Benigne diseases of stomach are one of the serious conditions of our world.... so here u get littlebit information about these diseases...hope it will help you for your future study about these diseases... thank you.

1. Presented By :-
Biswanath Das.
Student of AGMC.

2. Types BDS
 Gastritis
 PUD
 Gastric polyp
 Gastric lymphoma
 Acute Gastric dilatation
 Gastric volvulus
 Menetrier’s disease

3. Gastritis

4. Definition
 The term gastritis is used to denote inflammation
associated with mucosal injury
 Gastritis is mostly a histological term that needs
biopsy to be confirmed
 Gastritis is usually due to infectious agents (such as
Helicobacter pylori) and autoimmune and
hypersensitivity reactions.

5. Continue..
It also occurs after cholecystectomy, gastric surgery
& also for prolonged use of NSAIDS……………………

6. Acute Gastritis

7. Types of gastritis
 Type A gastritis
 Type B gastritis
 Reflux gastritis
 Erosive gastritis
 Stress gastritis
 Lymphocytic gastritis
 Menetrier’s gastritis

8. PEPTIC ULCER DISEASE
(PUD)

9. An ulcer is defined as disruption of the
mucosal integrity .So ‘peptic ulcer’ refers
to an ulcer in the lower oesophagus,
stomach or duodenum, in jejunum after
surgical anastomosis to stomach or rarely
in the ileum adjacent to meckel’s
diverticulum leading to local defect or
excavation due to active inflammation.
DEFINITION

10. Although the prevalence of peptic ulcer is
decreasing in many western countries it still affects
approximately 10% of all adults at some time in
their lives. The male to female ratio for duodenal
ulcers varies from 5:1 to 2:1 whilist for gastric ulcers
is 2:1 or less.
INCIDENCE

11. Classification
A . Depending on the site—
-Chronic duodenal ulcer
-Chronic gastric ulcer
-Combind ulcer
-Anastomotic ulcer
B . Depending on the duration-
-Acute peptic ulcer
-Chronic peptic ulcer

12. Despite the constant attack on gastroduodeual
mucosa by a host of noxious agents (acid,
pepsin, bile, pancreatic enzymes, drugs &
bacteria) integrity is maintained by an intricate
system that provides mucosal defense & repair.
GASTRIC PHYSIOLOGY

13. Gastroduodenal defense
mechanisms
 Mucus layer on surface
 Bicarbonate section in mucosa
 Adequate mucosal blood flow
 Epithelial regenerative capacity
 Postaglandin secretion
 Intracellular tight junction
 Apical surface membrane transport.

14. Causes of PUD

15. Acute peptic ulcer
Drugs such as
aspirin,steroids
By stress (Stress ulcer):-
May be following
endotoxic shock :
 Hypotension,
 Haemorrhage or
 Cardiac infarction.

16. Sepsis.
After trauma or
neurosurgical
operations (Curling’s
ulcers).
After burns (curling’s
ulcers).
Patient on steroids
(Steroids ulcers).The size of peptic ulcer
Acute peptic ulcer

17. CHRONIC PEPTIC ULCERS
GASTRIC ULCERS
1. NSAIDs.
2. H.pylori infection
3. Deficient mucous barriers.
4. Mucosal trauma.
5. Local Ischaemia.
6. Antral stasis.
7. Decrease mucosal resistance
8. Pyloroduodenal reflex

18. DUODENAL ULCER
1. Acid hyper secretion.
2. Genetics factor.
3. Endocrine organ
dysfunction.
4. Liver abscess.
5. Emotional factors.
6. Diet & smoking.
7. Helicobacter pylori.
8. Decrease in
bicarbonate
production.
CHRONIC PEPTIC ULCERS

19. Pathogenesis
NSAIDs migrate across lipid membrane of epithelial cells.
Trapped in an ionized form.
Related with NSAIDs
Cell injury.
Topical NSAIDs.
Alter surface mucous layer.
back diffusion of H+ & Pepsin.
Further cell damage.

20. Figure shows machanisms by which NSAIDs may
induce nucosal injury :

21. Risk factors for NSAIDs – induced Gastroduodenal ulcers
Established
Advanced age.
History of ulcer.
Concomitant use of
glucocorticoids.
High dose of NSAIDs.
Multiple NSAIDs.
Concomitant use of
anticoagulants serious or
multi system disease.
Possible
Concomitant infection
with H. pylori.
Cigarette smoking.
Alcohol consumption.

