BY DR PRIYANKA.

1. APPLIED ANATOMY AND
PHYSIOLOGY OF
STOMACH

2. QUADRANTS OF ABDOMEN

3. STOMACH
Muscular organ- most dialated part of alimentary
canal.
J shaped enlargement of GI tract.
It occupies epigastric, umblical and left
hypochondraic regions.
Lies in upper left quadrant of abdominal cavity.

4. SHAPE AND SIZE OF
STOMACH
• Vertical- when the stomach is empty
• Piriform- when it is partially distended
• Horizontal – in obese persons
• High and transverse (steer horn type)- in
short fat individuals
• Low and elongated in tall and feeble
individuals
• About 10 inches (25 cm long)

5. SHAPES OF
STOMACH

6. ANATOMICAL DIVISIONS OF
THE STOMACH
NAL CARDIA FUNDUS BODY
PYLORIC PART

8. SURFACES OF
STOMACH
ANTERO-
SUPERIOR
SURFACE
POSTERO-
INFERIOR
SURFACE
CURVATURES OF
STOMACH
Greater
curvature
Lesser
curvature

9. ORIFICE OF
STOMACH PYLORIC
CARDIAC
SPINCHERS OF
STOMACH

11. RELATIONS
ANTERIOR
• Inf.surface of the left
lobe and quadrate lobe
• Left half of the
diaphragm
• Anterior abdominal wall
• SUPERIOR
• Left dome of diaphragm
POSTERIOR
• Diaphragm
• Gastric surface of
spleen
• Left supra renal gland
• Left kidney
• Pancreas
• Transverse meso colon
• Transverse colon

13. BLOOD
SUPPLY
ARTERIAL
SUPPLY
Supplied by celiac
artery or its
branches
Left gastric artery
Right gastric artery
Right gastro
epiploic artery
Short gastric artery
– branch of
spleenic artery
VENOUS
DRAINAGE
Left gastric vein
Right gastsric vein
Left gastro epiploic
vein
Right gastro
epiploic vein
Short gastric veins

15. LYMPHATIC
DRAINAGE
• The lymphatic of
stomach drained into :-
• Gastroepiploic nodes
• Inferior gastric nodes
• Pancreato- spleenic
group of lymph nodes
• Symphathetic-T6-T10
spinal segments from
the celiac and hepatic
plexus
• Para symphathetic-
anterior gastric (mainly
formed by left vagus)
• Posterior gastric(mainly
formed by right vagus)
NERVE SUPPLY

16. HISTOLOGY OF STOMACH
SEROUS LAYER
MUSCULAR
SUB MUCOUS
MUCUS
COAT
MUSCULAR
• Outer longitudinal
• Middle circular
• inner Oblique layer

17. CLINICAL ANATOMY

18. PYLORIC STENOSIS
• PATHOLOGY:
• Musculature of the
pylorus and antrum is
grossly hypertrophied
• Hypertrophy being
maximum in pylorus
• CLINICAL FEATURES
• First bone male child
affected
• Most commonly seen in 4
weeks after birth
• Vomitting is the
presenting symptom
• Forcible and projectile
• Only milk and no bile
• Weight loss
• Emaciated and
dehydrated
• Characteristic peristaltic
waves that can be seen
to pass across the upper
abdomen.

20. DIEULAFOYS
DISEASE
• Large tortous arteriole in
the stomach wall that
erodes and bleeds
• Can present in any part of
git
• Cause gastric hemorrhage
• Also called caliber
persistent artery or
aneurysm of gastric vessels
• Symptoms- recurrent
hemetemesis with melena

21. MENETRIER’S
DISEASE
• Rare disease
• Characterized by massive
overgrowth of mucous
cells in the mucous
membrane lining the
stomach resulting in large
gastric folds.
Symptom- pain in the upper
middle region of the
stomach (Epigastric pain)

22. GASTRIC ATROPHY
• Condition in which the muscles of the
stomach shrink and become weak
• Gastric glands also shrink resulting in the
deficiency of gastric juice
• Caused by loss of gastric glandular cells and
their eventual replacement by intestinal and
fibrous tissues.

