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Peptic Ulcer Disease




                                          PROFESSOR A. M. S. M.
                                               SHARFUZZAMAN
Sunday, November 18, 2012   DR. RUBEL, SSMC                 1
                                         PROFESSOR OF SURGERY
Learning Objectives
  To 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.



Sunday, November 18, 2012   DR. RUBEL, SSMC               2
Definition
Peptic Ulcer Disease is defined as an ulcer
occurring in a region that touches gastric acid
and pepsin and usually refers to gastric ulcer or
duodenal ulcer.
Sites:
Duodenum, ……(80%)
Stomach ……….(19%)
Duodenum and Stomach……(4%)
G-E junction
Gastro-jejunostomy site (1%)
Meckel’s diverticulum
Sunday, November 18, 2012   DR. RUBEL, SSMC    3
Erosion :
    a superficial lesion caused by
denudation of the surface epithelium



 Ulcer :
     a mucosal defect extending into the
   muscularis mucosa



Sunday, November 18, 2012   DR. RUBEL, SSMC   4
Epidemiology of peptic ulceration
Frequency
United 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.

Sex
There 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.

Age
The peak age for DU is increasing(25-50 years worldwide but higher in
developed countries), GU occurs in older age groups>50
    Sunday, November 18, 2012      DR. RUBEL, SSMC                                5
Mucosal defences against peptic ulceration
EXTRAMUCOSAL
     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.
  Sunday, November 18, 2012       DR. RUBEL, SSMC                              6
Pathogenesis;

                              Normal

                              Increased Attack
                                          Hyperacidity

                              Weak defense
                                        Helicobacter pylori
                                   Stress, drugs,
                              smoking
 Sunday, November 18, 2012   DR. RUBEL, SSMC                  7
Pathogenesis;




Damaging forces: - Acid
                               - Pepsin

Defensive forces:*Surface mucous, *Bicarbonate ion in mucous, *Mucosal
                             blood Flow, *Apical surface membrane transport, *Epithelial
                             regeneration, *Prostaglandins
 Sunday, November 18, 2012                DR. RUBEL, SSMC                            8
Etiology;
  H.Pylori
                        Urease – Ammonia stimulates gastrin release, increases
                        acid secretion
                        Protease – breaks glycoprotein of mucous
                        Lipopolysaccharide – attracts neutrophils
  Hyperacidity
                        Zollinger – Ellison Syndrome
                        multiple endocrine neoplasia (MEN-I)
                        Antral G cell hyperplasia
                        Systemic mastocytosis
                        Basophilic leukemias
  Drugs                                                    No effect of
                  NSAIDS
                  Corticosteroids
                                                           genetics and
  Systemic stresses                                        spicy foods
  Cigarette smoking, Alcohol
  Rapid gastric emptying
  Personality and stress

 Sunday, November 18, 2012           DR. RUBEL, SSMC                             9
Helicobacter pylori:
        Most common infection in the world (20%)
        10% of men, 4% women develop PUD
        Positive in 70-100% of PUD patients.
        H.pylori related disorders:
             Chronic gastritis – 90%
             Peptic ulcer disease – 95-100%
             Gastric carcinoma – 70%
             Gastric lymphoma
             Reflux Oesophagitis.
             Non ulcer dyspepsia
 Sunday, November 18, 2012   DR. RUBEL, SSMC   10
H. pylori – silver stain




Sunday, November 18, 2012   DR. RUBEL, SSMC   11
H. pylori – giemsa stain




Sunday, November 18, 2012   DR. RUBEL, SSMC   12
H. pylori – H & E stain




Sunday, November 18, 2012   DR. RUBEL, SSMC   13
H. Pylori
                                               S-shaped gram
                                               negative rod, flagella
                                               Produces urease,
                                               protease, cytotoxin
                                               Alters acid secretory
                                               function
                                               Binds to mucosal
                                               blood group antigen
                                               Colonization rate
                                               increases with age:
                                               up to 50% in persons
                                               >50 years

 Sunday, November 18, 2012   DR. RUBEL, SSMC                       14
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



