1. PEPTIC ULCER

2. • Erosion of GI mucosa resulting from digestive action of HCl
and pepsin.
• There are two main sites of peptic ulcer —
• 1. Gastric
• 2. Duodenal.
• Rare peptic ulcers may be seen in the
• (i) cardiac end of oesophagus;
• (ii) Meckel’s diverticulum (due to presence of ectopic
gastric mucosa);
• (iii) In any segment of bowel (anastomotic ulcer)
which has been surgically anastomosed to the gastric
fundus.
• Peptic ulcers may be acute ulcers, which are shallow
and multiple and chronic ulcers, which are single,
deep and scirrhous.

3. AETIOLOGY AND PATHOGENESIS
• ACUTE PEPTIC ULCERS
• (i) About half the patients give history of ingestion of
aspirin or butazolidin.
• (ii) Sometimes these acute ulcers may occur following
stress, when they are called ‘stress ulcers’.
• This may occur following hypotension from
haemorrhage, endotoxin shock or cardiac infarction,
• (iii) Sepsis is an important aetiologic factor. Undrained
pus may be responsible for acute stress ulcers.
• Upper G.I. bleeding from these ulcers may be seen in
critically ill patient and should be a signal to search for
pus.

4. • (iv) These acute ulcers may be seen after cerebral
trauma or neurosurgical operations (Cushing’s ulcer).
• Higher rate of acid secretion and higher gastrin level
suggest that patients with head injury may have
increased vagal activity,
• (v) After major bums acute ulcers may be seen
(Curling’s ulcer).
• Within first 48 hours multiple acute erosions may
develop anywhere in the body and fundus of the
stomach (antrum and duodenum usually escape).
• During convalescent period of such bum cases, acute
duodenal ulcer may occur which often become chronic,
• (vi) Patients on steroids may develop acute ulcers,
known as ‘steroid ulcers’.

5. • CHRONIC PEPTIC ULCERS.—
• 1.GASTRIC ULCER
• Gastric ulcer patients secrete either low
normal or below normal amounts of acid.
• Only 5% of patients may demonstrate acid
hypersecretion.

6. • 1. DIMINISHED MUCOSAL RESISTANCE
• 2. PYLORODUODENAL REFLUX
• 3. DEFICIENT MUCOUS BARRIER
• 4. MUCOSAL TRAUMA
• 5. LOCAL ISCHAEMIA
• 6. ANTRAL STASIS
• 7. NONSTEROIDAL ANTIINFLAMMATORY
DRUGS (NSAIDs)
• 8. HELICOBACTER PYLORI

7. 1. DIMINISHED MUCOSAL RESISTANCE
• This has been incriminated as the cause of
chronic gastric ulcer.
• This is due to lowering of the ability to resist
the effect of acid pepsin digestion.

8. 2. PYLORODUODENAL REFLUX
• Regurgitated bile and other duodenal juices
have been taken to be the prime cause of
preulcerative superficial gastritis.
• Though such biliary reflux may account for a
large number of gastric ulcer cases, it does not
seem possible to explain all of them on this
basis.
• Some gastric ulcers occur in the fundus or at
the cardia where such biliary effects would
seem least active.

9. 3. DEFICIENT MUCOUS BARRIER
• A surface layer of mucus protects normally
from the digestive effect of the hydrochloric
acid and pepsin.
• When this mucous barrier becomes deficient
gastric ulcer may develop.
• But it is a matter of clinical observation that in
most cases of gastric ulcer the stomach
produces large quantities of mucus.

10. 4. MUCOSAL TRAUMA
• 85% of gastric ulcers occur along the lesser
curve.
• This fact together with the observation that
fluids tend to pass through the lesser curve of
the stomach suggests that a mechanical
factor might be involved.
• This part of the stomach is exposed to
injurious effects of heat and trauma

11. 5. LOCAL ISCHAEMIA
• Microemboli artificially introduced into the
gastric circulation of dogs or interferencewith
blood supply by ligation of vessels or omental
stripping would cause gastric erosions and ulcers
todevelop.
• Arteriovenous shunts which are present in the
submucosa of the stomach are under the control
of sympatheticnervous system and excessive
stress and strain may cause diminution of blood
supply to the mucous membrane of the stomach
leading to ulcer formation.

12. 6. ANTRAL STASIS
• This usually produces increased acid secretion
and it is an accepted fact that the majority of
patients with gastric ulcers have low acid
content in the stomach.
• But it is seen that nearer the ulcer to the
pylorus more is the acid secretion of the
stomach.