23. DISPLACEMENT OF
STOMACH
• Pancreatic and psuedo cyst, abscess in the
omentum bursa can push the stomach
forward/anteriorly.
• This displacement is usually visible in the lateral
radiographic CT.
• The posterior wall of stomach may adhere to the
part of the posterior wall of the omentum bursa
that covers the pancreas
• This occurs due to the inflammation of pancreas
and the posterior wall of stomach is very close to
that.

24. PHYSIOLOGY OF STOMACH

25. GASTRIC GLANDS AND
OXYNTIC GLANDS
IN FUNDUS AND BODY
GASTRIC PIT COMMUNICATES
WITH SEVERAL GASTRIC
GLANDS
GASTRIC GLANDS ARE
DOMINATED BY 2 TYPE OF CELLS
CHIEF CELLS, PARIETAL CELLS-
THEY SECRETE ABOUT 1500 ML
GASTRIC JUICE EACH DAY
• Most important and most
numerous of the gastric
glands
• Several oxyntic glands open by
a common opening called
gastric pit
• Each gland contains types of
cells.neck mucus cells found in
neck region, paarietal or
oxyntic cells, secreting hcl and
intrinsic factor., peptic or chief
cells which contain zymogen
granules, secrete pepsinogen-
the precursor of pepsin, chief
cells secrete gastric lipase.

26. • PARIETAL CELLS
Intrinsic factor
HCL
• The secretory activities
of the parietal cells can
keep the stomach
contents at a ph of 1.5-
2.0.

27. CHIIEF CELLS
Abundant near
the base of
gastric gland
Cells secrete
pepsinogen
Pepsinogen
converted by the
acid into pepsin
Functions most
effectively at a
strongly acidic pH
of 1.5-2.0
In new borns-it
produces renin, also
known as chymosin
and gastric lipase

28. PYLORIC GLANDS
• Glands in the pylorus produce primarily mucous
rather than enzymes
• Enteroendocrine cells are scattered among mucus
secreting cells
• These cells produce 7 different hormones
• Most notably the hormone gastrin
• Gastrin is produced by G cells
• Most abundant in pyloric pits of gastric antrum

29. ENDOCRINE CELLS
RICHLY ENDOWED WITH
ENDOCRINE CELLS PRODUCE HISTAMINE
MUCOSA CONTAIN G
CELLS –PRODUCE
GASTRIN
LARGE NUMBER
OF STOMATO
STATIN
PRODUCING D
CELLS

30. FUNCTIONS OF
GASTRIN
THE PYLORIC GLANDS ALSO CONTAIN D CELLS,WHICH RELEAESE
STOMATO STATIN- HORMONE THAT INHIBITS GASTRIN RELEASE

31. REGULATION OF
GASTRIC ACTIVITY
CONTROLLED BY CNS
REGULATED OF SHORT REFLEXES
CORDINATED IN THE WALL OF THE
STOMACH
REGULATED BY DIGESTIVE TRACT
HORMONES
SEVERAL PHASES OF GASTRIC
CONTROL CAN BE IDENTIFIED

32. CEPHALIC
PHASE
Function- prepare stomach
for the arrival of food
Duration- short (minutes)
Mechanism-
Neural:Via preganglonic
fibres in vagus nerve and
synapses in sub mucosal
plexus
Actions ;primary- increased
volume of gastric juice by
stimulating mucus, enzyme,
and acid production
Secondary: stimulation of
gastrin release by g cells

33. GASTRIC PHASE
Functions:
Enhance secretion started
in cephalic stage,
homogenise and acidify
chyme
Initiate digestion of proteins
by pepsin
Duration:long(3-4hrs)
Mechanism: neural
response :short reflexes
triggered by
Stimulation of stretch
receptors as stomach fills
Stimulation of chemo
receptors as Ph increases
Hormonal
Stimulation of gastrin
release by G cells by
parasymphathetic activity
and presence of peptides
and amino acids in chyme
Local response: release of
histamine by mast cells as
stomach fills
Actions :
Increase acid and
pepsinogen production
Increased motility and
initiation of mixing waves.

