriH. pylori) is a ) is a gram negative spiral-shaped bacillus gram negative spiral-shaped bacillus found in the gastric mucous layer or found in the gastric mucous layer or adherent to the epithelial lining of the adherent to the epithelial lining of the stomach. stomach.

H. pyloriH. 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 with How do people get infected with H. pyloriH. pylori??

It is not known how It is not known how H. pyloriH. pylori is transmitted or is transmitted or why some patients become symptomatic while why some patients become symptomatic while others do not. others do not.

The bacteria are most likely spread from person The bacteria are most likely spread from person to person through fecal-oral or oral-oral routes. to person through fecal-oral or oral-oral routes.

Possible environmental reservoirs include:Possible environmental reservoirs include:– contaminated water sourcescontaminated water sources– Iatrogenic spread through contaminated endoscopes Iatrogenic spread through contaminated endoscopes

has been documented but can be prevented has been documented but can be prevented

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What can people do to prevent What can people do to prevent H. H. pylori pylori infection? infection?

Since the source of Since the source of H. pyloriH. pylori is not yet known, is not yet known, recommendations for avoiding infection have recommendations for avoiding infection have not been made. not been made.

In general, it is always wise for persons to wash In general, it is always wise for persons to wash hands thoroughly, to eat food that has been hands thoroughly, to eat food that has been properly prepared, and to drink water from a properly 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, spicy food, Before this bacterium was discovered, spicy food, acid, stress, and lifestyle were considered the acid, stress, and lifestyle were considered the major causes of ulcers. major causes of ulcers.

The majority of patients were given long-term The majority of patients were given long-term medications, such as H2 blockers, and more medications, such as H2 blockers, and more recently, proton pump inhibitors, without a chance recently, proton pump inhibitors, without a chance for permanent cure. for permanent cure.

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

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H. PyloriH. Pylori infection infection

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

Since we now know that most ulcers are caused Since we now know that most ulcers are caused by by H. pyloriH. pylori, appropriate antibiotic regimens can , appropriate antibiotic regimens can successfully eradicate the infection in most successfully eradicate the infection in most patients, with complete resolution of mucosal patients, with complete resolution of mucosal inflammation and a minimal chance for inflammation and a minimal chance for recurrence of ulcers.recurrence of ulcers.

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What illnesses does What illnesses does H. pyloriH. 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. pyloriH. pylori causes chronic active, chronic persistent, and atrophic causes chronic active, chronic persistent, and atrophic gastritis in adults and children. gastritis in adults and children.

Infection with Infection with H. pyloriH. pylori also causes duodenal and gastric also causes duodenal and gastric ulcers. Infected persons have a 2- to 6-fold increased ulcers. Infected persons have a 2- to 6-fold increased risk of developing gastric cancer and mucosal-risk of developing gastric cancer and mucosal-associated-lymphoid-type (MALT) lymphoma compared associated-lymphoid-type (MALT) lymphoma compared with their uninfected counterparts. with their uninfected counterparts.

The role of The role of H. pyloriH. pylori in non-ulcer dyspepsia remains in non-ulcer dyspepsia remains unclear. unclear.

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Peptic Ulcer Disease SymptomsPeptic Ulcer Disease Symptoms#1. Epigastric Pain#1. Epigastric Pain– BurningBurning– Occurs 1-3 hrs p/ mealsOccurs 1-3 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 outlet complete gastric outlet obstructionobstruction

DyspepsiaDyspepsia– Belching/ BloatingBelching/ Bloating

HeartburnHeartburnChest DiscomfortChest DiscomfortAnorexiaAnorexiaWeight loss Weight loss – In gastric ulcers (also in In 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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Chinese ProverbsChinese ProverbsMan with one chopstick go hungry.Man with one chopstick go hungry.

Man who scratch ass should not bite fingernails.Man who scratch ass should not bite fingernails.

  Man who eat many prunes get good run for money.Man who eat many prunes get good run for money.

Baseball is wrong: man with four balls cannot walk.Baseball is wrong: man with four balls cannot walk.

Panties not best thing on earth! But next to best thing on earth.Panties not best thing on earth! But next to best thing on earth.

Man who fight with wife all day get no piece at night.Man who fight with wife all day get no piece at night.