Sunday, November 18, 2012   DR. RUBEL, SSMC              15
Pathogenetic qualities of H.pylori;
        Adheres to gastric epithelium
        Lives within mucous gel layer overlying gastric epithelium
        Penetrates intercellular junctions
        Invades gastric glands and canaliculi of parietal cells
        Secretes urease to produce ammonia, which protects it from
               gastric acid
        Produces cytotoxins that may play role in pathogenicity
        Induces epithelial cytolysis and disrupts intercellular
               junctions
        Increases permeability of mucous layer to hydrogen ions
               and pepsin
        Enables gastric acid and pepsin to create ulcer craters
        Evades host immune defenses
        Damages tissue.
 Sunday, November 18, 2012   DR. RUBEL, SSMC                  16
Peptic Ulcer
  Size – variable; 0.3 – 4 cm in
 diameter
  Shape - round to oval
  Sharply demarcated, clean-cut,
 punched-out area with clean base
  Margins are usually level with
 surrounding mucosa or slightly
 elevated due to edema; the mucosa
 is undermined at the edges
  Radiating mucosal rugae
 80% 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.


 Sunday, November 18, 2012           DR. RUBEL, SSMC   17
Gastric Ulcer- Endoscopic Appearance




 Sunday, November 18, 2012   DR. RUBEL, SSMC   18
Gastric Ulcer- Gross Appearance


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

 Sunday, November 18, 2012   DR. RUBEL, SSMC               19
Acute Gastric Ulcer




 Sunday, November 18, 2012   DR. RUBEL, SSMC   20
Giant gastric ulcer




 Sunday, November 18, 2012   DR. RUBEL, SSMC   21
Gastric Ulcer




 Sunday, November 18, 2012   DR. RUBEL, SSMC   22
Duodenal Peptic Ulcers- Gross




 Sunday, November 18, 2012   DR. RUBEL, SSMC   23
Duodenal Peptic Ulcer-Gross




 Sunday, November 18, 2012   DR. RUBEL, SSMC   24
Microscopy:
                                                          Overhanging gastric
                                                          mucosal margins (A)
                  A
                             B                            Necrotic fibrinoid
                                 C, D                     debris (B)
                                                          Acute inflammatory
                                                          infiltrate (C)
                                                          Granulation tissue
                                                          (D)
                             E
                                                          Fibrotic scarred
                                                          base (E)

 Sunday, November 18, 2012              DR. RUBEL, SSMC                  25
Ulcer Base
                                              Superficial thin layer of
                                              necrotic fibrinoid debris
                                              Zone of inflammatory
                                              infiltrate with neutrophils
                                              Zone of granulation
                                              tissue with dilated blood
                                              vessels and lymphocytes
                                              Zone of fibrous scarring




Sunday, November 18, 2012   DR. RUBEL, SSMC                         26
H. Pylori - Lab Studies
     HP fecal antigen test
               Monoclonal antibody immunochromatography of
               stool samples.
               Very specific (98%) and sensitive (94%).
     13
     Carbon-urea breath test
     HP serology – IgG
     Biopsy/Histopathology
     CLO test,
     Culture
 Sunday, November 18, 2012   DR. RUBEL, SSMC                 27
PUD - Diagnosis
    Endoscopy upper GIT
    Barium meal – contrast x-ray
    Biopsy – bacteria & malignancy
    H.Pylori:
         CLO test
         Endoscopy cytology
         Biopsy – Special stains
         Culture - difficult
         13/14
               Carbon-Urea Breath test.
         H.pylori serology
 Sunday, November 18, 2012   DR. RUBEL, SSMC   28
Endoscopy upper GIT




Sunday, November 18, 2012   DR. RUBEL, SSMC   29
Video-endoscopy upper GIT




 Sunday, November 18, 2012   DR. RUBEL, SSMC   30
Video-endoscopy upper GIT




 Sunday, November 18, 2012   DR. RUBEL, SSMC   31
Typical radiographic features of
a duodenal ulcer;




  Sunday, November 18, 2012   DR. RUBEL, SSMC   32
Typical radiographic features of duodenal ulcer. This
duodenal bulb ulcer is associated with marked edema,
resulting in the appearance of radiating folds to the ulcer
crater. The bulb is also distorted secondary to previously
existing ulceration




  Sunday, November 18, 2012   DR. RUBEL, SSMC             33
Typical radiographic features of
a benign gastric ulcer;
   A large well-
   circumscribed
   ulcer is seen
   on the
   angularis




