This document provides an overview of benign diseases of the stomach. It begins with the gross anatomy and congenital abnormalities of the stomach. It then discusses various types of gastritis including acute, chronic, autoimmune, and H. pylori-related gastritis. The document also covers hypertrophic gastropathies, peptic ulcer disease, gastric ulcer classification and symptoms, and other benign stomach diseases.

2. DR.MEHMOOD-UR-REHMAN
PGR WARD 26 JPMC
BENIGN DISEASES
OF STOMACH

3. LAYOUT
 Gross anatomy of stomach
 Congenital abnomralities
 Gastritis,types and management
 Hypertrophic gastropathies
 Gastric ulcer,types and management
 Complications of gastric ulceration
 Post gastrectomy sequelae and syndromes
 Other benign diseases of stomach
 References.

4. Gross anatomy of stomach
Stomach is the dilated part of the alimentary canal
between esophgus and small intestine.
J shaped or steer horn shaped
It lies under the cover of ribs extending from left costal
margin to epigastrium and umblical region
Postion is not constant.
2 openings (cardiac and pyloric)
2 carvatures (greater and lesser)
2 surfaces (anterior and posterior).

7. Relations of stomach
ANTERIOR
o Ant. Abdomenal wall
o left costal margin
o left pleura and lung
o diaphragm
o left lobe of liver
POSTERIOR
o The lesser sac & pancreas
o Left suprarenal gland & kidney
o The spleen & spleenic artery
o The transverse mesocolon and
transverse colon
o The diaphragm.

8. Blood supply of stomach
ARTERIES
 Left gastric artery
 Right gastric artery
 Short gastric arteries
 Left gastroepiploic artery
 Right gastroepiploic artery
VEINS
 Left and right gastric vein (portal vein)
 Short gastric and left gastroepiploic vein (splenic vein)
 Right gastroepiploic vein (sup. Mesenteric vein)

11. Lymphatic drainage

12. Nerve supply of stomach

13. CONGENITAL
ABNORMALITIES

14.  Agastria
 Microgastria
 Atresia
 Congenital pyloric stenosis
 Duplication
 Diverticula
 Dextrogastria
 Volvulus

15. Pyloric stenosis
 Males 3:1 vs. Females
 ist week presentation
 May occur with Turner syndrome,
trisomy 18, esophageal atresia
Features:
 Narrowing of pyloris,hypertrophy and possibly
hyperplasia.
 Hypochloremia,hypokelemia and alkalosis
 Regurgitation (projectile !!)
 Aspiration
 dehdration

16. DIAGNOSIS
 O/E oval mass will be palpable (OLIVE)
 USG confirms diagnosis.
 Contrast study string sign.
TREATMENT (curative)
 Pyloromyotomy
(Ramstedt's Operation)
Open or lap

17. GASTRITIS

18.  Acute gastritis
 Chronic gastritis
a) Type A gastritis (autoimmune)
b) Type B gastritis (H.pylori)
c) Type C gastritis (Chemical/Reactive gastritis)
d) Other forms

19. ACUTE GASTRITIS
 Gastritis (inflammation of gastric mucosa)
 Transient inflammation (usually)
a) bleeding and erosion
b) sloughing of mucosa
 Pathogenesis not clear: associations
a) NSAID (e.g., aspirin)
b) alcohol
c) smoking
d) stress (trauma, burns, surgery)
e) uremia,infections

20. Factors involved: (1 or more)
 acid secretion with back diffusion
 Decreased HCO3- buffer
 Decreased blood flow
 Disruption of mucus layer
 Damage to epithelium
 Lots of patients have idiopathic acute
gastritis without any of the listed disorders !!
 Neutrophils above basement membrane
(Active inflammation)

21. Features
 may be asymptomatic
 Epigastric pain
 Stomach fullness
 loss of appetite
 indigestion
 black stools
 nausea
 vomiting
 bloody vomit that looks like used coffee grounds

22. Diagnosis
 History
 Examination
 A complete blood count (CBC), which is used to
check your overall health
 A blood, breath, or saliva test, which is used to check
for H. pylori
 A fecal test, for occult blood
 Endoscopy,
 Gastric tissue biopsy

