peptic ulcer. rubel ppt

Peptic Ulcer Peptic Ulcer DiseaseDisease

PROFESSOR A. M. S. M. SHARFUZZAMAN

PROFESSOR OF SURGERYTuesday, April 11, 2023Tuesday, April 11, 2023 DR. RUBEL, SSMCDR. RUBEL, SSMC 11

Tuesday, April 11, 2023Tuesday, April 11, 2023 DR. RUBEL, SSMCDR. RUBEL, SSMC

Learning ObjectivesTo be able to decide on the most

appropriate techniques to use in the investigation of patients with complaints relating to the stomach and duodenum.

To understand the critical importance of gastritis and Helicobacter pylori in upper gastrointestinal disease.

To be able to investigate and treat peptic ulcer disease and its complications.

22

DefinitionDefinition PePeptic Ulcer Diseaseptic Ulcer Disease is defined as is defined as an an ulcerulcer occurring in a region that occurring in a region that touches touches gastric acid gastric acid and and pepsinpepsin and and usually refers to usually refers to gastric ulcer or gastric ulcer or duodenal ulcer.duodenal ulcer.Sites:Duodenum, ……(80%)Stomach ……….(19%)Duodenum and Stomach……(4%)G-E junctionGastro-jejunostomy site (1%)

Meckel’s diverticulum Tuesday, April 11, 2023Tuesday, April 11, 2023 DR. RUBEL, SSMCDR. RUBEL, SSMC 33

ErosionErosion : :

a superficial lesion caused by a superficial lesion caused by denudation of the surface epitheliumdenudation of the surface epithelium

Ulcer Ulcer ::

a mucosal defect extending into the a mucosal defect extending into the muscularis mucosamuscularis mucosa

Tuesday, April 11, 2023Tuesday, April 11, 2023 DR. RUBEL, SSMCDR. RUBEL, SSMC 44

Epidemiology of peptic ulcerationEpidemiology of peptic ulcerationFrequencyUnited States:

One-year point prevalence is 1.8%. Lifetime prevalence is approximately 10%. PUD affects approximately 4.5 million people annually.

Internationally:

The prevalence of H pylori infection in developing countries is as high as 50-100%. The prevalence of PUD is increasing in developing countries.

SexThere is a 3 to 1 male to female ratio for GU and 4 to 1 for DU. Prevalence has shifted from predominance in males to similar occurrences for both sexes.

Lifetime prevalence is approximately 11-14% for men and 8-11% for women.

AgeThe peak age for DU is increasing(25-50 years worldwide but higher in developed countries), GU occurs in older age groups>50


Mucosal defences against peptic ulcerationEXTRAMUCOSAL

Mucous cap; a hydrophobic gel layer secreted by the mucus cells,

Buffer layer; hydrogen carbonate is trapped in the mucous cap buffering the acid,

Bicarbonate secretion: leads to a pH gradient from 2 in the lumen to 7 on the epithelial surface.

MUCOSAL

Luminal cells resistance to acid.

Mucosal integrity(prostaglandin helps to maintain this so is reduced when taking NSAIDs; other growth factors also help and are inhibited by alcohol)

Tight cell junctions.

MICROVASCULAR

The microcirculation neutralises acid and removes toxic substances; smoking-related microvascular disease reduces this blood flow.


NormalNormal

Increased AttackIncreased Attack

HyperacidityHyperacidity

Weak defenseWeak defense

Helicobacter pyloriHelicobacter pylori Stress, drugs, Stress, drugs, smokingsmoking

Pathogenesis;


Pathogenesis;Pathogenesis;

Damaging forces: - Acid- Pepsin

Defensive forces:*Surface mucous, *Bicarbonate ion in mucous, *Mucosal blood Flow, *Apical surface membrane transport, *Epithelial regeneration, *Prostaglandins


Etiology;Etiology;H.PyloriH.Pylori

Urease – Ammonia stimulates gastrin Urease – Ammonia stimulates gastrin release, increases acid secretionrelease, increases acid secretionProtease – breaks glycoprotein of mucousProtease – breaks glycoprotein of mucousLipopolysaccharide – attracts neutrophilsLipopolysaccharide – attracts neutrophils