 Sunday, November 18, 2012   DR. RUBEL, SSMC   34
Urease production test(CLO Test)




 Sunday, November 18, 2012   DR. RUBEL, SSMC   35
Acute Esophagitis & Gastritis




 Sunday, November 18, 2012   DR. RUBEL, SSMC   36
Acute Gastritis




 Sunday, November 18, 2012   DR. RUBEL, SSMC   37
Gastric erosions




Sunday, November 18, 2012   DR. RUBEL, SSMC   38
Typical endoscopic appearance of a benign gastric ulcer. The ulcer is
on the angularis, the most common location for a gastric ulcer, and is
well circumscribed without any associated mass effect. The
surrounding mucosa is mildly erythematous and without nodularity.




   Sunday, November 18, 2012   DR. RUBEL, SSMC                       39
A posterior duodenal ulcer




Sunday, November 18, 2012   DR. RUBEL, SSMC   40
Erosions in the duodenal bulb and a
posterior duodenal ulcer




  Sunday, November 18, 2012   DR. RUBEL, SSMC   41
Clinical presentation of PUD
Symptoms:
Abdominal pain
 located in the epigastric area
 burning in quality
 occurred on an empty stomach 2 to 4 hours after meals
 and/or at night (nocturnal pain);
 relieved by antacids and/or meals
 tend to wax and wane over months
           “acid dyspepsia”
Sunday, November 18, 2012   DR. RUBEL, SSMC        42
Abdominal pain(cont.)
   the majority of patients (approximately 70%)
   with epigastric distress (“dyspepsia”) do not
   have evidence of active ulcer disease;
   conversely up to 40% of patients with an
   active ulcer crater deny abdominal pain;
   patients can present with an ulcer-related
   complication, particularly hemorrhage,
   without antecedent symptoms

Sunday, November 18, 2012   DR. RUBEL, SSMC    43
Abdominal pain(cont.)
Despite being both insensitive and
non-specific, the symptom of
epigastric abdominal pain, particularly
burning after meals and at night and
relieved with food or antacid,
suggests the possibility of ulcer
disease.

 Sunday, November 18, 2012   DR. RUBEL, SSMC   44
Other symptoms
 gastro esophageal reflux including upright and supine
 reflux and non-cardiac chest pain

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




Sunday, November 18, 2012   DR. RUBEL, SSMC         45
Signs;
Physical examination is of limited value
in patients with uncomplicated ulcer.

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

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


 Sunday, November 18, 2012   DR. RUBEL, SSMC   46
Signs(cont.)
    In patients with free perforation or ulcer
    penetration into the pancreas, findings of
    peritonitis are usually present.

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




Sunday, November 18, 2012   DR. RUBEL, SSMC            47
Complications:
Hemorrhage
 The most common complication of ulcer disease (in approximately
  15% of patients) manifest as haematemesis and melena.
Perforation
  Duodenal ulcers: perforate anteriorly
  Gastric ulcers: perforate along the anterior wall of the lesser
  curvature of the stomach.
Penetration
  Mainly to posterior structure as pancreas.
Scarring and stenosis
  Stomach: tea-pot deformity, hour-glass contracture.
  Duodenum: pyloric stenosis as GOO.


  Sunday, November 18, 2012   DR. RUBEL, SSMC                       48
Hemorrhage
The most common complication of ulcer disease (in
approximately 15% of patients) manifest as
haematemesis and melena. Bleeding: Upper
gastrointestinal (UGI) bleeding secondary to peptic
ulcer is a common medical condition that results in
high patient morbidity UGI bleeding commonly
presents with hematemesis (vomiting of blood or
coffee-ground like material) and/or melena (black,
tarry stools).



Sunday, November 18, 2012   DR. RUBEL, SSMC           49
D.U-Hemorrhage




  Sunday, November 18, 2012   DR. RUBEL, SSMC   50
Perforated peptic ulcer.
Duodenal, antral, and gastric body ulcers account for 60, 20 and
20percent of perforations due to peptic ulcer, respectively . One-third
to one-half of perforated ulcers are associated with NSAID use; these
usually occur in elderly patients