22. Related to H. Pylori
Factors predisposing to higher colonization rate includes :-
Poor socio – economic status.
Less education.
Transmission :-
 Oral-oral.
 Fecal-oral route.

23. Role of H.pylori
 It secretes urease,portease & phospholipase.
 Urease generates ammonia that binds with H+ &
decreases acidity ,thus colonization & survival of
the organism is favoured.
 Protease damages the glycoprotein of gastric mucus
 Phospholipases damages the surface epithelium &
release leukotrines & eicosanoids.

24. Continue..
 Increase production of
proinflammatory
cytokines e.g-IL-1,IL-
6,TNF & IL-8
 May cause thrombotic
occlusion leading to
ischemia.
 Epithelial injury is
induced by VacA
regulated by CagA …..

25. Clinical feature
Acute peptic ulcers
Dyspepsia due to minor bleeding.
Haematemesis- fresh blood can cause hypotension & shock .
Present of abdominal pain due to erosions/perforation
Sometimes melaena is also present & drop in BP
Chronic Peptic ulcers

26. C/F along with comparison
Chronic gastric ulcers
Incidence –less common
Periodicity
Less marked
Attack lasts for several
weeks followed by
interval of freedom from
symmetrical for 2 – 6
months.
Chronic Duodenal ulcers
Common …..
Well marked
Attack lasts for several wks
with interval of freedom
from 2 – 6 months usually
appears in spring &
autumn.
Continued….

27. Chronic gastric ulcers
Pain
Strictly epigastric.
Pricking natures pain.
On ulcer penetration pain
radiate to back.
Site
Mid – epigastrium /
slightly to its left.
Chronic Duodenal ulcers
Pain more severe & spasmodic
in nature.
Pain on right hypocondrium..
Continued…..

28. Chronic gastric ulcers
Relation with food
 Almost immediately or any
time up to 1½ hr. after meal
as food irritates ulcer.
 Pain not felt empty
stomach.
 Pain not felt at night.
 Food aggravates pain.
Chronic Duodenal ulcers
 Starts usually 2½ - 3 hr. after
food.When stomach pushes
chyme into duodenum &
irritate ulcer.
 Felt empty stomach ‘Hunger –
Pain’.
 Pain at night, is characteristic.
 Food relieves pain.
Continued…

29. Chronic gastric ulcers
Vomiting
Noticeable in half cases.
Occur after food.
Relieves pain.
May be self induces.
Appetite
Good.
Patient afraid to take food.
Diet
Patient avoids fried & spicy
food.
Chronic Duodenal ulcers
Rare.
Quite good.
Eat frequently to around pain.
No particular food initiates
pain.
Continued…

30. Chronic gastric ulcers
Weight
Patient Losses weight.
Hemorrhage
Less common.
Haematemesis is more – than
melaena.
On Examination
Tenderness in midepigastric /
slightly to left of it.
Chronic Duodenal ulcers
 Patient gains the weight
 More common.
 Melaena more common than
haematemesis.
 Tenderness at right
hypocondrium..

31. SPECIAL INVESTIGETIONS
-OGD
-Barium meal study
-Test for H.pylori.
-USG
-Examination of blood.
-Examination of stool.
-Gastric function test

32. Endoscopy and radiology examination of PUD :

33. Treatment
Basic Treatment
 Rest.
 Diet (avoid spicy food, use balance
diet, no alcohol and smoking).

34. Medical Treatment
Antacids.
H2 receptor antagonistic.
Proton pump inhibitors.
Cytoprotective agents.
Bismuth – containing preparations.
Prostaglandin analogues.

35. Drugs used in Treatment of PUD
Drug Eg. Dose
Acid suppressing
drug ‘Antacids’.
Mylanta 100 – 140 mg /d
Maalox,
Tums,
120mg/d
H2 receptor
antagonists.
Roxatidine 75mg bd/6wks
Ranitidine 150mg bd/6wks
Famotidine 2o mg bd/6wks

36. Drugs used in Treatment of PUD
Drug Eg. Dose
Proton pump
inhibitors.
Omeprazol 20 mg /d
Lansoprazol 30 mg /d
Rabeprazol 20 mg /d
Pantoprazol 40 mg/d
Mucosal protective
agents.
Sucralfate. Sucralfatet 1g qid.
Prostaglandis
analogus.
Misoprostol 200 mcg. qid.
Bismuth –
containing
compounds.
Bismuth
subsalicylate
(BSS)
2 tablet qid.

