Peptic ulcer

DefinitionDefinition
• Acid peptic digestion of alimentary mucosa resulting in anAcid peptic digestion of alimentary mucosa resulting in an
ulcer is called peptic ulcer disease.ulcer is called peptic ulcer disease.
• The corrosive effects of acidThe corrosive effects of acid
++
• Proteolytic effect of pepsinProteolytic effect of pepsin

Gastritis is the precursor to PUD and it is clinically difficult toGastritis is the precursor to PUD and it is clinically difficult to
differentiate the twodifferentiate the two
Stomach (called gastric ulcer)Stomach (called gastric ulcer)
Duodenum (called duodenal ulcer)Duodenum (called duodenal ulcer)
Esophagus (called Esophageal ulcer)Esophagus (called Esophageal ulcer)
Meckel's Diverticulum (called Meckel's DiverticulumMeckel's Diverticulum (called Meckel's Diverticulum
ulcer)ulcer)
Anastomotic ulcer after GJ.Anastomotic ulcer after GJ.

Peptic Ulcer DiseasePeptic Ulcer Disease

Gastric Mucosa & SecretionsGastric Mucosa & Secretions
The inside of the stomach is bathed in about 2 liters ofThe inside of the stomach is bathed in about 2 liters of
gastric juice every daygastric juice every day
Gastric juice is composed of digestive enzymes &Gastric juice is composed of digestive enzymes &
concentrated hydrochloric acid, which can readily tearconcentrated hydrochloric acid, which can readily tear
apart the toughest food or microorganismapart the toughest food or microorganism
The gastroduodenal mucosal integrity is
determined by protective (defensive) & damaging
(aggressive) factors

Gastric Mucosa & SecretionsGastric Mucosa & Secretions
The Defensive Forces
Bicarbonate
Mucus layer
Mucosal blood flow
Prostaglandins
Growth factors
The Aggressive Forces
Helicobacter pylori
HCl acid
Pepsins
NSAIDs
Bile acids
Ischemia and hypoxia.
Smoking and alcohol
When the aggressive factors increase or the
defensive factors decrease, mucosal damage
will result, leading to erosions & ulcerations

Because of ImbalanceBecause of Imbalance
Imbalance primarily between Aggressive factorsImbalance primarily between Aggressive factors
and Defensive factors:and Defensive factors:
Aggressive
factors, e,g,
acid, pepsin,
bile etc.
Defensive
factors, e.g.
mucus,
HCO3, PG

Phases of gastric secretionPhases of gastric secretion
Phase Stimuli Pathway
Cephalic (stimulate) Sight, smell, taste or
thought of food
1) Vagus (M3 receptors)
2) Histamine (H2 receptor)
3) Gastrin
Gastric (stimulate) Food in the stomach 1) Stretch: local reflex (M3
receptors)
2) Chemical substances in food
(gastrin)
3) Increase pH: Inhibition of
somatostatin (GHIH) release
Intestinal (inhibit) Chyme in the
duodenum

Gastric secretionsGastric secretions
1.1. PepsinogensPepsinogens (Chief cells).(Chief cells).
2.2. HCl and intrinsic factorHCl and intrinsic factor (Parietal cells).(Parietal cells).
3.3. GastrinGastrin (G-cells).(G-cells).
4.4. Mucus, bicarbonateMucus, bicarbonate (mucus-secreting cells).(mucus-secreting cells).

What may contributeWhat may contribute
imbalance ?imbalance ?
Helicobacter pyloriHelicobacter pylori
NSAIDsNSAIDs
EthanolEthanol
TobaccoTobacco
Severe physiologicSevere physiologic
stress (Burns, CNS trauma,stress (Burns, CNS trauma,
Surgery, Severe medical illness)Surgery, Severe medical illness)
SteroidsSteroids

EtiologyEtiology
 Other uncommon causes include:Other uncommon causes include:
Gastrinoma (Gastrin secreting tumor)Gastrinoma (Gastrin secreting tumor)
Stress ulceration (trauma, burns, critical illness)Stress ulceration (trauma, burns, critical illness)
Viral infectionsViral infections
Vascular insufficiencyVascular insufficiency

Who are they ?Who are they ?
Barry J Marshall J. Robin Warren
Nobel Laureates
of Medicine –
2005
Discovery of
H. pylori & its
role in peptic
ulcer

EtiologyEtiology
 The two most common causes of PUD are:The two most common causes of PUD are:
Helicobacter pyloriHelicobacter pylori infection ( 70-80%)infection ( 70-80%)
Non-steroidal anti-inflammatory drugs (NSAIDS)Non-steroidal anti-inflammatory drugs (NSAIDS)

H.pyloriH.pylori as a cause of PUDas a cause of PUD

Pathogenesis ofPathogenesis of H. pyloriH. pylori infectioninfection
H. pyloriH. pylori is Gram-negative, spiral &is Gram-negative, spiral &
has multiple flagella at one endhas multiple flagella at one end
Transmitted from person-to-personTransmitted from person-to-person
by Oro–oral or feco-oral spreadby Oro–oral or feco-oral spread
Rhesus monkey is the only naturalRhesus monkey is the only natural
reservoir.reservoir.

Dynamics of H.pylori infectionDynamics of H.pylori infection
Dr.T.V.Rao MDDr.T.V.Rao MD 1818

Any acidity is buffered by theAny acidity is buffered by the
organism's production of theorganism's production of the
enzyme urease, which catalyzesenzyme urease, which catalyzes
the production of ammonia (NH3)the production of ammonia (NH3)
from urea & raises the pH therefrom urea & raises the pH there
The bacterium stimulates chronicThe bacterium stimulates chronic
gastritis by provoking a localgastritis by provoking a local
inflammatory response.inflammatory response.

- ↓ Somatostatin production from antral D-cells due to antral gastritis
- Low somatostatin will ↑Gastrin release from G-cell 
hypergastrinemia
- This will stimulate acid production by the parietal cells  leading to
further duodenal ulceration.
Effects of H. pylori on gastric Hormones
This effect is exaggerated among smokers!

Carcinogenic effect ofCarcinogenic effect of H. pyloriH. pylori
H. pylori
Host Factors
Other environmental
Factors
Antral gastritis Pangastritis
DU GU Gastritis Cancer

NSAIDSNSAIDS
Symptomatic GI ulceration occurs in 2% - 4% of patientsSymptomatic GI ulceration occurs in 2% - 4% of patients
treated with NSAIDs for 1 yeartreated with NSAIDs for 1 year
In view of the million of people who take NSAIDs annually,In view of the million of people who take NSAIDs annually,
these small percentages translate into a large number ofthese small percentages translate into a large number of
symptomatic ulcerssymptomatic ulcers
The effects of aspirin & NSAIDs on the gastric mucosa rangesThe effects of aspirin & NSAIDs on the gastric mucosa ranges
from mucosal hemorrhages to erosions & acute ulcersfrom mucosal hemorrhages to erosions & acute ulcers

NSAIDSNSAIDS
 Inhibits the production ofInhibits the production of prostaglandinsprostaglandins precursor fromprecursor from
membrane fatty acids resulting in:membrane fatty acids resulting in:
1. Decrease mucus & HCO3 production1. Decrease mucus & HCO3 production
2. Decrease mucosal blood flow2. Decrease mucosal blood flow
3. Reduce cell renewal3. Reduce cell renewal
 The drugs also generate oxygen-free radicals & products ofThe drugs also generate oxygen-free radicals & products of
the lipoxygenase pathway that may contribute to ulcerationthe lipoxygenase pathway that may contribute to ulceration

NSAIDSNSAIDS
 Gastric acid probably aggravates NSAID-induce mucosalGastric acid probably aggravates NSAID-induce mucosal
injury byinjury by
- Converting superficial injury to deeper mucosal necrosis,- Converting superficial injury to deeper mucosal necrosis,
- Interfering with haemostasis & platelet aggregation- Interfering with haemostasis & platelet aggregation
- Impairing ulcer healing- Impairing ulcer healing
• Users of NSAIDs are at approximately 3 times greater relativeUsers of NSAIDs are at approximately 3 times greater relative
risk of serious adverse gastrointestinal events than nonusersrisk of serious adverse gastrointestinal events than nonusers

Psychological Stress UlcersPsychological Stress Ulcers
Gastric mucosa of body of stomach undergoes a period ofGastric mucosa of body of stomach undergoes a period of
transient ischemia in association withtransient ischemia in association with
HypotensionHypotension
Severe injurySevere injury
Extensive burnsExtensive burns
Complicated surgeryComplicated surgery

Psychological Stress UlcersPsychological Stress Ulcers
Ischemia due to capillary blood flow or shunting of blood↓Ischemia due to capillary blood flow or shunting of blood↓
away from GI tract so that blood flow bypasses gastricaway from GI tract so that blood flow bypasses gastric
mucosamucosa
Imbalance between destructive properties of HCl acid andImbalance between destructive properties of HCl acid and
pepsin, and protective factors of stomachpepsin, and protective factors of stomach’’s mucosal barriers mucosal barrier

TypesTypes
AcuteAcute
ChronicChronic

Acute peptic ulcer (DUODENAL ORAcute peptic ulcer (DUODENAL OR
GASTRIC ULCER)GASTRIC ULCER)
They are usually multiple erosions due to disruption of theThey are usually multiple erosions due to disruption of the mucosalmucosal
barrier.barrier.
Causes - Stress, drugs like analgesics, steroids, surgeries.Causes - Stress, drugs like analgesics, steroids, surgeries.
Sudden onset of acute pain and tenderness in epigastric region.Sudden onset of acute pain and tenderness in epigastric region.
Vomiting with or without haematemesis.Vomiting with or without haematemesis.
Often acute peptic ulcers can lead to perforations.Often acute peptic ulcers can lead to perforations.
Acute ulcers after cerebral trauma or neurosur geries are called asAcute ulcers after cerebral trauma or neurosur geries are called as
Cushing’s ulcers .Cushing’s ulcers .
Acute ulcers after major burns are called as Curling’s ulcers .Acute ulcers after major burns are called as Curling’s ulcers .
Diagnosis is by gastroscopy.Diagnosis is by gastroscopy.