HyperacidityHyperacidityZollinger – Ellison SyndromeZollinger – Ellison Syndrome multiple endocrine neoplasia (MEN-I) multiple endocrine neoplasia (MEN-I) Antral G cell hyperplasia Antral G cell hyperplasia Systemic mastocytosis Systemic mastocytosis Basophilic leukemiasBasophilic leukemias

DrugsDrugsNSAIDSNSAIDSCorticosteroidsCorticosteroids

Systemic stressesSystemic stressesCigarette smoking, Alcohol Cigarette smoking, Alcohol Rapid gastric emptying Rapid gastric emptying Personality and stressPersonality and stress

No effect of genetics and spicy foods


Helicobacter pylori:Helicobacter pylori:Most common infection in the world Most common infection in the world (20%)(20%)

10% of men, 4% women develop PUD10% of men, 4% women develop PUD

Positive in 70-100% of PUD patients.Positive in 70-100% of PUD patients.

H.pylori related disorders:H.pylori related disorders:Chronic gastritis – 90%Chronic gastritis – 90%Peptic ulcer disease – 95-100%Peptic ulcer disease – 95-100%Gastric carcinoma – 70%Gastric carcinoma – 70%Gastric lymphomaGastric lymphomaReflux Oesophagitis.Reflux Oesophagitis.Non ulcer dyspepsiaNon ulcer dyspepsia


H. pylori – silver stainH. pylori – silver stain


H. pylori – giemsa stainH. pylori – giemsa stain


H. H. pyloripylori – H & E stain – H & E stain


H. PyloriH. Pylori

S-shaped gram S-shaped gram negative rod, negative rod, flagella flagella

Produces urease, Produces urease, protease, cytotoxin protease, cytotoxin

Alters acid Alters acid secretory function secretory function

Binds to mucosal Binds to mucosal blood group blood group antigen antigen Colonization rate Colonization rate increases with increases with age: up to 50% in age: up to 50% in persons >50 yearspersons >50 years


Risk factors for H.Pylori infection; Birth in a developing country

Low socioeconomic status

Crowded living conditions

Large families

Unsanitary living conditions

Unclean food or water

Presence of infants in the home

Exposure to gastric contents of infected individuals


Pathogenetic qualities of H.pylori;

Adheres to gastric epitheliumLives within mucous gel layer overlying gastric epitheliumPenetrates intercellular junctionsInvades gastric glands and canaliculi of parietal cellsSecretes urease to produce ammonia, which protects it from

gastric acidProduces cytotoxins that may play role in pathogenicityInduces epithelial cytolysis and disrupts intercellular

junctionsIncreases permeability of mucous layer to hydrogen ions

and pepsinEnables gastric acid and pepsin to create ulcer cratersEvades host immune defensesDamages tissue.


Peptic Ulcer Peptic Ulcer Size – variable; 0.3 – 4 cm in Size – variable; 0.3 – 4 cm in diameterdiameter

Shape - round to ovalShape - round to oval

Sharply demarcated, clean-Sharply demarcated, clean-cut, punched-out area with cut, punched-out area with clean baseclean base

Margins are usually level Margins are usually level with surrounding mucosa or with surrounding mucosa or slightly elevated due to slightly elevated due to edema; the mucosa is edema; the mucosa is undermined at the edgesundermined at the edges

Radiating mucosal rugaeRadiating mucosal rugae80% are solitary, 80% occur in the duodenum, of which 90% in the first part of the duodenum on the anterior wall’ within a few centimeter of the pyloric ring.19% occur in the stomach(usually at the lesser curvature at the border of the body and antrum.Tuesday, April 11, 2023Tuesday, April 11, 2023 DR. RUBEL, SSMCDR. RUBEL, SSMC 1717

Gastric Ulcer-Gastric Ulcer- Endoscopic AppearanceEndoscopic Appearance


Gastric Ulcer-Gastric Ulcer- Gross AppearanceGross Appearance

Sharply Sharply punched-out punched-out Large, Large, mucosal mucosal defect or defect or ulcer ulcer Radiating Radiating mucosal foldsmucosal folds