   Sunday, November 18, 2012   DR. RUBEL, SSMC                    51
Penetration
 Is similar pathologically to perforation,
 except that the ulcer crater burrows through
 the entire wall of the intestine, and instead
 of leaking digestive contents into the
 peritoneal cavity, the crater bores into an
 adjacent organ.
 Gastric ulcers most commonly penetrate
 into the left lobe of the liver, while duodenal
 ulcers penetrate posteriorly into the adjacent
 pancreas, sometimes leading to pancreatitis.
 Rarely, gastric ulcers may penetrate into the
 colon, resulting in a gastrocolic fistula
 Sunday, November 18, 2012   DR. RUBEL, SSMC       52
Gastric outlet obstruction (gastric retention
or pyloric stenosis);
  Gastric outlet obstruction is the least frequent ulcer
  complication. Most cases are associated with duodenal
  or pyloric channel ulceration, with gastric ulceration
  accounting for only 5 percent of cases.

  functional impairment of antral motility due to the
  effects of acute inflammation and edema;
  mechanical obstruction due to scarring near the
  gastroduodenal junction;
  manifest as gastroesophageal reflux, early satiety,
  weight loss, abdominal pain, and vomiting;
  As the degree of retention increases, the quantity of
  vomitus also increases, often containing food ingested
  12 or more hours previously.
  Sunday, November 18, 2012   DR. RUBEL, SSMC         53
Barium upper gastrointestinal study
demonstrates the size of the stomach.

 Pyloric
 stenosis




  Sunday, November 18, 2012   DR. RUBEL, SSMC   54
Endoscopy demonstrates the pyloric
obstruction with an active ulcer crater seen
in the pyloric channel.




  Sunday, November 18, 2012   DR. RUBEL, SSMC   55
Malignant transformation
                            (Gastric ulcer )




Sunday, November 18, 2012      DR. RUBEL, SSMC   56
Malignant transformation
                            (Gastric ulcer )




Sunday, November 18, 2012      DR. RUBEL, SSMC   57
Malignant transformation
                            (Gastric ulcer )




Sunday, November 18, 2012      DR. RUBEL, SSMC   58
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.

  Sunday, November 18, 2012   DR. RUBEL, SSMC                  59
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.



  Sunday, November 18, 2012   DR. RUBEL, SSMC               60
Surgical Care
 With 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.

    Sunday, November 18, 2012      DR. RUBEL, SSMC                           61
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.
  Sunday, November 18, 2012        DR. RUBEL, SSMC                               62
Diet
No special diet is required.

Medication
Treat 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

    Sunday, November 18, 2012      DR. RUBEL, SSMC                           63
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..




    Sunday, November 18, 2012      DR. RUBEL, SSMC                           64
PPI-based triple therapies consist of a 14-day treatment of the
following:
        Omeprazole (Prilosec): 20 mg PO bid or
        Lansoprazole (Prevacid): 30 mg PO bid or
        Rabeprazole (Aciphex): 20 mg PO bid or
        Esomeprazole (Nexium): 40 mg PO qd
                 Plus:
        Clarithromycin (Biaxin): 500 mg PO bid and
        Amoxicillin (Amoxil): 1 g PO bid

The alternative combination therapy consists of the following
treatments administered for 14 days:
        Omeprazole (Prilosec): 20 mg PO bid or
        Lansoprazole (Prevacid): 30 mg PO bid or
        Rabeprazole (Aciphex): 20 mg PO bid or
        Esomeprazole (Nexium): 40 mg PO qd
                 Plus:
        Clarithromycin (Biaxin): 500 mg PO bid and
        Metronidazole (Flagyl): 500 mg PO bid
   Sunday, November 18, 2012    DR. RUBEL, SSMC           65
Quadruple therapies
for 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 and
Bismuth 525 mg PO qid and
Metronidazole 500 mg PO qid and
Tetracycline 500 mg PO qid




 Sunday, November 18, 2012   DR. RUBEL, SSMC          66
Further Outpatient Care
  Endoscopy 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 Meds
  Consider 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.




