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
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.
Extends b/w cardiac & pyloric orifice forming right
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
In contracted state mucosa is folded to form RUGAE.
They are Longitudinal & more marked towards pyloric &
Actually they are large folds in sub mucosal connective tissue
Obliterated when stomach is distended
honey combed due to small
gastric pits (foveola). Base of
gastric pits (foveola) receives
gastric glands which
extend deep into lamina
Epithelium is simple columnar
Found In body & fundus
Situated near the cardia
numerous mucous & entero
endocrine cells predominate
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
◦ 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
◦ Hydrochloric acid
◦ Intrinsic factor
Located in body & fundus
In proximal 80%of stomach
◦ Mucus- protection
Located in the antrum
In the distal 20% of
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
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
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
Gastric mucosal protection:
Intraluminal concentration of H+ is 3 million times greater than
blood and tissue.
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
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
• H. cinaedi and H. fennelliae are associated with proctitis in
• 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
: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
• 20 – 50% prevalence in middle age adults in
• >80% prevalence in middle age adults in developing
:may reflect poorer living conditions
• Oral ingestion of bacterium
within families (esp children)
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
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.
-lifetime risk 3% in US, 25% Japan
-eradication provides long-term cure
-strong evidence of increased risk 0.1-3%
-unclear whether eradication reduces the
risk of gastric cancer
-72%→ 98% of MALT lymphoma
infected with H. pylori
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
Definition: Chronic inflammatory cells, predominately lymphocytes and plasma
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
Parietal cell Antibodies 20% of patients over age 60
20% of patients with – hypoparathyroidism
– Addison’s disease
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
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
- Biopsy of the G.M. provides the most reliable means of identifying and
-Several biopsies of suspected areas, when safe and possible, are recommended.
In type A.G. + pernicious anemia
Vit. B12 – indefinite regular parental administration
- corrosive chemicals antrum injury
(HCl, H2SO4, NaOH)
burning of the mouth, throat, retrosternal area
hemorrhage / perforation
Treatment: supportive therapy
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
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
Chron’s disease produce: ulceration
Diagnostic: biopsies + cytology to exclude malignancy
surgical exploration if the diagnostic is not established
by biopsy at endoscopy.