TreatmentTreatment
Intravenous ranitidine 50 mg, 8th hourly.Intravenous ranitidine 50 mg, 8th hourly.
IV fluids. IV pantoprazole/rabeprazole/omeprazole.IV fluids. IV pantoprazole/rabeprazole/omeprazole.
Blood transfusions if there is bleeding.Blood transfusions if there is bleeding.
Most of the time surgery is not required for acute ulcers.Most of the time surgery is not required for acute ulcers.
During follow-up patients are advised to take antiulcer drugsDuring follow-up patients are advised to take antiulcer drugs
for 4-6 weeks—ranitidine, omeprazole or lanso prazole.for 4-6 weeks—ranitidine, omeprazole or lanso prazole.

Curling’s UlcersCurling’s Ulcers
They are acute ulcers which develop after major burns,They are acute ulcers which develop after major burns,
presenting as pain in epigastric region, vomiting orpresenting as pain in epigastric region, vomiting or
haematemesis.haematemesis.
Treatment is conservative—IV ranitidine. IV pantoprazoleTreatment is conservative—IV ranitidine. IV pantoprazole
80 mg in 100 ml DNS—slow, later 40 mg IV maintenance.80 mg in 100 ml DNS—slow, later 40 mg IV maintenance.

Cushing’s UlcersCushing’s Ulcers
They are acute ulcers which develop after cerebral trauma orThey are acute ulcers which develop after cerebral trauma or
after neurosurgical operations.after neurosurgical operations.
It is commonly single, deeper ulcer more frequentlyIt is commonly single, deeper ulcer more frequently
perforates.perforates.
It can occur in oesophagus and duodenum also. Treatment isIt can occur in oesophagus and duodenum also. Treatment is
conservative by IV ranitidine.conservative by IV ranitidine.

Chronic ulcersChronic ulcers
Two major variants in peptic ulcers are commonly encountered in theTwo major variants in peptic ulcers are commonly encountered in the
clinical practice:clinical practice:
1)1) Duodenal UlcerDuodenal Ulcer (DU)(DU)
2)2) Gastric UlcerGastric Ulcer (GU)(GU)

Gastric ulcerGastric ulcer
It occurs due to imbalance between protective and damagingIt occurs due to imbalance between protective and damaging
factors of gastric mucosa.factors of gastric mucosa.
Atrophic gastritis, duodenogastric bile reflux, gastric stasis,Atrophic gastritis, duodenogastric bile reflux, gastric stasis,
abnormalities in acid and pepsin secretion.abnormalities in acid and pepsin secretion.
Acid becomes ulcerogenic even to normal gastric mucosa.Acid becomes ulcerogenic even to normal gastric mucosa.
Smoking, alcohol, NSAIDs, steroids.Smoking, alcohol, NSAIDs, steroids.
Helicobacter pylori infection (70%).Helicobacter pylori infection (70%).
There is either normochlorhydria or hypochlorhydria.There is either normochlorhydria or hypochlorhydria.
Altered mucosal barrier mechanism.Altered mucosal barrier mechanism.
Lower socioeconomic group.Lower socioeconomic group.

Gastric ulcerGastric ulcer
Factors Involved in Gastric Ulcer FormationFactors Involved in Gastric Ulcer Formation
Duodenogastric reflux—reflux containing bile salts andDuodenogastric reflux—reflux containing bile salts and
lysolecithin break the mucosal barrier making it morelysolecithin break the mucosal barrier making it more
vulnerable for injury, action of drugs and pepsin injury.vulnerable for injury, action of drugs and pepsin injury.
Gastric stasis.Gastric stasis.
Ischaemia of the gastric mucosa.Ischaemia of the gastric mucosa.
Type II and III gastric ulcers show acid hypersecretion.Type II and III gastric ulcers show acid hypersecretion.

PathologyPathology
Gastric ulcer is large in size, usually lies in the lesserGastric ulcer is large in size, usually lies in the lesser
curvature, its floor being formed by the muscular layer.curvature, its floor being formed by the muscular layer.
Posteriorly it may penetrate into the pancreas; it may causePosteriorly it may penetrate into the pancreas; it may cause
torrential bleeding by eroding left gastric (commonly) vesslestorrential bleeding by eroding left gastric (commonly) vessles
or splenic vessels or vessels in the gastric ulcer wall.or splenic vessels or vessels in the gastric ulcer wall.
Microscopically, it shows ulcer crater with chronicMicroscopically, it shows ulcer crater with chronic
inflammatory cells and granulation tissue, endarteritisinflammatory cells and granulation tissue, endarteritis
obliterans and epithelial proliferation.obliterans and epithelial proliferation.

(Ulcer to the right of the incisura is malignant unless proved(Ulcer to the right of the incisura is malignant unless proved
otherwise).otherwise).
Gastric ulcer > 3 cm is called as giant gastric ulcer. It has gotGastric ulcer > 3 cm is called as giant gastric ulcer. It has got
6-23% chances to turn into malignancy.6-23% chances to turn into malignancy.
Grossly, margin of the benign gastric ulcer is clear; deep;Grossly, margin of the benign gastric ulcer is clear; deep;
near lesser curve; edge is not everted with gastric mucosalnear lesser curve; edge is not everted with gastric mucosal
folds converging towards the base of the ulcer.folds converging towards the base of the ulcer.
95% of benign gastric ulcer occurs towards lesser curve, as it95% of benign gastric ulcer occurs towards lesser curve, as it
takes more burden of passage of food and so more of weartakes more burden of passage of food and so more of wear
and tear. Benign gastric ulcer is rare in greater curvature,and tear. Benign gastric ulcer is rare in greater curvature,
fundus and cardia.fundus and cardia.

Clinical featuresClinical features
Equal in both sexes. It is becoming more common inEqual in both sexes. It is becoming more common in
females.females.
Common after the age of 40 years.Common after the age of 40 years.
PainPain in epigastric region after taking food, lasting up to twoin epigastric region after taking food, lasting up to two
hours. Pain is uncommon during night. It is relieved byhours. Pain is uncommon during night. It is relieved by
vomiting or by inducing vomiting.vomiting or by inducing vomiting.

PeriodicityPeriodicity: Symptom free interval may be 2-6 months.: Symptom free interval may be 2-6 months.
Often with seasonal variation.Often with seasonal variation.
VomitingVomiting relieves pain and often it is induced by the patient forrelieves pain and often it is induced by the patient for
relief of pain.relief of pain.
Haematemesis and melaenaHaematemesis and melaena: Haematemesis is more: Haematemesis is more common.common.
Appetite is good but hesitant to eat, because eating induces painAppetite is good but hesitant to eat, because eating induces pain
and that results in loss of weight.and that results in loss of weight.
But once complications occur, appetite decreases. Aversion toBut once complications occur, appetite decreases. Aversion to
spicy, fried foods occurs.spicy, fried foods occurs.
On deep palpation, tenderness is felt in epigastric region.On deep palpation, tenderness is felt in epigastric region.

Differential diagnosisDifferential diagnosis
Hiatus hernia.Hiatus hernia.
Cholecystitis.Cholecystitis.
Chronic pancreatitis.Chronic pancreatitis.
Chronic gastritis.Chronic gastritis.
Dyspepsia.Dyspepsia.
Carcinoma stomach.Carcinoma stomach.

Barium meal X-rayBarium meal X-ray
Barium meal showing Niche in theBarium meal showing Niche in the
lesser curve aslesser curve as benign gastric ulcer.benign gastric ulcer.
Niche on the lesser curve with notch onNiche on the lesser curve with notch on
the greater curvaturethe greater curvature
Ulcer crater projects beyond the lumenUlcer crater projects beyond the lumen
of the ulcerof the ulcer
Regular/round margin of the ulcerRegular/round margin of the ulcer
crater—stomach spoke wheel patterncrater—stomach spoke wheel pattern
Overhanging mucosa at the margins ofOverhanging mucosa at the margins of
a benign gastric ulcer—projects inwardsa benign gastric ulcer—projects inwards
towards the ulcer—Hamptom’s linetowards the ulcer—Hamptom’s line
Converging mucosal folds towards theConverging mucosal folds towards the
base of the ulcerbase of the ulcer
Symmetrical normal gastric mucosalSymmetrical normal gastric mucosal
foldsfolds

GastroscopyGastroscopy
Gastroscopy is done toGastroscopy is done to
see the location, type ofsee the location, type of
ulcer and also to takeulcer and also to take
biopsy (10 biopsies).biopsy (10 biopsies).
Gastric ulcer in the body of theGastric ulcer in the body of the
stomach.stomach.

