Stomach Flashcards
what are the anatomic divisions of the stomach?
cardia ( Esoph )
Fundus ( diaph )
body ( acid )
pylorus
greater curvature
lesser curvature
rugae ( the lining of the stomach )
what is the blood supply of the stomach?
all 3 classic branches of the celiac axis supply the stomach
common hepatic
left gastric
splenic
what is the venous drainage of the stomach?
portal vein
what are the type of mucous cells?
surface mucous
mucous neck cell
what is the function of mucous cells?
secrete mucous
pepsinogen 2
what is the function of chief cells?
produce pepsinogen 1
both pepsinogen 1 and 2 are activated into pepsin when it comes in contanct with acid produced by gastric parietal cells ( HCL )
what is the function of parietal cells?
HCL and intrinsic factor
what is the function of enteroendocrine cells?
ECL —> histamine
somatostatin —> D cells
endothelin
describe the glands lining the cardia?
mucin secreting cells ( Mucous cells ) with shallow glands
shallow glands at the cardia because no digestion happen there
describe the glands found in the antrum ( antral glands )?
antral glands are similar but contain endocrine cells —>
G cells –> release gastrin to stimulate luminal acid secretion ( HCL ) by partietal cells
shallow like cardia cuz no digestion happen here
describe the glands found in the body and fundus?
well developed glands
oxyntic glands
parietal cells —> HCL
chief cells ———-> release pepsin to aid in digestion
well developed glands cuz digestion happen here
what are the damaging forces on the mucosa of the stomach?
gastric acidity
peptic enzymes
what are the defensive forces of the stomach mucosa?
Surface mucous layer
Bicarbonate secretion into mucus ( to neutralize acid )
Mucosal blood flow ( To help regenerate )
apical surface
membrane transport
epithelial regenerative capacity
elaboration of prostaglandins
what is the function of prostaglandin ?
prostaglandin E
decreases ACID
increase Mucous
help in protection of the stomach mucosa
NSAIDS stop prostaglandin so nsaids will cause stomach ulcer
what stuff can decrease the mucosal defense and increase the damage?
H pylori infections –> proinflammation
Ischemia
NSAIDS
Alcohol
cigarettes
gastric hyperacidity
Duodenal gastric reflux
Shock ( no blood supply )
delayed gastric emptying —> LEAD TO INCREASED ACID
Host factors
what is the most common site for ulcer?
1st part of the duodenum
Note :
Stomach is less common and cancer present as ulcer in the stomach
what is gastritis?
inflammatory disease of the stomach
Very common
what are the types of gastritis?
Acute
chronic
Autoimmune
other types :
Eosinophilic
allergic
lymphocytic
Granulomatous
GVH
describe acute gastritis ?
hemorrhagic
Transient mucosal ( superficial ) inflammatory process
what is the clinical presentation of acute gastritis ?
Asymptomatic
or
Variable degrees of epigastric pain, nausea, vomiting
or
in severe cases : mucosal erosions, ulceration , hemorrhage , hematemesis , melena ( bleeding in the rectum )
what are the causes of acute gastritis?
NSAIDS ( Particularly aspirin ) cuz it reduces prostaglandin and bicarbonate
Excessive alcohol consumptions
Heavy smoking
Severe stress ( trauma , burns , surgery )
chemotherapy
gastric irradiation or freezing
ischemia and shock
suicidal attempts as with acids and alkali
mechanical ( nasogastric intubation - tube from the nose to the stomach )
Distal gastrectomy
what is the problem with ulceration in GIT?
cause leakage of content —> Sepsis
this is why appendicitis is critical luli as it can rupture and release its contents into the peritoneum
describe the basic histology of acute/ hemorrhagic gastritis ?
erosion
hemorrhage
NEUTROPHILS
describe the histology of MILD acute gastritis?
surface epithelium is intact
Scattered neutrophils
describe the histology of SEVERE acute gastritis ?
severe mucosal damage
Erosions
Loss of superficial epithelium
mucosal neutrophilic infiltrates ( neutrophils in the mucosa )
Purulent exudate
what is the different between erosion and ulcer?
erosions are more superficial and involve upper layers
describe the histology of acute erosive hemorrhagic gastritis?
