GASTRIC ULCER AETIOLOGY It occurs due to imbalance between protective and damaging factors of gastric mucosa. Atrophic gastritis duodenogastric bile reflux gastric stasis abnormalities in acid and pepsin secretion. Acid becomes ulcerogenic even to normal gastric mucosa.

1. en love da Homoeopathy
GASTRIC
ULCER

2. GASTRIC
ULCER

3. GASTRICULCER
AETIOLOGY
• It occurs due to imbalance
betweenprotective and
damaging factors of
gastricmucosa.
• Atrophicgastritis
• duodenogastricbile reflux
• gastricstasis
• abnormalities in acid and
pepsinsecretion.
• Acid becomes ulcerogenic
evento normal gastric
mucosa.
• Smoking, alcohol,
NSAIDs, steroids.
• Helicobacter pylori
infection(70%).
• There is either
normochlorhydriaor
hypochlor hydria.
• Alteredmucosal barrier
mechanism.
• Lower socioeconomic
group.

4. FACTIORSINVOLVED
• Factors Involvedin Gastric
Ulcer Formation
• Duodenogastricreflux—
reflux containing bile salts
and lysolecithinbreakthe
mucosal barrier making it
more vulnerablefor injury,
action of drugs and pepsin
injury.
• Gastric stasis.
• Ischaemia of the gastric
mucosa.
• Type II and III gastriculcers
show acid hypersecretion
Types of GastricUlcer (Daintree
Johnson)
Type Location Incidence Acid
level
Type I In the antrum, near the
lesser curve 55%Normal
Type II Combined gastriculcer
(inthe body) 25%High with
duodenal ulcer
Type III Prepyloric ulcer 15%
High
Type IV Gastriculcer in the
proximal stomach 5%Normal

5. PATHOLOGY
• Gastric ulcer is large in size,
↓
usually lies in the lesser
curvature
↓
its floor being formedby the
muscular layer.
↓
Posteriorly it may penetrateinto
the pancreas
↓
it may cause torrential bleeding
↓
by eroding left gastric
(commonly)vessles or splenic
vessels or vessels in the
gastriculcer wall.
↓
Anteriorlyit may perforate or
penetrateinto the liver
↓
It may lead intohour glass
contracture, or tea-pot
deformity

6. ↓
Microscopically, it shows ulcer
crater with chronic
inflammatorycells
↓
and granulation tissue,
endarteritis obliterans and
epithelial proliferation.
↓
(Ulcer to the right of the incisura
is malignant unlessproved
otherwise).
↓
Gastric ulcer >3 cm is calledas
giant gastric ulcer.
↓
It has got 6–23%chances to
turninto malignancy.
↓
Incidence of perforation and
bleeding is also veryhigh.
↓
Endoscopy and biopsyshouldbe
done to rule out malignancy.
↓
Follow-up endoscopy is a must if
drug therapy is usedfor
treatmentto confirmthe
complete healing of the ulcer.

7. ↓
Grossly, marginof the benign
gastriculcer is clear; deep; near
lesser curve; edge is not everted
with gastricmucosal folds
converging towards the base of
the ulcer.
↓
Ninty-five per cent of benign
gastriculcer occurs towards
lesser curve, as it takes more
burdenof passage of food
and so more of wear and tear.
↓
Benigngastriculcer is rare in
greater curvature, fundus
and cardia.

8. CLINICALFEATURES
• Acute ulcer:
• It is confined to mucosa
and submucosa.
• It is commonly due to
NSAIDs.
• Chroniculcer:
• It penetrates muscularis
layer of stomach.
• Equal in both sexes
• It is becoming more common
in females.
• Common after the age of 40
years.
PAIN
• Painin epigastricregion
after taking food, lasting up
to two hours.
• Painis uncommonduring
night. It is relievedby
vomiting or by inducing
vomiting.
• Periodicity: Symptomfree
interval may be 2–6 months.
Oftenwithseasonal
variation.
• Vomiting relieves pain and
often it is induced by the
patient for relief of pain.

