Peptic ulcer disease, h.pylori virulence factors, pathogenesis, definition, classification, diagnosis, management, upper gastrointestinal tract bleeding management

1. Peptic ulcer disease
Munkhtulga G.
2015
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2. Introduction
• Burning epigastric pain exacerbated by fasting and
improved with meals is a symptom complex associated with
peptic ulcer disease (PUD).
• An ulcer is defined as disruption of the mucosal
integrity of the stomach and/or duodenum leading
to a local defect or excavation due to active
inflammation.
• Ulcers occur within the stomach and/or duodenum and are often
chronic in nature.
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3. №85 - 3,9
№91 - 3,6
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4. 20th death
cause of
total
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Mucous
HCl, Intrinsic factor
(pepsinogen, mucous)
Histamine
Pepsinogen

6. Mucosal defense
• 3 level barrier:
1. Pre-epithelial
Physicochemical, mucus-
HCO3-phospholipid layer
2. Epithelial
3. Subepithelial
Microvascular system, HCO3,
micronutrients, oxygen
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7. Mucosal barrier – epithelial level
• Mucus production, epithelial
cell ionic transporters that
maintain intracellular pH
bicarbonate production, and
intracellular tight junctions.
• Heat shock proteins that
prevent protein denaturation
and protect cells (increased
temperature, cytotoxic
agents, or oxidative stress.)
• Trefoil factor family peptides
and cathelicidins,  surface
cell protection and
regeneration.
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8. Restitution (epithelial level)
• If the preepithelial barrier were
breached, gastric epithelial cells
bordering a site of injury can migrate
to restore a damaged region (
restitution ).
• This process occurs independent of
cell division and requires
uninterrupted blood flow and an
alkaline pH in the surrounding
environment.
• Epidermal (EGF), TGFα and basic
fibroblast growth factor (FGF),
modulate the process of restitution.
• Larger defects - require cell
proliferation.
• Epithelial cell regeneration is
regulated by prostaglandins and
growth factors such as EGF and TGF-
α.
• Angiogenesis
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9. Prostaglandins (epithelial defence)
• Regulate release of
mucosal HCO3, mucus
• Inhibit parietal cell
secretion
• Maintain mucosal blood
flow, epithelial restitution
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11. Prostaglandins E and I
• PGE receptors: EP1, 2, 3, 4
• In addition to stimulating
epithelial cells to release
more bicarbonate and
mucus,
• prostaglandins can reduce
the permeability of the
epithelium and thus reduce
acid back-diffusion
PI2 = Prostacyclin
IP = Prostacyclin receptor
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12. Nytric oxide (NO)
• Stimulate gastric
mucus
• Increase mucosal
blood flow
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13. Essentials of gastric secretion
• Basal acid production occurs in a circadian pattern
• Highest – night
• Lowest – morning hours
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14. Why blocking only one receptor type
decreases acid secretion that activate
different ways?
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15. Regulation of gastric acid secretion
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16. Ulcer
• Ulcers are defined as breaks in the mucosal surface
>5 mm in size, with depth to the submucosa.
• Duodenal ulcers (DU)
• 1st portion of duodenum (95%) with ~90% located within
3 cm of pylorus
• Usually ≤1 cm (3-6cm, giant ulcer)
• Gastric ulcers (GU)
• Distal to junction between antrum and acid secretory
mucosa
• Prepyloric area
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19. H. Pylori
• 90% of all DUs were associated with H.Pylori
• H.Pylori is present in only 30-60% of individuals
with GUs
• 50-70% of those with DUs
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20. Gastric ulcer
• Abnormalities in resting and stimulated pyloric sphincter
pressure with a concomitant increase in
• Duodenal gastric reflux
• Bile acids, lysolecithin, and pancreatic enzymes may injure
gastric mucosa
• Delayed gastric emptying of solids