13. 7. NONSTEROIDAL ANTIINFLAMMATORY
DRUGS (NSAIDs)
• Ingestion of these drugs in patients suffering from
arthritis as a long term basis is a significant aetiologic
factor at present time.
• The drugs of this group are often called ulcerogenic
drugs.
• These drugs seem to disrupt the prostaglandin-driven
support of the mucosal barrier.
• These prostaglandins are related to the production of
mucosal gel layer in the stomach, which provides a
protective barrier to the gastric and duodenal lining.
• So disruption of this mucosal barrier allows even
minimal amount of acid to cause ulceration.

14. 8. HELICOBACTER PYLORI
• It is a spirochaetal bacterium which exists in the
deep mucosal layer of the antrum mainly and
duodenum rarely.
• Upto l/5th of normal population harbours this
bacterium.
• In almost 100% of cases of duodenal ulcer
patients H.pylori have been demonstrated.
• Eradication of this bacteria has led to decreased
recurrence rate of ulcer cases.
• So presence of H.pylori clearly predisposes to
peptic ulceration.

15. • 2. Duodenal ulcer
• CAUSES
• 1. ACID HYPERSECRETION
• 2. GENETIC FACTORS
• 3. ENDOCRINE ORGAN DYSFUNCTION
• 4. LIVER DISEASE
• 5. EMOTIONAL FACTORS
• 6. DIET AND SMOKING
• 7. HELICOBACTER PYLORI
• 8. DECREASE IN BICARBONATE PRODUCTION

16. 1. ACID HYPERSECRETION
• Pathogenesis of duodenal ulceration is seemingly
simplified at first sight by a clear relationship to over-
production of hydrochloric acid by the stomach.
• In most collected series, the mean basal and maximal
acid output of duodenal ulcer patients is approximately
2 times more than those of the control patients.
• It has also been shown that the stomachs of duodenal
ulcer patients have almost twice the number of
parietal cells (increased parietal cell mass) compared to
normal stomachs.
• Serum group I pepsinogen level is also increased in
duodenal ulcer patients.

17. • It has got a direct relationship with the acid
secretory potential of the stomach.
• Duodenal ulcer patients also show increased
gastrin stimulation.
• They also show an increased rate of gastric
emptying.
• Diminished acid inhibition of gastrin release is
also noticed.
• Increased vagal excitation has also been
assumed to underlie theduodenal ulcer
diathesis.

18. 2. GENETIC FACTORS
• Diminished power of resistance of the mucosa has
also been incriminated to cause duodenal ulcer.
• In a great number of cases the acid production may be
within the high side of the normal range and in these
cases ulceration cannot be explained except the
diminished mucosal resistance to normal acid
secretion.
• A genetic background can be well explained.
• There is a significant relationship between blood group
‘0’ and the development of duodenal ulcer.
• Persons of blood group ‘0’ who do not possess AB
antigen are peculiarly apt to develop duodenal ulcers.

19. 3. ENDOCRINE ORGAN DYSFUNCTION
• In addition to the Zollinger-Ellison syndrome, in which
there is over-production of gastrin by pancreatic
tumour tissue with consequent hyperacidity and ulcer
formation, other endocrine adenomata may be
associated with duodenal ulcer.
• In Cushing’s syndrome, the high level of endogenous
steroids may be responsible for duodenal ulcer.
• In parathyroid tumour hyperacidity may be either due
to hypercalcaemia orother causes have been noticed.
• Some bronchial carcinomas do produce hyperacidity.
• Multiple adenoma syndrome, where adenoma in
pituitary, adrenal, parathyroid and pancreas have been
noticed, may cause hyperacidity.

20. 4. LIVER DISEASE
• Ulceration of both stomach and duodenum
has co-existed with disease of the liver
particularly cirrhosis.
• It may be due to increase in the blood supply
to the gastric mucosa and over-production of
histamine in the stomach wall to stimulate the
parietal cells.

21. 5. EMOTIONAL FACTORS
• Anxiety, stress and strain have always been
incriminated to cause peptic ulcer.

22. 6. DIET AND SMOKING
• Irregular diet, spicy food and excessive drinking of tea
and coffee have always provoked formation of peptic
ulcer.
• Opinions vary regarding alcohol. Some have found a
clear relationship whereas others could not find any
definite relation.
• Smoking does appear to predispose ulcer formation.
• Cigarette smoking has a definite relation with ulcer
formation.
• The exact cause is not yet clearly understood, but it
seems that smoking diminishes mucosal defence
mechanism almost similar to NSAIDs

23. 7. HELICOBACTER PYLORI
• As mentioned in the aetiology of chronic
gastric ulcer, H.pylori have been isolated in
100% of duodenal ulcer cases.
• Its irradication has definitely led to decrease in
recurrence rate and this clearly indicates its
importance in the aetiology of duodenal ulcer.