TreatmentTreatment
Drugs like H2 blockers, proton pump inhibitors,Drugs like H2 blockers, proton pump inhibitors,
carbenexolone (Biogastrone, Sucralfate, prostag landinscarbenexolone (Biogastrone, Sucralfate, prostag landins
which coats the ulcer and so creates a mucosal barrier) helpswhich coats the ulcer and so creates a mucosal barrier) helps
in reducing or eliminating the symptoms.in reducing or eliminating the symptoms.
But asymptomatic ulcer may exist silently and may turn intoBut asymptomatic ulcer may exist silently and may turn into
malignancy.malignancy.
So surgery is the preferred line of treatment. PartialSo surgery is the preferred line of treatment. Partial
gastrectomy and Billroth I gastroduodenal anastomosis isgastrectomy and Billroth I gastroduodenal anastomosis is
done.done.

Type IV proximal gastric ulcer is difficult to manage. It is treated byType IV proximal gastric ulcer is difficult to manage. It is treated by
subtotal gastrectomy. Often distal gastrectomy with selective sleeve likesubtotal gastrectomy. Often distal gastrectomy with selective sleeve like
extension cut along the lesser curve to remove the ulcer is done—extension cut along the lesser curve to remove the ulcer is done—
Pauchet’s procedure.Pauchet’s procedure.
Other surgical procedures:Other surgical procedures:
1. de Miguel’s antrectomy : Distal antrectomy, pylorectomy with1. de Miguel’s antrectomy : Distal antrectomy, pylorectomy with
excision of ulcer along with gastroduodenal anastomosis is done. Itexcision of ulcer along with gastroduodenal anastomosis is done. It
preserves gastric reservoir function, shows less recurrence rate and lesspreserves gastric reservoir function, shows less recurrence rate and less
operative morbidity.operative morbidity.
2. Mak’s pylorus preserving gastrectomy : Hemigastrectomy with2. Mak’s pylorus preserving gastrectomy : Hemigastrectomy with
excision of pyloric ulcer but retaining 2 cm prepyloric stomach. It isexcision of pyloric ulcer but retaining 2 cm prepyloric stomach. It is
only used in type I gastric ulcer. Even though it has got feweronly used in type I gastric ulcer. Even though it has got fewer
incidences of postoperative diarrhoea and dumping, it has got highincidences of postoperative diarrhoea and dumping, it has got high
recurrence raterecurrence rate

3. HSV with excision of ulcer.3. HSV with excision of ulcer.
4. Kelling Madlener procedure : It is antrectomy and4. Kelling Madlener procedure : It is antrectomy and
excision of proximal gastric ulcer Type IV.excision of proximal gastric ulcer Type IV.
5. Csendes procedure : It is subtotal gastrectomy with sleeve5. Csendes procedure : It is subtotal gastrectomy with sleeve
extended resection along the lesser curve forextended resection along the lesser curve for type IVtype IV
proximal gastric ulcer.proximal gastric ulcer.

ComplicationsComplications
1. Hour glass contracture : It occurs1. Hour glass contracture : It occurs
exclusively in women , is due toexclusively in women , is due to
cicatricial contracture of lesser curvecicatricial contracture of lesser curve
ulcer. Here stomach is divided intoulcer. Here stomach is divided into
two compartments.two compartments.
• Clinical features– Loss of periodicity.Clinical features– Loss of periodicity.
Persistent pain.Persistent pain. Vomiting.Vomiting. Loss ofLoss of
appetite and weight.appetite and weight.
• DiagnosisDiagnosis– Barium meal: It shows fi– Barium meal: It shows fi
lling only in the proximal stomach orlling only in the proximal stomach or
double pouched stomach.double pouched stomach.––
Gastroscopy.Gastroscopy.
• TreatmentTreatment
• Partial gastrectomy wherein gastricPartial gastrectomy wherein gastric
ulcer with lower compartment of theulcer with lower compartment of the
stomach is removed and Billrothstomach is removed and Billroth
anastomosis is done.anastomosis is done.

• Tea-pot deformityTea-pot deformity
(Hand-bag stomach): It is(Hand-bag stomach): It is
due to cicatrisation anddue to cicatrisation and
shortening of the lessershortening of the lesser
curvature.curvature.
• They present withThey present with
features of pyloricfeatures of pyloric
stenosis.stenosis.
• Treatment is partialTreatment is partial
gastrectomy with Billrothgastrectomy with Billroth
I anastomosis.I anastomosis.

• 3. Perforation— most frequent.3. Perforation— most frequent.
• 4. Bleeding by erosion into the left gastric and rarely splenic4. Bleeding by erosion into the left gastric and rarely splenic
vessels or to vessels in the wall of ulcer —35%. It is commonvessels or to vessels in the wall of ulcer —35%. It is common
in type II and III gastric ulcers.in type II and III gastric ulcers.
• 5. Penetration posteriorly into pancreas, anteriorly into liver5. Penetration posteriorly into pancreas, anteriorly into liver
• 6. Malignant transformation usually into adenocar cinoma6. Malignant transformation usually into adenocar cinoma
of stomach (2-5%)..of stomach (2-5%)..

Duodenal ulcerDuodenal ulcer
• AetiologyAetiology
• Common in people with blood group O +ve.Common in people with blood group O +ve.
• Stress, anxiety—‘hurry, worry, curry’.Stress, anxiety—‘hurry, worry, curry’.
• Helicobacter pylori infection is an important aetiology forHelicobacter pylori infection is an important aetiology for duodenalduodenal
ulcer (90%).ulcer (90%).
• NSAIDs, steroidsNSAIDs, steroids
• Endocrine causes: Zollinger-Ellison syndrome, MENEndocrine causes: Zollinger-Ellison syndrome, MEN syndrome,syndrome,
hyperparathyroidism.hyperparathyroidism.
• Other causes: Alcohol, smoking, vitamin defi ciency.Other causes: Alcohol, smoking, vitamin defi ciency.
• Dragstedt dictum : “No acid – No ulcer”.Dragstedt dictum : “No acid – No ulcer”.

• PathologyPathology
• Ulcer occurs in the fi rst part of duodenum, usually with in theUlcer occurs in the fi rst part of duodenum, usually with in the
first inch,involving the muscular layer.first inch,involving the muscular layer.
• Sites:Sites:
• a. In the bulb (bulbar)—95%.a. In the bulb (bulbar)—95%.
• b. Post-bulbar (5%).b. Post-bulbar (5%).
• Eventually it shows cicatrisation causing pyloric stenosis. SerosaEventually it shows cicatrisation causing pyloric stenosis. Serosa
overlying the site of duodenal ulcer shows petechial haemorrhagesoverlying the site of duodenal ulcer shows petechial haemorrhages
with speckled red dots, appearing like sprinkledwith speckled red dots, appearing like sprinkled cayenne pepper .cayenne pepper .

• Microscopically, ulcer with chronic inflammation withMicroscopically, ulcer with chronic inflammation with
granulation tissue, gastric metaplasia of duodenal mucosa,granulation tissue, gastric metaplasia of duodenal mucosa,
endarteritis obliterans are visualised.endarteritis obliterans are visualised.
• Sometimes two opposing ulcers, i.e. over anterior andSometimes two opposing ulcers, i.e. over anterior and
posterior surfaces of duodenum are present and are called asposterior surfaces of duodenum are present and are called as
kissing ulcers.kissing ulcers.
• An anterior ulcer perforates commonly, posterior ulcerAn anterior ulcer perforates commonly, posterior ulcer
bleeds or penetrates commonly.bleeds or penetrates commonly.

Clinical featuresClinical features
• PainPain is more before food, in early morning and decreases after taking food. Itis more before food, in early morning and decreases after taking food. It
is classically called as hunger pain as it is relieved by taking food. Night painsis classically called as hunger pain as it is relieved by taking food. Night pains
are common.are common.
• PeriodicityPeriodicity is more common than in chronic gastric ulcer with seasonalis more common than in chronic gastric ulcer with seasonal
variation.variation.
• In India, ratio of duodenal ulcer to gastric ulcer is 30 : 1. A very highIn India, ratio of duodenal ulcer to gastric ulcer is 30 : 1. A very high
incidence.incidence.
• It is common in all socioeconomic group, more with stressed professionalsIt is common in all socioeconomic group, more with stressed professionals
(Type A personality).(Type A personality).
• Common in males .Common in males .
• Water-brash, heart burn, vomiting may be present.Water-brash, heart burn, vomiting may be present.
• Melaena is more common, haematemesis also can occur.Melaena is more common, haematemesis also can occur.

• Appetite is good and there is gain in weight. It decreasesAppetite is good and there is gain in weight. It decreases
once stenosis develops.once stenosis develops.
• Eats more frequently without any restriction.Eats more frequently without any restriction.
• Chronic duodenal ulcer can be uncomplicated orChronic duodenal ulcer can be uncomplicated or
complicated.complicated.

• Barium meal X-rayBarium meal X-ray
shows deformed orshows deformed or
absence of duodenal capabsence of duodenal cap
(because of spasm).(because of spasm).
Appearance of ‘trifoliate’Appearance of ‘trifoliate’
duodenum is due toduodenum is due to
secondary duodenalsecondary duodenal
diverticula which occursdiverticula which occurs
as a result of scarring ofas a result of scarring of
ulcer.ulcer.

