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GI2 E1 > stomach > Flashcards

stomach Flashcards

robbins

1
Q

differentiate between acute gastritis and gastropathy

A

acute gastritis= acute gastric mucosal inflammation with neutrophils present

gastropathy= mucosal injury without inflammatory cells (or rare inflammatory cells)

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2
Q

what are the two examples of hypertrophic gastropathy

A

ménétrier ds

zollinger-ellison syndrome

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3
Q

what factors will cause gastropathy

A

NSAIDs, alcohol, bile, and stress induced injusry

ulcers, lesions s/p decreased perfusion, portal HTN –> gastropathy –> gastritis

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4
Q

list the protective and damaging factors that effect gastric mucosa

A

protective=
mucus secretions, bicarb, blood flow, epithelial barrier + regeneration capacity, prostaglandins

damaging=
acidity, peptic enzymes, H. Pylori, NSAIDs, tobacco, alc, duodenal-gastric reflux, ischemia, shock

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5
Q

what is the function of foveolar cells

A

secrete mucin, bicarb

complete replacement of the surface foveolar cells every 3-7 days is essential for the maintenance of the epithelial layer

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6
Q

what is the function of parietal cells

A

secrete HCl into the gastric lumen and bicard into the mucosal vasculature

= capillary ‘alkaline tide”

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7
Q

what are the two functions of mucosal vasculature in the stomach

A

delivers O2 and nutrients while washing away acid that has back diffused into the lamina propria and delivering bicarb

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8
Q

relate the use of NSAIDS to gatritis

A

NSAIDs inhibit COX–> inhibit synthesis of prostaglandins E2+ I2

greatest injury with nonselective COX inhibitors= aspirin, ibuprofen, naproxen

also injurious to have COX2 specific inhibition= celecoxib

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9
Q

how does H. Pylori cause injury leading to gastritis

A

urease secreting H. Pylori can inhibit gastric bicarb transporters by ammonium ions

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10
Q

reduced mucin and bicarb secretion in ______ patients predisposes them to developing gastritis

A

older

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11
Q

relate high altitudes to developing gastritis

A

decreased O2= decreased protective factors produced

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12
Q

foveolar cell hyperplasia, slight vasculature congestion, corkscrew profiles and epithelial proliferation

mucosal infiltrate and fibrin containing purulent exudate int he lumen, with possible hemorrhage and dark punctae in hyperemic mucosa

A

gastropathy and mild acute gastritis

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13
Q

(in stomach) the presence of _____ above the basement membrane and in direct contact with epithelial cells signifies active gastritis

A

neutrophils

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14
Q

describe the clinical presentation of NSAID-induced gastropathy

A

asymptomatic or persistent epigastric pain that responds to antacids or PPIs

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15
Q

describe the clinical presentation associated with bile reflux induced gastropathy

A

pain is refractory to therapy and may be accompanied by occasional bilious vomiting

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16
Q

more than 75% of critically ill patients develop endoscopically visible ___ _____ during the first 3 days of their illness

A

gastric lesions

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17
Q

___ ____ are the most common in people with shock, sepsis, or severe trauma

A

stress ulcers

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18
Q

______ are ulcers associated with severe burns and trauma, that occur in the ____ ____

A

curling ulcer, proximal duodenal

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19
Q

________ are ulcers associated with intracranial disease that arise in the ____, _____, and ____. they carry a ____ incidence of perforation

A

cushing ulcers
stomach, duodenum, esophagus
high

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20
Q

describe the etiology of how stress ulcers form

A

stress from systemic hypotension or reduced blood flow

upregulation of inducible NO synthase and endothelin 1–> ischemic gastric mucosal injury

intracranial injury–> direct stimulation of vagal nuclei–> hypersecretion of gastric acid –> lowering intracellular pH of mucosal cells

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21
Q

found anywhere in the stomach, rounded and less than 1 cm. stained brown/black by acid digestion at the base, can be associated with transmural inflammation and local serositis, sharply demarcated next to normal adjacent mucosa

A

acute STRESS ulcer (not a peptic ulcer)

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22
Q

differentiate between the morphology of an acute and chronic stress ulcer in the stomach

A

chronic do not have scarring and blood vessel thickenings that are in acute stress ulcers