24. 8. DECREASE IN BICARBONATE
PRODUCTION
• DECREASE IN BICARBONATE PRODUCTION by the
stomach and/or duodenum leads to peptic
ulceration.
• Those with decreased bicarbonate production
cannot maintain a pH-neutral microlayer
between the mucosal lining below and mucous
gel layer above.
• That is why the drugs which increase bicarbonate
production are being investigated to be used in
the treatment of peptic ulcer disease.

25. PATHOLOGY
• Gastric ulcer is large in size, usually lies in the
lesser curvature, its floor being formed by the
muscular layer.
• Posteriorly it may penetrate into the pancreas; it
may cause torrential bleeding by eroding left
gastric (commonly) vessles or splenic vessels or
vessels in the gastric ulcer wall.
• Anteriorly it may perforate or penetrate into the
liver.
• It may lead into hour glass contracture, or tea-pot
deformity.

26. • Microscopically, it shows ulcer crater with
chronic inflammatory cells and granulation
tissue, endarteritis obliterans and epithelial
proliferation.

27. • Gastric ulcer >3 cm is called as giant gastric ulcer.
It has got 6–23% chances to turn into malignancy.
• Incidence of perforation and bleeding is also very
high.
• Endoscopy and biopsy should be done to rule out
malignancy.
• Follow-up endoscopy is a must if drug therapy is
used for treatment to confirm the complete
healing of the ulcer.
• If complete remission has not occurred then
partial gastrectomy should be done.

28. • Grossly, margin of the benign gastric ulcer is
clear; deep; near lesser curve; edge is not
everted with gastric mucosal folds converging
towards the base of the ulcer.
• Ninty-five per cent of benign gastric ulcer
occurs towards lesser curve, as it takes more
burden of passage of food and so more of
wear and tear.
• Benign gastric ulcer is rare in greater
curvature, fundus and cardia.

29. • Acute ulcer: It is confined to mucosa and
submucosa.
• It is commonly due to NSAIDs.
• Chronic ulcer: It penetrates muscularis layer
of stomach.

30. Clinical Features
• Equal in both sexes.
• It is becoming more common in females.
• Common after the age of 40 years.
• Pain in epigastric region after taking food, lasting
up to two hours.
• Pain is uncommon during night. It is relieved by
vomiting or by inducing vomiting.
• Periodicity: Symptom free interval may be 2–6
months.
• Often with seasonal variation.
• Vomiting relieves pain and often it is induced by
the patientfor relief of pain.

31. Clinical Features
• Haematemesis and melaena:
• Haematemesis is more common.
• Appetite is good but hesitant to eat, because
eating induces pain and that results in loss of
weight.
• But once complications occur, appetite
decreases.
• Aversion to spicy, fried foods occurs.
• On deep palpation, tenderness is felt in
epigastric region.

32. Type &Location
• Type I: In the antrum,
near the lesser curve.
• Type II: Combined
gastric ulcer (in the
body) with duodenal
ulcer
• Type III: Prepyloric
ulcer
• Type IV: Gastric ulcer
in the proximal
stomach or cardia

33. Investigations
• Barium meal X-ray to see niche and notch.
• Barium meal X-ray features of benign gastric ulcer:
• Niche on the lesser curve with notch on the greater
curvature
• ™
Ulcer crater projects beyond the lumen of the ulcer
• ™
Regular/round margin of the ulcer crater—stomach
spoke wheel pattern
• ™
Overhanging mucosa at the margins of a benign gastric
ulcer— projects inwards towards the ulcer Hamptom’s
line
• ™
Converging mucosal folds towards the base of the ulcer
• ™
Symmetrical normal gastric mucosal folds

35. • Gastroscopy is done to see the location, type
of ulcer and also to take biopsy (10 biopsies).
• Ultrasound abdomen mainly to rule out other
diseases and to confirm associated diseases.
Multiple ulcers visualised on
gastroscopy
(A) Gastric ulcer in the body of the stomach;
(B) Gastric ulcer in prepyloric region.

36. Treatment
• Drugs like H2 blockers, proton-pump
inhibitors, carbenoxolone (biogastrone,
sucralfate, prostaglandins which coats the
ulcer and so creates a mucosal barrier) helps
in reducing or eliminating the symptoms.
• But asymptomatic ulcer may exist silently and
may turn into malignancy.

37. • So surgery is the preferred line
of treatment. Partial
gastrectomy and Billroth I
gastroduodenal anastomosis is
done.
• Type IV proximal gastric ulcer is
difficult to manage.
• It is treated by subtotal
gastrectomy.
• Often distal gastrectomy with
selective sleeve like extension
cut along the lesser curve to
remove the ulcer is done—
Pauchet’s procedure.

