PUD

2. Anatomy of stomach and duodenum

5. • Mucous cells in the gastric
pits secrete mucus
• parietal cells secrete
hydrochloric acid
• G cells, which are present
predominantly only in the
antrum of the stomach,
secrete gastrin
• ECL cells secrete histamine
• chief cells secrete
pepsinogen

8. Control of acid secretion.
Gastrin released from antral G cells
in response to food binds to
cholecystokinin receptors (CCK-
2R) on the surface of
enterochromaffin-like (ECL) cells,
which in turn release histamine.
The histamine binds to H2
receptors on parietal cells and
this leads to secretion of
hydrogen ions, in exchange for
potassium ions at the apical
membrane. Parietal cells also
express CCK-2R and it is thought
that activation of these
receptors by gastrin is involved
in regulatory proliferation of
parietal cells. Cholinergic (vagal)
activity and gastric distension
also stimulate acid secretion;
somatostatin, vasoactive
intestinal polypeptide (VIP) and
gastric inhibitory polypeptide
(GIP) inhibit it.

14. Epidemiology

16. Etiology

21. Etiology of PUD
• Normal
• Increased Attack
Hyperacidity
• Weak defense
Helicobacter pylori*
Stress, drugs, smoking

33. A gastric ulcer caused by
H.pylori
A duodenal ulcer caused by
H.pylori

34. Risk factors
 Older than 60 years of age
 Previous peptic ulcer
 Previous ulcer-related upper GI
complication
 Concomitant use of corticosteroid
 High-dose NSAIDs
 Multiple NSAID use or NSAID plus
aspirin use
 Aspirin (including
cardioprotective dosages)
 Concomitant use of anticoagulant
 Concomitant use of antiplatelet
drug such as clopidogrel
 Concomitant use of selective
serotonin reuptake inhibitor
 Chronic illness (e.g.,
cardiovascular disease)
 NSAID-related dyspepsia
 Helicobacter pylori infection
 Rheumatoid arthritis (extent of
disability)
 Alcohol consumption
 Cigarette smoking

35. Symptoms
The most common symptom of peptic ulcers is abdominal pain.
The pain is usually in the upper middle part of the abdomen,
above the belly button and below the breastbone.
The pain can feel like burning or gnawing, and it may go through
to the back.
Pain often comes several hours after a meal when the stomach is
empty.
The pain is often worse at night and early morning.
It can last anywhere from a few minutes to several hours.
The pain may be relieved by food, antacids, or vomiting.

36. Other symptoms of peptic ulcers include the following:
Nausea
Vomiting
Loss of appetite
Loss of weight
Severe ulcers may cause bleeding in the stomach or duodenum. Bleeding is
sometimes the only symptom of an ulcer. This bleeding can be fast or slow.
Fast bleeding reveals itself in one of the following ways:
Vomiting of blood or dark material that looks something like coffee grounds: This is
an emergency and warrants an immediate visit to an emergency department.
Blood in the stool or black, tarry, sticky-looking stools
Slow bleeding is often more difficult to detect, because it has no dramatic symptoms.
The usual result is low blood cell count.
The symptoms of anemia are tiredness (fatigue), lack of energy (lethargy),
weakness, rapid heartbeat (tachycardia), and pales skin (pallor).

37. Pathogenesis
A physiologic imbalance between aggressive factors (gastric acid and pepsin) and
protective factors (mucosal defense and repair) remain important issues in the
pathophysiology of gastric and duodenal ulcers

38. THANKYOU
 Gram negative, Spiral bacilli
 Spirochetes
 Do not invade cells – only mucous
 Breakdown urea - ammonia
 Break down mucosal defense
 Chronic Superficial inflammation

39. Factors which influence the virulence of H. pylori

40. Dynamics of H.pylori infection

41. Pathogenesis of H.pylori infection

42. NSAIDs Induced PU

43. PUD - Diagnosis
Endoscopic tests
Histology
Microbiologic examination using various stains
Culture of biopsy
Biopsy (rapid) urease
HP urease generates ammonia, which causes a color change
Nonendoscopic tests
Antibody detection(laboratory-based)
Detects antibodies to HP in serum; in the U.S., only FDA-approved anti-HP lgG
antibody should be Used
Antibody detection (can be performed in office or near patient)
Detects lgG antibodies to HP in whole blood or finger stick
Urea breath test (UBT)
HP urease breaks down ingested labeled C-urea, patient exhales labeled CO2
Stool antigen Identifies
HP antigen in stool, leading to color change that can be detected visually or by
spectrophotometer
Barium meal – contrast x-ray
ELISA