When GUs develop in the presence of minimal acid levels,
impairment of mucosal defense factors may be present.
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21. Role of H. pylori
Virulence Factors
1. cag PAI
2. VacA vacuolating factor
3. Acid resistance
4. Adhesins and outer membrane proteins
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22. 1. Cytotoxin associated gene A (CagA)
• 140kD, highly immunogenic
• Encoded by cagA gene – 50-70% of H.pylori strains
• CagA+ strains  higher inflammatory  PUD, G.cancer
• Type-IV secretion apparatus (syringe like structure)
• CagA, Peptidoglycan and others
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23. Src kinase
mediates
Lifelong colonization of the host
CagA эсэд транслокацилагдан орсны дараа
EPIYA motif /Glu-Pro-Ile-Tyr-Ala/ хэмээх амин
хүчлүүдийн дараалалынхаа тирозин а/х дээр
Src бүлгийн киназа ферментийн
оролцоотойгоор фосфорждог.
Гэхдээ эргээд CagA нь Src киназа ферментээ
дарангуйлах нөлөө үзүүлснээр сөрөг эргэх
холбооны механизм адил байгаа бөгөөд энэ
нь яагаад H.Pylori маш удаанаар оршин
тогтнодгийг тайлбарлаж байна.
carcinogenesis
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24. 2. Vac A – vacoulating cytotoxin
• 50% of all H. Pylori strain secrete
• 95 kD
• Membrane channel formation
• Disruption of endosomal and lysosomal activity
• Effect on integrin R-induced cell signaling
• Interference with cytoskeleton-dependent cell function
• Induction of apoptosis
• Immune modulation
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25. 1. Directly delivered to cell
2. Secreted VacA binds to
surface R
3. Directly taken up by cell
4. Taken up by pinocytosis
5. Form membrane channel
 leakage of nutrients to
ECS
6. Pass through tight
junction
Nature reviews Microbiology
Acid secretion ↓
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27. 3. Acid resistance
• H. pylori is able to colonize acidic gastric
environment
• Bacterium is not acidophile
• pH of gastric mucosa 4-6.5
• Growth occurs pH5.5-8.0
• Brief exposure to pH<4
• UREASE  Ammonia  pH↑ (neutralize)
• Also associated with outer membrane
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29. 3. Acid resistance
• Ammonia  cytotoxic to epithelium
• HCO3  suppress bactericidal effect of
peroxynitrite, nitric oxide metabolite
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30. 4.Adhesins
OipA - Proinflammatory
response-inducing
protein
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31. Pathophysiology – H.pylori
• Chronic active gastritis – 10-15%  PUD
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32. Summary of bacterial factors
• Vac A:
• CD4 T cells inhibiting their proliferation
• disrupt normal function of B cells, CD8 T cells, macrophages and mast cells.
• CagA+ strains  higher inflammatory  PUD, G.cancer
• Urease  NH3  epithelial cell
• Surface factors that are chemotactic for neutrophils and monocytes,
which in turn contribute to epithelial cell injuries.
• H. pylori makes proteases and phospholipases that break down the
glycoprotein lipid complex of the mucous gel, thus reducing the efficacy
of this first line of mucosal defense.
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33. Host factors
• Genetic predisposition
• Recruitment of neutrophils, lymphocytes (T and B),
macrophages, and plasma cells
• ↑ cytokines in the gastric epithelium: (IL1α/β, IL-2, IL-6, IL-
8, TNFα, and IFN-γ).
• Mucosal and a systemic humoral response, which does not
lead to eradication of the bacteria but further compounds
epithelial cell injury.
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34. Duodenal ulceration
• The reason - unclear.
• H. pylori - may be more virulent.
• Certain specific bacterial factors such as the duodenal ulcer-
promoting gene A ( dupA ), may be associated
• Gastric metaplasia  high acid exposure, permits H. pylori to bind to it
and produce local injury secondary to the host response.
• H. pylori antral infection could lead to increased acid production,
increased duodenal acid, and mucosal injury.
• Basal and stimulated [meal, gastrin-releasing peptide (GRP)] gastrin
release are increased, and somatostatin secreting D cells may be
decreased.
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NSAIDs induced PUD