It take many nails to build crib, but one screw to fill it.It take many nails to build crib, but one screw to fill it. Man who drive like hell, bound to get there.Man who drive like hell, bound to get there.

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Who should be tested and Who should be tested and treated for treated for H. pylori H. pylori ??

Persons with active gastric or duodenal Persons with active gastric or duodenal ulcers or documented history of ulcers ulcers or documented history of ulcers should be tested for should be tested for H. pyloriH. pylori, and if found , and if found to be infected, they should be treated. to be infected, they should be treated.

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

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PUD TestsPUD TestsLaboratory Test:Laboratory Test:– Routine tests are of little importance. Having a CBC is Routine 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– AmylaseAmylase– ElectrolytesElectrolytes– Serum Gastrin level if ZE syndrome is suspectedSerum Gastrin level if ZE syndrome is suspected

Frequently occurring duodenal ulcers or multiple Frequently occurring duodenal ulcers or multiple Duodenal Ulcers*Duodenal Ulcers*

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How is How is H. pyloriH. pylori infection diagnosed? infection diagnosed? Several methods may be used to diagnose Several methods may be used to diagnose H. pylori H. pylori infection.infection. Serological testsSerological tests that measure specific that measure specific H. pylori H. pylori IgG IgG antibodies 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 AssayUrea Breath testUrea Breath test – In this test, the patient is given either 13C- or 14C-labeled urea to In this test, the patient is given either 13C- or 14C-labeled urea to

drink. drink. – H. pylori H. pylori metabolizes the urea rapidly, and the labeled carbon is metabolizes the urea rapidly, and the labeled carbon is

absorbed. absorbed. – This labeled carbon can then be measured as CO2 in the patient's This 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%. – PPI’s can give false negative resultsPPI’s can give false negative results

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How is How is H. pyloriH. pylori infection in PUD infection in PUD diagnosed? diagnosed?

UpperUpper 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. pyloriH. pylori by Endoscopy by EndoscopyDuring endoscopy, biopsy specimens of the During endoscopy, biopsy specimens of the stomach and duodenum are obtained and the stomach and duodenum are obtained and the diagnosis of diagnosis of H. pylori H. pylori can be made by several can be made by several methods: methods: – The biopsy urease test - a colorimetric test based on The biopsy urease test - a colorimetric test based on

the ability of the ability of H. pylori H. pylori to produce urease; it provides to produce urease; it provides rapid testing at the time of biopsy. rapid testing at the time of biopsy.

– Histologic identification of organisms - considered the Histologic identification of organisms - considered 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, which which requires an experienced laboratory and is necessary requires an experienced laboratory and is necessary when antimicrobial susceptibility testing is desiredwhen antimicrobial susceptibility testing is desired

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Peptic Ulcer Disease TherapyPeptic Ulcer Disease TherapyNon-Pharmacological Non-Pharmacological – Diet change is of no valueDiet change is of no value– Smoking CessationSmoking Cessation

Smoking delays healingSmoking delays healing

– DC medications that enhance the progressionDC medications that enhance the progressionNSAIDSNSAIDS

Pharmacological TherapyPharmacological Therapy– Inhibit secretion of acidInhibit secretion of acid– Neutralizing gastric acidsNeutralizing gastric acids– Augmentation of protection of mucosaAugmentation of protection of mucosa– Antibiotics prnAntibiotics 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

AntacidsAntacids

Proton pump inhibitorsProton pump inhibitors

AnticholinergicsAnticholinergics

ProstaglandinsProstaglandins

Augmentation protectionAugmentation protection

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Peptic Ulcer Disease TherapyPeptic Ulcer Disease TherapyAntacids Antacids (magnesium, aluminum, & calcium based) (magnesium, aluminum, & calcium based)

– cause diarrheacause diarrhea

Moderate to high doses of H2 blockers result in Moderate to high doses of H2 blockers result in improved healing ratesimproved healing rates– Used 1 hr PC & HS for 6-8 wksUsed 1 hr PC & HS for 6-8 wks– Side effects:Side effects:

Hypermagnesemia (careful in renal patients)Hypermagnesemia (careful in renal patients)Aluminum causes phosphate depletion & osteoporosisAluminum causes phosphate depletion & osteoporosisSodium overload in CHFSodium overload in CHFHypercalcium causing Milk alkali syndromeHypercalcium causing Milk alkali syndromeInhibits 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,K-ATPase pumpInhibit the H,K-ATPase pump– Healing rate 80-100%Healing rate 80-100%– Prilosec (Omeprazole)Prilosec (Omeprazole)