23. Management
Lifestyle Changes:
 avoiding or limiting alcohol consumption
 avoiding spicy, fried, and acidic foods
 eating frequent, small meals
 reducing stress
 avoiding drugs that can irritate the stomach lining, such
as NSAIDs or aspirin or steroids
Medications
 H2 receptor antagonist (cimetidine)
 PPI (omeprazole)
 Antibiotics if h.pylori is there

24. Chronic gastritis
 presence of chronic mucosal inflammation
a) leading to mucosal atrophy
b) intestinal metaplasia
c) usually no erosion
d) epithelial changes may lead to dysplasia
>basis for CA

25. Pathogenesis
 chronic infection (H. pylori)
 autoimmune (pernicious anemia)
 alcohol,
 smoking
 post surgery (i.e., gastric)
 radiation

26. Presentation
 Nausea or recurrent upset stomach
 Abdominal bloating
 Abdominal pain
 Vomiting
 Indigestion
 Burning feeling in the stomach between meals or at night
 Hiccups
 Loss of appetite
 Vomiting blood or coffee ground-like material
 Black, tarry stools

27. Types A gastritis
 Autoimmune gastritis
 10% of gastritis cases
 Ab against H+-K+-ATPase in perietal cells , gastrin
and IF
a) Mucosal atrophy (body) - Loss of acid production
b) Pernicious anemia (lack of IF from body)
 seen with other autoimmune disease
a) type 1 diabetes
b) Addison's disease
c) Hashimoto thyroiditis

28.  High risk of gastric CA and endocrine Tumors
(carcinoid tumors)
 Diffuse mucosal damage
a) Fundus and body
b) Lymphocytes and plasma cells
c) Active inflammation neutrophils !
d) Atrophy is frequently associated with pangastritis
(H. pylori)
e) Hyperplasia of G cells of antrum (Inc. gastrin)
i. Gastremia (Inc. gastrin>ECL cell hypertrophy)

29. Decreased acid production  increased gastrin from G
cells  increased stimulation of ECL cells for histamin
secretion  hypertrophy of ECL cells in body 
microadenomapotential for transformation into
malignant tumor.
(TYPE A GASTRITIS PATIENTS ARE PREDISPOSED
TO GASTRIC CANCER.ENDOSCOPIC SERVIALANCE
IS APPROPRIATE FOR SCREENING)

30. Type B gastritis
 H.PYLORI most important etiologic association
with chronic gastritis
 Gram neg microaerophilic flagellated urease
producing spiral shaped bacteria found in stomach.
 Urease breaks down urea into ammonia and CO2
which produce a neutral area around bacteria.
 Urease is important for producing chronic infection
 Upto 50% of worlds population affected.
 RISK FECTORS overcrowding, inc number of
siblings, sharing a bed, and lack of running water.

31.  Transmission fecal/oral and oral/aral
 plays role in other diseases:
a) peptic ulcer
b) gastric carcinoma
c) gastric MALT lymphoma
“mucosa-associated lymphoid tissue”
(B-cells produce igG and igA against bacteria locally.B cells are
stimulated by T cells of host.prolonged stimulation can produce
B cell lymphomas in rare cases)

33. 1. Antral type gastritis
G cell stimulation by bacteria
increased acid production
causes peptic ulcers
1. Pangastritis
concomitant autoimmune gastritis
multifocal gastric atrophy
decreased acid production
inc risk of adenocarcinoma

34. Diagnosis
 CBC for anemia and infection
 Serologic test for gastrin level,antiperietal cell
antibodies
 Fecal test for blood
 Fecal bacteria detection
 Urea breath test
 An endoscopy
 Gastric biopsy (culture)- histology visualization
(proximal stomach for Autoimmune gastritis)

35. Management
 Life style modifications
 Avoidance of drugs like NSAIDs and steroids
 H2 receptor antagonist
 PPI
 FOR AUTOIMMUNE VERIETY immunosupressive
drugs and chemotherpy
 Iron and B12 supplements (autoimmune gastritis)