38. Risk factors
• Cigarette smoking
• Decrease healing rates, impair response to therapy, and increase
ulcer-related complications such as perforation. The mechanism
responsible for increased ulcer diathesis in smokers is unknown.
• gastric emptying, decreased proximal duodenal bicarbonate
production, increased risk for H. pylori infection, and cigarette-
induced generation of noxious mucosal free radicals
• Genetic predisposition, Increased frequency of blood
group O
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39. Risk factors
• Psychological stress
• Diet
• Specific chronics:
• Strong association: systemic mastocytosis, chronic
pulmonary disease, chronic renal failure, cirrhosis,
nephrolithiasis, and α 1 -antitrypsin deficiency.
• Possible association: (1) hyperparathyroidism, (2) coronary
artery disease, (3) polycythemia vera, and (4) chronic
pancreatitis
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41. DIAGNOSIS
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42. Burning epigastric
“hunger” pain
tends to occur when acid is secreted in the absence
of food buffer (e.g., 2–3 h after meals) and at night, usually
between 23.00 and 02.00
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43. • Pain rarely occurs before breakfast.
• Alkali, food, and antisecretory agents produce relief
such that “classic” patients tend to “feed” their ulcers.
• Not specific for PUD
• Asymptomatic
• Food relief is more likely to occur with peptic ulcer,
• Food provocation of symptoms (postprandial pain or
food intolerance) and nausea have negative predictive
value for underlying PUD
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GERD

45. • Complete symptom resolution at 3 months had a 98%
positive predictive value for successful eradication of Hp
infection
• Persisting symptoms had only a 25% positive predictive
value for persisting Hp infection
• ~1/3 of Hp+ ulcer patients  1-3 years symptoms after
Hp eradication
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46. Complaints
• Loss of appetite
• Chest heartburn
• Belching
• Acidy regurgitation
• Hematemesis: bloody vomitus
• Melena: tarry stool passage
• Maroon: tarry- bloody stool passage
• Hematochezia: bloody stool passage
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47. Physical examination:
• Inspection: pale, weight loss, coating of tongue …
• Palpation: left or epigastric tenderness, pain radiation,
Vasilenko’s sign
• Percusion: Mendel’s sign
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48. Laboratory
• CBC: Anemic signs, inflammatory sign ±
• Biochemistry: Gastrin ↑, secretin and somatostatin ↓
• Immunology: H.Pylori +
• Gregerson test +
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49. Gastric ulcer
• Type I: gastric body, low
gastric acid production;
• Type II: antrum and
gastric acid can vary from
low to normal;
• Type III occur within 3 cm
of the pylorus and are
commonly accompanied
by duodenal ulcers and
normal or high gastric acid
production
• Type IV are found in the
cardia and low gastric
acid production.
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51. Stages Manifestation
Active stage
A1
The surrounding mucosa is edematously swollen and no regenerating epithelium is
seen endoscopically
A2
The surrounding edema has decreased, the ulcer margin is clear, and a slight amount of regenerating
epithelium is seen in the ulcer margin. A red halo in the marginal zone and a white slough circle in the
ulcer margin are frequently seen. Usually, converging mucosal folds can be followed right up to the ulcer
margin
Healing stage
H1
The white coating is becoming thin and the regenerating epithelium is extending into the ulcer base.
The gradient between the ulcer margin and the ulcer floor is becoming flat. The ulcer crater is still
evident and the margin of the ulcer is sharp. The diameter of the mucosal defect is about one-half to
twothirds that of A1
H2
The defect is smaller than in H1 and the regenerating epithelium covers most of the ulcer floor. The area
of white coating is about a quarter to one-third that of A1
Scarring stage
S1
The regenerating epithelium completely covers the floor of ulcer. The white coating has disappeared.
Initially, the regenerating region is markedly red. Upon close observation, many capillaries can be seen.
This is called ‘‘red scar’’
S2
In several months to a few years, the redness is reduced to the color of the surrounding mucosa. This is
called ‘‘white scar’’
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51
Endoscopic Stage Classification of Gastric Ulcer by Sakita-Miwa

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54. Gastric ulcer stages using
a six-stage system
Stage Finding
A1 (active stage 1) Ulcer that contains mucus coating, with marginal elevation because of
edema
A2 (active stage 2) Mucus-coated ulcer with discrete margin and less edema than active
stage 1
H1 (healing stage 1) Unhealed ulcer covered by regenerating epithelium < 50%, with or
without converging folds
H2 (healing stage 2) Ulcer with a mucosal break but almost covered with regenerating
epithelium
S1 (scar stage 1) Red scar with rough epithelialization without mucosal break
S2 (scar stage 2) White scar with complete re-epithelialization
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World J Gastrointest Endosc. 2010 January 16; 2(1): 36–40.
Published online 2010 January 16. doi: 10.4253/wjge.v2.i1.36.