37. Two wks Regimens recommended for
eradication of H. pylori :
Drug Dose
1. Lansoprazole 30+ Amoxicillin1000+ clarithromycin 500 all
BD
2. Lansoprazole 30 +Tinidazole 500 + Clarithromycin 250 all
BD
3. Lansoprazole 30 + Tinidazole 500 + amoxicillin 750 all BD

38. RECOMMENDED TREATMENT FOR NSAID – RELATED
MUCOSAL INJURY :
Active ulcer
--NSAID discontinued.
--Prophylactic therapy.
--H. Pylori infection.
H2 receptor antagonist or
PPI.
Misoprostol.
Selective Cox – 2 inhibitor.
Eradication if active ulcer
present or there is a past
history of PUD.

39. Surgical therapy
Indications
When ulcer fails to heal with medical
management (2 months for gastric ulcer &
6 month for duodenal ulcers).
Patient in need of quick relief.
Long-standing non – healing ulcer.
Ulcer producing obstruction.
Haemorrhagic ulcers.
Perforation of ulcers.
Suspicion of malignancy.
Continued…

40. Surgical therapy
Surgical procedures
A. For Duodenal Ulcer---
• Billroth II gastrectomy
• Gastrojejunostomy
• Truncal vagotomy & drainage
• HSV
• Tv & antrectomy
B.For Gastric Ulcer----
• Billroth I gastrectomy.
Continued…

41. Billroth II gastrectomy
 The lower 2/3 rd of the
stomach is removed and
the remainder is
anastomosed to the
jejunum

42. Gastroenterostomy
 Jejunum is anastomosed to
the post. Dependent wall of
stomach
 Gastroenterostomy
allows regurgitation of
alkaline duodenal contents
into the stomach
 Creates a passage between the
body of stomach to small
intestines
 Keeps acid away from
ulcerated area

43. Vagotomy
 Two types—
A . Total truncal
vagotomy with
gastrojejunostomy—
mayo or pyloroplasty
B . Highly selective
vagotomy

44. Pyloroplasty
 Pyloroplasty
 Widens the pylorus to
guarantee stomach
emptying even
without vagus nerve
stimulation
 Two types-
A.Heinecke-Mickulicz
Pyloroplasty
B. Finney pyloroplasty

45. Vagotomy & antrectomy
 Vagotomy is done
followed by
 Antrectomy/
Subtotal
Gastrectomy
 Lower half of
stomach (antrum)
makes most of the
acid
 Removing this
portion
(antrectomy)
decreases acid
production

46. Billroth I Gastrectomy
 The lower half of the
stomach is removed
 The remainder is
anastomosed to the first
part of duodenum.

47. Postoperative Care
 NG tube – care and management
 Monitor for post-operative complications

48. Postoperative complication
 Bleeding
 Occurs at the anastomosed site
 First 24 hours and post-op days 4-7
 Duodenal stump leak
 Billroth II
 Severe abdominal pain
 Bile stained drainage on dressing
 Gastric retention
 WILL NEED TO PUT NG TUBE BACK IN

49. Post-op Complications
 Recurrent ulceration
 Small stomach syndrome
 Bile vomiting
 Post vagotomy diarrhoea
 Malignant transformation
 Nutrional consequences
 Early & late dumping

50. Dumping Syndrome
 Rapid emptying of food and fluids from the
stomach into the jejunum
 Symptoms
 Weakness
 Faintness
 Palpitations
 Fullness
 Discomfort
 Nausea
 diarrhoea

51. Minimize Dumping Syndrome
 Decrease high carbohydrate intake
 Eat slowly
 Avoid fluids during meals
 Increase fat
 Eat small, frequent meals

52. Management of PU

53. Complications
A. Acute complication
-Perforation
- Haematemesis & melaena
B. Sub acute complication-Residual abscess
C. Chronic complication
-Gastric outlet obstruction
-Teapot deformity
-Hourglass contracture of stomach
-penetration into surrounding structure
-Ca stomach

54. Perforated peptic ulcer
 Common in man . Ratio 8:1
 Anterior duodenal ulcer perforate & posterior duodenal
ulcer bleed . Posterior stomach wall also perforate to the
lesser sac
 Chronic use of NSAIDS & H.pylori infection are the
common cause.
 Mortality rate 5-10%
 Golden time to operate within 6hrs.

