Al-Hayat Medical University
Gastroenterology
Batch III Medical Students
Lecturer : Dr Abdulfatah Abdullahi Jama
Diseases of the Stomuch
Date: 26/03/2023

Most dilated part of GIT occupies in the epigastric, umbilical and
left hypochondral areas, occupying a recess bounded by
upper abdominal viscera, completed above& anterolateraly
by anterior abdominal wall &diaphragm

Roughly J Shaped at rest
Size and Shape varies with
a) Volume of food or fluid it contains
b) Position of body
c) Phase of respiration
High and transverse in obese and short persons
Elongated in thin persons

Cardiac orifices
Situated to the left of midline behind 7th costal cartilage
2.5cm from its sternal junction at the level of T11
10 cm from ant abdominal wall.

Can be identified by prepyloric vein crossing its anterior
surface vertically.

Lesser curvature
Extends b/w cardiac & pyloric orifice forming right
border
Incisura angularis is a notch in the most dependent part
,its position varies with gastric distension
Gives attachment to lesser omentum

4 to 5 times longer than lesser curvature
Starts at cardiac incisure
Arches upwards & postero laterally & to Lt
Highest convexity is fundus Lt 5th
Finally turns right to end at the pylorus Attachments

 A large globular Lt
part & a narrow
tubular Rt part

Mucosa
Sub mucosa
Muscularis externa
Serosa
Mucosa
Thick, smooth surface
Reddish brown to pink in colour

In contracted state mucosa is folded to form RUGAE.
They are Longitudinal & more marked towards pyloric &
greater curvature
Actually they are large folds in sub mucosal connective tissue
Obliterated when stomach is distended

Epithelium
Lamina propria
Muscularis mucosa

 Epithelium
Appears as
honey combed due to small
gastric pits (foveola). Base of
gastric pits (foveola) receives
gastric glands which
extend deep into lamina
propria
 Epithelium is simple columnar
mucous cells

Principal
 Found In body & fundus
Cardiac glands
 Situated near the cardia
Pyloric glands
numerous mucous & entero
endocrine cells predominate

 Highly differentiated
 Found In body & fundus
Are made of different types of cells
Chief
Parietal
Mucous
Entero endocrine

Cardiac glands
 Situated near the cardia
 Mucous secreting cells predominate
Pyloric glands
 numerous mucous & entero endocrine cells
predominate

 Muscularis mucosa
 Inner circular
 Outer longitudinal
 Ext circular in some places
 Sub mucosa
 Loose connective tissue
 Collagen, elastin,sub mucosal plexus of stomach

Oblique fibres
 Limited to gastric body
 Most developed near the cardiac orifice
Circular fibres
 Form a uniform layer external to oblique
fibres
 At the pylorus form annular pyloric sphincter


Parasympathetic sympathetic

[ vagus]
Anterior br Posterior br
(frm rt vagus) ( frm Lt vagus)

o Functions of stomach
o Gastric secretion
 Mechanism of HCl formation
 Gastric digestive enzymes
 Neural & hormonal control of gastric secretion
 Phases of gastric secretion
o Motor functions of the stomach
o Stomach Emptying

 Stores food
 Digestion
◦ Mechanical – mix
◦ Chemical – protein digestion
 Gastric juice: converts meal to acidic chyme
◦ HCl: kills bacteria, denatures proteins
◦ Pepsin: enzyme breaks down proteins
 Rugae = large folds
 Mucus = protects lining of stomach

oxyntic (gastric) glands Pyloric glands
 Secrete:
◦ Hydrochloric acid
◦ Pepsinogen
◦ Intrinsic factor
◦ Mucus
 Located in body & fundus
 In proximal 80%of stomach
 Secrete:
◦ Mucus- protection
◦ Gastrin
◦ Pepsinogen
 Located in the antrum
 In the distal 20% of
stomach
 In addition to mucus secreting cells that line the
stomach and secrete alkaline mucus there is two
important types of tubular glands:

