Year three 2022

Dr. Nadia A. Gheni

 Acid protection
üMucous.
üHCO3-.
üEpithelial barrier.
üBlood flow.
üProstaglandin E, I. incrase all other protective mechanisms

promotor for all protective mechanisms

 Congenital anomalies
not affected the esophagus
1. Diaphragmatic hernia. defect or abcense a part of diaphragm

2. Pyloric stenosis.
tissue of organ in other organ
3. Pancreatic heterotopia. ectopic normal ilets of pancrease within the
gastric mucosa or gastric mucosa within
4. Gastroschisis. the pancreas

5. Omphalocele.
Pathology:
üProtrusion of abdominal viscera into the chest
cavity.
üResult from abnormal development of diaphragm in
utero.
üHigh mortality rate. because the comppresing effect on the heart and lungs
üIncomplete diaphragm formation →abdominal
organs protrude into chest cavity → physical
obstruction of heart, lung formation/function →
pulmonary hypoplasia, surfactant deficiency,
• Partial or total absence of a region of a diaphragm,
usually on the left, the abdominal content may
herniate into the thorax, including left kidney,
perinephric fat, stomach, and small intestine.

• Differ from the hiatal hernia in that the defect

in the diaphragm does not involve the
hiatal orifice. gases and loops of bowel

• Hernial wall composed of peritoneum

and pleura.
• Pathology
• Constriction of pylorus due to pyloric sphincter
hypertrophy → gastric outflow obstruction.
• Congenital hypertrophy of pyloric smooth muscle.
• Risk factors:
• Firstborn, male: female 3-4:1.
• parents with pyloric stenosis.
result in increase intragasrtic pressure
x-ray features
distended stomach with minimal intestinal gases
because of obstruction
• Complications:
• Dehydration.
• Malnourishment.
• Acid-base imbalance.
• Mic. microscopicaly
• Hypertrophy of muscularis propria of pylorus.
• Signs & symptoms:
• Classically presented two weeks after birth.
• Projectile nonbilious vomiting.
• Visible peristalsis.from eso. to stomach neutophils seen in gastritis
• Dehydrated undernourished.
• Abdominal olive-like mass.
X-ray: could be palpated

• Distended stomach.
• Minimal intestinal gas.
Surgery:
• Pyloromyotomy.
more common in females
 contents are expused
(not covered) stomch spliting
• Congenital malformation
of abdominal wall.
• Leads to exposure of
abdominal contents.

failure of two bilateral process to

fusion completly
 omphalo=umblical cord
cele=cyst the gastric contens are within a bubble
(peritonial and amenun)

• Persistent herniation of
bowel into the umblical
cord.
• due to failure of
herniated intestine to
return to body cavity
during development.
• contents are covered
by peritoneum &
amnion of umblical
 chronic:-
1) Autoimmune
2) H.pylori

• Inflammation of gastric mucosa.

• Types: eneutophils seen in gastritis

• Acidic damage to mucosa.

• Due to imbalance between mucosal defenses and
acid environment.

• Micro.: neutrophils infiltration, erosion and necrotic

debris.
 Acute gastritis
superfecial Erosion of mucosa
Hemorrhage.
neutrophils neutophils seen in gastritis
 Risk factors(stress related ulcer)
• Extensive burn(Curling ulcer) hypovolimic shock so deminished blood
flow from organs like stomach to incr. it
in the vital organs like brain and heart
• NSAIDs. By production of cox
impairs the prostaglanden secretion

• Alcohol consumption. directly toxic to the epithelial cells

• Chemotherapy. damaging the cells regeneration and growth (DNA)
• Increased intracranial pressure (Cushing
ulcer) by vagal stimulation gastric acute ulceration releated to reccent brain abnormality
• Shock.
• Severe psychological stress.
These patients develope gastric ulcer within
few days
 • Strongly acidic gastric lumen aids in digestion but also has the
potential to damage the mucosa.

• Mechanisms those protect gastric mucosa:

üMucin secretion by foveolar cells.

üBicarbonate secretion into mucous by surface
epithelial cells.
üRich mucosal blood supply.
imp.
üEpithelial regeneration.
üProstaglandin synthesis.
vNSAID: inhibit COX-dependent prostaglandin
synthesis(PG stimulates all the defense
mechanisms: mucous, bicarbonate, and
mucosal blood flow)
 Most often due to , hypotension, and
splanchnic vasoconstriction induced by stress.
Increased secretion of the vasoconstrictor
endothelin-1.
Direct excessive stimulation of vagal nuclei with
excess acid secretion in ICD.
imp.
Systemic acidosis may lower the mucosal cell pH
with resultant damage to these cells.
• Superficial inflammation. eroneutophils seen in gastritis
• Erosion (loss of epithelium) just the 1st layer of mucosa is lost
• Ulcer (loss of mucosa) all layers are damaged
so will exposured sub mucosa
epithelium
lamina properia
mascularis mucosae
 causes of impaired physiological change

Reduced mucin and bicarbonate secretion in

elderly. elderly people have reduced gladular secretions of almost all glands
Hypoxemia and decreased oxygen supply to the
mucosa in high altitudes and smoking.
Chemicals’ ingestion: acid, base, directly toxic
to epithelial and stromal cells.
Also, for alcohol consumption, NSAID, radiation.
Chemotherapy: inhibit DNA synthesis and
mitosis.
 neutrophils is indecator for active reccent

Morphology inflammation

Hyperemia, edema and vascular congestion.