• Gastroscopy reveals the type, location of ulcer, narrowing ifGastroscopy reveals the type, location of ulcer, narrowing if
any.any.
• Biopsy also can be taken to look for the presence ofBiopsy also can be taken to look for the presence of
Helicobacter pylori .Helicobacter pylori .
• Usually biopsies are taken from duodenum, pylorus, antrum,Usually biopsies are taken from duodenum, pylorus, antrum,
body, fundus, and confirmed by rapid urease test or C13 orbody, fundus, and confirmed by rapid urease test or C13 or
C14 breath tests.C14 breath tests.
• Estimation of serum gastrin level, serum calcium level.Estimation of serum gastrin level, serum calcium level.

Differential diagnosisDifferential diagnosis
• Carcinoma stomach (pylorus)Carcinoma stomach (pylorus)
• Dyspepsia due to other causesDyspepsia due to other causes
• –– Hiatus herniaHiatus hernia
• –– OesophagitisOesophagitis
• –– CholecystitisCholecystitis
• –– Chronic pancreatitisChronic pancreatitis

Diagnosis:Diagnosis:
1)1) Diagnosis of ulcerDiagnosis of ulcer
2)2) Diagnosis of H. pyloriDiagnosis of H. pylori

 EndoscopyEndoscopy
 Barium meal – contrast x-rayBarium meal – contrast x-ray
 Biopsy – bacteria & malignancyBiopsy – bacteria & malignancy
 H.Pylori:H.Pylori:
 Endoscopy cytologyEndoscopy cytology
 Biopsy – Special stainsBiopsy – Special stains
 Culture - difficultCulture - difficult
 Urease Breath test.Urease Breath test.
PUD - DiagnosisPUD - Diagnosis

Diagnosis of PUDDiagnosis of PUD
In most patients routine laboratory tests are usuallyIn most patients routine laboratory tests are usually unhelpfulunhelpful
Diagnosis of PUD depends mainly on endoscopic and
radiographic confirmation

EndoscopyEndoscopy
• Most sensitive and specific .Most sensitive and specific .
• Direct visualization of the mucosa,Direct visualization of the mucosa,
• Biopsy to rule out malignancy orBiopsy to rule out malignancy or Hpylori.Hpylori.
• Identifies lesions too small to detect by Ba exam, forIdentifies lesions too small to detect by Ba exam, for
evaluation of atypical radiographic abnormalities, or toevaluation of atypical radiographic abnormalities, or to
determine if an ulcer is a source of blood loss.determine if an ulcer is a source of blood loss.

Doudenal Ulcer on EndoscopyDoudenal Ulcer on Endoscopy
Doudenal UlcerNormal doudenal bulb

Gastric Ulcer on EndoscopyGastric Ulcer on Endoscopy
Chronic Gastric Ulcers

Diagnosis ofDiagnosis of H. pyloriH. pylori
 Non-invasiveNon-invasive
• CC1313
or Cor C1414
Urea Breath TestUrea Breath Test
• Stool antigen testStool antigen test
• H. pylori IgG titer (serology)H. pylori IgG titer (serology)
 InvasiveInvasive
• Gastric mucosal biopsyGastric mucosal biopsy
• Rapid Urease testRapid Urease test

Non-invasive
1. C13 or C14 Urea Breath Test
The best test for the detection
of an active infection

Non-invasiveNon-invasive
1)1) Serology forSerology for H pyloriH pylori
a.a. Serum Antibodies (IgG) toSerum Antibodies (IgG) to H pyloriH pylori (Not for active(Not for active
infection)infection)
b.b. Fecal antigen testing (Fecal antigen testing (Test for active HPTest for active HP))

InvasiveInvasive
• Upper GI endoscopyUpper GI endoscopy
– Highly sensitive testHighly sensitive test
– Patient needs sedationPatient needs sedation
– Has bothHas both diagnosticdiagnostic && therapeutictherapeutic rolerole

Invasive (endoscopy)Invasive (endoscopy)
– DiagnosticDiagnostic::
– Detect the site and the size of the ulcer, even smallDetect the site and the size of the ulcer, even small
and superficial ulcer can be detectedand superficial ulcer can be detected
– Detect source of bleedingDetect source of bleeding
– Biopsies can be taken forBiopsies can be taken for rapid urease testrapid urease test,,
histopathologyhistopathology && cultureculture

• Rapid urease test ( RUT)Rapid urease test ( RUT)
o Considered the endoscopicConsidered the endoscopic diagnostic test of choicediagnostic test of choice
o Gastric biopsy specimens are placed in the rapidGastric biopsy specimens are placed in the rapid
urease test kit. Ifurease test kit. If H pyloriH pylori are present, bacterialare present, bacterial
urease converts urea to ammonia, which changesurease converts urea to ammonia, which changes
pH and produces apH and produces a CCOOLLOORR changechange

* Histopathology* Histopathology
o Done if the rapid urease test result is negativeDone if the rapid urease test result is negative
* Culture* Culture
o Used in research studies and is not availableUsed in research studies and is not available
routinely for clinical useroutinely for clinical use

TreatmentTreatment
• Aim of therapy:Aim of therapy:
• To relieve symptoms;To relieve symptoms;
• To heal ulcer;To heal ulcer;
• To prevent recurrence.To prevent recurrence.
• I. General measuresI. General measures::
• Avoid alcohol, NSAIDs, smoking, spicy foods. HaveAvoid alcohol, NSAIDs, smoking, spicy foods. Have
• more frequent food.more frequent food.
• II. Specific measures:II. Specific measures:
• Intragastric pH should be maintained above 5.Intragastric pH should be maintained above 5.

ClassificationClassification
1.1. Acid Neutralizing agents: (ANTACIDS)Acid Neutralizing agents: (ANTACIDS)
• Systemic: Sodium Bicarbonate and Sod. CitrateSystemic: Sodium Bicarbonate and Sod. Citrate
• Nonsystemic: Magnesium hydroxide, Mag. Treisilicate, AluminiumNonsystemic: Magnesium hydroxide, Mag. Treisilicate, Aluminium
hydroxide gel, Magaldrate and calcium carbonatehydroxide gel, Magaldrate and calcium carbonate
1.1. Reduction in Gastric acid secretion:Reduction in Gastric acid secretion:
• H2 antihistamines:H2 antihistamines: Cimetidine, Ranitidine, Famotidine,Cimetidine, Ranitidine, Famotidine,
Nizatidine and RoxatidineNizatidine and Roxatidine
• Proton pump inhibitors:Proton pump inhibitors: Omeprazole, LansoprazoleOmeprazole, Lansoprazole
Pantoprazole, Rabeprazole and EsomeprazolePantoprazole, Rabeprazole and Esomeprazole
• Anticholinergics:Anticholinergics: Pirenzepine, Propantheline andPirenzepine, Propantheline and
OxyphenoniumOxyphenonium
• Prostaglandin analogue:Prostaglandin analogue: MisoprostolMisoprostol

Classification – contd.Classification – contd.
3.3. Ulcer protectives: Sucralfate, Colloidal Bismuth sudcitrateUlcer protectives: Sucralfate, Colloidal Bismuth sudcitrate
4.4. Anti-H. pylori Drugs: Amoxicillin, Clarithromycin,Anti-H. pylori Drugs: Amoxicillin, Clarithromycin,
metronidazole, tinidazole and tetracyclinemetronidazole, tinidazole and tetracycline

AntacidsAntacids
• Weak bases that neutralize acidWeak bases that neutralize acid
• Also inhibit formation of pepsinAlso inhibit formation of pepsin
(As pepsinogen converted to pepsin at acidic pH)(As pepsinogen converted to pepsin at acidic pH)
• Acid Neutralizing Capacity:Acid Neutralizing Capacity:
– Potency of AntacidsPotency of Antacids
– Expressed in terms of Number ofExpressed in terms of Number of mEqmEq ofof 1N HCl1N HCl that are broughtthat are brought
down to pH 3.5 in 15 minutes by unit dose of a preparation (1 gm)down to pH 3.5 in 15 minutes by unit dose of a preparation (1 gm)

Antacids - The Oldest RemedyAntacids - The Oldest Remedy
• Sodium Bicarbonate:Sodium Bicarbonate:
– Potent neutralizing capacity and acts instantlyPotent neutralizing capacity and acts instantly
– ANC: 1 gm = 12 mEqANC: 1 gm = 12 mEq
• NOT USED ANYMORE FOR ITS DEMERITS:NOT USED ANYMORE FOR ITS DEMERITS:
– Systemic alkalosisSystemic alkalosis
– Distension, discomfort and belching – CO2Distension, discomfort and belching – CO2
– Rebound acidityRebound acidity
– Sodium overloadSodium overload

AntacidsAntacids
• Present day antacids :Present day antacids :
– Aluminium Hydroxide (ANC 1-2.5mEq/g)Aluminium Hydroxide (ANC 1-2.5mEq/g)
– Magnesium Hydroxide (ANC 30 mEq) – milk of magnesiaMagnesium Hydroxide (ANC 30 mEq) – milk of magnesia
– Magnesium trisilicate (ANC 1mEq/g)Magnesium trisilicate (ANC 1mEq/g)
• Duration of action : 30 min when taken in empty stomach and 2Duration of action : 30 min when taken in empty stomach and 2
hrs when taken after a mealhrs when taken after a meal
• Side effects :Side effects :
– Aluminium antacids –Aluminium antacids – constipationconstipation (As they relax gastric smooth(As they relax gastric smooth
muscle & delay gastric emptying) – also hypophosphatemia andmuscle & delay gastric emptying) – also hypophosphatemia and
osteomalciaosteomalcia
– Mg2+ antacids – OsmoticMg2+ antacids – Osmotic diarrhoeadiarrhoea
• In renal failure Al3+ antacid – Aluminium toxicityIn renal failure Al3+ antacid – Aluminium toxicity
& Encephalopathy& Encephalopathy
(Magaldrate – hydrated hydroxy magnesium aluminate)(Magaldrate – hydrated hydroxy magnesium aluminate)