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56. Forrest classification system with
predictive prognosis
Forrest Classification
Rebleeding
Incidence
Surgical
Requirement
Incidence of
Death
Type I: Active Bleed
Ia: Spurting Bleed
Ib: Oozing Bleed
55-100% 35% 11%
Type II: Recent Bleed
Ila: Non-Bleeding Visible Vessel (NBVV)
Ilb: Adherent Clot
40-50% 34% 11%
20-30% 10% 7%
Type III: Lesion without Bleeding
Flat Spot
Clean Base
10% 6% 3%
5% 0.5% 2%
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57. Tactic
• AI, Forrest Ia, Ib, IIa  Department of surgery
• AII, Forrest IIb, III  Department of Gastroenterology
• H-I, H-II, Forrest III  Home
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58. Forrest Ia ulcer bleeding
in a small gastric ulcer
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Arterial hemorrhage (Forrest Ia) from
an ulcer on top of a submucous tumor
of the gastric body

59. A: A spurting bleeding
of the gastric ulcer
(Forrest Ia)
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B. Oozing bleeding of the gastric
ulcer (Forrest Ib);
C: Non-bleeding visible vessel
of the gastic ulcer (Forrest IIa).

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61. A. Active pumping
B. Active oozing
C. Vessel exposure
D. Red or black clot
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65. Radiology of PUD
• http://radiopaedia.org/articles/peptic-ulcer-disease
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gastric ulcer with bull's eye sign

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Benign gastric ulcer
gastric ulcer

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Benign Antral Ulcer
Duodenal ulcer

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Double-contrast upper gastrointestinal series. Posterior
wall duodenal ulcer.
Lateral view of a posterior wall ulcer
in the same patient
Duodenal ulcer in imaging: http://emedicine.medscape.com/article/367878-overview

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70. • Stomach acid test
• Atropine test
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1. Ходоодны шүүрлийн шинжилгээ хийх заалт
Туйлын заалт:
 Мэс заслын дараах дахисан шарх, залгадас дээрх шархлаа (анастомозын
шарх) (*PAO>15ммол/цаг)
 Zollinger-Ellison syndrome сэжиглэсэн тохиолдол, G эсийн гиперплази,
гиперпаратиреодизм (**ВАО>15ммол/цаг, ВАҮ/РАО<0.6)
Харьцангуй заалт:
 Мэс заслын хэлбэрийг сонгох
 Мэс заслын дараах үр дүнг хянах
 Пернициоз анемиг сэжиглэх
2. Гастрины сорил хийх заалт (секретин судсаар)
• Zollinger-Ellison syndrome сэжиглэсэн тохиолдол (сийвэнгийн гастрин >100%
ихсэнэ)
• G эсийн гиперплази сэжиглэсэн тохиолдол (сийвэнгийн гастрин <50% ихсэнэ)

71. K25 – Gastric ulcer
K26 – Duodenal ulcer
.0 Acute with haemorrhage
.1 Acute with perforation
.2 Acute with both haemorrhage and perforation
.3 Acute without haemorrhage or perforation
.4 Chronic or unspecified with haemorrhage
.5 Chronic or unspecified with perforation
.6 Chronic or unspecified with both haemorrhage and perforation
.7 Chronic without haemorrhage or perforation
.9 Unspecified as acute or chronic, without haemorrhage or perforation
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45
45