Presence of neutrophils above the basement
membrane indicate active inflammation.
In severe case hemorrhage and erosion
developed: acute erosive hemorrhagic
gastritis(upper GIT bleeding).
acute mean within few days

.
acute erosive, hyperemic pin-point hemorrhagic spots (not one ulcer like peptic ulcer)
 two types;-

1) 90% H.pylori
microscopically neutrophils is indecator for active reccent inflammation 2) 10% ((rare type)
*there are no inflammatory cells within the normal stomach
two types;-

1) 90% H.pylori
diffuse peripheral gastritis 2) 10% rare type) autoimmune

• Is the presence of chronic mucosal inflammatory

changes leading to epithelial metaplasia, mucosal
atrophy and gland loss. atrophic because of mucosa is atrophy parietal cells are
destructed epithelial metaplasia (goblet cell metaplasia)

• Metaplasia: reversible change of one type of

epithelium into another in response to stress.
• Intestinal metaplasia: goblet cells. normally present within colon
mucosal atrophy only in chronic conditions ( long standing, damaging t-cell cyto toxicity cause mucosal
cells destruction glandular atrophy), notttt in acuteee
• Two main causes:
• H. pylori associated.
• Autoimmune.
extacellular bacteria

most common cause(90%).

S- shaped G- negative.
antrum and body. the parietal cells locations
increase with age.
H. pylori colonization of mucosa leads to impaired healing
and inflammation.
Role in metabolic cellular alterations due to infection,
bacterial toxins, and host inflammatory response.
Response to antimicrobials. treat. pharmacologically
risk of ulcer and cancer.
extacellular bacteria, could be seen within the lumen (mucos layer), present in almost all casses of gastric and
duodenal ulcers, and other gasric pathologies (gasritis, adenocarcenoma, gastric lymphoma) mainly inhabiting the
antrum (antral gasritis) H.pylori associated gasritis
• Present in almost all cases of gastric and duodenal
ulcers.
• Antral gastritis with increased acid secretion→→
peptic ulcers in stomach and duodenum.

• In some patients H. pylori gastritis extends to

destruct parietal cells in the body and fundus as in
autoimmune gastritis→→ reduced acid secretion
and hypergastrinemia. rebound hypersecretion of HCL
• Extensive gastritis of body and fundus may→→
intestinal metaplasia and risk of cancer.
body and fundus for (autoimmune gastritis,.
• In early stages: lymphocytes and plasma cellstwointypes;-
lamina propria upper third = chronic superficial1) 90% H.pylori
gastritis. 2) 10% (rare type)

• In severe cases: inflammatory cell infiltration in all

mucosal thickness with lymphoid aggregates.
• Additional features:
• 1- activity: if neutrophils→ active gastritis.
• 2- regenerative changes: enlarged hyperchromatic
cells with mitotic activity in mucosal cells.
• 3- metaplasia: goblet intestinal cells.
• 4- atrophy: glandular loss.
• 5- H pylori found on mucosal cells.
• 6- dysplasia cytologic changes with atypia in severe
cases→ intestinal-type gastric adenocarcinoma.
body and fundus for (autoimmune gastritis), antrum (H.pylori)

Chronic gastritis
*there are no inflammatory cells within the normal stomach, but if there are alot of inflammatory cells within mucosa
will incurrage the cell to transform (metaplastic) to another cells that are present in surrounding of inflammatiom

LYMPHOIS AND
INFLAMMATORY CELLS
AGGRIGATES, IN ALL THCKNESS
OF MUCOSA (SEVERE CASSES)
 *there are no inflammatory cells within the normal stomach

the interstitium normally back to bcak (close to each others)

delicated (hard to seen)

Gastric
intestinal
metaplasia
reversble after proper treatment, but if not
treated can predisposing to intetinal tight
adenocarcinoma.

in this pic. widening of interstitium (glandular atrophy)

reduce acid secretion and hyper gasrenmia, rebound hypersecretion of HCL

fovular cells, fulled with goblet cell metaplasia developing in asiting of inflammatory backgroung
• Cytotoxin-associated gene A (CagA);
carcinogenic virulence factor of H. pylori.
• Normal gastrin levels, no achlorhydria.
• no anti-parietal cell/anti-intrinsic factor
antibodies (compared to autoimmune
atrophic gastritis; achlorhydria,
antiparietal/anti-intrinsic factor antibodies)
1) secrete urease to split urea into amonia (neutralization to
• Gastric ulcers. acidic medium)
2) it have lysosomal or digestive enzymes like (protease and
urease).
3) these mechanisms of H.pylori (g cell hyperplasia to stimulate
gastren secretion in antrum to stimulate the secretion of HCL
this process called rebound acis secretion
10% of chronic gastritis.
Damage limited to gastric body & fundus.
Inherited autoimmunity against intrinsic factor in
parietal cells→ inhibition of gastric acid
secretion→ achlorhydria→ ↓ intrinsic factor→
B12 malabsorption→ pernicious anemia.
Associated with other autoimmune diseases.
 Features of AG:
• Ab to parietal cells and IF in the serum.
• Decreased s. pepsinogen I.
• Antral endocrine cell hyperplasia.
• Vit. B12 deficiency.
• Defective gastric acid secretion→ impaired iron
absorption, G- cell hyperplasia→ hypergastrinemia
↑neuroendocrine tumor formation.
• ↑risk of neuroendocrine tumor.
• ↑ risk of gastric adenocarcinoma.
 Morphology:
ØDamage to the oxyntic acid producing
mucosa in the body and fundus.
ØAbsent antral and cardia damage.
ØDiffused atrophy, and rugal folds atrophy.
ØLymphocytes, plasma cells and macrophages
in the LP. lamina properia
ØParietal and chief cell loss with intestinal
metaplasia.
 Autoimmune gastritis
lamina properia dystruction, rich in inflammatory cells (lymphoid aggregate),early glandular atrofy,

inflammed stroma and interstetium

AI gastritis same
Thank you