35. INTESTINAL
PHASE
Function:
Control rate of chyme entry
into duodenum
Duration : long (hrs)
Mechanism
Neural: short
reflexes(entero gastric
reflex) triggered by
extension of duodenum
Hormonal
Primary: stimulation of CCK,
GIP, and secretin realease
by presence of acid,
carbohydrate and lipids
Secondary:release of
gastrin stimulated by
presence of undigested
proteins and peptides
Actions
feed back inhibition of
gastric acid and pepsinogen
production
Reduction of gastric motility

37. DIGESTION AND
ABSORPTION IN THE
STOMACH
Preliminary digestion of
proteins by pepsin.
Permits the digestion of
carbohydrates and lipids by
salivary amylase and lingual
lipase
Although digestion occur in
stomach , no nutrient
absorption there because:
The epithelial cells are covered
by a blanket of alkaline mucus
and are not exposed to the
chyme.
The epithelial cells lack the
specialized transport
mechanism of cells that line
small intestine
The gastric lining is relatively
impermeable to water
Digestion has not proceeded
to completion by the time
chyme leaves the stomach. At
this stage ,most
carbohydrates, lipids and
proteins are partially broken
down.

38. LAYER OF
STOMACH
CELLS SECRETION REGION OF
STOMACH
ISTHMUS OF
GLAND
FOVEOLAR CELLS MUCUS GEL LAYER FUNDUS, CARDIA,
PYLORIC
BODY OF GLAND PARIETAL CELLS GASTRIC ACID (HCL)
AND INTRINSIC
FACTOR
FUNDUS ONLY
BASE OF GLAND CHIEF CELLS PEPSINOGEN AND
GASTRIC LIPASE
FUNDIC ONLY
BASE OF GLAND ENTEROENDOCRIN
E CELLS
HORMONE,
GASTRIN,
HISTAMINE,
ENDORPHINS,
SEROTONIN,
CHOLECYSTOKININ,
SOMATOSTATIN
FUNDUS , CARDIAC
AND PYLORIC

39. HORMONES FUNCTIONS
GASTRIN INCREASE IN THE SECRETION OF HCL FROM THE PARIETAL CELLS
AND PEPSINOGN FROM CHIEF CELLS IN THE STOMACH,INCREASED
MOTILITY IN STOMACH, GASTRIN RELAESE BY G CELLS IN
STOMACH IN RESPONSE TO DISTENTION OF ANTRUM , IT IS
INHIBITED BY A Ph LESS THAN 4(HIGLY ACIDIC),AS WELL AS THE
HORMONE SOMATOSTATIN
CHOLECYSTOKININ CCK HAS MOST EFFECT ON GB, CAUSING GB CONTRACTIONS BUT
IT ALSO DECREASES GASTRIC EMPTYING AND INCREASE RELEASE
OF PANCREATIC JUICE WHICH IS ALKALIN AND NEUTALIZES THE
CHYME
SECRETIN SECRETIN PPRODUCE IN THE SMALL INTESTINE, HAS MOST EFFECT
ON PANCREAS, BUT WILL ALSO DIMINISH ACID SECRETION IN THE
STOMACH
GASTRIC
INHIBITORY
PEPTIDE
GIP DECREASES BOTH GASTRIC ACID RELAESE AND MOTILITY
ENTEROGLUCAGON DECREASES BOTH GASTRIC ACID AND MOTILITY

40. SECRETIONS OF
THE STOMACH
Chyme: ingested food +stomach secretions
Mucus- surface and neck mucus cells
Viscous and alkalin
Protects from acidic chyme and enzyme
pepsin
Irritation of stomach mucosa causes
greater mucus
Intrinsic factor:parietal cells ,binds with vit
b12 and helps for the absorption.
Hcl:parietal cells
Kills bacteria
Stops carbohydrate digestion by
inactivating salivary amylase
Denatures proteins
Helps convert pepsinogen to pepsin
Pepsinogen: chief cells,packed in zymogen
granules.
pepsin catalyses breaking of covalent bonds
in proteins
G cells: secrete the hormone gastrin which
stimulates hcl secretion from parietal cells.