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74. Ulcer Healing
• Repair of ulcers is that involves inflammation, cell proliferation
(particularly at the ulcer margin), formation of granulation tissue
at the base of the ulcer, and angiogenesis (new blood vessel
growth).
• In response to ulceration, a new type of cell appears in the ulcer
margin which secretes large amounts of epithelial growth factor
(EGF), acting as a potent stimulus for reepithelialization.
• Glandular structure is gradually reestablished, along with the
mucosal microcirculation.
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75. Ulcer healing - Platelet
• Platelets contribute significantly to ulcer healing, at least in part
through the delivery of numerous growth factors that can
promote angiogenesis and epithelial cell proliferation.
• Of course, platelets are also an important element in hemostasis,
and bleeding of ulcers is a very important clinical concern.
• Some of the clinical benefit of drugs that suppress gastric acid
secretion may be related to a facilitation of platelet
aggregation; thus platelet aggregation will not occur at a pH <5.4.
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76. Ulcer healing - PGs
• Prostaglandins also trigger the release of vascular endothelial
growth factor (VEGF), which has been shown to make an
important contribution to ulcer healing, likely via stimulation of
angiogenesis.
• Selective COX-2 inhibitors impair gastric ulcer healing, and
mice deficient in COX-2 exhibit impaired ulcer healing. The
beneficial effects of PGE2 on gastric ulcer healing in rodents
appear to be mediated via the EP4 receptor.
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77. • Clinical algorithm for the
management of peptic ulcer
bleeding adopted at the Prince of
Wales Hospital, Hong Kong.
• 2006
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78. Management of Patients
with Ulcer Bleeding
American College of Gastroenterology – Practice guideline
2012
The American Journal of GASTROENTEROLOGY
2015-04-07 78Am J Gastroenterol 2012; 107:345–360; doi: 10.1038/ajg.2011.480; published online 7 February 2012

79. Includes:
Initial management of UGIB*
1. Initial assessment and risk stratification,
2. Pre-endoscopic use of medications
3. Gastric lavage
4. Timing of endoscopy.
Endoscopic and medical management of ulcer disease:
5. Endoscopic findings and their prognostic implications,
6. Endoscopic hemostatic therapy
7. Post-endoscopic medical therapy and disposition
8. Prevention of recurrent ulcer bleeding.
2015-04-07 79*UGIB – Upper GastroIntestinal Bleeding

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Initialassessmentand
riskstratification
1. Hemodynamic status should be assessed immediately upon presentation and
resuscitative measures begun as needed (Strong recommendation).
2. Blood transfusions should target hemoglobin ≥ 7 g / dl, with higher hemoglobins
targeted in patients with clinical evidence of intravascular volume depletion or
comorbidities, such as coronary artery disease (Conditional recommendation).
3. Risk assessment should be performed to stratify patients into higher and lower
risk categories and may assist in initial decisions such as timing of endoscopy, time of
discharge, and level of care (Conditional recommendation).
4. Discharge from the emergency department without inpatient endoscopy may be
considered in patients with urea nitrogen < 18.2 mg / dl; hemoglobin ≥ 13.0 g / dl for
men (12.0 g / dl for women), systolic blood pressure ≥ 110 mm Hg; pulse < 100 beats
/ min; and absence of melena, syncope, cardiac failure, and liver disease, as they
have < 1 % chance of requiring intervention (Conditional recommendation).

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Pre-endoscopicmedicaltherapy 5. Intravenous infusion of erythromycin (250 mg ~ 30 min (20-60min)
before endoscopy) should be considered to improve diagnostic yield and
decrease the need for repeat endoscopy. However, erythromycin has not
consistently been shown to improve clinical outcomes (Conditional
recommendation). IMPROVE VISUALIZATION AT EGD, ↓ 2ND EGD
6. Pre-endoscopic intravenous PPI (e.g., 80 mg bolus followed by 8 mg / h
infusion) may be considered to decrease the proportion of patients who
have higher risk stigmata of hemorrhage at endoscopy and who receive
endoscopic therapy. However, PPIs do not improve clinical outcomes such
as further bleeding, surgery, or death (Conditional recommendation).
7. If endoscopy will be delayed or cannot be performed, intravenous PPI
is recommended to reduce further bleeding (Conditional
recommendation).

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Gastric lavage
8. Nasogastric or orogastric lavage is NOT REQUIRED in patients with UGIB for diagnosis,
prognosis, visualization, or therapeutic effect (Conditional recommendation).
Timingofendoscopy
9. Patients with UGIB should generally undergo endoscopy within 24 h of admission,
following resuscitative efforts to optimize hemodynamic parameters and other medical
problems (Conditional recommendation).
10. In patients who are hemodynamically stable and without serious comorbidities
endoscopy should be performed as soon as possible in a non-emergent setting to
identify the substantial proportion of patients with low-risk endoscopic findings who can
be safely discharged (Conditional recommendation).
11. In patients with higher risk clinical features (e.g., tachycardia, hypotension, bloody
emesis or nasogastric aspirate in hospital) endoscopy within 12 h may be considered to
potentially improve clinical outcomes (Conditional recommendation).