55. Stages
Stages of duodenal peritonitis
Stages of reaction
Stage of bacterial peritonitis

56. Investications
 Complete blood picture & electrolyte study
 Plain x-ray chest or abdomen in erect position
 CT of abdomen

57. Perforated PU

58. Treatment
A. Aspiration of stomach content.
B. Blood grouping & cross matching.
C. Chrats-tp/bp/pulse/uo.
D. Drugs-antibiotics .
E. Exploratory laparotomy .
F. Fluids .

59. Haemorrhage from PU
 Haemorrhage from pu in acute case causes anaemia
bt in chronic case causes haematemesis & melaena.
 Commonest site- post. Duodenal wall & in case of
stomach lesser curvature.
 Precipiting factor-Chronicity
-Irritants
-Atherosclerosis

60. Risk factors
 Increased age
 Male
 CVD
 DM & RD
 Increased nmb of
medication
 Oral anticoagulant use

61. Clinical Feature
 Previous h/o PU+ abdominal pain
 H/o haematemesis / melaena one/more attack.
 Features of haemorrhagic shock.
Feeble , thready pulse , hypotension , syncope ,
oliguria , brainstem hypoxia , mild abdominal
distension.

62. Managment
 Emergency upper OGD
 Resuscitation
 Endoscopy
A. Conservative management-
-emergency replacement of blood.
-ryle’s tube is passed & cold saline stomach wash .
-cold antacids , every 3hrly,about 10-20ml
-IV Ranitidine 50mg,8 hrly /IV Pantoprazole 40mg is
given to reduce the acidity.

63. Continue….
B. Non surgical treatment—
-Laser coagulation
-Sclerotherapy
- Haemoclip application.
C. Surgical control of bleeding—

64. Continue…
INDICATION
-Failure of endoscopic haemostasis.
-Rebleeding in hospita
- 6 units blood already given.
- Elderly patient with rebleeding.
-Massive haemorrhage leading to shock or cardiac
instability.
-Recurrent haemorrhage require hospitalization.
.

65. Continue..
TYPES OF SURGERY
1. Surgery for bleeding duodenal ulcer---
- Laparotomy & anterior gastroduodenotomy
- Visualise the bleeding site.
- Under-running ulcer base by direct suture/4 quadrant
ligation of gd artery.
- followed by gastroduodenotomy incision in converted
into a pyloroplasty followed by vagotomy .

66. Continue..
2. Surgery for bleeding gastric ulcer ..
-Laparotomy , gastrotomy & visualise the site.
-Under-running of the ulcer base.
-Partial gastrectomy is the best treatment.
-Haemostatic method include thermotherapy.
-When bleeding is controlled employed long term medical
therapy-pph / H.pylory t/t….
-If H.pylori infection present then eradication therapy also
should be performed.

67. D/D of Haematemesis
 Stress ulceration.
 Gastric erosions
 Mallory-Weiss tear
 Dieulafoy’s disease.
 Tumours
 Portal hypertension
 portal gastropathy
 Aortic enteric fistula

69. Gastric outlet obstruction
-Earlier it was called as pyloroc stenosis.
-Chronic cicatrisation of a duodenal ulcer or juxtapyloric
ulcer
narrowing of pyloric antrum
pyloric stenosis
-More common in South India
-Metabolic changes such as paradoxical aciduria are
usually seen…

70. Symptoms
 Hunger pain of DU disappears.
 It may be replaced by dull aching pain bec of gastric
distention
 Colicky pain is due to hyperperistalsis of stomach
 Vomiting is profuse , projectile , foul smelling &
nonbilious
 May be distension of upper abdomen with epigastric
fullness.

71. Signs
 VGP
 Succussion splash
 Auscultopercussion test/auscultoscraping test.

72. Investigations
A . Barium meal x-ray
-hugely dilated stomach
-mosaic appearance at the
gastrodeodenal junction
B. Gastroscopy
C . Electrolyte study----
hypochloraemic alkalosis,
hyponatraemai,hypokalaemia,
paradoxical aciduria

73. Barium meal x-ray- Hugely dilated
stomach

74. Treatment
A. Aspiration of stomach content.
B. Blood grouping & cross matching.
C. Chrats-tp/bp/pulse/uo.
D. Drugs-antibiotics
E. Exploratory laparotomy . Vagotomy followed by GJ is
done. Pyloplasty is contraindicated.
F. Fluids .