Antacids – contd.Antacids – contd.
• SimethiconeSimethicone: Decrease surface tension thereby reduce bubble: Decrease surface tension thereby reduce bubble
formation - added to prevent refluxformation - added to prevent reflux
• Alginates:Alginates: Form a layer of foam on top of gastric contents &Form a layer of foam on top of gastric contents &
reduce refluxreduce reflux
• Oxethazaine:Oxethazaine: Surface anaestheticSurface anaesthetic

Sucralfate – ulcer protectiveSucralfate – ulcer protective
• Salt ofSalt of sucrosesucrose complexed to sulfated aluminium hydroxidecomplexed to sulfated aluminium hydroxide
(basic aluminium salt)(basic aluminium salt)
• MOA:MOA:
– In acidic pHIn acidic pH polymerisespolymerises to viscous gel that adheres to ulcer crater -to viscous gel that adheres to ulcer crater -
more on duodenal ulcermore on duodenal ulcer
– Precipitates protein on surface proteins and acts as physical barrierPrecipitates protein on surface proteins and acts as physical barrier
– Dietary proteins get deposited on this layer forming another coatDietary proteins get deposited on this layer forming another coat
– Delays gastric emptying and causes gastric PG synthesis – protectiveDelays gastric emptying and causes gastric PG synthesis – protective
actionaction

Sucralfate – contd.Sucralfate – contd.
• Taken on empty stomach 1 hr. before mealsTaken on empty stomach 1 hr. before meals
• Concurrent antacids, HConcurrent antacids, H22 antagonist avoided (as it needs acid forantagonist avoided (as it needs acid for
activation)activation)
• Uses:Uses:
– NSAID induced ulcersNSAID induced ulcers
– Patients with continued smokingPatients with continued smoking
– ICUICU
– Topically – burn, bedsore ulcers, excoriated skinsTopically – burn, bedsore ulcers, excoriated skins
• Dose: 1 gm 1 Hr before mealsDose: 1 gm 1 Hr before meals
• ADRs: Constipation, hypophosphatemiaADRs: Constipation, hypophosphatemia

Chemical reactions of antacids with HCl in theChemical reactions of antacids with HCl in the
stomachstomach

AntacidsAntacids
Capsules & Tablets:Capsules & Tablets:
• PowdersPowders
• Chewable tabletsChewable tablets
• SuspensionsSuspensions
• Effervescent granules and tabletsEffervescent granules and tablets

HH22 AntagonistsAntagonists
• Cimetidine, Ranitidine, Famotidine, Roxatidine, NizatidineCimetidine, Ranitidine, Famotidine, Roxatidine, Nizatidine
andand
• MOA:MOA:
– Reversible competitive inhibitors of HReversible competitive inhibitors of H22 receptorreceptor
– Highly selective, no action on HHighly selective, no action on H11 or Hor H33 receptorsreceptors
– All phases of gastric acid secretionAll phases of gastric acid secretion
– Very effective in inhibiting nocturnal acid secretion (as it dependsVery effective in inhibiting nocturnal acid secretion (as it depends
largely on Histamine )largely on Histamine )
– Modest impact on meal stimulated acid secretion (as it depends onModest impact on meal stimulated acid secretion (as it depends on
gastrin, acetylcholine and histamine)gastrin, acetylcholine and histamine)
– Volume of pepsin content and IF are also reducedVolume of pepsin content and IF are also reduced
– Volume reduced by 60 – 70% - anti ulcerogenic effectVolume reduced by 60 – 70% - anti ulcerogenic effect
– No effect on motilityNo effect on motility

HH22 antagonistsantagonists
• Kinetics:Kinetics:
– All drugs are absorbed orally adequatelyAll drugs are absorbed orally adequately
– Bioavailability upto 80 %Bioavailability upto 80 %
– Absorption is not interfered by presence of foodAbsorption is not interfered by presence of food
– Can cross placental barrier and reaches milkCan cross placental barrier and reaches milk
– Poor CNS penetrationPoor CNS penetration
– 2/32/3rdrd
of the drugs are excreted unchanged in bile and urineof the drugs are excreted unchanged in bile and urine
• Preparations: available as tablets, injectionsPreparations: available as tablets, injections

HH22 antagonists - ADRsantagonists - ADRs
• Extremely safe drugs and well toleratedExtremely safe drugs and well tolerated
• Main ADRs are related to Cimetidine:Main ADRs are related to Cimetidine:
– AntiandrogenicAntiandrogenic effectseffects
– IncreasesIncreases prolactinprolactin secretion and inhibits degradation ofsecretion and inhibits degradation of estradiolestradiol byby
liverliver
– Cytochrome P450 inhibition – theophylline, metronidazole, phenytoin,Cytochrome P450 inhibition – theophylline, metronidazole, phenytoin,
imipramine etc.imipramine etc.
– AntacidsAntacids
• Others:Others:
– Headache, dizziness, bowel upset, dry mouthHeadache, dizziness, bowel upset, dry mouth
– Bolus IV – release histamine – bradycardia, arrhythmia, cardiac arrestBolus IV – release histamine – bradycardia, arrhythmia, cardiac arrest
– Elderly - precautionElderly - precaution

HH22 antagonists - Usesantagonists - Uses
Promote the healing of gastric and duodenal ulcersPromote the healing of gastric and duodenal ulcers
• Duodenal ulcer – 70 to 90%Duodenal ulcer – 70 to 90%
• Gastric Ulcer – 50 to 75% (NSAID ulcers))Gastric Ulcer – 50 to 75% (NSAID ulcers))
• Stress ulcer and gastritisStress ulcer and gastritis
• GERDGERD
• Zollinger-Ellison syndromeZollinger-Ellison syndrome
• Prophylaxis of aspiration pneumoniaProphylaxis of aspiration pneumonia
• UrticariaUrticaria
Doses:Doses:
• 300 mg/40 mg/150 mg at bed time of R, F, Rox respectively for healing300 mg/40 mg/150 mg at bed time of R, F, Rox respectively for healing
• Maintenance: 150/20/150 mg BD of R, F, RoxMaintenance: 150/20/150 mg BD of R, F, Rox

HH22 blockers Tablets in Peptic ulcerblockers Tablets in Peptic ulcer
Cimetidine 800mg bedtime /400mgBd 400mg bedtime
Ranitidine 300 mg bedtime/150mg BD 150 mg bedtime
Famotidine 40 mg bedtime 20 mg bedtime
Roxatidine 150 mg bedtime 75 mg bedtime

Proton Pump InhibitorsProton Pump Inhibitors
• Most effective drugs in antiulcer therapyMost effective drugs in antiulcer therapy
• ProdrugsProdrugs requiring activation in acid environmentrequiring activation in acid environment
• Block enzymes responsible for secreting HCl - bindsBlock enzymes responsible for secreting HCl - binds
irreversiblyirreversibly toto H+K+ATPaseH+K+ATPase
• Prototype:Prototype: Omeprazole (Prilosec)Omeprazole (Prilosec)
• Examples:Examples:
– LansoprazoleLansoprazole
– PantoprazolePantoprazole
– RabeprazoleRabeprazole
– EsomeprazoleEsomeprazole
Omeprazole

Pharmacokinetics - PPIPharmacokinetics - PPI
 Given on an empty stomach because food affectsGiven on an empty stomach because food affects
absorptionabsorption
 They should be given 30 minutes to 1 hour before foodThey should be given 30 minutes to 1 hour before food
intake because an acidic pH in the parietal cell acidintake because an acidic pH in the parietal cell acid
canaliculi is required for drug activation, and foodcanaliculi is required for drug activation, and food
stimulates acid productionstimulates acid production
 Concomitant use of other antisecretory drugs - H2 receptorConcomitant use of other antisecretory drugs - H2 receptor
antagonists – reduces actionantagonists – reduces action
 Highly protein bound and rapidly Metabolized by the liverHighly protein bound and rapidly Metabolized by the liver
by CYP2C19 and CYP3A4 – dose reduction necessary inby CYP2C19 and CYP3A4 – dose reduction necessary in
severe hepatic failuresevere hepatic failure
 Excreted in Kidneys minimally (no dose reduction neededExcreted in Kidneys minimally (no dose reduction needed
in renal failure and elderly)in renal failure and elderly)

Adverse EffectsAdverse Effects
 The most common are GIT troubles in the form of nausea,The most common are GIT troubles in the form of nausea,
abdominal pain, constipation, flatulence, and diarrheaabdominal pain, constipation, flatulence, and diarrhea
 Subacute myopathy, arthralgias, headaches, and skin rashesSubacute myopathy, arthralgias, headaches, and skin rashes
 Prolonged use:Prolonged use:
 Gynaecomastia, erectile dysfunctionGynaecomastia, erectile dysfunction
 Leucopenia and hepatic dysfunctionLeucopenia and hepatic dysfunction
 Vitamin B12 deficiencyVitamin B12 deficiency
 Hypergastrinemia which may predispose to reboundHypergastrinemia which may predispose to rebound
hypersecretion of gastric acid upon discontinuation of therapy andhypersecretion of gastric acid upon discontinuation of therapy and
may promote the growth of gastrointestinal tumors (carcinoidmay promote the growth of gastrointestinal tumors (carcinoid
tumors )tumors )