Erosion + hemorrhage may occur —–> manifest as DARK PUNCTA when it supposed to be HYPEREMIC MUCOSA
what is the grossly feature of acute gastritis ?
red dots indicating the hemorrhage and erosion
in microscope u will see neutrophilic infiltrates
describe chronic gastritis ?
less severe symptoms
More persistent
NO EROSIONS
NO HEMORRHAGE
what are the causes of chronic gastritis ?
Chronic infection by H pylori ( most common )
Autoimmune gastritis ( atrophic gastritis )
alcohol and cigarette smoking
Postsurgical , reflux of bile
Motor and mechanical : obstructions , bezoars ( luminal concretions ) , gastric atony
Radiations
granulomatous conditions ( crohn disease )
what are 2 most important causes of chronic gastritis ?
Autoimmune —> Type A ( A- autoimmune )
H pylori —-> Type B ( Bylori )
what is the most cause chronic gastritis?
H pylori
also most important because it causes both PEPTIC ULCERS and pro inflammation
what is the anatomical location of Type A ( Autoimmune )?
Body
what is the anatomical location of Type B ( bylori ) ?
Antrum
what type of antibodies is found in type A chronic gastritis ( Autoimmune )?
antibodies against the parietal cells ( H/K atapase ) + intrinsic factor
what type of antibodies is found in type B ( byloric ) chronic gastritis ?
Antibodies against H pylori
compare the 2 types in term of acid production ?
in Type A ( autoimmune ) —> antibodies will destroy parietal cells –> LESS ACID
in Type B ( byolri ) —> inflammation due to infection and more ACID
compare the 2 types in term of Gastrin secretion ?
In Type A we have low acid cuz parietal cells are destroyed —> Gastrin will increase to compensate
in Type B –> normal gastrin
how diagnose what type of chronic gastritis it is?
Serology test
what are the histological features of chronic gastritis ?
NO EROSION OR HEMORRHAGE
perhaps some neutrophils
Lymphocytes , Lymphoid follicles
what are the regenerative changes that happen in chronic gastritis?
Metaplasia—> intestinal —> due to prolonged inflammation
Atrophy —> Mucosal hypoplasia —> thinning —> ONLY IN AUTOIMMUNE
Dysplasia —-> due to metaplasia due to prolonged inflammation
what do you usually see under the microscope in both types of chronic gastritis?
Type A —> Lymphocytes and lymphoid follicle + ATROPHY
Type B —–> inflammatory cells like neutrophils
Regeneration in both
describe the prevelence of helicobacter pylori gastritis?
90% of gastritis
Acute + chronic
what parts of the stomach is affected by H pylori gastritis ?
Type B –> antrum
what does H pyolri do to the acid secretion?
Increase acid secretion —-> peptic ulcer disease of the stomach or duodenum
what does H pyolri produce?
Ureases —> urea to ammonia CO2 which is toxing to epithelial cells but protects bug from acid
Proteases
Vacuolating cytotoxin A ( VacA ) —–> damage epithelium , cause apoptosis , disrupt tight junction
Cytotoxin-associated gene A ( CagA )
Phosoplipases
all of these damage the endothelium especially the ureases
what does H pylori infection increase the risk of ?
increase the risk of gastric cancer
what are the 4 features of H pylori virulence ?
Flagella —-> Motile in viscous mucus
Urease —> Generate ammonia from endogenous urea —> elevate local gastric PH around organism and protect the bacteria from acidity
Adhesins —> Enhance bacterial adherence to surface cells
Toxins
how does H pyloric gastritis cause inflammatory polyps ?
inflammation—-> overcrowding of cells and hyperplasia occur to the point where they start bulging out of the lumen epithelium
what happens in autoimmune gastritis?
destruction of parietal cells
what is the location of autoimmune gastritis ?
Type A —-> body and fundus
what type of hypersensitivity is autoimmune gastritis ?
T cell mediated
+
Antibodies against intrinsic factor and parietal cells
SO TYPE 4 HYPERSENSITIVTY
what are the characteristics of autoimmune gastritis ?
Atrophy of mucosa
Decreased acid production —> achlorhydria —-> INCREASED GASTRIN LEVELS TO COUNTER THE LOW ACID
Megaloblastic - pernicious anemia —> because antibodies destroy the intrinsic factors from parietal cells so no Vitamin B12 binding to the factor and no vitamin B12-IF complex to be absorbed in the terminal ileum
IT IS THE MOST COMMON CAUSE FOR VITAMIN B12 DEFICIENCY
what happens to the G cells in autoimmune gastritis ?