44. Endoscopy

45. Endoscopy

46. Capsule endoscopy
-tiny camera
-light source
-radio transmitter
2 picture in every
second(totally 8
hours)

47. Barium X-Ray

48. Histological examination

49. Urea breath test

51. Urease test
T he Endosc-Hp® Test consists
of a twin well cartridge
containing urea, phenol red
and buffer salts when
reconstituted, and a buffer. If
the urease enzyme of
Helicobacter pylori is present
in a biopsy specimen, the rise
in pH associated with the
hydrolysis of urea causes a
change in colour from yellow to
pink/red. The colour change
indicates a positive reaction
and confirms the presence of
Helicobacter pylori. (30minute)
Urease is a constitutively expressed enzyme that
hydrolyzes urea to carbon dioxide and ammonia.
(NH2)2CO + H2O → CO2 + 2NH3
Urease test media contain 2% urea and phenol red as a
pH indicator. An increase in pH due to the production of
ammonia results in a color change from yellow (pH 6.8)
to bright pink (pH 8.2).

52. Rapid test for H.Pylori
CLIAwaived H. pylori Whole Blood
Rapid Test. A rapid qualitative
immunoassay intended to detect
the presence of IgG antibodies
specific to Helicobacter pylori (H.
pylori) in human whole blood.

53. ELISA
Enzyme-linked immunosorbent assay

54. Indirect ELISA
A sandwich ELISA. (1) Plate is coated with a
capture antibody; (2) sample is added, and any
antigen present binds to capture antibody; (3)
detecting antibody is added, and binds to
antigen; (4) enzyme-linked secondary antibody
is added, and binds to detecting antibody; (5)
substrate is added, and is converted by enzyme
to detectable form.

55. TREATMENT OF PUD

56. TREATMENT OF PUD
• The treatment selected for PUD depends on
the following factors:
(1)the etiology of the ulcer
(2)whether the ulcer is new or recurrent
(3)the presence of any ulcer-related
complications.
• Overall treatment is aimed-
relieving ulcer pain
healing the ulcer
preventing ulcer recurrence
and reducing ulcer-related complications.

57. The goals of PUD therapy are to--
(1) resolve symptoms
(2) reduce acid secretion
(3) promote epithelial healing
(4) prevent ulcer-related complications
(5) Prevent ulcer recurrence.
(6) For HP-related PUD, eradication of HP is
an additional goal

58. NONPHARMACOLOGIC THERAPY
• Patients with PUD should eliminate or
reduce psychological stress, cigarette
smoking, and the use of nonselective
NSAIDs (including aspirin).
• Although there is no “antiulcer diet,” the
patient should avoid foods and beverages
(e.g., spicy foods, caffeine, and alcohol)
that cause dyspepsia or that exacerbate
ulcer symptoms.
• If possible, alternative agents such as
acetaminophen, nonacetylated salicylate

59. Surgical therapy
VAGOTOMY

60. PYLOROPLASTY
This surgery enlarges the opening through which
stomach contents are emptied into the intestine, allowing
the stomach to empty more quickly.

61. ANTRECTOMY
Remove the lower part of the stomach (antrum), which
produces a hormone that stimulates the stomach to
secrete digestive juices. A vagotomy is usually done in
conjunction with an antrectomy.

62. GASTRO-JEJUNOSTOMY

63. TREATMENT OF GASTRIC BLEEDING
PHOTOCOAGULATION( LASER)

64. ELECTROCOAGULATION ( heat is generated by high
frequency electrical current)

65. INJECTION THERAPY ( Adrenalin or saline)

66. Angiographic therapy

67. Guidelines for the evaluation and management of a
patient who presents with dyspeptic or ulcer-like
symptoms. COX-2, cyclooxygenase-2; GERD,
gastroesophageal reflux disease; HP,Helicobacter
pylori; H2-RA, H2-receptor antagonist; PPI, proton
pump inhibitor; NSAID, nonsteroidal anti-inflammatory
drug; NUD, nonulcer dyspepsia.