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Endoscopic
diagnosis
12. Stigmata of recent hemorrhage should be recorded as they predict risk of further
bleeding and guide management decisions. [active spurting, non-bleeding visible
vessel, active oozing, adherent clot, flat pigmented spot, and clean base] (Strong
recommendation). [table 3]
Endoscopictherapy
16. Epinephrine therapy should not be used alone. If used, it should be combined with
a second modality (Strong recommendation).
17. Thermal therapy with bipolar electrocoagulation or heater probe and injection of
sclerosant (e.g., absolute alcohol) are recommended because they
reduce further bleeding, need for surgery, and mortality (Strong recommendation).
18. Clips are recommended because they appear to decrease further bleeding and
need for surgery. However, comparisons of clips vs. other therapies yield
variable results and currently used clips have not been well studied (Conditional
recommendation).
19. For the subset of patients with actively bleeding ulcers, thermal therapy or
epinephrine plus a second modality may be preferred over clips or sclerosant alone to
achieve initial hemostasis (Conditional recommendation).

84. 12.
• Serious bleeding does not occur from an erosion due to
absence of vessels in the mucosa
• When ulcer erodes into vessels in submucosa or deeper
• Ulcer surface area dimensions or diameter can be
estimated with the use of a device of known dimension,
such as an open biopsy forceps.
• Ulcers larger than 1 – 2 cm are associated with increased
rates of further bleeding with conservative therapy and aft
er endoscopic therapy
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85. 12.
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13. 14. 15.
20.
20.
21.
Decrease re-
bleeding,
surgery and
mortality

87. Endoscopic hemostatic therapy
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• Bipolar accessories complete a
circuit without the use of a
grounding pad. (a) Schematic of
bipolar circuit; (b) Bipolar
hemostasis probe with active
and return electrodes closely
spaced at the probe's tip

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A. Initial endoscopic finding
B. Post state of epinephrine
injection+argon plasma coagulation
C. Re-bleeding occurred 2 days after
the initial endoscopic treatment
D. Second endoscopic therapy with
epinephrine injection+argon plasma
coagulation
E. Post state of 2nd endoscopic therapy

91. 91
Medical
therapyAFTER
endoscopy Figure 1, green
Repeatendoscopy
22. Routine second-look endoscopy, in which repeat endoscopy is performed 24 h
after initial endoscopic hemostatic therapy, is not recommended. (Conditional
recommendation).
23. Repeat endoscopy should be performed in patients with clinical evidence of
recurrent bleeding and hemostatic therapy should be applied in those with higher risk
stigmata of hemorrhage (Strong recommendation).
24. If further bleeding occurs after a second endoscopic therapeutic session, surgery or
interventional radiology with transcathether arterial embolization is generally
employed (Conditional recommendation).
2nd look EGD  significant reduction in rebleeding with no significant benefit in reducing SURGERY OR DEATH
Single Endoscopy + high dose IV PPI vs 2nd EGD without PPI  rebleeding 8,2 vs 8,7%

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Long-term prevention of
recurrent bleeding ulcers
Figure 2
27, 28, 29, 30
Hospitalization
25. Patients with high-risk stigmata (active bleeding, visible vessels, clots) should
generally be hospitalized for 3 days assuming no rebleeding and no other
reason for hospitalization. They may be fed clear liquids soon after endoscopy
(Conditional recommendation).
26. Patients with clean-based ulcers may receive a regular diet and be discharged
after endoscopy assuming they are hemodynamically stable, their hemoglobin
is stable, they have no other medical problems, and they have a residence where
they can be observed by a responsible adult (Strong recommendation).