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23
Q

____ _____ may blunt the impact of stress ulceration in critically ill patients, but the most important determinant of clinical outcome is the ability to _____________

A

prophylactic PPIs

correct the underlying condition

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24
Q

what are the two non-stress related causes of gastric bleeding

A

dieulafoy lesions and gastric antral vascular ectasia (GAVE)

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25
Q

what is the etiology of a dieulafoy lesion

A

= a submucosal A that doesn’t branch properly within the wall of the stomach, resulting in an A up to 10x the size of mucosal capillaries

bleeding is self-limited and can be associated with NSAID use (recurrent)

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26
Q

where are dieulafoy lesions most commonly found

A

the lesser curvature of the stomach

near the GE junction

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27
Q

(in the stomach) ‘longitudinal stripes of edematous erythematous mucosa that alternate with less severely injured, paler mucosa” “watermelon stomach”

A

GAVE (gastric antral vascular ectasia)

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28
Q

in the stomach, histology of antral mucosa shows reactive gastropathy with dilated capillaries containing fibrin thrombi

A

GAVE (gastric antral vascular ectasia)

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29
Q

while most often ___, GAVE can be associated with ___ and ______. patients usually present with ________ or _________

A

idiopathy
systemic sclerosis
occult fecal blood
iron deficiency anemia

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30
Q

the most common cause of chronic gastritis

A

H. Pylori

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31
Q

the most common cause of diffuse atrophic gastritis

A

autoimmune gastritis

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32
Q

clinical presentation of H. Pylori

A

less severe and more persistent compared to acute gastritis

nausea, upper abd pain, vomiting

RARELY hematemesis

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33
Q

H. Pylori is a __-shaped or ____bacilli and is present in almost all patients with ____ ulcers

A

spiral, curved

duodenal

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34
Q

acute H. Pylori does not produce _____ _____ to be caught. in most cases, it is the ___ ___ that causes individuals to seek trx

A

sufficient sx

chronic gastritis

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35
Q

what epidemiological factors are associated with H. Pylori

A

poverty, household crowding, limited education, African Americans+ Mexican Americans, rural areas, birth outside of the US

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36
Q

H. Pylori is transmitted via the _____ route and is typically acquired in ______ and persists throughout life _____

A

fecal-oral

childhood, without trx

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37
Q

H. Pylori most often presents as …

A

a predominantly antral gastritis with normal or increased acid production

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38
Q

As in the case of H. Pylori, when ____ is limited to the antrum, increased ____ production results in a greater disk for duodenal ulcers

A

inflammation

acid

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39
Q

H. Pylori gastritis spreading to the body and fundus is called ___ ____ ____. In this condition, there is an ____ risk of gastric adenocarcinoma. thus, there is an ___ relationship between duodenal ulcer and gastric adenocarcinoma

A

multifocal atrophic gastritis
increased
inverse

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40
Q

the virulence of H. Pylori is linked to what factors

A

flagella
urease, elevating local gastric pH to allow for survival
adhesins, adhese to foveolar cells
toxins = CagA

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41
Q

Cag A, produced by _____, leads to an increased risk of _______

A

H. Pylori,

gastric adenocarcinoma

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42
Q

(in the context of H. Pylori infection) genetic mutations that lead to increased production of __ and ___ or decreased expression of ____ are associated with increased risk of pangastritis, atrophy, and gastric CA. __ ___ may also be risk factor of H. Pylori associated-gastric C

A

TNF, IL-1B
IL-10
iron deficiency

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43
Q

where in the stomach are H. Pylori most often found, which is directly related to the increased risk of ___ ____

A

antrum

duodenal ulcers

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44
Q

gastric antrum viewed endoscopically is erythematous and has a coarse/nodular appearance, with neotrophils within the lamina propria accumulating in the lumen to create abscesses

A

H. Pylori infected antrum

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45
Q

the presence of what two cell types is characteristic of H. Pylori infection

A

intraepithelial neutrophils

subepithelial plasma cells

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46
Q

long standing H. pylori gastritis can spread to the body and fundus, causing a loss in ___ and ___ cells, causing the oxyntic mucosa to take on the appearance of antral mucosa

A

parietal , chief

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47
Q

what are the diagnostic tests for H. Pylori infection

A

noninvasive serologic tests for Ab against H. Pylori
fecal bacterial detection
urea breath test
gastric biopsy–> rapid urease test, bacterial culture, PCR

