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