 Vagus nerve (neural effector) either by releasing Ach (direct
activation of parietal cells) or by releasing Gastrin releasing
peptide, GRP (indirect activation).
 Gastrin (hormonal effector)
 Enterochromaffin-like cells release Histamine activates H2
receptor (parietal cells)  increases acid secretion
 Cimetidine (H2 receptor blocker) peptic ulcer and
gastroesophageal reflux

 3 motor functions of the stomach:
◦ Storage of large quantities of food
◦ Mixing of food with gastric secretions to produce chyme
◦ Slow emptying of chyme into the small intestine at a suitable
rate for proper digestion & absorption

 Digestion of carbohydrate in mouth & stomach
◦ Food mixed with saliva that contain ptyalin (an α amylase)
secreted by parotid gland
◦ It hydrolysis starch to maltose
◦ It continues in stomach for 1 hr
◦ Gastric acid deactivate it

 Digestion of proteins in the stomach
◦ Pepsin
 secreted by chief (peptic) cells
 It is active at pH 2-3 and inactive at pH 5
 Initiate protein digestion (10-20% of protein digestion)
 Can digest collagen
◦ Hydrochloric acid
 secreted by parital (oxyntic) cells

 Stomach is a poor absorptive area of GIT
◦ It lacks the villous type of absorptive membrane
◦ It has tight junctions between epithelial cells
◦ Only a few highly-lipid soluble substances can be absorbed
such as:
 Alcohol
 Aspirin

2500 ml/day
Contents
cations Na,K,Mg,H+
anions Cl,HPO2,so4
pepsin
lipase
Mucus
IF

Gastric mucosal protection:
Intraluminal concentration of H+ is 3 million times greater than
blood and tissue.
“Mucosal barrier”
1] Mucous secretion.
2] Bicarbonate secretion.
3] Epithelial barrier (rapid regeneration).
4] Mucosal blood flow (to sweep away hydrogen ions).
5] Prostaglandin protection (help maintain blood flow).

1983-discovered by Warren and Marshall in Australia
Discovery revolutionised the treatment of duodenal and gastric
ulcers.
Earned them the Nobel Prize for Medicine in 2005.
Formerly known as Campylobacter pyloridis.

• Nearly 20 species of Helicobacter are now recognised
• The gastric helicobacters colonise the stomachs of
animals. The monkey, cat, dog, all harbour their own
species
• H. cinaedi and H. fennelliae are associated with proctitis in
homosexual men.
• H. pylori are found in the human stomach. Molecular
studies suggest transmission from an animal source.

Gram-negative spiral bacillus
Fastidious in terms of growth requirements
:strictly micro-aerophilic
:require C02 for growth
Has a tuft of sheathed unipolar flagella; specially adapted to
colonise mucous membranes

Hallmark of the species is production of urease enzyme
-urease breaks urea down to C02+NH3
-amonia is a strong base
-process helps H. pylori survive
strongly acidic stomach conditions
Very fragile (a point of importance
when referring samples to the lab)

• H. pylori infection occurs worldwide
• Prevalence varies greatly among countries and population
groups
• 20 – 50% prevalence in middle age adults in
industrialised countries
• >80% prevalence in middle age adults in developing
countries
 :may reflect poorer living conditions

• Oral ingestion of bacterium
 within families (esp children)
 person-person contact
 faecal-oral transmission


Highly adapted organism that lives only on gastric mucosa
Gastric antrum is the most favoured site
Present in the mucus that overlies the mucosa

After several days incubation period, patients suffer mild attack
of acute gastritis
-abdominal pain
-nausea
-flatulence
-bad breath
Symptoms can last but hypochlorhydria can last up to one year

Despite a substantial antibiotic response, infection and
chronic gastritis persist
After decades there may be progression to atrophic
gastritis (conditions which are inhospitable for the
bacteria) and numbers reduce.