Acute Gastric UlcerAcute Gastric Ulcer


Giant gastric ulcerGiant gastric ulcer


Gastric UlcerGastric Ulcer


Duodenal Peptic Ulcers- Duodenal Peptic Ulcers- GrossGross


Duodenal Peptic Ulcer-Duodenal Peptic Ulcer-GrossGross


Microscopy:Microscopy:Overhanging gastric Overhanging gastric mucosal margins (mucosal margins (AA))

Necrotic fibrinoid Necrotic fibrinoid debris (debris (BB))

Acute inflammatory Acute inflammatory infiltrate (infiltrate (CC))

Granulation tissue Granulation tissue ((DD))

Fibrotic scarred Fibrotic scarred base (base (EE) )

A

B

C, D

E


Ulcer BaseUlcer Base

Superficial thin layer of Superficial thin layer of necrotic fibrinoid debris necrotic fibrinoid debris

Zone of inflammatory Zone of inflammatory infiltrate with neutrophils infiltrate with neutrophils

Zone of granulation Zone of granulation tissue with dilated blood tissue with dilated blood vessels and lymphocytes vessels and lymphocytes

Zone of fibrous scarringZone of fibrous scarring


H. Pylori - Lab StudiesH. Pylori - Lab Studies

HP fecal antigen testHP fecal antigen testMonoclonal antibody Monoclonal antibody immunochromatography of stool immunochromatography of stool samples. samples.

Very specific (98%) and sensitive (94%).Very specific (98%) and sensitive (94%). 1313Carbon-urea breath test Carbon-urea breath test

HP serology – IgGHP serology – IgG

Biopsy/HistopathologyBiopsy/Histopathology

CLO test,CLO test,

CultureCultureTuesday, April 11, 2023Tuesday, April 11, 2023 DR. RUBEL, SSMCDR. RUBEL, SSMC 2727

PUD - DiagnosisPUD - Diagnosis

Endoscopy upper GITEndoscopy upper GITBarium meal – contrast x-rayBarium meal – contrast x-rayBiopsy – bacteria & malignancyBiopsy – bacteria & malignancyH.Pylori:H.Pylori:

CLO testCLO test

Endoscopy cytologyEndoscopy cytologyBiopsy – Special stainsBiopsy – Special stainsCulture - difficultCulture - difficult 13/1413/14Carbon-Urea Breath test.Carbon-Urea Breath test.H.pylori serologyH.pylori serology


EndoscopyEndoscopy upper GIT upper GIT


Video-endoscopyVideo-endoscopy upper upper GITGIT


Video-endoscopy upper Video-endoscopy upper GITGIT


Typical radiographic features of Typical radiographic features of a duodenal ulcer;a duodenal ulcer;


Typical radiographic features of duodenal ulcer.Typical radiographic features of duodenal ulcer... Typical radiographic features of duodenal ulcer. This Typical radiographic features of duodenal ulcer. This duodenal bulb ulcer is associated with marked edema, duodenal bulb ulcer is associated with marked edema, resulting in the appearance of radiating folds to the ulcer resulting in the appearance of radiating folds to the ulcer crater. The bulb is also distorted secondary to previously crater. The bulb is also distorted secondary to previously existing ulcerationexisting ulceration


Typical radiographic features of Typical radiographic features of a benign gastric ulcer;a benign gastric ulcer;

A large A large well-well-circumscricircumscribed ulcer bed ulcer is seen on is seen on the the angularisangularis


Urease production Urease production test(CLO Test)test(CLO Test)


Acute Esophagitis & GastritisAcute Esophagitis & Gastritis


Acute GastritisAcute Gastritis


Gastric erosionsGastric erosions


Typical endoscopic appearance of a benign gastric ulcer. The ulcer is Typical endoscopic appearance of a benign gastric ulcer. The ulcer is on the angularis, the most common location for a gastric ulcer, and is on the angularis, the most common location for a gastric ulcer, and is well circumscribed without any associated mass effect. The well circumscribed without any associated mass effect. The

surrounding mucosa is mildly erythematous and without nodularity.surrounding mucosa is mildly erythematous and without nodularity.