• Therapeutic uses:Therapeutic uses:
1.1. Gastroesophageal reflux disease (GERD)Gastroesophageal reflux disease (GERD)
2.2. Peptic Ulcer - Gastric and duodenal ulcersPeptic Ulcer - Gastric and duodenal ulcers
3.3. Bleeding peptic UlcerBleeding peptic Ulcer
4.4. Zollinger ellison SyndromeZollinger ellison Syndrome
5.5. Prevention of recurrence of nonsteroidal antiinflammatory drugPrevention of recurrence of nonsteroidal antiinflammatory drug
(NSAID) - associated gastric ulcers in patients who continue(NSAID) - associated gastric ulcers in patients who continue
NSAID use.NSAID use.
6.6. Reducing the risk of duodenal ulcer recurrence associated withReducing the risk of duodenal ulcer recurrence associated with
H. pylori infectionsH. pylori infections
7.7. Aspiration PneumoniaAspiration Pneumonia

PPI – Dosage schedulePPI – Dosage schedule
• Omeprazole 20 mg o.d.Omeprazole 20 mg o.d.
• Lansoprazole 30 mg o.d.Lansoprazole 30 mg o.d.
• Pantoprazole 40 mg o.d.Pantoprazole 40 mg o.d.
• Rabeprazole 20 mg o.d.Rabeprazole 20 mg o.d.
• Esomeprazole 20 - 40 mg o.d.Esomeprazole 20 - 40 mg o.d.

Muscarinic antagonistsMuscarinic antagonists
Atropine:Atropine:
– Block the MBlock the M11 class receptorsclass receptors
– Reduce acid productionReduce acid production
– Abolish gastrointestinal spasmAbolish gastrointestinal spasm
Pirenzepine and TelenzepinePirenzepine and Telenzepine
Mechanism of action:Mechanism of action:
• Reduce meal stimulated HCl secretion by reversible blockade of muscarinicReduce meal stimulated HCl secretion by reversible blockade of muscarinic
(M1) receptors on the cell bodies of the intramural cholinergic ganglia(M1) receptors on the cell bodies of the intramural cholinergic ganglia
(receptors on parietal cells are M3).(receptors on parietal cells are M3).
• Unpopular as a first choice because of high incidence ofUnpopular as a first choice because of high incidence of
anticholinergic side effects (dry mouth and blurredanticholinergic side effects (dry mouth and blurred vision)vision)

Prostaglandin analoguesProstaglandin analogues
• Inhibit gastric acid secretionInhibit gastric acid secretion
• Exhibit ‘cytoprotective’ activityExhibit ‘cytoprotective’ activity
• Enhance local production of mucus or bicarbonateEnhance local production of mucus or bicarbonate
• Promote local cell regenerationPromote local cell regeneration
• Help to maintain mucosal bloodHelp to maintain mucosal blood

Prostaglandin analogues -Prostaglandin analogues -
MisoprostolMisoprostol
Actions:Actions:
Inhibit histamine-stimulated gastric acid secretionInhibit histamine-stimulated gastric acid secretion
Stimulation of mucin and bicarbonate secretionStimulation of mucin and bicarbonate secretion
Increase mucosal blood flowIncrease mucosal blood flow
(Reinforcing of mucous layer buffered by HCO3(Reinforcing of mucous layer buffered by HCO3
secretion from epithelial cells)secretion from epithelial cells)
Therapeutic uses:Therapeutic uses:
Prevent ion of NSAID-induced mucosal injuryPrevent ion of NSAID-induced mucosal injury
(rarely used because it needs frequent(rarely used because it needs frequent
administration – 4 times daily)administration – 4 times daily)

MisoprostolMisoprostol
• Doses: 200 mcg 4 times a day (Misoprost)Doses: 200 mcg 4 times a day (Misoprost)
• ADRs:ADRs:
– Diarrhoea and abdominal crampsDiarrhoea and abdominal cramps
– Uterine bleedingUterine bleeding
– AbortionAbortion
– Exacerbations of inflammatory bowel disease and shouldExacerbations of inflammatory bowel disease and should
be avoided in patients with this disorderbe avoided in patients with this disorder
Contraindications:Contraindications:
1.1. Inflammatory bowel diseaseInflammatory bowel disease
2.2. Pregnancy (may cause abortion)Pregnancy (may cause abortion)

ProglumideACh
PGE2
Histamine
Gastrin
Adenyl
cyclase
_
+
ATP cAMP
Protein Kinase
(Activated)
Ca++
+
Ca++
Proton pump
KK+
H+
Gastric acid
Parietal cell
Lumen of stomach
Antacid
Omeprazole
Ranitidine
H2M3
Misoprostol
_
_
_
_
+
PGE
receptor
+
+
Gastrin
receptor+
+
+

Eradication of H.pylori
Omeprazole
Amoxicillin
Clarithromycin
Metronidazole

Triple Therapy
The BEST among all the Triple therapy regimen is:
Omeprazole / Lansoprazole - 20 / 30 mg bd
Clarithromycin - 500 mg bd
Amoxycillin / Metronidazole - 1gm / 500 mg bd
Given for 14 days followed by P.P.I for 4 – 6 weeks
Short regimens for 7 – 10 days not very effective

Triple Therapy – cont …
Bismuth subsalicylate – 2 tab qid
Metronidazole - 250 mg qid
Tetracycline - 500 mg qid
Some other Triple Therapy Regimens are
Ranitidine Bismuth citrate - 400 mg bd
Tetracycline - 500 mg bd
Clarithromycin / Metronidazole - 500 mg bd

Bismuth subsalicylateBismuth subsalicylate
Pharmacological actions:Pharmacological actions:
• Undergoes rapid dissolution in the stomach into bismuth andUndergoes rapid dissolution in the stomach into bismuth and
salicylatessalicylates
• Salicylates are absorbedSalicylates are absorbed
• Bismuth coats ulcers and erosions protecting them from acidBismuth coats ulcers and erosions protecting them from acid
and pepsin and increases prostaglandin and bicarbonateand pepsin and increases prostaglandin and bicarbonate
productionproduction
• Uses:Uses:
• Treatment of dyspepsia and acute diarrhoeaTreatment of dyspepsia and acute diarrhoea

Surgery for Uncomplicated DUSurgery for Uncomplicated DU
• Indications for surgical intervention for chronic DUIndications for surgical intervention for chronic DU
(Uncomplicated(Uncomplicated DU):DU):
• 1. Uncomplicated DU, not responding to drug therapy of 8-1. Uncomplicated DU, not responding to drug therapy of 8-
12 weeks—intractable duodenal ulcer12 weeks—intractable duodenal ulcer
• 2. Repeated recurrences2. Repeated recurrences
• Presently most of the uncomplicated DU does not requirePresently most of the uncomplicated DU does not require
surgerysurgery

• Highly selective vagotomy (HSV). In HSV, only fibresHighly selective vagotomy (HSV). In HSV, only fibres
supplying the parietal cells are ligated. Nerve of Latarjetsupplying the parietal cells are ligated. Nerve of Latarjet
which supplies the antrum pump is retained and so nowhich supplies the antrum pump is retained and so no
drainage procedure is required in HSV.drainage procedure is required in HSV.
• HSV is also called as parietal cell vagotomy or superselectiveHSV is also called as parietal cell vagotomy or superselective
vagotomy .vagotomy .
• Here nerve fibres in last 6 cm of stomach, just proximal toHere nerve fibres in last 6 cm of stomach, just proximal to
pylorus are preserved (Crow’s foot).pylorus are preserved (Crow’s foot).
• Vagotomy reduces acid secretion, hence ulcer heals. No acid,Vagotomy reduces acid secretion, hence ulcer heals. No acid,
No ulcer .No ulcer .

• Selective vagotomy with pyloroplasty (SV + P).Selective vagotomy with pyloroplasty (SV + P).
• Truncal vagotomy with gastrojejunostomy (TV + GJ).Truncal vagotomy with gastrojejunostomy (TV + GJ).
• Posterior truncal vagotomy with anteriorPosterior truncal vagotomy with anterior
seromyotomy— Taylor’s operation.seromyotomy— Taylor’s operation.
• Posterior truncal vagotomy with HSV without drainagePosterior truncal vagotomy with HSV without drainage
• Linear gastrectomy with posterior truncal vagotomyLinear gastrectomy with posterior truncal vagotomy

Types of vagotomy. (A) Highly selective vagotomy,Types of vagotomy. (A) Highly selective vagotomy,
(B) Selective vagotomy with pyloroplasty, (C) Truncal(B) Selective vagotomy with pyloroplasty, (C) Truncal
vagotomy withvagotomy with
gastrojejunostomy.gastrojejunostomy.

Evaluation/Follow-up/Evaluation/Follow-up/
• H. Pylori Positive: retesting for tx efficacyH. Pylori Positive: retesting for tx efficacy
• Urea breath test—no sooner than 4 weeks after therapy to avoid falseUrea breath test—no sooner than 4 weeks after therapy to avoid false
negative resultsnegative results
• Stool antigen test—an 8 week interval must be allowed after therapy.Stool antigen test—an 8 week interval must be allowed after therapy.
• H. Pylori Negative:H. Pylori Negative:
• evaluate symptoms after one month. Patients who are controlledevaluate symptoms after one month. Patients who are controlled
should cont. 2-4 more weeks.should cont. 2-4 more weeks.