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48
Q

what are the effective trx for H. Pylori

A

abx and PPIs for at least 10-14 days

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49
Q

in contrast to H. Pylori associated, autoimmune gastritis typically spares the __ and is associated with _____

A

antrum

hypergastrinemia

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50
Q 
autoimmune gastritis is associated with 
Ab against \_\_\_\_\_\_ and \_\_\_\_
\_\_\_\_ levels of serum pepsinogen I
endocrine cell \_\_\_\_\_
Vit \_\_\_ deficiency
\_\_\_\_ gastric acid secretion ( \_\_\_\_\_)
A 
parietal cells, intrinsic factors
reduced
hyperplasia
B12
defective, achlorhydria
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51
Q

what are the inflammatory infiltrates for H. Pylori associated and autoimmune gastritis

A

H. Pylori = Nø, subepithelial plasma cells

autoimmune= lymphocytes, Mø

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52
Q

describe acid production in H. Pylori associated and autoimmune gastritis

A

H. Pylori= increased to slightly decreased

autoimmune= decreased

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53
Q

describe gastric levels in H. Pylori associated and autoimmune gastritis

A

h pylori= normal to decreased

autoimmune= increased (neuroendocrine hyperplasia)

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54
Q

describe the gastric mucosa lesions associated with H. Pylori associated and autoimmune gastritis

A

h pylori –> hyperplastic/inflammatory polyps

autoimmune= neuroendocrine hyperplasia

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55
Q

describe the serology results in H. Pylori associated and autoimmune gastritis

A

h pylori= ab against h pylori

autoimmune= ab against parietal cells (H/K ATPase, intrinsic factor)

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56
Q

what are the sequelae of H. Pylori associated and autoimmune gastritis

A

h pylori = peptic ulcer, adenocarcinoma, MALToma

autoimmune= atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor

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57
Q

what conditions are associated with autoimmune gastritis

A

thyroiditis, DM, Graves disease

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58
Q

describe how autoimmune gastritis results in pernicious anemia

A

Ab-parietal cells –> x parietal cells –> decreased intrinsic factor –> decreased B12 absorbed in intestine –> pernicious anemia

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59
Q

describe how autoimmune gastritis results in hypergastrinemia

A

Ab-parietal cells –> x parietal cells –> decreased gastric acid –> increased gastrin production + hyperplasia of G cells in antrum –> super increased gastrin production = hypergastrinemia

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60
Q

_______ are considered to be the principal agents of injury in autoimmune gastritis, attacking parietal cell components like the _______

A

CD4 T cells

H/K ATPase

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61
Q

in autoimmune gastritis, reduced ______ results from chief cell destruction, which is achieved through ___________ during the autoimmune attack on parietal cells

A

serum pepsinogen 1 concentration,

gastric gland destruction

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62
Q

Ab are not thought to be pathogenic in autoimmune gastritis because

A

neither secreted IF nor luminally oriented PPIs are accessible to circulating Abs

63
Q

oxyntic mucosa appears markedly thinned and rugal folds are lost.
when incomplete can get a nodular appearance, or intestinal metaplasia characterized by the presence of goblet cells and columnar absorptive cells

A

diffuse gastric atrophy related to autoimmune gastritis

64
Q

in autoimmune gastritis, if Vit B12 loss is extensive, it can lead to what kind of change

A

megaloblastic change= nuclear enlargment

65
Q

describe the clinical presentation of autoimmune gastritis

A

because it takes decades to progress, the median age of diagnosis is 60, with more women than men

have sx of anemia,
atrophic glossitis secondary to Vit B12 deficiency,
epithelial megaloblastosis,
malabsorptive diarrhea,
peripheral neuropathy, spinal cord lesions, and cerebral dysfunction, parasthesias and numbness

66
Q

in autoimmune gastritis, the demyelination of the ___ and ___ spinal tracts can give rise to ___ ____ ____ __ ____ ____, resulting in the following clinical signs: ____

A

dorsal, lateral, subacute combined degeneration of the cord

loss of vibration and position sense, sensory ataxia with a + Romberg sign, limb weakness, spasticity, extensor plantar responses, mild personality changes and memory loss to psychosis

67
Q

in autoimmune gastritis, unlike anemia, neurologic changes are _____ by Vit B replacement