A posterior duodenal ulcerA posterior duodenal ulcer


Erosions in the duodenal bulb and a Erosions in the duodenal bulb and a

posterior duodenal ulcerposterior duodenal ulcer


Clinical presentation of Clinical presentation of PUDPUD

Symptoms:Symptoms:Abdominal painAbdominal pain

located in the epigastric arealocated in the epigastric areaburning in qualityburning in qualityoccurred on an empty stomach 2 to 4 hours occurred on an empty stomach 2 to 4 hours after meals and/or at night (after meals and/or at night (nocturnal painnocturnal pain););relieved by antacids and/or mealsrelieved by antacids and/or mealstend to wax and wane over monthstend to wax and wane over months

““acid dyspepsiaacid dyspepsia” ” Tuesday, April 11, 2023Tuesday, April 11, 2023 DR. RUBEL, SSMCDR. RUBEL, SSMC 4242

Abdominal pain(cont.)Abdominal pain(cont.)the majority of patients (approximately the majority of patients (approximately 70%) with epigastric distress 70%) with epigastric distress ((““dyspepsiadyspepsia””) do not have evidence of ) do not have evidence of active ulcer disease;active ulcer disease;conversely up to 40% of patients with conversely up to 40% of patients with an active ulcer crater deny abdominal an active ulcer crater deny abdominal pain;pain;patients can present with an ulcer-patients can present with an ulcer-related complication, particularly related complication, particularly hemorrhage, without antecedent hemorrhage, without antecedent symptomssymptoms


Abdominal pain(cont.)Abdominal pain(cont.) DDespite being both insensitive and espite being both insensitive and non-specific, the symptom of non-specific, the symptom of epigastric abdominal pain, particularly epigastric abdominal pain, particularly burning after meals and at night and burning after meals and at night and relieved with food or antacid, relieved with food or antacid, suggests the possibility of ulcer suggests the possibility of ulcer disease.disease.


Other symptomsOther symptoms

gastro esophageal reflux including gastro esophageal reflux including upright and supine reflux and non-upright and supine reflux and non-cardiac chest paincardiac chest pain

symptoms of indigestion occurring with symptoms of indigestion occurring with or shortly after eating and characterized or shortly after eating and characterized by epigastric fullness and discomfort by epigastric fullness and discomfort belching bloating nausea early satiety belching bloating nausea early satiety and specific food intolerances.and specific food intolerances.


Signs;Signs;Physical examination is of Physical examination is of limited value in patients with limited value in patients with uncomplicated ulcer.uncomplicated ulcer.

For epigastric tendernessFor epigastric tenderness on deep on deep palpation, the sensitivity and specificity palpation, the sensitivity and specificity are all approximately 50% or less. are all approximately 50% or less.

Furthermore, many patients with non-Furthermore, many patients with non-ulcer diseases also have epigastric ulcer diseases also have epigastric tenderness on physical examination.tenderness on physical examination.


Signs(cont.)Signs(cont.) In patientsIn patients with with free perforationfree perforation or or ulcer penetrationulcer penetration into the pancreas, into the pancreas, findings of findings of peritonitis peritonitis are usually are usually present.present.

In patientsIn patients with with gastric retentiongastric retention who who have been fastinghave been fasting for a few hours, a for a few hours, a succussion splashsuccussion splash (produced by (produced by auscultating auscultating the abdomen while the abdomen while rocking the patient back and forth),rocking the patient back and forth), suggestssuggests retained gastric contents.retained gastric contents.


Complications:Complications:HemorrhageHemorrhage The most common complication of ulcer disease (in The most common complication of ulcer disease (in

approximately 15% of patients)approximately 15% of patients) manifest asmanifest as haematemesis and melena.haematemesis and melena.