69. PHARMACOLOGIC THERAPY

71. Proton pump inhibitor
Omeprazole is inactive at neutral pH, but at pH < 5
rearranges to two charged cationic forms (a sulphenic acid
and a sulphenamide configurations) that react covalently
with SH groups of the H+/K+ATPase enzyme and inactivate it
irreversibly, especially when two molecules of omeprazole
react with one molecule of the enzyme. After diffusing into
the parietal cell from blood, it gets concentrated in the
acidic pH of the canaliculi because the charged forms
generated there are unable to diffuse back.

73. Sucralfate (CARAFATE) consists of the octasulfate of
sucrose to which Al(OH)3 has been added. In an acid
environment (pH <4), sucralfate undergoes extensive
cross-linking to produce a viscous, sticky polymer that
adheres to epithelial cells and ulcer craters for up to 6
hours after a single dose.Colloidal bismuth compound
(i) Increased secretion of mucus and bicarbonate through
stimulation of mucosal PGE2 production.
(ii) CBS and mucus form a glycoprotein-Bi complex which
coats the ulcer and acts as a diffusion barrier to HCl.
(iii) Detaches H pylori from the surface of mucosa and
directiy kills this organism involved in causation of ulcers
and relapses.

74. Treatment and dosing recommendations to heal peptic ulcers
or provide maintenance therapy are shown here---

75. Treatment of Helicobacter pylori–Associated Ulcers
The primary goal of HP therapy is to completely
eradicate the organism using an effective antibiotic-
containing regimen.
Eradication therapy with a PPI-based three-drug regimen
should be considered for all patients who test positive for
HP and have an active ulcer or a documented history of
either an ulcer or ulcer-related complication. Different
antibiotics should be used if a second course of HP
eradication therapy is required.
The first-line regimen should contain a PPI plus
clarithromycin and either amoxicillin or metronidazole.

76. Drug Regimens to Eradicate Helicobacter pylori

77. Treatment of NSAID-Induced Ulcers
For patients discontinuing NSAID therapy, PPIs,
H2RAs, or sucralfate are all effective for ulcer
healing.
PPI therapy heals NSAID ulcers faster than
H2RAs.
For patients continuing NSAID therapy, PPIs are
preferred over H2RAs or sucralfate.
If the decision is made to continue NSAID
therapy, adjunctive strategies may be required to

78. Prevention of NSAID-Induced Ulcers
Prophylactic regimens against PUD are often required in
patients who require long-term NSAID or aspirin therapy
for osteoarthritis, rheumatoid arthritis, or cardioprotection.
Misoprostol, H2RAs, PPIs, and COX-2 selective inhibitors
have been evaluated in controlled trials to reduce the risk
of NSAID-induced PUD.Treatment of Refractory Ulcers
The presence of refractory ulcers [ulcers that persist
beyond 8 weeks (DU) or 12 weeks (GU)] requires thorough
assessment, including evaluation of medication
compliance.
The patient should be questioned regarding recent
NSAID ingestion.
Tolerance has been reported with as few as 4 weeks of
H2RA therapy, and thus a change to PPI therapy should be
considered in this situation.
Other assessments that may be considered include an

79. Patient Care and Monitoring
General Recommendations: HP-Associated and NSAID Induced Ulcers
1. Assess the severity of signs and symptoms. Identify the
presence of any alarm signs and symptoms.
2. Educate the patient on monitoring for alarm signs and
symptoms.
3. Obtain a history of prescription medication, over-the counter
medication, and dietary supplement use.
4. Encourage lifestyle modifications such as reducing tobacco
use and ethanol ingestion and decreasing psychological stress.
5. Determine the appropriate duration of therapy for acid
suppressive therapy.
6. Define the current impact of PUD on the patient’s quality of life
and the improvement in these outcomes sought with drug
therapy.
7. Evaluate current drug therapy for potential adverse drug
reactions and drug interactions.
Helicobacter pylori–Associated Ulcers
1. Recommend an appropriate drug regimen that will eradicate

80. 4. Recommend different antibiotics if this treatment
regimen is a result of failure of a prior HP regimen.
5. Educate the patient on the importance of adherence to
eradication therapy.
NSAID-Associated Ulcers
1. Assess for risk factors for NSAID ulcers and recommend
an appropriate strategy to reduce ulcer risk.
2. Monitor for signs and symptoms of complications
associated with NSAID-related ulceration.
3. Recommend an appropriate treatment regimen to
achieve the desired outcomes.
4. Assess and counsel patients on potential adverse drug
events and drug interactions.
5. Inform patients who are receiving prophylactic therapy
on the importance of its use, potential adverse drug
events, and the possible alarm symptoms associated with