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

39. Complications of Gastric Ulcer
• Hour glass
contracture

40. • Tea-pot deformity
(Hand-bag
stomach)
Complications of Gastric Ulcer

41. Complications of Gastric Ulcer
• Perforation
• Penetration posteriorly into pancreas,
anteriorly into liver.
• Malignant transformation usually into
adenocarcinoma of stomach.

42. DUODENAL ULCER

43. 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-Ellison syndrome,
MEN syndrome, hyperparathyroidism.
• Other causes: Alcohol, smoking, vitamin
deficiency.
• “No acid – No ulcer”.

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

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

46. Clinical Features
• In India, ratio of duodenal ulcer (DU) to gastric
ulcer is 30 : 1.
• A very high incidence.
• It is common in all socioeconomic group, more
with stressed professionals (Type A
personality).

47. • Pain is 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 pains are common.
• Common in males.
• Periodicity is more common than in chronic
gastric ulcer with seasonal variation.
• Water-brash, heart burn, vomiting may be
present.
• Melaena is more common, haematemesis also
can occur.

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

49. Complications of Duodenal Ulcer
• 1. Pyloric stenosis: Due to scarring and
cicatrisation of first part of the duodenum.
• 2. Bleeding (10%).
• 3. Perforation (5%). Both acute and chronic
ulcers can perforate.
• Anterior ulcers perforate.
• 4. Residual abscess.
• 5. Penetration to pancreas.

50. NOTE
Chronic duodenal ulcer will not turn into
malignancy.
Ulcer which is more than 2 cm is called as giant
duodenal ulcer.

51. Investigations
• x Barium meal X-ray
shows deformed or
absence of duodenal
cap (because of
spasm).
• Appearance of
‘trifoliate’
duodenum is due to
secondary duodenal
diverticula which
occurs as a result of
scarring of ulcer.

52. • 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 taken from duodenum,
pylorus, antrum, body, fundus, and confirmed
by rapid urease test or C13 or C14 breath
tests.
• Estimation of serum gastrin level, serum
calcium level.

54. Differential diagnosis
• Carcinoma stomach (pylorus)
• ™
. Dyspepsia due to other causes
–– Hiatus hernia
–– Oesophagitis
–– Cholecystitis
–– Chronic pancreatitis

55. Treatment
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 maintained above 5.

56. Drugs
• 1. H2 Blockers
• 2. Proton-pump inhibitors
• 3. Antacids
• 4. Sucralfate
• 5. Anti-Helicobacter pylori regime
• 6. Colloid bismuth sulphate
• 7. Misoprostol

57. Surgery for Uncomplicated Duodenal
Ulcer
• Indications for surgical intervention for
chronic DU (Uncomplicated DU):
• 1. Uncomplicated DU, not responding to drug
therapy of 8–12 weeks—intractable duodenal
ulcer
• 2. Repeated recurrences
Presently most of the uncomplicated DU does
not require surgery

58. • Highly selective vagotomy (HSV).
• Selective vagotomy with pyloroplasty (SV + P).
• Truncal vagotomy with gastrojejunostomy (TV +
GJ).
• Posterior truncal vagotomy with anterior
seromyotomy.
• Vagotomy with antrectomy
• Posterior truncal vagotomy with HSV without
drainage procedure (Kim’s) often through
laparoscopy is also done.
• Linear gastrectomy with posterior truncal
vagotomy through laparoscopy.

59. HOMOEOPATHIC
TREATMENT

60. • Argentum nitricum . For abdominal bloating with
belching and pain.
• Arsenicum album . For ulcers with intense burning
pains and nausea; especially for people who cannot
bear the sight or smell of food and are thirsty.
• Kali bichromicum . For burning or shooting abdominal
pain that is worse in the hours after midnight.
• Lycopodium . For bloating after eating with burning
that lasts for hours; especially for people who feel
hungry soon after eating and wake up hungry.

61. • Nitric acid . For sharp, shooting pain that worsens at
night and is accompanied by feelings of hopelessness
and even fear of dying.
• Nux vomica . For digestive disturbances (including
heartburn and indigestion) that worsen after eating;
particularly for those who crave alcohol, coffee, and
tobacco.
• Phosphorus . For burning stomach pain that worsens at
night; those for whom this remedy is appropriate tend
to feel very thirsty, craving cold beverages.
• Pulsatilla . For symptoms that vary (that is, change
abruptly) and pain that gets worse from fatty foods;
appropriate people are distinctly not thirsty.