36. Eradication therapy for H.Pylori

37. Reactive/chemical gastropathy
absence of active inflammation (no neutrophils)
causes:
a) Bile reflux (post surgery)
b) Alcohol
c) NSAIDS
Diagnosis made on biopsy
Risk of carcinoma in bile reflux gastritis

38. OTHER FORMS
 Eosinophilic gastritis
 Lymphocytic gastrits
 Allergicgastrtis
 Granulomatous gastritis

39. HYPERTROPHIC
GASTROPATHIES

40. Ménétrier's disease
• hypoproteinemic hypertrophic
gastropathy
• Gross hypertrophy of gastric mucosal folds
• Mucus production,hypochlorhydra,anemia and
hypoproteinemia (80%).
• Overexpression of TGF-α
• CMV AND H.PYLORI association
• Detected on contrast study and endoscopy
• Cituximab ist line treatment
• Gastrectomy in resistance (Malignant potential)

41. Zollinger Ellison Syndrome
 Caused by gastrinoma
 Cmmon sites pancreas,duodenum and abd L/N.
 Massive secretion of HCL and ulcers due to ectopic
gastrin production from tumor
 Associated w/ type I (MEN) PPP (25%)
 20% multiple, 2/3 malignant, w/ slow growing
 Parietal cell mass is increased

42.  Diagnosis
• Endoscopy
• Secretion stimulation test
• Basal gastrin level 36 times normal
• Gastric PH
• MRI
 Treatment
H2 rec blockers ,PPI and excision of primary tumor.

43. PEPTIC ULCER
DISEASE (PUD)

44. A circumscribed ulceration of the gastrointestinal
mucosa occurring in areas exposed to acid and
pepsin and most often caused by Helicobacter pylori
infection and NSAIDS.

45. Gastric ulcer Duodenal ulcer

46. Pud demographics
 Higher prevalence in developing countries
• H. Pylori is sometimes associated with socioeconomic status
and poor hygiene
 In the US:
• Lifetime prevalence is ~10%.
• PUD affects ~4.5 million annually.
• Hospitalization rate is ~30 pts per 100,000 cases.
• Mortality rate has decreased dramatically in the past 20 years
• approximately 1 death per 100,000 cases

47. GASTRIC ULCER
 common in late middle age
• incidence increases with age
 Male to female ratio—2:1
 More common in patients with blood group A
 Use of NSAIDs - associated with a three- to four-fold
increase in risk of gastric ulcer
 related to H. pylori ~ 75%,90% in case of duodenum.
 10 - 20% of patients with a gastric ulcer have a
concomitant duodenal ulcer

48. CLASSIFICATION

49. Etiology
 A peptic ulcer is a mucosal break, 3 mm or greater,
that can involve the stomach or duodenum.
 Contributing factors are H pylori, NSAIDs, acid, and
pepsin.
 Aggressive factors include smoking, ethanol, bile acids,
aspirin, steroids, and stress.
 Protective factors are mucus, bicarbonate, mucosal
blood flow, prostaglandins, hydrophobic layer, and
epithelial renewal.
 When an imbalance occurs, PUD might develop
 1% due to Zollinger Ellison Syndrome

50. SIGNS AN SYMPTOMS
 Pain— ”gnawing”, “aching”, or “burning”
• Duodenal ulcers: occurs 1-3 hours after a meal and may
awaken patient from sleep. Pain is relieved by food, antacids,
or vomiting.
• Gastric ulcers: food may exacerbate the pain while vomiting
relieves it.
 Nausea, vomiting, belching, dyspepsia, bloating, chest
discomfort, anorexia, hematemesis, &/or melena may
also occur.
• nausea, vomiting, & weight loss more common with Gastric
ulcers

51.  Epigastric tenderness
 Succussion splash resulting from scaring or edema due
to partial or complete gastric outlet obstruction
• A succussion splash describes the sound obtained by shaking
an individual who has free fluid and air or gas in a hollow
organ or body cavity.
• Usually elicited to confirm intestinal or pyloric obstruction.
• Done by gently shaking the abdomen by holding either side of
the pelvis. A positive test occurs when a splashing noise is
heard, either with or without a stethoscope. It is not valid if the
pt has eaten or drunk fluid within the last three hours.