  Sunday, November 18, 2012      DR. RUBEL, SSMC                           67
PREVENTION
 Primary 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
 Sunday, November 18, 2012      DR. RUBEL, SSMC                          68
Prognosis
       When 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 Education
       Stop smoking.
       Avoid NSAID and aspirin use.
       Avoid heavy alcohol use.
       Stress reduction counseling might be helpful in individual cases but is
       not needed routinely.
       .
                                 DR. RUBEL, SSMC                          69
   Sunday, November 18, 2012
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.
 Sunday, November 18, 2012   DR. RUBEL, SSMC                   70
Sunday, November 18, 2012   DR. RUBEL, SSMC   71

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Peptic ulcer. rubel ppt

  • 1. Peptic Ulcer Disease PROFESSOR A. M. S. M. SHARFUZZAMAN Sunday, November 18, 2012 DR. RUBEL, SSMC 1 PROFESSOR OF SURGERY
  • 2. Learning Objectives To 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. Sunday, November 18, 2012 DR. RUBEL, SSMC 2
  • 3. Definition Peptic Ulcer Disease is defined as an ulcer occurring in a region that touches gastric acid and pepsin and usually refers to gastric ulcer or duodenal ulcer. Sites: Duodenum, ……(80%) Stomach ……….(19%) Duodenum and Stomach……(4%) G-E junction Gastro-jejunostomy site (1%) Meckel’s diverticulum Sunday, November 18, 2012 DR. RUBEL, SSMC 3
  • 4. Erosion : a superficial lesion caused by denudation of the surface epithelium Ulcer : a mucosal defect extending into the muscularis mucosa Sunday, November 18, 2012 DR. RUBEL, SSMC 4
  • 5. Epidemiology of peptic ulceration Frequency United 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. Sex There 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. Age The peak age for DU is increasing(25-50 years worldwide but higher in developed countries), GU occurs in older age groups>50 Sunday, November 18, 2012 DR. RUBEL, SSMC 5
  • 6. Mucosal defences against peptic ulceration EXTRAMUCOSAL 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. Sunday, November 18, 2012 DR. RUBEL, SSMC 6
  • 7. Pathogenesis; Normal Increased Attack Hyperacidity Weak defense Helicobacter pylori Stress, drugs, smoking Sunday, November 18, 2012 DR. RUBEL, SSMC 7
  • 8. Pathogenesis; Damaging forces: - Acid - Pepsin Defensive forces:*Surface mucous, *Bicarbonate ion in mucous, *Mucosal blood Flow, *Apical surface membrane transport, *Epithelial regeneration, *Prostaglandins Sunday, November 18, 2012 DR. RUBEL, SSMC 8
  • 9. Etiology; H.Pylori Urease – Ammonia stimulates gastrin release, increases acid secretion Protease – breaks glycoprotein of mucous Lipopolysaccharide – attracts neutrophils Hyperacidity Zollinger – Ellison Syndrome multiple endocrine neoplasia (MEN-I) Antral G cell hyperplasia Systemic mastocytosis Basophilic leukemias Drugs No effect of NSAIDS Corticosteroids genetics and Systemic stresses spicy foods Cigarette smoking, Alcohol Rapid gastric emptying Personality and stress Sunday, November 18, 2012 DR. RUBEL, SSMC 9
  • 10. Helicobacter pylori: Most common infection in the world (20%) 10% of men, 4% women develop PUD Positive in 70-100% of PUD patients. H.pylori related disorders: Chronic gastritis – 90% Peptic ulcer disease – 95-100% Gastric carcinoma – 70% Gastric lymphoma Reflux Oesophagitis. Non ulcer dyspepsia Sunday, November 18, 2012 DR. RUBEL, SSMC 10
  • 11. H. pylori – silver stain Sunday, November 18, 2012 DR. RUBEL, SSMC 11
  • 12. H. pylori – giemsa stain Sunday, November 18, 2012 DR. RUBEL, SSMC 12
  • 13. H. pylori – H & E stain Sunday, November 18, 2012 DR. RUBEL, SSMC 13
  • 14. H. Pylori S-shaped gram negative rod, flagella Produces urease, protease, cytotoxin Alters acid secretory function Binds to mucosal blood group antigen Colonization rate increases with age: up to 50% in persons >50 years Sunday, November 18, 2012 DR. RUBEL, SSMC 14
  • 15. 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 Sunday, November 18, 2012 DR. RUBEL, SSMC 15