Perforation Perforation Duodenal ulcersDuodenal ulcers: perforate anteriorly: perforate anteriorlyGastric ulcersGastric ulcers:: perforate along the anterior wall of the perforate along the anterior wall of the lesser curvature of the stomach.lesser curvature of the stomach.

PenetrationPenetrationMainly to posterior structure as pancreas.Mainly to posterior structure as pancreas.

Scarring and stenosisScarring and stenosisStomach:Stomach: tea-pot deformity, hour-glass contracture. tea-pot deformity, hour-glass contracture.DuodenumDuodenum: pyloric stenosis as GOO.: pyloric stenosis as GOO.


HemorrhageHemorrhageThe most common complication of The most common complication of ulcer disease (in approximately 15% of ulcer disease (in approximately 15% of patients)patients) manifest asmanifest as haematemesis haematemesis and melena. Bleeding: Upper and melena. Bleeding: Upper gastrointestinal (UGI) bleeding gastrointestinal (UGI) bleeding secondary to peptic ulcer is a common secondary to peptic ulcer is a common medical condition that results in high medical condition that results in high patient morbidity UGI bleeding patient morbidity UGI bleeding commonly presents with hematemesis commonly presents with hematemesis (vomiting of blood or coffee-ground (vomiting of blood or coffee-ground like material) and/or melena (black, like material) and/or melena (black, tarry stools).tarry stools).



D.U-HemorrhageD.U-Hemorrhage

Perforated peptic ulcer.Perforated peptic ulcer.Duodenal, antral, and gastric body ulcers account Duodenal, antral, and gastric body ulcers account for 60, 20 and 20percent of perforations due to for 60, 20 and 20percent of perforations due to peptic ulcer, respectively . One-third to one-half of peptic ulcer, respectively . One-third to one-half of perforated ulcers are associated with NSAID use; perforated ulcers are associated with NSAID use; these usually occur in elderly patients these usually occur in elderly patients


PenetrationPenetration Is similar pathologically to Is similar pathologically to perforationperforation, except that the ulcer , except that the ulcer cratercrater burrowsburrows through the entire through the entire wall of the intestine, and instead of wall of the intestine, and instead of leaking digestive contents into the leaking digestive contents into the peritoneal cavity, the crater boresperitoneal cavity, the crater bores into an adjacent organ. into an adjacent organ. Gastric ulcersGastric ulcers most commonly most commonly penetrate into the left lobe of the penetrate into the left lobe of the liver, while liver, while duodenal ulcersduodenal ulcers penetrate penetrate posteriorly into the adjacent posteriorly into the adjacent pancreas, sometimes leading to pancreas, sometimes leading to pancreatitis. Rarely, gastric ulcers pancreatitis. Rarely, gastric ulcers may penetrate into the colon, may penetrate into the colon, resulting in a gastrocolic fistularesulting in a gastrocolic fistula


Gastric outlet obstructionGastric outlet obstruction ((gastric gastric retentionretention

oror pyloric stenosispyloric stenosis); ); Gastric outlet obstruction is the least frequent Gastric outlet obstruction is the least frequent ulcer complication. Most cases are associated ulcer complication. Most cases are associated with duodenal or pyloric channel ulceration, with duodenal or pyloric channel ulceration, with gastric ulceration accounting for only 5 with gastric ulceration accounting for only 5 percent of cases. percent of cases.

functional impairment of antral motilityfunctional impairment of antral motility due to due to the effects of acute inflammation and edema;the effects of acute inflammation and edema;mechanical obstructionmechanical obstruction due to scarring near due to scarring near the gastroduodenal junction;the gastroduodenal junction;manifest as gastroesophageal reflux, early manifest as gastroesophageal reflux, early satiety, weight loss, abdominal pain, and satiety, weight loss, abdominal pain, and vomiting;vomiting;As the degree of retention increases, the As the degree of retention increases, the quantity of vomitusquantity of vomitus also increases, often also increases, often containing food ingested 12 or more hours containing food ingested 12 or more hours previously.previously.Tuesday, April 11, 2023Tuesday, April 11, 2023 DR. RUBEL, SSMCDR. RUBEL, SSMC 5353

Barium upper gastrointestinal Barium upper gastrointestinal study demonstrates the size of the study demonstrates the size of the stomach.stomach.