• Upper digestive bleedingUpper digestive bleeding is the most common complication.is the most common complication.
• Sudden large bleeding can be life-threatening.Sudden large bleeding can be life-threatening.
• It occurs when the ulcer erodes one of the blood vessels, such as theIt occurs when the ulcer erodes one of the blood vessels, such as the
gastroduodenal artery.gastroduodenal artery.

• PerforationPerforation often leads to catastrophic consequences.often leads to catastrophic consequences.
• Erosion of the gastro-intestinal wall by the ulcer leads toErosion of the gastro-intestinal wall by the ulcer leads to
spillage of stomach or intestinal content into the abdominalspillage of stomach or intestinal content into the abdominal
cavity.cavity.
• Perforation at the anterior surface of the stomach leads toPerforation at the anterior surface of the stomach leads to
acuteacute peritonitisperitonitis, initially chemical and later bacterial, initially chemical and later bacterial
peritonitis. The first sign is often sudden intense abdominalperitonitis. The first sign is often sudden intense abdominal
pain.pain.
• Posterior wall perforation leads toPosterior wall perforation leads to pancreatitispancreatitis; pain in this; pain in this
situation often radiates to the back.situation often radiates to the back.
• Perforation in the CBD- aerobilia,Perforation in the CBD- aerobilia, cholangitischolangitis

• PenetrationPenetration is when the ulcer continues intois when the ulcer continues into
adjacent organs such as the liver and pancreas.adjacent organs such as the liver and pancreas.
• Gastric outlet obstructionGastric outlet obstruction - scarring and swelling- scarring and swelling
due to ulcers causes pyloric narrowing. Patientdue to ulcers causes pyloric narrowing. Patient
often presents with severe vomiting.often presents with severe vomiting.
• CancerCancer is included in the differential diagnosisis included in the differential diagnosis
(elucidated by biopsy), Helicobacter pilory as the(elucidated by biopsy), Helicobacter pilory as the
etiological factor making it 3 to 6 times moreetiological factor making it 3 to 6 times more
likely to develop stomach cancer from the ulcer.likely to develop stomach cancer from the ulcer.

Diagnosis of perforatedDiagnosis of perforated
peptic ulcer diseasepeptic ulcer disease
 History and physical examinationHistory and physical examination
 UprightUpright chest radiographschest radiographs will showwill show pneumoperitoneumpneumoperitoneum
((““free airfree air””) in 80) in 80––90% of the cases.90% of the cases.
 If pneumoperitoneum is identified on plain radiographs, there is no need for further studies.If pneumoperitoneum is identified on plain radiographs, there is no need for further studies.
 Ultrasound is less sensitive for detecting free air but could be used to identifyUltrasound is less sensitive for detecting free air but could be used to identify other indirect findings of perforationother indirect findings of perforation such assuch as
free fluidfree fluid andand decreased peristalsisdecreased peristalsis when the diagnosis remains in question.when the diagnosis remains in question.
 Computerized tomography (CT) scans are more sensitiveComputerized tomography (CT) scans are more sensitive
for detecting pneumoperitoneum than the other modalitiesfor detecting pneumoperitoneum than the other modalities
but should ideally be performed at least 6 h following the onsetbut should ideally be performed at least 6 h following the onset
of symptoms.of symptoms.
the use ofthe use of oral contrast medium with CT scanningoral contrast medium with CT scanning to identifyto identify
thethe site of perforationsite of perforation and theand the presence of ongoing leakage.presence of ongoing leakage.

Indications for surgery inIndications for surgery in
patients with peptic ulcer diseasepatients with peptic ulcer disease
 The indications for surgery for PUD have recently beenThe indications for surgery for PUD have recently been
limited to the treatment of complicated PUD.limited to the treatment of complicated PUD.
 because of the high mortality rate following emergencybecause of the high mortality rate following emergency
surgery for perforated PUD, many are suggestingsurgery for perforated PUD, many are suggesting
nonoperative management rather than surgicalnonoperative management rather than surgical
management in high-risk patients.management in high-risk patients.
 High risk is defined asHigh risk is defined as
the presence of severe comorbidities,the presence of severe comorbidities,
perforation greater than 24 h,perforation greater than 24 h,
and hypotension on presentation.and hypotension on presentation.

 Crofts et al. determined that nonoperative managementCrofts et al. determined that nonoperative management
with nasogastric suction, fluid resuscitation, andwith nasogastric suction, fluid resuscitation, and
antibioticsantibiotics
can be effective in the treatment of perforated PUD if thecan be effective in the treatment of perforated PUD if the
site of perforation has sealed.site of perforation has sealed.
 Failure to improve within 24 h should then prompt anFailure to improve within 24 h should then prompt an
operation.operation.
 Each case must be individualized, and nonoperativeEach case must be individualized, and nonoperative
management should not be undertaken if a contrastmanagement should not be undertaken if a contrast
study of the upper gastrointenstinal tract showsstudy of the upper gastrointenstinal tract shows
continuing free perforationcontinuing free perforation..

Treatment options forTreatment options for
perforated peptic ulcer diseaseperforated peptic ulcer disease
 Surgery for PUD has a long history with many surgicalSurgery for PUD has a long history with many surgical
options.options.
 Many procedures have gone out of favor due toMany procedures have gone out of favor due to
complications, side effects, and inadequacy, leavingcomplications, side effects, and inadequacy, leaving
 highly selective vagotomy (HSV) orhighly selective vagotomy (HSV) or
 Truncal vagotomy with pylorplasty or gastrojejunosotomy,Truncal vagotomy with pylorplasty or gastrojejunosotomy,
 Vagotomy with antrectomy, andVagotomy with antrectomy, and
 Omental patch closureOmental patch closure
as the current options.as the current options.

Omental patch closureOmental patch closure
 Omental patch closureOmental patch closure is a quick and simple procedure that isis a quick and simple procedure that is
very useful in perforated PUD.very useful in perforated PUD.
 It has long been the recommended treatment in patients withIt has long been the recommended treatment in patients with
multiple comorbiditiesmultiple comorbidities, those that are, those that are
hemodynamically unstablehemodynamically unstable andand
those with exudative peritonitis.those with exudative peritonitis.
 It is not useful inIt is not useful in Type IV gastric ulcersType IV gastric ulcers and may not be theand may not be the
optimal treatment in a stable patient with a perforated Type Ioptimal treatment in a stable patient with a perforated Type I
gastric ulcergastric ulcer
 Numerous authors in recent years have prospectively investigated peptic ulcer recurrence rates after simple patch closure and H. pylori eradication and have reportedNumerous authors in recent years have prospectively investigated peptic ulcer recurrence rates after simple patch closure and H. pylori eradication and have reported
high success rateshigh success rates

Highly selective vagotomyHighly selective vagotomy
 HSV is a tedious but safe operation , that can be performedHSV is a tedious but safe operation , that can be performed
laparoscopically,laparoscopically,
with minimal side effects.with minimal side effects.
 It has a higher recurrent ulcer rate thanIt has a higher recurrent ulcer rate than
the other procedures (10the other procedures (10––20%).20%).
 It is not useful for Type II or Type IIIIt is not useful for Type II or Type III
gastric ulcers or for complicated PUD.gastric ulcers or for complicated PUD.

Truncal vagotomyTruncal vagotomy
 Truncal vagotomy and drainage procedure is very useful inTruncal vagotomy and drainage procedure is very useful in
complicated ulcer disease.complicated ulcer disease.
 It reduces peak acid secretion by 50%.It reduces peak acid secretion by 50%.
 It has a significant side effect profile and has a recurrentIt has a significant side effect profile and has a recurrent
ulcer rate of 10%.ulcer rate of 10%.

Truncal vagotomy.Truncal vagotomy.

Vagotomy with antrectomyVagotomy with antrectomy
 Vagotomy with antrectomy isVagotomy with antrectomy is most effective at reducing acid secretionmost effective at reducing acid secretion andand
has a recurrence rate of 0has a recurrence rate of 0––2%.2%.
But, this operation has a 20% rate of post-gastrectomyBut, this operation has a 20% rate of post-gastrectomy
and post-vagotomy syndromes and has a significant associated mortality.and post-vagotomy syndromes and has a significant associated mortality.
 The mortality risk increases with patient comorbiditiesThe mortality risk increases with patient comorbidities
and with emergency surgery for complicated PUD.and with emergency surgery for complicated PUD.
 It should be avoided in hemodynamically unstableIt should be avoided in hemodynamically unstable
paitents and those with extensive inflammation since the anastamosis maypaitents and those with extensive inflammation since the anastamosis may
be compromised.be compromised.

postoperative morbidity and mortality associatedpostoperative morbidity and mortality associated
with repair of a perforated peptic ulcer diseasewith repair of a perforated peptic ulcer disease
 Despite current advances in medical and surgical therapy, theDespite current advances in medical and surgical therapy, the
morbidity and mortality associatedmorbidity and mortality associated
with perforated PUD remains very high andwith perforated PUD remains very high and
this area has remained a topic of current research efforts.this area has remained a topic of current research efforts.
 ComorbiditiesComorbidities andand preoperative shockpreoperative shock are well-establishedare well-established
independent risk factors for a poorindependent risk factors for a poor
outcome following emergency surgery.outcome following emergency surgery.
 Kocer et al. addedKocer et al. added ageage,, time before surgerytime before surgery, and, and performance of aperformance of a
definitive operationdefinitive operation to the listto the list
of significant risk factors.of significant risk factors.