A

not reversible

68
Q

(stomach) tissue damage associated with dense infiltrates of eosinophils in the mucosa and muscularis, in the antrum or pyloris

A

eosinophilic gastritis

69
Q

what are the most common causes of eosinophilic gastritis

A

allergies to dairy and soy

70
Q

in what population is lymphocytic gastritis most common

A

women, those with celiac ds

71
Q

in stomach= thickened folds covered by small nodules with central aphthous ulceration, marked increase in the number of intraepithelial T lymphocytes

A

lymphocytic gastritis/ varioliform gastritis

72
Q

what are the most common causes of granulomatous gastritis

A

Crohn ds, sarcoidosis, infections

73
Q

what are risk factors of PUD

A

PUD is a complication of chronic gastritis

risk with H. Pylori, cigarettes, CV disease, COPD, illicit drugs, NSAIDs, alcoholic cirrhosis, psych stress, zollinger ellison, vital infection with CMV, herpes

74
Q

the most common form of PUD occurs within the gastric ____ or _____ as a result of chronic ______-associated gastritis associated with increased ______ and decreased _________ secretions

A

atrum, duodenum
H. Pylori
gastric acid, duodenal bicard

75
Q

PUD within the gastric ____ or ____ are generally protected form ___ and ____ because, which they have increased acid production, they don’t make enough

A

fundus, body

antral and duodenal ulcers

76
Q

growing incidence of PUD is seen in patients _______ because of increased ____ use

A

older than 60 y.o

NSAID

77
Q

because PUD results from an imbalance between mucosal protection and damage, it usually develops on a background of ______, though they are most common in the _____

A

chronic gastritis,

proximal duodenum

78
Q

gastric peptic ulcers are mostly located _____, near the interface of the ___ and ____

A

lesser curvature, body and antrum

79
Q

(in the stomach) usually solitary lesions. round-oval, sharply punched out defect and usually level with the surrounding mucosa

A

peptic ulcers

80
Q

perforation of peptic ulcers is a ___ ___, and may be identified by ____

A

surgical emergency,

detection of free air under the diaphragm on upright radiographs of the abdomen

81
Q

malignant transformation of peptic ulcers is

A

very rare

82
Q

the majority of peptic ulcers come to clinical attention because of ____, though some also come in because of

A

epigastric burning or aching pain

iron deficiency anemia, hemorrhage, or perforation

83
Q

describe clinical sx of PUD

A

pain occurs 1-3 hours after meals during the day, worse at night, relieved by alkali or food
N/V, bloating, belching

84
Q

trx of PUD

A

H. Pylori eradication, neutralization of gastric acid with PPIs, withdraw offending agents

85
Q

2/3 of deaths due to PUD occur because

A

perforation

86
Q

H Pylori gastritis induces _____ that can give rise to B cell lymphomas ( __ )

A

MALT

MALTomas

87
Q

the risk of adenocarcinoma is greatest in _____ gastritis

A

autoimmune

88
Q

epithelial exposure to ___ and ____ with chronic gastritis can lead to dysplasia

A

free radicals and proliferative stimuli

89
Q

hyperchromasia and nuclear enlargement of histologic changes associated with

A

dysplasia

90
Q

reactive epithelial cells ____ as they reach the mucosal surface, while dysplastic lesions remain ___. this shows as normal growth becoming ___ to the basement membrane, while dysplasia stays ___

A

mature
immature
perpendicular
parrallel

91
Q

(in the stomach) reactive epithelial proliferation in responde to trauma, can mimic invasive adenocarcinoma

A

gastritis cystica

92
Q

giant “cerebriform” enlargement of the rugal folds due to epithelial hyperplasia without inflammation

A

hypertrophic gastropathies

93
Q

what are the two examples of hypertrophic gastropathies

A

menetrier ds and zollinger ellison syndrom

94
Q

what is the etiology and histologic change associated with menetrier ds

A

-excessive secretionof TGFα,

diffuse hyperplasia of the foveolar epithelium of the body and fundus of the stomach, irregular enlargement of teh gastric rugae with the antrum generally spared
glands elongated in corkscrew appearance and cystic dilation