Pyloric stenosis


Endoscopy demonstrates the Endoscopy demonstrates the pyloric obstruction with an pyloric obstruction with an active ulcer crater seen in the active ulcer crater seen in the pyloric channel.pyloric channel.


Malignant Malignant transformationtransformation

(Gastric ulcer )(Gastric ulcer )



Malignant transformation

(Gastric ulcer )

TREATMENT;Medical treatment

Given the current understanding of the pathogenesis of PUD, most patients with PUD are treated successfully with cure of H pylori infection and/or avoidance of NSAIDs, along with the appropriate use of antisecretory therapy.

A number of treatment options exist for patients presenting with symptoms suggestive of PUD or ulcerlike dyspepsia, including empiric antisecretory therapy, empiric triple therapy for H pylori infection, endoscopy followed by appropriate therapy based on findings, and H pylori serology followed by triple therapy for patients who are infected. Breath testing for active H pylori infection may be used.


Medical treatment(cont.)

Computer models have suggested that obtaining H pylori serology followed by triple therapy for patients who are infected is the most cost-effective approach; however, no direct evidence from clinical trials provides confirmation.

Perform endoscopy early in patients older than 45-50 years and in patients with associated so-called alarm symptoms, such as dysphagia, recurrent vomiting, weight loss, or bleeding.


Surgical CareWith the success of medical therapy, surgery has a very limited role in the

management of PUD.

Potential indications for surgery include refractory disease. Complications of PUD include the following:

Refractory, symptomatic peptic ulcers, though rare with the cure of H pylori infection and the appropriate use of antisecretory therapy, are a potential complication of PUD.

Perforation usually is managed emergently with surgical repair. However, this is not mandatory for all patients.

Obstruction can complicate PUD, particularly if PUD is refractory to aggressive antisecretory therapy, H pylori eradication, or avoidance of NSAIDs. Obstruction may persist or recur despite endoscopic balloon dilation.


Surgical Care(cont.)Penetration, particularly if not walled off or if a gastrocolic fistula develops, is a potential complication of PUD.

Bleeding can complicate PUD, particularly in patients with massive hemorrhage and hemodynamic instability, recurrent bleeding on medical therapy, and failure of therapeutic endoscopy to control bleeding.

The appropriate surgical procedure depends on the location and nature of the ulcer.

Many authorities recommend simple oversewing of the ulcer with treatment of the underlying H pylori infection or cessation of NSAIDs for bleeding PUD.

Additional surgical options for refractory or complicated PUD include vagotomy and pyloroplasty, vagotomy and antrectomy with gastroduodenal reconstruction (Billroth I) or gastrojejunal reconstruction (Billroth II), or a highly selective vagotomy.


DietNo special diet is required.

MedicationTreat all patients with peptic ulcers and associated H pylori infection with proton pump inhibitor (PPI)-based triple therapy, which results in a cure rate of infection and healing in approximately 85-90% of cases. Ulcers can relapse in the absence of successful H pylori eradication.

Dual therapies, which are alternative regimens for treating H pylori infection, are usually not recommended as first-line therapy because of a variable cure rate that is significantly less than the cure rate achieved with triple therapy.

Active ulcers associated with NSAID use are treated with an appropriate course of PPI therapy and the cessation of NSAIDs. For patients with a known history of ulcer, and in whom NSAID use is unavoidable, the lowest possible dose and duration of the NSAID and co-therapy with a PPI or misoprostol are recommended


Medication(contd.)PPI-based triple therapies for H pylori are considered the first-line therapies for the treatment of H pylori in the United States with a cure rate of 85-90%. These regimens consist of a PPI, amoxicillin, and clarithromycin for 7-14 days. A longer duration of treatment (14 d vs 7 d) appears to be more affective and is currently the recommended duration of treatment. Amoxicillin should only be substituted by metronidazole in penicillin-allergic patients because of the high rate of metronidazole resistance.