Strain virulence
Host genotype
Environmental
factors

PUD
-lifetime risk 3% in US, 25% Japan
-eradication provides long-term cure
Gastric carcinoma
-strong evidence of increased risk 0.1-3%
-unclear whether eradication reduces the
risk of gastric cancer
MALT lymphoma
-72%→ 98% of MALT lymphoma
infected with H. pylori

Aim: to understand the pathogenesis of gastritis, peptic ulcer
disease and cancer of stomach.

Definition of Gastritis:
Inflammation of the gastric mucosa.
group of disorders with inflammatory changes in the
gastric mucosa (G.M.) that have different clinical
features, histological characteristics and pathogenesis.
A. Acute Gastritis
B. Chronic Gastritis

ACUTE GASTRITIS + HELICOBACTER PYLORI
- short spiral – shaped, microaerophitic gram - bacillus
- in gastric samples by histological examination, culture, increase
activity, by endonuclease analysis.
- UBT 13C, 14C
- antibodies (Ig G, Ig A) to H.P.
90 – 100 % Hp + antral biopsy specimens of DU patients
70 % - G.U.
80 % - chronic gastritis involving the antral mucosa

CHRONIC GASTRITIS
Definition: Chronic inflammatory cells, predominately lymphocytes and plasma
cells.
HISTOLOGIC CLASSIFICATION
I. SUPERFICIAL GASTRITIS
- Inflammatory changes in the lamina propia of the superficial mucosa of the upper
half of G.M. and the glands are preserved
II. ATROPHIC GASTRITIS
- the inflammatory infiltrate extends to the deep positions of the mucosa
- profound loss of the glandular structures which are separated widely by connective
tissue, with a greatly reduced / absent inflammatory infiltrate.
Gastritis progresses – changes in the morphology of the gastric glandular elements.
Intestinal metaplasia – conversion of gastric glands to the small-intestinal mucosal
glands with goblet cells.

CHRONIC GASTRITIS – TYPES A & B
Type A – involves the body and fundus of the stomach
– from that may lead to pernicious anemia
Antibodies to parietal cells, intrinsec factor in serum  immuno / autoimmuno
pathogenesis
Parietal cell Antibodies 20% of patients over age 60
 20% of patients with – hypoparathyroidism
– Addison’s disease
– vitiligo
Antibodies to intrinsec factor 40 % of those with pernicious anemia.
The risk of stomach cancer in patients with type A gastritis and pernicious anemia is
three times than the general population
Type B:
In younger patients  involves the antrum
In elderly patients  involves entire stomach
The incidence increases with age
- Strong associations of H. pylori with type B gastrities

DIAGNOSIS
- Biopsy of the G.M. provides the most reliable means of identifying and
classifying gastritis.
-Several biopsies of suspected areas, when safe and possible, are recommended.
TREATMENT
In type A.G. + pernicious anemia
Vit. B12 – indefinite regular parental administration

CORROSIVE GASTRITIS
- corrosive chemicals  antrum injury
(HCl, H2SO4, NaOH)
Symtoms:
burning of the mouth, throat, retrosternal area
epigastric pain
vomiting
hemorrhage / perforation
Treatment: supportive therapy

INFECTIOUS GASTRITIS
Phlegmonous G – necrosis, sepsis
- streptococci, staphylococci, Proteus, Escherichia coli
TREATMENT i.v. antibiotics
fluids + electrolyte replacement
gastrectomy – in lack of response
It can occur in immuno-compromised patients  cytomegalovirus

EOSINOPHILIC GASTRITIS
extensive eosinophilic infiltration (e.i) of the wall of the stomach
-biopsy reveals .
- antrum is more frequently involved than gastric body and fundus.
SYMPTOMS: epigastric pain
nausea, vomiting
TREATMENT: glucocorticoids

GRANULOMATOUS GASTRITIS
Chron’s disease produce: ulceration
granulomatous infiltration
stricture formation
Other’s: histoplasmosis
candidosis
syphilis
tuberculoses
Diagnostic: biopsies + cytology to exclude malignancy
surgical exploration if the diagnostic is not established
by biopsy at endoscopy.