41. HELICOBACTER
PYLORI
• Spiral shaped organism
• Difficult to culture outside
the mucous layer of the
stomach
• It has the ability to
hydrolyse urea,resulting in
the production of ammonia
• Effect of amonia antral g
cells release of gatrin
hypergastrinaemia in
patients with peptic ulcer
disease, inturn result in
gastric acid hyper secretion
• Infection disruption
of the gastric mucous
barrier by the enzymes
produced by the organism
• And the inflammation in
duced in the gastric
epithelium.
• H.pylori infection resullts in
chronic gastritis
• This may progress to gastric
ulceration

42. PEPTIC ULCER
• Open sores that develop on
the inside lining of stomach
• Epigastric pain,
• Nature of pain- gnawing,
may radiate to the back
• Eating may sometime
relieve pain
• Intermittent pain
• Comon site- lesser
curvature
• Symptoms-
• Burning stomach pain
• Feeling of fullness , bloating
or belching
• Heart burn
• nausea/vomitting
• Alteration in weight
• Bleeding- acute
presentation with
hemetemesis and melena
• Risk factors- smoking,
alcohol, untreated stress,
spicy food

43. GASTRITIS
• Inflammation of the gastric
mucous membrane
• Causes
• Swallowed drugs, including
alchohol, aspirin,
• After severe emotional or
physical stress
• Bacterial infection of the
gastric wall, ingestion of
strongly acidic or alkaline
chemicals.
• Acute or chronis
• ACUTE GASTRITIS
• Inflammation of the
superficial layers of mucous
membrane
• Infiltration with leukocytes
mostly neutrophills
• CHRONIC GASTRITIS:
• Inflammation of deeper
layers
• Infiltration with more
lymphocytes
• It results in the atrophy of
the gastric mucosa with loss
of chief cells and parietal
cells
• Secretion of gastric juice
decreases.

44. TYPE A GASTRITIS
• Autoimmune condition in
which there are circulating
antibodies to the parietal
cell.
• Results in atrophy of the
parietal cell mass, hence
hypochlorhydria and
achlorhydria
• Antrum is not effected
• Predisposed to the
development of gastric
cancer
TYPE B GASTRITIS
• Associated with H-pylori.
• Effects the antrum
• Prone to peptic ulcer
• Helico bacter associated
with pan gastritis- common
manifestation of infection
• More prone to the
development of gastric
cancer

45. EROSIVE GASTRITIS
• When the acid residing
wihin the stomach begin to
erode and will wear away
the mucosal lining.
• Cause- NSAIDS, Alcohol
• These agents will disturb
the mucosal barrier.
• Typically acute
,infllammation will be less
but can lead to bleeding
• Even lead to stomach
cancer
STRESS GASTRITIS
• CAUSE- Reduction in the
blood supply to superficial
mucosa of the stomach
• Can cause mucosal erosions
and superficial hemorhhage
• Symptoms- coffee ground
vomittus

46. Rare
Characterise by the infiltration of the gastric mucosa by
inflammatory cells
Probably associated with H-pylori infection
Pattern of inflammation resembles- coeliac disease or
lymphocytic colits
Symptoms are nausea, vomitting, abdominal pain, diarrhoea,
weight loss
• LYMPHOCYTIC GASTRITIS

47. STOMACH CANCER
• Also known as gastric
cancer
• Developing from the
lining of stomach
• Because of the lymphatic
vessels of the mucus
membrane and the
submucosa of the
stomach are in continuity,
it is possible for cancer
cells to travel different
parts of the stomach.

48. CONCLUSION
• Creates a reservoir of food.
• Blends food with gastric secretions to create a
semifluid substance referred to as chyme.
• Controls the speed of delivery of chyme into the
small intestine to enable proper digestion and
absorption in the small intestine.
• Hydrochloric acid secreted by the gastric glands
ruins bacteria existing in the food and bevarage.
• Citadels intrinsic factor within the gastric juice
helps in the absorption of vitamin B12 in the
small intestine.