9. • Haematemesis and melaena:
• Haematemesis is more
common.
• Appetite is good but hesitant
to eat, because eating
induces painand that
results in loss of weight.
• But once complications
occur, appetite decreases.
Aversionto spicy, friedfoods
occurs.
• On deep palpation,
tendernessis felt in
epigastric region.
INVESTIGATION
• Bariummeal X-rayto see
niche and notch
• Gastroscopy is done to see
the location, type of ulcer
and also to take biopsy (10
biopsies).
• Ultrasoundabdomen
mainly to rule out other
diseases and to confirm
associateddiseases.

10. DIFFERENTIAL DIAGNOSIS
• Hiatus hernia ™
• Cholecystitis ™
• Chronicpancreatitis ™
• Chronicgastritis ™
• Dyspepsia ™
• Carcinoma stomach.
TREATMENT
• Drugs like H2 blockers,
proton-pumpinhibitors,
carbenoxolone (biogastrone,
sucralfate, prostag landins
whichcoats the ulcer and so
creates a mucosal barrier)
helps in reducing or
eliminating the symptoms.
• But asymptomatic ulcer may
exist silentlyand may turn
into malignancy

11. SURGERY
• So surgery is the
preferredline of
treatment.
• Partial gastrectomyand
BillrothI gastroduodenal
anasto mosis is done.
Other surgical procedures:
1. de Miguel’s antrectomy
2. Maki’s pylorus
preserving gastrectomy
3. HSV with excision of
ulcer
4. Kelling Madlener procedure:
It is antrectomy and excision of
proximal gastric ulcer TypeIV
5. Csendes procedure
COMPLICATION
1. Hour glass contracture:
• It, occurs exclusivelyin
women, is due to cicatricial
contracture of lesser curve
ulcer.
• Here stomachis divided into
twocompartments. Clinical
features – Loss of
periodicity.

12. • Persisting pain, Loss of
Appatitie, Vomitting, Loss of
Weight.
2. Tea-pot deformity (Hand-
bag stomach):
• It is due to cicatrisation and
shortening of the lesser
curvature.
• They present withfeatures
of pyloric stenosis.
• Treatment is partial
gastrectomy with BillrothI
anastomosis.
3. Perforation—most frequent.
4. Bleeding by erosion into the
left gastricand rarely splenic
vessels or to vessels in the wall
of ulcer—35%. It is common in
typeII and III gastric ulcers
5. Penetrationposteriorly into
pancreas, anteriorlyinto liver.
6. Malignant transformation
usually intoadenocarcinoma of
stomach(5–10%).

13. Differential Diagnosis
• Hiatus hernia.
• Cholecystitis.
• Chronicpancreatitis.
• Chronicgastritis.
• Dyspepsia.
• Carcinoma stomach.
DUODENALULCER
Aetiology
• Common in people with
blood group O +ve.
• Stress, anxiety—‘hurry,
worry, curry’.
• Helicobacter pylori infection
is an important aetiology for
duodenal ulcer (90%).
• NSAIDs, steroids.
• Endocrine causes:
Zollinger–Ellisonsyndrome
• MEN syndrome
• hyperparathyroidism.

14. • Other causes:Alcohol,
smoking, vitamin
deficiency.
Pathology
• Ulcer occurs in the first part
of duodenum, usually with
in the first inch,involvingthe
muscular layer.
Sites:
• a. In the bulb (bulbar)—
95%.
• b. Postbulbar (5%). •
• Eventually it shows
cicatrisation causing pyloric
stenosis.
• Serosaoverlying thesite of
duodenal ulcer shows
petechial haemorrhages
with speckled red dots,
appearing like sprinkled
cayenne pepper.
• It appears like cayenne
pepper.
Microscopically
• ulcer withchronic
inflammationwith
granulation tissue, gastric
metaplasia of duodenal
mucosa, endarteritis
obliterans are visualised. •

15. • Sometimes two opposing
ulcers, i.e. over anterior
and posterior surfaces of
duodenumare present
and are called as kissing
ulcers. •
• An anterior ulcer
perforates commonly,
posterior ulcer bleeds or
penetrates commonly.
Clinical Features
• In India, ratio of duodenal
ulcer to gastriculcer is 30 :
1. A veryhigh incidence.
• It is common in all socio-
economic group, more
with stressed professionals
(TypeA personality).
• Painis more before food,
in earlymorning and
decreases after taking
food. It is classically called
as hunger painas it is
relievedby taking food.