93. Figure 2 . Recommended management to prevent recurrent
ulcer bleeding based on etiology of ulcer bleeding.
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1.6 vs 14.8% recurrent ulcer
H.Pylori erad+PPI : Without PPI

94. Recurrent bleeding risk
• H.Pylori (+) bleeding ulcer  12 months  recurrent
bleeding 26%
• NSAIDs user + H.Pylori (+) with bleeding ulcer only
H.Pylori eradication  ulcer healing  6 months 
recurrent bleeding 19%
• Low dose aspirin + H.pylori (+)  15%
• Idiopathic bleeding ulcers  7 ys  42%
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95. Recommendation for PPI usage
• PPIs can cause falsely negative H.pylori in 1/3 cases
• PPIs should be discontinued 2 weeks before testing
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96. NSAIDs ulcer
• Celecoxib vs Diclofenac+PPIs  6 ms  4.8 : 6.4%
recurrent bleeding
• Recurrent ulcer 19 : 26%
• [Celecoxib + PPIs bid] vs [Celecoxib+placebo[  0 vs 8.9%
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97. Medication Cost Cost for CI x 72 hours
IV pantoprazole (Protonix®)
Bolus: 80 mg
CI: 8 mg/hr
$55.00
$132.00/day
N/A
$396.00
2015-04-07 97
Table 3: Average Wholesale Price (AWP) of IV Pantoprazole22

98. • Clinical algorithm for the
management of peptic ulcer
bleeding adopted at the Prince of
Wales Hospital, Hong Kong.
• 2006
2015-04-07 98

99. Uncomplicated ulcer
• Regimen (inpatient or outpatient)
• Diet: 3-4 hours apart, 5-7 times/day
• Bleeding risk: food denial for 24h
• H.Pylori eradication
• Acid reducing agents and gastroprotector: PPIs, H2RA
• 6-8weeks – gastric ulcer
• 4-6 weeks – duodenal ulcer
2015-04-07 99

100. Drugs used in Tx of
PUD
2015-04-07 100

101. 2015-04-07 101

102. Complication of PUD
Acute hemorrhage
2015-04-07
102
Nonshock state
preterminal
event
Blood transfuse!Restoration of IV fluid

103. 2015-04-07 103
6100₮
7800₮
12500₮
13500₮
23100₮
650₮

104. 2015-04-07 104
4,550 ₮
54,000 ₮
2,300 ₮
1,600 ₮
6,500 ₮
Мизопростол 200мкг – 3500 ₮

105. Reference:
• Г.Энхдолгор, Н.Бира, Х.Оюунцэцэг нар, Хоол боловсруулах эрхтэний эмгэг, 2014 он, ху214-244
• Harrison’s Principles of Internal Medicine, 18th ed, volume 2, part 14, section 1, chapter 293, pp2438-2459
• Watson et al. Gastrin — active participant or bystander in gastric carcinogenesis?, Nature Reviews Cancer 6, 936–
946 (December 2006) | doi:10.1038/nrc2014
• John L. Wallace, Prostaglandins, NSAIDs, and Gastric Mucosal Protection: Why Doesn't the Stomach Digest Itself?
Physiol Rev 88: 1547–1565, 2008; doi:10.1152/physrev.00004.2008.
• Koji Takeuchi et al, Prostaglandin EP Receptors Involved in Modulating Gastrointestinal Mucosal Integrity, J
Pharmacol Sci 114, 248 – 261 (2010)
• S.J. Konturek et al, Brain-gut and appetite regulating hormones in the control of gastric secretion and mucosal
protection
• Johannes G. Kusters et al, Pathogenesis of Helicobacter pylori Infection, CLINICAL MICROBIOLOGY REVIEWS,
July 2006, p. 449–490 Vol. 19, No. 3, 0893-8512/06/$08.000 doi:10.1128/CMR.00054-05
• Tadataka Yamada et al, Principles of clinical gastroenterology, 2008, chapter 7, pp99-120
• Nicholas J. Talley et al, Practice guidelines, Guidelines for the Management of Dyspepsia, American Journal of
Gastroenterology ISSN 0002-9270, 2005 by Am. Coll. of Gastroenterology doi: 10.1111/j.1572-0241.2005.00225.x
• Loren Laine, MD and Dennis M. Jensen, MD, Management of Patients With Ulcer Bleeding, Am J Gastroenterol
2012; 107:345–360; doi: 10.1038/ajg.2011.480; published online 7 February 2012
• Guillermo Gutierrez et al, Clinical review: Hemorrhagic shock, Critical Care 2004, 8:373-381 (DOI 10.1186/cc2851)
2015-04-07 105

106. Thank you for your
attention!
2015-04-07 106