95
Q

what are the clinical sx of menetrier ds

A

weight loss, diarrhea, and peripheral edema (due to hypoproteinemia

96
Q

menetrier ds in children is different than in adults in that in children the ds is usually ____ and often follows a _____

A

self-limited, respiratory infection

97
Q

which hypertrophic gastropathies and gastric polyps are associated with adenocarcinoma

A

menetrier ds
gastric adenoma
FAP syndrome (fundic gland polyps)

98
Q

what are the main sx of zollinger ellison ds

A

peptic ulcers

99
Q

what is the clinical presentation of inflammatory and gastric polyps

A

look like chronic gastritis

100
Q

what is the clinical presentation of gastric adenoma

A

presents like chronic gastritis

101
Q

what is the inflammatory infiltrate in menetriere ds

A

limited, if any they’re lymphocytes

102
Q

what is the inflammatory infiltrate in zollinger-ellison syndrome

A

neutrophils

103
Q

what sx present with zollinger ellison syndrome

A 
peptic ulcers (duodenal)
chronic diarrhea
104
Q

what is the inflammatory infiltrate in inflammatory and hyperplastic polyps

A

neutrophils and lymphocytes

105
Q

what is the inflammatory infiltrate in gastric cystica

A

neutrophils and lymphocytes

106
Q

what inflammatory infiltrates are present in fundic gland polyps

A

NONE

107
Q

in what hypertrophic gastropathies/gastric polyps is mucous cells the predominant cell type

A

menetriere ds
inflammatory and hyperplastic polyps
gastritis cystica

108
Q

in what hypertrophic gastropathies/gastric polyps is parietal cells the predominant cell type

A

zollinger ellison syndrome

109
Q

in what hypertrophic gastropathies/gastric polyps is parietal and chief cells the predominant cell type

A

fundic gland polyps

110
Q

what is the mean patient age for menetrier ds

A

30-60

111
Q

what is the mean patient age for zollinger ellison syndrome

A

50

112
Q

what is the mean patient age for inflammatory and hyperplastic polyps

A

50-60

113
Q

what is the mean patient age for fundic gland polyps

A

50

114
Q

what is the population most commonly seen with gastric adenomas

A

50-60, men

115
Q

what is the treatment for menetriere ds

A

IV albumin and parenteral nutritional supplementation

agents that block TGF a mediated activation of epidermal GF

116
Q

what is the cause of zollinger ellison syndrome

A

gastrin secreting tumors

117
Q

doubling of oxyntic mucosal thickness due to 5x increase in the number of parietal cells,

A

zollinger ellison syndrome

118
Q

____ induces hyperplasia of mucous neck cells, mucin hyperproduction, and proliferation of endocrine cells in ___ syndrome

A

gastrin

zollinger-ellson

119
Q

what is the treatment of zollinger ellison syndrome

A

blockade of acid hypersecretion- PPIs

treatment of the gastrinoma is the main determinant of long-term survival

120
Q

in zollinger ellison syndrome, though slow growing, most gastrinomas are ____. 1/4 of them are associated with _____

A

malignant

MEN1

121
Q

what risk factors lead to presence of fundic gland polyps

A

FAP= familial adenomatous polyposis

increased use of PPIs

122
Q

risk of adenocarcinoma in gastric adenomas is related to the _____ of the lesion, and is particularly increased in lesions _____

A

size, >2 cm in diameter

123
Q

risk of gastric adenomas

gastric adenomas (>/=) intestinal adenomas

A

>

124
Q

the most common malignancy of the stomach

A

adenocarcinoma

125
Q

most common sites of gastric CA metastasis

A 
supraclavicular sentinal LN (virchow node)
periumbilical LN
L axillary LN
ovary
pouch of Douglas
126
Q

what are risk factors for gastric CA

A

lower SES

multifocal mucosal atrophy, intestinal metaplasia

127
Q

white PUD does not increase risk for gastric CA, those who have partial ____ have a higher risk of developing CA in the ____

A

gastrectomies

residual gastric stump

128
Q

____, caused by loss of function of ___, is the key step to developing diffuse gastric CA

other genetic mutations that increase risk of diffuse gastric CA are ___ and ____