Anticholinergics: reduce acid by 50% and Anticholinergics: reduce acid by 50% and cause blurred vision cause 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 in Inhibit 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 to Primary role is to be used as a prophylactic agent to

prevent NSAID induced ulcers. Not used as a prevent NSAID induced ulcers. Not used as a primary 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 & pepsinAbsorbs bile & pepsin

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Screw the environment carpooling Screw the environment carpooling is badis bad

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What are the treatment regimens used for What are the treatment regimens used for H. pylori H. pylori eradication?eradication?

Current therapy for Current therapy for H. pylori H. pylori infection consists of infection consists of 10 days to 2 weeks of one or two effective 10 days to 2 weeks of one or two effective antibiotics, antibiotics, – amoxicillin, amoxicillin, – tetracycline tetracycline

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 (pepto-bismol), bismuth subsalicylate (pepto-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 with proton pump inhibitor in conjunction with the antibiotics helps the antibiotics helps – alleviate ulcer-related symptoms (i.e., alleviate ulcer-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 antibiotics and may enhance efficacy of the antibiotics against against H. pylori H. pylori at the gastric mucosal at the gastric mucosal surface.surface.

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

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

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FDA-approved treatment optionsFDA-approved treatment options1. Omeprazole 40 mg QD + clarithromycin 500 mg TID x 2 wks, 1. Omeprazole 40 mg QD + clarithromycin 500 mg TID x 2 wks, then omeprazole 20 mg QD x 2 wks then omeprazole 20 mg QD x 2 wks

-OR- -OR-

2. (Zantac) Ranitidine bismuth citrate (RBC) 400 mg BID + 2. (Zantac) Ranitidine bismuth citrate (RBC) 400 mg BID + clarithromycin 500 mg TID x 2 wks, then RBC 400 mg BID x 2 clarithromycin 500 mg TID x 2 wks, then RBC 400 mg BID x 2 wks wks

-OR--OR-

3. Bismuth subsalicylate (Pepto Bismol®) 525 mg QID + 3. Bismuth subsalicylate (Pepto Bismol®) 525 mg QID + metronidazole 250 mg QID + tetracycline 500 mg QID* x 2 wks + metronidazole 250 mg QID + tetracycline 500 mg QID* x 2 wks + H2 receptor antagonist therapy as directed x 4 wksH2 receptor antagonist therapy as directed x 4 wks

-OR--OR-

4. Lansoprazole 30 mg BID + amoxicillin 1 g BID + clarithromycin 4. Lansoprazole 30 mg BID + amoxicillin 1 g BID + clarithromycin 500 mg TID x 10 days 500 mg TID x 10 days

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FDA-approved treatment options FDA-approved treatment options (cont.)(cont.)

5. -OR- Lansoprazole 30 mg TID + amoxicillin 1 g TID x 5. -OR- Lansoprazole 30 mg TID + amoxicillin 1 g TID x 2 wks** 2 wks**

6. -OR- Rantidine bismuth citrate 400 mg BID + 6. -OR- Rantidine bismuth citrate 400 mg BID + clarithromycin 500 mg BID x 2 wks, then RBC 400 mg clarithromycin 500 mg BID x 2 wks, then RBC 400 mg BID x 2 wks BID x 2 wks

7. -OR- Omeprazole 20 mg BID + clarithromycin 500 mg 7. -OR- Omeprazole 20 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days BID + amoxicillin 1 g BID x 10 days

8. -OR- Lansoprazole 30 mg BID + clarithromycin 500 8. -OR- Lansoprazole 30 mg BID + clarithromycin 500 mg BID + amoxicillin 1 g BID x 10 days mg BID + amoxicillin 1 g BID x 10 days

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Long-term consequences of Long-term consequences of H. H. pyloripylori infection? infection?

Recent studies have shown an association between Recent studies have shown an association between long-term infection with long-term infection with H. pylori H. pylori and the and the development of development of gastric cancergastric cancer. .