Adjunctive medical treatments followingAdjunctive medical treatments following
operation for perforated PUDoperation for perforated PUD
 Proton Pump InhibitorsProton Pump Inhibitors
 Discontinuation of Nonsteroidal Anti-inflammatory DrugsDiscontinuation of Nonsteroidal Anti-inflammatory Drugs
 Medications for Mucosal CytoprotectionMedications for Mucosal Cytoprotection
 Treatment of Helicobacter pylori and verification ofTreatment of Helicobacter pylori and verification of
eradicationeradication

keypoints to remember in managingkeypoints to remember in managing
patients withpatients with perforated PUDperforated PUD
 Biopsy of all perforated gastric ulcers is required.Biopsy of all perforated gastric ulcers is required.
 No single approach is ideal for all patients. Surgeons must beNo single approach is ideal for all patients. Surgeons must be
prepared to individualizeprepared to individualize
all treatment plansall treatment plans
 Any patient admitted to a hospital because of peptic ulcer diseaseAny patient admitted to a hospital because of peptic ulcer disease
should be placed on lifelong acid suppression.should be placed on lifelong acid suppression.
 Patients who regularly take NSAIDs or aspirin should takePatients who regularly take NSAIDs or aspirin should take
concomitant acid suppressiveconcomitant acid suppressive medicationmedication if they are more than 60if they are more than 60
years old.years old.
 Lifelong acid suppressive medication may be equivalent to surgicalLifelong acid suppressive medication may be equivalent to surgical
vagotomy in preventingvagotomy in preventing recurrent peptic ulcerrecurrent peptic ulcer oror ulcerulcer
complicationscomplications..

Management of upper GIManagement of upper GI
HemorrhageHemorrhage

ManagementManagement Upper GITUpper GIT
BleedingBleeding
Complete history:Complete history:
alcohol use, cirrhosis, heart burn, reflux, and medications.alcohol use, cirrhosis, heart burn, reflux, and medications.
ExamExam ::
signs ofsigns of cirrhosiscirrhosis including spider angiomata, palmer erythema,including spider angiomata, palmer erythema,
prominent abdominal veins, caput medusa, and ascites.prominent abdominal veins, caput medusa, and ascites.
mucous membranes for melanin spots associated with Puetz-mucous membranes for melanin spots associated with Puetz-
Jeghers syndrome.Jeghers syndrome.

Physical ExamPhysical Exam
Vital signs:Vital signs: instability, respiratory distress,instability, respiratory distress,
beware of beta blockadebeware of beta blockade
signs of anemia, dehydrationsigns of anemia, dehydration
Abdominal examAbdominal exam::
Rectal examRectal exam::
Look for perianal causes of bleeding.Look for perianal causes of bleeding.
check for occult blood in the stool.check for occult blood in the stool.

Laboratory studies:Laboratory studies:
• Type and CrossType and Cross
• CBC: anemia?CBC: anemia?
• hepatic dysfunction and renalhepatic dysfunction and renal
compromisecompromise
• Coags: coagulopathyCoags: coagulopathy
• ABG: probe for acidosisABG: probe for acidosis

Interventions to considerInterventions to consider
• ABCABC’’ss
 Ensure adequateEnsure adequate airwayairway protection andprotection and
adequate respirations:massive bleedingadequate respirations:massive bleeding
considered forconsidered for intubationintubation
 Start 2 large boreStart 2 large bore IVIV’’ss..
 FluidFluid bolus either NS or LRbolus either NS or LR
 3-for-1 rule: Replace each milliliter of blood3-for-1 rule: Replace each milliliter of blood
loss with 3 mL of crystalloid fluid.loss with 3 mL of crystalloid fluid.

PharmacotherapyPharmacotherapy
• Proton pump inhibitors (PPIs),Proton pump inhibitors (PPIs),
orally or intravenously as an infusionorally or intravenously as an infusion
• OctreotideOctreotide is a somatostatin analog: shunt blood away from theis a somatostatin analog: shunt blood away from the
splanchnic circulation. variceal and non-variceal upper GI hage.splanchnic circulation. variceal and non-variceal upper GI hage.
• vasopressinvasopressin analog most commonly for variceal upper GI hage.analog most commonly for variceal upper GI hage.
• Anti-fibrinolytic drugsAnti-fibrinolytic drugs such assuch as
tranexamic acidtranexamic acid
•
Factor VIIFactor VII for variceal hemorrhagefor variceal hemorrhage

TubesTubes
• Foley CatheterFoley Catheter
• NG with gastric lavageNG with gastric lavage:: If theIf the
stomach contains bile but no blood,stomach contains bile but no blood,
UGIB is less likelyUGIB is less likely
• Iced saline lavageIced saline lavage
• STAT UpperSTAT Upper endoscopyendoscopy

Early EndoscopyEarly Endoscopy
• Both As A Diagnostic And Therapeutic:Both As A Diagnostic And Therapeutic:
1.1. Injection of adrenaline or sclerotherapyInjection of adrenaline or sclerotherapy
2.2. Electrocautery:Electrocautery: thermalthermal
3.3. Endoscopic clippingEndoscopic clipping
4.4. Banding of varicesBanding of varices
5.5. Argon plasma coagulation.Argon plasma coagulation.
6.6. Cryotherapy ablation is another possibilityCryotherapy ablation is another possibility

Stigmata of high riskStigmata of high risk
• Active bleedingActive bleeding
• OozingOozing
• Visible vesselsVisible vessels
• Red SpotsRed Spots

Visiblevessels
oozing bleeding
Active bleeding
Red Spots

Contraindications to endoscopyContraindications to endoscopy
• UncooperativeUncooperative
• severesevere cardiaccardiac decompensation,decompensation,
acute myocardial infarctionacute myocardial infarction
• perforatedperforated viscusviscus ((eg, esophagus,eg, esophagus,
stomach, intestinestomach, intestine).).

Refractory casesRefractory cases
• RepeatRepeat esophagogastroduodenoscopyesophagogastroduodenoscopy
• AngiographyAngiography EmbolizationEmbolization the feeder vesselthe feeder vessel
• Balloon tamponadeBalloon tamponade
• SurgerySurgery, to oversew or remove, to oversew or remove

PU bleeding TREATMENTPU bleeding TREATMENT
• MedicalMedical
• Anti-ulcer medicationAnti-ulcer medication
• H. pylori treatmentH. pylori treatment
• Stop NSAIDsStop NSAIDs
• Follow up EGD for gastric ulcer in 6Follow up EGD for gastric ulcer in 6
weeksweeks

PU TREATMENTPU TREATMENT
• Endoscopic interventionsEndoscopic interventions
• Thermal coagulationThermal coagulation
• Injected agentsInjected agents
Success rateSuccess rate
» 95% initailly95% initailly
» 80% will not rebleed80% will not rebleed

PU TREATMENTPU TREATMENT
• Surgical interventionSurgical intervention
– Only 10% of patientsOnly 10% of patients
– IndicationsIndications
1.1. Failure of endoscopyFailure of endoscopy
2.2. Significant rebleeding after 1Significant rebleeding after 1stst
endoscopyendoscopy
3.3. Ongoing transfusion requirementOngoing transfusion requirement
4.4. Need for >6 units over 24 hoursNeed for >6 units over 24 hours
5.5. Earlier for elderly, multiple co-morbiditiesEarlier for elderly, multiple co-morbidities

PU Surgical interventionPU Surgical intervention
• Doudenal ulcerDoudenal ulcer
– Expose ulcer with duodenotomy or duodenopyloromyotomyExpose ulcer with duodenotomy or duodenopyloromyotomy
– Direct suture ligation,Direct suture ligation,
– The gastroduodenalThe gastroduodenal artery may be ligatedartery may be ligated if necessaryif necessary
– the pyloric channel is closed vertically resulting in athe pyloric channel is closed vertically resulting in a
Heineke-Mikulicz pyloroplastyHeineke-Mikulicz pyloroplasty
– Anti-secretory procedureAnti-secretory procedure
» Truncal, parietal cell vagotomyTruncal, parietal cell vagotomy
» can use medscan use meds

PU Surgical interventionPU Surgical intervention
• Gastric ulcerGastric ulcer
– 10% are maliganant10% are maliganant
– 30% will rebleed30% will rebleed
with simple ligationwith simple ligation
ResectionResection
• Distal gastrectomyDistal gastrectomy
Bilroth I or IIBilroth I or II
• Subtotal gastrectomySubtotal gastrectomy

Angiographic obliterationAngiographic obliteration
• of the bleeding vessel is considered inof the bleeding vessel is considered in
patients with poor prognosespatients with poor prognoses

SummarySummary
 A peptic ulcer is a break in superficial epithelial cells penetratingA peptic ulcer is a break in superficial epithelial cells penetrating
down to muscularis mucosadown to muscularis mucosa
 Duodenal > gastric ulcersDuodenal > gastric ulcers
 Can be asymptomaticCan be asymptomatic
 H pylori is a predominant risk factorH pylori is a predominant risk factor
 H pylori diagnosed by c urea breath test, stool antigen or ifH pylori diagnosed by c urea breath test, stool antigen or if
validated serology, treated with PAC500 or PMC250 regimevalidated serology, treated with PAC500 or PMC250 regime
 Complications of PUD can lead to acute emergency of upper GIComplications of PUD can lead to acute emergency of upper GI
bleedbleed

H. pyloriH. pylori
Thank UThank U


Peptic ulcer

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