52. Differential Diagnosis
 Neoplasm of the stomach
 Pancreatitis
 Pancreatic cancer
 Diverticulitis
 Non ulcer dyspepsia (also called functional
dyspepsia)
 Cholecystitis
 Gastritis
 GERD
 MI—not to be missed if having chest pain

53. Diagnostic Plan
 Guaiac test for occult blood loss
 Labs: CBC , LFTs, amylase, and lipase.
 H. Pylori can be diagnosed by urea breath test, blood
test, stool antigen assays, & rapid urease test on a
biopsy sample.
 Upper GI Endoscopy: Any pt >50 yr with new onset of
symptoms or those with alarm markings including
anemia, weight loss, or GI bleeding.
• Preferred diagnostic test b/c its highly sensitive for dx of ulcers
and allows for biopsy to rule out malignancy and rapid urease
tests for testing for H. Pylori.

54. MANAGEMENT (NON SURGICAL)
Lifestyle Changes
 Discontinue NSAIDs and use Acetaminophen for pain
control if possible.
 Acid suppression--Antacids
 Smoking cessation
 Avoidance of alcohol
 No dietary restrictions unless certain foods are
associated with problems.
 Stress reduction

55. Plan: H. Pylori
 Medications: Triple therapy for 14 days is considered the
treatment of choice.
 Goal: complete elimination of H. Pylori. Once achieved
reinfection rates are low.

56. Plan: Non H. Pylori
 Medications—treat with Proton Pump Inhibitors or
H2 receptor antagonists to assist ulcer healing
 2 months duration.

57. Complications
 Perforation & Penetration—into pancreas, liver and
retroperitoneal space
 Peritonitis
 Bowel obstruction, Gastric outflow obstruction, &
Pyloric stenosis
 Bleeding--occurs in 25% to 33% of cases and
accounts for 25% of ulcer deaths.
 Gastric CA

58. Algorithm for managing complications

59. MANAGEMENT (SURGICAL)
 People who do not respond to medication, or who
develop complications:
• BI, BII resection
• Trancal vagotomy and drainage
• Highly selective vagotomy

60. BILLROTH I
 Gastro-duodenoanastomosis end-to-end
BILLROTH II
 gastro-jejunoanastomosis end-to-side with blind
closure of duodenum

62. VAGOTOMY
Trancal vagotomy and drainage
• Nerve sectioned from trunk dec acid production
• S/E; Gastric stasisPyloroplasty or gastrojejunostomy
gall bladder stasisgall stones
Highly selective Vagotomy
• Only perietal cell mass denervated
• S/E Epigastric fullness (loss of receptive relaxation of
stomach)
Trancal vagotomy and antrectomy

63. Algorithm for evalvation and treatment

64. Giant Gastric Ulcer
 Giant gastric ulcer: >2cm;10 30% malignancy risk
 Subtotal gastrectomy with Roux-en-Y (high
morbidity and mortality)
 Kelling-Madlener procedure: less aggressive,
antrectomy, BI reconstruction, bilateral truncal
vagotomy, multiple biopsies, cautery of ulcer

65. Complications after stomach resection
 Recurrent ulceration,
 stenosis of anastomosis,
 bleeding, pancreatitis,obstructive icterus,
 fistulation,
 stasis,
 intestinal obstruction from adhesions and
intussusception
 early dumping syndrome
 late dumping syndrome
 Anemia,diarrhea,weight loss and bile vomiting

66. Early dumping syndrome
 group of symptoms approved shortly after meal
 appears after BII resection
 vasomotoric sy. - face redness, fall of blood pressure,
dizziness
 GI sy. - vomiting, diarrhoea
 Management: diet, no sugar, low quantities of food,
change BII to BI resection

67. Late dumping syndrome
 hypoglycaemia (sugar is not enough digested)
 appears after BII resection
 weakness, perspiration, dizziness, tremor 3h after meal
Management.: no sugar, change BII to BI resection

68. References
 Bailey and love short practice of surgery 26th
addition
 Sabiston 19th addition
 Wikipedia

69. THANKYOU