In the setting of active ulcers caused by H pylori, treatment with a PPI beyond the 14-day course of antibiotics and until the confirmation for the eradication of

H pylori is recommended for complicated ulcers..


PPI-based triple therapies consist of a 14-day treatment of the following:

Omeprazole (Prilosec): 20 mg PO bid orLansoprazole (Prevacid): 30 mg PO bid orRabeprazole (Aciphex): 20 mg PO bid orEsomeprazole (Nexium): 40 mg PO qd

Plus:Clarithromycin (Biaxin): 500 mg PO bid andAmoxicillin (Amoxil): 1 g PO bid

The alternative combination therapy consists of the following treatments administered for 14 days:

Omeprazole (Prilosec): 20 mg PO bid orLansoprazole (Prevacid): 30 mg PO bid orRabeprazole (Aciphex): 20 mg PO bid orEsomeprazole (Nexium): 40 mg PO qd

Plus:Clarithromycin (Biaxin): 500 mg PO bid andMetronidazole (Flagyl): 500 mg PO bid


Quadruple therapiesfor H pylori infection are generally reserved for patients who have failed a course of treatment and are administered for 14 days. The treatment includes the following drugs:

PPI PO bid andBismuth 525 mg PO qid andMetronidazole 500 mg PO qid andTetracycline 500 mg PO qid


Further Outpatient CareEndoscopy is required to document healing of gastric ulcers and to rule out gastric cancer. This usually is performed 6-8 weeks after the initial diagnosis of PUD.

Documentation of H pylori cure with a noninvasive test, such as the urea breath test or fecal antigen test, is appropriate in patients with complicated ulcers

In/Out Patient MedsConsider maintenance therapy with half standard doses of H2-receptor antagonists at bedtime in patients with recurrent, refractory, or complicated ulcers, particularly if cure of H pylori has not been documented or if an H pylori-negative ulcer is present.


PREVENTIONPrimary prevention of NSAID-induced ulcers includes the following:

Avoid unnecessary use of NSAIDs.

Use acetaminophen or nonacetylated salicylates when possible.

Use the lowest effective dose of an NSAID and switch to less toxic NSAIDs, such as the newer NSAIDs or cyclooxygenase-2 (COX-2) inhibitors, in high-risk patients without cardiovascular disease.

Consider prophylactic or preventive therapy for the following patients:

Patients with NSAID-induced ulcers who require chronic, daily NSAID therapy

Patients older than 60 years

Patients with a history of PUD or a complication such as

gastrointestinal bleeding Patients taking concomitant steroids or anticoagulants or patients with

significant comorbid medical illnesses Tuesday, April 11, 2023Tuesday, April 11, 2023 DR. RUBEL, SSMCDR. RUBEL, SSMC 6868

PrognosisWhen the underlying cause is addressed, the prognosis is excellent. Most patients are treated successfully with the cure of H pylori infection, avoidance of NSAIDs, and the appropriate use of antisecretory therapy.

Cure of H pylori infection changes the natural history of the disease, with a decrease in the ulcer recurrence rate from 60-90% to approximately 10-20%. However, this is a higher recurrence rate than previously reported, suggesting an increased number of ulcers not caused by H pylori infection.

Patient EducationStop smoking.Avoid NSAID and aspirin use.Avoid heavy alcohol use.Stress reduction counseling might be helpful in individual cases but is not needed routinely..

Tuesday, April 11, 2023Tuesday, April 11, 2023DR. RUBEL, SSMCDR. RUBEL, SSMC 6969

Summary Most PU are caused by H. pylori or NSAIDs

and changes in epidemiology mirror changes in these principle etiological factors.

DU are more common than GU, but the symptoms are indistinguishable.

GU may become malignant and an ulcerated GU may mimic a benign ulcer.

Gastric antisecretory agents and H. pylori eradication therapy are the mainstay of treatment, and elective surgery is not now commonly performed.

The common complication of peptic ulcer are perforation, bleeding and stenosis.

The treatment of the perforated PU is primarily surgical, although some patients may be managed conservatively.


peptic ulcer. rubel ppt

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