Hypertrophy because theres an increased production of Gastrin due to low acid cuz again parietal cells are getting attacked
what disease happen due to pernicious anemia and vitamin B12 deficiency?
peripheral neuropathy
what risk is elevated cuz of autoimmune gastritis?
Gastric adenocarcinoma :
due to chronic inflammation and intestinal metaplasia
due to inflammatory infiltrate
metaplasia due to lymphocyte signaling
autoimmune gastritis results in ?
Atrophy of gastric body glands
results in decreased acid production
Antral G cell hyperplasia, acholrhydra, vitamin B12 deficiency
what is the definition of erosion ?
epithelial disruption within the mucosa BUT NO BREACH OF MUSCULARIS MUCOSA
What is the definition of Ulcer?
Breach in the mucosa that extend through the muscularis mucosa into SUBMUCOSA OR DEEPER or could even involve all the layers
peptic ulcer disease is associated with which disease ?
H pylori infection
NSAID ( aspirin )
what is the most common location for peptic ulcer disease ?
First portion of the duodenum (90% )
Gastric antrum
what is most important pathogenesis of peptic ulcer disease ?
Gastric hyperacidity —> most important one
other one is cigarrete cuz it causes inflammation
what could lead to gastric hyperacidity ?
H pylori infection
parietal cell hyperplasia
excessive secretory responses
impaired inhibition of stimulatory mechanism such as gastrin release
what are cofactors that could increase the ulcerogenesis?
Cigarette smoking —> impairs mucosal blood flow and healing
High dose corticosteroids –> suppress Prostaglandins synthesis and impair healing
Alcoholic , cirrhosis , chronic obstructive pulmonary disease , chronic renal failure , hyperparathyroidism
describe the gross morphology of Peptic ulcer?
80% —-> Solitary , 20% –> multiple
shallow lesions —> less than 0.3 cm
deep lesions —–> more than 0.6 cm
what are the characteristics of classic peptic ulcer?
round to oval in shape
punched out defect
the base is smooth and clean —> peptic digestion of exudate
what is the extract location of stomach peptic ulcer?
few cm of the pyloric valve
located near the interface of the body and antrum
4 times in the proximal duodenum than the stomach
most prone part is the pylorus
in regard to malignancy in which type of peptic ulcer its most common in?
duodenal ulcers are nearly never malignant - duodenal so carcinoma is very very rare
gastric ulcer maybe due to gastric carcinoma
what are benign tumors of the stomach?
Polyps —-> hyperplastic or adenomatous
Leiomyomas —> same gross and micro as smooth muscles ( lie = smooth muscle )
Lipomas —> same gross and micro adipose tissue ( lipo = fat )
what are the malignant cancers of the stomach?
adeno- carcinoma
lymphoma : 5% —> mucosa associated lymphoid tissue MALTS / maltomas
what are the POTENTIAL malignant tumors of the stomach?
G.I.S.T —> Gastro Intestinal Stromal Tumor
Carcinoid –> neuroendocrine
describe gastric polyps ?
Nodules or masses projecting above the level of the surrounding mucosa
5% of upper GIT endoscopies
gastric polyps result form what?
Epithelial or stromal cell —> hyperplasia, inflammation, neoplasia
how prevalent are inflammatory and hyperplastic polyps?
75% of gastric polyps —> most common
50-60 years of age
what is the background of inflammatory and hyperplastic polyps ?
Chronic gastritis –> reactive hyperplasia
H pylori gastritis polyps regress after bacterial eradication
what are the characteristics of Polyps?
Multiple , ovoid , less than 1 cm , smooth surface cover
irregular , cystically dilated, elongated foveolar glands
Larger polyps more than 1.5cm HIGHER RISK FOR DYSPLASIA
What are the causes of fundic gland polyps ?
Sporadic —> no cancer risk
familial polyposis —> dysplasia and cancer
Proton pump inhibitors
how does PPI cause fundic gland polyps ?
Decrease acid production —-> increase gastrin secretion —-> gastrin stimulates parietal cells —> glandular hyperplasia
what are the characteristics of fundic gland polyps?
Well circumscribed
occur in gastric body and fundus
Multiple , irregular glands lined by flattened PARIETAL AND CHIEF CELLS
BOTH FUNDIC AND INFLMMATORY AND HYPERPLASTIC POLYPS ARE NON NEOPLASTIC
what is the prevalence of gastric adenoma ?