16. • Night pains are common.
• Common in males.
• Periodicityis more
commonthan in chronic
gastriculcer with seasonal
variation.
• Water-brash
• heartburn
• vomiting may be present.
• Melaenais more common,
haematemesis also can
occur.
• Appetite is good and there
is gain in weight.
• It decreases oncestenosis
develops.
• Eats more frequently
without any restriction.
• Chronicduodenal ulcer
can be uncomplicatedor
complicated.
Complications of Duodenal
Ulcer
• 1. Pyloricstenosis: Due to
scarring and cicatrisation
of first part of the
duodenum.
• 2. Bleeding (10%).

17. INVESTIGATION
Bariummeal X-ray
• shows deformedor absence
of duodenal cap (becauseof
spasm).
• Appearance of ‘trifoliate’
duodenumis due to
secondary duodenal
diverticula
3. Perforation (5%). Bothacute
and chroniculcers can perforate.
Anterior ulcers perforate.
4.Residual abscess.
5.Penetrationto pancreas.
• whichoccurs as a result of
scarring of ulcer.
Gastroscopy
• reveals the type, location
of ulcer, narrowing if any.
• Biopsy also can be taken
to look for the presence of
Helicobacter pylori.
• Usually biopsies are
takenfromduodenum,
pylorus, antrum, body,
fundus, and confirmed
by rapidurease test or
C13 or C14breathtests.

18. • Estimationof serum
gastrin level, serum
calciumlevel.
DIFFERENTIAL DIAGNOSIS
• Carcinoma stomach
(pylorus) ™
• Dyspepsia due to other
causes
• Hiatus hernia
• Oesophagitis
• Cholecystitis
• Chronicpancreatitis
Aim of therapy:
• To relieve symptoms; to
heal ulcer; to prevent
recurrence.
I. General measures:
• Avoid alcohol,
NSAIDs, smoking,
spicy foods
• Have more frequent
food.
II. Specific measures:
• Intragastric pH should be
maintainedabove 5.

19. • Drugs
1. H2 Blockers
2. Proton-pumpinhibitors
3. Antacids:
• Neutralises the HCl to form
water and salt and also
inhibits peptic activity.
• Aluminiumhydroxide and
magnesiumtrisilicate are
commonly used.
• Dose is 2 grams 2 hours
after food.
4.Sucralfate
• It is an aluminiumsalt of
sulfatedsucrose
• whichprovides a protective
coat to ulcer crater thereby
promotes healing.
• It inhibits peptic activity.
5. Anti-Helicobacter pylori
regime:
• It is veryuseful, givenfor 7–
14 days—later the proton-
pump inhibitors are
continued.

20. • Triple or quadruple
(tetracycline, bismuth,
tinidazole, pantoprazole)
regimes are used
6. Colloidbismuth sulphateis a
good drug for ulcer
7. Misoprostol (200 mg tid) is
the only prostaglandin agonist
accepted
SURGERY
• Highlyselective vagotomy
(HSV).
• Selective vagotomy with
pyloroplasty(SV+ P).
• Truncal vagotomy with
gastrojejunostomy (TV + GJ).
• Posterior truncal vagotomy
with anterior seromyo
tomy—Taylor’s operation.
• It can be done through
laparoscopy.

21. • Vagotomy with antrectomy
• Posterior truncal vagotomy
• Linear gastrectomy with
posterior truncal vagotomy
through laparoscopy.
REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

22. A
Special Thanks
To A Very
Special Doctor