A

loss of E-cadherin, CHD-1

x BRCA2, xTP53

129
Q

genetic mutations that lead to sporadic intestinal type gastric CA

A

increase Wnt pathway signalling

LOF of APC gene,
GOF of B-catenin encoding genes
LOF of TGFB, BAX, CDKN2A

130
Q

most adenocarcinoma of the stomach exist in the ___, along the ____ curvature

A

antrum

lesser

131
Q

due to _____, some gastric adenocarcinomas will not form glands but rather have large mucin vacuoles that push the nucleus to the periphery, called ____ morphology

A

E-cadherin loss

signet-ring cell

132
Q

diffuse gastric infiltrative tumors often evoke a desmoplastic reaction that ____, cause diffuse rugal ___ and caused thick walls with leather bottle like appearance called ___ ____

A

stiffens
flattening
linitis plastica

133
Q

intestinal type gastric CA, as opposed to antral type, predominates in what populations

A

high risk areas, those with precursor lesons

males over 55 yo

134
Q

what is the most powerful prognostic indicator in gastric CA

A

depth of invasion and extent of nodal and distal metastases

135
Q

what is the trx and prognosis of gastric CA

A

surgical resection

5 year survival rate= 90%

136
Q

what is the most common inducer of MALTomas in the stomach

A

H. Pylori

137
Q

what genetic translocations are commonly associated with MALTomas

A

t(11;18)(q21;q21) –> create chimeric AP12-MLT fusion gene

t)1;14)(p22;q32) –> increased expression of MALT1 and BLC-10 proteins

both –> constituitively activate NFKB–> promot B cell growth and survival

138
Q

describe the connection between H Pylori trx and the trx of MALToma

A

if MALToma is caused by H Pylori–>eradication slashes recurrence rates and allows durable remission

if MALToma caused by genetic translocation–> eradication does nothing

139
Q

what are the most common presenting sx of MALTomas

A

dyspepsia and epigastric pain

hematemesis, melena, weight loss

140
Q

what are the most common sites of carcinoid tumors

A

small intestine, tracheobronchial tree, lungs

141
Q

what conditions are associated with carcinoid tumors

A

endocrine cell hyperplasia
autoimmune chronic atrophic gastritis
MEN-1
zollinger, ellison gastritis

142
Q

in what population are carcinoid tumors seen in

A

patients > 60 yo

143
Q

what are the sx of carcinoid tumor

A

depends on what hormones are being elaborated

make gastrin? –> zollinger-ellison syndrome

ileal tumor —> carcinoid syndrome (too many vasoactive substances being secreted into systemic circulation)

144
Q

what is the most important prognostic factor for GI carcinoid tumors- elborate

A

location

foregut (before the ligament of treitz) = rarely metastasize, cured by resection

midgut= aggressive, greater depth of local invasion, increased size, have necrosis and mitoses and associated with worse prognosis

hindgut= (appendix and colorectal) = incidental findings, almost always benign, usually found when small

145
Q

what is the most common mesenchymal tumor of the abd

A

GI stromal tumor

146
Q

in what population will you find GISTs

A

peak age= 60 y.o

147
Q

what is a Carney triad

A

uncommon presentation in which you have GIST in children

in young females
=GIST , paraganglioma, and pulmonary chondrome

148
Q

what genetic mutations are common in GISTs

what does it result in

A

most have gain of function of receptor tyrosine kinase KIT

another mutation is of PDGFRA, both increase intracellular signals for proliferation and survival

also have mutations in genes coding for succinate dehydrogenase comples (SDH_) = inherited in Carney-Stratakis syndrome
=dysregulation of HIF-1a–> increased transcription of VEGF and IGF1R

149
Q

deletion of ch 9p, less of cell cycle regulator ____, is involved in many gastric CAs

A

CDKN2A

150
Q

what is the most useful diagnostic marker of GIST

A

KIT gene

151
Q

(in the stomach)a large fleshy mass with a whorled appearance, either spindle cell type or epithelioid type

A

GIST

152
Q

where do GISTs metastasize to?

A

peritoneal cavity

liver

153
Q

what are the clinical sx of GISTs

A

mucosal ulceration–? blood loss, anemia

can be an incidental finding

154
Q

what is the trx and prognosis of GIST

A

trx= surgical resection
GISTs with KIT/PDGFRA mutations usually respond to trx with imatinib, though resistance is common

prognosis depends on size, mitotic index, and location
-gastric GISTs are less aggressive than intestinal GISTs

GI2 E1 (19 decks)

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