  • 16. Pathogenetic qualities of H.pylori; Adheres to gastric epithelium Lives within mucous gel layer overlying gastric epithelium Penetrates intercellular junctions Invades gastric glands and canaliculi of parietal cells Secretes urease to produce ammonia, which protects it from gastric acid Produces cytotoxins that may play role in pathogenicity Induces epithelial cytolysis and disrupts intercellular junctions Increases permeability of mucous layer to hydrogen ions and pepsin Enables gastric acid and pepsin to create ulcer craters Evades host immune defenses Damages tissue. Sunday, November 18, 2012 DR. RUBEL, SSMC 16
  • 17. Peptic Ulcer Size – variable; 0.3 – 4 cm in diameter Shape - round to oval Sharply demarcated, clean-cut, punched-out area with clean base Margins are usually level with surrounding mucosa or slightly elevated due to edema; the mucosa is undermined at the edges Radiating mucosal rugae 80% 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. Sunday, November 18, 2012 DR. RUBEL, SSMC 17
  • 18. Gastric Ulcer- Endoscopic Appearance Sunday, November 18, 2012 DR. RUBEL, SSMC 18
  • 19. Gastric Ulcer- Gross Appearance Sharply punched-out Large, mucosal defect or ulcer Radiating mucosal folds Sunday, November 18, 2012 DR. RUBEL, SSMC 19
  • 20. Acute Gastric Ulcer Sunday, November 18, 2012 DR. RUBEL, SSMC 20
  • 21. Giant gastric ulcer Sunday, November 18, 2012 DR. RUBEL, SSMC 21
  • 22. Gastric Ulcer Sunday, November 18, 2012 DR. RUBEL, SSMC 22
  • 23. Duodenal Peptic Ulcers- Gross Sunday, November 18, 2012 DR. RUBEL, SSMC 23
  • 24. Duodenal Peptic Ulcer-Gross Sunday, November 18, 2012 DR. RUBEL, SSMC 24
  • 25. Microscopy: Overhanging gastric mucosal margins (A) A B Necrotic fibrinoid C, D debris (B) Acute inflammatory infiltrate (C) Granulation tissue (D) E Fibrotic scarred base (E) Sunday, November 18, 2012 DR. RUBEL, SSMC 25
  • 26. Ulcer Base Superficial thin layer of necrotic fibrinoid debris Zone of inflammatory infiltrate with neutrophils Zone of granulation tissue with dilated blood vessels and lymphocytes Zone of fibrous scarring Sunday, November 18, 2012 DR. RUBEL, SSMC 26
  • 27. H. Pylori - Lab Studies HP fecal antigen test Monoclonal antibody immunochromatography of stool samples. Very specific (98%) and sensitive (94%). 13 Carbon-urea breath test HP serology – IgG Biopsy/Histopathology CLO test, Culture Sunday, November 18, 2012 DR. RUBEL, SSMC 27
  • 28. PUD - Diagnosis Endoscopy upper GIT Barium meal – contrast x-ray Biopsy – bacteria & malignancy H.Pylori: CLO test Endoscopy cytology Biopsy – Special stains Culture - difficult 13/14 Carbon-Urea Breath test. H.pylori serology Sunday, November 18, 2012 DR. RUBEL, SSMC 28
  • 29. Endoscopy upper GIT Sunday, November 18, 2012 DR. RUBEL, SSMC 29
  • 30. Video-endoscopy upper GIT Sunday, November 18, 2012 DR. RUBEL, SSMC 30
  • 31. Video-endoscopy upper GIT Sunday, November 18, 2012 DR. RUBEL, SSMC 31
  • 32. Typical radiographic features of a duodenal ulcer; Sunday, November 18, 2012 DR. RUBEL, SSMC 32
  • 33. Typical radiographic features of duodenal ulcer. This duodenal bulb ulcer is associated with marked edema, resulting in the appearance of radiating folds to the ulcer crater. The bulb is also distorted secondary to previously existing ulceration Sunday, November 18, 2012 DR. RUBEL, SSMC 33
  • 34. Typical radiographic features of a benign gastric ulcer; A large well- circumscribed ulcer is seen on the angularis Sunday, November 18, 2012 DR. RUBEL, SSMC 34
  • 35. Urease production test(CLO Test) Sunday, November 18, 2012 DR. RUBEL, SSMC 35
  • 36. Acute Esophagitis & Gastritis Sunday, November 18, 2012 DR. RUBEL, SSMC 36
  • 37. Acute Gastritis Sunday, November 18, 2012 DR. RUBEL, SSMC 37
  • 38. Gastric erosions Sunday, November 18, 2012 DR. RUBEL, SSMC 38
  • 39. Typical endoscopic appearance of a benign gastric ulcer. The ulcer is on the angularis, the most common location for a gastric ulcer, and is well circumscribed without any associated mass effect. The surrounding mucosa is mildly erythematous and without nodularity. Sunday, November 18, 2012 DR. RUBEL, SSMC 39
