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PATHOLOGYY2S2 > Stomach > Flashcards

Stomach Flashcards

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1
Q

what are the anatomic divisions of the stomach?

A

cardia ( Esoph )

Fundus ( diaph )

body ( acid )

pylorus

greater curvature

lesser curvature

rugae ( the lining of the stomach )

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2
Q

what is the blood supply of the stomach?

A

all 3 classic branches of the celiac axis supply the stomach

common hepatic

left gastric

splenic

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3
Q

what is the venous drainage of the stomach?

A

portal vein

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4
Q

what are the type of mucous cells?

A

surface mucous

mucous neck cell

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5
Q

what is the function of mucous cells?

A

secrete mucous

pepsinogen 2

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6
Q

what is the function of chief cells?

A

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 )

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7
Q

what is the function of parietal cells?

A

HCL and intrinsic factor

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8
Q

what is the function of enteroendocrine cells?

A

ECL —> histamine

somatostatin —> D cells

endothelin

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9
Q

describe the glands lining the cardia?

A

mucin secreting cells ( Mucous cells ) with shallow glands

shallow glands at the cardia because no digestion happen there

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10
Q

describe the glands found in the antrum ( antral glands )?

A

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

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11
Q

describe the glands found in the body and fundus?

A

well developed glands

oxyntic glands

parietal cells —> HCL

chief cells ———-> release pepsin to aid in digestion

well developed glands cuz digestion happen here

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12
Q

what are the damaging forces on the mucosa of the stomach?

A

gastric acidity

peptic enzymes

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13
Q

what are the defensive forces of the stomach mucosa?

A

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

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14
Q

what is the function of prostaglandin ?

A

prostaglandin E

decreases ACID

increase Mucous

help in protection of the stomach mucosa

NSAIDS stop prostaglandin so nsaids will cause stomach ulcer

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15
Q

what stuff can decrease the mucosal defense and increase the damage?

A

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

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16
Q

what is the most common site for ulcer?

A

1st part of the duodenum

Note :

Stomach is less common and cancer present as ulcer in the stomach

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17
Q

what is gastritis?

A

inflammatory disease of the stomach

Very common

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18
Q

what are the types of gastritis?

A

Acute

chronic

Autoimmune

other types :

Eosinophilic

allergic

lymphocytic

Granulomatous

GVH

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19
Q

describe acute gastritis ?

A

hemorrhagic

Transient mucosal ( superficial ) inflammatory process

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20
Q

what is the clinical presentation of acute gastritis ?

A

Asymptomatic

or

Variable degrees of epigastric pain, nausea, vomiting

or

in severe cases : mucosal erosions, ulceration , hemorrhage , hematemesis , melena ( bleeding in the rectum )

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21
Q

what are the causes of acute gastritis?

A

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

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22
Q

what is the problem with ulceration in GIT?

A

cause leakage of content —> Sepsis

this is why appendicitis is critical luli as it can rupture and release its contents into the peritoneum

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23
Q

describe the basic histology of acute/ hemorrhagic gastritis ?

A

erosion

hemorrhage

NEUTROPHILS

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24
Q

describe the histology of MILD acute gastritis?