Gastric cancer is the second most common cancerGastric cancer is the second most common cancer worldwideworldwide; it is most common in countries such as ; it is most common in countries such as Colombia and China, where Colombia and China, where H. pyloriH. pylori infects over infects over half the population in early childhood. half the population in early childhood.

In the United States, where In the United States, where H. pyloriH. pylori is less common is less common in young people, gastric cancer rates have in young people, gastric cancer rates have decreased.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 of BRBPR in stool)Hematochezia (passage of BRBPR 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: “coffee-grounds”Slow bleed: “coffee-grounds”

MelenaMelena– Black tarry stoolBlack tarry stool– Source:Source:

Upper GIUpper GIOr lower GI to right colonOr lower GI to right colon

HematocheziaHematochezia– Bright red blood in stoolBright red blood in stool– Source:Source:

Lower GILower GIOr Upper GI if massiveOr Upper GI if massive

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Occult bloodOccult bloodHemacult/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 day Obtain 2 different samples from 2 stools over a 3 day periodperiodLaxatives alter results causing both false-positive and Laxatives alter results causing both false-positive and false-negative resultsfalse-negative resultsFalse positive results from food rich in peroxidaseFalse positive results from food rich in peroxidase– Bloody meatsBloody meats– BroccoliBroccoli– TurnipsTurnips– CauliflowerCauliflower

False negatives from taking Vit. C or food containing False negatives from taking Vit. C or food containing vitamin Cvitamin CNeoplasms 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 GI Upper GI – #1 PUD#1 PUD

DuodenalDuodenalGastricGastric

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

– Mallory-Weiss tear Mallory-Weiss tear (Mucosal laceration @ EG (Mucosal laceration @ EG junction)junction)

– GastritisGastritis

Lower GI Lower GI – #1 Hemorrhoids#1 Hemorrhoids– #2 Anal Fissure#2 Anal Fissure– DiverticulosisDiverticulosis– IBDIBD– IntussusceptionIntussusception

Upper & Lower GIUpper & Lower GI– NeoplasmsNeoplasms– Angiodysplasias Angiodysplasias

(Osler’s disease)(Osler’s disease)

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GI BleedGI BleedGI bleeding is a powerful laxativeGI bleeding is a powerful laxative

GI 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 bleeding until proven otherwiseuntil proven otherwise

GI bleeding is secondary GI bleeding is secondary to cancer until proven to cancer until proven otherwiseotherwise

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GI BleedGI BleedNature & duration helps with evaluationNature & duration helps with evaluation

Presence 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 CANCERALWAYS R/O CANCER

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Upper GI bleedUpper GI bleed

4x more common than lower GI 4x more common than lower GI bleedbleed

R/O upper GI source by NG tube R/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 disease Signs 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 alcohol Acute bleeding after heavy alcohol ingestion or retching suggests a ingestion or retching suggests a Mallory-Weiss tear.Mallory-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 Treitz Defined as below ligament of Treitz – (divides duodenum/ jejunum)(divides duodenum/ jejunum)

95% from Colon95% from Colon

Less likely than Upper GI bleed to present Less likely than Upper GI bleed to present in 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 & coagulation coagulation

Multi-organ failureMulti-organ failure

Hemodynamic collapseHemodynamic collapse

Hyper-ammonia toxicityHyper-ammonia toxicity

Hepatorenal failureHepatorenal failure

EncephalopathyEncephalopathy

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MCC of GI Bleeding MCC 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 dsAnorectal ds

Inflammatory bowel dsInflammatory bowel ds

– Over 50 y/o c Major BleedOver 50 y/o c Major BleedDiverticulosisDiverticulosis

Vascular ectasiasVascular ectasias

MalignancyMalignancy

ischemiaischemia

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LABS1.CBC

2.PT/PTT/Thrombin time- DIC panel (FSP fibrin split products, fibrinogen, FDP fibrin degradation products, clotting time, D dimer assay)

3.Electrolytes/BUN/creatinine

4.Blood Type and Cross match

5.CXR/ AXR rarely helpful only if perforated

GI BLEED

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CXR PneumoperitoneumCXR Pneumoperitoneum

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Anoscopy/ Sigmoidoscopy VS. Anoscopy/ Sigmoidoscopy VS. ColonoscopyColonoscopy

Anoscopy/ Anoscopy/ SigmoidoscopySigmoidoscopy– Acceptable in <45 yo Acceptable in <45 yo

otherwise healthy to otherwise healthy to evaluate for:evaluate for:

Anorectal ds.Anorectal ds.