  • 40. A posterior duodenal ulcer Sunday, November 18, 2012 DR. RUBEL, SSMC 40
  • 41. Erosions in the duodenal bulb and a posterior duodenal ulcer Sunday, November 18, 2012 DR. RUBEL, SSMC 41
  • 42. Clinical presentation of PUD Symptoms: Abdominal pain located in the epigastric area burning in quality occurred on an empty stomach 2 to 4 hours after meals and/or at night (nocturnal pain); relieved by antacids and/or meals tend to wax and wane over months “acid dyspepsia” Sunday, November 18, 2012 DR. RUBEL, SSMC 42
  • 43. Abdominal pain(cont.) the majority of patients (approximately 70%) with epigastric distress (“dyspepsia”) do not have evidence of active ulcer disease; conversely up to 40% of patients with an active ulcer crater deny abdominal pain; patients can present with an ulcer-related complication, particularly hemorrhage, without antecedent symptoms Sunday, November 18, 2012 DR. RUBEL, SSMC 43
  • 44. Abdominal pain(cont.) Despite being both insensitive and non-specific, the symptom of epigastric abdominal pain, particularly burning after meals and at night and relieved with food or antacid, suggests the possibility of ulcer disease. Sunday, November 18, 2012 DR. RUBEL, SSMC 44
  • 45. Other symptoms gastro esophageal reflux including upright and supine reflux and non-cardiac chest pain symptoms of indigestion occurring with or shortly after eating and characterized by epigastric fullness and discomfort belching bloating nausea early satiety and specific food intolerances. Sunday, November 18, 2012 DR. RUBEL, SSMC 45
  • 46. Signs; Physical examination is of limited value in patients with uncomplicated ulcer. For epigastric tenderness on deep palpation, the sensitivity and specificity are all approximately 50% or less. Furthermore, many patients with non- ulcer diseases also have epigastric tenderness on physical examination. Sunday, November 18, 2012 DR. RUBEL, SSMC 46
  • 47. Signs(cont.) In patients with free perforation or ulcer penetration into the pancreas, findings of peritonitis are usually present. In patients with gastric retention who have been fasting for a few hours, a succussion splash (produced by auscultating the abdomen while rocking the patient back and forth), suggests retained gastric contents. Sunday, November 18, 2012 DR. RUBEL, SSMC 47
  • 48. Complications: Hemorrhage The most common complication of ulcer disease (in approximately 15% of patients) manifest as haematemesis and melena. Perforation Duodenal ulcers: perforate anteriorly Gastric ulcers: perforate along the anterior wall of the lesser curvature of the stomach. Penetration Mainly to posterior structure as pancreas. Scarring and stenosis Stomach: tea-pot deformity, hour-glass contracture. Duodenum: pyloric stenosis as GOO. Sunday, November 18, 2012 DR. RUBEL, SSMC 48
  • 49. Hemorrhage The most common complication of ulcer disease (in approximately 15% of patients) manifest as haematemesis and melena. Bleeding: Upper gastrointestinal (UGI) bleeding secondary to peptic ulcer is a common medical condition that results in high patient morbidity UGI bleeding commonly presents with hematemesis (vomiting of blood or coffee-ground like material) and/or melena (black, tarry stools). Sunday, November 18, 2012 DR. RUBEL, SSMC 49
  • 50. D.U-Hemorrhage Sunday, November 18, 2012 DR. RUBEL, SSMC 50
  • 51. Perforated peptic ulcer. Duodenal, antral, and gastric body ulcers account for 60, 20 and 20percent of perforations due to peptic ulcer, respectively . One-third to one-half of perforated ulcers are associated with NSAID use; these usually occur in elderly patients Sunday, November 18, 2012 DR. RUBEL, SSMC 51