A

surface epithelium is intact

Scattered neutrophils

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25
describe the histology of SEVERE acute gastritis ?
severe mucosal damage Erosions Loss of superficial epithelium mucosal neutrophilic infiltrates ( neutrophils in the mucosa ) Purulent exudate
26
what is the different between erosion and ulcer?
erosions are more superficial and involve upper layers
27
describe the histology of acute erosive hemorrhagic gastritis?
Erosion + hemorrhage may occur -----> manifest as DARK PUNCTA when it supposed to be HYPEREMIC MUCOSA
28
what is the grossly feature of acute gastritis ?
red dots indicating the hemorrhage and erosion in microscope u will see neutrophilic infiltrates
29
describe chronic gastritis ?
less severe symptoms More persistent NO EROSIONS NO HEMORRHAGE
30
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 )
31
what are 2 most important causes of chronic gastritis ?
Autoimmune ---> Type A ( A- autoimmune ) H pylori ----> Type B ( Bylori )
32
what is the most cause chronic gastritis?
H pylori also most important because it causes both PEPTIC ULCERS and pro inflammation
33
what is the anatomical location of Type A ( Autoimmune )?
Body
34
what is the anatomical location of Type B ( bylori ) ?
Antrum
35
what type of antibodies is found in type A chronic gastritis ( Autoimmune )?
antibodies against the parietal cells ( H/K atapase ) + intrinsic factor
35
what type of antibodies is found in type B ( byloric ) chronic gastritis ?
Antibodies against H pylori
36
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
37
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
38
how diagnose what type of chronic gastritis it is?
Serology test
39
what are the histological features of chronic gastritis ?
NO EROSION OR HEMORRHAGE perhaps some neutrophils Lymphocytes , Lymphoid follicles
40
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
41
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
42
describe the prevelence of helicobacter pylori gastritis?
90% of gastritis Acute + chronic
43
what parts of the stomach is affected by H pylori gastritis ?
Type B --> antrum
44
what does H pyolri do to the acid secretion?
Increase acid secretion ----> peptic ulcer disease of the stomach or duodenum
45
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
46
what does H pylori infection increase the risk of ?
increase the risk of gastric cancer
47
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
48
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
49
what happens in autoimmune gastritis?
destruction of parietal cells
50
what is the location of autoimmune gastritis ?
Type A ----> body and fundus
51
what type of hypersensitivity is autoimmune gastritis ?
T cell mediated + Antibodies against intrinsic factor and parietal cells SO TYPE 4 HYPERSENSITIVTY
52
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
53
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
54
what disease happen due to pernicious anemia and vitamin B12 deficiency?
peripheral neuropathy
55
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
56
autoimmune gastritis results in ?
Atrophy of gastric body glands results in decreased acid production Antral G cell hyperplasia, acholrhydra, vitamin B12 deficiency
57
what is the definition of erosion ?
epithelial disruption within the mucosa BUT NO BREACH OF MUSCULARIS MUCOSA
58
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
59
peptic ulcer disease is associated with which disease ?
H pylori infection NSAID ( aspirin )
60
what is the most common location for peptic ulcer disease ?
First portion of the duodenum (90% ) Gastric antrum
61
what is most important pathogenesis of peptic ulcer disease ?
Gastric hyperacidity ---> most important one other one is cigarrete cuz it causes inflammation
62
what could lead to gastric hyperacidity ?
H pylori infection parietal cell hyperplasia excessive secretory responses impaired inhibition of stimulatory mechanism such as gastrin release
63
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
64
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
65
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
66
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
67
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
68
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 )
69
what are the malignant cancers of the stomach?
adeno- carcinoma lymphoma : 5% ---> mucosa associated lymphoid tissue MALTS / maltomas
70
what are the POTENTIAL malignant tumors of the stomach?
G.I.S.T ---> Gastro Intestinal Stromal Tumor Carcinoid --> neuroendocrine
71
describe gastric polyps ?
Nodules or masses projecting above the level of the surrounding mucosa 5% of upper GIT endoscopies
72
gastric polyps result form what?
Epithelial or stromal cell ---> hyperplasia, inflammation, neoplasia
73
how prevalent are inflammatory and hyperplastic polyps?
75% of gastric polyps ---> most common 50-60 years of age
74
what is the background of inflammatory and hyperplastic polyps ?
Chronic gastritis --> reactive hyperplasia H pylori gastritis polyps regress after bacterial eradication
75
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
76
What are the causes of fundic gland polyps ?
Sporadic ---> no cancer risk familial polyposis ---> dysplasia and cancer Proton pump inhibitors
77
how does PPI cause fundic gland polyps ?
Decrease acid production ----> increase gastrin secretion ----> gastrin stimulates parietal cells ---> glandular hyperplasia
78
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
79
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
80
what is the location of gastric adenoma?
antrum
81
what is the background of gastric adenoma?
chronic gastritis AND atrophy and intestinal metaplasia ( autoimmune gastritis )
82
which type of adenoma has higher cancer risk? gastric adenoma or intestinal adenoma?
Gastric
83
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
84
what is the prevalence of gastric adenocarcinoma ?
90% of all gastric cancer more common in females
85
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
86
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
87
why is cancer of the gastric cardia raising ?
barret esophagus Chronic GERD obesity
88
what are the pathogenesis for gastric adenocarcinoma ?
Mutations H. Pylori EBV --> epstein barr virus
89
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
90
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
91
describe the H. Pylori pathogenesis ?
induce chronic gastritic increased production of proinflammatory proteins ---> IL-1B and TNF
92
describe EBV pathogenesis?
10% of gastric adenocarcinoma
93
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
94
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
95
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
96
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
97
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
98
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
99
what is the most common form mesenchymal neoplasm of GIT ?
Gastro intestinal stromal tumor ( GIST ) 10% of the whole Gastric cancers --> 90% are adenocarcinoma
100
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
101
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

PATHOLOGYY2S2 (12 decks)

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