10% of all gastric polyps
increases with age ( 50 and 60 years of age )
more common in males 3:1
what is the location of gastric adenoma?
antrum
what is the background of gastric adenoma?
chronic gastritis AND atrophy and intestinal metaplasia ( autoimmune gastritis )
which type of adenoma has higher cancer risk? gastric adenoma or intestinal adenoma?
Gastric
what are the characteristics of gastric adenoma?
intestinal type columnar epithelium
exhibit epithelial dysplasia —> low or high grade
large size adenoma MORE THAN 2 CM could become adenocarcinoma
what is the prevalence of gastric adenocarcinoma ?
90% of all gastric cancer
more common in females
what is the most common disease associated with gastric adenocarcinoma?
H. pylori ( MASSIVELY )
other risk factors :
alcohol
smoking
Socioeconomically : excessive consumption of salted fish, pickled vegetables and cured meats
what is the most common countries for gastric adenocarcinoma?
japan
Chile
costa rica
eastern europe
there are mass endoscopic screening programs in japan
35% of the newly detected cases are early gastric cancer
incidence dropped in USA and western countries due to environmental and dietary factors
why is cancer of the gastric cardia raising ?
barret esophagus
Chronic GERD
obesity
what are the pathogenesis for gastric adenocarcinoma ?
Mutations
H. Pylori
EBV –> epstein barr virus
describe the mutation pathogenesis?
Majority are not hereditary
Loss E-Cadherin function 50% of cases —-> Diffuse gastric cancer ( familial gastric cancers )
Patients with familial adenomatous polyposis (FAP) with germline mutations in adenomatous polyposis coli (APC ) genes have increased risk FOR :
Intestinal type gastric cancer
what are the mutations for sporadic adenocarcinoma ?
P53 mutations
APC —> FAP folks also at risk
Familial : loss of function of CDH1 mutation / silencing ——> CODES FOR E CADHERIN
describe the H. Pylori pathogenesis ?
induce chronic gastritic
increased production of proinflammatory proteins —> IL-1B and TNF
describe EBV pathogenesis?
10% of gastric adenocarcinoma
what are the classifications of adenocarcinoma ?
Classified according their locations in the stomach as well as gross and histology morphology
Lauren classifications : intestinal and diffuse type
describe intestinal gastric cancer ?
area of intestinal metaplasia
Tumor cells are well differentiated
Grow slowly and tend to form glands
men > women
older people
Form either an exophytic mass or an ulcerated tumor
Elevated mass with heaped up borders and central ulcerations :
most at the lesser curvature of antrum
Due to chronic inflammation
describe the diffuse type of gastric cancer?
Infiltrate deeply without mass but SPREAD WIDELY in the gastric wall
poorly differentiated , behave aggressively
men = women
younger age
the gastric wall is markedly thickened and rugal folds are partially lost:
No E cadherin -No attachment - hence diffusely distribute
what are the grossly characteristics of diffuse infiltrative adenocarcinoma ?
Linitis plastica :
Grows diffusely through ALL LAYERS OF STOMACH
Greatly thickening its wall + giving the stomach classic LEATHER BOTTLE appearance —> horrible prognosis
what are the microscopic of diffuse infiltrative gastric adenocarcinoma ?
Large mucin vacuoles
expand the cytoplasm and push the nucleus to the periphery creating a signet ring cell —> poorly differentiating cells
what are the other microscopic patterns of diffuse infiltrative gastric adenocarcinoma ?
all of them are glandlike structure :
Papillary
Tubular
Mucinous : ocean of mucin
adenosquamous —> squamous pattern
all of them are gland like structure but different variations
what is the most common form mesenchymal neoplasm of GIT ?
Gastro intestinal stromal tumor ( GIST )
10% of the whole Gastric cancers –> 90% are adenocarcinoma
what are the characteristics of GIST?
Stroma and not glandular
can behave and/or look benign or malignant
Look like smooth muscles i.e stroma, spindly, thin, whirly and poorly differentiated ——> hard to diagnosis cuz look similar to smooth cells
what do the cells usually express in GIST?
positive for c-KIT ( CD117 ) —> express this antigen on immunochemical staining —> diagnosis
immunochemistry IS IMPORTANT FOR DIAGNOSIS