  • 52. Penetration Is similar pathologically to perforation, except that the ulcer crater burrows through the entire wall of the intestine, and instead of leaking digestive contents into the peritoneal cavity, the crater bores into an adjacent organ. Gastric ulcers most commonly penetrate into the left lobe of the liver, while duodenal ulcers penetrate posteriorly into the adjacent pancreas, sometimes leading to pancreatitis. Rarely, gastric ulcers may penetrate into the colon, resulting in a gastrocolic fistula Sunday, November 18, 2012 DR. RUBEL, SSMC 52
  • 53. Gastric outlet obstruction (gastric retention or pyloric stenosis); Gastric outlet obstruction is the least frequent ulcer complication. Most cases are associated with duodenal or pyloric channel ulceration, with gastric ulceration accounting for only 5 percent of cases. functional impairment of antral motility due to the effects of acute inflammation and edema; mechanical obstruction due to scarring near the gastroduodenal junction; manifest as gastroesophageal reflux, early satiety, weight loss, abdominal pain, and vomiting; As the degree of retention increases, the quantity of vomitus also increases, often containing food ingested 12 or more hours previously. Sunday, November 18, 2012 DR. RUBEL, SSMC 53
  • 54. Barium upper gastrointestinal study demonstrates the size of the stomach. Pyloric stenosis Sunday, November 18, 2012 DR. RUBEL, SSMC 54
  • 55. Endoscopy demonstrates the pyloric obstruction with an active ulcer crater seen in the pyloric channel. Sunday, November 18, 2012 DR. RUBEL, SSMC 55
  • 56. Malignant transformation (Gastric ulcer ) Sunday, November 18, 2012 DR. RUBEL, SSMC 56
  • 57. Malignant transformation (Gastric ulcer ) Sunday, November 18, 2012 DR. RUBEL, SSMC 57
  • 58. Malignant transformation (Gastric ulcer ) Sunday, November 18, 2012 DR. RUBEL, SSMC 58
  • 59. 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. Sunday, November 18, 2012 DR. RUBEL, SSMC 59
  • 60. 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. Sunday, November 18, 2012 DR. RUBEL, SSMC 60
  • 61. Surgical Care With 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. Sunday, November 18, 2012 DR. RUBEL, SSMC 61
  • 62. 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. Sunday, November 18, 2012 DR. RUBEL, SSMC 62
  • 63. Diet No special diet is required. Medication Treat 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 Sunday, November 18, 2012 DR. RUBEL, SSMC 63
  • 64. 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.. Sunday, November 18, 2012 DR. RUBEL, SSMC 64
  • 65. PPI-based triple therapies consist of a 14-day treatment of the following: Omeprazole (Prilosec): 20 mg PO bid or Lansoprazole (Prevacid): 30 mg PO bid or Rabeprazole (Aciphex): 20 mg PO bid or Esomeprazole (Nexium): 40 mg PO qd Plus: Clarithromycin (Biaxin): 500 mg PO bid and Amoxicillin (Amoxil): 1 g PO bid The alternative combination therapy consists of the following treatments administered for 14 days: Omeprazole (Prilosec): 20 mg PO bid or Lansoprazole (Prevacid): 30 mg PO bid or Rabeprazole (Aciphex): 20 mg PO bid or Esomeprazole (Nexium): 40 mg PO qd Plus: Clarithromycin (Biaxin): 500 mg PO bid and Metronidazole (Flagyl): 500 mg PO bid Sunday, November 18, 2012 DR. RUBEL, SSMC 65
  • 66. Quadruple therapies for 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 and Bismuth 525 mg PO qid and Metronidazole 500 mg PO qid and Tetracycline 500 mg PO qid Sunday, November 18, 2012 DR. RUBEL, SSMC 66
  • 67. Further Outpatient Care Endoscopy 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 Meds Consider 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. Sunday, November 18, 2012 DR. RUBEL, SSMC 67
  • 68. PREVENTION Primary 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 Sunday, November 18, 2012 DR. RUBEL, SSMC 68
  • 69. Prognosis When 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 Education Stop smoking. Avoid NSAID and aspirin use. Avoid heavy alcohol use. Stress reduction counseling might be helpful in individual cases but is not needed routinely. . DR. RUBEL, SSMC 69 Sunday, November 18, 2012
  • 70. 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. Sunday, November 18, 2012 DR. RUBEL, SSMC 70
  • 71. Sunday, November 18, 2012 DR. RUBEL, SSMC 71