Inflammatory bowel ds.Inflammatory bowel ds.

Infectious colitisInfectious colitis

– If lesion found, no If lesion found, no further eval neededfurther eval needed

ColonscopyColonscopy– Used Diagnostically Used Diagnostically

and Therapeuticallyand Therapeutically– All >40-45 yo c/ + All >40-45 yo c/ +

guiaic or Fe+ guiaic or Fe+ deficiency anemiadeficiency anemia

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Flex SigFlex Sig

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Anoscopy/ Rigid SigmoidoscopyAnoscopy/ Rigid Sigmoidoscopy

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Super Duper Pooper ScooperSuper Duper Pooper Scooper

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ColonoscopyColonoscopy

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Urgent management of Upper GI Urgent management of Upper GI bleedsbleeds

2 Large bore IV lines need started c/ colloid solution 2 Large bore IV lines need started c/ colloid solution started until PRBC can be infused, if needed.started until PRBC can be infused, if needed.OctreotideOctreotide- Decreases portal HTN (it is administered - Decreases portal HTN (it is administered promptly 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 be and 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 PUDEndoscopyEndoscopy– 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 embolizationAngiographic embolization– Transvenous shunts (for portal HTN, and variceal bleeds)Transvenous shunts (for portal HTN, and variceal bleeds)

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Chinese ProverbsChinese Proverbs

Man who stand on toilet is high on pot.Man who stand on toilet is high on pot.

Man who live in glass house should change Man who live in glass house should change clothes in basement.clothes in basement. Man who fish in other man's well often catch Man who fish in other man's well often catch crabs.crabs. Man who fart in church sit in own pew.Man who fart in church sit in own pew. Crowded elevator smell different to midget.Crowded elevator smell different to midget.

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ReviewReviewAcute Erosive GastritisAcute Erosive Gastritis– D/C NSAIDS or add misoprostolD/C NSAIDS or add misoprostol– If bleeding caused by ASA; consider platelet If bleeding caused by ASA; consider platelet

administrationadministration– 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

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ReviewReviewPeptic Ulcer DiseasePeptic Ulcer Disease– Almost all need Pepsin, Acid, & Almost all need Pepsin, Acid, & H. pyloriH. pylori to form ulcer to form ulcer– Eradicate H. pylori Eradicate H. pylori – Endoscopic bx to exclude adenocarcinoma Endoscopic bx to exclude adenocarcinoma

recommended for all patientsrecommended for all patients– If refractory: obtain fasting serum gastrin levels to If refractory: obtain fasting serum gastrin levels to

exclude Zollinger-Ellisonexclude Zollinger-Ellison– Consider parietal cell vagotomy. Consider parietal cell vagotomy.

Partial gastrectomy c/ gastro-duodenostomy (Billroth I) or Partial gastrectomy c/ gastro-duodenostomy (Billroth I) or gastrojejunostomy (Billroth II) are rarely used now.gastrojejunostomy (Billroth II) are rarely used now.

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ReviewReviewUpper GI BleedUpper GI Bleed– Evaluate hemodynamic status, stabilizeEvaluate hemodynamic status, stabilize– Nasogastric tubeNasogastric tube– OctreotideOctreotide– Endoscopy if bleeding is severe enough to Endoscopy if bleeding is severe enough to

require blood transfusionsrequire blood transfusions– Bleeding from esophageal varices: endoscopic Bleeding from esophageal varices: endoscopic

sclerotherapy preferredsclerotherapy preferred

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ReviewReviewLower GI BleedLower GI Bleed– The most common cause of significant bleeding is The most common cause of significant bleeding is

diverticular bleeding; that of intermittent minor diverticular bleeding; that of intermittent minor hematochezia is hemorrhoidal bleedinghematochezia is hemorrhoidal bleeding

– Evaluate hemodynamic status, stabilizeEvaluate hemodynamic status, stabilize– Colonoscopy if bleeding is severe or patient >50 yrs Colonoscopy 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 Intra-arterial bleeding is slow or intermittent), or Intra-arterial vasopressin or embolization.vasopressin or embolization.

– Surgery as last resortSurgery as last resort

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